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103-theme 2 > platelets and haemostasis > Flashcards

platelets and haemostasis Flashcards

1
Q

what do endothelial cells do when intact? when injured?

A
  • contributes to preventing clots

- promotes clotting on exposed basement membrane

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2
Q

what is extravasation?

A

active movement of fluid out of blood vessels

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3
Q

what is haemostasis? 7

A
  • a process which causes bleeding to stop
  • clotting
  • keeps blood within a damaged vessel
  • opposite is haemorrhage
  • first stage of wound healing
  • endothelium secrets inhibitors of haemostasis normally
  • when injured, the endothelium stops secreting inhibitors and instead secretes von willebrand factor
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4
Q

explain platelets for primary haemostatic plug due to vessel wall injury? 3

A
  • platelet adhesion
    to exposed collagen in the basement membrane
  • platelet activation
    exocytose dense granules (serotonin, ADP, calcium)
    -platelet aggregation
    stimulated by ADP, blocked by prasugrel, via fibrinogen
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5
Q

what does coagulation do for clotting? 3

A
  • makes a meshwork on the clot
  • enzyme cascade- each activates the next enzyme
  • part of coagulation requires platelets membrane
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6
Q

what does vasoconstriction do for blood clotting? 4

A
  • platelets release vasoconstrictors and pro-thrombotic agents
  • serotonin
  • ADP
  • thromboxane A2
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7
Q

what happens if you go down the common myeloid progenitor pathway? 2

A
  • it can become a megakaryocyte which is found in the bone marrow
  • each one will produce many thrombocytes (platelets)
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8
Q

what is thrombocytopenia?

A

low platelet count in the blood

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9
Q

what is platelet activation? 5

A
  • exocytose + change shape + increased respiratory rate
  • required for haemostasis
  • extracellular ADP leads to the activation of P2Y receptor which causes a cation flow
  • platelets release thromboxane A2 (TXA2)
  • ADP causes positive feedback on platelets
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10
Q

explain how coagulation works? 5

A
  • many clotting factors circulate as inactive precursors
  • factor Xa is activated version of factor X
  • most are enzymes which will cleave other factors to activate them
  • factor V and factors VIII are not enzymes, but are cofactors allowing enzymes to function which are also initially inactive
  • initial activating factor is segregated
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11
Q

what pathways lead to a blood clot? 3

A
  • extrinsic pathway can make Xa
  • intrinsic pathway can make Xa
  • Xa works in the common pathway
  • this leads to a clot
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12
Q

what happens if blood is left standing in a lab? 2

A
  • it will clot

- this is stopped with citrate or heparin

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13
Q

what is plasma?

what is serum?

A
  • fluid portion of blood
  • fluid left after clotting, almost identical to plasma except its missing its fibrinogen, clotting factors II, V and VIII
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14
Q

describe the common pathway? 5

A
  • fibrinogen
  • thrombin
  • fibrin
  • XIII +Ca2+
  • fibrin cross-linked, is a stable clot
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15
Q

explain the 2 coagulation cascades? 6

A
  • extrinsic (tissue factor) pathway
  • requires the secretion of tissue factor to occur
  • initiation of coagulation
  • intrinsic (contact activation) pathway
  • all factors/ proenzymes are already in place
  • amplification of process through positive feedback
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16
Q

how do we activate thrombin? 3

A
  • activated by factor Xa, but poorly
  • factor Va is a cofactor of factor Xa
  • together they activate thrombin well
17
Q

what are the pathways to activate factor X? 3

A
  • extrinsic Xase- tissue factor (under endothelium) and factor VIIa
  • intrinsic Xase- factor VIIIa and factor IXa
  • thrombin also activates it via positive feedback
18
Q

explain positive feedback in coagulation?

A

-thrombin activates upstream cofactors to activate itself

19
Q

what are the coagulation factors? 11

A
  • prothrombin group
  • factors II, VII, IX, X
  • enzymes
  • vitamin K needed for synthesis
  • requires Ca2+ for activation
  • stable
  • thrombin group
  • factors I, V, VIII
  • thrombin activates them
  • V and VIII are cofactors
  • factor I is fibrinogen
  • increased in inflammation, pregnancy and with oral contraceptives
20
Q

what is vitamin K? 5

A
  • clotting factor made by the liver
  • liver dysfunction, cirrhosis or hepatitis can cause a clotting deficiency
  • a class of related fat-soluble vitamins
  • required to synthesise coagulation factors prothrombin II, VII, X (calcium dependent proteases)
  • essential for gamma carboxylation of clotting enzymes
21
Q

what does fibrinolysis and inhibition of coagulation need to balance with?

A

clot formation

22
Q

what happens if there is too much fibrinolysis and inhibition of coagulation? 2

A
  • blood vessel accumulating damage

- haemorrhage

23
Q

what happens if there is too much clot formation?

A

clot obstructs the vessel lumen

24
Q

what is plasmin? 4

A
  • lyses fibrin- stops and destroys clots
  • starts as inactive plasminogen (plasma protein made by the liver)
  • requires tissue plasminogen activator (tPA) to mature
  • tPA is on the surface of endothelial cells
25
Q

what is protein C? 6

A
  • coagulation inhibitor
  • starts as an inactive enzyme
  • made in the liver
  • activated on surface of endothelial cells
  • inactivates factor Va and factor VIIIa
  • works with cofactor protein A to inactivate Va
26
Q

what is antithrombin III? 6

A
  • peptide in blood made by liver
  • blocks the activity of thrombin
  • heparin increases AT III activity
  • heparin is reversible by protamine sulphate
  • AT III deficiency leads to risk of thrombotic disease
  • recombinant form of AT III is used medically for thrombotic disorders
27
Q

what is a vitamin K deficiency? 5

A
  • results in clotting insufficiency
  • rare as vitamin K is made by bacteria of the large intestines and found in leafy green veg
  • caused by GI disease or no fat absorption
  • liver disease- no bile salts
  • warfarin prevents the recycling of vitamin K and depletes the active vitamin K after a few days
28
Q

what is haemophilia A? 5

A
  • clotting disorder
  • affects larger blood vessels
  • wounds that bleed for days due to congenital lack of factor VIII
  • X-linked, so only males have symptoms
  • treat with purified factor VIII (expensive and rare)
  • christmas disease/ haemophilia B is a lack of factor IX, the symptoms are the same
29
Q

what is atherogenesis- a disease of inflammation? 7

A
  • a disease of inflammation
  • monocytes enter lesion and become macrophages and consume cholesterol esters
  • become foam cells
  • die and release contents which attract more monocytes
  • cytokines
  • chemo-attractants
  • inflammation and haemostasis have synergistic effects on each other
30
Q

what is atherogenesis- a disease of lipids? 4

A
  • LDL deposits lipids in lesion
  • cholesterol esters are non-aqueous which can make them solid/hard
  • cholesterol esters are oxidised making oxygen radicals which makes them immunogenic
  • oxidised lipids are consumed by macrophages which become foam cells, which explode, which attract more monoctyes
31
Q

what is atherogenesis- a disease of the endothelium? 3

A
  • endothelium expresses chemoattractant for monocytes to find and enter lesions
  • when endothelium is lost, collagen stimulates coagulation, endothelium normally covers the collagen and the basement membrane
  • when endothelium is lost, the vessel cannot control it dilation as it cannot produce NO
32
Q

explain pharmacological control of blood clotting? 3

A
  • anti-platelet agents block platelet activation which makes it good for treating arterial disease
  • anti-coagulants block production or activity of clotting factors and are used to treat venous disease
  • fibrinolytics are used to dissolve fibrin in arterial disease
33
Q

describe antiplatelet agents? 8

A
  • prevent clotting in arteries where anticoagulants have limited effects
  • used in acute coronary syndromes
  • aspirin is a cyclo-oxygenase (COX) inhibitor
  • blocks the formation of thromboxane A2 in platelets
  • lengthens bleeding time
  • does not increase coagulation time
  • prophylaxis for MI
  • ADP receptor inhibitors= prasugrel/ clopidogrel
34
Q

describe anti-coagulants? 7

A
  • prevent clotting in veins and low-pressure pulmonary system
  • deep vein thrombosis
  • pulmonary embolism
  • heparin inhibit coagulation with ATIII by inhibiting factor Xa
  • novel oral anticoagulants (NOACs)
  • dabigatran (thrombin inhibitor)
  • rivaroxaban (factor Xa inhibitor)
35
Q

describe fibrinolytics? 6

A
  • clotting in arteries (high pressure)
  • used during acute coronary syndromes
  • tissue plasminogen activator (tPA)
  • streptokinase
  • urokinase
  • also called thrombolytic drugs

103-theme 2 (9 decks)

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