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Pathology > Atheroma, Thrombosis, Embolism and Infarction > Flashcards

Atheroma, Thrombosis, Embolism and Infarction Flashcards

1
Q

What is ischaemia?

A

Result of impaired vascular perfusion depriving the affected tissue of nutrients, inc. oxygen

Can be REVERSIBLE depending on speed of onset, local demand and duration - amongst other factors

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2
Q

What is infarction?

A

ISCHAEMIC NECROSIS of a tissue/organ secondary to occlusion/reduction of arterial supply/venous drainage

Recovery depends on tissue’s regenerative ability, e.g: scarring or, in liver, regeneration may occur

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3
Q

Haemostasis regulates?

A

Maintain blood in a fluid, clot free state in normal vessels

Induce rapid, localised haemostatic plug at site of vascular injury

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4
Q

What is thrombosis?

A

Pathological corruption of haemostasis - forms a solid/semi-solid mass from blood constituents, WITHIN the VASCULAR system, during LIFE

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5
Q

Virchow’s Triad?

A

Changes in VESSEL WALLS (endothelial injury)

Changes in BLOOD CONSTITUENTS (hypercoagulability)

Changes in BLOOD FLOW

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6
Q

Functions of platelets?

A

Close small breaches in vessel walls

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7
Q

Haemostatic contents of platelets?

A

α-granules: adhesion components (promote clotting), e.g: fibrinogen, fibronectin, Platelet-Derived Growth Factor - PDGF, anti-heparin, etc)

Dense granules: contents cause platelet aggregation, e.g: ADP

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8
Q

Functions of endothelial cells?

A

Maintains a permeability barrier

Elaborates anti-coagulant, anti-thrombotic, fibrinolytic regulators, e.g: heparin-like molecules, plasminogen activator

Elaborates pro-thombotic molecules, e.g: vWF, tissue factor (TF), plasminogen activator inhibitor

Produces EC matrix

Modulates blood flow and vascular activity, using vasoconstrictors and dilators

Regulates inflammation and immunity by altering, e.g: IL-1, IL-6, chemokines and adhesion molecule expression

Regulates cell growth, using growth stimulators, e.g: PDGF, and growth inhibitors, e.g: heparin

Role in LDL oxidation

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9
Q

Causes of endothelial injury?

A 
Hyperlipidaemia
Hypertension
Smoking
Toxins
Vasculitis
Viruses
Immune reactions
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10
Q

Effects of stasis and turbulence on platelets?

A

Disrupt laminar blood flow so:
Platelets come into contact with endothelium
Activated clotting factors are not diluted by normal, rapid flow
Inflow of anti-coagulant factors is slowed, allowing thrombi to persist
Activation of endothelial cells is promoted

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11
Q

Situations where turbulence and stasis commonly cause thrombosis?

A

Impairing venous drainage of the lower limbs, predisposing to DVT
Non-contractile areas of myocardium following MI
Aneurysms
AF
Mitral valve stenosis and left atrial dilation (poor flow)

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12
Q

What is hypercoagulability?

A

Any alteration in the coagulation pathway that predisposes to thrombosis

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13
Q

Two categories of diseases causing hypercoagulability?

A

Acquired genetic

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14
Q

Acquired hypercoagulable states that are high risk?

A 
MI
Immobilisation
Tissue damage
Cancer
Prosthetic heart valves 
DIC (disseminated intravasculat coagulation - proteins controlling blood clotting become overly active)
Heparin-induced thrombocytopaenia
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15
Q

Acquired hypercoagulable states that are lower risk?

A 
AF
Oral contraceptive use
Late pregnancy and post-partum
Sickle cell anaemia
Smoking
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16
Q

Genetic hypercoagulable states?

A

Factor V mutations
Defects in anti-coagulant pathways -antithrombin III deficienct
Defects in fibrinolysis

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17
Q

Morphology of arterial thrombi?

A

Often occlude LUMEN, in common sites like coronary, cerebral and femoral arteries
Associated with ATHEROMA and have a firm attachment to the wall

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18
Q

Appearance of arterial thrombi?

A

Show LINES OF ZAHN - laminated due to alternating pale (platelet and fibrin) and dark (rbc/wbc) bands

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19
Q

Morphology of venous thrombi?

A

Most occlude VEIN LUMEN, often STASIS related

Evokes inflammation - thrombophlebitis

20
Q

Most important and common venous thrombi?

A

DVT of calf - most important
Less common are popliteal, femoral, iliac and pelvic thrombi

Large vessel thrombi are prone to embolise

21
Q

Fates of thrombi?

A

Propagation proximally, small to large vessel

Embolisation

Resolution (fibrinolysis)

Organisation (granulation tissue, recanalisation)

DIC

22
Q

Most common emboli?

A

Thromboemboli

23
Q

Types of embolism?

A

Thromboembolism

Fat embolism

Marrow embolism

Air embolism

Septic embolism

Amniotic fluid embolism

Tumour embolism

24
Q

Difference between red and white infarct?

A

White infarct (lack of rbs accumulation) - usually in organs with only one circulation

Red infarct - cause by haemorrhage, usually in organs with 2 circulations, e.g: lungs

25
Q

Rare occasions where venous emboli cause infarcts in peripheral arterial circulation?

A

Venous emboli do NOT cause infarcts in peripheral arterial circulation unless:
Atrial/ventricular septal defect
Paradoxical embolus
…rare

26
Q

Causes of fat embolism?

A

Major soft tissue trauma

Major bone fractures:
Fatty marrow enters venules, most globules arrest in lungs to cause dyspnoea
Some reach peripheral circulation to cause skin rashes, CNS confusion

Potentially fatal

27
Q

Causes of gas/air embolism?

A

Barotrauma - in divers
During delivery or abortion
Iatrogenic

Frothy bubbles occlude major vessels - at least 100ml gas required to enter venous circulation

28
Q

Describe amniotic fluid embolism

A

Post-partum (high mortality)

Amniotic fluid (prostaglandin-rish) and debris enters torn veins and embolises to lungs - causes marked oedema, often DIC (leads to heamorrhage)

29
Q

Origins of systemic emboli?

A

Most from thrombi within heart chambers/on valves, e.g:
In AF
Mural thrombus, post-MI (formation of a thrombus in contact with the endocardial lining of a cardiac chamber, or a large blood vessel)
Aneurysm

30
Q

Destinations of systemic emboli?

A

Legs - gangrene
Brain - infarct/CVA
Visceral - GI, kidney, spleen
Arms - gangrene

31
Q

What does arteriosclerosis mean?

A

Hardening of the arteries

32
Q

Three disease patterns under arteriosclerosis?

A

Atherosclerosis - disease of intima
Monckeberg Medial Calcific Sclerosis - calcification of medium-sized arteries, in those > 50 years of age
Arteriolosclerosis - disease of small arteries and arterioles (hyaline and hyperplastic types); assoc. with diabetes mellitus and hypertension

33
Q

Main targets of atherosclerosis?

A

Aorta - aneurysm
Coronary arteries - MI, chronic myocardial ischaemia (anginal pain/cardiac failure)
Cerebral arteries

34
Q

Genetic polymorphisms associated with atherosclerosis?

A 
Lipoprotein Lp(a) (apo-B100+apo-A)
Inflammatory Markers (CRP)
Fibrinolytic Markers (PAI-1)
35
Q

Which infections can contribute atherosclerosis?

A

Inflammation arises from:

Chlamydia

36
Q

Constituents of atherosclerotic plaque?

A

Raised focal lesion of intima
Lipid core of cholesterol, esters and lipoproteins
Fibrous cap

37
Q

How is the artery wall structure medial to the plaque degraded?

A

Weakening of arterial wall

Aneurysm development

38
Q

Key stages in atherosclerosis?

A 
Chronic endothelial injury
Endothelial dysfunction
Macrophages activation 
Lipoprotein oxidation
Foam cell formation, fatty streak
Plaqure formation and growth
39
Q

What does endothelial dysfunction involve?

A

Increased permeability
Monocyte adhesion
Monocyte emigration
Platelet adhesion

40
Q

Roles of activated macrophages in atherosclerosis?

A

Generation of reactive oxygen species leading to oxidation of lipoproteins

Production of cytokines which promote chemotaxis and adhesion of further leucocytes

Production of growth factors contributing to smooth muscle proliferation

41
Q

Why are lipoproteins oxidised in atherosclerosis (functions)?

A

More easily ingested by macrophages
Act as chemotactic factors for monocytes
Increase monocyte adhesion
Inhibit macrophage motility, Trapping macrophages within the plaque
Stimulate cytokine and growth factor release
Directly damage endothelial and smooth muscle cells
Induce an antibody response

42
Q

What does foam cells and fatty streak formation involves?

A

Macrophages and smooth muscle cells engulf lipid to become foam cells

43
Q

How can fatty streak be reversed?

A

At this stage, which is visible as a fatty streak on the wall of the artery, the process may still be reversible if the level of blood cholesterol is reduced.

44
Q

What does plaque formation and growth involve?

A

When hypercholesterolaemia persists, smooth muscle proliferation and collagen deposition convert the fatty streak into a mature fibrofatty atheroma

45
Q

Common areas of atherosclerosis?

A

Thoracic aorta - mainly arch branch points
Carotid artery bifurcations - esp. internal carotic
Circle of Willis
Coronary arteries - part. ostia and LAD

46
Q

What happens after atherosclerosis?

A

Resolution: reabsorb lipid at fatty streak stage (pre-extracellular lipid) - maybe using high-dose statins

Repair: stabilisation by fibrosis (scarring), thick cap or total fibrosis; omega-3 fish oils promote this. Also, calcification

47
Q

Complications of atherosclerosis?

A

Ulceration of atheromatous plaque and THROMBOSIS

Haemorrhage into plaque, causing rupture and embolism of plaque contents; leads to critical stenosis or aneurysm formation

Pathology (25 decks)

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