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Your patient is undergoing surgery and is given a medication to relax his muscle before the surgery commences.  He immediately develops bronchoconstriction and hypotension. State the reason for this presentation and mention at least 3 drugs that can cause this effect and describe their mechanism of action?

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Your patient is undergoing surgery and is given a medication to relax his muscle before the surgery commences.  He immediately develops bronchoconstriction and hypotension. State the reason for this presentation and mention at least 3 drugs that can cause this effect and describe their mechanism of action?

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Describe the steps of neurotransmission in the picture.

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Describe the steps of neurotransmission in the picture.

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Your patient presents with diarrhea, stooling vomiting and muscle twitching.
Describe the receptors and the signaling mechanisms associated with this symptoms?

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List examples of Muscarinic and Nicotinic agonists.

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List examples of Muscarinic and Nicotinic agonists.

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Muscarinic agonists- Bethanechol, Carbachol, Pilocarpine, Methacholine.

Nicotinic agonists- Nicotine, Succinylcholine, Varenicline.

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Examples of Muscarinic and Nicotinic agonists 

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Examples of Muscarinic and Nicotinic agonists 

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Muscarinic agonists- Bethanechol, Carbachol, Pilocarpine, Methacholine.
Nicotinic agonists- Nicotine, Succinylcholine, Varenicline,

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Nicotinic agonist- Varenicline,acetylcholine ,Nicotine
Muscarinic agonist-Pilocarpine,Methacholine,donipizil

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If your patient complains of dry mouth what drugs would you give the patient.

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If your patient complains of dry mouth what drugs would you give the patient.

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Describe the mechanism of action of the drugs including secondary messengers?

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pilocarpine and cevimelin

Mechanism of action
muscarinic cholinergic M3 receptor agonist, increases salivation.

Secondary messenger

The inhibition of adenylyl cyclase results in a decreased level of intramolecular cAMP. Reduced levels of cAMP as a second messenger decreases an activity of cAMP-dependent protein kinase

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If your patient complains of dry mouth what drugs would you give the patient? and describe the MOA of the drug including secondary messengers.

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If your patient complains of dry mouth what drugs would you give the patient? and describe the MOA of the drug including secondary messengers.

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The patient is facing xerostomia which is the sensation of oral dryness due to no saliva production.
To treat it I would give pilocarpine which is a cholinergic muscarinic agonist that stimulates the secretion of exocrine glands.

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Pilocarpine (Salagen) is a cholinergic agonist, meaning it activates cholinergic receptors in your body. This causes your saliva glands to make more saliva so that your mouth is less dry.

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If your patient explains he took a muscarinic agonist poison. He presents with initial muscle twitching and then flaccid muscles. 

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If your patient explains he took a muscarinic agonist poison. He presents with initial muscle twitching and then flaccid muscles. 

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What receptors are associated with this presentation and why did he present or develop flaccid muscles?

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Patient took a muscarinic agonist can cause poisoning such the symptoms can be muscle twitching of the facial muscles and it is due to cholinesterase inhibitor as it results to increased levels of Ach in the synapses and Muscarinic receptors is involved in it.

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If your patient explains he took a muscarinic agonist poison. He presents with initial muscle twitching and then flaccid muscles.What receptors are associated with this presentation and why did he present or develop flaccid muscles?

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If your patient explains he took a muscarinic agonist poison. He presents with initial muscle twitching and then flaccid muscles.What receptors are associated with this presentation and why did he present or develop flaccid muscles?

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Patient took a muscarinic agonist over intake can cause poisoning such the symptoms can be muscle twitching of the facial muscles and it is due to cholinesterase inhibitor as it results to increased levels of Ach in the synapses Muscarinic receptors are associated with the presentation.

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In large doses, such as can occur in poisoning, anticholinesterases initially cause twitching of muscles. This is because spontaneous ACh release can give rise to endplate potentials that reach the firing threshold. Later, paralysis may occur due to depolarisation block, which is associated with the build-up of ACh.

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Muscarinic agonists are agents that activate the muscarinic acetylcholine receptor.

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Describe the effect of muscarinic activation in the eye?

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Describe the effect of muscarinic activation in the eye?

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How does this differ from sympathetic activation of the eye?

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Atropine- Dicyclomine
Cyclopentolate- Tropicamide
Ipratropium- Tiotropium
Tolterodine- Oxybutinin

Hyoscine

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Atropine, Scopolamine, Ipratropium, Tiotropium bromide, Glycopyrrolate, Oxybutynin

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atropine, scopolamine, and ipratropium

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If your patient takes night shade berry which has an antimuscarinic as active. What will be the clinical presentation. Suggest a potential management. 

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If your patient takes night shade berry which has an antimuscarinic as active. What will be the clinical presentation. Suggest a potential management. 

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Acetylcholine will release in the terminal due to calcium influx, due to which soma get more negative and it will exite and acetylcholine release in the Clift , then it bind to muscarinic receptor and Nicotinic receptor of postsynaptic nerve , after that acetylcholine esterase  will break the acetylcholine into acetyl and choline which will be reused again in process.

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Synthesis of Neurotansmitter

1) Acetyl Co-A joins with Choline to form Acetylcholine which is the neurotransmitter.

Pathway of Activation & Deactivation of Neurotransmitter

1) when there is a influx of calcium causes negative which helps transmissions by excitation into pre synaptic cleft, where Acetylcholine released, this acetylcholine binds to muscarnic and nicotine receptors in the post synaptic cleft which helps in activation.

2) Later Acetylcholine Esterase will helps in breakdown of acetylcholine which will be reuse.

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Nightshade berries contain atropine, which is a potent antimuscarinic agent
clinical presentations of atropine toxicity include:

1. Dry mouth

2. Blurred vision and dilated pupils (mydriasis)

3. Increased heart rate (tachycardia)

4. Decreased gastrointestinal motility, which can lead to constipation

5. Urinary retention

6. Confusion, agitation, and hallucinations

Management of atropine toxicity involves supportive care and the administration of antidotes. The main antidote for atropine toxicity is physostigmine, a cholinesterase inhibitor

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Carbachol - Stimulation of muscarinic receptors in the eye which can make constriction of the ciliary muscle and contract the iris which Increases the aqueous humor outflow and decreases the intraocular pressure for miosis of the eye.

Pilocarpine - Stimulation of muscarinic receptors in the eve to increase intraocular pressure.

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If your patient takes nightshade berry which has an antimuscarinic as active. What will be the clinical presentation? Suggest potential management.

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If your patient takes nightshade berry which has an antimuscarinic as active. What will be the clinical presentation? Suggest potential management.

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Nightshade berries contain atropine which is a potent antimuscarinic drug. it can cause Xerostomia, mydriasis with blurred vision, Constipation, Tachycardia, Fever, and Tremors.

Potential management could be the administration of physostigmine, IV fluids to maintain hydrated, Support blood pressure, and Administration of Benzodiazepines to control agitation and seizures.

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Nightshade berries contain atropine, antimuscarinic agent clinical presentations of atropine toxicity include:Dry mouth, Blurred, Dilated pupils, Increased heart rate,  Decreased gastrointestinal motility and other anticholinergic effects. Management of atropine toxicity involves supportive care and the administration of antidotes.(Physostigmine)

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Nightshade berries contain atropine, antimuscarinic agent clinical presentations of atropine toxicity include:Dry mouth, Blurred, Dilated pupils, Increased heart rate,  Decreased gastrointestinal motility and other anticholinergic effects. Management of atropine toxicity involves supportive care and the administration of antidotes.(Physostigmine)

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Describe the effect of muscarinic activation in the eye? How does this differ from sympathetic activation of the eye?

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Describe the effect of muscarinic activation in the eye? How does this differ from sympathetic activation of the eye?

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Carbachol - Stimulation of muscarinic receptors in the eye which can make constriction of the ciliary muscle and contract the iris which Increases the aqueous humor outflow and decreases the intraocular pressure for miosis of the eye.

Pilocarpine -  Stimulation of muscarinic receptors in the eye to increase intraocular pressure.

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Choline is transported into the presynaptic nerve

terminal by a sodium-dependent choline transporter (CHT). This transporter can be inhibited by hemicholinium drugs. In the cytoplasm, acetylcholine is synthesized from choline and acetyl-COA(AcCOA) by the enzyme choline acetyltransferase (ChAT)Acetylcholine is then transported into the storage vesicle by a second carrier. the vesicle-associated transporter (VAT) which can be inhibited by vesamicol. Peptides(P)

adenosine triphosphate (ATP) and proteoglycan are also stored in the vesicle.

Release or transmitter occurs when voltage-sensitive calcium

channels in the terminal membrane are opened. allowing an influx of calcium.

the resultant increase in intracellular calcium causes fusion of

vesicles with the surface membrane and exocytotic expulsion of acetylcholine and cotransmitters into the junctional cleft . This step can be blocked by botulinum toxin. Acetylcholine's action is terminated by

the enzyme acetyl cholinesterase. Receptors on the

presynaptic nerve ending modulate transmitter release.

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Muscarinic agonists act mainly via muscarinic M₃ cholinoceptors to cause contraction of the iris sphincter, ciliary muscle and trabecular meshwork as well as increase outflow facility of aqueous humour.

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It cause the anticholinergic effect

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Pilocarpine or cevimeline, a selective M3 agonist, can be used to increase salivation and lacrimal secretion in patients with dry mouth or dry eyes .When pilocarpine binds to muscarinic receptors on the salivary glands, it triggers the production of secondary messengers such as IP3 and DAG, which, as described earlier, help to increase the production of saliva.

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Synthesis of Ach is due to Acetyl Co-A with choline in process of sodium influx by CHT.
When the calcium channels open there will be an influx of calcium, causing a negative.
Excitatory neurotransmission in the presynaptic cell causes Ach release into the synaptic cleft and can bind to the nicotinic receptor and muscarinic receptor of the postsynaptic cell.
Later acetylcholinesterase breaks down the Ach into the Acetyl Co-A and choline to continue the process again.

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The patient may be presenting with signs of adverse reaction to non-depolarizing blockade works a the neuromuscular junction. Three such drugs are 1. Mivacurium- It is inactivated by plasma cholinesterase and cause excessive hypotension. The histamine effect causes broncho-constriction 2. Atracurium- Has a slightly histamine effect and causes hypotension. 3. Tubocurarine- causes histamine effect.

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The patient may be presenting with signs of adverse reaction to non-depolarizing blockade works a the neuromuscular junction. Three such drugs are 1. Mivacurium- It is inactivated by plasma cholinesterase and cause excessive hypotension. The histamine effect causes broncho-constriction 2. Atracurium- Has a slightly histamine effect and causes hypotension. 3. Tubocurarine- causes histamine effect.

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What is the difference in mechanism of action between Suxamethomium  and pancuronium?

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What is the difference in mechanism of action between Suxamethomium  and pancuronium?

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Suxamethonium (Succinylcholine) is a depolarizing blockaded that acts a acetylcholine receptor agonist causing depolarization initially causing muscle twitching, preventing muscle contraction and causes hypotension.  as oppose to Pancuronium- which is a non-depolarizing blockade that has an antimuscarinc effect which causes tachycardia and hypertension. It can be overcome by increase Acetylcholine concentration.

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Suxamethonium (Succinylcholine) is a depolarizing blockaded that acts a acetylcholine receptor agonist causing depolarization initially causing muscle twitching, preventing muscle contraction and causes hypotension.  as oppose to Pancuronium- which is a non-depolarizing blockade that has an antimuscarinc effect which causes tachycardia and hypertension. It can be overcome by increase Acetylcholine concentration.

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suxamethonium is a depolarizing NMBA that mimics the action of acetylcholine at the neuromuscular junction, causing sustained muscle depolarization and relaxation. Pancuronium is a non-depolarizing NMBA that competes with acetylcholine for binding to the receptor, but does not activate it, leading to muscle relaxation.

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Identify the neuromuscular blockers that would be dependent on appropriate liver function.

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Identify the neuromuscular blockers that would be dependent on appropriate liver function.

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Suxamethonium is a neuromuscular blockade that is dependent on liver function because the liver cannot break down Suxamethonium. Suxamethonium is cleared from the blood with plasma cholinesterase which is synthesize in the liver and reduces its activity.

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Suxamethonium is a neuromuscular blockade that is dependent on liver function because the liver cannot break down Suxamethonium. Suxamethonium is cleared from the blood with plasma cholinesterase which is synthesize in the liver and reduces its activity.

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If your patient is having malignant hyperthermia what symptoms will he show and how will you manage it?

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If your patient is having malignant hyperthermia what symptoms will he show and how will you manage it?

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Patient with malignant hyperthermia would present with muscle rigidity or spams, tachycardia, brachypnea, threatening high body temperature, excess sweating. It can be succinylcholine induces. Treatment with Dantrolene (Dantrium) which is a ryanodine receptor antagonists is most effective.

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Patient with malignant hyperthermia would present with muscle rigidity or spams, tachycardia, brachypnea, threatening high body temperature, excess sweating. It can be succinylcholine induces. Treatment with Dantrolene (Dantrium) which is a ryanodine receptor antagonists is most effective.

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What are the clinical features of Organophosphate poisoning?

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What are the clinical features of Organophosphate poisoning?

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The clinical feature of Organophosphate poisoning include those of nicotinic and muscarinic effect/parasympathetic activity such as  muscle twitching and muscle paralysis, tachycardia, hypertension, sweating, nausea, vomiting, increase salivation, lacrimation, diarrhea, blurred vision and mitosis. An effective antidote is Atropine and pralidoxime (reactivation of cholinesterase)

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The clinical feature of Organophosphate poisoning include those of nicotinic and muscarinic effect/parasympathetic activity such as  muscle twitching and muscle paralysis, tachycardia, hypertension, sweating, nausea, vomiting, increase salivation, lacrimation, diarrhea, blurred vision and mitosis. An effective antidote is Atropine and pralidoxime (reactivation of cholinesterase)