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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
Q

Diseases causing increase in ammonia:

A
  • Hepatocellular disease (dec uptake)
  • Hepatic vascular shunts (PSS)
  • Urea cycle disorders (rare)
  • Urea toxicosis in ruminants
26
Q

Sample collection for ammonia testing

A
  • put on ice immediately
  • send with control normal sample
  • in vitro generation of ammonia can falsly increase
27
Q

CBC and biochem panel changes with pancreatitis

A
  • CBC
    • neutrophilia with left shift +/- toxicity
    • lymphopenia
    • eosinopenia
  • Chem
    • hypercholesterolemia
    • inc ALT
    • inc ALP
    • hyperbilirubinemia
    • hypocalcemia
    • hyperglycemia
28
Q

Amylase

A
  • 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
Q

Lipase

A
  • 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
Q

Canine: spec cPL

canine pancreatic lipase

A
  • 0-200 NRI
  • 201-399 questionable range
  • > 400 consistent wtih pancreatitis
31
Q

feline spec fPL

feline pancreatic lipase

A
  • < /=3.5 unlikely animal has pancreatitis
  • 3.6-5.3 cat may have pancreatitis
  • >/= 5.4 consistent with pancreatitis
32
Q

SNAP cPL/fPL test

A
  • qualitative
  • spot lighter than reference spot => normal
  • spot same color as reference spot => elevated
  • Spot darker than reference spot => consistent with pancreatitis
33
Q

Triaditis

A
  • Inflammatory process in cats involving
    • liver-cholangiohepatitis
    • pancreas-pancreatitis
    • small intestine-inflammatory bowel disease
34
Q

Maldigestion

A
  • not enough digestive enzymes from pancreas to breakdown food
  • EPI (Exocrine pancreatic insufficiency)
35
Q

Malabsorption

A
  • GI or GI lymphatic disease
36
Q

CBC and biochem changes with EPI

A
  • 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
Q

TLI

A
  • serum trypsin like immunoreactivity
  • Dogs:
    • below 2.5 ug/L diagnostic for EPI
  • Cats:
    • below 8.0 ug/L diagnostic for EPI
38
Q

Differentials for PLE/Malabsorptive disease

A
  • IBD (inflammatory bowel disease)
  • triaditis in cats
  • Lymphagiectasia (dogs only)
  • Pythiosis (dogs only)
  • GI histoplasmosis
39
Q

CBC and biochem changes with PLE

A
  • 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
Q

Folate

A
  • In food
  • Produced by bacteria
  • absorbed in proximal SI
41
Q

Cobalamin

A
  • In food
  • absorption decreased by bacteria
  • absorbedin duodenum and ileum
42
Q

Cobalamin and folate panels

A
  • id need for supplementation
  • id bacterial overgrowth
  • help localize GI dz
43
Q

Folate/Cobalamin panel

  • EPI
  • Bact overgrowth
  • Prox SI disease
  • Distal SI disease
  • Diffuse SI disease
A
44
Q

Fecal Alpha1-Proteinase Inhibitor

A
  • Plasma protein lost in GI lumen when mucosal intestinal integrity is compromised
  • useful when PLE suspected
  • >/=21 is abnormal => PLE
45
Q

Other helpful modalitis besides lab data for dx of pancreatitis or PLE

A
  • Serum cobalamine and folate
46
Q

Common clinicopathologic abnormalities seen in hypothyroidism

A
  • CBC
    • mild, regenerative anemia
    • codocytes (target cells)
  • Chem
    • fasting hypercholesterolemia
    • fasting hypertriglyceridemia
47
Q

Common clinicopathologic abnormalities seen in hyperadrenocorticism

A
  • 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
Q

Common clinicopathologic abnormalities seen in hypoadrenicorticism

A
  • 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
Q

Common clinicopathologic abnormalities seen in diabetes mellitus

A
  • 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
Q

causes of Hypercholesterolemia

A
  • Diabetes Mellitlus
  • Hyperadrenocorticism
  • Hypothyroidism
  • Cholestasis
  • Pancreatitis
  • Nephrotic syndrome
  • Post prandial (mild inc)
  • Breed related (Schnauzer/others)
51
Q

Causes of hypocholesterolemia

A
  • Malabsorption/maldigestion
  • Dec liver function of failure
  • Hypoadrenocorticism
52
Q

Conditions other than kidney disease that could result in azotemia and dec urine concentrating ability

A
  • 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
Q

Important sources for enzymes

  • Creatine Kinase (CK)
  • Aspartate aminotransferase (AST)
  • Alanine aminotransferase (ALT)
  • Sorbitol Dehydrogenase (SDH)
  • Alkaline Phosphatase (ALP)
  • Gamma glutyltransferase (GGT)
A
54
Q

Hypocholremic metabolic alkalosis with paradoxical aciduria

NAVLE

A
  • 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
Q

Hypercalcemia Causes

GOSHDARNIT

A
  • 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
Q

If proteins decrease (ie: hypoalbuminemia or liver failure) the anion gap….

A

Decreases

57
Q

Decreased bicarb causes

A
  • 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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