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Adv. Diagnostics > Clin Path > Flashcards

Clin Path Flashcards

1
Q

What is an inflammatory leukogram in a small animal patient?

A

(Neutrophilia with a left shift and toxic changes, sometimes might see monocytosis and lymphopenia)

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2
Q

What is an inflammatory leukogram in a large animal patient?

A

(Neutrophilia with a left shift and toxic changes, hyperfibrinogenemia, and sometimes see monocytosis)

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3
Q

What are the two differentials for lymphopenia?

A

(Acute inflammation and stress)

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4
Q

What are the three differentials for a mild normocytic, normochromic, non-regenerative anemia?

A

(Inflammation, pre-regen, or chronic dz)

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5
Q

What are the differentials for hypoalbuminemia?

A

(Hepatic failure (confirm with other blood work parameters), PLN (confirm with protein in urine), PLE (typically will see overall decrease in TP unless paired with enteritis), and inflammation)

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6
Q

What are the differentials for hyperglobulinemia?

A

(Dehydration, inflammation, and neoplasia)

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7
Q

How can you go about supporting a diagnosis of prerenal vs. renal vs. post-renal azotemia?

A

(Prerenal: should be paired with signs of dehydration + ruling out renal and post-renal, renal: should be paired with an isosthenuric USG, post-renal: should be paired with a PE that supports lower urinary dz and electrolyte abnormalities (low Na, low Cl, and high P))

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8
Q

What impact will hypoalbuminemia have on the anion gap and TCO2?

A

(If severe enough will decrease the anion gap and TCO2 will increase to compensate)

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9
Q

You are presented with a foal with a low MCV on their CBC, how can you further evaluate that CBC to determine if the foal has iron deficiency or not?

A

(Look at MCHC (hemoglobin/iron per volume of RBC), if its normal the foal has plenty of iron)

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10
Q

How will bilirubin be impacted on a chem in a fasted/anorexic horse?

A

(There will be hyperbilirubinemia specifically indirect bilirubin will be elevated)

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11
Q

Describe a stress leukogram.

A

(Leukocytosis (specifically mature neutrophilia), mild monocytosis, lymphopenia, and eosinopenia)

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12
Q

What are the two possible differentials for non-worrisome (aka no other signs of diabetes or sepsis) hyperglycemia?

A

(Stress or excitement/epinephrine)

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13
Q

What are your differentials for a titrational metabolic acidosis?

A

(Ketones, lactate, uremic acids, and ethylene glycol)

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14
Q

If a patient has hypercalcemia, what other values would you look at to indicate Addison’s dz?

A

(Sodium (low), chloride (low), and potassium (high))

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15
Q

If a patient has hypercalcemia, what other values would you look at to indicate vitamin D toxicosis?

A

(Phosphorus (elevated))

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16
Q

What test can be used to differentiate a neoplastic vs. idiopathic cause of hypercalcemia?

A

(Malignancy profile which measures PTHrP, if elevated = neoplasia)

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17
Q

What things can cause eosinophilia?

A

(Worms, wheezes, and weird diseases)

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18
Q

What neoplasms can induce eosinophilia?

A

(Lymphoma and MCT)

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19
Q

What would move mild normocytic, normochromic nonregenerative anemia caused by renal failure higher on your differential list?

A

(If it is paired with severe azotemia, typically do not see anemia until it is end stage kidney disease)

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20
Q

Why should you look at the blood smear when there is thrombocytopenia?

A

(To check for clumped platelets)

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21
Q

What is the singular differential for hyperalbuminemia?

A

(Dehydration)

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22
Q

What are the two differentials for a marked anemia paired with a mild, inadequate reticulocytosis?

A

(1) bone marrow is not forming retics appropriately, 2) acute on chronic anemia)

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23
Q

What are differentials for acanthocytes?

A

(Liver disease and erythrocyte fragmentation)

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24
Q

What are differentials for keratocytes?

A

(Iron deficiency, liver disease, myelodysplastic syndrome, erythrocyte fragmentation)

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25
Q

There are lots of differentials for schistocytes (severe iron deficiency, microangiopathic hemolytic anemia, heart failure, etc.) but they all cause what in particular?

A

(Erythrocyte fragmentation)

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26
Q

Which of the following values are used for evaluating hepatocellular injury?

  • AST
  • ALP
  • Bilirubin
  • Cholesterol
  • Bile Acids
  • ALT
  • Albumin
  • Glucose
  • ALP
  • SDH
  • GGT
  • Coag factors
  • BUN
A

(AST, ALT, and SDH)

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27
Q

Which of the following values are used for evaluating a patient for cholestasis?

  • AST
  • ALP
  • Bilirubin
  • Cholesterol
  • Bile Acids
  • ALT
  • Albumin
  • Glucose
  • ALP
  • SDH
  • GGT
  • Coag factors
  • BUN
A

(ALP, GGT, Cholesterol, bilirubin, and bile acids)

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28
Q

Which of the following values are used for evaluating liver function?

  • AST
  • ALP
  • Bilirubin
  • Cholesterol
  • Bile Acids
  • ALT
  • Albumin
  • Glucose
  • ALP
  • SDH
  • GGT
  • Coag factors
  • BUN
A

(Glucose, BUN, albumin, cholesterol, and coag factors)

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29
Q

How do glucocorticoids and phenobarbital (and other drugs associated with increased liver enzymes) induce increased liver enzymes?

A

(By triggered normal, uninjured hepatic cells to increase production of enzymes)

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30
Q

Prehepatic causes (such as hemolysis, or fasting/anorexic in large animal species) for hyperbilirubinemia will increase unconjugated/conjugated (choose) bilirubin.

A

(Unconjugated)

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31
Q

Hepatic causes (markedly reduced functional mass) for hyperbilirubinemia will increase unconjugated/conjugated (choose) bilirubin.

A

(Unconjugated)

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32
Q

Post hepatic causes (biliary obstruction, sepsis causing functional cholestasis) for hyperbilirubinemia will increase unconjugated/conjugated (choose) bilirubin.

A

(Conjugated)

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33
Q

In cases of cholestasis, cholesterol will be increased/decreased/normal (choose) and triglycerides will be increased/decreased/normal (choose).

A

(Cholesterol is increased or normal, triglycerides are normal)

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34
Q

What can cause hyponatremia, hypokalemia, and hypochloremia to all occur in one patient?

A

(GI or third space loss)

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35
Q

What is the most common explanation for a hypochloremic metabolic alkalosis?

A

(Vomiting)

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36
Q

(T/F) If you have a patient with a cholestasis liver enzyme pattern and both hypercholesterolemia and hypertriglyceridemia, both of those findings can be explained by the cholestasis.

A

(F, cholestasis does not increased triglycerides, so this would more likely be explain by other causes of hyperlipidemia (hypothyroid, DM, cushings, acute pancreatitis, or postprandial))

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37
Q

(T/F) Leptospirosis most typically causes a cholestatic liver enzyme pattern.

A

(T, but can do whatever as well so just be careful)

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38
Q

Why does cholesterol tend to rise before bilirubin does in cases of cholestasis?

A

(Bc the kidneys are particularly good at filtering out bilirubin so cholesterol will go up first and will be followed by bilirubin once there is enough to overwhelm the kidneys)

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39
Q

What are the possible explanations for hyperchloremic metabolic acidosis?

A

(Secretional (diarrhea) or renal tubular (toxic, drug, infectious, or congenital causes) acidosis)

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40
Q

(T/F) Any amount of acanthocytes and keratocytes in the blood of a goat (or cow, or pig) are normal.

A

(F, only normal in low numbers)

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41
Q

What is the purpose of PARR?

A

(PARR is used to determine whether a population of lymphocytes is neoplastic or not; typically monoclonal = neoplasia, polyclonal = inflammation)

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42
Q

What are some infectious agents that can cause a monoclonal response that looks a lot like lymphoma (so they need to be ruled out)?

A

(Ehrlichia and Leishmania)

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43
Q

What is the purpose of flow cytometry?

A

(Flow cytometry is used to provide more information (determine cell lineage) when neoplasia is suspected cytologically; can distinguish between myeloid vs lymphoid leukemia, also allows for phenotyping lymphoma which is a useful prognostic indicator)

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44
Q

For the following scenarios, would you request PARR or flow cytometry:

  • Cytology shows a population of lymphocytes which are suspicious for but not conclusive for neoplasia
  • Cytology shows lymphoid neoplasia
  • Cytology shows lymphoid neoplasia or leukemia of uncertain etiology
A
  • Cytology shows a population of lymphocytes which are suspicious for but not conclusive for neoplasia (PARR)
  • Cytology shows lymphoid neoplasia (Flow cytometry for phenotyping/prognosis)
  • Cytology shows lymphoid neoplasia or leukemia of uncertain etiology (Flow cytometry to determine cell of origin)
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45
Q

Do you expect calcium to be high or low with an acidemia?

A

(High → calcium is being displaced from albumin)

46
Q

Do you expect potassium to be high or low with acidemia?

A

(High → transcellular shifting)

47
Q

If you have a primary respiratory acidosis (so a high pCO2) and a compensatory metabolic response, what value do you expect to change to indicate that and how would it change?

A

(TCO2 would change and it would increase for a compensatory metabolic alkalosis)

48
Q

What portions of the kidney prevent large molecules (primarily proteins) from entering filtrate?

A

(Glomerulus)

49
Q

What is the purpose of the renal tubules?

A

(Reabsorb water and small molecules, regulate acid-base, secrete some electrolytes or water, and endocrine stuff (EPO, calcitriol))

50
Q

What blood work values are an indirect measurement of GFR?

A

(Creatinine, BUN, and SDMA)

51
Q

What lab work value can indicate glomerular leakage?

A

(Urine protein)

52
Q

What lab work values can clue you in on tubular function?

A

(USG and urine pH)

53
Q

GFR is mediated primarily by renal plasma flow rate which is impacted by what physiological characteristic of an animal?

A

(Blood volume, cardiac output, number of functional glomeruli, and constriction/dilation of afferent/efferent glomerular arterioles)

54
Q

What can affect BUN besides decreased GFR?

A

(Dietary protein intake, GI urea recycling (ruminants), and hepatic function)

55
Q

What can affect creatinine besides decreased GFR?

A

(Muscle mass)

56
Q

(T/F) Creatinine is usually a better estimate of GFR when compared to BUN in mammals.

A

(T)

57
Q

(T/F) SDMA can be used to determine decreased GFR even when a patient is dehydrated.

A

(F, prerenal and post renal causes can still increase SDMA so need to rule those out before trusting an increased SDMA = decreased GFR because of a renal issue)

58
Q

Which of the following indicate prerenal azotemia?

A - Azotemia, USG 1.050
B - Azotemia, USG 1.015
C - Azotemia, tacky MM
D - Azotemia, dogs tries to bite you when palpating abdomen with a fluid wave

A

(A, C)

59
Q

Which of the following indicate renal azotemia?

A - Azotemia, USG 1.050
B - Azotemia, USG 1.015
C - Azotemia, tacky MM
D - Azotemia, dogs tries to bite you when palpating abdomen with a fluid wave

A

(B)

60
Q

Which of the following indicate post renal azotemia?

A - Azotemia, USG 1.050
B - Azotemia, USG 1.015
C - Azotemia, tacky MM
D - Azotemia, dogs tries to bite you when palpating abdomen with a fluid wave

A

(D)

61
Q

How does nephrogenic diabetes insipidus cause a low USG?

A

(ADH is unable to function properly, why that happens depends on the cause, some causes are hypercalcemia, hypokalemia, canine pyometra, and hepatic failure)

62
Q

What disease causes osmotic diuresis?

A

(Diabetes mellitus)

63
Q

How do hyponatremia, Addison’s, liver failure, and psychogenic polydipsia cause a decreased USG?

A

(They cause medullary washout)

64
Q

What diseases lead to a decreased ADH and therefore a decreased USG?

A

(Central diabetes insipidus and Cushing’s dz)

65
Q

(T/F) Isosthenuria is any USG value less than 1.020.

A

(F, isosthenuria is specifically between two given values (1.008-1.012 per Idexx), anything lower than the isosthenuria values indicates hyposthenuria which still indicates a normal functioning kidney because you need your kidneys to excrete excess water too)

66
Q

What are prerenal causes of proteinuria?

A

(Hemoglobin (hemolysis), myoglobin (rhabdomyolysis), and bence-jones proteins (multiple myeloma))

67
Q

(T/F) There is no such thing as physiologic renal proteinuria.

A

(F, as long as it is mild and transient it is normal for there to be proteinuria associated with a fever or even strenuous activity)

68
Q

What are some possible causes of moderate to marked hypoglycemia in an adult animal?

A

(Insulinoma, xylitol toxicosis, hypoadrenocorticism, hepatic failure, lactational, sepsis, and iatrogenic insulin overdose)

69
Q

What are some of the causes of a decreased Na:K (< 27)?

A

(Addison’s, urinary obstruction/rupture, whipworms, diarrhea, AKI, and diabetes mellitus)

70
Q

What are causes of a hyperchloremic metabolic acidosis?

A

(Secretional acidosis (diarrhea) or renal tubular acidosis (rare))

71
Q

An elevated anion gap indicates what acid base disturbance?

A

(Titrational metabolic acidosis)

72
Q

What are some causes of hypocholesterolemia?

A

(Hepatic failure/PSS, Addison’s, and PLE)

73
Q

What are the causes of hypercalcemia?

A

(Granulomatous inflammation, osteolysis, spurious, hyperparathyroidism, hypervitaminosis D, Addison’s, renal failure, and neoplasia)

74
Q

What are two explanations for a reticulocytosis without anemia?

A

(Previous hemorrhage and dehydration masking anemia)

75
Q

What are all of the contributors to hemostasis?

A

(Platelets, clotting factors, and blood vessels)

76
Q

(T/F) Stress hyperglycemia is not typically associated with glucosuria.

A

(T)

77
Q

What are possible causes of hyperphosphatemia?

A

(Decreased GFR, vitamin D toxicity, intestinal ischemia, rhabdomyolysis/tumor lysis, hyperthyroidism, and hyperadrenocorticism)

78
Q

What are possible causes of hypocalcemia?

A

(Hypoalbuminemia, hypomagnesemia, maternal, CKD, acute pancreatitis, rhabdomyolysis/tumor lysis, and metastatic mineralization)

79
Q

What should be at the top of your differential list when a dog is showing signs of both hepatic and renal disease?

A

(Leptospirosis, other possibilities are acute pancreatitis with an AKI, toxins, sepsis, multicentric neoplasia, and fungal dz)

80
Q

What protein and TNCC value indicate a transudate?

A

(Protein < 2.5 g/dL and TNCC <1,500/uL)

81
Q

What protein and TNCC value indicate a modified transudate?

A

(Protein > 2.5 g/dL and TNCC 1,000-5,000/uL)

82
Q

What protein and TNCC value indicate an exudate?

A

(Protein > 2.5 g/dL and TNCC >5,000/uL)

83
Q

What should you be looking for on blood work to indicate a transition cow is experiencing milk fever?

A

(Calcium < 5.5 mg/dL)

84
Q

What should you be looking for on blood work to indicate a transition cow is experiencing grass tetany?

A

(Calcium < 5.5 mg/dL and magnesium < 1.4 mg/dL)

85
Q

What should you be looking for on blood work to indicate a transition cow is experiencing hepatic lipidosis?

A

(Elevated bilirubin, +/- AST elevation, GGT elevation)

86
Q

What are differentials for hypocalcemia?

A

(Hypoparathyroidism, blister beetles, pancreatitis, oxalates (ethylene glycol, plants), cell tumor, low albumin, rhabdomyolysis, CKD, decreased intake or intestinal disease, union with phosphorus (metastatic mineralization), and maternal (milk fever, periparturient paresis, puerperal tetany, eclampsia))

87
Q

If there is an acidemia, potassium should typically be high/low (choose).

A

(High from cellular shifting)

88
Q

What are some differentials for a negative energy balance (which can be indicated by an elevated BHB)?

A

(Lactation, diabetes mellitus, starvation, displaced abomasum, and endurance racing in horses/dogs)

89
Q

Anorexia in a large animal species will increase which type of bilirubin?

A

(Indirect/unconjugated)

90
Q

What are differentials for an increased BUN with a normal creatinine?

A

(GI bleeding, high protein diet, dehydration or low muscle mass)

91
Q

What are differentials for hypertriglyceridemia?

A

(Postprandial (most common), hypothyroidism, acute pancreatitis, diabetes mellitus, hyperadrenocorticism, and congenital hyperlipidemia)

92
Q

What CBC finding is indicative of chronic inflammation?

A

(Neutrophilia > 2x the RR)

93
Q

What is the best explanation for a mild hyperphosphatemia?

A

(Decreased GFR)

94
Q

Which of the zones of the adrenal cortex are typically involved in hypo/hyperadrenocorticism?

A

(Zona glomerulosa and zona fasiculata)

95
Q

Where does cortisol normally have negative feedback?

A

(Both the hypothalamus and pituitary gland)

96
Q

(T/F) Primary hyperadrenocorticism is adrenal dependent.

A

(T, secondary is pituitary)

97
Q

Is pituitary or adrenal hyperadrenocorticism more common?

A

(Pituitary)

98
Q

Describe secondary hyperadrenocorticism.

A

(There is either pituitary hyperplasia or a tumor that causes an excess release of ACTH which triggers the adrenals to excrete excess cortisol, adrenals will bilaterally enlarge due to the excess stimulation, cortisol still have negative feedback on hypothalamus and pituitary but the pituitary doesn’t respond as it does in a healthy animal)

99
Q

Describe primary hyperadrenocorticism.

A

(There is a tumor associated with one of the adrenals that secretes excess cortisol, that cortisol has negative feedback on the hypothalamus and pituitary so ACTH secretion will be minimal and so the other adrenal will atrophy due to have no stimulation)

100
Q

What are the screening tests for hyperadrenocorticism?

A

(Urine cortisol-creatinine ratio, low dose dexamethasone suppression test, and ACTH stimulation test)

101
Q

What tests can be used for confirmation and/or differentiating hyperadrenocorticism?

A

(Endogenous ACTH, LDDST, HDDST (not used much anymore), abdominal ultrasound, and head/abdominal CT/MRI)

102
Q

The urine cortisol-creatinine ratio test is very sensitive/specific (choose) and has poor specificity/sensitivity (choose).

A

(Is very sensitive, has poor specificity i.e. you can trust negatives but cannot trust positives so this is a good screening/ruling out test)

103
Q

How is a LDDST performed?

A

(You take a baseline cortisol, administer dexamethasone, then measure cortisol again at 4 and 8 hours; the 4 hour value can aid in differentiation between PDH/ADH and the 8 hour value rules in/out HAC)

104
Q

When is an LDDST best used to rule in or out HAC?

A

(Best to use with patients who have classical clinical and CBC/chem features of HAC)

105
Q

Which LDDST curve(s) indicates PDH?

A

(Partial suppression or no suppression; also technically complete suppression but that is considered a false negative)

106
Q

Which LDDST curve indicates ADH?

A

(A no suppression curve can indicate PDH or ADH, will need further testing to determine which it is)

107
Q

What is the purpose of a high dex dose suppression test?

A

(To differentiate between PDH and ADH but ultrasound has better diagnostic yield so its not used much anymore)

108
Q

How is an ACTH stimulation test performed?

A

(You take a baseline cortisol, administer ACTH, measure cortisol again in 1-2 hours; ACTH is meant to trigger cortisol excretion from the adrenals)

109
Q

If you want an HAC test that you can trust a positive result from to indicate a patient has HAC (say it is a patient with a weird presentation but you have some suspicion), which test would you choose?

A

(ACTH stimulation test, has the highest specificity of any of the HAC test)

110
Q

How do you use endogenous ACTH to differentiate between ADH and PDH?

A

(ADH will have low ACTH bc excess cortisol from the adrenal tumor will suppress hypothalamus and pituitary, PDH will have high ACTH because hyperplastic pituitary or tumor will secrete excess ACTH)

111
Q

What values (low/high) do you expect to see on an insulin:glucose test if a dog has an insulinoma?

A

(High insulin (bc it is being secreted by the tumor) and low glucose (bc it is being shoved into cells))

Adv. Diagnostics (5 decks)

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