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15 Endocrine > 15.10-11 Adrenal Cortex + Medulla > Flashcards

15.10-11 Adrenal Cortex + Medulla Flashcards

1
Q

You do adrenal imaging on pt with Cushing’s syndrome to determine cause. Think what in these results? How to differentiate btwn similar presentations?

  1. one enlarged adrenal, one atrophied
  2. bilateral hypertrophy
  3. bilateral atrophy
A
  1. adrenal adenoma/carcinoma/
  2. high ACTH (may be Cushing’s disease or paraneoplastic ACTH tumor)
    - in order to distinguish btwn both, do a high-dose dexamethasone test. Pituitary tumor will respond, but ectopic will not
  3. exogenous glucocorticoids
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2
Q

Low and high dose dexamethasone test results in these Cushing syndrome causes:

  1. exogenous glucocorticoids
  2. Cushing’s disease (ACTH secreting pit adenoma)
  3. ectopic ACTH secretion (paraneoplastic)
  4. primary adrenal adenoma, hyperplasia, carcinoma
A

Low:

all: no suppression

high dose:

  1. N/A
  2. suppression
  3. no suppression
  4. N/A
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2
Q

Acute adrenal insufficiency

  • most common cause
  • another important cause
  • clinical presentation
A
  1. abrupt withdrawal of glucocorticoids (must wean pt off of it)
  2. Waterhouse -Friedrichsen syndrome
    - presents as weakness and hypotension (shock)
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3
Q

Cortisol effect on immune function (3)

A
  1. block phospholipase A2 (decrease prostaglandins, LTs)
  2. block IL-2 (block T cell activation)
  3. block histamine release from mast cells
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4
Q

ACTH levels in these causes of Cushing syndrome

  1. exogenous glucocorticoids
  2. Cushing’s disease (ACTH secreting pit adenoma)
  3. ectopic ACTH secretion (paraneoplastic)
  4. primary adrenal adenoma, hyperplasia, carcinoma
A
  1. low
  2. high (androgen excess may be present)
  3. very high (androgen excess and hyperpigmentation may be present)
  4. low
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4
Q

Addison’s disease

  • clinical presentation (3 mechs)
  • mnemonic
A
  1. low aldo–hypotension, hyponatremia, hypovolemia, hyperkalemia, met acidosis
  2. low cortisol–hypotension, vomiting, diarrhea, weakness
  3. increased ACTH–hyperpigmentation

“A3”– Adrenal Atrophy with Absence of hormone production.

All 3 cortical divisions (medulla spared)

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5
Q

Primary hyperaldosteronism

-tx

A

Aldosterone blocker

  • spironolactone, eplerenone
  • surgery for adenoma
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6
Q

17 OHlase deficiency

  • clinical presentation
  • Tx
A
  1. HTN and mild hypokalemia:

excess mineralocorticoids, resulting in low renin and therefore low Aldo. buildup of mineralocorticoid activity with 11-DOC and corticosterone

  1. Primary amenorrhea, lack of female pubic hair. pseudohermaphroditism in males.
    - loss of androgens
  2. still have glucocorticoid activity with corticosterone

Tx: glucocorticoids, also sex steroids

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7
Q

Cushing syndrome

-dx tests (3)

A
  1. 24 hr urine cortisol (increased in Cushing syndrome)
  2. late night salivary level (increased)
  3. low-dose dexamethasone suppression test. (fails to suppress cort in all cases of Cushing syndrome)
    - In primary Cushing syndrome, high dexamethasone has no suppression effect. In Cushing disease (pituitary), high dexamethasone has suppression effect
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8
Q

In Cushing syndrome, pt presents with HTN, hypokalemia, and met alkalosis

-mechs (2)

A
  1. high cortisol has mineralocort activity
  2. cort upregulates alpha 1 receptors in vasculature, causing vasoconstriction
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9
Q

Imaging reveals what in each cause of Cushing’s syndrome?

  1. exogenous glucocorticoids
  2. Cushing’s disease (ACTH secreting pit adenoma)
  3. ectopic ACTH secretion (paraneoplastic)
  4. primary adrenal adenoma, hyperplasia, carcinoma
A
  1. bilateral adrenal atrophy
  2. bilateral adrenal hypertrophy
  3. bilateral adrenal hypertrophy
  4. one adrenal is hypertrophied, other atrophies
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10
Q

Adrenal medulla

-composed of what embryologic cells?

A

neural crest-derived chromaffin cells

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11
Q

causes of renovascular HTN (2)

A
  1. fibromuscular dysplasia (young women)
  2. atherosclerosis (elderly)
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11
Q

Neonate presents with life-threatening hypotension. Also has hyponatremia and hyperkalemia.

think what?

A
  • Think lack of mineralocorticoid and glucocorticoids
  • So, think CAH (21 OHlase deficiency)
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12
Q

Addison’s disease

-causes (3)

A

chronic adrenal insufficiency

  • progressive destruction of adrenal glands
    1. autoimmune (most common in west)
    2. TB (most common in developing world)
    3. metastatic cancer (esp from lung!)
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13
Q

Glucocorticoid-remediable aldosteronism (GRA)

  • mech
  • clinical presentation
A
  • rare cause of familial hyperaldosteronism
  • aberrant expression of aldosterone synthase in fasciculata (normally only in glomerulosa)
  • presents in children as HTN, hypokalemia, high Aldo, low renin (secondary hyperaldosteronism)
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14
Q

Cushing syndrome

-causes (4)

A

think source of cort/ACTH

  1. exogenous glucocorticoids
  2. Cushing’s disease (ACTH secreting pit adenoma)
  3. ectopic ACTH secretion (paraneoplastic)
  4. primary adrenal adenoma, hyperplasia, carcinoma
16
Q

Primary hyperaldosteronism

  • most common cause
  • other causes (2)
A
  • bilateral adrenal hyperplasia
    1. Conn’s syndrome (adrenal adenoma)
    2. Adrenal carcinoma
17
Q

Waterhouse-Friderichsen syndrome

  • mech
  • classic cause
A
  • classic cause of acute adrenal insufficiency
  • hemorrhagic necrosis of adrenal glands, classically due to DIC in young children with Neisseria meningitidis infection
  • lack of cortisol exacerbates hypotension, leading to death
18
Q

metastic carcinoma in adrenal gland.

-What organ source is highly assoc with adrenal metastasis?

A

Lung cancer

19
Q

How to differentiate intra-adrenal pheochromocytoma from extra-adrenal catecholamine secreting tumor?

A

Intra-adrenal will have serum metanephrine and normetanephrine, while extra-adrenal secretes mainly normetanephrine.

NE is converted to Epi mainly inside the medulla because of the enzyme PNMT, which is stimulated by Cortisol present in medulla

20
Q

Pheochromocytoma

  • tumor of what specific cell type?
  • how to dx? (2)
A
  • chromaffin cells of the adrenal medulla
  • dx with:
    1. increased serum metanephrines
    2. increased 24 hr urine metanephrines and VMA
20
Q

Pheochromocytoma

  • tx
  • what to be aware about in tx
A
  • Surgery
  • Must use alpha-blocker (phenoxybenzamine) before surgery to prevent deadly release of catecholamines. (HTN crisis)
22
Q

phenoxybenzamine

A

alpha blocker, used before pheochromocytoma surgery

23
Q

How can TB affect the adrenal gland?

A

-destruction of adrenal glands leads to Addison’s disease (chronic adrenal insufficiency)

24
Q

Pheochromocytoma

-rule of 10s (4)

A
  1. 10% bilateral
  2. 10% familial
  3. 10% malignant
  4. 10% located outside the adrenal medulla (eg bladder wall or organ of Zuckerkandl)
25
Q

21 OHlase deficiency vs 11 OHlase deficiency

-how do symptoms and tx compare

A

Both lead to CAH.

11 OHlase deficiency has weak mineralocorticoid production with 11-DOC, while 21 OHlase has no mineralocorticoid activity.

So, there is HTN and mild hypokalemia in 11 OHlase deficiency, whereas there is hypotension and hyperkalemia in 21 OHlase deficiency.

Tx: glucocorticoids for both, mineralocorticoids for 21 OHlase

26
Q

Pheochromocytoma

-clinical presentation (5)

A

symptoms due to increased catecholamines

5 P’s:

Pressure (high BP)

Pain (headache)

Perspiration

Palpitations

Pallor

28
Q

Neonatal female patient has clitoral enlargement, HTN, and hyperkalemia. Aldosterone is low.

think what?

A

Think CAH caused by 11 OHlase deficiency.

  • similar to CAH from 21 OHlase deficiency, except there is mineralocorticoid activity from 11-DOC.
  • Low Aldosterone b/c renin is low
29
Q

Congenital Adrenal Hyperplasia

  • most common enzyme deficiency?
  • how does it present? (classic (4) and nonclassic)
A
  • 21 OHlase deficiency
  • classic form presents in neonates:
    1. hyponatremia
    2. hyperkalemia
    3. hypovolemia (life threatening hypotension)
    4. clitoral enlargement in females
  • nonclassic form presents later in life: precocious puberty in males, hirsuitism with menstrual irregulaties in females
30
Q

describe metabolism of catecholamines

A

Tyr –> DOPA –> DA –> NE –> Epi

NE –> normetanephrine —MAO–> VMA

Epi –> metanephrine —MAO–> VMA

metanephrines and VMA (vanillylmandelic acid) excreted in urine

31
Q

Pheochromocytoma

-assoc with what syndromes? (4)

A
  1. MEN 2A (MPP–medullary thyroid carcinoma, pheo, parathyroid)
  2. MEN 2B (MPN–medullary thyroid carcinoma, pheo, neuroma)
  3. Hippel-Lindau disease
  4. neurofibromatosis type 1
32
Q

Congenital Adrenal hyperplasia

-how to screen

A
  • look at 17 OH-progesterone levels
  • increased in 21 OHlase and 11 OHlase deficiencies
  • decreased in 17 OHlase deficiency
33
Q

Secondary hyperaldosteronism

-causes

A

-activation of RAAS

(eg CHF, renovascular HTN)

34
Q

Aldosterone

-fxn in nephron

A

Principal cells: reabsorb Na, secrete K

alpha-intercalated cells: secrete H+

35
Q

Primary hyperaldosteronism vs Secondary hyperaldosteronism

-renin levels

A

Primary: low renin levels

secondary: high renin

37
Q

Cushing syndrome–mech of each:

  1. muscle weakness, thin extremities (muscle wasting)
  2. moon facies, buffalo hump, truncal obesity
  3. abdominal striae
  4. HTN, hypokalemia, met alkalosis
  5. osteoporosis
A
  1. cortisol promotes proteolysis for gluconeogenesis
  2. high insulin (from hyperglycemia) deposits fat cenrally
  3. lower fibroblast activity
  4. high cortisol acts on mineralocorticoid receptors. also, cortisol upregulates A1 receptors
  5. cort decreases osteoblast activity
38
Q

Child pt presents with HTN, hypokalemia, and metabolic alkalosis

  • think what?
  • how to dx?
  • Tx
A

Looks like hyperaldosteronism, probably genetic since child.

  1. GRA–glucocorticoid remediable aldosteronism (aberrant expression of Aldo synthase in fasciculata)
  2. Liddle syndrome (decreased degradation of tubular Na channels)

So, measure Aldo levels! In Liddle, there is low aldo b/c it has nothing to do with Aldo.

  1. GRA: Tx with Aldo blockers (spironolactone, eplerenone)
  2. Liddle: Tx with tubular Na channel blockers (amiloride, triamterene) NOT aldo blockers
39
Q

Child with meningitis:

-what adrenal gland problem to be concerned about?

A

Waterhouse-Friedrichsen syndrome

  • classically presents as young child due to DIC with Neiserria meningitidis infection
  • hemorrhagic necrosis of adrenal glands. Loss of cortisol exacerbates the hypotension, leading to death
40
Q

Liddle syndrome

  • mech
  • clinical presentation
  • Tx
A
  • decreased degradation of sodium channels in collecting ducts
  • (mimics hyperaldosteronism) presents as HTN, hypokalemia, met alkalosis in a young pt
  • tx: (tubular Na channel blockers) Amiloride/triamterene

Note: Aldo blockers (spironolactone) NOT EFFECTIVE

41
Q

How to distinguish primary from secondary adrenal insufficiency?

(2)

A

In primary:

  1. hyperpigmentation (MSH from POMC)
  2. hyperkalemia (aldo still governed by RAAS system)
42
Q

Conn syndrome

A

primary hyperaldosteronism, from aldosterone secreting tumor

15 Endocrine (7 decks)

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