Anti-anginal & Anti-thrombotic

Question 1

Nitrates

Answer 1

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

Question 2

Nitrate side effects

Answer 2

Hypotension
Headache
Flushing
Light headedness

Question 3

Nitrates; specific agents

Answer 3

Nitroglycerin

Isosorbide mononitrate

Question 4

Isosorbide Mononitrate

Indication

Answer 4

Angina pectoris

Question 5

Isosorbide mononitrate

Contraindication

Answer 5

Avoid use with PDE-5 inhibitors

Ie. sildenafil

Question 6

Isosorbide mononitrate

Pharmacokinetics

Answer 6

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

Question 7

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

Answer 7

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

Question 8

Are nitrates more specific to arterial or venous blood?

Answer 8

Venous

Question 9

Beta Blockers

Answer 9

Blocks beta adrenergic receptors

Question 10

Beta blocker side effects

Answer 10

Bradycardia
Heart block
HA
Fatigue

Question 11

beta blocker interactions

Answer 11

Avoid use with intrinsic sympathomimetic activity

ISA - aka partial agonist

Question 12

Beta 1 receptors

Beta2 receptors

Answer 12

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)

Question 13

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

Answer 13

Abrupt discont. Leads to reflex tachycardia

Question 14

CNS adverse effects of beta blockers

Answer 14

Dizziness, fatigue, depression

Question 15

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

Answer 15

Beta blocker
Cardioselective (B1) competitive antagonist

Indications: MI, CHF, angina, HTN

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

Question 16

Atenolol

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

Answer 16

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

Question 17

Propranolol

Receptors?
Indications?
Avoid?
Metabolism pathways?
Interactions?

Answer 17

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)

Question 18

Carvedilol

Answer 18

Nonselective (A1 adrenergic blockade activity)

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

Avoid: heart block, severe bradycardia

Metab: CYPs

Interactions: grapefruit juice

Question 19

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

Answer 19

???/

Question 20

Which BB covers both beta and alpha receptors?

Answer 20

??

Question 21

Calcium Channel blockers

Answer 21

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)

Question 22

Dihydropyridine

Answer 22

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

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

Question 23

Non-dihydropiriines

Answer 23

Diltiazem, verapamil

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

Question 24

Amlodipine

Answer 24

DHP Ca channel blocker

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

No contraindications

Question 25

Verapamil

Answer 25

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

Question 26

Diltiazam

Answer 26

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

Question 27

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

Answer 27

DHP - acts in periphery NonDHP - more in heart

Question 28

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

Answer 28

They inhibit CYPs

Question 29

Aspirin

Answer 29

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

Question 30

Do other NSAIDs like aspirin have effects on platelets?

Answer 30

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

Question 31

Clopidogrel

Answer 31

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..

Question 32

Ticagrelor

Answer 32

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

Question 33

Prasugrel

Answer 33

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

Question 34

Warfarin = coumadin

Answer 34

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

Question 35

Rivaroxaban = Xarelto

Answer 35

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

Question 36

Apixaban = Eliquis

Answer 36

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