Exam 4 Flashcards by AE G

petechiae, ecchymoses, mucosal bleeding – melena, hematochezia, hematuria, epistaxis are all clinical signs of what disease?

thrombocytopenia

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causes of thrombocytopenia due to decreased production

bone marrow cancer
infection
immune-mediated disease
chemotherapeutics

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causes of thrombocytopenia due to increased consumption

vasculitis, DIC, envenomation

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causes of thrombocytopenia due to increased destruction

immune-mediated diseases

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causes of thrombocytopenia due to sequestration

enlarged spleen

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what is the most common cause of thrombocytopenia

destruction - immune-mediated

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miscellaneous causes of thrombocytopenia

platelet clumps
breeds w/ macrothrombocytes (cavalier king charles spaniels)
EDTA pseudothrombocytopenia
preanalytical factors

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plts < 20,000

immune-mediated TP

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plts < 60,000

DIC

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where is von willebrand factor in blood vessel structure

subendothelial collagen

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3 steps of platelet plug formation

adhesion
release reaction
aggregation

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factors of the intrinsic pathway
tests

8,9,11,12
measured by aPTT, ACT

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factors of the extrinsic pathway
tests

7
PT

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factors of the common pathway

1,2,5,10

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what factor is responsible for stabilization of fibrin clot

13a

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lab results of vascular disorders

prolonged bleeding time
normal-decreased platelets
plasma/blood assays normal

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lab results of decreased production & increased destruction

prolonged bleeding time
ACT normal-prolonged
plasma assays normal
decreased platelets

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lab results of von willebrand disease

prolonged bleeding time
decreased VWF
normal platelets

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differentiate types I, II, III of von willebrand disease

type I - decreased in VWF:AG & all multimeres
type II - decreased VWF:Ag & decrease in high MW multimere
type III - VWF undetectable

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which type of VWF disease are dobermans more likely to have

type I

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lab results due to vitamin K antagonists

prolonged ACT, aPTT, PT
QF normal

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lab results due to hepatic failure

prolonged ACT, aPTT, PT
low QF

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inherited coagulation disorders?

7 - prolonged PT
8 - hemophilia A - prolonged aPTT, ACT
9 - hemophilia B - prolonged aPTT, ACT

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DIC is due to what 2 things?

thrombocytopenia & coagulopathy

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causes of DIC?

pancreatitis, heat stroke, severe hypoxia, endotoxemia/sepsis, IMHA

lab results of DIC

everything abnormal decrease plt count prolonged bleeding time prolonged ACT, aPTT, PT low QF increase FDPs & D-dimers

3 phases of DIC

hypercoagulable phase consumption of plt & coag factors hypocoagulable phases

what is prolonged bleeding time indicative of

primary hemostasis disorder

what is renal threshold for glucose what happens if BG > renal threshold

The kidney has a limit on how much glucose can be absorbed “renal threshold” if blood glucose > renal threshold then there will be glucosuria

what is a good measurement to use for distinguishing DM from excitement, assessing diabetic remission, confirming DM in cats and looking at the preceding 2-3 weeks [BG]

serum fructosamine

when should insulin be decreased normally?

with BG <60 mg/gL

describe equine metabolic syndrome associated with ____ 3 components:

horses associated with laminitis 3 component: regional adiposity, hyperinsulinemia, insulin resistance obesity = insulin resistance and glucose intolerance

lab finding of equine metabolic syndrome

hyperglycemia/normoglycemia hyperinsulinemia increased GGT, AST, SDH hyperlipidemia

limitations of serum amylase & lipase in the diagnosis of pancreatitis in dogs/cats what suggests pancreatic injury?

both not Se or Sp - can be normal in patients with pancreatitis can be increased with any decrease in GFR/renal failure due to inactivation by kidney steroids can increase lipase 5x upper RI >3-4x upper RI

Know how measuring peritoneal amylase and lipase may aid in the diagnosis of pancreatitis

damage to pancreas can lead to leakage of enzymes peritoneal level > serum = suggestive of pancreatitis but could also be perforation or trauma

how would pancreatitis affect serum liver enzymes

increased liver enzymes

how is serum PLI is used to help confirm the diagnosis of pancreatitis in dogs and cats

specific for pancreatic origin lipase very Se not affected by renal dz or steroids 0-200 normal > 400 pancreatitis

positive PLI snap in a dog

with clinical suspicion, PPV is high but other diagnostics should be confirm

negative PLI snap in a dog

likely accurate in ruling out acute pancreatitis

what is the difference between EPI and malabsorption in regard to proteins

EPI - maintain proteins malabsorption - hypoproteinemia

what are the limitations of quantifying fecal fat in differentiating malabsorption from maldigestion (EPI)

screens for undigested fats positive can be suggestive for maldigestion (EPI) but many EPI animals will not have detectable fat

what test would you run to confirm EPI

trypsin-like immunoreactivity (TLI)

TLI results in dogs < 2.5 ug/L > 5 ug/L 2.5-5 ug/L

< 2.5 is EPI > 5 intestinal disease - do biopsy gray zone 2.5-5 repeat in a few weeks

TLI results in cats < 8 ug/L

< 8 is EPI often also have decreased B12

↓ folate & B12

malabsorption

↓ folate only

proximal SI defect

↓ B12 only

distal SI defect EPI in cats

↑ folate, ↓ B12

bacterial overgrowth

weight loss, voluminous unformed stools, PUPD, polyphagia are clinical signs suggestive of what

EPI or malabsorption

what breeds are at an increased risk for pancreatitis

mini schnauzers and yorkshire terriers

what endocrine diseases are associated with increased serum lipids

hypothyroidism Cushings/PPID diabetes mellitus equine metabolic syndrome

increased cholesterol only

cholestasis

increased triglycerides only

extreme negative energy balance (pregnancy, lactation, anorexia, obesity)

increased cholesterol & triglycerides (hyperlipidemia)

endocrinopathies corticosteroids post-prandial pancreatitis nephrotic syndrome familial hyperlipidemic syndrome (schnauzers & ponies)

decreased cholesterol

malabsorption/maldigestion liver failure addison's disease

ALT

small animals liver & severe m injury increase with glucocorticoids

AST

small & large animals parallel with ALT increase in SA liver & muscle injury

SDH

large animals liver injury

ALP

increases with bone, hepatic, glucocorticoids (dogs), growing animals, anticonvulsants, cushings (dogs) & hyperthyroidism (cats) NOT affected by drugs or corticosteroids in cats

GGT

more sensitive for cholestasis in horses/cattle increased with neonates (except horses) & glucocorticoids

causes of increased serum bile acids

1. severe liver damage 2. obstruction 3. shunting of blood (PSS) 4. secondary due to cholestasis

when would you not want to run a serum bile acids

if ALP and GGT are already increased due to cholestasis