Family Medicine Keywords Defined - 2005
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Medtext keyword books give you an overview of the topics that have been presented on the board exam during the last couple of years. All keywords are defined and include current references with page numbers.

Samples:

EN001          Adrenal Insufficiency
Cortisol is the predominant corticosteroid secreted from the adrenal cortex in humans. Many diseases and treatments can interfere with the normal corticosteroid response to illness and thus induce tissue corticosteroid insufficiency. These etiologies include, head injury, central nervous system depressants, pituitary infarction, adrenal hemorrhage from septicemia and coagulopathy, destruction of adrenal tissue by tumors or infection such as HIV, or exogenous agents such as etomidate (anesthetic agent), ketoconazole medroxyprogesterone, and megestrol acetate treatment. Exogenous corticosteroid therapy in patients generally receiving more than 30 mg. of hydrocortisone per day (7.5 mg of prednisolone or 0.75 mg of dexamethasone per day) for more than three weeks can suppress the hypothalamic-pituitary-adrenal axis and induce adrenal atrophy that may persist for months after the cessation of corticosteroid treatment.

Features of corticosteroid insufficiency include symptoms such as weakness, anorexia, nausea, vomiting, abdominal pain, myalgia, arthralgia, dizziness, headaches, memory impairment, depression, amenorrhea, cold intolerance, and salt cravings. Findings on physical exam may include postural hypotension, fever, tachycardia, increased pigmentation, decreased body hair, and vitiligo. Clinical problems include hyponatremia, hypoglycemia, hyperkalemia, eosinophilia, elevated thyrotropin levels, hemodynamic instability, and multiple-organ dysfunction.

Making the diagnoses can be difficult but helpful laboratory measurements include checking random cortisol levels and/or the cortisol response to the corticotropin stimulation test.

Treatment with corticosteroid during intercurrent and acute illnesses for the adrenal insufficiency depends upon the extent to the disease and the patient’s condition. Replacement doses may be given for minor trauma, surgery or fever. Larger doses need to be given for major surgery, major trauma, or critical illness such as septic shock. For patients with persistent adrenal deficiency, long-term hydrocortisone treatment ranging from 15-25 mg per day is generally indicated. Many patients with adrenal disease may also require mineralocorticoid replacement with 0.05 to 0.2 mg of fludrocortisone per day. These patients need to increase their doses during periods of acute illnesses, stress, trauma, or surgery.

1. Cooper, MS, and Stewart, PM. Corticosteroid Insufficiency in Acutely Ill Patients. NEJM. 2003;348:727-34.

GE004          B12 Deficiency
Vitamin B12 (cobalamin) has an important role in DNA synthesis and neurologic function. The role it plays in hyperhomocysteinemia and atherosclerosis is still being uncovered. Old ideas about oral supplementation are now being shown to be not true.

The true prevalence in the population of B12 deficiency is unknown. Studies have shown that in patients over 65 the incidence may be as high as 15%. The use of gastric acid blocking agents can lead to decreased B12 levels.

Clinical signs of B12 deficiency are hematologic, neurologic and psychiatric. Hematologically you can see megaloblastic anemia and pancytopenia. Neurologically paresthesias, peripheral neuropathy and combined systems disease may be seen. Irritability, personality change, mild memory impairment, dementia, depression and psychosis may be some of the psychiatric changes seen. Now research says that an increased risk of myocardial infarction and stroke may be tied to B12 deficiency.

It is felt that low B12 levels produce hyperhomocysteinemia which is an independent risk factor for cardiovascular disease.

Only two enzymatic reactions are known to be dependent on B12. Methylmalonic acid is converted to succinyl-CoA using B12 as a cofactor. Low B12 results in increased levels of methylmalonic acid. Secondly homocysteine is converted to methionine by using B12 and folic acid. Low B12 equals high homocysteine levels.

B12 absorption is dependent on several variables. Gastric acid breaks down B12 that is bound to food. Intrinsic factor (from the parietal cells in the stomach) binds to B12 in the duodenum. It is this B12/Intrinsic factor complex that eventually gets absorbed in the terminal ileum. There may be an alternate source of absorption that is independent of intrinsic factor or even an intact terminal ileum. This is why the old belief that oral B12 supplementation could only occur with intrinsic factor and a terminal ileum present is no longer true. Obviously the interruption of any of these steps in the uptake may lead to a B12 deficiency.

Diagnosis is typically based on measurement of serum B12 levels. It should be noted that about half of those with subclinical disease have normal B12 levels. A more sensitive test for screening may be measurement of serum methylmalonic acid and homocysteine levels for reasons noted above. The use of a Schilling test in pernicious anemia has been replaced in the most part by serologic testing for Parietal cell and Intrinsic factor antibodies. Remember that low folic acid levels can result in low B12 levels as well.

Causes of B12 deficiency include nutritional deficiency as B12 is found in meat and diary products. The typical reserve in humans is large and can maintain a patient for two to five years. The elderly on a “tea and toast” diet may be at high risk as are chronic alcoholics. Malabsorption syndromes including autoimmune dysfunction and the body attacking parietal cells account for most cases of pernicious anemia. The widespread and prolonged use of H2 blockers and Proton Pump Inhibitors for ulcer disease may cause impaired breakdown of B12 from food rendering it unfit for absorption.

Supplementation of B12 can be oral but in the past has been mostly through IM injections. Now that we know that oral supplementation is reliable the dosage of B12 supplementation is 1,000 to 2,000 mcg per day for one to two weeks followed by a maintenance dosage of 1,000 mcg per day for life. IM injections have typically been 100 to 1,000 mcg every day for one to two weeks followed by a maintenance dosage of 100 to 1,000 mcg every one to three months.

Follow up should show an increase in reticulocytes if the treatment is for anemia. This can be seen as early as one to two weeks after start of therapy. In mild deficiency states usually follow up includes rechecks of B12, homocysteine and methylmalonic acid levels in two to three months after starting therapy.

1. Robert C Oh, CPT MC USA, David L Brown, Maj MC USA. Vitamin B12 Deficiency. Am Fam Physician 2003;67:979-86, 993-4.

GI011          Upper and Lower GI bleeds
Gastrointestinal bleeding is blood loss that comes from anywhere in the gastrointestinal tract from the mouth to the anus. Bleeding is defined as upper GI in origin if the source is proximal to the ligament of Treitz. Bleeding distal to the ligament of Treitz is designated as lower GI bleeding. Bleeding that is not symptomatic and is found incidentally or with screening is defined as occult GI bleeding. Occult bleeding may be either upper or lower in origin, but in U.S. adults an upper source is more common.

Presentations of upper GI bleeding include hematemesis (vomiting of red or “coffee ground” blood) and melena (dark or black stools). Though less common, 10% of patients presenting with red blood per rectum will be found to have an upper GI source. Lower GI bleeding presents most often as hematochezia (blood mixed with stool) or purely as red blood per rectum. In addition to the bleeding, patients should be evaluated for signs and symptoms to help decide how severe the bleeding is. Symptoms of orthostasis or dizziness, or signs of shock (tachycardia, hypotension) indicate the severity of the bleed.

The common causes of upper GI bleeding in order of frequency are:
1) Peptic ulcer disease
2) Portal hypertension (varicele bleeding)
3) Mallory-Weiss tears
4) Gastritis
5) Esophagitis

The causes of major lower GI bleeding in order of frequency are:
1) Diverticulosis
2) Angiodysplasia
3) Neoplasms
4) Inflammatory bowel disease
5) Anorectal disease

Initial evaluation includes a focused history and physical exam looking for clues as to the etiology of the bleed and to try to determine if it is upper or lower in origin. As part of the initial evaluation, basic lab tests should be obtained including a CBC, coagulation studies, a comprehensive metabolic panel, and blood should be typed and cross-matched for 2-4 units of blood. Vascular access should be secured with two 18 gauge IV lines. Unless the patient’s complaint is bright red blood per rectum, a nasogastric tube should be inserted and aspiration of the gastric contents should be done looking for red or coffee ground blood. An anorectal exam along with a digital rectal exam and testing of stool for blood should be done.

Volume replacement and transfusion therapy are the mainstays of treatment. Initial volume support should be with normal saline or lactated ringers solution at a bolus dose of 20 ml/kg. If there are signs or symptoms of shock, transfusion of packed red blood cells should be done. In the face of acute bleeding, the hemoglobin and hematocrit are not reliable indicators of volume status. Transfusion of other blood products will depend on the clinical picture. Platelet transfusion should be done for patients with counts less than 50,000/?l. Patients with abnormal coagulation studies, or who receive more than four units of packed RBCs should be given fresh frozen plasma.

Medical management of acute bleeding includes acid suppression medications if an upper source is suspected. Proton pump inhibitors are the preferred agents and should be given by the IV route. To decrease the splanchnic blood flow and reduce portal pressure in GI hemorrhage, a continuous IV infusion of octreotide (100µg bolus followed by 50 µg/hr infusion) is recommended.

Acute endoscopic management is recommended once the patient has been hemodynamically stabilized. Endoscopy has three main purposes:
1) To document the source of bleeding
2) To help determine the risk of re-bleeding
3) To render endoscopic therapy.

Endoscopic therapy for upper GI bleeding includes vasoconstrictor injections into bleeding sites, direct cauterization and band ligation of varices. Injection and cautery treatments are also effective for lower GI bleeding from diverticulosis or angiodysplasia.

1. Tierney LM, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment. 44th Ed. McGraw-Hill. New York NY. 2005:533-540.

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