CARDIAC DRUGS

Question 1

moa unfractionated heparin/

Answer 1

activates antithrombin III which inhibits thrombin, factor IXa, Xa, XIa and XIIa

Question 2

concurrent use of which drugs can make clopidogrel less effective?

Answer 2

PPIs - definitely with omeprazole and esomeprazole

Question 3

moa of LMWH?

Answer 3

activates antithrombin III which inhibitors factor Xa

Question 4

examples of LMWH?

Answer 4

dalteparin sodium, enoxaparin sodium, and tinzaparin sodium

Question 5

why are LMWHs often used over unfractionates heparins?

Answer 5

they are as effective and they have a lower risk of heparin-induced thrombocytopenia

Question 6

MOA of fondaparinux?

Answer 6

this is a synthetic heparin that activates antithrombin III which inhibits factor Xa

Question 7

moa of warfarin?

Answer 7

inhibits epoxide reductase which prevents reduction of vitamin K to its active form
this means there is not enough vitamin K to cofactor 2,7,9,10 and protein C

Question 8

management of pts on warfarin undergoing emergency surgery?

Answer 8

stop warfarin & give four-factor prothrombin complex

Question 9

management of pts on warfarin if surgery can wait for 6-8 hours?

Answer 9

stop warfarin and give 5mg IV vitamin K

Question 10

4 examples of DOACs?

Answer 10

apixaban
rivaroxaban
dabigatran
edoxaban

Question 11

MOA of apixaban?

Answer 11

direct factor Xa inhibitor

Question 12

MOA of rivaroxaban?

Answer 12

direct factor Xa inhibitor

Question 13

MOA of dabigatran?

Answer 13

direct thrombin inhibitor

Question 14

MOA of edoxaban?

Answer 14

direct factor Xa inhibitor

Question 15

reversing agents for apixavan?

Answer 15

andexanet alfa

Question 16

reversing agents for rivaroxaban?

Answer 16

andexanet alfa

Question 17

reversing agents for dabigatran?

Answer 17

idarucizumab

Question 18

MOA of nicorandil? what is it used for?

Answer 18

K+ channel activator and vasodilator = drops BP = reduced myocardial oxygen demand

used as an anti-anginal

Question 19

MOA of ivabradine? what is it used for?

Answer 19

acts on If (funny) ion currents which are highly expressed in the SAN which reduces cardiac pacemaker activity and decreases the HR
anti-anginal

Question 20

MOA of ranalozine? what is it used for?

Answer 20

an inhibitor of late Na+ channels which reduces Ca2+ accumulation and lowers cardiac wall tension in the ventricles, reducing myocardial oxygen demand
anti-anginal

Question 21

MOA of aspirin at low and high doses?

Answer 21

at low doses aspirin selectively inhibits COX1 whereas at higher doses it inhibits both isoenzymes
this reduces production of thromboxane A2 and therefore reduces platelet aggregation

Question 22

examples of irreversible P2Y12 receptor antagonists?

Answer 22

clopidogrel
prasugrel
ticlodipine

Question 23

examples of reversible P2Y12 receptor antagonists?

Answer 23

ticagrelor
cangrelor

Question 24

examples of GPIIb/IIIa receptor antagonist?

Answer 24

tirofiban
eptifibatide
abciximab

Question 25

MOA of dipyridamole?

Answer 25

inhibiting the function of phosphodiesterase and adenosine deaminase. this prevents the degradation of cAMP which is an inhibitor of platelet function

Question 26

moa of alteplase and tenecteplase? how are they different?

Answer 26

they are recombinant tissue plasminogen antagonists that convert plasminogen to plasmin in a fibrin-dependant process i..e they bind to fibrin-rich clots tenecteplase has a longer half life and a higher binding specificity to fibrin

Question 27

MOA of lidocaine?

Answer 27

1b - Na+ channel blocker

Question 28

MOA of flecainide?

Answer 28

1c- Na+ channel blocker

Question 29

MOA of sotalol?

Answer 29

III - K+ channel blocker

Question 30

MOA of atropine on the heart?

Answer 30

antimuscuarininc that increases HR and improves AV condition by blocking parasympathetic Ach effects

Question 31

MOA of amiodarine?

Answer 31

III - K+ channel blocker

Question 32

how do beta blockers work to help angina

Answer 32

they decrease HR, reduce the force of cardiac contraction and lower bp by reducing CO overall this reduces the myocardial oxygen demand

Question 33

how do calcium channel blockers work to help angina

Answer 33

dihydropyridines - peripheral arterial dilation non-dihydropyridines - negative chronotropic effect and reduces cardiac contractility overall they reduce myocardial oxygen demand

Question 34

outline the differences in moa of diydropyridines and non-dihydropyridines?

Answer 34

non- dihydropyridines exhibit frequency-dependant receptor bindings and gain access to Ca2+ channels when in its open state dihydropyridines preferentially bind to the channel in its inactivated state. more Ca2+ channels are in the inactive state in relaxed vascular smooth muscle than in cardiac muscle so these CCBs selectively bid to vascular smooth muscle Ca2+ channels. this is why non-dihydropyridines have anti arrhythmic properties and the dihydropyridines cause vasodilatation

Question 35

initial drug therapy for all ACS?

Answer 35

aspirin 300mg oxygen if sats <94% morphine if severe pain sublingual or IV nitrates

Question 36

management of STEMI after initial drug Tx

Answer 36

if PCI is possible within 120mins then give another anti platelet (prasugrel or clopidogrel if already taking an oral anticoagulant) AND unfractionates heparin and bailout GPIIb/IIIa inhibitor f using radial access if not possible within 120 mins then given a antithrombin (e.g. fondaparinux), fibrinolysis and following the procedure give ticagrelor

Question 37

management of NSTEMI after initial drug Tx?

Answer 37

fondaparinux if no immediate PCI is planned estimate 6 month mortality using GRACE. if low risk give ticagrelor if high risk then offer PCI within 72 hours. give prasugrel or ticagrelor and unfractional heparin

Question 38

management of acute HF?

Answer 38

IV loop diuretics oxygen if sats <94% if concomitant MI, severe hypertension or regurgitant aortic/mitral valvular heart disease then give nitrates

Question 39

first line therapy for chronic HF?

Answer 39

ACEi and BB - start 1 drug at a time!

Question 40

second line therapy for chronic HF?

Answer 40

aldosterone antagonist (remember to monitor K+ due to ACEi and aldosterone antagonist use) SGLT2 inhibitor

Question 41

third line therapy for chronic HF?

Answer 41

initiate by specialist... ivabradine sacbitril-valsartan hydralazine and nitrate digoxin cardiac resynchronisation therapy

Question 42

which drugs can be used for pharmacological cardioversion in AF?

Answer 42

amiodarone flecainide less commonly - quinidine, dofetilide, ibutilide, propafenone

Question 43

CI to flecainide?

Answer 43

structural heart disease

Question 44

which anticoagulants should be used I AF?

Answer 44

DOACs (second line is warfarin)

Question 45

what drugs can be used for rate-control in AF?

Answer 45

BB rate-limiting CCB such as verapamil monotherapy digoxin monotherapy

Question 46

monitoring f amiodarne?

Answer 46

TFT, LFT, U&E, CXR prior to treatment TFT and LFTs every 6 months

Question 47

which drugs can be used to maintain sinus rhythm in pts with AF?

Answer 47

BB dronedarone amiodarine - particularly if coexisting HF

Question 48

adverse effect of amiodarone?

Answer 48

thyroid dysfunction corneal deposits pulmonary fibrosis liver fibrosis or hepatitis peripheral neuropathy and myopathy photosensitivity slate-grey appearance thrmbophlebitis bradycardia QT prolongation

Question 49

management of VT?

Answer 49

if adverse signs -> immediate cardioversion otherwise... amiodarone 300mg IV over 20-60 mins then 900mg over 24 hours other choices include lidocaine and procainamide (VERAPAMIL SHOULD NOT BE USED)

Question 50

when is warfarin still used in preference to DOACs for AF?

Answer 50

if the pt has a mechanical heart valve

Question 51

management of regular SVT i.e. not AF!?

Answer 51

vasalva manoeuvre adenosine 6mg rapid IV bolus. if not effective give 12mg and then a further 12mg electrical car diversion

Question 52

drugs given in ALS non-shockable rhythm?

Answer 52

adrenaline 1mg repeat every 3-5 minutes

Question 53

drugs given in ALS when pts are in VF or pulseless VT after 3 shocks have been administered?

Answer 53

amiodarine 300mg further dose of amiodarine 150mg after 5 shocks administered (if not available use lidocaine)

Question 54

drug management of life-threatening adult bradycardia?

Answer 54

give 500mcg IV atropine. You can repeat this to a maximum of 3mg, or you could try transcutaneous pacing or isoprenaline/adrenaline infusion if nothing works seek expert help and arrange transvenous pacing

Question 55

most common adverse effects of statins?

Answer 55

myalgia (measure CK and if concentration is >5 ULN discontinue) headache and GI disturbances sleep disorders arthralgia dizziness

Question 56

potentially serious SE of statins?

Answer 56

myopathy/myositis rhabdomyolysis raise liver enzymes/drug-induced hepatitis very influent reports of new-set myasthenia graves

Question 57

when should statins be avoided?

Answer 57

caution with hepatic impairment reduce dose in renal disease as excreted by the kidneys discontinue 3 months before trying to conceive and 1 month after - congenital anomalies avoid in breastfeeding in inadequately managed hypothyroidism

Question 58

what affects the metabolism of statins?

Answer 58

CYP450 inhibitors leads to an accumulation of statins in the body putting pt at increased risk of adverse effects. most worryingly this is induced muscle injury - most common with simvastatin e.g. pts should avoid grapefruit juice and some drugs

Question 59

monitoring of statins?

Answer 59

before stating - 1 full lipid profile, TSH, U&Es, eGFR, LFTs, CK, HbA1c or fasting BG if high risk of diabetes LFTs should be repeated at 3 months and 12 months. as long as serum transaminases are less than 3x ULN then continue recheck diabetes at 3 months only check CK if muscle pain

Question 60

when should a patient take simvastatin?

Answer 60

before bed as its short acting and this maximises their effect as HMG-CoA reductase is more active at night (longer acting statins e.g. atorvastatin can be taken at night or morning)