atheroscelorosis Flashcards

1
Q

vascular endothelial cells:
* Serve as —
* Maintain — interface - — , —
* Modulate — and — – —
* Regulate — and — reactions- —- , – factors
* Alter– and – permeability
* Transcytosis — in — wall → —
* Lipoprotein lipase
* RA System-ACE and ACE2 enzymes (Covid-19)

A

semipermeable membrane
blood tissue
anti platelet and anticoagulant
vascular tone and blood flow
nitric oxide NO
immune and inflammatory
cytokines and growth factors
flow and leakage
lipoproteins
arterial
atheroma

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2
Q
  • Atherosclerosis and atheroma are used interchangeably
  • Definition - ‘ — of the – ’, a —
    disease in which fibro fatty deposits accumulate in the — layer of — and — sized — - progressive accumulation of inflammatory, immune, smooth muscle cells, lipids and connective tissue in intima
  • Deposition of atheroma occurs on — or— (not — )
  • Definition:
     Atheroma is a fibrolipid plaque-atherosclerotic or atheromatous plaque - raised lesion protruding into the lumen, — core, — cap
A

hardening
arteries
complex chronic
intima
elastic and medium sied artries
larger elastic and muscular artries
not veins
cholesterol lipid
fibrous

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3
Q

why’s it important to understand consequences of the atherocolesrosis:
1. — – cell — due to – blood flow
2. —
3. Source for — to break off
4. Vessel wall —/— (— )
other consequences are:
 Myocardial infarction/ischaemic heart disease
 Cerebral infarction (stroke)
 Peripheral vascular disease
 Aortic aneurysms
 Mesenteric occlusion – ischaemic bowel
 Ischaemia/Infarction can occur from plaque occluding
artery or from an embolus from the plaque

A

infraction
necrosis
low
ischaemia
emboli
dilation/repture
aneurysm

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4
Q

atherosclerosis pathogenesis:
* — injury → — potential
* Accumulation of — (LDL with — cholesterol) in vessel wall
* Monocytes and leukocytes –> — of blood vessel → transform to —
* Factors from platelets and macrophages cause — of smooth muscle cells from – of artery to—
* Smooth muscle cells –> — accumulation giving a — i.e. —
more causes :
- Endothelial dysfunction
(e.g., increased — , leukocyte — )
Monocyte — and — .
- Smooth muscle emigration from –
to – . — activation
- Macrophages and smooth muscle cells engulf –
- smooth muscle — and collagen , extracellular lipid

A

chronic endothelial injury ( this injury can be caused by * Hyperlipidemia
* Hypertension
* Smoking
* Homocysteine
* Hemodynamic factors
* Toxins
* Viruses)
thrombotic
lipoprotein
high
intima
macrophages
migration
media
intima
collagen
fibrolipid plaque
atheroma
permeability
adhesion
adhesion and emigration
media to intima
macrophages
lipid
proliferation

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5
Q

stable/unstable plaque:
* Stable plaque - — fibrous cap, —
* Unstable plaque - – fibrous cap, —
* Unstable plaques – likely to get complications – – into plaque, or – of surface with –

A

thick
calcification
thin
inflammation
more
haemorrhage
erosion
thrombosis

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6
Q

atherosclerosis consequence:
—- , — in plaque (causing — size of plaque), — , —
* Complete occlusion of artery ( — into plaque, — ) —> —
* Partial occlusion of artery– > — e.g.—
* Thrombus formation:
 — size of plaque –> —occlusion
 Embolisation of:
- —
- –
- —
* — formation
* — e.g. Aorta
* —

A

occlusion
thrombus
increase
embolus
aneruysm
haemorrhage
thrombosis
infraction
ischaemia
angina
increase
increase
thrombus
cholestrol
platelt
aneurysm
dissection
calcification

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7
Q

risk factors of atheroma:
major :
1- nonmodifiable are — , — , —
2- potentially controllable ; ——
3- lesser/uncertain/nonquantified atherscolrosis: — ,—- , —-

A

age gender and genetic abnormalities
controllable:
- hyperlipidemia
- hypertension
- ciggerate smoking
- diabetes
lesser/uncertain:
- postmenipasual oestrogen deficiency
- stress type A personality
- obesity
- physical inactivity
-hardened tras unsaturated fat intake
- alcohol
chlamydophilia pneumonia

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8
Q

risk factors ATHEROMA/ATHEROSCLEROSIS:
* Age:
 Death rates from IHD rise with each decade
 Between ages – and –the incidence of — increases — fold
* Gender
 Other factors being equal, — are more prone to atherosclerosis
 After — , the incidence of atherosclerosis-related diseases increases in — probably owing to a
decrease in natural — levels
* Genetics
 Familial predisposition to atherosclerosis is most likely —
* — , failure to clearance of low density lipoproteins
—-density lipoprotein (LDL) delivers cholesterol to peripheral tissues
—-density lipoprotein (HDL) mobilizes cholesterol, transporting it to the liver for excretion in the bile
 High dietary intake of cholesterol and saturated fats,
(egg yolk & animal fats) raises the plasma cholesterol level

A

40-60
myocardial infraction
5
males
menopause
women
osterogen
polygenic
hyperlipidemia
low
high

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9
Q

more risk factors :
* — around branches
 Men between ages 45 and 62 whose blood pressure exceeds 169/95 mm Hg have a more than fivefold
greater risk of IHD than those with blood pressures of 140/90 mm Hg or lower. Why?
 Both systolic and diastolic levels are important
* Cigarette smoking
 Smoking one or more packs of cigarettes per day for
several years increases the death rate from IHD by up to 200%
* —
 Induces hypercholesterolemia and a markedly
increased predisposition to atherosclerosis
 Incidence of — is twice as high in
diabetics as in non-diabetics
—-fold increased risk of atherosclerosis-induced
gangrene of the lower extremities
other risk factors:
* Lack exercise
* Elevated CRP
* Homocysteinaemia
* Obesity
* Gout
* Drugs COX-2 inhibitors
* Rheumatoid arthritis, SLE

A

hypertension
diebetes mellitus
myocardial infraction
100

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10
Q

distribution of atheroma:
* Abdominal aorta, esp. around ostia of its major
branches. Why around ostia?
* Coronary arteries
* Popliteal arteries
* Descending thoracic aorta
* Internal carotid and arteries of Circle of Willis
* Often widespread within an individual
* “Atheropath”
summary:
- — (fibro lipid plaque) commonest arterial cause of — and —
* Leading cause of –
* Related to — damage
* Must know pathogenesis and risk factors
* Major cause of —
* Often complicated by — formation on plaque +-subsequent systemic embolization (platelets, cholesterol,
thrombus, plaque)
* May cause — and –

A

atherosclerosis
ischaemia and infraction
death
endothelial
ishcemia/infraction
thrombus
aneurysm and rupture

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11
Q
  • Atheroma
     —
  • Atherosclerosis
     Atheroma of — with –/—
  • Arteriolosclerosis
     Narrowing of — due to —
A

fibrolipid plaque
larger artries
fribsois/narrowing
small arterioles
hypertension

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12
Q

ARTERIOLOSCLEROSIS - SUMMARY
* Narrowing of — - fibromuscular intimal — ,elastin and connective tissue
* Due to —
* Narrows — (intimal hyperplasia) arteriole
* Common in — - hyaline arteriolosclerosis
* Common in —
* Malignant — - fibrinoid necrosis followed by smooth muscle cell — “— skin” appearance

A

arterioles
thickening
hypertension
lumen
diabetic
kidney
hypertension
proliferation
onion skin

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