Student Name:
Case THREE “Liam”________________________
Analyses
Grader Initials: __________________
Description of abnormalities in
appropriate medical terminology
COMPLETE BLOOD COUNT
Erythrogram and
1,) Normocytic, hyperchromic,
morphology
regenerative anemia
2.) Moderately icteric plasma
3.) Polychromasia
4.) Metarubricytosis
5.) Reticulocytosis
Mechanistic explanation with supporting data
-Leukogram and
morphology
1.) Leukocytosis
2.) Mature Neutrophilia
3.) Regenerative left shift
4.) Monocytosis
5.) Metamyelocytosis
6.) Reactive lymphocytes
1-4) Inflammatory Leukogram supported by mature
neutrophilia, presence of regenerative left shift and
monocytosis.
5.) Metamyelocytosis is rare and can be seen in
conditions of increased demand (such as
inflammation).
6.) Reactive lymphocytes usually seen with antigenic
stimulation.
1.)Thrombocytopenia
2.) Prolonged PT, PTT
2.) Increased FDPs
Prolonged PT, PTT, increased FDPs and
thrombocytopenia are suggestive of disseminated
intravascular coagulation (DIC), a mixed hemostatic
defect.
1.) BUN 2X URI
The increase in BUN in the absence of increased
creatinine is due an increased production of urea
which is seen in cases hemorrhage from gastro-
1.) Normocytic, hyperchromic (artifact), regenerative
anemia is most likely due to acute blood loss. The
increased MCHC is likely due to presence of icterus.
Anemia of acute blood loss is supported by
hypoproteinemia and the presence of reticulocytes
indicating that it a regenerative process as well as the
presence of a coagulopathy.
2.) Icteric plasma due to hyperbilirubinemia.
3.) Polychromasia is due to the increased number of
reticulocytes in circulation.
4.) Metarubricytosis indicating marrow endothelial
damage likely due to hypoxia.
5.) Reticulocytosis indicates marrow response to
anemia.
COAGULOGRAM
PT, PTT, Platelets,
FDPs
CHEMISTRY
BUN, Creatinine
Remember to
incorporate UA
Grader comments
Student Name:
Ca, P, Mg
Proteins
Case THREE “Liam”________________________
1.) Calcium- do not interpret
2.) P, Mg- Normal
hypoproteinemia
Electrolytes (Na,
Normal
Cl, K)
Acid/base (Cl,
Normal
Bicarbonate, Anion
gap)
Bilirubin
Hyperbilirubinemia
ALP/GGT
1.) ALP 5X URI
2.) GGT 2X URI
Grader Initials: __________________
intestinal tract The nitrogenous compounds from the
blood are re-absorbed as they pass through the
remaining GIT and then broken down to urea by the
liver. Increased BUN in the presence of relativley
normal creatinine could also be due to poor tissue
profusion.
--------------------------------------------------------The hypoproteinemia in this case is likely due to
acute blood loss. The hypoproteinemia could be do to
decreased liver function however one would look for
hypocholesterolemia, hypoglycemia, and low BUN
which are all normal or increased in this situation,
suggesting blood loss is more likely. Further testing
should be done to investigate decreased liver function
because there is prolonged PT and PTT, along with a
cholesterol level that is low normal.
------------------------------------------------------------------------------------------------------------------------
The hyperbilirubinemia in this case is likely due to
cholestasis. This is supported by a severe
bilirubinemia, increases in the cholestatic enzymes:
ALP and GGT. Hemolysis is less likely because of a
lack of supporting erythrocyte morphology such as
spherocytes, agglutination, Heinz bodies, ect. Also,
hyperbilirubinemia due to decreased liver function is
less likely as it usually causes mild to moderate
hyperbilirubinemia, along with low albumin,
cholesterol, glucose and BUN.
1.) The five fold increase in ALP is likely due to
cholestasis that is increasing the production and
leakage of cholestatic enzymes from either/or
Student Name:
Case THREE “Liam”________________________
ALT/AST/SDH
1.) ALT 3X URI
2.) AST 8X URI
Amylase
CK
Glucose,
cholesterol
OTHER DATA
Urinalysis
Fluid
analysis/cytology
data
Normal
n/a
1.) Cholesterol: normal
2.) do not interpret glucose
n/a
n/a
Grader Initials: __________________
hepatocytes and biliary epithelium.
2.) In the presence of increased ALP the 2 fold
increase in GGT is also likely elevated by the same
mechanism as ALP.
1.) The 3 fold increase in ALT is a specific marker of
hepatocyte damage in dogs and cats.
2.) The 8 fold increase in AST is likely also due to
hepatocellular damage supported by the increase in
ALT which is specific for hepatocyte damage.
However, a less likely contributing factor to the
increased AST could be hemolysis which can result
when red blood cells are forced through altered
vascular channel such as vessels containing fibrin
strands, and can be associated with DIC. Hemolysis
would further be supported by the finding of
shistocytes and keratocytes on erythrocyte
morphology.
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Mechanistic explanation with supporting data: mechanisms could include things such as inflammation, oxidative damage, impaired
production, increased losses. You must be specific. For example, if the mechanism is oxidative damage, suggest some specific causes (ie
Red Maple leaf, acetaminophen, etc) For increased losses, you MUST indicate likely sites (GI, renal, third space, cutaneous) and support for
your conclusion (presence of diarrhea, azotemia with proteinuria, abdominal effusion, etc).
Student Name:
Case THREE “Liam”________________________
Grader Initials: __________________
Differential diagnoses: Make a list of 2-3 differential diagnoses and support your differentials with supporting data/information. List
confirmatory testing if you think some is recommended. You will be given guidance as to how specific it is possible to be for individual
cases.
Summary: The clinical findings of acute blood loss anemia, inflammatory leukogram, increased BUN, DIC, hyperbilirubinemia, and
increased ALT, AST, ALP, GGT , suggest that "Liam" is likely suffering from liver disease due primarily from hepatocellular damage with
secondary cholestasis most likely caused by neoplasia or hepatitis (further supported by reactive lymphocytes). Although, while the
laboratory findings indicate the highest increase in enzymes associated with hepatocellular damage these values are not dramatically
increased compared to those indicating cholestasis, therefore it is not easily identified which process occurred first as liver disease is not
mutually exclusive and often occur together (if one process is of sufficient severity, it can cause the other types of pathology to occur.);
especially if a component of AST is hemolysis which increases the value slightly, the increase in value between AST and ALP could be
very similar along with the similar values of GGT and ALT. Liver function should be evaluated as some lab findings could be suggestive of
decreased liver function. Severe liver damage and cholestasis can lead to decrease liver function. To evaluate liver function serum bile acids
and blood ammonia should be preformed.
Differential Diagnosis:
1.) Neoplasia
2.) Hepatitis
3.) Decreased Liver function
Additional testing:
1.) Ultrasound & radiographs
2.) Liver biopsy
3.) Serum bile acids
4.) Blood Ammonia