Au,cirrhosis

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Au,cirrhosis

  1. 1. Topic --- CIRRHOSIS
  2. 2.  Should be able to define cirrhosis Should be able to classify cirrhosis Should be able to work up CLD be able to mention complications of CLD
  3. 3.  Introduction -------------------- 1’ Definition ------------------------0.5’ Etiologic classification----------25’ Pathogenesis ---------------------3’ Clinical presentation ------------10’ Diagnosis --------------------------10’ Staging ----------------------------- 3’ Management outline--------------3’
  4. 4.  liver -- receives a dual blood supply; ~20% of the blood flow is oxygen-rich blood from the hepatic artery, and 80% is nutrient-rich blood from the portal vein arising from the stomach, intestines,pancreas,andspleen (almost from entire GI- through Superior / Inferior mesentry)
  5. 5.  hepatocytes, constitute 2/3 stellat(13% ) Kupffer cells endothelial cells and blood vessels, bile ductular cells, and supporting structures
  6. 6. Liver cells :1-- hepatocytes, constitute 2/3.has distinct polarity; Disse space & microvilli with passive and active uptake of nutrients, proteins, and other molecules. Plays vital roles in maintaining homeostasis and health; synthesis serum proteins (albumin, carrier proteins, coagulation factors, many hormonal and growth factors), the production of bile and its carriers (bile acids, cholesterol, lecithin, phospholipids), the regulation of nutrients (glucose, glycogen, lipids, cholesterol, amino acids), and metabolism and conjugation of lipophilic compounds (bilirubin, anions, cations, drugs) for excretion in the bile or urine.
  7. 7. 2-- Kupffer cells (reticuloendothelial system), lie within the sinusoidal vascular space and represent the largest group of fixed macrophages in the body.3---stellate (Ito,fat-storing ) 13%- (retinoid;vitA metabolite storage), not prominent unless activated, when they produce collagen and matrix in large.4-- endothelial cells and blood vessels, bile ductular cells, and supporting structures.
  8. 8.  Def : cirrhosis is irreversible hepatic damage ; histologically characterized by loss of hepatic architecture with fibrosis & nodular regeneration.
  9. 9. ALCOHOLHEPATOTROPHIC VIRAL HEPATITIS: - HCV -HBV -HV-Coinfection(HBV+HCV, HBV+HDV) -HV-Coinfection with HIV -HV-Alcohol abuseAUTOIMMUNE HEPATITIS (AIH)BILLIARY DISEASES:  PRIMARY(Psc/PBC)  SECONDARY: obstructive;cholangitis
  10. 10.  HERIDETARY METABOLIC DISEASES -HEMOCHROMATOSIS -WILSON’S DISEASE -ALPHA1-ANTITRYPSIN DEFICIENCY(AAT ) -CYSTIC FIBROSIS -GLYCOGEN DISEASEVASCULAR DISEASES: -VENO-OCCLUSIVE DISEASE(VOD) -BUDD-CHIARI SYNDROME(BCS) -CHF/ Percarditis( CARDIAC CIRRHOSIS)Drugs: Metotrixate, amiodarone,Toxins: Carbon tetrachloride, diethylmitrosamideIdiopathic Indian childhood cirrhosis Cryptogenic
  11. 11.  Alcoholic cirrhosis :Chronic & excessive ingestionRisk factors:A, quantity-M-60-80g/d for 10-20yrs F -20-40g alcohol/d for shorter NB-1beer =12g alcohol(ethanol)B, duration –chronic consumptionC, genderD, concurrent hepatitisE,genetic –genepolymorphism; ADHF, malnutrition –obesity – fatty liver
  12. 12. ADH ALDHAlcohol ---------- acetaldehyde --Acetate  highly reactive with protein(by reactive O2) & form adduct  Stellate cells ACTIVATION  COLLAGEN PRODUCTION
  13. 13. HCVPredictive factors for diseases progression :A-host factor ; age 40+ at acquisition,Cimminity –rapid pB-viral factors : d/t genotype,viral loadC- alcohol intakeD- HIV –coinfection  HCC
  14. 14.  Progression vary with :1-function of age(viralrepli/immunit-interplay)NB –perinatal infection  90%cirrhosis - adult infection  < 5%2 –alcohol consumption3 –concomitant HDV ,HIV infection
  15. 15.  HBsAg Anti-HBs IgM anti-HBc IgG anti-HBc HBeAg Anti-HBe viral copies/mL Interpretation + − + − + − + Acute infection; occasionally ―reactivation‖ of chronic hepatitis B − + − + − −/+ − Prior infection with immunity − + − − − − − Vaccination with immunity + − − + − + <105 Chronic hepatitis B without replication + − − + + − >105 Chronic hepatitis B with replication + − − + − + >105 Chronic hepatitis B with precore mutant Anti-HBc, hepatitis B core antibody; anti-HBe, hepatitis B e antibody; anti-HBs, hepatitis B surface antibody; HBeAg, hepatitis B e antig
  16. 16. Risk : obesity, hyperlipidemia,DM,Histology: fatty change & inflammation
  17. 17.  Primary biliary cirrhosis(PBS) : progressive granulomatous inflamm interlobular bile ducts damage cirrhosisCause : unknown ? Autoimmune ,Affect : 90% middle age women
  18. 18.  Primary sclerosing cholangitis(PSC)Progressive obliterative inflamm of intra & extra hepatic bile ducts fibrosis cirrhosisCause : unknown ? Autoimmune >70% asssociate with Ulcerative colitis
  19. 19.  Hemochromatosis:Autosom disorder of Fe metabol X-ed by high Fe absorption deposition in multiple organs (LIVER, PANCREASE, HEART ,PITIUTARY, JOINT)Affect : middle age men, loss through mensus protect women.
  20. 20.  Wilson’s Disease : Inherited disorder X-ed by failure to excrete copper(failure to prepare Cu,transportingATPase , for biliary excretion)  accummulation of toxicCu in LIVER&BRAINKayser-Fleischer ring : pathognomonic(usually) brownish pigment ring at the periphery of cornea
  21. 21.  Alpha 1-antitrypsin deficiency Inherited disorder causes abnormal folding of AATprotien  failure of Liver secretion  accumulationin hepatocytes  Liver damageNEONATE :cholestasisearlychildhood cirrhosisADULT :- cirrhosis HCC
  22. 22. NB:-lung is affected due to destrucion ELASTASEAAT -Elastin (protien)  destruction of protien
  23. 23. LIVER INJURY( CHRONIC) OF ANY CAUSE  ACTIVATION STELLATE,Endothelial,Kupffer,..Cells Collagen production Fibrogenesis(wound healing) 
  24. 24. Hepatocytes microvilli & Endothelial fenestration lost Micro/Macronodular Regeneration Metabolic &synthetic dysfunction of hepatocytes DECOMPANSETED LIVER  END STAGE
  25. 25.  1/3 asymptomatic History: Hx of alcohol, drug abuse, blood Tx, familly ds, Weakness, fatigue, wt loss, anorexia, flatulent dyspepsia,abdominal pain, impotence/↓libido, jaundice, leg/abdo m swelling, GI/skin hemorrhage
  26. 26.  may present with life-threatening complications: ~variceal hemorrhage, ~ascites, ~spontaneous bacterial peritonitis (SBP) ~hepatic encephalopathy.
  27. 27.  Physical signs: Fever Atrophic legs and arms Parotid enlargement Testicular atrophy Ascites & edema, hydrothorax/effusion Portal HTN/splenomegally Asterixis, confusion,fetor hepaticus
  28. 28.  Spider angiomas/nevi,  Abdominal collaterals(found in 50% pregnant)  Axillary & pubic hair Telangectasias loss Palmar erythema  Kayser-Fleischer ring( Pigmentation cornea) Purpura, white nails  Asterixic(flapping) Finger clubbing,  Testicular atrophy Dupytrens contructure
  29. 29.  Spiderangiomata/ spider telangiectasias-- are vascular lesions consisting of a central arteriole surrounded by many smaller vessels on trunk, face, and upper limbs. pathogenesis is incompletely understood, believed to result from alterations in sex hormone metabolism; in men increase in the estradiol/free testosterone rationot specific for cirrhosis can be seen during pregnancy , severe malnutrition. As a general rule, the number and size of spider angiomata correlate with the severity of liver disease . Patients with numerous and large spider angiomata may be at increased risk for variceal hemorrhage.
  30. 30.  Palmar erythema — exaggeration of the normal speckled mottling of the palm, believed to be caused by altered sex hormone metabolism . on the thenar and hypothenar eminences while sparing the central portions of the palm. not specific for liver disease ,can be seen in pregnancy rheumatoid arthritis, hyperthyroidism, and hematological malignancies.
  31. 31.  Muehrckes nails --paired horizontal white bands separated by normal color. caused by hypoalbuminemia .not specific for cirrhosis, also be seen in other conditions with hypoalbuminemia. Clubbing — angle b/n nail plate and proximal nail fold >180degree. severe form[grade4] is drum stick. more common in biliary causes of cirrhosis (particularly primary biliary cirrhosis) ,but not specific for liver disease.
  32. 32.  Dupuytrenscontracture — thickening and shortening of the palmar fascia with flexion deformity ,fibroblastic proliferation and disorderly collagen deposition with fascial thickening. The pathogenesis is unknown but may be related to free radical formation generated by the oxidative metabolism of hypoxanthine
  33. 33.  Gynecomastia — benign proliferation of the glandular tissue of the male breast and clinically by the presence of a rubbery or firm mass extending concentrically from the nipple(s). Fat deposition without glandular proliferation is termed pseudogynecomastia ( obese men). These two entities can be distinguished by having the patient lie on his back with his hands behind his head. The examiner then places his or her thumb and forefinger on each side of the breast, and slowly brings them together. caused by increased production of androstenedione from the adrenals, enhanced aromatization of androstenedione to estrone, and increased conversion of estrone to estradiol. Men may also develop other features reflecting feminization such as loss of chest or axillary hair and inversion of the normal male pubic hair pattern. Gynecomastia can be seen in a variety of conditions other than cirrhosis.
  34. 34.  Testicular atrophy — Hypogonadism is manifested by impotence, infertility, loss of sexual drive, and testicular atrophy. It is a feature seen predominantly in patients with alcoholic cirrhosis and hemochromatosis. More than one mechanism appears to be involved. In some cases, primary gonadal injury appears to be more prominent, as suggested by increased serum FSH and LH concentrations, while in others suppression of hypothalamic or pituitary function appears to have a primary role, as suggested by serum LH concentrations that are not elevated. The toxic effects of alcohol or iron may also contribute to its development.
  35. 35.  Hepatomegaly — cirrhotic liver may be enlarged, normal sized, or small. While the presence of a palpable liver may indicate liver disease, a non-palpable liver does not exclude it. When palpable, the cirrhotic liver has a firm and nodular consistency. Splenomegaly — caused by congestion as the result of portal HTN . other several ddx are possible.. Ascites — accumulation of fluid in the peritoneal cavity. The accuracy of physical findings is variable depending in part upon the amount of fluid present, the technique used to examine the patient, and the clinical setting (eg, detection may be more difficult in patients who are obese). In one study, the absence of flank dullness was the most accurate predictor against the presence of ascites; the probability of ascites being present was less than 10 percent in such patients . However, approximately 1500 mL of fluid had to be present for flank dullness to be detected. Shifting dullness is more specific.
  36. 36.  Caput medusae — The veins of the lower abdominal wall normally drain inferiorly into the iliofemoral system while the veins of the upper abdominal wall drain superiorly into the veins of the thoracic wall and axilla. When portal hypertension occurs as the result of cirrhosis, the umbilical vein, normally obliterated in early life, may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, causing them to become prominent. This appearance has been said to resemble the head (caput) of the mythical Gorgon Medusa.
  37. 37.  Dilated abdominal veins can also be seen in the IVCS and SVCS (if obstruction includes the azygous system) . In these conditions, collateral veins tend to be more prominent in the lateral aspect of the abdominal wall. One maneuver that has been proposed to distinguish vena caval obstruction from portal hypertension is to pass the finger along dilated veins located below the umbilicus to strip them of blood and determine the direction of blood flow during refilling. In portal-systemic collateral veins, the blood flow should be directed inferiorly away from the umbilicus in contrast to vena caval collateral vein flow in which the flow should be cephalad. However, the actual ability of this maneuver to discriminate between the two is poor since in both conditions the dilated veins may lack valves and thus have bidirectional blood flow .
  38. 38.  Fetor hepaticus — A sweet, pungent smell to the breath of a cirrhotic patient may occasionally be encountered. It is caused by increased concentrations of dimethylsulphide, the presence of which suggests underlying severe portal-systemic shunting . Jaundice — yellow coloring of the skin and mucus membranes that results from increased serum bilirubin. It is usually not detectable until Tbil > 3 mg/dL. The hyperbilirubinemia may also cause the urine to appear dark or "coca-cola" colored. Yellow discoloration to the skin can also be caused by excessive consumption of carotene ( carrots). But can be distinguished from jaundice by the absence of yellow discoloration in the sclera in the former.
  39. 39.  Asterixis— bilateral but asynchronous flapping motions of outstretched, dorsiflexed hands ,is seen in patients with hepatic encephalopathy, ?may also be seen in patients with uremia and severe heart failure.
  40. 40.  In most instances can be made accurately by a careful history, physical examination, and application of a few laboratory tests. In some circumstances, radiologic examinations are helpful or, indeed, diagnostic. Liver biopsy is considered the "gold standard" in evaluation of liver disease but is now needed less for diagnosis than for grading and staging disease.
  41. 41. LabLFT can be normal, >3-5x UNL or  1, AST(SGOT) ALT(SGPT) <40Iu/ml AST/ALT <0.8 , >2 in alcoholic LD 2,Alk ph - usually elevated but <3X theupper normal limit. Higher levels in psc &pbc
  42. 42. 3,Bilirubin (N T <1mg/dl;17microg/dl ,D<0.3 N in compensated,  in advanced cirrhosis4,Albumin-  as the synthetic function of the liverdeclines with worsening cirrhosis;helps to grade the severitof cirrhosis.But not specific for liver disease,can be seenCHF, NS, protein losing enteropathy, or malnutrition.
  43. 43. 5, Prothrombin time liver synthesize 11 blood coagulation proteins; Factor I (fibrinogen), II (prothrombin), V , VII , IX , X , XII and XIII can be measured individually or indirectly by more general measures of clotting ability such as the PT. CoagFactors ( liver capacity to synthesize) = PT prolongGlobulins- in cirrhosis(infection), IgG in AIH ,IgM in PBC
  44. 44. Serum Na+ — Hyponatremia is common in cirrhosis with ascites &severe in ESLD ; inability to excrete free water; high levels of ADHsecretion.Hematologic abnormalities Anemia — multifactorial ; acute and chronic GI blood loss, folate deficiency, direct toxicity due to alcohol, hypersplenism,BMsuppression,ACD (inflammation), & hemolysis may all contribute.
  45. 45. Thrombocytopenia - portal HTN congestive splenomegaly sequestration of up to 90 % of circulating platelet mass. -  thrombopoietinLeukopenia and neutropenia — due to hypersplenism
  46. 46. Imaging studies : U/S, Ctscan,MRI Angiography , ERCP/MRCP, UGIE,Echo LIVER BIOPSY
  47. 47.  Alcoholic liver disease- History of alcohol abuse , AST/ALT >2 Chronic hepatitis C- ELISA assay for anti-HCV ,PCR for HCV-RNA PBC- Antimitochondrial antibodies PSC holangitis - Strong association with IBD, cholangi AIH -Hypergammaglobulinemia ,AntinuclearASMA,ALKA Chronic hepatitis B - HBsAg and HBeAg and, HBV DNA Hereditary hemochromatosis- Family history of cirrhosis ,Serum ferritin & iron,transferritin satur>80% , TIBC ,biopsy- hepatic Fe index,genetic tes Wilsons disease - Family or personal history of cirrhosis at a young age ,serum ceruloplasmim,biopsy -Co AATdeficiency- Family or personal history of cirrhosis at a young age,serumAAT,phenotyping NASH - History of diabetes mellitus or metabolic syndrome, hepatic imaging , biopsy
  48. 48. parameter score 1 2 31.ASCITES Abscent Slight Moderat2.BILIRUBIN <2mg/dl 2-3 >33.ALBUMIN >3.5g/dl 2.8-3.5 <2.84.PT <4sec 4-6 >6 INR <1.7 1.7-2.3 >2.35.HENCEPH None Grade1-2 G3-4
  49. 49.  grade A- total score of 5-6 ;well-compensated disease ;100-85% of 1-2yr survival grade B- total score7-9 ;significant functional compromise ;80-60%of 1-2yr survival gradeC- total score 10-15 decompensated disease ;45-35% 0f 1-2yr survival.
  50. 50. goals :- Slowing or reversing the progression of liver disease- Preventing superimposed insults to the liver-Preventing and treating the complications-Determining the appropriateness and optimal timing for liver transplantation
  51. 51.  Abstinence from alcohol . Interferon therapy to HCVslows the progression,fibrosis &risk of HCC. Rx of chronic HB with lamivudinsignificant improvement in liver function and histology & risk of HCC Rx autoimmune hepatitis with immunosuppressive agents10yr survi 90 %
  52. 52.  Phlebotomy , Chelation ,Dietary restriction of iron – for HH Chelating –for wilson D
  53. 53. AVOID substance abuse; alcohol, acetaminophen ,NSAIDs hepatotoxic drugs & herbal remedies. Give Vaccination — against HAV & HBV can prevent a superimposed insult to a liver Pneumococcal vaccine yearly influenza vaccination
  54. 54. xumura ULFAADHA !
  55. 55. COMPLICATION OF END-STAGE CLD
  56. 56. AT THE END : Mention the complication. Rescribe the mechanism Work up principile Outline the managment
  57. 57.  Portal hypertension -------------------------5’ Variceal hemorrhage -----------------------10’ Ascites -----------------------------------10’ Spontaneous bacterial peritonitis ------10’ Hepatic encephalopathy ------------------10’
  58. 58.  Portalhypertension Variceal hemorrhage Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Hepatic encephalopathy Hepatopulmonary syndrome Hepatocellular carcinoma Coagulopathy malnutrition
  59. 59.  Def Causes Types consequence
  60. 60.  Def: hepatic venous pressure gradient (HVPG)> 5 mmHg.Portal pressure = Portal venous flow x portal venous outflow resistance -R blood flow - vasodilatation within the splanchnic vascular bed  splanchnic blood flow. Cause : cirrhosis-commonst >60% : noncirrhotic : ?idiopathic
  61. 61. 1 Prehepatic :Portal &/ or splenic vein thrombosis , : Massive splenomegaly (Bantis syndrome)2 Hepatic :commonst type 95%2a PresinusoidalSchistosomiasis –fibrosis,Congenital hepaticfibrosis2b Sinusoidal  Cirrhosis2c Postsinusoidalsinusoidal obstruction syndrome(VOD),BCS3 Posthepatic : IVC obstruction , : Budd-Chiari syndrome : Cardiac causes ;RCM Constrictive pericarditis
  62. 62.  1-- UGIB 2-- ascites 3—splenomegaly with hypersplenism.
  63. 63.  Def Location Risk Dx Rx
  64. 64. VARICES - are collateral vessels that develop because of PHT; 1/3of pts with cirrhosis & 1/3 of them will develop bleeding.LOCATION— -distal esophagus (commonst) ; thinnest coat and at risk to bleed, - stomach, -Rectum, - Umbilicus,…FACTORS  risk of bleeding : --PHTN >12mmhg ,-- severity of cirrhosis (Childs class),--size of the varix ,--location of the varix,-- endoscopic stigmata(red wale signs& …)
  65. 65. Endoscopy.Abdominal imaging, CT or MRI demonstrenodular lesionThrombocytopenia
  66. 66. a--Pharmacologic =nonselective beta blockade (propranolol ,nadolol )b--Endoscopic variceal band ligation(EVL) &/or variceal injection therapy (sclerotherapy)
  67. 67. a --- fluid and blood product replacementb ---medical ;1-somatostatin or Octreotide , Vasopressin= direct splanchnic vasoconstrictor, is given at dosages of 50–100 g/h by continuous infusion.c---surgical ;1-Balloon tamponade (Sengstaken-Blakemore tube or Minnesota tube)2- endoscopic therapy ( first-line to control active-vigorous bleeding by EVL & /or variceal injection therapy (sclerotherapy)3- transjugular intrahepatic portosystemic shunt (TIPS)under angiographic guidance
  68. 68. a---repeated variceal band ligation until varices are obliterated.b---adjunctive Beta blockade (for recurrent variceal band ligation ,But no need once obliteration achieved)c---TIPS
  69. 69.  Highrisk group to develop reccurrent variceal bleeding ? Prognosis of variceal bleeding ? Other causes for UGIB ?
  70. 70. Risk factors for recurrent variceal hemorrhage Age >60 years Severity of initial bleed Renal failure Severity of liver failure Ascites Hepatoma Active alcoholism Active bleeding on endoscopy Increasing varix size Red signs yes coagulopathy Portal pressures
  71. 71.  Def Mechanism Dx Rx
  72. 72.  def: pathologic accumulation of fluid in the peritoneal cavity mechanism: multifactors1] PORTAL HYPERTENSIONis the first step toward fluid retention in cirrhosis.>12 mmHg required.cirrhosis without PHT do not develop ascites ascites disappear if <12 mmHg■Portal hypertension exerts a local hydrostatic pressure hepatic and splanchnic production of lymph &transudation of fluid into the peritoneal cavity.
  73. 73. 2] Na RETENTION :splanchnic vasodilatation-Arterial underfilling- Activation Renin-Ang-Aldos -- Na retent-3] HYPOALBUMINEMIA : synthetic function of cirrhotic liver  Hypoalbuminemia   plasma oncotic pressure  loss of fluid from the vascular compartment into the peritoneal cavity.
  74. 74.  incidious abdominal distension ;( high Na diet,HCC ,splanchnic vein thrombosis Precipitate) Abdominal pain ; SBP Respiratory distress ( Rt pleural effussion ) Malnourish; muscle wasting and excessive fatigue and weakness. bulging flanks, fluid Waves ,shifting dullness +v ,sign of pleural effussion.
  75. 75.  abdominal imaging ; U/s , CT scan Paracentesis : AnalysisColor (clear,straw,cloudy,bloody,milky,brown)cirrhosis –straw/clear(if n-Bilir, protien)SBP –cloudyHCC –bloody
  76. 76. test1-Cell cout & diff - N >250  SBP2-Gram stain,AFB and culture -3-Protein -3.1 SAAG -3.2 [total protein]4-Cytology - for malignant cells.5-Amylase - to exclude pancreatic ascites
  77. 77. test1-Cell cout & diff - N >250 SBP2-Gram stain,AFB and culture -3-Protein- serum ascites-to-albumin gradient (SAAG) ; [total protein] in ascites is quite low in cirrhosis; <1 g/dLSAAG=serum alb minus ascitic albumin ( not ratio ) >1.1 g/dL indicates PHT-cirrhosis with 97%accuracy & High-gradient (transudative remains stable unless PHT <1.1 g/dl indicates abscence of PHT,Low-gradient (exudative) but infectious(opsonization) or malignant (peritoneal carcinomatosis, tuberculous peritonitis, pancreatitis, serositis, pyogenic peritonitis, and nephrotic syndrome)4-Cytology - for malignant cells.5-Amylase - to exclude pancreatic ascites
  78. 78.  Bilirubin — in brown ascites. As mentioned above, an ascitic bilirubin > of serum suggests bowel or biliary perforation into ascites Glucose — Lactate dehydrogenase Triglycerides — milky/ Chylous ascites has TG > 200 mg/dL
  79. 79.  dietary sodium restriction spironolactone at 100–200 mg/d- 400–600mg furosemide 40–80 mg/d- 120–160 mg/d repeated large-volume paracentesis(refractory ascites) TIPS (refractory ascites)liver transplantation prognosis of cirrhosis with ascites is poor, survive 2 years <50%
  80. 80.  LIST Other causes of ASCITES
  81. 81.  Def Etiology Precipitant Distinction from secondary BP Dx Rx
  82. 82.  Def:ascitic fluid infection without an evident intraabdominal surgically-treatable source. ETIOLOGIES ?
  83. 83.  Escherichia coli 43% Klebsiella pneumoniae 11% Streptococcus pneumoniae 9% Other streptococcal species 19% Enterobacteriaceae 4% Staphylococcus 3% Pseudomonas 1% Miscellaneous* 10%
  84. 84.  cirrhosis,& associated conditions Ascitic [total protein] <1 g/dL (<10 g/L) Prior episode of SBP Serum [total bilirubin] > 2.5 mg/dL Variceal hemorrhage malnutrition Proton pump inhibitors Nephrotic ascites
  85. 85.  Subtel- due to separation of visceral & parietal peritoneum Fever 69 Abdominal pain 59 Altered mental status 54 Abdominal tenderness 49 Diarrhea 32 Paralytic ileus 30 Hypotension 21 Hypothermia 17
  86. 86. Def : ascitic fluid infection in which there is a positive ascitic fluid bacterial culture and an ascitic fluid PMN count ≥ 250 cells/mm3 with an evident intraabdominal surgically- treatable source of infection .Two varieties :1--perforation peritonitis (eg, perforated peptic ulcer into ascites)2--nonperforation peritonitis (eg, perinephric abscesNB-mortality 100% if treatment consists only of antibiotics with no surgical intervention . And 80% if a patient with SBP receives an unnecessary exploratory laparotomy .
  87. 87. Clinical — both can be ( even frank perforation) subtle b/c peritoneum separation by AscitesAnalysis — PMN count ≥ 250 with two or more of[Total protein ] >1 g/dL (10 g/L)[ Glucose ]<50 mg/dL[ LDH >UNL for serumImaging studies — plain and upright abdo minal films water-soluble gut contrast studies( extravasation of contrastSBP-Rx response follow up --- with repeat analysis after 48hrs ; PMN is lower
  88. 88.  Ascitic fluid analysis :1] Cell count --- absolute PMNcount≥ 2502] Culture ---- positive3] SAAG ----- Low-gradient4] [Total protien] -----lowest[ ] ; < 1g/dl5] [glucose] > 50mg/dl6] LDH (released from lysed PMNs) --[43 +/- 20mU/mL ]7] [Amylase ]--- in pancreatitis and gut perforation8] [ bilirubin] if dark/brown ascites----if > serum value  choleperitoneum ;GBperforation
  89. 89.  1- third-generation cephalosporin?2-combination of ampicillin and gentamicin .Third-gener + metronidazolFor secondary BP
  90. 90. third-generation cephalosporin benefits over ampic/genta-combination:A-- A higher rate of resolution of the infection — 85 versus 56 %B--No /less nephrotoxicity versus 5 % with ampicillin- gentamicinC-- No superinfection versus 14 percent with ampicillin- gentamicin.
  91. 91.  Def Mechanism Precipitant Stages Rx
  92. 92.  Def : ?potentially reversible neuropsychiatric syndrome seconday to liver diseases CLD,END-STAGE Or acute fulminant hepatic failure.
  93. 93. Ammonia — cause in >90% + other neurotoxinsProduced--- colonic bacterial catabolism of nitrogenous source; ingested protein and secreted urea.  Enters the circulation via the portal vein Liver clears almost all by converting into glutamine & prevent entry into the systemic circulation In cirrhosis ,portal blood bypasses the liver via the collaterals and the toxicmetabolites pass directly to the brain ( impaired liver  blood ammonia ) Induced alteration of brain neurotransmitter balance - especially at the astrocyte-neurone interface
  94. 94.  PRECIPITANTS ?
  95. 95.  High dietary protein GI- haemorrhage Constipation Vomiting /Diarrhea Infection; SBP , sepsis Fluid and electrolyte ( k+ )disturbance due to:diuretic therapy,paracentesis Drugs (e.g. anyCNSdepressant) Benzodiazepines,Narcotics ,Alcohol Portosystemic shunt operations, TIPS Any surgical procedure Progressive liver damage Development of hepatocellular carcinoma
  96. 96. change in personalityconfusedCan be quite violent and difficult to manageOr very sleepy and difficult to arouseAsterixis "liver flap‖hepatic coma due Brain edema -herniation
  97. 97.  mainstay lactulose--, a nonabsorbable disaccharide eliminat nitrogenous source R x of precipitats ?Restriction of dietary protein neomycin + metronidazole =Poorly absorbed antibiotics as adjunctive therapies or alternative to lactulose rifaximin. ?Zinc supplementation Prognostic worse as stage progress
  98. 98.  refers === development of acute renal failure in advanced liver disease, severe alcoholic hepatitis, (less often) metastatic tumor, and acute fulminant hepatic failure from any cause. MECHANISM : portal hypertension -splanchnic vasodilatation - hypotension-induced activation of the renin-angiotensin and sympathetic nervous system- renal perfusion ( GFR )
  99. 99.  Type I HRS--- more serious type; progressive impairment in renal function and a significant reduction in creatinine clearance ( 50% )within in <2wks,serum Cr.2.5mg/dl , oliguria Type II HRS ; less severe. GFR and Cr
  100. 100.  midodrine --is a systemic vasoconstrictor alpha1–agonist-- octreotide -- inhibitor of endogenous vasodilator , in combination intravenous albumin liver transplantation prognosis is poor unless transplant can be achieved within a short period of time
  101. 101.  90% of primary hepatic malignancy One of the most common malignancies ,4th leading death , affecr men commonly 1 million/yr with MR=250,000/yr Liver cirrhosis, HBV, HCV are most important risk factors Most Asymtomatic or present with abdomen pain or liver failure s/s Px=survive 2-6 months if unRxed
  102. 102.  Causes of HCC: Viral infection: B,C,D; cirrhosis from HBV,HCV, HH --at highest risk, while AIH,NASH &Wilsons d lower risk.HBV even at carrier state is high risk. Toxins:Alcohol, aphlatoxin B1, tobaco,Thorium oxide, Vinyl chloride monomers Metabolic liver ds: hemochrom,alpha1,PCT,glycogen storageI, II Others: BCS, Liver flukes, androgeic anabolic hormones, etc
  103. 103.  S/S:nonspecific similar Hard irregular hepatomegally with bruit and cachexia and splenomegally Portal vein thrombosis Coagulopathy Multiorgan failure Portal HTN
  104. 104. Extrahepatic -- most common sites are lung, intraabdominal lymph nodes, bone, and adrenal gland; brain metastases are extremely rare . Extrahepatic metastases are more common in patients with intrahepatic tumors >5 cm in diameter
  105. 105.  DDX of primary hepatic malignancy: 1.Epithelial : HCC;cholangioca;bilary cystadenoca;Sq cell ca; mucoepidermoid ca 2. Mesenchymal: Angiosercoma, hemangioendothelioma, Leimyosarcoma, fibrosercoma, embryonal , sercoma, rhabdomyosercoma, Malignant schewanoma/ histosercoma, lymphoma
  106. 106.  3.Mixed tumors: Hepatoblastoma Mixed HCC &cholangiocellular Ca carcinsarcoma
  107. 107.  Treatment & prevention Quarterly U/s & AFP for CLD for early HCC DX RX: Ethanol, chemoembolz, resection, LTx, palliative care; RT, HormonalRx Mass HBV vaccination and CLD Rx for prevention
  108. 108. can be asymptomatic OR can present with complication of cirrhosisRUQ pain ,weight loss , early satiety, or a palpable mass in the upper abdomen.Obstructive jaundice r ,dyspnea ( metastases), Intraperitoneal bleeding ( tumor rupture)Hepato/splenomegaly with bruitParaneoplastic syndromes — hypoglycemia, erythrocytosis, hypercalcemia, se vere watery diarrhea,and cutaneous manifestation
  109. 109.  Patterns of metastatic spread —Extrahepatic -- most common sites are lung, intraabdominal lymph nodes, bone, and adrenal gland; brain metastases are extremely rare . Extrahepatic metastases are more common in patients with intrahepatic tumors >5 cm in diameter .
  110. 110.  Alpha-fetoprotein --- glycoprotein that is normally produced during gestation by the fetal liver and yolk sacr can pregnancy, with tumors of gonadal origin, and chronic liver disease ;acute or chronic viral hepatitisNORMAL=10 and 20 mcg/L >500 mcg/L in high risk group is suggest to HCCIMAGINGBIOPSY
  111. 111.  Surgical Livertransplant Radiotherapy/chemotherapy
  112. 112.  regulationof protein and energy metabolism catabolic, and muscle protein is metabolized,poor dietary intake, alterations in gut nutrient absorption, and alterations in protein metabolism.Dietary supplementation is helpful
  113. 113.  Coagulopathy is almost universal in cirrhosis.  synthesis of clotting factors and impaired clearance of anticoagulants. thrombocytopenia from hypersplenism  Vitamin K absorption – AFFECTdependent CF ( II, VII, IX, & X )
  114. 114.  anemia from --persplenism, hemolysis, iron deficiency, and perhaps folate deficiency from malnutrition. Macrocytosis Neutropenia from -hypersplenism.
  115. 115.  Osteoporosis- malabsorption of vitamin D & calcium ingestion
  116. 116.  HARRISON’S PRINCIPLES OF INT.MEDICINE 17th EDITION UpTODate 17.2 KUMAR CLINICAL MEDICINE 6th EDITION

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