Drugs Flashcards
Name a ß-1 antagonist and what it is used to treat
atenolol used to treat hypertension
decrease HR & force of contraction
name an a1-antagonist and what it is used to treat
doxazosin
treat hypertension through vasodilation (anti-hypertensive drug), inhibits NA on vascular SM
name a mixed adrenoceptor antagonist
carvedilo
not used as too much side effects
Name a ß1 agonist and when it is used
dobutamine
relax SM, cardiogenic shock (pump failure)
Name a ß2-agonist and when it is used
salbutamol treat asthma (bronchodilation)
What is a muscarinic agonist and when is it used?
pilocarpine used to treat glaucoma (cause constriction)
binds to M3 receptor
Wha is a muscarinic antagonist and what are the effects?
atropine
M2: increase HR
M3: cause bronchial (dilation) relaxation (normally M3 cause constriction, parasympathetic)
dilate pupils
Name an Na+ blocker and when it is used and how it works
Lidocaine
used after MI to prevent V.tachycardia
acts in open / inactivate state, dissociates rapidly for next AP
stops afterdepolarisation (high Ca2+, long QT)
Name a ß-adrenoceptor antagonist and what it does
sympathetic increases after an MI which causes ventricular arrhythmia (tachycardia)
so ß-blocker reduces O2 demand and less Ca2+ (decrease HR & contractility)
slows AVN conduction - prevent supraventricular tachycardia & ventricular rate
slows down funny current (HCN), increasing PR interval from 3-5ss
less cAMP produced, less PKA phosphorylates L-type VOCC, less bind to RyR (decrease force & rate)
what is the function of K+ channel blockers and when are they used?
lengthens ARP (phase 3), not used as pro-arrhythmic except amiodarone in W-P-W (re-entry loops, multiple foci, affects QRS) treat tachycardia prolongs QT
Function of Ca2+ blockers and when they are used?
blocks L-type Ca2+ channels (upstroke of SAN - depolarisation)
decrease Ca2+ decreasing force of contraction & HR (SAN), doesn’t affect ventricles as Ca2+ in ventricles only affect plateau
slows AVN as SAN i slowed - lengths PR (P also widens)
cause peripheral & coronary vasodilation
if used with ß-blocker cause HF
What is adenosine used? what does it act on?
can be produced endogenously
acts on A1 receptors on AV node
phosphorylates K+ channels - hyperpolarise cells of conduction tissues
stops heart arrhythmia: low dose of high conc K+ stops heart suddenly to start again - restore sinus rhythm quickly - like ‘defib’
Name an example of a cardiac glycoside and how it functions
digoxin
blocks Na+/K+/ATPase, increases intracellular Na+, so NCX reverses to pump 3Na+ out and 1Ca2+ in, increasing force of contraction and CO
increases vagal nerve (parasympathetic) - slows down HR
How do organic nitrates work?
released from endothelial cells, reacts with thiol (-SH) of SM, produces NO2- reduced to NO
causes venodilation (decrease pre-load
dilate collateral arteries
all reduce workload of the heart
Which drugs do you give to reduce work load of the heart?
ACE-inhibitors (decrease angiotensin II, less Na+, less water retention, less blood volume)
diuretics
ß-blockers (decrease AC, decrease cAMP, decrease Ca2+ for force of contraction)