SFP: adrenal pathology I Flashcards

1
Q

Describe the hypothalamic pituitary adrenal axis

A
  1. CRH released from the hypothalamus signals the anterior pituitary to release ACTH. 2. ACTH is released and travels to the adrenal glands. 3. Adrenal steroids aka cortisol is released. Once adequate levels are reached, cortisol feeds back to the pituitary/hypothalamus to reduce CRH and ACTH secretion.
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2
Q

What is Cushing’s syndrome?

A

Anything causing too many glucocorticoids being released.

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3
Q

What are the main causes of Cushing’s syndrome?

A

Hypersecretion of ACTH (Cushing’s disease), lesion in the adrenal gland, paraneoplastic syndromes, and iatrogenic (taking too many glucocorticoids).

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4
Q

What is Cushing’s disease?

A

Too much cortisol production resulting from increased ACTH.

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5
Q

What is the most common cause of Cushing disease?

A

An ACTH producing microadenoma in the pituitary.

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6
Q

What happens to the adrenal gland in Cushing’s disease?

A

Bilateral adrenal hyperplasia that may be diffuse or nodular.

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7
Q

What happens to the adrenal gland in paraneoplastic syndromes?

A

Adrenal hyperplasia.

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8
Q

What is the main lesion in the adrenal gland associated with Cushing’s syndrome?

A

An adenoma.

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9
Q

Compare ACTH in adrenal vs pituitary hypercortisolism.

A

In pituitary causes, ACTH will be way up. In adrenal causes, ACTH will be down due to the negative feedback loop.

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10
Q

What happens to the cortex with a functional adenoma?

A

Atrophy of the cortex adjacent to the adenoma, since they are not getting ACTH stimulation.

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11
Q

What is a big cause of paraneoplastic Cushing syndrome?

A

Small cell carcinoma of the lung.

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12
Q

What happens to ACTH in paraneoplastic Cushing syndrome?

A

It’s way up.

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13
Q

What happens to the adrenal gland when we take too many exogenous glucocorticoids?

A

Adrenal atrophy, but the zona glomerulosa will have normal thickness.

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14
Q

What are clinical features of Cushing syndrome?

A

Upper body obesity with thin arms/legs, “buffalo hump”, high BP, high blood sugar, thin skin, bruising.

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15
Q

How do we check cortisol?

A

24-hour urinary free cortisol or midnight salivary cortisol.

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16
Q

When is cortisol typically highest?

A

Early in the morning.

17
Q

What is the low-dose dexamethasone suppression test?

A

A small amount of dexamethasone is administered, which should reduce cortisol the following day. If cortisol is elevated, this indicates the feedback loop isn’t working right.

18
Q

What is the high-dose dexamethasone suppression test?

A

Used as a confirmatory test for Cushing’s disease; it will suppress urinary free cortisol.

19
Q

What is primary hyperaldosteronism?

A

Chronic excess aldosterone secretion.

20
Q

What is the pathophysiology of hyperaldosteronism?

A

Increased aldosterone causes excess retention of salt and water, as well as excess excretion of potassium, leading to hypertension and hypokalemia.

21
Q

What are common causes of primary hyperaldosteronism?

A

Adrenocortical hyperplasia, adenomas.

22
Q

What is CYP11B2?

A

Aldosterone synthase gene; if overactivated it can lead to adrenocortical hyperplasia and hyperaldosteronism.

23
Q

What is a big cause of secondary hyperaldosteronism?

A

Dysfunction of RAAS.

24
Q

What can cause a ramped up RAAS system?

A

Decreased renal perfusion, hypovolemia and edema, pregnancy (estrogen-caused).

25
What is Conn syndrome?
Adenoma in the adrenal gland producing aldosterone.
26
What are spironolactone bodies?
Eosinophilic laminated cytoplasmic inclusions found in adenomas causing hyperaldosteronism.
27
What happens to the adrenal gland in primary hyperaldosteronism?
Nothing! Excess aldosterone won’t shut off ACTH/won’t cause excess ACTH production, so there isn’t hyperplasia or atrophy.