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 (82 cards)

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
2 contraindications for alginate preparations use and why
Hypertensive pts - sodium content of preparation | Diabetic pts - glucose content of preparations
26
How do H2 receptor antagonists work?
Inhibit histamine H2 receptors reducing production of stomach acid
27
What 2 conditions are H2 receptor antagonists used for?
Gastro oespophageal reflux disease | Peptic ulcer disease
28
True or false, H2 receptor antagonists and alginate preparations have few ADRs?
True
29
How do proton pump inhibitors work?
Inhibit the exchange of protons for potassium ions preventing the production of gastric acid.
30
What 3 conditions are proton pumps used for?
Gastro oesophageal reflux disease Peptic ulcer disease Dyspepsia
31
5 ADRs of proton pump inhibitors
``` GIT discomfort Headache Rash x2 increase in risk of C.Diff ? increased risk of osteoporosis ```
32
What bacteria causes chronic gastritis? | ?gram
Helicobacter pylori | Gram -ve
33
What % of duodenal ulcers are caused by helicobacter pylori infections?
95%
34
What % of gastric ulcers are caused by helicobacter pylori infections?
70-80%
35
What is the treatment for helicobacer infections?
Abx and a proton pump inhibitor
36
5 causes of gastro oesophageal reflux disease
Bile Acid Relaxation/dysfunction of lower oesophageal sphincter Motility dysfunction of lower oesophageal sphincter Life style factors
37
What 2 features of pregnancy increase the incidence of gastro oesophageal disease?
Increased abdominal pressure | Increased progesterone levels that causes smooth muscles to relax
38
What are the 3 stages of treatment for GORD in pregnancy?
1. Alginate preparation 2. H2 receptor antagonist 3. PPI
39
What is the treatment for GORD in an infant? And for what duration?
Alginate preparation for 1-2 weeks
40
What is the treatment for GORD in children and the duration?
H2 antagonist/PPI for 1 month
41
What is the aim of GORD treatment in adults?
To improve intrinsic factors (prostaglandins, blood flow, bicarbonate, mucus) that protect GIT mucosa and reduce contact of gastric acid with oesophagus
42
5 non-pharmacological lifestyle alterations to reduce GORD
``` Stop smoking Loose weight Avoid trigger foods e.g. fats Sleeping with head raised Avoid alcohol ```
43
What is the treatment for GORD in adults and duration?
PPI for 1-2 months, titrating down to the lowest dose to treat symptoms.
44
What are 2 reasons why pt would remain on max dose of PPI?
Severe GORD or strictures
45
7 causes of nausea / vomiting
``` Drugs Motion Endogenous toxins e.g. dialysis pt Over indulgence Viral infection Gastroenteritis Migraine ```
46
5 classes of anti-emetics
``` H1 receptor antagonists AchM receptor antagonists Anti-dopaminergics 5HT3 receptor antagonists Others- cannibinoids ```
47
What endogenous chemical do H1 receptor antagonists interfere with?
Histamine
48
What 3 conditions are H1 receptor antagonists most effective for?
Post op nausea and sickness Motion sickness Pregnancy sickness
49
2 ADRs of H1 receptor antagonists
Drowsiness | Antimuscarinic
50
What are AchM receptor antagonists most effective for?
Motion sickness
51
2 routes for AchM receptor antagonists
Transdermal patch | Sublingual tablet
52
3 ADRs of AchM receptor antagonists
Dry mouth Blurred vision Sedation
53
What are 2 subcategories of anti-dopaminergics?
Phenothiazines and butrophenones
54
How do phenothiazines work? | what area do they inhibit
Inhibit agents that stimulate the chemoreceptor trigger zone
55
What 2 situations are phenothiazines most effective in treating?
Post op nausea and vomiting | Palliative care nausea and vomiting
56
How do butyrophenones work? | which receptor do they inhibit where, GIT motility
Work as antagonists on dopamine receptors in chemoreceptor trigger zone. Increase GIT motility
57
What are butyrophenones most effective in treating?
Nausea and vomiting associated with chemotherapy
58
3 ADRs of anti-dopaminergics
Arrythmias Hyperolactinaemia Involuntary movements
59
Mechanism of how antiemetics work
Antagonists stopping propagation of action potentials from nausea/vomiting receptors
60
How do 5HT3 receptor antagonists work?
Inhibit receptors in the chemoreceptor trigger zone
61
What are 5HT3 receptor antagonists most effective in treating?
Chemotherapy related nausea/ vomiting | Post op nausea vomiting
62
What is an ADR of 5HT3 receptor antagonists?
Increase in arrythmias by increasing the QT interval
63
2 routes of administration for 5HT3 receptor antagonists
Orally | IV
64
Explain the mechanism of nausea/vomiting
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
Which structure detects motion sickness?
Vestibular apparatus
66
4 neurotransmitters involved in nausea/vomiting
Dopamine Histamine Acetylcholine 5 hydroxytriptamine
67
What neurotransmitter do D2 receptors bind to and where are they located?
Dopamine | Chemoreceptor trigger zone
68
What neurotransmitter do Ach Muscanaric receptors bind to and where are they located?
Acetylcholine | Vomiting centre and vestibular apparatus
69
What neurotransmitter binds to H1 receptors and where are they located?
Histamine | Vomiting centre and vestibular apparatus
70
What neurotransmitter binds to 5HT3 receptors and where are they located?
5 hydroxytripramine | Chemoreceptor trigger zone and in GIT
71
5 causes of constipation
``` Immobility Inadequate diet Lack of dietary fibre Drugs Disease ```
72
4 classes of laxatives
Osmotic Bulk Stimulants Softeners
73
Name type of bulk laxative and mechanism of effect
Ispagulahusk | Increases faecal mass, increasing the pressure on GIT wall stimulating peristalsis
74
What is an instruction for use in bulk laxatives?
Stay hydrated
75
Name type of osmotic laxative and mechanism of effect
Macrogols | Increase influx of water into faecal matter softening stool
76
2 ADRs of osmotic laxatives
Bloating | Flatulence
77
How do faecal softeners work?
Increase absorption of water into faecal matter decreasing surface tension
78
How do stimulant laxatives work?
Stimulate the gut wall increasing GIT motility
79
ADR of stimulant laxatives
Cramping
80
4 causes of diarrhoea
Infection Disease Drugs Diet
81
Treatment for diarrhoea
Fluid and electrolyte replacement, isotonic solution containing glucose, sodium, potassium, chloride and bicarbonate ions
82
What is the risk electrolyte wise in diarrhoea?
Risk of hypokalaemia caused by dehydration