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Infect & Immune 2 AM > AM L3 Thrombosis and diabetes > Flashcards

AM L3 Thrombosis and diabetes Flashcards

1
Q

What is plaque erosion?

A

focal areas of endothelium become denuded (stripped) and expose underlying connective tissue

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2
Q

MMPs are ____-dependent ____.

A

zinc dependent endopeptidases

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3
Q

Role of MMPs in plaque erosion?

A

degrade components of the extracellular matrix and basement membrane

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4
Q

2 main ways plaque erosion occurs?

A
  1. endothelial cell desquamation (scraping off) due to lysis of the extracellular matrix (caused by MMPs)
  2. endothelial cell death (including apoptosis)
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5
Q

MMPs subdivided into….

A

5 classes including collagenases, gelatinases and stromelysins

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6
Q

How does plaque erosion cause thrombosis?

A

The basement membrane is exposed, including collagen. This is prothrombotic. Platelet aggregation is trigger which can result in thrombosis.

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7
Q

Where does the thrombos lie in plaque erosion?

A

On top of the fibrous cap

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8
Q

Plaque rupture is….

A

a structural defect (gap) in the fibrous cap that separates the necrotic lipid core of an ATS plaque from the lumen, resulting in exposure of the necrotic core to the blood.

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9
Q

Trauma activates which clotting pathway

A

Extrinsic.

Activates VIIa.

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10
Q

The plaque expresses high levels of ….

A

tissue factor.

This results in the clotting cascade being activated when the legionis ruptured as large amounts are exposed.

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11
Q

Markers of vulnerable plaques

5

A

Large lipid core (>50% volume of plaque)
High density of macrophages
Low density of smooth muscle cells in the cap
High Tissue Factor content
Thin cap in which the collagen structure is disorganised

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12
Q

Why is high density of macrophages a risk factor?

A

Express tissue factor and MMPs.

Risky, particularly at the edges

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13
Q

If the thrombosis is in the surface of the plaque it is as a result of….

A

Superficial erosion

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14
Q

If the thrombosis is coming out of the necrotic lesion it is as a result of….

A

Rupture of the fibrous cap

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15
Q

Plaque rupture accounts for …. of fatal MI in men

Plaque erosion accounts for …. of MI in women

A

80%
50%
So basically it is very bad

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16
Q

What is a risk factor

A

something that changes your chances of having a disease.

May be modifiable or fixed

17
Q

Modifiable risk factors in terms of LDL and HDL

A

Raised LDL

Low HCL

18
Q

Modifiable risk factors include

A 
Diabetes
Obesity
Hypertension
Smoking
Physical inactivity
19
Q

Is homocysteine modifiable or fixed risk factor?

A

Elements of both - diet can change the level

20
Q

What is the leading cause of mortality in diabetes?

A

CHD (50% of all deaths)

21
Q

How does the body respond to an increase in blood glucose?

A

beta islet cells of the pancreas produce insulin

this causes adipocytes, liver and muscle to take up glucose

22
Q

How does the body respond to a decrease in blood glucose?

A

Pancreatic alpha cells produce glucagon.

Causes liver to increase ketone synth, gluconeogenesis and glycogenolysis

23
Q

What process is stopped in type 1 diabetes?

A

Pancreatic beta cells don’t produce insulin

24
Q

What process is stopped in type 2 diabetes?

A

Response to circulating insulin

25
Q

Diabetes causes ….(4)… thus increasing cardiovascular risk

A

increase endothelial dysfunction
increase blood viscosity
increase blood coagulation
secondary dyslipidemia

26
Q

Most complications of diabetes arise from

A

damage to blood vessels

27
Q

ATS is accelerated in diabetes particularly in what 3 arteries?

A

coronary, carotid and femoral

macrovascular damage

28
Q

Microvascular damage of diabetes occurs where? (3)

A

Retina, kidney, nervous system

29
Q

Hyperglycemia causes ….(4) … resulting in endothelial dysfuntion

A

Constriction
Growth promotion
Pro-thrombosis
Pro-inflammation

30
Q

Endothelial dysfunction is…

A

imbalance between the production of vasoconstricting and vasorelaxing mediators

31
Q

Sign of endothelial dysfunciton

A

decreased production of nitric oxide

32
Q

enzyme that produces nitric oxide?

A

phosphorylated eNOS (endothelial nitric oxide synthase)

33
Q

what is necessary to maintain the enzyme that makes NO

A

insulin is needed to activate AKt kinase
this phosphorylates eNOS to make it active
this produces NO

34
Q

unphosphorylated eNOS causes….

A 
endothelial dysfunction
(via:
reduced blood flow
thrombosis
inflammation
neointima formation)
35
Q

low NO also results in

A 
more ROS
more NADPH (precursor)
36
Q

what happens in mice with insulin receptor knock out?

A

decreased eNOS and impaired endothelial vasodilator funciton.
Impaired NO bioavailability and defects in PI3kinase/Akt system, what ever that is ….

Infect & Immune 2 AM (11 decks)

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