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Gastrology > Cirrhosis Complications > Flashcards

Cirrhosis Complications Flashcards

1
Q

Portal Hypertension definition

A

Increased resistance to flow and sustained increase in pressure

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2
Q

Aetiology

A

Pre hepatic - blockage of portal vein before the liver

  • Portal vein thrombosis
  • AV fistula

Hepatic - disruption or change of liver architecture

  • cirrhosis
  • alcoholic hepatitis

Post-hepatic - blockage of the venous system after the liver

  • Budd-chiaris syndrome
  • right-sided heart failure

Cirrhosis is the most common cause of PHTN

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3
Q

Anatomy of the portal vein

A

Union of superior mesenteric (from the gut) and splenic vein (from the spleen) and carries 75% of hepatic vascular inflow (25% via hepatic artery)

  • entera via the hilum (porta hepatits) and blood passes into the hepatic sinusoids via the portal tracts
  • leaves via the hepatic veins to join the inferior vena cava
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4
Q

Clinical features of portal hypertension

A

Could only be splenomegaly

  • GI bleeding from oesophageal or gastric varices - covered in separate topic
  • ascites
  • hepatic encephalopathy
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5
Q

Investigations

A
  • endoscopic examination of the upper GI tract - varices
  • USS- splenomgaly and indicate the cause
  • CT and MRI angio- portal vein clot
  • thrombocytopenia- hypersplenism
  • leucopenia
  • anaemia
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6
Q

Ascites definition

A

Abnormal collection of fluid in the peritoneal cavity and is common complication of portal hypertension

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7
Q

Pathogenesis of ascites

A
  • Na+ and water retention, due to peripheral and arterial vasodilation.
  • Decreased blood volume activates RAAS system + SNS
  • Local hydrostatic pressure increases due to PHTN - increased lymph production in hepatic and splanchinic regions
  • impaired synthesis of albumin by the liver
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8
Q

Clinical features of ascites

A
  • fulness in flanks
  • shifting dullness
  • tense ascites is uncomfortable and produces respiratory distress
  • pleural effusion - right sided
  • peripheral oedema
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9
Q

Investigations of ascites

A

A diagnostic aspiration of 10-20ml of ascitic fluid

Appearance -

  • Straw- serious effusion
  • bloody - trauma, malignancy
  • turbid - SBP
  • milky- malignancy, lymphoma

measure Serum-ascites albumin gradient - SAAG

SAAG >1.1g/dL causes

  • portal hypertension
    • Pre-hepatic: portal vein thrombosis
    • hepatic: cirrhosis, chronic hepatits
    • post-hepatic: right heart failure, constrictive pericarditis

SAAG <1.1g/dL

  • Other causes
    • hypoalbuminameia: nephrotic syndrome, malnutrtion
    • peritoneal disease: intra-abdominal malignacy SBP
    • others: pancreatitis, pancreatic psuedocyst

Tests

  • cells
    • cell count - raised SBP
    • MC&S - infective agent
    • cytology-malignant
  • albumin - SAAG
  • amylase - pancreatitis
  • glucose - decreased in TB and malignancy
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10
Q

Management of ascites

A
  • Diet - salt restriction (allows diuresis as pt no has more fluid than salt)
  • Diuretics
    • Spironolactone 100mg- diuretic action on dital part of nephron to inhibit aldosterone
    • Furosemide 20-40mg daily - loop diuretic
  • Approach is to lose about 0.5kg per day because the maximum rate of trasnfer between compartments is about 700ml/day. Too rapid causes intracascular volume depletion adn hypokalaemia
  • Paracentesis - resistant to medical therapy or severe, ascites drained. May cause depletion of serum albumin, so give albumin infusion
  • TIPS - transjugular intrahepatic portosystemic shunt - artifical channel within the liver that establishes communication between the inflow portal vein and outflow hepatic vein
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11
Q

Complications of ascites

A

Spontaneous bacterial peritonitis

  • Escherichia coli
  • diagnostic aspiraiton
  • empiral antibiotic therapy - 3rd generation cephalo (cefotaxime)
  • sepsis six protocol
  • patients recoverng from one episode of SBP should receive prophylaxis with iral norofloxacin
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12
Q

Encephalopathy

A

Neuropsychiatric syndrome which occurs with advanced hepatocellular disease, either chronic (cirrhosis) or acute (fulimant hepatic failure)

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13
Q

Pathophysiology of encephalopathy

A
  • normally, ammonia from porteins are metabolised in the liver
  • this cannot occur due to portal hypertension where the portal blood bypasses the liver via the collaterals and the toxix metabolites pass directly to the brain
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14
Q

Symptoms of encephalopathy

A
  • inability to concentrate
  • loss of memory
  • confusion
  • decreased conscioussness
  • increased tone and hyperreflexia
  • reversal of sleep pattern
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15
Q

Signs of heptatic encephalopathy

A
  • fetor hepaticus (sweet smell to breath)
  • flapping tremor of outstretched hand (asterixis)
  • inability to draw five point star (construcitonal apriaxa)
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16
Q

Investgations of hepatic encephalopathy

A

Clinical diagnosis

  • EEG
  • VERS
  • arterial blood ammonina
17
Q

Management of hepatic encephalopathy

A
  • identify and treat precipitating cause and minimise absoprtion of nitrogenous material
  • Laxative - oral lactulose (10-30ml day) is an osmotic purgative that reduces colonic pH and limitis ammonia absorption. It may be given via a nasograstric tube if the patient is comatose
  • dose should be titrated to result in 2-4 soft stools daily
  • Antibiotics- to reduce number of bowel organsisms and hence production of ammoia. Rifaximin or oral metronidazole
  • maintenance of nutrition with adequate calories - protein is restricted initially
18
Q

Hepatic pulmonary syndrome

A

Pulmonary vasodilation induced by NO. Insufficeint oxygen due to different pressure in capillary and alveoli. ALso causes difficult in breathing. Ultimately due to secretion of hormones by the liver suffering advanced cirrhosis such as endothelin 1

19
Q

Diagnosis of hepatic pulmonary syndrome

A
  • transthoracic echo - shows intrapulmonary shunting and ABGs confirm the arterial oxygen desaturation
20
Q

Treatment of hepatorenal syndrome

A
  • Liver transplant is only definitive treatment
21
Q

Haemorrhoids/ anorectal varices

A

Dilation of collateral submucosal vessels due to backflow in the vein of the rectum. Occurs due to PHTN which shunts bloo from the portal system through the portosystemic anastomosis into the systemic venous system.

22
Q

Pathogenesis of anorectal varices

A
  • blood from the superior portion of the rectum normally drains into the superior rectal vein and via the inferior mesenteric vein to the liver
  • Blood from the middle and inferior portions of the rectum is drained via the middle and inferior rectal veins
  • In portal hypertension, venous resistance is increased within the PVS, when the pressure in the portal veins increases above that of teh systemic, blood is shunted through the portosystemic anastomoses.
  • shunting of blood and consequential increase pressure through the collateral veins causes varicosities
23
Q

Treatment of anorectal varices

A
  • TIPS
  • treatment if underlying portal hypertension

Gastrology (19 decks)

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