Dyspepsia and Peptic Ulcer Disease Flashcards

(43 cards)

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
what is somatostatin
inhibitor of gastrin release (and insulin and glucagon)
26
what happens when the acidity of the the stomach increases
gastrin release decreased due to increased somatostatin
27
what does an increased duodenal acid load result in
gastric metaplasia, H Pylori colonisation, ulceration
28
how is H pylori infection diagnosed
gastric biopsy (urease test, histology, culture/ sensitivity) urease breath test faecal antigen test (FAT) serology (IgA antibodies)- not accurate with older patients
29
how does H pylori affect the pH of its microenvironment
increases pH- via the enzyme urease, splits urea and produces ammonium bicarbonate
30
how is are all PUD treated
anti secretory therapy (PPI) tested for presence of H pylori withdraw NSAIDs lifestyle surgery (infrequent)
31
what does a +ve H pylori test mean for management
eradication needed
32
how are non HP and non NSAIds ulcers treated
nutrition and optimise comorbidities
33
what are the anti-secretory therapies
PPIs; omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole and rabeprazole (OLEs) histamine 2 receptor antagonists (H2RAs); cimetidine, ranitidine, famotidine and nizatidine (TIDINE)
34
what is the H pylori eradication treatment
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
what are the common S/E of eradication therapy and the consequences of this
nausea and diarrhoea- reduces patient compliance
36
what are the complications of PUD
amaemia, bleeding, perforation, gastric outlet. duodenal obstruction- fibrotic scar, malignancy
37
what are the symptoms of gastric cancer
dyspepsia + alarm symptoms: wight loss, anaemia, mass, recurrent vomiting
38
what is achlorhydria and how is it associated with gastric cancer
loss of HCL in gastric secretions caused by e.g pernicious anaemia, previous gastric surgery
39
what causes pernicious anaemia
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
what is the pathway from normal stomach to neoplasia (correa's hypothesis)
normal- (h pylori, salt, antioxidants, N- nitroso compounds)- chronic gastritis, atrophy- (smoking)- intertestinal metaplasia- dysplasia- neoplasia
41
what does H pylori do to gastric acid secretion
inhibits it- effect of body inflammation cause by infection, direct effect of bacterial product
42
what gene disposes patients to having a hypochlorhydric response to H pylori
IL- IB gene (powerful acid inhibitor and IB associates with pro inflammatory responses)
43
what determines whether mucosal inflammation from H pylori infection develops into cancer
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