7. Upper GI Flashcards
A 45 year old woman presents with a 2 month history of upper abdominal pain, occurring 2 – 3 hours after meals. The GP orders some blood tests, with the relevant results shown below:
RBC low, HCT low, MCV low
All other tests in range
Which of these is the most likely diagnosis?
A. GORD B. Duodenal ulcer C. Gastric ulcer D. Biliary colic E. Cholecystitis
B. Duodenal ulcer
All are possible causes of upper abdominal pain. However, the blood tests suggest a biliary cause is not likely (although this happens a few hours after meals as well) because LFTs are normal.
In addition, the patient has microcytic anaemia, suggestive of iron deficiency anaemia. This means the patient may likely have a source of blood loss – an ulcer being the only option on the list that could explain this. The fact it occurs a few hours after meals points more towards duodenal ulcers, gastric would cause pain sooner.
A 61 year old man presents to his GP with a 3 month history of upper abdominal pain following meals. On questioning, he describes this pain as burning and is able to point to the pain on his abdomen. He reports having noticed his clothes have been looser recently, and has a long standing history of headaches. Which of these is the most important investigation to arrange?
H. Pylori breath test Full Blood Count OGD Endoscopy Trial of Proton pump inhibitor (PPI) Abdominal X-ray
OGD Endoscopy
This question has a few parts to it. Firstly we need to think of what the diagnosis is. It is most likely an ulcer, given the burning pain following meals and the fact the patient can point to the pain – pointing sign.
However there are some worrying symptoms – particularly the weight loss. This makes us fear it could be gastric cancer (which could have developed from peptic ulcer disease). The man is also over 55 and so we are more fearful of malignancy. For this reason we want to carry out an OGD endoscopy to (hopefully) rule this out.
The headaches could be interpreted 2 ways. Firstly it could be metastases to brain, but unlikely as they have been occurring prior to the upper abdominal pain. Instead, patient may take aspirin or other NSAID for their headaches, which has contributed to ulcer formation. We don’t know! But in an OSCE setting it would be vital to ask how the patient manages their pain.
Would still want to carry out FBC to look for IDA, and H. Pylori breath test would be best investigation if we only suspected PUD. Trial of PPI more for GORD and AXR will provide us with little information. Remember the question is most important, so the investigation that would have the worst consequences if you failed to do it.
Define PUD
Break in the epithelial lining of the stomach or duodenum
Duodenal - more common
Gastric
Symptoms of PUD
Pt. can be asymptomatic or have any dyspeptic symptoms
- Recurrent epigastric pain (gnawing/burning) after meals (immediate = gastric, 2 hours = duodenal)
- Early Satiety
- Nausea & Vomiting
- Potential anorexia & weight loss
Signs of PUD
Epigastric tenderness Pointing sign (pt points to where pain is)
What are some complications of PUD?
Problem as can lead to blood loss and consequent anaemia, can also perforate
In patients with duodenal ulcers, the abdominal pain may be severe and radiate to the back as a result of penetration of the ulcer posteriorly into the pancreas
Duodenal vs Gastric ulcers
Duodenal: 2-3 hrs after eating, antacid relief, overeat - weight gain, awake pts at night (50-80%)
Gastric: shortly after eating, antacid = minimal relief, avoids eating - wt loss, awake less pts. at night (30-40%)
Following a meal, the pylorus closes – relieves duodenal ulcers
Pathophysiology of PUD
Anything that damages mucosa can lead to ulcer formation. Following this, anything that increases pH of the environment around ulcer can result in symptoms.
If erode to BV then can bleed, if further then can perforate
Pepsin is a protease (precursor is pepsinogen), that acts in the stomach to break down proteins. Certain foods like pineapple contain bromelain which acts like pepsin.
Risk factors of PUD
Main: H.Pylori - LEDC and NSAIDs - MEDC Smoking (slows mucosal healing) Bisphosphonates (dmg lining) Head trauma - Cushing's Burns - Curling's Age (?NSAID use) Zollinger Ellison Syndrome
Why do NSAIDs cause PUD?
What should we note?
(Ibuprofen, Aspirin, Naproxen)
By inhibiting COX 1, suppress gastrin prostaglandin synthesis. Consequently, barrier properties of GI mucosa are impaired, reduction of gastric mucosal blood flow also, preventing repair.
Many NSAID induced ulcers are silent. Look out for conditions that may have lead to long term NSAID use, e.g. MI and Stroke for aspirin
Helicobacter Pylori Prevalence and Pathophysiology
Gram-negative flagellate
Prevalent in up to 50% of population
10% of these may develop an ulcer
Leads to inflammation of stomach and duodenum by producing urease, producing ammonia –> dmg mucosa
Helicobacter Pylori is a RF for…?
PUD
Stomach Cancer
Lymphoma
Investigations for H pylori
13C urea breath test: ingestion 13C urea then measure 13-CO2 in breath after using mass spectrometry (As H.pylori produces urease not normally found in stomach)
- stop PPI before test
Stool Antigen Test
Management of H pylori
One-week 2x/day triple therapy as first-line: full dose proton pump inhibitor, with amoxicillin 1g, and clarithromycin 500mg,
OR (in the case of penicillin hypersensitivity) metronidazole 400mg and clarithromycin 250mg
Zollinger-Ellison Syndrome Pathophysiology
Neuroendocrine tumour in pancreas (gastrinoma) - produces gastrin –> hypergastrinaemia –> hypertrophy of gastric mucosa & stimulation of acid secreting cells –> dmg mucosa and ulceration –> malabsorption, inctivation of pancreatic enzymes
a/w MEN1 (25%), or sporadic
How many of ZE pts. develop PUD, and how many PUD pts have ZE?
90% of Z-E pts –> gastric and duodenal ulcers
0.1 – 1% of all patients with duodenal ulcers
When should you consider Zollinger-Ellison, and what Investigations should you do?
Multiple ulcers refractory to treatment
Family history/other symptoms of MEN
Fasting serum gastrin (elevated)
Serum calcium (?ParaThy function if suspect MEN)
Gastric acid secretory tests, stimulation tests, Imaging
Treatment and prognosis for ZE
PPI
Surgical resection if PPI insufficient/malig
Prognosis = good if not metastatic
Cushing Ulcers
Raised ICP thought to stimulate efferent fibres of vagus nerve release Acetycholine onto M3 receptors of parietal cells. This causes insertion of hydrogen potassium ATPase vesicles into apical plasma membrane, increasing secretion of gastric acid secretion. This leads to ulceration of gastric mucosa.
Curling Ulcers
Reduced plasma volume leads to ischaemia and necrosis of gastric muscosa
Investigations of PUD
Under 55 and no red flag symptoms: H pylori most likely - confirm:
- Breath test/stool antigen
- (FBC, stool occult blood, serum gastrin)
The other tests may be carried out if other causes or complications are suspected, e.g. FBC in anaemia, serum gastrin in Zollinger Ellison syndrome
Over 55 or
Red flag: weight loss, bleeding, anaemia, vomiting, early satiety, or dysphagia or Tx failed
- OGD (uGI) endoscopy - most specific and sensitive.
- Histology (if ulcer –> ?neoplasia) + biopsy urease testing
- If ulcer is present then arrange follow up UGI endoscopy to confirm resolution and rule out malignancy.
Management of PUD
Risk factor Modification
Diet - avoid foods that increase Sx
Smoking/ETOH - stop
NSAIDs and bisphosphonates - stop or ALT
Pharmacological
H. Pylori positive: triple therapy (lanso, ome, panto-prazole)
H. Pylori negative: PPI or H2 antagonist (block Hr, decrease gastric acid production - niza, famo, cime, rani -tidine)
May need to treat anaemia (resolve after ulcer heals; may give ferrous fumarate)
Tx of PUD complications
Bleed:
Endoscopy to visualise +/- therapy, e.g. adrenaline (VC), cauterise, clip application
IV PPI (immediate)
+/- Blood transfusion (if lots of blood loss)
Perforate
NBM + IV Antibiotics to prevent GI contents exiting GIT and infection risk
Surgery to repair
Gastric outlet obstruction: active ulcer –> inflammation and oedema/scarring –> blocked outflow –> stomach full of gastric juice, infested food and fluid –> vomiting without pain
Scarring and stricturing
Malignancy
Perforation of PUD X-Ray signs
Air under diaphragm, peritonitis, pneumoperitoneum
Gastric Cancer RF and symptoms
Adenocarcinoma most common
RF: Smoking, H pylori, chronic gastritis e.g. PUD (asympt NSAID ulcer could present yrs later as malig)
Symptoms: overlap w/ PUD
Epigastric pain (perineural invasion of the tumour)
Nausea, vomiting ±blood
Anorexia
Weight loss (anorexia, but also due to increased metabolic demands of the cancer)
Gastric cancer Signs
Palpable epigastric mass
Virchow’s node/Troisier’s sign - Lymphadenopathy in the left supraclavicular fossa
Sister Mary Joseph node - Metastatic nodule on umbilicus
All suggestive of met. abdo ca
Define Gastro-oesophageal Reflux Disease + its epidemiology
Reflux of stomach contents –> oesophagus
Very common condition, accountable for up to 50% of non-cardiac chest pain.
Symptoms and signs of GORD
Oesophageal ‘typical’ symptoms (most common and the most specific)
- Heartburn (most common) a retrosternal sensation of burning or discomfort usually after eating or when lying supine/bending over.
- Regurgitation: effortless return of gastric and/or oesophageal contents into the pharynx. Regurgitation can induce respiratory complications if gastric contents spill into the tracheobronchial tree.
- Dysphagia in 1/3 of pts - sensation food is stuck, particularly in the retrosternal area.
Extra-oesophageal (atypical)
- Coughing/wheeze: Aspiration of stomach contents into tracheobronchial tree/vagal reflex art
- Hoarseness/sore throat: irritation of vocal cords
- Non-cardiac chest pain – as oesophagus builds up with pressure it presses on the heart
- Dental manifestation e.g. enamel erosions due to HCl regurgitated into mouth
No real signs on examination
Risk factors for GORD
Anything leading to opening/damage of LOS and consequent reflux of stomach contents:
Increased Intra-abdominal Pressure:
Obesity
Pregnancy
Lower oesophageal sphincter hypotension:
Drugs: anti-muscarinics, CCBs, nitrates, smoking - relax LOS
Overtreatment of achalasia (botox)
Hiatus hernia
Gastric hypersecretion: - build up until ultimately refluxes
Diet - fat, chocolate, coffee or alcohol ingestion, large meals
Smoking - rest and digest (LOS relax, stomach acid increase)
Zollinger Ellison syndrome
Hiatus Hernia Definition
Portion of the stomach prolapses through the diaphragmatic oesophageal hiatus, predisposing to reflux or worsening existing reflux
Sometimes found incidentally on chest X ray or endoscopy.
RF for HH
Increased IAP, defect in containing wall
Muscle weakening and loss of elasticity with age
Pregnancy
Obesity
Abdominal ascites
Types of HH
Can be congenital or acquired.
Acquired hiatal hernias are divided further into nontraumatic (more common) and traumatic hernias.
Non-traumatically acquired hernias are divided yet further into 2 types:
(1) sliding hiatal hernia
(2) paraoesophageal hiatal hernia (a mixed variety is also possible)
