Hyperadrenocorticism (Cushing's Dz) Flashcards

1
Q

Describe the position and function of the adrenal glands

A
  • craniomedially to each kidney
  • assist in maintaining blood pressure, electrolyte and water homeostasis, and sexual differentiation; aiding stress response of body
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2
Q

Define hyperadrenocorticism

A

excessive secretion of cortisol

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3
Q

2 forms of Cushing’s & what causes them

A

pituitary-dependent (PDH)
-presence of functional adenoma (usually benign) within the pituitary gland

adrenal-dependent (ADH)
-presence of functional adrenal tumor (benign or malignant)

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4
Q

3 general effects of hypercortisolemia upon the body

A
  • increased production and mobilization of glucose by the liver and decreased utilization of glucose by the tissues
  • promotes catabolism, resulting in decrease in proteins in almost all tissues (exceptions: liver and plasma proteins)
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5
Q

List common CS of Cushing’s

A
  • Polyuria w/ compensatory polydipsia
  • Polyphagia
  • Weight gain
  • Pot-bellied appearance
  • Alopecia
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6
Q

Underlying pathology of Cushing’s CS: polyuria w/ compensatory polydipsia

A

suspected that cortisol interferes with kidney’s ability to conserve water, resulting in diuresis

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7
Q

Underlying pathology of Cushing’s CS: Polyphagia

A

due to decreased ability of tissues to use glucose for energy, the CNS things that energy is needed; this results in a catabolic state and a constantly hungry pet; also possible that cortisol has direct effect on hunger center

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8
Q

Underlying pathology of Cushing’s CS: weight gain

A

secondary to enlargement of liver (hepatomegaly) as a result of hepatic effects of cortisol

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9
Q

Underlying pathology of Cushing’s CS: pot-bellied appearance

A

mobilization of fat to the abdomen combined with catabolism of muscle proteins and excess abdominal weight leads to sagging of abdominal musculature

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10
Q

Underlying pathology of Cushing’s CS: alopecia

A

unknown; can be very dramatic; often symmetric and non-pruritic

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11
Q

Common physical appearance of Cushing’s pet

A

overweight
pot-bellied
alopecia
hepatomegaly w/ abd. palpaption

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12
Q

Cushing’s changes to CBC

A

stress response leukogram

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13
Q

Cushing’s changes to serum chem

A

+/- mild hyperglycemia due to increased glucose production but decreased glucose utilization

  • elevated hepatic enzymes as result of direct effect of cortisol on hepatocytes and hepatic blood flow
  • hypercholesterolemia –> lipid metabolism is interfered so there is an increase in circulating cholesterol and triglycerides
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14
Q

Cushing’s changes to UA/other urine test

A
  • dilute SG due to polyuria

- Cortisol:creatinine ration –> increased amount of cortisol as compared to urinary creatinine concentration

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15
Q

What are the 2 screening lab tests used to determine if Cushing’s is present?

A

ACTH Stimulation Test

Low Dose Dexamethasone Suppression Test (LDDS)

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16
Q

What are ACTH Stim tests results for a Cushing’s patient?

A

baseline sample will have excess cortisol and post ACTH admin. sample will have even more cortisol

17
Q

LDDST is designed to do what

A

take advantage of negative feeback system of cortisol upon ACTH

18
Q

How is the LDDST done?

A

Baseline serum cortisol sample is taken, then an injection of dexamethasone is given followed by 2 additional blood samples at specified times

19
Q

What is dexamethasone?

A

a synthetic corticosteroid

20
Q

What are the results of a LDDST test in a Cushing’s patient? Explain.

A

cortisol level will not change or will be even higher

Reason: a pathological process is inhibiting the negative feedback loop, so the dex doesn’t decrease the cortisol level like in normally would

21
Q

Mutual con of ACTH stim and LDDST

A

many outside influences can alter test results and make them difficult to interpret

22
Q

Which test is more resistant to outside influence?

A

LDDST

23
Q

Which test is more specific?

A

ACTH Stim

24
Q

How do you determine between PDH and ADH?

A

Abdominal Ultrasound

  • bilateral adrenal gland enlargement = PDH or bilateral adrenal tumor
  • unilateral adrenal gland enlargement = suggestive of primary adrenal tumor

Eval of endogenous ACTH concentrations of High Dose Dexamethasone Suppression Test

25
Q

2 Meds for PDH and what they do

A

Mitotane- causes significant necrosis of all 3 zona layers of adrenal cortex
Trilostane- inhibits adrenal cortex’s ability to produce cortisol

26
Q

Cons of PDH meds

A

may induce Addison’s if not careful

27
Q

2 therapeutic options for ADH

A
  • surgical removal of adrenal tumor from gland

- mitotane at higher doses than for PDH if not surgical candidate