A 40-year-old alcoholic male presents with a 6-day history of binge drinking. Serum chemistry tests reveal the following: Electrolytes (mmol/L): Na+ 145; K+ 5.0; Cl- 105; HCO3- 15
BUN: 7.1 mmol/L (20 mg/dL)
Creatinine: 133 g/L (1.5 mg/dL)
Glucose: 9.6 mmol/L (172 mg/dL)
The nitroprusside (Acetest) agent gives a minimally positive result. Optimal therapy to ameliorate the patient's acid-base disorder would include 5% dextrose in
A: water
B: normal saline
C: normal saline, insulin, and sodium bicarbonate
D: half normal saline and insulin
E: half normal saline, insulin, and sodium bicarbonate
The correct answer is B. normal saline
A reasonable way to approach the diagnosis of metabolic acidosis is to separate patients into those with an increased anion gap and those with a normal anion gap (hyperchloremic acidosis). A calculation of these unmeasured anions consists of the sum of plasma bicarbonate and chloride minus the plasma sodium concentration (the normal value is 8 to 16 mmol/L). Reasons for increased acid production include diabetic ketoacidosis, alcoholic ketoacidosis (as in this patient), starvation, lactic acidosis caused by circulatory failure, certain drugs and toxins, and poisoning resulting from salicylates, ethylene glycol, or methanol. Finally, renal failure increases the anion gap because sulfate, phosphate, and organic acid ions are not excreted normally. Normal anion gap acidosis is due to renal tubular dysfunction or colonic losses. Since the ratio of beta-hydroxybutyrate to acetoacetate is high in alcoholic ketoacidosis, ketonemia can be missed by the routinely employed nitroprusside (Acetest) reagent, which detects acetoacetate but not beta-hydroxybutyrate. Patients suffering from alcoholic ketoacidosis do well on infusions of glucose and saline. Neither insulin nor alkali is required in these situations unless the acidosis is extreme (bicarbonate less than 6 to 8 mmol/L).
Each of the following patients was noted to have an abnormally high serum cholesterol and was placed on a reduced calorie, cholesterol, and fat diet for the past 3 months. None has any history of ischemic heart disease. In which of the following patients would it be most appropriate to recommend lipid-lowering drug therapy at this time?
A: A 52-year-old smoker and diabetic with an LDL cholesterol value of 3.2 mmol/L (120 mg/dL)
B: A 60-year-old hypertensive woman with an LDL cholesterol value of 3.5 mmol/L (140 mg/dL)
C: A 50-year-old man with cholesterol of 6 mmol/L (230 mg/dL)
D: A 45-year-old man with LDL cholesterol of 5 mmol/L (200 mg/dL)
E: A 58-year-old male smoker with cholesterol of 5.5 mmol/L (220 mg/dL) and LDL cholesterol of 4 mmol/L (150 mg/dL)
The correct answer is D. A 45-year-old man with LDL cholesterol of 5 mmol/L (200 mg/dL)
Given the clearly defined benefits of lipid lowering in patients at risk for ischemic heart disease, screening measurement of blood cholesterol levels (nonfasting) is recommended for all adult patients, especially young patients with a family history of premature heart disease. If hyperlipidemia is detected, secondary causes such as hypothyroidism, nephrotic syndrome, and uremia should be considered, along with stopping drugs that can aggravate the condition, including oral contraceptives, estrogens, thiazides, and beta blockers. Once these effects are considered, the primary step is attention to diet. Attempts should be made to bring the patient to normal weight and encourage the patient to undergo dietary therapy with reduced intake of calories, cholesterol, and saturated fat. However, patients who remain at high risk after 3 months of an intensive regimen of dietary therapy should be strongly considered for lipid-lowering drug therapy. Such therapy is recommended for any adult patient whose LDL cholesterol remains greater than 4.9 mmol/L (190 mg/dL) or greater than 4.1 mmol/L (160 mg/dL) in the presence of two or more risk factors. A more aggressive approach is recommended for patients with a prior history of ischemic heart disease. Other risk factors for early atherosclerosis include diabetes mellitus, hypertension, familial hyperlipidemias, hypothyroidism, systemic lupus, and homocysteinemia. Drugs that act to lower LDL cholesterol include bile acid-binding resins such as cholestyramine, nicotinic acid, and hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors.
hi i took step3 last week.it is just like step 2 but more emphasis on treatment and management.you need to be able to read fast because the case histories are sometimes very long.swansons seems to cover a lot of the questions asked on the exam.also a lot of quesstions on drugs.
When did you give your exam?For which state did you take it? how many months did you prepare? what books did you read?. I hope you have done very well in your exam. Give me some information regarding the exam.Thank you very much in advance.
I TOOK THE EXAM FOR THE STATE OF CONNECTICUT IN OCTOBER 2000. I READ MAINLY SWANSON FAMILY PRACTICE FOR THE BOARDS AND CURRENT MEDICAL DIAGNOSIS AND TREATMENT. THE TIME TAKEN TO PREPARE FOR THE SAME DEPENDS ON THE PERSON AND THEIR STYLE OF PREPARATION. SINCE I AM THE LAST MINUTE CRAMMMER TYPE I STUDIED FOR ABOUT THREE WEEKS WITHOUT ANY BREAKS.IT IS EASIER TO STUDY AND DO THE EXAM WELL IF YOU HAVE SOME CLINICAL EXPERIENCE BUT IT IS NOT ABSOLUTELY NECESSARY. I CAN SAY THIS BECAUSE I MYSELF AM FROM A PARACLINICAL BACKGROUND. WITH THE ABOVE AMOUNT OF STUDY I MANAGED TO PASS THE EXAM, THANK GOD. HOPE THIS HELPS. IT IS NOT VERY DIFFICULT, SO DON'T WORRY. IF YOU HAVE ANY MORE QUESTIONS I WILL BE GLAD TO ANSWER THEM.
read swansons review for family practice boards and supplement it with current medical diagnosis and treatment. some of my friends found blueprints for step 3 very useful.
NMSR recent live lecture audio tapes needed (step one)
by
Hi ,
I am looking for the Audio tapes from a recent live lecture series on step one. Please email me if you have them taped. I cannot afford the live lectures so I might be able to buy the tapes. Please offer a decent price.
Good prognostic factors for schizophrenia include:
Female gender
Married status
Good premorbid functioning
Late onset disease (>45 years of age)
Affective symptoms
High quotient of intelligence
Predominantly positive symptoms
Acute onset of disease with precipitating factor
Few prior episodes of schizophrenia
Phasic pattern of episodes and remissions
Paranoid subtype schizophrenia
No family history of schizophrenia
Family history of affective disorder
Good support systems
1. Both cyclophosphamide and melphalan can cause leukemia and bladder cancer.
2. Thorotrast has been implicated in causing angiosarcoma of the liver.
3. Tamoxifen can cause endometrial carcinoma.
A 75-year-old man presents with recurrent episodes of shortness of breath on minimal exertion. He has no prior significant past medical history. Physical examination reveals blood pressure of 110/70 without pulsus paradoxus, heart rate of 110, respiratory rate of 25, and temperature of 37°C (98.6°F) orally. Jugular veins are distended and the heart sounds are distant, but there are third and fourth extra heart sounds. The liver is enlarged, and pedal edema is present. The electrocardiogram shows nonspecific ST-T wave changes and occasional premature ventricular contractions. The chest x-ray reveals clear lung fields and a mildly dilated cardiac silhouette. Echocardiography reveals normal systolic function and thickened ventricular walls with a "speckled" appearance. Which of the following conditions is most consistent with the patient's clinical presentation?
The correct answer is C. Amyloidosis
The restrictive cardiomyopathies are characterized pathophysiologically by an impairment to ventricular filling. The cardiac silhouette is usually mildly, if at all, enlarged. Electrocardiography typically displays low-voltage QRS complexes, atrioventricular conduction defects, and a host of nonspecific arrhythmias. Echocardiography frequently reveals normal systolic and increased left ventricular wall thickness. In amyloidosis, the left ventricular wall appears to be "speckled." While primary cardiac amyloidosis typically produces diastolic dysfunction or restrictive cardiomyopathy as in this question, systolic dysfunction, arrhythmias, and orthostatic hypotension may be alternative presentations. Hemochromatosis also may cause a restrictive picture, but the speckled appearance noted in the echocardiogram would be absent. Alcoholism and viral infections typically cause dilated cardiomyopathies. Chronic tuberculous pericarditis can manifest clinical symptoms similar to those seen in restrictive cardiomyopathy. Patients with constrictive pericarditis have clinical presentations similar to those of patients with restrictive cardiomyopathy but tend to have normal ventricular wall thickness on echocardiography, pericardial calcification, and the absence of third or fourth heart sounds on chest auscultation.
Major resik factors:
Diabetes - the greatest risk factor of all
Smoking - the # 1 preventable risk factor
Hypertension
Hypercholesterolemia
Family history
Minor risk factors:
obesity, age, low estrogen, homocystinuria