Drugs 1 Flashcards
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what is Lidocaine
blocks volatge gated NA+ channels local anaesthetic only blocks in open/inactive state aka blocks damaged depolarised tissue blocks during depoalrisation dissociated in time for next AP blocks after an AP has occurred
when would you use lidocaine
after an MI - only if patient shows signs of ventricular tacycardia
give IV
not used prophyaltically following MI
what is propranolol
b-adrenoreceptor antagonist
describe b-adrenoreceptor anatgonists
e..g propranol
prevent supraventricualr tachycardia - slows conduction in AV node, slows Ventriuclar rate in patients with AF
used following an MI - becaue MI causes increased symathetiic actiivty.
b-blockes prevent ventricular arrythmais
reduced O2 demand - reduces myocardial ischaemia therefore good following MI
descrbie the mechanism of beta blockers on APs
decreases slope of pacemakrer potential in SA
slows conduction at AV node - stops supraventricular tachycardia going through (AF)
get a more normal ventricular rate
decribe class 4, L type Ca2+ channel blockers
decreases slope of AP at SA node
decreases AV nodal conduction
decreases force of contraction = negative ionotrophy (iron man= ionoptropy)
coronary and peripheral vasodilation
give 2 examples of Ca2+ channel blockers
Dihydropridine Ca2+ channel blockers
describe what adenosine is and uses
G alpha 1
produced endogenosuly at physillgical levels but can be given IV
Acts on receptors at AV node
v.short half life
enhances K+ conductance - hyperpolarises cells of conducting tissue
anti-arryhtmics - useful for terminating re-enterant SVT
describe class 3 anti arryhtmia drugs
prolong AP
block K+ channels = lengthens refractory period
can be pro-aryhtmic - prolongs QT interval
when would you use class 3 drugs
treat tachycardia associated with Wolff-parkinson White syndrome as this has a re-entry loop due to an extra conduction pathway)
effective for suppressing ventricular arrhyhtmias post MI
give an exam[ple of an ACE inhibitor
Perindopril
what is function of ace inhibitor
inhibits action of angiotensin converting enzyme (angiotensin 1 into 2)
acts on kidneys to increase Na+ and water reabsoprtion and is a vasoconstrictor
decreases vasomotor tone (decreases BP) = reduces afterload of heart
decreases fluid retention (decreases blood volume) = reduces preload of heart
when would you use ACE inhibitors
hypertension
heart failure
what problem do you get with ace inhibitors
can cause dry cough due to excess bradykinin (these get broken down into peptides)
what type of drug do you give to someone who cannot tolerate ACE inhibitors?
Angiotensin 2 receptor blockers (ARBs)
give an example of ARBs
Losartan
what is furosemide
diuretic
describe the mechanism of diuretics
loop of henle
reduces pulmoanry and peripheral oedema
when would you give diuretics
heart failure
hypertension
congestive heart failure
how does amlopidine, nicardipine work
ca2+ channel blockers
decreases peripheral resistance
decreases arterial bp
reduce workload of heart by reducing afterload
how does verampamil work
act on heart
ca2+ channel blockers
reduce workload by reducing force of contraction
when would you use ca2+ channel blockers
hypertension
angina
coronary artery spasms
SVTs - supraventricular tachycardias
give an exmaple of a cardiac glycoside
digoxin
how do cardiac glcosides work
increased vagal activity - action via CNS, slow AV conduction, slows HR
Positive inotropes
blocks Na+ K+ ATPase
Ca2+ is extruded via Na+ and Ca2+ exhancges driven by Na+ moving down conc gradient
leads to raise in [Na+] intracellular = decrease in activity of Na+ Ca2+ exchanger
cause increase in intracellular Calcium = more calcium stored in SR
incresaed force of contraction (inotropy)
