Gastrointestinal Flashcards
Define achalasia
An oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter (LOS) to relax in response to swallowing
Explain the aetiology of achalasia
The degeneration of ganglion cells of the myenteric plexus in the oesophagus
Summarise the epidemiology of achalasia
Annual incidence is about 1 in 100000. Usual presentation age: 25–60 years.
What are the presenting symptoms of achalasia?
Insidious onset and gradual progression of:
. intermittent dysphagia involving solids and liquids;
. difficulty belching;
. regurgitation (particularly at night);
. heartburn;
. chest pain (atypical/cramping, retrosternal);
. weight loss.
What are the signs of achalasia on physical examination?
May reveal signs of complications: aspiration pneumonia, malnutrition and weight loss may result
What are the appropriate investigations for achalasia?
1st line:
Upper gastrointestinal endoscopy- mucosa obscured by retained saliva (and to exclude malignancy)
Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak- shaped). Loss of peristalsis and delayed oesophageal emptying
Oesophageal Manometry:
. incomplete LOS relaxation
. Elevated resting LOS pressure (>45 mmHg);
. absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.
CXR:may show a widened mediastinum and double right heart border (dilated oesophagus), an air-fluid level in the upper chest and absence of the normal gastric air bubble.
What is acute cholangitis?
Also known as ascending Cholangitis
- Infection of the biliary tree, most commonly caused by obstruction
- In its less severe form, there is biliary obstruction with inflammation and bacterial seeding and growth in the biliary tree
What is the aetiology of acute cholangitis?
- Most commonly gallstones leading to choledocholithiasis (gallstones in the bile duct) and biliary obstruction.
- Iatrogenic biliary tract injury, most commonly caused via surgical injury cholecystectomy, can lead to benign strictures, which in turn can lead to obstructions
- Acute prancreatitis
- Malignant strictures (restricts flow)
What is the epidemiology of acute cholangitis?
Relatively uncommon
Male: female ratio is equal
Median age of presentation is 50-60
What are the presenting signs of acute cholangitis?
Pale stools
Pruritus
Hypotension
Mental status changes
What are the investigations for acute cholangitis?
FBC: Raised WBC, decreases platelets
Serum urea: Raised in severe cases
Serum creatinine: Raised in severe cases
ABG: Metabolic acidosis
LFT: Hyperbilinuraemia
CRP: Raised
Serum K & Mg: May be decreased
Blood cultures: Bacteria usually gram negative, but gram positive bacteria and anaerobes are also implicated in cholangitis
Tansabdominal USS: dilated bile duct, common bile duct stones- order CT with contrast if USS is negative
ERCP: best first intervention, can assist in the diagnosis of cholangitis by finding stones causing obstruction and is also therapeutic, as the procedure can be used for biliary stone extraction
What are the presenting symptoms of acute cholangitis?
Jaundice
Fever
Upper abdominal pain
Right upper quadrant tenderness
How is acute cholangitis managed?
Initial stabilisation:
-borad spectrum IV antibiotics
-correct any electrolyte imbalances and coagulation abnormalities
- give adequate analgesia
Biliary decompression:
-ERCP
-surgical incision of the common bile duct (choledochotomy with a T tube replacement)
- cholecystectomy
Consider endoscopic lithotripsy- physical destruction of gallstones
What are the possible complications of acute cholangitis?
- Acute prancreatitis
- Inadequate biliary drainage following performance of endoscopy, radiology or surgery
- Hepatic abscess
What is the prognosis of acute cholangitis?
If adequate biliary drainage is quickly obtained, most patients experience rapid clinical improvement
Outcome worse for patient’s with underlying medical conditions
What is Alcoholic hepatitis?
Inflammatory liver injury and necrosis caused by chronic heavy intake of alcohol
What are the three stages of Alcoholic liver disease?
- Fatty liver (steatosis)
- Alcoholic Hepatitis
- Alcoholic Liver Cirrhosis
What is the aetiology Alcoholic hepatitis?
The middle stage between fatty liver (steatosis) and alcoholic liver cirrhosis.
Inflammatory liver injury, liver histopathology shows:
-centrilobar ballooning degeneration
-necrosis of hepatocytes
-steatosis (abnormal retention of lipids)
-neutrophilic inflammation
-cholestasis (impaired secretion of bile from hepatocytes and so decrease flow of bile)
-Mallory hyaline inclusions and giant mitochondria
What is the epidemiology of Alcoholic hepatitis?
10-35% of heavy drinkers develop this form of liver disease
What are the presenting symptoms of Alcoholic hepatitis?
May remain asymptomatic and undetected unless they present for other reasons May be mild illness with: -Nausea -Malaise -Epigastric or right hypochondrial pain -Low-grade fever May be more severe with: -Jaundice -Abdominal discomfort or swelling -Swollen ankles -GI bleeding
Women tend to present with more florid (fully complete) illness than men
There is a history of heavy alcohol intake (15–20 years of excessive intake necessary for development of alcoholic hepatitis)
There may be trigger events (e.g. aspiration pneumonia or injury)
What are the signs of Alcoholic hepatitis on physical examination?
Signs of alcohol excess: -Malnourished -Palmar erythema -Dupuytrens contracture -Facial telangiectasia -Parotid enlargement -Spider naevi -Gynaecomastia -Testicular atrophy -Hepatomegaly -Easy bruising Signs of severe alcoholic hepatitis: -Febrile (50% of patients) -Tachycardia -Jaundice (>50% of patients) -Bruising -Encephalopathy (e.g. hepatic foetor-breath has a strong, musty smell, liver flap, drowsiness, unable to copy a five-pointed star, disoriented) -Ascites (30–60% of patients) -Hepatomegaly (may be tender on palpation) -Splenomegaly
What are the appropriate investigations for Alcoholic hepatitis?
Bloods:
-FBC: reduced Hb, raised MCV, raised WCC, reduced platelets
-LFT (raised transminases, raised bilirubin, reduced albumin, raised AlkPhos, raised GGT)
-U&Es: Urea and K+ levels tend to be low, unless significant renal impairment
*Clotting: Prolonged PT is a sensitive marker of significant liver damage
Ultrasound scan: For other causes of liver impairment (e.g. malignancies)
Upper GI endoscopy: To investigate for varices
Liver biopsy: Percutaneous or transjugular (in the presence of coagulopathy) may be helpful
to distinguish from other causes of hepatitis
Electroencephalogram: For slow-wave activity indicative of encephalopathy
What is the management of Alcoholic hepatitis?
Acute:
- Thiamine, Vitamin C and other multivitamins (initially parenterally)
- Monitor and correct K+ , Mg2+ and glucose abnormalities
- Ensure adequate urine output
- Treat encephalopathy with oral lactulose and phosphate enemas
- Ascites is managed by diuretics (spironolactone with or without furosemide) or therapeutic paracentesis
- Glypressin and N-acetylcysteine for hepatorenal syndrome (treatment of bleeding oesophageal varices)
Nutrition:
-Nutritional support with oral or nasogastric feeding is important with increased caloric intake
-Protein restriction should be avoided unless the patient is encephalopathic
-Total enteral nutrition may also be considered as this improves mortality rate
Nutritional supplementation and vitamins (B group, thiamine, folic acid) should be started parenterally initially and then continued orally after
Steroid therapy: Meta-analyses show that steroids reduce short-term mortality for severe alcoholic hepatitis
What are the complications of Alcoholic hepatitis?
Acute liver decompensation
Hepatorenal syndrome (renal failure secondary to advanced liver disease)
Cirrhosis
What is the prognosis of Alcoholic hepatitis?
Mortality in first month is about 10%; 40% in first year
If alcohol intake continues, most progress to cirrhosis within 1–3 years
Prognostic scores:
-Maddreys discriminant function (MDF):
MDF= (bilirubin/17) + (prolongation of PT x 4.6)
If MDF > 32, this indicates >50% 30-day mortality
-Glasgow alcoholic hepatitis score (GAHS):
Age (years)
WCC (109/L)
Urea (mmol/L)
PT ratio
Bilirubin (mmol/L)
If GAHS> 9 from Day 1 to 9, this indicates >50% 30-day mortality
What is amyloidosis?
A (heterogenous) group of diseases characterised by extracellular deposition of amyloid fibrils
What are the two main subtypes of amyloidosis?
Type AA: serum Amyloid A protein
-non-familial secondary amyloidosis: inflammatory polyarthropathies account for 60% of cases
Type AL: immunoglobulin light chain amyloidosis (primary amyloidosis)
Which are the main 2 organs affected by amyloidosis?
Kidneys
Heart
What is the epidemiology of amyloidosis?
In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year, with around 60 new cases annually- RARE
What are the presenting symptoms of amyloidosis?
PMH of inflammatory conditions (RF) Chronic infections (RF) Positive FH (RF) Fatigue Weight loss Dyspnoea on exertion
What are the signs of amyloidosis on physical examination?
Jugular venous distension- high right-sided filling pressure
Lower extremity oedema (nephrotic syndrome)
Macroglossia- most specific finding for AL
Diffuse muscular weakness
Shoulder pad sign- psudeohypertrophy of amyloid
What are the appropriate investigations for amyloidosis?
1st line:
Serum/ urine immunofixation- presence of monoclonal protein
Immunoglobulin free light chain assay- diagnosing AL
Bone marrow biopsy- clonal plasma cells
Others:
Tissue biopsy, ECG (for conduction abnormalities)
What is an anal fissure?
A split in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding
What is the aetiology of anal fissures?
Passage of a hard stool bolus may precipitate an anal fissure (however, only a minority of patients are constipated at the onset of symptoms)
The fissure may begin during an episode of loose stool, or often occurs spontaneously with no obvious precipitating factor
*Opiate analgesia is associated with constipation and a subsequent increased incidence of anal fissure
What are the presenting symptoms of an anal fissure?
Pain on defecation 'Tearing' sensation on passing stool Fresh blood on stool or on wiping Anal spasm These symptoms are intermittent
What are the appropriate investigations for an anal fissure?
*Clinical diagnosis
Others:
-Anal manometry: in patients with resistant fissures: low resting pressure
-Anal ultrasound: patients with suspected anal sphincter deficits
What is the management for anal fissures?
- Conservative measures: consisting of a
- High-fibre diet
- Increased fluid intake
- Sitz baths (warm-water bath covering the hips and buttocks)
- Stool softeners and analgesics (more severe cases)
Additional treatment:
- Topical nitrates or calcium channel blockers
- Treatment with diltiazem - because of dose-limiting headaches following topical nitrates
- Topical treatment must be continued for 6 to 8 weeks to allow re-epithelialisation of the fissure- otherwise early relapse
If a fissure is resistant to topical treatments, diagnosis of primary idiopathic fissure should be confirmed
What is the management for anal fissures?
- Conservative measures: consisting of a
- High-fibre diet
- Increased fluid intake
- Sitz baths (warm-water bath covering the hips and buttocks)
- Stool softeners and analgesics (more severe cases)
Additional treatment:
- Topical nitrates or calcium channel blockers
- Treatment with diltiazem - because of dose-limiting headaches following topical nitrates
- Topical treatment must be continued for 6 to 8 weeks to allow re-epithelialisation of the fissure- otherwise early relapse
If a fissure is resistant to topical treatments, diagnosis of primary idiopathic fissure should be confirmed, treatment is surgery
What are the complications of an anal fissure?
Chronic anal fissures: while many acute anal fissures spontaneously heal, a proportion will become chronic if left untreated
Recurrence: most likely if a patient stops treatment too early
Incontinence after surgery
What is the prognosis for anal fissures?
Approximately 60% of patients will achieve healing of their fissure at 6 to 8 weeks
A further 20% will heal after a course of topical diltiazem Some of these patients may subsequently relapse and may require a surgical option
What is Appendicectomy?
The removal of the appendix either laparoscopically (mainly) or open surgery with general anaesthesia
What are the indications for an Appendicectomy?
Appendicitis: indicated in all cases of suspected nonperforated appendicitis
Carcinoid tumors are the most common malignancy of the appendix; most of these are small (<1 cm)
What are the possible complications of an Appendicectomy?
Wound infection- prophylactic antibiotics may be given
Haematoma
Scarring
Abscess
Hernia – at the site of incision
Bowel obstruction
*Laparascopic appendectomy has been shown to decrease the incidence of overall complications
What is Appendicitis?
An acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix
What is the aetiology of Appendicitis?
Obstruction of the lumen of the appendix is the main cause of acute appendicitis
Faecolith (a hard mass of faecal matter),normal stool or lymphoid hyperplasia are the main causes for obstruction
What are the risk factors for Appendicitis?
WEAK
Smoking
<6 months of breastfeeding
Low dietary fibre
What is the epidemiology of Appendicitis?
One of the most common acute surgical abdominal emergencies
May occur at any age but is most commonly seen in early teens to late 40s
Slight predominance for males however females have a greater risk for an appendectomy
What are the presenting symptoms of Appendicitis?
Abdominal pain: -Initially epigastric -Later right iliac fossa Nausea and vomiting Fever
What are the signs of Appendicitis on physical examination?
Diminished bowel sounds
Fever
Tachycardia
*Rovsing’s sign: Pressing the left side of the abdominal cavity elicits pain in right lower quadrant
*Psoas sign: Extending the right thigh on left lateral position elicits pain in right lower quadrant
*Obturator sign: Pain is elicited in the right lower quadrant of abdomen by internal rotation of the flexed right thigh
What are the appropriate investigations for Appendicitis?
Bloods: *FBC (mild leukocytosis), high discriminatory power when combined with history
*Abdominal and pelvic CT scan:
-Abnormal appendix (diameter >6 mm) identified or calcified appendicolith seen in association with peri-appendiceal inflammation, fat stranding
-Wall thickening, wall enhancement, and inflammatory changes in the surrounding tissues are additional findings
Urinary pregnancy test: if positive, the possibility of ectopic pregnancy should be considered
Others:
- Abdominal ultrasound: aperistaltic (Absence of peristalsis) or non-compressible structure with outer diameter >6 mm, fluid collection if perforated, fat stranding, appendicolith -preferred in children
- Urinalysis: if abnormal could suggest renal colic or UTI cause
- Abdominal and pelvic MRI in pregnancy: In pregnant women presenting with features of appendicitis, an abdominal sonogram should be performed to identify the appendix: abnormal appendix (diameter >6 mm)
What is the management for Appendicitis?
Uncomplicated presentation:
- Once the diagnosis is made, patients should be nil by mouth
- IV fluids, such as lactated Ringer’s solution, should be started
- Use of prophylactic intravenous broad-spectrum antibiotic such as cefoxitin is recommended for uncomplicated appendicitis to reduce the risk of wound infection
- Prompt appendectomy remains the treatment of choice
Complicated presentation: occur in 4% to 6% of patients and include gangrene with subsequent perforation or intra-abdominal abscess
- IV fluids, such as lactated Ringer’s solution, should be started
- Antibiotics should be started immediately: e.g. cefoxitin and should be continued until patient becomes afebrile and the leukocytosis is corrected
- Interval appendectomy is performed after 6 weeks if the symptoms are not completely resolved
What are the complications of Appendicitis?
Perforation
generalised peritonitis
Appendicular mass (usually due to delay in medical treatment)
Appendicular abscess: usually occurs as a progression of the disease process, particularly after perforation
Surgical wound infection
What is the prognosis of Appendicitis?
If patients are treated in a timely fashion, the prognosis is good
Wound infection and intra-abdominal abscess are potential complications associated with appendectomy
Laparascopic appendectomy has been shown to decrease the incidence of overall complications
What is Autoimmune Hepatitis?
A chronic inflammatory disease of the liver of unknown aetiology, characterized by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies
What is the aetiology of Autoimmune Hepatitis?
In a genetically predisposed individual, an environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens which then become the focus of a principally T-cell-mediated autoimmune attack
The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis
What is the epidemiology of Autoimmune Hepatitis?
Type 1 autoimmune hepatitis occurs in all age groups (although mainly in young women)
Type 2 is generally a disease of girls and young women.
Type 1 is the most common form
What are the two types of Autoimmune Hepatitis?
Type I (classic): ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA) Type 2: Antibodies to liver/kidney microsomes (ALKM-1, directed at an epitope of CYP2D6), antibodies to a liver cytosol antigen (ALC-1)
What are the environmental factors that can cause Autoimmune Hepatitis in a genetically predisposed individual?
Measles Hepatitis viruses (A,C and D) Cytomegalovirus Epstein-Barr virus Drugs such as methyldopa, atorvastatin, interferon and infliximab
What are the presenting symptoms of Autoimmune Hepatitis?
Fatigue/malaise Anorexia Abdominal discomfort Pruritus Arthralgia Nausea Fever
What are the signs of Autoimmune Hepatitis on physical examination?
Hepatomegaly
Jaundice
Abdominal discomfort
Spider angioma: dilation of vessels below the skin: central, red spot and reddish extensions which radiate outward like a spider’s web
What are the appropriate investigations for Autoimmune Hepatitis?
*Liver function tests:
-Aspartate transaminase (AST): 200 to 300 international units/L (indicator of inflammation)
-Alanine transaminase (ALT): 200 to 300 international units/L (indicator of inflammation)
-Bilirubin: mildly to moderately increased
-GGT: mildly to moderately increased
-Alkaline phosphatase: mildly to moderately increased
-Serum albumin: decreased
-Prothrombin time: prolonged
Others:
-Anti-nuclear antibodies (TYPE 1)
-Smooth muscles antibodies (TYPE 1)
-Other antibodies
-Abdominal ultrasound: if extra-hepatic biliary obstruction is suspected
*-Liver biopsy: Essential to establish the diagnosis, evaluate disease severity, and determine the need for treatment: plasma cell infiltration
*When GGT and Alk Phosphate are markedly increased: bile duct injury should be suspected
What raises GGT levels (LFT)?
Alcohol abuse, intra-hepatic or extra-hepatic cholestasis and biliary obstruction, hepatocellular disease of other origin, and hepatic malignancies
What raises Alkaline phosphatase levels (LFT)?
Intra-hepatic or extra-hepatic cholestasis, hepatocellular disease of other origin, and some bone diseases
What decreases albumin level (LFT)?
Reduced in most forms of chronic liver disease, particularly cirrhosis.
Decreased also in nephrotic syndrome, malnutrition and malabsorption, chronic infection, and loss from bloodstream (haemorrhage, burns, exudates) or gastrointestinal tract (protein-losing enteropathies)
What is Barrett’s oesophagus?
A change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia
-associated with gastro-oesophageal reflux, even if the reflux is asymptomatic
What is the aetiology of Barrett’s oesophagus?
The primary aetiological factor involved in Barrett’s oesophagus is gastro-oesophageal reflux
Combined acid and bile reflux are the primary causative agents
What are the risk factors for Barrett’s oesophagus?
Acid/bile reflux or GORD Increased age White ethnicity Male sex FH Obesity Smoking
What is the epidemiology of Barrett’s oesophagus?
Between 0.5% and 2.0% of the general population due to the increased prevalence of GORD
Becomes more prevalent with age and Men and white people seem to have a higher prevalence
What are the presenting symptoms/signs of Barrett’s oesophagus?
Heartburn Nausea Regurgitation: expulsion of material from the pharynx, or oesophagus Chest pain Dysphagia: difficulty swallowing
What are the appropriate investigations for Barrett’s oesophagus?
**Oesophago-gastroduodenoscopy (OGD): abnormal epithelium characteristic of Barrett’s oesophagus proximal to the gastro-oesophageal junction (includes biopsy for histology)
Others:
-Barium oesophagogram: Cannot diagnose Barrett’s oesophagus but can evaluate for a mass lesion or stricture before endoscopy
-Chromoendoscopy: staining
What is the management for Barrett’s oesophagus?
Non-dysplastic Barrett’s oesophagus:
- Proton-pump inhibitors and surveillance: reduce acid exposure of the distal oesophagus
- Anti-reflux surgery: such as laparoscopic Nissen fundoplication, eliminate acid and bile reflux in more than 90% of patients
- Recommend AGAINST radiofrequency ablation (RFA)
Barrett’s oesophagus with low-grade dysplasia:
- Endoscopic eradication therapies such as RFA
- *Endoscopic mucosal resection (EMR) is the optimal diagnostic and therapeutic technique when mucosal nodularity is discovered
Barrett’s oesophagus with high-grade dysplasia:
High risk of adenocarcinoma!
-Endoscopic mucosal resection
-Endoscopic sub-mucosal dissection
-radiofrequency ablation (RFA) BEST OPTION*
OR: Oesophagectomy is a definitive treatment option, related to significant procedure-related mortality and long-term morbidity
What are the complications of Barrett’s oesophagus?
Oesophageal stricture (abnormal narrowing )
Affect on quality of life
Dysplasia and adenocarcinoma
What is the prognosis for Barrett’s oesophagus?
Patients are at a greater risk of developing adenocarcinoma
Proton-pump inhibitor treatment does not lead to regression of Barrett’s oesophagus but anti-reflux surgery and surgery lowers the risk for progression to adenocarcinoma
What are cholangiocarcinomas?
Cancers arising from the bile duct epithelium. These can be divided depending on their location in the biliary tree:
intrahepatic or extrahepatic (perihilar and distal)
What is the aetiology of cholangiocarcinomas?
There is a close association between infection, inflammation, and malignancy
What are the risk factors for cholangiocarcinomas?
Age > 50 years
Cholangitis
Choledocholithiasis (gall stones)
Structural disorders of the biliary tract e.g. bile duct adenoma
Ulcerative colitis
Primary sclerosis cholangitis (high association with UC)
Non-specific cirrhosis, alcoholic liver disease
HIV
Hepatitis B and C
What is the epidemiology of cholangiocarcinomas?
Slight male predominance
Approximately 2/3rds of cholangiocarcinomas occur in patients between 50 and 70 years of age
Highest rates in Thailand and South American Countries
What are the presenting symptoms of cholangiocarcinomas?
Painless jaundice (90% of patients) Others which are less common: -Weight loss -Abdominal pain -Itchiness -Dark urine and pale stools (obstructive jaundice)
What are the signs of cholangiocarcinomas on physical examination?
Jaundice
Triad of: fever, jaundice and right upper quadrant pain (acute cholangitis- 10% of patients)
Palpable gallbladder (RARE)
Hepatomegaly (RARE)
What are the appropriate investigations for cholangiocarcinomas?
Bloods:
-Serum bilirubin: Conjugated bilirubin is elevated in obstructive jaundice
-Serum alkaline phosphate: Suggests obstructive (or cholestatic) pattern of elevated LFTs, along with GGT, AST and ALT
-Serum prothrombin time: increased in prolonged obstruction of the common bile or hepatic duct
Tumour marker: Ca 19-9- elevated in up to 85% of patients with cholangiocarcinoma
Imaging:
-Abdominal ultrasound: intrahepatic cholangiocarcinoma may be seen as a mass lesion
-Abdominal CT: intrahepatic mass lesion, dilated intrahepatic ducts, and localised lymphadenopathy
-Abdominal MRI/angiography: staging tool/extent of tumour
-*ERCP (Endoscopic Retrograde Cholangiopancreatography) : a filling defect or area of narrowing will be seen if a tumour is present- INVASIVE
Others:
MRCP (extent of duct involvement)
Percuatneous transhepatic cathertisation (invasive procedure that is used when the tumour causes complete obstruction of the biliary tree)
What is a Cholecystectomy?
The surgical removal of the gallbladder
What are the indications for a Cholecystectomy?
Gallbladder trauma
Cholangiocarcinoma
Acute cholecystitis
Cholelithiasis- gallstones
What are the complications of a Cholecystectomy?
Bile leak
Bleeding
Infection
Injury to nearby structures, specifically bile duct injury. Also liver and small intestine
Greater risk of DVT
Risks from general anaesthetic: allergic reaction, death
Post-cholecystectomy syndrome: thought to be due to bile leaking into areas such as the stomach, or by gallstones being left in the bile ducts
-tummy pain
-indigestion
-diarrhoea
-yellowing of the eyes and skin (jaundice)
-high temperature (fever) of 38C or above
What is Cholecystitis?
Acute gallbladder inflammation, and one of the major complications of cholelithiasis or gallstones
What is the aetiology of Cholecystitis?
At least 90% of patients have gallstones:
- It develops in up to 10% of patients with symptomatic gallstones.
- In most cases it is caused by complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct, which leads to inflammation within the gallbladder wall
In 5% of cases, acute cholecystitis occurs in the absence of gallstones, causing an acalculous cholecystitis. Predisposing factors are:
-Starvation
-Total parenteral nutrition
-Narcotic analgesics
-Immobility
This leads to bile inspissation (due to dehydration) or bile stasis (due to trauma or severe systemic illness) which can block the cystic duct
What is the epidemiology of Cholecystitis?
The distribution and incidence of acute cholecystitis follow that of cholelithiasis because of the close relationship between the two
- Cholelithiasis occurs in approximately 15% of adults
- It is 3X more common in women than in men up to the age of 50 years, and is about 1.5 X more common in women than in men thereafter
What are the presenting symptoms of Cholecystitis?
Pina in the upper right quadrant Fever/rigors Nausea Right shoulder pain (referred pain) Anorexia (associated with biliary disease)
What are the signs of Cholecystitis on physical examination?
Tenderness in the right upper quadrant
Palpable mass: distended, tender gallbladder may be palpable as a distinct mass
Signs of infection: unwell, tachycardia, fever
What are the appropriate investigations for Cholecystitis?
If sepsis is suspected: CT or MRI of the abdomen:
- Irregular thickening of the gallbladder wall
- Poor contrast enhancement of the gallbladder wall (interrupted rim sign)
- Increased density of fatty tissue around the gallbladder
- Gas in the gallbladder lumen or wall
- Membranous structures within the lumen (intraluminal flap or intraluminal membrane)
- Peri‐gallbladder abscess
- If sepsis is not suspected: Abdominal ultrasound (first line for suspected gallstones)
- Pericholecystic fluid
- Distended gallbladder
- Thickened gallbladder wall (>3 mm)
- Gallstones
- Positive sonographic Murphy’s sign
Bloods:
- FBC: WCC
- CRP: inflammation
- Bilirubin: elevated may indicate acute focal cholestasis in adjacent liver tissue or due to common bile duct stones
- LFTs: if raised may indicate whether further imaging is required, such as MRCP
- Serum lipase/amylase: exclude acute pancreatitis
- Blood cultures/ bile cultures: infective organism suspected
Others:
- Magnetic resonance cholangiopancreatography (MRCP): if ultrasound has not detected common bile duct stones but the bile duct is dilated and/or liver function test results are abnormal
- Endoscopic ultrasound: May detect stones not identified by MRCP or abdominal ultrasound
What is a positive Murphy’s sign?
Firmly placing a hand at the costal margin in the right upper abdominal quadrant and asking the patient to breathe deeply
If the gallbladder is inflamed, the patient will experience pain and catch their breath as the gallbladder descends and contacts the palpating hand
A similar manoeuvre in the left upper quadrant should not elicit discomfort
What is the management for Cholecystitis?
Initial treatment: analgesia, fluid resuscitation, and antibiotics (if infection is suspected)
Arrange urgent laparoscopic cholecystectomy (surgery within 72 hours of onset is preferable)
What are the possible complications of Cholecystitis?
- Gangrenous cholecystitis: Associated inflammation leads to ischaemic necrosis of the wall
- Perforation of the gallbladder (10%)
- Suppurative cholecystitis: Thickened gallbladder wall with white cell infiltration, intra-wall abscesses, and necrosis -may result in perforation of the gallbladder and a pericholecystic abscess formation
- Bile duct injury due to surgery
- Gallstone ileus: gallstone passing from the biliary tract into the intestinal tract (through a fistula), leading to small-intestinal obstruction. Treatment is with enterotomy and stone extraction
- Cholecystoenteric fistulas: Decompression of the gallbladder because of a fistula may cause resolution of the acute cholecystitis (common sites duodenum and the hepatic flexure of the colon)
What is the prognosis of Cholecystitis?
Removing the gallbladder and the contained gallstones when biliary pain starts will prevent further biliary attacks and reduce the risk of developing cholecystitis
If the gallbladder perforates, mortality is 30%
*Untreated acute acalculous cholecystitis is life-threatening and is associated with up to 50% mortality
What is Cirrhosis?
End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes
Decompensated when there are complications such as ascites, jaundice, encephalopathy or GI bleeding
What is the aetiology of Cirrhosis?
Cirrhosis can derive from any chronic liver disease:
-Chronic alcohol misuse: Most common UK cause
-Chronic viral hepatitis: Hepatitis B/C are the most common causes worldwide
-Non-alcoholic fatty liver disease (NAFLD and associated steatohepatitis): associated with obesity, diabetes, total parenteral nutrition
-Chronic biliary diseases: Primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), biliary atresia (condition in infants in which the bile ducts outside and inside the liver are scarred and blocked)
-Autoimmune hepatitis
Drugs: e.g. methotrexate, hepatotoxic drugs
Inherited: a1-Antitrypsin deficiency, haemochromatosis, Wilsons disease, galactosaemia, cystic fibrosis
Vascular: Budd–Chiari syndrome (occlusion of the hepatic veins that drain the liver) or hepatic venous congestion.
What is the triad in Budd–Chiari syndrome?
Abdominal pain, ascites, and liver enlargement
What is the epidemiology of Cirrhosis?
Among the top 10 leading cause of deaths worldwide, liver disease is the third biggest cause of premature mortality in the UK
What are the precipitating factors of Decompensation?
Infection GI bleeding Constipation High-protein meal Electrolyte imbalances Alcohol and drugs Tumour development Portal vein thrombosis
What are the presenting symptoms of Cirrhosis?
Early non-specific symptoms: -Anorexia -Nausea -Fatigue -Weakness -Weight loss Symptoms caused by reduced liver synthetic function: -Easy bruising -Abdominal swelling -Ankle oedema Reduced detoxification function: -Jaundice -Personality change -Altered sleep pattern -Amenorrhoea Portal hypertension: -Abdominal swelling -Haematemesis -PR bleeding or melaena
What are the signs of Cirrhosis on physical examination?
Stigmata of chronic liver disease: Asterixis (liver flap) Bruises Clubbing Dupuytrens contracture Erythema (palmar) Others: -Jaundice -Gynaecomastia, -Leukonychia (hypoalbuminaemia) -Parotid enlargement -Spider naevi -Scratch marks (due to pruritus) -Ascites (shifting dullness and fluid thrill) -Enlarged liver (shrunken and small in later stage) -Testicular atrophy -Caput medusae (dilated superficial abdominal veins) -Splenomegaly (indicating portal hypertension)
What are the appropriate investigations for Cirrhosis?
- LFTs:
- Deranged
- AST and ALT levels increase with hepatocellular damage
- Raised AlkPhos, GGT and bilirubin
- Reduced Albumin (marker of hepatic synthetic dysfunction)
- Clotting: Prolonged PT (reduced synthesis of clotting factors)
- Serum alpha-fetoprotein (AFP): elevated in chronic liver disease, but high levels may suggest hepatocellular carcinoma*
- FBC: low Hb, low platelets as a result of hypersplenism
Others (to investigate cause):
- Viral serology (HBsAg, HBsAb, HCV ab)
- a1-antitrypsin (155 of patients can develop cirrhosis)
- caeruloplasmin (Wilsons disease)
- Iron studies: serum ferritin, iron, total iron binding capacity (haemochromatosis)
- Anti-mitochondrial antibody (PBC)
- Anti-nuclear antibodies (ANA), SMA (autoimmune hepatitis)
- Liver biopsy: architectural distortion of the liver parenchyma with formation of regenerative nodules (not always necessary)
Imaging:
- Abdominal ultrasound/CT: COMPLICATIONS: liver surface nodularity, small liver, possible hypertrophy of left/caudate lobe, ascites, splenomegaly, increased diameter of the portal vein (≥13 mm), or collateral vessels
- OGD: presence of gastro-oesophageal varices or portal hypertensive gastropathy secondary to portal hypertension
What is the management for Cirrhosis?
Treat the cause if possible such as such as hepatitis B and C virus infections
Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
Nutrition is very important and if intake is poor, dietitian review and enteral supplements should be given; nasogastric feeding may be indicated
Treatment of the complications
*Liver transplantation is the only curative measure
What are the possible complications of Cirrhosis and their management?
Encephalopathy:
-Treat infections
-Exclude a GI bleed
-Lactulose, phosphate enemas and avoid sedation
Portal Hypertension-Ascites:
-Diuretics (spironolactone/furosemide)
-Dietary sodium restriction (88meq or 2g/day),
-Therapeutic paracentesis (with human albumin replacement IV)
-Monitor weight daily
-Fluid restriction in patients with plasma sodium <120mmol/L
-Avoid alcohol and NSAIDs.
Spontaneous bacterial peritonitis:
-Antibiotic treatment (e.g. cefuroxime and metronidazole), prophylaxis against recurrent SBP with ciprofloxacin
Surgical:
-Consider insertion of TIPS to relieve portal hypertension (if recurrent variceal bleeds or diuretic-resistant ascites) although it may precipitate encephalopathy
Other complications include: Hepatocellular carcinoma, Renal failure (hepatorenal syndrome), Pulmonary hypertension (hepatopulmonary syndrome)
What is the prognosis of Cirrhosis?
Depends on the aetiology and complications
Generally poor; overall 5-year survival is 50%
In the presence of ascites, 2-year survival of 50%
What is Coeliac disease?
Inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption
What is the aetiology of Coeliac disease?
Systemic autoimmune disorder triggered by gluten peptides from grains including wheat, rye, and barley
Almost all people with coeliac disease carry one of two major histocompatibility complex class-II molecules (HLA-DQ2 or -DQ8) that are required to present gluten peptides in a manner that activates an antigen-specific T cell response
FH of coeliac disease is a RF as is PMH of autoimmune diseases such as TYPE 1 DM, autoimmune thyroid disease, IBD (UC and Crohn’s disease)
What is the epidemiology of Coeliac disease?
Coeliac disease is a common disorder in the US and in Europe
Women are slightly more likely to be affected (2/3)
Can present at any age
What are the presenting symptoms of Coeliac disease?
May be asymptomatic
Abdominal discomfort, pain and distention (bloating)
Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away)
Diarrhoea
Tiredness, malaise, weight loss (despite normal diet)
Failure to thrive in children, amenorrhoea in young adults
What are the signs of Coeliac disease on physical examination?
Signs of anaemia: Pallor
Signs of malnutrition: Short stature, abdominal distension (bloating) and wasted buttocks in children
Triceps skinfold thickness gives an indication of fat stores
Signs of vitamin or mineral deficiencies (e.g. osteomalacia, easy bruising)
Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)-UNCOMMON
What are the appropriate investigations for Coeliac disease?
FBC and blood smear: -Iron deficiency (microcytic) anaemia is the most common clinical presentation in adults -Folate (and rarely vitamin B12) deficiency may lead to a macrocytic anaemia *Immunoglobulin A- tissue transglutaminase (IgA-tTG): titre above normal range for laboratory Endomysial antibody (EMA): more expensive alternative to IgA-tTG Skin biopsy: patient with skin lesions suggestive of dermatitis herpetiformis: granular deposits of IgA IgG DGP or IgA/IgG DGP (deamidated gliadin peptide): test of choice for patients with IgA deficiency (common,1 in 50 with coeliac disease) Small bowel endoscopy and biopsy: -Direct visualization shows villous atrophy in the small intestine (particularly the jejunum and ileum) giving the mucosa a flat smooth appearance -Biopsy shows villous atrophy with crypt hyperplasia of the duodenum -The epithelium adopts a cuboidal appearance, and there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria
What is the management of Coeliac disease?
Advice:
-Strict lifelong gluten-free diet with avoidance of all wheat, rye and barley products
-Education and expert dietary advice is essential- the Coeliac Society offers patient support and advice
Medical:
-Vitamin and mineral supplements
-Oral corticosteroids may be used if the disease does not subside with gluten withdrawal
What are the complications of Coeliac disease?
Iron, folate and Vitamin B12 deficiency Osteomalacia Ulcerative jejunoileitis Gastrointestinal lymphoma (particularly T cell) Bacterial overgrowth Rarely, can cause cerebellar ataxia
What is the prognosis of Coeliac disease?
With strict adherence to gluten-free diet, most patients make a full recovery
Symptoms usually resolve within weeks but histological changes may take longer to resolve
A gluten-free diet needs to be followed for life
What is Colonoscopy?
A procedure that uses a long, narrow, flexible, telescopic camera called a colonoscope to look at the lining of your large bowel
What are the indications for a Colonoscopy?
Lower GI bleeding Screening and surveillance of colorectal polyps and cancers: -Colon cancer -Surveillance after polypectomy -Colorectal cancer post-resection surveillance -Inflammatory bowel diseases Acute and chronic diarrhoea Therapeutic indications for colonoscopy: -Excision and ablation of lesions -Treatment of lower GI bleeding -Colonic decompression -Dilation of colonic stenosis -Foreign body removal Miscellaneous indications: -Abnormal radiological examinations -Isolated unexplained abdominal pain -Chronic constipation -Preoperative and intraoperative localization of colonic lesions
What are the possible complications for a Colonoscopy?
Intestinal perforations
Bleeding
Adverse reaction to anaesthetic
Infection
What is colorectal cancer?
Malignancy of the large bowel - the majority of colorectal cancers are adenocarcinomas derived from epithelial cells
What is the aetiology of colorectal cancer?
Colorectal cancer represents a complex interaction of genetic and environmental factors:
Genetic: next to age, FH is the most common risk factor
*Family cancer syndromes: familial adenomatous polyposis (FAP) and Lynch syndrome
Environmental: Obesity, high energy intake, and physical inactivity are synergistic risk factors (low fibre diet)
Also: inflammatory bowel disease, acromegaly
What is the epidemiology of colorectal cancer?
Second most common cause of cancer death in the West
Average age at diagnosis 60–65 years.
What are the presenting symptoms of colorectal cancer?
Left-sided colon and rectum:
- Change in bowel habit (increased frequency, looser stools)
- Rectal bleeding or blood/mucous mixed in with stools
- Rectal masses may also present as tenesmus (sensation of incomplete emptying after defecation)
Right-sided colon:
-Later presentation, with symptoms of anaemia, weight loss and non- specific malaise or, more rarely, lower abdominal pain
Up to 20% of tumours will present as an emergency with pain and distension caused by large bowel obstruction, haemorrhage or peritonitis as a result of perforation
What are the signs of colorectal cancer on physical examination?
Anaemia may be only sign, particularly in right-sided lesions
Abdominal mass, low-lying rectal tumours may be palpable on rectal examination
Metastatic disease: Hepatomegaly, shifting dullness of ascites
What are the appropriate investigations for colorectal cancer?
Blood: FBC (for anaemia), LFT (often normal), tumour markers (CEA to monitor treatment response or disease recurrence)
Stool: Occult or frank blood in stool (screening test)
Endoscopy:
-Sigmoidoscopy, colonoscopy: may see ulcerating or exophytic (growing outward) mucosal lesion that may narrow the bowel lumen
-Allows visualization and biopsy. Polypectomy can also be performed if isolated small carcinoma in situ
Barium contrast studies: Apple core stricture on barium enema
Abdominal ultrasound scan for hepatic metastases
Other staging investigations include:
-CXR
-CT: colonic wall thickening, enlarged lymph nodes, liver metastases, ascites, lung secondaries
-MRI, endorectal ultrasound
What is Crohn’s disease?
Chronic granulomatous transmural inflammatory disease that can affect any part of the gastrointestinal tract
Grouped with ulcerative colitis and together they are known as inflammatory bowel disease
What is the aetiology of Crohn’s disease?
Cause has not yet been elucidated, but thought to involve an interplay between genetic and environmental factors
Inflammation can occur anywhere along GI tract (40% involving the terminal ileum) and skip lesions with inflamed segments of bowel interspersed with normal segments is not unusual
What is the epidemiology of Crohn’s disease?
Annual UK incidence is 5–8 in 100,000
Prevalence is 50–80 in 100,000
The peak age of onset is between 15 and 40 years, and there is a smaller second peak between 60 and 80 years (*teens or twenties)
CD is equally prevalent among men and women
What are the presenting symptoms of Crohn’s disease?
Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction)
Diarrhoea (may be bloody or steatorrhoea)
Fever, malaise, weight loss
Symptoms of complications
What are the presenting symptoms of Crohn’s disease?
Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction)
(Prolonged) Diarrhoea (may be bloody or steatorrhoea)
Fever, malaise, weight loss
Symptoms of complications
What are the signs of Crohn’s disease on physical examination?
Weight loss
Clubbing
Signs of anaemia (pallor)
Aphthous ulceration of the mouth
Perianal skin tags, fistulae and abscesses
Signs of complications (eye disease, joint disease, skin disease)
What are the appropriate investigations for Crohn’s disease?
Bloods:
-FBC: due to chronic inflammation: anaemia, leukocytosis, may be thrombocytosis- marker of active inflammation
-ESR/CRP: elevated
-Iron studies: normal, or may demonstrate changes consistent with iron deficiency (GI bleeding or malabsorption of iron)
-Serum B12/folate: may be low secondary to malabsorption
-Metabolic profile: hypoalbuminaemia, hypocholesterolaemia, hypocalcaemia due to chronic or severe disease
Stool microscopy and culture: To exclude infective colitis
Plain abdominal x-ray: small bowel or colonic dilation; calcification; sacroiliitis; intra-abdominal abscesses
CT abdomen: skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae
MRI/abdomen pelvis: superior to CT, used when contraindicated: same as CT findings
Others: (helpful in differentiating with UC)
-Colonoscopy with intubation of the ileum is the definitive test to diagnose CD: aphthous ulcers (painful, clearly defined, round shallow), hyperaemia, oedema, cobblestoning, discontinuous-skip lesions
-Tissue biopsy: confirmatory rather than diagnostic
-faecal calprotectin: elevated (proteins released into faeces when neutrophils gather at the site of any GI tract inflammation)
What are the histological findings for Crohn’s disease?
Significant inflammation in the colonic wall, widening of submucosa, and dense lymphoid aggregates in the submucosa
Cryptitis with morphological distortion of the crypts accompanied by inflammation and abundant lymphatic and plasma cells
Inflammation of deeper layers and presence of non-caseating granulomas
What is the long term management for Crohn’s disease?
Symptomatic treatment: managing diarrhoea, abdominal pain, and malabsorption
-Antidiarrhoeal agents should be avoided in patients with active colitis, given the risk of developing toxic megacolon
Medical therapy:
-Immunomodulators (azathioprine, mercaptopurine, methotrexate), reduce relapses- MYELOSUPPRESION, HEPATOOXICITY, LUNG FIBROSIS
-TNF-alpha inhibitors (infliximab- Biosimilars), effective agents in achieving and maintaining remission- RISK OF TB
-Severely active disease: Oral or intravenous corticosteroids and combination of immunomodulator therapy and TNF-alpha inhibitor therapy
Advice: Stop smoking, dietician referral. Education and advice (e.g. from inflammatory bowel disease nurse specialists)
Surgery:
- Indicated for failure of medical treatment, failure to thrive in children or the presence of complications
-This involves resection of affected bowel and stoma formation, although there is a risk of disease recurrence (due to discontinuous skip lesions)
What is the management for an acute exacerbation of Crohn’s disease?
Fluid resuscitation
IV or oral corticosteroids
Immunmodulators (azathioprine and methotrexate) may induce a remission in colonic Crohns disease
Analgesia
Elemental diet may induce remission (more often used in children)
Parenteral nutrition may be necessary
Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin)
Assess for complications
What are the complications of Crohn’s disease?
GI:
-Haemorrhage
-Bowel strictures
-Toxic megacolon (colon expands, dilates, and distends- high risk of rupture which is life threatening)
-Perforation
-Fistulae (between bowel, bladder, vagina)
-Perianal fistulae and abscess
-GI carcinoma (5% risk in 10 years)
-Malabsorption
Extraintestinal features:
-Uveitis
-Episcleritis
-Gallstones
-Kidney stones
-Arthropathy
-Sacroiliitis
-Ankylosing spondylitis
-Erythema nodosum
-Pyoderma gangrenosum: painful pustules or nodules become ulcers that progressively grow
-Amyloidosis
What is the prognosis for Crohn’s disease?
Chronic relapsing condition
Two-thirds will require surgery at some stage and two-thirds of these >1 surgical procedure
What is Diverticular disease?
The presence of outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel (diverticulosis) associated with complications, e.g. haemorrhage, infection, fistulae
What is Diverticulitis?
Acute inflammation and infection of colonic diverticulae
What is the aetiology of Diverticular disease?
Multi-factorial aetiology- both genetic and environmental factors are described as causative, especially a *low dietary fibre intake*, which in Western populations is deemed as the predominant contributing factor Other predisposing factors include: -Decreased physical activity -Obesity -Increased red meat consumption -Tobacco smoking -Excessive alcohol and caffeine intake -Steroids -Non-steroidal anti-inflammatory drugs
What is the pathogenesis of Diverticular disease?
- A low-fibre diet leads to loss of stool bulk
- Consequently, high colonic intraluminal pressures must be generated to propel the stool, leading to herniation of the mucosa and submucosa through the muscularis
- Proposed diverticular obstruction by inspissated faeces can lead to bacterial overgrowth, toxin production and mucosal injury and diverticulitis- perforation, abscess, ulceration and fistulation or stricture formation
- Diverticulae are most common in the sigmoid and descending colon but can be right sided
What is the epidemiology of Diverticular disease?
Common, 60% of people living in industrialized countries will develop colonic diverticula (can be difficult to determine because most patients are asymptomatic)
Rare < 40years
What are the presenting symptoms of Diverticular disease?
Often asymptomatic (80–90%)
Complications include:
-PR bleeding
-Diverticulitis: typically, left iliac fossa or lower abdominal pain
-Fever
-Diverticular fistulation into bladder: pneumaturia (passage of gas mixed with urine), faecaluria (presence of faeces in the urine) and recurrent UTI
What are the signs of Diverticular disease on physical examination?
Diverticulitis: -Tender abdomen -Signs of local or generalized peritonitis if perforation has occurred: Abdominal pain or tenderness Signs of ascites: flank dullness, shifting dullness, fluid wave, and auscultatory percussion Signs of sepsis may be present: -Hypothermia -Hypotension -Tachycardia
What are the appropriate investigations for Diverticular disease?
*FBC: Polymorphonuclear leukocytosis is present in acute diverticulitis (elevated CRP), cross match if bleeding
*CT abdomen: (imaging modality of choice), thickening of bowel wall, mass, abscess, streaky mesenteric fat; may show gas in the bladder in cases of fistula
Others:
-Abdominal x-ray: (considered when acute diverticulitis is suspected), pneumoperitoneum, ileus, soft tissue densities; free air in bowel perforation
-Abdominal USS: if CT cannot be obtained, signs of abscess, perforation, obstruction
-CXR: normal, or free air under diaphragm if perforation
-Contrast enema: (when initial acute symptoms have resolved to confirm diagnosis), diverticuli, abscess, perforation, obstruction, fistula
-Colonoscopy/Sigmoidoscopy: when diagnosis is unclear and malignancy is suspected Single, multiple, or scattered diverticula, with or without acute mucosal inflammation
-Blood culture: patients with suspected sepsis
-Angiogram/isotope labelled RBC nuclear scan: in acute bleeding
What is the management of Diverticular disease?
Asymptomatic:
-Soluble high-fibre diet (20–30 g/day)
GI bleed:
-PR bleeding is often managed conservatively with IV rehydration, antibiotics, blood transfusion if necessary. -Angiography and embolization or surgery if severe
Diverticulitis:
-Uncomplicated: low-residue diet and oral antibiotics
-Complicated: IV antibiotics and IV fluid rehydration and bowel rest, localised collections or abscesses may be treated by radiologically sited drains
Surgery: ‘Hartmanns procedure’
-Individual basis depending on age, frequency, and severity of recurrent symptoms, previous complications
(e.g. perforation and peritonitis) and presence of co-morbidities
-Surgical treatment can be by open or laparoscopic approaches:
**More recently, laparoscopic drainage, peritoneal lavage and drain placement can be effective
What are the complications of Diverticular disease?
Diverticulitis Pericolic abscess Perforation Faecal peritonitis Colonic obstruction Fistula formation (bladder, small intestine, vagina) Haemorrhage low risk: colorectal neoplasm
What is the prognosis for Diverticular disease?
Most patients with uncomplicated diverticulitis recover following medical treatment and do not require surgical intervention
Diverticular disease recurs in 1/3 of patients following response to medical treatment, mostly within 5 years- risk is higher in young patients and those with abscess formation at diagnosis
Recurrent disease is associated with high mortality
What is Endoscopic retrograde cholangiopancreatography (ERCP)?
A procedure that combines upper gastrointestinal (GI) endoscopy and x-rays to treat problems of the bile and pancreatic ducts
During an ERCP, stents can be inserted into the bile ducts, to allow drainage of bile into the intestine and biopsies can be taken
What are the indications for Endoscopic retrograde cholangiopancreatography (ERCP)?
When your bile or pancreatic ducts have become narrowed or blocked:
- Jaundice
- Choledocholithiasis (gallstones)
- Infection
- Acute/chronic pancreatitis
- Abnormal LFTs
- Trauma or surgical complications in your bile or pancreatic ducts
- Pancreatic pseudocysts
- Suspected malignancy of the bile ducts or pancreas
- More used as a treatment rather than diagnostic test as it is invasive (MRCP is preferred)
What are the possible complications of Endoscopic retrograde cholangiopancreatography (ERCP)?
Pancreatitis (most common)
Infection
Bleeding
Perforation
Prolonged pancreatic stenting is associated with stent occlusion, pancreatic duct obstruction and pseudocyst formation
What is Endoscopy?
A procedure to examine internal organs by placing an endoscope (camera) inside the body
What are the indications for Endoscopy?
Investigate symptoms such as:
-Dysphagia
-Abdominal pain that is persistent
-Frequent diarrhoea, or nausea and vomiting
-Unintentional weight loss
-Frequent heartburn or indigestion
-PR bleeding
More effective at identifying inflammation, ulcers, and tumours than other imaging techniques
Can also take biopsies and treat some conditions by surgical removal
What are the complications of Endoscopy?
Infection
Perforation/ bleeding
What are the different types of Endoscopy?
Gastroscopy Colonoscopy Bronchoscopy Hysteroscopy Cystoscopy Flexible sigmoidoscopy Endoscopic ultrasound Endoscopic retrograde cholangiopancreatography (ERCP)
What is Enteral feeding?
The administration of feed and/or fluid via a tube going into the gastrointestinal tract. Can also be used:
- To administer medication
- For gastric aspiration
- For gastric decompression
What is Parenteral feeding?
The administration of specialist nutritional products to a person intravenously, bypassing the usual process of eating and digestion (GI tract)
What are the indications for Feeding (enteral & parenteral)?
Stroke, which may impair ability to swallow
Malignancy which may cause fatigue, nausea, and vomiting that make it difficult to eat
Critical illness or injury, which reduces energy or ability to eat
Failure to thrive or inability to eat in young children or infants
Serious illness, which places the body in a state of stress, making it difficult to take in enough nutrients
Neurological or movement disorders that increase caloric requirements while making it more difficult to eat
GI dysfunction or disease
Parenteral feeding can be a life-saving option in many circumstances. However, it’s preferable to use enteral nutrition if at all possible
What are the possible complications of Feeding (enteral & parenteral)?
Aspiration
Refeeding syndrome, dangerous electrolyte imbalances that may occur in people who are very malnourished and start receiving enteral feeds
Infection of the tube or insertion site
Nausea and vomiting that may result from feeds that are too large or fast, or from slowed emptying of the stomach
Skin irritation at the tube insertion site
Diarrhoea due to a liquid diet or possibly medications
Tube dislodgement or blockage, which may occur if not flushed properly
What are the different types of Enteral Feeding?
Nasogastric tube (NGT) starts in the nose and ends in the stomach
Orogastric tube (OGT) starts in the mouth and ends in the stomach
Nasoenteric tube starts in the nose and ends in the intestines (subtypes include nasojejunal and nasoduodenal tubes)
Oroenteric tube starts in the mouth and ends in the intestines
Gastrostomy tube is placed through the skin of the abdomen straight to the stomach (subtypes include PEG, PRG, and button tubes)
Jejunostomy tube is placed through the skin of the abdomen straight into the intestines (subtypes include PEJ and PRJ tubes)
What is Functional dyspepsia?
A term to describe a symptom or a combination of symptoms where UGI endoscopy did not reveal a potential cause for the dyspepsia
(It is generally reserved for patients with a normal endoscopy whose symptoms do not suggest GORD)
What is the aetiology of Functional dyspepsia?
- Post-prandial distress syndrome (PDS), which is characterised by meal-induced dyspeptic symptoms, such as discomfort, pain, nausea, and fullness
- Epigastric pain syndrome (EPS), which refers to epigastric pain, or epigastric burning, that does not occur exclusively post-prandially, can occur during fasting, and can even be improved by meal ingestion
- Overlapping PDS and EPS, which is characterised by meal-induced dyspeptic symptoms and epigastric pain or burning
What is the epidemiology of Functional dyspepsia & irritable bowel syndrome (IBS)?
There is much overlap between functional dyspepsia and IBS
Patients who have both disorders have a substantially greater symptom burden and are more likely to consult a physician
Women who have experienced emotional or physical abuse appear to be particularly vulnerable to developing functional dyspepsia and irritable bowel syndrome (IBS)
What is Irritable bowel syndrome (IBS)?
A chronic condition characterised by abdominal pain associated with bowel dysfunction, the pain is often relieved by defecation and is sometimes accompanied by abdominal bloating
What is the aetiology of Irritable bowel syndrome (IBS)?
No specific endoscopic, biochemical, anatomic, microbiological, or histological findings in IBS that make the aetiology clear
Stress and emotional tension can frequently trigger bouts of IBS
What are the presenting symptoms/signs of Functional dyspepsia?
Epigastric pain or burning
Early satiety and post-prandial fullness
Belching
Bloating
Nausea
Discomfort in the upper abdomen
What are the presenting symptoms/signs of Irritable bowel syndrome (IBS)?
Abdominal discomfort
Altered bowel habits
Abdominal bloating or distension
Normal abdominal examination
What are the appropriate investigations for Functional dyspepsia & irritable bowel syndrome (IBS)?
Exclude other causes:
- FBC: normal, anaemia may suggest another cause
- Stool studies: normal
- Anti-endomysial antibodies/anti-tissue transglutaminase: if coeliac disease is suspected
- Plain abdominal x-ray: normal no abnormal bowel pattern to suggest obstruction
- Endoscopy: colonoscopy/sigmoidoscopy or gastroscopy are normal
What are gallstones?
Also known as cholelithiasis is the presence of solid concretions in the gallbladder
Gallstones form in the gallbladder but may exit into the bile ducts (choledocholithiasis)
What is biliary colic?
A dull pain in the middle to upper right quadrant of the abdomen and occurs when a gallstone blocks the bile duct
What is the aetiology of gallstones?
90% of gallstones are composed of cholesterol
Different types:
-Mixed stones: Contain cholesterol, calcium bilirubinate, phosphate and protein. Associated with older age, female, obesity, parenteral nutrition, drugs (OCP, octreotide), family history, ethnicity (e.g. Pima Indians), interruption of the enterohepatic recirculation of bile salts (e.g. Crohns disease), terminal ileal resection
-Pure cholesterol stones: Similar associations as mixed stones
-Approximately 2% of all gallstones are black pigment stones: Black stones made of calcium bilirubinate (elevated bilirubin secondary to haemolytic disorders, cirrhosis). Associated with haemolytic disorders (e.g. sickle cell, thalassemia, hereditary spherocytosis)
What is the epidemiology of gallstones?
Cholelithiasis occurs in approximately 10% to 15% of adults in the US and Europe
The highest prevalence of cholelithiasis arises in American Indian populations
Age, obesity, and female sex hormones are important aetiological factors
What are the presenting symptoms of gallstones?
Asymptomatic (90%): Found incidentally
Biliary colic:
-Sudden onset, severe RUQ or epigastric pain, constant in nature
-May radiate to right scapula, often precipitated by a fatty meal
-Can last hours, may be associated nausea and vomiting
Acute cholecystitis:
-Patient systemically unwell, fever, prolonged upper abdominal pain that may be referred to the right shoulder (due to diaphragmatic irritation)
Ascending cholangitis:
-Classical association between RUQ pain, jaundice and rigors/fever (Charcots triad)
-If combined with hypotension and confusion, it is known as Reynolds pentad
What are the signs of gallstones on physical examination?
Biliary colic:
-RUQ or epigastric tenderness: typically increases in intensity and lasts for several hours
Acute cholecystitis:
-Tachycardia
-Pyrexia
-Right upper quadrant or epigastric tenderness.
-There may be guarding with/without rebound
-*Murphys sign is elicited by placing a hand at the costal margin in the RUQ and asking the patient to breathe deeply, patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers
Ascending cholangitis:
-Pyrexia
-RUQ pain
-Jaundice
What are the appropriate investigations for gallstones?
Bloods:
-FBC: elevated WBC in cholecystitis or cholangitis
-LFTs: Normal in cholelithiasis, Elevated alkaline phosphatase (suggests obstruction of the cystic or bile duct) and elevated bilirubin in choledocholithiasis
-Serum lipase and amylase: elevated (>3 times upper limit of normal) in acute pancreatitis
-*Abdominal ultrasound: *best single diagnostic test for cholelithiasis:
=cholelithiasis: stones in the gallbladder =choledocholithiasis: stones in the bile duct with or without bile duct dilation
=assess increased thickness of gallbladder wall
Others:for suspected choledocholithiasis that is not confirmed by abdominal ultrasound:
-MRCP
-Endoscopic USS
-ERCP: preferred intervention for patients with high risk of bile duct stones (positive imaging, symptoms, and/or blood tests) as it offers both diagnosis and therapy, removing the stones
-Abdominal CT: can be used to investigate suspected ascending cholangitis or gallstone pancreatitis
What is the management of gallstones?
Asymptomatic cholelithiasis does not require any treatment (advice: avoidance of fat in diet)
Laparoscopic cholecystectomy is the procedure of choice for symptomatic cholelithiasis
For Choledocholithiasis:
1. ERCP stone extraction
2. Following this cholecystectomy represents definitive treatment to reduce the risk of recurrent biliary events, in particular cholangitis or pancreatitis
For most patients with simultaneous gallbladder and bile duct stones, early laparoscopic cholecystectomy should generally follow within 72 hours after ERCP and stone extraction
What is the management of severe biliary colic?
Admission, IV fluids, analgesia, antiemetics and antibiotics if there are signs of infection (cholecystitis or cholangitis)
If symptoms fail to improve or worsen, a localized abscess or empyema should be suspected
This can be drained percutaneously by cholecystostomy and pigtail catheter
If there is evidence of obstruction, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram
What are the complications of gallstones?
Stones within gallbladder:
-Biliary colic, cholecystitis, mucocoele or gallbladder empyema, porcelain gallbladder, predisposition to gallbladder cancer (rare)
Stones outside gallbladder:
-Obstructive jaundice, pancreatitis, ascending cholangitis, perforation and pericholecystic abscess or bile peritonitis, cholecystenteric fistula, gallstone ileus
-Mirizzi syndrome: large gallstone can become lodged in the cystic duct and compress or damage the common hepatic duct, resulting in biliary obstruction and jaundice
Surgical complications:
-ERCP associated pancreatitis
-Cholecystectomy: Bleeding, infection, bile leak, bile duct injury (0.3% laparoscopic, 0.2% open), post-cholecystectomy syndrome (persistent dyspeptic symptoms), port-site hernias
What is the prognosis for gallstones?
In most cases gallstones are (asymptomatic) benign and do not cause significant problems
If they become symptomatic, surgery is an effective treatment
Risk factors for recurrent choledochal problems are common: bile duct dilatation to >15mm, gallbladder being left intact, diverticulum, brown pigmented stones
What is gastric cancer?
A neoplasm that can develop in any portion of the stomach and may spread to the lymph nodes and other organs, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma
What is the aetiology of gastric cancer?
Most cases are probably caused by environmental insults in genetically predisposed individuals that lead to mutation and subsequent unregulated cell growth
Risk factors include:
-Helicobacter pylori infection
-Atrophic gastritis
-Diet high in smoked, processed foods and nitrosamines
-Smoking
-Alcohol
What is the epidemiology of gastric cancer?
Common cause of cancer death worldwide, with highest incidence in Asia, especially Japan
Sixth most common cancer in UK (annual incidence is 15 in 100000)
M: W is 2:1
Age>50 years
*Cancer of the antrum/body is becoming less common, while that of the cardia and gastro- oesophageal junction is increasing
What are the presenting symptoms of gastric cancer?
In the early phases, it is often asymptomatic
Early satiety or epigastric discomfort
Weight loss, anorexia, nausea and vomiting
Haematemesis, melaena, symptoms of anaemia
Dysphagia (tumours of the cardia)
Symptoms of metastases, particularly abdominal swelling (ascites) or jaundice (liver involvement)
What are the signs of gastric cancer on physical examination?
Physical examination may be normal Epigastric mass Abdominal tenderness Ascites Signs of anaemia Many eponymous signs: **Virchows node/Troisiers sign: Lymphadenopathy in left supraclavicular fossa Sister Mary Joseph node: Metastatic nodule on umbilicus Krukenbergs tumour: Ovarian metastases
What are the appropriate investigations for gastric cancer?
*Upper gastrointestinal endoscopy with biopsy: ulcer or mass or mucosal changes
Bloods: FBC (for anaemia), LFT
CT/MRI: Staging of tumour and planning of surgery (metastatic lesions)
Ultrasound of liver: Staging of tumour (metastatic lesions)
Bone scan: Staging of tumour (metastatic lesions)
Endoscopic ultrasound: Assesses depth of invasion and lymph node spread (determines clinical tumour (T) and node (N) stage)
Laparoscopy: May be needed to determine if tumour is resectable
What is Gastro-oesophageal reflux disease (GORD)?
Inflammation of the oesophagus caused by reflux of gastric acid and/or bile
What is the aetiology of Gastro-oesophageal reflux disease (GORD)?
The lower oesophageal sphincter (LOS) regulates food passage from the oesophagus to the stomach and contains both intrinsic smooth muscle and skeletal muscle
Episodes of transient lower oesophageal sphincter relaxation are a normal phenomenon, but they occur *more frequently in GORD, causing reflux of gastric contents into the oesophagus
It is more likely to occur if there is a hiatal sac containing acid- Patients with severe reflux often have a hiatus hernia and decreased resting lower oesophageal sphincter pressure (can have high/moderate pressure too)
FH link
What is the epidemiology of Gastro-oesophageal reflux disease (GORD)?
GORD is a common condition that affects between 10% and 30% of people in developed countries
There is global variation, with less than 10% prevalence in East Asia
All age groups are affected but risk increases with age and obesity
What are the presenting symptoms of Gastro-oesophageal reflux disease (GORD)?
Substernal burning discomfort or heartburn aggravated by lying supine, bending or large meals and drinking alcohol
Regurgitation of gastric contents
Dysphagia (caused by formation of peptic stricture after long-standing reflux)
Bloating/ early satiety
-Pain relieved by antacids
Waterbrash: stomach acid gets into throat resulting in sudden flow of saliva
RARE: Aspiration may result in voice hoarseness, laryngitis, nocturnal cough and wheeze with (out) pneumonia
What are the signs of Gastro-oesophageal reflux disease (GORD) on physical examination?
Usually normal
Occasionally, epigastric tenderness, wheeze on chest auscultation, dysphonia (hoarse voice)
What are the appropriate investigations for Gastro-oesophageal reflux disease (GORD)?
Diagnosis is clinical- a therapeutic trial of a proton-pump inhibitor (PPI) can serve for both diagnosis and initial treatment (e.g. omeprazole)
Others:
-OGD: indicated for alarm symptoms or symptoms suggesting complicated disease (atypical, persistent, or relapsing symptoms): may show oesophagitis (erosion, ulcerations, strictures) or Barrett’s oesophagus
-Ambulatory (24h) pH monitoring: can demonstrate abnormal exposure to oesophageal acid in the absence of oesophagitis, pH <4 more than 4% of the time is abnormal
-Oesophageal manometry: may suggest achalasia, oesophageal spasm, or other motor disorders
-Barium swallow: may be useful in patients with dysphagia for whom endoscopy is contraindicated or unavailable- To detect hiatus hernia, peptic stricture, extrinsic compression of the oesophagus can be visualized
-Oesophageal capsule endoscopy: swallowing a capsule endoscope to visualise the oesophagus, may show oesophagitis or Barrett’s oesophagus, less-invasive, safe alternative to upper endoscopy
-CXR: finding of hiatus hernia (gastric bubble behind cardiac shadow)
What is the management of Gastro-oesophageal reflux disease (GORD)?
Advice: Lifestyle changes, weight loss, elevating head of bed, avoid provoking factors, stopping smoking, lower fat meals, avoiding large meals late in the evening
Medical:
-Proton-pump inhibitors (PPIs) are the most effective drugs (adverse effects: increased risk of bone fracture, decreased efficacy of clopidogrel, hypomagnesaemia)
-If there is absent or inadequate response, treatment can proceed to high-dose PPI and endoscopy (investigate cause)
Endoscopy: Annual endoscopic surveillance for Barretts oesophagus; may be necessary for stricture dilation or stenting
Surgery:
-Antireflux surgery for those with symptoms despite optimal medical management or in those intolerant of medication (people who do not respond to PPIs will probably not respond to surgery)
-Bariatric surgery: Patients with GORD who are obese may benefit
What are the complications of Gastro-oesophageal reflux disease (GORD)?
Low risk:
Oesophageal ulceration-anaemia if perforated
Peptic stricture
Barretts oesophagus (risk increases with positive smoking history or hiatus hernia)
Oesophageal adenocarcinoma
What is the prognosis of Gastro-oesophageal reflux disease (GORD)?
50% respond to lifestyle measures alone
Most patients respond to treatment with proton-pump inhibitors (PPIs)
Maintenance PPI therapy is recommended for those who have symptoms when the PPI is discontinued, as well as for those with erosive oesophagitis and Barrett’s oesophagus
Most patients relapse off PPI therapy however, there are risks associated with long-term use
What is Gastroenteritis?
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
What is Infectious Colitis?
Inflammation of the colon due to a virus or bacteria
What is the aetiology of Gastroenteritis and Infectious Colitis?
Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water
What are the common causative organisms of Gastroenteritis and Infectious Colitis?
Viral: Rotavirus, adenovirus, astrovirus
Bacterial: Campylobacter jejuni, Escherichia coli, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica
Protozoal: Entamoeba histolytica
Toxins: From Staphylococcus aureus, Clostridium botulinum, Bacillus cereus, mushrooms, heavy metals, seafood
Commonly contaminated foods: Improperly cooked meat (S. aureus, C. perfringens), old rice (B. cereus, S. aureus), eggs and poultry (Salmonella), milk and cheeses (Listeria,
Campylobacter), canned food (botulism)
What is the epidemiology of Gastroenteritis and Infectious Colitis?
Common, and often under-reported, a serious cause of morbidity and mortality in the developing world
What are the presenting symptoms of Gastroenteritis and Infectious Colitis?
Sudden onset nausea, vomiting, anorexia
Diarrhoea (bloody or watery)
Abdominal pain or discomfort
Fever and malaise
*Enquire about recent travel, antibiotic use and recent food intake (how cooked, source andwhether anyone else ill)
Time of onset:
-Toxins (early; 1–24 h)
-Bacterial/viral/protozoal (12 h or later)
Effect of toxin:
-Botulinum causes paralysis
-Mushrooms can cause fits, renal or liver failure
What are the signs of Gastroenteritis and Infectious Colitis on physical examination?
Diffuse abdominal tenderness
Abdominal distension
Bowel sounds are often increased
If severe:
-Pyrexia
-Dehydration
-Hypotension
-Peripheral shutdown
What are the appropriate investigations for Gastroenteritis and Infectious Colitis?
Blood:
-FBC
-Blood culture (helps identification if bacteriaemia present)
-U&Es: dehydration
Stool:
-Faecal microscopy for polymorphs, parasites, oocysts, culture, electron microscopy (used to diagnose viral infections)
-Analysis for toxins, particularly for pseudomembranous
colitis (Clostridium difficile toxin)
AXR or ultrasound:
-To exclude other causes of abdominal pain
Sigmoidoscopy:
-Often unnecessary unless inflammatory bowel disease needs to be excluded
What is the management for Gastroenteritis and Infectious Colitis?
Bed rest
Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt)
IV rehydration may be necessary in those with severe vomiting
*Most infections are self-limiting
-Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter)
Botulism: Botulinum antitoxin IM and manage in ITU.
Public health:
-Often a notifiable disease
-Educate on basic hygiene and cooking
What are the complications of Gastroenteritis and Infectious Colitis?
Dehydration
Electrolyte imbalance
Pre-renal failure
Secondary lactose intolerance (particularly in infants)
Sepsis and shock (particularly Salmonella and Shigella)
Haemolytic uraemic syndrome is associated with toxins from E. coli
Guillian–Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis
*Botulism: Respiratory muscle weakness or paralysis
What is the prognosis for Gastroenteritis and Infectious Colitis?
Generally good, as the majority of cases are self-limiting
What is Gastrointestinal perforation?
Also known as ruptured bowel
May occur at any anatomical location from the upper oesophagus to the anorectal junction
