COMMON GI CONDITIONS

1. Oesophagus
Barrett's Oesophagus
Pathology
Squamous cells go through metaplasia to columnar cells - adaptive change
for protection against acid environment
Could be small patchy areas or the entire length of the oesophagus
Changes visible on endoscopy
40x increased risk of oesophageal adenocarcinoma
Management
Biopsy for histology
Pre malignant changes (high grade dysplasia)
Oesophageal resection (in younger, fit patients)
Mucosal ablation (in other patients)
No premalignant changes
Regular endoscopy and biopsy
Intensive anti-reflux measures (including long term PPI)
Oesophageal Cancer
Incidence
9 / 100,000 a year in UK
Risk factors
Diet, alcohol excess, smoking, obesity
Achalasia, reflux oesophagitis, Barrett's oesophagus
Signs / symptoms
Dysphagia, weight loss, retrosternal chest pain
Hoarseness, cough
Tests
Barium swallow, CXR, oesophagoscopy with biospsy
CT / MRI
Staging
Spread
Directly by submucosal infiltration and local spread
To nodes, or later via blood
Tis - carncinoma in situ; T1 - invading submucosa; T2 - invading muscularis
propria; T3 - invading adventitia; T4 - invading adjacent structures
(T)NM - as usual
Treatment
Poor prognosis with or without treatment
If T1 / T2 radical curative
oesophagectomy
Pre-op chemo improves survival but
causes some morbidity
If surgery is not indicated chemo +
radiotherapy is better than radiotherapy
alone
Palliation in advanced disease aims to restore swallowing with
chemo, radiotherapy, stenting, and laser use
Fistula Abnormal connection between two epithelial surfaces
Stricture Abnormal narrowing of gut
Oesophagitis
Range of endoscopic findings from mild
redness to severe bleeding
Excessive mucosal exposure to acid and pepsin can lead to distal oesophageal ulceration in patients with reflux
Metaplasia can lead to adenocarcinoma
Bleeding is common but rarely life threatening
Mallory Weiss Tear Retching / vomiting causing haematemesis via oesophageal tear
Hiatus hernia
Increased patency of lower oesophageal sphincter
Principles of Grading & Staging
Grading
Histological appearance
Differentiated > Metaplasia (low to high) > Dysplasia (low to high)
Degree of differentiation
Staging
Guides management options
TNM
Tis - in situ (on mucosa)
T1 - submucosa
T2 - into muscle (muscularis propria)
T3 - into serosa
Swallowing Difficulties
Alarm Symptoms
Progressive
Prolonged
Clinical features
Difficulty swallowing
solids and liquids from
onset?
Yes: motility disorder or pharyngeal cause
No: stricture (solids then liquids)
Difficultly to make
swallowing movement?
Yes: bulbar palsy
Swallowing painful?
Yes: cancer, oseophagitis, oseophageal spasm
Intermittent or constant?
Intermittent: oesophageal spasm
Constant: malignant stricture
Neck bulge / gurgle
on drinking?
Yes: pharyngeal pouch
Causes
Mechanical block
Malignant stricture: oesophageal Ca,
gastric Ca, pharyngeal Ca
Benign stricture
Extrinsic pressure: lung Ca, mediastinal lymph nodes, AA, goitre
Pharyngeal pouch
Motility
Achalasia (failue of relaxation of lower oesophageal sphincter)
Oesophageal spasm
Bulbar palsy
Others
Oesophagitis: infection, reflux
Categories
Dysphagia with fluid = neurological / muscle deficit
Dysphagia with solids = physcial / mechanical deficit
Oesophagus.mmap - 07/09/2010 -

2. Peptic Ulcer Disease 1
Dyspepsia
Symtpoms: epigastric pain, bloating, heartburn
Alarm symptoms: Anaemia (iron deficiency), weight loss, anorexia, melaena, haematemesis, swallowing difficulty
Management
If > 55yrs or alarm symptoms refer for urgent endoscopy
Simple anatacids for 4 weeks
Test for H. Pylori and eradicate if present; otherwise PPI for 2 weeks
Management
Lifestyle
Avoid food that worsens symptoms
Stop smoking (smoking slows healing in
GU and increases relapses in DU)
Clinical
H. Pylori eradication
Triple therapy
PAC500 regime: PPI, amoxicillin & clarithromycin
PMC 250: PPI, metronidazole & clarithromycin
Upto 85% effective
For 7 days
Drugs to reduce acid
PPIs Lansoprazole 30mg / 24hrs
H2 Receptor Antagonists
Ranitidine 300mg nocte
Cimetidine 800mg nocte
Ulcers
Duodenal
4x more common than gastric
Major risk factors: H. Pylori (90%), drugs (aspirin, NSAIDs, steroids)
Minor risk factors: increased gastric acid secretion, increased gastric emptying (lowers
duodenal pH), blood group O, smoking, ?stress
Symptoms: epigastric pain (before meals / night) relieved by eating or drinking milk,
asymptomatic (50%), recurrent
Signs: epigastric tenderness
Diagnosis: upper GI endoscopy (stop PPI 2 week prior), H. Pylori test
Gastric
Occur mainly in the elderly
Risk factors: H. Pylori (80%), smoking, NSAIDs, duodenal reflux, delayed gastric emptying, stress
Symptoms: asymptomatic, epigastric pain (related to meals / relieved by antacids) +/- weight loss
Tests: upper GI endoscopy (to exclude Ca), biopsies from ulcer rim and base (histology / H. Pylori)
Complications
Bleeding
Perforation Presenting features depends on how ulcer bursts
Malignancy
Gastric outflow obstruction
H. Pylori
Infection
Spiral shaped gram negative urease producting bacterium
Found in gastric antrum and in areas of gastric metaplasia in the duodenum
Pathogenesis
Colonisation in the antrum
Inflammation of the gastric mucosa (gastritis)
Gastric inflammation may lead to gastric or duodenal ulcer formation
Diagnosis
13C Urea breath test
Very sensitive (98%) and specific (95%)
Breath test also used to demonstrate eradication
Laparotomy
Post-op complications
General
Pain
Pyrexia
Confusion
Dyspnoea / Hypoxia
Hypo / Hypertension
Oliguria
Nausea / Vomiting
Hyponaturaemia
Specific
Wound breakdown / dehiscence (esp.
elderly and malnourished)
May lead to burst abdomen
A&P
Stomach
Anatomy
Cardia
Abundant mucous glands to protect oseophagus
Fundus
In contact with the diaphragm
Body
Contains the gastric glands secreting
enzymes and acids
Pylorus
Pyloric antrum and pyloric canal
Pyloric sphincter regulates release into duodenum
Glands secrete mucous and digestive hormones
Glands
Gastric
Parietal cells
Proximal portion of gland
Secrete hydrochloric acid (H+ via proton pump along with Cl-)
and intrinsic factor (absoprtion of B12)
Chief cells
Abundant near base of gland
Secrete pepsinogen
Pyloric
Cells primarily produce a mucous secretion
G Cells
Abundant in gastric pits of pyloric antrum
Secrete gastrin (stimulates parietal and chief cells)
D Cells
Continually release somatostatin, inhibiting gastrin release
Overridden by neural and hormonal stimuli
Histiology
Columnar epithelium
Peptic Ulcer Disease.mmap - 07/09/2010 -

3. Peptic Ulcer Disease 2
Peritonitis
Peritonitis
Perforated ulcer
Perforated diverticulum
Perforated appendix
Perforated bowel
Perforated gall bladder
Signs
Prostration; shock; lying still; positive cough test
Tenderness; abdo rigidity, guarding, absent bowel sounds
Erect CXR may show gas under diaphragm (pneumoperitoneum)
Management
Usually requires a laparotomy
Acute pancreatitis causes these signs but does not require a laparotomy -
check serum amylase (massively raised in acute pancreatitis)
Endoscopy
Pre procedure
Stop anti acid therapy 2 weeks before
hand (can mask adenocarcinomas)
Nil by mouth for 8 hrs; water up till 4 hrs
Procedure
Sedation
Pharynx sprayed wirh local anaesthetic and flexible endoscope passed
Suction to prevent aspiration
Complications
Transient sore throat
Amnesia following sedation
Perforation (< 0.1%)
Consent
Consent
Patient must have capacity to give consent
Before intervention is initiated
Intervention is understood by the patient
(risks, benefits, complications,
alternatives, consequences)
Voluntarily given
Capacity
Adult is assumed to have capacity unless
proven otherwise
Four parts
Understand and accept information is true
Remember what has been said
Show reason (to weigh up choices)
Communicate decision
Upper Abdo Pain
Dudodenal ulcer
Non-ulcer dyspepsia
Duodenal Crohn's
TB, lymphoma
Pancreatic Ca
Dyspepsia
Non- ulcer dyspepsia
Duodenal ulcer
Duodenitis
Gastritis / Gastric ulcer
Gastric malignancy
GORD
Oesophagitis
Pneumoperitoneum
Perforation
Gas forming infection
Iatrogenic (surgery)
Per vaginam (water ski-ing,
vigorous intercourse)
Interposition of bowel between
liver and diaphragm
Peptic Ulcer Disease 2.mmap - 07/09/2010 -

4. Malabsorption
IBD
Ulcerative Colitis
Relapsing / remitting inflammatory disorder of colonic mucosa; never spreads proximal to ileocaecal valve
Pathology
Hyperaemic / haemorrhagic granular colonic mucosa +/- pseudopolyps
Inflammation is normally not transmural
Histology
Inflammatory infiltrate; goblet cell
depletion; glandular distortion; mucosal
ulcers; crypt abscesses
Epidemiology
Prevalence: 100 - 200 / 100,000
Incidence: 10 - 20 / 100,000 a year
Most present 15 - 30 yrs; 3 x more common in non-smokers
Symptoms / Signs
Symptoms
Gradual onset of diarrhoea (+/- blood and mucus); crampy abdo
pain; increased frequency of bowels; systemic symptoms
common during attacks (fever, malaise, anorexia, weight loss)
Signs
May be none
In acute / severe episodes: fever, tachycardia, tender / distended abdo
Peripheral Manifestations
Clubbing; oral ulcers; erythema nodosum (purple, painful nodules on
shins); conjuctivitis; iritis (inflammation of iris); large joint arthritis; fatty liver
Tests
Usual bloods FBC, ESR, CRP, U&E, LFT, cultures
Stool cultures to exclude infection
AXR: no faecal shadows, mucosal thickening
Sigmoidoscopy: inflamed, friable mucosa
Rectal biopsy: inflammatory infiltrate, goblet cell depletion, mucoal ulcers, crypt abscesses
Complications
Perforation and bleeding
Toxic dilatation of colon; venous thrombosis; colonic cancer
Management
Inducing remission
Mild UC (< 4 motions / day) Prednisolone for 2 weeks (oral or retention enemas)
Moderate UC (4 - 6 motions / day) Oral Prednisolone for 2 weeks + 5-ASA + steroid enemas
Severe UC (> 6 motions / day) Treat as inpatient
Maintaining remission
5-ASA
Infliximab
Surgery
20% will require surgery at some point
Proctocolectomy and terminal ileostomy
Indications for surgery
Perforation; haemorrhage; toxic dilatation;
failure of medical therapy
Crohn's Disease
Chronic inflammatory disease characterised by transmural granulmatoud inflammation; can affect any part
of the gut but favours terminal ileum and proximal colon; skip lesions (unaffected bowel areas between
areas of disease) differentiate Crohn's from UC
Epidemiology
Prevalence: 50 - 100 / 100,000
Incidence: 5 - 10 / 100,000 per year
Associations: high sugar, low fibre diet, altered cell mediated immunity, smoking, NSAIDs
Symptoms / Signs
Symptoms
Diarrhoea, abdo pain, weight loss
Fever, malaise, anorexia (with active disease)
Signs
Abdo tenderness, right iliac fossa mass,
perianal absecess / fistulae / skin tags,
anal / rectal strictures
Peripheral Manifestations
Ahthous ulceration (oral mucous ulcer),
clubbing, erythema nodosum, iritis, fatty
liver, large joint arthritis
Complications
Small bowel obstruction; toxic dilatation; abscess formation; fistulae;
rectal haemorrhage; colonic cancer (rarer than in UC)
Tests
Usual bloods FBC, ESR, CRP, U&E, LFT, cultures, serum iron, vit B12
Colonoscopy to assess disease extent
Management
Mild attacks Prednisolone
Severe attacks
IV steroids, nil by mouth, IV hydration
Hydrocortisone IV, topical steroids for rectal disease
Nutrients required for Health
Vitamin B12
Absorbed in the terminal ileum
Deficiency causes: macrocytic anaemia,
neuropathy, glossitis
Vitamin C
Absorbed in the proximal ileum
Deficiency causes: scurvy
Malabsorption
Common in UK: coeliac disease, chronic
pancreatitis, Crohn's
Decreased bowel; pancreatic
insufficiency; small bowel mucosa;
bacterial overgrowth; infection; intestinal
hurry
Malabsorption Syndromes
Coeliac disease
T cell mediated autoimmune disease of small bowel in which prolamin
intolerance causes villous atrophy and malabsorption
Presentation
Can occur at any age (peaks in infancy and 50s)
One third are asymptomatic
Steatorrhoea; abdo pain; bloating; nausea & vomiting; angular
stomatitis; weight loss; fatigue; incidental iron def anaemia
Diagnosis
An IgA antibody, 95% specific
Duodenal biopsy via endoscopy: villous atropy and crypt
hyperplasia - reversing on gluten free diet
Management
Lifelong gluten free diet
Rice, maize, soya, potatoes, oats and sugar are Ok
Gluten free biscuits, flour, bread and pasta are prescribable
Complications
Anaemia; secondary lactose intolerance; increased risk of malignancy
Chronic pancreatitis
Causes
Typically alcohol
Rarely familial, CF. haemochromatosis,
pancreatic duct obstruction
Presentation
Epigastric pain through to pack (relieved by sitting forward or hot
water bottles on epigastrium / back)
Bloating, steatorrhoea, weight loss, brittle diabetes
Symptoms relapse and worsen
Tests
Ultrasound (pseudocyst), CT, AXR
(speckled pancreatic calcification)
Management
Drugs
Analgesia
Lipase + fat soluble vitamins
Diet
No alcohol; low fat diet
Surgery
Indications: unremitting pain, weight loss
Complications
Pseudocyst; diabetes; bilary obstruction;
local arterial aneruysm; gastric varices
Malabsorption.mmap - 07/09/2010 -

5. Irritable Bowel
Syndrome
Clinical features
Presentation
Typically 20 - 40 years; female predominance
Symptoms
Abdo pain (relieved by defecation); bloating; altered
bowel habit; tenesmus; muscus PR
Less commonly: nausea; dyspareunia; pain in back /
thigh / chest; change in urinary frequency; depression
Chronic > 6 months, exacerbated by
stress, menstruation, or gastroenteritis
Signs
Examination often normal, although
generalised tenderness is common
Insufflation of air during sigmoidoscopy may reproduce pain
Red flags
Factors suggesting disease
other than IBS
Age > 40 yrs; history < 6 months
Anorexia; weight loss; waking at night
(pain / diarrhoea)
Mouth ulcers; abnormal
investigations; PR bleeding
Management
Rarely 100% effective
Particularly medical therapy
Be pragmatic
Food intolerance
Try exclusion diets Although may lead to obsessions
Constipation
Increase fibre intake gradually
Non fermentable fibre (Fybogel) is better than fermenting
(Lactulose) - increased gas production adds to bloating
Diarrhoea
Bulking agent +/- loperamide after each loose stool
Colic & bloating
Anti spasmodics may help
Dyspeptic symptoms
Antacids
Psychological therapy
Emphasise positive prognosis 50% improve after one year
Tricyclics in low dose can be helpful
Diagnosis of Exclusion
Aetiology
Heterogeneous group of abdo symptoms
with no found organic cause
Probably due to disorders of intestinal motility or
enhanced visceral perception (brain gut axis)
Exclude other diagnoses
Young with classic history
FBC, ESR, LFT, coeliac serology
Urinalysis, sigmoidoscopy
Patient aged > 45 years or
evidence of organic disease
Colonoscopy
Prominent diarrhoea
LFT, stool culture, B12 & folate
TSH, antiendomysial antibodies
(coeliac) barium follow through
Further investigation guided
by symptoms
Upper GI endoscopy (dyspepsia)
Duodenal biopsy (coeliac)
Small bowel radiology (CD)
ERCP (chronic pancreatitis) or MRCP
(active pancreatitis)
When to refer
Changing symptoms in known IBS
To dietician with food intolerance
For psych input with pronounced depression
For gynae with cyclical pain
Irritable Bowel Syndrome.mmap - 07/09/2010 -

6. Bowels Bowel Cancer
Epidemiology
2nd most common cause of cancer death
32,000 cases per year, 50% mortality
More common in urban than rural areas
Genetic links / family history
No close relative affected CRC risk = 1 / 50
1 close relative CRC risk = 1 / 17
2 close relatives CRC risk = 1 / 10
Predisposing / protective factors
Predisposing: neoplastic polyps, UC, Crohn's, FAP, HNPCC, previous
Ca, low fibre diet, red meat
Protective: NSAIDs and aspirin
Presentation
Left sided bleeding / mucus PR, altered bowel habits, tenesmus, PR mass
Right sided Weight loss, low Hb, abdo pain
Either abdo mass, obstruction, perforation, haemorrhage, fistula
Significant symptoms
Rectal bleeding & change in bowel habit (35% risk of CRC); abdo /
rectal mass (30% risk of CRC); iron def anaemia (30% risk of CRC)
Tests
FBC (microcytic anaemia), FOB
Proctoscopy, sigmoidoscopy, barium enema,
colonoscopy (can be done virtually via CT)
CEA
Blood tumour marker for CRC
Crude screening method
Better for monitoring reoccurence
Distribution
15 % caecum & ascending colon, 10% transverse colon
5% descending colon, 25% sigmoid colon, 45% rectum
At least half are located in the sigmoid or rectum
Staging
Dukes
A - confined to bowel wall (90% 5 yr survival)
B - through bowel wall (65% 5 yr survival)
C - lymph node involvement (30% 5 yr survival)
D - distant mets (<10% 5 yr survival)
TNM
Tis - in situ (on mucosa)
T1 - submucosa
T2 - into muscle (muscularis propria)
T3 - into serosa
Spread
Local, lymphatic, by blood (liver, lung, bone), or transcoelomic
Management
T1
Could use transanal resection 5% chance of leaving behind involved lymph nodes
T2
Surgery alone
Autonomic nerves can be affected by
removal of rectal cancer Risk of sexual and bladder dysfunction
T3
Pre-op radiotherapy (due to risk of leaving cancer behind)
Then surgery
T4
Pre-op radiotherapy + / - chemotherapy
Then surgery
Diverticular Disease
Definitions
Diverticulum
Outpouching of the gut wall
Diverticulosis
Diverticula are present
Diverticular disease
Implies diverticula are symptomatic
Diverticulitis
Inflammation of diverticulum
Pathology
Patient has had motions which are hard to pass and becomes constipated
Acquired colonic diverticula are the most common type
Most occur in the sigmoid colon (95% complication occur at this site)
Lack of dietary fibre leads to high intraluminal pressure >
forces mucosa to herniate through muscle layers of gut wall
30% of westerners have diverticulosis by 60 yrs
Diagnosis
PR; sigmoidoscopy, barium enema, colonoscopy; CT
Management
Symptoms / Signs: altered bowel habit, left sided
colic (relieved by defecation, nausea, flatulence
High fibre diet
Antispasmodics
Surgical resection may be resorted to
Stool softeners
Complications
Diverticulitis
Features: pyrexia, raised WCC & CRP /
ESR, tender colon, localised peritonism
Treatment: analgesia, NBM, IV fluids, antibiotics
Pain - left iliac fossa
Perforation
Features: ileus, peritonitis, shock
40% mortality
Treated as acute abdo
Haemorrhage
Usually sudden and painless
Common cause of big rectal bleeds
Fistulae
Enterocolic, colovaginal ir colovesical
Treatment is surgical
Abscesses
Features: swinging fever, leucocytosis, localised signs
Treatment: antibiotics with ultrasound guided drainage
Post infective strictures
May form in the sigmoid colon
Investigations
Red Flags (for 2 week referral)
Rectal bleeding & change in bowel habit for 6 weeks
Rectal bleeding without anal symptoms in those over 45 yrs
Iron deficiency anaemia without obvious cause
Palpable abdo / rectal mass
2 episodes of FOB+ separated by a period of time
Value of investigations
FOB
CRC national screening programme
Aged 60 - 69; two yearly
2% FOB + (10% of these will have CRC)
Test is not very sensitive, although is used for risk reduction
Sigmoidoscopy
Screen for left sided lesions
90% sensitivity & 99% specificity
Limitations
Acceptability and cost
Does not pick up right sided lesions
Colonoscopy
Examines the entire colon
Perforation rate (0.2%) is higher than sigmoidoscopy (0.01%)
Limitations
Costs, need for sedation, acceptability,
limited availability of trained staff
Bowels.mmap - 21/10/2009 -

7. Liver 1
Immunity
Vaccine - attenuated strain of virus
Innoculation - IgG
IgM - immediate release
IgG - long term and base line protection
Cirrhosis
Irreversible liver damage - loss of normal hepatic architecture with
fibrosis and nodular regeneration
Causes
Chronic alcohol abuse
HBV and HCV infection
Signs
May be done other than abnormal LFTs
Leuconychia, clubbing, palmar erythema, hyperdynamic circulation
Dupuytren contracture, spider naevi, gynaecomastia,
parotid enlargement, hepatomegaly
Complications
Hepatic failure
Coagulopathy
Encephalopathy
Liver flap
Confusion / coma
Hypoalbuminaemia Oedema
Sepsis
Spontaneous bacterial peritonitis
Hypoglycaemia
Portal hypertension
Ascites
Splenomegaly
Oesophageal varices
Caput medusae
Management
General
Good nutrition; low salt diet; alcohol abstinence
Avoid NSAIDs, sedatives and opiates`
Interferon alpha
Ascites
Bed rest, fluid restriction
Spironolactone
SBP
Common organisms E Coli, Klebsiella and Strept
Antibiotics
Liver Transplant
Increases 5 yr survival in end stage
disease from 20% to 70%
Prognosis
5 yr survival 50%
Hepatitis
Hepatic Encephalopathy
As liver fails nitrogenous waste builds up and enters the circulation; astrocytes in the
brain clear it (involving conversion of glutamate to glutamine - excess glutamine shifts
the osmotic balance and fluid enters cells creating cerebral oedema
Grade I: altered mood / behaviour, sleep disturbance
Grade II: drowsiness, confusion, slurred speech
Grade III: stupor, incoherence, restlessness
Grade IV: coma
Liver Function Tests
Enzymes
AST / ALP / ALT / Bilirubin
ALT - also raised with muscle damage
ALP - also raised with renal damage, Paget's disease, children, and fractures
Functions
Clotting
Treat with: FFP / cryoprecipitate, vitamin K, keep warm (clotting less
effective when cold)
Avoid colloids
Colloids can disrupt clotting factors - in
worse case can lead to DIC in
predisposed patients (septic)
Stop warfarin and aspirin
Albumin
If falls can lead to massive interstitial oedema
Treat with human albumin solution
Glucose
Alcoholic Liver Disease
AST ++
ALT +
AST : ALT > 2
Hep C
AST + or =
ALT ++
AST : ALT < 1
Non Alcoholic Fatty Liver Disease
AST +
ALT ++
AST : ALT < 1
Portal Hypertension
Causes
Pre-hepatic
Portal vein thrombosis; splenic vein thrombosis
Hepatic
Cirrhosis; schistosomiasis; sarcoidosis; myeloproliferative diseases
Post hepatic
Budd-Chiari syndrome; right sided heart failure
Varices
Portal HT causes dilated collateral veins at sites of portosystemic anastomosis
Commonly occur in the lower oesophagus, but also around the umbilicus snd in the rectum
Develop in patients with cirrhosis when portal pressure > 10 mmHg
Variceal bleeding may develop when portal pressure > 12 mmHg (up to 50% mortality)
Gallstones
Bile contains cholesterol, bile pigments (Hb) and phospholipids
Acute Cholecystitis
Stone impactation in neck of gallbladder
Continuous epigastric pain (referred to R shoulder), vomiting, fever
Treatment: NBM, analgesia, antibiotics, cholecystectomy
Chronic Cholecystitis
Stones cause chronic inflammation +/- colic
Abdo discomfort, distension, nausea, fat intolerance
Investigate with ultrasound
Treatement: cholecystectomy
Liver.mmap - 07/09/2010 -

8. Liver 2 Hepatitis B (DNA virus)
Spread
Blood products, IVDU, sexual intercourse, direct contact
Risks
At risk groups
IVDU & sexual partners; health workers; haemophiliacs
Haemodialysis; sexually promiscuous; close family members of carriers;
staff of long term institutions
Endemic in Far East, Africa, Mediterarranean
Incubation
1 - 6 months
Symptoms & Signs
Resembles hep A
Extra hepatic features are more common
Tests
Antigens
HBsAg
Surface
Present 1 - 6 months after exposure
Persistent for 6 months implies carrier status
HBcAg Core
HBeAg
DNA material
Present after acute illness
Implies high infectivity
Antibodies
Abs Implies vaccine or previous infection
Abc Implies previous infection
Management
Vaccination
May be universal or for high risk groups
Passive immunisation may be given following high risk exposure
Given HBsAg to allow body to produce Abs
Treatment
Supportive
Avoid alcohol
Complications
Fulminant hepatic failure (rare); relapse; prolonged cholestasis; chronic hepatitis
(10%); cirrhosis; hepatocellular carcinoma (upto 60 x increased risk)
Hepatitis C (RNA flavivirus)
Spread
Blood; IVDU; sexual; acupuncture
Course
Early infection is often mild / asymptomatic
85% develop chronic infection; 25% develop cirrhosis; a few get hepatocellular cancer
Tests
LFTs; anti-HCV antibodies; HCV-PCR
Liver biopsy if HCV-PCR +ive to assess liver damage
Management
Interferon alpha & ribavirin in chronic infection
Interferon alpha in acute stage may reduce progression to chronic disease
Hepatitis A (RNA virus)
Spread
Faecal-oral route
Often in travellers / institutions
Incubation
2 - 6 weeks
Symptoms & Signs
Prodrome
Fever, malaise, anorexia, nausea, arthralgia
Jaundice +/- hepatosplenomegaly
Tests
Serum transaminases rises 3 weeks after exposure
IgM rises from day 25; IgG remains detectable for life
Management
Prevention
Passive immunisation
Human Ig gives upto 3 months immunity to
those at risk (travellers, household contacts)
Active immunisation
I year immunisation; extended to 10 years
after 6 months booster
Treatment
Symptomatic relief
Prognosis
Usually self limiting
Fulminant hepatitis occurs rarely; chronic liver disease does not occur
Liver 2.mmap - 07/09/2010 -