Upper GI Pharmacology Flashcards

1
Q

Why are obesity and pregnancy risk factors for GORD?

A

. Obesity increases intra-abdominal pressure, so easier for stomach contents to be pushed up into oesophagus
. Pregnancy causes increased intra-abdominal pressure, and also hormones cause upper oesophageal sphincter to relax

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2
Q

What is a common drug treatment for pregnant women with GORD?

A

Antacids because they are very safe for pregnancy

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3
Q

What is the most common cause of duodenal ulcers? How does it cause ulcers?

A

. H.pylori bacterial infection

. Chronic gastritis can lead to ulceration

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4
Q

Give 3 tests for H.pylori

A

. Urea breath test
. Biopsy- test for urease activity
. Antigen testing/ antibodies present in stool, saliva, blood

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5
Q

Why is the production of urease important for the survival of H. pylori’s?

A

. Urease converts urea to ammonia and carbon dioxide

. Ammonia neutralises stomach acid to allow H. pylori to survive

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6
Q

What is melaena? What is it a sign of?

A

Melaena are black tarry stools, often occurring with gastric bleeds when blood is partially digested and comes out black

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7
Q

Name three substances which act to increase acid secretion

A

Histamine (binds to H2-receptors in stomach), gastrin, acetylcholine (binds to M3 receptors) –> switch on proton pump

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8
Q

Name two substances which act to decrease acid secretion

A

Prostaglandins (switches off proton pump), bicarbonate

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9
Q

What do antacids do?

A

Neutralise stomach acid to relieve GORD symptoms (doesn’t treat underlying problem though)

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10
Q

How do alginates work?

A

Alginic acid combines with saliva to form a viscous foam, which sits on top of gastric contents as a protective raft –> protects oesophagus during reflux

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11
Q

How do histamine H2 antagonists work?

A

Block H2-receptors, which blocks signal to proton pump so less H+ pumped out in stomach acid

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12
Q

Why are H2 antagonists used to treat peptic ulcers/GORD but antimuscarinics aren’t?

A

Blocking H2 receptors (histamine action) or M3 receptors (prostaglandin action) both block the signal to PPIs, but blocking M3 receptors would have systemic effects because they’re not specific to the PPI pathway

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13
Q

What is the difference between H1 and H2 receptors?

A

Histamine H1 receptors involved in allergies, histamine H2 receptors involved in gastric PPI stuff

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14
Q

PPIs are irreversible, well tolerated, and very effective. What is the main adverse effect of PPIs?

A

. Inhibit proton pumps so stomach acid less acidic, so weaker defence against invading bacteria
. Higher risk of food poisoning due to achlorhydria (lack of HCl)

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15
Q

Outline the triple therapy approach to peptic ulceration

A

. 2 antibiotics from: amoxicillin, clarithromycin, metronidazole (to prevent infection while having less acidic stomach acid)
. Plus PPI/H2-antagonist (to deal with ulcer)

. Triple therapy for a week, then just PPI alone

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16
Q

Why do NSAIDs increase the risk of gastric ulcers?

A

. Inhibit CoX
. CoX has two isoforms (CoX1 = gastric protection, CoX2=inflammation via prostaglandin)
. NSAIDs aim to reduce inflammation but can then reduce gastric protection at the same time, giving rise to ulcers