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MUSCLE RELAXANTS AND ANTICHOLINERGIC
DRUGS
Q1) types of muscle relaxant& how they work (the difference), how to confirm
position of endotracheal tube
Type1:
*Depolarizing , Non competitive, agonist.(Succinylcholine)
*work :succinylcholine Bind nicotinic cholinergic receptors at end plate lead to
depolarization of muscle fibers (so called depolarizing)>>In contrast to Ach ,it resists
the hydrolysis by Ach-estrase enzyme so remains attached to receptors for longer
time>>constant, continuous stimulation of receptors lead to repeated action potentials
& initial phase of muscles fasciculation>>This continuous stimulation of receptors
lead to receptors desensetization (unresponsiveness) then muscle exhaustion &
paralysis>>Drug remains binding to Ach receptors causing desensatization till it
diffuse away from end plate to plasma>>In plasma it undergo spontaneous hydrolysis
by endogenous plasma cholinesterase (pseudocholieesterase),
Type2:
*Non depolarizing, Competitive, antagonist.(Tubocurarine )
work: These drugs combine with nicotinic receptors and prevent binding of
acetylcholine so prevent depolarization of the muscle cell membrane so inhibiting
muscle contraction, these drugs competitively block the receptors this means that you
can overcome their action by increase Ach concentration by giving Ach esterase
inhibitors such as pyridostigmine or neostigmine …
Q2) What do you know about NMB in details? What the reverse?
1. Two classes: 1. Depolarizing, Non competitive, agonist. As
Succinylcholine
2. Non depolarizing, Competitive, antagonist. As Tubocurarine
3. NMB’s are co-administrated with anasthetics in the induction phase to
induce muscle paralysis
4. facilitate the surgery, especially intra-abdominal and intra-thoracic
surgeries
5. Facilitate endotracheal intubation.
It is reversed by anticholinesterases, neostigmine, and edrophonium
Q3) What do you know about succinylcholine?
MOA & Termination
succinylcholine
Bind nicotinic
cholinergic
receptors at end
plate lead to
depolarization
of muscle fibers
(so called
depolarizing)
In contrast to
Ach ,it resists
the hydrolysis by
Ach-estrase
enzyme so
remains
attached to
receptors for
longer time
NOTES :
• No drug to
antagonize it.
• It has shorter DOA
compared to
competitive
blockers
For more about MOA
refer to HANDOUT &
read about phase I &
phase
II12block .
March
This continuous
stimulation of receptors
lead to receptors
desensetization
(unresponsiveness)
then muscle exhaustion
& paralysis
constant,
continuous
stimulation of
receptors lead to
repeated action
potentials & initial
phase of muscles
fasciculation
Drug remains
binding to Ach
receptors
causing
desensatization
till it diffuse
away from end
plate to plasma
In plasma it undergo
spontaneous
hydrolysis by
endogenous plasma
cholinesterase
(pseudocholieesteras
e), not
acetylcholinesterase
Dr. Med. Khaled Radaideh
11
Pharmacodynamics
CNS :
•
MSS :
•
NO effect on
consciousness, pain
threshold & cerebral fnx
↑ IOP
↑ ICP
•
•
•
•
•
Skeletal muscles
paralysis
Myalagia
Myoglobinemia,
myoglobinurea
Messeter muscle spasm
Dynamics
CVS :
•
•
Bradycardia
Dysarrythmia
•
Sinus arrest
GU:
•
Resp:
•
March 12
Respiratory
muscles paralysis
Dr. Med. Khaled Radaideh
Coz metabolites
excreted by
kidneys, pts with
RF may have
hyperkalemia
14
Indications:
1. Non Fasting (emergency, CS)
2. Predicted difficult intubation
3. Prior to ECT
4. Operations of short duration where muscle relaxation is needed.
Absolute contra- indications:
1. Inability to maintain airways
2. Lack of resuscitative equipment
3. Known allergy / hypersensetivity
4. Positive Hx of malignant hyperthermia
5. Myotonia (M. congenita, M.dystrophica, paramyotonia congenita), why ?
6. Patient have risk of a hyperkalemic response to succinylcoline, previously
mentioned.
Relative contra- indications:
1. Known Hx of plasma cholinestrase deficiency
2. Myasthenia gravis & myasthenic syndrome
3. Familial periodic paralysis
4. Open eye injury
Q4) What are the side effects for succinycholine ??
Bradycardia
Dysarrythmia
Sinus arrest
myalagia
myoglobinemia , myoglobinurea
↑ intra-ocular pressure
↑ intracranial pressure
Q5) So why do we use it although it has a lot of side effects?
o It’s hydrolyzed in plasma & the metabolites are excreted by kidneys.
o Peak effect reached within 60 sec
o The blocking effect dissipates over the next 5-10 min.
o It is used in the following cases:
 Non Fasting (emergency, CS)
 Predicted difficult intubation
 Prior to ECT
 Operations of short duration where muscle relaxation is needed.
Q6) what is the drug from non depolarizing muscle relaxant that is metabolized
by hofmann elimination??
Atracurium
Q7) mention 5 side effects of suxamethonium?
Hyperthermia, apnea, hyperkalemia, constipation, muscle pain,
acute rhabdomyolysis..
Q8) What do you know about atracurium? What is the most imp cause of post op
airway obstruction, give other causes?
Q9) talk about the uses and side effects of atropine and neostigmine ?
Neostagmine:
1. In anesthesia at the end of an operation to reverse the effect of non polarizing
muscle relaxants
2. It can be used for urinary retention resulting from general anesthesia
3. In the treatment of myasthenia gravis
Side effects of neostagmine:
1.
2.
3.
4.
5.
6.
7.
8.
Salivation
Flushing
Sweaty skin
Meiosis
Bronchospasm
Bradycardia, decrease BP
Abdominal pain, nausea
Urinary urgency
Atropine:
1. Blocks the effect of acetylchline that result from cholinesterase inhibitors like
Neostigmine
2. Blocks secretions prior to surgery
3. Ophthalmic: mydiasis and cycloplegia to facilitate the examination of retina &
optic disc
4. GIT: antispasmodic agents
5. Urinary: reduce hypermotility states f the urinary bladder and occasionally used in
enuresis
6. CNS disorder: Parkinson and motion sickness
7. Antidote for organophosphate & some types of mushroom poisoning.
Side effects of atropine:
1.
2.
3.
4.
5.
6.
Dry mouth
Blurred vision
Tachycardia
Constipation
Confusion, delirium ,agitation
Collapse of the circulatory & RS.
Talk abt hypo/hyperkalemia?
•
Hypo..sym/signs:

Autonomic neuropathy

Skeletal muscle weakness

Increased sensitivity to Digoxin

Cardiac
• Decreased myocardial contractility
• Electrical conduction abnormalities
• Arrhythmias
• Tachycardia
• Ventricular fibrillation
• Hyper…sym/signs:
 Areflexia
 Weakness
 Paralysis
 Paresthesia
 Cardiac conduction abnormalities