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  • nitrogenous wastesevere liver disease
  • Glycogenolysisgluconeogenesis
  • Chronic liver disease in the clinical context is a disease process of the liver that involves a process of progressive destruction and regeneration of the liver parenchyma leading to fibrosis andcirrhosis.
  • at the University of Malaya Medical Centre.2006
  • Indeed, patients with hepatitis C may have chronic hepatitis for as long as 40 years before progressing to cirrhosis
  • Portosystemic vascular shunts are anomalous (abnormal) blood vessels that shunt blood away from the liver. This diversion of blood leads to liver failure and the collection of toxins in the blood, which most frequently cause behavioral changes, seizures or coma.
  • Gallstones and CholecystitisCholedocholithiasischolangitis
  • females are twice as susceptible to alcohol-related liver disease, and may develop alcoholic liver disease with shorter durations and doses of chronic consumption. The lesser amount of alcohol dehydrogenase secreted in the gut, higher proportion of body fat in women, and changes in fat absorption due to the menstrual cycle may explain this phenomenon
  •  inflammation of the liver with concurrent fataccumulation in liver
  •  It protects tissues from enzymes of inflammatory cells
  • Cirrhosis

    1. 1. MED STUDENT OF UniSZA CIRRHOSIS Nurfarhana binti Lazim Nazihah bt Mohamad Siti Aisyah binti Mat Jusoh Noor Azira binti Sharif Siti Hamidah binti Mahbud
    2. 2. LIVER • the second largest organ and the largest gland • predominantly occupies the right hypochondrium but the left lobe extends to the epigastrium • shape: prism or wedge • is pinkish brown in color, with a soft consistency, and is highly vascular and easily friable
    3. 3. • covered by peritoneum with the exception of the ‘bare area’. • the upper surface of the liver is percussed at the level of the fifth intercostal space • the anterior surface is separated from the inferior (visceral) surface by a sharp anterior (inferior) border that is clinically palpable.
    4. 4. Segmental Division Anatomical division Physiological division divided by Falciform ligament (ant) Ligamentum venosum (post) Fossa for gall bladder Fossa for IVC
    5. 5. • The liver has a unique dual blood supply (about 1500 mL/min) both from the proper hepatic artery (20-40%) and from the portal vein (60-80%)
    6. 6. • formed of hexagonal lobules with a central vein in the center and portal triad at the corners. • plates are separated by blood sinusoids lined by endothelium and contain VonKupffor cells. • hepatocytes at the periphery of the lobules facing portal tracts are called the limiting plates.
    7. 7. Portosystemic anastomosis Gastroesophageal junction Left gastric vein Around umbilicus Anal area Paraumbilical vein Azygos vein Superior rectal vein Middle & inferior rectal vein Veins of anterior abdominal wall
    8. 8. Physiology of the liver FUNCTIONS OF THE LIVER
    9. 9. PROTEIN METABOLISM synthesis and storage • the liver is the principal site of synthesis of all circullating protein apart from γ-globulin which are produced in the reticulo endothelial system. • the liver receives amino acid from the intestine and muscles and, by controlling the rate of gluconeogenesis and transamination, regulate levels in the plasma. •Plasma cotains 60-80 g/L of protein, mainly in the form of albumin, globulin and fibrinogen
    10. 10. • albumin has a half life of 16-24 days, and 10-12 g are synthetized daily. • its main function are: - to maintain the intravascular oncotic ( colloid osmotic) pressure - to transport water- insoluble substances such as *bilirubin, *hormones *fatty acid *drugs • reduced synthesis of albumin over prolonged periods  hypoalbuminaemia ( in chronic liver disease and malnutrition) •Hypoalbuminaemia also found in : - hypercatabolic states ( trauma with sepsis) - diseases where there is an excessive loss ( nephrotic syndrome, protein losing enteropathy )
    11. 11. • transport or carrier proteins such as transferrin and caeruloplasmin, acute phase and other proteins such as: - α1- antitrypsin - α- fetoprotein are also produced in liver. • the liver also synthesized all factors involved in coagulation ( apart from one-third of factor VII ) that is : - fibrinogen - prothrombin - factors V,VII,IX,X and XII - protein C and S - antithrombin - complement system • the liver stores: - large amounts of vitamins, particularly A, D and B12 - lesser amounts of others vitamin K and folate - also minerals ( iron in ferritinhaemosiderin and copper
    12. 12. Degradation (nitrogen excretion) This is the major pathway for the elimination of nitrogenous waste Failure of this process occurs in severe liver disease
    13. 13. CARBOHYDRATE METABOLISM Major function of the liver : - Glucose homeostasis - Maintenance of blood sugar Liver stores – 80 g of glycogen Immediate fasting state Prolonged starvation • blood glucose mantained by glycogenolysis or by gluconeogenesis Ketone bodies and fatty acids • source of gluconeogenesis - lactate - pyruvate - amino acids from muscle (mainly alanine and glutamine) - glycerol from lipolysis of fat stores
    14. 14. LIPID METABOLISM Fats are insoluble in water and are transported in the plasma as protein lipid complexes ( lipo proteins) The liver has a major role in the metabolism of lipoproteins It synthesizes : •VLDLs •HDLs •LCAT • IDLs • LDLs • triglycerides ( mainly of dietary origin) • Cholesterol ( dietary origin )
    15. 15. FORMATION OF BILE • Bile secretion and bile acid metabolism bile consist of water , electrolytesbile acids, cholesterol,phospholipids and conjugated bilirubin • bilirubin metabolism Bilirubin is produced mainly from the breakdown of mature red cells in the kuffer cells of the liner and in the reticuloendothelial system
    16. 16. HORMONE AND DRUG INACTIVATION •The liver catabolizes hormones such as: - insulin - glucagon - oestrogens - growth hormone - glucocorticoids - parathyroid homones • it is the major site for the metabolism of drugs and alcohol
    17. 17. IMMUNOLOGICAL FUNCTION The liver act as ‘sieve’ for the bacterial and other antigens carried to it via the portal tract from the gastrointestinal tract - kuffer cell ( macrophage, sp. Memb. Receptor for degrade without ab ) - the reticulo endothelial sys.  tissue repair - T and B lymphocyte interaction - cytotoxic activity in disease processes ligands ag
    18. 18. Liver Cirrhosis BY: SITI AISYAH MAT JUSOH
    19. 19. cirrhosis • Consequence of chronic liver disease characterized by replacement of liver tissue by diffuse hepatic fibrosis, scar tissue and regenerative nodules • The liver architecture is diffusely abnormal and this interferes with liver blood flow and function • Occur at any age, has significant morbidity and is an important cause of hepatic death
    20. 20. Epidemiology • According to World Health Organization (WHO) every year 34 million people are infected by Hepatitis C. About 150 million people are chronically infected and at risk of developing liver cirrhosis and/or liver cancer. And more than 350,000 people die every year from Hepatitis C-related liver disease. • In Malaysia, according to the Malaysian Liver Foundation (MLF), an estimated 2.5 million people suffer from chronic Hepatitis, and this doesn’t include other serious liver afflicted diseases such as Jaundice, Alcoholic liver disease (ALD), Non-Alcoholic fatty liver disease (NAFLD) and Liver Cirrhosis brought about by toxins from everyday products and alcohol consumption.
    21. 21. • Indian had a high prevalence of alcoholassociated chronic liver disease • Hepatitis B was the predominant etiology in Malay and Chinese compared to Indians • Hepatitis C cirrhosis was highest in Malay University of Malaya Medical Centre(2006)
    22. 22. pathogenesis • Cardinal features of cirrhosis: – an increase in fibrous tissue – progressive and widespread death of liver cells – inflammation leading to loss of the normal liver architecture
    23. 23. • Following liver injury, stellate cells in space of Disse are activated by cytokines and their receptors, reactive oxygen intermediates and other paracrine and autocrine signals produced by Kupffer cell, activated platelets and hepatocytes • This transform stellate cell into myofibroblast-like cell, capable of producing collagen, proinflammatory cytokines and other mediators which promote hepatocyte damage and cause tissue fibrosis • The progression of liver injury to cirrhosis may occur over weeks to years
    24. 24. • Destruction of liver architecture causes distortion and loss of normal hepatic vasculature with the development of portosystemic vascular shunts and the formation of nodules • It evolves slowly over years to decades and normally continues to progress even after removal of the aetiological agent
    25. 25. • Can be classified histologically into two types: – Micronodular cirrhosis – Macronodular cirrhosis
    26. 26. Micronodular cirrhosis characterised by small nodules about <3mm in diameter and seen in alcoholic or biliary tract disease
    27. 27. Macronodular cirrhosis characterised by larger nodules of various sizes and normal acini may be seen within larger nodules, areas of previous collapse of the liver architecture are evidenced by larger fibrous scars. This types often seen following chronic viral hepatitis
    28. 28. Etiology Common Others • • • • • Biliary cirrhosis: primary or secondary • Autoimmune hepatitis • Hereditary Haemochromatosis • Hepatic venous congestion • Budd Chiari Syndrome • Wilson’s Disease • Drugs • Alpha 1 Antitrypsin deficiency • Cystic Fibrosis • Galactosemia • Glycogen storage disease • Veno-occlusive disease • Idiopathic (Cryptogenic) Alcohol Hepatitis B Hepatitis C Non-alcoholic fatty liver disease
    29. 29.  Long-term heavy drinking of alcohol – Estimated that the development of cirrhosis requires, on average, the ingestion of 80 grams of ethanol daily for 10 to 20 years – This corresponds to approximately one liter of wine, eight standard sized beers, or one half pint of hard liquor each day – Chronic consumption of alcohol  secretion of proinflammatory cytokines (TNF-alpha, IL6 and IL8), oxidative stress, lipid peroxidation, and acetaldehyde toxicity  inflammation, apoptosis and eventually fibrosis of liver cells – females are twice as susceptible to alcohol-related liver disease, with shorter durations and doses of chronic consumption
    30. 30. Chronic viral hepatitis type B, C and D o Infection with the hepatitis C virus causes inflammation of the liver and a variable grade of damage to the organ that over several decades can lead to cirrhosis  the most common reason for liver transplant – Hepatitis D is dependent on the presence of hepatitis B and accelerates cirrhosis in coinfection
    31. 31. • Non-alcoholic steatohepatitis – fat builds up in the liver and eventually causes scar tissue – associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications • Primary biliary cirrhosis – more common in women – an autoimmune disease of the liver – slow progressive destruction of the small bile ducts of the liver, with the intralobular ducts (Canals of Hering) affected early in the disease. When these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the tissue
    32. 32. • Autoimmune chronic active hepatitis – uncommon condition that results in the body's immune system attacking and destroying liver cells. – abnormal immune response results in inflammation of the liver • Haemochromatosis – too much iron is absorbed by the body and the excess is deposited in the liver and cause liver to enlarge and becomes damaged, – Causes: hereditary haemochromatosis(HHC), a genetic disorder, and transfusional iron overload, which can result from repeated blood transfusion.
    33. 33. • Wilson’s disease – an autosomal recessive genetic disorder in which copper accumulates in tissues; this manifests as neurological or psychiatric symptoms and liver disease – When the amount of copper in the liver overwhelms the proteins that normally bind it, it causes oxidative damage through a process known as Fenton chemistry; this damage eventually leads to chronic active hepatitis, fibrosis (deposition of connective tissue) and cirrhosis
    34. 34. • Alpha-1 antitrypsin deficiency – Alpha-1 antitrypsin (A1AT) is a protein produced by the liver that protects the lungs – a genetic disorder that causes defective production of alpha 1-antitrypsin(A1AT), leading to decreased A1AT activity in the blood and lungs, and deposition of excessive abnormal A1AT protein in liver cells. – Because A1AT is expressed in the liver, certain mutations in the gene encoding the protein can cause misfolding and impaired secretion, which can lead to liver cirrhosis • Galactosaemia – the enzymes needed for further metabolism of galactose are severely diminished or missing entirely, leading to toxic levels of galactose 1-phosphate in various tissues resulting in hepatomegaly and cirrhosis
    35. 35. Symptom of liver disease Signs of chronic liver disease Complication of cirrhosis
    36. 36. Symptoms Acute liver disease • • • • Malaise Anorexia Fever Jaundice
    37. 37. Symptoms chronic liver disease • • • • • • right hypochondrial pain abdominal distension ankle swelling haematemesis and melaena pruritus breast swelling (gynaecomastia), loss of libido and amenorrhoea • confusion and drowsiness
    38. 38. Signs of chronic liver disease
    39. 39. INVESTIGATION OF CIRRHOSIS Siti hamidah bt mahbud
    40. 40. To assess severity Liver function test. Serum albumin and prothrombin time (marker for synthetic function of liver) •the outlook is poor with an albumin level below 28 g/L. •prothrombin time ^ = ^ severity of the liver disease
    41. 41. Liver biochemistry. Aminotransferases (ALT and AST) – present in hepatocytes and leak to blood when cell damage. • AST(mitochondrial enzyme: present in heart ,muscle ,kidney & brain)= ^ in hepatic necrosis, MI, muscle injury, congestive cardiac failure. • ALT (cytosomal enzyme: present in liver) = ^ in lever disease. Alkaline phosphate (ALP) –present in canalicular & sinusoidal membranes of the liver, bone, intestine, placenta. • ^ in cholestasis, may also ^ in metastases to liver and cirrhosis
    42. 42. can be normal, depending on the severity of cirrhosis. In most cases there is at least a slight elevation in the serum ALP and serum aminotransferases. Bilirubin = ^ in liver disease
    43. 43. Serum electrolytes. low sodium indicates severe liver disease due to a defect in free water clearance or to excess diuretic therapy. Serum creatinine. An elevated concentration > 130 μmol/L is a marker of worse prognosis.
    44. 44. Type of cirrhosis This can be determined by: ■ viral markers ■ serum autoantibodies Anti-mitochondrial antibody (AMA) = primary biliary cirrhosis ■ serum immunoglobulins ^ igM = primary biliary cirrhosis.
    45. 45. ■ iron indices and ferritin ■ copper & α1-antitrypsin Serum copper and serum α1-antitrypsin should always be measured in young cirrhotics.  Total iron-binding capacity (TIBC) and ferritin should be measured to exclude hereditary haemochromatosis; genetic markers are also available
    46. 46. Imaging Ultrasound examination. can demonstrate changes in size and shape of the liver. Fatty change and fibrosis produce a diffuse increased echogenicity. In established cirrhosis there may be marginal nodularity of the liver surface and distortion of the arterial vascular architecture.
    47. 47. CT scan CT scan showing an irregular lobulated liver. There is splenomegaly and enlargement of collateral vessels beneath the anterior abdominal wall (arrows) as a result of portal hypertension.
    48. 48. Endoscopy performed for the detection and Treatment of varices, and portal hypertensive gastropathy.. MRI scan. This is useful in the diagnosis of benign tumours such as haemangiomas. Liver biopsy necessary to confirm the severity and type of liver disease.
    49. 49. Complication & effect of cirrhosis • Portal hypertension and gastrointestinal haemorrhage • Ascites • Portosystemic encephalopathy • Hepatorenal syndrome • Hepatocellular carcinoma • Bacteraemias, infections • Malnutrition
    50. 50. Portal hypertension • Elevation of hepatic venous pressure gradient to > 5mm Hg. • It is caused by combination of 2 simultaneously occuring hemodynamic processes : 1. Increased intrahepatic resistance to passage of blood flow through liver 2. Increased splanchnic blood flow secondary to vasodilation
    51. 51. Portal hypertension
    52. 52. Ascitis • Accumulation of fluid within the peritoneal cavity • Most common complication of cirrhosis • Two-year survival of patients with ascites is approximately 50 percent
    53. 53. Ascitis • Assessment of ascites – Grading • Grade 1 — mild; Detectable only by US • Grade 2 — moderate; Moderate symmetrical distension of the abdomen • Grade 3 — large or gross asites with marked abdominal distension • Therapy: diuretics paracentesis
    54. 54. Portosystemic encephalopathy • Toxic substances (ammonia) bypass the liver via collaterals and gain access to the brain • Symptoms: lethargy mild confusion anorexia reversal of sleep pattern disorientation coma
    55. 55. Hapatorenal syndrome • acute renal failure coupled with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or severe alcoholic hepatitis) • characterized by: – – – – Oliguria benign urine sediment very low rate of sodium excretion progressive rise in the plasma creatinine concentration
    56. 56. Hepatorenal syndrome • Reduction in GFR often clinically masked • Prognosis is poor unless hepatic function improves • Nephrotoxic agents and overdiuresis can precipitate HRS
    57. 57. Management of cirrhosis
    58. 58. • Treatment options for cirrhosis depend on the cause and the level of liver damage. The goals of treatment are to prevent further liver damage and reduce complications. • When cirrhosis cannot be treated, the liver will not be able to work and a liver transplant may be needed
    59. 59. way to manage cirrhosis • Maintain a healthy lifestyle (eat a healthy diet and exercise regularly) • Limit salt in your diet to prevent or reduce fluid build up • Avoid raw shellfish • Stop drinking alcohol • Talk to your doctor about hepatitis A and hepatitis B vaccinations • Do not share needles, razors, toothbrushes or other personal items with others
    60. 60. REFERENCES BOOK • Kumar & Clarks; Clinical Medicine; 7th Edition WEB 1. Cirrhosis: Diagnosis, Management, and Prevention ; American family physician By : S. PAUL STARR, MD, and DANIEL RAINES, MD, Louisiana State University Health Sciences Center School of Medicine at New Orleans, New Orleans, Louisiana 2. Cirrhosis ; American liver foundation