Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
308 Cards in this Set
- Front
- Back
|
Fat cow syndrome is also called what?
|
-hepatic lipidosis
-lipid mobilization syndrome |
|
|
What is the typical signalment of a cow with hepatic lipidosis?
|
-post partum dairy cows
-overconditioned beef cows -obesity |
|
|
Cows affected with fat cow syndrome typiccaly have other disease such as waht?
|
-metritis
-mastitis -LDA -retained fetal membranes -hypocalcemia |
|
|
Do these cows respond well to tx?
|
No, respond poorly
|
|
|
How is fat cow syndrome defined?
|
A dz that results from prolonged negative energy balance occurring immediately after calving (at onset of lactation), tends to affect obese cows
|
|
|
What does lactation do to energy balance?
|
Increase energy demands (cows tend to have less appetite at this time)
|
|
|
What happens as a result of the increased energy demands?
|
Mobilization of body fat
|
|
|
What happens to obese cows at this time?
|
Go completely off fedd near calving
|
|
|
More fat is immobilized n the obese cow, what happens in the liver?
|
An avalanche of fatty acids is sent to the liver
|
|
|
What happens to NEFA's in the liver?
|
Either oxidized or re-esterified with glycerol to form TGs
|
|
|
If there is insufficient oxaloacetate to to enter the TCA cycle, what happens to the Nefa's?
|
Ketone bodies are formed
|
|
|
What is the result of a high amount of ketones?
|
-reduces feed intake
-perpetuates negative energy balance |
|
|
When the hepatic lipooprotein synthesis is depressed, the live ris overwhlemed with free fatty acids and TGS which are stored where?
|
Within the hepatocytes
|
|
|
What is the major contributing facotr of the accumulation of hepatic TG's in cows?
|
An increase in circulating TG's- NOT a decline in apolipoprotein output
|
|
|
What are the clinical signs of hepatic lipidosis?
|
-weakness
-recumbency -pronounced anorexia -decreased milk production -ketosis that does not respond well to tx |
|
|
What dxs are used for fatty cow syndrome?
|
-ketonuria
-incr liver enzymes if < 25% of liver is functional -hypoglycemia can check for -serum Nefa concentration -liver bx -leukopenia |
|
|
What clin path results might you see with a cow with hepatic lipidosis?
|
-serum Nefas > 1000
- increased AST -leukopenia -do liver bx |
|
|
What would you see in a liver bx of hepatic lipidosis?
|
Clear fat droplets/globules distending cells and displacing the nucleus
|
|
|
What is the tx for hepatic lipidosis?
|
-IV glucose
-insulin (inhibits lipolysis) -abx -antioxidants |
|
|
How can fatty cow syndrome be prevented?
|
-prevent obesity in late lactation
-match energy/feed to production |
|
|
What are the common causes of liver abscess in adult cattle?
|
-2ndary to grain overload (lactic acidosis)
-erosion of ruminal epithelium-->ruminitis-->portal circulation from ruminoreticulum to liver |
|
|
What are the common causes of liver abscess in neonates and young cows?
|
naval infection- extending from umbilical vein to liver
|
|
|
What is the most common pathogen associated with liver abscess?
|
Fusobacterium necrophorum
|
|
|
What are the general signs of the subclinical form of abscess?
|
-reduced gain and productivity
|
|
|
What are the clinical signs of liver abscess?
|
-decreased gain
-wt loss -decreased milk production -periods of pyrexia -anorexia -abd pain |
|
|
What is a rare clinical form of liver abscess?
|
-acute hepatitis (fever, arched back, hepatic swelling)
|
|
|
What is a serious complication to liver abscess?
|
caudal vena cava syndrome
|
|
|
What are the potential outcomes of caudal vena cava syndrome?
|
-sudden death
-thrombosis of CVC -multifocal pulmonary abscess |
|
|
What causes caudal vena cava syndrome?
|
-abscess forms in the liver and encapsulates
-erosion on the hepatic vessels, thrombic emboli -bacteria carried to heart and lungs |
|
|
What clin path results might you see with a liver abscess?
|
-inflammatory leukogram with incr fibrinogin
+/- incr SDH, AST chronic: CBC may be normal, anemia., incr globulin |
|
|
What is the tx for liver abscess?
|
-responds poorly...can use PCN or oxytet
|
|
|
How can liver abscesses be prevented?
|
-prevent rumenitis (slowly incr grain amounts)
-provide long stem roughage -feed additive abx -prevent umbilical infection in young |
|
|
What is the common liver fluke of cattle?
|
Fasciola hepatica
|
|
|
Which fluke is a problem with bovine sharing pastures with deer?
|
Fascioloides magna (giant liver fluke)
|
|
|
What is the difference in response to F hepatica between cattle and sheep?
|
cattle: develop resistance, subclinical dz
sheep: no resistance, acute hepatitis and biliary obstruction |
|
|
What is the definitive host for F magna?
|
white tail deer
|
|
|
What is the difference in response to F magna between cattle and sheep?
|
Cattle: fibrotic capsule forms
Sheep: extensive hepatic migration and destruction, often fatal |
|
|
What are the clinical signs of liver fluke infestation?
|
-poor productivity
-wt loss -edema -pale mm -diarrhea -death (sheep) |
|
|
Liver flukes can produce what changes seen on clin path?
|
-anemia
-eosinophilia -cholestasis 9icterus) -incr GGT, alk phos, SDH, AST -hypoalbuminemia |
|
|
How do you dx liver flukes?
|
-response to flukicide
-hx of access to snails -fecal eggs -Elisa (not accurate) On necropsy: acute: enlarged hemorrhagic liver chronic: shrunken liver, fibrosis of bile ducts |
|
|
When do you tx with flukicide?
|
Spring in Pacific NW
Fall in Gulf States |
|
|
What is Black Disease?
|
Infectious, necrotic hepatitis
|
|
|
In sheep, what is the causal organism of Black dz?
|
Clostridium novyi, type B
|
|
|
What damage does C novyi cause in the liver?
|
-hepatic necrosis
-endothelial damage -neuronal damage |
|
|
How do the spores infect the liver?
|
absorbed form the GIT and move to the liver, fluke migration create an anaerobic envrionment in damaged liver tissue--> C novyi proliferation
|
|
|
C novyi Type B exotoxin targets which cells?
|
-endothelial cells (subcu hemorrhage occurs)
|
|
|
What are the clinical signs of Black dz?
|
-usually found dead, no red urine or external bleeding
|
|
|
What is seen on liver necropsy of Black dz?
|
hemorrhage of subcu tissue resulting in black discoloration
|
|
|
How is Black dz dx?
|
FA of liver tissue
|
|
|
How is Black Dz prevented?
|
-vaccination
-control flukes |
|
|
What is another name for Redwater?
|
Bacillary hemoglobinuria
|
|
|
What is the causative agent of Bacillary hemoglobinuria?
|
Clostridium novyi Type D (C hemolyticum)
|
|
|
The C novyi type D spores are quiescent in the liver until when?
|
An anaerobic environment is created by fluke migration
|
|
|
What are the clinical signs of Bacillary hemoglobinuria?
|
-found dead
-dark red-brown urine -pale mm or icterus -thin blood -tachypnea -rapidly progressive shock -RBC membrane in blood stream may activate coagulation cascade resulting in DIC |
|
|
Clin path is raely performed for redwater but what would you see?
|
-decreased PCV
-incr TP -incr total and indirect bilirubin |
|
|
What is the tx and prevention for Bacillary hemoglobinuria?
|
-antitoxin to C hemolytica
-PCN -blood transfusion -vaccination |
|
|
What are the signs of toxic plant ingestion?
|
-depression
-diarrhea -tenesmus -ascites -recumbency -coma -icterus not common in cattle (it is common in horses) |
|
|
What is the chemical the causes plant toxicity?
|
Pyrrolizidine alkaloids
|
|
|
What plants contain PA
|
-tansy ragwort
-grounsel -tarweed -fiddleneck -rattlebox -hound's tongue |
|
|
What is the pathopysiology of PA toxicity?
|
-PA converted to pyrroles in the gut, pyrroles cross-link hepatocyte DNA arresting mitosis, hepatocytes enlarge (megalocytes) then die. Dead hepatocytes replaced by fibrous tissue, cirhhosis results
|
|
|
What is the triad of signs of PA toxicosis?
|
-megalocytosis
-fibrosis -bile duct hyperplasia |
|
|
PA toxicity is a subclinical dz until how many hepatocytes are destroyed?
|
80%
|
|
|
What are the clinical signs of liver failure?
|
-weight loss
-poor productivity -nutrient metabolism impaired -ascites:poor alubumin output by failing liver -portal hypertension |
|
|
Peripheral edema is a result of what condition?
|
Hypoalubinemia
|
|
|
Hypoalubinemia and gut wall edema can lead to what?
|
diarrhea
|
|
|
What signs of hepatic encephalopathy might be see?
|
-tenesmus
-head pressing -profound depression/somnolence -possible coma |
|
|
Clin path results for PA toxicity would show what?
|
-incr GGT, ALP (poss SDH, AST)
-incr total, direct and indirect bilirubin -decreased alb, glu, urea |
|
|
Cattle need to ingest how much of a toxic plant to see an effect?
|
2-5% of bwt...is cumulative
|
|
|
What is the tx for PA toxicosis?
|
None
|
|
|
Bovine parturient paresis is also called what?
|
-hypocalcemia
-milk fever |
|
|
Which type of cows are more likely to get parturient paresis?
|
Dairy
beef cows get prepartum hypocalcemis |
|
|
What is the typical signalment for a parturient paresis cow?
|
-dairy cow
-occurs within 24 hrs of calving -6% have dystocia |
|
|
How many stages of milk fever are there?
|
3
|
|
|
What are the clinical signs of stage 1 of milk fever?
|
-hypersensitive, excited, nervous
-weak -shift wt side to side -ataxia, tachycardia -mild hyperthermia -feces firm |
|
|
what is the classic position of a coe in stage 2 of milk fever?
|
-sternal recumbency
-head tucked to side -S shaped curve to neck |
|
|
What are the other signs of stage 2?
|
-muscle fasiculations
-tachycardia (< 90) -decr intensity of heart sounds -cold extremities -mild bloat |
|
|
What are the signs of stage 3 of milk fever?
|
-lat recumbency
-progressive loss of consciousness -severe bloat -heart sounds inaudible -tachycardia -coma, death |
|
|
Milk fever can lead to what type of nerve damage?
|
Peripheral nerve i.e. peroneal
|
|
|
How do you differentiate endotoxemia from milk fever?
|
-poor CRT
-fever -diarrhea -tightly constricted pupils -injected scleral vessels -abnormal milk |
|
|
Milk fever is also defined as hypocalcemia, what level is considered to be stage 1?
|
<7.5 mg/dl
|
|
|
What other e'lyte levels will be seen with milk fever?
|
-hyperglycemia (impaired insulin release)
-hypophospahtemia -hypokalemia -sometimes hypermagnesemia |
|
|
Why does hypocalcemia lead to flaccid paralysis?
|
Ca++ is required for release of Ach at the NMJ and for muscle contraction
|
|
|
What leads to a depletion of serum ionized Ca++?
|
rapid onset of milk production
|
|
|
Why is it difficult for a milk fever cow to increase Ca++?
|
-osteoclasts are temporarily refractive to PTH, increase bone resorption takes 48 hrs following incr PTH
-1,25 hydroxyvitamin D production is inadequate to increase intestinal absorption, (takes 24 hrs) |
|
|
Which condition promotes hypocalcemia....acidic or alkaline pH
|
Alkaline
|
|
|
What is the tx for milk fever?
|
Stage 1: oral ca++ gel, subcu ca++ gluconate
Stage 2,3: IV Ca++ salts |
|
|
What caution do you need to be aware of when giving IC Ca++?
|
Ca++ is directly caridotoxic ,must give slowly while ausculting the heart
|
|
|
How can you tell if milk fever tx is successful?
|
-eructation, defecation, urination resumes
-incr intesnsity of heart sounds, -stands before you leave the farm |
|
|
Nursing care of milk fever cows includes what?
|
-good footings
-keep cows sternal -don't force them up -roll side to side if recovery is prolonged -provide fresh water |
|
|
True or False, relapse of milk fever occurs more often in older cows?
|
True (25-30% relapse)
|
|
|
How can a relapse of milk fever be prevented?
|
oral Ca++ gel
subcu ca++ (no dextrose) |
|
|
What caution should you take when using oral Ca++ gel?
|
It is caustic and can cause oral ulcers
|
|
|
Can milk fever be prevented?
|
yes- Ca++ restricted diets in late gestation
-dietary Ca++ at < or = to 15 g/dl 10 days prepartum |
|
|
What results would acidification of the diet give?
|
- incr urinary excretion of Ca++
- incr resorption of Ca++ from bone -osteoclasts exchange Ca++ for H+ -incr Vit D formation |
|
|
What is the purpose of the dietary cation difference (DCAD)
|
Estimates whether a diet has the potential to be acidogenic or alkalogenic. Goal is to create a diet which is more negatively charges (higher in anions)
|
|
|
During the dry period, which e'lyte should be limited?
|
K+
|
|
|
The clinical signs of nutritional secondary hyperparathyroidism are due to what?
|
Resulting bone resorption to maintain plasma Ca++ levels during dietary deficiency
|
|
|
What are the clinical signs of nutritional secondary hyperparathyroidism?
|
-intermittent shifting lameness
-bones of head affected -low serum ca++ with high phosphorus -Alk phos may elevate -urinary fractional excretion is dx |
|
|
If phosphorus levels remain high in the diet, what can result?
|
-prolonged stimulation of bone resorption leads to osteoporosis and replacement with fibrous connective tissue
|
|
|
What role does phosphorus play in the body?
|
-component of cellular molecules
-acid-base buffer system -major component of bone, saliva, milk production and fetal development |
|
|
Chronic mild hyperphosphatemia leads to what general condition?
|
reduced growth and productivity
|
|
|
Rickets causes what clinical signs/findings?
|
-stiffness and shifting leg lameness
-enlarged painful swelling of physis and metaphysis of long bones and CCj (string of pearls) |
|
|
True or false, osteomalacia can cause fxs that don't heal?
|
True
|
|
|
What causes a downer cow?
|
-severe acute HYPOphosphatemia, associated with hypocalcemia and hypomagnesemia--milk fever relapse
|
|
|
What are signs of hypophosphatemia?
|
-impaired reproductivitiy
-failure to grow -inappetance -pica -recumbent but alert |
|
|
Post parturient hemolobinuria can be seen in which cows?
|
-high producing dairy w/in 6 weeks of parturition
|
|
|
What are the findings of Post parturient hemoglobinuria?
|
-decr milk production
-intravascular hemolysis -anemia, jaundice, hemoglobinuria |
|
|
Clin path of Post parturient hemoglobinuria might show what results?
|
-anemia (Heinz body on smear)
-U/a: hbguria -copper and Se deficiency |
|
|
Acute hypophospahtemia can be caused by what conditions?
|
-milk and colostrum production
draws large amounts of phosphorus |
|
|
What causes rickets?
|
Failure of mineralization in growing animals (and Vit D deficiency)
|
|
|
Demineralization in adults is called what?
|
Osteomalacis- normal rate of osteoclastic activity without concurrent osteoblastic activity
|
|
|
What is the potential pathophys behind Post parturient hemolobinuria?
|
Hypophosphatemia results in decreased ATP synthesis by RBCs, intracellular Na+ rises, cells sweel and lyse
|
|
|
What is the tx for severe acute hypophosphatemia?
|
IV phosphorus administration (fleet enema in an IV)
Oral phosphorus has a more prolonged effect |
|
|
What are the txs for Post parturient hemolobinuria?
|
-phosphorus supplementation
-blood transfusion -isotonic fluids -Se and copper supps |
|
|
How can hypophosphatemia be prevented?
|
Cattle producing milk should be fed a diet containoing .42% phosphorus, Ca++ to phos ratios of 2:1
|
|
|
What is another name for hypomagnesemia?
|
Grass tetany
|
|
|
Why is magnesium important?
|
-vital to normal nerve conduction, muscle function and bone mineral formation
|
|
|
What clinical syndrome can a Mg imbalance cause?
|
-hypomagnesemia (grass tetany)
-transport tetany -milk tetany -winter tetany |
|
|
The incidence of hypomagnesemia is seen more when?
|
Lactating beef cattle within 60 days of calving when put out on cold season grasses
|
|
|
What are the clinical signs of hypomagnesemia?
|
(more rapid and sever with concurrent hypocalcemia)
-decreased food intake -nervousness -decr milk production and total milk fat -alert, hyperexcitibility -erect ears, ear twitch , hyperesthesia |
|
|
What are the signs of severe hypomagnesemia?
|
-twitching of muscles of face
-decreased rumen motility -ptyalism -irritable -tetanic muscle spasm -nystagmus |
|
|
What are the ddx's for the aggressiveness from hypomagnesemia?
|
-rabies
-nervous ketosis -nervous coccidiosis -claviceps pupura -staggers -lead toxicity |
|
|
Why might Mg levels be normal in a cow with convulsions?
|
Muscle damage and leakage of Mg from intracellular pool
|
|
|
How must Mg be supplied?
|
diet
|
|
|
What causes the tetany?
|
Mg is important to maintain the resting membrane potential, excessive release ofAch at myoneuronal junction (low Mg : Ca++ promotes Ach release)leads to sustained myofiber contractions
|
|
|
What are some examples of forages low in Mg?
|
-lush growing grasses
-fescue -orchard grass -small grain grasses |
|
|
What is the tx for hypomagnesemia?
|
Slow IV of calcium gluconate w/ 5% Mg hypophosphate subcu
-oral Mg -Mg enema |
|
|
How can hypomagnesemia be prevented?
|
Supplement Mg daily (add to ration)
-Mg feeding blocks -offer legumes |
|
|
What is the importance of potassium?
|
Maintenance of resting membrane potential
|
|
|
Inflow of potassium is dependent on what?
|
Diet
outflow through renal, salivary and milk |
|
|
Cows that have hypokalemia share what history?
|
-had moderate to sever ketosis
-delivered a calf less than 30 days ago -all tx with isopredone acetate |
|
|
What are the clinical signs of hypokalemia?
|
-muscle fasiclualtion
-skeletal muscle weakness -profound muscle flaccidity -neck muscles affected (head against flank) -cardiac arrhythmia |
|
|
What are the potential causes of external imbalance of potassium regulation?
|
-anorexia
-glucocorticoid administration |
|
|
What are the potential causes of an imbalance of interal potassium homeostasis?
|
-alkalosis: cellular uptake of K+ in exchange for H+
-ketosis tx: insulin and glucose (uptake of glucose is accompanied by intracellular movement of K+) |
|
|
What is the tx for hypokalemia?
|
IV and oral K+ (IV not effective alone)
|
|
|
What is ketosis?
|
A biological process that results when sufficient glucose is not available from dietary CHO and the body switches to mobilizing fat stores
|
|
|
What are the metabolic events that lead to ketosis?
|
negatie energy balance-->negative glucose balance-->adipose mobilization-->elevation of plams Nefa concentration
|
|
|
Where in the body are nefa's converted to ketone bodies?
|
Mitochondria of the liver
|
|
|
What are the 2 potential fates of nefas in the liver?
|
-ketogensesis
-triglyceride synthesis |
|
|
In peak lactation ketosis, which metabolic process dominates?
|
Ketogenesis
|
|
|
In post partum ketosis, which metabolic process dominates?
|
Triglyceride production
|
|
|
What are the 3 types of ketones synthesized?
|
-aceotacetic acid
-acetone -B hydroxybutyrate |
|
|
Primary ketosis is a result of what?
|
Metabolci dz, no underlying etiology
|
|
|
Secondary ketosis is a result of what?
|
Complication of another dz
-mastitits -metritis -peritonitis |
|
|
What is the typical signalment of a ketotic cow?
|
-post partum dairy cow
-late gestation beef cow |
|
|
What are the clinical signs of ketosis?
|
-vague
-anorexic -sharp drop in milk production -dull coat -depression |
|
|
What nervous dysfunction might be seen with ketosis?
|
-licking, chewing, hypersalivation
-gait distubances -bellowing, head pressing, aggressiveness |
|
|
How is ketosis tx?
|
2ndary ketosis: tx primary dz
-IV glucose, dex, insulin, propylene glycol |
|
|
What are the 3 key ingredients in ketosis prevention?
|
-manage late gestation dry cows
-maximize dry matter intake at start of lactation -maintain adequate energy/fiber/protein levels in lactating diet |
|
|
What are the classic scenarios of pregnancy toxemia in cows?
|
-multiple fetuses
-last month of gestation -second or later gestation |
|
|
What is the pathogenesis of pregnancy toxemia?
|
disruption of glucose homeostasis-->rumen doesn't have room to expand to increase dry matter intake, dam mobilizes body fat
|
|
|
What are the clinical signs of pregnancy toxemia?
|
-gradual decrease of food intake
-depression of activity -down and unable to rise -tremors, weak, grinding of teeth -death |
|
|
How is pregnancy toxemia tx?
|
-determine if dam or fetus is more important
-c-section |
|
|
What medical management steps can be taken for pregnancy toxemia?
|
-IV dextrose
-adequate nutrition -if recumnbent: deep bedding, turn side to side |
|
|
How can pregnancy toxemia be prevented?
|
U/S to determine the number of feti, can feed extra grain
-balance late pregnancy diet |
|
|
How many upper incisors does a cow have?
|
None
|
|
|
The 3rd incisors euprt at what age?
|
36 months
|
|
|
What are some of the dental problems cattle can have?
|
-dental caries
-premature dental attrition (sandy soil_ -fx teeth -periodontal dz |
|
|
If the animal is losing wt, what should be included in your PE?
|
Complete oral exam
|
|
|
In which species is a tooth root abscess common
|
Camelids
|
|
|
what ddx needs to rh ruled out for tooth root abscess?
|
lumpy jaw - take rads
|
|
|
What is the only cure for tooth root abscess?
|
sx removal with long term abx
|
|
|
What is ptalyism?
|
excess saliva production
|
|
|
What are potential causes of ptyalism?
|
-esophageal obstruction
-stomatitis -rumen dysfunction -rabies -pseudorabies -toxicants WEAR GLOVES! |
|
|
What is the causative organism of wooden tongue.
|
Actinobacillus lignieresi
|
|
|
What type of lesion does wooden tongue cause?
|
Granulomatous absecss
|
|
|
What are the clinical signs of actinobacillus?
|
--difficulty prehending food
-excess salivation -tongue may protrude from mouth -foreign objects in moiuth -oral abscess |
|
|
How is actinobacillus dx?
|
Bx and culture of lesion
-pus crushed between 2 slides will show sulphur granules |
|
|
What is the tx for actinobacillus?
|
IV sodium iodide
|
|
|
What are the potential side effects of sodium iodide?
|
-abortion
-monitor for toxicity (SLUD, dandruff) |
|
|
Actinomyces bovis causes what condition?
|
Lumpy jaw
|
|
|
What physical sign does actinomyces cause?
|
Immovable, non-painful bony mass on mandible
|
|
|
What are the r/o's for actinomyces?
|
-tooth root abscess
-fx -tumor |
|
|
How do you dx actinomyces?
|
Pus crushed between 2 slides shows sulphur granules
-rads show area of radiolucence and osteomyelitits surrounded by periosteal new bone and fibrous tissue |
|
|
What is the tx for lumpy jaw?
|
Sodium iodide IV
|
|
|
What is the common cause of pharyngeal trauma?
|
-use of a balling gun, long dose syringe, speculum etc
|
|
|
pharyngeal trauma results in what kind of injury?
|
-cellulitis
-abscess -hematoma formation |
|
|
What are the clinical signs of pharyngeal trauma/abscess?
|
-anorexia
-salivation -malodorous breath -extension of the head and neck -feed coming from nares -swelling, fever, dyspnea |
|
|
What is the first step in dx pharyngeal trauma/abscess?
|
careful digital palpation of the pharynx
|
|
|
What other diagnostics are helpful in diagnosing the site of the lesion and extent of cellulitis or presence of f.b.?
|
-endoscopy
-U/S -rads |
|
|
What signs would you see if there is damage to the pharyngeal branch of the vagus nerve?
|
Pharyngeal phase of swallowing is disrupted, reflux of food through the nares
|
|
|
What sign might you see if the cranial laryngeal nerve is affected?
|
Diminished cough reflex
|
|
|
Forestomach stasis could be a consequence of pharyngeal trauma if which nerve is inflammed?
|
Vagus
|
|
|
What is the tx for pharyngeal trauma/abscess?
|
-aggressive abx
-supportive tx -Nsaids -once the animal can drink w/o reflux, green grass or mash can be offered |
|
|
How do you treat a discrete retropharyngeal abscess?
|
-drain it into the pharynx through the original laceration
|
|
|
name the vesicular diseases
|
-bluetongue
-bovein papular stomatitis -vesicular stomatitis -FMD -BVD -malignant catarrhal fever |
|
|
Bluetonuge virus is in which family?
|
Reoviridae (orbivirus)
|
|
|
Bluetongue is non-contagious, how is it spread and which spp is the primary host?
|
-insect borne
-sheep host |
|
|
How is Bluetongue transmitted?
|
-biting midges (culicoides)
-ticks -sheep keds -in utero -mechanical -? venereal |
|
|
What are the general clinical signs of Bluetongue?
|
-fever, de[pression, salivation, facial swelling, dyspnea, panting, nasal discharge, hyperemia of muzzle lips and ears
pregnancy: resoprtion, abortion, dummy lambs |
|
|
What are the specific clinical signs of bluetongue?
|
-oral erosion, ulceration
-tongue swollen, protruding, cyanotic Feet: soft hoove, lameness, coronitis |
|
|
How is Bluetongue dx?
|
-clin signs
-hx -virus ioslation while febrile -Elisa -AGID -complement fix |
|
|
What is the tx for bluetongue?
|
-no specific tx
-support (fluids, abx -control of vectors |
|
|
What is the medical name for Orf?
|
Contagious ecthyma
|
|
|
Where do the lesions of orf occur?
|
-mouth
-face -feet -teats -genitalia |
|
|
How is Contagious ecthyma transmitted?
|
-direct contact
-environmental contaminants -pox virus enters through abrasion (coarse plants and feeds injure mucosa) |
|
|
Which age of sheep are most susceptible?
|
3-6 month old feeders
|
|
|
True of false, to promote healing scabs of orf lesions should be removed?
|
false- can delay healing
|
|
|
How can Contagious ecthyma be prevented?
|
-maintain virus-free herd
-vacc available...but it is a live vacc |
|
|
Why should farmers be cautious of Orf?
|
highly zoonotic
|
|
|
What is sotmatitis?
|
Inflammation of the oral cavity, painful for the animal to eat o drink, lots of drooling, different cuases
|
|
|
Bovine papular stomatitis is a mild dz of which age of cattle?
|
Young
|
|
|
What is a pathognmonic sign of Bovine papular stomatitis?
|
-proliferative lesions in and around the mouth
-rat tail syndrome (feedlot cattle) |
|
|
Vesicular stomatitis is a rhabdoviridae dz that causes sporadic outbreaks in what spp?
|
-cattle
-horse -donkey -mule -pigs |
|
|
Where should you look for lesions with vesicular stomatitis?
|
-mouth
-teat -interdigital space |
|
|
What are the clinical signs of vesicular stomatitis?
|
-incubation of 9 days
-fever -oral lesions -progress to ulcers -difficulty eating/drinking -decr milk production -lameness |
|
|
How is vesicular stomatitis transmitted?
|
-cow to cow
-milking machine -shared feed/water -insects |
|
|
What is the tx for vesicular stomatitis?
|
supportive care (reportable dz)
|
|
|
FMD survives where?
|
-milk
-milk products -bone marrow -lymph glands |
|
|
What effects can FMD have?
|
-fever
-vesicles -abortion -death in your animals |
|
|
How quickly do animals recover from FMD?
|
2 weeks unless there is a 2ndary infection
|
|
|
What are the oral lesions of FMD
|
-vesicles on tongue, dental pad, gums, soft palate, nostrils, muzzle, e
-excess salivation -drooling -serous nasal discharge |
|
|
Teat lesions from FMD cause what?
|
Decreased milk production
|
|
|
What foot lesions are caused by FMD?
|
-in the interdigital space
-coronary band -lamness -reluctance to move |
|
|
How is FMD dx?
|
-complement fix
-Eloisa |
|
|
What is the tx for FMD?
|
-No tx, support
|
|
|
Malignant catarrhal fever is caused by which virus?
|
Herpes
|
|
|
What are the 2 types of Malignant catarrhal fever?
|
-African (Wildebeest- more contagious)
-Sheep associated |
|
|
Cattle are dead in host for Malignant catarrhal fever, what dz does MCF cause in wildebeest and sheep?
|
None
|
|
|
What is the mortality of MCF?
|
100%
|
|
|
What pathopysiologic effects does MCF have?
|
Proliferation of T lymphocytes, vasculitis from vascular endo thelial damage, vascultitis from lymphoid cell infiltration, all epithelail surfaces affected
|
|
|
What are the 4 forms of MCF?
|
--peracute
-head and eye -encephalitic -skin |
|
|
What are the clinical signs of MCF?
|
-oral erosions/salivation
-dairrhea -keratocoonjunctivitis -mucopurulent nasal discharge -thickening, cracking skin -encephalitis, high fever, lympadenopathy |
|
|
MCF lesions include what?
|
Hyperemic to hemorrhagic nasal mucosa
-necrotic and ulcerated oral mucosa -ulcers in GIT, ellarged lymph nodes, tonsil's peyer's patches, swollen liver, hyperemia of eyes all are lesions of vascultitis |
|
|
How do you control MCF?
|
-separate sick animals
-keep cattle away fro wildebeest and sheep -vaccinate |
|
|
What are the 2 biotypes of Bovine Viral Diarrhea?
|
-cytopathic
-noncytopathic |
|
|
Noncytopathic, persistantly infected cattle become infected when?
|
Infection of th fetus (at less than 125 days gestation = PI)
|
|
|
BVDV Type 2 causes what dz?
|
Mucosal dz
|
|
|
What happens if a PI cow comes into contact with the cytopathic strain?
|
Nasty TCP
|
|
|
How can BVDv enter a herd?
|
-inadequate immunization
-purchased animals |
|
|
What is the clinical presentation of BVDV?
|
-Acute/peracute: high fever, off feed, diarrhea, death within 48 hrs
-pneumonia, hemorrhagic syndrome, sever platlet depression, repor problems, abortion |
|
|
How is BVDV transmitted?
|
-vertical
-horizontal (direct, short aerosol, oral contamination of feed and water |
|
|
Immunosuppression from BVD can lead to what condition?
|
-leucopenia
-fever -2ndary bacterial infection |
|
|
How do you test for BVD?
|
-virus isolation (nasal swab or buffy coat)
-antigen detection nucleic acid detection |
|
|
Which BVD vaccine is best?
|
MLV- not for pregnant
|
|
|
What is the usual cause of choke in a horse?
|
Ingestion of fruits or vegetables (hedge apple)
|
|
|
What 2ndary complication can occur from choke and be considered an emergency?
|
bloat due to esophageal obstruction
|
|
|
What are the clinical signs of choke?
|
Anxiety
-ptyalism -dysphagia anorexia -repeated attempts to swallow -bloat |
|
|
What other effects can choke have on the esophagus?
|
--erode the esophagus
-pressure necrosis -perforate--gas and pus can dissect through fascial planes to enter thorax (pyothorax) |
|
|
What is tx for choke of the anterior esophagus?
|
Place fist in jugucalr groove, true to push object into pharyngeal area
|
|
|
What is the tx for choke if the f.b. is at the thoracic inlet, heart base or cardia?
|
Attempt to push into stomach with tube
|
|
|
What method is used if the f.b. is at the cardia and can't be pushed to the stomach?
|
rumenostomy
|
|
|
,megaesophagus (camelids) has been observed resulting from what conditions?
|
-pharyngeal trauma
-congenital disorders -sarcocystis |
|
|
What are the clinical signs of megaesophagus?
|
-regurgitation
-wt loss -aspiration pneumonia |
|
|
How is megaesophagus dx and tx?
|
Dx: contrast rads
Tx: feed upright, metclopramide, sucralfate |
|
|
How is rumen fluid collected?
|
-stomach tube
-rumenocentesis |
|
|
Analysis of rumen fluid includes what parameters?
|
-color
-consistency -odor -pH -methylene blur rxn -protozoa -rumen chloride levels |
|
|
Simple rumen indigestion has what features?
|
-group problem
-feed related -anorexic -decr production -rumen microflora and pH disrupted |
|
|
How is simple indigestion tx?
|
-transfaunation
-grass diet |
|
|
CHO engorgement causes what condition in the rumen?
|
lactic acidosis
|
|
|
Which feeds can cause CHO engorgement?
|
-cereal grains
-inductrial by poducts -frutis, tubers -finely round feeds -hay and grass -corn silage |
|
|
Grain overload leads to ruminal acidosis and what else?
|
Rapid production of VFAs by Gram + bacteria
|
|
|
What effect do the VFAs have overall?
|
VFA's pull plasma water into the lumen of the ruemn resultin gin dehydration, hemoconcentration
acids absorbed = metabolic acidosis |
|
|
As the pH of the rumen drops lower, what happens?
|
G- bacteria killed off
-endotoxin from cell walls absorbed into circulation -results in shock, dehydration,laminitis |
|
|
Bacteria entering the portal venous blood causes what dz in the liver?
|
Abscess
|
|
|
Bacteria species results in destruction of thiamine which leads to what condition?
|
Polioencephalomalcia
|
|
|
At his point, the rumen is invaded with fungi, usually of which speceis?
|
Aspergillus
|
|
|
What are the sequelae to ruminal acidosis?
|
-liver/lung abscess
-septicemia -diarrhea -rumen ulcers -rumen perf |
|
|
What are the clinical signs of ruminal acidosis?
|
-elevated temp
-HR 80-140 -RR elevated -rumen fluid pH 5 sour odor -protozoa dead -G+ bacteria predominate -abd pain, dehydration, blaot, scleral injection |
|
|
What clin path findings are associated with ruminal acidosis?
|
-metabolic acidosis
-Incr PCV -Incr TP -Incr BUN/Cr -Incr anion gap -decreased Ca++ |
|
|
what is the tx for ruminal acidosis?
|
-abx
-fluids -nsaids -laxative -rumenotomy -B vits -transfaunation |
|
|
what dietary changes can be made to prevent ruminal acidosis?
|
-adding abx
-HCO3 -ionophore |
|
|
What does SARA stand for?
|
Subacute rumen acidosis
|
|
|
What s the cause of fresh cow acidosis?
|
-7-20 days after calving
-rumen papillae need time to elongate -rumen microflor shoft to digest high energy ration |
|
|
What is adapted acidosis?
|
40-150 days in milk
-diet may not have enough functional fiber |
|
|
What are the clinical signs of SARA?
|
-depressed feed intake
-decreased milk prod -hoof lesions (paint brush laminitis) on necropsy: liver abscess, endocarditis, pulmonary embolus |
|
|
Hoe do you dx SARA?
|
-group dx
-measure rumen pH (12 or more animals, if >25% have pH <5.5 you have a problem |
|
|
What is vagal indigestion syndrome?
|
Motor disturbances which impair passage of ingesta from the reticulorumen and abomasum to the lower GIT
- a collection of diseases |
|
|
What are the clinical signs of vagal indigestion?
|
-slow loss of production
-slow wt loss -poor appetite -scant pasty feces -papple shape -bradycardia |
|
|
What can cause inflammation of the vagus nerve?
|
-pharyngeal trauma
-penumonia -hardware dz -abomasum volvulus |
|
|
What is the appearance of a cow with vagal indigestion?
|
-slab sided abd contour
-abd has normal fullness even w/ anorexia -rectal exam reveals ventral sac of rumen distended to the right |
|
|
How many classifications of vagal indigestion are there?
|
4
|
|
|
How is Type I vagal indigestion defined?
|
f.b. or esophageal compression, failure of eructation
|
|
|
How is Type II vagal indigestion defined?
|
Impariment of transport of ingesta from reticulum through omasal canal into abomasum
|
|
|
How is Type III vagal indigestion defined?
|
-primary abomasal impaction
-secondary abomasal impaction (decreased emptying from hardware dz) |
|
|
How is Type IV vagal indigestion defined?
|
difficult to define
occurs in dairy cattle late in pregnancy |
|
|
How is vagal indigestion tx?
|
-correct underlying problem
-rumen lavage -rumenotomy |
|
|
What is a ruminal drinker?
|
Calves with chronic indigestion because milk is deposited into the rumen as a result of the failure of the esophageal groove reflex during drinking
|
|
|
Which calves are at greatest risk?
|
bucket fed calves, gulp rather than sip
|
|
|
What is the pathophys of a ruminal drinker?
|
Milk retaine din the rumen ferments to acids, lowers rumen pH
|
|
|
What are the clinical signs of a ruminal drinker?
|
-inappetance
-ventral abdomen distention -poor growth -sticky clay like feces -fluid splashing spounds while drinking -rancid smelling material from stomach tube |
|
|
What is the tx for ruminal drinkers?
|
-remove fermented material from rumen
-flush with saline -transfaunation -add hay -induce sucking (on fingers) |
|
|
What is the cause f bloat? (rumen tympany?
|
Occurs if eructation is prevented for any reason
|
|
|
What are the clinical findings of bloat?
|
-distended left paralumbar fossa
-discomfort -open mouth breathing -anorexia -salivation -depressed -sudden death |
|
|
What is primary bloat?
|
Eructation normal but gas cannot be expelled (frothy bloat from legumes or grain)
|
|
|
What is 2ndary bloat?
|
Failureof eructation from:
esoph f.b. -vagal indigestion -psotional -hypocalcemis -pharyngitis -pneumonia |
|
|
What is the tx for free gas bloat?
|
-stomach tube
-exercise -admin ca++ -rumen trochar |
|
|
What is the tx for frothy bloat?
|
reduce surface tension of bubbles, consolidation of tiny bubbles into free gas bloat
|
|
|
What are the suggested step of tx for bloat?
|
chronic: incr fiber decr grain
-transfaunation |
|
|
Define traumatic reticuloperitonitis?
|
Hardware dz... ingestion of a f.b. casuing perforation of the reticulum resulting in contamination of the body cavities and organs
|
|
|
What are the 4 possible outcomes of f.d. ingestion?
|
1. object attached to magnet
2. penetration of the reticular wall, no penetration into peritoneal cavity -3. peforation of pertoneal cavity 4. migration of f.b. |
|
|
What is a typical hx of a cow with hardware dz?
|
-rarelt < 2 years old
-dairy -acute drop in milk production -reluctance to walk, stand, lie down -abd pain, rigid stance, arched back |
|
|
What are the signs of peritonitis?
|
-fever
-abd pain -wt loss -diarrhea -pneumonia -endocarditis -bradycardia |
|
|
What clin path changes are seen with hardware dz?
|
-leukocytosis with left shift
-incr fibrinogen -incr globulin -anemia |
|
|
How is hardware dz dx?
|
-abdominocentesis
-rads -fluoro -U/S |
|
|
What are the indications for an abdominocentesis?
|
-eval of accumulated abd fluid
-dx of abd dz |
|
|
For which abdominal condtions would you do an abdominocentesis?
|
-hardware dz
-peritonitis -abomasal ulcers -abomasl rupture -neoplasia |
|
|
In monograstrics and camelids where is the abdominocentesis performed?
|
Most ventral aspect on midline
|
|
|
What is effusion?
|
Fludi that escapes the blood vessels or lymphatics into tissue or body cavities
|
|
|
Define transudate.
|
Serous fluid accumulation due to alteration in pressure
clear, colorless, protein < 2.5g nuc cell <5000 |
|
|
What are the causes of a transudate?
|
-incr capillary pressure
-decr plsma oncotic pressure -CRF -parasitism -starvation -GI protein loss |
|
|
Define exudate?
|
-turbid
-protein > 3 g/dl -nuc cell count > 10,000 |
|
|
Classification of inflammtory fluids are based on cells, what defines an acute inflammation?
|
80-85% neutrophils
|
|
|
What defines exudate of a chronic inflammation?
|
50-70 non-degenerate neutrophils, 20-50% monos/macs
|
|
|
How would you describe chronic inflammation?
|
75% mono/macs
|
|
|
How do you dx hardware dz?
|
-compaas over reticulum for magnet
-laporotomy -rumenotomy |
|
|
What medical tx can be used for hardware dz?
|
-abx
-nsaids -orla magnet -fluids and support |
|
|
What is the sx tx for hardware dZ?
|
left paralumbar fossa exploratory lap
|
