Gastrointestinal Pharmacology notes and learning objectives Flashcards
This set of 30 flashcards covers Gastrointestinal Pharmacology, organised by pathophysiology, drug classes, mechanisms of action, therapeutic rationale, and the roles of the enteric and autonomic nervous systems. (30 cards)
What percentage of prescriptions are for gastrointestinal (GI) disorders?
- About 8% of all prescriptions
- Many OTC medications are also used
Why is understanding GI pathophysiology important for pharmacology?
- Explains rationale for treatment
- Helps understand drug mechanisms
- Aids in anticipating side effects
What are the functional components of the GI system?
- Alimentary canal + accessory organs (liver, pancreas, gallbladder)
- Regulated by muscular sphincters
- Functions: motility, secretion, digestion, absorption
What are the histological layers of the GI tract?
- Mucosa
- Submucosa
- Muscularis (circular & longitudinal layers)
- Serosa/Mesentery (nerves + vessels)
What is the enteric nervous system (ENS)?
- Autonomous “second brain” of the gut
- Contains sensory/motor neurons
- Generates slow waves (pacemaker: interstitial cells of Cajal)
How does the autonomic nervous system influence the GI tract?
- Parasympathetic: Stimulates activity (“rest & digest”)
- **Sympathetic: **Inhibits GI activity (“fight or flight”)
What brain structures control vomiting?
- Vomiting Centre (VC) - integrates signals
- Chemoreceptor Trigger Zone (CTZ) - detects blood-borne toxins (outside BBB)
What are common neurotransmitters involved in emesis?
Histamine (H1), Acetylcholine (M1), Dopamine (D2), Serotonin (5-HT3), Substance P (NK1)
Which pathways trigger the vomiting reflex?
- Cortical input (pain, smells)
- Vestibular system (motion)
- GI tract (toxins/chemotherapy)
- Blood (via CTZ)
What class of drugs is best for motion sickness?
- H1 antihistamines (e.g., promethazine)
- Muscarinic antagonists (e.g., hyoscine)
What is the mechanism of dopamine (D2) antagonists in emesis?
- Block D2 receptors in CTZ
- Some enhance GI motility
Name three key D2 antagonists and their differences.
- Metoclopramide: central + peripheral; crosses BBB
- Domperidone: peripheral only; fewer CNS side effects
- Prochlorperazine: blocks D2, H1, and M1; EPS risk
How do 5-HT3 antagonists like ondansetron work?
- Block serotonin at CTZ, GI tract, and vomiting centre
- Used in chemo/post-op nausea
What do NK1 antagonists like aprepitant block?
- Block substance P at NK1 receptors
- Used in chemo-induced nausea (often with 5-HT3 antagonist + steroid)
What are the three stimulatory receptors on parietal cells?
- H2 (histamine)
- M3 (acetylcholine)
- CCK2 (gastrin)
What inhibits acid secretion in the stomach?
- Somatostatin
- Prostaglandins (PGE2, PGI2)
What is the indirect dominant acid secretion pathway?
Gastrin → stimulates ECL → releases histamine → binds H2 on parietal cells
What are the protective roles of prostaglandins in the stomach?
- Inhibit acid secretion
- Promote mucus + bicarbonate production
How do antacids work?
- Weak bases that neutralize stomach HCl
- Rapid symptom relief only
Name common antacid components and their side effects.
- Aluminium: constipation
- Magnesium: diarrhoea
- Carbonate: bloating (CO₂)
What is the MOA of H2 receptor antagonists?
- Block H2 receptors on parietal cells
- ↓ Histamine-mediated acid secretion (~90%)
What is a major interaction concern with cimetidine?
Inhibits CYP450 enzymes → increases levels of other drugs
How do PPIs reduce acid secretion?
- Irreversibly inhibit H⁺/K⁺ ATPase (proton pump)
- Block final step of acid production
What are key side effects of PPIs?
- Infection risk (↓ acid defense)
- Rebound acid hypersecretion
- Hypomagnesemia (long-term)
