1 Flashcards
When should screening for colon cancer begin in the patient with no family history of colon cancer?
Screening for colon cancer should begin at 50 with colonoscopy every 10 years. Annual fecal occult blood testing, sigmoidoscopy every 5 years, and barium enema are also options.
What are the screening mammography recommendations for breast cancer?
Every 1–2 years from age 40 and over. Breast examination by physician for ages 20–30, every 3 yrs. Patients with multiple first–degree relatives with breast cancer should receive prophylactic tamoxifen.
What is the prophylaxis for hepatitis A for travelers?
If a patient is leaving within 2 wks to a nonindustrialized country, vaccine and immune serum globulin are given. A booster shot given 6 months after the initial vaccination confers immunity for 10 years.
Which travelers should receive hepatitis B vaccine?
Patients who will work with indigenous, engage in sex, receive medical/ dental care, on remain abroad >6 mth in a country where prevalence is intermediate or high.
What is the recommended prophylaxis for malaria for travelers?
Traveling to Mexico, Central America (except Panama), or Caribbean, chloroquine is prophylaxis for malaria. For travelers to areas where chloroquine resistance common, mefloquine recommended.
At what age is meningococcal vaccine usually given?
Meningococcal is routinely given at age 11.
What are the recommendations for prevention of traveler’’s diarrhea?’
Patients who experience loose stools without fever or blood may take loperamide. Treatment with a fluoroquinolone or azithromycin is reserved for patients with bloody diarrhea.
What are the recommendations for tetanus and diphtheria vaccination in adults who were never vaccinated?
Adults who were never vaccinated should receive three doses, the first two are given 1 to 2 months apart, with the third dose given 6 to 12 months later. A booster vaccination should be given every 10 years for life.
What are the recommendations for influenza vaccination?
Annually for adults >50. Cardiopulmonary disease, diabetes, hemoglobinopathy, or who are in chronic care facilities should receive annual. Pregnant women who will be in 2nd or 3rd trimester during influenza season.
What are the indications for pneumococcal vaccination?
Adults >65; sickle–cell, splenectomy, cardiopulmonary disease, alcoholism, cirrhosis, Alaskan natives, Native Americans; immunocomp (heme malignancies, CRF, nephrotic, HIV; immunosuppressives).
What are the indications for hepatitis B vaccination?
IV drug abuse, male homosexuality, household or sexual contact with hepatitis B carriers, frequent exposure to blood, chronic liver disease. Immunity can be confirmed serologically.
What are the recommendations for hepatitis A vaccine?
Hepatitis A vaccine is recommended for travelers to endemic areas, day–care employees, homosexual men, and chronic liver disease.
What are the indications for varicella vaccine?
Varicella vaccine is recommended for all adults who lack a history of childhood infection; should not be given to immunocompromised or pregnant because it is live attenuated.
What are the recommendations for measles, mumps, rubella vaccine?
Measles, mumps, rubella vaccine is a live attenuated vaccine given in childhood. Healthy adults should receive 1 dose if never vaccinated. Pregnant and immunocompromised not vaccinated.
What are the recommendations for osteoporosis screening?
All women older than age 65 should be given DEXA scans every 1–2 years. Begin at age 60, if there is low body weight or increased risk of fractures.
What are the recommendations for screening for abdominal aortic aneurysm?
Ultrasound should be given once in male smokers older than age 65.
What are the recommendations for cholesterol screening?
Cholesterol screening should begin at age 35 in men and 45 in women who have no risk factors. For patients with risk factors for coronary artery disease, screening should be done routinely after age 20.
What are the recommendations for screening for diabetes?
Obesity, impaired fasting glucose, African–Americans, native Americans and/or positive family history.
What is the criteria for the diagnosis of diabetes?
Diabetes mellitus is diagnosed when two fasting are greater than 126 mg/dL, or when a random glucose is >200 mg/dL.
What clinical test should be used to screen for alcohol abuse?
CAGE: Have you ever felt the need for Cut down? Have you ever felt Annoyed by criticism of your drinking? Have you ever Guilty about your drinking? Have you ever taken Eye opener? Positive is 2 yes
What pathological conditions are associated with hyperprolactinemia?
Excess of prolactin occurs with prolactinomas (most common functioning pituitary adenomas, 60% of pituitary tumors.
What medications cause hyperprolactinemia?
Decreased inhibitory action of dopamine caused by drugs that block dopamine synthesis (phenothiazines, metoclopramide) and dopamine–depleting agents (alpha–methyldopa).
What is the presentation of hyperprolactinemia?
Women have galactorrhea, amenorrhea/oligomenorrhea, osteoporosis, infertility, gynecomastia; men have hypogonadism, erectile dysfunction, decreased libido, gynecomastia and infertility.
How is hyperprolactinemia diagnosed?
Always exclude pregnancy, lactation, hypothyroidism and medications before starting the evaluation of hyperprolactinemia. Prolactin levels >100 ng/mL suggest probable pituitary adenoma.
What is the management of hyperprolactinemia?
For prolactinomas: cabergoline or bromocriptine (dopamine agonist) reduce prolactin levels. Surgery for adenomas not responsive to cabergoline or bromocriptine, or if the tumor causes neurologic effects.
What is acromegaly?
Excessive secretion of growth hormone in an adult. In children, gigantism occurs. In adults acromegaly occurs, which is bony and soft tissue overgrowth. Pituitary adenoma that overproduces growth hormone. Only 1% are malignant.
How is acromegaly diagnosed?
The best initial test is insulin–like growth factor–1 levels. Confirmatory testing involves the measurement of GH after 100 g of glucose is given orally.
What is the management of acromegaly?
Transsphenoidal surgery. Hypopituitarism occurs after surgery in 10–20%. Octreotide is a somatostatin analog that reduces GH in two thirds of patients and causes partial tumor regression in 20–50% of patients.
What are the causes of hypopituitarism?
Tumors, cysts, sarcoidosis, Tb, syphilis, eosinophilic granuloma, Hashimoto, gastric atrophy. Trauma, radiation, surgery, infections, hypoxia. Sheehan postpartum necrosis, hemochromatosis, amyloidosis.
What are the signs of hypopituitarism?
Amenorrhea, genital atrophy, loss pubic hair. Growth fail. Thyrotropin deficiency: hypothyroidism. Adrenocorticotropin def: fatigue, anorexia, wt loss, decreased skin pigment, hypotension, hypoNa.
How is hypopituitarism diagnosed?
Measure GH, TSH, LH, and insulin–like–GF1.
How is ACTH deficiency diagnosed?
Insulin tolerance test: give insulin and measure serum cortisol. Metyrapone tests for decreased ACTH production. Metyrapone blocks cortisol production, which should increase ACTH levels.
How is gonadotropin deficiency diagnosed?
To diagnose gonadotropin deficiency in women, measure LH, FSH, and estrogen. In males, gonadotropin deficiency is detected by measuring LH, FSH, and testosterone.
How is thyroid stimulating hormone deficiency diagnosed?
To diagnose TSH deficiency, measure serum thyroxine (T4), and free triiodothyronine (T3), which are low, with a normal to low TSH.
What is central diabetes insipidus?
CDI is neurohypophyseal deficiency of vasopressin (ADH), which results in excessive, dilute urine and increased thirst with hypernatremia. Nephrogenic DL is caused by renal resistance to vasopressin.
What are the causes of central diabetes insipidus?
Adenomas, craniopharyngiomas; leukemias, sarcoid histocytosis. Pituitary/hypothalamic surgery, radiotherapy, severe head injuries, anoxia, hypertension, and meningitis. Idiopathic; encephalitis, TB, and syphilis.
What are the causes of nephrogenic diabetes insipidus?
Nephrogenic DL: idiopathic or caused by hyperCa, hypoK, sickle cell, amyloidosis, myeloma, pyelonephritis, sarcoidosis, Sjögren syndrome, lithium, demeclocycline, colchicine.
What are the clinical signs of diabetes insipidus?
Polyuria, excessive thirst, polydipsia (16–20 L/d), hypernatremia with high serum osmolarity, decreased urine specific gravity, dehydration, weakness, fever, altered mental status, and death.
How is diabetes insipidus diagnosed?
Water deprivation test: Uosm after dehydration versus Uosm after vasopressin. Normal response to fluid restriction is increased urine osm, decrease urine vol. DL urine vol remains high despite vol depletion.
How is nephrogenic diabetes insipidus differentiated from central diabetes insipidus?
ADH levels will be low in central DL and high in nephrogenic DL.
What is the differential diagnosis of diabetes insipidus?
Psychogenic polydipsia, drug–induced polydipsia from chlorpromazine, anticholinergic drugs, or thioridazine, and hypothalamic diseases.
What is the management of central diabetes insipidus?
Hormone replacement with vasopressin. For nephrogenic DL, HCTZ or amiloride increase the reabsorption of fluid from the proximal tubule.
What are the causes of syndrome of inappropriate secretion of ADH?
Small cell CA, pancreas CA, ectopic ADH; TB, pneumonia, lung abscess; head injury, stroke, encephalitis; chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine.
What are the clinical signs of syndrome of inappropriate ADH?
Water retention and ECF expansion without edema or hypertension. Hyponatremia. Hyponatremia and concentrated urine (Uosm >300 mOsm), no edema or dehydration.
What are the CNS signs of SIADH?
Cerebral edema from hyponatremia causes irritability, confusion, seizures, coma.
What are the laboratory findings in syndrome of inappropriate secretion of ADH?
Hyponatremia 20 mEq/L (inappropriate natriuresis). Low BUN, low creatinine, low urate, low albumin.
What is the management of SIADH?
Treat cause. Fluid restrict 800 mL/d. Demeclocycline. If severe confusion, convulsions, or coma: hypertonic saline (3%) 200–300 mL IV over 3–4 h. The rate of correction 0.5–1 mmol/L/h of serum Na.
What is the most sensitive test for thyroid diseases?
The most sensitive test in thyroid diseases is the TSH. If the TSH is normal, then the patient is euthyroid.
What are the effects of thyroid binding globulin levels on the thyroxine levels?
Increased TBG in pregnancy, OCP will increase total T4 but free T4 level is normal. Decreased TBG levels in nephrotic syndrome and androgens. Decreased TBG will decrease total T4, but free or active T4 normal.
What are the signs of thyrotoxicosis?
Graves disease, diffuse goiter, exophthalmos, dermopathy. More in women in the fourth decade.
What is the cause of Grave disease?
Autoantibodies bind to TSH receptor and stimulate thyroid. Intrinsic thyroid autonomy can result from a hyperfunctioning adenoma (toxic) or toxic multinodular goiter of the elderly.
What are the causes of transient hyperthyroidism?
Subacute thyroiditis (painful) and lymphocytic thyroiditis (painless, postpartum). Thyrotoxicosis factitia and ectopic thyroid tissue (struma ovarii, functioning follicular carcinoma).
What are the cardiovascular signs of Graves disease?
Anxiety, insomnia; atrial fibrillation, tremors, frequent bowel movements, excessive sweating, heat intolerance. Weight loss, increased appetite, weakness. Dyspnea, palpitations, angina, or cardiac failure.
What are the dermatologic signs of Grave disease?
Skin is warm and moist, palmar erythema; fine, silky hair. Staring, infrequent blinking, oligomenorrhea; osteoporosis and hypercalcemia.
What are the laboratory findings in Graves disease?
Low TSH; increased serum free T4 and T. RIAU is increased. Antithyroglobulin and antimicrosomal antibodies are elevated in Graves disease and autoimmune thyroiditis.
What is the treatment of hyperthyroidism?
Popranolol, propylthiouracil (safe in preg) or methimazole. Both can cause agranulocytosis. Ablation with radioactive iodine. Subtotal thyroidectomy only in pregnancy and children.
What is a thyroid storm?
Thyrotoxicosis precipitated by stress, infection, surgery, or trauma. Extreme irritability, delirium, coma, tachycardia, restlessness, vomiting, jaundice, diarrhea, hypotension, dehydration, and fever.
What is the treatment for thyroid storm?
Glucose, hydration, glucocorticoids, oxygen, cooling blanket. Propylthiouracil, beta–blockers, and iodine inhibit hormone release.
What is the affect of antithyroid drugs on uptake of radioactive iodine?
Antithyroid drugs should be stopped several days before radioactive iodine treatment because the antithyroid medications block the uptake of the radioactive iodine.
What are the causes of primary hypothyroidism?
Hypothyroidism is from thyroid in 95%. Can be caused by chronic thyroiditis (Hashimoto), postablative or radioactive iodine, heritable defects, iodine deficiency; lithium, aspirin, amiodarone, interferon, sulfonamides.
What is the most common cause of goitrous hypothyroidism?
Hashimoto disease is most common cause of goitrous hypothyroidism.
What are the clinical signs in congenital hypothyroidism?
Cretinism, jaundice, hoarse, constipation, somnolence, feeding problems; delayed milestones, dwarf, protruding tongue, broad flat nose, wide eyes, sparse hair, dry skin, potbelly, umbilical hernia, impaired mental.
What are the signs and symptoms of hypothyroidism in the adult?
Lethargy, constipation, cold intolerance, cramping, carpal tunnel, menorrhagia. Slow intellectual/motor; appetite decrease, weight increase; dry hair/skin. Deep voice, prolonged DTR. Myxedema: expressionless, sparse hair, periorbital puffiness, Lg tongue.
What is the treatment of hypothyroidism?
Levothyroxine (T4) should be administered with monitoring of TSH/T3 levels (6 weeks to steady state after dosing changes).
What is myxedema coma?
Severe hypothyroidism with hypothermic, stuporous state; frequently fatal; respiratory depression. Precipitated by cold exposure, trauma, infections, and CNS depressants. Treatment is very high doses of T4 and T3.
What are the causes of subacute thyroiditis?
Granulomatous, giant cell, and de Quervain thyroiditis. In the fourth and fifth decades. Viral origin and follows upper respiratory infection; malaise, fever, pain over the thyroid. Thyroid enlarged and firm.
What are the laboratory findings in subacute thyroiditis?
Elevated erythrocyte sedimentation rate (ESR), decreased radioactive iodine uptake, initial elevation in T4 and T3, followed by hypothyroidism.
What is the treatment of subacute thyroiditis?
Aspirin, prednisone, and Popranolol.
What is Hashimoto thyroiditis?
Chronic autoimmune inflammatory process with lymphocytic infiltration. Common disorder most frequently in middle–aged women; most common cause of sporadic goiter in children.
What are the clinical signs of Hashimoto thyroiditis?
Goiter that is painless, rubbery and hypothyroidism.
How is Hashimoto thyroiditis diagnosed?
TSH increases, and T4 and T decrease. Antimicrosomal and antithyroperoxidase antibodies.
What is the management of Hashimoto thyroiditis?
Replacement with L–thyroxine (T4).
What is chronic lymphocytic thyroiditis?
Self–limiting thyrotoxicosis; more common women. Thyroid is painless, nontender, firm, symmetrical, and enlarged. T4 and T3 are elevated, RAIU is low, ESR normal. Lasts for 2–5 months. Treatment with Popranolol.
What is Reidel thyroiditis?
Fibrosis of the thyroid and mediastinal and retroperitoneal fibrosis.
What is papillary carcinoma?
Most common thyroid CA; radiation exposure. 70% of all thyroid CA. Women 3 times more than men. Second decade and later. Treatment is surgery or suppression with levothyroxine.
What is follicular carcinoma of the thyroid?
Follicular carcinoma accounts for 15% of thyroid cancers. Elderly women. More malignant than papillary carcinoma. Spreads hematogenously.
What is the treatment of follicular thyroid cancer?
Treatment is near–total thyroidectomy with postoperative radioiodine ablation.
What is anaplastic thyroid carcinoma?
10% of all thyroid cancer. Elderly women. Highly malignant, painful enlargement. Eighty percent of patients die.
What is medullary thyroid carcinoma?
5% of all thyroid cancers. More malignant than follicular carcinoma. Often produces calcitonin. Medullary carcinoma is a component of two types of multiple endocrine neoplasias.
What is the treatment of medullary thyroid cancer?
Treatment is thyroidectomy. Calcitonin levels can also be increased from cancer of the lung, pancreas, breast, and colon.
What are the clinical signs of thyroid carcinoma?
Growth of thyroid or mass with no tenderness or hoarseness. History of radiation. Men and elderly have a higher incidence of thyroid malignancy. Solitary; may produce calcitonin.
What is the significance of psammoma bodies in the thyroid?
Calcifications such as psammoma bodies suggest papillary carcinoma; increased density is associated with medullary carcinoma.
What is the significance of finding hyperthyroidism in association with a thyroid nodule?
Hyperthyroidism is never associated with cancer.
What is the diagnostic approach to solitary nonfunctioning nodule?
Fine–needle aspiration for cytology is the initial procedure. The first test for a thyroid nodule is the TSH; if TSH is normal, then proceed to an FNA. If TSH is low, the nodule is benign. Ultrasound to distinguish cysts.
What is the function of parathyroid hormone?
Maintains calcium concentration. PTH acts on bone and kidney, indirectly on intestine (effects synthesis 1,25–dihydroxy–cholecalciferol) to increase serum calcium. Regulated by serum–ionized calcium.
What is the effect of parathyroid hormone on the bones?
PTH increases osteoclast, which releases Ca. PTH inhibits PO4 reabsorption kidney which decreases PO4 and favors Ca release from bones. PTH activates vitamin D, increases GI Ca absorption. Calcitonin decreases Ca.
What is the most common cause of hypercalcemia?
Primary hyperparathyroidism. Hypercalcemia of malignancy caused by PTH–like protein. Sarcoidosis, Tb, berylliosis, histoplasmosis, coccidioidomycosis increase vitamin D.
What are the rare causes of hypercalcemia?
Rare causes: vitamin D, thiazides, lithium, Paget, immobilization, hyperthyroidism.
What are the signs of hypercalcemia?
Lethargy, confusion, constipation, anorexia, nausea, vomiting. Pancreatitis because of precipitation of Ca pancreas. Polyuria, polydipsia. Ca precipitates kidney, resulting in nephrolithiasis. HTN in 50%.
What are the ECG signs of hypercalcemia?
ECG shows short QT.
What is the treatment for hypercalcemia?
Saline or half–normal and furosemide, which promote calcium loss. Bisphosphonates such as alendronate, zoledronate, risedronate, pamidronate inhibit osteoclasts and stimulate osteoblasts. Calcitonin.
What are the causes of primary hyperparathyroidism?
Gland adenoma (80%). Parathyroid CA rare (
What the effects of hyperparathyroidism on bone?
Osteitis fibrosa cystica occurs because of osteoclastic bone resorption; bone pain, fractures, swelling, deformity, bone cysts, and brown tumors (punched–out lesions). One half asymptomatic.
How is primary hyperparathyroidism diagnosed?
Serum calcium >10.5 mg/dL, with elevated PTH level. In every other cause of hypercalcemia the PTH level will be low. Serum phosphate is low (
What is the management of primary hyperparathyroidism?
Removal of parathyroids. Bisphosphonates if surgery is contraindicated or if serum Ca
What are the causes of hypocalcemia?
Most common: hypoparathyroidism, renal failure, hyperphosphatemia, hypoMg. Loop diuretics, phenytoin, alendronate, foscarnet. Lack of renal activated 1,25–vitamin D, leads to decreased Ca absorption.
What are the signs of hypocalcemia?
Hypocalcemia results in neural hyperexcitability, seizures, tetany, circumoral numbness, and tingling. Cataracts.
What are the ECG signs of hypocalcemia?
Arrhythmias may develop because of a prolonged QT.
What is the most common cause of hypoparathyroidism?
Thyroidectomy. Low PTH levels are also seen in hereditary hypoparathyroidism and hypoMg. Mg deficiency prevents release of PTH. High PTH levels in renal failure because decreased active vitamin D.
What are the neurologic signs of hypoparathyroidism?
Neuromuscular irritability, tetany, laryngospasm, cramps, seizures, impaired memory. Chvostek sign: percussion of facial nerve contraction face. Trousseau: inflation of cuff elicits flexion metacarpophalangeal.
What are the cardiovascular signs of hypocalcemia?
QT prolongation, CHF, and/or hypotension. Circumoral tingling and tingling of the hands and feet.
How is hypoparathyroidism diagnosed?
Low calcium may be due to a low albumin. Ionized calcium is best test. PTH low. Low Ca with high PO4 can be due to renal failure, tissue destruction, hypoparathyroidism, pseudohypoparathyroidism.
What are the causes of a low calcium with low phosphorous?
Low calcium with low phosphorous is caused by low vitamin D.
What is the management of hypoparathyroidism?
Calcium gluconate IV. Maintenance oral calcium 2–4 g/d, vitamin D, and if there is hyperphosphatemia, diet restriction and phosphate binders (CaCO3).
What is the usual age of onset of type 1 diabetes?
The age of onset is usually
What is the usual age of onset of type 2 diabetes?
Usually >40; males > females. >20% of first–degree relatives are affected with 90–100% occurrence in identical twins. Obese.
What is the cause of type 2 diabetes?
90% of diabetes is type 2, caused by abnormal insulin secretion and resistance to insulin.
What are the clinical signs of diabetes?
Hyperglycemia causes polyuria, polydipsia, polyphagia, coma (ketoacidosis for type I diabetes and hyperosmolar coma for type 2 diabetes).
How is diabetes diagnosed?
Polyuria, polydipsia, ketonuria, weight loss, plasma glucose >200 mg/dL in these patients is sufficient for diagnosis. In asymptomatic patients, fasting plasma glucose 126 mg/dL on two occasions is diagnostic of diabetes.
What is glycosylated hemoglobin A1c?
HgA1c is condensation of glucose with free amino groups on Hb. It is used to follow glucose control. HgA1C is high in diabetics with chronic hyperglycemia during the preceding 8–12 weeks.
What is the glycosylated hemoglobin A1c goal?
The goal of therapy is to have an HgA1c
What is the management of type 2 diabetes?
Metformin in obese. Contraindicated: renal insufficiency. Does not cause hypoglycemia. If diabetes is not controlled with metformin, add a sulfonylurea; then either switch to insulin or add glitazone.
What is the dosage for insulin in type 2 diabetes?
0.5 U/kg, with two–thirds given AM (2/3 NPH, 1/3 reg) and one–third in PM (½ NPH, ½ reg). Glucose measurements before each meal and at bedtime.
What is the dosage for glargine insulin?
Once–a–day injection along with 2–3 times/day ultra short–acting insulin (such as lispro or aspart before meals). Glargine causes less hypoglycemia compared with NPH.
What is the acute complication of uncontrolled type 1 diabetes mellitus?
Diabetic ketoacidosis results from severe insulin insufficiency in type 1 diabetics. Precipitating factors of DKA include interrupted insulin therapy, infection, emotional stress, and excessive alcohol.
What are the clinical signs of diabetic ketoacidosis?
Anorexia, nausea, vomiting, abdominal pain, rapid breathing (Kussmaul), fruity breath odor (acetone), dry skin/mucous membranes, poor skin turgor, altered consciousness to coma. Arrhythmias, hyperkalemia fatal.
What is the treatment of diabetic ketoacidosis?
K is low because of the urinary loss of K. As soon as K
What acid–base disorder is associated with uncontrolled diabetes?
Elevated blood glucose, increased acetoacetate, acetone, hydroxybutyrate result in metabolic acidosis (low serum bicarbonate and low blood pH), and increased anion gap [sodium – (bicarbonate + chloride)].
What is hyperosmolar nonketotic coma?
HONK occurs in type 2 diabetes; severe hyperglycemia without ketosis. Precipitated by noncompliance plus inability to drink. Elderly, infections, strokes, steroids, immunosuppressants, diuretics.
What is the presentation of hyperosmolar nonketotic coma?
Profound dehydration results from hyperglycemic diuresis. Weakness, polyuria, polydipsia, lethargy, confusion, convulsions, and coma.
What are the laboratory findings in hyperosmolar nonketotic coma?
Elevated blood glucose (>1,000 mg/dL) and extremely high serum osmolality.
What is the treatment of hyperosmolar non–ketotic coma?
High–volume fluid and electrolyte replacement and insulin.
What are the chronic ocular complications of diabetes?
Retinopathy is the leading cause of blindness; background or proliferative (microaneurysms, hemorrhages, exudates, retinal edema).
What are the ophthalmic screening recommendations for diabetes?
Diabetics should be screened for retinopathy once a year. Proliferative retinopathy is treated with laser photocoagulation.
What are the renal complications of diabetes?
Nephropathy affects 40% of type 1 and 30% of type 2 diabetics. Proteinuria and end–stage renal disease can develop. Diffuse widening of glomerular basement membrane and mesangial thickening.
What is the treatment of diabetic nephropathy?
Management of nephropathy involves strict control of diabetes, angiotensin–converting enzyme inhibitors, and dialysis or renal transplantation.
What are the screening recommendations for proteinuria in diabetics?
All diabetics should be screened for proteinuria annually. Microalbuminuria is >30/day. Treated with ACE inhibitors. Diabetes is the most common cause of end stage renal disease.
What are the cardiovascular complications of diabetes?
75% of deaths in diabetes are from myocardial infarction, congestive failure, or stroke. Coronary artery bypass should be performed in a diabetic patient even if there is only two–vessel coronary disease.
What is the lipid management of diabetes?
Diabetes is equivalent of coronary disease for management of hyperlipidemia. The target LDL in a diabetes is 100 mg/dL. Statin for an LDL >100 mg/dL.
What is the management of diabetic retinopathy?
Screening for retinopathy annually. In type 1 diabetes, the first screening should take place 5 years after diagnosis, then annually. Proliferative retinopathy with vitreous hemorrhages or neovascularization is treated with laser.
What is the treatment of diabetic gastroparesis?
Metoclopramide or erythromycin.
What is the treatment of diabetic erectile dysfunction?
Occurs in 50% of patients after 10 years of diabetes. Treatment is sildenafil.
What is the screening for diabetic peripheral neuropathy?
Podiatric examination annually. Neuropathy leads to increased injury. Diabetes is responsible for 50% of all nontraumatic amputations.
What are the characteristics of diabetic peripheral neuropathy?
Peripheral neuropathy is symmetrical, with numbness, paresthesia, pain; absent reflexes and loss of vibratory. Mononeuropathy (mononeuritis multiplex) is foot drop, wrist drop, or paralysis of 3, 4, 6 cranial nerve.
What are the signs of diabetic autonomic neuropathy?
Difficulty swallowing, delayed gastric emptying (gastroparesis), constipation, or diarrhea. Bladder dysfunction or paralysis.
What is the treatment for peripheral neuropathy?
Analgesics, gabapentin, pregabalin, amitriptyline, and carbamazepine
What is the Somogyi effect?
Rebound hyperglycemia in the morning because of counterregulatory hormone release after hypoglycemia at night.
What is the dawn phenomenon?
Early morning rise in plasma glucose, requiring increased amounts of insulin to maintain euglycemia.
What are the symptoms of hypoglycemia?
Sweating, tremor, tachycardia, anxiety, hunger. Dizziness, headache, clouding vision, blunted mental, fine motor loss, confusion, abnormal behavior, convulsions, loss consciousness. Major symptoms
What are the causes of hypoglycemia?
Panhypopituitarism, adrenal insufficiency, enzyme defects, malnutrition, pregnancy, liver disease, alcohol, Popranolol, salicylates. Insulinoma, exogenous insulin, sulfonylureas, quinine, endotoxic shock, insulin receptor Ab.
What are the clinical signs of insulinoma?
Insulinoma (pancreatic B–cell tumor) can cause hypoglycemia. Benign symptoms of hypoglycemia are blurred vision, headache, feelings of detachment, slurred speech, and weakness.
How is insulinoma diagnosed?
Serum insulin level of >8 mg/mL in the presence of blood glucose values
What are the causes of factitious hyperinsulinism?
Administration of insulin or ingestion of Equal or oral sulfonylureas. It is common.
What are the laboratory abnormalities in factitious hyperinsulinism?
Hypoglycemia, high insulin and suppressed plasma C peptide is pathognomonic of exogenous insulin. Ethanol–hypoglycemia with starvation.
What is Cushing syndrome?
Group of abnormalities. Glucocorticoid therapy is most common cause. Others: adrenal hyperplasia, which can be caused by pituitary ACTH in pituitary dysfunction or pituitary ACTH–adenomas
What is Cushing disease?
Pituitary adenoma that secretes ACTH, causing hypercortisolism.
What percentage of Cushing syndrome is caused by ACTH–producing pituitary adenomas?
ACTH–producing pituitary adenomas cause 40% of Cushing cases.
What types of cancers can cause adrenal hyperplasia by producing ACTH?
ACTH or corticotropin–releasing hormone is secreted by bronchogenic, thymus, or pancreatic CA. Adrenal adenoma or carcinoma and adrenal nodular hyperplasia account for 30% Cushing.
What are the clinical signs of Cushing syndrome?
Moon face, buffalo hump, truncal obesity; HTN, weakness, osteoporosis; striae, bruises. Acne, hirsutism, oligomenorrhea. Depression, psychosis. Hyperglycemia, delayed healing, nephrolith; glaucoma, polyuria, infections.
What are the laboratory signs of Cushing syndrome?
Cushing’’s is associated with hypokalemia and leukocytosis. Hypokalemia occurs because of the mineralocorticoid effect of steroids.’
How is Cushing syndrome diagnosed?
1– mg overnight dexamethasone suppression test and the 24–hour urine free cortisol. The tests used to establish the etiology of the cortisol excess are the ACTH level, high–dose Dex suppress test, MRI.
What is the 1–mg overnight dexamethasone suppression test?
Best initial diagnostic test of glucocorticoid excess. Give dexamethasone 11 PM; cortisol at 8 AM should be normal. Single random cortisol levels are not reliable. Abnormal 1–mg test confirmed with 24h urine cortisol.
How is the etiology of the Cushing syndrome established?
ACTH levels are elevated with either a pituitary source of ACTH (adenoma or ectopic). If the ACTH level is low, then the etiology is adenoma, cancer, or adrenal hyperplasia.
When there is a high ACTH level, how is the precise etiology of Cushing syndrome determined?
MRI of the pituitary for an adenoma or a CT scan of the chest looking for an ectopic focus.
What is hyperaldosteronism?
Aldosterone reabsorbs sodium and excretes K and acid (H+). Hyperaldosteronism is caused by: primary aldosteronism from the adrenal; and secondary aldosteronism, in which the stimulus is extraadrenal.
What are the causes of primary hyperaldosteronism?
Unilateral adrenal adenoma (70%). Bilateral hyperplasia accounts for 25–30%. Excessive licorice ingestion (licorice has aldosterone–like qualities).
How is primary hyperaldosteronism diagnosed?
High urine aldosterone and low plasma renin levels confirm a diagnosis of primary hyperaldosteronism. High–salt diet before the test should suppress aldosterone. Confirm the diagnosis with a CT scan of the adrenals.
What is the treatment of bilateral adrenal hyperplasia?
Bilateral adrenal hyperplasia is treated with spironolactone, which blocks aldosterone.
What is Bartter syndrome?
Secondary hyperaldosteronism without edema or hypertension; defect in the loop of Henle; severe hypokalemic alkalosis, defect in renal conservation of sodium or chloride.
What is congenital adrenal hyperplasia?
Most common adrenal disorder of infancy and childhood. CAH is an autosomal recessive mutation, which produce deficiencies of enzymes that are necessary for the synthesis of cortisol.
What are the common enzymatic defects associated with congenital adrenal hyperplasia?
Enzymatic defects include alpha–21 hydroxylase deficiency in 95% of all cases. Alpha–21 hydroxylase deficiency is associated with reduction in aldosterone secretion in one third of patients.
What are the signs of congenital adrenal hyperplasia?
Adrenal virilization with salt–losing tendency caused by aldosterone deficiency (hyponatremia, hyperkalemia, dehydration, hypotension). Ambiguous genitalia, enlarged clitoris, labial fusion, virilization. Males have macrogenitosomia, precocious puberty.
How is congenital adrenal hyperplasia diagnosed?
Failure to thrive, adrenal insufficiency, salt wasting, HTN. Decreased testosterone, androstenedione, dehydroepiandrosterone, 17–hydroxy–progesterone, urinary 17–ketosteroid,, pregnanetriol.
What is the management of congenital adrenal hyperplasia?
Glucocorticoid (hydrocortisone) replacement.
What are the two types of adrenal deficiency disorders?
Adrenal insufficiency is divided into primary adrenocorticoid deficiency (Addison disease) and secondary failure in elaboration of ACTH. Primary adrenocortical insufficiency results from adrenal hypofunction.
What are the causes of Addison disease?
Caused by destruction of gland. Autoimmune destruction accounts for 80%. Destruction by surgical removal, Tb, fungal, CMV, Mycobacterium avium complex, hemorrhagic, trauma, metastatic invasion.
What are the clinical signs of Addison disease?
Weakness, paresthesias, cramping, stress intolerance, irritability. Small heart, wt loss, sparse axillary hair. Hyperpigmentation only with primary insufficiency. Addisonian crisis is fever, hypotension, low Na, high K, acidosis.
How is primary adrenocortical insufficiency diagnosed?
Rapid ACTH, then measurement of cortisol. Moderate neutropenia, lymphocytosis, eosinophilia; elevated K, BUN; low Na; low blood glucose; low plasma cortisol and urinary 17–hydroxycorticosteroid.
What is the cosyntropin or ACTH stimulation test?
A cortisol level is obtained before and after administering ACTH. A normal person should show a rise in cortisol level after ACTH administration.
What is the management of Addison disease?
Glucocorticoid, mineralocorticoid, and sodium chloride replacement.
What is an adrenal crisis?
Fever, vomiting, abdominal pain, altered mental, vascular collapse. Previously undiagnosed adrenal insufficiency after surgery, serious infection, stress; bilateral adrenal infarction/hemorrhage, withdrawal from glucocorticoids.
What is the treatment of adrenal crisis?
Measure cortisol level, then rapidly administer fluids and IV hydrocortisone.
What is pheochromocytoma?
Pheochromocytoma is a rare, usually benign, tumor that arises from the chromaffin cells of the sympathetic nerves. 90% in adrenals; 10% extraadrenal, 10% malignant, 10% in children, 10% bilateral, 10% not HTN.
What substances are secreted by pheochromocytomas?
Epinephrine secretion causes tachycardia, sweating, flushing, and hypertension. Norepinephrine is secreted by all extraadrenal pheochromocytomas.
What are the clinical signs of pheochromocytoma?
Paroxysms lasting a few minutes to several hours, with headache, profuse sweating, palpitations, and apprehension. Pain in the chest or abdomen, nausea and vomiting. Hypertension with tachycardia.
How is pheochromocytoma diagnosed?
24–h urine collection for free catecholamines, urinary metanephrines and vanillylmandelic acid, plasma catecholamine. Plasma metanephrine is initial test. Chromogranin levels correlate tumor size. CT/MRI.
What is the management of pheochromocytomas?
Control BP with alpha–adrenergic blocker (phentolamine, phenoxybenzamine). No other antihypertensive drugs should be used before adequate control of blood pressure. Surgery after BP stabilization.
What are the causes of primary hypogonadism?
Primary hypogonadism (hypergonadotropic: increased LH, FSH) from Klinefelter syndrome (small testes, eunuchoid, XXY), anorchia, castration or radiotherapy, mumps, TB, leprosy, or chemotherapeutic agents.
What are the causes of secondary hypogonadism?
Secondary hypogonadism (low LH, FSH) can result from hypopituitarism caused by idiopathic, tumors, hypothalamic lesions, Kallmann syndrome (hypergonadotrophic hypogonadism, decreased smell).
What are the clinical signs of prepubertal hypogonadism?
External genitalia are underdeveloped, voice is high–pitched, beard does not grow, lacks libido and potency. Youthful appearance, with obesity, long extremities, small Adam’’s apple, gynecomastia.’
What are the laboratory abnormalities in hypogonadism?
Urinary 17–ketosteroid is low to normal, and serum testosterone low. Serum FSH and LH are low in hypothalamic or pituitary origin and elevated in primary testicular failure. Treatment is testosterone.
What are the causes of postpubertal hypogonadism?
Pituitary lesion or testes damage by trauma, radiation, infection, drugs. Loss of libido, potency, hair; sterility. Testosterone low. FSH, LH are low with pituitary lesions and high with testicular failure. Rx testosterone.
What is Klinefelter syndrome?
1 of every 500 males. Caused by a supernumerary X chromosomes. 47,XXY. Gynecomastia with elevated levels of LH and FSH. Sterility and lack of libido. The testes are small. Mental retardation may be present.
What are the laboratory abnormalities in Klinefelter syndrome?
Urinary 17–ketosteroids are low normal; serum testosterone is low to normal, LH and FSH are elevated, and serum estradiol is elevated. 20x increased risk of breast cancer. Treatment is testosterone.
What are the basic synovial fluid tests?
Cell count, crystals, cultures, and Gram stain.
What are the synovial fluid cell count in osteoarthritis?
OA and traumatic arthritis have 200–2,000 white blood cells (WBC)/mm3 in the synovial fluid. Inflammatory diseases (RA, gout) have 5,000–50,000 WBC/mm3. Septic arthritis has >50,000 WBC/mm3.
What are antinuclear antibodies?
Antinuclear antibodies are Ab that bind to structures within nucleus. ANAs are found in SLE, Sjögren syndrome, and systemic sclerosis, and 5% of normal people.
How is the ANA test performed?
The ANA test is performed by exposing the antibodies in the serum to laboratory test cells. It is then determined whether the antibodies react with various parts of the nucleus.
What subsets of ANAs are associated with systemic lupus erythematosus?
Anti ds–DNA and anti–SM antibodies are found in patients with SLE; anti–histone antibodies are found in patients with drug–induced lupus.
What is the significance of a positive ANA test?
95% of SLE have positive ANA. Neg ANA excludes SLE. Pos ANA in asymptomatic patient is a false pos (5% of population); a positive ANA with arthritis, proteinuria, pleural effusion is likely SLE.
What are rheumatoid factors?
Autoantibody against Fc portion of IgG. RF found in 70% of RA. Not specific for RA and are found in 5% of healthy. RF is neither sensitive nor specific for the diagnosis of RA. High titers causes more aggressive disease.
What is the significance of a positive cyclic citrullinated peptide?
Cyclic citrullinated peptide is associated with rheumatoid arthritis.
What are antineutrophil cytoplasmic antibodies?
ANCAs are antibodies directed against cytoplasm of neutrophils in Wegener granulomatosis. Perinuclear ANCA is found in polyarteritis nodosa and Churg–Strauss syndrome.
What is antiphospholipid antibody syndrome?
Hypercoagulable state with Ab against phospholipids or cardiolipins (lupus anticoagulant or anticardiolipin antibodies). Elevated PTT, false–positive VDRL.
What is the presentation of antiphospholipid antibody syndrome?
Presents with spontaneous abortions or thromboembolism. If two first–trimester spontaneous abortions occur, antiphosolipid antibodies should be checked.
A 28–year–old woman with joint swelling and stiffness. Stiffness for 2 h in morning. Fatigue, fever. Wrist, MCPs, and PIPs red and swollen. DIPs are not involved. Fluid in wrist joints. What is the diagnosis?
Rheumatoid arthritis.
What is rheumatoid arthritis?
Chronic, symmetric, inflammatory synovitis. Inflammation destroys cartilage and causes bone erosions, deforming joint. Triggered by infectious agent. Women 3x more than men; 35–50 years.
What is the diagnostic criteria for rheumatoid arthritis?
4 of the following: Morning stiffness. Swelling of wrists, MCPs, PIPs. Swelling of three joints. Symmetric joint swelling. Joint erosions on x–rays. RF positive. Rheumatoid nodules.
