endo path Flashcards
cushings etiology
increased cortisol d/t
- endogenous corticosteroids
- primary adrenal adenoma, hyperplasia, or carcinoma
- ACTH-secreting pit adenoma (Cushings disease) or pareneoplasitc ACTH secretion
endogenous corticosteroids
decreased ACTH
b/l adrenal atrophy
MCC
primary adrenal adenoma, hyperplasia, or carcinoma
decreased ACTH
atrophy of uninvolved adrenal gland
can also present w/pseudohyperaldosteronism
ACTH secreting adenoma or paraneoplastic ACTH secretion
results in increased ACTH
b/l adrenal hyperplasia
cushings findings
HTN weight gain moon facies truncal obestiy buffalo hump skin changes osteoporosis hyperglycemia amenorrhea immunosupression
Dexamethasone suppression test
cushings disease will suppress
ectopic ACTH secretion will not supress
CRH stimulation test
cushings dis-> increase in ACTH and cortisol
ectopic ACTH secretion -> no increase
symptoms of adrenal insufficiency
weakness fatigue orthostatic hypotension mm aches weight loss GI sugar and/or salt cravings
Dx of adrenal insufficiency
measurement of serum electrocluces am cortisol ACTH ACTH stimulation test metyrapone stimulation test
metyrapone stimulation test
blocks last step of cortisol synthesis
normal response in decreased cortisol and increased ACTH
in adrenal insufficiency ACTH does not increase
primary adrenal insufficiency
hypotension hyperkalemia metaboic acidosis skin and mucosal hyperpigmentation chronic -> addisons disease
causes of addisons
autoimmune (MC)
TB
mets
Waterhouse-friderichsen syndomre
N. menigitidis
secondary adrenal insufficiency
decreased ACTH
no hyperpigmentation
no hyperkalemia
tertiary adrenal insufficiency
pt w/chronic exogenous steroid use precipitated by abrupt withdrawal
aldosterone unaffected
neuroblastoma
MC tumor of adrenal medulla in kids
usually
neuroblastoma presentation
distended abdomen firm irregular mass that can cross midline (wilms-tumor) opsoclonus-myoclonus sundroem HVA and VMA increased in urine bombesin and neuron-specific enolase _ rarely causes HTN N-myc
pheo etiology
MC tumor of adrenal medulla in adults
derived from chromaffin cells from neural crest
pheo rule of 10’s
10% malignant 10% b/l 10% extra-adrenal 10% calcify 10% kids
pheo symptoms
5 Ps pressure (increased BP) pain (HA) perspiration palpitations pallor
pheo associations
NF1
VHL
MEN2A and 2B
pheo findings
increased catecholamines and metanephrines in urine and plasma
Tx of pheo
irreversilbe alpha antagonists (phenoxybenzamine)
followed by BB prior to tumor resection
if BB first -> HTN crisis
hypothyroidism symptoms
cold intolerance weight gain, decreased appetite hypoactivity, lethargy, fatigue, weakness constipation decreased reflexes myxedema (facial/periorbital) dry, cool skin, coarse brittle hair bradycardia, dyspnea on exertion
hypothyroidism labs
increased TSH (best test)
decreased free T3/4
hypercholesterolemia (d/t decreased LDL R)
hyperthyroidism symptoms
heat intolerance weight loss, increased appetite hyperactivity diarrhea increased reflexes pretibial myxedema periorbital edema warm moist skin, fine hair chest pain, palpitations, arrhythmias (increased number and sensitivity of betaRs)
hyperthyroidism labs
decreased TSH if primary
increased free or total T3/4
hypocholesterolemia (d/t increased LDL R)
hashimotos
MCC of hypothyroidism in iodine sufficient regions anti-thyroid peroxidase anti-microsomal anti-thyroglobulin HLA-DR5 increased risk of Hodgkin lymphoma
hashimotos presentation
may have transient hyperthyroid stage d/t thyrotoxicosis during follicular rupture
moderately enlarged, non-tender thyroid
hashitmotos histo
Hurthle cells
lymphoid aggregate w/germinal centers
congenital hypothyroidism/cretinism
severe fetal hypothyroidism
thyroid dsygenesis MCC in US