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Phase 2a - ICS > Thrombosis, embolism, ischaemia and infarction > Flashcards

Thrombosis, embolism, ischaemia and infarction Flashcards

1
Q

Definition of thrombus

A

Solid mass of blood constituents formed within the vascular system in life.

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2
Q

Predisposing factors = Virchow’s triad

A

Abnormalities of the vessels wall (intima).

Abnormalities of blood flow.

Abnormalities of blood constituents.

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3
Q

Arterial thrombosis is most commonly superimposed by…

A

Atheroma

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4
Q

Venous thrombosis most commonly due to…

A

Stasis

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5
Q

What are the clinical consequences of thrombosis?

A

Arterial: tissue infarction distally

Venous: (oedema due to impaired venous drainage) and embolism.

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6
Q

Platelets

A

Angular in appearance, anucleated.
Derived from megakaryocytes.
Contain mitochondria and cytoskeletal elements.

Platelets also contain alpha granules and dense granules.

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7
Q

Alpha granules in platelets:

A

Stores substances involved in platelet adhesion to damaged vessel walls (fibrinogen, fibronectin, PDGF, antiheparin).

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8
Q

Dense granules in platelets:

A

Substances such as ADP which is needed for aggregation.

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9
Q

What activates platelets?

A

When they come into contact with collagen or with polymerising fibrin.

Platelets change shape and extend pseudopodia; granules release content and forms a mess until endothelial cells regenerate.

If this happens in an intact vessel= thrombus.

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10
Q

True or false?

All three of the predisposing factors have to happen for thrombosis to happen?

A

False.

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11
Q

Arterial thrombosis (early phase)

A

Atheromatous plaque= slightly raised fatty streak on the intimal surface of any artery.

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12
Q

Arterial thrombosis (later phase)

A

Plaque enlarges, raised enough to protrude into the lumen and cause a degree of turbulence.

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13
Q

What is the result of turbulence?

A

Loss of intimal cells - denuded plaque surface is now presented to blood cells.

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14
Q

Turbulence itself predisposes to:

A

Fibrin deposition and platelet clumping. The bare luminal surface will have collagen exposed and platelets will adhere to this.

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15
Q

What factors are altered in a smoker?

A

All three - changes in blood constituents are now present too.

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16
Q

Why is this process self-perpetuating?

A

Alpha granules release PDGFs - proliferation of arterial smooth muscle cells = important constituent of atheromatous plaque.

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17
Q

Layers of thrombus

A

Platelet layer is first.

Fibrin meshwork on top which entraps RBCs.

These bands are alternating.

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18
Q

How is turbulence affected in thrombus?

A

Greatest at the downstream side of arterial thrombi and on the upstream side of venous thrombi.
Therefor thrombi grow in the direction of blood flow = PROPAGATION.

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19
Q

Where do most venous thrombi begin?

A

BP is lower so thrombi is not due to atheroma.

Most being at valves.

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20
Q

What is the reason this (most common place for venous thrombi to occur)?

A

Valves naturally produce a degree of turbulence because they protrude into the vessel lumen.

They can also be damaged by trauma/stasis and occlusion.

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21
Q

What are two scenarios that allow thrombus formation?

A

If BP falls during surgery or following an infarct.

Venous return is highly dependent on muscle pumps - immobilisation enhances risks.

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22
Q

What are the clinical effects of arterial thrombosis?

A

Loss of pulses distal to the thrombus and signs of impaired blood supply: cold, pale, painful and tissue dies resulting in gangrene.

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23
Q

What are the clinical effects of venous thrombosis?

A

95% occurs in leg veins - area becomes tender, swollen and reddened. (blood is still carried to the site by arteries but cannot be taken away).
Tenderness is due to ischaemia in the vein wall.

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24
Q

Fate of thrombi?

A

1- Best case: resolves.

2- May become organised into a scars (due to the invasion of macrophages= clears it away) then fibroblasts which lay collagen; occasionally leaving a mural nodule or web that narrows the vessel.

3 - Intimal cells may proliferate - small capillaries grow into the thrombus: later fuse into large vessels = recanalisation.

4 - Causes death due to affecting vital centres.

5 - Fragments can break off - forming embolism.

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25
Q

Definition of an embolus:

A

A mass of material in the vascular system which able to become lodged within a vessels and block it.

26
Q

What are most emboli derived from?

A

Thrombi.

27
Q

Give examples of other type of embolic material:

A

Atheromatous plaque material.

Vegetation on heart valves (IE).

Fragments of tumour (causing metastasis).

Amniotic fluid, gas and fat as well.

28
Q

What is the most common embolism?

A

Pulmonary embolism as a result of DVT.

29
Q

PE

A

As a result of venous thrombosis: 95% in legs, small fraction in pelvic veins and minimal occur in the venous sinuses of the brain.

30
Q

Paradoxical embolism

A

If it arrives into the arterial side of circulation due a defect in septum etc…

31
Q

The effects of small PE

A

Depends on size.

Small one may be lysed and go unnoticed.

May accumulate and cause resp. deficiency. Over time, can lead to idiopathic pulmonary hypertension.

32
Q

The effects of larger PE

A

Can cause acute respiratory and cardiac problems.

Chest pain and SOB due to the effective loss of area supplied by the BV leading to an infarct. Recovery but loss of lung function.

33
Q

The effect of third class (largest emboli)

A

Sudden death. Often found at the bifurcation of one of the major pulmonary arteries= saddle embolus.

34
Q

Systemic embolism

A

Arise in arterial system.

Thrombi generally form in the heart or on atheromatous plaque.

35
Q

How do thrombi arise in the heart after MI?

A

May arise from cardiac muscle that died (MI). General endothelial lining is lost -> collagen is exposed = platelets come in contact.

Area of dead myocardium is adynamic= turbulence occurs.

36
Q

What other causes in the heart can lead to thrombus formation?

A

AFib.
Ineffective movement - blood stagnant - thrombus. When normal rhythm is restored it may break off.

37
Q

What happens to emboli formed in the heart?

A

Usually starts in LA/LV.

  1. Can be disloged in at the bifurcation of the aorta (saddle embolus). Cuts off circulation to lower limbs - need to act ASAP.
  2. Small ones can travel and dislodge in the periphery and cause gangrene of the digits.
  3. May travel to kidney or spleen where remain asymptomatic but cause death of distal tissue supplied by the artery = ischaemic scars.
38
Q

Example of a more dramatic consequence of an embolism?

A

SMA occlusion can cause death of a whole section of the bowel. Bowel depends upon the whole organ to be intact to function.

Can lead to perforation and peritonitis.

39
Q

Embolic atheroma

A

Fragments of atheromatous plaque causes ischaemic stroke of the toes.

40
Q

Platelet emboli

A

Emboli from early lesions may be composed solely of platelets. They are tiny therefore pose little risk; unless in brain.

TIA - risk for subsequent major stroke event.

41
Q

Infective embolism

A

Vegetations on the heart valve. Infective agents causes weakening of the wall.

42
Q

Fat embolism

A

Resulting from break in bone, trauma, severe burns - free fat in circulation.

43
Q

Gas embolism

A

Several forms are iatrogenic.

Surgical - 100mL of air is needed to be injected into a vein to cause death.

Opening of vessels to air poses a risk.

44
Q

Caisson disease

A

Divers
Rapid transfer from high/low pressure environments or vice versa.

  • High pressure increased volume of gas dissolves.
  • During rapid decompression these come out as bubbles: Nitrogen is a problem!
45
Q

Amniotic embolism

A

Increased pressure in uterus - fluid might be forced into maternal uterine veins. Can be lodged in the lungs -> respiratory problems.

46
Q

Tumour embolism

A

Small break offs that penetrate vessels. Not cause acute problems but major form of metastasis.

47
Q

Embolism of foreign matter

A

Talc is a common contaminant of fluids injected IV.

Granulomatous reaction in the organs in which they lodge - i.e. liver.

48
Q

Infarction

A

Ischaemic death of tissue. They elicit an inflammatory reaction.

49
Q

Reperfusion injury

A

Many effects take place during reperfusion. Much of the damage is oxygen dependent - so when blood flow is restored it reaches cells that have been disrupted (Ca out of the mitochondria) - free radicals.
Polymorphs and macrophages enter and bring their own intrinsic O2 free radicals.

50
Q

Gangrene

A

Whole areas of limb or gut have their arterial supply cut off = larger areas of mixed tissue die.

51
Q

What are the two types of gangrene?

A

Dry gangrene: tissue dies and becomes mummified and healing occurs above it. The dead area drops off. Sterile process - seen in diabetic foot.

Wet gangrene: bacterial infection - gangrene spread proximally and PT dies due to sepsis.

52
Q

What other mechanism can result in gangrene?

A

Torsion - gut may twist on a lax mesentery. Ovary testes may twist around their pedicle = leading to occlusion in venous return.
Organ swells - oedema further compresses the drainage.
Ischaemia -> infarction.

53
Q

Describe gas gangrene

A

Infection of ischaemic tissue by gas-producing anaerobic bacteria i.e. Clostridium perfringens.

54
Q

Capillary ischaemia

A

Frostbite damages capillaries - area supplied by them becomes ischaemic and dies.

55
Q

Trenched foot

A

Exposure to cold causes constriction followed by fixed dilation.

55
Q

What are other ways by which capillaries get blocked by?

A

Parasites
Abnormal cells Sickle cell disease
DIC.

56
Q

Example of end artery systems

A

Retinal artery - blockage leads to blindness.

57
Q

Low-inflow infarction

A

Impaired blod flow leads to infarction.
Watershed areas
Tissues perfused by portal vasculature
Tissues distal to pathological arterial stenoses
Metabolically active tissues

58
Q

Watershed areas

A

Tissue at the interface between the adjacent territories of two arteries is prone to infarction if there is an impairment. There is no collateral supply.

Splenic flexure - between SMA and IMA
Regions of cerebral hemispheres - around major cerebral arteries
Myocardium - between sub-endocardial myocardium

59
Q

Portal vasculature

A

Already passed through one set of capillaries. There is a drop in intravascular pressure in the first set of capillaries and a reduction in O2 saturation - makes the second set more susceptible to ischaemic injury.

60
Q

Arterial stenoses

A

Atheromatous narrowing or stenosis of arteries. In hypotensive individuals - distal tissue may become infarcted.

61
Q

Transient arterial spams can cause what?

A

Infarction in vulnerable tissues such as the brain and heart.

Phase 2a - ICS (43 decks)

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