Exam 4 Flashcards
petechiae, ecchymoses, mucosal bleeding – melena, hematochezia, hematuria, epistaxis are all clinical signs of what disease?
thrombocytopenia
causes of thrombocytopenia due to decreased production
bone marrow cancer
infection
immune-mediated disease
chemotherapeutics
causes of thrombocytopenia due to increased consumption
vasculitis, DIC, envenomation
causes of thrombocytopenia due to increased destruction
immune-mediated diseases
causes of thrombocytopenia due to sequestration
enlarged spleen
what is the most common cause of thrombocytopenia
destruction - immune-mediated
miscellaneous causes of thrombocytopenia
platelet clumps
breeds w/ macrothrombocytes (cavalier king charles spaniels)
EDTA pseudothrombocytopenia
preanalytical factors
plts < 20,000
immune-mediated TP
plts < 60,000
DIC
where is von willebrand factor in blood vessel structure
subendothelial collagen
3 steps of platelet plug formation
- adhesion
- release reaction
- aggregation
factors of the intrinsic pathway
tests
8,9,11,12
measured by aPTT, ACT
factors of the extrinsic pathway
tests
7
PT
factors of the common pathway
1,2,5,10
what factor is responsible for stabilization of fibrin clot
13a
lab results of vascular disorders
prolonged bleeding time
normal-decreased platelets
plasma/blood assays normal
lab results of decreased production & increased destruction
prolonged bleeding time
ACT normal-prolonged
plasma assays normal
decreased platelets
lab results of von willebrand disease
prolonged bleeding time
decreased VWF
normal platelets
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
which type of VWF disease are dobermans more likely to have
type I
lab results due to vitamin K antagonists
prolonged ACT, aPTT, PT
QF normal
lab results due to hepatic failure
prolonged ACT, aPTT, PT
low QF
inherited coagulation disorders?
7 - prolonged PT
8 - hemophilia A - prolonged aPTT, ACT
9 - hemophilia B - prolonged aPTT, ACT
DIC is due to what 2 things?
thrombocytopenia & coagulopathy
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
- severe liver damage
- obstruction
- shunting of blood (PSS)
- 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
