NM DRUGS (NM19 & 20)

Drug Name Action Category Other

DRUGS AFFECTING NA
Carbidopa - inhibits DOPA decarboxylase in PNS. Therefore, - affects NA synthesis Used in parkinsons disease
decreasing dopamine.
a-methyltyrosine - inhibits tyrosine hydroxylase. - affects NA synthesis
- Tyrosine is converted to a-methyldopa and a-
methylnoradrenaline and released as false transmitter. They
act on a2 receptors causing decrease in blood pressure.
Reserpine - prevents accumulation of NA in synaptic vesicles - affects NA storage - used in treatment of severe
- depletes NA storage hypertension, may cause depression.
Guanethidine, - Guanethidine, is taken up via Uptake 1 mechanism into - depletes NA
Bretyllium terminal, stored in synaptic vesicles and released by - adrenergic neuron blocking drug
stimulation.
- This causes slow and long lasting depletion of NA.
- synaptic vesicles unable to fuse with cell
Tyramine, - its taken up via uptake system 1 and displaces NA from - Indirectly acting sympathomimetic - tyramine is precursor of NA and
Amphetamine, vesicles. amines leads to increased level of NA,
Ephedrine - it may also act at adrenergic receptors, producing post increasing BP.
synaptic effects. - no tyramine via MAO inhibitors
Cocaine - uptake system 1 blocked by tricyclic antidepressants such - inhibits NA uptake
as desipramine, cocaine
Phenoxybenzamine - blocks extraneuronal uptake (uptake system 2) - inhibits NA uptake - corticosteroids have similar effect
AUTONOMIC ADRENERGIC AGONIST (direct sympathomimetics)
Adrenaline/ - Used for anaphylactic shock, cardiac arrest, acute asthma - Naturally occurring catecholamine
Noradrenaline - prevents capillary bleeding - acts on ALL adrenergic receptors
Dopamine - Moderate dose: stimulates DA receptors to cause - naturally occurring catecholamine Therapeutic uses: shock and
vasodilation in mesenteric and renal vascular beds; also, refractory congestive heart failure.
stimulate B1 receptors in heart to increase HR & contraction.
- High dose: stimulate a1 receptor to cause vasoconstriction
Isoprenaline - It relaxes smooth muscle and increases heart rate - Synthetic catecholamine Therapeutic uses: cardiac arrest and
- non selective Beta AGONIST branchospasm during ansethesia
Phenylephrine - increases BP, reflex bradycardia (decr HR), and mydriasis - ALPHA 1 selective over alpha 2 Therapeutic uses: hypotensive states
(excessive dilation of pupil) and Nasal decongestants
Clonidine - reduces sympathetic outflow, HR and peripheral resistance - ALPHA 2 agonist Therapeutic uses: hypertension
Dobutamine - its an inotropic agent (increases heart rate) - Synthetic catecholamine Therapeutic uses: shock and
-S/E: increase HR, BP. -Beta 1 AGONIST refractory congestive heart failure.
Tertbutamine - causes rapid branchodilation. It also raises cAMP to relax - BETA 2 agonist Therapeutic uses: asthma, bronchitis
smooth muscle and inhibition of inflammatory mediators
 Drug Name Action Category Other
AUTONOMIC ADRENERGIC ANTAGONIST (direct sympatholytics)
Phentolamine - its reversible antagonist. - blocks both ALPHA receptors Therapeutic uses: hypertension
- decreases peripheral resistance, positive inotropic and
chronotropic effects, and causes vasodilation
Phenoxybenzamine - irreversible antagonist - blocks both ALPHA receptors
Prazocin, - selective for alpha 1 - blocks ALPHA 1 receptor Therapeutic uses: hypertension
Doxazocin
Propanolol - acts on both B1 and B2 - NON SELECTIVE B-RECEPTOR Therapeutic uses: hypertension,
- It decreases cardiac output and reduce sympathetic outflow antagonist cardiac arrhythmias, glaucoma,
via CNS. angina pectoris
- S/E: bradycardia, cardiac failure, branchoconstriction - Lipophilic and extensive 1st pass
metabolism
Atenolol - it reduces risk of bronchospasm and also as ACE inhibitor - selective B1 blocker Therapeutic uses: hypertension,
angina, myocardial infarction
- Lipophilic and crosses placental
barrier
DRUGS AFFECTING CHOLINERGIC TRANSMISSION
Hemicholinum - Competitive inhibitor of choline uptake - affects ACh SYNTHESIS
Vesamicol - Inhibition of packaging of acetylcholine into vesicles - affects ACh SYNTHESIS
Triethylcholine - inhibits choline uptake, taken up and acetylated to - affects ACh SYNTHESIS
acetyltriethylcholine. Stored as false transmitter.
Botulin toxin - It prevents release of vesicles by degrading SNAP-23 - affects ACh RELEASE - Originates from C. botulinum
(SNARE protein). Use: muscle spasms, migrane and
cosmetically to paralyze facial
muscles to alleviate wrinknes.
MUSCURANIC AGONIST AND ANTAGONIST
Carbachol, - muscuranic agonist resemble the effects of parasympathetic - MUSCURANIC AGONIST
Bethanrchol stimulation. It increase GI motility.
Atropine - It’s a competitive antagonist vs ACh. - MUSCURANIC ANTAGONIST
- Eyes: mydriasis (pupil dilation), increases intraocular
pressure. GI: reduce hypermotility state, antispasmodic agent
to relax GIT and bladder. Cardiovascular: at low doses
decreases cardiac rate and higher doses, increases CR.
Secretions: blocks salivary glands (xerostomia), sweat
glands, lacrimal glands.
 Drug Name Action Category Other
ANTICHOLINESTERASES
Myasthenia Gravis:
- It’s a neuromuscular disorder characterized by muscle weakness and rapid fatigue.
Symptoms: ptosis (drooping eyelids), difficulty breathing, weakness of skeletal muscle.
Cause: autoimmune response. Sero positive for Abs to mAChRs and Seronegative for Abs to MuSk
Treatment: diagnose it with edrophonium (tensilon) which is a short duration AChE inhibitor and relieves ptosis. Treat it wih Neostigmine, which is AChE inhibitor
Alzherimers Disease:
-Tacrine (AChE inhibitor for AD), Donepezil (Reversible AChE inhibitor), Rivastigmine, and Galantamine (Competitive, reversible AChE inhibitor).
Edrophonium - it binds to anionic site only. The ionic bond is reversible - DIAGNOSE Myasthenia Gravis Uses: diagnosing MG
- SHORT TERM AChE
Neostgimine, - positively charged nitrogen that binds to anionic site. These - TREATMENT for Myasthenia Gravis Uses: glaucoma
pyridostigmine, compounds are carbamyl (not acetyl) ester which carbmylate - MEDIUM TERM AChE
physostigmine serine. They hydrolyze much slower than acetyl groups
Isoflurophate - irreversible organophosphate. - IRREVERSIBLE AChE Uses: ophthalmic ointment for
- covalent phosphorylation of serine hydroxyl groups. glaucoma
NON-DEPOLARIZING AGENTS
D-Tubocurarine - It binds and blocks nicotinic receptor at NMJ as - blocks NICOTINIC receptor Uses: relaxant during surgery to stop
competitive antagonist which causes decrease in end-plate - thus, prevent depolarization muscle spasms
potential and relaxation of skeletal muscle. It causes motor
paralysis (eyes first, respiratory last). It lowers blood
pressure because it blocks ganglia and releases histamine. It
produces bronchoconstriction.
DEPOLARIZING BLOCKING DRUGS
Succinylcholine - the block is caused by membrane depolarization (Phase 1 - causes DEPOLARIZATION Uses: anesthesis – muscle relaxation.
Block) so it act as agonists. Normally, ACh will be degraded
by AChE. However, this drug has longer duration of effect.
- It maintains the membrane potential above threshold and it
doesn’t allow the muscle to repolarize which may lead to
fasciculations (muscle twitching), muscle reverts to flaccid
state, rather than tetany.
AChE REACTIVATION
Pralidoxime - It has a quaternary nitrogen group. It promotes transfer of -ACTIVATES AChE Uses: treat nerve gas/
phosphorylated covalent bond from the esteric site on organophosphate victims
cholinesterase, thus, removing the block.