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M1 > week 12 > Flashcards

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
Q

what are the three components of virchow’s triad

A

hypercoaguability
blood stasis
vascular damage

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25
Q

how does pregnancy cause hyperocoagulability

A

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

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26
Q

how does hormone replacement therapy increase coagulation

A

increases fibrinogen and some clotting factors

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27
Q

how does advanced carnioma cause increased coagulation 2ways

A

venous stasis due to tumour compression

some tumours can express tissue factor which activates the extrinsic coagulation pathway

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28
Q

heriditary thrombophilic conditions 3

A

factor 5 leiden mutation
activated protein c resistance
antithrombin deficiency

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29
Q

risk factors of coagulopathies 4

A

male
old age
obesity
previous venous thrombotic event

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30
Q

how can a DVT lead to a PE (define PE)

A

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
Q

what is prothrombin time

A

this is part of an investigatve test which measures how long blood takes to clot

it is presented as an INR

32
Q

investigations in diagnosis of coagulopathies 10

A
  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
Q

what is activated partial thromboplastin time

A

evaluates the clotting function of the intrinsic pathway

34
Q

thrombin time

A

ability for blood to form a fibrin clot by measuring the time after thrombin addition

35
Q

clinical feature of a venous thrombosis 5

A

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
Q

clinical features of a pulmonary embolism 5

A

dyspnoea

pleuritic chest pain

tachycardia

haemoptysis

syncope

37
Q

different components of blood avaiable for transfusion 4

A

red cell
platelets
plasma
cryoprecipitate

38
Q

fractionated blood products 3

A

immunoglobulins
albumin
clotting factors

39
Q

what is cryprecipitate

A

supernatant from lightly thawed fresh frozen plasma

40
Q

what are the mandatory testings required when someone donates their blood 4

A

ABO and RHD blood group

red cell antibody screening

syphillis screening

viral screening

41
Q

what is rhesus blood typing and what does an incompatability mean?

A

Routine rhesus typing is done to test for the absence or presnece of D antigen

RHD + means present
RHD - means absent

42
Q

complications of a blood transfusion 6

A

haemolytic reaction

allergic reaction

infection transmission

iron overload

volume overload

febrile non haemolytic reaction

43
Q

what are the three pillars of patient blood management

A

optimising haemoglobin
minimising blood loss
appropriate transfusion

44
Q

what happens as a result of volume overload in an iron transfusion 2

A

too much fluid too quickly resulting in:
- congestive heart failure
- pulmonary oedema

45
Q

what is febrile non maermolytic reaction in blood transfusion complication

A

immune response to the white blood cells in the transfused blood

46
Q

what is primary haemostasis bleeding disorder (give three examples)

A

platelet disorders affected the platelet plug formation including
thrombocytopenia
platelet dysfunction
von Willebrand factor deficiency

47
Q

what is secondary haemostasis bleeding disorder (give two examples)

A

affects the fibrin mesh formation and clotting cascade
heriditary = haemophilia
medication induced

48
Q

what is increased clot degredation bleeding disorder (2)

A

hyperfibrinolysis
causes include:
hereditary
prostate cancer

49
Q

causes of acquired bleeding disorders 7

A

cancer
disseminated intravasuclar coagulation
drug related
thrombocytopenia
immune thrombocytopenia purpura
renal failure
myeloma and lymphoma

50
Q

how does disseminated intravascular coagulation work 2

A

characterised by systemic coagulation activation causing:
- fibrin clots formation
- consumption of platelets and coag factors

51
Q

how does immune thrombocytopenia purpura work

A

autoimmune disorder characterised by igG antibodies which destroy platelets

52
Q

inherited bleeding disorders 3

A

von willebrand disease
haemophilia a and b

53
Q

what is the most common bleeding disorder

A

von willebrand disease

54
Q

what is haemophilia a deficiency of

A

factor 8

55
Q

what is haemophilia b a deficiency of

A

factor 9

56
Q

clinical features with bleeding disorders 6

A

bruising
purpura
bleeding post surgery
menorrhagia
haematuria
epistaxis

57
Q

what are the two functions of von willebrand factor

A

platelet adhesion
prevention of factor 8 degredation

58
Q

anticoagulants 5

A

heparins
vitamin k antagonists
DOACs: apixaban, rivaoxaban
Dabigatran

59
Q

example of thrombolytic agent

A

tPA (tissue plasminogen activator) catalyses plasminogen conversion to plasmin increasing fibrinolysis

60
Q

what is factor replacement therapy and what three are done

A

re-supply clotting factors to prevent/treat haemorrhage/internal bleeding

the three diseases treated are:
vWF deficiency
haemophilia a
haemophilia b

61
Q

contraindications generally for anticoagulants and antiplatelets 3

A

active/recent haemorrhage
recent surgery
severe thrombocytopenia

62
Q

complications of oral antiplatelets (2 examples of these drugs)

A

ex. aspirin, tricagrelor
bleeding, Gi ulceration

63
Q

unfractionated heparin characteristics 6

A

administered intravenously
fully reversible
independent of renal failure
more complex dosage
requires frequent monitoring
high risk of HITS

64
Q

Low molecular weight heparin 3

A

subcutaneous injection
partially reversible
longer half life

65
Q

side effects of heparins 4

A

bleeding
Heparin induced thrombocytopenia syndrome = HITS
alopecia
osteoporosis

66
Q

what are the two types of ways that one can give heparin in terms of aim of procedure

A

prophylactic: prevention of VTE
therapeutic: treatment of VTE

67
Q

warfarin when is it used 2

A

in severe kidney disease and in patients with a mechanical heart valve

68
Q

side effects of warfarin 4

A

high drug interactions
high bleeding risks
alopecia
liver dysfunction

69
Q

to whom do we not give warfarin to

A

when pregnant

70
Q

key DOACS

A

apixaban and rivaroxaban

71
Q

limitation of DOACs 3

A

cant give to pregnant
cant give in severe renal failure
no reversal mechanisms

72
Q

benefits of DOACs

A

few drug interactions
simple dosages
low bleeding risk

73
Q

desmopressin

A

releases endothelial stored coagulation factors including:
von willebrand factor
factor 8

74
Q

heparin function 3

A

activates antithrombin
inhibits factor ten
inhibits thrombin

75
Q

what are the tests to do in coagulopathies 11

A

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
Q

what are 3 thrombophilic conditions

A

factor V leiden mutation
active protein c resistance
antithrombin deficiency

M1 (13 decks)

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