Pathology: Thrombosis, Embolism and Infarction

Question 1

define thrombosis

Answer 1

formation of a blood clot inside a blood vessel, obstructing flow of blood

Question 2

define embolus

Answer 2

a piece of clot that breaks free and begins to travel around the body

Question 3

define embolism

Answer 3

lodging of an embolus inside a blood vessel.

Question 4

define ischaemia

Answer 4

restriction of blood supply to tissues, causing a shortage of oxygen and glucose needed to keep the tissue alive

Question 5

define infarction

Answer 5

obstruction of blood supply to an organ/ region of tissue, typically caused by a thrombus/ emboli - causing local tissue death

Question 6

clots are intravascular/ extravascular?

Answer 6

extravascular

Question 7

thrombi are intravascular/ extravascular?

Answer 7

intravascular

Question 8

3 elements of Virchow’s triad?

Answer 8

• stasis
• hypercoagulability
• endothelial damage

Question 9

what two main stages lead to thrombosis?

Answer 9

1. platelet activation

2. fibrin production via coagulation cascade

Question 10

endothelial damage exposes _____ , leading to platelet activation

Answer 10

collagen
(the exposed collagen, and vWF bind to glycoprotein Ia/ IIb on platelets - there is then an increase in platelet integrins)

Question 11

activated platelets release granules such as vWF, platelet activating factor (PAF), thromboxane A2 (TXA2), ADP. What is the purpose of this?

Answer 11

to attract other platelets

Question 12

what is activated partial thromboplastin time for?

Answer 12

it’s a medical test that characterises blood clotting. Detects clotting abnormalities, but also monitors treatment effects with heparin

Question 13

what is the function of thromboplastin (AKA tissue factor)?

Answer 13

it’s a plasma protein which aids clotting, by catalysing the conversion of prothrombin to thrombin

Question 14

why doesn’t thrombosis occur in the arterial system (unless there is underlying atherosclerosis)?

Answer 14

because the arterial system is high flow, and so pro-coagulant materials are washed along before being able to do anything. BUT you can get deep VEIN thrombosis - because pro-coagulant materials are not washed along.

Question 15

why is there typically increased endothelial damage where arteries branch?

Answer 15

due to turbulent flow at bifurcations

Question 16

Poiseuille’s law states that for a small reduction in lumen, there is a big/ small reduction in blood flow?

Answer 16

BIG

Question 17

what can cause endothelial injury?

Answer 17

toxins
infectious agents
smoking
autoimmune disease (e.g. primary vasculitis - Ig directed at vessel walls)
previous DVT
turbulence (also causes stasis)

Question 18

stasis is more likely to occur in arterial/ venous system? Why?

Answer 18

venous
faulty valves would mean the blood cannot keep flowing
venous insufficiency may cause pooling in the legs (often caused by varicose veins)

Question 19

what are factors promoting clot lysis?

Answer 19

plasmin

anti-clotting proteins: protein C, protein S, and anti-thrombin III

Question 20

hypercoagulability can be primary (due to genetic causes). Give examples?

Answer 20

• factor V Lieden thrombophilia (factor V - which helps blood to clot - is mutated so that an anticoagulant protein cannot inhibit it)
• deficiencies of protein C/ S, or AT III

Question 21

hypercoagulability can be secondary. Give examples?

Answer 21

prolonged immobility
significant tissue injury (burns, RTA)
antiphospholipid syndrome (autoimmune)
MI
atrial fibrillation
cancer (tumour may produce TF, mucin, inflammatory cytokines)
therapy (chemo)
marantic endocarditis (NBTE)
low risk:
the pill
smoking
renal disease
cardiomyopathy