GI Flashcards
Describe the pathophysiology of Primary Biliary Cholangitis
Autoimmune condition affecting interlobular bile ducts (in the liver), causing inflammation and damage = obstruction of bile flow (cholestasis)
Name 3 things released by the gallbladder and how these cause symptoms of Primary Biliary Cholangitis
1) Bile Acids (help with absorption/digestion of fats) = itching/pruritus, greasy stools, fat malabsorption
2) Bilirubin = pale stools and dark urine, jaundice
3) Cholesterol = xanthelasma (deposits in the skin) and xanthomas (larger nodules in skin/joints)
Symptoms of Primary Biliary Cholangitis
RUQ pain
Hepatomegaly
Itching/Pruritus
Pale/Greasy Stools
Dark Urine
Fatigue
Xanthelasma and Xanthomas
Jaundice
Hyperpigmentation
Management for Primary Biliary Cholangitis?
1st Line - Ursodeoxycholic Acid
Cholestyramine (for pruritus)
Fat Soluble Vitamin Supplements (A, D, E, K)
How do we test for Primary Biliary Cholangitis?
LFTs - raised ALP
Raised Serum AMA (Anti-Mitochondrial Antibodies) - most specific to PBC
Raised Serum ANA Anti-Nuclear Antibodies)
Raised Serum IgM
Imaging (excludes extrahepatic cause) - RUQ ultrasound or MRCP
Complications of Primary Biliary Cholangitis?
Cirrhosis = Portal Hypertension = Ascites, Variceal Haemorrhage
Osteomalacia and Osteoporosis (due to VitD deficiency)
Increased risk of HCC
What diseases are associated with Primary Biliary Cholangitis
Sjogren’s Syndrome (80%)
Rheumatoid Arthritis
Thyroid Disease
What is the pathophysiology of Primary Sclerosing Cholangitis?
Inflammation and sclerosis (fibrosing/thickening) of the intra and extra-hepatic bile ducts
What is the difference between Primary Biliary Cholangitis and Primary Sclerosing Cholangitis?
PBC affects only the intra-hepatic bile ducts while PSC affects both
What are the investigations for Primary Sclerosing Cholangitis
LFTs - raised ALP
MRCP - shows strictures in the bile ducts
ERCP
p-ANCA may be positive
What are the symptoms of Primary Sclerosing Cholangitis
RUQ pain
Itching/Pruritus
Fatigue
Jaundice
Hepatomegaly
What is the management of Primary Sclerosing Cholangitis
Dilation of strictures using stents guided by ERCP
Cholestyramine - pruritus
Fat Soluble Vitamin Supplements
What are the complications of Primary Sclerosing Cholangitis
Biliary Strictures
Cholangiocarcinoma
Cirrhosis
Osteoporosis
Acute Bacterial Cholangitis
What disease is Primary Sclerosing Cholangitis associated with?
Ulcerative Colitis - 70/80% of patients with PSC have UC
What is the pathophysiology of Acute Cholangitis
Infection and inflammation of the bile ducts
High mortality due to sepsis and septicaemia
What are the 2 main causes of Acute Cholangitis
Obstruction of bile flow (i.e. Gallstone)
Infection during ERCP
Most common organisms causing Acute Cholangitis
E.coli
Klebsiella species
Enterococcus species
Symptoms of Acute Cholangitis
RUQ pain
Fever
Jaundice
N+V
Pruritus
Pale stools
Dark Urine
What is Charcot’s triad
RUQ pain
Fever
Jaundice (raised bilirubin)
What is the management of Acute Cholangitis
Treat for sepsis:
Take blood cultures
Check lactate
Check urine output
Give Oxygen
Give IV fluids
Give IV antibiotics
Nil by mouth
ERCP to remove stone
Percutaneous transhepatic cholangiogram - drain through skin, liver and bile ducts relieves obstruction (for patients less suitable for ERCP or if it has failed)
What are the investigations for Acute Cholangitis
FBC - raised WBCs
LFTs - raised Bilirubin, ALP, GGT
Raised CRP
MRCP
ERCP
Abdominal Ultrasound
Pathophysiology of Acute Cholecytitis
Inflammation of the gallbladder
Causes of Acute Cholecystitis
Calculous AC - stone in the neck of gallbladder or cystic duct
Acalculous AC - patients on TPN or long periods of fasting where gallbladder is not being stimulated and leads to build-up pressure
Presentation of Acute Cholecystitis
RUQ pain (may radiate to right shoulder)
Fever
N+V
Murphy’s Sign
Tachycardic and tachypnoeic
Investigations for Acute Cholecystitis
FBC - raised WCC
Raised Inflammatory markers
Abdominal Ultrasound
MRCP - visualise stones
What is Murphy’s Sign
Place a hand in RUQ and apply pressure
Ask the patient to take a deep breath in
The gallbladder will move downwards during inspiration and come in contact with your hand
Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration
What would an Abdominal Ultrasound show in Acute Cholecystitis
Thickening of gallbladder wall
Stones/Sludge in gallbladder
Fluid around gallbladder
Treatment of Acute Cholecystitis
Nil by mouth
IV Fluids
IV antibiotics
ERCP - to remove potential stones
Cholecystectomy
Complications of Acute Cholecystitis
Sepsis
Gallbladder perforation
Gallbladder empyema (infected tissue and pus collecting in the gallbladder) - IV antibiotics and cholecystectomy/cholecystostomy
Main risk factor for cholangiocarcinoma
Primary Sclerosing Cholangitis
Presentation of cholangiocarcinoma
Jaundice
Weight loss
Pale stools
Dark urine
Palpable Gallbladder
RUQ pain
Hepatomegaly
What is Courvoisier’s law
Palpable Gallbladder + Jaundice = cholangiocarcinoma
2 causes of painless jaundice
cholangiocarcinoma
pancreatic cancer
Tumour marker of cholangiocarcinoma and pancreatic cancer
CA19-9 (remembering tip: 9 looks like a pancreas and 9 is also a ‘g’ for gallbladder)
Investigations of cholangiocarcinoma
CT TAP for staging
CA19-9 (carbohydrate antigen)
MRCP - assess obstruction
Treatment of cholangiocarcinoma
None
ERCP - relieve obstruction and gain biopsy of tumour
Risk factors for biliary colic
4 F’s
Fat - enhanced cholesterol synthesis and secretion
Female
Fertile - pregnancy increases risk
Forty
Why does biliary colic occur
Gallbladder contracting against a stone in the cystic duct
Presentation of biliary colic
Severe colicky epigastric or RUQ pain often after meals
N+V
What triggers contraction of the gallbladder
Fatty meals = release of cholecystokinin (CKK) = contraction
Investigations for gallstones
LFTs - bilirubin may be raised if flow is blocked, raised ALP and less raised ALT/AST
Ultrasound - gallstones in gallbladder or ducts, duct dilatation
MRCP
ERCP
Treatment for gallstones
Cholecystectomy for symptomatic patients
What is a Kocher incision
a right subcostal “Kocher” incision is used in cholecystectomies
Complications of cholecystectomy
Bleeding
Infection
Perforation
Stones left over
Damage to nearby organs
What is Post-cholecystectomy syndrome
Non-specific symptoms that can occur after a cholecystectomy
They may be attributed to changes in the bile flow after removal of the gallbladder. Symptoms often improve with time. Symptoms include:
Diarrhoea
Indigestion
Epigastric or right upper quadrant pain and discomfort
Nausea
Intolerance of fatty foods
Flatulence
Causes of acute pancreatitis
IGETSMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion Venom
Hyperlipidaemia
ERCP
Drugs (furosemide, thiazide diuretics, and azathioprine)
What drugs can cause acute pancreatitis
Furosemide
Thiazide diuretics
Azathioprine
Presentation of acute pancreatitis
Severe epigastric pain radiating through to the back
Epigastric tenderness
Vomiting
Systemically unwell - low grade fever and tachycardia
What is Cullen’s and Grey-Turner’s sign
Sign of pancreatitis
Cullen’s - peri-umbilical discolouration (yellow/blue/purple bruising)
Grey-Turner’s - flank discolouration (yellow/blue/purple bruising)
What tool do we use for assessing severity of acute pancreatitis? What is measured in it? What is the scoring system?
Glasgow-Imrie scoring system:
P - Pao2 < 8KPa (hypoxic)
A - Age > 55
N - Neutrophils (WBC > 15)
C - Calcium < 2mmol/L
R - uRea > 16mmol/L
A - Albumin < 32g/L
S - Sugar (Glucose < 10mmol/L)
0 or 1 = mild
2 = moderate
3 or more = severe
Investigations for acute pancreatitis
Amylase - raised more than 3 times normal limit
Lipase - more sensitive and specific than amylase
CRP
Ultrasound - to assess for gallstones
CT abdomen - assess for complications
Management of acute pancreatitis
IV fluids - aim for > 0.5ml/kg/hr
IV Analgesia
Nil by mouth - parenteral or enteral nutrition (to stop activation of pancreas in response to food in duodenum)
Antibiotics - only if there is evidence of necrosis or abscess formation
Cholecystectomy - if gallstones
ERCP - if obstructed biliary tree
Surgical drainage if necrosis
Difference between total parenteral and enteral nutrition
Enteral nutrition - feeding though a tube inserted into the stomach, duodenum or jejunum
TPN - feeding through a vein
Complications of acute pancreatitis
Necrosis of pancreas
Infection of necrosed area
Abscess formation
Peripancreatic fluid collection
Pseudocysts in pancreas
Chronic pancreatitis
Presentation of chronic pancreatitis
Chronic epigastric pain
Loss of exocrine function - less lipase hence steatorrhea
Weight loss
Loss of endocrine function - diabetes develops
Formation of pseudocysts and abscess
Investigations for chronic pancreatitis
CT - shows atrophy and calcification of pancreas
Faecal elastase - assesses exocrine function
Management of chronic pancreatitis
Analgesia
Drinking and smoking abstinence
Creon - pancreatic enzyme replacement
Subcutaneous insulin regimes - to treat diabetes
What are the stages of Alcohol Related Liver Disease?
1) ALcoholic Fatty Liver (hepatic steatosis) - accumalation of fat droplets in the liver
2) Alcoholic hepatitis
3) Cirrhosis - functional liver tissue replaced with scar tissue
What is the reccomended alcohol consumption per wee?
14 units
Presentation of Alcohol Related Liver Disease
Jaundice
RUQ pain
Hepatomegaly
Peripheral oedema
Palmar erythema (abnormal oestrogen = raised NO synthase = dilation)
Clubbing
Dupuytren’s contracture
Xantomas
Spider angiomas
Investigations for Alcohol Related Liver Disease
ALT - raised
AST - raised
AST:ALT ratio > 2:1
GGT raised
ALP raised
Bilirubin raised
Serum Albumin raised
Prolongues prothrombin time
Liver ultrasound - can show farrt cganges and cirrhosis
Fibroscan - shows degree of fibrosis
Management for Alcohol Related Liver Disease
Alcohol abstinence
Glucocorticoids - prednisolone
Pentoxyphylline
Nutritional support - vitamin B1
How do you screen for harmful alcohol use?
CAGE questionnaire
C – CUT DOWN? Do you ever think you should cut down?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Do you ever feel guilty about drinking?
E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?
What withdrawals symptoms can occur 6-12hours after alcohol abstinence?
Tremor
Sweating
Headaces
Tachycardia
Anxiety
What can occur 12-24 hours after alcohol abstinence?
Hallucinations
What can occur 36 hours after alcohol abstinence?
Seizures
What can occur 3 days after alcohol abstinence?
Delirium Tremens (DT = day three)
Pathophysiology of alcohol withdrawal
alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
extreme excitability of the brain and excessive adrenergic (adrenalin-related) activity.
Feature of delirium tremens
Confusion
Severe agitation
Auditory and visual hallucinations
Delusions
Tremor
Ataxia
Fever
Tachycardia
Treatment of delirium tremens
Lorazepam (benzodiazepine)
How to treat alcohol withdrawal
1st line = Chlordiazepoxide hydrochloride
Diazepam (Alternative)
Carbamazepine
Pabrinex (High dose vitamin B) given IM or IV
Followed by oral thiamine (if diet is deficient)
What drug reduces alcohol cravings?
Acamprosate (agonist of NMDA receptors = improved abstinence)
What drug promotes abstinence of alcohol?
Disulfiram (causes severe reaction after alcohol consumption)
What causes Wernicke’s encephalopathy
Thiamine deficiency due to alcohol excess
Thiamine poorly absorbed in presence of alcohol
Excess alcohol use = decreased absorption of Thiamine = Wernicke’s encepholopathy
Feature of Wernicke’s encephalopathy
ACON:
Ataxia
Confusion
Opthalmoplegia
Nystagmus
Treatment of Wernicke’s encephalopathy
Urgent replacement of Thiamine
If Wernicke’s encepholopahy goes untreated what may develop?
Korsakoff syndrome
What are the features of Korsakoff syndrome?
Anterograde and Retrograde amenesia
Confabulation
+ symptoms of Wernicke’s encephalopathy
What are the symptoms of anal fissures
Bright red rectal bleeding
Pain around the anus
Pruritus ani
Discharge
Constipation
What is the management of Acute (<1wks) and Chronic (>1wks) anal fissures
Acute:
Soften stool - through a high fiber and water diet OR bulk-forming laxatives (1st line)
Lubricants
Topical anesthetics
analgesia
Chronic :
Topical GTN
If Topical GTN not working then:
Sphincterotomy or Botulinum toxin
Symptoms of appendicitis
Peri-umbilical abdominal pain that migrates to the right iliac fossa
N+V
Anorexia
Fever
Guarding
Rigidity
What is Rosving’s sign?
Palpation of left iliac fossa results in pain in the right iliac fossa
What signs are present if the appendix has potentially been perforated?
Rebound and percussion tenderness
Investigations for appendicitis
Raised inflammatory markers
Nuetrophil dominant leucocystosis
Urinalysis - exclude pregnancy, UTI and renal colic
Ultrasound - exclude gynaecological/obstetric causes
Differential for appendicits
Ectopic pregnancy
Ovarian cyst torsion/rupture
Mesenteric adenitis
Meckel’s diverticulum
Treatment for appendicitis
Appendectomy
Prophylactic antibiotics
Potential complications of appendectomy
Bleeding
Removal of normal appenix
Perforation
Damage to nearby organs
VTE
How do we determine the cause of ascites
using serum-ascites albumin gradient
If > 11g/L then indicated portal hypertension
If < 11g/L then indicates other cause
What are the possible causes of ascites if the SAAG is > 11g/L
Liver disorders:
cirrhosis/alcoholic liver disease
acute liver failure
liver metastases
Cardiac:
righ heart failure
constrictive pericarditis
Other
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive crisis
myxodema
What are the possible causes of ascites if the SAAG is <11g/L
Hypoalbuminaemia:
nephrotic syndrome
severe malnutrition (e.g. kwashiorkor)
Malignancy:
peritoneal carcinomatosis
Infections:
tuberculous peritonitis
Other:
pancreatitis
bowel obstruction
biliary ascites
post-operative lymphatic leak
serositis in connective tissue disease
Management for ascites
Reduce dietary sodium
Aldosterone antagonist - spironolactone
Drainage - therapeutic abdominal paracentesis
Prophylactic antibitoics for SBP
How is cirrhosis diagnosed
Transient elastography (Fibroscan)
+ upper endoscopy to check for varices in patients with new diagnosis of cirrhosis
Individuals carrying which haplotypes are genetically predisposed to coeliac disease?
HLA-DQ2 or HLA-DQ8
What are the GI related symptoms of coeliac disease
Diarrhoea
Abdominal pain or bloating
Steatorrhoea
N+V
What are the extraintestinal symptoms of coeliac disease
Dermatitis herpatiformis
Mouth ulcers
Iron deficiency anaemia
Weight loss
Bone pain, fractures, osteoporosis or osteopenia - impaired vitamin D absorption
Peripheral neuropathy
Fatigue
Investigations for coeliac disease
Serum anti-tTG antibodies (highest sensitivity and specificity)
Serum anti-EMA antibodies
Total serum IgA antibodies - excludes selective IgA deficiency
Duodenal biopsy (gold standard)
What 3 things are seen on a duodenal biopsy in coeliac disease
Crypt hyperplasia
Villous atrophy
Increased intraepithelial lymphocytes
Management for coeliac disease
Gluten free diet
Supplements for any deficiencies
Pneumococal vaccine (for functional hyposplenism)
What other conditions is coeliac disease linked with
T1DM
Thyroid disease
(autoimmune)
Complications of coeliac disease
Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism
Ulcerative jejunitis
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
Risk factors for bowel cancer
Familial adenomatous polyposis
Hereditary non-polypsis colorectal cancer
IBD
Increased age
Diet (high in red/processed meat and low fibre)
Smoking
Obesity
Alcohol
Presentation of bowel cancer
Change in bowel habit
Rectal bleeding
Unexplained abdominal pain
Iron deficiency anaemia
Abdominal or rectal mass
What is the screening for bowel cancer
Faecal Immunochemical Test (FIT test) - detects amount of human heamoglobin in stools
From what age are you offered routine bowel cancer screening
FIT test every two years from 50-74
What is the tumour marker for bowel cancer
Carcinoembryonic antigen (CEA)
Investigations for bowel cancer
Colonoscopy
Sigmoidoscopy (if only rectal bleeding is present)
CT colonogrophy (for patients less fit for colonoscopy)
Staging TAP CT scan
What two classification systems are used for bowel cancer
Dukes’
TNM
Summarise Dukes’ classification for bowel cancer
Dukes A - confined to mucosa and part of the muscle of the bowel wall
Dukes B - extending through the muscle of the bowel wall
Dukes C - lymph node involvement
Dukes D - metastatic disease
Summarise TNM classification for bowel cancer
T for Tumour:
TX – unable to assess size
T1 – submucosa involvement
T2 – involvement of muscularis propria (muscle layer)
T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa
T4 – spread through the serosa (4a) reaching other tissues or organs (4b)
N for Nodes:
NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes
M for Metastasis:
M0 – no metastasis
M1 – metastasis
Management for bowel cancer
Surgical resection
Chemotherapy
Radiotherapy
Palliative care
Define the following:
Right hemicolectomy
Left hemicolectomy
High anterior resection
Low anterior resection
Abdomino-perineal resection (APR)
Hartmann’s procedure
Right hemicolectomy -removal of the caecum, ascending and proximal transverse colon.
Left hemicolectomy -removal of the distal transverse and descending colon.
High anterior resection -removing the sigmoid colon (may be called a sigmoid colectomy).
Low anterior resection -removing the sigmoid colon and upper rectum but sparing the lower rectum and anus.
Abdomino-perineal resection (APR) - removing the rectum and anus (plus or minus the sigmoid colon) and suturing over the anus. It leaves the patient with a permanent colostomy.
Hartmann’s procedure (usually an emergency procedure) - the removal of the rectosigmoid colon and creation of an colostomy.
What is and what are the features of low anterior resection syndrome
occur after resection of a portion of bowel from the rectum, with anastomosis between the colon and rectum
Urgency and frequency of bowel movements
Faecal incontinence
Difficulty controlling flatulence
What is meaured during follow up of curative bowel cancer surgery
CEA
CT TAP
What is diverticular disease
herniation of colonic mucosa through the muscular wall of the colon
Where does diverticular disease commonly occur
The site between the taenia coli where vessels pierce the muscle to supply the mucosa. For this reason, the rectum, which lacks taenia, is often spared.
Symptoms of diverticular disease
Altered bowel habit (constipation)
Rectal bleeding
Abdominal pain (left lower quadrant)
Investigations for diverticular disease
Colonoscopy
CT cologram
Barium enema
What is the name of the classification system of diverticular disease?
Hinchey Classification:
I - Para-colonic abscess
II - Pelvic abscess
III - Purulent abscess
IV - Faecal peritonitis
Treatment of diverticular disease
Increase dietary fibre intake
Define diverticulitis
The infection of a diverticulum
Difference between diverticulosis and diverticulitis
Diverticulosis = presenceof diverticula
Diverticulitis = infection of a diverticula
Risk factors for diverticulitis
Age
Lack of dietary fibre
Obesity
Sedentary lifestyle
Symptoms of diverticulitis
Severe abdominal pain (left iliac fossa although may be right in Asian people)
N+V
Fever
Change in bowel habit
Urinary frequency, urgency or dysuria (irritation of bladder by inflamed bowel)
PR bleeding
Guarding, rigidity and rebound tenderness
Investigations for diverticulitis
FBC - raised WCC
CRP - riased
ERECT CXR - pneumoperitoneum in case of perforation
AXR - dilated bowel loops, obstruction or abscess
CT - may show abscess
Colonoscopy - should be avoided initially due to perforation risk
Management of diverticulitis
Oral antibiotics - co-amoxiclav for at least 5 days
Analgesia - NSAIDs or opiates
Liquid diet
If symptoms dont settle within 72 hours = IV antibiotics (cephalosporin + metronidazole), IV fluids , Analgesia, Nil by mouth
Complications of diverticulitis
Perforation
Peritonitis
Pereidiverticular abscess
Large haemorrhage
Fistula between colon and bladder (= pneumaturia or faecaluria) or vagina (vaginal passage of flatus or faeces)
Ileus or obstruction
Most prevalant type of gastric cancer
Gastric adenocarcinoma (arises from glandular epithelium in stomach lining)
Risk factors for gastric cancer
Helicobacter Pylori - inflammation of lining = atrophy and intestinal metaplasia = dysplasia
Pernicious anaemia caused atrophic gastritis
Diet high in salt, nitrates and salt preserved foods
Smoking
Ethnicity - Japanese and Chinese
Feature of gastric cancer
Abdominal pain (vague epigastric pain)
Weight loss and anorexia
N+V
Dysphagia (if originated in proximal stomach)
Upper GI bleeding
Virchows node and Sister Mary Joseph’s node (if lymphatic spread)
Where are Virchow’s node and Sister Mary Joseph’s node
Virchow = left supraclavicular lymph node
Sister MJ node = Periumbilical node
Investigations for gastric cancer
OGD with biopsy (may see signet ring cells)
CT CAP for staging
Management of gastric cancer
Surgery:
- Endoscopic mucosal resection
- Partial gastrectomy
- Total gastrectomy
Chemotherapy
Define GORD
The flow of stomach acid from the stomach into the oesophagus through the lower oesophageal sphincter
What type of epithelium is in the stomach and oesophagus
Stomach = columnar
Oesophagus = squamous
Risk factors for GORD
Greasy and spicy foods
Smoking
Obesity
H.pylori
Hiatus hernia
Stress
NSAIDs
Alcohol
Coffee and tea
Presentation of GORD
Dyspepsia:
Heartburn
Retrosternal or epigastric pain
Reflux of stomach acid into oesophagus
Bloating
Nocturnal cough
Hoarse voice
Odynophagia (painful swallowing)
GORD red flags
Dysphagia
Age over 55
Weight loss
Upper abdominal pain and mass
Reflux
Treatment-resistant dyspepsia
N+V
Anaemia (from bleeding)
Raised platelet count
What can an OGD be used for?
Gastritis
Peptic ulcers
Upper gastrointestinal bleeding
Oesophageal varices (in liver cirrhosis)
Barretts oesophagus
Oesophageal stricture
Malignancy of the oesophagus or stomach
What is a hiatus hernia and what are the four types?
Herniation of the stomach up through the diaphragm
Type 1: Sliding
Type 2: Rolling (a separate portion of the stomach (i.e., the fundus), folds around and enters through the diaphragm opening)
Type 3: Combination of sliding and rolling
Type 4: Large opening with additional abdominal organs entering the thorax (pancreas, bowel etc)
Investigations for hiatus hernia
CXR
CT
Endoscopy
Barium swallow test
Investigations for GORD
Upper GI endoscopy (OGD) if:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss
If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)
Management of GORD
Lifestyle changes
Review meds (stop NSAIDs)
Antacids (gaviscon)
PPIs (omeprazole or lansaprozole) for 4 weeks
Histamine H2-receptor antagonists (famotidine) - if inadequate response to PPIs
Surgery
What is the surgery for GORD called and what does it involve
Laproscopic fundoplication (Nissen’s) - tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.
What type of bacteria is H.pylori
Gram negative aerobic bacteria
Mechanism of action of H.pylori
H. pylori produces ammonium hydroxide, which neutralises the acid surrounding the bacteria. It also produces several toxins. The ammonia and toxins lead to gastric mucosal damage.
Investigations for H.pylori
Stool antigen test
Urea breath test using radiolabelled carbon 13
H.pylori antibody test (blood)
Rapid urease test - biopsy of stomach from endoscopy added to medium containing urea, urease enzyme from H.pylori neutralises the acid = change in colour of pH indicator
What is the H.pylori eradication scheme
Triple therapy:
PPI + 2 antibiotics (amoxicillin and clarithromycin) for 7 days
What is Barret’s oesophagus
It refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium.
Risk factors for Barret’s oesophagus
GORD
Male
Smoking
Obesity (central)
Symptoms for Barret’s oesphagus
same as GORD
Management of Barret’s oesophagus
High dose PPI
Endoscopy every 3-5 years
If dysplasia present - Radiofequency ablation
or
Endoscopic mucosal resection
What is Zollinger-Ellison syndrome
Condition characterised by excessive levels of gastrin secondary to a gastrin-secreting tumour. The majority of these tumours are found in the first part of the duodenum, with the second most common location being the pancreas.
Triad of features for Zollinger-Ellison syndrome
Multiple gastroduodenal ulcers
Diarrhoea
Malabsorption
Investigations for Zollinger-Ellison syndrome
Fasting gastrin levels
Secretin stiumlation test:
Gastrin levels measured –> given an injection of secretin –> Gastrin levels will be measured again –> If Zollinger-Ellison present = gastrin levels will rise dramatically
What is the typical location of haemorrhoids (mucosal vascular cushions) in the anal canal
Left lateral
Right posterior
Right anterior portions of the anal canal
(3 o’clock, 7’o’clock and 11 o’clock respectively)
Features of haemorrhoids
Painless rectal bleeding
Pruritus
Pain (only significant if piles are thrombosed)
Soiling may occur with thrid or fourth degree piles
What are the two different types of haemorrhoids
External:
- Originate below dentate line
- Prone to thrombosis
Internal:
- Originate above dentate line
- Do not generally cause pain
Define haemorrhoids nased on grading them from Grade I to IV
I - do not proplapse out of anal canal
II - prolapse on defecation but reduce spontaneously
III - can be manually reduced
IV - cannot be reduced
Investigations for haemorrhoids
Based on examination
External - visible on inspection
Internal - PR exam
Proctoscopy - required for proper visualise and insepction
Management of haemorrhoids
Non-surgical:
Soften stool - high fibre diet and increase fluid intake
Topical local anaesthetics (Anusol) and sterois (Anusol HC)
Germaloids cream - contain lidocaine
Proctosedyl ointment (contains cinchocaine and hydrocortisone – short term only)
Rubber band ligation
Injection sclerotherapy
Surgical:
Haemorrhoid artery ligation
Haemorrhoidectomy
Staple haemorrhoidectomy
Features of thrombosed haemorrhoid and management of them
Appear as:
Purplish, very tender, swollen lumps around the anus.
Resolve with time
If extremely painful - surgery
What type of virus is Hepatitis A
RNA
What is the four stages of liver infection?
Incubation phase (period between coming into contact with virus and developing symptoms)
Prodromal phase (period where symptoms develop before fully developed acute illness)
Icteric phase (period of established infection)
Convalescent phase (period of recovery after acute illness)
What is the mode of transmission of Hepatitis A
Faecal-oral route
What are the symptoms of Hepatitis A
Incubation phase: none
Prodromal phase:
Flu like prodromol symptoms
N+V
Diarrhoea
Fever
Abdominal pain (RUQ)
Icteric phase:
Tender hepatomegaly
Jaundice
Pruritus
Dark urine
Pale stools
Convalescent phase:
Muscle weakness
Malaise
Anorexia
Hepatic tenderness
Investigations for Hepatitis A
PCR test for Hepatitis A RNA
Hepatitis A virus Immunoglobulin M (HAV-IgM = produced when person is first infeced) and HAV-IgG (past exposure/immunity)
Positive IgM and Positive IgG = acute Hep A infection
Positive IgM and Negative IgG = past infection or immunity
High IgG and Moderate IgM = recent infection
LFTs = raised ALT and AST
Raised ALP (but less than 2 time normal)
Management of Hepatitis A
no specific treatment as usually self limiting
Pain relied
Anti-emetics etc.
Is there a vaccine for Hepatitis A
Yes
What type of virus is Hepatitis B
Double-stranded DNA
What is the mode of transmission of Hepatitis B
Blood or bodily fluids
E.g. sexual intercourse, sharing needles, vertical transmission (from mother to to child during pregnancy)
What do the following markers mean?
HBsAg (surface antigen)
HBeAg (E antigen)
HBcAb (Core antibodies)
HBsAb (Surface Antibodies)
HBV DNA (Hep B DNA)
HBsAg = active infection (is what is injected through vaccines)
HBeAg = marker of infectivity
HBcAb = distinguishes between acute, chronic or past infection
Has two versions: IgM and IgG versions
- IgM = active infection - high titre in acute and low titre in chronic
- IgG = past ingection
HBsAb = immune response to HBsAg
HBV DNA = direct count of viral load
What are the symptoms of Hep B
Asymptomatic
None specific symptom:
Fever
Malaise
Anorexia
Fatigue
Symptoms of chronic liver disease:
Palmar erythema
Spider angiomata
Asterixis
Easy bruising
Symptoms of cirrhosis and portal hypertension:
Ascites
Hepatomegaly
Splenomegaly
Peripheral oedema
Caput medusae
Extra-hepatic manifestiations:
Polyarteritis nodosa
Investigations for Hepatitis B
LFTs: raised ALT and AST
ALP and GGT raised but not much
Raised AST:ALT ratio (but not more than 2)
Previous vaccine: Positive HBsAb everything else negative
Previous Infection:
Positive HBsAb, Positive HBcAb
Acute HBV:
Positive HBsAg, Positive HBcAb (IgM), negative HBsAb
Chronic Infection:
Positive HBsAg, Positive HBcAb (IgG), Negative HBsAb
FBC: Hb and MCV (to check for bleeding)
U+Es: usually normal
Synthetic function:
Albumin: reduced
Prothrombin time and INR : prolonged
Management of Hepatitis B (Acute and Chronic)
Acute:
Tenofovir or Entecavir (antivirals) until HBsAg is normal
Chronic:
Antiviral therapy - first-line treatments are entecavir, tenofovir or peginterferon alfa 2a (if no cirrhosis), and entecavir or tenofovir (if cirrhosis present)
Complications of Hepatitis B
Cirrhosis
HCC
FLuminant hepatic failure
What is the treatment of Hepatitis B in pregnancy
Babies born to mothers who are chronically infected with hepatitis B or to mothers who’ve had acute hepatitis B during pregnancy should receive a complete course of vaccination + hepatitis B immunoglobulin
What type of virus is Hepatitis C
RNA
What is the mode of transmission of Hepatitis C
Blood and bodily fluids
Vertical Transmission
Symptoms of Hepatitis C
Transient rise in ALT & AST
Fatigue
Arthralgia
Investigations for Hepatitis C
HCV RNA
Management of Acute and Chronic Hepatitis C
Combination of protease inhibitors (e.g.
Daclatasvir + sofosbuvir
or
Sofosbuvir + simeprevir
with or without ribavirin are used
Complications of Hepatitis C
Eyes: Sjogrens
Rheumatological: arthralgia, arthritis
Cirrhosis
HCC
What type of virus is Hepatitis D
RNA
What is the mode of transmission of Hepatitis D
Blood and bodily fluids
What disease is Hepatitis D associated with
Hepatitis B
Difference between co-infection and superinfection of Hepatitis D
Co-infection = Hep B and D infection at same time
Superinfection = Hep B positive patient develops Heb D (associated with high risk of fluminant hepatitis, cirrhosis, chronic hepatitis)
Investigation of Hepatitis D
Reverse polymerase chain reaction of hepatitis D RNA
Treatment of Hepatitis D
Pegylated interferon alpha
What type of virus is Hepatitis E
RNA
Mode of transmission of Hepatitis E
Faecal-oral
How many types of autoimmune hepatitis are there
3
What antibodies are present in all 3 autoimmune hepaitits
I:
ANA (anti-nuclear antibodies)
SMA (anti-smooth muscle antibodies)
II:
LKM1 (anti-liver/kidney microsomal tpe 1 antibodies)
III:
Soluble licer-kidney antigen
Symptoms of autoimmune hepatitis
Signs of chronic liver disease
Fever
Jaundice
Amenorrhoea
Investigations for autoimmune hepatitis
Serum ANA/SMA/LKM1antibodies
IgG levels: raised
Liver biopsy
Management of autoimmune hepatitis
Steroids - prednisolone
Immunosuppresants - azathioprine
Liver transplant
What gender are more likely to get inguinal hernias
Male
Symptoms of inguinal hernia
Groin lump - superior and medial to pubic tubercle (disappears on pressure/when patient lies down)
Discomfort and ache - worse with activity
Strangulation- rare
Management of inguinal hernias
Mesh repair - unilateral is open and bilateral is laprascopic
Complications of inguinal hernia repair
Early - bruising and wound infection
Late - chronic pain and reoccurence
Risk factors for abdominal wall hernias
obesity
ascites
increasing age
surgical wounds
What is a femoral hernia
Section of bowel or any other part of the abdominal viscera pass into the femoral canal via the femoral ring
Symptoms of a femoral hernia
Lump in groin
Typically non-reducible
Cough impule is absent
What gender are more likely to get femoral hernias
Women - during pregnancy there is increased intra-abdominal pressure
Differentials for femoral hernia
Lymphadenopthy
Abscess
Femoral artery aneurysm
Hydrocoele or varicocele in males
Lipoma
Inguinal hernia
Complications of femoral hernia
Incarceration - where herniated tissue cannot be reduced
Strangulation - can follow on from incarceration and is a surgical emergency
Bowel obstruction
Bowel iscaemia and resection
Management of femoral hernia
Surgery - via laparotomy or laproscopic
Symptoms of strangulated inguinal hernia
Pain
Fever
Increase in hernia size
Erythema of overlying skin
Guarding and localised tenderness
Bowel obstruction - distension and N+V
Bowel iscaemia - bloody stools
What does a strangulated inguinal hernia show on bloods
Leukocytosis
Raised lactate
Causes of hyposplenism
Sickle cell disease
Coeliac disease
Dermatitis herpatiformis
Graves’ disease
SLE
Amyloid
Splenectomy
Symptoms of hyposplenism
Fever
Headache
Myalgia
Investigations for hyposplenism
Blood smears:
Howell-Jelly bodies
Siderocytes
What is postoperative/paralytic ileus
Complication after surgery involving extesive handling of the bowel
Results in reduction in peristalsis = pseudo-obstruction
Symptoms of paralytic ileus
Abdominal distension/bloating
Abdominal pain
N+V
Inability to pass flatus
Inability to tolerate oral diet
Differential for paralytic ileus
Deranged electrolytes - check K+, Mg, Phosphate
Inflammation/infection to nearby bowel
Injury to bwel
Treatment of paralytic ileus
Nil-by-mouth initiall - may progress to small sips of fluid
NG tube if vomiting
IV fluids to maintain normovolaemia
TPN - required for severe/prolonged cases
What mnemonic can be used to remember the features of ulcerative colitis
CLOSE UP
Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis is associated
Symtpms of ulcerative colitis
Diarrhoea
Abdominal pain
Rectal bleeding
Weight loss
Fatigue
Blood or mucus in the stool
Investigations for ulcerative colitis
FBC - may show anaemia, leukocytosis or thrombocytosis
CRP/ESR - raised
Faecal calprotectin - raised
Colonoscopy/sigmoidoscopy + biopsy - gold standard
Abdominal and pelvic CT - for complications (abscess, strictures or perforation)
Why would a sigmoidoscopy be preferred rather than a colonoscopy for ulcerative colitis diagnosing
Performing colonoscopy in patients with severe UC may cause perforations
What would a colonoscopy show in ulcerative colitis
Red, raw mucosa that bleeds easily
No inflammation beyond submucosa
Widespread ulceration
What does a barium enema show in ulcerative colitis
Loss of haustrations
Superficial ulceration
Pseudopolyps
Drainpipe colon - colon is narrow and short
How do you determine the severity of a patients ulcerative colitis
Mild: < 4 stools/day, only a small amount of blood
Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
Severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
What is the treatment of ulcerative colitis (inducing and maintaining remission)
INDUCING REMISSION
Mild-moderate UC:
Proctitis - topical aminosalicylates (mesalazine)
- if remission not achieved within 4 weeks = add an oral ASA
- if remission still not achieved add oral corticosteroid
Proctosigmoiditis:
- topical ASA
- if remission not acheived in 4 weeks then add oral ASA
- If still no remission then use oral ASA and oral corticosteroid
Extensive:
- topical ASA + oral ASA
- if no remission in 4 weeks offer oral ASA + oral corticosteroid
Severe UC:
First line = IV steroids (hydrocortisone)
IV cyclosporins is second line
If not improved within 72 hours then add IV ciclosporins to IV hydrocortisone
MAINTAINING REMISSION
- oral ASA
- topical ASA
- topical ASA + oral ASA
Severe relapse or >= 2 exacerbatopns in past year = oral azathioprine or mercaptopurine
Surgery
- Panproctocolectomy with an ileostomy or ileo-anal anastomosis (J-pouch)
Complications of IBD
Colorectal cancer
What is the mnemonic for learning the features of crohn’s disease
crow’s NESTS
No blood or mucus
Entire GI tract affected
Skip lesions on endoscopy
Terminal ileum most affected and Transmural inflammation
Smoking is a risk factor
Symptoms of crohn’s disease
Abdominal pain
Diarrhoea
Weight loss
Perianal disease - skin tags, ulcers, anal fissures, perianal abscess or fistulas
Investigations for crohn’s disease
FBC - anaemia
Vitamin B12 and D - low
Faecal calprotectin - raised
ESR/CRP - raised
Colonoscopy - deep ulcer and skip lesions - cobblestone appearance
Histology of biopsy - inflammation in all layers, goblet cells and granulomas
What will a small bowel enema show in crohn’s disease
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae
What is the treatment of crohn’s disease (inducing and maintaining remission)
INDUCING REMISSION
Corticosteroids - prednisolone
+ azathioprine or mercaptopurine
or
+ methotrexate
or
+ infliximab or adalimumab
2nd line to corticosteroids = ASA
+ enteral nutrition
MAINTAINING REMISSION
First line = azathioprine or mercaptopurine
2nd line = methotrexate
Surgery
- Distal ileum resection
- Treating strictures
- Treating fistulas
What do you assess before offering azathioprine or mercaptopurine
Thiopurine methyltransferase (TPMT) activity
Complications of crohn’s disease
Colorectal cancer
Small bowel cancer
Osteoporosis
How do you make a diagnosis of IBS
Abdominal pain or discomfort present for at least 6 months and:
- Is either relieved by defecation or associated with altered bowel frequency or stool form
Plus at least 2 of the following:
- Altered stool passage (straining, urgency, incomplete evacuation)
- Abdominal bloating, distension, hardness or tenison
- Made worse by eating
- Passage of mucus
Extra-instestinal features of IBS
Lethargy
Nausea
Back pain
Headache
Investigations for IBS
FBC - check for anaemia
ESR/CRP - check for IBD
Anti-TTG/EMA - for coeliacs
Treatment for IBS
Diarrhoea - loperamide
Constipation - bulk-forming laxatives (isaghula husk) - LINACLOTIDE is alternative
Cramps - antispasmodics (mebeverine, hyoscine butylbromide) - TCAs (amitriptilyine) is second line then SSRIs (citalopram)
CBT
What dietary advice can you give someone for IBS
Regular meals and take time
Avoid missing meals
Drink at least 8 cups of water
Restrict caffeine (tea and coffee) and alcohol
Consider high fibre diet
What is mesenteric adenitis?
Inflamed lymph nodes within the mesentery
It can cause similar symptoms to appendicitis
What is malnutrition defined as
BMI of less than 18.5 OR
unintentional weight loss greater than 10% within the last 3-6 months OR
a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
What tool is used for screening for malnutrition and what is included in it
MUST (Malnutrition Universal Screening Tool)
Takes into account BMI, recent weight change and the presence of acute disease
Managment of malnutiriton
Dietician support
Food first approach
Oral nutritional supplements
Are gastric ulcers or duodenal ulcers more common
Duodenal
What are the risk factors for peptic ulcers
H.pylori infection
NSAIDs
Stress
Alcohol
Caffeine
Smoking
Spicy foods
What medications increase the risk of a peptic ulcer bleeding
NSAIDs
Aspirin
Anticoagulants (DOACs)
Steroids
SSRIs
What are the symptoms of peptic ulcers
Epigastric pain
N+V
Duodenal ulcers - epigastric pain when hungry relieved by eating
Gastric ulcers - epigastric pain worsened by eating
Investigations for peptic ulcers
H.pylori testing - urease breath test or stool antigen test
Endoscopy (OGD)
Management of peptic ulcers
Stopping NSAIDs
PPIs (lansoprazole or omeprazole) - if H.pylori -ve
Treating H.pylore infections - triple therapy = PPI + 2 antibiotics (amoxicillin and clarithromycin) for 7 days
Complications of peptic ulcer disease
Bleeding
Perforation
What artery is the source of bleeding in peptic ulcer disease
Gastroduodenal artery
Symptoms of a bleeding associated with peptic ulcer disease
Haematemesis
Coffee ground vomiting
Melaena
Hypotension
Tachycardic
Treatment for a GI bleed associated with peptic ulcer disease
ABCDE approach
IV PPIs
1st line = endoscopic intervention
2nd line = urgent interventional angiograpy with transarterial embolisation
OR surgery
Symptoms of a perforation associated with peptic ulcer disease
Epigastric pain which becomes more generalised
Syncope
Investigation and treatment for a perforation associated with peptic ulcer disease
Erect CXR - free air under the diaphragm
Treatment - surgery
What viruses commonly cause viral gastroenteritis
Rotavirus
Norovirus
Adenovirus (tends to cause respiratory symptoms)
What bacterial organisms can cause gastroenteritis
E.coli
Campylobacter Jejuni
Shigella
Salmonella
Bacillus Cereus
Yersinia Enterocolitica
Staphylococcus Aureus
What parasite can cause gastroenteritis
Giardiasis
What are the symptoms of gastroenteritis
Abdominal pain/cramps
Diarrhoea (at least 3 times in 24 hours)
N+V
Fever
General malaise
What gastroenteritis-causing bacteria produce the Shiga toxin
E.coli 0157
shigella
What bacteria can cause bloody diarrhoea in the context of gastroenteritis
E.coli
Shigella
Amoebiasis
What bacteria can cause Haemolytic Uraemic Syndrome in the context of gastroenteritis
Shiga toxin producing organisms:
E.coli 0157
Shigella
Investigations for gastroenteritis
Clinical diagnosis but can consider:
Stool culture and sensitivity
What is the treatment of gastroenteritis for the following causative organisms:
C.jejuni
Giardiasis
(Other organisms do not require antibiotics)
Oral rehydration salt (ORS) - diaoralyte
C.jejuni = clarithromycin (if severe symptoms i.e. high fever, bloody and/or high output diarrhoea)
Giardiasis = metronidazole 2000mg once daily for 3 days
What are possible complications of gastroenteritis
Lactose intolerance
IBS
Reactive arthritis
Guillain–Barré syndrome
Haemolytic uraemic syndrome
How is C.jejuni spread
Raw or improperly cooked poultry
Untreated water
Unpasteurised milk
How is salmonella spread
Eating raw eggs or poultry
How is Bacillus Cereus spread
It grows on food not immediately refrigerated after cooking (e.g., fried rice or cooked pasta left at room temperature)
Produces cerulide toxin
What gastroenteritis causing organism can mimic appendicitis
Yersinia Enterocolitica
Can present with right sided abdominal pain (mesenteric lymphadenitis) and fever
What is a volvulus
Torsion of the colon around it’s mesenteric axis resulting in compromised blood flow and closed loop obstruction.
What are the 2 types of volvulus
Sigmoid volvulus - more common in older patients and caused by chronic constipation
Caecum volvulus - more common in younger patients
What are the symptoms of a volvulus
Constipation
Abdominal bloating
Abdominal pain
N+V (green bilious vomiting)
Investigations for volvulus
Abdominal film (X-ray) - coffee bean sign (dilated and twisted sigmoid colon looks like a giant coffee bean)
Large, dilated loop of colon, often with air-fluid levels
Contrast CT
Management of volvulus
Nil by mouth, NG tube, IV fluids
Sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion
Caecal volvulus: management is usually operative. Right hemicolectomy is often needed
What is the most common site of pancreatic cancers?
Head of pancreas
What are the risk factors for pancreatic cancer
Increased age
Smoking
Diabetes
Chronic pancreatitis
BRCA2 gene
KRAS gene
Hereditary non-polyposis colorectal carcinoma
Multiple endocrine neoplasia
Symptoms of pancreatic cancer
Painless jaundice - pale stools, dark urine, pruritus
Hepatomegaly, Gallbladder, Epigastric mass may be palpable
Steatorrhea - loss of exocrine function
Diabetes - loss of endocrine function
Atypical back pain
Migratory thrombophlebitis
Investigation for pancreatic cancer
CT abdomen for diagnosis and staging (CT CAP)
CA19-9
MRCP - assess obstruction
ERCP - for stent insertion and obtain biopsies
Biopsy
Management of pancreatic cancer
Surgery to remove tumour:
Total pancreatectomy
Distal pancreatectomy
Pylorus-preserving pancreaticoduodenectomy (PPPD) (modified Whipple procedure)
Radical pancreaticoduodenectomy (Whipple procedure) - Head of pancreas, pylorus, duodenum, gallbladder, bile duct, lymph nodes all removed
Also:
Stent insertion - for palliation
Chemotherapy
Radiotherapy
What is the most common type of oesophageal cancer
Adenocarcinoma (near the gastroesophageal junction)
What are the two types of oesophageal cancer
Adenocarcinoma - lower two thirds
Squamous cell carcinoma - upper two thirds
What are the risk factors of oesophageal adenocarcinoma
GORD
Barret’s oesophagus
Smoking
Obesity
What are the risk factors for oesophageal squamous cell carcinoma
Smoking
Alcohol
Achalasia
Plummer-Vinson syndrome
Diets rich in nitrosamines
Symptoms of oesophageal cancer
Dysphagia
Anorexia
Weight loss
Vomiting
Odynophagia
Hoarse voice
Melaena
Cough
Investigations for oesophageal cancer
Upper GI endoscopy
Endoscopic ultrasound - for locoregional staging
CT CAP - initial staging
Treatment of oesophageal cancer?
Surgical resection - Ivor-Lewis esophagectomy
Adjuvant chemotherapy
Causes of generalised abdominal pain
Peritonitis
Ruptured abdominal aortic aneurysm
Intestinal obstruction
Ischaemic colitis
Causes of right upper quadrant pain
Biliary colic
Acute cholecystitis
Acute cholangitis
Causes of epigastric pain
Gastritis
Peptic ulcer disease
Pancreatitis
Ruptured AAA
Causes of central abdominal pain
Ruptured AAA
Intestinal obstruction
Ischaemic colitis
Early stages of appendicitis
Causes of right iliac fossa pain
Acute appendicitis
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion
Meckel’s diverticulitis
Causes of left iliac fossa pain
Diverticulitis
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion
Causes of suprapubic pain
Lower urinary tract infection
Acute urinary retention
Pelvic inflammatory disease
Prostatitis
Causes of loin to groin pain
Renal colic (kidney stones)
Ruptured AAA
Pyelonephritis
Symptoms of spontaneous bacterial peritonitis
Ascites
Abdominal pain
Fever
Investigations for spontaneous bacterial peritonitis
Paracentesis - neutrophil count over 250 cells/ul
Most common organism causing spontaneous bacterial peritonitis
E.coli
Management of spontaneous bacterial peritonitis
IV cefotaxime
What is haemochromatosis
Autosomal recessive genetic condition resulting in iron overload. There is excessive total body iron and deposition of iron in tissues.
Symptoms of haemochromatosis
Lethargy
Joints - arthralgia, arthritis
Gonads - erectile dysfunction, menstrual irregularities
Abdominal pain
Mood disturbances
Complications of haemochromatosis
Skin - bronze pigmentation
Pancreas - diabetes mellitus
Liver - features of chronic liver disease: hepatomegaly, cirrhosis
Heart - cardiomyopathy
Joints - arthritis in the hand specifically - ‘iron fist’ sign
Gonads - hypogonadism
Investigations for haemochromatosis
Serum ferritin - raised
Transferrin saturation - raised
Genetic testing - for HFE gene
LFTs
Liver biopsy
MRI - helps visualise iron concentration in liver
Management of haemochromatosis
Venesection - aim for transferrin saturation below 50% and serum ferritin concentration below 50ug/l
Desferrioxamine - second line
What is Wilson’s disease
Autosomal recessive genetic condition resulting in the excessive accumulation of copper
Symptoms of Wilson’s disease
Liver: hepatitis and cirrhosis
Neurological:
- Tremor
- Dystonia
- Parkinsonism - tremor, bradykinesia, rigidity
Psychiatric:
- Abnormal behaviour
- Depression
- Psychosis
- Cognitive impairment
Kayser-Fleischer ring in cornea
Can also have Haemolytic anaemia and Renal tubular acidosis
Investigations for Wilson’s disease
Slit lamp examination - for Kayser-Fleischer ring
Serum caeruloplasmin (carries copper in the blood)- reduced
Total serum copper - reduced (As all is bound to caeruloplasmin)
Free serum copper - raised
24hr urinary copper excretion - raised
Genetic analysis
Management of Wilson’s disease
Penicillamine - chelates copper
Trientine hydrocholoride - second line chelating agent
Zinc salts (inhibit copper absorption in the gastrointestinal tract)
How is diarrhoea defined
> 3 loose or watery stool per day
What are the acute causes of diarrhoea
Gastroenteritis
Diverticulitis
Antibiotics
Constipation causing overflow
Chronic causes of diarrhoea
IBS
IBD
Colorectal cancer
Coeliac disease
Define constipation
Less than 3 stools a week
Hard stools that are difficult to pass
Rabbit dropping stools
Straining and painful passages of stools
What is the management of constipation
Treat underlying cause
Increase dietary fibe
Ensure adequate fluid intake
Ensure adequate activity levels
1st Line = bulk-forming laxative - ispaghula
2nd Line = osmotic laxative - macrogol
Complications of constipation
Overflow diarrhoea
Acute urinary retention
Haemorrhoids
What is Gilbert’s Syndrome
Autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase.
Feature of Gilbert’s syndrome
Unconjugated hyperbilirubinemia (i.e. not in urine)
Jaundice may only be seen during an intercurrent illness, exercise or fasting
What are the risk factors for developing hepatocellular carcinoma
Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C
Rarer causes (e.g., primary sclerosing cholangitis)
What is the tumour marker for HCC
AFP - alpha-fetoprotein
How often are patients with liver cirrhosis screened for HCC? What tests does this include?
Every 6 months
Ultrasound
Alpha-fetoprotein (AFP)
Symptoms of HCC
Tends to present late
Jaundice
RUQ pain
Ascites
Hepatomegaly
N+V
Pruritis
Weight loss
Investigations for HCC
Ultrasound
AFP
CT and MRI for staging
Biopsy
Management of HCC
Surgical resection - for early disease
Liver transplant
Radiofrequency ablation
Transarterial chemoembolisation (TACE)
Sorafenib: a multikinase inhibitor
Causes of cirrhosis
Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
What are the examination findings of liver cirrhosis
Cachexia (wasting of the body and muscles)
Jaundice caused by raised bilirubin
Hepatomegaly (enlargement of the liver)
Small nodular liver as it becomes more cirrhotic
Splenomegaly due to portal hypertension
Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)
Palmar erythema caused by elevated oestrogen levels
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising due to abnormal clotting
Excoriations (scratches on the skin due to itching)
Ascites (fluid in the peritoneal cavity)
Caput medusae (distended paraumbilical veins due to portal hypertension)
Leukonychia (white fingernails) associated with hypoalbuminaemia
Asterixis (“flapping tremor”) in decompensated liver disease
What does a non-invasive liver screen consist of
Ultrasound - to diagnose fatty liver
Hepatitis B and C serology
Autoantibodies - autoimmune hepatitis, PBC, PSC
Immunoglobulins
Caeruloplasmin
Alpha-1-antitrypsin levels
Ferritin and Transferrin saturation
What will LFTs look like in decompensated cirrhosis
Raised Bilirubin, ALT, AST, ALP
Low albumin
Increased PT time
Thrombocytopenia
Hyponatraemia - occurs with fluid retention
What does the enhanced liver fibrosis (ELF) blood test test for
Fibrosis in NAFLD
What are the enhanced liver fibrosis blood test ranges
10.51 or above – advanced fibrosis
Under 10.51 – unlikely advanced fibrosis (NICE recommend rechecking every 3 years in NAFLD)
What does an ultrasound show in liver cirrhosis
Nodularity on surface
‘corkscrew’ appearance to hepatic arteries
Enlarged portal vein with reduced flow
Ascites
Splenomegaly
Who is a fibroscan recommended for
Patients at risk of cirrhosis:
Chronic Hepatitis B and C
ARLD
Heavy alcohol drinkers
NAFLD
What does the Child-Pugh score assess?
Assesses the severity of cirrhosis and prognosis
What is used in the Child-Pugh score
ABCDE mnemonic
Albumin
Bilirubin
Clotting - INR
Dilation - ascites
Encephalopathy
What are the 6 complications of liver cirrhosis
Malnutrition
Portal hypertension
Varices (bleeding varices possible)
Ascites
SBP
Hepatorenal syndrome
Hepatic encephalopathy
How does cirrhosis cause malnutrition and how to treat it
Reduced appetite
Deranged protein metabolism and production in the liver
Deranged glucose storage and glycogen storage
Regular meals
High protein and calorie intake
Avoid alcohol
what is the most common site of varices due to liver cirrhosis
Distal oesophagus (oesophageal varices)
Anterior abdominal wall (caput medusae)
How to treat oesophageal varices
Prophylactic beta blockers - propranolol
Variceal band ligation - if BB contraindicated
How to treat bleeding oesophageal varices
Blood transfusion
Treat any coagulopathy (e.g., with fresh frozen plasma)
Vasopressin analogues (e.g., terlipressin or somatostatin)
Prophylactic broad-spectrum antibiotics (shown to reduce mortality)
Urgent endoscopy with variceal band ligation
Consider intubation and intensive care
TIPS
How to manage ascites
Low sodium diet
Aldosterone antagonists (e.g., spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics (ciprofloxacin or norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
Transjugular intrahepatic portosystemic shunt (TIPS) is considered in refractory ascites
Liver transplantation is considered in refractory ascites
How does hepatorenal syndrome develop in patients with cirrhosis
Portal hypertension causes the portal vessels to release vasodilators, which cause significant vasodilation in the splanchnic circulation (the vessels supplying the gastrointestinal organs). Vasodilation leads to reduced blood pressure. The kidneys respond to the reduced pressure by activating the renin-angiotensin-aldosterone system, which leads to vasoconstriction of the renal vessels. Renal vasoconstriction combined with low systemic pressure results in the kidneys being starved of blood and significantly reduced kidney function.
How does cirrhosis cause hepatic encephalopathy
Build up of ammonia - produced by intestinal bacteria
What factors can trigger or worsen hepatic encephalopathy
Constipation
Dehydration
Infection
High protein diet
Management of hepatic encephalopathy
Lactulose - to prevent constipation
Rifaximin - reduced number of intestinal bacteria producing ammonia
What is the MELD score used for and what is included in the scoring system?
The MELD score estimates a patient’s chances of surviving their disease during the next three months
Includes:
Bilirubin
Creatinine
INR
What is the MELD score used for and what is included in the scoring system?
The MELD score estimates a patient’s chances of surviving their disease during the next three months
Includes:
Bilirubin
Creatinine
INR
What is the difference between compensated and decompressed liver cirrhosis
Compensated: liver is still able to function relatively well, despite scarring from the disease
Decompensated: liver is no longer able to function properly, and patients experience serious symptoms and complications
What is the difference between compensated and decompressed liver cirrhosis
Compensated: liver is still able to function relatively well, despite scarring from the disease
Decompensated: liver is no longer able to function properly, and patients experience serious symptoms and complications
What are the three stages of non-alcoholic fatty liver disease
Steatosis
Steatohepatitis
Cirrhosis
Risk factors for non-alcoholic fatty liver disease
Obesity
T2DM
Hyperlipidaemia
Sudden weight loss/starvation
Jejunoileal bypass
What are the symptoms of NAFLD?
Hepatomegaly
ALT greater than AST
Increased echogenicity on liver ultrasound
Management of NAFLD
Lifestyle changes (particularly weight loss) and monitoring
What are the oesophageal causes of an upper GI bleed?
Oesophageal varices
Oesophagitis
Cancer
Mallory-Weiss tear
What are the gastric causes of an upper GI bleed?
Gastritis
Gastric cancer
What are the duodenal causes of an upper GI bleed?
Duodenal ulcer
Aorta-enteric fistula
What scoring systems are used for upper GI bleeds and what is included in them?
Blatchford bleeding score - helps clinicians decide whether patients can be managed as outpatients or not
Includes:
Hb
Urea
Initial systolic BP
Sex
Heart rate > 100
Malaena present
Recent syncope
Hepatic disease history
Cardiac failure present
Rockfall scoring system - provides a percentage risk of rebleeding and mortality
Includes:
Age
Shock
Comorbidities
Diagnosis
Major stigmata of recent haemorrhage
How to treat an upper GI bleed
ABCDE approach with wide bore cannula access
Platelet transfusion if actively bleeding
FFP for patients with reduced fibrinogen or prolonged PT time
Endoscopy after ABCDE
If non-variceal bleed then: give PPIs
If variceal bleed:
Terlipressin
Band ligation
TIPS - if not controlled with above
What are the extra-intestinal manifestations of IBD?
Erythema nodosum
Pyoderma gangrenosum
Inflammatory arthritis
Scleritis
Uveitis
Primary sclerosing cholangitis (more so with UC)
What is infectious colitis
Colonic infection by bacteria, viruses, or parasites
What are the common causative organisms of infectious colitis
Bacterial:
C.jejuni
Salmonella
E.coli
Shigella
Viral:
Norovirus
Rotavirus
Adenovirus
CMV
Parasitic:
Entamoeba
STDs:
Neisseria gonorrhoeae
Chlamydia trachomatis
Herpes simplex 1 and 2
Investigations for infectious colitis
Stool MCS
FBC
ESR/CRP
Treatment for infectious colitis
Treat according to causative agent
What organism causes rice water stools
Cholera
Define bowel obstruction
When the passage of food, fluids and gas through the intestines becomes blocked
What is third-spacing
Abnormal loss of fluid in bowel obstruction. GI tract releases fluids which are later reabsorbed in the colon. If there is a blockage, they cannot be reabsorbed meaning fluid is lost from the intravascular space into the GI tract. This leads to hypovolemia and potentially shock.
What are the three main causes of bowel obstruction
Hernias
Malignancies (tumor)
Adhesions
What is the most common cause of large bowel obstruction
Tumors - most common
Volvulus
Diverticular disease
What is the most common cause of small bowel obstruction
Adhesions
followed by hernias
What are the 4 main causes of intestinal adhesion
Abdominal or pelvic surgery
Peritonitis
Abdominal or pelvic infection (e.g. PID)
Endometriosis
Define a closed loop obstruction
Where there are two points of obstruction along the bowel, meaning the middle section is sandwiched between the two obstructions
What are the causes of a closed loop obstruction
Adhesions
Volvulus
Hernias
A single point of obstruction in the large bowel with a competent ileocaecal valve (the valve doesn’t allow contents to pass back through it)
What are the symptoms of large bowel obstruction
Absence of passing stools or flatus
Abdominal pain
Abdominal distension
N+V
Peritonism - if bowel perforation is present
What are the symptoms of small bowel obstruction
Diffuse central abdominal pain
N+V (typically bilious vomiting)
Constipation and lack of flatulence
Abdominal distension (more apparent in lower level obstructions)
Tinkling bowel sounds
Investigations for bowel obstruction
Abdominal X-ray - 1st line
CT scan - gold standard
U&Es - assess electrolytes
VBG - metabolic acidosis due to vomiting stomach acid
Lactate - raised due to bowel ischaemia
What is shown on an x-ray in small bowel obstruction
Distended small bowel loops with fluid levels
Consider dilated if the small bowel is >3cm in diameter
What is shown on an x-ray in large bowel obstruction
Diameter greater than the normal diameter limits, which are:
Caecum: 10-12cm
Ascending colon: 8cm
Recto-sigmoid colon: 6.5cm
What might indicate bowel perforation on an abdominal x-ray
The presence of free intra-peritoneal gas (air under the diaphragm) indicates colonic perforation
What are the normal limits for the diameter of the small bowel, caecum, ascending colon and recto-sigmoid colon and why are these relevant
Small bowel: 3m
Caecum: 10-12cm
Ascending colon: 8cm
Recto-sigmoid colon: 6.5cm
They are relevant as anything over this might indicate bowel obstruction
What is the initial management of bowel obstruction
‘Drip and suck’:
Nil by mouth
IV fluids
NG tube with free drainage
What is the management of bowel obstruction if the initial management is not successful
Surgery, to either:
Find the cause with explorative surgery
To treat adhesions - adhesiolysis
Hernia repair
Emergency resection of the obstructing tumour (or stents to push tumour out of the way)
What would the management of bowel obstruction be if there was a perforation as well
Emergency surgery
IV antibiotics
What is achalasia
Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated
Symptoms of achalasia
Dysphagia of both liquids and solids
Heartburn
Regurgitation of foods - may lead to cough or aspiration pneumonia
Investigations for achalasia
Oesophageal manometry - excessive LOS tone which doesn’t relax on swallowing
Barium swallow - bird beak appearance
CXR - wide mediastinum and fluid level
Treatment of achalasia
Pneumatic (balloon) dilation
Surgery - Heller cardiomyotomy
Intra-sphincteric injection of botulinum toxin
