Gastrointestinal Flashcards
Define achalasia
An oesophageal motor disorder characterised by a LACK OF OESOPHAGEAL PERISTALSIS and failure of the lower oesophageal sphincter to relax in response to swallowing.
Explain the aetiology of achalasia
Degeneration of the ganglion cells of the myenteric plexus due to unknown aetiology
What are the risk factors for alchalasia?
Infection (herpes and measles virus), autoimmunity, genetics, allgrove syndrome
Epidemiology of achalasia
1 in 100,000.
Can occur at any age but peak in those over 60.
Equal incidence in men and women.
What are the presenting symptoms of achalasia?
Intermittent DYSPHAGIA of solids and liquids Difficulty belching Regurgitation of bland, undigested food or saliva (especially at night) - NOT ACIDIC Heartburn Chest pain Weight loss Nocturnal cough when lying down Pain relived by drinking cold water
What are the signs of achalasia on physical examination?
Nil signs of note
Any signs would be signs of complications eg aspiration pneumonia and malnutrition
What would be appropriate investigations for achalasia and what would their results be?
Upper GI endoscopy - normal, excludes malignancy
Barium swallow - Dilated oesophagus which smoothly tapers down to the sphincter (beak shaped)
Oesophageal manometry - high resting LOS pressure
CXR - absence of gastric gas bubble, widened mediastinum, double right heart border, air-fluid level in upper chest
Define acute cholangitis
Infection of the bile ducts
Explain the aetiology of acute cholangitis
Obstruction of bile duct by gallstones allows bacteria to ascend up the bile duct.
ERCP
Tumours (e.g. pancreatic, cholangiocarcinoma)
Bile duct stricture or stenosis
Parasitic infection
What are the risk factors for acute cholangitis?
Age >50 years
Cholelithiasis
Benign or malignant stricture
Post-procedure injury of bile ducts
What is the epidemiology of acute cholangitis?
Equal in males and females
Median age of presentation: 50-60 yrs
Racial distribution follows that of gallstone disease -
fair skinned people, fat, female, fertile, forty
What are the presenting symptoms of acute cholangitis?
CHARCOT’S TRIAD - RUQ pain, jaundice, fever +/- rigors
REYNOLD’S PENTAD - RUQ pain, jaundice, fever +/- rigors, mental confusion, septic shock
Pruritis (itchy skin)
What are the signs of acute cholangitis on examination?
Fever RUQ tenderness Mild hepatomegaly Jaundice Mental status changes Sepsis Hypotension Tachycardia
What would the appropriate investigations for acute cholangitis be and what would the results be?
Bloods: FBC - High WCC CRP/ESR - possibly raised LFTs - raised ALP + GGT U&Es - urea and creatinine raised, potassium and magnesium low Blood cultures - check for sepsis
Imaging:
ERCP
Abdo USS - see dilated bile duct and stones
If suspecting but negative: contrast-enhanced CT, MRCP or PTC
What is the management of acute cholangitis?
Intravenous antibiotics, intensive medical management and non-operative biliary decompression (ERCP or PTC) with endoscopic lithotripsy to fragment stones if necessary
Analgesics
Second line: surgical biliary decompression via cholecystectomy or choledochotomy (incision into CBD)
Identify the possible complications of acute cholangitis?
Hepatic abscess Liver failure Bacteraemia Gram-negative sepsis Septic shock AKI Organ dysfunction Complications of PTC or ERCP eg abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage
Summarise the prognosis of patients with acute cholangitis
Rapid clinical improvement once adequate biliary drainage is achieved
Patients with significant underlying medical conditions or delayed decompression, poorer prognosis
Hyperbilirubinaemia, high fever, leukocytosis, older age, hypoalbuminaemia are predictive of poor prognosis
17-40% mortality
Define alcohol withdrawal
A syndrome which occurs in patients with chronic alcoholism or alcohol dependence 4-12 hours following the abrupt cessation or decrease of alcohol consumption.
Explain the aetiology of alcohol withdrawal
Chronic alcohol use:
- upregulates post-synaptic STIMULATORY NMDA receptors
- downregulates post-synaptic INHIBITORY GABA type A receptors.
- ethanol activates the inhibitory receptors.
On cessation there is an imbalance between GABA and NMDA stimulation - increased excitation of NMDA.
What are the risk factors for alcohol withdrawal syndrome?
History of alcohol withdrawal syndrome and delirium tremens.
Abrupt cessation of alcohol.
Summarise the epidemiology of alcohol withdrawal syndrome
50% of alcohol dependent patients will experience AWS on abrupt cessation of consumption.
8% of all patients admitted to hospital are at risk of alcohol withdrawal.
What are the presenting symptoms of alcohol withdrawal?
Change in mental status Hallucinations Seizures Delusions Nausea and vomiting Tremor
What are the signs of alcohol withdrawal?
Hypertension
Tachycardia
Hyperthermia
What are the investigations for alcohol withdrawal?
Serum urea and creatinine - check for dehydration
LFTs - if increased, alcoholic hepatitis
Ethanol - high = more severe AWS
Electrolytes - hypokalaemia = severe AWS, DT
FBC - rule out infection
CT head and CXR to rule out other cause.
Generate a management plan for alcohol withdrawal
First line = long acting benzodiazepines - diazepam (oral if mild, if moderate or severe then i.v.) or clomethiazole
Supportive treatment to prevent relapse and relieve symptoms.
Phenobarbital if patient needs large benzodiazepine dose
Vitamin supplementation (thiamine, magnesium).
If severe AWS with or without benziodiazepine-resistance, ICU admission.
What are the possible complications of alcohol withdrawal?
Oversedation from treatment
Delirium tremens
Alcohol-withdrawal seizures - less than 3% of these progress to status epilepticus
What is the prognosis of alcohol withdrawal?
Some patients experience persistent insomnia and autonomic symptoms for few months.
50% remain abstinent for a year.
Define alcoholic hepatitis
Inflammatory liver injury caused by chronic heavy alcohol intake.
Explain the aetiology of alcoholic hepatitis
Histopathology shows: Steatosis Ballooning and necrosis of hepatocytes Mallory bodies (cytoplasmic inclusions in hepatocytes). Neutrophilic inflammation Cholestasis Giant mitochondria
One of the THREE forms of liver disease caused by excessive alcohol intake - the spectrum consists of:
Alcoholic fatty liver (steatosis)
Alcoholic hepatitis
Chronic cirrhosis
What are the risk factors of alcoholic hepatitis?
Excessive alcohol intake for 10-15 years
Presence of hepatitis C
Summarise the epidemiology of alcoholic hepatitis
Occurs in 10-35% of heavy drinkers
What are the presenting symptoms of alcoholic hepatitis?
Rapid onset jaundice Nausea Malaise Anorexia RUQ pain Drowsiness, confusion Fever Abdominal distension (ascites) Swollen ankles GI bleeding
What are the signs of alcoholic hepatitis on examination?
Febrile Tachycardia Jaundice Bruising Encephalopathy Ascites Hepatomegaly Splenomegaly Palmar erythema Dupuytren’s contracture Spider naevi Gynaecomastia
What are appropriate investigations for alcoholic hepatitis?
Bloods
- FBC: low Hb, high MCV, high WCC, low platelets
- LFTs: high AST + ALT, high bilirubin, high ALP + GGT, low albumin
- U&Es: low urea and K+
- Clotting: prolonged PT
Ultrasound - exclude malignancy, abscess etc
Upper GI Endoscopy - investigate varices
Liver Biopsy
EEG - slow-wave activity indicates encephalopathy
Generate a management plan for alcoholic hepatitis
Acute:
- IV Thiamine, Vit C and multivitamins
- Monitor and correct K, Mg and glucose abnormalities
- Ensure adequate urine output
- Treat encephalopathy: oral lactulose and phosphate enemas
- Treat ascites: diuretics, paracentesis
- Treat hepatorenal syndrome: glypressin, N-acetylcysteine
Nutrition
- Oral or nasogastric feeding (high protein diet)
- Vitamin supplementation (IV then oral B vitamins, thiamine, folic acid)
Note: if have encephalopathy then protein restriction
Steroid therapy
- 40mg/day for 4 weeks
Long term
- Stop drinking/reduce alcohol intake
What is hepatorenal syndrome?
The development of renal failure in patients with advanced chronic liver disease
What are the possible complications of alcoholic hepatitis?
Hepatorenal syndrome
Cirrhosis
Acute liver decompensation
What is the prognosis for patients with alcoholic hepatitis?
Mortality in the first month = 10%
Mortality in the first year = 40%
If alcohol intake continues, most will progress to cirrhosis within 1-3 years.
Define amyloidosis
The accumulation of misfolded proteins known as amyloid in organs and tissues.
Amyloid demonstrates apple green birefringence under polarised light with Congo red stain.
Amyloid deposition is disruptive to tissues and so amyloidosis manifests its clinical sequelae by the dysfunction of those organs in which it deposits
What are the different types of amyloidosis?
Primary amyloidosis (AL): Produce immunoglobulin light chains that are inherently prone to misfolding into an insoluble beta-pleated sheet configuration. Primary target organ = kidney (disruption of glomerular basement membrane) Also deposits in heart (conduction abnormalities) and nerves (vasa nervorum)
Secondary amyloidosis (AA): Improper processing of serum amyloid A protein - not broken down enough. Affects kidney, GI tract, thyroid.
What are the risk factors/causes of amyloidosis?
AL: MGUS, Multiple myeloma. No underlying genetic, environmental or occupational risk factors.
AA:
Inflammatory polyarthropathies - RA, psoriatic arthritis, ankylosing spondylitis
Chronic infections - bronchiectasis, TB, osteomyelitis
IBD – Crohn’s
Malignancy - Hodgkin’s lymphoma, renal cell carcinoma
Castleman’s disease - lymphoproliferative disorder
What is the epidemiology of amyloidosis?
Rare, more common in males, median age of diagnosis is 64, potentially twice as common in black people than white
What are the presenting symptoms and sign on examination of amyloidosis?
Depends on where amyloid deposits
Cardiomyopathy/heart failure
- Fatigue
- Weight loss
- SOBOE
- Raised JVP
- Oedema
- Postural hypotension
GI involvement
- Nausea
- Abdominal cramps
- Change in bowel habit
- Weight loss
- Hepatomegaly
Nephrotic syndrome
- Fatigue
- Oedema
- Postural hypotension
Neurological
- Peripheral neuropathy (paraesthesia)
- Autonomic neuropathy (bladder/bowel dysfunction)
- Carpal tunnel syndrome
Other
- Periorbital purpura/eyelid petechiae (raccoon eyes)
- Macroglossia (AL only)
- Shoulder pad sign (enlarged shoulders)
What are the appropriate investigations for amyloidosis?
Serum and urine immunofixation - presence of monoclonal antibody, light chain protein in urine indicative of multiple myeloma and amyloidosis
Immunoglobulin free light chain assay - abnormal kappa to lamda ratio
Bone marrow biopsy - would find clonal plasma cells
Define anal fissure
A painful tear in the squamous lining of the lower anal canal
What is the aetiology/risk factors of anal fissures?
Idiopathic IBD Constipation/passage of hard stool Opiate analgesics (can cause constipation) Pregnancy
Rare: syphillis, herpes, trauma, anal cancer, psoriasis
Summarise the epidemiology of anal fissures
Affects both sexes equally
Can occur at any age but most often 15-40 year olds
Incidence around 1 in 350 adults
What are the presenting symptoms of anal fissure?
Tearing pain on defecation - described as passing broken glass
Fresh PR bleeding
Anal spasm
Anal itching (pruritus ani)
What are the signs on examination of anal fissure?
Visible tear in squamous lining of anus
Anal spasm
Sentinel pile (harmless growth hanging off skin around outside of anus)
What are the appropriate investigations for anal fissure?
Examine the anus - inspection only as DRE is too painful
Anal manometry - patients with resistant fissures have low resting pressure
Anal ultrasound - check for anal sphincter defects
What is the management of anal fissures?
Conservative management
- High fibre diet
- Increased fluid intake
- Topical analgesia: lidocaine ointment
- Laxatives
Medical
- GTN ointment (relaxes anal sphincter and promotes healing)
- Diltiazem ointment (relaxes anal sphincter and promotes healing)
- Botulinum toxin injection if chronic
Surgical
- Lateral subcutaneous internal sphincterotomy
- 2nd line = anal advancement flap
What are the possible complications of anal fissures and their management?
Chronic anal fissure
Recurrence
Perianal abscess or anal fistula in IBD
Incontinence after surgery
What is the prognosis of anal fissures?
60% of fissures heal in 6-8 weeks
30% require a surgical intervention
Define appendicitis
Acute inflammation of the appendix
What is the aetiology/risk factors of appendicitis?
Lumen obstruction by faecolith, normal stool, infective agents or lymphoid hyperplasia
Gut organisms then invade appendix wall
Leads to oedema, ischaemic necrosis and perforation
What is the epidemiology of appendicitis?
Can occur at any age but less likely in extremes
Most common between 10 and 20 years old
Males slightly more likely
What are the presenting symptoms of appendicitis?
Periumbilical pain which moves to RIF Anorexia Nausea and vomiting Constipation Diarrhoea Fever
What are the signs on examination of appendicitis?
Fever Tachycardia McBurney’s sign - RIF tenderness Rosving’s sign - palpation of LIF causes more pain in RIF than in left RIF guarding and rebound tenderness Tender mass Psoas sign - pain on extending the hip Cope sign - pain in flex ion and internal rotation of the hip Diminished bowel sounds Fetor
What are the appropriate investigations for appendicitis?
Bloods
FBC - high white cell count
CRP - high
CT abdo and pelvis - appendix diameter more than 6mm Urine pregnancy test Abdominal ultrasound Urinalysis - negative Abdo and pelvic MRI if pregnant
What is the management for appendicitis?
IV fluids
Prompt appendicectomy
Antibiotics - cefoxitin and metronidazole
What are the possible complications of appendicitis?
Perforation Appendix mass when appendix becomes covered with omentum Appendix abscess Peritonitis Surgical wound infection
What is the prognosis of appendicitis?
In uncomplicated appendicitis most people recover with no long term complications
Define autoimmune hepatitis
Chronic inflammatory disease of the liver of unknown aetiology characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoantibodies
What are the risk factors of autoimmune hepatitis?
Female HLA-DR3/DR4 Other autoimmune conditions eg pernicious anaemia, thyroiditis, coeliac Measles virus Cytomegalovirus Epstein-Barr virus Hepatitis A, C or D virus Drugs
What are the two types of autoimmune hepatitis?
Type 1:
Anti-nuclear antibodies, anti-smooth muscle antibodies, anti-actin antibodies, anti-soluble liver antigen
Type 2:
Anti-liver/kidney microsomes, anti-liver cytosol antigen
Describe the epidemiology of autoimmune hepatitis?
Highest among people with northern European ancestry.
Can occur in any age group.
Type 1 had a bimodal age distribution - between 10-30 and 40-60 years.
Type 2 mainly affects children between the ages of 2 and 14 years.
Women are affected more frequently than men.
What are the presenting symptoms of autoimmune hepatitis?
Insidious
Malaise Fatigue Anorexia Weight loss Nausea Jaundice Amenorrhoea Epistaxis Pruritis
Acute presentation: Fever Anorexia Jaundice Nausea/Vomiting/Diarrhoea RUQ pain Arthralgia Polyarthritis Maculopapular rash
What are the signs on examination of autoimmune hepatitis?
Stigmata of chronic liver disease = hepatomegaly, spider naevi, jaundice, splenomegaly
Late features = Ascites, oedema, hepatic encephalopathy
What are the appropriate investigations for autoimmune hepatitis?
Bloods
LFTs: high AST, ALT, GGT, ALP, Bilirubin. Low albumin (in severe disease)
Clotting: High PT (in severe disease)
FBC: Low Hb, platelets and WCC
Serum globulin - hypergammaglobulinaemia with presence of ANA, ASMA and Anti-LKM antibodies
Liver Biopsy - establish diagnosis and check whether hepatitis or cirrhosis
To rule out other causes of liver disease: Viral serology Urinary copper/caeruloplasmin Ferritin and transferrin saturation Alpha-1 antitrypsin Anti-mitochondrial antibodies (PBC)
US, CT or MRI of liver and abdomen - visualise structural lesions
ERCP - rule out PSC
What is the definition of Barrett’s oesophagus?
Metaplastic change in the lower oesophageal mucosa from oesophageal stratified
squamous epithelium to intestinal simple columnar epithelium secondary to prolonged
acid reflux
SQAUMOUS -> COLUMNAR
What are the risk factors of Barrett’s oesophagus?
Central obesity Age White ethnicity Male Smoking Family history of Barrett's oesophagus or oesophageal adenocarcinoma GORD Hiatus hernia - makes GORD more likely
Describe the epidemiology of Barrett’s oesophagus
0.5-2.0% of the general population
Rare in children - more prevalent with increasing age
More common in white men
What are the presenting symptoms of Barrett’s oesophagus?
Same as symptoms of GORD: Heartburn Nausea Water-brash (sour taste in the mouth) Bloating Belching Burning pain when swallowing Dysphagia Regurgitation
What are the signs on examination of Barrett’s oesophagus?
Nil of note
What are the appropriate investigations for Barrett’s oesophagus?
Upper GI endoscopy with biopsy - violaceous epithelium proximal to the gastro-oesophageal junction.
Barium oesophagogram - not diagnostic but can look for mass or stricture before endoscopy if having dysphagia
What is the treatment of Barrett’s oesophagus?
Non-dysplastic Barrett’s oesophagus:
- PPI and surveillance
- Radiofrequency ablation in high-risk patients
- If PPI ineffective, anti-reflux surgery and surveillance
Low-grade dysplasia:
- Radiofrequency ablation with or without endoscopic mucosal resection if nodular
High-grade dysplasia:
- Radiofrequency ablation with or without endoscopic mucosal resection and PPI
- 2nd line = oesophagectomy
What are the complications of Barrett’s oesophagus?
Dysplasia and oesophageal adenocarcinoma
Oesophageal stricture
What is the prognosis of Barrett’s oesophagus?
Adenocarcinomas discovered while screening for Barrett’s oesophagus are early-stage lesions and have good prognosis (5-year survival >85%).
5-10% of those with Barrett’s oesophagus will develop adenocarcinoma over 10-20 years.
Define cholangiocarcinoma
Cancers arising from the bile duct epithelium which are mostly adenocarcinomas
What are the risk factors for cholangiocarcinoma?
Age >50 years Cholangitis Choledocolithiasis Cholecystolithiasis Structural disorders of biliary tree UC Primary sclerosing cholangitis Liver disease - Cirrhosis, Alcoholic liver disease Hepatitis B or C virus Parasitic infections
What is the epidemiology of cholangiocarcinoma?
Mostly between 50-70 years old
Males slightly more likely
More common in developing world due to increased prevalence of parasitic infections
What are the presenting symptoms of cholangiocarcinoma?
Painless jaundice Weight loss Malaise Anorexia Abdominal pain Obstructive jaundice symptoms: Pruritis, yellow sclera, pale stool, dark urine
What are the signs on examination of cholangiocarcinoma?
Palpable gallbladder
Hepatomegaly
Courvoisier’s Law - in the presence of jaundice, a palpable gallbladder (that is non-tender) is unlikely to be due to gallstones (i.e. cancer of the pancreas
or biliary tree is more likely)
What are the appropriate investigations for cholangiocarcinoma?
Bloods:
LFTs - high conjugated bilirubin, ALP, GGT, slight increase AST and ALT
Clotting screen - increased PT
Tumour markers - high CA19-9, CEA, CA-125
Abdo USS - identify malignant vs benign
Abdo CT if necessary
Abdo MRI
MR angiography for staging
ERCP/MRCP/PTC to show extent of duct involvement
Define cholecystitis
Acute inflammation of the gallbladder
Describe the aetiology of cholecystitis
Complete cystic duct obstruction due to impacted gallstone in gallbladder neck or cystic duct
Blockage of bile flow.
Gall bladder distension which leads to inflammation within the gallbladder wall.
What are the risk factors of cholecystitis?
Age Female Fat Diabetes mellitus Drugs (OCP, octreotide) Family history Ethnicity (Caucasian) Pregnancy TPN Terminal ileum disease Female, fat, fertile, fair, forty
Pigment Stone Risk Factors (caused by increased bilirubin due to haemolysis): haemolytic disorders (e.g. sickle cell anaemia)
Summarise the epidemiology of cholecystitis
3 times more common in women
More common with increasing age
10-15% of adults have gallstones
What are the presenting symptoms of cholecystitis?
RUQ pain Pain referred to right shoulder Fever Systemically unwell Anorexia Nausea Previous episodes of biliary pain
What are the signs on examination of cholecystitis?
Positive Murphy's sign - ask patient to exhale, palpate right costal margin and ask patient to inhale. Patient stops breathing in and winces. Tachycardia Pyrexia RUQ guarding or rebound tenderness Rare: abdominal mass
What are the appropriate investigations for cholecystitis?
Bloods: FBC - high WCC High CRP LFTs - high ALP, GGT and bilirubin Blood cultures Amylase (exclude pancreatitis)
Ultrasound - shows gallstones, increased thickness of gallbladder wall, dilatation of biliary tree
HIDA if USS shows nothing - shows failure of gallbladder filling
AXR
Other imaging - to exclude differentials (e.g. erect CXR, ERCP)
What is the treatment of cholecystitis?
Conservative:
If only mild biliary colic - low-fat diet
Medical: NBM IV fluids Analgesia Anti-emetics Antibiotics (if infection is present) If symptoms persist despite antibiotics, suspect localised abscess or empyema - drainage Urgent biliary drainage by ERCP PTC
Surgical:
Laparoscopic Cholecystectomy
What are the possible complications of cholecystitis?
Perforation
Abscess
Necrosis
Gallstone ileus
Cholecystectomy complications: Bile duct injury Bleeding Infection Bile leak
What is the prognosis of cholecystitis?
Gallstones are usually asymptomatic
Surgery offers an excellent chance of cure if they were to become symptomatic
Define cirrhosis
End-stage of chronic liver damage with replacement of normal liver architecture with abnormal diffuse fibrosis and nodules of regenerating hepatocytes.
Decompensation occurs when there is evidence of complications e.g. portal hypertension,
varices, encephalopathy, jaundice, ascites
What are the causes of cirrhosis?
Chronic alcohol misuse - MOST COMMON UK CAUSE
Chronic viral hepatitis B/C - MOST COMMON WORLDWIDE CAUSE
Autoimmune hepatitis
Drugs (e.g. methotrexate, hepatotoxic drugs)
Inherited
-Alpha1-antitrypsin deficiency
-Haemochromatosis
-Wilson’s disease
-Galactosaemia
-Cystic Fibrosis
Vascular
-Budd-Chiari Syndrome
-Hepatic Venous Congestion
Chronic Biliary Diseases - primary sclerosing cholangitis, primary biliary cirrhosis, biliary atresia
Non-Alcoholic Steatohepatitis (NASH)
What are the risk factors for cirrhosis?
Alcohol misuse IVDU Unprotected sex Blood transfusion Obesity Diabetes Total parenteral nutrition Short bowel syndromes Hyperlipidaemia Drugs (e.g. amiodarone, tamoxifen)
Summarise the epidemiology of cirrhosis
Common in alcoholics
What are the presenting symptoms of cirrhosis?
Early non-specific symptoms: Anorexia Nausea Fatigue Weakness Weight loss
Symptoms due to decreased liver synthetic function:
Easy bruising
Abnormal swelling
Ankle oedema
Symptoms due to reduced detoxification function: Jaundice and pruritis Personality change Altered sleep pattern Amenorrhoea Galactorrhoea
Symptoms due to portal hypertension:
Abdominal swelling
Haematemesis - coffee ground vomit
PR bleeding or melaena
What are the signs on examination of cirrhosis?
Asterixis Bruises Clubbing Dupuytren's contracture Palmar erythema Fetor hepaticus Jaundice Gynaecomastia Leukonychia Parotid enlargement Spider naevi and facial telangiectasia Scratch mark (from cholestatic pruritis) Ascites (Hepatomegaly) - in early phase however shrinks at later phases Testicular atrophy Caput medusae Splenomegaly Liver flap
What are the appropriate investigations for cirrhosis?
Bloods
FBC: low platelets due to hypersplenism as a result of portal hypertension
LFTs: high AST, ALT, ALP, GGT and bilirubin, ALT highest. Serum albumin: low
Serum sodium: low
Clotting: prolonged PT
Investigations to determine CAUSE
Hepatitis C antibodies
Hepatitis B surface antigen
Viral serology
Alpha-1 antitrypsin
Iron studies: serum ferritin, iron, total iron binding capacity (TIBC) - check for haemochromatosis
Anti-mitochondrial antibody, ANA, ASMA - chec for autoimmune hepatitis
Serum ceruloplasmin - low in Wilson’s disease
Ascitic Tap
MC&S - check for infection
Biochemistry (protein, albumin, glucose, amylase)
Cytology
ASCITIC TAP WITH NEUTROPHILS > 250/mm3 = spontaneous bacterial peritonitis (SBP)
US, CT or MRI
Endoscopy - To examine varices
What is the management of cirrhosis?
Treatment of underlying chronic liver disease
Prevent superimposed hepatic injury - avoid alcohol and hepatotoxic drugs e.g. NSAIDs, high doses of paracetamol. Immunisation against hep A and B for susceptible patients, management of metabolic risk factors, maintenance of adequate nutrition, and regular exercise
Monitoring for complications
Sodium restriction and diuretics for ascites - spironolactone and furosemide if not responding
2nd line = liver transplantation
Treatment of complications:
- Encephalopathy - liver cannot break down ammonia in GI tract so goes to brain and exerts toxic effects
Treat infections
Exclude GI bleed
Lactulose (decrease gut absorption of ammonia) and phosphate enemas
Avoid sedation - Ascites
Diuretics (spironolactone with/without furosemide)
Dietary sodium restriction
Therapeutic paracentesis (with human albumin replacement)
Monitor weight
Fluid restrict if plasma sodium < 120 mmol/L
Avoid alcohol and NSAIDs - Spontaneous Bacterial Peritonitis
Antibiotics (e.g. cefuroxime and metronidazole
Prophylaxis against recurrent SBP with ciprofloxacin - Surgical
TIPS (transjugular intrahepatic portosystemic shunt) -reduce portal hypertension
What are the possible complications of cirrhosis?
Portal hypertension with ASCITES Hepatic encephalopathy Variceal haemorrhage Spontaneous Bacterial Peritonitis Hepato Cellular Carcinoma Renal failure (hepatorenal syndrome) AKI Pulmonary hypertension (hepatopulmonary syndrome
What is the prognosis of cirrhosis?
The overall median survival of patients with cirrhosis is approximately 10 years
Likelihood of transitioning to decompensated cirrhosis within 10 years is 50%.
The median survival time in patients with decompensated cirrhosis is approximately 2 years.
