Gastroenterology Flashcards
Mechanical causes of dysphagia
Malignancy - pharyngeal, oesophageal, gastric cancers
Benign strictures - oesophageal web, peptic stricture
Extrinsic pressure - lung cancer, mediastinal LNs, aortic aneurysm, retrosternal goitre
Pharyngeal pouch
Motility disorders that cause dysphagia
Achalasia
Oesophageal spasm
Systemic sclerosis
Neurological bulbar palsy - Parkinson’s disease, MG, multiple sclerosis, CVA
Dysphagia - Causes of difficulty swallowing solids and liquids from the start?
Motility disorder - achalasia, CNS, pharyngeal
Dysphagia - causes of difficulty swallowing solids and then liquids
Stricture - malignancy and benign stricture
Dysphagia - causes of difficulty initiating swallowing movement
Bulbar palsy - especially if patient coughs on swallowing
Dysphagia - causes of painful swallowing (odynophagia)
Ulceration - malignancy, oesophagitis, viral infection, candida, spasm.
Dysphagia - causes of intermittent and constant/getting worse
Intermittent - oesophageal spasm
Constant/getting worse - malignant stricture
Dysphagia - cause of neck bulge on drinking?
Pharyngeal pouch
Investigations of dysphagia
Bloods - FBC, U&E
Upper GI endoscopy and/or biopsy
For motility disorders - fluoroscopic swallowing studies
For pharyngeal pouch - contrast swallow
Symptoms of dyspepsia (including red flag symptoms)
Epigastric pain Fullness after eating Heartburn Tender epigastrium Red flags (ALARMS) - Anaemia, Loss of weight, Anorexia, Recent onset symptoms, Melaena, swallowing difficulty
Dyspepsia - Requirements of urgent referral for 2 week wait endoscopy
All patients who have got dysphagia
All patients with upper abdominal mass consistent with stomach cancer
Patients aged >= 55 years who have got weight loss and any of the following - upper abdominal pain, reflux, dyspepsia
Dyspepsia - Requirements for non-urgent referral for endoscopy
Patients with haematemesis
Patients aged >=55 years who have got either - treatment resistant dyspepsia, upper abdominal pain with low Hb levels, raised platelet count, or nausea and vomiting
Dyspepsia - management for patients who do not meet referral criteria
- Review medications for cause - eg NSAIDS
- Lifestyle advice
- Trial of full-dose PPI for 1 month OR ‘test and treat’ approach for H. pylori
Test for H.pylori
Urea breath test
Treatment for H.pylori
PPI + amoxicillin + clarithromycin for 7 days
Risk factors for peptic ulcer disease
H.pylori
Drugs - NSAIDs, SSRIs, Steroids, Bisphosphonates
Zollinger-Elison syndrome (excessive levels of gastrin)
Alcohol
Smoking
Symptoms of peptic ulcer disease
Epigastric pain
Nausea
Duodenal Ulcers - epigastric pain when hungry, relieved by eating
Gastric ulcers - epigastric pain worsened by eating
What is zollinger-ellison syndrome
Gastrin secreting tumour of either duodenum or pancreas causing excessive levels of gastrin
Features - multiple ulcers, diarrhoea, malabsorption
Diagnosis - fasting gastrin levels, secretin stimulation test
Complications of peptic ulcer disease
Bleeding, perforation, malignancy, reduced gastric outflow
Causes of GORD
Lower oesophageal sphincter hypotension Hiatus hernia Oesophageal dysmotility Obesity Gastric acid hypersecretion Smoking Alcohol Pregnancy Drugs - TCA, anticholinergics, nitrates H.pylori
Symptoms of GORD
Heartburn Belching Acid brash Waterbrash - increased salivation Odynophagia Extra-oesophageal - nocturnal asthma, chronic cough, laryngitis, sinusitis
Complications of GORD
Oesophagitis
Ulcers
Iron-deficiency anaemia
Barrett’s oesophagus (metaplasia from squamous to columnar)
Investigations of GORD
Endoscopy if dysphagia
Endoscopy if >=55 and have dysphagia, relapsing symptoms, weight loss etc
If endoscopy negative - 24 hours oesophageal pH monitoring
Treatment of GORD
Lifestyle - weight loss, smoking cessation, small regular meals, reduce alcohol, avoid eating >3 hours before bed
+ve endoscopy - full dose PPI for 1-2 months. If responding, use low dose treatment PRN. If not responding, double-dose PPI for 1 month
-ve endoscopy - full dose PPI for 1 month. If responding, use low dose PPI PRN. If not responding, H2RA or pro kinetic for 1 month.
What are the two types of Hiatus Hernia?
Sliding (95%) - gastroesophageal junction moves above diaphragm
Rolling - gastroesophageal junction remains below diaphragm, but a separate part of the stomach herniates through the oesophageal hiatus.
What is Achalasia?
Features of achalasia
Investigations for achalasia
Treatment of achalasia
Failure of oesophageal peristalsis and loss of LOS relaxation due to loss of Auerbach’s plexus ganglia.
Common in middle-aged men and women
Features - dysphagia of solids and liquids, heartburn, regurgitation of food
Investigations - oesophageal manometry (excessive LOS tone which doesn’t relax on swallowing). Barium swallow (bird’s beak appearance). CXR (wide mediastinum, fluid level)
Treatment - injection of botulinum toxin. Heller cardiomyotomy. Balloon dilation.
What’s the definition of diarrhoea
> 3 loose or watery stool per day.
Acute - <14 days
Chronic - >14 days
Lifestyle treatment of constipation
Encourage fluid intake
Diet/exercise advice
High fibre diet
Types of laxatives
Bulking agents - increase faecal mass, stimulating peristalsis. Isphagula husk, fybogel, celevac.
Stimulant laxatives - increase intestinal motility. Senna, docusate, bisacodyl
Stool softeners - arachis oil enemas
Osmotic agents - retain fluid in bowel. Lactulose, macrogol (movicol), phosphate enemas.
Symptoms and signs of Crohn’s disease
Diarrhoea - non-bloody Abdominal pain Weight loss Failure to thrive Fatigue, fever, malaise, anorexia
Extra-intestinal symptoms of Crohn’s disease
Arthritis (most common) Erythema nodosum Episcleritis Osteoporosis Uveitis Pyoderma gangrenosum
Investigations for Crohn’s disease
Bloods - FBC, ESR, CRP, U&E, LFT, INR, B12, folate, ferritin, TIBC
Stool - MC&S, faecal calprotectin
Colonoscopy + biopsy
Capsule endoscopy for proximal bowel disease
Crohn’s disease management
Lifestyle - stop smoking, avoid NSAIDs, COCP
Inducing remission - Prednisolone first line. Elemental diet. Mesalazine used second-line.
Azathioprine or mercaptopurine used as add-on therapy.
Infliximab for refractory disease.
Maintaining remission - Azathioprine or mercaptopurine used first-line.
Methotrexate second-line.
5-ASA if patient has had previous surgery.
Surgery - ileocaecal resection.
Complications of Crohn’s disease
Small bowel cancer, colorectal cancer, osteoporosis, small bowel obstruction, toxic dilatation, abscess formation.
Symptoms of Ulcerative Colitis
Bloody diarrhoea LLQ Abdominal pain Urgency Tenesmus Systemic symptoms in attacks - fever, malaise, anorexia, reduced weight
Extraintestinal symptoms of Ulcerative Colitis
Arthritis (most common) Episcleritis Erythema nodosum Pyoderma gangrenosum conjunctivitis Primary sclerosis cholangitis Uveitis Ankylosing spondylitis
Investigations of Ulcerative Colitis
Bloods - FBC, U&E, ESR, CRP, LFT, blood culture
Stool -faecal calprotectin
AXR - loss of haustrations, superficial ulceration (pseudo polyps), drainpipe colon.
Lower GI endoscopy - limited flexible sigmoidoscopy.
How to differentiate between mild, moderate and severe ulcerative colitis
Mild - <4 stools daily, no systemic disturbance, normal ESR and CRP
Moderate - 4-6 stools daily, minimal systemic disturbance
Severe - >6 stools daily, containing blood. Systemic disturbance eg fever, tachycardia, abdominal tenderness, distension of reduced bowel sounds, anaemia, hypoalbuminaemia
Signs on bowel enema in Crohn’s disease
Strictures - Kantor’s string sign
Proximal bowel dilation
Rose thorn ulcers
Fistulae
Management of Ulcerative Colitis
Induction (mild to moderate)
Proctitis - Rectal mesalazine first line. If remission not achieved in 4 weeks, add oral mesalazine. If still not remission, add topical or oral corticosteroid.
Proctosigmoiditis and left-sided UC - rectal mesalazine. If no remission within 4 weeks, add high-dose oral mesalazine. If still no remission, give oral mesalazine and oral corticosteroid.
Extensive disease - rectal mesalazine and high dose oral mesalazine. If remission not achieved within 4 weeks, stop topical and give high-dose oral mesalazine and oral corticosteroid.
Induction (severe)
Treat in hospital. IV steroids
If not improvement after 72 hours, IV ciclosporin or surgery.
Maintaining remission
Mild-moderate - rectal mesalazine daily or oral and rectal mesalazine.
Severe - oral azathioprine or oral mercaptopurine.
Key differences between CD and UC
Crohn’s disease -
Non-bloody diarrhoea
Weight loss more prominent
Upper GI symptoms, mouth ulcers, perianal disease, mass in RIF
Gallstones
Obstruction, fistula, colorectal cancer
Lesions anywhere from mouth to anus, skip lesions
Inflammation in all layers from mucosa to serosa
Deep ulcers, skip lesions (cobble-stone appearance)
Ulcerative Colitis - Bloody diarrhoea, pain in LLQ, tenesmus Primary sclerosis cholangitis Risk of colorectal cancer higher in UC Inflammation starts at rectum and never spreads beyond ileocaecal valve Continuous disease No inflammation beyond submucosa Pseudopolyps (ulceration with preservation of adjacent mucosa which has appearance of polyps.
Symptoms of malabsorption
Diarrhoea Weight loss Steatorrhoea Bloating Lethargy
Causes of malabsorption
Intestinal - Coaeliac disease Crohn's disease Whipple's disease Giardiasis Brush border enzyme deficiencies
Pancreatic -
Chronic pancreatitis
Cystic fibrosis
Pancreatic cancer
Biliary -
Biliary obstruction
Primary biliary cirrhosis
Others -
Bacterial overgrowth
Short bowel syndrome
Lymphoma
Symptoms of coeliac disease
Chronic or intermittent diarrhoea
Failure to thrive
Persistent or unexplained GI symptoms - nausea and vomiting
Prolonged fatigue
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia
Autoimmune thyroid disease Dermatitis herpetiformis IBS Type 1 DM First-degree relatives with coeliac disease
Complications of coeliac disease
Anaemia Dermatitis herpetiformis Hyposplenism Osteoporosis, osteomalacia Lactose intolerance Subfertility Enteropathy-associated T-cell lymphoma of small intestine
Investigations for coeliac disease
If already on gluten-free diet, introduce gluten for at least 6 weeks prior to testing.
Immunology - TTG antibodies or endomyseal antibody (IgA)
Duodenal/jejunal biopsy - villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propriety infiltration with lymphocytes.
Management of coeliac disease
Gluten-free diet - eg rice, potatoes, corn
Gluten-free biscuits, flour, bread and pasta are prescribable.
Monitor response by symptoms and repeat serology.
Immunisation - due to having a degree of functional hyposplenism, offered pneumococcal vaccine. Influenza vaccine given on an individual basis.
Diagnosis of IBS
Consider if have had the following for at least 6 months -
Abdominal pain
Bloating
Change in bowel habit
Positive diagnosis if patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form in addition to 2/4 symptoms: Altered stool passage Abdominal bloating Symptoms made worse by eating Passage of mucus
Investigations of IBS
FBC
ESR/CRP
Coeliac screen
Management of IBS
First line -
Pain - antispasmodic agents (hyoscine butyl bromide)
Constipation - laxatives (avoid lactulose)
Diarrhoea - loperamide
Second-line -
Low-dose TCA (amitriptyline)
Others -
Psychological - if symptoms don’t improve after 12 months consider CBT, hypnotherapy or psychological therapy.
Conservative management - Have regular meals and take time to eat Avoid missing meals Plenty of fluids Restrict tea and coffee to 3 cups a day Reduce alcohol Limit intake of high fibre food
Risk factors for pancreatic cancer
Age Smoking Diabetes Chronic pancreatitis HNPCC MEN BRCA2 gene
Symptoms of pancreatic cancer
Painless jaundice
Courvoisier’s law - presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
Anorexia, weight loss, epigastric pain
Steatorrhoea
DM
Back pain
Migratory thrombophlebitis (eg arm swelling)
Investigations for pancreatic cancer
Bloods - CA 19-9
Imaging - ultrasound, CT
Biopsy
MRCP
Management of pancreatic cancer
Less than 20% are suitable for surgery at diagnosis
Whipple’s resection (pancreaticoduodenectomy)
Adjuvant chemotherapy
ERCP with stenting for palliation
What is a carcinoid tumour
Tumours of enterochromaffin cell origin, capable of producing serotonin.
Symptoms of carcinoid tumour
Carcinoid syndrome (mets in liver) Flushing Diarrhoea Bronchospasm Hypotension Right heart valvular stenosis ACTH and GHRH increased
Investigations of carcinoid tumour
Urinary 5-HIAA
Plasma chromogranin A y
Management of carcinoid tumour
Somatostatin analogues - octreotide
Loperamide for diarrhoea
Surgery is only definitive cure
What is carcinoid crisis
Tumour outgrows blood supply
Life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia.
Treat with high-dose octreotide, supportive measures, careful management of fluid balance
What is hepatic encephalopathy
As liver fails, ammonia builds up in circulation and passes to the brain. Astrocytes clear it converting glutamate to glutamine.
This excess glutamine causes osmotic imbalance, and shift of fluid into these cells - hence cerebral oedema.
Features of hepatic encephalopathy
Grade 1 - altered mood/behaviour, sleep disturbance, dyspraxia, poor arithmetic, no liver flap
Grade 2 - increased drowsiness, confusion, slurred speech, liver flap, inappropriate behaviour
Grade 3 - incoherent, restless, liver flap, stupor
Grade 4 - coma
Management of hepatic encephalopathy
First-line - lactulose
Secondary prophylaxis - rifaximin (decrease ammonia production)
Treatments for complications of liver failure
Cerebral oedema - 20% mannitol IV, hyperventilate.
Ascites - restrict fluid, diuretics
Bleeding - vitamin K, platelets, FFP
Blind treatment of infection - ceftriaxone
Reduced blood glucose - glucose IV if <2
Hepatic encephalopathy - lactulose, rifaximin
What are the 2 types of hepatorenal syndrome
HRS 1 - rapidly progressive. Doubling serum creatinine to >221
Very poor prognosis
HRS 2 - slowly progressive
Poor prognosis, but patients may live longer
Treatment of hepatorenal syndrome
Vasopressin analogues - terlipressin (cause vasoconstriction of splanchnic circulation
Volume expansion with 20% albumin
Transjugular intrahepatic portosystemic shunt.
Signs of liver cirrhosis
Leuconychia Clubbing Palmar erythema Hyperdynamic circulation Dupuytren's contracture Spider naevi Xanthelasma Gynaecomastia Small nodular liver Ascites Splenomegaly
Investigations for liver cirrhosis
Transient elastography and acoustic radiation force impulse imaging
Enhanced liver fibrosis score for patients with NAFLD
Upper endoscopy for varices
Liver ultrasound every 6 months (+/- alpha-feto protein) for check for hepatocellular cancer
Biopsy
Features, diagnosis and management of spontaneous bacterial peritonitis
Seen in patients with ascites secondary to liver cirrhosis
Features - ascites, abdominal pain, fever
Diagnosis - paracentesis - neutrophil count >250
Management - IV cefoxamine
Prophylaxis for patients with ascites if:
Have had episode of SBP
Patients with fluid protein <15 and either Child-Pugh score of at least 9 or hepatorenal syndrome
Features of hepatitis B
Fever
Jaundice
Elevated liver transaminases
Complications of hepatitis B
Chronic hepatitis Hepatocellular carcinoma Glomerulonephritis Polyarteritis nodosa Cryoglobulinaemia
Hepatitis B serology
Surface antigen (HBsAg) is first marker to appear and causes production of anti-has
HBsAg implies acute disease (1-6 months)
If HBsAg present for >6 months, chronic disease
Anti-HBs implies immunity (either exposure or immunisation). Negative in chronic disease.
Anti-HBc implies previous or current infection.
IgM in acute phase.
IgG persists.
HbeAg results from breakdown of core antigen from infected liver cells, marker of infectivity.
Management of hep B
Tenofovir
Entecavir
Telbivudine
Interfern-alpha
Aim is to clear HBsAg
When is Hep B given for vaccinations
2, 3 and 4 months
How to interpret anti-HBs levels after being vaccinated
> 100 - adequate response. Booster at 5 years
10-100 - suboptimal, one additional vaccine dose should be given.
<10 - non-responder. Test for current or past infection. Give further vaccine course with testing following. If still fail to response, HBIG given for protection if exposed to virus.
Outcome of hepatitis C infection
15-15% clear virus after acute infection
55-85% develop chronic hepatitis C
Complications of chronic hepatitis C
Arthralgia, arthritis Sjogren's syndrome Cirrhosis Hepatocellular carcinoma Cryoglobulinaemia Porphyria cutanea tarda Membranoproliferative glomerulonephritis.
Management of hepatitis C
Protease inhibitors (daclatasvir + sofosbuvir) with or without ribavarin
Signs and symptoms of alcohol withdrawal
10-72 hours after last drink
Tachycardia, hypotension, tremor, confusion, fits, hallucinations (delirium tremens)
Delirium tremens at 48-72 hours.
Management of alcohol withdrawal
First line - benzodiazepine
Carbamazepine
Management of alcohol addiction
Disulfiram - promotes abstinence.
Acamprosate - reduces cravings. NMDA receptor antagonist.
management of alcoholic ketoacidosis
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration
Infusion of saline and thiamine. Thiamine avoids Wernicke encephalopathy or Korsakoff psychosis
Features of Wernicke encephalopathy
Nystagmus Opthalmoplegia Ataxia Confusion, altered GCS Peripheral sensory neuropathy
Features of Korsakoff syndrome
Addition of anterograde and retrograde amnesia and confabulation in addition to the symptoms of Wernicke encephalopathy.
What are the 3 types of autoimmune hepatitis
Type 1 - ANA and anti-smooth muscle antibodies (SMA). Affects both adults and children
Type 2 - Anti-liver/kidney microsomal type 1 antibodies (LKM1). Affects children only
Type 3 - Soluble liver-kidney antigen. Affects adults in middle-age
Features of autoimmune hepatitis
Signs of chronic liver disease Fever, jaundice Amenorrhoea (common) Raised IgG levels Liver biopsy - inflammation extending beyond limiting plate 'piecemeal necrosis', bridging necrosis
Management of autoimmune hepatitis
Steroids, azathioprine
Liver transplantation
What is Wilson’s disease
Autosomal recessive disorder
Excessive copper deposition in tissues
Onset between 10-25 years.
Features of Wilson’s disease
Liver - hepatitis, cirrhosis
Neurological - basal ganglia degeneration, speech, behavioural, psychiatric problems. Also asterisks, chorea, dementia, parkinsonism
Kayser-Fleischer rings (dark rings around the eye)
Renal tubular acidosis
Haemoylsis
Blue nails
Investigations for Wilson’s disease
Reduced serum ceruloplasmin
Reduced serum copper
Increased 24 hour urinary copper excretion
Management of Wilson’s disease
Avoid foods with high copper content Lifelong penicillamine (chelates copper) If severe liver disease - liver transplantation.
Features of haemochromatosis
Fatigue, erectile dysfunction, arthralgia
Bronze skin pigmentation
DM
Liver - stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition.
Cardiac failure (2nd to dilated cardiomyopathy)
Hypogonadism
Arthritis of hands.
Reversible and irreversible complications of haemochromatosis
Reversible - cardiomyopathy, skin pigmentation
Irreversible - liver cirrhosis, DM, hypogonadotrophic hypogonadism, arthropathy
Investigations for haemochromatosis
Bloods - LFT, increased ferritin, increased transferrin saturation, low TIBC
Genotyping HFE mutation
Joint x-ray - chonedrocalcinosis
Liver biopsy - Perl’s stain
Management of haemochromatosis
Venesection
What is the scoring system for liver cirrhosis
Child-Pugh or MELD
What are the metabolic consequences of refeeding syndrome
Hypophosphataemia
Hypokalaemia
Hypomagnesaemia - may predispose to torsades to pointes
Abnormal fluid balance
How to prevent refeeding syndrome
If haven’t eaten for >5 days, aim to re-feed at no more than 50% of requirements for first 2 days.
What is melanosis Coli
Disorder of pigmentation of bowel wall.
Histology - pigment-laden macrophages
Associated with laxative abuse (senna)
Features, investigation and management of Gilbert’s syndrome
Autosomal recessive condition
Defective bilirubin conjugation due to deficiency in UDP glucoronosyltransferase.
Features - unconjugated hyperbilirubinaemia, jaundice seen during intercurrent illness, exercise or fasting
Investigations - rise in bilirubin following prolonged fasting or IV nicotinic acid
No treatment required.
What other test would you need to do to determine whether a raised ALP is from liver or bone
Gamma-glutamyltransferase
Which tests determine liver function
Serum albumin, serum bilirubin, PT (INR)
Which tests determine liver injury
AST, ALT
ALP
GGT
What is the AST/ALT ratio in alcoholic liver disease
2:1 or more
Features of alpha-1 antitrypsin deficiency
Lungs - panacinar emphysema
Liver - cirrhosis, hepatocellular carcinoma in adults, cholestasis in children.
Investigations of alpha-1 antitrypsin deficiency
A1AT concentrations
Spirometry - obstructive pattern
Management of alpha-1 antitrypsin deficiency
No smoking
Supportive - bronchodilators, physiotherapy
IV A1AT protein concentrates
Surgery - lung volume reduction surgery, lung transplantation.
