Week 5 Stomach part 2- conditions

Question 1

describe the prevalence and incidence of common stomach disorders

Answer 1

gastritis- acute, chronic (bacterial, autoimmune)
peptic ulcer disease
zollinger-ellison disease
stress ulcers
cancer of the stomach

Question 2

What is dyspepsia and how common is it?

Answer 2

Upper GI symptoms- 40% of adults supper from this every year

Question 3

What is GORD, what is it caused by and what are the symptoms?

Answer 3

Gastro- oesophageal reflux disease
Causes- lower oesophageal sphincter not working properly, delayed gastric emptying- raised Intra gastric pressure, hiatus hernia, obesity
Results in reflux of stomach contents into oesophagus
Heartburn, cough, sore throat, dysphagia

Question 3

What mechanisms are in place to stop reflux?

Answer 3

Lower oesophageal sphincter, oesophagus enters at an acute angle making it difficult for food to go back up and the diaphragm wraps around the top stopping reflux

Question 4

What problems does GORD cause?

Answer 4

Oesophagitis
Fibrous strictures- narrow lumen of oesophagus can cause dysphagia (when happened more than once)
Barrett’s oesophagus- metaplasia of squamous epithelial to columnar due to acid in oesophagus- increased risk of adenocarcinoma (30-40x)

Question 5

What is the treatment for GORD?

Answer 5

• Lifestyle modifications- changes in diet- smaller meals, not lying down straight after eating
• pharmacological-
  - antacids- if mild,
  - H2 antagonists- blocking histamine receptor on parietal cell
  - PPI- blocking H pump of parietal cell
• surgery- rare

Question 6

what is acute gastritis, what are some common causes and what symptoms are often seen?

Answer 6

acute mucosal inflammatory process
causes- heavy use of NSAIDS, lots of alcohol, chemo, bile reflux- deposited in duodenum- reverse peristalsis= bile in stomach
sympts- asymptomatic or pain, nausea, vomiting, occasionally bleeding which can be fatal

Question 7

what are the 2 main causes and symptoms of chronic gastritis?

Answer 7

1. bacterial- H pylori infections- most common cause- half of population have h. Pylori in stomach and don’t know
   -symptoms- asymptomatic or similar to acute gastritis
   - may develop due to complications- peptic ulcers,
   adenocarcinoma, MALT lymphoma
2. autoimmune- antibodies to gastric parietal cells- can lead to pernicious anaemia
   symptoms- anaemia, glossitis (tongue inflammation), anorexia- don’t feel like eating, neurological symptoms- visual disturbance/ gait problems/ associated with B12 deficiency

Also chemical/ reactive causes- chronic alcohol abuse, NSAIDs, chronic bile reflux

Question 8

what is peptic ulcer disease, what are the criteria to be classed as a ulcer and where do they commonly occur?

Answer 8

Defects in gastric/duodenal mucosa- must extend through muscularis mucosa, most common in first part of duodenum- acidic chyme, commonly affects lesser curve of stomach

Question 9

what are the common causes of peptic ulcer disease and what normal defence mechanisms are in place?

Answer 9

caused by mucosal injury by- stomach acid, H pylori, NSAIDS,- following on from gastritis

• smoking contributes to relapse of ulcer disease
• massive physiological stress- burns

normal defences
- mucus, bicarbonate, adequate mucosal blood flow- can remove acid that diffuses through injured mucosa, prostaglandins- stimulate previous, epithelial renewal

Question 10

what are the symptoms of peptic ulcer disease and serious problems associated with it?

Answer 10

epigastric pain- sometimes back pain

• burning/gnawing
• follows meal times
• often at night

serious symptoms

• bleeding/ anaemia- gastroduodenal artery lies behind duodenum- can erode into this= haemoptasis- coughing up blood
• satiety- feel full quickly
• weight loss

Question 11

how is functional dyspepsia (upper GI symptoms) linked to ulcer disease?

Answer 11

have same symptoms as ulcer disease but there is no physical evidence of disease when investigate therefore this is a diagnosis of exclusion- if excluded other things can give a diagnosis of this

Question 11

how is a diagnosis of gastric pathology made and what results will be seen?

Answer 11

• upper GI endoscopy
  biopsies- benign/malignant ulcerations, H pylori
• urease breath test - detects h pylori- based on ability of h pylori to convert urea and ammonia and carbon dioxide
• erect chest x ray- perforation- see gas- dark under diagphram instead of liver up close to it
• blood test- anaemia

Question 13

what are modern ulcer treatments?

Answer 13

• eradicate h pylori- triple therapy- PPI (block parietal cell- acid), clarithromycin and amoxicillin
• stop NSAIDS
• endoscopy for bleeding ulcers- and follow up for treated gastric ulcers- PPI

Question 14

what pharmacological interventions can be used to reduce gastric acid secretions?

Answer 14

H2 blockers- block H2 receptors that histamine binds to when released from ECL cells
- cimetidine, ranitidine
proton pump inhibitors (PPI) - black H pump in parietal cells secreting acid

Question 15

describe helicobacter pylori, how it spreads and protects itself from acid?

Answer 15

h pylori spread oral to oral / faecal to oral

• helix shaped gram -ve, microaerophilic- want some O2 but too much damaging
• produces urease- converts urea to ammonia/bicarbonate- increases local pH- ammonia creates small alkali cloud around itself protecting itself from acid in stomach , also uses chemotasis to move to alkali areas
• has a flagellum- good motility, lives in mucus layer/adheres to gastric epithelia damaging it creating an inflammatory response against epithelia

Question 16

how does h pylori cause chronic gastritis and how does it change gastric physiology?

Answer 16

problems

• releases cytotoxins- direct epithelial injury
• expresses enzymes- urease- ammonia toxic to epithelia
• possibly degrades mucus layer
• promotes inflammatory response- self injury

Question 17

where does H pylori colonise, what affects does this have and how does this lead to disease?

Answer 17

if colonises in antrum- where G cells are= increases gastrin secretion or decreases D cell activity (secrete somatostatin to inhibit gastrin)
- increases parietal cell acid secretion= more acidic chyme= duodenal epithelial metaplasia, usually h pylori cannot survive in duodenum but if becomes more acidic it can then colonise in duodenum= duodenal ulceration

if in antrum and body- asymptomatic

if predominantly in body- atrophic effect- withering of parietal cells- lower acid- gastric ulcer, leads to intestinal metaplasia- dysplasia- cancer

Question 18

what is zollinger ellison syndrome?

Answer 18

non beta islet cell gastrin secreting tumour of the pancreas
Can be part of MEN1- multipe endocrine neoplasia- several sites producing acid via gastrin
- proliferation of parietal cells- lots of acid production = severe ulceration of stomach and small bowel= abdo pain, diarrhoea

Question 19

what are stress ulcers?

Answer 19

symptoms of gastritis/ulceration

following- severe burns, raised intracranial pressure, sepsis, severe trauma, multiple organ failure

Question 20

describe stomach cancer- presentation, risk factors

Answer 20

third most common cancer in world
usually presents late- large before get symptoms= dysphagia, loss of appetite, malaena (dark, sticky faeces), weight loss, nausea/vomiting, virchows nodes- left supraclavicular region of lymph nodes

risk factors- male, h pylori, dietary factors, smoking

Question 20

what are the common types of stomach cancers and how are they diagnosed/treated?

Answer 20

majority adenocarcinoma- intestinal, diffuse
small no. of lymphomas, carcinoid, stromal

diagnosed via bloods- anaemia, upper GI endoscopy, CT,
treatment- surgery, chemo, radiation