Newman Flashcards

(30 cards)

1
Q

What’s the pneumonic for the adrenal cortex structures and products?

A

Go find rex, make good sex

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2
Q

What’s the medulla stimulated by?

A

Sympathetic nervous system

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3
Q

What is the tx for an adrenal crisis?

A

Replacement tx, hydrocortisone + fluids

Treat hyperkalemia if needed (elevated T waves on ECG)

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4
Q

Lack of ADH causes?

A

High K, low Na, metabolic acidosis, high serum renin

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5
Q

What test would you order in someone w/ suspected CAH?

A

17-hydroxyprogesterone levels (should be high if 21 is defective)

Cortisol test also fine, would be low
Androstenedione would be high

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6
Q

What is Addison dx? What’s its most common cause? Most common infection? What are its genetics? What’s the most common presentation?

A

Chronic adreno-cortical deficiency d/t destruction of AC
Autoimmune, auto-antibodies to 21 or 17
TB
X-linked recessive disorder may mimic MS
Weakness and fatigue, hyper-pigmentation of the skin, hypoglycemia, hypotension

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7
Q

What is Waterhouse-Friderichsen Syndrome? What causes it? What’s the morph presentation? Pt presentation?

A

Bilateral adrenal hemorrhage
Neisseria menengitidis
Adrenals converted to sacs of clotted blood
Hypotension/shock + DIC + body-wide purpura

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8
Q

What is familial GC def? What are the genetics? Common presentation? What is the only def?

A

ACTH R resistance on adrenal cortex
Autosomal recessive
Hyperpigmentation d/t excess ACTH release and build-up (MSH, which is also a product of precursor POMC)
Cortisol

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9
Q

What is CAH? What’s impaired? Which enzymes is blood pressure/salt-wasting not a factor?

A

Metabolic disorder d/t enzyme loss causing virilization in females and perhaps other things (depends on what enzyme)
Most commonly 21-hydroxylase (def) causing def in aldosterone and cortisol but excess of androgens
17 and 11 (17 isn’t in aldosterone pathway, 11 allows for product synthesis that can inc BP)

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10
Q

Lab findings in primary adrenal insuff?

A

Low: Na, GC, MC, blood glucose, BP, serum epi (cortisol req)
High: K, H (metabolic acidosis), Ca, renin

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11
Q

What lab test should be run to confirm diagnosis of primary adrenal insuff/during adrenal crisis?

A

Cosyntropin (synthetic ACTH) stimulation test

  • IM delivery will NOT inc cortisol levels in 45 min (adrenal glands are the problem)
  • if IM delivery DOES inc cortisol, problem is secondary (hypothalamic or pituitary) because ACTH isn’t being made.. adrenals are waiting for it!
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12
Q

What’s the tx for primary adrenal insuff?

A

GC (hydrocortisone, prednisone) and MC (Fludrocortisone) replacement tx

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13
Q

What are some sxs of an acute adrenal crisis?

A

Abd or flank pain, confusion, dehydration, fatigue, fever, loss of appetite, low BP, N/V, rapid heart and resp rate

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14
Q

What are some ways cortisol interacts with the systems of the body?

A

Reduces collagen synth -> thin skin
Interacts w/ neutrophils -> dec immune function
Limits cytokine mobilization in wounds -> poor wound healing
Re-allocates fat deposits -> skinny arms and legs, fat trunk
Inc BP (d/t inc ACTH)
Easy brusibility

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15
Q

When is Cushing ACTH-dep? When is it not? What scenario makes it Cushing dx?

A

Pituitary adenoma or ectopic (small cell carcinoma of the lung)
Exogenous corticosteroid use or adrenocortical tumor
Pituitary adenoma

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16
Q

What test is used as a screening test for Cushing syndrome? How does it work?

A

Dexamethasone suppression test
Draw a baseline ACTH -> high dose Dexamethasone given at night -> draw cortisol lvls in AM
Results dictate what is going on (pituitary adenomas/Cushing dx only scenario to show response to Dexamethasone test of dec cortisol because pituitary still has capability of responding to outside stimuli and dec ACTH secretions)

17
Q

What are adrenal incidentalomas? What must be done about them?

A

Benign lesions

Plasma fractionated free metanephrines lab (pheo test)

18
Q

What is primary aldosteronism? What’s the most common cause? What’s an inc risk?

A

Inappropriately high levels of aldosterone in the serum that doesn’t suppress adequately with Na-loading (normally the juxtaglomerular apparatus can shut down renin release and thus aldosterone), causes early-onset HTN that’s resistant to tx

Adrenal hyperplasia

CV complications higher in primary aldosteronism vs reg HTN

19
Q

What labs are seen in primary aldosteronism?

A

High: Na, BP (severe HTN above 160/100)
Low: K (metabolic alkalosis, tetany, muscle weakness, paresthesias, HA), renin levels

20
Q

What is Conn Syndrome? What’s the genetic factor in 40% of cases?

A

Primary aldosteronism d/t adrenal adenoma that secretes aldosterone
Mutation in K channel

21
Q

What’s required in all pts w/ biochemically confirmed primary hyperaldosteronism?

A

Thin slice CT scan of the adrenals to screen for adrenal adenomas

22
Q

What are pheochromocytomas?

A

Neoplasms of the adrenal medulla (sympathetic nervous system) arising from chromaffin cells that release catecholamines (epi, NE), 10% can be paragangliomas

23
Q

What does epi do? What does NE do?

A

Tacyarrhythmias

HTN

24
Q

What mutation can predispose to a pheochromocytoma?

A

VHL (autosomal dominant)

25
What lab is run to check for pheochromocytomas?
Plasma fractioned free metanephrines levels, single most sensitive test for secretory pheos and paragangliomas
26
What can occur during/post surgical removal of a pheochromocytoma?
Seeding of the abd (pheochromocytomatosis) -> multifocal recurrent tumors
27
What is the tx for pheos pre-surgery?
Alpha-blockers (Phenoxybenzamine)
28
Can pheos and paragangliomas be declared malignant soley based on morphology?
No
29
What are the MEN syndromes?
Autosomal dominant traits | Predispose to dev of tumors in two or more different endocrine glands
30
What MEN syndromes are associated w/ pheos?
MEN 2 and 3