Endocrine Flashcards
Follicular cells
in thyroid
produce and store T3 and T4, thyroglobulin
Parafollicular cells
in thyroid
aka C cells
secrete calcitonin
Thyroid Nodule
F>M
Features: feeling of choking, difficulty breathing or swallowing
Dx: TSH level, Fine-needle aspiration, US
Tx: low risk = observe 3-6 months, give oral TH
high risk = surgical resection
Graves Disease
Cause: ab to TSH receptors
Features: diffuse goiter with hyperthyroidism, exophthalmos, tachycardia, tremor, heat intolerance, weight loss, pretibial myxedema.
Dx: thyroid function tests.
Tx: 1. medical blockade (PTU, methimazole)
2. radioiodine ablation
3. surgical resection
beta blockers ameliorate some effects of TH, used for short term management until surgery
Toxic Adenoma
solitary tumor of thyroid causing excessive amounts of TH and hyperthyroidism.
Features: similar to graves disease
Dx: high T3 and T4, suppressed TSH, thyroid normal or small with nodule on exam.
Tx: thyroid lobectomy and isthmectomy
Plummer’s Disease
aka toxic multinodular goiter
Tx: total thyroidectomy
Papillary Carcinoma of Thyroid
from follicular cells.
most common thyroid malignancy
Features: psammoma bodies (layers of calcium), grow slowly, good prognosis.
Bad prognosis = over 50yr, male, larger than 4cm
Tx: surgery
Metastases = bones and lungs
Follicular Carcinoma of Thyroid
second most common thyroid malignancy
from follicular cells.
Features: similar to follicular adenomas but have capsular and vascular invasion, good prognosis.
Tx: surgery
Medullary Carcinoma of Thyroid
in parafollicular cells.
20% AD inheritance or MEN2A or 2B
in both thyroid lobes.
50% 10 yr survival
Dx: plasma screening with elevated calcitonin, Ca and Pentagastrin infusion test show increased calcitonin.
Tx: without LN mets = total thyroidectomy and central lymph node dissection
LN mets = radical lymph node dissection
Anaplastic Carcinoma of Thyroid
aggressive, undifferentiated
from follicular cells
Bad prognosis
<2yr survival
Lymphoma of Thyroid
Features: present as thyroid mass.
Dx: core needle or open biopsy
Primary Hyperparathyroidism
Cause: pituitaryr adenoma (prolactinoma), parathyroid hyperplasia, or parathyroid carcinoma
Features: urolithiasis, bone disease, abdominal pain, muscle/joint pains, fatigue/lethargy, depression/psychosis.
“stones, bones, groans, moans, psych overtones”
Dx: elevated PTH, low serum phosphate, normal renal function, hypercalcemia
Adenoma = one large gland
Hyperplasia = all glands large
Tx: acute severe hypercalcemia = large volume saline infusion, furosemide
surgery
Secondary Hyperparathyroidism
in renal failure patients.
Cause: phosphate retention and low calcium from renal failure. leads to high PTH, parathyroid hyperplasia, hyperphosphatemia. Also from lack of Vit D
Featuers: bone pian, calcinosis, pruritus
Dx: high PTH, high Cr, hyperphosphatemia
Tx: dialysis, vit D supplement, oral phosphate binders, cinacalcet
renal transplant
Tertiary Hyperparathyroidism
secondary hyperparathyroidism with one or more glands that autonomically produce PTH.
Dx: high PTH even after renal transplant, hypercalcemia
Tx: acute severe hypercalcemia = large volume saline infusion, furosemide
Adrenal Cortex
3 layers:
- zona glomerulosa = mineralocorticoids = aldosterone
- zona fasciculata = cortisol
- zona reticularis = sex steroids
Aldosterone
t1/2 = 15 min
metabolized by liver
regulated by RAS and plasma potassium concentration
causes Na resorption in kidney, K wasting
hypersecretion = Conn’s syndrome
Conn’s Syndrome
hypersecretion of aldosterone (primary aldosteronism)
cause: adrenal adenoma, diffuse hyperplasia, nodular/adenomatous hyperplasia of adrenal cortex, ACC
Features: hypokalemia, HTN, muscle weakness, metabolic alkalosis, hypomagnesemia, tetany, 2:1 F:M, 30’s - 50 yrs, not suppressed by salt loading.
Dx: elevated serum and urinary aldosterone, suppressed renin, elevated aldosterone-to-renin ratio, sodium loading to rule out secondary cause, CT abdomen, adrenal venous sampling
Tx: unilateral aldosteronoma = spironolactone and then lap adrenalectomy unilateral
bilateral adrenal hyperplasia = spironolactone
Cushing Syndrome
ACTH-dependent or -independent hypercortisolism
1. ACTH-independent = exogenous steroid use, adenoma, adrenal cortical carcinoma, bilateral adrenal hyperplasia
2. ACTH-dependent = excessive CRH, pituitary adenoma, extrapituitary ACTH-producing tumors
Features: 20-40yrs old, 4:1 F:M, truncal obesity, HTN, diabetes, weakness, purple striae, hirsutism, moon facies, buffalo hump
If due to ectopic ACTH and pituitary tumors then melanotropins are secreted and have increased skin pigmentation.
Dx: urinary free cortisol , late-night salivary cortisol, 1mg dexamethasone suppression test.
then measure plasma ACTH, suppressed = primary adrenal tumor.
increased ACTH => pituitary MRI
Cushing Disease
pituitary adenoma producing bilateral adrenal cortical hyperplasia.
Features: truncal obesity, HTN, diabetes, weakness, purple striae, hirsutism, moon facies, buffalo hump
Dx: bilateral cortical hyperplasia, pituitary adenoma
Tx: temporary = metyrapone, ketoconazole, aminoglutethimide, radiation.
surgery = transsphenoidal microadenomectomy, if fails then bilateral lap adrenalectomy/radiotherapy/hypophysectoy.
Side effects of bilateral adrenalectomy = Nelson’s syndrome = hyperpigmentation, headaches, exophthalmos, visual field loss.
Adrenal Adenoma
number one cause of primary adrenal hypercoritsolism (Cushing syndrome)
Features: increased cortisol, decreased ACTH, atrophy of remaining ipsilateral adrenals and contralateral adrenals.
Tx: lap unilateral adrenalectomy, perioperative steroids, postop perdnisone until normal adrenal function
Adrenal Cortical Carcinoma
causes Cushing syndrome
Features: peak incidence 30-50yrs, L>R, F>M, hormone hypersecretion, poor prognosis, large (>6cm), friable, necrotic center and hemorrhage, stippled calcifications, extension through adrenal vein into renal vein or IMV, virilizing/feminizing, aldosterone secreting
Dx: CT
Tx: open unilateral adrenalectomy
Primary Adrenal Hyperplasia
causes Cushing syndrome
both sides hyperplastic
either:
1. PPNAD = primary pigmented nodular adrenocortical disease
2. AIMAH = ACTH-independent macronodular adrenal hyperplasia
Tx: bilateral adrenalectomy laparascopically
Bilateral adenomas
cortisol secreting
Tx: bilat cortical-sparing lap adrenalectomy
Incidentaloma
arenal mass discovered on CT, MRI, or US.
80% non-functioning, 5% subclinical Cushing syndrome,5% pheochromocytoma
Dx: dexamethosone suppression test, plasma metanephrines, adrenal biopsy if a met
Tx: f/u radiographic testing 3-6 months then 1-2 yrs and hormonal disturbance evals
pheos should be resected
