Name: Karl Jasper C.

Cabagnot, RPh Date: August 10, 2022

Course and Section: BS Pharmacy Major in Clinical Pharmacy 5B

Subject: Pathophysiology 1

Concepts of Health and Disease: Seatwork 1

This section was obtained from the abdominal aorta of a 58-year-old man who had died as the result of a
myocardial infarct. The aorta was slightly wider than normal and was inelastic. The intima, especially in the
ascending and abdominal portion, contained numerous yellowish plaques, some of which were ulcerated and/or
calcified. A "porridge" like material was seen within some of these plaques when they were sectioned.

1. What are the possible risk factors for developing atherosclerosis in this patient?

Answer:

Atherosclerosis is defined as the disease which is characterized by the narrowing and hardening of
arterial walls due to the formation of plaques in the arteries. The formation of plaques on the arteries leads to
obstruction of blood flow of heart muscles which will later lead on the rupture of arteries creating thrombus.

In the given case, possible risk factor for this patient will be:

a) Being obese and be having High triglycerides and LDL (Low Density Lipoprotein) levels. This is because
it is stated the case that the patient has yellowish plaques in the abdominal portions. Having high
amounts or concentration of LDLs and triglycerides can be deposited in the tunica intima which will
later cause development of thrombus will lead to the disease formation.
b) Having High blood pressure. As a 58-year-old man, this patient possibly be having high blood pressure
because it is evident that the aorta is slightly wider and inelastic thus manifests high blood pressure
which can damage the blood vessels and arterial walls affecting its elasticity and sensitivity.
Additionally, LDL and triglycerides can gather on to damage areas and can cause clogging the arteries
leading to atherosclerosis.
c) Having High saturated fat diet and Alcoholism. High fat intake can lead to increase concentration of
bad cholesterols (LDL) in blood and Alcoholism having heavy alcohol consumption can weaken and thins
heart muscles which disrupts efficient blood flow.
d) Smoking. The chemicals inhaled when smoking e.g., nicotine and other chemicals present in cigarettes
may damage the heart muscle elasticity and sensitivity and build-up of plaques can be intensified.

2. How does atherosclerosis cause Myocardial Infarction?

Answer:

Myocardial Infarction comes from the Greek words “myo” which means “muscle”; “kardia” which
means “heart” and Latin word “infarcire” which means “to stuff into”. Together, Myocardial Infarction or
commonly known as “heart attack” is defined as the decreased or complete cessation of blood flow on the heart
muscle. Myocardial Infarction is the result of the cascade of complex events and process of thrombus formation
which is termed as atherosclerosis.

Atherosclerosis is the primary underlying disease process of Myocardial Infarction. The accumulation
of lipid (and other substances which is called foam cells) in the layer of tunica intima, together with the
inflammation brought about by the white blood cells forms thrombus and driven by vascular inflammation
triggers impede or complete blockade of the blood vessels. As this event continues, large parts of the arteries
do not receive oxygenated blood. Prolonged deprivation of oxygen can later result to myocardial deterioration
and cell death which therefore results to heart attack or Myocardial Infarction. This disease is usually
characterised by chest discomfort and/ or chest pain (angina), shortness of breath, vomiting, nausea and
fainting.
3. How does atherosclerosis develop?

Answer:

Atherosclerosis can develop in the layers of the arterial walls. The layer consists of first, the
endothelium, next the tunica intima, then the tunica media containing smooth muscle cells. Outside the
endothelium is the lumen where the LDL (Low Density Lipoproteins) resides. In the case of Atherosclerosis, there
is an endothelial cells dysfunction where the endothelium allows LDL to move into the tunica intima layer.

When the LDL enters the tunica intima, the dysfunctional endothelial cells release ROS (Reactive
Oxygen Species) and other enzymes such as metalloproteases which will oxidize the LDL. When the LDLs are
oxidized, it cannot leave the tunica intima and is trapped inside. The dysfunctional endothelium and the oxidized
LDL triggers to express adhesion molecules for white blood cells such as monocytes and it attaches to the
receptors and consequently moves into the tunica intima.

When that happens, the Monocytes will become Macrophages. Macrophages has a scavenger receptor
which will engulfs the oxidized LDL and eventually become foam cells. Foam cells could attract more
macrophages by releasing chemokines. Also, foam cells can release IGF-1 which is a growth factor and can cause
smooth muscle cells from the tunica media to migrate and cause smooth muscle cell proliferation into the tunica
intima. More smooth muscle cells facilitate the production of more collagen. Additionally, foam cells can also
die releasing their lipid contents including DNA materials which will then attracts neutrophils because of
inflammation. Foam cells can also release pro-inflammatory cytokines and ROS. This, together with neutrophils
can elevate inflammation in the area. The are is now termed as the plaque, which is basically composed of dead
foam cells, smooth muscle cells. When this has happened, there will be an increase of blood supply to the layer
of the tunica intima to the vessels called vasa vasorum.

T-cells has also a role in the process. They combine into adhesion receptors which are expressed on
the endothelial cells and enter the plaque area and can also be activated by macrophages and release substances
such as interferon gamma (INF-y) which also promotes inflammation and activates endothelial cells to attract
more white blood cells. The process continues to grow and can rupture which can cause thrombosis and forms
thrombus to further aggregate the area in which causes the obstruction of blood flow.