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Chest Pain

The document discusses the process of atherosclerosis, which is the buildup of plaque in the arteries. It begins with risk factors that increase low-density lipoprotein (LDL) and decrease high-density lipoprotein (HDL), such as smoking, diabetes, and obesity. This leads to fat deposition and accumulation in the artery wall. Macrophages are recruited and secrete substances that damage the endothelium, causing the formation of fatty streaks and eventually more complex plaques called atheromas. Over time, these plaques can rupture, leading to thrombosis and blockages that reduce blood flow and oxygen delivery, potentially causing chest pain, heart attack, or other cardiovascular problems.

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kokotam
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368 views1 page

Chest Pain

The document discusses the process of atherosclerosis, which is the buildup of plaque in the arteries. It begins with risk factors that increase low-density lipoprotein (LDL) and decrease high-density lipoprotein (HDL), such as smoking, diabetes, and obesity. This leads to fat deposition and accumulation in the artery wall. Macrophages are recruited and secrete substances that damage the endothelium, causing the formation of fatty streaks and eventually more complex plaques called atheromas. Over time, these plaques can rupture, leading to thrombosis and blockages that reduce blood flow and oxygen delivery, potentially causing chest pain, heart attack, or other cardiovascular problems.

Uploaded by

kokotam
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOC, PDF, TXT or read online on Scribd
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Cigarette Smoking

Hypertension
Diabetes Mellitus
Obesity
Hypercholesterolemia
use oral contraceptive pills
Behavioral Patterns
Excessive intake of high cholesterol
diet
Genetic Predisposition

↑ LDL: ↓ HDL

Fat Deposition & accumulation @ intima

Formation of fatty streaks Invasion of macrophages

Inflammatory Response
Secretes injurious free Concentration of
radicals (superoxides) swollen cells
Platelet adherence Altered vessel wall
& ↑ permeability
Damage to endothelium Minor elevation of
Release of GF’s the intima
(Platelet-derived growth factor)

ATHEROMA

Proliferation of Deposition of Promote


smooth muscle cells collagen, elastin & chemotaxis
connective tissue
matrix
Fibrous cap

Progressive narrowing of
arterial lumen

Shortness of
breath upon Partial hypoxia Necrosis in the media
exertion

Deterioration of media
Vasodilation Activation of formation of Smooth muscle
anastomoses atrophy

Function may resume Ruptures easily due to ↑ pressure Destruction of internal


2◦ to collateral circulation elastic lamina

Enlargement of lesion
Gradual weakening of
arterial wall

Chest Loss of normally firm


Pain support

Activation of intrinsic Surface ulceration


coagulation pathway
Release of lactic
acid Exposes interior of the
Thrombosis to the surface atheroma to blood
of plaque

Anaerobic
respiration
Thromboembolism Pallor,
a
sweating, ↑
BP,
Angin
Imbalance of Obstruction of large
demand over coronary artery tachycardia
perfusion

Gradual weakening of ↓ cardiac output ↑ workload : ↓heart Physical response


myocardium contractility to stress
on
infarcti
Myocardial ischemia dial Inability of the heart to
Myocar compensate for the
increased demand
Necrosis
c shock
Cardiogeni
Release of Formation of
cardiac fibrous tissue failure
enzymes Heart
↓ extensible
CK, LDH,
Troponin

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