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CVS drugs Flashcards

1
Q

Medication to aid smoking cessation?

A

Nicotine Gum
Varenicline
Bupropion

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2
Q

Varenicline MOA, when to start, side effects

A

Oral selective nicotine receptor partial agonist
Start one week before target stop date and gradually increase the dose.
SEs: appetite change; dry
mouth; taste disturbance; headache; drowsiness; dizziness; sleep disorders; abnormal
dreams; depression; suicidal thoughts; panic; dysarthria

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3
Q

Bupropion: Alternative name? When to consider? SEs?

A

Amfebutamone
consider if varenicline and nicotine gum fails
SEs: seizures, insomnia, headache

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4
Q

Drugs that cause long QT interval?

A

Anti-arrhythmics (Quinidine, amiodarone, procainamide, sotalol)
antimicrobials (Erythromycin, levofloxacin, pentamidine, halofantrine)
antihistamines (Terfenadine, astemizole)
Motility drugs (Domperidone)
Psychoactive drugs (Haloperidol, risperidone, tricyclics, SSRIs)

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5
Q

Terfenadine

A

Antihistamine

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6
Q

Drug causes of sinus bradycardia

A

beta blockers
digoxin
amiodarone

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7
Q

Drug causes of 2nd degree heart block

A

digoxin

beta blockers

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8
Q

Signs of digoxin toxicity

A

Downward slowing ST depression
3rd degree HB
Inverted T wave in V5- V6
Any arrythmia can occur (ventricular ectopics and nodal bradycardia are common)

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9
Q

drug cause of low voltage QRS

A

doxorubicin cardiotoxicity

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10
Q

Drugs that can be used in stress echo if patient cannot exercise

A

Dobutamine

Dipyridamole

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11
Q

Aspirin MOA, uses and dosage

A

Aspirin irreversibly acetylates cyclo-oxygenase, preventing production
of thromboxane A2, thereby inhibiting platelet aggregation.
low dose
(eg 75mg/24h PO) for secondary prevention following MI, TIA/stroke, and for patients
with angina or peripheral vascular disease.

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12
Q

ADP receptor antagonists three drugs. MOA. compare with aspirin. uses

A 
clopidogrel, prasugrel, ticagrelor
Block platelet aggregation
less gastric irritation.
uses: truly intolerant
of aspirin; with aspirin after coronary stent insertion; and in acute coronary
syndrome
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13
Q

Name a Glycoprotein IIb/IIIa antagonists. uses?

A

tirofiban

unstable angina/MI

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14
Q

What are the two types of DOACs? Examples? Review? CIs? Interactions?

A

Direct factor Xa inhibitor - Apixaban, rivaroxaban
Direct thrombin inhibitor - Dabigatran, bivalirudin
Others: Fondaparinux (pentasaccharide Xa inhibitor) - used in ACS or in place of LMWH for prophylaxis

do not require regular monitoring and
dose adjustment; just a quarterly assessment and annual blood test.
CI: severe renal/liver impairment; active bleeding; lesion
at risk of bleeding; reduced clotting factors. Interactions: heparin, clopidogrel.

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15
Q

Anticoagulation for mechanical valves?

A

Warfarin

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16
Q

Anticoagulants used in ACS?

A

treatment dose LMWH, fondaparinux (Xa inhibitor), & bivalirudin (thrombin inhibitor)

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17
Q

Main indications for anticoagulants?

A

Therapeutic: Venous thromboembolic disease: DVT and PE.
Prophylactic: Prevention of DVT/PE in high-risk patients eg post-op.
Prevention of stroke, eg in chronic AF or prosthetic heart valves.

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18
Q

LMWH examples? MOA? Route? Use?

A

dalteparin, enoxaparin, tinzaparin
inactivates factor Xa
SC
prevention and initial treatment of VTE

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19
Q

Unfractionated heparin route? MOA? Use?

A

IV or SC

binds to antithrombin to increaseits ability to inhibit thrombin, factor Xa, and IXa

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20
Q

SEs of heparin. CIs?

A

Bleeding (eg at operative site, gastrointestinal, intracranial), heparininduced
thrombocytopenia (HIT), osteoporosis with long-term use, hyperkalaemia

CIs: Bleeding disorders, platelets <60x10^9/L, previous HIT, peptic ulcer, cerebral
haemorrhage, severe hypertension, neurosurgery.

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21
Q

Compare UFH and LMWH.

A

Half life if 2- to 4- old longer than UFH and more predictable response.
UFH requires monitoring- may need to adjust dose (with APTT).
HIT and osteoporosis is less common with LMWH than UFH.

22
Q

Warfarin route? Frequency? MOA? CIs?

A

PO
OD
inhibits the reductase
enzyme responsible for regenerating the active form of vitamin K, producing
a state analogous to vitamin K deficiency
CI: Peptic ulcer, bleeding disorders, severe
hypertension, pregnancy

23
Q

Warfarin interactions?

A

increased by alcohol, allopurinal, amiodar one, aspirin, chloramphenicol, cimetidine, ciprofl oxacin, co-trimoxazole,
danazol, dipyridamole, disulfi ram, erythromycin (and broad-spectrum
antibiotics), gemfi brozil, glucagon, ketoconazole, metronidazole, miconazole, nalidixic
acid, neomycin, NSAIDS, phenytoin, quinidine, simvastatin (but not pravastatin),
sulfi npyrazone, sulfonamides, tetracyclines, levothyroxine.

reduced by: aminoglutethimide, barbiturates, carbamaz epine,
contraceptive steroids, dichloralphenazone, griseofulvin, rifampicin, phenytoin,
vitamin K.

24
Q

How do you transition from heparin to warfarin?

A

give heparin in combination and
continue until INR is in target therapeutic range on 2 consecutive days. Start warfarin at 5–10mg given at 18.00 on days 1 and 2, then check INR
on day 3 (it takes 48–72h for anticoagulant effect to develop).
Adjust subsequent doses according to the INR, which needs to be measured on alternate days until
stable, then weekly or less often.

25
Q

UFH overdose Tx?

A

stop infusion

if bleeding: protamine sulphate (discuss with a haematologist)

26
Q

DOAC overdose Tx?

A

challenging and evolving area (including monoclonal
anti-drug antibodies eg idarucizumab for dabigatran
discuss with haematologist

27
Q

Warfarin overdose Tx:

A

INR 5-8, no bleed: Withold 1–2 doses. Restart warfarin at a lower maintanence
dose once INR <5.
INR 5-8, minor bleed (including epistaxis): Stop warfarin and admit for urgent IV vitamin K (give
slowly). Restart warfarin when INR <5.
INR >8, no bleed: Stop warfarin and seek haematology advice.
INR >8, minor bleed: Stop warfarin and admit for urgent IV vitamin K. Check INR
daily—repeat vitamin K if INR too high after 24h. Restart
warfarin at a lower dose when INR <5.
Any major
bleed (including
intracranial
haemorrhage): Stop warfarin. Give prothrombin complex concentrate 50
units/kg (if unavailable, give FFP 15mL/kg ≈ 1L for a 70kg
man) and 5–10mg vitamin K IV. Discuss with haematologist.

28
Q

Warfarin uses and target INR? Duration of treatment in DVT/PE

A

Pulmonary embolism and DVT. Aim for INR of 2–3; 3.5 if recurrent PE or DVT
whilst anticoagulated.
Atrial fibrillation: for stroke prevention (p130). Target INR 2–3.
Prosthetic metallic heart valves: for stroke prevention. Target INR 2–3 if aortic
valve or 2.5–3.5 if mitral valve.

1st episode: at least 3 months - extended to 6 months if more extensive, life-threatening clot at presentation, for those with transient but
persistent risk factors (eg prolonged immobility) or if evidence of persistent clot at 3 months.

For those with recurrent unprovoked emboli or underlying thrombophilia consider bleeding risks against benefits of indefinite treatment.

29
Q

Beta blockers MOA? selectivity? uses? CI? SEs?

A

MOA: Blocking beta1-receptors is negatively inotropic and chronotropic; blocking
beta2-receptors induces peripheral vasoconstriction and bronchoconstriction
propanolol is non-selective, bisoprolol is relatively beta 1 selective

uses: Angina,
hypertension, anti dysrhythmic, post MI (reduces mortality), heart failure (with caution).
CI: Severe asthma/COPD, heart block.
SEs: Lethargy, erectile dysfunction, reduced joie de vivre,
nightmares, headache, bronchospasm, heart failure, cold peripheries

30
Q

ACEi uses? SEs? CIs?

A

hypertension, heart failure, post-MI

SEs: dry cough, urticaria, renal failure, angio-oedema

CIs: bilateral renal artery or aortic valve stenosis

31
Q

How to start ACEi in CCF patients?

A

reduce diuretic dose initially and use long-acting ACE-i. Monitor U&E when starting or
raising ACE-i dose, a creatinine rise of >20% is concerning. If the patient starts ACE-i
prior to discharge, ask the GP to check U&E in 1–2 weeks.

32
Q

Types of diuretics and examples? uses? MOAs? SEs?

A

loop: furosemide - heart failure - inhibit the Na/2Cl/K
co-transporter. SES: dehydration, reduced Na+, reduced K+, reduced Ca2+, ototoxic

thiazide and thiazide like diuretics: indapamide (hypertension), metolazone (heart failure), bendroflumethiazide - SE: low K+, raised Ca2+, low Mg2+, raised urate (±gout), impotence

potassium sparing diuretics: aldosterone antagonists (spironolactone, eplerenone) - block aldosterone receptors
amiloride - blocks the epithelial
sodium channel in the distal convoluted tubules.

33
Q

Vasodilators uses? MOA?

A

heart failure, IHD, and hypertension
nitrates preferentially
dilate veins and the large arteries, reduce filling pressure (pre-load), while hydralazine
(often used with nitrates) primarily dilates the resistance vessels, thus reducing BP(after-load). Prazosin (an alpha-blocker) dilates arteries and veins.

34
Q

CCB MOA? types, examples, effects, uses? SEs? CI?

A

reduce cell entry of Ca2+ via voltage-sensitive channels in
smooth muscle, thereby promoting coronary and peripheral vasodilation and reducing
myocardial oxygen consumption. All current drugs block L-type Ca2+ channels.

dihydropyridines: nifedipine, amlodipine - peripheral vasodilators
(also dilate coronary arteries) and cause a refl ex tachycardia, so are often used
with a beta-blocker. They are used mainly in hypertension and angina.

non-dihydropyridines—verapamil and diltiazem— slow conduction at the AV and SA nodes- used to treat hypertension, angina, and dysrhythmias. Don’t give non-dihydropyridines with beta-blockers (risk of severe bradycardia ± LVF).

SEs: Flushes, headache, ankle oedema (diuretic unresponsive), reduced LV function, gingival
hypertrophy.
CI: heart block

35
Q

What drugs should you not give with dihydropyridines and why?

A

beta blockers - risk of severe bradycardia ± LVF

36
Q

Digoxin MOA? uses? dosage and monitoring? half life? CIs? SEs? How to manage digoxin toxicity?

A

blocks Na+/K+ pump.
slow pulse in fast AF, heart failure in sinus rhythm if symptomatic despite optimal ACE-i therapy (reduces admissions for worsening CCF)

measure plasma level >6h post dose. Typical dose: 500mcg stat PO, repeated after 12h, then 125mcg (if elderly) to 250mcg/d PO OD

IV dose: 0.75–1mg in 0.9% NaCl
over 2h.
T0.5 = 36hrs
CIs: HCM, WPW syndrome
SEs: Any arrhythmia (supravent ricular tachycardia with AV block is suggestive), nausea, reduced appetite, yellow vision, confusion, gynaecomastia.

Mx: ECG, check digoxin levels, check K+, Mg2+, and Ca2+. If toxicity confirmed: stop
digoxin, correct electrolyte imbalances, treat arrhy thmias, and consider IV DigiFab

37
Q

what factors increase risk of digoxin toxicity?

A

low K+, low Mg+, raised Ca2+,

38
Q

Classes of anti-arrhythmics and examples?

A

Class 1 - sodium channel blockers
1a: Procainamide, 1b: Lidocaine, 1c: Flecainide
Class 2: Beta blockers
Class 3: Potassium channel blockers (Amiodarone)

39
Q

Na+ channel blockers examples? uses? CIs?

A

Procainamide (1a), lidocaine (1b) - can be used to terminate VT
Flecainide (1c) - AF cardioversion, arrhythmia prophylaxis in patients with WPW or troublesome paroxysmal AF.

CI: Heart
failure, IHD, valve disease, and heart block.

40
Q

Amiodarone MOA? uses? SEs? Monitoring?

A

Amiodarone prolongs the cardiac action
potential, reducing the potential for tachyarrhythmias.
Used in both supra-ventricular
and ventricular tachycardias, including during cardiac arrest.
SEs include: thyroid disease, liver disease, pulmonary fibrosis and peripheral
neuropathy.
Monitor TFTs and LFTs every 6 months.

41
Q

Ivabradine MOA? uses? CIs? interactions?

A

Blocks the pacemaker ‘funny current’, slowing pulse rate without significantly dropping blood pressure

angina, heart failure, and (off -licence)
in autonomic tachycardia syndromes.
CI: Acute MI, bradycardia, long QT syndrome,
shock. Many drug interactions, including with calcium antagonists.

42
Q

Statins MOA? SEs? CIs?

A

inhibit the enzyme HMG-COA reductase, which
causes de novo synthesis of cholesterol in the liver. This increases LDL receptor expression
by hepatocytes leading to reduced circulating LDL cholesterol. More effective if given at night

SES:
Muscle aches, abdominal discomfort, raised transaminases (eg ALT), raised CK, myositis, rarely
rhabdomyolysis (more common if used with fi brates).

CIs: porphyria, cholestasis, pregnancy

43
Q

Mx of hyperlipidaemia? what drugs to use for hypertriglyceridaemia?

A

1st line: Atorvastatin 20mg PO at night, for primary prevention, and 80mg
for secondary prevention and primary prevention in those with kidney disease.
Simvastatin 40mg, is an alternative. Aim for >40% plasma cholesterol reduction in those with CVD.

2nd line: Ezetimibe—a cholesterol absorption inhibitor, may be used in
statin intolerance or combination with statins to achive target reduction.

3rd line: Alirocumab—a monoclonal antibody against PCSK9 (acts to
reduce hepatocyte LDL receptor expression). Very effective in reducing LDL, but
expensive and needs to be given by injection every 2 weeks.

others: fibrates, eg
bezafibrate (useful in mixed hyperlipidaemias); anion exchange resins, eg colestyramine;
nicotinic acid (raised HDL; reduced LDL; SE: severe flushes; aspirin 300mg ½h pre-dose
helps this)

Hypertriglyceridaemia: Responds best to fi brates, nicotinic acid, or fish oil.

44
Q

Mx of angina?

A

Address exacerbating factors.
Secondary prevention of cardiovascular disease - smoking, exercise, diet, hypertension, diabetes - 75mg aspirin daily

PRN symptom relief - GTN spray or sublingual tabs

antianginal medication: 
beta blockers
CCB
long-acting nitrates eg. isosorbide mononitrate(alternative GTN skin patches)
ivabradine
Ranolazine
nicorandil

revascularisation: Considered when optimal medical therapy proves inadequate.
PCI - insert stent to reduce re-stenosis. use dual antiplatelet therapy for at least 12 month after stent insertion to reduce risk of instent thrombosis
CABG

45
Q

GTN SEs? usage?

A

Low BP, headaches

Advise the patient
to repeat the dose if the pain has not gone after 5min and to call an ambulance
if the pain is still present 5min after the second dose.

46
Q

ranolazine MOA? use? when to be cautious?

A

inhhibits late Na+ current
antianginal
Caution if heart failure,
elderly, weight <60kg or prolonged QT interval.

47
Q

nicorandil MOA? CI?

A

K+ channel activator

CI: acute pulmonary oedema,
severe hypotension, hypovolaemia, LV failure

48
Q

CABG vs PCI

A

CABG less likely to need repeat
revascularization and those with multivessel disease can expect better outcomes.
However, CABG is open heart surgery and so recovery is slower and the patient is left with two large wounds (sternal and vein harvesting).

49
Q

Hypertension Mx guidelines?

A

<55yrs, and black patients of any age - 1st lines is a Ca2+-channel antagonist or thiazide.
<55yrs 1st line is ACE-i or ARB
beta-blockers are not 1st line for hypertension, but consider in younger people, particularly
if: intolerance or contraindication to ACE-i/ARB, she is a woman of child-bearing
potential, or there is increased sympathetic drive.

2nd line: ACE-i + Ca2+-channel antagonist
3rd line: ACE-i, Ca2+-channel antagonist, and thiazide
4th line: consider spironolactone or
higher-dose thiazide (monitor U+Es). Or beta blocker or selective alpha blocker

50
Q

ACEi example? SEs? When would ACE-i be first choice for hypertension

A

lisinopril

51
Q

ARB example? when to be cautious? monitoring? SEs?

A

candesartan
caution if valve disease or cardiomyopathy; monitor K+.
SE: vertigo, urticaria, pruritus.

52
Q

How to acheive AV node blockade? Why would you want to do this?

A

do this is AVNRT or AVRT -
Vagal manoeuvres: carotid sinus massage, Valsalva manoeuvre (eg blowing into
a syringe).
2 IV adenosine

Drugs (12 decks)

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