coagulation and inflammation Flashcards

1
Q

what does tissue factor do

A

it triggers the clotting cascade

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2
Q

what do anticoagulants and anti-platelets do

A

block calcium signals to spot them from activating

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3
Q

what does antithrombin III do

A

it helps to stop the coagulation pathway from carrying on further down the blood vessesl

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4
Q

what happens to the blood vessels when there is damage

A
  • subendothelial lining is removed
  • barrier stopping clotting cascade has gone
  • platelets begin to bind
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5
Q

how do platelets start to bind after damage to the vessel

A

bind to the subendothelial matric through collagen receptors

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6
Q

what does reflex vasoconstriction do

A

reduces the blood flow to the damaged vessels

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7
Q

why does reflex vasoconstriction occur

A

-endothelin release from endothelium vasoconstricts
- loss of NO causes smooth muscle cells to be disinhibited
- serotonin release maintains vasoconstriction

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8
Q

what is primary haemostasis

A

the platelets plug the hole in the damaged vessel

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9
Q

why does primary haemostasis occur

A
  • platelets stick to subendothelial collagen by von Willebrand Factor
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10
Q

what happens in a loss of von willebrand factor

A

causes bleeding disorders and platelets can’t bind to subendothelial layer

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11
Q

how are platelets activated

A

adhesion via glycoproteins trigger their activation by a rise in cytosolic Ca concentration

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12
Q

what happens once platelets bind

A
  • positive feedback
  • pathway triggers more platelets to bind
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13
Q

what do activated platelets produces

A
  • secretory vesicles/ granules released - ATP, ADP and serotonin
  • produce thromboxane A2
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14
Q

what do activated platelets trigger

A

conversion of glycoprotein IIb/IIIa into active form
- platelets can adhere to fibrogen to create a plug to restrict blood flow

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15
Q

why are ADP antagonists used to treat for antiplatelets

A
  • block the positive feedback loop
  • stop the clotting you don’t want but don’t stop it fully
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16
Q

what is immune thrombocytopenia

A
  • bleeding disorder from a low platelet count
  • cytotoxic T cells target own platelets
  • more blood leaves in microvascular damage making small spots
17
Q

what is secondary haemostasis

A

fibrin production stabilises and strengthens the growing clot

18
Q

why is thrombin needed in secondary haemostasis

A

it cleaves fibrinogen to fibrin

19
Q

how does fibrin stabilise the clot

A

cross linking due to factor 13 increase strength, making an insoluble fibrin mesh to stop clot movement

20
Q

what does the extrinsic pathway do in clotting

A

it initiates coagulation

21
Q

how is excessive blood clotting prevented by fibrin

A
  • circulating tissue factor bind to the platelet plasma membrane (calcium-dependent)
  • helps localise all components of coagulation cascade to platelet surface
22
Q

when does fibrinogen do

A

helps the wall to contract to get endothelial wall build up to replace the platelets

23
Q

how does warfarin work

A
  • inhibits vitamin K of clotting factors in the liver
  • means platelets cant bind to platelets plasma membrane
24
Q

how does haemophilia A work

A
  • factor VIII deficiency
  • prevents normal production of tenase complex
25
Q

how is the clotting cascade ‘turned off’

A
  • thrombin mediated
  • protein C bind to surface of endothelial cell
  • it binds and becomes activated and cleave factor 5 and 8a
26
Q

what is the triad of death

A
  • coagulopathy
  • acidosis
  • hypothermia
27
Q

how does the triad of death

A
  • fluid resuscitation dilutes coagulopathy
  • loss bicarbonate you go into acidosis
  • acidosis slows down the clotting cascade
28
Q

what causes systemic activation of coagulation

A
  • pregnancy complications
  • hyperthermia
  • sepsis
  • burns
  • trauma
  • cancer
  • transfusion
29
Q

what happens in fibrinolysis

A

resolution of clot by breaking down fibrin

30
Q

how is fibrin broken down

A
  • endothelial cells release tissue plasminogen activation
  • thrombin activates protein C to disinhibit t-PA
  • t-PA activates plasminogen
  • plasmin then cleaves fibrin to break down clot
31
Q

what does recombinant tPA do

A

used to remove unwanted clots formed during a stroke

32
Q

what does TXA do

A

prevents heavy nose or menstrual bleeding following trauma or surgery

33
Q

what causes venous thrombosis

A

endothelial inflammation due to loss of blood flow triggering vWF

34
Q

how are white blood cells involved in acute inflammation

A
  • inflammatory mediators triggered causing redness, heat and swelling
  • more blood flow to area makes if read and warm
35
Q

why is the swelling in acute inflammation

A
  • more filtration as intracellular junction broken down
  • fluid and proteins can move faster causing swelling
36
Q

what does factor 12 trigger

A
  1. 12 -> prekallikrein -> kallikrein -> joins HMW kininogen -> bradykinin (inflmation)
  2. 12 -> prekallikrein -> kallikrein -> joins plasminogen -> plasmin
37
Q

what does serotonin cause

A
  • vasodilation
  • increased vascular permeability
38
Q

what does histamine cause

A
  • vasodilation
  • increased vascular permeability
39
Q

what do leukocytes and platelets cause

A
  • PGD2 - vasodilation
  • PGE2 - vasodilation and pain