PHARMACOLOGY Flashcards
mechanism of ivabradine
selective blocker of HCN channels
effect of ivabradine on the pacemaker potential
reduces the slope
ivabradine effect
slows HR
reduces oxygen consumption
ivabradine uses
angina
tachycardia
mild to moderate chronic heart failure
side effects of ivabradine
arrhythmias
hypotension
name B-adrenoreceptor agonists
dobutamine
adrenaline
noradrenaline
which channels is dobutamine selective for?
B1
mechanisms of B-adrenoreceptor agonists
results in stimulation of adenylyl cyclase and production of cAMP which generates protein kinase A
phosphorylation increases Ca++ influx and release of Ca++ from the SR
effect of B-adrenoreceptor agonists
increase contractility, force and rate
decrease cardiac efficiency
use of B-adrenoreceptor ligands
infarction cardiogenic shock cardiomyopathies inotropic support heart failure (dobutamine) asthma emergency (adrenaline) anaphylactic shock
side effects of B-adrenoreceptor agonists
arrhythmias
acute MI
name B blockers
propranolol
metoprolol
atenolol
which of the B blockers is non selective?
propranolol
which of the B blockers are selective for B1?
metoprolol
atenolol
effect of B blockers
decrease in heart rate, contractility, MAP and O2 consumption
use of B blockers
angina
hypertension
heart failure
side effects of B blockers
asthma fatigue cold peripheries heart failure bradycardia (heart block) hypoglycaemia
which patients could have heart failure as a side effect of beta blockers?
in patients who rely on sympathetic drive to maintain CO
name the muscarinic antagonist which is non selective for M2 receptors
atropine
effect of atropine (muscarinic antagonist)
increase in heart rate
use of atropine (muscarinic antagonist)
reverse bradycardia following an MI
side effects of atropine
arrhythmias
hallucinations
confusion
name the cardiac glycoside
digoxin
mechanism of action of digoxin
competes with K+ and at alpha subunit blocks the Na/K ATPase pump
effect of digoxin
increase in contractility, force and CO
indirect- increased vagal discharge and slows SA node discharge
shortens action potential and refractory period
when are the effects of digoxin dangerously enhanced?
hypokalaemia
use of digoxin
heart failure
atrial fibrillation
side effects of digoxin
heart block
dysrhythmias
myocarditis
name the calcium sensitiser
levosimendan
mechanism of levosimendan
binds to troponin C in myocytes, sensitising them to Ca2+
effect of levosimendan
increase in contractility
use of levosimendan
acutely decompensated congestive heart failure
side effects of levosimendan
headaches
arrhythmias
hypokalaemia
class I anti arrhythmic drug
A = disopyramide B = lignocaine C = flecainide
mechanism of class I
voltage activated Na+ channels
reduces Na+ channel current
use of class I
rhythm control
side effects of class I
negative inotropic effects
class II anti arhythmic drug
B-blockers eg propranolol
use of class II
rate control
class III anti arhythmic drug
amiodaron sotalol
mechanism of amiodaron sotalol
voltage activated K+ channels
action potential prolongation
use of amiodaron sotalol
rhythm control
class IV anti arrhythmic drug
Ca2+ channel antagonist eg verapamil
use of class IV
rate control
name nitrates
isosobide mononitrate
GTN spray
mechanism of nitrates
mimic the effect of endothelium produce nitric oxide NO causes efflux of Ca++ producing hyperpolarisation and relaxation cGMP is also produced which regulates protein kinase G activity causing relaxation endothelin is also produced venorelaxation arteriolar dilatation increase in coronary blood flow
name ACE inhibitors
prills eg ramipril
mechanism of ACE inhibitors
block the conversion of angiotensin I to angiotensin II so aldosterone and ADH are not stimulated
effect of ACE inhibitors
vasodilation and arterial dilation
use of ACEis
hypertension
heart failure
side effects of ACEis
renal dysfunction
oedema
dry cough
when are ACEi and ARBs contraindicated?
pregnancy
name the ARBs
tans eg losartan
mechanism of ARBs
blocks angiotensin II receptors
use of ARBs
hypertension
heart failure
intolerance of dry cough of ACEi
side effects of ARBs
renal dysfunction
oedema
name calcium antagonists
amlodipine
verapamil
diltiazem
mechanism of calcium antagonists
decrease conduction at SA and AV node
effect of calcium antagonists
decrease in heart rate
use of calcium antagonists
hypertension
angina
supraventricular arrhythmias
side effects of calcium antagonists
ankle oedema
bradycardia (caution when using beta blockers)
name the main alpha blocker
doxazosin
mechanism of alpha blockers
block alpha adrenoreceptors to cause vasodilation
use of alpha blockers
hypertension
prostatic hypertrophy
side effect of alpha blockers
postural hypertension
name potassium channel openers
DILS
minoxidil
nicroandil
mechanism of potassium channel openers
causes hyper polarisation which switches off calcium channels
mediated by ATP
effect of potassium channel openers
relaxation of vascular smooth muscle
use of potassium channel openers
severe hypertension
angina
side effects of potassium channel openers
tachycardia
salt and water retention
name a thiazide diuretic
bendrofluazide
name a loop diuretic
furosemide
mechanism of thiazide diuretics
inhibit NaCl reabsorption in distal tubules by blocking NaCl co-transporter
mechanism of loop diuretics
inhibit NaCl reabsorption in the thick ascending limb of the loop of henle
use of diuretics
hypertension
heart failure
effect of diuretics
increase in excretion of Na, Cl and water
side effects of diuretics
hypokalaemia arrhythmias fatigue hyperglycaemia increase in uric acid = gout
name statins
simvastatin
atorvastatin
mechanism of statins
blocks HMG coA reductase which inhibits the formation of cholesterol
effect of statins
decrease in LDL and total cholesterol inflammation
stabilised atherosclerotic plaque and decreases thrombosis
use of statins
hypercholesterolemia
side effects of statins
used in caution with hypothyroidism and history of liver disease
myalgia, myopathy, myositis
name fibrates
bezafibrate
gemfibrozil
mechanism of action of fibrates
agonist of nuclear receptors which enhances transcription of lipoprotein lipase which hydrolyses triglycerides to fatty acids and glycerol
use of fibrates
high triglyceride levels
side effect of fibrates
myositis
name bile acid binding resins
colestyramine
colestipol
colsevelam
mechanism of bile acid binding resins
cause the excretion of bile salts resulting in more cholesterol to be converted to bile salts
bile resins bind bile in the intestine so it is not absorbed in the duodenum
liver uses metabolises cholesterol to compensate for its lost
use of bile acid binding resins
decreased absorption of triglycerides
increased LDL receptor expression
side effect of bile acid binding resins
GI tract irritation
mechanism of action of ezetimibe
inhibits transport proteins and reduces absorption of cholesterol
use of ezetimibe
to lower LDL cholesterol
side effects of ezetimibe
diarrhoea
abdominal pain
headache
when is ezetimibe contraindicated?
in breast feeding
name anticoagulants
warfarin
heparin
LMWH
orally active inhibitors
mechanism of action of warfarin
acts as a vitamin K antagonist which prevents production of mature coagulation factors
use of anticoagulants
DVT
PE
NSTEMI
AF
side effect of warfarin
haemorrhage anywhere
reversed by vitamin K
mechanism of action of anticoagulants (except warfarin)
binds to antithrombin III, increasing its affinity for serine proteases to greatly increase their rate of inactivation
side effects of anticoagulants
haemorrhage
osteoporosis
hypoaldosteronism
hypersensitivity reactions
name anti platelets
aspirin
clopidogrel
mechanism of action of anti platelets
prevent new thrombosis
blocks COX, inhibiting formation of TXA2 which causes cross linking of platelets
blocks ADP from binding to P2Y12 receptor and formation of fibrin
use of anti platelets
angina
acute MI
cerebral vascular incident (CVA) and TIA
patients at risk of above
side effects of anti platelets
haemorrhage
peptic ulcer
aspirin sensitivity -> asthma
name fibrinolytic drugs
streptokinase
tissue plasminogen activator
alteplase duteplase
mechanism of fibrinolytic drugs
fibrinolytic cascade opposes coagulation cascade
activate formation of plasmin from plasminogen which lysis fibrin into fibrin fragments causing lysis of the clot
use of fibrinolytics
STEMI
PE
stroke
reopen acclude arteries
side effect of fibrinolytics
haemorrhage risk (controlled by tranexamic acid which inhibits plasminogen activation)
