Adrenal Pathophysiology Flashcards

(34 cards)

1
Q

What are three main hallmarks of Cushing’s syndrome?

A
  1. Loss of diurnal variation of cortisol secretion
  2. Autonomy from “central” ACTH control (loss of response to feedback inhibition)
  3. Excess cortisol secretion
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2
Q

What are two broad categories of of Cushing’s syndrome?

A

ACTH-dependent and ACTH independent

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3
Q

What is most common cause os Cushing’s Syndrome?

A

Exogenous use of glucocorticoids

Next is Cushing’s disease (ACTH producing pituitary adenoma)

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4
Q

What are basic metabolic derangements due to excess corticosteroids? (3)

A

Stimulates gluconeogensis: hyperglycemia
Increases lipogenesis, insulin resistance: increased FFA
Increased gluconeogenesis results in catabolism of proteins

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5
Q

Signs and symptoms of Cushing’s Syndrome: Effects of fat metabolism (4)

A

Dewlap (neck)/round face
Supraclavicular fat pads
Buffalo hump
Skinny limbs with big stomach

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6
Q

Other effects of cortisol excess: immunity, hematopoetic, eyes and musculoskeletal (3)

A

Impaired immunity
Hypercoagulability
Cataract formation
MS: proximal myopathy, osteoperosis, redistribution of body fat

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7
Q

What are cardiovascular effects of cortisol excess? (3)

A

Hypertension, cardiomyopathy, increased thromboembolic events (atherosclerosis, strokes, PE, etc)

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8
Q

What are dermatological effects of cortisol excess? (6)

A
Thin skin
Easy bruisability
Striae
Acne
Hyperpigmentation
Hirsutism
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9
Q

What are CNS effects of cortisol excess? (2)

A

Pyschiatric disturbances

Cognition/psychosocial functioning

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10
Q

What are mineralocorticoid and androgen effects of excess cortisol? (4)

A

HTN and hypokalemia (hk more associated with ectopic ACTH production)
Testosterone increased in females
Abnormal menses
Marked virilization worrisome for malignant adrenal tumor

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11
Q

ACTH-dependent Cushing’s is characterized by ______

A

Bilateral adrenal hyperplasia

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12
Q

What hormone levels do we observe in ACTH-independent Cushing’s? Why?

A

High cortisol; low ACTH

This is because cortisol is providing negative feedback on ACTH

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13
Q

How do you measure loss of diurnal variation of cortisol secretion?

A

Late night salivary cortisol: measures free cortisol and can be easily collected at home

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14
Q

Dexamethasone suppression: what it does….why do you do it?

A

Exogenous dexamethasone substitutes for ACTH in suppressing ACTH release
Should have low cortisol….if not, it indicates inappropriate cortisol secretion

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15
Q

24 hour urinary free cortisol: what indicates Cushing’s?

A

If cortisol > 3x upper limit of normal

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16
Q

How do you localize source of problem?

A

Look at plasma ACTH– if low, Cushing’s is from adrenal source….if high, Cushing’s from pituitary or ectopic ACTH source….also if exogenous, ACTH is low

17
Q

Treatment of Cushing’s: Unilateral adrenal adenoma

A

Adrenalectomy

18
Q

Treatment for pituitary adenoma

A

Hypophysectomy

19
Q

How long do symptoms of hypercortisolism take to resolve?

A

Up to 12 months

Not all sequelae completely resolve (especially psych ones0

20
Q

Primary adrenal failure (Addison’s disease): main features (4)

A

90% of cortex destroyed before presentation
Elevated ACTH
Usually indolent course
Can lose adrenal hormones

21
Q

Symptoms of primary adrenal failure are consistent with ____ and _____ deficiency, and include _____ (3)

A

Mineralocorticoid and glucocorticoid deficiency

Hyponatremia, hyperkalmeia, hypotension

22
Q

Clinical characteristics of primary adrenal failure: (6)

A
Hyperpigmentation
Weight loss
Muscle/joint pains
Fatigue
Nausea, abdominal pain
Hypoglycemia (reduced gluconeogenesis)
23
Q

Etiologies of Addison’s Disease (5)

A
Autoimmune destruction (60%)
Infectious: TB, fungus, HIV
Bilateral hemorrhage/infarct
Metastatic cancer
Drugs: aminoglutethimide, ketoconazole, etomidate, rifampin, phenytoin
24
Q

Diagnosis of Addison’s disease (2)

A

Early AM cortisol/ACTH concentration: look for low cortisol and high ACTH

Cosyntropin stimulation testing: look at IM injection of synthetic ACTH and measure cortisol

25
What is an adrenal crisis? What are the clinical characteristics? (big list)
Acute deficiency in cortisol/mineralocorticoids Hypotension, shock, fatigue, weakness, malaise, fever, lethargy, abdominal pain/nausea/vomiting, anorexia, hypoglycemia
26
Etiologies of Adrenal Crisis (4)
New primary adrenal failure Known adrenal insufficiency with acute illness or under-replacement of meds Acute withdrawal of high dose glucocorticoids Pituitary apoplexy
27
Treatment of Adrenal Crisis (3)
Rehydration: saline IV and electrolytes Dexamethasone Monitor BP
28
Autoimmune adrenalitis are associated with _____
Other autoimmune disorders-- polyglandular syndromes Type 1: hypoparathyroidism, candidiasis, primary hypogonadism Type 2: T1DM, autimmune thyroiditis, vitiligo, hypogonadism
29
Primary Hyperaldosteronism: Findings (5)
Mineralocorticoid excess: | Hypertension, hypokalemia, hypernatremia, metabolic alkalosis, muscle weakness
30
Who should be screened for primary hyperaldosteronism? (4)
Pts under 30 with HTN, no obesity or family history Pts with unexplained hypokalemia and hypertension Pts with resistant HTN Ptts with adrenal incidentaloma/HTN
31
Dx of Primary Hyperaldosteronism
Look at aldosterone: renin ratio >20 suggestive, but not diagnostic
32
What do you do for hyperaldosteronism patients over 35? Why?
Sample adrenal vein prior to surgery-- differentiate between unilateral adenoma and bilateral adrenal hyperplasia
33
How do you distinguish unilateral adenoma vs. bilateral hyperplasia?
Lateral disease has aldosterone concentration 4x greater than the contralateral side
34
How do you treat unilateral adenoma vs. bilateral hyperplasia?
Unilateral aldosterone-secreting adenoma: surgical resection Bilateral adrenal hyperplasia: mineralocorticoid antagonist