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Clin Path > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Case # 65: 6yo K9 presents weak, vomiting, & blood/chem panel reveals:

Lymphocytosis,
Monocytosis,
Hypercalcemic, 
Hyponatremic,
Hyperkalemic,
Dec. TCO2,
AG: 32

Diagnostic interpretation?

A

Addison’s! (This is a “TEXTBOOK” case!)

*esp because the hyponatremia is coupled with hyperkalemia!

The hypercalcemia could be related to decreased glucocorticoids (they reduce GI calcium uptake), or calcium retention by kidneys (due to sodium loss).

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2
Q

Squamous epithelial cells present in urine sediment would be coming from where and indicating what?

A

Distal urethra, vaginal tract, skin;
Not necessarily indicative - often seen in free catch urine
rarely pathogenic: sertoli cell tumors causing squamous metaplasia

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3
Q

Transitional epithelial cells present in urine sediment are coming from where and indicating what?

A

Renal pelvis, ureter, bladder, proximal urethra;

Could indicate:
Hyperplasia (associated w/inflammation),
Or
Transitional cell tumors (benign & malignant)

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4
Q

What is necessary for concentration of urine?

A

1) >33% functional nephrons

2) production and responsiveness to ADH; maintenance of medullary hypertonicity (production of BUN & aldosterone)

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5
Q

How would you differentiate a patient with Ehrlichiosis vs. a patient with multiple myeloma?

A

Both can demonstrate hyperglobulinemia, but multiple myeloma might result in hypocholesterolemia

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6
Q

What are possible causes of coagulopathy in patients with multiple myeloma?

A

???

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7
Q

Which animals have auto antibodies?

A

Dogs,

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8
Q

What is fraction excretion?

A

???

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9
Q

How do we differentiate CENTRAL Diabetes Insipidis from RENAL Diabetes Insipidis from Renal FAILURE…?

A

???

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10
Q

Laboratory findings you would expect to see with glomerulonephropathy…?

A

Moderate-marked Hypoalbuminemia,

Moderate-marked proteinuria,

Hypercoagulability

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11
Q

What is the most common cause of hyponatremia?

A

Hypovolemia - due to loss from GIT, kidney, or cutaneous (skin)

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12
Q

A diabetic patient is markedly hyperglycemic; what do you expect the sodium concentration to be? What is the mechanism?

A

Decreased!

Water shifts from the ICF–>ECF

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13
Q

When chloride loss parallels sodium loss proportionately, we can attribute the loss of both ions to causes of Hyponatremia.

When chloride loss is truly greater than sodium loss, what is the most common cause? Why?

A

Hypochloremic metabolic alkalosis!

The small intestine is not resorbing HCl secretions; bicarbonate increases

Monogastrics will have severe vomiting/pyloric outflow obstruction

Ruminants will have abomasal disorders / high GI obstructions (ileum)

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14
Q

Hyperventilation and hyperthermia go with which acid-base disturbance?

A

Respiratory alkalosis!

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15
Q

What is the most common acid-base disturbance observed in patients hypoventilating/under anesthesia?

A

Respiratory acidosis

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16
Q

What are the 2 mechanisms that result in Metabolic Acidosis?

A

1) increase in acid (titrational acidosis)

2) loss of base (bicarbonate)

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17
Q

What do we expect to see as far as acid-base disturbances in a patient with an increase in nonvolatile acids and a high AG?

A

Most likely “titrational acidosis” or “high anion-gap acidosis” - is metabolic acidosis due to increase in nonvolatile acids (KLUE)

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18
Q

How can paradoxical aciduria occur?

A

Hypochloremic metabolic alkalosis

+ dehydration!

First, the kidney preserves water -> then aldosterone pulls in Na+ - but since we have a hypochloremic metabolic alkalosis, there’s not enough Cl- to compensate, so it pulls bicarbonate back

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19
Q

What is the short-term compensation for a Metabolic Acidosis?

A

Increased ventilation (respiratory alkalosis)

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20
Q

If a metabolic alkalosis results from loss of H+ at the level of the kidney, what can we attribute the disturbance to?

A

Diuretics,
Hypokalemia,
Chronic respiratory acidosis (>3-5 days)

21
Q

How can a cow have mixed acid-base disturbance?

A

Case of abomasal volvulus (hypochloremic metabolic alkalosis):

Distended abomasum presses on the caudal vena cava, decreasing blood flow to heart, leading to hypoxia and subsequent lactic ACIDOSIS

22
Q

What is the most common cause of hyperphosphatemia?

A

Decreased GFR (whether a result of prerenal azotemia or renal disease)

*but also ruptured bladder, urethral obstruction

23
Q

What constitutes “apparent hypocalcemia” as opposed to TRUE hypocalcemia?

A

The fraction of Ca2+ bound to albumin is decreased, as the available albumin is decreased…

Total calcium - albumin + 3.5 = corrected calcium

24
Q 
What do 
Renal dz,
Ethylene glycol toxicosis,
Pancreatitis,
Eclampsia, 
Sepsis

Have in common?

A

Common causes of hypocalcemia!

*also Hypoparathyroidism if coupled with hyperphosphatemia in absence of azotemia

25
Q

What is the gold standard for total circulating T4?

A

Radioimmunoassay (RIA)

26
Q

What is the gold standard for measuring UNBOUND (free) T4?

A

Equilibrium dialysis

27
Q

Middle-aged, pure-bred dog CBC & chemistry present:

Mild-moderate nonregenerative anemia,
Fasting hypercholesterolemia,
Fasting hypertriglyceridemia,
TT4 decreased,
FT4 decreased,
And TSH increased

What’s your primary differential?

A

Primary hypothyroidism

28
Q

Thyroid function testing in a dog reveals:

TT4 decreased,
FT4 decreased,
And TSH decreased

What is your top differential?

A

Secondary Hypothyroidism

29
Q

How can we differentiate euthyroid sick syndrome from hypothyroidism?

A

Euthyroid is seen in sick animals that do not show clinical signs for hypothyroidism as well as this pattern in the thyroid function tests:

TT4 decreased,
FT4 NORMAL -> decreased,
TSH NORMAL -> increased

30
Q

What is the typical pathogenesis of feline hyperthyroidism?

A 
Functional adenoma (hyperplasia) 
- usually bilateral
31
Q

What diagnostics on a CBC might support feline hyperthyroidism?

A

Polycythemia

Heinz-body formation that is NOT associated w/hemolytic anemia!

32
Q

What diagnostics on a chemistry might support feline hyperthyroidism?

A

Mild-moderate elevation in ALT,
Possible increased ALP,
Azotemia

33
Q

How can azotemia be “masked” in feline hyperthyroidism?

A

Increased cardiac output–>increased GFR–>lowers the BUN

These patients are usually cachexic, so the lack of muscle mass will yield a lower basal Crea…

With hyperthyroid treatment, it can be unmasked!

34
Q

How do we diagnose hyperthyroidism in cats?

A

TT4! It’s reliable!!

35
Q

What is a protein-losing nephropathy that leads to abdominal effusion and requires 5 things?

A

Nephrotic syndrome! (Glomerulonephropathy)
Requires:
1) proteinuria (glomerular dz)
2) hypoalbuminemia (losing Alb)
3) abdominal effusion (loss of oncotic pressure)
4) hypercholesterolemia/hypertriglyceridemia
5) hypercoagulability (loss of antithrombin)

36
Q

You’re presented with a patient exhibiting the following:

Good BCS, but sudden vomiting, diarrhea, halitosis, depression, and oliguria to anuria, azotemia…

A

Acute RF!

37
Q

How is Chronic RF set apart from acute?

A

Patients are usually cachexic, have a nonregenerative anemia, presence of a metabolic acidosis, hyperphosphatemia in CRF, whereas these signs are not present in ARF

38
Q

When is a high CREA concentration diagnostic for Uroabdomen?

A

When the [CREA] of the peritoneal effusion is 2x > the [CREA] of the plasma (upon abdominal centesis)

39
Q

On protein electrophoretogram, a patient has presented decreased albumin and multiple increased globulin fractions… What can we interpret?

A

A polyclonal gammopathy!

40
Q

On protein electrophoresis, a patient demonstrates normal albumin and a single large peak in the gamma fraction… what can we conclude?

A

Monoclonal gammopathy!

41
Q

What is the most severe type of proteinuria?

A

Renal, glomerular! This is the only time you will also see hypoalbuminemia!!

42
Q

If ALP is increased withOUT hyperbilirubinemia (in a dog), what are we thinking?

A

Steroid/anticonvulsant medication induction

43
Q

Why is GGT a better indicator than ALP of cholestasis in cats?

A

Because ALP has a half life of only 6 hours in cats! (Compared to 70 hours in the dog)

44
Q

When might ALP be a better indicator of cholestasis in cats?

A

Hepatic lipidosis

45
Q

If Albumin is low and globulin is high, what is our primary differential?

A

Liver dz

46
Q

Which enzyme will typically be increased for 1-2 months following cessation of steroid therapy?

A

ALP

47
Q

If we see a decrease in BUN, cholesterol, AND albumin, what’s our most likely diagnosis?

A

Liver failure - it makes all of these

48
Q

What is maldigestion typically called?

A

EPI (exocrine pancreatic insufficiency) - not enough enzymes

49
Q

What is malabsorption usually a sign/consequence of?

A

Diffuse liver disease that has done something to the mucosa to inhibit nutrient absorption

Clin Path (1 decks)

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