Peptic Ulcer Disease and Reflux Esophagitis PDF

Part 1 1: Pep ptic Ulce er Disea ase and Reflux Esophag E gitis █ PEP PTIC ULCE ER Definittion: ulcera ation of the...

Part 1 1: Pep ptic Ulce er Disea ase and Reflux Esophag E gitis █ PEP PTIC ULCE ER Definittion: ulcera ation of the e duodenuum or stom mach due tot imbalannce betwee en local invasive force (e.g g. HCl andd pepsin) a and protecttive mecha anisms. Invasiv ve factors:  ess: ↑ HCl and pepsin secretion Stre n by pariettal cells.  Diett: coffee, alcohol a and d spices.  Druugs: NSAID Ds, corticosteroids, m morphine, methylxan nthines, etcc.  ection with Infe h Helicoba acter pylorri. H. ppylori is sppiral gram –ve flageellates foun nd in the antrum a of human sttomach. Cerrtain enzym mes and toxins t prooduced by y the bacteria causee tissue damage. d Infe ection with h H. pylori can be d diagnosed by endosc copic biop psy or serological marrkers. Defens sive mech hanisms:  Muccus prod duction by gasttric muccosa.  Pan ncreatic bic carbonate secretion.  Goo od mucosa al blood flo ow.  Loc cal PGE2 annd PGI2 production. Regula ation of HC Cl secretio on  Ach h: ↑ HCl seecretion thrrough M1 rreceptors → ↑ intrace ellular Ca2+.  Gasstrin: ↑ HC n through G receptorrs → ↑ intra Cl secretion acellular Caa2+.  Histamine: ↑ HCl secretion througgh H2 rece eptors → ↑ intracellulaar cAMP. 251  Both C Ca2+ and cAMP activate H+ /K+ ATPase e at the membrane ofo the pari etal + cell to secrete H into the gastric lum men “proton pump”.  PGE E2 and PGI2: act on PG P recepto ors → ↓ cAMP → ↓ HCl secre etion. Clinica al picture  Epig gastric paiin: charactterized by: – DDiffuse annd worsen ns by food d in GGU. – L Localized (point ten nderness) a and rrelieved byy food in DU. D  Signns of comp plications e.g. bleediing, ane emia, etc. Diagno osis – End doscopy: visualizatio v cer. n of the ulc – Rad diologic: byy barium meal. m █ The erapy of peptic p ulcer ▌Non-d drug thera apy = life style s mod dification  Resst and Sedation: theyy improve hhealing and relief pain of DU.  Stopp Smoking g, Spices, alcohol, coffee, an nd tea: beccause theyy ↑ HCl.  Avo oid Stress: because stress s ↑ HC Cl.  Avo oid ulcerogenic drugs s: e.g. NSAAIDs.  Diett: – Frequeent small meals m in DU U in order to buffer high acidityy. – Encourage milk anda fats. – Avoid Spices S and d fried foodd ▌Pharm macologic cal therapy y Dru ugs that neutralize HCl: H antac cids ugs that ↓ HCl secre Dru etion: 252  – Selective M1 blockers: pirenzepine, telenzepine. – H2 blockers: cimetidine, ranitidine, famotidine. – Proton pump inhibitors: omeprazole, lanzoprazole, etc. Drugs that ↑ mucosal defense mechanisms: – Sucralfate – Colloid bismuth compounds: e.g. bismuth subcitrate. – Carbenoxolone – PGE1 analogues: misoprostol. Antimicrobial drugs for H. pylori: see later. Adjuvant therapy: Sedatives and multivitamins to ↓ stress to enhance healing. █ ANTACIDS  Antacids are weak bases that are taken orally and partially neutralize gastric acid and reduce pepsin activity.  They are used as symptomatic relief of hyperacidity and should not be used as long-term treatment. Sodium bicarbonate Calcium carbonate Magnesium and aluminum salts (Mg hydroxide and Aluminium hydroxide)  It can be absorbed  Partially absorbed ant-  They are poorly ab- systemically leading to acid. sorbed from GIT and salt & water retention,  Ca2+ may act directly to have no systemic and metabolic stimulate gastrin secre- effects. alkalosis. tion leading to acid  The unabsorbed Mg  It is contraindicated in rebound. salts cause osmotic di- hypertension and heart  It is contraindicated in arrhea; the unabsorbed failure. hypercalcemia and Al salts cause  It has rapid onset and renal stones. constipation. short duration.  They have slow onset. Adverse effects Change in bowel habits: Al3+ hydroxide causes constipation, while Mg2+ hydroxide cause diarrhea. For this reason, both salts are combined together to manage this problem. 253