Fundamentals Tutorial Week 6

Frage	Antworten
A 41 year-old man was admitted to the hospital with acute abdominal pain, which was diagnosed as a perforated duodenal ulcer. Intubation for the purpose of inserting a camera into the stomach was scheduled under general anaesthesia. At the close of the surgical procedure, reversal of their muscular blockade was required. a. Which drug is most probably used to aid the intubation? b. What is the MOA of that drug? c. What drug might be given to restore neuromuscular function and why?	Suxamethionium because it is a depolarizing neuromuscular blocking agent Keeps depolarisation happening and causes muscle to be flaccid Give a cholinergic to reverse -> Neostigmine to increase ACh levels and displace the neuromuscular blocking agent from nicotinic receptors
Why is myasthenia gravis treated with tymectomy (surgical removal of the thymus gland) apart from drug treatment with neostigmine?	Myasthenia gravis • Nicotinic receptors blocked by antibodies produced by thymus gland. • Antibodies inactivate nicotinic receptors, reduced ACh transmission results in muscle weaknes • Ideally to increase Ach transmission (direct acting cholinergics) • Neostigmine indirect acting inhibits breakdown of ACh • Immunosuppressive options = thymectomy – remove thymus responsible in production of T and B lymphocytes - > T and B lymphocytes fail to recognize self and hence the interaction with the nicotinic receptors. • Corticosteroids
Why is the major effect of nicotinic receptor blockade skeletal muscle weakness?	• ACh binds to nicotinic receptors • NN found on neuronal end plate • NM found at musculature system muscle end plate Nicotinic receptors mediate nerve activation of the muscles at the neuromuscular junction; blockade of nicotinic receptors supresses that activation and it is first experienced as muscle weakness
Why is atropine an antidote for the effects of Sarin, a potent chemical weapon?	• Sarin is a cholinergic • Atropine is an anticholinergic • Sarin is a potent organophosphate *irreversible acetylcholinesterase) • Results in increased ACh transmission • Reversed using atropine • Atropine blocks the M receptors, reducing ACh transmission
Explain the MOA by which neostigmine treatment results in the data obtained in third graph from the top (after neostigmine)	• MG inactivation of N receptors inhibits binding of ACh • Presence of AChE within synapse reduces to Ach • Results in muscle weakness (reduced depolarization) • Neostigmine inhibits AChE • Allows ACh transmission across any remaining receptors (increased depolarisation observed)
Lambert-Eaton syndrome (another autoimmune disease), is a presynaptic disorder in which acetylcholine release is impaired due to production of autoantibodies. Knowing about the regulation of acetylcholine release, what would be the most probable target for those autoantibodies?	• Production of ACh is normal at pre-ganglion • Pathophysiology o T and B lymphocytes attack Ca2+ channels o ACh can only be released with an influx of Ca2+ into the pre-ganglion o Minimal release of ACh o Additional AChE reducds ACh concentration o Lack of ACh interacting with cholinoceptors at post-ganglion
Suxamethonium is also known as succinylcholine. (SCh) • What is the MOA of Suxamethonium? • What are the most dangerous physiological effects of Suxamethonium? • Why is Suxamethonium called a “perfect murder weapon”	• SCh is a depolarizing non-competitive blocker at the neuromuscular junction • Blocks ACh transmission, results in muscle relaxation • SCh can bind onto receptors on smooth muscle Excessive relaxation of the diaphragm
What is the difference between direct- and indirect-acting cholinomimetics?	• Cholinomimetic drugs mimic the action of cholinergic neurotransmitter • Direct acting cholinomimetic drugs to reproduce their pharmacological effect by receptor and activation • Indirect acting rugs inhibit ACh • Direct acting acts on ACh receptors • Indirect acts on the AChE
Which sympathetic mediators are made in adrenal medulla and why	Noradrenaline and Adrenaline They are the only mediators that can enter the adrenal medulla. Medualla expresses all the necessary enzymes
Which sympathetic mediators are made in sympathetic nerves and why?	Only noradrenaline, because nerves do not have methyl transferase and cannot proceed reaction
Which neurotransmitter is made in Substantia nigra and why?	Dopamine, because substantia nigra does not have dopamine hydroxylase or methyl transferase
What is the rate limiting step in catecholamine synthesis in all of those tissues (adrenal medulla, sympathetic nerves and Substantia nigra?	Conversion of tyrosine to DPOA by tyrosine hydroxylase
can you use anticholinergic drugs in people suffering tachycardia?	In general, anticholinergic drugs should be avoided in patients suffering increased heart rate (tachycardia) anti-cholinergics can cause tachycardia
In 1996 a patent was awarded for pilocarpine containing chewing gum. Which condition is intended to be treated with such product?	Cholinergic (SLUDGE EFFECT) Dry-mouth xerostomia • Innervated by PNS • Pilocarpine stimulates PNS to increase saliva production
Instead of SLUDGE, some authors group the cholinergic effects into another short description: DUMBBELLS. Compare the two options and identify which of the symptoms are different between DUMBBELLS and SLUDGE group?	Gastric motility Miosis Bradycardia
Why are both arterioles (sending blood from the heart to the body) and veins (sending blood from the body to the heart) predominantly innervated by sympathetic nerves?	• Parasympathetic nervous system taking over circulatory system results in hypotension and decrease in heart rate, pooling of blood in the extremities – orthostatic-hypotension • Sympathetic sends blood back up to the heart SV = CO x TPR BP = HR x SV Regulated by SNS mainly for proper blood flow, BP, CO and HR and SV If PNS takes over, opposite effects, hypotension, bradycardia (low heart rate), decreased venous return, and orthostatic-hypotension
Why blockade of parasympathetic-cholinergic action on the heart creates tachycardia (increased heart beat)?	When parasympathetic nerves are blocked, sympathetic action becomes predominant and its role is to increase heart beat.
If cholinergic blockade of GI tract causes reduced tone and motility; constipation and decreased secretions (see table) thereby negatively affecting GI function, when is the use of Mebeverine warranted?	Drug class: Muscarinic antagonist (antimuscarinic) Only in conditions such as IBS where cholinergic nerves are overstimulating -> treats gastric spasm. COMT and MAO enzymes that break down adrenaline in synaptic space (???)

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Fundamentals Tutorial Week 6

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