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REVISION > CARDIAC DRUGS > Flashcards

CARDIAC DRUGS Flashcards

1
Q

moa unfractionated heparin/

A

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

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2
Q

concurrent use of which drugs can make clopidogrel less effective?

A

PPIs - definitely with omeprazole and esomeprazole

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3
Q

moa of LMWH?

A

activates antithrombin III which inhibitors factor Xa

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4
Q

examples of LMWH?

A

dalteparin sodium, enoxaparin sodium, and tinzaparin sodium

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5
Q

why are LMWHs often used over unfractionates heparins?

A

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

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6
Q

MOA of fondaparinux?

A

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

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7
Q

moa of warfarin?

A

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

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8
Q

management of pts on warfarin undergoing emergency surgery?

A

stop warfarin & give four-factor prothrombin complex

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9
Q

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

A

stop warfarin and give 5mg IV vitamin K

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10
Q

4 examples of DOACs?

A

apixaban
rivaroxaban
dabigatran
edoxaban

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11
Q

MOA of apixaban?

A

direct factor Xa inhibitor

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12
Q

MOA of rivaroxaban?

A

direct factor Xa inhibitor

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13
Q

MOA of dabigatran?

A

direct thrombin inhibitor

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14
Q

MOA of edoxaban?

A

direct factor Xa inhibitor

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15
Q

reversing agents for apixavan?

A

andexanet alfa

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16
Q

reversing agents for rivaroxaban?

A

andexanet alfa

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17
Q

reversing agents for dabigatran?

A

idarucizumab

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18
Q

MOA of nicorandil? what is it used for?

A

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

used as an anti-anginal

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19
Q

MOA of ivabradine? what is it used for?

A

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

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20
Q

MOA of ranalozine? what is it used for?

A

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

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21
Q

MOA of aspirin at low and high doses?

A

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

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22
Q

examples of irreversible P2Y12 receptor antagonists?

A

clopidogrel
prasugrel
ticlodipine

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23
Q

examples of reversible P2Y12 receptor antagonists?

A

ticagrelor
cangrelor

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24
Q

examples of GPIIb/IIIa receptor antagonist?

A

tirofiban
eptifibatide
abciximab

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25
Q

MOA of dipyridamole?

A

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

26
Q

moa of alteplase and tenecteplase? how are they different?

A

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

27
Q

MOA of lidocaine?

A

1b - Na+ channel blocker

28
Q

MOA of flecainide?

A

1c- Na+ channel blocker

29
Q

MOA of sotalol?

A

III - K+ channel blocker

30
Q

MOA of atropine on the heart?

A

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

31
Q

MOA of amiodarine?

A

III - K+ channel blocker

32
Q

how do beta blockers work to help angina

A

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

33
Q

how do calcium channel blockers work to help angina

A

dihydropyridines - peripheral arterial dilation
non-dihydropyridines - negative chronotropic effect and reduces cardiac contractility

overall they reduce myocardial oxygen demand

34
Q

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

A

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

35
Q

initial drug therapy for all ACS?

A

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

36
Q

management of STEMI after initial drug Tx

A

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

37
Q

management of NSTEMI after initial drug Tx?

A

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

38
Q

management of acute HF?

A

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

39
Q

first line therapy for chronic HF?

A

ACEi and BB - start 1 drug at a time!

40
Q

second line therapy for chronic HF?

A

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

SGLT2 inhibitor

41
Q

third line therapy for chronic HF?

A

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

42
Q

which drugs can be used for pharmacological cardioversion in AF?

A

amiodarone
flecainide

less commonly - quinidine, dofetilide, ibutilide, propafenone

43
Q

CI to flecainide?

A

structural heart disease

44
Q

which anticoagulants should be used I AF?

A

DOACs

(second line is warfarin)

45
Q

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

A

BB
rate-limiting CCB such as verapamil monotherapy
digoxin monotherapy

46
Q

monitoring f amiodarne?

A

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

47
Q

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

A

BB
dronedarone
amiodarine - particularly if coexisting HF

48
Q

adverse effect of amiodarone?

A

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

49
Q

management of VT?

A

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)

50
Q

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

A

if the pt has a mechanical heart valve

51
Q

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

A

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

52
Q

drugs given in ALS non-shockable rhythm?

A

adrenaline 1mg
repeat every 3-5 minutes

53
Q

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

A

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

54
Q

drug management of life-threatening adult bradycardia?

A

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

55
Q

most common adverse effects of statins?

A

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

56
Q

potentially serious SE of statins?

A

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

57
Q

when should statins be avoided?

A

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

58
Q

what affects the metabolism of statins?

A

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

59
Q

monitoring of statins?

A

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

60
Q

when should a patient take simvastatin?

A

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)

61
Q
A

REVISION (25 decks)

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