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clin med IV > Adrenals > Flashcards

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
Q

fat changes associated with cushings

A
  • moon face
  • supraclavicular fat deposition
  • buffalo hump
  • torso/ central adiposity
26
Q

skin changes assoc with cushings

A
  • purple/ red striae
  • thin skin
  • easy bruising
27
Q

non skin/fat changes assoc with cushings

A
  • psych manifestations- esp depression
  • if adenoma: HA, vision change, polyuria, nocturia
  • increased infections
  • poor wound healing
  • osteoporosis and pathologic fxs
  • HTN
28
Q

dx of endogenous cushing’s

A
  • stepwise approach
    1. 24 hour urine
    1. 1 mg dexamethasone suppressive test
    1. CRH/Dex suppression if above inconclusive
  • ACTH should be low in early afternoon
29
Q

what do you do after dx of cushing’s is made and ACTH is high

A
  • cranial MRI

- high dose dex suppression test

30
Q

what do you do after dx of cushing’s is made and ACTH is low-normal

A
  • get abd ct/ MRI

- suspect it is being made from adrenal tumor

31
Q

treatment for endogenous cushing’s

A
  • transphenoidal resection if pituitary mass
  • if fails -> radiation
  • adrenalectomy with failed resection, adrenal mass, ectopic ACTH from another mass unable to resect
32
Q

what is addison’s disease

A
  • primary adrenocortical def

- d/t autoimmune destruction of adrenal cortex or TB

33
Q

si/sx of addison’s

A
  • insidious onset
  • weakness/ fatigue. initially asthenia
  • hypotension, orthostasis, dehydration
  • weight loss, anorexia
  • +/- hyperpigmentation of skin and mucosa
  • N/V/D, abd pain
34
Q

how is addison’s disease diagnosed

A
  • cortrosyn stim test (cosyntropin) -> minimal/ no change
  • stimulates ACTH
  • tests functional ability of adrenal cortex to synthesis cortisol
35
Q

what are the lab findings for addison’s

A
  • low Na
  • high K
  • increased urine Na
  • increased BUN/Cr
36
Q

work up for addison’s

A
  • CMP
  • EKG: peak T, wide QRS, sine wave d/t hyperK
  • CXR and PPD to assess for TB
  • abd CT
37
Q

what to atrophic adrenals suggest on abd ct

A
  • idiopathic autoimmune addison’s
38
Q

secondary adrenal insufficiency

A
  • similar to Addison’s but no hyperpigmentation
  • panhypopituitarism
  • usu d/t prolonged exogenous steroids
  • low levels of ACTH
39
Q

what is addison’s assoc with hyperpigmentation

A
  • precursor to ACTH is same precursor to melanocyte stim hormone
40
Q

treatment for adrenal insufficiency

A
  • glucocorticoids: cortef
  • mineralocorticoids: florinef
  • ample Na intake
  • education
  • closely follow up
41
Q

adrenal crisis

A
  • 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
Q

what is waterhouse- friderichsen syndrome

A
  • hemorrhagic destruction of bilat adrenals
  • occurs in ICU pts
  • d/t pseudomonas, meningococcemia
43
Q

common stressors for adrenal crisis

A
  • infection
  • trauma/ surgery
  • V/D
  • emotional turmoil
44
Q

si/sx of adrenal crisis

A
  • hypotension -> vascular collapse
  • N/V, abd pain
  • hyperpyrexia or none
  • lethargy, somnolence, mental status changes
  • hypoglycemia
  • hypoNa
  • hyperK
  • metabolic acidosis
45
Q

tx for adrenal crisis

A
  • IVF resuscitation

- stress hydrocortisone 100 mg IV q 6 hours

46
Q

MEN I

A
  • autosomal dominant genetic disorder of oncogenes
  • “three P’s”
  • parathyroid
  • pancreas
  • pituitary
47
Q

what is the most common manifestation of MEN I

A
  • hyperparathyroid
48
Q

what are the pancreatic issues assoc with MEN I

A
  • gastrin -> zollinger ellison
  • insulin -> insulinoma
  • VIP -> water diarrhea syndrome
  • somatostatin
49
Q

dx of MEN I

A
  • depends on sx
  • hormone/ electrolyte assays
  • provocative testing: secretin stim test, fast to test serum insulin and c-peptide levels
  • dexamethasone suppression test
50
Q

treatment of MEN I

A
  • surgical resection- usu multiple required
  • transphenoidal sx for pituitary tumors
  • parathroidectomy + thyroidectomy
  • medical mgmt with dopamine agonists, H2 blockers, PPIs
51
Q

MEN 2a

A
  • MTC
  • pheo
  • hyperparathyroidism
  • MTC typically dev in childhood, > 1 cm tumor, local and distant mets
52
Q

MEN 2b

A
  • MTC
  • pheo
  • mucosal neuromas
  • marfanoid body habitus
  • MTC dev earlier and more aggressive than 2a
53
Q

treatment for MEN2

A
  • 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

clin med IV (23 decks)

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