Week 28 / Haemostasis 1 Flashcards

1
Q

Q: What is the definition of haemostasis?

A

A: Haemostasis is the natural process and body’s physiological response that prevents significant blood loss after vascular injury by forming a localized plug in injured vessels, while keeping blood fluid and clot-free in normal blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Q: What is haemostasis?

A

A: Haemostasis is the process that prevents and stops bleeding, or the cessation of blood flow following injury to a blood vessel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Q: What is thrombosis?

A

Thrombosis refers to the formation of blood clots inside a blood vessel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Q: What is haemostasis?

A

A: Haemostasis is a finely tuned and complex biochemical process that prevents and stops bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Q: What are the major players in haemostasis?

A

A
The blood vessel wall
Platelets and other blood cells
Coagulation proteins and other proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Q: What are the four steps in haemostasis?

A

A:
Localised vasoconstriction - reduces blood flow to the injury site and retards blood loss.

Primary haemostasis - formation of a platelet plug to plug the breach in the blood vessel.

Secondary haemostasis - blood clotting/coagulation strengthens and reinforces the platelet plug.

Tertiary haemostasis - fibrinolysis, which dissolves the clot once blood vessel integrity has been restored.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Q: What happens during localised vasoconstriction in haemostasis?

A

A: In localised vasoconstriction, the injured blood vessel constricts, mediated by reflex neurogenic mechanisms and locally released vasoconstrictors like endothelin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Q: How long does localised vasoconstriction last?

A

A: Localised vasoconstriction is transient and typically lasts for up to 30 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Q: What is the effect of localised vasoconstriction?

A

A: It briefly reduces blood flow to the injury site and retards blood loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Q: What is the role of intact endothelium in primary haemostasis?

A

A: Intact endothelium acts as a physical barrier, separating circulating platelets from thrombogenic substances in the extravascular space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Q: What triggers primary haemostasis after vascular injury?

A

A: Vascular injury exposes the procoagulant subendothelial matrix to circulating platelets, initiating four events:

Platelet adhesion
Platelet activation
Platelet aggregation
Platelet plug formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Q: What happens during platelet adhesion in primary haemostasis?

A

A: Upon endothelial injury, platelets bind to exposed subendothelial matrix proteins (e.g., collagen) through transmembrane glycoprotein receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Q: What are the key glycoprotein receptors involved in platelet adhesion?

A

A: The key glycoprotein receptors involved in platelet adhesion include:

GP1b-IX-V complex binds to von Willebrand factor
GPVI and α2β1 (GPIa-IIa) bind directly to collagen
GP1c/IIa binds to fibronectin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Q: What happens during platelet activation in primary haemostasis?

A

A: Platelets undergo several key changes:

Shape change: Platelets transform from a normal discoid shape to elongated cells with cytoplasmic extensions.

Granule release: Platelets release the contents of preformed cytoplasmic granules.

α-granules: Contain von Willebrand factor (vWF), P-selectin, FV, and FXIII.
Dense granules: Contain ADP, serotonin, and calcium (Ca²⁺), etc.

Membrane phospholipid metabolism: Increases thromboxane A₂ (TXA₂) production.

Activation and expression of GPIIb/IIIa receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Q: What happens during platelet aggregation and plug formation in primary haemostasis?

A

A: Agonist-activated platelet GPIIb/IIIa receptors bind fibrinogen, creating cross-bridges with adjacent platelets and forming a primary haemostatic plug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Q: Is the primary haemostatic plug sufficient to stop haemorrhage in all blood vessels?

A

A: The primary haemostatic plug is sufficient to stop haemorrhage in small blood vessels, but not in larger vessels or those with severe injury.

17
Q

Q: What role do aggregated platelets play in secondary haemostasis?

A

A: The activated and aggregated platelets form the phospholipid membrane surface necessary for the clotting process in secondary haemostasis.

18
Q

Q: What is secondary haemostasis also called?

A

A: Secondary haemostasis is also called the Coagulation Cascade.

19
Q

Q: What is the main goal of secondary haemostasis?

A

A: The main goal is to form a stable fibrin clot at the site of injury.

20
Q

Q: How does secondary haemostasis contribute to clot formation?

A

A: Secondary haemostasis involves the serial activation of coagulation factors, leading to the formation of insoluble, cross-linked fibrin, which stabilizes the primary platelet plug and forms a compact, solid, irreversible clot (secondary haemostatic plug).

21
Q

Q: What is the Coagulation Cascade?

A

A: The Coagulation Cascade is a sequence of enzymatic reactions involving blood-borne coagulation or clotting factors.

22
Q

Q: What are the key components required for the major activation reactions in the Coagulation Cascade?

A

A: The major activation reactions require a negatively charged phospholipid-rich membrane surface, an enzyme (activated coagulation factor), a substrate (proenzyme form of downstream coagulation factor), a cofactor, and Ca²⁺.

23
Q

Q: How is the Coagulation Cascade traditionally divided?

A

A: It is traditionally divided into three distinct pathways: the intrinsic, extrinsic, and common pathways.

24
Q

Q: What happens during the Coagulation Cascade?

A

A: The Coagulation Cascade involves serial activation of inactive plasma proteins (a & B globulins) to active enzymes and cofactors, leading to the conversion of fibrinogen to fibrin by the activated enzyme thrombin.

25
Q

Q: What are the enzymes in the Coagulation Cascade?

A

A: All enzymes in the Coagulation Cascade are serine proteases.

26
Q

Q: How are the coagulation or clotting factors identified?

A

A: The coagulation or clotting factors are identified with Roman numerals (I-XIII), according to the order of their discovery. The activated form of the factor is denoted by a lowercase “a” after the factor number.

27
Q

Q: Where are most of the coagulation factors synthesized?

A

A: Most of the coagulation factors are synthesized in the liver.

28
Q

Q: Which coagulation factors belong to the Contact Group?

A

A: The Contact Group includes factors XII, XI, prekallikrein, and HMW Kininogen. They require contact with a negatively charged surface for activation.

29
Q

Q: Which coagulation factors belong to the Prothrombin Group?

A

A: The Prothrombin Group includes factors II, VII, IX, and X. They require vitamin K for synthesis.

30
Q

Q: Which coagulation factors belong to the Fibrinogen Group?

A

A: The Fibrinogen Group includes factors I, V, VIII, and XIII. These are large molecules and are absent from serum.

31
Q

OPEN PP MAHRAN LOVE UUU XX

A

OPEN PP MAHRAN LOVE UUU XX

32
Q

KEEP GOING MAHRAN THESE MF GOT NOTHING ON YOU

A

KEEP GOING MAHRAN THESE MF GOT NOTHING ON YOU