CIRRHOSIS Flashcards

1
Q

Asterixis (liver flap), confusion and coma in a patient with liver cirrhosis is caused by what?

A

Hyperammonaemia

Liver normally converts ammonia into urea, this does not happen in liver damage

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2
Q

How does lactulose work to lower hyperammonaemia?

A
  • Synthetic disaccharide broken down in colon by bacteria to fatty acids
  • This lowers colonic pH which favours formation of NH4+ over NH3
  • NH4+ not absorbed → trapped in colon
  • Result ⇒ lower plasma ammonia concentrations
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3
Q

Explain why people with liver cirrhosis get the following symptoms:

  • Jaundice
  • Hypoglycaemia
  • Coagulopathy
  • Ascites/oedema
A
  • Jaundice: loss of bilirubin metabolism
  • Hypoglycaemia: loss of gluconeogenesis
  • Coagulopathy: loss of clotting factors
  • Ascites/oedema: loss of production of albumin
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4
Q

Which two forces control movement of fluid out of capillaries and into tissues?

A
  • Hydrostatic pressure: drives fluid out of capillaries
  • Oncotic pressure: proteins pull water into capillaries
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5
Q

Oestrogen levels rise in liver cirrhosis. Explain why and list three symptoms this would cause

A

Oestrogen is normally removed by the liver

  • Gynaecomastia in men
  • Spider naevi
  • Palmar erythema
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6
Q

What does cirrhosis of the liver cause to blood flow through it? What condition will this cause?

A

Obstructed blood flow through liver → increased pressure in portal vein → portal hypertension

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7
Q

In liver disease which normally constitutively expressed vasodilator is produced in large amounts?

► this causes which hallmark sign seen in cirrhosis?

A

Nitric oxide (NO)

Reduced systemic vascular resistance → reduced blood pressure

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8
Q

Patients with cirrhosis but without portal hypertension will not develop which condition?

A

Ascites

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9
Q

Define ascites. How would you diagnose?

how is it treated?

A

Abnormal buildup of fluid in peritoneal cavity

  • Diagnosis → physical exam, history, bloods, USS / CT, paracentesis
  • Paracentesis → needle inserted through abdominal wall and fluid removed
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10
Q

Which blood vessels are responsible for many of the side-effects caused by portal hypertension? Explain why. Give 4 clinical consequences of this condition

A

Venous collaterals​ → Portosystemic collaterals (varices) develop spontaneously via engorgment of pre-existing normally collapsed anastomoses between portal and systemic venous systems. Shunt blood away from liver to systemic system, to reduce portal pressure. Not sufficient for normalising pressure.

  • Umbilicus: caput medusa
  • Oesophagus: varicose, upper GI bleed
  • Stomach: upper GI bleed
  • Rectum: haemorrhoids
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11
Q

Where is most oesophageal venous blood drained? Where is the rest drained? How does this relate to formation of varices in portal hypertension?

A
  • Most drain into oesophageal veins → superior vena cava
  • Small amount drains to left gastric vein (AKA coronary vein) → portal vein

♦ There are normally small collapsed collaterals between oesophageal veins and left gastric vein. In portal HTN these become engorged.

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12
Q

How does portal hypertension cause gastric varices? Which blood vessels are involved?

A

Small and normally collapsed collateral vessels between left gastric vein and splenic vein become engorged in portal hypertension

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13
Q

Which veins are involved in the collaterals causing this condition?

A

Caput Medusa

paraumbilical and epigastric veins: collaterals become engorged in portal hypertension

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14
Q

What are haemorrhoids? Where do internal haemorrhoids occur? Which vessels are involved when they are caused by portal hypertension?

A
  • Vascular cushions
  • Help maintain faecal continence and ensure no liquid escapes through sphincter
  • If they become swollen → pathological
  • Seen in constipation, straining, raised intra-abdominal pressure (pregnancy, ascites)

Internal: Above dentate line

Vessels involved in haemorrhoids in portal HTN: superior rectal vein and middle/inferior rectal veins

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15
Q

Why do you many patients with liver cirrhosis have low platelets? 2 points

A

Hypersplenism caused by engorgement of spleen as a result of portal hypertension → splenic sequestration

Depressed thrombopoietin levels

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16
Q

A patient with acute onset abdominal pain, splenomegaly, all the symptoms of portal hypertension but a normal liver biopsy is likely to have which condition?

A

Portal vein thrombosis

17
Q

Give two reasons for new/worsening ascites in liver disease. How can you differentiate?

A
  • Portal hypertension
  • Malignancy causing leaky vasculature

► Sample ascitic fluid via paracentesis and work out difference between serum albumin and albumin in ascites

Serum albumin - ascites albumin = SAAG (serum ascites albumin gradient)

18
Q

What is the treatment for ascites?

A
  • Sodium restriction
  • Spironolactone (drug of choice), loops 2nd line
  • Paracentesis
  • TIPS: transjugular intrahepatic portosystemic shunt
19
Q

What infection are people with ascities more likely to get?

Which bacteria is normally implicated?

What symptoms would you expect to see?

How would you treat?

A
  • Spontaneous bacterial peritonitis: ascitic fluid infection
  • Gut bacteria → E. coli or klebsiella
  • Fever, abdominal pain, tenderness
  • Third-generation cephalosporin: achieves good levels in ascitic fluid
20
Q

Describe some of the ways liver cirrhosis is diagnosed

A
  • Gold standard: biopsy. Not if diagnosis clear from history, done only when it will change management
  • Imaging: may show small, nodular liver but not sensitive or specific
  • Clinical: ascites, low platelet, spider angiomata
21
Q

Which cells are activated in liver disease and proliferate to produce fibrous tissue? What do they normally do in the liver?

A
  • Stellate cells
  • Perisinusoidal cells, normally storage site for retinoids (vit A metabolites)
  • High yield fact: major contributor to liver cirrhosis