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Clinical Pathology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

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

A

thrombocytopenia

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2
Q

causes of thrombocytopenia due to decreased production

A

bone marrow cancer
infection
immune-mediated disease
chemotherapeutics

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3
Q

causes of thrombocytopenia due to increased consumption

A

vasculitis, DIC, envenomation

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4
Q

causes of thrombocytopenia due to increased destruction

A

immune-mediated diseases

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5
Q

causes of thrombocytopenia due to sequestration

A

enlarged spleen

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6
Q

what is the most common cause of thrombocytopenia

A

destruction - immune-mediated

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7
Q

miscellaneous causes of thrombocytopenia

A

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

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8
Q

plts < 20,000

A

immune-mediated TP

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9
Q

plts < 60,000

A

DIC

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10
Q

where is von willebrand factor in blood vessel structure

A

subendothelial collagen

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11
Q

3 steps of platelet plug formation

A
  1. adhesion
  2. release reaction
  3. aggregation
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12
Q

factors of the intrinsic pathway
tests

A

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

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13
Q

factors of the extrinsic pathway
tests

A

7
PT

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14
Q

factors of the common pathway

A

1,2,5,10

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15
Q

what factor is responsible for stabilization of fibrin clot

A

13a

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16
Q

lab results of vascular disorders

A

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

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17
Q

lab results of decreased production & increased destruction

A

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

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18
Q

lab results of von willebrand disease

A

prolonged bleeding time
decreased VWF
normal platelets

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19
Q

differentiate types I, II, III of von willebrand disease

A

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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20
Q

which type of VWF disease are dobermans more likely to have

A

type I

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21
Q

lab results due to vitamin K antagonists

A

prolonged ACT, aPTT, PT
QF normal

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22
Q

lab results due to hepatic failure

A

prolonged ACT, aPTT, PT
low QF

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23
Q

inherited coagulation disorders?

A

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

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24
Q

DIC is due to what 2 things?

A

thrombocytopenia & coagulopathy

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25
Q

causes of DIC?

A

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

26
Q

lab results of DIC

A

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

27
Q

3 phases of DIC

A

hypercoagulable phase
consumption of plt & coag factors
hypocoagulable phases

28
Q

what is prolonged bleeding time indicative of

A

primary hemostasis disorder

29
Q

what is renal threshold for glucose

what happens if BG > renal threshold

A

The kidney has a limit on how much glucose can be absorbed “renal threshold”

if blood glucose > renal threshold then there will be glucosuria

30
Q

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]

A

serum fructosamine

31
Q

when should insulin be decreased normally?

A

with BG <60 mg/gL

32
Q

describe equine metabolic syndrome

associated with ____
3 components:

A

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

33
Q

lab finding of equine metabolic syndrome

A

hyperglycemia/normoglycemia
hyperinsulinemia
increased GGT, AST, SDH
hyperlipidemia

34
Q

limitations of serum amylase & lipase in the diagnosis of pancreatitis in dogs/cats

what suggests pancreatic injury?

A

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

35
Q

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

A

damage to pancreas can lead to leakage of enzymes

peritoneal level > serum = suggestive of pancreatitis but could also be perforation or trauma

36
Q

how would pancreatitis affect serum liver enzymes

A

increased liver enzymes

37
Q

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

A

specific for pancreatic origin lipase
very Se
not affected by renal dz or steroids

0-200 normal
> 400 pancreatitis

38
Q

positive PLI snap in a dog

A

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

39
Q

negative PLI snap in a dog

A

likely accurate in ruling out acute pancreatitis

40
Q

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

A

EPI - maintain proteins
malabsorption - hypoproteinemia

41
Q

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

A

screens for undigested fats

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

42
Q

what test would you run to confirm EPI

A

trypsin-like immunoreactivity (TLI)

43
Q

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

A

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

44
Q

TLI results in cats
< 8 ug/L

A

< 8 is EPI
often also have decreased B12

45
Q

↓ folate & B12

A

malabsorption

46
Q

↓ folate only

A

proximal SI defect

47
Q

↓ B12 only

A

distal SI defect
EPI in cats

48
Q

↑ folate, ↓ B12

A

bacterial overgrowth

49
Q

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

A

EPI or malabsorption

50
Q

what breeds are at an increased risk for pancreatitis

A

mini schnauzers and yorkshire terriers

51
Q

what endocrine diseases are associated with increased serum lipids

A

hypothyroidism
Cushings/PPID
diabetes mellitus
equine metabolic syndrome

52
Q

increased cholesterol only

A

cholestasis

53
Q

increased triglycerides only

A

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

54
Q

increased cholesterol & triglycerides (hyperlipidemia)

A

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

55
Q

decreased cholesterol

A

malabsorption/maldigestion
liver failure
addison’s disease

56
Q

ALT

A

small animals
liver & severe m injury
increase with glucocorticoids

57
Q

AST

A

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

58
Q

SDH

A

large animals
liver injury

59
Q

ALP

A

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

60
Q

GGT

A

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

61
Q

causes of increased serum bile acids

A
  1. severe liver damage
  2. obstruction
  3. shunting of blood (PSS)
  4. secondary due to cholestasis
62
Q

when would you not want to run a serum bile acids

A

if ALP and GGT are already increased due to cholestasis

Clinical Pathology (7 decks)

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