Dyspepsia and PUD Flashcards
Dyspepsia
epigastric pain/burning
post-prandial fullness
early satiety
Causes of dyspepsia
> Peptic ulcer disease
H pylori
NSAIDs
Gastric cancer
Idiopathic (majority) - FUNCTIONAL
No evidence of culprit structural disease
GORD may coexist
Dyspepsia - o/e
Uncomplicated - epigastric tenderness
complicated - cachexia, mass, evidence of gastric outflow obstruction, peritonism
gastric outflow obs - succussion (sloshing)
If no ALARM symptoms - treatment?
Check H pylori
Eradicate if infected
If HP -ve, treat with acid inhibition.
What is HEARTBURN/reflux?
Gastro Oesophageal Reflux Disease
Functional dyspepsia?
Presence of one of:
epigastric pain/burning
post-prandial fullness
early satiety
No evidence of structural disease.
Peptic Ulcer Disease
> Pain is predominant dyspepsia
Cause of dyspepsia
Aggravated or relieved by eating
Relapsing and remitting chronic illness
Causes of peptic ulcer disease
H pylori
NSAIDs
Helicobacter pylori
> Acquired in infancy
Gram negative microaerophilic flagellated bacillus
> Oral-oral, faecal-oral spray
> Consequences do not arise until later in life
Consequences of H pylori infection
- Nothing
- Peptic Ulcer Diseaese
- Gastric cancer (rare)
What does H pylori do?
Causes an increase in acid secretion and gastrin release (leading to more acid secretion)
Duodenal acid load increases –> gastric metaplasia in the duodenum
H pylori can then colonise these “islands” of metaplasia leading to ULCERATION
If edges of ulcer are irregular, what could that entail?
Possible cancer
Gastric atrophy - appearance of mucosa
No rugae
Flat AF
Acute gastritis - appearance
Folds are puffed up and flattened out
H pylori - diagnosis
Gastric biopsy
Urease test
Histology
Culture/sensitivity
Urease breath test
Faecal antigen test
IgA antibodies
What does H pylori use as one of its energy sources?
Urea
Hence urease breath test is used to detect presence of h pylori
Treatment of peptic ulcer disease
ALL antisecretory therapy (PPI, Histamine receptor antagonists): 4-8 wks therapy
OMEPRAZOLE in particular
Test for presence of H pylori//
If positive - eradicate and confirm
If negative - antisecretory therapy
Withdraw NSAIDs
Nutrition for non HP/NSAID ulcers.
H pylori eradication therapy
Triple therapy for 1 week
- PPI + amoxycillin (1g bd) + clarithromycin 500mg bd
- PPI + metronidazole 400mg bd + clarithromycin 250mg bd
2 week regimens//
higher eradication rates
poorer compliance
Peptic ulcer disease - complications
-
anaemia
bleeding
perforation
gastric outlet obstruction
Gastric ulcer follow up
Endoscopy at 6/8 wks
Ensure healing and no malignancy
IL-1B (interleukin 1B) inflammatory host H pylori causes?
Gastric cancer
Acid HYPOsecretion (not the usual high acid)
Body predominate gastritis
Atrophic gastritis
Cancer
What does the oesophagus NOT possess?
A serosa
Main cancers of the oesophagus?
Adenocarcinoma (mainly)
Squamous cell carcinoma
Barrett’s Oesophagus
- related to
Chronic GORD related
replacement of stratified squamous epithelium by columnar epithelium
Metaplasia
THEN becomes dysplastic –> Adenocarcinoma
New onset dysphagia in an over 55 = [investigation]
Endoscopy
Mucosal abnormality = x biopsies
6
Staging of oesophageal cancer
PET CT - more sensitive for distal node disease
Endoscopic ultrasound - regional nodal disease
TNM staging for oesophageal cancer
T = how far primary tumour has grown into wall N = Cancer spread to nearby lymph nodes M = Metastasis
Tis = tumour in situ
T1a = endoscopic management of cancer
T1b -> T4b - must be removed by oesophagectomy
Where are squamous cell carcinomas more commonly found in oesophagus
More proximally
Squamous cell carcinoma treatment
Localised SCC - radical chemoradiotherapy
Adenocarcinoma
May be suitable for endoscopic resection (if Tis or T1b)
No metastases –> consider oesophagectomy ± chemo
Upper GI haemorrhage - the “100” rule
Poor prognostic group Systolic BP < 100mmHg Pulse > 100 Hb < 100g/l Age> 60 Comorbid disease Postural drop in blood pressure
Upper GI bleed - endscopy
Identify cause
Therapeutic manoeuvres
Assess risk of rebreeding
Blatchford Score
0-1 = low risk GI bleed
2-5 = indeterminate risk
≥ 6 = HIGH RISK GI BLEED
Treatment of GI bleed
If witnessed significant bleeding or stigmata - IV omeprazole infusion
If stigmata of cirrhosis/ known liver disease = TERLIPRESSIN
For high risk –> endoscopy ASAP
What drug is used for an intermediate/high risk GI bleed??
TERLIPRESSIN (if stigmata of liver cirrhosis/disease)vis
Endoscopic treatment of peptic ulcers
- Injection
- Heater probe coagulation
- Combinations
- Clips
- Haemospray
Peptic ulcer endoscopic treatment
1st line - adrenaline injection/ heater probe
If re-bleed, use omeprazole infusion
Further therapy.
Bleed stops.
Then omeprazole
H pylori eradication as appropriate
If bleeding continues –> SURGERY
Variceal bleeding - risk factors
Portal hypertension > 12mmHg
Cirrhotics with varies will bleed < 2 years
Degree of liver failure
High mortality
Variceal bleeding - haemostasis
- Terlipressin
- Endoscopic variceal ligation (banding)
- Sclerotherapy
- Sengstaken-Blakemmore balloon
- TIPS
Where are varices most common?
Bottom 5cm of the oesophagus
Terlipressin
Vasopressin prodrug
Splanchnic vasoconstrictor
Beneficial for renal perfusion
If endoscopic homeostasis fails, what then?
Sengstaken-Blakemore Tube
balloon; inflate balloon and pul back - puts pressure on GO junction
TIPSS (Transjugular intrahepatic portosystemic shunt)
Uncontrollable bleeding gastric varices
FINAL LINE
Acute oesophagitis
Rare
CORROSIVE damage following chemical ingestion
Chronic Oesophagitis
Common
REFLUX disease
(rare causes include Crohn’s)
Reflux oesophagitis
- due to
- raised intra-abdo pressure in…
Inflammation of the oesophagus due to reflux of gastric content (acidic)
Defective sphincter ± hiatus hernia
Raised intra-abdominal pressure due to obesity or pregnancy
What are the cells most associated with chronic inflammation?
Macrophages and lymphocytes
Reflux oesophagitis - histology
Basal zone expansion
Increased proliferation to compensate for increased cell desquamation
Elongation of papillae
Complications of reflux
> Ulceration
Stricture
BARRETT’S OESOPHAGUS (untreated)
Barrett’s oesophagus (looks like a material)
Red velvety oesophagus
What is metaplasia at risk of developing into?
Dysplasia and cancerous growth
Is Barrett’s oesophagus a pre malignant condition?
Yes
Allergic Oesophagitis
- ## what kind of cells?
Eosinophilic oesophagitis
Asthma/allergy
Corrugated (feline) oesophagus
Looks like a trachea
Allergic oesophagitis - treatment
Steroids, chromoglycate, montelukast
Benign Oesophageal Tumours
> Squamous papilloma
- Related to HPV - Rare
> Leiomyomas
Lipomas
Fibrovascular polyps
Granular cell tumours
Malignant oesophageal tumours
> Squamous cell carcinoma - “islands of malignant cells”
> Adenocarcinoma
DYSPHAGIA
Squamous cell carcinoma is more common amongst?
Iranians, Chinese
Very hot tea
HIGH grade dysplasia
Cells look malignant but have not yet intended basement membrane
Mechanisms of metastases
> Direct invasion
Lymphatic permeation
Vascular invasion
General symptoms of malignancy
> Anaemia
Weight loss, loss of energy
Due to effects of metastases
Boerhaave syndrome
Spontaneous perforation of the oesophagus due to retching or vomiting (also barretts)
Most commonly occurs in distal oesophagus
Left
Severe retrosternal chest pain
Odynophagia
Mediastinal/ free peritoneal air
Oral Squamous Cell carcinoma
White, red, speckled, ulcer, lump.
Floor of mouth, lateral border and ventral tongue
Soft palate
Chemical gastritis
Due to NSAIDs, alcohol, bile reflex
Direct injury to mucous layer
Hyperplasia and little inflammation
Erosions/Ulcers form
Chronic duodenal ulcers
50% of patients with duodenal ulceration have increased acid secretion
Excess acid in duodenum –> metaplasia –> H pylori infection –> inflammation –> ulceration
Peptic ulcer - microscopic
Layered
Floor of necrotic pus
Inflammation
Fibrotic scar tissue (deepest)
Complications of peptic ulcers
Peforation Penetration Haemorrhage Stenosis Intractable pain
Autoimmune gastritis
Rare
Anti-parietal and anti intrinsic factor antibodies
Atrophy/intestinal metaplasia
Pernicious anaemia due to B12 deficiency
Malignancy risk
Gastric Adenocarcinoma - premalignant conditions
H pylori is a big cause
Pernicious anaemia
Partial gastrectomy
lynch syndrome
menetrier;s disease
Gastric adenocarcoma - subtypes
> Intestinal type// exophytic/polypoid mass cauliflower like raised edges heaped up border not very well defined borders
> Diffuse type//
expands/infiltrates stomach wall
signet ring sign
can spread
they do not aggregate
WORSE PROGNOSIS
Maltoma (MALT)
Derived from mucosa associated lymphoid tissue
H pylori infection
Continuous inflammation induces an evolution into a clonal B cell proliferation
If unchecked becomes a high grade lymphoma
“creamy”
“Fleshy”
Benign gastric tumours
Polyps
Hyperplastic polyps
Cystic fund gland polyps
Linitis plastica
Diffuse type
“Leather bottle stomach”
Malignant
GORD
3 factors
> Incompetent LOS
Poor oesophageal clearance
Barrier function/visceral sensitivity
Symptoms of GORD
Heartburn Acid reflux Waterbrash Dysphagia Odynophagia Weight loss Chest pain Hoarseness Coughing
GORD - Ix
Endoscopy
Oesophageal manometry & pH studies
Management of GORD
Symptom relief//
Stop smoking
lose weight
prop up the bed head
antacids - PPIs***, H2RAs
Healing oesophagitis//
surgery (nissen fundoplication)
Prevent complications//
Nissen Fundoplication (GORD)
Controls symptoms of GORD well
Heals oesophagitis
Young patients
Severe/ unrespons disease
Wrapping fundus around oesophagus - reinforcing the closing function of the LOS
Dysplasia management
Surveillance every 3 months
Endoscopy
Optimise PPI dose
Gastroparesis
Delayed emptying of stomach
No physical obstruction
Fullness Nausea Vomiting Weight loss Upper GI pain
Causes of gastroparesis
Idiopathic
Diabetes mellitus
Cannabis
Medication - opiates, anti ACh
Gastroparesis - management
Removal of drugs
Liquid diet
Eat little and often
Promotility agents
Achalasia
What is it?
What happens to the food?
Failure of sphincter smooth muscle to relax
Food backed up in oesophagus
Heller myotomy
Heller myotome
Muscles of cardia are cut, allowing food and liquids to pass into stomach .
Consequences of vomiting
Dehydration Hypochloraemic Metabolic alkalosis Hypokalaemia Mallory weiss tear Aspiration of vomitus
