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GI > Dyspepsia and Peptic Ulcer Disease > Flashcards

Dyspepsia and Peptic Ulcer Disease Flashcards

1
Q

what is dyspepsia

A

indigestion

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2
Q

what are the symptoms in romes criteria of dyspepsia

A

epigastric pain/ burning, postprandial fullness, early satiety

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3
Q

where does the foregut start and end

A

cricopharyngeus to ampulla of vater

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4
Q

what structures are in the foregut

A

oesophagus, stomach, duodenum, pancreas, gallbladder

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5
Q

what is dyspepsia more common with

A

if H pylori infected, NSAID use, overlap with IBS/GORD

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6
Q

what are the causes of dyspepsia

A

organic causes;
peptic ulcer disease, drugs, gastric cancer

idiopathic causes (75%)

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7
Q

what is the difference between dyspepsia and heartburn/ relfuc

A

heartburn/ reflux is a burning sensation in the epigastric region

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8
Q

what is GORD

A

gastro- oesophageal reflux disease

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9
Q

what should be found on exam of uncomplicated dyspepsia

A

epigastric tenderness only

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10
Q

what might be found on examination of uncomplicated dyspepsia

A

cachexia, mass, evidence of gastric outflow obstruction (vomiting, splish and splash of gastric content around blockage), peritonism

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11
Q

how is dyspepsia treated

A

check H pylori status- eradicate if infected which will cure ulcer disease and remove risk of gastric cancer

if HP -ve treat with acid inhibItion

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12
Q

what lifestyle factors could cause dyspepsia

A

diet (spicy food, drink, infrequent meals)

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13
Q

what is functional dyspepsia

A

when there in no evidence of structural disease that explain the symptoms- idopathic

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14
Q

what can cause functional dyspepsia

A 
visceral hypersensitivity, 
disrupted gut-immune interactions,
 abnormal upper GI motor and reflex functions,
physiological factors, 
genetic factors,
altered brain- gut interactions
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15
Q

what is peptic ulcer disease

A

a common cause of dyspepsia- pain predominant dyspepsia (which radiates to back) cause by gastric or duodenal ulcers

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16
Q

what is the onset/ aggravating factors of peptic ulcer disease

A

often nocturnal, relapsing and remitting chronic illness- aggravated/ relieved by eating

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17
Q

who is peptic ulcer disease more common in

A

lower socio-economic groups, people with FH of it

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18
Q

what are the causes of peptic ulcer disease

A

H pylori, NSAIDs (COX1, COX2, PGE),

gatric dysmobility and outflow obstruction thought to be associated

19
Q

describe H pylori

A

gram -ve microaerophilic, flagellated bacillus

20
Q

how is H pylori aquired

A

in infancy by oral-oral/ faecal oral spread

21
Q

what gastric cancers area associated with peptic ulcer disease

A

almost all non-cardia gastric adenocarcinoma

low grade B-cell gastric lymphomas

22
Q

is H pylori more common in develop/ developing world?

A

developing- possibly reflect sanitation

23
Q

what effect does food have on the acidity of the stomach

A

food increases pH which stimulates G cells to release gastrin which stimulates parietal cells of the fundus to produce HCL

24
Q

what happens when H pylori affects the distal stomach

A

If affects distal stomach G cells stimulated which lead to over stimulation of parietal cells which creates hyper acidic state which creates gastric metaplasia.
Duodenal mucosa cant be infected with h pylori but the gastric metaplasia can cause duodenal ulcer. Will move proximally causing an increased amount of gastrin but acid making ability defect so excessive amount of gastrin= alkaline stomach+ hypertrophy= risk of gastric cancer

25
Q

what is somatostatin

A

inhibitor of gastrin release (and insulin and glucagon)

26
Q

what happens when the acidity of the the stomach increases

A

gastrin release decreased due to increased somatostatin

27
Q

what does an increased duodenal acid load result in

A

gastric metaplasia, H Pylori colonisation, ulceration

28
Q

how is H pylori infection diagnosed

A

gastric biopsy (urease test, histology, culture/ sensitivity)

urease breath test

faecal antigen test (FAT)

serology (IgA antibodies)- not accurate with older patients

29
Q

how does H pylori affect the pH of its microenvironment

A

increases pH- via the enzyme urease, splits urea and produces ammonium bicarbonate

30
Q

how is are all PUD treated

A

anti secretory therapy (PPI)

tested for presence of H pylori

withdraw NSAIDs

lifestyle

surgery (infrequent)

31
Q

what does a +ve H pylori test mean for management

A

eradication needed

32
Q

how are non HP and non NSAIds ulcers treated

A

nutrition and optimise comorbidities

33
Q

what are the anti-secretory therapies

A

PPIs; omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole and rabeprazole (OLEs)

histamine 2 receptor antagonists (H2RAs); cimetidine, ranitidine, famotidine and nizatidine (TIDINE)

34
Q

what is the H pylori eradication treatment

A

triple therapy for 1 week;

PPI + amoxycillin 1g bd + clarithromycin 500mg bd

or
PPI + metronidazole 400mg bd + clarithromycin 250mg bd

bd= twice a day

35
Q

what are the common S/E of eradication therapy and the consequences of this

A

nausea and diarrhoea- reduces patient compliance

36
Q

what are the complications of PUD

A

amaemia, bleeding, perforation, gastric outlet. duodenal obstruction- fibrotic scar, malignancy

37
Q

what are the symptoms of gastric cancer

A

dyspepsia + alarm symptoms: wight loss, anaemia, mass, recurrent vomiting

38
Q

what is achlorhydria and how is it associated with gastric cancer

A

loss of HCL in gastric secretions caused by e.g pernicious anaemia, previous gastric surgery

39
Q

what causes pernicious anaemia

A

The most common cause of pernicious anemia is the loss of stomach cells that make intrinsic factor. Intrinsic factor helps the body absorb vitamin B12 in the intestine

40
Q

what is the pathway from normal stomach to neoplasia (correa’s hypothesis)

A

normal- (h pylori, salt, antioxidants, N- nitroso compounds)- chronic gastritis, atrophy- (smoking)- intertestinal metaplasia- dysplasia- neoplasia

41
Q

what does H pylori do to gastric acid secretion

A

inhibits it- effect of body inflammation cause by infection, direct effect of bacterial product

42
Q

what gene disposes patients to having a hypochlorhydric response to H pylori

A

IL- IB gene (powerful acid inhibitor and IB associates with pro inflammatory responses)

43
Q

what determines whether mucosal inflammation from H pylori infection develops into cancer

A

IL-1B pro-inflammatory Host genotype

if Yes:
Acid hyposecretion
Body predominant gastritis
Atrophic gastritis
Cancer

if No
Normal or high acid
Antral predominant gastritis
DU or No Disease

GI (64 decks)

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