TSH: Clinical sx, Lab abnormalities ( elevated cholesterol, prolactin CPK, low Na, anemia, Goiter, Previous thyroid disorder, Down's, Turner's, MS, FHx of autoimmune thyroid disorder, primary pulmonary HTN, radiation to the neck, Drugs ( lithium, amiodarone, and interferon alpha, Pituitary disorder. | When do you screen for hypothyroid and with what? |
Levothyroxine 1.6 mcg/kd/d. | How much thyroid replacement do you give for hypothyroid? |
Mild elevation of TSH ( 4-10) with normal free T4 | How do you diagnose subclinical hypothyroid? |
Pregnant, memory problem in elderly, hypercholesterolemia. | Who do you treat for subclinical hypothyroid? |
Low TSH, and high T4. If T4 normal check T3. Positive TPO ( thyroid peroxidase AB in Graves Dz) | How do you dx hyperthyroid? |
Measure function with RAIU. Gives a picture of thyroid whether it's active (hot) or inactive ( cold) | What is the w/u of hyperthyroid? |
Graves, toxic multi nodular goiter, Toxic adenoma | What disorder seen with High RAIU? |
Lymphocitic thyroiditis, thyroxine supplement, amiodarone, and subacute thyroiditis. | What disorder is seen with low RAIU? |
Low TSH with normal free T3 and T4. Recheck in 2-3 mo | How do you diagnose subclinical hyperthyroid? |
Over 60 with TSH < 0.1 or TSH 0.1-0.4 with heart disease or osteoporosis. | When do you treat subclinical hyperthyroid? |
Radioactive iodine ablation. Causes thyroid ablation over 6-18 wk.
Most remain euthyroid.
Monitor with TSH and T4 in 6 wk and 8 wk, then TSH every 6-12 mo for life. | How do you treat hyperthyroid? |
BB ( Atenolol ) for sx,
Methimazole, PTU only in pregnant pt, ( both hepatotoxic and cause agranulocytosis. Monitor for sx.)
Radioactive iodine: curative but iatrogenic hypothyroid produced within 10 years
Treat with surgery if cold nodule or previous irradiation. | How do you treat Graves disease? |
Anterior neck pain, dysphagia, sweat, tremor and wt loss. Ass with viral infection. Self limiting 2 mo. | What are the sx of subacute thyroiditis? |
Low RAIU and high sed rate > 50. Initially hyperthyroid, then euthyroid by 18 mo. | How do you dx subacute thyroiditis? |
ASA,Steroid, and BB | How do you treat subacute thyroiditis? |
Prior neck irradiation, solitary nodule, Large size > 4 cm and rapid growth, dysphagia, dysphonia, male, age < 20 and > 70, Hypoechoic on US with micro calcification. | Thyroid nodules: Risk factor for malignancy |
Hot on RAIU and cystic | What suggest a benign nodule? |
Check TSH. If low, check RAIU
Thyroid US
FNA for solid lesion > 1 cm and all lesions > 2 cm and all cold nodules.
Repeat US in 1 year if FNA negative but suspicious.
Purely cystic nodule < 1 cm do not need FNA, but monitor 6-12 mo for 2 years.
Surgical excision for nodules > 4 cm. | What is the w/u of thyroid nodule? |
If symptomatic, treat with unilateral thyroid lobectomy or ablation.
If asymptomatic monitor with US 6-12 mo for 2 years. Repeat FNA if change in volume > 20% or new sx. | What is the treatment of benign nodular disease? |
Hot nodule on RAIU. Rx with Ablative with radioactive iodine or surgery. | How do you treat thyroid adenoma? |
High calcium, Low PO4 and normal or elevated PTH level. | How do you dx. primary hyperparathyroid? |
Mostly adenoma, only 3% malignant. | What causes hyperparathyroid? |
Stones, bones, abdominal groans and psychic moans. Osteoporosis, pancreatitis, depression, kidney stones, | What are the sx of hyperparathyroid? |
Repeat with free Ca, check albumin to calculate corrected Ca, CMP, Mg, Vit D( can cause secondary hyperparathyroid) and PTH | How do you work up hypercalcemia? |
Asymptomatic ( Most) Monitor for sx, monitor Ca and Cr and check bone density.
Symptomatic, osteoporosis, and age < 50: Surgery.
Treat hypercalcemia > 14 with hydration and biophosphanate. Lasix promotes calciuria. | How do you treat hyperparathyroid? |
Neuroleptics, reglan, doperidone, methyldopa, reserpine, verapamil, cimetidine, estrogen renal failure hypothyroid, and nipple stimulation. | Which drugs cause hyperprolactin? |
Women : galactorrhea, ameorrhea, hirsutism, infertility
Men: Impotence, fatigue, osteoporosis, and gynecomastia.
Headache and visual changes. | How does hyperprolactin present ? |
functional micro adenoma < 1cm with prolactin levels < 200
Prolactin, LH, FSH, TSH, Free T4, 24 hour urine free cortisol, testosterone, and estradiol, Cr | Prolactinoma definition and work up. |
Prolactin level > 100 | When do you check MRI with elevated prolactin? |
Bromocriptine or Carbergoline: better tolerated ( dopamine agonist)
90% efficacious with response in 2-3 wk. Continue treatment for 2 years and repeat MRI
Transphenoidal surgery if visual changes or near sx. if failure of meds or adenoma > 3 cm. | How do you treat prolactinoma? |
Pituitary adenoma with excess Growth Hormone. | What causes Acromegaly? |
Stimulation of insulin like growth factor which decreases the effect of insulin.
Too much GH before epiphyseal plates have closed results in giantism
Excess GH after plates close results in acromegaly: growth of soft tissue, fatigue, prox muscle weakness, decrease libido and mentrual changes. | What are the effects of excess growth hormone? |
Screen with Insulin like growth factor. If > 3, +
Confirm with 100 gm glucose load and check GH in 2 hours. If it does not decrease < 5 then positive test. | How do you diagnose Acromegaly? |
Glucose intolerance, hypogonadism, large hands and feet, large tongue and coarse facial features. Prone to skin tags and colon polyps, carpal tunnel and visual field defect with large tumor. | What are the signs of acromegaly? |
transsphenoidal surgery followed by radiation or radiation alone.
Can use bromocriptine for shrink tumor before surgery. | How do you treat acromegaly? |
Neurogenic DI results of decrease ADH from pituitary and Nephrogenic is due to decrease effect of ADH on kidney. | What is the difference between Neurogenic and nephrogenic Diabetes Insipidus? |
Polyuria, Polydypsia with Hypernatremia | What are the symptoms of DI |
Idiopathic ( most common) CNS trauma- post surgery, infection or malignancy, autoimmune | What causes Neurogenic DI? |
Lithium 20%, Elevated Ca and low K, hereditary | Which drugs can cause nephrogenic DI? |
Water deprivation test with measurement of ADH and Plasma and Urine Osmolality. If normal see increase in plasma Osmo, but with neurogenic DI increase in plasma osmo does not increase ADH. | How do you diagnose Neurogenic DI? |
Water deprivation test with hourly measurment of ADH, plasma and urine osmo. See increase in ADH, but NO increase in urine osmo. | How do you diagnose Nephrogenic DI? |
Desmopresssin DDAVP oral, nasal or SQ | How do you treat neurogenic DI? |
Thiazide diuretics. | How do you treat nephrogenic DI? |
Too much ADH. Cause: CNS trauma, infection, small cell carcinoma, and drugs( chlorpropamide , carbamazepine, and chlorothiazide and clofibrate) | What is SIADH? and what causes it? |
Low Na. Euvolemic, hyposomolar with inappropriate urine concentration. | What are the manifestation of SIADH. |
Fluid restriction to 1000 cc/d.if asymptomatic
If Na < 120 or seizure treat with hypertonic saline followed by fluid restriction.
Chronic SIADH is treated with demclocycline which decreases kidney sensitivity to ADH. | How do you treat SIADH? |
AR with 21 hydroxylase deficiency causing an increase in DHEA.
Can also cause elevated 17 hydroxyprogesterone. | congenital adrenal hyperplasia, cause and lab abnormality. |
Ambiguous genetalia in children, hirsutism and menstrual irregularity in older girls. | How does congenital adrenal hyperplasia manifest? |
Excessive glucocorticoid production or Steroid therapy.
Manifests with proximal muscle weakness, striae, buffalo hump, fluid retention, HTN, mood face, easy bruising, Low K and osteopenia and DM. | Cushing Syndrome definition |
Check a 24 hour urine cortisol level. If > 100 mcg = elevated
Do a dexamethasone suppression test by giving 1 mg of dexamethasone at 11 pm and check a serum cortisol 8 am. Normally you would see a suppressed cortisol level. If > 5 mcg/ diagnostic of Cushing Syndrome. | How do you diagnose Cushing Syndrome? |
Increase pituitary ACTH and subsequent increase in DHEA
Manifests with hirsutism. | What is Cushing Disease? |
Elevated serum cortisol and elevated ACTH. ( Normally should be suppressed)
To differentiate if ACTH coming from pituitary or ectopic do an overnight dexamethasone suppression test with 8 mg. If level of ACTH is suppressed to less than 1/2 or normal diagnostic of Cushing Disease.
Next is to image brain with MRI.
To r/o ectopic ACTH form malignancy check 17 hydroxysteroid. Elevated | How do you diagnose Cushing Disease? |
Adrenal gland is not making enough hormones. Plasma ACTH is high.
Cause is autoimmune adrenalitis. | What is primary Addisons Disease? |
Steroid withdrawal from chronic therapy. ACTH is low. | What causes secondary Addison's Disease? |
Low Cortisol, low aldosterone and high renin. Wt loss, N/V weakness, orthostatic hypotension, increase skin pigmentation.
Lab abnormalities: Low Na and High K. | How does Addison's disease manifest? |
ACTH stimulation test. Draw baseline cortisol and aldosterone, then check ACTH in 1 hour. If cortisol is low < 20 mcg, then have primary adrenal insufficiency. | How do you diagnose Addison's? |
Acutely with Dexamethasone, then oral prednisone.
Chronic treatment with hydrocortisone and fludrocortisone. | How do you treat Addison's? |