1 Assessment details Assessment 1: Case Study Weighting: 40% Word count: 1250 words Marking criteria and standards: See pages XXXXXXXXXXAim of assessment The purpose of this assessment is for the...

PATHOPHYSIOLOGY OF ISCHAEMIC DISEASE OF THE CEREBRAL
HEMISPHERE
Ischemic Heart Disease
IHD is caused due to Imbalance between supply and demand of the blood. The
Narrowing and hardening of the arteries leads to this kind of imbalance for cardiac
muscle .
Symptoms of IHD
Angina pectoris – which is referred as the cardiac pain resulting from myocardial
ischemia , Usually occurs in substernal region, jaw, neck, or arms, may also be in
epigastrum and interscapular regions. The Symptoms are feeling pressure,
heaviness, fullness, squeezing, burning, aching, choking, or even dyspnea.
The Emerging evidence strongly suggests that coronary heart disease (CHD),which
is the result of vesselocclusion deposition of lipids, is a manifestation of a chronic
inflammatory response . Elevated plasma cholesterol levels is already established
as risk factors for CHD, and lowering cholesterol levels, particularly low-density
lipoprotein cholesterol (LDL-C), is the main focus of the prevention of CHD.
Evidence suggests that there are lipid-lowering modes of therapy which also
reduce inflammation, thereby reducing the risk of cardiovascular events, even for
individuals with LDL-C levels in the normal range (130 mg/dL) based on the
National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP
III) guidelines. The frequent presence of fatty streaks in young children is
consistent with the chronic nature of atherosclerotic progression. the possible
events that can initiate fatty streak formation are such as - LDL-C, modified by
oxidation, glycation, and association with proteoglycans and immune complexes,
which can become trapped in the arterial wall, thereby injuring the endothelium
and vascular smooth muscle.
Once when trapped, LDL-C particles become progressively more oxidized, and
form lipid peroxides, and hence facilitate accumulation of cholesterol esters. Also,
modified LDLC is chemotactic for circulation of monocytes and stimulates the
proliferation of macrophages already in the lession. The Inflammatory mediators
increase the binding of LDL-C to endothelial cells and vascular smooth muscle
cells which have migrated into the lesion. As the plaque becomes thicker, the
arterial wall responds by “remodeling,” that is, gradual dilation to maintain the
diameter of the vessel lumen. Eventually, macrophages may be...