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Mechanism of Disease > Atheroma, Thrombosis & Embolism > Flashcards

Atheroma, Thrombosis & Embolism Flashcards

1
Q

Define atherosclerosis

A
  • Degeneration of arterial walls characterised by fibrosis, lipid deposition, inflammation limiting blood circulation & predisposes to thrombosis
  • Primary pathological abnormality of arterial thrombosis
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2
Q

Which blood vessels are commonly affected by atherosclerosis?

A
  • Bifurcations (turbulent flow)
  • Abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Carotid vessels
  • Circle of Willis
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3
Q

What are risk factors for atherosclerosis?

A 
Non-modifiable= Age, male, FH, genetic
Modifiable= Smoking, diabetes, hypertension, hyperlipidaemia/cholestrolaemia, CRP, physical inactivity
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4
Q

What are the causes and the first step in atherosclerosis?

A
  • Haemodynamic injury, chemicals, irradiation, immune complex deposition
  • First step= endothelial injury
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5
Q

What is the pathophysiology of atherosclerosis?

A
  • Due to chronic injury & repair of endothelium
  • Prescence of hyperlipidaemia lipid will accumulate in inner vessel (intima)
  • Monocytes migrate into intima & ingest lipid = foam cells
  • Stage known as fatty streak
  • Foam cells secrete chemokines attracting more monocytes, lymphocytes & s.muscle cells
  • S.muscle proliferate & secrete connective tissue
  • Atherosclerotic plaque formed from fat, extracellular material, leukocytes & S.muscle
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6
Q

What are the components of an atheromatous plaque?

A

-Fibrous cap (S.muscle, marophages, foam cells, lymphocytes, collagen, elastin)
-Necrotic centre (Cell debris, cholesterol crystals, Ca & foam cells)
Adhered to media

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7
Q

What sequences can follow atherosclerosis?

A
  • Occlusion
  • Weakening of vessel walls (aneurysm formation)
  • Erosion (thrombosis formation)
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8
Q

What is thrombosis and how is this different to a clot?

A
  • Solidification of blood contents formed in the vessel during life
  • Different in pathogenesis & morphology
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9
Q

How is a clot different from a thrombus?

A

C= Stagnant blood, enzymatic process, elastic, adopts shape of vessel

T=Within body during life, firm, dependant on platelets

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10
Q

What are platelets?

A

-Fragments of megakaryocytes in bone marrow
-Circulate in bloodstream
Bind to collagen exposed by endothelial damage & activate
-Secrete: a granules (PDGF, fibronectin,fibrinogen) dense granules (chemotactic chemicals)

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11
Q

What are the components of Virchow’s triad?

A
  • For platelet adhesion & thrombus formation
  • Change in intimal surface of the vessel (damage)
  • Blood constituents (hypercoagulability)
  • Pattern of blood flow (stasis)
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12
Q

Describe cardiac thrombi

A
  • Known as mural thrombi
  • Occur over areas of endomyocardial injury (MI, myocarditis)
  • Can occur with arrhythmias & cardiomyopathy
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13
Q

What are possible consequences of thrombosis?

A
  • Occlusion of vessel
  • Resolution
  • Incorporation into vessel wall
  • Recanalisation
  • Embolisation
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14
Q

What is an embolus?

A

A mass of material in the vascular system able to lodge in a vessel and block it

  • may be endo/exogenous
  • May be solid/liquid/gas
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15
Q

What is the most common type of emboli?

A

Pulmonary emboli
common cause of hospital morbidity& mortality
Risk factors=genetic & acquired

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16
Q

What are risk factors for an embolism?

A
  • Acquired= Immobility, malignancy, heart failure, obesity, pregnancy, oestrogens, renal disease, smokers
  • Genetic= thrombotic disorders (protein S deficiency, FV leiden)
17
Q

What are the clinical effects of a pulmonary (or central) emboli?

A
  • Small= asymptomatic multiple may result in pulmonary hypertension
  • Medium= Acute respiratory & cardiac failure (V/Q mismatch, RV strain)
  • Large= Death ‘saddle emboli’
18
Q

What are causes of a systemic emboli?

A
  • Arise within the heart- MI/AF

- Arise within arterial circulation-atheroma

19
Q

What is an infective emboli?

A
  • Usually from vegetations on infected heart valves
  • Effects compunded by infective nature
  • May lead to mycotic aneurysm formation
20
Q

What is a tumour emboli?

A
  • Bits break off as tumour penetrates vessel
  • Not usually cause of immediate physical problems
  • Major route of dissemination
21
Q

What is a gas emboli?

A
  • Air (obstetric procedures/ chest wall injury) >100ml to cause clinical effects
  • Nitrogen (decompression sickness, divers, tunnel workers), nitrogen bubbles enter bones, joints, lungs
22
Q

What is an amniotic fluid emboli?

A
  • Inc uterine pressure during labour may force amniotic fluid into maternal uterine veins
  • Lodge in lungs causing respiratory distress
  • Can shed skin cells histologically
23
Q

What is a fat embolism?

A
  • Microscopic fat emboli in 80% patients with significant trauma at post mortem
  • Sudden onset of respiratory distress
  • Fatal in 15%
24
Q

What is a foreign body emboli?

A
  • Particles injected intravenously

- Leads to a granulomatous reaction

25
Q

What is the pathogenesis of a venous thrombus?

A
  • Venous stasis
  • Hypercoagulable states
  • Thrombi predominantly composed of fibrin lesser role of platelet accumulation & aggregation
26
Q

What are risk factorsfor VTE?

A

-Active cancer or cancer treatment
-Over 60
-Critical care
-Dehydration
-Major trauma
-Surgery
-Immobility
-Obesity
-Varicose veins with phlebitis
-Contraceptive pill
Hormone replacement therapy
-Personal/1st degree family history of VTE

27
Q

What is thrombophilia?

A

-Familial or acquired disorders of the haemostatic mechanism which predispose to thrombosis
OR
-Patients who develop VTE spontaeously, at an early age, recurrently, disproportionate severity

28
Q

Name some heritable thrombophilias

A

-Antithrombin deficiency
-Protein C & S deficiencies
-Activated protein C resistance/FV leiden
Prothrombin 20210A
-Dysfibrinogenaemia

29
Q

Name an acquired thrombophilia

A

-Antiphospholipid syndrome= antiphospholipid antibodies on at least 2 occassions 8 weeks apart with VT/AT/recurrent fetal loss

30
Q

What are the clinical features of thrombophilia?

A
  • DVT/PE
  • Superficial thrombophlebitis
  • Arterial thrombosis
  • Obstetric complications
  • Coumarin induced skin necrosis
  • Thrombosis of cerebral, axillary, portal, mesenteric veins
31
Q

What is factor V leiden?

A

-FV resistant to cleavage by APC
-Single mutation in factor V gene
-Most common familial thrombophilia
-

32
Q

Describe prothrombin 20210A

A
  • Point mutation in 3’ untranslated region of prothrombin gene
  • Increased prothrombin levels

Mechanism of Disease (18 decks)

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