Thrombosis and Infarction

Question 1

what two factors prevent blood clotting unnecessarily?

Answer 1

1. laminar flow - cells travel in centre of arterial vessels, and don’t touch the sides
2. endothelial cells which line vessels are not ‘sticky’ when healthy

Question 2

describe basic clot formation

Answer 2

coagulation cascade results in formation of a fibrin meshwork that entraps the cells into a solid but elastic clot
commonly form after death

Question 3

what is a thrombus?

Answer 3

a solid mass of blood constituents formed within an intact vessel in life

Question 4

what 3 things make up Virchow’s triad?

Answer 4

abnormalities of vessel wall; abnormalities of blood flow; abnormalities of blood constituents

Question 5

why do we need clot-forming cells and proteins in the blood?

Answer 5

to stop massive haemorrhage if we cut/scratch our selves

Question 6

what is the first stage of thrombosis?

Answer 6

platelet aggregation

Question 7

describe the process of platelet aggregation

Answer 7

upon coming into contact with collagen, platelets release chemicals (e.g. ADP) from dense granules that cause the aggregation of other platelets, and set off the clotting cascade.

chemicals released from alpha granules cause platelet adhesion to damaged vessel walls.

Question 8

after platelet aggregation, what is next in the process of thrombosis?

Answer 8

platelet aggregation sets off clotting cascade, so a fibrin mesh begins to form - traps red blood cells

Question 9

what tends to initiate arterial thrombosis?

Answer 9

atheromatous plaque protrudes into lumen, causing turbulent blood flow.
turbulence leads to loss of intimal cells.
denuded plaque surface exposed to blood flow - platelets will settle on exposed collagen.
thrombus forms.

Question 10

give an example of what may cause damage to endothelial wall?

Answer 10

cigarette smoking causing endothelial cell injury - change in vessel wall and change in blood flow over injured cells

Question 11

describe the layers seen in an arterial thrombus

Answer 11

first layer = platelet layer - due to platelet aggregation on damaged wall
second layer = fibrin mesh and trapped red blood cells
these alternating layers = lines of Zahn

Question 12

what typically initiates venous thrombosis?

Answer 12

most form at valves - they naturally cause a degree of turbulence - may be damaged by trauma, stasis and occlusion

Question 13

what predisposes someone to venous thrombosis?

Answer 13

fall in blood pressure, causing slowing of blood flow over turbulent areas - eg during surgery, or following MI.
immobility is a big risk for venous thrombosis in calf - stasis, as no contraction of surrounding muscles.

Question 14

define embolism

Answer 14

the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel

Question 15

list the possible causes of embolus

Answer 15

FATBAT
Fat
Air
Thrombus
Bacteria (endocarditis vegetation)
Amniotic fluid
Tumour

Question 16

describe the path of an embolus in the venous system

Answer 16

vena cava&raquo_space; through R side of heart&raquo_space; lodge somewhere in pulmonary arteries.
will not pass through lungs as blood vessels split down to capillary level.

Question 17

describe the path of an embolus in the arterial system

Answer 17

can travel anywhere downstream of its entry point

Question 18

what is the most common cause of a pulmonary embolism?

Answer 18

deep vein thrombosis of the leg becomes dislodged, makes way to pulmonary arterial system and occludes

Question 19

define ischaemia

Answer 19

a reduction in blood flow to a tissue without any other implications

Question 20

define infarction

Answer 20

reduction in blood flow to a tissue to such an extent that it can no longer support maintenance of cells and they die.
“ischaemic death of tissue in living body”

Question 21

what is the most common cause of infarction?

Answer 21

thrombosis of an artery to the extent it occludes it

Question 22

what makes an organ more susceptible to damage by infarction?

Answer 22

end arterial supply - if this supply is interrupted they have no other way of getting nutrients/O2

Question 23

name organs which have a dual arterial supply

Answer 23

liver - portal venous and hepatic artery
lungs - pulmonary venous and bronchial artery
brain - around circle of Willis

Question 24

list some causes infarction/ischaemia

Answer 24

Obstruction:
THROMBOSIS
arterial embolism
atherosclerotic plaques
Compression:
tumour/volvulus/hernia
Vasoconstriction:
e.g. cocaine vasoconstriction --> MI
Rupture of artery due to trauma

Question 25

what are the risk factors for atherosclerosis?

Answer 25

increasing age
male gender
hypertension
smoking
diabetes
hypercholesterolaemia - high LDL, low HDL

Question 26

what is a fatty streak? what is it composed of?

Answer 26

first stage of atheroma formation - yellow elevation of intima.
masses of lipid-laden macrophages.

Question 27

describe the structure of fully developed atherosclerotic plaque

Answer 27

central lipid core
cap of fibrous tissue covered by the arterial endothelium
cap contains macrophages, T lymphocytes and mast cells

Question 28

what provides the structural strength of an atherosclerotic plaque?

Answer 28

connective tissues in the fibrous cap (collagens) - produced by SMCs

Question 29

describe atheromatous lesions

Answer 29

rich in cellular lipids and cellular debris.
soft, semi-fluid, highly thrombogenic lesions.
bordered by a rim of foam cells

Question 30

what are foam cells?

Answer 30

macrophages that have phagocytosed oxidised lipoproteins via a membrane-bound scavenger receptor.
large amounts of cytoplasm, with foamy appearance.

Question 31

what are the two basic steps in the development of an atheromatous lesion?

Answer 31

1. injury to the endothelium of the arterial wall

2. tissue response of vascular wall to injury

Question 32

what arteries are commonly affected by atheroma?

Answer 32

aorta (esp abdo aorta)
coronary arteries
cerebral arteries
common iliac/femoral arteries

Question 33

what are the key stages in development of atherosclerosis?

Answer 33

1. chronic endothelial injury
2. plasma proteins (inc. LDL) diffuse into intima
3. monocytes bind receptors expressed (due to step 1), differentiate into macrophages
4. macrophages take up LDL to form foam cells - on death, release contents to form extracellular lipid pools
5. platelet adhesion
6. release of cytokines and growth factors by platelets/activated macrophages - migration of SMCs to site
7. these are repair SMCs, producing collagen in attempt to stabilize the lesion

Question 34

what is the function of SMCs in the development of atherosclerosis?

Answer 34

act as repair SMCs, producing collagen to try and stabilize the legion

Question 35

what causes the formation of extracellular lipid pools in atherosclerotic plaques?

Answer 35

death of foam cells - spill out their lipid-rich contents

Question 36

describe what happens in acute atherothrombotic occlusion

Answer 36

plaque rupture exposes thrombogenic plaque contents (collagen, lipid, debris).
activation of coag cascade and rapid thrombotic occlusion of vessel occurs.

Question 37

describe what happens in a ruptured abdominal atherosclerotic aneurysm

Answer 37

rupture of a weakened dilated atheromatous abdominal aneurysm - retroperitoneal haemorrhage and death