Adrenal disorders: Howell Flashcards

1
Q

Incidence and etiology of addisons disease

A

-insidious onset, progressive
- 80% due to idiopathic (AI) atrophy of adrenal cortex
- other: granulomatous infections, necrosis

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2
Q

pathogenesis of addisions disease

A

-primary hypofunction of adrenal gland
- lack of aldosterone: hyponatremic, hyperkalemia, dehydration
-lack of cortisol: hypoglycemia, myocardial weakness, hyperpigmentation
-lack of androgens: lack of pubic and axillary hair in females

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3
Q

Signs and sx of addison’s disease

A
  • H/A, nausea and vomit, malaise, anorexia
    -increased skin pigmentation (especially at creases)
    -orthostatic hypotension
    -decreased cold tolerance
    -fatigue, weakness
    depression
    wt loss and dehydration in later stages
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4
Q

what sx of addisons dz can occur at later stages

A

weight loss and dehydration

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5
Q

signs and sx of addisonian crisis

A

sudden onset:

-hyperpyrexia
-severe v/d
-severe abdominal and low back pain
-peripheral vascular collapse
-cyanosis
-confusion

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6
Q

Diagnostic labs in addison’s disease

A

-hyponatremia
-hyperkalemia
-metabolic acidosis: as potassium increases in the blood, hydrogen ions increase as well
-increased renin and ACTH levels: renin due to decrease in aldosterone
-morning cortisol levels will be low

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7
Q

what is the most common cause of cushings syndrome

A

prolonged or high doses of exogenous corticosteroids

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8
Q

which cushing’s etiology is more common in women

A

endogenous causes 5X more common in women
(pituitary adenoma secreting ACTH)

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9
Q

cushings syndrome vs disease

A

syndrome: group of signs and symptoms

disease: pituitary adenoma

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10
Q

signs and sx of cushings

A

-impaired collagen production: spontaneous bruising, poor wound healing, purple striae over abdomen

  • proximal muscle weakness
    -bone loss
    -hyperglycemia
    -hypertension
    -increased central fat deposit
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11
Q

dx labs for cushings

A

-electrolytes: ACTH issue? normal electrolyses, adrenal adenoma? abnormal electrolytes

  • elevated serum and 24 hour urinary cortisol levels
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12
Q

ddx pituitary adenoma and SCC lung

A

dexa suppression test:
-give dexametha(cortisonic) and look at response of ACTH
-If pituitary adenoma: ACTH goes down 50% bc its bening and responds to higher cortisol

-if SCC of lung: no change bc cancer is rogue and does what it wants

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13
Q

Secondary adrenal insufficiency etiology

A

-Sheehans syndrome
-tumors, trauma
-discontinuation of exogenous steroids

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14
Q

Signs and sx of secondary adrenal insufficiency

A
  • similar to addisons dx however there is no hyperpigmentation (low ACTH)
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15
Q

DX of secondary adrenal insufficiency

A

-electrolytes and aldosterone will be normal (not under control of ACTH)
-ACTH stimulation test results in increase cortisol levels

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16
Q

another name for primary hyperaldosteronism

A

conn syndrome

17
Q

sx of conn syndrome

A
  • muscle weakness
  • palpitation, HTN
    -H/A
    -fatigue
    -metabolic alkolosis
18
Q

incidence of conn syndrome

A

2x more common in women

19
Q

dx labs for conn syndrome

A
  • hypokalemia
    -hypernatremia
    -aldosterone to renin ratio greater than 20:1
    -normal ACTH and glucose
    -abdominal CT scan for adenoma : distinguishes hyperplasia from primary hyperaldosterone
20
Q

Etiology of conn syndrome

A

50% due to unilateral adenomas
40% due to bilateral hyperplasia

21
Q

etiology of secondary hyperaldosteronism

A

stimulation by renin-angiotensin system (not adrenal gland)

-CHF
-liver cirrhosis
-nephrotic syndrome

22
Q

sx of secondary hyperaldosteronism

A

symptoms similar to primary but more HTN and edema

23
Q

pheochromocytoma incidence

A

adrenal medulla disorder
-rare
-young adults 20-40 yrs old
-95% are bening tumors

24
Q

what is pheochromocytoma assocaited with

A

men II

25
Q

sx of pheochromocytoma

A
  • tremors, nervousness, H/A, sweating
    -HTN, palpitations, tachycardia

may be episodic

26
Q

dx of pheochromocytoma

A
  • 24 hour urine for catecholamines and metabolites
    -CT or MRI of the adrenal medulla
27
Q

inheritance pattern in congenital adrenal hyperplasia

A

autosommal recessive

28
Q

pathogenesis of congenital adrenal hyperplasia

A

21-hydroxylase deficiency in over 90% of cases
unable to make cortisol and aldosterone —- precursors shift to androgen synth

29
Q

severe sx of congenital adrenal hyperplasia

A

-virilization of female genital
-V/D, dehydration
-failure to thrive, salt wasting
- accelerated skeletal and pubertal maturation in males (lead to short stature bc growth plates close early in age)

30
Q

mild sx of congenital adrenal hyperplasia

A

-hirsutism
-oligomenorrhea
-infertility
-acne
-orthostatic hypotension
-frequent illness
-poor response to stress

31
Q

labs congenital adrenal hyperplasia

A

-hyponatremia
-hyperkalemia
-metabolic acidosis
-low aldosterone
low cortisol
hypoglycemia

32
Q
A