Endocrine Flashcards
Hyperprolactinemia- etiology? presentation? tests? treatment?
ETIOLOGY: Can be cosecreted with GH due to acromegaly; hypothyroidsm can lead to hyperprolactinemia because extremely high TRH will stimulate prolactin secretion
Physiological causes are pregnancy, intesne exercise, renal insuffiency, increased chest wall stimulation; cutting pituitary stalk
Drugs- antipsychotics, methyldopa, metoclopromide, opioids, TCA, verapamil
PRESENTATION: women present with galactorrhea, amenorrhea, infertility; men present with erectile dysfunction, decreased libido, gynecomastia.
DIAGNOSTIC TEST: thyroid function test, pregnancy test, BUN/CRE (kidney disease elevates prolactin), LFT (cirrhosis elevates prolactin)
MRI is done after high prolactin is confirmed, secondary causes like medications is excluded AND patient is NOT pregnant.
TREATMENT: 1. Dopa agonists such as Cabergoline and bromocriptine. 2. Transphenoidal surgery for those not responding to meds
Hypothyroidism- etiology? diagnostic test? treatment?
ETIOLOGY: almost always from a single cause such as failure of thyroid gland from burnt out hashimoto’s, dietary deficiency of iodine and amiodarone are also causes.
DIAGNOSTIC TEST: all thyroid disorders tested first with serum TSH levels. If suppressed, measure free T4.
When TSH is high (double normal) with a normal free T4 level, replace with TH! When TSH is less than double the normal, check for antibodies to antithyroid peroxidase/anti thyroglobulin. If positive, replace with TH.
TREATMENT: Synthroid (thyroxine)
Hyperthyroidism- etiology? diagnostic test? treatment?
GRAVES- low TSH, elevated RAIU, confirm by positive antibody testing
SUBACUTE THYROIDITIS- low TSH, decreased RAIU, confirm by tenderness
PAINLESS THYROIDITIS- low TSH, decreased RAIU, no confirmatory test
EXOGENOUS TH USE- low TSH, decreased RAIU, confirmed by hx and involuted non palpable gland
TREATMENT: Graves- Radioactive iodine S.A thyroiditis- Aspirin Painless thyroiditis- none Exogenous TH use- stop use pituitary adenoma- surgery
Acute hyperthyroidism and “Thyroid storm” TX
- propanolol- blocks target organ effect, inhibits peripheral conversion of T4 to T3.
- Thiourea drugs (Methimazole and PTU) block hormone production
- Iodinated contrast material blocks peripheral conversion of T4 to active T3 and blocks release of existing hormone
- Steroids
- radioactive iodine: ablates gland for permanent cure
Thyroid nodules- Dx test?
> 1cm MUST be biopsied by FNA if there is normal T4/TSH. Nodules in those who are euthyroid should be biopsied.
Hypercalcemia- etiology? presentation? treatment?
ETIOLOGY: MCC is Primary hyperparathyroidsm (most are asymptomatic) and malignancy (in those with severe, acute symptomatic hypercalcemia). Other causes are VIT d intoxication, sarcoidosis/granulomatous diseases, thiazides, hyperthyroidism, mets to bone, Multiple Myeloma
PRESENTATION: acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy and constipation. Cardio-Short QT syndrome and HTN; Bone lesions- osteoporosis, Renal- Nephrolithiasis, DI, Renal insufficiency
TREATMENT of acute hypercalcemia: 1) Saline hydration at high volume 2) bisphosphonates (pamidronate, zoledronic acid)
If saline and bisphosphonates don’t correct the hypercalcemia, give calcitonin
Hyperparathyroidism- etiology? presentation? Dx test? Treatment?
ETIOLOGY: solitary adenoma (80-85%), Hyperplasia of all 4 glands (15-20%), Parathyroid malignancy (1%)
PRESENTATION: often asymptomatic with elevation of calcium levels no CBC. More often, there are slower manifestations than severe hypercalcemia, such as- osteoporosis, nephrolithiasis/renal insufficiency, muscle weakness, anorexia, nausea, vomiting, abdominal pain, PUD (calcium stimulates gastrin)
DX TEST: high Calcium, PTH, low Phosphorous, high Chloride, elevated BUN/Cr; EKG with short QT, Alk phos may be elevated from effect of PTH on bone.
TREATMENT: surgical removal of involved glands. If surgery is not possible, give CINACALCET.
Hypocalcemia- Etiology? Presentation? Dx test? Treatment?
ETIOLOGY: primary hypoparathyroidism often a complication of prior neck surgery (thyroidectomy), hypomagnesemia (Mg is necessary for PTH to be released from gland. low Mg leads to increase loss of calcium), renal failure (kidney can’t convert to more active 1,25 hydroxy D), hypoalbuminemia (for every point decrease in albumin, total calcium decreases by 0.8, free calcium level is normal), vitamin D def, malabsorption
PRESENATION: neural hyperexcitability- chvostek sign, carpopedal spasm, perioral numbness, mental irritability, seizures, tetany (trousseau sign)
DX TEST: EKG prolonged QT, slit lamp shows early cataracts
TREATMENT: replace Calcium and vitamin D.
Hypercortisolism- Diagnostic tests and treatment?
DX TEST: 1) Best initial- 24 hour urine cortisol or 1mg overnight DEXA suppression test; 24 hour is more specific, DEXA test can be false positive (due to depression, alcohol, and obesity) 2) if ACTH is elevated and does not suppress with high dose DEXA, do a MRI scan. If MRI does not show a clear pituitary lesion, sample the inferior petrosal sinus for ACTH, possibly after stimulating the patient with CRH (elevated level of ACTH from venous drainage confirms pituitary as a source). If ACTH is elevated and MRI and Petrosal sinus sample do not show clear lesions, scan the chest for an ectopic source of ACTH.
TREATMENT: transphenoidal surgery for pituitary sources; laparoscopic removal for adrenal sources.
Evaluation of Adrenal “Incidentaloma” of an unexpected asymptomatic adrenal lesions found on CT?
- metanephrines of blood or urine to exclude pheochromocytoma
- renin and aldosterone levels to exclude hyperaldosteronism
- 1mg overnight DEXA suppression test
