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120 Cards in this Set
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pituitary adenomas
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<1cm --> microadenoma
>1cm macroadenoma and associated with panhypopituitarism and visual symptoms prolactin 50-60%; GH 15-20%; ACTH 10-15%; LH/FSH 10-15% |
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hyperprolactinemia definition
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excess prolactin release results in galactorrhea-amenorrhea syndrome
prolactin inhibits the LH surge that causes ovulation by inhibition of hypothalamus (LHRH) which results in the amenorrhea possible but rare in males |
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hyperprolactinemia etiology
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physiologic --> pregnancy, early nursing, hypoglycemia, seizure, exercise, stress, sleep, nipple stimulation
prolactinoma block of pituitary stalk and dopamine by tumors, cranippharyngioma, meningioma, dysgerminoma, empty sella, trauma pharmacologic --> dopamine synthesis blockers (phenothiazines, metoclopramide), dopamine-depleting agents (methyldopa, reserpine), tricyclics, narcotics, cocaine, SSRIs, risperidone also high TRH due to primary hypothyroidism stimulates prolactin (always check TSH) |
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hyperprolactinemia clinical presentation
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women: galactorrhea, menstrual abnormalities, osteoposoris, osteopenia, infertility, gynecomastia
men: hypogonadism, erectile dysfunction, decreased libido, gynecomastia, infertility |
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hyperprolactinemia diagnosis
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exclude pregnancy, lactation, hypothyroidism and medications
prolactinomas may co-secrete GH normal basal fasting PRL level is <20mg/L >100ng/mL in nonpregnant --> probable pituitary adenoma --> MRI of pituitary |
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hyperprolactinemia management
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1st line: cabergolide or bromocriptine (reduces prolactin to <10% of pre-treatment levels)
if no response or compressive neurologic symptoms --> surgery only 30% of macroadenomas can be resected and >50% recurr |
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acromegaly etiology
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GH-secreting pituitary adenomas (75% are macroadenomas); rarely ectopic GH or GHRH-secreting tumors
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acromegaly clinical presentation
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enlargement of hands and feet, coarse facial features, thick skin folds; shoe, hat, glove, ring size increase; prognathism and separation of teeth; deeper voice; increased sweating; obstructive sleep apnea; visceromegaly, osteoarthritis, entrapment neuropathy; menstrual problems (prolactin is co-secreted); 30% get cardiac pathologies (cardiomyopathy, hypertension, arrythmia, hypertrophy, diastolic dysfunction, premature atherosclerosis); impaired glucose tolerance (80%), diabetes (13-20%), hypertension (33%), joint disease (articular cartilage proliferation)
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acromegaly diagnosis
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Initial test: IGF-1 levels
confirmation: GH level >5ng/mL after glucose load (should supress GH) if GH excess is confirmed --> MRI (detects tumor in 90%) or CT to localize tumor |
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acromegaly management
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1st line --> surgery
2nd line --> octeotride (↓GH in 66%) bromocriptine/carbegolide (↓GH in 25%) pegvisomant (GH analog receptor antagonist) 3rd line --> radiotherapy surgery and radiotherapy can result in hypopituitarism (10-20%) |
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acromegaly complications
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tumor pressure or rupture into brain or sinuses
cardiac failure (MCCOD) diabetes mellitus cord compression visual defects |
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hypopituitarism etiology
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Tumors:
pituitary adenomas, cysts, hypothalamic tumors (craniopharyngioma, meningioma, glioma); Inflammatory: sarcoidosis, TB, syphilis, eosinophilic granuloma, autoimmune lymphocytic hypophysitis Vascular: Sheehan postpartum necrosis, pituitary apoplexy, hemochromatosis, amyloidosis, CVA/stroke Other: trauma, radiation, surgery, infections, hypoxia |
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hypopituitarism presentation
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defficiencies in order
gonadotropin deficiency (amenorrhea, genital atrophy/impotence, infertility, decreased libido, loss of axillary and pubic hair) GH deficiency (maybe assymptomatic, hypersensitivity to insulin, hyperlipidemia, short stature in children) TSH deficiency ( hypothyroidism, fatigue, weakness, hyperlipidemia, cold intolerance, dry skin, no goiter) ACTH deficiency (secondary adrenal insuficiency, hypocortisolism, fever, hypotension, hyponatremia [minimal], decreased response to stress, weightloss) |
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hypopituitarism diagnosis
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measure hormones:
GH --> insulin-induced hypoglycemia ↓ glucose to <40mg/dL which ↑ GH > 10mg/L - if <10mg/L there is deficiency; or arginine infusion; ACTH --> insulin tolerance test should increase plasma cortisol to > 19mg/dL or metyrapone test should suppress cortisol and increase serum ACTH, failure indicates deficiency; measure LH, FSH, estrogen/testosterone TSH --> low T4/T3 levels with normal to low TSH |
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hypopituitarism management
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treat underlying cause; hormone replacement therapy specially cortisol
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Empty sella syndrome (ESS)
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herniation of suprasellar subarachnoid space through diaphragm; no pituitary seen on MRI or CT; can be idiopathic or secondary to trauma or radiotherapy; presentation: obesity, multiparoous women, headeache and 30% will have hypertension; therapy is reassurance.
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diabetes insipidus definition
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disorder of the neurohypophyseal system (hypothalamus or neurohypophisis) results in ADH deficiency (central DI); or renal resistance to the action of ADH (nephrogenic DI)
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central diabetes insipidus etiology
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neoplastic/infiltrative lessions in hypothalamus or pituitary (60% have adenohypophisis deficiency):
Craniopharyngiomas Encephalitis Meningitis Trauma Tuberculosis Radiotherapy Adenomas Anoxia Leukemia Histocytosis Hypertension Idiopathic syphillis surgery "CEMTTRAAL HHIgh" |
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nephrogenic diabetes insipidus etiology
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Demeclocycline
Idiopathic Sickle cell Sarcoidosis Sjogren Colchicine Lithium Amyloidosis Myeloma Pyelonephritis or secondary to hypercalcemia, hypokalemia "DIureSSSis CLAMP" |
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diabetes insipidus presentation
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polyuria
polydipsia hypernatremia urine specific gravity <1,010 severe dehydration weakness fever altered mental state prostration nocturia |
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diabetes insipidus diagnosis
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Diagnosis: Water Deprevation test (plasma/urine osmolarity ratio while pt. doesnt drink water) high plasma Osm, urine Osm doesnt change in DI. Add ADH to water depravation test and if response is normal : CDI still low Urine Osm : NDI CDI: low ADH NDI: Normal ADH |
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diabetes insipidus differential
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primary polydipsia
drug-induced polydipsia from chlorpromazine, anticholinergics, thioridazine hypothalamic disease Diabetes insipidus |
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diabetes insipidus management
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CDI: ADH hormone replacement (dessmopressin ddavp) or ADH secretion stimulators (chlorpropamide, clofibrate, carbamazepine)
NDI: HCTZ or amiloride (k sparing) as well as correction of calcium balance |
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SIADH etiology
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cancer: small cell lung CA, pancreas CA, ectopic ADH secretion
infections: TB, lung abscess CNS: head injury, Stroke, encephalitis drugs: chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine "inappropriate CCCCancer VVIBE" Cancer, 4 C drugs, 2 V drugs, Infections, Brain, Ectopic |
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SIADH presentation
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water retention
ECF expansion without edema or hypertension (natriuresis) hyponatremia concentrated urine signs of cerebral edema when hyponatremia is severe (irritability, confusion, seizures, coma) |
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SIADH diagnosis
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high ADH is most accurate test
hyponatremia <130mEq/L urine sodium > 20mEq/L; maintained hypervolemia ↓RAA low electrolytes in blood (BUN, creatinine, uric acid) low albumin |
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SIADH management
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treat underlying cause
fluid restriction to 800-1000mL/d demeclocycline (AVP inhibitor) in case of cerebral edema: hypertonic 3% saline 200-300mL IV in 3-4h |
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hyperthyroidism etiology
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Graves (toxic diffuse goiter)(most common)
hyperfunctioning adenoma, Plummer disease (toxic multinodular goiter) amiodarone excess TSH (rare) transient hyperthyroidism due to subacute thyroiditis (painful) lymphocytic thyroiditis (painless) thyrotoxicosis factitia ectopic thyroid tissue (struma ovarii, functioning follicular CA) |
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hyperthyroidism presentation
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Cardiac:
atrial fibrillation, dyspnea, palpitations, angina, heart failure Adrenergic: nervousness, insomnia, irritability, tremors, frequent bowel movements, excessive sweating, heat intolerance, warm moist skin Metabolic: weight loss, weakness, palmar erythema, oligomenorrhea, osteoporosis/hypercalcemia Eye: staring, infrequent blinking, lid lag Graves has diffuse goiter + exopthalmus + dermopathy-pretibial myxedema and may be associated with PA, MG or DM "CAME" |
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hyperthyroidism diagnosis
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history and PE plus lab confirmation:
TSH (↓ in primary, ↑ in secondary) ↑ free T4/T3 ↑RAIU TSI in Graves ↑ anti-thyroglobulin and antimicrosomal Ab in Graves and Hashimoto's |
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hyperthyroidism differential
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Pheochromocytoma
Acromegaly Cardiac (A fib) Mania Myasthenia Anxiety Neurosis MG and orbital tumors can cause opthalmoplegia and exopthalmus if primary, need to specify Graves or thyroiditis "hyperthyroid PACMMAN" |
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hyperthyroidism management
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immediate: propranolol, PTU, methimazole (can cause agranulocytosis)
later: radioactive iodine ablative therapy or thyroidectomy if 2nd trimester pregnancy, children or compressive symptoms levothyroxine hormone replacement may be needed to avoid hypothyroidism |
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thyroid storm presentation
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endocrine emergency precipitated by stress, infection, surgery, trauma; presents with:
Tachychardia Hypotension Hot (fever Vomiting Restlessness Irritability Icteric Coma Diarrhea Dehydration Delirium "Thyroid HHVRIICaneD" |
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thyroid storm management
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saline/glucose hydration, oxygen, cooling blanket;
1. PTU, 100mg every 2h 2. iodine (inhibits hormone release) 3. propranolol 4. dexamethasone (inhibits hormone release, impairs peripheral generation of T3 and adrenal support) PTU blocks uptake of RAI and should be stopped 1-2 weeks before and after RAIU treatment |
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hypothyroidism etiology
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95% primary:
Congenital defects Lithium Aspirin Amiodarone Surgery (postablative) Sulfonamides Iodine (radioactive and deficiency) Interferon Hashimoto (MCC) also secondary (pituitary) and tertiary (hypothalamus) "hypothyroidism due to CLAASSIIc Hashimoto" |
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hypothyroidism presentation in newborn
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Cretinism
Cry hoarsely Coarse features Constipation Retardation (mental and skeletal) Eating problems Eyes widely set Tongue protruding Teeth problems Nose broad and flat Sommnolence Sparse hair Skin is dry Jaundice Abdomen protrudes with umbilical hernia Milestones delayed Migit (dwarfism) "CCCCREETTiNSS JAM" |
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hypothyroidism presentation in adult
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lethargy, constipation, cold intolerance, mental dullness, anorexia with weight increase, dry skin and hair, deep hoarse voice, myxedema, slow tendon reflexes with prolonged relaxation, pale cool dry skin
hypercholesterolemia, expressionless face, sparse hair, periorbital puffiness, macroglosia, hypokinesis, deafness, hyponatremia, anemia, stiffness, muscle cramps, carpal tunnel syndrome, menorrhagia, |
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hypothyroidism diagnosis
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history and PE plus lab confirmation:
↑ TSH (primary) or normal/↓ TSH (secondary) ↓T4 and FT4 ↓ T3 also may have hypercholesterolemia ↑ CPK ↑ AST hyponatremia ↑ LDH and 12% have PA |
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hypothyroidism management
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gradual metabolic restoration with levothyroxine (monitor TSH/T3)
if suspicion of 2dary or 3ary give hydrocortisone first then hormone replacement if myxedema coma signs (respiratory depression and ↑CO2 retention) use very high doses of T4 and T3 |
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subacute thyroiditis
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also called granulomatous or De Quervain; viral etiology
presents with upper respiratory symptoms plus painful enlarged and firm thyroid lab confirmation is made by ↑ ESR, ↓ RAIU and initial ↑ of T3/T4 then ↓ symptomatic management: aspirin, prednisone, propanolol differential: Graves (there's ↑ RAIU); subsides to normal function |
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Hashimoto etiology
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chronic autoimmune lymphocytic infiltration of the thyroid with antimicrosomal and antithyroglobulin antibodies
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Hashimoto presentation
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painless asymmetrical nontoxic goiter of firm/rubbery consistency with signs and symptoms of hypothyroidism
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Hashimoto diagnosis
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history and PE
confirmation with needle biopsy labs: normal or ↑ TSH normal or ↓ T4/T3 antimicrosomal antithyroglobulin antiperoxidase antibodies |
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Hashimoto management
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levothyroxin hormone replacement
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Lymphocytic thyroiditis
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self-limiting episode of thyrotoxicosis associated with chronic lymphocytic thyroiditis
thyroid is nontender, firm, symemetrical and slightly enlarged normal ESR, ↑T4/T3, ↓RAIU antithyroid antibodies may be present but in low titer; its recurrent symptomatic treatment with propranolol |
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Reidel thyroiditis
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intense fibrosis and enlargement of the thyroid
surgery is needed associated with mediastinal and retroperitoneal fibrosis |
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thyroid adenomas
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may be nonfunctioning or hyperfunctioning
slow growth types are follicular (most common), papillary and Hurthle treat with ablation surgery or RAI |
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papillary thyroid carcinoma
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most common and differentiated
more common in women, bimodal frequency slow growing; lymphatic spread psamomma bodies seen in X-rays treat with surgery alone (small) or surgery + radiotherapy and also TSH suppression with levothyroxine |
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follicular thyroid carcinoma
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2nd most common
more frequent in elderly women hematogenous spread with metastasis to lung and bone total thyroidectomy with postoperative ablative radiation |
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anaplastic thyroid carcinoma
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3rd most common; more frequent in elderly women; highly malignant with rapid and painful enlargement; 80% die in 1 year of diagnosis; direct spread
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medullary thyroid carcinoma
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least common
arises from parafollicular cells and produces calcitonin associated with MEN IIa and MEN IIb thyroidectomy is indicated differentiate paraneoplastic calcitonin production in lung, breast, pancreas and colon cancer |
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thyroid cancer diagnosis
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recent growth of thyroid mass with nontenderness or hoarseness
solitary nodule, ↑ calcitonin, x-ray calcifications or increased density suggest malignancy first test is TSH if normal TSH --> FNA procedure (preferred) or scintillation scanning functioning nodules are most likely adenomas while nonfunctioning nodules are malignant in 20% of cases; ultrasound is usefull to distinguish cyst from solid nodule |
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metabolism of calcium
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regulated by PTH via osteoclast activation, vitamin D activation and distal tubule reabsorption; 80% of ingested calcium is excreted, 20% absorbed; 2% of total calcium is in blood 50% free, 40% protein-bound and 10% bound to citrate or phosphate buffers
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hyperparathyroidism etiology
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most common is primary hyperPTH
malignancies (lung) produce PTH-like peptide granulomatous diseases (sarcoidosis, TB, berylliosis, histoplasmosis) vitamin D intoxication thiazides lithium Paget disease acidosis |
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hyperparathyroidism presentation
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CONfusion
CONstipation Nephrolithiasis Anorexia Nausea Pancreatitis Polyuria Polydipsia Hypertension (30-50%) short QT wave, ulcers, lethargy "CONstANt PPPtH" |
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hyperparathyroidism management
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Fluid replacement, furosemide (loop diuretics), biphosphonates (alendronate)
calcitonin if can't wait 2 days for biphosphonates to make effect |
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primary hyperparathyroidism etiology
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one gland adenoma (80%), gland hyperplasia (20%), MEN I or II
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primary hyperparathyroidism presentation
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Pancreatitis
Peptic ulcer Polyuria Polydipsia Psychiatric disorders Nephrocalcinosis Stones Osteitis fibrosa cystica Fatigability Constipation hypertension short QT arrhythmia "PaNS OF Calcium" osteitis fibrosa cystica: bone pain, fractures, deformities, localized demineralization, bone cysts, brown tumors |
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primary hyperparathyroidism management
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parathyroidectomy if symptoms of hypercalcemia, bone disease, renal disease, pregnancy
medical RX if calcium <11.5mg/dL: biphosphonates, restriction of dietary calcium, oral hydration, phosphate supplements emergency RX: IV normal saline, furosemide, IV biphosphonates and calcitonin if rapid effect is necessary |
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secondary hyperparathyroidism management
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cinacalcet: calcimimetic agent shuts off parathyroids; used in secondary hyperPTH caused by hemodialisis and parathyroid OA
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hypocalcemia etiology
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hypoparathyroidism
renal failure hyperphosphatemia hypomagnasemia alkalosis low albumin levels (pseudo hypocalcemia) massive blood transfusion |
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hypocalcemia presentation and RX
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neural hyperexcitability (seizures, tetany, numbness, tingling), prolonged QT arrhythmia; treat with calcium and vitamin D supplementation
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hypoparathyroidism etiology
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most common is surgical removal of parathyroids
hypomagnesemia, hereditary note: chronic renal failure and low vitamin D produce high levels of PTH but signs and symptoms of hypocalcemia. |
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hypoparathyroidism presentation
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neuromuscular irritability
tetany laryngospasm cramps seizures Chevostek Trousseau QT prolongation arrhythmia refractory CHF hyperventilation worsens hypoPTH due to alkalosis |
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hypoparathyroidism diagnosis
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signs and symptoms
low serum calcium or albumin suggests hypoPTH preferable to measure ionized calcium PTH may be high or low |
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hypoparathyroidism management
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acute: calcium gluconate IV
maintenance: oral calcium, vitamin D and phosphate binders if hyperphosphatemia |
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diabetes etiology
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type I: genetically susceptible autoimmune destruction of beta cells following viral infection
type II: unknown but theres abnormal insulin secretion and resistance to insulin |
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diabetes presentation
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polyuria
polydipsia polyphagia hyperglycemia ketoacidosis or hyperosmolar coma signs and symptoms of complications may exist |
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diabetes diagnosis
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random plasma glucose >200mg/dL plus symptoms or 2 fasting plasma glucose >126mg/dL; glucose tolerance test may be required to show >200mg/dL at 2h and at least one earlier sample; HgA1c >7% suggests diabetic patient has been noncompliant with treatment for the previous 8-12 weeks
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type II diabetes management
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patient education, weight reduction, low fat diet and physical activity
if this fails to keep HgA1c below 7% then drugs; 1st line: sulfonylurea (thin patients) or metformin (obeese patients); 2nd line: add sulfonylurea or metformin; 3rd line: add glitazone or switch to insulin 0.5U/kg; |
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diabetes complications
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acute: DKA or HONK
chronic: myocardial infarction (#1 cause of death in diabetics) hyperlipidemia diabetic nephropathy (#1 cause of chronic renal failure) diabetic retinopathy gastroparesis erectile dysfunction diabetic foot neuropathy |
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diabetic ketoacidosis presentation
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Kussmaul respiration
Acidosis Anorexia Abdominal pain Consciousness altered Dehydration Vinegar breath Vomiting and hyperkalemia "Keto AAACiD & Vinegar" |
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diabetic ketoacidosis diagnosis
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signs and symptoms plus elevated plasma glucose, elevated levels of acetoacetate and hydroxybutirate, metabolic acidosis and increased anion gap
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diabetic ketoacidosis management
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insulin bolus with 5-10 units; potassium if plasma levels <4 mEq/L; fluid and electrolyte replacement
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hyperosmolar nonketotic coma presentation
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Water (profound dehydration)
Weakness Polyuria Polydipsia Confusion Coma SEizures lethargy "dehydrated CCOMAtoSE" |
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hyperosmolar nonketotic coma diagnosis
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elevated plasma glucose (1000 mg/dL)
extremely high serum osmolality high BUN mild metabolic acidosis (bicarbonate around 20 mEq/L) without ketosis |
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hyperosmolar nonketotic coma management
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high-volume fluid and electrolyte replacement + insulin
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myocardial infarction risk in diabetes
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#1 cause of death in diabetics (75%); for every 1% reduction in HgA1c there's 14% risk reduction; for every 10 point decrease in blood pressure there's additional 12% risk reduction
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lipid management in diabetics
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target LDL is <100mg/dL
if 100-130mg/dL: recommend diet, exercise and consider statin if >130mg/dL statin is recommended |
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diabetic nephropathy
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affects 30-40% of type I and 20-30% of type II diabetics
diffuse membrane and mesangial thickening is most common nodular glomerulosclerosis is also common (Kimmelstiel-Wilson syndrome) screen for proteinuria annually proteinuria is >300mg of albumin in 24 hour urine microalbuminuria is first stage and between 30-300mg all diabetics with proteinuria should be given ACE inhibitor or ARB |
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diabetic retinopathy
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screen type II diabetics at diagnosis and annually thereafter
screen type I diabetics 5 years after diagnosis and annually thereafter proliferative retinopathy shows vitreous hemorrhages and/or neovascularization and is treated with laser photocoagulation |
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diabetic gastroparesis and erectile dysfunction
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treat gastroparesis with metoclopramide or erythromycin
50% of diabetics have erectile dysfunction after 10 years, treat with sildenafil |
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diabetic foot
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due to trauma and infection in presence of diabetic neuropathy
podiatric examination annually responsible for 50% of nontraumatic amputations |
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diabetic neuropathy
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peripheral neuropathy: most common, symmetrical, numbness, paresthesia, pain, absent reflexes, loss of vibratory sense (treat with gabapentin (best), pregabalin (best), analgesics, amitriptyline, carbamazepine)
mononeuropathy: sudden foot drop, wrist drop or paralysis of III, IV or VI nerves autonomic neuropathy: orthostatic hypotension, syncope, gastroparesis and constipation or diarrhea, bladder dysfunction and urinary retention, impotence and retrograde ejaculation |
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hypoglycemia presentation
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excessive secretion of epinephrine -->
sweating, tremor, tachychardia, anxiety, hunger CNS --> dizziness, headache, clouded vision, loss of fine motor skills, confusion, seizures, coma |
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posprandial hypoglycemia
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due to alimentary hyperinsulinism after gastrectomy, vagotomy, etc…; idiopathic or galactosemia
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fasting hypoglycemia
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underproduction of glucose due to hormone deficiencies (panhypopituitarism, adrenal insufficiency), enzyme defects, malnutrition, late pregnancy, acquired liver disease, alcohol, propanolol, salicylates, hyperinsulinism (insulinoma, exogenous insulin, sulfonylureas, quinine, endoteoxic shock, autoimmune insulin receptor antibodies)
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insulinoma
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subacute or chronic hypoglycemia causes blurred vision, headache, slurred speech, weakness
diagnosis: serum insulin level > 8mg/mL with blood glucose <40mg.dL CT, ultrasound or arteriography to localize tumor surgical, diet and medical treatment |
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factitious hyperinsulinism
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due to self-administration of insulin, Equal or sulfonylureas
hypoglycemia, high immunoreactivity, high insulin and low C peptide |
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ethanol-induced hypoglycemia
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glycogen is depleted in 18-24 hours and gluconeogenesis is blocked by ethanol concentration of 45mg/dL in blood
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classification of hypoglycemia
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posprandial, fasting, insulinoma, factitious, ethanol-induced
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Cushing syndrome etiology
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MCC is prolonged use of glucocorticoids; adrenal hyperplasia secondary to pituitary adenomas (40%), nonendocrine ACTH-producing tumors; adrenal neoplasia (30%)
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Cushing syndrome presentation
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Buffalo hump
Weakness Wound healing Fat deposition Amenorrhea Leukocytosis Osteoporosis Hypertension Hirsutism Potassium Psychiatric disorders Striae Stones Glucose intolerance Immune depression "BWWFALO HHumPPSS & DIabetes" |
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Cushing syndrome diagnosis
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Initial test: 1mg overnight dexamethasone suppression test;
if abnormal or false+ --> 24-hour urine free cortisol; if normal, exclude Cushing, if abnormal Cushing syndrome diagnosis; determine etiology: high dose dexamethasone suppression if supression to <50% of control --> pituitary adenoma; if no response then ACTH-producing tumor or adrenal hyperplasia measure ACTH level if high, then it's ACTH-producing tumor (do chest CT) if low it's adrenal hyperplasia --> urinary 17KS, DHEA-S, abdominal CT: if high and >4cm mass then its adrenal CA if normal or <4cm mass then adrenal adenoma |
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hyperaldosteronism etiology
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primary hyperaldosteronism (low renin) due to unilateral adrenal adenoma (70%)
or bilateral hyperplasia (25-30%) secondary hyperaldosteronism (high renin) due to |
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primary hyperaldosteronism presentation
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diastolic hypertension
muscle weakness polyuria polydipsia hypokalemia hypernatremia metabolic alkalosis no edema |
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secondary hyperaldosteronism presentation
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hypokalemia
metabolic alkalosis may or may not have muscle weakness polyuria polydipsia edema no diastolic hypertension no hypernatremia |
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primary hyperaldosteronism diagnosis
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high urine aldosterone levels and low plasma renin levels (give high-salt diet before lab tests); confirm with CT scan of adrenals
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primary hyperaldosteronism management
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adrenal adenomas are removed surgically
bilateral hyperplasia --> spironolactone |
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Bartter syndrome
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defect in Na-K-2CL transporter of loops of Henle, acts as furosemide-secreting tumor loosing NaCl which stimulates renin and aldosterone secretion
presentation: secondary hyperaldosteronism with no hypertension, no edema and severe hypokalemic alkalosis |
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syndrome of adrenal androgen excess
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excess DHEA and androstenidione which are then converted to testosterone due to congenital adrenal hyperplasia or adrenal neoplasia
presentation: hirsutism, oligomenorrhea, acne, virilization; |
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congenital adrenal hyperplasia etiology
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enzyme deficiencies: 21-beta hydroxylase, 17-hydroxylase, 11-hydroxylase
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congenital adrenal hyperplasia presentation
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21-beta hydroxylase deficiency (95%): low aldosterone in 1/3 (salt-loss, hyponatremia, hyperkalemia, dehydration, hypotension), female pseudohermaphroditism or precocious puberty in males
11-hydroxylase deficiency: virilization and hypertension/hyperkalemia due to 11-deoxycorticosterone; 17-hydroxylase deficiency: hypogonadism (17KS are blocked), hypokalemia, hypertension (11-deoxycorticosterone) |
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congenital adrenal hyperplasia diagnosis
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suspect infants with failure to thrive, adrenal insufficiency, salt-wasting and/or hypertension
lab studies: serum testosterone, androstenidione, dehydroepiandrostenidione, 17-hydroxyprogesterone, urinary 17KS and pregnanetriol |
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congenital adrenal hyperplasia management
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hydrocortisone
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Adisson disease etiology
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autoimmune destruction of the adrenals (80%), idiopathic destruction of the adrenals; surgical removal of the glands, destruction due to infection (TB, fungal, CMV, mycobacterium avium); hemorrhage, trauma, metastatic invasion
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Adisson disease presentation
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Acidosis
Weakness Weight loss Pressure is low (in primary) Pigmentation (in primary) Paresthesia Potassium is high Intolerance to stress Cramping Sparse axillary hair Sodium is low "Addison WWith PPPPICmentSS" |
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Addison disease diagnosis
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initial test: plasma cortisol after 250um of consyntropin -->
subnormal increase in cortisol --> measure ACTH --> if high it's primary adrenal insufficiency; if low its secondary adrenal insufficiency also hemogram (neutropenia, lymphocytosis, eosinophiliaa); elevated potassium and BUN; low sodium; low glucose; low plasma cortisol and low urinary 17-hydroxycorticosteroid |
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Addison disease management
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glucocorticoid, mineralocorticoid (fludrocortisone) and NaCl replacement; patient education
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Adrenal crisis
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due to major stress in previously undiagnosed patient, bilateral adrenal infarction or hemorrhage, abrupt glucocorticoid withdrawal
presentation: FEver, Vomit, Abdominal pain, Altered mental status, Hypotension "glucocorticoid withdrawal causes FeVAAH" Rx: fluid replacement + hydrocortisone |
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pheochromocytoma epidemiology
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10% Malignant
10% Children 10% no Hypertension 10% Bilateral 10% Extraadrenal "10% MuCH BEtter adrenaline" 5% autosomal dominnant alone MEN II MEN III von Recklinghousen neurofibromatosis von Hippel-Lindau retinal cerebellar hemangioblastomatosis affects 0.1% of hypertensives |
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pheochromocytoma presentation
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paroxystic crisis of sudden onset
headache profuse sweating palpitations chest or abdomen pain nausea/vomit hypertensive crisis and tachychardia anxiety tremor weight loss |
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pheochromocytoma diagnosis
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screening:
plasma metanephrine (no smoking 4 hours before test) urinary free catecholamines urinary metanephrines urinary vanillylmandelic acid plasma catecholamines if screening equivocal --> clonidine suppression test if screening is positive --> CT or MRI if not shown --> MIBG scan serum chromogranin levels correlate with tumor size |
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pheochromocytoma differential
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essential hypertension
anxiety attacks factitious crisis intracranial lesions autonomic epilepsy |
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pheochromocytoma management
|
if crisis: phentolamine or phenoxybenzamine
after stabilization may use other antihypertensives and surgery |
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primary (hypergonadotropic) hypogonadism etiology
|
Klinefelter
anorchia surgical or accidental castration radio therapy chemotherapy mumps TB leprosy |
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secondary (hypogonadotropic) hypogonadism etiology
|
hypopituitarism
Kallman syndrome (hypogonadism and decreased sense of smell) |
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hypogonadism presentation
|
undeveloped external genitalia, no seondary sexual characteristics, low libido and potency, retarded bone age;
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hypogonadism diagnosis and Rx
|
low-normal urinary 17KS
low serum testosterone low LH/FSH in pituitary origin high LH/FSH in primary testicular failure Rx: testosterone |
|
|
Klinefelter syndrome
|
47XXY
hypogonadism gynecomastia sterility small testes high LH/FSH low-normal serum testosterone low urinary 17KS high serum estradiol |
