Anda di halaman 1dari 29

Drug Classes – ANS

The Nervous System


 Cholinergic Drugs
 Acetylcholinesterase drugs
 Cholinergic agonists
 Atropine
 Adrenergic Drugs
 Direct-acting
 Indirect-acting
 Dual-acting
 -blockers

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Sites of Action
 5 sites of action
 Synthesis
 Release
 Storage
 Action
 Termination of
action

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Cholinergic = Parasympathetic
 Cholinergic drugs
 Promote action of neurotransmitter (NT)
acetylcholine (Ach)

 2 types
 Cholinergic agonists
 AntiACh-ase drugs

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Cholinergic Agonists
 Directly stimulate cholinergic receptors

 Look like ACh but not

 Acts like Ach so would have similar


action

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Cholinergic Agonists – PK
 Rarely given by IV or IM injection

 WHY?
 Acetylcholinesterase  breaks down drugs
before the can act
 Act quickly, may cause “cholinergic crisis”

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Cholinergic Agonists – PK
 Commonly given PO, SC, eye drops
 All drugs metabolized by
cholinesterases
 At receptor sites
 In plasma
 In liver
 Excreted by kidney

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Cholinergic Agonists – PT

 Treat weak bladder conditions

 Post-op / post-partum urinary retention

 Post-op abdominal distention

 GI atony

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
AChase Inhibitors
 Inhibit acetylcholinesterase enzyme
 Enzyme found in synaptic clefts (between nerve
and effector cell)
 Normal function = break down ACh

 Thus, AChase Inhibitors allow ACh to hang


around longer

 Can be reversible or irreversible

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Anticholinesterase – PK
 Readily absorbed from GI, SC
 Can be given IM, IV
 Only physostigmine cross BBB
 Most metabolized throughout the body
 Excreted by kidneys

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Anticholinesterase – PT
 Increase bladder tone
 Reduce eye pressure (glaucoma, surg)
 Improve tone, peristalsis in GI tract
 Treat overdose of cholinergic blocking
drugs, TCA, Narcotics

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Cholinergic Blocking Drugs
 Interrupt parasympathetic nerve
impulses
 Cholinergic blockers only block
muscarinic receptors
 Ex. ATROPINE

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Atropine - PK
 Absorption from eyes, GI, mm, skin
 Distributed, mostly, throughout body
 “Alkaloids” readily cross BBB
 Others don’t
 Low to moderate protein binding
 Metabolized in liver, excreted in feces +
pee

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Atropine – PT
 Pre-op > reduce oral/gastric secretions
 Prevent drop in heart rate

 My dad!
 Syncope because of drop in heart rate
and blood pressure
 Give atropine > wakes up!

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Atropine – PD
 Without the drug
 ACh released by vagal nerve onto SA node
 SA node = pacemaker of the heart
 Slows electrical conduction between atria and
ventricles
 Heart rate slows down
 With the drug
 Competes with ACh for binding site in SA node
 Atropine speeds up the heart!

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Adrenergic Drugs
 Sympathomimetic drugs

 Catecholamines
 Noncatecholamines

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Adrenergic Drugs
 Direct-acting
 Direct effect on a target organ
 Indirect-acting
 Triggers neurotransmitter
 NT takes over from there
 Dual-acting
 Always work both ways

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Catecholamines
 Can’t be taken orally > destroyed by
enzymes
 Sublingually
 SC absorption slow
 WHY?
 IM absorption more rapid
 WHY?

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Catecholamines
 Metabolized by liver (predominantly)
 Excreted primarily in urine
 Some in feces and breast milk

 Primarily direct acting


 Act on alpha or beta receptors
 See attached sheet
© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Catecholamines – PT
 Norepinephrine has most pure -
activity
 Dobutamine and isoproterenol have
only -related uses
 Epinephrine stimulates - and -
receptors
 Dopamine acts on dopamine receptors

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Noncatecholamines - PT
 Local or systemic constriction of blood
vessels (eg. phenylephrine)
 Nasal and eye decongestion (eg.
ephedrine)
 Dilation of bronchioles (eg. albuterol)
 Smooth-muscle relaxation

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Adrenergic Blockers
 Alpha-adrenergic blockers
 Relax smooth muscle in blood vessels
 Increase dilation of blood vessels
 Decrease blood pressure

 Learn about orthostatic hypotension in


your book

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Alpha-blockers – PT
 Used to treat
 Hypertension
 Peripheral vascular disorders (Raynaud’s)

 Use has become controversial


 New study recently showed lots of side-
effects
 Almost last-line treatment
© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Beta-Blockers
 BIG BIG BIG BIG BIG MONEY!
 Cheap drugs, but prescribed a lot!

 1 sites mostly in heart


 2 sites mostly in bronchi, blood
vessels, uterus
 Nonselective -blockers also exist

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
-blockers – PK
 Absorbed rapidly and well from GI
 Protein-bound to some extent
 Onset of action is primarily dose- and drug-
dependent
 When given IV, reach peak levels fast
 Distribution: lots in heart, liver, lungs, saliva
 Metabolized by liver, excreted by kidneys

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
-blockers – V/ IMPORTANT!

We will talk about these a lot more


when we come to cardiovascular
related case-studies.

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
-blockers – V/ IMPORTANT!
 Reduce blood pressure
 Reduce heart rate and excitability
 Slow conduction of electrical impulse
 Decreased force of heart’s contraction
 Constriction of bronchioles
 Constriction of peripheral blood vessels

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Sample Question
Patient with hypertension is prescribed a
drug. Which would be your first
choice?
(A) Alpha-blocker

(B) Beta-blocker

(C) Alpha-agonist

(D) Beta-agonist

(E) Epinephrine

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001
Sample Question
Which of the following would be the
LEAST expected side-effect from
therapy with that agent?
(A) Orthostatic hypotension

(B) Nausea and vomiting

(C) Dizziness

(D) Hypertension

(E) Flatulence

© Johns Hopkins University, Baltimore, Maryland /// Contributed by: Andrew Healey, 2001