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Benjamin's Pathology > Atherosclerosis, thrombosis, embolism, ischaemia and infarction. > Flashcards

Atherosclerosis, thrombosis, embolism, ischaemia and infarction. Flashcards

1
Q

What is ischaemia

A

Loss of blood supply to a tissue because of a blocked blood vessel

Results in tissue coagulative necrosis

Mostly due to blockage of artery

Sometimes due to blockage of vein

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2
Q

What is infarction

A

Death of tissue (necrosis) secondary to ischaemia following abrupt interference with the blood supply.

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3
Q

What is arterial infarction (white)?

A

Follows sudden obstruction to the arterial supply to a tissue or organ.

Shpaed according to the territory of vessel supply

Pale with red hyperaemic border late stages scarring.

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4
Q

What is venous infarction (red)?

A

Follows sudden and persistent obstruction to venous drainage of an organ or tissue.

Congestion, increased pressure leading to rupture of small vessels, red / black (haemorrhagic).

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5
Q

What are the consequences of infarct?

A

Insufficient oxygen

Insufficient nutrients

Excess waste products

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6
Q

How does ischaemia affect the cells?

A

Cells like homeostasis

If there are slight changes the cells can adapt

If the changes are too great:

Cell injury

Cell (necrosis)

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7
Q

Is ischaemia acute or chronic?

A

Both

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8
Q

More details on infarct. Where, causes, acute or chronic?

A

Area of ischaemic necrosis within a tissue or organ

From acute arterial or venous occlusion

Most caused by arterial thrombosis or embolism

Acute

Heal by organization and fibrosis

Different cells types have differing vulnerabilities to ischaemia

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9
Q

Where do pale infarcts occur?

A

In tissues supplied by end arteries.

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10
Q

What is a haemorrhagic infarct?

A

Venous occlusion

Tissues with a dual or rich collateral blood supply

Reperfusion

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11
Q

What is thrombosis?

A

Normal haemostasis

Thrombus formation: Clotted mass of blood forming within the CVS during life: pathologic

Complex process involving the interaction of blood vessel walls, platelets and various plasma proteins.

Balance between factors that promote thrombogenesis and those that promote thrombolysis

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12
Q

What is the endothelial walls role in thrombus formation?

A

Barrier

Antithrombic: Molecules on surface
Molecules released into blood: Prostacyclin annd NO inhibit platelet aggregation

Can be prothrombotic

Secrete vasodilators and vasocontrictors

Normally resistant to leukocyte adhesion.

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13
Q

Platelets role in thrombus formation?

A

Flow in center of stream

Do not normally adhere to endothelium

Activated by collagen exposed following vessel injury

Release chemicals leading to activation and aggregation of more platelets

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14
Q

What do you need to know about clotting cascade?

A

Normal blood flows through steadily through endothelial lumen. At some stages there is an increase in clotting agents that cause blood to clot.

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15
Q

What is a thrombus?

A

Clotted mass of blood forming within the cardiovascular system during life.

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16
Q

What is virchows triad. Explain the components.

A

Alterations in blood flow - plays an important role in both venous and arterial thrombosis

Hypercoagulability - plays greater role in venous thrombosis than arterial thrombosis

Damage to endothelium - plays a greater role in arterial thrombosis

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17
Q

More details of virchows triad - Alterations in blood flow

A

Turbulence:

In aneurysms

Over atherosclerotic plaques

Around abnormal cardiac valves

Slowing:

restricted mobiligy e.g. elder, post surgical, unconscious

Cardiac failure

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18
Q

More details of virchows triad - Hypercoagulability of blood.

A

Post operative

Genetic

Certain malignancies

High oestrogens: peri-partum, some oral contraceptives

Injury to endothelium or endocardium:

Direct trauma

Inflammation

Atherosclerosis

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19
Q

What is an arterial thrombi?

A

Most caused by atherosclerosis (endothelial injury)

or aneurysms (turbulence)

20
Q

What is a cardiac thrombi?

A

Occurs in left ventricle:

Following infarction

in LV aneurysms

Left atrium in atrial fibrillation

21
Q

What is venous thrombi?

A

Slowing of blood flow and hypercoagulability are especially important

Deep leg and pelvic veins important sites

22
Q

What can happen to the thrombus?

A

Embolisation

Fibrinolysis (breakdown)

Organisation

Persistence e.g. thrombi in aortic aneurysms

23
Q

What are some complications of thrombosis?

A

Obstruction to blood flow (usually arterial)

Embolism (Both arterial and venous)

24
Q

Define Embolus

A

Intravascular solid, liquid or gaseous mass carried in the blood stream to some site remote from its origin or point of entrance into the blood stream

e.g. thrombo-emboli

athero-emboli

septic emboli

gaseous nitrogen bubbles in ‘the bends’

25
Q

What is Deep vein thrombosis (DVT)?

A

Thrombi form within deep veins of lower limbs and embolise to lungs

26
Q

What are risk factors for DVT? (hint virchows)

A

Stasis: immobilisation

Cardiac failure

Hypercoagulable states: Post - operative

High oestrogens: post partum, oral contraceptive pill

Some malignancies

Genetic abnormalities in coagulation

Obesity

Local endothelial injury: Trauma, sugical injury, smoking

27
Q

2 Common veins DVT formed in?

A

Popliteal vein

Femoral vein

28
Q

Give the route of a pulmonary embolism.

A

Beings in the leg (above the knee) travels to inferior vena cava to right side of heart to pulmonary artery to be lodged in lung.

29
Q

List some possible consequences of a pulmonary embolism.

A

Asymptomatic and small (60-80%) undergo organization and incorporated into vessel wall.

If medium sized may present with haemoptysis, cough and breathlessness

Pulmonary haemorrhage (due to dual blood supply)

Pulmonary infarct (RARE)

Pulmonary hypertension (Multiple emobli over time)

Sudden death when 60% of the pulmonary circulation is obstructed. Death by Cor Pulmonale right heart failure.

30
Q

Identify what is cause of death, and where.

A
31
Q

Brief definition of Atherosclerosis, % of deaths in developed world and where highest incidence occurs.

A

Extremely common

Underlying cause of most heart attacks and strokes

Chronic accumulation of lipids in intima and medium sized arteries.

Causes 50% of deaths in developed world

Highest incidence in:

North America

Europe

Australia, NZ

Russia

32
Q

What are the risk factors for Atherosclerosis?

A

Main:

Cigarette smoking

Hypertension

Diabetes mellitus

Dyslipidaemia

Increasing age

Male

Other:

Genetic

Obesity, lack of exercise, stress

33
Q

What is Atherosclerosis?

A

A disease caused by the formation of plaques on the walls of arteries

Plaques consist of:

Central lipid core (cholesterol)

Fibrous cap

Plaques narrow the vessel —-> ischaemia

Plaques + thrombus —-> infarction

plaques + acute plaque event —-> sudden increase in ischaemia

34
Q

List the seven steps of atherosclerosis in the response to injury hypothesis.

A
  1. Chronic endothelial injury yields an increase in permeability causing WBC adhesion and thrombotic potential
  2. Insudation of lipoproteins (LDLs) into the intima of vessel wall.
  3. Blood monocytes adhere and migrate into intima transforming into macrophages, engulfing lipid and becoming foam cells
  4. Platelets adhere
  5. Activated platelets, foam cells and vascular cells release cytokines and growth factors e.g platelet-derived growth factor causing migration of smooth muscle cells from media into intima
  6. The smooth muscle cells proliferate, exposing ECM and accumulation of collagen and proteoglycans
  7. More lipid accumulates - fibrofatty atheroma
35
Q

What is the morphology of atherosclerosis?

A

Fatty streaks:

Lipid filled foam cells in the intima

Flat lesions

Children from the age of 10 years

Not all will progress

36
Q

Named what the arrows are pointing to.

A
37
Q

Where does atherosclerosis occur?

A

Elastic Arteries:
Aorta, carotid arteries; iliac arteries

Large and medium muscular arteries:
Coronary arteries, popliteal arteris, cerebral arteries

38
Q

What happens to people with atherosclerosis?

A

Decreased blood flow through an artery:

Ischaemic heart disease

Peripheral vascular disease

Cerebrovascular disease

Predisposition to thrombosis on plaques:

Collagen fibres in plaque are exposed to the circulating blood initiating thrombus formation

Complete occlusion of small vessels

In large vessels pieces may break off and enter circulation (emoblism) or block an artery elsewhere.

Bleeding into a plaque: Sudden ballooning out

Rapid narrowing of lumen

Weakening of the vessel wall:

Aneurysm formation.

39
Q

Normal artery

A

Acute plaque event: Atherosclerosis and thrombus

40
Q

Examples of complications of atherosclerosis.

A
41
Q

Examples of complications of atherosclerosis.

A
42
Q

Examples of complications of atherosclerosis.

A
43
Q

What is an Aneurysm?

A

Abnormal focal dilatation in wall of vessel or a cardiac chamber

Arise due to weakening of media

44
Q

What causes an Aneurysm?

A

Atherosclerosis

Congenital weakness in the wall: probable predisposing factor of berry aneurysms around the circle of Willis

Systemic hypertension —-> microaneurysms in cerebral arterioles from arteriolar damage (hyaline arteriolosclerosis)

Infection in an artery wall (mycotic aneurysm)

Other

45
Q

What are some complications of an aneurysm?

A

Thrombosis

Rupture

46
Q
A

Benjamin's Pathology (10 decks)

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