A. Mark Clarfield, MD

Having spent several years as a family doctor before becoming a consultant geriatrician, I have stood on both sides of the fence. As a primary-care physician, I was subjected to the humiliations dished out by many a consultant. Yet, to my chagrin, in later years, I found myself perpetrating similar outrages on physicians seeking my help.

As patients, the elderly are particularly vulnerable to getting caught in the crossfire when consultant and consultee do not see eye to eye. The main reason for this is that no one needs the services of good primary care with appropriate consultant backup more than the older patient.

In this article as well as in the March issue, I shall describe mistakes that I have made (or seen colleagues make) on both sides of the great divide between consultant and consultee.

Sins of the Consultant

1. Arrogance: Chapter 1

The specialist has, by definition, a very comprehensive knowledge of a specific area of medicine. This knowledge can be used to beat the consultee over the head with implied or overt criticism.

Philip Dopp, BSc

Alzheimer's Disease (AD) is a neurological disorder that is characterized by a slowly degenerative process affecting cognitive function. At a histopathological level, AD patients are characterized by the deposition of senile plaques within the brain, as well as within the walls of cerebral blood vessels.^1-5 It is believed that through an unknown mechanism, these senile plaques exert a toxic effect on surrounding neurons, resulting in the neuronal degeneration found in AD patients.^1,5

The primary constituent of these senile plaques is amyloid b peptide (Ab). Two proteases, b-secretase and g-secretase cleave this peptide from a larger precursor protein, b-amyloid precursor protein (APP).^1,5-6 Essentially, b-secretase cleaves APP to produce an APPsb soluble fragment and C99, a membrane bound fragment, whereas a-secretase can prohibit Ab formation by cleaving APP within the Ab sequence to produce APPsa and C83.⁶ Ultimately, g-secretase acts on C99 to produce Ab, or on C83 to produce a nonpathogenic p3 peptide.

Anna Liachenko, BSc, MSc

Canadian postmenopausal women now have a new drug option for treatment of established osteoporosis and/or relief of pain associated with osteoporotic fractures--synthetic salmon calcitonin administered as a nasal spray (Miacalcin Nasal Spray or Miacalcin NS). Already available in over 70 countries, the drug was approved in Canada in September of 1999. The nasal spray is very safe and has been shown in various studies to increase bone mineral density (BMD) in vertebrae, the primary site of fractures in postmenopausal osteoporosis. Several months ago a large clinical trial confirmed that Miacalcin NS lowers the risk of vertebral fractures, making it an important agent for osteoporotic therapy.⁶

Calcitonin is a peptide hormone secreted by the thyroid gland and its secretion is under the direct control of blood calcium levels. In humans, no definite effects on calcium levels are seen in states of calcitonin deficiency or excess. Calcitonin was discovered over 35 years ago by Dr. Harold Copp at the University of British Columbia. Secretion calcitonin is estrogen-dependent and is decreased after menopause.^7,8 Osteoporotics have lower levels of serum calcitonin than both premenopausal and healthy menopausal females. It is likely that the deficiency in the hormone plays some role in postmenopausal bone loss, and studies have found that calcitonin counteracts both early and established osteoporosis.

Dr. Michael J. Taylor

The following article attempts to add insight into the complex and difficult issue of physician assisted suicide by approaching it from a broad perspective. The article will begin with a brief and informal historical survey of attitudes toward physician assisted suicide. It will then address the arguments both for and against this issue, and conclude with an examination of some of the evidence that is available to support concerns of those on both sides of the debate. Included in the article are some inferences as to the direction debates about physician assisted suicide might take in the future. Though terms such as euthanasia and physician assisted suicide are often used to denote different entities both by the lay public and within the medical literature, for the purposes of this article, the term physician assisted suicide is used to describe the active involvement of a physician in ending the life of a patient at the patients specific request (i.e. through the prescription or administration of lethal medications). The act of ending the life of a patient without his or her specific request (i.e. "mercy killing"), and the decision to forgo life sustaining treatment (including the use of ventilators, dialysis or feeding tubes) are not included within the definition of physician assisted suicide as discussed in this article.

Nariman Malik, BSc

Introduction
Mitral regurgitation is a common valvular heart disease, especially in the elderly.¹ It is defined as a condition in which there is an abnormal flow of blood from the left ventricle to the left atrium across an incompetent mitral valve during ventricular systole.² The mitral valve consists of four main components: the annulus, anterior and posterior leaflets, the chordae tendinae and the papillary muscles. Mitral regurgitation has a number of underlying etiologies that can be broadly classed into two groups: mitral regurgitation due to organic disease (e.g. rheumatic disease or infective endocarditis) or mitral regurgitation due to functional causes (regurgitation results from myocardial dysfunction as opposed to valvular problems). In developed countries, the etiologic profile of mitral regurgitation has changed over recent years due to the decreased incidence of rheumatic heart disease.³ Mitral regurgitation is most frequently due to degenerative and ischemic causes in the western world.⁴ See table 1

D'Arcy L. Little MD, CCFP
York Community Services, Toronto

Relenza (zanamivir), an orally-inhaled anti-viral medication effective against all known strains of the influenza virus, was approved by the Therapeutic Products Program of Health Canada on November 3, 1999.

Epidemiology
It is estimated that in Canada influenza affects between 10 to 15% of the population (between 3 and 5 million people) each year. The number of affected persons can be as high as 80% of nursing home residents. In addition, these infections result in about 75,000 hospitalizations and 7,000 deaths yearly.¹ In economic terms, flu-related costs to the Canadian economy during the 1997-98 flu season were estimated to be over $1 billion.²

The Mainstay of Treatment for Influenza
The influenza vaccine has been and remains the mainstay of prophylactic protection against influenza, and is recommended for elderly and high-risk patients, their household contacts, and health-care personnel. Under ideal circumstances, in healthy, young adults, vaccine effectiveness is in the range of 70-90%, with much lower effectiveness in the elderly (30-50%).³ For optimal results, it is recommended as a single 0.5 ml IM dose to be given from October through mid-November, although it can be given from September to the end of the influenza season.

Jason Park, BSc

Chronic aortic regurgitation is common in the elderly. Indeed, a Finnish study looking at the prevalence of aortic valve abnormalities found that 13% of a random, asymptomatic elderly population had moderate to severe evidence of aortic regurgitation when imaged with echocardiography.¹ Although chronic aortic regurgitation is usually insidious in its course, it can progress to cause permanent myocardial damage and congestive heart failure. Major indications for surgical correction of severe chronic aortic regurgitation are the onset of more than mild symptoms, such as dyspnea, or echocardiographic evidence of left ventricular systolic dysfunction. Surgery should be performed before systolic dysfunction is significant in order to limit progression of the disease and possible irreversible myocardial dysfunction. Careful follow-up of patients with chronic aortic regurgitation is required, including a detailed history, physical examination, and echocardiography, in order to optimize the benefits of surgery and limit the possibility of permanent myocardial damage.

Etiology and Pathophysiology
Chronic aortic regurgitation results from incomplete closure of the aortic valve due to disease of either the aortic root or the aortic valve itself. A frequent cause of aortic regurgitation is idiopathic aortic root dilatation, which is associated with hypertension.

Sheldon Singh, BSc

Valvular heart disease is an increasingly common cause of congestive heart failure in the elderly population. Stenosis of the aortic valve is one type of valvular heart disease that can lead to congestive heart failure. Approximately 28,000 aortic valve replacements were performed in the United States in 1994. Sixty-one per cent of these were performed in individuals over age 65. This procedure is the second most common open-heart procedure performed in the elderly after coronary bypass grafting.

In adults, aortic stenosis may be due to previous rheumatic disease or calcification of a congenital bicuspid valve or normal tricuspid aortic valve. Although common worldwide, rheumatic disease is uncommon in North America and Europe. However, because of the increasing aging population, degenerative aortic valve calcification constitutes a substantial health problem.¹

Anatomy
A normal aortic valve is tricuspid. Each leaflet is flexible and composed of three layers covered with endothelium on each side. Degenerative calcific disease is characterized by discrete focal lesions on the aortic side of the leaflet. It is typically an active inflammatory process that bears some resemblance to atherosclerosis; there are protein and lipid infiltration as well as macrophages, foam cells, and the occasional T cell.² The risk factors for aortic valve disease include age, male gender, lipoprotein a, hypertension, smoking, cholesterol and diabetes.

Joyce So, BSc

While thrombolytic therapy has become an established part of treatment for acute ischemic heart disease, the controversy continues regarding its potential and practical use in acute ischemic stroke. In a situation where time is of the essence, is thrombolysis the best available solution?

Acute ischemic stroke (AIS), or "brain infarction", is most commonly a result of intracerebral artery occlusion due to embolism from proximal sites such as the internal carotid arteries, heart or aorta. Unlike cardiac arrest, where brain viability is measured in minutes, AIS presents with a mixture of salvageable tissue, allowing for a therapeutic window that can last several hours. While the definitive time frame has yet to be pinned down, the generally accepted mantra "Time is Brain" reflects the notion that prognosis is improved by early intervention. The question now is whether there is a role for thrombolytic therapy in the management of AIS.

The two most prominent candidates for use in thrombolytic AIS therapy are streptokinase and recombinant tissue plasminogen activator (rtPA), both serine proteases that catalyze the conversion of plasminogen to plasmin, which digests fibrin clots.

D'Arcy L. Little, MD, CCFP
York Community Services, Toronto, ON

Introduction
Every year there are approximately 50,000 strokes in Canada. Currently, close to 300,000 Canadians are stroke survivors. As stroke is an age-related condition, the number of strokes is predicted to increase as the Canadian population ages. The resultant national cost, which is estimated at 2.7 billion annually, will also increase unless improvements are made to prevention and treatment.¹ Approximately 1 in 6 survivors of a first stroke experiences a recurrent stroke over the next 5 years, of which 25% are fatal within 28 days.² The above statistics suggest that attention to secondary stroke prevention would be important in reducing the morbidity, mortality and cost to society of stroke. The purpose of this article is to review the role of anti-platelet and anticoagulant agents in the secondary prevention of stroke.

Goals of Therapy
Therapeutic measures in secondary stroke prevention aim to prevent recurrent stroke or transient ischemic attacks, with the aim of preventing morbidity and mortality from incremental neurological deficits, as well as preventing associated cardiac ischemic events.