Gastro Med + Upper GI Surg COMPLETE Flashcards
Gastroenterology and Upper GI Surgery combined revision set. Created 06/12/24., finished 11/01/25.
Give some drugs that reduce lower oesophageal sphincter tone and can precipitate / worsen reflux.
Theophylline
Caffeine
Cigarettes
CCB
BB
Anticholinergics
How long is the washout period for a PPI before testing for H.pylori?
2 weeks
Discuss the management options available for GORD.
First line is lifestyle advice and full dose PPI for 4 weeks.
Consider a further 4 weeks if not responding, and change in PPI.
H2-receptor antagonist e.g. famotidine can be considered as well if nocturnal symptoms.
Alginate e.g. gaviscon can also be used, create a ‘foam raft’ to stop reflux symptoms.
What is the management for a positive H.pylori result?
7 DAYS High dose PPI, then continue for 2 months + AMOXICILLIN + Metronidazole OR Clarithromycin, BD.
Test for H.pylori 4-8 weeks after completion of eradication therapy.
Occasionally surgery is indicated for a hiatus hernia. What is the surgical procedure and what occurs in it?
Nissen Fundoplication.
The fundus of the stomach is wrapped around the LOS to prevent reflux.
What are the 2 different types of hiatus hernia and what are the differences?
Sliding (80%). The GOJ ‘slides’ through the oesophageal hiatus into the thorax.
Rolling (20%). The LOS actually stays below the diaphragm but part of the stomach rolls up into the chest, next to the oesophagus. Can result in gastric volvulus, severe pain and need for surgery.
What cell changes occur in Barrett’s oesophagus?
Intestinal metaplasia from squamous to columnar epithelium due to chronic acid reflux.
How is Barrett’s oesophagus diagnosed, and why is it significant?
Following endoscopic biopsy, even though it is visible macroscopically.
Pre-malignant change for oesophageal adenocarcinoma.
https://www.clinicalkey.com/student/content/book/3-s2.0-B9780443115387000306
What is achalasia?
Failure of relaxation of the distal end of the oesophagus due to a neuromuscular problem, usually involving the ganglionic cells of the myenteric plexus.
Leads to progressive dilatation of the proximal end, tortuosity, incoordination of peristalsis and hypertrophy of the proximal oesophagus.
Achalasia is diagnsosed after a barium swallow, endoscopy and manometry. What are the management options?
It is incurable so only symptomatic relief is available.
Botulinum toxin or endoscopic balloon dilation can provide symptomatic relief.
Surgery can sometimes be done (Heller cardiomyotomy) but this can cause reflux oesophagitis.
Describe the differences in types of oesophageal cancer in terms of where in the oesophagus it arises.
Upper 2/3 = squamous. Most common worldwide.
Lower 1/3 = adenocarcinoma. Columnar epithelium transformation.
Squamous cell carcinoma and adenocarcinoma of the oesophagus share a lot of risk factors but also have some independent ones. Outline specific risk factors for these types of cancers.
Squamous: alcohol intake, smoking.
Adenocarcinoma; GORD, Barrett’s oesophagus, obesity.
Give some risk factors for oesophageal cancer, regardless of type.
Advancing age
Achalasia
Plummer-Vinson syndrome
Tylosis (AD palmar and plantar keratosis)
What is Plummer-Vinson syndrome?
Classical triad of post-cricoid dysphagia, iron deficiency anaemia and oesophageal webs.
Increases risk of oesophageal cancer, mainly SCC.
It has associations with Coeliac disease, thyroid disease, rheumatoid arthritis and Crohn’s.
Patients with oesophageal cancer are often asymptomatic until a late stage. Clinically, how may they present when they do have symptoms?
Odonyphagia
Dysphagia; progressive, solids to liquids
Dyspepsia
Weight loss
Hoarseness
Vomiting
Anorexia
Haematemesis
Upper abdo pain
Anaemia
Give 4 differential diagnoses for oesophageal cancer.
Achalasia
Benign stricture
Barrett’s oesophagus
Gastric cancer
Who would get an upper GI endoscopy on the 2 weeks USOC list?
Dysphagia or over 55 + weight loss + one of [upper abdo pain, reflux, dyspepsia]
What investigation methods are used to stage oesophageal cancer after it has been picked up via upper GI endoscopy?
Endoscopic US
CT CAP
+/- laparoscopy for occult peritoneal disease
Discuss the management options for oesophageal cancers.
Only 1/3 of lesions at presentation are suitable for surgical resection (Ivor-Lewis), which carries a high mortality risk.
Risks of this include anastomotic leak resulting in mediastinitis.
Neo/adjuvant chemotherapy is used (epirubicin, cisplatin +/or 5-flurouracil).
Oesophageal stenting is a symptomatic palliative option.
Peptic Ulcer Disease has a prevalence of 15-20%. Where is it most likely to occur, give 5 sites in order of the most common.
Duodenum
Stomach
Oesophagus
Jejunum
Also may occur in a Meckel diverticulum with ectopic gastric mucosa.
What causes Zollinger-Ellison syndrome and what are the clinical features?
Caused by a gastrin-secreting duodenal or pancreatic adenoma. (Most common in first part of duodenum).
Causes diarrhoea, steatorrhoea, malaborption, multiple gastroduodenal ulcers.
Raised fasting gastrin level helps to diagnose.
30% of gastrinomas arise as part of what syndrome?
MEN I
Why does Zollinger-Ellison syndrome cause diarrhoea, steatorhoea and pancreatic insufficiency?
Diarrhoea due to low pH in the upper intestinal tract.
Steatorrhoea due to reduced lipase activity due to low pH.
The low lipase / other pancreatic enzymes are dysfunctional due to the low pH, manifesting as pancreatic insufficiency.
What are the top 2 causes of peptic ulcer disease? + give 3 drug types that increase risk.
H.pylori (95% of duodenal ulcers, 80% gastric ulcers)
NSAID use (remember to ask about OTC medications)
SSRIs
Steroids
Bisphosphonates
What are the 3 main complications secondary to peptic ulcer disease?
Bleeding
Perforation
Pyloric Stenosis (due to the oedema around the ulcerated area, or from scar formation from ulcer healing)
What is the pattern of pain of a duodenal vs gastric ulcer?
Before meals or at night, relieved by eating = duodenal
Pain associated with eating, relieved by antacids = gastric
Give 5 causes of acute gastritis / ulceration.
NSAIDs
Alcohol
Steroids
Smoking
Severe stress
Peptic ulcers can perforate, and these symptoms often present suddenly. Give some clinical features of a perforated peptic ulcer, and what investigation should be done (even though it is often a clinical diagnosis).
Epigastric pain, becoming more generalised.
Sudden onset pain.
Syncope may be present.
Erect CXR to check for free air under the diaphragm.
Bleeding is the most common complication of peptic ulcer disease, accounting for around 75% of problems. Which artery is most likely to be involved, and give 4 clinical features that may be present.
Gastroduodenal artery
Haematemesis
Melaena
Hypotension
Tachycardia
What scores are used during an upper GI bleed for risk assessment?
Glasgow Blatchford (initially) and Rockall (post-endoscopy) scores.
Pre-endoscopy Blatchford score of 0 = consider early discharge.
Blatchford indicates whether patients should be managed as an inpatient or not.
Rockall is done post endoscopy to provide % risk of rebleeding and mortality; includes age, shock features, comorbidities, aetiology of bleeding and endoscopic features of recent haemorrhage.
An upper GI haemorrhage indicates need for endoscopy. Which patients should be done immediately, and which patients should be done within 24 hours of admission?
Haemodynamically unstable = immediately.
All other patients = within 24 hours.
A significant upper GI bleed is a medical emergency. An A-E approach should be used. Describe management strategies that would commonly be used in this situation.
Airway safe.
Oxygen if hypoxic.
IV fluids whilst awaiting crossmatched blood. 2 large bore IV access.
Clotting should be corrected; platelets (if <50x10^9 / L), FFP (if PT or APTT >1.5x normal) if actively bleeding / unstable.
Prothrombin complex concentrate e.g. Beriplex and vit K to reverse warfarin if necessary.
If there is active bleeding during an endoscopy, what interventions can be used to stop it?
Adrenaline injection (NOT as monotherapy)
Clipping / banding ligates varices
Heat probe / laser therapy coagulates varices
Specific management for variceal bleeding:
(One of the most significant complications of portal hypertension is oesophageal varices).
IV antibiotics (quinolones e.g. )
IV terlipressin
Oesophageal = band ligation, then consider TIPS.
Gastric = endoscopic injection of N-butyl-2-cyanoacrylate if gastric varices. TIPS if not controlled.
Sengstaken-Blakemore tube ?
STOP NSAIDs, but continue low dose aspirin for secondary prevention of vascular event if haemostasis has been achieved.
Give 4 adverse prognosticators of variceal bleeding i.e. other features of decompensated liver failure.
Jaundice
Hypoalbuminaemia
Encephalopathy
Ascites
Upper GI bleeding is common. What are the top 2 causes, and describe 3 clinical features that may be seen regardless of cause.
Oesophageal Varices
Peptic Ulcer Disease
Haematemesis (bright red or coffee ground)
Melaena (black, tarry, due to passage of altered blood per rectum)
Raised urea due to protein meal of the blood
What is the physiology of how a TIPS procedure works in variceal bleeding?
Transjugular intra-hepatic porto-systemic shunt; lowers portal pressure by creating a shunt to the systemic circulation. Reduces bleeding due to lower pressure.
Enlargement of the left supraclavicular fossa lymph node is known as what, and what does it indicate? + one other sign of this.
Virchow’s node
Indicates lymphatic spread of gastric cancer (mets)
+ Periumbilical node = Sister Mary Joseph nodule
Give some local and systemic features of gastric cancer.
Local:
Dysphagia
Dyspepsia
N&V
GI bleed and IDA
Palpable mass / tenderness
Systemic:
Weight loss
Anorexia
Where is gastric cancer most likely to metastasise to?
Liver, bones, breast, lung
What is a Krukenberg tumour?
Ovarian tumour due to transcoloemic (across a body cavity e.g. peritoneal) spread of gastrointestinal cancer.
Malignant, mucin-secreting signet-ring cell adenocarcinoma.
Account for 5% of ovarian tumours.
What is the most common type of gastric cancer and where is is most likely to arise within the stomach?
Adenocarcinoma from glandular epithelium of stomach lining
Pylorus and antrum
Outline some of the risk factors for gastric cancer.
Male (2:1)
Increased age (half of patients are >75)
Japanese heritage (increased nitrosamines in diet ?fish)
Atrophic gastritis e.g. due to chronic gastritis
Pernicious anaemia
Blood group A
H.pylori
Alcohol use
Smoking
Diet: salt + salt preserved foods, + high processed meat and nitrate diet
Why is H.pylori a risk factor for gastric cancer?
Triggers inflammation of the gastric mucosa, leads to atrophy and intestinal metaplasia and then dysplasia
Paraneoplastic features of gastric cancer are rare, but there are 2 to be aware of. What are they?
Acanthosis nigricans
Dermatomyositis
Investigations for gastric cancer are used for diagnosis and staging. Give the different ones used respectively.
OGD with biopsy = diagnostic
CT CAP = staging +/- endoscopic US
A large number of abnormal cells are seen on a biopsy with a patient with suspected gastric cancer. What type of cells might these be, and what does the number indicate?
Signet ring cells; large vacuole of mucin that displaces the nucleus to one side.
Higher number = worse prognosis
Surgery is really the only curative option for gastric cancer. What are the 3 surgical options? + one potential pharmacological one
Endoscopic mucosal resection if early stage
Partial gastrectomy
Total gastrectomy
Herceptin if HER2-receptor positive
Tyrosine kinase inhibitors are biological agents used amongst some cancers. Give 2 types of cancer that TKIs are used for, and give the name of one of the agents.
Imatinib
CML
Gastrointestinal stromal tumours
What is a GIST?
Gastrointestinal stromal tumour; mesenchymal tumour of GI tract.
Commonly benign, usually solitary.
Clinical features are dependent on size, and include nausea, vomiting and occult bleeding.
What genetic condition would a GIST be associated with?
Neurofibromatosis type I
Outline the exocrine functions of the pancreas.
Pancreatic acinar cells produce digestive enzymes.
These include lipase, amylase, proteases inc trypsin and chymotrypsin.
The enzymes are trnasported to the duodenum in high-volume pancreatic secretion from the ductal cells. It contains high amounts of bicarbonate to neutralise the gastric acid, as enzyme activity is pH dependent.
Outline the endocrine functions of the pancreas. (inc 5 main types of islet cells).
The endocrine pancreas consists of hormone producing cells arranged in islets (islets of Langerhans). The hormones are secreted directly into the circulation.
5 main types of islet cell:
Beta = insulin
Alpha = glucagon
D = somatostatin
PP = pancreatic polypeptide
Enterochromaffin cells = serotonin
Chronic pancreatitis is a chronic, irreversible inflammation and or fibrosis of the pancreas, resulting in exocrine and endocrine insufficiency.
Give 5 causes of chronic pancreatitis, highlighting the most common one.
Alcohol abuse = number 1
Cystic fibrosis
Haemachromatosis
Ductal obstruction e.g. stones, tumour, structural abnormalities including pancreas divisum and annular pancreas.
Drugs including thiazides, azathioprine and tetracyclines.
Describe the clinical features that chronic pancreatitis would start with and progress to.
Intermittent abdominal pain, radiating to back. Worse 15-30 minutes after eating.
Weight loss
Generally unwell
Intermittent or persistent obstructive jaundice
Steatorrhoea, between 5-20 years post onset of pain, secondary to malaborption from reduction in pancreatic exocrine function e.g. lipase.
Diabetes ~ 20 years post onset of pain, due to pancreatic islet beta cell destruction.
Pseudocysts and abscesses.
Discuss the management of chronic pancreatitis.
Avoid alcohol.
Low fat diet due to malabsorption.
Analgesia.
Fat soluble vitamins, pancreatic enzyme e.g. Creon, and calcium given.
Manage diabetes if present.
ERCP if stricture.
ESWL if stones present.
Which scans + one other test are often done when investigation chronic pancreatitis?
AXR; 30% will show calcification.
CT is more sensitive at detecting calcification.
Faecal elastase can detect exocrine function.
What blood tests might be checked when suspecting chronic pancreatitis, and discuss what they might show.
FBC might show elevated WCC, CRP may be raised due to inflammation.
Fasting serum glucose is often raised.
LFTs may show an obstructive pattern.
Check Calcium, magnesium and phosphate.
Note: amylase may not be raised because pancreas has reduced function.
What is the main type of pancreatic carcinoma and where is it most likely to occur?
Adenocarcinoma
75% in head of pancreas
What are some risk factors for pancreatic carcinoma?
Smoking
Chronic pancreatitis
Diabetes
Associated with KRAS mutation
Familial cancer syndromes, inc BRCA2 and HNPCC
Increased age
General features of pancreatic carcinoma include weight loss, lethargy and anorexia. Other symptoms are quite vague, making it hard to pick up and often resulting in late diagnosis. Describe some clinical features of pancreatic carcinoma.
Painless jaundice
?Epigastric pain that radiates to the back
Dyspepsia
Steatorrhoea
Obstructive jaundice
Palpable gallbladder
New onset depressive symptoms
? acute pancreatitis due to obstruction of pancreatic duct
? hepatomegaly due to biliary obstruction or mets
What is Trousseau’s sign and what does it indicate?
Trousseau’s = superficial venous thrombosis, repeated attacks at different sites.
= thrombophlebitis migrans. Due to procoagulant factors of cancer. 10% of patients with pancreatic cancer will have this.
What is Courvoisier’s sign?
Palpable gallbladder, usually painless.
Usually in context of obstructive jaundice
What is the pathophysiology of obstructive jaundice in the context of pancreatic cancer?
Tumour of the head of the pancreas / ampulla compresses the distal common bile duct.
Pancreatic cancer is usually diagnosed too late, with less than 20% presenting with a localised tumour suitable for resection. What is the curative procedure for tumours of the head or neck of the pancreas, and give 2 side effects.
Whipple = pancreatoduodenectomy. Adjuvant chemotherapy is often giving too.
Dumping syndrome
Peptic ulcer disease
What are the investigations generally done in suspected pancreatic cancer?
US; sensitivity 60%
High resolution contrast CT; gold standard to confirm
EUS can be useful if lesions are <2cm and not picked up on CT
What tumour marker may be useful when monitoring response to treatment in pancreatic cancer, or can be helpful diagnostically if it rises over time?
CA19-9
The mainstay of treatment for pancreatic cancer is palliative and symptom management. Chemotherapy maybe also be given. Give options for symptom management.
Stenting if obstructive jaundice or duodenal obstruction.
Pancreatic enzyme supplementation.
Pain management via pain team, usually opioids.
What sign may be present on a CT scan in suspected pancreatic cancer?
Double duct sign; simultaneous dilation of common bile and pancreatic ducts.
Eosinophilic oesophagitis?
After a meal, pancreatic exocrine secretion is regulated by 3 different inputs. What are these?
Cephalic; behavioural cues related to sight, smell and taste of food.
Gastric; gastric distention causes secretion of enzyme rich fluid, little bicarb or water.
Intestinal; protein, fat and gastric acid enter duodenum.
Which hormones play a role in digestive enzyme secretion?
Cholecystokinin; produced in I cells of SI mucosa, secreted in response to intraluminal food. Acts on vagal afferent fibres to stimulate pancreatic secretion.
Secretin; direct effect on pancreatic acinar cells, as well as ductal cells - results in a bicarb-rich pancreatic secretion.
Give 3 causes of upper GI bleeding:
Gastric or duodenal ulcer
Oesophageal varices
Mallory-Weiss tear
What are oesophageal varices, and what causes them?
Dilated submucosal distal oesophageal veins that connect the portal and systemic circulations, and are important portosystemic collaterals.
They occur secondary to portal hypertension and cirrhosis, and serve as a collateral pathway between the portal vein and the SVC via the azygos vein.
Most common ^ (‘downhill’ varices also occur but much less common and different pathology).
Name 4 pancreatic neuroendocrine tumours.
Gastrinoma (resulting in Zollinger-Ellison syndrome)
Insulinoma (sporadic or MEN. 95% benign. Fasting hypoglycaemia.)
Glucagonoma
Somatostatinoma
What does gastrin do?
Stimulate secretion of gastric acid from parietal cells.
Produced by G cells.
What is Whipple’s triad for diagnosis of an insulinoma?
Symptoms associated with fasting or exercise (diplopia, sweating, palpitations, weakness, confusion, LOC, tonic clonic seizure)
Hypoglycaemia confirmed during these episodes
Glucose relieves symptoms
Alcohol can produce a wide spectrum of liver disease. What are the 3 categories?
Fatty liver; metabolism of alcohol produces fat in the liver; steatosis occurs where the cells are swollen with fat. Can be reversed at this stage.
Alcoholic hepatitis; steatosis + leucocyte infiltration = hepatocellular necrosis. +/- Mallory bodies.
Cirrhosis; abnormal liver architecture interfering with blood flow and function, leading to portal hypertension and liver failure.
What are the NICE recommendations for screening for liver cirrhosis?
Transient elastography / Fibroscan for:
People with HCV infection
Men who drink over 50 and women who drink over 35 units of alcohol per week
People diagnosed with alcohol-related liver disease
People diagnosed with NAFLD adn advanced stage liver disease as assessed by an ELF score of >=10.51
What would liver biochemistry testing reveal in a patient with alcoholic hepatitis?
Leucocytosis
Elevated:
Serum bilirubin
Serum AST and ALT (AST>ALT ratio >3 is strongly suggestive)
Serum ALP
Serum PT
( + low serum albumin)
GGT characteristically elevated in all alcoholic liver disease
Alcoholic hepatitis can be severe and lead to acute decompensation. Nutrition must be maintained with enteral feeding and maybe vitamin supplementation. What is the pharmacological management for alcoholic hepatitis, and how is it decided who would benefit from it?
Glucocorticoid e.g. prednisolone often used during acute episodes of alcoholic hepatitis.
Maddrey’s Discriminant Function is often used to determine who would benefit. Calculated using PT and Br concentration.
DF > 32 NICE recommends use of steroids; improves 1 months survival, but no effect on >3 month survival.
The Glasgow score of more than 9 indicates necessity of steroids as >9 has a 28 mortality of 75%, but <9 is 50%.
The MELD score also indicates survival at 1 year but does not describe need for steroids.
What are the common causes of cirrhosis (4)
Alcohol
Hepatitis B+/-D
Hepatitis C
NAFLD
Describe the blood supply to the liver.
Accounts for 25% of cardiac output.
25% of supply comes via hepatic artery, a branch of the coeliac axis. Autoregulation of flow occurs, ensuring constant total blood flow.
75% comes from portal vein which drains most of the GI tract and spleen. Normal pressure is 5-8 mmHg, and flow increases after meals.
State the functions of the liver.
Protein metabolism
Synthesis and storage (of proteins, vitamins etc.)
Nitrogen excretion (amino acid degradation)
Lipid metabolism
Production of bile
Immune response
Liver ‘function’ tests do not always accurately assess the synthetic function of the liver. Which 2 of the standard tests are best to consider when looking for liver synthetic function?
Prothrombin time
Albumin level
Acute liver failure describes rapid onset hepatocellular dysfunction. State 4 causes.
Paracetamol overdose
Acute fatty liver of pregnancy
Alcohol
Viral hepatitis, usually A or B
Discuss the use of serum albumin when assessing liver disease.
Serum albumin is a marker of synthetic function.
It’s useful to assess the severity of chronic liver disease, as a falling albumin can be a bad prognostic factor.
In acute liver disease, albumin levels may be normal.
Low albumin can be difficult to interpret when there are other causes of hypoalbuminaemia also present, e.g. malnutrition, urinary protein loss or sepsis.
Why does vitamin K deficiency commonly occur in biliary obstruction?
Low intestinal concentrations of bile salts lead to poor absorption of vitamin K.
Why is prothrombin time a sensitive predictor of both acute and chronic liver disease?
Short half life
What would you see on a FBC in patient affected by liver disease?
Thrombocytopenia, often aggravated by alcohol-induced bone marrow suppression.
Macrocytic red cells if alcohol excess.
Discuss alpha1-antitrypsin, AFP and copper studies in liver disease.
Alpha 1-antitrypsin deficiency can cause cirrhosis.
AFP normally produced by fetal liver. Appearance in high levels in adulthood = HCC.
Increased levels in pregnancy = fetal NTD.
Slightly raised in hepatitis, CLD and teratomas in regenerative liver tissue.
Urinary copper is raised, and serum copper and caeruloplasmin are low in Wilson’s disease.
Which serum autoantibody is found in over 95% of patients with PBC?
AMA
What are the classic symptoms of gallstones, when does it occur and why?
Colicky, RUQ pain occurring post prandially.
It is worst following a fatty meal, when CCK levels are at their highest and gallbladder contraction is maximal.
2 most important test in suspected gallstones?
Abdominal US
LFTs
Preoperative MRCP is usually indicated.
What are the two main types of gallstone?
Cholesterol stone (85% in western world). Formation of these stones is a consequence of cholesterol crystallization from bile.
Pigment stone
Why are statins effective at treating hypercholesterolaemia?
They inhibit HMG-CoA reductase, which catalyses the rate limiting step of cholesterol synthesis.
Management of asymptomatic gallstones:
Asx stones in the gallbladder = NO TREATMENT
Asx stones in CBD = consider surgery due to risk of cholangitis ad pancreatitis
4 risks of ERCP:
Bleeding
Duodenal perforation
Pancreatitis
Cholangitis
There are two types of bile pigment stones. What are they and how do they arise?
Black: calcium bilirubinate. Hyperbilirubinaemia is a critical risk factor, so all major haemolytic anaemias are associated e.g. HS, SCD and thalassaemia, also subclinical haemolysis from prosthetic valve replacements, malaria, hypersplenism etc. Also Gilbert’s.
Brown: calcium salts of fatty acids + calcium bilirubinate. Bile stasis and biliary infection precipitate them.
What is Mirizzi syndrome?
A gallstone in the neck of the gallbladder or in the cystic duct compressing and obstructing the common bile duct, causing deranged LFTs (LFTs are actually often normal in acute cholecystitis).
The initial event in acute cholecystitis is the obstruction of gallbladder emptying, most commonly by a stone. This obstruction results in increased gallbladder glandular secretion and distension which may compromise vascular supply to the gallbladder, and inflammation is also a consequence. What is Murphy’s sign that can often be elicited in acute cholecystitis?
Pain on inspiration when examiner’s fingers are in the approximate location of the gallbladder.
Describe blood results you would expect to see in acute cholecystitis.
Leukocytosis
Raised CRP
Bilirubin and ALP raised significantly = indicates bile duct obstruction.
Aminotransferases can be raised.
90% of acute cholecystitis develops secondary to gallstones. What may cause acalculous cholecystitis, the missing 10%?
Often seen in severely ill, hospitalised patients.
Gallbladder stasis, hypoperfusion and infection can contribute.
May develop secondary to Cryptosporidium or CMV in immunocompromised patients.
Initial management of acute cholecystitis:
Conservative: NBM, fluids, IV antibiotics and opiate analgesia.
Cholecystectomy is usually delayed for a few days to allow symptoms to settle before surgery, but NICE recommends within 1 week.
US is the first line choice of investigation for acute cholecystitis. If the diagnosis remains unclear what could you use next?
HIDA scan: cholescintigraphy, injection of labelled HIDA and taken up selectively by hepatocytes, secreted into bile to visualise biliary tree.
In obstruction, the gallbladder will not be visualised.
What is ascending cholangitis, and what is the most likely organism to cause it, and classic triad of symptoms?
E.coli
Bacterial infection of the common bile duct, causing Charcot’s triad of symptoms:
RUQ pain
Fever
Jaundice
Hypotension and confusion are also often present (‘Reynold’s Pentad’)
Management of ascending cholangitis?
IV abx
ERCP after 24-48 hours to relieve any obstruction
PSC is characterised by inflammation of intra and extrahepatic bile ducts. What are some associations of it?
UC (80% of patients with PSC have UC)
Crohn’s, but less than UC
HIV
Clinical features of PSC include jaundice & pruritis (cholestatic symptoms), RUQ and fatigue. What investigations / scans might be done and what would they show?
Raised Br
Raised ALP
ERCP / MRCP showing beaded appearance from multiple biliary strictures.
p-ANCA may be positive
?liver biopsy has a limited role but may show obliterative cholangitis
Which 2 types of cancer are patients with PSC at an increased risk of getting?
Cholangiocarcinoma
CRC
PBC is thought to be an autoimmune condition, affecting women over men. The classic clinical picture would be a middle aged woman presenting with itching. What are 4 commonly associated diseases with PBC?
Sjogren’s
Systemic sclerosis
RA
Thyroid disease
What is the pathophysiology of PBC thought to be?
Chronic inflammatory process (?autoimmune) causing damage to interlobular bile ducts, causing progressive cholestasis which may eventually progress to cirrhosis.
What is the first line medication for PBC, and also another for symptomatic control?
Ursodeoxycholic acid
Cholestyramine
+ fat soluble vitamin supplementation, liver transplant if bilirubin is >100.
As PBC has the potential to cause cirrhosis, what are the potential complications, and also give 3 other potential complications.
Portal hypertension, ascites, variceal haemorrhage.
Osteoporosis and osteomalacia.
HCC risk x20
Describe the clinical features of PBC, from early to late.
Early; may be asx, isolated ALP rise on LFTs. Fatigue, pruritis.
Cholestatic jaundice, RUQ pain, hyperpigmentation.
Clubbing, hepatosplenomegaly.
Late, may progress to liver failure.
Give 3 immunology tests that would be present / raised in PBC.
AMA M2 subtype in 98%
Smooth muscle antibodies in 30%
Raised serum IgM
Imaging is required before diagnosis of PBC to rule out extrahepatic biliary obstruction. Which imaging is usually done?
RUQ US
or
MRCP
What is the mechanism of acute alcohol withdrawal?
Chronic alcohol consumption enhances GABA inhibition in the CNS (similar to benzos) and inhibits NMDA glutamate transmission.
Alcohol withdrawal symptoms occur due to reversal of this system when alcohol is removed and GABA is decreased, revealing a more excitatory state.
What is the first line pharmacological management for alcohol withdrawal?
Chlordiazepoxide reducing dose, or diazepam as they are long acting. (lorazepam preferred in patients with hepatic failure).
Why is lorazepam the preferred choice of benzodiazepine for patients with liver cirrhosis?
Lorazepam is metabolized through glucuronidation, which is affected less by liver function.
Chlordiazepoxide is oxidised via the p450 system, therefore in cirrhosis there is major risk of accumulation and risk of toxicity, which include sedation and hepatic encephalopathy.
Acute liver failure is defined as:
Acute liver injury with encephalopathy and deranged coagulation with INR >1.5 in a patient with a previously normal liver.
Sometimes, patients may have previous liver damage e.g. D superinfection in a HBsAg positive carrier, Budd-Chiari syndrome or Wilson’s disease.
Histology wise, there is multiacinar necrosis involving a substantial part of the liver.
The time from jaundice development to the development of hepatic encephalopathy can be defined as hyperacute, acute and subacute. What time frames correspond to these headings?
Hyperacute = 7 days
Acute = 8-28 days
Subacute = 21-26 weeks
What is one of the most common causes of acute liver failure in the UK?
Paracetamol overdose
In which 3 causes of acute liver failure is severe fatty change seen?
Acute fatty liver of pregnancy
Reye’s syndrome
IV tetracycline administration e.g. doxy, lymecycline
Describe the stages of hepatic encephalopathy.
I: Irritability
II: Confusion, inappropriate behaviour
III: Incoherent, restless
IV: Coma +/- convulsions
The aetiology of hepatic encephalopathy is not fully understood, but describe the general consensus.
Excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.
Can be seen in acute and also chronic disease (e.g. mild cognitive impairment in patients with liver cirrhosis).
What does NICE recommend for treatment of hepatic encephalopathy?
Lactulose; promotes excretion of ammonia and increases metabolism of ammonia by gut bacteria.
Rifaximin abx for secondary prophylaxis; modulate gut flora resulting in decreased ammonia production.
Give some precipitating factors for hepatic encephalopathy.
Infection e.g. SBP
Renal failure
Hypokalaemia
Constipation
GI bleed
Post TIPS procedure
Drugs including sedatives and diuretics
Give some clinical features of acute (severe) liver failure
Jaundice
Small liver
Hepatic encephalopathy
Fetor hepaticus (breath of the dead, shunting allows thiols to pass directly to lungs)
Fever, vomiting, hypoglycaemia
Spasticity and hyperreflexia
Complications of acute liver failure.
Cerebral oedema (causing ICH and brain herniation)
Bacterial and fungal infections
AKI from hepatorenal syndrome and ATN
GI bleeding
Respiratory arrest
Pancreatitis
What would be seen on LFTs in acute liver failure?
Raised bilirubin
Raised AST and ALT (though not useful for indicating course of disease as they fall with albumin with deteriorating liver function)
LOW coagulation factors, including prothrombin and factor V
EEG and US (small liver) may also be useful
Which electrolyte abnormalities are expected in acute liver failure and what should be done to correct them?
HYPO glycaemia, kalaemia, magnaesaemia, calcaemia, phosphataemia, natraemia
Correct with 10% glucose infusion, k, mag, calc, phos supplements and hypertonic saline.
Coagulopathy corrected with vitamin K, platelets, blood or FFP.
Transfer criteria for patients in acute liver failure to specialist unit (post paracetamol overdose):
INR >3
Hepatic encephalopathy
Hypotension post fluid resuscitation
Metabolic acidosis
[Prothrombin time in seconds > time since paracetamol overdose in hours]
The portal vein is formed by the union of which 2 veins?
Superior mesenteric
Splenic
Portal hypertension is mainly due to cirrhosis, but can have pre-hepatic, intrahepatic or post hepatic causes. Discuss these.
Pre-hepatic = blockage of portal vein before the liver e.g. portal vein thrombosis.
Intrahepatic = disruption of liver architecture.
1. Presinusoidal from schistosomiasis
2. Sinusoidal from cirrhosis, congenital hepatic fibrosis.
3. Post sinusoidal from veno-occlusive disease or Budd Chiari syndrome
Post hepatic is rare (RHD, constrictive pericarditis, IVC obstruction).
What is the normal pressure for the portal vein, and above what pressure do collaterals form within the systemic venous system?
5-8 mmHg
Above 10-12 mmHg collaterals will start to form.
How does portal hypertension arise, and what factors act to sustain it?
Liver injury and fibrosis causes activation of myofibroblasts and contraction, increasing the resistance in the portal vein, causing portal hypertension.
There is hyperdynamic circulation in cirrhosis, caused by nitric oxides etc, and plasma volume expansion due to sodium retention, and these maintain portal hypertension.
What are the lobes of the liver?
Right, left, caudate and quadrate
Ascites can be evaluated based on the serum albumin: ascitic albumin gradient. Discuss the results of SAAG levels and what potential causes these would indicate.
SAAG >11g/L indicates PORTAL HYPERTENSION.
Liver: cirrhosis / alcoholic liver disease, acute liver failure, liver mets.
Cardiac: RHF, constrictive pericarditis.
Other: Budd Chiari syndrome, portal vein thrombosis, veno-occlusive disease, myxoedema.
SAAG <11g/L
Hypoalbuminaemia e.g. nephrotic syndrome, malnutrition
Malignancy
Infections e.g. tuberculous peritonitis
Pancreatitis, bowel obstruction, biliary ascites,
Discuss the management of ascites.
Low sodium diet
Aldosterone antagonist e.g. spironolactone
Drain if tense ascites, with albumin ‘cover’.
Prophylactic antibiotics for people with cirrhosis and ascites with either previous SBP or ascitic protein <15g/L, until ascites has resolved.
Gastritis is just inflammation of the stomach lining. NSAIDs can often cause it. What differentials exist for a gastritis picture, of symptoms including epigastric pain, remitting and relapsing symptoms, vomiting etc.
PUD
Gastric / oesophageal cancer
GORD
Acute pancreatitis
Functional dyspepsia
Using the NESTS mnemonic, what are features favouring Crohn’s over UC?
No blood
Entire GI tract
Skip lesions
Transmural / terminal ileum
Smoking is a risk factor
Give some clinical features specific to UC.
Bloody diarrhoea
Continuous
Limited to colon and rectum
Smoking may be protective
PSC is associated with UC
Use aminosalicylates e.g. mesalazine
Extra-intestinal symptoms of IBD are very common. State 4 that are related to disease activity.
Arthritis (pauci-articular, asymmetrical)
Erythema nodosum
Episcleritis (Crohn’s>UC)
Osteoporosis
Give 6 blood tests that would be relevant in the investigation of IBD symptoms and explain why.
FBC (anaemia, and platelets increase in inflammatory state)
LFTs (albumin, protein lost in bowel, sign of late / severe)
CRP (inflammation, correlates well with disease activity in Crohn’s)
Anti-TTG and IgA (ddx Coeliac disease)
TFTs (hyperthyroidism can cause diarrhoea)
U+Es (electrolyte imbalance and kidney function)
Give 4 methods of investigation in IBD (not blood tests).
Stool microscopy and culture (for infective DDx)
Faecal calprotectin
Colonoscopy and biopsy
Imaging for complications such as fistulae etc
Crohn’s and UC can both have extraintestinal eye disease presentations. What are the most commonly seen eye diseases for Crohn’s and UC respectively.
UC = Uveitis
Crohn’s = episcleritis (NOT painful classically)
Extra-intestinal symptoms of IBD are very common. State 5 that are unrelated to disease activity.
Arthritis (polyarticular, symmetrical)
Uveitis (UC>C)
Pyoderma gangrenosum
Clubbing
PSC (UC mainly)
(Unrelated Arthritis Causing Proper Problems)
IBD management follows the induction of remission and maintenance of remission pathway. How is induction of remission in CROHN’S achieved?
- Oral prednisolone or IV hydrocortisone
- ?Aminosalicylate e.g. mesalazine
?Enteral nutrition if steroids CI e.g. child worried about growth being affected by steroids.
Add ons:
Azathioprine or mercaptopurine, but not as monotherapy.
Infliximab if refractory or fistulating.
Metronidazole if isolated perianal disease.
IBD management follows the induction of remission and maintenance of remission pathway. How is induction of remission in UC achieved in mild - moderate cases?
Induction of remission depends on the area affected by UC.
Proctitis:
Topical mesalazine
If after 4 weeks no improvement, add oral mesalazine.
If still no imp, add topical or oral steroid
(topical mes, oral mes, steroid)
Procto-sigmoid + Left sided:
topical mes
4 weeks: high dose oral mes OR high dose oral mes + topical steroid
Later; stop topical mes, high dose oral mes + oral steroid
Extensive:
high does oral mesalazine
add oral steroid if not controlled
IBD management follows the induction of remission and maintenance of remission pathway. How is maintenance of remission in CROHN’S achieved?
Azathioprine or mercaptopurine but measure TPMT activity first.
Methotrexate is second line.
STOP SMOKING
IBD management follows the induction of remission and maintenance of remission pathway. How is maintenance of remission in UC achieved in mild - moderate cases?
If procto-sigmoid:
Topical mesalazine +/- oral mesalazine
If left-side involvement / extensive:
Low maintenance dose of oral aminosalicylate e.g. mesalazine.
Describe the classification of UC in terms of severity.
MILD
<4 stools / day
Minimal blood
MODERATE
4-6 stools / day
Some blood / varying amounts
No systemic features
SEVERE
>6 stools per day
Lots of blood
Systemic features inc pyrexia, tachycardia, anaemia, raised inflammatory markers
Discuss the induction and maintenance of remission of UC in severe cases.
HOSPITAL BASED
IV hydrocortisone.
If not working, add IV ciclosporin after 72 hours.
If still not working, consider surgery.
What is the investigation of choice for perianal fistulae in Crohn’s, and how might they be treated?
MRI is imaging of choice.
Metronidazole
?Infliximab
If complex, insert draining seton suture to prevent formation of abscess.
Abscess; incision and drainage + antibiotics
If there is strictly terminal ileum disease in Crohn’s then ileocecal resection may be considered.
Which type of cancer are patients with IBD more at risk of, but UC more than Crohn’s?
Colorectal cancer
When should a diagnosis of IBS be considered?
If any of the following for > 6 months:
Abdominal pain
Bloating
Change in bowel habit
When should a positive diagnosis of IBS be confirmed, and what are 3 suggested primary care (blood) investigations that should be done?
Abdominal pain relieved by defecation / associated with altered bowel frequency / stool form + 2/4 of:
- Altered stool passage e.g. straining / urgency / incomplete evacuation
- Abdo bloating
- Worsened by eating
- Passage of mucous
FBC
ESR / CRP for inflammation
Coeliac screen / anti-TTG
State 2 surgical options in advanced UC.
Panproctocolectomy with either:
ileostomy
OR
ileo-anal anastomosis with J pouch
2 main mechanisms of H.pylori for surviving the acidic gastric environment:
Chemotaxis away from low pH areas, burrows into mucosal linings.
Secretes urease –> converted to NH3 –> alkalinisation of the acidic environment
4 associated conditions of H.pylori:
PUD
Gastric cancer
MALT lymphoma
Atrophic gastritis
