查看完整版本 : ▲寵物全方位解說篇▲

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[size=12px][b][size=5][color=magenta]NONSTEROIDAL 抗發炎藥物[/color][/size][/b]

行動機制
所有nonsteroidal 抗發炎藥物(NSAIDs) 行動通過一個相似的機制, 將禁止前列腺素(PGs) 綜合通過cyclo oxygenase (考克斯) 酵素的禁止。

一些被禁止的PGs 促進炎症, 當一些執行重要身體作用。

NSAIDs 裝於罐中或禁止激動PGs (通過COX-2) 或重要結構性PGs (通過COX-1) 或兩個(非有選擇性) 。更舊的NSAIDs 譬如ibuprofen, phenylbutazone, naproxen, piroxicam, 並且flunixin 無選擇性和禁止COX-1 和COX-2 。更新的NSAIDs 譬如COXIB (celecoxib), carprofen 和meloxicam, 溫和地是COX-2 有選擇性和相對地COX-1 饒恕, 雖然這根據體外研究並且它也許變化在種類之中。最近被介紹的deracoxib 和firocoxib 是COX-2 有選擇性的藥物, 並且tepoxalin 是考克斯和lipo oxygenase (LOX) 抗化劑。

  
類型NSAIDs

COX-2 有選擇性的 (COXIB) Deracoxib(Deramaxx®), firocoxib (Previcox®) 。
溫和COX-2 有選擇性的 Carprofen (Rimadyl®), meloxicam (Metacam®) 。
考克斯和LOX 抗化劑 Tepoxalin (Zubrin®); 這個產品不是有選擇性的為COX-2, 而是有某一LOX 禁止。

  
NSAIDs 出版比較
被證明的好處未建立根據效力或安全, 一另, 但是有少量好研究比較不同的藥物。在firocoxib 和etodolac 的比較研究中, 在效力上的區別或安全未被發現, 但是研究在美國比較tepoxalin 和carprofen, 並且在歐洲比較tepoxalin 和meloxicam 發現tepoxalin 有一個輕微的趨嚮往更好的效力和安全。根據endoscopic 研究, carprofen 被顯示有好處在阿斯匹靈根據GI toxicosis 。

  
Toxicosis 從NSAIDs

GI toxicosis
COXIBs 溫和地COX-2 有選擇性的藥物沒有被證明的好處從受控研究進行在狗或貓。
需要是機警的對研究看胃損害, 如同更加嚴厲的損害傾向於位於接近小腸。
糧食與藥物管理局接受了GI 潰瘍一些報告與相關deracoxib 管理; 主要介入小小腸潰瘍。
缺乏信心預先處理deracoxib 事例的起因但它可以是, 已存在GI 損傷導致COX-2 的upregulation, 充當在癒合的一個角色GI 短文。
動物與低蛋白質也許是在增加的風險為副作用由於NSAIDs 的高度protein-bound 本質(不是absolute 禁忌症候, 但需要仔細地藥量這些動物和嚴密監測他們) 。


肝toxicosis
任何NSAIDS 可能導致深刻, 有氣質hepatotoxicosis 。Deracoxib 並且是磺胺, 因此它應該小心地被使用在養殖事先安排好對磺胺過敏症(Doberman pinscher 、薩莫耶特人和其它白色上漆的養殖, 微型schnauzer) 。
它是不定的是否比其它NSAIDs 經常carprofen 起因肝toxicosis, 但它同肝臟問題聯繫在一起更多比其它藥物根據糧食與藥物管理局的有害事件報告資料。
沒有證據證明肝疾病預先預先處理對NSAID 導致的肝臟傷。已存在肝臟酵素海拔不是肝toxicosis 的預報因子從NSAIDs 。
雖然這些藥物是全部由肝臟高度代謝為多數藥物, 已存在肝臟病不似乎影響新陳代謝(由於肝功能儲備) 。


腎臟toxicosis
COX-1 和COX-2 在腎臟作用的兩個戲劇重要角色。
NSAIDs 大劑量也許造成腎臟損傷(筒形局部缺血和退化), 雖然這很少被看見在治療藥量。
動物以已存在腎臟損傷和那些以被減少的腎臟血流也許是事先安排好的對腎臟toxicosis 。


對小片作用的作用(COX-1 禁止)
NSAIDs 是能禁止小片作用和因此不被推薦為患者事先安排好對或以前退出的hemostatic 混亂(即馮Willebrand 疾病、血友病, thrombopathia) 。
任一NSAID 以看得出的COX-1 禁止作用能影響小片作用(即ketoprofen), 雖然盲目的臨床試驗未證實這關心。

監視狗在NSAIDs
  
患者應該有前管理臨床和定期實驗室評估。治療、肝臟酵素或膽紅素的二個星期崗位_蒙應該被檢查。為長期療法, 臨床和實驗室評估應該是至少逐年, 或許每6 個月。

  
對NSAIDs 的用途在貓
  
NSAIDs 不登記貓在美國, 但是meloxicam 和ketoprofen 登記貓在加拿大和歐洲, 和看來是相對地安全的在貓。

藥量由一些獸醫使用(標記): Meloxicam, 可利用作為可注射和風味糖漿(容量小因此貓似乎容忍口味), 在0.1 mg/kg q24h 2-3 天最初, 那麼0.025-0.05 mg/kg 2 -3x 每星期至於較長期使用。

Ketoprofen, 可利用以可注射和口頭形式, 在2 mg/kg 一次; 然後1 mg/kg 每日。

Carprofen 被批准在歐洲為貓, 但至於短期使用唯一。

  
Tramadol 氯化物(Ultram®)
  
Tramadol 有溫和的鎮痛藥物產和行動多個方式, 以一些鴉片製劑作用但這不是一種受控物質。藥物學地, tramadol 有一個 α2 苦悶者作用, 和antiserotonin 和鴉片製劑感受器官作用, 但對痛覺缺失貢獻的機制是未知的。藥物是低廉, 和可利用的作為普通產品。沒有研究被報告提供它的安全和效力, 雖然有一項約物動力學的研究被報告定義它的吸收和性格在狗。它傾向於不導致嘔吐和以opioids 。它被執行了與NSAIDs 沒有任何瞭解的問題。

試驗未完成在狗建立藥量。根據約物動力學的研究, 藥量在5mg/kg 狗每6 個小時口頭將導致血漿集中認為是在治療範圍。藥量為貓未建立。

  
藥物選擇
  
為劇痛, 譬如在perioperative 用途, 獸醫執行了可注射的NSAIDs 以好結果。藥物被使用在這些事例包括ketoprofen, flunixin meglumine, carprofen, tolfenamic 酸(Tolfedine®, 可利用在美國之外), 和ketorolac tromethamine (Toradol®) 。這些藥物被使用1-2 天減少熱病和痛苦從手術或精神創傷。前有效的射入carprofen 對狗證明是有利減少手術後痛苦在狗在ovariohysterectomy 以後。

口頭NSAIDs 也許還被使用為myositis 、關節炎, 和手術後痛苦的深刻治療, 或他們也許慢性地被執行為骨關節炎。被執行在美國對狗的糧食與藥物管理局登記的藥物有: carprofen, etodolac 、deracoxib 、meloxicam, 和tepoxalin 。有時被使用的人的藥物標記包括阿斯匹靈, piroxicam, ketoprofen, 和naproxen 。為貓, 多數經驗是與meloxicam 、ketoprofen, 和"兒童的" 阿斯匹靈。在美國之外, carprofen, ketoprofen, tolfenamic 酸, 並且meloxicam 登記骨關節炎的治療在狗。在北美洲和歐洲, 所有這些藥物被執行了以飲食補充譬如氨基葡萄糖和軟骨素sulfate 。

有研究可利用為各種藥物顯示劑量養生之道, 和效力與安慰劑比較, 為痛苦的治療與相關骨關節炎。當藥物與互相比較, 它難展示區別在這些藥物之間為減少痛苦在動物中。一些研究試圖顯示哪些上述藥物是最安全的。當carprofen, meloxicam, 和ketoprofen 被比較了在狗由endoscopic 評估, 沒有重大不利影響導致, 或區別在藥物之中談到gastroduodenal 損害。阿斯匹靈, 至少在深刻管理以後, 被顯示導致黏膜傷害、胃炎, 和出血在狗。在管理carprofen 以後, 阿斯匹靈, 和etodolac 在被推薦的藥量對狗28 天, 那裡是較少gastroduodenal 損害從極大carprofen 和etodolac 與阿斯匹靈比較。作用carprofen 並且etodolac 是沒有與那些安慰劑不同。

  
總結
  
有幾個選擇為對待狗以骨關節炎與NSAIDs 。像人, 那裡比有區別在藥物之中也許是更加巨大的區別在個體之中在他們的反應。一些獸醫選擇了阿斯匹靈作為一種最初的藥物, 因為這是低廉和知交多數寵物所有者。但, 其它獸醫喜歡選擇糧食與藥物管理局批准的藥物譬如etodolac, carprofen, deracoxib 、meloxicam 和tepoxalin 為治療在狗。一些獸醫仍然依靠人的藥物被使用在額外標記方式治療患者加工困難對批准的動物藥物。這些藥物包括piroxicam (Feldene®), naproxen (Aleve®), 和ketoprofen (Orudis®) 。這些未接受安全和效力試驗在美國。在美國之外, 在加拿大和歐洲, 其它普遍的NSAIDs 被使用在小動物包括ketoprofen 和tolfenamic 酸。他們有相對地好安全外形並且臨床結果被提供了。

為痛苦的治療與NSAIDs 在貓, 無登記在美國, 並且唯一ketoprofen 和meloxicam 是批准至於使用在其它國家和顯示是安全的。在美國, ketoprofen 是可利用的因為12.5mg 片劑為人, 可利用不用處方(Orudis 千噸®) 。阿斯匹靈有時被使用在貓, 與"小孩子的阿斯匹靈" 被執行(81 毫克片劑) 在20 mg/kg 藥量每48 個小時。

Mechanism of Action
All nonsteroidal anti-inflammatory drugs (NSAIDs) act via a similar mechanism, which is to inhibit synthesis of prostaglandins (PGs) via inhibition of the cyclo-oxygenase (COX) enzyme.

Some of the inhibited PGs promote inflammation, while some perform important body functions.

NSAIDs can either inhibit the inflammatory PGs (via COX-2) or the important constitutive PGs (via COX-1) or both (non selective). Older NSAIDs such as ibuprofen, phenylbutazone, naproxen, piroxicam, and flunixin are nonselective and inhibit both COX-1 and COX-2. Newer NSAIDs such as the COXIB (celecoxib), carprofen and meloxicam, are mildly COX-2 selective and relatively COX-1 sparing, although this is based on in vitro studies and it may vary among species. The recently introduced deracoxib and firocoxib are COX-2 selective drugs, and tepoxalin is a COX and lipo-oxygenase (LOX) inhibitor.

  
Types of NSAIDs

COX-2 selective (COXIB) Deracoxib(Deramaxx®), firocoxib (Previcox®).
Mildly COX-2 selective Carprofen (Rimadyl®), meloxicam (Metacam®).
COX and LOX inhibitors Tepoxalin (Zubrin®); this product is not selective for COX-2, but has some LOX inhibition.

  
Published Comparisons of NSAIDs
No proven advantage has been established in terms of efficacy or safety, of one over another, but there are few good studies comparing the different drugs. In a comparison study of firocoxib and etodolac, no difference in efficacy or safety was found, whereas studies in the US comparing tepoxalin and carprofen, and in Europe comparing tepoxalin and meloxicam found that tepoxalin had a slight trend toward better efficacy and safety. Based on endoscopic studies, carprofen has been shown to have an advantage over aspirin in terms of GI toxicosis.

  
Toxicosis from NSAIDs

GI toxicosis
No proven advantage of COXIBs over mildly COX-2 selective drugs from controlled studies conducted in dogs or cats.
Need to be wary of studies looking at gastric lesions, as more severe lesions tend to be located in the proximal small intestine.
FDA has received some reports of GI ulceration associated with deracoxib administration; mostly involving small intestinal ulcers.
Unsure of predisposing causes of the deracoxib cases but it may be that pre-existing GI damage results in upregulation of COX-2, which plays a role in healing of the GI tract.
Animals with low protein may be at increased risk for side effects due to the highly protein-bound nature of NSAIDs (not an absolute contraindication, but need to dose these animals carefully and monitor them closely).


Hepatic toxicosis
Any of the NSAIDS can cause acute, idiosyncratic hepatotoxicosis. Deracoxib is also a sulfonamide, so it should be used with caution in breeds predisposed to sulfonamide hypersensitivity (Doberman pinscher, Samoyed and other white-coated breeds, miniature schnauzer).
It is uncertain whether carprofen causes hepatic toxicosis more often than other NSAIDs, but it has been associated with liver problems more than other drugs according to the FDA's adverse event reporting data.
There is no evidence that prior hepatic disease predisposes to NSAID-induced liver injury. Pre-existing liver enzyme elevation is not a predictor of hepatic toxicosis from NSAIDs.
Although these drugs are all highly metabolized by the liver for most drugs, pre-existing liver disease does not seem to affect metabolism (due to liver function reserve).


Renal toxicosis
COX-1 and COX-2 both play important roles in renal function.
High doses of NSAIDs may cause renal damage (tubular ischemia and degeneration), although this is seen rarely at therapeutic doses.
Animals with pre-existing renal damage and those with reduced renal blood flow may be predisposed to renal toxicosis.


Effects on platelet function (COX-1 inhibition)
NSAIDs are capable of inhibiting platelet function and so are not recommended for patients predisposed to or with pre-exiting hemostatic disorders (e.g. von Willebrand disease, hemophilia, thrombopathia).
Any NSAID with appreciable COX-1 inhibitory function could affect platelet function (e.g. ketoprofen), although no blinded clinical trials have confirmed this concern.
Monitoring Dogs on NSAIDs
  
Patients should have a pre-administration clinical and routine laboratory evaluation. Two weeks post-initiation of treatment, liver enzymes or bilirubin should be checked. For long-term therapy, clinical and laboratory evaluation should be at least yearly, perhaps every 6 months.

  
Use of NSAIDs in Cats
  
No NSAIDs are registered for cats in the US, but both meloxicam and ketoprofen are registered for cats in Canada and Europe, and appear to be relatively safe in cats.

Dose that has been used by some veterinarians (off-label): Meloxicam, available as injectable and flavored syrup (volume is small so cats seem to tolerate taste), at 0.1 mg/kg q24h for 2-3 days initially, then 0.025-0.05 mg/kg 2 -3x per week for longer term use.

Ketoprofen, available in injectable and oral forms, at 2 mg/kg once; then 1 mg/kg daily.

Carprofen is approved in Europe for cats, but for short-term use only.

  
Tramadol hydrochloride (Ultram®)
  
Tramadol has mild analgesic properties and multiple modes of action, with some opiate effects but it is not a controlled substance. Pharmacologically, tramadol has an α2-agonist effect, and antiserotonin and opiate receptor effects, but the mechanism that contributes to analgesia is unknown. The drug is inexpensive, and available as the generic product. There are no studies reported to document its safety and efficacy , although there is a pharmacokinetic study reported to define its absorption and disposition in dogs. It tends not to cause vomiting as with opioids. It has been administered with NSAIDs without any known problems.

Trials have not been done in dogs to establish doses. Based on pharmacokinetic studies, a dose in dogs of 5mg/kg orally every 6 hrs will produce plasma concentrations considered to be in the therapeutic range. Doses have not been established for cats.

  
Drug Selection
  
For acute pain, such as in perioperative use, veterinarians have administered injectable NSAIDs with good results. Drugs used in these instances include ketoprofen, flunixin meglumine, carprofen, tolfenamic acid (Tolfedine®, available outside the U.S.), and ketorolac tromethamine (Toradol®). These drugs have been used for 1-2 days to decrease fever and pain from surgery or trauma. Pre-operative injections of carprofen to dogs were shown to be beneficial to decrease post-operative pain in dogs after ovariohysterectomy.

Oral NSAIDs also may be used for acute treatment of myositis, arthritis, and post-operative pain, or they may be administered chronically for osteoarthritis. FDA-registered drugs that are administered in the US to dogs include: carprofen, etodolac, deracoxib, meloxicam, and tepoxalin. Human drugs that are sometimes used off-label include aspirin, piroxicam, ketoprofen, and naproxen. For cats, most experience has been with meloxicam, ketoprofen, and "children's" aspirin. Outside the US, carprofen, ketoprofen, tolfenamic acid, and meloxicam are registered for treatment of osteoarthritis in dogs. In North America and Europe, all these drugs have been administered with dietary supplements such as glucosamine and chondroitin sulfate.

There are studies available for each drug showing dosage regimens, and efficacy in comparison to placebo, for the treatment of pain associated with osteoarthritis. When drugs are compared to one another, it is difficult to demonstrate differences between these drugs for reducing pain in animals. Some studies have attempted to show which of the above drugs is safest. When carprofen, meloxicam, and ketoprofen were compared in dogs by endoscopic evaluation, there were no significant adverse effects produced, or differences among the drugs with respect to gastroduodenal lesions. Aspirin, at least after acute administration, has been shown to induce mucosal injury, gastritis, and hemorrhage in dogs. After administration of carprofen, aspirin, and etodolac at recommended doses to dogs for 28 days, there was significantly less gastroduodenal lesions from carprofen and etodolac as compared to aspirin. The effects of carprofen and etodolac were no different from those of placebo.

  
Summary
  
There are several choices for treating dogs with osteoarthritis with NSAIDs. Like people, there may be greater differences among individuals in their response than there are differences among the drugs. Some veterinarians have selected aspirin as an initial drug, because it is inexpensive and familiar to most pet owners. But, other veterinarians prefer to select an FDA-approved drug such as the etodolac, carprofen, deracoxib, meloxicam and tepoxalin for treatment in dogs. Some veterinarians still rely on human drugs used in an extra-label manner to treat patients refractory to approved animal drugs. These drugs include piroxicam (Feldene®), naproxen (Aleve®), and ketoprofen (Orudis®). These have not undergone safety and efficacy trials in the US. Outside the US, in Canada and Europe, other popular NSAIDs used in small animals include ketoprofen and tolfenamic acid. They have a relatively good safety profile and clinical results have been documented.

For treatment of pain with NSAIDs in cats, none are registered in the US, and only ketoprofen and meloxicam are approved for use in other countries and shown to be safe. In the US, ketoprofen is available as a 12.5mg tablet for people, available over-the-counter (Orudis-KT®). Aspirin is sometimes used in cats, with a "children's aspirin" administered (81 mg tablet) at a dose of 20 mg/kg every 48 hours.[/size]
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[size=12px][b][size=5][color=magenta]犬 FOODBORNE AFLATOXICOSIS[/color][/size][/b]

黃麴黴毒素是幾個真菌的種類產品在類 麴黴菌 (即, A.flavus 和 A. parasiticus) 並且毛叢, 也許增長在各種各樣的莊稼包括玉米、花生、棉籽、核桃和胡桃。它可能被生產在領域在收穫之前或在食物存貯期間。汙染的玉米認為是黃麴黴毒素的來源在最近嚴肅的狗與食物相關的爆發。

黃麴黴毒素特別是瞄準它被酵素激活的肝臟。毒性adduct 熱中地束縛與DNA 和蛋白質, 修改包含的hepatocytes 的新陳代謝的能力。100 份每十億(ppb) 黃麴黴毒素在狗食裡同似犬病症聯繫在一起; 這是玉米在填裝, 45 英尺筒倉, 直徑16 英尺100 kernals 等值!

  
臨床標誌
臨床標誌起始是陰險的, 也許被延遲3 個星期或長在曝光以後。標誌最初地依然是隱晦和可能進步對inappetence, 慵倦, 嘔吐和減重。其它標誌包括polyuria/polydipsia 、溫和的黃疸、hematochezia 、melena, hematemesis, 挫傷, 胃腸膨脹、修改過的transudate 進步對一個出血性的身體洞, 流出, 和周邊腫鼓。嚴厲地受影響的動物也許屈服對嚴厲食道失血、肝腦病和嚴厲hypogylcemia 。

  
診斷
根據當前的理解, 極小的資料庫為查出對黃麴黴毒素的暴露是飲食回顧、詳盡的體格檢查、CBC 、生化外形和尿分析。antithrombin III 和蛋白質C 的被減少的集中被報告是aflatoxicosis 早期的顯示。肝臟損傷從黃麴黴毒素曝光也許仍然是存在既使實驗室試驗的結果是在正常極限內。

  
Clinicopathologic 特點
血液學外形通常是正常的, 但也許顯示嗜中性白細胞減少症、貧血症並且/或者thrombocytopenia; 生化外形顯示易變溫和減輕在ALT 的增量, 適度地低膽固醇, 高的總膽紅素(在5-9 mg/dL 之間); 凝固外形展示高的APTT 和PT, 和顯著被降下的antithrombin 和蛋白質C 活動; 尿分析顯露稀釋尿和顆粒狀塑像當毒力升級。在肝臟細胞學有microvesicular 肥膩vacuolation, 並且肝臟病理組織學顯露hepatocellular 肥膩vacuolation 和perivenular 炎症。當情況進步, 那裡也許是門高血壓、胃腸流出, 和靈菌深刻起始入末端小腸和冒號。

在深刻案件, 病理組織學顯露出血和壞死以肝繩子的離解。更加慢性的損害包括lipidosis, 膽汁增生和門纖維變性與滲入淋巴細胞和巨噬細胞。壞死焦點並且被注意。

Aflatoxin is a product of several species of fungus in the genera Aspergillus (e.g., A. flavus and A. parasiticus) and Penicillium, which may grow on a variety of crops including corn, peanuts, cottonseed, walnuts and pecans. It can be produced in the field before harvest or during food storage. Contaminated corn is believed to have been the source of aflatoxin in the recent serious dog food-related outbreak.

Aflatoxin especially targets the liver where it is activated by enzymes. The toxic adduct avidly binds with DNA and proteins, altering the metabolic abilities of involved hepatocytes. 100 parts per billion (ppb) aflatoxin in dog food has been associated with canine illness; this is the equivalent of 100 kernals of corn in a filled, 45-foot silo, 16 feet in diameter!

  
Clinical Signs
The onset of clinical signs is insidious and may be delayed for 3 weeks or longer after exposure. Signs remain vague initially and can progress to inappetence, lethargy, vomiting and weight loss. Other signs include polyuria/polydipsia, mild jaundice, hematochezia, melena, hematemesis, bruising, abdominal distention, modified transudate progressing to a hemorrhagic body cavity, effusions, and peripheral edema. Severely affected animals may succumb to severe gastrointestinal blood loss, hepatic encephalopathy and severe hypogylcemia.

  
Diagnosis
Based on current understanding, the minimum data base for detecting exposure to aflatoxin is a dietary review, thorough physical examination, CBC, biochemistry profile and urinalysis. Decreased concentrations of antithrombin III and protein C are reported to be an early indicator of aflatoxicosis. Liver damage from aflatoxin exposure may still be present even if results of laboratory tests are within normal limits.

  
Clinicopathologic Features
Hematology profile is usually normal, but may show neutropenia, anemia and/or thrombocytopenia; biochemistry profile shows variable mild to moderate increases in ALT, moderately low cholesterol, high total bilirubin (between 5-9 mg/dL); coagulation profile shows high APTT and PT, and significantly lowered antithrombin and protein C activity; urinalysis reveals dilute urine and granular casts as toxicity escalates. On liver cytology there is microvesicular fatty vacuolation, and liver histopathology reveals hepatocellular fatty vacuolation and perivenular inflammation. As the condition progresses, there may be acute onset of portal hypertension, abdominal effusion, and bleeding into the distal small intestine and colon.

In acute cases, histopathology reveals hemorrhage and necrosis with dissociation of hepatic cords. More chronic lesions include lipidosis, biliary hyperplasia and portal fibrosis with infiltrates of lymphocytes and macrophages. Foci of necrosis are also noted[/size]
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[size=12px][color=magenta][b][size=5]尿分析的重要性[/size][/b]
[/color]
尿分析的重要性
尿的評估為它的物理和化工物產, 和微觀沉積考試是任一名健康或不適的患者的臨床和實驗室考試的重要組分。定期尿分析的組分包括出現、比重、酸鹼度、蛋白質和葡萄糖內容、酮或glucosuria 膽紅素、隱密血液出現, 泌尿沉積的出現, 和考試為白血球、紅血球、上皮細胞、塑像、細菌、酵母、真菌, 和水晶出現。另外, 腎臟作用被估計在定期血液化學外形由小圓麵包、肌氨酸酐、電解質、澱粉酵素, 和白蛋白的測量在堅持proteinuria 情況下。

  
彙集方法
尿可能由cystocentesis, 導尿收集, 並且中途任意捉住(無效) 。但是, 無效的中途收藏通常產生充分標本只如果結果是消極的, 作為細胞計數的解釋, 蛋白質含量, 並且這些標本文化可以給引入歧途的結果。細菌出現在尿收集了由cystocentesis 表明一個感染過程, 但是細菌也許是存在在變化的數字在插入導管的或中途無效的樣品。在後者情況, 這些有機體通常是汙染物在彙集過程期間。

  
樣品穩定
定期運輸時間不影響尿分析或尿文化結果, 如果樣品適當地被收集了和被安置了在正確類型不育的容器[ 參見下面] 。

出版資訊從尿的研究從31 條健康狗收集了並且八隻健康貓估計了存儲時間和溫度的作用在酸鹼度、比重, 和水晶形成。所有貓樣品由cystocentesis 收集了, 但是大多狗樣品由中途獲得了任意捉住(27); 殘餘的四尿由cystocentesis (2) 和導尿(2) 收集了。整除數各尿樣被分析了在60 分鐘內彙集和在存貯以後在室或冷藏溫度六個和24 小時。結果表明, 水晶形成了在樣品從11 動物(28%), 但增加的存儲時間和被減少的存貯溫度同在鈣乙二酸酯水晶的數量的重大增量聯繫在一起形成了。水晶的更加了不起的數字形成了在尿整除數被存放24 小時比在那些被存放六個小時。沒有存儲時間和溫度的重大作用在酸鹼度或比重。研究的結論是, 尿樣應該被分析在60 彙集分鐘內使對體外水晶形成的溫度和非定常作用減到最小。水晶出現被觀察在被存放的樣品應該因此由新鮮的尿的再估價確認。

水晶共同地是存在在狗和貓尿和通常是一點診斷意義。鳥糞石、無定形的磷酸鹽, 和乙二酸酯是也許被發現在正常尿樣水晶的例子。

Importance of Urinalysis
Evaluation of the urine for its physical and chemical properties, and microscopic sediment examination are important components of the clinical and laboratory examination of any healthy or ill patient. The components of a routine urinalysis include appearance, specific gravity, pH, protein and glucose content, bilirubin, presence of ketones or glucosuria, presence of occult blood, and examination of the urinary sediment for the presence of leukocytes, erythrocytes, epithelial cells, casts, bacteria, yeast, fungi, and crystals. In addition, renal function is assessed in the routine blood chemistry profile by measurements of BUN, creatinine, electrolytes, amylase, and albumin in the case of persistent proteinuria.

  
Collection Method
Urine can be collected by cystocentesis, catheterization, and midstream free catch (voided). However, voided midstream collections usually yield adequate specimens only if results are negative, as interpretation of cell counts, protein content, and culture of these specimens may give misleading results. The presence of bacteria in urine collected by cystocentesis indicates an infectious process, whereas bacteria may be present in varying numbers in catheterized or midstream voided samples. In the latter situations, these organisms are usually contaminants during the collection process.

  
Sample Stability
Routine transport time does not influence urinalysis or urine culture results, if the sample has been collected appropriately and placed in the correct type of sterile container [see below].

Published information from a study of urine collected from 31 healthy dogs and eight healthy cats assessed the effects of storage time and temperature on pH, specific gravity, and crystal formation. All the cat samples were collected by cystocentesis, whereas most of the dog samples were obtained by midstream free catch (27); the remaining four urines were collected by cystocentesis (2) and catheterization (2). Aliquots of each urine sample were analyzed within 60 min of collection and after storage at room or refrigeration temperatures for six and 24 hrs. Results indicated that crystals formed in samples from 11 of the animals (28%), but that increased storage time and decreased storage temperature were associated with a significant increase in the number of calcium oxalate crystals formed. Greater numbers of crystals formed in the urine aliquots stored for 24 hrs than in those stored for six hrs. There was no significant effect of storage time and temperature on pH or specific gravity. The conclusions of the study were that urine sample should be analyzed within 60 min of collection to minimize temperature- and time-dependent effects on in vitro crystal formation. Presence of crystals observed in stored samples should therefore be validated by reevaluation of fresh urine.

Crystals commonly are present in the urine of dogs and cats and usually are of little diagnostic significance. Struvite, amorphous phosphates, and oxalates are examples of crystals that may be found in normal urine samples.[/size]
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[size=12px][b][size=5][color=magenta]什麼是Addison 的疾病[/color][/size][/b]

我們開始以Addison 的疾病簡要的概要。  這是共同的名字對於hypoadrenocorticism, 或腎上腺不足。  這是一種疾病以對許多其它疾病是共同, 使診斷困難和有時過程排除的症狀。  但一旦Addison 的正確地被診斷, 一條適當地被對待的狗能居住正常, 活躍生活。

腎上腺, 一個在各個腎臟, 被彌補二層、外皮和骨髓。  外面區域, 或外皮, 藏匿類皮質激素激素譬如+化皮質酮和醛甾酮。  骨髓, 一部分的有同情心的神經系統, 藏匿epinephrine (腎上腺素), 由Addison 的一般不影響。

有Addison 的疾病的三個形式:  主要, 次要和非典型。  主要和非典型Addison 的通常是免疫斡旋的損傷的結果對封墊的。次要hypoadrenocorticism 是從pituitary 的疏忽刺激腎上腺與促腎上腺皮質的激素(促腎上腺皮質激素) 。  它是重要為您知道哪類型Addison 的疾病您的狗被對待為。

  我沒有一個診斷- 什麼是症狀?
Addison 的疾病症狀可能是隱晦的。  更加重要地, 他們與許多不同的問題症狀是相似。  最初地, 狗也許是無精打采的, 或似乎壓下。  許多狗被描述像似乎, 或丟失正常閃閃發光在他們的眼睛。  缺乏胃口是好顯示。  其它症狀包括食道問題像嘔吐和腹瀉。  痛苦在後腿肉, 或廣義肌肉弱點譬如無法跳床或長沙發的狗如同他從前做了不是不凡的。  發抖或肌肉震顫也許並且是存在。  最重要的事記住是, 您知道您的狗更好比任何人。  如果某事似乎amiss, 安排它被檢查。

這些症狀也許打蠟和減少經過幾個月或幾年使診斷困難。  如果腎上腺持續惡化, 狗最後將有一個深刻情節稱Addisonian 危機。  鉀水平舉起和打亂心臟的正常作用。  心率失常可能收效和血壓下落對危險地低水平。  小圓麵包和肌氨酸酐水平, 顯示的腎臟一般起作用, 經常被舉起。  這時許多動物被診斷以腎衰竭, 因為腎臟無法適當地起作用。  動物典型地被給IV 解答為再水化, 也許導致幾乎神奇的補救。  這, 是一個了不起的徵兆, 腎上腺的失敗而不是的腎臟創造症狀。

  症狀

嘔吐

腹瀉

慵倦

消沉

缺乏胃口

震顫或震動

肌肉弱點

痛苦在後面處所
您怎麼可以是肯定的這是Addison 的?

第一事的當中一個看Addison 的疾病被懷疑是電解質水平。  二是憂慮是鈉(Na) 並且鉀(k) 。  除看這些價值之外, 它是重要看比率在二之間。  這個數字由劃分獲得K 成Na, 應該是在27 和40 之間。  例如, 一條狗以Na 水平的145 和K 水平的4.5 會有比率32 。  一條狗在Addisonian 危機典型地將有一個低Na 水平、被舉起的K 和低比率。

當電解質水平是重要顯示, 他們不是明確的測試確定Addison 的疾病。  實際上, 以次要和非典型hypoadrenocorticism, 電解質水平不能是受影響的。  為明確的診斷狗被給促腎上腺皮質激素刺激或反應測試。  這測試腎上腺封墊的能力生產類皮質激素激素+化皮質酮。

執行促腎上腺皮質激素刺激測試, 一個最初的血樣是拉長並且+化皮質酮水平被測量。  狗被注射以告訴腎上腺生產+化皮質酮腦下垂體的激素促腎上腺皮質激素的形式。  在一個小時以後, 血液再抽, 和+化皮質酮水平被測量。  休息的+化皮質酮應該範圍從1-4 μg/dl 在平均狗, 和應該是顯著高的, 在6-20 μg/dl 的範圍, 崗位刺激。 (這些數字也許變化根據實驗室。) 如果休息的+化皮質酮是降低並且狗有沒有或對刺激的一個低反應, 診斷是Addison 的疾病。  注意, 一些glucocorticoids, 譬如強體松, 可能影響促腎上腺皮質激素測試的結果, 當dexamethasone 不。

  
保持在它頂部

有幾個療程被使用對待Addison 的。  第一型作為礦物類皮質激素和替換醛甾酮- 激素負責任對維護電解質水平。  它用或一個口頭療程稱Florinef ( ™ fludrocortisone 醋酸鹽) 或可注射的Percorten-V 替換™ (desoxycorticosterone pivalate 或DOCP) 。為有非典型或次要Addison 的兩者都不這些療程被使用的狗因為醛甾酮的生產不被影響並且電解質保留在平衡。

除替換醛甾酮之外, +化皮質酮, 或glucocorticoids, 由腎上腺通常藏匿必須並且被替換。  這典型地做以強體松或□化可體松的一個口頭形式。  與非典型和次要Addison 的糖皮質激素是唯一的療程被給。  

  

底線

當您的狗以Addison 的疾病將需要療程和監視在他有生之年, 多數狗與Addison 的罐頭回到他們喜愛的活動。  您將學會讀您的狗, 瞭解是什麼他的重音觸發器並且跟隨您的天性在他的關心。  一起, 您將克服患難和從這經驗將學會。  您將幫助您的狗帶領正常, 活躍和樂趣被填裝的生活。
治療和療程

有幾個療程被使用對待Addison 的疾病。  第一型作為礦物類皮質激素和替換醛甾酮- 激素負責任對維護電解質水平。  它用或一個口頭療程稱Florinef ( ™ fludrocortisone 醋酸鹽) 或可注射的Percorten-V 替換™ (desoxycorticosterone pivalate 或DOCP) 。為有非典型或次要Addison 的兩者都不這些療程被使用的狗因為醛甾酮的生產不被影響並且電解質保留在平衡。

除醛甾酮之外, +化皮質酮, 或glucocorticoids, 由腎上腺通常藏匿必須並且被替換。  這典型地做以強體松或□化可體松的一個口頭形式。  在危機期間, 狗也許接受射入dexamethasone, 一有力和速效糖皮質激素。  狗也許最初地開始在強體松大劑量促進回歸到健康。  根據一個持續的依據, 糖皮質激素的藥量可能被減少和在某些情況下被消滅除了一個和需要的依據。  與非典型和次要Addison 的糖皮質激素是唯一的療程被給。  

礦物類皮質激素:

主要Addison 的疾病由替換對待礦物類皮質激素, 醛甾酮, 用或Florinef 片劑或可注射的Percorten-V 。  這些療程幫助維護電解質鈉(Na) 並且鉀(k) 的平衡。

Florinef 是名牌對於fludrocortisone 醋酸鹽。  這個療程是還可利用的以它的普通形式, fludrocortisone 醋酸鹽, 從配製藥劑師。  這是主要礦物類皮質激素, 而且有一些糖皮質激素的活動。  開始的藥量由默克獸醫指南推薦是0.05 - 0.1 mgs 每10 磅體重。  一些狗要求顯著大劑量維護正常電解質。

藥量也許同時被劃分和被給兩次每天或早晨被給, 通常。  50 磅狗會採取在0.25 和0.5 mgs 之間對開始。  名牌Florinef 片劑也許被購買直接地從您的狩醫或從藥房。  某些人民發現它更加有效和高效率有療程的適當的藥量由一位配製的藥劑師準備著以膠囊、液體, 或chewable 形式。

Percorten-V 是名牌對於desoxycorticosterone pivalate 。  這是一個可注射的療程以唯一礦物類皮質激素活動。  它沒有任何糖皮質激素的活動。  藥量由Novartis 推薦, 製造商, 是0.75 - 1.0 mgs 每一磅體重, 被給每21 - 30 天。  有25 mgs 在各機器語言(或cc) 療程。

50 磅狗會接受在37.5 - 50 mgs 或1.5 - 2.0 mls 之間。  一些狗充分地贍養在更低的藥量, 當一些狗要求更低的藥量使罕見的副作用減到最小。  Percorten-V 是可利用的只通過一位被准許的獸醫, 雖然一些獸醫藥房也許運載療程。

  
Glucocorticoids:

腎上腺封墊生產+化皮質酮, 糖皮質激素。  這是激素由促腎上腺皮質激素刺激測試測量被使用診斷Addison 的疾病。

所有狗與Addison 的要求glucocorticoids 的補充在重音時候。  許多需要glucocorticoids 根據一個更加規則的依據, 特別那些在DOCP 。  狗以非典型或次要Addison 的唯一的作為glucocorticoids 。

最共同的glucocorticoids 是強體松、□化可體松和dexamethasone 。  有另外的glucocorticoids 譬如prednisolone 和methylprednisolone 。  默克獸醫指南推薦0.1 - 0.2 mgs/lb. 強體松藥量每天。  這與0.4 - 0.8 mgs/lb. 是等效的每天□化可體松。

但是, 一些狗剩餘glucocorticoids 展示症狀在這些藥量。  這些問題也許包括過份喝和排尿、增加的胃口、復發的傳染, 被舉起的肝臟酵素, 氣喘, 不安定性和甚而關於行為的變動。  由於這些狗將是在療程在他們有生之年, 它重要優化劑量最大化好處, 當使不需要的副作用減到最小。  如果您工作減少glucocorticoids 您的狗藥量, 是肯定慢慢地工作與您的狩醫和更低數額。

確定什麼構成重音為您的狗, 當另外的glucocorticoids 是必要的, 是非常單獨的。  像人, 狗發現不同的情況緊張。  重音可能是以許多形式, 好和壞, 從物理對情感。  為一些狗到狩醫的一次旅行要求額外療程, 當為其他人這能是houseguests 或額外活躍娛樂時間。知道您的狗的觸發器是關鍵的。  它是根本嚴密監測狗並且準備給額外療程當需要出現
實驗室結果

驗血:

Addison 的疾病被診斷通過驗血叫做促腎上腺皮質激素刺激或反應測試。  這個測試典型地只完成一次診斷情況。  執行促腎上腺皮質激素刺激測試, 一個最初的血樣是拉長並且+化皮質酮水平被測量。  狗被注射以告訴腎上腺生產+化皮質酮腦下垂體的激素促腎上腺皮質激素的一個綜合性形式。  在一個小時以後, 血液再抽, 和+化皮質酮水平被測量。  休息的+化皮質酮應該範圍從1-4 μg/dl 在平均狗, 和應該是顯著高的, 在6-20 μg/dl 的範圍, 崗位刺激。  如果休息的+化皮質酮是降低並且狗有沒有或對刺激的一個低反應, 診斷是Addison 的疾病。  注意, 一些glucocorticoids, 譬如強體松, 可能影響促腎上腺皮質激素測試的結果, 當dexamethasone 不。

在診斷, 您的狗大概將有什麼指超級Chem 或Chem 盤區和CBC (完全血液計數) 看其它重要血液價值。  結果從這些驗血幫助確定如果器官譬如腎臟、肝臟和胰腺適當地起作用, 以及如果任何傳染的標誌是存在。  完全驗血應該被完成每6 個月到一年為一條狗以Addison 的疾病。

有特別是興趣在Addison 的疾病上的二個驗血結果。  他們是鈉(Na) 並且鉀(k) 。  激素醛甾酮調控這些電解質。  在主要Addison 的疾病, 腎上腺封墊不生產(足夠) 醛甾酮, 因此它必須用Florinef 或DOCP 替換。  這是您和您的狩醫將使用監測礦物類皮質激素的有效率的資訊(DOCP 或fludrocortisone) 。電解質頻繁地被檢查在開始確定正確療程水平。

正常範圍為這些價值也許變化根據實驗室和設備被使用。  典型地, 正常水平為鈉是在139 到154 mEq/L 之間並且鉀應該是在3.6 到5.5 mEq/L 之間。  除看這些價值之外, 它可能是有用看比率在二之間。  這個數字由劃分獲得K 成Na, 應該是在27 和40 之間。  例如, 一條狗以Na 水平的145 和K 水平的4.5 會有比率32 。  一條狗在Addisonian 危機典型地將有一個低Na 水平、被舉起的K 和低比率。 它重要學會在什麼水平您的狗感覺他最佳。


   
Let’s start with a brief overview of Addison’s disease.  It is the common name for hypoadrenocorticism, or adrenal insufficiency.  It is a disease with symptoms that are common to many other ailments, making diagnosis difficult and sometimes a process of elimination.  But once Addison’s is correctly diagnosed, a properly treated dog can live a normal, active life.

The adrenal, one on each kidney, is made up of two layers, the cortex and the medulla.  The outer area, or cortex, secretes corticosteroid hormones such as cortisol and aldosterone.  The medulla, part of the sympathetic nervous system, secretes epinephrine (adrenaline), which is generally not affected by Addison’s.

There are three forms of Addison’s disease:  primary, secondary and atypical.  Primary and atypical Addison’s are usually the result of immune mediated damage to the glands. Secondary hypoadrenocorticism is from failure of the pituitary to stimulate the adrenals with adrenocorticotropic hormone (ACTH).  It is important for you to know which type of Addison’s disease your dog is being treated for.

  I don’t have a diagnosis – what are the symptoms?
The symptoms of Addison’s disease can be vague.  More importantly, they are similar to the symptoms of many different problems.  Initially, the dog may be listless, or seem depressed.  Many dogs are described as just seeming off, or losing the normal sparkle in their eye.  Lack of appetite is a good indicator.  Other symptoms include gastro-intestinal problems like vomiting and diarrhea.  Pain in the hindquarters, or generalized muscle weakness such as a dog that can’t jump onto the bed or couch as he has done in the past is not uncommon.  Shivering or muscle tremors may also be present.  The most important thing to remember is that you know your dog better than anyone.  If something seems amiss, have it checked out.

These symptoms may wax and wane over months or years making diagnosis difficult.  If the adrenals continue deteriorating, ultimately the dog will have an acute episode called an Addisonian crisis.  Potassium levels elevate and disrupt normal function of the heart.  Arrhythmias can result and blood pressure drops to dangerously low levels.  BUN and creatinine levels, generally indicators of kidney function, are often elevated.  At this point many animals are diagnosed with renal failure, as the kidneys are unable to function properly.  Typically animals are given IV solutions for rehydration, which may produce an almost miraculous recovery.  This too, is a great indication that failure of the adrenals rather than of the kidneys is creating the symptoms.

  SYMPTOMS

Vomiting

Diarrhea

Lethargy

Depression

Lack of appetite

Tremors or shaking

Muscle weakness

Pain in hind quarters
How can you be sure it’s Addison’s?

One of the first things to look at when Addison’s disease is suspected are the electrolyte levels.  The two that are of greatest concern are sodium (Na) and potassium (K).  In addition to looking at these values, it is important to look at the ratio between the two.  This number is derived by dividing K into Na and should be between 27 and 40.  For example, a dog with a Na level of 145 and a K level of 4.5 would have a ratio of 32.  A dog in an Addisonian crisis will typically have a low Na level, elevated K and low ratio.
While electrolyte levels are important indicators, they are not the definitive test to determine Addison’s disease.  In fact, with secondary and atypical hypoadrenocorticism, electrolyte levels may not be affected.  For definitive diagnosis the dog is given the ACTH stimulation or response test.  This tests the ability of the adrenal glands to produce the corticosteroid hormone cortisol.

To perform the ACTH stimulation test, an initial blood sample is drawn and the cortisol level is measured.  The dog is injected with a form of the pituitary hormone ACTH that tells the adrenals to produce cortisol.  After an hour, blood is drawn again, and the cortisol level measured.  Resting cortisol should range from 1-4 μg/dl in the average dog, and should be significantly higher, in the range of 6-20 μg/dl, post-stimulation. (These numbers may vary depending on the lab.) If resting cortisol is low and the dog has no or a low response to the stimulation, the diagnosis is Addison’s disease.  Be aware that some glucocorticoids, such as prednisone, can affect the results of the ACTH test, while dexamethasone does not.

  


Primary Addisons requires the
replacement medications of mineralocortioids. ____________________

Atypical and Secondary require  
the replacement of  
glucocorticoids only.
____________________

Atypical Addison's  
can become Primary and requires  
careful monitoring of your dog.
____________________

Addison's dogs require additional glucocorticods during periods of stress,

injury or surgery.



Keeping on top of it

There are several medications used to treat Addison’s.  The first type acts as a mineralocorticoid and replaces the aldosterone – the hormone responsible for maintaining electrolyte levels.  It is replaced with either an oral medication called Florinef ™ (fludrocortisone acetate) or the injectable Percorten-V™ (desoxycorticosterone pivalate or DOCP). For dogs that have atypical or secondary Addison’s neither of these medications are used because the production of aldosterone isn’t effected and electrolytes remain in balance.

In addition to replacing the aldosterone, the cortisol, or glucocorticoids, normally secreted by the adrenals must also be replaced.  This is typically done with an oral form of prednisone or hydrocortisone.  With atypical and secondary Addison’s the glucocorticoid is the only medication given.  

  

The bottom line

While your dog with Addison’s disease will need medications and monitoring for the rest of his life, most dogs with Addison’s can return to their favorite activities.  You will learn to read your dog, understand what his stress triggers are and follow your instincts in his care.  Together, you will overcome ADversity and learn from this experience.  You will help your dog lead a normal, active and fun-filled life.


Treatment and Medications

There are several medications used to treat Addison’s disease.  The first type acts as a mineralocorticoid and replaces aldosterone – the hormone responsible for maintaining electrolyte levels.  It is replaced with either an oral medication called Florinef ™ (fludrocortisone acetate) or the injectable Percorten-V™ (desoxycorticosterone pivalate or DOCP). For dogs that have atypical or secondary Addison’s neither of these medications are used because the production of aldosterone isn’t effected and electrolytes remain in balance.

In addition to aldosterone, the cortisol, or glucocorticoids, normally secreted by the adrenals must also be replaced.  This is typically done with an oral form of prednisone or hydrocortisone.  During a crisis, the dog may receive an injection of dexamethasone, a potent and fast-acting glucocorticoid.  The dog may be started initially on high doses of prednisone to facilitate a return to health.  On an on-going basis, the glucocorticoid dose can be reduced and in some cases eliminated except on an as-needed basis.  With atypical and secondary Addison’s the glucocorticoid is the only medication given.  

Mineralocorticoids:

Primary Addison’s disease is treated by replacing the mineralocorticoid, Aldosterone, with either tablets of Florinef or the injectable Percorten-V.  These medications help maintain the balance of the electrolytes Sodium (Na) and Potassium (K).

Florinef is the brand name for fludrocortisone acetate.  This medication is also available in its generic form, fludrocortisone acetate, from compounding pharmacists.  It is primarily a mineralocorticoid, but also has some glucocorticoid activity.  The starting dose recommended by the Merck Veterinary Manual is 0.05 – 0.1 mgs per 10 lbs of bodyweight.  Some dogs require significantly higher doses to maintain normal electrolytes.

The dose may be divided and given twice per day or given all at once, usually in the morning.  A 50-pound dog would take between 0.25 and 0.5 mgs to start.  The brand name Florinef tablets may be purchased directly from your vet or from a pharmacy.  Some people find it more cost effective and efficient to have the proper dose of the medication prepared by a compounding pharmacist in capsule, liquid, or chewable form.

Percorten-V is the brand name for desoxycorticosterone pivalate.  It is an injectable medication with only mineralocorticoid activity.  It does not have any glucocorticoid activity.  The dose recommended by Novartis, the manufacturer, is 0.75 – 1.0 mgs per one lbs. of bodyweight, given every 21 – 30 days.  There are 25 mgs in each ml (or cc) of the medication.

A 50-pound dog would receive between 37.5 – 50 mgs or 1.5 – 2.0 mls.  Some dogs are adequately maintained on lower doses, while some dogs require lower doses to minimize rare side effects.  Percorten-V is available only through a licensed veterinarian, although some veterinary pharmacies may carry the medication.

   Glucocorticoids:

The adrenal glands produce cortisol, a glucocorticoid.  It is the hormone measured by the ACTH Stimulation test used to diagnose Addison’s disease.

All dogs with Addison’s require the supplementation of glucocorticoids in times of stress.  Many need glucocorticoids on a more regular basis, particularly those on DOCP.  Dogs with atypical or secondary Addison’s only take glucocorticoids.

The most common glucocorticoids are prednisone, hydrocortisone and dexamethasone.  There are additional glucocorticoids such as prednisolone and methylprednisolone.  The Merck Veterinary manual recommends a prednisone dose of 0.1 – 0.2 mgs/lb. per day.  This is equivalent to 0.4 – 0.8 mgs/lb. per day of hydrocortisone.

However, some dogs show symptoms of excess glucocorticoids on these doses.  These problems may include excessive drinking and urination, increased appetite, recurring infections, elevated liver enzymes, panting, restlessness and even behavioral changes.  Because these dogs will be on medications for the rest of their lives, it is important to fine-tune the dosages to maximize benefits, while minimizing unwanted side effects.  If you are working to reduce your dogs dose of glucocorticoids, be sure to work with your vet and lower the amount slowly.

Determining what constitutes stress for your dog, when additional glucocorticoids are necessary, is very individual.  Like people, dogs find different situations stressful.  Stress can be in many forms, both good and bad, from physical to emotional.  For some dogs a trip to the vet requires extra medication, while for others it could be houseguests or extra active playtime. Knowing your dog’s triggers is crucial.  It is essential to monitor the dog closely and be prepared to give extra medication when the need arises



More about ACTH test

Reading your dogs blood work

Determining Electrolyte Ratio

Electrolyte ratio is determined by dividing the "NA" number by the "K" number.

145÷ 4.5 = 32

Electrolyte Calculator[/size]

minibabyqq 2006-12-20 04:19

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[size=12px][b][size=5][color=magenta]危害健康從蚤和壁虱產品[/color][/size][/b]

毒物在寵物
健康危害從蚤和壁虱產品


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這個2000 日11月NRDC 報告突出潛在的健康危害對人和寵物從蚤衣領和其它蚤和壁虱控制產品。報告推薦EPA 禁令對這些產品整個組的用途-- 那些使用有機磷酸鹽。它並且提供對寵物所有者的推薦在與交戰的蚤和壁虱以各種各樣簡單的非化學製品步並且/或者由應用更加安全的產品, 包括昆蟲生長調節器。

行政總結
每年, 美國人嚮他們的寵物購買和應用浩大的一些毒性化學製品意欲殺害蚤和壁虱。這些產品被設計毒害昆蟲, 並且他們通常做那。但他們能並且毒害處理他們的寵物和人民。而且, 當這些產品被結合在家, 當他們經常是, 與其它毒性化學製品在共同的使用-- 殺蟲劑、除草藥, 和其它產品-- 他們可能形成一個嚴肅的健康風險, 特別是孩子。

成人是在危險中從這些蚤和壁虱產品-- 寵愛嚮動物每天應用殺蟲劑的工作者, 例如。但這是是最脆弱的孩子。由於children.s 身體仍然顯現出, 他們比成人能是敏感的對毒性化學製品的作用。研究與實驗動物提出了詢問在孩子暴露於確定殺蟲劑在寵物產品的科學家之中-- 在水平認為是安全的為成人-- 面對更高的風險, 不僅為深刻毒化, 而且為有腦子作用和其它嚴肅的疾病的較長期問題。而且, children.s 行為經常使他們脆弱比成人。特別是, 小孩hand-to-mouth 傾向使它容易對含毒物被咽下-- 和不僅由寵愛家庭狗和然後投入他們的手在他們的嘴的孩子。孩子花費含毒物從寵物產品傾向於積累的他們的時間-- 爬行在地毯, 演奏與寵物玩具, 處理家庭塵土的儲積, 和更多。

許多和或許多數美國人相信, 商業可利用的殺蟲劑, 譬如那些被發現在寵物產品, 由政府緊緊調控。實際上, 他們不是。不是直到1996 的段落年法律集中於殺蟲劑在食物裡做了環境保護代辦處(EPA) 開始審查風險從殺蟲劑在寵物產品正經。對這天, EPA 允許寵物產品製造和銷售包含危害殺蟲藥以一點點或沒有示範, 對這些成份的child.s 暴露會是安全的。正因為這些產品是在貨架不意味他們被測試了或能是被假定的保險櫃。

當然, 一樣壞像這些產品也許為寵物所有者和照料者, 他們經常是壞為寵物。根據非常有限的資料可利用, 看起來, 上百和數以萬計寵物被傷害了或大概被殺害了通過對寵物產品的暴露包含殺蟲劑。和與小孩子, 寵物無法報告they.re 被毒害在低藥量。

更加健康的選擇對這些殺蟲劑是欣然可利用的。容易的物理措施像頻繁沐浴和梳寵物可能使用途殺蟲劑不必要。寵物產品包含非殺蟲劑生長調節器可能還停止蚤從成功地再生產。另外, 更新的殺蟲藥, 被噴灑或被察覺是有效的反對蚤和壁虱沒有是毒性的對人的神經系統的寵物, 被開發了。這些選擇的安全和有效率悲劇地做持續的用途更舊, 更加毒性的寵物產品多餘。




寵物殺蟲劑在工作
大約美國家庭的百分之90 使用殺蟲劑。達成協議對一項研究, 家庭的百分之80 被勘測使用了殺蟲劑在家甚而當一名婦女在家庭懷孕, 並且百分之70 使用了他們在child.s 第一期間六個月生活。被勘測的家庭的一半報告了使用殺蟲藥控制蚤和壁虱在寵物。更多比十億美元一年在蚤和壁虱產品上被花費。

不幸地, 對這些產品的寬用途是沒有徵兆, 他們是安全的。相當相反, 他們介紹入家的殺蟲劑包括是危害的對人腦和神經系統、化學製品也許打亂人的激素的化學製品(內分泌) 系統, 並且殺蟲劑被懷疑導致癌症。

蚤控制產品在市場上現在包括七具體"有機磷酸鹽殺蟲藥" (OPs) 。OPs 工作在阻攔body.s 信使化學製品, acetylcholine 的故障旁邊, 因此干涉神經傳輸發信號在昆蟲、寵物和人腦子和神經系統。在OPs 面前, acetylcholine 加強在身體。收效的干涉以神經傳輸是這樣巨大, 它實際上殺害昆蟲。在藥劑過量, OPs 可能並且殺害人和寵物。但以對蚤控制產品的正常用途包含OPs, 寵物並且孩子也許是處於危險中。

七OPs 是chlorpyrifos, dichlorvos, phosmet, naled, tetrachlorvinphos 、二秦農地亞農和馬拉松殺蟲劑。他們是有效成分在許多寵物產品。產品一張全面名單發表在表1 。它包括主要寵物殺蟲劑品牌, 譬如Alco, Americare, Beaphar, 雙義務, Ford.s, 自由五, 愉快的傑克, Hartz, Hopkins, 殺害Ko, 保護、Rabon 、Riverdale 、軍士、Unicorn 、狩醫Kem 、勝利和Zema 。

有機磷酸鹽化學製品並且被使用在食物和在其它共同的家庭產品被設計殺害非寵物出生的昆蟲。為家庭暴露於這些毒性化學製品, 然而, 路線入家和具體怎樣化學製品工作比簡單的事實較不相關的他們造成健康威脅。從健康立場, person.s 聯合的暴露到這些的當中一個OPs, 不問它各自的用途, 是什麼重要。進一步, 因為各種各樣的OPs 所有作用由攻擊同樣化學製品在身體, acetylcholine, 對各種各樣的暴露OPs 能有聯合的衝擊。




EPA 的角色
孩子和成人實際暴露對OPs 在寵物產品充分地未被測量, 並且這樣研究未必需製造者尋求把新寵物殺蟲劑產品放在市場上。的確, 直到1996 的段落年食物質量保護行動, EPA 典型地被承擔那裡是沒有風險從這些產品, 經常以一點點或沒有科學依據。換句話說, EPA 考慮到數十年產品製造和銷售包含寵物殺蟲劑沒有示範, 對產品的child.s 暴露會是安全的。

1996 年法律要求新事EPA: 它估計對 特殊 殺蟲劑的人的積累作用被使用在食品, 佔不僅曝光從食物, 但從所有來源。因為OPs 被使用在寵物產品並且被使用在食用農作物, 法律適用於這些殺蟲劑。起作用相似法律的其它供應要求EPA 估計對一個人的漸增作用從對所有殺蟲劑的暴露和其它化學製品。由於各操作作用由攻擊同樣化工信使在身體, 對各種各樣的家庭暴露另外OPs 應該被期望有漸增健康衝擊。新法律指揮EPA 佔這個漸增作用在它的風險評估。

迄今, EPA.s 遵照食物質量保護Act.s 供應是殘缺不全的。它的風險評估由用於保守地說風險從寵物產品的有缺陷和不一致的假定妨礙了。例如, 在暴露計算的風險對一種化學製品的, EPA 假設, 成人 從未 擁抱他們的狗, 並且在一定數量的事例, EPA 做各種各樣不切實際的假定多久孩子花費與他們的寵物聯繫。

而且, 四年在法案的制定, EPA 有依從代辦處帳戶為多OPs 的漸增衝擊或的其它化學製品起作用用同樣方式的要求之後。這裡再, 結果是保守地說暴露健康危害對含毒物的在寵物產品的風險評估。終於, 仍然今天, EPA 長期從未接受了充分毒力測試為這些殺蟲劑產品在市場上。七種化學製品是這個報告焦點, 只有一個-- chlorpyrifos -- 充分地被測試了為它的對child.s 腦子和神經系統的衝擊。並且, 當緊張系統測試對於chlorpyrifos 最近被完成了, 結果如此令人困擾, 製造商採取了實際上對化學製品的所有室內用途市場。

與那些重要失敗在EPA.s 方法學, Agency.s 正式風險評估為七OPs 發現兩寵愛並且其它產品應該驚動寵物所有者和父母: EPA 現在計算, 對單獨OPs 的child.s 暴露在寵物產品在治療的那天單獨可能超出安全水平在500 次-- 百分之50,000 以前。 對孩子的暴露被計算在一個更長的時期可能超出安全水平對更加了不起的程度。是EPA 計算風險從這些產品使用酣然的假定關於怎樣對人的暴露發生在現實世界, 並且/或者是它依從法律規定, 它計算漸增作用的這些OPs 和的產品作用相似, 風險的EPA 估計從這些產品會是更加荒涼的平靜。

自然資源防禦委員會是一肩並肩投入各自的風險評估為殺蟲劑從寵物產品, 突出整體風險對孩子。EPA 繼續看這些操作風險只一種化學製品一次。代辦處簡單地從未傳播對估計漸增風險兒童面孔從他們暴露對所有另外OPs 的無數的用途。一旦EPA 如此, 漸增風險是肯定超出EPA.s 安全水平對更加了不起的程度。




風險
雖則對風險的EPA.s 評估從OPs 在產品是新的寵物, EPA 一般長期辨認了OPs 作為是在殺蟲劑之中形成最高的風險人類健康。工作者暴露於這些化學製品, 例如, 體驗了視覺問題, 緩慢的認為, 和記憶缺乏。實際上, 然而, 主要風險為人是可能的對幼兒和胎兒腦子和神經系統, 因為他們的系統仍然顯現出當他們暴露於OPs 。風險進來二形式: 風險從毒化, 和風險從對腦子和神經系統的長期作用。


深刻毒化Children.s 風險。 OPs 被認為最危險的殺蟲劑為深刻毒化, 特別為孩子更加年輕比六。在事件之中向毒物控制中心報告, 孩子暴露於OPs 比暴露於其它類型殺蟲劑的孩子是三倍可能五倍可能住醫院, 四倍可能被承認一個重要關心單位, 和死, 遭受生活威脅的病症, 或開發永久傷殘, 。


Children.s 長期健康效應。 child.s 顯現出的腦子和神經系統是特別脆弱的對OPs 的毒性作用因為這些系統不充分地被開發出生時, 必須繼續形成在早期的童年期間。腦子發展要求某些細胞對首先增長, 那麼移居在腦子之內, 和互相然後連接。化學製品譬如OPs 可能中斷和有不可逆的作用在這發展。研究並且表示, 孩子暴露於OPs 也許面對增加的風險為如此後在生活問題像癌症和Parkinson.s 疾病。一項最近流行病學的研究, 例如, 表示, 人們以任一在家暴露的歷史對殺蟲藥的, 像OPs, 以後裝更多比Parkinson.s 於罐中雙重風險在生活中。另外, 四OPs 被使用在產品增加癌症在實驗動物的寵物, 和也許因此導致癌症在人。看, 尤其, 孕婦暴露於蚤和壁虱產品的一項流行病學的研究, 被發現他們的孩子比那些百分之250 可能在控制群被診斷以腦癌在他們的第五個生日之前。

當然, 這是不僅是在危險中的孩子。寵物和寵物工作者是脆弱的。
寵物毒化。 近年來, 上百, 如果沒有數以萬計, 寵物由殺蟲劑產品未毒害具體地被設計至於使用在寵物。產品包含OPs 是在最壞的罪犯之中。EPA 發現這些寵物產品頻繁地被誤用並且這樣的誤用應該由製造者期望。貓是特別脆弱的, 因為他們經常缺乏關鍵酵素為代謝或解毒OPs 。和與孩子, cat.s 小大小和獨特的行為-- 在這種情況下, 修飾-- 運作反對他們, 使他們特別脆弱對操作毒化。


寵物工作者毒化。 在一個最近四期間, 至少26 個成人服務以殺蟲劑寵物垂度被毒害了。近一半這些箱子介入了操作, phosmet 。而且, 服務與蚤控制產品幾乎700 個成人的勘測發現這些工作者是二和一半時間可能有衛生問題比工作者沒暴露於這樣產品。怨言統計地包括在被弄髒的視覺, 皮膚沖洗和哮喘的重大增量。
雖然我們看的每個OPs 有不安全的寵物用途, 這些產品物產變化, 和因此他們造成有些不同的威脅人民暴露於他們。一些例子:

寵物"被浸洗" 以phosmet 。寵愛一條大狗天它的治療和然後投入他們的手指在他們的嘴將接受超過500 倍這種化學製品的安全水平的小孩, 根據EPA 估計。


蚤衣領包含dichlorvos (DDVP) 。EPA.s 初步估計是, 小孩暴露於寵物佩帶蚤衣領包含dichlorvos 會暴露於安全水平從殺蟲藥吸入散發從衣領的21 倍。成人暴露於同樣產品會體驗曝光十個次大於安全水平。


蚤衣領包含naled 。EPA 沒有發現用途naled 是安全的為兒童年齡八和以下的蚤衣領。小孩曝光被計算是儘量十倍更多比EPA.s 保險櫃水平。


蚤衣領包含chlorpyrifos 。EPA 估計, 小孩暴露於狗佩帶這些衣領能得到超過水平EPA 僅僅認為安全的從擁抱或寵愛他們的狗的七倍。


寵物噴灑了或拂去了灰塵與tetrachlorvinphos 。EPA 發現小孩暴露了在中等或被噴灑了或拂去了灰塵與tetrachlorvinphos 產品像EPA.s 保險櫃水平能面對曝光幾乎兩次高的大型狗。


浸洗或搽粉寵物與tetrachlorvinphos 。EPA 確定, 搽粉或浸洗一隻唯一寵物與tetrachlorvinphos, 在終身中, 每年兩次會形成癌症風險人浸洗寵物幾乎六到七個次更加高級比可接受的EPA 水平。浸洗或搽粉多隻寵物, 或那麼更加頻繁地做, 會提高癌症風險更高。



更加安全的選擇
兒童, 寵物和動物工作者持續的暴露對OPs 包含在寵物產品是更加困厄的因為更加安全的選擇是欣然可利用的。容易的物理措施單獨, 像頻繁洗滌物和梳寵物和吸塵的地毯和傢具, 可能使溫和的蚤大批出沒在控制之下。選擇包括昆蟲生長調節器、或拘捕幼小蚤的成長的IGRs, 不是殺蟲劑, 但寧可化學製品。這些包括methoprene, fenoxycarb 和pyriproxyfen 和普遍的lufenuron (節目®) 。選擇並且包括更新的殺蟲劑產品被噴灑或被察覺寵物, 譬如fipronil (前線®) 或imidacloprid (好處®) 。特別當使用與物理措施的組合, 這些更新的化學製品的安全和有效率使持續的用途寵物產品包含OPs -- 和他們的乘務員風險為人和寵物-- 輕率和不必要。




推薦
威脅造成人和寵物由OPs 在寵物殺蟲劑是難容的。自然資源防禦委員會推薦以下:

寵物所有者應該開始使用更加安全的產品在他們的寵物, 避免基於操作的寵物產品。更加安全的產品與像掠過通常寵愛與蚤梳子當檢查蚤, 和頻繁地割在區域寵物花費多數時間戶外的如此簡單的物理措施最好被結合。


孕婦和家庭與孩子應該停止立刻使用基於操作的產品。


孩子應該從未應用蚤香波, 拂去灰塵, 垂度, 等包含OPs 對他們的寵物。EPA 俯視了和低估了特殊性風險對孩子當評估這些產品安全至於家庭使用。


販商應該從他們的架子去除操作產品和尋求教育顧客關於優點更加安全的選擇。


EPA 應該立刻行動取締對寵物殺蟲劑的用途包含OPs 。


EPA 應該考慮並且取締包含氨基甲酸袂-- 殺蟲藥組緊密地與OPs, 和分享相關與OPs 害處同樣基本的生物機制的寵物產品。同樣, 房主和販商應該避免這些氨基甲酸袂包含的產品購買和銷售。


EPA 應該採取步驟更好通知獸醫、寵物所有者和公眾關於更加安全的選擇為蚤和壁虱控制在寵物。
為多數寵物所有者, 家庭狗或貓是家庭的一名心愛的成員。不幸地, 產品經常被使用保護寵物免受蚤和壁虱運載嚴肅的健康危害-- 不僅為寵物, 但為演奏與他們的孩子, 關心為他們, 和愛他們。更加安全的選擇是可利用的-- 有效地將保護寵物免受昆蟲沒有介紹難容的健康危害入家的選擇。消費者、製造者、獸醫、販商和政府全部有一個重要角色扮演在消滅這些危險的寵物產品和帶領更加安全的選擇進入共同的用途。

表1:
EPA 登記的寵物產品包含有機磷酸鹽殺蟲藥
殺蟲藥 狗產品 貓產品
Chlorpyrifos Zema 11 個月的衣領* Sulfodene Scratchex 蚤和壁虱衣領為貓*
Sergeant.s 蚤+ 壁虱衣領 愉快的傑克3-X 蚤、壁虱和Mange 衣領為貓
Sergeant.s 快速行動的蚤& 壁虱衣領為狗 勝利II 充分的季節貓衣領
Hartz 330 天蚤& 壁虱衣領為狗   
Sandoz Dursban 衣領為狗(RF-9411)
Methoprene/Chlorpyriphos 組合衣領為狗
愉快的傑克Tri-Plex 蚤和Mange 衣領
Sardex
Sulfodene Scratchex 蚤和壁虱衣領為狗
勝利12 一整年衣領與Dursban 為大狗
Dichlorvos Sergeant.s 哨兵衣領為狗 Sergeant.s 哨兵衣領為貓
Sergeant.s 快速行動的蚤& 壁虱衣領為狗 蚤衣領為貓
Sergeant.s 雙倍行動蚤和壁虱衣領為狗 Alco 蚤衣領為Cats.White
蚤衣領為狗 Alco 蚤衣領為Cats.Clear
Alco 蚤衣領為狗- 黑, 清楚& 閃爍 Alco 蚤衣領為Cats.Glitters
自由清楚的狗項圈 自由清楚的貓衣領
Naled Sergeant.s 哨兵IV 蚤& 壁虱衣領(為狗) * Sergeant.s 哨兵IV 蚤& 壁虱衣領*
Sergeant.s (r) 哨兵V 蚤& 壁虱衣領為狗* Sergeant.s (r) 哨兵V 蚤& 壁虱衣領為貓*
Sergeant.s 蚤+ 壁虱衣領*   
Phosmet Unicorn 殺蟲塵土*   
狩醫Kem Kemolate 能乳化的液體* (為浸洗)
Tetrachlorvinphos Hartz 2 在1 個衣領裡為狗* Hartz 2 在1 個衣領裡為貓*
Hartz 2 在1 個蚤和壁虱控制衣領裡與14.5% Rabon * Hartz 2 在1 個正持久衣領裡為貓*
Hartz 2 在1 加上七個月衣領為狗* Hartz 2 在1 個正7 個月的衣領裡為貓*
Hartz Rabon 衣領與Methoprene Hartz Rabon 衣領與Methoprene
Americare Rabon 蚤& 壁虱衣領為狗 Americare Rabon 蚤& 壁虱衣領為貓
Rabon 塵土為狗和貓 Rabon 塵土為狗和貓
Hartz 2 在1 粒蚤& 壁虱粉末為狗* Hartz 2 在1 粒蚤& 壁虱粉末為貓
清洗莊稼家畜1% Rabon 塵土 清洗莊稼家畜1% Rabon 塵土
Hartz 2 在1 個蚤& 壁虱泵浦裡為狗II Hartz 2 在1 個蚤& 壁虱泵浦裡為貓II *
Hartz Rabon 浪花以Methoprene 泵浦公式化 Hartz Rabon 浪花以Methoprene 泵浦公式化*
Hartz Rabon 蚤和壁虱垂度為狗和貓* Hartz Rabon 蚤和壁虱垂度為狗和貓*
Hartz 2 在1 朵蚤和壁虱浪花與防臭劑為狗III *   
Hartz 蚤和壁虱放水劑, 包含1% Rabon *
馬拉松殺蟲劑 殺害Ko 馬拉松殺蟲劑集中 殺害Ko 馬拉松殺蟲劑集中
Riverdale 馬拉松殺蟲劑5 Riverdale 馬拉松殺蟲劑5
Ford.s 50% 馬拉松殺蟲劑能乳化的集中 SMCP 5% 馬拉松殺蟲劑塵土
SMCP 5% 馬拉松殺蟲劑塵土 Hopkins 馬拉松殺蟲劑57% 能乳化的液體殺蟲藥B
Hopkins 馬拉松殺蟲劑57% 能乳化的液體殺蟲藥B 50% 馬拉松殺蟲劑能乳化的集中
50% 馬拉松殺蟲劑能乳化的集中 55% 馬拉松殺蟲劑集中
55% 馬拉松殺蟲劑集中 50% 馬拉松殺蟲劑
50% 馬拉松殺蟲劑 Micro.Gro Cythion 優質成績馬拉松殺蟲劑E-5
微Gro Cythion 優質成績馬拉松殺蟲劑E-5 Fyfanon 57 EC
Fyfanon 57 EC   
二秦農地亞農 保護150 反射的蚤和壁虱衣領為狗 保護150 反射的蚤和壁虱衣領為貓
保護加上150 蚤和壁虱衣領為狗與EFA 保護加上蚤和壁虱衣領為貓
保護150 蚤和壁虱衣領為狗和大狗 保護150 蚤和壁虱衣領為貓
保護300 蚤和壁虱衣領為狗 雙義務加上蚤& 壁虱衣領與Nutrisorb 為貓
二秦農地亞農Pyriproxyfen 衣領為狗和小狗# 1, # 2, #3 雙義務反射的蚤& 壁虱衣領為貓
雙義務加上蚤& 壁虱衣領與Nutrisorb 為狗 自由五蚤和壁虱衣領為貓
雙義務反射的蚤& 壁虱衣領   
自由五蚤和壁虱衣領為狗
Beaphar 壁虱& 蚤衣領為狗
雙義務蚤& 壁虱衣領為狗
來源: 詹姆斯山毛櫸, 美國EPA 辦公室殺蟲劑節目, 寵物產品登記七有機磷酸鹽, 2000 年6月3 日。

注: 產品在規則型是那些向EPA 登記2000 年自6月3 日。星號表明寵物產品知道形成為EPA.s 風險評估的依據為那種化學製品。Dichlorvos 、二秦農地亞農和馬拉松殺蟲劑風險評估沒有列出特殊產品。用斜體字印刷的產品是那些, 隨後對風險評估, 製造商現在表明他們不再將維護產品的註冊。在多數, 如果沒有所有這一類案件, 然而, 產品保留在使用中在這個報告準備了時候。  
EXECUTIVE SUMMARY
Each year, Americans purchase and apply to their pets a vast array of toxic chemicals intended to kill fleas and ticks. These products are designed to poison insects, and they usually do just that. But they can also poison pets and the people who handle them. Moreover, when these products are combined in the home, as they often are, with other toxic chemical products in common use -- pesticides, herbicides, and other products -- they can pose a serious health risk, especially to children.


TABLE 1:
EPA Registered Pet Products Containing Organophosphates Insecticides
Insecticide Dog Product Cat Product
Chlorpyrifos Zema 11-month collar* Sulfodene Scratchex Flea and Tick Collar for Cats*
Sergeant𠏋 Flea + Tick Collar Happy Jack 3-X Flea, Tick And Mange Collar For Cats
Sergeant𠏋 Fast-Acting Flea & Tick Collar For Dogs Victory II Full Season Cat Collar
Hartz 330 Day Flea & Tick Collar For Dogs   
Sandoz Dursban Collar For Dogs (RF-9411)
Methoprene/Chlorpyriphos Combination Collar For Dogs
Happy Jack Tri-Plex Flea And Mange Collar
Sardex
Sulfodene Scratchex Flea And Tick Collar For Dogs
Victory 12 Full Year Collar With Dursban For Large Dogs
Dichlorvos Sergeant𠏋 Sentry Collar For Dogs Sergeant𠏋 Sentry Collar For Cats
Sergeant𠏋 Fast-Acting Flea & Tick Collar For Dogs Flea Collar For Cats
Sergeant𠏋 Dual Action Flea And Tick Collar For Dogs Alco Flea Collar For Cats𦂤hite
Flea Collar For Dogs Alco Flea Collar For Cats䊼lear
Alco Flea Collar For Dogs - Black, Clear & Glitters Alco Flea Collar For Cats𨧼litters
Freedom Clear Dog Collar Freedom Clear Cat Collar
Naled Sergeant𠏋 Sentry IV Flea & Tick Collar (for dogs)* Sergeant𠏋 Sentry IV Flea & Tick Collar*
Sergeant𠏋 (R) Sentry V Flea & Tick Collar For Dogs* Sergeant𠏋 (R) Sentry V Flea & Tick Collar For Cats*
Sergeant𠏋 Flea + Tick Collar*   
Phosmet Unicorn Insecticidal Dust*   
Vet-Kem Kemolate Emulsifiable Liquid* (for dipping)
Tetrachlorvinphos Hartz 2 In 1 Collar For Dogs* Hartz 2 in 1 Collar for Cats*
Hartz 2 in 1 Flea and Tick Control Collar with 14.5% Rabon* Hartz 2 in 1 Plus Long Lasting Collar for Cats*
Hartz 2 In 1 Plus Seven Month Collar For Dogs* Hartz 2 in 1 Plus 7-month Collar for Cats*
Hartz Rabon Collar With Methoprene Hartz Rabon Collar With Methoprene
Americare Rabon Flea & Tick Collar For Dogs Americare Rabon Flea & Tick Collar For Cats
Rabon Dust For Dogs And Cats Rabon Dust For Dogs And Cats
Hartz 2 In 1 Flea & Tick Powder For Dogs* Hartz 2 in 1 Flea & Tick Powder for Cats
Clean Crop Livestock 1% Rabon Dust Clean Crop Livestock 1% Rabon Dust
Hartz 2 In 1 Flea & Tick Pump For Dogs II Hartz 2 In 1 Flea & Tick Pump For Cats II*
Hartz Rabon Spray With Methoprene Pump Formulation Hartz Rabon Spray With Methoprene Pump Formulation*
Hartz Rabon Flea and Tick Dip for Dogs and Cats* Hartz Rabon Flea and Tick Dip for Dogs and Cats*
Hartz 2 In 1 Flea And Tick Spray With Deodorant For Dogs III*   
Hartz Flea and Tick Repellent, containing 1% Rabon*
Malathion Kill-Ko Malathion Concentrate Kill-Ko Malathion Concentrate
Riverdale Malathion 5 Riverdale Malathion 5
Ford𠏋 50% Malathion Emulsifiable Concentrate SMCP 5% Malathion Dust
SMCP 5% Malathion Dust Hopkins Malathion 57% Emulsifiable Liquid Insecticide-B
Hopkins Malathion 57% Emulsifiable Liquid Insecticide-B 50% Malathion Emulsifiable Concentrate
50% Malathion Emulsifiable Concentrate 55% Malathion Concentrate
55% Malathion Concentrate 50% Malathion
50% Malathion Micro𨧼ro Cythion Premium Grade Malathion E-5
Micro-Gro Cythion Premium Grade Malathion E-5 Fyfanon 57 EC
Fyfanon 57 EC   
Diazinon Protection 150 Reflecting Flea And Tick Collar For Dogs Protection 150 Reflecting Flea And Tick Collar For Cats
Protection Plus 150 Flea And Tick Collar For Dogs With EFA Protection Plus Flea And Tick Collar For Cats
Protection 150 Flea And Tick Collar For Dogs And Large Dogs Protection 150 Flea And Tick Collar For Cats
Protection 300 Flea And Tick Collar For Dogs Double Duty Plus Flea & Tick Collar With Nutrisorb For Cats
Diazinon-Pyriproxyfen Collar For Dogs And Puppies #1, #2, #3 Double Duty Reflecting Flea & Tick Collar For Cats
Double Duty Plus Flea & Tick Collar With Nutrisorb For Dogs Freedom Five Flea And Tick Collar For Cats
Double Duty Reflecting Flea & Tick Collar   
Freedom Five Flea And Tick Collar For Dogs
Beaphar Tick & Flea Collar For Dogs
Double Duty Flea & Tick Collar For Dogs
Source: James Beech, U.S. EPA Office of Pesticide Programs, Pet Products Registered for Seven Organophosphates, June 3, 2000.[/size]
[/td][/tr][tr][td]
[/td][/tr][/table]

minibabyqq 2006-12-20 04:19

轉貼自4682

[size=12px][b][size=5][color=magenta]甲狀腺 THE THYROID DILEMMA[/color][/size][/b]

甲狀腺機能不足是犬最共同的內分泌混亂, 並且80% 案件應該起因於自動免疫的(lymphocytic) 甲狀腺炎。它採取破壞至少75% 甲狀腺由被瞄準的T 淋巴細胞, 在甲狀腺機能不足的古典臨床標誌被體現之前。因而, 導致對甲狀腺機能不足似犬自動免疫的甲狀腺炎早期賠償階段的準確診斷買得起重要基因和臨床選擇為及時干預和案件管理。這混亂的可遺傳的本質擺在重大基因涵義為良種畜。

竟管甲狀腺官能不良是寵物最頻繁地被認可的內分泌混亂, 它經常難做一個明確的診斷。因為甲狀腺調控所有身體多孔的作用新陳代謝, 被減少的甲狀腺作用可能導致大範圍臨床顯示, 有時隱晦, 其他計時古典, 和偶爾地非常異常。許多這些臨床標誌仿造那些起因於其它起因和因此甲狀腺功能考驗的情況和解釋的認識可能疑難。進一步, 甲狀腺官能不良的發展是從常態開始和逐漸進步在幾個月對幾年對結束階段疾病的連續流。

  
  
基礎線甲狀腺外形
完全基礎線甲狀腺外形應該被測量和典型地包括總T4, 自由T4, 甲狀腺自身抗體, 和也許並且包括總T3 、自由T3 和TSH 。如果包括在甲狀腺外形, T3 和freeT3 分析用試樣通常反射甲狀腺炎當兩個假地被舉起的歸結於T3 出現自身抗體。自身抗體(AA) 分析用試樣(T3.AA, T4.AA, TgAA) 是特別重要在掩護良種畜為可遺傳的自動免疫的甲狀腺病。

正常參考範圍為健康成人動物甲狀腺analytes 傾向於是相似為伴侶動物多數養殖。例外是有更低的基礎水平狗的sighthound 和大的養殖。典型的甲狀腺成水平為健康sighthounds, 這樣作為退休的賽跑的靈獅, 是在或在建立的實驗室參考範圍之下, 但是健康大的養殖有優選的水平在這些範圍之間末端和中點。

進一步, 因為幼小動物仍然增長並且青少年成熟, 優選的甲狀腺水平被預計是在參考範圍的上半方。為老年醫學的動物, 基礎新陳代謝通常減速, 和因此優選的甲狀腺水平可能是離中等長度範圍較近甚至輕微地降下。

所有動物不是相同
小狗有更高的基礎甲狀腺水平比成人

醫學有更低的基礎甲狀腺水平比成人

Large/giant 養殖有更低的基礎甲狀腺水平

Sighthounds 有更低的基礎甲狀腺水平

基因掩護為甲狀腺病
甲狀腺炎多數案件舉起了清液TgAA 水平, 但是只大約20-40% 案件舉起了流通的T3 並且/或者T4 AA 。被舉起的T3 並且/或者T4 AA 出現支持自動免疫的甲狀腺炎診斷但低估它的流行, 因為診斷只由發現在某些情況下顯露被舉起的TgAA 或lymphocytic 滲入在甲狀腺切片檢查法之內。測量AA 水平並且允許混亂的早期的認識, 和促進基因建議。它建議受影響的狗不被使用作為良種畜。

商業TgAA 測試可能給假的消極結果如果狗接受了甲狀腺補充在早先90 天之內。假的消極TgAA 結果可能還發生在大約8% 狗中被核實有高的T3.AA 並且/或者T4.AA 。低檔假的正面TgAA 結果也許被獲得如果狗被接種了在早先40-90 天之內, 或偶爾地在非thyroidal 病症案件(NTI) 。出版研究比男性表明, 甲狀腺炎的流行直接地同體重聯繫在一起, 是最高的在狗2-4 年年紀, 和像其它自動免疫的混亂, 可能發生在女性。

掩護為似犬甲狀腺官能不良
完成甲狀腺抗體外形更喜歡
TSH 惡劣有預測性, 不同於人, 作為一些狗有TSH 一  輕微地另外bioform 由分析用試樣沒認可
基礎水平由某些藥物(類固醇、苯巴比妥, 磺胺  ) 影響
基礎水平降下了由女性荷爾蒙; 由孕酮[ 性荷爾蒙週期  作用] 上升
甲狀腺素治療是最佳每日兩次被給
劃分每日藥量q 12 個小時避免"峰頂和谷" 作用
達到更好的穩定狀態24 小時; 半衰期12-16 個小時
藥量一次每日結果在不受歡迎的峰頂和谷裡
藥量應該直接地被給以口而不是在食物碗裡, 作為  鈣困境甲狀腺素, 可能減速吸收
測試的動物在甲狀腺素療法
監視為臨床標誌的決議
血樣應該被畫4-6 個小時崗位藥片為出價的療法
甲狀腺抗體外形更喜歡; a 必須為甲狀腺炎案件
極小值測試需要是T4
FreeT4 是還有用的, 因為T4 可能被壓制與一致NTI
FT4(ED) 應該使用在T4.AA 出現, 避免自身抗體  干涉
崗位藥片治療範圍應該是在鞋幫1/3 到1/3 在  參考範圍之上
測試的更舊的貓
基礎甲狀腺水平在更舊的貓應該低比成人
其它病症經常降低T4, 掩沒甲狀腺機能亢進
FT4(ED) 敏感, 但較不具體比T4 為診斷的  甲狀腺機能亢進
FT4(ED) 應該總被評估與T4 一起
基礎水平降下了由女性荷爾蒙; 由孕酮[ 性荷爾蒙週期  作用] 上升  
甲狀腺測試對於基因掩護目的是較不可能是意味深長的在青春期之前。掩護被創始, 因此, 一旦健康狗和母狗到達了性成熟(在10-14 個月之間在男性和在第一anestrous 期間為女性跟隨他們的少女熱) 。因為女性性週期是淡靜在anestrus 期間, 性激素的任一影響對基礎線甲狀腺作用將減到最小。這個期間一般開始12 個星期從早先熱的起始和持續一個月或長期。結果的解釋從基礎線甲狀腺外形在原封女性願他更加可靠當他們被測試在anestrus 。一旦最初的甲狀腺外形被獲得, 狗和母狗應該每年被復校估計他們的甲狀腺作用和整體健康。獲得每年測試結果提供允許顯現出的甲狀腺官能不良的早期的認識的比較。這考慮到及時治療, 表明, 避免臨床標誌的出現或推進與相關甲狀腺機能不足的地方。

掩護為似犬自動免疫的甲狀腺炎
完成甲狀腺抗體外形要求
測試原封母狗在anestrus 期間
需要T3.AA, T4.AA, TgAA; 不僅freeT4, TSH, TgAA
OFA 甲狀腺登記是一個有限的盤區
一些案件(~8%) 是T3.AA 並且/或者T4.AA +, 但TgAA -
對待似犬自動免疫的甲狀腺炎
對待盒+ 為T3.AA 並且/或者T4.AA, 或TgAA 與甲狀腺素
當有爭議, 臨床證據支持這種方法而不是  等待直到狗得到不適或有出軌行為†
如果唯一低檔TgAA +, 再實驗外形在2-4 裡mos
款待以甲狀腺素出價; 重測外形在2-4 裡mos
總監測以甲狀腺抗體外形
最近接種, 等待90 天在再實驗之前
不要養殖狗以自動免疫的甲狀腺炎
可遺傳的特徵, 不管臨床狀態
屏幕親戚每年從青春期
考慮為養殖, 如果陰性, 在年齡三以後
†資料從人和狗以甲狀腺炎表示, AA 水平逐漸成為減少在5-10 個月中。這應該起因於腦下垂體的TSH 生產的負反饋禁止, 反過來, 減少感受器官刺激斡旋甲狀腺acinar 細胞的被瞄準的lymphocytic 破壞。

Hypothyroidism is the most common endocrine disorder of canines, and up to 80% of cases are believed to result from autoimmune (lymphocytic) thyroiditis. It takes destruction of at least 75% of the thyroid gland by targeted T-lymphocytes, before classical clinical signs of hypothyroidism are manifested. Thus, accurate diagnosis of the early compensatory stages of canine autoimmune thyroiditis that lead up to hypothyroidism affords important genetic and clinical options for prompt intervention and case management. The heritable nature of this disorder poses significant genetic implications for breeding stock.

Despite the fact that thyroid dysfunction is the most frequently recognized endocrine disorder of pet animals, it is often difficult to make a definitive diagnosis. As the thyroid gland regulates metabolism of all body cellular functions, reduced thyroid function can produce a wide range of clinical manifestations, sometimes vague, other times classical, and occasionally very unusual. Many of these clinical signs mimic those resulting from other causes and so recognition of the condition and interpretation of thyroid function tests can be problematic. Further, development of thyroid dysfunction is a continuum that begins with normalcy and progresses gradually over months to several years to end-stage disease.

  
  
Baseline Thyroid Profiles
A complete baseline thyroid profile should be measured and typically includes total T4, free T4, thyroid autoantibodies, and may also include total T3, free T3 and cTSH. If included in thyroid profiles, the T3 and freeT3 assays usually reflect thyroiditis when both are spuriously elevated due to presence of T3 autoantibody. The autoantibody (AA) assays (T3AA, T4AA, TgAA) are especially important in screening breeding stock for heritable autoimmune thyroid disease.

The normal reference ranges for thyroid analytes of healthy adult animals tend to be similar for most breeds of companion animals. Exceptions are the sighthound and giant breeds of dogs which have lower basal levels. Typical thyroid levels for healthy sighthounds, such as retired racing greyhounds, are at or just below the established laboratory reference ranges, whereas healthy giant breeds have optimal levels between the lower end and midpoint of these ranges.

Further, because young animals are still growing and adolescents are maturing, optimal thyroid levels are expected to be in the upper half of the references ranges. For geriatric animals, basal metabolism is usually slowing down, and so optimal thyroid levels are likely to be closer to midrange or even slightly lower.

All animals are not the same
Puppies have higher basal thyroid levels than adults

Geriatrics have lower basal thyroid levels than adults

Large/giant breeds have lower basal thyroid levels

Sighthounds have much lower basal thyroid levels
Genetic Screening for Thyroid Disease
Most cases of thyroiditis have elevated serum TgAA levels, whereas only about 20-40% of cases have elevated circulating T3 and/or T4 AA. The presence of elevated T3 and/or T4 AA supports a diagnosis of autoimmune thyroiditis but underestimates its prevalence, as the diagnosis in some cases is revealed only by finding an elevated TgAA or lymphocytic infiltrates within thyroid biopsies. Measuring AA levels also permits early recognition of the disorder, and facilitates genetic counseling. It is recommended that affected dogs not be used as breeding stock.

The commercial TgAA test can give false negative results if the dog has received thyroid supplement within the previous 90 days. False negative TgAA results also can occur in about 8% of dogs verified to have high T3AA and/or T4AA. Low-grade false positive TgAA results may be obtained if the dog has been vaccinated within the previous 40-90 days, or occasionally in cases of non-thyroidal illness (NTI). Published studies indicate that prevalence of thyroiditis is directly associated with body weight, is highest in dogs 2-4 years old, and like other autoimmune disorders, more likely to occur in females than males.

Screening for Canine Thyroid Dysfunction
Complete thyroid antibody profile preferred
cTSH poorly predictive, unlike humans, as some dogs have a slightly  different bioform of TSH not recognized by the assay
Basal levels affected by certain drugs (steroids, phenobarbital,  sulfonamides)
Basal levels lowered by estrogen; raised by progesterone [sex hormonal  cycle effects]
Thyroxine treatment is best given twice daily
Dividing the daily dose q 12 hrs avoids "peak and valley" effect
Achieves better steady state over 24 hrs; half life 12-16 hrs
Dosing once daily results in undesirable peaks and valleys
Dosing should be given directly by mouth rather than in food bowl, as  calcium binds thyroxine and can retard absorption
Testing animals on thyroxine therapy
Monitoring for resolution of clinical signs
Blood samples should be drawn 4-6 hrs post-pill for BID therapy
Thyroid antibody profile preferred; a must for thyroiditis cases
Minimum testing needed is T4
FreeT4 is also helpful, as T4 can be suppressed with concurrent NTI
FT4(ED) should be used in presence of T4AA, to avoid autoantibody  interference
Post-pill therapeutic ranges should be at upper 1/3 to 1/3 above the  reference ranges
Testing older cats
Basal thyroid levels in older cats should be lower than adults
Other illnesses often lower T4, masking hyperthyroidism
FT4(ED) more sensitive, but less specific than T4 for diagnosing  hyperthyroidism
FT4(ED) should always be evaluated together with T4
Basal levels lowered by estrogen; raised by progesterone [sex hormonal  cycle effects]

Thyroid testing for genetic screening purposes is less likely to be meaningful before puberty. Screening is initiated, therefore, once healthy dogs and bitches have reached sexual maturity (between 10-14 months in males and during the first anestrous period for females following their maiden heat). As the female sexual cycle is quiescent during anestrus, any influence of sex hormones on baseline thyroid function will be minimized. This period generally begins 12 weeks from the onset of the previous heat and lasts one month or longer. The interpretation of results from baseline thyroid profiles in intact females will he more reliable when they are tested in anestrus. Once the initial thyroid profile is obtained, dogs and bitches should be rechecked on an annual basis to assess their thyroid function and overall health. Obtaining annual test results provides comparisons that permit early recognition of developing thyroid dysfunction. This allows for prompt treatment, where indicated, to avoid the appearance or advancement of clinical signs associated with hypothyroidism.

Screening for Canine Autoimmune Thyroiditis
Complete thyroid antibody profile required
Test intact bitches during anestrus
Need T3AA, T4AA, TgAA; not just freeT4, TSH, TgAA
OFA Thyroid Registry is a limited panel
Some cases (~8%) are T3AA and/or T4AA +, but TgAA -
Treating Canine Autoimmune Thyroiditis
Treat cases + for T3AA and/or T4AA, or TgAA with thyroxine
While controversial, clinical evidence supports this approach rather than  waiting until dog gets ill or has aberrant behavior†
If only low-grade TgAA + , retest profile in 2-4 mos
Treat with thyroxine BID; retest profile in 2-4 mos
Always monitor with thyroid antibody profile
For recently vaccinates, wait 90 days before retesting
Do not breed dogs with autoimmune thyroiditis
Heritable trait, regardless of clinical status
Screen relatives annually from puberty
Consider for breeding, if negative, after age three
†Data from humans and dogs with thyroiditis show that AA levels gradually become reduced over a period of 5-10 months. This is believed to result from negative feedback inhibition of pituitary TSH production, which in turn, reduces stimulation of receptors mediating the targeted lymphocytic destruction of thyroid acinar cells.

[To be continued next month, with discussion of diagnostic profile recommendations and interpretations][/size]

minibabyqq 2006-12-20 04:20

[table][tr][td]轉貼自4682

[size=12px][b][size=5][color=magenta]膀胱癌 BLADDER CANCER[/color][/size][/b]

過渡細胞癌(TCC) 是尿道癌症的最共同的形式在狗和包括幾乎2% 所有似犬癌症。TCC 的流行增加了過去25 年在狗審查在獸醫教的醫院在北美洲的730% 。在狗, TCC 風險同肥胖病, 女性, TCC, 和都市住宅的familial 歷史聯繫在一起, 但不是對對被動香煙煙或家庭化學製品的暴露。蘇格蘭狗是養殖在TCC (18 時間更加高級比被混合的養殖狗) 最高的風險, 雖然TCC 顯著增加的風險並且被發現wirehaired 狐狸狗、西部高地白色狗, 和Shetland sheepdogs 。這建議基因素質對TCC 在狗, 特別是在蘇格蘭狗。這些研究結果表明, 獸醫應該推薦執行定期(即, 兩次逐年) cytologic 尿考試在蘇格蘭狗和其它高風險養殖經過6 年紀。

二完成了情形控制研究被審查是否對草坪或庭院的對典型蚤和壁虱產品的用途和暴露被對待與除草藥和殺蟲藥增加了TCC 的發生在蘇格蘭狗。基因上事先安排好的研究狗所有者被吸收了通過私有獸醫實踐並且美國蘇格蘭狗俱樂部[ 狗以其它與健康有關的情況的所有者87 條成人狗與TCC (案件) 並且83 成人(控制) 完成一張書面83 條成人狗查詢表在第一研究中, 和所有者每個TCC 和控制群完成了一張查詢表在第二項研究中] 。

  
對蚤和壁虱殺蟲劑的暴露
暴露的歷史對蚤和壁虱產品的1 年在TCC 之前診斷是案件狗的一個研究要求並且一個可比較的期間被勘測了為控制狗。TCC 風險聯繫了對蚤的暴露並且壁虱產品是堅定的通過單變量和多邏輯斯諦的回歸分析。

在調整以後為主人因素, 蘇格蘭狗被對待與典型斑點在蚤和壁虱產品包含fipronil 或imidacloprid 沒有TCC 一種增加的風險, 比較沒暴露於任何蚤和壁虱產品的蘇格蘭狗。TCC 風險聯繫了對更舊的典型蚤的用途並且壁虱產品譬如香波、垂度、粉末、浪花, 和衣領不能被評估由於所有者的編號下限在使用了這樣產品的研究人口。結論: 結果建議, 用途對典型斑點在蚤和壁虱產品不增加TCC 風險在蘇格蘭狗。

  
對除草藥和殺蟲藥的暴露
暴露的歷史對草坪或庭院化學製品的1 年在TCC 之前診斷是案件狗的一個研究要求並且一個可比較的期間被勘測了為控制狗。

TCC 風險顯著被增加了在狗之中暴露於草坪或庭院被對待與除草藥和殺蟲藥(可能性比率, 7.19) 或與除草藥單獨(可能性比率, 3.62) 。狗暴露於草坪或庭院被對待與殺蟲藥單獨不極大有一小, 但, 增加的風險TCC (可能性比率1.62) 比較狗暴露於未經治療的草坪。TCC 風險是高的在狗暴露於含苯氧基的酸除草藥(可能性比率, 4.42), 最常用的化學製品在農業, 或nonphenoxy 酸除草藥(可能性比率, 3.49 之中), 比較狗暴露了在沒有接受除草藥應用的草坪或庭院。 結論: 蘇格蘭狗所有者應該減少他們的對草坪或庭院的狗的暴露被對待與共同的除草藥、特殊含苯氧基的除草藥和可能nonphenoxy 除草藥。

飲食菜消耗量和維生素補充
第三項情形控制研究審查了潛在的飲食風險因素為92 條蘇格蘭狗> 6 年紀與TCC (案件) 並且一個可比較的小組83 條蘇格蘭狗沒有尿道疾病(控制的) 最近歷史。狗所有者完成了一張查詢表關於維生素補充他們的狗的飲食和進水閘在去年。乾商業狗食是主要食物類型被消耗的日報> 95% 案件和控制狗, 並且時間狗被維護了在被報告的飲食是7.9 ± 3.1 年。

在調整以後為年齡、重量、中性狀態, 和外套顏色, 菜的消耗量至少3 times/wk 同對開發TCC 風險的70% 整體減少聯繫在一起(可能性比率, 0.30) 。最頻繁地被消耗的菜是在橙黃小組, 用紅蘿蔔經常被餵養。為各自的菜型, 開發TCC 風險被減少了90% 以所有綠色葉茂盛菜(可能性比率, 0.12 的) 消耗量並且70% 與任何橙黃菜(可能性比率, 0.31) 。這些研究結果應該與類胡蘿卜素和松香油出現關係在綠色和黃色菜, 明顯地表達一個防護作用反對顯現出的膀胱癌在人和在膀胱化工導致的瘤在嚙齒目動物。

十字花科的菜的消耗量並且減少了開發TCC 風險, 但不極大(可能性比率, 0.22), 由於不充分的樣本大小作為研究人口175 可能產生了唯一60% 力量查出TCC 80% 被減少的風險。同樣, 研究的力量查出對TCC 風險的50% 減少聯繫了每日維生素補充(維生素E 和C) 是還降低(25%) 由於不充分的樣本大小。 結論: 結果建議, 某些菜的消耗量也許防止或減慢TCC 的發展在蘇格蘭狗。

測試可利用為查出TCC:
BTA (膀胱腫瘤抗原)—測試編碼4383 。樣品要求, 2 機器語言新鮮的尿; 測試s ensitivity 90%, 測試特異性78% 。
尿細胞學, 更喜歡的尿分析方法以cytospin 準備的評估。

參考: Glickman 等, JAVMA 224:1290-1297 2004 年; Raghavan 等、JAVMA 225:389-394,2004 和JAVMA 227:94-100 2005 年。

  
MRSA 殖民化的治療
人們: 使用典型軟膏(Bactroban., mupiricin), 鼻, q 12 h 為5 d 。

寵物: 傳染與MRSA 在狗被報告了但他們潛在的角色作為一個水庫為人的傳染是有爭議的。所有MRSA 報告了在寵物迄今露出人的孤立genomic 署名, 表明人對寵物遷移。 葡萄球菌aureus 通常不是一個長期拓殖的有機體在寵物。如果發現在鼻或剝皮一隻無症狀寵物的拖把, 有機體是更加可能的瞬變病原生物從一個人的主人而不是一個真實的拓殖的有機體。所有人的證明和或 治療 在家庭是主要重要的事物。寵物的角色作為人的病原生物慢性載體不是好瞭解, 雖然慎重是明智的。寵物不應該允許直接聯繫與任何是immunocompromized 的個體直到寵物是被開化的陰性為MRSA 。做法未被展示是有效的在decontaminating 寵物。MRSA 載體狀態的剷除從人在家庭通常將是有效的在去除有機體從寵物。

  
2,6 - 二甲氧基苯青黴素抗性葡萄球菌(夫人)
更多重要的事物在獸醫方面是在主人適應的Staphylococcal 種類的潛力獲取抵抗樣式看在MRSA 。 葡萄球菌intermedius 是coagulase-positive commensal 葡萄球菌spp 。 狗和貓。

大多數 葡萄球菌intermedius 孤立在狗和貓不顯示2,6 - 二甲氧基苯青黴素抵抗。

文學報告關於 葡萄球菌intermedius 孤立從狗和貓和 2,6 - 二甲氧基苯青黴素 抵抗給了矛盾結果: 資料從田納西大學與57 葡萄球菌intermedius 孤立, 只2 是2,6 - 二甲氧基苯青黴素抗性, 雖然50% 有mecA 基因由PCR 查出測試, 建議, 它不可以被表達了。從伊利諾伊大學, 25 2,6 - 二甲氧基苯青黴素抗性 葡萄球菌intermedius 孤立, 23 有mecA 基因, 並且非2,6 - 二甲氧基苯青黴素抗性孤立沒有mecA 基因。進一步工作是需要的確定mecA 基因偵查的價值在獸醫孤立。

凝固酵素消極 葡萄球菌spp 。 孤立(譬如 葡萄球菌schleiferi) 在狗和貓比凝固酵素正面孤立看上去通常被查出以2,6 - 二甲氧基苯青黴素抵抗。這些通常被報告從似犬膿皮病。

  
治療選擇為夫人
缺乏對對任一b 酮抗生素的用途的臨床反應(即青黴素或頭孢菌素)—既使測試在試管內表明他們是敏感的—表明, 這些抗生素不應該被使用對待夫人傳染。

其它選擇:

TMS
比平均成功反對夫人, 但不是藥物改善共同地被推薦在獸醫方面, 由於在有害反應的潛力。

Quinolones

Vancomycin
幾不利: 非常毒害腎臟在狗; 需要是被執行的q 6 h 由IV 路線。

Zyvox (Linezolid)
抗生素(oxazalinozodes) 新家庭的成員; 能enterally 或腸外地被執行。約物動力學的評估在狗表明有效劑量是20-30 mg/kg q 12 h. 低毒力, 但非常昂貴的。使用只如果沒有其它選擇; 例如, 在多藥物抗性夫人Zyvox 是還有效的反對vancomycin 抗性腸球菌。  
Transitional cell carcinoma (TCC) is the most common form of urinary tract cancer in dogs and comprises nearly 2% of all canine cancers. The prevalence of TCC has increased 730% over the past 25 years in dogs examined at veterinary teaching hospitals in North America. In dogs, TCC risk is associated with obesity, female sex, familial history of TCC, and urban dwelling, but not to exposure to passive cigarette smoke or household chemicals. Scottish terriers are the breed at highest risk of TCC (18-times higher than mixed breed dogs), although significantly increased risk of TCC is also found in wirehaired fox terriers, West Highland white terriers, and Shetland sheepdogs. This suggests a genetic predisposition to TCC in terriers, especially in Scottish terriers. These findings indicate that veterinarians should recommend performing routine (e.g., twice yearly) cytologic urine examinations in Scottish Terriers and other high risk breeds over 6 years of age.

Two completed case-control studies examined whether use of topical flea and tick products and exposure to lawns or gardens treated with herbicides and insecticides increased the incidence of TCC in Scottish terriers. Owners of genetically predisposed study dogs were recruited through private veterinary practices and the Scottish Terrier Club of America [owners of 87 adult dogs with TCC (cases) and 83 adult dogs with other health-related conditions (controls) completed a written questionnaire in the first study, and owners of 83 adult dogs each of the TCC and control groups completed a questionnaire in the second study].

  
Exposure to flea and tick pesticides
History of exposure to flea and tick products 1 year prior to diagnosis of TCC was a study requirement for case dogs and a comparable period was surveyed for control dogs. Risk of TCC associated with exposure to flea and tick products was determined by means of univariate and multiple logistic regression analysis.

After adjustment for host factors, Scottish terriers treated with topical spot-on flea and tick products containing fipronil or imidacloprid did not have an increased risk of TCC, compared with Scottish Terriers that had never been exposed to any flea and tick products. The risk of TCC associated with use of older topical flea and tick products such as shampoos, dips, powders, sprays, and collars could not be evaluated because of the low number of owners in the study population that had used such products. Conclusion: Results suggest that use of topical spot-on flea and tick products does not increase the risk of TCC in Scottish terriers.

  
Exposure to herbicides and insecticides
History of exposure to lawn or garden chemicals 1 year prior to diagnosis of TCC was a study requirement for case dogs and a comparable period was surveyed for control dogs.

The risk of TCC was significantly increased among dogs exposed to lawns or gardens treated with both herbicides and insecticides (odds ratio, 7.19) or with herbicides alone (odds ratio, 3.62). Dogs exposed to lawns or gardens treated with insecticides alone had a small, but not significantly, increased risk of TCC (odds ratio, 1.62) compared with dogs exposed to untreated lawns. The risk of TCC was higher among dogs exposed to phenoxy acid herbicides (odds ratio, 4.42), the most commonly used chemical in agriculture, or nonphenoxy acid herbicides (odds ratio, 3.49), compared with dogs exposed to lawns or gardens that did not receive an herbicide application. Conclusion: Owners of Scottish terriers should decrease their dogs' exposure to lawns or gardens treated with common herbicides, particularly phenoxy herbicides and possibly nonphenoxy herbicides.
Dietary vegetable consumption and vitamin supplementation
A third case-control study examined the potential dietary risk factors for 92 Scottish terriers > 6 years of age with TCC (cases) and a comparable group of 83 Scottish terriers with no recent history of urinary tract disease (controls). Dog owners completed a questionnaire regarding their dogs' diet and intake of vitamin supplements in the previous year. Dry commercial dog food was the predominant food type consumed daily by > 95% of the case and control dogs, and the length of time dogs were maintained on the reported diet was 7.9 ± 3.1 yr.

After adjustment for age, weight, neuter status, and coat color, consumption of vegetables at least 3 times/wk was associated with a 70% overall reduction in risk of developing TCC (odds ratio, 0.30). The most frequently consumed vegetables were in the yellow-orange group, with carrots fed most often. For individual vegetable types, the risk of developing TCC was reduced 90% with consumption of any green leafy vegetables (odds ratio, 0.12) and 70% with any yellow-orange vegetables (odds ratio, 0.31). These findings are believed to relate to the presence of carotenoids and retinol in green and yellow vegetables, which apparently convey a protective effect against developing bladder cancer in humans and in chemically-induced neoplasms of the bladder in rodents.

Consumption of cruciferous vegetables also reduced the risk of developing TCC, but not significantly (odds ratio, 0.22), possibly because of inadequate sample size as the study population of 175 yielded only a 60% power to detect an 80% decreased risk of TCC. Similarly, the power of the study to detect a 50% reduction in TCC risk associated with daily vitamin supplementation (vitamins E and C) was also low (25%) because of inadequate sample size. Conclusion: Results suggest that consumption of certain vegetables may prevent or slow the development of TCC in Scottish terriers.

Tests Available for Detecting TCC:
BTA (Bladder Tumor Antigen)—Test Code 4383. Sample requirement, 2 mL fresh urine; test s ensitivity 90%, test specificity 78%.
Urine Cytology, preferred urinalysis method with evaluation of cytospin preparation.

References: Glickman et al, JAVMA 224:1290-1297, 2004; Raghavan et al, JAVMA 225:389-394,2004 and JAVMA 227:94-100, 2005.

  
Treatment of MRSA Colonization
People: Use topical ointment (Bactroban? mupiricin), nasally, q 12 h for 5 d.

Pets: Infections with MRSA in dogs have been reported but their potential role as a reservoir for human infection is controversial. All MRSA reported to date in pets bare the genomic signature of human isolates, indicating a human-to-pet migration. Staph. aureus is not normally a long-term colonizing organism in pets. If found in a nasal or skin swab of an asymptomatic pet, the organism is more likely a transient pathogen from a human host rather than a true colonizing organism. Identification and or treatment of all humans in the household is of primary concern. The role of pets as chronic carriers of human pathogens is not well understood, although prudence is wise. Pets should not be allowed direct contact with any individual who is immunocompromized until the pets have been cultured negative for MRSA. No procedure has been demonstrated to be effective in decontaminating pets. Eradication of the MRSA carrier state from people in the household usually will be effective in removing the organism from the pet.

  
Methicillin-Resistant Staphylococcus (MRS)
Of more concern in veterinary medicine is the potential for host adapted Staphylococcal species to acquire the resistance patterns seen in MRSA. Staph. intermedius is the coagulase-positive commensal Staph. spp. of dogs and cats.

The vast majority of Staph. intermedius isolates in dogs and cats do not show methicillin resistance.

Literature reports on Staph. intermedius isolates from dogs and cats and methicillin resistance have given conflicting results: Data from University of Tennessee with 57 Staph. intermedius isolates, only 2 were methicillin resistant, although 50% had the mecA gene detected by PCR testing, suggesting that it may not have been expressed. From the University of Illinois, of 25 methicillin-resistant Staph. intermedius isolates, 23 had mecA gene, and the non-methicillin-resistant isolates did not have the mecA gene. Further work is needed to determine the value of mecA gene detection on veterinary isolates.

Coagulase negative Staphylococcus spp. isolates (such as Staph. schleiferi) in dogs and cats appear to be more commonly detected with methicillin-resistance than do the coagulase positive isolates. These are usually reported from canine pyodermas.

  
Treatment Options for MRS
Lack of clinical response to use of any b-lactam antibiotic (e.g. penicillins or cephalosporins)—even if in vitro testing indicates that they are sensitive—indicates that these antibiotics should not be used to treat an MRS infection.

Other choices:

TMS
Better than average success against MRS, but not a drug commonly recommended in veterinary medicine, because of potential for adverse reactions.

Quinolones

Vancomycin
Several disadvantages: very nephrotoxic in dogs; needs to be administered q 6 h by IV route.

Zyvox (Linezolid)
Member of new family of antibiotics (oxazalinozodes); can be administered enterally or parenterally. Pharmacokinetic evaluation in dogs indicates the effective dose is 20-30 mg/kg q 12 h. Low toxicity, but very expensive. Use only if no other choice; for example, in multi-drug resistant MRS. Zyvox is also effective against vancomycin-resistant enterococcus.[/size]
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[size=12px][b][size=5][color=magenta]糖尿病MELLITUS[/color][/size][/b]

一致混亂
  
糖尿病mellitus (DM 的) 管理也許被複雜化在狗以一致混亂由於在櫃臺管理激素, 譬如胰高血糖素, 兒茶酚胺、類皮質激素, 或生長激素的集中的增量。

在221 條糖尿病狗的研究中, 平均年齡在診斷的時期是8.9 ± 2.9 年, 並且性人口統計是89 spayed 女性、78 個被閹割的男性、38 個原封男性和16 位原封女性。純血統狗佔163 221 個案件(74%), 並且最頻繁地影響的養殖是微型schnauzers (27 個案件), 拉布拉多獵犬(18), 和微型長捲毛狗(16); 58 條狗(26%) 是混雜的養殖。第二項最近研究介入了45 條狗以DM 被評估為一致癩。

最共同的一致疾病是:

糖尿病ketoacidosis (酮尿和新陳代謝的酸中毒) 被診斷了在15% 狗中。
尿道傳染是存在在21% 159 被開化的尿樣中, 並且最共同的細菌被隔絕是E. 桿菌。
Cushing 的綜合症狀被診斷了在51 (23%) 案件中。診斷由歷史、臨床腎上腺功能考驗在50 條狗和屍體檢驗的標誌, 和結果建立了在一條狗。低藥量dexamethasone 鎮壓(LDDS) 測試結果是反常的在41 50 條狗中被測試。五條狗有促腎上腺皮質激素刺激測試一致與Cushing 的綜合症狀, 並且四他們並且有反常LDDS 測試。另外47 狗被測試有正常腎上腺功能考驗。
甲狀腺機能不足被診斷了在8 (4%) 狗中根據臨床標誌和TSH 刺激測試(5 條狗), 低T4 和高的TSH (2 條狗) 並且屍體檢驗(1 條狗) 。
深刻胰腺炎是存在在28 (13%) 案件中根據臨床標誌、胃腸超聲波或histologic 研究結果。另外, 更多比狗的一半有高澱粉酵素和脂肪分解素含量。
Dermatologic 混亂最共同地看在45 條糖尿病狗學習了包括: 細菌皮炎(84%), otitis (58%), 過敏皮炎(49%), malassezia 導致的皮炎(42%), 和endocrinopathies (~40%) 。也被看見以DM: demodecosis, 經常被推斷在狗; 皮膚淋巴瘤特別是在貓, 而且在狗; 並且necrolytic 遷移紅斑(aka hepatocutaneous 綜合症狀) 。過敏pruritic 癩是存在在22 45 條狗中(49%) 並且在DM 之前在至少2 年以前。
為更大的研究(221 個案件), 臨床標誌的卑鄙期間是1.3 ± 1.9 月。煩渴和polyuria 是存在在82%, 慵倦(57%), inappetence (45%), 嘔吐(40%), 減重(39%), polyphagia (22%), 和腹瀉(13%) 。多數狗(48%) 是超重, 雖然19% 是重量不足。多數狗(50%) 很好水合了, 僅32% 適度地被脫水了並且18% 嚴厲地被脫水了。其它研究結果包括hepatomegaly (61%), 大瀑布(26%) 並且心臟病私語(26%) 。

在dermatologic 研究中, 21 45 條狗(47%) 最近接受了類皮質激素療法。九他們斷斷續續地接受了類皮質激素抗發炎藥量一年或更多, 並且5 條狗比一個月被給了類皮質激素免疫抑制的藥量在DM 之前診斷。那些以過敏癩(22 條狗), 3 有食物過敏, 1 有蚤過敏皮炎, 並且18 有遺傳性過敏症的皮炎。

細菌皮膚傳染是存在在38 條狗, 28 有唯一表面傳染, 6 有表面和深刻的膿皮病, 並且4 最共同地有唯一深刻的傳染以interdigital 根瘤的形式。大多狗陳列了pruritis 。26 條狗與提出在DM 以後起始的otitis, 細胞學顯露了酵母、細菌, 或兩個的混合物。

皮炎從malassezia 被查出了在19 條狗, 並且13 這些有過敏皮炎一個預先的診斷。6 條殘餘的狗與malassezia, 4 有necrolytic 遷移紅斑(並且叫做hepatocutaneous 綜合症狀、新陳代謝的表皮壞死, 或表面necrolytic 皮炎) 。一條其它狗在這45 專題研究中有necrolytic 遷移紅斑並且它未同酵母傳染聯繫在一起。最共同的站點為酵母繁茂是interdigital 空間(10 條狗) 並且爪摺疊(8 條狗) 。

Hyperadrenocorticism 是存在在13 45 條(29%) 狗中以DM 和癩。甲狀腺機能不足被診斷了在5 45 中(11%) 這個小組狗。

在122 專題研究中, 多數狗是hyperglycemic 在最初的考試之時。被電離的鈣在不到狗的一半內是正常的。不定的起因Hypocalcemia 被發現了在多數狗以反常被電離的鈣含量。AST 的被舉起的水平, ALT, 並且阿爾卑斯被發現了在多數狗, 並且澱粉酵素和脂肪分解素含量是高的在更多比一半箱子。大約狗的半有新陳代謝的酸中毒。

尿分析顯露, 81% 狗集中了尿, 83% 有glucosuria, 52% 有proteinuria, 44% 有血尿, 並且36% 有酮尿。

幅射線照相的研究包括胃腸ultrasonography 在127 條狗, 胃腸射線照相在46 條狗, 和胸部射線照相在100 條狗。有27 條狗以hepatomegaly, 104 條狗與hyperechoic 肝臟, 48 條狗與hyperechoic 腎臟外皮, 27 條狗與hypoechoic 胰腺和hyperechoic 腸繫膜一致與深刻胰腺炎, 23 條狗以腹膜流出, 11 條狗以十二指腸牆壁變厚, 15 條狗以肺齒齦音樣式, 和9 條狗以cardiomegaly 。

  
結論
  
一致混亂是共同在狗以DM 。不適當地反應胰島素療法的狗以糖尿病應該被評估為也許導致胰島素抗性的各種各樣的混亂。許多糖尿病狗以一致癩有一個已存在過敏預先的類皮質激素管理的情況, 歷史, 或其他endocrinopathy 可能導致或加重癩。

Management of diabetes mellitus (DM) may be complicated in dogs with concurrent disorders due to an increase in concentrations of counter-regulatory hormones, such as glucagon, catecholamines, corticosteroids, or growth hormone.

In a study of 221 diabetic dogs, the mean age at time of diagnosis was 8.9 ± 2.9 years, and the sex demographic was 89 spayed females, 78 neutered males, 38 intact males and 16 intact females. Purebred dogs accounted for 163 of the 221 cases (74%), and the most frequently affected breeds were miniature schnauzers (27 cases), Labrador retrievers (18), and miniature poodles (16); 58 dogs (26%) were mixed breeds. A second recent study involved 45 dogs with DM evaluated for concurrent skin disease.

The most common concurrent diseases were:

Diabetic ketoacidosis (ketonuria and metabolic acidosis) was diagnosed in 15% of dogs.
Urinary tract infection was present in 21% of 159 cultured urine samples, and the most common bacterium isolated was E. coli.
Cushing's syndrome was diagnosed in 51 (23%) of cases. Diagnosis was established by history, clinical signs, and results of adrenal function tests in 50 dogs and necropsy in one dog. Low-dose dexamethasone suppression (LDDS) test results were abnormal in 41 of the 50 dogs tested. Five dogs had ACTH stimulation tests consistent with Cushing's syndrome, and four of them also had abnormal LDDS tests. Another 47 dogs tested had normal adrenal function tests.
Hypothyroidism was diagnosed in 8 (4%) of the dogs based on clinical signs and TSH stimulation tests (5 dogs), low T4 and high cTSH (2 dogs) and necropsy (1 dog).
Acute pancreatitis was present in 28 (13%) of cases based on clinical signs, abdominal ultrasound or histologic findings. In addition, more than half of the dogs had high amylase and lipase concentrations.
Dermatologic disorders most commonly seen in the 45 diabetic dogs studied included: bacterial dermatitis (84%), otitis (58%), allergic dermatitis (49%), malassezia-induced dermatitis (42%), and endocrinopathies (~40%). Also seen with DM are: demodecosis, often generalized in dogs; cutaneous lymphoma especially in cats, but also in dogs; and necrolytic migratory erythema (aka hepatocutaneous syndrome). Allergic pruritic skin disease was present in 22 of the 45 dogs (49%) and preceded the DM by at least 2 years.

For the larger study (221 cases), the mean duration of clinical signs was 1.3 ± 1.9 months. Polydipsia and polyuria were present in 82%, lethargy (57%), inappetence (45%), vomiting (40%), weight loss (39%), polyphagia (22%), and diarrhea (13%). Most dogs (48%) were overweight, although 19% were underweight. Most dogs (50%) were well hydrated, but 32% were moderately dehydrated and 18% were severely dehydrated. Other findings included hepatomegaly (61%), cataracts (26%) and cardiac murmurs (26%).

In the dermatologic study, 21 of the 45 dogs (47%) had received corticosteroid therapy recently. Nine of them had received anti-inflammatory doses of corticosteroids intermittently for a year or more, and 5 dogs had been given immunosuppressive doses of corticosteroids less than a month before the diagnosis of DM. Of those with allergic skin disease (22 dogs), 3 had food allergies, 1 had flea allergic dermatitis, and 18 had atopic dermatitis.

Bacterial skin infection was present in 38 dogs, of which 28 had only superficial infections, 6 had both superficial and deep pyoderma, and 4 had only deep infections most commonly in the form of interdigital nodules. Most of the dogs exhibited pruritis. Of the 26 dogs with otitis which presented after the onset of DM, cytology revealed yeast, bacteria, or a mixture of both.

Dermatitis from malassezia was detected in 19 dogs, and 13 of these had a prior diagnosis of allergic dermatitis. Of the 6 remaining dogs with malassezia, 4 had necrolytic migratory erythema (also called hepatocutaneous syndrome, metabolic epidermal necrosis, or superficial necrolytic dermatitis). One other dog in this 45 case study had necrolytic migratory erythema and it was not associated with yeast infection. The most common sites for yeast overgrowth were interdigital spaces (10 dogs) and claw fold (8 dogs).

Hyperadrenocorticism was present in 13 of 45 (29%) dogs with DM and skin disease. Hypothyroidism was diagnosed in 5 of 45 (11%) of this group of dogs.

In the 122 case study, most dogs were hyperglycemic at the time of initial examination. Ionized calcium was normal in less than half of the dogs. Hypocalcemia of uncertain cause was found in most dogs with abnormal ionized calcium concentrations. Elevated levels of AST, ALT, and ALP were found in most dogs, and amylase and lipase concentrations were high in more than half of the cases. About half of the dogs had metabolic acidosis.

Urinalysis revealed that 81% of the dogs had concentrated urine, 83% had glucosuria, 52% had proteinuria, 44% had hematuria, and 36% had ketonuria.

Radiographic studies included abdominal ultrasonography on 127 dogs, abdominal radiographs on 46 dogs, and thoracic radiographs on 100 dogs. There were 27 dogs with hepatomegaly, 104 dogs with hyperechoic livers, 48 dogs with hyperechoic renal cortices, 27 dogs with hypoechoic pancreas and hyperechoic mesentery consistent with acute pancreatitis, 23 dogs with peritoneal effusions, 11 dogs with duodenal wall thickening, 15 dogs with pulmonary alveolar pattern, and 9 dogs with cardiomegaly.

  
Conclusions
  
Concurrent disorders are common in dogs with DM. Dogs with diabetes that fail to respond appropriately to insulin therapy should be evaluated for a wide variety of disorders which may cause insulin resistance. Many diabetic dogs with concurrent skin disease have a pre-existing allergic condition, history of prior corticosteroid administration, or another endocrinopathy likely causing or aggravating the skin disease.[/size]
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minibabyqq 2006-12-20 04:21

[table][tr][td]轉貼自4682

[size=12px][color=magenta][b][size=5]BARTONELLOSIS疾病[/size][/b]
[/color]
Bartonella vinsonii, 亞種berkhoffii, 被報告導致心率失常、心內膜炎、心肌炎、和granulomatous 淋巴腺炎和鼻炎在狗。 Bartonella henselae 並且向起因肝臟病(peliosis 肝炎報告) 在狗。當傳染媒介未被辨認為Bartonella spp., 壁虱認為是可能的傳染媒介。有co 傳染的一種高速率在狗與ehrlichiosis 、babesiosis 和bartonellosis 。任一條狗被對待為Babesia spp. 或Ehrlichia spp. 傳染和不完全地反應應該被測試為Bartonella spp. 傳染。Immunosuppression 起因於bartonellosis, 並且這也許削弱狗的能力對清楚的一致傳染。

大約700 個清液樣品由Breitschwerdt 博士的實驗室篩選, 90 (11%) 是seropositive 為Bartonella spp., 比早先著名的3% 率高級。這些90, 30 條狗沒有其它抗體反對傳染物質並且24 有完全病歷。在這些24 狗之中, 30% 有耳朵要訣和leukocytoclastic 脈管炎erosion/scabbing 的dermatologic 變動在切片檢查法。一些狗有關節痛, 並且20% 有uveitis 有或沒有視網膜出血。百分之二十一有神經學疾病, 數有變化在CSF 上像GME, 並且21% 有AIHA 。狗的一半有thrombocytopenia, 並且大約三分之一有neutrophilia 、monocytosis 、嗜酸性白血球過多, 和貧血症。

在貓, Bartonella henselae 也許導致熱病、齒齦炎和口腔炎, 和lymphadenopathy 。診斷根據血清學和PCR 。
Bartonellosis 湧現如同一種更加重要的zoonotic 疾病比早先體會。

當 Bartonella spp 。 普遍並且認出在許多種類, 最重大的臨床疾病發生在貓、狗和人(貓抓痕疾病, CSD) 。五個種類現在被認可在貓: Bartonella henselae 、B. clarridgeiae 、B. kochlerae 、B. weissii 和 B. elizabethae。在狗, 最共同的種類是 B. vinsonii, 雖然 B. henselae 並且向起因病症報告。 B. henselae 是最共同的種類看在人。傳輸傳染媒介最近被辨認包括共同的家養的貓和狗蚤, 和鹿壁虱。一致傳染以Lyme 疾病(疏螺旋體burgdorferi) 並且 B. henselae 導致了CNS 疾病在人, 並且狗有co 傳染的一種高速率與Ehrlichia spp. 和Babesia spp 。

  
臨床綜合症狀
人。 早先被描述的疾病有: CSD 、桿菌的angiomatosis 和peliosis 、熱性的菌血症、lymphadenopathy 、心內膜炎、植物生長的valvular 疾病、uveitis 、神經混亂、貧血症、neuroretinitis, 和骨髓炎。最近被描述的疾病有: 激動腸疾病, 單核白細胞增多症像綜合症狀, 肺滲入, meningoencephalitis 、關節痛、少年關節炎、皮膚疹和紫斑症、皮膚肉芽腫, 和disciform 角膜炎。

貓。 有Bartonella 的大流行 spp 。 傳染在貓, 通常是無症狀載體。但是, 研究發現了一個協會在Bartonella 傳染和慢性口頭疾病(齒齦炎、口腔炎, 和口頭潰瘍之間), lymphocytic plasmacytic 結膜炎和uveitis 、上部呼吸傳染、激動腸疾病, 和慢性腎衰竭。蚤傳送傳染在貓之中並且流行是高的在迷路者和風雨棚貓之中, 和multicat 家庭。流行地理上並且變化; 有機體興旺在節肢動物傳染媒介被發現的高濕熱。傳染可能堅持幾年來, 並且貓能成為reinfected 在Bartonella 抗體面前。

狗。 Bartonella spp 。 可以導致心內膜炎、granulomatous 淋巴腺炎、鼻炎、肝臟病、dermatologic 損害、關節痛、uveitis 、神經學疾病、貧血症、白血球增多和thrombocytopenia 。

診斷
考慮應該被給予測試的貓以口頭疾病為Bartonella, 並且為FeLV 和FIV 傳染。健康貓與聯繫immunocompromised 人應該並且被測試為Bartonella 傳染。

Bartonella 血清學當前是診斷更喜歡的方法。Bartonella 西部汙點血清學測試更喜歡在貓, 將查出傳染以所有種類已知傳染貓。(Bartonella 西部汙點, 測試編碼S16890; 要求0.5ml 清液; TAT 是5lj 幾天。)

Bartonella 血清學在狗可能執行使用西部汙點測試或IFA 測試(Bartonella Vinsonii 滴定量; 測試編碼16891 為東部和測試明確客戶, 測試編碼85162 為西部客戶; 要求0.5ml 清液; TAT 是7-14 天。)

PCR 測試對於Bartonella 是可利用的和並且查出所有 Bartonella spp 。 知道傳染貓和狗。較少比為人所知關於血清學測試目前為人所知關於Bartonella 敏感性PCR 測試。(Bartonella PCR; 測試編碼S1315; 要求血液1ml 在LTT; TAT 是5-7 天。)

Bartonella 有機體可能並且被開化從被傳染的動物血液。這個測試敏感性是不定的。(Bartonella 文化; 測試編碼S16001; 要求血液1ml 在LTT; TAT 是4 個星期。)

  
治療
選擇的治療一次每日口頭是azithromycin 在10 mg/kg 10 天。為貓以口頭疾病, 執行牙齒規程和對待與azithromycin 。嚴謹蚤控制是根本的為貓和環境, 並且壁虱控制並且被勸告。健康被傳染的貓應該被對待與azithromycin 。寵物所有者應該避免咬住或抓, 並且azithromycin 的液體形式也許是容易執行比片劑。

Doxycyline 可能並且使用每日兩次治療Bartonella 傳染在貓在藥量50 毫克6 個星期。

抗體滴定量應該被復校6 個月post-treatment, 與2 摺疊或降低滴定量看在成功地被對待的盒。

Bartonella vinsonii, subspecies berkhoffii, has been reported to cause cardiac arrhythmia, endocarditis, myocarditis, and granulomatous lymphadenitis and rhinitis in dogs. Bartonella henselae also has been reported to cause liver disease (peliosis hepatitis) in dogs. While vectors have not been identified for Bartonella spp., ticks are believed to be likely vectors. There is a high rate of co-infection in dogs with ehrlichiosis, babesiosis and bartonellosis. Any dog being treated for Babesia spp. or Ehrlichia spp. infection and not responding completely should be tested for Bartonella spp. infection. Immunosuppression results from bartonellosis, and this may impair ability of the dog to clear concurrent infections.

Of about 700 serum samples screened by Dr. Breitschwerdt's laboratory, 90 (11%) were seropositive for Bartonella spp., which is higher than the previously noted 3% rate. Of these 90, 30 dogs had no other antibodies against infectious agents and 24 had complete medical records. Among these 24 dogs, 30% had dermatologic changes of erosion/scabbing of ear tips and leukocytoclastic vasculitis on biopsy. Some dogs had joint pain, and 20% had uveitis with or without retinal hemorrhages. Twenty-one percent had neurological disease, several had changes in the CSF like GME, and 21% had AIHA. Half of the dogs had thrombocytopenia, and about one third had neutrophilia, monocytosis, eosinophilia, and anemia.

In cats, Bartonella henselae may cause fever, gingivitis and stomatitis, and lymphadenopathy. Diagnosis is based on serology and PCR.
Bartonellosis is emerging as a more important zoonotic disease than previously realized.

While Bartonella spp. are widespread and recognized in many species, the most significant clinical disease occurs in cats, dogs and people (cat scratch disease, CSD). Five species are now recognized in cats: Bartonella henselae, B. clarridgeiae, B. kochlerae, B. weissii and B. elizabethae. In dogs, the most common species is B. vinsonii, although B. henselae also is reported to cause illness. B. henselae is the most common species seen in people. Transmission vectors recently identified include the common domestic cat and dog fleas, and the deer tick. Concurrent infections with Lyme disease (Borrelia burgdorferi) and B. henselae have produced CNS disease in humans, and dogs have a high rate of co-infection with Ehrlichia spp. and Babesia spp.

  
Clinical Syndromes
Humans. Previously described diseases include: CSD, bacillary angiomatosis and peliosis, febrile bacteremia, lymphadenopathy, endocarditis, vegetative valvular disease, uveitis, neurological disorders, anemia, neuroretinitis, and osteomyelitis. Newly described diseases include: inflammatory bowel disease, mononucleosis-like syndrome, pulmonary infiltrates, meningoencephalitis, arthralgia, juvenile arthritis, cutaneous rash and purpura, cutaneous granuloma, and disciform keratitis.

Cats. There is a high prevalence of Bartonella spp. infection in cats, which are usually asymptomatic carriers. However, research has found an association between Bartonella infection and chronic oral disease (gingivitis, stomatitis, and oral ulcers), lymphocytic-plasmacytic conjunctivitis and uveitis, upper respiratory infection, inflammatory bowel disease, and chronic renal failure. Fleas transmit the infection among cats and the prevalence is higher among stray and shelter cats, and multicat households. Prevalence also varies geographically; the organism thrives in high heat and humidity where arthropod vectors are found. Infection can persist for years, and cats can become reinfected in the presence of Bartonella antibody.

Dogs. Bartonella spp. may cause endocarditis, granulomatous lymphadenitis, rhinitis, liver disease, dermatologic lesions, joint pain, uveitis, neurological disease, anemia, leukocytosis and thrombocytopenia.

Diagnosis
Consideration should be given to testing cats with oral disease for Bartonella, as well as for FeLV and FIV infection. Healthy cats in contact with immunocompromised people should also be tested for Bartonella infection.

Bartonella serology is currently the preferred method of diagnosis. The Bartonella Western Blot serology test is preferred in cats and will detect infection with all species known to infect cats. (Bartonella Western Blot, Test code S16890; Requires 0.5ml serum; TAT is 5lj days.)

Bartonella serology in dogs can be performed using the Western Blot test or an IFA test. (Bartonella Vinsonii titer; Test code 16891 for East and Test Express clients, Test code 85162 for West clients; Requires 0.5ml serum; TAT is 7-14 days.)

PCR testing for Bartonella is available and also detects all Bartonella spp. known to infect cats and dogs. Less is presently known about the sensitivity of Bartonella PCR testing than is known about serology testing. (Bartonella PCR; Test code S1315; Requires 1ml of blood in a LTT; TAT is 5-7 days.)

Bartonella organisms can also be cultured from the blood of infected animals. The sensitivity of this test is uncertain. (Bartonella culture; Test code S16001; Requires 1ml of blood in a LTT; TAT is 4 weeks.)

  
Treatment
The treatment of choice is azithromycin at 10 mg/kg orally once daily for 10 days. For cats with oral disease, perform dental procedures and treat with azithromycin. Rigorous flea control is essential for the cat and the environment, and tick control also is advised. Healthy infected cats should be treated with azithromycin as well. Pet owners should avoid being bitten or scratched, and the liquid form of azithromycin may be easier to administer than tablets.

Doxycyline can also be used to treat Bartonella infections in cats at a dose of 50 mg twice daily for 6 weeks.

Antibody titers should be rechecked 6 months post-treatment, with a 2-fold or more lowering of the titer seen in successfully treated cases.[/size]
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minibabyqq 2006-12-20 04:22

轉貼自4682

[size=12px][b][size=5][color=magenta]帚形菌屬OTITIS EXTERNA[/color][/size][/b]

背景
帚形菌屬spp., 最共同地P. aeruginosa, 是狗外在耳道的共同的機會主義的病原生物, 他們對otitis externa 貢獻。在慢性案件, 這傳染經常導致otitis 媒介。

處理的帚形菌屬otitis 案件的一個重要和經常頻繁地被忽略的方面將辨認和對待預先處理耳道對次要傳染的部下的疾病。如果這不做, 帚形菌屬傳染可能將復發, 因此促進有機體張力的發展以多藥物抵抗。

帚形菌屬otitis 的共同的根本原因有: 食物過敏或過敏症、遺傳性過敏症、keratinization 混亂(主要seborrhea), 甲狀腺機能不足、Cushing 的綜合症狀, 和聽覺外國身體。

當典型地方治療由所有主張, 有當前爭論關於對系統抗生素的用途在帚形菌屬otitis externa 的治療。一個小組相信, 系統抗生素長的時期(4-16 個星期) 是需要的消滅傳染, 特別是如果有中耳介入。另一小組不再使用系統抗生素(除了有流體在中耳裡或tympanic 教宗通諭所蓋之圓璽的骨多的病勢漸退的幅射線照相的證據) 的地方, 相信, 足夠的組織水平高不被到達在耳朵殺害帚形菌屬。這些同事運用清洗運河和提供典型抗生素的典型治療(通常enrofloxacin 的) 高濃度在耳道和中耳之內。系統抗生素對抗藥性抵抗並且貢獻更多看在週期性otitis 案件externa/media 。

  
臨床研究結果
典型的臨床研究結果在介紹有: 厭食; 耳朵殘骸的證據, 放電, 嚴厲指責, 自已切斷, 骯髒的氣味, painfulness, 過份抓, 筆直耳朵的崩潰; 並且降下和震動頭。在耳鏡檢法, 有耳道的增生和炎症。

  
診斷
在otitis 慢性或無答復的案件, 被懷疑或coinfirmed otitis 媒介, 或當許多rod-shaped 細菌被看見在細胞學, 診斷取決於耳朵拖把或針文化aspirate 以微生物的隔離和證明, 被細菌敏感性的決心跟隨。帚形菌屬otitis 有差別的診斷有: Malassezia spp 、其它otitis externa (葡萄球菌intermedius 、腸球菌spp, 變形蟲spp, 鏈球菌spp, 和大腸埃希氏菌的) 次要細菌起因, 和耳的瘤形成或外國身體反應(即狐狸尾巴) 。

管理和治療
  
最初或溫和的傳染

整個耳道應該被審查下來對tympanic 膜、樣品被採取為細胞學和文化, 和耳朵周到地被清洗去除殘骸和油脂。為溫和的案件, 耳道可能柔和地被清洗與ceruminolytic 代理和寬鬆棉花; 更加嚴肅的案件也許要求耳朵的清潔在麻醉之下。
清潔和乾燥劑應該是應用的在洗滌運河以後。
典型治療選擇, 根據滲出液細胞學從耳道: a) 使用一個Tris Edta 產品(TrizEDTA, DermaPet) 運用了15 分鐘在典型fluoroquinolone 之前q 12 h. 的應用[ Tris Edta 從細胞信封提取二價的正離子, 造成phospholipids 和細胞脆弱發行。保險櫃使用既使tympanic 膜被打亂。] 安置典型fluoroquinolone 產品在耳道和按摩很好。產品有: Baytril 耳(enrofloxacin/silver sulfadiazine, 貝爾), 或可注射的enrofloxacin 的1 份在22.7 mg/mL 和增加4 份的Synotic (fluocinolone 丙酮化合物在DMSO, 堡壘推託), 1% □化可體松, 或鹽; Ciloxan 眼科解答、Alcon, 或Floxin 耳, Daiichi 。b) 使用可注射的enrofloxacin 、tris EDTA 、dexamethasone 並且/或者DMSO 的解答在耳道q 裡12 個小時(12 機器語言Tris EDTA 、100 毫克enrofloxacin, 4-8 毫克dexamethasone, 1-2 機器語言醫療成績DMSO) 。c) 使用包含一aminoglycoside 譬如gentamycin 、新黴素、amikacin, 或脫普黴素的典型耳朵治療(Gentocin 耳或Otomax, Schering 耕犁; Tresaderm, Merial; Tobrex 或TobraDex, Alcon) 。d) 使用典型polymyxin B, 與□化可體松並且/或者新黴素的組合。[ 被配製的解答或其它公式化被考慮額外標記治療。]
系統治療: 因為otitis 媒介可能是高的與帚形菌屬otitis externa, 4-16 個星期系統抗生素, 根據文化和敏感性結果由一些專家主張。如果文化結果不是可利用的, 嘗試enrofloxacin 在20 mg/kg/day 或marbofloxacin 在5.5 mg/kg/day 。
包括典型類皮質激素減少膨脹和滲出在耳道。

為慢性或抗性傳染

系統抗生素, 根據文化和敏感性結果由一些專家主張。為otitis 媒介, 系統抗生素也許是需要的12-16 個星期。對典型抗生素的一致耳朵清潔和用途是根本的。
如果上述典型治療未運作, 那麼嘗試這些準備的當中一個: a) 變成銀色sulfadiazine 1 % (Silvadene, 國君) 奶油(混合一份以9 份澆灌和適用於耳朵) 。b) 可注射的ticarcillin (增加30 機器語言不育的水來3 g 瓶ticarcillin; 然後需要1.8 機器語言混合物和增加98.2 機器語言丙烯甘醇) 。冷藏和以前震動很好使用; 槽櫪至少2 個星期。

支援和預防療法

適當的療法被設立為任何部下或伴隨系統疾病。
為週期性或抗性案件, 考慮治療的不適當的治療或期間, 部下的疾病譬如遺傳性過敏症或食物過敏, otitis 媒介, 或耳道相應一致問題(stenotic 運河、長的懶散的耳朵、大量, 等) 。帚形菌屬otitis externa 所有案件應該階段性地被復校(10-14 天) 確定反應對治療, 和對手錶為再現的標誌。療法應該繼續4 個或更多星期保證otitis 立刻不復發, 或堅持以慢性形式。  
Background
Pseudomonas spp., most commonly P. aeruginosa, are common opportunistic pathogens of the external ear canals of dogs, where they contribute to otitis externa. In chronic cases, this infection often leads to otitis media.

A critical and often frequently overlooked aspect of managing Pseudomonas otitis cases is to identify and treat the underlying disease that predisposes the ear canals to secondary infection. If this is not done, the Pseudomonas infection will likely recur, thereby promoting development of strains of organisms with multiple drug resistance.

Common underlying causes of Pseudomonas otitis include: food allergy or hypersensitivity, atopy, keratinization disorders (primary seborrhea), hypothyroidism, Cushing's syndrome, and aural foreign bodies.

While topical local treatment is advocated by all, currently there is a controversy regarding use of systemic antibiotics in the treatment of Pseudomonas otitis externa. One group believes that systemic antibiotics for long periods of time (4-16 weeks) are needed to eliminate the infection, especially if there is middle ear involvement. The other group no longer uses systemic antibiotics (except where there is radiographic evidence of fluid in middle ear or bony lysis of the tympanic bulla), believing that high enough tissue levels are not reached in the ear to kill Pseudomonas. These colleagues utilize topical treatments that clean the canals and provide high concentrations of topical antibiotics (usually enrofloxacin) within the ear canal and middle ear. Systemic antibiotics also contribute more to antibiotic resistance seen in cases of recurrent otitis externa/media.

  
Clinical Findings
Typical clinical findings at presentation include: anorexia; evidence of ear debris, discharge, excoriation, self-mutilation, foul odor, painfulness, excessive scratching, collapse of erect ear; and lowering and shaking of head. On otoscopy, there is hyperplasia and inflammation of the ear canal.

  
Diagnosis
In chronic or unresponsive cases of otitis, suspected or coinfirmed otitis media, or when numerous rod-shaped bacteria are seen on cytology, diagnosis depends upon culture of ear swabs or needle aspirate with isolation and identification of microorganisms, followed by determination of bacterial sensitivity. Differential diagnosis of Pseudomonas otitis includes: Malassezia spp, other secondary bacterial causes of otitis externa (Staphylococcus intermedius, Enterococcus spp, Proteus spp, Streptococcus spp, and Escherichia coli), and otic neoplasia or foreign body reaction (e.g fox tail).

  
Management and Treatment
  
Initial or Mild Infections

The entire ear canal should be examined down to the tympanic membrane, samples taken for cytology and culture, and the ears thoroughly cleaned to remove debris and lipids. For mild cases, the ear canal can be gently cleaned with a ceruminolytic agent and loose cotton; more serious cases may require cleaning of the ear under anesthesia.
A cleaning and drying agent should be applied after cleansing the canals.
Topical treatment alternatives, based on cytology of exudate from ear canal: a) Use A Tris-EDTA product (TrizEDTA, DermaPet) applied 15 min prior to application of topical fluoroquinolone q 12 h. [Tris-EDTA extracts divalent cations from the cell envelope, causing release of phospholipids and cell fragility. Safe to use even if tympanic membrane is disrupted.] Place topical fluoroquinolone product in the ear canal and massage well. Products include: Baytril Otic (enrofloxacin/silver sulfadiazine, Bayer), or 1 part of injectable enrofloxacin at 22.7 mg/mL and add 4 parts of Synotic (fluocinolone acetonide in DMSO, Fort Dodge), 1% hydrocortisone, or saline; Ciloxan Ophthalmic Solution, Alcon, or Floxin Otic, Daiichi. b) Use solution of injectable enrofloxacin, tris EDTA, dexamethasone and/or DMSO in ear canals q 12 hr (12 mL of Tris EDTA, 100 mg enrofloxacin, 4-8 mg dexamethasone, 1-2 mL of medical grade DMSO). c) Use topical ear treatments that contain an aminoglycoside such as gentamycin, neomycin, amikacin, or tobramycin (Gentocin Otic or Otomax, Schering-Plough; Tresaderm, Merial; Tobrex or TobraDex, Alcon). d) Use topical polymyxin B, in combination with hydrocortisone and/or neomycin. [Compounded solutions or other formulations are considered extra-label treatments.]
Systemic treatment: As the likelihood of otitis media is high with Pseudomonas otitis externa, 4-16 weeks of systemic antibiotics, based on culture and sensitivity results are advocated by some experts. If no culture results are available, try enrofloxacin at 20 mg/kg/day or marbofloxacin at 5.5 mg/kg/day.
Include topical corticosteroids to decrease swelling and exudation in the ear canal.

For Chronic or Resistant Infections

Systemic antibiotics, based on culture and sensitivity results are advocated by some experts. For otitis media, systemic antibiotics may be needed for 12-16 weeks. Concurrent ear cleanings and use of topical antibiotics are essential.
If the above topical treatments have not worked, then try one of these preparations: a) Silver sulfadiazine 1 % (Silvadene, Monarch) cream (mix one part with 9 parts water and apply to ears). b) Injectable ticarcillin (add 30 mL sterile water to a 3 g bottle of ticarcillin; then take 1.8 mL of mixture and add 98.2 mL propylene glycol). Refrigerate and shake well before using; stable for at least 2 weeks.

Supportive and Preventive Therapy

Appropriate therapy is instituted for any underlying or accompanying systemic diseases.
For recurrent or resistant cases, consider inappropriate treatment or duration of treatment, underlying disease such as atopy or food allergy, otitis media, or ear canal conformation issues (stenotic canals, long floppy ears, masses, etc). All cases of Pseudomonas otitis externa should be rechecked periodically (10-14 days) to determine the response to treatment, and to watch for signs of recurrence. Therapy should be continued for 4 or more weeks to ensure the otitis does not immediately recur, or persists in chronic form.[/size]

minibabyqq 2006-12-20 04:22

[table][tr][td]轉貼自4682

[size=12px][b][size=5][color=magenta]淋巴球過多症[/color][/size][/b]

Clonality 分析用試樣
clonality 分析用試樣的目的(PCR 為抗原感受器官重新整理, PARR) 將確定是否淋巴細胞的人口易反應或造形術。分析用試樣使用polymerase 鏈式反應(PCR) 放大免疫球蛋白基因(為B 細胞) 或T 細胞感受器官基因(為T 細胞) 。有無數的可能的PCR 產品大小當淋巴細胞的混雜的人口被測試。當被放大的DNA 產品是相同大小, 淋巴細胞人口從同樣前體被獲得和是暗示的一個造形術過程, 雖然慢性E. canis 傳染還導致這和應該被調查。PARR 能並且表明是否淋巴細胞的clonal 人口是B 細胞或T 細胞。

Clonality 分析用試樣被提供在貓但看來是較不敏感的為辨認造形術淋巴細胞人口比在狗。

  
適當的標本
樣品可能包括或者: 血液在LTT; 血液汙跡; 淋巴結或骨髓吐氣(在幻燈片或在LTT); 或身體洞流出。被弄髒了的細胞學準備可能被使用, 僅甲醛水固定的樣品 無法被使用為PARR 。

  
測試評估
淋巴結被評估了從72 條狗以lymphadenopathy 。PARR 的結果表明了85% 敏感性為淋巴腺敵意以92% 特異性(即8% 假的正面) 。假正面案件包括狗與 E. canis (2 個案件); Lyme 疾病、芽苞黴菌病, 和RMSF 1 案件每個) 。

周邊血液的評估由PARR 在86 條狗以multicentric LSA 被證實的診斷由PARR 顯露, 85% 狗有周邊血液介入。在文學, 當由血液汙跡, 20-60% 狗評估與multicentric LSA 有周邊血液介入。研究結果的寬廣的範圍這裡表明視覺血液汙跡分析固有主觀。

評估由~ 20 狗PARR 以 E. canis seropositivity 和周邊血液淋巴球過多症表示, 一些他們有淋巴細胞的clonal 人口。

淋巴細胞Phenotyping
淋巴細胞phenotyping 的用途流程cytometry 和被標記的monoclonal 抗體指揮了反對各種各樣的淋巴細胞CD 抗原。通常, 淋巴細胞phenotyping 可能提供關於白細胞人口的本質的更加詳細的資訊, 因為多個標誌可能同時被審查。Phenotyping 由流程cytometry 可能使用評估堅持淋巴球過多症確定是否細胞是造形術對易反應。

  
適當的標本
樣品可能包括或者: 血液在LTT; 淋巴結或骨髓吐氣(注射吐氣入鹽包含的~ 10% 清液~ 200 uL); 或身體洞流出。骨髓從貓是unabled 被評估此時。

  
用途和研究結果
這個測試是有用的為 評估周邊血液淋巴球過多症 在狗以成熟淋巴球過多症。慢性lymphocytic 白血病(CLL) 幾乎總是T 細胞起源。細胞像造形術傾向於有出軌表現型(丟失了某些細胞表面標誌) 並且因而能被辨認。

這也許幫助以 預知為lymphosacoma 案件。 狗以B 細胞起源LSA 傾向於反應更好治療(平均生存~ 12 m) 比狗以T 細胞起源LSA (GI 和皮膚LSA 在狗傾向於是T 細胞和同一種更加粗劣的預測聯繫在一起) 。大約80% 似犬LSA 案件是B 細胞起源。

淋巴細胞phenotyping 可能幫助在評估胸膜流出在貓。 在LSA, 大多數細胞典型地將是B 淋巴細胞, 但是以chylothorax 有淋巴細胞的混雜的人口, 並且與thymoma, 細胞有細胞有獨特的顯形特徵。

  
FIV 被傳染的貓和CD4:CD8 評估
這類型評估不認為是非常有用的在評估的immunosuppression 或預測在FIV 被傳染的貓。


Clonality Assay
The purpose of the clonality assay (PCR for antigen receptor rearrangements, PARR) is to determine whether a population of lymphocytes are reactive or neoplastic. The assay uses the polymerase chain reaction (PCR) to amplify the immunoglobulin gene (for B cells) or the T-cell receptor gene (for T cells). There are innumerable possible PCR product sizes when a mixed population of lymphocytes is tested. When the amplified DNA products are the same size, the lymphocyte population is derived from the same precursor and is suggestive of a neoplastic process, although chronic E. canis infection also can cause this and should be investigated. PARR can also indicate whether a clonal population of lymphocytes are B-cells or T-cells.

Clonality assay is offered in cats but appears to be less sensitive for identifying neoplastic lymphocyte populations than in dogs.

  
Suitable Specimens
Samples can include either: Blood in LTT; blood smears; lymph node or bone marrow aspirates (on slide or in LTT); or body cavity effusions. Cytological preparations that have been stained can be used, but formalin-fixed samples cannot be used for the PARR.

  
Test Evaluation
Lymph nodes were evaluated from 72 dogs with lymphadenopathy. Results of PARR indicated 85% sensitivity for lymphoid malignancy with 92% specificity (i.e. 8% false positive). The false-positive cases included dogs with E. canis (2 cases) ; Lyme disease, blastomycosis, and RMSF 1 case each).

Evaluation of peripheral blood by PARR in 86 dogs with confirmed diagnosis of multicentric LSA by PARR revealed that 85% of dogs had peripheral blood involvement. In the literature, when evaluated by blood smears, 20-60% of dogs with multicentric LSA have peripheral blood involvement. The broad range of findings here indicates the inherent subjectivity of visual blood smear analysis.

Evaluation by PARR of ~ 20 dogs with E. canis seropositivity and peripheral blood lymphocytosis showed that a few of them have clonal populations of lymphocytes.

Lymphocyte Phenotyping
Lymphocyte phenotyping uses flow cytometry and labeled monoclonal antibodies directed against a variety of lymphocyte CD antigens. Generally, lymphocyte phenotyping can give more detailed information about the nature of the white blood cell populations, because multiple markers can be examined simultaneously. Phenotyping by flow cytometry can be used to evaluate persistent lymphocytosis to determine whether the cells are neoplastic versus reactive.

  
Suitable Specimens
Samples can include either: Blood in LTT; lymph node or bone marrow aspirates (inject aspirates into ~ 200 uL of saline containing ~ 10% serum ); or body cavity effusions. Bone marrow from cats is unabled to be evaluated at this time.

  
Uses and Findings
This test is useful for evaluating peripheral blood lymphocytosis in dogs with mature lymphocytosis. Chronic lymphocytic leukemia (CLL) is almost always of T-cell origin. Cells tend to have an aberrant phenotype (have lost certain cell surface markers) and are thus able to be identified as neoplastic.

This may help with prognostication for lymphosacoma cases. Dogs with B-cell origin LSA tend to respond better to treatment (average survival ~ 12 m) than dogs with T-cell origin LSA (GI and cutaneous LSA in dogs tend to be T-cell and are associated with a poorer prognosis). Approximately 80% of canine LSA cases are of B-cell origin.

Lymphocyte phenotyping can help in evaluating pleural effusions in cats. In LSA, the vast majority of cells will typically be B lymphocytes, whereas with chylothorax there is a mixed population of lymphocytes, and with thymoma, the cells have cells have unique phenotypic characteristics.

  
FIV infected cats and CD4:CD8 evaluation
This type of evaluation is not considered to be very helpful in evaluating immunosuppression or prognosis in FIV-infected cats.[/size]
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minibabyqq 2006-12-20 04:22

轉貼自4682

[size=12px][b][size=5][color=magenta]鈣混亂 CALCIUM DISORDERS[/color][/size][/b]

_ 背景
_ 鈣(加州) 是required 為許多重要細胞內和細胞外身體作用, 以及為骨骼支持。_ 關於50-60% 總加州是在這ionized 形式(Ca++), 是required 為各種各樣作用, 包括: _ enzymatic 反應, 膜運輸和穩定, 血液凝固, 神經傳導, neuromuscular 傳輸, 肌肉收縮, 血管光滑肌肉口氣, 激素分泌物, 骨頭形成和吸回, 控制肝糖朊新陳代謝, 和細胞成長和分裂。_ 反常清液加州集中可以是診斷價值, 和可以貢獻對發展損害和臨床標誌疾病。

_ _ 章程清液加州集中是複雜和要求這聯合行動副甲狀腺激素, 維生素D 代謝產物和calcitonin 。_ 副甲狀腺激素和calcitriol 是這主要管理者加州homeostasis 。_ 副甲狀腺激素是大負責任為這分鐘對分鐘控制清液Ca++ 集中, 但是calcitriol 維護每日控制。_ 這肚腑, 腎臟, 和骨頭是這主要目標器官受影響由加州管理激素。_ 這些互作用允許保護加州在這細胞外流體容量由腎臟筒形重吸收, increased 小腸運輸加州從這節食, 和內部再分配加州從骨頭。_ 這骨骼服務和主要供應加州和磷當小腸吸收和腎臟重吸收是不充分對維護正常清液加州集中。_ 骨頭加州動員是重要在這深刻章程血液加州。

_ _ 細胞外Ca++ 集中是這分數總加州是活躍regulated 。_ 當血液加州集中下落, PTH 分泌物是stimulated 。_ 副甲狀腺激素施加指揮作用在骨頭和腎臟和間接作用在這肚腑通過calcitriol 。_ PTH 增加綜合calcitriol, 反過來, 增加加州吸收從這肚腑。

_ _ Calcitonin 是小多縮氨基酸激素synthesized 由C 細胞在這甲狀腺封墊, 和服務重要角色在limiting 這程度postprandial hypercalcemia 。_ 這行動, 在音樂會與PTH, 行動對維護清液Ca++ 集中在之內狹窄範圍。

_ _ 維生素D (calciferol) 是classified 和secosteroid 激素, 與幾重要活躍代謝產物。_ 這最重要步在bioactivation 維生素D 發生當這25-hydroxyvitamin 形式是進一步羥基化對calcitriol 在這接近tubule 這腎臟。

竟管唯一Ca++ 分數是生理地活躍的, 動物的加州狀態典型地根據清液共計加州集中的評估, 因為總清液加州集中被承擔直接地是比例與Ca++ 。在狗, 總清液加州集中被改正或 “定期地” 也 “被調整” 相對清液共計白蛋白, 每當白蛋白含量是在3.5 mg/dL 以下。但是, 問題依然是是否總清液加州可能被使用準確地預言Ca++ 。1500 個案件的一項最近回顧展研究發現了診斷discordance 在總加州和Ca++ 27-37% 之間和在36-54% 狗的亞人口之間以慢性腎衰竭。因而, hypercalcemia 被過高估計, 並且hypocalcemia 被低估。在> 400 個似貓的案件平行的回顧展回顧, discordancy 在總加州之間和Ca++ 是~25% 。因而, 清液Ca++ 必須被測量準確地估計加州狀態。

  
Ca++ 的測量
Ca++ 的準確決心要求, 樣品正確地被收集和被處理。酸性酸鹼度傾向加州的離解從蛋白質和增加相當數量Ca++ 在樣品, 但是鹼性酸鹼度減少相當數量Ca++ 。混合清液與空氣導致被減少的Ca++ 和增加的酸鹼度。

當Ca++ 可能被測量在被肝素化的整體血液, 這不被推薦當肝素也許干涉Ca++ 的測量。硅樹脂分離器管不應該被使用因為被電離的加州集中增加的歸結於加州發行從硅樹脂膠凝體。

清液應該被收集通過vacutainer 直接地入清液vacutainer 管。血液應該允許凝結, 和由離心法然後分離。從管去除清液, 管不能被打開。針附有到一個空的注射器應該被使用撤出清液從vacutainer 管, 通過紅頂。這清液然後轉移到第二支清液vacutainer 管通過針避免介紹任一空氣入樣品。清液(絕氧) 收集了這樣並且存放在4C 是穩定的7 天, 允許時刻為發貨對參考實驗室為Ca++ 的測量。

Background
Calcium (Ca) is required for many vital intracellular and extracellular body functions, as well as for skeletal support. About 50-60% of total Ca is in the ionized form (Ca++), which is required for a wide variety of functions, including: enzymatic reactions, membrane transport and stability, blood coagulation, nerve conduction, neuromuscular transmission, muscle contraction, vascular smooth muscle tone, hormone secretion, bone formation and resorption, control of hepatic glycogen metabolism, and cell growth and division. Abnormal serum Ca concentrations may be of diagnostic value, and may contribute to development of lesions and clinical signs of disease.

Regulation of serum Ca concentration is complex and requires the integrated actions of parathyroid hormone, vitamin D metabolites and calcitonin. Parathyroid hormone and calcitriol are the main regulators of Ca homeostasis. Parathyroid hormone is largely responsible for the minute-to-minute control of serum Ca++ concentration, whereas calcitriol maintains day-to-day control. The intestine, kidney, and bone are the major target organs affected by Ca regulatory hormones. These interactions allow conservation of Ca in the extracellular fluid volume by renal tubular reabsorption, increased intestinal transport of Ca from the diet, and internal redistribution of Ca from bone. The skeleton serves as a major supply of Ca and phosphorus when intestinal absorption and renal reabsorption are inadequate to maintain normal serum Ca concentrations. Bone Ca mobilization is important in the acute regulation of blood Ca.

Extracellular Ca++ concentration is the fraction of total Ca that is actively regulated. When blood Ca concentration falls, PTH secretion is stimulated. Parathyroid hormone exerts direct effects on bone and kidney and indirect effects on the intestine through calcitriol. PTH increases synthesis of calcitriol, which, in turn, increases Ca absorption from the intestine.

Calcitonin is a small polypeptide hormone synthesized by C-cells in the thyroid gland, and serves an important role in limiting the degree of postprandial hypercalcemia. This action, in concert with PTH, acts to maintain serum Ca++ concentration within a narrow range.

Vitamin D (calciferol) is classified as a secosteroid hormone, with several important active metabolites. The most important step in bioactivation of vitamin D occurs when the 25-hydroxyvitamin form is further hydroxylated to calcitriol in the proximal tubule of the kidney.

Despite the fact that only the Ca++ fraction is physiologically active, the Ca status of animals has typically been based on evaluation of serum total Ca concentration, as total serum Ca concentration has been assumed to be directly proportional to Ca++. In dogs, total serum Ca concentrations are also routinely “corrected” or “adjusted” relative to the serum total albumin, whenever the albumin concentration is below 3.5 mg/dL. However, a question has remained about whether total serum Ca can be used to accurately predict Ca++. A recent retrospective study of over 1500 cases found diagnostic discordance between total Ca and Ca++ of 27-37% and between 36-54% of the subpopulation of dogs with chronic renal failure. Thus, hypercalcemia is overestimated, and hypocalcemia is underestimated. In a parallel retrospective review of > 400 feline cases, discordancy between total Ca and Ca++ was ~25%. Thus, serum Ca++ must be measured to accurately assess Ca status.

  
Measurement of Ca++
Accurate determination of Ca++ requires that samples be collected and processed correctly. Acidic pH favors dissociation of Ca from protein and increases the amount of Ca++ in the sample, whereas alkaline pH decreases the amount of Ca++. Mixing of serum with air results in decreased Ca++ and increased pH.

While Ca++ can be measured in heparinized whole blood, this is not recommended as heparin may interfere with measurement of Ca++. Silicone-separator tubes should not be used because ionized Ca concentration is increased due to release of Ca from the silicone gel.

Serum should be collected via vacutainer directly into a serum vacutainer tube. Blood should be allowed to clot, and then separated by centrifugation. To remove serum from the tube, the tube must not be opened. A needle attached to an empty syringe should be used to withdraw serum from the vacutainer tube, through the red top. This serum is then transferred to a second serum vacutainer tube through the needle to avoid introducing any air into the sample. Serum collected this way (anaerobically) and stored at 4C is stable for up to 7 days, which permits time for shipment to a reference laboratory for measurement of Ca++.[/size]

minibabyqq 2006-12-20 04:23

[table][tr][td]轉貼自4682

[size=12px][b][size=5][color=magenta]犬貧血症[/color][/size][/b]

狗(或貓的) 臨床介紹以貧血症隨部下的疾病變化隨貧血症的嚴肅和期間, 和。那裡也許是少量歷史研究結果與貧血症有關並且它經常是偶然發生的發現labwork 執行。也許並且被描述作為慵倦、弱點或被減少的鍛煉容忍) 的無精打采(並且inappetence, 雖然共同的怨言在狗以貧血症, 是未指明的研究結果。其它歷史怨言看在有貧血症病人可能包括崩潰、出血或hemolysis 的中略語, 和證據(icterus 或pigmenturia) 。您可能需要請求客戶更加具體的問題顯露這背景。

仔細的體格檢查可能提供有用的資訊關於貧血症。體格檢查研究結果在狗以貧血症取決於貧血症部下的疾病過程和嚴肅。研究結果也許包括黏膜pallor, 呼吸迫促, 心動過速, 一句軟的心臟收縮的心臟私語(不大聲比等級III/IV), 並且脈衝改變(運動過強的大腿骨脈衝) 。動物以出血性的震動有上述研究結果除了脈衝將是微弱的, 肢冷卻, 並且心臟私語也許或不能是存在。其它研究結果與相關具體類型貧血症也許包括icterus (hemolysis), 熱病(感染, 免疫被斡旋, 或造形術疾病), 出血(hemostatic 問題, 精神創傷), hepatosplenomegaly (免疫斡旋的疾病、瘤形成、spenic 扭力, 傳染), 和內分泌脫髮症(甲狀腺機能不足) 。

  
貧血症的實驗室分類
  
貧血症的分類是重要步在確定起因、最佳的方法對治療, 和預測。

嚴肅根據血流比容計 (被包裝的細胞容量, PCV) 。一個任意分類
嚴肅
PCV

溫和
30-37%

適度
20-30%

嚴厲
10-20%

重要
< 10%


溫和, non-regenerative 貧血症由慢性疾病造成, 經常不能值得追求。慢性疾病貧血症在狗典型地不生產一個血流比容計< 20%, 因此巨大貧血症可能是非常有用的在確定起因。
再生對non-regenerative
有許多實驗室顯示, 貧血症也許是再生的, 包括macrocytosis 和或許hypochromasia (被減少的MCHC), 增加的Howell 快活的身體、normoblastemia 、polychromasia, 和reticulocytosis anisocytosis, 和出現。Antech 診斷等級polychromasia 在以下等級:
等級
% 多色的RBCs

1+
2-5%

2+
6-10%

3+
11-15%

4+
> 15%


黃金本位制為評估是否貧血症再生或non-regenerative 是出現或缺乏和程度reticulocytosis 。校正的reticulocyte 百分比(%) 或absolute reticulocyte 數字必需改正未加工的reticulocyte % 為貧血症的作用。
為什麼這是重要?
  
為例, 考慮一reticulocyte % 5 。五% reticulocytes 在一條狗與PCV 20% 是兩次許多reticulocytes 作為5% reticulocytes 在一條狗與PCV 10% 。有2 種方式改正reticuloycte % 為程度貧血症, 如下:

校正的retic. % =

reticulocyte % x
(患者PCV%)
40


一校正的reticulocyte % < 1% 表明non-regenerative 貧血症。更高校正的價值, 更加強烈再生反應。

Absolute reticulocyte 數字= reticulocyte % x RBC 計數

absolute reticulocyte 計數< 60,000 cells/.l 表明non-regenerative 貧血症。更高reticulocyte 計數, 更加強烈再生反應。

這些2 個方法確切地做同樣事(改正為貧血症的作用) 並且給同樣解釋。

reticulocyte 生產索引, 是校正的reticulocyte % 的修改, 不是根本價值和它的有效性被問了。


  
規則出口為再生貧血症
  

出血

Peracute (分鐘對幾小時) 並且深刻(小時對幾天) 失血最初地non-regenerative 。一個充分的再生反應的發展需要5-7 天在貧血症以後起始。

慢性失血貧血症也許成為non-regenerative 和microcytic 由於鋼缺乏。

出血也許歸結於一種coagulopathy 或對某一地方疾病(即, 腫瘤、潰瘍, 精神創傷) 。

出血經常隱密, 這樣, 缺乏可看見的靈菌無法使用排除它作為起因為貧血症。


Hemolysis (被減少的RBC 壽命)

願發生內部或額外vascularly, 和願歸結於內在紅細胞異常(譬如丙酮酸鹽kinase 或phosphofructokinase 缺乏) 或混亂在紅細胞之外(AIHA 、鋅或蔥toxicoses 、hypophosphatemia 、蛇envenomation, 和DIC) 。

深刻溶血貧血症也許non-regenerative 。一個充分的再生反應的發展需要5-7 天在貧血症以後起始。

免疫斡旋的溶血貧血症可能還non-regenerative, 如果它介入骨髓前體攻擊。

耐心對某人特徵的描述, 或pigmenturia 、橙色凳子, 或毒素曝光(蔥, 鋅) 客戶報告可能增加懷疑臨床索引為hemolysis 。支持hemolysis 的實驗室反常性當貧血症的起因有: 明顯再生貧血症出現與Heinz 身體一正常總蛋白含量、hyperbilirubinemia 、反常bilirubinuria 、hemoglobinemia 、hemoglobinuria 、紅細胞autoagglutination 、出現或許多spherocytes 一起。


  
何時骨髓評估是必要的?
  
徵兆為骨髓評估包括non-regenerative 血細胞減少貧血症沒有明顯的起因, 出現或貧血症和嗜中性白細胞減少症, 並且"疾風" 或非典型細胞報告在周邊血液抹上回顧。

  
規則出口為Non-Regenerative 貧血症:
  

慢性疾病貧血症

腎衰竭

Endocrinopathies

Addison.s 疾病

甲狀腺機能不足

AIHA 與骨髓介入(成熟性拘捕或紅細胞發育不全) 。

骨髓疾病譬如myelodysplasia 、hematopoietic 瘤形成、myelophthisis (擁擠在骨髓外面由癌細胞), 發育不全的貧血症(phenylbutazone 、女性荷爾蒙、苯巴比妥, 輻射), ehrlichiosis, 和系統真菌病。

營養

鋼缺乏

葉酸缺乏(偶爾地參見在嚴厲小腸疾病)

蛋白質卡路里營養不良

早期的出血或hemolysis

Clinical presentation of dogs (or cats) with anemia varies with the severity and duration of the anemia, and with the underlying disease. There may be few historical findings related to anemia and often it is an incidental finding when labwork is performed. Listlessness (which may also be described as lethargy, weakness or reduced exercise tolerance) and inappetence, although common complaints in dogs with anemia, are non-specific findings. Other historical complaints seen in patients with anemia can include collapse, syncope, and evidence of hemorrhage or hemolysis (icterus or pigmenturia). You may need to ask the client more specific questions to reveal this background.

A careful physical examination can provide helpful information regarding anemia. Physical examination findings in dogs with anemia depend on the underlying disease process and severity of anemia. Findings may include mucous membrane pallor, tachypnea, tachycardia, a soft systolic heart murmur (not louder than grade III/IV), and pulse changes (hyperkinetic femoral pulses). Animals with hemorrhagic shock have the above findings except that pulses will be weak, extremities cool, and a heart murmur may or may not be present. Other findings associated with specific types of anemia may include icterus (hemolysis), fever (infectious, immune-mediated, or neoplastic disease), hemorrhages (hemostatic problem, trauma), hepatosplenomegaly (immune-mediated disease, neoplasia, spenic torsion, infection), and endocrine alopecia (hypothyroidism).

  
Laboratory Classification of Anemia
  
Classification of anemia is an important step in determining the cause, best approach to treatment, and prognosis.

Severity based on hematocrit (packed cell volume, PCV) ?an arbitrary classification
Severity
PCV

Mild
30–37%

Moderate
20–30%

Severe
10–20%

Critical
<10%


Mild, non-regenerative anemias are often caused by chronic disease and may not be worth pursuing. Anemia of chronic disease in dogs typically does not produce a hematocrit <20%, so the magnitude of anemia can be very helpful in determining cause.
Regenerative versus non-regenerative
There are many laboratory indicators that an anemia may be regenerative, including macrocytosis and perhaps hypochromasia (decreased MCHC), increased anisocytosis, and presence of Howell Jolly bodies, normoblastemia, polychromasia, and reticulocytosis. Antech Diagnostics grades polychromasia on the following scale:
Grade
% Polychromatic RBCs

1+
2–5%

2+
6–10%

3+
11–15%

4+
>15%


The gold standard for evaluating whether anemia is regenerative or non-regenerative is the presence or absence and degree of reticulocytosis. A corrected reticulocyte percentage (%) or absolute reticulocyte number is required to correct the raw reticulocyte % for the effect of anemia.

Why is this Important?
  
As an example, consider a reticulocyte % of 5. Five % reticulocytes in a dog with a PCV of 20% is twice as many reticulocytes as 5% reticulocytes in a dog with a PCV of 10%. There are 2 ways to correct the reticuloycte % for the degree of anemia, as follows:

Corrected retic. % =

reticulocyte % x
(patient PCV%)
40


A corrected reticulocyte % of < 1% indicates a non-regenerative anemia. The higher the corrected value, the stronger the regenerative response.

Absolute reticulocyte number = reticulocyte % x RBC count

An absolute reticulocyte count of <60,000 cells/µl indicates a non-regenerative anemia. The higher the reticulocyte count, the stronger the regenerative response.

These 2 methods do exactly the same thing (correct for the effect of anemia) and give the same interpretation.

The reticulocyte production index, which is a modification of the corrected reticulocyte %, is not an essential value and its validity has been questioned.


  
Rule Outs for Regenerative Anemia
  

Hemorrhage

Peracute (over minutes to hours) and acute (over hours to days) blood loss will initially be non-regenerative. Development of a full regenerative response takes 5–7 days after the onset of anemia.

Chronic blood loss anemia may become non-regenerative and microcytic due to iron deficiency.

Hemorrhage may be due to a coagulopathy or to some local disease (eg, tumor, ulcer, trauma).

Hemorrhage is often occult, such that the lack of visible bleeding cannot be used to exclude it as a cause for anemia.


Hemolysis (decreased RBC lifespan)

May occur intra- or extra-vascularly, and may be due to intrinsic red cell abnormalities (such as pyruvate kinase or phosphofructokinase deficiencies) or disorders outside the red cell (AIHA, zinc or onion toxicoses, hypophosphatemia, snake envenomation, and DIC).

Acute hemolytic anemia may be non-regenerative. Development of a full regenerative response takes 5–7 days after the onset of anemia.

Immune-mediated hemolytic anemia also can be non-regenerative, if it involves attack of bone marrow precursors.

Patient signalment, or client report of pigmenturia, orange stool, or toxin exposure (onion, zinc) can increase the clinical index of suspicion for hemolysis. Laboratory abnormalities that support hemolysis as a cause of anemia include: presence of marked regenerative anemia along with a normal total protein, hyperbilirubinemia, abnormal bilirubinuria, hemoglobinemia, hemoglobinuria, red cell autoagglutination, presence of Heinz bodies or numerous spherocytes.


  
When is Bone Marrow Evaluation Necessary?
  
Indications for bone marrow evaluation include non-regenerative anemias without apparent cause, presence of pancytopenia or anemia and neutropenia, and reports of "blasts" or atypical cells on peripheral blood smear review.

  
Rule Outs for Non-Regenerative Anemias:
  

Anemia of chronic disease

Renal failure

Endocrinopathies

Addison𠏋 disease

Hypothyroidism

AIHA with bone marrow involvement (maturation arrest or red cell hypoplasia).

Bone marrow disease such as myelodysplasia, hematopoietic neoplasia, myelophthisis (crowding out of marrow by cancer cells), aplastic anemia (phenylbutazone, estrogen, phenobarbital, radiation), ehrlichiosis, and systemic mycoses.

Nutritional

Iron deficiency

Folic acid deficiency (seen occasionally in severe intestinal disease)

Protein-calorie malnutrition

Early hemorrhage or hemolysis[/size]
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[/td][/tr][/table]

minibabyqq 2006-12-20 04:24

[table][tr][td]轉貼自4682

[size=12px][color=magenta][b][size=5]標準根運河療法 STANDARD ROOT CANAL THERAPY[/size]  [/b]
[/color][size=12px]這是最共同的治療完成在我們的提及牙齒實踐。執行主要為深齲損害在人, 但主要為破碎的牙在動物中。所有牙死亡的起因是一個徵兆為這個做法。

[b]徵兆[/b] [indent]任何牙死亡的起因
A 。 [b][i]破碎的(被傷的) 牙[/i][/b]
B 。[b][i] 深洞[/i][/b]
C. 精神創傷對導致死亡的牙, 但沒有牙破裂
D 。 [b][i]下頜破裂[/i][/b] 對牙的那損傷供血。
E 。 [b][i]嚴厲地破舊的牙[/i][/b]
[/indent][b]技術[/b]
[indent]1 。患者沉著並且牙被探索確定是否齲或
破裂延伸到黏漿狀物質分庭。
2. 牙齒射線照相被暴露確定是否牙是足夠成熟的
接受這個療法的形式。並且確信, 沒有根破裂或
會減少預測為做法的其它牙齒疾病。
3. 根據介入的牙和類型破裂, 訪問對根運河被製作
被做通過破裂站點或其他站點促進清洗和填裝
運河。
4. 使用endodontic 文件, 害病的神經、血管和牙結構是
從運河去除。運河被洗滌(漂洗) 用一種抗菌解答。當運河被清洗, 它被烘乾以不育, 吸收劑紙點(被滾動紙。
5. 根運河被填裝(obturated) 避免牙成為re 傳染。
6. 手術後射線照相被暴露保證運河的適當的積土
7. 存取孔和破裂站點被填裝。
[/indent]牙現在是一樣強的像它曾經, 並且制約不被安置在吃在崗位麻醉劑期間以後是結束(通常12 個小時) 。復校射線照相被推薦在6 個月和然後每年或如此。如果額外力量或大小渴望, [b][i]冠療法[/i][/b] 可能執行。



[b]STANDARD ROOT CANAL THERAPY[/b]

This is the most common treatment done in our referral dental practice. Performed mostly for deep caries lesions in people, but mostly for fractured teeth in animals. Any cause of tooth death is an indication for this procedure.

[b]INDICATIONS[/b]
[indent]Any cause of tooth death
A. [b][i]Fractured (broken) teeth[/i][/b]
B.[b][i] Deep Cavities[/i][/b]
C. Trauma to tooth that causes death, but without fracture of tooth
D. [b][i]Jaw fractures[/i][/b] that damages blood supply to tooth.
E. [b][i]Severely worn teeth[/i][/b]
[/indent][b]TECHNIQUE[/b]
[indent]1. The patient is sedated and the tooth is explored to determine whether caries or
fracture extends into pulp chamber.
2. A dental radiograph is exposed to determine whether the tooth is mature enough to
undergo this form of therapy. Also to make sure that there is no root fractures or
other dental disease that would decrease the prognosis for the procedure.
3. Depending on the tooth involved and type of fracture, access to the root canal made
be made through the fracture site or another site to facilitate cleaning and filling the
canal.
4. Using endodontic files, the diseased nerves, blood vessels and tooth structure are
removed from the canal. The canal is lavaged (rinsed) with an antibacterial solution. When the canal is cleaned, it is dried with sterile, absorbent paper points (rolled up pieces of paper.
5. The root canal is filled (obturated) to avoid the tooth becoming re-infected.
6. A post-operative radiograph is exposed to ensure proper fill of the canal
7. The access hole and fracture site are filled.
[/indent]The tooth is now as strong as it will ever be, and no restrictions are placed on eating after the post-anesthetic period is over (usually 12 hours). Recheck radiographs are recommended at 6 months and then every year or so. If extra strength or size is desired, [b][i]crown therapy[/i][/b] can be performed.[/size][/size]
[/td][/tr][tr][td]
[/td][/tr][/table]

minibabyqq 2006-12-20 04:24

[table][tr][td]轉貼自4682

[size=12px][size=5][color=magenta][b]重要PULPOTOMY VITAL PULPOTOMY[/b][/color][/size]  [url=http://www11.discuss.com.hk/misc.php?action=emailfriend&tid=2813906][img]http://www11.discuss.com.hk/images/discuss_style/emailtofriend3.gif[/img][/url]

[size=12px]這個做法與根運河不同因為牙活(重要) 。
這是一個更加容易的做法執行因為唯一頂面(冠狀) 部份被去除。
有二個主要原因, 這個做法執行在獸醫牙科方面: [list=1][*][b][i]冠減少 [/i][/b]。為二個不同原因
a. 正牙學問題導致精神創傷對口頭軟的組織
b. 解除武裝的規程減少損傷由狠毒動物造成。[*][b][i]牙新鮮的破裂[/i][/b]
這做允許牙繼續成熟和獲取力量。這是最可貴的在發育未全的牙裡, 做法執行希望它將保留對生活至關重要或至少長期足夠將成熟(apexify) 並且將接受一個 [b][i]標準根運河做法[/i][/b]。[/list][b]技術[/b]
[list=1][*]前有效的牙齒射線照相被暴露確定成熟水平和如果任何
其它病理學是存在。[*]患者接受一完全牙齒預防(清潔) 並且嘴被漂洗以一種抗菌解答減少細菌汙染。[*]地方麻醉的射入被執行減少痛苦在期間和以後
麻醉。[*]冠被降下(如果需要) 。[*]所有害病的黏漿狀物質組織被去除與高速bur (牙齒鑽子) 。[*]靈菌被控制以不育的紙點在運河允許凝塊形成。[*]+氧化鈣被安置入運河:
這是抗菌的, 和還將激怒黏漿狀物質和將導致它制定牙結構(牙質) 防護層數。這將減少未來細菌汙染的機會。[*]中間層數被安置在+氧化鈣絕緣黏漿狀物質和行動作為一個基地為最後的恢復。[*]最後的補藥被安置在通入站點。[*]手術後射線照相被暴露保證適當的積土。
復校射線照相是重要的在這些規程。有失敗的機會沒有向外臨床標誌。多數寵物將遭受在沉默。[/list]
[b]破舊的牙[/b]

[align=left]有許多起因為破舊的牙在狗或貓。最共同是pruritis (發癢和嚼), 因為頭髮是非常磨蝕。這共同地將導致嚴厲佩帶門牙, 雖然犬可能並且是受影響的。這對gumline, 和偶爾地下面可能一直進步。嚼在網球或其它磨蝕玩具的狗(認為網球作為一個計分的墊), 經常將佩帶他們的更小的前面面頰牙(前臼齒), 和犬的後面方面。這磨蝕won.t 做在一天中, 但嚼每天幾年來可能導致重大穿戴。其它起因嚼在事如籬笆, 將磨損犬的後側方。終於, 咬合不良可能導致二顆牙一起來和佩帶在彼此。 [/align][align=left]破舊的牙看起來像破碎的牙, 但通常不是一個重大問題。如果穿戴慢慢地發生, 牙反應將由制定額外牙結構(牙質) 以回應牙損失保護黏漿狀物質。這與我們的牙反應深洞的方法是相似。如果這發生, 牙一般將停留活, 和不會要求任一種另外的療法。被暴露的牙質在牙中間將弄髒淺棕褐色對中等褐色。儀器不會能進入根運河。[/align][align=left]如果牙是殘破的, 或穿戴發生太快速或繼續太, 牙將變得endodontically 包含。這些牙一般將有黑褐色染黑中心, 將允許儀器入運河。這些牙要求或 [b][i]根運河療法[/i][/b] 或 [b][i]提取[/i][/b]。 [/align][align=left]有事例, 然而, 牙don.t 跟隨上述描述。偶爾, 穿戴可能發生足夠迅速傳染牙, 然而牙將居住足夠長期制定牙質防護層數在它死之前。這些牙將看起來像一顆重要, 被佩帶的牙在外部, 但將是死在裡面。唯一的方式肯定告訴是由牙齒放射學。死的牙將有一條更寬的根運河比他們的重要鄰居。因此, 我推薦射線照相在所有顯著破舊的牙。[/align][align=left]This procedure differs from a root canal in that the tooth is still alive (vital).
It is an easier procedure to perform as only the top (coronal) portion is removed.
There are two main reasons that this procedure is performed in Veterinary Dentistry:[/align][list=1][*][b][i]Crown Reduction [/i][/b]?for two different reasons
a. Orthodontic problems causing trauma to oral soft tissues
b. Disarming procedures to reduce the damage caused by vicious animals.[*][b][i]Fresh fractures of teeth[/i][/b]
This is done to allow the tooth to continue to mature and gain strength. This is most valuable in immature teeth, where the procedure is performed in the hopes that it will remain vital for life or at least long enough to mature (apexify) and accept a [b][i]standard root canal procedure[/i][/b].[/list][b]Technique[/b]
[list=1][*]A pre-operative dental radiograph is exposed to determine maturity level and if any
other pathology is present.[*]The patient receives a complete dental prophylaxis (cleaning) and the mouth is rinsed with an antimicrobial solution to reduce bacterial contamination.[*]A local anesthetic injection is administered to decrease pain during and after
anesthesia.[*]The crown is lowered (if necessary).[*]All diseased pulp tissue is removed with a high-speed bur (dental drill).[*]Bleeding is controlled with sterile paper points in the canal allowing a clot to form.[*]Calcium hydroxide is placed into the canal:
This is antibacterial, and also will irritate the pulp and cause it to lay down a protective layer of tooth structure (dentin). This will decrease the chance of future bacterial contamination.[*]An intermediate layer is placed over the calcium hydroxide to insulate the pulp and act as a base for the final restoration.[*]The final restorative is placed over the access site.[*]A post-operative radiograph is exposed to ensure proper fill.
Recheck radiographs are critical in these procedures. There is a chance of failure without outward clinical signs. Most pets will suffer in silence.[/list][b]WORN TEETH[/b]
[align=center][table=90%][tr][td=1,1,70%][align=left]There are many causes for worn teeth in a dog or cat. The most common is pruritis (itching and chewing), because hair is very abrasive. This will commonly cause severe wearing of the incisors, although the canines can also be affected. This can progress all the way to the gumline, and occasionally below. Dogs that chew on tennis balls or other abrasive toys (think of tennis ball as a scoring pad), will often wear their smaller front cheek teeth (premolars), and the back aspect of the canines. This abrasion won㦙 do much over the course of one day, but chewing every day for years can cause significant wear. Another cause is chewing on things like fences, which will wear down the backside of the canines. Finally, malocclusions can cause two teeth to come together and wear on each other. [/align][/td][td=1,1,30%][align=center][img=255,195]http://www.avds-online.org/images/resourceimages/wornteeth1.jpg[/img]
The wear on this tooth is from the mandibular canine.[/align][/td][/tr][/table][/align]
[align=left]Worn teeth look like fractured teeth, but usually are not a significant problem. If the wear occurs slowly, the tooth will respond by laying down extra tooth structure (dentin) in response to the tooth loss to protect the pulp. This is similar to the way that our teeth respond to deep cavities. If this occurs, the tooth will generally stay alive, and not require any additional therapy. The exposed dentin in the middle of the tooth will stain a light tan to medium brown. An instrument will not be able to enter the root canal. [/align][align=center][table=90%][tr][td=1,1,40%][align=center][img=255,195]http://www.avds-online.org/images/resourceimages/wornteeth2.jpg[/img]
Chronic wear many times results in deposition of reparative dentin, the dark discoloration seen on this tooth. If wear is slow the tooth may survive by this mechanism. Rapid wear rarely produces a significant response and tooth vitality may be compromised.[/align][/td][td=1,1,60%][align=left]If the tooth is broken, or the wear occurs too fast or continues too far, the tooth will become endodontically involved. These teeth will generally have a dark brown to black center, which will allow an instrument into the canal. These teeth require either [b][i]root canal therapy[/i][/b] or [b][i]extraction[/i][/b]. [/align][align=left]There are instances, however, that the teeth don㦙 follow the above descriptions. On occasion, wear can occur quickly enough to infect the tooth, however the tooth will live long enough to lay down a protective layer of dentin before it dies. These teeth will look like a vital, worn tooth on the outside, but will be dead on the inside. The only way to tell for sure is by dental radiology. Dead teeth will have a wider root canal than their vital neighbors. For this reason, I recommend radiographs on all significantly worn teeth.[/align][/td][/tr][/table][/align][/size][/size]
[/td][/tr][tr][td]
[/td][/tr][/table]

minibabyqq 2006-12-20 04:25

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[size=12px][size=5][color=magenta][b]一般Patellar Luxation 資訊[/b][/color][/size][/size]
[size=12px][size=5][color=red][/color][/size] [/size]
[size=12px][size=5][color=red][/color][/size] [/size]
[size=12px][size=5][color=black][b]General Patellar Luxation Information[/b][/color][/size]  [url=http://www11.discuss.com.hk/misc.php?action=emailfriend&tid=2816210][img]http://www11.discuss.com.hk/images/discuss_style/emailtofriend3.gif[/img][/url]

[size=12px]什麼是Patellar Luxation?臏骨, 或膝蓋骨, 是抑止聯接(膝蓋的) 一部分。在patellar luxation 、膝蓋骨luxates, 或流行音樂不恰當, 或在一個中間或側向位置。
[url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fglossary.html#bilateral][color=#800080]雙邊[/color][/url] 介入是最共同, 但單邊不是不凡的。動物能是受影響的當他們是8 個星期年齡的時候。最著名發現是敲膝蓋(膝valgum) 姿態。臏骨通常是可減少的, 並且中間抵押韌帶的laxity 也許是顯然的。抑止聯接的中間retinacular 組織經常變厚, 並且腳能看側向地扭轉當重量被安置在肢體。
Patellar Luxation 類別Patellar luxations 歸入幾個類別: [/size]
[size=12px][list=1][*][url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fpatluxgeninfo.html#medial][b][color=#800080]中間luxation; 玩具、縮樣, 和大養殖[/color][/b][/url][*][b][url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fpatluxgeninfo.html#lateraltoy][color=#800080]側向luxation; 玩具和縮樣養殖[/color][/url][/b][*][b][url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fpatluxgeninfo.html#laterallarge][color=#800080]側向luxation; 大和巨人養殖。 [/color][/url][/b][*]Luxation 起因於精神創傷; 各種各樣的養殖, 沒有對證明過程的重要性。[/list][/size]
第號1, 2 和3 或為人所知是可遺傳的或強烈被懷疑。

中間Luxation 在玩具、縮樣, 和大養殖雖然luxation 不能是存在出生時, 導致這些luxations 的解剖殘疾是存在在那時間和負責對隨後週期性patellar luxation 。Patellar luxation 應該被認為一種被繼承的疾病。 [b][color=#003399][/color][/b][b][color=#003399]臨床標誌 [/color][/b]
患者三類是可識別的:
[list=1][*]他們開始走的出生不滿一月的嬰兒和更舊的小狗經常顯示反常hind-leg 支架和作用的臨床標誌從時間; 這些禮物等級3 和4 一般。[*]年輕人成熟動物與等級2 到3 luxations 陳列了反常或斷斷續續地反常步態所有他們的生活但通常被提出當問題symptomatically 惡化。[*]更舊的動物與等級1 和2 luxations 也許陳列瘸的突然的標誌由於軟的組織進一步故障結果較小精神創傷的或由於惡化退化聯接疾病痛苦。[/list]標誌隨程度luxation 顯著變化。在等級1 和2, 瘸是顯然的只當臏骨是在luxated 位置。腿運載與抑止聯接被屈曲但也許被接觸對地面每第三或第四步在快速的步態。分級3 並且4 個動物陳列蹲下, bowlegged 姿態(膝varum) 以腳轉動了內部和與大多數重量轉移到前面腿。

永久luxation 使quadriceps 無效在擴大抑止。抑止的引伸將允許luxation 的減少對等級1 和2 。痛苦是存在在某些情況下, 特別是當臏骨和大腿骨髁的chondromalacia 是存在。多數動物; 但是, 似乎顯示一點激怒在 [url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fglossary.html#palpation][color=#800080]觸診[/color][/url]。
側向Luxation 在玩具和縮樣養殖 側向luxation 在小養殖後經常被看見在動物的生活中, 從5 到8 年紀。遺傳能力是未知的。骨骼反常性是相對地較小在這綜合症狀, 似乎代表一次故障在軟的組織, 陰暗的骨骼精神錯亂。因而, 多數側向luxations 是等級1 和2, 並且骨多的變動是相似, 但在對面, 與那些被描述為中間luxation 。狗有更加功能的傷殘與側向luxation 比與中間luxation 。
[b][color=#003399][/color][/b][b][color=#003399]臨床標誌 [/color][/b]
在成熟動物, 標誌也許迅速地顯現出和也許同較小精神創傷或吃力活動聯繫在一起。敲膝蓋或膝valgum 姿態, 有時被描述和封印像, 典型的。

突然的雙邊luxation 也許使動物無法站立和因此模仿神經學疾病。體格檢查是如所描述為中間luxation 。
側向Luxation 在大和巨人養殖 並且叫的膝valgum, 這個情況通常被看見在大和巨人養殖。一個基因樣式被注意了, 用了不起的丹麥人、聖Bernards, 和愛爾蘭Wolfhounds 是最共同地受影響的。hip 發育異常組分, 譬如髖關節valga (大腿骨脖子的傾向增加的角度) 並且大腿骨脖子的增加的anteversion, 與側向patellar luxation 有關。這些殘疾導致股骨的內部自轉以末端股骨的側向扭力和valgus 殘疾, 側向地偏移quadriceps 機制和臏骨。
[b][color=#003399][/color][/b][b][color=#003399]臨床標誌 [/color][/b]
雙邊介入是最共同。動物看上去影響當他們是5 個到6 個月年齡的時候。最著名發現是敲膝蓋(膝valgum) 姿態。臏骨通常是可減少的, 並且中間抵押韌帶的laxity 也許是顯然的。抑止聯接的中間retinacular 組織經常變厚, 並且腳能經常看側向地扭轉當重量被安置在肢體。

診斷Patellar Luxation 考試和證明狗是被審查的醒的(化工克制不被推薦) 並且由出席的獸醫分類根據應用和總說明指示。獸醫然後完成 [url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2fplappbw.pdf][color=#800080]申請表[/color][/url] 表明狗的臏骨評估的結果。
應用和 [url=http://66.94.231.168/babelfish/translate_url_content?lp=en_zt&trurl=http%3a%2f%2fwww.offa.org%2ffees.html][color=#0000ff]費[/color][/url] 可能然後被郵寄對OFA 。出席的獸醫和所有者被鼓勵遞交所有評估, 是否正常或反常, 為資料的完整性的目的。沒有OFA 費為輸入臏骨的一個反常評估在資料庫中。
養殖資料庫數字將被發布對所有狗被發現正常在12 個月年齡或更舊。養殖資料庫數字將包含年齡在評估並且它建議狗階段性地被再檢查因為一些luxations 不會是顯然的在最新生活內。
初步評估狗的評估在12 個月年齡之下被鼓勵如果所有者渴望養殖在這年齡。時機會集助長資料在在6-8 個星期年齡在小狗的發行之前對新所有者。
Patellar Luxation 等級
Patellar Luxation 資料庫是為狗12 個月和。考試少於執行了在狗12 個月對待咨詢並且OFA 養殖數字不會被分配。
分類程度方法luxation 和骨多的殘疾是有用的為診斷, 和可能嚮或中間或側向luxations 被申請由扭轉中間側向定向參考。臏骨的位置可能容易地是palpated 開始在tibial 節結和工作接近沿patellar 韌帶對臏骨。
等級1手工臏骨容易luxates 在抑止聯接的充分的引伸, 但回到trochlea 當發布。crepitation 不是明顯的。中間, 或非常偶爾地, tibial 冠的側向偏差(與臏骨的側向luxation) 是只最小的, 和那裡是非常脛骨的輕微的自轉。抑止的彎曲和引伸是在一條直線沒有飛腓節的綁架。
等級2有頻繁patellar luxation, 在某些情況下, 變得更或較不永久。肢體有時運載, 雖然重量軸承定期地發生與抑止餘留輕微地被屈曲。特別是在麻醉之下它經常是可能減少luxation 由側向地手工轉動脛骨, 但臏骨reluxates 容易地當聯接的手工緊張被發布。儘量30 個程度中間tibial 扭力和tibial 冠的輕微的中間偏差可以存在。當臏骨中間休息飛腓節輕微地被拐騙。如果情況是雙邊的, 更多重量被投擲forelimbs 。

許多狗以這個等級與情況合理地很好許多年, 但臏骨的恆定的luxation 在臏骨的明確表達的表面的trochlea 起因侵蝕的中間trochlear 土坎和並且中間嘴唇的接近區域居住。這導致crepitation 變得明顯當臏骨是手工luxated 。
等級3臏骨是永久地luxated 以在30 度和50 度之間tibial 冠的脛骨和偏差的扭力從cranial/caudal 飛機。雖然luxation 不是斷斷續續的, 許多動物使用肢體以抑止舉行在一個半被屈曲的位置。trochlea 是非常淺甚至鋪平。
等級4脛骨中間被扭轉並且tibial 冠也許中間顯示進一步偏差以結果它說謊50 度到90 度從cranial/caudal 飛機。臏骨是永久地luxated 。臏骨說謊在中間髁之上並且空間可能palpated 在patellar 韌帶和股骨之間的末端末端。trochlea 是缺席甚至凸面。肢體運載, 或動物移動在一個蹲下的位置, 與肢體被屈曲。

What is Patellar Luxation?The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position.
[url=http://www.offa.org/glossary.html#bilateral][color=#0000ff]Bilateral[/color][/url] involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
Patellar Luxation CategoriesPatellar luxations fall into several categories:
[list=1][*][url=http://www.offa.org/patluxgeninfo.html#medial][b][color=#800080]Medial luxation; toy, miniature, and large breeds[/color][/b][/url][*][b][url=http://www.offa.org/patluxgeninfo.html#lateraltoy][color=#800080]Lateral luxation; toy and miniature breeds[/color][/url][/b][*][b][url=http://www.offa.org/patluxgeninfo.html#laterallarge][color=#800080]Lateral luxation; large and giant breeds. [/color][/url][/b][*]Luxation resulting from trauma; various breeds, of no importance to the certification process.[/list]Numbers 1, 2 and 3 are either known to be heritable or strongly suspected.

[color=#000000]Medial Luxation in Toy, Miniature, and Large Breeds[/color]Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation should be considered an inherited disease.
[b][color=#003399]Clinical Signs [/color][/b]
Three classes of patients are identifiable:
[list=1][*]Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.[*]Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.[*]Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.[/list]Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs.

Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals; however, seem to show little irritation upon [url=http://www.offa.org/glossary.html#palpation][color=#0000ff]palpation[/color][/url].
[color=#000000]Lateral Luxation in Toy and Miniature Breeds [/color]Lateral luxation in small breeds is most often seen late in the animal's life, from 5 to 8 years of age. The heritability is unknown. Skeletal abnormalities are relatively minor in this syndrome, which seems to represent a breakdown in soft tissue in response to, as yet, obscure skeletal derangement. Thus, most lateral luxations are grades 1 and 2, and the bony changes are similar, but opposite, to those described for medial luxation. The dog has more functional disability with lateral luxation than with medial luxation.
[b][color=#003399]Clinical Signs [/color][/b]
In mature animals, signs may develop rapidly and may be associated with minor trauma or strenuous activity. A knock-knee or genu valgum stance, sometimes described as seal-like, is characteristic.

Sudden bilateral luxation may render the animal unable to stand and so simulate neurological disease. Physical examination is as described for medial luxation.
[color=#000000]Lateral Luxation in Large and Giant Breeds [/color]Also called genu valgum, this condition is usually seen in the large and giant breeds. A genetic pattern has been noted, with Great Danes, St. Bernards, and Irish Wolfhounds being the most commonly affected. Components of hip dysplasia, such as coxa valga (increased angle of inclination of the femoral neck) and increased anteversion of the femoral neck, are related to lateral patellar luxation. These deformities cause internal rotation of the femur with lateral torsion and valgus deformity of the distal femur, which displaces the quadriceps mechanism and patella laterally.
[b][color=#003399]Clinical Signs [/color][/b]
Bilateral involvement is most common. Animals appear to be affected by the time they are 5 to 6 months of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can often be seen to twist laterally as weight is placed on the limb.
Examination and CertificationThe dog is examined awake (chemical restraint is not recommended) and classified by the attending veterinarian according to the application and general information instructions. The veterinarian then completes the [url=http://www.offa.org/plappbw.pdf][color=#800080]application form[/color][/url] indicating the the results of the dog's patella evaluation.
The application and [url=http://www.offa.org/fees.html][color=#0000ff]fee[/color][/url] can then be mailed to OFA. The attending veterinarian and owner is encouraged to submit all evaluations, whether normal or abnormal, for the purpose of completeness of data. There is no OFA fee for entering an abnormal evaluation of the patella in the data bank.
A breed database number will be issued to all dogs found to be normal at 12 months of age or older. The breed database number will contain the age at evaluation and it is recommended that dogs be periodically reexamined as some luxations will not be evident until later in life.
Preliminary EvaluationsEvaluation of dogs under 12 months of age is encouraged if the owner desires to breed at this age. The most opportune time to gather breeding data is at 6-8 weeks of age prior to the puppy's release to the new owner.


The Patellar Luxation Database is for dogs 12 months and over. Examinations performed on dogs less than 12 months will be treated as Consultations and no OFA breed numbers will be assigned.
A method of classifying the degree of luxation and bony deformity is useful for diagnosis, and can be applied to either medial or lateral luxations by reversing the medial-lateral directional references. The position of the patella can easily be palpated starting at the tibial tubercle and working proximal along the patellar ligament to the patella.
Grade 1Manually the patella easily luxates at full extension of the stifle joint, but returns to the trochlea when released. No crepitation is apparent. The medial, or very occasionally, lateral deviation of the tibial crest (with lateral luxation of the patella) is only minimal, and there is very slight rotation of the tibia. Flexion and extension of the stifle is in a straight line with no abduction of the hock.
Grade 2There is frequent patellar luxation, which, in some cases, becomes more or less permanent. The limb is sometimes carried, although weight bearing routinely occurs with the stifle remaining slightly flexed. Especially under anesthesia it is often possible to reduce the luxation by manually turning the tibia laterally, but the patella reluxates with ease when manual tension of the joint is released. As much as 30 degrees of medial tibial torsion and a slight medial deviation of the tibial crest may exist. When the patella is resting medially the hock is slightly abducted. If the condition is bilateral, more weight is thrown onto the forelimbs.

Many dogs with this grade live with the condition reasonably well for many years, but the constant luxation of the patella over the medial trochlear ridge of the trochlea causes erosion of the articulating surface of the patella and also the proximal area of the medial lip. This results in crepitation becoming apparent when the patella is luxated manually.
Grade 3The patella is permanently luxated with torsion of the tibia and deviation of the tibial crest of between 30 degrees and 50 degrees from the cranial/caudal plane. Although the luxation is not intermittent, many animals use the limb with the stifle held in a semi flexed position. The trochlea is very shallow or even flattened.
Grade 4The tibia is medially twisted and the tibial crest may show further deviation medially with the result that it lies 50 degrees to 90 degrees from the cranial/caudal plane. The patella is permanently luxated. The patella lies just above the medial condyle and a space can be palpated between the patellar ligament and the distal end of the femur. The trochlea is absent or even convex. The limb is carried, or the animal moves in a crouched position, with the limb flexed.[/size][/td][/tr][tr][td]

[/td][/tr][/table]

minibabyqq 2006-12-20 04:25

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[size=12px][size=5][color=magenta][b]先天心臟病疾病體檢[/b][/color][/size][/size]
[size=12px][size=5][color=red][/color][/size] [/size]
[size=12px][size=5][color=black][b]Congenital Cardiac Disease Physical Exam[/b][/color][/size]  [url=http://www11.discuss.com.hk/misc.php?action=emailfriend&tid=2815293][img]http://www11.discuss.com.hk/images/discuss_style/emailtofriend3.gif[/img][/url]

[size=12px][color=#000000]心臟病檢查[/color]臨床心臟病考試應該被舉辦以系統的方式。動脈和多血脈性的脈衝、黏膜, 和precordium 應該被評估。心率應該被獲得。臨床考試應該由個體執行以先進的訓練在心臟病診斷。
上證明由獸醫內科美國學院, 心臟病學專業由美國獸醫醫療協會考慮作為臨床熟練的基準為獸醫在臨床心臟病學方面, 並且考試由這個專業委員會Diplomate 被推薦。其它獸醫也許能執行這些考試, 假設他們接受了先進的訓練在subspecialty 先天心臟病。
[b][color=#003399]Ascultation[/color][/b][color=#003399][/color]心臟病聽診應該進行在一個安靜, 無分心環境。動物應該是常設和克制, 但鎮靜劑應該被避免。氣喘必須是受控的並且如果需要, 狗應該被給時刻休息和順應對環境。臨床工作者如果能辨認心臟病閥門區域為聽診。稽查應該逐漸移動聽診器橫跨所有閥門區域和應該還auscultate 在subaortic 區域、上升的主動脈、肺動脈, 和左craniodorsal 心臟病基地。從事左precordium 的考試, 正確的precordium 應該被審查。 [/size]
[size=12px][list][*]二尖瓣區域被找出和立刻背部對可觸知的左頂端衝動和由觸診辨認以手指的要訣。聽診器然後被安置在僧帽形的區域和心音被辨認。[*]動脈閥區域是背部和1 或2 肋間的空間頭蓋骨在頂端衝動左面。第二心音將是最強烈的當聽診器被集中在動脈閥區域。私語起源於或放熱對聽診subaortic 範圍是顯然立刻caudoventral 對動脈閥區域。私語起源於或放熱入上升的主動脈將是顯然craniodorsal 對動脈閥, 也許並且射出對正確的頭蓋骨胸部和對頸動脈在脖子。[*]pulmonic 閥門區域是腹和一肋間的空間頭蓋骨對動脈閥區域。私語起源於或放熱入主要肺動脈將是顯然背對pulmonic 閥門在左hemithorax 。[*]tricuspid 閥門區域是一個相對地大區域位於正確的hemithorax, 對面和輕微地頭蓋骨對二尖瓣區域。[*]臨床工作者應該並且auscultate 沿腹正確的precordium (正確的sternal 疆界) 並且是正確的craniodorsal 心臟病疆界。[*]所有心臟病私語或反常聲音應該是著名。私語應該被描述依照下面被表明。[/list][/size]
[b][color=#003399]心臟病私語的描述[/color][/b][color=#003399][/color]心臟病私語的一個完整描述如果做和記錄在病歷。 [list][*]私語應該被選定作為心臟收縮, 舒張, 或連續。[*]點最大的私語強度應該被表明如上所述。當precordial 興奮是可觸知的, 私語一般將是最強烈的在這振動。[*]私語斷斷續續地只被查出得或是易變的應該是因此表明了。[*]私語的輻射應該被表明[/list][b][color=#003399]心率、心臟節奏, 和鍛煉的作用 [/color][/b][color=#003399][/color]一些心臟私語變得顯然或大聲以變化在自主神經系統的活動、心率, 或心臟病週期長度上。這樣變動也許被鍛煉或其他導致重音。評估心臟私語的重要性在鍛煉以後當前是未解決的。看起來, 一些狗以先天subaortic 狹窄或以動態流出短文阻礙也許有只變得顯然以增加的有同情心的活動的私語或在長時期的心臟病填裝的期間在明顯靜脈竇心率失常期間它應該還注意到之後, 一些正常, 無辜的心臟私語也許增加在強度在鍛煉以後。此外, 氣喘人工製品也許是一個問題在鍛煉以後。 它是很可能審查狗在鍛煉導致增加的敏感性對軟的私語但大概被減少的特異性診斷之後。心臟隨後而來的鍛煉的聽診是在審查的獸醫的謹慎。
此時OFA 不要求一次崗位鍛煉考試在對心臟私語的評估在狗; 但是, 這實踐也許被修改如果明確的資訊變得可利用。

Echocardiographic 檢查echocardiographic 考試應該被舉辦在一件系統的事情。稽查必須能執行二維, 搏動揮動多譜勒儀, 和連續波心臟的多譜勒儀考試。顏色多譜勒儀的可及性是可貴但不根本的為多數考試。echocardiographic 考試應該由個體執行和解釋以先進的訓練在心臟病診斷。
上證明由獸醫內科美國學院, 心臟病學專業由獸醫醫療協會美國學院考慮作為臨床熟練的基準為獸醫在臨床心臟病學方面, 並且考試由這個專業委員會Diplomate 被推薦。其它獸醫也許能執行這些考試提供了他們有適當的設備和接受了先進的訓練在echocardiography 方面。
想像pericardial 空間、兩心房、兩個心室、偉大的船, 和四個心臟病閥門當有必要應該是印象的使用長的軸, 短軸, 頂端, 和有角度的圖像飛機執行心臟的一次完全考試。命名原則應該跟隨那由心臟病學獸醫內科專業美國學院推薦。一個解剖診斷也許是可能的根據二維想像; 但是, 心臟病私語的起源應該並且被評估運用多譜勒儀方法。
多譜勒儀
所有心臟病閥門的多譜勒儀考試應該執行和被記錄。反常流程應該被定量使用搏動的波浪或連續波多譜勒儀技術。價值被獲得應該與參考價值比較。所有鎮定藥的抑制作用或鎮靜劑必須被考慮當測量高峰流程速度。顏色多譜勒儀echocardiography 應該被使用如果可利用估計正常和反常血流樣式。反常流程橫跨心臟病中隔或分流器的證明在偉大的船的水平是最佳由顏色和搏動的波浪多譜勒儀技術的組合完成。典型的echocardiographic 特點共同先天
心臟瑕疵被表明在表一個。
評估特別留意應該被指揮對對流程樣式和速度的評估在左心室出口和下降的主動脈。優選的對準線以血流應該被尋找使準確速度被報告。這也許要求對sub-xiphoid (subcostal) 變換裝置的用途
位置並且左頂端(尾部parasternal) 變換裝置安置。除高峰速度的測量之外使用搏動的或顏色波浪多譜勒儀, 搏動的波浪樣品容量應該逐漸被推進從subaortic 區域入acsending 的主動脈為了辨認突然的加速度在流程速度、動盪, 或大動脈反流。
錄影帶Echocardiographic 研究應該被報告關於錄影帶為隨後分析並且反常研究結果一個書面紀錄應該被輸入病歷。
Echocardiographic 研究結果 [table=98%][tr][size=2][color=#ffffff]先天不足[/color][/size][size=2][color=#ffffff]典型的Auscultatory 特點[/color][/size][size=2][color=#ffffff]診斷Echocardiographic 和多譜勒儀Echocardiographic 特點[/color][/size][/tr][tr][td]專利ductus arteriosus[/td][td]連續的心臟私語以最大的強度在左頭蓋骨背部心臟病基地[/td][td]連續倒退流程從專利ductus arteriosus 入肺動脈[/td][/tr][tr][td]心室氏族的瑕疵[/td][td]心臟收縮的私語以最大的強度在正確的腹precordium; 較不經常最大的強度是在pulmonic 閥門區域和肺動脈[/td][td]氏族的瑕疵可能經常是印象的在多架想像飛機裡。反常, 一般高速度, 心臟收縮的流程橫跨氏族的瑕疵是顯然的。[/td][/tr][tr][td]Atrial 氏族的瑕疵[/td][td]心臟收縮的私語以最大的強度在pulmonic 閥門區域和肺動脈。第二心音也許廣泛被分裂[/td][td]氏族的瑕疵可能一般是印象的在多架想像飛機裡。反常血流也許被辨認橫跨氏族的瑕疵入正確的心房。[/td][/tr][tr][td]Pulmonic 狹窄[/td][td]心臟收縮的私語以最大的強度在pulmonic 閥門區域和肺動脈[/td][td]反常肺閥門和/or subvalvular 解剖學。血流的突然的加速度在正確的心室出口以動盪, 高速度心臟收縮的流程橫跨肺閥門和入主要肺動脈。[/td][/tr][tr][td]Valvular 和subvalvular 大動脈狹窄[/td][td]心臟收縮的私語以最大的強度在subaortic 或動脈閥區域和放熱入上升的主動脈。私語也許並且是突出的在正確的頭蓋骨胸部。[/td][td]反常subvalvular 或大動脈valvular 解剖學也許是顯然的。血流的突然的加速度入左心室流出短文以動盪, 高速度心臟收縮的流程橫跨動脈閥和入上升的主動脈。一致大動脈反流通常是存在。[/td][/tr][tr][td]二尖瓣發育異常[/td][td]心臟收縮的私語以最大的強度在左尖頂和僧帽形的區域[/td][td]二尖瓣用具的反常解剖學。高速度後退心臟收縮的流程橫跨二尖瓣入左心房。一致二尖瓣狹窄也許是存在。[/td][/tr][tr][td]Tricuspid 閥門發育異常[/td][td]心臟收縮的私語以最大的強度在tricuspid 閥門區域[/td][td]tricuspid 閥門用具的反常解剖學。高速度後退心臟收縮的流程橫跨tricuspid 閥門入正確的心房。一致tricuspid 閥門狹窄也許是存在。[/td][/tr][tr][td]正確對左心臟病分流器[/td][td]可變物—一句心臟收縮的私語在左基地經常被查出; 青紫是一個重要臨床標誌[/td][td]反常解剖學與例子有的心臟病畸形關係了: Fallot, 專利ductus arteriosus 四聯劇以肺高血壓, 肺或tricuspid 閥門狹窄以atrial 氏族的瑕疵。正確對左邊轉軌可以相反echocardiography 提供靠多譜勒儀技術並且/或者。[/td][/tr][/table][color=#000000]The Cardiac Exam[/color]The clinical cardiac examination should be conducted in a systematic manner. The arterial and venous pulses, mucous membranes, and precordium should be evaluated. Heart rate should be obtained. The clinical examination should be performed by an individual with advanced training in cardiac diagnosis.
Board certification by the American College of Veterinary Internal Medicine, Specialty of Cardiology is considered by the American Veterinary Medical Association as the benchmark of clinical proficiency for veterinarians in clinical cardiology, and examination by a Diplomate of this specialty board is recommended. Other veterinarians may be able to perform these examinations, provided they have received advanced training in the subspecialty of congenital heart disease.
[b][color=#003399]Ascultation[/color][/b][color=#003399][/color]Cardiac auscultation should be performed in a quiet, distraction-free environment. The animal should be standing and restrained, but sedative drugs should be avoided. Panting must be controlled and if necessary, the dog should be given time to rest and acclimate to the environment. The clinician should able to identify the cardiac valve areas for auscultation. The examiner should gradually move the stethoscope across all valve areas and also should auscultate over the subaortic area, ascending aorta, pulmonary artery, and the left craniodorsal cardiac base. Following examination of the left precordium, the right precordium should be examined. [list][*]The mitral valve area is located over and immediately dorsal to the palpable left apical impulse and is identified by palpation with the tips of the fingers. The stethoscope is then placed over the mitral area and the heart sounds identified.[*]The aortic valve area is dorsal and 1 or 2 intercostal spaces cranial to the left apical impulse. The second heart sound will be most intense when the stethoscope is centered over the aortic valve area. Murmurs originating from or radiating to the subaortic area of auscultation are evident immediately caudoventral to the aortic valve area. Murmurs originating from or radiating into the ascending aorta will be evident craniodorsal to the aortic valve and may also project to the right cranial thorax and to the carotid arteries in the neck.[*]The pulmonic valve area is ventral and one intercostal space cranial to the aortic valve area. Murmurs originating from or radiating into the main pulmonary artery will be evident dorsal to the pulmonic valve over the left hemithorax.[*]The tricuspid valve area is a relatively large area located on the right hemithorax, opposite and slightly cranial to the mitral valve area.[*]The clinician should also auscultate along the ventral right precordium (right sternal border) and over be right craniodorsal cardiac border.[*]Any cardiac murmurs or abnormal sounds should be noted. Murmurs should be described as indicated below.[/list][b][color=#003399]Description of Cardiac Murmurs[/color][/b][color=#003399][/color]A full description of the cardiac murmur should made and recorded in the medical record. [list][*]Murmurs should be designated as systolic, diastolic, or continuous.[*]The point of maximal murmur intensity should be indicated as described above. When a precordial thrill is palpable, the murmur will generally be most intense over this vibration.[*]Murmurs that are only detected intermittently or are variable should be so indicated.[*]The radiation of the murmur should be indicated[/list][b][color=#003399]Effects of heart rate, heart rhythm, and exercise [/color][/b][color=#003399][/color]Some heart murmurs become evident or louder with changes in autonomic activity, heart rate, or cardiac cycle length. Such changes may be induced by exercise or other stresses. The importance of evaluating heart murmurs after exercise is currently unresolved. It appears that some dogs with congenital subaortic stenosis or with dynamic outflow tract obstruction may have murmurs that only become evident with increased sympathetic activity or after prolonged cardiac filling periods during marked sinus arrhythmia It also should be noted that some normal, innocent heart murmurs may increase in intensity after exercise. Furthermore, panting artifact may be a problem after exercise. It is most likely that examining dogs after exercise will result in increased sensitivity to diagnosis of soft murmurs but probably decreased specificity as well. Auscultation of the heart following exercise is at the discretion of the examining veterinarian.
At this time the OFA does not require a post exercise examination in the assessment of heart murmurs in dogs; however, this practice may be modified should definitive information become available.

[color=#000000]The Echocardiographic Exam[/color]The echocardiographic examination should be conducted in a systematic matter. The examiner must be able to perform two-dimensional, pulsed-wave Doppler, and continuous wave Doppler examinations of the heart. The availability of color Doppler is valuable but not essential for most examinations. The echocardiographic examination should be performed and interpreted by individuals with advanced training in cardiac diagnosis.
Board certification by the American College of Veterinary Internal Medicine, Specialty of Cardiology is considered by the American College of Veterinary Medical Association as the benchmark of clinical proficiency for veterinarians in clinical cardiology, and examination by a Diplomate of this Specialty Board is recommended. Other veterinarians may be able to perform these examinations provided they have appropriate equipment and have received advanced training in echocardiography.
[color=#000000]Imaging[/color]The pericardial space, both atria, both ventricles, the great vessels, and the four cardiac valves should be imaged using long axis, short axis, apical, and angled image planes as necessary to perform a complete examination of the heart. Nomenclature should follow that recommended by the American College of Veterinary Internal Medicine Specialty of Cardiology. An anatomic diagnosis may be possible based on two-dimensional imaging; however, the origin of cardiac murmurs should also be evaluated using Doppler methods.
[color=#000000]Doppler[/color]
Doppler examination of all cardiac valves should be performed and recorded. Abnormal flow should be quantified using pulsed wave or continuous wave Doppler techniques. Values obtained should be compared to reference values. The depressant effects of any tranquilizers or sedative must be considered when measuring peak flow velocities. Color Doppler echocardiography should be employed if available to assess normal and abnormal blood flow patterns. Identification of abnormal flow across the cardiac septa or shunts at the level of the great vessels is best done by a combination of color and pulsed wave Doppler techniques. Typical echocardiographic features of common congenital
heart defects are indicated in table one.
[color=#000000]Assessment[/color]Special attention should be directed to the assessment of flow patterns and velocities in the left ventricular outlet and descending aorta. Optimal alignment with blood flow should be sought for accurate velocities to be reported. This may require the use of sub-xiphoid (subcostal) transducer
positions as well as left apical (caudal parasternal) transducer placements. In addition to measurement of peak velocity using pulsed or color wave Doppler, the pulsed wave sample volume should be gradually advanced from the subaortic area into the acsending aorta in order to identify sudden accelerations in flow velocity, turbulence, or aortic regurgitation.
[color=#000000]Videotape[/color]Echocardiographic studies should be reported on videotape for subsequent analysis and a written record of abnormal findings should be entered into the medical record.
[color=#000000]Echocardiographic Findings[/color] [table=98%][tr][size=2][color=#ffffff]Congenital Defect[/color][/size][size=2][color=#ffffff]Typical Auscultatory Features[/color][/size][size=2][color=#ffffff]Diagnostic Echocardiographic and Doppler Echocardiographic Features[/color][/size][/tr][tr][td]Patent ductus arteriosus[/td][td]Continuous heart murmur with maximal intensity over the left cranial dorsal cardiac base[/td][td]Continuous retrograde flow from the patent ductus arteriosus into the pulmonary artery[/td][/tr][tr][td]Ventricular septal defect[/td][td]Systolic murmur with maximal intensity over the right ventral precordium; less often maximal intensity is over the pulmonic valve area and pulmonary artery[/td][td]The septal defect can often be imaged in multiple imaging planes. Abnormal, generally high velocity, systolic flow across the septal defect is evident.[/td][/tr][tr][td]Atrial septal defect[/td][td]Systolic murmur with maximal intensity over the pulmonic valve area and pulmonary artery. The second heart sound may be widely split[/td][td]The septal defect can generally be imaged in multiple imaging planes. Abnormal blood flow may be identified across the septal defect into the right atrium.[/td][/tr][tr][td]Pulmonic stenosis[/td][td]Systolic murmur with maximal intensity over the pulmonic valve area and pulmonary artery[/td][td]Abnormal pulmonary valve and /or subvalvular anatomy. Sudden acceleration of blood flow in the right ventricular outlet with turbulent, high velocity systolic flow across the pulmonary valve and into the main pulmonary artery.[/td][/tr][tr][td]Valvular and subvalvular aortic stenosis[/td][td]Systolic murmur with maximal intensity over the subaortic or aortic valve area and radiating into the ascending aorta. The murmur may also be prominent over the right cranial thorax.[/td][td]Abnormal subvalvular or aortic valvular anatomy may be evident. Sudden acceleration of blood flow into the left ventricular outflow tract with turbulent, high velocity systolic flow across the aortic valve and into the ascending aorta. Concurrent aortic regurgitation is usually present.[/td][/tr][tr][td]Mitral valve dysplasia[/td][td]Systolic murmur with maximal intensity over the left apex and mitral area[/td][td]Abnormal anatomy of the mitral valve apparatus. High velocity retrograde systolic flow across the mitral valve into the left atrium. Concurrent mitral valve stenosis may be present.[/td][/tr][tr][td]Tricuspid valve dysplasia[/td][td]Systolic murmur with maximal intensity over the tricuspid valve area[/td][td]Abnormal anatomy of the tricuspid valve apparatus. High velocity retrograde systolic flow across the tricuspid valve into the right atrium. Concurrent tricuspid valve stenosis may be present.[/td][/tr][tr][td]Right to left cardiac shunt[/td][td]Variable—a systolic murmur at the left base is often detected; cyanosis is an important clinical sign[/td][td]Abnormal anatomy related to the cardiac malformations examples include: tetralogy of Fallot, patent ductus arteriosus with pulmonary hypertension, pulmonary or tricuspid valves stenosis with atrial septal defect. Right to left shunting may be documented by Doppler techniques and/or by contrast echocardiography.[/td][/tr][/table][/size][/td][/tr][tr][td]

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minibabyqq 2006-12-20 04:26

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[size=12px][size=5][color=magenta][b]退化聯接疾病(骨關節炎)[/b][/color][/size][/size]
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[size=12px][color=red][size=5][b][color=black]Degenerative Joint Disease (Osteoarthritis)[/color]  [url=http://www5.discuss.com.hk/misc.php?action=emailfriend&tid=2823574][img]http://www5.discuss.com.hk/images/discuss_style/emailtofriend3.gif[/img][/url] [/b][/size][/color]

[size=12px]取決於誰您談話與, 期限' 骨關節炎的和' 退化聯接疾病' 可以或不可以被使用描述同樣事。在這次討論, 我們互換性將使用用語。

什麼是退化聯接疾病(DJD)?

退化聯接疾病為報道和保護骨頭的末端在可移動的光滑的軟骨的損失描繪(synovial) 聯接。軟骨沒有神經當它接觸其它骨頭軟骨, 那裡如此是沒有痛苦。當軟骨磨損, 骨頭被暴露。骨頭有神經如此當二個骨頭末端在一種聯合接觸它導致痛苦和 炎症。在退化聯接疾病我們也看小骨多的投射(osteophytes) 形成在是緊挨聯接的骨頭。這增加來痛苦。退化聯接疾病是進步, 意味它繼續得到更壞。

什麼導致退化聯接疾病?

退化聯接疾病可能發生由於磨損在否則正常聯接和發生作為狗年齡。這叫做主要退化聯接疾病。退化聯接疾病也許並且發生由於其它情況影響聯接譬如 hip 發育異常 或 手肘發育異常。然後這叫做次要退化聯接疾病。

哪條狗是在危險中開發退化聯接疾病?

某任一條狗以一個 先天 聯合問題, 像 發育異常 或臏骨luxation 是有傾向對開發退化聯接疾病。有傷害對聯接譬如破裂介入聯接的狗, 或一條 被爆裂的先前cruciate 韌帶 在膝蓋將是可能開發退化聯接疾病。

什麼是退化聯接疾病症狀?

退化聯接疾病症狀將變化至於哪聯接是包含的, 狗的年齡, 和疾病的嚴肅。總之, 第一症狀也許是修改過的 步態 因為狗將設法把更多它的重量放在未受影響的肢體上。那裡也許是肌肉萎縮(對肌肉的大小的減少) 在受影響的肢體因為狗使用它, 或至少把較少重量放在它上。例如, 在一條狗以hip 發育異常介入兩後面肢體, 後面肢體的肌肉也許是稀薄的, 但是, 胸口的肌肉和肩膀也許被增加在大小因為狗把更多重量放在前面腿上。

許多時間狗也許發現它難起來在躺下以後和看上去僵硬。狗也許無法跳入汽車。許多狗發現它難下來或臺階。

取決於相當數量痛苦狗體驗, 也許那裡在變化在胃口和行為(即, 狗上也許去單獨經常) 。聯接一般不是圓鼓的並且痛苦是愚鈍的酸疼的型, 因此狗不vocalize 或經常不大聲呼喊在痛苦中。一些狗將舔或將咬住在是痛苦的區域。一些將尋找溫暖或軟的地方睡覺。

退化聯接疾病怎麼被診斷?

獸醫將獲得狗的標誌的好歷史從所有者和將執行一次完全體檢。射線照相被採取, 並且更加進一步的實驗室試驗或受影響的joint(s) 的被選派的檢查也許執行。

退化聯接疾病怎麼被對待?

退化聯接疾病可能 醫療上 和外科地被對待。

某種退化聯接疾病的形式可能被對待以手術。例如, hip 替換在狗以hip 發育異常變得更加共同。其它規程可能並且執行僅他們的成功休息在多少骨多的變動發生□在和在聯接附近。請看文章在具體聯合疾病為關於外科治療選擇的延長的討論為那種疾病。

什麼是預測為狗以退化聯接疾病?

退化聯接疾病是進步- 它將繼續惡化。有我們能醫療上對待疾病減速進步的方式並且許多狗反應很好和能舒適地居住幾年來。在更加嚴厲的案件, 手術也許做包括實際聯合替換。在這些情況下, 補救通常是非常好的。
Depending upon whom you talk to, the terms 'osteoarthritis' and 'degenerative joint disease' may or may not be used to describe the same thing. In this discussion, we will use the terms interchangeably.

What is degenerative joint disease (DJD)?

Degenerative joint disease is characterized by the loss of the smooth cartilage that covers and protects the end of the bones in a movable (synovial) joint. The cartilage has no nerves so when it touches the cartilage of another bone, there is no pain. When the cartilage wears away, the bone is exposed. The bone does have nerves so when the two bone ends in a joint touch each other it results in pain and inflammation. In degenerative joint disease we also see small bony projections (osteophytes) form on the bone that is close to the joint. This adds to the pain. Degenerative joint disease is progressive, meaning it continues to get worse.

What causes degenerative joint disease?

Degenerative joint disease can occur as a result of wear and tear on an otherwise normal joint and occurs as the dog ages. This is called primary degenerative joint disease. Degenerative joint disease may also occur as a result of another condition affecting the joint such as hip dysplasia or elbow dysplasia. Then it is called secondary degenerative joint disease.

Which dogs are at risk of developing degenerative joint disease?

Certainly any dog with a congenital joint problem, like dysplasia or patella luxation is going to be more prone to developing degenerative joint disease. Dogs who have had injury to a joint such as a fracture involving the joint, or a ruptured anterior cruciate ligament in the knee will be more likely to develop degenerative joint disease.

What are the symptoms of degenerative joint disease?

The symptoms of degenerative joint disease will vary as to which joints are involved, the age of the dog, and the severity of the disease. In general, the first symptoms may be an altered gait since the dog will try to put more of its weight on the unaffected limbs. There may be muscle atrophy (reduction in the size of the muscle) in the affected limb because the dog is using it less, or at least putting less weight on it. For instance, in a dog with hip dysplasia involving both hind limbs, the muscles of the hind limbs may be thin, whereas, the muscles of the chest and shoulders may be increased in size because the dog is putting more weight on the front legs.

Many times the dog may find it difficult to get up after lying down and appears stiff. The dog may be unable to jump up into the car. Many dogs find it difficult to go up or down stairs.

Depending upon the amount of pain the dog is experiencing, there may be changes in appetite and behavior (e.g., the dog may go off by itself more often). The joints are generally not swollen and the pain is the dull aching type, so dogs do not often vocalize or cry out in pain. Some dogs will lick or bite at the area that is painful. Some will seek out warmth or soft places to sleep.

How is degenerative joint disease diagnosed?

The veterinarian will obtain a good history of the dog's signs from the owner and perform a complete physical exam. Radiographs are taken, and further laboratory tests or more detailed exams of the affected joint(s) may be performed.

How is degenerative joint disease treated?

Degenerative joint disease can be treated medically and surgically.

Some forms of degenerative joint disease can be treated with surgery. For example, hip replacements in dogs with hip dysplasia are becoming more common. Other procedures can also be performed but their success rests upon how many bony changes have occurred in and around the joint. Please see the article on the specific joint disease for extended discussion on the surgical treatment options for that disease.

What is the prognosis for dogs with degenerative joint disease?

Degenerative joint disease is progressive - it will continue to worsen. There are ways we can medically treat the disease to slow down the progression and many dogs respond well and can live comfortably for years. In more severe cases, surgery may be performed including actual joint replacements. In these cases, the recovery is usually very good.[/size][/size]
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minibabyqq 2006-12-20 04:26

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[size=12px][color=red][size=5][b][color=magenta]關節炎& 其它聯合疾病的起因和管理[/color]  [url=http://www5.discuss.com.hk/misc.php?action=emailfriend&tid=2823136][img]http://www5.discuss.com.hk/images/discuss_style/emailtofriend3.gif[/img][/url] [/b][/size][/color]

[size=12px]許多寵物開發某種聯合疾病的形式在他們的生活期間。它可能是溫和的, 甚而unnoticeable 對寵物所有者, 或它可能致衰弱, 嚴厲地影響寵物的生活水平, 甚至造成完全瘸。多數案件之間跌倒某處。

當一些寵物也許開發聯合疾病在前半他們的生活, 標誌通常沒出現直到後者一半生活, 變化根據您的寵物的養殖。狗比貓是易受關節炎, 並且更大的狗養殖比更小的養殖脆弱的。

聯合疾病的最共同的標誌包括僵硬, 跛行, 或傾向肢體- 特別在睡眠以後或休息, 無能上升, 勉強跳躍甚至攀登臺階, 和引人注目的痛苦。

關節炎的起因

有影響狗聯接的許多疾病, 那麼許多, 實際上, 有10 個主要分類。

聯合疾病發生由於:

韌帶、腱, 或肌肉疾病, 即, 爆裂了先前cruciate 韌帶

破裂介入聯接

發展混亂, 即, hip 發育異常, 手肘發育異常, osteochondritis dissecans, Legg-Perthes 疾病

先天混亂, 即, Wobbler 的綜合症狀 (子宮頸spondylomyelopathy), luxated 臏骨

飲食和荷爾蒙疾病, 即, hyperparathyroidism, 肥胖病

新陳代謝的混亂, 即, 馮Willebrand 的疾病 (血友病) 在狗

巨蟹星座

退化聯接疾病 (骨關節炎)

激動聯合疾病, 即, Lyme 疾病, 類風濕病的關節炎

退化脊髓聯合疾病, 即, 椎間的圓盤疾病, cauda equina 綜合症狀

關節炎的管理

hip 發育異常和骨關節炎的藥物治療近幾年來很大地改進了由於幾種新補充和藥物介紹和認同。由於hip 發育異常(和其它類型發育異常) 是主要 被繼承的 情況, 沒有防止他們的發展的產品在市場上。通過適當的飲食、鍛煉、補充、anti-inflammatories, 和鎮痛, 您也許能減少退化聯接疾病進步, 但鬆散性在聯接或骨多的變動極大不會改變。

醫療管理被表明為兩條幼小狗以臨床標誌和為更舊的狗以慢性骨關節炎。由於高費用被介入以許多手術, 醫療管理是許多時間唯一的現實選擇為許多寵物所有者。醫療管理multifaceted 。為最佳的結果, 數以下形式應該被設立。為多數動物, 獸醫從第一推薦開始和工作他們的方式在這張名單下作為需要控制痛苦和炎症與相關退化聯接疾病。

重量管理

重量管理是必須演講的第一事。所有外科和醫療過程將是更加有利的如果動物不是超重。考慮, 由寵物的一半決定在美國超重, 有一個公平的機會許多狗與臀部dysplasia/osteoarthritis 並且是超重。幫助狗丟失磅直到他到達他的被推薦的重量, 和保留它那裡, 可以是所有者能做為寵物的最重要的事。但是, 這也許是治療的最堅硬的部份, 但它值得它。您, 作為所有者, 掌握什麼您的狗吃。如果您哺養適當的食物在一個適當的水平和保留款待對極小值, 您的狗將丟失重量。

鍛煉

鍛煉是下重要步。行使提供行動的好範圍並且肌肉大廈和極限磨損在聯接是最佳。皮帶走, 游泳, 走在踏車, 緩慢跑步, 和去在臺階上下是優秀低衝擊鍛煉。一個鍛煉節目應該被賦予個性為各條狗根據狗的骨關節炎、重量, 和情況的嚴肅。總之, 太少許鍛煉比太多可能損傷的, 然而錯誤類型鍛煉可能導致害處。當觀看狗戲劇飛碟是非常令人愉快和樂趣為狗, 它是非常堅硬的在狗的聯接。記住, 它是重要對鍛煉 每日; 只行使週末, 例如, 比好可以導致更多害處如果動物疼痛為星期的剩餘和勉強行動根本。溫暖肌肉在鍛煉之前和跟隨鍛煉以"溫暖下來的" 期間是有利的。與您的獸醫協商關於一個鍛煉節目適當為您的狗。

溫暖和好睡覺區域

多數人民以關節炎發現標誌傾向於惡化在冷, 潮濕的天氣裡。保持您的寵物溫暖, 可以幫助他是更加舒適的。寵物毛線衣將幫助保留聯接取暖器。您可以想要考慮保留溫度在您的家一臺小的取暖器, 也是。

提供企業, 矯形泡沫床幫助許多狗以關節炎。床與dome-shaped, 矯形泡沫均勻地分佈重量和減少壓力在聯接。他們並且是容易對寵物出去。安置床在一個溫暖的斑點從草稿。

按摩和物理療法

您的獸醫或獸醫職員能顯示您怎麼執行物理療法和按摩在您的狗幫助放鬆僵硬的肌肉和促進行動的一個好範圍在聯接。記住, 您的狗是在痛苦中, 因此慢慢地開始和建立信任。開始由寵愛區域和工作由柔和地揉肌肉決定在聯接附近與您的指尖使用小, 圓行動。逐漸工作您的出口對周圍的肌肉。潮濕熱是還有利的。

使每日活動較不痛苦

去在臺階上下經常是困難的為關節炎寵物, 並且為狗, 它可能做去外面小便和排糞非常困難。許多人修造或買舷梯, 特別是在臺階導致外部, 使它容易對狗去外面。

更大的養殖狗能特別是受益於舉起他們的食物和水碗。被舉起的飼養者做吃和喝舒適為關節炎寵物, 特別如果有僵硬在脖子或後面。

口頭疾病修改骨關節炎代理

氨基葡萄糖和軟骨素: 氨基葡萄糖和軟骨素 是成為了廣泛使用在對待動物和人為骨關節炎補充的二種成份。由於巨大成功在治療患者以骨關節炎, 這些產品來了到療法最前方和今天成為最普遍的產品為處理的關節炎。

氨基葡萄糖是主要糖被發現在glycosaminoglycans 和hyaluronate, 是重要積木在軟骨綜合和維護在聯接。軟骨素提高glycosaminoglycans 綜合和禁止殘損的 酵素 在聯接。

當狗有hip 發育異常或其它骨關節炎, 聯接反常地佩帶並且防護軟骨在聯接的表面得到磨損並且總值骨頭對骨頭聯絡創造痛苦。他們需要綜合新軟骨和修理現有的損壞的軟骨的氨基葡萄糖和軟骨素給軟骨形成的細胞(chondrocytes) 積木。這些產品不是止痛藥; 他們運作在實際上癒合造成了的損害旁邊。這些產品一般需要至少六個星期開始癒合軟骨並且多數動物需要贍養在這些產品剩餘他們的生活防止進一步軟骨故障。這些產品是非常安全的和顯示非常少量副作用。有許多不同的glucosamine/chondroitin 產品在市場上, 但他們不是全部創造了均等。我們看了最佳的結果從包含純淨的成份是人的成績在質量的產品。產品譬如Drs. Foster 和史密斯聯合關心和Gluco-C, 或獸醫被賣的產品Cosequin 是數適合這個類別。

S Adenosyl L 氨基甲硫基丁酸(同樣, Denosyl SD4): 一個最近產品, Denosyl SD4, 主張了為骨關節炎的管理在人。這個產品效力為骨關節炎的管理在動物中不充分地被確定了, 然而它被使用作為治療為肝臟病在狗和貓。它有抗發炎和痛苦解除物產。

Perna 淡菜: Perna 小管, 或綠色lipped 淡菜, 是可食的貝類被發現在離紐西蘭的附近岸。軟的組織被分離從殼, 被洗滌多次, 結冰, 和被冰凍乾燥。它被處理成一粒美好的粉末和然後增加來產品。它被彌補61% 蛋白質、13% 碳水化合物、12% glycosaminoglycans (堵嘴), 5% 油脂(包括eicosatetraenoic 酸, 或ETAs), 5% 礦物, 和4% 水。它並且包含氨基葡萄糖, 堵嘴前體和軟骨的當中一個積木。氨基葡萄糖、堵嘴(複雜糖沒有枝的鏈子) 並且ETAs (類型Ω3 脂肪酸) 是化合物在淡菜應該對它的有利作用貢獻。ETAs 是幫助在抗發炎活動和從而關節痛的減少的關鍵成份。堵嘴是軟骨和synovial 流體主要組分被發現在聯接。

四圜素: 某四圜素譬如doxycycline 和二甲胺四環素被顯示禁止劃分軟骨的酵素。一項研究研究的結果建議, doxycyline 減少了軟骨的退化在狗與被爆裂的cruciate 韌帶。進一步研究需要完成評估這些四圜素的好處在骨關節炎的治療在狗。

可注射的疾病修改骨關節炎代理

Polysulfated Glycosaminoglycan (Adequan): Adequan 是被執行作為射入的產品。一系列的射擊被放棄幾星期和非常經常有有利結果。費用和每週射入不便是一個威懾物對一些所有者, 特別是從口頭氨基葡萄糖產品是很有效的。這個產品幫助防止軟骨故障, 也許幫助以新軟骨綜合。這個產品的行動完全機制不完全地被瞭解, 但看上去從事幾個不同的區域在軟骨保護和綜合。

Hyaluronic 酸(傳奇): Hyaluronic 酸是聯合流體一個重要組分。包括它在骨關節炎的managment 可以保護聯接由增加聯合流體的黏度, 減少炎症和換氣自由基。大多數對hyaluronic 酸的研究完成在人和馬, 但它也許並且是有效的在狗。這是被執行直接地入聯接的一個可注射的產品。

其它口頭補充

甲醇sulfonyl 甲烷(MSM): MSM 是一種自然, sulfur-containing 化合物由海帶生產在海洋。MSM 被報告提高結締組織結構正直, 和幫助減少傷痕組織由修改對傷痕形成貢獻的cross-linkages 。MSM 被促進了作為有強有力抗發炎和痛苦減少物產。

肌酸: 肌酸 是氨基酸衍生物被形成在肝臟、腎臟, 和胰腺從氨基酸氨基胍基戊酸、氨基乙酸, 和氨基甲硫基丁酸。它被發現在紅肉和魚。肌酸是沒有一位肌肉建造者, 而是助手在adenosine triphosphate 的身體生產(ATP), 燃料, 為短小, 能量強烈的爆炸。在人, 它建立精瘦的身體大量由幫助肌肉工作更長, 允許你艱苦訓練, 練習更多舉重, 和有更多重複。這是在導致大廈肌肉的鍛煉的增量, 不是肌酸單獨。肌酸也許是有用的在狗以肌肉萎縮與相關骨關節炎。

維生素C: 維生素C 作為抗氧劑和是重要營養素在膠原和軟骨綜合。由於狗和貓能製造他們自己的維生素C, 不要求它在他們的飲食像人, 使用維生素C 效力在骨關節炎的管理在狗依然是不明。補充用維生素C 在一個合理的水平不會導致毒力, 也許證明有一個有利作用。

Ω3 脂肪酸: Ω3 脂肪酸 經常被使用為遺傳性過敏症的標誌的管理在狗。由於他們的抗發炎物產, 一些主張了他們的用途在狗以骨關節炎。研究研究實施中將確定他們的有效率在骨關節炎的管理。

Duralactin: 最近, 一種給予專利的成份被獲得從草食的母牛牛奶被學習了和被銷售了為musculoskeletal 混亂的管理在狗。這稱Duralactin, 有抗發炎物產, 和是non-prescription 產品。它也許使用作為主要支援營養援助幫助處理炎症或與non-steroidal 抗發炎藥物(NSAIDs) 或類皮質激素一道。

抗發炎藥物

緩衝的阿斯匹靈: 緩衝的阿斯匹靈是一劑優秀抗發炎和止痛藥在狗(不要給您的貓阿斯匹靈除非由您的獸醫規定) 。它可能被使用與glucosamine/chondroitin 產品一起。與所有阿斯匹靈產品被使用在狗, 有小腸翻倒風險或在罕見的案件, 胃 潰瘍。由於這些問題, 它建議如果狗開發GI 翻倒的標誌, 產品被中斷直到獸醫檢查可能執行。(由給阿斯匹靈以膳食, 您可以能減少副作用的可能性。) 使用緩衝的阿斯匹靈被公式化為狗使劑量和管理更加容易。

Carprofen (Rimadyl), Etodolac (EtoGesic), Deracoxib (Deramaxx), Ketoprofen, Meloxicam: 這些是non-steroidal 抗發炎藥物(NSAIDs) 被開發用於狗以骨關節炎。他們是強和有效的止痛藥和抗發炎代理。他們是處方產品並且由於潛在的副作用, 仔細的緊持對藥量的數量和頻率必須被跟隨。製造商推薦週期性bloodwork 做在是在這個產品監測任一顯現出的肝臟 或 其它問題起因於他們的用途的動物。這些產品最初地經常被使用以氨基葡萄糖療法並且然後當氨基葡萄糖產品開始運作, NSAID 藥量也許被減少甚至被消滅。任何NSAID 不應該被使用與阿斯匹靈、類皮質激素, 或其它NSAIDs 。Acetaminophen (Tylenol), 和ibuprofen 有許多潛在的副作用和不被推薦沒有獸醫教導。

類皮質激素: 類皮質激素被使用許多年對待痛苦並且 炎症 與相關骨關節炎, 然而, 他們的用途是有爭議的。類皮質激素作為一有力抗發炎, 但不幸地, 有許多不受歡迎的短和長期副作用。由於這些副作用和出現更新, 更加具體的藥物, 類皮質激素一般只被使用在更舊的動物以所有其它痛苦控制產品失敗了的突然起燃。類皮質激素是處方產品和進來藥片和可注射的形式。
Many pets develop some form of joint disease during their lives. It can be mild, even unnoticeable to the pet owner, or it can be debilitating, severely affecting the pet's quality of life, or even causing complete lameness. The majority of cases fall somewhere in between.

While some pets may develop joint disease in the first half of their lives, signs usually do not appear until the latter half of life, which varies depending on your pet's breed. Dogs are more susceptible to arthritis than cats, and the larger dog breeds are more vulnerable than smaller breeds.

The most common signs of joint disease include stiffness, limping, or favoring a limb - particularly after sleep or resting, inability to rise, reluctance to jump or even climb stairs, and noticeable pain.

Causes of arthritis

There are many diseases that affect the joints of dogs, so many, in fact, that there are 10 major classifications.

Joint diseases occur as a result of:

Ligament, tendon, or muscle disease, e.g., ruptured anterior cruciate ligament

Fractures involving the joint

Developmental disorders, e.g., hip dysplasia, elbow dysplasia, osteochondritis dissecans, Legg-Perthes disease

Congenital disorders, e.g., Wobbler's syndrome (cervical spondylomyelopathy), luxated patella

Dietary and hormonal disease, e.g., hyperparathyroidism, obesity

Metabolic disorders, e.g., von Willebrand's disease (hemophilia) in dogs

Cancer

Degenerative joint disease (osteoarthritis)

Inflammatory joint disease, e.g., Lyme disease, rheumatoid arthritis

Degenerative spinal joint disease, e.g., intervertebral disc disease, cauda equina syndrome

Management of arthritis

Medical treatment of hip dysplasia and osteoarthritis has greatly improved in the last several years thanks to the introduction and approval of several new supplements and drugs. Because hip dysplasia (and other types of dysplasias) are primarily inherited conditions, there are no products on the market that prevent their development. Through proper diet, exercise, supplements, anti-inflammatories, and pain relief, you may be able to decrease the progression of degenerative joint disease, but the looseness in the joint or bony changes will not change significantly.

Medical management is indicated for both young dogs with clinical signs and for older dogs with chronic osteoarthritis. Because of the high cost involved with many surgeries, medical management is many times the only realistic option for many pet owners. Medical management is multifaceted. For the best results, several of the following modalities should be instituted. For most animals, veterinarians begin with the first recommendations and work their way down this list as needed to control the pain and inflammation associated with degenerative joint disease.

Weight Management

Weight management is the first thing that must be addressed. All surgical and medical procedures will be more beneficial if the animal is not overweight. Considering that up to half of the pets in the U.S. are overweight, there is a fair chance that many of the dogs with hip dysplasia/osteoarthritis are also overweight. Helping a dog lose pounds until he reaches his recommended weight, and keeping it there, may be the most important thing an owner can do for a pet. However, this may be the hardest part of the treatment, but it is worth it. You, as the owner, have control over what your dog eats. If you feed an appropriate food at an appropriate level and keep treats to a minimum, your dog will lose weight.

Exercise

Exercise is the next important step. Exercise that provides for good range of motion and muscle building and limits wear and tear on the joints is the best. Leash walking, swimming, walking on treadmills, slow jogging, and going up and down stairs are excellent low-impact exercises. An exercise program should be individualized for each dog based on the severity of the osteoarthritis, weight, and condition of the dog. In general, too little exercise can be more detrimental than too much, however the wrong type of exercise can cause harm. While watching a dog play Frisbee is very enjoyable and fun for the dog, it is very hard on a dog's joints. Remember, it is important to exercise daily; only exercising on weekends, for instance, may cause more harm than good if the animal is sore for the rest of the week and reluctant to move at all. Warming the muscles prior to exercise and following exercise with a "warm-down" period are beneficial. Consult with your veterinarian regarding an exercise program appropriate for your dog.

Warmth and good sleeping areas

Most people with arthritis find that the signs tend to worsen in cold, damp weather. Keeping your pet warm, may help him be more comfortable. A pet sweater will help keep joints warmer. You may want to consider keeping the temperature in your home a little warmer, too.

Providing a firm, orthopedic foam bed helps many dogs with arthritis. Beds with dome-shaped, orthopedic foam distribute weight evenly and reduce pressure on joints. They are also much easier for the pet to get out of. Place the bed in a warm spot away from drafts.

Massage and physical therapy

Your veterinarian or the veterinary staff can show you how to perform physical therapy and massage on your dog to help relax stiff muscles and promote a good range of motion in the joints. Remember, your dog is in pain, so start slowly and build trust. Start by petting the area and work up to gently kneading the muscles around the joint with your fingertips using a small, circular motion. Gradually work your way out to the surrounding muscles. Moist heat is also beneficial.

Making daily activities less painful

Going up and down stairs is often difficult for arthritic pets, and for dogs, it can make going outside to urinate and defecate very difficult. Many people build or buy ramps, especially on stairs leading to the outside, to make it easier for the dogs to go outside.

Larger breed dogs can especially benefit from elevating their food and water bowls. Elevated feeders make eating and drinking more comfortable for arthritic pets, particularly if there is stiffness in the neck or back.

Oral Disease-Modifying Osteoarthritis Agents

Glucosamine and Chondroitin: Glucosamine and chondroitin are two ingredients of supplements that have become widely used in treating both animals and humans for osteoarthritis. Due to the overwhelming success in treating patients with osteoarthritis, these products have come to the forefront of therapy and are becoming the most popular products for managing arthritis today.

Glucosamine is the major sugar found in glycosaminoglycans and hyaluronate, which are important building blocks in the synthesis and maintenance of cartilage in the joint. Chondroitin enhances the synthesis of glycosaminoglycans and inhibits damaging enzymes in the joint.

When a dog has hip dysplasia or other osteoarthritis, the joint wears abnormally and the protective cartilage on the surface of the joint gets worn away and the resultant bone-to-bone contact creates pain. Glucosamine and chondroitin give the cartilage-forming cells (chondrocytes) the building blocks they need to synthesize new cartilage and to repair the existing damaged cartilage. These products are not painkillers; they work by actually healing the damage that has been done. These products generally take at least six weeks to begin to heal the cartilage and most animals need to be maintained on these products the rest of their lives to prevent further cartilage breakdown. These products are very safe and show very few side effects. There are many different glucosamine/chondroitin products on the market, but they are not all created equal. We have seen the best results from products that contain pure ingredients that are human grade in quality. Products such as Drs. Foster and Smith Joint Care and Gluco-C, or the veterinary-sold product Cosequin are several that fit this category.

S-Adenosyl-L-methionine (SAMe, Denosyl SD4): A recent product, Denosyl SD4, has been advocated for the management of osteoarthritis in people. The efficacy of this product for the management of osteoarthritis in animals has not been fully determined, however it is being used as a treatment for liver disease in dogs and cats. It has both anti-inflammatory and pain relieving properties.

Perna Mussels: Perna canaliculus, or green-lipped mussel, is an edible shellfish found off the shores of New Zealand. The soft tissue is separated from the shell, washed several times, frozen, and freeze-dried. It is then processed into a fine powder and added to products. It is made up of 61% protein, 13% carbohydrates, 12% glycosaminoglycans (GAGs), 5% lipids (including eicosatetraenoic acids, or ETAs), 5% minerals, and 4% water. It also contains glucosamine, a GAG precursor and one of the building blocks of cartilage. Glucosamine, GAGs (unbranched chains of complex sugars) and ETAs (a type of Omega-3 fatty acids) are the compounds in the mussel believed to contribute to its beneficial effects. ETAs are the key ingredients that help in the anti-inflammatory activity and thereby the reduction of joint pain. GAGs are the main components of cartilage and the synovial fluid found in joints.

Tetracyclines: Some tetracyclines such as doxycycline and minocycline have been shown to inhibit enzymes that break down cartilage. The results of one research study suggested that doxycyline reduced the degeneration of cartilage in dogs with ruptured cruciate ligaments. Further studies need to be done to evaluate the benefit of these tetracyclines in the treatment of osteoarthritis in dogs.

Injectable Disease-Modifying Osteoarthritis Agents

Polysulfated Glycosaminoglycan (Adequan): Adequan is a product that is administered as an injection. A series of shots are given over weeks and very often have favorable results. The cost and the inconvenience of weekly injections are a deterrent to some owners, especially since the oral glucosamine products are so effective. This product helps prevent the breakdown of cartilage and may help with the synthesis of new cartilage. The complete mechanism of action of this product is not completely understood, but appears to work on several different areas in cartilage protection and synthesis.

Hyaluronic Acid (Legend): Hyaluronic acid is an important component of joint fluid. Including it in the managment of osteoarthritis may protect the joint by increasing the viscosity of the joint fluid, reducing inflammation and scavenging free radicals. Most of the research on hyaluronic acid has been done in people and horses, but it may also be effective in dogs. This is an injectable product which is administered directly into the joint.[/size][/size]
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[color=Magenta][size=5][b]Lumbosacral 狹窄(Cauda Equina 綜合症狀)   [/b][/size][/color]

Lumbosacral 狹窄 並且被命名了lumbosacral 不穩定、lumbosacral 畸形、lumbosacral malarticulation 、腰部脊髓狹窄、lumbosacral spondylolisthesis 、lumbosacral 神經根壓縮, 和cauda equina 綜合症狀。所有這些期限描述聯接的關節炎在最後腰部椎骨和sacrum 之間, 是骨頭的當中一個組成骨盆。這關節炎使脊髓和神經通過的運河狹窄。椎間的圓盤在椎骨和sacrum 之間經常是反常的, 更加進一步使運河狹窄。關節炎和圓盤疾病施加壓力在神經結束脊髓。lumbosacral 狹窄症狀, 然後, 是神經傷的結果。

什麼是lumbosacral 狹窄症狀?

cauda equina 綜合症狀的最共同的標誌是痛苦。痛苦也許發生在後面, 在一條或兩條後腿裡, 或尾巴。狗通常有困難上升從躺下, 但一旦他開始走他解決僵硬。那裡也許是肌肉損失在一條或兩條後方腿裡。狗也許有困難小便或排糞由於痛苦, 也許變得incontinent, 或也許無法小便。一些狗無法移動他們的尾巴, 或有嚴厲痛苦如果尾巴被移動。經常狗將有拖曳的 步態, 和拖著腳走路他們的腳趾。一些狗將嚼在他們的骨盆區域、後面肢體, 或尾巴, 有時創造可觀的損傷由這自已切斷。

許多標誌看以lumbosacral 狹窄可能仿造那些hip 發育異常, 並且二個條件需要被區分。

哪個動物在危險中有lumbosacral 狹窄?

Lumbosacral 狹窄最共同地發生在大養殖狗。德國牧羊人看來是可能開發這個情況。情況可能被獲取, 意味狗開始在法線之外和然後開發了這個情況。或, lumbosacral 狹窄可能是一個 先天 情況, 意味狗出生以反常性。不管怎樣, 症狀一般不發生直到狗在在3 和7 年紀之間。

Lumbosacral 狹窄很少看在貓。

lumbosacral 狹窄怎麼被診斷?

獸醫將要求所有者歷史的何時症狀被開發, 等。一次體檢然後將執行。後面肢體將被操作以各種各樣的方式確定哪個位置是痛苦的。獸醫並且將做神經學檢查, 包括測試反射, 確定哪根神經也許受傷。

射線照相(X-射線) 被採取評估脊椎和骨盆。研究結果可能是非常暗示的lumbosacral 狹窄, 但不是充足做診斷。達到診斷, 特別規程必須由注射染料入受影響的區域和re 射線照相執行。根據染料被安置的地方, 做法叫做myelography 、epidurography, 或diskography 。這些規程必須完成在麻醉之下。染料的位移由反常性在骨頭和椎間的圓盤證實lumbosacral 狹窄診斷。

lumbosacral 狹窄怎麼被對待?

根據情況的嚴肅, 動物體驗的相當數量痛苦, 動物的整體健康, 財政制約, 並且其它因素, lumbosacral 狹窄外科地或nonsurgically 被對待。

Nonsurgical 治療: 如果情況是溫和的, 狗也許被對待以 嚴密的 休息6 個到8 個星期。抗發炎療程譬如prednisolone 被給。在許多情況下, 這可能解除症狀。但是, 當狗變得更加活躍, 症狀可能返回。

外科治療: 有二個不同外科技術使用對待lumbosacral 狹窄。在一, 骨頭一起被熔化在一樣正常位置儘可能。這防止反常行動在他們之間, 和減少進一步關節炎風險。在第二個技術, 一部分的骨頭和椎間的圓盤被去除減少壓力在脊髓和神經。

無論如何, 狗必須被限制2 個到4 個星期在手術以後, 和也許並且被安置在prednisolone 療法。為有困難或無法小便的狗, 膀胱必須手工被表達多次一天。

什麼是預測為狗以lumbosacral 狹窄?

外型為狗以lumbosacral 狹窄依靠症狀嚴肅在治療之前。是溫和地受影響的狗也許能返回到正常作用。為那些無法incontinent 或小便在治療之前, 預測是窮的
Lumbosacral stenosis has also been termed lumbosacral instability, lumbosacral malformation, lumbosacral malarticulation, lumbar spinal stenosis, lumbosacral spondylolisthesis, lumbosacral nerve root compression, and cauda equina syndrome. All these terms describe arthritis of the joint between the last lumbar vertebra and the sacrum, which is one of the bones that makes up the pelvis. This arthritis narrows the canal through which the spinal cord and nerves pass through. The intervertebral disc between the vertebra and the sacrum is often abnormal as well, further narrowing the canal. The arthritis and disc disease put pressure on the nerves coming off the spinal cord. The symptoms of lumbosacral stenosis, then, are a result of nerve injury.

What are the symptoms of lumbosacral stenosis?

The most common sign of cauda equina syndrome is pain. The pain may occur in the back, in one or both hind legs, or the tail. The dog usually has difficulty rising from lying down, but once he begins to walk about he works out of the stiffness. There may be muscle loss in one or both rear legs. The dog may have difficulty urinating or defecating because of the pain, may become incontinent, or may be unable to urinate. Some dogs are unable to move their tail, or have severe pain if the tail is moved. Often dogs will have a shuffling gait, and scuff their toes. Some dogs will chew on their pelvic area, hind limbs, or tail, sometimes creating considerable damage by this self-mutilation.

Many of the signs seen with lumbosacral stenosis can mimic those of hip dysplasia, and the two conditions need to be differentiated.

Which animals are at risk of having lumbosacral stenosis?

Lumbosacral stenosis occurs most commonly in large breed dogs. German Shepherds appear to be more likely to develop this condition. The condition can be acquired, meaning the dog started out normal and then developed this condition. Or, lumbosacral stenosis can be a congenital condition, meaning the dog was born with the abnormality. Either way, the symptoms generally do not occur until the dog is between 3 and 7 years of age.

Lumbosacral stenosis is rarely seen in cats.

How is lumbosacral stenosis diagnosed?

The veterinarian will ask the owner for a history of when the symptoms developed, etc. A physical exam will then be performed. The hind limbs will be manipulated in various ways to determine which positions are painful. The veterinarian will also do a neurological exam, including testing the reflexes, to determine which nerves may be injured.

Radiographs (x-rays) are taken to evaluate the spine and pelvis. The findings can be very suggestive of lumbosacral stenosis, but are not sufficient to make the diagnosis. To achieve a diagnosis, special procedures must be performed by injecting dye into the affected area and re-radiographing. Depending on where the dye is placed, the procedure is called myelography, epidurography, or diskography. These procedures must be done under anesthesia. Displacement of the dye by the abnormalities in the bones and intervertebral disc confirms the diagnosis of lumbosacral stenosis.

How is lumbosacral stenosis treated?

Depending on the severity of the condition, amount of pain the animal is experiencing, overall health of the animal, financial restrictions, and other factors, lumbosacral stenosis is treated surgically or nonsurgically.

Nonsurgical treatment: If the condition is mild, dogs may be treated with strict rest for 6 to 8 weeks. Anti-inflammatory medications such as prednisolone are given. In many cases, this can relieve the symptoms. However, when the dog becomes more active, the symptoms can return.

Surgical treatment: There are two different surgical techniques used to treat lumbosacral stenosis. In the first, the bones are fused together in as normal a position as possible. This prevents abnormal motion between them, and reduces the risk of further arthritis. In the second technique, part of the bone and the intervertebral disc are removed to reduce pressure on the spinal cord and nerves.

In either case, dogs must be confined for 2 to 4 weeks after surgery, and may also be placed on prednisolone therapy. For dogs who have difficulty or are unable to urinate, the bladder must be manually expressed several times a day.

What is the prognosis for dogs with lumbosacral stenosis?

The outlook for dogs with lumbosacral stenosis is dependent on the severity of symptoms before treatment. Dogs who are mildly affected may be able to return to normal function. For those who are incontinent or unable to urinate prior to treatment, the prognosis is much poorer.

minibabyqq 2006-12-20 19:42

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[size=12px][color=red][size=5][b][color=magenta]Luxating 臏骨 Luxating Patella[/color]  [url=http://www5.discuss.com.hk/misc.php?action=emailfriend&tid=2824049][img]http://www5.discuss.com.hk/images/discuss_style/emailtofriend3.gif[/img][/url] [/b][/size][/color]
[size=12px]一條狗從更小的養殖的當中一個運行橫跨庭院追逐一個被扔的球。在中間大步, 他叫喊在痛苦中和成功他的左後腿地面。在一秒鐘以後, 他持續跛行three-legged 時尚。在十分鐘以後, 後方腿下落退卻對地面並且他通常使用它。這個情節發生可能每週一次。它從未真正地似乎打擾他– 痛苦, 瘸的一個短的期間yelp, 和在幾分鐘他是回到他的老自已。典型地, 他是小或玩具養殖譬如拉薩Apso, Pekingese 、Pomeranian, 長捲毛狗, 或波士頓公牛。
一塊luxating 的臏骨也許更加嚴厲地影響一些動物。他們也許握腿幾天和顯示可觀的難受。有一塊luxating 的臏骨在兩條後腿的狗也許改變他們的整個姿勢, 由投下他們的後腿肉和握後方腿更遠從身體當他們走。那些最嚴厲地受影響不能甚而使用他們的後方腿, 走由完全地平衡在他們的前面腿像馬戲節目, 或拿著他們的後腿肉地面。

正常膝蓋解剖學

臏骨是我們知道作為膝蓋蓋帽的骨頭。一條凹線在最後股骨的允許臏骨上上下下滑動當膝蓋關節彎曲反覆。這樣做, 臏骨引導quadriceps 肌肉的行動在更低的腿。臏骨並且保護膝蓋關節。

看股骨(大腿骨頭的) 更低的前面部份在一條正常狗, 您將注意形成一條相當深刻的凹線在上下臏骨應該滑的二個骨多的土坎。這些結構限制patella’s 運動對一個被制約的地方, 並且這樣做, 控制quadriceps 肌肉的活動。

整個系統由聯合流體經常潤滑。這有效以便有行動總自由在結構之間。

什麼發生當臏骨是luxated?

在一些狗, 由於畸形或精神創傷, 土坎形成patellar 凹線不是突出的, 並且一條太淺凹線被創造。在一條狗以淺凹線, 臏骨意志luxate (跳出凹線) 斜向一邊, 特別是往裡面。這導致腿對' 關起來' 以腳被握地面。

當臏骨luxates 從股骨, 它的凹線無法通常返回到它的正常位置直到quadriceps 肌肉放鬆和增加在長度。這解釋為什麼受影響的狗也許被迫握他的腿幾分鐘或如此在最初的事件以後。當肌肉被收縮並且臏骨是luxated 從它的正確位置, 聯接被拿著在被屈曲的或彎曲的位置。yelp 是從痛苦由膝蓋蓋帽造成滑橫跨股骨的骨多的土坎。一次在位置外面, 動物不感覺難受和繼續他的活動。

哪條狗在危險中有a luxated 臏骨?

狗, 特別微型和玩具長捲毛狗更小養殖, 有臏骨luxation 的最高的發生。遺傳學可能充當角色。

在安排極端短的腿譬如Basset 追逐或Dachshund 的某些養殖, patellar luxation 認為是次要對股骨和脛骨的反常形狀。骨頭的曲度在這些養殖運作與quadriceps 肌肉的力量一道偏移臏骨對裡面。請不要誤會– 沒有所有這些養殖的成員影響與patellar luxation, 唯一一個小部份。

什麼是症狀?

多數狗是中年, 以斷斷續續的(在再再) 瘸的歷史在受影響的後方leg(s) 。一條受影響的狗共同地停止和大聲呼喊在痛苦中當他跑。受影響的腿將被擴大rearward, 並且有一陣子, 狗無法屈曲它回到正常位置。

什麼是風險?

未更正, patellar 土坎將佩帶, 凹線將變得更淺並且狗將變得進步地更瘸。關節炎過早地將影響聯接, 導致一個永久地圓鼓的膝蓋以粗劣的流動性。所以, 一個好評估需要由您的獸醫完成及早在情況防止長期關節炎致殘。

治療為luxating 的臏骨

和會被期望, 醫療療法有一點矯正能力在這混亂並且手術必需因此和是選擇的治療。一種外科治療不是必要的在每個體以這個情況。

手術可能修改受影響的結構和臏骨的運動。凹線在股骨的基地也許外科地被加深更好包含膝蓋蓋帽。膝蓋蓋帽也許' 被栓在' 側向地下(在外部) 防止它中間偏離(往裡面) 。骨多的隆起在quadriceps 腱的附件的站點在脛骨, 也許被切除和然後被再依附在一個更加側向的位置。所有這些規程運作得很好並且型執行依靠單獨案件和臨床工作者。動物應該迅速反應在手術和通常完全地恢復在三十天之內, 使用他的腿以正常時尚之後。

助長考慮

由於牢固的基因關係, 我們真正地認為, 動物以這混亂不應該被使用為養殖。他們能仍然是優秀寵物- 並且那些要求手術通常將帶領完全正常生活沒有對活動的任何制約。
   
A dog from one of the smaller breeds runs across the yard chasing a tossed ball. In mid-stride, he yelps in pain and pulls his left hind leg off of the ground. After a second, he continues limping on in a three-legged fashion. After ten minutes, the rear leg drops back down to the ground and he uses it normally. This episode occurs maybe once a week. It never really seems to bother him that much – a yelp of pain, a short period of lameness, and in a few minutes he is back to his old self. Typically, he is a small or toy breed such as a Lhasa Apso, Pekingese, Pomeranian, Poodle, or Boston Bull.
A luxating patella may affect some animals much more severely. They may hold the leg up for several days and show considerable discomfort. Dogs who have a luxating patella on both hind legs may change their entire posture, by dropping their hindquarters and holding the rear legs farther out from the body as they walk. Those most severely affected may not even use their rear legs, walking by balancing themselves on their front legs like a circus act, or holding their hindquarters completely off the ground.

Normal knee anatomy

The patella is the bone we know as the knee cap. A groove in the end of the femur allows the patella to glide up and down when the knee joint is bent back and forth. In doing so, the patella guides the action of the quadriceps muscle in the lower leg. The patella also protects the knee joint.

Looking at the lower front portion of the femur (the thigh bone) in a normal dog, you will notice two bony ridges that form a fairly deep groove in which the patella is supposed to slide up and down. These structures limit the patella’s movement to one restricted place, and in doing so, control the activity of the quadriceps muscle.

The entire system is constantly lubricated by joint fluid. It works so that there is total freedom of motion between the structures.

What occurs when the patella is luxated?

In some dogs, because of malformation or trauma, the ridges forming the patellar groove are not prominent, and a too-shallow groove is created. In a dog with shallow grooves, the patella will luxate (jump out of the groove) sideways, especially toward the inside. This causes the leg to 'lock up' with the foot held off the ground.

When the patella luxates from the groove of the femur, it usually cannot return to its normal position until the quadriceps muscle relaxes and increases in length. This explains why the affected dog may be forced to hold his leg up for a few minutes or so after the initial incident. While the muscles are contracted and the patella is luxated from its correct position, the joint is held in the flexed or bent position. The yelp is from the pain caused by the knee cap sliding across the bony ridges of the femur. Once out of position, the animal feels no discomfort and continues his activity.

Which dogs are at risk of having a luxated patella?

Smaller breeds of dogs, especially Miniature and Toy Poodles, have the highest incidence of patella luxation. Genetics can play a role.

In certain breeds that have extremely short legs such as the Basset Hound or Dachshund, patellar luxation is thought to be secondary to the abnormal shape of the femur and tibia. The curvatures of the bones in these breeds work in conjunction with the forces of the quadriceps muscles to displace the patella to the inside. Please do not misunderstand – not all members of these breeds are affected with patellar luxation, only a small portion.

What are the symptoms?

Most dogs are middle-aged, with a history of intermittent (on-again-off-again) lameness in the affected rear leg(s). An affected dog commonly stops and cries out in pain as he is running. The affected leg will be extended rearward, and for a while, the dog is unable to flex it back into the normal position.

What are the risks?

Uncorrected, the patellar ridges will wear, the groove will become even shallower and the dog will become progressively more lame. Arthritis will prematurely affect the joint, causing a permanently swollen knee with poor mobility. Therefore, a good evaluation needs to be done by your veterinarian early in the condition to prevent long-term arthritic crippling.

Treatment for luxating patellas

As would be expected, medical therapy has little corrective ability in this disorder and surgery is therefore required and is the treatment of choice. A surgical treatment is not necessary in every individual with this condition.

Surgery can alter both the affected structures and the movement of the patella. The groove at the base of the femur may be surgically deepened to better contain the knee cap. The knee cap itself may be 'tied down' laterally (on the outside) to prevent it from deviating medially (toward the inside). The bony protuberance at the site of the attachment of the quadriceps tendon on the tibia, may be cut off and then re-attached in a more lateral position. All of these procedures work well and the type performed depends on the individual case and the clinician. The animal should respond quickly after surgery and is usually completely recovered within thirty days, using his legs in normal fashion.

Breeding considerations

Because of the strong genetic relationships, we really feel that animals with this disorder should not be used for breeding. They can still be excellent pets - and those that do require surgery will usually lead perfectly normal lives without any restrictions on activity.[/size][/size]

minibabyqq 2006-12-20 19:42

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[size=12px][size=5][color=magenta][b]白內障   Cataracts[/b][/color][/size]

大瀑布是共同的問題的當中一個影響狗的眼睛。有許多大瀑布形成的不同的形式和起因。他們影響所有狗的養殖和年齡, 但某些型通常出現在某些養殖。竟管他們是非常共同, 仍然有很多, 我們不知道關於似犬大瀑布。唯一的當前的治療選擇是手術, 但是以正確耐心選擇結果是非常好的。這篇文章將解釋一些大瀑布的不同的形式包括他們的起始的年齡和他們的治療選擇。
什麼是大瀑布?

詞大瀑布逐字地意味' 劃分。' 這次故障提到透鏡纖維或它的膠囊的正常安排的中斷。這中斷導致透明度損失和對視覺的總值減少。大瀑布看上去有白色或被擊碎的冰出現和經常被發現在眼睛的透鏡。

核硬化

我們經常得到帶領一條更舊的狗進入診所訴說大瀑布形成在他們的狗的眼睛的人。時間的大多數, 狗沒有大瀑布, 而是有更加共同的情況以' 核硬化著名。' 核硬化是發生在更舊的狗透鏡的正常變動。核硬化出現作為一輕微graying 透鏡。它同時通常發生在兩隻眼睛和發生在多數狗經過六年紀。透明度損失發生由於線性纖維的壓縮在透鏡。情況極大不影響狗的視覺並且治療不被推薦。

大瀑布怎麼形成?

竟管有幾大瀑布的不同的形式和起因, 他們全都相似地顯現出。正常透鏡被維護在一個被脫水的狀態。它包括66% 水和33% 蛋白質。有一個複雜的鈉水泵系統在保留這water/protein 平衡在檢查的透鏡。當biomechanical 系統在透鏡被損壞, 這條泵裝置開始失敗並且額外水搬入透鏡。另外, 不能溶解的蛋白質的百分比增加。這些變動導致透明度和大瀑布形成損失。

起始的年齡

狗開發大瀑布的年齡是非常重要在分類類型大瀑布。起始的年齡是特別重要為確定如果大瀑布是一個遺傳性特徵的結果在狗某些養殖。

先天大瀑布: 這些是是存在出生時的大瀑布。這些大瀑布通常發生在兩隻眼睛。竟管動物是出生與他們, 他們不一定 被繼承。傳染或毒素也許導致這些大瀑布的形成當小狗是在子宮內。主要先天大瀑布譬如那些被發現在微型Schnauzers, 然而, 被繼承。

發展(早期的起始) 大瀑布: 發展大瀑布是那些在初期顯現出在生活中。和與先天大瀑布, 他們也許由外部來源繼承或造成譬如精神創傷、 糖尿病mellitus、傳染, 或毒力。被繼承的大瀑布在這年齡是共同在幾養殖包括阿富汗追逐和標準長捲毛狗。

老態龍鍾的(晚起始) 大瀑布: 發生在狗經過六年紀的大瀑布叫做老態龍鍾的大瀑布。他們頻繁地發生較少在狗比在人。核硬化, 不認為是一個醫療課題, 與大瀑布經常被混淆在這年齡。

被繼承的大瀑布

被繼承的大瀑布在狗也許發生獨立地或與其它 視覺 疾病有關係。看上去開發被繼承的大瀑布與他們的起始一起的年齡的養殖下面是列出的。如果狗被診斷與被繼承的大瀑布, 狗不應該明顯地被使用為養殖由於使疾病永存可能在子孫。

養殖 起始的年齡
阿富汗追逐
6-12 個月
美國斗雞家Spaniel
6 + 幾個月
波士頓狗
先天
切塞皮克灣獵犬 1 + 幾年
德國牧羊人 8 + 幾星期
金黃獵犬
6 + 幾個月
拉布拉多獵犬
6 + 幾個月
微型Schnauzer
先天或6 + 幾個月
老英國Sheepdog
先天
西伯利亞愛斯基摩
6 + 幾個月
Staffordshire 公牛狗
6 + 幾個月
標準長捲毛狗 1 + 幾年
威爾士Springer Spaniel 先天
西部高地白色狗 先天

最共同的新陳代謝的混亂造成大瀑布形成在狗是糖尿病mellitus 。如果糖尿病狗被跟隨一年或更, 幾乎所有會開發大瀑布。在糖尿病狗, 葡萄糖含量在透鏡增加。額外葡萄糖被轉換成山梨糖醇, 導致在水彙集的增量對透鏡。增量在水中導致透鏡纖維和收效的大瀑布的故障。大瀑布在糖尿病狗可能極端迅速地顯現出, 如果狗不被調控。他們一般影響兩隻眼睛。透鏡的外科撤除可能成功地進行在糖尿病狗, 如果動物成功地被調控了至少三個月。

精神創傷

刺、獵槍藥丸, 或其它對象的精神創傷從車禍, 或滲透也許損壞透鏡並且大瀑布也許顯現出。這些類型大瀑布通常只發生在一隻眼睛, 可能成功地被對待以外科撤除。

治療

治療為似犬大瀑布包括透鏡的外科撤除。有當前沒有好non-surgical 治療為這個情況。以在獸醫外科技巧和設備的增量, 外科手術去除問題透鏡變得越來越共同。有幾個不同的技術使用去除受影響的透鏡包括; 整個透鏡的撤除和周圍的膠囊, 透鏡的透鏡的撤除離開周圍的膠囊, phacoemulsification, 和 透鏡的志向和乾燥作用。所有這些技術可能提供優秀結果。為一個成果, 受影響的動物必須接受一次詳盡的考試確定如果這是一名好外科候選人。不被調控的糖尿病動物, 難對待日報, 或動物在粗劣或failing 健康的進取的動物, 不是好外科候選人。如果您懷疑您的狗開發大瀑布, 那麼您應該嚴密工作以獸醫眼科醫生採取最佳和最有效的治療過程為狗。
Cataracts are one of the most common problems affecting the eyes of the dog. There are many different forms and causes of cataract formation. They affect all breeds and ages of dogs, but certain types show up more commonly in certain breeds. Despite the fact that they are very common, there is still a lot that we do not know about canine cataracts. The only current treatment option is surgery, but with correct patient selection the outcome is very good. This article will explain some of the different forms of cataracts including their age of onset and their treatment options.
What are cataracts?

The word cataract literally means 'to break down.' This breakdown refers to the disruption of the normal arrangement of the lens fibers or its capsule. This disruption results in the loss of transparency and the resultant reduction in vision. Cataracts often appear to have a white or crushed ice appearance and are found in the lens of the eye.

Nuclear sclerosis

We often get people that bring an older dog into the clinic complaining of cataract formation in their dogs' eyes. The vast majority of the time, the dog does not have cataracts, but has the much more common condition known as 'nuclear sclerosis.' Nuclear sclerosis is a normal change that occurs in the lens of older dogs. Nuclear sclerosis appears as a slight graying of the lens. It usually occurs in both eyes at the same time and occurs in most dogs over six years of age. The loss of transparency occurs because of compression of the linear fibers in the lens. The condition does not significantly affect the vision of the dog and treatment is not recommended.

How do cataracts form?

Despite the fact that there are several different forms and causes of cataracts, they all develop in a similar fashion. The normal lens is maintained in a dehydrated state. It consists of 66% water and 33% protein. There is a complicated sodium water pump system in the lens that keeps this water/protein balance in check. When the biomechanical system in the lens is damaged, this pump system begins to fail and extra water moves into the lens. In addition, the percentage of insoluble protein increases. These changes result in the loss of transparency and cataract formation.

Age of onset

The age at which a dog develops cataracts is very important in classifying the type of cataract. The age of onset is particularly important for determining if the cataracts are the result of a hereditary trait in certain breeds of dogs.

Congenital Cataracts: These are cataracts that are present at birth. These cataracts usually occur in both eyes. Despite the fact that the animal is born with them, they are not necessarily inherited. Infections or toxins may cause the formation of these cataracts while the puppies are still in utero. Primary congenital cataracts such as those found in Miniature Schnauzers are, however, inherited.

Developmental (Early Onset) Cataracts: Developmental cataracts are those that develop early on in life. As with congenital cataracts, they may be inherited or caused by outside sources such as trauma, diabetes mellitus, infection, or toxicity. Inherited cataracts at this age are more common in several breeds including Afghan Hounds and Standard Poodles.

Senile (Late Onset) Cataracts: The cataracts that occur in dogs over six years of age are called senile cataracts. They occur much less frequently in dogs than in humans. Nuclear sclerosis, which is not considered to be a medical problem, is often confused with cataracts at this age.

Inherited cataracts

Inherited cataracts in the dog may occur independently or in association with other ocular disease. The breeds that appear to develop inherited cataracts along with their age of onset are listed below. If a dog is diagnosed with inherited cataracts, the dog should obviously not be used for breeding because of the likelihood of perpetuating the disease in the offspring.

Breed Age of Onset
Afghan Hound
6-12 months
American Cocker Spaniel
6 + months
Boston Terrier
Congenital
Chesapeake Bay Retriever 1 + years
German Shepherd 8 + weeks
Golden Retriever
6 + months
Labrador Retriever
6 + months
Miniature Schnauzer
Congenital or 6 + months
Old English Sheepdog
Congenital
Siberian Husky
6 + months
Staffordshire Bull Terrier
6 + months
Standard Poodle 1 + years
Welsh Springer Spaniel Congenital
West Highland White Terrier Congenital

The most common metabolic disorder resulting in cataract formation in the dog is diabetes mellitus. If diabetic dogs are followed for a year or more, almost all of them would develop cataracts. In diabetic dogs, the glucose concentrations in the lens increases. The extra glucose is converted into sorbitol, which causes an increase in the influx of water to the lens. The increase in water causes a breakdown of the lens fibers and a resulting cataract. Cataracts in diabetic dogs can develop extremely rapidly, if the dog is not regulated. They generally affect both eyes. Surgical removal of the lens can be successfully performed in the diabetic dog, if the animal has been regulated successfully for at least three months.

Trauma

Trauma from an automobile accident, or penetration of a thorn, shotgun pellet, or other object may damage the lens and a cataract may develop. These types of cataracts usually only occur in one eye and can be treated successfully with surgical removal.

Treatment

Treatment for canine cataracts consists of surgical removal of the lens. There is currently no good non-surgical treatment for this condition. With the increase in veterinary surgical skill and equipment, the surgical procedure to remove the problem lens is becoming increasingly more common. There are several different techniques used to remove the affected lens including; the removal of the entire lens and surrounding capsule, the removal of the lens leaving the surrounding capsule, phacoemulsification of the lens, and aspiration and desiccation of the lens. All of these techniques can offer excellent results. For a successful outcome, the affected animal must undergo a thorough examination to determine if it is a good surgical candidate. Diabetic animals that are not regulated, aggressive animals that are difficult to treat daily, or animals in poor or failing health, are not good surgical candidates. If you suspect your dog is developing cataracts, then you should work closely with a veterinary ophthalmologist to take the best and most effective course of treatment for the dog.[/size]
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[/td][/tr][/table]

minibabyqq 2006-12-20 19:43

轉貼自4682

[size=12px][color=red][color=red][b][size=5][color=magenta]攝護腺擴大 Prostate Enlargement[/color][/size]   [/b][/color][/color]


當人到達年齡的80, 他們有攝護腺的顯現出的癌症的一次80% 機會。這經常是 可能 難對待和生活威脅的一個惡性形式。當unneutered 公狗到達8 年紀, 他有顯現出的攝護腺疾病的一次大於80% 機會, 但它很少是癌的(良性 或惡性) 。封墊發揮同樣作用在作為它做在人和遭受所有同樣疾病的狗。幸運地為狗, 然而, 威脅生命的情況的發生是更低。但是, 多數unneutered 犬一次願或另, 遭受很多難受如果不嚴厲痛苦由於攝護腺封墊。
什麼是攝護腺封墊?

攝護腺封墊是在骨盆之間在膀胱之後和直接地在直腸之下的一個bi-lobed 結構。在四十磅狗, 這通常是大約直徑一到二英寸。它圍攏和是開放對尿道它的封墊的整個長度。小管或輸送管放置流體由攝護腺生產直接地入尿道作為它追獵通過攝護腺。攝護腺開始顯現出在狗到達青春期和獲得它的最大大小之前當狗二歲的時候。從那點, 它的大小由男性激素睪甾酮並且/或者各種各樣的疾病條件確定。

攝護腺封墊被分類作為輔助性封墊。這意味著, 它在某個方面是重要為成功養殖, 但直接地不生產精液。Prostatic 流體是總被突然叫喊的液體的大部分, 和重要兩個在養育精液細胞和提供更加了不起的容量對突然叫喊使他們的運動更加容易。精液細胞實際上是唯一共計的非常小百分比突然叫喊和必須一直旅行從男性的睪丸到女性的卵巢。這也許是距離大於三英尺根據養殖。雖然精液細胞能獨自行動, 大多數實際運動來自尿道、子宮頸, 和子宮體的收縮的肌組織推擠流體。更大的可變的容量使它容易對這些結構推進精液細胞必要的距離。Prostatic 流體並且有保護精液加上減退機會為傳染在女性的抗菌物產。

閹割的作用在攝護腺

被閹割 的狗 在青春期有很少prostatic 組織之前。沒有被生產在睪丸之內的男性激素睪甾酮, 攝護腺封墊不顯現出。如果我們將外科地探索這個區域在這些狗的當中一個中, 只有微小的船腹會被注意在尿道。小大小不導致害處對狗, 因為攝護腺的唯一的已知的作用是精液細胞的支持和養料。如果一條成熟狗被閹割, 封墊將收縮對較少它的早先大小的那四分之一。在幾個月內, 它的功能細胞將停止所有或幾乎支援流體的總產量。

攝護腺疾病的標誌

在人, 害病的攝護腺通常導致痛苦或困難的排尿。這有道理因為當圓鼓, 它可能關閉和減少尿道的大小。痛苦來自, 因此, 身體設法驅逐尿通過一個有限的開頭。並且, 當身體使用過份力量逐出尿, 它增加壓力在痛苦的攝護腺之內。這件同樣事在犬, 但稍微發生。

古典地, 在狗, 擴大的攝護腺導致痛苦的排糞。記住, 攝護腺封墊謊言在直腸之下在骨多的骨盆之內。運河通過骨盆只是很大和它不能得到任何大在一條單獨狗。所以, 當攝護腺增加在大小, 它推擠反對直腸, 很大地減少空間可利用為直腸。當凳子通過從 大腸 通過直腸在排糞期間, 有經常不是足夠的室容納一切。狗將勞損並且張力驅逐凳子和凳子施加壓力在圓鼓和痛苦的攝護腺。這是便秘和糞便勞損的同道會在公狗。

狗與痛苦的攝護腺反常地經常將走。他們試圖保留任何東西從乘坐反對或施加壓力在圓鼓, 痛苦的封墊。他們的後方腿將是僵硬的並且平直在膝蓋和飛腓節和他們通常將採取非常短的步驟。一些所有者提到這像' 走在蛋。'

其它標誌直接地與相關prostatic 傳染是放電從陰莖包括血液和pus, 勞損小便, 和在罕見的案件, 腹膜炎, 顯現出當細菌從攝護腺洩漏和進入胃腸洞。

類型prostatic 疾病在狗

良性Prostatic 增生: 在狗, 最共同的prostatic 疾病顯然是良性Prostatic 增生(BPH) 。這由細菌不造成或病毒傳染和這不是癌症的形式。這是, 寧可, 封墊的一個正常老化過程。當狗繼續成熟, 腺組織在攝護腺之內接受肥大。也就是說有在大小和細胞的數量的增量在腺組織之內。另外, 囊腫 顯現出在封墊裡面並且這些逐漸增加在大小。這兩個因素擴大攝護腺的整體大小施加內部壓力在殘餘的組織。幾乎所有狗經過4-5 年紀將顯示某一程度prostatic 擴大由BPH 造成。在許多, 封墊不也許是痛苦的, 但是當情況繼續通過年齡, 這依照陳述至少將是源泉的恆定的難受, 但, 它能和經常造成有排尿和背叛的問題。

細菌傳染: 大概, prostatic 疾病的次要個共同的形式在狗是細菌傳染。細菌可能進入攝護腺通過血液系統或從尿道。在後者, 細菌可能來自膀胱或過來尿道通過陰莖。膀胱傳染是共同在狗和容易地被對待。可能口頭被採取的許多抗生素排泄從身體由腎臟和被放置因此unchanged 入膀胱。到了能迅速消滅細菌當前。一旦有機體做了他們的方式入和拓殖攝護腺, 然而, 傳染更難控制或消滅。很少如果被放置入膀胱通過腎臟的任何抗生素做他們的方式成攝護腺封墊即使尿道通過它。另外, 有一個生理障礙在血液和攝護腺封墊之間。也就是說正因為一種物質像抗生素由血液運載, 它不一定將進入攝護腺封墊。唯一某些療程有通過在這個障礙的化工物產。這限制抗生素我們的選擇。以細菌傳染, 那是不幸的, 如同各自的細菌人口可能由某些抗生素只殺害。另外, 在時間期間, 這些敏感性的樣式對抗生素也許改變。然後細菌, 是否它是在耳朵、創傷, 或攝護腺之內, 可能不再被對待以同樣產品和新的必須被選擇。

這個封墊的細菌傳染是或者 深刻, 慢性的, 或被提出作為膿腫。任一傳染早期被命名深刻和是極端痛苦的。他們將影響不僅攝護腺, 但細菌也許傳播對身體的剩餘導致熱病和另外的標誌根據什麼身體的其它結構細菌拓殖。鑰匙這裡將確定, 源泉的傳染是在攝護腺之內和因此指揮治療的大部分在那個區域。

慢性傳染跟隨這個深刻階段, 也許繼續幾年來。他們難對待, 因為細菌可能成為設陷井在封墊的結疤的組織之內。它幾乎不可能讓療程進入這些區域。慢性階段是較不痛苦的, 但仍然是潛在的源泉的細菌傳播對其它區域。重覆了膀胱傳染的多數狗是正義是連續reinfected 與細菌從害病的攝護腺。膿腫是口袋pus 顯現了出在封墊之內細菌傳染的一個慢性形式。

巨蟹星座: 不同於人, prostatic 癌症是不凡的在狗。一些會描述他們像罕見。當他們發生, 他們通常是惡性和潛在地生活威脅。癌症也許metastasize, 傳播在身體過程中由血液系統和' 通常播種' 肝臟、肺, 或腎臟。他們能當地並且傳播入地方 淋巴結 和後面和骨盆的骨頭。這時及時, 我們沒有治療prostatic 癌症並且無是可能的在不遠的將來。唯一短期寬恕並且/或者安心是可能的通過輻射和醫療療法。

診斷

當攝護腺由良性成長、囊腫、癌症, 或傳染影響, 它得到更大並且它得到痛苦對接觸。在我們的實踐, 我們審查所有成熟狗攝護腺在慣例物理期間。這由插入一個gloved 手指入直腸和palpating 做攝護腺。由執行這次直腸考試, 獸醫能感覺攝護腺和注意它的大小, 一貫性, 對稱, 形狀, 和如果任一痛苦是存在。經常, 尿樣由一支導尿管採取在檢查以後將包含更多細胞從攝護腺。這些樣品被審查與一個顯微鏡為傳染、炎症, 或癌症的證據。

在未被閹割的狗, 精液評估可能是非常有用的在確定診斷。射線照相(X-射線) 或 超聲波 考試經常被使用更好估計攝護腺和周圍的組織。攝護腺的切片檢查法也許被採取證實診斷。

治療和預防

每當我們遇到任何攝護腺的上述問題在狗(有其他人, 但這些牌子98% 共計事例), 我們應付長期和經常昂貴的療法。例如, 慢性細菌前列腺炎的成功的治療通常將需要6 個到8 個星期連續的口頭療程、射入、泌尿導尿、灌腸, 和可能的手術。在幾乎所有案件, 這是選擇, 患者被閹割, 因為在睪甾酮被取消之後, 封墊將收縮並且情況更加容易對待。這當然不會有作用在癌症是包含的案件。

90% 所有prostatic 疾病會防止在所有狗期間生活如果動物被刪改了在第一該年生活。閹割不會有作用在癌症的發生, 而是記住這是非常罕見的。
   



When men reach the age of 80, they have about an 80% chance of developing cancer of the prostate. It is often a malignant form that can be difficult to treat and life threatening. When an unneutered male dog reaches 8 years of age, he has a greater than 80% chance of developing prostate disease, but it is rarely cancerous (benign or malignant). The gland serves the same function in the dog as it does in man and suffers from all the same diseases. Fortunately for the dog, however, the incidence of life-threatening conditions is much lower. Still, most unneutered canines will at one time or another, suffer a lot of discomfort if not severe pain due to the prostate gland.
What is the prostate gland?

The prostate gland is a bi-lobed structure that lies within the pelvis just behind the bladder and directly below the rectum. In a forty-pound dog, it is normally about one to two inches in diameter. It surrounds and is open to the urethra its entire length of the gland. Small tubes or ducts deposit the fluids produced by the prostate directly into the urethra as it courses through the prostate. The prostate starts to develop before the dog reaches puberty and attains its maximum size by the time the dog is two years old. From that point on, its size is determined by the male hormone testosterone and/or various disease conditions.

The prostate gland is classified as an accessory sex gland. This means that in some way it is important for successful breeding, but does not directly produce the sperm. Prostatic fluid is a major portion of the total ejaculated liquid, and is important both in nourishing the sperm cells and providing a greater volume to the ejaculate to make their movement much easier. The sperm cells are actually only a very small percentage of the total ejaculate and must travel all the way from the testicles of the male to the ovaries of the female. This may be a distance of greater than three feet depending on the breed. Although sperm cells are able to move on their own, most of the actual movement comes from the contracting musculature of the urethra, cervix, and uterus pushing the fluid along. A larger fluid volume makes it easier for these structures to propel the sperm cells the necessary distance. Prostatic fluids also have antibacterial properties that protect the sperm plus decrease the chances for infection in the female.

Effect of neutering on the prostate

Dogs that are neutered before puberty have very little prostatic tissue. Without the male hormone testosterone that is produced within the testicles, the prostate gland does not develop. If we were to surgically explore this area in one of these dogs, only a tiny bulge would be noted in the urethra. The small size causes no harm to the dog, since the only known function of the prostate is support and nourishment of the sperm cells. If a mature dog is neutered, the gland will shrink to less that one-fourth of its previous size. Within a few months, its functional cells will cease all or nearly all production of the supportive fluids.

Signs of prostate disease

In man, a diseased prostate usually causes painful or difficult urination. This makes sense because when swollen, it can close down and decrease the size of the urethra. The pain, therefore, comes from the body trying to force urine out through a restricted opening. Also, when the body uses excessive force to expel the urine, it increases pressures within the painful prostate. This same thing happens in the canine, but to a lesser degree.

Classically, in the dog, an enlarged prostate causes painful defecation. Remember, the prostate gland lies right below the rectum within the bony pelvis. The canal through the pelvis is only so big and it cannot get any bigger on an individual dog. Therefore, when the prostate increases in size, it pushes up against the rectum, greatly decreasing the space available for the rectum. When stools pass from the large intestine through the rectum during defecation, there often is not enough room to accommodate everything. The dog will strain and strain to force the stool out and the stool puts pressure on the swollen and painful prostate. This is the most common cause of constipation and fecal straining in the male dog.

Dogs with painful prostates will often walk abnormally. They are attempting to keep anything from riding against or putting pressure on the swollen, painful gland. Their rear legs will be stiff and straight at the knee and hock and they will usually take very short steps. Some owners refer to this as 'walking on eggs.'

Other signs directly associated with prostatic infection are discharges from the penis including blood and pus, straining to urinate, and in rare cases, peritonitis, which develops when bacteria from the prostate leak out and enter the abdominal cavity.

Types of prostatic disease in the dog

Benign Prostatic Hyperplasia: In the dog, by far the most common prostatic disease is Benign Prostatic Hyperplasia (BPH). This is not caused by bacterial or viral infection and it is not a form of cancer. It is, rather, a normal aging process of the gland. As the dog continues to mature, the glandular tissue within the prostate undergoes hypertrophy. That is to say that there is an increase in both the size and the number of the cells within the glandular tissue. Additionally, cysts develop inside the gland and these gradually increase in size. Both of these factors enlarge the overall size of the prostate putting internal pressure on the remaining tissue. Almost all dogs over 4-5 years of age will show some degree of prostatic enlargement caused by BPH. In many, the gland may not yet be painful, but as the condition continues with age, it will at the very least be a source of constant discomfort, but as stated, it can and often does cause problems with both urination and defection.

Bacterial Infections: Probably, the second most common form of prostatic disease in the dog is bacterial infection. Bacteria can get into the prostate via the blood system or from the urinary tract. In the latter, bacteria can come from the bladder or come up the urethra through the penis. Bladder infections are common in the dog and easily treated. Many antibiotics that can be taken orally are excreted from the body by the kidneys and are therefore deposited unchanged into the bladder. Here they can quickly eliminate the bacteria present. Once the organisms have made their way into and colonized the prostate, however, the infections are much more difficult to control or eliminate. Very little if any of the antibiotics that are deposited into the bladder via the kidneys make their way into the prostate gland even though the urethra passes through it. Additionally, there is a physiological barrier between the blood and the prostate gland. That is to say that just because a substance like an antibiotic is being carried by the blood, it will not necessarily get into the prostate gland. Only certain medications have chemical properties that pass over this barrier. This limits our choice of antibiotics. With bacterial infections, that is unfortunate, as individual bacterial populations can only be killed by certain antibiotics. Additionally, over time, these patterns of sensitivity to the antibiotics may change. Then the bacteria, whether it is within an ear, wound, or prostate, can no longer be treated with the same product and a new one must be chosen.

Bacterial infections of this gland are either acute, chronic, or are presented as abscesses. The early stages of any infection are termed acute and are extremely painful. They will affect not only the prostate, but bacteria may spread to the rest of the body causing fevers and additional signs depending on what other structures of the body the bacteria colonizes. The key here is to determine that the source of the infection is within the prostate and therefore direct a major portion of the treatment at that area.

Chronic infections follow this acute phase and may go on for years. They are difficult to treat, as bacteria can become trapped within scarred tissue of the gland. It is almost impossible to get medications into these areas. The chronic stage is less painful, but still is a potential source of bacterial spread to other areas. Most dogs that have repeated bladder infections are just being continuously reinfected with bacteria from the diseased prostate. Abscesses are a chronic form of bacterial infection in which pockets of pus have developed within the gland.

Cancer: Unlike humans, prostatic cancers are uncommon in the dog. Some would describe them as rare. When they do occur, they are usually malignant and potentially life threatening. The cancer may metastasize, spreading throughout the body by the blood system and usually 'seeding' the liver, lungs, or kidneys. They can also spread locally into regional lymph nodes and the bones of the back and pelvis. At this point in time, we have no cure for prostatic cancer and none is probable in the near future. Only short-term remission and/or relief is possible through radiation and medical therapy.

Diagnosis

When the prostate is affected by benign growth, cysts, cancer, or infection, it gets bigger and it gets painful to the touch. In our practice, we examine the prostate of all mature dogs during a routine physical. This is done by inserting a gloved finger into the rectum and palpating the prostate. By performing this rectal examination, the veterinarian is able to feel the prostate and note its size, consistency, symmetry, shape, and if any pain is present. Often, urine samples taken by a catheter after the exam will contain more cells from the prostate. These samples are examined with a microscope for evidence of infection, inflammation, or cancer.

In dogs who have not been neutered, semen evaluation can be very helpful in determining the diagnosis. Radiographs (x-rays) or ultrasound examinations are often used to better assess the prostate and surrounding tissues. Biopsies of the prostate may be taken to confirm a diagnosis.

Treatment and prevention

Whenever we encounter any of the above problems of the prostate in the dog (there are others, but these make up over 98% of the total cases), we are dealing with long-term and often expensive therapy. For example, the successful treatment of a chronic bacterial prostatitis will usually require 6 to 8 weeks of continuous oral medication, injections, urinary catheterizations, enemas, and possible surgery. In almost all cases, where it is an option, the patient is neutered, because after the testosterone is removed, the gland will shrink and the condition is much easier to treat. This would of course have no effect on a case where cancer was involved.

Over 90% of all prostatic diseases would be prevented during the life of all dogs if the animal was castrated in the first year of life. Neutering will have no effect on the incidence of cancer, but remember this is very rare.[/size]

minibabyqq 2006-12-20 19:44

[table][tr][td]轉貼自4682

[size=12px][color=red][size=5][b][color=magenta]Osteosarcoma (骨癌)[/color] [/b][/size][/color][/size]
[size=12px][color=red][size=5][/size][/color] [/size]
[size=12px][color=black][size=5][b]Osteosarcoma (Bone Cancer)   [/b][/size]
[/color]

Osteosarcomas 佔只5% 所有似犬 腫瘤, 但80-90% 敵意介入骨頭。共同在大養殖狗, osteosarcoma 是經常要求受影響的肢體截肢術被結合與化療提供臨時安心從 這種 進取的疾病骨頭的進取的癌症。
哪條狗是在危險中為開發osteosarcomas?

Osteosarcomas 一般影響更舊的大或巨型養殖狗。大的養殖在最巨大的風險為開發osteosarcoma 包括了不起的丹麥人、聖徒Bernards, 偉大的比利牛斯、Newfoundlands 、Bernese 山狗, 和愛爾蘭Wolfhounds 。大養殖譬如Rottweilers 、Labradors 、金黃獵犬、牧羊人、Dobermans 、Weimaraners, 和拳擊手並且是在一種增加的風險。這不是一個非常共同的腫瘤在小養殖狗和很少不發生在貓。稱80 磅的狗60 倍可能證明是至少開發osteosarcoma 比狗稱少於75 磅。當更舊的狗通常開發osteosarcomas, 那裡看來是增加的發生在一到二歲中尾隨。馬律狗有osteosarcomas 的增加的發生。

它是未知的為什麼一些狗開發osteosarcomas, 但一種理論建議迅速地增長的細胞被發現在成長板材在骨頭基因上是在變化一種更加巨大的風險。其它理論是, 腫瘤顯現出在精神創傷站點。增加的多孔的活動在破裂或精神創傷的站點能導致癌細胞的發展。現實是, 這兩可以是真實的並且那裡也許是其它起因不被發現。

什麼是osteosarcomas 症狀?

osteosarcomas 症狀經常嚴密同他們的地點聯繫在一起。多數osteosarcomas 顯現出在狗肢體在手肘之下或臨近膝蓋。腫瘤通常形成在或者靠近成長板材。受影響的狗經常將有發出音的骨頭膨脹。 X-射線 經常顯露, 被結合與歷史和養殖, 也許表明osteosarcoma 的發展的一個典型骨頭樣式。這些腫瘤經常導致痛苦在可能首先被查出作為瘸在受影響的肢體的聯接。90% 這些腫瘤將有 轉移 對肺在診斷之時, 但由於轉移的小最初的大小, 少於10% 最初地將出現在胸部X光。由於這轉移的高發生, 所有狗與osteosarcomas 被對待好像他們有轉移對肺不管研究結果在最初的肺X-射線。Osteosarcomas 偶爾地將出現在不同的地點並且其它腫瘤類型可能最初地同樣看來是osteosarcoma 。由於這種可能性, 切片檢查法 總被推薦。黴菌骨頭傳染可能導致相似的症狀和出現在X-射線, 因此黴菌文化經常執行幫助澄清診斷。

什麼是治療為osteosarcoma?

Osteosarcoma 是要求一個進取的治療協議的進取, 高度變形的癌症。一旦腫瘤正面地被辨認了作為osteosarcoma, 受影響的肢體通常被截肢。在腫瘤是在正確的地點的罕見的案件, 一些肢體饒恕的手術做了, 但那通常不是實際情形。在截肢術以後, 化療路線通常開始。最成功的藥物是carboplatin 和cisplatin 。Carboplatin 更加昂貴, 但更加安全和更加容易執行。Doxorubicin 有時被使用。一位合格的獸醫癌症醫師經常是最佳的資訊源並且他或她意識到最新的化療協議。一條狗的估計壽命與一適當地辨認的和被對待的osteosarcoma 很大地變化, 但可能接近一年或長期。

osteosarcoma 是可防止的嗎?

不看起來, osteosarcoma 是可防止的。由於一些強的養殖交互作用, 有的任一條養殖線osteosarcoma 的歷史應該被審查嚴密在養殖前。不幸地, 我們不完全地瞭解osteosarcoma 的起因, 但有希望地當我們的知識改善, 我們能繼續提供更加有效的治療和早期診斷測試。

Osteosarcomas account for only 5% of all canine tumors, but 80-90% of malignancies involving the bone. Much more common in large breed dogs, osteosarcoma is an aggressive cancer of the bone that often requires amputation of the affected limb coupled with chemotherapy to provide temporary relief from this aggressive disease.
Which dogs >><<

Osteosarcomas generally affect older large or giant breed dogs. The giant breeds >><<eat Danes, Saint Bernards, Great Pyrenees, Newfoundlands, Bernese Mountain Dogs, and Irish Wolfhounds. Large breeds such as Rottweilers, Labradors, Golden Retrievers, Shepherds, Dobermans, Weimaraners, and Boxers are also at an increased risk. It is not a very common tumor in small breed dogs and rarely occurs in cats. Dogs that weigh over 80 pounds have been shown to be at least 60 times more likely to develop an osteosarcoma than dogs weighing less than 75 pounds. While older dogs more commonly develop osteosarcomas, there does appear to be an increased incidence in one to two year old dogs as well. Male dogs have an increased incidence of osteosarcomas.

It is unknown why some dogs develop osteosarcomas, but one theory suggests that the rapidly growing cells found at the growth plates in the bones are genetically >><<ased cellular activity at the site of a fracture or trauma could result in the development of cancer cells. The reality is that both of these may be true and there may be other causes not yet discovered.

What are the symptoms of osteosarcomas?

The symptoms of osteosarcomas are often closely associated with their location. Most osteosarcomas develop on the limbs of dogs below the elbow or near the knee. The tumors usually form at or near the growth plates. Affected dogs will often have a pronounced bone swelling. X-rays often reveal a characteristic bone pattern that, coupled with history and breed, may indicate the development of an osteosarcoma. These tumors often produce pain in the joint that can first be detected as lameness in the affected limb. Up to 90% of these tumors will have metastasis to the lungs at the time of diagnosis, but because of the small initial size of the metastases, less than 10% will initially show up on a chest x-ray. Because of this high incidence of metastasis, all dogs with osteosarcomas are treated as if they have metastasis to the lungs regardless of the findings on the initial lung x-rays. Osteosarcomas will occasionally show up at different locations and likewise other tumor types can initially appear to be an osteosarcoma. Because of this possibility, a biopsy is always recommended. Fungal bone infections can produce similar symptoms and appearance on an x-ray, so a fungal culture is often performed to help clarify the diagnosis.

What is the treatment for osteosarcoma?

Osteosarcoma is an aggressive, highly metastatic cancer that requires an aggressive treatment protocol. Once the tumor has been positively identified as an osteosarcoma, the affected limb is usually amputated. In rare cases where the tumor is in the right location, some limb-sparing surgeries have been performed, but that is not usually the case. After the amputation, a course of chemotherapy is usually begun. The most successful drugs have been carboplatin and cisplatin. Carboplatin is more expensive, but safer and easier to administer. Doxorubicin is sometimes used as well. A qualified veterinary oncologist is often the best source of information and he or she will be aware of the newest chemotherapy protocols. The life expectancy of a dog with a properly identified and treated osteosarcoma varies greatly, but can approach a year or longer.

Is osteosarcoma preventable?

It does not appear that osteosarcoma is preventable. Because of some strong breed correlations, any breed line that has a history of osteosarcoma should be examined closely prior to breeding. Unfortunately, we do not completely understand the cause of osteosarcoma, but hopefully as our knowledge improves, we can continue to provide more effective treatments and early diagnostic tests.[/size]
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minibabyqq 2006-12-20 19:45

[size=12px][color=red][size=5][b][color=magenta]腫瘤[/color]   [/b][/size][/color]


乳房腫瘤是最共同的 腫瘤 在不是spayed 的母 狗。乳房腫瘤可能是小, 簡單的根瘤或大, 進取, 變形的 成長。以早檢測和及時治療, 甚而一些更加嚴重的腫瘤可能成功地被對待。貓並且遭受乳房腫瘤並且他們有被談論在一篇分開的文章的他們自己獨特的套問題。
哪條狗是在危險中為開發乳房腫瘤?

乳房腫瘤是更加共同unspayed, 中年母狗(那些在5 和10 年紀之間), 雖然他們可能, 極少數情況下, 被發現在狗一樣年輕像2 年。這些腫瘤是罕見的在是spayed 在2 年紀之下的狗。偶爾地, 乳房腫瘤將顯現出在公狗並且這些通常是非常進取的和有一種粗劣的預測。

乳腺癌風險幾乎被消滅在是spayed 在 他們的 第一熱之前的狗。
Spaying 很大地減少一條母狗的機會開發這個情況。在那些女性spayed 在他們的第一個熱週期, 乳腺癌之前是非常, 非常罕見。惡性乳房腫瘤風險在狗spayed 在他們的第一熱之前是0.05% 。它是8% 為狗spayed 在一熱以後, 並且26% 在狗spayed 在某些荷爾蒙因素排除或減少導致降低疾病的發生在狗的他們的第二heat.It 被相信之後是spayed 。這些因素大概會是 女性荷爾蒙、 孕酮、相似的激素或可能組合的二或更多這些。

什麼是類型乳房腫瘤在狗?

有多類型乳房腫瘤在狗。所有乳房腫瘤的大約二分之一在狗是 良性的, 並且一半 惡性。所有乳房腫瘤應該被辨認通過切片檢查法和病理組織學(組織的微觀考試) 幫助在那特殊類型的治療腫瘤。

似犬乳房腫瘤的最共同的良性形式實際上是幾不同的類型混合物細胞。使一個唯一腫瘤擁有更多比一個親切癌細胞實際上是罕見的在許多種類。這組合癌症在狗稱' 良性混雜的乳房腫瘤' 和包含腺和結締組織。其它良性腫瘤包括複雜腺瘤、fibroadenomas 、輸送管papillomas, 和簡單的腺瘤。

惡性乳房腫瘤有: 筒形腺癌、乳頭狀的腺癌、乳頭狀的囊狀腺癌、堅實癌、整形的癌、osteosarcomas 、fibrosarcomas, 和惡性混雜的腫瘤。

什麼是乳房腫瘤症狀?

乳房腫瘤提出作為堅實大量或作為多脹大。當腫瘤升起在乳房組織, 他們通常容易查出由柔和地 palpating 乳房封墊。當腫瘤首先出現他們將感覺像豌豆石渣小片斷在皮膚之下。他們是非常堅硬的和難行動在皮膚之下。他們能迅速地增長在一個短的時期, 加倍他們的大小每個月或如此。

狗通常有五個乳房封墊, 每個與它自己的乳頭, 在它的更低的腹部的正確和左邊。雖然乳腺癌能和發生總計封墊, 它最頻繁地通常發生在4th 和5th。在箱子的一半, 超過一成長被觀察。良性成長經常是光滑, 小和緩慢生長。惡性腫瘤的標誌包括迅速增長、不規則的形狀、牢固的附件對皮膚或部下的組織, 靈菌, 和 潰瘍。偶爾地是小長期以來時間的腫瘤也許迅速和進取地突然增長, 但這是例外不是規則。

它非常難確定類型腫瘤根據物理檢查。 切片檢查法 或腫瘤撤除和分析是幾乎總需要的確定如果腫瘤良性或惡性, 並且辨認什麼型這是。腫瘤, 是更加進取的也許metastasize 和傳播對周圍的 淋巴結 或對肺。淋巴結的胸部X光和物理檢查經常將幫助在證實這。

乳房癌症傳播對身體的剩餘通過各自的癌細胞發行從各種各樣的腫瘤入lymphatics 。淋巴系統包括特別船和 淋巴結。有地方淋巴結在身體的正確和左邊在前面和後方腿之下。他們稱 ' 輔助' 和' 腹股溝' 淋巴結, 各自地。乳房封墊1, 2, 和3 排泄和塗他們的腫瘤細胞今後對輔助淋巴結, 當細胞從3, 4, 和5 傳播對腹股溝部分。新腫瘤形成在這些站點和然後發布去其它器官譬如肺、肝臟, 或腎臟的更多細胞。

什麼是治療?

外科撤除: 在發現任一大量在狗的乳房之內, 外科撤除被推薦除非患者是非常老的。如果手術及早完成這種疾病其間, 癌症可能完全被消滅完全成功50% 箱子有癌症的一個惡性形式。區域被切除取決於實習者的評斷和特選。一些只將取消大量。其他人, 考慮到怎麼癌症傳播, 將去除大量和排泄與封墊乳房組織和淋巴結的剩餘。例如, 如果成長被查出了在第號2 封墊在左邊, 我們會去除因此封墊, 1, 2, 和3 和輔助淋巴結在那邊。如果它被發現了在第號4 封墊在右邊, 然後封墊3, 4, 5, 和腹股溝淋巴結在那邊完全地會被去除。以一些腫瘤類型, 特別是肉瘤, 完全撤除是非常困難的並且許多這些箱子將有腫瘤再生物在早先被去除的腫瘤的站點。

所有者也許與一項根本乳房切除術混淆一個乳房封墊的外科撤除在狗在人, 與所有伴生的問題。在人, 這類型手術會影響使補救複雜化的部下的肌肉組織。在狗, 然而, 所有乳房組織和相關lymphatics 是在肌肉層數外面, 因此我們只需要穿過皮膚和乳房組織。這使手術更加容易和補救更加快速。一項根本乳房切除術在狗意味所有乳房, 皮膚覆蓋物他們, 並且四個淋巴結全部同時被去除。雖然這真實地是主要手術, 縫合撤除通常發生在10 到14 天以正常活動那時恢復。

許多獸醫願spay 狗有乳房切除術(除非她是非常老的) 。這的價值在減少腫瘤再現是有爭議的。

化療和放射治療: 化療不是一種非常成功亦不廣泛被應用的治療為乳房腫瘤在狗。但是, 與改變和經常改善使可利用服麻醉劑, 獸醫癌症醫師應該被咨詢發現如果有一種有效的藥物可利用為您的狗的特殊類型乳房癌症。放射治療的有效率不周到地被研究了。一些反荷爾蒙藥物養生之道被測試在狗。這時及時, 腫瘤的外科撤除是選擇的治療。

我怎麼可以防止乳房癌症在我的狗?

有一樣容易地被防止像乳房癌症在狗的少量癌症。有一個直接和有大量文件證明的鏈接在早期spaying 母狗和對發生的減少之間在乳房癌症。狗spayed 在進入他們的第一熱之前有曾經患乳房癌症的一次極端小機會。狗比spayed 在他們的第一熱但在2.5 年之前是在更多風險之後, 僅較少風險是的那狗從未spayed, 或以後spayed 在生活中。我們全部知道spaying 的女性的巨大的好處在童年年齡, 但每天, 獸醫仍然應付這種容易地可防止的疾病。及早spaying 仍然是所有者能做改進健康和保證長壽為他們的狗的一個最佳的事寵物。

結論

乳房癌症是非常共同的癌症, 可能成功地經常被對待, 如果及早捉住。如果所有非育種的狗和貓是spayed 在他們的第一熱這種疾病能幾乎完全地被消滅之前。如果您發現成長或lump 在您的狗乳房組織, 您應該立刻通知您的獸醫和不採取"等待和不看" 態度


Mammary tumors are the most common tumors in female dogs who have not been spayed. Mammary tumors can be small, simple nodules or large, aggressive, metastatic growths. With early detection and prompt treatment, even some of the more serious tumors can be successfully treated. Cats also suffer from mammary tumors and they have their own unique set of problems that are discussed in a separate article.
Which dogs >><<

Mammary tumors are more common in unspayed, middle-aged female dogs (those between 5 and 10 years of age), although they can, on rare occasions, be found in dogs as young as 2 years. These tumors are rare in dogs that were spayed under 2 years of age. Occasionally, mammary tumors will develop in male dogs and these are usually very aggressive and have a poor prognosis.

The risk of breast cancer is almost eliminated in dogs that are spayed before their first heat.
Spaying greatly reduces the chances of a female dog developing this condition. In those females spayed prior to their first heat cycle, breast cancer is very, very rare. The risk of malignant mammary tumors in dogs spayed prior to their first heat is 0.05%. It is 8% for dog spayed after one heat, and 26% in dogs spayed after their second heat.It is believed that the elimination or reduction of certain hormonal factors causes the lowering of incidence of the disease in dogs that have been spayed. These factors would probably be estrogen, progesterone, a similar hormone or possibly a combination of two or more of these.

What are the types of mammary tumors in dogs?

There are multiple types of mammary tumors in dogs. Approximately one-half of all mammary tumors in dogs are benign, and half are malignant. All mammary tumors should be identified through a biopsy and histopathology (microscopic examination of the tissue) to help in the treatment of that particular type of tumor.

The most common benign form of canine mammary tumors is actually a mixture of several different types of cells. For a single tumor to possess more than one kind of cancerous cell is actually rare in many species. This combination cancer in the dog is called a 'benign mixed mammary tumor' and contains glandular and connective tissue. Other benign tumors include complex adenomas, fibroadenomas, duct papillomas, and simple adenomas.

The malignant mammary tumors include: tubular adenocarcinomas, papillary adenocarcinomas, papillary cystic adenocarcinomas, solid carcinomas, anaplastic carcinomas, osteosarcomas, fibrosarcomas, and malignant mixed tumors.

What are the symptoms of mammary tumors?

Mammary tumors present as a solid mass or as multiple swellings. When tumors do arise in the mammary tissue, they are usually easy to detect by gently palpating the mammary glands. When tumors first appear they will feel like small pieces of pea gravel just under the skin. They are very hard and are difficult to move around under the skin. They can grow rapidly in a short period of time, doubling their size every month or so.

The dog normally has five mammary glands, each with its own nipple, on both the right and left side of its lower abdomen. Although breast cancer can and does occur in all of the glands, it usually occurs most frequently in the 4th and 5th. In half of the cases, more than one growth is observed. Benign growths are often smooth, small and slow growing. Signs of malignant tumors include rapid growth, irregular shape, firm attachment to the skin or underlying tissue, bleeding, and ulceration. Occasionally tumors that have been small for a long period of time may suddenly grow quickly and aggressively, but this is the exception not the rule.

It is very difficult to determine the type of tumor based on physical inspection. A biopsy or tumor removal and analysis are almost always needed to determine if the tumor is benign or malignant, and to identify what type it is. Tumors, which are more aggressive may metastasize and spread to the surrounding lymph nodes or to the lungs. A chest x-ray and physical inspection of the lymph nodes will often help in confirming this.

Mammary cancer spreads to the rest of the body through the release of individual cancer cells from the various tumors into the lymphatics. The lymphatic system includes special vessels and lymph nodes. There are regional lymph nodes on both the right and left sides of the body under the front and rear legs. They are called the 'axillary' and 'inguinal' lymph nodes, respectively. Mammary glands 1, 2, and 3 drain and spread their tumor cells forward to axillary lymph nodes, while cells from 3, 4, and 5 spread to the inguinal ones. New tumors form at these sites and then release more cells that go to other organs such as the lungs, liver, or kidneys.

What is the treatment?

Surgical Removal: Upon finding any mass within the breast of a dog, surgical removal is recommended unless the patient is very old. If a surgery is done early in the course of this disease, the cancer can be totally eliminated in over 50% of the cases having a malignant form of cancer. The area excised depends on the judgment and preference of the practitioner. Some will only remove the mass itself. Others, taking into consideration how the cancer spreads, will remove the mass and the rest of the mammary tissue and lymph nodes that drain with the gland. For example, if a growth were detected in the number 2 gland on the left side, we would therefore remove glands, 1, 2, and 3 and the axillary lymph node on that side. If it were found in the number 4 gland on the right side, then glands 3, 4, 5, and the inguinal lymph node on that side would be completely removed. With some tumor types, especially sarcomas, complete removal is very difficult and many of these cases will have tumor regrowth at the site of the previously removed tumor.

Owners may confuse a surgical removal of a mammary gland in the dog with a radical mastectomy in humans, with all of the associated problems. In humans, this type of surgery would affect the underlying muscle tissue which complicates the recovery. In the dog, however, all of the breast tissue and the related lymphatics are outside of the muscle layer, so we only need to cut through the skin and the mammary tissue. This makes the surgery much easier and recovery much faster. A radical mastectomy in a dog means all the breasts, the skin covering them, and the four lymph nodes are all removed at the same time. Although this is truly major surgery, suture removal usually occurs in 10 to 14 days with normal activity resuming at that point.

Many veterinarians will spay a dog having a mastectomy (unless she is very old). The value of this in decreasing the recurrence of tumors is still controversial.

Chemotherapy and Radiation Therapy: Chemotherapy has not been a very successful nor widely used treatment for mammary tumors in dogs. However, with the constantly changing and improving drugs available, a veterinary oncologist should be consulted to find out if there is an effective drug available for your dog's particular type of mammary cancer. The effectiveness of radiation therapy has not been thoroughly researched. Some anti-hormonal drug regimens are being tested in dogs. At this point in time, surgical removal of the tumors is the treatment of choice.

How can I prevent mammary cancer in my dog?

There are few cancers that are as easily prevented as mammary cancer in dogs. There is a direct and well-documented link between the early spaying of female dogs and the reduction in the incidence in mammary cancer. Dogs spayed before coming into their first heat have an extremely small chance of ever developing mammary cancer. Dogs spayed after their first heat but before 2.5 years >><<n life. We all know the huge benefits of spaying females at an early age, but every day, veterinarians still deal with this easily preventable disease. Early spaying is still one of the best things pet owners can do to improve the health and ensure a long life for their dogs.

Conclusion

Mammary cancer is a very common cancer and can often be successfully treated, if caught early. If all non-breeding dogs and cats were spayed before their first heat this disease could be almost completely eliminated. If you find a growth or lump in the mammary tissue of your dog, you should inform your veterinarian immediately and not take a "wait and see" attitude.[/size]

minibabyqq 2006-12-20 19:45

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[size=12px][color=red][size=5][b][color=magenta]狗瘟 Distemper[/color]   [/b][/size][/color]


大多數我們聽說了慍怒傳染為狗和會集它是非常壞。基本的疫苗為狗是the 接種反對慍怒、parvovirus 和一些較小 狗窩 咳嗽代理的慍怒射擊, 。。幸運地, 這是所有多數人民曾經聽說慍怒。如果您讀這, 然而, 您大概有被懷疑有這畏懼的傳染的一條狗。

典型的慍怒嫌疑犯是搶救或寵物商店狗或小狗, 通常以可疑的接種歷史或一個殘缺不全的接種系列。狗或小狗被安置了與其它搶救狗。症狀開始與:

. 黏的眼睛和鼻子放電
. 來和經常未被注意) 的熱病(
. 粗劣的胃口
. 咳嗽和肺炎的發展

病毒攻擊身體以環境(黏膜) 並且開始的接口以呼吸道, 因此肺炎, 而是它不停止那裡。病毒行動向產物:

. 嘔吐和腹瀉
. 鼻子和腳墊(因此的Callusing 老名字的當中一個對於慍怒。堅硬墊疾病)

在完成以後什麼叫mucosal 階段。傳染環境接口被攻擊(如所描述由上述GI 和呼吸疾病), 病毒進行對中央神經系統為它的neurologic 階段導致:

. 奪取(古典地從進步對整體的抽風的攫取或tremoring 下頜開始。這個慍怒經典標誌稱口香糖適合。) 奪取不是唯一的慍怒標誌通過任何手段。震顫、不平衡狀態, 和肢體弱點全部也許發生。標誌也許進步對死亡或也許變得non-progressive 和永久。補救是還可能的。

這意味著, 狗看上去恢復1 個到3 個星期以後只打破以神經學疾病。更加年輕的小狗或個體以微弱的免疫經常死在黏膜階段期間當更強的個體也許有相對地溫和的黏膜標誌和不看上去不適直到神經學階段觸擊。

病毒



   

似犬慍怒病毒與人的痲疹病毒相關緊密地並且, 實際上, 在更舊的時期, 小狗免疫了為慍怒與疫苗反對痲疹。它說, 一個孩子在狗的家被接種與活慍怒病毒疫苗將成為暴露在病毒和免疫反對痲疹(我們在家雖則不推薦這樣實驗)

慍怒病毒包括核糖核酸一條唯一子線, 被裝箱在再被裝箱在一個肥膩信封的蛋白質外套。這聽起來神秘但肥膩信封牌子所有區別在世界上。肥膩信封容易地被打亂在牌子它不可能使感染病毒堅持在環境的環境裡。由於一個原封肥膩信封必需為傳染, 病毒傳輸必須介入狗尾隨聯絡或至少聯絡以極端新(少於30 分鐘年紀) 被傳染的身體分泌物。和與其它病毒, 生存病毒結冰和愉快地能生存幾年來如果保持結冰和被保護免受光。定期消毒作用和清潔欣然殺害慍怒病毒在狗窩設置。

傳輸和傳染

被傳染的狗典型地傳染其它狗通過咳嗽被傳染的呼吸分泌物雖然病毒是棚子在多數其它身體分泌物包括尿。病毒輸入新主人通過鼻子或嘴和及時地開始複製。病毒由免疫系統的細胞吞噬叫做巨噬細胞。想法是, 病毒將被吞噬, 將被圍住在細胞之內和將被酵素然後毀壞。不幸地為新主人, 這個過程不損壞病毒按照計劃使病毒使用巨噬細胞作為交通工具通過host.s 身體。在24 小時之內, 病毒到肺的淋巴結旅行了。在第6 天以前, 病毒移居了對脾臟、胃、小腸, 和肝臟。熱病這時顯現出。

在天8 或9 以前一個重要緊要關頭被到達在傳染時間表。  主人登上一個免疫反應在這時間期間並且結果依賴於怎樣快速地和多麼恰當這是成功的。一個強烈的免疫反應開始這時清除病毒和消滅了病毒所有蹤影沒有病症症狀在Day 14 以前。一個微弱的免疫反應允許病毒到達上皮細胞, 排行每個接口身體有與外部世界的細胞。嫩上皮細胞排行腦子的分庭被傳染。主人開始病態當病毒傳播而是作為host.s 免疫反應生長症狀減少。這種現象佔寬可變性在症狀; 一些狗得到唯一幾種溫和的症狀當其他人得到一個充分的致死的組合。

在清除從多數內臟以後, 病毒能掩藏起來長的時期在神經系統和皮膚。由於這種現象, callusing 皮膚或, 更壞, 奪取可以長期發生在傳染被認為被清除之後。

多數受害者在美國是小狗。(初乳哺乳了在第一天或因此生活將提供他們以他們的mother.s 免疫的堅實反射。這由年齡減少了16 個星期留給小狗脆弱如果疫苗未被執行為進一步保護。  在我們的社會多數母親狗接受了某種接種的形式和因而能傳遞至少一些免疫, 將有一些能力保護自己。在接種不是共同的社會, 慍怒攻擊所有年齡狗。)

證實慍怒傳染

好像它不足夠壞這傳染有一個窮地被定義的終點因此一個從未知道你肯定是在樹林外面, 它幾乎不可能證實慍怒診斷。因此, 慍怒是一個臨床診斷, 意味那而不是證實的傳染以測試是消極或正面的, 獸醫必須看整體圖片: 什麼症狀是那裡, 是歷史典型, 等。病毒保留逃避以便正面測試結果是意味深長的在證實傳染, 但消極結果不排除它。  下列是可能被使用的測試:

慍怒包括身體 。Distemper 包括身體是是可看見的在顯微鏡下在被傳染的細胞之內的實際叢病毒。死後的包括身體是欣然可看見的在泌尿膀胱組織如此使確認慍怒在死亡以後相對地容易。在生存患者, 我們典型地有對eye.s conjunctival 膜(眼球孔的桃紅色公園的血細胞和細胞的就緒存取) 。提高包括身體的可見性,  immunocytology 使用。在這個技術, 抗體反對慍怒病毒用螢光標誌被標記。抗體束縛對病毒如果這是存在有效地死包括身體以發光在這黑暗的螢光顏色。  包括身體出現證實慍怒傳染。缺乏可發現的包括身體不排除慍怒傳染當包括身體最後變得上漆與host.s 擁有反之阻攔螢光被標記的抗體被使用在測試的抗體。




   


如果callusing 攔路賊或鼻子是顯然的, 這個組織切片檢查法可能相當後被測試為包括身體在傳染。

慍怒抗體水平 。慍怒滴定量(其它antibody 水平的詞。) 或者IgM 。  型(導致在傳染早期) 並且IgG. 類型(導致在最新階段傳染) 可能被檢查。問題是, 慍怒接種導致這些同樣抗體並且慍怒嫌疑犯經常有最近接種。高IgM 滴定量表明最近傳染或最近接種。沒有方式告訴哪些。

腦脊髓流體抗體水平 。在神經學慍怒案件, 腦脊髓流體經常被輕拍和慍怒抗體水平被檢查。慍怒抗體在腦脊髓流體裡是高度表示的慍怒傳染因為疫苗導致的抗體不橫渡血腦障壁障礙入CSF 流體。

治療為慍怒

許多異常的協議湧現了在時間期間當我們摸索為意味深長的抗病毒療法。事實遺骸的, 補救從慍怒是所有關於免疫和唯一的真正的治療是支援關心當患者登上它自己的免疫反應。如果患者有肺炎, 抗生素被使用在次要細菌傳染。導氣管擴張肌被使用依照必要。物理療法使用促進咳嗽。如果患者有腹瀉, 靜脈內流體被使用防止失水等。

慍怒是極端易變的在它的能力導致症狀並且補救發生在任何個階段。這導致了被分類的療法相信作用當什麼是更加可能的被目擊是傳染的自然撤除由host.s 免疫系統。
神經學慍怒特別難對待。但是, 它是可能為狗恢復以適於居住的缺乏從neurodistemper; 無痛苦的死亡最好動身去進步, 不適於神經學症狀。

防止傳染

如果證實的診斷和療法是慍怒陷阱, 預防是容易的部份。  有效的慍怒接種是可利用的從50 年代在普遍接種, 慍怒之前是似犬社區的鞭, 消除愛犬整個townfuls 。今天, 慍怒是一種罕見的疾病除了在風雨棚、搶救, 和寵物商店世界。

distemper 射擊。是基本的免役為狗。它與疫苗一般被結合為似犬 parvovirus 為parainfluenza 、腺病毒2, 細螺旋體病, 和有時coronavirus 。小狗爾後是被接種的起點在年齡6-8 個星期和然後每2 個到4 個星期直到年齡16 個星期。下疫苗是一年後。以後, 隨後接種助推器被給每1 到3 年或根據抗體水平根據監督的動物醫院的政策。

疫苗是可利用的在傳統修改過的活病毒格式, 慍怒病毒不被修改導致免疫反應而是沒有病症。  疫苗是還可利用的在活無害的病毒的再組合格式(不是根本修改的慍怒病毒或否則) 被使用運載慍怒病毒的部份引起免疫反應。再組合格式的好處是, 它是完全地不可能的使慍怒或慍怒腦炎發生由於接種。這些複雜化是極為罕見的但可能與修改過的活病毒疫苗。

對人的痲疹病毒的用途接種反對似犬慍怒現今主要passe 。免疫獲得了這樣一樣長期不持續和不是像成功作為那被獲得與修改過的活或再組合慍怒疫苗。


常見問題解答

看起來這裡我們有一個致死的結果是可能的沒有不測試證實傳染和方式確定的一種疾病如果傳染真實地是結束與。  慍怒嫌疑犯的所有者將有許多問題並且這裡我們試圖回答不可以公開地報道了在上述文本的問題。

I 擁有一條幼小狗與非常非常被弄髒的和挖坑的牙。我被告訴這也許表明她有慍怒作為小狗。  慍怒怎麼會導致這?
慍怒病毒攻擊epithelial 細胞。這些是排行接口以環境的細胞, 嘴包括。在puppyhood 永久牙的芽仍然顯現出(從上皮細胞) 。慍怒傳染(和伴生的熱病) 可能留下這些牙芽永久地被損壞以便成人牙進來與被弄髒的和挖坑的搪瓷。這叫做enamel 發育不全。

有是任何方式預言是否一條狗以慍怒將進步對神經學階段?
不真正地。  在病毒之前進入中央神經系統的階段傳染是皮膚被攻擊的階段。鼻子和腳墊的Callusing 傾向於同神經學慍怒的發展聯繫在一起。從黏膜階段恢復的大約50% 狗概括來說將進步對neurodistemper 。狗開發neurodistemper, 它說, 大約50% 將做如此在一個月之內或二黏膜階段。我們的印象是, 50% 大概是一點過高估計。風險進步對neurodistemper 是較少在成人狗因為他們比小狗傾向於登上更加有效的免疫反應。

我們擁有了死和被懷疑有慍怒的一條狗。我們怎麼應該消毒我們的家在一條新狗被介紹之前?
慍怒的當中一個少數個正面方面是, 病毒無法居住沒有新分泌物; 它被撤消在分鐘在生存host.s 身體之外。最小的消毒作用是必要的。

多久一條恢復的狗是傳染性的?
一條恢復的狗也許流灑病毒2 個到3 個月。它重要保留這在頭腦當採取任何地方其它狗是存在的一隻恢復的寵物。最強烈的病毒流出發生在第一2 個星期傳染。

什麼是Old 狗腦炎? 。
情況叫做Old Dog 腦炎提到可能發生在狗有慍怒許多歲月預先的慢性腦子炎症。  這些腦子損害與那些是相同的在進步對一慢性神經學慍怒作為他們的傳染一部分衝擊的狗。由於種種原因, 在一些個體, 狗居住幾乎所有它的生活作為慍怒倖存者只打破以neurodistemper 在老年齡。

什麼是Vaccinial 慍怒? 。狗可以實際上得到慍怒從它的疫苗嗎?
Vaccinial 慍怒提到neurodistemper 的發展10 到21 天在修改過的活慍怒疫苗以後(它的管理不是可能有這反應當再組合疫苗被使用) 。

人可以得到傳染與似犬慍怒病毒嗎?
人能得到傳染與病毒意味病毒似乎能複製在人體但沒有病症結果。一次, 多發性硬化症被認為同對似犬慍怒病毒的暴露聯繫在一起但進一步研究建議這實際上是也許是罪犯的人的痲疹病毒(似犬慍怒的一個近親) 。不看起來, 有任一種人的危險在似犬慍怒病毒。

Most of us have heard of distemper infection for dogs and gather it is very bad. The basic vaccine for dogs is 懀he distemper shot,?which vaccinates against distemper, parvovirus and some minor kennel cough agents. Luckily, this is all most people ever hear of distemper. If you are reading this, however, you probably have a dog that is suspected of having this dreaded infection.

The typical distemper suspect is a rescue or pet store dog or puppy, usually with questionable vaccination history or an as yet incomplete vaccination series. The dog or puppy has been housed with other rescue dogs. Symptoms begin with:

?nbsp;Gooey eye and nose discharge
?nbsp;Fever (which often comes and goes unnoticed)
?nbspoor appetite
?nbsp;Coughing and the development of pneumonia

The virus is attacking interfaces of the body with the environment (the mucous membranes) and starts with the respiratory tract, hence the pneumonia, but it does not stop there. The virus moves on to produce:

?nbsp;Vomiting and diarrhea
?nbsp;Callusing of the nose and foot pads (hence one of the old names for distemper ?hard pad disease)

After completing what is called the 𢘫ucosal phase?of infection where environmental interfaces are attacked (as described by the above GI and respiratory disease), the virus proceeds to the central nervous system for its 忛eurologic phase?leading to:

?nbsp;Seizures (classically starting with snapping or tremoring of the jaws that progress to convulsions of the whole body. This distemper classic sign is called a chewing gum fit.) Seizures are not the only distemper sign by any means. Tremors, imbalance, and limb weakness all may occur. Signs may progress to death or may become non-progressive and permanent. Recovery is also possible.

This means that the dog appears to recover only to break with neurologic disease 1 to 3 weeks later. Younger puppies or individuals with weak immunity often die during the mucosal phase while stronger individuals may have relatively mild mucosal signs and not appear ill until the neurologic phase strikes.

The Virus Itself



   

The canine distemper virus is closely related to the human measles virus and, in fact, in older times, puppies were immunized for distemper with vaccine against measles. It has been said that a child in the home of a dog vaccinated with live distemper virus vaccine will become exposed to the virus and immunized against the measles (though we do not recommend such experiments at home)

The distemper virus consists of a single strand of RNA, encased in a protein coat which is again encased in a fatty envelope. This sounds esoteric but the fatty envelope makes all the difference in the world. The fatty envelope is easily disrupted in the environment which makes it impossible for infectious virus to persist in the environment. Because an intact fatty envelope is required for infection, virus transmission must involve dog to dog contact or at least contact with extremely fresh (less than 30 minutes old) infected body secretions. As with other viruses, living virus happily freezes and can survive for years if kept frozen and protected from light. Routine disinfection and cleaning readily kills the distemper virus in the kennel setting.

Transmission and Infection

The infected dog typically infects other dogs via coughing infected respiratory secretions though the virus is shed in most other body secretions including urine. The virus enters the new host via the nose or mouth and promptly begins to replicate. Virus is engulfed by cells of the immune system called macrophages. The idea is that the virus will be engulfed, walled off within the cell and then destroyed by enzymes. Unfortunately for the new host, this process does not damage the virus as intended enabling the virus to use the macrophage as a means of transportation through the host𠏋 body. Within 24 hours, the virus has traveled to the lymph nodes of the lung. By the 6th day, the virus has migrated to the spleen, stomach, small intestine, and liver. Fever is developing at this point.

By day 8 or 9 an important crux is reached in the timetable of infection.  The host is mounting an immune response during this time and the outcome depends on how fast and how well this is accomplished. A strong immune response begins to clear the virus at this point and has eliminated all traces of virus with no symptoms of illness by Day 14. A weak immune response allows the virus to reach the epithelial cells, the cells which line every interface the body has with the outside world. The tender epithelial cells lining the chambers of the brain are infected as well. The host begins to get sick as the virus spreads but as the host𠏋 immune response grows symptoms wane. This phenomenon accounts for the wide variability in symptoms; some dogs get only a few mild symptoms while others get a full lethal combination.

After clearing from most internal organs, the virus is able to hide out for long periods of time in the nervous system and skin. Because of this phenomenon, callusing of skin or, much worse, seizures may occur long after the infection was thought to be cleared.

Most victims in the U.S. are puppies. (The colostrum suckled in the first day or so of life will provide them with a solid reflection of their mother𠏋 immunity. This will have waned by age 16 weeks leaving the puppy vulnerable if vaccines have not been administered for further protection.  In our society most mother dogs will have received some form of vaccination and thus be able to pass on at least some immunity and will have some ability to protect herself. In societies where vaccination is not common, distemper attacks all age dogs.)

Confirming the Distemper Infection

As if it is not bad enough that this infection has a poorly defined endpoint so one never knows for sure one is out of the woods, it is almost impossible to confirm a distemper diagnosis. Because of this, distemper is a clinical diagnosis, which means that rather than confirming infection with a test that is negative or positive, the veterinarian must look at the whole picture: what symptoms are there, is the history typical, etc. The virus itself remains elusive so that positive test results are meaningful in confirming the infection, but negative results do not rule it out.  The following are tests that can be used:

Distemper Inclusion Bodies ?璌istemper inclusion bodies?are actual clumps of virus that are visible under the microscope within infected cells. Post-mortem inclusion bodies are readily visible in the urinary bladder tissue thus making confirmation of distemper after death relatively easy. In the living patient, we typically have ready access to blood cells and cells of the eye𠏋 conjunctival membranes (the pink park of the eye socket). To enhance the visibility of inclusion bodies,  immunocytology is used. In this technique, antibodies against distemper virus are tagged with fluorescent markers. The antibodies bind to virus if it is present effectively dying the inclusion body with glow-in-the-dark fluorescent color.  The presence of inclusion bodies confirms distemper infection. The lack of detectable inclusion bodies does not rule out distemper infection as inclusion bodies ultimately become coated with the host𠏋 own antibodies which in turn block the fluorescent-tagged antibodies used in the test.




   


If callusing of the footpads or nose is evident, a biopsy of this tissue can be tested for inclusion bodies fairly late in infection.

Distemper Antibody Levels ?Distemper titers (another word of 弌ntibody level? of either the 𨧻gM?nbsp; type (produced in early stages of infection) and the 𨧻gG?type (produced in later phases of infection) can be checked. The problem is that distemper vaccination induces these same antibodies and often distemper suspects have had recent vaccination. A high IgM titer indicates recent infection or recent vaccination. There is no way to tell which.

Cerebrospinal Fluid Antibody Levels ?In neurologic distemper cases, cerebrospinal fluid is often tapped and distemper antibody levels checked. Distemper antibodies in cerebrospinal fluid is highly indicative of distemper infection as vaccine-induced antibodies do not cross the blood-brain barrier into the CSF fluid.

Treatment for Distemper

Many bizarre protocols have emerged over time as we grope for meaningful anti-viral therapy. The fact remains that recovery from distemper is all about immunity and the only real treatment is supportive care while the patient mounts its own immune response. If the patient has pneumonia, antibiotics are used on the secondary bacterial infections. Airway dilators are used as needed. Physical therapy is used to promote cough. If the patient has diarrhea, intravenous fluids are used to prevent dehydration etc.

Distemper is extremely variable in its ability to produce symptoms and recovery occurs at any stage. This has led to assorted therapies being credited with effect when what was more likely witnessed was the natural removal of the infection by the host𠏋 immune system.
Neurologic distemper is particularly difficult to treat. Still, it is possible for dogs to recover with livable deficits even from neurodistemper; euthanasia is best left for progressive, incapacitating neurologic symptoms.

Preventing Infection

If confirming diagnosis and therapy are the pitfalls of distemper, prevention is the easy part.  Effective distemper vaccination has been available since the 1950s. Prior to widespread vaccination, distemper was the scourge of the canine community, wiping out entire townfuls of pet dogs. Today, distemper is a rare disease except in the shelter, rescue, and pet store world.

The 𡞫istemper shot?is the basic immunization for dogs. It is generally combined with vaccine for canine parvovirus as well for parainfluenza, adenovirus 2, leptospirosis, and sometimes coronavirus. Puppies are vaccinated beginning at age 6-8 weeks and then every 2 to 4 weeks thereafter until age 16 weeks. The next vaccine is one year later. After that subsequent vaccination boosters are given every 1 to 3 years or based on antibody levels depending on the policy of the supervising animal hospital.

Vaccine is available in the traditional modified live virus format, where distemper virus is modified to induce immune-response but not illness.  Vaccine is also available in the recombinant format where a live harmless virus (not the distemper virus at all modified or otherwise) is used to carry the portion of the distemper virus which generates the immune-response. The benefit of the recombinant format is that it is completely impossible for distemper or distemper encephalitis to occur as the result of vaccination. These complications are exceedingly rare but still possible with modified live virus vaccine.

The use of the human measles virus to vaccinate against canine distemper is largely passe nowadays. Immunity obtained this way does not last as long and is not as successful as that obtained with a modified live or recombinant distemper vaccine.[/size]
[/td][/tr][tr][td]
[/td][/tr][/table]

minibabyqq 2006-12-20 19:46

[table][tr][td]轉貼自4682

[size=12px][size=5][color=magenta][b]青光眼  Glaucoma[/b][/color][/size] [table=98%][tr][td=2,1]青光眼是我們面對作為獸醫的最富挑戰性的眼科疾病的當中一個。情況是痛苦的和經常導致永久視覺損失。海拔在眼內壓力發生由於含水幽默被削弱的流出通過iridocorneal 角度。青光眼也許發生次要對許多條件包括透鏡luxation 和uveitis 但多數案件是主要和繼承, 通常影響狗在3-6 年紀之間。典型的案件提出以易變的期間的赤紅和多雲的歷史。當只一隻眼睛是受影響的, 症狀也許被忽略有一段時間了直到地球擴大是最後著名。這一般表明, 壓力是超出40-50 mmHg (法線上限是25 mmHg) 幾星期並且不可逆的視覺損失收效了。當第二隻眼睛變得受影響(這一點通常是案件伴隨著被繼承的青光眼), 患者那麼出席以深刻盲目性的歷史。當只一隻眼睛是受影響的, "正常" 眼睛的考試由gonioscopy (對隱形眼鏡和裂縫燈的用途直接地審查iridocorneal 角度) 可能幫助在預言是否這隻眼睛可能變得受影響。在某些情況下典型療程也許prophylactically 被使用。
[align=center][img=413,266]http://www.veterinaryvision.com/pictures/eyedrawing-glaucoma.gif[/img] [/align][size=+1][size=+1]養殖事先安排好對被繼承的青光眼 [table=250][tr][td=2,1][list][*]阿拉斯加的Malamute[*]美國斗雞家[*]Spaniel[*]Basset 追逐[*]小獵犬[*]Bouvier des Flandres[*]Bullmastiff[*]石標狗[*]食物食物[*]Dalmatian[*]狐狸狗[*]了不起的丹麥人[*]Keeshound[*]挪威Elkhound[*]長捲毛狗[*]薩莫耶特人[*]Shar Pei[*]西伯利亞愛斯基摩[/list][/td][/tr][/table][table=450][size=+2]青光眼症狀 [tr][td=1,1,50%][size=+1]症狀 [/td][td=1,1,50%][size=+1]起因 [/td][/tr][tr][td=1,1,50%]Scleral 射入[/td][td=1,1,50%]被舉起的IOP 結果在被削弱的多血脈性的回歸[/td][/tr][tr][td=1,1,50%]角膜腫鼓[/td][td=1,1,50%]對角膜內皮的直接壓力作用[/td][/tr][tr][td=1,1,50%]Pupillary 擴張[/td][td=1,1,50%]對pupillary 括約肌肌肉的直接壓力作用, 表明壓力超出40 mmHg[/td][/tr][tr][td=1,1,50%]輸入視覺缺乏(願是反演性的如果< 72 個小時) [/td][td=1,2]對視網膜和視覺神經的壓力作用[/td][/tr][tr][td=1,1,50%]盲目性[/td][/tr][tr][td=1,1,50%]地球擴大[/td][td=1,1,50%]慢性壓力海拔的作用, 表明永久視覺損失[/td][/tr][tr][td=1,1,50%]透鏡luxation[/td][td=1,1,50%]願是主要(通常先前luxation) 或次要(後部luxation/subluxation) 由於地球zonule 纖維擴大和故障[/td][/tr][/table][table=500][tr][td][img=212,188]http://www.veterinaryvision.com/pictures/glaucoma_1.jpg[/img][/td][td][img=205,188]http://www.veterinaryvision.com/pictures/glaucoma_secondary.jpg[/img][/td][/tr][/table][/td][/tr][tr][td=2,1][size=+2]治療 治療為青光眼被指揮在恢復視覺和舒適。這要求對壓力海拔的程度和期間的一個準確評估。在有在功能視覺的眼睛(沒有地球擴大, 期間回歸的潛力少於一個星期), 直接醫療療法使用最初地減少壓力。這被外科選擇選擇跟隨試圖永久地正常化壓力。醫療管理很少是成功的長期由於週期性壓力海拔和藥物毒力。
二極管laser 最近變得可利用為ciliary 身體的photocoagulation 。一根1 毫米探針嚮sclera 被應用2-2.5 毫米後部對異色邊緣提供2.5-3.5 焦耳(2.5 mwatts 為1000-1400 毫秒) 能量對ciliary 身體20-30 個站點。這導致ciliary 身體的分泌皮膜的地方化的破壞如此減少含水幽默生產。有並且在extrascleral 流出的一些增量含水在這做法進一步減少的眼內壓力以後。我們是幸運的, 這樣laser 由Iris Medical 使可利用對我們在山景。這個做法被使用了在窗簾和視覺眼睛以令人鼓舞的結果。手術後地, 眼睛是舒適的以最小的炎症。laser 做法可能被重覆如果需要。 [table=450][size=+2][size=+2]醫療療法為青光眼 [tr][td=1,1,24%][size=+1]藥物 [/td][td=1,1,25%][size=+1]藥量 [/td][td=1,1,51%][size=+1]評論 [/td][/tr][tr][td]甘露醇20%[/td][td]5 ml/lb BW IV[/td][td]評估小圓麵包首先, 扣壓水但螢幕為失水[/td][/tr][tr][td]甘油[/td][td]0.25 ml/lb BW PO[/td][td]可利用在櫃臺; 可能是重覆的q 5 個小時為2-3 藥量[/td][/tr][tr][td]Daranide (dichlorphenamide)[/td][td=1,2]1-2 mg/lb PO BID-TID[/td][td=1,2]導致hypokalemia, 經常沒被容忍的長期[/td][/tr][tr][td]Methazolamide[/td][/tr][tr][td]Timolol 0.5%[/td][td]典型BID-TID[/td][td][/td][/tr][tr][td]Dorzolamide (Trusopt)[/td][td]典型BID-TID[/td][td][/td][/tr][tr][td]Propine[/td][td]典型BID-TID[/td][td]偶爾的地方激怒[/td][/tr][/table][table=450][size=+2]外科選擇為視覺眼睛 [tr][td=1,1,33%][size=+1]做法 [/td][td=1,1,33%][size=+1]行動方法 [/td][td=1,1,34%][size=2]Advantages/Disadvantages[/size] [/td][/tr][tr][td=1,1,33%][b]Laser cyclophotocoagulation[/b]
[img=185,190]http://www.veterinaryvision.com/pictures/glaucoma_3_post-laser.jpg[/img][/td][td=1,1,33%]減少含水生產[/td][td=1,1,34%]專業設備要求易變的成功70% 在狗, 較少在貓[/td][/tr][tr][td=1,1,33%][b]後部sclerectomy-[/b]
[b]cyclodialysis-transcleral
iridencleisis[/b][/td][td=1,1,33%]增加含水流出[/td][td=1,1,34%]易變的成功: 75% 短期, 50% 長期[/td][/tr][tr][td=1,1,33%][b]Gonio 種入[/b][/td][td=1,1,33%]增加含水流出[/td][td=1,1,34%]extrememly 易變的成功
[/td][/tr][/table][/td][/tr][/table][table=98%][tr][td=2,1][size=+2]一隻瞎的眼睛的化妝保存
雖然它不能總是可能保存視覺, 它應該是在我們的力量之內使我們的患者舒適。進一步治療必要為是瞎的眼睛取決於, 當然, 盲目性的起因。最後導致盲目性的許多情況是還痛苦的。特別是, 青光眼也許長期導致慢性難受在visionis 以後丟失。雖然許多動物以被舉起的眼內壓力不會斜眼看或不會摩擦在受影響的眼睛, 一些將變得進步地lethargic 所有者也許簡單地歸因於"老年齡" 。人們影響以青光眼描述強烈的"頭疼" 類型痛苦。窗簾的外科撤除, 痛苦的眼睛總是選擇解除痛苦並且, 為一些所有者, 這不提供最簡單的選擇以複雜化的最少可能性和病後調養必需。但是, 為許多所有者, 眼睛的撤除運載心理意義在視覺作用之外損失。所有者附上對他們的寵物的物理出現不應該被低估的重要性。
有選擇為是否則瞎和痛苦的眼睛的化妝保存。首要, 它是根本建立, 視覺不可逆地的確丟失了。第二, 根本原因(即眼內腫瘤、系統疾病導致視網膜獨立小分隊或uveitis) 必須被辨認。第三, 對難受的評估應該被做。通常這要求眼內壓力的測量和視覺炎症的評估。
[/td][/tr][tr][td=2,1]
[img=287,264]http://www.veterinaryvision.com/pictures/post-laser.jpg[/img][/td][/tr][tr][td=2,1][b]Laser Cyclophotocoagulation (CPC)[/b] 介入ciliary 身體的部份的有選擇性的破壞減少含水幽默生產。這個做法運用二極管laser transclerally 被應用。這是選擇做法在有潛力恢復視覺深刻青光眼的案件。 [/td][/tr][tr][td=2,1][img=360,291]http://www.veterinaryvision.com/pictures/prosthesis1.jpg[/img][/td][/tr][tr][td=2,1]一條 [b]眼內假肢[/b] 是黑色、硅樹脂球形被種入入corneoscleral 殼在uveal 短文的外科撤除以後, 透鏡和視網膜。

[b]藥物Ciliary 身體燒蝕[/b] 介入志向玻璃被艮他黴素和dexamethasone 的組合的射入跟隨。艮他黴素證明是高度毒性的對ciliary 身體(並且視網膜) 並且因而導致含水幽默的被減少的生產。雖然這個做法是相對地低廉的, 結果是相當易變的, 與大瀑布形成和增加的角膜不透明看並且ciliary 身體的過份破壞造成地球萎縮(phthisis) 。這個做法一般是後備的為它是必要避免一般麻醉深度和期間必需為其它外科手術的那些動物。
[/td][/tr][tr][td=2,1][table=400][size=+2][size=+2]選擇為瞎的眼睛的治療 [tr][td][/td][td]Laser CPC [/td][td]眼內假肢 [/td][td]藥物燒蝕 [/td][td]Enucleation [/td][td]沒有治療[/td][/tr][tr][td]青光眼[/td][td]+[/td][td]+[/td][td]+[/td][td]+[/td][td]-[/td][/tr][tr][td]眼內腫瘤[/td][td]-[/td][td]-[/td][td]-[/td][td]+[/td][td]-[/td][/tr][tr][td]Uveitis[/td][td]-[/td][td][align=center]可能[/align][/td][td]-[/td][td]+[/td][td]-[/td][/tr][tr][td]視網膜獨立小分隊[/td][td]-[/td][td]-[/td][td]-[/td][td]-[/td][td][align=center]+/- laser retinopexy[/align][/td][/tr][tr][td]視網膜退化[/td][td]-[/td][td]-[/td][td]-[/td][td]-[/td][td]+[/td][/tr][tr][td]不可彌補的穿孔的精神創傷[/td][td]-[/td][td][align=center]可能[/align][/td][td]-[/td][td]+[/td][td]-[/td][/tr][tr][td=5,1][/td][td=1,6][/td][/tr][tr][td]費用[/td][td]+++[/td][td]++[/td][td]+[/td][td]++[/td][/tr][tr][td]專業設備[/td][td][align=center]是[/align][/td][td][align=center]是[/align][/td][td][align=center]是[/align][/td][td][align=center]不[/align][/td][/tr][tr][td]病後調養[/td][td][align=center]3-4 個星期[/align][/td][td][align=center]3-4 個星期[/align][/td][td][align=center]2 個星期[/align][/td][td][align=center]無[/align][/td][/tr][tr][td]成功率[/td][td][align=center]60%[/align][/td][td][align=center]90%[/align][/td][td][align=center]75%[/align][/td][td][align=center]99%[/align][/td][/tr][tr][td]最後的出現[/td][td][align=center]優秀[/align][/td][td][align=center]好[/align][/td][td][align=center]易變(phthisis, 大瀑布也許發生)[/align][/td][td][align=center]看法不同的問題[/align][/td][/tr][/table][/td][/tr][/table][table=98%][tr][td]
[/td][/tr][/table][table=98%][tr][td=2,1]Glaucoma is one of the most challenging ophthalmic diseases we face as veterinarians. The condition is painful and often results in permanent vision loss. The elevation in intraocular pressure occurs due to impaired outflow of aqueous humor through the iridocorneal angle. Glaucoma may occur secondary to many conditions including lens luxation and uveitis but most cases are primary and inherited, usually affecting dogs between 3-6 years of age. The typical case presents with a history of redness and cloudiness of variable duration. When only one eye is affected, the symptoms may be overlooked for some time until globe enlargement is finally noted. This generally indicates that the pressure has been in excess of 40-50 mmHg (upper limit of normal is 25 mmHg) for weeks and that irreversible vision loss has resulted. When the second eye becomes affected (as is usually the case with inherited glaucoma), the patient then presents with a history of acute blindness. When only one eye is affected, examination of the "normal" eye by gonioscopy (use of a contact lens and a slit lamp to directly examine the iridocorneal angle) can help in predicting whether this eye is likely to become affected. In some cases topical medication may be used prophylactically.
[align=center][img=413,266]http://www.veterinaryvision.com/pictures/eyedrawing-glaucoma.gif[/img] [/align][size=+1]Breeds Predisposed to Inherited Glaucoma [table=250][tr][td=2,1][list][*]Alaskan Malamute[*]American Cocker[*]Spaniel[*]Basset Hound[*]Beagle[*]Bouvier des Flandres[*]Bullmastiff[*]Cairn Terrier[*]Chow Chow[*]Dalmatian[*]Fox Terrier[*]Great Dane[*]Keeshound[*]Norwegian Elkhound[*]Poodle[*]Samoyed[*]Shar Pei[*]Siberian Husky[/list][/td][/tr][/table][table=450][size=+2]Symptoms of Glaucoma [tr][td=1,1,50%][size=+1]Symptom [/td][td=1,1,50%][size=+1]Cause [/td][/tr][tr][td=1,1,50%]Scleral injection[/td][td=1,1,50%]elevated IOP results in impaired venous return[/td][/tr][tr][td=1,1,50%]Corneal edema[/td][td=1,1,50%]direct pressure effect on corneal endothelium[/td][/tr][tr][td=1,1,50%]Pupillary dilation[/td][td=1,1,50%]direct pressure effect on pupillary sphincter muscle, indicates pressure in excess of 40 mmHg[/td][/tr][tr][td=1,1,50%]Afferent vision deficit (may be reversible if < 72 hours) [/td][td=1,2]pressure effect on retina and optic nerve[/td][/tr][tr][td=1,1,50%]Blindness[/td][/tr][tr][td=1,1,50%]Globe enlargement[/td][td=1,1,50%]effect of chronic pressure elevation, indicates permanent vision loss[/td][/tr][tr][td=1,1,50%]Lens luxation[/td][td=1,1,50%]may be primary (usually anterior luxation) or secondary (posterior luxation/subluxation) due to globe enlargement and breakdown of zonule fibers[/td][/tr][/table][table=500][tr][td][img=212,188]http://www.veterinaryvision.com/pictures/glaucoma_1.jpg[/img][/td][td][img=205,188]http://www.veterinaryvision.com/pictures/glaucoma_secondary.jpg[/img][/td][/tr][/table][/td][/tr][tr][td=2,1][size=+2]Treatment Treatment for glaucoma is directed at restoring both vision and comfort. This requires an accurate assessment of the extent and duration of the pressure elevation. In eyes which have the potential for return of functional vision (no globe enlargement, duration less than one week), immediate medical therapy is used to initially reduce the pressure. This is followed by a choice of surgical options to attempt to permanently normalize the pressure. Medical management is rarely successful long-term due to recurrent pressure elevation and drug toxicity.
The diode laser has recently become available for photocoagulation of the ciliary body. A 1 mm probe is applied to the sclera 2-2.5 mm posterior to the limbus to deliver 2.5-3.5 joules (2.5 mwatts for 1000-1400 msec) of energy to the ciliary body over 20-30 sites. This results in localized destruction of the secretory epithelium of the ciliary body thus reducing aqueous humor production. There is also some increase in extrascleral outflow of aqueous after this procedure further reducing intraocular pressure. We are fortunate that such a laser has been made available to us by Iris Medical in Mountain View. This procedure has been used in both blind and visual eyes with encouraging results. Postoperatively, the eyes are comfortable with minimal inflammation. The laser procedure can be repeated if necessary. [table=450][size=+2]Medical Therapy for Glaucoma [tr][td=1,1,24%][size=+1]Drug [/td][td=1,1,25%][size=+1]Dose [/td][td=1,1,51%][size=+1]Comments [/td][/tr][tr][td]Mannitol 20%[/td][td]5 ml/lb BW IV[/td][td]evaluate BUN first, withhold water but monitor for dehydration[/td][/tr][tr][td]Glycerine[/td][td]0.25 ml/lb BW PO[/td][td]available over the counter; can be repeated q 5 hours for 2-3 doses[/td][/tr][tr][td]Daranide (dichlorphenamide)[/td][td=1,2]1-2 mg/lb PO BID-TID[/td][td=1,2]induces hypokalemia, often not tolerated long-term[/td][/tr][tr][td]Methazolamide[/td][/tr][tr][td]Timolol 0.5%[/td][td]topical BID-TID[/td][td][/td][/tr][tr][td]Dorzolamide (Trusopt)[/td][td]topical BID-TID[/td][td][/td][/tr][tr][td]Propine[/td][td]topical BID-TID[/td][td]occasional local irritation[/td][/tr][/table][table=450][size=+2]Surgical options for visual eyes [tr][td=1,1,33%][size=+1]Procedure [/td][td=1,1,33%][size=+1]Method of action [/td][td=1,1,34%][size=2]Advantages/Disadvantages[/size] [/td][/tr][tr][td=1,1,33%][b]Laser cyclophotocoagulation[/b]
[img=185,190]http://www.veterinaryvision.com/pictures/glaucoma_3_post-laser.jpg[/img][/td][td=1,1,33%]decreases aqueous production[/td][td=1,1,34%]specialized equipment required variable success 70% in dogs, less in cats[/td][/tr][tr][td=1,1,33%][b]Posterior sclerectomy-[/b]
[b]cyclodialysis-transcleral
iridencleisis[/b][/td][td=1,1,33%]increase aqueous outflow[/td][td=1,1,34%]variable success: 75% short-term, 50% long-term[/td][/tr][tr][td=1,1,33%][b]Gonio-implant[/b][/td][td=1,1,33%]increase aqueous outflow[/td][td=1,1,34%]extrememly variable success
[/td][/tr][/table][/td][/tr][/table][table=98%][tr][td=1,1,2%][/td][td][table=98%][tr][td=2,1][size=+2]Cosmetic Preservation of a Blind Eye
Although it may not always be possible to preserve vision, it should be within our power to make our patients comfortable. The necessity of further treatment for an eye which is blind depends, of course, on the cause of the blindness. Many conditions which ultimately result in blindness are also painful. In particular, glaucoma may cause chronic discomfort long after the visionis lost. Although many animals with elevated intraocular pressure will not squint or rub at the affected eye, some will become progressively lethargic which owners may attribute simply to "old age". People affected with glaucoma describe an intense "headache" type of pain. Surgical removal of a blind, painful eye is always an option to relieve the pain and, for some owners, this offers the simplest choice with the least possibility of complications and no aftercare required. However, for many owners, removal of an eye carries a psychological significance beyond the loss of visual function. The importance that owners attach to their pet's physical appearance should not be underestimated.
There are alternatives for cosmetic preservation of an eye which is otherwise blind and painful. First and foremost, it is essential to establish that vision has indeed been irreversibly lost. Secondly, the underlying cause (i.e. intraocular tumor, systemic disease leading to retinal detachment or uveitis) must be identified. Thirdly, an assessment of discomfort should be made. Usually this requires measurement of intraocular pressure and an evaluation of ocular inflammation.
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[img=287,264]http://www.veterinaryvision.com/pictures/post-laser.jpg[/img][/td][/tr][tr][td=2,1][b]Laser Cyclophotocoagulation (CPC)[/b] involves selective destruction of a portion of the ciliary body to decrease aqueous humor production. This procedure utilizes a diode laser applied transclerally. This is the procedure of choice in cases of acute glaucoma where there is the potential to restore vision. [/td][/tr][tr][td=2,1][img=360,291]http://www.veterinaryvision.com/pictures/prosthesis1.jpg[/img][/td][/tr][tr][td=2,1]An [b]Intraocular Prosthesis[/b] is a black, silicone sphere implanted into the corneoscleral shell after surgical removal of the uveal tract, lens and retina.

[b]Pharmacologic Ciliary Body Ablation[/b] involves aspiration of vitreous followed by injection of a combination of gentamicin and dexamethasone. Gentamicin has been shown to be highly toxic to the ciliary body (as well as the retina) and thus results in reduced production of aqueous humor. Although this procedure is relatively inexpensive, the results are quite variable, with cataract formation and increased corneal opacity seen as well as excessive destruction of the ciliary body resulting in globe atrophy (phthisis). This procedure is generally reserved for those animals where it is necessary to avoid the depth and duration of general anesthesia required for the other surgical procedures.
[/td][/tr][tr][td=2,1][table=400][size=+2]Options for Treatment of Blind Eyes [tr][td][/td][td]Laser CPC [/td][td]Intraocular Prosthesis [/td][td]Pharmacologic Ablation [/td][td]Enucleation [/td][td]No Treatment[/td][/tr][tr][td]Glaucoma[/td][td]+[/td][td]+[/td][td]+[/td][td]+[/td][td]-[/td][/tr][tr][td]Intraocular tumor[/td][td]-[/td][td]-[/td][td]-[/td][td]+[/td][td]-[/td][/tr][tr][td]Uveitis[/td][td]-[/td][td][align=center]possible[/align][/td][td]-[/td][td]+[/td][td]-[/td][/tr][tr][td]Retinal detachment[/td][td]-[/td][td]-[/td][td]-[/td][td]-[/td][td][align=center]+/- laser retinopexy[/align][/td][/tr][tr][td]Retinal degeneration[/td][td]-[/td][td]-[/td][td]-[/td][td]-[/td][td]+[/td][/tr][tr][td]Irreparable perforating trauma[/td][td]-[/td][td][align=center]possible[/align][/td][td]-[/td][td]+[/td][td]-[/td][/tr][tr][td=5,1][/td][td=1,6][/td][/tr][tr][td]Cost[/td][td]+++[/td][td]++[/td][td]+[/td][td]++[/td][/tr][tr][td]Specialized Equipment[/td][td][align=center]yes[/align][/td][td][align=center]yes[/align][/td][td][align=center]yes[/align][/td][td][align=center]no[/align][/td][/tr][tr][td]Aftercare[/td][td][align=center]3-4 weeks[/align][/td][td][align=center]3-4 weeks[/align][/td][td][align=center]2 weeks[/align][/td][td][align=center]none[/align][/td][/tr][tr][td]Success rate[/td][td][align=center]60%[/align][/td][td][align=center]90%[/align][/td][td][align=center]75%[/align][/td][td][align=center]99%[/align][/td][/tr][tr][td]Final appearance[/td][td][align=center]excellent[/align][/td][td][align=center]good[/align][/td][td][align=center]variable (phthisis, cataract may occur)[/align][/td][td][align=center]a matter of opinion[/align][/td][/tr][/table][/td][/tr][/table][/td][/tr][/table][/size]
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minibabyqq 2006-12-20 19:48

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[size=12px][size=5][color=magenta][b]注意眼睛上的顏色變化Pigmented Ocular Masses[/b][/color][/size] [table=98%][tr][td=2,1]一個變化在眼睛上的顏色由多數所有者迅速地注意。眼睛的被著色的損害很大地變化在他們的出現和他們的臨床意義上
[b]Limbal 黑瘤[/b] 起源於melanocytes 外緣通常被發現在角膜和sclera 的連接點之內。這些腫瘤是組織學上良性的但進步地擴大以眼內iridocorneal 角度的引伸、入侵和次要青光眼。那裡看來是養殖素質為大養殖, 與金黃獵犬和拉布拉多獵犬在最共同地受影響的養殖之中。當這些腫瘤影響狗少於5 年紀, 他們傾向於更加迅速地進步以早期治療被表明。
[/td][/tr][tr][td=2,1][img=172,180]http://www.veterinaryvision.com/pictures/limbalmmpre.jpg[/img][img=208,180]http://www.veterinaryvision.com/pictures/limbalmmpost.jpg[/img][/td][/tr][tr][td=2,1]這些腫瘤幸運地是順應的對 [i]二極管laser photocoagulation[/i]。部份外科切除執行以殘餘的受影響的limbal 組織的治療與laser 被交付通過經營的顯微鏡。這些相片以前說明一個典型的limbal 黑瘤和6 個星期的出現在治療以後與二極管laser 。雖然一些角膜不透明依然是, 有是腫瘤的沒有進步三年。
[b]眼皮黑瘤[/b] 並且是典型地良性的。當少於25% 眼皮邊際是包含的, 外科切除是選擇的治療。但是, 當損害是更大或多, laser 治療有價值。
[/td][/tr][tr][td=2,1]相片這系列說明多個眼皮黑瘤在一條五年老Vizsla 狗。在初期三個星期期間手術後, 有壞死在laser 治療站點。以時間, 脫落被對待的區域導致光滑, 功能眼皮邊際。使用常規外科切除, 一個嫁接的做法會是必要的。
[/td][/tr][tr][td=2,1][img=176,144]http://www.veterinaryvision.com/pictures/lidmmpre.jpg[/img][img=157,144]http://www.veterinaryvision.com/pictures/lidmmpost1.jpg[/img]
[/td][/tr][tr][td=2,1][img=163,144]http://www.veterinaryvision.com/pictures/lidmmpost2.jpg[/img] [/td][/tr][tr][td=2,1][b]Conjunctival 黑瘤[/b] 有經常是非常與其它視覺黑瘤不同的生物行為。這些腫瘤類似嚴密黑瘤與相關其它黏膜(即口頭mucosa 黑瘤) 並且也許高度惡性。進取的外科切除, 包括enucleation 如果需要, 被表明。[/td][/tr][tr][td=2,1][img=144,149]http://www.veterinaryvision.com/pictures/conjmm.jpg[/img] [/td][/tr][tr][td=2,1][b]Uveal 黑瘤[/b] 代表最共同的主要眼內腫瘤。虹膜是經常受影響的, 與ciliary 身體並且/或者脈絡膜由引伸次要地影響。這些腫瘤出現如同密集地被著色的, 地方化的大量在虹膜之內。在狗, uveal 黑瘤一般是良性的以轉移的非常低發生。在許多情況下, lesin 不是著名或提到直到腫瘤延伸到iridocorneal 角度並且/或者posteriorly 入ciliary 身體。在這些情況下, 沒有選擇為治療並且, 青光眼最後發生需要enucleation 。
[/td][/tr][tr][td=2,1][img=180,127]http://www.veterinaryvision.com/pictures/uvealmmcanine1.jpg[/img][img=179,127]http://www.veterinaryvision.com/pictures/uvealmmcanine2.jpg[/img] [/td][/tr][tr][td=2,1][img=142,122]http://www.veterinaryvision.com/pictures/irismmdogpre.jpg[/img][img=144,123]http://www.veterinaryvision.com/pictures/irismmdogpost.jpg[/img]更加早期的虹膜黑瘤在狗可能成功地被對待使用二極管laser photocoagulation 以視覺的優秀結果和保存。這些相片說明一個小虹膜黑瘤在一隻3 年拉布拉多獵犬。損害transcorneally 被對待了使用二極管laser 。一年手術後, 被對待的區域陳列虹膜萎縮和一個小虹膜瑕疵沒有殘餘的腫瘤。

[/td][/tr][/table][table=98%][tr][td=2,1]A change in color of the eye is rapidly noted by most owners. Pigmented lesions of the eye vary greatly in their appearance and their clinical significance
[b]Limbal melanomas[/b] originate from the rim of melanocytes normally found within the junction of the cornea and sclera. These tumors are histologically benign but progressively enlarge with intraocular extension, invasion of the iridocorneal angle and secondary glaucoma. There appears to be a breed pre-disposition for large breeds, with Golden retrievers and Labrador retrievers among the most commonly affected breeds. When these tumors affect dogs less than 5 years of age, they tend to progress more rapidly with early treatment indicated.
[/td][/tr][tr][td=2,1][img=172,180]http://www.veterinaryvision.com/pictures/limbalmmpre.jpg[/img][img=208,180]http://www.veterinaryvision.com/pictures/limbalmmpost.jpg[/img][/td][/tr][tr][td=2,1]Fortunately these tumors are amenable to [i]diode laser photocoagulation[/i]. Partial surgical excision is performed with treatment of the remaining affected limbal tissue with the laser delivered through the operating microscope. These photographs illustrate the appearance of a typical limbal melanoma before and 6 weeks after treatment with the diode laser. Although some corneal opacity remains, there has been no progression of the tumor for over three years.
[b]Eyelid melanomas[/b] are also typically benign. When less than 25% of the eyelid margin is involved, surgical excision is the treatment of choice. However, when the lesions are larger or multiple, laser treatment is of value.
[/td][/tr][tr][td=2,1]This series of photographs illustrates multiple eyelid melanomas in a five year old Vizsla dog. During the initial three weeks postoperatively, there was necrosis at the site of laser treatment. With time, sloughing of the treated area resulted in a smooth, functional eyelid margin. Using conventional surgical excision, a grafting procedure would have been necessary.
[/td][/tr][tr][td=2,1][img=176,144]http://www.veterinaryvision.com/pictures/lidmmpre.jpg[/img][img=157,144]http://www.veterinaryvision.com/pictures/lidmmpost1.jpg[/img]
[/td][/tr][tr][td=2,1][img=163,144]http://www.veterinaryvision.com/pictures/lidmmpost2.jpg[/img] [/td][/tr][tr][td=2,1][b]Conjunctival melanomas[/b] have biological behavior that is often very different from other ocular melanomas. These tumors more closely resemble melanomas associated with other mucous membranes (i.e. oral mucosa melanomas) and may be highly malignant. Aggressive surgical excision, including enucleation if necessary, is indicated.[/td][/tr][tr][td=2,1][img=144,149]http://www.veterinaryvision.com/pictures/conjmm.jpg[/img] [/td][/tr][tr][td=2,1][b]Uveal melanomas[/b] represent the most common primary intraocular tumor. The iris is most often affected, with the ciliary body and/or choroid affected secondarily by extension. These tumors appear as a densely pigmented, localized mass within the iris. In dogs, uveal melanomas are generally benign with a very low incidence of metastasis. In many cases, the lesin is not noted or referred until the tumor has extended into the iridocorneal angle and/or posteriorly into the ciliary body. In these cases, there are no options for treatment and, ultimately glaucoma occurs necessitating enucleation.
[/td][/tr][tr][td=2,1][img=180,127]http://www.veterinaryvision.com/pictures/uvealmmcanine1.jpg[/img][img=179,127]http://www.veterinaryvision.com/pictures/uvealmmcanine2.jpg[/img] [/td][/tr][tr][td=2,1][img=142,122]http://www.veterinaryvision.com/pictures/irismmdogpre.jpg[/img][img=144,123]http://www.veterinaryvision.com/pictures/irismmdogpost.jpg[/img]Earlier iris melanomas in dogs can be successfully treated using diode laser photocoagulation with excellent results and preservation of vision. These photos illustrate a small iris melanoma in a 3 year old Labrador retriever. The lesion was treated transcorneally using a diode laser. One year postoperatively, the treated area exhibits iris atrophy and a small iris defect with no remaining tumor.
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minibabyqq 2006-12-20 19:49

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[size=12px][size=5][color=magenta][b]系統高血壓   Systemic Hypertension[/b][/color][/size] [table=98%][tr][td=2,1][size=+2]起因 海拔在血壓經常發生作為一種次要現象對已存在系統疾病。腎功能不全包括glomerular 並且細胞間的疾病是次要高血壓的同道會在狗和貓(通過renin-angiotensin 系統和鈉保留的活化作用) 。相反地然而, 高血壓可能並且導致腎功能不全通過進步局部缺血。因而, 在許多慢性案件, 它也許難確定哪種疾病首先來了。在一次勘測(Cowgill, UCD), 73% 狗以腎臟病被發現有被舉起的血壓。
[size=+2][size=+2]視覺標誌 視覺疾病與相關系統高血壓發生由於小船和血管流出破裂。那裡也許並且是一個次要先前或平底鍋uveitis 。經常視覺標誌(深刻視覺損失和pupillary 擴張由於視網膜獨立小分隊) 也許是第一症狀由所有者注意。
[size=+2][size=+2]診斷 系統血壓的測量也許由測量直接地(通過動脈cannulation) 或間接地完成相當數量外在壓力必需遮沒血流在肢。多譜勒儀血壓計是血壓測量間接方法被使用在我們的實踐。壓力袖口適用於尾巴或forelimb 或hindlimb 。做法容易地執行以最小的克制; 幾反覆讀書被獲得使人工製品減到最小。正常收縮壓是120 毫米百克; 動物陳列高血壓retinopathy 經常有壓力超出200 毫米百克。
[size=+2][size=+2]治療 成功的療法要求對部下的情況的患者的一般健康和證明的綜合評估。如果腎臟作用是法線, 系統利尿藥經常是成功的在導致subretinal 流體的吸回以視網膜re-attachment 。當治療為腎衰竭(再水化, 增加的鹽進水閘) 並且高血壓(利尿藥, 被減少的鹽進水閘) 是在直接反對互相, 腎臟導致的高血壓的治療是最富挑戰性。療法通常介入藥物的組合, 仔細地被滴定為各名患者。

[/td][/tr][tr][td=2,1][table=98%][tr][td=2,1][b]視覺標誌[/b][/td][/tr][tr][td=1,1,50%][img=211,216]http://www.veterinaryvision.com/pictures/hypertens_2.jpg[/img][/td][td][img=207,216]http://www.veterinaryvision.com/pictures/hypertens_1.jpg[/img][/td][/tr][tr][td=2,1][table=225][tr][td][list][*]深刻盲目性[*]Pupillary 擴張[*]Hyphema[*]玻璃出血[*]視網膜獨立小分隊[*]視網膜出血[/list][/td][/tr][/table][/td][/tr][/table][/td][/tr][tr][td=2,1][table=425][size=+2]藥物□去□常對待系統高血壓 [tr][td=1,1,22%][size=+1]藥物 [/td][td=1,1,15%][size=+1]劑量 [/td][td=1,1,63%][size=+1]行動機制 [/td][/tr][tr][td]Amlodipine[/td][td]0.625 毫克SID[/td][td]鈣渠道預鍛模[/td][/tr][tr][td]Hydrochlorothiazide[/td][td]1.0-2.0 mg/kg[/td][td]利尿, 減退細胞外可變的容量[/td][/tr][tr][td]心得安[/td][td]0.5-2.0 mg/kg[/td][td]b 腎上腺素能的預鍛模, 減退腎素, 小時, CO[/td][/tr][tr][td]Captopril[/td][td]0.5-1.0 mg/kg[/td][td]禁止血管緊縮素轉換的酵素[/td][/tr][tr][td]Prazosin[/td][td]1.0-2.0 mg/kg[/td][td]腎上腺素能的預鍛模, 血管舒張劑, 減少TPR[/td][/tr][tr][td]Hydralazine[/td][td]0.5-1.0 mg/kg[/td][td]鈣渠道預鍛模, 血管舒張劑, 減退TPR, 增加小時[/td][/tr][tr][td]強體松[/td][td]0.5-1.0 mg/kg[/td][td]減少血管流出[/td][/tr][/table][/td][/tr][/table][table=98%][tr][td=2,1][size=+2]Causes Elevation in blood pressure occurs most often as a secondary phenomenon to pre-existing systemic disease. Renal insufficiency including glomerular as well as interstitial disease is the most common cause of secondary hypertension in dogs and cats (through activation of the renin-angiotensin system and sodium retention). Conversely however, hypertension can also cause renal insufficiency through progressive ischemia. Thus, in many chronic cases, it may be difficult to determine which disease came first. In one survey (Cowgill, UCD), 73% of dogs with renal disease were found to have elevated blood pressure.
[size=+2]Ocular Signs Ocular disease associated with systemic hypertension occurs as a result of rupture of small vessels and vascular effusion. There may also be a secondary anterior- or pan-uveitis. Often the ocular signs (acute vision loss and pupillary dilation due to retinal detachment) may be the first symptoms noted by the owner.
[size=+2]Diagnosis Measurement of systemic blood pressure may be done directly (through arterial cannulation) or indirectly by measuring the amount of external pressure required to occlude blood flow in an extremity. The Doppler sphygmomanometer is the indirect method of blood pressure measurement used in our practice. The pressure cuff is applied to the tail or a forelimb or hindlimb. The procedure is easily performed with minimal restraint; several repetitive readings are obtained to minimize artifact. Normal systolic pressure is 120 mm Hg; animals exhibiting hypertensive retinopathy often have pressure in excess of 200 mm Hg.
[size=+2]Treatment Successful therapy requires an overall assessment of the patient's general health and identification of the underlying condition. If renal function is normal, systemic diuretics are often successful in causing resorption of the subretinal fluid with retinal re-attachment. As the treatment for renal failure (rehydration, increased salt intake) and hypertension (diuretics, reduced salt intake) are in direct opposition to each other, treatment of renal-induced hypertension is most challenging. Therapy usually involves a combination of drugs, carefully titrated for each patient.

[/td][/tr][tr][td=2,1][table=98%][tr][td=2,1][b]OCULAR SIGNS[/b][/td][/tr][tr][td=1,1,50%][img=211,216]http://www.veterinaryvision.com/pictures/hypertens_2.jpg[/img][/td][td][img=207,216]http://www.veterinaryvision.com/pictures/hypertens_1.jpg[/img][/td][/tr][tr][td=2,1][table=225][tr][td][list][*]Acute blindness[*]Pupillary dilation[*]Hyphema[*]Vitreous hemorrhage[*]Retinal detachment[*]Retinal hemorrhage[/list][/td][/tr][/table][/td][/tr][/table][/td][/tr][tr][td=2,1][table=425][size=+2]Drugs Used to Treat Systemic Hypertension [tr][td=1,1,22%][size=+1]Drug [/td][td=1,1,15%][size=+1]Dosage [/td][td=1,1,63%][size=+1]Mechanism of Action [/td][/tr][tr][td]Amlodipine[/td][td]0.625 mg SID[/td][td]calcium channel blocker[/td][/tr][tr][td]Hydrochlorothiazide[/td][td]1.0-2.0 mg/kg[/td][td]diuretic, decreases extracellular fluid volume[/td][/tr][tr][td]Propranolol[/td][td]0.5-2.0 mg/kg[/td][td]b-adrenergic blocker, decreases renin, HR, CO[/td][/tr][tr][td]Captopril[/td][td]0.5-1.0 mg/kg[/td][td]inhibits angiotensin converting enzyme[/td][/tr][tr][td]Prazosin[/td][td]1.0-2.0 mg/kg[/td][td]a-adrenergic blocker, vasodilator, decreases TPR[/td][/tr][tr][td]Hydralazine[/td][td]0.5-1.0 mg/kg[/td][td]calcium channel blocker, vasodilator, decreases TPR, increases HR[/td][/tr][tr][td]Prednisone[/td][td]0.5-1.0 mg/kg[/td][td]decreases vascular effusion[/td][/tr][/table][/td][/tr][/table][/size]
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minibabyqq 2006-12-20 19:50

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[size=12px][size=5][color=magenta][b]視網膜退化    Retinal Degeneration[/b][/color][/size]


進步視網膜萎縮(PRA) 是導致標尺和錐體退化在視網膜以不可逆的視覺損失的一種被繼承的疾病。在繼承方式被辨認了的所有養殖, 它是autosomal 隱性。PRA 的被繼承的形式寬廣地被分類至於是否標尺或錐體是主要受影響和作為或[b]發育異常[/b]( 光感受器的 發展反常性- 典型一個非常早期的起始的形式臨床標誌在一年紀之前) 或 [b]退化[/b] (一個最新起始情況發生在光感受器的正常成熟性以後) 。
起始和前進速度的年齡變化從養殖到養殖。在許多情況下, 視覺損傷的臨床標誌發生當狗是6-8 年紀。第一標誌被觀察通常是夜視損失, 進步, 通常在幾個月內, 對白天視覺損失。此時, pupillary 擴張也許並且是著名。
雖然視網膜退化多數案件被繼承, 有這個情況變形叫做 [b]Sudden Acquired 的視網膜退化(SARD)[/b]。受影響的動物提出以深刻盲目性和雙邊pupillary 擴張的歷史; 有通常沒有系統或神經學疾病暴露或症狀的歷史對毒素的。視網膜和視覺神經的Ophthalmoscopic 考試不顯露反常性在疾病的早期。
被繼承的視網膜退化診斷可能由臨床考試通常做使用檢眼計審查視網膜。變薄視網膜和視網膜船的被減少的大小被觀察。偶爾地, 大瀑布也許發生次要對視網膜退化。在這些情況下, 大瀑布手術明顯地是沒有好處。但是, 狗不能經常提出為眼科考試直到大瀑布進步了以便詳細的fundus 考試由透鏡不透明防止。在這些情況下, 視網膜電圖描記術是根本做這個診斷和防止多餘的手術。
視網膜電圖描記術是電子反應被記錄當視網膜由光刺激。在角膜不透明或大瀑布面前, 充足的光到達視網膜導致反應在視網膜是工作條件下。徵兆為視網膜電圖描記術有:
1) 視網膜作用的preoperative 評估在大瀑布提取之前為了查出那些動物影響在PRA 的同時。
2) 沒有ophthalmoscopically 明顯的損害視網膜疾病的證明; 即突然的被獲取的視網膜退化(SARD), 夜視症; 與視覺損失特別區別這些(amaurosis 的) CNS 起因。
3) 動物的證明基因上影響與PRA 在他們陳列臨床標誌或是可發現的由檢眼計考試之前。這是特別重要在選擇會被使用為養殖在多數PRA 的動物(6-9 年的) 形式起始之前的年齡。
視網膜電圖描記術要求一般麻醉和專業設備。隱形眼鏡電極被安置在眼睛和參考針電極的表面在耳朵和鼻梁的pinna 。多數測試執行使用白色或紅燈唯一閃光。查出錐體反常性, 技術叫做忽悠融合使用。這辨認在之外各自的爾格反應不是可發現的刺激的頻率。這價值通常是75-80/second 。在狗影響以夜視症, 錐體有選擇性地影響, 忽悠融合頻率也許是一樣降低像5-10/second 。 [table=450][size=+2][size=+2]養殖影響與PRA [tr][td=1,1,50%][size=+1]養殖 [/td][td=1,1,50%][size=+1]評論 [/td][/tr][tr][td]Akita[/td][td]起始2-3 年[/td][/tr][tr][td]阿拉斯加的Malamute[/td][td]夜視症; 具體錐體退化[/td][/tr][tr][td]小獵犬[/td][td][/td][/tr][tr][td]疆界大牧羊犬[/td][td][/td][/tr][tr][td]俄國獵狼犬[/td][td]2 型描述了[/td][/tr][tr][td]Briard[/td][td]起始12-18 個月[/td][/tr][tr][td]切塞皮克灣獵犬[/td][td]2 型: 起始8-12 個月或4 到7 年[/td][/tr][tr][td]食物食物[/td][td][/td][/tr][tr][td]美國斗雞家Spaniel[/td][td][/td][/tr][tr][td]大牧羊犬[/td][td]標尺錐體發育異常類型II, 起始6-8 個月; 還典型的PRA, 起始6-9 年[/td][/tr][tr][td]英國斗雞家Spaniel[/td][td]起始1-3 年[/td][/tr][tr][td]英國Springer Spaniel[/td][td]起始3-5 年[/td][/tr][tr][td]德國牧羊人[/td][td][/td][/tr][tr][td]金黃獵犬[/td][td][/td][/tr][tr][td]愛爾蘭安裝員[/td][td]標尺錐體發育異常類型I, 起始< 6 個月[/td][/tr][tr][td]拉布拉多獵犬[/td][td]2 型: PRA 和中央PRA (RPE 影響)[/td][/tr][tr][td]拉薩Apso[/td][td][/td][/tr][tr][td]微型Schnauzer[/td][td]標尺錐體發育異常, 起始10-12 個月[/td][/tr][tr][td]挪威Elkhound[/td][td]標尺發育異常, 輕率在1-2 年以前[/td][/tr][tr][td]長捲毛狗[/td][td][align=center]標尺錐體退化, 起始6-9 年[/align][/td][/tr][tr][td]Rottweiler[/td][td][/td][/tr][tr][td]薩莫耶特人[/td][td][/td][/tr][tr][td]Shar Pei[/td][td][/td][/tr][tr][td]Shetland Sheepdog[/td][td][/td][/tr][tr][td]Shih Tzu[/td][td][/td][/tr][tr][td]西伯利亞愛斯基摩[/td][td][/td][/tr][tr][td]西藏狗[/td][td]起始8-12 個月[/td][/tr][/table][table=98%][tr][td=1,1,50%][img=253,310]http://www.veterinaryvision.com/pictures/retina-dog_normal.jpg[/img][/td][td=1,1,50%][img=249,310]http://www.veterinaryvision.com/pictures/retina-dog_pra.jpg[/img][/td][/tr][/table]Progressive retinal atrophy (PRA) is an inherited disease which results in degeneration of the rods and cones in the retina with irreversible vision loss. In all breeds in which the mode of inheritance has been identified, it is autosomal recessive. The inherited forms of PRA are broadly classified as to whether the rods or cones are primarily affected and as either a form of [b]dysplasia [/b](developmental abnormality of the photoreceptors - typically a very early onset of clinical signs prior to one year of age) or [b]degeneration[/b] (a later onset condition occurring after normal maturation of the photoreceptors).
The age of onset and rate of progression varies from breed to breed. In most cases, clinical signs of vision impairment occur when the dog is 6-8 years of age. The first sign observed is usually a loss of night vision, which progresses, usually within a few months, to a loss of daylight vision as well. At this time, the pupillary dilation may also be noted.
Although most cases of retinal degeneration are inherited, there is a variant of this condition called [b]Sudden Acquired Retinal Degeneration (SARD)[/b]. Affected animals present with a history of acute blindness and bilateral pupillary dilation; there is usually no history of exposure to toxins or symptoms of systemic or neurologic disease. Ophthalmoscopic examination of the retina and optic nerve reveals no abnormalities in the early stages of the disease.
Diagnosis of inherited retinal degeneration can usually be made by clinical examination using an ophthalmoscope to examine the retina. Thinning of the retina and reduced size of the retinal vessels are observed. Occasionally, cataracts may occur secondary to retinal degeneration. In such cases, cataract surgery is obviously of no benefit. However, often a dog may not present for ophthalmic examination until the cataracts have progressed so that detailed fundus examination is prevented by the lens opacity. In such cases, electroretinography is essential to make this diagnosis and prevent an unnecessary surgery.
Electroretinography is the electrical response recorded when the retina is stimulated by light. Even in the presence of a corneal opacity or cataract, sufficient light reaches the retina to cause a response provided that the retina is functional. Indications for electroretinography include:
1) preoperative evaluation of retinal function before cataract extraction in order to detect those animals affected concurrently with PRA.
2) identification of retinal diseases which do not have ophthalmoscopically apparent lesions; e.g. Sudden Acquired Retinal Degeneration (SARD), hemeralopia; particularly to distinguish these from CNS causes of vision loss (amaurosis).
3) identification of animals genetically affected with PRA before they exhibit clinical signs or are detectable by ophthalmoscope examination. This is particularly important in selecting animals which would be used for breeding before the age of onset of most forms of PRA (6-9 years).
Electroretinography requires general anesthesia and specialized equipment. A contact lens electrode is placed on the surface of the eye and reference needle electrodes on the pinna of the ear and the bridge of the nose. Most tests are performed using a single flash of white or red light. To detect cone abnormalities, a technique called flicker fusion is used. This identifies the frequency of stimulation beyond which individual ERG responses are not detectable. Normally this value is 75-80/second. In dogs affected with hemeralopia, in which the cones are selectively affected, the flicker fusion frequency may be as low as 5-10/second. [table=450][size=+2]Breeds Affected with PRA [tr][td=1,1,50%][size=+1]Breed [/td][td=1,1,50%][size=+1]Comment [/td][/tr][tr][td]Akita[/td][td]onset 2-3 yrs[/td][/tr][tr][td]Alaskan Malamute[/td][td]Hemeralopia; specific cone degeneration[/td][/tr][tr][td]Beagle[/td][td][/td][/tr][tr][td]Border Collie[/td][td][/td][/tr][tr][td]Borzoi[/td][td]2 types described[/td][/tr][tr][td]Briard[/td][td]onset 12-18 months[/td][/tr][tr][td]Chesapeake Bay Retriever[/td][td]2 types: onset 8-12 months or 4 to 7 yrs[/td][/tr][tr][td]Chow Chow[/td][td][/td][/tr][tr][td]American Cocker Spaniel[/td][td][/td][/tr][tr][td]Collie[/td][td]Rod-cone dysplasia type II, onset 6-8 months; also typical PRA, onset 6-9 yrs[/td][/tr][tr][td]English Cocker Spaniel[/td][td]onset 1-3 yrs[/td][/tr][tr][td]English Springer Spaniel[/td][td]onset 3-5 yrs[/td][/tr][tr][td]German Shepherd[/td][td][/td][/tr][tr][td]Golden Retriever[/td][td][/td][/tr][tr][td]Irish Setter[/td][td]Rod-cone dysplasia type I, onset < 6 months[/td][/tr][tr][td]Labrador Retriever[/td][td]2 types: PRA and Central PRA (RPE affected)[/td][/tr][tr][td]Lhasa Apso[/td][td][/td][/tr][tr][td]Miniature Schnauzer[/td][td]Rod-cone dysplasia, onset 10-12 months[/td][/tr][tr][td]Norwegian Elkhound[/td][td]Rod dysplasia, blind by 1-2 yrs[/td][/tr][tr][td]Poodle[/td][td][align=center]Rod-cone degeneration, onset 6-9 yrs[/align][/td][/tr][tr][td]Rottweiler[/td][td][/td][/tr][tr][td]Samoyed[/td][td][/td][/tr][tr][td]Shar Pei[/td][td][/td][/tr][tr][td]Shetland Sheepdog[/td][td][/td][/tr][tr][td]Shih Tzu[/td][td][/td][/tr][tr][td]Siberian Husky[/td][td][/td][/tr][tr][td]Tibetan Terrier[/td][td]onset 8-12 months[/td][/tr][/table][table=98%][tr][td=1,1,50%][img=253,310]http://www.veterinaryvision.com/pictures/retina-dog_normal.jpg[/img][/td][td=1,1,50%][img=249,310]http://www.veterinaryvision.com/pictures/retina-dog_pra.jpg[/img][/td][/tr][/table][/size]
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