Cirrhosis Flashcards

1
Q

If a patient has normal platelets most likely they don’t have cirrhosis

A
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2
Q

What is liver cirrhosis?

A

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

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3
Q

What the causes of liver cirrhosis?

A

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.

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4
Q

Th pathophsyology of liver cirrhosis?

A

 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

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5
Q

Cirrhosis can be classified histologically into?

A

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.

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6
Q

What are the clinical features of liver cirrhosis?

A

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,

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7
Q

What are the features of chronic liver failure?

A

• Worsening synthetic liver
function:
Prolonged prothrombin time and Low albumin.

• Jaundice
• Portal hypertension.
• Variceal bleeding

• Hepatic encephalopathy.
*Ascites:

Spontaneous bacterial

peritonitis

Hepatorenal failue.

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8
Q

What are the investigation of liver cirrhosis?

A

 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

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9
Q

How to manage liver cirrhosis?

A

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)

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10
Q

Cirrhosis has a lot of complications, describe each one using numbers like

A
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11
Q

1- portal hypertension?

A

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)

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12
Q
  1. Esophageal/gastric Varices?
A

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.

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13
Q

3- ascites?

A

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

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14
Q

Causes of ascites ?

A

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.

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15
Q
  1. Hepatic encephalopathy?
A

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.

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16
Q

5- Hepatorenal syndrome?

A

 Progressive renal failure in advanced liver disease,
secondary to renal hypoperfusion resulting from
vasoconstriction of renal vessels.
 This is a functional renal failure.

  • Clinical features:
     Azotemia( build up nitrogenous products like BUN, creatinine in the blood)
     Oliguria
     hyponatremia
     Hypotension  low urine sodium (<10 mEq/L).

Treatment:  Liver transplantation is the only cure.

17
Q

6- SBP (spontaneous bacterial peritonitis)?

A

Infected ascitic fluid; occurs in up to 20% of patients hospitalized for ascites. Has a high recurrence rate (up to 70% in first year).

Clinical features:
 Abdominal pain
 Fever
 Vomiting
 Rebound tenderness
 SBP may lead to sepsis.

*Diagnosis :
 Paracentesis and examination of ascitic fluid for WBCs
(especially PMNs), Gram stain with culture, and
sensitivities.
 WBC >500, PMN >250.  Positive ascites culture; culture-negative SBP is common as
well.

*Treatment:  Broad-spectrum antibiotic therapy: Give specific antibiotic
once organism is identified.  Clinical improvement should be seen in 24 to 48 hours

18
Q

7- coaguopathy?

A

 Prolonged prothrombin time (PT);
 PTT may be prolonged with severe disease.
 Vitamin K ineffective because it cannot be used by diseased liver.
 Treat coagulopathy with fresh frozen plasma.

19
Q

8- Hepatocellular carcinoma (HCC) ?

A

Present in 10% to 25% of patients with cirrhosis.

20
Q

Prognosis of cirrhosis?

A

The overall prognosis is poor.