Case Studies Flashcards
(35 cards)
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.
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
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.
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
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.
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
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.
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
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.
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.
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.
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
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.
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.
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.
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
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)
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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
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.
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.
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.
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.
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.
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
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.
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
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.
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?)
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.
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
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.
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
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.
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
