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
Q

Pathophysiology of rheumatic fever

A
  • 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
Q

What is an Aschoff body

A
  • a focus of chronic inflammatory cells, necrosis and activated macrophages
  • seen in the heart in acute rheumatic fever
27
Q

Vegatations of heart disease may lead to what?

A

-can be infective/thrombotic nodules which develop in valave leaflets impairing the normal valve mobility. Can also embolise

28
Q

Effect of pancarditis

A
  • 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
Q

What is rheumatic HD

A

-main cause of mitrals tenosis and can cause mitral regurigation

30
Q

add to valvular HD lecture

A

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