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CARDIOLOGY TO IMPRESS - The Ultimate Guide for Students and Junior Doctors©
Imperial College Press
http://www.worldscibooks.com/medsci/p704.html
 
107
Chapter 4
Commonly EncounteredConditions
 Attending outpatient clinics can be an extremely valuable learningexperience. However, with increasing time restraints on senior staff, itis important to be proactive in making the most of the availableopportunities. If you let it all float past, you can end up sitting in thecorner while the clinic happens around you, catching the odd pathol-ogy ‘here and there’ without making the best of your opportunitiesto gain understanding and experience.In this chapter we will explore the most commonly encounteredconditions, thus enabling you to be better prepared to get the mostout of your time in clinic. We recommend reading the chapters beforethe clinic sessions so that you can concentrate on improving therecognition of key symptoms and signs, examining the patient andunderstanding the current management protocol in both out andin-patient clinical settings.Remember you are NOT expected to know everything thereisto know about these conditions, but you will impress your sen-iorsby demonstrating a practical knowledge of these commonconditions.
4.1Atherosclerosis
 Atherosclerosis is a multifactorial, chronic inflammatory processcharacterised by the build-up of an
atheromatous plaque 
 which narrowsthe luminal diameter of an artery.
 
CARDIOLOGY TO IMPRESS - The Ultimate Guide for Students and Junior Doctors©
Imperial College Press
http://www.worldscibooks.com/medsci/p704.html
 
Five steps to understanding the pathogenesisof atherosclerosis:1.Damage to the arterial endothelium
— caused by repeatedinjury to the endothelial cells. This makes the endothelium morepermeable to lipids and low density lipoprotein (LDL) allowingthem to migrate into the tunica intima.
2.Formation of a fatty streak 
— macrophages are also ‘attracted’ tothe injured endothelium and migrate into the intima. They then takeup the oxidised LDL to form foam cells. The foam cells together with activated platelets trigger the movement of smooth muscle cellsfrom the tunica media into the intima.
3.Lipid plaque
— the build up of smooth muscle cells, foam cellsand free lipids creates the lipid plaque.
4.Fibrous plaque
— as the plaque grows, the smooth muscle cellsare replaced by collagen. The collagen layer forms a fibrous plaque.
5.Thrombus formation
— when the plaque fissures, this results infurther platelet aggregation and the formation of a thrombus,causing further narrowing of the luminal diameter of the vessel.
108
Chapter 4 
Figure 4.1
Layers of the endothelium
Let’s begin by examining a ‘normal’ blood vessel — composed of endothelial cells. The endothelium has three layers: tunica intima,tunica media, and tunica adventia.
 
CARDIOLOGY TO IMPRESS - The Ultimate Guide for Students and Junior Doctors©
Imperial College Press
http://www.worldscibooks.com/medsci/p704.html
 
The plaque that forms has several clinical implications:
•
Stable angina
is caused by progressive stenosis (narrowing) of the vessel. This reduces the blood supply to the tissues during exercise/exertion known as
ischaemia 
resulting in hypoxic damage to thecells causing pain.
Commonly Encountered Conditions 
109Figure 4.2
Formation of an atheromatous plaque
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