Gastrointestinal (4) Flashcards
Define volvulus
A twisting of a loop of bowel around itself and the axis of its surrounding mesentery. This can result in obstruction and ischaemia.
Mostly sigmoid, then caecal. Can have midgut volvulus neonatorum which occurs in neonates
Summarise the aetiology of volvulus
Pregnancy Constipation Long sigmoid colon Long mesentery Mobile caecum Adhesions Chagas disease Parasitic infections Malrotation (risk factor in neonates) Hirschsprung disease - causes severe consitpation
Summarise the epidemiology of volvulus
Sigmoid volvulus usually occurs in pregnant women or elderly patients
Caecal volvulus occurs in young adults
Midgut volvulus occurs in babies and young children due to malrotation of bowel - presents around 3 months
What are the presenting symptoms of volvulus?
Abdominal bloating/distension Severe colicky abdominal pain Constipation or absolute constipation Bloody stool Vomiting
What are the signs on physical examination of volvulus?
Palpable abdominal mass
Tinkling or absent bowel sounds
Abdominal distension
If perforation occurs: Fever Severe abdominal tenderness Lying very still Tachycardia Hypotension
Signs of dehydration:
Reduced skin turgor
Dry mucous membranes
What are the appropriate investigations for volvulus?
Erect CXR - check for perforation
AXR - coffee bean sign if sigmoid volvulus, foetus sign if caecal volvulus, see large or small bowel dilatation
Barium enema (CONTRAINDICATED IF RISK OF PERFORATION) - shows bird beak sign at site of obstruction
Sigmoidoscopy/colonoscopy
DRE
CT scan
Define primary biliary cirrhosis
An autoimmune chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis, fibrosis, and, ultimately, cirrhosis.
Summarise the aetiology of primary biliary cirrhosis
Autoimmune condition
Anti-mitochondrial antibodies (PDC-E2) attack the bile duct cells, leading to destruction and allowing bile to exit the ducts and move into the interstitium and blood
An environmental trigger may cause bile duct epithelial injury
This leads to a T-cell mediated AI response directed against bile duct epithelial cells
Summarise the epidemiology of primary biliary cirrhosis
More common in women 9:1
Peak age between 55-65
Affects middle aged women
What are the presenting symptoms of primary biliary cirrhosis?
Inisidious onset Fatigue Jaundice Pruritis Smelly, fatty, light coloured stool Weight loss Joint pain
Rarely, it may cause discomfort in the RUQ
May present with a complication of liver decompensation (jaundice, ascites, variceal haemorrhage)
May present with symptoms of associated conditions (e.g. Sjogren’s syndrome, arthritis, Raynaud’s phenomenon)
What are the signs on physical examination of primary biliary cirrhosis?
Early, there may be no signs Jaundice Skin pigmentation Scratch marks (indicates pruritis) Xanthomas (secondary to hypercholesterolaemia) Hepatomegaly Ascites Signs of chronic liver disease
What are the appropriate investigations of primary biliary cirrhosis?
LFTS:
Elevated conjugated bilirubin
Elevated ALP
Elevated GGT
ALT and AST - normally initially but will become abnormal as disease progresses
Albumin - decreased to indicate impaired liver function
PT - prolonged as impaired liver function
Anti-mitochondrial antibodies present
Polycloncal elevation of IgM and IgG
Hypercholesterolaemia
Abdo USS - shows no obstructive lesion within bile duct causing abnormal LFTs
Liver Biopsy:
Chronic inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes
Define viral hepatitis
Inflammation of the liver caused by one of the five hepatitis viruses.
Hepatitis A virus is an RNA virus, transmitted by the faecal-oral route. Prevalent in environments with improper hygiene and is common in travellers.
Hepatitis B virus is a DNA virus transmitted by percutaneous and permucosal routes - blood, bodily fluids and birthing.
Hepatitis C virus is an infectious, hepatotropic RNA virus belonging to the Flavivirus family.
Hepatitis D is transmitted by blood and body fluids and cannot be obtained without Hepatitis B infection.
Hepatitis E is spread by the faecal oral route and occurs in entermic areas. In pregnant woman it can cause fulminant hepatitis.
Summarise the epidemiology of viral hepatitis
Hepatitis A - faecal oral route, travellers, contaminated food and water
Hepatitis B - transmitted through blood and bodily fluid - IVDU, unprotected sex, blood transfusions, birthing
Hepatitis C - blood and bodily fluid
Hepatitis D requires HBV infection
Hepatitis E - faecal oral route, causes fulminant hepatitis in pregnant women
What are the risk factors for hepatitis A and hepatitis B/C?
Risk factors for Hepatitis A:
Living in endemic regions
Personal contact with infected person
Risk factors for Hepatitis B/C: Recipients of blood products IV drug users Tattooing Sexual activity
Summarise the epidemiology of viral hepatitis?
Hepatitis A:
Endemic in the developing world and infection often occurs sub-clinically
Less common in the developed world due to better sanitation
Age of exposure is higher in developed world
Common in travellers
Hepatitis B:
Common, causing 1-2 million deaths annually
Hepatitis C:
Common, with different genotypes having different geographical prevalence
What are the presenting symptoms of viral hepatitis?
Incubation period of HAV and HEV: 3-6 weeks
Incubation period of HBV is 3-6 months
HCV: 90% of acute infections are asymptomatic, 10% get jaundiced with mild flu-like illness
Jaundice RUQ pain Fever Fatigue Pruritis Dark urine Light coloured stool Nausea and vomiting Malaise Anorexia Headache
Hepatitis C:
Causes extrahepatic manifestations eg cryoglobulinaemia causing headaches, palpable purpura, arthritis
What are the signs on physical examination of viral hepatitis?
Jaundice
Hepatomegaly
Pyrexia
Splenomegaly
Cervical lymphadenopathy (in 10-20% of patients)
Occasionally: urticaria and maculopapular rash
Hepatitis B and C may have signs of chronic liver disease or decompensation - asterixis, bruising, dupytren’s, palmar erythema etc
Absence of stigmata of chronic liver disease in HAV (although spider naevi may be present)
What are the appropriate investigations for viral hepatitis?
LFTs: high AST, ALT, ALP and bilirubin (ALT GREATER THAN AST)
High ESR
Low albumin + high platelets (if severe)
Prolonged PT and PTT if severe
Viral Serology:
Hepatitis A:
Anti-HAV IgM (acute)
Anti-HAV IgG (recovery phase and lifelong persistence)
Hepatitis B:
HBsAg, IgM anti-HBcAg, HBeAg, HBV DNA - acute
Anti-HBs, total antiHBc - chronic
Hepatitis C:
HCV IgM - acute
HCV IgG - chronic or past exposure
Hepatitis E:
Anti-HEV IgM (raised 1-4 weeks after onset)
Urinalysis: Positive for bilirubin and raised urobilinogen
Liver biopsy: in HBV and HCV to assess liver disease
What is the appropriate management for viral hepatitis?
Hepatitis A - fluids, bed rest, symptomatic treatment eg antipyretics, antiemetics, cholestyramine for severe pruritis, vaccination
Hepatitis E - fluids
Hepatitis B:
HEP B IS A NOTIFIABLE DISEASE
Acute: Symptomatic treatment (antipyretics, antiemetics and cholestyramine) and bed rest.
Chronic: interferon alpha (standard or pegylated) is given.
Hepatitis C: Pegylated interferon-alpha and ribavirin (guanosine nucleotide analogue).
What are the possible complications of viral hepatitis?
Hepatitis A:
Fulminant hepatic failure (more common in pregnant women)
Cholestatic hepatitis with prolonged jaundice and pruritus can develop after HAV infection
Post-hepatitis syndrome: continued malaise for weeks to months
Hepatitis B:
1% get fulminant hepatic failure
CHRONIC HBV INFECTION IN NEONATES (10% of adults, much higher in neonates)
CIRRHOSIS
EXTRAHEPATIC immune complex disorders (e.g. glomerulonephritis, polyarteritis nodosa)
Hepatocellular carcinoma
Hepatitis C: Fulminant hepatic failure Chronic carriage of HCV HEPATOCELLULAR CARCINOMA Less common: porphyria cutanea tarda, cryoglobulinaemia, glomerulonephritis
HEPATITIS E = FULMINANT HEPATITIS IN PREGNANT WOMEN
Summarise the prognosis of viral hepatitis
HAV: Recovery is usually within 3-6 weeks. Occasionally patients may relapse during recovery. There are no chronic sequelae.
Fulminant hepatic failure has a mortality of 80%.
HBV: 10% of infections become chronic. Of the chronic infections, 20-30% will develop cirrhosis.
HCV: 80% of exposed will progress to chronic carriage. Of these, 20-30% will develop cirrhosis over 10-20 years.
Define portal hypertension
An increased pressure in the hepatic portal vein - clinically significant when >10mmHg
Summarise the aetiology of portal hypertension
Restriction of blood flow through hepatic portal vein and into IVC causes back flow of blood and pressure build up
The most common cause is cirrhosis
Pre-hepatic causes: Blockage of hepatic portal vein due to: Congenital stenosis Portal vein thrombosis Splenic vein thrombosis Extrinsic compression
Hepatic:
Cirrhosis
Schistomiasis
Sarcoidosis
Post-hepatic:
Right heart failure
Constrictive pericarditis
Budd-Chiari syndrome
Summarise the epidemiology of portal hypertension
It is a common complication of cirrhosis
What are the presenting symptoms of portal hypertension?
Jaundice if due to cirrhosis Haematemesis Melana Distended abdomen Distended abdominal veins Abdominal pain and fever - spontaneous bacterial peritonitis
Symptoms of hepatic encephalopathy: Confusion Nausea Fatigue Changes in sleep
What are the signs on physical examination of portal hypertension?
Caput medusae
Ascites
Altered consciousness if hepatic encephalopathy
Splenomegaly
Signs of liver failure: Aterixis Bruising Clubbing Dupytren's contracture Palmar erythema Fetor hepaticus Gynaecomastia Spider naevi Jaundice Testicular atrophy
What are the appropriate investigations for portal hypertension?
Hepatic venous pressure gradient measurement
Upper GI endoscopy - eosophageal varices
Abdominal USS - liver and spleen size, portal blood flow, cirrhosis
Doppler USS
Liver CT/MRI - if other imaging methods inconclusive - ascites, cirrhosis, splenomegaly, IVC dilatation
Investigations to identify cause: Viral serology Autoantibodies - ANAs, ASMA for autoimmune hepatitis LFTs Clotting - prolonged PT is sign of liver failure Ferritin: haemochromatosis alfa1-antitrypsin levels Caeruloplasmin: Wilson's disease
Liver Biopsy if indicated
What is the appropriate management of portal hypertension?
Ascites - sodium restriction, diuretics
Treatment of oesophageal varices if present - sclerotherapy, variceal ligation, balloon tamponade, octreotide
Non-selective beta-blockers: reduces portal pressure and reduces risk of variceal bleeding
Terlipressin: can reduce portal venous pressure
Transjugular Intrahepatic Portosystemic Shunt (TIPS): surgical shunt placed between the hepatic portal vein and the hepatic vein to ease congestion in the portal vein
Liver transplant
What are the possible complications of portal hypertension?
Portosystemic shunts
Bleeding oesophageal varices - haematemesis
Bleeding rectal varices - meleana
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Ascites complications: hepatorenal syndrome, hepatic hydrothorax
Pulmonary complications:
Porto-pulmonary hypertension
Hepatopulmonary syndrome: triad hepatic dysfunction, hypoxaemia, extreme vasodilation (intrapulmonary vascular dilatation)
Liver failure
Cirrhotic cardiomyopathy
Summarise the prognosis of portal hypertension
Depends on the underlying cause
Variceal haemorrhages have a 1-year mortality of 40%
Define ulcerative colitis
A type of inflammatory bowel disease with a relapsing and remitting nature, involving mucosal and submucosal inflammation from the rectum moving proximally through the colon.
Summarise the aetiology of ulcerative colitis
Aetiology unknown
Genetic factors - often family history present - HLA-DRB1
Environmental factors eg diet, stress often involved in flares
T cell destruction of large intestinal lining cells
Often associated with pANCA and primary sclerosing cholangitis
Summarise the epidemiology of ulcerative colitis
Often affects young women
More common in Caucasians and Eastern European Jews
Uncommon before the age of 10 years
Peak onset: 20-40 years
Equal sex ratio up to the age of 40 years (higher in males from then on)
What are the presenting symptoms of ulcerative colitis?
Bloody diarrhoea Weight loss Mucous diarrhoea Fatigue Fever LLQ pain Cramping Bloating Tenesmus Feacal urgency
Extraintestinal symptoms: Uveitis Episcleritis Pyoderma gangrenosum Erythema nodosum Arthritis
What are the signs on physical examination of ulcerative colitis?
Pallor Erythema nodosum LLQ tenderness Abdominal distension Fever Dehydration Clubbing Tachycardia Blood, mucus and tenderness on PR examination
What are the appropriate investigations for ulcerative colitis?
FBC - macrocytic, megaloblastic anaemia Iron studies - iron deficiency anaemia ESR/CRP - elevated Albumin - decreased Faecal calprotectin - elevated Stool studies - negative culture AXR - rule out toxic megacolon
Colonoscopy and biopsy: Crypt abscesses Neutrophils Ulcers Paneth cells in descending colon Lead pipe colon NO granulomas Mucosal and submucosal inflammation
Barium Enema: Shows mucosal ulceration with granular appearance and filling defects (due to pseudo polyps). Narrowed colon and loss of haustral pattern – leadpipe appearance. Colonoscopy and barium enema may be DANGEROUS during an acute exacerbation - risk of perforation.
What is the appropriate management of ulcerative colitis?
Depends on severity of disease
Acute Exacerbation: IV rehydration, IV corticosteroids and bowel rest Parenteral feeding may be necessary Antibiotics If toxic megacolon - proctocolectomy
Mild Disease:
Oral or rectal anti-inflammatories - 5-ASA derivatives (e.g. mesalazine, olsalazine, sulphasalazine) and/or rectal steroids.
Moderate to Severe Disease:
Oral steroids
Oral 5-ASA
Immunosuppression (with azathioprine, cyclosporine, 6-mercaptopurine OR biologics - infliximab (anti-TNF monoclonal antibody)
Advice:
Patient education and support.
Treat complications
Regular colonoscopic surveillance
Surgical: If medical treatment fails, presence of complications or to prevent colonic carcinoma - colectomy
What are the possible complications of ulcerative colitis?
Toxic megacolon Strictures Colorectal cancer - adenocarcinoma Perforation Infection Pseudopolys Primary sclerosing cholangitis GI haemorrhage
Extra-gastrointestinal Manifestations: Uveitis, renal calculi, arthropathy, sacroiliitis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, osteoporosis (from chronic steroid use), amyloidosis
Summarise the prognosis of ulcerative colitis
Only colectomy is curative
Colonic adenocarcinoma develops in 3-5% of population
Most common cause of death is toxic megacolon
Normal life expectancy
Poor prognostic factors: Low albumin (< 30 g/L) PR blood Raised CRP Dilated loops of bowel 8+ bowel movements per day Fever
Define Wilson’s disease
An autosomal recessive disease of ATP7B, leading to impaired transport and biliary excretion of copper, leading to copper deposition particularly in the brain, liver and cornea.
Summarise the aetiology of Wilson’s disease
An autosomal recessive mutation in the ATP7B protein on the long arm of chromosome 13 prevents (copper transporting protein in hepatocytes)
Prevents copper transport into bile for excretion
Summarise the epidemiology of Wilson’s disease
No sex or ethnicity differences
Presentation usually at 10-40 years old
First presentation in children is usually liver disease
First presentation in adults usually neurological deficits
What are the presenting symptoms of Wilson’s disease?
Hepatic: Abdominal pain Can present with hepatitis, cirrhosis or liver failure Jaundice Easy bruising Variceal bleeding Encephalopathy Asterixis Spider naevi Ascites Gynaecomastia
Neurological: Change in personality Dysarthria Tremor - intention, resting, flapping Parkinsonism Dystonia Ataxia Dementia Rigidity Dyskinesia Drooling Dysphagia
Fatigue
What are the signs on physical examination?
Hepatosplenomegaly RUQ tenderness Jaundice Spider naevi Gynaecomastia Ascites
KAYSER-FLEISCHER RINGS
What are the appropriate investigations for Wilson’s disease?
FBC - haemolytic anaemia, low WBC Serum ceruloplasmin - decreased Serum copper - elevated AST and ALT - elevated Albumin - decreased PT prolonged
24 urinary copper excretion - increased >100mg
Liver biopsy - increased copper content
Define primary sclerosing cholangitis
A chronic, progressive cholestatic liver disease characterised by fibrosis and destruction of intra and extra-hepatic bile ducts, often associated with Ulcerative Colitis
Summarise the aetiology of primary sclerosing cholangitis
Aetiology unknown
Likely genetic and environmental causes
Associated with ulcerative colitis, increased IgM antibodies and increased pANCA
HLA-B8, HLA-DR3
Summarise the epidemiology of primary sclerosing cholangitis?
Common in middle aged men (30s-50s) with Ulcerative Colitis
What are the presenting symptoms of primary sclerosing cholangitis?
Pruritis Jaundice RUQ pain Fatigue Weight loss Steatorrhoea - greasy light coloured foul-smelling stool
May present with episodes of fever and rigors caused by acute cholangitis (less common)
What are the signs on physical examination of primary sclerosing cholangitis?
May have no signs Jaundice Hepatosplenomegaly Spider naevi Palmar erythema Ascites Excoriations
What are the appropriate investigations for primary sclerosing cholangitis?
LFTs - elevated ALP, GGT, conjugated bilirubin, AST and ALT may be elevated
pANCA positive in 70%
IgG high in children, IgM high in adults
ASMA and ANA present in 30%
ERCP - alternating strictures and fibrosis and dilation of bile ducts - beaded pattern
Abdo USS - abnormal bile ducts
Serum albumin - may be normal or low
PT may be prolonged
Liver biopsy - confirm diagnosis and allow staging
Define rectal prolapse
Protrusion of full thickness or just the mucosal layer of rectum through the anus due to loss of attachments inside the body allowing rectal telescope out.
Summarise the aetiology/risk factors of rectal prolapse
Chronic straining Constipation Diarrhoea Pelvic floor damage Increasing age Female Pregnancy Abnormal rectum anatomy or physiology Decreased anal sphincter pressure Previous trauma to the anus Neurological conditions - MS, cauda equina syndrome
Causes in children:
Increased intraabdominal pressure
Cystic fibrosis
Diarrhoea
Summarise the aetiology of rectal prolapse
Common in elderly
Common in young children <3
What are the presenting symptoms of rectal prolapse?
Mass protruding from rectum - dark red, often comes out on defecation, straining, coughing, sneezing
Mass may need digital replacement
Seepage at the site - mucus, rectal bleeding
Pain at site
Faecal incontinence
Diarrhoea
Constipation
What are the signs on physical examination of rectal prolapse?
Mass protruding from anus
May be necrotic or ulcerated if poor vascular supply
Decreased anal sphincter tone
What are the appropriate investigations for rectal prolapse?
Mainly clinical diagnosis Proctosigmoidoscopy Defecating proctogram Pudendal nerve studies Anal sphincter manometry Sweat chloride test - check for cystic fibrosis in children
Define gastritis and peptic ulcer disease
Gastritis = inflammation of the gastric mucosa
Peptic ulcer disease = erosion of the GI tract leading to ulceration due to chronic exposure to gastric acid and peptic juices
Summarise the aetiology of gastritis and peptic ulcer disease
Caused by an imbalance between the damaging action of acid and pepsin and the mucosal protective mechanisms.
Acute gastritis:
Alcohol, NSAIDs, physiological stress (sepsis, shock, trauma)
Chronic gastritis:
H. pylori
Autoimmune
Gastric ulcers:
H. pylori
NSAIDs
Duodenal ulcers:
H. pylori
Zollinger-Ellison syndrome - gastrinoma in duodenum or pancreas
Summarise the epidemiology of gastritis and peptic ulcer disease
COMMON (annual incidence: 1-4/1000)
More common in males
Mean age for duodenal ulcer is in the 30s
Mean age for gastric ulcers is in the 50s
Helicobacter pylori is usually acquired in childhood
Prevalence is roughly equal to age in years
What are the presenting symptoms of gastritis and peptic ulcer disease?
Gastritis: epigastric pain, nausea, vomiting
Epigastric pain Worse after eating - gastric ulcer Relieved by eating - duodenal ulcer Weight loss - gastric ulcer Weight gain - duodenal ulcer Post-prandial belching Bloating Vomiting Early satiety
Zollinger-Ellison:
Epigastric pain
Diarrhoea
Symptoms of malabsorption
Present with complications: haematemesis, melaena (haemorrhage), diffuse abdo pain (perforation)
What are the signs on physical examination of gastritis and peptic ulcer disease?
Epigastric tenderness
Signs of complications eg anaemia (conjunctival pallor)
What are the appropriate investigations for gastritis and peptic ulcer disease?
FBC - anaemia if bleeding
Serum amylase - exclude pancreatitis
Upper endoscopy and biopsy
H pylori testing:
Serum IgG antibody against H. pylori
Stool antigen test
C-13 Urea breath test - radio-labelled urea given orally, C13 detected when breathed out
Campylobacter-like organism test: Gastric biopsy is placed with a substrate of urea and a pH indicator. If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red
Test for Zollinger-Ellison syndrome:
Secretin test - does not cause decrease in gastrin following IV secretin
Serum gastrin elevated
What is the appropriate management of gastritis and peptic ulcer disease?
Acute:
Fluid resuscitation if perforation or bleeding (IV colloids/crystalloids)
Endoscopy
Surgical treatment
Bleeding ulcer:
Haemostasis via injection sclerotherapy, laser coagulation, electrocoagulation
Surgery: Indicated if the ulcer has perforated or if the bleeding ulcer can’t be controlled
Conservative:
Stop NSAIDs, avoid alcohol, smoking, caffeine
H. pylori negative:
PPIs and H2 antagonists
Use misoprostol (prostaglandin E1 analogue) if NSAID use is necessary
H. pylori:
Triple therapy for 1-2 weeks - clarithromycin, amoxicillin, PPI eg omeprazole (2 antibiotics and PPI)
What are the possible complications of gastritis and peptic ulcer disease?
Haemorrhage
Perforation
Obstruction
Summarise the prognosis of gastritis and peptic ulcer disease
Overall lifetime risk = 10%
Outlook is generally good; peptic ulcers associated with H. pylori are cured by eradication
Define pilonidal sinus
An abnormal epithelial-lined tract which is filled with hairs which opens onto the skin surface in the natal cleft.
Summarise the aetiology of pilonidal sinus
Forceful insertion/penetration of hairs into the skin of the natal cleft in the sacrococcygeal region, leading to an inflammatory reaction which forms an epithelialised sinus.
Intermittent negative pressure draws in more hair, perpetuating the cycle
Risk factors: Deep, narrow natal cleft Broken skin Hirsutism Spending long time sitting down
Summarise the epidemiology of pilonidal sinus
Common
Affects men of working age (80% of patients are men)
Mean age of presentation = 20 years old
What are the presenting symptoms of pilonidal sinus?
Painful natal cleft in sacrococcygeal area
Discharge from natal cleft
Swelling of natal cleft
Often recurrent problem
What are the signs on physical examination of pilonidal sinus?
Midline openings or pits between the buttocks in the natal cleft
Hair may protrude out from these pits
Swelling of sacrococcygeal region
Tenderness of region
Discharge of blood-stained fluid or pus on compression
What are the appropriate investigations for pilonidal sinus?
Clinical diagnosis
If suspect infection:
FBC - elevated WBC
Fasting glucose - increased risk of infection in diabetics
What is the appropriate management of pilonidal sinus?
Conservative prevention - hair removal and local hygeine
Acute pilonidal abscess - incision and drainage, antibiotic as adjunct if needed
Chronic pilonidal sinus - surgical excision under GA or repair
What are the possible complications of pilonidal sinus?
Pain Infection Abscess Recurrence Post-operative collection deep to sutures Necrotizing fasciitis
Summarise the prognosis of pilonidal sinus
Good with drainage
Shaving will cure in most cases
Usually resolves by the age of 40
Depending on the surgical technique chosen, recurrence rates are variable and average 6.9%
Recurrence less likely after healing by secondary intention compared with primary wound closure
Define non-alcoholic steatohepatitis
Part of a spectrum of conditions characterised by the build up of fat in the liver, not caused by excessive alcohol use or viruses. Necrosis of the hepatocytes due to fat deposit degradation causes inflammation, leading to non-alcoholic steatohepatitis.
Summarise the aetiology of non-alcoholic steatohepatitis
Fat droplets form in hepatocytes, often associated with insulin resistance
If fat persists, it can cause inflammation and fibrosis (steatohepatitis) due to its vulnerability to degradation resulting in radical formation and subsequent damage to hepatocytes
Risk factor: Obesity Metabolic syndrome Hypertension Diabetes Hyperlipidaemia Hypertriglyceridaemia Smoking Age >50
Summarise the epidemiology of non-alcoholic steatohepatitis
Affects 20-40% of Western world
Majority of patients 40-60 years old
Most common cause of chronic liver disease in Western world
What are the presenting symptoms of non-alcoholic steatohepatitis?
Often asymptomatic
RUQ pain Fatigue Malaise Jaundice Unexplained weight loss
Symptoms of cirrhosis later
What are the signs on physical examination of non-alcoholic steatohepatitis?
RUQ tenderness
Hepatomegaly
Jaundice
Signs of cirrhosis if it further develops
What are the appropriate investigations for non-alcoholic steatohepatitis?
LFTs - elevated ALT and AST (ALT greater elevation)
USS imaging - hepatomegaly, fatty infiltrates, show steatosis
Biopsy and histology - >5% fat content, cellular ballooning, mallory-denk bodies
What is the management of non-alcoholic steatohepatitis?
REVERSIBLE
Control of risk factors and metabolic syndrome:
First line - weight loss, exercise
Medical management of metabolic co-morbidities eg diabetes, hypercholesterolaemia, hypertension
Smoking cessation
If develops to cirrhosis:
Liver transplant
TIPS
What are the possible complications of non-alcoholic steatohepatitis?
Cirrhosis: Ascites Oesophageal varices Variceal haemorrhage Hepatic encephalopathy Hepatocellular carcinoma End-stage liver failure
Summarise the prognosis of non-alcoholic steatohepatitis
Increased mortality
9-20% of patients develop to cirrhosis
Define perineal abscess and fistulae
Perineal abscess - collection of pus in the perineal region
Perineal fistulae - abnormal communication between anal canal and external skin which is chronically infected
Summarise the aetiology of perineal abscess and fistulae
Bacterial infection, usually by enteric gut infection, causes abscess
Abscess blocks deep intramuscular gland duct - fistulae develop
Associated with: Perianal sepsis Abscess Crohn's TB Diverticular disease
Summarise the epidemiology of perineal abscess and fistulae
More common in men
Perineal fistulae common in people with recurrent anal abscesses
What are the presenting symptoms of perineal abscess and fistulae?
Abscess:
Fever
Pain
Swollen, warm, red mass
Fistula: Can be painless or painful Drainage of mucous/pus/faeces from skin Skin excoriations Bleeding, red, itchy swelling Pain on sitting or moving Recurrent abscesses
What are the signs on physical examination of perineal abscess and fistulae?
Red, tender, swollen, fluctuant mass in perineal area - abscess
Fever
Fistula:
Abnormal opening in perineal region
Surrounding skin granulation tissue - red, inflammed, tender
Mucuous/serous/faeces discharge
What are the appropriate investigations for perineal abscess and fistulae?
FBC - elevated WCC in abscess
CRP/ESR - elevated in abscess
MRI
Endoanal USS
What is the management of perineal abscess and fistulae?
Abscess - incision and drainage, antibiotics if needed
Fistula:
Superficial fistula not involving much of anal sphincter - FISTULOTOMY
High up fistula or involves lots of sphincter - seton suture which is tightened over time
What are the possible complications of perineal abscess and fistulae?
Recurrence
Damage to internal anal sphincter
Incontinence
Perisiting pain
Summarise the prognosis of perineal abscess and fistulae
High recurrence rate without complete excision
Define liver abscess and cyst
Abscess: liver infection resulting in a walled off collection of pus
Cyst: liver infection resulting in a walled off collection of cyst fluid
Summarise the aetiology of liver abscess and cyst
Pyogenic (producing pus):
Escherichia coli, Klebsiella, Enterococcus, Bacteroides, Streptococci, Staphylococci
60% are caused by biliary tract disease (e.g. gallstones, strictures, congenital cysts)
15% have unknown cause
Amoebic abscess: Caused by Entamoeba histolytica
Hydatid cyst: Caused by tapeworm Echinococcus granulosis
Other causes: TB
Summarise the epidemiology of liver abscess and cyst
Pyogenic is the most common type of liver abscess in the industrialised world
Amoebic liver abscess: most common WORLDWIDE
Hydatid cysts: common in sheep-rearing countries
What are the presenting symptoms of liver abscess and cyst?
Fever Malaise, nausea and weight loss Anorexia Night sweats RUQ/epigastric pain that may be referred to the shoulder (irritation of the diaphragm) Jaundice Diarrhoea Pyrexia of unknown origin IMPORTANT: make sure you ask about foreign travel
What are the signs on physical examination of liver abscess and cyst?
Fever: continuous or spiking
Jaundice
Tender hepatomegaly (right lobe affected more than left)
Right lung base:
Dullness to percussion
Reduced breath sounds
Due to reactive pleural effusion
What are the appropriate investigations for liver abscess and cyst?
FBC: Mild anaemia, leucocytosis, high eosinophils (if hydatid disease) LFTs: High ALP, high bilirubin High ESR and CRP Blood cultures Amoebic and hydatid serology
Stool MC&S: for E. histolytica
Liver US or CT/MRI: localises structure of mass
CXR: check for right pleural effusion or atelectasis, raised hemidiaphragm
Aspiration and culture of the abscess material: Most pyogenic liver abscesses are polymicrobial. Amoebic abscesses have fluid of necrotic hepatocytes and trophozoites.
Vitamin A deficiency signs and symptoms
Poor vision (sometimes complete loss of vision) Loss of vision in darkness Poor immune function Zinc deficiency Fat malabsorption
Vitamin B deficiency signs and symptoms
BeriBeri syndrome Weak muscles and very little energy Anaemia Cataracts Decreased thyroid function
Vitamin C deficiency signs and symptoms
Scurvy (bleeding gums, eye manifestations) Wounds take longer to heal Muscular and nervous irritability Muscle cramps and tetany Depression Hypertension
Vitamin D deficiency signs and symptoms
Rickets (bones are soft and bend)
Prone to fracture
Osteoporosis
Poor calcium absorption
Vitamin E deficiency signs and symptoms
Red cell lysis Anaemia Bruising Hot flashes Skin disorders: psoriasis, eczema, poor wound healing
Vitamin K deficiency signs and symptoms
Excessive bleeding (vitamin-K-dependent clotting factor synthesis hindered)
History of bruising
Appearance of ruptured capillaries
Menorrhagia
