M.Sc. Nursing 1st year HCN, SRHU Anatomy of liver location Upper right quadrant (Right hypochondriac region) of the abdominal cavity. it rests just below the diaphragm, to the right of the stomach and overlies the gallbladder. • Size about 15 cm • Shape wedge-shaped • Weight 1.44–1.66 kg (3.2–3.7 lb) • Colour reddish-brown
• It is both the heaviest internal organ and the
largest gland in the human body. Layers Covered by visceral peritoneum layer falciform ligament
Lobe and lobules
• The liver has two lobes larger right lobe and a smaller left lobe, divided by the falciform ligament. • Each lobe is further divided into eight segments. • Each segment has an estimated 1,0000 lobules, or small lobes. • Each of these lobules has a small tube (duct) that flows toward the common hepatic duct. Ducts Blood Supply The liver is connected to two large blood vessels: the hepatic artery and the portal vein. • The hepatic artery carries oxygen-rich blood from the aorta, • And the portal vein carries blood rich in hepatic artery digested nutrients from the entire gastrointestinal tract and also from the spleen and pancreas. portal vein • These blood vessels subdivide into small capillaries known as liver sinusoids, hepatic lobules 1. Metabolic Functions Liver actively participates in carbohydrate metabolism, lipid, protein, mineral and vitamin metabolisms. 2.Hematological and synthetic functions Liver participates in formation of blood (particularly in embryo) • Synthesis of plasma proteins (albumin and prothrombin),and hormones e.g angiotensinogen, insulin-like growth factor and triiodothyronine. • Destruction of erythrocytes (Bilirubin) 3.Protective functions & detoxification Kuffer cells of liver perform phagocytosis to eliminate foreign compounds. 4.Storage functions Glycogen, vitamins A,D and B12 5.Excretory Functions Bile pigments, bile salts and cholesterol are excreted in bile, into intestine. 8.Breakdown The liver is responsible for the breakdown of insulin and other hormones Cirrhosis of liver • Cirrhosis is a condition in which the liver does not function properly due to long term damage of liver • The development of cirrhosis is an insidious, prolonged course, usually after decades of chronic liver disease. DEFINITION Cirrhosis of liver is a chronic progressive disease of liver characterised destruction and replacement of normal tissue by scar tissue. Causes: • excessive alcohol consumption (40%) • hepatitis B (30%) • Hepatitis C (20%) • Injury • Obesity and diabetic • Prolonged use of Steroid medication • Biliary cirrhosis • New over growth of fibrous connective tissue (alteration in blood flow) • Wilson’s disease (excess copper accumulation in liver) Pathophysiology Hepatocyte injury with necrosis fibrosis, regeneration and eventual degeneration
Diminished parenchymal cell mass causes regeneration of tissue with
nodular areas of proliferating hepatocytes
Hepatocyte respond to injury with deposition of collagen that forms
fibrous connective tissue
This scar tissue and nodular areas of regeneration impaired the intra hepatic blood flow Ongoing necrosis
Failure of hepatocellular function and portal hypertension occurs
Ascites, severe calcification, scaring, fibrosis, encephalopathy (hepatic
coma) and G.I. bleeding CLINICAL MANIFESTATION Early manifestation: Usually no symptoms or may be non specific such as- headache fatigue jaundice. Later manifestation- • May be severe and result from liver failure and portal hypertension. Hematologic problem: It include- • leukopenia • anaemia • coagulation disorder • thrombocytopenia Endocrine problem • Men show- gynecomastia (benign growth of the glandular tissue of the male breast) • Loss of axillary and pubic hair • Testicular atrophy Female show- • amenorrhea • Vaginal bleeding (older women) Skin lesion: Spider angiomas- small dilated blood vessels with a bright red centre point and spinder like branches. Usually occur in neck, nose, cheeks, upper trunks and shoulder.
• Palmar erythema- is a rare skin
condition where the palms of both hands become reddish. • Usually affects the base of the palm and the area around the bottom of thumb and little finger JAUNDICE Ascites Hepatomegaly
Clubbing of finger splenomegaly
• Peripheral neuropathy- Due to dietary deficiency of thymine folic acid and cobalamin. • Itching DIAGNOSTIC EVALUATION History collection present health history past health history Physical examination Skin colour Enlarge left hepatic lobe splenomegaly • Gold standard test for diagnosis is liver biopsy through a percutaneous transjuglar, laparoscopic of fine needle approach • LFT (liver function test) • RFT (Renal function test) • Blood investigation for hepatitis b and c • CBC (complete blood count) • Ct scan • MRI • Ultrasonography MANAGEMENT MEDICAL MANAGEMENT • Fluid build-up in the belly (ascites). It can be deadly if it is not controlled. Treatment can include: • Following a low-sodium diet. • Medicines such as diuretics. • Removing fluid with a needle(paracentesis) • Bleeding from enlarged veins. Variceal bleeding in the digestive tract can be treated with: • Beta-blocker such as carvedilol • Antibiotic therapy for infection • Fluid restriction >1000ml/day • Monitor daily weight and abdominal girth INJ.of vit.k 1amp.iv- OD for 3 days Analgesic such as Surgical management: • Transjuglar intrahepatic portosystemic shunt (TIPS). by useing imaging guidance connect the portal vein to the hepatic vein in the liver. • A small metal device called a stent is placed to keep the connection open and allow it to bring blood draining from the bowel back to the heart while avoiding the liver. . • Liver transplantation 1-Pain related to liver tissue damage as evidence by patient verbalization. Goal- to reduce pain Intervention- Provide comfortable position Provide calm environment Administer analgesic medication 2-Imbalanced Nutrition Less Than Body Requirements related to Inadequate diet as evidence by Weight loss • Goal: improve the nutritional status • Intervention • Measure dietary intake by calorie count • Encourage patient to eat explain reasons for the types of diet • Give small, frequent meals • Provide tube feedings if indicated 3- Increased isotonic fluid retention related to compromised regulatory mechanisms evidenced by Edema • Goal: stabilized fluid volume • Intervention: • Measure I&O, weigh daily, and note gain of more than 0.5 kg/day. • abdominal vein distension • Assess degree of peripheral Edema • Measure abdominal girth daily 4-Risk for Impaired Skin Integrity related to presence of Edema as evidence by patient appearance • Goal : Maintain skin integrity • Intervention: • Inspect pressure points and skin surfaces closely and routinely • Recommend elevating lower extremities • Keep linens dry and free of wrinkles • Administer medications as prescribed by COMPLICATION Edema: As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt and water in the body. The excess salt and water first accumulates in the tissue beneath the skin of the ankles and legs because of the effect of gravity when standing or sitting. This accumulation of fluid is called peripheral Edema Ascites: • As cirrhosis worsens and more salt and water are retained, fluid also may accumulate in the abdominal cavity between the abdominal wall and the abdominal organs. • This accumulation of fluid (called ascites) causes swelling of the abdomen, abdominal discomfort, and increased weight. Spontaneous bacterial peritonitis (SBP): • Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow. • Normally, the abdominal cavity contains a very small amount of fluid that is able to resist infection well, and bacteria that enter the abdomen (usually from the intestine) are • killed or find their way into the portal vein and to the liver where they killed. • In cirrhosis, the fluid that collects in the abdomen is unable to resist infection normally. In addition, more bacteria find their way from the intestine into the ascites. • Therefore, infection within the abdomen and the ascites, referred to as spontaneous bacterial peritonitis or SBP, is likely to occur. SBP is a life- threatening complication. • Some patients with SBP have no symptoms, while others have no symptoms, • while others have fever, chills, abdominal pain and tenderness, diarrhoea, and worsening ascites. Bleeding from oesophageal varices: • In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart from the intestines and raises the pressure in the portal vein Portal hypertension. When pressure in the portal vein becomes high enough, it causes blood to flow around the liver through veins with lower pressure to reach the heart. The most common veins through which blood bypasses the liver are the veins lining the lower part of the oesophagus and the upper part of the stomach. As a result of the increased flow of blood and the resulting increase in pressure, the veins in the lower oesophagus and upper stomach expand and then are referred to as oesophageal and gastric • varices; the higher the portal pressure, the larger the varices and the more likely a patient is to bleed from the varices into the oesophagus or stomach. Bleeding from varices usually is severe and, without immediate treatment, can be fatal. • Symptoms- vomiting blood (the vomitus can be red blood mixed with clots or "coffee grounds" in appearance, the latter due to the effect of acid on the blood), passing stool that is black and tarry due to changes in the blood as it passes through the intestine (melena), and orthostatic dizziness or fainting (caused by a drop in blood pressure especially when standing up from a lying position). • Bleeding also may occur from varices that form elsewhere in the intestines, for example, the colon, but this is rare. Hepatic encephalopathy: • Some of the protein in food that escapes digestion and absorption is used by bacteria that are normally present in the intestine. • While using the protein for their own purposes, the bacteria make substances that they release into the intestine. • These substances then can be absorbed into the body. Some of these substances, for example, ammonia, can have toxic effects on the brain. Ordinarily, these toxic substances are carried from the intestine in the portal vein to the liver where they are removed from the blood and detoxified. • liver cells cannot function normally either because they are damaged or because they have lost their normal relationship with the blood. In addition, some of the blood in the portal vein bypasses the liver through other veins. • The result of these abnormalities is that toxic substances cannot be removed by the liver cells, and, instead, the toxic substances accumulate in the blood. • When the toxic substances accumulate sufficiently in the blood, the function of the brain is impaired, a condition called hepatic encephalopathy. • Symptoms: Sleeping during the day rather than at night (reversal of the normal sleep pattern). • Other symptoms include irritability, inability to concentrate or perform calculations, loss of memory, confusion, or depressed levels of consciousness. Ultimately, severe hepatic encephalopathy causes coma and death. Hepatorenal syndrome: • It is a functional problem in the kidneys, meaning there is no physical damage to the kidneys • The hepatorenal syndrome is defined as progressive failure of the kidneys to clear substances from the blood and produce adequate amounts of urine while other important functions of the kidney, such as retention of salt, are maintained. • If liver function improves or a healthy liver is transplanted into a patient with hepatorenal syndrome, the kidneys usually begin to work normally again. • This suggests that the reduced function of the kidneys is the result of either the accumulation of toxic substances in the blood or abnormal liver function when the liver fails. Hepatopulmonary syndrome: • some patients with advanced cirrhosis can develop hepatopulmonary syndrome. These patients can experience difficulty breathing because certain hormones released in advanced cirrhosis cause the lungs to function abnormally. • The basic problem in the lung is that not enough blood flows through the small blood vessels in the lungs that are in contact with the alveoli (air sacs) of the lungs. • Blood flowing through the lungs is shunted around the alveoli and cannot pick up enough oxygen from the air in the alveoli. • As a result the patient experiences shortness of breath • experiences shortness of breath, particularly with exertion • Hepatopulmonary syndrome: • Rarely, some patients with advanced cirrhosis can develop hepatopulmonary syndrome. • These patients can experience difficulty breathing because certain hormones released in advanced cirrhosis cause the lungs to function abnormally. • The basic problem in the lung is that not enough blood flows through the small blood vessels in the lungs that are in contact with the alveoli (air sacs) of the lungs. • Blood flowing through the lungs is shunted around the alveoli and cannot pick up enough oxygen from the air in the alveoli. • As a result, the patient experiences shortness of breath, particularly with exertion. Hypersplenism: The spleen normally acts as a filter to remove older red blood cells, white blood cells, and platelets (small particles that are important for the clotting of blood). The blood that drains from the spleen joins the blood in the portal vein from the intestines. As the pressure in the portal vein rises in cirrhosis, it increasingly blocks the flow of blood from the spleen. Liver cancer (hepatocellular carcinoma: • Cirrhosis due to any cause increases the risk of primary liver cancer (hepatocellular carcinoma). Primary refers to the fact that the tumour originates in the liver. • A secondary liver cancer is one that originates elsewhere in the body and spreads (metastasizes) to the liver.