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Alimentary System > Clinical Pharmacology of Alimentary > Flashcards

Clinical Pharmacology of Alimentary Flashcards

1
Q

List the main drug classes used in the treatment of acid suppression.

A
  • Antacids
  • H2 receptor antagonists
  • Proton pump inhibitors
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2
Q

List the main drug classes used to affect GI motility.

A
  • Antiemetics
  • Anti-muscarinics/other antispasmodics
  • Anti-motility
  • Laxatives
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3
Q

List the main drug classes used in the treatment of IBD.

A
  • Aminosalicylates
  • Corticosteroids
  • Immunosuppressants
  • Biologics
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4
Q

List the main drug classes used to affect intestinal secretions.

A
  • Bile acid sequestrates

- Ursedeoxycholic acid

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5
Q

Describe antacids and give an example.

A
  • Used in treatment of acid suppression
  • Contain magnesium or aluminium
  • Neutralise gastric acid
  • Taken when symptoms occur
    e. g. Maalox
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6
Q

Describe alginates and give an example.

A
  • Used in treatment of acid suppression
  • Form a viscous gel that floats on stomach contents and reduced reflux
    e. g. Gaviscon
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7
Q

Describe mucosal protectors and give examples.

A
  • Used in treatment of acid suppression

e. g. bismuth, sucralfate, misoprostol

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8
Q

Describe H2 receptor antagonists and give an example.

A
  • Used in treatment of acid suppression
  • Block histamine receptor thereby reducing acid secretion
  • Indicated in GORD/peptic ulcer disease
  • Given orally or intravenously
    e. g. Ranitidine
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9
Q

Describe proton pump inhibitors and give an example.

A
  • Used in treatment of acid suppression
  • Block proton pump thereby reducing acid secretion
  • Indicated in GORD/peptic ulcer disease
  • Oral or IV administration
  • Widely used (overused?)
  • Triple therapy treatment of PU/DU associated with H. pylori
  • Problems with GI upset and predisposition to C. difficile infection, hypomagnesaemia, B12 deficiency
    e. g. Omeprazole
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10
Q

Describe prokinetic agents and give examples.

A
  • Increase gut motility and gastric emptying
  • MoA: not clear but involves parasympathetic nervous system control of smooth muscle and sphincter tone (via ACh)
  • Also stop vomiting
    e. g. gastroparesis, GORD, antiemetics, Metoclopramide and Domperidone (dopamine antagonists - habit post-synaptic cholinergic neurons)
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11
Q

Describe classes of drugs that decrease GI motility and give examples.

A
  • Can be used for clinical benefit (anti-diarrhoea) or cause unwanted effects (constipation)
  • MoA: decrease ACh release via opiate receptors, decrease in smooth muscle contraction, increase in anal sphincter tone
    e. g. Loperamide (Immodium), Opiods
  • Loperamide has few central opiate effects as it is not well absorbed across the blood-brain barrier
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12
Q

Describe anti-spasmodics and give examples.

A
  • Can be used to reduce symptoms in IBS, renal colic

Three mechanisms;

  • Inhibit smooth muscle constriction in gut wall –> muscle relaxation –> reduces spasm
    e. g. anti-cholinergic muscarinic antagonists (hyoscine, buscopan, mebeverine)
  • Direct smooth muscle relaxants
  • CCBs (peppermint oil) reduce Ca –> smooth muscle relaxation
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13
Q

Describe laxatives and give examples.

A
  • Pharmacological treatment may not be needed

Four types;

  • Bulk e.g. Isphagula
  • Osmotic e.g. Lactulose
  • Stimulant e.g. Senna
  • Softeners e.g. Arachis oil
  • Work by increasing bulk or drawing fluid into gut

Issues;

  • Obstruction
  • Route of administration: oral or rectal
  • Need for other measures: osmotic laxatives will not work without adequate fluid intake
  • Misuse
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14
Q

Describe aminosalicylates and give examples.

A
  • Treatment of IBD
  • MoA: unclear but anti-inflammatory
  • Oral or rectal administration
  • Chemically related to salicylates so avoid if allergic
  • Caution in renal impairment
    e. g. Mesalazine, Olsalazine

Adverse effects;

  • GI upset
  • Blood dycrasias
  • Headches
  • Renal impairment
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15
Q

Describe corticosteroids.

A
  • Treatment of IBD
  • Anti-inflammatory effects
  • Given orally, IV or rectally

Concerns and contraindications;

  • Osteoporosis
  • Cushingoid features e.g. weight gain, DM, HT
  • Increased susceptibility to infection
  • Addisonian crisis with abrupt withdrawal
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16
Q

Describe immunosuppressants and give an example.

A
  • Treatment of IBD
  • Prevent formation of purine required for DNA synthesis –> reduce immune cell proliferation
  • Numerous drug interactions
  • Specialist use and close monitoring required
    e. g. Azathioprine

Adverse effects;

  • Mainly bone marrow suppression
  • Azathioprine hypersensitivity
  • Organ damage (lung, liver, pancreatitis)
17
Q

Describe biologics (anti-TNFA antibodies) and given an example.

A
  • Treatment of IBD
  • Mouse-human chimeric antibody to TNF-alpha
  • Prevents action of TNF-alpha (key cytokine in inflammatory response)
  • Also used in psoriasis, RA
  • Addresses inflammatory response but not underlying disease process so course of disease after discontinuation is unclear
    e. g. Infliximab
18
Q

Describe infliximab and its cautions/contraindications and adverse effects.

A
  • Biologics used in treating IBD

Cautions/contraindications;

  • Current TB or other serious infection
  • Multiple sclerosis (can cause onset too)
  • Pregnancy/breast feeding

Adverse effects;

  • Risk of infection, particularly TB (screen all patients)
  • Infusion reaction (itch, fever)
  • Anaemia, thrombocytopenia, neutropenia
  • ?Demyelination
  • Pleurodenia
  • Malignancy
19
Q

Describe cholestyramine.

A
  • Affects biliary secretion
  • Pruritis from biliary cause
  • Reduces biliary salts by binding with them in the gut and then excreting insoluble complex
  • May affect absorption other drugs so should be taken separately
  • May affect fat soluble vitamin absorption so may decrease vitamin K levels (affecting clotting and Warfarin)
20
Q

Describe ursodeoxycholic acid.

A
  • Affects biliary secretion
  • Used to treat gallstones and primary biliary cirrhosis (PBC)
  • Inhibits an enzyme involved in formation of cholesterol, altering amount in bile and slowly dissolving non-calcified stones
21
Q

Describe the problems with absorption.

A
  • GI symptoms may necessitate a change in route of administration
  • Absorption (rate and total): pH, gut transit, transit time
22
Q

Describe the problems with distribution.

A
  • Low albumin –> decreased binding and increased free drug concentration
23
Q

Describe the problems with metabolism.

A
  • Liver enzymes (may be inhibited or reduced but generally toxic)
  • Increased gut bacteria (metabolise drugs so increases doses needed)
  • Liver blood flow (drugs with high extraction ratio)
24
Q

Describe the problems with excretion.

A
  • Biliary excretion (increased toxicity if hepatobiliary disease)
25
Q

Describe GI adverse effects.

A
  • GI upset very common with medication (20-40% of ADRs)

Diarrhoea/constipation;

  • Acute/chronic
    e. g. cholinergic, NSAIDs, antimicrobials, opioids, anti-cholinergic
  • Multiple mechanisms

GI bleeding/ulceration;

  • 6.5% of hospital admissions due to ADRs
    e. g. low dose aspirin, NSAIDs, warfarin
  • Mechanisms include ulcer causation and increased bleeding tendency
  • Other drugs implicated e.g. SSRIs

Changes to gut bacteria;

  • Mainly antibiotics
  • Loss of OCP activity
  • Reduced vitamin K absorption (increased prothrombin time)
  • Overgrowth of pathogenic bacteria e.g. C. difficile
26
Q

Describe drug-induced liver injury.

A

Type A ADR: intrinsic hepatotoxicity (predictable, dose–dependent, acute)

Type B ADR: idiosyncratic hepatotoxicity (unpredictable, not dose dependent, and may occur at any time – may be part of a hypersensitivity reaction);

  • May be due to drug, herbal product or active metabolite
  • Can range from asymptomatic increase in LFTs to fulminant liver failure and death
  • Generally hepatitis or cholestasis, but can mimic any pattern of acute or chronic liver disease
27
Q

Describe the risk factors of drug-induced liver injury.

A
  • Age: elderly
  • Sex: female
  • Alcohol consumption
  • Genetic factors
  • Malnourishment
28
Q

Consider the severity of liver disease.

A
  • Child-Pugh classification

- Individual scored summed and grouped as <7 = A, 7-9 = B, >9 = C

29
Q

Describe prescribing in liver disease.

A

Care with avoidance of;

  • Drugs that can be toxic due to changes in pharmacokinetics: liver metabolism, therapeutic index, biliary excretion (if biliary/cholestatic disease)
  • Hepatotoxic drugs e.g. methotrexate, azathioprine
  • Drugs that may worsen the non-liver aspect of disease (e.g. encephalopathy) e.g. benzodiazepines

Particular drugs;

  • Warfarin/anticoagulants: clotting factors already low
  • Aspirin/NSAIDs: increase bleeding time, in combo with low clotting factors, NSAIDs can worsen ascites due to fluid retention
  • Opiates/benzodiazepines: may precipitate encephalopathy by increasing sedation

Alimentary System (43 decks)

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