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Gastrointestinal system > GI pharmacology > Flashcards

GI pharmacology Flashcards

1
Q

Causes of nausea

A
  • GI irritation
  • Migraine, pain
  • Motion sickness, pregnancy
  • Psychogenic - stress/emotional trauma
  • Radiation
  • Drugs
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2
Q

Effects of nausea

A
  • Dehydration
  • Alkalosis - excreting stomach acid
  • Hypokalaemia - volume depletion
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3
Q

How is vomiting controlled?

A
  • Sensory input → vomiting centre (smooth muscle contraction)
  • Vestibular organ → vestibular nucleus → CTZ → vomiting centre
  • CTZ screens blood fot toxins etc
  • Sensory afferents from GIT via vagus nerve into NTS = vomiting centre for contractile response
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4
Q

Anti-emetic drugs

A
  • H1 antagonists - target vestibular nuclei
  • Muscarinic ACh antagonists - target vestibular nuclei and vomiting centre
  • 5-HT3 antagonists - targets CTZ and visceral afferents
  • D2 antagonists - targets CTZ
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5
Q

What do H1 antagonists target?

A

Vestibular nuclei

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6
Q

What do muscarinic ACh antagonists target?

A

Vestibular nuclei and vomiting centre

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7
Q

What do 5-HT3 antagonists target?

A

CTZ and visceral afferents

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8
Q

When are D2 dopamine antagonists needed, example

A

Post operative nausea and vomiting, metoclopramide

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9
Q

When are H1 histamine antagonists needed, example

A

Most nausea and vomiting, cyclising

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10
Q

When are muscarinic ACh antagonists needed, example

A

Motion sickness

Hyoscine

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11
Q

When are 5-HT3 antagonists needed, example

A

Post operative sickness and nausea

Ondansetron

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12
Q

Controlling acid secretion

A
  • Neuronal - ACh - via vagus nerve to acts on msucarinic receptors on mast-like cells in gut (enterochromaffin cells) and parietal cells
  • Parietal cells secrete acid
  • Endocrine - gastrin - peptide from endocrine mucosa in duodenum - acts on mast-like cells to activate proton pumps and acid secretion
  • Paracrine - histamine acts on H2 receptors in parietal cells
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13
Q

Pathological consequences of gastric acid

A
  • Protective factors: NaHCO3, mucus, epithelial cell regeneration and tight junctions, blood supply
  • Aggressive factors: H+, pepsin, helicobacter pylori
  • Dyspepsia - discomfort due to acid production
  • GORD - oesophageal sphincters are not strong - flows to oesophagus
  • Gastric and duodenal ulcers - protective factors in gut overcome
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14
Q

Helicobacter pylori

A
  • Gram -ve bacterium
  • Risk factor for gastritis, gastric cancer, peptic ulcer
  • 95% of duodenal ulcer presentations
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15
Q

Pharmacotherapy

A
  • Addresses primary problems and controlling acid secretion and mucus production
  • Proton pump inhibitors
  • H2 antagonists
  • Synthetic PGs to increase mucus production and inhibit parietal cell activation
  • Antacids
  • Antibiotics eradicate H.pylori - amoxicillin plus clarithromycin or metronidazole
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16
Q

What do H2 antagonists target?

A

H2R

17
Q

What do NSAIDs target?

A

AA - PGE2 = no mucus

18
Q

Function of misoprostol

A

Replaces PGs

19
Q

When are PPIs needed, example

A

GAstric/duodenal ulcers, GORD

Omeprazole

20
Q

When are H2 antagonists needed, example

A

Only if PPI contraindicated

Ranitidine

21
Q

When are synthetic PGs needed, example

A

Gastric/duodenal ulcers/NSAID

Misoprostol

22
Q

When are antacids needed, example

A

Ulcer dyspepsia, GORD

Aluminium hydroxide

23
Q

What is constipation

A

Definition: small, hard stools with a frequency below pts normal function

24
Q

Causes of constipation

A
  • Dietary, fluid/electrolyte disturbance
  • Misconceptions about normal bowel habit
  • IBS
  • Poor bowel habit
  • Laxative abuse
  • Pregnancy
  • Endocrine disorders - hypothyroidism
  • Anorectal disease - fissures and haemorrhoids
  • Parkinson’s/stroke
  • Mechanical obstruction
  • Nerve damage
  • Immobility
  • Drugs
25
Q

Drugs affecting GIT

A
  • Decreasing motility: autonomic effects - atropine
  • Opiates increase muscle tone, suppress peristalsis, raise sphincter tone and reduce sensitivity to rectal distension
  • Increase motility - metoclopramide, osmotic effects (magnesium), fat malabsorption (orlistat), microbial proliferation (antibiotics)
26
Q

Laxative function

A

Colon adjusts fluid and sodium balance

27
Q

Bowel cleansing solutions

A
  • Picolax - sodium picosulphate (stimulant)

- Magnesium citrate (osmotic)

28
Q

What is diarrhoea?

A

Failure of intestinal uptake of sodium and water = watery bowel movements

29
Q

Effects of diarrhoea

A

Dehydration and acidosis

30
Q

Treatment of diarrhoea

A
  • Symptomatic - correction of fluid and electrolyte loss
  • Antimotility drugs - opioids (loperamide)
  • Bulking agents - ispaghula
31
Q

What do bulk laxatives do, example

A

Increase faecal mass

Bran/ispaghula husk

32
Q

What do osmotic laxatives do, example

A

Increase fluid in bowel

Lactulose

33
Q

What do stimulant laxatives do, example

A

Increased intestinal motility

Senna

34
Q

What do faecal softeners do, example

A

Lubricate and soften

Arachis (peanut) oil

Gastrointestinal system (27 decks)

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