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week 12 Flashcards

1
Q

what are two tissue factors which aid in platelet adhesion when BVs get damaged

A

subendothelial collagen
von willebrand factor

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2
Q

process of platelet adhesion to damaged blood vessles 4

A

exposed extracellular matrix including subendothelial collagen and von willebrand factor

platelets bind

binding triggers platelet activation resulting in a shape change and granule secretion

glyocprotein IIb/IIIa receptors on platelets bind irreversibly to fibrinogen

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3
Q

role of glycoprotein IIb/IIIa

A

it is activated by platelet activation and allows the irreversible binidng of platelets to fibrinogen

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4
Q

role of ADP in platelet adhesion

A

secreted by activated platelets activating other platelets

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5
Q

role of thromboxane in platelet adhesion

A

diffuses out of activated platelets activating more platelets

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6
Q

what are the four different mechanisms of actions in antiplatelets

A

COX inhibitors
ADP receptor antagonists
Phosphodiesterase inhibitors
GPIIb/IIIA

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7
Q

mechanism of COX inhibitors

A

inhibits COX1 enzyme used to produce thromboxane
therefore reduces platelet activation

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8
Q

mechanisms of ADP receptor antagonists

A

prevents ADP binding to platelets

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9
Q

mechanism of GPIIb/IIA inhibitors

A

prevents activation og GPIIB/IIIA receptors preventing platelet adhesion to fibrinogen

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10
Q

mechanism of phosphodiesterase inhibitors

A

inhibit platelet activation but mechanism unknown

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11
Q

intrinsic pathway of blood coagulation

A

activation of mulitple factors which leads to the activation of factor x

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12
Q

extrinsic pathway of coagulation

A

tissue factor which along with factor 7 activates factor 10

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13
Q

common pathway steps 5

A

factor 10 converted to factor 5

causes activation of factor 2 (prothrombin to thrombin)

thrombin (akak actiavted factor 2) turns factor one into its active form (fibrinogen to fibrin)

fibrin laid on pleatlet plug

stabilised with factor 13 whcih is fibrin stabilising factor

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14
Q

what is factor 2

A

prothrombin

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14
Q

what is factor 1

A

fibrinogen

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15
Q

what is factor 13

A

fibrin stabilising factor

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16
Q

what triggers activation of coagulation 2

A

breach in endothelium
foreign surfaces

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17
Q

process of fibrinolysis 3 steps

A

tissue plasminogen factor released

converts plasminogen into its active form plasmin

breaks down the fibrin

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18
Q

tranexamic acid function and mech

A

inhibits fibrinolysis

it is a competitive inhibitor which binds to plasminogen preventing it from converting to plasmin and binding to fibrin to initiate fibrinolysis

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19
Q

types of anticoagulants 5:

A

antithrombin
protein c
vitamin k anatgonsits
factor 10 inhibitors
direct oral anticoagulants

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20
Q

how does activated protein C cause anticoagulation 3

A

inhibits clotting factors and prothrombinase

produced when thrombin is produced

acts in a negative feedback loop to keep thrombin levels in check

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21
Q

how does activated antithrombin cause anticoagulation

A

neutralises clotting factors

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22
Q

how does vitamin k anatagonists cause anticoagulation 3

A

they inhibit clotting factors which are dependent on vitamin k for synthesis

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23
Q

which clotting factors are affected by vitamin k anatagonists

A

2, 7, 9 and 10

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24
what are the three components of virchow's triad
hypercoaguability blood stasis vascular damage
25
how does pregnancy cause hyperocoagulability
to prevent blood loss there are multiple coagulant mechanisms including: - decreased venous blood flow - increased clotting factors - increased protein c resistance -incr inhibitors of fibrinolysis
26
how does hormone replacement therapy increase coagulation
increases fibrinogen and some clotting factors
27
how does advanced carnioma cause increased coagulation 2ways
venous stasis due to tumour compression some tumours can express tissue factor which activates the extrinsic coagulation pathway
28
heriditary thrombophilic conditions 3
factor 5 leiden mutation activated protein c resistance antithrombin deficiency
29
risk factors of coagulopathies 4
male old age obesity previous venous thrombotic event
30
how can a DVT lead to a PE (define PE)
PE is an embolism which reaches pulmonary ciruclation and then gets occluded DVT can dislodge becoming an embolus and then reach pulmonary circulation to become a PE
31
what is prothrombin time
this is part of an investigatve test which measures how long blood takes to clot it is presented as an INR
32
investigations in diagnosis of coagulopathies 10
1. prothrombin time 2. activated partial thromboplastin time 3. fibrinogen level 4. thrombin time 5. CBE 6. genetic testing 7. antithrombin activity 8. protein c activity 9. blood film 10. VWD and factor 8
33
what is activated partial thromboplastin time
evaluates the clotting function of the intrinsic pathway
34
thrombin time
ability for blood to form a fibrin clot by measuring the time after thrombin addition
35
clinical feature of a venous thrombosis 5
unilateral chest pain due to inflammation peripheral oedema = due to increased fluid erythema due to increased blood flow tenderness due to inflammation rubor due to warmth
36
clinical features of a pulmonary embolism 5
dyspnoea pleuritic chest pain tachycardia haemoptysis syncope
37
different components of blood avaiable for transfusion 4
red cell platelets plasma cryoprecipitate
38
fractionated blood products 3
immunoglobulins albumin clotting factors
39
what is cryprecipitate
supernatant from lightly thawed fresh frozen plasma
40
what are the mandatory testings required when someone donates their blood 4
ABO and RHD blood group red cell antibody screening syphillis screening viral screening
41
what is rhesus blood typing and what does an incompatability mean?
Routine rhesus typing is done to test for the absence or presnece of D antigen RHD + means present RHD - means absent
42
complications of a blood transfusion 6
haemolytic reaction allergic reaction infection transmission iron overload volume overload febrile non haemolytic reaction
43
what are the three pillars of patient blood management
optimising haemoglobin minimising blood loss appropriate transfusion
44
what happens as a result of volume overload in an iron transfusion 2
too much fluid too quickly resulting in: - congestive heart failure - pulmonary oedema
45
what is febrile non maermolytic reaction in blood transfusion complication
immune response to the white blood cells in the transfused blood
46
what is primary haemostasis bleeding disorder (give three examples)
platelet disorders affected the platelet plug formation including thrombocytopenia platelet dysfunction von Willebrand factor deficiency
47
what is secondary haemostasis bleeding disorder (give two examples)
affects the fibrin mesh formation and clotting cascade heriditary = haemophilia medication induced
48
what is increased clot degredation bleeding disorder (2)
hyperfibrinolysis causes include: hereditary prostate cancer
49
causes of acquired bleeding disorders 7
cancer disseminated intravasuclar coagulation drug related thrombocytopenia immune thrombocytopenia purpura renal failure myeloma and lymphoma
50
how does disseminated intravascular coagulation work 2
characterised by systemic coagulation activation causing: - fibrin clots formation - consumption of platelets and coag factors
51
how does immune thrombocytopenia purpura work
autoimmune disorder characterised by igG antibodies which destroy platelets
52
inherited bleeding disorders 3
von willebrand disease haemophilia a and b
53
what is the most common bleeding disorder
von willebrand disease
54
what is haemophilia a deficiency of
factor 8
55
what is haemophilia b a deficiency of
factor 9
56
clinical features with bleeding disorders 6
bruising purpura bleeding post surgery menorrhagia haematuria epistaxis
57
what are the two functions of von willebrand factor
platelet adhesion prevention of factor 8 degredation
58
anticoagulants 5
heparins vitamin k antagonists DOACs: apixaban, rivaoxaban Dabigatran
59
example of thrombolytic agent
tPA (tissue plasminogen activator) catalyses plasminogen conversion to plasmin increasing fibrinolysis
60
what is factor replacement therapy and what three are done
re-supply clotting factors to prevent/treat haemorrhage/internal bleeding the three diseases treated are: vWF deficiency haemophilia a haemophilia b
61
contraindications generally for anticoagulants and antiplatelets 3
active/recent haemorrhage recent surgery severe thrombocytopenia
62
complications of oral antiplatelets (2 examples of these drugs)
ex. aspirin, tricagrelor bleeding, Gi ulceration
63
unfractionated heparin characteristics 6
administered intravenously fully reversible independent of renal failure more complex dosage requires frequent monitoring high risk of HITS
64
Low molecular weight heparin 3
subcutaneous injection partially reversible longer half life
65
side effects of heparins 4
bleeding Heparin induced thrombocytopenia syndrome = HITS alopecia osteoporosis
66
what are the two types of ways that one can give heparin in terms of aim of procedure
prophylactic: prevention of VTE therapeutic: treatment of VTE
67
warfarin when is it used 2
in severe kidney disease and in patients with a mechanical heart valve
68
side effects of warfarin 4
high drug interactions high bleeding risks alopecia liver dysfunction
69
to whom do we not give warfarin to
when pregnant
70
key DOACS
apixaban and rivaroxaban
71
limitation of DOACs 3
cant give to pregnant cant give in severe renal failure no reversal mechanisms
72
benefits of DOACs
few drug interactions simple dosages low bleeding risk
73
desmopressin
releases endothelial stored coagulation factors including: von willebrand factor factor 8
74
heparin function 3
activates antithrombin inhibits factor ten inhibits thrombin
75
what are the tests to do in coagulopathies 11
vWF and subendoethlila collagen tests CBE Blood film Prothrombin time activated partial thromboplastin time Thrombin time Fibrinogen level antibody testing genetic testing protein c activity
76
what are 3 thrombophilic conditions
factor V leiden mutation active protein c resistance antithrombin deficiency

M1 (13 decks)

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