Top 100 drugs (Not finished) Flashcards
What is the common indication for adenosine?
As a first-line diagnostic and therapeutic agent in supraventricular tachycardia (SVT).
What is the mechanism of action of adenosine in cardioversion (allowing the depolarisations from the SA node to resume normal control of the heart)?
Adenosine is an agonist of adenosine receptors on cell surfaces. In the heart, activation of these GPCRs induces a number of effects: reducing the frequency of spontaneous depolarisations (automaticity) and increaseing resistance to depolarisation (refractoriness). In turn, this transiently slows the sinus rate, conduction velocity, and increases atrioventricular node refractoriness. Increasing the refractoriness in the AV node breaks the re-entry circuit, which allows normal depolarisations from the SA node to resume normal control of heart rate.
What is the mechanism of action of adenosine in atrial flutter?
Does not induce cardioversion, however by blocking conduction to the ventricles. It allows closer inspection of the atrial rhythm on the ECG. Which may reveal the diagnosis.
What are the important adverse effects of adenosine?
It interferes with the function of the SA and AV nodes so adenosine can induce bradycardia and even asytole (flat line). Sinking feeling, impending doom, breathlessness.
What type of patients are especially sensitive to the effects of adenosine?
Those who have had a heart transplant.
Which patients should not be administered adenosine?
Those who cannot tolerate the transient bradycardic effects, hypotensive patients, those with coronary ischaemia or decompressed heart failure. As adenosine may also induce bronchospasm it should be avoided in those such as people with asthma or copd or may be suceptible.
Why would we avoid adenosine in a COPD patient?
As adenosine may also induce bronchospasm it should be avoided in those such as people with asthma or copd or may be suceptible.
What is the interaction between adenosine and dipyridamole?
Dipyridamole (is a medication that inhibits blood clot formation when given chronically and causes blood vessel dilation when given at high doses over a short time) blocks cellular uptake of adenosine, which prolongs and potentiates the effects of adenosine.The adenosine dose should be halved.
What is the interaction between adenosine and theophylline, aminophylline and caffeine?
Theophylline, aminophylline and caffeine are all competitive antagonists of adenosine receptors and may reduce its effect - may require higher doses.
How is adenosine given and at what doses? where would it be found on the drug chart?
IV, once-only section, 6mg IV or 12mg in selected cases.
What are the three main indications for Aldosterone antagonists?
- Ascities and oedema due to liver cirrhosis - spironolactone is the first - line diuretic.2. Chronic heart failure of at least moderate severity or arising within 1 month of a MI, usually as an addition to a B-blocker and an ACEI/ATRB.3. Primary hyperaldosteronism for patients awaiting surgery or for those who surgery is not an option.
What are the two common examples of aldosterone antagonists?
Spironolactone + epleronone
What is the first - line diuretic for ascities and oedema due to liver cirrhosis?
Spirinolactone
What is the place in the heart failure therapy of an aldosterone antagonist?
Moderate severity heart failure or heart failure within 1 month of a MI.Used in addition to a B-blocker and an ACEi/ATRB
When are aldosterone antagonists used in the treatment of primary hyperaldosteronism?
While awaiting surgery or when surgery is not an option.
Where is aldosterone produced and what is its mechanism of action?
Mineralcorticoid produced in the adrenal cortex which acts on mineralcorticoid receptors in the distal tubules of the kidney to increase the activity of luminal epithelial sodium channels ENaC.This increases the reabsorption of sodium and water (which elavates blood pressure and heartload) with the by-product of increased potassium excretion.
What is the by-product of the increased sodium and water retention caused by aldosterones? (electrolyte)
Increased potassium excretion = hypokaleamia
What is an important adverse effect of aldosterone antagonists?
Hyperkalaemia (aldosterone can cause hypokalaemia).But also liver impairment, jaundice and Stevens-Johnson syndrome which is a T-cell mediated hypersensitivity reaction.
What are the symptoms of hyperkalaemia caused by aldosterone antagonists?
Muscle weakness, arrhythmias and even cadiac arrest.
What is the most common reason males stop taking spironolactone?
Gynaecomastia + impotence. These are benign and reversible and may abate on dose reduction.
Aldosterone antagonists such as epleronone and spironolactone are contraindicated in which patient groups? [4]
- Severe renal impairment2. Hyperkalaemia 3. Addisons disease (aldosterone deficient) 4. Aldosterone antagonists can cross placenta and appear in breast milk so should be avoided in pregnant/breast feeding women when possible.
The combination of an aldosterone antagonist with ACE inhibitors and aniotensin receptor blockers increases the risks of what?
Hyperkaleamia.
Epleronone is an aldosterone antagonist which is only licensed for the treatment of
heart failure, spironolactone: acities/oedema due to liver cirrhosis, primary hyperaldosteronism + heart failure.
What are the typical starting doses for spironolactone in the treatment of ascities and heart failure?
Ascities: 100mg dailyHeart failure: 25mg daily.
Which aldosterone antagonist is also available as a combined preparation with a thiazide or loop diuretic?
Spironolactone: Lasilactone 20mg/50mg capsules: furosemide (LD).CO-FLUMACTONE: Hydroflumethiazide
When should spironolactone generally be taken?
With food.
What monitoring is needed for Aldosterone antagonists?
Efficacy: patient reporting and clinical findings i.e. reduction in ascities or blood pressure.Safety: renal function and serum K+ concentration due to risk of renal impairment and hyperkalaemia.
Why should spironolactone be prescribed instead of epleronone?
A month of spironolactone = £1.50, epleronone = £40 as it is still protected by patent.
Why is spironolactone usually precribed alongside a loop or thiazide diuretic?
It is a relatively weak diuretic that takes several days to start having an effect.
In the treatment of ascities due to chronic liver failure, spironolactone and furosemide are generally used together in a ratio of what?
5:1 eg spironolactone 200mg, furosemide 40mg.
What are the common indications of alpha-blockers?
- First-line medical option to improve symptoms in benign prostatic hyperplasia, which lifestyle changes are insufficient. [5alpha-reductase inhibitors may be added in selected cases, surgical treatment is also an option - especially if evidence of urinary tract damage]2. As an add-on treatment in resistant hypertension, when other medicines (eg CCB, ACEI, thiazide diuretics) are insufficient.
Why is the term alpha blocker not the most accurate when describing drugs such as doxazosin, tamsulosin and alfuzosin?
They are highly selective for the alpha-1 adrenoreceptor which are found mainly in smooth muscle, including blood vessels and the urinary tract. Stimulation induces contraction; blockade induces relaxation. Alpha-blockers therefore cause vasodilation and a fall in blood pressure, and reduced resistance to bladder outflow.
What is the mechanism of action of doxazosin, tamsulosin and alfuzosin in the treatment of BPH and resistant hypertension?
They are highly selective for blocking the alpha-1 adrenoreceptor which is found mainly in smooth muscle, including blood vessels and the urinary tract. The blockade induces relaxation and a fall in blood pressure, and reduced resistance to bladder outflow.
What are the important adverse effects of alpha-blockers?
Predictably from their effects on vascular tone, alpha-blockers can cause postural hypotension, dizziness and syncope.
When are the adverse effects of alpha-blockers most prominent?
After the first dose - similar to ACE inhibitors and angiotensin receptor blockers.
In what patients should alpha blockers not be used in?
In those patients with existing postural hypotension.
What are the important interactions with regard to the use of alpha blockers?What adjustments to a patients existing medicines regime may need to be made?
Combining anti-hypertensive drugs results in additive blood pressure lowering effects. In order to avoid pronounced first-dose hypotension, we may need to omit doses of one or more existing anti-hypertensive drugs on the day the alpha blocker is started. This is particularly the case for B-blockers, which inhibit the reflex tachycardia that forms part of the compensatory response to vasodilation.
What is the main difference between the licensing for Doxazosin and Tamsulosin?
Doxazosin is licensed both for BPH and hypertension, tamsulosin is only licensed for BPH - this is because it has a less pronounced blood pressure lowering effect.
What is the typical starting dose for Doxazosin for both BPH and hypertension?
1mg daily and increased at 1-2 weeks intervals according to response.
When is the best time to take doxazosin, at least initially?
Because of the pronounced blood pressure lowering effect of doxazosin, it is best taken at bedtime, at least initially.
Why might we introduce an alpha blocker at an earlier stage in the hypertension treatment pathway for a man?
They may also have BPH and thus an alpha blocker could relieve symptoms of both with the use of a single drug.
Why would we use modified release forms of alpha blockers?
There is little convincing evidence that MR forms are any more effective than standard-release forms and since they are taken at the same frequency (daily) they do not improve convenience for patients. As they are branded products they are more expensive for the NHS.
Long acting nitrates are used for what?
Isosorbide nitrate is used for the prophylaxis of angina where a beta blocker and/ or a ccb has been insufficient or not tolerated
What are intravenous nitrates used for?
IV nitrates are used in the treatment of pulmonary oedema usually in combination with furosemide and oxygen
What are short acting nitrates used for?
Treatment of acute angina and the chest pain associated with acute coronary syndrome
What is the mechanism of action of nitrates?
Nitrates are converted to nitric oxide (NO) which increases cGMP synthesis and reduces intracellular calcium in smooth muscle cells causing them to relax and a reduction in cardiac preload and ventricular filling.
What are the important adverse effects of nitrates?
They are vasodilator so can cause: flushing, headaches, lightheadedness and hypotension. Sustained nitrate use can cause tolerance thus a nitrate free period overnight needs to be adhered to: take morning and afternoon
In who should the use of nitrates be contraindicated?
Patients with severe aortic stenosis as can cause cardiovascular collapse. Patients with haemodynamic instability such as hypotension.
What is an important prescribing issue when dealing with prescriptions for generic modified release isosorbide mononitrate?
It must be prescribed by brand are there are important differences between preparations.
What are the practical communication points regarding a prescription for nitrates?
Patient may develop headache when starting nitrates but normally passes.Patient should use sublingual GTN before tasks that normally bring on their angina. Due to the risks of postural hypotension, it is a good idea to advise them to sit down and rest before and for 5 minutes after taking sublingual GTN.Due to the risk of tolerance, doses should be taken morning and afternoon with twice daily isosorbide mononitrate.
What are the major interactions to be aware of with nitrate drugs?
Contraindicated in patients using phosphodiesterase inhibitors such as sildenafil, as they enhance and prolong the hypotensive effect of nitrates.Nitrates should also be used with care in patients on antihypertensive medication as they may precipitate hypotension.
What are the common indications for aspirin use?
- Treatment of ACS and acute ischaemic stroke - where the rapid inhibition of platelet aggregation can prevent or limit arterial thrombosis and reduce mortality.2. Secondary prevention of thrombotic arterial events in patients with cardiovascular, cerebrovascular and peripheral arterial disease.3. As an alternative to warfarin and novel anticoagulants to reduce the risk of intracranial thrombus and embolic stroke in AF 4. Mild to moderate pain relief and fever.
What is the mechanism of action of aspirin?
Aspirin irreversibly inhibits COX to reduce the production of the pro-aggregatory factor thromboxane from arachidonic acid, reducing platelet aggregation and the risk of arterial occlusion.The antiplatelet effect of aspirin occurs at low doses and lasts for the lifetime of the platelet as they do not have Nuclues and thus no ability to synthesis New COX.
What are the important adverse effects of aspirin?
GI upset but more serious include gastrointestinal ulceration, bronchospasm etc. In regular high dose aspirin therapy tinnitus can occur.ASPIRIN is life threatening in overdose: hyperventilating, metabolic acidosis, confusion followed by convulsions, cardiovascular collapse and respiratory arrest.
Why should aspirin not be given to people under the age of 16?
There is the risk of Reye’s syndrome, a rare but life threatening illness that principally affects the liver and brain.
Can aspirin be used by people with asthma?
Yes, but it should not be taken by people with aspirin hypersensitivity.
Can aspirin be used safely in pregnancy?
Aspirin should not be used in the third trimester or pregnancy because prostaglandin inhibition may lead to premature closure of the ductus arteriosus.
Can someone taking allopurinol use aspirin?
Aspirin should be avoided in people with gout as it can precipitate an attack.
What are the main interactions for aspirin?
Aspirin acts synergistically with other antiplatelet agents which can cause increased risk of bleeding so caution must be used when using it with clopdigrel, warfarin etc,
What are the common indications for clopidogrel?
- Treatment of acute coronary syndrome, where rapid inhibition of platelet aggregation can prevent or limit arterial thrombosis and mortality.2. To prevent occlusion of coronary artery stents3. For long term secondary prevention of thrombotic arterial events in patients with cardiovascular, cerebrovascular and peripheral arterial disease. 4. To reduce the risk of intracardiac thrombus and embolic stroke in atrial fibrillation where warfarin and novel oral anticoagulants are contraindicated.
How does clopidogrel inhibit platelet aggregation?
Clopidogrel binds irreversibly to adenosine diphosphate (ADP) receptors ( the p2712 subtype) n the surface of platelets. As this process is independent of the cyckoxygenase pathway, it’s actions are synergistic with those of aspirin.
What are the main risks of clopidogrel use?
Bleeding in the GI tract and thrombocytopenia
Who should clopidogrel not be used in?
Anyone with active bleeding and may need to be stopped 7 days before elective surgery. It should also be used with caution in patients with renal and hepatic impairment.
Why may clopidogrel efficacy be reduced by cytochrome p450 inhibitors such as omeprazole, erythromycin, ciprofloxacin, some antifungals and SSRIs?
Clopidogrel is a pro drug that requires metabolism by hepatic p450 enzymes to be activated.
Why is omeprazole not first line for GI protection in patients taking clopidogrel?
Clopidogrel is a pro drug which needs activation by hepatic metabolism via p450 enzymes and omeprazole is a cyp450 enzyme inhibitor which can lead to reduced levels of clopidogrel. Lansoprazole and pantoprazole are preferred
Why must clopdigrel be stopped 7 days before elective surgery?
It acts irreversibly on the ADP surfacer receptor therefore the effect lasts for the lifespan of the platelet 7-10 days.
What are the clinical indications for the use of loop diuretics?
Relief of breathlessness in acute pulmonary oedema in conjunction with 02 and nitrates (IV).Symptomatic relief of fluid overload in chronic heart failure.Symptomatic relief of fluid overload in other oedematous states, eg renal failure, liver failure, where they may be given in conjunction with other diuretics
How do loop diuretics work? (2)
Act on the ascending limb of the loop of Henle. They inhibit the Na+/K+/2Cl-co-transporter which is the protein responsible for transporting sodium, potassium and chloride ions from the tubular lumen into the epithelial cell. Water then follows by osmosis. Inhibiting this process has a potent diuretic effect. In addition, loop diuretics also cause dilution of capacitance veins.In acute heart failure, this reduces preload and improves contractile function of the overstretched heart muscle.
Why, when taken chronically, can loop diuretics worsen gout?
They inhibit Uric acid excretion.
Why can loop diuretics cause practically any low electrolyte state?
Inhibiting the Na+/K+/2Cl- co transporter increases urinary losses of sodium, potassium, and chloride ions. Indirectly, this also increases excretion of magnesium, calcium and hydrogen ions.
How can loop diuretics, at high doses lead to hearing loss and tinnitus?
A similar sodium potassium chloride co transporter to the one they inhibit in the ascending limb of the loop of henle is present in the ear and is responsible for regulating endolymph composition.
In who are loop diuretics contra indicated?
Patients with severe hypovolemia or dehydration.
In who should the use of loop diuretics only be used with caution?
Patients at risk of hepatic encephalopathy (where hypokalaemia can cause or worsen coma.Those with severe hypokalaemia and or hyponatraemia.Taken chronically, loop diuretics have the potential to affect uric acid excretion and worsen gout.
What are two examples of loop diuretics?
Furosemide and bumetanide.
Loop diuretics have the potential to affect drugs that are excreted by the kidneys. What are 3 drugs/drug classes that this is clinically relevant to?
Lithium levels are increased due to reduced excretion. The risk of digoxin toxicity is increased due to the diuretic associated hypokalaemia.The ototoxicity and nephrotoxicity of aminoglycosides can be increased.
In the context of severe fluid overload, why might furosemide be given via IV?What could be an alternative and why?
The proportion of furosemide absorbed from the gut, its bioavailability, is highly variable both between and within individuals.In cases of severe fluid overload this is particularly the case, presumably due to gut wall oedema. This can be circumvented by using it via IV but not always desirable. Bumetanide has a more predictable BA and may be a better choice. 1mg of bumetanide is the equivalent of 40mg furosemide.
What is the dose equivalence between furosemide and bumetanide?
1mg bumetanide = 40mg furosemide
When should oral maintenance doses of a loop diuretic, such as furosemide or bumetanide, be taken and why?
In the morning and with a second in the afternoon if needed to avoid causing nocturia
What is the most important patient counselling point for loop diuretics?
Will make them pee more so should not be taken at night.
How does warfarin treatment differ regarding tissue heart valve replacement and mechanical heart valve replacement?
Short term after tissue replacement. Long-term after mechanical.
Why is warfarin not used for the prevention of ARTERIAL thrombosis?
Myocardial infarction, thrombotic stroke etc are driven by platelet aggregation, which are prevented by anti-platelet agents such as aspirin and clopidogrel.
How does warfarin work?
Warfarin inhibits hepatic production of vitamin-k dependent coagulation factors and co factors.Vitamin k must be in its reduced form for the synthesis of coagulation factors.It is then oxidised and then reactivated by vitamin k epoxide reductase. Warfarin inhibits vitamin k epoxide reductase, preventing the reactivation of vitamin k and hence coagulation factor synthesis.
Who should not take warfarin?
Those with active bleeding, those with at immediate risk of haemorrhage, people with liver diseases are less able to metabolise the drug and thus are at an increased risk of overanticoagulation.Warfarin should not be used in the first trimester because it can cause fetal malformations and should not be used towards term as it can cause maternal haemorrhage at delivery.
How do many antibiotics cause an increase in anticoagulation in warfarin patients?
Many antibiotics can increase anticoagulation in patients on warfarin by killing gut flora which synthesises vitamin K
What effect do cytochrome p 450 inhibitors have on the metabolism of warfarin?
Cytochrome p 450 inhibitors decrease warfarin metabolism and this increase the risk of bleeding. Relevant examples include fluconazole, macrolides and protease inhibitors.
What effect do cytochrome p 450 inducers such as phenytoin, rifampicin and carbamazepine have on the metabolism of warfarin?
Increase it and thus increased risk of clots occurring.
Warfarin is taken orally once-a-day. The dose is 5-10 mg on day one with a lower dose used for patients who are elderly lighter and increased risk of bleeding due to interacting medicines for example.How are subsequent warfarin doses calculated?
INR.
After starting warfarin it takes several days for full anticoagulation to be achieved.Patients requiring immediate Anticoagulation are normally started on warfarin and what other drug?
Heparin as it has a fast onset of action. Heparin is with drawn one full anticoagulation with warfarin is achieved.
Single episode of VTE requires treatment with warfarin of what duration?
Treatment may last for between three and six months. Lifelong warfarin may be required for recurrent VTE or for cardiac disease.
When is warfarin normally taken and why?
Warfarin is normally taken around 6 PM every day for consistent effects on the INR in the following morning
What is the INR?
This is the prothrombin time as a person on warfarin divided by that of a non-wharf a nice control person.
What is the INR target of a patient with AF or in VTE?
2.0-3.0
What are the costs of warfarin?
Warfarin costs about 1 pound per month but the associated monitoring costs at this. Novel oral anticoagulants such as The bigger tram and River rocks are banned have a similar efficacy to warfarin slightly better safety profiles and require less intensive monitoring however they are more expensive and this cost is likely a barrier to the NHS adopting them
How is digoxin used in AF and atrial flutter?
Digoxin is used in atrial flutter and AF to reduce the ventricular rate.However, a beta blocker of a non-dihydropyridine calcium channel blocker is usually more effective.
When is digoxin used in severe heart failure?
Third line treatment in people who are already taking an ACEi, beta blocker and either an aldosterone antagonist Or an angiotensin receptor blocker.It is used at an earlier stage in patients with co-existing AF.
How does digoxin work? What is it’s mechanism of action?
Digoxin is negatively chronotopic. This means it reduces the heart rate. Digoxin is ask positively inotropic, this means it increases the force of the heart contraction. So it has the effect of slowing the heart rate down and increasing the force with which it beats.
What is the therapeutic effect of digoxin in treating atrial flutter and atrial fibrillation?
Via an indirect route involving increased vagal (parasympathetic) tone. This reduces conduction at the atrioventricular node, preventing some impulses from being transmitted to the ventricles, thereby reducing the ventricular rate.
How does digoxin work in heart failure?
In heart failure, digoxin has a direct effect on myocytes via inhibition the sodium potassium ATPase pumps, causing sodium to accumulate in the cell. As the cellular extrusion of calcium ions requires low sodium levels intracellularly, elevation of the intracellular sodium causes calcium ions to accumulate in the cell, increasing the contractile force.
How is digoxin eliminated?
Renally, so the dose needs to be reduced in renal impairment.
Certain Electrolyte abnormalities increase the risk of the jocks in toxicity, Which of these disturbances is probably the most important? Why?
Potassium disturbance is probably the most important as digoxin competed with potassium to bind the sodium potassium ATPase pump, thus when serum potassium levels are low, more digoxin can bind at the pump and thus more therapeutic effect is seen which can cause toxicity.
What are the main side effects of digoxin? Less serious and serious.
Bradycardia, gastrointestinal upset, rash, dizziness and even visual disturbances ( blurred or yellow vision).Serious: a wide range of arrhythmia can be caused by digoxin and these may be life threatening.
What is the common indication for nicorandil?
Prevention and treatment of chest pain in people with STABLE angina. The first choice treatments for stable angina are beta blockers and CCB, individually or in combination. Nicorandil (or a long -acting nitrate) may be used if these drugs are insufficient or not tolerated.
What is the mechanism of action of nicorandil?
Nicorandil causes both arterial and venous vasodilation through its action as a nitrate. (NO = more GMP= more CA leave cell, more relaxation). IT also works by activating K+-ATP channels. Efflux of K+ through activated K+-ATP channels leads to hyperpolarisation of the cell membrane and subsequent inactivation of voltage-gated Ca2+ channels, the net effect is a decrease in free intracellular calcium.
What are the unwanted effects of nicorandil use?
Vasodilation causes flushes, dizziness and headache. Nicorandil can also cause nausea, vomting and hypotension. Less frequently it can cause GI, skin or mucosal ulceration which responds to withdrawal of treatment.
What are the warnings associated with nicorandil usage?
Not to be used in patients with poor left ventricular function, hypotension or pulmonary oedema. This is because it can worsen these conditions. As wth nitrates, the hypotensive side effects of nicorandil are significantly enhanced by phosphodiesterase inhibitors (e.g. sildenafil) and they should not be prescribed together.
How is nicorandil inititated?
It is started at a low dose of 5-10mg twice daily and increased to 20-30mg twice daily as the patient becomes tolerant of the vasodilatory adverse effects.
What are the two indications for the use of dipyridamole?
- In cerebrovascular disease for secondary prevention of stroke.Dipyridamole is currently first-line therapy following a transient ischaemic attack, and second-line therapy following an ischaemic stroke where clopidogrel is contraindicated or not tolerated. Should usually be given with aspirin but monotherapy is possible if aspirin not used. 2. To induce tachycardia during a myocardial perfusion scan in the diagnosis of ischaemic heart disease.
What are the antiplatelet mechanisms of action of dipyridamole?
The end effect is an increase in intra-platelet cyclic adenosine monophosphate (cAMP) that inhibits platelet aggregation, reducing the risk of arterial occlusion. Its vasodilatory effects are due to blocking the cellular uptake of adenosine, prolonging its effect on blood vessels to produce vasodilation.
How does dipyridamole produce vasodilation?
Blocks cellular uptake of adenosine, prolonging its effect on blood vessels to produce vasodilation. Its antiplatelet effects are due to an increase in intra-platelet adenosine monophosphate (cAMP) that inhibits platelet aggregation, reducing the risk of arterial occlusion.
What are the important adverse effects of dipyridamole?
They relate to its vasodilatory (headache, flushing, dizziness, GI symptoms) and antiplatelet effects (increased bleed risk, and rarely thrombocytopenia).
Why should dipyridamole be used with caution in patients with ischaemic heart diease, aortic stenosis and heart failure?
It causes vasodilation and tachycardia that can exacerbate these conditions.
What are the important interactions with dipyridamole?
Dipyridamole + other antiplatelets/anticoagulants = increased sick of bleeding.Prolongs the effects of adenosine.
Current evidence is strongest for the use of what form and strenght of dipyridamole?
mr 200MG BD, should be taken with food and not crushed but swallowed whole.
When is amiodarone used?
In the management of tachyarrhythmias, including AF, atrial flutter, supraventricular tachycardia, ventricular tachycardia and refractory ventricular fibrillation. It is generally only used when other therapeutic options (drugs or electrical cardioversion) have been ineffective or not tolerated.
How does amiodarone work?
Amiodarone has many effects on myocardial cells, including blockade of sodium, calcium and potassium channels and antagonism of alpha and beta adrenergic receptors.
When taken chronically amiodarone can have a number of adverse effects such as:
Pneumonitis (lungs)Bradycardia, AV block (heart)Hepatitis (liver)Photosensitivity and grey discolouration (skin)Thyroid abnormalities due to its high iodine content and structural similarities to thyroid hormone.
In what patients whould amiodarone be avoided?
Patients with severe hypotension, those with heart block and those with any active thyroid disease.
What are the most important drug interactions with amiodarone?
Amiodarone increases the plasma concentrations of:Digoxin VerapamilDiltiazem This may increase the risk of bradycardia, AV block and heart failure. The doses of these drugs should be halved if amiodarone is initiated.
When is atropine used?
First-line in the management of severe or symptomatic bradycardia to increase heart rate.
When is hyoscine butylbromide used?
- First-line for IBS due to antispasmodic effect2. End of life to reduce copious respiratory secretions.
How do antimuscarinic drugs achieve their actions?
Atropine, hyoscine butylbromide, glycopyrronium bind to the muscarinic receptor and act as competive inhibitors of acetylcholine. Stimulation of the muscarininc receptors brings about a range of parasympathetic ‘rest and digest’ effects. By blocking the receptor, antimuscarinics have the opposite effects: they increase heart rate and conduction, reduce smooth muscle tone and peristaltic contraction, including in the fut and urinary tract. They reduce secretions from glands in the respiratory tract and gut.
What are the adverse effects of drugs such as atropine, hyoscine butylbromide and glycopyrronium?
As they are antimuscarinic they have predictable side effects of tachycardia, dry mouth and constipation. By reducing destrusor muscle activity, they can cause urinary retention in patients with benign prostatic hypertrophy. The occular effects may cause blurred vision. Atropine has central effects so can cause drowsiness and confusion, particularly in the elderly.
In which patients should antimuscarinics be used with caution?
In patients susceptible to angle-closure glaucoma, in whom they can precipitate a dangerous rise in intraocular pressure. They should generally be avoided in patients at risk of arrhythmias unless the indication for use is bradycardia.
What is the main clinical difference between atropine and glycopyrronium?
Glycopyrronium does not cross the BB and hence causes less drowsiness but it is not widely available on hospital wards.
What are the indications for amlodipine use?
First line in over 55 or black as step 1 hypertension management, also see nifedipine to a lesser degree
All calcium channel blockers can be used to control symptoms in people with what? What is the main alternative?
Stable angina, beta blockers being the main alternative
Diltiazem and Verapamil are used to control cardiac rate in people with what’s?
supraventricular arrhythmia including supraventricular tachycardia, atrial flutter and atrial fibrillation
How do calcium channel blockers work in hypertension management?
CCBS decrease calcium entry into vascular and cardiac cells, reducing intracellular calcium concentration. This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure.
How do ccbs function in the management of stable angina?
In the heart, ccbs reduces myocardial contractility, they suppress cardiac contraction, particularly across the atrioventricular node, slowing the ventricular rate. Reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand, preventing angina.
