Result from dilated veins in the walls of the lower part of the esophagus and sometimes the upper part of the stomach.
are a life-threatening complication of portal hypertension.
Tests to visualize the varices include EGD (esophagogastroduodenoscopy).
symptoms are

1) Vomiting
2) Vomiting blood
3) Black, tarry stools
4) Bloody stools
5) Decreased urine output
6) Symptoms of chronic liver disease (such as cirrhosis)
7) Excessive thirst
8) Paleness
9) Light-headedness


Physical examination:

1) Signs of chronic liver disease or cirrhosis
2) Low blood pressure
3) Rapid heart rate
4)Bloody or black stool on rectal exam

Tests to visualize the varices include EGD (esophagogastroduodenoscopy).

manage persistent varices with medical and procedural therapies:
1) endoscopic therapy
2) balloon tamponade
3) the transjugular intrahepatic portosystemic shunt (TIPS) procedure
4) Octreotide and vasopressin are medications that may be used to decrease portal blood flow and slow bleeding.
5) Emergency surgery may rarely be used to treat patients if other therapy fails

Bleeding esophageal varices are a serious complication of liver disease and carry a poor prognosis.

Liver transplantation should be considered.

Complication
1) Recurrence of bleeding after treatment
2) Hypovolemic shock
3) Esophageal stricture after surgery or endoscopic therapy
4) Worsening encephalopathy (confusion)
5) Infection (pneumonia, blood stream infection, peritonitis

Prevention

Treatment of the underlying causes of liver disease may prevent bleeding.

In hemochromatosis, the commonest mutation is C282Y. It is found in approximately 90% of cases.
The mutation is on chromosome 6, affecting the HFE gene.
There is an increased incidence in males.
The serum Fe is elevated (> 300 mg/dL).
The serum transferrin saturation is a sensitive parameter of increased Fe and merits evaluation when > 50%.
The serum ferritin is increased ferritin of >1000 μmol/l is suggestive (normal <200).> 2 mg/24 h) by the chelating drug deferoxamine (500 to 1000 mg IM based on the size of the patient), and this has been used as a diagnostic test.
In addition, when the Fe content in the liver is significantly increased, an MRI may reflect this change. Liver biopsy had been the gold standard in diagnosis; it now serves only to provide evidence of fibrosis (cirrhosis). Gene assay (Homozygosity C282y mutations) is the also an excellent diagnostic test.


Venesection is preferred therapy . Treatment consists of bi-weekly venesection removing approximately 500 ml per week. Desferrioxamine infusion (another iron chelator) can also be used.

Iron infiltrates the parathyroid glands and can cause hypoparathyroidism. In haemochromatosis , joint deposition of iron occurs, causing arthropathy. Increased iron deposition in the skin stimulates increased melanin production. Haemochromatosis is a recognised cause of restrictive cardiomyopathy. Cardiac damage is commonly seen with ferritin >2,000 ng/l

Wilson disease : The abnormal gene is the ATP7B gene on chromosome 13. It is autosomal recessive. Kayser-Fleischer rings are often seen on slit lamp, but not always. The best test is hepatic copper concentration (> 250 μg /g of dry weight). . Typically there is low serum copper levels but high urine excretion of copper. There is low liver production of caeruloplasmin (< style="font-weight: bold;">Non-alcoholic steatohepatitis (NASH) is a form of liver disease resembling alcoholic liver disease in a patient who does not consume significant amounts of alcohol. The natural course is relatively benign, but liver cirrhosis. together with all its sequelae, may develop; sometimes liver transplantation is indicated. NASH is associated increased prevalence of Insulin resistance/type 2 diabetes. There may also be lipid abnormalities and increased iron stores.

Abdominal tenderness is found in more than 50% of patients with Spontaneous Bacterial Peritonitis. Findings on the abdominal examination can range from mild tenderness to overt rebound and guarding. Traditionally, three fourths of SBP infections are caused by aerobic gram-negative organisms (50% of these being Escherichia coli), and one fourth of these infections are due to aerobic gram-positive organisms ( streptococcal species).
An ascitic fluid neutrophil count of > 250 cells/mL and ascites lactate level of >25 mg/dL are the single best predictors of SBP. A combination of an aminoglycoside and ampicillin or cefotaxime can be used.

Budd-Chiari syndrome is thrombosis of the hepatic vein, the major vein that leavesthe liver. Most patients have an underlying thrombotic tendency. About 10% have polycythemia vera, and about 10% have been on the OCP. The most common symptoms in Budd-Chiari syndrome are hepatomegaly, abdominal pain, ascites and jaundice.

Child's Pugh classification includes bilirubin, prothrombin tine, encephalopathy scores, ascites and albumin to measure the severity of liver disease.

Somatostatin its derivative, octreotide, and terlipressin are often used for emergency treatment of bleeding oesophageal varices in patients with cirrhosis of the liver.

Beta blockers (nadolol), nitrates, vasopressin analogues and somatostatin analogues can also be used for reducing rebleeding in oesophageal varices

Wernicke encephalopathy is a neurologic disorder of acute onset caused by a thiamine deficiency. The condition is characterized by ocular abnormalities, ataxia, and a global confusional state. Wernicke encephalopathy results from a deficiency in vitamin B-1 (ie, thiamine). The episode may have been precipitated by intravenous dextrose administration which exhausted his vitamin B reserves. B vitamins should be administered to all alcoholic patients requiring dextrose.

The main features of Korsakoff’s psychosis is short term memory loss and subsequent compensatory confabulation by patient. Other symptoms may include delirium, anxiety, depression, confusion, delusions and insomnia. The treatment is with intravenous thiamine.

Hepatorenal syndrome (HRS) is the development of renal dysfunction in patients with severe liver disease (acute or chronic) in the absence of any other identifiable causes of renal Pathology

Hepatitis A Virus is a picornavirus.
Hepatitis B Virus is a hepadnavirus.
Hepatitis C Virus is a flavivirus. It is a single-stranded RNA virus.


Hepatitis B
A positive anti-HBc (IgM) and HBsAg suggests acute infection.

When the infection resolves, HBsAg becomes negative and anti-HBc (IgG) is positive.

In patients who have been vaccinated, HBsAg is negative and anti-HBs is positive.

HbcAg is the first detectable antigen in acute infection but is also detectable in chronic infection.

HbsAg is detectable in chronic infection.

HbsAb is a sign of previous infection or immunisation.

HBeAg (not HBcAg) is the best marker of infectivity, and is used as an important criteria for selection of patients who have chronic hepatitis B for interferon (α-2B)
therapy.
HBV DNA and HBeAg levels are measured in response to the therapy and undetectable levels would be considered successful treatment.

10% of patients with hepatitis B develop chronic infection (as compared to hepatitis C where 80% develop chronic infection).

30% of patients with hepatitis C develop hepatocellular carcinoma over 30 years. 20% develop cirrhosis over 20 years.

The treatment options are ribavirin or PEG (polyethylene glycolated) interferon.

IFN α is only effective in clearing the virus in 25% of patients.

Meta-analysis of data strongly suggests a two to three-fold enhanced efficacy of interferon-ribavirin combination therapy over interferon monotherapy in all major subgroups of chronic hepatitis C patients.

In hepatitis C, response to therapy is determined by normalisation of hepatic transaminases and undetectability of hepatitis C RNA in plasma.

Hepatitis D (delta) is a superimposed infection to Hepatitis B.

Hepatitis E causes acute illnesses, and does not result in a chronic carrier state. It is usually transmitted in a faeco oral route (similar to hepatitis A). It occurs mostly in developing countries and is widespread in India, Asia, Africa and Central America.

Hepatitis G virus or GBV-C does not appear to cause progressive liver disease.

Autoimmune hepatitis occurs in younger to middle aged women. 25% present as acute hepatitis, but the onset is usually insidious. Amenorrhoea is relatively common. It is associated with hyperglobulinaemia rather than hypoglobulinaemia. 60% are associated HLAB8, DR3 and DW3. The sicca syndrome (xerostomia/dry eyes,keratoconjunctivitis sicca may occur).

Achalasia:

Achalasia is an esophageal motility disorder. It is diagnosed when there is a complete lack of peristalsis within the body of the esophagus. The lower esophageal sphincter does not relax to allow food to enter the stomach. Symptoms are difficulty swallowing both liquids and solids. Many people also have associated regurgitation, vomiting, weight loss, and atypical chest discomfort.

• Botulinum injections are most effective of all the options for relieving a lower oesophageal sphincter restriction which leads to achalasia.
• Nifedipine, nitrates or sildenafil can also be used, but are less effective.
• Surgically, Heller’s oesophageal myotomy is the best treatment option, it can be done via an abdominal incision or laparascopically.

• Barrett's Columnar replaces Squamous in Barrett’s oesophagus.
• This is also known as small intestinal (columnar) metaplasia.
• There is increased risk of oesophageal adenocarcinoma.
• Nitrates, caffeine and alcohol can help relieve symptoms by relaxing lower oesophageal tone.
• Not all patients with GORD should undergo an OGD (should be considered if GI bleeding or symptoms of dysphagia occur).
• Oesophagitis is present in half of GORD patients.
• Oesophageal manometry or oesophageal motility study measures the strength of the lower oesophageal sphincter. This would rule out achalasia.

• Mallory-Weiss tears are usually caused by forceful or prolonged vomiting or coughing.
• They may also be caused by epileptic convulsions.
• The tear may be followed by vomiting bright red blood or by passing blood in the stool.
• The incidence is 4 in 100,000 people. Achlorhydria (absence of gastric acid secretion) can be caused by immune destruction to the stomach wall, malnutrition and marijuana use. The pentagastrin testis used as a diagnostic aid for evaluation of gastric acid secretory function

PANCREATITIS

Coxsackie, mumps, ECHO and hepatitis viruses as well as hypothermia can cause acute pancreatitis.

The following are poor prognostic indicators in acute pancreatitis:

• Calcium <> 15
• Urea >16
• ALT >200
• PaO2 <8>
• Age > 55 years
• Glucose > 10

• Cullen's sign (periumbilical discolouration) can be present
• Grey Turner's sign (flank discoloration) can be present
• Purtscher's retinopathy (ischaemic areas in the retina) can be present

• Clotting of the hepatic vein, the major vein that leaves the liver
• It occurs in 1 out of 100000 individuals and is more common in females.
  
• Some 10-20% also have obstruction of the portal vein.
• Most patients have an underlying condition that predisposes to blood clotting
1. 10% have polycythemia vera
2. 10% of patients with Budd-Chiari syndrome take birth control pills
• Polycythemia vera and myelodysplastic syndrome are the most frequent cause.
• Thrombophilic conditions
• Antiphospholipid syndrome .
• Paroxysmal nocturnal hemoglobinuria in about 12 % of patients; PNH can also induce a VOD-like picture.
• Rarer causes include Behçets disease - often with involvement of the inferior vena cava , granulomatous idiopathic venulitis and hypereosinophilic syndrome . The latter two conditions may be steroid responsive.
• Occasionaly tumors such as atrial myxoma, Wilms tumor and cystic or alveolar echinococcosis can mimick BCS.
• Most Common Features is ascites, classical triad of ascites, abdominal pain and hepatomegaly.

• Anticoagulation starting at the time of diagnosis, initially using low-molecular heparin (conventional heparin being used only when rapid reversal of anticoagulation was anticipated) and switching to oral agents after an average of 2 weeks.
• Interventional radiological recanalization of the hepatic veins with angioplasty or stenting for short and long stenoses, respectively.
• If this failed, TIPS insertion via a hepatic vein stump or by transcaval approach
• OLT if TIPS failed or was not technically feasible.

• In general, nearly 2/3 of patients with Budd-Chiari survive 10 years.
• Important negative prognostic indicators include ascites, encephalopathy, elevated Child-Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin).

Colorectal carcinoma: is second most common cause of death from neoplastic diseases, with peak incidence in 60-79 years of age, and rare under the age of 40.

Risk factors:

• High fat, high protein, low fibre diets

• Presence of multiple sporadic adenomatous polyps

• Ulcerative colitis

• Familial adenomatous polyposis

Morphology:

Distribution is as follows….

• Caecum/ ascending colon (38%)

• Transverse colon (8%)

• Descending colon (8%)

• Rectosigmoid (35%)

• Multiple sites at presentation (1%)

Presentation may be:

• Polypoid, fungating masses; especially in capacious caecum and right (ascending) colon

• Annular, encircling masses with napkin-ring obstruction; characteristic of distal colorectum

Both forms penetrate bowel wall over years (diffuse infiltrative)

Clinical finding:

Colorectal carcinoma is asymptomatic for years, though:

• Fatigue

• Weakness

• Iron deficiency anaemia

• Abdominal discomfort

• Progressive bowel obstruction

• Liver enlargement (metastases)

Eventually occur.

Five-year survival depends on the depth of penetration and lymph node involvement and ranges from 100% for lesions limited to the mucosa to 25% for extensively invasive tumours. Surgery is the only hope for cure.

Cirrhosis: defined by three characteristics:

• Fibrosis: delicate band or broad septa

• Nodules: created by regeneration of hepatocytes

• Disruption of parenchymal architecture of the entire liver
  
  

Causes: cirrhosis is the end point of many disease processes, most of which are hepatitic:

• Alcoholic liver disease (60-70%)

• Viral hepatitis (10%)

• Biliary diseases (5-10%)

• Primary hemochromatosis (5%)

Others include Wilson disease, a₁-antitrypsin deficiency and cryptogenic cirrhosis.

Clinical consequences: cirrhosis may be clinically silent but ultimately leads to anorexia, weight loss, weakness, osteoporosis, and debilitation.

Ultimate causes of death are:

• Hepatic failure

• Complications of portal hypertension

• Hepatocellular carcinoma