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Clinical Pathology 2017 > Exam 4 > Flashcards

Exam 4 Flashcards

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1
Q

Leakage enzymes

A

CK, AST, ALT, SDH, GLDH

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2
Q

Induction enzymes

A

ALP, GGT

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3
Q

CK sources and half-life

A

Sources: skeletal, cardiac and smooth muscle; brain (highly specific/sensitive for myopathies)
Half-life: very short (hrs)

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4
Q

AST sources and half-life

A

Sources: skeletal muscle and hepatocytes mainly; also RBCs, other cells (sensitive, low specificity)
Half-life: hours/days

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5
Q

ALT sources and half-life

A

Sources: hepatocytes mainly, also skeletal muscle in dogs/cats (very specific/sensitive for liver, rarely increases with myopathy)
Half-life: hours/days

small animals only

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6
Q

SDH sources and half-life

A

Sources: hepatocytes
Half-life: hours

horses, ruminants, swine

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7
Q

GLDH sources and half-life

A

Sources: hepatocytes
Half-life: hours

large animals and exotics

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8
Q

Enzymes increased with myopathy (muscle disease)

A

CK, AST, ALT

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9
Q

Enzymes increased with hepatocellular injury

A

AST, ALT, SDH

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10
Q

Liver disease: all hepatic enzymes

A

Leakage: ALT, AST, SDH

Induced/cholestasis: ALP, GGT

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11
Q

Markers for cholestasis

A

Bilirubin, bile acids, cholesterol, ALP, GGT

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12
Q

Hepatic function tests and what happens with decreased liver function

A

Synthetic function tests: albumin
- albumin, BUN, cholesterol, glucose
- decreased liver function = decreased synthetic function tests (can’t make)
Excretory function tests: bilirubin
- bilirubin, bile acids, ammonia
- decreased liver function = increased excretory function tests (can’t excrete)

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13
Q

What causes elevated inducible enzymes (cholestatic enzymes)?

A

Increased synthesis from hyperplastic cells

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14
Q

ALP sources and half-life

A

Sources: hepatocytes, biliary epithelium, osteoblasts, colostrum (low specificity)
Half-life: dog 3 days, cat 6 hours

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15
Q

GGT sources and half-life

A

Sources: biliary epithelium mainly; also hepatocytes and colostrum (more specific for cholestasis than ALP)
Half-life: 3 days

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16
Q

Which enzymes are more sensitive to cholestasis (by species)?

A

Dog: ALP
Cat, horse, cattle: GGT
(in cats and horses, bilirubin increases before ALP)

ALP = more specific for all

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17
Q

Other considerations for elevated induced enzymes: ALP, GGT

A

Ingestion of colostrum in dogs, cats, ruminants
Steroids or PB use in dogs
ALP only: younger than 1 yr, or osteosarcoma

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18
Q

Pre-hepatic bilirubinemia

A

Mostly unconjugated increased

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19
Q

Causes of pre-hepatic bilirubinemia

A

Hemolytic disease

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20
Q

Hepatic bilirubinemia

A

Mixed conjugated and unconjugated

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21
Q

Causes of hepatic bilirubinemia

A

Defective uptake of unconjugated bilirubin: hepatic dysfunction, anorexia in horses
Defective conjugation/excretion of bilirubin: hepatic dysfunction, functional cholestasis (sepsis), intra and extra-hepatic cholestasis

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22
Q

Post-hepatic bilirubinemia

A

Mostly conjugated bilirubin increased

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23
Q

Unconjugated vs conjugated bilirubin

A 
Unconjugated = binds to albumin, accumulates in blood
Conjugated = water soluble, accumulates in urine
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24
Q

What increase occurs first, hyperbilirubinemia or bile acids?

A

Hyperbilirubinemia

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25
Different tests for bilirubin
``` Total bilirubin (routine chem) Bilirubin splits (direct = conjugated, indirect = unconjugated - good for anorexic horses) Urinary bilirubin (urine dipstick, never normal in cat) Urinary urobilinogen (not clinically important) ```
26
Bile acid metabolism
``` Synthesized by hepatocytes from cholesterol Conjugates and excreted into bile Stored in gall bladder CCK releases into duodenum Reabsorbed by ileum (portal vein) ```
27
Process of bile acid metabolism requires 3 working parts:
1. Healthy hepatocytes 2. Intestinal absorption 3. Portal circulation
28
Causes of increased bile acids
Decreased hepatic clearance: portosystemic shunt or microvascualr dysplasia Hepatocellular dysfunction Decreased hepatic biliary excretion: intra/extra-hepatic cholestasis, functional cholestasis (sepsis) Maltese dogs: normal
29
Indication for bile acid tests
When hepatic enzymes/function tests are minimally altered, but liver disease suspected NOT indicated with hyperbilirubinemia
30
Procedure for testing bile acids
1 fasted sample, 1 post-prandial sample (after gallbladder contraction, 1 sample in horses)
31
Ammonia source and clearance
Protein degradation by enteric bacteria, absorbed by intestines, cleared from portal circulation by hepatocytes via urea cycle
32
Significance of hyperammonemia
Accumulates during liver dysfunction - hepatocytes not converting ammonia to urea (increased ammonia, decreased BUN) Role in hepatic encephalopathy
33
Causes of hyperammonemia
Decreased blood clearance: hepatocellular dysfunction (decreased uptake), PSS, urea cycle disorders Increased production/intake: physiologic, urea toxicosis (cattle), intestinal disease (horses)
34
Analytes synthesized by hepatocytes = DECREASED WITH HEPATIC DYSFUNCTION
Albumin (late liver disease) Urea Cholesterol (may be increased with concurrent cholestasis) Glucose (late liver disease, may be increased with decreased hepatic intake) Clotting factors
35
BUN:Creat change with disease
High with pre-renal azotemia or GI hemorrhage
36
Total protein change with disease
Low with PLE - both albumin and globulins are low
37
Cholesterol changes with disease
Low with PLE
38
Calcium change with disease
Low with intestinal malabsorption or secondary to hypoalbuminemia
39
Magnesium change with disease
Low with decreased intake (anorexia) or decreased GI absorption
40
Phosphorous change with disease
Low with decreased intake (anorexia) or decreased GI absorption
41
Sodium changes with disease
High if pure water loss by GI tract | Low if isotonic fluid or Na rich fluid loss by GI tract
42
Potassium changes with disease
Low if lost in GI or anorexia
43
Chloride changes with disease
High if pure water loss by GI Low if isotonic fluid or CL rich fluid loss by GI Disproportionally elevated relative to Na if HCO3 being lost by GI
44
TCO2 changes with disease
High with upper GI disease and selective loss of HCl | Low if losing bicarbonate in diarrhea
45
Protein changes with hemorrhage, BLE, exudative lesion, SEVERE PLN or hepatopathy
Panhypoproteinemia
46
Protein changes with PLN or hepatopathies
Hypoalbuminemia
47
Protein changes with inflammation, hepatopathies
Hypoalbuminemia | Hyperglobulinemia
48
Protein changes with dehydration
Panhyperproteinemia
49
Pancreatitis: CBC changes
Neutrophilia with L shift +/- toxicity Lymphopenia Eosinopenia Thrombocytopenia
50
Pancreatitis: chem changes
Hypercholesterolemia Increased ALT (liver leakage), ALP (cholestatic) Hyper bilirubinemia d/t cholestasis Hypocalcemia (more so in cats) Hyperglycemia (hyperglucagonemia - alpha cells of pancreas, diabetes, stress)
51
Clinical signs of pancreatitis in dogs vs cats
Dogs: pain, V/D, fever Cats: dehydration, weight loss, hypothermic, icterus (less likely to see V and fever)
52
Exocrine pancreatic insufficiency (EPI)
Insufficient synthesis/secretion of digestive enzymes by pancreatic acinar tissue = maldigestion
53
Clinical signs of EPI
Chronic, severe weight loss despite and GOOD APPETITE | Cow patty diarrhea
54
Additional complications of EPI (3)
``` Concurrent with diabetes mellitus Secondary SIBO (lack of anti-bacterial factor or bicarbonate from pancreas) Secondary cobalamin/B12 deficiency (lack of IF from pancreas) ```
55
EPI: CBC changes
Maybe normal | +/- normocytic, normochromic anemia
56
EPI: chem changes
Often normal +/- low cholesterol +/- hyperglycemia +/- mild to moderate elevated ALT, AST, ALP
57
Pancreatic enzymes
Amylase, lipase, trypsin
58
Which pancreatic enzymes are decreased with EPI?
Lipase and trypsin
59
Amylase sources
Pancreatic acinar cells*, SI, salivary glands in pigs
60
Lipase sources
Pancreatic acinar cells*, gastric mucosal cells, SI, liver, adipocytes, myocytes
61
Trypsin sources
Pancreatic acinar cells, as trypsinogen
62
Causes of elevated amylase
Pancreatic disease*, GI disease, renal failure*, other causes of decreased GFR ( pre and post-renal)
63
Causes of elevated lipase
>3 fold = likely pancreatitis
64
Causes of elevated trypsin
Pancreatitis, pancreatic hypertrophy, renal disease, SI disease
65
What are each of the pancreatic enzymes tests used for?
Amylase: increases seen with pancreatitis, pancreatic neoplasia, enteritis Lipase: used to dx pancreatitis Trypsin: used to dx EPI
66
Maldigestion vs. malabsorption
``` Maldigestion = think pancreas Malabsorption = think GI ```
67
Malabsorption
Thickened GI = abnormal cell infiltration d/t inflammation/cancer Parasitism/infection GI lymphatic disease = lymphangestasia CS: V/D, colic, abomasal disease
68
Effect of EPI on folate, cobalamin, TLI
Folate: normal/increased Cobalamin: decreased TLI: decreased
69
Effect of bacterial overgrowth on folate, cobalamin, TLI
Folate: increased Cobalamin: decreased TLI: normal
70
Effect of proximal SI disease on folate, cobalamin, TLI
Folate: decreased Cobalamin: normal TLI: normal
71
Effect of distal SI disease on folate, cobalamin, TLI
Folate: normal Cobalamin: decreased TLI: normal
72
Effect of diffuse SI disease on folate, cobalamin, TLI
Folate: decreased Cobalamin: decreased TLI: normal
73
Folate vs cobalamin
Folate = B9 - produced by bacteria, increased with ARE, absorbed in proximal SI Cobalamin = B12 - absorption decreased by bacteria, decreased with ARE, absorbed in duodenum and mostly ileum with IF from pancreas
74
Causes of hypocholesterolemia
Decreased hepatic synthesis = hepatic disease, PSS Decreased intestinal absorption = PLE Maldigestion = EPI
75
Clinical signs of hypoglycemia
Lethargy, incoordination, exercise intolerance, seizures, coma
76
Causes of hypoglycemia
Increased insulin secretion (insulinoma, xylitol toxicity) Decreased insulin antagonists (cortisol) Decreased gluconeogenesis (liver insufficiency, dec cortisol, starvation) Increase glucose utilization (lactational, exertional) Sepsis/neoplasm Pharmacological (insulin, sulfonylurea)
77
Causes of hyperglycemia
Catecholamine induced (fractious animal, pheochromocytoma) Endocrine (DM, Cushing’s, acromegaly, hyperpituitarism) Drugs (dextrose, xylazine, ketamine) Hyperglucagonemia (glucagonoma) Pancreatitis Other

Clinical Pathology 2017 (4 decks)

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