Case Studies

Question 1

Dog with anemia, elevated retics, anisocytosis in the RBCs and polychromasia, elevated WBCs (segs) and platelets and a decreased total protein and albumin. There is increased MCV and low MCHC.

Answer 1

Indicative of blood loss and increased MCV/macrocytosis and low MCHC/hypochromasia are due to reticulocytosis. Retics are large young and anucleate RBCs. Thrombocytosis consistent with chronic hemorrhage d/t release from spleen and increased thrombocytopoiesis. Mature neutrophilia also often d/t hemorrhage.
This dog had Ancylostoma hookworms. pg 385

Question 2

Dog with Anemia with increased retics and nucleated reds.
Anisocytosis, polychromasia and spherocytes.
Elevated Neuts, segs, bands and monos, low lymphs.
Elevated ALP, ALT, total Bili and unconjugated bili.
Platelets are low and there is bilirubinuria.

Answer 2

Macrocytic, hypochromic (d/t the retics that lack their full complement of Hgb and are big), regenerative anemia.
Regenerative anemia with icterus, hyperbilirubinemia with a predominance of unconjugated bilirubin indicates hemolysis. Extravascular hemolysis.
This was IMHA and there was a positive Coombs/direct Ab test and spherocytosis.
Neutrophilic leukocytosis with left shift, monocytosis and lymphopenia > d/t hemolysis and steroid admin. Neutrophilia commonly seen with IMHA d/t extravascular hemolysis.
Platelets are low with increased MPV means Evans syndrome and concurrent immune mediated destruction of plts.
Elevated ALT d/t hypoxia induced liver injury from anemia. Increased ALP d/t steroid admin. Bilirubinuria, which is conjugated, d/t hemolysis. pg 387

Question 3

Anemic horse with increased MCH and MCHC with Heinz bodies and eccentrocytes.
WBCs are high including segs.
Fibrinogen is elevated.
Creatinine and Total protein are elevated.
AST and Bilirubin are elevated and Methemoglobin is elevated.
Urine is brown with 3+ protein, 1+ Bilirubin, 4+ blood, and there are Ca carbonate crystals and mucus. USG is 1015
There is icterus, chocolate colored blood, dark brown urine and orange red plasma.

Answer 3

This animal
Problems: There is hemolytic anemia. The presence of Hyperbilirubinemia, hemoglobinemia and hemoglobinuria indicates intravascular hemolysis.
You know there is hemoglobinemia cause of the red plasma and increased MCHC. Heinz bodies and eccentrocytes indicate oxidative damage to RBCs from ingestion of Red Maple leaves.
REMEMBER: HORSES do not EVER show reticulocytes so all their anemias look nonregenerative.
Methemoglobinemia > oxidation of heme iron from ferrous to ferric form. Causes brown discoloration of mucous membranes and it may accompany oxidative hemolysis.
Neutrophilic leukocytosis commonly observed with hemolytic anemias. High fibrinogen associated with inflammation.
Azotemia may be renal or prerenal but low USG suggests renal and may be a component of hemoglobinuric nephrosis.
AST is in liver, muscle and RBCs so hemolysis can elevate it. Check SDH and CK to rule out the first two.
Unconjugated hyperbilirubinemia usually suggests hemolysis, which is true in this case, but in horses unconjugated bilirubin always predominates in all types of icterus and it also may accompany ANOREXIA in horses.
Brown urine suggests either hematuria, hemoglobinuria or myoglobinuria, in this case there are no RBCs in sediment and there is hemoglobinemia so you know its hemoglobrinuria. (can confirm with ammonium sulfate precipitation test, precipitates hgb from the urine.)
Low SG (renal dz), proteinuria (d/t hgb or glomerular/tubular damage), and bilirubinuria (even though hyperbilirubinemia in horse is due to unconjugated bilirubin, some may be conjugated and spill into the urine, remember, bilirubinuria is always due to conjugated bilirubin.) Also remember bilirubinuria precedes detectable hyperbilirubinemia. p389

Question 4

Dog with low HCT, Hgb and RBC.
Absolute retics are low, platelets are low, and WBCs (segs) are low.
Urinalysis > USG 1035 with 1+ bilirubin and 1+protein. Many WBCs on sediment with squamous cells. The marrow was hypocellular with mostly stromal cells consistent with Aplastic anemia.

Answer 4

This is aplastic anemia / pancytopenia.
Non regen anemia with normal RBC indices, neutropenia and thrombocytopenia indicate aplastic anemia suggesting a multipotential stem cell disorder.
Urinary tract inflammation with squamous cells present suggests squamous metaplasia of the prostate epithelium secondary to estrogens.
This dog had a Sertoli cell tumor in a retained testicle which was producing estrogen, myelosuppression as a paraneoplastic syndrome. THere was squamous metaplasia in the prostate with purulent inflammation explaining the UA results. Squamous metaplasia can result in prostatitis. p392

Question 5

Dog.Anemia with low Hgb, MCV, MCH and MCHC. Retics are high and there are nRBCs.
There is anisocytosis and polychromasia.
WBCs are high including both segs and bands.
The serum ALT is increased.
The serum Fe is low and the percent saturation of Hgb is low and fecal occult blood is positive.
On marrow aspirate there is hypercellular particles with increased megakaryocytes and a high normal M:E ration. There is absence of macrophage iron and increased late rubricytes and metarubricytes.

Answer 5

Microcytic, hypochromic, regenerative anemia = iron deficiency anemia form blood loss, eventually becoming non regen. The decreased marrow macrophage iron low serum iron and decreased saturation of transferrin confirm iron deficiency.
Neutrophilia is commonly seen with regenerative anemia.
Thrombocytosis commonly seen with hemorrhagic anemia.
Increased ALT from centrilobular hepatic damage from hypoxia d/t anemia.
The protein is normal cause maybe it was dehydrated and the protein was actually low.
The marrow is hypercellular d/t neutrophilia and megas are high d/t thrombocytopenia. The RBC precursors are high d/t the anemia and Fe deficiency causes ineffective erythropoiesis.
This dog had a bleeding intestinal mass, and it as resected and anastomosis performed.

Question 6

This horse has an elevated Hct but low WBC including low Segs but high bands. WBC’s have cytoplasmic vacuolation and basophilia.
Fibrinogen is elevated, BUN, total protein and albumin are elevated.
Na is low.
TCO2 is low and AG is low.
On blood gas bicarb is low and PCO2 is low. pH is also low.

Answer 6

Polycythemia d/t dehydration, also resulting in elevated TP and albumin.
Leukopenia, neutropenia, degen left shift, toxic change in neuts and lymphopenia suggest bad prognosis d/t infection or endotoxemia. Neutropenia means bad infection.
Degenerative left shift (that means bands in circulation and segs are low, if segs high it would be regenerative) means bad prognosis as the marrow storage pool is depleted and can’t keep up.
The toxic changes in the neuts means messed up cellular maturation in the marrow and associated with severe infection/inflammation.
Very high fibrinogen means bad inflammation.
Azotemia prerenal d/t dehydration but need UA to verify its not renal.
Hyponatremia means Na is being lost in greater amounts than water which is typical of acute diarrhea in horses, total body Cl is also likely low. K+ also comes depleted in acidosis as it shifts from ICF to ECF and is also likely lost to some degree in diarrhea.
Metabolic acidosis (low bicarb and TCo2) is present and low PCO2 means there i s respiratory compensation. The pH is very low, loss of bicarb (secretory acidosis) likely as NaHC03- in the intestine is indicated by the normal or low anion gap and normal Cl- in the face of severe hyponatremia. Basically acidosis shifts K+ from ICF to ECF which is balanced by the loss of K+ in diarrhea. The normal AG excludes titration of bicarb as a cause of acidosis. (see pg 165) Its a secretory acidosis, basically a bicarb loss acidosis but the Cl increases via resorption in the kidney, but the Na and K+ (the two main cations) are also low which also means Cl- is probably low and AG is low too to maintain electroneutrality.
Salmonella was confirmed at necropsy. pg 398

Question 7

Cat with Anemia with low Hgb but no retics.
WBC Segs and Bands are all high.
Total protein is high, albumin is low.
Alpha and beta globulins are low but Gamma globulins are high.
A:G is low and there is a polyclonal gammopathy on the electrophoretic.
There is ascites with cloudy viscous fluid that has a high cell count with nondegen neutrophils, macrophages and a granular proteinic background. The protein in the fluid is high, the albumin is low but the gamma globulins are what is high.

Answer 7

Normochromic, normocytic non regen anemia with normal RBC morphology and no other cytopenias = chronic inflammation / chronic dz.
Leukocytosis with neutrophilia and left shift > appropriate response to bad inflammation.
Hyperproteinemia d/t polyclonal gammopathy from Ig characteristic of chronic antigenic stimulation. Low albumin d/t negative acute phase, or renal loss or cachexia.
Purulent peritonitis but the Non degen neutrophils suggest a NON bacterial etiology.
The low A:G also suggests FIP, also the granular background suggests high protein content characteristic of FIP.
This cat had FIP pg 401.

Question 8

Dog with low HCT, Hgb and RBC but retics are normal and RBC morphology is normal.
WBCs are high with high segs and bands (the bands outnumber the segs), metamyelocytes and monos. WBC morph shows cytoplasmic basophilia and vacuolation.
Serum chemistry shows azotemia with high TP.
Glucose is low and Na and Cl are both low. Acid Base is normal.
UA is voided with 1.020 USG and 2+ protein and both blood and WBC on urine sediment.

Answer 8

Normochromic, normocytic, non-regen anemia with no other cytopenias indicates = Anemia of chronic dz.
Leukocytosis with left shift and toxic changes and the fact bands outnumber segs (termed “degenerative left shift”) means storage pool depleted and suggests worse prognosis. Toxic changes suggest bacterial infection (means disturbed maturation in the marrow).
Azotemia may be renal cause the USG is pretty low but could also be prerenal.
Hyperproteinemia with normoalbumin and decreased A:G. The hyperprotein suggests increased globulins cause the Alb is normal so likely not dehydration unless the Alb is actually low. There may also be Alb loss in the urine and thus there may actually be dehydration causing a normal albumin and increased GLob, but with the leukogram changes the Glob is probably high from inflammation.
Hypoglycemia suggests sepsis (or insulinoma).
Low Cl and Na are from vomiting and diuresis (note there was a PU/PD described in the history, classic for this condition).
Low USG with pyuria, hematuria and proteinuria. (but note the urine sample was voided.)
Endotoxin can prevent collecting tubules from responding to ADH to conserve water resulting in polyuria (interestingly Ca does this too), (can’t completely rule out primary renal dz).
This dog had a pyometra and after surgery there was a slight leukamoid response with neuts going up but eventually WBC count normalized. pg404

Question 9

10 month old cat with vomiting, dehydration and enlarged periph LNs.
The HCT and Hgb are high. WBCs are low including segs (bands are higher than segs) and lymphs and monos are increased. RBC and WBC morphology are normal.
UA cystocentesis has USG of 1.065.
Serum chemistry shows elevated BUN and TP as well as albumin.
Electrolytes are normal but TCO2 is low but Anion gap is normal.
FeLV is negative but a bone marrow aspirate is hypocellular with Low M:E and normal erythroid maturation, only early myeloid precursors present and megakaryocytes are adequate.
There was a lymph node aspirate with mostly small lymphs, many plasma cells and some large lymphs. (lymphoid hyperplasia)

Answer 9

RBC’s high from dehydration.
There is leukopenia and neutropenia with a degenerative left shift and granulocytic hypoplasia of the bone marrow.
Neutropenia is caused by decreased production of neutrophils, overwhelming tissue consumption of neutrophils or shift from circulating pool to marginated pool. Degen left shift means the marrow is depleted of segmenters and granulopoiesis is failing to meet tissue demand for neutrophils. The low M:E also suggests granulocytic hypoplasia.
Lymphopenia suggests viral dz and suggests parvovirus as it destroys dividing lymphs, hematopoietic cells and intestinal crypt epi cells. Stress may also contribute to lymphopenia.
Azotemia with high USG and high albumin means dehydration.
Na is normal suggesting it was also lost with water so its isotonic dehydration. Even though K+ is normal there is probably a deficit d/t the acidemia and loss in vomiting and diarrhea.
Low bicarb with normal AG means its not a titrational acidosis so it must be a secretory acidosis with bicarb lost in diarrhea.
Lymph node hyperplasia is from infection/AG stimulation and redist to LNs.
This cat had Panleukopenia. It destroys all hematopoietic precursors approx 3-4 days after viral infection and result in neutropenia as they have the shortest half life adn there is increased demand with infection, endotoxemia etc. Anemia may be masked by dehydration. pg 407

Question 10

4 YO dog with bilateral enlargement of multiple LNs.
The HCT, Hgb and RBC are low.
RBC morphology is normal and Plts are adequate.
WBC are high including segs and Monos.
Some large lymphocytes are present in blood but lymphocyte numbers are normal.
Marrow aspirate showed normocellular particles and a mildy increased M:E. (mild granulocytic hyperplasia)
In the LN there is a monomorphic population of large lymphocytes.
BUN/Crea are increased. Ca is mildy elevated.
On UA the USG is low and there are some granular casts but its otherwise normal.

Answer 10

This is lymphoma and it has a leukemic blood profile. The dx of lymphoma is evident from clinical signs and the presence of large lymphocytes. in the blood and LN. Since large lymphocytes were not described in the marrow this suggests leukemic lymphoma and not leukemia.
Anemia is anemia of chronic dz, its normocytic and normochromic and non regenerative where you get mild erythroid hypoplasia which was confirmed by marrow aspirate with the high M:E.
Hypercalcemia is common in lymphoma.
Azotemia with isosthenuria suggests renal failure especially with granular casts indicating a renal tubular lesion of unknown severity. This dog may have nephrocalcinosis from hypercalcemia.
This dog had multicentric leukemic lymphoma.

Question 11

Dog with epistaxis, oral ecchymotic hemorrhages and abdominal pain.
The HCT, Hgb and RBC are low and there are schistocytes.
Platelets are low and the MPV is high.
WBC are high including segs and bands and metamyelocytes, ie left shift. Monos are also high but WBC morphology is normal.
On chemistry the TP is high, albumin is normal and the A:G is low.
On the clotting tests:
BMBT, APTT, PT and TT are all high.
FDPs are also high.

Answer 11

The anemia is normochromic, normocytic non regen so its anemia of chronic dz. Neutrophils are adequate which suggests a selective RBC problem and even though its non regen, presence of schistocytes suggests a hemolytic component with fragmentation of RBCs.
The leukogram is inflammatory with a regenerative left shift.
The thrombocytopenia with increased clotting times suggests DIC. Thrombocytopenia occurs either d/t increased consumption as in DIC, lack of production or immune mediated destruction. Increased MPV suggests increased plt turnover.
Increased BMBT is d/t thrombocytopenia or possibly platelet dysfunction d/t DIC and FDP’s coating platelets.
Consumption of clotting factors in DIC has increased APTT, PT and TT.
**The increased TT tells you the fibrinogen is increased, remember prolonged TT is the most sensitive measure of decreased fibrinogen concentration.
Increased FDPs means increased fibrin clot lysis and fibrinogen degradation. Excess FDPs can also interfere with plt function and BMBT and TT too.
The Fibrin strands in vasculature will result in the presence of schistocytes.
THe high TP, normal albumin and low A:G tells you that globulin is high which may be related to prolonged antigenic stimulation. You need electrophoresis to tell you the exact type of globulinemia you have.
This animal had a unilateral adrenal abscess causing inflammation and DIC.

Question 12

Horse with anorexia, ataxia and head pressing and icterus.
RBC normal.
WBC high including segs and bands. (left shift)
Fibrinogen is high and BUN is low.
GGT, AST and SDH are high.
Anion Gap is high.
T. bili, D. bili, bile acids and NH3/ ammonia are high.

Answer 12

Increased SDH and AST mean hepatocellular damage and release of leakage enzymes.
High Bili and increased GGT suggest cholestasis. Remember unconjugated bilirubin predominates in all cases of hyperbilirubinemia in the horse. So if there is no anemia then high bilirubin suggests hepatic dz. Anorexia may increased bili in the horse but not to this magnitude.
Increased bile acids also suggests cholestasis.
High ammonia and decreased BUN suggests decreased hepatic functional mass with failure to convert ammonia to urea in the hepatic urea cycle. Albumin synthesis is not affected.
Inflammatory leukogram with left shift means intense inflammation as does hyperfibrinogenemia.
This horse had hepatocellular necrosis with periportal to bridging fibrosis with biliary hyperplasia, probably due to Aflotoxins or PA toxicity.
There was also purulent colitis which explains the leukogram.

Question 13

Dog with low MCV and codocytes-target cells, otherwise RBCs are normal.
WBC are normal.
There is low BUN, low TP, albumin and low A:G.
ALP and ALT are increased and glucose is low.
Ca is low.
T. bili and pre and post prandial bile acids are high.
NH3/ammonia is high.
Cholesterol is low.
UA shows very low USG 1.006 (hyposthenuria) with 1+ protein and 3+ bilirubin.
Blood is negative in urine but there are ammonium biurate crystals.

Answer 13

This dog is in liver failure.
There is increased pre and post bile acids and low cholesterol, both of which are hepatic function tests (increased pre and post BA may mean PSS). There is fasting hyperammonemia and low BUN which means either liver failure of a portosystemic shunt. The high ammonia may cause CNS signs (hepatic encephalopathy) including depression, ataxia and seizures.
There is low albumin d/t decreased hepatic synthesis and there may also be renal loss with 1+ protienuria in a dilute urine.
Hypoglycemia likely d/t liver failure d/t decreased hepatic glycogen if a insulinoma isn’t present.
Increased ALT means hepatocellular injury.
High bili means hepatobiliary dz as does increased ALP, there is probably cholestasis.
Hypocalcemia likely d/t hypoalbuminemia.
Microcytosis in the RBCs is consistent with PSS.
Hypotonicity to the urine is likely d/t lack of medullary tonicity from decreased BUN concentration and medullary washout from polyuria.
Ammonium biurate crystals in the urine likely d/t hyperammonemia.
Bilirubinuria d/t cholestasis.
Proteinuria in a dilute urine is significant. There is renal protein loss likely d/t glomerular or tubular lesion.
This dog had a PSS, extrahepatic and on histo of liver there was hepatic chord atrophy and microvascular dysplasia.

Question 14

Dog with distended abdomen and abdominal pain. The WBC are high as are the segs and bands (bands are lower than segs). There is cytoplasmic basophilia and vacuolation. The monos are also high.
There is azotemia with high TP and Albumin.
ALP, ALT and Glucose are also elevated.
The Ca is low and the amylase and lipase are high. The USG is 1045 and there is 1+ glucose but no ketones.

Answer 14

There is an inflammatory leukogram characterized by neutrophilia with a left shift. Purulent inflammation likey due to peritonitis. Toxic changes in the neuts indicate systemic toxemia in this case this is all due to pancreatitis and steatitis.
Prerenal azotemia with high ALbumin and USG means dehydration and decreased renal perfusion.
Very high lipase and amylase suggest a pancreatic origin but is also likely due to prerenal azotemia and decreased GFR.
Cholestasis and liver injury d/t close proximity of the common bile duct and the man pancreatic duct where the enter the duodenum, pancreatitis can cause partial obstruction of the common bile duct.
Hyperglycemia is due to pancreatic necrosis and also caused glucosria.
Hypocalcemia is d/t glucagon released from the necrotic pancreas which stimulates calcitonin release reducing blood Ca concentration. (there may also be a little precipitation of Ca in fat saponification but that’s not the main cause).
Extensive pancreatic necrosis was observed at necropsy in this case.

Question 15

Poodle with vomiting weight loss and PU/PD. The HCT, Hgb and RBC are all low and there are no retics but the RBC morphology is normal.
UA shows a 1.012 specific gravity, 4+ glucose moderate ketones, 1+ bili and few RBC, WBC and transitional cells on sediment.
ON serum chemistry there is azotemia with elevated ALP, mild ALT elevation and hyperglycemia.
Na and Chloride are low.
TCO2 is low. AG is high.
Calcium is low and Phos is high.
Fecal trypsin is low.
TLI is low, folate is high and cobalamin is low.
BT-PABA is low.

Answer 15

Decreased TLI and BT-PABA cleavage indicates deficiency in trypsinogen and chymotrypsin respectively.
High folate and low cobalamin means bacterial overgrowth d/t lack of bacteriostatic pancreatic enzymes.
Hyperglycemia, ketonemia, glycosuria and ketonuria = Diabetes mellitus (neg energy balance).
Liver dz present based on elevated ALP with cholestasis (glycogen swollen hepatocytes compressing bile canaliculi) but in diabetes dogs can have induction of steroid isoenzyme of ALP too. DM promotes hepatic glycogen loading and hepatic lipidosis causing hepatocyte swelling as Glucose is produced from AA via gluconeogenesis and lipids are consumed for energy via Beta oxidation (to ketones I think). Bilirubinuria also d/t cholestasis. Elevated ALT also likely due to increased membrane permeability as its only mildly elevated.
Renal failure indicated by low USG with azotemia and high Phos and low Calcium. The kidney makes less 1,25 dihydroxycholecalciferol. The Ca X Phos is also above 70 so there is potential for soft tissue mineralization.
Normochromic, normocytic non regen anemia means anemia of chronic dz. Also may be d/t renal dz and decreased EPO production.
Metabolic acidosis with high AG means unmeasured anions likely uremic acids and ketones with a titrational acidosis.
Hyponatremia and hypochloremia with normokalemia (d/t acidosis). Glucosuria results in osmotic diuresis, K+ is also lost but with an acidosis its moving ICF to ECF so normokalemia is maintained. Cl also lost in vomiting.
This dog had exocrine pancreatic insufficiency, diabetes mellitus, chronic renal failure, I think the liver changes are from glycogen and lipid storage due to the DM most likely. pg 421

Question 16

A dog with a history do diarrhea and weight loss.
There is lymphopenia.
UA there is a USG of 1.033 with negative protein.
Chemistry: The total protein and albumin are low
The glucose are Calcium are low. There is fat in the feces including split fats. The plasma is clear pre and post feeding.
TLI is normal.
The D–xylose absorption at 60, 90 and 120 minutes is low.

Answer 16

The fecal fat / steatorrhea means malabsorption. The presence of split fats means means pancreatic lipase is being produced.
Deficient d-xylose absorption suggests malabsorption as it is a simple sugar that should be readily absorbed and appear in the blood.
Normal TLI means the problem is not EPI so this all means its an absorptive problem and not digestive problem.
Low TP and albumin means pan hypoproteinemia (normal AG ratio). Means loss in the GI and not kidney as no evidence of decreased production as liver values are normal and no bleeding, no anemia. The suggests enteric protein loss / malabsorption.
Hypoglycemia d/t malabsorption of carbs.
Hypocalcemia is d/t hypoalbuminemia.
Lymphopenia d/t loss of intestinal afferent lymph which is lymphocyte rich and lost into intestine lumen concurrent with protein loss.
This dog had IBD on intestinal bx. > PLE, lymphocyte loss and malabsorption of fat.
Intestinal bacterial overgrowth is likely responsible for the abnormal D xylose test cause simple sugars are absorbed into portal blood and not lymphatics. pg 425

Question 17

Horse with pain and sweating.
The WBC is high including bands and segs (but segs are higher than bands.)
Fibrinogen is high
Plasma is pale yellow colored.
BUN and Crea are high so there is azotemia.
Protein is normal.
AST and CK are high and Phosphorus is high.
Urine is brown with a USG of 1.020 and 2+ protein. Occult blood is 4+ and there are only few RBC on sediment but also 4-5 WBC per HPF and some granular casts as well as some CaCO3 crystals.

Answer 17

Inflammatory leukogram with regenerative left shift also supported by elevated fibrinogen which is an acute phase protein.
Myoglobinuria as evidenced by red brown discoloration of urine but this can also occur with hemoglobinuria and hematuria but its not hematuria cause the RBC on sediment is low and its not hemoglobinuria cause the plasma is pale golden colored so it must be myoglobinuria. The positive reaction for occult blodo can occur with all three cause of the peroxidase activity of the strips. Myoglobinuria is also supported by the elevated AST and CK. (AST can also be prsent with hemolysis but the plasma is a normal color.) Liver enzymes are normal so its not liver.
Myoglobinuria, inflammation and loss of albumin can all result in protienuria. In this case its probably myoglobinuria and there is some WBCs present too.
Azotemia with a low USG and no evidence of dehydration - Albumin is normal and HCT is normal (ie its renal azotemia).
Also the Phos is elevated which points to renal dz.
Granular casts also indicate tubular damage.
This horse has primary muscle dz with rhabomyolysis, like tying up, with secondary myoglobinuric nephrosis and renal failure.

Question 18

A lethargic dog.
There is elevated HCT, Hb and RBC and RBC morphology is normal.
WBC are also high as are segs and bands (but segs are higher than bands).
Urinalysis: The USG is 1.011 and there is 1+ protein and glucose.
Serum Chem: There is azotemia with an elevated TP and albumin is normal.
Glucose is elevated, K+ is elevated, Cl- is low and TCO2 is low.
AG is elevated.
Ca is low and Phos is high.
Blood Gas: The pH is low, HCO3- is low and PCO2 is low.

Answer 18

There is renal failure based on the azotemia and isosthenuria.
Hyperphosphatemia also indicates renal dz and decreased GFR. This dog also had Oxalate monohydrate crystals on UA sediment (ethylene glycol tox) and the rust inhibitor in antifreeze can also be a source of phosphate.
There is metabolic acidosis and its titrational based on the elevated AG. Metabolites of ethylene glycol and the uremic acids elevated the AG. There is respiratory compensation based on the low PC02. The Cl is probably low cause of vomiting.
Polycythemia with elevated HCT is from dehydration, also elevated TP from dehydration. (The A/G ratio is normal).
Proteinuria from renal dz.
Mild hyperglycemia glucosuria from catecholamine release and maybe some in the urine is due to acute renal necrosis/dz d/t destruction of epi cells and inability to reclaim the glucose so in that case it can be seen in the urine with even mild hyperglycemia.
Na isnt’ elevated cause its being lost and its not low cause of dehydration. Low Cl from vomiting. Acidemia caused a shift of K from intra to extracellular and I guess oliguria prevents K+ from being lost in the urine (in renal failure you can get absence of urine production if things are really bad.)
Hypocalcemia in renal failure via several mechanisms and in this case also cause formation of Ca oxalate crystals and cause of the elevated Phos.
Inflammatory leukogram with left shift suggests clinically signficant inflammation.
Dx: This dog had oxalate nephrosis with renal failure and high AG, hypoclacemia and Ca oxalate crystalluria, all classic for antifreeze tox. There is a test for antifreeze so you can detect it early in plama as long as the test is done within 12 hours of exposure before its turned into toxic metabolites. Propylene glycol (food preservative) and glycerol can interfere with the test.

Question 19

A dog with low HCT, Hb and RBC. RBC morph is normal and there are no retics.
The WBC is high mostly due to high segs but there are no bands.
UA: Its cloudy with low USG (1.016) and there is 4+ protein with both glc and ketones being negative. There are few RBC and WBC and there are granular casts and amorphous crystals.
Chemistry: BUN and Crea are high.
Total protein, Albumin and A:G are all low.
Calcium is low and Phos and Cholesterol are high.
ON the abdominal fluid analysis its clear and colorless, the nucleated cell count is high at 200/ul and includes non degen neutrophils, macrophages and mesothelial cells, protein is 2.5 and it was interpreted as a transudate.
Urine Protein Creatinine ratio is 12.2.

Answer 19

Anemia of chronic renal dz as evidenced by the normocytic, normochromic, non regenerative anemia accompanied by azotemia. There is likely loss of EPO secreting peritubular cells.
The leukogram is a stress leukogram: Neutrophilia without a left shift and a low normal lymphocyte count (SMILED, segs monos increased, lymphs, eos decreased)
LIkely early renal failure with low USG in the face of azotemia and proteinuria. (remember azotemia can also be pre renal and post renal). This animal also was PU/PD which fits with low USG.
Note - with primary glomerular lesions (like amyloidosis or glomerulonephritis) azotemia may PRECEDE the loss of urine concentrating ability (so initially it may look prerenal). This may be referred to as Glomerulotubular imbalance because tubule dysfunction usually precedes glomerular dysfunction in renal failure. (so I guess the glomerulus is in charge of preventing azotemia - based on nephron function, and tubules resorb protein).
Proteinuria of renal origin based on the normal sediment exam, this is albumin loss which is supported by the low serum albumin and low A:G. IN some cases of amyloidosis when severe globulins may be lost.
*ALso a urine protien crea ratio of > 3 suggests protienuria is of glomerular origin. (ie its a shitload of protein). The highest UPC rations are observed with renal amyloidosis.
Hypocalcemia is d/t low albumin (40% of Ca in blood is Alb bound and 50% is ionized). Hypocalcemia can be seen in renal failure in some cases but need the iCa++ to determine that.
Hyperphosphatemia is seen due to renal dz and means the GFR is decreased.
High cholesterol is seen d/t the low albumin which is thought to stim lipoprotein synthesis in the liver.
This animal also had dependent edema and ascites d/t hypoalbuminemia, decreased plasma oncotic pressure, it can be generalized and would be called anasarca too in some cases but is most often dependent.
Renal amyloidosis was dx’d by biopsy in this case.
This is nephrotic syndrome based on the Edema, Azotemia, Hypoalbuminemia, proteinuria, and hypercholesterolemia. Nephrotic syndrome is due to Primary glomerular disease. pg 434

Question 20

A cat with an elevated WBC count, mostly segs, no bands present and lymphocytes are a little low. WBC morphology is normal.
UA: On cysto the color is reddish brown and cloudy and USG is 1.031. There is 3+ protein and 4+ blood. There are lots of RBC and WBC on sediment as well as triple phosphate crystals and 3+ bacterial rods.
Chemistry: BUN/Crea are high.
Glucose is high, Na is low, K+ is high, Cl is low.
TCO2 is low. Anion gap is high.
Calcium is normal and Phos is high.

Answer 20

The WBC changes are a stress leukogram based on neutrophilia with no left shift, lymphopenia and eosinopenia (remember SMILED).
Pos urine protien and occult blood = hematuria; pyuria is present based on the sediment exam and there is bacteriuria so there is a UTI. Thus overall interp is Hemorrhagic bacterial cystitis.
The azotemia is likely post renal.
Hyperglycemia is likely stress / catecholamine release.
High anion gap metabolic acidosis due to presence of uremic acids and is titrational (not secretory) based on the high AG. Lactic acid may also contribute in this case. Low TC)2/bicarb from titration by uremic and/or lactic acids.
Hyponatremia from low total body Na and the low Cl is from vomiting in this case.
Hyperkalemia d/t acidosis and urinary obstruction (excess body K+ is eliminated in the urine).
Hyperphosphatemia from reduced GFR (follows BUN/Crea).
Summary: This cat was obstructed and had a UTI. pg436

Question 21

Holstein cow with low segs, and high bands (higher than segs), and also has other precursors in circulation.
WBCs have cytoplasmic vacuolation and basophilia.
Fibrinogen is elevated.
AST and Glucose are elevated.
High Anion Gap. TCO2 is normal.

Answer 21

Leukogram = Neutropenia with degenerative left shift and toxic changes in neutrophils. This is peracute inflammatory dz in cattle (as also evidenced by high fibrinogen). The neutrophil storage pool is exhausted. Toxic changes reflect severe bacterial infection and toxemia in this cow.
Increased AST could be liver dz, muscle dz or hemolysis. (there is no other evidence of hemolysis); elevated SDH would point to liver and elevated CK would point to muscle.
Hyperglycemia from catecholamine release.
High Anion gap from ummeasured anions and in this case may be lactate production from shock. This could also be related to ketosis. Both of these would cause a titrational metabolic acidosis. TCO2 is normal so there must be a concurrent alkalosis in this case (like from abomasal reflux of Cl- I think) so this would be a mixed metabolic alkalosis and acidosis.
This cow had a hot udder and acute septic mastitis and an occult acidosis based on the high AG. What type of mastitis do you think this is (ie whats the organism?)

Question 22

8% Dehydrated Cow with elevated Segs but not bands. The lymphs are low but WBC morphology is normal.
Fibrinogen is high.
UA: Voided, red and cloudy with USG of 1.018, 3+ protien and 2+ glucose.
Ketones and Bili are negative.
Blood is 4+
Sediment there are many RBCs and 1-2 granular casts per hpf.
Chemistry: The BUN/Crea are high.
Total protein and Alb are high but A:G is normal.
Glucose is high.
Na, K+, Cl- are all low.
TCO2 is high and Anion gap is high.
Ca is low and Phos is high.
Blood Gas: HCO3- is high and PCO2 is normal and pH is high.

Answer 22

Neutrophilia and leukopenia with normal total WBC count means either stress or mild inflammation. (remember SMILED).
Hyperfibrinogenemia from inflammation.
Azotemia likely renal or pre renal (not post renal as the sample was voided). Low USG in this case with the dehydration suggests renal failure.
Protienuria and hematuria may be from the renal lesion or from the bladder.
Granular casts indicate a tubular lesion of unknown severity.
High albumin and by calculation with the A:G, the globulins are also high. Likely from the dehydration present in this cow and its severe.
Hyperglycemia and glucosuria may be seen in extremely ill cattle.
Hyponatremia and hypokalemia > bovine renal dz causes loss of Na and low K+ may be due to external shifts of K like from decreased intake and loss in the urine, and also from internal shifts from the alkalosis.
There is a mixed metabolic acidosis and alkalosis (Low TCO2 and bicarb) and the hypochloridemia are all common in bovine renal dz d/t upper GI stasis and functional loss or trapping of abomasal HCl.
Normal pCO2 means resp compensation has not occurred.
High AG is from extra anions/acids present (uremic acids, phosphoric acids (high P concentration) and perhaps high lactic acid (shock). Its a mixed acidosis alkalosis in this csae but the alkalosis is winning.
Hypocalcemia and hyperphosphatemia is from bovine renal dz.
This cow had unilateral perirenal and renal hemorrhage, and bilateral nephrosis was dx’d. The etiology was not determined. You wonder about Bracken Fern, enzootic hematuria though, with renal damage and abomasal stasis. pg 442

Question 23

A cow with normal RBCs but elevated WBCs including Segs, but bands are normal..
Fibrinogen is elevated.
UA is pale and clear with USG of 1.012. Protein is negative and glucose is 2+ and ketones are negative. Ph is 5 in the urine so its acidotic.
Chemistry shows elevated glucose at 231.
Potassium is low
Chloride is low
TCO2 is high but Anion Gap is normal.
Blood Gas: HCO3- is high, PCO2 is high and pH is high.

Answer 23

There is a neutrophilic leukocytosis without a left shift which can occur in non inflammatory conditions like displaced abomasum. In this case the fibrinogen is elevated which says there is some inflammatoin.
Hyperglycemia and glucosuria, in cattle this can be induced by endogenous catecholamine or steroid release and as in this case it may exceed the renal threshold.
There is a metabolic alkalosis with respiratory compensation based on the elevated HCO3- and TCO2 combined with a high PCO2 (to compensate).
Abomasal displacement causes sequestration of HCl so HCO3- must go up (Cl is low in this case).
Normally with alkalemia bicarb would be lost in the urine with retention of H+, but in this case there is a deficiency of Cl- so bicarb is resorbed from the filtrate
There is also a deficiency of K+, so as Na+ is resorbed H+ (acid) is secreted in the urine which worsens the alkalosis and causes paradoxic aciduria.
The AG in this case is normal so there is no titrational metabolic acidosis in this case.
They hypokalemia is due to anorexia in a herbivore, which commonly causes low K+ in these guys (decreased intake and continued renal loss) and also the fact there is an alkalosis so most K+ is intracellular. Additionally there is also loss of K+ in gastric and intestinal fluids with the displacement.
This cow had an Right displaced abomasum. pg 443

Question 24

Vomiting dog with elevated hematocrit. It has rapid respiration and is being administered fluids.
The UA was clear with a USG of 1.015.
BUN is elevated on chemistry.
Na, K+ and Cl- are all low.
TCO2 is high and Anion Gap is high.
Blood Gas: HCO3- is high, pH is high and PO2 is low. PCO2 is normal.

Answer 24

The polycythemia is probably from dehydration that was severe from the vomiting. (absolute polycytemia would be from stuff like L to R shunting, high altitude, chronic hypoxia, lung dz, renal cysts or neoplasms).
Azotemia with a low USG may indicate renal failure but low USG may also be diuresis from fluid therapy.
Hyponatremia, hypochoremia and hypokalemia. Hyponatremia likely due to overhydration or inadequate Na in the fluid administered, and Cl- normally parallels Na but may also be low from vomiting. The Hypokelemia is often a sequela of long term fluid admin, esp if the fluids are alkalizing, causing an internal shift of K+ from ECF to ICF. Diuresis produces kaliuresis when fluids are administered.
Hypoxemia with a normal PCO2 means a perfusion/diffusion abnormality, ie oxygen is not getting where it needs to get in the alveoli as in pneumonia, pulmonary edema, or pulmonary thrombosis.
There is an uncompensated mixed metabolic acidosis (high AG) and alkalosis (high TC02 and bicarb and pH). There is lack of respiratory compensation cause PCO2 is normal. The hypoxia is maintaining respiratory drive preventing hypoventilation needed to compensate for the alkalosis.
High AG suggests a titrational acidosis like uremic acids or lactic acids. Lots of lactated ringers fluids can also increase lactate and AG. Lactate can also be converted to bicarb and cause an elevated bicarb or maybe they added bicarb to the fluids.
BLUF: This dog had Paraquat toxicosis, which is a herbicide that causes interstitial pneumonia, type II pneumocyte hyperplasia, pulmonary fibrosis and comprimised respiratory function (which explains the hypoxia). It was dx’d with nephrosis, pulmonary hemorrhage and pulmonary edema on necropsy.
pg446

Question 25

A dog that had lameness, hyphema and hematuria. The Hct, Hgb and RBC are all low. The retics are elevated and the absolute retics are elevated. There is polychromasia.
The WBCs are elevated including the segs but the bands are not. The Monos are also increased. WBC morphology is normal.
UA: The urine is red with a USG of 1040. The pH is 6.5 and the protein is 4+, blood is 4+. Glucose, ketones and bilirubin are negative. WBC are TNTC and the RBCs are also high..
Chemistry: Total protein and albumin are low.
Clotting tests: The activated clotting time is high, the APTT is high and the PT is high. TT is normal and FDPs are low.
ON synovial fluid analysis its red and cloudy with poor mucin clot quality some nucleated cells, numerous RBCs with 20% neuts and 80% monocytes and lymphocytes.
There is erythrophagocytosis by macrophages.
The interpretation was hemarthrosis or bleeding into the joint.

Answer 25

There is a normochromic, normocytic regenerative anemia. Its consistent with a hemorrhagic anemia.
Leukocytosis, neutrophilia and monocytosis commonly occur after hemorrhage.
Hypoalbumin and hypoproteinemia is from hemorrhage, A:G is normal cuase both are lost in blood.
Both PT (extrinsic) and APTT (intrinsic) are elevated so its either a problem in the common pathway (1, 2, 5, 10), or multiple factors are low for the extrinsic (3, 7) and intrinsic (8, 9, 11, 12).
It could be vitamin K dependent factor defeciency (2, 7, 9, 10).
Hemophilia A is factor 8 def. Hemophilia B is factor 9 def. so its not either of these. Its not VWD cause they don’t effect PT or PTT. Its not DIC cause plts, fibrinogen and FDPs are normal. Coumarin rodenticide toxicity is likely. Liver dz is unlikely cause liver enzymes are not elevated and the other liver function tests are normal.
Hematuria likely from hemorrhage. RBCs in the joint with erythrophagocytosis also consistent with hemrorhage.
This dog was exposed to an anticoagulant rodenticide like coumarin. It was treated with vitamin K administration. pg 448

Question 26

This dog was PU/PD with alopecia etc and has elevated WBCs including segs but not bands. Lymphs are low and monocytes are high. RBC and WBC morphology are normal.
UA: clear yellow with USG of 1.006. The pH is 7 and there are squamous cells on sediment.
Chemistry: ALP is elevated and ALP post Levam is high still and the remaining ALP that suppressed with levamisole is normal (ie the difference between the ALP and ALP post levam).
ALT is high and glucose is mildy elevated.
On other testing the ACTH stim test showed pre-ACTH cortisol as 2.1 and post ACTH cortisol as 21.1.
Low dose dex suppression had a pre dex cortisol of 2.28 and an 8 hour post cortisol as 1.78.

Answer 26

Leukocytosis with neutrophilia, monocytosis, lymphopenia and eosinopenia with lack of a left shift is consistent with corticosteroid administration.
Increased ALP with resistance to levamisole inhibition. Its the steroid isoenzyme of ALP which is resistant to levamisole inhibition (unlike bone and liver isoenzymes which are suppressed by it).
You get some elevation in ALT cause of swelling of hepatocytes with glycogen and blocking of canaliculi and cholestasis with detergent action on plasma membranes.
Hyperglycemia from gluconeogenesis due to steroids.
Hyperadrenocorticism: Overstimulation with ACTH (too high of a response) and failure to suppress plasma cortisol with Dex indicates cushings but does not diff b/t adrenal or pituitary dependent, you would need HDDST for that. Most cases of pituitary dependent cushings respond to HDD but not adrenal dependent. If this was iatrogenic cushings the adrenal gland would fail to respond to ACTH stimulation.
Very low Urine SG due to medullary washout and reduced medullary tonicity caused by the steroid induced polyuria. You would need gradual water deprivation test to determine if renal failure is present.
A pituitary adenoma was discovered at necropsy with this dog. pg 451

Question 27

Cat with PU/PD, fleas and tachycardia and wt loss.
The HCT, Hgb and RBC are all high. RBC morphology is normal.
WBCs are high including segs, but bands are normal. Lymphs are low and eos are high.
UA: Voided, USG is 1.060 and there is 2+blood. Many RBCs on sediment and some fat droplets.
Chemistry: BUN is high but Crea is normal.
ALP, ALT and Glucose are high.
Total T4 is high. There is pleural fluid prensent and it has a volume of 200ml with 3.4 protein and 2000 nucleated cell count consisting of many small lymphs, a few non degen neutrophils macs and mesothelial cells.
Interpretation is a modified transudate of cardiac disease.

Answer 27

Polycythemia probably a little from dehydration but also from absolute polycythemia from the hyperthyroidism with stimulation of erythropoiesis.
Leukocytosis with neutrophilia, eosinophilia and lymphopenia is part from stress but the Eos elevated is probably from the fleas or flea allergy dermatitis.
Increased BUN is from increased protein catabolism in hyperthyroidism. Azotemia and high USG usually means prerenal. GFR problems or renal azotemia unlikely in this case cause Crea is normal.
INcreased ALP usually means biliary dz but hepatic centrilobular lesions seen with heart dz don’t usually don’t cause cholestasis. Hyperthyroidism is thought to cause increased bone turnover so it may be the bone isoenzyme of ALP.
Increased ALT likely due to centrilobular hepatic necrosis from hypoxia due to the cardiac dz that’s causing the pleural effusion (likely HCM).
Hyperglycemia from catecholamine release or from gluconeogenesis in response to cachexia and muscle catabolism related to hyperthyroidism.
INcreased TT4 means hyperthyroidism, when very high its diagnostic. Due to an adenoma or nodular / adenomatous thyroid hyperplasia.
HCM resulting in the pleural effusion is a sequela of the disease.
The three most common causes of lymphocyte rich pleural effusion in cats is lymphoma, cardiac disease and chylothorax.
This cat was hyperthyroid with HCM. pg 455

Question 28

A dog with vaginal bleeding. It has normal hematology. On UA the sample is voided and pink and the USG is 1.036. The blood is 2+ and there are many rbcs on sediment but only rare WBCs.
Serum chemistry is normal. Platelet count is normal.
Clotting tests: BMBT is high but all other clotting tests are normal. Von Willebrand’s factor antigen is low.

Answer 28

Von Willebrand’s disease causes platelet dysfunction and prolonged BMBT. Other ddx for increased BMBT when there is a normal platelet count include uremia or increased FDPs which are not supported by the lab data in this case.
Coag factor VIII deficiency accompanies deficiency of vWF but its usually not that low and so the APTT is generally not prolonged (remember APTT is intrinsic with factors 8, 9, 10, 11).
vWD is confirmed documenting decreased vWD factor antigen.
Hematuria in this case is likely of genital tract origin.
BLUF: This dog had VW disease. Fresh frozen plasma can be used to control bleeding associated with vWD. Plts are NOT needed because the defect is a lack of a plasma glycoprotein VW factor, the platelets are normal.

Question 29

A cow with a large splashy atonic rumen and muscle tremors.
The HCT, Hgb and RBC are low. RBC morphology shows slight anisocytosis.
WBC are elevated and segs are elevated and Monos are elevated.
protein is high and Fibrinogen is high.
UA: The USG is 1.029. The pH is 8. There is 1+ glucose and the ketones are negative.
Blood and bilirubin are negative. There are many triple phosphate crystals on UA.
BUN is high and Total protein is high.
GGT and AST are high, SDH is high and CPK is very high and ALT is high.
Na and Cl- are high.
Anion gap is high.
Total bilirubin is high.
Other tests include plasma NH3 (urea) and Rumen NH3 which are both high.

Answer 29

The polycythemia may be due to dehydration.
The anisocytosis with a little variation in RBC size is a no
normal finding in cattle.
The leukocytosis and neutrophilia is due to excitement and also probably inflammation.
Monocytosis is from acute or chronic inflammation.
Hyperproteinemia and hyperfibrinogenemia are from inflammation (fibrinogen contributes to the TP).
High anion gap may be due to lactic acid from shock but the TCO2 is normal so you really need a blood gas to get a better assessment.
Hypernatremic hypovolemia is due to the presence of a bunch of extra small molecular substances (urea) increasing tonicity in the rumen fluid. Little urea diffuses out of the rumen but water can enter and it enters with Na, depelting Na. Total body water is normal but water has accumulated in the GI tract.
There is K depletion although it measures normal. It leaks from damaged muscle and there is decreased ECF K cause the animal is anorectic. There is a cardiac arrhythmia that may be due to K+ ICF depletion.
Hyperchloridemia d/t increased NaCl. The Na is decreased higher than the Cl so there may be some sequestration of HCl in the GI tract due to the rumen disorder.
Increased BUN is possibly due to absorption of the Urea from the GI tract or increased hepatic synthesis of urea from ammonia as the body tries to clear excess ammonia and there may be some prerenal azotemia too.
Increased AST is likely from liver as SDH is also increased but CK is really high so it may also be from muscle (it can also come from hemolysis don’t forget, butt there is no evidence of that here.)
Marked increase in CK is from muscle injury from being a downer cow.
Increased ALT - remember LT for little animals, this is not useful for cows, it probably came from the muscle injury.
GGT is what is measured in large animals to assess for biliary dz, not ALP. There is likely some cholestasis in this cow.
Increased SDH indicates hepatocellular damage (remember SDH for large animals, remember Simmental Damaged Hepatocytes, SDH).
Hyperammonemia in this case is due to rumen microflora converting urea to ammonia which can be absorbed into the blood to form NH3. Ammonia contributes to neurologic abnormalities and muscle weakness.
Normal glucose with glucosuria is probably from excitement and catecholamine release followed by storage of urine and sampling for a period after the excitement subsides.
Anorectic cattle might have a little increase in T. bili.
You would expect an anorectic animal to excrete an acid urine but its alkaline in this case cause of excretion of excess ammonia, and the triple phosphate crystals form in alkaline urine.
BLUF: This animal was accidentally fed toxic levels of urea. Urea toxicosis resulted in shifts of fluid into the rumen causing hypernatremic dehydration. The rumen flora convert urea to ammonia and some is absorbed leading to hyperammonia and ammonia toxicity and you see disorientation, muscle weakness, neuro signs etc. Further muscle damage from being down. pg 458

Question 30

A 2 year old dog with polyuria, resp distress and pulmonary edema.
The platelets are low, WBC are high including segs but not bands.
Lymphs are also low.
UA: USG is 1.010 and the protein is 1+. There are few RBC, WBC and amorphous crystals on sediment.
BLood gas: The pH is a little low. PCO2 is high, PO2 is low and HCO3- is low. The base excess is also low.
Chemistry: The BUN is high and Crea is also high.
Total protein and albumin are low. The A:G and glucose are also low.
The K+ is high. The TCO2 is low. The Anion Gap is high.
Ca is high and Phos is high. (CaXPhos is > 70).

Answer 30

Leukocytosis with neutrophilia and lymphopenia, likely from stress, this is a stress leukogram.
There is hypoventilation based on the low O2, high CO2, there is a respiratory acidosis. The animal has increased respiratory effort so its a problem with the alveoli (and not decreased drive) if there is no upper airway obstruction.
There is mixed metabolic and respiratory acidosis based on the high anion gap from uremic acids and phosporic acid from the renal disease, the metabolic acidosis based on the low bicarb and TCO2. Its titrational based in the high AG.
Hyperkalemia is from end stage renal disease. (oliguric renal disease). K+ also goes up in acidosis due to internal/intracellular shifts. .
Hypercalcemia and hyperphophatemia with elevated Ca Phos produce means tissue mineralization. Elevated Ca and Phos may be seen in congential renal disease.
Azotemia with markedly high crea and moderately high BUN consistent with bad renal dz.
Hypoglycemia may reflect exhaustion of glucose stores.
Hypoalbumin / hypoproteinemia (The A:G is low, globulin isn’t normally lost in urine) are from loss in the kidney as the urine is very dilute but there is a 1+ protein on the dipstick that would be albumin.
Isosthenuria and mild proteinuria, ie low USG with proteinuria are consistent with end stage renal dz.
BLUF: This dog had congenital renal dz progressing to end stage renal dz and the pulmonary stuff is from mineralization of alveolar walls througout the lungs (so called uremic pneumonitis). Mineralization causes lack of elasticity in the alveoli, inability to expire air and obstructive, hypoventilatory pulmonary dz. The kidneys were small and fibrotic / end stage. pg 463

Question 31

A dog with a total T4 of 0.78 (1.5-4.0)
TT3 104 (78-260)
fT4 0.7 (0.9 - 2.3)
Anti thyroglobulin autoantibodies: neg
Anti T4 Abs: 6% (<10%)
Anti T3 Abs: 0% (<2%)
cTSH 1.2 (<0.6)

Answer 31

Low TT4 and fT4 and increased TSH are consistent with early primary hypoparathyroidism.
T3 is normal as tissues and the thyroid can produce a larger percentage of T3.
There is no obvious evidence of immune mediated thyroiditis in this case because anti thyroglobulin, anti T4, and anti T3 autoantibody concentrations are WNL.
BLUF: This dog had early hypothyroidism. pg 465

Question 32

A dog that is obese and being treated with prednisolone for pruritis and has a bad hair coat. The total T4 is: <0.5 (1.5-4) and the cTSH is 0.2 (<0.6).

Answer 32

A decreased TT4 and TSH may be due to hypothyroidism but could also be something else like the pred txmentt (I think this is called euthyroid sick).
The TSH is suppressed by the pred apparently but this has not been demonstrated experimentally. Also, some dogs with hypothyroidism may have a normal TSH (appox 25%). This recommends weaning off the pred and retesting the TSH and TT4 but I wonder why not just do a fT4? pg466

Question 33

A miniature poodle wiht persistent lipemia and being treated for epilepsy with phenobarb. It has lethargy and hair loss.
The fT4 is 0.4 (0.9-2.3).
cTSH 3.2 (<0.6).

Answer 33

There is decreased fT4 and increased TSH.
Decreased fT4 and TT4 are known to occur with phenobarb txent but usually they are mild and not severe as in this case.
These lab results are consistent with primary hypothyroidism and should be tx’d with supplementation.

Question 34

A dog with elevated MCV and MCH and occasional macrocytes for the RBC morphology.
The WBCs are high including the segs and bands (segs are higher than bands). Monos are also high.
The WBC morphology shows cytolasmic basophilia and vacuolation.
Modified knotts test shows Dirofilaria immitis present.
Urinalysis:
Its a catheterized sample and its dark yellow and cloudy. The USG is 1.039 and pH is 8.0. There is 2+protein and 2+ glucose. Ketones are 1+. There are moderate numbers of WBC and RBC on sediment exam.
There are 1-4 granular casts/hpf, bacilli, spermatozoa and fat globules.
Blood Gas: Ph is low and PCO2 is high and PO2 is normal and HCO3- is low.
Serum chemistry: BUN and Crea are high.Na is high.
Total protein and albumin are high.
ALT and ALP are high. ALP with levam is normal but only suppresed about 20% of the total ALP.
TCO2 is low and Anion gap is high..
Phosphorus is high.
Amylase and lipase are high.
Other: baseline cortisol, low dose dexamethasone and high does dexamethasone are all high.

Answer 34

Macrocytosis without polychromasia and a normal RBC count represents congenital macrocytosis seen occasionally in poodles (if there was polychromasia/reticulocytes that would explain it.)
Increased MCH but MCHC is WNL, usually these values follow the same trend but when the disagree you should go with the MCHC, its more accurate than the MV and MCH because it does not require the RBC count for its calculation. Thus in this case the RBC population is normocytic.
There is a leukocytosis with left shift and monocytosis as well as toxic change so this is inflammatory. (note the left shift is pretty minimal).
This patient has a UTI cause there is bacteria in the urine.
This patient has heartworm but does not have an eosinophilia or basophilia which may suggest cortisol release in this dog.
There is pyuria, bacteuria, hematuria, proteinuria, glucosuria and ketonuria and thus there is a UTI an that is also increasing the urine pH as the bacteria degrade urea to ammonia. Note the protein reagent pad will falsely detect protein in an alkaline urine and thus proteinuria should be confirmed by another technique.
Glucosuria and hyperglycemia are suggestive of diabetes mellitus.
Ketonuria suggests a negative energy balance often seen in DM. This also explains the titrational metabolic acidosis that is present.
There is an uncompensated metabolic acidosis that is titrational based on the high AG (actic acid or ketoacids) with normal high PCO2 - this patient is hypoventilating for some unexplained reason.
There is hypernatremia probably from dehydration and I would expect the chloride to be high cause of the acidosis but its probably being lost in vomiting otherwise it would be high (remember when Cl is lost bicarb goes up).
Azotemia is probably prerenal as the USG is high.
The albumin is high from dehydration.
ALT is high from either pancreatic enzymes leaking, cholestasis with detergent action of bile acids, steroid hepatopathy with membrane compromise and leakage.
Increased ALP with mostly resistance to levamisole txment indicates its mostly the steroid isoenzyme of ALP that is high. SOme cholestasis related to the pancreatitis may have resulted in cholestasis too.
Hyperphosphatemia with increased CaXPhos product. The high Phos might be from decreased GFR and the high Ca Phos product means soft tissue mineralization is imminent.
Hyperlipasemia and hyperamylasemia suggest acute pancreatitis but if there is a decreased GFR that can also mean the clearance of these enzymes is prolonged.
Increased baseline cortisol with failure to suppress with low and high does dex suggests adrenal cortical neoplasm, in this case its likely adrenal and not pituitary cause it didn’t suppress with the HDDS test.
BLUF: This dog had Cushings and diabetes complicated by ketoacidosis, pancreatitis and a UTI. Necrotizing pancreatitis resulted in diabetes and exocrinne pancreatic insufficiency. The dog had an adrenal cortical tumor. pg 470

Question 35

A dog with seizures and vomiting and diarrhea.
The Hgb is high and the MCH and MCHC area also high. RBC morphology is normal.
There is lipemia and hemolysis in the sample.
WBC are high including segs and bands but segs are higher bands.
WBC cells look old, differential count may be inaccurate and there is slight toxic basophilia.
Chemistry:
BUN and Crea are high. Total protein is high.
Albumin and Globulins are high.
ALT is high. Glucose is low.
Potassium is high.
TCO2 is low and Anion Gap is high.
Calcium is high and Phosphorus is low.
CK is high. Amylase is high and Lipase is low.
There was no urinalysis reported.

Answer 35

There is increased hemoglobin, MCH and MCHC. Recall RBCs never produce too much hemoglobin so the presnce of hyperchromia means there is hemolysis and this is confirmed by the plasma color and if the hemoglobin is falsely elevated the calculated MCH and MCHC will be erroneous.
There is a leukocytosis with a left shift, neutrophilia, toxic change and degenerative leukocytes. So there is severe inflammation based on the left shift and possible toxic change.
Can’t tell if azotemia is renal or prerenal cause no urine was submitted. Could also be post renal.
Hyperproteinemia with both high albumin and globulin. If the hemolysis is severe it may increase the TP due to hemoglobin and lipemia can also result in false high values. There may also be dehydration.
Elevated ALT can occur with hemolysis but could also mean liver leakage/damage.
The hypoglycemia is likely artifactual as the sample sat on the clot for an extended period.
Hyperkalemia can be seen in acidosis, anuria/renal failure or ruptured bladder. Could also be due to the K+ content in RBCs that ruptured.
Low TCO2 with elevated AG is an titrational metabolic acidosis but lactic acid can also build up if the serum isn’t removed from the clot right away and titrate the plasma bicarb resulting in fictitous acidosis.
The bad lipemia and well as bad hemolysis can both elevate calcium a little.
The elevated Phos is unusual and probably from hemolysis.
Increased CK is because the analytical method used to detect CK is messed up by hemolysis resulting in a false CK reading on the assay.
Increased amylase is from pancreatitis or decreased renal clearance.
Decreased lipase is from the hemolysis which directly inhibits lipase.
BLUF: The blood and serum are of limited use due to the hemolysis, lipemia and delayed processing of the sample. Samples should always be fasted and processed right away. pg 472