Cirrhosis Flashcards
If a patient has normal platelets most likely they don’t have cirrhosis
What is liver cirrhosis?
Cirrhosis is a chronic liver disease characterized by fibrosis, disruption
of the liver architecture, and widespread nodules in the liver.
Irreversible (some expectation in early cases ).
Cirrhosis is a histological diagnosis
What the causes of liver cirrhosis?
1- aLcohol.
2- chronic viral hepatitis (B,C).
3- non alcoholic fatty liver disease.
4- immune: primary sclerosing cholangitis, autoimmune liver disease.
5- biliary: primary biliary cholangitis, secondary biliary cirrhosis, and cystic fibrosis.
6- genetics: heamochromatosis, Wilson’s disease, and a1-antitrypsin deficienty
7- cryptogenic( unknown).
8- chronic venous outflow obstruction
9- any chronic liver disease.
Th pathophsyology of liver cirrhosis?
Liver injury
Kupffer cells and hepatocytes.
Activated by cytokines Transforms the stellate cell into a myofibroblast-like cell, capable of producing collagen, pro-
inflammatory cytokines and other mediators that promote hepatocyte damage and tissue fibrosis Over years as progressive fibrosis
Cirrhosis can be classified histologically into?
1- Micronodular cirrhosis, characterised by small nodules about 1 mm in diameter and typically
seen in alcoholic cirrhosis.
2-Macronodular cirrhosis, characterised by larger nodules of various sizes. Areas of previous
collapse of the liver architecture are evidenced by large fibrous scars.
What are the clinical features of liver cirrhosis?
Some patients have no overt clinical findings, especially early in the disease.
Patients may have signs or symptoms suggestive of one or more of the complications of cirrhosis.
1- Hepatomegaly (although liver may also be small in HCV?)
• Jaundice
• Ascites
• Circulatory changes: spider telangiectasia( spider angioma or spider neavus) , palmar erythema,
cyanosis
• Endocrine changes: loss of libido, hair loss
*Men: gynaecomastia, testicular atrophy, impotence
* Women: breast atrophy, irregular menses, amenorrhoea
• Haemorrhagic tendency: bruises, purpura, epistaxis
• Portal hypertension: splenomegaly, collateral vessels, variceal
bleeding
• Hepatic (portosystemic) encephalopathy
• Other features: pigmentation, digital clubbing, Dupuytren’s
contracture.
also,
What are the features of chronic liver failure?
• Worsening synthetic liver
function:
Prolonged prothrombin time and Low albumin.
• Jaundice
• Portal hypertension.
• Variceal bleeding
• Hepatic encephalopathy.
*Ascites:
Spontaneous bacterial
peritonitis
Hepatorenal failue.
What are the investigation of liver cirrhosis?
Definitive diagnosis is histologic (liver biopsy)
other tests may be suggestive.
CBC:
o fall in platelet count <150 is the earliest finding.
o Rise in INR( prothrombin time test) .
o fall in albumin.
o Rise in bilirubin
Hypoglycemia but this is more often a feature seen in severe acute liver failure FibroTest: combination of various clinical and biochemical markers that can predict degree of fibrosis
Imaging
o U/S is the primary imaging modality but only finds advanced cirrhosis
o CT to look for varices, nodular liver texture, splenomegaly, ascites
o transient elastography (FibroScan®): non-invasive tool using elastography for measuring liver compliance (variable
availability)
Gastroscopy: varices or portal hypertensive gastropathy
How to manage liver cirrhosis?
Treat underlying disorder .
Maintenance of nutrition Decrease insults (e.g. alcohol cessation, hepatotoxic drugs, immunize for hepatitis A and B if nonimmune) .
Follow patient for complications (esophageal varices, ascites, HCC)
Prognosis: Child-Pugh Score and MELD score
Liver transplantation for end-stage disease; use MELD score (e.g. MELD ≥15)
Cirrhosis has a lot of complications, describe each one using numbers like
1- portal hypertension?
Clinical features :
Liver cirrhosis symptoms
o Bleeding
o Hematemesis
o Melena
and Hematochezia.
*Diagnose:
Based on above features.
Paracentesis can help in diagnosis.
*Treatment :
ABC
Blood transfusion if need it
Endoscopy
Transjugular intrahepatic portal-systemic shunt
(TIPS)
- Esophageal/gastric Varices?
Caused by portal hypertension.
Clinical features :
Massive hematemesis Melena
Exacerbation of hepatic encephalopathy .
Treatment :
ABC
IV antibiotics
IV octreotide
Urgent upper GI endoscopy :
o variceal ligation
o sclerotherapy.
o Cautery
Give nonselective β-blockers (propranolol, timolol,
nadolol) as long-term therapy to prevent rebleeding.
3- ascites?
Accumulation of fluid in the peritoneal cavity due to portal HTN.
Clinical features:
abdominal distention
shifting dullness
fluid wave.
Diagnostic paracentesis : Indications include new-onset ascites
worsening ascites
suspected spontaneous bacterial peritonitis (SBP):
o Examine cell count
o ascites albumin
o Gram stain, and culture to rule out infection
o Measure the serum ascites albumin gradient. If it is
>1.1 g/dL, portal HTN is very likely. If <1.1 g/dL, portal
HTN is unlikely, and other causes must be considered..
Treatment:
Bed rest
a low-sodium diet
diuretics (furosemide and spironolactone)
Therapeutic paracentesis:
o tense ascites
o shortness of breath
Causes of ascites ?
o Measure the serum ascites albumin gradient. If it is
>1.1 g/dL, portal HTN is very likely. If <1.1 g/dL, portal
HTN is unlikely, and other causes must be considered.
- Hepatic encephalopathy?
Toxic metabolites (ammonia ) .
Occurs in 50% of all cases of cirrhosis, with varying severity.
Risk factor :
alkalosis,
hypokalaemia
sedating drugs
GI bleeding,
systemic infection
hypovolemia.
Clinical features:
Decreased mental function(Hepatic encephalopathy).
Asterixis (“flapping tremor)
Rigidity, hyperreflexia. Fetor hepaticus: musty odor of breath.
Treatment:
Lactulose
Rifaximin (antibiotic): kills bowel flora Diet :limit protein to 30 to 40 g/day.