1 Flashcards
(495 cards)
1
Q
When should screening for colon cancer begin in the patient with no family history of colon cancer?
A
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.
2
Q
What are the screening mammography recommendations for breast cancer?
A
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.
3
Q
What is the prophylaxis for hepatitis A for travelers?
A
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.
4
Q
Which travelers should receive hepatitis B vaccine?
A
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.
5
Q
What is the recommended prophylaxis for malaria for travelers?
A
Traveling to Mexico, Central America (except Panama), or Caribbean, chloroquine is prophylaxis for malaria. For travelers to areas where chloroquine resistance common, mefloquine recommended.
6
Q
At what age is meningococcal vaccine usually given?
A
Meningococcal is routinely given at age 11.
7
Q
What are the recommendations for prevention of traveler’’s diarrhea?’
A
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.
8
Q
What are the recommendations for tetanus and diphtheria vaccination in adults who were never vaccinated?
A
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.
9
Q
What are the recommendations for influenza vaccination?
A
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.
10
Q
What are the indications for pneumococcal vaccination?
A
Adults >65; sickle–cell, splenectomy, cardiopulmonary disease, alcoholism, cirrhosis, Alaskan natives, Native Americans; immunocomp (heme malignancies, CRF, nephrotic, HIV; immunosuppressives).
11
Q
What are the indications for hepatitis B vaccination?
A
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.
12
Q
What are the recommendations for hepatitis A vaccine?
A
Hepatitis A vaccine is recommended for travelers to endemic areas, day–care employees, homosexual men, and chronic liver disease.
13
Q
What are the indications for varicella vaccine?
A
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.
14
Q
What are the recommendations for measles, mumps, rubella vaccine?
A
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.
15
Q
What are the recommendations for osteoporosis screening?
A
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.
16
Q
What are the recommendations for screening for abdominal aortic aneurysm?
A
Ultrasound should be given once in male smokers older than age 65.
17
Q
What are the recommendations for cholesterol screening?
A
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.
18
Q
What are the recommendations for screening for diabetes?
A
Obesity, impaired fasting glucose, African–Americans, native Americans and/or positive family history.
19
Q
What is the criteria for the diagnosis of diabetes?
A
Diabetes mellitus is diagnosed when two fasting are greater than 126 mg/dL, or when a random glucose is >200 mg/dL.
20
Q
What clinical test should be used to screen for alcohol abuse?
A
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
21
Q
What pathological conditions are associated with hyperprolactinemia?
A
Excess of prolactin occurs with prolactinomas (most common functioning pituitary adenomas, 60% of pituitary tumors.
22
Q
What medications cause hyperprolactinemia?
A
Decreased inhibitory action of dopamine caused by drugs that block dopamine synthesis (phenothiazines, metoclopramide) and dopamine–depleting agents (alpha–methyldopa).
23
Q
What is the presentation of hyperprolactinemia?
A
Women have galactorrhea, amenorrhea/oligomenorrhea, osteoporosis, infertility, gynecomastia; men have hypogonadism, erectile dysfunction, decreased libido, gynecomastia and infertility.
24
Q
How is hyperprolactinemia diagnosed?
A
Always exclude pregnancy, lactation, hypothyroidism and medications before starting the evaluation of hyperprolactinemia. Prolactin levels >100 ng/mL suggest probable pituitary adenoma.
25
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.
26
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.
27
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.
28
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.
29
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.
30
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.
31
How is hypopituitarism diagnosed?
Measure GH, TSH, LH, and insulin–like–GF1.
32
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.
33
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.
34
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.
35
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.
36
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.
37
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.
38
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.
39
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.
40
How is nephrogenic diabetes insipidus differentiated from central diabetes insipidus?
ADH levels will be low in central DL and high in nephrogenic DL.
41
What is the differential diagnosis of diabetes insipidus?
Psychogenic polydipsia, drug–induced polydipsia from chlorpromazine, anticholinergic drugs, or thioridazine, and hypothalamic diseases.
42
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.
43
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.
44
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.
45
What are the CNS signs of SIADH?
Cerebral edema from hyponatremia causes irritability, confusion, seizures, coma.
46
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.
47
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.
48
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.
49
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.
50
What are the signs of thyrotoxicosis?
Graves disease, diffuse goiter, exophthalmos, dermopathy. More in women in the fourth decade.
51
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.
52
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).
53
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.
54
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.
55
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.
56
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.
57
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.
58
What is the treatment for thyroid storm?
Glucose, hydration, glucocorticoids, oxygen, cooling blanket. Propylthiouracil, beta–blockers, and iodine inhibit hormone release.
59
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.
60
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.
61
What is the most common cause of goitrous hypothyroidism?
Hashimoto disease is most common cause of goitrous hypothyroidism.
62
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.
63
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.
64
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).
65
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.
66
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.
67
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.
68
What is the treatment of subacute thyroiditis?
Aspirin, prednisone, and Popranolol.
69
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.
70
What are the clinical signs of Hashimoto thyroiditis?
Goiter that is painless, rubbery and hypothyroidism.
71
How is Hashimoto thyroiditis diagnosed?
TSH increases, and T4 and T decrease. Antimicrosomal and antithyroperoxidase antibodies.
72
What is the management of Hashimoto thyroiditis?
Replacement with L–thyroxine (T4).
73
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.
74
What is Reidel thyroiditis?
Fibrosis of the thyroid and mediastinal and retroperitoneal fibrosis.
75
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.
76
What is follicular carcinoma of the thyroid?
Follicular carcinoma accounts for 15% of thyroid cancers. Elderly women. More malignant than papillary carcinoma. Spreads hematogenously.
77
What is the treatment of follicular thyroid cancer?
Treatment is near–total thyroidectomy with postoperative radioiodine ablation.
78
What is anaplastic thyroid carcinoma?
10% of all thyroid cancer. Elderly women. Highly malignant, painful enlargement. Eighty percent of patients die.
79
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.
80
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.
81
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.
82
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.
83
What is the significance of finding hyperthyroidism in association with a thyroid nodule?
Hyperthyroidism is never associated with cancer.
84
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.
85
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.
86
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.
87
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.
88
What are the rare causes of hypercalcemia?
Rare causes: vitamin D, thiazides, lithium, Paget, immobilization, hyperthyroidism.
89
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%.
90
What are the ECG signs of hypercalcemia?
ECG shows short QT.
91
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.
92
What are the causes of primary hyperparathyroidism?
Gland adenoma (80%). Parathyroid CA rare (
93
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.
94
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 (
95
What is the management of primary hyperparathyroidism?
Removal of parathyroids. Bisphosphonates if surgery is contraindicated or if serum Ca
96
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.
97
What are the signs of hypocalcemia?
Hypocalcemia results in neural hyperexcitability, seizures, tetany, circumoral numbness, and tingling. Cataracts.
98
What are the ECG signs of hypocalcemia?
Arrhythmias may develop because of a prolonged QT.
99
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.
100
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.
101
What are the cardiovascular signs of hypocalcemia?
QT prolongation, CHF, and/or hypotension. Circumoral tingling and tingling of the hands and feet.
102
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.
103
What are the causes of a low calcium with low phosphorous?
Low calcium with low phosphorous is caused by low vitamin D.
104
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).
105
What is the usual age of onset of type 1 diabetes?
The age of onset is usually
106
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.
107
What is the cause of type 2 diabetes?
90% of diabetes is type 2, caused by abnormal insulin secretion and resistance to insulin.
108
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).
109
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.
110
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.
111
What is the glycosylated hemoglobin A1c goal?
The goal of therapy is to have an HgA1c
112
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.
113
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.
114
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.
115
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.
116
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.
117
What is the treatment of diabetic ketoacidosis?
K is low because of the urinary loss of K. As soon as K
118
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)].
119
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.
120
What is the presentation of hyperosmolar nonketotic coma?
Profound dehydration results from hyperglycemic diuresis. Weakness, polyuria, polydipsia, lethargy, confusion, convulsions, and coma.
121
What are the laboratory findings in hyperosmolar nonketotic coma?
Elevated blood glucose (\>1,000 mg/dL) and extremely high serum osmolality.
122
What is the treatment of hyperosmolar non–ketotic coma?
High–volume fluid and electrolyte replacement and insulin.
123
What are the chronic ocular complications of diabetes?
Retinopathy is the leading cause of blindness; background or proliferative (microaneurysms, hemorrhages, exudates, retinal edema).
124
What are the ophthalmic screening recommendations for diabetes?
Diabetics should be screened for retinopathy once a year. Proliferative retinopathy is treated with laser photocoagulation.
125
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.
126
What is the treatment of diabetic nephropathy?
Management of nephropathy involves strict control of diabetes, angiotensin–converting enzyme inhibitors, and dialysis or renal transplantation.
127
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.
128
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.
129
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.
130
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.
131
What is the treatment of diabetic gastroparesis?
Metoclopramide or erythromycin.
132
What is the treatment of diabetic erectile dysfunction?
Occurs in 50% of patients after 10 years of diabetes. Treatment is sildenafil.
133
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.
134
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.
135
What are the signs of diabetic autonomic neuropathy?
Difficulty swallowing, delayed gastric emptying (gastroparesis), constipation, or diarrhea. Bladder dysfunction or paralysis.
136
What is the treatment for peripheral neuropathy?
Analgesics, gabapentin, pregabalin, amitriptyline, and carbamazepine
137
What is the Somogyi effect?
Rebound hyperglycemia in the morning because of counterregulatory hormone release after hypoglycemia at night.
138
What is the dawn phenomenon?
Early morning rise in plasma glucose, requiring increased amounts of insulin to maintain euglycemia.
139
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
140
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.
141
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.
142
How is insulinoma diagnosed?
Serum insulin level of \>8 mg/mL in the presence of blood glucose values
143
What are the causes of factitious hyperinsulinism?
Administration of insulin or ingestion of Equal or oral sulfonylureas. It is common.
144
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.
145
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
146
What is Cushing disease?
Pituitary adenoma that secretes ACTH, causing hypercortisolism.
147
What percentage of Cushing syndrome is caused by ACTH–producing pituitary adenomas?
ACTH–producing pituitary adenomas cause 40% of Cushing cases.
148
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.
149
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.
150
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.'
151
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.
152
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.
153
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.
154
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.
155
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.
156
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).
157
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.
158
What is the treatment of bilateral adrenal hyperplasia?
Bilateral adrenal hyperplasia is treated with spironolactone, which blocks aldosterone.
159
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.
160
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.
161
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.
162
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.
163
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.
164
What is the management of congenital adrenal hyperplasia?
Glucocorticoid (hydrocortisone) replacement.
165
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.
166
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.
167
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.
168
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.
169
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.
170
What is the management of Addison disease?
Glucocorticoid, mineralocorticoid, and sodium chloride replacement.
171
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.
172
What is the treatment of adrenal crisis?
Measure cortisol level, then rapidly administer fluids and IV hydrocortisone.
173
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.
174
What substances are secreted by pheochromocytomas?
Epinephrine secretion causes tachycardia, sweating, flushing, and hypertension. Norepinephrine is secreted by all extraadrenal pheochromocytomas.
175
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.
176
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.
177
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.
178
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.
179
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).
180
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.'
181
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.
182
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.
183
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.
184
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.
185
What are the basic synovial fluid tests?
Cell count, crystals, cultures, and Gram stain.
186
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.
187
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.
188
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.
189
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.
190
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.
191
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.
192
What is the significance of a positive cyclic citrullinated peptide?
Cyclic citrullinated peptide is associated with rheumatoid arthritis.
193
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.
194
What is antiphospholipid antibody syndrome?
Hypercoagulable state with Ab against phospholipids or cardiolipins (lupus anticoagulant or anticardiolipin antibodies). Elevated PTT, false–positive VDRL.
195
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.
196
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.
197
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.
198
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.
199
Which joints are never involved in rheumatoid arthritis?
Distal interphalangeal joints and joints of the lower back.
200
What are the systemic symptoms of rheumatoid arthritis?
Two–thirds of the patients present with fatigue, anorexia, weight loss, generalized weakness before the onset of the arthritis.
201
What are the extraarticular manifestations of rheumatoid arthritis?
Damage to the ligaments and tendons. Radial deviation of the wrist with ulnar deviation of the digits. Boutonniere deformity. Swan–neck deformity. Rheumatoid nodules.
202
What are the laboratory findings in rheumatoid arthritis?
Rheumatoid factor, anemia, increased ESR, X–rays erosions.
203
What is the initial treatment for rheumatoid arthritis?
Nonsteroidal antiinflammatory drugs (NSAIDs) have fewer side effects than aspirin.
204
What is the mechanism of selective COX–2 inhibitors?
Cyclooxygenase 2 inhibitors selectively block the COX–2 enzyme at the site of inflammation. Benefit of COX–2 inhibitors is not inhibiting COX–1, an enzyme that produces protective stomach lining.
205
What is the mechanism of action of nonselective NSAIDS?
Nonselective of NSAIDs block both COX–2 and COX–1, which can lead to increased risk for gastrointestinal side effects (bleeding).
206
What is the beneficial effect of selective NSAID COX–2 inhibitors?
Selective COX–2 inhibitors (celecoxib) reduce risk of gastric ulcers, but COX–2 inhibitors double risk of MI and stroke because COX–2 enzyme creates protective fatty acids that prevent thromboses.
207
What is the treatment of rheumatoid arthritis that does not respond to NSAIDs?
Glucocorticoids. Disease–modifying agents: antimalarials, gold, sulfasalazine, methotrexate, and tumor necrosis factor receptor inhibitors: infliximab (Remicade), adalimumab (Humira), etanercept (Enbrel)
208
What is atlantoaxial subluxation?
Occurs in rheumatoid arthritis when there is excessive movement between atlas (Cl) and axis (C2). Neck pain, C2 radicular pain (hands), myelopathy, paraplegia, quadriplegia.
209
What is a ruptured Baker cyst?
Extension of inflamed synovium into the popliteal space; swollen, painful calf.
210
34–year–old woman with confusion, malar rash, HTN, symmetrical joint swelling of wrists and MCPs. Creatinine of 2.5, proteinuria. What is the diagnosis?
Systemic lupus erythematosus.
211
What is systemic lupus erythematosus?
Systemic disease in which tissues and multiple organs are damaged by autoantibodies and immune complexes. Ninety percent of cases are women. Ultraviolet light may cause flares.
212
What is the diagnostic criteria for systemic lupus erythematosus?
4 required: malar/discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal; neurologic (seizures, psychosis); hematologic (hemolysis, leukopenia); immunologic (ANA).
213
What are the skin manifestations of systemic lupus erythematosus?
Malar rash and photosensitivity (diffuse, maculopapular) flare with exposure to UV–B light and resolve with no scarring. Discoid lupus is a circular rash with a raised rim over scalp and face; central atrophy and scarring.
214
What are the joint manifestations of systemic lupus erythematosus?
Arthritis is systemic, non–erosive of wrists, MCPs, PIPs.
215
What are the psychiatric manifestations of systemic lupus erythematosus?
Change in personality and psychosis with CNS lupus. Libman–Sacks endocarditis is noninfectious endocarditis that is rare in lupus
216
What are the laboratory findings in lupus?
Positive ANA supports diagnosis but is not specific. Complement levels are decreased in lupus. ds–DNA antibodies with active lupus are very specific: increase likelihood of nephritis, and active SLE.
217
What is the treatment for systemic lupus?
NSAIDs for arthritis, pleurisy. Corticosteroid for rashes. Hydroxychloroquine and corticosteroids for arthritis. Cytotoxics (azathioprine, cyclophosphamide) for nephritis, carditis, pleuritis. Sunscreen.
218
What drugs cause drug–induced lupus?
Hydralazine, isoniazid, procainamide, quinidine.
219
What is the presentation of drug–induced lupus?
Arthritis, fatigue, fever, and rarely pleurisy. There is no skin disease, kidney disease, and milder symptoms than SLE. Causes positive ANA. Symptoms resolve within 2 weeks.
220
35–year–old woman with skin tightness and painful fingertips with exposure to cold. BP 170/100; shiny, thickened skin. Elevated creatinine. What is the diagnosis?
Scleroderma.
221
What is systemic sclerosis?
Thickening of the skin caused by accumulation of connective tissue; involvement of GI, lungs, kidneys. All scleroderma patients have Raynaud phenomenon.
222
What are the gastrointestinal signs of systemic sclerosis?
Esophageal dysmotility and achalasia, hypomotility of the small intestine with bacterial overgrowth and malabsorption, and dilatation of the large intestine with diverticula.
223
What are the pulmonary manifestations of scleroderma?
Pulmonary fibrosis with restrictive lung disease and cor pulmonale.
224
What are the renal manifestations of scleroderma?
Renal crisis in which malignant hypertension acute renal failure. Treated with angiotensin–converting enzyme inhibitors.
225
What is limited scleroderma (CREST syndrome)?
Variant of scleroderma: Calcinosis, Raynaud, Esophageal dysfunction, Sclerodactyly, Telangiectasias. Calcium deposits in fingers, knees, elbows, ulcerate. Sclerodactyly is skin thickening of fingers, toes.
226
What are the laboratory findings in limited scleroderma?
Limited scleroderma has positive ANA test. Antibodies to Sc–70 are negative in limited scleroderma and positive in diffuse scleroderma.
227
What is Raynaud phenomenon?
Pallor, cyanosis in cold. Vasoconstriction. Raynaud disease is not associated underlying disease. Secondary Raynaud phenomenon is associated with disease (scleroderma). 5% population Raynaud disease. Young women.
228
What is the treatment for systemic sclerosis?
No cure. D–penicillamine may be used. Raynaud phenomenon: use calcium–channel blockers; for hypertension use angiotensin–converting enzyme inhibitors.
229
A 43–year–old woman with dry eyes and sensation of sand in her eyes; painful swallowing. Parotid enlargement. ANA positive. What is the diagnosis?
Sjögren syndrome.
230
What is Sjögren syndrome?
Autoimmune lymphocytic infiltration of exocrine glands; xerostomia, dry eyes. Sjögren syndrome may be primary or with autoimmune diseases (secondary), RA or SLE. Lungs, kidneys, malignant lymphoma.
231
What is the presentation of Sjögren syndrome?
Itchy eyes, sandy feeling under their eyes destruction of the corneal epithelium (keratoconjunctivitis sicca), and dysphagia.
232
What are diagnostic tests for Sjögren syndrome?
Schirmer''s test shows decreased tear production. ANA positive; anti–Ro (SSA) and anti–La (SSB) are positive. Treatment is artificial tears.'
233
Which autoimmune diseases have arthritis plus multiple organ involvement?
SLE, systemic sclerosis (scleroderma), and Sjögren syndrome.
234
25–year–old man with lower back stiffness and pain in morning \>2 h, improving with exercise. Murmur over second right intercostal space and decreased range–of–motion of lumbar spine. What is the diagnosis?
Ankylosing spondylitis.
235
What allele is associated with the spondyloarthropathies?
B–27 allele.
236
What is ankylosing spondylitis?
Inflammatory disorder that affects axial skeleton and peripheral joints. Second to third decade (rare after 40). Men 3–4 times that of women. Positive for HLA B–27.
237
What is the presentation of ankylosing spondylitis?
Chronic lower back pain, young man (20s–30s). Morning stiffness 1 h, improves with exercise. Cervical spine not affected. Anterior uveitis, aortic insufficiency, CHF, heart block. Decreased spine mobility, fractures.
238
What are the x–ray abnormalities in ankylosing spondylitis?
Sacroiliitis and fusing of the sacroiliac joint. Bamboo spine and squaring of the vertebral bodies.
239
What is the treatment for ankylosing spondylitis?
NSAIDs, physical therapy, exercise. TNF blockers (infliximab, adalimumab, etanercept).
240
What is reactive arthritis?
Seronegative arthropathy after infection, non–gonococcal urethritis. Keratoderma blennorrhagica (waxy, palms/soles), circinate balanitis, oral/genital ulcers, conjunctivitis, arthritis. Campylobacter, Salmonella.
241
What is the treatment for reactive arthritis?
Severe form of reactive arthritis in HIV patients improves with antiretroviral medications. NSAIDS, tumor necrosis factor blockers.
242
What is psoriatic arthritis?
Arthritis involves the DIP joints and associated with psoriatic nail disease (pitting of the nails); sausage–shaped digit.
243
What is enteropathic arthropathy?
Joint arthropathy with ulcerative colitis or Crohn disease; associated with pyoderma gangrenosum and erythema nodosum.
244
A 66–year–old man with knee pain and pain in distal interphalangeal joints. Knee crepitations. What is the diagnosis?
Osteoarthritis
245
What is osteoarthritis?
Most common joint disease. Articular cartilage destruction with hypertrophy of bone. Osteoarthritis, unlike RA, is not an inflammatory disease. Knee osteoarthritis is leading cause of chronic disability in elderly.
246
What are the major risk factors for osteoarthritis?
Age, female sex, genetic factors, major joint trauma, repetitive stress, and obesity. The most common joint to be affected is the knee; base of the thumb.
247
What is the presentation of osteoarthritis?
Weight–bearing joints (hip, knee), small finger joints (PIPs, DIPs). Oligoarticular–asymmetric. Progressive, irreversible. Pain with exercise, relieved by rest. Morning stiffness
248
What X–ray findings are associated with osteoarthritis?
Osteophytes and unequal joint space PIP osteophytes are called Bouchard''s nodes, in the DIP are called Heberden''s nodes.'
249
What is the treatment of osteoarthritis?
Acetaminophen, analgesic ibuprofen is 1,200 mg/d, antiinflammatory dose is 2,400 mg/d. Caution in elderly with NSAIDs. COX–2 inhibitors may be used in patients at high risk for ulcers (celecoxib).
250
What are the crystal–induced arthropathies?
Monosodium urate, calcium pyrophosphate, calcium oxalate, calcium hydroxyapatite caused by deposition in joints; they have identical presentations and can only be distinguished by synovial fluid analysis.
251
What is gout?
Gout affects middle–aged men and presents with acute monoarthritis. Deposition of urate crystals in connective tissue (tophi) and kidneys.
252
What is the presentation of acute gout?
First toe is commonly affected (podagra); knee, ankle, PIPs, or DIPs may be initially involved. First episode occurs at night with severe joint pain. Warm, red, tender. Pain resolves within 3–14 days.
253
What are the factors that can precipitate gout?
Excessive alcohol, trauma, surgery, infection, steroid withdrawal, hydrochlorothiazide, furosemide; pyrazinamide and ethambutol, and serious medical illnesses.
254
How is gout diagnosed?
Uric acid maybe normal. Many have elevated uric acid levels and never develop gout. Serum uric acid level is of no value in diagnosis of gout. Synovial fluid: negatively birefringent needles. WBCs 5000–50000.
255
What is the treatment of acute gouty arthritis?
Indomethacin 50 mg three times a day. Colchicine, 0.6 mg every hour until symptoms resolve. Steroids, intraarticular or oral in elderly patients who cannot tolerate NSAIDs, colchicine or in renal impairment.
256
What is the treatment of recurrent gouty attacks?
Hypouricemic therapy in recurrent gouty. Probenecid used in undersecretors (\>80%). Allopurinol in overproducers, undersecretors, with renal failure/stones. Allopurinol should not be initiated during attack.
257
What is pseudogout?
Calcium pyrophosphate crystal deposition is more common in the elderly population and preexisting joint damage. Hyperparathyroidism, hemochromatosis, hypophosphatemia, hypomagnesemia.
258
What are the clinical signs of pseudogout?
The knee is the most commonly affected joint; other joints are the wrist, shoulder, and ankle.
259
How is pseudogout diagnosed?
Rhomboid, positive birefringent crystals on synovial fluid evaluation. Linear radiodense deposits in joint menisci or articular cartilage (chondrocalcinosis).
260
What is the treatment for calcium pyrophosphate crystal deposition disease?
NSAIDS, colchicine, corticosteroid. Prevent frequent recurrences with low doses of colchicine.
261
A 65–year–old woman with history of rheumatoid arthritis with left shoulder pain for 2 days; low–grade fever. decreased range of motion, erythema. What is the next step?
Perform arthrocentesis
262
What is the most common cause of infectious arthritis in patients younger than 40 years old?
Gonorrhea, which accounts for 70% of episodes in patients younger than 40 years old.
263
What is the most common cause of infectious arthritis in older patients?
Staphylococcus aureus is most common cause of infectious arthritis and occurs in preexisting joint destruction from other rheumatic diseases. RA is highest risk.
264
What are the synovial fluid findings in gonococcal infectious arthritis?
Infected joints with gonococci will not have positive cultures, and the Gram stain will be negative.
265
What treatment should be prescribed for a young woman with acute monoarticular arthritis with \>50,000 WBCs in synovial fluid without crystals?
A young woman with acute monoarticular arthritis who is found to have \>50,000 WBCs in the synovial fluid without crystals should be treated with ceftriaxone.
266
What treatment should be ordered for an elderly man with RA and acute monoarticular arthritis and \>50,000 WBCS in synovial fluid?
An elderly man with infectious arthritis should be treated with IV nafcillin or vancomycin.
267
What is Wegener granulomatosis?
Small vessel vasculitis of any organ, but mainly the sinuses, nose, trachea, lungs and kidneys. Rhinitis, sinusitis, and nasal ulcers. Cough, hemoptysis, and dyspnea. Kidney involvement in 80%. Arthritis in 60%.
268
How is Wegener granulomatosis diagnosed?
Associated with antineutrophil cytoplasmic antibodies (C–ANCA). Confirm diagnosis by biopsy of an involved organ (nasal septum), vasculitis and granulomas.
269
What is the treatment of Wegener granulomatosis?
Glucocorticoid and immunosuppressive agent (cyclophosphamide).
270
What is polyarteritis nodosa?
Multisystem disease with fever, malaise, weight loss, anorexia, and abdominal pain. Affects any site in the body, except the lungs. Predisposition for skin, kidney, nerves, GI.
271
What is the presentation of polyarteritis nodosa?
Peripheral neuropathies. abdominal pain and gastrointestinal bleeding. Biopsy of skin, symptomatic nerves, or muscles medium–size arteritis.
272
What is the treatment of polyarteritis nodosa?
Corticosteroids, immunosuppressive drugs (cyclophosphamide).
273
What is Churg–Strauss syndrome?
Vasculitis can involve any organ; asthma, eosinophilia, lung involvement.
274
What is the presentation of Churg–Strauss syndrome?
Middle aged individual with new–onset asthma, mononeuropathy, transient pulmonary infiltrates, paranasal sinus abnormalities, nasal polyps, allergic rhinitis.
275
What are the biopsy findings in Churg–Strauss syndrome?
Biopsy: medium arteritis. Treatment is prednisone and cytotoxic agent.
276
What is temporal arteritis?
Temporal arteritis is a vasculitis of large arteries that supply the head, eyes, and optic nerves. New–onset headache in any patient older than 50 years; may cause permanent vision loss.
277
What is the presentation of temporal arteritis?
Headache, pain in temples. Scalp tenderness, jaw claudication, decreased vision, tongue numbness, sudden loss of vision. 25% also have polymyalgia rheumatica.
278
How is temporal arteritis diagnosed?
ESR is first test (100% sensitive); always confirm by biopsy of temporal artery for giant cells. If temporal arteritis is suspected and the ESR elevated, prednisone should be started immediately (before biopsy).
279
A 73–year–old woman with new right–sided headache, fever, decreased vision. What is the first step?
Check the ESR; if elevated, start prednisone 60 mg daily.
280
43–year–old woman with proximal weakness for 2 months. Diffuse lilac rash over sun–exposed areas. Weakness in upper and lower proximal muscles. CPK and aldolase positive. What is the diagnosis?
Dermatomyositis
281
What are the inflammatory myopathies?
Inflammatory muscle diseases with progressive muscle weakness. Polymyositis, dermatomyositis, and inclusion body myositis.
282
What are the clinical signs of inflammatory myopathies?
Proximal muscle weakness: lifting objects, combing hair, rising from chair. Ocular muscles never involved, which differentiates inflammatory myopathies from myasthenia.
283
What is the presentation of dermatomyositis?
Dermatomyositis will have weakness with heliotrope rash, which is a purple–lilac discoloration of the face, eyelids, and sun–exposed areas of body.
284
What are the laboratory findings in inflammatory myopathies?
Inflammatory destruction of muscles causes an elevation of the muscle enzymes creatine kinase and aldolase. EMG shows of myopathic potentials; confirmed by biopsy.
285
What is the treatment for polymyositis and dermatomyositis?
Steroids are useful in polymyositis and dermatomyositis.
286
What is achalasia?
Idiopathic loss of nerves of lower esophageal sphincter; inhibitory neurons lost, inability to relax LES. Unknown etiology. Very small number can be from Chagas disease, gastric carcinoma, lymphoma.
287
What is the presentation of achalasia?
Achalasia presents with progressive dysphagia to both solids and liquids; regurgitation.
288
How is achalasia diagnosed?
Barium esophagography shows dilation of esophagus, which narrows into bird''s beak at end. Esophageal manometry shows increased lower esophageal sphincter resting pressure. Treatment is dilation.'
289
A 65–year–old man with difficulty swallowing solids, weight loss. reflux esophagitis, smoking, enlarged left supraclavicular lymph node. What is the diagnosis?
Esophageal cancer.
290
What are the causes of esophageal cancer?
Alcohol, tobacco for squamous cell cancer in proximal two–thirds of esophagus. Adenocarcinoma in the distal third, associated with gastroesophageal reflux disease and Barretts esophagus.
291
What is the presentation of esophageal cancer?
Progressive dysphagia first for solid food, then liquids, weight loss. Halitosis, regurgitation, hoarseness, and hypercalcemia.
292
How is esophageal cancer diagnosed?
Barium swallow first; endoscopy is mandatory for biopsy. CT scan assesses local spread; bronchoscopy detects spread into the bronchi. Endoscopic ultrasound for staging.
293
What is the presentation of esophageal spasm?
Intermittent chest pain, dysphagia, with no relationship to exertion or eating. The pain is precipitated by drinking cold liquids.
294
How is esophageal spasm diagnosed?
Barium studies show a corkscrew pattern. The most accurate test is manometric studies.
295
What is the treatment of esophageal spasm?
Nifedipine and nitrates.
296
What is Schatzki''s ring?'
Schatzki''s rings are thin, epithelial membranes; intermittent dysphagia; painless. More distal and located at the squamocolumnar junction proximal to the lower esophageal sphincter.'
297
What is Plummer–Vinson syndrome?
Plummer–Vinson syndrome causes a more proximal ring in the hypopharynx. Associated with iron–deficiency anemia and progression to squamous cell cancer. Middle–aged women.
298
How is Plummer–Vinson syndrome diagnosed?
Diagnosed with a barium swallow.
299
What is the treatment of Plummer–Vinson syndrome?
May respond to treatment of iron deficiency. Dilation procedures are used.
300
What is the most common infectious cause of esophagitis?
Candida albicans. HIV positive with a CD4
301
What is the treatment of esophagitis?
If the patient is HIV positive, empiric treatment is with fluconazole.
302
What medications are associated with esophagitis?
Pills that cause esophagitis are alendronate, quinine, risedronate, vitamin C, potassium chloride, doxycycline, NSAIDs, and iron sulfate.
303
What is a Zenker diverticulum?
Outpocketing of posterior pharynx. Older patients have bad breath and difficulty initiating swallowing. Repeated clearing of throat; regurgitation of food eaten several days ago.
304
How is Zenker diverticulum diagnosed?
The diagnosis is made by barium studies. Treated with surgical resection.
305
What is Mallory–Weiss syndrome?
Tear of the lower esophagus caused by retching and vomiting. Painless upper gastrointestinal bleeding. Melena or hematemesis. Diagnosed by upper endoscopy.
306
What is the treatment for Mallory–Weiss tears?
Resolve spontaneously. Injection of the tear with epinephrine or cauterization.
307
What are the causes of epigastric pain?
Ulcer disease, pancreatitis, gastroesophageal reflux disease, gastritis, and gastric cancer.
308
What organism causes gastric ulcers, duodenal ulcers, and gastritis?
Helicobacter pylori is most strongly associated with the development of duodenal ulcers, gastric ulcers, and gastritis.
309
What is the most common cause of epigastric tenderness?
Pancreatitis is the most common cause for epigastric tenderness and pain. Ulcer disease is associated with epigastric tenderness in
310
What is the most common cause of epigastric pain?
The most common etiology of epigastric pain is nonulcer dyspepsia, a functional disorder of persistent pain with normal tests.
311
How is Helicobacter pylori disease diagnosed?
H. pylori can be diagnosed with serology, urea breath testing, stool antigen detection. Endoscopy not needed, but biopsy and is the most accurate. When testing for eradication, use breath test or stool antigen.
312
When is endoscopy indicated for patients with ulcer disease?
All patients with epigastric pain and \>45 years or alarm symptoms, such as weight loss, dysphagia, odynophagia, or heme–positive stool, should undergo endoscopy to exclude gastric cancer.
313
What is the treatment of Helicobacter pylori disease?
Ulcers, reflux disease, and gastritis treated empirically. Young, healthy patients can be treated empirically with H2 blockers, antacids, or proton–pump inhibitors, and then endoscopy if there is no improvement.
314
What is the cause of gastroesophageal reflux disease?
Abnormal flow of the acid gastric contents backward from the stomach up into the esophagus through the lower esophageal sphincter.
315
What factors decrease tone of the lower esophageal sphincter?
Nicotine, alcohol, caffeine, peppermint, chocolate, anticholinergics, calcium–channel blocking agents, and nitrates.
316
What is the clinical presentation of GERD?
Epigastric pain, sore throat; a bad, metal–like taste in the mouth; hoarseness; and cough and wheezing. Pain in the substernal area. 24–hour pH monitoring is not necessary.
317
What is the treatment for GERD?
PP–inhibitors: omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole increase pH. Avoid nicotine, alcohol, caffeine, chocolate, late meals. Elevate bed. 5% require Nissen fundoplication.
318
What is Barrett esophagus?
Complication of long–standing reflux disease where epithelium of lower esophagus changes from normal squamous epithelium to columnar epithelium. Treatment is proton–pump inhibitors.
319
What are the causes of peptic ulcer disease?
Ulcers are caused by NSAIDs, H pylori, stomach CA, Zollinger–Ellison, Crohn, burns, head trauma, mechanical ventilation. Ulcers not caused by smoking, alcohol, steroids.
320
What is the pathophysiology of peptic ulcer disease?
Prostaglandins stimulate mucous production that forms a protective barrier. Prostaglandins are inhibited by NSAIDs. Parietal cells produce acid.
321
What hormones stimulate acid production?
Stimulants of acid production are gastrin, acetylcholine, histamine. Histamine is released by stomach cells and stimulates acid release.
322
What is the mechanism of action of H2 blockers?
H2 blockers, such as cimetidine, famotidine, and ranitidine, inhibit acid release by blocking histamine effect on parietal cells.
323
What is Zollinger–Ellison syndrome?
Zollinger–Ellison syndrome is the excessive production and release of gastrin from G cells.
324
What is the most common cause of ulcer disease?
The most common cause of ulcer disease is Helicobacter pylori followed by the use of NSAIDs. Eighty to 90% of duodenal ulcers and 70 to 80% of gastric ulcers are associated with H. pylori.
325
How is ulcer disease diagnosed?
Ulcer is best diagnosed with endoscopy. In patients 45, wt loss, anemia, or heme–positive, endoscopy should be performed.
326
How is H. pylori disease diagnosed?
Diagnosis of H. pylori is based on serology, urea breath test, stool antigen, or biopsy. Serology is the least expensive and has high sensitivity. Serology does not distinguish between old disease and new disease.
327
What is the advantage of breath testing for H pylori over serology?
Advantage of breath testing and stool antigen detection is same sensitivity as serology and are able to distinguish new versus old disease. After treatment, breath/stool tests become neg and used as a test for cure.
328
What is the treatment of H pylori ulcer disease?
PPI, clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole are all equal. PPI/clarithromycin/amoxicillin is \>90% effective. Therapy 10–14 d.
329
What is the approach to patients who fail therapy for H pylori?
In those who fail therapy, a urea breath test should be performed. If the organism was not eradicated, then re–treat with PPI, tetracycline, metronidazole and bismuth subsalicylate.
330
What is gastritis?
Inflammation, erosion of the gastric lining. Unlike ulcer disease, gastritis can be caused by alcohol; also NSAIDs, Helicobacter, head trauma, burns, mechanical ventilation. Associated with increased gastric acid.
331
What is the presentation of gastritis?
Most patients with gastritis present with asymptomatic bleeding. Other patients have epigastric pain, nausea and vomiting, hematemesis or melena.
332
How is gastritis diagnosed?
The diagnosis of H. pylori is based on either serology, urea breath testing, stool antigen testing, or biopsy with histology.
333
When should endoscopy be performed in patients with gastritis?
If
334
How is gastritis treated?
PPI combined with clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole are equal. Duration of therapy is 10 to 14 days.
335
How is pernicious anemia diagnosed?
B12 deficiency and pernicious anemia are diagnosed with low B12 level and increased methylmalonic acid level. Pernicious anemia is confirmed by antiparietal cell Ab and anti–intrinsic factor Ab.
336
What is Zollinger–Ellison syndrome?
Hypergastrinemia caused by cancer of gastrin–producing cells. Half of gastrinomas are in duodenum, and quarter are in pancreas.
337
What is the presentation of Zollinger–Ellison syndrome?
Present with ulcer.
338
How is Zollinger–Ellison syndrome diagnosed?
Gastrin level must be elevated while the patient is off antisecretory therapy for several days. Nuclear somatostatin–receptor scintigraphy is sensitive metastatic disease. Most sensitive test endoscopic ultrasound.
339
What is gastroparesis?
Weak stomach. Cause is diabetes. Presents with early satiety, postprandial nausea, and sense of increased abdominal fullness. Abdominal pain and bloating and diabetes, with retinopathy, neuropathy, nephropathy.
340
What is the treatment for gastroparesis?
Increase motility of the stomach with erythromycin or metoclopramide.
341
What are the symptoms of inflammatory bowel disease?
Fever, diarrhea, weight loss, and abdominal pain and bleeding. Episcleritis, scleritis and iritis, sclerosing cholangitis, joint pains, and pyoderma gangrenosum or erythema nodosum.
342
What are skip lesions in inflammatory bowel disease?
Skip lesions are areas of normal tissue in between the areas of disease; associated with Crohn disease.
343
What are the characteristics of ulcerative colitis?
UC that is a mucosal disease which is limited to the large bowel. UC has no skip lesions, no fistula formation, and no oral or perianal involvement. UC is more likely to cause bloody diarrhea.
344
Which type of inflammatory bowel disease can lead to colon cancer?
Both forms of IBD can lead to colon cancer after 8 to 10 years of involvement of the colon.
345
What are the complications of Crohn disease?
Complications of Crohn disease are calcium oxalate kidney stones, diarrhea, and cholesterol gallstones.
346
How is inflammatory bowel disease diagnosed?
Colonoscopy. Antineutrophil cytoplasmic antibody is associated with UC.
347
What laboratory abnormalities are associated with Crohn disease?
B12, calcium, vitamin K, iron deficiencies because malabsorption. Anti–saccharomyces cerevisiae antibodies. PT increased because vitamin K malabsorption. Kidney stones because increased absorption oxalate.
348
What is the treatment of inflammatory bowel disease?
Pentasa is a form of mesalamine released in upper and lower bowel; hence, it is used in CD. Asacol is a form of mesalamine released in the large bowel, and it is most useful for UC. Rowasa is used for rectal disease.
349
What is the treatment of exacerbations of inflammatory bowel disease?
Acute exacerbations of IBD are treated with high–dose steroids. Budesonide has a strong local effect when used orally, but is largely cleared by the liver in a first–pass effect.
350
What is the treatment of Crohn perianal disease?
Ciprofloxacin and metronidazole are used for CD with perianal disease. Infliximab is used for CD fistulae or refractory disease.
351
What is the role of surgery in inflammatory bowel disease?
Surgery is curative in UC; almost 60% will require surgery within 5 years after the diagnosis of UC due to refractory symptoms or severe disease. Surgery is less effective in CD and the disease reoccurs after surgery.
352
What is the laboratory evaluation of inflammatory bowel disease?
Stool should be evaluated for fecal leukocytes, culture, and ova and parasite examination. Clostridium difficile toxin and stool Giardia–antigen testing.
353
What are the most common causes of infectious diarrhea?
Campylobacter and Salmonella.
354
What is the presentation of Bacillus cereus diarrhea?
Ingestion of refried Chinese food. Short incubation period (1–6 hours). Vomiting is prominent. Blood is never present.
355
What type of diarrhea is associated with reactive arthritis and Guillain–Barre syndrome?
Campylobacter
356
What type of diarrhea occurs in HIV–positive patients with
Cryptosporidium and Isospora.
357
What type of food is associated with E. coli 0157:H7?
Hamburger meat. Shiga toxin may cause hemolytic uremic syndrome when organism dies; therefore, antibiotics are contraindicated. Platelet transfusions exacerbate the disease.
358
What type of ingestion is associated with Giardia diarrhea?
Unfiltered water on a camping trip. Giardia never causes blood in stool. There is abdominal fullness, bloating, and gas. Giardia can also simulate celiac disease by causing a fat and vitamin malabsorption.
359
What type if diarrhea is associated with ingestion of chicken and eggs, dairy products?
Salmonella
360
What type of ingestion is associated with scombroid poisoning?
Contaminated fish, resulting in vomiting, diarrhea, flushing, wheezing within minutes. Bacteria invade, producing and then releasing histamine into the flesh of fish, such as tuna, mahi mahi, mackerel and amberjack.
361
What is the presentation of Yersinia diarrhea?
Yersinia can mimic appendicitis. Also common in people with iron overload, e.g., hemochromatosis.
362
What type of ingestion is associated with Vibrio parahaemolyticus?
Ingestion of raw shellfish, such as mussels, oysters, and clams.
363
What type of ingestion is associated with Vibrio vulnificus?
Raw shellfish; high incidence in people with underlying liver disease or disorders of iron metabolism. Associated with the development of skin bullae.
364
What population is predisposed to viral diarrhea?
Children in day–care centers; absence of blood and white cells
365
Ingestion of what type of foods is associated with Staphylococcus aureus gastroenteritis?
Ingestion of dairy products, eggs, salads. Short incubation period (1–6 hours); nausea/vomiting predominate; rarely diarrhea.
366
Ingestion of what type of food is associated with ciguatera–toxin?
2–6 hours after ingestion of grouper fish, red snapper, and barracuda. Neurological symptoms include paresthesia, weakness, and reversal of heat and cold.
367
How is acute diarrhea diagnosed?
Fecal leukocytes is most useful test. Found when there has been invasion of the intestinal mucosa, as in dysentery, which is a bacterial infection of the bowel, producing diarrhea and bloody stool.
368
What are the invasive organisms that cause infectious diarrhea?
Salmonella, Shigella, Campylobacter, V parahaemolyticus, Yersinia, E coli, Vibrio vulnificus. Invasive organisms need 24 h to produce effect. The most definitive test for these bacteria is stool culture.
369
How is cryptosporidiosis diagnosed?
Cryptosporidiosis is diagnosed with a modified acid–fast test.
370
How is giardia diagnosed?
Giardia is diagnosed with an ELISA stool antigen test. 90% sensitivity.
371
What is the treatment of acute infectious diarrhea?
Antibiotics are used if there is abdominal pain, blood in the stool, and fever. Empiric therapy for infectious diarrhea is ciprofloxacin.
372
What is the treatment for scombroid poisoning?
Scombroid poisoning is treated with diphenhydramine.
373
What is the treatment of Giardia?
Giardia is treated with metronidazole. A newer agent for Giardia is tinidazole, which is effective in a single dose.
374
What is the treatment of Cryptosporidiosis?
Cryptosporidiosis is treated with paromomycin and raise the CD4 count to \>100/mm3 with antiretrovirals.
375
What is antibiotic–associated diarrhea?
Most common cause is Clostridium difficile. Any antibiotic may cause diarrhea, although clindamycin may have one of the highest frequencies. Stool test for C. difficile toxin.
376
What is the treatment for antibiotic–associated diarrhea?
Metronidazole. Oral vancomycin only if not resolve with metronidazole.
377
What is the presentation of lactose intolerance?
Diarrhea with gas and bloating; never has blood or leukocytes. Weight loss does not occur. High prevalence. Increased stool osmolality and increased osmolar gap.
378
How is lactase deficiency diagnosed?
Remove milk, cheese, ice cream, and all other dairy products (except yogurt) from the diet; resolution of symptoms should occur within 24 to 36 hours. Dietary changes are the best therapy; lactase supplements.
379
What is irritable bowel syndrome?
Pain syndrome in which there is increased frequency of peristaltic contractions.20% have constipation. Some have diarrhea alone or diarrhea alternating with constipation. No nocturnal symptoms. History of abuse.
380
How is irritable bowel syndrome diagnosed?
No specific diagnostic test. Exclude lactose intolerance, inflammatory bowel disease, celiac disease, carcinoid, Giardia infection, and anatomic defects of the bowel.
381
What is the Rome criteria for irritable bowel syndrome?
Pain relieved by a bowel movement or by a change in bowel habit. Fewer symptoms at night. Diarrhea alternating with constipation. No fever, weight loss, anorexia, or anemia.
382
What is the treatment for irritable bowel syndrome?
High–fiber, loperamide, diphenoxylate. Antispasmodics: hyoscyamine, dicyclomine, belladonna. Tricyclics. Tegaserod in constipation–predominant; may cause diarrhea. Alosetron reduces diarrhea.
383
What is carcinoid syndrome?
Tumors that cause neuroendocrine syndrome. Located in appendix and ileum. Symptoms appear after liver has been overwhelmed by metastatic disease. Bronchial carcinoids are rare but are highly symptomatic.
384
What is the presentation of carcinoid syndrome?
Diarrhea, flushing, tachycardia, hypotension. Tricuspid insufficiency and pulmonic stenosis.
385
How is carcinoid syndrome diagnosed?
Urinary 5–hydroxyindolacetic acid level (5–HIAA).
386
What is the treatment of carcinoid syndrome?
Control diarrhea with octreotide (somatostatin analog). Very few carcinoids are localized enough for surgical resection.
387
What are causes of fat malabsorption?
Celiac disease and chronic pancreatitis; tropical sprue and Whipple disease are extremely rare causes.
388
What is the presentation of fat malabsorption?
Greasy diarrhea, oily, floating, foul smelling. Weight loss. Malabsorption of the fat–soluble vitamins A, D, E, K. Hypocalcemia, easy bruising; prolongation PT. Iron malabsorption, macrocytic anemia.
389
What type of malabsorption causes Vitamin B12 deficiency?
Vitamin B12 malabsorption occurs from damage or loss of the mucosal surface of the terminal ileum from celiac disease.
390
What is the most common presentation of celiac disease?
Iron deficiency anemia. Dermatitis herpetiformis is a vesicular skin rash on the extensor surfaces of the body in 10%.
391
What is the most common cause of fat malabsorption?
Celiac disease is the most likely cause of fat malabsorption because it is the most common.
392
What is the presentation of malabsorption caused by chronic pancreatitis?
Patients with chronic pancreatitis will give a history steatorrhea with repeated episodes of pancreatitis from alcohol or gallstones.
393
What type of malabsorption is associated with travel to a tropical country?
Tropical sprue is suspected when there is a history of being in a tropical country.
394
What is the presentation of Whipple disease?
Whipple disease is the rarest cause of fat malabsorption; dementia (10%), arthralgias (80%), and ophthalmoplegia. Caused by the bacterium Tropheryma whipplei.
395
How is celiac disease diagnosed?
Antigliadin, antiendomysial, and antitransglutaminase antibodies. Small bowel biopsy shows flattening of villi. Just removing gluten (wheat, oats) from diet is not effective for diagnosis because antibodies.
396
What is the presentation of chronic pancreatitis?
Chronic pancreatitis is diagnosed from the history of repeated episodes of pancreatitis and is confirmed by finding calcification of the pancreas on x–ray and CT scan.
397
How is tropical sprue diagnosed?
Tropical sprue and Whipple disease are diagnosed by finding organisms on a bowel–wall biopsy. A positive Tropheryma Whippelii biopsy shows foamy macrophages that are PAS positive.
398
What is the treatment of malabsorption?
Chronic pancreatitis can be managed by orally replacing, amylase, lipase, trypsin. Tropical sprue is treated with sulfamethoxazole/trimethoprim or doxycycline.
399
What is the treatment of Whipple disease?
Whipple disease is treated with sulfamethoxazole/trimethoprim or doxycycline or ceftriaxone for 1 year.
400
What is diverticulosis?
Diverticulosis is caused by a lack of fiber in the diet and an increase in intracolonic pressure, leading to outpocketing of the colon. 50% of persons are over the age of 50.
401
What is the presentation of diverticulosis?
Asymptomatic. Left lower quadrant abdominal pain that can be colicky in nature.
402
How is diverticulosis diagnosed?
Colonoscopy. Diverticula are more on left in sigmoid, but bleeding occurs more often from diverticula on the right because of thinner mucosa and more fragile blood vessels. Bleeding is painless.
403
What is the treatment for diverticulosis?
Dietary fiber in bran, or bulking agents, such as psyllium husks.
404
What is the presentation of diverticulitis?
Fever, tenderness, pain, and elevation of white blood cell count.
405
How is diverticulitis diagnosed?
CT scanning. Barium studies and endoscopy are relatively contraindicated in diverticulitis.
406
What is the treatment for diverticulitis?
Cipro and metronidazole. Other choices are ampicillin/sulbactam, piperacillin/ tazobactam, or the combination of cefotetan or cefoxitin with gentamicin. Mild disease treated with amoxicillin/ clavulanate.
407
What are the causes of constipation?
Lack of fiber; calcium–channel blockers, oral ferrous sulfate, hypothyroidism, opiate analgesics, anticholinergics, and tricyclic antidepressants.
408
What is the lifetime risk of colon cancer?
\>6%. Most cases occur sporadically. Diets that are high in red meat, fat and smoking increase the risk.
409
What is the presentation of colon cancer?
Heme–positive, brown stool; chronic anemia when the cancer in right side of colon. Left–sided lesions cause obstruction and decreased stool caliber.
410
What type of cancer is associated with endocarditis caused by Streptococcus bovis?
Colon cancer is associated with endocarditis by Streptococcus bovis and Clostridium septicum.
411
What is the treatment for colon cancer?
Localized disease easily be cured. Once the disease has spread, then surgical resection will not be effective. Widespread disease is treated with resection and 5–FU.
412
What is the screening for colon cancer?
Annual fecal occult blood testing, colonoscopy every 10 years, and sigmoidoscopy every 5 years. Screening should occur after the age of 50 years.
413
What are the causes of a false–positive stool guaiac test?
False–positive stool guaiac tests can be caused by aspirin, NSAIDs, red meat, and poultry. False–negative tests can be caused by vitamin C.
414
What is hereditary polyposis colorectal cancer syndrome?
Genetic defect causing colon cancer. 3 family members in at least 2 generations with colon CA. 30% develop endometrial/ovarian cancer. Screening should start at the age of 25 with colonoscopy every 1 to 2 years.
415
What is familial adenomatous polyposis?
100% adenomas by 35 yrs and of colon cancer by 50. Polyps by age 25. Screening flexible sigmoidoscopy should be done every 1 to 2 years beginning at age 12. If polyps are found, a colectomy should be performed.
416
What is the colon cancer risk in juvenile polyposis syndrome?
Juvenile polyposis syndrome has 10% risk of colon cancer. Hamartomas have very little risk of developing into cancer.
417
What is Gardner syndrome?
Gardner syndrome is colon cancer with multiple, osteomas, lipomas, cysts, and fibrosarcomas. The osteomas have predilection for the mandible.
418
What is Peutz–Jeghers syndrome?
Hamartomatous polyps in the large and small intestine with hyperpigmented spots. Melanotic spots on lips, buccal, skin. Risk of cancer increased. Intussusception, obstruction.
419
What is the usual outcome of gastrointestinal bleeding?
80% of cases of gastrointestinal bleeding will resolve spontaneously with supportive management, irrespective of etiology.
420
What is the initial management of gastrointestinal bleeding?
Fluid resuscitation with NS. CBC, PT, T&C. If PT is elevated, give FFP. Platelets if count is
421
What medications should be given to patients with gastrointestinal bleeding?
Patients with gastritis or ulcer disease should be treated with PPIs empirically. H2 blockers have no efficacy in acute gastrointestinal bleeding.
422
What medication reduces portal hypertension in patients with cirrhosis of the liver and gastrointestinal bleeding?
If a history of cirrhosis of the liver, or if long–term alcoholic, octreotide should be added to this initial management plan to decrease portal hypertension.
423
What are the indications for transfusion in acute bleeding?
Hematocrit should be maintained \>30% in older patients or CAD. Younger patients do not need to be transfused, unless their hematocrit is
424
What is the treatment of bleeding esophageal varices?
Octreotide to lower portal pressure. If ineffective, endoscopy to place bands. If banding is not effective, then transjugular intrahepatic portosystemic shunting.
425
What is transjugular intrahepatic portosystemic shunting?
Creates shunt between the systemic circulation of hepatic vein and portal circulation of portal vein.
426
What is the primary complication of TIPS?
Complication of transjugular intrahepatic portosystemic shunting is worsening of encephalopathy.
427
What are the indications for a Blakemore tube?
A Blakemore tube tamponades the site of bleeding in the stomach or esophagus; rarely used and is only a temporary bridge to surgery.
428
What medication reduces risk of bleeding in portal hypertension?
Propranolol is a nonselective beta–blocker that used in the long–term management of portal hypertension to decrease the frequency of bleeding.
429
What are the most common causes of upper gastrointestinal bleeding?
Ulcers, gastritis, Mallory–Weiss, esophagitis, gastric cancer. Variceal bleeding is common in portal hypertension from cirrhosis.
430
What is the anatomic definition of upper gastrointestinal bleeding?
Upper gastrointestinal bleeding is defined as bleeding proximal to the ligament of Treitz.
431
What are the causes of lower gastrointestinal bleeding?
Diverticulosis, angiodysplasia, hemorrhoids, cancer, and inflammatory bowel disease.
432
What is the clinical presentation of lower gastrointestinal bleeding?
Red blood in stools; upper gastrointestinal bleeding presents with black stool or melena.
433
What degree of blood loss is indicated by the finding of orthostasis?
Orthostasis is a \>10 rise in pulse or \>20 drop in systolic BP when the patient goes from supine to standing or sitting. Orthostasis indicates a 15–20% blood loss.
434
If the resting pulse is \>100 bpm, what amount of blood loss has occurred?
Pulse above 100/min or a systolic blood pressure under 100 indicates \>30% blood loss.
435
How is lower gastrointestinal bleeding diagnosed?
Endoscopy is the most accurate test for upper and lower GI bleeding. If endoscopy is unrevealing, nuclear bleeding scan can detect low volume bleeds 0.1–0.5 mL/min. Small bowel bleeding detected capsule endoscopy.
436
What are the causes of acute pancreatitis?
Majority from alcoholism/gallstones. Pentamidine, didanosine, azathioprine, sulfas (sulfamethoxazole/trimethoprim thiazides). Hypercalcemia, hypertriglyceridemia. ERCP, trauma, mumps.
437
What is the pathophysiology of pancreatitis?
Premature activation of trypsinogen into trypsin while in the pancreas. Autodigestion of the pancreas.
438
What is the clinical presentation of acute pancreatitis?
Midepigastric pain with tenderness, nausea, and vomiting; radiates to the back. Septic shock; fever, hypotension, respiratory distress from ARDS, elevation of the white cell count; rigid abdomen.
439
How is acute pancreatitis diagnosed?
Lipase is more specific than amylase. Elevated WBC, hypoxia, glucose, LDH, AST. Calcium decreases because malabsorption of fat allows fat to bind with Ca. BUN increases because volume depletion.
440
What test determines the severity of pancreatitis?
The most accurate test to determine the severity of pancreatitis is the CT scan, which will demonstrate inflammation, necrosis, pseudocysts, abscesses, and ductal stones. Findings on the CT scan are a more
441
What are the signs of severe necrotizing pancreatitis?
Cullen sign: blue around umbilicus caused by hemoperitoneum. Turner''s: Purple flanks caused by tissue Hb. Best test for biliary/ pancreas is ERCP. Urinary trypsinogen activation peptide predicts severity.'
442
What are the complications of pancreatitis?
Ascites (high in amylase); pleural effusion (transudate, amylase); splenic vein thrombosis.
443
What is the treatment of pancreatitis?
Intravenous fluids, bowel rest, and pain medication. ERCP removes stone in the pancreatic duct or and to dilate a stricture.
444
What as the management of pancreatic necrosis?
Necrosis on CT is an indication imipenem or cefuroxime. Fever is an indication to perform a percutaneous needle biopsy. Infection of the pancreas and necrosis requires debridement.
445
What is the management of pancreatic pseudocysts?
Pseudocysts develop 2 weeks after pancreatitis. Pseudocysts should be drained if pain, fistula, rupture, or if expanding. Small, asymptomatic pseudocysts
446
What is the pathophysiology of cirrhosis of the liver?
Cirrhosis develops when there is chronic inflammation of the liver. When at least 70 to 80% of liver function has been lost, the synthetic capacity of the liver is diminished.
447
What are the causes of cirrhosis of the liver?
The most common cause of cirrhosis is alcohol. Other causes of cirrhosis are primary biliary cirrhosis, sclerosing cholangitis, alpha–1 antitrypsin deficiency, hemochromatosis, and Wilson disease.
448
What are the signs of hepatic cirrhosis?
Esophageal varices, ascites, edema; spider angiomata, palmar erythema, asterixis, encephalopathy, jaundice, low albumin. PT prolonged because of inability to make clotting factors.
449
What is spontaneous bacterial peritonitis?
Idiopathic infection of ascites. Gram stain is rarely positive. Culture of the fluid is the most specific test. White cell count of \>500 or the presence of \>250 neutrophils are criteria for infection.
450
What is the treatment of spontaneous bacterial peritonitis?
Cefotaxime and ceftriaxone are the drugs of choice for SBP and albumin infusion decreases risk of hepatorenal syndrome.
451
What is the serum–ascites albumin gradient?
Ascitic albumin is normally 1.1, portal hypertension is cause. When SAAG is
452
What is the treatment of cirrhotic edema?
Edema and fluid overload in third spaces, such as ascites, are managed with spironolactone.
453
What is the treatment of cirrhotic portal hypertension?
Portal hypertension and varices are managed with propranolol to prevent bleeding. Encephalopathy is managed with neomycin or lactulose. Vitamin K is not effective.
454
What is primary biliary cirrhosis?
Idiopathic autoimmune disorder in middle–aged women. Bilirubin levels do not elevate until 5 years. Association with Sjögren syndrome, rheumatoid arthritis, and scleroderma.
455
What is the presentation of primary biliary cirrhosis?
Fatigue, pruritus. Asymptomatic with an elevated alkaline phos. Osteoporosis. Transaminases normal. GGTP, IgM elevated. Antimitochondrial Ab specific. Biopsy diagnostic.
456
What is the treatment for primary biliary cirrhosis?
Bile acid–binding medication, such as ursodeoxycholic acid and cholestyramine. Ultraviolet light. Liver transplant.
457
What is the presentation of primary sclerosing cholangitis?
Fatigue, pruritus; increased alkaline phos. Idiopathic disorder of biliary system associated more often ulcerative colitis, also with Crohn. Cancer of biliary system in 15%.
458
How is primary sclerosing cholangitis diagnosed?
Elevated alkaline phosphatase; the antimitochondrial antibody test is negative. The most specific test for primary sclerosing cholangitis is an ERCP or transhepatic cholangiogram.
459
What is the treatment for primary sclerosing cholangitis?
Bile acid–binding resins. Liver transplant.
460
What is hemochromatosis?
Common genetic disease of overabsorption of iron in duodenum. Hepatic inflammation, fibrosis, cirrhosis. Hepatocellular CA in 20%. Restrictive cardiomyopathy 15%. Arthralgias, skin hyperpigmentation, diabetes.
461
What are the laboratory findings in hemochromatosis?
Decreased iron–binding capacity. Ferritin is elevated. Liver biopsy.
462
What is the treatment of hemochromatosis?
Phlebotomy to remove iron.
463
What is Wilson disease?
Autosomal recessive; diminished ability to excrete copper. Copper in liver, brain, cornea. Basal ganglia movement disorder. Kayser–Fleischer rings in eye on slit–lamp. Fanconi syndrome and type II RTA.
464
How is Wilson disease diagnosed?
Low ceruloplasmin level. High urinary copper level. Liver biopsy is most specific.
465
What is the treatment for Wilson disease?
Penicillamine is a copper chelator. Liver transplantation is curative.
466
What is alpha–1 antitrypsin deficiency?
Autosomal recessive disorder leading to deficient alpha–1 antitrypsin levels. Cirrhosis, emphysema developing at a young age in a nonsmoker.
467
How is alpha–1 antitrypsin deficiency diagnosed?
Low level of the enzyme in a person with COPD confirms diagnosis.
468
What is the treatment of alpha–1 antitrypsin deficiency?
Replacement of the enzyme and stop smoking.
469
How is chronic hepatitis B and C diagnosed?
Persistence of hepatitis B surface antigen for more than 6 mth confirms chronic hepatitis B. Ab to hepatitis C and elevated viral load by PCR confirms chronic hepatitis C. Liver biopsy most accurate.
470
What is the treatment for chronic hepatitis B?
Chronic hepatitis B is treated with interferon, lamivudine, or adefovir.
471
What is the treatment for chronic hepatitis C?
Chronic hepatitis C is treated with the combination of pegylated interferon and ribavirin.
472
What are the important aspects of the chest pain history?
Duration, quality, location, radiation, frequency, alleviating or precipitating factors (exercise), associated symptoms. For acute coronary syndromes the quality of chest pain is described as tightness, or pressure.
473
What is the clinical presentation of inferoposterior myocardial ischemia?
Nausea and vomiting are sometimes the main symptoms in inferoposterior wall ischemia. In inferoposterior wall ischemia, vagal reflexes may cause bradycardia and hypotension.
474
What are the characteristics of pain that is less likely to be caused by ischemia?
Sharp chest pain that the patient can pinpoint is not likely caused by ischemia, especially if pain is reproduced by position or palpation. Diaphoresis, tachypnea, anxiety indicate a life–threatening process.
475
What is the usual amount of time that myocardial infarction pain is present?
Myocardial infarction lasts more than 20–30 minutes.
476
What etiology is suggested if pain is relieved by nitroglycerine?
Relief of chest pain with nitroglycerin indicates ischemia or esophageal spasm. Chest pain that worsens with nitroglycerin occurs with gastroesophageal reflux disease.
477
What is the presentation of acute coronary syndrome in women?
Acute coronary syndromes in women present with atypical symptoms: dyspnea, shortness of breath, fatigue.
478
What are the physical examination findings that suggest aortic dissection?
Blood pressure a difference between arms of over 20 mm Hg systolic suggests aortic dissection.
479
What etiologies of chest pain are suggested by hypotension?
Massive pulmonary embolism or cardiac shock. Fever may suggest pneumonia or esophageal rupture. Corneal lipid rings, narrowed retinal arteries, murmurs; pigment and hair–loss on legs indicate coronary syndrome.
480
What etiology is suggested by wide splitting of the second heart sound?
Wide physiologic splitting of the second heart sound (splitting wider with inspiration) can be found in right ventricular infarction.
481
What is the significance of fourth heart sound in patients with chest pain?
A new fourth heart sound can occur with angina or infarction. An S3 is may be caused by underlying heart failure.
482
What etiology is suggested by the finding of a murmur of aortic regurgitation in patients with ischemic chest pain?
Significant aortic regurgitation occurs in over half of patients with aortic dissection, while mitral regurgitation can occur in patients with angina or infarction and is due to papillary muscle dysfunction.
483
What are the 12–lead ECG signs of an acute myocardial infarction?
50% of persons with acute MI will have diagnostic findings (ST elevation or Q waves \>0.04 sec), while 35% will have findings consistent with ischemia (ST depression and/or T wave inversion).
484
What is the role of creatine kinase MB isoenzyme in patients with an acute coronary syndrome?
CK–MB isoenzyme is cardiac specific and is useful for early diagnosis of MI.
485
At what time after an acute myocardial infarction does the CK–MB become elevated?
CK–MB detectable 4–6 hrs after ischemia onset, peaks 12–24 hrs, normalizes 2–3 d; can be used to detect early reinfarction. CK–MB levels are obtained at admission to ED and repeated 6–12 hrs.
486
What are cardiac troponins?
Troponins (T, I, C) are in striated and cardiac muscle. T and I are preferred markers for diagnosis of myocardial injury. Troponin T and I have similar sensitivity and specificity for MI.
487
What is the difference between troponin T and I?
Unlike troponin I levels, troponin T levels may be elevated in patients with renal disease, polymyositis, or dermatomyositis.
488
What is the significance of an elevated troponin level and a normal CK–MB in a patient with chest pain?
Patients with a normal CK–MB level but elevated troponin levels have sustained minor myocardial damage, or microinfarction. Elevations of both CK–MB and troponins is acute MI.
489
How much time is required before cardiac troponins return to normal after an acute myocardial infarction?
The cardiac troponins may remain elevated up to two weeks after symptom onset, which makes them useful as late markers of recent acute myocardial infarction.
490
What is the role of the chest x–ray in patients with chest pain?
Pneumothorax, pneumomediastinum, effusion, infiltrates. Aortic dissection can cause widening of mediastinum. Loss of lung volume or unilateral loss of vascular markings suggest PE.
491
What are the symptoms of aortic dissection?
Pain is sharp, tearing, severe; radiates to back; loss of pulses; aortic insufficiency murmur; mediastinum is widened; confirmed by MRI, CT scan, transesophageal echocardiogram, or aortography.
492
What are the symptoms of pulmonary embolism?
Dyspnea, tachycardia, hypoxemia; pleuritic pain.
493
How is pulmonary embolism diagnosed?
ECG may show an S wave in lead I, Q wave in lead III, or inverted T wave in lead III. Diagnosis is confirmed by spiral chest CT, lung scan, or pulmonary angiogram.
494
What are the symptoms of pericarditis?
Pain is sharp, positional, pleuritic, and relieved by leaning forward; preceded by viral illness; pericardial rub.
495
What are the ECG signs of acute pericarditis?
Diffuse ST elevation occurs without evolution of Q waves; CK level usually normal.
