Adrenals Flashcards

1
Q

what hormones does the adrenal cortex

A
  • glucocorticoids
  • mineralocorticoids
  • adrogens
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2
Q

how is cortisol releeased

A
  • diurnal basal rate
  • bursts d/t stress
  • regulated by ant pituitary and ACHT neg feedback
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3
Q

role of cortisol

A
  • suppress immune sys
  • anti-inflammatory
  • gluconeogenesis -> elevated BS
  • causes increase WBCs but functionally suppressed
  • inhibit insulin
  • ketogenesis
  • elevated RBC and platelet levels
  • reduce bone formation
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4
Q

what is the role of aldosterone

A
  • Na retention (water follows)

- K secretion

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5
Q

what is produced in the adrenal medulla

A
  • catecholamines: epi, NE, dopamine
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6
Q

what are chromaffin cells

A
  • produce and store catecholamines in adrenal medulla
  • have CNS origin without dendrites/ axons
  • surrounded by BV -> rapid direct release of catecholamines
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7
Q

pheochromocytoma

A
  • adrenal medulla tumor
  • rare
  • produces, stores, and secretes catecholamines
  • usu unilat and benign
  • make up small portion of HTN
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8
Q

si/sx of pheo

A
  • HTN- sustained or labile
  • paroxysmal sx:
  • HA, diaphoresis, palpitations*
  • chest pain
  • N/V, abd pain
  • anxiety
  • pallor and/or flushing
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9
Q

dx of pheo

A
  • get 24 hour urine: looking for catecholamine metabolites

- CT or MRI*

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10
Q

tx of pheo

A
  • surgically remove tumors

- before surgery MUST do alpha block for 10-14 days, BB for 2 days

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11
Q

what alpha blockade is used prior to pheo surgery

A
  • phenoxybenzamine
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12
Q

what beta blockers are used prior to pheo surgery

A
  • propranolol

- nadolol

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13
Q

what do alpha and beta blockade before pheo removal

A
  • prevent intra-operative HTN crisis d/t catecholamine release
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14
Q

what do plasma renin levels look like in primary hyperaldosteronism

A
  • plasma renin low

- high aldo causes RAAS to shut off

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15
Q

what do plasma renin levels look like in secondary hyperaldosteronism

A
  • plasma renin high

- aldo elevates in response

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16
Q

what is Conn’s syndrome

A
  • primary hyperaldo
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17
Q

classic findings for primary hyperaldo

A
  • diastolic HTN -> HA
  • hypoK: muscle weakness and fatigue
  • metabolic alkalosis: H loss with K
  • low plasma renin
  • generally: HA + high na + low K
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18
Q

work up for primary hyperaldo

A
  • hypoK, hyperNa, metabolic alkalosis
  • low plasma renin
  • EKG: U wave, ST depression, prominent P
  • CXR: possible cardiomegaly
  • proteinuria on UA
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19
Q

criteria for dx of primary hyperaldo

A
  • diastolic HTN without edema
  • decreased secretion of renin when stimulated via volume depletion
  • increased secretion of aldo that cant be suppressed by volume expansion
  • cannot be on diuretics during testing
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20
Q

tx of primary hyperaldo

A
  • surgical excision if adneom
  • diet- Na restriction
  • spironolactone
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21
Q

cushing’s syndrome

A
  • prolonged exposure to glucocorticoids

- either endogenous or exogenous cortisol

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22
Q

exogenous exposure of steroids -> cushings

A
  • most common cause of cushings
  • ACTH doesnt get released -> atrophy of adrenals
  • HPA suppression can last a year after d/c
23
Q

cushing’s disease

A
  • pituitary overproduction of ACTH d/t adenoma
24
Q

endogenous exposure of steroids -> cushings

A
  • hypersecretion of cortisol
  • pituitary adenoma (cushings dz)
  • adrenal primary mass
  • small cell lung ca
  • thyroid neoplasm
  • pancreatic neoplasm
25
fat changes associated with cushings
- moon face - supraclavicular fat deposition - buffalo hump - torso/ central adiposity
26
skin changes assoc with cushings
- purple/ red striae - thin skin - easy bruising
27
non skin/fat changes assoc with cushings
- psych manifestations- esp depression - if adenoma: HA, vision change, polyuria, nocturia - increased infections - poor wound healing - osteoporosis and pathologic fxs - HTN
28
dx of endogenous cushing's
- stepwise approach - 1. 24 hour urine - 2. 1 mg dexamethasone suppressive test - 3. CRH/Dex suppression if above inconclusive - ACTH should be low in early afternoon
29
what do you do after dx of cushing's is made and ACTH is high
- cranial MRI | - high dose dex suppression test
30
what do you do after dx of cushing's is made and ACTH is low-normal
- get abd ct/ MRI | - suspect it is being made from adrenal tumor
31
treatment for endogenous cushing's
- transphenoidal resection if pituitary mass - if fails -> radiation - adrenalectomy with failed resection, adrenal mass, ectopic ACTH from another mass unable to resect
32
what is addison's disease
- primary adrenocortical def | - d/t autoimmune destruction of adrenal cortex or TB
33
si/sx of addison's
- insidious onset - weakness/ fatigue. initially asthenia - hypotension, orthostasis, dehydration - weight loss, anorexia - +/- hyperpigmentation of skin and mucosa - N/V/D, abd pain
34
how is addison's disease diagnosed
- cortrosyn stim test (cosyntropin) -> minimal/ no change - stimulates ACTH - tests functional ability of adrenal cortex to synthesis cortisol
35
what are the lab findings for addison's
- low Na - high K - increased urine Na - increased BUN/Cr
36
work up for addison's
- CMP - EKG: peak T, wide QRS, sine wave d/t hyperK - CXR and PPD to assess for TB - abd CT
37
what to atrophic adrenals suggest on abd ct
- idiopathic autoimmune addison's
38
secondary adrenal insufficiency
- similar to Addison's but no hyperpigmentation - panhypopituitarism - usu d/t prolonged exogenous steroids - low levels of ACTH
39
what is addison's assoc with hyperpigmentation
- precursor to ACTH is same precursor to melanocyte stim hormone
40
treatment for adrenal insufficiency
- glucocorticoids: cortef - mineralocorticoids: florinef - ample Na intake - education - closely follow up
41
adrenal crisis
- rapid/ severe adrenal collapse - can cause coma/death - typically due to exacerbation of chronic adrenal insuff with stress precipitant - may also be d/t hemorrhagic destruction, anticoagulation, or pregnancy
42
what is waterhouse- friderichsen syndrome
- hemorrhagic destruction of bilat adrenals - occurs in ICU pts - d/t pseudomonas, meningococcemia
43
common stressors for adrenal crisis
- infection - trauma/ surgery - V/D - emotional turmoil
44
si/sx of adrenal crisis
- hypotension -> vascular collapse - N/V, abd pain - hyperpyrexia or none - lethargy, somnolence, mental status changes - hypoglycemia - hypoNa - hyperK - metabolic acidosis
45
tx for adrenal crisis
- IVF resuscitation | - stress hydrocortisone 100 mg IV q 6 hours
46
MEN I
- autosomal dominant genetic disorder of oncogenes - "three P's" - parathyroid - pancreas - pituitary
47
what is the most common manifestation of MEN I
- hyperparathyroid
48
what are the pancreatic issues assoc with MEN I
- gastrin -> zollinger ellison - insulin -> insulinoma - VIP -> water diarrhea syndrome - somatostatin
49
dx of MEN I
- depends on sx - hormone/ electrolyte assays - provocative testing: secretin stim test, fast to test serum insulin and c-peptide levels - dexamethasone suppression test
50
treatment of MEN I
- surgical resection- usu multiple required - transphenoidal sx for pituitary tumors - parathroidectomy + thyroidectomy - medical mgmt with dopamine agonists, H2 blockers, PPIs
51
MEN 2a
- MTC - pheo - hyperparathyroidism - MTC typically dev in childhood, > 1 cm tumor, local and distant mets
52
MEN 2b
- MTC - pheo - mucosal neuromas - marfanoid body habitus - MTC dev earlier and more aggressive than 2a
53
treatment for MEN2
- early thyroidectomy - genetic testing - annual screening with urine metanephrine/ VMA - measure serum Ca PTH q2-3 years - surgery very effective - pheo tends to recur- consider uni vs bilat resection - remove 3.5 parathyroid, place 0.5 in forearm