Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LCRS Pharma > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

examples of pro-coagulants (plasma)

A

prothrombin
F5, F7-F13
fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

examples of anti-coagulants (plasma)

A

plasminogen
TFPI (Tissue Factor Pathway Inhibitor)
Protein C & S
anti-thrombin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why does surgery make you susceptible to thrombosis?

A

immobility post-op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the difference between a red thrombus and a white thrombus?

A

red thrombus:

  • veins
  • high in fibrin content (fat clot)
  • form in the vessel lumen

white thrombus:

  • arteries
  • high in platelets (hence use of antiplatelets)
  • within atherosclerotic plaque i.e. within the endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the 3 components of Virchow’s Triad?

A

1) rate of blow flow (stasis)
2) consistency of blood(coagulability)
3) blood vessel wall integrity (wall injury)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does rate of blow flow affect thrombosis?

A

slow flow means that anti-coagulant factors are not replenished and promotes coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does consistency of blood affect thrombosis?

A

If there is an imbalance in the pro and anti-coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does blood vessel wall integrity affect thrombosis?

A

damage to the wall causes exposure of collagen to pro-coagulation factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the three steps in coagulation?

A

1) Initiation – small scale production of thrombin.
2) Amplification – large scale production of thrombin (on platelet surfaces).
3) Propagation – generation of fibrin strands by thrombin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what targets the initiation step?

A

anti-coagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what targets the amplification step?

A

anti-platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what targets the propagation step?

A

thrombolytics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does the Two-level Well score determine?

A

the higher the score, the more likely for thrombosis to occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does the D-dimer test detect and determine?

A

it detects fibrin breakdown products

a positive tests determine DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what occurs during the initiation step in coagulation?

A

1) Tissue Factor presenting cells activate F10 and F5 forming the prothrombinase complex.
2) the prothombinase complex activates F2 (pro-thrombin) into F2a (thrombin)
3) F2a (thrombin) and F10a is inactivated by anti-thrombin (AT-III)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what makes up the prothrombinase complex?

A

F5a and F10a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the anti-coagulant drugs that can target “initiation”?

A

o Dabigatran – inhibits thrombin.
o Rivaroxaban – inhibits F10a.
o Heparin – activates AT-III.
o Warfarin – vitamin k antagonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is dabigatran?

A

direct oral anticoagulant
–>inhibits thrombin
oral

not used often due to GI bleeding side effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is rivaroxaban?

A

direct oral anti-coagulant
- ->inhibits F10a
oral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is heparin?

give an example of a heparin

A

activates antithrombin-III
e.g. dalteparin
IV, SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

name a LMW heparin.

A

dalteparin (given SC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is warfarin?

A

vitamin K epoxide reductase inhibitor/antagonist

vitamin K creates F2, 7, 9, 10 and therefore is considered an indirect acting drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the indications for the use of anti-coagulants?

A
  • VTE
  • DVT and PE
  • thrombosis during surgery
  • atrial fibrillation (prophylaxis to stroke)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what occurs in amplification stage?

A

1) thrombin (produced in large scale) activates platelets in a +ve FB effect
2) activated platelets change shape and become sticky causing aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe the platelet activation process

A
  1. Thrombin binds to the PAR (Protease Activated Receptor).
    - thrombin is that protease
  2. PAR activation causes a rise in intracellular [Ca2+].
  3. Raised [Ca2+] causes exocytosis of ADP from dense granules.
  4. ADP binds to another platelet’s P2Y12R, having auto- and paracrine effects, activating platelet.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does activation of PAR lead to alongside the rise in intracellular calcium?

A

liberates arachidonic acid (AA) which is turned into TXA2 by COX enzymes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the role of TXA2 in platelet aggregation?

A

induces the expression of GlpIIb/IIIa integrin receptor, which enables aggregation

28
Q

what converts AA into TXA2?

A

COX enzymes

29
Q

what are the anti-platelet drugs that can be used in “amplification”?

A

o Clopidogrel – ADP/P2Y12R antagonist.
o Aspirin – irreversible COX1 inhibitor.
o Abciximab – Glp2b/3a antagonist.

30
Q

what is Clopidogrel?

what is its mechanism of action?

A
  • anti-platelet
  • ADP/P2Y12R antagonist
  • competes with ADP, produced by platelet, for the P2Y12 receptor
  • prevents platelet activation

oral

31
Q

what is aspirin?

what is its mechanism?

A

irreversible COX1 inhibitor:

  • covalent binding to COX-1
  • reduces the production of TXA2
  • no activation of platelet as a result

aspirin is also an NSAID
oral
lower doses have fewer side effects and can be just as effective as higher doses

32
Q

what is abciximab?

A
  • anti-platelet
  • GlpIIIa/IIb antagonist
  • monoclonal antibodies that target the integrin receptors
  • prevents platelet aggregation

IV, SC
have limited, specialist uses

33
Q

what are the indications for the use of anti-platelet drugs?

A

o Acute coronary syndromes – MI.

o Atrial fibrillation – prophylaxis of strokes.

34
Q

what happens in the propagation step?

A

1) activated platelets cause the large scale production of thrombin
2) the thrombin binds to fibrinogen and converts it to fibrin strands

35
Q

why are thrombolytics used in “propagation” and what are the drugs?

A

Anticoagulants and antiplatelet drugs do not remove pre-formed clots, thrombolytics will.

Alteplase – recombinant tissue-type plasminogen activator (rt-PA).

36
Q

what is alteplase?

what is its mechanism of action

A
  • thrombolytic
  • recombinant tissue plasminogen activator analogue.
  • Converts plasminogen to plasmin which then degrades fibrin and dissolves the clot.

IV

37
Q

what are the indications for the use of thrombolytics?

A
  • arterial thrombi
  • VTE
  • stroke (first line)
  • ST elevated MI (more serious than NSTEMI)
38
Q

what can a red thrombus cause and what a white thrombus cause?

A

red thrombus –> DVT

white thrombus–> NSTEMI and STEMI

39
Q

what is DVT?

what is it caused by?

A

red thrombus of the deep veins of the leg (e.g. popliteal vein)
Caused by stasis of blood and damage to endothelium

40
Q

how is a DVT managed?

A

Reduce levels of anticoagulant factors – anticoagulants.

E.G. Dabigatran, Rivaroxaban, Heparin, Warfarin.

41
Q

what is the difference between NSTEMI and STEMI?

A

NSTEMI caused by a partially occluded coronary artery

STEMI is caused by a fully occluded coronary artery

42
Q

drug: target
- clopi
- aspirin
- Abciximab

A
  • P2Y12R
  • COX-1
  • GlpIIb/IIIa
43
Q

what causes the white thrombus in STEMI and NSTEMI?

A

1) Atheroma formation.
2) Damage to endothelium.
3) Platelet aggregation–> thrombus

44
Q

how is NSTEMI managed?

A

Reduce lipid formation and platelet aggregation/activation

use antiplatelets:

E.G. Clopidogrel, aspirin, Abciximab.

45
Q

how is STEMI managed?

A

Reduce lipid formation, platelet aggregation/activation and dissolve thrombus

use antiplatelets and thrombolytics:

  • APs – Clopidogrel, aspirin, Abciximab.
  • TLs – Alteplase.
46
Q

why is a CT scan important in stroke in an emergency?

A

to eliminate haemorrhagic stroke (bleeding) or determine ischaemic stroke

47
Q

what treatment would ischaemic stroke receive?

A

alteplase therapy

48
Q

what is the role of plasminogen?

A

converted to plasmin which degrades fibrin strands

too much plasmin can however cause excessive bleeding

49
Q

what is the treatment for a suspected clot?

A

thrombolytics

50
Q

what is the treatment for predicted clot in the venous system?

A

anti-coagulants

51
Q

what is the treatment for predicted clot in the arterial system?

A

antiplatelets

52
Q

summary of disease and drugs:

1) anti-coagulant
2) antiplatelets
3) thrombolytics

A

1) DVT, PE, AF
2) stroke, acute coronary syndromes, AF, AAneurysm, peripheral arterial disease
3) stroke, acute coronary syndromes, PE

53
Q

what are the arterial and venous disease?

A

arterial:
- stroke
- acute coronary syndromes
- AF
- aortic aneurysm
- peripheral arterial disease

venous:

  • DVT
  • PE
54
Q

what conversion that warfarin prevent?

A

2,7,9,10

reduced vitamin K epoxide is needed to convert glutamate to gamma-carboxyglutamate

55
Q

what is NSTEMI?

A

Non-ST-elevated MI due to partially occluded coronary artery

56
Q

how is NSTEMI treated?

A

aspirin
clopidogrel
heparin tp reduce DVT risk

57
Q

what is STEMI?

A

ST elevated MI

fully occluded coronary artery

58
Q

how is STEMI treated?

A

aspirin
clopidogrel
thrombolysis (if onset within 12 hours)

59
Q

what is the logic behind using anti-platelets for acute coronary syndrome?

A

prevent further thrombus formation

thrombus formation makes use of platelets

60
Q

what is aspirin, an anti-platelet, used for?

A

strokes
MI
aortic aneurysm
atrial fibrillation

61
Q

what are the side effects of aspirin?

A
  • gastric irritation and ulceration
  • bronchospasm (PGE2 made by COX-1)
  • prolonged bleeding
  • nephrotoxicity
62
Q

name a thrombolytic

A

alteplase (tPA)

63
Q

name 3 anti-platelet drugs

A

aspirin
clopidogrel
abciximab

64
Q

what are anti-platelets used for generally?

A

arterial disease

e.g. strokes and heart attacks

  • blood here is usually faster so coagulation risk due to stasis is not an issue
  • once a clot has formed, its growth further is the problem
65
Q

what are anticoagulants used for generally?

A

venous disease
disease of static blood

e.g. atrial fibrillation, DVT, PE

66
Q

what are the exceptions in the use of anti-platelets and anticoagulants?

A

Antiplatelets are still often given for stroke prevention in people with AF, despite anticoagulants being superior at preventing stroke compared to aspirin in AF

Anticoagulants are given in stroke and ACS if the patient has AF or is being kept in hospital and so is at risk of DVT

67
Q

what does the suffix “-ban” mean?

A

inhibits factor 10a

LCRS Pharma (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions