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Endocrinology > Adrenal Pathophysiology > Flashcards

Adrenal Pathophysiology Flashcards

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
Q

What is an adrenal crisis? What are the clinical characteristics? (big list)

A

Acute deficiency in cortisol/mineralocorticoids

Hypotension, shock, fatigue, weakness, malaise, fever, lethargy, abdominal pain/nausea/vomiting, anorexia, hypoglycemia

26
Q

Etiologies of Adrenal Crisis (4)

A

New primary adrenal failure
Known adrenal insufficiency with acute illness or under-replacement of meds
Acute withdrawal of high dose glucocorticoids
Pituitary apoplexy

27
Q

Treatment of Adrenal Crisis (3)

A

Rehydration: saline IV and electrolytes
Dexamethasone
Monitor BP

28
Q

Autoimmune adrenalitis are associated with _____

A

Other autoimmune disorders– polyglandular syndromes
Type 1: hypoparathyroidism, candidiasis, primary hypogonadism
Type 2: T1DM, autimmune thyroiditis, vitiligo, hypogonadism

29
Q

Primary Hyperaldosteronism: Findings (5)

A

Mineralocorticoid excess:

Hypertension, hypokalemia, hypernatremia, metabolic alkalosis, muscle weakness

30
Q

Who should be screened for primary hyperaldosteronism? (4)

A

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
Q

Dx of Primary Hyperaldosteronism

A

Look at aldosterone: renin ratio

> 20 suggestive, but not diagnostic

32
Q

What do you do for hyperaldosteronism patients over 35? Why?

A

Sample adrenal vein prior to surgery– differentiate between unilateral adenoma and bilateral adrenal hyperplasia

33
Q

How do you distinguish unilateral adenoma vs. bilateral hyperplasia?

A

Lateral disease has aldosterone concentration 4x greater than the contralateral side

34
Q

How do you treat unilateral adenoma vs. bilateral hyperplasia?

A

Unilateral aldosterone-secreting adenoma: surgical resection

Bilateral adrenal hyperplasia: mineralocorticoid antagonist

Endocrinology (26 decks)

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