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FA17 Endocrine > Adrenal Disease > Flashcards

Adrenal Disease Flashcards

1
Q

when are cortisol levels the lowest?

A

middle of the night (2AM)

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2
Q

effects of cortisol?

A
  1. metabolic
  2. calcium homeostasis/connective tissue
  3. Cardiovascular
  4. Immunity
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3
Q

cortisol metabolic effects

A

increases catabolism (breakdown)

increases insulin levels and gluconeogenesis

inhibits growth and reproductive axes

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4
Q

iatrogenic adrenal insufficiency

A

often acquired due to withdrawal of glucocorticoids (suddenly)

Prednisone, dexamthasone

can be inhaled

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5
Q

primary adrenal insufficiency

A

issue is with gland itself

MC cause of adrenal insufficiency

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6
Q

hypothalamic-pituitary-adrenal axis

A

CRH is released in hypothalamus

travels to anterior pituitary to make ACTH

ACTH stimulates adrenal glands to release cortisol

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7
Q

Etiologies of adrenal insufficiency

A 
Autoimmune/Addison's
Tuberculosis 
Bilateral adrenal hemorrhage/infarctions
Congenital causes 
Infiltrative 
Iatrogenic
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8
Q

addison’s disease

A

accounts for majority of adrenal insufficiency in developed world

anti-adrenal ABs - destruction of entire cortex

BOTH cortisol and aldosterone synthesis

women 30-50

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9
Q

TB

A

mc cause of adrenal insufficiency in areas where TB is endemic

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10
Q

congenital cause of adrenal hyperplasia

A

21-hydroxylase def.

can’t make glucocorticoid, precursor is shunted to other hormone pathways

lading to virilization, ambiguous genitalia, salt wasting

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11
Q

symptoms of adrenal insufficiency (5)

A

hyperpigmentation (bc melanostimulating molecule)

weakness, fatigue, dizziness, orthostasis

weight loss and poor appetite

myalgia/arthralgia

heightened senses + salt craving

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12
Q

signs of primary adrenal insufficiency

A

pigmentation change in skin

hypotension/low BP

dehydration

scant axillary or pubic hair in women

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13
Q

lab findings of primary adrenal insufficiency

A

hyponatremia and hyperkalemia

hypoglycemia

metabolic acidosis and renal failure

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14
Q

secondary adrenal disease

A

NO hyper pigmentation, salt cravings, or hyperkalemia

YES s/s of endocrine diseases (issues with gland, more than one axis)

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15
Q

non emergent Dx of cortisol deficiency

A

random serum cortisol (if you have high levels it excludes)

DIAGNOSTIC- cosynotropin stimulation test

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16
Q

cosyntropin stimulation test

A

diagnostic of adrenal insufficiency

synthetic ACTH that is injected and cortisol + aldosterone levels are measured

normally: increase in aldosterone and cortisol
positive insufficiency if levels do not rise

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17
Q

tx of adrenal insufficiency

A

must wear medic alert

lifelong glucocorticoid and mineralocorticoid (hydrocortisone/cortef and fludrocortisone/florinef)

may use DHEA

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18
Q

Hydrocortisone/cortef

A

on PO use is adrenal insufficiency

cytochrome P450 will reduce serum concentrations so have to dose up to avoid crisis

have to stress dose it

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19
Q

adrenal insufficiency pt becomes ill

minor illness

A

doubling of glucocorticoid dose and close outpatient followup

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20
Q

adrenal insufficiency pt becomes ill

major illness

A

trauma, surgery with anesthesia

hydrocortisone 50-100mg q6-8 hrs

weaned following surgery/illness

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21
Q

prognosis of adrenal insufficiency

A

cautious of stressors which may precipitate adrenal crisis

decreased life expectancy\risk of death is 2x average

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22
Q

adrenal crisis cause

A

medical emergency of cortisol deficiency

stress in a patient with mild adrenal insufficiency who isn’t diagnosed

sudden withdrawal of corticosteroids

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23
Q

signs of symptoms of adrenal crisis

A

acute illness

hypotension and dehydration 
metabolic acidosis 
HA, confusion, coma 
N/v abdominal pain 
fever and hyperpryrexia
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24
Q

inducers of cytochrome P50

A

will have to increase dose bc it uses it all faster

AEDs, Mycobacteria ABX. St. John’s wort, Estrogen/progesterone, steroids

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25
Q

inhibitors of cytochrome P50

A

will have to decrease dose

antiretrovirals, azoles, macrolide abx, FQ, CCBs

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26
Q

diagnosis of adrenal crisis

A

random ACTH levels, aldosterone levels

consider other causes (shock, hyperkalemia, hyponatremia, acute abdomen - decrease WBC)

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27
Q

treatment of acute adrenal crisis

A
  1. steroid stress dosing w/100 mg cortef then infusion util weaned back down
  2. aggressive IV fluid replacement
  3. electrolyte correction
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28
Q

what is MC etiology of adrenal insufficiency in US

A

autoimmune destruction

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29
Q

what is mc symptom of adrenal insufficiency in an otherwise healthy patient?

fevers/chills
HTN/tachycardia
Weakness/Fatigue
anorexia/paradoxical weight gain

A

Weakness/Fatigue

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30
Q

Cushing’s syndrome pathophysiology

A

excessive exogenous corticosteroid

could be caused by ACTH hypersecretion of by benign pituitary adenoma

non-pituitary adenoma that secretes ACTH

excesses autonomous cortisol secretion

31
Q

cushion’s DISEASE

A

excessive ACTH secretion by a benign pituitary adenoma

70% of cases, F > M

decreased CRH b/c increased ACTH/cortisol

autonomous ACTH secretion by tumor in pituitary

32
Q

paraneoplastic syndrome

A

carcinoid, SCLC

non-pituitary tumor secretes ACTH autonomously

elevated ACTH, low CRH

pituitary gland and hypothalamus appropriately turned off

33
Q

adrenal tumor

A

tumor on adrenal gland secretes cortisol autonomously

low CRH and ACTH bc tumor is doing the work

34
Q

S/s of Cushing’s Syndrome (10!)

A

purple striae

hirsutism (male hair growth, chest in women, deepening voice)

skin finding (thin skin, easy bruising, SLOW HEALING)

immunologic impairment

central obesity (+ wasted extremities)

moon face (flushed)

buffalo hump/supraclavicular fat pads

hypertension + diabetes mellitus

proximal muscle weakness, osteoporosis

renal calculi

35
Q

tests used to diagnose Cushings

A

dexamethasone supression test

salivary cortisol level

random urinary free cortisol

36
Q

dexamethasone supression test

A

give dose at night and check AM levels

normal: cortisol levels will be low in the AM
cushing’s: cortisol levels will still be high

37
Q

salivary cortisol tests

A

take a swab of saliva at 11PM

should have low cortisol at the this time, high suggests cortisol

38
Q

how do you localize source in cushings

A

serum ACTH levels
CRH stimulation test
pituitary MRI + contrast
CT scan of chest/abdomen/pelvis

39
Q

serum ACTH test

A

used to localize bushings

high = pituitary or ectopic source 
undetectable = adrenal source
40
Q

CRH stimulation test

A

increasing ACTH and cortisol (pituitary source)

constant ACTH and cortisol (ectopic source)

41
Q

primary tx of pituitary adenoma

A

surgical

42
Q

tx of adrenal adenoma

A

mc adrenal source

laparoscopic adrenal resection

43
Q

tx of adrenal carcinoma

A

highly suggested by androgen excess

aggressively resected openly with laparotomy

44
Q

ectopic source

surgical resection

A

first line

must find source then resect

45
Q

carcinoid tumors

A

mc ectopic source

lung, proximal GI tract

slo growing by may be malignant with distant metastases

46
Q

neuroendocrone tumors

A

MEN syndrome

pancreas, pheomedullary thyroid CA

47
Q

medical therapy ectopic source of cushing’s tx

A

SCLC or another primary would be used if source is paraneoplastic

48
Q

how do you treat chushings if you can’t find source?

A

medical suppression via ketoconazole

49
Q

prognosis of Cushings

A

untreated - Lethal and typically caused by excess steroid

  1. CAD compilcations
  2. diabetes
  3. infections
  4. perforated viscera
    increased fracture risk
50
Q

pesudocushing’s syndrome

A

recognized conditions that occurs in people who ingest large quantities of alcohol

develop s/s and biochemical abnormalities w/o high cortisol levels

abstinence from alcohol will reverse the process

51
Q

tx of choice for Cushing’s dz by adrenal adenoma

A

unilateral adrenal resection

52
Q

which of following is NOT s/s of cushings?

purple, angry stretch marks
nonhealing wounds
HTN
pear shape obesity

A

pear shape obesity

53
Q

RAAS system (6 steps)

A
  1. renin release from kidney due to DECREASED renal perfusion
  2. renin converts angiotensinogen to angiotensin I
  3. angiotensin I is converted to angiotensin II by ACE in lungs and other tissue
  4. angiotensin II causes vasoconstriction and stimulates aldosterone secretion from adrenal gland
  5. Aldosterone causes Na+ reabsorption and K+/H+ secretion
  6. increased [Na+] raises the BP and stops renin release
54
Q

hypoaldosteronism

A

def. of aldosterone

typically secondary to deficient renin production by a diseased kidney

55
Q

hyporeninemic hypoaldosteronism

A

cause by diabetic nephropathy or chronic tubulointerstitial kidney disease

56
Q

hypoaldosteronism pt presents with

A

hyperkalemia and non-anion gap metabolic acidosis

no excretion of K+ in urine - bc holds onto K+ to keep positive ion

non anion gap metabolic acidosis caused by normally functioning kidneys that fail to acidify urine (sodium is normal + volume decreased)

57
Q

symptoms of hypoaldosteronism

A

not many, decreased blood pressure

angiotensin II and norepinephrine activation to maintain sodium balance

58
Q

when should you consider hypoaldosteronism?

A

pt has persistent hyperkalmeia w/0 another cause

repeat K check and do EKG, calculate urine anion gap

59
Q

Tx of hypoaldosteronism

A

if primary adrenal deficiency present - tx with fludrocortisone to prevent orthostasis and normalize K+

can exacerbate HTN and edema

not often used in hyporeninemic hypoaldosteronism

60
Q

primary hyperaldosteronism

caused by

A 
aldosterone producing adenoma 
bilateral adrenal hyperplasia 
adrenal CA (rare)
61
Q

pathophysiology of primary hyperaldosteronism

A

will have sodium retention, HTN, hypokalemia (not always seen) and metabolic alkalosis

hold onto too much sodium, so waste away K+ and H+

62
Q

when do you suspect primary hyperaldosteronism

A

present with significant HTN at 30-50 y/o (F>M)

pt with persistent hypokalemia and resistant hypertension

63
Q

hyperaldosteronism s/s

A

due to low K+

fatigue, weakness, nocturia, HA

polydipsia, polyuria, parasthesisas

may have tetany, Trousseau’s or Chvostek

bp may be elevated

64
Q

diagnosing hyperaldosteronism

A

BP meds stopped

controlled with non-dihydropuridine CCBs
correct renal impairment and hypokalemia

65
Q

aldosterone to renin ratio (ARR)

A

compared serum aldosterone to production of angiotensin I from angiotensinogen (measure plasma renin activity)

normal person = increase renin then increase aldosterone

in hyperaldosteronism = renin always low, aldosterone is always high

66
Q

diagnosis of hyperaldosteronism

A

following ARR

confirm diagnosis of hyperaldosteronism

distinguish b/w adrenal adenoma and adrenal hyperplasia

67
Q

tx of hyperaldosteronism

A

adrenal adenoma is treated surgically

adrenal hyperplasia is treated with aldactone

68
Q

pheochromocytoma

A

secrete norepinephrine and other catecholamines

most often found in adrenal medulla

may be a feature of MEN

69
Q

MEN 1

A

parathyroid adenoma, pituitary tumors, entero[ancreatic tumor and skin tumors

70
Q

MEN 2A

A

medullary thyroid CA
pheochromocytoma
parathyroid hyperplasia

71
Q

MEN 2B

A

medullary thyroid CA
pheochromocytoma
GI tumors/marfanoid habitus

72
Q

symptoms of pheochromocytoma

A 
paroxysmal HTN 
headache 
palpitations 
sweating 
chest pain 
BP fluctuations
73
Q

diagnosis of pheochromocytoma

A

24 hr urine creatinine collection

total catecholamines

metanephrine

vanillylmandelic acid levels

abdominal MRI

74
Q

pheochromocytoma tx

A

hypertension resistent to stnd meds

pre op alpha blockage then beta blocker is added if needed then open up for adrenalectomy

serum free metanephrine levels normalize and should be checked

FA17 Endocrine (10 decks)

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