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Pathophysiology of the heart and circulatory system > Lecture 8 > Flashcards

Lecture 8 Flashcards

Vascular pathology (62 cards)

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1
Q

What does a plaque contain?

A

Cholesterol, macrophages and triglycerides

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2
Q

How can you know under the microscope that something is a clot?

A

Because unclotted blood would have washed away in the preparation

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3
Q

Is a plaque chronic or acute? And what of a clot?

A

A plaque is chronic and a clot is acute

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4
Q

What is the consequence of atherosclerosis on the vessel wall?

A

It leads to thinning of the muscular layer of the vessel wall

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5
Q

What is used to measure LDL?

A

The cholesterol to HDL ratio

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6
Q

Which vessel does basal constriction?

A

The arteriole

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7
Q

What does morbidity mean?

A

The existence of symptoms

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8
Q

What is essential hypertension?

A

When a specific cause cannot be appointed

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9
Q

What is the function of collagen?

A

It gives structure and protects against mechanical factors

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10
Q

What leads to a continuous strain on the vessels?

A

Blood pressure and flow

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11
Q

What happens when LDL is transported into the endothelium?

A

It gets oxidized and is now considered to be MM-LDL

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12
Q

How do monocytes get into the endothelium?

A

Via adhesion molecules

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13
Q

What is the function of monocytes?

A

They process cytokines (which increase the expression of adhesion molecules) and chemokines (which attract specific cells)

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14
Q

Why do monocytes transform to macrophages?

A

To take up the toxic MM-LDL

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15
Q

What happens when LDL oxidation progresses?

A

The proteins that usually bind to the receptor are also oxidized and now bind the scavenger receptor

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16
Q

What doe macrophages activate?

A

T cells

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17
Q

What do T cells do to the plaque?

A

They weaken the cap of the plaque

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18
Q

What is the function of Nitric Oxide (NO)?

A

It is a vasodilater and control the normal vascular function, clotting and control where the blood flows

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19
Q

Where is NO produced?

A

In the endothelium

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20
Q

What functions does the endothelium have?

A

Resistance/flow/volume
Angiogenesis/arteriogenesis
Barrier function
Infiltration of leukocytes
Thrombosis/haematosis

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21
Q

What is the quickest vasodilator?

A

Adenosine

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22
Q

What is the most powerful vasodilator?

A

Endothelin

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23
Q

What is the quickest vasoconstrictor?

A

The sympathetic tone

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24
Q

What molecule lowers blood pressure?

A

Angiotensin

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25
What are some characteristics of NOS-I?
It is neural, calcium-dependent, it is a neurotransmitter
26
What are some characteristics of NOS-II?
It is calcium-independent, the expression is induced by TNF-a, thus it is inducible and mediates an immune response to eg bacteria
27
What are some characteristics of NOS-III?
It is endothelial, calcium-dependent, is activated by shear stress through phosphorylation and it controls blood flow/thrombosis and inflammation
28
What is argenine used for?
To produce NO
29
What is NO production with Argenine controlled by?
Calcium influx, which is triggered by acetylcholine
30
What does shear stress activate?
It activates Akt
31
What is the function of Akt?
It results in a stable eNOS increase, which leads to arteriogenesis
32
How can eNOS be inhibited?
Via the pseudo substrate ADMA
33
How is ADMA degraded?
By DDAH
34
How do leukocytes invade in the endothelium?
Via adhesion factors that are expressed on leukocytes and endothelium (all adhesion factors need to be expressed), this controls where they van infiltrate
35
What is vasculitis?
An inflammation of all arteries, the leukocytes can enter everywhere
36
Where can most of the endothelium be found?
In the microvasculature, thus capillaries and vaso vasorum
37
What is the consequence of smoking on plaque formation?
It leads to quicker LDL oxidation and it damages the endothelium, which increases the expression of adhesion factors and decreases its barrier function
38
How is LDL transported?
From the liver to tissue
39
How is HDL transported?
From the tissue to the liver
40
How can coronary heart disease (CHD) be predicted?
With LDL
41
Which processes determine cholesterol levels?
Cholesterol synthesis Intestinal uptake of cholesterol Reverse cholesterol transport Hepato/intestinal clearance
42
What happens when HMG-CoA is inhibited?
The cholesterol in the liver is lowered
43
What happens when more cholesterol is taken up?
It heightens the clearance
44
What is the function of the drug Ezetimibe?
It lowers cholesterol absorption from the duodenum by blocking NPCILI, but thickening of the intima is not reduced
45
What is the consequence of bile acids binding to resins?
It inhibits cholesterol absorption and increases triglycerides and increased fecal elimination of bile acids
46
What is the function of statins on LDL?
It powerfully lowers LDL and it does so dose-dependently
47
What are the two function of statins?
Lowering plaque formation and improving endothelial function
48
When is C-reactive protein secreted?
When there is an inflammation
49
Which organ produces C-reactive protein?
The liver
50
What is the function of Canakinumab?
It targets Il-Ib as an anti-inflammatory protein for CVD. It lowers C-reactive protein
51
What is the function of Colchiane?
It is from a plant and has a bigger effect on CVD than Canakinumab
52
What is the result of spastic arterioles?
Diziness and chest pain
53
How do arterioles control arterial pressure?
By regulating the capillary pressure
54
What can be a consequence of high blood pressure?
Bad eye sight and kidney failure
55
What can be a consequence of long-term high blood pressure?
The kidney will regulate the blood pressure via ADH, which stimulates ion and water secretion
56
What is the downside of infusing adenosine?
It is too powerful
57
What is the consequence of a lower flow reserve?
There cardiomyovascular function worsens
58
When should the flow reserve go up?
When adenosine is infused
59
When can the response to adenosine lower?
In later stage diabetic patients
60
How can the blood flow be also stimulated?
By putting eg a hand in cold water (produce noradrenaline)
61
What is rarifection?
The disappearing of a capillary, it can happen in eg kidney diseases, which lowers the microvessel density
62
Which factors contribute to rarifection?
Inflammation, toxin and hypertension

Pathophysiology of the heart and circulatory system (11 decks)

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