Module 4 Part 2 - Edema, Haemorrhage, Thrombus, Embolus and Infarction

Question 1

Edema

Answer 1

Accumulation of excess fluid in the tissue
Can be local or general
This occurs if hydrostatic pressure in vessels increases i.e. more fluid leaves capillaries
More fluid leaves with reduced plasma oncotic (osmotic) pressure
- leads to hypoproteinaemia
- e.g. liver fails to produce albumin
More fluid leaves if vascular permeability is altered
- acute inflammation

Question 2

Causes of Hypoproteinaemia

Answer 2

Decrease of protein production
Excessive loss of protein
Elevated catabolism of protein

Question 3

Pulmonary and Subcutaneous Edema

Answer 3

Pulmonary
- accumulation of fluid in the alveoli of the lung
- caused by increased hydrostatic pressure in the pulmonary vascular bed, resulting from failure of the left side of the heart
Subcutaneous
- accumulation of fluid in subcutaneous tissue
- caused by increased hydrostatic pressure in the systemic venous system, resulting from failure of the right side of the heart

Question 4

Haemorrhage

Answer 4

Caused by rupture of blood vessels
Massive exsanguination usually caused by trauma to a major artery or vein but may also result from bursting or a vessel weakened by disease

Question 5

Haematoma

Answer 5

An accumulation of blood within soft tissue

It is usually due to traumatic damage to vessels but occasionally follow spontaneous rupture of diseased vessels

Question 6

Haemorrhage - Petechiae and Purpura

Answer 6

Petechiae (1-2 mm diameter) and purpura (2-10 mm diameter) are small tissue haemorrhages often seen in the skin
Due to:
- abnormal small vessel fragility
- abnormal blood clotting
- abrupt increase in pressure within small venules and capillaries

Question 7

Thrombosis

Answer 7

A clotted mass of blood forming in the circulation
It is a structured, solid mass composed of blood constituents that forms in the cardiovascular system
It is due to the activation of the normal coagulation system
- aggregation of platelets, held together with meshwork of fibrin
- normal haemostatic mechanism, occurring constantly to plug small defects in blood vessel walls

Question 8

Factors Contributing to Thrombus Formation

Answer 8

Damage to endothelium
- e.g. atheromatous ulceration of an artery or damage to endocardium
Alterations in blood flow
- turbulence in arteries (plaques) and stasis in veins (morbidity) interrupts the laminar flow of blood and allows platelets to come into contact with endothelium
Composition of blood OCP

Question 9

4 Main Outcomes following Vascular Occlusion by a Thrombus

Answer 9

1. Thrombus may enlarge along the vessel (process termed propagation)
2. Thrombus will undergo lysis by the fibrinolytic system
3. There may be organisation of the thrombus by ingrowth of granulation tissue from the vessel wall
   - gradually the thrombus is replaced by granulation tissue and new vascular channels develop, bridging the site of occlusion and re-establishing flow (this is termed recanalisation)
4. Fragments may break off the thrombus and be carried by the circulation to impact in other vessels (process termed thromboembolism)

Question 10

What happens once the thrombus is plugged effectively and the vessel wall repairs?

Answer 10

The small platelet/fibrin thrombus is normally removed by fibrinolysis

Question 11

Thrombus in Different Vessels and what they Cause

Answer 11

Systemic veins
- travel round to the heart to impact pulmonary arterial system
- causes pulmonary thromboembolism and massive saddle like emboli
In the Heart
- travel via the aorta to the systemic arterial circulation
- there they commonly impact in arteries leading to the brain, kidneys, spleen, gut and lower limbs
Common carotid arteries
- impact in the cerebral arterial system
Abdominal aorta
- commonly impact in the renal arteries and arteries of the lower limbs

Question 12

Pulmonary Embolus

Answer 12

Usually follows thrombosis in leg veins
Small pulmonary emboli impact in peripheral branches of pulmonary artery cause pulmonary infarcts
Large pulmonary emboli may impact in, and obstruct, a major pulmonary artery, causing sudden death (massive pulmonary embolus)
A small pulmonary embolus (with infarction) may be followed by a much larger, fatal embolus (premonitary embolus)
Prevention of leg vein thrombosis is the best way of preventing pulmonary embolus

Question 13

Infarction

Answer 13

Lack of perfusion of tissues by oxygenated blood leads to infarction
Failure of adequate blood supply causes cell damage through ischaemia
Tissue damage due to interference with local blood flow is termed infarction
The ischaemic damage results in coagulative necrosis

Question 14

Infarction and Necrosis

Answer 14

Blockage of an artery generally causes coagulative necrosis in the target organ
An exception being liquefactive necrosis in the brain

Question 15

What is seen in an Infarction?

Answer 15

Immediately follwoing arterial occlusion, a damaged area is typically poorly defined, pale and swollen
WIthin about 48 hours the dead tissue becomes better demarcated and is pale and yellow
As an acute inflammatory response develops in adjacent viable tissue, a red hyperemic border becomes visible, separating normal tissue from the area of infarction
After 10 days or so, ingrowth of granulation tissue and organisation are advanced, infarcted area is ultimately replaced by collagenous scarring

Question 16

The Body’s Reaction to Infarction

Answer 16

Systemic reaction to necrotic tissue
Fever and raised ESR
Neutrophilia
Enzymes from dead and dying cells
Aspartate transaminase (AST), LDH, creatine kinase from infarcts of the heart

Question 17

Aneurysm

Answer 17

An abnormal focal dilation of an artery
Can cause symptoms by:
- local mass effect (pressing against adjacent structures)
- rupture of vessel (predisposition to thrombosis)
Most frequent cause is atherosclerosis
Can also caused by an abnormality that weakens the media
- common factor in this type of pathology is the loss of elastin and muscle in the arterial wall mediated by a local inflammatory response

Question 18

Cardiac Tamponade

Answer 18

When blood bursts through the ventricular wall into the pericardial cavity
The sudden rise in pressure prevents cardiac filling, leading to rapid death
Can be due to an infarct (can occur between 2-10 days after an infarct)

Question 19

Formation of Atherosclerosis

Answer 19

1. Damage to the endothelium due to an irritant
   - e.g. lipids (LDL cholesterol), toxins from smoking, hypertension
2. Cholesterol collects under the damaged endothelium forming a fatty streak
3. Cholesterol is oxidised (LDL modification hypothesis) which sends out a signal to the immune system, attracting monocytes
4. Monocyte will try to break up the fatty streak and it will then be converted to a macrophage
5. Macrophage takes up so much cholesterol that it dies off (foam cells) and release cytokines to attract more monocytes
6. Cholesterol and foam cells build up to form a plaque
7. Smooth muscle cells migrate out of the tunica media into the plaque and secrete a fibrous cap
8. The smooth muscle cells then deposit calcium into the plaque (this is what hardens the arteries)

Question 20

What happens when a plaque from atherosclerosis ruptures?

Answer 20

The thrombogenic plaque material is exposed to the blood

This forms a blood clot that blocks the blood flow through the artery