Adrenals Flashcards
what hormones does the adrenal cortex
- glucocorticoids
- mineralocorticoids
- adrogens
how is cortisol releeased
- diurnal basal rate
- bursts d/t stress
- regulated by ant pituitary and ACHT neg feedback
role of cortisol
- 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
what is the role of aldosterone
- Na retention (water follows)
- K secretion
what is produced in the adrenal medulla
- catecholamines: epi, NE, dopamine
what are chromaffin cells
- produce and store catecholamines in adrenal medulla
- have CNS origin without dendrites/ axons
- surrounded by BV -> rapid direct release of catecholamines
pheochromocytoma
- adrenal medulla tumor
- rare
- produces, stores, and secretes catecholamines
- usu unilat and benign
- make up small portion of HTN
si/sx of pheo
- HTN- sustained or labile
- paroxysmal sx:
- HA, diaphoresis, palpitations*
- chest pain
- N/V, abd pain
- anxiety
- pallor and/or flushing
dx of pheo
- get 24 hour urine: looking for catecholamine metabolites
- CT or MRI*
tx of pheo
- surgically remove tumors
- before surgery MUST do alpha block for 10-14 days, BB for 2 days
what alpha blockade is used prior to pheo surgery
- phenoxybenzamine
what beta blockers are used prior to pheo surgery
- propranolol
- nadolol
what do alpha and beta blockade before pheo removal
- prevent intra-operative HTN crisis d/t catecholamine release
what do plasma renin levels look like in primary hyperaldosteronism
- plasma renin low
- high aldo causes RAAS to shut off
what do plasma renin levels look like in secondary hyperaldosteronism
- plasma renin high
- aldo elevates in response
what is Conn’s syndrome
- primary hyperaldo
classic findings for primary hyperaldo
- diastolic HTN -> HA
- hypoK: muscle weakness and fatigue
- metabolic alkalosis: H loss with K
- low plasma renin
- generally: HA + high na + low K
work up for primary hyperaldo
- hypoK, hyperNa, metabolic alkalosis
- low plasma renin
- EKG: U wave, ST depression, prominent P
- CXR: possible cardiomegaly
- proteinuria on UA
criteria for dx of primary hyperaldo
- 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
tx of primary hyperaldo
- surgical excision if adneom
- diet- Na restriction
- spironolactone
cushing’s syndrome
- prolonged exposure to glucocorticoids
- either endogenous or exogenous cortisol
exogenous exposure of steroids -> cushings
- most common cause of cushings
- ACTH doesnt get released -> atrophy of adrenals
- HPA suppression can last a year after d/c
cushing’s disease
- pituitary overproduction of ACTH d/t adenoma
endogenous exposure of steroids -> cushings
- hypersecretion of cortisol
- pituitary adenoma (cushings dz)
- adrenal primary mass
- small cell lung ca
- thyroid neoplasm
- pancreatic neoplasm
fat changes associated with cushings
- moon face
- supraclavicular fat deposition
- buffalo hump
- torso/ central adiposity
skin changes assoc with cushings
- purple/ red striae
- thin skin
- easy bruising
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
dx of endogenous cushing’s
- stepwise approach
- 24 hour urine
- 1 mg dexamethasone suppressive test
- CRH/Dex suppression if above inconclusive
- ACTH should be low in early afternoon
what do you do after dx of cushing’s is made and ACTH is high
- cranial MRI
- high dose dex suppression test
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
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
what is addison’s disease
- primary adrenocortical def
- d/t autoimmune destruction of adrenal cortex or TB
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
how is addison’s disease diagnosed
- cortrosyn stim test (cosyntropin) -> minimal/ no change
- stimulates ACTH
- tests functional ability of adrenal cortex to synthesis cortisol
what are the lab findings for addison’s
- low Na
- high K
- increased urine Na
- increased BUN/Cr
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
what to atrophic adrenals suggest on abd ct
- idiopathic autoimmune addison’s
secondary adrenal insufficiency
- similar to Addison’s but no hyperpigmentation
- panhypopituitarism
- usu d/t prolonged exogenous steroids
- low levels of ACTH
what is addison’s assoc with hyperpigmentation
- precursor to ACTH is same precursor to melanocyte stim hormone
treatment for adrenal insufficiency
- glucocorticoids: cortef
- mineralocorticoids: florinef
- ample Na intake
- education
- closely follow up
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
what is waterhouse- friderichsen syndrome
- hemorrhagic destruction of bilat adrenals
- occurs in ICU pts
- d/t pseudomonas, meningococcemia
common stressors for adrenal crisis
- infection
- trauma/ surgery
- V/D
- emotional turmoil
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
tx for adrenal crisis
- IVF resuscitation
- stress hydrocortisone 100 mg IV q 6 hours
MEN I
- autosomal dominant genetic disorder of oncogenes
- “three P’s”
- parathyroid
- pancreas
- pituitary
what is the most common manifestation of MEN I
- hyperparathyroid
what are the pancreatic issues assoc with MEN I
- gastrin -> zollinger ellison
- insulin -> insulinoma
- VIP -> water diarrhea syndrome
- somatostatin
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
treatment of MEN I
- surgical resection- usu multiple required
- transphenoidal sx for pituitary tumors
- parathroidectomy + thyroidectomy
- medical mgmt with dopamine agonists, H2 blockers, PPIs
MEN 2a
- MTC
- pheo
- hyperparathyroidism
- MTC typically dev in childhood, > 1 cm tumor, local and distant mets
MEN 2b
- MTC
- pheo
- mucosal neuromas
- marfanoid body habitus
- MTC dev earlier and more aggressive than 2a
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
