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;
48 Cards in this Set
- Front
- Back
- 3rd side (hint)
What is hemolytic anemia? What are the 2 types?
|
Premature RBC destruction
-intravascular -extravascular, in macrophage system Increased RBC fragility |
|
|
What are the 3 clinical signs of hemolytic anemia?
|
1) Anemia
2) Icterus 3) Hemoglobinurea IF: -intravascular -Hb exceeds amount of haptoglobin to bind it |
|
|
What are 8 clinical signs of hemolytic anemia?
|
1) Hemoglobinurea if intravascular
2) Low RBC count 3) Low PCV 4) Hb varies with time 5) High MCHC early -sine Hb not in RBC 6) Heinz bodies +/- 7) Elevated total biliruben 8) Blood hemolyzed, not iatrogenic |
|
|
What are 8 toxic causes of hemolytic anemia?
|
1) Copper
2) Onions 3) Rape 4) Kale 5) Other brassica 6) Red maple in horses 7) Cold water in calves 8) Snake bite |
|
|
What are some non-toxic causes of hemolytic anemia?
|
Leptospirosis, babesia, equine infectious anemia, neonatal isoerythrolysis, anaplasmosis
|
|
|
What are 2 ways that the body can have excess copper?
|
1) Excess copper
2) Deficiency in Molybdenum -binds with copper & necessary for metabolism |
|
|
What are 6 sources of copper?
|
1) CuSO4- foot baths
2) Fungicides 3) Algicides 4) Excessive supplementation -poultry or horse minerals to sheep -Injectable supplements 5) Fertilizing pastures w/ poultry manure 6) anti-helmentics |
|
|
What is the mode of action of copper toxicity?
|
-interaction w/ molybdenum (excess Cu or deficient Mo)
-Copper released into circulation -Copper oxidizes erythrocyte membrane--> increases fragility of RBC, hemolysis, formation of methemoglobin may aggravate the affect |
|
|
Copper is absorbed in the ______ intestine, circulates bound to ____ and is stored in the _____.
|
Small intestine
Albumin Liver |
|
|
What is copper used for in the body?
|
1) Ceruloplasmin
2) Erythrocuprein 3) Cu containing enzymes |
|
|
What 2 compounds are needed to metabolize copper metabolism?
|
1) SO4
2) Molybdenum |
|
|
What is the pathophysiology of copper toxicity?
|
-Stored copper in liver not a problem until excessive
-sudden release of copper--> accumulation of excess copper (when saturated hepatocyte dies) & other stress or toxicity to liver -Copper damages RBC membrane |
|
|
What animals are most susceptible to copper toxicity? Compare goats, sheep, and calves.
|
Sheep!!! very susceptible
Goats 3-4 x more resistant Cattle even more resistant |
|
|
What are 4 clinical pathologies associated with copper toxicity?
|
1) whole blood cu > 0.7 - 1.3 ppm
2) Liver cu > 150 ppm wet base 3) Elevated SDH, LDH, AST 4) Elevated serum bilirubin |
|
|
What are 3 postmortem findings of animals with copper toxicity?
|
1) Icterus
2) Gun-metal kidney -copper plugs kidney tubules 3) Enlarged spleen |
|
|
What are 2 treatments for copper toxicity?
|
1) Ammonium tetrathiomolybdate
-binds Cu for excretion -not always available 2) D-penicillamine -expensive$$$$ |
|
|
What are 2 ways to prevent copper poisoning?
|
Limit copper intake
Provide Molybdenum -add to supplement -Cu: MO < 6:1 |
|
|
When are onions more toxic to ruminants?
|
When large amount consumed and rumen not accustomed to it bc rumen organisms haven't adjusted
|
|
|
What is the mode of action of onion toxicity?
|
Contains N-propyl disulfide (in edible bulb)
-denatures hemoglobin -heinz body formation -acute hemolysis |
|
|
**What is the main clinical sign of onion toxicity?
|
Hemolytic anemia****
|
|
|
What are 2 treatments for copper toxicity?
|
1) Ammonium tetrathiomolybdate
-binds Cu for excretion -not always available 2) D-penicillamine -expensive$$$$ |
|
|
What are 2 ways to prevent copper poisoning?
|
Limit copper intake
Provide Molybdenum -add to supplement -Cu: MO < 6:1 |
|
|
When are onions more toxic to ruminants?
|
When large amount consumed and rumen not accustomed to it bc rumen organisms haven't adjusted
|
|
|
What is the mode of action of onion toxicity?
|
Contains N-propyl disulfide (in edible bulb)
-denatures hemoglobin -heinz body formation -acute hemolysis |
|
|
**What is the main clinical sign of onion toxicity?
|
Hemolytic anemia****
|
|
|
What are 3 components of treating onion toxicity?
|
1) Stop feeding onions for a while
2) Blood transfusions $$$ 3) Diuresis -iv fluids |
|
|
What is the mode of action of Brassica (mustard family and Rape & kale (glucosinolates)?
|
Contain glucosinolates such as S-methyl cystine sulfoxide--> reduced to dimethyl disulfide--> denatures hemoglobin--> causes heinz body hemolytic anemia
|
|
|
What are 4 toxins present in kale, rape and brassica?
|
1) Glucosinolates
2) Some contain thiocyanate 3) Some are goitrogens 4) Some contain tryptophan |
|
|
What are 4 possible clinical signs seen with kale, rape or brassica?
|
1) Hemolytic anemia (heinz body)
2) Goiter 3) ABPEE 4) Polioencephalomalacia if thiaminase |
|
|
How do you diagnose kale, brassica or rape toxicity?
|
History of consuming plants
Lab evidence of heinz body hemolytic anemia |
|
|
What are 3 components of treating kale, rape or brassica toxicity without emphysema present?
|
1) Remove from source
2) avoid respiratory distress 3) Blood transfusion$$$ |
|
|
What 3 additional treatments should you do if an animal with kale, rape or brassica toxicity has emphysema?
|
1) corticosteroids
2) Diuretics 3) Oxygen $$$$ -costs more than sheep |
|
|
What are 3 ways to prevent kale, rape or brassica toxicity?
|
1) introduce to new feed gradually
2) Feed other roughages 3) wait til after freeze to feed |
|
|
What are 3 circumstances of poisoning from cold water in calves?
|
1) Calves just weaned or taken off milk
2) Aren't accustomed to drinking water 3) When finally decide to drink, consume an excessive amount of cold water |
|
|
What is the mechanism of action of cold water in calves?
|
-Massive intake of water
-Hypotonicity of body fluids -Decrease in serum osmolality?? -Lysis of erythrocytes -Hemolytic anemia |
|
|
What is the primary clinical sign of cold water in calves?
|
**Hemolytic anemia
-may see hyponatremia |
|
|
What are 3 components of treating cold water in calves?
|
1) Restrict water
2) Hypertonic saline IV 3) Mannitol -most survive without treatment |
|
|
What are 6 causes of bone marrow depression?
|
1) Bracken fern in cattle
2) T-2 mycotoxins 3) Aspirin in small animals 4) Chloramphenicol 5) Chemotherapeutic agents 6) Neoplasia of bone marrow -lymphosarcoma |
|
|
What cell lines are affected by bracken fern in cattle?
|
All cell lines
-thrombocytopenia -anemia -neutropenia |
|
|
What are 2 harmful effects of bracken fern in cattle?
|
Bone marrow depression
Bladder tumors---> hematuria |
|
|
What are 3 circumstances of bracken fern toxicosis in cattle?
|
1) On poor feed or pasture
2) Fern available & being consumer over a period of time -usually over a month 3) Several animals ill, appear to have other infectious diseases |
|
|
What is the toxin in bracken fern that affects cattle?
|
Ptaquiloside a lactone
-responsible for bone marrow suppression -aplastic anemia -thrombocytopenia -granulocytopenia |
-
|
|
What are the 2 primary signs of bracken fern toxicosis in cattle?
|
1) Other Infections, pneumonia
2) Hemorrhage |
|
|
What are 3 laboratory pathologies found in cattle with bracken fern toxicosis?
|
1) Anemia
2) Thrombocytopenia 3) granulocytopenia |
|
|
What is the life span of a RBC?
|
> 100 days
|
|
|
What are 2 ways to diagnose bracken fern toxicity in cattle?
|
1) Bone marrow aspirate
-aplastic: decreased megalocytes & other precursors of both RBCs & granulocytes 2) Evidence of consuming bracken fern over long period of time |
|
|
What are 2 components of treating bracken fern toxicosis in cattle?
|
1) DL Batyl alcohol
-hard to find 2) Whole blood transfusions $$ -don't last: platelets 2 d, neutrophils 1 d |
|
|
What is the prognosis of bracken fern toxicity in cattle?
|
Going to die
|
|