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Pharm Drug List

Pharm Drug List

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Published by: sxymd321 on Feb 17, 2013
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Drug List – Autonomics and Cardiovascular
CHOLINERGIC DRUGSMuscarinic Agonists – ch. 4
– Eye (M3): topical application produces rapid miosis andcontraction of ciliary muscle
accommodation and loss of far vision. One of themost potent stimulators of secretions (sweat, tears, saliva, etc.) but is non-specifica.
Clinical use:
for glaucoma
lowering intraocular pressure of bothnarrow-angle (closed angle) and wide angle (open angle) glaucoma b.
Side Effects: can enter the brain and cause CNS disturbances; stimulates profuse sweating and salivation. Stinging and local irritation as well2.
– directly stimulates muscarinic receptors, causing
intestinalmotility and tone. Also stimulates the detrusor muscles of the bladder, but not thetrigone and sphincter 
expulsion of urine. PO, renal excretion,
not degraded bycholinesterase
Clinical: stimulates atonic bladder (particularly in non-obstructive urinaryretention) b.
Side effects: generalized cholinergic stimulation including: sweating,salivation, flushing,
BP, nausea, abdominal pain, diarrhea, bronchospasm, and miosis.c.
Contraindications: asthmatics (due to bronchoconstriction)3.
– has both muscarinic and nicotinic actions. Effects both the CVsystem and the GI system because of its ganglion-stimulating activity, maystimulate then depress these systems. Can cause epinephrine release from theadrenal medulla by nicotinic action. In the eye, it mimics the effects of ACh
Clinical: glaucoma treatment in the eye as a miotic agent by causing papillary constriction
intraocular pressure b.
Side effects: none when used ophthamalogically
Anticholinesterases – ch. 4
– has cholinergic, nicotinic, and muscarinic actions. It is acholinesterase inhibitor, but is also a tertiary amine and therefore
can cross the BBB
intestinal and bladder motility for atony. In the eye
miosisand spasm of accommodation (glaucoma). Also used to treat overdoses of anticholinergics (atropine, phenothiazine, and tricyclic anti-depressants) b.
Side effects: convulsions, respiratory and cardiovascular depression.Possible paralysis of skeletal muscle, but rare in therapeutic doses5.
– cholinesterase inhibitor 
carbamylates cholinesterase’s activesite making the enzyme resistant to hydration (preventing activation)
 accumulation of ACh at the neuromuscular junction.
 Bowel and bladder smoothmuscle
: causes
motility, sphincter relaxation.
Skeletal muscle
: reversesnondepolarizing (i.e. competitive) neuromuscular blockade. Also used for sympathetic and parasympathetic stimulation of the heart (parasympatheticdominates). Effects last 30min – 2hr 
GI motility, stimulates bladder contraction (in atony), treatsmyasthenia gravis[MG] (degrades the nicotinic receptors at theneuromuscular junction so there are fewer receptors that get attacked bythe autoimmune antibodies of MG) b.
Side effects: general cholinergic stimulation (salivation, flushing,
d BP,nausea, abdominal pain, diarrhea, bronchospasm)6.
– Reversibly binds ACh-esterase at the neuromuscular junction(NMJ). Short acting (10-20min), IV, renal excretion, inactivated by plasmaesterasesa.
Clinical: Used to diagnose MG but not treat it because it is too shortacting.i.
Tensilon Test:
ACh at NMJ can overcome ACh receptor ab’s
 sudden, short-lasting improvement followed by
d muscle strengthii.
Used to differentiate worsening MG vs. overmedication
willmake overmedication worse, but will improve worsening MG7.
– similar to edrophonium. Has a long half-life and is used mainlyfor treatment of myasthenia gravis8.
(DFP) – an organophosphate that covalently binds to a serine-OHat the active site of ACh-esterase
permanent inactivation of ACh-esterase.Restoration of ACh-esterase activity requires synthesis of new ACh-esterase.a.
Clinical: Ophthalmic ointment used for chronic treatment of open-angleglaucoma. Effects can last up to a week  b.
Actions: generalized cholinergic stimulation, paralysis of motor functions
breathing difficulties; convulsions, intense miosis9.
(2-PAM) – reactivates inhibited ACh-esterase, but is unable to gointo the CNS. It can displace organophosphates like isoflurophate as long as
loss of the alkyl group
irreversible binding
) hasn’t occurreda.
Clinical: Used to treat overdose of ambenonium,
, and pyridostigmine that are used to treat myasthenia gravis. Usually used incombination with atropine to offset effects of DFP
Muscarinic Antagonists – ch. 5
– a tertiary amine belladonna alkaloid that acts competitively onmuscarinic receptors in CNS and PNS (parasympathetics)
prevents ACh binding to muscarinic receptorsa.
Clinical: Treatment of bradycardia.i.
Cholinesterase inhibitor overdose
treats bradycardias caused byvagal hyperactivityii.
causes cycloplegia (
 paralysis of ciliary muscle
) andmydriasis (
 pupil dilation
GU: treatment of cramping and urgent bladder in mild cystitis.Reduces hypermotility of bladder iv.
Low dose:
bronchial secretion,
Med. Dose: mydriasis, cycloplegia,
HR vi.
Large Dose: inhibition of urination;
GI tone, motility, andsecretions
3 b.
Side Effects: “red as a beet, blind as a bat, dry as a bone, mad as a hatter.”Dilation of superficial blood vessels
atropine flush; blurred vision;
 secretions; hyperthermia; delirium, hallucinationsc.
Contraindications: Narrow-angle glaucoma (relaxation of iris
 obstruction of Schlemm’s canal
in intraocular pressure)11.
– tertiary amine belladonna alkaloid similar to atropine; has greater action on CNS and longer duration of action in comparison to atropinea.
Clinical: used for motion sickness prophylaxis, block of short termmemory b.
Side Effects: similar to atropine
Neuromuscular Blocking Agents – ch. 5Competitive Blockers
– competitive nicotinic receptor antagonist. Produces anondepolarizing blockade (
 blocks nicotinic receptors without depolarizing the target cell
).At high doses it enters and blocks ion channels at the motor end plate. Drug preferentially blocks nicotinic receptors at motor end plates over nicotinicreceptors at autonomic ganglia.
This results in surmountable skeletal muscle paralysis
. Causes
CO, blocks NE uptake and stimulates NE release. IV,onset of action is 3-5 min; renal excretion; T
= 12.5 mina.
Clinical: Nondepolarizing skeletal muscle relaxant
used as a surgicaladjuvant for muscle relaxation b.
Side effects: can cause histamine release at higher doses
flushing,edema, erythema, hypotension, tachycardia13.
the purified active ingredient of curare
; is the prototype for nondepolarizing neuromuscular blockersa.
Side effects: causes considerable histamine release14.
– similar to Pancuronium
Depolarizing Agents
– slowly and reversibly binds ACh receptors,
causing thechannels to open and the neuromuscular membrane to depolarize
causes allreceptors to remain in inactive state, prevents response to endogenous ligand binding. Depolarizing blockades are
reversed by cholinesterase inhibitors.Rapidly hydrolyzed by plasma and liver pseudocholinesterases.a.
Clinical: Skeletal muscle relaxation for brief surgical procedures. IVdrips for longer procedures b.
Side effects: Malignant hyperthermia; hypotension, arrhythmias,respiratory collapse;
intraocular pressure

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