Upper GI Flashcards
Why do people usually get Upper GI conditions?
Usually due to ACID:
- Hence acid being in the wrong location (e.g. reflux to the oesophagus or over flow to the duodenum)
- Over production of acid
- Faults with protective mechanisms (e.g. if sphinters are not working properly etc)
- Dyspepsia (indigestion, discomfort in your upper abdomen)
What are the aims of treatment for upper GI conditions?
- Prevent acid from relocating
- Reduce acid production or neutralise it
- Remove cause of the underlying problems
What factors aid in susceptibility of gastric cancer?
- More common in smokers and drinkers (due to reduction in protective mechanisms)
- Related to H.Pylori infection
- Increased salt intake (changes in diet)
- Less common in vegetarian
- Age (mainly over 75) and sex (males rate is double than female) are risk factors in gastric cancer
What is the pathophysiology of gastric (stomach) secretions?
The Chief cells and mucus glands secrete pepsinogen. Pepsinogen breaks down proteins. For the activation of pepsinogens and pepsin activity we need acid conditions in the stomach, so we need a pH of less than 3 (very acidic).
Parietal cells secrete hydrochloric acid (gastric acid) and intrinsic factor. Parietal cells are located in the glands found in the Fundus (upper part of the stomach). HCl activates pepsinogen and kills bacteria that enters the stomach.
We need intrinsic factor for B12 absorption from the small intestines. Without it we can get problems with RBC production.
What 3 things is acid secretion via parietal cells controlled by? (food)
- Cephalic Phase - Nervous control (brain) - parasympathetic
- Thought, smell, taste or sight of food
- Gastric secretion is under nervous control, its the parasympathetic nervous system and occurs via the vagus nerve - and get a production of ACh
- About 30% of acid production happens before food enters the stomach, due to the thought of food, smell, taste or sight etc - nervous control which prepares the body for eating. - Gastric phase - Local control (stomach) - parasympathetic
- Distension of stomach and chemical make up and the gastric contents are stimulating receptors and release of gastrin which is involved in the production of stomach acid.
- Around 50-60% of acid is released during this phase. - Intestinal phase - hormonal control (small intestines)
- Food in duodenum (chyme) causes secretion of somatostatin which inhibits acid production - hence a negative feedback mechanism which inhibits vagal stimulation of the stomach
These phases can overlap and occur simultaneously.
What is the physiology of gastric secretion?
There’s secretion of H+ ions from the parietal cells which is stimulated by histamine, gastrin and acetylcholine (ACh).
Gastrin:
- Gastrin is produced in response to vagal stimuli, a rise in pH (hence decrease in acidity - negative feedback) and ingested protein and calcium (chemical stimulation from food contents).
- Gastrin stimulates the growth of gastric mucosa hence has a protective function
Within the parietal cells, H+ is produced via the proton/protein pump, and theres exchange in H+ and K+ in the gastric lumen.
What is gastric cytoprotection?
It is an important protective feature otherwise we would end up essentially eating ourselves - digesting our stomach from inside out.
AUTO-DIGESTION of the stomach is prevented by a thin layer above the mucosa surface.
- We have this complex matron of bicarbonate and mucus around pH 7 (neutral) and this is called the unstirred layer.
- So in this layer, blood flow inside the mucosa removes H+ ions that have diffused back from the lumen. Hence the build up of concentrated acid is removed and taken away by the submucosal blood flow.
If someone goes into shock and theres low blood pressure and poor blood perfusion, hence causing a decrease in blood flow, then the protection mechanism is disrupted and can lead to:
- Necrosis of the mucosa and therefore we get an increase in H+ concentration and decrease in oxygen levels.
- Stress ulcer in shocked or critically ill patients
How does prostaglandins play a role in gastric cytoprotection?
Prostaglandins such as Somatostatin, increases mucus secretion, increase in bicarbonate production, increase in blood flow and DECREASE in acid production.
NSAIDs interfere with prostaglandin synthesis via the COX pathway. Hence why patients who are prescribed NSAIDs are more likely to suffer with ulcers etc hence why they need additional protection if they’re gonna be on NSAIDs longterm as we’re taking away some of the body natural protection.
How does Oesophageal protection play a role in gastric cytoprotection?
The lower oesophageal sphincter is in a permanent state of tonic contraction and it relaxes to allow passage of food. Hence this part is kind of sealed of unless when were passing food into the stomach.
May experience small amount of reflux which is occasionally normal (may be due to food, alcohol etc).
- But if it becomes a regular thing then it might suggest a fault here.
What is gastritis?
Gastritis is inflammation of the gastric mucosa. It is an inflammatory response to the bacteria H.Pylori. It can lead to a chronic gastritis, peptic ulcer disease and ultimately to gastric cancer.
Symptoms include dyspepsia, indigestion, burning stomach pain or a feeling of sickness etc.
But most patients are asymptomatic.
Gastritis is a precursor, is precedes (comes before) ulceration.
What is H.Pylori bacteria? (Helicobacter Pylori)
H.pylori bacteria are adapted to surviving in acidic environments. They protect themselves by hydrolysing urea to produce ammonia, effectively buffer H+ ions - so they can survive in acidic environments by creating a buffer around themselves.
They colonise beneath the mucus layer in the antrum -> Leads to chronic inflammation -> Decrease in somatostatin -> Increased gastrin production -> INCREASE IN ACID PRODUCTION
So this INCREASE in acid production leads to CHRONIC INFLAMMATION in the duodenum, and H.Pylori moves (follows the acidic site) into the duodenum and reduces local protection -> DUODENAL ULCER
H.Pylori causes GASTRITIS throughout the stomach, which leads to DAMAGED cells and DECREASED acid production and DECREASED mucosa (decrease in protection), which long term leads to Gastric Ulcer and GASTRIC CANCER
How do we identify if patient has H.Pylori?
Can do identified breath test or stool antigen test:
- Give patient radio labelled urea and CO2 produced in breath - UREA BREATH TEST
- As H.Pyloris secrete ureas to create that buffer and the urea and the CO2 can be radio labelled. - Stool test
- Stools need to be stored at -20 degrees before testing.
- Individual will need to avoid antibiotics for weeks before the test to avoid false negatives
Patients with duodenal ulcers have over 90% H.Pylori present
Patients with Stomach (gastric) Ulcer have around 70-80% H.Pylori present.
Eradication (removal) of infection improves healing rates and reduces relapse rates.
Eradication (removal) IS A CURE for H.Pylori associated ulcers.
What is peptic ulcer disease (PUD)?
This is your gastric ulcers and duodenal ulcers.
Factors causing peptic ulcers:
- Age
- Gastric hyper secretion
- Reduced mucosal resistance - smokers (less natural protection)
Duodenal Ulcer - HIGHER THAN AVERAGE ACID OUTPUT
Gastric Ulcer - LOWER MUCOSAL RESISTANCE
What are the risk fairs for Peptic Ulcer disease?
- H.Pylori is the major cause of PUD
- NSAIDs are common cause of PUD - may be due to self medication
- More common in smokers:
- Increase number of cigarettes in a day INCREASES peptic ulcer prevalence
- Rate of healing slower in smokers and relapse twice as common - Genetic link with people with parents with PUD - 3 times more likely
- Salty diets
What drugs induce Dyspepsia?
- NSAIDs, risks increased further if:
- Elderly
- History of peptic ulcer
- Smoker - Sulfasalazine
- Iron preparations
- Corticosteroids
- Potassium (MR forms)
- Bisphophonates
Etc.
1/3 of patients with RA suffer with PUD
- Ibuprofen is the safest NSAID so hence suggested if NSAID is required
Patients on low dose aspirin is also at increased risk.
NSAIDs inhibit prostaglandin synthesis via COX pathway:
- COX-1 Pathway -> Protective prostaglandins (e.g. GI mucosa)
- COX-2 Pathway -> Inflammatory prostaglandins
SAFER NSAIDs HAVE LESS INHIBITORY EFFECT ON COX-1
Celecoxib (COX 2 selective) very little COX-1 activity
What are the signs and symptoms of Peptic ulcer disease?
- Gastric symptoms:
- Pain of eating
- Epigastric pain (below the sternal and above the navel (belly) ) - Duodenal symptoms:
- Localised pain occurring between meals and at night
- Relieved by eating (fatty foods may aggravate) - Other symptoms for both
- Bloating, nausea, anorexia (eating disorder) and belching (burping)
- Haematemesis (vomiting of blood) and melaena (dark sticky faeces containing partially digested blood) present if bleed occurred
What is GORD?
Gastro-oesophageal reflux disease.
Condition where acid contents of the stomach leaks into the oesophagus.
Caused by gastric juice and occasionally duodenal contents in oesophagus
The defective lower oesophageal sphincter is the most important abnormality.
What are the factors that can lower the pressure of the lower oesophageal sphincter?
- Dietary factors (larger meals, fatty meals, energy rich foods etc)
- Fat, chocolate, caffeine, alcohol
These cause the sphincter to relax allowing the contents of the stomach to pass through to the oesophagus. This reflux causes symptoms of heartburn - burning sensation in your food pipe. - Cigarette smoking
- Endocrine factors
- High levels of oestrogen and progesterone
HRT and oral contraceptive has been associated with GORD. Pregnant women experience heartburn symptoms - Drugs
What is hiatus hernia?
When part of the stomach is pushed up through the diaphragm.
This prevents the lower oesophagus sphincter from closing properly, allowing stomach contents to escape up into the oesophagus.
Hiatus Hernia very prevalent
Majority of patients asymptomatic
May present as GORD
Which drugs lower the lower oesophageal sphincter pressure?
- Anticholinergics
- Beta-2 agonists
- CCBs
- Diazepam
- Nitrates
- Alcohol
- Progesterones
- Oral contraceptives
- Theophylline
Which drugs can cause oesophageal ulcerations?
- NSAIDs
- Bisphosponates
- Clindamycin
- Clotrimoxazole
- Doxycycline
- Potassium
- Theophylline
- Tetracycline
Hence why we ensure patients wash down tablets with a full glass of water so medications as such do not have prolonged contact with the oesophagus if not it can cause ulcerations.
Antibiotics are responsible for 50% of drug induced oesophagitis.
What symptoms are seen in patients with GORD?
- Motility of oesophagus may be abnormal in patients with GORD
- Gastric emptying delayed in 40% of patients with GORD
- Main symptom is heartburn
- May also suffer dysphagia or odyhophagia (pain on swallowing)
- Complications of gord can include Barretts oesophagus (risk factor for cancer, and it is when the cells lining the oesophagus change to resemble that of the intestine), haemorrhage, stricture
- Endoscopy only method of diagnosis (camera tube)
What is functional dyspepsia?
This is dyspepsia that has been investigated, so patients who have symptoms but no evidence of organic disease detected.
May be due to hypersensitivity to gastric acid.
Occurs in 4 groups of people:
- Ulcer like symptoms
- Dysmotility like symptoms
- Reflux like symptoms - ongoing presentation for heartburn etc
- Non-specific set of symptoms
Eradicate (eliminate) H priority if present.
Neutralise acid or prevent acid production (symptomatic relief)
Periodic monitoring - may be a precursor
What is done in terms of management of stomach and duodenal ulcers?
- Identify and eradicate (eliminate) H.Pylori bacteria
Therapy for H.Pylori would include 7 day triple therapy, which involves a proton pump inhibitor and 2 antibiotics e.g. amoxicillin and clarithromycin.
- Stop inappropriate therapy
Such as NSAIDs. In these cases a Proton pump inhibitor or H2 antagonist for around 8 weeks. Once the ulcer is healed, we check for H.Pylori and if H.Pylori is present, we subsequently offer that eradication therapy as well.
- Reduce acid production to reduce gastritis and enable mucosa to repair
- Block H2 (H2 antagonist) or Proton Pump inhibitor for 4-8 weeks
If the patient presents later and the ulcer is unhealed, this may be due to:
- Adherence:- With triple therapy for example have they completed the course, taken the medications appropriately for example.
- NSAIDs:- Have they stopped the NSAIDs or have carried on with them due to pain or they’ve stopped the prescribed NSAIDs but they’ve been using OTC NSAIDs etc.
- Other disease present:- E.g. Chrohns disease or malignancy.
