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FA17 Endocrine > Adrenal Disease > Flashcards

Adrenal Disease Flashcards

(74 cards)

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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
inhibitors of cytochrome P50
will have to decrease dose antiretrovirals, azoles, macrolide abx, FQ, CCBs
26
diagnosis of adrenal crisis
random ACTH levels, aldosterone levels consider other causes (shock, hyperkalemia, hyponatremia, acute abdomen - decrease WBC)
27
treatment of acute adrenal crisis
1. steroid stress dosing w/100 mg cortef then infusion util weaned back down 2. aggressive IV fluid replacement 3. electrolyte correction
28
what is MC etiology of adrenal insufficiency in US
autoimmune destruction
29
what is mc symptom of adrenal insufficiency in an otherwise healthy patient? fevers/chills HTN/tachycardia Weakness/Fatigue anorexia/paradoxical weight gain
Weakness/Fatigue
30
Cushing's syndrome pathophysiology
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
cushion's DISEASE
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
paraneoplastic syndrome
carcinoid, SCLC non-pituitary tumor secretes ACTH autonomously elevated ACTH, low CRH pituitary gland and hypothalamus appropriately turned off
33
adrenal tumor
tumor on adrenal gland secretes cortisol autonomously low CRH and ACTH bc tumor is doing the work
34
S/s of Cushing's Syndrome (10!)
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
tests used to diagnose Cushings
dexamethasone supression test salivary cortisol level random urinary free cortisol
36
dexamethasone supression test
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
salivary cortisol tests
take a swab of saliva at 11PM should have low cortisol at the this time, high suggests cortisol
38
how do you localize source in cushings
serum ACTH levels CRH stimulation test pituitary MRI + contrast CT scan of chest/abdomen/pelvis
39
serum ACTH test
used to localize bushings ``` high = pituitary or ectopic source undetectable = adrenal source ```
40
CRH stimulation test
increasing ACTH and cortisol (pituitary source) | constant ACTH and cortisol (ectopic source)
41
primary tx of pituitary adenoma
surgical
42
tx of adrenal adenoma
mc adrenal source laparoscopic adrenal resection
43
tx of adrenal carcinoma
highly suggested by androgen excess aggressively resected openly with laparotomy
44
ectopic source surgical resection
first line must find source then resect
45
carcinoid tumors
mc ectopic source lung, proximal GI tract slo growing by may be malignant with distant metastases
46
neuroendocrone tumors
MEN syndrome pancreas, pheomedullary thyroid CA
47
medical therapy ectopic source of cushing's tx
SCLC or another primary would be used if source is paraneoplastic
48
how do you treat chushings if you can't find source?
medical suppression via ketoconazole
49
prognosis of Cushings
untreated - Lethal and typically caused by excess steroid 1. CAD compilcations 2. diabetes 3. infections 4. perforated viscera increased fracture risk
50
pesudocushing's syndrome
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
tx of choice for Cushing's dz by adrenal adenoma
unilateral adrenal resection
52
which of following is NOT s/s of cushings? purple, angry stretch marks nonhealing wounds HTN pear shape obesity
pear shape obesity
53
RAAS system (6 steps)
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
hypoaldosteronism
def. of aldosterone typically secondary to deficient renin production by a diseased kidney
55
hyporeninemic hypoaldosteronism
cause by diabetic nephropathy or chronic tubulointerstitial kidney disease
56
hypoaldosteronism pt presents with
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
symptoms of hypoaldosteronism
not many, decreased blood pressure angiotensin II and norepinephrine activation to maintain sodium balance
58
when should you consider hypoaldosteronism?
pt has persistent hyperkalmeia w/0 another cause repeat K check and do EKG, calculate urine anion gap
59
Tx of hypoaldosteronism
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
primary hyperaldosteronism caused by
``` aldosterone producing adenoma bilateral adrenal hyperplasia adrenal CA (rare) ```
61
pathophysiology of primary hyperaldosteronism
will have sodium retention, HTN, hypokalemia (not always seen) and metabolic alkalosis hold onto too much sodium, so waste away K+ and H+
62
when do you suspect primary hyperaldosteronism
present with significant HTN at 30-50 y/o (F>M) pt with persistent hypokalemia and resistant hypertension
63
hyperaldosteronism s/s
due to low K+ fatigue, weakness, nocturia, HA polydipsia, polyuria, parasthesisas may have tetany, Trousseau's or Chvostek bp may be elevated
64
diagnosing hyperaldosteronism
BP meds stopped controlled with non-dihydropuridine CCBs correct renal impairment and hypokalemia
65
aldosterone to renin ratio (ARR)
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
diagnosis of hyperaldosteronism
following ARR confirm diagnosis of hyperaldosteronism distinguish b/w adrenal adenoma and adrenal hyperplasia
67
tx of hyperaldosteronism
adrenal adenoma is treated surgically adrenal hyperplasia is treated with aldactone
68
pheochromocytoma
secrete norepinephrine and other catecholamines most often found in adrenal medulla may be a feature of MEN
69
MEN 1
parathyroid adenoma, pituitary tumors, entero[ancreatic tumor and skin tumors
70
MEN 2A
medullary thyroid CA pheochromocytoma parathyroid hyperplasia
71
MEN 2B
medullary thyroid CA pheochromocytoma GI tumors/marfanoid habitus
72
symptoms of pheochromocytoma
``` paroxysmal HTN headache palpitations sweating chest pain BP fluctuations ```
73
diagnosis of pheochromocytoma
24 hr urine creatinine collection total catecholamines metanephrine vanillylmandelic acid levels abdominal MRI
74
pheochromocytoma tx
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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