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PBHD - FINAL EXAM > Lecture 9 - cardiovascular > Flashcards

Lecture 9 - cardiovascular Flashcards

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1
Q

what is atheroscelorosis?

A

The accumulation of lipids and fats within the walls of the arteries of the body. Means the hardening of atherosclerosis.

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2
Q

how does atherosclerosis occur?

A

When the fatty streaks (there are fatty streaks in every individual) develops into a plaque. Arteries become calcified and somewhat scarred in the process of plaque formation, which results in them being not as elastic and not as able to change and vary according to blood pressure needs within different parts of the body.

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3
Q

atherosclerosis leads to

A

heart attack, stroke, embloisms, death or myocardial infarction. very dangerous

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4
Q

Why is atherosclerosis asymptomatic for many years?

A

Very slow development, for clinical symptoms to show; ischaemia, infarction, altered blood pressure, thrombosis and embolism.

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5
Q

Atherosclerosis is the biggest killer in the…..

A

western world, as it leads to many deadly diseases n fatalities.

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6
Q

Which arteries does atheroscleorsis affect?

A

Any artery, most common in large arteries; aorta and most clinically impacted arteries are coronary a, cerebral a.

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7
Q

Why does atherosclerosis affect men more?

A

Testosterone directly leads to the hardening of arteries independent of atheroscelorosis, this compounded with the calcification we see in atherosclerosis, leads to more chances of developing atherosclerosis than females.

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8
Q

Identify atherosclerotic plaques.

A

the following features will be seen in atherosclerotic arteries:
- fatty white streaks, that predispose atherosclerotic plaque formation. fatty streaks are when lipids have gotten into the blood vessel wall, completely asymptomatic. Plaques is bodies reaction to fatty streaks.
- necrotic dark plaques, which are calcified.
- broken, fragmented plaques on the aorta.
- severity of atherosclerosis can vary.

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9
Q

what are the risk factors of atherosclerosis?

A

age, exercise, weight, diet, smoking, cholesterol levels in bloodstream (HDL:LDL lipid to protein ratio-high or low - LDL is predisposing factor), diabetes, high resting blood pressure.

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10
Q

Normal vessel wall vs developed plaque - Atherosclerosis Development

A

ELL FILM CAP

E – Endothelial Dysfunction due to stress, smoking, diabetes
L – Lipoprotein Entry and Modification in the intima
L – Leukocyte Recruitment to the plaque site
F – Foam Cell Formation as macrophages engulf LDL
I – Intimal Thickening from SMC proliferation and leukocyte activity
L – Luminal Narrowing causes restricted blood flow
M – Macrophages try to clear lipids and become foam cells
C – Calcification and Fatty Streak Evolution
A – Apoptosis of SMCs in fibrous cap formation
P – Plaque Disruption due to size vs. stability balance, leading to ACS

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11
Q

What separates smooth muscle cells from the basement membrane and endothelial cells in a normal vessel wall?

A

An elastic lamina separates smooth muscle cells from the basement membrane and endothelial cells.

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12
Q

Where do lipids begin to accumulate in atherosclerosis?

A

Lipids start to build up between the endothelial cells and the internal elastic lamina.

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13
Q

What is a key feature of plaque development in atherosclerosis?

A

The presence of smooth muscle cells around the plaque.

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14
Q

What are fatty streaks, and do they occur in everyone?

A

Fatty streaks are lipid build-ups in vessel walls and occur in everyone.

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15
Q

When does a fatty streak become classified as a plaque?

A

When the body’s inflammatory response is triggered, recruiting macrophages and promoting smooth muscle cell proliferation into the affected area.

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16
Q

What role do macrophages play in plaque formation?

A

Macrophages attempt to absorb lipids, becoming foam cells, but they often fail to break down the lipids fully, leading to lipid build-up and plaque formation.

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17
Q

What happens to macrophages that ingest too much lipid?

A

They become bloated, may die, and release lipids back into the area, creating a cycle of macrophage recruitment and death.

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18
Q

Why are macrophages in plaques called “foam cells”?

A

They appear foamy under a microscope due to the lipid content they absorb.

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19
Q

What is a “fibrous cap” in atherosclerosis?

A

A fibrous cap is a layer of smooth muscle cells, fibroblasts, and collagen that forms over the lipid accumulation to isolate it from the bloodstream.

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20
Q

Why does the body form a fibrous cap over a plaque?

A

To prevent the plaque from rupturing and releasing lipids into the bloodstream, which could lead to embolisms.

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21
Q

What are the dangers of a developed plaque rupturing?

A

Lipids entering the bloodstream can cause embolisms, leading to blockages and potential downstream health issues.

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22
Q

What happens to plaques as they become more advanced?

A

They may calcify, form more necrotic and fragmented regions, and, in rare cases, cause embolisms due to infection or rupture.

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23
Q

What materials make up the fibrous cap over a developed plaque?

A

The fibrous cap consists of smooth muscle cells, fibroblasts, collagen, and sometimes fibrin, forming a barrier around the lipid core.

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24
Q

What triggers the body’s inflammatory response in atherosclerosis?

A

The build-up of lipids triggers the inflammatory response, leading to macrophage recruitment and smooth muscle cell infiltration.

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25
Why can't macrophages effectively metabolize the lipids in plaques?
Macrophages are not efficient at breaking down or metabolizing lipids, leading to lipid accumulation and the formation of foam cells.
26
What happens when macrophages fail to process lipids within the plaque?
The excess lipids can crystallize, leading to "soapification," which can contribute to calcification and hardening of the plaque.
27
How does the body respond to the ineffective lipid breakdown by macrophages?
The body attempts to isolate the lipid accumulation by forming a fibrous cap over the plaque, creating a scar-like capsule to protect the bloodstream.
28
Why is lipid accumulation in the bloodstream a problem?
Lipids are lipophilic and hydrophobic, meaning they can form embolisms if released into the bloodstream, causing downstream issues.
29
What are the consequences of advanced plaque calcification?
Calcification makes the plaque stiff and can increase the risk of rupture, potentially leading to embolisms and more severe complications.
30
What initiates endothelial dysfunction in atherosclerosis?
Shear stress, high LDL concentration, smoking, and diabetes.
31
What happens to lipoproteins after entering the intima?
they undergo oxidation and glycation, becoming more inflammatory.
32
How do leukocytes get attracted to the site of plaque development?
Endothelial and smooth muscle cells express adhesion molecules and release chemoattractants to recruit immune cells.
33
What causes the thickening of the intimal layer in atherosclerosis?
Smooth muscle cell proliferation and continued leukocyte recruitment.
34
What are the effects of luminal narrowing due to plaque growth?
It limits blood flow, causing claudication in peripheral vessels or angina in coronary circulation.
35
What is the significance of the fibrous cap in plaque stability?
The fibrous cap stabilizes the plaque but can be vulnerable if it becomes thin, increasing rupture risk.
36
How does plaque disruption lead to acute coronary syndrome (ACS)?
Plaque rupture releases lipids into the bloodstream, potentially causing blockages and triggering ACS.
37
What are the key features of developed plaque compared to normal vessel walls?
Normal Vessel Wall: - Clear separation between endothelium and smooth muscle by elastic lamina. - Smooth muscle cells are well-organized and confined within the media layer. - Minimal lipid accumulation. Developed Plaque: - Lipid accumulation between endothelium and internal elastic lamina. - Infiltration of inflammatory cells like macrophages (forming foam cells). - Proliferation and migration of smooth muscle cells into the intima. - Formation of a fibrous cap over the lipid core. - Potential calcification, necrosis, and stiffening of the plaque.
38
What role do monocytes play in plaque development?
Monocytes adhere to the vessel wall, enter the intima, and differentiate into macrophages.
39
What do macrophages do with oxidized lipids in plaque formation?
Macrophages take up oxidized lipids, becoming foam cells.
40
What growth factor do macrophages release, and what is its effect?
Macrophages release Platelet-Derived Growth Factor (PDGF), which activates smooth muscle cells.
41
Which cytokines do macrophages release to increase leukocyte adhesion?
Macrophages release IL-1 (Interleukin-1) and TNF (Tumor Necrosis Factor) to increase leukocyte adhesion.
42
What is the role of MCP-1 in atherosclerosis, and which cells release it?
Macrophages release Monocyte Chemoattractant Protein-1 (MCP-1) to attract more monocytes to the plaque area.
43
what does PDGF stand for?
Platelet-Derived Growth Factor
44
What effect do PDGF and other growth factors have on smooth muscle cells in plaque formation?
They stimulate smooth muscle cell proliferation.
45
Where do smooth muscle cells migrate during plaque development?
Smooth muscle cells migrate into the intima layer of the vessel wall.
46
What do smooth muscle cells produce after migrating into the intima?
They synthesize collagen and glycoproteins, contributing to the extracellular matrix.
47
What are the three key steps of smooth muscle cell activity in plaque formation?
1) Migration to the intima, 2) Proliferation through mitosis, and 3) Elaboration of the extracellular matrix.
48
What effect do platelets have on smooth muscle cells?
Platelets activate smooth muscle cells, promoting their proliferation and migration.
49
How do platelets contribute to thrombus (blood clot) formation?
Platelets promote thrombus formation by aggregating at the site of vessel injury and releasing factors that initiate clotting.
50
Why is platelet activation significant in atherosclerosis?
Platelet activation contributes to plaque stability and increases the risk of thrombus formation if a plaque ruptures, potentially leading to vessel blockage.
51
What role do smooth muscle cells play in the pathogenesis of atherosclerosis?
Smooth muscle cells proliferate and migrate into the intima, contributing to plaque development.
52
How do macrophages contribute to plaque formation in atherosclerosis?
Macrophages proliferate in the intima, take up oxidized lipids, and transform into foam cells, promoting inflammation and plaque buildup.
53
What type of tissue is laid down during plaque formation, and why is it important?
Connective tissue, including collagen, is laid down to form the extracellular matrix, providing structural support to the developing plaque.
54
Where do lipids accumulate in the process of atherosclerosis?
Lipids accumulate in the intima layer, becoming oxidized and contributing to plaque formation.
55
What factors can lead to endothelial injury or dysfunction, initiating atherosclerosis?
factors include hyperlipidemia, hypertension, smoking, toxins, hemodynamic forces, immune reactions, and viruses.
56
What are the main components of a developed atherosclerotic plaque?
A developed plaque contains a fibrofatty atheroma, lipid debris, lymphocytes, and collagen, forming a structured lesion in the artery wall.
57
What are the structural regions seen in a cross-section of developed plaque?
The regions include the Lumen (L), Fibrous cap (F), and Core of lipid and cellular debris (C).
58
What is a fibrous cap, and why is it important in plaque stability?
The fibrous cap is a layer of connective tissue that covers the lipid core in a plaque, helping to stabilize it and prevent rupture.
59
What are the possible complications of an advanced atherosclerotic plaque?
Complications include thrombosis, plaque rupture, hemorrhage, wall weakening, and calcification.
60
At what age might clinical complications of atherosclerosis, such as myocardial infarction or cerebral infarction, become more likely?
Clinical complications typically become more common from age 40 onwards.
61
What serious conditions can result from plaque progression in atherosclerosis?
Conditions include myocardial infarction, cerebral infarction (stroke), gangrene of extremities, and abdominal aortic aneurysm.
62
How does a fatty streak differ from a fibrous plaque?
A fatty streak is an early lipid accumulation in the intima, while a fibrous plaque includes a fibrous cap over a lipid-rich core, representing a more advanced stage of atherosclerosis.
63
What is essential hypertension?
Essential hypertension is a sustained elevation in blood pressure with no obvious cause and accounts for the majority of all hypertension cases.
64
What is the normal blood pressure range for adults?
The normal range is typically 60-90 mmHg diastolic and 100-140 mmHg systolic, though some people may have values outside this range and still be healthy.
65
Why is essential hypertension called "essential"?
Because it has no obvious or identifiable cause.
66
What are the main risk factors for essential hypertension?
Family history, age, high salt intake, obesity, and excess sympathetic nervous system activity.
67
How does family history impact the risk of developing essential hypertension?
A family history of hypertension increases the likelihood of developing it, suggesting a genetic component.
68
Why is excess sympathetic activity a risk factor for hypertension?
Excess sympathetic activity can increase heart rate and vasoconstriction, raising blood pressure over time.
69
How does sodium retention affect blood pressure?
Sodium retention increases blood volume, leading to expanded cardiac output and elevated blood pressure.
70
What is the relationship between body sodium and blood pressure?
There is a positive correlation; higher body sodium levels can lead to higher blood pressure.
71
How does raised cellular sodium influence peripheral vascular resistance (PVR)?
Raised cellular sodium impairs calcium transport out of smooth muscle cells, leading to increased PVR.
72
How does sympathetic activity influence blood pressure?
Sympathetic activity increases both cardiac output (CO) and peripheral vascular resistance (PVR), raising blood pressure.
73
What could heightened sensitivity to circulating catecholamines result in?
Increased sensitivity may lead to elevated adrenergic neural activity, contributing to higher blood pressure.
74
Which neurotransmitters are associated with increased sympathetic activity?
Catecholamines like dopamine, norepinephrine, and epinephrine influence sympathetic activity and blood pressure.
75
How does increased renin-angiotensin-aldosterone activity affect blood pressure?
It elevates peripheral vascular resistance (PVR) and causes blood volume expansion, leading to higher blood pressure.
76
Are elevated renin levels common in all patients with hypertension?
No, raised renin plasma levels are only present in a small subset of individuals with hypertension.
77
Which medication is effective for individuals with high renin-angiotensin-aldosterone activity?
ACE inhibitors are often effective for these individuals by blocking the conversion of angiotensin I to angiotensin II.
78
What role does angiotensin II play in blood pressure regulation?
Angiotensin II causes vasoconstriction and stimulates aldosterone release, both of which raise blood pressure.
79
What is the function of aldosterone in the renin-angiotensin-aldosterone system?
Aldosterone promotes sodium reabsorption in the kidneys, increasing blood volume and pressure.
80
Which genetic and acquired conditions affect the RAAS and may lead to hypertension?
Conditions include GRA (aldosterone synthase excess), AME (11β-HSD deficiency), Liddle syndrome, and others related to abnormal sodium handling.
81
How does the renin-angiotensin-aldosterone system (RAAS) pathway start?
The RAAS is activated when renin is released in response to low blood pressure or low sodium levels, converting angiotensinogen to angiotensin I.
82
Which conditions may respond to ACE inhibitors in the treatment of hypertension?
Conditions with high renin activity and increased angiotensin II levels often respond to ACE inhibitors.
83
What cardiovascular conditions are associated with increased risk due to hypertension?
Atherosclerosis, left ventricular hypertrophy, and heart failure.
84
What cerebrovascular condition is a risk factor due to hypertension?
Intracerebral hemorrhage.
85
What vascular change is associated with hypertension and leads to a homogenous vessel wall appearance?
Hyaline vascular change.
86
What is a key management strategy for hypertension related to risk factors?
Attending to risk factors, such as lifestyle modifications and addressing underlying health issues.
87
What medications are commonly used to reduce peripheral vascular resistance in hypertension management?
ACE inhibitors, diuretics, angiotensin II blockers, and vasodilators.
88
How do ACE inhibitors help manage hypertension?
They reduce peripheral vascular resistance by inhibiting the renin-angiotensin-aldosterone system.
89
What is a myocardial infarction?
Myocardial infarction, or heart attack, is myocardial damage due to ischemia (lack of blood flow).
90
What causes myocardial infarction?
MI is caused by ischemia, which restricts blood flow to the heart muscle, leading to tissue damage.
91
What are common symptoms of a myocardial infarction related to the sympathetic response?
Nausea, vomiting, diaphoresis (sweating), pale and cool skin, and increased heart rate.
92
Which symptom of myocardial infarction is due to low cardiac output?
Decreased blood pressure is associated with low cardiac output (CO) resulting from heart damage.
93
How does inflammation manifest as a symptom of myocardial infarction?
Inflammation occurs as the body responds to necrotic (dead) heart tissue following the ischemic event.
94
What conduction disturbances might occur during a myocardial infarction?
MI can lead to irregular heartbeats or arrhythmias due to necrosis of the heart tissue affecting electrical pathways.
95
What type of necrosis occurs in myocardial tissue after an infarction?
Coagulative necrosis.
96
What early visual changes can be seen in the myocardium following an infarction?
Pallor of the affected tissue due to loss of blood supply.
97
What inflammatory changes occur in the myocardium a few days after infarction?
Hyperaemia (increased blood flow) and neutrophil infiltration.
98
When does granulation tissue begin to form in the myocardium after an infarction?
Granulation tissue typically forms 4-10 days post-infarction.
99
What process occurs in the myocardium over time after an infarction, leading to scarring?
Gradual fibrosis, resulting in the formation of fibrous tissue (scar) after about 6 weeks.
100
What happens to the myocardium's zone of perfusion immediately after coronary artery obstruction?
The zone of perfusion becomes ischemic, leading to necrosis over time if blood flow is not restored.
101
How does the zone of necrosis progress over time in myocardial infarction?
The necrotic area expands from the endocardium toward the epicardium within hours if blood flow remains obstructed.
102
How long does ischemia need to last for irreversible damage in myocardial cells?
Ischemia becomes irreversible in the myocardium after 30-40 minutes.
103
What metabolic shift occurs in myocardial cells due to reduced oxygen supply?
Cells switch to anaerobic glycolysis due to reduced oxygen supply.
104
What is the result of anaerobic glycolysis in myocardial cells?
It leads to increased lactic acid, decreased pH, and eventual failure of anaerobic glycolysis.
105
What happens to ATP levels during myocardial ischemia?
ATP levels decrease, affecting cellular functions.
106
How does decreased ATP affect ion pumps in myocardial cells?
Failure of membrane ion pumps occurs, leading to ion imbalance.
107
What cellular change results from the influx of solutes and water in ischemic cells?
Swelling of the endoplasmic reticulum (ER) and cellular edema.
108
What happens to protein synthesis and metabolic reactions in ischemic myocardial cells?
There is a decrease in metabolic reactions and protein synthesis.
109
How does ischemia disrupt the cell's structural integrity?
Ischemia disrupts the cytoskeleton and damages the mitochondrial membrane.
110
What major cellular events occur as ischemic damage progresses?
Mitochondrial swelling, release of lysosomal enzymes, breakdown of DNA/RNA, nucleus dissolution, and coagulation of cell proteins.
111
describe MI histology
features of MI 1 day post-infarction: Coagulative necrosis with wavy fibers and early infiltration of neutrophils. 3-4 days post-infarction: Heavy infiltration of neutrophils, breakdown of myocyte nuclei, and ongoing coagulative necrosis. 7-10 days post-MI: Macrophages replace neutrophils, clearing debris, and early formation of granulation tissue. MI at 10 days: Established granulation tissue with abundant macrophages and beginning fibrosis. MI at >10 days: Dense collagenous scar tissue and fibrosis, indicating the formation of mature scar tissue.
112
Heart Failure caused by:
reduced cardiac output → arterial underfilling
113
What are the main goals of myocardial infarction management?
Increase oxygen supply, decrease oxygen demand, prevent and detect arrhythmias, provide pain relief, and treat the underlying cause.
114
How can oxygen supply be increased in the management of myocardial infarction?
Oxygen therapy, medications like nitroglycerin to dilate coronary arteries, and in some cases, procedures to restore blood flow.
115
Why is it important to decrease oxygen demand in myocardial infarction?
Reducing oxygen demand helps relieve stress on the heart, preventing further damage to ischemic tissue.
116
How does streptokinase assist in managing myocardial infarction?
Streptokinase activates plasminogen to form plasmin, which breaks down fibrin in blood clots, helping to dissolve the clot blocking the coronary artery.
117
What is the role of plasmin in fibrinolysis?
Plasmin degrades fibrin into fibrin degradation products, helping to dissolve blood clots.
118
What enzymes activate plasminogen besides streptokinase?
Tissue plasminogen activator (tPA) and urokinase also activate plasminogen to form plasmin.
119
Why is it important to monitor for arrhythmias in myocardial infarction management?
Arrhythmias can lead to life-threatening complications; early detection and treatment are crucial for patient stability.
120
What is the function of α2-antiplasmin in the fibrinolytic pathway?
α2-antiplasmin inhibits plasmin, helping to regulate the breakdown of fibrin and control excessive clot dissolution.
121
How does increased sympathetic activity act as a compensatory response in cardiovascular conditions?
It increases heart rate, contractile force, and redistributes blood to raise blood pressure, increase venous return, and boost preload.
122
What are the effects of activating the renin-angiotensin-aldosterone system (RAAS) as a compensatory response?
RAAS causes vasoconstriction to raise blood pressure and promotes sodium and water retention to increase preload.
123
How does ventricular hypertrophy serve as a compensatory mechanism?
Ventricular hypertrophy increases the force of heart contractions, helping to maintain cardiac output under stress.
124
What is the role of elevated 2,3-DPG in compensatory responses?
Elevated 2,3-DPG decreases hemoglobin's affinity for oxygen, allowing more oxygen to be released to tissues.
125
What effect does increased preload have on the heart?
Increased preload stretches the heart muscle, enhancing contractility and improving cardiac output.
126
What is a disadvantage of fluid retention as a compensatory response?
Fluid retention can lead to systemic venous congestion and dependent edema, as well as pulmonary venous congestion and pulmonary edema, causing decreased compliance and dyspnea.
127
How does arteriole vasoconstriction negatively impact the body in compensatory responses?
Arteriole vasoconstriction can lead to decreased urine output, muscle weakness, and increased afterload, which strains the heart.
128
What is a downside of ventricular hypertrophy as a compensatory mechanism?
Hypertrophy increases myocardial oxygen demand, which can strain the heart and worsen ischemia.
129
What are some methods to reduce preload in heart failure management?
Preload can be reduced through dietary modifications, diuretics, and vasodilators.
130
How can contractility be augmented in heart failure management?
Contractility can be increased with inotropic medications, which strengthen heart contractions.
131
What strategies are used to reduce afterload in heart failure management?
Afterload reduction can be achieved through vasodilation and by inhibiting the renin-angiotensin-aldosterone (RAA) system.
132

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