Lecture 28 - Clinical Case Review Flashcards
List 2 differential for the glucose change
- Marked hyperglycemia (consistent with Diabetes mellitus)f, DDx stress-
induced hyperglycemia but the elevated magnitude and the species
makes is unlikely
Can you explain the change of the Urea?
Liver insufficiency or portosystemic shunts –> BUN will decrease
Was there something about the sample that could interfere with
spectrophotometry and which analytes will be affected?
- Plasma being lipemic, leads to interference with spectrophotometric
essays. So the HYPERPhosphatemia, Total protein concentrate and
Globulin concentration are most likely Falsely increased
How would you interpret the Albumin levels?
- The Slight HYPERalbuminemia is consistent w hypovolemia. Clinically,
signs of dehydration should be evaluated
What is your evaluation of the lipids in this patient?
Moderate hypertriglyceridemia and mild hypercholesterolemia are frequently observed in patients suffering from Diabetes
Mellitus due to accelerated synthesis of the lipids. DDx is Hyperadrenocorticism.
What about the liver enzymes? What is your interpretation ? Is there hepatocellular injury or cholestasis?
Slight to moderate Elevated ALT, indicative of hepatocellular damage, mostly likely due to a metabolic disorder such as Lipidosis,
which is frequently associated with Diab. Mellitus. Moderate increase ALP suggests intra to post hepatic cholestasis with
induction of the liver-specific ALP isoenzyme. Cholestasis may result from metabolic disease (Diab. Mellitus, Lipidosis,
hyperadrenocorticism. (remember the list of causes of elevated L-ALP on lecture 25)
- Describe and discuss the significant urinalysis findings
a. what are the most remarkable changes?
b. what would you say about the glucose in urine and what should
you compare it in the biochemical profile? - Based on the short Hx and lab results, What is the most likely disease
in this Dog? - What further tests would you recommend and why?
a. what are the most remarkable changes? Glucosuria,
proteinuria
b. what would you say about the glucose in urine and what
should you compare it in the biochemical profile? Glucosuria
in the face of hyperglycemia, indicated the reabsorption
capacity of the renal proximal tubules for glucose is
exceeded.
3. Based on the short Hx and lab results, What is the most
likely disease in this Dog? This dog most likely has Diab.
Mellitus with subsequent hepatocellular disease, most likely
hepatic Lipidosis
- What further tests would you recommend and why?
Ultrasound and pancreatic enzymes to rule out
pancreatitis as a probable cause of diab. Mellitus.
Potential hepatic Lipidosis should also be evaluated w US.
Could use fine needle aspirate of the liver to confirm
hepatic Lipidosis and cholestasis
Urine culture, may be recommended as diabetic patients
frequently develop urinary tract infections due to
glucosuria, and it may occur in absence of Pyuria (pus in
urine)
Phosphate and Protein concentrations should be repeated
in a non-lipemic sample. Ultracentrifugation may be used
to clear lipemia sample, if available. Believe or not,
putting sample in the freezer may separate the “cream”
layer at the top of the tube and clear serum below this
layer
If Diab. Mellitus is difficult to stabilize,
hyperadrenocorticism may be contributing. An ACTH
stimulation test may be performed (we will talk about this
in the chapter of endocrine diseases)
- What are your main interpretation for the hematology findings?
a. Lymphopenia: in the absence of other abnormalities most likely indicates a stress (endogenous or
exogenous glucocorticoids) response
Interpretation of the biochemical profiles one by
one:
1. CK
severely increased CK enzyme activity
resulting from excessive muscle damage
after hypoxia and squeezing while the cat
was stuck in the window.
Interpretation of the biochemical profiles one by
one:
1. ALT
is mildly to moderately increased.
Muscle damage is the most likely reason for
elevated ALT, although hepatocellular
damage may contribute.
Interpretation of the biochemical profiles one by
one:
1. Creatinine
There is a moderate azotemia
consistent with a reduced GFR because of
pre-renal, renal or post-renal causes. A pre-
renal cause may be possible because of the
hypoxia and/or dehydration. Renal disease
may contribute as the accident may have
resulted in direct kidney damage.
Interpretation of the biochemical profiles one by
one:
1. Glucose
The slight hyperglycemia most
likely is due to a stress response.
Theoretically, diabetes mellitus cannot be
excluded, but the history makes this less
likely
Would you like to order any further analyses?
a. Urinalysis to help differentiate pre-renal from renal causes for the azotemia and evaluate
renal function
b. Repeated glucose measurements and possibly a fructosamine assay to exclude diabetes
mellitus.
This is a case of muscle damage due to hypoxia.
1.Which info from the CBC and/or the
biochemistry panel can help you to
evaluate or identify DEHYDRATION?
2.Is there evidence of inflammation?
- See below:
a. Increased RBC, Increased Hgb,
Increased HCT, increased Total protein,
and increased albumin support
dehydration
b.Dehydration is suggested by partial
anorexia and removal of abomasal
reflux - See below:
a. Yes, by the presence of neutrophilia
and increased fibrinogen
- What is your interpretation of the creatinine?
- What test could help you to interpret question 3?
- a. Increased Creatinine may be due to: pre-renal (dehydration), or post-renal conditions.
- a. Urinalysis and measurement of USG is recommended to help determine if conditions other
than dehydration may be contributing
Lets go over the Biochemical findings one by one:
1. What is the most striking finding? And what is
that consistent with?
a. the markedly increased feline pancreatic
lipase (fPLI) concentration
b. It is consistent with pancreatitis, matches
the non-specific clinical signs in this cat.
What other findings do you see and what are DDx for the changes?
a. MILD hyperbilirubinemia: Hyperbilirubinemia may occur in the face of pre-hepatic (e.g.
hemolysis), hepatic or post-hepatic disease. As no hemolysis has been reported and anemia
is not present, pre-hepatic causes can be excluded. Pancreatitis may lead to impaired bile
flow through the common bile duct, thereby leading to post-hepatic hyperbilirubinemia.
Patients with pancreatitis frequently have concurrent disease, such as hepatic lipidosis,
hepatitis, intestinal inflammation or intestinal neoplasia.
b. Slight increase in ALP and ALT enzyme activities. Increased enzyme activity of ALP may also
point to cholestasis due to impaired bile flow. In cats, increased ALP is also reported with
hepatic lipidosis, another possible cause for hepatic bilirubinemia. Hepatic lipidosis may also
be the reason for hepatocellular damage as exemplified by the increased ALT enzyme
activity. Extension of the pancreatic inflammation to the liver may further contribute to
increased ALT enzyme activity.
What are the Urea and creatinine suggesting and the phosphorus?
a. Mild azotemia characterized ( increase urea & creatinine concentrations) + mild
hyperphosphatemia. This is consistent with a decreased GFR and may be pre-renal, renal or
post- renal in origin. As the patient shows a decreased appetite, diminished fluid intake
leading to dehydration as a pre- renal cause for the azotemia should be considered. In the
face of severe pancreatitis, vascular leakage may also contribute to pre-renal azotemia as
extravasation of fluid in the third space takes place.
- What test do you need to assess/classify the
interpretation from the Urea/creatinine? - What is the interpretation of the Proteins?
- a. Definitive exclusion of renal or post-renal
disease is only possible by urinalysis.
Special consideration should be given to
the USG as well as signs of lower urinary
tract disease. - a. Mild hypoproteinemia based on a mild
hypoalbuminemia may occur in the face of
vascular leakage, malnutrition, impaired
intestinal absorption of protein and/or
diminished hepatic albumin synthesis. The
exact reason for the hypoalbuminemia
cannot be determined based on the
present results
- What is the interpretation of the Glucose?
.mild hyperglycemia is present and may be stress
induced in a chronically ill cat. In addition, the
inflamed pancreas may release glucagon in higher
concentrations than insulin. Glucagon leads to
increased gluconeogenesis and glycogenolysis, thus
augmenting glucose serum concentration. Diabetes
mellitus is another risk factor for pancreatitis and, of
course, should also be considered, although the
hyperglycemia is only slight
- Would a Feline trypsin-like immunoreactivity (fTLI) help you assessed this case?
Feline trypsin-like immunoreactivity (fTLI) may be
assessed in a cat with pancreatitis, but sensitivity
and specificity are not as good as fPLI and negative
results do not rule out pancreatitis. fTLI may further
be increased in the face of intestinal disease, which
is a common risk factor for pancreatitis
