PT
● MODULE 12 / 20
Gastrointestinal Pharmacology
Connect acid suppression, emesis pathways, motility and fluid replacement to gastrointestinal treatment.
Quick revision ↓ Medical Dictionary
FULL CHAPTER EXPLANATION
Deep Learning — Module 12
Read this section in sequence. It moves from drug targets to therapeutic effects, adverse reactions and safe use.
01
Acid suppression and mucosal protection
Proton-pump inhibitors suppress gastric H-K ATPase activity, while H2 antagonists reduce histamine-stimulated acid secretion. Antacids neutralize existing acid and may interact with absorption of other medicines. Sucralfate forms a protective barrier in an acidic environment; misoprostol is a prostaglandin analogue that can protect gastric mucosa but also stimulates uterine activity. Relief of dyspepsia does not exclude serious disease. Helicobacter pylori eradication requires an appropriate multidrug regimen based on resistance and current guidance.
02
Antiemetics and prokinetics
Emesis integrates gut, vestibular and central signals. Ondansetron blocks 5-HT3 receptors; metoclopramide blocks dopamine D2 pathways and promotes upper gut motility. Dopamine blockade can produce extrapyramidal reactions, and some antiemetics prolong QT. H1 and muscarinic antagonists are useful for selected vestibular causes. Aprepitant blocks neurokinin-1 signaling. A prokinetic is unsuitable when mechanical obstruction is suspected because increasing movement does not remove an obstructing lesion.
03
Constipation therapies
Bulk-forming agents retain water and increase stool mass when fluid intake and bowel patency are adequate. Osmotic agents such as polyethylene glycol draw water into the lumen; lactulose is metabolized in the colon and also helps reduce ammonia absorption in hepatic encephalopathy. Stimulant laxatives increase intestinal secretion or motility. Choose according to cause, duration and comorbidity. New constipation with concerning features warrants assessment rather than indefinite escalation of laxatives.
04
Diarrhea and rehydration
Oral rehydration solution exploits preserved sodium-glucose cotransport to replace water and electrolytes. Antimotility therapy such as loperamide reduces propulsive movement through peripheral opioid activity but does not correct dehydration. It may be inappropriate in invasive diarrhea or settings with risk of toxic dilation. Antimicrobials are reserved for defined indications rather than every loose stool. The priority is assessing hydration, severity and cause, especially in children and vulnerable patients.
05
Inflammatory and functional bowel disease
Aminosalicylates have a role particularly in ulcerative colitis; corticosteroids can induce remission but are unsuitable as routine long-term maintenance because of toxicity. Immunomodulators and biologics require specialist selection and monitoring. Irritable bowel syndrome management depends on predominant symptoms and may include dietary strategies, antispasmodics or selected bowel-directed medicines. Functional symptoms, inflammatory disease and mechanical obstruction require different reasoning even when all produce abdominal pain.
High-Yield Revision
- Rehydration and symptom suppression are different interventions.
- Match antiemetic class to the pathway and patient risk.
- Exclude obstruction before stimulating gastrointestinal motility.
Common Exam & Concept Pitfalls
- Acid suppression alone does not eradicate H. pylori.
- Do not give antimotility drugs automatically for bloody or invasive diarrhea.
Sources & Further Reading
Curriculum scope checked 23 September 2026. These original study notes summarize established principles; current institutional guidance and product information govern clinical use. Faculty review is pending.
RAHBAR study structure: target → drug action → therapeutic use → adverse effects → monitoring. Use institutional curriculum and faculty guidance for local sequencing, practical requirements and assessment specifications.