Drugs Flashcards
Denosumab
Monoclonal antibody
RANK-L
Alternative to bisphosphonates
Used in treatment of osteoporosis
Pirfenidone
Anti-fibrotic agent given in (idiopathic) lung fibrosis
Oxybutinin (type of drug, mode of action, usage, side effects)
Anti-muscarinics
Work on receptors in the bladder (bladder has M3 receptors but it is a non specific drug)
Treatment for urinary incontinence
Side effects - dry eyes, dry mouth, confusion, constipation
Phenylephrine
Drops
Dilates the pupil
Alpha 1 adrenergic agonist
Tropicamide
Eye drops
Dilates the pupil
Anti-muscarinic
Name the most common enzyme inducers (HINT: think PC BRAS)
Phenytoin Carbamazepine Barbiturates Rifampicin Alcohol XS Sulphonylureas
Name the most common enzyme inhibitors (HINT: think AO DEVICES)
Allopurinol Omeprazole Disulfiram Erythromycin Valproate Isoniazid Cirprofloxacin Ethanol - acute intoxication Sulphonamides
Name the drugs which should be stopped before surgery, and when. (HINT: think I LACK OP)
Insulin - variable
Lithium - 24 hours before
Anticoagulants - variable
COCP (and HRT) - 4 weeks
K-sparing diuretics - day of surgery
Oral hypoglycaemic - variable, usually from when patient is NBM to prevent hypo
Perindopril (ACEi) - day of surgery
Give some examples of drugs that require therapeutic drug monitoring
Lithium Vancomycin Aminoglycosides Phenytoin Carbamazepine Digoxin Cyclosporine Theophylline
What is the maximum dose of paracetamol in 24 hours?
4G
Cyclizine - uses, dose and contraindications
Antiemetic Prescribed if a patient is feeling nauseous 50mg 8 hourly IM/IV/P.O. Do not use of patient had heart failure
Name the antiemetic and doss prescribed for patients that cannot have cyclizine (eg heart failure patients)
Metoclopramide 10mg 8 hourly
IM/IV
What is the target INR in patients on warfarin?
2.5
What is target INR in warfarin patients with metallic heart valves?
3.5
Furosemide / Bumetanide
- MOA
- SE
- CI
Loop diuretics
SE - LOW Na, K, Ca + postural hypotension
CI - LOW K, anuric AKI
Bendrofluazide
- MOA
- SE
- CI
Thiazide-like diuretics
SE - LOW Na, K + postural hypotension + inc glucose in DM
CI - LOW K, gout, severe CKD/AKI
Spironolactone
- MOA
- SE
- CI
Aldosterone antagonist
SE - HIGH K + gynaecomastia
CI - Addison’s
What is the MOA of thrombolytics (such as stretokinase or tPA)?
Convert plasminogen to plasmic which assists in the breakdown of fibrin
Linsopril / Captopril / Ramipril
- MOA
- SE
- CI
- Interactions and monitoring
ACE inhibitor SE - HIGH K+, dry cough, angioedema CI - RAS, angioedema Interactions - - ACEi + NSAIDs = RF - ACEi + Diuretics = hypotension Monitoring - U&Es
Candesartan / Lorsartan
- MOA
- Indication
- SE
ARB - angiotensin II receptor antagonist (blocker)
Indication - often reserved for those that cannot tolerate ACEi
SE - HIGH K+
List some of the indications for ACEi (or ARB) prescription
HF HTN Post-MI Angina Diabetic neuropathy
List some of the indications for B-blocker prescription
Angina HF (not severe) Acute MI Arrhythmias HTN Long QT Anxiety Migraine prophylaxis Glaucoma
Name two cardioselective b-blockers
Bisoprolol
Atenolol
Name two non-selective b-blockers
Propranolol
Labetolol
Which two b-blockers are lipophilic? What is the implication of this?
Metorpolol and Propranolol
More likely to cause nightmares as can cross the BBB
List two considerations when treating diabetics or pre-diabetics with b-blockers (HINT: think about drug interactions)
Increased risk of new onset DM if concurrent thiazide therapy
Increase risk of unnoticed hypoglycaemia if concurrent insulin therapy
Phentolamine
Alpha blocker - used mainly to treat HTN in phaeochromocytoma patients
Doxazosin
Alpha blocker - used mainly to treat BPH but has anti-HTN effects
Methyldopa
alpha-2 agonist - used mainly to treat HTN in pregnancy
Name two dihydropyridine CCBs
Nifedipine
Amlodipine
Name two non-dihydropiridine CCBs
Diltiazem
Verapamil
What is the main mode of action of dihydropyridine CCBs
Vasodilation - acts on arterial smooth muscle
What is the main mode of action of non-dihydropyridine CCBs
Negative ionotropic effect to decrease contractility
List some of the indications for treatment with dihydropiridine CCBs
Angina
HTN
List some of the indications for treatment with non-dihydropiridine CCBs
Angina
HTN
Arrhythmias
What class of drugs are Class I Vaughan-Williams anti-arrhythmics?
Sodium channel blockers (i.e. local anaesthetics)
Name one drug from each of the following Vaughan-Williams classes:
- 1a
- 1b
- 1c
1a = procainamide 1b = lignocaine 1c = flecanide
What are the MOAs for the Vaughan-Williams drugs (HINT: think “some block potassium channels)
Class I - Sodium channel blockers
Class II - B-blcokers
Class III - Potassium channel blockers
Class IV - Calcium channel blockers
Name a Class 1a anti-arrhythmic drug and describe (a) how it works and (b) its indication
Procainamide - works by prolonging repolarisation thereby increasing action potential duration
Indication - ventricular arrhythmias
Name a Class 1b anti-arrhythmic drug and describe (a) how it works and (b) its indication
Lignocaine - works by shortening reploarisation
Indication - post-MI ventricular arrhythmias
Name a Class 1c anti-arrhythmic drug and give its indication
Flecanide - Wolff-Parkinson-White, acute AF
Name some Class II anti-arrhythmic drugs
B-blockers = metoprolol, propranolol, atenolol
Describe how Class II anti-arrhythmic drugs work
Increase refractory period at AVN thereby slowing conduction and preventing arrhythmias due to sympathetic discharge
List some of the indications for Class II anti-arrhythmic drugs
Post-MI arrhythmias
AF - rate control
SVT
Name some Class III anti-arrhythmic drugs
Potassium channel blockers - amiodarone, sotalol
Describe how Class III anti-arrhythmic drugs work
Block potassium channels therby increasing the refractory period, this increases the QT interval
List some of the indications for Class III anti-arrhythmic drugs
Ventricular arrhythmias
Supraventricular arrhythmias
Wolff-Parkinson-White
Name some Class IV anti-arrhythmic drugs
Calcium channel blockers - non-dihydropyridines: verapamil, diltiazem
Are Class IV anti-arrhythmic drugs dihydropyridines or not?
Non-dihydropyridine CCBs
List some of the indications for Class IV anti-arrhythmic drugs
Prevention of SVt recurrence
AF - rate control
Acute SVT
Describe how Class IV anti-arrhythmic drugs work
Slow AVN conduction
How does digoxin work?
(1) Positive inotropic effect - increases force of contraction by inhibiting Na/K ATPase (therefore increasing their concentration)
(2) Negative chronotropic effect - increases HR at rest by increasing AVN refractory period
How does adenosine cause transient AV block?
By hyperpolarising myocytes via A1 receptors in cardiac tissues
Name a short-acting nitrate and (a) its MOA and (b) its indication
GTN
(a) vasodilation
(b) pain relief in angina and ACS
Name a long-acting nitrate and (a) its MOA and (b) its indication
ISMN / ISDN (isosorbide mono/dinitrate)
(a) vasodilation
(b) CHF
List some of the contraindications for nitrate prescription
Aortic stenosis
Mitral stenosis
Hypotension
Glaucoma
Name a non-nitrate treatment for angina
Nicorandil
What is a major contraindication for most anti-arrhythmic drugs?
Heart block
List some of the indications for Rx with anti-platelet therapy
ACS
Secondary prevention in IHD, stroke, TIA, PVD
Primary prevention in those with high CVD risk and hypertension
Heart valve replacements
How does aspirin work?
Aspirin is an irreversible non-selective COX inhibitor
(1) inhibition of COX enzymes
(2) prevention of platelet activation
(3) prevention of platelet adhesion and aggregation
List some of the contraindications for aspirin Rx
Paediatrics (except Kawasaki’s)
Active peptic ulcer disease
Bleeding disorders
How does clopidogrel work?
Irreversible adenosine receptor antagonist
(1) Binds to adenosine receptor
(2) Inhibits ADP-induced binding of fibrinogen to GP11b/IIIa
List some of the indications for treatment with statins
Known CVD
Diabetes mellitus >40 years old
High 10 year CVD risk (>20%)
How do statins work?
Statins are HMG-CoA reductase inhibitors - they block the rate limiting step in cholesterol synthesis
What are the major (useful) downstream effects of statins?
Decrease LDL cholesterol
Increase HDL cholesterol
Decrease triglycerides
Can statins be used in pregnancy?
No - pregnancy is CI
What natural substance interacts with statins and should be avoided?
Grapefruit juice
How do inhaled corticosteroids work?
They act over weeks to decrease inflammation and prevent long-term decline in lung function
How do inhaled corticosteroids decrease inflammation?
Decrease cytokine production Decrease prostaglandin synthesis Decrease leukotriene synthesis Decrease IgE secretion Decrease leukocyte recruitment
What is the MOA of theophylline?
Increases cAMP causing bronchodilation
Which patients cannot be treated with antihistamines>
Hepatic Disease
Long QT
BPH
Closed angle glaucoma
Name a non-sedating antihistamine
Certirizine
Name a sedating antihistamine
Chlorphenamine (piriton)
How do antihistamines work?
H1 (histamine 1 receptor) antagonists
What kind of drug is montelukast and how does it work?
Leukotriene receptor antagonists - blocks leukotrienes and prevents inflammator response seen in asthma
Name some osmotic laxatives
Laculose
Movicol / macrogol
Phosphate enema
Name a stimulant laxative
Senna
Is ramipril safe during pregnancy? If not, suggest a suitable alternative
No - ramipril is teratogenic
Labetolol is the first-line alternative
How often is warfarin (INR) monitoring required?
Weekly until INR has stabilised, then monthly after that
What affect does potassium have on warfarin?
Because of the MOA of warfarin (competitive binding for Na/K ATPase), changes to [K] can alter the drugs effectiveness:
- High concentrations of potassium = limit drug effect
- Low concentrations of potassium = augment drug effect
List some drugs that interact with alcohol, explain the interaction
Metformin + alcohol = lactic acidosis
NSAIDs + alcohol = GI bleeds
Warfarin + alcohol = excessive anticogaulation
MAO inhibitors + alcohol = hypertensive crisis
Metronidazole + alcohol = sweating, nausea, vomiting
Opioids + alcohol = sedation
Benzos + alcohol = sedation
Barbiturates + alcohol = sedation
Why should you not co-prescribe NSAIDs and ACEi?
NSAIDs have an effect on the afferent arteriole (cause constriction by inhibiting prostaglandins) thereby lowering renal perfusion
ACEi have an effect on the efferent arteriole (cause vasodilation) thereby lowering renal perfusion
Together, their effects are synergistic therefore renal perfusion is lowered to dangerous levels
