Detailed table of all the drugs mentioned throughout the course and textbook along with their mechanisms of actions, side effects, uses, etc. Useful for the MCQ
Samenvatting Rang & Dale's Pharmacology hoofdstukken Farmacologie
A summary of benzodiazepines and their uses to treat CNS disease
Samenvatting van alle hoorcolleges, werkcolleges en zelfstudies van de cursus Algemene Farmacologie Thema 1: Farmacokinetiek (BMW30405)
Alles voor dit studieboek
(31)
Geschreven voor
University College London (UCL)
University College London
PHAR0007 Introductory Pharmacology (PHAR0007)
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DRUGS AFFECTING NORADRENERGIC
TRANSMISSION
Main Unwanted Pharmacokinetic
Type Drug Uses/function
action effects effects
Adrenoceptor Poorly absorbed by mouth
Not used
agonists à Rapid removal by tissues
clinically
directly Metabolized by MAO and
acting COMT
Transmitter at
sympathomi
postganglionic
metic drugs Bind to adrenoceptors to
sympathetic Hypertension
Norepinephri stimulate a response
neurons and in Vasoconstricti
ne
α1/2/β1 CNS on
/ Stimulates a1-
agonist Tachycardia
Noradrenalin adrenoceptor mediated
Hormone of Ventricular
e vasoconstriction to
adrenal medulla dysrhythmias
increase cardiac output
Treats
Simulates B1-mediated
circulatory
vasoconstriction to
shock with drop
increase force and rate of
in BP
contraction
α1/2/β1
Adrenaline
agonist
β1/2
Isoprenaline
agonist
Asthma,
anaphylactic
Hypertension
shock, cardiac
Vasoconstricti Poorly absorbed by mouth
arrest, added to
on Rapid removal by tissues
Epinephrine α/β agonist local anesthetic
Tachycardia Metabolized by MAO and
solutions
Ventricular COMT
Main hormone
dysrhythmias
of adrenal
medulla
Relieves decongestion
Hypertension
Phenylephrin Nasal through a1-mediated
α1 agonist Reflex
e decongestion vasoconstriction to shrink
bradycardia
the blood vessels
Stimulates B2-
adrenoceptors on skeletal
muscle arterioles to
produce vasodilation
Drop in diastolic blood
pressure à activates
Asthma baroreceptor reflex to
Not endogenous increase sympathetic
Methoxamin Tachycardia
α agonist substance stimulation
e Dysrhythmias
Nasal
decongestant Stimulates B1-
adrenoceptors to increase
heart rate
Relieves decongestion
through a1-mediated
vasoconstriction to shrink
he blood vessels
Clonidine α2 agonist Hypertension Drowsiness Stimulation of a1-
Migraine Orthostatic adrenoceptors and post-
, hypertension synaptic a2-
Oedema adrenoceptors on blood
Weight gain vessels at high
Rebound concentrations causes
hypertension vasoconstriction
Causes pupil dilation via
stimulation of a2-
Brimonidine α2 agonist Glaucoma adrenoceptors on ciliary
body to reduce aqueous
humour production
Stimulates B2-mediated
Tachycardia bronchodilation
Asthma Dysrhythmias Stimulates B2-
Salmeterol β2 agonist Premature Tremor adrenoceptor relaxation
labour Peripheral on uterine smooth muscle
vasodilation Given by aerosol
Tachycardia A short-acting analogue of
Dysrhythmias Salmeterol, used for
Salbutamol β2 agonist Asthma Tremor asthma treatment. At high
Peripheral doses may cause
vasodilation hypokalemia in liver.
Tachycardia
Asthma Dysrhythmias
Terbutaline β2 agonist Delay of Tremor
parturition Peripheral
vasodilation
Tachycardia
Anabolic action Dysrhythmias
Clenbuterol β2 agonist to increase Tremor
muscle strength Peripheral
vasodilation
Tachycardia
Dysrhythmias
Delay of
Ritodrine β2 agonist Tremor
parturition
Peripheral
vasodilation
Binds to B1
adrenoceptors
Powerful Increases levels of
contraction of Angina cAMP
cardiac Arrhythmias Increases PKA
β1 myocytes Tachycardia activation
Dobutamine
agonists Short term Anxiety
Dopamine Phosphorylation of
continuous Fatigue
support in heart Headache L-type Ca2+
failure channels
Increased cellular
Ca2+ and
contraction
Relaxes bladder smooth
muscle to treat overactive
Treat overactive Cannot treat bladder
Mirabegron β3 agonist bladder obesity in Found on brown
Anti-obesity adults adipocytes à stimulate
non-shivering
thermogenesis
Indirectly Hypertension
acting Vasoconstricti
Destroyed by MAO in the
sympathomi No clinical use on
Tyramine NA release gut
metic agent Present in foods Tachycardia
Does not enter brain
Ventricular
dysrhythmias
Amphetamin NA release CNS stimulant in Well absorbed orally
, MAO narcolepsy
inhibitor Hyperactive Penetrates freely into
NET children brain
e
inhibitor Appetite Excreted unchanged in
CNS suppressant urine
stimulant Drug of abuse
When NA is released from
presynaptic nerve
terminal by exocytosis,
Hypertension
some stimulates post
Tachycardia
synaptic adrenoceptors
Insomnia
Acute
NA release Signal terminated quickly
psychosis with
Β agonist by reuptake of NA into
Nasal overdose
Ephedrine Weak CNS presynaptic nerve
decongestion Dependence
stimulant terminals
action
Uptake blockers bind to
NA transport to prevent
NA from being taken back
up in the presynaptic
terminal
α- α- Postural
adrenoceptor antagonist hypotension
antagonists non- Flushing
Phenoxyben Phaeochromocy
selective Tachycardia
zamine toma
irreversible Nasal
uptake 1 congestion
inhibitor Impotence
Postural
α1/2- Rarely used hypotension
antagonist Anti- Flushing
Phentolamin
non- hypertensive Tachycardia
e
selective Higher NA Nasal
vasodilator release congestion
Impotence
Blocks a1-adrenoceptors
Postural
α1 on arterioles stopping
hypotension
Antagonist vasoconstriction action
Flushing
competitiv lowering blood pressure
Prazosin Hypertension Tachycardia
e
Nasal
reversible Blocks a1-mediated
congestion
contraction of the smooth
Impotence
muscle
Blocks a1-mediated
α1 Prostatic Failure of
Tamsulosin contraction of the smooth
Antagonist hyperplasia ejaculation
muscle
α2 Not clinically Blocks presynaptic a2-
Excitement
Yohimbine Antagonist used arenoceptors causing
Hypertension
aphrodisiac increased release of NA
Blocks a1-adrenoceptors
on arterioles stopping
vasoconstriction action
Hypertension
α1 lowering blood pressure
Doxazosin Benign prostatic
Antagonist
hyperplasia
Blocks a1-mediated
contraction of the smooth
muscle
Blocking presynaptic a2-
α2
Mirtazapine Antidepressant adrenoceptors causes
antagonist
increased release of NA
Consequence of a1-adrenoceptor antagonist:
Adrenaline reversal in vivo
- Adrenaline normally causes rise in BP by a-adrenoceptors à vasoconstriction
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