College of Physicians
Academy of Medicine of Malaysia
|COLLEGE OF PHYSICIANS VOL. 10 NO. 1 (FOR MEMBERS ONLY)
Table of Contents
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Message from the President
“Maintaining standards in housemanship training - Quality in the face of quantity”
The medical grapevine has been buzzing actively on various issues challenging our healthcare system. One of the more persistent issues has been the failure to address the problem of persistent brain drain and the persistent disparity of healthcare standard between urban and rural areas.
In some urban areas such as the Klang Valley, the doctor-patient ratio is about 1:390 which surpasses the World Health Organization’s (WHO) benchmark of 1:600.
On the other hand, in many rural areas, the deficit of medical manpower continues, especially in states like Sabah and Sarawak where the doctor-patient ratio could be as high as 1:4000.
Since the 1980s, the key strategy has been to “flood the market” with increasing the production of doctors to counter the “brain drain” and to address the doctor-patient ratio disparity in rural areas. In addition, it was hoped that with improving service conditions in the public sector, more doctors would be encouraged to stay and serve beyond the three years of compulsory national service.
Unfortunately, this strategy has had limited results. Thirty years down the road we are still faced with the same old scenario. We are producing more and more doctors each year. Doctors continue to leave for the lure of the private sector and doctors continue to want to work in urban setting where there are better facilities and opportunities for career development. More than two out of five of public medical posts are yet to be filled. In addition, this escalating production of doctors has itself resulted in an acute new problem and that is of falling standards in housemanship training.
Over the past 20 years, the mushrooming of medical schools has put a severe strain in providing sufficient and appropriate hands-on training facilities. Virtually all major public hospitals are now teaching hospitals for medical schools. The escalating commercialization of medical education has rapidly translated into more doctors produced each year in a relatively short time span. Today, we have about 22 medical schools in Malaysia that annually produce 4,000 medical graduates for a country of 27 million people. There are rumblings in the grapevine that there are plans to produce up to 5000 doctors yearly within the next five years. Superficially this appears to be a good thing except for the fact that there will now be an increasing shortage of places for comprehensive housemanship training.
Comprehensive housemanship training is a fundamental process in the finishing school for a good medical training. In the early 80s, it was sheer hard work. House officers were on active call, every other night. It provided trainees with the valuable hands-on experience needed to manage patients under supervision. With the current annual production of 4,000 medical graduates, there are just not enough patients and training posts in government hospitals for all these new medical graduates.
The situation will worsen further over the next five to seven years with more medical schools, both locally and overseas, churning out doctors by the thousands.
The recent move by the Ministry of Health to extend the housemanship training to two years is recognition of the fact of the matter. Unfortunately, by doing so, the problem is made acutely worse because immediately, there now needs to be 8,000 (4,000 x 2) houseman posts yearly.
It is now known that in some hospitals, house officers go on call once a week or once in two weeks. Some even have to share patients with their fellow housemen in the wards. At the end of the day, they will be inadequately exposed to the critical mass of patients that is essential for basic training to prepare them for their next job as medical officers where they are expected to deal with patients independently and also to supervise the next generation of house officers. On the other hand, we also hear of complaints that in some hospital units, some house officers have been so severely overworked to the extent that their quality of life and quality of care of patients may be compromised. Either way, the situation does not auger well for the system.
The discordance between production of doctors and the ability to provide sufficient housemenship training will eventually affect the overall quality of healthcare delivery in the years to come. It is clear that the strategy to flood the market with doctors will do more damage than good. It is now time to critically look at how to improve the qualitative aspects and move away from the quantitative aspects of medical training.
DR STEVEN KW CHOW
College of Physician, AMM
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ATP III At-A-Glance: Quick Desk Reference
STEP 1: Determine lipoprotein levels - obtain complete lipoprotein profile after 9- to 12-hour fast.
ATP III Classification of LDL, Total, and HDL Cholesterol (mg/dL)
LDL Cholesterol - Primary Target of Therapy
||Near Optimal/Above Optimal
||Near Optimal/Above Optimal
STEP 2: Identify presence of clinical atherosclerotic disease that confers high risk for coronary heart disease (CHD) events (CHD risk equivalent):
- Clinical CHD
- Symptomatic carotid artery disease
- Peripheral arterial disease
- Abdominal aortic aneurysm.
STEP 3: Determine presence of major risk factors (other than LDL):
Major Risk Factors (Exclusive of LDL Cholesterol) That Modify LDL Goals
- Cigarette smoking
- Hypertension (BP 140/90 mmHg or on antihypertensive medication)
- Low HDL cholesterol (<40 mg/dl)*
- Family history of premature CHD (CHD in male first degree relative <55 years; CHD in female first degree relative <65 years)
- Age (men 45 years; women 55 years)
* HDL cholesterol 60 mg/dL counts as a "negative" risk factor; its presence removes one risk factor from the total count.
Note: in ATP III, diabetes is regarded as a CHD risk equivalent.
STEP 4: If 2+ risk factors (other than LDL) are present without CHD or CHD risk equivalent, assess 10-year (shortterm) CHD risk (see Framingham tables).
Three levels of 10-year risk:
- >20% -- CHD risk equivalent
STEP 5: Determine risk category:
- Establish LDL goal of therapy
- Determine need for therapeutic lifestyle changes (TLC)
- Determine level for drug consideration
LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Different Risk Categories.
LDL Level at
|LDL Level at
Which to Consider
|CHD or CHD
||>130 mg/d (100-129
mg/dL: drug optional)*
|2+ Risk Factors
||10-year risk 10-20%:
|10-year risk <10%:
||>190 mg/dL (160-189
* Some authorities recommend use of LDL-lowering drugs in this category if an LDL cholesterol <100 mg/dL cannot be achieved by therapeutic lifestyle changes. Others prefer use of drugs that primarily modify triglycerides and HDL, e.g., nicotinic acid or fibrate. Clinical judgment also may call for deferring drug therapy in this subcategory.
** Almost all people with 0-1 risk factor have a 10-year risk <10%, thus 10-year risk assessment in people with 0-1 risk factor is not necessary.
STEP 6: Initiate therapeutic lifestyle changes (TLC) if LDL is above goal.
- TLC Diet:
- Saturated fat <7% of calories, cholesterol <200 mg/day
- Consider increased viscous (soluble) fiber (10-25 g/day) and plant stanols/sterols (2g/day) as therapeutic options to enhance LDL lowering
- Weight management
- Increased physical activity
STEP 7: Consider adding drug therapy if LDL exceeds levels shown in Step 5 table:
Consider drug simultaneously with TLC for CHD and CHD equivalents
Consider adding drug to TLC after 3 months for other risk categories.
Drugs Affecting Lipoprotein Metabolism
||Agents and Daily Doses
|HMG CoA reductase
|Lovastatin (20-80 mg),
Simvastatin (20-80 mg),
Fluvastatin (20-80 mg),
Atorvastatin (10-80 mg),
Cerivastatin (0.4-0.8 mg)
Active or chronic liver disease
Concomitant use of certain
|Cholestyramine (4-16 g)
Colestipol (5-20 g)
Colesevelam (2.6-3.8 g)
TG No change or increase
of other drugs
TG >400 mg/dL
TG >200 mg/dL
(crystalline) nicotinic acid
(1.5-3 gm), extended release
nicotinic acid (Niaspan ®)
(1-2 g), sustained release
nicotinic acid (1-2 g)
Hyperuricemia (or gout)
Upper GI distress
Chronic liver disease
Peptic ulcer disease
||Gemfibrozil (600 mg BID)
Fenofibrate (200 mg)
Clofibrate (1000 mg BID)
(may be increased in
patients with high TG)
Severe renal disease Severe
* Cyclosporine, macrolide antibiotics, various anti-fungal agents, and cytochrome P-450 inhibitors (fibrates and niacin should be used with appropriate caution).
STEP 8: Identify metabolic syndrome and treat, if present, after 3 months of TLC.
Clinical Identification of the Metabolic Syndrome - Any 3 of the Following:
>102 cm (>40 in)
>88 cm (>35 in)
* Overweight and obesity are associated with insulin resistance and the metabolic syndrome. However, the presence of abdominal obesity is more highly correlated with the metabolic risk factors than is an elevated body mass index (BMI). Therefore, the simple measure of waist circumference is recommended to identify the body weight component of the metabolic syndrome.
** Some male patients can develop multiple metabolic risk factors when the waist circumference is only marginally increased, e.g., 94-102 cm (37-39 in). Such patients may have a strong genetic contribution to insulin resistance. They should benefit from changes in life habits, similarly to men with categorical increases in waist circumference.
Treatment of the metabolic syndrome
- Treat underlying causes (overweight/obesity and physical inactivity):
- Intensify weight management
- Increase physical activity
- Treat lipid and non-lipid risk factors if they persist despite these lifestyle therapies:
- Treat hypertension
- Use aspirin for CHD patients to reduce prothrombotic state
- Treat elevated triglycerides and/or low HDL (as shown in Step 9 below)
STEP 9: Treat elevated triglycerides.
ATP III Classification of Serum Triglycerides (mg/dL)
Treatment of elevated triglycerides (>150 mg/dL)
- Primary aim of therapy is to reach LDL goal.
- Intensify weight management.
- Increase physical activity.
- If triglycerides are >200 mg/dL after LDL goal is reached, set secondary goal for non-HDL cholesterol (total - HDL) 30 mg/dL higher than LDL goal.
Comparison of LDL Cholesterol and Non-HDL Cholesterol Goals for Three Risk Categories
|CHD and CHD Risk Equivalent
(10-year risk for CHD >20%)
|Multiple (2+) Risk Factors and
10-year risk <20%
|0-1 Risk Factor
If triglycerides 200-499 mg/dL after LDL goal is reached, consider adding drug if needed to reach non-HDL goal:
intensify therapy with LDL-lowering drug, or
add nicotinic acid or fibrate to further lower VLDL.
If triglycerides >500 mg/dL, first lower triglycerides to prevent pancreatitis:
very low-fat diet (15% of calories from fat)
weight management and physical activity
fibrate or nicotinic acid
when triglycerides <500 mg/dL, turn to LDL-lowering therapy.
Treatment of low HDL cholesterol (<40 mg/dL)
First reach LDL goal, then:
Intensify weight management and increase physical activity.
If triglycerides 200-499 mg/dL, achieve non-HDL goal.
If triglycerides <200 mg/dL (isolated low HDL) in CHD or CHD equivalent, consider nicotinic acid or fibrate.
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Update Article / Short Review
The efficacy of endoscopic sphincterotomy after cholecystectomy in patients with sphincter-of-Oddi dysfunction
Geenen JE, Hogan WJ, Dodds WJ, Toouli J, Venu RP
Division of Gastroenterology, Medical College of Wisconsin, Milwaukee
Forty-seven patients thought to have dysfunction of the sphincter of Oddi were randomly assigned to undergo endoscopic sphincterotomy or sham sphincterotomy in a prospective double-blind study. All the patients had pain resembling biliary pain, had previously undergone a cholecystectomy, and had clinical characteristics suggesting biliary obstruction. The patients were randomly assigned to the treatment (n = 23) or nontreatment (n = 24) group before manometric examination of the sphincter of Oddi was performed. Sphincterotomy resulted in improvement in pain scores at one-year follow-up in 10 of 11 patients with elevated sphincter pressure. In contrast, there was improvement in only 3 of 12 patients with elevated basal sphincter pressures who underwent the sham procedure. In patients with normal sphincter pressure, pain scores were similar regardless of treatment. After one year, sphincterotomy was performed in 12 symptomatic patients who had undergone the sham procedure--7 with elevated sphincter pressures and 5 with normal sphincter pressures. Forty patients were followed for four years. Of the 23 patients with increased sphincter pressure, 10 of the original 11 who underwent sphincterotomy remained virtually free of pain; 7 others who subsequently underwent sphincterotomy also benefited from it. Thus, 17 of 18 patients with sphincter-of-Oddi dysfunction verified by manometry benefited from sphincterotomy. In patients with normal sphincter pressure, sphincterotomy was no more beneficial than sham therapy. Our observations suggest that endoscopic sphincterotomy offers long-term relief of pain in a group of patients with verified sphincter-of-Oddi dysfunction.
Manometry based randomised trial of endoscopic sphincterotomy for sphincter of Oddi dysfunction
J Toouli, I Roberts-Thomson, J Kellow, J Dowsett, G Saccone, P Evans, P Jeans, M Cox, P Anderson, C Worthley, Y Chan, N Shanks and A Craig
GI Surgical Unit, Flinders Medical Centre, Adelaide, Australia.
BACKGROUND—Endoscopic sphincterotomy for biliary-type pain after cholecystectomy remains controversial despite evidence of efficacy in some patients with a high sphincter of Oddi (SO) basal pressure (SO stenosis).
AIM—To evaluate the effects of sphincterotomy in patients randomised on the basis of results from endoscopic biliary manometry.
METHODS—Endoscopic biliary manometry was performed in 81 patients with biliary-type pain after cholecystectomy who had a dilated bile duct on retrograde cholangiography, transient increases in liver enzymes after episodes of pain, or positive responses to challenge with morphine/neostigmine. The manometric record was categorised as SO stenosis, SO dyskinesia, or normal, after which the patient was randomised in each category to sphincterotomy or to a sham procedure in a prospective double blind study. Symptoms were assessed at intervals of three months for 24 months by an independent observer, and the effects of sphincterotomy on sphincter function were monitored by repeat manometry after three and 24 months.
RESULTS—In the SO stenosis group, symptoms improved in 11 of 13 patients treated by sphincterotomy and in five of 13 subjected to a sham procedure (p = 0.041). When manometric records were categorised as dyskinesia or normal, results from sphincterotomy and sham procedures did not differ. Complications were rare, but included mild pancreatitis in seven patients (14 episodes) and a collection in the right upper quadrant, presumably related to a minor perforation. At three months, the endoscopic incision was extended in 19 patients because of manometric evidence of incomplete division of the sphincter.
CONCLUSION—In patients with presumed SO dysfunction, endoscopic sphincterotomy is helpful in those with manometric features of SO stenosis.
Keywords: sphincter of Oddi; manometry; endoscopic sphincterotomy; motility; bile duct; pancreas
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ECG Quiz / Self Assessment
1. Write a report on this ECG.
2. What is the likely significance of the T waves in this ECG?
1. Name five ECG diagnoses.
A 50 year old man presented with nausea and vomiting 1 week prior to admission. He was recently diagnosed to be hypertensive and was prescribed Moduretic by the private practitioner. He was found to be hyponatremic (sodium 110 mmol/L) and was given saline infusion. The following day, he was found to be confused. A brain MRI was performed. What complication had occurred?
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||Atrial 88 per minute, ventricular 25 per minute
||Complete heart block with variable ventricular
||Duration: 0.12-0.16 secs
Configuration: Q in AVL, I and V4
||Giant inversion, particularly V2-4
2 The T waves are nearly pathognomonic of a recent syncopal attack
Comments: The axis cannot be worked out as some of the complexes are right ventricular and some left ventricular in origin. This patient recovered spontaneously. He died a month later from bronchopneumonia. There was left ventricular hypertrophy at post-mortem and small areas of fibrosis in the left ventricle, but no area on infartion greater than 0.06 cm diameter. The brain was macroscopically normal.
||100 per minute
||Sinus rhythm. PR interval 0.36 secs
Duration: 0.12 secs
Configuration: RSR ' in AVR and V1. Slurred S
in II, AVL and V6. Deep Q waves in II, III, AVF,
V2 to V6
||Elevation in II and III
||Flat in III. Each T waves is deformed by presence
of a P waves
(a) First degree heart block
(b) Complete right bundle-branch block
(c) Left axis deviation
(d) Transmural inferior myocardial infarction
(e) Transmural anterior myocardial infarction
A: Central pontine myelinolysis
MRI T1-weighted image shows a hypointense lesion in the pontine area which appears hyperintense on T2-weighted image.
Central pontine myelinolysis (CPM) is characterized primarily by the symmetric destruction of myelin sheaths in the pons. Most patients who develop pontine myelinolysis have had documented hyponatremia, and serum sodium levels were corrected rapidly to normal or supranormal levels. This condition has been associated with chronic alcoholics, undernutrition and dehydrated patients resulting from vomiting, diarrhea or diuretic therapy. The main underlying factor is related to the rapid correction of serum sodium levels.
The clinical manifestations vary from asymptomatic to comatose. Neurologic signs and symptoms appear within 2 to 3 days after rapid correction of sodium levels. Findings include dysarthria, mutism, behavioral abnormalities, ophthalmoparesis, bulbar and pseudobulbar palsy, hyperreflexia, quadriplegia, seizures, and coma. Extra pontine involvement may affect the cerebellum, putamen, thalamus, corpus callosum, subcortical white matter, claustrum, caudate, hypothalamus, lateral geniculate bodies, amygdala, subthalamic nuclei or substantia nigra.
Computed tomography abnormalities include symmetric areas of hypodensity in the pons or extrapontine regions without associated mass effect. Lesions appear hypointense on TIWI and hyperintense on T2WI MRI. Cerebrospinal fluid levels of protein and myelin basic protein may be elevated.
In animal studies, after administration of hypertonic saline in hypotonic rats, there is opening of the blood brain barrier followed by swelling of the inner loop of the myelin sheath, oligodendrocyte degeneration and release of macrophage derived factors leading to eventual breakdown of myelin.
Prevention of myelinolysis includes judicious correction of hyponatremia with saline ( not more than 12 mmol/L in 24 hours) and free water restriction, discontinuation of diuretic therapy, correction of metabolic abnormalities and medical complications.
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