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Clin path test 4 > Learner objectives > Flashcards

Learner objectives Flashcards

1
Q

Inflammatory leukogram

A
  • immature neutrophils (more than 300 bands)
  • often toxicity as well
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2
Q

Physiologic leukogram

A
  • from stress/excitement
  • mature neutrophilia
  • lymphocytosis
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3
Q

Stress leukogram

A
  • Think cortisol
  • Mature neutrophilia
  • Monocytosis
  • Lymphopenia
  • eosinopenia

*can often have combo of inflammatory and stress leukogram

  • more than 300 bands
  • lymphopenia
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4
Q
  1. Which enzymes are from muscle leakage?
  2. Which enzymes are from liver leakage?
A
  1. CK, AST, LDH => injured skeletal myocytes
  2. ALT, AST, SDH => hepatocellular injury
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5
Q

What does an inc in leakage enzymes tell you?

A

The relative amount of cells injured, not extent of injury (reversible/irreversible).

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6
Q

Which enzymes are cholestatic enzymes?

A
  • ALP, GGT
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7
Q

What does an increase in a cholestatic enzyme mean?

A
  • cholestasis induces synthesis of ALP, and GGT
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8
Q

What are other causes/sources for increases in cholestatic enzymes?

A
  • ALP on canicular surface of hepatocytes is cleaved by pohspholipases
    • activated by increased bile acids during cholestasis
  • Cholestasis causes biliary epithelium to undergo hyperplasia
    • synthesizes more GGT
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9
Q

Are any cholestatic enzymes species specific?

A
  • Cats: any increase in ALP is significant
  • Dogs: increased ALP can be induced by glucocorticoid induction
  • GGT: more sensitive in cattle, horses, cats
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10
Q

With muscle damage, how might patterns of leakage inzymes change over time?

A
  • CK goes up and down quickly
    • short half life
  • AST takes longer to increase, and remains elevated longer
    • longer half life
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11
Q

What will happen if you take a sample a few days after muscle injury?

A
  • AST will be elevated, not CK
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12
Q

What pattern of increase do you expect for leakage enzymes and cholestatic enzymes with liver disease?

A
  • Leakage enzymes elevate before cholestatic
    • leakage enzymes released immediately
    • takes days to elevate enzyme activity
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13
Q

What magnitude of increase in enzymes is clinically significant?

Exceptions:

A
  • 2-3 fold increases over RI

Exceptions

  • ALP in cats
  • GGT in dogs and cats
  • SDH
  • low grade inflammatory lesion
  • Decreased number of target cells
  • Inhibitors of enzyme activity
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14
Q

Species specific differences in biomarkers:

ALT

SDH

ALP

ALP

GGT

A
  • ALT: very good in dog and cat
  • SDH: very specific used in horses, ruminants, swine
  • ALP: any increase in cat is important
  • ALP: very good indicator of cholestasis in dog
  • GGT: more specific for cholestasis, more sens for cat, horse, cattle
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15
Q

Markers of cholestasis in addition to cholestatic enzymes that are present on a routine chem panel:

Not on a routine chem panel

A

On routine chem panel

  • Bilirubin
  • Cholesterol

Not on routine chem panel

  • Bile acids
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16
Q

Definition of cholestasis:

Types of cholestasis:

A

Def:

  • impaired biliary flow occuring between hepatocytes and duodenum

Intrahepatic

  • canaliculi and hepatic biliary duct flow affected

Extrahepatic

  • gall bladder and common bile duct flow affected
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17
Q

Liver function tests on routine biochem panel:

A
  • Exretory:
    • bilirubin
  • Synthetic:
    • albumin
    • urea (BUN)
    • cholesterol
    • glucose
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18
Q

How would liver function tests change with decreased liver function?

A

Bilirubin: High (excretory test)

Albumin: Low (synthesis test)

BUN: Low (synthesis test)

Cholesterol: Low (synthesis test)

Glucose: Low (synthesis test)

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19
Q

Additional liver function tests not on routine biochem panel:

A
  • Bile acids
  • ammonia
  • coagulation factors
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20
Q

Categories of hyperbilirubinemia:

A
  • Pre-hepatic: mostly unconjucated
  • Hepatic: conjugated + unconjugated
  • Post-hepatic: mostly conjugated
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21
Q
  1. Cause of pre-hepatic hyperbilirubinemia in all species:
  2. Horses:
A
  1. hemolytic anemia
  2. fasting
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22
Q

Significance of positive urine bilirubin test:

A
  • Dog: small amounts can be common in concentrated urine
  • Cat: ANY bilirubin is significant
    • higher renal threshold for bilirubin
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23
Q

Conditions that cause increase bile acids:

A
  • Portosystemic shunts
  • Hepatocellular disease
24
Q

Breed specific issues with bile acid measurements:

A
  • Healthy maltese dogs can have elevated bile acids
25
Diseases causing increase in ammonia:
* Hepatocellular disease (dec uptake) * Hepatic vascular shunts (PSS) * Urea cycle disorders (rare) * Urea toxicosis in ruminants
26
Sample collection for ammonia testing
* put on ice immediately * send with control normal sample * in vitro generation of ammonia can falsly increase
27
CBC and biochem panel changes with pancreatitis
* CBC * neutrophilia with left shift +/- toxicity * lymphopenia * eosinopenia * Chem * hypercholesterolemia * inc ALT * inc ALP * hyperbilirubinemia * hypocalcemia * hyperglycemia
28
Amylase
* produced by pancreatic acinar cells * cleared by kidney * increased in pancreatic disease * inflammation * trauma * necrosis * neoplasia * renal failure * severe dehydration * greater than 3 fold increase usualy from pancreatitis
29
Lipase
* produced by pancreatic acinal cells * many other sources * cleared by the kidney * increase greater than 3 fold =\> likely pancreatic disease * decrease =\> EPI (exocrine pancreatic insufficiency)
30
Canine: spec cPL canine pancreatic lipase
* 0-200 NRI * 201-399 questionable range * \> 400 consistent wtih pancreatitis
31
feline spec fPL feline pancreatic lipase
* \< /=3.5 unlikely animal has pancreatitis * 3.6-5.3 cat may have pancreatitis * \>/= 5.4 consistent with pancreatitis
32
SNAP cPL/fPL test
* qualitative * spot lighter than reference spot =\> normal * spot same color as reference spot =\> elevated * Spot darker than reference spot =\> consistent with pancreatitis
33
Triaditis
* Inflammatory process in cats involving * liver-cholangiohepatitis * pancreas-pancreatitis * small intestine-inflammatory bowel disease
34
Maldigestion
* not enough digestive enzymes from pancreas to breakdown food * EPI (Exocrine pancreatic insufficiency)
35
Malabsorption
* GI or GI lymphatic disease
36
CBC and biochem changes with EPI
* CBC * often normal * +/- normocytic, normochromic anemia (chronic dz, not inflammatory dz) * Chemistry * often normal * +/- low cholesterol * hyperglycemia * mild to moderate inc ALT and ALP
37
TLI
* serum trypsin like immunoreactivity * Dogs: * below 2.5 ug/L diagnostic for EPI * Cats: * below 8.0 ug/L diagnostic for EPI
38
Differentials for PLE/Malabsorptive disease
* IBD (inflammatory bowel disease) * triaditis in cats * Lymphagiectasia (dogs only) * Pythiosis (dogs only) * GI histoplasmosis
39
CBC and biochem changes with PLE
* CBC =\> normal * Chem * High BUN/Creat with pre-renal azotemia * Low TP * low albumin * low globulins * low cholesterol * low Ca * high/low Na * Low K * high/low Cl * high or low TCO2 \* Na, CL =\> high if pure water loss by GI \* Na, Cl =\> low if isotonic fluid or NaCl rich fluid loss by GI tract \* TCO2 =\> high if selective loss of HCl-upper GI disease \* TCO2 =\> low if losing bicarb in diarrhea
40
Folate
* In food * Produced by bacteria * absorbed in proximal SI
41
Cobalamin
* In food * absorption decreased by bacteria * absorbedin duodenum and ileum
42
Cobalamin and folate panels
* id need for supplementation * id bacterial overgrowth * help localize GI dz
43
Folate/Cobalamin panel * EPI * Bact overgrowth * Prox SI disease * Distal SI disease * Diffuse SI disease
44
Fecal Alpha1-Proteinase Inhibitor
* Plasma protein lost in GI lumen when mucosal intestinal integrity is compromised * useful when PLE suspected * \>/=21 is abnormal =\> PLE
45
Other helpful modalitis besides lab data for dx of pancreatitis or PLE
* Serum cobalamine and folate
46
Common clinicopathologic abnormalities seen in hypothyroidism
* CBC * mild, regenerative anemia * codocytes (target cells) * Chem * fasting hypercholesterolemia * fasting hypertriglyceridemia
47
Common clinicopathologic abnormalities seen in hyperadrenocorticism
* CBC * may have mild elevation in PCV * +/- stress leukogram * +/- thrombocytosis * Chem * inc ALP (dog only) * inc ALT * inc cholesterol * inc fasting blood glucose (cortisol =\> insulin resistence) * U/A * proteinuria * UTI * Dilute urine (cortisol =\> blocks ADH)
48
Common clinicopathologic abnormalities seen in hypoadrenicorticism
* CBC * mild to moderate anemia * inc PCV if dehydrated * lack of stress leukogram in sick patient (should see leukopenia but don't) * relaxed leukogram * Chem * azotemia * low Na, high Cl * high K * hypoglycemia * hypocholesterolemia * hypercalcemia * dec Na to K ration (\<24) * U/A * USG low even if dehydrated * chronic hyponatremia causes medullary washout
49
Common clinicopathologic abnormalities seen in diabetes mellitus
* CBC * normal if uncomplicated * an inflammatory leukogram indicates underlying dz * Chem * hyperglycemia * hypercholesterolemia * elevated ALP * marked inc think diabetes + hyperadrenocorticism * elevated ALP * U/A * glucosuria * inappropriately concentrated urine for dehydration * +/- ketonuria * +/- UTI
50
causes of Hypercholesterolemia
* Diabetes Mellitlus * Hyperadrenocorticism * Hypothyroidism * Cholestasis * Pancreatitis * Nephrotic syndrome * Post prandial (mild inc) * Breed related (Schnauzer/others)
51
Causes of hypocholesterolemia
* Malabsorption/maldigestion * Dec liver function of failure * Hypoadrenocorticism
52
Conditions other than kidney disease that could result in azotemia and dec urine concentrating ability
* Inhibition of ADH * Hypercalcemia * Hypercortisolemia * medullary washout (not enough solute ie Na in renal medulla to move water back inside) * liver failure/dec function (low urea) * Hypoadrenocorticism (low Na) * Osmotic diuresis (tubules have ton of solute so water doesn't move back inside) * diabetes mellitus
53
Important sources for enzymes * Creatine Kinase (CK) * Aspartate aminotransferase (AST) * Alanine aminotransferase (ALT) * Sorbitol Dehydrogenase (SDH) * Alkaline Phosphatase (ALP) * Gamma glutyltransferase (GGT)
54
**Hypocholremic metabolic alkalosis with paradoxical aciduria** **NAVLE**
* Upper GI dz (LDA) * dehydration (not drinking) * hypokalemic (not eating) * loss of HCl (Cl sequestered in stomach) * leads to metabolic alkalosis * Dehydration leads to * RAAS activation =\> Cl resporption & K excretion * Loss of HCl leads to * metabolic alkalosis =\> alkaline urine \*sequestered Cl=\> resportion of bicarb instead of Cl =\> paradoxical acid urine \*hypokalemia =\> can't excrete K =\> H+ excretion which exacerbates the condition
55
Hypercalcemia Causes GOSHDARNIT
* G: Granulomatous * O: Osteolysis * S: Spurious * H: Hyperparathyroidism (Primary) * D: Vitamin D Toxicosis * A: Addison's; Age * R: Renal Disease * N: Neoplasia * I: Idiopathic * T: Temp =\> Hypothermia
56
If proteins decrease (ie: hypoalbuminemia or liver failure) the anion gap....
Decreases
57
Decreased bicarb causes
* diarrhea (Cl inc to compensate =\> normal anion gap) * titrated (bound up by acids =\> inc anion gap)

Clin path test 4 (9 decks)

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