Essay On Pharmacology


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Pharmacology


What is the mechanism of action of NSAIDS?

Aspirin and other NSAIDS function by blocking the prostaglandins which are crucial in sensitizing the peripheral pain receptors. These drugs have three effects including anti-inflammation, antipyretic and analgesic functions (Foye, Lemke, & Williams, 2013).The anti-inflammatory and analgesic functions act on both the Central and Peripheral Nervous systems while antipyretic functions primarily on the CNS. When the tissues are traumatized, various cytokines are produced with both stimulatory and sensitizing functions (Foye, Lemke, & Williams, 2013).The arachidonic cascade through the action of 5-lipo-oxyegenase and cyclooxygenase (COX) synthesizes prostaglandins and leukotrienes. There are two types of Cyclooxygenases inhibited by NSAIDs; COX1 and COX2. NSAIDS have inhibitory effects on the two enzymes since the two classes of cytokines sensitize the pain receptors.

What are the actions of NSAIDS against pain and inflammation?

The mechanism of action of NSAIDS is divided on the effects the drugs have on fever, pain and inflammation. For their anti-inflammatory effects, the drugs inhibit the cyclooxygenase (COX), an enzyme catalyzing the conversion of arachidonic acid to prostaglandins and thromboxane (Pazdernik & Kerecsen, 2010).When used for analgesic purposes, they have the significant effect on pain which arises from peripheral sensitization during inflammation. The drugs lead nociceptors to respond to stimuli which are painless. They function by blocking COX2 an enzyme responsible for synthesis of cytokines responsive to pain. For antipyretic effects, NSAIDS function through the inhibition of synthesis of prostaglandin E2. The prostaglandin is of relevance in triggering the hypothalamus which contributes to an increment in temperature during the inflammation process.

What is the mechanism of action of acetaminophen?

Acetaminophen has both analgesic and antipyretic effects. The exact site of mechanism of action of acetaminophen for analgesic purposes has not been elucidated. It is believed that the potential mechanism involves inhibitory effects on nitric oxide pathway (Kee, Hayes, & McCuistion, 2014). The inhibitory effects are mediated by several neurotransmitters receptors including substance P and N-methyl-D-aspartate. Leukocytes cause an elevation of Prostaglandin E in CSF. Fever arises when elevated levels of PGE acts on anterior hypothalamus thus decreasing heat loss while leading to heat gain. Acetaminophen inhibits the action of pyrogens in the heat regulatory centers of the brain by inhibiting prostaglandin synthesis (Kee, Hayes, & McCuistion, 2014). Unlike salicylates, acetaminophen does not rely upon the activation of arginine vasopressin V-1 receptors.

What is the pathway that leads to hepatotoxicity in acetaminophen overdose?

Acetaminophen overdose cause fatal hepatic centrilobular necrosis. There are various possible mode of actions that contribute to hepatotoxicity with findings showing that acetaminophen is activated by the cytochrome P450 enzymes (Kee, Hayes, & McCuistion, 2014). It is converted to its reactive metabolite N-acetyl-p-benzoquinone imine that binds and depletes the glutathione levels (GSH). Glutathione plays a significant role in the prevention of necrosis from the action of peroxides and superoxide. Studies reveal the presences of nitrated residues as well as acetaminophen adducts in the necrotic cells following acetaminophen overdoses. In situations of overdose NAPQI contributes to the depletion of glutathione. Unconjugated NAPQI binds to cellular proteins and other organelles leading to necrosis and eventual liver failure. N-acetylcysteine, an antidote of APAP poisoning reduces the extent of hepatotoxicity by increasing GSH synthesis (Kee, Hayes, & McCuistion, 2014).

What are the different mechanisms of action of bulk forming laxatives, saline laxatives, osmotic laxatives, and stimulant laxatives?

Bulk forming laxatives are recommended treatments for constipation. They are naturally derived from agar, kelp and gum while others are synthetic, for example, methylcellulose. They swell in the intestines lubricating and softening the stool for passage (Foye, Lemke, & Williams, 2013).They absorb water, and swells forming a gelatinous mass that keeps faeces soft. The bulk then stimulates reflexes in the contraction of the intestinal wall causing emptying. Osmotic laxatives on the other hand functions by increasing water available to intestines and colon. They include sorbitol and magnesium citrate (Panchmatia, 2010). By increasing water in the small intestines and colon, they enhance the pliability of the stool. Stimulant laxatives work by increasing the motor activity of the bowels by stimulating the nerve plexus in the intestinal wall. An example of the stimulant laxative is senna and bisacodyl (Foye, Lemke, & Williams, 2013).Saline laxatives draw large amounts of water from other parts of the body to the intestines which increase pressure on intestinal walls triggering bowel movement.

What is the mechanism of action of antidiarrheals?

Diarrhea is a medical condition characterized by passage of watery stools. Antidiarrheal fall under different categories depending on the active agent. Drugs such as Loperamide binds to the µ receptors with the stimulation of the receptor decreasing the tone of longitudinal muscle and thus increasing the transit time of the stool (Classen, Tytgat, & Lightdale, 2011).The drug thus reduces the GIT motility while increasing the transit time (Botting, 2000).Others, function through the adsorption or electrolytes and decreasing fluid secretion while contributing to vasoconstriction of the blood vessels in the small intestines and colon.

What are the different classes of antacids? What are their mechanisms of action?

All antacids despite their different formulations have the same mode of action (Classen, Tytgat, & Lightdale, 2011).They function by decreasing the acidity of gastric secretion and provide a buffering action through neutralizing the acid in the stomach. Antacids are categorized based on the active compounds. (Bardsley, 2009). There are four types of antacids including the sodium bicarbonate type, calcium carbonate, aluminum and calcium containing antacids (Baning, 2012). According to Mosby’s Critical Care Drug Reference. (2013) they work by raising the pH while neutralizing excessive gastric juice.
What is the role of H. pylori in intestinal ulcer formation?

Helicobacter pylori is a bacteria that thrives under extreme acidic pH. H. pylori infects the antral portions of the stomach. The maintenance of balance between the release of gastric juice by G-cells and histamine from the ECL is played by somatostatin (Daniels, & Schmelzer, 2013). H. pylori acts directly on the ECL cells which release histamine thus increasing the secretory activity of the parietal cells (Duncan, 2013). The bacteria further down regulate proton pumps involving H+/Na+-ATPase resulting in elevated amounts of hydrochloric acid. Presence of H. pylori in the gastric antrum contributes to gastric hypersecretion eventually leading to the development of ulcers. (Edmund, 2014)

References
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Bardsley, A. (2009). Assessment and management of faecal incontinence. Journal of Community Nursing 23(4), 4-10.
Bennett, S. (2013). Pharmacology of paracetamol and prescribing consideration. Nurse Prescribing 11(1), 28-33.
Botting RM. (2000). Mechanism of action of acetaminophen: is there a cyclooxygenase 3? Clinical Infectious Diseases 31(5), 202-10.
Brunton, L., Chabner, B. & Knollman, B. (2011). Goodman and Gilman's The Pharmacological Basis of Therapeutics, (12th.ed). New York: The McGraw-Hill Companies, Inc.
Classen, M., Tytgat, G. N., & Lightdale, C. J. (2011). Gastroenterological endoscopy. Stuttgart [Germany: Thieme.
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Duncan, M.A. (2013). Popular pain killers: NSAIDS. Arthritis Today 27(3), 46-49.
Edmunds, M. (2014). Pharmacology for the Primary Care Provider, (4th.ed). Elsevier.
Foye, W. O., Lemke, T. L., & Williams, D. A. (2013). Foye's principles of medicinal chemistry. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Gum, S., Cho, M. (2013). Recent Updates on Acetaminophen Hepatotoxicity: The Role of Nrf2 in Hepatoprotection. York: the McGraw Hill-Companies, Inc. ISBN:978-0071764011
Kee, J. L., Hayes, E. R., & McCuistion, L. E. (2014). Pharmacology: A patient-centered nursing process approach.
Mosby’s Critical Care Drug Reference. (2013). Antidiarrheal medications.
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