Parasympatholytics

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Skeletal muscle relaxants work by inhibiting nerve impulse transmission at the neuromuscular junction. Curare, derived from South American plants, was historically used as an arrow poison and paralyzes animals. It is a natural source of neuromuscular blocking agents. These agents have classifications including depolarizing and nondepolarizing blockers. D-tubocurarine, a nondepolarizing blocker derived from curare-containing plants, acts as a competitive antagonist at nicotinic receptors on the motor endplate, reversibly blocking acetylcholine transmission and initially paralyzing smaller muscles before affecting larger ones. It does not cross the blood-brain barrier or placenta.

Introduction
Definition
These are the Drug produce relaxant of skeletal muscle by
inhibiting
the transmission of nerve impulse at neuromuscular junction
History
CURARE:- it is the generic name for certain plant extracts
used by South America tribal's as arrow
poison for game Hunting.
 the animal get paralyzed even if not killed.
natural source of curare- Strychnos toxifera,
- Chondrodendron tomentosus
Uses
• general anesthetics to provide muscle Relaxant for surgery
•Painful muscle spasms
•Spastic neurological condition

Classifications
I.Neuromuscular BlockingAgent
A. Nondepolarizing (Competitive) blockers)
1.Long acting: d-Tubocurarine, Pancuronium, Doxacurium, Pipercu
2. Intermediate acting: Vecuronium,Atracurium, Cisatracurium, Rocu
Rapacuronium
3. Short acting: Mivacurium
B. Depolarizing blockers
-Succinylcholine, Decamethonium
II.Directly acting agent
-Dantrolene sodium
-Quinine

d-Tubocurarine
Source: (CURARE)
Chondrodendron tomentosus,
Strychnos lethalis
It is dextro rotatory competitive
blockers.
Mainly used as an Arrow poison in
hunting
animals

MOA
It binds to the Nicotinic receptors on the motor
end
plate N thus blocks the action of Ach by
competitive blockade
If the concn of Ach varies (increase) d-
Tubocurarine bockade is reversed

Pharmacological Action
Skeletal muscle
initially paralyses smaller muscle (finger, toes eyes ear)
latter bigger muscle (limbs, neck, trunk followed by intercostal
muscles)
Diaphragm is affected at last N recovery is reversed.
CNS
don’t cross BBB & PB i.e no effect on CNS
Autonomic ganglia
partially blockade both autonomic ganglia & adernal medulla
resulting fall of B.P
Histamine Release
directly act on mast cell & produce Histamin causes >bronchospasm
>increase salivary

Pharmacokinetics:
A not absorb from GIT but well
absorbed through IM
D doesn't pass BBB &PB
M in liver
E  urine

Skeletal muscle relaxants can be classified as peripherally or centrally acting. Peripherally acting drugs relax muscles by blocking the neuromuscular junction or directly acting on muscles. Non-depolarizing blockers like atracurium and vecuronium competitively inhibit nicotinic receptors. Succinylcholine is a depolarizing blocker that stimulates nicotinic receptors. Dantrolene and quinine directly act on skeletal muscle. Centrally acting drugs like benzodiazepines, baclofen, and tizanidine act in the central nervous system to relieve muscle spasms and spasticity. These drugs are used to facilitate surgery and treat conditions like sp

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Curare alkaloids are neuromuscular blocking agents obtained from plants that are used as adjuvants in surgical anesthesia to relax skeletal muscles. Tubocurarine is a prototypical curare alkaloid that was later purified and used clinically. It acts by blocking nicotinic receptors at the neuromuscular junction. Several semi-synthetic and synthetic neuromuscular blocking agents were later developed with varying durations of action and safety profiles for use in surgery and diagnosis of conditions like myasthenia gravis. Structure-activity relationship studies led to derivatives with improved potency and duration of action.

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- Residual block - Prolonged action of relaxant - Organ dysfunction (liver, kidney) - Atypical pseudocholinesterase - Drug interactions - Hypothermia - Neuromuscular disease Consider sugammadex in these cases. Sugammadex - Cyclodextrin that encapsulates Rocuronium and Vecuronium molecules - Removes them from the neuromuscular junction - Rapid reversal of even profound block - No side effects of anticholinesterases - Dose dependent reversal - 2 mg/kg reverses moderate block - 4 mg/kg reverses profound block - 16 mg/kg reverses

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Skeletal muscle relaxants are drugs that induce skeletal muscle relaxation. They are classified as peripherally acting, centrally acting, or direct acting. Peripherally acting drugs like atracurium and mivacurium act by blocking neuromuscular junctions, while centrally acting drugs like baclofen and diazepam facilitate GABA action in the central nervous system. Direct acting drugs such as dantrolene act directly on skeletal muscles to interfere with calcium release and muscle contraction. These drugs are used to treat muscle spasms, relax muscles during anesthesia, and prevent malignant hyperthermia among other uses.

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Parasympatholytics

2. Introduction Definition These are the Drug produce relaxant of skeletal muscle by inhibiting the transmission of nerve impulse at neuromuscular junction History CURARE:- it is the generic name for certain plant extracts used by South America tribal's as arrow poison for game Hunting.  the animal get paralyzed even if not killed. natural source of curare- Strychnos toxifera, - Chondrodendron tomentosus Uses • general anesthetics to provide muscle Relaxant for surgery •Painful muscle spasms •Spastic neurological condition

3. Classifications I.Neuromuscular BlockingAgent A. Nondepolarizing (Competitive) blockers) 1.Long acting: d-Tubocurarine, Pancuronium, Doxacurium, Pipercu 2. Intermediate acting: Vecuronium,Atracurium, Cisatracurium, Rocu Rapacuronium 3. Short acting: Mivacurium B. Depolarizing blockers -Succinylcholine, Decamethonium II.Directly acting agent -Dantrolene sodium -Quinine

4. d-Tubocurarine Source: (CURARE) Chondrodendron tomentosus, Strychnos lethalis It is dextro rotatory competitive blockers. Mainly used as an Arrow poison in hunting animals

5. MOA It binds to the Nicotinic receptors on the motor end plate N thus blocks the action of Ach by competitive blockade If the concn of Ach varies (increase) d- Tubocurarine bockade is reversed

6. Pharmacological Action Skeletal muscle initially paralyses smaller muscle (finger, toes eyes ear) latter bigger muscle (limbs, neck, trunk followed by intercostal muscles) Diaphragm is affected at last N recovery is reversed. CNS don’t cross BBB & PB i.e no effect on CNS Autonomic ganglia partially blockade both autonomic ganglia & adernal medulla resulting fall of B.P Histamine Release directly act on mast cell & produce Histamin causes >bronchospasm >increase salivary

7. Pharmacokinetics: A not absorb from GIT but well absorbed through IM D doesn't pass BBB &PB M in liver E  urine

8. ADR

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