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Systems: Alimentary AB > Clinical Pharmacology of the Alimentary System > Flashcards

Clinical Pharmacology of the Alimentary System Flashcards

1
Q

What are the main types of drugs used in alimentary disease?

A
  • Acid suppression
  • Drugs affecting GI motility
  • Laxatives
  • Drugs for IBD
  • Drugs affecting intestinal secretions
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2
Q

What can be used for acid suppression?

A
  • Antacids
  • H2 receptor antagonists
  • Proton pump inhibitors
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3
Q

What type of drugs can affect GI motility?

A
  • Anti-emetics

- Anti-muscarinics/other anti0spasmodics

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4
Q

What types of drugs can be used for IBD?

A
  • Amino salicylates
  • Corticosteroids
  • Immunosuppressant’s
  • Biologicals
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5
Q

What types of drugs can affect intestinal secretions?

A

-Bile acid sequestrants and ursodeoxycholic acid

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6
Q

What is the mechanism of action of antacids?

A

Act on hydrogen ions pumped into the stomach lumen to neutralise them

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7
Q

What is the mechanism of action of PPIs?

A

Inhibit the proton pump that pumps H ions into the stomach lumen to prevent decrease in stomach pH

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8
Q

What is the mechanism of action of H2 antagonists?

A

Prevents stimulation of the proton pump which decreases the number of H ions being pumped into the stomach lumen, preventing decrease in pH

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9
Q

What do antacids such as Maalox contain?

A

Magnesium or aluminium

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10
Q

What do antacids do?

A

Neutralise gastric acid

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11
Q

When are antacids taken?

A

When symptoms occur

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12
Q

Give example of a well-known alginate.

A

Gaviscon

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13
Q

What do alginates do?

A

Forma viscous gel that floats on stomach contents and reduces reflux

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14
Q

Give 3 examples of other mucosal protectors apart from antacids and alginates.

A
  • Bismuth
  • Sucralfate
  • Misoprostol
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15
Q

Give an example of a H2 receptor antagonist and a common brand that its found in.

A

Ranitidine found in Zantac

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16
Q

What do H2 receptor antagonists do?

A

Block histamine receptor thereby reducing acid secretion

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17
Q

When are H2 receptor antagonist indicated?

A
  • GORD

- Peptic ulcer disease

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18
Q

How are H2 receptor antagonists administered?

A
  • Orally

- IV

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19
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

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20
Q

What do PPIs do?

A

-Irreversibly block proton pump and thereby reduce acid secretion

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21
Q

When are PPIs indicated?

A
  • GORD

- Peptic ulcer disease

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22
Q

How are PPIs administered?

A
  • Orally

- IV

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23
Q

What can long term PPI use predispose you to?

A
  • C diff infection
  • Hypomagnesaemia
  • B12 deficiency
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24
Q

What can PPIs be given with antibiotics as triple therapy for?

A

Ulcers associated with H pylori

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25
Q

What do pro-kinetic agents do?

A

Increase gut motility and gastric emptying

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26
Q

What are pro-kinetic agents used for?

A
  • Gastro paresis
  • GORD
  • Anti-emetics
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27
Q

Give 2 examples of pro-kinetic agents.

A
  • Metoclopramide

- Domperidone

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28
Q

What is the mechanism of action of pro-kinetics?

A

Mechanism of action is not clear but involves parasympathetic nervous system control of smooth muscle and sphincter tone (via ACh)

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29
Q

How does domperidone probably work?

A

By blocking dopamine receptors which inhibit post-synaptic cholinergic neurones

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30
Q

How can motion induce vomiting?

A
  • Vestibular nuclei

- Vomiting centre in the medulla

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31
Q

How can the smell and sight of vomit induce vomiting?

A
  • Cerebral cortex

- Vomiting centre in the medulla

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32
Q

How can drugs and toxins induce vomiting?

A
  • Chemoreceptor trigger zone

- Vomiting centre in the medulla

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33
Q

How can gastroenteritis, radiotherapy and some drugs induce vomiting?

A
  • Pharynx and GIT

- Vomiting centre in the medulla

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34
Q

What types of drugs act on the pharynx and GIT to prevent vomiting?

A
  • 5HT3 antagonists

- Dopamine antagonists

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35
Q

What type of drugs act in the vestibular nuclei to prevent vomiting?

A

Anti-histamines

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36
Q

What type of drugs act on the chemoreceptor trigger zone to prevent vomiting?

A
  • Dopamine antagonists
  • 5HT3 antagonists
  • Cannabinoids
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37
Q

What type of drugs act on the vomiting centre in the medulla to prevent vomiting?

A
  • Anti-muscarinics

- Anti-histamines

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38
Q

What can drugs which decrease motility be used for?

A

Clinical benefit (anti-diarrhoea) however, the may cause unwanted effects (constipation)

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39
Q

What is the mechanism of action for drugs which decrease GI motility?

A
  • Via the opiate receptors in the GIT to decrease ACh release
  • Decrease in smooth muscle contraction
  • Increase in anal sphincter tone
40
Q

Why does loperamide have few central opiate effects?

A

It is not well absorbed across the blood-brain barrier

41
Q

What can anti-spasmodics be used for?

A

Reduce symptoms due to IBS and renal colic

42
Q

What are the 3 mechanisms of anti-spasmodics?

A
  • -Anti-cholinergic muscarinic antagonists (hyoscine, buscopan, meberverine) that inhibit smooth muscle constriction in the gut wall, producing muscle relaxation and reduction spasm
  • Direct smooth muscle relaxants
  • Calcium channel blockers reduce calcium required for smooth muscle contraction
43
Q

What is an example of a calcium channel blocker?

A

Peppermint oil

44
Q

What are the 4 types of laxatives and an example?

A
  • Bulk: isphagula
  • Osmotic: lactulose
  • Stimulant: senna
  • Softeners: arachis oil
45
Q

How do laxatives work?

A

Work by increasing bulk or drawing fluid into gut

46
Q

What are the issues with laxatives?

A
  • Obstruction
  • Route of administration (oral or rectal)
  • Need for other measures (osmotic laxatives will not work without adequate fluid intake)
  • Misuse
47
Q

What is the mechanism of action of aminosalicylates?

A

Unclear but anti-inflammatory

48
Q

How can aminosalicylates be administered?

A
  • Oral

- Rectal

49
Q

What are aminosalicylates chemically related to?

A

Salicylates

50
Q

What are the possible adverse effects of aminosalicylate?

A
  • GI upset
  • Blood dyscrasias
  • Renal impairment
51
Q

Give 3 examples of aminosalicylates.

A
  • Mesalazine
  • Olsalzine
  • Sulfasalazine
52
Q

What effect for corticosteroids have?

A

-Anti-inflammatory

53
Q

How can corticosteroids be administered?

A
  • Oral
  • IV
  • Rectal
54
Q

What are the usual concerns and contrainidications for corticosteroids?

A
  • Osteoporosis
  • Cushingoid features including weight gain, DM, HT
  • Increased susceptibility to infection
  • Addisonian crisis with abrupt withdrawal
55
Q

Give an example of an immunosuppressant.

A

Azathioprine

56
Q

How do immunosuppressant’s work?

A

Prevent the formation of purines required for DNA synthesis so reduces immune cell proliferation

57
Q

What adverse side effects are related to immunosuppressants?

A

-Mainly related to bone marrow suppression but also azathioprine hypersensitivity and organ damage (lung, liver, pancreatitis)

58
Q

Give an example of an anti-TNFa antibodies biological?

A

Infliximab

59
Q

How do anti-TNFa antibodies work?

A
  • Mouse-human chimeric antibody to TNFa
  • Prevents action of TNFa (key cytokine in inflammatory response)
  • Addresses inflammatory response but not underlying disease process so course of disease after discontinuation is unclear
60
Q

What are biologicals used in outside of the GIT?

A
  • Psoriasis

- Rheumatoid arthritis

61
Q

What cautions/contraindications are there for infliximab?

A
  • Current Tb or other serious infection
  • Multiple sclerosis
  • Pregnancy/breast feeding
62
Q

What are the adverse effects of infliximab?

A
  • Risk of infection, particularly TB so all patients should be screened
  • Infusion reaction
  • Anaemia, thrombocytopenia, neutropenia
  • Demyleination
  • Pleurodynia
  • Malignancy
63
Q

Other than infliximab give examples of 5 other biologicals.

A
  • Certolizumab
  • Adalimumab
  • Natalizumab
  • Golimumab
  • Vendolizumab
64
Q

Certolizumba

A

Fab fragment of humanized anti-TNFa monoclonal antibody

65
Q

Adalimumab

A

Humanized recombinant antibody to TNF

66
Q

Natalizumab

A

Anti-integrin monoclonal antibody

67
Q

Vendolizumab

A

Binds to integrin a4B7

68
Q

What drugs affect biliary secretions?

A
  • Cholestyramine

- Ursodeoxycholic acid

69
Q

What is cholestryamine given to relieve?

A

Prurutus from biliary cause

70
Q

How does cholestyramine work?

A

Reduces bile salts by binding with them in the gut and then excreting as insoluble complex

71
Q

What may cholestyramine affect?

A
  • Absorption of other drugs so should be taken separately

- Fat soluble vitamin absorption so may decrease vitamin K levels (affect clotting and warfarin)

72
Q

What is ursodeoxycholic acid used to treat?

A
  • Gallstones

- Primary biliary cirrhosis

73
Q

How does ursodeoxycholic acid work?

A

Inhibits an enzyme involved in the formation of cholesterol, altering amount in bile and slowly dissolving non-calcified stones

74
Q

GI or liver disease ca affect the processes of drug …

A
  • Absorption
  • Distribution
  • Metabolism
  • Excretion
75
Q

What is absorption dependent on?

A
  • pH
  • Gut length
  • Transit time
76
Q

What problems are there with distribution in chronic liver disease?

A

-Low albumin (decreased binding and increased free drug concentration)

77
Q

What problems with metabolism are there in chronic liver disease?

A
  • Liver enzymes (variability in effects but generally toxicity)
  • Increased gut bacteria (metabolise drugs so increased dose needed)
  • Gut wall metabolism (disease may reduce first pass metabolism)
  • Liver blood flow (drugs with a high extraction ratio)
78
Q

What problems with excretion are there in chronic liver disease?

A

Biliary excretion (increased toxicity if hepatobiliary disease)

79
Q

How does liver disease affect sedation with benzodiazepines?

A

Exaggerated response

80
Q

How does liver disease affect diuresis with loop diuretics?

A

Reduced response

81
Q

How does liver disease affect aminoglycosides?

A

Increased nephrotoxicity

82
Q

What GI adverse effects can there be with medication?

A
  • Diarrhoea/constipation
  • Bleeding/ulceration
  • Changes to gut bacteria
  • Drug induced liver injury
83
Q

What are the mechanisms for diarrhoea/constipation as an adverse drug reaction?

A

Multiple mechanisms

  • Osmotic
  • Secretory
  • Shortened transit time
  • Protein losing
  • Malabsorption
84
Q

What are the most common causes of GI bleeding/ulceration as an adverse drug effect?

A
  • Low dose aspirin
  • NSAIDs
  • Warfarin
85
Q

What drugs are mainly responsible for changes to gut bacteria?

A

Antibiotics

86
Q

What do changes in gut bacteria lead to?

A
  • Reduced vitamin K absorption (increased prothrombin time)

- Overgrowth of pathogenic bacteria

87
Q

What type A ADR can occur with drug induced liver injury?

A

Intrinsic hepatotoxicity (predictable, dose dependent, acute)

88
Q

What type B ADR can occur with drug induced liver injury?

A

Idiosyncratic hepatotoxicity (unpredictable, not dose dependent and may occur at any time- may be part of hypersensitivity reaction)

89
Q

Describe type B ADR drug induced liver injury.

A
  • May be due to the drug itself or an active metabolite
  • Can range from asymptomatic increase in LFTs to fulminant liver failure and death
  • Generally hepatitis or cholestasis but can mimic any pattern or acute or chronic liver disease
90
Q

What are the risk factors for ADR?

A
  • Age
  • Female
  • Alcohol consumption
  • Genetic factors
  • Malnourishment
91
Q

What is the most common reason for withdrawal of a drug from the marker?

A

Hepatotoxicity

92
Q

What scale is used to consider the severity of liver disease?

A

Child-Pugh classification

93
Q

What drugs should there be extra care/avoidance with in liver disease?

A
  • Drugs which can be toxic due to changes in pharmokinetics: (Liver metabolism, therapeutic index, biliary excretion)
  • Drugs which are hepatotoxic
  • Drugs which may worsen the non-liver aspects of liver disease
94
Q

Why should warfarin/anti-coagulants be avoided in liver disease?

A

Clotting factors are already low

95
Q

Why should aspirin/NSAIDs be avoided in liver disease?

A
  • Can increase bleeding time, in combination with deficiency in clotting factors
  • NSAIDs can worsen ascites due to fluid retention
96
Q

Why should opiates/benzodiazepines be avoided in liver disease?

A

-May precipitate encephalopathy by increasing sedation

Systems: Alimentary AB (37 decks)

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