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1-5 GIT > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What can GORD lead to?

A

Ulcerative oesophagitis which can lead to cancer

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2
Q

Common antacid therapies

A
  • gaviscon: float on stomach contents
  • Antacid tablets coat oesophagus and neutralise acid in stomach
  • H2 receptor antagonists: inhibitor of H2 receptor - prevent histamine action on parietal cell
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3
Q

GI causes of nausea and vomiting

A
  • outflow obstruction
  • dysmotility
  • mucosal inflammation
  • infections
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4
Q

Other causes of nausea and vomiting

A

Chemical - drugs, radiotherapy, toxins
Vestibular - motion sickness, cerebellar tumour
CNS - anxiety, raised ICP
Pregnancy

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5
Q

4 Main sources of afferent input that are associated with the pathophysiology of nausea and vomiting

A
  1. chemoreceptor trigger zone
  2. vestibular system
  3. vagal and spinal afferent serves from GI tract
  4. CNS
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6
Q

Mechanism of action of metoclopramide

A

¥ Enhances response to acetylcholine in the upper GI tract
¥ Blocks dopamine receptors in the CTZ
¥ At higher doses also blocks CTZ serotonin receptors

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7
Q

Adverse effects of metoclopramide

A
  • Extra pyramidal symptoms – more common in younger patients (and female)
  • Rarely causes tardive dyskinesia, higher risk with longer treatment
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8
Q

Mechanism of action of domperidone

A
  • effective at the CTZ

- blocks dopamine receptors in the upper GI tract resulting in increased motility

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9
Q

Mechanisms to cross the blood brain barrier (3)

A
  1. transmembrane diffusion
  2. transport systems
  3. transcellular pathway
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10
Q

Examples of serotonin antagonists

A

Ondansetron, granisteron, palonosetron

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11
Q

Major and minor effects of serotonin antagonists

A

Major - effect - block released serotonin in upper GI tract

Minor - acts at the vomiting centre

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12
Q

Short term and long term side effects of steroids

A

Short term - increased BSL, hunger, increased BP, psychosis

Long term - osteoporosis, steroid induced DM, myopathy, thin skin

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13
Q

Action of hycosine

A

Anticholinergic at muscarinic receptors

- minor histamine and serotonin antagonism

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14
Q

Treating nausea and vomiting in pregnant women

A

Cat A: metoclopramide, pyridoxine
Cat B1: Odansetron
Cat C: Prochlorperazine

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15
Q

If medication is required for children with acute gastroenteritis (nausea/vomiting), what should be given?

A

Odansetron

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16
Q

Accompanying signs and symptoms to nausea and vomiting

A
  • abdominal pain, distention, peritonism
  • diarrhoea
  • fever, neck stiffness
  • vertigo
  • focal neurology
17
Q

3 Pharmacokinetic changes in hepatic insufficiency

A
  1. bioavailability
  2. protein binding, and therefore distribution
  3. hepatic clearance
    - phase 1 (cytochrome p450)
    - phase 2 (glucourinidation and sulphation)
18
Q

How does liver disease affect flow dependent clearance?

A

Chronic hepatic disease
scarring obstructed blood vessels shunting drug in portal and arterial blood bypasses hepatocytes increased bioavailability and reduced clearance of flow dependent drugs

19
Q

Flow dependent drugs

A
  • nitrates
  • opiates
  • beta-adrenoceptor blockers
  • calcium channel blockers
  • lignocaine
20
Q

Enzyme dependent drugs

A
  • Most anti-convulsants
  • Warfarin
  • Benzodiazepines
  • Theophylline
  • Most NSAID’s
  • Amiodarone
21
Q

Effects of hepatic disease on enzyme dependent drugs

A
  • impaired clearance

- alcohol induces some P450 isoenzymes

22
Q

Liver failure and reduced albumin

A

Hypoalbuminaemia: reduced bound fraction of highly albumin bound drugs
Results in increased extravascular water volume and reduced intravascular water volume – altered distribution volume for highly water soluble drugs

23
Q

How does hepatic disease effect anticoagulant use?

A

Reduced clotting factor synthesis = increased effectiveness of anticoagulants and increased bleeding risk
CONTRAINDICATED

24
Q

How does hepatic disease effect sedative use?

A
  • increased sensitivity to sedatives - bento’s and opiates
  • increased risk of over sedation and hepatic encephalopathy
    TAKE WITH CARE
25
Q

How does hepatic disease effect diuretic use?

A
  • Reduced plasma albumin reduced plasma osmotic pressure
  • Increased tissue fluid and reduced plasma volume
  • Reduced renal flow
  • Increased renin increased angiotensin II increased aldosterone
  • Na+ and H2O retention and K+ loss
    AVOID K+ DEPLETING AGENTS
26
Q

Therapeutic goals in inflammatory bowel disease

A
  • manage exacerbations swiftly
  • suppress chronic inflamm
  • surveillance for complications
  • manage GIT complications as well as extra intestinal disease
27
Q

Role of aminoslicylates in IBD

A
  • maintaining remission in UC, limited in Crohn’s
28
Q

Role of corticosteroids in IBD

A
  • potent anti-inflammatory

- used for moderate and severe relapses of UC and Crohn’s

29
Q

Action and adverse effects of thiopurines

A 
- result in immunomodulation via induction of T cell apoptosis
Adverse affects 
antiproliferative 
• Antiproliferative actions: bone marrow failure (↓WCC,
↓platelets)
• Hepatotoxicity
• Allergic skin rash
• Teratogenicity risk
30
Q

Role of anti-TNF-alpha antibodies in IBD (infliximab, adalimumab)

A

TNF-alpha regulates immune cells

31
Q

Osmotic laxatives used in constipation

A
  • increase water content of stools
    • Polyethylene glycol (PEG) Movicol – lower dose as aperient ColonLytely - larger doses as bowel prep
    • Magnesium citrate
    Epson salts, some Mg absorbed
    • Sodium phosphate
    Risk of electrolyte disorders (↑PO4, ↓Ca, ↓K), used in enemas
    • Nonabsorbable carbohydrates Lactulose/sorbitol
32
Q

Stimulants used in constipation

A

Encourage bowel motility
• Senna
Converted into active Sennosides A & B by colonic bacteria
• Docusate sodium (Coloxyl) Detergent, also stool softener
• Sodium picosulphate Picoprep
• Bisacodyl
Oral and suppository formulations

33
Q

Drugs used in diarhoea

A

Mu opioid receptor antagonists: Diphenoxylate, loperamide, codeine sulfate
Bulking agents: plant fibre, guar gum

1-5 GIT (7 decks)

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