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Pharmacology > Anti-anginal & Anti-thrombotic > Flashcards

Anti-anginal & Anti-thrombotic Flashcards

1
Q

Nitrates

A 
Anti-angina
Immediate sxs relief & prevention
Relaxation of vascular sm 
Venous dilation
Reduced preload
Reduced O2 consumption
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2
Q

Nitrate side effects

A

Hypotension
Headache
Flushing
Light headedness

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3
Q

Nitrates; specific agents

A

Nitroglycerin

Isosorbide mononitrate

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4
Q

Isosorbide Mononitrate

Indication

A

Angina pectoris

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5
Q

Isosorbide mononitrate

Contraindication

A

Avoid use with PDE-5 inhibitors

Ie. sildenafil

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6
Q

Isosorbide mononitrate

Pharmacokinetics

A

Onset time: 30-40min
Duration of action: >6hrs (IR), 12-24hr(ER)

Metabolism: extensive first pass metabolism in the liver
Some non-hepatic metabolism via rbcs and vascular walls

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7
Q

Natural things with hypotensive properties enhance the effects of nitrates… some of these include:

A

Coleus - additive coronary vasodilation
Hawthorn - additive coronary vasodilation
L-citrulline (converted to L-arginine) - additive coronary vasodilation
NAC - sever hypotension, intolerable HA, antocoagulation

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8
Q

Are nitrates more specific to arterial or venous blood?

A

Venous

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9
Q

Beta Blockers

A

Blocks beta adrenergic receptors

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10
Q

Beta blocker side effects

A

Bradycardia
Heart block
HA
Fatigue

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11
Q

beta blocker interactions

A

Avoid use with intrinsic sympathomimetic activity

ISA - aka partial agonist

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12
Q

Beta 1 receptors

Beta2 receptors

A

B1 - Found primarily on the heart
B2 - lungs, but also the heart
B3 - adipose tissue and heart

(At high doses, selective beta blockers become non-selective)

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13
Q

Why should you not discontinue beta blockers abruptly and instead taper down gradually?

A

Abrupt discont. Leads to reflex tachycardia

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14
Q

CNS adverse effects of beta blockers

A

Dizziness, fatigue, depression

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15
Q

Metoprolol
Which receptors does it bind?
what are its specific indications?
When should it be avoided?

A

Beta blocker
Cardioselective (B1) competitive antagonist

Indications: MI, CHF, angina, HTN

Avoid: ppl with heart block or severe bradycardia (HR<60)

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16
Q

Atenolol

Receptors?
Specific indications?
Avoid when?
Major interactions?
Major concerns?
A

cardioselective (b1) BB, competative antagonist

Indicated for MI, HTN, angina

Avoid: heart block, severe bradycardia

Metabolism: limited hepatic

Major interaction with apples (reduced atenolol interactions)

Concerns: higher mortality than with other BBs … except when it comes to silent ischemia, then atenolol has greater benefit

17
Q

Propranolol

Receptors?
Indications?
Avoid?
Metabolism pathways?
Interactions?
A

Nonselective (b1&2) BB

Indications: MI (tx and prevent), HTN, angina, migraine prophylaxis, supraventricular arrythmias

Avoid: heart block, severe bradycardia

Metabolism: CYPs

Interactions: indian snakeroot (enhances propranolol), St. John’s Wort (increased metabolism)

18
Q

Carvedilol

A

Nonselective (A1 adrenergic blockade activity)

Indications: MI, HTN, CHF, angina (off label use)

Avoid: heart block, severe bradycardia

Metab: CYPs

Interactions: grapefruit juice

19
Q

Which BBs are more likely to interact with beta-agonists used in asthma?

A

???/

20
Q

Which BB covers both beta and alpha receptors?

A

??

21
Q

Calcium Channel blockers

A

Blocks Ca influx thus leading to smooth muscle relaxation

For prophylactic tx, decrease BP, dilate coronary bv, dilates peripheral bv

Sides effects = tachycardia, edema, HA, fatigue, exercise intolerance, hypotension

The agents differ based on their selectivity towards dihydropyridine (DHP) receptors which are predominantly found in the periphery

Second line therapy for angina, first line for other conditions like variant angina

Abrupt discont. Leads to withdrawal sxs (not huge concern)

22
Q

Dihydropyridine

A

Nifedipine (1st gen)
Felodipine (2nd gen)
Amlodipine (3rd gen)

Pts with compromised L ventricular function or reduced HR maybe candidates from dihydropyridines CCB

23
Q

Non-dihydropiriines

A

Diltiazem, verapamil

Avoid in pt with ejection fraction <35 (heart failure)
Avoid in combo with BB therapy (dec HR)

24
Q

Amlodipine

A

DHP Ca channel blocker

For HTN, chronic stable angina, variant angina, prophylaxis for disorder of cv system

No contraindications

25
Q

Verapamil

A

Non-DH Ca channel blocker

For HTN, CSA, variant angina, angina, SVT, Afib/Aflutter

Avoid with hypotension, LVEF <30%, AV block without pacemaker, sick0sinus syndrom without pm, certain arrythmias

26
Q

Diltiazam

A

Non-DHP Ca channel blocker

For atrial arrythmias, HTN, SVT, angina

Avoid with hypotension, LVEF less than 30%, av block without pm, SSS w/o pm, certain arrythmias

27
Q

How do the mechanism of action different between SHP and nonDHP CCBs?

A

DHP - acts in periphery

NonDHP - more in heart

28
Q

Why are CCBs more likely to have drugs interactions with other therapeutic moreties

A

They inhibit CYPs

29
Q

Aspirin

A

NSAID
Irreversibly inhibits the COX ez ***
Nonselective - so no preference between cox1 or 2.. pretty balanced
Avoid with anyone under age of 18 to prevent reyes syndrome
[Naproxen is not irreversible thats the difference]

Adverse effects: GI bleeding, disruption of renal perfusion

Metab: hydrolyzed to salicylate = the active form (hydrolyzed by esterases in the GI mucosa, RBCs, synovial flui, and blood)
Metabolized quickly.. less than 3 hrs via hepatic conjugation
Interactions: Coca-Cola, danshen, don quai, evening primrose, willow bark – all inc cbleeding

30
Q

Do other NSAIDs like aspirin have effects on platelets?

A

Yes, but they affects platelets more so you are more likely to see bleeding with those other ones (like ibuprophen)…..?

31
Q

Clopidogrel

A

Targets P2Y12 which is on ADP receptors on platelets

Reduces platelet aggregation by preventing the activation of GPIIb/IIIa receptor complex

Fewer risks, esp with GI bleeding

7-10 days duration of effects

Interactions are pretty much the same as aspirin
Also grapefruit and SJW which inc CYPs and thus inc metab..

32
Q

Ticagrelor

A

Reversibly blocks P2Y12 of ADP receptors on platelets

Regents activation of the GPIIb/IIIa complex thus reducing platelet aggregation

Duration depends on concentration.. up to 24 hrs

Again, similar interactions as the others

33
Q

Prasugrel

A

IRREVERSIBLE blocking of P2Y12 of ADP receptors on platelet surfaces
Prevents activ of GP IIb/IIIa complex
Reduces platelet aggregation

Rapid metabolism

34
Q

Warfarin

= coumadin

A

Inhibits vit K oxide reductase
(This is the EZ responsible for regenerating vit K so it can activate clotting factors)

Vit k dependent clotting factors = 2, 7, 9, 10

Cannot inhibit active clotting factors

Reversal = vit K

35
Q

Rivaroxaban

= Xarelto

A

Direct reversible inhibition of factor Xa
Prevents activation of thrombin/factorII
And downstream prevents conversion of fibrinogen to fibrin

Dose once a day

36
Q

Apixaban

= Eliquis

A

Direct REVERSIBLE inhibition of factor Xa
Prevents activation of thrombin/factor II
And prevents conversion of fibrinogen to fibrin

Pharmacology (3 decks)

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