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110 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Three basic types of hepatic disease processes
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Hepatocellular disease/damage
Biliary disease (cholestasis) Hepatic insufficiency |
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Increased: AST, ALT
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Hepatocellular damage
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Increased: ALP, cholesterol
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Steroid excess
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Increased: AST, ALT
Decreased: T. Protein, Albumin, Cholesterol, BUN |
Hepatocellular damage
Hepatic insufficiency |
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Increased: ALP, bilirubin, cholesterol
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Cholestasis
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Increased: AST, ALT, ALP, bilirubin, globulin, cholesterol
Decreased: Glucose, T. protein, albumin, BUN |
Hepatocellular damage
Hepatic insufficiency Cholestasis |
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Decreased: Glucose, T. protein, Albumin, cholesterol, BUN
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Hepatic insufficiency
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Renal failure
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Kidney function is inadequate to maintain health
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Impaired renal function
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Loss of functional nephrons
Characteristic lab abnormalities Clinical signs |
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Azotemia
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Excess nonprotein nitrogen
(BUN and creatinine) |
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Uremia
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Clinical signs related to renal failure
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Examples of pre-renal azotemia
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Dehydration
Hypovolemia |
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Examples of renal azotemia
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Renal failure (acute or chronic)
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Examples of post-renal azotemia
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Urinary obstruction
Uroabdomen |
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Classic pattern for renal failure
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Azotemia
Inadequately concentrated urine |
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Adequate concentrations for dogs, cats, horses, and cattle
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Dogs >1.030
Cats > 1.040 Cattle & Horses > 1.025 |
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Functional reserve of kidneys
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Large (>50%)
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__________ are _________ markers of renal disease
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Azotemia and impaired concentrating ability are insensitive and nonspecific markers of renal disease
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Markers of renal GFR
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Urea nitrogen, creatinine, phosphorus
Serum concentrations increase as GFR decreases |
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Cause of azotemia with Addison's
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pre-renal (dehydration)
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End-stage or acute renal failure findings
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oliguric/anuric
hyperkalemia |
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oliguric/anuric
hyperkalemia |
End-stage or acute renal failure
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Chronic/early renal failure findings
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Polyuria
Hypokalemia |
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Polyuria
Hypokalemia |
Chronic/early renal failure
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Horses with renal failure
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Often hypercalcemic and HYPOPHOSPHATEMIC
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Differentials for urine discoloration
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Hemoglobin
Myoglobin Hematuria (RBC's) Bilirubin |
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Provides information about concentrating ability
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Specific gravity
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Provides information about glomerular permeability
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Urine protein
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Basic components of a urinalysis
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Description of time and method of collection and storage
Description of gross appearance and odor Specific gravity Urine biochemistry -pH, glucose, ketones, protein, heme, bilirubin, etc. Microscopic examination -RBC's, WBC's, epithelial cells, casts, bacteria, crystals, lipid |
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Hyposthenuria
Isosthenuria Hypersthenuria |
<1.007
1.007-1.013 >1.013 |
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Reliable and unreliable urine dipstick tests
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Reasonably accurate: Glucose, bilirubin, ketones, protein
Unreliable: pH, specific gravity, leukocytes Very sensitive: Blood/heme Of little clinical value: Urobilinogen Nitrite |
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Feline SG measurement on human refractometer: 1.023
Actual SG? |
1.019
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If not temperature compensated, how are SG measurements affected on a refractometer?
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Underestimates SG at temps >68F
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Correction of SG for proteinuria
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1g/dL protein adds 0.003-0.005
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Correction of SG for glycosuria
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1g/dL glucose adds 0.004-0.005
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Platelet lifespan
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1 week
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Ability to measure a substance of interest and only that substance
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Analytical specificity
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Specificity- definition
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Ability to measure a substance of interest and only that substance
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Detection limit definition
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Smallest possible concentration (quantity) of a substance (analyte) That can be detected with reasonable certainty
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Consistently giving results that are higher or lower
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Constant bias
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Two tests agree well at low analyte concentrations but agree less well at higher concentrations
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Proportional bias
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What determines a properly validated test?
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Random error is not large enough to impact clinical decision-making (will always be present)
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Can have high correlation without
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Agreement
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When will a glucometer reading and chemistry analyzer results be similar
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At glucose concentrations between 70 and 250mg/dL
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Reference interval definition
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Lower and upper reference limit
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Large animal cholestatic marker
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GGT (Gamma-glutamyltransferase)
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Why is GGT not measured in dogs and cats?
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Typically parallels the activity of ALP
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Why is shit brown?
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Stercobilinogen
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Rate-limiting step of Bilirubin metabolism
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Conjugated bilirubin going from hepatocyte into biliary tract
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How does bilirubin circulate in the blood?
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Bound to albumin
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Steps in bilirubin metabolism taking place in macrophage
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Hemoglobin from RBCs broken down into Heme and protein
Heme converted to biliverdin (green) Biliverdin converted to unconjugated bilirubin (orange) |
n/a
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Steps in bilirubin metabolism taking place in the hepatocyte
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Albumin leaves, unconj. bilirubin enters hepatocyte
Bilirubin conjugated (to conjugated bilirubin) |
n/a
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ALT sources
1/2 life |
Hapatocytes
Muscle (very minor) Cytosol Inducible |
2-3 days (dogs)
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AST sources
1/2 life |
Hepatocytes
Myocytes Erythrocytes Cytosol and mitochondria |
<1 day (dogs)
7-8 days (horse) |
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SDH sources
1/2 life |
Hepatocytes (large animals)
Leakage from cytosol |
<12 hours (horse)
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GDH sources
1/2 life |
Hepatocytes (Birds)
Leakage from cytosol and mitochondria |
????
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ALP sources
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Hepatocytes and biliary cells
Bone Placenta |
~3 days (dogs)
<8 hours (cats) |
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GGT sources
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Hepatocytes and biliary cells (large animals)
Mammary Synthesis from cell membranes |
~3 days (horse)
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CK sources
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Myocytes
Leakage from cytosol |
<2 hours (dogs)
~2 hours (horses) |
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LDH
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Lactate dehydrogenase
Hepatocytes Myocytes Erythrocytes Not used (very non-specific) |
<6hr (dogs)
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Sign of resolution of myocyte insult
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Persistently high serum AST activity with normalizing CK
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ALP in cats vs. dogs
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Cats have lower hepatic ALP activity and shorter 1/2 life
Therefore less sensitive but more specific in cats (9/10 with inc. ALP have current cholestasis) |
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Action and timeline of corticosteroids and ALP
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Only in dogs
Endogenous (Cushing's) or exogenous GC's and anticonvulsants (primidone and phenobarbital) induce production of L-ALP --> inc. serum levels in a few days Induces production of C-ALP after ~1 week (later than L-ALP) |
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Normal contribution of C-ALP to total ALP
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~10-30% (only found in DOGS)
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Magnitude of response of ALP to steroids
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Total ALP (C-ALP and L-ALP) may be <2x to >20x URL
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Scottish Terriers
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Have higher ALP activities (1350 U/L, compared to 230U/L in control dogs)
Not related to disease |
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When is proteinuria an abnormal finding?
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Always
Except in dogs with specific gravity >1.019; may be trace to +1 on dipstick |
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Reasons for increased ALP
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Intrahepatic and posthepatic cholestasis (Accumulation of bile acids promotes L-ALP synthesis in hepatocytes and biliary epithelial cells)
Glucocorticoids-Dogs Anticonvulsants-Dogs Endogenous corticosteroids-Dogs Young, rapidly growing animals (B-ALP) Lytic or proliferative bone lesions (osteosarcoma, osteomyelitis) Fracture healing (B-ALP) Hyperparathyroidism (active bone reabsorption) (B-ALP) Hyperthyroid cats (B-ALP and L-ALP) P-ALP Scottish Terriers |
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ALP in hyperthyroid cats
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Typically <4xURL
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Reasons for increased P-ALP
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Only in late-term pregnant cats (mild increase)
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Renal tubular damage and GGT
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Increase in urine GGT, but no effect on serum GGT
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Causes of hypernatremia
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Water deficits
-Inadequate intake (Deprivation, defective thirst response in hypothalamus) -Pure loss (Panting, hyperventilation, fever, diabetes insipidus) -H2O loss>Na loss (Renal osmotic diuresis, osmotic diarrhea, phosphate enemas, paintball toxicosis) Na excess (Salt poisoning, Administration of hypertonis saline or sodium bicarbonate) Decreased renal excretion (Hyperaldosteronism) |
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Sodium levels with vomiting
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Normonatremic, or hyponatremic
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Sodium levels with diarrhea
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Normonatremic, or hyponatremic
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Causes of normonatremia/hyponatremia with edema or transudate
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Congestive heart failure
Hepatic cirrhosis Nephrotic syndrome |
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RBC metabolism
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Rely on glycolysis for energy (no organelles = no mitochondria)
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RBC lifespan
Dogs, cats, horses, cattle, humans |
Dogs- 100 days
Cats- 70 days Cows & Horses- 150 days Humans- 120 days |
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Colloidal osmotic pressure
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Caused by large molecules (proteins, mostly albumin)
Opposes exit from VASCULAR SYSTEM |
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Extracellular (Serum) Osmolality
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Electrolytes and small molecules (glucose, urea)
Changes cause shifts between ECF and ICF |
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Measuring total protein
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Biuret method-detects peptide bonds, highly specific, 1-10 g/dL
Precipitation and dye binding methods, quantify small amounts of protein (mg/dL) in urine and CSF Refractometry- Changes in refractive index; 1-10 g/dL, Lipemia and Hemolysis may interfere |
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Bromcresol green
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Most used way to measure albumin in veterinary medicine
Not reliable in birds and reptiles |
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Bromcresol purple
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Accurate in humans but inaccurate in animals
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Proteins in acute phase reaction
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Increased: Alpha and beta globulins, fibrinogen, serum amyloid A (SAA), C-reactive protein (dogs)
Decreased: Albumin, Transferrin |
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Proteins in chronic inflammation
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Increased within 1-3 weeks after onset of inflammation
Increased: Gamma immunoglobulins (IgG), complement (C3); polyclonal gammopathy |
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Hypofibrinoginemia
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DIC (fibrinogen consumed)
Congenital deficiency (rare) Manifest as bleeding |
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Endotoxic shock effect on RBCs
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Hemoconcentration resulting in erythrocytosis
From fluid shifting from intravascular space to extravascular space |
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Secondary appropriate erythrocytosis
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Right-to left shunts (hypoxia)
Pulmonary disease (hypoxia) Hyperthyroidism (inc. tissue demand) |
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Primary erythrocytosis
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Polycythemia vera
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Secondary inappropriate erythrocytosis
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Renal lesions (neoplasia, cysts, etc.) secreting Epo.
Extra-renal lesions secreting Epo |
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Non-pathologic erythrocytosis
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Breed variations- Thoroughbreds, greyhounds
Physiologic-Altitude, training Doping Idiopathic |
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Absolute reticulocyte concentration reference interval
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<80,000
<60,000 in cats |
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Horse erythrogram
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Won't see reticulocytosis
May see macrocytos, but only in hemolytic cases |
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Level of anemia with different conditions
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Marrow increases erythroid component 2-3x with blood loss and 6-8x with hemolysis
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Findings associated with hemolytic anemias but not with blood loss anemias
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Poikilocytosis (schistocytes, spherocytes) or inclusions (Heinz bodies, organisms)
Neutrophilic leukocytosis (presence of immunocomplexes stimulates inflammation) Higher degree of reticulocytosis (iron rapidly recycled) Splenomegaly (Splenic macrophage hyperplasia) |
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FeLV is a risk factor for what?
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Myelodysplastic syndrome (MDS)
Less than 20-30% blasts in the bone marrow Cytopenia of more than one cell line |
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Stress-induced neutrophil response
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Increased marrow release
Shift from MNP to CNP Decreased emigration into tissues |
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Neutrophilia-acute vs. chronic inflammation
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Acute- Marrow release exceeds tissue emigration
Chronic-Increased marrow release, increased granulopoiesis, inc. tissue emigration |
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chronic myeloid leukemia diagnosis
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Done by ruling out other differentials
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Extreme neutrophilia- magnitude and differentials
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Dogs >50,000; cats >30,000
Pyometra, pyothorax Hemolytic diseases (esp. IMHA) Hepatozoon americanum G-CSF or GM-CSF secreting tumor Granulocytic leukemia Leukocyte adhesion deficiency |
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Eosinophilia differentials
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Parasitism
Allergic/hypersensitivity reactions Paraneoplastic Mast cell tumor Addison's Leukemia Idiopathic |
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Eosinopenia differentials
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Corticosteroid-induced
Physiologic response Acute inflammation Not very diagnostically significant |
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Lymphocytosis differentials
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Chronic inflammation
Physiologic response Addison’s Disease Persistent lymphocytosis of cattle Lymphoid leukemia |
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Lymphopenia differentials
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Corticosteroid-induced
Acute inflammation Depletion Lymphoid hypoplasia or aplasia |
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Monocytosis differentials
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Inflammation-acute and chronic
Corticosteroid- or Stress-induced Neoplasia (monocytic leukemia) Secondary to neutropenia |
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Broad categories of neutropenia etiologies
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Excess tissue demand
Sequestration- Endotoxin (margination), Pseudoneutropenia Decreased granulopoiesis- Cancer therapies, viral/rickettsial infxns, estrogen Ineffective granulopoiesis- viral infxns and myelodysplastic syndromes Peripheral destruction-immune-mediated |
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Cutoff for IMT
Cutoff for DIC |
Platelets <20,000/uL
Platelets decreased but >50,000/uL |
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Triad of findings for DIC
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Thrombocytopenia
Prolonged coagulation time Decreased fibrinogen/increased fibrin degradation products (FDP's, D-dimer) |
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Causes of IMT
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Primary- Idiopathic (more in young-middle aged bitches)
Secondary- Drugs, infection (FeLV, A. platys), neoplasia, vaccination? |
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DIC is ALWAYS secondary to another disease. Which ones?
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Neoplasia
Sepsis Endotoxemia Shock Heat stroke Intravascular hemolysis Obstetrical complications |
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Causes of increased platelet COMSUMPTION
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DIC, vasculitis (RMSF, immune-mediated)
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