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;
144 Cards in this Set
- Front
- Back
|
What are the 3 parasites that most commonly cause liver disease in large animals?
|
1) *Fasciola hepatica
2) Fascioliodes magna 3) Dicrocoelium dendritium -usually normal flora in the liver and don't cause pathology, but if have them probably have hepatica too |
|
|
Why is the liver so important in ruminants?
|
***ruminants do not absorb glucose, need liver to make glucose
|
|
|
Why do we worry about liver flukes in large animals?
|
Flukes migrate and create an anaerobic environment---> clostridial infections
|
|
|
Where is Fasciola hepatica distributed?
|
South central US and Florida, Pacific NW
-depends on distribution of intermediate host |
|
|
What is the intermediate host of fasciola hepatica?
|
Snails
-where fasciola hepatica does a lot of asexual reproduction |
|
|
What type of weather do snails, the intermediate host of fasciola hepatica, live in?
|
-Small temporary water habitats
-Prefer habitats wet for > 6 months / year |
|
|
True or false. Fasciola can be introduced to a new area in livestock and infect local species of snails.
|
True, and infected snails can introduce fasciola to new areas
-so if snails brought in on truck can infect pasture |
|
|
Why is the transmission of F. hepatica different in the wet northwest and the wet southeast?
|
Because important part of life cycle of snail is that it depends on the number of days above 50 degrees
-need like 14 or 21 days above 50 degrees, 24 hours a day |
|
|
How is the seasonality of F. hepatica different in tropical regions?
|
They're always present, bc it's above 50 degrees year round and wet
|
|
|
**How long does it take for F. hepatic to reach the liver after the metacercarie are ingested on the vegetation?
|
Takes 6-7 weeks to see liver flukes
|
|
|
How long does it take F. hepatica to reach sexual maturity once inside the liver?
|
2-4 weeks*****
|
|
|
How long does it take after ingestion of metacercariae on vegetation before you can diagnose F. hepatica?
|
6-7 weeks + 2-4 weeks= 8-11 weeks before can diagnose
-unless do a liver biopsy then can diagnose after 6-7 weeks |
|
|
What are the 3 ways clinical disease of F. hepatica can present?
|
1) Subclinical disease and production loss
2) Anemia, ill thrift and hepatic dysfunction due to fluke migration and feeding 3) Acute illness and sudden death from Cl. novyi and Cl. haemolyticum |
|
|
Why can F. hepatic result in production loss?
|
Because the liver is there to make glucose, so results in production loss
|
|
|
How can you tell an animal is ill-thrift? (i.e. what are some clinical signs of an ill-thrift animal?)
|
Skinny, poor haircoat
-in beef cattle see the rate of daily gain decrease -Dairy cows have decreased milk production -might se abortion or issues w/ reproduction if not enough glucose |
|
|
How do animals present with black disease? Red water?
|
Black disease: Dead- black on ventrum from bruising and hemolysis from hemorrhage
Red water: dead w/ hematuria |
|
|
What kills an animal with a clostridium infection? Is it the bacteremic shower or acute toxemia?
|
it's the acute toxemia that kills the animal, not the bacteria
|
|
|
Can you diagnose C. haemolyticum (Bacillary hemoglobinuria) with a urinalysis?
|
NO, toxin is present in urine, not the organism
|
|
|
F. hepatica commonly causes subclinical infection, what are the only clinical signs?
|
Reduced weight and feed efficiency
|
|
|
In cattle, economic loss occurs with > or equal to ______ flukes/ animal.
|
40
|
|
|
Clinical disease occurs in cattle with > or equal to ______ flukes/ animal.
|
200
|
|
|
What are the clinical signs of subclinical disease due to F. hepatica? (3)
|
Poor condition, reduced lactation and slower return to estrus in breeding cattle
-can look at how much food they're given : how much they're growing |
|
|
What are 6 differential diagnosis for cattle with poor condition, reduced lactation and slower return to estrus in breeding cattle, especially in the SE USA?
|
1) F. hepatica
2) BVDV 3) IBR (Bovine herpesvirus-1) 4) Leptospirosis* 5) Neospora* 6) Fescue toxicity** -estrogen like toxin |
|
|
What cattle will first show clinical signs of F. hepatica?
|
Those with the heaviest burden
|
|
|
What are the clinical signs of F. hepatica (like those cattle w/ heaviest burdens)?
|
-Weight loss, emaciation, depression, anorexia, rough coat
-anemia, hypoproteinemia, 'bottle jaw' -rarely mild icterus |
|
|
Why do you get hypoproteinemia w/ liver flukes?
|
Because damaging the liver= major production organ of proteins in the body
|
|
|
What are 5 differential diagnoses for a young cow with low protein and submandibular edema?
|
1) Ostertagia ostertagia
2) BVD* -protein losing enteropathy 3) Salmonella -diarrhea 4) Coronavirus -winter dysentery 5) Iatrogenic: too much fluids *not Johne's= cows 2-3 years old *E. coli= calves < 5 days old |
|
|
Why do we rarely see bilirubinuria or therefore icterus in cattle?
|
Rumen microbes use up all the bilirubin
-don't even usually see icterus w/ high bilirubin |
|
|
Are sheep and goats more or less susceptible than cattle to F. hepatica?
|
More susceptible
|
|
|
Why can flukes be fatal in sheep & goats?
|
Fluke entry to bile ducts can be fatal
-ascites, hemoabdomen, pallor and icterus if heavy burden of 1000-5000 |
|
|
What type of disease is more common in small ruminants with F. hepatica? What are the clinical signs?
|
Chronic disease
-burdens > 200 flukes -edema, ascites, emaciation (can get right sided heart failure) -extensive fibrosis occurs as liver heals |
|
|
Why do small ruminants get higher fluke burdens of F. hepatica than cattle?
|
Don't develop immunity like cattle do
-also why they tend to get chronic disease |
|
|
What are 4 ways that disease results from F. hepatic results from maturation of the flukes in bile ducts?
|
1) Hyperplastic cholangitis
2) Plasma protein loss 3) Blood loss 4) Flukes produce proline which creates depression anemia and biliary hyperplasia |
|
|
How long does it take cattle to mount an immune response to F. hepatica infection?
|
5-6 months post infection
-****few flukes survive > 12 months -after 12 months worry about secondary healing of liver |
|
|
What are 3 reasons that fluke maturation in bile ducts results in blood loss?
|
1) Lack of clotting factors
2) Blood cells get sheared in liver 3) Hemolysis **blood loss from hemolysis and hemorrhage |
|
|
What are 4 components of diagnosing F. hepatica?
|
1) History and geographic area
2) Clinical signs 3) CBC and chemistry 4) Fecal sediment examination for ova *not fecal float |
|
|
What do you see on CBC and chemistry of an animal with F. hepatica infections?
|
-anemia, hypoproteinemia
-mild eosinophilia -elevated heaptic enzymes: **GGT (parasites crawling through bile ducts), next look at SDH Secondary: AST, ALP |
|
|
True or false. Fecal floats diagnosis trematodes not nematodes.
|
False, Does not find trematodes, but does find nematodes
-hence fecal floats do not work to diagnose F. hepatica |
|
|
When performing a fecal sedimentation F. hepatica must be distinguished from What? Why?
|
Paramphistomum is smaller, rounded and nonpathogenic rumen fluke
-these 2 are often transmitted together bc same climate and intermediate host, so presence of paramphistomum may indicate presence of F. hepatica |
|
|
Why do you have to treat animals with F. hepatica at least twice?
|
Because flukecides do not kill the larvae, so must kill the adults, then wait and retreat
|
|
|
What are the 2 antiparasitics used to kill F. hepatica flukes?
|
Albendazole and clorsulon
|
|
|
What is the optimal timing for using albendazole or clorsulon to treat F. hepatica flukes?
|
Time treatment to ensure susceptibility (flukes >12 weeks after transmission season) but remove while < 6 m old and less pathogenic
|
|
|
***What is the only flukecide for F. hepatica that can be used in lactating animal?
|
Albndazole****
|
|
|
What determines if cattle need twice a year treatment for F. hepatica?
|
Burden load and hence the year (climate)
|
|
|
How can you prevent F. hepatica?
|
Single treatment in fall or early winter after transmission season kills adults before winter stress
-prevents egg shedding and snail infection next season 2) Fence off or drain snail habitat 3) pasture rotation 4) Molluscides (toxic to fish & wildlife) 5) public fluke monitoring -talk to neighbors |
|
|
What an you do differently to prevent F. hepatica on high risk properties or in high risk years?
|
-spring treatment on high risk properties or in high risk years to remove flukes acquired during late extended transmission on irrigated pastures or wet coastal regions
-check 10 random animals |
|
|
How do the tunnels of coagulative necrosis from F. hepatica appear on necropsy?
|
-Diffuse hepatic fibrosis, particularly ventral lobe
-can cause liver condemnation |
|
|
What are 3 findings on necropsy that are due to mechanical damage and feeding and growth of F. hepatica flukes in the biliary tract?
|
1) Proliferative cholangiohepatitis
2) Fibrosis and thickening of ducts w/ eventual calcification (in cattle) 3) Dark bile- excreted fluke products |
|
|
What is the common name of Fascioloides magna?
|
Large american liver fluke
|
|
|
What animals are affected by F. magna?
|
Sheep and cattle grazing common areas w/ natural hosts
-deer, elk and moose |
|
|
F. magna and F. hepatica have similar life cycles, but how is F. magna different?
|
Greater number of and variety of snail hosts
-broader geographic distribution since hosts tolerate a wider range of habitat and temperature |
|
|
What type of host are cattle for F. magna?
|
Dead end hosts
-rapidly encapsulate parasite |
|
|
True or false. F. magna can be diagnosed in cattle via fecal sedimentation.
|
False, cannot be diagnosed bc of a lack of fecal egg production
|
|
|
What is the main significance of F. magna infection in cattle?
|
Condemnation of liver and other organs
|
|
|
Is F. magna a bigger issue in small ruminants or cattle?
|
SHEEP AND GOATS
-parasite has unlimited migration -1-2 flukes can kill or cause severe hepatic insufficiency |
|
|
What is the treatment for F. magna in sheep and goats?
|
Albendazole
-avoid early in pregnancy |
|
|
What is the common name for Dicrocoelium dendriticum?
|
Lancet fluke
|
|
|
Compare the disease of dicrocoelium dendriticum to that of fasciola flukes.
|
Chroinc, less severe disease
|
|
|
What is the relative size of dicrocoelium dendriticum?
|
Small fluke (<1 cm)
|
|
|
What is the intermediate host of Dicrocoelium dendriticum?
|
Indirect life cycle w/ snail and ant hosts
|
|
|
What type of host are goats, sheep and cattle for dicrocoelium dendriticum?
|
Definitive hosts
|
|
|
Where do adult Dicrocoelium dendriticum reside in the body?
|
In bile ducts and shed eggs
|
|
|
What is the life cycle of dicrocoelium dendriticum? (5)
|
-eggs ingested by snails--> cercariae
-cercariae expelled & ingested by ants -infectious metacercariae develop in ants and cause paralysis -ants ingested by grazing livestock -Young flukes excyst in SI and enter the common bile duct to migrate to the liver |
|
|
What is the prepatent period of Dicrocoelium dendriticum?
|
8-12 weeks
|
|
|
Dicrocoelium dendriticum are common in ______.
|
North america
-prevalence as high as 45% in endemic areas |
|
|
Dicrocoelium dendriticum are less pathogenic, but can be present in high numbers. So what kind of damage do they cause?
|
Progressive inflammation of the biliary tree, cirrhosis and hepatic insufficiency
|
|
|
What are the clinical signs of Dicrocoelium dendriticum? (5)
|
Weight loss
Depression Anemia Hypoproteinemia Submandibular edema |
|
|
How do you diagnose Dicrocoelium dendriticum?
|
*Fecal sedimentation
-eggs are smaller, dark brown, operculated |
|
|
What are the 4 differential diagnoses for Dicrocoelium dendriticum?
|
1) Nematodes
2) Trematodes -F. hepatica -F. magna 3) Bacterial 4) Viral |
|
|
When and what do we use to treat Dicrocoelium dendriticum?
|
Albendazole, base treatment on using it on animals with highest worm burdens
|
|
|
What are the 4 scenarios where large animals tend to get hepatic lipidosis?
|
1)Fat cow syndrome of dairy cattle
2) protein energy malnutrition of beef cattle 3) pregnancy ketosis or 'twin lamb disease' of ewes and does 4) hyperlipidemia/ hyperlipemia of equids |
|
|
What is the normal consequence of a negative energy balance in a large animal?
|
-minor drop in blood glucose and drop in the insulin: glucagon ratio
-hormone sensitive lipases convert fat to FFA's and glycerol -mobilization of FFA to liver results in triglyceride storage in cells w/ eventual export as VLDL's |
|
|
What goes wrong with normal pathophysiology that results in hepatic lipidosis?
|
Lipidosis occurs when hepatic triglyceride formation exceeds FA oxidation and release of VLDLs
|
|
|
Why do ruminants tend to get hepatic lipidosis?
|
Have poor ability to export VLDL's possibly due to inadequate production of apolipoprotein A
|
|
|
What are 7 options for treating hepatic lipidosis?
|
1) Eliminate negative energy balance and the factors creating it
2) IV glucose infusion (most common) 3) Insulin 4) Niacin (B3) 5) Corticosteroids 6) Vitamin E/ Se 7) Transfaunation |
|
|
Why do we give IV glucose infusion to patients with hepatic lipidosis?
|
-Give some nutritional support
-Can increase Insulin: glucose ratio to decrease hormone sensitive lipase mobilization of FFA's and may stimulation production of VLDL's= trying to stop fat mobilization |
|
|
Why do we give insulin to patients with hepatic lipidosis?
|
To alter the insulin: glucagon ratio directly
|
|
|
Why can niacin (B3) be given to patients with hepatic lipidosis?
|
May reduce tissue lipolysis and fat load presented to liver
-better preventative |
|
|
Why do you give an animal with hepatic lipidosis corticosteroids?
|
Increase appetite
Reduce milk production Induce gluconeogenesis |
|
|
Why do we give vitamin E and selenium to animals with hepatic lipidosis?
|
Free radical scavengers
|
|
|
What's the purpose of transfaunation in an animal with hepatic lipidosis?
|
Enhance forestomach digestion and absorption of VFA's for energy and glucose precursors
|
|
|
What is fat cow syndrome?
|
Multifactorial condition characterized by mobilization of fat to the liver of post parturient dairy cows
|
|
|
Why do cows with Fat Cow Syndrome get fat in the first place?
|
They have too long of a lactation, when get long into lactation they are still on lactating cow diets= too many calories in and not enough calories out bc not producing enough milk
|
|
|
Why do cats with Fat Cow Syndrome mobilize fats?
|
Because when long in lactation or long dry off and eating lots of food and not making much milk and then go into next lactation (freshen or calf= high stress time) so start milking and metabolic demand goes way up before appetite does = ketosis
|
|
|
Why is it a problem when cows with Fat Cow Syndrome mobilizes fats?
|
If overconditioned cow and start mobilizing fats then lipoproteins go into liver to be repackaged and used because not taking in enough food
-cows are really poor at making lipoproteins in liver so all the mobilization of fat gets stuck in the liver ***Doesn't happen in horses or cats |
|
|
Fat Cow Syndrome is complicated by concurrent ________ disease that result in reduced feed intake and further increase energy demand.
|
Peri-parturient diseases
|
|
|
What is type I ketosis? What's the treatment?
|
Primary (lots of milk not enough appetite), happens b/w 7-10 days after freshening
-just give glucose |
|
|
What is type II ketosis?
|
Ketosis due to some other reason- like liver not working because full of fat, low calcium, retained placenta (can cause displacement of abomasum then not eating at all and get mobilization of fat)
-happens 3-5 days after calving |
|
|
You are examining 3 cows, with BAS scores of: 1.5, 3, and 4.5. If one of them has a peri-parturient disease, which one would you suspect has it?
|
The 1.5, can see all the transverse processes
|
|
|
What is the number range for BAS scoring of beef cattle?
|
1-9 scale
Dairy cows= 1-5 |
|
|
What are 5 components that will help diagnose Fat Cow Syndrome?
|
1) Physical exam
2) Liver enzymes frequently normal 3) Possible hypoglycemia -but usually have stress response 4) *Ketonuria 5) Refractory to treatment 6) Liver biopsy -problematic |
|
|
Why is a liver biopsy problematic when trying to diagnose Fat Cow Syndrome?
|
-Lipidosis (15-30%) present in normal cows
-Liver fat values > 34% correlate to clinical signs -don't usually biopsy |
|
|
What are the 3 ketones present in the urine?
|
Acetate
Beta-hydroxybutyrate Acetoacetate (what's measured with strips) |
|
|
What is the prognosis of Fat Cow Syndrome?
|
Guarded- mortality 25%
|
|
|
What is the treatment for Fat Cow Syndrome?
|
Identify and treat any predisposing disease
-address negative energy balance and lipidosis |
|
|
How do you prevent Fat Cow Syndrome?
|
-Dietary management of stock during late lactation and dry period
-Prompt treatment of peri-parturient diseases -adequate protein is critical in the dry period |
|
|
What will pathologies will you find in a liver of a cow that suffered fat cow syndrome on necropsy? (3)
|
1) Enlarged yellow and swollen liver
2) Floats in formalin 3) Fatty infiltration of hepatocytes *Search carefully for other diseases |
|
|
How do you diagnose ketonuria in a cow with Fat Cow Syndrome?
|
Ketone strips
|
|
|
Why can't you use prednisolone in ruminants?
|
Don't use oral corticosteroids bc of the rumen
|
|
|
How do you prevent Fat Cow Syndrome?
|
-Dietary management of stock during late lactation and dry period
-Prompt treatment of peri-parturient diseases -adequate protein is critical in the dry period |
|
|
How can you make sure to prevent obesity in late lactation?
|
-12-13 month calving interval
-match requirements to milk production in late lactation -make changes before the dry period |
|
|
What will pathologies will you find in a liver of a cow that suffered fat cow syndrome on necropsy? (3)
|
1) Enlarged yellow and swollen liver
2) Floats in formalin 3) Fatty infiltration of hepatocytes *Search carefully for other diseases |
|
|
How do you diagnose ketonuria in a cow with Fat Cow Syndrome?
|
Ketone strips
|
|
|
Why can't you use prednisolone in ruminants?
|
Don't use oral corticosteroids bc of the rumen
|
|
|
How can you make sure to prevent obesity in late lactation?
|
-12-13 month calving interval
-match requirements to milk production in late lactation -make changes before the dry period |
|
|
How do you make sure to provide adequate protein during the period in order to prevent Fat Cow Syndrome?
|
-Good quality roughage
-Additional grain 2-4 weeks prior to calving to allow adjustment to the expected post calving ration |
|
|
What animals get protein- energy malnutrition?
|
Disease of pregnant beef cows on marginal diets
|
|
|
When do the signs of protein-energy malnutrition arise?
|
In winter
|
|
|
What are 3 reasons that protein-energy malnutrition arises in winter?
|
1) Increased energy demands from inclement weather and developing fetus
2) Heifers predisposed (growth demands) 3) Primary diseases, snow cover, unpalatable feed |
|
|
What are the clinical signs of protein-energy malnutrition?
|
Syndrome of weight loss, weakness and depression
-animals often thin w/ a long hair coat -Die in 7-14 days of becoming recumbent |
|
|
What are 4 components of diagnosing protein-energy malnutrition?
|
1) Rule out other possible causes
-keep open mind 2) Demonstrate inadequate caloric intake -take feed samples, pictures, look at whole property 3) Ketonuria unusual -bc no energy drain 4) Look for metabolic bone disease -Cows with huge heads- not enough calcium and too much phosphorus--> bony proliferation |
|
|
Is treatment of protein-energy malnutrition very successful?
|
No, usually difficult and unrewarding
|
|
|
What are 3 components of treating protein-energy malnutrition?
|
1) Force feeding alfalfa slurry
2) Propylene glycol -glucose precursor 3) Address concurrent disease (s) -micronutrient deficiencies |
|
|
What are 3 findings on necropsy of an animal with protein-energy malnutrition?
|
1) Atrophy of fat
2) Pathologic fractures 3) Poor rumen development |
|
|
What are 4 ways to prevent protein-energy malnutrition in beef cattle?
|
1) Appropriately address energy requirements of 3rd trimester and in cold weather
2) Provide good quality forage in adequate amounts 3) Maintain good BC scores (5-7) in cows entering third trimester 4) Look at your cattle |
|
|
When does pregnancy toxemia occur in ewes and does?
|
Final 2-4 weeks gestation
|
|
|
What is the pathophysiology of pregnancy toxemia?
|
Inability to meet energy demands w/ rapid fetal growth and inadequate caloric intake
-nutritional and physiological stress increase the incidence |
|
|
What ewes usually get pregnancy toxemia?
|
Ewes with >1 fetus
-affected ewes often in very good body condition |
|
|
When does pregnancy toxemia occur in ewes and does?
|
Final 2-4 weeks gestation
|
|
|
What are the clinical signs of pregnancy toxemia?
|
-Anorexia, weakness, and depression
-Separation from the herd -Apparent blindness -Tremors, star gazing, ataxia, circling and bruxism |
|
|
What is the pathophysiology of pregnancy toxemia?
|
Inability to meet energy demands w/ rapid fetal growth and inadequate caloric intake
-nutritional and physiological stress increase the incidence |
|
|
What are the differential diagnoses for a blind small ruminant that is walking around that is not pregnant?
|
-Thiaminase
-Sulfur toxicity -Listeria -lead toxicity -salt toxicity |
|
|
What ewes usually get pregnancy toxemia?
|
Ewes with >1 fetus
-affected ewes often in very good body condition |
|
|
What are the clinical signs of pregnancy toxemia?
|
-Anorexia, weakness, and depression
-Separation from the herd -Apparent blindness -Tremors, star gazing, ataxia, circling and bruxism |
|
|
What are the differential diagnoses for a blind small ruminant that is walking around that is not pregnant?
|
-Thiaminase
-Sulfur toxicity -Listeria -lead toxicity -salt toxicity |
|
|
What do you find on physical exam and lab findings of an animal with pregnancy toxemia?
|
-Ketonuria
-acidosis w/ low serum K+ and calcium -elevated FFA and BHB -Does may develop marked neutrophilia (stress?) |
|
|
What do you find on necropsy of an animal with pregnancy toxemia?
|
Friable and fatty liver
|
|
|
What is the mortality of pregnancy toxemia?
|
High without aggressive therapy
-economic question of mom or fetus |
|
|
What is the treatment of pregnancy toxemia?
|
1) C-section or induce parturition
-Dexamethason in ewes 2) Continuous infusion of glucose 3) Adjunct therapies -B vitamins for gluconeogenesis, transfaunation -Glucose precursors: propylene glycol, calcium propionate |
|
|
What are 3 components of preventing pregnancy toxemia in does and ewes?
|
1) Predisposed if they enter 3rd trimester over or under-conditioned
2) Provide excellent quality forage 3) Serial measurement of plasma BHB to assess nutritional adequacy |
|
|
What large animals most commonly get hyperlipemia/ hyperlipidemia?
|
Ponies, donkeys and miniature horses
|
|
|
What is hyperlipemia/ hyperlipidemia associated with? What animals are predisposed?
|
A sudden drop in dietary carbohydrates
-sudden starvation or anorexia -Lactating animals predisposed -fat mobilization w/ hepatic accumulation |
|
|
What causes hyperlipemia/ hyperlipidemia?
|
Production of an abnormal VLDL
|
|
|
Why are horses predisposed to hyperlipidemia/ hyperlipemia?
|
Make huge lipoproteins (package into giant fat molecules) and they get stuck in capillaries like in the feet, liver and kidney
|
|
|
What is hyperlipidemia?
|
Mild metabolic dysfunction with mild elevation of triglycerides
<500 mg/dL and plasma is clear -no evidence of hepatic dysfunction |
|
|
What is the treatment for hyperlipidemia?
|
Usually readily reversible if caloric intake increased
|
|
|
Why does hyperlipidemia often occur when animals are azotemic?
|
Prevents lipid removal from the blood by inhibiting LPL
|
|
|
What is hyperlipemia?
|
More severe dysfunction
Triglycerides>>>500 mg/dL |
|
|
What are the clinical signs of hyperlipemia? (3)
|
1) Anorexia, depression, weakness, incoordination and diarhea
2) White coating of tongue and concurrent myopathy common 3) Insulin resistant hyperglycemia |
|
|
What is the mortality of hyperlipidemia?
|
often high
|
|
|
*Why is laminitis a frequent complication of hyperlipemia/ hyperlipidemia?
|
Giant fat molecules can get stuck in the feet --> laminitis
|
|
|
What are 4 sequela to hyperlipemia/ hyperlipidemia syndromes?
|
1) Severe metabolic dysfunction and death
2) Liver rupture -hemoabdomen and sudden death 3) Laminitis a frequent complication 4) Lipid can accumulate in liver, kidney, heart and skeletal muscle and cause signs associated with dysfunction of these organs |
|
|
What are 6 components to diagnosing hyperlipemia/ hyperlipidemia?
|
1) History
2) Triglycerides 3) White or yellow opalescence of plasma 4) elevated bilirubin and FFA's 5) Metabolic acidosis in severe cases 6) Ultrasound -hepatomegaly -increased echogenicity -some loss of normal hepatic architecture |
|
|
What are 3 components to treating hyperlipemia/ hyperlipidemia?
|
1) Correct primary disease to alleviate anorexia
-teeth? 2) Correct negative energy balance -IV dextrose infusions -force feeding alfalfa slurry and/ or complete diets -intravenous nutrition 3) Insulin reduces fat mobilization |
