You are on page 1of 48

The Liver

The Liver

Largest gland of the body, weighing about 1500 g. Has two main lobe- the right and left Supplied with blood from two sources: the hepatic artery and the portal vein

The Liver
Functions:

Metabolism of carbohydrate, protein, and fat Storage and activation of vitamins and minerals Formation and excretion of bile Conversion of ammonia to urea Action as filter and food chamber

ACUTE VIRAL HEPATITIS


Acute viral hepatitis is a widespread inflammation of the liver and is caused by hepatitis virus A, B, C, D, and E.

MINOR AGENTS CAUSING HEPATITIS


Epstein-Barr virus Cytomegalovirus Herpes simplex Yellow fever Rubella

HEPATITIS A VIRUS (HAV)

Transmitted by the fecal-oral route and is contracted through contaminated drinking water, food and sewage.

Symptoms:

Anorexia (most frequent symptom) Nausea Vomitting Right upper quadrant abdominal pain Dark urine Jaundice (icterus)

HEPATITIS B VIRUS (HVB) AND HEPATITIS C VIRUS (HCV)


Transmitted via blood, blood products, semen and saliva. They can be spread from contaminated needles, blood transfusion, open cuts or wounds, splashes of blood into the mouth or eyes and through sexual contact

HEPATITIS D VIRUS (HDV)


Dependent on the HBV for survival and propagation in humans. May be a coinfection or superinfection.

HEPATITIS E VIRUS (HEV)


Transmitted by oral-fecal route Rare in America, frequent in southeastern, eastern and central Asia,northern, eastern and western Africa and Mexico.

Sources of contamination

Contaminated water appears to be the source of infection, which usually afflicts people living in crowded and unsanitary conditions. HEV is generally acute rather than chronic.

Phases of symptoms of acute viral hepatitis

PRODROMAL PHASE

Affects 25% of the patients Causes fever, arthraglia, rash and angiodema

ICTERIC PHASE

Appearance of jaundice

CONVALESCENT PHASE

Jaundice and other symptoms begin to subside. Complete recovery is expected in 95% of HAV cases, 90% of acute HBV cases, 1530% in HCV cases. Chronic hepatitis does not develop with HEV, and symptoms and liver function tests usually normalize within 6 weeks.h

FULMINANT HEPATITIS

A syndrome in which severe liver dysfunction is accompanied by hepatic encepalopathy A disease defined by the absence of pre existing liver disease and the development of hepatic encepalopathy within 8 weeks of onset of illness.

CAUSES OF FULMINANT HEPATITIS


Viral hepatitis Chemical toxicity (acetaminophen, drug reactions, poisonous mushrooms, industrial poisons) Wilsons disease, fatty liver of pregnancy, Reyes syndrome, hepatic ischemia, hepatic vein obstruction, and dessiminated malignancies.

EXTRAHEPATIC COMPLICATIONS

Cerebral edema, coagulopathy, bleeding, cardiovascular abnormality, renal failure, pulmonary complications, acid-base disturbances, electrolyte imbalances, sepsis and pancreatitis.

CHRONIC HEPATITIS

To be defined, a patient must have at least 6month course of hepatitis and clinical evidence of liver disease Can have autoimmune, viral, metabolic, and toxic etiologies

ALCOHOLIC LIVER DISEASE

Alcohol problems are highest among young adults 18-29 years of age and lowest among adults 65 years and older Acetaldehyde, a toxic product of alcohol metabolism causes damage to mitochondrial membrane structure and function

PATHOGENESIS OF ALCOHOLIC LIVER DISEASES


HEPATIC STEATOSIS ALCOHOLIC HEPATITIS CIRRHOSIS

HEPATIC STEATOSIS

Caused by the culmination of the following metabolic disturbances: Increase in the mobilization of fatty acids from adipose tissue Increase in hepatic synthesis of fatty acids Increase in triglyceride production Trapping of trigyceride in the liver Hepatic steatosis is reversible with the abstinence in from alcohol and conversely if abuse continues and can develop into cirrhosis

Chronic liver disease due to diffuse necrosis and regeneration leading to an increase in fibrous tissue formation disrupting the normal liver structure.

EXTERNAL SYMPTOMS:
Icteric sclerea Alopecia Asterixis Spider angioma Palmar erythema Gynecomastia

EXTERNAL SYMPTOMS:
Jaundice Bruising Caput medusae Ascites Muscle Wasting

EXTERNAL SYMPTOMS: Altered hair distribution Testicular atrophy Edema

INTERNAL SYMPTOMS:
Encephalopathy Esophageal varices Portal hypertension Cirrhosis Hepatrorenal syndrome Tea-colored urine Clay-colored stool

Malnutrition - plays a major role in the pathogenesis of liver injury and has a
profound negative impact on prognosis. - Maldigestion or mal absorption - Anorexia - Early Satiety - Nausea and Vomiting - Altered Metabolism - Restricted Diets

Causes:

Ascites accumulation of fluids in the abdominal cavity. Portal Hypertension increases blood flow and can result in varices in the gastrointestinal tract. Hyponatremia often occurs because of the decreased ability to excrete water because of the persistent release of antidiuretic hormone, sodium losses via paracentesis, excessive diuretic use or overly aggressive sodium restriction. Hepatic Encephalopathy characterized by impaired mentation, neuromuscular disturbances and altered conciousness. Fat Malabsorption Glucose Alteration

Renal insufficiency and Hepatorenal Syndrome - is a renal failure associated with severe liver disease without intrinsic kidney abnormality. It is characterized by reductions in renal blood flow, cortical perfusion and glumerular filtration rate. Ostepenia

Increase energy intake via small, frequent meals Sodium restriction for fluid retention Fluid restriction for hyponatremia Carbohydrates controlled diets for hypoglycemia Vitamins and minerals supplements Oral liquid supplements or enteral feeding (consider BCAA formulas for encephalopathy)

Diseases of the gallbladder

Diseases of the gallbladder

1. 2. 3. 4. 5.

Cholelithiasis Cholecystitis Acute Cholangitis Sclerosing cholangitis Cholestasis

Cholelithiasis
-the formation of the gallstones (calculi) in the absence of the infection of the gallbladder -it develops when stones slip into the bile ducts, producing obstruction pain, and cramps if the passage of the bile into the duodenum is interrupted, cholecystasis can develop. -treatment of these diseases includes surgical removal of the gallbladder

Cholecystitis

- it is the inflammation of the gallbladder - it may be chronic or acute - it is usually caused by gallstones obstructing the bile ducts, leading to the back up of bile -acute cholecytitis w/out stone may occur in critically ill patients - this disease can only be treated through surgical intervention - in acute cholecystitis, a hydrolized low fat formula or an oral diet consisting of 30 to 45 grams of fat per day can be given as for chronic, it may require a long term fat diet that contains 25% to 30% of k/cal as fat

Acute

Cholangitis

- inflammation of the bile ducts -it requires resuscitation w/ fluids & broad-spectrum antibiotics, if the patients doesnt improve w/ conservative treatment, placement of a percutaneos bilary treatment placement of a percutaneous bilary stent or cholecystectomy may be needed

Scherosing

Choloangitis

- it results from sepsis & liver failure

- patients are generally on broad spectrum antibiotics


- patients may require chronic antibiotics therapy when sepsis is recurrent

Cholestasis

- it

is a condition of sludge like bulid up in the gallbladder as a result of stimulation or re;ease of bile\ - it occurs in patients w/out aoral or enteral feeding for a long period of time. - prevention includes stimulation of intestinal & biliary motility & secretions - drug therapy is also used when not possible

Diseases of the Exocrine Pancreas

Pancreatis

- is the inflammation of the pancreas and is charaacterized by edema. Cellular exudates and fat necrosis. - diseases can range form mild an d self limiting to severe, with auto digestion, necrosis and hemorrhage of pancreatic tissue - it is classified as either Acute or Chronic - Pancreatic destruction so extensive that exocrine and endocrine functions are severely diminished and maldigestion and diabetes may result

Causes:

- Billiary Tract Disease - Chronic Alcoholism - Gallstones - Hypertriglycerimia - Hyperglycemia - Trauma - Certain drugs, some viral indections

Symptoms:

- indigestion of food - Nausea - Vomiting - Abdominal pain and Distension - Steatorrhea

Severe

cases:

- Hypotension - Oliguria - Dyspnesia (It may also lead to Hemorrhage, Shock or even Death)

Acute

Pancreatitis

- withhold oral and enteral feeding - support with intravenously fluid - if the oral nutrition cannot be initiated in 5 to 7 days, start nutrition support - for severe, prolonged cases in acute pancreatitis, (PN) Parenteral nutrition should be iniated - if Triglycerides (Tgs) are < 400 mg / dl before PN initiation. Use a 3 in 1 solution and monitor TG level - if TGs are elevated (>400 mg/dl), use a dextrose based solution, monitor serum glucose frequently, and treat as needed w/ insulin.

Acute

Pancreatitis

- Once oral nutrition is started, provide: * easily digestible foods * adequate protein intake * low-fat diet * increased calories * 6 small meals - H2 receptor antagonists may be prescribed to decreased hydrochloric acid production, which will reduce stimulation of the pancreas - Somatostatin is considered the best inhibitor of the pancreatic secretion and may be added to the PN solution.

Chronic
- provide

Pancreatitis

oral diet as in acute pahse - TF can be used when oral diet is inadequate - supplement pancreatic enzymes - supplement fat-soluble vitamins and vitamin B12 - manage intestinal pH w/ * antacids * H2-recept antagonists proton pump inhibitors * administer insulin for glucose intolerance

Submitted to: Dr. Roosevelita A. Cruz


Submitted by: 1. Limjoco, Levin Vergel A. 2. Gacias, Martin P. 3. Felipe, Philippine Andrew T. 4. Poscablo, Ma. Glenn Erica R. 5. Tingzon, Bethel P.
Section B. 7:03-10:30, Saturday

You might also like