Cirrhosis Flashcards

1
Q

Cirrhosis Facts

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2
Q

Causes of Cirrhosis

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3
Q

Complications of Cirrhosis

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4
Q

Normal Vascular Anatomy vs. Sinusoidal Portal Hypertension

A

Because the blood cannot flow through the portal vein it will flow around the liver via portal systemic collaterals. The portal venous system is separated from the systemic venous system. Thus the IVC is NOT impacted by portal hypertension.

This causes two problems:

  • varices
  • blood that does not flow through the liver does not get toxins removed from it. E.g. ammonia AND leading to hepatic encephalopathy.
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5
Q

Measuring Portal Hypertension

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6
Q

Decompensated Cirrhosis

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7
Q

Child-Turcotte-Pugh Classification

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8
Q

Ascites in Cirrhosis

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Portal hypertension leads to the pooling of blood in the splanchnic capillary bed.

This leads to reduced effective arterial volume because the blood cant get to the heat to be circulated through the body.

Due to the reduced arterial volume, the kidney senses a reduced blood volume assuming that the person is hypovolemic/dehydrated

BUT in this situation the patient is wet hypovolemic there is too much fluid its all sitting in the splanchnic capillary bed. The kidney will retain Na+ and H20 and lower oncotic pressure due to low albumin. This leads to the accumulation of fluid in the abdomen → ascites

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9
Q

Ascites in Cirrhosis

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10
Q

Serum-Ascites Albumin Gradient

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11
Q

Ascites: Abdominal Paracentesis

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12
Q

Complications of Ascites

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13
Q

What is the infection of the ascites fluid due to and the risk factors of Spontaneous Bacterial Peritonitis (SBP)?

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14
Q

SBP: Clinical Presentation

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15
Q

Management of Ascites due to Cirrhosis

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16
Q

Spontaneous Bacterial Peritonitis (SBP)?

A
17
Q

Variceal Bleeding

A
  • When HVPG > 10mm Hg, mostly >12
    • increased resistance to flow
      • hepatic fibrosis
      • intrahepatic vasoconstriction
    • and increase in portal blood flow
      • splanchnic vasodilatation
  • prevalence correlates with severity liver disease
    • 40% CTP A
    • 85% CTP C
  • Variceal hemorrhage occurs 5-10% yearly
  • predictors of bleeding
    • size of varices
    • decompensated cirrhosis
    • presence of red wale signs
18
Q

Laplace’s Law

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19
Q

Variceal bleeding treatment

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  • Prevention of rebleeding
    • repeat band ligation until eradication of varices
    • non-selective beta blocker
      • I.e. nadolol or propanolol
      • reduction in cardiac output (anti-b1 effect)
      • reduction in portal pressure through antagonism of endogenous b2 activity in splanchnic circulation
20
Q

Hepatic Encephalopathy: definition, symptoms, and pathogenesis

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21
Q

Stages of Hepatic Encephalopathy

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22
Q

Hepatic Encephalopathy Precipitants

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23
Q

Hepatic Encephalopathy Treatment

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24
Q

Hepatorenal Syndrome

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25
Q

Hepatorenal Syndrome Pathogenesis

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26
Q

Type 1 Hepatorenal Syndrome

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27
Q

Hepatorenal Syndrome Therapies

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28
Q

Hepatopulmonary Syndrome

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29
Q

Portopulmonary Hypertension

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