PITUITARY- SIADH, DI, GH excess and deficiency, prolactinoma, adenoma Flashcards
SIADH
- define
- patho
excess production of ADH causes body to retain excess amt of water leading to hyponatremia
patho
- ADH from pos pituitary or ectopic
- waer retention and urine concentration = inc volume, dec Na
- but NO edema in SIADH due to ANP release
SIADH causes
common- pulm, CNS ds+certain meds
- malignancy: lung SCLC
- CNS d/o: CVA, head trauma, surgery
- pulm: pneum, TB, mech vent
- medication: vasopressin, SSRI, carbamazepine, oxcarbazepine, thiazides, NSAIDS
SIADH presentation
- acute v. chronic
hyponatremia cause body to retain water while getting rid of Na (<135)
- osmotic shift inot intracell space
- acute–> sweeling to brain, n/v, lethargy, can lead to seizure/coma/death
- chronic—> asx, anorexia, n/v, CNS sx
SIADH dx
- serum and urine values
LOW serum osmo + HIGH urine osmo
serum: Na <135, osm <275, inc ADH
urine: Na>40, osm >100
SIADH management
- Asx
- sx
Asx
- water restrict FIRST, then follow w salt tabs if needed
- urine osm >500 ADD FUROSEMIDE
Sx
- water restrict
- ADH recep antag (Tolvaptan if refractory to tx)
- isotonic or hypertonic IV saline if Na<120 (severe, can cause neuro sx)
SIADH management warning
- correct v. incorrect
DO NOT CORRECT SODIUM TOO QUICKLY
- correct: <8 mEq/L per 24h (check q3-4h)
- overcorrection risk—> osmotic demyelination syndrome
diabetes insipidus (DI)
- hallmark sign
- 2 types
not enough or ineffective ADH
hallmark sign is POLYURIA
- central = pos pit not secreting enough ADH
- nephrogenic = pos pit secretes, but renal tubules NOT RESPONDING to ADH
DI causes
- central
- nephrogenic
Central
- idiopathic MCC
- head trauma/neurosurgery
- damage to hypothal/pituitary (tumors, TB, syph, etc)
- fam/congenital d/o
nephrogenic
- chronic lithium use MCC
- hypercalcemia
- hypokalemia
- kidney ds
- children—genetic mutation
DI presentation
- polyuria/nocturia (5-15 L/day, dilute)
- thirst/polydipsia
- hypernatremia (mild)
DI dx - screening
Screen
- urine: dec specific gravity, dec osmo (<300)
- plasma: inc osmo (>280)
if pt consistent w DI, undergo water deprivation test to confirm dx and type
nl plasma osm: 250-290
DI dx- water deprivation test
- how does it work
- results
no fluid intake for several hrs, check urine osmo every hr
- once urine osm stable (<30 rise over 3 hrs), inject 2g desmopressin (synth ADH) sc
- check urine osm 1 hr later
(+) response = central DI
no response = nephronic DI
(+) = low urine osm, inc urine vol, low ADH in blood
DI management
- central
- nephrogenic
Central
- desmopressin SC
- chlorpropamide
Nephrogenic
- low sodium, low protein diet
- thiazide diuretic (HCTZ)
- if pt needs to stay on lithium–> add amiloride
- GH effect
- GH disorders
GH- inc body mass and general growth
- works with insulin like growth factor 1(IGF-1) to promote normal growth bones and tissues
- beneficial effect on lipid profile, dec insulin sensitivity
disorders
- acromegaly/gigantism = too much GH
- GH deficiency/pituitary dwarfism = not enough GH
Acromegaly v. Gigantism
ACROMEGALY
GH excess in ADULThood
- bones inc in size but after growth plate fusion, so no excess height
GIGANTISM
- GH excess in childhood
- arises before growth plates fuse, excess height
Acromegaly/gigantism causes
MCC- GH secreting pituitary adenoma
rare- ecotpic GH secreting tumor (paraneoplastic)
(pancreatic, ovarian, lung, or hematopoeitic)
acromegaly presentation
- growth
- CV
- metabolic
- parasellar
- misc
growth: hands and feet, (inc glove/ring size), enlarged jaw, coarse facial features, macroglossia, spaced teeth
CV: inc risk LVH, dilated CM, HTN, sleep apnea
metabolic: gluc intolerance–>DM
parasellar sx: H/A, bitemp hemianopia
misc: inc risk colonic polyps/CA
gigantism presentation
similar to acromegaly but with RAPID LINEAR growth
- often develop obesity
- large hands/feat
- coarse facial features (forehead protrude, jaw projection)
- parasellar Sx (HA, visual field defects, other pit hormones dec–> FSH/LH)
acromegaly/gigantism Dx
- inc IGF-1 levels for age
- inc GH
- confirm with oral gluc suppression test (No GH suppression = positive –> GH inc despite gluc pos)
if both pos===> PITUITRY MRI to check for adenoma
acromegaly/gigantism Tx
transsphenoidal resection of pituitary adenoma (for both)
- check IGF-1 after surgery, if still elevated—> radiation therapy, +/- oral agent
- somatostatin analog: octreotide or lanreotide
- dopamine agonist: cabergoline (preferred for compliance since somatostain is inhib of many endocrine hormones)
acromegaly/gigantism outcomes post op
- nl pit function
- soft tissue swell will improve, bone changes are permanent
- HTN/cardiac changes persist
- PT need lifeline follow up and GH + IGF-1 monitoring to assess for recurrent tumor
- radiation tx can cause some hypopituitarism
GH deficiency
in childhood: growth pattern delay, short stature
adults: low bone density, low muscle mass (NO bone growth effect)
GH deficiency causes
- hypothal or pituitary dysfunction (tumor, radiation, head trauma, sheehan syndrome)
- genetic mutation (ex: laron syndrome)
GH deficiency
sheehan syndrome
post partum hypopituitarism secondary to necrosis and dec pituitary blood flow to pit gland during excess blood loss
- leads to severe hypotension peri post partum
GH presentation
- childhood
- adulthood
childhood
- newborns: hypoglycemia, jaundice, micropenis
- delayed bone growth for age-short stature
adulthood
- often undiagnosed
- dec muscle mass and bone density
- inc LDL
