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Into three groups first antimuscarinic agents second ganglionic blockers also known as anticholinergic drugs these agents block primarily muscarinic well known medications that belongs to this group is atropine sweat and lacrimal glands now antimuscarinic activity of atropine in the eye known as mydriasis inability to focus visually also known as cycloplegia are used before
An eye exam or eye surgery as well as to treat certain action other antimuscarinic agents such as cyclopentolate and tropicamide can produce mydriasis that lasts for hours atropine’s effects can last for results in reduction of gi motility from stomach to colon this translates into atropine can also effectively block m2 receptors on the sa node and av node atropine produces
Dry mouth dry skin and ultimately causes body temperature to much greater effect on the cns as well as longer duration of action for that prevention of motion sickness and post-operative nausea and vomiting it is antimuscarinic group that i want to talk about are ipratropium and tiotropium ipratropium and tiotropium block muscarinic acetylcholine receptors without in the
Lungs which in turn leads to bronchodilation and reduction of mucus maintenance treatment of bronchospasms in patients with copd ipratropium rhinorrhea which is runny nose the main difference between ipratropium and is dosed once daily while ipratropium is a short-acting agent that typically group are used for treatment of overreactive bladder these include tolterodine
Darifenacin solifenacin oxybutynin trospium which is the main receptor involved in bladder function however the overall benztropine and trihexyphenidyl which through their ability to suppress parkinson-like disorders now before we move on to the next group i wanted to us to remember anticholinergic adverse effects where a stands for agitation d stands for dry mouth and s
Stands for stasis of urine and sweating now we can ganglionic blockers the main agent in this group is nicotine which is a main it is also considered a functional antagonist because of its ability to nicotinic receptors of both parasympathetic and sympathetic neurotransmitters such as dopamine serotonin and norepinephrine just to convulsions and then it depresses cns which
Can lead to respiratory paralysis blood pressure and heart rate but at higher doses it can cause blood pressure and vomiting last but not least use of nicotine in any form can cause addiction well-being overall other than to help people quit smoking nicotine is not very talk about neuromuscular blockers neuromuscular blocking agents simply nicotinic receptors on the skeletal
Muscle so if we zoom in on this part nicotinic receptors to which acetylcholine of these channels let’s sodium ions to enter the muscle fiber and trigger surrounds those cylindrical structures known as myofibrils then the action and then the arrival of action potential causes calcium to be released from the see all these steps in action so action potential causes release
Of calcium gets released and muscle contracts it’s that easy with these nicotinic acetylcholine receptors we can divide these agents for all of you who need a quick review of membrane depolarization i strongly potential so let’s talk about nondepolarizing agents first these don’t induce ion channel opening what that means is that they prevent muscle contraction in clinical
Practice these agents are used to facilitate muscle relaxation during surgery which allows for lower doses of general intravenously time to onset of action is administered these agents paralyze small fast contracting muscle first that is diaphragm on the other hand these muscles recover in the reverse manner agent typically depends on the desired onset and duration of the
Muscle time measured from administration to recovery of 25% of baseline muscle following cisatracurium which has clinical duration of about 90 minutes with clinical duration of about 40 minutes vecuronium which also has clinical duration as well now when it comes to side-effects atracurium causes bronchoconstriction it also has toxic metabolite called laudanosine which this
Is why atracurium has been largely replaced by its isomer cisatracurium its metabolism is independent of hepatic or renal function therefore and rocuronium are metabolized by liver with hepatic dysfunction but overall in urine and one of its main side effects is increase in heart rate now receptor agonists they mimic the acetylcholine however they are much more resistant to
Degradation by acetylcholinesterase and therefore produce persistent is succinylcholine so succinylcholine binds to the nicotinic receptor and open which results in membrane depolarization now because prolonged depolarization which leads to a transient fasciculations and finally channel closes and membrane repolarizes however due to continued stimulation preventing formation
Of further action potentials this is referred to as commonly used to facilitate rapid sequence endotracheal intubation in muscle relaxation during electroconvulsive therapy following intravenous administration succinylcholine causes complete muscle relaxation redistribution and hydrolysis by plasma pseudocholinesterase and that brings us succinylcholine can lead to prolonged
Apnea next prolonged into the extracellular fluid which can result in hyperkalemia however in those with elevated potassium tissue damage succinylcholine can cause serious ekg changes and even in severe malignant hyperthermia symptoms of malignant hyperthermia include severe as 43 degrees celsius and with that i wanted to thank you for watching and i
Transcribed from video
Pharmacology – ANTICHOLINERGIC & NEUROMUSCULAR BLOCKING AGENTS (MADE EASY) By Speed Pharmacology
