Cardio Drugs Flashcards
ACE inhibitors
- What side effects can be experienced?
- What are their cautions and contraindications?
- What monitoring is required?
- cough
- angioedema
- hyperkalaemia
- pregnancy + breastfeeding
- aortic stenosis (hypotension)
- hereditary idiopathic angioedema
- renovascular disease
+ K+ >5.0 get specialist review
3.
U+Es checked at initiation and after increasing the dose
serum creatinine increase <30% and K+ up to 5.5 are acceptable
may get significant renal impairment in patients with undiagnosed bilateral renal artery stenosis
Adenosine
- What medications can
a) potentiate their action
b) inhibit their action - What does it do?
- How should it be administered?
- What are its possible adverse effects?
1
a) dipyridamole
b) theophylline
- cause transient AV node block
(half life of 8-10s) - wide-calibre cannula due to its short half-life
- chest pain
- bronchospasm (therefore cannot give to asthmatics)
- transient flushing (feeling of warmth)
- can enhance accessory pathways (therefore could lead to increase in HR)
Amiodarone
- What is its mechanism of action (and therefore antiarrhythmic drug class)
- What does it decrease the metabolism of?
- What are its possible adverse effects?
- What monitoring is required?
1. blocks potassium channels (class III) can also block sodium channels (class I effect)
- warfarin
- pulmonary fibrosis / pneumonitis
- prolonged QT
- liver fibrosis / hepatitis
- slate-grey appearance
- photosensitivity
- thyroid dysfunction (hypo or hyper)
- corneal deposits
- neuropathy/myopathy
- thrombophlebitis (therefore ideally inserted into central vein)
mnemonic - think one for each system
- CXR, U+Es, LFTs, TFTs at initiation
- LFTs + TFTs 6 monthly
Beta blockers
What are their:
- SEs
- Contraindications
NOTE: these apply to systemic beta blockers and not all necessarily to cardio-specific beta blockers e.g. atenolol
1.
- bronchospasm
- cold peripheries
- sleep disturbance (incl. nightmares)
- fatigue
- Erectile dysfunction
mnemonic: cold peripheries claire not allowed, I wouldn’t be allowed because of bottom 3
- asthma
- uncontrolled HF
- sick sinus syndrome (damage to SA node)
- use with verapamil: severe bradycardia
Dabigatran
- What is its mechanism of action?
- When is it indicated?
- When should it not be prescribed?
- How can you reverse its effects?
- anticoagulant - direct thrombin inhibitor
- hip or knee replacement surgery
- stroke prevention in non-valvular AF if one of the following:
- previous stroke / TIA / embolism
- LV ejection fraction <40%
- symptomatic HF NYHA class 2 or above
- > 75 years old
- > 65 years old and one of CAD, hypertension or DM
- GFR<30 (doses reduced in CKD)
- mechanical heart valves
- Idarucizumab
Ivabradine
- When is it used and what is its mechanism of action?
- What are its side effects?
- anti-anginas drug working by reducing HR
acts on the funny current in the SA node
- visual effects
- headache
- bradycardia
Loop diuretics
e.g. furosemide, bumetanide
- What is their mechanism of action?
- What should be done in patients with poor renal function?
- When are they given?
- What are their possible SEs?
- inhibit Na-K-Cl transporter in the thick ascending limb of Henle
(therefore reduce reabsorption of NaCl) - increased dose required to achieve sufficient concentration in the tubules
- HF (acute + chronic)
- resistant hypertension
- low ions:
- hypokalaemia
- hyponatraemia
- hypocalcaemia
- hypomagnesaemia
- hypochloraemic alkalosis
- hypotension
- hyperglycaemia
- ototoxicity
- gout
- renal impairment
Nicorandil
- What is it used to treat and what is its mechanism of action?
- What are its possible side effects?
- When is it contraindicated?
- vasodilator by being potassium channel activator, activating guanylate cyclase increasing cGMP
- headache
- flushing
- ulcers (eyes, skin, mucosal, GI)
- LV failure
NOTE: think that makes sense if LV failure will not be able to reach adequate BP to perfuse tissues with dilated blood vessels
Nitrates
- What is their mechanism of action?
- What are their SEs?
- Patients can develop a tolerance: how should this be managed?
- release of nitric oxide in smooth muscle activates guanylate cyclase, increasing cGMP
this dilates coronary arteries + reduced venous return reducing O2 demand in the heart
- headaches
- flushing
- hypotension
- tachycardia
- take second dose after 8 hrs rather than 12 hrs
Statins
- What is their mechanism of action?
- What are their side effects?
- What are their contraindications?
- Who should receive a statin?
- What dose should be given when?
- What monitoring is required?
- inhibit HMG-CoA reductase (rate limiting enzyme of hepatic synthesis)
- myopathy
- liver impairment
- macrolide therapy (e.g. clarithromycin, erythromycin)
(therefore statins stopped during the course) - pregnancy
- previous intracerebral haemorrhage
- macrolide therapy (e.g. clarithromycin, erythromycin)
- CV disease (ischaemic heart disease, peripheral arterial disease, previous stroke / TIA)
- 10 year CV risk >10%
- assess T2DM on QRISK2
- T1DM: diagnosed over 10 year ago OR over 40 OR peripheral neuropathy
- 20mg:
primary prevention:
- cv risk >10% in 10 years
- DM
CKD: GFR<60
80mg secondary prevention - ischaemic heart disease - stroke - peripheral arterial disease
- due to possible liver impairment:
LFTs at baseline, 3 months and 12 months
if rise to 3x upper limit of reference range treatment should be discontinued
NOTE: anti-fungals can also cause liver impairment and also require 3 monthly monitoring hence if patient gets thrush give anti-fungal pessary instead
Thiazide diuretics
- What is their mechanism of action?
- What are their common SEs?
- inhibit NaCl symporter in distal convoluted tubule
- dehydration
- postural hypotension
- hypokalaemia, hyponatraemia, hypercalcaemia
- gout
- impaired glucose tolerance
- impotence
NOTE: hypercalcaemia leads to hypocalciuria reducing likelihood of renal stones
Warfarin
- What is its mechanism of action?
- What are its indications?
- What is the INR?
- What are its SEs?
- inhibits epoxide reductase preventing reduction of Vitamin K to its active form
this in turn helps as a cofactor in the carboxylation of clotting factors II, VII, IX, X and protein C (1972 last full year of vietnam WARfarin)
- mechanical heart valves
- secondary to DOACs in AF and VTE
- international normalised ratio
patients prothrombin time / normal prothrombin time - haemorrhage
- teratogenic (but safe in breastfeeding)
- skin necrosis (red painful skin before over days becoming hard to touch and purpuric)
- purple toes
Warfarin interactions
- Which factors can potentiate warfarin?
- P450 system
a) What can induce it (therefore decrease INR)
b) What can inhibit it
(therefore increase INR)
- liver disease
- cranberry juice
- displace warfarin from plasma albumin (NSAIDs)
- inhibit platelet function (NSAIDs)
- P450 enzyme inhibitors
- a) BARSAS
- barbiturates (phenobarbitone)
- anti epileptics: phenytoin, carbamazepine
- rifampicin
- St John’s wort
- alcohol intake (chronic)
- smoking
b) CIIAAAASS
- cimetidine + omeprazole
- imidazoles: ketoconazole, fluconazole
- isoniazid
- allopurinol
- amiodarone
- antibiotics: cipro. clari. erythro.
- acute alcohol intake
- SSRIs
- sodium valproate
Warfarin Management
How is warfarin managed in the following situations?
- major bleeding
- INR>8 minor bleeding
- INR>8 no bleeding
- INR 5-8 minor bleeding
- INR 5-8 no bleeding
- stop warfarin
- IV Vit K 5mg
- prothrombin complex concentrate (can give FFP ONLY if PCC not available)
- stop warfarin
- IV vit K 1-3mg
- repeat if INR still high 24 hrs later
- restart warfarin when INR <5
3.
- stop warfarin
- oral vit K 1-5mg
- repeat if INR still high 24 hrs later
- restart when INR<5
- stop warfarin
- IV vit K 1-3mg
- restart warfarin when INR <5
- withold 1/2 doses
- reduce maintenance dose
What is the mechanism of action of fondaparinux?
activates antithrombin III which in turn inhibits factor Xa
