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EndoRepro 2 Exam 2 > Adrenal HYHO - Newman > Flashcards

Adrenal HYHO - Newman Flashcards

1
Q

what zone of the adrenal cortex produces mineralocorticoids?

A

glomerulosa

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2
Q

what zone of the adrenal cortex produces glucocorticoids?

A

fasciculata

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3
Q

what zone of the adrenal cortex produces sex steroids?

A

reticularis

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4
Q

what does the short term stress response involve?

A

stimulation of the adrenal medulla via preganglionic sympathetic fibers resulting in the release of catecholamines (Epi and NE)

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5
Q

what are the side effects of short term stress response?

A
  • increased HR
  • increased BP
  • glycogen conversion to glucose in the liver
  • dilaation of bronchioles
  • changes in blood flow patterns leading to decreased digestive system activity and reduced urine output
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6
Q

what does the long term stress response involve?

A

CRH stimulation of the anterior pituitary, stimulation of the adrenal cortex by ACTH, and release of mineralocorticoids and glucocorticoids

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7
Q

what are the effects of mineralocorticoid (aldosterone) release?

A
  • retention of Na and H2O by kidneys

- increased blood volume and blood pressure

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8
Q

what are the effects of glucocorticoids (cortisol) release?

A
  • protein and fat are converted to glucose or broken down for energy
  • increased blood glucose
  • suppression of immune system
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9
Q

what does the RAAS system regulate?

A

renal, cardiac and vascular physiology

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10
Q

what stimulates renin secretion?

A

decreased renal perfusion and/on increased sympathetic activity

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11
Q

what does renin do?

A

it converts Angiotensinogen -> Ang I

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12
Q

what does Ang II stimulate?

A

aldosterone secretion from the adrenal cortex

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13
Q

what is the MCC of ambiguous genitalia in a female?

A

congenital adrenal hyperplasia (causing virilization of the genitalia)
- CAH can be life threatening MUST be on the differential is ambiguous genitalia are found

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14
Q

what is the most common form of CAH?

A
  • *21-hydroxylase deficiency**

- results in deficiency of aldosterone and cortisol, increase in testosterone

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15
Q

signs/symptoms of what?

  • failure to thrive
  • recurrent vomiting
  • dehydration
  • hypotension
  • hyponatremia
  • hyperkalemia
  • shock
A

CAH

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16
Q

what are the levels of aldosterone, cortisol and androgens in CAH?

A
  • aldosterone = low
  • cortisol = low
  • androgens = high
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17
Q

what is the essential treatment of an infant in crisis due to CAH?

A
    • hydrocortisone (IV or IM)**
  • fluids/glucose
  • manage hyperkalemia
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18
Q

what is the purpose of mandatory newborn screening?

A

to detect potentially fatal or disabling conditions in newborns as early as possible, hopefully before serious illness develops

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19
Q

what are the three categories of adrenal gland defects responsible for primary adrenal insufficiency?

A
  • adrenal dysfunction (usually autoimmune)
  • adrenal dysgenesis
  • impaired steroidogenesis
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20
Q

what are the clinical signs/symptoms that nearly ALL patients complain of with primary adrenal insufficiency?

A
  • fatigue
  • reduced stamina
  • weakness
  • anorexia
  • weight loss
  • skin hyperpigmentation
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21
Q

what are the clinical signs/symptoms that most patients complain of with primary adrenal insufficiency?

A
  • abdominal pain/N/V
  • MSK pain
  • psychiatric sx (depression, anxiety, irritability)
  • HA, vomiting
  • salt craving
  • low BP (orthostatic)
22
Q
  • moderate neutropenia
  • low serum sodium
  • high serum potassium
  • fasting hypoglycemia
  • low MORNING plasma cortisol
A

lab findings of pt with primary adrenal insufficiency

23
Q

what are the signs/symptoms of acute adrenal crisis?

A
  • dehydration
  • dizziness/light headedness
  • rapid HR
  • rapid RR
  • confusion
  • N/V
  • fever
  • HA
  • abdominal pain/flank pain
24
Q
  • low serum cortisol
  • low blood sugar
  • low serum sodium
  • high serum potassium
  • metabolic acidosis
  • inadequate bump in cortisol level with ACTH stimulation test
A

lab findings of acute adrenal crisis

25
Q

what are the main components of acute adrenal crisis treatment?

A
  • hydrocortisone
  • fluids/glucose
  • fludrocortisone (after hydrocortosone)
  • treat hyperkalemia
26
Q

what would lower than normal serum cortisol typically result in, if everything was working normally?

A

increased serum ACTH

27
Q

what does a lack of pituitary secretion of ACTH in response to low serum cortisol indicate?

A

the problem is “higher” than the adrenal glands

- pituitary issue

28
Q

what is low serum ACTH in the setting of low serum cortisol consistent with?

A

secondary adrenal insufficiency

29
Q

what aer the signs/symptoms of Cushing disease?

A
  • obesity/asymmetric weight gain (trunk/abd)
  • moon face
  • buffalo hump
  • hirsutism/acne
  • thirst, polyuria
  • HTN
  • dark purple striae
  • mental symptoms (difficulty concentrating)
  • impaired wound healing
  • susceptibility to opportunistic infections
30
Q

what are elevated midnight cortisol levels indicative of?

A

Cushing syndrome

31
Q

what is the best screening method for Cushing syndrome?

A

dexamethasone stimulation test

  • dexamethasone should suppress ACTH from pituitary
  • low dose given at night
  • serum cortisol is drawn in the morning
  • results are used in conjunction with serum ACTH levels drawn before dex was given
32
Q

what does it mean if the serum cortisol is low after dexamethasone test?

A

Cushing syndrome can be excluded with certainty

33
Q

what should be considered if ACTH is undetectable/low, and cortisol is not suppressed by high or low doses?

A 
primary hypercortisolism (not driven by ACTH_
- possible adrenal tumor
34
Q

what should be considered if ACTH is elevated in the hundreds, and cortisol is not suppressed by high or low doses?

A

ectopic ACTH syndrome

- often associated with small cell carcinoma of the lung!

35
Q

what should be considered if ACTCH is normal to elevated, and cortisol is not suppressed by low doses, but suppressed by high doses?

A

Cushing disease

36
Q

what are most patients with primary aldosterone (hyperaldosteronism) hypertensive?

A

excessive aldosterone production increases Na retention, which increases water retention -> increasing BP

37
Q

what dx would you expect if patient has:

  • treatment-resistant HTN
  • severe HTN
  • early onset HTN
  • low renin HTN
  • HTN with family hx of early onset HTN or CVA
  • 1st degree relative with aldosteronism
A

primary aldosteronism

38
Q

what does Newman want us to remember about primary aldosteronism?

A
  1. low renin
  2. hypokalemia
  3. metabolic acidosis
39
Q

what was initially used to describe the condition in which a unilateral aldosterone producing adrenal adenoma resulted in hypertension

A

Conn syndrome

40
Q

what is Conn syndrome now used interchangeably with?

A

primary hyperaldosteronism, whether the pt has an adenoma or not

41
Q

what is the primary location and secretion of a pheochromocytoma?

A
  • location: adrenal medulla

- secretes: catecholamines (Epi and NE)

42
Q

what is the primary location and secretion of a paraganglioma?

A
  • location: outside the adrenal gland

- secretes: catecholamines (Epi and NE), OR can be NON-secreting

43
Q

what are the symptoms of pheochromocytoma and paraganglioma?

A

disease of P’s

  • paroxysmal
  • pressure elevated (HTN)
  • pounding pain (HA)
  • panic
  • palpitations
  • pallor
44
Q

what is the most sensitive test for diagnosing secretory pheochromocytomas and paragangliomas?

A

plasma fractionated free metanephrines

45
Q

what is the inheritance pattern of von Hippel-Lindau disease type 2

A

autosomal dominant

- 20% develop pheochromocytomas

46
Q
  • retinal capillary hemangiomas/hemangioblastomas (blood vessel tumors)
  • hemangioblastomas of CNS
  • increased risk for renal cysts that transform into renal cell carcinoma
A

von Hipple-Lindau diseae type 2

47
Q

why do you always treat pheochromocytoma with an alpha-blocker prior to the use of beta-blockers?

A

unopposed alpha receptor stimulation can lead to further elevation of BP
- after alpha blockage has been established, beta blockers can be started

48
Q

what is the alpha blocker example that Newman gave for treating pheochromocytoma?

A

phenoxybenxamine

49
Q

these tumors are usually found incidentally on abd CT/MRI

  • most are benign adrenal adenomas, but they can also be malignant tumors of several types
  • if greater than 4cm, and not obviously benign, cyst, or hemorrhage -> resect
  • if hx of malignancy exists in pt -> resect
A

adrenal gland incidentaloma

50
Q

what do pts with adrenal incidentalomas require clinical assessment for? (3)

A
  • Cushing syndrome
  • hyperaldosteronism
  • testing for pheochromocytoma (plasma fractionated free metanephrines)
51
Q

what does Newman want us to recognize about MEN syndromes?

A

they are caused by gene mutations and therefore tend to run in families

EndoRepro 2 Exam 2 (10 decks)

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