Upper Gastrointestinal Flashcards

1
Q

How do NSAIDs lead to mucosal damage?

A

increased neutrophil adherence

damage from neutrophil derived free radicals & proteases

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2
Q

What do G cells secrete?

A

gastrin

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3
Q

What does gastrin stimulate? How?

A

enterochromaffin-like cells

action at gastrin/cholecystokinin2 receptors

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4
Q

What receptor is found on parietal cells?

A

gastrin receptors

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5
Q

What do enterochromaffin-like cells release? What is this enhanced by?

A

histamine

enhanced by gastrin and acetylcholine

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6
Q

What does Somatostatin inhibit?

A

release of gastrin
histamine
acid from parietal cells

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7
Q

How do Prostaglandins protect gastric mucosa?

A

increasing bicarbonate secretion
increase protective mucus production
reduce gastric acid secretion

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8
Q

Tests to detect presence of Helicobacter pylori

A

carbon-13 urea breath test
stool antigen test
lab-based serology test

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9
Q

How to treat functional dyspepsia if H.pylori is not present

A

4 week-course of proton pump inhibitor

or H2 blocker

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10
Q

H.pylori mechanism of action

A

produces urease, releases ammonium chloride
increase pH stimulates G cells
inflammatory mediators inhibit D cells
G cells increase release of gastrin
increased acid secretion, increased risk of ulcer formation

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11
Q

What do D cells release?

A

Somatostatin

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12
Q

First line treatment for H.pylori

A

7 day, twice daily
PPI
amoxicillin, clarithromycin/metronidazole

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13
Q

Second line treatment for H.pylori

A

out of clarithromycin/metronidazole

whichever wasn’t used first

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14
Q

Treatment for gastro-oesophageal reflux disease

A

full dose of PPI for 4 or 8 weeks

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15
Q

Treatment for GORD, if inadequate response to PPI?

A

offer H2 receptor Antagonist

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16
Q

Treatment for GORD, if oesophageal stricture present?

A

long-term, full-dose PPI treatment

17
Q

Examples of Proton-pump inhibitors

A

omeprazole

lansoprazole

18
Q

Where do Proton-Pump Inhibitors concentrate?

A

canaliculi of parietal cells

19
Q

What do Proton-Pump Inhibitors target?

A

H+/K+ ATPase pump

20
Q

The active form of omeprazole

A

sulfanemide form

21
Q

Suffix of PPIs

A

’‘-prazole’’

22
Q

Clinical uses of PPIs (5)

A
gastric and duodenal ulcer
hypersecretory states
GORD
NSAID associated ulcer
dyspepsia relief
23
Q

H2 receptor analogue examples

A

Ranitidine
Famotidine
Cimetidine

24
Q

H2 receptor analogue suffix

A

’‘-tidine’’

25
Q

H2 receptor analogue mechanism of action

A

competitive antagonists

reduced action of histamine in acid production

26
Q

Antacid examples

A

Sodium bicarbonate salts
Magnesium hydroxide
Magnesium carbonate
Aluminium hydroxide gel

27
Q

Antacid mechanism of action

A

weak bases
quickly neutralise hyperacidity of stomach
in dyspepsia
short term

28
Q

Bismuth Salts mechanism of action

A

toxic to H.pylori
interfere with adherence to gastric mucosa
treatment of mild dyspepsia

29
Q

What is Sucralfate made up of?

A

aluminium hydroxide

sulfated sucrose

30
Q

Sucralfate mechanism of action

A

provides protective coating on the mucus