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simplified parkinsons and schitx > peptic ulcers simplified > Flashcards

peptic ulcers simplified Flashcards

1
Q

What are the investigations that you would perform with a presentation of epigastric pain, burning sensation that occurs after meals?

A

Carbon-urea breath test

Stool antigen test

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2
Q

What can the carbon urea and stool antigen test tell you?

A

If carbon is positive, likely to be H.pylori and this is confirmed by a positive stool test.

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3
Q

Summarise the pathophysiology of H.pylori

A

In the gastrum antrum, epithelia produces a mucous layer protective, H.pylori dissolves the mucous layer and causes epithelial cell death increasing exposure to acidity cause an ulcer.

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4
Q

What can you get as a result of severe ulceration?

A

Severe bleeding

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5
Q

What is the treatment for H.pylori peptic ulcer?

A

Amoxicillin and Clarithromycin(penicillin)/metronidazole - antibiotics
Protein pump inhibitor to reduce the secretion of stomach acid.
Triple therapy = 2 antibiotics and PPi

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6
Q

Is H.pylori gram negative or positive?

A

Negative

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7
Q

Give some basic information about Helicobacter Pylori

A

Gram negative
motile
microaerophilic bacterium (requires little free oxygen)
Resides in human GI exclusively colonising gastric type epithelium

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8
Q

Which type of bacterium to antibodies tend to be effective against?

A

Aerobic

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9
Q

How does helicobacter pylori lead to ulcer formation?

A

Increased gastric acid formation - increased gastrin or decreased somatostatin
Gastric metaplasia - cells transform due to excess acid
Downregulation of defence - reduced epidermal growth factor and reduced bicarbonate production

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10
Q

Summarise the virulence of helicobacter pylori

A

UREASE - catalyses urea into ammonium chloride and monochloramine which damages epithelial cells
Urease is antigenic and does evoke an immune response
Certain virulent strains produce CagA(antigenic) or VacA(cytotoxic) leads to more intense inflammation.
UREASE IS AN ENZYME PRODUCED BY H.PYLORI

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11
Q

What would be different in the case of chronic H.pylori positive peptic ulcer?

A

1st line therapy wasn’t effective so consider quinolone, tetracycline.
Proton pump inhibitor 4-12 weeks rather than 7 days, OMEPRAZOLE
Additive - bismuth sucralfate which is a chelating agent that reduces aciditiy of environment.

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12
Q

Physiological action of proton pumps?

A

H+/K+/ATPase pump expressed on secretory vesicles within parietal cells
Increased calcium leads to increase cAMP, translocation of secretory vesicle to apical parietal surface leading to H+ secretion.

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13
Q

How do proton pumps cause ulceration?

A

INCREASED ACTIVITY leading to increased H+ secretion reducing gastric pH

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14
Q

What percentage of peptic ulcers are H.pylori positive in developed world?

A

70%

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15
Q

What is the case when the carbon urea and stool antigen test come back negative with same presentation?

A

Usually a result of NSAID use

These patients tend to use NSAIDs

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16
Q

Describe the pathophysiology of NSAIDs

A

Directly cytotoxic
reduces mucus production
Increased likelihood of bleeding (large blood supply to stomach)
Increased acidity of stomach = ulcer

17
Q

What is treatment for NSAID associated peptic ulcer?

A

Remove NSAID - however not always an option if the patient requires it for heart condition, anticoagulant properties etc.
In that case
PPi or H2 receptor antagonist (RANITIDINE) 4-8 weeks

18
Q

Why are H2 receptor antagonists useful as a drug class in treatment of peptic ulcers?

A

h2 receptors increase acid secretion

19
Q

How does acetylcholine regulate gastric acid production?

A

Released from vagus neurone, act on M3 receptors and increased intracellular calcium
INCREASE GASTRIC ACID

20
Q

How does Prostaglandins regulate gastric acid production?

A

Released from local cells act on EP3 receptors and decrease cAMP
LESS GASTRIC ACID

21
Q

How does histamine regulate gastric acid production?

A

Released from enterochromaffin like cells, and act on H2 receptors to increase cAMP
INCREASE GASTRIC ACID

22
Q

How does gastrin regulate gastric acid production?

A

Released from G cells and act on cholecystokinin B receptors to increase intracellular calcium
INCREASE GASTRIC ACID

23
Q

Summarise gastric acid secretion

A

INCREASE cAMP and calcium lead to translocation of secretory vesicles to parietal cell apical surface leading to H+ secretion.

24
Q

Describe the effect of somatostatin

A

Inhibits G cells, ECL cells and parietal cells hence decreasing H+ secretion

simplified parkinsons and schitx (3 decks)

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