endocrine disorders Flashcards
(36 cards)
pit gland
anterior: TSH, ACTH - acts on adrenal cortex to stim production and release others -> cortisol, aldosterone
posterior: ADH (vassopressin), oxytocin
adrenal gland
sit on top of kidneys
inner medulla (epi and norepi - SNS and f/f) and outer cortex secrete cortisol, aldosterone, androgens
respond to ACTH -> these are not stored, secreted on demand - cortisol (glucocorticoids), aldosterone (mineralcorticoids), androgens (sex steroids)
cushings
too much ACTH (hypercortisolism)
causes:
primary hyperfunction - disease of cortex
secondary hyperfunction - ant pit
exogenous steroids = management of other disease, most common
ACTH
monitor levels to dx adrenal cortex dysF
cortisol function = increase BS, protect against stress, suppress immune and inflam processes, breakdown P and fat (high chol and BP)
if always on , like in cushings, body doesnt respond by releasing more when actually stressed and therefore the body doesnt get protective effects
cushings: cm
look like long term steroids
high glucose avail: glucose intol, hypergly
maintain vascular system: htn, capillary friability (ecchymoses - capillaries are squeezed)
P breakdown: muscle wasting, muscle weak, thin skin, osteoporosis and bone pain and fractures
fat breakdown: redistributed to abd, shoulders, face, thin limbs
suppress immune and inflam: decreased wound healing, r/o infection
CNS excitability: mood swings, insomnia
red cheeks, buffalo hump fat pad, bruise easily, abd striae, pendulous abd, thin arms and legs, skin is thin and fragile, htn d/t increased Na and H2O retention, gluconeogenesis, hirsutism, thinning hair, gynecomastia, moon face, apple shaped
cushings: tm
depends on cause
pituitary or adrenal tumor: sx or radiation
exogenous steroids? -> taper
drugs: aminoglutethimide + ketoconazole -> relieve cortisol issue but not primary choice
addisons
hyposecretion of adrenocorticoid hormones - lack of cortisol!
etiology: idiopathic, autoimmune, other
addisons: patho
adrenal gland destroyed or damaged, s when 90% non functional - so disease at advanced state at time of dx, ACTH and MSH secreted in large amounts
adrenal gland doesnt secrete cortisol -> no negative feedback, therefore, ant pit increase secretion of ACTH and MSH to stim cortisol production
addisons: cm
early: anorexia, weight loss, weak, malaise, apathy, e imbalance, skin hyperpig (MSH)
hypoaldosterone:
hypoT - decreased vascular tone, CO, circulating BV
salt craving - decreased serum Na, hyperK, dehyd -> stim ADH which leads to FVE
hypocortisolism = decreased E - hypogly, weak and fatigue, unsuppressed ACTH, hyperpig
addisons: tm
adrenal insufficiency requires lifelong corticosteroid replacement therapy
all pt require glucocorticoid and may need mineralcorticoid (fludrocortisone)
hydrocortisone is #1 - has gluco and mineral action,
prednisone, dexamethasone
shouldnt have many SE, should just be functioning
addisons: tm - pharm issues
dosing mimics natural release
timing! - bed, consistent
small doses to decrease SE
never abruptly stop -> addisonian crisis
increase dose when stressed -> sx, trauma, infection; 3x3 rule (3x usual dose for 3 days but consult hcp)
always have emergency supply -> injection and oral
medic alert bracelet
adrenal crisis - severe cushing s
acute emergency, massive increase in cortisol (serum, random) or 24 hr urine cortisol 4x upper limit, severe hypoK, sepsis, opportunistic infection, uncontrolled htn, HF, lots of others
adrenal crisis - addisonian crisis
sudden insufficiency of corticosteroids, med emergency, prevent with drugs and teaching
adrenal medulla disorder
pheochromocytoma
tumor -> produce excessive catecholamines, mostly benign
rf: young - middle age
patho: SNS stim -> excessive release of epi and norepi
epi stim alpha and beta -> heart, lungs, vessels
norepi stim just alpha
epi and norepi cause htn!
adrenal medulla disorder: cm
can have sporadic episodes when SNS stimulated - stress, exercise, excitement, smoking
htn -> HA, tachy, diaphoresis, stroke!
therefore, we should decrease stim and enhance relaxation
adrenal medulla disorder: tm
sx is preferred
principal cause of htn is activation of alpha 1 receptors on blood vessles
alpha blockers until sx or inoperable (10-14 days prior and then after sx)
ADH disorders
released if increase in serum osmolality and/or hypoT
function -> water retention via action in the kidneys
SIADH and DI
SAIDH
too much (s of inappropriate ADH)
abn production or sustained secretion
fluid retention, serum hypoosmolality and hypoNa, [] urine
SAIDH: etiology
malignant tumor -> small cell carcinoma of lung (adenocarcinoma) - release ADH
CNS disorders -> head trauma, stroke, brain tumor
drug therapy -> morphine, SSRI’s, some chemo
miscellaneous conditions -> hypothyroidism, infection
SAIDH: patho
elevated ADH -> increased H2O reabs in tubules -> increased IVF -> dilutional hypoNa and decreased serum osmolality, [] urine
SAIDH: cm
decreased serum osmolality, increased urine osmolality and specific gravity, Na decreased, UO decreased, weight increased
retain H2O witout Na therefore s/s hypoNa and FVE
cm depend on severity and rate of onset of hypoNa
s/s hypoNa
dyspnea, fatigue
neuro: lethargy, confusion, dulled sensorium
muscle twitch, convulsion
GI: impaired taste, anorexia, v, cramps
severe s when Na: 100 - 115 -> irreversible neurologic damage
SAIDH: water intoxication
serum Na lower than inside cells -> swell
neuro -> confusion, lethargy, coma, death
SAIDH: pharm
not first line
tm directed at cause
head trauma = wait
med OD = stop
democlocycline = chronic SIADH
loop diuretics (Na >125) + salt tablets
