Upper GI Disease Flashcards
Dyspepsia Definition
group of symptoms
• PAIN/DISCOMFORT IN UPPER ABDOMEN • RETROSTERNAL PAIN, HEARTBURN • ANOREXIA, NAUSEA, VOMITING BLOATING, FULLNESS/EARLY SATIETY
Dyspepsia Investigations
Hx + examination
* Drug hx = NSAIDs, steroids, bisphosphonates, CCB, nitrates, theophyllines, anti-muscarinics, OTT drugs to help symptoms * Lifestyle/PMHx hx = diet (fat, alcohol, large meals, coffee), systemic sclerosis, achalasia rx, hiatus hernia, pregnancy/obesity, smoking, exercise
Bloods = FBC, ferritin, LFTs, U+Es, calcium, glucose, coeliac serology, serum IgA
ALARMS Symptoms
ANOREXIA (UNEXPLAINED)
LOSS OF WGT. (UNEXPLAINED)
ANAEMIA: IRON DEFICIENCY - COULD SIGNIFY LESION IN GI THAT IS BLEEDING
RECENT ONSET»_space; 55YRS/PERSISTENT DESPITE TREATMENT
MELAENA/HAEMATEMESIS/MASS
SWALLOWING PROBLEMS - DYSPHAGIA (esp. if constant & increasing in freq.)
Dyspepsia Aetiology
Organic/Functional
H. PYLORI
Upper GI = peptic ulcer, gastritis, non-ulcer dyspepsia, gastric cancer
Hepatic Causes, Pancreatic Disease, Gallstones
Lower GI = coeliac disease, IBS, colonic cancer
Psychological
Drugs
Other system disease = metabolic, cardiac, hypercalcaemia, DM
H. pylori - bacterial characteristics, outcomes + what do outcomes depend on
gram -ve bacteria + microaerophilic + spiral shaped + flagellated - faecal-oral route
can only colonise gastric-type mucosa + reside in surface mucus layer - uses flagella to burrow into mucus layer to survive aci & produces urease to produce alkaline layer ~ it
evokes immune response in underlying mucosa - depends on host factors
Outcome depends on = site of colonisation, bacterial characteristics, host factors, environmental factors
Can result in = ASYMPTOMATIC/CHRONIC GASTRITIS (most likely), CHRONIC ATROPHIC GASTRIC & INTESTINAL METAPLASIA, GASTRIC/DUDENAL ULCER, GASTRIC CANCER; MALT LYMPHOMA (v. unlikely)
H. pylori - diagnosis
Non-invasive = serology (IgG against H. pylori - unspecific), 13C/14C UREA BREATH TEST (looks for urease presence by measuring CO2), STOOL ANTIGEN TEST (ELISA, off PPI for 2 weeks)
Invasive = gastric biopsies (for histology + culture), RAPID SLIDE UREASE TEST (CLO) - looks for urease presence by looking for ammonia
Gastritis
Aetiology:
A = autoimmine, rare, autoantibodies attack parietal cells - lose specialised epithelium = reduced acid secretion + pernicious anaemia
B = BACTERIAL, H. PYLORI
C = CHEMICAL, BILE, DRUGS e.g. NSAIDs, alcohol
Peptic Ulcer Disease Risk Factors
H. pylori Smoking Alcohol Drugs e.g. NSAIDs Stress
Rare = crohn’s disease, Zollinger-Ellison syndrome, hyperparathyroidism
Peptic Ulcer Disease Epidemiology
COMMON, decreased incidence in developing countries
MEN > WOMEN & DU > GU (but both common in elderly)
Peptic Ulcer Disease Presentation
- EPIGASTRIC PAIN = MAIN FEATURE; MAY BE RELIEVED BY ANTACIDS
- NOCTURNAL/HUNGER PAIN (MORE COMMON IN DU = may be due to malabsorption due to ulcer)
- BACK PAIN (MAY SUGGEST PENETRATION OF POSTERIOR DU; as DU would be low down & back pain will be evident if ulcer perforates & damages posterior structures)
- NAUSEA, VOMITING (occasionally; IF BLEEDING ULCER = HAEMATEMESIS &/OR MELAENA, ANAEMIA), ANOREXIA, WGT. LOSS
- EPIGASTRIC TENDERNESS MAY BE ONLY SIGN
Peptic Ulcer Disease Management
• MEDICAL:
○ ERADICATION THERAPY IF ULCERS CAUSED BY H. PYLORI ○ ANTACIDS - PPI (omeprazole)/H2 ANTAGONISTS (ranitidine) ○ IF NSAIDS INVOLVED = STOPPED/IF CONTINUED MUST RECEIVE PROTECTIVE AGENTS FOLLOWING ERADICATION THERAPY ○ TREAT COMPLICATION AS THEY ARISE • SURGERY: ONLY FOR COMPLICATED PUD