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1
Q

Name 2 anatacids

A

Gavisgon and peptac

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2
Q

What is the mechanism by which antacids work?

A

Contain alginate and >1 anatacid e.g. sodium bicarb, calcium carb, magnesium or aluminium salts

Buffer stomach acid and increase stomach viscosity, reducing damage to mucosa and preventing GORD

Might also inhibits pepsin production

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3
Q

What are the indications for antacids?

A
  1. GORD

2. Dyspepsia

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4
Q

What are the CIs for antacids?

A

Usually well tolerated and safe in pregnancy

Avoid combo with thick, milk preperations - may thicken stomach contents, causing bloating and nausea

Caution Na/K containing antacids in hyperK+/fluid overload

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5
Q

What are the SEs of antacids?

A

Few, depends on preparation.

Aluminium salts may cause constipation

Magnesium salts may cause diarrhoea

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6
Q

What are the interactions of antacids?

A

Alginate may bind to drugs and reduce their concentration

Antacids may increase the concentration of drugs by reducing stomach acid

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7
Q

When should antacids be taken?

A

Just after meal, before bed or when Sx occur

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8
Q

Should antacids be used long term?

A

No - temporary measure. Discuss lifestyle for why GORD is occurring

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9
Q

Name one H2 receptor antagonist

A

Ranitidine

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10
Q

What is the mechanism by which H2 receptors work?

A

Histamine (released by local paracrine cells) regulate parietal cell proton pumps that exchange K+ for H+ into the lumen

Ranitidine blocks histamine receptor so reduces gastric acid secretion

However, proton pump can be activated through different mechanisms so H2 blockers do not completely stop gastric acid secretion

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11
Q

What are the indications for H2 receptor antagonists?

A
  1. GORD/dyspepsia - relieves Sx. Alternative treatment = PPIs which are often preferred
  2. Peptic ulcer - prevention and treatment of gastric, duodenal and NSAID associated ulcers. PPIs usually preferred
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12
Q

What are the CIs for H2 receptor antagonists?

A
  • May disguise Sx of gastric cancer - should fully investigate cause of Sx
  • Renal impairment - dose reduction
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13
Q

What are the SEs of H2 receptor antagonists?

A

Few
May cause GI upset (e.g. diarrhoea or constipation)
Headache
Dizziness

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14
Q

What are the interactions of H2 receptor antagonists?

A

No major drug interactions

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15
Q

How is H2 receptor antagonists excreted?

A

Renally

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16
Q

What should patients avoid when taking H2 receptor antagonists?

A

Alcohol and smoking.

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17
Q

Name 3 proton pump inhibitors

A

Omeprazole, pantoprazole, lansoprazole

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18
Q

What is the mechanism by which PPIs exert their action

A

Irreversibly block the H+/K+ ATPase channels of gastric parietal cells, thereby reducing gastric acid secretion

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19
Q

What are the indications for PPIs?

A
  1. Peptic ulcer - prevention and Tx of gastric and duodenal ulcers (including NSAID associated)
  2. Dyspepsia and GORD - treatment of
  3. Eradication of H Pylori Infection (in addition to ABx)
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20
Q

What are the CIs for PPIs?

A
  • May disguise the symptoms/signs of gastric cancer - should explore warning/red flag signs
  • Increased risk of # in elderly (osteoporosis)
  • Increases absorption of digoxin
  • Dose reduction in hepatic impairment
21
Q

What are the SEs of PPIs?

A
  • Gastric upset and headache
  • Increased gastric pH - reduced host defences may result in infection, particularly in elderly - C Diff
  • Hypomagnesia - arrhythmia/tettany
  • Hypersecretion of gastric acid upon secretion
22
Q

What are the interactions of PPIs?

A

Increase absorption of digoxin

CYP450 inhibitor e.g. reduce platelet reducing effect of clopidogrel, increase risk of bleeding with warfarin

23
Q

How are PPIs excreted?

24
Q

Name 2 anti-motility/anti-diarrhoea drugs?

A

Loperamide (imodium), codeine phosphate

25
Q

What is the mechanism by which loperamide/codeine phosphate (anti-diarrhoreals) worK

A
  • Inhibit opioid ų-receptors in GI system - reduces peristalsis and smooth muscle tone.
  • Increases bowel transit time and increases anal sphincter tone
  • Increases time for water absorption (hardens stools)
26
Q

What are the indications for loperamide/codeine phosphate?

A
  1. Diarrhoea - in context of IBS or gastroenteritis
27
Q

What are the CIs for loperamide/codeine phosphate?

A
  • Acute ulcerative colitis - reducing peristalsis increases risk of megacolon/perforation
  • C Diff infection (may signify infection)
  • Acute bloody diarrhoea (dysentry) - may signify infection. Particularly relevant for E Coli 0157 (haemolytic uraemia syndrome; HUS - anti-mobility drugs increases risk)
28
Q

What are the SE’s of loperamide/codeine phosphate?

A

Predictable

  • Constipation
  • Abdo cramping
  • Flactulence
29
Q

What are the interactions of loperamide/codeine phosphate?

A

No significant interactions

30
Q

Name one stimulant laxative

31
Q

What is the mechanism by which stimulant laxatives work?

A
  • Increase H2O and electrolyte secretion from mucosa into lumen. Increases volume of intestinal contents and peristalsis.
  • Pro-peristaltic action - senna broken down by bacteria in gut. Metabolites act directly on enteric nervous system. Increases peristalsis.
32
Q

What are the Indications for stimulant laxatives

A
  1. Constipation

2. Suppositories for faecal impaction

33
Q

What are the SEs of stimulant laxatives?

A
  1. Diarrhoea
  2. Abdo pain/cramping
  3. Melanosis Coli - pigmentation of intestinal wall with chronic use
34
Q

What are the CI for stimulant laxatives?

A
  1. GI obstruction - may increase risk of perforation

2. Anal fissures/haemorrhoids - avoid rectal preparations

35
Q

What are the possible drug interactions for stimulant laxatives?

A

No clinically significant drug interactions

36
Q

Name one Aminosalicylates

A

Mesalazine

37
Q

What is the mechanism by which aminosalicylates work?

A

Exert therapeutic effect by releasing 5-ASA

Unknown mechanism but has anti-inflammatory and immunosuppressive effect in the gut

38
Q

What are the indications for aminosalicylates?

A
  1. 1st line treatment for ulcerative colitis and remission of Crohn’s disease
39
Q

What are the CIs for aminosalicylates

A
  1. Contain salicylates (like aspirin) - contraindicated in individuals with hypersensitivity to aspirin
  2. Renal impairment
40
Q

What are the SEs of aminosalicylates?

A
  • Headache
  • GI disturbance
  • Blood abnormalities (rare for serious e.g. leucopenia, thrombocytopenia
  • Hypersensitivity reaction
  • Renal impairment
41
Q

What are the drug interactions for aminosalicylates?

A
  • Has pH sensitive coating which may react with other drugs that alter drug pH e.g. PPIs

Lactulose reduce pH in stools. May prevent release of 5ASA in the colon

42
Q

How are aminosalicyltes eliminated?

43
Q

Name one anti-emetic

A

metoclopramide

44
Q

What is the mechanism by which metoclopramide/anti-emetics work?

A

Act on various receptors that input into the vomiting centre of the medulla of the brain

  • Block dopamine (D2) receptors of the chemoreceptor trigger zone and gut
  • Block histamien and acetylcholine receptors of the vomiting centre and the vestibular system
45
Q

What are the indications for metoclopramide/anti-emetics?

A
  1. Treatment and prophylaxis of nausea and vomiting in wide range of scenarios e.g. vertigo
  2. First generation antipsychotics (atypical) treatment of psychotic disorders e.g. schizophrenia
46
Q

What are the contraindications for the use of metoclopramide/anti-emetics?

A
  • Sedative effect and potentially hepatotoxic (hepatic failure and drivers, elderly etc)
  • Those who are susceptible to anti-cholinergic side effects e.g. prostatic hypertrophy - may cause urine retention
  • reduce in the elderly
47
Q

What are the side effects of anti-emetics/metoclopramide?

A
  • Drowsiness/sedation
  • Gynaecomastia
  • Postural hypotension/dizziness
  • Movement abnormalities:
    Short term Tx - acute dystonic
    disorders e.g. oculogyric crisis
        Long term Tx - extrapyramidal 
    symptoms e.g. Tardive dyskinesia 
    (irreversible, involuntary movements 
    of face, body and limbs)
  • Prolong QT interval (like antipsychotics)
48
Q

What are drug interactions of anti-emetic/metoclopramide?

A
  • Anything that prolongs the QT interval e.g. anti-psychotics, SSRIs, ciprofloxin, macrolides, quinines
  • D2 containing drugs
  • Parkinson drugs
49
Q

How are anti-emetics/metoclopramide eliminated?

Drugs (9 decks)

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