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Human Physiology - Cardiopulmonary Physiology > Platelets and Haemostasis > Flashcards

Platelets and Haemostasis Flashcards

1
Q

what are platelets
what is their function

A

small cell fragments formed by megakaryocytes
clotting

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2
Q

how are platelets formed
describe their origin cells

A

shed off from megakaryocytes
extraordinarily large bone-marrow cells

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3
Q

describe clot formation when a vessel is injured

A
  • circulating platelets adhere to and are activated by exposed collagen
  • Von Willebrand factor activates platelets causing them to have protrusions
  • activated platelets release ADP and thromboxane A2
  • these further activate more platelets to join the newly forming plug and release further ADP and thromboxane A2
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4
Q

how soon after injury does a blood vessel constrict

A

vasoconstriction occurs within seconds

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5
Q

what prevents platelet aggregation under normal conditions and confines aggregation to plug sites

A

normal uninjured endothelium releases prostacyclin and nitric oxide to inhibit it

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6
Q

what is the effect of aspirin

A

acts as a blood thinner by inhibiting the COX1 pathway which normally releases prostaglandins that stimulate clotting

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7
Q

what is haemostasis
what is the functions

A

arrest of bleeding from a broken blood vessel; stopping a haemorrhage
prevents blood loss from damaged small vessels

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8
Q

features of platelets

A

no nucleus
some organelles round when inactive, protrusions when active

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9
Q

how does blood clot formation get triggered

A

chain reaction involving plasma clotting factors

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10
Q

fibrinogen

A

plasma protein important for clotting but must be converted to fibrin

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11
Q

when is prothrombin converted to thrombin

A

when blood clotting is desirable

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12
Q

what is the clotting cascade
what is the final step

A

series of sequential reactions that occurs until thrombin catalyses the conversion of fibrinogen to fibrin

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13
Q

describe the formation of fibrin mesh

A
  • thrombin cleaves fibrinogen to make a fibrin monomer
  • thrombin also cleaves factor 13 -> 13a
  • fibrin monomers cross link into a fibrin strand
  • cross linked stands form a mesh stabilised by factor 13 cross linking
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14
Q

intrinsic clotting pathway

A

precipitates clotting within damaged vessels, and clotting of blood samples e.g. in test tubes

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15
Q

extrinsic pathway

A

initiates clotting blood that has escaped into the tissues

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16
Q

clot retraction

A

platelets trapped within the clot contract and shrink the fibrin mesh
pulls the edges of the damaged vessel closer together allowing healing

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17
Q

at what point do the intrinsic and extrinsic pathway converge

A

factor 10 activation

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18
Q

factor 10 function

A

together with Ca2+ and factor 5 converts prothrombin to thrombin

19
Q

what activates factor 13

A

thrombin

20
Q

what are the results of thalassaemia and haemophilia

A

poor blood clotting and excessive bleeding

21
Q

how is the extrinsic pathway activated when there is damage from outside

A
  • tissue thromboplastin (factor 3) is released from damaged tissue
  • acts together with factor 7 and Ca2+ to activate factor 10
22
Q

when damage affects both pathways, which activates factor 10 first

A

extrinsic

23
Q

what other factors does factor 10 require to act

A

factor 5 and Ca2+

24
Q

how is the intrinsic pathway activated

A
  • when factor 12 (Hageman factor) is activated by contact with exposed collagen at the surface of damaged vessels
  • or by contact with a foreign surface (glass in test tubes)
25
Q

order of factor activation in the intrinsic pathway

A

12, 11, 9, 10

26
Q

what factor is required between factor 11 and 9
what factor is required between factor 9 and 10

A

4
8

27
Q

where are clotting factors synthesised
what vitamin do many of them require

A

liver
vitamin K

28
Q

what cells form a scar at vessel defects

A

fibroblasts

29
Q

what dissolves clots
how

A

plasmin
becomes trapped in the clot and later dissolves it by slowly breaking down the fibrin meshwork

30
Q

what is the continuous role of plasmin

A

preventing inappropriate clot formation

31
Q

why would you want to pharmacologically inhibit tissue plasminogen activator

A

it cleaves plasminogen into active plasmin
when you want clotting e.g. haemophilia

32
Q

why would you want to pharmacologically inhibit plasmin
what is the physiological inhibitor of plasmin when does it act

A

when you want clotting
alpha2-antiplasmin, when plasmin in blood is 6-8X exceeding therapeutic dose

33
Q

what is a thrombus
what is a thromboembolism - what can they cause

A

abnormal intravascular clot attached to a vessel wall
free floating abnormal intravascular clot - stroke

34
Q

causes of strokes

A

thromboembolism, brain bleed, hypoxia

35
Q

why is liver disease a blood clotting disorder

A

liver synthesises procoagulants and most clotting factors
also produces bile to absorb fat and vitamin K

36
Q

why is vitamin K deficiency a blood clotting disorder

A

essential for the synthesis of clotting factors

37
Q

why does long term antibiotic use result in bleeding disorders

A

results in vit K deficiency because half of our Vit K comes from gut bacteria (other half diet)

38
Q

thrombocytopenia definition
results
cause
treatment

A

number of circulating platelets is too low
spontaneous, widespread haemorrhage, visible by small purple spots on the skin
caused by damaged bone marrow or cancer
treated with whole blood transfusions or platelet transfusion

39
Q

thrombosis definition
causes
results

A

inappropriate clotting
caused by roughened surface of a vessel, endothelial cell injury (collagen exposed), disrupted flow (stasis - no laminar flow)
can cause DVT, ischemia, and tissue death

40
Q

coronary thrombosis
cerebral thrombosis

A

thrombus in a blood vessel of the heart can cause a heart attack
thrombus in a blood vessel of the brain can cause a stroke

41
Q

atherosclerosis

A

build up of oxidised LDL, fatty plaques in vessels

42
Q

what do blood types depend on

A

surface antigens on erythrocytes

43
Q

when does haemolytic disease of the new-born occur
explain why

A
  • occurs when the mother is Rh- during the second or later pregnancies with a Rh+ child
  • when Rh+ blood from previous pregnancy caused her body to synthesise anti-Rh Abs
  • mothers Abs cross the placenta and cause agglutination and haemolysis of foetal RBCs
44
Q

how is haemolytic disease of the new-born prevented

A

injected anti-Rh antibodies eliminate Rh+ cells

Human Physiology - Cardiopulmonary Physiology (10 decks)

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