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First Year med - dundee > 82. Atheroma/Atherosclerosis > Flashcards

82. Atheroma/Atherosclerosis Flashcards

1
Q

name some atheroma synonyms

A

atherosclerosis
hardening of the arteries
coronary artery disease
ischemic heart disease

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2
Q

atheromas are extremely common in……………….world

A

developed

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3
Q

ichaemic heart disease and stokes account for …… of all deaths

A

1/3

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4
Q

what is the epidemiology of atheroma (aetiology)

A
  • cigarette smoking
  • hypertension
  • hyperlipidemia
  • diabetes
  • age
  • sex - males
  • genetics
    endothelial injury
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5
Q

what is the main ‘how’ of atheromas

A

endothelial injury or anything that increases endothelial cell injury can initiate the process of atherosclerosis

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6
Q

what kind of blood flow in vessels is said to be smooth in parallel layers

A

laminar

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7
Q

where does haemodynamic injury occur

A
  • sites of turbulent flow
  • any branching site - change of flow (aka not laminar)
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8
Q

Smoking a pack of cigarrettes a day increased the risk of angina etc. by over …………

A

200X

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9
Q

does high or low blood pressure damage endothelium

A

HBP

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10
Q

what is one of the biggest risk factors of atheromas

A

Hyperlipidemaemia

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11
Q

name a type of hyperlipidaemia

A

hypercholesterolaemia

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12
Q

High density Lipoprotein - good or bad?

A

Good

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13
Q

Low Density Lipoprotein - good or bad?

A

Bad

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14
Q

diabetes causes an increase of what

A

cholesterol levels

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15
Q

what is it that causes elastci strands in blood vessels to become rigid (diabetes)

A

advanced glycation end products (AGE)

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16
Q

what does Advanced Glycation End Products (AGE) cause

A

abnormal cross linking
loss of elasticity
trap cholesterol (LDL)

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17
Q

What is abnormal cross linking

A

They induce abnormal cross-linking of collagen and other proteins in the vessel walls. This cross-linking makes the vessel walls more rigid and less elastic.

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18
Q

what age is most at risk of atheromas

A

40-60

19
Q

what age is earliest atherosclerosis started and what age is all started to develop

A

1 and then 10

20
Q

why are males at higher risk

A

No one knows for sure as its an “independent risk factor”

21
Q

genetic variation in what 3 areas can cause atheromas

A
  • 1 – cholesterol metabolism
  • 2 – inflammatory response
  • 3 – control of blood pressure
22
Q

in 4 steps describe how atheromas happen

A
  1. Primary endothelial injury
  2. Accumulation of lipids and macrophages
  3. Migration of smooth muscle cells
  4. Increase in size
23
Q

when endothelial injury occurs what happens in terms of WBCs and perm… and (Hint- VC..)

A

increase permeability and increased WBC adhesion
increase VCAM-1: Vascular Cell Adhesion Molecule-1

24
Q

In the blood stream they are called ………..and not in blood stream they are called …………….

A

In the blood stream they are called Monocytes and not in blood stream they are called macrophages

25
Q

after endothelial injury, what attaches and migrates through wall

A

monocytes and once they are through they are macrophages

26
Q

what do the macrophages do to the cholesterol

A

gobble it up

27
Q

when the Macrophages ingest LDL cholesterol and can become …….cells if overloaded.

A

foam

28
Q

when the Macrophages ingest LDL cholesterol and can become overloaded foam cells what happens to them

A

they become trapped and LDL is deposited in the arterial cell wall

29
Q

what does the HDL do

A

High-density lipoprotein (HDL) cholesterol helps remove excess cholesterol from macrophages and other cells. HDL transports cholesterol back to the liver, where it can be processed and excreted from the body.

30
Q

smooth muscle migrates from where to where

A

tunuica media into intima

31
Q

when smooth muscle cells are migrating they get ……………… and take on………

A

stuck and take on cholesterol

32
Q

after smooth muscle gets stuck and takes on cholesterol, what does it produce

A

Extracellular matrix - eg. Collagen

33
Q

after smooth muscle gets stuck and takes on cholesterol and starts to produce ECM like collagen, what does it change from - to

A

Changes lesion from fatty streak to fibrofatty plaque

34
Q

on a histogram how can you tell if something is skeletal muscle

A

striations

35
Q

describe progression of an atheroma

A
  • More cholesterol
    • More macrophages
    • More smooth muscle and collagen etc
      Eventually too much cholesterol and a pool of extracellular cholesterol forms the centre of the plaque
36
Q

what is the Poiseuille equation

A

Q= (Pi)(Pr^4) over (8)(n)(l)
Q - flow rate
P - pressure
r- Radius
n- Fluid Viscosity
l- Length of tubing

37
Q

what is this equation called
Q= (Pi)(Pr^4) over (8)(n)(l)

A

Poiseuille

38
Q

As atheromatous plaques enlarge blood flow is ….

A

compromised

39
Q

Progression is associated with further loss of ………. and …………

A

luminal patency (the state of being openness obstructed) and arterial wall weakness

40
Q

Whats the difference between fatty streak and fibrofatty plaque

A

Fatty Streak: Early, simpler lesions mainly composed of foam cells.

Fibrofatty Plaque: More advanced, complex lesions with additional cellular and extracellular components, and a higher risk of causing clinical problems.

41
Q

ATHEROMATOUS NARROWING OF AN ARTERY IS LIKELY TO PRODUCE CRITICAL DISEASE IF

A
  • It is the only artery supplying an organ or tissue (i.e. There is no collateral circulation)
  • The artery diameter is small (e.g coronary artery versus common iliac artery)
  • Overall blood flow is reduced (i.e. cardiac failure)
42
Q

what is a proliferative atheroma

A

cells proliferate and extracellular matrix production causes plaque growth

43
Q

what is a complicated atheroma

A

plaque rupturing - thrombosis etc

First Year med - dundee (41 decks)

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