Drugs Flashcards

1
Q

Name a ß-1 antagonist and what it is used to treat

A

atenolol used to treat hypertension

decrease HR & force of contraction

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2
Q

name an a1-antagonist and what it is used to treat

A

doxazosin

treat hypertension through vasodilation (anti-hypertensive drug), inhibits NA on vascular SM

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3
Q

name a mixed adrenoceptor antagonist

A

carvedilo

not used as too much side effects

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4
Q

Name a ß1 agonist and when it is used

A

dobutamine

relax SM, cardiogenic shock (pump failure)

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5
Q

Name a ß2-agonist and when it is used

A
salbutamol
treat asthma (bronchodilation)
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6
Q

What is a muscarinic agonist and when is it used?

A

pilocarpine used to treat glaucoma (cause constriction)

binds to M3 receptor

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7
Q

Wha is a muscarinic antagonist and what are the effects?

A

atropine
M2: increase HR
M3: cause bronchial (dilation) relaxation (normally M3 cause constriction, parasympathetic)
dilate pupils

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8
Q

Name an Na+ blocker and when it is used and how it works

A

Lidocaine
used after MI to prevent V.tachycardia
acts in open / inactivate state, dissociates rapidly for next AP
stops afterdepolarisation (high Ca2+, long QT)

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9
Q

Name a ß-adrenoceptor antagonist and what it does

A

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)

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10
Q

what is the function of K+ channel blockers and when are they used?

A
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
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11
Q

Function of Ca2+ blockers and when they are used?

A

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

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12
Q

What is adenosine used? what does it act on?

A

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’

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13
Q

Name an example of a cardiac glycoside and how it functions

A

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

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14
Q

How do organic nitrates work?

A

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

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15
Q

Which drugs do you give to reduce work load of the heart?

A

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)

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16
Q

When are antithrombotic drugs used?

A
acute fibrillation (HF)
acute MI
mechanical prosthetic heart valves
17
Q

how do ACE-inhibitors work?

A

decrease pre-load (blood volume decrease)
decrease afterload (vasodilate, decrease vasomotor tone, decrease peripheral vessels resistance)
chronic heart failure