Pharmacology - GASTROINTESTINAL AND ANTIEMETIC DRUGS (MADE EASY)

[@Askify]

My transcript notes of the video: 00:01 In this lecture we are going to cover the pharmacology of drugs acting on gastrointestinal system so let's get right into it the gastrointestinal tract is a part of 00:12 the human digestive system which includes the mouth esophagus stomach and intestines plus the accessory organs of digestion such as the salivary glands pancreas liver and gallbladder now the nervous system and endocrine 00:26 system work together to control gastric secretions and motility associated with the movement of food throughout the gastrointestinal tract digestion starts with a side thought or smell of food when the brain anticipates 00:39 an incoming meal the vagus nerve sends a message to the stomach to stimulate gastric secretion the mucosal lining of the stomach contains numerous gastric glands these glands open to the surface of the mucosa 00:52 through tiny holes called gastric pits there are a few different types of cells that make up the gastric glands surface and neck mucous cells which produce jelly-like substance called mucus that protects the lining of the 01:05 stomach parietal cells which produce hydrochloric acid that creates a low ph environment in the stomach chief cells which produce pepsinogen and gastric lipase enzymes that are 01:17 responsible for digestion of dietary proteins and fat enterochromafin-like cells which produce histamine that helps to induce the production of acid and g cells which produce peptide 01:30 hormone gastrin that is responsible for regulation of gastric activity now the vagus nerve is the single neural link between the brain's higher functions and gastric secretion in response to food intake vagus nerve 01:45 becomes excited and begins to release acetylcholine acetylcholine exerts its effects in the stomach directly through activation of muscarinic m3 receptors on parierle cells as well as indirectly through 01:57 activation of m1 receptors on enterochromafin-like cells to initiate histamine release and m3 receptors on g-cells to initiate gastrin release subsequently parieral cells are stimulated by histamine via h2 receptors 02:13 and by gastrin which acts on ecl cells cholecystokinin b receptors to enhance the histamine release in addition to directly stimulating parietal cells which also express cholecystokinin b receptors 02:28 now the activation of h2 receptor by histamine causes intracellular cnp levels to increase while the activation of m3 receptor by zero coin and cholecystokinin b receptor by gastrin causes intracellular calcium levels to 02:41 increase these independent pathways then converge to activate protein kinase cascade that in turn triggers translocation of hydrogen potassium 80 base also known as the proton pump from cytoplasm to the 02:53 apical surface the proton pump is the terminal staging gastric acid secretion being directly responsible for the active transport of hydrogen ions out of the cell in exchange for potassium ions 03:06 chloride ions are also secreted from parietal cells into the lumen by simple diffusion in the stomach lumen hydrogen chloride and water combine to form hydrochloric acid which creates a highly acidic 03:18 environment for digestion now understanding the physiology of gastric acid secretion and the pathophysiology of acid-related diseases such as gastroesophageal reflux and peptic ulcer has led to the development 03:31 of various ways to decrease acid exposure one of the pharmacological approaches aimed at neutralizing secreted acid is to prevent stimulation of the parietal cell 03:42 this can be achieved with the use of drugs called h2 receptor antagonists which work by competitively inhibiting histamine binding at h2 receptors on the parietal cells resulting in reduction of 03:53 histamine-mediated acid secretion drugs that belong to this class include cymetidine fomotidine nizadidine and ranitidine now another pharmacological approach is to directly disrupt the functioning of 04:08 the proton pump responsible for acid secretion this can be achieved with the use of drugs called proton pump inhibitors which work by binding to the hydrogen potassium atpase and suppressing the 04:19 secretion of hydrogen ions into the gastric lumen drugs that belong to this class include dexalonsoprazole esomeprazole lansoprazole omeprazole pantoprazole and rebeprazole 04:34 all right so while h2 receptor antagonists and proton pump inhibitors can provide a sustained suppression of gastric acid secretion patients needing immediate relief from their symptoms may benefit from a faster acting agent 04:47 belonging to a drug class known as non-systemic antacids members of this class include aluminum hydroxide magnesium hydroxide and calcium carbonate unlike the other acid-reducing agents 05:00 non-systemic antacids do not decrease acid secretion but instead act primarily by directly neutralizing hydrochloric acid this happens as a result of simple chemical reaction that combines a metal 05:12 ion from an antacid compound with a gastric acid binding group to form a salt and water this in turn raises the ph of the stomach contents and provides rapid relief from hyper acidity To get the full transcript and PDF notes with screenshot - Try Askify notes chrome extension tool

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Antibacterial medications called 'nitroimidazoles' primarily used to treat infections caused by protozoans & bacteria should have been added to the video. Edit: Thanks a lot for uploading videos.

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Do some of these gastrointestinal drugs cause serious side effects

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[@tpy....]

Mataclopramide is a pro kinetic agent and chlopromazine and prochlorperazine is neuroleptics so how can we use neuroleptics to counter act d2 receptor

[@SpeedPharmacology]

Neuroleptics like chlorpromazine and prochlorperazine counteract D2 receptors primarily by antagonizing them, leading to therapeutic effects such as antiemesis and antipsychotic actions. This antagonism helps reduce dopamine activity, alleviating symptoms like nausea, vomiting, and psychosis. While they are not primarily prokinetic agents like metoclopramide, their D2 receptor antagonism can indirectly affect gastrointestinal motility in certain cases

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8:45 I wished you also mentioned Domperidon.