Alimentary pharmacology

22 flashcards · Other · by Anonymous Sloth

1. What are the main classes of drugs used in the treatment of alimentary disease

   Acid suppression Antacids H2-receptor antagonist Proton pump inhibitor Drugs affecting GI motility Anti-emetics Anti-muscarinics Anti-motility IBD drugs Aminosalicylates Corticosteroids Immunosuppressants Biologics Intestinal secretion drugs bile acid sequestrates Ursodeoxycholic acid

2. Mechanism, indication, contraindication of antacids

   Contain magnesium or aluminium Neutralise acid Taken to suppress symptoms

3. Mechanism, indication, contraindication of alginates

   Form thick gel layer on stomach content Prevent further reflux E.g Gaviscon

4. Mechanism, indication, contraindication of H2 receptor antagonists

   Bind and block the histamine receptor in the parietal cell Prevents further acid secretion Indicated for GORD and peptic ulcer disease IV or oral route

5. Mechanism, indication, contraindication of proton pump inhibitors

   Block the proton pump Reduces acid secretion Indicated for GORD and peptic ulcer disease Given orally or IV

6. Mechanism, indication, contraindication of prokinetic agents

   Increase gut motility and gastric emptying Unclear mechanism however involves parasympathetic control of the smooth muscle and sphincter tone. Used in Gastroparesis GORD Anti-emetics

7. Mechanism, indication, contraindication of GI motility inhibitory agents

   Decrease the release of acetylcholine in the opiate receptors of the GI tract Decreases smooth muscle contraction and increases anal sphincter tone

8. Mechanism, indication, contraindication of anti-spasmodic agents

   Reduce symptoms of IBS and renal colic (stones) Mechanism anti-cholinergic muscarinic antagonists (inhibit smooth muscle constriction in gut wall) Peppermint calcium-channel blocker Decreases muscle contraction

9. What are the four types of laxatives

   Bulk Osmotic Stimulant Softeners All work by increasing bulk or drawling fluid into the gut

10. Issue associated with laxatives

    Obstruction Oral or rectal administration Osmotic laxatives do not work without adequate fluid intake Misuse (eating disorder)

11. Mechanism, indication, contraindication of aminosalicylates

    Unclear mechanism but performs as an anti-inflammatory Oral or rectal administration Contraindication for renal impairment Adverse reaction GI upset blood upset Renal impairment

12. Mechanism, indication, contraindication of Corticosteroids

    Anti-inflammatory Oral, IV or rectal Contraindication osteoporosis Cushings disorder Infection susceptibility

13. Mechanism, indication, contraindication of immunosuppressants

    Prevent purine formation in DNA synthesis (reduces immune cell growth) Adverse reaction bone marrow suppression organ damage Drug interaction

14. Mechanism, indication, contraindication of biologics

    Prevents action of TNF -alpha antibodies Used for psoriasis and rheumatoid arthritis Addresses inflammatory response but not the underlying disease Contraindication TB infection MS Pregnancy/ breastfeeding Adverse reaction Infection risk Infusion reaction (pruritus, fever Anaemia, thrombocytopenia, neutropenia Malignancy

15. Mechanism, indication, contraindication of cholestyramine

    Reduces bile salt reabsorption by bind and forming an insoluble complex Affects fat soluble vitamin absorption (decrease vitamin k levels)

16. Mechanism, indication, contraindication of ursodeoxycholic acid

    Inhibition of enzyme involved in cholesterol formation Dissolves non-calcified stones Treatment of gallstones and primary biliary cirrhosis

17. How does the GI system affect drug pharmacokinetics

    Alimentary system is directly in drug pharmacokinetics, diseases in the system can affect drug processing. Route of administration must be altered in the presence of GI symptoms

18. Describe the problems of pharmacokinetics (ADME) in the alimentary system

    Absorption is dependent on pH Gut length Transit time Distribution Low albumin (decreased binding of fat soluble drugs and increased free drug concentration) Metabolism Liver enzymes ( variability directly affects drug toxicity) Increased gut flora cause increased metabolism Reduced first pass metabolism Hepatic portal blood flow Excretion Accummulation of toxins in hepatic-biliary disease Spironolactone

19. Common GI adverse effects

    GI upset Diarrhoea/ constipation 25% drug-induced diarrhoea due to antimicrobials Acute or chronic GI bleeding/ ulceration Low dose acorn/ NSAIDS Warfarin NOAC Due to higher bleeding tendency and ulcer causation Changes to gut flora Antibiotics Reduced vitamin K absorption (increased clotting time) Overgrowth of pathogenic bacteria

20. Describe drug induced liver injury

21. Principles of prescribing for patients with liver disease

    Care and avoidance of: Drugs that become toxic due to changes in pharmacokinetics (liver metabolism, therapeutic index, biliary excretion) Drugs with hepatotoxicity Drugs that worsen non-liver factors of liver disease (encephalopathy)

22. What drugs in particular worsen liver disease

    Particular drugs Warfarin/ anti-coagulants (liver produces less clotting factors) Aspirin/ NSAIDS (increases prothrombin time and worsens ascites( Opiates/ benzodiazepines (can cause encephalopathy by increasing sedation)