Please enable JavaScript.
Coggle requires JavaScript to display documents.
Gastrointestinal Pharmacology - Coggle Diagram
Gastrointestinal Pharmacology
Antacids
Often relieve symptoms of dyspepsia and GORD
They are best given when symptoms occur/are expected (usually between meals or at bedtime)
Aluminium and magnesium containing antacids being relatively insoluble in water, are long-acting if retained in the stomach. They are suitable for most antacid purposes
Magnesium containing antacids tend to be laxative whereas aluminium containing antacids may be constipating; antacids containing both may reduce these side-effects
Calcium containing antacids can induce rebound acid secretion: prolonged high doses also cause hypercalcaemia
MOA: neutralises HCl
Most widely used is aluminium hydroxide and magnesium hydroxide
Hydroxide reacts with H+ to give water
Magnesium and aluminium react with bicarbonate and phosphates to form salts
Sodium bicarbonate – reacts with HCl to give water carbon dioxide and salt
Calcium carbonate – reacts with HCl to form calcium chloride and carbon dioxide
Adverse effects:
Magnesium hydroxide – diarrhoea and avoid in chronic kidney failure as can lead to hypermagnesemia
Aluminium hydroxide – constipation and can bind phosphate causing hypophosphatemia
Sodium bicarbonate – can get sodium retention in patients with hypertension/fluid overload
Calcium carbonate – can cause constipation
Alginates
Taken in combination with antacids
They increase the viscosity of the stomach contents and can protect the oesophageal mucosa from acid reflux
MOA: some alginate-containing preparations form a viscous gel (‘raft’) that floats on the surface of the stomach contents and stops it travelling back up, thereby reducing symptoms of reflux
Proton Pump Inhibitors (PPIs)
Effective short-term treatment for gastric/duodenal ulcers. They are also used to treat dyspepsia and GORD
Examples: omeprazole, lansoprazole, and pantoprazole
MOA: block the H+/K+ ATPase (proton pump). They are used 1st line for many GI related conditions
Side effects: abdominal pain, constipation, diarrhoea, dizziness, dry mouth, GI disorders, headache, insomnia, nausea, skin reactions, and vomiting
Excretion is mainly renal
Poor metaboliser (there is decreased clearance so increased acid inhibition)
There is potential for drug-drug interactions with other drugs metabolised by 2C19 (such as warfarin and carbamazepine)
H-2 receptor antagonists
MOA: reversible and competitive antagonists at the histamine H2 receptor. H2 receptor activation increases cAMP activating protein kinase and increasing H+ production
Examples: cimetidine and famotidine
Side effects: constipation, diarrhoea, dizziness, fatigue, and headaches
Elimination is mainly by hepatic routes (some are renal)
Rapid absorption – reaches peak plasma concentration in 1-3 hours
They have several drug-drug interactions
Crosses placenta and is secreted in breast milk
Aminosalicylates
MOA: not fully understood. Thought to work on the cells lining the gut to change the way cells release certain chemicals. These chemicals can contribute to making the gut inflamed, and may be a factor in causing the symptoms of inflammatory bowel diseases
Sulfazine – combination of 5-aminosalicylic acid (5-ASA) and sulfapyridine (acts only as a carrier to the colonic site of action but still causes side-effects)
In the newer aminosalicylates, mesalazine (5-ASA), balsalazide sodium (a pro-drug of 5-ASA) and olsalazine sodium (a dimer of 5-ASA which cleaves in the lower bowel), the sulfonamide-related side-effects of sulfasalazine are avoided, but 5-ASA alone can still cause side-effects (including blood disorders and lupus-like syndrome also seen with sulfasalazine)
Antispasmodics
Smooth muscle relaxants – may relieve abdominal pain/spasm
Examples – peppermint oil, and alverine citrate
Antimuscarinic (used to be anticholinergics) – reduce intestinal motility and are used for GI smooth muscle spasm
They include the tertiary amines atropine sulfate and dicycloverine hydrochloride, and the quaternary ammonium compounds propantheline bromide and hyoscine butylbromide
The quaternary ammonium compounds are less lipid soluble than tertiary amines and are less likely to cross the blood–brain barrier; therefore, have a lower risk for CNS side-effects. They are also less well absorbed from the GI tract
Anti-motility drugs
Examples: loperamide hydrochloride (Brand name: Imodium)
They have opioid-like activity
Side effects: drowsiness, abdominal cramps, and dizziness
MOA: activate presynaptic receptor in ENS, decreasing ACh release and peristalsis
Laxatives
Used to treat constipation
Bulk-forming laxatives
Examples: ispaghula husk (fybogel) and methylcellulose
MOA: causes an increase in bowel content volume, triggering stretch receptor in the intestinal wall. This leads to reflex contractions (peristalsis) that propels the bowel content forward
Onset of action = up to 72 hours
They are non-digestible and fluid intake must be maintain to avoid intestinal obstruction
Particularly useful is adults with small, hard stools which can’t increase fibre in their diet
May exacerbate symptoms of flatulence, bloating, and cramping
Stimulant laxatives
Examples: bisacodyl (sodium picosulfate) and members of the anthraquinone group (senna, co-danthramer and co-danthrusate)
MOA: increase intestinal motility and often cause abdominal cramps
Should be avoided in intestinal obstruction
Indications: severe constipation
Can be taken between 6-12 hours to work
Faecal softener laxatives
Examples: docusate sodium and glycerol suppositories (have softening properties)
MOA: act by decreasing surface tension and increasing penetration of intestinal fluid into the faecal mass
Osmotic laxatives
MOA: increase amount of water in the large bowel, either by drawing fluid from the body into the bowel or by retaining the fluid they were administered with
Example: Macrogols (Brand: Movicol) are inert polymers of ethylene glycol which sequester fluid in the bowel; giving fluid with macrogols may reduce the dehydrating effect sometimes seen with osmotic laxatives