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Pharmacology > Gastrointestinal disease > Flashcards

Gastrointestinal disease Flashcards

Dyspepsia; Gastric acid secretion; Antacid; Alginate preparations; H2 receptor antagonists; Proton pump inhibitors; Gastro oesophageal reflux disease; Nausea and vomiting; H1 receptor antagonists; anti dopaminergics; 5HT3 receptor antagonists; Constipation; Laxatives; Diarrhoea

1
Q

What area of the GIT is affected by dyspepsia and what are the 4 main causes?

A

Symptoms effecting the upper GIT

Caused by underlying conditions, drugs, smooth muscle relaxants and gastric acid

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2
Q

6 symptoms of dyspepsia

A 
Retrosternal/epigastric pain 
Fullness 
Bloating 
Wind 
Heart burn 
Nausea/vomiting
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3
Q

3 underlying conditions mistaken for dyspepsia

A

Peptic ulcer disease
Gastro oesophageal reflux disease
Non-ulcer dyspepsia

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4
Q

6 drugs that can cause dyspepsia

A 
Nitrates 
Theophyllines 
Bisphosphonates 
NSAIDs 
Corticosteroids 
Calcium antagonists
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5
Q

Explain why smooth muscle relaxants cause dyspepsia

A

Cause smooth muscle of oesophageal sphincter to relax allowing stomach contents to rise up and come into contact with unprotected oesophagus

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6
Q

Explain how gastric acid causes dyspepsia

A

Over production

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7
Q

What cell is gastric acid secreted from and what type of acid is it

A

Parietal cells by proton pumps

Hydrochloric acid

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8
Q

Name 4 drug groups used for gastric acid

A

Antacids
H2 receptor antagonists
Alginate preparations
Proton pump inhibitors

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9
Q

3 chemicals that stimulate gastric acid secretion

A

Histamine
Acetylcholine
Gastrin

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10
Q

What cell produces histamine?

A

Enterochromaffin like cells (ELC)

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11
Q

What nerve is stimulated to release acetylcholine

A

Vagus nerve

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12
Q

What cell is gastrin secreted by?

A

G cells

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13
Q

Explain how gastric acid is secreted?

A

Gastrin, histamine and acetylcholine all stimulate proton pumps of parietal cells to transport hydrogen ions into the gastric lumen- in exchange for potassium ions.
Chloride and potassium ions passively diffuse out into the gastric lumen.
Gastrin and acetylcholine indirectly stimulate histamine release further stimulating gastric acid production.

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14
Q

4 intrinsic GIT mucosa protective factors

A

Blood flow
Bicarbonate
Prostaglandins
Mucus

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15
Q

3 aggravating intrinsic factors for GIT mucosa

A

Refluxed bile
Acid
Pepsin

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16
Q

How do antacids work on dyspepsia symptomatic relief?

A

Neutralise stomach acid

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17
Q

4 forms antacids come as

A

Tabs
Liquids
Single agents
Combinations

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18
Q

2 interactions of antacids

A

Reduce absorption rate from GIT

Interfere with drugs that have enteric coatings

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19
Q

4 ADRs of antacids

A

Constipation
Diarrhoea
Unpalatable
Alter sodium and aluminium absorption

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20
Q

How do alginate preparations work?

A

Work as rafting agents, providing a protective coating of the oesophagus wen stomach contents rise up

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21
Q

What condition are antacids used for?

A

Dyspepsia

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22
Q

What 2 conditions are alginate preparations used for?

A

Gastro oesophageal reflux disease (GORD)

Dyspepsia

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23
Q

True or false, alginate preparations are safe for use in pregnancy

A

True - minimal side effects

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24
Q

What time of day are alginate preparations advised to be taken at?

A

Bed time or with evening meal

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25
Q

2 contraindications for alginate preparations use and why

A

Hypertensive pts - sodium content of preparation

Diabetic pts - glucose content of preparations

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26
Q

How do H2 receptor antagonists work?

A

Inhibit histamine H2 receptors reducing production of stomach acid

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27
Q

What 2 conditions are H2 receptor antagonists used for?

A

Gastro oespophageal reflux disease

Peptic ulcer disease

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28
Q

True or false, H2 receptor antagonists and alginate preparations have few ADRs?

A

True

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29
Q

How do proton pump inhibitors work?

A

Inhibit the exchange of protons for potassium ions preventing the production of gastric acid.

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30
Q

What 3 conditions are proton pumps used for?

A

Gastro oesophageal reflux disease
Peptic ulcer disease
Dyspepsia

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31
Q

5 ADRs of proton pump inhibitors

A 
GIT discomfort 
Headache 
Rash 
x2 increase in risk of C.Diff 
? increased risk of osteoporosis
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32
Q

What bacteria causes chronic gastritis?

?gram

A

Helicobacter pylori

Gram -ve

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33
Q

What % of duodenal ulcers are caused by helicobacter pylori infections?

A

95%

34
Q

What % of gastric ulcers are caused by helicobacter pylori infections?

A

70-80%

35
Q

What is the treatment for helicobacer infections?

A

Abx and a proton pump inhibitor

36
Q

5 causes of gastro oesophageal reflux disease

A

Bile
Acid
Relaxation/dysfunction of lower oesophageal sphincter
Motility dysfunction of lower oesophageal sphincter
Life style factors

37
Q

What 2 features of pregnancy increase the incidence of gastro oesophageal disease?

A

Increased abdominal pressure

Increased progesterone levels that causes smooth muscles to relax

38
Q

What are the 3 stages of treatment for GORD in pregnancy?

A
  1. Alginate preparation
  2. H2 receptor antagonist
  3. PPI
39
Q

What is the treatment for GORD in an infant? And for what duration?

A

Alginate preparation for 1-2 weeks

40
Q

What is the treatment for GORD in children and the duration?

A

H2 antagonist/PPI for 1 month

41
Q

What is the aim of GORD treatment in adults?

A

To improve intrinsic factors (prostaglandins, blood flow, bicarbonate, mucus) that protect GIT mucosa and reduce contact of gastric acid with oesophagus

42
Q

5 non-pharmacological lifestyle alterations to reduce GORD

A 
Stop smoking 
Loose weight 
Avoid trigger foods e.g. fats 
Sleeping with head raised
Avoid alcohol
43
Q

What is the treatment for GORD in adults and duration?

A

PPI for 1-2 months, titrating down to the lowest dose to treat symptoms.

44
Q

What are 2 reasons why pt would remain on max dose of PPI?

A

Severe GORD or strictures

45
Q

7 causes of nausea / vomiting

A 
Drugs 
Motion 
Endogenous toxins e.g. dialysis pt 
Over indulgence 
Viral infection 
Gastroenteritis 
Migraine
46
Q

5 classes of anti-emetics

A 
H1 receptor antagonists
AchM receptor antagonists 
Anti-dopaminergics 
5HT3 receptor antagonists 
Others- cannibinoids
47
Q

What endogenous chemical do H1 receptor antagonists interfere with?

A

Histamine

48
Q

What 3 conditions are H1 receptor antagonists most effective for?

A

Post op nausea and sickness
Motion sickness
Pregnancy sickness

49
Q

2 ADRs of H1 receptor antagonists

A

Drowsiness

Antimuscarinic

50
Q

What are AchM receptor antagonists most effective for?

A

Motion sickness

51
Q

2 routes for AchM receptor antagonists

A

Transdermal patch

Sublingual tablet

52
Q

3 ADRs of AchM receptor antagonists

A

Dry mouth
Blurred vision
Sedation

53
Q

What are 2 subcategories of anti-dopaminergics?

A

Phenothiazines and butrophenones

54
Q

How do phenothiazines work?

what area do they inhibit

A

Inhibit agents that stimulate the chemoreceptor trigger zone

55
Q

What 2 situations are phenothiazines most effective in treating?

A

Post op nausea and vomiting

Palliative care nausea and vomiting

56
Q

How do butyrophenones work?

which receptor do they inhibit where, GIT motility

A

Work as antagonists on dopamine receptors in chemoreceptor trigger zone.
Increase GIT motility

57
Q

What are butyrophenones most effective in treating?

A

Nausea and vomiting associated with chemotherapy

58
Q

3 ADRs of anti-dopaminergics

A

Arrythmias
Hyperolactinaemia
Involuntary movements

59
Q

Mechanism of how antiemetics work

A

Antagonists stopping propagation of action potentials from nausea/vomiting receptors

60
Q

How do 5HT3 receptor antagonists work?

A

Inhibit receptors in the chemoreceptor trigger zone

61
Q

What are 5HT3 receptor antagonists most effective in treating?

A

Chemotherapy related nausea/ vomiting

Post op nausea vomiting

62
Q

What is an ADR of 5HT3 receptor antagonists?

A

Increase in arrythmias by increasing the QT interval

63
Q

2 routes of administration for 5HT3 receptor antagonists

A

Orally

IV

64
Q

Explain the mechanism of nausea/vomiting

A

Chemoreceptor trigger zone, located outside the blood brain barrier, able to detect noxious stimuli such as chemicals, ingested substances, endogenous toxins.
Impulses pass from chemoreceptor trigger zone to vomiting centres in the ventricles of the brain.
Vomit centre controls the smooth muscle of the stomach, when stimulated causing the stomach contents to be expelled.

65
Q

Which structure detects motion sickness?

A

Vestibular apparatus

66
Q

4 neurotransmitters involved in nausea/vomiting

A

Dopamine
Histamine
Acetylcholine
5 hydroxytriptamine

67
Q

What neurotransmitter do D2 receptors bind to and where are they located?

A

Dopamine

Chemoreceptor trigger zone

68
Q

What neurotransmitter do Ach Muscanaric receptors bind to and where are they located?

A

Acetylcholine

Vomiting centre and vestibular apparatus

69
Q

What neurotransmitter binds to H1 receptors and where are they located?

A

Histamine

Vomiting centre and vestibular apparatus

70
Q

What neurotransmitter binds to 5HT3 receptors and where are they located?

A

5 hydroxytripramine

Chemoreceptor trigger zone and in GIT

71
Q

5 causes of constipation

A 
Immobility 
Inadequate diet 
Lack of dietary fibre 
Drugs 
Disease
72
Q

4 classes of laxatives

A

Osmotic
Bulk
Stimulants
Softeners

73
Q

Name type of bulk laxative and mechanism of effect

A

Ispagulahusk

Increases faecal mass, increasing the pressure on GIT wall stimulating peristalsis

74
Q

What is an instruction for use in bulk laxatives?

A

Stay hydrated

75
Q

Name type of osmotic laxative and mechanism of effect

A

Macrogols

Increase influx of water into faecal matter softening stool

76
Q

2 ADRs of osmotic laxatives

A

Bloating

Flatulence

77
Q

How do faecal softeners work?

A

Increase absorption of water into faecal matter decreasing surface tension

78
Q

How do stimulant laxatives work?

A

Stimulate the gut wall increasing GIT motility

79
Q

ADR of stimulant laxatives

A

Cramping

80
Q

4 causes of diarrhoea

A

Infection
Disease
Drugs
Diet

81
Q

Treatment for diarrhoea

A

Fluid and electrolyte replacement, isotonic solution containing glucose, sodium, potassium, chloride and bicarbonate ions

82
Q

What is the risk electrolyte wise in diarrhoea?

A

Risk of hypokalaemia caused by dehydration

Pharmacology (10 decks)

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