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Biochemistry > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What does the clotting process consist of?

A
  1. Platelet clumping
  2. Aggregation of fibrin
  3. Vasoconstriction
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2
Q

What are platelets?

A

cell fragments produced by bone marrow

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3
Q

Do platelets contain a a nucleus, mitochondria or vesicles?

A

contain vesicles that contain blood-clotting factors

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4
Q

When is collagen exposed?

A

when the blood vessel surface is damaged

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5
Q

Explain the outline of the blood clotting process?

A
  1. platelets adhere to the exposed collagen surface
  2. activated to form platelet plug and release clotting factors
  3. Promote vasoconstriction and platelet aggregation
  4. Clotting cascade causes fibrin to be deposited and cross-linked.
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6
Q

Are rbcs and platelets visible in a light microscope?

A

yes, rbcs large circles and platelets are smaller circles

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7
Q

What are factors and where are they located?

A

proteins found in the plasma

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8
Q

What is the normal of normal platelets?

A

Bi-concave

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9
Q

What happens to the platelets when they become active?

A

shape change
aggregation (starting to stick together) and adhesion
degranulation ( release of chemicals to control haemostasis)

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10
Q

How do platelets become activated?

A

exposure to collagen and von-willebrand factor

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11
Q

what is the 3 step process for clot formation?

A

Platelet plug => activating clotting factors
fibrin mesh => covering the plug (soft clot)
clot solidified => formation of crosslinks ( hard clot)

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12
Q

What are pro-enzymes and why are said to be inactive?

A

inactive enzymes

they have a N-terminal region that blocks the active site of the enzyme

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13
Q

How can pro-enzymes be activated?

A

Hydrolysing the backbone at the right place using proteases.
Pro-region is removed (no further interest)
Active enzyme can now change substrate to product

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14
Q

What are zymogens?

A

Proenzymes

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15
Q

Which are the active components fibrin or fibrinogen or thrombin or pro-thrombin?

A

fibrin and thrombin

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16
Q

What is the role of thrombin?

A

• Activation of platelets.
• Activation of Factors V,
VIII and XIII.
• Activation of Protein C

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17
Q

What starts the whole of the blood clotting process?

A

activation of prothrombin

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18
Q

What are cofactors?

A

proteins that bind to activate the factors

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19
Q

Why is it called clotting cascades?

A

both intrinsic and extrinsic pathways

20
Q

When is the intrinsic pathway used?

A

damaged tissue (exposed collagen)

21
Q

what protein is released after exposure to collagen and what are the chain of active factors produced?

A

Kininogen/Kallikrein - protein

active factors - 12a => 11a =>9a

22
Q

What co-factors are needed for the conversion of IXa to be converted to Xa?

A

thrombin needed to convert VIII to VIIIa
ca
Phospholipids

23
Q

Why is factor Xa important?

A

needed to form thrombin from prothrombin which is then need to convert fibrinogen into fibrin

24
Q

What happens if there’s a deficiency in VIIIa (or any of the co-factors) in the intrinsic pathway?

A

No Xa meaning no thrombin, pathway stops at factor IXa

25
Q

If there is a deficiency in factor Va?

A

BOTH intrinsic and extrinsic pathways will stop at factor Xa

26
Q

Why are there co-factors?

A

They bind to proteins to make them active

27
Q

What is the common pathway of the clotting cascade?

A

process from formation of factor Xa to fibrin

28
Q

are factor VIII and V proteases?

A

no they are co-factors

29
Q

What is the underlying concept of the intrinsic pathway of the clotting cascades?

A

one molecule of XIIa can produce many molecules of XI which can produce many molecules IXa
Evolving a large response from a very small signal

30
Q

What happens if there is a small [thrombin] in circulation?

A

cycle produces lots more

31
Q

How many chains is fibrin made up?

A

6, 2 alpha, 2 beta and 2 gamma

32
Q

Why is the alpha and beta end of the fibrin highly negative?

A

These chains contain highly acidic residues

33
Q

What does the thrombin do to the fibrin?

A

cleaves/removes highly negative region of the fibrin allowing cross-links to form

34
Q

How are the fibrin chains held together?

A

disulphide bridges

35
Q

What happens to the fibrin after thrombin has acted?

A

forms a fibrin monomer, this goes onto form a fibrin polymer (network formed by crosslinks)

36
Q

How are the crosslinks between fibrin molecules formed?

A

Factor XIIIa (needs thrombin cofactor) forms covalent bonds between glutamine and lysine side chains on the fibrin molecules.

37
Q

How is the clotting process and fibrinolysis switched off?

A

using enzyme inhibitors

38
Q

how does clot limitation occur?

A

Anti‐thrombin inhibits thrombin and factors VIIa, IXa, Xa, XIa, XIIa
Protein C hydrolyses factors V and VIII.
alpha 1‐antitrypsin and alpha 2‐macroglobulin act as protease inhibitors

39
Q

what stops fibrinolysis?

A

plasminogen ( cofactors- tissue plasminogen activator and urokinase) => plasmin cleaves fibrin => blood clot lysis

40
Q

what are anticoagulants? examples?

A

they thin the blood by stopping the blood-clotting cascade

warfarin and dicoumarol

41
Q

how do anticoagulants work?

A

They inhibit post- translational modification required by several factors

42
Q

What are the effects Ptm?

A

the factors contain modified amino acids - so instead of one acidic side group they contain two
Enzyme required to do this needs vit K

43
Q

what anticoagulants do to glutamate?

A

inhibits vit K, resulting in factors not being able to initiate clotting

44
Q

What drugs are given to reduce blood clotting in blood sample?

A

Heparin: a negatively charged polysaccharide, enhances antithrombin activity so low thrombin
Aspirin: prevents platelet aggregation so low protease activity
Citrate: used in stored blood, binds Ca2+ reduces heart attack

45
Q

What clotting disorders are there increase clotting time?

A

Haemophilia A (Factor VIII deficiency, prevalence
~1:12,000)
Haemophilia B (Factor IX deficiency, prevalence
~ 1:30,000)
Von Willebrand’s disease (decreased platelet
aggregation)
Severe liver disease
Conditions may present as persistent gingival bleeding or
excess bleeding after tooth extraction/oral surgery

46
Q

What clotting disorders are there decrease clotting time?

A

Antithrombin deficiency

Protein C defects

47
Q

Why are clotting disorders not fatal?

A

still got extrinsic pathway for clotting

Biochemistry (3 decks)

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