Cardiac Pharmacology Flashcards

1
Q

What are the main side effects of ACEIs?

A
  • Dry cough
  • Hyperkalaemia
  • 1st dose Hypotension
  • Angioedema
  • Renal failure
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2
Q

What are the effects of NSAIDs and Alcohol on ACEIs?

A

NSAIDs antagonise the anti-hypertensive effects

Alcohol can cause a compound hypotensive effect

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3
Q

What is the effect of ACEIs on the glomerular vessels?

A

Vasodilation of the efferent arteriole, lowering eGFR

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4
Q

What are the 3 main classes of CCBs?

A

Dihydropyridines - target the peripheral vessel Ca channels more selectively
Non-dihydropyridines - target the cardiac Ca channels more selectively
Mixed selectivity

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5
Q

Give examples of each of the 3 main classes of CCBs

A

Dihydro: Amlodipine and Nifedipine
Non-dihydro: Verapamil
Mixed: Diltiazem

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6
Q

What are the side effects of CCBs?

A

Dizziness
Peripheral oedema - Amlodipine especially can cause ankle swelling
CI in HF - use non-dihydro

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7
Q

How do Beta blockers reduce production of renin?

A

Blocking the beta 1 receptors in the JGA

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8
Q

What 2 main conditions are Beta blockers typically contraindicated in? Why?

A

Asthma
COPD
Blockage of the B2 receptors, preventing bronchodilation

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9
Q

What are the main side effects of Nitrates?

A

Headache
Dizziness
Palpitations
Tolerance (loss of efficacy)

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10
Q

What is the target INR in most individuals? What does an INR that is too low or too high mean?

A

2-3
Too high = too runny, risk of bleed and haemorrhage
Too low = too sludgy and risk of thrombosis

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11
Q

If anticoagulation is needed in pregnancy, what is the drug of choice?

A

LMWH

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12
Q

In what 3 main circumstances is Warfarin given over DOACs?

A

Metallic heart valve
Severe renal impairment
Anti-phospholipid syndrome

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13
Q

What coagulation factor does Apixaban, Rivaroxaban and Edixaban inhibit? What about Dabigatran?

A

Xa

IIa

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14
Q

What are some of the reasons DOACs are now first line over warfarin?

A
No monitoring required 
Quicker onset and shorter half life 
No need for initiation by heparin 
Fewer interactions 
50% less chance of intracranial bleed 
Lower bleeding risk, especially of major bleeds
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15
Q

How do you reverse DOACs? What about Warfarin?

A

Prothrombin concentrate +/- tranexamic acid

Vitamin K supplement

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16
Q

What are the requirements for stopping DOACs for surgery?

A

24hrs before for minor bleed risk, 48 for major
Same time to wait after before you re-start it
LMWH can be used to bridge if at a particularly high risk of thrombosis

17
Q

What is the mechanism of heparin? What about LMWH?

A

Activation of antithrombin III, which inhibits Thrombin/IIa and Xa
LMWH only inhibits Xa
Allows dissocation and subsequent repeat inhibition

18
Q

Are anti-PLT drugs used for arterial or venous clots? What about anticoagulative drugs?

A

Anti-PLT: arterial

Anticoagulation: venous

19
Q

How do fibrinolytic drugs work? Can you name two examples?

A

Promotes conversion of plasmin into plasminogen on fibrin strands, increasing fibrin and clot breakdown
Alteplase and Streptokinase

20
Q

How do pro-haemostatic drugs work? Can you given an example?

A

Prevent conversion of plasmin into plasminogen (generally).

Tranexamic acid