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Module 5: Alimentary > Alimentary Pharmacology > Flashcards

Alimentary Pharmacology Flashcards

1
Q

Liver disease: Identify patients with impaired liver function

A
  • Use albumin and PT to establish synthetic function of the liver
    • These parameters tend to decrease in the advanced stages of liver failure
    • NOTE: PT and INR may be decreased due to Vitamin K deficiency
  • LFR tests do not provide information on synthetic abilty, only on damage
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2
Q

Liver disease: Discuss how pharmacokinetic parameters alter due to liver disease

A

Absorption:

  • Decreased due to decreased GI motility
  • Decreased first pass metabolism causes increased bioavailabilty

Distribution:

  • Ascites and oedema change distribution
  • Hypoalbuminaemia: Decreased transport

Metabolism:

  • Decreased levels of hepatic metabolic enzymes
  • Lipid soluble drugs not metabolised to water soluble
  • Drugs with high extraction ratio will experience decreased clearance
    • Extraction ratio: The amount of parent drug that is irreversibly removed from the blood with each pass through the liver
  • Determined by blood flow through the liver

Excretion:

  • Reduced renal clearance. For drugs with narrow therapeutic window this is particularly detrimental
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3
Q

Liver disease: Describe how pharmacodynamic properties may alter and list 3 medicines affected

A

↑ response, ↓ effect, ↑ toxicity (RET)

  1. Benzodiazopines (sedatives)
  2. anticoagulants
  3. Opiates
  4. diuretics
  5. nephrotoxic medicines
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4
Q

Liver disease: List 5 medicines/medicine classes to use with caution or avoid in patients with impaired liver function

A
  1. Electrolyte disturbing medicines e.g. diuretics
  2. Constipating medications
  3. Herbal medicines
  4. Encephalopathy inducing medicines e.g. diuretics
  5. Hepatotoxic medicines
  6. Nephrotoxic medicines
  7. Medicines with haematological effects e.g. warfarin
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5
Q

Liver disease: List general considerations for prescribing in patients with impaired liver function

A
  • Age
  • Gender
  • Alcohol abuse
  • Nutritional status
  • Systemic disease
  • Other medications
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6
Q

Adverse drug reactions: Define ADR

A

ADR: An unwanted/unpleasant effect that occurs at the desired dose of a medication

☆Toxicity occurs above the desired dose

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7
Q

Adverse drug reactions: Discuss what types of ADR can occur

A

On-target: Occur due to the action of the drug on its target receptor

Off-target: Occur due to the action of the drug on an unintended target

A-E classification:

  • Augmented: Exaggeration of effects (on-target) can be reduced with dose. Predictable and preventable
  • Bizarre: Not predictable. Normally very serious
  • Continuing: Persist for long periods
  • Delayed: Occur following use of a medication
  • End of use: Associated with withdrawal of medicines
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8
Q

Adverse drug reactions: State 2 types of ADR and distinguish between them

A

Bizarre: Unpredictable. Anaphylaxis to beta-lactams.

Augmented: Linked to on-target, e.g. ACE inhibitors acting at receptors in other regions

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9
Q

Adverse drug reactions: Identify factors which predispose patients towards developing an ADR

A
  • Polypharmacy
  • Decreased hepatic/renal function
  • Age
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10
Q

Adverse drug reactions: Outline how the safety of medicines is tested and monitored

A

Tested: Laboratory tests, testing on healthy individuals, clinical tests of small group large group clinical trial, drug licensed and marketed

Monitored: Pharmacovigilance. Yellow card scheme to report side-effects

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11
Q

Adverse effects: Suggest ways to avoid ADRs

A
  • Low doses
  • Avoid polypharmacy
  • Short courses
  • Low first dose
  • Avoid in women of child bearing age
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12
Q

Drug interactions: State the pharmacokinetic and pharmacodynamic mechanisms that underlie most drug interactions

A

Pharmacokinetics:

  1. Absorption: Presence of food, GI emptying, chelation,
  2. Metabolism: CytP450 can be affected by food and medications
  3. Distribution: Displacement from binding protein, increases bioavailabilty
  4. Excretion: Changes in GFR

Pharmacodynamics:

Toxicity

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13
Q

Drug interactions: Recogise which drugs are likely to pose a problem

A

Warfarin

Insulin

Lithium

Digoxin

C

A

T

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14
Q

Outline the physiological mechanisms in nausea and vomiting and the transmitter involved

A

Triggers:

  • Severe emotion, disturbing site etc. Th frontal cortex signals to the vomiting centre
  • The CTZ may signal to the vomiting centre
  • Signals from the stomach (via vagus) to the vomiting centre
  • Signals from the vestibular centre to the vomiting centre

CTZ: D2, 5-HT (CDS)

Vestibular centre: H1, Muscarinic

Vomiting centre: Muscarinic, 5-HT, H1 (M&S H)

Stomach: Vagus through release of 5-HT

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15
Q

Anti-emetics: H1 antagonists

A
  • Effective against most causes of emesis, particularly vestibular
  • Some antimuscarinic action
  • Example: Cyclizine

ADR:

  • Sedation, antimuscarinic effects
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16
Q

Anti-emetics: D2 antagonists

A
  • Effective against CTZ and GIT receptor induced emesis
  • Some of this group also have antimuscarinic and antihistaminic effects

ADRs:

  • EPSE (problems with movement e.g. dystonia)
  • Dizziness
  • Drowsiness
17
Q

Anti-emetics: Antimuscarinics

A
  • More effective than antihistamines but less well tolerated
    • Due to antimuscarinic side effects e.g. dry mouth, drowsiness, blurred vision and urinary retention
  • Effective for motion sickess and post-operative vomiting

Example: hyoscine butylbromide

18
Q

Anti-emetics: Serotonin antagonist (5-HT)

A
  • Highly effective against cancer chemotherapy induced emesis
  • Post-operative

Mild side effects:

  • Constipation
  • Flushing
  • Headache
  • Fatigue
19
Q

Anti-emetics:

Dexamethasome, neurokinin 1-receptor antagonists, nabilone, benzodiazepines

A

Dexamethosone: Chemotherapy and post-operative

Neurokinin 1-receptor antagonists: Cisplatin

Nabilone

Benxodiazepenes: Anticipatory N&V

20
Q

Constipation: List drugs that commonly cause constipation

A
  • Iron salts
  • Antimuscarinics
  • Calcium channel blockers
  • Opiates
  • Diuretics
  • Calcium
21
Q

Laxatives: Bulk-forming laxatives

A

MOA:

  • Addition of indigestable polysaccharides
  • Causes the retention of fluid in faecal mass and subsequent stretching
  • This activates stretch receptors and promotes peristalsis
  • Example: Husk

Notes:

  • Take several days to work
  • Adequate fluid intake essential

Side effects:

  • Flatulence
  • Abdominal distension
  • Bloating
  • DO NOT USE WITH OPIATES
22
Q

Laxatives: Osmotic laxatives

A

MOA:

  • Semisynthetic disaccharide or poorly absorbed ions
  • Draw in fluid via osmotic effect, increasing faecal volume

Notes:

  • Takes 2-3 days to work
  • Need to take regularly
  • Requires high fluid intake

Side effects:

  • Bloating
  • Flatulence
  • Cramps
  • Electrolyte disturbances
23
Q

Laxatives: Stool softeners

A

MOA:

  • Reduce the surface tension of faeces, increasing the amount of fluid able to be taken into the faeces
  • Soften the faeces

Notes:

  • Effect occurs after 1-3 days
24
Q

Laxatives: Stimulant laxatives

A

MOA:

  • Directly stimulate the colonic nerves, prompting propulsive movements
  • Example: Senna

Notes:

  • Effect within 8-12 hours
  • Use with opioids

Side effects:

  • Abdominal crmap
  • Caution with long term use
  • Avoid in intestional obstruction
25
Q

Diarrhoea: List drugs that cause diarrhoea

A
  • Beta-blockers
  • Digoxin
  • Antibiotics
  • Metformin
  • Antacids with magnesium
  • PPIs
26
Q

Management of diarrhoea: Fluid replacement

A

Oral rehydration therapy

27
Q

Management of diarrhoea: Racecadotril

A
  • Prodrug
  • Enkephalinase inhibitor
  • Inhibits the breakdown of endogenous opioids → reducing intestinal secretions
  • Used for uncomplicated diarrhoea
28
Q

Management of diarrhoea: Anti-motility agents

A

Examples: Opioids, Codeine, loperamide

  • Eluxadoline: Used for irritable bowel syndrome

MOA: Enhance segmental contractions in the colon. Prolong transit time by inhibiting propulsive movements of the small intestine and colon.

Module 5: Alimentary (13 decks)

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