Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Biochemistry > Revision lecture B31 > Flashcards

Revision lecture B31 Flashcards

1
Q

What are the 3 major steps of Haemostasis

A

1) vascular spasm
2) formation of platelet plug
3) blood coagulation (clotting)

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

Why must Haemostasis be appropriately controlled

A

To avoid inappropriate clot formation
Clots must be eventually degraded
Clots are temporarily solution

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

What si the vascular spasm

A

Vasoconstriction
Muscle cell contracts reducing blood flow nd limit blood loss
Opposing endothelial cell surfaces are pressed together and adhere

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

What si the vascular spasm mediated by

A

Platelet derived products - serotonin and thromboxane A2

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

What does normal endothelium produce

A

Vasodilators - nitric oxide

And inhibitors of aggregation - prostaglandin

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

What are platelets also known as

A

Thrombocytes

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

Where are platelets derived form

A

Megakaryocytes in the bone marrow

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

What doe platelets contain

A

No nuclei but other organelles for energy production

Contain high concentrations of actin and myosin therefore can contract

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

What are some factors involved in platelet activation

A

ADP - released by platelets, erythrocytes and endothelial cells

Thrombin - made by enzyme cleavage of prothrombin

Collagen - in the connective tissue, exposed by vessel damage

PAF - platelet activating factor (phospholipid) form the vessel wall and other cells

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

What are the effects of platelet activation

A

Change shape form disc to sphere with extended pseudopodia which facilitate aggregation and coagulant activity

Release compounds involved in Haemostasis
Aggregate
Adhere to vessel wall
Synthesis thromboxane A2 a potent labile mediator of platelet activation and vasoconstriction

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

What si the general formation of the platelet plug

A

Platelets aggregate to form primary plug

To prevent being washed away by blood flow platelets release Chems which enhance blood coagulation, incomrp fibrin

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

What is vWF

A

Von Willebrand Factor

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

What sit he role of vWF

A

Binding platelets together

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

What are Gplb and Gpllb/llla

A

Glycoproteins and receptors

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

What si the most common defect with platelets

A

Von Willebrand disease which is a group of autosomal dieases affecting vWF

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

What are less common disorders affecting platelets

A

Affect the receptors found in the platelet membrane involved in platelet adhesion and aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Wat are anti platelet drugs used to treat

A

Arterial thrombosis blood clot in a vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do anti ppateelt durgs work

A

They decrease platelet aggregation and inhibit thrombus formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some examples of anti platelet drugs

A

Aspirin (reduces thromboxane A2)
Platelet receptor antagonists (target Gpllb which binds vWF)
Platelet ADP receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What do blood coagulation factors interact to form

A

The secondary fibrin rich, Haemostatic plug in small vessels and the secondary fibrin thrombus In arteries and veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What si the intrinsic pathway for blood coagulation

A

Activated by exposure of flowing blood to subendothelial collagen exposed by damaged vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the extrinsic pathway of blood coagulation

A

Activated by tissue damage which exposes flowing blood to a protein called tissue factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does the intrinsic and extrinsic pathways of blood coagulation lead to

A

A final common pathway resulting in conversion of fibrinogen to fibrin

24
Q

What is the clot formation

A

Fibrin clot from red by interaction of intrinsic, extrinsic and final common pathways

A clot on top of platelet plug strengthens the lug reinforces the seal

25
What is fibrin
Insoluble, threadlike molecule Forms a loose, mesh that trans blood cells Generated form fibrinogen which is a large soluble plasm protein syn by the liver
26
What si the key role of thrombin
Catalyses conversion of fibrinogen to fibrin | Activated factor 13
27
Where do cross links form
Between adjacent fibrin strands Strengthens and stabilises clot Catalysed by factor 13
28
What si the blood clotting cascade in intrinsic pathway
Initiates clotting in a damaged vessel Activated by factor 12 comes into contact with collagen or foreign stance Aggregated platelets secrete platelet factor (PF3) which is essential for the cascade and platelet aggregation Activation of factor 10 a protease can digest prothrombin to thrombin
29
What si the blood clotting cascade for the extrinsic pathway
Requires contact with tissue factors to blood Traumatised tissue = release tissue factor which with factor 7 activates factor 10
30
What si fibrinogen
Soluble plasma protein | 6 polypeptide chains
31
What does thrombin do
Converts fibrinogen to fibrin Cleaves four peptide bonds in fibrinogen relapsing fibrinopeptides and fibrin monomers
32
What do the fibrin monomers do
Spontaneously assemble into ordered fibrous arrays called fibrin whci is insoluble
33
What factor causes the cross linking of fibrin
Factor 13
34
What si thrombins dual action
Catalyses formation of fibrin but also initaties the deactivation of the clotting cascade
35
As well as thrombin in terminating clotting what else is essential
Specific inhibitors
36
Clotting factors are labile and short lived due to ...
Dilution by blood flow Removal by liver Degradation by proteases
37
What si the complete list of the roles of thrombin
1) converts fibrinogen to fibrin 2) activates factor 13 to stabilise the fibrin meshwork by cross linking 3) stimulates its own activation by positive feedback 4) enhances platelet aggregation
38
What si vitamin k essential for
Synthesis of prothrombin and other clotting factors (8, 9 and 10)
39
What does prothrombin have in its N terminus
Glutamate residues
40
What is vitamin k enzymatic ally converted to, where and how
Conv to - gamma- carboxyglutamate in the liver
41
What does the gamma carboxyglutamate do
Binds calcium which facial takes conversion to thrombin
42
What si the role of calcium
Binding of calcium anchors prothrombin to the platelet mem surfaces after injury Brings prothrombin knot proximity of clotting factors required for its activation to thrombin Activation frees thrombin
43
What are some examples of vitamin k antagonists
Discoumarol | Warfarin - anti coagulant sun prothrombin without gamma carboxyglutamate
44
What sit he substance which prevents inappropriate clotting
Anti- thrombin Heparin Protein C Tissue factor pathway inhibitor
45
Where is anti thrombin produced
In the liver
46
What does anti thrombin do
Inactivates thrombin
47
Where is heparin syn and what does it do
Syn in mast cell | Activates anti thrombin and used as an anti coag
48
Where is protein c and its cofactors syn and what do they do
Syn in the liver | Degrade clotting factors
49
What does the tissue factor pathway inhibitor do
Inhibit the tissue factor VIIa complex blocking activation of factor 10
50
What is fibrinolysis
Dissolving the clot
51
What happens in fibrinolysis
Circulating plasminogen binds to fibrin Factor 12 activates conversion to plasmin Plasmin slowly degrades fibrin (phagocytes remove debris) Tissue plasminogen activator also activates plasmin to do this
52
What is plasminogen
A serum protein which is produced int he liver
53
Excessive bleeding may result from
congenital or acquired disease of any of the stages of Haemostasis
54
What does congenital mean
Present form birth
55
What are some congenital reasons for excessive bleeding
``` Disorder collagen syn - vessel wall VWF deficiency (or receps) - platelets Coag factors deficiency (factors) - coagulation Anti plasmin deficiency - fibrinolysis ```
56
What are some acquired disorders for excessive bleeding
Vit c deficiency - vessel wall Anti platelet drugs - platelets Vit k def - coagulation Fibrinolytic drugs - fibrinolysis
57
What is Haemostasis
The arrest of bleeding

Biochemistry (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions