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LIVER (SPECIAL IX (urine, faeces, haematological investigations - rbc…

- - - - as a cause of GI haemorrhage
      - as one of the causes of ascites
        
        CAUSES OF ASCITES
        
        heart failure
        
        renal failure
        
        Carcinomatosis eg ovarian malignancy
        
        chronic peritonitis eg tuberculous
        
        liver failure and portal HTN
        
        pancreatitis
      - ddx of jaundice or hepatomegaly
      - treatment
        
        treat uncomplicated portal htn involves treatment of the underlying condition eg abstinence of etoh, treat underlying viral infection, metabolic condition or autoimmune liver disease
        
        if large oesophageal varices are visible on endoscopy, prophylaxis with medication or band ligation of varices is performed, since first episode of variceal haemorrhage is associated with a 15-20% mortality
        
        Manageemnt of haemorrhage from gastro-oesophageal varices
        
        encephalopathy may be precipitated by absorbing meal of blood within intestine
        
        prophylaxis against haemorrhage varices- beta blocker = reduce splanchnic blood flow and lower portal venous pressure
        endoscopic band ligation in larger varices
        
        establishing the diagnosis
        
        not necessarily varices
        
        prone to bleeding from gastric erosions and commonly affected by peptic ulceration
        
        immediate treatment
        
        airway protection, emergency resuscitation, stabilise prior to endoscopy
        
        prevent aspiration - pts with liver disease have impaired consciousness = risk of aspirate
        
        rescusitation with fluid and blood - if coag abnorm give FFP
        
        antimicrobial therapy- 3rd gen cephalosporin
        
        STOPPING HAEMORRHAGE
        
        IV terlipressin - vasopressin analogue = reduce portal venous pressure and temporary cessation of bleeding by mesenteric arteriolar constriction
        
        endoscopic variceal band ligationor sclerotherapy to oesophageal varices
        
        cyanoacrylate injection into gastric varices
        
        balloon tamponade
        
        transjugular intrahepatic portosystemic shunt (TIPS)
        
        Surgical portocaval shunt - anastamose portal vein to IVC or splenic vein to left renal vein - ow superseded by TIPS - common complication of shunts when anastamosis made between portal and systemic circ is hepatic encephalopathy
        
        oesophageal transection
        
        TREATING ASCITES
        
        diuretic - spirinolactone often combined with a thiazide or loop diuretic
        
        paracentesis
        
        diet - low Na, high protein
        
        TIPS
  - - - inferior vena cavagram - can demonstrate hepatic venous occlusion
      - portal pressure measurement
      - liver biopsy - determine cause of cirrhosis
- - - - primary biliary cirrhosis
      - primary sclerosing cholangitis
      - autoimmune chronic liver disease
    - - Fe overload - haemachromatosis
      - Cu overload - wilson's disease
      - NAFLD
      - alpha1 antitrypsin associated liver disease
    - - budd chiari syndrome (hepatic venous occlusion)
      - severe chronic congestive cardiac failure
    - - 2o to prolonged biliary obstruction (2o biliary cirrhosis)
      - cystic fibrosis
      - cryptogenic
      - parenteral nutrition related
  - - - mental changes, flapping tremor, hepatic coma
    - - arise from obstruction in portal drainage
        
        hepatic
        
        eg cirrhosis
        
        post hepatic
        
        congenital obliteration
        
        blockage of hepatic veins by tumour invasion
        
        idiopathic hepatic venous thrombosis in young adults of both sexes - this is a manifestation of a prothrombotic tendency, which may be hereditary or acquired due to myeloproliferative disease, other systemic conditions or drugs
        
        prehepatic
        
        occlusion by tumour or pancreatitis
        
        hepatic sarcoidosis
        
        portal vein thrombosis
        
        portal vein sclerosis
        
        congen malform
        
        normal portal pressure between 5 and 10 mmHg
        
        pathological effects
        
        4 important effects of portal HTN:
        
        splenomegaly
        
        ascites (in hepatic and post hepatic portal HTN only)
        
        the development of collateral portosystemic venous drainage
        
        the manifestations of hepatic failure (in severe cirrhosis)
        
        collateral channels
        
        caput medusae
        
        varices lead to potential GI haemorrhage
        
        splenomegaly
        
        result of portal congestion and hypertrophy of splenic subtance itself
        
        often assoc w/ haematological changes of hypersplenism: leucopenia and thrombocytopaenia
        
        anaemia accompanying splenomegaly can be accounted for by GI bleeding and is not necessarily a result of splenic enlargement
        
        ascites
        
        raised portal venous pressure
        
        serum albumin synthesis (via liver) is reduced = lower serum osmotic pressure
        
        splanchnic vasodilation = blood pools = systemic hypotension = renal hypoperfusion = trigger RAAS = retain water and Na
- - - - fibroalmellar carcinoma, uncommon variant of hepatoma affecting young adults and children
      - cholangiocarcinoma
        
        adenocarcinoma arising from bile duct
        
        present with jaundice and may complicate primary sclerosing cholangitis
        
        20% of 1o tumours
        
        if early amenable to extended liver resection
        
        relieve jaundice at ERCP
      - hepatocellular carcinoma
        
        common in central africa and south east asia
        
        80% of cases arise in pts with cirrhosis
        
        cirrhosis caused by
        
        haemachromatosis
        
        alcoholic liver disease
        
        hep c infection - may take 25 yrs after
        
        NAFLD
        
        hep b infection - the most common cause of HCC worldwide
        
        clinical features
        
        in absence of cirrhosis = massive liver swelling, weight loss, ascites possibly
        
        in presence of advanced disease - rapid deterioration, decompensation with encephalopathy ascites and impaired synthetic function
        
        SPECIAL IX
        
        serum alpha fetoprotein raised but not sens or spec for carcinoma, rises in other diseases
        
        cross sectional imaging US and contrast enhanced CT or MR confirm tumour presence
        
        selective hepatic angiography distinguish generative nodules from small HCCs or reveal multifocal
        
        TREAT
        
        in absence of cirrhosis, 1o hepatocellular carcinoma confined to one lobe treat by hemi-hepatectomy
        
        in presence of cirrhosis, removing liver substance may precipitate hepatic decompensation and death = do radiofrequency ablation or transarterial chemoembolisation (TACE) - further lesions are likely to develop - only alternative is liver transplant
    - - systemic blood spread (from lung, breast, testis, melanoma, etc)
      - direct spread (from gallbladder, stomach and hepatic flexure of colon)
      - portal spread (from alimentary tract_
      - CLINICAL EFFECTS
        
        hepatomeg
        
        jaundice
        
        hepatic failure
        
        portal vein obstruction --> varices and ascites
        
        IVC obstruction --> leg oedema
      - resection of these tumours not appropriate in disseminated malignancy
        but maybe when deposits can be surg excised leaving adequate residual liver