The Complete Study Guide for the MCCEE & MCCQE1

The Ottawa Notes is a complete review of all the major medical topics covered in the Canadian Medical Licensing Exams.  It comes complete with over 250 integrated colour pictures, diagrams, and radiology images.  Topics include the following:




Emergency Medicine




Infectious Disease

Medical Ethics







Physical Medicine and Rehabilitation




Sports Medicine




The Ottawa Notes POWER REVIEW

The New Ottawa Notes Power Review is a fully printed and bound 80 page review book designed to help students cover the most commonly tested topics on the MCCEE and MCCQE1.  Each subject helps you pinpoint the disease, diagnosis, and treatment with key words and phrases most commonly seen on the exams.  This book can be used as a quick refresher or constant review tool to keep learned information fresh and at your fingertips.  An excellent tool to keep your memory and medical facts sharp.

Example of topics covered:

Cushing’s Syndrome

Cushing's syndrome is a constellation of clinical abnormalities caused by chronic high blood levels of cortisol or related corticosteroids. Cushing's disease is Cushing's syndrome that results from excess pituitary production of ACTH, usually secondary to a pituitary adenoma. Typical symptoms include moon facies and truncal obesity with thin arms and legs. Diagnosis is by history of receiving corticosteroids or by finding elevated serum cortisol. Treatment depends on the cause.


A pheochromocytoma is a catecholamine-secreting tumor of chromaffin cells typically located in the adrenals. It causes persistent or paroxysmal hypertension. Diagnosis is by measuring catecholamine products in blood or urine. Imaging tests, especially CT or MRI, help localize tumors. Treatment involves removal of the tumor when possible. Drug therapy for control of BP includes α-blockade, usually combined with β-blockade. The catecholamines secreted include norepinephrine, epinephrine, dopamine, and dopa in varying proportions. About 90% of pheochromocytomas are in the adrenal medulla, but they may also be located in other tissues derived from neural crest cells.

Primary Aldosteronism (Conn’s Syndrome)

Primary aldosteronism is aldosteronism caused by autonomous production of aldosterone by the adrenal cortex (due to hyperplasia, adenoma, or carcinoma). Symptoms and signs include episodic weakness, elevated BP, and hypokalemia. Diagnosis includes measurement of plasma aldosterone levels and plasma renin activity. Treatment depends on cause. A tumor is removed if possible; in hyperplasia, spironolactone or related drugs may normalize BP and eliminate other clinical features.

Secondary Aldosteronism

Secondary aldosteronism is increased adrenal production of aldosterone in response to nonpituitary, extra-adrenal stimuli, including renal artery stenosis and hypovolemia. Symptoms are those of primary aldosteronism. Treatment involves correcting the cause. Secondary aldosteronism is caused by reduced renal blood flow, which stimulates the renin-angiotensin mechanism with resultant hypersecretion of aldosterone. Causes of reduced renal blood flow include obstructive renal artery disease (eg, atheroma, stenosis), renal vasoconstriction (as occurs in accelerated hypertension), and edematous disorders (eg, heart failure, cirrhosis with ascites, nephrotic syndrome). Secretion may be normal in heart failure, but hepatic blood flow and aldosterone metabolism are reduced, so circulating levels of the hormone are high.

The Ottawa Notes CD Study Guide



Lichen planus (LP) is a pruritic, papular eruption characterized by its violaceous color; polygonal shape; and, sometimes, fine scale. Lichen planus is most commonly found on the flexor surfaces of the upper extremities, on the genitalia, and on the mucous membranes. Lichen planus is most likely an immunologically mediated reaction.


Most cases of lichen planus (LP) are insidious.


In addition to the cutaneous eruption, lichen planus (LP) can involve the mucous membranes, the genitalia, the nails, and the scalp. The clinical presentation of lichen planus has several forms: actinic, annular, atrophic, erosive, follicular, hypertrophic, linear, pigmented, and vesicular/bullous. The papules are violaceous, shiny, and polygonal; varying in size from 1 mm to greater than 1 cm in diameter . They can be discrete or arranged in groups of lines or circles. Characteristic fine, white lines, called Wickham stria, are often found on the papules.


Lichen planus (LP) is a self-limited disease that usually resolves within 8-12 months. Mild cases can be treated with fluorinated topical steroids. More severe cases, especially those with scalp, nail, and mucous membrane involvement, may need more intensive therapy.


A 71-year-old man presents to his physician for follow-up of a recent emergency department visit. The patient has a 2-year history of mild congestive heart failure in the setting of long-standing hypertension. He reports that yesterday he sought care at the local emergency department for palpitations and shortness of breath. He was told that his heart was "fibrillating", but later, the fibrillation had "stopped on its own." His medications include a thiazide diuretic and an ACE inhibitor. On physical examination, he appears well and in no distress. His blood pressure is 130/80 mm Hg, and his pulse is 100/min and regular. His lungs have scant bibasilar rales, and no gallops are appreciated. He has a grade 2 holosystolic murmur heard best at the apex. His jugular venous pressure (JVP) is 10 cm at 30 degrees. An ECG taken in the office reveals atrial fibrillation at a rate of 94/min with normal ST segments. Which of the following is the most appropriate next step in management?

A. Discontinue the ACE inhibitor
B. Initiate amiodarone therapy
C. Initiate beta blocker therapy
D. Initiate digoxin therapy
E. Initiate furosemide therapy


The correct answer is D. An important concept to recognize in the treatment of medical conditions is that certain medications overlap syndromes and are efficacious in many areas. This "co-treatment" option maximizes the benefits of each drug in a regimen and often addresses two or more issues simultaneously. In this case, ACE inhibitors have been shown to be very beneficial in prolonging the survival of patients with congestive heart failure (CHF). They are also useful antihypertensive agents. Given this, discontinuing his ACE inhibitor (choice A) is clearly incorrect. This patient requires rate control for his atrial fibrillation, that, even at moderately elevated rates, causes cardiovascular embarrassment and pulmonary edema. Short of restoring this patient's atrial contractions, rate control is the best method to ensure adequate management of atrial fibrillation. Digoxin, with or without a nodal agent such as a beta blocker, has been shown to be reasonably effective at rate control.

Amiodarone therapy (choice B) is a pharmacologic method to convert atrial fibrillation to normal sinus rhythm. It has about the same efficacy as electrical cardioversion. It does nothing, however, in the short term, to control the rate.

Beta blocker therapy (choice C) alone is not as efficacious as digoxin alone. In addition, although some beta blockers (carvedilol) are being used clinically in CHF, not all beta blockers have been shown to be safe for use with this condition. Therefore, although digoxin plus a beta blocking agent would be preferred, there is good reason to initiate digoxin therapy alone for this patient.

Furosemide therapy (choice E) is partially correct. Although furosemide will help clinically with the failure, the underlying cause for the pulmonary edema will not be addressed solely by giving a diuretic. The more appropriate therapy is to control the rate, then the edema will resolve.

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