Theraputics Flashcards
examples of long acting insulin
levemir, lantus
How quickly does long acting insulin take efffect and how long does the effect of long acting insulin last?
2-4 hours, 24 hours approx
How quickly does short acting insulin take efffect and how long does the effect last?
5 minutes, 2-4 hours
examples of intermediate and short mixed acting insulin
novomix 30, hunulogue, humulin m3
examples of short acting insulin
actrapid, novorapid
what none-diabetes drug therapy is associated with hypoglycaemia?
b-blockers
what 3 criteria need to be met for a diagnosis of DKA
raised blood glucose (>11mmol/l), ketonuria (>3 mmmol/l), acidosis (pH < 7.35/bicarb <15mmmol/l)
what medications can cause hyper/hypothyroidism
lithium and amamiodarone (treats irregular heartbeats,
drug treatment for hypothyroidism and basics about this drugs
levothyroxine, once a day before breakfast, long half life, can miss doses
drug treatment for hyperthyroidism and basics about this drug
carbimazole, several weeks for effect, monitor for signs of blood disorders (thrombocytopenia, leukopenia,etc)
what medication provides symptomatic relief from hyperthyroidism
b-blockers, eg propanolol
causes of hyperthyroidism
Graves, thyroid nodules, medications
causes of hypothyroidism
autoimmune thyroiditis, surgical removal of thyroid gland, iodine deficiency, medications, other types of thyroiditis, pituitary gland, congenital (rare)
what is the most dangerous side effect of carbimazole and how should patients monitor for it
bone marrow suppression causing agranulocytosis/leukopenia (very lowered WBC count, particularly neutrophils) Report immediately any signs of fever, sore throat, mouth ulcers
what are the main side effects of carbimazole?
rash/pruritus common but can be treated with antihistamine and carbimazole stopped, bone marrow suppression rare but serious, FBC and stop immediately if neutrophil depletion, jaundice and liver problems rare but caution in pts with liver disease
what are the NICE targets for treatment of hypertension?
systolic >140mmhg, diastolic >90 or 80 in diabetics, clinical diastolic <140/90 clinically if under 80, 150/90 if over 80, at home diastolic 135/85 or 145/85
Goals for treatment of hypertension
Reduction in cardiovascular damage.
Preservation of renal function.
Limitation or reversal of left ventricular hypertrophy.
Prevention of IHD.
Reduction in mortality due to stroke and MIs
how do ace inhibitors work?
inhibiting the ACE, they lead to reductions in angiotensin II, which leads to:
Reductions in arterial and venous vasoconstriction
Reduced aldosterone production leads to reductions in salt and water retention
Also potentiate bradykinin – cough
what are the commonest adverse reactions to ACE inhibitors?
hypotension/dizziness, especially after 1st dose, Dry cough (bradykinin), hyperkalemia (avoid potassium supplements, allergic reactions including severe reaction affecting gut wall and causing abdo pain, angiodema (peripheral swelling, specially round face)
when should Ace I’s be avoided, what precautions should be taken?
Should be avoided in renovascular disease
Renin-dependent hypertension, ACEIs lead to renal underperfusion and severe hypotension
May lead to a worsening of renal function – if this occurs discontinue
Monitor creatinine before and during use
examples of rate limiting Ca channel blockers
Verapamil and Diltiazem (work slightly differently)
Examples of none- rate limiting Ca channel blockers
Dihydropyridines - non rate limiting
Amlodipine, Felodipine, Nifedipine
What is the difference in the MOA of rate limiting vs none-rate limiting Ca channel blockers?
Verapamil exerts most of its effects on the heart compared with dihydropyridine effects, which are greater on arteriole smooth muscle
what is the MOA of Ca channel blockers?
Inhibit voltage operated calcium channels on vascular smooth muscle, leading to vasodilatation and a reduction in BP
a-blockers examples
Alpha-blockers
e.g. doxazosin, prazosin
a-blockers MOA
These are competitive receptor antagonists of a1-adrenoceptors
a-blockers are last choice antihypertensives for what reason?
Widespread side effects, which makes them poorly tolerated
side effects of a-blockers
dizziness, postural hypotension, nasal congestion, fluid retention
side effects of Ca channel blockers
Peripheral oedema Postural hypotension Peripheral oedema (ankles) headaches flushing of face Constipation (some)
side effects and cautions of thiazide diuretics
hypokalemia, Postural hypotension
Impaired glucose control
Do not use in gout
MOA B-Blockers
Mechanism of action unclear:
Reduction in sympathetic drive to the heart, reducing cardiac output
A reduction in sympathetically evoked renin release
why since 2006 have NICE stopped recommending B-Blockers as first line treatment for blood pressure
2006: NICE no longer recommended as reduced effectiveness at preventing stroke and increased risk of diabetes
Side effects, B-Blockers
•dizziness •excessive tiredness •blurred vision •cold hands and feet •slow heartbeat •diarrhoea and nausea bronchospasm (specially asthmatics)
Less common side effects include:
- sleep disturbance (insomnia)
- lack of sex drive (loss of libido)
- depression
- in men, problems getting an erection (impotence)
which thiazide diuretic remains effective in renal impairment?
metolazone
Most ….. are innefective in moderate/severe renal impairment except metolazone. Creatinine levels should be taken before and during treatment
Most thiazide diuretics are innefective in moderate/severe renal impairment except metolazone. Creatinine levels should be taken before and during treatment
Most thiazide diuretics are innefective in …… except metolazone. Creatinine levels should be taken before and during treatment
Most thiazide diuretics are innefective in moderate/severe renal impairment except metolazone. Creatinine levels should be taken before and during treatment
Most thiazide diuretics are innefective in moderate/severe renal impairment except …… Creatinine levels should be taken before and during treatment
Most thiazide diuretics are innefective in moderate/severe renal impairment except metolazone. Creatinine levels should be taken before and during treatment
Most thiazide diuretics are innefective in moderate/severe renal impairment except metolazone. …. should be taken before and during treatment
Most thiazide diuretics are innefective in moderate/severe renal impairment except metolazone. Creatinine levels should be taken before and during treatment
MOA thiazide diuretics
Inhibit Na+/Cl- in distal convoluted tubule
Reduction in circulating volume
Also causes vasodilatation
caution should be taken when using B-Blockers in …., particularly B2 selective agents as ….
caution should be taken when using B-Blockers in asthmatic and COPD patients, particularly B2 selective agents as they may block bronchial B2 receptors
lifestyle factors which will help reduce BP
Reduce their overall cardiovascular risk:
Alcohol consumption should be reduced
Alcohol increases BP in a significant proportion of pts
Weight reduction
Reduce excess caffeine
Reducing fat and salt intake
Increasing fruit and oily fish in the diet
Increasing exercise
Smoking cessation
For what conditions are B-Blockers indicated/contra-indicated
Indicated MI, IHD, CHF
- Asthma/COPD
- Heart block
For what conditions are ACE inhibitors/AT1 receptor antagonists indicated/contra-indicated
+ Heart failure
+ Left ventricular hypertrophy
+ Diabetic nephropathy
- Renovascular disease
For what conditions are Ca channel blockers indicated/contra-indicated
+ Afro-Caribbean ethnicity
+ DHPs in isolated systolic HT
Diltiazem/verapamil in angina but not CHF
For what conditions are thiazide diuretics indicated/contra-indicated
+ Elderly
- Gout
?? Diabetes?? Unclear
For what conditions are a- blockers indicated/contra-indicated
prostatic hypertrophy, when others have been ineffective
ACE inhibitors are the 1st line antihypertensive for patients who are ….
ACE inhibitors are the 1st line antihypertensive for patients who are none-black/under 55
…… are the 1st line antihypertensive for patients who are over 55/black (low renin)
Ca channel blockers are the 1st line antihypertensive for patients who are over 55/black (low renin)
Ca channel blockers are the 1st line antihypertensive for ……
Ca channel blockers are the 1st line antihypertensive for patients who are over 55/black (low renin)
….. are the 1st line antihypertensive for patients who are none-black/under 55
ACE inhibitors are the 1st line antihypertensive for patients who are none-black/under 55
What is the 3rd line treatment for hypertension
thiazide diuretic
what drugs can be used as 4th line treatment for hypertension
Add alpha blocker
or spironolactone
or other diuretic
Or beta blocker
what situations may B-Blockers be used to treat hypertension?
In patients with angina or past MI
Child bearing
Increased sympathetic drive
Intolerance to ACEIs / ATRA
what are the stages of hypertension
Stage 1: >140/>90
Stage 2: >160/>100
Severe: >180/>110
when should hypertension be treated?
Stage 1 with one or more of End organ damage Diabetes CV disease High CV risk (>20% over 10 years – see rear of BNF)
all with stage 2
The …… demonstrated that the statin, simvastatin reduced cardiovascular events in high risk (e.g. hypertensive) pts – even with ‘normal cholesterols’
Statins should be considered for all high risk patients irrespective of cholesterol level.
The Heart Protection Study (2002) demonstrated that the statin, simvastatin reduced cardiovascular events in high risk (e.g. hypertensive) pts – even with ‘normal cholesterols’
Statins should be considered for all high risk patients irrespective of cholesterol level.
The Heart Protection Study (2002) demonstrated that ….
the statin, simvastatin reduced cardiovascular events in high risk (e.g. hypertensive) pts – even with ‘normal cholesterols’
Statins should be considered for all high risk patients irrespective of cholesterol level.
study by Ascot 2005 ….
study by Ascot 2005 Compared atenolol (plus bendroflumethiazide as required) and amlodipine (plus perindopril as required).
Equal BP control
Amlodipine reduced cardiovascular events more and induced less diabetes
Suggest that amlodipine-based therapy is superior in patients at moderate risk of CV disease
how does prinzmetals angina differ from angina pectoris?
symptoms more at rest (eg; waking up at night), more vasospasm than atheroma. Approx 2/3 of cases associated with atherosclerosis but often not to degree that it would cause the level of angina, ST elevation not depression,
MOA nitrates
Via release of nitric oxide and cGMP which causes:
Venodilatation, leading to a decrease in preload and a reduction in cardiac work
Coronary vasodilatation, improves coronary blood flow
Why are B-blockers effective in preventing coronary events?
-ve inotropic and chronotropic (decrease amount muscle works, decrease HR) effects reducing cardiac work and preventing symptoms.
Coronary flow only occurs during diastole, then by slowing the heart the diastolic period will be increased, as will the time for coronary blood flow.
Anti-arrhythmic effects and reduce the risk of myocardial infarction
Calcium channel blockers exert a class …antiarrhythmic effect
4
Class …. antiarrhythmic medicines slow the electrical impulses in the heart by blocking the heart’s potassium channels. Amiodarone, sotalol, and dofetilide are examples of class III medicines
Class III antiarrhythmic medicines slow the electrical impulses in the heart by blocking the heart’s potassium channels. Amiodarone, sotalol, and dofetilide are examples of class III medicines
Class …. antiarrhythmic medicines slow the electrical impulses in the heart by blocking the heart’s potassium channels. Amiodarone, sotalol, and dofetilide are examples of class III medicines
3
Class 3 antiarrhythmic medicines …… Amiodarone, sotalol, and dofetilide are examples of class III medicines
Class 3 antiarrhythmic medicines slow the electrical impulses in the heart by blocking the heart’s potassium channels. Amiodarone, sotalol, and dofetilide are examples of class III medicines
Class 3 antiarrhythmic medicines slow the electrical impulses in the heart by blocking the heart’s potassium channels. …. are examples of class III medicines
Class 3 antiarrhythmic medicines slow the electrical impulses in the heart by blocking the heart’s potassium channels. Amiodarone, sotalol, and dofetilide are examples of class III medicines
Class II antiarrhythmic medicines are …. which work by blocking the impulses that may cause an irregular heart rhythm and by interfering with hormonal influences (such as adrenaline) on the heart’s cells. By doing this, they also reduce blood pressure and heart rate. Propranolol, metoprolol, and atenolol are examples of class II medicines
Class II antiarrhythmic medicines are beta-blockers, which work by blocking the impulses that may cause an irregular heart rhythm and by interfering with hormonal influences (such as adrenaline) on the heart’s cells. By doing this, they also reduce blood pressure and heart rate. Propranolol, metoprolol, and atenolol are examples of class II medicines
Class II antiarrhythmic medicines are beta-blockers, which work by blocking the impulses that may cause an irregular heart rhythm and by interfering with hormonal influences (such as adrenaline) on the heart’s cells. By doing this, they also reduce ….. Propranolol, metoprolol, and atenolol are examples of class II medicines
Class II antiarrhythmic medicines are beta-blockers, which work by blocking the impulses that may cause an irregular heart rhythm and by interfering with hormonal influences (such as adrenaline) on the heart’s cells. By doing this, they also reduce blood pressure and heart rate. Propranolol, metoprolol, and atenolol are examples of class II medicines
Class II antiarrhythmic medicines are beta-blockers, which work by blocking the impulses that may cause an irregular heart rhythm and by interfering with hormonal influences (such as adrenaline) on the heart’s cells. By doing this, they also reduce blood pressure and heart rate. …..l are examples of class II medicines
Class II antiarrhythmic medicines are beta-blockers, which work by blocking the impulses that may cause an irregular heart rhythm and by interfering with hormonal influences (such as adrenaline) on the heart’s cells. By doing this, they also reduce blood pressure and heart rate. Propranolol, metoprolol, and atenolol are examples of class II medicines
Class I antiarrhythmic medicines are ….., which slow electrical conduction in the heart. Quinidine, procainamide, disopyramide, flecainide, propafenone, tocainide, and mexiletine are examples of class I medicines.
Class I antiarrhythmic medicines are sodium-channel blockers, which slow electrical conduction in the heart. Quinidine, procainamide, disopyramide, flecainide, propafenone, tocainide, and mexiletine are examples of class I medicines.
Class I antiarrhythmic medicines are sodium-channel blockers, which ….. Quinidine, procainamide, disopyramide, flecainide, propafenone, tocainide, and mexiletine are examples of class I medicines.
Class I antiarrhythmic medicines are sodium-channel blockers, which slow electrical conduction in the heart. Quinidine, procainamide, disopyramide, flecainide, propafenone, tocainide, and mexiletine are examples of class I medicines.
Class I antiarrhythmic medicines are sodium-channel blockers, which slow electrical conduction in the heart. ….. are examples of class I medicines.
Class I antiarrhythmic medicines are sodium-channel blockers, which slow electrical conduction in the heart. Quinidine, procainamide, disopyramide, flecainide, propafenone, tocainide, and mexiletine are examples of class I medicines.
…. antiarrhythmic medicines are sodium-channel blockers, which slow electrical conduction in the heart. Quinidine, procainamide, disopyramide, flecainide, propafenone, tocainide, and mexiletine are examples of class I medicines.
class 1
why are Ca channel blockers useful to use in IHD?
Vasodilatation and improve coronary blood flow, so preventing symptoms.
Verapamil (and to a lesser extent diltiazem) also have myocardial depressant and bradycardic actions, so reducing cardiac work and myocardial O2 demand
The … trial indicated that ramipril reduced mortality in patients with IHD
HOPE trial indicated that ramipril reduced mortality in patients with IHD
HOPE trial indicated that …..
HOPE trial indicated that ramipril reduced mortality in patients with IHD
aspirin MOA
Favours prostacyclin production over thromboxane as inhibits both endothelial and platelet cyclo-oxygenase (COX). Endothelial cell as nucleated and can regenerate COX, platelets lack nuclei and can not
Ibuprofen may oppose beneficial actions
what drug may oppose beneficial actions of aspirin?
ibruprofen
Clopidogrel MOA
ADP receptor antagonist (prevents platelet aggregation)
Equally effective aspirin
Used in pts who can not receive aspirin (e.g. in asthma)
which class of drugs only relieve symptoms of angina and don’t decrease risk of MI
Ca channel blockers
what would be first line therapy for unstable/stable angina?
B-blocker
what treatment would be used for unstable/stable angina if B-blockers are ineffective/contraindicated?
Ca channel blocker, usually diltiazem/veramipil (cardioselective) or long acting Dihydropyridine (amlodipine)
K channel activators, eg Nicorandil work by …
: combined NO donor and activator of ATP-sensitive K-channels.
The target is the ATP-sensitive K+-channel (KATP):
……… work by combined NO donor and activator of ATP-sensitive K-channels.
The target is the ATP-sensitive K+-channel (KATP):
K channel activators, eg Nicorandil
what drug drug is particularly effective at treating prinzmetal angina? why?
Ca channel blockers, particularly effective at reversing vasospasm
Which Ca channel blockers can/can’t be added to B-Blocker to treat angina?
DHPs, not veramipil
what prevention measures should be taken in patients with stable angina or high CV risk?
BP >140/85, statins, aim to reduce >5mmol/l or 3mm/l LDL or 30%, lifestyle advice
what medications can be added to a regime for patients with refractory angina
long acting nitrate (eg; isosorbide mononitrate), Ca channel blocker (but not veramipil), nicorandil (K channel activator)
side effects and cautions of nitrates
flushing, headache, tolerance, do not use with viagra (can cause very low bp), do not use with hypertrophic cardiomyopathy
which conditions should nitrates not be used?
hypertrophic myopathy, using viagra
thiazide diuretics are ineffective in pts with GFR <
30
Why should verapamil not be added to a b-blocker?
Do not combine verapamil with a beta blocker, as the risk of bradycardia is very high
how can tolerance of nitrates be avoided
8-12 hour nitrate free periods in regime
MOA statins
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors
Decrease hepatic cholesterol synthesis
Reduced hepatocyte cholesterol levels trigger increased expression of LDL receptors
Increased clearance of LDL from the plasma
Bile Acid sequestrants (e.g. colestyramine)
…….
Interfere with the absorption of fat soluble vitamins
May cause constipation
Other drugs to be taken 1 hour before or 4 hours after
……
Inhibits intestinal absorption of cholesterol
Ezetimibe
Inhibits intestinal absorption of cholesterol
Fibrates (e.g. bezafibrate)
……
Fibrates (e.g. bezafibrate)
Act mainly by decreasing serum triglycerides
…….
Act mainly by decreasing serum triglycerides
Fibrates (e.g. bezafibrate)
Act mainly by decreasing serum triglycerides
Ezetimibe
……
Ezetimibe
Inhibits intestinal absorption of cholesterol
……. Interfere with the absorption of fat soluble vitamins
May cause constipation
Other drugs to be taken 1 hour before or 4 hours after
Bile Acid sequestrants (e.g. colestyramine Interfere with the absorption of fat soluble vitamins
May cause constipation
Other drugs to be taken 1 hour before or 4 hours after
What other antianginal agents can be used if therapies aren’t tolerated
Ivabradine
Lowers heart rate with its action on the sinus node
Ranolazine
An adjunctive therapy or if patients are intolerant of 1st line agents
which lifestyle factors have been shown to be most effective in reducing bp?
Diet rich in fruit, veg, low-fat dairy with reduced content of saturated and total fat (8-14 systolic reduction), weight loss to normal BMI (5-10 systolic reduction per 10kg lost) . reg aerobic exercise (30 mins most days, 4-9), reduce dietary NaCL >6g, 1tsp/day, 2-8)
What interventions should be implemented for somebody suffering acute MI
Reassure
O2 (high flow, 100% trauma mask if sats >94/88 COPD)
Morphine (5-10 mg slow IV injection followed by further of same doses. Add 10mg IV metochlopramide usually)
Asprin 300mg chew
Nitrate (GTN, sublingual/spray), IV if continued pain
Clopidogrel 300mg oral if ECG changes or troponin +ve
Enoxaparin if ECG changes or troponin +ve 1mg/kg twice daily for 2-8 days until >24 hours pain free or discharge (minimum 2 days)
how long should clopidogrel be continued after MI
1 Month for STEMI
12 Month for NSTEMI
how long should aspirin be continued after MI? what other medication may be needed
indefinitely, PPI
which medications should be given for secondary prevention of MI
Aspirin 75mg OD
Clopidogrel 75mg OD
Simvastatin 40mg ON
Beta-blocker-titrated to maximum tolerated dose
ACE inhibitor-titrated to maximum tolerated dose
All patients with left ventricular systolic dysfunction should receive an …..
Angiotensin-Converting Enzyme inhibitor: ACEI
…… are now recognised as having an important role and should be used first line in moderate/stable heart failure
Beta-blockers are now recognised as having an important role and should be used first line in moderate/stable heart failure
Beta-blockers are now recognised as having an important role and should be used first line in ….
Beta-blockers are now recognised as having an important role and should be used first line in moderate/stable heart failure
important points about ACE inhibitors which make them helpful in HF
Reduce afterload and pre-load, prolong life and relieve symptoms, oppose neurohormonal adaptation and may prevent cardiac remodelling.
ACE inhibitors should not be used with…
NSAIDs
What blood results should be monitored when using ACE I
urea/creatinine
Ace inhibitors should be titrated…
upwards to max tolerable dose, may exceed max licensed dose in HF
What alterations could be made to conteract hypotension in ACE Is
give at night, withdraw diuretics for a few days
Thiazides / loop diuretics may cause …. – this is less of a problem if they are used with ACEIs
Thiazides / loop diuretics may cause hypokalaemia – this is less of a problem if they are used with ACEIs
Thiazides / loop diuretics may cause hypokalaemia – this is less of a problem if they are used with ….
Thiazides / loop diuretics may cause hypokalaemia – this is less of a problem if they are used with ACEIs
hypokalaemia in HF can be caused by ….. diuretics. It can enhance the effect of digoxin
hypokalaemia in HF can be caused by loop diuretics/thiazide diuretics. It can enhance the effect of digoxin
hypokalaemia in HF can be caused by loop diuretics/thiazide diuretics. It can enhance the effect of ….
hypokalaemia in HF can be caused by loop diuretics/thiazide diuretics. It can enhance the effect of digoxin
Digoxin is generally reserved for ……
Digoxin is generally reserved for heart failure with atrial fibrillation
or when other treatments fail to control the condition
Digoxin doses should be…. to ensure ventricular rate does not fall below 60 beats/min as this indicates toxicity
Digoxin doses should be titrated to ensure ventricular rate does not fall below 60 beats/min as this indicates toxicity
Digoxin doses should be titrated to ensure ventricular rate does not fall below … beats/min as this indicates toxicity
Digoxin doses should be titrated to ensure ventricular rate does not fall below 60 beats/min as this indicates toxicity
digoxin is contra-indicated in ….
concurrent heart block or bradycardia
In HF,…. has been shown in a Low dose 25 mg (non-diuretic dose) to reduce mortality by 35%
In HF, Spironolactone has been shown in a Low dose 25 mg (non-diuretic dose) to reduce mortality by 35%
In HF, Spironolactone has been shown in a ….. to reduce mortality by 35%
In HF, Spironolactone has been shown in a Low dose 25 mg (non-diuretic dose) to reduce mortality by 35%
In HF, Spironolactone has been shown in a Low dose 25 mg (non-diuretic dose) to …..
In HF, Spironolactone has been shown in a Low dose 25 mg (non-diuretic dose) to reduce mortality by 35%
…. are especially useful in HF associated with ischaemia
B-Blockers are especially useful in HF associated with ischaemia
B-Blockers are especially useful in HF associated with ….
B-Blockers are especially useful in HF associated with ischaemia
what qualities of B-blockers make them effective treatment for HF
Reduce sympathetic stimulation, HR and O2 consumption
Antiarrhythmic activity reduces sudden death
WILL ALSO CONTROL RATE IN ATRIAL FIBRILLATION
Oppose the neurohormonal activation which leads to myocyte dysfunction
which B-Blockers are used to treat HF
Metoprolol, bisoprolol, nebivolol, carvedilol also an a-blocker/antioxidant
why are diuretics useful in treating HF
Cause reduction in circulating volume, reduce preload and after load
Also cause venodilatation, reduce preload
diuretics are generally used in HF when there is
peripheral/pulmonary odema
symptoms of digoxin toxicity
anorexia, nausea (suggest dose too high), visual disturbances, diarrhoea
…..
Remains the 1st line medication for stroke prevention. Should aim for INR range 2-3 for AF
Warfarin
Remains the 1st line medication
INR range 2-3 for AF
Warfarin
Remains the 1st line medication for stroke prevention. Aim for
INR range …. for AF
2-3
What treatment can be used in stroke prevention if warfarin is not suitable?
aspirin 75MG
Why would a dose higher than 75mg/day of aspirin not be considered?
Pharmacologically, near-complete platelet inhibition is achieved with aspirin 75 mg/day. Therefore there is no need for a larger dose as all that is seen is an increase in side effects.
which cardiac drugs can be used for rate control?
B-blockers (eg bisoprolol/atenolol), Non DHP Ca channel blockers (Verapamil, diltiazim), digitalis glyclosides (digoxin, digitoxin), amioderone, dronedarone
Digoxin only controls….
Only controls ventricular rate at rest
what affect does digoxin exert on the heart
Increase the force of myocardial contraction and reduces conductivity within the AV node
SEs of amioderone
Corneal microdeposits Optic neuritis/optic neuropathy Phototoxic reactions Hypothyroidism/Hyperthyroidism Hepatotoxicity Fibrosis
which drugs should be avoided in HF?
Thiazolidinediones, Cause worsening of HF
Calcium Channel Blockers
Have a negative inotropic effect
NSAID’s Cause sodium and water retention
What drugs have been shown to have no benefits in HF?
Statins
Oral Anticoagulants
No reduction in mortality/morbidity compared to placebo or aspirin
Ca channel blockers should be avoided in HF because…
they have a -ve inotropic effect
NSAIDs should be avoided in HF because…
cause Na and water retention
The chance of a poor outcome in HF is highest ….
early after the onset of HF
what would be the treatment for HF with sustained ejection fraction
Use of diuretics for the relief of congestion and oedema Treatment of co-morbidity Hypertension IHD Diabetes
what benefits do spironolactones/mineralocorticoids have on patients with HF
Significant reductions of both morbidity and mortality
Reduce left ventricular hypertrophy
what needs monitored with use of spironolactones/mineralocorticoids
renal function and K+
what would be the first choice(s) of drugs to treat tonic-clonic seizures
1st choice valproate or carbamazepine or lamotrigine (in females of childbearing age)
2nd levetiracetam
what would be the first choice(s) of drugs to treat absence seizures
1st choice: ethosuximde
2nd choice: valproate/lamotrigine
what would be the choice(s) of drugs to treat myoclonic seizures
Sodium Valproate, Clonazepam and Levetiracetam
what would be the choices of drugs to treat atypical seizures
Sodium Valproate, Lamotrigine and Clonazepam
MOA sodium valproate
Potentiates GABA and causes sodium channel blockade
side effects sodium valproate
Side effects: sedation, weight gain, tremor
Need to carry out LFT’s. Ass with liver damage. Associated with birth defects, avoid in child bearing age
MOA Carbimazapine
Carbamazepine
Use dependent blockade of sodium channels
side effects carbamazapine
Side effects: rash, dizziness, double vision
Patients need to be able to recognise signs of blood disorders Many interactions: induction leads to acclerated metabolism of interacting drugs. Associated with birth defects
features of lamotigrine
Use-dependent blockade of Na-channels, reduces release of glutamate
Not particularly sedating
Withdraw if the patient develops a rash/flu-like illness – risk of life threatening skin conditions and associated with bone marrow toxicity, (aplastic anaemia)
which epilepsy treatment(s) are associated with thrombocytopenia
valproate
which epilepsy treatments are associated with altered liver function
Carbamazepine & valproate may affect hepatic function ~ altered liver function tests (LFTs)
LFT (essential with valproate) & INR monitoring
which epilepsy treatment(s) are associated with severe skin disorders eg;stevens johnson syndrome
carbamazepine, lamotrigine, phenytoin, valproate)
why may epilepsy drugs become less effective during pregnancy
Due to enzyme induction and increased volume of distribution
what would be appropriate treatment for status epilepticus?
Lorazepam i.v. Or Diazepam: i.v. or as rectal solution Or Clonazepam Or Phenytoin slow i.v. Failing the above a general anaesthetic such as propofol
explain why phenytoin is not a first line drug choice for long term epilepsy therapy
metabolism saturates and so get disproportionate increases in plasma concentration on increasing dose
Rates of metabolism varies between patients
– requires plasma conc monitoring
which factors increase gastric acid secretion
Increase acid secretion
Histamine via H2 receptors
Gastrin
Acetylcholine via M-receptors – M3 on parietal cells
which factors decrease gastric acid secretion
Decrease acid secretion
Prostaglandins (E2 and I2)
Also cytoprotective via bicarbonate and mucus release
How do H2 receptor antagonists work
Histamine H2 receptors: coupled via adenylyl cyclase to increase cAMP which activates the proton pump:
examples of H2 receptor antagonists
ranitidine, cimetidine, famotidine (tagamet, zantac, pepcid)
H2 antagonists are best given…
at night
which impoportant interaction does cimetidine have. Which other drug in its class doesn’t have this effect?
Cimetidine - inhibits cytochrome P450 and therefore the metabolism of other drugs, resulting in important drug interactions e.g.
Oral anticoagulants
Phenytoin
Carbamazepine
Tricyclic antidepressants
Ranitidine does not interact in this way and is thus favoured
