Haemostasis & Coagulation

Question 1

Haemostasis

Answer 1

The normal response of the vessel to injury by forming a clot that serves to limit haemorrhage

Question 2

Is coagulation related to the platelet side of things

Answer 2

NO

Question 3

Intrinsic Pathway of Clotting

Answer 3

Activated when blood comes into contact with foreign tissue - exposed collagen from injured blood vessel wall, test tube

Question 4

Extrinsic Pathway of Clotting

Answer 4

Tissue is damaged and releases thromboplastin

Question 5

Purpose of the Amplification Cascade

Answer 5

Each step of clotting is amplified such that a lot of fibrin is released with little prompt

Question 6

Describe the amplification cascade

Answer 6

Something like one active factor X activates 10,000 Prothrombins into thrombin (amplification)

Thrombin gets you factor XIII and chops up fibrinogen into fibrin, which is stabilised by factor III

Fibrin leads to the clotting

Question 7

Which is more of a cardiovascular risk; too much or too little fibrinogen?

Answer 7

Too much fibrinogen is a cardiovascular risk as it predisposes to clot formation

Question 8

Role of platelets (don’t just say clotting!!)

Answer 8

Forming a mechanical plug during blood vessel injury

Question 9

Two main reactions of platelets

Answer 9

Adhesion

Aggregation

Question 10

Describe the adhesion reaction of platelets

Answer 10

They adhere to the subendothelial surface on damaged tissue; supported by
Von Willebrand’s factor
They release 5-HT, ADP and thromboxane

Question 11

Describe the aggregation reaction of platelets

Answer 11

Platelets begin to clump and stick together due to thromboxane and ADP which signal them to stick together

Once ADP binds to a platelet, it results in the expression of glycoprotein IIb-IIIa, allowing them to become cross linked via vWF and fibrinogen

Question 12

Bleeding time test

Answer 12

Incision made on forearm with venous cuff

Bleeding time increases with platelet dysfunction/thrombocytopaenia

Question 13

International Normalised Ratio (INR)

Answer 13

Test for Prothrombin time;
Blood test measuring the ability of blood to clot - time for Coagulation following addition of thromboplastin

Standard is 1 (12 seconds is 1); if someone has an INR of 2, they take longer than normal to clot

Prolonged by abnormalities of blood factors, liver disease or warfarin

FOCUS ON THIS ONE!!

Question 14

Activated Partial Thromboplastin Time (APTT)

Answer 14

Examines the intrinsic pathway of clotting; altered by changes in clotting factors

Outdated mostly and somewhat irrelevant

Question 15

Thrombosis

Answer 15

Formation of unwanted blood clots in the bloodstream

Question 16

What happens in atrial fibrillation

Answer 16

SA Node normally fires across the atrium causing a pulse; in this pathology, other tissues take the role of pacemaker and cause a very uncoordinated contraction

Leads to a very irregular heart rate and tachychardia

Usually a result of tissue damage

Question 17

What is a consequence of atrial fibrillation

Answer 17

Blood is stagnant so a clot forms; it is shot into the brain causing a stroke

High risk of stroke with AF

Think of it like clotty cream getting all mixed up and condensed

Question 18

What is the main cause of myocardial infarctions

Answer 18

Patient gets atherosclerotic plaque in coronary arteries; blood is blocked from going downstream of that plaque and boom heart attack baby

Question 19

Compare the relevance of cloagulation factors and platelets in venous vs arterial thrombosis

Answer 19

Venous Thrombosis is more of a coagulation factor event

Arterial thrombosis is more of a platelet event

Question 20

Examples of arterial thrombosis

Answer 20

Myocardial Infarctions

Ischaemic Strokes

Question 21

What is the cause of Haemophilia A

Answer 21

X-linked genetic disorder causing low factor VIII of the clotting cascade

Question 22

How is haemophilia treated

Answer 22

Previously, it was treated via regular infusions of factor VIII

Alternatively, sometimes analogue of ADH was used which increases patients factor VIII release

Then Emicizumab was introduced

Question 23

Emicizumab

Answer 23

Modern monoclonal antibody treatment of haemophilia A; given via monthly sc injections; activates factor IX and X so bypasses role of factor VIII

Very effective and high half life compared to transfusion

Question 24

Haemophilia B

Answer 24

(Christmas disease since factor was discovered on christmas)

Deficiency of factor IX

Treated via prophylactic factor IX

Question 25

Von Willebrand’s Disease

Answer 25

Heridary lack or defect in vWF

Leads to increased bruising, nose bleeds, mucosal bleeding

Question 26

Treatment of Von Willebrand’s Disease

Answer 26

Analogue of ADH/Vasopressin, factor VIII or vWF

Question 27

Effect of liver disease on clotting

Answer 27

Reduced synthesis of clotting factors leads to increased bleeding; increased prothrombin time

Question 28

Thrombocytopaenia

Answer 28

Reduced platelet count; leads to spontaneous skin bleeding

Question 29

Causes of thrombocytopaenia

Answer 29

Idiopathic
Viral
Drug-induced
Toxins

Question 30

Can Drugs cause thrombocytopaenia

Answer 30

Yes; if it does, change the prescription

Question 31

Disseminated Intravascular Coagulation

Answer 31

DIC
Large amounts of fibrin generated by procoagulant material like amniotic fluid

Leads to vast consumption of clotting factors and platelets; causes widespread haemorrhage but also maybe thrombosis

DEATH IS COMING (not always but its very bad - medical emergency)

Question 32

Treatment of DIC (Disseminated Intravascular Coagulation)

Answer 32

Platelets and fresh frozen plasma

you do defrost the plasma lmao

Question 33

Factor V Leiden mutation

Answer 33

Single nucleotide polymorphism

Abnormal Factor V

Less susceptible to deactibation so leads to increased risk of venous (only) thrombosis - especially with oral contraceptives/pregnancy

Question 34

How is haemophilia treated

Answer 34

Previously, it was treated via regular infusions of factor VIII

Alternatively, sometimes analogue of ADH was used which increases patients factor VIII release

Then Emicizumab was introduced