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05 Endo > Adrenal Gland Disorders > Flashcards

Adrenal Gland Disorders Flashcards

1
Q

bp guidelines in ph

A

> 140 systolic

>90 diastolic

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2
Q

when to screen for secondary hpn

A

drug-resistance (uncontrolled bp with at least 3 drugs, 1 being diuretic)
abrupt onset
young age
excessive target end organ damage
diastolic hpn
unprovoked/excessive hypokalemia with elevated bp

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3
Q

____ causes predominate in secondary hpn causes

A

adrenal dependent

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4
Q

adrenal cortical hormones

A

mineralocorticoids: aldosterone
glucocorticoids: cortisol
sex hormonres: testosterone -> dht or estradiol

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5
Q

adrenal medullary hormones

A

epinephrine and norepinephrine (degraded by mao and comt)

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6
Q

hormones that can cause hpn

A

mineralocorticoids
glucocorticoids
catecholamines
(all except sex)

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7
Q

t/f acth only acts on mineralocorticoids

A

f, it acts on the entire adrenal cortex. not just cortisol that will be produced when acth is secreted (also other hormones and metabolites)

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8
Q

mechanisms of hpn in cushing’s

A
  • increased production of 11-deoxycorticosterone
  • enhanced pressor sensitivity to endogenous vasoconstrictors
  • increased co
  • activation of the raas by the increased hepatic production of angiotensinogen
  • cortisol activation of the mineralocorticoid receptor
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9
Q

how to workup cushings

A

screening
confirmation of diagnosis
classification

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10
Q

who to screen for cushings?

A

people with hpn

people with clinical manifestations of co-morbid conditions associated with cushing’s

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11
Q

clinical presentations of cushing’s

A

fat-related
cutaneous
muscular
emotional and cognitive

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12
Q

screening tests for cushing’s

A

24 hour urinary free cortisol
overnight 1 mg dexamethasone suppression
late night salivary cortisol

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13
Q

normal or abnormal results for screening tests for cushings

A

24h urinary: levels > 3-4x upper limit of normal is suggestive of cushings
overnight 1 mg dexamethasone: normal should suppress plasma cortisol to <1.8 mcg/dl or 50 nmol/dl
saliva: normal is <145 ng/dl or < 4nmol/dl

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14
Q

conditions associated with hypercortisolism with clinical features of cushings

A 
pregnancy
depression or other psych
alcohol dependance
morbid obesity
poorly controlled dm
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15
Q

causes of acth dependent cushing’s

A

pituitary adenoma

non-pituitary neoplasm (ectopic)

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16
Q

causes of acth independent cushing’s

A

iatrogenic: glucocorticoid intake and megestrol acetate intake
adrenal neoplasm
nodular adrenal hyperplasia
factitious

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17
Q

most common cause of cushing’s

A

pituitary adenoma (acth dependent)

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18
Q

initial imaging studies for cushings

A

abdominal ct for primary adrenal problem

pituitary mri for pituitary source

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19
Q

specialized imaging studies for cushings

A

inferior petrosal sinus sampling study: for lateralizing occult lesion in the pituitary and guiding surgical therapy
chest and abdominal ct for suspected ectopic acth

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20
Q

test done after confirming cushing’s diagnosis

A

check serum acth

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21
Q

results of acth tests for cushings

A

acth suppressed: acth independent cushing from adrenal glands
acth is normal/high: acth dependent cushings from pituitary or ectopic source

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22
Q

how to differentiate pituitary vs ectopic source

A

high dose dexamethasone suppression test

suppressed: pituitary
not suppressed: ectopic

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23
Q

last resort test for cushings diagnosis

A

inferior petrosal sinus sampling

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24
Q

initial treatment of choice for cushings

A

surgical resection (TSS)

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25
second line treatment for cushings
medical treatment with or without radiation
26
medical treatment in cushings is primary for
ectopic autonomous secretion of cortisol in patients with occult or metastatic eas
27
medical treatment is adjunctive therapy for
adrenocortical carcinoma, to reduce cortisol levels
28
indications for radiation therapy in cushings
concerns about mass effects or invasion associated with corticotroph adenomas patients who have failed tss or recurrent cushing's
29
t/f you need to confirm that medical therapy is effective in normalizing cortisol before administering radiation therapy
true
30
treatment for acth dependent cushings, ectopic and no tumors
steroidogenesis i gc receptor antagonist bilateral adrenalectomy
31
treatment for acth dependent cushings, pituitary source or >6 mm mass
tumor resection via tss if failed, repeat tss, pituitary directed medical treatment, or radiation treatment and steroidogenesis inhibitors
32
treatment for acth independent cushing's
bilateral/unilateral adrenalectomy and treat metastatic disease
33
effects angiotensin II
causes vasoconstriction of arterioles stimulation of adrenal cortex to release aldosterone (inc sodium water reabsorption, inc secretion of potassium to urine)
34
the most common specifically treatable and potentially curable form of hpn
primary aldosteronism
35
clinical presentation of primary aldosteronism
``` inc aldosterone secretion inc renal sodium reabsorption extracellular fluid volume expansion suppression of renin hypertension hypokalemia ```
36
screening test for primary aldosteronism
plasma renin/aldosterone ratio PAC:PRA ratio >30 = investigate for primary aldosteronism
37
indications for screening for primary aldosteronism
``` sustained bp 150/90 resistant hypertension bp controlled with 4 drugs spontaneous adrenal incidentaloma obstructive sleep apnea family history cva at young age first degree relative with primary aldosteronism ```
38
false positives from ARR
impaired renal function advancing age medicaitons (b adrenergic blockers, methyldopa, clonidine, nsaids)
39
false negatives from ARR
hypokalemia dietary salt restriction pregnancy medications (diuretics, CCB, ACEI, ARB)
40
confirmation tests for primary aldosteronism
iv saline suppression | captopril challenge test
41
results for iv saline suppression
measures pac baseline and 4h normal: <5 ng/dl at 4h indeterminate: 5-19 ng/dl at 4h abnormal: >/= 15 ng/dl at baseline and >/= 10 ng/dl at 4h
42
results of captopril challenge test
measures pac baseline and 1-2 h normal: pac suppressed by 30% abnormal: no suppression
43
subtypes of primary aldosteronism
bilateral idiopathic adrenal hyperplasia or idiopathic hyperaldosteronism* aldosterone producing adenoma
44
gold standard test for subtype classification
adrenal venous sampling
45
other tests for subtype classification
adrenal scintigraphy | adrenal ct and mri
46
algorithm for PA
hypertension w/ risk factor -> arr -> arr >30 -> confirmatory test -> subtype classification
47
what do you do when patient is positive for ARR and unwilling to proceed with tests
treat with mineralocorticoid receptor antagonist
48
indications to proceed with MR antagonist
very low potassium with very low renin and >20 ng/dl PAC if patient doesnt want to undergo surgery
49
treatment if AVS shows bilateral adrenal hyperplasia
surgery with MR antagonist or MR antagonist only (if surgery not desired)
50
treatment if AVS shows unilateral adrenal mass
laparoscopic adrenalectomy
51
criteria for laparoscopic adrenalectomy
marked PA young age positive in adrenal ct unilateral adrenal mass
52
MR antagonists
spironolactone - available in ph | eplerenone
53
other drugs for PA
amiloride: aldosterone independent antagonist of renal tubular sodium transport CCBs ACEi blocks intraadrenal raas
54
after successful laparoscopic adrenalectomy in a unilateral mass, patients will be normotensive even after ____
5 years
55
___ and ___ are tumors that produce catecholamines
pheochromocytoma (intra adrenal) and paraganglioma (extra adrenal)
56
when to screen for ppgl?
``` paroxysmal symptoms paradoxic bp responses to certain medication resistant hpn incidental adrenal mass previous ppgl family history syndromic features ```
57
most common symptoms in ppgl
headache diaphoresis forceful heartbeat
58
ppgl biochemical phenotypes, adrenergic
adrenal medulla associated with kinase pathway mutations more paroxysmal symptoms
59
ppgl biochemical phenotypes, noradrenergic
adrenal medulla or extra renal associated with hypoxic signaling pathway mutations less paroxysmal symptoms
60
medications that can trigger ppgl crisis
``` d2 receptor antagonists b-adrenergic receptor blockers sympathomimetics opioid analgesics NE reuptake inhibitors SSRI MAO inhibitors corticosteroids peptides neuromuscular blocking agents ```
61
syndromes associated with ppgl
MEN 2a/2b VHL syndrome NF 1
62
metabolites measured in ppgl confirmation
fractionated catecholamines | fractionated metanephrines
63
tests for ppgl confirmation
plasma free metanephrines | 24h urinary fractionated metanephrines
64
drugs that can cause false positive ppgl
mao-i, sympathomimetics, cocaine, levodopa, b blockers
65
plasma free metanephrine results
normal: no ppgl | elevated >3x upper limit: highly predictive of ppgl
66
24h urinary fractionated metanephrine results
normal: excludes ppgl | elevated >2x upper limit: highly predictive of ppgl
67
when to do imaging for ppgl
when there is clear biochemical evidence
68
first choice for ppgl imaging
ct scan: thorax abdomen and pelvis
69
other types of imaging for ppgl
mri: skull base and neck mibg scintigraphy: metastatic pdg pet/ct scan: preferred for metastatic
70
t/f genetic testing is required prior to starting treatment for ppgl
false
71
management for ppgl
surgical: minimally invasive adrenalectomy or open resection
72
peri-operative treatments before surgery
non-pharma: high sodium and fluid intake | pharma
73
pharma peri-operative treatments for ppgl
table 6
74
t/f we dont need to follow the sequence when giving presurgical medical prep for ppgl
false, bblockers ahead of adrenergic blockers can precipitate a hypertesive crisis
75
measure plasma or urine levels of metanephrines at ___
2-4 weeks after surgery
76
t/f lifelong biochemical testing is needed after ppgl surgery
true

05 Endo (16 decks)

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