Pathophysiology of Thrombosis and embolism Flashcards

1
Q

What is meant by laminar blood flow?

A

-Normal blood flow of blood that moves parallel and

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2
Q

Types of abnormal blood flow

A

Stasis
-stagnation of flow

Turbulence
-forceful, unpredictable flow

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3
Q

State conditions that may affect blood flow

A
  • thromb embolism
  • atheroma
  • hyperviscosity, spasm
  • external compression
  • vasculitis
  • vascular steal
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4
Q

State Virchow’s triad

A

Factors causing thrombosis

  • changes in BV wall
  • changes in blood constituents
  • changes in pattern of blood flow
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5
Q

Describe the pathogenesis of thrombosis

A
  • Endothelial injury
  • stasis OR turbulent blood flow
  • hypercoagulability of blood

(Virchows triad)

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6
Q

Describe pathogenesis of thrombosis in an athermatous coronary artery

A

-turbulent blood flow ( fibrin deposition, platelet clumping)
-loss of intimal cells, rupture occurs an collagen is exposed + platelets will adhere
-fibrin meshwork, RBCs will be trapped + alternating bands ( linez of zahn) formed?
-

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7
Q

Examples of changes in vessel wall

A

atheromatous coroanry artery

-hypercholesterolaemia

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8
Q

Changes in blood constituents examples

A
  • hypervisccity

- post traumatic hypercoaguability

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9
Q

Changes in blood flow examples

A
  • stasis ‘’ ecconomy class syndrome ‘’ post op

- turbulence; atheramatous plaque, aortic aneurysm

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10
Q

What is an embolism?

A

-movement of abnormal material in bloodstream and may block vessels lumen

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11
Q

What is an embolus?

A

-detached intravascular solid/liquid/gaseous mass

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12
Q

Sources of systemic/arterial thromboembolus

A
  • mural thrombus ; adheres the vessel wall ( associated with MI/ left atrial dilation + atrifal fibrilation)
  • aortic aneurtysms
  • atheromatous plaques
  • valvular vegetations ( venous thrombi - paradocical emboli)
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13
Q

Systemic thromboembolus

A
  • mainly travels to lower limbs, brain + other organs

- can lead to ischaemia, calibre of occluded vessel, collateral circulation + infarction

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14
Q

Types of embolus

A
  • systemic/arterial thromboembolus
  • venous thromboembolus
  • fat
  • gas
  • air
  • tumour
  • trophoblast
  • septic material
  • amniotic fluid
  • bone marrow
  • foreign bodies
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15
Q

Venous thromboembolus

A
  • originates from deep venous thromboses ( lower limbs)
  • travels to pulmonary arterial circulation
  • can cause occlusion of main pulmonary artery, bifurcation( saddle embolus), smaller arteries
  • most common form of thromboemmbolic disease
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16
Q

Consequences of pulmonary thromboembolisk

A
  • silent, pulmonary hamorrhage/infaction, right heart failure, sudden death
  • if multiple over time > pulmonary hypertension and RVF
17
Q

Risk factors for DVT and pulmonary thromboembolism

A

-cardiac failure, severe trauma/burns, post op/post partum, nephrotic sundrome, disseminated malignancy, oral contraceptive, age, bed rest/immbolisation, obesity, PMH

18
Q

Surgical patients at risk of DVT/pulmonary thromboembolism

A

recieve prophylacis : TEDS, s/c heparin

19
Q

When may a fat embolis occur?

A
  • after major fracture

- sundrome of fat embolism: brain, kidneys and skin is affected

20
Q

When may a gas embolus occur?

A
  • if you have decompression sickness; N2 forms as bubbles which lodges in brain capillaries
  • air embolus due to head, neck wounds, surgery + CV lines
21
Q

Examples of trophoblast and septic material in association with embolus

A

Trophoblast - pregnant women > lungs

Septic material - infective endocarditis

22
Q

Why may amniotic fluid, bone marrow + foregin bodies be an embolus?

A

amniotic fluid - cause of collapse and can cause death in child birth

Bone marrow - fractures; CPR

Forwign bodies - intravascular cannulae tipes, sutures

23
Q

What is rheumatic fever?

A
  • disease of disordered immunity
  • inflammatory changes in heart,joints + has neurological symptoms
  • affects children 5-15 years, boys>girls
24
Q

Presentation of rheumatic fever

A
  • polyarthritiss of large joints + skin rashes + dever

- pancarditis ( inflammation of endocardium, myocardium AND pericardium) and in acute; heart murmurs will be common

25
Pathophysiology of rheumatic fever
- Beta group A haemolytic strep infection - strong antibody reaction to strep which may cross react with unknown antigens in connective tissues - damage to heart tissue may be caused by combination of antibody mediated and T cell mediated reactions
26
What is an Aschoff body
- a focus of chronic inflammatory cells, necrosis and activated macrophages - seen in the heart in acute rheumatic fever
27
Vegatations of heart disease may lead to what?
-can be infective/thrombotic nodules which develop in valave leaflets impairing the normal valve mobility. Can also embolise
28
Effect of pancarditis
- acute can > chronic rheumatic heart disease which affects valves - inflammation of endocardium + left sided valves results in fibrinoid necrosis of the valve/cusps/chordae tendinae which ( along with line of closure ) forms small vegetations -fibrotic valvvular disease ( mainly valve ) will involve leaflet thickening, commissural fusion + shortening, thicening + fusion of chordae tendinae
29
What is rheumatic HD
-main cause of mitrals tenosis and can cause mitral regurigation
30
add to valvular HD lecture
Can cause mitral regurgitation but now most commonly due to ischaemic heart disease Now only rarely causes aortic stenosis – most due to calcific aortic valve disease Potentially still causes aortic regurgitation/incompetence Tricuspid valve involvement infrequent; pulmonary valve involvement rare