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Pathobiology of Human Disease > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

How common is CV disease?

A

Main cause of death in Western countries
Responsible for half of deaths in Europe

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2
Q

What is Cardiovascular disease described as?

A

A term used to describe conditions which affect blood vessels or the heart
Group of disorders, Frequently fatal because efficient blood flow supports the whole of the body and organs

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3
Q

What is the structure of Arteries?

A
  • Tunica Intima
  • Tunica Media
  • Tunica Adventitia
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4
Q

What is the Tunica Intima?

A

Inner layer of the artery (closest to lumen)
Single layer of endothelial cells (like blood vessels)
In direct contact with blood

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5
Q

What is the endothelium?

A

Physical barrier
Controls passage of substances from blood to tissues and vice versa

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6
Q

What are the functions of the Endothelium?

A

Participates in many functions e.g.
- Regulates vascular function
- Dilation or constriction of muscle to control artery lumen size
- Inflammatory responses (e.g. cytokines)

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7
Q

What is the function of the Tunica Intima?

A

Thin layer of connective tissue and internal elastic lamina separates the endothelium from the next layer
Basement membrane
Role is to support the endothelium (anchors it to the arterial wall)

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8
Q

What is the Tunica Media?

A

‘Middle layer’
Smooth muscle cells : arranged in concentric circles which permits the artery to change in diameter

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9
Q

What is the external elastic lamina?

A

The connective tissue which separates the tunica media from the outer layer of the vessel
Also provides structural support

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10
Q

What is the Tunica Adventitia?

A

Outer layer of blood vessel wall
Composed of cells (e.g. fibroblasts) and connective tissue
The connective tissue helps maintain the structure and integrity of the blood vessel

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11
Q

How do vessels work in Tunica Adventitia?

A

Large vessels have their own blood supply (vaso vasorum)
Oxygen and nutrients cannot diffuse from the lumen to the outer layer

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12
Q

What is artheroscelrosis?

A

Is initiated caused by the deposition of lipids in the arterial wall

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13
Q

What are lipoproteins composed of?

A

Composed from lipid and protein
Are a family of substances that have different functions and properties
Size, density, composition

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14
Q

What is the common function of lipoproteins?

A

To transport lipids

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15
Q

What is the structure of lipoproteins?

A
  • Spherical
  • Hydrophobic lipid core e.g. cholesterol
  • Outer layer of phospholipids and apolipoproteins important for structure and targeting)
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16
Q

What are the different lipoproteins (from big to small)?

A
  • Chylomicrons
  • Very low density lipoproteins (VLDL)
  • Intermediate density lipoproteins (IDL)
  • Low density lipoproteins (LDL)
  • High density lipoproteins (HDL)
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17
Q

What different lipids can lipoproteins carry?

A

Cholesterol, cholesterol esters, triglycerides, fatty acids, phospholipids

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18
Q

Where are lipoproteins produced?

A

Are mainly produced in the liver and intestine
Within the circulation, they are dynamic structures
Constant state of flux

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19
Q

What are chylomicrons?

A

Made in the intestine
Derived from lipids in the diet
Made by intestinal epithelium and secreted into blood
Deliver dietary fats (mainly triglycerides) to peripheral tissues which is used for energy

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20
Q

Where are VLDL’s synthesized?

A

Synthesized in the liver
Secreted into blood

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21
Q

Where is VLDL taken up?

A

By peripheral tissues
Lipid used for energy and storage by body
VLDL is converted to IDL and LDL (in blood/peripheral tissues/liver)

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22
Q

Where are LDL’s taken up and what is the main lipid component?

A

LDL taken up by cells via LDL receptors
(receptor mediated endocytosis)
Main lipid component- cholesterol

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23
Q

How is excess LDL removed and what is the main protein component of LDL?

A

Excess LDL removed by liver and this controls circulating concentration of LDL
(apo)B100 is the main protein component of LDL

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24
Q

What happens during receptor mediated endocytosis?

A

Cells take up LDL particles from the bloodstream by using LDL receptors on their surface
The LDL is broken down to release cholesterol which the cell uses or stores as needed

25
Q

How is LDL plasma concentration regulated?

A

Is regulated primarily by the liver, which removes excess LDL from the blood via LDL receptors. When blood LDL levels are high, the liver increases receptor activity to take up and clear more LDL, lowering the concentration

26
Q

What is hyperlipidemia?

A

condition characterized by abnormally high levels of lipids (fats) in the blood, primarily cholesterol and triglycerides

27
Q

What are the main features and risks of artherscelrosis?

A

LDL accumulation in the arterial wall is a prominent feature
Hyperlipidemia is the main risk factor for artherscelrosis
Elevated LDL concentration in blood

28
Q

What are the sub classes of LDL?

A

Small, dense LDL (Subclass A)
Large, buoyant LDL (Subclass B)
Small, dense LDL is more pathogenic

29
Q

Where are HDL’s synthesised?

A

by the liver

30
Q

What do HDL’s remove?

A

HDL removes excess lipid from tissues/circulation and delivers it to the liver
This process is called Reverse cholesterol transport (RCT)
LDL broken down and converted to bile salts- eliminated via faeces

31
Q

What functions do HDL’s have?

A

HDL has protective functions
Can remove LDL from circulation/artheroscelerotic lesions
Inverse predictor of CVD
Low levels promote artheroscelrosis

32
Q

What is the structure of triglycerides?

A

One molecule of glycerol and 3 fatty acids
Energy (e.g source of fuel for muscles) and energy storage

33
Q

What is the structure of cholesterol?

A

Structure has 4 carbon rings
Critical component of membranes (structure)
Many other functions e.g. used for synthesis (precursor) of hormones and bile salts, myelin sheath

34
Q

What is the structure of cholesterol esters?

A

Cholesterol attached to fatty acids
Can be de-esterfied

35
Q

How do artheroscelrotic plaques develop?

A

Develop over decades
Plaques are the fatty lesions that form in arteries
Occur due to a blockage of blood flow

36
Q

What are the clinical effects of artheroscelrosis?

A

A sudden blockage of the affected artery happens due to clot formation
Heart attack/stroke
Often with fatal consequence
Chronic effects of high blood pressure

37
Q

What are the 3 hypotheses for artheroscelrotic plaque formation?

A

Response to (endothelial) injury
Response to retention
Response to oxidation

38
Q

What are the main causes of hyperlipidemia?

A

Diet and lifestyle
Genetic predisposition
Familial hypercholesterolemia
Mutations produce non-functional LDL receptors

39
Q

How does response to injury give rise to artherosclerotic plaques?

A

Whole of the arterial system exposed to high LDL but lesions form at specific sites

40
Q

What are the different physical forces on blood vessels that result in artherscelrosis?

A

Hemodynamic factors (blood flow) play a key role in artherogenesis
Endothelial shear stress (ESS)

41
Q

How do hemodynamic factors contribute to artherscelrosis?

A

Controls the sites at which the lipid accumulate in the arterial tree
Endothelial cells respond to changes in blood flow to promote

42
Q

How does ESS contribute to arthersclerosis?

A

It is the frictional force exerted by flowing blood on the endothelium
Low ESS makes arteries vulnerable to arthersclerosis development

43
Q

How does turbulent laminar flow cause arthersclerosis?

A

Disrurbed laminar flow causes low endothelial shear stress and promotes artheroscelrosis

44
Q

How must LDL’s be transported for arthersclerosis to develop?

A

LDL must be transported across the arterial wall for artherosclerosis to develop
Low Endothelial shear stress causes damage to the endothelium
- Enhances LDL transport
- Endothelium more permeable to LDL

45
Q

What are the 3 main pathways of LDL transport?

A
  1. Transcytosis (through endothelial cells)
  2. Paracellular (between endothelial cells)
  3. Leaky junction pathway- Permeability of endothelium is enhanced due to cell damage/death (caused by low ESS)
46
Q

What happens when LDL’s move from blood in the arterial wall via leaky junctions?

A

The higher the circulating level of LDL, the higher the level of transport
Smaller LDL are transported more easily
LDL is retained in the arterial wall

47
Q

What do LDL’s attach to?

A

Proteoglycans in the arterial wall
Binding mediated by ApoB100 in LDL
Promotes accumulation of LDL
Response to retention

48
Q

What must LDL be to be pathogenic?

A

LDL in it’s native state is not artherogenic
LDL must be pathogenic

49
Q

How does response to oxidation promote artherosclerosis?

A

Oxidised LDL is formed in the arterial wall (OxLDL)
Acquires new functions
Triggers inflammatory response

50
Q

What does OxLDL do?

A

Activates endothelial cells
Release of monocyte chemoattractants
Increase in adhesion molecule expression on endothelial cells

51
Q

What is MCP-1?

A

Monocyte chemotactic protein (MCP-1) is the chemokine that attracts circulating monocytes to the site of oxLDL accumulation

52
Q

What happens after MCP-1 attracts monocytes?

A

Monocytes migrate into the arterial wall
Following recruitment monocytes differentiate to macrophages
oxLDL is taken up (internalised) by macrophages
Lipid accumulates in the cytoplasm of cells and foam cells form

53
Q

What does the accumulation of foam cells lead to?

A

Leads to formation of a fatty streak
The initial lesion of artherosclerosis

54
Q

How does Arthersclerosis progress/transition?

A

Over time the morphology of the lesion changes
Developing lesion: continued foam cell formation and macrophage accumulation plaque size increases

55
Q

What are the characteristics that develop over time in arthersclerosis?

A

A fibrous cap forms
1. Thin fibrous cap
2. Stable fibrous lesion forms

56
Q

What happens for a plaque to rupture?

A

Clinical events occur due to an abrupt, catastrophic change in plaque morphology

57
Q

What makes the plaque vulnerable to rupture?

A

Previously thought there was a gradual narrowing of the lumen
Rupture exposes the plaque contents to artery lumen
Arterial blood comes into direct contact with the plaque interior

58
Q

What is thrombosis?

A

Formation of blood clot within a blood vessel, which can partially or fully block blood flow

59
Q

When does thrombosis occur in arthersclerosis?

A

As a complex lesion, rupture and thrombosis occurs

Pathobiology of Human Disease (16 decks)

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