Haemodynamic disorders, thrombosis and shock

Question 1

What is meant by microcirculation?

Answer 1

The exchange of fluid, nutrients and waste products between blood and cells taht takes place through the interstitium and microcirculation.

Question 2

What is the interstitium?

Answer 2

Space between cells. Composed of structural, adhesive and absorptive components

Question 3

Describe the fluid distribution in the body

Answer 3

Body= 80% water (2/3 intracellular. 1/3 extracellular)

extracellular= 80% in the interstitium and 20% in plasma

Question 4

What helps control distribution of fluid nutrients and waste between blood/ interstitium and cells?

Answer 4

• Physical barriers
• Pressure
• Concentration gradients

Question 5

What is the definition of oedema?

Answer 5

Accumulation of excess interstitial fluid

Question 6

What are the mechanisms of oedema?

Answer 6

• Increased microvascular permeability
• incrased intravascular hydrostatic pressure
• decreased intravascular osmotic pressure
• decreased lymphatic drainage

Question 7

What are the causes of increased microvascular permeability?

Answer 7

• Inflammation
• Toxins
• Anaphylaxis
• Clotting abnormalities

Question 8

What are the causes of increased intravascular hydrostatic pressure

Answer 8

• Portal hypertension
• Pulmonary hypertension
• Localised hypertension
• Localised venous obstruction
• Fluid overload
• Hyperaemia

Question 9

What are the causes of decreased intravascular osmotic pressure?

Answer 9

• Decreased albumin production
• Increased albumin loss
• Water intoxication

Question 10

What are the causes of decreased lymphatic drainage?

Answer 10

• Lymphatic obstruction/ compression
• Lymphagitis
• Lyphatic aplasia/ hypoplasia

Question 11

What is the definition of haemostasis?

Answer 11

Arrest of bleeding.

• The physiologic response to vascular damage, mechanism to seal an injured vessel
• Interactions between endothelium, platelets and coagulation factors

Question 12

What are the three stages of haemostasis?

Answer 12

1) formation of platelet plug (primary haemostasis)
2) formation of fibrin network (secondary haemostasis)
3) Removal of platelet/ fibrin plug (fibrinolysis) (thrombus retraction)

Question 13

Explain the extrinsic coagulation pathway

Answer 13

Occurs outside the blood vessel wall when shed blood contacts tissue debris. Involves THROMBOPLASTIN.

Question 14

Explain the intrinsic coagulation pathway

Answer 14

Triggered by presence of abnormal surfaces on components normally present in the blood (all the coagulation factors). Finishes with activation of Factor X.

Question 15

What is the other name for Factor 3 in the coag cascade?

Answer 15

Tissue factor/ Thromboplastin

Question 16

What is Factor VII in the coag cascade?

Answer 16

Proconvertin

Question 17

Which factor is at the terminus of the extrinsic and intrinsic pathways of the coag cascade?

Answer 17

Factor X

Question 18

What is the end product of the coag cascade?

Answer 18

Fibrin

Question 19

What is the name for too low concentration of platelets?

Answer 19

Thrombocytopenia

thrombocytopathy= name for abnormal platelet function

Question 20

What is Petechia?

Answer 20

Pinpoint haemorrhage (1-2mm)

Question 21

What is ecchymosis?

Answer 21

Haemorrhage of up to 2-3cm

Question 22

What does the thrombosis Virchow triad include?

Answer 22

Endothelial injury
Abnormal blood flow
Hypercoagulability
Thrombosis in the centre

Question 23

What is an embolus?

Answer 23

A piece of free floating foreign material within the blood e.g. fat, cartilage, thrombus fragment

Question 24

What is a thromboembolus?

Answer 24

Embolus derived from fragments of a thrombus

Question 25

Where do venous thromboemboli typically lodge?

Answer 25

Pulmonary circulation

Question 26

Where do arterial thromboemboli normally lodge?

Answer 26

Sites of vascular bifurcation.

Question 27

What does disseminated intravascular coagulation (DIC) mean?

Answer 27

Serious manifestation of abnormal coagulation, severe dyshomeostasis caused by the generation of excess thrombin. Various causes e.g. diffuse vascular damage or systemic infections

Question 28

What is the mechanism for DIC?

Answer 28

Excess thrombin- platelet aggregation and fibrin formation- widespread microvascular clots- consumption of coagulation factors- widespread haemorrhages

Question 29

Describe hyperaemia

Answer 29

Increased blood flow- active engorgement of vascular beds -increased inflow via arteriolar dilation -outflow remains normal or is decreased. -causes: heat (skin_ postprandial (GI) pathologic cause= inflammation

Question 30

Describe congestion

Answer 30

- Decreased blood flow, passive engorgement of vascular beds with a decrease outflow and normal or increased inflow. - Causes: acute-heart failure/ euthanasia. Chronic- obstruction of venous outflow, heart failure, pulmonary disease

Question 31

What are the causes of decreased tissue perfusion?

Answer 31

- Obstruction of a blood vessel - Local vascular congestion - Decreased cardiac output

Question 32

What factors influence development of an infarct?

Answer 32

- nature of the vascular supply - rate at which occlusion develops - vulnerability to hypoxia (neurons/ myocardial cells vulnerable) - oxygen content of the blood

Question 33

What would an arterial obstruction lead to?

Answer 33

loss of blood downstream resulting in abrupt coagulative necrosis

Question 34

What would venous obstruction lead to?

Answer 34

Reduction/ loss of venous return

Question 35

List the events of shock

Answer 35

Hypotension- decreased tissue perfusion- cellular hypoxia- shift to anaerobic metabolism- cellular degeneration- cell death

Question 36

What are the different types of shock?

Answer 36

1) cardiogenic: failure of heart to pump adequately 2) hypovolaemic: decreased circulating blood volume due to blood/ fluid loss 3) blood maldistribution: Anaphylactic (generalised type 1 hypersensitivity), neurogenic (trauma to NS), septic (peripheral vasodilation caused by components of bacteria/ fungi inducing release of vascular/ inflammatory mediators)