Brainscape's Knowledge GenomeTM

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


See full index

Y2 - CPT > Lecture 11 - Antiplatelets And Fibrinolytics > Flashcards

Lecture 11 - Antiplatelets And Fibrinolytics Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

What are 2 examples of bleeding disorders?

A

Haemophilia (A and B)
Von Wille Brand disease

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

What is haemophilia A?

A

Dysfunction or absence of clotting factor VIII

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

What is haemophilia B?

A

Dysfunction or absence in clotting factor IX

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

What is Von Willebrand disease?

A

Dysfunction or absence of Von willebrand factor
Von willebrand factor allows platelets to adhere to blood vessel walls for clots to form

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

What is a thrombus?

A

A clot adhered to a vessel wall

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

What is an embolus?

A

An intravascular clot distal to the site of origin

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

What are some common thromboembolic disease?

A

DVT
PE
Can be caused by AF

Can lead to TIA, iscahmic stroke and MI

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

What part of the atria do thrombi most commonly form in atrial fibrillation?

A

Oracles

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

What usually causes venous thrombosis?

A

Stasis of blood
Damage to the veins

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

What usually causes arterial thrombosis?

A

Atherosclerotic plaque rupture

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

What are usually the contents of a venous thrombus?

A

High red cell count
High fibrin
Low platelet content EVENLY DISTRIBUTED

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

What are usually the contents of an arterial thrombus?

A

Lower fibrin content
Much higher platelet

Appearance has Lines Of Zahn

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

What is the triad that increases the risk of thrombosis?

A

Virchows triad

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

What is the triad for virchows traid?

A

Increased coagulability
Blood vessel injury
Reduced blood flow (Stasis)

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

What can causes blood stasis?

A

A fib
Long distance travel
Varicose veins
Immobility

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

What can cause increased blood coagulability?

A

Sepsis
Smoking
Coagulation disorders
Malignancy

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

What can cause blood vessel injury?

A

Trauma
Invasive procedures
Hypertension

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

What substance does healthy endothelium produce which inhibits platelet aggregation?

A

PGI2 (prostacyclin)

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

What is the action of PGI2 (prostacyclin) produced by healthy endothelium?

A

Inhibits platelet aggregation

PGI2 binds to platelet receptors causing increased cAMP in platelets
High cAMP in platelets leads to low Ca2+ in platelets
Low Ca2+ prevents platelet aggregation and keeps platelet aggregators agents low

This stabilises the GPIIb and GPIIIa receptors on the platetlet surface

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

Where are GPIIb/IIIa receptors located?

A

On surface of platelets

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

What is the lifespan of a platelet?

A

8-10 days

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

How can atherosclerosis lead to thrombus formation?

A

Fibrous cap thin, plaque ruptures and clotting factors released

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

How do platelets become activated?

A

Bind to exposed collagen fibres and release platelet granules contains ADP, Thromboxane A2, platelet activation factor and thrombin

This leads to increased calcium and decreased cAMP in platelet

The inc calcium activates GPIIb/IIIa receptors and fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does omega 3 fish oils help prevent thrombus formation?

A

Contains substance that acts like PGI2 so prevents platelets adhering to endothelium

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

What colour are platelet rich arterial thrombi?

A

White

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What type of drugs are given for arterial thrombi?

A

Anitplatelet
Fibrinolytics

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

What type are drugs are given for lower platelet content Red VENOUS thrombi?

A

Parenteral anticoagulants like heparins and oral anticoagulants like warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What type of drug is aspirin?

A

COX inhibitor (Cyclo-oxygenase inhibitor)

Antiplatelelt

29
Q

How does Aspirin work as an antiplatelet?

A

Inhibits COX1 production of Thromboxane A2 so leads to irreversible platelet aggregation

30
Q

Why does aspirin not completely inhibit all platelet aggregation?

A

Only prevents Thromboxane A2 production from COX

Their are other aggregating factors

31
Q

What is a low non-analgesic dose of aspirin?

A

75mg

32
Q

What is a loading dose of aspirin used in acute coronary syndromes?

A

300mg

33
Q

What dose aspirin do at its low 75mg dose?

A

Anti-platelet aggregation

No analgesic effect

34
Q

How can higher doses of aspirin affect PGI2?

A

Can inhibit it (bad?)

35
Q

How is aspirin normally absorbed?

A

Passive diffusion

36
Q

1.) What type of drug is aspirin?
2.) what is it used for?
3.) MoA?
4.) Adverse effects?
5.) Contra-indications?
6.) Drug-drug interaction?

A

1.) COX inhibitor
1.) antiplatelet aggregation
3.) prevents COX producing Thromboxane A2 which normally helps elevate platelet Ca2+ contetn leading to aggregation
4.) GI irritation, GI bleeding (peptic ulcer), haemorrhagic stroke, aspirin hypersensitivity
5.) Reye’s syndrome
Aspirin hypersensitivity
3rd. Trimester of pregnancy leads to closure of ductus Arterioles
6.) other antiplatelets and anticoagulants

37
Q

What is given to help close ductus arteriosus?

A

Ibruprofen

38
Q

What is given to help keep ductus arteriosus open?

A

Prostaglandins

39
Q

Why does the antiplatelet effect of aspirin last the life span of a platelet so 7-10 days?

A

The dont have nuclei so cant make more Thromboxane A2

40
Q

When is aspirin given?

A

AF patients post stroke
Secondary prevention of stroke and TIA
2ndary prevention of Acute Coronary syndromes
Post primary percuatneous coronary intervention and stent

41
Q

What type of drug is given alongside long term use aspirin?

A

Proton pump inhibitors like omeprazole for gastric protection

42
Q

What doses of aspirin are given for NSTEMI and STEMI?

Acute ischamic stroke?/

A

NSTEMI/STEMI = 1 300mg loading dose

Acute ischameic stroke = initial 300mg daily for 2 weeks

43
Q

What are some examples of ADP receptor antagonists?

A

Clopidogrel
Prasugrel
Ticagrelor

44
Q

What is the general mechanism of action of clopidogrel, prasugrel and ticagrelor?

A

ADP receptor antagonists

Prevent ADP binding to P2Y12 which prevents the activation of GPIIb/IIIa receptors

45
Q

What is the difference in the mechanism of action for Clopidogrel and prasugrel compared to ticagrelor?

A

Clopidogrel and prasugrel are irreversible inhibitors of P2Y12
They are also booth prodrugs also need hepatic metabolism

Ticagrelor acts reversibly at a different site

46
Q

How are the ADP receptor antagonists typically taken?

A

Orally

47
Q

1.) What type of drug is clopidogrel, prasugrel and ticagrelor?
2.) what is it used for?
3.) MoA?
4.) Adverse effects?
5.) Contra-indications?
6.) Drug-drug interaction?

A

1.) ADP receptor antagonists
2.) Antiplatelet therapy
3.) Clopidogrel adn prasugrel bind irreversibly to. P2Y12 preventing ADP binding and inhibiting activation of GPIIb/IIIa receptors
Ticagrelor accts reversibly elsewhere

4.) BLEEDING, GI upset, dyspepsia, diarrhoea, rarely thrombocytopenia
5.)high bleedrisk patients with renal or heptaic impairment.

6.) CYP inhibitors (CYP2C19 needed to activate clopidogrel), Omeprazole, ciprofloxacin, erythromycin some SSRIs

Other antiplatelets, anticoagulants or NSAIDs

48
Q

What area the indications for using ADP receptor antagonists?

A

Ischamic stroke (and TIA)
Clopidogrel long term mono therapy where aspirin is contraindicated

NSTEMI take with aspirin
Percutaneous coronary intervention (prasugrel)

49
Q

What is an example of a phosphodiesterase inhibitor?

A

Dipyridamole

50
Q

What is the mechanism of action of dipyridamole (phosphodiesterase inhibitor)?

A

Inhibits cellular reuptake of adenosine leading to increased concentration of adenosine, this inhibits platetlet aggregation via adenosine (A2) receptors

Also prevents cAMP degradation which prevents expression of GPIIb/IIIa

51
Q

1.) What type of drug is dipyridamole?
2.) what is it used for?
3.) MoA?
4.) Adverse effects?
5.) Contra-indications?
6.) Drug-drug interaction?

A

1.) phosphodiesterase inhibotr
2.) secondary prevention of ischameic stroke and TIAs, prophylaxis for thromboembolism following valve replacement
Stroke

3.)inhibits cellular reuptake of adenosine, leads to increased conc of adenosine inhibiting platelet aggregation via adenosine A2 receptors
4.)Vomitng, diarrhoea and dizziness

5.) ???
6.) antiplatelets, anticoagulants and adenosine

52
Q

What is an example of Glycoprotein IIb/IIIa inhibitor?

A

Abciximab

53
Q

What is the mechanism of action of GPIIb/IIIa inhibitors like abciximab?

A

Antibodies block GPIIb/IIIa receptors preventing the binding of fibrinogen and Von Willebrand factor to the GPIIb/IIIa receptors preventing aggregation

54
Q

How is abciximab administered?

A

IV

55
Q

1.) What type of drug is abciximab?
2.) what is it used for?
3.) MoA?
4.) Adverse effects?
5.) Contra-indications?
6.) Drug-drug interaction?

A

1.) GPIIb/IIIa inhibitors
2.) high risk Percutaneous transluminal coronary angioplasty patients with other drugs

3.) antibodies block GPIIb/IIIa receptors preventing fibrinogen and Von Willebrand factor from binding reducing aggregation

56
Q

What is the general mechanism that fibrinolytics work by?

A

Dissolve the fibrin meshwork of thrombus

57
Q

What are 2 examples of fibrinolytic drugs that inhibit the conversion of plasminogen to plasmin?

A

Streptokinase
Alteplase

58
Q

Why can streptokinase only be used once?

A

Antibodies will develop to it other wise since it’s extracted from haemolytic streptococci

59
Q

What type of drug is alteplase?

A

Recombinant tissue plasminogen activator

60
Q

When is aletplase typically I used?

A

Acute ischamic stroke must be given less than 4.5hrs from symptoms

In some following STEMI
PE

61
Q

What is tranexamic acid?

A

Drug which inhibits plasminogen

Given for epistaxis or Haemorrhagia so stops bleeding

62
Q

What are some adverse effects and drug interactions of alteplase and streptokinase?

A

Adverse = bleeding

Drug = antiplatelets and anticoagulants

63
Q

When is Percutaneous coronary intervention used over thrombolytics follwing an STEMI?

A

When presentation is within 12hrs of onset of symptoms and primary PCI can be done within 120mmins of the time where fibrinolytics could have been given

64
Q

What is a negative consequence of PCI following a STEMI?

A

Reperfusion injury

65
Q

What is reperfusion injury?

A

When a tissue becomes re perfused with blood, further damage occurs due to increased production of ROS, inflammatory mediators and plasma membrane disruption

66
Q

What drugs can be given as a secondary prevention of acute coronary syndrome once haemodynamically stable?

A

ACEi (ARBs if ACEi contraindicated)

B blocker
Dual antiplatelet therapy so 75mg aspirin + ADP receptor antagonist (clopidogrel or ticagrelor)

Statin (80mg Atorvastatin starting point)

67
Q

Why do GPIIb/IIIa inhibitors afford more complete anti-platelet aggregation than other agents?

A

Targets the final common pathway

68
Q

What is the overall function of phosphodiesterase

A

Controls the production of secondary messengers like cAMP and cGMP

69
Q

Why are antiplatelet drugs used in secondary prevention of ACS and TIA?

A

Reduce risk of cardiovascular events be preventing platelet aggregation

Y2 - CPT (30 decks)

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