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2a ILAs > atherosclerosis > Flashcards

atherosclerosis Flashcards

1
Q

describe the structure of the normal arterial vessel WALL

A
  1. tunica intima (innermost, next to lumen, simple squamous)
  2. tunica media (smooth muscle layer)
  3. adventitia (outermost)
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2
Q

4 components of an atherosclerosis plaque

A

Lipid
Necrotic core
Connective tissue
Fibrous “cap

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3
Q

what are the 3 main headings to plaque formation mechanism

A
  1. damage to endothelial wall
  2. LDLs begin formation of fatty streak
  3. plaque growth
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4
Q

list non-modifiable risk factors for atherosclerosis

A

Age
Gender
Race
Family History
type 1 diabetes

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5
Q

list modifiable risk factors for atherosclerosis

A

Smoker
Lack of exercise
Weight
(Borderline) Diabetes (type 2)
Hypertension
High cholesterol

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6
Q

why is smoking a risk factor for atherosclerosis?

A

Releases free radicals, nicotine + CO into the body/blood → These damage endothelial cells → increased risk of plaque formation

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7
Q

why is hypertension a risk factor for atherosclerosis?

A

Increased pressure →increased damage of the vessel wall → increased risk of plaque formation

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8
Q

why is poorly controlled Diabetes a risk factor for atherosclerosis?

A

High glucose levels in the blood

Increased Free radicals leads to Increased oxidation of LDLs

Loss of nitric oxide (NO) , Which normally allows relaxation of vessel + increased flow

Promotes platelet aggregation

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9
Q

why is High cholesterol levels a risk factor for atherosclerosis?

A

High LDLs

Can pass in and out of the arterial wall in excess, accumulates in arterial wall,

undergoes oxidation….

plaque formation etc

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10
Q

why is obesity a risk factor for atherosclerosis?

A

Increases proinflammatory cytokines levels

More LDLs

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11
Q

why is a lack of exercise a risk factor for atherosclerosis?

A

exercise helps rebalance of low- and high-density lipoproteins

Reduces blood pressure

Therefore lack of exercise can lead to high levels of LDLs, hypertension, obesity

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12
Q

why is age a risk factor for atherosclerosis?

?

A

Risk increases with age as plaque builds up over time

The trend shows: If fatty streaks develop in 20s, these don’t establish into plaques until 30-50s, and only in you 40s-80s do these plaques cause compilations such as thrombosis or angina

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13
Q

why is race/ethnicity a risk factor for atherosclerosis?

A

Certain ethnic minority groups are at greater risk of heart disease

Rates of cardiovascular disease (CVD) and diabetes are higher among Black and South Asian groups in the UK

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14
Q

why is family history a risk factor for atherosclerosis?

A

Lipid levels, hypertension and diabetes, all appear to have an inheritable component.

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15
Q

what are primary preventative measures for atherosclerosis?

A

Exercise more
- Helps rebalance of low- and high-density lipoproteins
- Reduces blood pressure

Eat more healthily
- Less salt + sat fats
- Less sugar- diabetes risk

Stop smoking
- Less free radicals, nicotine + CO into the body/blood
- Therefore less damage endothelial cells

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16
Q

what are secondary preventions for atherosclerosis?

A

Statin
- to help lower the level of low-density lipoprotein (LDL) cholesterol in the blood.

Antihypertensives:
Calcium channel blockers (CCB) eg. Nifedipine
ACE inhibitors (ACEi) eg. ramipril
angiotensin receptor blockers (ARB) eg. Candesartan
Diuretics eg. chlorthalidone
Beta blockers eg. propranolol

Diabetes control:
- Eg. Metformin medication

Social and green prescribing
- Weight loss groups
- Gym vouchers
- Join a walking group

17
Q

Define the term ‘co-benefits’ in relation to health and climate change?

A

Co-benefits:the positive effects that a policy or measure aimed at one objective might have on other objectives

Implementation of climate policies has many co benefits including reducing health risks

Climate change and health are interlinked, for instance, measures to prevent air pollution will also help breathing quality

18
Q

what is the most accepted theory on the mechanism of atherosclerosis plaque formation

A

the endothelial damage theory

19
Q

explain step 2 of plaque formation:

  1. endothelial wall damage
A

Due to high levels of LDLs in blood stream (hyperlipidemia)
Smoking or air pollution (free radicals)
High cholesterol
Hypertension - causes physical injury
Turbulent blood flow, for example, where arteries branch
Chronically elevated blood glucose levels

20
Q

explain step 2 of plaque formation:

  1. LDLs begin formation of fatty streak
A

Dysfunctional endothelial cells allow Low density lipoproteins (LDLs) to move from lumen into tunica intima layer

The Dysfunctional cells release reactive oxygen species (eg. metalloproteases) which oxidise the LDLs

Oxidised LDLs cannot leave the intima, they are trapped

Dysfunctional endothelial cells + oxidised LDLs trigger endothelial cells to express adhesion molecules for WBCs (monocytes + T helper cells)

These monocytes attach and move into intima where they are now called macrophages

Macrophages have scavenger receptors that will engulf the oxidised LDLs to become a foam cell ( a macrophage containing lipids, essential to inflammation)

A fatty streak has formed

21
Q

explain step 3 of plaque formation:

  1. Plaque growth
A

Foam cells release products, then die and release their contents. this forms the fibrous cap, the bulk of the plaque and increases inflammation.

Products released:
- chemokines, to attract more macrophages

  • IGF-1 ( a growth factor), that causes smooth muscle cells to proliferate and migrate from the media to the intima layer. These cells make collagen, which forms a hard, fibrous cap to the plaque
  • proinflammatory cytokines and reactive oxygen species increase inflammation
  • When the foam cells die they release lipid content, containing DNA materials which attract neutrophils to the site of Inflammation
22
Q

what 2 other factors increase plaque growth

A
  1. increased blood supply to plaque
  2. T cells
  • they bind onto endothelial cells
  • enter plaque area
  • are activated by macrophages to release IFN-Y
  • this promotes inflammation and activates endothelial cells to attract more WBCs
  • as a result inflammation increases and plaque grows

2a ILAs (3 decks)

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