GASTRO Flashcards
Define Achalasia
A condition in which the normal muscular activity of the oesophagus is disturbed (absent or uncoordinated) due to failure or incomplete relaxation of the lower oesophageal sphincter
- Delay in the passage of swallowed material into the stomach
Aetiology of Achalasia
Caused by a degeneration of the ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause
- Oesophageal infection with Trypanosoma Cruzi seen in Central/ South America produces a similar disorder (CHAGAS disease)
Epidemiology of achalasia
- It may occur at any age (mainly 25-60 yrs)
- Affects both sexes equally
- Annual incidence 1/100,000
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 (because they are eating less)
Signs of achalasia on physical examination
• May show signs of complications:
o Aspiration pneumonia
o Malnutrition
o Weight loss
Investigations for achalasia
• CXR may show:
o Widened mediastinum
o Double right heart border (dilated oesophagus)
o Air-fluid level in the upper chest
o Absence of the normal gastric air bubble
• Barium swallow may show:
o Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)
• Endoscopy to exclude malignancy (which could mimic achalasia)
• Manometry (used to assess pressure at the LOS) may show:
o Elevated resting LOS pressure (> 45 mm Hg)
o Incomplete LOS relaxation
o Absence of peristalsis in the smooth muscle portion of the oesophagus
• NOTE: you may do serology for antibodies against T. cruzi if CHAGAS DISEASE is a possibility (and blood film may detect parasites)
Define Acute Cholangitis
Infection of the bile duct
Aetiology/ Risk factors of acute cholangitis
• There are several causes:
o Obstruction of the gallbladder or bile duct due to stones
o ERCP
o Tumours (e.g. pancreatic, cholangiocarcinoma)
o Bile duct stricture or stenosis
o Parasitic infection (e.g. ascariasis)
Epidemiology of acute cholangitis
- 9% of patients admitted to hospital with gallstone disease will have acute cholangitis
- Equal in males and females
- Median age of presentation: 50-60 yrs
- Racial distribution follows that of gallstone disease - fair-skinned people
Presenting symptoms of acute cholangitis
• Most patients present with Charcot’s Triad of symptoms:
o RUQ Pain
o Jaundice
o Fever with rigors
• This list of symptoms has been extended to include the following two symptoms, forming the Reynolds’ Pentad:
o Mental confusion
o Septic shock
• Patients may also complain of pruritus
Signs of acute cholangitis on physical examination
- Fever
- RUQ tenderness
- Mild hepatomegaly
- Jaundice
- Mental status changes
- Sepsis
- Hypotension
- Tachycardia
- Peritonitis (uncommon - check for alternative diagnosis)
Investigations for acute cholangitis
• Bloods
o FBC: High WCC
o CRP/ESR: possibly raised
o LFTs: typical pattern of obstructive jaundice (raised ALP + GGT)
o U&Es: may be signs of renal dysfunction
o Blood cultures: check for sepsis
o Amylase: may be raised if the lower part of the common bile duct is involved
• Imaging
o X-ray KUB: look for stones
o Abdominal ultrasound: look for stones and dilation of the common bile duct
o Contrast-enhanced CT/MRI: good for diagnosing cholangitis
o MRCP: may be necessary to detect non-calcified stones
Management plan for acute cholangitis
• Resuscitation: may be required if the patient is in septic shock
• Broad-spectrum antibiotics: given once blood cultures have been taken (select drugs that are effective against anaerobes and Gram-negative organisms: e.g. cefuroxime +
metronidazole)
• Most patients respond to antibiotics but endoscopic biliary drainage is usually required
to treat the underlying obstruction
• Management depends on severity:
o Stage 1 (Mild)
• Antimicrobial therapy
• Percutaneous, endoscopic or operative intervention for non-responders (depending on aetiology)
o Stage 2 (Moderate)
• Early percutaneous or endoscopic drainage
• Endoscopic biliary drainage is recommended
o Stage 3 (Severe)
• NOTE: severe cholangitis counts as including shock, conscious disturbance,
acute lung injury, AKI, hepatic injury or DIC
• Treatment of organ failure with ventilatory support, vasopressors etc.
• Urgent percutaneous or endoscopic drainage
• Definitive treatment required once the clinical picture improves
Possible complications of acute cholangitis
• Liver abscesses • Liver failure • Bacteraemia • Gram-negative sepsis • Septic shock • AKI • Organ dysfunction • Percutaneous or endoscopic drainage can lead to: o Intra-abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage
Prognosis for patients with acute cholangitis
• Mortality between 17M40%
Define Alcoholic Hepatitis
Inflammatory liver injury caused by chronic heavy intake of alcohol
Aetiology/ Risk Factors of alcoholic hepatitis
• One of the THREE forms of liver disease caused by excessive alcohol intake - the spectrum consists of:
o Alcoholic fatty liver (steatosis)
o Alcoholic hepatitis
o Chronic cirrhosis
• Histopathological features of alcohol hepatitis:
o Centrilobular ballooning
o Degeneration and necrosis of hepatocytes
o Steatosis
o Neutrophilic inflammation
o Cholestasis
o Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of
cytokeratin intermediate filaments)
o Giant mitochondria
Epidemiology of alcoholic hepatitis
• Occurs in 10-35% of heavy drinkers
Presenting symptoms of alcoholic hepatitis
• May remain asymptomatic and undetected
• May be mild illness with symptoms such as:
o Nausea
o Malaise
o Epigastric pain
o Right hypochondrial pain o Low-grade fever
• More severe presenting symptoms include:
o Jaundice
o Abdominal discomfort or swelling
o Swollen ankles
o GI bleeding
• NOTE: a long history of heavy drinking is required for the development of alcoholic hepatitis (around 15-20 years)
• There may be events that trigger the disease (e.g. aspiration pneumonia, injury)
Signs of alcoholic hepatitis on physical examination
• Signs of Alcohol Excess o Malnourished o Palmar erythema o Dupuytren's contracture o Facial telangiectasia o Parotid enlargement o Spider naevi o Gynaecomastia o Testicular atrophy o Hepatomegaly o Easy bruising • Signs of Severe Alcoholic Hepatitis o Febrile (in 50% of patients) o Tachycardia o Jaundice o Bruising o Encephalopathy (e.g. liver flap, drowsiness, disorientation) o Ascites o Hepatomegaly o Splenomegaly
Investigations for alcoholic hepatitis
• Bloods
o FBC:
• Low Hb
• High MCV
• High WCC
• Low platelets
o LFTs:
• High AST + ALT
• High bilirubin
• High ALP + GGT • Low albumin
o U&Es:
• Urea and K+ tend to be low
o Clotting: prolonged PT is a sensitive marker for significant liver damage
• Ultrasound - check for other causes of liver impairment (e.g. malignancy)
• Upper GI Endoscopy - investigate varices
• Liver Biopsy - can help distinguish from other causes of hepatitis
• EEG - slow-wave activity indicates encephalopathy
Management plan for alcoholic hepatitis
• Acute
o Thiamine
o Vitamin C and other multivitamins (can be given as Pabrinex)
o Monitor and correct K+, Mg2+ and glucose
o Ensure adequate urine output
o Treat encephalopathy with oral lactulose or phosphate enemas
o Ascites - manage with diuretics (spironolactone with/without furosemide)
o Therapeutic paracentesis
o Glypressin and N-Macetylcysteine for hepatorenal syndrome
• Nutrition
o Via oral or NG feeding is important
o Protein restriction should be avoided unless the patient is encephalopathic
o Nutritional supplementation and vitamins (B group, thiamine and folic acid)
should be started parenterally initially, and continued orally
• Steroid Therapy - reduces short-term mortality for severe alcoholic hepatitis
NOTE: hepatorenal syndrome - the development of renal failure in patients with advanced chronic liver disease
• Thought to arise because of abnormalities in blood vessel tone in the kidneys
• Blood vessels in the kidney constrict because of the dilatation of blood vessels in the splanchnic circulation (supplying the intestines), which is mediated by factors released
by the kidneys
• The splanchnic vasodilation leads to reduced effective volume of blood detected by
the juxtaglomarular apparatus, leading to activation of the RAS and vasoconstriction of
vessels in the kidney
• This leads to kidney failure
identify possible complications of alcoholic hepatitis
- Acute liver decompensation
- Hepatorenal syndrome
- Cirrhosis
Prognosis for patients with alcoholic hepatitis
• Mortality:
o First month = 10%
o First year = 40%
• If alcohol intake continues, most will progress to cirrhosis within 1-3 years
Define Anal Fissure
A painful tear in the squamous lining of the lower anal canal
- 90% of all anal fissures are posterior (anterior anal fissures tend to occur after childbirth)
Epidemiology of anal fissures
- Affects 1/10 people during their life time
- Both sexes are affected equally
- Can occur at any age
- Most cases occur in children and young adults: 10-30 yrs
Aetiology / Risk factors of anal fissure
• Most are caused by hard faeces
• Anal sphincter spasm can constrict the inferior rectal artery, causing ischaemia and
impairing the healing process
• Rare causes: syphilis, herpes, trauma, Crohn’s, anal cancer, psoriasis
Presenting symptoms of anal fissure
- Tearing pain when passing stools
- There may be a little bit of blood in the faeces or on the paper
- Anal itching (pruritus ani)
Signs of anal fissure on physical examination
• Tears in the squamous lining of the anus on examination
Investigations for anal fissure
Examine the anus
Management plan for anal fissure
• Conservative
o High-fibre diet
o Softening the stools (laxatives)
o Good hydration
• Medical
o Lidocaine ointment (local anaesthetic)
o GTN ointment (relaxes the anal sphincter and promoted healing)
o Diltiazem (relaxes the anal sphincter and promotes healing)
o Botulinum toxin injection
• Surgical
o Lateral sphincterotomy
o This relaxes the anal sphincter and promotes healing but it has complications
(e.g. anal incontinence) so it is reserved for patients who are intolerant or not
responsive to non-surgical treatments
Possible complications of anal fissure
Chronic anal fissure
Prognosis for patients with anal fissure
• In most people, the fissure will heal within a week or so
• Treatment revolves around easing pain by keeping the stools soft and relaxing the anal
sphincter to promote healing
Define Appendicitis
Inflammation of the appendix
Epidemiology of appendicitis
- The MOST COMMON surgical emergency
- Can occur at any age
- Most commonly occurs between 10-20 yrs
Aetiology/ Risk factors of appendicitis
- Gut organisms invade the appendix wall after lumen obstruction (e.g. by lymphoid hyperplasia, faecolith or filarial worms)
- This leads to oedema, ischaemic necrosis and perforation
Presenting symptoms of appendicitis
- Periumbilical pain that moves to the right iliac fossa
- Anorexia is an important feature
- Vomiting (may occur after pain)
- Constipation
- Diarrhoea
Signs of appendicitis on physical examination
• General Signs
o Tachycardia
o Fever
o Furred tongue
o Lying still
o Coughing hurts
o Foetor with/without flushing
o Shallow breaths
• RIF Signs
o Guarding
o Rebound and percussion tenderness
o PR pain on the right side (sign of low-lying pelvic appendix)
• Special Signs
o Rovsing’s Sign - palpation of the left iliac fossa causes more pain in the right iliac fossa than the left
o Psoas Sign - pain on extending the hip (caused by retrocaecal appendix)
o Cope Sign - pain on flexion and internal rotation of the hip (occurs if the appendix is in close proximity to the obturator internus)
• Variations in clinical picture
o Inflammation of retrocaecal/retroperitoneal appendix may cause flank pain or RUQ pain
• The only sign may be tenderness on the right on DRE
o A child may have vague abdominal pain and will not eat their favourite food
o A shocked confused 80+ year old who is not in any pain
Investigations for appendicitis
• Bloods o High WCC (mainly neutrophils) o High CRP • Ultrasound may help • CT - high diagnostic accuracy
Management plan for appendicitis
• Prompt appendicectomy • Antibiotics: o Cefuroxime o Metronidazole • Laparoscopy - diagnostic and therapeutic advantages
Possible complications of appendicitis
• Perforation
• Appendix mass
o Occurs when the inflamed appendix becomes covered with omentum
• Appendix abscess
o May occur if appendix mass fails to resolve
o Treatment involves drainage and antibiotics
Prognosis for patients with appendicitis
- Uncomplicated appendicitis - most people recover with no long-term problems
- Ruptured appendix - greater risk of complications/death
Define Autoimmune hepatitis
Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies
Aetiology/ Risk Factors 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 raised titre of anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (ASMA) and anti-liver/kidney microsomes (anti-LKM) are NOT thought to directly injure the liver
• 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
• TWO major forms of autoimmune hepatitis:
o Type 1 (Classic)
• ANA
• ASMA
• Anti-actin antibodies (AAA)
• Anti-soluble liver antigen (antiMSLA)
o Type 2
• Antibodies to liver/kidney microsomes (ALKM-1)
• Antibodies to liver cytosol antigen (ALCM1)
Summarise the epidemiology of autoimmune hepatitis
- Type 1: occurs in ALL age groups (but mainly young women)
* Type 2: generally occurs in girls and young women
Presenting symptoms of autoimmune hepatitis
• May be asymptomatic and discovered incidentally through abnormal LFT • Insidiously present with: o Malaise o Fatigue o Anorexia o Weight loss o Nausea o Jaundice o Amenorrhoea o Epistaxis • Acute hepatitis (25%) presents with: o Fever o Anorexia o Jaundice o Nausea/ Vomiting/ Diarrhoea o RUQ pain o Some may present with serum sickness (e.g. arthralgia, polyarthritis, maculopapular rash) • NOTE: check for personal or family history of other autoimmune diseases • A full history is important to rule out other causes of hepatitis (e.g. viral, alcoholic)
Signs of autoimmune hepatitis on physical examination
- Stigmata of chronic liver disease (e.g. spider naevi)
- Ascites, oedema and hepatic encephalopathy are late features
- Cushingoid features may be present even before the administration of steroids
Investigations for autoimmune hepatitis
• Bloods:
o LFTs:
• High: AST, ALT, GGT, ALP and Bilirubin
• Low: albumin (in severe disease)
o Clotting:
• High PT (in severe disease)
o FBC:
• Low Hb, platelets and WCC (if hypersplenism from portal hypertension)
o Hypergammaglobulinaemia
• Presence of ANA, ASMA and Anti-LKM antibodies
• Liver Biopsy:
o Needed to establish diagnosis and check whether hepatitis or cirrhosis
• To rule out other causes of liver disease:
o Viral serology
o Urinary copper/caeruloplasmin
o Ferritin and transferrin saturation
o alpha1 antitrypsin
o AntiMmitochondrial antibodies (PBC)
• US, CT or MRI of liver and abdomen
o Visualise structural lesions
• ERCP
o To rule out PSC
Define Barrett’s Oesophagus
Prolonged exposure of the normal squamous epithelium to reflux ate of GORD leads to mucosal inflammation and erosion , leading to replacement of the mucosa with metaplastic columnar epithelium
- Metaplastic change: squamous –> columnar
- Main problem: Barrett’s could progress to oesophageal adenocarcinoma
Aetiology/ Risk Factors of Barrett’s oesophagus
• Reflux will occur if the cardiac sphincter is not working properly (most of the time it is
unclear why it is not working properly)
• Hiatus hernia make GORD more likely
Epidemiology of Barrett’s Oesophagus
- 1/10 adults have heart burn every day
* 3-5% of people with GORD will develop Barrett’s oesophagus
Presenting symptoms of Barrett’s Oesophagus
• Patients are likely to experience symptoms of GORD:
o Heartburn
o Nausea
o Water-brash (sour taste in the mouth)
o Bloating
o Belching
o Burning pain when swallowing
Investigations for Barrett’s Oesophagus
• OGD and Biopsy
o This will show the replacement of the squamous epithelium with columnar epithelium
Management plan for Barrett’s Oesophagus
• Pre-malignant/High grade dysplasia:
o Oesophageal resection
o Eradicative mucosectomy
o NOTE: this is appropriate if the patients are young and fit
• Other techniques:
o Endoscopic targeted mucosectomy
o Mucosal ablation by epithelial laser, radiofrequency (HALO) or photodynamic
ablation (PD)
• Low-grade dysplasia - annual endoscopic surveillance is recommended
• No pre-malignant changes found:
o Surveillance endoscopy and biopsy performed every 1-3 years
o Anti-reflux measures (e.g. high dose PPI)
Complications of Barrett’s Oesophagus
- MAIN COMPLICATION: development of oesophageal adenocarcinoma
- Risk of dysplasia
Prognosis for patients with Barrett’s Oesophagus
• Barrett’s oesophagus carries a 30-60 times higher risk of oesophageal adenocarcinoma
than the general population
• Most patients, however, do not develop oesophageal adenocarcinoma
• 5-10% of those with Barrett’s oesophagus will develop adenocarcinoma over 10-20
years
Define Biliary Colic
Pain resulting from obstruction of the gallbladder or common bile duct, usually by a stone. The pain, which is very severe, is usually felt in the upper abdomen (in the midline or to the right) but can also be poorly localised due to its visceral nature
Aetiology/ Risk Factors of Biliary Colic
• Occurs due to contractions of the biliary tree in an attempt to relieve an obstruction (e.g. due to a stone) • Risk factors of gallstones: o Fair (Caucasian) o Fat o Fertile o Forty o Female
Epidemiology of Biliary Colic
- 10-15% of people in the adult Western world will develop gallstones
- Biliary colic is the most common presentation of gallstone disease
Presenting symptoms of biliary colic
- Crampy RUQ pain
- Nausea and vomiting
- Pain may radiate to the right scapula
- The pain does NOT fluctuate and has a tendency to persist
- Individuals may present with pain following ingestion of a fatty meal
Biliary colic on physical examination
• RUQ pain and epigastric tenderness
Investigations for biliary colic
• Urinalysis, CXR and ECG to exclude other causes (e.g. basal pneumonia, inferior MI)
• Ultrasound
o Look for dilatation of the CBD
o Gallbladder wall may be thickened
• LFT
• ERCP - useful diagnostically and therapeutically
• CT - may be useful if other forms of imaging have been insufficient
Management plan for biliary colic
• Analgesia • IV fluids • NBM • Surgical o Laparoscopic cholecystectomy • ERCP can also be used to help remove stones or stent a blocked bile duct
Complications of biliary colic
• Complications of surgery
o Injury to the bile duct
o Fat intolerance - due to inability to secrete a large amount of bile into the
intestine because the patient no longer has a gallbladder
o Post-cholecystectomy syndrome - presence of abdominal symptoms (e.g.
dyspepsia, nausea/vomiting, RUQ pain) after the removal of the gallbladder
Prognosis for patients with biliary colic
• GOOD prognosis with appropriate treatment
Define Cholecystitis
Inflammation of the gallbladder
Aetiology/ Risk Factors of cholecystitis
• Types of Stones
o Mixed Stones (80%)
• Contains cholesterol, calcium bilirubinate, phosphate and protein
• Form due to an imbalance between bile salts, phospholipids, cholesterol,
nucleation factors and gallbladder motility
o Pure Cholesterol Stones (10%)
o Pigment Stones (10%)
• Black stones made of calcium bilirubinate
• Form due to increased bilirubin (e.g. due to haemolysis)
• Risk Factors
o Age
o Female
o Fat
o Diabetes mellitus
o Drugs (OCP, octreotide)
o Family history
o Ethnicity (Caucasian)
o Pigment Stone Risk Factors: haemolytic disorders (e.g. sickle cell anaemia)
Epidemiology of cholecystitis
- Very COMMON
- UK prevalence of gallstone disease = 10%
- 3 x more common in FEMALES
- More common with increasing age
Presenting symptoms of cholecystitis
- Systemically unwell
- Fever
- Prolonged abdominal pain
- Pain may be referred to right shoulder (due to diaphragmatic irritation)
Signs of Cholecystitis on physical examination
- Tachycardia
- Pyrexia
- RUQ pain or epigastric tenderness
- May be guarding or rebound tenderness
- Murphy’s sign positive
Investigations for cholecystitis
• Bloods
o FBC - high WCC in cholecystitis and cholangitis
o LFT - high ALP + GGT in ascending cholangitis
o Blood cultures
o Amylase (exclude pancreatitis)
• Ultrasound
o Shows gallstones
o Increased thickness of gallbladder wall
o Dilatation of biliary tree
• AXR - but only 10% of gallstones are radio-opaque
• Other imaging - to exclude differentials (e.g. erect CXR, ERCP)
Management plan for cholecystitis
• Conservative
o If only mild biliary colic - follow a low-fat diet
• Medical
o NBM
o IV fluids
o Analgesia
o AntiMemetics
o Antibiotics (if infection is present)
o NOTE: if symptoms persist despite antibiotic treatment, suspect a localised
abscess or empyema, which would require drainage
o If there is an obstruction, urgent biliary drainage by ERCP or via a percutaneous
route is necessary
• Surgical
o Laparoscopic Cholecystectomy
Complications of cholecystitis
• Stones within the gallbladder o Biliary colic o Cholecystitis o Gallbladder empyema o Gallbladder cancer (RARE) • Stones outside the gallbladder o Obstructive jaundice o Pancreatitis o Ascending cholangitis o Cholecystoduodenal fistula o Gallstone ileus o Bouveret syndrome (gallstones cause gastric outlet obstruction) o Mirizzi syndrome • Complications of cholecystectomy o Bleeding o Infection o Bile leak o Post-cholecystectomy syndrome o Port-site hernia
Prognosis for patients with cholecystectomy
- Gallstones do NOT cause symptoms most of the time
* Surgery offers an excellent chance of cure if they were to become symptomatic
Define Cirrhosis
End-stage of chronic liver damage with replacement of normal liver architecture with diffuse-fibrosis and nodules of regenerating hepatocytes
- Cirrhosis is considered DECOMPENSATED if it becomes complicated by any of:
- ascites
- jaundice
- encephalopathy
- GI bleed
Decompensation can be precipitated by infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein thrombosis
Aetiology/ Risk Factors of Cirrhosis
• Chronic alcohol misuse (most common in the UK) • Chronic viral hepatitis (hep B/C - most common worldwide) • Autoimmune hepatitis • Drugs (e.g. methotrexate, hepatotoxic drugs) • Inherited o alpha1-antitrypsin deficiency o Haemochromatosis o Wilson's disease o Galactosaemia o Cystic Fibrosis • Vascular o Budd-Chiari Syndrome o Hepatic Venous Congestion • Chronic Biliary Diseases o PBC o PSC o Biliary atresia • Unknown: 5-10% • Non-Alcoholic Steatohepatitis (NASH) o Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs (e.g. amiodarone, tamoxifen)
Presenting symptoms of Cirrhosis
• Early non-specific symptoms: o Anorexia o Nausea o Fatigue o Weakness o Weight loss • Symptoms due to decreased liver synthetic function: o Easy bruising o Abnormal swelling o Ankle oedema • Symptoms due to reduced detoxification function: o Jaundice o Personality change o Altered sleep pattern o Amenorrhoea o Galactorrhoea • Symptoms due to portal hypertension: o Abdominal swelling o Haematemesis o PR bleeding or melaena
Epidemiology of Cirrhosis
One of the top 10 causes of death worldwide
Signs of cirrhosis on physical examination
These are all signs of chronic liver disease • Asterixis • Bruises • Clubbing • Dupuytren's contracture • Palmar erythema • Jaundice • Gynaecomastia • Leukonychia • Parotid enlargement • Spider naevi • Scratch mark (from cholestatic pruritis) • Ascites • Enlarged liver (may be shrunken in the later stages) • Testicular atrophy • Caput medusae • Splenomegaly
Investigations for cirrhosis
• Bloods
o FBC: low platelets + Hb = because of hypersplenism as a result of portal
hypertension
o LFTs - may be normal but often get:
• High AST, ALT, ALP, GGT and bilirubin
• Low albumin
o Clotting: prolonged PT
o Serum AFP (alpha-fetoprotein = tumour marker for liver cancer):
• Raised in chronic liver disease
• High levels may suggest hepatocellular carcinoma
• Investigations to determine CAUSE
o Viral serology
o alpha1-antitrypsin
o Caeruloplasmin
• This is a copper-carrying complex that is LOW in Wilson’s disease
o Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) -check for
haemochromatosis
o AntiMmitochondrial antibody (PBC)
o ANA, ASMA (autoimmune hepatitis)
• Ascitic Tap
o MC&S - check for infection
o Biochemistry (protein, albumin, glucose, amylase)
o Cytology
o IMPORTANT: ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial
peritonitis (SBP)
• Liver Biopsy
o Performed either:
• Percutaneously
• Transjugular - if clotting deranged or ascitic
o Histopathological features of cirrhosis:
• Periportal fibrosis
• Loss of normal liver architecture
• Nodular appearance
o Grade - indicates degree of inflammation
o Stage - degree of architectural distortion (from mild portal fibrosis –> cirrhosis)
• Imaging
o US, CT or MRI - to detect complications such as:
• Ascites
• HCC
• Hepatic or portal vein thrombosis
• Exclude biliary obstruction
o MRCP (if PSC suspected)
• Endoscopy
o To examine varices
• Child-Pugh Grading - score for estimating the prognosis in chronic liver
disease/cirrhosis. It is based on 5 factors:
o Albumin
o Bilirubin
o PT
o Ascites
o Encephalopathy
• Cirrhosis can be divided into Classes using the Child-Push grading system:
o Class A: 5-6
o Class B: 7-9
o Class C: 10-15
Management plan for cirrhosis
• Treat the CAUSE if possible
• Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver
• Nutrition is important
• Enteral supplements should be given
• NG feeding may be indicated
• Treating Complications:
o Encephalopathy
• Treat infections
• Exclude GI bleed
• Use lactulose and phosphate enemas
! Normally, the liver breaks down ammonia that is absorbed in the GI tract, however, in Cirrhosis the ammonia can go through the liver without being broken down and exert toxic effects on the brain
! IMPORTANT: lactulose reduces the absorption of ammonia from the gut
! This helps prevent encephalopathy caused by ammonia reaching the brain
• Avoid sedation
o Ascites
• Diuretics (spironolactone with/without furosemide)
• Dietary sodium restriction
• Therapeutic paracentesis (with human albumin replacement)
• Monitor weight
• Fluid restrict if plasma sodium < 120 mmol/L
• Avoid alcohol and NSAIDs
o Spontaneous Bacterial Peritonitis
• Antibiotics (e.g. cefuroxime and metronidazole)
• Prophylaxis against recurrent SBP with ciprofloxacin
o Surgical
• Consider TIPS (transjugular intrahepatic portosystemic shunt) - this helps reduce portal hypertension
! However, it may precipitate encephalopathy because it is providing a route for blood from the GI tract to bypass the liver
• Liver transplantation is the only curative method
Complications of Cirrhosis
- Portal hypertension with ascites
- Hepatic encephalopathy
- Variceal haemorrhage
- SBP
- HCC
- Renal failure (hepatorenal syndrome)
- Pulmonary hypertension (hepatopulmonary syndrome)
Prognosis for patients with cirrhosis
• Depends on aetiology and complications
• Generally poor prognosis
o Overall 5 year survival = 50%
o If ascites, 2 year survival = 50%
Define Coeliac Disease
An inflammatory disease caused by intolerance to Gluten, causing chronic intestinal malabsorption.
It leads to subtotal villous atrophy and crypt hyperplasia
Aetiology/ Risk Factors of Coeliac disease
• Due to sensitivity to the GLIADIN component of gluten
• Exposure to gliadin triggers and immunological reaction in the small intestine leading
to mucosal damage and loss of villi
• 10% risk of firstMdegree relatives being affected
• Clear genetic susceptibility associated with HLA-B8, HLA-DR3 and HLA-DQW2 haplotypes
Epidemiology of coeliac disease
- UK: 1/2000
- West Ireland: 1/300
- Rare in East-Asia
Presenting symptoms of coeliac disease
- May be asymptomatic
- Abdominal discomfort, pain and distention
- 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
Signs of Coeliac disease on physical examination
• Signs of anaemia: pallor • Signs of malnutrition:
o Short stature
o Abdominal distension
o Wasted buttocks in children
o Triceps skinfold thickness gives indication of fat stores
• Signs of vitamin/mineral deficiencies: osteomalacia, easy bruising
• Intense, itchy blisters on elbows, knees or buttocks (dermatitis herpetiformis)
Investigations for coeliac disease
• Blood:
o FBC (low Hb, iron and folate)
o U&E
o Albumin
o Calcium
o Phosphate
• Serology:
o IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic
o NOTE: IgA deficiency is quite COMMON (1/50 with coeliac) so Ig levels should be measured to avoid false negatives
• Stool: culture to exclude infection, faecal fat tests for steatorrhoea
• DJxylose test: reduced urinary excretion after oral xylose indicates small bowel
malabsorption
• Endoscopy: allows direct visualisation of villous atrophy in the small intestine (mucosa
appears flat and smooth)
o Biopsy will show villous atrophy and crypt
hyperplasia in the duodenum
o The epithelium adopts a cuboidal appearance
- there is an inflammatory infiltrate of lymphocytes and plasma cells in the lamina propria
Management plan for coeliac disease
- Advice: avoid gluten (wheat, rye and barley products)
* Medical: vitamin and mineral supplements. Oral corticosteroids if disease does not subside with avoidance of gluten
Possible complications of coeliac disease
- Iron, folate and B12 deficiency
- Osteomalacia
- Ulcerative jejunoileitis
- GI lymphoma (particularly T cell)
- Bacterial overgrowth
- Cerebellar ataxia (rarely)
Prognosis for patients with coeliac disease
- FULL RECOVERY in most patients who strictly adhere to a gluten-free diet
- Symptoms usually resolve within weeks though histological changes may take longer • Gluten-free diet must be followed for life
Define Crohn’s disease
Chronic granulomatous inflammatory disease that. can affect any part of the GI tract. Grouped with UC and known, together, as IBD
Aetiology/ Risk factors of Crohn’s
• Cause unknown but thought to be due to interplay between genetic and
environmental factors
• Though inflammation can occur anywhere from mouth to anus, 40% involves the
terminal ileum
Epidemiology of Crohn’s disease
- UK annual incidence: 5-8/100,000
- UK prevalence: 50-80/100,000
- Affects any age but peaks in teens, 20s and 40s
Presenting symptoms of Crohn’s disease
- Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)
- Diarrhoea (may be bloody or steatorrhoea)
- Fever, malaise, weight loss
- Symptoms of complications
- Sometimes right iliac fossa pain due to inflammation of terminal ileum
Signs of Crohn’s disease on physical examination
- Weight loss
- Clubbing
- Signs of anaemia
- Aphthous ulcers in mouth
- Perianal skin tags, fistulae and abscesses
- Uveitis, erythema nodosum, pyoderma gangrenosum
Investigations for Crohn’s disease
• Blood:
o FBC - low Hb, high platelets, high WCC
o U&Es
o LFTs - low albumin
o High ESR (suggests chronic inflammation)
o CRP may be high or normal
• Stool microscopy and culture: exclude infective colitis
• AXR: could show evidence of toxic megacolon
• Erect CXR: if there is a risk of perforation
• Small bowel barium follow-through could show:
o Fibrosis/strictures (string sign of Kantor - part of the intestine looks like a piece of string, showing incomplete filling of the intestinal lumen)
o Deep ulceration (rose thorn ulcers)
o Cobblestone mucosa
• Endoscopy (OGD, colonoscopy) and biopsy may show:
o Could help differentiate UC and CD
o Useful for monitoring malignancy and disease
progression
o Can show mucosal oedema and ulceration with
‘rose thorn fissures’ (occurs when there is a
cobblestone mucosa)
o Fistulae and abscesses
o Transmural chronic inflammation with infiltration
of macrophages, lymphocytes and plasma cells
o Granulomas with epithelioid giant cells may be seen in blood vessels and lymphatics
• Radionucide-labelled neutrophil scan: can localise the inflammation (when other
investigations are contraindicated)
Management plan for Crohn’s disease
• Acute Exacerbation
o Fluid resuscitation
o IV/oral corticosteroids
o 5-ASA analogues (e.g. mesalazine and olsalazine)
o Analgesia
o Parenteral nutrition may be necessary
o Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb
• Long-Term
o Steroids - for acute exacerbations
o 5-ASA analogues - decreases the frequency of relapses (useful for mild to
moderate disease)
• NOTE: more commonly used in UC
o Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6- mercaptopurine, methotrexate) reduces the frequency of relapses
o Anti-TNF agents: (e.g. infliximab and adalimumab) - very effective at inducing and maintaining remission. Usually reserved for refractory Crohn’s.
• General Advice:
o Stop smoking
o Dietician referral (low fibre diet necessary if there are stricture present)
• Surgery indicated it:
o Medical treatment fails
o Failure to thrive in children in the presence of complications
o Involves resection of affected bowel and stoma formation - NOTE: there is a risk of disease recurrence
Possible complications of Crohn’s disease
• GI: o Haemorrhage o Strictures o Perforation o Fistulae (between bowel, bladder, vagina) o Perianal fistulae and abscesses o GI cancer o Malabsorption • Extraintestinal Features: o Uveitis o Episcleritis o Gallstones o Kidney stones o Arthropathy o Sacroiliitis o Ankylosing spondylitis o Erythema nodosum o Pyoderma gangrenosum o Amyloidosis
Prognosis for patients with Crohn’s disease
- It is a chronic relapsing condition
- 2/3 of patients will require surgery at some stage
- 2/3 of these patients require more than 1 operation
Define Diverticulosis, Diverticular disease, Diverticulitis and the Hinchley Classification of Acute Diverticulitis
- Diverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel
- Diverticular disease: diverticulosis associated with complications e.g. haemorrhage, infection, fistulae
- Diverticulitis: actue inflammation and infection of colonic diverticulae
- Hinchey Classification of Acute Diverticulitis :
Ia: phlegm
Ib and II: localised abscesses
III: perforation and purulent peritonitis
IV: faecal peritonitis
Aetiology/ Risk Factors of diverticular disease
• Aetiology:
o A low-fibre diet leads to loss of stool bulk
o This leads to the generation of high colonic intraluminal pressures to propel the
stool out
o This, in turn, leads to the herniation of the mucosa and submucosa through the
muscularis
• Pathogenesis:
o Diveticulae are most commonly found in the sigmoid and descending colon
o However, they can also be right-sided
o Diverticulae are NOT found in the rectum
o Diverticular are found particularly at sites of nutrient artery penetration
o Diverticular obstruction by thickened faeces can lead to bacterial overgrowth, toxin production and mucosal injury
o Which can then lead to diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation
Epidemiology of diverticular disease
- Diverticular disease is VERY COMMON
- 60% of people living in industrialised countries will develop colonic diverticulae
- Rare < 40 yrs
- Right-sided diverticulae are more common in Asia
Presenting symptoms of diverticular disease
• Often ASYMPTOMATIC (80-90%)
• Complications can lead to symptoms such as:
o PR bleeding
o Diverticulitis (causing LIF and lower abdominal pain and fever)
o Diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
Signs of diverticular disease
• Diverticulitis - tender abdomen and signs of local or generalised peritonitis if a
diverticulum has perforated
Investigations for diverticular disease
• Bloods:
o FBC: increased WCC, increased CRP
o Check clotting and cross-match if bleeding
• Barium Enema (with or without air contrast):
o Shows presence of diverticulae (saw-tooth appearance of lumen)
o This reflects pseudohypertrohy of circular muscle
o IMPORTANT: barium enema should NOT be performed in the acute setting
because there is a high risk of perforation
• Flexible Sigmoidoscopy and Colonoscopy:
o Diverticulae can be visualised and other pathology (e.g. polyps and tumours) can
be excluded
• In ACUTE setting: CT scan for evidence of diverticular disease and complications may be performed
Management plan for diverticular disease
• Asymptomatic:
o Soluble high-fibre diet (20-30 g/day)
o Some drugs are under investigation for their use in preventing recurrent flares of
diverticulitis (such as probiotics and anti-inflammatories)
• GI Bleed:
o PR bleeding usually managed conservatively with IV rehydration, antibiotics and blood transfusion if necessary
o Angiography and embolisation or surgery if severe
• Diverticulitis:
o IV antibiotics
o IV fluid rehydration
o Bowel rest
o Abscesses ma be drained by radiologically sited drains
• Surgery:
o May be necessary in patients with recurrent attacks or complications (e.g. perforation and peritonitis)
Open surgery:
• Hartmann’s procedure (proctosigmoidectomy leaving a stoma)
• One-stage resection and anastomosis (risk of leak) - with or without
defunctioning stoma Laparoscopic drainage, peritoneal lavage and drain placement can be effective
Complications of diverticular disease
- Diverticulitis
- Pericolic abscess
- Perforation
- Faecal peritonitis
- Colonic obstruction
- Fistula formation (bladder, small intestine, vagina)
- Haemorrhage
Prognosis for patients with diverticular disease
• 10-25% have one or more episodes of diverticulitis
Define Gastroenteritis
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort
Aetiology/ Risk Factors of gastroenteritis
• Caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water (faecal-oral route) • Viral: o Rotavirus o Adenovirus o Astrovirus o Calcivirus o Norwalk virus o Small round structures viruses • Bacterial: o Campylobacter jejuni o Escherichia coli (particularly O157) o Salmonella o Shigella o Vibrio cholerae o Listeria o Yersinia enterocolitica • Protozoal: o Entamoeba histolytica o Cryptosporidium parvum o Giardia lamblia • Toxins from: o Staphylococcus aureus o Clostridium botulinum o Clostridium perfringens o Bacillus cereus o Mushrooms o Heavy metals o Seafood • Commonly contaminated foods: o Improperly cooked meat o Old rice o Eggs and poultry o Milk and cheeses o Canned food
Epidemiology of gastroenteritis
- COMMON
* Serious cause of morbidity and mortality in the developing world
Presenting symptoms of gastroenteritis
• Sudden onset nausea, vomiting, anorexia
• DIARRHOEA (bloody or watery)
• Abdominal pain or discomfort
• Fever and malaise
• IMPORTANT: enquire about recent travel, antibiotic use and recent food intake (how
the food was cooked, sourced and whether anyone else is ill)
• Time of Onset:
o Toxins = early (1-24 hours)
o Bacterial/viral/protozoal = 12+ hours
• Pay attention to the other effects of toxins:
o Botulinum causes paralysis
o Mushrooms can cause fits, renal or liver failure
Signs of gastroenteritis on physical examination
- Diffuse abdominal tenderness
- Abdominal distension
- Bowel sounds are often INCREASED
- In SEVERE gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown
Very important to check hydration status immediately as any diarrhoeal condition can lead to dehydration
Investigations for gastroenteritis
- Bloods: FBC, blood culture (identify bacteraemia), U&Es (dehydration)
- Stool: faecal microscopy and analysis for toxins (particularly for the toxin causing pseudomembranous colitis (C. difficile toxin)
- AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation)
- Sigmoidoscopy: usually unnecessary unless inflammatory bowel disease needs to be excluded
Management plan for gastroenteritis
• Bed rest
• Fluid and electrolyte replacement with oral rehydration solution (contains glucose and
salt)
• IV rehydration may be necessary in those with severe vomiting
• Most infections are selfJlimiting (so will go away with time)
• Antibiotic treatment is only used if severe or if infective agent has been identified
• NOTE: if botulism is present (due to Clostridium botulinum) treat with botulinum
antitoxin (IM) and manage in ITU
• NOTE: this is often a notifiable disease and is an important public health issue
Possible complications of gastroenteritis
• Dehydration
• Electrolyte imbalance
• Prerenal failure (due to dehydration)
• Secondary lactose intolerance (particularly in infants)
• Sepsis and shock
• Haemolytic uraemic syndrome (associated with toxins from E. coli O157)
• Guillain-Barre Syndrome may occur weeks after recovery from Campylobacter
gastroenteritis
• NOTE: botulism can lead to respiratory muscle weakness or paralysis
Prognosis for patients with gastroenteritis
• Good prognosis because most cases are self-limiting
Define Gastrointestinal perforation
Perforation of the wall of the GI tract with spillage of bowel contents
Aetiology/ Risk Factors of GI perforation
• Large Bowel o COMMON: • Diverticulitis • Colorectal cancer • Appendicitis o Others: volvulus, ulcerative colitis (toxic megacolon) • Gastroduodenal o COMMON: • Perforated duodenal or gastric ulcer o Others: gastric cancer • Small Bowel (RARE) o Trauma o Infection (e.g. TB) o Crohn's disease • Oesophagus o Boerhaave's perforation - rupture of the oesophagus following forceful vomiting • Risk Factors o Risk factors of cause (e.g. gastroduodenal - NSAIDs, steroids, bisphosphonates)
Epidemiology of GI perforation
Incidence depends on cause
Presenting symptoms of gastrointestinal perforation
• Depends on CAUSE
• Large Bowel
o Peritonitic abdominal pain
o IMPORTANT: make sure you rule out ruptured AAA • Gastroduodenal
o Sudden-onset severe epigastric pain - worse on movement
o Pain becomes generalised
o Gastric malignancy - may have accompanying weight loss and nausea/vomiting
• Oesophageal
o Severe pain following an episode of violent vomiting
o Neck/chest pain and dysphagia develop soon afterwards
Signs of gastrointestinal perforation on clinical examination
- Very UNWELL
- Signs of shock
- Pyrexia
- Pallor
- Dehydration
- Signs of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds)
- Loss of liver dullness (due to overlying gas)
Investigations for gastrointestinal perforation
• Bloods o FBC, U&E, LFTs o Amylase - will be raised with perforation (but should not be astronomical (as seen in pancreatitis)) • Erect CXR o Shows air under the diaphragm • AXR o Shows abnormal gas shadowing • Gastrograffin Swallow o For suspected oesophageal perforations
Management plan for gastrointestinal perforation
• Resuscitation
o Correct fluid and electrolytes
o IV antibiotics (with anaerobic cover)
• Surgical
o Large Bowel
• Identify site of perforation
• Peritoneal lavage
• Resection of perforated section (usually as part
of a Hartmann’s procedure) o Gastroduodenal
• Laparotomy
• Peritoneal lavage
• Perforation is closed with an omental patch
• Gastric ulcers are biopsied
• Helicobacter pylori eradication if positive for H. pylori
o Oesophageal
• Pleural lavage
• Repair of ruptured oesophagus
Possible complications of gastrointestinal perforation
- Large and Small Bowel - peritonitis
* Oesophagus - mediastinitis, shock, overwhelming sepsis and death
Prognosis for patients with gastrointestinal perforation
• Gastroduodenal
o Gastric ulcers have higher morbidity and mortality than duodenal ulcers
o POOR prognosis for perforated gastric carcinomas
• Large Bowel
o High risk of faecal peritonitis if left untreated
o This can lead to DEATH from septicaemia and multiorgan failure
Define GORD
Inflammation of the oesophagus caused by reflux of gastric acid and/ or bile
Aetiology/ Risk Factors of GORD
• Caused by disruption of mechanisms that prevent reflux
• Mechanisms that prevent reflux:
o Lower oesophageal sphincter
o Acute angle of junction
o Mucosal rosette
o Intra-abdominal portion of oesophagus (diaphragm acts as a sphincter)
• Prolonged oesophageal acid clearance contributes to 50% of cases
Epidemiology of GORD
- COMMON
* 5-10% of adults
Presenting symptoms of GORD
• Substernal/epigastric burning discomfort or ‘heartburn’
• Aggravated by:
o Lying supine
o Bending
o Large meals
o Drinking alcohol
• Pain is relieved by antacids
• Waterbrash (regurgitation of an excessive accumulation of saliva from the lower part
of the oesophagus often with some acid material from the stomach)
• Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze
• Dysphagia - caused by formation of peptic stricture after long-standing reflux
Signs of GORD on physical examination
- Usually NORMAL
* Occasionally - epigastric tenderness, wheeze on chest auscultation, dysphonia
Investigations for GORD
• Often a CLINICAL diagnosis
• Upper GI endoscopy, biopsy and cytological brushings
o Confirms presence of oesophagitis and can exclude malignancy
• Barium Swallow can detect:
o Hiatus hernia
• NOTE: operation to repair hiatus hernia is called Nissen fundoplication
o Peptic stricture
o Extrinsic compression of the oesophagus
• CXR:
o This is NOT specific for GORD
o However, a CXR can lead to the incidental finding of a hiatus hernia (gastric bubble behind the cardiac shadow)
• 24 hr oesophageal pH monitoring:
o pH probe places in lower oesophagus determines the temporal relationship
between symptoms and oesophageal pH
Management plan for GORD
• Advice:
o Weight loss
o Elevating head of bed
o Avoid provoking factors
o Stop smoking
o Lower fat meals
o Avoid large meals late in the evening
• Medical:
o Antacids
o Alginates
o H2 antagonists (e.g. ranitidine)
o Proton pump inhibitors (e.g. lansoprazole, omeprazole)
• Endoscopy:
o Annual endoscopic surveillance - looking for Barrett’s Oesophagus
o May be necessary for stricture dilation or stenting
• Surgery:
o Antireflux surgery if refractory to medical treatment
• Nissen Fundoplication:
o Fundus of the stomach is wrapped around the lower oesophagus - helps reduce
the risk of hiatus hernia and reduce reflux
Possible complications of GORD
- Oesophageal ulceration
- Peptic stricture
- Anaemia
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
- Associated with asthma and chronic laryngitis
Prognosis of patients with GORD
- 50% respond to lifestyle measures alone
- In patients that require drug therapy, withdrawal is often associated with relapse
- 20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
Define Haemorrhoids
Anal vascular cushions become enlarged and engorged with a tendency to protrude, bleed or prolapse in the anal canal
- Classification of Haemorrhoids:
o Internal
• Arise from the superior haemorrhoidal plexus
• Lie ABOVE the dentate line
o External
• Lie BELOW the dentate line
o NOTE: dentate line = a line that divides the upper 2/3 and the lower 1/3 of the anal canal and represents the hindgut-proctodeum junction
- Degrees of Haemorrhoids
o 1st Degree - haemorrhoids that do NOT prolapse
o 2nd Degree - prolapse with defecation but reduce spontaneously
o 3rd Degree - prolapse and require manual reduction
o 4th Degree - prolapse that CANNOT be reduced
Aetiology/ Risk Factors of haemorrhoids
• Exact cause is disputed • Caused by disorganisation of the fibromuscular stroma of the anal cushions • Risk Factors o Constipation o Prolonged straining o Derangement of the internal anal sphincter o Pregnancy o Portal hypertension
Epidemiology of haemorrhoids
- COMMON
* Peak age: 45-65 yrs
Presenting symtpoms of haemorrhoids
• Usually ASYMPTOMATIC
• Bleeding
o Bright red blood that is on the toilet paper and drips into the pan after passage of stool
o Blood will NOT be mixed with the stool
• ABSENCE of alarm symptoms (weight loss, anaemia, change in bowel habit, passage of
clotted or dark blood, mucus mixed with the stool)
• Other symptoms:
o Itching
o Anal lumps
o Prolapsing tissue
• NOTE: external haemorrhoids that have thrombosed can be very PAINFUL
