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path 300 > Cardiovascular 1 > Flashcards

Cardiovascular 1 Flashcards

1
Q

What are the different types of blood vessels and their functions?

A
  • The aorta is a large blood vessel with a thick wall and elastic tissue because it has to withstand high pressure.
  • As the blood goes forward it goes to smaller and smaller arteries, diameter gets smaller and walls get thinner (less elastic tissue),
  • until the capillary which only have 1 layer in the wall since is made for exchange.
  • Veins are bigger since they are made for capacity (at any moment they contain the majority of the blood in the body).
  • They also have valves (in the larger ones) in order to control the one-way flow and can also contract to some extent.
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2
Q

What is atherosclerosis and what does it cause?

A

Atherosclerosis is a pathological change in the wall of the artery and is the fundamental cause of many circulatory problems. It causes cardiovascular disease and cerebrovascular disease.

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3
Q

Describe the timeline of atherosclerosis.

A

The initial event is endothelial injury and dysfunction, leading to the formation of a fatty streak. This can advance and buildup, leading to the abnormal buildup of atheroma (fibrous tissue) within the intima. This can progress from mild to moderate to severe, with plaques sticking into the wall of the aorta.

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4
Q

What are the consequences of atherosclerosis?

A

Atherosclerosis can be asymptomatic until highly advanced. It can cause angina, myocardial infarct, transient ischemic attacks, stroke, and peripheral arterial disease. The stability/fragility of the atherosclerotic plaque can also be determined depending on the thickness of the wall of the plaque.

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5
Q

What are capillaries made for?

A

They are made for exchange, hence they only have 1 layer in the wall.

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6
Q

What is the function of veins?

A

They are made for capacity and contain the majority of the blood in the body at any moment

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7
Q

What is a fatty streak in atherosclerosis?

A

It’s the normal lipid accumulation in proliferating intimal smooth muscle and extracellular matrix.

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8
Q

What happens in the preclinical phase of atherosclerosis?

A

There is formation of a normal fatty streak, which can advance and buildup, but no symptoms are felt as there is enough space for blood to flow.

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9
Q

What happens in the clinical phase of atherosclerosis?

A

This phase can involve rupture/fissuring of the surface of the plaque, erosion/ulceration, or hemorrhage in the plaque. All can lead to aneurysm and rupture of aorta, occlusion by a thrombus, or critical stenosis (complete block by fat).

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10
Q

What is a stable plaque in atherosclerosis?

A

A stable plaque has a small lipid core with a thick fibrous cap, allowing enough blood to pass through.

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11
Q

What is an unstable plaque in atherosclerosis?

A

An unstable plaque has a big lipid core with a thin fibrous cap, which has much more potential to rupture.

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12
Q

What is the function of valves in veins?

A

They control the one-way flow of blood.

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13
Q

What is the role of endothelial cells in blood vessels?

A

They release signaling molecules and can alter coagulation, inflammation, blood flow, etc. in response to injury or stress.

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14
Q

What is the consequence of a ruptured atherosclerotic plaque?

A

It can lead to aneurysm and rupture of aorta, occlusion by a thrombus, or critical stenosis.

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15
Q

What is an aneurysm in the context of atherosclerosis?

A

It’s a weakening of the wall of the blood vessel, which can rupture and cause significant bleeding.

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16
Q

What is the key component of multifactorial risk in pathogenesis?

A

The key components are endothelial dysfunction and chronic inflammation.

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17
Q

What is a critical feature in atherosclerosis?

A

Endothelial injury is a critical feature in atherosclerosis.

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18
Q

What may cause chronic endothelial injury?

A

Chronic injury may be due to hyperlipidemia, hypertension, smoking, etc.

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19
Q

What are the most vulnerable places for injury and plaque formations? Why?

A

Branch points are the most vulnerable places for injury and plaque formations since blood is flowing through here and has to hit the endothelial to diverge

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20
Q

What changes can inflammation within the arterial intima lead to?

A

It can lead to cytokine release promoting cellular changes.

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21
Q

What are the most important cells in the pathogenesis?

A

Macrophages and T-cells are the most important cells in the pathogenesis.

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22
Q

What happens when cells migrate through the altered endothelium into the intima?

A

They alter their properties, which can lead to injury induced smooth muscle cell proliferation

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23
Q

What are foam cells?

A

Foam cells are macrophages filled with lipids, which causes the buildup up lipid in the vessel wall.

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24
Q

What is the structure and function of lipoproteins?

A

Lipoproteins have an outside phospholipid membrane with cholesterol and is surrounded by different apoproteins. Inside is triglycerides and cholesterol esters but varies with their types. They have different functions based on their different apoprotein receptor signaling

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25
Q

What happens when oxidized LDL is internalized by scavenger receptors on macrophages within the intima?

A

Macrophages can then accumulate LDL and becomes foam cells. This also activates inflammatory response: releases cytokines, chemokines, ROS, etc.

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26
Q

What are the functions of smooth muscle cells?

A

They can accumulate lipid, become foam cells, and synthesize collagen, elastin, and glycoproteins

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27
Q

What changes can smooth muscle cells undergo?

A

They can change from contractile (normal) to secretory when responding to secreted factors. They can also exhibit many other phenotypes: mesenchymal, fibroblast, macrophage, osteogenic, adipocyte, contractile.

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28
Q

What is the result of hypercholesterolemia in the context of pathogenesis?

A

In hypercholesterolemia, monocytes attach and migrate along the wall of the vessel.

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29
Q

What happens when foam cells die?

A

If foam cells die, they then release all their accumulated lipid in the circulation.

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30
Q

What is the role of LDL in the pathogenesis?

A

LDL can contribute to the pathogenesis since they deliver cholesterol in cells throughout the body, and many cells do not need cholesterol.

31
Q

What is the function of HDL in the pathogenesis?

A

HDL removes cholesterol from cells in the periphery and take it back to the liver – called reverse cholesterol transport. HDL also has many protective roles: they can release anti-inflammatory, antioxidants, and anticoagulants.

32
Q

What is the function of lipoproteins?

A

Lipoproteins have different functions based on their different apoprotein receptor signaling. They supply energy and cholesterol to cells, most LDL returns to the liver. Some of the LDL/remnants can contribute to the pathogenesis.

33
Q

What is the role of macrophages in the pathogenesis?

A

Macrophages have many scavenger receptors which allows them to take in (internalize) lipids. Oxidized LDL is internalized by scavenger receptors on macrophages within the intima, macrophages can then accumulate LDL and becomes foam cells.

34
Q

What happens after chronic endothelial injury in the sequence of pathogenesis in atherosclerosis?

A

It causes endothelial dysfunction (increased permeability, and leukocyte and monocyte adhesion/migration).

35
Q

What is the role of macrophages and smooth muscle cells in the sequence of pathogenesis?

A

Macrophages are activated, smooth muscle cells are recruited, and there is an accumulation of lipids in the vessels wall. Macrophages and smooth muscle cells engulf lipids (can eventually become foam cells).

36
Q

What are the risk factors for pathogenesis?

A

The risk factors are additive: hypertension, smoking, high LDL, low HDL, elevated triglycerides, lack of exercise, diabetes mellitus.

37
Q

How does smoking increase the risk of pathogenesis?

A

Smoking increases the risk of platelet aggregation, CO damages endothelium, release NA, more likely to have hypertension.

38
Q

What is the effect of a rare genetic defect in LDL receptor?

A

It leads to familial hypercholesterolemia. Monozygotic is very dangerous, can develop problems early in life. Heterozygotic is not as bad, but still earlier onset.

39
Q

What is the difference between saturated and unsaturated lipids in terms of serum cholesterol level?

A

Saturated lipids increase serum cholesterol level (and decrease LDLR).

40
Q

What is thrombosis?

A

Thrombosis is a blood clot forming within the vessel.

41
Q

What are the risks of thrombosis?

A

The risks are endothelial injury, altered composition of blood, hypercoagulability, and abnormal blood flow.

42
Q

What is embolism?

A

Embolism is any clot that moves (does not have to be a blood clot).

43
Q

What is familial hypercholesterolemia and how does it affect the risk of pathogenesis?

A

Familial hypercholesterolemia is a rare genetic defect in LDL receptor. Monozygotic is very dangerous, can develop problems early in life. Heterozygotic is not as bad, but still earlier onset.

44
Q

How does diabetes increase the risk of pathogenesis?

A

Diabetes, especially type 2, is linked to obesity and western diet. As BMI increases, the risk of type 2 increases greatly. It can cause metabolic syndrome, which causes abdominal obesity, hyperinsulinemia, high fasting plasma glucose, impaired glucose tolerance, hypertriglyceridemia, low HDL, and hypertension.

45
Q

What is embolism and how does it occur?

A

Embolism is any clot that moves (does not have to be a blood clot). Most common is a venous thrombus that gets detached – resulting in either poor circulation or increased blood clotting after trauma.

46
Q

What happens if you decrease the diameter of a vessel in peripheral vascular disease?

A

If you decrease the diameter, you greatly reduce the flow.

47
Q

What is intermittent claudication in the context of peripheral vascular disease?

A

Intermittent claudication refers to just getting enough blood for resting state in the periphery.

48
Q

What is an aneurysm?

A

An aneurysm is a weakening of the wall of the vessel usually due to atherosclerosis.

49
Q

What are the different types of aneurysms?

A

Aneurysms can be circumferential (all around the vessel), localized (a bulge forms), micro-aneurysms (associated with hypertension and usually occurs in smaller arteries - in brain and retina), saccular (like a sac sticking out), fusiform (all the way around), or berry aneurysms (at the base of the brain in the circle of Willis).

50
Q

What are the potential consequences of an aneurysm in the aorta?

A

An aneurysm in the aorta can break through the wall of the aorta (aortic dissection), leading to complications such as death and organ ischemia. It can also cause the blood to flow backwards, compressing the heart.

51
Q

What are varicose veins?

A

Varicose veins are bulges in the veins, usually in the legs. They tend to occur in people who stand a lot and don’t move a lot (prolonged standing, pregnancy, obesity). More blood will tend to be in the veins in the lower body than the upper body.

52
Q

What happens to the blood flow in varicose veins?

A

Normally, when muscles in the leg contract, it will cause the blood to flow up towards the heart, but in varicose veins, even when the valve is closed, blood will flow downwards.

53
Q

What is the solution for intermittent claudication in peripheral vascular disease?

A

The solution for intermittent claudication can be surgery, including graft, bypass, or angioplasty.

54
Q

What are the complications of an aortic dissection?

A

The complications of an aortic dissection can include death and organ ischemia.

55
Q

What are the conditions that can lead to varicose veins?

A

Conditions that can lead to varicose veins include prolonged standing, pregnancy, and obesity.

56
Q

What is the effect of an aneurysm on blood flow?

A

An aneurysm can cause the blood to flow backwards, compressing the heart.

57
Q

What is a micro-aneurysm and where does it usually occur?

A

A micro-aneurysm is associated with hypertension and usually occurs in smaller arteries, such as arterioles in the brain and retina.

58
Q

What is a berry aneurysm and where is it located?

A

A berry aneurysm is located at the base of the brain, in the circle of Willis.

59
Q

which vessels have their own blood supply?

A

large arteries

60
Q

what is angina?

A

terrible chest pain when increased physical effort

61
Q

what are transient ischemic attacks?

A

when blood flow to a section of the brain in borderline adequate, so can case symptoms transiently.

62
Q

what are symptoms/pathology of peripheral arterial disease?

A

rest pain, gangrene, necrosis

63
Q

what happens to the arterial walls in atherosclerosis?

A

the elastic wall is weakened

64
Q

pathogenesis leading to alteration of smooth muscle cells and macrophage functions in atherosclerosis.

A
  • many cells (e.g. monocytes, platelets, lymphocytes) can release growth factors for smooth muscle cells, which can cause them to migrate to the endothelium, where they can start proliferating.
  • Then, lipoproteins can enter the cells and accumulate:
  • LDL enters vessels wall, macrophages engulf them and accumulates them until they become foam cells.
65
Q

sequence of events for atherosclerosis pathogenesis.

A
  1. Chronic endothelial injury due to a variety of things (e.g. hyperlipidemia)
  2. Causes endothelial dysfunction (increased permeability, and leukocyte and monocyte adhesion/migration)
  3. Macrophages are then activated, smooth muscle cells are recruited, and there is an accumulation of lipids in the vessels wall.
  4. Macrophages and smooth muscle cells engulf lipids (can eventually become foam cells)
  5. Smooth muscle cells proliferate, which causes increase synthesis of collagen and extracellular matrix, making a deposition layer.
66
Q

effect of PCSK9 mutation

A

loss of function of PCSK9, there is less LDLR, so less lipids in the liver.

67
Q

effect of microvascular disease

A
  • causes capillary vasoconstriction, permeability increase, and abnormal ECM,
  • which leads to edema, ischemia, and neovascularization.
68
Q

how does diabetes cause atherosclerosis (pathology)?

A
  • Causes endothelial damage (due to insulin resistance and hyperglycemia), cause damage to ECM (glucose-derivatives react with intracellular and extracellular proteins), and may involve ROS production by the mitochondria.
  • Normally, insulin causes translocation of glucose transporter from intracellular sites to the plasma membrane, but in obesity, there is insulin resistance.
69
Q

how is the blood composition altered in thrombosis?

A
  • increase in platelets, fibrinogen and prothrombin after surgery or childbirth.
  • Causing change in platelet adhesiveness
70
Q

common sites for thrombosis

A

heart, brain, and periphery

71
Q

possible outcomes of venous thrombosis

A

Resolution, embolization to lungs, propagation towards the heart, organized and recanalized (or incorporated into the wall).

72
Q

what causes a thrombus in an artery and a vein?

A
  • In artery: usually caused by plaque rupture and endothelial injury.
  • In vein: usually caused by altered blood flow, coagulation, and injury (usually in a region of low blood flow)
  • Deep vein thrombosis: a risk with immobilization (e.g. air travel)
73
Q

what happens when a venous clot forms in the periphery?

A
  • it will go straight into the heart, and if it is small enough, it will get pumped to the lungs.
  • Lungs have dual blood supply, and depending on the size, you will or will not get an infarct.
  • If they are small, there is enough collateral flow that there will not be death of the lung, but if it is large, it will block a larger branch, blocking off the blood flow in a portion of the lung.
74
Q

what happens of there is an arterial clot?

A

the damage depends on the location (whether or not there is collateral flow) – but if in heart, there is not collateral flow, so can cause infarct.

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