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
H pylori
- diagnosis
Non-invasive testing
- Breath test
- Antibody measurement (serology)
- > Tells you that in some point have been in contact with helicobacter
- Stool HP antigen test
Invasive
- Culture - used if want antibiotic sensitivity
- Histology
- Urease (CLO) test
- > Changes to red (high pH due to ammonia)
- > Used bedside at endoscopy
H pylori
- treatment
- SE
1st line (90% efficacy) Triple therapy for 1 week
PPI - Lansoprazole 30mg 2x daily (or omeprazole 20mg BD)
Clarithromycin 500mg 2x daily
Metronidazole 400mg 2x daily
2nd line (85-90% efficacy) - 1 week
- Lansoprazole 30mg 2x daily (or omeprazole 20mg BD)
- Clarithromycin 500mg 2x daily
- Amoxycillin 1g 2x daily
Eradication not always necessary / eradication may cause regression of some gastric lymphomas – MALTomas
SE: diarrhoea (30-50% - mild, C difficile colitis can occur),
Amoxicillin: penicillin-sensitivity rash, diarrhoea
Clarithromycin: GI upset, enzyme inhibitor
Metronidazole: metallic taste, flushing/vomiting if taken with alcohol, nausea, vomiting, abdominal cramps, headaches, rash
NSAID induced peptic ulcer disease
- pathology
- RF
- treatment
Tissue injury → release of phospholipids → arachidonic acid
- Leukotrienes (bronchoconstriction)
- Cox-1 (constitutional)
Cytoprotective prostaglandins -> Protective for gastric mucosa lining; Aid platelet aggregation
- Cox -2 (inducible) - Recruit inflammatory white cells; Sensitize skin pain receptor; Stimulate hypothalamic fever response
All NSAIDs also inhibit COX-1 → increase risk of developing ulcers due to reduced protection from acid
Prostaglandins stimulate bicarbonate and mucus secretion and increase mucosal blood flow
RF
- Age >60 y/o (atrophic gastritis)
- Past history of peptic ulcer disease
- Past history of adverse events with NSAIDs
- Concomitant corticosteroid use
- High dose or multiple NSAIDs
- Individual NSAID – lower with ibuprofen
Treatment
- Offending drug should be removed
- NSAIDs should be used at lowest effective dose
- Co-prescription of a PPI will heal most ulcers
- Prescription of a COX-2 specific drug will limit GI toxicity -> Celecoxib
Diverticular disease DD
colorectal cancer ischaemic colitis appendicitis IBD Infection
What is the function of the pancreas?
Exocrine – digestive function – releases juices into ducts
- Trypsin & chymotrypsin → proteins
- Amylase → carbohydrates
- Lipase → fats
•
Endocrine – releases hormones into blood; regulates blood sugar
Congenital abnormalities of the pancreas
Pancreas divisum (a single pancreatic duct has not formed – remain as two distinct: dorsal and ventral)
Annular pancreas (ring of pancreatic tissue continuous with head of pancreas surrounds 2nd part of duodenum → constriction)
What is acute pancreatitis?
- pathology
Acute inflammatory process of the pancreas - variable involvement of other regional tissues/ remote organ systems
Epidemiology: 40/100,000; 3% of all admissions with abdominal pain
Mild: Minimal organ dysfunction; Uneventful recovery
Severe: Organ failure and/or local complication; Necrosis
Pathology
- Premature intracellular trypsinogen activation → proteases released and digest pancreas
- Nuclear factor kappa activated → mitochondrial dysfunction, autophagy, inflammatory response
Aetiology of pancreatitis
I Get Smashed
I - idiopathic
G – gall stones
E – ethanol
T – trauma
S – steroids M – mumps A – Autoimmune S – scorpion bite H – hypoglycaemia, hypocalcaemia E – ERCP D – dehydration; drugs
Idiopathic; Gall stones; Ethanol; Trauma; Steroids; Mumps; Autoimmune; Scorpion bite; ERCP; vascular disease hypothermia
Hypoglycaemia, hypocalcaemia, hyperparathyrodism
Dehydration; drugs - Furosemide; didanosine; oestrogens; azathioprine, thiazide diuretics; sulphonamides; tetracyclines; sulindac; mercaptopurine
Malignancy –periampullary cancer
Acute pancreatitis presentation
- Variable
Severe abdominal pain radiating to back
- Relieved when lean forward; worse with movements
Associated with vomiting, nausea, fever, tachycardia
Organ failure – respiratory, renal; ARDS
Jaundice, cholangitis
Grey Turner’s sign (bruising of flanks → retroperitoneal bleeding)
Cullen’s sign (bruising around umbilicus due to liberated pancreatic enzymes →diffusion of fat necrosis and inflammation with retroperitoneum or intraabdominal bleeding)
Grey Turner’s sign
bruising of flanks → retroperitoneal bleeding
Cullen’s sign
bruising around umbilicus due to liberated pancreatic enzymes →diffusion of fat necrosis and inflammation with retroperitoneum or intraabdominal bleeding
Acute pancreatitis diagnosis and investigations
Age – 40-50 years; Epigastric tenderness
Exam
(1) In early stages – guarding & rebound tenderness absent as inflammation principally retroperitoneal
- -> Opposite to perforated peptic ulcer
(2) Bowel sounds may becomes absent → paralytic ileus
Determine cause
- Gallstones; alcohol; medications; FH; viral illness
Initial:
- Pancreatic enzymes (amylase, lipase) – 3-4 times elevated serum amylase
elevated - Supports but is not pathogonomic
- LFTs
- US of gallbladder and biliary tree
2nd line
- Fasting plasma lipids
- Fasting plasma Calcium (after acute episode)
- Viral antibody titres
- Autoantibody / IgG4 titres
- MRCP / CT scan of pancreas
3rd line
- Repeat gallbladder US
- Endoscopic US
- ERCP (bile for crystals)
- Sphincter of oddi manometry
DD of acute pancreatitis
Biliary colic
perforated peptic ulcer - will have guarding and rebound tenderness
Acute mesenteric ischaemia, Acute MI
Basal pneumonia
What is the prognosis of acute pancreatitis?
80% resolve spontanously
20% develop complications
Acute pancreatitis treatment
Supportive treatment
Fluid resuscitation IV crystalloids (Ringer’s lactate) Analgesia - Morphine sulphate IV; fentanyl; ketorolac Correct electrolyte abnormalities Nutrition Nil by mouth initially if vomiting; Feeding; Dietician Monitor early warning signs Organ dysfunction Critical care support ? antibiotics - not given unless there is actual inflammation of the pancreas due to bacteria!! if cause is gallstones, do not give antibiotics!
Acute pancreatitis - surgery options and indications
Surgery
- Doubt in diagnosis
- Early cholecystectomy if have gallstones
- ERCP
Acute cholangitis Jaundice dilated bile duct on US Necrosectomy -> MIRP / Open Bleeding Pancreatic abscesses Pancreatic pseudocyst
Possible complications of acute pancreatitis
Local - Peripancreatic fluid collection - Pancreatic necrosis; abscess - Infected necrosis → May lead to shock Treatment: carbapanems, quinolones, metronidazole
Pseudocyst
- May be caused by inflammation of parenchyma
Biliary/gastric obstruction
General
- Respiratory failure; Renal failure; Circulatory failure
- Malnutrition
Acute pancreatitis death rates
Two peaks in death rates – Early death - 1st week / late death - 2nd week
Week 1 – Initial attack → SIRS → MODS
-Death due to multi-organ system failure
Week 2- Pancreatic necrosis → sepsis → MODS
- Death due to infected pancreatic necrosis
Acute pancreatitis - Glasgow criteria for prognosis
> 3 = severe disease
P- PaO2 <8 kPa (60mmHg) A- Age (>55) N- Neutrophils (WCC >15x10^9/L) C- Calcium (decreased Ca = severe/ increased Ca may have caused pancreatitis) R- renal function (urea >16mmol/L) E- enzymes (delayed LFTs) alanine aminotransferase >200U/L A- albumin S – sugar (high BM) >10mmol/L
+ lactate dehydrogenase
Chronic pancreatitis
- what is it?
- symptoms?
12/100,000
Continuing inflammatory disease of pancreas - irreversible, morphologic change that typically causes pain or permanent loss of function or both
Progressive; Inflammatory change, necrosis, fibrosis
Symptoms
Loss of exocrine and endocrine elements
Epigastric pain that bores through to the back
Relieved by sitting forward; hot water bottle (epigastrium /back)
Bloating; steatorrhoea
Reduced weight
Symptoms relapse and worsen
Causes of chronic pancreatitis
TIGARO
T= toxic-metabolic
- Alcohol; tobacco; hyperCa, chronic kidney disease
I = idiopathic
- Tropical/ early or late onset types
G = genetic
- Hereditary pancreatitis (cationic trypsinogen mutation)
- SPINK-1 mutatino
- Cystic fibrosis
- Haemochromatosis (iron builds up in body)
A = auto-immune
- Consider in older patients
R = recurrent and severe acute pancreatitis
- Reccurent; post-necrotic
O = obstructive
- Ductal adenocarcinoma
- Intraductal papillary mucinous neoplasia
- Pancreas divisum
- Sphincter of Oddi stenosis
Chronic pancreatitis investigations
Nutritional assessment
- Clinical; Anthropometry; Biochemistry
Morphology of pancreas
(1) US + CT scan
CT – pancreatic calcifications, enlargement, ductal dilation
MRCP/ MRI pancreas; ERCP
Pancreatic function tests
- Collect pure pancreatic juice after secretin injection – invasive & seldom used
- Endocrine - May have elevated blood glucose/ diabetes occurs in advanced cases
Exocrine: Direct; Indirect
Direct testing of exocrine function of pancreas
Secretin stimulation tests
Indirect testing of exocrine function of pancreas
Faecal elastase, pancreolaurlyl
Chronic pancreatitis treatment
Analgesia
- Coeliac-plexus block
Lipase (Creon)
Insulin needs may be high/variable – beware hypos
Identify cause
Alcohol counselling
Dietician – nutritional supplements
Fat soluble vitamins
No alcohol; low fat
Role
- Relieve symptoms – pain
- Treat complications – obstruction (biliary/gastric), pseudocyts, pseudo-aneurysm
PPI may be given optimise duodenal pH for pancreatic enzyme activity
Surgery
Decompression of pancreatic/bile duct
- Peustow’s lateral pancreatico-jejunostomy
- Hepatico-jejunostomy
Resectional surgery
- Whipples pancreatico-duodenectomy
- Distal pancreatectomy
Combined
- Frey’s surgery
- Beger’s procedure
Auto-immune pancreatitis
- presentation
- lab results
- CT results
Form of chronic pancreatitis
Mimic cancer but responds to glucocorticoids
- Some may require azathioprine
Abdo pain, weight loss or obstructive jaundice
NO acute attacks of pancreatitis
Increased serum IgG or IgG4
Diffusely enlarged pancreas, narrowing of pancreatic duct, structuring of lower bile duct
Pancreatic carcinoma
- RF
- pathology
- symptoms
- examination
- diagnosis
- treatment
- prognosis
600-700/year in Scotland
Late presentation Typically male (2:1) , >70 years old
RF: smoking, alcohol, carcinogens, DM, chronic pancreatitis, increased waist circumference
Pathology
- Mostly ductal adenocarcinoma (metastasize early, present late)
- 60% pancreas head; 25% body; 15% tail
- 95% mutation in KRAS2 gene
Symptoms Non-specific abdominal symptoms Epigastric pain radiating to back Obstructive jaundice Weight loss, anorexia May have diabetes or acute pancreatitis
Exam:
- May have epigastric mass, hepatomegaly, splenomegaly, lymphadenopathy, ascites
Diagnosis
- Bloods: Cholestatic jaundice
- US / CT
Staging – CT abdomen & chest +/- laparoscopy
Treatment
Resection
- Pancreatoduodenectomy/Whipple’s – head of pancreas, duodenum, portion of stomach removed
Chemotherapy
- Post-op – delays progression
Prognosis
Dismal – mean survival <6 months; 5 year survival 3%
Pancreatic exocrine insufficiency
Pancreas produces 1.5L/day of bicarbonate and enzyme-rich fluid (digestion of fat, protein, carbohydrate)
Lipolytic activity declines first so fat absorption mainly affected
Steatorrhoea, weight loss, vitamin deficiency (A,D,E,K)
Causes: chronic pancreatitis, pancreatic cancer, CF, haemachromatosis, pancreatic resection, gastric resection
Treatment: pancreatic enzyme replacement, taken with meals and snacks, gastric acid suppression (supplements work at higher pH), vitamin supplements
Small bowel overgrowth (SIBO)
- causes
- treatment
Causes (1) Stasis: strictures (Crohns, TB), Hypomotility (Old age, opiate analgesics, diabetes, systemic sclerosis) (2) Blind loops, diverticulae (3) Immunodeficiency
Treatment: 2 weeks antibiotics
Bile acid malabsorption
Bile acids absorbed in ileum → cause secretory diarrhoea in colon
Type 1 – ileal disease or resection
Type 2 – idiopathic
Type 3 – assoc. with cholecystectomy, rapid transit, coeliac, SIBO, chronic pancreatitis
Investigation: Serum 7-alpha cholestenone
Treatment: cholestyramine, colesevelam
Giardia lamblia
Non-invasive pathogen
Malabsorption due to brush border damage; reduction in absorptive surface; bile acid utilization; induction of hypermotility; enterotoxin
Treatment: metronidazole
Causes of malabsorption
Coeliac disease Pancreatic exocrine insufficiency Small bowel overgrowth Bile acid malabsorption Giardia lamblia
Functional dyspepsia
- clinical features
- Important points to consider
- investigations
- management
Chronic dyspepsia in absence of organic disease
-May have early satiety, fullness, bloating, nausea
Cause poorly understood – probably mucosal, motility, psychiatric disorders
Clinical features
- Usually young <40 years; W:M, 2:1
- Abdominal discomfort with other dyspeptic symptoms
- Nausea, satiety, bloating after meals
- Morning symptoms are characteristic, pain, nausea may occur on waking
- History - may have symptoms of IBS
- Inappropriate tenderness on abdominal pain
- NO weight loss
- Symptoms may be disproportionate to clinical well-being
Must consider:
- Peptic ulcer disease
- Intra-abdominal malignancy – older people
- Depressive illness?
- Alcohol misuse – early-morning nausea, retching
Investigations
- Rule out pregnancy before radiological investigations!
- Check for H. pylori infection -> Offer treatment if +ve ; SE: worsening of underlying GORD
- > 55 years old – endoscopy to exclude mucosal disease
Management
- Explanation and reassurance
- Explore psychological factors
- Idiosyncratic and restrictive diets little benefit – but may try smaller portions, fat restriction
Drugs
- Antacids sometimes helpful - hydrotalcite
- Prokinetic drugs
Metoclopramide (SE: extrapyramidal – tardive dyskinesia in young patients), domperidone
Given before meals if nausea, vomiting, bloating prominent
H2 –receptor antagonist
- If night pain or heartburn
Low dose tricyclic agents
Functional bowel disease
Persistent & unexplained symptoms - no structural abnormality/ pathological process
Disordered physiological function
- Attributable to mid or lower GI tract
Peak in 20-40 year olds
Mainly female = 3:1
Coexisting conditions common: non-ulcer dyspepsia, chronic fatigue syndrome, dysmenorrhoea, fibromyalgia
Causes of functional bowel disease
Likely multifactorial: Chemical / stress/ hormonal changes / food / genetic / infection / anxiety / medications / depression / trauma – panic disorder
May be state of low-grade gut inflammation/immune activation, not detectable by tests
- Raised number of mucosal mast cells that sensitise enteric neurones by releasing histamine and tryptase
- Some respond to Ketotifen – mast cell stabiliser
Post infective IBS
- 6-17% - onset of symptoms attributed to acute gastroenteritis episode
- Salmonella; Campylobacter
- 25% continue with altered bowel habits (6 months post episode)
- Hypotheses: Increased response to inflammatory stimuli
Emotional factors
- Psychological factor – 80%
- Previous depressive illness – 40%; Current psychiatric illness – 70%
- Sometimes associated with history of physical/sexual abuse
- BENEFIT from psychologically based therapy
Physiological factors: Serotoninergic disorder – increased release of 5-HT in D-IBS & deficiency in constipation-predominant diarrhoea
Luminal factors
- SIBO – gut dysbiosis present in some
Respond to probiotics & non-absorbable antibiotic - rifaximin (for C-IBS)
- Chemical food intolerance to poorly absorbed, short-chain carbohydrates (lactose, fructose and sorbitol) – fermentation in colon leads to bloating, pain, wind and altered bowel habits.
Dysfunction with motor & sensory aspects – altered gut reactivity (motility and secretion) in response to stimuli, may be environmental, or luminal
Enteric nervous system
Controls intestinal motility & secretory functions
Semi-autonomous
- Parasympathetic (cholinergic) and sympathetic NS (adrenergic)
Functions independently
Contains many neurotransmitters – including 5-hydroxytryptamine (5-HT)
- IBS = 5-HT mediated visceral hypersensitivity and gut motility
5HT
- Distribution: CNS – 5% / GI tract 95%
- Enterochromaffin cells – contain serotonin
- Act as transducers detecting changes in chemical environment intestinal lumen
- Releases serotonin → serotonin receptors on sensory nerves → initiate peristalsis
- Enterocytes SERT (transporter)
- Inactivate response
- Stimulation of 5HT receptors on intrinsic sensory neurones → triggers peristaltic reflex and colonic mass movement
IBS
- symptoms
- exam
- diagnosis
- management
THINK ABC
A - abdominal pain or discomfort
B - bloating
C - change in bowel habit
Symptoms
- Recurrent abdominal discomfort, bloating worsens throughout day, alternate between episodes of diarrhoea and constipation
- Good to classify as predominantly diarrhoea or constipation
- May pass mucus; rarely have nocturnal symptoms
- Abdominal pain may be variable – Cancer would be in one place!
- No weight loss; overall appear well
- Dyspepsia 87%
- Tiredness 97%
- Backache 79%
- Dyspareunia 69%
- Urinary frequency 56%
- Headache 50%
- Nocturia 48%; Sleep disorder 28%
- Fibromyalgia 20%
Exam: Usually unremarkable – some tenderness to palpation
Diagnosis
- No test – diagnosis by exclusion
Only do FBC, ESR, CRP, Antibody testing for coeliac
- Absence of biological/physiological markers
- Symptoms based criteria: Rome IV
Abdominal pain and 2 of:
- Pain related to defecation
- Change in stool frequency
- Change in stool form
Symptoms over 6 months on average weekly for last 3 months
Management
Identify Patient’s Concerns
Explain nature of the condition
Reassure:
IBS is a recognised clinical entity
Involve patient:
- Symptoms can fluctuate
- Diet or stress may precipitate symptoms
Provide continuity: - ongoing review may be important to patient
- Set realistic expectations
- Symptom monitoring with diary – may help find precipitating factors
Diarrhea - 1st line = loperamide
IBS alarm symptoms
Rectal bleeding Documented weight loss or fever Persistent diarrhoea or vomiting Constant and recent abdominal distension Anaemia &/or GIH New onset in patients >50 years Family history of bowel cancer, IBD Frequent Nocturnal symptoms Absence of psychological distress Urinary sediment - haematuria
IBS DD
Food intolerance
Infection: Giardiasis, amoebiasis, TB
IBD
Bacterial overgrowth
Diveritcular disease
Colon cancer
Bile salt malabsorption
CHO malabsorption: Lactose/ fructose/ sucrose
Hormonal syndromes: Medullary thyroid cancer; Gastrinoma / Vipoma; Glucagonoma
Rarer types of colitis: Gold colitis; Collagenous / lymphocytic
Pseudo-obstruction: Myopathy / neuropathy
