NAVLE Study Guide

NAVLE Clinical Pathology High-Yield Guide: CBC, Chemistry, Urine

Clinical pathology questions on the NAVLE hand you a CBC, chemistry panel or urinalysis and ask what pattern it shows and what to do next. The patterns are finite: three leukograms, two kinds of anemia, three locations of azotemia, two families of liver enzymes, a short list of electrolyte signatures and a handful of endocrine and coagulation tests. This guide sets them out with the species differences and cut-offs that the exam uses, drawn from the Merck Veterinary Manual; where a number could not be verified, it has been left out so that you do not learn a wrong one.

Why Clinical Pathology Is High-Yield

Lab interpretation is embedded in almost every species block. A canine Addison's question is really a Na:K question; a feline CKD question is really a USG and creatinine question; an equine colic question hands you a peritoneal fluid analysis; a bovine ketosis question is a BHB question. Because the same patterns are tested across species, this material pays off in several blocks at once. And because image and data interpretation is part of the exam format (see the complete NAVLE guide), you will see actual lab tables in the stems, not just descriptions.

Complete Blood Count Patterns

The Three Leukograms

PatternNeutrophilsLymphocytesEosinophilsOtherTypical cause
Stress (glucocorticoid)Mature neutrophilia, no bandsLymphopeniaEosinopeniaMonocytosis in dogsEndogenous cortisol from illness, exogenous steroids, Cushing's
InflammatoryNeutrophilia with left shift (bands), toxic changeVariableVariableMonocytosis if chronicBacterial infection, tissue necrosis, immune-mediated disease
Physiologic (epinephrine)Mild mature neutrophiliaLymphocytosis (especially cats)NormalTransient, resolves in under an hourFear, excitement, exertion, the fractious cat at the clinic
  • Left shift: Increased band neutrophils. A regenerative left shift has more segmented neutrophils than bands with an overall neutrophilia; a degenerative left shift has bands equal to or exceeding segmented cells, usually with a normal or low total count, and signals that demand is outrunning marrow supply. Degenerative left shift carries a worse prognosis.
  • Gotcha: Cattle have a small neutrophil reserve, so acute severe inflammation presents as neutropenia with a degenerative left shift, and lymphocytes normally outnumber neutrophils. A persistent lymphocytosis in an older dog or cow raises lymphoma or bovine leukosis.

Regenerative Versus Non-Regenerative Anemia

  • Regenerative: Marrow responding to blood loss or hemolysis. Merck's thresholds: absolute reticulocytes above about 60,000/mcL in dogs and above 50,000 aggregate reticulocytes/mcL in cats, or a corrected reticulocyte percentage above 1%. Expect polychromasia, anisocytosis, increased MCV and nucleated red cells. Regeneration takes 3 to 5 days to appear, so a fresh hemorrhage looks non-regenerative on day one.
  • Non-regenerative: Anemia of inflammatory disease (mild, normocytic), chronic kidney disease, marrow disease (FeLV, estrogen, chemotherapy), iron deficiency (microcytic, hypochromic, from chronic GI loss or fleas), hypothyroidism.
  • Gotcha: Cats have aggregate and punctate reticulocytes; only aggregate reticulocytes are counted for regeneration. Horses do not release reticulocytes into blood at all, so equine regeneration is judged by serial PCV, MCV and marrow examination. Ruminants release reticulocytes only with strong regeneration.

Immune-Mediated Hemolytic Anemia

  • Findings: Regenerative anemia (after the first few days), spherocytes (the hallmark in dogs; hard to identify in cats because their normal red cells lack central pallor), autoagglutination that persists after saline dilution, positive Coombs (direct antiglobulin) test, hyperbilirubinemia and bilirubinuria, hemoglobinemia or hemoglobinuria if intravascular, inflammatory leukogram, often thrombocytopenia (Evans syndrome).
  • Gotcha: Saline dilution disperses rouleaux but not true agglutination. Look for triggers (Mycoplasma haemofelis and FeLV in cats; drugs, babesiosis, zinc in dogs). Thromboembolism is a leading cause of death in canine IMHA; Merck flags pulmonary thromboembolism as a risk in these hypercoagulable dogs.

Thrombocytopenia

  • Causes by mechanism: Decreased production (marrow disease, estrogen, chemotherapy, FeLV); increased destruction (primary immune-mediated thrombocytopenia, drug-induced, Evans syndrome); consumption (DIC, vasculitis, severe hemorrhage); sequestration (splenomegaly); infectious (Ehrlichia canis, Anaplasma platys, Rickettsia rickettsii, Babesia, Leishmania).
  • Gotcha: Cavalier King Charles Spaniels have hereditary macrothrombocytopenia with normal function. Check a smear for clumps before believing a low count. Petechiae mean platelets; hematomas and cavity bleeding mean factors.
Leukogram shortcut: no bands and no lymphocytes means stress; bands and toxic neutrophils mean inflammation; lymphocytes up in a frightened cat means epinephrine. Anemia shortcut: count the reticulocytes, then wait 3 to 5 days before you call it non-regenerative.

Serum Chemistry

Azotemia: Prerenal, Renal, Postrenal

TypeBUN and creatinineUrine specific gravityKey clue
PrerenalRaised, BUN often proportionally moreConcentrated: dog above 1.030, cat above 1.035Dehydration, shock, heart failure; resolves with fluids; GI bleeding raises BUN alone
RenalRaisedInadequately concentrated for the degree of dehydration; isosthenuric in CKDKidney cannot concentrate; CKD, AKI, leptospirosis, ethylene glycol, lilies in cats
PostrenalRaised, often with hyperkalemiaVariableObstruction or uroabdomen; palpate the bladder, check the abdomen
  • Gotchas: Azotemia with dilute urine in a dehydrated animal is renal unless something else has removed concentrating ability: hypoadrenocorticism (medullary washout), diuretics, hypercalcemia, pyometra or glucocorticoids. Cats retain some concentrating ability into renal failure, hence the higher feline cut-off.
  • IRIS staging uses fasting creatinine in a stable, hydrated patient: dogs stage 1 below 1.4 mg/dL, stage 2 from 1.4 to 2.8, stage 3 from 2.9 to 5, stage 4 above 5; cats stage 1 below 1.6, stage 2 from 1.6 to 2.8, stage 3 from 2.9 to 5, stage 4 above 5. SDMA rises earlier than creatinine and is less affected by loss of muscle mass. Substaging uses UPC and blood pressure.

Liver Enzymes: Hepatocellular Versus Cholestatic

EnzymeCategoryDogs and catsHorses and ruminants
ALTHepatocellular leakageLiver-specific in dogs and cats; rises higher and recovers faster than ASTNot useful; little hepatic ALT
ASTHepatocellular leakage plus muscleLess specific than ALT; check CK to exclude muscleUsed, but always pair with CK
SDH and GLDHHepatocellular leakageRarely runThe liver-specific leakage enzymes; GLDH rises with hepatic necrosis
ALPCholestatic and inducedDog: long half-life (days), steroid and bone isoenzymes, values in the thousands suggest steroids; cat: short half-life (hours) and low activity, so any rise is significantNon-specific; wide reference ranges; not the preferred cholestatic marker
GGTCholestaticMore specific than ALP for cholestasis in cats (hepatic lipidosis raises ALP more than GGT)The cholestatic marker of choice in horses and ruminants; very high in colostrum-fed neonates
  • Function tests: Enzymes measure damage, not function. Function is assessed by bile acids (paired pre- and postprandial in dogs and cats; horses have no gallbladder so a single sample suffices), ammonia, albumin, BUN, glucose, cholesterol and clotting factors. Bile acids are the screening test for portosystemic shunt and are uninterpretable once the patient is icteric because cholestasis alone raises them.
  • Bilirubin: Prehepatic, hepatic or posthepatic. Bilirubinuria in a cat is always abnormal; anorexic horses develop mild hyperbilirubinemia without liver disease.
  • Gotcha: Young growing animals have bone ALP; hyperthyroid cats have raised ALP; a dog on prednisone will have a striking ALP rise that does not mean liver failure; the canine steroid isoenzyme has no equivalent in cats.

Electrolytes

  • Hyponatremia with hyperkalemia: The Addison's signature. Merck cites a Na:K ratio below 27 as suggestive but not pathognomonic, because whipworm infection, uroabdomen, chylothorax and repeated drainage of effusions, severe GI disease and pregnancy can mimic it. Confirm with an ACTH stimulation test; a baseline cortisol above 2.0 mcg/dL effectively excludes hypoadrenocorticism, a value below that requires the stimulation test. Atypical Addison's has normal electrolytes.
  • Hyperkalemia causes: Decreased excretion (urethral obstruction, uroabdomen, anuric renal failure, Addison's), translocation (acidosis, insulin deficiency in DKA, reperfusion, massive tissue trauma), and artifact (hemolysis in Akitas and other Japanese breeds whose red cells carry potassium, marked thrombocytosis or leukocytosis in serum samples). ECG changes progress from tall tented T waves to absent P waves, wide QRS and bradycardia.
  • Hypokalemia: Anorexia plus fluid therapy, vomiting, chronic kidney disease in cats, diuretics, insulin treatment of DKA, hyperaldosteronism. Cervical ventroflexion in cats and muscle weakness are the tested signs.
  • Hypercalcemia differentials: Malignancy (lymphoma, anal sac apocrine gland adenocarcinoma, multiple myeloma; PTHrP high, PTH suppressed), primary hyperparathyroidism (PTH inappropriately normal or high with low-normal phosphorus), renal failure, hypoadrenocorticism, vitamin D toxicosis (cholecalciferol rodenticide, calcipotriene creams; phosphorus high), granulomatous disease, bone disease, and idiopathic hypercalcemia, which Merck lists as the most common form in cats. Always confirm with ionized calcium and interpret with phosphorus and PTH.
  • Hypocalcemia: Eclampsia in lactating small-breed bitches, milk fever, hypoparathyroidism after feline thyroidectomy, ethylene glycol, pancreatitis, and hypoalbuminemia (total low, ionized normal).
  • Chloride and acid-base: Hypochloremic, hypokalemic metabolic alkalosis means gastric or abomasal chloride loss (pyloric obstruction, displaced abomasum). High anion gap acidosis: DKA, ethylene glycol, lactate, renal failure.

Practice reading lab tables under exam conditions

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