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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
Q

Hepatic tests allow clinicians to

A
  • 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
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26
Q

Best indicator of ongoing hepatocellular injury

A

increasd activity of hepatic cytosolic enzymes

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27
Q

Magnitude of increased activity of enzyme correlates with

A

Number of hepatocytes injured not severity (reversible/irreversible)

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28
Q

Alanine aminotransferarse (ALT)

A
  • 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
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29
Q

AST must be analyzed with

A
  • ALT in small animals
  • CK in all species

*hemolysis (real or from sample collection) will inc AST activity

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30
Q

Sorbitol dehydrogenase (SDH)

A
  • Tissue sources
    • hepatocytes of all species
  • Half-life
    • 4 hours in dogs
  • Clinical application
    • prim used in large animal
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31
Q

Intrahepatic cholestasis

A
  • Canicular or ductular bile flow impeded w/in liver by
    • swollen hepatocytes
    • inflammatory/neoplastic cell infiltrates
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32
Q

Differentiating between the two types of cholestasis

A
  • cannot be done with lab tests
  • must use imaging, bx, etc
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33
Q

Alkaline phosphatase (ALP)

A
  • 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
Q

cholestasis

(All species)

A
  • 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
Q

Hepatic lipidosis in cats

A
  • Causes bigger increase in ALP than cholangiohepatitis
36
Q

ALP:GGT

A
  • most useful in cats
  • distinguishes between hepatic lipidosis and cholangiohepatitis
37
Q

ALP and Glucocorticosteroids in dogs

A
  • 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
Q

ALP and Non-steroidal drug induction in dogs

A
  • Phenobarb induces synthesis of hepatic isoenzyme ALP
  • differentiate from cholestasis
39
Q

Young animals and ALP

(< 1 to 1.5 yrs old)

A
  • inc in ALP
    • synthesis of bone ALP isoform by osteoblasts
    • occurs in all species
40
Q

hyperplasia or neoplasia and ALT

A
  • 2-3 X normal inc with
    • osteosarc
    • fracture healing
    • excessive periosteal bone proliferation
    • cats with hyperthyroidism
41
Q

ALP and colostrum ingestion

A
  • Puppies and kittens
  • occurs some in calves not in foals
42
Q

Gamma glutamytransferase (GGT)

A
  • 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
Q

GGT and renal tubular necrosis

A
  • Can be detected by inc GGT in urine not in serum
44
Q

GGT and cholestasis

A
  • 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
Q

Cats and GGT

A
  • More sensitive indicator of cholangiohepatitis
46
Q

Horses and GGT

A
  • inc GGT associated with right dorsal displacement of large colon
    • compression of bile duct = extrahepatic cholestasis
47
Q

when assessing cholistasis

A
  • better to have both ALP and GGT to assess cholestasis
48
Q

GGT and colostrum

A
  • inc in neonatal calves and puppies only
49
Q

Evaluating decreased hepatic excretory function

A
  • bilirubin
  • bile acids ammonia
50
Q

Bile Acids

A
  • 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
Q

Indications for bile acid analysis

Procedure

A
  • 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
Q

Hepatic causes of inc serum/plasma bile acids

A

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
Q

Maltese dogs and bile acids

A
  • often have fasting and post-prandial bile acid concentrations 2-4 X higher than normal
54
Q

Inc fasting bile acid conc and post prandial normal bile acid

A
  • Not clinically significant
55
Q

If you suspect a falsly low concentration of bile acids in a liver dysfunction patient

A

run an ammonia test

56
Q

Bilirubin

A
  • classical test of hepatic function
  • less sensitive than bile acid tests
    • liver has excess capacity to uptake and metabolize bilirubin
57
Q

Bilirubin metabolic pathway

A
  • 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
Q

Lab tests for serum bilirubin

a. total bilirubin
b. bilirubin splits
c. urinary bilirubin

A
  • 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
Q

Interpretation of higher unconjugated bilirubinemia

A
  • 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
Q

Interpretation of higher conjugated bilirubinemia

A
  • 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
Q

Interpretation of Mixed hyperbilirubinemia

A
  • 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
Q

BIlirubin splits utility

A
  • 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
Q

Ammonia normal metabolism

A
  • 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
Q

Hyperammonemia

A
  • 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
Q

Ammonia assay procedure

A
  • 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
Q

Causes of hyperammonemia

A
    1. Decreased hepatocellular uptake
    1. Vascular shunts around liver (PSS)
    1. Congenital deficiency of urea-cycle enzumes
      * all other tests of liver function will be unremarkable so ammonia test is indicated
    1. Urea toxicosis/ammoniated forage toxicosis in ruminants
67
Q

Main use of ammonia testing

A
  • 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
Q

Decreased hepatic synthetic functions

A
  • 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
Q

Albumin

A
  • 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
Q

Hyperglobulinemia and liver disease

A
  • 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
Q

Dec Albumin:globulin

A

can also occur with chronic inflammatory diseases

72
Q

Urea

A
  • 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
Q

Hypocholesterolemia

A
  • can occur secondary to liver failure (hepatocytes synthesize and control cholesterol)
74
Q

Hypercholesterolemia

A
  • when cholestasis cause by liver disease leads to decreased cholesterol excretion
75
Q

Glucose

A
  • liver disease is an unlikely cause of hypoglycemia
  • hyperglycemia possible
    • due to liver disease the decreases hepatic uptake of glucose
76
Q

Coagulopathies

A
  • 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
Q

Pre-surgical work up to obtain liver biopsy

A
  • coagulation tests indicated although clinical bleeding problems are uncommon in liver dz
78
Q

Blue top

A

Na Citrate

79
Q

Electrolytes Sample Collection

A
  • 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
Q

Electrolyte artifacts due to K-EDTA

A
  • INC potassium => from K in anticoagulant
  • Dec Divalent cations (Ca2+, Mg2+) => chelated by EDTA
  • Dec Bicarb => EDTA is acidic and titrates it out
81
Q

Electrolyte artifacts due to Na-Citrate

A
  • 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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