Core conditions Flashcards
What is diverticular disease?
- pathology
- RF
- Clinical features
- Investigations
- Treatment
- Complications
PATHOLOGY
- High intraluminal pressures force mucosa & submucosa to herniate through muscle layers of gut at weak points, adjacent to penetrating vessels (where vasa recti penetrate the colonic wall)
- Most within sigmoid colon (95% complications at this site)
- Can affect small or large bowel
- repeated attacks of inflammation –> thickening of bowel wall, narrowing of lumen - eventual obstruction
RF
- Low fibre diet
- age >50
CLINICAL FEATURES
- majority asymptomatic
- altered bowel habit (usually constipation) + left iliac fossa/ colicky pain (relieved on defecation)
- nausea & vomiting
- sigmoid colon may be palpable
INVESTIGATIONS
- CT abdomen - especially if acute (colonoscopy may cause perforation in acute diverticulitis), confirm diagnosis, assess severity, show complications?
TREATMENT
- Bowel rest
- antibiotics may be needed (given by GP or in hospital, may need to be IV)
- treatment of constipation
- Surgery
COMPLICATIONS
- bleeding
- segmental colitis
- perforation
- abscess
- fistulas
- obstruction
What is coeliac disease?
- Common digestive condition – 1 in 150-300; 1% in UK
- Females 2x as often as males
- Peak in infancy after initial exposure to gluten, larger peak in 40-50s
- Inflammatory disorder of small bowel
- Hypersensitivity reaction to glutamine-rich proteins in wheat, barley & rye (gliadins, hordeins, secalins) NOT allergy/intolerance
- Gluten = specific peptide fraction of protein
- Autoimmune condition → damage to lining villi of small intestine.
- Strong link to certain HLA class II genes (HLA-DQ2 [95%] and HLA-DQ8)
- However most DQ2/DQ8 +ve people never develop coeliac
- Villi increase absorptive surface & have blood vessels to absorb nutrients.
- Damaged→ malabsorption (Vits, minerals, calcium, carbohydrates, protein, fats)
Symptoms of coeliac
Variable
- Lethargy – tired all the time
- Anaemia (Fe, folate, B12 and mixed)
- Malabsorption
- Abdominal pain
- Non-specific abdominal symptoms (bloating)
- Diarrhea
- Weight loss
- Oral ulceration
- Osteoporosis
- Sub-fertility
Diagnosis of coeliac
(1) IgA-tTG
- consider IgG tests if IgA deficient
(2) biopsy from 2nd part of duodenum
- at least 4 biopsies taken and one from duodenal bulb
Histological features of coeliac
- chronic inflammation
- villous atrophy
- crypt hyperplasia
- decreased villi to crypt ratio
- loss of enterocyte height
- lamina propria infiltration
- increased intra-epithelial lymphocytes
- Increased mitotic activity
- epithelial damage
What is the treatment for coeliacs disease?
- gluten free diet (avoid wheat, rye and barley - oats probably okay)
if non-responsive - consider prednisolone (7.5-20mg) - or immunomodulator (AZA)
- Check for common deficiencies
GIVE Calcium and Vitamin D.
Fe only given if deficient.
Bone mineral density should be done for baseline. Re-evaluate 1 year after starting gluten free diet.
Conditions associated with coeliac
Range of extra-intestinal conditions
- Endocrine – Type 1 diabetes, thyroid disorders
- Liver – primary biliary scleorosis, autoimmune hepatitis
- Skin – dermatitis herpetiformis
- Neruological
- Cardiac
- IgA deficiency
- SBBO – small bowel bacterial overgrowth
8% non-responsive coeliac patients
Symptoms: Diarrhea, pain, weight loss, bloating, flatulence, nausea, steatorrhoea
Nutritional deficiencies - Vit D (tetany), Vit A (night blindness), Cobalamin (neuropathy), VitB12 (macrocytosis)
Investigation: H2 Lactose / Glucose breath test
Treatment: 7-10/7 course of- CO-amoxiclav + metronidazole
- Cephalexin + co-trimoxazole
- Gentamicin + metronidazole
Hyposplenism
- 80%
- Howell Jolly bodies, target cells, thrombocytopenia
- Treatment:
- Meningococcal, pneumococcal, HIB vaccinatinos
- Prophylactic antibiotics
- ALL patients with new diagnosis of coeliac require annual flu vaccines and also pneumococcal vaccine
Autoimmune conditions
- Thyroid disease, Type 1 diabetes, addison’s, Sjogrens syndrome
What is dermatitis herpetiformis?
Patches of intensely itchy blisters on elbows, knees, back, buttocks
- 2-3% of people with coeliac have it
- IgA deposition at basement membrane
Treatment:
Gluten free diet
In some can try: Dapsone (100-150mg daily)
Peptic ulcer disease
- what is it?
- what is the prevalence?
- gender preference?
- other RF
Ulcer in oesophagus and/or stomach and/or duodenum
Affects 10% of population
M>F = 5:1
Commonest in blood group A
family history
Duodenal ulcers
- RF
- diagnosis
4x commoner than gastric ulcer
RF: helicobacter pylori, drugs (NSAID, steroids, SSRI), increased gastric acid secretion, increased gastric empyting, smoking
Diagnosis: Upper GI endoscopy; Test for H pylori
Gastric ulcers
- RF
- diagnosis
mainly in elderly on lesser curve
RF H pylori smoking NSAIDs reflux of duodenal contents delayed gastric emptying stress
Diagnosis: Upper GI endoscopy, multiple biopsies. Repeat endoscopy after 6-8 weeks to confirm healing and exclude malignancy
Causes of peptic ulcer disease
H. pylori (>90% duodenal ulcers, >70% gastric ulcers)
- If <55 years old – test & treat
NSAIDs – deplete mucosal defence
Stress – burn injury, sepsis, prolonged hospitalisation
Smoking – causes increased risk/ delayed healing
Familial predisposition
- ?HP cluster? Genetic?
Rare
- Acid-pepsin versus mucosal resistance
Zollinger Ellison syndrome
Zollinger-Ellison syndrome
- What is it?
- Features?
Gastric acid hyper secretion due to a gastrin secreting tumour of islet cell of pancreas
- Leads to peptic ulceration
2/3 malignant but slow growing
20-60% have co-existing adenomas of parathyroid and pituitary (MEN-1)
Gastrin hypersecretion → hyperacidity and ulcers
Pancreatic enzymes inactivated due to low pH & bile salts precipitate causing diarrhoea & steatorrhoea
Features
- Multiple ulcers often unusual sites
- Poor response to standard therapy
- Complications common
- Diarrhoea can be presenting feature
- Serum gastrin levels grossly elevated / secretin stimulation further increases levels
Tumour localisation difficult
- CT; Selective angiography and sampling; EUS
Management
- Surgical resection if tumour localised
- PPI’s high dose
- Octreotide injections to reduce gastrin levels
5y survival 60-75%
Peptic ulcer disease
- symptoms
Often difficult to differentiate from gastric cancer
- Epigastric pain (relief by food)
Duodenal
- Several hours post-prandially or awakened the patient from sleep or both
- “pain decreases with food” - Often eating food seems to help “feed the ulcer”
Gastric ulcers
- Pain felt shortly after meals and eating food does not stop pain “pain greater with eating”
- Dyspeptic constellation & bloating
- No symptoms – silent ulcers common in elderly & may be NSAID induced
- NO specific signs i.e epigastric tenderness
Nausea Fullness Bloating Hunger pain Heartburn (retrosternal pain)
Alarm symptoms of peptic ulcer disease
Vomiting
Pain radiation
Early satiety
Nocturnal pain
Sinister symptoms → malignancy
Vomiting (?gastric outlet obstruction)
Pain radiation = pancreatic pathology
A - anaemia L - loss of weight A - anorexia R - recent onset/progressive symptoms M - malaria/haematemesis S - swallowing difficulty
Peptic ulcer disease investigations
Endoscopy - take biopsy from raw edges of ulcer
Barium meal examination
H. Pylori status
Peptic ulcer disease management
Stop smoking; Avoid aspirin, NSAIDs; Alcohol in moderation
Depends on cause: H pylori / NSAIDs
Maintenance treatment
- Not necessary after successful helicobacter pylori eradication
- If cannot avoid NSAIDs or aspirin may require long term protection
Medications: Short-term awaiting HP status - PPI
Bleeding - 30-50% due to peptic ulcer - Mortality remains 6-10% - Haematemesis, malaena Treatment: - IV access - Define circulatory status& co-morbidity - Blood tests: FBC, U&Es, LFTs - Cross-match blood - Resuscitation – crystalloids, colloids, blood - Intensive monitoring - Early endoscopy - HP eradication - PPIs - Surgery
Peptic ulcer disease surgical management
- emergency
- elective
Emergency
- Perforation of ulcer (more common in duodenal)
- Peritonitis, shock
- Sudden severe pain initially in upper abdomen then generalised; Shoulder tip pain (irritation of diaphragm)
- Air under diaphragm (bilateral)
- Absent bowel sounds
- Mortality 10%
- Bleeding (that cannot be controlled endoscopically)
Elective
- Chronic non-healing gastric ulcer
- Partial gastrectomy
- Complications of surgery: dumping (rapid gastric empyting), bile reflux gastropathy, diarrhoea, maldigestion,
Gastric outflow obstruction
- Nausea, vomiting of previously eaten food, abdominal distension
- Visible gastric peristalsis, succession splash, dehydration
- Management: IV fluids, correction of acidosis, nasogastric suction, endoscopy
Recurrent ulcer following surgery
Signs of ulcer perforation
- Peritonitis, shock
- Sudden severe pain initially in upper abdomen then generalised; Shoulder tip pain (irritation of diaphragm)
- Air under diaphragm (bilateral)
- Absent bowel sounds
- Mortality 10%
H pylori
- where does it cause ulcer most often?
Duodenal > gastric
H pylori
- long term consequences
Gastric cancer
gastric-marginal B cell lymphoma (MALT)
non-ulcer dyspepsia
NSAID induced gastropathy
H pylori
- what kind of bacteria is it
Spiral shaped gram –ve acidophilic bacterium
4-6 flagella - multiple sheathed flagella
Strong urease activity
Shape, motility & enzymatic action → penetrate beneath mucosal layer
H pylori
- Epidemiology
- For who is probability of being infected greater?
Associated with lower economic status – rather than race
Probability of being infected is greater:
- For older persons (>50 years)
- Minorities (African-Americans 40%)
- Immigrants from developing countries (Latino, Eastern Europe)
H pylori
- pathology
Oral transmission
Stomach colonisation
Lives next to epithelium
- Prefers antrum - if H+ secretion very high
- Protected by stomach mucus & ability to produce urea to buffer acidic pH
Provokes inflammatory response releasing cytokines
- Vacuolating cytotoxin (vacA) – formation of vacuoles, induction of apoptosis, disruption of epithelial junctions, blockage of T cell response
- Cytotoxin-associated gene (cagA) – alteration of signalling pathways, alteration of tight junctions
Adhesins – attachment to epithelial cells
LPS – induction of inflammatory response
Urease – Urea → NH3 + CO2.
- Ammonia provides a neutral microenvironment favourable to H. pylori
Antral stomatostatin is depleted and increased gastrin release by G cells
Hyperacidity occurs with mucosal damage
Duodenum develops gastric like tissue (metaplasia) with further colonisation and hyperacidity
Depletion of antral D-cell somatostatin
Increased gastrin release from G cells
Increased acid secretion
Increased acid load in duodenum leads to gastric metaplasia
Inflammation & eventual ulceration
May lead to glandular atrophy of gastric mucosa and intestinal metaplsia
H pylori
- 3 mechanisms of injury
Hypergastrinemia
- Negative feedback for gastrin is blocked – resulted in uncontrolled excess gastrin → hyperacidity
Direct mucosal injury
- Cytotoxins cause increased production of ammonia (toxin to epithelial cells)
Inflammatory response
- Mediated by macrophages, neutrophils, T-cell
