Clinical Pathology Board

Clinical Pathology
Review
Blood Made Simple!
• Hematology
• Coagulation
• Liz Little • Urinalysis
• emills@vet.upenn.edu • Biochemisty
• Rosenthal 305 • *** items more
important

Hemoglobin
Hematology
Eccentrocyte Heinz bodies

• Hemoglobin: 4 globin chains and 1 heme group

– Thalassemia syndrome: abnormally low
levels of Hb
– Porphyrins are intermediates of heme
biosynthesis- enzyme deficiencies can lead
to excessive accumulation = porphyrias
• Oxidative damage***:
– Denaturation of HB with Heinz body formation. Cats
have a low to moderate frequency of HB normally.
– Oxidation and cross-linking of membrane proteins
with eccentrocyte formation
– Oxidation of HB iron (Fe2+, ferrous) to methemoglobin
(Fe3+, ferric ). It interferes with O2 transport. May instill
brown color to mucous membranes.
– RBCs are lysed or prematurely removed from
circulation
– Visible with new methylene blue stain

Oxidative Damage*** Iron

• Cats and dogs: acetaminophen, benzocaine,
onions, H2O2
• Cats: phenazopyridine, propylene glycol,
methionine, methylene blue.
• Dogs: Vit K1, Vit K3, napthalene,
phenylhydrazine, zinc.
• Horses: onions, phenothiazine, red maple (Acer
rubrum) leaves, wilted or dry.
• Ruminants: Brassica spp. (kale, rape), copper
toxicosis, IV H2O2, molybdeum deficiency,
onions, rye grass
• Endogenous: secondary to inflammation.
• Serum Iron: if very low, diagnostic for Fe
deficiency, but normal levels are maintained until
deficiency is severe.
• Serum ferritin: most reliable method for
evaluation of Fe stores-sent to KS State. It does
not contain Fe, but is a good index of stores
because it is in equilibrium with tissue ferritin,
which DOES contain Fe.
• Stainable iron is not normally present in
• feline marrow.

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 Red Blood Cells
• Lifespan: 120/90 days (dog/cat)
• Erythropoiesis stimulated by:
– Kidney (⇑ EPO) in response to low O2
tension***
– Lung/nasal/cardiac disease
– Hyperthyroidism: increased metabolic rate
and increased need for O2 in tissues.
Reticulocytes
• Reticulocytes = polychromatophilic RBCs
• Uncorrected: % as counted
• Corrected: % retics x patient’s PCV
normal PCV (45 dog, 37 cat)
• ***Absolute: If know RBC count, can calculate absolute. % retics x
RBC count
– > 60,000 cells/ul in cats, > 80,000 in dogs = regenerative
– Horses don’t produce retics, will see ⇑MCV
• Cats: two types of reticulocytes
– Punctate: long-lived, not counted in retic count
– Aggregate: indicative of bone marrow production
• Cattle: reticulocytosis and basophilic stippling

Erythropoiesis suppression RBC Indicies

• Estrogen • Copper deficiency • MCV (Hct/RBC x 10):
• TNF (chronic disease, • Iron deficiency – ⇓ with Fe deficiency,
Akitas, Shiba, sheep,
neoplasia, • Myelodysplastic goats
inflammation) syndrome – ⇑ with regenerative
• CRF*** • Herefords and anemia, Poodles
• Immune-mediated English Springer • MCHC: more accurate
Spaniels-congenital than MCH since not
• Myelophthisis
dependent on RBC count
• Ehrlichiosis dyserythropoiesis
(Hb/PCV x 100)
• RDW: estimation of the
degree of anisocytosis

Anemia***
• Normocytic, normochromic: chronic disease, non-
regenerative
• Macrocytic, hypochromic: regenerative response
after blood loss or hemolysis, IMHA
• Macrocytic, normochromic: regneration or due to
defective erythropoiesis (FeLV, Poodle
macrocytosis)
• Microcytic, hypochromic: Fe deficiency, pyridoxine
deficiency
• Microcytic, normochromic: Fe deficiency, hepatic
failure (PSS)
Anemia
• IMHA***: spherocytosis, positive direct Coombs test,
+/- agglutination, regenerative
– Dogs: idiopathic, vaccines
– Cats: H. felis, LSA
– Horses: penicillin, LSA
• Hemolytic, regenerative
– Extravascular: parasitic, IMHA
– Intravascular: toxin, complement mediated, transfusion reaction,
• Hemorrhagic: regenerative, low TP
– Trauma, coagulopathy,neoplasia, parasitism, hematuria, GI ulcers
• Non-regenerative: decreased RBC production, chronic
– Inflammatory disease, CRF
– Marrow hypoplasia/aplasia: myelitis, toxicosis, irradiation, infiltrative
– Erythroid hypoplasia/ineffective: PRCA, FeLV, nutritional,
hypothyroidism, Addisons, liver disease or failure.

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 RBC Morphology
• Acanthocyte: neoplasia, HSA,
post-splenectomy
• Blister cell: DIC; focal
thrombus
• Schistocyte:***
microangiopathic hemoysis,
DIC, neoplasia,
glomerulonephritis, severe
burns, focal thrombus
• Target cell: regenerative
anemias, Fe deficiency, liver
disease, splenectomy
• Eccentrocyte and heinz
bodies***: oxidative
damage
• Spherocytes***: IMHA
(many), DIC, oxidants,
zinc, snakebites, post-
transfusion
• Stomatocytes: Alaskan
malamutes, schnauzers
RBC Morphology
• Howell-Jolly bodies: • Rouleaux: common in
nuclear remnants, normal horses, +/- cats;
to see occasionally in hyperglobulinemia,
cats, dysfunctional hyperfibrinogenemia
spleen, steroid use,
dyserythropoiesis, • Agglutination: hemolysis,
vincristine, regenerative IMHA. Confirm with saline
anemias agglutination test.
• Basophilic stippling:
pathologic precipitation of Agglutination
ribosomes; common in
regenerative anemias of
cats and cattle;
dyserythropoiesis; Rouleaux
anomaly in some poodles

RBC Morphology Leukocytes

• Neutrophils and lymphocytes most common
• One or the other typically predominates
– Mice & rats: lymphs >>> neuts
– Dogs & cats: neuts >>> lymphs
Target cell Basophilic stippling Howell-Jolly body – Horses: neuts ≈ lymphs
– Ruminants/hamsters: lymphs > neuts
• Life Span
– Neutrophil: 5-10 hours
– Lymphoctye: hours-years
– Eosinophil:mins-hours
Blister cell Schistocyte
Acanthocyte
Keratocyte
– Basophil: 6 hours
– Monocytes: months

Leukocyte profiles Neutrophils

• Stress leukogram (corticosteroids)***: neutrophilic Neutrophilia
leukocytosis, monocytosis, eosinopenia, lymphopenia • Inflammatory: infections,
• Excitement (epinephrine): leukocytosis, lymphocytosis, IMHA, necrosis
no left shift
• GCC-associated: stress,
• Left shift: increased numbers of immature neutrophils Cushings, exogenous,
(bands) ACTH therapy
• Degenerative left shift: leukopenia, neutropenia, • Physiologic: Fight or Flight,
immature forms out number matures catecholamine injections
• Right shift: increased numbers of hypersegmented • Neoplastic: granulocytic
neutrophils (myelogenous leukemia),
• Lymphopenia: consider viral infection paraneoplastic
• Leukemoid reaction: reactive, usually >100,000 cells/ul • Others: LAD, estrogen
toxicosis
Neutropenia
• Inflammation: overwhelming
tissue demand (eq.
Salmonellosis, parvovirus,
eq. Influenza), endotoxemia
• Peripheral destruction:
immune-mediated,
hemophagocytic syndromes
• Granulocytic hypoplasia:
infections (parvo, FeLV,
Toxo, Ehrilichia), neoplasia,
toxic, marrow necrosis,
myelofibrosis
• Ineffective production
• Cyclic hematopoiesis

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 Lymphocytes& Monocytes Eosinophils
• Eosinophilia
• Lymphocytosis • Monocytosis (basophilia)
• Chronic inflammation • Inflammation • Hypersensitivity (allergic)
• Parasitism
• Physiologic: fight or flight • GCC associated
• Idiopathic eosinophilic
• Neoplasia: LSA, lymphocytic leukemia • Monocytic leukemia conditions
• Addison’s • Secondary to immune • Mast cell degranulation
• Lymphopenia neutropenia • Mast cell neoplasia
• Cyclic hematopoiesis (cutaneous lesions in dogs
• Acute inflammation
• G-CSF administration especially)
• GCC associated • Addison’s
• Depletion-lymphoid effusion • Monocytopenia
• Neoplastic eosinophilia
• Lymphoid hypoplasia/aplasia • Difficult to document because
there can be relatively few
• Eosinopenia
blood monocytes. It is not • GCC associated
considered a significant • Acute inflammation
finding. • Aplastic marrow

Coagulation Coagulation
• Primary hemostasis***: vascular • Secondary hemostasis***:
endothelium, vWF, platelets = coagulation factors to form
formation of an unstable platelet
plug.
secure fibrin clot.
PT • Primary hemostatic defects • Secondary hemostatic
• Thrombocytopenia disorders
PTT
– IM • Coagulopaties-hereditary
ACT
– Hemophilia A(VIII) & B(IX)
– Ehrlichia & infections
– Factor deficiencies (VII, X, XI,
– BM disease XII)
• Thombopathia • Acquired
– Hereditary or Drugs (aspirin) – Anticoagulant rodenticides
• von Willebrand’s disease – Vitamin K deficiency
TT
• Vasculopathies – Drugs (heparin, coumarin)
• Clinical signs: Mucosal bleeding – Liver disease
• Clinical signs: Cavity bleeding

Coagulation
• Factors II, VII, IX, & X require Vit K for production
• VII: shortest half life (6.5 hours)
• ATIII inhibits coagulation by binding to and inactivating
caogulation factors. Heparin accelerates activity of ATIII.
• vW disease: VIII-related antigen decreased
– Normal APTT and PT
– Bleeding commonly involves mucosal surfaces
– Autosomal incomplete dominant
– Dobermans most common
Coagulation
• ⇑ PT (OSPT): extrinsic and common
– Acquired deficiencies: hepatic disease, Vit K
antagonism/deficiency
– Hereditary deficiencies in I, II, V, VII, X
– ***In early Vit D antagonism, PT is the first to be
prolonged, due to short half-life of FVII
• ⇑ APTT: intrinsic and common
– Acquired: see above
– Increased coagulation factor inactivation/consumption
(DIC)
– Hereditary
– Inhibition of factors by heparin, FDPs, Abs to
phospholipids and/or coagulation factors.

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 Coagulation
• ACT: similar to APTT (instrinsic and common),
easy, less sensitive
• BMBT: platelet function and coagulation
• TT: amount and activity of fibrinogen
• PIVKA: Proteins invoked by vitamin K absence
– Precursors to Vit K dependent factors
accumulate in the rER of the hepatocytes and
eventually enter the peripheral blood when
intrahepatic vitamin K is depleted by
anticoagulant rodenticides or intestinal
malabsorption.
Transfusion medicine
• Most DSH cats in US are type A (>95%)
• Exotic breeds more likely type B than DSH
• AB very rare
• Type B cats have strong naturally occurring anti-
A alloantibodies. Anti-B alloantibodies of type A
cats have weak activity. Type AB cats do not
have alloantibodies.
• There are at least 13 dog erythrocyte antigens
(DEAs).
• The most antigenic is DEA 1.1. DEA 1.1 positive
should not be given to DEA 1.1 negative dogs.
URINE!
• Specific Gravity: assesses solute
concentration in urine.
• Isosthenuria: USG=1.008-1.012
– Similar to SG of plasma, suspect of tubular
dysfunction
• Hyposthenuria: USG <1.008
– Some dilution of the glomerular ultrafiltrate,
some functional tubular capacity.
• Hypersthenuria: USG > 1.025-1.035
depending on species.
– Adequately concentrated
Platelets
• Platelet: anucleated cell fragment found in mammalian species
and derived from megakaryocyte cytoplasm.
• Production takes about 4 day; T ½= 7-10 days
• Thrombocytopenia: significant bleeding not seen until platelet
count < 40,000/ul unless multiple disturbances present.
– Decreased production:drugs, Ehrlichia, neoplasia
– Increased destruction/consumption: ITP, DIC, RMSF
• Thrombocytosis: may be associated with bleeding if severe
(>1,000,000/ul)
– Reactive: Fe deficiency, chronic inflammation
– Primary: essential thrombocythemia, megakaryocytic
leukemia
Neonatal
isoerythrolysis***
• Ingested maternal colostral alloantibodies are
absorbed by the intestine, enter blood, and
attach to neonate’s paternal-derived
erythrocyte antigens. The Ab-coated RBCs are
then lysed by macrophages or complement.
• Cats: Type B queen passes her anti-A
alloantibodies to a Type A or Type AB kitten.
• Horses: NI may occur if a mare negative for
Aa or Qa antigens has acquired alloantibodies
against such antigens during prior pregnancies
or transfusion, and her foal is postive for Aa or
Qa alloantigen (paternal derived).
Specific Gravity
• Assessed in conjunction with azotemia.
• Pre-renal: azotemia with adequate
concentration
– Dehydrated animals should have hypersthenuric
urine if renal concentrating ability is intact
• Renal: azotemia with inadequate urine
concentration
– Loss of 75% nephron mass will impair GFR and
tubular concentrating ability
• Post-renal: azotemia with variable urine
concentration
– Suspect obstruction
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 Urinalysis Urinalysis
• Glucosuria: indicates that the renal
• Proteinuria: threshold has been exceeded, except for
– Pre-renal: increased permeability of glomerulus rare cases when the blood glucose is
from fever, stress, seizures, exercise normal, but tubular dysfunction results in
– Overload: myoglobin, hemoglobin, BJ proteins impaired glucose reabsorption. (Fanconi
– Renal: damage to glomerulus from Abs, immune syndrome)
complexes, amyloidosis, inflammation
– Post-glomerular: tubular dysfunction from inflammation or
hemorrhage (bladder) • Ketonuria: reflects excessive fat
– Urine protein should be interpreted in the context of degradation and /or deficiency in
sediment evaluation. carbohydrate metabolism due to DM, cattle
• Urine protein:creatinine ratio minimizes the effects of variable ketosis, pregnancy disease of ewes,
urine concentration
• Nephrotic syndrome:edema, hypoalbuminemia, proteinuria,
starvation, low carbohydrate high fat diet.
hypercholesterolemia-primary glomerular disease

Urinalysis Urine Sediment

• Occult blood: erythrocytes, hemoglobin,
myoglobin. RBCs will clear with • Cells: squamous epithelial cells,
centrifugation. transitional epithelial cells, leukocytes
• Bilirubinuria: disruption of bile flow. • Casts: renal tubular damage(except
– Dogs and cattle may normally have trace to hyaline)
1+
– Any bilirubinuria is significant in the cat • Crystals: crystalluria is not diagnostic of
• pH: ⇓ acidosis, fever urolithiasis
– ⇑ delayed analysis, urine retention in bladder, – Acidic: calcium oxalates, cystine
bacterial infection/contamination, alkalosis, – Alkaline: struvites (MAP), calcium
post-prandial alkaline tide carbonates, ammonium biurate

Crystals Chemsitry
Acidic

• Serum: water,
electrolytes,
Calcium oxalate dihydrate Cystine
•Healthy mammals Calcium oxalate monohydrate •Rare
metabolites, proteins,
•Hypercalciuria •Hypercalciuria •Liver disease glucose, minerals,
•Hyperoxaluria (EG toxicity) •Hyperoxaluria
lipids, hormones,
vitamins, enzymes,
Alkaline

drugs, toxins.
• No fibrinogen

Struvite (MAP) Ammonium urate

Calcium carbonate
•alkalinuria •Healthy mammals
•Healthy herbivores
•Dalmations
•PSS

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 • Hypercalcemia
Chemistry
– Malignancy: lymphoma,
apocrine gland tumor of anal
sac, multiple myeloma,
metastatic neoplasia (rare)
– Endocrine: Addison’s
disease, primary
hyperparathyroidism.
– Vit D toxicity: iatrogenic (tx of
hypoparathyroidism), rat
poison, toxic plants (day
blooming jessamine,
Solanum)
– Granulomatous disease-
macrophages produce Vit D.
– +/- Renal failure
– Young animals, large breed
Hypocalcemia
• Hyperparathyroidism
• Addison’s
• Hypoalbuminemia***:
• Renal Disease
– correctedCa= measuredCa (mg.dl) – albumin (g/dl) + 3.5
• D, Vitamin • Primary hypoparathyroidism
• Osteolytic lesions • Renal secondary hyperparathyroidism-CRF
• Puerperal tetany or eclampsia***-dogs, mares, ewes.
• Neoplasia
• Systemic Fungal • Parturient hypocalcemia*** (milk fever in cattle) ⇓PO4
Infection • Ethylene glycol toxicity***
• ARF
• Pancreatitis
• Blister beetle toxicity (cantharidiasis)-horses
• Phosphate enema in cats

Hypocalcemia Calcium/Phosphorus
• Oxalate toxicity (rhubarb, greasewood, kikaye)-horses
• Hypomagnesaemia (grass tetany): PTH responses are • ⇑Ca ⇓PO4
mediated by Mg
• Myopathies
– Neoplasia
– Transport tetany in horses-sweating-hypochloremic alkalosis- • Paraneoplastic
increased binding of calcium to albumin hypercalcemia
– Exertional rhabdomyolysis, malignant hyperthermia, selenium – Hyperparathyroidism My dog
myopathy
• Rumen overload- lactic acidosis- increased phosphate • ⇓ Ca ⇑PO4
and decreased binding of Ca to phosphate and lactate in – Renal failure
renal tubules
– Hypoparathyroidism
• Iatrogenic-thyroidectomy
– Nutritional secondary hyperparathyroidism
from excess PO4 intake

Hyperphosphatemia Hypophosphatemia
• Young animals*** • Diets with low
• Renal failure*** Ca:PO4 ratio • Hyperparathyroidism* • Translocation
• Hypoparathyroidism • Hepatic lipidosis – Insulin administration
• Prerenal and
• Decreased intestinal – Bicarbonate
postrenal azotemia • In vitro hemolysis
administration
• Rodenticide- • Phosphate enema absorption:
– IV Glucose
cholecalciferol*** phosphate-binding
• Osteolytic bone • Defective Mobilization
antacids
• Hypervitaminosis D lesions of PO4 from bone***
• Increased urinary
– Eclampsia
excretion
– Milk fever***
– Hypercalcemia of
malignancy*** • Renal failure in
– Diabetic ketoacidosis horses

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 Hyperkalemia
• Decreased urinary
excretion
– Addisons
– Urethral obstruction
– Anuric or oliguric renal
failure
– Ruptured bladder/ureter
– Selected GI disease
(trichuriasis, salmonellosis,
perforated duodenal ulcer)
– Chylothorax
– Hyperkalemic periodic
paralysis (horse, dog)
• Translocation
– Metabolic acidosis
– Muscle necrosis
– Seizures
– Selenium deficiency
– Pseudohyperkalemia
in Akitas and Shibas,
horses, pigs, cattle
– Thrombocytosis
Hypokalemia
• Increased loss:
– GI: vomiting, diarrhea
– Urinary: CRF (especially in cats), post-obstructive
diuresis, inappropriate fluid therapy, drugs (loop
diuretics, thaizide diuretics)
– Sweating: horses
• Translocation:
– Insulin therapy-shifts K into cells
– Alkalosis-increased HCO3 in renal tubules and
increased K secretion
• Decreased Intake:
– anorexia (esp. herbivores), dietary deficiency

Glucose Hypoalbuminemia
• Hyperglycemia • Hypoglycemia
– Decreased production • Decreased production • Increased loss
– DM*** (persistent)
• Juveniles: esp toy – Chronic hepatic – Renal:
– Stress (transient, breeds glomerulonephritis,
insufficiency
cats) • Hunting dogs amyloidosis
– Inadequate intake – GI: PLE, IBD, LSA,
– Cushings • Severe hepatic disease
• Addison’s – Maldigestion histoplasmosis,
– Drugs-transient lymphangiectasia
– Increased Utilization – Malabsorption
• GCC – Cutaneous (burns)
• Diazoxide • Insulinoma (beta cell) • Sequestration
• Extrapancreatic – Whole blood loss
• Thaizide diuretics – Body cavity effusions
neoplasia • PLN: lose albumin and
(hepatocellular CA, – Vasculopathy ATIII
HAS • PLE: lose albumin and
• Sepsis globulin
Stressed?

⇑Globulins Blood Urea Nitrogen

• Increased
• Polyclonal-chronic antigenic stimulation • Decreased
• Decreased • Increased Loss
– Infectious: elimination – Any cause of PU
• Bacterial: Brucellosis, pyoderma, bacterial endocarditis
– Pre-renal – Young animals: increased
• Viral: FIP, FIV, FeLV Ehrlichia
urine output, high anabolic
• Systemic fungal infections – Renal
state, PD
• Rickettsial: Ehrlichiosis – Post-renal obstruction • Decreased Production
• Monoclonal • Increased production – Hepatic (PSS, cirrhosis)
– Severely restricted protein
– Neoplasia: MM (IgG or IgA), LSA, Waldenstrom’s – High protein diets
diet (U/D)
macroglobulinemia (IgM) – Catabolic drugs
– Infectious: Ehrlichosis (rare, IgG), Leshmaniasis, FIP (steroids,
(rare) tetracyclines)
– GI hemorrhage**

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 PU/PD Alanine aminotransferase
• CRF • Hypercalcemia
• DM • Hypokalemia • Cytoplasmic enzyme
• Drugs • Pyelonephritis • Half-life
• Cushing’s • Primary renal – Cats: 4-6 hours
• Pyometra glycosuria – Dogs: 60 hours
• Hyperthyroidism • Addisons • ⇑ ALT:
• Severe hepatic Dz • Central DI – hepatocellular leakage/necrosis (3X normal)
• Congenital – Hepatic parenchymal disease:
nephrogenic DI cholangiohepatitis, cirrhosis, trauma, chronic
• Primary polydipsia hepatitis
– Iatrogenic-drug induced

Aspartate aminotransferase Alkaline phosphatase

• Cytoplasmic and mitochondrial enzyme
• Half-life • Three isoenzymes: liver, steroid (dogs), bone
– Cats: 77 minutes
• Half-life (L-ALKP)
– Dogs: 5 hours
– Cats: 8 hours
• ⇑ AST
– Dogs: 3 days
– Hepatic disease-neoplasia, lipidosis, CAH, cirrhosis,
PSS • Species differences
– Muscle disease (inflammation or necrosis) – Dogs: sensitivity for cholestasis may be increased
– Hemolysis before icterus develops
– DM – Cats & Horses: poor diagnostic sensitivity, typically
– Cushing’s icteric before increased
– Hyperthyroidism or hypothyroidism – Cattle: moderate sensitivity for cholestasis, but these
disorders uncommon in cattle

Alkaline phosphatase GGT

• ⇑ ALKP
– Drugs: steroids*, pheobarb, primidone, phenytoin
– Biliary tract abnormalities: cholestasis*, pancreatitis
– Hepatic parenchymal disease: cholangiohepatitis,
chronic hepatitis, cirrhosis/fibrosis, hepatic lipidosis
(normal GGT), FIP, hepatic neoplasia
– Bone disease (due to osteoblast activity)
• Rickets, hyperparathyroid, bone tumors, fractures
– Miscellaneous: pregnancy (⇑ placental ALP), benign
familial hyperphosphatemia in Siberian Huskies (B-
ALP), young dogs*, DM, hyperthyroidism, Cushing’s*
• Inducible enzyme, not leakage
• Increases usually parallel ALKP
• ⇑ GGT
– Cholestatic liver disease
– Cortisol excess (dogs)
– Neonatal cows, dogs, sheep (large amount in colostrum)
– Horses: better diagnostic sensitivity than ALP for
cholestasis or other biliary disorders
• SDH: enzyme of choice in horses and cows
– Indicates hepatocyte damage/hepatoxicities, often
acute, may return to normal 4-5 days after insult.

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 Diseases and Diagnostic
Findings
Italics = < 50% cases
• Addisons: Azotemia, hyponatremia, hypochloremia, hyperkalemia,
Na:K < 27:1, normochromic-normocytic anemia, lymphocytosis,
eosinophilia, hypoglycemia, hypercalcemia
• Borreliosis: non-septic, suppurative polyarthritis. IgM Abs, or
increasing IgG Abs.
• Cholangiohepatitis, cats: Hyperbilirubinemia, increased ALT, ALKP,
elevated resting and post-prandial BA. Hyperglobulinemia in chronic
disease.
• Cholecalciferol toxicity: Hypercalcemia, hyperphosphatemia,
azotemia, hyposthenuria
• Chylous effusions: fluid TRIG>serum TRIG
• Cushing’s: increased ALKP (dogs), neutrophilia, lymphopenia,
eosinopenia, hypercholesterolemia, low urine SG, positive urine
culture, hyperglycemia
Diseases
• Eclampsia: severe hypocalcemia (<6.5mg/dl)
• Ehrlichia canis: IgG Ab titer > 1:20, thrombocytopenia,
bone marrow plasmacytosis, hyperglobulinemia, non-
regenerative anemia, pancytopenia, neutropenia
(horses)
• EG toxicity: 4-24hrs: increased anion gap and osmolality,
acidemia, EG in blood or serum. 12-72 hours: azotemia,
isosthenuria, Ca oxalate monohydrate crystals in urine,
hypocalcemia, hyperglycemia.
• Exocrine pancreatic insufficiency: TLI < 2 ug/L (dogs),
decreased fTLI (cats)
• FIV: anemia, lymphopenia, neutropenia
Diseases
• Hepatic lipidosis: increased ALKP, hyperbilirubinemia,
ALKP increased more than ALT or AST, increased BA,
hyperglycemia
• Hepatic necrosis, acute: markedly increased ALT, ALKP,
hyperbilirubinemia, hypoglycemia, inflammatory leukogram
• Hepatitis, chronic: increased ALT, ALKP,
hyperbilirubinemia, hypoalbuminemia, increased BA,
acites
• Hyperparathyroidism(primary): hypercalcemia with high
PTH, hypophosphatemia, low urine SG
• Hyperthyroidism: increased PCV, ALT, ALKP, AST,
hyperphosphatemia
• Hypothyroidism: mild normocytic, normochromic anemia,
hypercholesterolemia
Diseases
• DI: hyposthenuria, lack of response to modified water
deprivation, positive response to ADH if central DI,
hypernatremia
• DM: Persistent fasting hyperglycemia and glycosuria,
increased ALKP, hypercholesterolemia; proteinuria,
bacteriuria, pyuria
• Diabetic ketoacidosis: persistent fasting hyperglycemia
and glycosuria, ketonuria, metabolic acidosis, increased
anion gap, increased ALKP, hypercholesterolemia,
leukocytosis, hypokalemia, hyponatremia, azotemia,
lipemia
• Dirofilariasis: eosinophilia, basophilia, proteinuria,
hyperglobulinemia
• DIC: three of the following
– Prolonged PT, Prolonged PTT, Decreased ATIII,
thrombocytopenia, increased FDPs, +/- schistocytosis
Diseases
• FIP: hyperproteinemia and polyclonal gammopathy,
hypoalbuminemia, decreased serum alb:glob ratio,
elevated AST, anemia; non septic pyogranulomatous
exudate with high protein and relatively low cell count in
effusive form
• FeLV: IFA or ELISA, anemia, neutropenia, lymphopenia
• Glomerulonephropathy: proteinuria despite no hematuria
or pyuria, urine P:C ratio > 3, azotemia,
hypercholesterolemia, hypoalbuminemia, acites
• Hepatic cirrhosis: increased BA, ALT, ALKP,
hypoalbuminemia, decreased BUN, hyperbilirubinemia,
acites, hypoglycemia, hypocholesterolemia
Diseases
• Primary hypoparathyroidism: hypocalcemia, low PTH,
hyperphosphatemia
• IBD: decreased albumin and globulin
• Insulinoma: fasting hypoglycemia with high normal or
increased serum insulin.
• Leptospirosis: azotemia, leukocytosis,
thrombocytopenia, increased ALKP, hyperbilirubinemia
• LSA: hypercalcemia, anemia, leukocytosis or leukopenia,
increased ALT, increased ALKP, azotemia, positive FeLV
• Parvovirus: neutropenia
• Peritonitis: neutrophilia or neutropenia,
hypoalbuminemia, acidemia, hyperkalemia
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 Diseases Diseases
• RMSF: mild thrombocytopenia, leukopenia (2-4 days)
• PSS: increased post-prandial BA, hypoalbuminemia, then leukocytosis.
hyperammonemia, microhepatia, hypoglobulinemia, • Rodenticide (warfarin-type): prolonged PT, PTT, w/o
decreased BUN, hypocholesterolemi, microcytosis increased FDPs, thrombocytopenia
• PLE: decreased albumin and globulins, • Uroabdomen: azotemia, abdominal fluid > serum
hypocholesterolemia, lymphopenia creatinine, hyponatremia, hyperkalemia
• Pyometra: neutrophilia, azotemia, hyperglobulinemia,
isosthenuria, proteinuria
• ARF: azotemia, hyperphosphatemia, isosthenuria,
hyperkalemia
Good Luck!!!
• CRF: non-regenerative anemia, isosthenuria, azotemia,
hyperphosphatemia, hypokalemia

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