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Clin path test 4 > Clinical Chemistry notes > Flashcards

Clinical Chemistry notes Flashcards

1
Q

Red top vacutainer

A
  • no anticoagulant
  • silica particles
  • don’t use for urinalysis/CSF
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2
Q

Tiger Top

A
  • Clot-separator gel
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3
Q

Green top tube

A
  • heparinized
  • used when tests needed STAT (susp hyperkalemia, hypoglycemia)
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4
Q

Purple top, KEDTA

A
  • chelates cations
  • falsely lowers activity of certain enzymes
  • falsely low Ca, Mg
  • falsely inc K
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5
Q

Lysis of cells

A
  • releases
    • AST
    • LDH
    • Magnesium
    • Phophorus
    • Potassium
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6
Q

Leakage of enzyme

A
  • Fragmentation of peripheral cytoplasm
  • Cell necrosis
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7
Q

Induction of enzyme synthesis

A
  • Pathologic stimuli
  • Proliferation of cells
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8
Q

Cause of inc enzyme activity in serum after tissue injury

A
    1. Leakage
    1. Induction
    1. Dec in activation, clearance or excretion
    1. Absorption of maternal enzymes from colostrum
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9
Q

When the number of cells which are the cource of enzyme is markedly decreased

A
  • enzymatic activity can eventually decline
  • e.g. cirrhosis
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10
Q

Enzyme inhibitors

A
  • released during tissue injury
  • can dec activity measured by analyzier
  • e.g acute pancreatitis inhibits
    • amylase and lipase
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11
Q

Immunoassays not affected by inhibitors

A
  • TLI
  • PLI
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12
Q

No clnical significance attached to …

A
  • low enzyme activity
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13
Q

Laboratory detection of muscle disease

A
    1. Trauma
    1. Exertion
    1. Degenerative myopathies
    1. Inflammation
    1. Nutritional myopathies
    1. Ischemic myopathies
    1. Metabolic myopathies
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14
Q

Increases in serum/plasma activity correlates with

A
  • number of myocytes injured
  • NOT type of injury (mild, reversible/irreversible)
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15
Q

Creatine kinase (CK)

A
  • Tissue sources:
      1. skeletal muscle (card. m., s.m., brain)
  • Half life
    • about 2 hours
  • Clnical applications
    • inc specific and sensitive for m. damage
    • inc can be > 20X RI
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16
Q

Aspartate aminotransferase (AST)

A
  • Tissue source
    • most tissues
    • hepatocytes
    • skeletal and cardiac muscle
    • erythrocytes
  • Half-life
    • < 1 day in small animal
    • 7 days in large animals
  • Clincal applications
    • Inc AST and CK = myopathies
    • Inc AST and Normal CK = suggestive of liver disorder/resolved muscle inj
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17
Q

Lactate dehydrogenase (LDH)

A
  • Tissue source
    • skeletal and cardiac muscle
    • liver
    • kidney
    • erythrocytes
    • leukocytes
  • Half life
    • not useful
  • Clinical applications
    • little utility: non-specific
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18
Q

Inc activity of ALT

A
  • rare
  • specific for hepatocellular leakage
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19
Q

Myoglobin

A
  • small, monomeric protein found in muscle
  • rapidly excreted in urine
  • myoglobinemia rarely observed
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20
Q

Positive hemoglobin rxn in urine is myoglobin if

A
    1. absence of hematuria
    1. absence of conditions that would lyse erythrocytes in urine
      * high pH low SG
    1. absence of hemolytic anemia and hemoglobinemia
    1. presence of myopathy (INC CK activity)
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21
Q

Natriuretic peptides

A
  • made/released by cardiac muscle in reponse to inc stretch
  • Counter-act renin-angiotensin system
  • NT ProBNP measured
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22
Q

Lab detection of hepatocellular disease and their causes

Hepatocellular injury

A

Causes

  • hypoxia
  • toxins
  • inflammation
  • abscesses
  • lipidosis
  • neoplasm
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23
Q

Lab detection of cholestasis and causes

A
  • hepatocellular swelling
  • neoplasm
  • inflammation
  • cholelith
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24
Q

Causes of Dec hepatic function

A
  • congenital/acquired shunts
  • chronic hepatic dz
    • dec synthesis
    • dec excretion
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25
Hepatic tests allow clinicians to
* Detect presence of lesions/disease in liver * Localize disease to hepatocellular and/or cholestatic * severity of dz and prognosis with hepatic function tests * Monitor progression/resolution of dz and response to therapy
26
Best indicator of ongoing hepatocellular injury
increasd activity of hepatic cytosolic enzymes
27
Magnitude of increased activity of enzyme correlates with
**Number** of hepatocytes injured **not severity** (reversible/irreversible)
28
Alanine aminotransferarse (ALT)
* Tissue sources * hepatocytes * skeletal/cardiac muscle cats and dogs * half life * 2-3 days in dogs * Clinical applications * very sensitive and specific indicator of hepatocellular injury * Not sensitive in horses, ruminants and pigs
29
AST must be analyzed with
* ALT in small animals * CK in all species \*hemolysis (real or from sample collection) will inc AST activity
30
Sorbitol dehydrogenase (SDH)
* Tissue sources * hepatocytes of all species * Half-life * 4 hours in dogs * Clinical application * prim used in large animal
31
Intrahepatic cholestasis
* Canicular or ductular bile flow impeded w/in liver by * swollen hepatocytes * inflammatory/neoplastic cell infiltrates
32
Differentiating between the two types of cholestasis
* cannot be done with lab tests * must use imaging, bx, etc
33
Alkaline phosphatase (ALP)
* Tissue source * all tissues * membranes of hepatocytes (Canalicular surface) * Osteoblasts * biliary epithelium * Half-life * varies with tissue isoforms/species * Clinical application * cholestasis * glucocorticosteroids in dogs * Drug induction dogs * young animals * hyperplasia/neoplasm * colostrum * mammary neoplasm
34
cholestasis | (All species)
* ALP increases most dramatic in dogs * higher hepatic production * longer ALP half life * Cats * shorter half-life * **minimal increases over RI are clincally significant**
35
Hepatic lipidosis in cats
* Causes bigger increase in ALP than cholangiohepatitis
36
ALP:GGT
* most useful in cats * distinguishes between hepatic lipidosis and cholangiohepatitis
37
ALP and Glucocorticosteroids in dogs
* Hyperadrenocorticism and exogenous cortisol inc specific ALP isoform * half life: 3 days **in the dog** * ALP inc occurs 5-10 days after exogenous administration and persists 2 to 4 weeks
38
ALP and Non-steroidal drug induction in dogs
* Phenobarb induces synthesis of hepatic isoenzyme ALP * differentiate from cholestasis
39
Young animals and ALP | (\< 1 to 1.5 yrs old)
* inc in ALP * synthesis of bone ALP isoform by osteoblasts * occurs in all species
40
hyperplasia or neoplasia and ALT
* 2-3 X normal inc with * osteosarc * fracture healing * excessive periosteal bone proliferation * cats with hyperthyroidism
41
ALP and colostrum ingestion
* Puppies and kittens * occurs some in calves **not in foals**
42
Gamma glutamytransferase (GGT)
* Tissue Source * All tissues * **cell membranes of biliary epithelium** * **cell membranes of pancreas** * **renal tubular epthelial cells** * **​**Half life * 3 days in dogs and horses * Clinical application * cholestasis * colostrum ingestion * drug induction
43
GGT and renal tubular necrosis
* Can be detected by inc GGT in urine not in **serum**
44
GGT and cholestasis
* GGT more specific than ALP in all species (fewer tissue sources) * GGT more sensitive than ALP * cats * ruminants * horses * DOG: ALP MORE SENSITIVE INDICATOR OF CHOLESTASIS THAN GGT
45
Cats and GGT
* More sensitive indicator of cholangiohepatitis
46
Horses and GGT
* inc GGT associated with right dorsal displacement of large colon * compression of bile duct = extrahepatic cholestasis
47
when assessing cholistasis
* better to have both ALP and GGT to assess cholestasis
48
GGT and colostrum
* inc in neonatal calves and puppies only
49
Evaluating decreased hepatic excretory function
* bilirubin * bile acids ammonia
50
Bile Acids
* function as detergents * essential for intestinal absorption of lipids and hepatic excretion of cholesterol * metabolism * hepatocellular synthesis from cholesterol * conjugated by hepatocytes =\> inc water solubility * Excreted into bile (Most stored in gall bladder * cholecystokinin stimulated contraction of gall bladder (ind by fat) * Intestinal absorption in Ileum, entry into portal veins * 90% first pass metabolism cleared from portal blood by hepatocytes
51
Indications for bile acid analysis Procedure
* when routine hepatic tests (enzyme and function) are normal * dog/cat * 2 serum/plasma samples collected after 12 hour * 1 tube after 8-12 hour fast * 1 tube after feeding small portion canned maintenance \*horses aren't fasted =\> can inc bile acids
52
Hepatic causes of inc serum/plasma bile acids
Sensitive and specific in dogs/cats/horses/cattle for * Portosystemic vascular shunts * dec clearance since portal circulation bypasses liver * Hepatocellular disease * decreased hepatocellular uptake of bile acids from portal blood * Cholestasis * dec excretion of bile acids/regurgitation
53
Maltese dogs and bile acids
* often have fasting and post-prandial bile acid concentrations 2-4 X higher than normal
54
Inc fasting bile acid conc and post prandial normal bile acid
* Not clinically significant
55
If you suspect a falsly low concentration of bile acids in a liver dysfunction patient
run an ammonia test
56
Bilirubin
* classical test of hepatic function * less sensitive than bile acid tests * liver has excess capacity to uptake and metabolize bilirubin
57
Bilirubin metabolic pathway
* Originates as degradation of heme from hemoglobin by macrophages * unconjugated bilirubin (water soluble) produced by macs, transported to liver in blood bound to albumin * hepatocytes uptake bilirubin * bilirubin conjugated to glucuronides/glucose in horses to make it water soluble * bilirubin excreted into canaliculi * Once secreted intestinal bacteria convert conjugated bilirubin to metabolites * urobilinogens/stercobilin
58
Lab tests for serum bilirubin a. total bilirubin b. bilirubin splits c. urinary bilirubin
* total bilirubin: * conjugated + unconjugated * available on routine panels * bilirubin splits * don't do at UF * Total bilirubin - direct bilirubin = indirect * Urinary bilirubin * bilirubinuria precedes bilirubinemia * In most animals some bilirubinuria is normal * **cats: bilirubinuria always indicates abnormality** * higher renal threshold for bilirubinuria
59
Interpretation of higher unconjugated bilirubinemia
* Pre-hepatic * fasting horses * anorexia/fasting equine hepatocytes less efficient at uptake of uncon bili * hemolytic anemias **(esp extravascular hemolysis)** * Inc internal blood-loss into body cavities (rare) * Congenital deficiency of enzyme/receptor required for hepatocellular uptake/conjugation
60
Interpretation of higher conjugated bilirubinemia
* Considered hyperbilirubinemia when \> 50% of total is conjugated/horses: \> 25% is conjugated * more specific for hepatic dz, not considered **sensitive** * Cholestasis * higher percentage of conjugated, \> likelihood of extrahepatic cholestasis * dogs only: inc ALP, GGT occurs before hyperbilirubinemia from cholestasis * horses/cattle: less likely to dev w/ obstructive cholestasis * Sepsis * inflammatory cytokines (TNF, IL-6) inhibit hepatic excretion conj bili by hepatocytes * dogs and cats with extra-hepatic bacterial infection * no liver lesion present =\> functional cholestasis * mild to no change in ALP or GGT * Congenital deficiency of enzyme required for hepatocellular excretion of conj bili
61
Interpretation of Mixed hyperbilirubinemia
* hepatocellular dz * dec exretion conj bili + hepatocel swelling = intrahepatic cholestasis * hepatocytes fail to uptake bilirubin =\> unconjucated bili also present * chronic hemolytic anemia * anemia induced hypoxia causes liver dysfunction * excretion of conjugated bili is compromised
62
BIlirubin splits utility
* Only useful in horses * determines if anorexia is causing inc unconjugated bilirubin * chronic liver dz and hemolytic anemia cause inc in both conj and unconj * Can also use PCV/Retics to tule out hemolytic anemia as cause of hyperbilirubinemia * other tests can be used to detect hepatobiliary dz
63
Ammonia normal metabolism
* produced by bacterial deamination of amino acids prom protein in intestines * absorbed in intestines and enters portal circulation * hepatocytes uptake ammonia from blood and convert it to urea (urea cycle)
64
Hyperammonemia
* occurs in liver dz when 60% of liver functional mass lost * diminished hepatic clearance of portal vein ammonia * altered hepatic metabolism also leads to inc neurotoxic mediators * hepatic encephalopathy=\> ataxia, stupor, blindness
65
Ammonia assay procedure
* Tricky, ammonia can rapidly form in vitro after collection * heparinized blood sample should be immediately placed on ice back after collection * Plasma should be separated by centrifugation ASAP and assayed or frozed * control sample should be collected from a fasted healthy animal to rule out sampling handling error * **at UF: collect heparinized venous blood 8-12 hours after fast**
66
Causes of hyperammonemia
* 1. Decreased hepatocellular uptake * 2. Vascular shunts around liver (PSS) * 3. Congenital deficiency of urea-cycle enzumes * all other tests of liver function will be unremarkable so ammonia test is indicated * 4. Urea toxicosis/ammoniated forage toxicosis in ruminants
67
Main use of ammonia testing
* rule in/out hepatic encephalopathy * bile acids usually as good as a liver function test as ammonia * except rare disorders when bile acids would be WRI * urea-cycle enzyme deficiency * urea toxicosis * when bile acids not intestinally reabsorbed * liver dz with concurrent PLE
68
Decreased hepatic synthetic functions
* liver dz causes decreased plasma conc of proteins and urea * not specific or very sensitive for early detection * significant mass must be damaged first
69
Albumin
* short half life: 8-10 days * preserved function of hepatocytes * Hypoalbuminemia * secondary to liver dz occurs late in hepatic failure * must rule out other causes * inflammation * renal loss * intestinal loss * blood loss
70
Hyperglobulinemia and liver disease
* liver disease = dec Kupffer cells (macs in liver) * inc antigenic load from infection escapes liver clearance and contacts immune system * hyperglobulinemia from liver dz more likely in horses
71
Dec Albumin:globulin
can also occur with chronic inflammatory diseases
72
Urea
* dec synthesis of urea in liver dz manifested as decreased serum/plasma BUN * dec dietary protein also causes decreased blood urea * Dec urea can lead PU/PD =\> medullary washout and dilute urine
73
Hypocholesterolemia
* can occur secondary to liver failure (hepatocytes synthesize and control cholesterol)
74
Hypercholesterolemia
* when cholestasis cause by liver disease leads to decreased cholesterol excretion
75
Glucose
* liver disease is an unlikely cause of hypoglycemia * hyperglycemia possible * due to liver disease the decreases hepatic uptake of glucose
76
Coagulopathies
* Clotting factors synthesized in liver * liver dz =\> prolonged PT and PTT and hypofibrinogemia * Hepatocellular dz and bile duct obstruction can dec absorption Vit K * DIC likely in massive hepatic necrosis * thrombocytopenia, prolonged clotting, increased D-dimers and FDPs, decreased antithrombin * Lack of Kupffer cells * inc Fibrin Degradation Products (FDPs) * Thrombocytopenia * portal hypertension =\> inc splenic sequestration of platelets * hepatocytes primary source of thrombopoietin (stim platelet prod in marrow)
77
Pre-surgical work up to obtain liver biopsy
* coagulation tests indicated although clinical bleeding problems are uncommon in liver dz
78
Blue top
Na Citrate
79
Electrolytes Sample Collection
* Fasted serum sample separated from clot asap * red top tube: no anticoagulant * dec artifacts due to * postprandial lipemia (Calcium) * Leakage of intracellular components (potassium) * Heparinized plasma may be used * Green top: lithium heparin * **DO NOT USE** * Purple top: Potassium EDTA * Blue top: Sodium Citrate
80
Electrolyte artifacts due to K-EDTA
* INC potassium =\> from K in anticoagulant * Dec Divalent cations (Ca2+, Mg2+) =\> chelated by EDTA * Dec Bicarb =\> EDTA is acidic and titrates it out
81
Electrolyte artifacts due to Na-Citrate
* INC sodium =\> Na in anticoagulant * Dec divalent cations (Ca2+, Mg2+) =\> citrate chelates cations * Dec bicarb =\> citrate is acidic * Dec Cl =\> dilution due to excess anticoagulant

Clin path test 4 (9 decks)

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