Gastroenterology Flashcards
Most common cause of pancreatitis?
Gallstones
Causes of pancreatitis?
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune disease (e.g. systemic lupus erythematosus, Sjogren’s syndrome)
Scorpion stings
Hypercalcaemia, hypertriglyceridemia, hypothermia
ERCP
Drugs (e.g. thiazides, azathioprine, sulphonamides)
How is Glasgow score of pancreatitis interpreted?
A score over 3 indicates severe, score 1 point for each of the following
PaO2 < 8kPa
Age > 55 years
Neutrophils > 15
Calcium < 2
Renal i.e. Urea > 16
Enzymes i.e. LDH > 600 or AST > 200
Albumin < 32
Sugar i.e. Glucose > 10
When should glasgow score for pancreatitis be calculated?
Within 48 hours of admission
Symptoms of pancreatitis?
Epigastric pain which radiates to the back
Nausea and vomiting
Diarrhoea
Signs of pancreatitis?
Abdominal tenderness
Peritonism
Tachycardia/ hypotension
Grey- Turners sign; bruising in flank
Cullens sign; bruising around umbilicus
Fox sign; bruising around inguinal ligament
Differentials for pancreatitis?
ACS
Perforated peptic ulcer
Ruptured abdominal aortic aneurysm
Bowel obstruction
Cholecystitis
Investigations to diagnose pancreatitis?
ABG; pO2
ECG
Pregnancy test
Capillary glucose
FBC, CRP, LFT, U+E, amylase, lipase, LDH, lipid profile
autoimmune markers
Coagulation
Abdominal USS
CXR, MRCP, CT
Management of pancreatitis?
Catheterise and monitor urine input and output
NG tube
Enteral nutrition
IV fluids
Anti-emetics
Antibiotics
Laparoscopic cholecystectomy
Complications of pancreatitis?
Pancreatic pseudocyst
Pancreatic necrosis
Peripancreatic fluid collections
Haemorrhage
Pancreatic fistulae
Acute respiratory distress syndrome
AKI
DIC
Sepsis
Multi-organ failure
Hypocalcaemia
Hyperglycaemia
What is porphyria?
Abnormalities in haem synthesis resulting in structural/ functional alterations in enzyme
Classified as acute or non-acute
Triggers for acute porphyria?
Antibiotics - Rifampicin, Isoniazid, Nitrofurantoin
Anaesthetic agents - Ketamine, Etomidate
Sulfonamides
Barbiturates
Antifungal agents
Symptoms of acute porphyria?
Abdominal pain
Nausea
Confusion
Hypertension
Seizures
Investigations to diagnose porphyria?
Urinary porphobilinogen; elevated
Urine appears red/ purple
Management of acute porphyria?
Supportive
Haem arginate
Risk factors for alcoholic liver disease?
Genetic predisposition
Concurrent liver disease
Nutritional status
High alcohol consumption
What does chronic alcohol consumption lead to?
Fatty liver
Alcoholic hepatitis
Cirrhosis
Signs of Alcoholic hepatitis?
Jaundice
Fever
Hepatomegaly
Nausea
Vomiting
Malaise
Signs of cirrhosis?
Jaundice
Ascites
Hepatic encephalopathy
Bleeding
Spider naeviae
Palmar erythema
Differentials for alcoholic liver disease?
Non alcoholic liver disease
Viral hepatitis
Haemochromatosis
Wilsons disease
Autoimmune hepatitis
Primary biliary cirrhosis
Bloods to diagnose liver disease?
FBC, LFT, Coagulation, serum albumin, viral serology, autoimmune markers, serum iron, ferritin, transferrin, ceruloplasmin
Ultrasound scan
CT/ MRI
FibroScan
Liver biopsy
Management of alcoholic liver disease?
Alcohol withdrawal
1-3 months prednisolone in hepatitis
Coagulopathy; vit K or FFP
Manage complications
Complications of alcoholic liver disease?
Reversible;
Alcoholic fatty liver
Early alcoholic hepatitis
Irreversible;
Cirrhosis
Hepatocellular carcinoma
What is alpha 1 anti-trypsin deficiency?
Alpha 1 antitrypsin is a serine protease inhibitor that inhibits neutrophil elastase. Deficiency leads to damage to alveoli and liver
Signs and symptoms of alpha 1 antitrypsin deficiency?
COPD in young individuals
Neonatal jaundice
Deranged LFTs in those with no identifiable cause for cirrhosis
Differentials for alpha 1 antitrypsin deficiency?
COPD
Hepatitis
Alcoholic liver disease
NAFLD
Viral hepatitis
Investigations to diagnose alpha 1 antitrypsin deficiency?
Spirometry; obstructive picture
Alpha 1 antitrypsin levels
Genotyping
Imaging; CXR, CT thorax (panacinar emphysema)
Liver fibroscan
Liver biopsy
Management of alpha 1 antitrypsin deficiency?
Smoking cessation
IV alpha 1 antitrypsin
Liver transplantation
Anti-emetics and their mechanism of action?
H1 receptor antagonists (cyclizine), indicated in vestibular disturbance
D2 receptor antagonists (domperidone, metoclopramide), indicated in post operative nausea, motion sickness
5HT3 receptor antagonist (ondansetron), indicated in acute gastroenteritis, post operative nausea, radiotherapy/ chemotherapy induced
Anti-muscarinic (hyoscine hydrobromide), indicated in vestibular disturbance, palliative care
Which anti-emetics should be avoided in parkinsons?
Prochlorperazine, clorpromazine, haloperidol
Antibodies in pernicious anaemia?
Intrinsic factor
Antibodies in coeliac disease?
Anti-tissue transglutaminase IgA
Anti- endomysial IgA
Anti- deaminated gliadin peptide IgG
Antibodies in primary biliary cirrhosis?
Antimitochondrial antibodies IgM
Antibodies in autoimmune hepatitis?
Anti smooth muscle antibodies IgG
What is ascites?
Abnormal accumulation of fluid within peritoneal cavity
Aetiology of ascites?
Liver disease; cirrhosis, acute liver failure, liver metastases
Cardiac disease; right heart failure
Budd- Chiari, Portal vein thrombosis
Nephrotic syndrome, kwashiorkor, peritoneal carcinomatosis, peritoneal metastases, infection
Signs and symptoms of ascites?
Abdominal distension
Abdominal discomfort or pain
Dyspnea
Reduced mobility
Anorexia and early satiety due to pressure on the stomach
Tense abdomen
Shifting dullness
Stigmata of the underlying cause (see below)
Investigations to find cause of ascites?
Ascitic tap
Bloods; FBC, U+E, LFT, CRP
Imaging; CT abdomen, CXR
Serum ascites albumin gradient SAAG; serum albumin concentration - ascites albumin concentration
Causes of high SAAG (>11g/ L)?
Cirrhosis
Heart failure
Budd Chiari syndrome
Constrictive pericarditis
Hepatic failure
Causes of low SAAG (<11g L)?
Cancer of the peritoneum, metastatic disease
Tuberculosis, peritonitis and other infections
Pancreatitis
Hypoalbuminaemia - nephrotic syndrome, Kwashiokor
Management of ascites?
High SAAG; salt and fluid restriction
Spironolactone
Therapeutic paracentesis
If ascitic tap shows neutrophils >250mm3 treat with IV piperacillin- tazobactam
Refractory ascites in portal hypertension consider TIPS
What is autoimmune hepatitis?
Chronic inflammatory disease of liver as a result of immune attack to hepatic cells
Epidemiology of autoimmune hepatitits?
More common in young middle aged women
Associated with other autoimmune conditions such as pernicious anaemia, ulcerative collitis, hashimotos/ graves, autoimmune haemolytic anaemia, primary sclerosing cholangitis
Symptoms of acute hepatitis?
Acute hepatits; Fever, Jaundice, Malaise, Abdominal pain, Utricarial rash, Polyarthritis, Pulmonary infiltration, Glomerulonephritis
Chronic liver disease; ascites, jaundice, leuconychia, spider naevi
Signs of autoimmune hepatits?
Fatigue
Anorexia
Hepatomegaly
Splenomegaly
Differentials for autoimmune hepatitis?
Acute; Hepatitis A/ E/ B, paracetamol poisoning, ischaemia
Chronic; alcohol, NAFLD, hepatitis B/ C
Investigations to diagnose autoimmune hepatitis?
Bloods; raised ALT, bilirubin, normal ALP
Management of autoimmune hepatitis?
Prednisolone induction therapy
Maintenance therapy with azathioprine
Liver transplantation
What is barrett’s oesophagus?
When any part of the distal squamous epithelium has undergone dysplasia and replaced with metaplastic columnar epithelium
Epidemiology of Barrett’s oesophagus?
Most commonly affecting males over 50 with longstanding GORD
Higher risk in obese people
Risk factors for Barrett’s oesophagus?
GORD- main risk factor
Obesity
Smoking
Hiatus hernia
Increasing age
Signs and symptoms of Barrett’s oesophagus?
Pain in the upper abdomen and chest
Heartburn
Acid taste in the mouth
Bloating
Belching
Anaemia
Weight loss
Anoerxia
Melaena
Investigations to diagnose Barrett’s oesophagus?
OGD- gold standard
What is the 2 week wait referral criteria for Barrett’s oeosphagus?
Dysphagia
>55 years with either weightloss, upper abdominal pain, reflux or dyspepsia
Non urgent direct access for upper GI endoscopy
Management for Barrett’s oesophagus?
If short segment (<3cm) without intestinal metaplasia no further surveillance
If longer segment (>3cm) repeat OGD every 2-3 years
Short segment with intestinal metaplasia OGD every 3-5 years
Indefinite dysplasia every 6 months
Visible high grade dysplasia; endoscopic ablation
Complications of Barrett’s oeosphagus?
Oesophageal adenocarcinoma
What is Budd- Chiari Syndrome?
Obstruction of hepatic venous outflow which impedes drainage of blood from liver leading to hepatomegaly, ascites and liver dysfunction
Causes of Budd- Chiari Syndrome?
Primary; Thrombosis
Polycythaemia
Essential thrombocytosis
Paroxysmal nocturnal haemoglobinuria
Antiphospholipid syndrome
Factor V leiden mutation
Protein C, protein S or antithrombin deficiency
Secondary;
Compression of hepatic veins
Inflammatory conditions
Infections
Pathoph?ysiology of Budd- Chiari Syndrome
Obstruction of hepatic venous outflow leads to increased hepatic sinusoidal pressure causing congestion and ischaemia
Results in hepatocyte injury, fibrosis, cirrhosis
Symptoms of Budd- Chiari Syndrome?
Abdominal pain (RUQ)
Hepatomegaly
Jaundice
Ascites
Peripheral oedema
Splenomegaly
Variceal bleeding
Differentials for Budd Chiari Syndrome?
Cirrhosis
Right heart failure
Constrictive pericarditis
Portal vein thrombosis
Hepatic veno-occlusive disease
Investigations to diagnose Budd Chiari Syndrome?
LFT, FBC, coagulation, serum albumin
USS with doppler
CT/ MRI angiography
Hepatic venography
Liver biopsy
Management of Budd Chiari Syndrome?
Ascites; diuretics, sodium restriction
Nutritional support to avoid hepatotoxic substances
Anticoagulation
Thrombolytic therapy
Angioplasty and stenting
TIPS
Liver transplantation
Complications of Budd Chiari syndrome?
Chronic liver disease and cirrhosis
Portal hypertension -> variceal bleeding
Liver failure
Hepatocellular carcinoma
What is a carcinoid tumour?
Neuroendocrine tumour that secretes serotonin often originating from appendix or small intestine
Where do carcinoid tumours originate from?
Neuroendocine cells most commonly found in GI tract and lungs
Presentation of carcinoid tumour?
Abdominal pain
Diarrhoea
Flushing
Wheezing
Pulmonary stenosis
Differentials for carcinoid tumour?
IBS
IBD
Mastocytosis
Investigations to diagnose carcinoid tumours?
Hormone levels; 5-HIAA which is a breakdown of serotonin
CT/MRI
Octreotide scans
Tissue biopsy
Management of carcinoid tumour?
Octreotide
Surgery
Embolisation
Radiofrequency ablation
What is the cause of cholera?
Vibrio cholerae O1 and O139 gram negative comma shaped bacteria with single polar flagellum
Symptoms of cholera?
Sudden onset of watery diarrhoea
Abdominal cramps
Nausea
Vomiting
Excessive thirst
Dry mouth
Dry skin
Oliguria
Drowsiness or lethargy
Irritability
Differentials for cholera?
Acute gastritis
Rotavirus
Traveler’s diarrhoea
Investigations for cholera?
Stool culture
Rapid diagnostic test
FBC, U+E
Management of cholera?
A-E
Aggressive fluid replacement
Antibiotics; doxycycline
Notifiable disease
What is alcohol dependance?
Primary chronic disease with genetic, psychological and environmental factors influencing its development and manifestation
Screening tools to identify chronic alcoholism?
AUDIT questionnaire
SADQ questionnaire
Indications for inpatient alcohol withdrawal?
Patients drinking >30 units per day
Scoring over 30 on the SADQ score
High risk of alcohol withdrawal seizures (previous alcohol withdrawal seizures or delirium tremens, or history of epilepsy)
Concurrent withdrawal from benzodiazepines
Significant medical or psychiatric comorbidity
Vulnerable patients
Patients under 18
When is assisted alcohol withdrawal required?
If drinking more than 15 units per day
If scoring over 20 points in AUDIT questionnaire
What medications can be used in medically assisted alcohol withdrawal?
Chlordiazepoxide
Acamprosate
Naltrexone/ disulfiram
Psychological intervention; CBT
What is pancreatitis?
Persistent inflammation and fibrosis of exocrine and endocrine components of the pancreas
Epidemiology of pancreatits?
80% of cases are due to chronic alcohol use
Causes of chronic pancreatitis?
Alcohol excess
Genetics; cystic fibrosis
Obstructive causes; pancreatic cancer
Metabolic
Pathophysiology of pancreatitis?
Progressive inflammation and development of fibrotic tissue in pancreas results in loss of exocrine and endocrine function function
Presentation of chronic pancreatitis?
Epigastric pain exacerbated after eating fatty foods and relieved by leaning forward
Bloating
Weight loss
Exocrine dysfunction; Malabsorption and steatorrhoea, reduced absorption of fat soluble vitamins A/D/E/K
Diabetes
Differentials for chronic pancreatitis?
Acute pancreatitis
Pancreatic cancer
Peptic ulcer disease
Abdominal aortic aneurysm
Investigations to diagnose chronic pancreatitis?
Blood glucose
Faecal elastase
Abdominal Xray
CT scan- more sensitive to detect calcification
Management of chronic pancreatitis?
Abstinence from alcohol
Endocrine dysfunction; insulin
Exocrine dysfunction; creon containing mixture of amylase, lipase and protease
Coeliac plexus block, pancreatectomy
Complications from chronic pancreatitis?
Pseudocyst
Pancreatic cancer
Diabetes mellitus
Steatorrhoea
What type of bacteria is clostridium difficile?
Gram positive anaerobic bacteria which produces spores which release exotoxin causing intestinal damage
Classification of clostridium difficile infection?
Non severe;
WWC<15
Rise in creatinine <50% of baseline
Temperature <38.5
Severe;
WWC>15
Rise in creatinine >50% of baseline
Temperature >38.5
Fulminant;
Systemic; hypotension, septic shock, rapid deterioration in condition
Local; ileus, toxic megacolon or bowel perforation
Causes of clostridium difficile infection?
Recent treatment with broad-spectrum antibiotics – nearly all antibiotics can cause C. difficile infection, with common culprits being:
Clindamycin
Ciprofloxacin
Third-generation cephalosporins (eg. Ceftriaxone)
Penicillins including Piperacillin-tazobactam (Tazocin)
Carbapenems (eg. Meropenem)
Increased length of stay in hospital
Age over 65 years
Predisposing conditions including inflammatory bowel disease (IBD), cancer or kidney disease, and immunosuppression (diabetes or HIV infection, or as side effect of chemotherapy or steroids)
Prolonged proton pump inhibitor (PPI) usage
Signs and symptoms of clostridium difficile?
Watery diarrhoea, which can be bloody
Painful abdominal cramps
Nausea
Signs of dehydration, such as dry mucous membranes, tachycardia and oliguria
Fever
Loss of appetite and weight loss
Confusion
Investigations to diagnose clostridium difficile?
Stool culture
Bloods; FBC, U+E, CRP
Abdominal Xray
Management of clostridium difficile?
A-E/ sepsis six
Evaluate antibiotics and stop unnecessary medications
Move to a side room and barrier nursing
Rehydration
Oral vancomycin
Second line fidaxomicin
Third line vancomycin and metronidazole
Surgical resection in life threatening toxic megacolon; subtotal colectomy
Management of clostridium difficile?
Pseudomembranous colitis
Toxic megacolon
Systemic toxicity
What is coeliac disease?
T cell mediated autoimmune disorder affecting the small intestine
Epidemiology of coeliac disease?
Affects females more
More prevalent in Irish descent
Cause of coeliac disease?
Positive family history
HLA-DQ2
History of other autoimmune disease
Symptoms of clostridium difficile?
Gastrointestinal symptoms; abdominal pain, distension, nausea and vomiting, diarrhoea, steatorrhoea
Systemic symptoms; fatigue, weight loss, failure to thrive
Signs of coeliac disease?
Pallor
Short stature
Signs of malabsorption such as bruising
Dermatitis herpetiformis
Abdominal distention
Differentials for coeliac disease?
IBS
IBD
Food intolerance
Gastroenteritis
Malabsorption
Investigations to diagnose coeliac disease?
Stool culture
Bloods; FBC, U+E, Bone profile, LFT, Iron, B12, Folate
anti-TTG, anti- endomysial, anti-gliadin
OGD; villous atrophy, crypt hyperplasia intraepithelial lymphovytes
Management of coeliac disease?
Lifelong gluten free diet
Dermatitis herpetiformis managed with dapsone
Complications of coeliac disease?
Mixed anaemia
Hyposplenism
Osteoporosis
Enteropathy associated T cell lymphoma
What is the Rome IV criteria for constipation?
Fewer than three bowel movements per week
Hard stool in more than 25% of bowel movements
Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements
Excessive straining in more than 25% of bowel movements
A need for manual evacuation of bowel movements
Classification of constipation?
Primary; no organic cause due to dysregulation of the function of colon
Secondary; diet, medication, metabolic, endocrine or neurological
Risk factors for constipation?
Advanced age
Inactivity
Low calorie intake
Low fibre diet
Certain medications
Female sex
Aetiology of constipation?
Dietary factors
Behavioral; inactivity, avoid defecation
Electrolyte disturbance; hypercalcaemia
Medications; opiates, CCB, antipsychotics
Neurological disorder; spinal cord lesion, parkinsons disease, diabetic neuropathy
Endocrine; hypothyroidism
Colon; malignancy, strictures
Anal fissures, proctitis
Signs and symptoms of constipation
Infrequent bowel movements (less than 3 per week)
Difficulty passing bowel motions
Tenesmus
Excessive straining
Abdominal distension
Abdominal mass felt at the left or right lower quadrants (stool)
Rectal bleeding
Anal fissures
Haemorrhoids
Presence of hard stool or impaction on digital rectal examination
Red flags of constipation?
Anaemia
Weight loss
Anorexia
Recent onset
Melaena
Haematemesis
PR bleeding
Swallowing difficulties
Investigations to diagnose constipation?
2WW; constipation with weight loss in anyone over 60
PR exam
Stool culture; MC&S
FIT test
FBC, U+E, TFT, calcium
Abdominal Xray
Barium enema
Colonoscopy
Management of constipation?
Lifestyle intervention
Bulking agents; ispaghula husk
Stimulant; senna
Stool softeners; sodium docusate, macrogol
Osmotic laxative; lactulose
Phosphate enema
Properties of bulk forming laxative?
Increases faecal mass and stimulate peristalsis
Features of stimulant laxative?
Increases intestinal motility
Used for short term relief
Features of stool softeners?
Softens stool to make passage of bowel movement easier
Used in anal fissures with anticipatory withholding
Features of osmotic laxatives?
Retains fluid in bowel and discourage ammonia producing microorganisms
First line for hepatic encephalopathy
Features of phosphate enema?
Used for rapid bowel evacuation before medical procedures
What is Crohn’s disease?
Chronic relapsing inflammatory bowel disease characterised by transmural granulomatous inflammation affecting any part of the GI tract
Aetiology of crohn’s disease?
Family history
Smoking
Diet high in refined carbohydrates and fats
Epidemiology of Crohn’s disease?
More common in northern climates
Increased incidence in Europe in Northern America
More common in 15-40 year olds and 60-80 year olds
Signs and symptoms of Crohn’s?
Crampy abdominal pain
Non bloody diarrhoea
Systemic symptoms; weight loss, fever
Aphthous ulcers in mouth
Right lower quadrant tenderness
Right iliac fossa mass
Perianal tags
Fistulae
Perianal abscess
Erythema nodosum; painful erythematous nodules/ plaques
Pyoderma gangrenosum; well defined ulcer with a purple overhanging edge
Anterior uveitis
Episcleritis
Enteropathic arthropathy
Axial spondyloarthropathy
Gallstones
AA amyloidosis
Investigations to diagnose Crohn’s?
Stool culture
Faecal calprotectin
Bloods; raised WCC, raised ESR/ CRP, thrombocytosis, anaemia, low albumin, haematinics
Endoscopy
MRI- upper GI series shows string of Kantour
Colonoscopy + biopsy; intermittent inflammation, cobblestone appearance, rose thorn ulcers, non caseating granuloma
Management of Crohn’s?
Induce remission;
Glucocorticoids; oral prednisolone or IV hydrocortisone
Maintaining remission;
Azathioprine or mercaptopurine
Methotrexate
Biological; infliximab, adalimumab
Surgical;
If severe disease consider surgery to control fistulae, resection of strictures, rest/ defunctioning of bowel
Management of peri-anal fistulae;
Drainage seton
Fistulotomy
Sphincter saving
Management of peri-anal abscess;
Ceftriaxone + Metronidazole
Examination under anaesthesia, incision and drainage
What should be considered when starting patients on Azathioprine or mercaptopurine?
Assess for thiopurine methyltransferase activity, underactivity increases risk of bone marrow suppression
Complications of Crohns?
Fistulas
Strictures
Abscesses
Malabsorption
Perforation
Nutritional deficiency
Increased risk of colon cancer
Osteoporosis
Intestinal obstruction
Toxic megacolon
Medications which induce CYP450 enzyme?
Carbemazepines
Rifampicin
Alcohol
Phenytoin
Griseofulvin
Phenobarbitone
Sulphonylureas
Medications which inhibit CYP450 enzymes?
Sodium valproate
Isoniazid
Cimetidine
Ketoconazole
Fluconazole
Alcohol & Grapefruit juice
Chloramphenicol
Erythromycin
Sulfonamides
Ciprofloxacin
Omeprazole
Metronidazole
Effect of CYP450 inducers on contraceptives?
COCP and POP are hepatically metabolised so inducers will reduce their effectiveness
What is dyspepsia?
Group of gastrointestinal symptoms such as epigastric pain, bloating, early satiety and nausea
Causes of dyspepsia?
Multifactorial
Dietary habits
Lifestyle choices
Psychological stressors
Helicobacter pylori infection
GORD
Medication uses
Underlying gastrointestinal disorders
Signs and symptoms of dyspepsia?
Epigastric pain or discomfort
Bloating
Belching
Nausea and early satiety
Patients may also report heartburn, regurgitation, or sour taste in the mouth if associated with GORD.
Differentials for dyspepsia?
GORD
Peptic ulcer disease
Gastritis
Gallbladder disease
Pancreatic disorders
Inferior MI
Investigations to identify cause of dyspepsia?
FBC
H.pylori; urea breath test, stool helicobacter antigen test
OGD
2WW; if dysphagia over 55 years with weight loss and any of the following; upper abdominal pain, reflux, dyspepsia
Management of dyspepsia?
Lifestyle; stop smoking, weight loss, avoid trigger foods, eat smaller meals, reduce alcohol
Medication review; exacerbating medications include aspirin, alpha blockers, anticholinergic, benzodiazepines, calcium channel blockers, corticosteroids, nitrates, NSAIDs, TCA
Medical management;
PPI
Treat H.pylori infection
What is dysphagia?
Swallowing difficulty which involves problems in oral, pharyngeal or oesophageal stages of swallowing
Aetiology of dysphagia?
Neurological: Conditions like cerebrovascular disease, Parkinson’s disease, motor neurone disease, myasthenia gravis, and bulbar palsy.
Motility disorders: Including achalasia, diffuse oesophageal spasm, and systemic sclerosis.
Mechanical/obstructive causes: Such as benign strictures, malignancy, pharyngeal pouch, and extrinsic pressure from lung cancer, mediastinal lymph nodes, or retrosternal goitre.
Other: Causes such as oesophagitis, globus (psychological causes), and Plummer-Vinson syndrome.
How to differentiate presentation of dysphagia in relation to cause?
Motility disorders; liquids and solids equally affected from the start
Benign or malignant stricture; progressive dysphagia of solids and then liquids
Neurological; Difficulty in swallowing motion
Candida; painful dysphagia
Pharyngeal pouch; bulging neck on swallowing, gurgling or halitosis
Plummer- Vinson syndrome; upper oesophageal web, post cricoid dysphagia,
Diffuse oesophageal spasm; intermittent dysphagia
Investigations to identify cause of dysphagia?
2WW; dysphagia over 55 years with weight loss and any of upper abdominal pain/ reflux or dyspepsia
FBC
Iron studies
Barium swallow
Manometry
24 hour pH
Management of dysphagia?
SALT assessment
PPI
Iron supplementation
Dilation in achalasia, removal of malignancy
What is enteric fever?
Typhoid or paratyphoid
Infection caused by salmonella typhi and salmonella paratyphi
Epidemiology of enteric fever?
Paratyphoid A,B and C are prevalent in inadequate sanitation and poor water supply
Paratyphoid fever is less common
Highest incidence in south asia, southeast asia, sub saharan africa
Primarily affect children and young adults
Risk factors for contracting typhoid?
Poor sanitation
Poor hygiene
How is typhoid spread?
Ingestion of food or water contaminated with faeces of infected infividual
Signs and symptoms of enteric fever?
Generally well 6-30 days post exposure
Gradual onset with high fever developing over several days
Paratyphoid is a milder illness with shorter incubation period
Weakness & myalgia
Relative bradycardia
Abdominal pain
Constipation (more common than diarrhoea)
Headaches
Vomiting (not usually severe)
Skin rash with rose-colored spots (uncommon, but common in exams!)
Confusion (if severe)
without treatment symptoms persist for weeks
Investigations to diagnose enteric fever?
Measure urine output
ECG
FBC, U+E, CRP, ABG, VBG (lactate), LFT, Group and Save, clotting
Blood culture, stool culture
Bone marrow aspirate- gold standard
MRI if ?osteomyelitis
Management of enteric fever?
Sepsis 6
Azithromycin/ ceftriaxone, some are sensitive to ciprofloxacin
Notifiable disease
Complications of typhoid?
Osteomyelitis
GI bleed/ perforation
Meningitis
What is GORD?
Reflux of gastric contents into oesophagus due to defective lower oesophageal sphincter leading to dyspepsia
Epidemiology of GORD?
10% of UK adults experience GORD
More common in over 50
Pathophysiology of GORD?
Defective LOS enabling reflux of gastric contents into oesophagus
Risk factors for GORD?
Obesity
Alcohol use
Smoking
Intake of coffee, citrus foods, spicy food, fat
Signs and symptoms of GORD?
Typical symptoms; dyspepsia, sensation of acid regurgitation
Atypical symptoms; epigastric/ chest pain, nausea, bloating, belching, blobus, laryngitis, tooth erosion
Alarm symptoms; weight loss, anaemia, dysphagia, haematemesis, melaena, persistent vomiting
Differentials for GORD?
Gastric ulcers
Oesophageal cancers
Functional dyspepsia
Hiatus hernia
Investigations to diagnose GORD?
H.pylori; Urea breath test, stool antigen test
OGD
Oesophageal manometry
Referral criteria for OGD in reflux?
2WW; over 55 years with weight loss and dyspepsia/ reflux
Non urgent;
55 and above with treatment resistant dyspepsia
Raised platelet count
Nausea and vomiting
Management of GORD?
Lifestyle; weight loss, dietary changes, elevation of head at night, avoid late night eating
PPI therapy
H.pylori eradication therapy
Complications of GORD?
Oesophageal ulcer
Oesophageal stricture
Barrett’s oesophagus
Adenocarcinoma of the oesophagus
What is gastroenteritis?
Enteric infection causing acute-onset diarrhoea +/- associated symptoms
What is dysentery?
Is acute infectious diarrhoea with blood & mucus, often with associated symptoms
Causes of diarrhoeal illness?
Norovirus
Rotavirus
Adenovirus
Campylobacter
E.coli
Salmonella
Shigella
Bacillus cereus
Staphylococcus aureus
Cryptosporidium
Entamoeba histolytica
Giardia
Signs and symptoms of gastroenteritis?
Sudden-onset diarrhoea, with or without blood
Faecal urgency
Nausea & vomiting
Fever, malaise
Abdominal pain
Associated symptoms specific to the cause
Investigations to diagnose gastroenteritis?
Stool culture
Bloods; FBC, U+E, CRP, LFT, TFT
VBG
Monitor urine output
Management of gastroenteritis?
A-E
Sepsis 6
Fluids
Anti-emetic
Anti-biotics;
Campylobacter; clarithromycin
Amoeba, giardia; metronidazole
Cholera; tetracycline
Notifiable disease
Complications of gastroenteritis?
Dehydration, electrolyte disturbance, acute kidney injury
Haemorrhagic colitis, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura
Reactive arthritis
Toxic megacolon
Sepsis
Faltering growth
IBS
Lactose intolerance
What is gastroparesis?
Chronic medical condition characterised by delayed gastric emptying without mechanical obstruction due to impaired activity of stomach muscles which delays gastric emptying
Epidemiology of gastroparesis?
Commonly associated with diabetes mellitus
Pathophysiology of gastroparesis?
Autonomic neuropathy
More likely in diabetes, parkinsons, certain medications, multiple sclerosis
Signs and symptoms of gastroparesis?
Nausea
Vomiting
Early satiety (feeling of fullness after a few bites)
Abdominal pain
Bloating
Diabetics; poor glucose level
Differentials for gastroparesis?
Peptic ulcer disease
Gastric outlet obstruction
GORD
Investigations to diagnose gastroparesis?
Solid meal gastric scintigraphy allowing visualisation of rate of gastric emptying
Management of gastroparesis?
Dietary modifications; low fibre, smaller frequent meals, pureed or mashed food
Pharmacological; metoclopramide
What is Giardiasis?
Infectious gastroenteritis cause by protozoan parasite giardia lamblia
Risk factors for giardiasis?
Exposure to contaminated water
Spread via faecal- oral route
Consumption of uncooked fruit or vegetables
Poor hand hygiene
Signs and symptoms of giardiasis?
Explosive, watery, non-bloody diarrhoea
Bloating
Flatulence
Nausea
Weight loss
Anorexia
Differentials for giardiasis?
Parasitic infections; cryptosporidium, entamoeba histolytica
Bacterial gastroenteritis
Viral gastroenteritis
Investigations for giardiasis?
Stool microscopy; repeat 3 times on separate days
Stool antigen test, stool PCR
Duodenal aspirates ad biopsy
Management of giardiasis?
Metronidazole
What is gilberts syndrome?
Inherited autosomal recessive disorder where liver does not process bilirubin due to mutation in UGT1A1 gene resulting in reduced activity of UGT enzyme which conjugates bilirubin with glucuronic acid
Signs and symptoms of gilberts syndrome?
Asymptomatic
Intermittent mild jaundice triggered by stress, fasting, infection, exercise
Differentials for gilberts syndrome?
Hepatitis
Haemolytic anaemia
Cholestasis
Investigations to diagnose gilberts syndrome?
Elevated bilirubin
LFT- otherwise normal
FBC
Management of gilberts syndrome?
No treatment
Monitor condition
What is H.pylori?
Gram negative spiral shaped bacterium
Signs and symptoms of H.pylori infection?
Dyspepsia symptoms
Abdominal discomfort or pain, typically in the upper abdomen
Bloating
Nausea
Loss of appetite
Weight loss
Differentials for H.pylori?
Gastritis
GORD
Gastric cancer
Investigations to diagnose H.pylori?
Stool antigen test
Carbon 13 urea breath test
OGD
Management of H.pylori infection?
First line; amoxicillin + clarithromycin + PPI
Metronidazole if penicillin allergy
After 4-8 weeks retest for H.pylori if still present commence another course of triple therapy with Metronidazole/ clarithromycin + amoxicillin +PPI
If after 2nd course consider PPI+ amoxicillin + tetracycline/ quinolone
If after 2 courses refer to gastroenterologist
Complications of H.pylori?
Duodenal ulcer, gastric ulcer
Gastric cancer
B cell MALT lymphoma
Atrophic gastritis
Causative agents of hepatitis?
Hepatitis A, B, C, D, E
EBV
CMV
Leptospirosis
Malaria
Alcohol
Drugs
Toxins
Autoimmune
Signs and symptoms of hepatitis?
Acute liver failure;
Hepatitis A and E
Fever, malaise, anorexia, Nausea and vomiting
Acute hepatitis;
RUQ pain, jaundice, tender hepatosplenomegaly
Chronic liver failure;
Hepatic encephalopathy, jaundice, ascites, coagulopathy
What type of virus is hepatitis A?
RNA picornavirus transmitted by faecal oral route
Epidemiology of hepatitis A?
High in developing countries
Greatest mortality and morbidity in over 50 years
Presentation of hepatitis A infection?
Flu like symptoms
Jaundice
Pale stools
Dark urine
Abdominal pain
Investigations to diagnose hepatitis A infection?
LFT; raised ALT/ AST
Serology
Management of hepatitis A infection?
Supportive management
Fluid intake
Electrolyte replacement
In which situation is hepatitis E infection associated with higher mortality?
Pregnancy, upto 20% mortality
What type of virus is hepatitis B?
dsDNA virus of hepadenaviridae family
60-90 day incubation period
Epidemiology of hepatitis B?
Most common cause of hepatitis globally
High prevalence in sub saharan africa, asia and pacific islands
Decline in incidence due to vaccination
Transmission of hepatitis B?
Vaginal/ anal intercourse
Transfusion
Vertical transmission
Needle stick injury
Serology results in hepatitis B?
HBsAg (Hepatitis B Surface Antigen); Indicates current infection; persists >6 months
Anti-HBs (Hepatitis B Surface Antibody); Indicates immunity from past infection or vaccination
HBeAg (Hepatitis B e Antigen); Indicates active viral replication; higher infectivity
Anti-HBe (Hepatitis B e Antibody); Indicates lower infectivity; seroconversion is associated with reduced viral replication
HBcAb (Hepatitis B Core Antibody); IgM indicates acute infection; IgG indicates past infection or vaccination
HBV DNA (Hepatitis B Virus DNA); Quantifies viral load; used to monitor response to treatment
Management of hepatitis B infection?
Pegylated interferon can prevent liver disease
Antiviral therapy in adults over 30 years with HBV DNA greater than 2000 and abnormal ALT on 2 consecutive tests 3 months apart
If sudden deterioration in hepatitis B patients consider co-infection with hepatitis D
What is hepatitis C?
RNA virus of flaviviridae family
Complications of hepatitis C infection?
15-25% clear virus
70% go on to develop chronic hepatitis
1-4% develop hepatocellular carcinoma
2-5% develop liver failure
Arthralgia/ arthritis
Sjorgen’s syndrome
Cryoglobulinaemia
Porphyria cutanea tarda
Membranoproliferative glomerulonephritis
Management of hepatitis C?
Nucleoside analogues; sofobuvir, daclatsavir
What is hepatocellular carcinoma?
Primary malignancy of liver predominantly in patients with underlying chronic liver disease and cirrhosis
Epidemiology of hepatocellular carcinoma?
6th most common cancer
Leading cause is chronic hepatitis B infection
Aetiology of hepatocellular carcinoma?
Chronic viral hepatitis (Hepatitis B or C)
Cirrhosis
Non-alcoholic fatty liver disease
Primary biliary cirrhosis
Inherited metabolic diseases
Alcohol misuse
Obesity
Type 2 Diabetes
Rare diseases: Wilson’s disease, porphyria cutanea tarda, alpha-1-antitrypsin deficiency
Signs and symptoms of hepatocellular carcinoma?
Can present with decompensated liver disease or liver failure
Abdominal pain
Weight loss
Jaundice
Ascites
Hepatomegaly, with a ‘craggy’ liver edge on examination
Encephalopathy
Differentials for hepatocellular carcinoma?
Metastatic liver disease
Cirrhosis
Hemangioma
Pancreatic cancer
Cholangiocarcinoma
Investigations to diagnose hepatocellular carcinoma?
Bloods; FBC, U+E, CRP, LFT, coagulation, viral serology, AFP
Abdominal USS
Liver biopsy with CT of chest, abdomen and pelvis
Monitoring of hepatocellular carcinoma?
6 monthly liver ultrasound and AFP measurement
Management of hepatocellular carcinoma?
Surgical resection of early stage tumour
Liver transplant
Radiotherapy
Chemotherapy
Biologicals
Palliative care
What is haemochromatosis?
Autosomal recessive disorder of iron metabolism characterised by accumulation of iron in body
Epidemiology of haemochromatosis?
Common in northern european descent
Affects 1 in 200 people
C282Y homozygous mutation is more common in celtic heritage
Aetiology of haemochromatosis?
Most common genotype is homozygosity for HFE C282Y on chromosome 6
This disrupts control of iron absorption leading to excessive accumulation in the body
Signs and symptoms of haemochromatosis?
Bronze skin
Type 2 diabetes mellitus
Fatigue
Joint pain
Sequalae of chronic liver disease/cirrhosis
Adrenal insufficiency
Testicular Atrophy
Differentials for haemochromatosis?
Wilson’s disease
Alpha- 1 antitrypsin deficiency
Porphyria cutanea tarda
Addisons disease
Investigations to diagnose haemochromatosis?
Transferrin saturation >55%
Raised iron
Low TIBC
Genetic testing for HFE gene mutation
MRI brain to identify higher iron deposition
Liver biopsy to confirm iron stores
Management of haemochromatosis?
Venesection
Desferrioxamine; iron chelating agents
Avoid undercooked seafood, high risk of listeria which thrive on iron
Complications of haemochromatosis?
Dilated cardiomyopathy
Bronze skin
Cirrhosis
Diabetes mellitus
Hypogonadotropic hypogonadism
Arthropathy
What is a hiatus hernia?
Abdominal contents protrude through enlarged oesophageal hiatus in diaphragm
Risk factors for hiatus hernia?
Obesity
Prior hiatal surgery
Increased intra-abdominal pressure, such as from chronic cough, multiparity, or ascites
Increasing age
Types of hiatus hernia?
Sliding hiatal hernia; GOJ slides up into chest resulting in less competent sphincter and consequent acid reflux
Rolling hiatal hernia; GOJ stays in abdomen but part of stomach protrudes into chest alongside oeshphagus
Which type of hiatal hernia is more common?
Sliding hiatal hernia, 80%
Which type of hiatal hernia requires more urgent treatment?
Rolling due to risk of volvulus
Signs and symptoms of hiatal hernia?
Heartburn
Dysphagia
Regurgitation
Odynophagia
Shortness of breath
Chronic cough
Chest pain
Differentials for hiatal hernia?
GORD
Gastritis
Peptic ulcer
Gallstones
Investigations to diagnose hiatal hernia?
Barium swallows
Endoscopy
Oesophageal manometry
Management of hiatal hernia?
Conservative;
Weight loss
Elevating head of bed
Avoid large meals 3-4 hours before bedtime
Avoid alcohol and spicy food
Smoking cessation
Caffeine, fatty foods , chocolate, peppermint, CCB, nitrates and beta blockers should be avoided
Medical;
PPI trial for 4-8 weeks
Surgical;
Nissen’s fundoplication
Complications of hiatal hernia?
Haemorrhage
Volvulus
Ischaemia
Necrosis
Obstruction
Medications which can cause diarrhoea?
Magnesium
Antibiotics, specifically penicillins
Chemotherapy agents
Proton pump inhibitors such as omeprazole
H2 blockers like cimetidine and ranitidine
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Metformin
Medications which can cause constipation?
Anti-depressants
Anti-psychotics
Levodopa
Aluminium-based antacids
Iron supplements
Opiates
Management of iatrogenic constipation/ diarrhoea?
Review and adjust dosage of offending drugs
Consider alternate medications
Anti-diarrhoeal/ laxative for short term use
Encourage hydration and dietary modification
What is IBS?
Chronic GI disorder of abdominal pain/ discomfort associated with altered bowel habits without identifiable structural or biochemical abnormalities
Epidemiology of IBS?
10-20% of adults affected worldwide
Aetiology of IBS?
Genetic predisposition, altered gut microbiota, low grade inflammation and abnormalities in gut-brain axis
Signs and symptoms of IBS?
Abdominal pain or discomfort relieved by defecation or associated with altered bowel frequency or stool form
Altered stool passage
Abdominal bloating
Symptoms worsened by eating
Passage of mucus
Lethargy, nausea, backache
Differentials for IBS?
IBD
Coeliac disease
Colorectal cancer
Investigations to diagnose IBS?
Diagnosis of exclusion, investigations to rule out other causes
Faecal calprotectin
FBC
ESR
CRP
Coeliac serology
Consider abdominal USS, sigmoidoscopy, colonoscopy, TFT, FIT test, faecal ova and parasite test, hydrogen breath test
Management of IBS?
Regular exercise, stress management
Low FODMAP diet
Low dose TCA
Psychotherapy, CBT, hypnotherapy
Aetiology of jaundice?
Pre-hepatic; gilberts disease, crigler-naajjar, haemolysis, rifampicin
Hepatic;
Viruses (hepatitis, CMV, EBV)
Drugs, including paracetamol overdose, nitrofurantoin, halothane, valproate, statins, tuberculosis antibiotics
Alcohol
Cirrhosis
Liver mass (abscess or malignancy)
Haemochromatosis
Autoimmune hepatitis
Alpha-1 antitrypsin deficiency
Budd-Chiari
Wilson’s disease
Failure to excrete conjugated bilirubin (Rotor and Dubin-Johnson syndromes)
Post hepatic;
Primary biliary cirrhosis
Primary sclerosing cholangitis
Common bile duct gallstones or Mirrizi’s syndrome (CBD compression from a gallstone in the cystic duct)
Drugs, including coamoxiclav, flucloxacillin, steroids, sulfonylureas
Malignancy, such as head of the pancreas adenocarcinoma, cholangiocarcinoma
Caroli’s disease
Biliary atresia
Signs and symptoms of jaundice?
Pre-hepatic: haemolysis, anaemia (fatigue, chest pain, palpitations, lightheadedness)
Hepatic: RUQ pain, fever, viral illness, risk factors include: IVDU/tattoo, UPSI
Post-hepatic: dark urine, pale stools, itch
What is courvoisier’s law?
Jaundice and palpable painless gallbladder not due to gallstones. Painless jaundice – red flag for pancreatic cancer or cholangiocarcinoma
What is liver cirrhosis?
Irreversible scarring of the liver with loss of normal hepatic architecture
Causes of liver cirrhosis?
Commonest causes:
Alcohol
Hepatitis B and C
Non-alcoholic fatty liver disease (NAFLD)
Less common causes:
Autoimmune: Autoimmune hepatitis, Primary biliary cirrhosis, Primary sclerosis cholangitis, Sarcoid
Genetic: Haemochromatosis, Wilson’s disease, Alpha-1-antitrypsin deficiency
Drugs: Methotrexate, Amiodarone, Isoniazid
Others: Budd-Chiari Syndrome, Heart failure, Tertiary syphilis
Signs and symptoms of liver cirrhosis?
Compensated;
Fatigue and anergia
Anorexia and cachexia
Nausea or abdominal pain
Spider naevi
Gynaecomastia
Finger clubbing
Leuconychia
Dupuytren’s contracture
Caput medusae
Splenomegaly
Decompensated;
Ascites and oedema
Jaundice
Pruritus
Palmar erythema
Gynaecomastia and testicular atrophy
Easy bruising
Encephalopathy/confusion
Liver ‘flap’
Differentials for Liver cirrhosis?
Hepatic steatosis
Chronic hepatitis
Congestive heart failure
Investigations to diagnose cirrhosis?
LFT; AST, ALT, ALP, GGT, albumin, bilirubin
FBC; leukocytosis, thrombocytopenia, anaemia
U+E
INR
Hepatitis serology
Peritoneal tap
Doppler USS
Fibroscan
Liver biopsy
What is the child pugh score?
Assess severity of liver cirrhosis
Takes into account bilirubin, albumin, PT, encephalopathy, ascites
A; <7 points
B; 7-9 points
c; >9 points
Interpretation of MELD score?
6-9; Low risk of mortality; Class I (less than 10%)
10-19; Intermediate risk of mortality; Class II (19%)
20-29; High risk of mortality; Class III (52%)
30-39; Severe risk of mortality; Class IV (71%)
≥40; Very severe risk of mortality; Class V (95%)
Management of liver cirrhosis?
Nutrition and no alcohol
Avoid NSAIDs, sedatives and opiates
6 month scans and serum AFP
Upper GI endoscopy
Cholestyramine for pruritus
Ascites; fluid restriction, low salt diet, spironolactone, furosemide, therapeutic paracentesis, albumin infusion
Liver transplant
Complications of liver cirrhosis?
Ascites
Spontaneous bacterial peritonitis
Liver failure
Hepatocellular carcinoma
Oesophageal varices +/- haemorrhage
Renal failure
What is liver failure?
Loss of liver function and development of complications including coagulopathy, jaundice, encephalopathy
Aetiology of liver failure?
Acute liver failure; viral hepatitis, drug induced liver injury (paracetamol halothane, isoniazid), toxic exposure, vascular disorder (budd- chiari syndrome, hepatic vein obstruction)
Chronic liver failure; alcohol misuse, chronic viral hepatitis, non alcoholic fatty liver disease, autoimmune liver disease (autoimmune hepatitis, primary biliary cholangitis), wilson’s disease, alpha-1 antitrypsin deficiency
Signs and symptoms of liver failure?
Hepatic encephalopathy
Abnormal bleeding
Jaundice
Pathophysiology of hepatic encephalopathy?
Ammonia accumulates in blood and crosses blood brain barrier and is metabolised by astrocytes to form glutamine.
Glutamine disrupts osmotic balance and astrocytes begin to swell resulting in cerebral oedema
Stages of hepatic encephalopathy?
Altered mood and behaviour, disturbance of sleep pattern and dyspraxia
Drowsiness, confusion, slurring of speech and personality change
Incoherency, restlessness, asterixis
Coma
Investigations to diagnose liver failure?
INR, coagulation studies
LFT, albumin
FBC, U+E, haematinics
Viral serology
Ascitic drain
Abdominal ultrasound scan
Doppler ultrasound scan
OGD
Management of liver failure?
Hepatic encephalopathy; lactulose, rifaximin, mannitol
Coagulopathy; vitamin K, FFP
Spontaneous bacterial peritonitis; IV piperacillin- tazobactam
TIPSS
Liver transplant
What is hepatorenal syndrome?
Cirrhosis
Ascites
Renal failure
Criteria for liver transplant if paracetamol induced?
Arterial pH <7.3 24h after ingestion OR
Pro-thrombin time >100s
AND creatinine >300µmol/L
AND grade III or IV encephalopathy.
Non paracetamol induced liver transplant criteria?
Prothrombin time >100s OR
Any three of:
Drug-induced liver failure
Age under 10 or over 40 years
1 week from 1st jaundice to encephalopathy
Prothrombin time >50s
Bilirubin ≥300µmol/L.
What is malabsorption?
Clinical syndrome characterised by impaired absorption of nutrients, vitamins or minerals from diet resulting in nutritional deficiencies
Aetiology of malabsorption?
Gastric causes; post gastrectomy
Small bowel causes; coeliac, crohns, small bowel resection
Pancreatic causes; chronic pancreatitis, pancreatic cancer, cystic fibrosis
Hepatobiliary causes; primary biliary cirrhosis, ileal resection, post cholecystectomy
Infective; giardasis, whipple’s disease, bacterial overgrowth
Signs and symptoms of malabsorption?
Diarrhoea
Steatorrhoea
Weight loss
Nutritional deficiency leading to anaemia, osteoporosis, peripheral neuropathy
What is malnourishment?
A body mass index (BMI) of less than 18.5 kg/m2.
Unintentional weight loss greater than 10% within the last 3–6 months.
A BMI of less than 20 kg/m2 and unintentional weight loss greater than 5% within the last 3–6 months.
What is melanosis coli?
Histological condition due to laxative abuse characterised by presence of dark brown pigmentation of the macrophages in the lamina propria of the colon
Epidemiology of melanosis coli?
Prolonged laxative use
Higher in elderly and young females
Aetiology of melanosis coli?
Laxative use, especially senns
Signs and symptoms of melanosis coli?
Chronic constipation
Abdominal discomfort
Anorexia nervosa/Bulimia - patients may be young and underweight with a history of purging.
Nausea
Differentials for melanosis coli?
IBD
Colorectal cancer
Ishcaemic colitis
Investigations to diagnose melanosis coli?
Colonoscopy
Histology; presence of pigmented macrophages in lamina propria
Management of melanosis coli?
Cessation of laxatives
What is MALT lymphoma?
Low grade non hodgkins lymphoma that originates from B lymphocytes in the marginal zone
Aetiology of MALT lymphoma?
H.pylori infection
Chronic inflammation
Signs and symptoms of MALT lymphoma?
Abdominal pain
Nausea and vomiting
Symptoms of anaemia
Weight loss
Differentials for MALT lymphoma?
Gastric adenocarcinoma
Gastritis
Peptic ulcer disease
Investigations to diagnose MALT lymphoma?
Endoscopy and biopsy
Immunohistochemistry
CT/ PET scan
Management of MALT lymphoma?
H. pylori eradication therapy
Chemotherapy/ radiotherapy
What is NAFLD?
Excessive fat accumulation in the liver in the absence of significant alcohol consumption
Epidemiology of NAFLD?
Affects 23-30%
Risk factors for NAFLD?
Obesity
Type 2 diabetes mellitus
Hyperlipidaemia (high triglycerides and low HDL)
Hypertension
Jejunal bypass surgery
Rapid weight loss or prolonged starvation
Polycystic ovary syndrome (PCOS)
Hypothyroidism
Obstructive sleep apnoea
Pathophysiology of NAFLD?
Steatosis; fat accumulates in the hepatocytes
Non alcoholic steatohepatitis; inflammation and hepatocellular injury in addition to fat accumulation leading to fibrosis
Fibrosis and cirrhosis; progressive scarring of the liver tissue leading to liver failure and increased risk of hepatocellular carcinoma
Signs and symptoms of NAFLD?
Fatigue
Right upper quadrant discomfort
Hepatomegaly
Jaundice
Ascites
Peripheral oedema
Hepatic encephalopathy
Differentials for NAFLD?
Alcoholic liver disease
Chronic hepatitis B and C
Autoimmune hepatitis
Wilson’s disease
Haemochromatosis
Drug induced liver injury
Investigations to diagnose NAFLD?
Bedside; History and examination
ALT, AST, GGT, ALP, albumin, clotting, FBC, lipid profile, viral serology
Ultrasound scan, fibroscan
Liver biopsy
Management of NAFLD?
Lifestyle modification, abstain from alcohol, vaccination against hepatitis A and B, avoid hepatotoxic medications
Control diabetes, hyperlipidaemia, hypertension
Vitamin E, pioglitazone
Complications of NAFLD?
Steatosis
Progression to cirrhosis
Liver failure
Hepatocellular carinoma
CVD due to metabolic syndrome
What is varices?
Dilated veins which are formed due to portal hypertension
Epidemiology of varices?
Common in patients with advanced liver disease
Occur in 50% of patients with cirrhosis
Variceal bleeding is leading cause of mortality
Gastric varices are less common than oesophageal
Causes of oesophageal varices?
Result of portal hypertension which can be due to cirrhosis, portal vein thrombosis, schistosomiasis, hepatic fibrosis
Signs and symptoms of a variceal bleed?
Haematemesis (vomiting of blood)
Melena (black, tarry stools)
Palpitations
Syncope (fainting)
Hypotension (low blood pressure)
Differentials for oesophageal varices?
Gastric ulcers
Duodenal ulcers
Mallory- weiss tears
Investigations to diagnose oesophageal varices?
Endoscopy
OGD
Management of oesophageal varices?
In acute bleed; correct clotting abnormalities, FFP and platelet transfusion
Trelipressin
Broad spectrum antibiotics to reduce risk of spontaneous bacterial peritonitis
Variceal band ligation
Sengstaken- Blakemore
Thiamine
Prevention; beta blocker, variceal band ligation, TIPSS
What is oesophagitis?
Inflammation of the oesophagus commonly due to reflux of gastric contents
Aetiology of oesphagitis?
Reflux of gastric contents, the most common cause
Medications e.g. NSAIDs
Infections
Allergens, as seen in eosinophilic oesophagitis
Presentation of oesophagitis?
‘Heartburn’ or retrosternal burning pain
Nausea with or without vomiting
Odynophagia, or painful swallowing
Differentials for oeosphagitis?
GORD
Gastritis
Peptic ulcer disease
Investigations to diagnose oesophagitis?
Endoscopy
Oesophageal pH monitoring
Management of oeosphagitis?
Lifestyle changes; weight loss, cessation of smoking, reduce alcohol intake
Pharmacological treatment; PPI for 1 month
What is oral candida?
White patches in mouth due to fungal infection, patches can be scraped off with friable mucosa underneath satellite lesions
Risk factors for oral candida?
Old age
Diabetes mellitus
Immunosuppression
Long term corticosteroids
Malignancy
Antibiotics
Treatment of oral candida?
Nystatin
Fluconazole
Aetiology of hairy leukoplakia?
EBV and is a sign of underlying HIV
Difference between candida and hairy leukoplakia?
Candida can be scrapped of but hairy leukoplakia cannot
What is peptic ulcer disease?
Painful sores/ ulcers in the lining of the stomach/ duodenum
Epidemiology of peptic ulcer disease?
Duodenal ulcers are 4 times as common as gastric ulcers
H.pylori accounts for 90% of duodenal ulcers
Risk factors for duodenal ulcers?
H.pylori infection
NSAIDs
Chronic use of steroids
SSRIs
Increased secretion of gastric acid
Smoking
Blood group O
Accelerated gastric emptying
Risk factors for gastric ulcers?
NSAIDs
H. Pylori infection
Smoking
Delayed gastric emptying
Severe stress
Presentation of gastric ulcer?
Abdominal pain exacerbated by eating
Nausea
Vomiting
Loss of appetite
Unexplained weight loss
Duodenal ulcer causes epigastric abdominal pain relieved by eating
Differentials for peptic ulcer disease?
Gastritis
GORD
Stomach cancer
Investigations to diagnose peptic ulcer disease?
Over 55 with dyspepsia and weight loss should ave 2WW
C-13 urea breath test
Endoscopy + biopsy
Management of peptic ulcer disease
Smoking cessation
Reducing alcohol intake
Regular, small meals and avoiding eating 4 hours before bedtime
Avoidance of acidic, fatty or spicy foods, and coffee
Weight loss if overweight
Stress management
Avoidance of NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs, and crack cocaine
Over-the-counter antacids
H.pylori eradication;
If associated with NSAID use; 8 week PPI then eradication therapy of amoxicillin + clarythromycin/ metronidazole
if not associated with NSAID then start PPI with eradication therapy
What is pernicious anaemia?
Autoimmune destruction of parietal cells in the gastric mucosa resulting in an intrinsic factor deficiency and hence vitamin B12
Pathological processes in pernicious anaemia?
Autoimmune attack
Intrinsic factor deficiency
Vitamin B12 deficiency
Megaloblastic changes
Haemolysis
Epidemiology of pernicious anaemia?
More common in Northern European, Scandinavian and African descent affecting adults aged 60
More common in those with other autoimmune disease
Signs and symptoms of pernicious anaemia?
Fatigue
Pallor
Glossitis - inflammation of the tongue, leading to a smooth, beefy-red appearance.
Neurological Symptoms and subacute combined degeneration of the cord: Pernicious anaemia may cause neuropathy, affecting balance, sensation, and coordination.
Jaundice - due to haemolysis
Cognitive Impairment - memory problems, confusion, and mood changes may occur
Differentials for pernicious anaemia?
Iron deficiency anaemia
Folate deficiency anaemia
Myelodysplastic syndromes
Investigations to diagnose pernicious anaemia?
FBC; low Hb, high MCV, high MCH, normal MCHC, low reticulocyte count
Blood smear; abnormally large oval shaped RBC
Haematinics, B12 assay
Parietal cell antibodies
Bone marrow aspiration and biopsy
Management of pernicious anaemia?
Lifelong hydroxycobalamin replacement
Consider folate replacement
Complications of pernicious anaemia?
Gastric cancer
Peripheral neuropathy
Subacute combined degeneration of the cord
Optic atrophy
Dementia
Hypothyroidism
Vitiligo
What is a Zenker’s diverticulum?
Pharyngeal pouch characterised by herniation of the pharyngeal mucosa through a point of weakness between thyropharyngeus and cricopharyngeus muscle in the inferior constrictor of the pharynx
Epidemiology of pharyngeal pouch?
Affects older adults over the age of 70 years
More common in males with ratio of 2:1
Signs and symptoms of pharyngeal pouch?
Dysphagia
Regurgitation of undigested food, resulting in halitosis
Aspiration
Chronic cough
Weight loss
Management of pharyngeal pouch?
If small and asymptomatic; watch and wait
Surgical; resection of the diverticulum, incision of the circopharyngeus
What is primary biliary cholangitis?
Autoimmune disease of the bile ducts that leads to scarring and inflammation leading to eventual liver cirrhosis
Epidemiology of primary biliary cholangitis?
More commonly affects women
25% of patients are under 40 years
10% of patients are male
Risk factors for PBC?
Previous family history of PBC
Female
Smoking
Predisposition to other autoimmune conditions (80% have Sjogren’s)
Signs and symptoms of PBC?
Extreme fatigue
Pruritus (itching)
Xerosis (dry skin)
Sicca syndrome (dry eyes)
RUQ pain
Xanthelasma
Clubbing
Jaundice
Late signs include sequalae of chronic liver disease
Increased risk of HCC
Differentials for PBC?
Autoimmune hepatitis
Chronic viral hepatitis
Primary sclerosing cholangitis
Alcoholic liver disease
Investigations to diagnose PBC?
Deranged LFTs
Positive AMA
Raised serum IgM
Abdominal USS
MRCP- Gold standard for visualising liver and bile duct
Liver biopsy
Management of PBC?
Ursodeoxycholic acid to slow disease progression by promoting bile flow
Cholestyramine for relief of pruritus
Vitamin supplements to manage deficiencies
Liver transplantation in advanced cases, often once bilirubin is >100 this is considered (Note: PBC may recur after transplantation)
Complications of PBC?
Chronic liver disease
Osteomalacia
What is primary sclerosing colangitis?
Chronic cholestatic disorder characterised by inflammation and fibrosis of intrahepatic and extrahepatic bile ducts leading to multifocal biliary strictures
Epidemiology of PSC?
More common in those with IBD, especially UC, 80% of PSC patients have UC
Associated with increased risk of colorectal and hepatobiliary cancers
Aetiology of PSC?
Autoimmune disease associated with positive anti- smooth muscle, antinuclear and p-ANCA antibodies
Signs and symptoms of PSC?
Hepatomegaly
Jaundice
Right upper quadrant pain
Fatigue, weight loss, fevers, and sweats
Associated with ulcerative colitis
Differentials of PSC?
Autoimmune hepatitis
Cholangiocarcinoma
Primary biliary cholangitis
Investigations to diagnose PSC?
Deranged LFT
Positive anti-smooth muscle , antinuclear and p-ANCA antibodies
Hypergammaglobulinaemia
MRCP/ ERCP
Liver biopsy
Management of PSC?
Lifestyle changes such as alcohol avoidance
Symptomatic management such as cholestyramine for pruritus
Supplementation of fat soluble vitamins (A,D,E,K)
Strictures may be dilated via ERCP
Liver transplantation may be indicated in cases complicated by chronic liver disease and/or hepatobiliary malignancies.
Complications of PSC?
Cholangiocarcinoma
Colorectal cancer
What is Ulcerative collitis?
Chronic relapsing-remitting inflammatory disease affecting large bowel typically starting at the rectum which spreads proximally upto the ileocaecal valve
Epidemiology of ulcerative collitis?
More prevalent in those 15-25 years and 55-65 years
Signs and symptoms of UC?
Diarrhoea often containing blood and/or mucus
Tenesmus or urgency
Generalised crampy abdominal pain in the left iliac fossa
Weight loss
Fever
Malaise
Anorexia
Extra-intestinal manifestations;
Dermatological; erythema nodosum, pyoderma gangrenosum
Ocular; anterior uveitis, episcleritis, conjunctivitis
Musculoskeletal; clubbing, non- deforming asymmetrical arthritis , sacroiliitis
Hepatobiliary; jaundice
AA amyloidosis
Differentials for Ulcerative collitis?
Crohns disease
Infective collitis
Ischaemic collitis
Investigations to diagnose ulcerative collitis?
Stool microscopy
Faecal calprotectin
FBC
CRP/ ESR
LFT
Abdominal xray to rule out to toxic megacolon/ perforation
Endoscopy/ colonoscopy
Biopsy
Barium enema
System to determine severity of ulcerative collitis?
Truelove and Witt’s criteria
Management of ulcerative collitis?
Mild to moderate disease;
Proctitis/ proctosigmoiditis; aminosalicylate, oral prednisolone, consider tacrolimus
Left sided/ extensive disease; high dose oral aminosalicylate, oral prednisolone
Acute severe disease;
IV corticosteroids
If no improvement in 72 hours IV ciclosporin
Surgery
Complications of ulcerative collitis?
Toxic megacolon
Massive lower GI haemorrhage
Colorectal cancer
Cholangiocarcinoma
Colonic strictures
Primary sclerosing cholangitis
Inflammatory pseudopolyps
Increased risk of VTE
What is whipples disease?
Rare systemic infectious disorder caused by bacterium tropheryma whipplei and affects GI system, joints and nervous system
Aetiology of whipples disease?
Tropheryma whipplei
Signs and symptoms of whipples disease?
Chronic diarrhoea
Abdominal pain
Joint pain
Weight loss
Heart failure
Neurological disturbance
Differentials for whipples disease?
IBD
Rheumatoid arthritis
Malabsorption syndrome
Investigations to diagnose whipples disease?
Small bowel biopsy; presence of acid- schiff positive macrophages
Electron microscopy shows macrophages containing causative bacterium
Management of whipples disease?
Long term co- trimoxazole
What is Wilson’s disease?
Autosomal recessive hereditary disorder characterised by impaired copper metabolism
Aetiology of wilsons disease?
Mutation in ATP7B gene which encodes a protein vital for copper transportation and elimination in the body resulting in copper accumulation in the liver and brain
Signs and symptoms of wilsons disease?
Hepatic manifestations: These range from asymptomatic disease with minor transaminase elevation, acute hepatitis, acute-on-chronic liver failure, to cirrhosis. Copper release into the bloodstream may cause Coomb’s negative haemolytic anaemia, characterized by transient low-grade haemolysis and jaundice.
Neurological manifestations: These include akinetic-rigid syndrome similar to Parkinson’s disease, pseudosclerosis dominated by tremor, ataxia, and a dystonic syndrome leading to severe contractures. Additional neurological findings may include drooling, spasticity, chorea, athetosis, myoclonus, micrographia, dyslalia, hypomimia, and dysarthria.
Psychiatric manifestations: These may precede hepatic or neurological signs in up to a third of patients and may include decreased academic performance, personality changes, sexual exhibitionism, impulsiveness, labile mood, inappropriate behaviour, depression, paranoia, schizophrenia, and, in rare cases, suicide.
Ocular manifestations: Include the presence of Kayser-Fleischer rings and sunflower cataracts, which are attributed to copper deposition in the Descemet’s membrane and the anterior and posterior capsule of the lens in the former and latter, respectively.
Differentials for wilsons disease?
Hepatitis; viral, autoimmune
Parkinsons disease
Cirrhosis
Psychiatric disorder; schizophrenia, paranoia, depression
Management of wilsons disease?
The first line blood test is serum caeruloplasmin - <140mg/L i.e. low, is pathogonomic. Can also measure total serum copper (low).
A 24-hour urine collection for measuring urinary copper excretion, which is typically high.
Genetic analysis of the ATP7B gene to confirm the diagnosis.
Imaging: MRI brain – may show basal ganglia degeneration
Invasive: Liver biopsy – increased hepatic copper
Management of wilsons disease?
Avoid chocolate, nuts, liver
Chelators; D-penicillamine, trientine
Zinc salts
For severe disease liver transplantatin
Prognosis of wilsons disease?
Good prognosis with early diagnosis
Untreated disease can lead to liver failure
What is zollinger ellison syndrome?
Tumour that sits in the pancreas or duodenum. There is uncontrolled release of gastrin from gastrinoma resulting in development of ulcerations in the stomach and duodenum
Epidemiology of zollinger ellison syndrome?
0.5-2 per million
Aetiology of Zollinger Ellison syndrome?
MEN type 1
Signs and symptoms of zollinger ellison syndrome?
Abdominal pain, particularly in the epigastric region
Diarrhoea
Ulceration of the duodenum, which can often lead to gastrointestinal bleeding
Non-responsiveness to simple Proton Pump Inhibitors (PPIs)
Differentials for zollinger ellison syndrome?
Peptic ulcer disease
Gastritis
GORD
Investigations to diagnose zollinger ellison syndrome?
Gastrin levels
Secretin stimulation test
Somatostain receptor scintigraphy
Endoscopy
Management of zollinger ellison syndrome?
Surgical resection
PPI
Chemotherapy, somatostatin analogues
