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Gastro Week 3

Gilbert S. Octavius 2014


Hepatitis Introduction
Hepatitis A
Risk Factors:
a) Poor hygiene
b) Contact with infected people
c) Anal-oral contact
d) Travelling to endemic places
e) Use of needles (very rare)
Hep A
• Has 4 genotypes
• Resistant to bile salts since it is not enveloped
• Resistant towards cold, hot (not very high
temp), detergent and acid
• Inactivated by formalin, chlorine and >38.5C
• It can survive in a dry environment from 2
hours to 60 days
Transmission
• Main transmission: Fecal-oral
• Sexual

• Use of needles, blood transfusion (very rare)


Natural History
• S&S develop 15-50 (mean 25-30 days) after
infection
• 1-2 weeks after S&S develops, the feces is
infectious
Viremia: 3 days – 5 weeks post-infection
Detected in feces: 1-5 weeks PI
Clinical manifestations: 2-8 weeks PI
Inrease in AST/ALT: 2 weeks PI, peak 4 weeks
IgM anti HAV: 1 week PI
IgG anti HAV: 3 weeks PI
Clinical Symptoms
Signs
• Chills
• Cough
• Myalgia
• Arthralgia
• Diarrhea
• Constipation
• Urticaria
• Pruritus
• Skin Rash
Symptoms
• Fever
• Bradycardia
• Icteric
• Lymphadenopathy
• Hepatosplenomegaly
Lab
• Increase in SGPT is more than increase in
SGOT
• Increase in biliruin, Gamma-GT, AP, PT
Treatment
• Symptomatic: antipyretic, antiemetic
• Enough hydration
• Adequate nutrition

Indication for hospitalization:


• Not enough food intake due to massive vomitting
• Dehydration
• Signs of liver failure: encephalopathy,
coagulopathy
Minimalizing Risk of Infection
• Adult  2 weeks before and 2 weeks after
onset
• Kids and Immunocompromised  lasts up to
6 months after onset
Hep A
• Hepatitis A tends to be more symptomatic in
adults; therefore, paradoxically, as the
frequency of HAV infection declines, the
likelihood of clinically apparent, even severe,
HAV illnesses increases in the susceptible
adult population
Hepatitis B
Transmission
Natural History
Phases of Infections
Hep B
Covalently closed circular DNA (ccc)  enables
Hep B to directly cause HCC without the
cirrhotic phase
Progression of Dz
Lab
• Seroconversion: HbeAg (-) and anti-Hbe (+)
• Active replication of virus has diminished
tremendously
• Seroconversion HbeAg is used to judge
clinically the improvement in chronic Hep B
Lab
• Anti-Hbc  to diagnose whether someone is
currently having an acute infection or not
Lab
• DNA Hep B  the most accurate way to know
the viral load
• This way, we can predict whether the patient
is going to develop a full blown cirrhosis or
HCC
Treatment
Hepatitis C
Transmission
Lab
• Anti HCV  shows that someone has been
infected before
• No protection effect
• Formed 7-8 weeks post infection
Lab
• HCV RNA  to know the presence & quantity
of virus in the body
• Formed 7-10 days post infection
Treatment Goal
• Therapy goal  CURE
Treatment
Hepatitis D
• Hepatitis D  Co-infection with Hepatitis B
Ascites
• Ascites is present when there is accumulation of free
fluid in the peritoneal cavity.
• Small amounts of ascites are asymptomatic, but with
larger accumulations of fluid (> 1 L) there is abdominal
distension, fullness in the flanks, shifting dullness on
percussion and, when the ascites is marked, a fluid
thrill.
• Other features include eversion of the umbilicus,
herniae, abdominal striae, divarication of the recti and
scrotal oedema. Dilated superficial abdominal veins
may be seen if the ascites is due to portal hypertension
Diagnosis
• USG  best means of detecting ascites
• Paracentesis  obtain fluid
• SAAG  differentiate between exudate or
transudate
• <25 g/L  usually cirrhotic patient 
transudate
Treatment
• Sodium and water retention
• Diuretics
• Paracentesis
• TIPS
• Peritoneo-venous shunt
Hepatic Encephalopathy
• Hepatic encephalopathy is a neuropsychiatric
syndrome caused by liver disease.
• As it progresses, confusion is followed by coma.
• Features include changes of intellect, personality,
emotions and consciousness, with or without
neurological signs. The degree of encephalopathy
can be graded from 1 to 4, depending on these
features, and this is useful in assessing response
to therapy
• When an episode develops acutely, a
precipitating factor may be found
Signs and symptoms
• The earliest features are very mild and easily overlooked but, as the
condition becomes more severe, apathy, inability to concentrate,
confusion, disorientation, drowsiness, slurring of speech and
eventually coma develop. Convulsions sometimes occur.
Examination usually shows a flapping tremor (asterixis), inability to
perform simple mental arithmetic tasks or to draw objects such as a
star (constructional apraxia), and, as the condition progresses,
hyper-reflexia and bilateral extensor plantar responses.
• Hepatic encephalopathy rarely causes focal neurological signs; if
these are present, other causes must be sought. Fetor hepaticus, a
sweet musty odour to the breath, is usually present but is more a
sign of liver failure and portosystemic shunting than of hepatic
encephalopathy. Rarely, chronic hepatic encephalopathy
(hepatocerebral degeneration) gives rise to variable combinations
of cerebellar dysfunction, Parkinsonian syndromes, spastic
paraplegia and dementia
Pathophysiology
• Patof  Ammonia overload
Diagnosis
• Diagnosis  made clinically
• In doubt  EEG  diffuse slowing of the
normal alpha waves with eventual
development of delta waves
Treatment
• Lactulose (15–30 mL 3 times daily) is increased
gradually until the bowels are moving twice daily. It
produces an osmotic laxative effect, reduces the pH of
the colonic content, thereby limiting colonic ammonia
absorption, and promotes the incorporation of
nitrogen into bacteria.
• Rifaximin (400 mg 3 times daily) is a well-tolerated,
non-absorbed antibiotic that acts by reducing the
bacterial content of the bowel and has been shown to
be effective. It can be used in addition, or as an
alternative, to lactulose if diarrhoea becomes
troublesome
Histology of Liver
Cirrhosis
• Cirrhosis is characterised by diffuse hepatic
fibrosis and nodule formation
• Worldwide, the most common causes are
chronic viral hepatitis, prolonged excessive
alcohol consumption and NAFLD. Cirrhosis is
the most common cause of portal
hypertension and its complications.
Pathophysiology
Types of Cirrhosis
• Cirrhosis is a histological diagnosis
• It evolves over years as progressive fibrosis and
widespread hepatocyte loss lead to distortion of the
normal liver architecture that disrupts the hepatic
vasculature, causing portosystemic shunts.
• Cirrhosis can be classified histologically into:
– Micronodular cirrhosis, characterised by small nodules
about 1 mm in diameter and typically seen in alcoholic
cirrhosis.
– Macronodular cirrhosis, characterised by larger nodules of
various sizes. Areas of previous collapse of the liver
architecture are evidenced by large fibrous scars.
Management
• Treat underlying causes
• Endoscopy  every 2 years
Portal Hypertension
The normal hepatic venous pressure gradient
(difference between the wedged hepatic venous
pressure and free hepatic venous pressure, see
below) is 5–6 mm Hg. Clinically significant portal
hypertension is present when the gradient
exceeds 10 mm Hg and risk of variceal bleeding
increases beyond a gradient of 12 mm Hg
Clinical Feature
• The clinical features result principally from
portal venous congestion and collateral vessel
formation
• Splenomegaly is a cardinal finding
Pathophysiology
• Increased portal vascular resistance leads to a
gradual reduction in the flow of portal blood to
the liver and simultaneously to the development
of collateral vessels, allowing portal blood to
bypass the liver and enter the systemic circulation
directly.
• Portosystemic shunting occurs, particularly in the
gastrointestinal tract and especially the distal
oesophagus, stomach and rectum, in the anterior
abdominal wall, and in the renal, lumbar, ovarian
and testicular vasculature.
Diagnosis
• Usually clinically
• Measure WHVP
• Endoscopy
• USG
• CT & MRI
Management
• Prevention of acute bleeding  beta blocker
Hepatocellular Carcinoma (Hepatoma)
• Cirrhosis is present in 75–90% of
individuals with HCC and is an important
risk factor for the disease. The risk is
between 1% and 5% in cirrhosis caused
by hepatitis B and C
• The risk is four times higher in HBeAg-positive
individuals than in those who are HBeAg-
negative
• Risk is higher in men as they age
HCC
• Macroscopically, the tumour usually appears
as a single mass in the absence of cirrhosis, or
as a single nodule or multiple nodules in the
presence of cirrhosis. It takes its blood supply
from the hepatic artery and tends to spread
by invasion into the portal vein and its radicals

• Can be caused by aflatoxin


Clinical Presentation
• Two types of presentation:
1. Underlying Cirrhosis
Deterioration in their liver function with
worsening ascites and/or jaundice or variceal
hemorrhage
Symptoms: weight loss, anorexia, abdominal
pain, hepatomegaly, right hypochondrial mass
2. Screening of patients at risk of HCC
Lab
• AFP  60% increase
• Imaging:
a) USG  focal liver lesion
b) CT w/ contrast  GOLD STANDARD
Barcelona Clinic Liver Cancer Staging
Primary Biliary Cirrhosis (PBC) &
Primary Sclerosing Cholangitis (PSC)
• Both present early with fatigue and pruritus
• Autoimmune disease
• PSC  Men, PBC  Women
Alcoholic Liver Disease
• A threshold of 14 units/week in women and
21 units/week in men is generally considered
safe. The risk threshold for developing ALD is
variable but begins at 30 g/day of ethanol
• Risk factors: Drinking pattern, gender, genetics
and nutrition
Pathophysiology
Treatment
• Nutrition
• Corticosteroids
• Pentoxifylline
• Liver Transplantation
Non-Alcoholic Fatty Liver Disease
(NAFLD)
• Non-alcoholic fatty liver disease (NAFLD)
represents a spectrum of liver disease
encompassing simple fatty infiltration
(steatosis), fat and inflammation (non-
alcoholic steatohepatitis, NASH) and cirrhosis,
in the absence of excessive alcohol
consumption (typically a threshold of < 20
g/day for women and < 30 g/day for men is
adopted)
Pathophysiology
Natural History
Lab
• Increase in AST & ALT
• USG  appears ‘bright’
• Liver biopsy  gold standard
Management
• Lifestyle
• HMG-CoA reductase inhibitor
• Tocoferol