Myocardial Ischemia Flashcards
1
Q
What occurs during myocardial ischemia?
A
Blood flow to the heart muscle (myocardium) is reduced, preventing it from receiving enough oxygen.
Myocardial ischemia is often a precursor to more severe cardiovascular issues.
2
Q
What usually causes reduced blood flow in myocardial ischemia?
A
A partial or complete blockage of the heart’s arteries, often due to atherosclerosis.
Atherosclerosis involves the accumulation of fatty deposits and other substances on arterial walls.
3
Q
What are common symptoms of myocardial ischemia?
A
Chest pain (angina), shortness of breath, fatigue, or it may be asymptomatic (silent ischemia).
Asymptomatic ischemia can make diagnosis challenging.
4
Q
What serious conditions can myocardial ischemia lead to if left untreated?
A
Heart attacks, heart failure, or arrhythmias.
Prompt treatment is crucial to prevent these severe outcomes.
5
Q
What are typical management strategies for myocardial ischemia?
A
Lifestyle changes, medications, and sometimes medical procedures like angioplasty or coronary artery bypass surgery.
These strategies aim to restore proper blood flow to the heart.
6
Q
Fill in the blank: Myocardial ischemia is often caused by _______.
A
[atherosclerosis]
7
Q
True or False: Myocardial ischemia can be asymptomatic.
A
True
This is referred to as silent ischemia.
8
Q
What is myocardial oxygen demand?
A
The amount of oxygen the heart muscle requires to function effectively.
This demand is influenced by various factors such as heart rate, contractility, wall tension, and myocardial mass.
9
Q
How does heart rate affect myocardial oxygen demand?
A
An increase in heart rate elevates the demand for oxygen because the heart is working harder and faster.
This leads to more frequent contractions.
10
Q
What does contractility refer to in the context of myocardial oxygen demand?
A
The inherent strength and vigor of the heart’s contractions.
Greater contractility increases oxygen demand as more energy and oxygen are needed for stronger contractions.
11
Q
What influences wall tension in the ventricles?
A
Preload and afterload.
Preload is the volume of blood returning to the heart, while afterload is the resistance the heart must overcome to eject blood.
12
Q
Define preload in relation to myocardial oxygen demand.
A
The volume of blood returning to the heart which stretches the heart muscle fibers.
An increase in preload raises oxygen demand as the heart works harder to pump the additional volume.
13
Q
What is afterload?
A
The resistance the heart must overcome to eject blood during systole.
Increased afterload elevates oxygen demand, often due to high blood pressure or aortic stenosis.
14
Q
How does myocardial mass affect oxygen demand?
A
A larger heart muscle mass demands more oxygen because there is more tissue to be supplied.
This is often seen in conditions like hypertrophy due to chronic high blood pressure.
15
Q
What can result from a disruption in the balance between oxygen supply and demand?
A
Conditions such as myocardial ischemia.
Increased demand without corresponding supply can lead to ischemic episodes.
16
Q
Name two types of medications that can help manage oxygen demand.
A
- Beta-blockers
- Calcium channel blockers
These medications reduce heart rate and contractility, thereby lowering oxygen demand.
17
Q
True or False: Increased afterload decreases myocardial oxygen demand.
A
False
Increased afterload elevates oxygen demand as the heart requires more energy to push against the resistance.
18
Q
Fill in the blank: An increase in _______ stretches the heart muscle fibers, raising oxygen demand.
A
[preload]
19
Q
What is myocardial ischemia?
A
A condition caused by reduced blood flow to the heart muscle
Myocardial ischemia can lead to chest pain and other cardiovascular complications.
20
Q
What is the most common cause of myocardial ischemia?
A
Atherosclerosis
Atherosclerosis involves the buildup of fatty deposits (plaques) in the coronary arteries.
21
Q
What does coronary artery spasm refer to?
A
A temporary tightening or constriction of the muscles in the artery wall
This can restrict blood flow temporarily, affecting both healthy and diseased arteries.
22
Q
What is coronary artery thrombosis?
A
Formation of a blood clot within a coronary artery
It can potentially lead to a complete blockage of blood flow.
23
Q
How does severe anemia contribute to myocardial ischemia?
A
By significantly reducing red blood cells or hemoglobin, impairing oxygen delivery
This affects the tissues including the heart muscle.
24
Q
What are tachyarrhythmias?
A
Rapid heart rhythms that increase oxygen demand while reducing coronary blood flow during diastole
They can exacerbate ischemic conditions.
25
How does hypertension affect the heart's oxygen demand?
It increases afterload and can lead to left ventricular hypertrophy
## Footnote
Both factors increase the heart’s oxygen demand.
26
What are congenital coronary artery anomalies?
Structural anomalies of the coronary arteries present at birth
## Footnote
These can lead to ischemia in affected individuals.
27
How do physical exertion and emotional stress contribute to myocardial ischemia?
They increase heart rate and contractility, thus elevating oxygen demand
## Footnote
This can lead to a mismatch between oxygen supply and demand.
28
What effect does cocaine use have on the coronary arteries?
It can cause severe coronary artery spasm and increase heart rate and blood pressure
## Footnote
This raises the risk of ischemia significantly.
29
What are some other factors that can contribute to myocardial ischemia?
Severe hypotension or hypoxia
## Footnote
These conditions restrict oxygen supply to the heart.
30
What are common approaches to address myocardial ischemia?
A combination of lifestyle changes, medical management, and interventional procedures
## Footnote
These aim to restore proper coronary blood flow and relieve symptoms.
31
What is Prinzmetal’s (Variant) Angina?
A form of angina caused by transient coronary artery spasm, leading to temporary narrowing of the coronary arteries.
## Footnote
Characterized by severe pain, often occurring at rest, particularly during the night or early morning.
32
What are the characteristics of Prinzmetal’s Angina?
* Occurs usually at rest
* Pain is severe and transient (lasting from a few minutes to 20 minutes)
* EKG shows ST-segment elevation during spasm
## Footnote
The ST-segment elevation typically resolves after the spasm subsides.
33
What triggers Prinzmetal’s Angina?
* Cold
* Stress
* Smoking
* Certain medications
## Footnote
These triggers lead to hyperreactivity of the coronary artery smooth muscle.
34
What is the management strategy for Prinzmetal’s Angina?
* Calcium channel blockers (e.g., nifedipine)
* Nitrates for acute spasms
* Avoidance of triggers
## Footnote
Calcium channel blockers help prevent spasms.
35
Define Chronic (Stable) Angina.
Predictable chest pain triggered by physical exertion or emotional stress, relieved by rest or nitrates.
## Footnote
It is a chronic condition with a consistent pattern over time.
36
What are the characteristics of Chronic Angina?
* Occurs during exertion or emotional distress
* Duration of less than 20 minutes
* EKG shows ST depression or T-wave inversion
## Footnote
The pattern remains consistent over time.
37
What is the mechanism behind Chronic Angina?
Due to a fixed atherosclerotic blockage in coronary arteries causing ischemia when oxygen demand exceeds supply.
## Footnote
This blockage limits blood flow during increased activity.
38
What management strategies are used for Chronic Angina?
* Lifestyle modifications
* Medications like nitrates, beta-blockers, and calcium channel blockers
* Revascularization procedures if needed
## Footnote
Management focuses on reducing symptoms and improving quality of life.
39
What defines Unstable Angina?
A more serious form of angina that occurs unpredictably, with increasing frequency, severity, or duration, often at rest.
## Footnote
It is considered an emergency situation.
40
What are the characteristics of Unstable Angina?
* Chest pain that can wake the patient from sleep
* Unrelieved by nitrates
* Duration typically longer than stable angina (>20 minutes)
* May be associated with new or worsening symptoms
## Footnote
This type of angina may indicate a higher risk of myocardial infarction.
41
What is the mechanism behind Unstable Angina?
Usually caused by a rupture of an atherosclerotic plaque with subsequent thrombus formation leading to partial or temporary occlusion.
## Footnote
This can critically compromise blood flow to the heart.
42
What are the risks associated with Unstable Angina?
Increased likelihood of progressing to myocardial infarction.
## Footnote
Urgent medical attention is necessary to prevent complications.
43
What is the management for Unstable Angina?
* Emergency treatment: nitrates, oxygen, antiplatelet agents (aspirin), anticoagulants
* Revascularization (angioplasty or surgery)
* Hospitalization and close monitoring
## Footnote
Rapid intervention is critical to mitigate risks.
44
True or False: Prinzmetal's Angina occurs predictably with exertion.
False
## Footnote
Prinzmetal's Angina typically occurs at rest and is not predictable.
45
Fill in the blank: Chronic Angina is relieved by _______.
[rest or nitrates]
## Footnote
This distinguishes it from unstable angina, which is not relieved by nitrates.
46
What EKG changes are associated with Unstable Angina?
May show ST depression, T wave inversion, or transient ST elevation.
## Footnote
These changes indicate varying levels of ischemia.
47
What are the ECG changes during an anginal episode in Chronic (Stable) Angina?
ST depression and T-wave inversion
## Footnote
ST depression is typically ≥1 mm below baseline, and T waves may become inverted, indicating ischemia.
48
What is typically observed on an ECG between episodes of Chronic (Stable) Angina?
Normal ECG
## Footnote
Resting ECGs may not show abnormalities, as ischemia is transient.
49
During an attack of Unstable Angina, what ECG changes are observed?
ST depression or T-wave inversion
## Footnote
Similar to stable angina, but no persistent ST elevation.
50
What is seen on the ECG at rest in cases of Unstable Angina?
Persistent ST depression or T-wave inversion
## Footnote
Ischemic changes may be transient or persistent in some cases.
51
What characterizes Prinzmetal’s (Variant) Angina during a spasm?
Transient ST elevation
## Footnote
Typically occurs during an ischemic spasm caused by coronary artery spasm.
52
What happens to the ECG after the spasm in Prinzmetal’s Angina?
ECG returns to baseline
## Footnote
T-wave inversion or ST depression may be seen after the episode.
53
What does ST segment elevation during angina indicate?
Acute ischemia
## Footnote
This is especially true in Prinzmetal’s angina.
54
What is common about the ECG changes during symptomatic episodes of angina?
Transient changes
## Footnote
May only be present during symptomatic episodes.
55
What is often required for accurate diagnosis of angina?
Serial ECG recordings during symptoms
## Footnote
This helps to capture transient ischemic changes.
56
What are the main goals of angina management?
Relieve symptoms, prevent progression, reduce risk of myocardial infarction and death
## Footnote
These goals guide the overall approach to treating angina.
57
List lifestyle modifications recommended for angina management.
* Smoking cessation
* Dietary changes (low fat, low salt)
* Regular physical activity
* Weight management
* Blood pressure control
* Lipid management
* Stress reduction
## Footnote
These modifications aim to improve overall cardiovascular health.
58
What is the role of nitrates in angina treatment?
Rapid relief of acute angina episodes and used prophylactically to prevent attacks
## Footnote
Sublingual nitroglycerin is a common nitrate used.
59
How do beta-blockers help in angina management?
Reduce heart rate, contractility, and oxygen demand
## Footnote
They are useful in both stable and unstable angina.
60
What are calcium channel blockers used for in angina?
Vasodilation, decrease afterload, relieve coronary spasm (Prinzmetal’s)
## Footnote
Examples include amlodipine, nifedipine, and verapamil.
61
When are ACE inhibitors or ARBs indicated in angina treatment?
If the patient has hypertension, heart failure, or diabetes
## Footnote
These medications help manage comorbid conditions.
62
What is the purpose of antiplatelet agents like aspirin in angina management?
Prevent thrombosis in coronary arteries
## Footnote
This reduces the risk of acute coronary events.
63
What role do statins play in angina treatment?
Lower LDL cholesterol and stabilize plaques
## Footnote
Statins are important for long-term cardiovascular risk reduction.
64
What additional measures may be taken during acute angina episodes?
* Oxygen therapy if hypoxic
* Anticoagulants (e.g., heparin) in unstable angina or NSTEMI
## Footnote
These measures aim to stabilize the patient in acute settings.
65
What is Percutaneous Coronary Intervention (PCI)?
Angioplasty and stenting for significant stenosis or refractory symptoms
## Footnote
PCI is a minimally invasive procedure to restore blood flow.
66
When is Coronary Artery Bypass Grafting (CABG) indicated?
In multiple-vessel disease or complex lesions
## Footnote
CABG is a more invasive surgical option for severe cases.
67
What is included in monitoring and follow-up for angina patients?
* Regular assessment of symptoms
* Lipid profile management
* Blood pressure control
* Cardiac function evaluation (echocardiography, stress testing)
## Footnote
Ongoing evaluation is crucial for effective management.
68
What are key components of patient education in angina management?
* Recognizing angina symptoms
* Use of sublingual nitrates
* Lifestyle modifications
* Medication adherence
## Footnote
Patient education helps empower individuals to manage their condition effectively.
69
Fill in the blank: The specific treatment plan for angina depends on the type of angina, severity, patient ________, and response to initial therapy.
comorbidities
## Footnote
Individualization of treatment is essential for optimal outcomes.
70
What are foundational lifestyle modifications for preventing atherosclerosis?
Dietary changes, regular physical activity, weight management, smoking cessation, blood pressure control, glycaemic control, limiting alcohol.
## Footnote
These lifestyle changes are essential for both prevention and management of atherosclerosis.
71
What dietary changes should be made to manage atherosclerosis?
Reduce saturated fats, trans fats, dietary cholesterol; increase fruits, vegetables, whole grains, lean proteins, omega-3 fatty acids.
## Footnote
A balanced diet can significantly impact cardiovascular health.
72
What is the recommended amount of physical activity to prevent atherosclerosis?
At least 150 minutes/week of moderate-intensity exercise.
## Footnote
Moderate-intensity exercise includes activities like brisk walking.
73
What is the importance of weight management in preventing atherosclerosis?
Achieve and maintain a healthy body weight.
## Footnote
Maintaining a healthy weight reduces risk factors associated with atherosclerosis.
74
What is the role of smoking cessation in managing atherosclerosis?
Complete avoidance of tobacco products.
## Footnote
Smoking is a significant risk factor for cardiovascular diseases.
75
How can blood pressure be controlled in the context of atherosclerosis?
Reduce salt intake, manage stress, adhere to antihypertensive therapy if prescribed.
## Footnote
Effective blood pressure management is crucial for cardiovascular health.
76
What is the goal of glycaemic control for diabetics in relation to atherosclerosis?
Maintain blood glucose within target ranges.
## Footnote
Proper glycaemic control helps reduce cardiovascular risks in diabetic patients.
77
What are the recommendations regarding alcohol consumption for atherosclerosis management?
Avoid excessive alcohol consumption.
## Footnote
Moderate alcohol intake may have some benefits, but excessive consumption poses risks.
78
What are the primary lipid-lowering agents used in pharmacological therapy for atherosclerosis?
* Statins
* Ezetimibe
* PCSK9 Inhibitors
* Fibrates
* Niacin
* Omega-3 Fatty Acids
## Footnote
These agents target lipid levels to reduce cardiovascular risk.
79
What is the primary function of statins in managing cholesterol levels?
Reduce LDL cholesterol significantly and have pleiotropic effects.
## Footnote
Pleiotropic effects include anti-inflammatory and plaque stabilization.
80
What is the role of Ezetimibe in cholesterol management?
Inhibits intestinal cholesterol absorption.
## Footnote
Ezetimibe is often used in conjunction with statins.
81
What are PCSK9 Inhibitors used for?
Very potent LDL reduction; used for familial hypercholesterolemia or statin intolerance.
## Footnote
These agents are a newer class of cholesterol-lowering medications.
82
What are the effects of Fibrates on lipid profiles?
Lower triglycerides, modest LDL reduction, raise HDL.
## Footnote
Fibrates are particularly effective in lowering triglyceride levels.
83
What is the function of Niacin in lipid management?
Raises HDL; lowers LDL and triglycerides.
## Footnote
Niacin can be used in certain patients to improve lipid profiles.
84
What are the cardiovascular benefits of Omega-3 Fatty Acids?
Lower triglycerides and have anti-inflammatory effects.
## Footnote
Omega-3 fatty acids can be found in fish oil and certain plant oils.
85
What is the function of antiplatelet agents like Aspirin in atherosclerosis management?
Inhibits platelet aggregation; reduces cardiovascular events.
## Footnote
Antiplatelet therapy is crucial for preventing heart attacks and strokes.
86
What are common antihypertensive agents used in atherosclerosis treatment?
* ACE inhibitors
* ARBs
* Calcium channel blockers
* Diuretics
## Footnote
These medications help control blood pressure and provide vascular benefits.
87
What is the role of Metformin in diabetes control for atherosclerosis management?
Maintain optimal glycaemic control.
## Footnote
Metformin is a first-line medication for type 2 diabetes.
88
What is Percutaneous Coronary Intervention (PCI)?
Angioplasty and stenting for significant stenoses.
## Footnote
PCI is a minimally invasive procedure to open blocked arteries.
89
What is Coronary Artery Bypass Grafting (CABG)?
Surgical procedure for multi-vessel disease or complex lesions.
## Footnote
CABG is often performed when angioplasty is not viable.
90
What is the definition of Plaque Rupture?
Disruption of the fibrous cap of an atherosclerotic plaque, exposing the lipid core to the bloodstream.
91
What mechanism leads to Plaque Rupture?
The fibrous cap tears open, exposing thrombogenic material like collagen and tissue factor, leading to rapid thrombus formation.
92
How does Plaque Rupture contribute to Myocardial Infarction (MI)?
It usually causes total occlusion of the coronary artery and is responsible for most cases of traumatic MI, especially in STEMI.
93
What type of infarction results from Plaque Rupture?
Full-thickness (transmural) infarction.
94
What is the definition of Plaque Erosion?
Denudation or loss of the endothelium over a plaque without rupture of the fibrous cap.
95
What mechanism leads to Plaque Erosion?
The endothelium is destroyed by inflammatory cells or shear stress, exposing the subendothelial matrix.
96
How does Plaque Erosion contribute to Myocardial Infarction (MI)?
It often causes sub-total occlusion and is more common in N-STEMI or unstable angina.
97
True or False: Plaque Erosion is usually associated with more extensive infarcts compared to Plaque Rupture.
False
98
Fill in the blank: Plaque Erosion triggers clot formation by exposing the _______.
subendothelial matrix
99
What does the endothelial layer indicate when it is intact or damaged?
Endothelial cells may appear disrupted above the plaque.
## Footnote
The condition of the endothelial layer is crucial for the cardiovascular health and can indicate the presence of atherosclerosis.
100
What are foam cells?
Lipid-laden macrophages that have engulfed oxidized LDL.
## Footnote
Foam cells are a key component in the development of atherosclerotic plaques.
101
What do cholesterol crystals appear as within the lipid core?
Clear, needle-shaped clefts.
## Footnote
Cholesterol crystals can indicate the presence of lipid-rich areas in atherosclerotic plaques.
102
What types of debris are found in the necrotic debris of a lipid core?
Dead cells and lipid material.
## Footnote
Necrotic debris is a sign of plaque instability and can lead to acute cardiovascular events.
103
What is the role of smooth muscle cells in the fibrous cap?
Proliferate and migrate from the media, forming a fibrous layer.
## Footnote
The fibrous cap is essential for plaque stability and is composed mainly of smooth muscle cells and extracellular matrix.
104
What substances strengthen the fibrous cap?
Collagen and extracellular matrix.
## Footnote
A robust fibrous cap is critical for preventing plaque rupture, which can lead to thrombosis.
105
Which inflammatory cells contribute to plaque progression?
Macrophages and T-lymphocytes.
## Footnote
These cells play a significant role in the inflammatory process associated with atherosclerosis.
106
What type of cells may be present during acute events in atherosclerosis?
Neutrophils.
## Footnote
The presence of neutrophils indicates an acute inflammatory response, often associated with plaque rupture.
107
What is indicated by the presence of calcium deposits in plaques?
Contributing to hardening.
## Footnote
Calcification is often seen in advanced atherosclerotic plaques and is associated with decreased arterial elasticity.
108
What does neovascularization refer to in the context of atherosclerotic plaques?
Small blood vessels may form within the plaque.
## Footnote
Neovascularization can supply nutrients to the plaque but may also contribute to its instability.
109
What is the initial trigger of endothelial injury?
Damage or dysfunction of the endothelial lining of arteries due to factors like hypertension, smoking, or high cholesterol.
## Footnote
Endothelial injury is crucial in the development of atherosclerosis.
110
What response occurs due to endothelial injury?
Increased permeability and recruitment of inflammatory cells.
## Footnote
This response can lead to further vascular complications.
111
What happens to LDL particles during lipid accumulation?
Low-density lipoprotein (LDL) particles penetrate the endothelium and become oxidized.
## Footnote
Oxidized LDL plays a significant role in atherosclerosis.
112
What is the role of oxidized LDL in endothelial injury?
Recognized as pathogenic, triggering further endothelial injury and inflammation.
## Footnote
This contributes to the progression of atherosclerosis.
113
What type of cells enter the vessel wall during inflammatory cell recruitment?
Monocytes.
## Footnote
These cells differentiate into macrophages that play a key role in the inflammatory response.
114
What do macrophages become after engulfing oxidized LDL?
Lipid-laden foam cells.
## Footnote
Foam cells are a hallmark of early atherosclerotic lesions.
115
What is a fatty streak?
An early lesion visible as fatty streaks due to foam cell accumulation.
## Footnote
Fatty streaks are considered a reversible stage in young individuals.
116
What occurs during smooth muscle cell proliferation?
Smooth muscle cells migrate from the media to the intima and proliferate, producing extracellular matrix components like collagen.
## Footnote
This process contributes to plaque stability.
117
What is formed during fibrous plaque development?
A fibrous cap formed by smooth muscle cells and collagen over a lipid core.
## Footnote
This is a critical stage in the development of advanced atherosclerotic plaques.
118
What characterizes advanced plaques?
Consists of a necrotic core (dead cells, cholesterol crystals), surrounded by a fibrous cap.
## Footnote
Advanced plaques are more prone to complications.
119
What happens when a thin fibrous cap ruptures?
Exposes the thrombogenic core, leading to platelet activation and thrombus (clot) formation.
## Footnote
This can result in acute cardiovascular events.
120
What clinical events can occur due to thrombosis?
Acute myocardial infarction or stroke if a thrombus occludes a vessel.
## Footnote
These events are major causes of morbidity and mortality.
121
What is a non-modifiable risk factor related to age?
Risk increases with age.
## Footnote
Age is a significant factor in assessing the likelihood of developing cardiovascular issues.
122
Which gender has a higher risk for heart disease?
Men have higher risk; post-menopausal women are also at increased risk.
## Footnote
Hormonal changes in women after menopause contribute to increased risk.
123
What familial factor increases the risk of heart disease?
A family history of early heart disease increases risk.
## Footnote
Genetics play a crucial role in the predisposition to cardiovascular diseases.
124
What is hyperlipidaemia?
High levels of LDL ('bad cholesterol') and low levels of HDL ('good cholesterol').
## Footnote
This condition is a significant modifiable risk factor for heart disease.
125
How does hypertension affect cardiovascular health?
High blood pressure can damage arteries.
## Footnote
Hypertension is a major contributor to heart disease and stroke.
126
What impact does smoking have on cardiovascular health?
Increases oxidative stress and endothelial damage.
## Footnote
Smoking is a critical risk factor that accelerates cardiovascular disease progression.
127
What condition does Diabetes Mellitus promote that affects heart health?
Promotes lipid abnormalities and endothelial dysfunction.
## Footnote
This can lead to increased cardiovascular risk.
128
How is obesity linked to cardiovascular risk?
Linked to dyslipidaemia and insulin resistance.
## Footnote
Obesity is a significant modifiable risk factor for heart disease.
129
What lifestyle factor contributes to obesity and cardiovascular risk?
Sedentary lifestyle.
## Footnote
Lack of physical activity is a well-known risk factor for various health issues.
130
What dietary components increase cardiovascular risk?
High in saturated fats, trans fats, and cholesterol.
## Footnote
These dietary choices can lead to increased LDL levels and heart disease.
131
How does alcohol consumption affect cardiovascular health?
Excessive intake can raise blood pressure and triglycerides.
## Footnote
Moderation is key to minimizing cardiovascular risks associated with alcohol.
132
What are elevated homocysteine levels linked to?
Linked to endothelial damage.
## Footnote
High homocysteine levels are considered an emerging risk factor for cardiovascular diseases.
133
What does C-Reactive Protein (CRP) indicate?
Marker of inflammation associated with atherosclerosis.
## Footnote
Elevated CRP levels can signal an increased risk of heart disease.
134
What is Lipoprotein(a)?
Genetic variant of LDL that can increase risk.
## Footnote
Lipoprotein(a) levels are influenced by genetics and can contribute to cardiovascular risk.
135
What are Triacylglycerols also known as?
Triglycerides
## Footnote
Triacylglycerols are the main form of stored energy in adipose tissue.
136
What is the structure of Triacylglycerols?
Composed of one glycerol molecule esterified with three fatty acids
## Footnote
The structure allows them to store energy efficiently.
137
What are the functions of Triacylglycerols?
* Main form of stored energy in adipose tissue
* Insulation and protection of organs
## Footnote
They play a crucial role in energy storage and organ protection.
138
What are the properties of Triacylglycerols?
* Hydrophobic
* Insoluble in water
* Fatty acids vary, influencing melting point and fluidity
## Footnote
These properties affect their behavior in biological systems.
139
What are Phospholipids composed of?
Glycerol backbone linked to two fatty acids, a phosphate group, and a polar head group
## Footnote
The composition is essential for their role in cell membranes.
140
What makes Phospholipids amphipathic?
The phosphate head is polar while the fatty acid tails are non-polar
## Footnote
This property is crucial for forming bilayers in cell membranes.
141
What are the functions of Phospholipids?
* Major components of cell membranes
* Maintaining fluidity and flexibility
* Involved in cell signalling
## Footnote
Their structure allows them to create barriers and facilitate communication in cells.
142
Name an example of a Phospholipid.
* Phosphatidylcholine (lecithin)
* Phosphatidylethanolamine
* Phosphatidylserine
## Footnote
These examples illustrate the diversity of phospholipids in biological membranes.
143
What is the structure of Cholesterol?
Steroid nucleus consisting of four fused rings with a hydroxyl group, a hydrocarbon tail, and a methyl group
## Footnote
This unique structure is important for its function in membranes and hormone synthesis.
144
What are the functions of Cholesterol?
* Structural component of cell membranes
* Providing fluidity
* Precursor for synthesis of steroid hormones, bile acids, and vitamin D
## Footnote
Cholesterol is vital for maintaining membrane integrity and for hormone production.
145
What are the properties of Cholesterol?
Amphipathic; hydroxyl group is polar, the rest is non-polar
## Footnote
This property contributes to its role in membrane fluidity.
146
What do chylomicrons transport?
Dietary triglycerides
## Footnote
Chylomicrons are lipoprotein particles that carry dietary lipids from the intestines to other locations in the body.
147
What is the primary function of VLDL?
Transport endogenous triglycerides
## Footnote
VLDL, or Very Low-Density Lipoprotein, is produced by the liver and carries triglycerides synthesized from carbohydrates.
148
What are IDL particles?
Transitional particles that can become LDL
## Footnote
Intermediate-Density Lipoproteins (IDL) are formed from the degradation of VLDL and can be converted into Low-Density Lipoproteins (LDL).
149
What is the function of LDL?
Deliver cholesterol to tissues
## Footnote
LDL, or Low-Density Lipoprotein, is often referred to as 'bad cholesterol' due to its association with atherosclerosis.
150
What is the protective effect of HDL?
Remove excess cholesterol
## Footnote
HDL, or High-Density Lipoprotein, is known as 'good cholesterol' because it helps remove cholesterol from the bloodstream and transport it to the liver for excretion.
151
What are lipoproteins composed of?
Spherical particles composed of hydrophobic lipids (triglycerides, cholesterol esters) and a surface of phospholipids, free cholesterol, and apolipoproteins
## Footnote
Apolipoproteins stabilize lipoprotein structure and serve as ligands for cell receptors
152
What is the core composition of lipoproteins?
Hydrophobic lipids, mainly triglycerides and cholesterol esters
## Footnote
The core is surrounded by a shell that includes phospholipids and free cholesterol
153
What are the main types of lipoproteins?
Chylomicrons, VLDL, LDL, HDL
## Footnote
Each type has a distinct composition and function in lipid transport
154
What characterizes chylomicrons?
Largest lipoproteins, mostly triglycerides, few apoproteins
## Footnote
Chylomicrons transport dietary lipids from the intestines to other locations in the body
155
What is the main function of LDL?
Delivery of cholesterol to peripheral tissues
## Footnote
LDL interacts with cell receptors to facilitate endocytosis
156
What is the core composition of LDL?
Mainly cholesterol esters (esterified cholesterol)
## Footnote
This composition is crucial for its role in cholesterol transport
157
What is the density range of LDL?
1.019–1.063 g/mL
## Footnote
Density is an important factor in the classification of lipoproteins
158
What is the primary apolipoprotein found in LDL?
Apolipoprotein B-100
## Footnote
This apolipoprotein is essential for LDL's function and receptor binding
159
What are the uses of cholesterol delivered by LDL?
* Cell membrane synthesis
* Hormone production (steroids)
* Storage in tissues
## Footnote
Cholesterol is vital for various cellular functions and processes
160
True or False: Elevated LDL levels are associated with atherosclerosis.
True
## Footnote
High LDL levels contribute to plaque formation in arterial walls
161
What role does LDL play in plaque formation?
Deposits cholesterol in the intima of arterial walls
## Footnote
This process is a key factor in the development of atherosclerosis
162
What are apolipoproteins?
Protein components of lipoproteins
## Footnote
They vary in size, amino acid composition, and specific functions.
163
What is the structural characteristic of apolipoproteins?
They are amphipathic, containing both hydrophilic and hydrophobic regions.
164
What is the role of apolipoproteins in lipoprotein particles?
Provide stability to lipoprotein particles.
165
Name the types of apolipoproteins.
* Apolipoprotein B (ApoB)
* Apolipoprotein A (ApoA)
* Apolipoprotein C (ApoC)
* Apolipoprotein E (ApoE)
166
Where is Apolipoprotein B (ApoB) found?
In chylomicrons, VLDL, LDL.
167
What is the predominant apolipoprotein in HDL?
Apolipoprotein A (ApoA).
168
In which lipoproteins is Apolipoprotein C (ApoC) present?
In chylomicrons, VLDL, HDL.
169
What is the role of Apolipoprotein E (ApoE)?
Facilitates clearance of chylomicron remnants and VLDL via hepatic receptors.
170
What is one of the functions of apolipoproteins concerning cell receptors?
Serve as recognition signals for specific cell surface receptors.
171
What enzyme does ApoC-II activate?
Lipoprotein lipase.
172
What is the function of ApoA-I in HDL?
Activates LCAT (lecithin-cholesterol acyltransferase).
173
What is the integral role of ApoB-100?
Integral for the formation of LDL.
174
What process does ApoB-100 facilitate?
LDL receptor-mediated endocytosis.
175
Fill in the blank: Apolipoproteins serve as _______ for specific cell surface receptors.
[ligands]
176
True or False: Apolipoproteins are only found in HDL.
False.
177
What regulatory roles do apolipoproteins play?
Modulate lipoprotein metabolism and synthesis.
178
What is the role of apolipoproteins as enzyme cofactors?
Activate enzymes involved in lipid metabolism.
179
What is the primary role of LDL in lipid transport?
LDL is the primary carrier of cholesterol in the bloodstream.
180
What is the main function of LDL?
Delivering cholesterol to peripheral tissues for cell membrane synthesis, hormone production, and storage.
181
What role does elevated LDL cholesterol play in atherosclerosis?
It is a major risk factor for developing atherosclerosis.
182
How do LDL particles contribute to atherosclerosis?
They infiltrate the arterial wall at sites of endothelial injury or dysfunction.
183
What happens to LDL once it infiltrates the arterial wall?
It becomes oxidized or modified, provoking an inflammatory response.
184
How are foam cells formed in atherosclerosis?
Oxidized LDL is taken up by macrophages via scavenger receptors.
185
What are fatty streaks in the context of atherosclerosis?
They are the earliest visible lesions formed by the accumulation of foam cells.
186
What leads to plaque development in atherosclerosis?
Continued accumulation of lipids, foam cells, and inflammatory cells.
187
What effect do high circulating LDL levels have on plaques?
They accelerate plaque growth and promote plaque instability, increasing the risk of rupture.
188
What clinical implications are associated with elevated LDL levels?
* Heart attacks (myocardial infarction) * Stroke * Peripheral artery disease
189
What is the therapeutic impact of lowering LDL levels?
It reduces the progression of atherosclerosis and decreases cardiovascular risk.
190
Fill in the blank: LDL becomes ________ or modified, which provokes an inflammatory response.
oxidized
191
True or False: Elevated LDL levels are linked with a lower incidence of heart attacks.
False
192
What is the mechanism of action of Statins?
Inhibit HMG-CoA reductase, leading to decreased intrahepatic cholesterol and increased clearance of LDL from circulation
## Footnote
Statins are HMG-CoA Reductase Inhibitors that significantly lower LDL cholesterol levels.
193
What is the primary effect of Statins on LDL cholesterol?
Significant reduction in LDL cholesterol (~20-50%)
## Footnote
Statins also cause a slight increase in HDL and a reduction in triglycerides.
194
What is the clinical use of Statins?
First-line treatment for hyperlipidemia and to reduce the risk of atherosclerotic cardiovascular disease (ASCVD)
## Footnote
Statins are used in both primary and secondary prevention.
195
What additional benefits do Statins provide?
Anti-inflammatory effects and plaque stabilization
## Footnote
These benefits enhance cardiovascular health beyond cholesterol reduction.
196
What is the mechanism of action of Ezetimibe?
Inhibits Niemann-Pick C1-Like 1 (NPC1L1) transporter in the small intestine
## Footnote
This action decreases dietary and biliary cholesterol absorption.
197
What is the main effect of Ezetimibe on LDL cholesterol?
LDL reduction of approximately 15-20% when added to statins
## Footnote
Ezetimibe is particularly useful for patients not reaching LDL goals.
198
What is the clinical use of Ezetimibe?
Adjunct therapy with statins and as an alternative for statin-intolerant patients
## Footnote
It is also useful in familial hypercholesterolemia.
199
What are the additional benefits of Ezetimibe?
Well tolerated with minimal side effects
## Footnote
This makes it a preferred option for many patients.
200
What is the mechanism of action of PCSK9 Inhibitors?
Monoclonal antibodies bind to PCSK9, preventing degradation of LDL receptors
## Footnote
This enhances clearance of LDL from blood.
201
What is the main effect of PCSK9 Inhibitors on LDL cholesterol?
Very potent LDL reduction (~50-70%)
## Footnote
This makes them particularly useful for specific high-risk populations.
202
What is the clinical use of PCSK9 Inhibitors?
Adjunct therapy when statins alone are insufficient and for patients intolerant to statins
## Footnote
They are especially beneficial in familial hypercholesterolemia.
203
What additional benefits do PCSK9 Inhibitors provide?
May have additional vascular benefits by stabilizing plaques
## Footnote
This contributes to overall cardiovascular health.
204
What are triglycerides (TGs)?
A type of lipid stored primarily in adipose tissue and circulate in the blood within lipoproteins like VLDL
205
What cardiovascular risk is associated with elevated plasma triglyceride levels?
Increased risk of atherosclerosis and cardiovascular disease (CVD)
206
What other risk factors often coexist with elevated triglyceride levels?
* Low HDL cholesterol
* High LDL
* Insulin resistance
* Metabolic syndrome
207
What are the mechanisms contributing to cardiovascular risk associated with high triglyceride levels?
* Linked with small, dense LDL particles that are more atherogenic
* Promote inflammation, endothelial dysfunction, and thrombosis
* Lead to formation of lipid-rich plaques prone to rupture
208
What is the significance of hypertriglyceridemia in lipid management?
Considered a cardiovascular risk factor when levels exceed 150 mg/dL
209
What can very high triglyceride levels (>500 mg/dL) cause?
Pancreatitis
210
What are fibrates and their examples?
* Gemfibrozil
* Fenofibrate
211
What is the mechanism of action of fibrates?
* Activate PPAR-α receptors
* Increase lipoprotein lipase activity
* Enhance clearance of triglyceride-rich lipoproteins
212
What is the effect of fibrates on triglyceride levels?
Reduce TG levels by 30-50% and slightly increase HDL
213
When are fibrates primarily used?
For severe hypertriglyceridemia (>500 mg/dL) to prevent pancreatitis
214
What are omega-3 fatty acids and their examples?
* Eicosapentaenoic acid (EPA)
* Docosahexaenoic acid (DHA)
* Combined formulations
215
What is the mechanism of omega-3 fatty acids?
Reduce hepatic VLDL synthesis and decrease circulating triglycerides
216
What is the effect of omega-3 fatty acids on triglyceride levels?
Reduce TG levels by 25-50%, especially at higher doses
217
What is the use of omega-3 fatty acids in therapy?
Adjunct therapy in hypertriglyceridemia and cardiovascular risk reduction
218
What is niacin (nicotinic acid) and its mechanism?
Inhibits lipolysis in adipose tissue, reducing free fatty acids and decreases VLDL and LDL synthesis
219
What is the effect of niacin on triglyceride levels?
Lower TG by 20-50% and appreciably increase HDL
220
What are the side effects of niacin?
* Flushing
* Hepatotoxicity
221
What is the primary function of statins?
LDL-lowering
222
What is the effect of statins on triglyceride levels?
Reduce TG levels modestly by 10-20%
223
In which patients are statins used?
Patients with mixed dyslipidemia
224
What is the primary function of HDL?
HDL collects excess cholesterol from peripheral tissues and atherosclerotic plaques and transports it back to the liver for excretion or recycling.
225
How does HDL provide a protective effect in the body?
It removes cholesterol from arterial walls, preventing or reducing plaque formation and limiting lipid accumulation within the arterial intima.
226
What are the anti-inflammatory effects of HDL?
HDL inhibits oxidation of LDL, reduces expression of adhesion molecules on endothelial cells, and suppresses recruitment of inflammatory cells (monocytes, T-cells).
227
What is the outcome of HDL's anti-inflammatory properties?
Diminishes vascular inflammation, a key factor in atherosclerosis progression.
228
What antioxidant properties does HDL possess?
HDL carries enzymes like paraoxonase that degrade oxidized lipids in LDL and cell membranes, protecting against oxidative damage to blood vessels.
229
How does HDL enhance endothelial function?
By promoting nitric oxide production, improving vasodilation, and reducing endothelial dysfunction, thereby maintaining vessel integrity.
230
What are the anti-thrombotic effects of HDL?
HDL can suppress platelet activation and aggregation, contributing to vascular homeostasis and reducing thrombosis risk.
231
Fill in the blank: HDL collects excess cholesterol from peripheral tissues and atherosclerotic plaques and transports it back to the _______.
[liver]
232
True or False: HDL enhances endothelial health by reducing nitric oxide production.
False
233
List the key functions of HDL as a defense mechanism.
* Reverse Cholesterol Transport
* Anti-inflammatory Effects
* Antioxidant Properties
* Endothelial Function
* Anti-thrombotic Effects
234
What is one of the leading causes of death worldwide?
Myocardial Infarction (MI)
## Footnote
MI has a higher prevalence in developed countries due to lifestyle factors.
235
How many people in the United States experience MI annually?
Approximately 1.5 million
## Footnote
This figure highlights the significant burden of MI in the U.S.
236
What is the estimated number of deaths due to MI each year in the United States?
About 370,000
## Footnote
This statistic underscores the severity of MI as a public health issue.
237
What factors are contributing to the rising incidence of MI in developing countries?
Increased risk factors like:
* Hypertension
* Smoking
* Unhealthy diets
## Footnote
Rapid urbanization and Westernization are also significant contributors.
238
At what age does the risk of MI significantly increase?
After 45–50 years
## Footnote
The highest incidence occurs in individuals over 60-70 years.
239
Which gender has a higher risk of MI before menopause?
Males
## Footnote
After menopause, the risk in women increases.
240
How much more likely are men to have MI at a younger age compared to women?
Approximately 2-3 times
## Footnote
This statistic emphasizes gender differences in MI risk.
241
List some modifiable risk factors for myocardial infarction.
* Hypertension
* Hyperlipidemia
* Smoking
* Diabetes mellitus
* Obesity
* Sedentary lifestyle
## Footnote
These factors can be altered to reduce MI risk.
242
What are some non-modifiable risk factors for myocardial infarction?
* Age
* Male gender
* Family history of coronary artery disease
## Footnote
These factors cannot be changed but influence risk assessment.
243
Where is the incidence of MI generally higher, urban or rural areas?
Urban areas
## Footnote
Lifestyle risks contribute to this increased incidence.
244
What is the overall acute MI mortality rate?
About 10-15%
## Footnote
This rate can vary significantly with healthcare access.
245
When do most deaths from MI occur?
Within the first hour
## Footnote
Sudden death is a critical concern in MI cases.
246
What has improved survival rates for MI patients?
Advances in reperfusion therapy and secondary prevention
## Footnote
These medical advancements have significantly impacted survivorship.
247
True or False: The incidence of MI is declining in all countries.
False
## Footnote
While some countries see a decline due to improved prevention and treatment, others are experiencing rising incidences.
248
What is hyperlipidemia (dyslipidemia)?
Elevated LDL cholesterol and low HDL cholesterol
## Footnote
Hyperlipidemia refers to abnormally elevated levels of lipids in the blood, which can lead to cardiovascular disease.
249
How does hypertension (high blood pressure) affect the body?
Damages arterial walls and promotes atherosclerosis
## Footnote
Hypertension can lead to the thickening and hardening of arteries, increasing the risk of heart attack and stroke.
250
What impact does smoking have on cardiovascular health?
Causes endothelial damage and promotes thrombosis
## Footnote
Smoking is a significant risk factor for cardiovascular diseases due to its harmful effects on blood vessels.
251
What role does diabetes mellitus play in cardiovascular disease?
Accelerates atherosclerosis and causes endothelial dysfunction
## Footnote
Diabetes is linked to increased risk of coronary artery disease due to its effects on blood vessels.
252
What are the associations of obesity with cardiovascular health?
Associated with dyslipidemia, hypertension, and insulin resistance
## Footnote
Obesity is a major risk factor for various cardiovascular conditions, impacting overall metabolic health.
253
How does physical inactivity contribute to cardiovascular risk?
Promotes obesity and metabolic syndrome
## Footnote
Lack of physical activity can lead to weight gain and increased risk of heart disease.
254
What constitutes an unhealthy diet in relation to cardiovascular health?
High saturated fats, trans fats, cholesterol intake
## Footnote
Diets high in unhealthy fats can lead to elevated cholesterol levels and increased heart disease risk.
255
What is the effect of excessive alcohol consumption on cardiovascular health?
Can increase blood pressure and contribute to obesity
## Footnote
Alcohol can have both direct and indirect effects on heart health.
256
How does chronic stress affect cardiovascular health?
Can elevate blood pressure and promote unhealthy lifestyles
## Footnote
Stress management is crucial for reducing cardiovascular risk.
257
What is the relationship between age and cardiovascular risk?
Risk increases with age, especially after 45 in men and 55 in women
## Footnote
Age is a significant non-modifiable risk factor for cardiovascular diseases.
258
How does gender influence cardiovascular risk?
Men have higher risk at a younger age; women’s risk increases after menopause
## Footnote
Hormonal changes in women post-menopause can increase their risk of heart disease.
259
What is the significance of family history in cardiovascular risk?
Genetic predisposition to early coronary artery disease
## Footnote
A family history of heart disease can indicate a higher risk for individuals.
260
Which ethnic groups have a higher prevalence of cardiovascular disease?
Certain populations, such as South Asians
## Footnote
Ethnicity can influence risk factors and prevalence of cardiovascular diseases.
261
What is the underlying cause of myocardial infarction?
Formation of atherosclerotic plaques in coronary arteries
## Footnote
Atherosclerosis is characterized by the buildup of fats, cholesterol, and other substances in and on the artery walls.
262
What makes atherosclerotic plaques vulnerable to rupture?
Plaques with a thin fibrous cap and large lipid core
## Footnote
These features increase the likelihood of plaque instability.
263
What is the triggering event for a myocardial infarction?
Plaque rupture or erosion
## Footnote
Both processes expose thrombogenic materials that initiate clot formation.
264
What happens when plaque ruptures?
Exposes thrombogenic material, activating coagulation cascade and leading to thrombus formation
## Footnote
Thrombogenic material includes tissue factor and other components that promote clotting.
265
What is the result of rapid clot formation in coronary arteries?
Partial or full occlusion of the coronary artery
## Footnote
Complete occlusion halts blood flow downstream, leading to ischemia.
266
What occurs during ischemia following myocardial infarction?
Oxygen supply to myocardium becomes severely reduced or stopped
## Footnote
This reduction leads to a switch in metabolism from aerobic to anaerobic.
267
What metabolic change occurs in myocytes during ischemia?
Switch from aerobic to anaerobic metabolism
## Footnote
This switch results in ATP depletion and lactic acid accumulation.
268
What are the early cellular injuries associated with myocardial infarction?
Disruption of cell membrane integrity and cytoplasmic enzyme leakage
## Footnote
Enzymes like troponins and CK-MB are commonly measured in the diagnosis.
269
How quickly do cellular changes begin after ischemia?
Within minutes
## Footnote
Full necrosis typically occurs after 20-30 minutes of persistent ischemia.
270
What is reperfusion injury?
Additional injury due to oxidative stress and inflammation after restoration of blood flow
## Footnote
This paradoxical effect can worsen the damage caused by the initial ischemia.
271
What is the process of healing after myocardial infarction?
Removal of necrotic tissue by macrophages and fibrosis leading to scar formation
## Footnote
The infarcted region eventually becomes a non-contractile scar.
272
List the summary of key events leading to myocardial infarction.
Plaque rupture/erosion → Thrombosis → Coronary occlusion → Ischemia → Myocyte necrosis → Healing by fibrosis
## Footnote
This sequence outlines the pathological progression of a myocardial infarction.
273
Fill in the blank: Myocytes switch from aerobic to _______ metabolism during ischemia.
anaerobic
274
True or False: Complete occlusion of a coronary artery can lead to ischemia.
True
275
What is the typical description of chest pain in myocardial infarction?
Severe, sudden, crushing, or constrictive
## Footnote
Often located substernally or retrosternally and may radiate to the left arm, neck, jaw, back, or epigastrium.
276
How long does chest pain usually last in classic myocardial infarction?
More than 20 minutes
## Footnote
Not relieved by rest or nitrates.
277
List associated symptoms of myocardial infarction.
* Dyspnea (shortness of breath)
* Diaphoresis (profuse sweating)
* Nausea and vomiting
* Palpitations or syncope
* Weakness or fatigue
## Footnote
Symptoms may vary in presentation.
278
What arrhythmias may occur during myocardial infarction?
* Ventricular tachycardia
* Ventricular fibrillation
* Complete heart block
## Footnote
These may present as palpitations, lightheadedness, or sudden collapse.
279
What hemodynamic changes may develop in extensive myocardial infarction?
* Hypotension
* Shock
* Pulmonary edema
## Footnote
Pulmonary edema is due to left ventricular failure.
280
What characterizes a silent myocardial infarction?
Minimal or no symptoms
## Footnote
More common in diabetics or the elderly.
281
What is referred pain in the context of myocardial infarction?
Pain that mimics gastrointestinal or musculoskeletal conditions
## Footnote
May be referred anteriorly or posteriorly.
282
What physical examination findings may indicate heart failure in myocardial infarction?
* S3 or S4 heart sound
* New murmurs
* Signs of heart failure (rales, elevated JVP, peripheral edema)
## Footnote
New murmurs may occur due to papillary muscle rupture or ventricular septal defect.
283
What is the difference in symptom chronology between stable angina and myocardial infarction?
Stable angina is predictable and relieved by rest; myocardial infarction is severe, persistent, at rest or with minimal exertion.
284
True or False: Chest pain in myocardial infarction is always relieved by nitrates.
False
## Footnote
Chest pain in classic MI is not relieved by rest or nitrates.
285
What is the key ECG feature of STEMI?
Persistent ST segment elevation (≥1 mm in contiguous leads)
## Footnote
Indicates transmural (full-thickness) myocardial injury
286
What does ST segment elevation in STEMI usually indicate?
Complete occlusion of a coronary artery
## Footnote
This leads to full-thickness myocardial injury
287
What additional ECG changes may develop in STEMI?
* Q waves may develop within hours to days
* T wave changes: usually inverted T waves during evolution
## Footnote
Q waves indicate tissue necrosis
288
What are the key ECG features of NSTEMI?
* ST segment depression
* T wave inversion
* No persistent ST elevation
## Footnote
Reflects subendocardial (partial-thickness) ischemia
289
What does the pathophysiology of NSTEMI reflect?
Subendocardial (partial-thickness) ischemia due to partial occlusion of coronary arteries
## Footnote
This condition leads to different ECG changes compared to STEMI
290
How may the ECG appear initially in NSTEMI?
ECG may be normal initially or show transient changes
## Footnote
This can make diagnosis challenging without further testing
291
What confirms myocardial necrosis in NSTEMI?
Elevated cardiac biomarkers (troponins)
## Footnote
These biomarkers are crucial for diagnosis alongside ECG findings
