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Cardiovascular system SA > Pathophysiology of atheroma > Flashcards

Pathophysiology of atheroma Flashcards

1
Q

What is the definition of an atheroma

A

Formation of Localised accumulation of lipid and fibrous tissue (plaques) in intima of arteries

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2
Q

What is arteriosclerosis

A

No atheromatous, thickening and hardening of the walls of the arteries, occurring typically in old age

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3
Q

What is the pathophysiology of arteriosclerosis

A

Smooth muscle hypertrophy, apparent reduplication of internal elastic laminae, intimal fibrosis → decrease in vessel diameter

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4
Q

When do the clinical effect of arteriosclerosis become more apparent

A

when CVS further stressed by haemorrhage, major surgery, infection, shock

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5
Q

What would you see in the development of early atheroma plague with no clinical significance

A

Fatty streaks - Smooth yellow patches in inner most coating of the arteries and Lipid-laden macrophages are present

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6
Q

What can be seen in full developed atheromatous plague

A

Central lipid core with fibrous tissue cap , covered by arterial endothelium

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7
Q

What is present in fibrous tissue cap

A

Collagen (produced by smooth muscle cells)

Inflammatory cells - macrophages, T-lymphocytes, mast cells (recruited from material endothelium)

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8
Q

What is present in the central lipid core in developed atheromatous plague

A

Central lipid core rich in cellular lipids

and debris derived from macrophages that died in the plague

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9
Q

What is the structure of the central lipid core

A

Soft,
highly thrombogenic,
often rim of “foamy” macrophages
(due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor)

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10
Q

What occurs in late plague development that leads to atherosclerosis

A

Dystrophic calcification extensive

Atheroma from arterial branching points as plague are merge together and cover large areas

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11
Q

What is the investigations for atheroma development - what can be seen

A

angiograms/CT

calcification of coronary arteries

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12
Q

What is the out come of Haemorrhage of plague

A

The plague ruptures, and travels though the blood vessels then causes a blockage - thrombosis

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13
Q

What is the most important risk factor in atheroma and why

A

Hypercholesterolaemia

- Causes plaque formation and growth in absence of other known risk factors

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14
Q

What is the signs of major Hypercholesterolaemia

A

Corneal arcus (premature) - cholesterol deposit in the iris

Tendon xanthomata - yellow patches caused by deposition of lipid on the knuckles and Achilles

Xanthelasmata - sharply demarcated yellowish deposit of fat underneath the skin, usually on or around the eyelids

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15
Q

What is the biochemistry of Hypercholesterolaemia

A

LDL, HDL, total cholesterol, triglycerides

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16
Q

What clinical history can show signs of Hypercholesterolaemia

A

Risk factors

Family history of MI/ atheroma

17
Q

What is the major risk factors for atheroma

A 
Smoking
Hypertension
Diabetes mellitus
Male
Elderly
Accelerate process of plaque formation driven by lipids
Hypercholesterolaemia
Obesity
18
Q

What is the process of atheromatous plaque development

A
  1. injury to endothelial lining of artery
  2. chronic inflammatory and healing response of vascular wall to agent causing injury
  3. Chronic exposure of arterial wall to these processes results in the formation of atheromatous plaques
19
Q

In more detail what is the pathogenesis of atheromatous plaques

A

Damaged Arterial endothelium leads to an:

inflammatory response in a process of tissue repair

  • Growth factors, cause proliferation of smooth muscle, synthesis more collagen, elastin and mucopolysaccharide as well as platelets, and macrophages
  • Platelet adhesion and smooth muscle proliferation results int the further recruitment of white blood cells and lipids
  • Monocyte adhesion to artery wall and transforms into foamy macrophage
  • T cell recruitment
  • Accumulation of LDL to the vessel wall due to extracellular (high permeability because of damage) and also the foamy macrophages

This chronic process resulting in thickened artery wall and proliferated intimal of smooth muscle therefore creating an atheromatous plaque

20
Q

What is the possible aetiologies of endothelial injury that leads on to atheroma

A

haemodynamic disturbances which result in a turbulent flow of blood

Hypercholesterolaemia

Endothelial loss -

21
Q

What is the characteristics of injured endothelia lining

A

Enhanced expression of cell adhesion molecules (ICAM-1, E-selectin)
High permeability for LDL
Increased thrombogenicity

Trigger inflammatory cells and lipids which deposit In the inner material layer and cause plaques

22
Q

What is the clinical manifestations of atheroma plaque formation

A

Progressive lumen narrowing due to high grade plaque stenosis

Embolisation of the distal arterial bed - blood clotting

23
Q

When atheroma is located in the coronary arteries, the clinical manifestation of atheromatous plaques results in what conditions

A

Myocardial Ischaemia
stable angina
Unstable angina with sever stenosis
Myocardial infarction

24
Q

What can, femoral and popliteal artery stenosis result in

A

intermittent claudication (peripheral arterial disease)

Cramping in leg induced by exercise

25
Q

Why is the rupture of the plaque a major complication

A

Leads on to an acute event as rupture exposes highly thrombogenic plaque contents to blood stream,

This activities coagulation of cascade and thrombotic occlusion in very short time - closing blood vessels

Acute atherothrombotic occlusion can then cause irreversible ischaemia and infarction

26
Q

Where is examples of places where infarction can occur as a result of ruptured in the plaque

A
  1. stroke (carotid, cerebral artery)
  2. Myocardial infarction (coronary artery)
  3. lower limb gangrene (ileal, femoral, popliteal artery)
27
Q

Due to the small foci of necrosis in the heart what can embolisation cause

A

life-threatening arrhythmias

28
Q

What happens in ruptured atheromatous abdominal aortic aneurysm and what is the characteristics

A

Excessive swelling (aneurysm) present and the media beneath atheromatous plaques becomes gradually weakened causing gradual dilatation of vessel, this can then cause a Sudden rupture → massive retroperitoneal haemorrhage

Slow but progressive, seen in elderly, often asymptomatic

29
Q

what size of aneurysm gives you a higher risk of rupturing

A

> 5cm

30
Q

What is the Preventative and therapeutic approaches to embolism

A 
Stop smoking
Control blood pressure
Weight-loss
Regular exercise
Dietary modifications
31
Q

What is the secondary prevention

A

Cholesterol lowering drugs, aspirin (inhibits platelet aggregation to decrease risk of thrombosis on established atheromatous plaques)

32
Q

What is a final approach to embolism

A

surgery

33
Q

What is an atheroma in the aorta cause

A

aneurysm

Cardiovascular system SA (43 decks)

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