Week 5 Stomach part 2- conditions Flashcards
(22 cards)
describe the prevalence and incidence of common stomach disorders
gastritis- acute, chronic (bacterial, autoimmune) peptic ulcer disease zollinger-ellison disease stress ulcers cancer of the stomach
What is dyspepsia and how common is it?
Upper GI symptoms- 40% of adults supper from this every year
What is GORD, what is it caused by and what are the symptoms?
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
What mechanisms are in place to stop reflux?
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
What problems does GORD cause?
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)
What is the treatment for GORD?
- 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
what is acute gastritis, what are some common causes and what symptoms are often seen?
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
what are the 2 main causes and symptoms of chronic gastritis?
- 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 - 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
what is peptic ulcer disease, what are the criteria to be classed as a ulcer and where do they commonly occur?
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
what are the common causes of peptic ulcer disease and what normal defence mechanisms are in place?
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
what are the symptoms of peptic ulcer disease and serious problems associated with it?
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
how is functional dyspepsia (upper GI symptoms) linked to ulcer disease?
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
how is a diagnosis of gastric pathology made and what results will be seen?
- 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
what are modern ulcer treatments?
- 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
what pharmacological interventions can be used to reduce gastric acid secretions?
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
describe helicobacter pylori, how it spreads and protects itself from acid?
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
how does h pylori cause chronic gastritis and how does it change gastric physiology?
problems
- releases cytotoxins- direct epithelial injury
- expresses enzymes- urease- ammonia toxic to epithelia
- possibly degrades mucus layer
- promotes inflammatory response- self injury
where does H pylori colonise, what affects does this have and how does this lead to disease?
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
what is zollinger ellison syndrome?
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
what are stress ulcers?
symptoms of gastritis/ulceration
following- severe burns, raised intracranial pressure, sepsis, severe trauma, multiple organ failure
describe stomach cancer- presentation, risk factors
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
what are the common types of stomach cancers and how are they diagnosed/treated?
majority adenocarcinoma- intestinal, diffuse
small no. of lymphomas, carcinoid, stromal
diagnosed via bloods- anaemia, upper GI endoscopy, CT,
treatment- surgery, chemo, radiation
