Pathology - endocrine Flashcards
bilateral vs. unilateral adrenal atrophy
bilateral - exogenous steroid use
unilateral - primary adrenal adenoma/hyperplasia/carcinoma on unaffected side
bilateral hyperplasia - Cushing disease (pituitary adenoma)
hypoercortisolism screening tests
incr. free cortisol on 24 hr urinalysis
incr. midnight salivary cortisol
if decr. ACTH, then adrenal tumor
if incr. ACTH, then do high-dose dexamethasone suppression and CRH stimulation
if ectopic, then no suppression and no increase with CRH
if pituitary tumor, then suppression and increase with CRH
adrenal insufficiency diagnosis
serum electrolytes (low Na, high K) random serum cortisol/ACTH response to ACTH stimulation
metyrapone stimulation (usually blocks last step in cortisol synth): normal response = decr. cortisol, incr. ACTH. in adrenal insufficiency, ACTH remains decr. after test
Primary vs. secondary vs. tertiary adrenal insufficiency
primary - loss of gland function. hyperpigmentation (incr. MSH from incr. ACTH). assoc w/ autoimmunity or meningococcemia (W-F syndrome)
secondary - decr. ACTH secretion from pituitary. spares skin/mucosa pigment. aldosterone synth preserved
tertiary - chronic exogenous steroid use, precipitated by abrupt withdrawal
neuroblastoma
adrenal medulla, derived from neural crest, N-myc oncogene
CHILDREN, crosses midline! (Wilm’s is unilateral)
dancing eyes, dancing feet
incr. homovanillic acid/vanillylmandelic acid in urine
pheochromocytoma
adrenal medulla, chromaffin cells, ADULTS
10%: malignant, bilateral, extra-adrenal, calcify, kids
seen w. NF1, MEN2A, MEN2B
5 P’s: pressure, pain, perspiration, palpitations, pallor
tx: phenoxybenzamine (a blocker) followed by B-blockers
thyroid abnormality skin findings
hyperthryoid - pretibial myxedema, periorbital edema
hypothyroid - myxedema (facial/periorbital)
Cholesterol and thyroid abnormality
Hypothyroid - high LDL (low LDL receptor expression)
Hyperthyroid - low LDL (incr. LDL receptor expression)
Hypothyroid etiologies (4 pathologies)
Hashimoto - HLA-DR5, incr. non-Hodgkin lymphoma
Congenital hypothyroidism - fetus is pot-bellied, puffy-faced, protuberant tongue, poor brain development
Subacute thyroiditis - s/p flu-like illness, jaw pain, tender thyroid
Riedel thyroiditis - fibrotic invasion, IgG4 systemic dz, rock-like goiter
Hyperthyroid etiologies (4 pathologies)
Graves - most common, autoAbs stimulate thyroid/retroorbital fibroblasts/dermal fibroblasts
toxic multinodular goiter - focal patches, independent of TSH, incr. release of T3/T4
thyroid storm - stress-induced thyrotoxicosis, incr. alk phos, tx: 3 P’s (propanolol, PTU, prednisolone)
Jod-Baselow - thyrotoxicosis s/p iodine replacement
Thyroid cancer (3 main subtypes)
Papillary: empty appearing nuclei w/ central clearing, psammoma bodies, lymphatic invasion
Follicular: good prognosis, invades thyroid capsule
Medullary: from parafollicular C cells, produces calcitonin, hematogenous spread, MEN 2A, 2B
Thyroid surgery complications
- hoarseness: recurrent laryngeal nerve damage
- hypocalcemia: removal of parathyroid glands
- transection of recurrent & superior laryngeal nerves: occurs during ligation of inferior and superior thryoid arteries (respectively)
Etiologies of hypoparathyroidism
Surgical excision of parathyroid glands
Autoimmune destruction
DiGeorge syndrome
PseudohypoPTH = Albright osteodystrophy, unresponsiveness of kidney to PTH, low Ca, shortened 4th/5th digits, short stature
PTH and Ca abnormalities
low PTH, low Ca = hypoparathyroidism
low PTH, high Ca = exogenous Ca intake
high PTH, low Ca = secondary hyperparathryoid (chronic renal failure, low Vit. D)
high PTH, high Ca = hyperplasia, adenoma, carcinoma
Hyperparathyroidism
Primary vs. secondary vs. tertiary
Primary: adenoma/hyperplasia, incr. PTH, serum Ca, urine Ca, alk phos, cAMP. look for stones, bones, groans, psych overtones
Secondary: chronic renal dz or low Vit. D = low Ca, high PO4, high alk phos, high PTH
Tertiary: refractory hyperPTH from chronic renal disease. extremely high PTH, elev. Ca
