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LSS Cardiovascular System > 11 Haemostasis > Flashcards

11 Haemostasis Flashcards

1
Q

Q: What are the functions of haemostasis? (2)

A

A: prevention of blood loss from intact vessels

arrest of bleeding from injured vessels

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2
Q

Q: Give an overview of the haemostatic process. (4)

A

A: (vessel injury)

  1. vessel constriction= first response and can prevent blood loss on its own
    - particularly important in small blood vessels
  2. PRIMARY HAEMOSTASIS: formation of unstable platelet plug
    - platelets in blood circulation interact with damaged vessels and cause formation
    - i) platelet adhesion
    - ii) platelet aggregation
  3. SECONDARY HAEMOSTASIS: stabilisation of the plug with fibrin
    - blood coagulation system is triggered and fibrin is formed-> consilidates platelet
    - means that the plug won’t breakdown to sheer stress within blood
  4. dissolution of clot and vessel repair via fibrinolysis
    - slower process = get remodelling of blood vessel and vessel repair
    - clot is gradually removed
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3
Q

Q: How does a thrombus formation compare to haemostasis?

A

A: thrombus formation= less stable

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4
Q

Q: What part of haemostasis is platelet adhesion part of? Describe mechanism one (3). Describe the alternative mechanism two.

A

A: primary haemostasis

  1. usually have layer of epithelial cells lining blood vessel -> disruption to this exposes underlying subendothelial connective tissue which contains collagen
  2. exposed collagen attracts Von Willebrand factor which circulates in the blood -> binds to exposed collagen
  3. said factor is able to capture circulating platelets via their glycoprotein 1b receptor -> platelet has adhered to site of injury

binding= adhesion reaction

  1. direct interaction of exposed collagen to platelet via glycoprotein 1a on platelet
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5
Q

Q: Compare the mechanisms of platelet adhesion in terms of conditions they occur under. In what state are the platelets when they bind?

A

A: 1= (indirect binding via VW factor) mechanism takes place under high sheer conditions- usually narrower blood vessels

2= direct mechanism takes place in areas of less sheer stress

inactivated form

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6
Q

Q: What happens following platelet adhesion? (3)

A

A: signals are sent through via glycoprotein 1b or 1a receptors = to activate platelet

causes release of ADP and prostaglandin from within platelet

RESULTS in initiation of platelet aggregation

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7
Q

Q: What part of haemostasis is platelet activation part of? Describe mechanism (3). What else contributes?

A

A: primary haemostasis

  1. when platelets are activated -> conformational change which activates glycoprotein 2b3a
  2. said GP binds to circulating fibrinogen
  3. acts like glue and clumps platelets together

coagulation system generates protease = THROMBIN= lots of functions in haemostasis inc platelet activation

-> causes more aggregation

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8
Q

Q: In what form do platelets circulate? What is platelet activation? how?

A

A: inactive- doesn’t interact directly with anything as long as blood vessel isn’t damaged

conversion from passive to interactive cell

progressively activated by engaging through receptors to damaged enothelial cells.. etc

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9
Q

Q: Describe activated platelets (3).

A

A: change shape

change membrane composition (important as coagulation enzyme is generated on surface of activated platelets)

present nre or activated proteins on their surface eg GpIIb/IIIa

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10
Q

Q: What does the blood coagulation system require? (2) Where are they from? (3)

A

A: lots of proteins and enzymes

most synthesis is in liver

some made in high local concentration in endothelium eg vWF

some in megakaryocytes-> packaged in platelets eg factor 5

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11
Q

Q: Draw the diagram for the blood coagulation system and label.

A

A: REFER

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12
Q

Q: What does being a cascade system mean?

A

A: can start off with 1 or 2 molecules that are activated-> can progressively amplify reaction -> get more at each stage generated

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13
Q

Q: Where does the intrinsic pathway it take place? Describe it (4). Catalyst?

A

A: = takes place on activated platelets

  • factor 12 (zymogen) -> 12a which is a protease
  • goes on to cleave factor 11 -> activated
  • that activated 9
  • that activates 10

10 to 10 a is catalysed by activated platelet with co factor 8a= generated from FVIII by trace amounts of thrombin

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14
Q

Q: Describe the extrinsic pathway. (2)

A

A: tissue factor is not normally found in blood

it’s expressed by cells outside normal endothelial cell barrier (sub endothelial tissue that express it)

when blood comes into contact with it, 10 -> 10a is catalysed directly by factor 7a

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15
Q

Q: What are the 2 ways to activate coagulation? Common end point?

A

A: extrinsic and intrinsic pathways

activated factor 10a

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16
Q

Q: Describe the common pathway. Catalyst? 2 further steps? Catalyst?

A

A: 1. 10a converts prothrombin to thrombonin (IIa)

co factor 5a = generated from FV by trace amounts of thrombin

  1. proteolytic action by thrombin to convert fibrinogen to fibrin
  2. fibrin forms cross linked fibrin

thrombin causes factor 13 -> F13a which catalyses [3] and cross links the fibrin = stabilises

17
Q

Q: What’s the role of CF 5 and 8?

A

A: large proteins that are not proteolytic enzymes

they enhance reactions

18
Q

Q: What is the role of tissue factor? Normal without vessel damage? What’s 12-> 12a mainly? useful?

A

A: ((physiological initiator of coagulation and formation of haemostatic plug ->)) trigger to initiate coagulation in vivo

usually don’t get 12-> 12a activation

(mainly an in vitro reaction)-> useful for some diagnostic tests

19
Q

Q: What is tPA? where is it made? Role? What does this allow?

Condition?

A

A: tPA (tissue plasminogen activator) = plasma protein, protease
-circulating precursor made in endothelial cells

convert plasminogen (circulates in blood at high concentrations) from an inactive zymogen to an active protease (PLASMIN)

protease dependant reaction of fibrinolysis

normally no contact between them but triggered when fibrin clot forms

20
Q

Q: What occurs during the process of fibrinolysis? (5)

A

A: 1. fibrin clot forms

  1. plasminogen and tPA bind to surface of fibrin clot
  2. tPA activates plasminogen by converting to plasmin
  3. plasmin= proteolytic and starts to breakdown fibrin clot
  4. FDP made= fibrin degradation products (fragments that clot is broken down into)
21
Q

Q: What can be readily measured in fibrinolysis? Forms basis of? Used when? eg? (2)

A

A: FDP, when clot is breaking down

forms basis of diagnostic test

used in situations where there’s more fibrin breakdown
eg. disseminated intravascular coagulation and active thrombosis

22
Q

Q: What’s the use in tPA and bacterial activators? Name? Use?

A

A: (streptokinase bacterial activator)

used in therapeutical thrombolysis for myocardial infarction (clot busters)

23
Q

Q: The clotting cascade is an amplification system, a small amount of factor VIIa producing a large amount of thrombin.

Why does blood not clot completely whenever clotting is initiated by vessel injury?

A

A: Coagulation inhibitory mechanisms prevent this (controls amount of coagulation that takes place)

24
Q

Q: How many coagulation inhibitory mechanisms are there? Describe 2. Include example.

A

A: 3

i) Direct Inhibition.
e. g. Antithrombin (sometimes known as antithrombin III), which is an inhibitor of thrombin and other clotting proteinases (found in blood stream)

(ii) Indirect inhibition.
e.g. Inhibition of thrombin generation by the protein C
anticoagulant pathway

25
Q

Q: Describe direct inhibition as a coagulation inhibitory mechanism (2). What’s affected? (4) What accelerates this process? Describe its use.

A

A: Antithrombin is a direct inhibitor of thrombin
and other proteinases (found in blood stream
-irreversibly forms inactive complexes (by binding)

  • XIa 11
  • IXa 9
  • Xa 10
  • thrombin (IIa)

Heparin accelerates the action of antithrombin= anticoag

Heparin is used for immediate anticoagulation in venous thrombosis and pulmonary embolism

26
Q

Q: Where are factor VIII and V found? what is their function? where? What activates them?

A

A: circulating in blood

VIII: X-> Xa via IXa

V: prothrombin -> thrombin (IIa) via Xa

work on platelet surface -> accelerate clotting reactions

Factors VIII and V are activated by trace amounts
of thrombin and become cofactors

27
Q

Q: In short what is indirect inhibition as a coagulation inhibitory mechanism? What’s the target? What happens when the target is slowed?

Describe the pathway. (5) Dual action?

A

A: the protein C pathway down-regulates thrombin generation

cofactors Va and VIIIa (accelerate thrombin formation about 10,000 fold)
-> get less thrombin generated

  1. thrombin produced in blood coag pathway (use of V and VIII) binds to receptor: thrombomodulin on endothelium cell membrane
  2. thrombin properties are changed
  3. while bound, it can activate protein C (protein C will bind)
  4. the activated protein C dissociates and binds to protein S = complex forms
  5. complex inactivates cofactors Va and VIIIa

thrombin can act in 2 ways- 1) activate FV and VIII to make coagulation factors but 2) binds to thrombomodulin and slows coagulation down by inactivating FVa and FVIIIa

28
Q

Q: Describe a variation that can restrict the effects of indirect inhibition as a coagulation inhibitory mechanism. What percentage of the population have it? How does it restrict effects? result?

A

A: Factor V Leiden: mutation in Arg506Gln -> a Polymorphism of factor V

4%

it’s not as easily inactivated by activated protein C- protein S complex -> coagulation cascade is not held in check as well (possibly due to the mutation being at the cleavage site)

-> means that there is more thrombin around

29
Q

Q: What can cause the Coagulation Inhibitory

Mechanisms Fail? (4) All?

A

A: 1. Antithrombin deficiency

  1. Protein C deficiency
  2. Protein S deficiency
  3. Factor V Leiden

all risk factors for thrombosis

LSS Cardiovascular System (17 decks)

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