Treatment of peptic ulcers Flashcards

1
Q

what is standard presentation for a H pylori positive uncomplicated peptic ulcer

A

epigastric pain, burning sensation after meals

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2
Q

what are investigations you would carry out for suspected peptic ulcer

A

carbon urea breath test

stool antigen test

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3
Q

if this is a h pylori positive peptic ulcer what results would you expect

A

+ve carbon urea breath test

+ve stool antigen test

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4
Q

briefly how does h pylori cause pathology

A

dissolves mucus layer
causes epithelial cell death
increases acidity
= peptic ulcer

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5
Q

where does H pylori reside

A

GI tract - exclusively colonising gastric-type epithelium

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6
Q

describe some features of h pylori

A

gram -ve, motile, microaerophilic bacterium

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7
Q

how does h pylori increase acidity

A

increases gastric acid formation

by increasing gastrin and decreasing somatostatin

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8
Q

how does it cause damage/ changes in epithelial cells

A

gastric metaplasia

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9
Q

how does h pylori gain access to the epithelial cells

A

down regulate defence factors

decrease in epidermal GF and decrease in HCO3- production

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10
Q

what is an important virulence factor of H pylori

A

Urease enzyme catalyses urea into ammonium chloride and monochloramine which cause damage to epithelial cells

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11
Q

what other property of urease allows it to cause damage and be identified in tests

A

antigenic - evokes immune response

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12
Q

what do more virulent strains of h pylori often contain

A

2 genes:

CagA (antigenic)
VacA (cytotoxic)

leads to more intense tissue inflamation

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13
Q

what is standard treatment for a H pylori positive uncomplicated peptic ulcer

A

2 Antibiotics (Amoxicillin + Clarithromycin)

PPI - ompreazole

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14
Q

what is the difference in presentation between complicated and uncomplicated peptic ulcers

A

complicated: burning sensation + epigastric pain constantly

not just after meals

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15
Q

what additional treatment considerations are made for complicated ulcers

A

consider Quinolone and tetracycline in addition to other 2 antibiotics

PPI for 4-12 weeks (longer)

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16
Q

what is the proper name for proton pump inhibitors

A

H+K+-ATPase

17
Q

where are proton pumps normally expressed

A

secretory vesicles in parietal cells

18
Q

what stimulates them to secrete H+ ions and what happens to these vesicles

A

Increase in Ca2+ = Increase in cAMP

Translocation of secretory vesicles to parietal cell apical surface

= reduction in gastric pH

19
Q

why do ulcers form (in relation to proton pump activity)

A

Increased activity = increased H+ secretion =

reduction in gastric pH

20
Q

how would you distinguish ulcer formation due to NSAIDS instead of H pylori

A

If NSAID is cause:

Carbon urea test = -ve
stool antigen test = -ve

21
Q

how do NSAIDS cause pathology (peptic ulcer)

A

directly cytotoxic

reduce mucus production

increase likelihood of bleeding

increase in acidity

22
Q

treatment of peptic ulcer cause by NSAIDs

A

remove NSAID

PPI or H2 rc antagonist

23
Q

give an example of a h2 rc antagonist

A

ranitidine

24
Q

what 4 molecules influence gastric acid secretion (nema receptors upon which they act

A

Ach - M3 rc
PGs - EP3 rc
Histamine - H2 rc
Gastrin - Cholecystokinin B rc

25
Q

where is gastrin released from

A

blood stream

26
Q

where is histamine released from

A

EC cells

27
Q

where is Ach released from

A

neurones (vagus/enteric)

28
Q

where are PGs released from

A

local cells

29
Q

via what mechanisms do these molecules affect Proton pumps

A

Ach and Gastrin: increase Ca2+

PGs and histamine: increase cAMP

30
Q

why is combination therapy the best current practice

A

targeting multiple pathways

target multiple mechanisms of increased acid secretion

decrease resistance

treat symptoms as well as cause

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