Gastrointestinal Flashcards
What is upper GI tract bleeding
A medical emergency
Involves some form of bleeding from the oesophagus, stomach or duodenum
What are the causes of upper GI bleeding
Oesophageal varices
Mallory-Weiss tear
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum
How does upper GI blleding present
Haematemesis (vomiting blood)
Coffee ground vomit (caused by vomiting digested blood that looks like coffee)
Melaena, which is tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic and other signs of shock (young fit patients may compensate well until they have lost a lot of blood)
Symptoms related to underlying pathology:
-Epigastric pain and dyspepsia in peptic ulcers
-Jaundice for ascites in liver disease with oesophageal varices
What is the Glasgow-Blatchford score
A scoring system used in suspected upper GI bleed on initial presentation
It scores patients based on their clinical presentation
It establishes their risk of having an upper GI bleed to help managment planning
Using an online calculator is the easiest way to calculate the score. A score > 0 indicates high risk for an upper GI bleed. It takes into account various features indicating an upper GI bleed:
-Drop in Hb
-Rise in urea
-Blood pressure
-Heart rate
-Melaena
-Syncopy
What is the Rockall Score
Used for patients that have had an endoscopy to calculate risk of rebreeding and overall mortality
It provides a percentage risk of rebleeding and mortality
Use an online calculator
Takes in to account these risk factors:
-Age
-Features of shock (e.g. tachycardia or hypotension)
-Co-morbidities
-Cause of bleeding (e.g. Mallory-Weiss tear or malignancy)
-Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels
How is an upper GI bleed managed
A – ABCDE approach to immediate resuscitation
B – Bloods
– Haemoglobin (FBC)
– Urea (U&Es)
– Coagulation (INR, FBC for platelets)
– Liver disease (LFTs)
– Crossmatch 2 units of blood
A – Access (ideally 2 large bore cannula)
T – Transfuse
– Transfuse blood, platelets and clotting factors (fresh frozen plasma) to patients with massive haemorrhage
– Transfusing more blood than necessary can be harmful
– Platelets should be given in active bleeding and thrombocytopenia (platelets < 50)
– Prothrombin complex concentrate can be given to patients taking warfarin that are actively bleeding
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
There are some additional steps if oesophageal varices are suspected, for example in patients with a history of chronic liver disease:
-Terlipressin
-Prophylactic broad spectrum antibiotics
The definitive treatment is oesophagogastroduodenoscopy (OGD) to provide interventions that stop the bleeding, for example banding of varices or cauterisation of the bleeding vessel.
NICE recommend against using a proton pump inhibitor prior to endoscopy, however you may find senior doctors that do this.
What is constipation
A common complaint that refers to the infrequent passage of stool, difficulty passing stool and/or a sensation of incomplete emptying of bowels
What are the two types of constipation
Primary:
-in the absence of an underlying cause
-aka functional or idiopathic
Secondary:
-due to an underlying pathology (eg. meds, GI disorder, endocrine disorder etc)
What are the sub types of primary constipation
Normal transit constipation: infrequent defaecation with evidence of normal colonic transit (most common)
Slow transit constipation: infrequent defaecation with evidence of slow colonic transit
Dyssynergic defecation: an inability to empty the rectum effectively. Due to paradoxical contraction or inadequate relaxation of pelvic floor muscles during defecation
What are the common causes of secondary constipation
Neurological: Parkinson’s disease, Hirschsprung disease, spinal cord injury, multiple sclerosis
Metabolic: Hypercalcaemia, diabetes mellitus, hypokalaemia
Endocrine: Panhypopituitarism, hypothyroidism
Medications: Iron supplements, antispasmodics, calcium-channel blockers, opiates, tricyclic antidepressants
Rheumatological: Systemic sclerosis, myotonic dystrophy, amyloid
Gastrointestinal: Irritable bowel syndrome, colonic strictures, inflammatory bowel disease, rectal prolapse
Pregnancy
What is faecal impaction
The retention of faeces in the rectum and colon to the extent that spontaneous evacuation is unlikely.
It may complicate a primary or secondary cause of constipation.
It is usually diagnosed on digital rectal examination or noted on imaging.
What is normal colonic function
The primary function of the colon is to absorb water and transport waste from the caecum to the rectum for evacuation. Colonic motility is important for the transport of faeces to the rectum where distension initiates the urge to defaecate. Defecation then relies on the coordinated relaxation of the internal anal sphincter and pelvic floor muscles with contraction of the diaphragm and abdominal muscles.
What are the types of colonic motility
Segmental activity: repetitive non-propulsive contractions that aid mixing and absorption
Propagated activity:
-large, coordinated contractions that aid the propulsion of stool from caecum to rectum.
-Divided into ‘low-amplitude propagated contractions (LAPC)’ and ‘high-amplitude propagated contractions (HAPC)’.
-LAPCs are frequent, low amplitude, and help transport content in the colon.
-HAPCs are less frequent, have high amplitude and act as powerful contractions involved in defecation itself.
What is the gastrocolic reflex
The association between eating and the urge to defecate
How does defecation happen
The initial part of defecation involves rectal filling. This activates receptors in the rectal wall that results in conscious awareness of needing to defecate. A small amount of faeces enters the anal canal by an involuntary relaxation of the internal anal sphincter. This is the rectoanal inhibitory reflex. If it is deemed socially acceptable to defecate, the person will find a toilet and adopt a sitting or squatting position. If not socially acceptable the rectal wall relaxes and the need to defecate subsides temporarily. During defecation, contraction of the abdominal muscles and diaphragm help to exert pressure on the abdominal viscera. At the same time, coordinated relaxation of the external anal sphincter and puborectalis helps to evacuate faeces down the created pressure gradient. After evacuation, there is a closing reflex with regaining external anal sphincter tone.
How is normal faecal continence maintained
The internal and external anal sphincters remain contracted.
In addition, a sling of muscle known as the puborectalis, which is part of the pelvic floor, tethers the rectum forming a tight angle that acts as a barrier to faeces entering the anus.
What are the Clinical features of constipation
Characterised by infrequent bowel motions, hard lumpy stools, straining, and incomplete emptying.
Infrequent stools are broadly defined as < 3 spontaneous bowel motions per week.
Symptoms
-Infrequent bowel motions
-Hard, lumpy stool
-Straining
-Manually extracting faeces
-Overflow diarrhoea (liquid stool leak around stool)
-Overflow incontinence (loss of control of defecation)
-Feeling incomplete emptying
Exam may show signs of secondary cause.
Examine abdomine
Nutritional status observation
PR exam to exclude structural problem and stength of sphincter function and defecation mechanism
What are the red flag symptoms of constipation
Weight loss
Rectal bleeding
Family history of colorectal cancer
Sudden change in bowel habit
Abdominal pain
Iron deficiency anaemia
What is the Rome IV criteria
Diagnosis of chronic idiopathic constipation
Must include two or more of the following:
-Straining during more than 25% of defecations
-Lumpy or hard stools (Bristol Stool Form Scale 1-2) more than 25% of defecations
-Sensation of incomplete evacuation more than 25% of defecations
-Sensation of anorectal obstruction/blockage more than 25% of defecations
-Manual maneuvers to facilitate more than 25% of defecations (e.g., digital evacuation)
-Fewer than three spontaneous bowel movements per week
-Loose stools are rarely present without the use of laxatives
-Insufficient criteria for irritable bowel syndrome
-The criteria must be fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis.
What are FDDs
Functional defecation disorders
The patient must satisfy diagnostic criteria for chronic idiopathic constipation and/or irritable bowel syndrome with constipation
During repeated attempts to defecate, there must be features of impaired evacuation, as demonstrated by 2 of the following 3 tests:
-Abnormal balloon expulsion test
-Abnormal anorectal evacuation pattern with manometry or anal surface electromyography (EMG)
-Impaired rectal evacuation by imaging
The criteria must be fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis.
FDDs may be subcategorised as dyssynergic defecation if there is an inappropriate contraction of the pelvic floor as measured with anal surface EMG or manometry with adequate propulsive forces during attempted defecation. The measurement of pelvic floor contraction is done through specialist anorectal physiology testing.
How is constipation investigated
Most people do not require extensive investigation
Exclude secondary causes
Investigate red flag features
Investiagte when refractory to initial therapy
Stool tests:
For ?IBD or ?colorectal cancer
-Faecal calprotectin (FCP)
-Quantitative faecal immunochemical test (qFIT)
Bloods:
To exclude secondary causes or to look for red flag features (eg thyroid problems or anaemia)
-Full blood count
-Renal profile
-Bone profile
-HbA1c
-Thyroid function tests
-Specialist: parathyroid hormone, cortisol, electrophoresis
Imaging:
-reserved for pts with a suspected secondary cause of constipation (eg diverticular stricture, malignancy)
-CT abdomen and pelvis
-MRI pelvis
-Abdominal xray (incidental findings of constipation)
Endoscopy:
-Colonoscopy in pts with new change of bowel habit to exclude sinister causes
-Recommended in pts with red flag features
– Age > 50 with unexplained rectal bleeding
– Age > 50 with rectal bleeding and change in bowel habit
– Age > 60 with change in bowel habits
Specialist investigations:
-In severe, refractory constipation that will be guided by gastroenterologists
-Colonic transit studies: use of radiopaque markers to assess colonic transit.
-Wireless motility capsule: ingestion of a wireless capsule to assess regional or whole gut transit time
-Defecography: assesses a patient evacuating barium solution to investigate structural problems contributing to defecatory disorders. A defecatory MRI proctogram is commonly requested
-Anorectal physiology: a series of investigations that can be used to assess sphincter function, rectal sensitivity, propulsive function, pressures (i.e. manometry), and ability to expel a balloon (simple form of defecography)
How is constipation managed
Most patients can be managed with simple lifestyle modifications or basic laxatives.
Address any secondary factors that have precipitated constipation.
The general treatment approach should be:
-Lifestyle modifications
-First-line laxatives (osmotic, bulk-forming, softeners)
-Second-line laxatives (stimulants, suppositories and/or enemas)
-Consider biofeedback (defecatory disorders)
-Newer therapies (prokinetics, secretagogues)
-Interventional treatments
What are the lifestyle modifications which can help manage contipation
Eat a healthy diet that is high in whole grains, fruit and vegetables
Slowly increase fibre in diet to 30g/day (too fast can lead to flatulence and bloating)
Maintain good fluid intake to avoid dehydration
Take regular exercise
Basic toilet regimens can be advised:
-Regular, unhurried routine to ensure complete defecation
-Respond immediately to sensation to defecate
-If limited mobility, ensure appropriate access to toilets and privacy
-Provide supported seating if unsteady on toilet
What are the types of laxatives available
Bulk forming laxative -> addition of osmotic laxative -> second line (stimulants) -> rectal therapies
The different types of laxatives include:
Bulk-forming (e.g. fybogel - ispaghula husk, methylcellulose):
-increase the ‘bulk’ of the stool that stimulates bowel function.
-usually take 2-3 days to work
-first line.
-important to drink plenty of water alongside bulk laxatives.
Osmotic (e.g. macrogol, lactulose):
-poorly absorbable molecules that exert an osmotic effect drawing water into the bowel lumen.
-very commonly used laxatives
-offered after bulk-forming laxatives.
-very effective in faecal impaction and infrequent bowel motions.
Stimulant (e.g. senna, bisacodyl, sodium picosulfate):
-stimulate the local nervous system within the gut wall that increases colonic contractility and secretions.
-work in 6-12 hours.
-may be used second-line
-better for patients with difficulty emptying rather than infrequent motions.
Softeners (e.g. arachis oil, sodium docusate):
-Docusate lowers the surface tension, which leads to water and fats penetrating the stool.
-typically combined with other laxatives (e.g. stimulants).
Suppositories (e.g. glycerol, bisacodyl):
-can be used to aid rectal emptying by stimulating the anal sphincter and initiating peristalsis.
-Glycerol is an osmotic type laxative
-Bisacodyl is a stimulant.
-May be combined with oral laxatives.
-Commonly used if inadequate response to oral, incomplete emptying, incontinence, or altered rectal sensitivity.
-Cause more rapid evacuation
Enemas (e.g. phosphate, sodium citrate, docusate):
-include osmotic, softeners, and/or weak stimulants.
-A phosphate enema contains 128 mL of liquid whereas others are ‘mini-enemas’ that come as only 5 mL.
-These can be combined with oral laxatives as needed.
-Like suppositories, they act quickly to bring about a more rapid evacuation.
What are the newer therapies being used in constipation management
Typically offered in ongoing contipation despite use of two conventional laxatives from two different classes for at least 6 months
Prokinetics (e.g. Prucalopride):
-Prucalopride is commonly used that works as a selective serotonin 5-HT4 receptor agonist.
-It simulates mass colonic movement and has an action on other areas of the gastrointestinal tract.
-It is contraindicated in colonic obstruction and should be used with caution in patients with ischaemic heart disease.
Secretagogues (e.g. Linaclotide, Lubiprostone):
-work by increasing intestinal chloride secretion that is associated with increased water secretion into the bowel lumen.
-Linaclotide activates the secretion of chloride through guanylcyclase C which activates CFTR chloride channels.
-Lubiprostone is derived from prostaglandin E1 and directly activates chloride channels and CFTR.
-Lubiprostone has been withdrawn in the UK market.
Opioid-antagonists (e.g. Naloxegol):
-Naloxegol is a peripherally acting opioid receptor antagonist.
-It decreases the constipating effects of opioids without altering their central analgesic effects.
How is faecal impaction treated
Typical regimen of high-dose macrogol which is an osmotic laxative
If there has been an inadequate response then macrogol can be combined with suppositories or enemas
After a few days of an osmotic laxative, or if stools are soft, a stimulant laxative can be used (avoid if stools are hard)
What is anorectal biofeedback
A treatment for patients with constipation related to disordered defecation or those with faecal incontinence.
It involves providing the patient with coaching and visual cues to help assist them with isolating and coordinating the pelvic floor muscles during defecation.
Anorectal biofeedback is run by experienced bowel nurse specialists and can be completed with or without the use of anorectal physiology. It essentially helps patients to strengthen or relax the pelvic floor muscles during defecation.
What are the surgical interventions for constipation
Rarely needed
In severe cases, surgical intervention may be offered (eg. subtotal colectomy, segmental colectomy, STARR procedure)
Mechanism behind contipation is important to determine to decide appropriate surgical intervention
Need to exclude gastrointestinal dysmotility that responds poorly to surgery.
What is diarrhoea
The passage of loose/ watery stool at least 3 times per 24hrs
How diarrhoea classified
Classification based on duration:
-Acute: <2 weeks
-Sub-acute: 2-4 weeks
-Chronic: >4 weeks
Classification based on etiology: mainly for acute
-Community acquired
-Hospital-acquired
What are the differentials for diarrhoea
GI:
-Infection
– gastroenteritis
– tropical infections
-Inflammation
– IBD
– diverticulitis
-Coeliac disease
-Lactose intolerance
-Colorectal carcinoma
-IBS
-Overflow
Endocrine:
-Thyroxicosis
-Addison’s
Drugs:
-Antibiotics
-PPIs
-Metformin
-Laxatives
-Digoxin
-Propanolol
-Alcohol
How is diarrhoea investigated
Extent of investigations depends on symptoms severity, chronicity, and red flags
Bloods:
-FBC
-U and Es
-LFTs
-TFTs
-Calcium
-Inflammatory markers
-Coeliac serology
-Faecal calprotectin
Stool:
-MC+S
-C.diff toxin
-Ova and parasites
-Faecal elastase (chronic pancreatitis)
-Gut hormones (gastronome, VIPoma)
Breath:
-13C breath test (H.pylori)
-Hydrogen breath test (lactose intolerance)
Endoscopy
How is diarrhoea managed
Usually spontaneously resolves
Manage underlying causes
Oral rehydration solution or IV fluids if severe dehydration
Consider loperamide
What is loperimide
u-opioid receptor agonist in the myenteric plexus, reducing smooth muscle tone
Doesn’t cross blood brain barrier so no CNS effects
Indications:
-Watery diarrhoea that interferes with daily function
-IBS
-Traveller’s diarrhoea
What is malnutrition
A sudden or chronic decrease in the intake of sufficient nutrition to support the body’s requirements for growth, healing and maintenance of life
Estimated that over 30% of patients admitted to hospital will experience a form of malnutrition
What is acute malnutrition
A brief period of inadequate nutrition that is most commonly in relation to an acute illness with a high inflammatory state and results in muscle wasting and rapid weight loss
What is chronic malnutrition
Inadequate nutrition that lasts longer than 3 months
Often secodnary to social, behavioural and economic factors in addition to illness related causes
What screening tools can be used for assessing malnutrition
Malnutrition Univeral Screening Tool (MUST)
Malnutrition Screening Tool (MST)
Mini-nutrtion Assessment (MNA)
What is the aetiology for malnutrition
As metabolic demand increase due to illness, injury or stressors such as exercise, people adapt their nutritional intake to meet the body’s requirements.
In settings of chronic disease and certain drugs, this normal course of adaptation because difficult and can lead to acute or chronic malnutrition
Three main reasons people may become malnourished:
-Inadequate amounts of nutrients (e.g. poor variety in diet)
-Difficulty absorbing nutrients (e.g. gastrointestinal dysfunction such as coeliac disease)
-Increased nutritional demands (e.g. post-surgery for healing)
What are the risk factors for malnutrition
Highest risk:
-those with chronic illnesses
-the elderly
-those living in supported accommodation
-patients drinking excessive amounts of alcohol over a prolonged period.
Other risk factors for malnutrition include:
-Being hospitalised for extended periods of time
-Problems with dentition, taste or smell
-Polypharmacy
-Social isolation and loneliness
-Mental health issues including grief, anxiety and depression
-Cognitive issues including confusion
What are the clinical features of malnutrition
-High susceptibility or long durations of infections
-Slow or poor wound healing
-Altered vital signs including bradycardia, hypotension, and hypothermia
-Depleted subcutaneous fat stores
-Low skeletal muscle mass
In children, other indicators are:
-Wasting: low weight for height
-Stunting: low height for age
-Underweight: low weight for age
What is the significance of serum albumin levels in malnutrition
Hypoalbuminaemia occurs in conditions where there is an excessive amount of protein being lost or where the production of albumin is impaired
Can also occur in the context of inflammatory states such as infections
Serum albumin should not be relied on in isolation to assess a patient’s nutritional state as there are a wide variety of factors which influence levels
What are the important areas to cover in malnutrition history taking
Weight history:
-current weight
-recent changes to weight
-changes to fit of clothes
Meal history:
-regularity of meals including skipping meals
Protein intake:
-intake of high-quality protein
Hydration:
-intake of fluids
How is a patient with suspected malnutrition examined clinically
Weight:
-unexpected weight loss from someone’s normal weight is indicative of a period of malnutrition.
-This includes people who are clinically overweight and obese.
Body mass index (BMI):
-a patient’s BMI indicates whether they might be malnourished.
-It is not however as accurate as history and clinical examination, and should never be used in isolation.
Review of muscle mass stores
Review of subcutaneous fat stores
Consideration could also be given to measuring:
-a patient’s grip strength
-triceps skin fold thickness
-mid-arm muscle circumference
How is malnutrition managed
Consideration of patients goals of care, prognosis and social factors
Dietician involvement
Treat reversible causes (eg infection or inflammatory state)
Oral nutrition used as long as possible with use of oralnutritional support such as high-energy-high-protein supplements and fortified food products
Minor changes to diet can have significant positive impact on patient’s nutritional status
If unable to safely swallow or unable to take sufficient calories orally, NG feeding should be considered.
For long term feeding, a gastrostomy (PEG or RIG) or jejunostomy should be considered
Parenteral nutrtion should be reserved for patients with intestinal failure or inaccessible givestive tracts
What is refeeding syndrome
A condition caused by rapid re-introduction of normal nutrition in patients who are chronically malnourished
In chronic malnutrition, a patient’s intracellular stores of key electrolytes become depleted.
If a patient then is suddenly provided with normal levels of nutrition, there is a sudden shift of these electrolytes from the extracellular to the intracellular compartment driven by a large insulin response and other factors.
Can ultimately lead to a sudden drop in extracellular levels of key electrolytes resulting in hypokalaemia and hypophosphataemia
This can subsequently lead to cardiac complications (eg arrhythmias)and seizures
How is refeeding syndrome prevented
Nutrition is re-introduced more gradually under the guidance of a dietician and the patients electrolytes are monitored closely, allowing deficiencies to be identified early and replaced appropriately
What are the potential complications of malnutrition
Impaired immunity (increased risk of infections)
Poor wound healing
Growth restriction in children
Unintentional weight loss, specifically the loss of muscle mass
Multi-organ failure
Death
What is GORD
Gastro-oesophageal reflux disease
Where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus
The oesophagis has a squamous epithelial lining making it more sensitive to the effects of stomach acid compared to the stomach which has columnar epithelial lining, which is more protected against stomach acid
How does GORD present
Dyspepsia
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
What are the red flag symptoms which indicate referral for endoscopy in a reflux type picture
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
How is GORD managed
Lifestyle advice
-Reduce tea, coffee and alcohol
-Weight loss
-Avoid smoking
-Smaller, lighter meals
-Avoid heavy meals before bed time
-Stay upright after meals rather than lying flat
Acid neutralising medication when required:
-Gaviscon
-Rennie
Proton pump inhibitors (reduce acid secretion in the stomach)
-Omeprazole
-Lansoprazole
Ranitidine
-This is an alternative to PPIs
-H2 receptor antagonist (antihistamine)
-Reduces stomach acid
Surgery
-laparoscopic fundoplication.
-involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.
What is H.pylori
H. pylori is a gram negative aerobic bacteria.
It lives in the stomach.
It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer.
It avoids the acidic environment by forcing its way into the gastric mucosa.
The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.
It also produces ammonia to neutralise the stomach acid.
The ammonia directly damages the epithelial cells.
Other chemicals produced by the bacteria also damage the epithelial lining.
How is H.pylori tested for
Offer a test for H. pylori to anyone with dyspepsia.
They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.
Tests
-Urea breath test using radiolabelled carbon 13
-Stool antigen test
-Rapid urease test can be performed during endoscopy.
– A rapid urease test is also known as a CLO test (Campylobacter-like organism test).
– It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa.
– Urea is added to this sample.
– If H. pylori are present, they produce urease enzymes that converts the urea to ammonia.
– The ammonia makes the solution more alkali giving a positive result on when the pH is tested.
How is H.pylori eradicated
The eradication regime involves triple therapy with a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.
The urea breath test can be used as a test of eradication after treatment. This is not routinely necessary.
What is Barretts oesophagus
Constant reflux of acid results in the lower oesophageal epithelium changing in a process known as metaplasia from a squamous to a columnar epithelium.
This change to columnar epithelium is called Barretts oesophagus.
When this change happens patients typically get an improvement in reflux symptoms.
Barretts oesophagus is considered a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus (3-5% lifetime risk with Barretts). Patients identified as having Barretts oesophagus are monitored for adenocarcinoma by regular endoscopy. In some patients there is a progression from Barretts oesophagus (columnar epithelium) with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.
Treatment of Barretts oesophagus is with proton pump inhibitors (e.g. omeprazole)
Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the epithelium so that it is replaced with normal cells.
This is not recommended in patients with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.
What are the major types oesophageal cancer
Squamous cell carcinoma (SCC): usually located in the upper or middle oesophagus. Accounts for >90% of cases worldwide.
Adenocarcinoma (AC): usually located in the lower oesophagus. Due to chronic reflux and development of a columnar metaplasia, which is a precursor lesion known as Barrett’s oesophagus.
Rarer forms of oesophageal cancers include small cell carcinoma, sarcoma, lymphoma, melanoma and choriocarcinoma.
What is the aetiology of oesophageal cancer
Two major risk factors:
-smoking
-alcohol
Oesophageal neoplasia develops due to sequential mutations that occur in the oesophageal epithelium, which allows cells to proliferate uncontrollably. Several risk factors for both SCC and AC increase the likelihood of developing these mutations.
What are the risk factors for squamous cell oesophageal cancer
Smoking
Alcohol consumption
Foods containing N-nitroso compounds
Chewing of areca nuts
Previous partial gastrectomy
Atrophic gastritis
Human papillomavirus (HPV): mainly genotypes 16 and 18
Tylosis: rare condition leading to hyperkeratosis of hands and feet
What are the risk factors for adenocarcinoma of oesophagus
Chronic reflux
Barrett’s oesophagus: 30-fold increase risk of AC
Smoking
Obesity
Zollinger-Ellison syndrome: gastrin-secreting tumour leading to excess hydrochloric acid.
What is the pathophysiology of oesophageal carcinoma
Squamous cell carcinoma
-Due to chronic alcohol consumption and smoking, which damage cellular DNA.
-Leads to development of genetic mutations that promote abnormal cell growth.
-Overtime, the cells proliferate uncontrollably leading to invasive cancer.
-SCC may be seen as an infiltrating and ulcerated mass in the middle oesophagus, especially if advanced.
-There is early invasion into surrounding lymph nodes and the tumour may metastasize to liver, bone and lung.
Adenocarcinoma
-Typically, chronic reflux leads to inflammation and damage of the lower oesophageal mucosa.
-This results in columnar metaplasia, which refers to the transformation of the mature squamous cell type to columnar cell type.
-This metaplastic epithelium may become dysplastic, which refers to cells with abnormal growth and development.
-The dysplastic epithelium acquires further genetic mutation that promotes development of invasive carcinoma.
-Most commonly located near the gastro-oesophageal junction and there is usually early lymph node involvement.
What are the clinical features of oesophageal carcinoma
The hallmark feature of oesophageal cancer is dysphagia, which refers to difficulty swallowing.
Symptoms
-Constitutional symptoms: fevers, anorexia, lethargy, weight loss
-Dysphagia: difficulty swallowing
-Weight loss: due to tumour-related anorexia and poor nutrition from swallowing difficulties
-Bleeding: haematemesis and melaena
-Pain: typically retrosternal pain
-Aspiration: cough, shortness of breath, fever
-Hoarseness: if there is extension to involve the recurrent laryngeal nerve
Signs
-Lymphadenopathy: if local tumour spread
-Cachexia
-Pallor: due to anaemia
-Hepatomegaly: if metastatic spread
What are the guidelines for referral in suspected oesophageal carcinoma
Urgent (two week wait) referral
-This means referring a patient for appropriate investigations (e.g. gastroscopy) for suspected oesophageal cancer within two weeks.
-It is usually combined with a clinic appointment and CT imaging.
-Dysphagia, OR
-> 55 years with weight loss and one of the following:
– Upper abdominal pain
– Reflux
– Dyspepsia
Non-urgent referral
-This means referral for a non-urgent gastroscopy to assess for oesophageal pathology.
-Usually performed within 6 weeks.
-Haematemesis, OR
-> 55 years with treatment resistant dyspepsia, OR
-> 55 years with upper abdominal pain and anaemia, OR
-Thrombocytosis with one of the following:
– Nausea/vomiting
– Weight loss
– Reflux
– Dyspepsia
–Upper abdominal pain
-Nausea/vomiting with one of the following:
– Weight loss
– Reflux
– Dyspepsia
– Upper abdominal pain
How is oesophageal cancer diagnosed
Using upper GI endoscopy and biopsy of suspected lesions
Gastroscopy:
-camera test that allows direct visualisation of the upper GI tract
-biopsies taken at the time and are sent for histological analysis for signs of malignancy
What investigations are performed in suspected oesophageal cancer
Gastroscopy and biopsy
Further investigations for assessment of distant spread anf key-organ function to help guide management:
-Bloods:
– Full blood count
– Serum iron, transferrin saturation, total iron binding capacity (TIBC)
– Urea & electrolytes
– Liver function tests
– Bone profile
– Clotting screen
– Renal function
-Imaging:
– CT CAP (for staging)
– Abdominal ultrasound (liver mets)
– PET-CT (for potential surgical candidates to assess distant disease not detected by convential CT)
Diagnostic laparoscopy (may be used to more accurately stage if it will alter management)
Endoscopic ultrasound (staging if will change management)
How is oesophageal cancer staged
Cancer stage is based on tumour size, presence of lymph node involvement and distant spread. We call these three factors ‘TNM’ (tumour, nodes, metastasis).
Tumour
TX: Primary tumour cannot be assessed
T0: No evidence of primary tumour
Tis: Carcinoma in situ/high-grade dysplasia
T1: Tumour invades lamina propria or submucosa
T1a: Tumour invades mucosa or lamina propria or muscularis mucosae
T1b: Tumour invades submucosa
T2: Tumour invades muscularis propria
T3: Tumour invades adventitia
T4: Tumour invades adjacent structures
T4a: Tumour invades pleura, pericardium, diaphragm or adjacent peritoneum
T4b: Tumour invades other adjacent structures such as aorta, vertebral body or trachea
Node
NX: Regional lymph nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis in 1–2 regional lymph nodes
N2: Metastasis in 3–6 regional lymph nodes
N3: Metastasis in 7 or more regional lymph nodes
Metastasis
MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
NOTE: Non-regional lymph node spread is considered M1a disease.
How oesophageal cancer managed
Depends on extent of cancer and pts fitness
Surgery: (treatment of choice where possible) resection of oesophageal or gastro-oesophageal tumours (e.g. oesophagectomy).
Endoscopic techniques: mucosal resection or submucosal dissection.
Radiotherapy: use of high energy rays to destroy cancer cells.
Chemotherapy: use of anti-cancer medications to destroy cancer cells.
Targeted cancer drugs: monoclonal antibodies against certain receptors (e.g. HER2).
Palliative care: use of chemotherapy/radiotherapy or stenting to control disease and/or symptoms without aiming to cure.
Best supportive care: focus primarily on symptoms and quality of life without systemic treatments.
The choice of treatment depends on whether the cancer is limited, locally advanced or advanced/metastatic.
-Limited: (Staging: T1-2, N0, M0) refers to small tumours without lymph node involvement or distant spread
-Locally advanced: (Staging: T3-4 or N1-2, M0) refers to larger tumours with/without lymph node involvement but without distant spread
-Advanced/metastatic: refers to metastatic disease with spread to distant sites
What are the paliative management options in oesophageal cancer
Palliative treatment should be considered in patients with locally advanced disease who are not operative candidates or not fit enough to undergo radical treatment (e.g. poor performance status, extensive co-morbidities).
Options include:
-Radiotherapy: if tumour lies within a radiotherapy field that allows high-doses to be applied.
-Chemotherapy: regimens depend on fitness of the patient.
-Local tumour treatment: endoscopic stenting, palliative radiotherapy.
-Best supportive care: focusing on symptom control only.
What is oesophageal stenting
Involves endoscopically placing a stent within the oesophagus to keep the lumen open and prevent dysphagia.
What is performance status
This describes a patients’ level of functioning in terms of their ability to care for themselves, what they can do as part of their daily activities and their physical ability.
Performance status can be measures using the World Health Organisation (WHO) / Eastern Cooperative Oncology Group (ECOG) scale.
Grade 0: Fully active, able to carry out all normal activities.
Grade 1: Restricted physical activity but ambulatory and able to carry out light sedentary work (e.g. office work).
Grade 2: Ambulatory and capable of all self care but unable to carry out any work activities. Out of bed >50% of day.
Grade 3: Capable of only limited self-care, confined to bed or chair > 50% of waking hours.
Grade 4: Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair.
Grade 5: Death.
What is the prognosis of oesophageal cancer
The five year survival of oesophageal cancer is poor at ~16%
Early diagnosis and treatment is potentially curative, especially if the disease is resectable.
However, oesophagectomy is a major operation with significant morbidity and mortality.
What are hernias
Hernias occur when there is a weak point in a cavity wall, usually affecting the muscle or fascia
This weakness allows a body organ that would normally be contained within that cavity to pass through the cavity wall
How do hernias present
There are many types of hernias that present differently depending on where they are and what organs are involved.
The typical features of an abdominal wall hernia are:
-A soft lump protruding from the abdominal wall
-The lump may be reducible (it can be pushed back into the normal place)
-The lump may protrude on coughing (raising intra-abdominal pressure) or standing (pulled out by gravity)
-Aching, pulling or dragging sensation
What are the potential complications of hernias
There are three key complications of hernias:
-Incarceration
-Obstruction
-Strangulation
Incarceration:
-The hernia cannot be reduced back into the proper position (it is irreducible).
-The bowel is trapped in the herniated position.
-Incarceration can lead to obstruction and strangulation of the hernia.
Obstruction:
-The hernia causes a blockage in the passage of faeces through the bowel.
-Presents with vomiting, generalised abdominal pain and absolute constipation (not passing faeces or flatus).
Strangulation
-The hernia is non-reducible (it is trapped with the bowel protruding) and the base of the hernia becomes so tight that it cuts off the blood supply, causing ischaemia.
-Presents with significant pain and tenderness at the hernia site.
-A surgical emergency.
-The bowel will die quickly (within hours) if not corrected with surgery.
-There will also be a mechanical obstruction when this occurs.
What is a Richter’s hernia
A very specific situation that can occur in any abdominal hernia.
Where only part of the bowel wall and lumen herniate through the defect, with the other side of that section of the bowel remaining within the peritoneal cavity.
Can become strangulated, where the blood supply to that portion of the bowel wall is constricted and cut off.
Strangulated Richter’s hernias will progress very rapidly to ischaemia and necrosis and should be operated on immediately.
What is Maydl’s Hernia
A specific situation where two different loops of bowel are contained within the hernia.
How are abdominal wall hernias managed
Conservative management:
-Leave the hernia alone.
-Most appropriate when the hernia has a wide neck (low risk of complications) and in patients that are not good candidates for surgery due to co-morbidities.
Tension-free repair:
-Placing a mesh over the defect in the abdominal wall.
-The mesh is sutured to the muscles and tissues on either side of the defect, covering it and preventing herniation of the cavity contents.
-Over time, tissues grow into the mesh and provide extra support.
-This has a lower recurrence rate compared with tension repair, but there may be complications associated with the mesh (e.g., chronic pain).
Tension repair:
-A surgical operation to suture the muscles and tissue on either side of the defect back together.
-Rarely performed and have been largely replaced by tension-free repairs.
-The hernia is held closed (to heal there) by sutures applying tension.
-This can cause pain and there is a relatively high recurrence rate of the hernia.
What are inguinal hernias and the two types
Inguinal hernias present with a soft lump in the inguinal region (in the groin). There are two types:
Indirect inguinal hernia
Direct inguinal hernia
What are the differentials for a lump in the inguinal region
Femoral hernia
Lymph node
Saphena varix (dilation of saphenous vein at junction with femoral vein in groin)
Femoral aneurysm
Abscess
Undescended / ectopic testes
Kidney transplant
What is an indirect hernia
Where the bowel herniates through the inguinal canal. (The inguinal canal is a tube that runs between the deep inguinal ring (where it connects to the peritoneal cavity), and the superficial inguinal ring (where it connects to the scrotum).)
In males, the inguinal canal is what allows the spermatic cord and its contents to travel from inside the peritoneal cavity, through the abdominal wall and into the scrotum.
In females, the round ligament is attaches to the uterus and passes through the deep inguinal ring, inguinal canal and then attaches to the labia majora.
During fetal development, the processus vaginalis is a pouch of peritoneum that extends from the abdominal cavity through the inguinal canal. This allows the testes to descend from the abdominal cavity, through the inguinal canal and into the scrotum. Normally, after the testes descend through the inguinal canal, the deep inguinal ring closes and the processus vaginalis is obliterated. However, in some patients, the inguinal ring remains patent, and the processus vaginalis remains intact. This leaves a tract or tunnel from the abdominal contents, through the inguinal canal and into the scrotum. The bowel can herniate along this tract, creating an indirect inguinal hernia.
There is a specific finding of indirect inguinal hernias that help you differentiate them from a direct inguinal hernias. When an indirect hernia is reduced and pressure is applied (with two fingertips) to the deep inguinal ring (at the mid-way point from the ASIS to the pubic tubercle), the hernia will remain reduced.
What is a direct inguinal hernia
Direct inguinal hernias occur due to weakness in the abdominal wall at Hesselbach’s triangle. The hernia protrudes directly through the abdominal wall, through Hesselbach’s triangle (not along a canal or tract like an indirect inguinal hernia). Pressure over the deep inguinal ring will not stop the herniation.
Hesselbach’s triangle boundaries (RIP mnemonic):
R – Rectus abdominis muscle – medial border
I – Inferior epigastric vessels – superior / lateral border
P – Poupart’s ligament (inguinal ligament) – inferior border
What are femoral hernias
Involve herniation of the abdominal contents through the femoral canal. This occurs below the inguinal ligament, at the top of the thigh.
The opening between the peritoneal cavity and the femoral canal is the femoral ring. The femoral ring leaves only a narrow opening for femoral hernias, putting femoral hernias at high risk of:
-Incarceration
-Obstruction
-Strangulation
Boundaries of the femoral canal (FLIP mnemonic):
F – Femoral vein laterally
L – Lacunar ligament medially
I – Inguinal ligament anteriorly
P – Pectineal ligament posteriorly
Don’t get the femoral canal confused with the femoral triangle. The femoral triangle is a larger area at the top of the thigh that contains the femoral canal. You can remember the boundaries with the SAIL mnemonic:
S – Sartorius – lateral border
A – Adductor longus – medial border
IL – Inguinal Ligament – superior border
Use the NAVY-C mnemonic to remember the contents of the femoral triangle from lateral to medial across the top of the thigh:
N – Femoral Nerve
A – Femoral Artery
V – Femoral Vein
Y – Y-fronts
C – Femoral Canal (containing lymphatic vessels and nodes)
What are incisional hernias
Occur at the site of an incision from previous surgery. They are due to weakness where the muscles and tissues were closed after a surgical incision. The bigger the incision, the higher the risk of a hernia forming. Medical co-morbidities put patients at higher risk due to poor healing.
Incisional hernias can be difficult to repair, with a high rate of recurrence. They are often left alone if they are large, with a wide neck and low risk of complications, particularly in patients with multiple co-morbidities.
What are umbilical hernias
Occur around the umbilicus due to a defect in the muscle around the umbilicus.
Umbilical hernias are common in neonates and can resolve spontaneously. They can also occur in older adults.
What are epigastric hernias
Simply a hernia in the epigastric region (upper abdo)
What are spigelian hernias
Occurs between the lateral border of the rectus abdominis muscle and the linea semilunaris. This is the site of the spigelian fascia, which is an aponeurosis between the muscles of the abdominal wall. Usually, this occurs in the lower abdomen and may present with non-specific abdominal wall pain. There may not be a noticeable lump.
An ultrasound scan can help establish the diagnosis.
Spigelian hernias generally have a narrower base, increasing the risk of incarceration, obstruction and strangulation.
What is diastasis recti
May also be called rectus diastasis and recti divarication. It refers to a widening of the linea alba, the connective tissue that separates the rectus abdominis muscle, forming a larger gap between the rectus muscles. It is not technically a hernia. This gap becomes most prominent when the patient lies on their back and lifts their head. There is a protruding bulge along the middle of the abdomen.
The linea alba is the aponeurosis of the two sides of the rectus abdominis muscle. The gap is created because the linea alba is stretched and broad.
This can be congenital (in newborns) or due to weakness in the connective tissue, for example following pregnancy or in obese patients.
No treatment is required in most cases, but surgical repair is possible.
What are obturator hernias
Where the abdominal or pelvic contents herniate through the obturator foramen at the bottom of the pelvis. They occur due to a defect in the pelvic floor and are more common in women, particularly in older age, after multiple pregnancies and vaginal deliveries. They are often asymptomatic but may present with irritation to the obturator nerve, causing pain in the groin or medial thigh.
Howship–Romberg sign refers to pain extending from the inner thigh to the knee when the hip is internally rotated and is due to compression of the obturator nerve.
It can also present with complications of:
-Incarceration
-Obstruction
-Strangulation
CT or MRI of the pelvis can establish the diagnosis. It may be found incidentally during pelvic surgery.
What is a hiatus hernia
Refers to the herniation of the stomach up through the diaphragm.
The diaphragm opening should be at the level of the lower oesophageal sphincter and should be fixed in place.
A narrow opening helps to maintain the sphincter and stop acid and stomach contents refluxing into the oesophagus.
When the opening of the diaphragm is wider, the stomach can enter through the diaphragm and the contents of the stomach can reflux into the oesophagus.
What are the types of hiatus hernia
Type 1: Sliding - the stomach slides up through the diaphragm, with the gastro-oesophageal junction passing up into the thorax.
Type 2: Rolling - a separate portion of the stomach (i.e. the fundus), folds around and enters through the diaphragm opening, alongside the oesophagus
Type 3: Combination of sliding and rolling
Type 4: Large opening with additional abdominal organs entering the thorax
What are the key risk factors for hiatus hernia
Increasing age
Obesity
Pregnancy
How do hiatus hernias present
Dyspepsia (indigestion), with symptoms of:
-Heartburn
-Acid reflux
-Reflux of food
-Burping
-Bloating
-Halitosis (bad breath)
How are hiatus hernias investigated
Can be intermittent, meaning they may not be seen on investigations.
May be seen on:
-Chest x-rays
-CT scans
-Endoscopy
-Barium swallow testing
How are hiatus hernias treated
Conservative (with medical treatment of gastro-oesophageal reflux)
Surgical repair if there is a high risk of complications or symptoms are resistant to medical treatment.
Involves laparoscopic fundoplication.
Involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.
What are peptic ulcers
Ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer)
Which type of peptic ulcers are more common
Duodenal
What is the pathophysiology of peptic ulceration
Stomach mucosa is prone to ulceration from:
-Breakdown of the protective layer of the stomach and duodenum
-Increase in stomach acid
The protective layer in the stomach is comprised of mucus and bicarbonate secreted by the stomach mucosa
The protective layer can be broken down by:
-Medications (eg steroids or NSAIDs)
-H. pylori
Increased acid can result from:
-stress
-alcohol
-caffeine
-smoking
-spicy foods
How does a peptic ulcer present
Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haemateemsis, coffee ground vomit and melaena
Iron deficiency anaemia (due to constant bleeding
Eating typically worsens the pain of gastric ulcers and improve the pain of duodenal ulcers
How are peptic ulcers managed
Diagnosed by endoscopy
During endoscopy a rapid ureas test (CLO test) can be performed to check for h. pylori
Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure
Medical treatment is the same as with GORD with high dose PPI
Endoscopy can be used to monitor the ulcer to ensure it heals and to assess for further ulcers
What are the potential complications of peptic ulcers
Bleeding fromt the ulcer is a common and potentially life threatening complication
Perforation resulting in an acute abdomen and peritonitis which requires urgent surgical repair (usually laparoscopic)
Scarring and strictures of the muscle and mucosa which can lead to narrowing of the pyloris causing difficulty emptying stomach contents. This is Pyloric stenosis.
What is the pylori
Exit of the stomach
How does pyloric stenosis present
Upper abdominal pain
Distension
Nausea and vomiting, particularly after eating
What is coeliac disease
An autoimmune condition where the exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel
What is the pathophysiology of coeliac disease
Auto-antibodies are created in response to exposure to gluten
These auto-antibodies target the epithelial cells of the intestine and lead to inflammation
The key auto-antibodies involved are:
-anti-tissue transglutaminase (anti-TTG)
-anti-endomysial (anti-EMA)
-deaminated gliadin peptides antibodies (anti-DGPs)
These antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment
Inflammation affects the small bowel, particularly the jejunum.
It causes atrophy of the intestinal villi
The intestinal cells have villi on them that help with absorbing nutrients from food passing through the intestine
Inflammation causes malabsorption of nutrients and symptoms of the disease
How does coeliac disease present
Often asymptomatic
Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
Rarely coeliac disease can present with neurological symptoms:
-peripheral neuropathy
-cerebral ataxia
-epilepsy
What are the genetic associations with coeliac disease
HLA-DQ2 gene (90%)
HLA-DQ8 gene
How is coeliac disease
Investigations must be carried out whilst the patient remains on a diet containing gluten otherwise it may not be possible to detect antibodies or inflammation in the bowel
Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies (which are IgA and if totally deficient then may give a false coeliac result):
-Raised anti-TTG antibodies
-Raised anti-endomysial antibodies
Endoscopy and intestinal biopsy show:
-crypt hypertrophy
-villious atrophy
Which conditions is coeliac disease associated with
Other autoimmune conditions:
-Type 1 diabetes
-Thyroid disease
-Autoimmune hepatitis
-Primary biliary cirrhosis
-Primary sclerosing cholangitis
What are the potential complications of untreated coeliac disease
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy associated T cell lymphoma (EATL) of the intestine
Non-hodgkin lymphoma
Small bowel adenocarcinoma (rare)
How is coeliac disease treated
Lifelong gluten free diet is essentially curative
Relapse will occur on consuming gluten again
Checking coeliac antibodies can be helpful in monitoring the disease
What are gallstones
Small stones that form within the gallbladder
They form from concentrated bile in the bile duct and most of them are made of cholesterol
They may be asymptomatic or can cause pain and lead to complications such as acute cholecystitis, acute cholangitis and pancreatitis (when gallstones block the drainage of the pancreas)
What is cholestasis
Blockage to the flow of bile
What is cholelithiasis
Gallstones are present
What is choledocholiathiasis
Gallstones in the bile duct
What is biliary colic
Intermittent right upper quadrant pain caused by gallstones irritating bile ducts by temporarily obstracting drainage of the gallbladder
They may get lodged at the neck of the gallbladder or in the cystic duct, then when they fall back into the gallbladder the symptoms resolve
Symptoms are:
-severe, colicky epigastric or RUQ pain
-Often triggered by meals (particularly high fat)
-Last between 30 mins to 8 hrs
-May be associated with nausea and vomiting
What is cholecystitis
Inflammation of the gallbladder
What is cholangitis
Inflammation of the bile ducts
What is a gallbladder empyema
Infected tissue and pus collecting in the gallbladder
Management involves IV antibiotics and one of two main options:
-cholecystectomy (to remove the gallbladder)
-cholecystostomy (inserting a drain into the gallbladder to allow the infected contents to drain)
What is cholecystectomy
Surgical removal of the gallbladder
Indicated in symptomatic patients or in those where gallstones are leading to complications
Stones in the bile ducts can be removed before by ERCP or during surgery
Laparoscopic is preferred to open (right subcostal Kocher incision) as it as fewer complications and a faster recover
What is cholecystostomy
Insertion a drain into the gallbladder
What are the risk factors for gallstones (4 F’s)
Fat, Fair, Female, Forty
How do gallstones present clinically
May be asymptomatic
Typical symptoms of biliary colic
Alternatively may present with complication of gallstones:
-acute cholecystitis
-acute cholangitis
-obstructive jaundice (if the stone blocks the ducts)
-pancreatitis
Why does avoiding fatty foods help ease biliary collic
Fat entering the digestive system causes cholecystokinin (CCK) secretion from the duodenum. CCK triggers contraction of the gallbladder which leads to biliary colic.
Therefore, those with gallstones and biliary colic are advised to avoid fatty foods to prevent CCK release and gallbladder contraction
What is the clinical significance of bilirubin test
Bilirubin normally drains from the liver, through the bile ducts and into the intestines
Raised bilirubin, jaundice with pale stools and dark urine represents an obstruction to flow within the biliary system
Obstruction may be caused by a gallstone in the bile duct or an external mass pressing on the bile ducts (eg cholangiocarcinoma or tumour of the head of the pancreas
What is the clinical relevance of alkaline phosphatase tests
Aka ALP or Alk Phos
A non-specific marker
It is an enzyme originating in the liver, bilary system and bone.
Abnormal results can indicate liver or bone problems
It is often raised in pregnancy due to production by the placenta
A raised ALP is consistent with biliary obstruction in the presence of right upper quadrant pain and/or jaundice
Can also be raised by:
-liver or bone malignancy
-primary biliary cirrhosis
-Paget’s disease of the bone
-etc
What is the clinical relevance of aminotransferases
Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are enzymes produced in the liver
A helpful marker of hepatocellular injury (damage to liver cells)
In patients with cholestasis (eg due to gallstones), ALT and AST can increase slightly with a higher rise in ALP (an obstructive picture)
IF ALT and AST are high compared with the ALP level, this is more indicative of a problem inside the liver with hepatocellular injury (a hepatitic picture)
How is ultrasound used in gallstone diagnosis
First line investigation for symptoms of gallstone disease
Most sensitive imagine for gallstones
Limited by the patient’s weight, gaseous bowel obstructing the view and discomfort from the probe
Findings:
-Gallstones in the gallbladder
-Gallstones in the ducts
-Bile duct dilatation (normally less than 6mm diameter)
-Acute cholecystitis (thickened gallbladder wall, stones or sludge in gallbladder and fluid around the gallbladder)
-The pancrease and pancreatic duct
What is magnetic resonance cholangio-panreatography (MRCP)
An MRI scan with a specific protocol that produces a detailed image of the biliary system
It is very sensitive and specific for biliary tree disease such as tones in the bile duct and malignancy
MRCP is used in many pictures eg identifying biliary strictures or congenital abnormalities
Used for further investigation in gallbladder disease if the ultrasound scan does not show stones in the duct but there is bile duct dilatation or raised bilirubin, suggestive of obstruction
What is endoscopic retrograde cholangio-panreatography (ERCP)
Involves inserting an endoscope down the oesophagus, past the stomach, to the duodenum and the opening of the common bile duct (the spincter of Oddi), giving access to the biliary system
Main indication for ERCP is to clear stones in the bile ducts
ERCP allows the operator to:
-Inject contrast and take x rays to visualise the biliary system and diagnose pathology (eg stones or strictures)
-Perform a sphincterotomy on the sphincter of Oddi if it is dysfunctional (blocking flow)
-Clear stones from the ducts
-Insert stents to improve bile duct drainage (eg with strictures or tumours)
-Take bipsies of tumours
What are the key complications of ERCP
Excessive bleeding
Cholangitis (infection in the bile ducts)
Pancreatitis
How is gallstone disease managed
Asymptomativ patients treated conservatively with no required intervention
Symptomatic patients or those with complications are treated with cholecystectomy, which is surgical removal of the gallbladder (dependent on fitness for surgery)
What is post-cholecystectomy syndrome
A group of non-specific symptoms that can occur after cholecystectomy
May be due to changes in the bile flow after removal of gallbladder
Will improve with time
Symptoms:
-Diarrhoea
-Indigestion
-Epigastric or RUQ pain or discomfort
-Nausea
-Intolerance of fatty foods
-Flatulence
What are the potential complications of cholecystectomy
Bleeding
Infection
Pain
Scars
Damage to bile duct including leakage and strictures
Stones left in the bile duct
Damage to the bowel, blood vessels or other organs
Anaesthetic risks
VTE
Post-cholecystectomy syndrome
What is acute cholecystitis
Infammation of the gallbladder caused by a blockage of the cystic duct preventing the gallbladder from draining
Key complication of gallstones (95% of cases caused by gallstones)
Gallstones may be trapped in the neck of the gallbladder or in the cystic duct
Can be caused by other things (rare) eg patients on TPN or long periods of fasting where gallbladder is not being stimulated by food to regularly empty leading to build up of pressure
How does acute cholecystitis present clinically
RUQ pain
Radiation to right shoulder
Fever
Nausea and vomiting
Tachycardia
Tachypnoea
RUQ tenderness
Murphy’s sign positive
Raised inflammatory markers and white blood cells
What is Murphy’s sign
Place a hand in RUQ and apply pressure
Ask patient to take a deep breath in
The gallbladder will move downwards during inspiration and come in contact with your hand
Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration
What imaging is indicated in acute cholecystitis
First line:
-Abdominal ultrasound showing:
– Thickened gallbladder wall
– Stones or sludge in gallbladder
– Fluid around the gallbladder
MRCP:
-May be used to visualise the biliary tree in more detial if a common bile duct stone is suspected but not seen on ultrasound scan (eg bile duct dilatation or raised bilirubin)
How is acute cholecystitis managed
Emergency admission for investigations and management
Conservative:
-Nil by mouth
-IV fluids
-Antibiotics (as per local guidelines)
-NG tube if required for vomiting
ERCP can be used to remove stones trapped in common bile duct
Cholecystectomy (removal of gallbladder) is usually performed during acute admission (within 72 hours of symptoms). In some cases it may be delayed 6-8 weeks after the acute episode to allow the inflammation to settle
What are the potential complicaitons of acute cholecystitis
Sepsis
Gallbladder empyema
Gangrenous gallbladder
Perforation
