Brainscape's Knowledge GenomeTM

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


See full index

CPT > L10 - Antiplatelets > Flashcards

L10 - Antiplatelets Flashcards

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

Venous thrombosis

A
  • associated with stasis of blood +/- damage to the vein
  • high RBC content
  • high fibrin content
  • low platelet content
  • red
  • soft and gelatinous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Arterial thrombosis

A

Forms at site of atherosclerosis following plaque rupture

  • low fibrin content
  • higher platelet content
  • white
  • lines of Zahn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Healthy endothelium

A
  1. Proastacyclin (PGI2) produced and released by endothelium cells
  2. PGI2 binds to the platelet receptors and increases cAMP in platelets
  3. The increased cAMP inhibits the release of sequestration calcium from stores
  4. Less calcium means less platelet aggregation
  5. Less release of platelet aggregatory mediators
  6. Glycoprotein IIb/IIIa receptors remains inactive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Glycoproteins IIb/IIIa

A
  • Integrin receptor complex found on platelets

- binds with fibrinogen and vWF to aid platelet aggregation

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

Platelet activation and aggregation

A
  1. Damage to endothelium e.g. by fibrous cap rupture exposes collagen fibres
  2. Adhesion and activation of platelets
  3. Chemical mediators are released by platelets granules e.g. thromboxane A2, ADP, serotonin, thrombin and platelet activation factor
  4. Further cascade of platelet aggregation as GP IIb/IIIa are activated which binds to fibrinogen and another platelet
  5. Ca2+ is released from its stores and cAMP decreases in platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Drug type for arterial and venous thrombi

A

Arterial thrombi: platelet rich, white

  • anti-platelet drugs
  • lesser extent fibrinolysis drugs

Venous thrombi: loser platelet content, red

  • parenteral anticoagulants - heparin
  • oral anticoagulants - warfarin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Secondary prevention in acute coronary syndrome

A

Combination of both anticoagulants, antiplatelets and fibrinolytics

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

Aspirin mechanism of action

A

Cyclo-oxygenase inhibitor

  • inhibits COX-1 mediated production of thromboxane A2 and irreversibly reduces platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why does aspirin not completely inhibit platelet aggregation

A

There are other methods that platelets use to aggregate, independent of COX 1

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

COX 1

A

Normally converts arachidonic acid into prostaglandin H2

Prostaglandin H2 is converted to thromboxane A2

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

Where is arachidonic acid produced from

A

Produced and accumulates around the phospholipid membrane

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

Dose actions of aspirin

A

Low dose - inhibits platelet aggregation

High dose

  • loading dose
  • analgesic
  • inhibits prostacyclin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Absorption of aspirin

A

Passive diffusion - hepatic hydrolysis when metabolised to salicylic acid

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

Side effects of aspirin

A

Prolonged bleeding time

  • haemorrhagic stroke
  • GI bleeding
  • peptic ulcers - to lesser extent
  • Reye’s syndrome
  • hypersensitivity
  • early closure of the ductus arteriosus in the 3rd trimester
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Reye’s syndrome

A

Occurs after a viral infection in children given aspirin
Can be fatal
Causes oedema and hepatic issues

Therefore do not give aspirin to children under 16

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

Cautionary measures with aspirin

A

Taken with other antiplatelets and and anticoagulants

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

Why does inhibitory effects of aspirin last the lifespan of a platelet (7-10 days)?

A

Platelets do not have nuclei therefore cannot reproduce COX - 1

18
Q

COX 1 polymorphism

A

Can cause lack of efficacy

May not acetylate COX 1 therefore reduces efficacy

19
Q

When is aspirin used?

A

In secondary prevention of:

  • stroke - initial 300mg daily for 2 weeks
  • TIA
  • acute coronary syndrome - initial once only chewable loading dose
  • MI in stable angina or peripheral vascular disease

Used in:
- post primary percutaneous coronary intervention (PCI) and stents to reduce ischaemic complications

20
Q

What is also given with long term aspirin?

A

PPI e.g. omeprazole form gastric protection

21
Q

ADP receptor antagonist examples

A

Clopidogrel
Prasugrel
Ticagrelor

22
Q

ADP receptor antagonists

A

Inhibits binding of ADP to P2Y12 receptor on platelets therefore less calcium release from stores, inhibiting the activation of GP IIb/IIIa receptors

(Independent of COX -1)

23
Q

Clopidogrel and prasugrel

A

Irreversible inhibitors of P2Y12

Pro drugs - require hepatic metabolites to activate them (CYPS)

24
Q

Onset speed for ADP receptor antagonists

A

Clopidogrel - slow onset of action without loading dose
Prasugrel - rapid onset but slower than ticagrelor
Ticagrelor - rapid onset (1-2 hours)

25
Q

Ticagrelor

A

Acts reversibly at different sites to clopidogrel

Has active metabolites

26
Q

Side effects of ADP receptor antagonists

A
  • Bleeding
  • GI upset - dyspepsia and diarrhoea
  • possible thrombocytopenia
  • clopidogrel needs stopping 7days prior to surgery
27
Q

Cautions with ADP receptor antagonists

A

Renal and hepatic impairment - due to excretion and activation

Clopidogrel requires CYPs for activation therefore (CYP inhibitors)

  • omeprazole
  • ciprofloxacin
  • erythromycin
  • SSRI

Ticagrelor can interact with CYP inhibitors and inducers

Co-prescribed with other antiplatelets and anticoagulant agents or NSAIDS

28
Q

When are ADP receptor antagonists used?

A
  • clopidogrel is used as monotherapy when aspirin is contraindicated
  • NSTEMI patients - up to 12months
  • STEMI with stent - up to 12 months

Long term secondary prevention for:

  • ischaemic stroke
  • TIA

Prasugrel with aspirin in ACS patients undergoing PCI for up to 12 months

29
Q

Glycoprotein IIb/IIIa inhibitors example

A

Abciximab - monoclonal antibody

Given as IV with bolus

30
Q

Glycoprotein IIb/IIIa inhibitor mechanism of action

A

Blocks the glycoproteins IIb/IIIa receptors therefore blocks the binding of fibrinogen and vWF to GP IIb/IIIa

Therefore inhibits aggregation of platelets at the terminal step - better efficacy

31
Q

Side effects and cautions of abciximab

A
  • bleeding (highest risk) - dose adjustments with body weight
  • thrombocytopenia
  • hypotension
  • bradycardia

Caution with other antiplatelets and anticoagulants
Specialist use in high risk percutaneous transluminal coronary angioplasty patients

32
Q

Phosphodiesterase inhibitor example

A

Dipyridamole

33
Q

Phosphodiesterase inhibitor mechanism

A

Inhibits the cellular reuptake of adenosine
Increased plasma adenosine
Inhibits platelet aggregation via A2 receptors

Also:
Prevents cAMP degradation
Less calcium released from stored
Less GP IIb/ IIIa receptor activation

34
Q

Side effects and cautions of dipyridamole

A

Flushing
Headache
Hypersensitivity

Caution with:

  • antihypertensives (higher adenosine plasma conc)
  • antiplatelets
  • anticoagulants
35
Q

Uses of dipyridamole

A

Secondary prevention of ischaemic stroke and TIAs

Adjunct for prophylaxis of thromboembolism following valve replacement

36
Q

Fibrinolytic agents

A

Streptokinase - promotes plasminogen expression
Alteplase - plasminogen activator

Plasmin causes fibrinolysis of a fibrin clot into fibrin degradation products

37
Q

Fibrinolysis inhibitor

A

Tranexamic acid

38
Q

When is Alteplase used

A

In acute ischaemic stroke - less that 4.5 hours

39
Q

Side effects of fibrinolytics

A

Bleeding

40
Q

Why can streptokinase only be used once?

A

Developed from streptococci therefore body will produce antibodies

CPT (23 decks)

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