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GI 2 > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

What are some common causes of Cirrhosis

A
  • Hepatitis B (D)
  • Hepatitis C
  • Alcohol
  • Hemochromatosis
  • Wilson’s Disease
  • Non-alcoholic steatohepatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
  • Alpha-1 antitrypsin deficiency
  • Budd-Chiari Syndrome
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2
Q

Examination findings of pt with Cirrhosis

A
  • Cachexia
  • Jaundice
  • Ascites
  • Spider angioma
  • Dupuytren’s contractures
  • Edema
  • Breast development
  • Testicular atrophy
  • Palmar erythema
  • Hair loss
  • Encephalopathy
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3
Q

Lab findings in pt with cirrhosis

A

• Elevated bilirubin
• Elevated transaminases
• Elevated alkaline
phosphatase
• Decreased albumin
• Elevated PT/INR
• Thrombocytopenia
• Leukopenia
• Renal insufficiency
• Hyponatremia

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4
Q

What type of muscle wasting do we see in pts with cirrhosis

A

muscle wasing and temporal wasting

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5
Q

What is specialy about spider angioma’s?

A

At level of collar and face, when you press on them, middle blanches and the legs fill out with blood

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6
Q

What are two things we see on pts hands with cirrhosis?

A

palmar erythema and dupuytrens contractures

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7
Q

What does a cirrhotic liver look like on CT?

A

smaller, nodular with increased fluid levels around it or ascites

spleen will also enlarge

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8
Q

What is the pahtology of hepatic fibrosis?

A

Stellate cells are activated and lay down collagen in space of Disse, obliterate space

Kupfner cells release cytokines and inflamatory cells

hepatocytes lose vili

***cause of cirrhosis is ongoing activation of stellate cells

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9
Q

What does it mean if pt is given a score of 5-7 for Child Pugh Score

A

Normal or health cirrhotic liver; no acites, no encephalopathy, normal INR and bilirubin

pts it compensated

Survival is 70-75%

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10
Q

What does it mean if pt is given a score of 7-9 for Child Pugh Score

A

They are cirrhotic and can control ascites with diuretics and enchephalopty with lactulose, they are decompensated with elevated INR and albumin

Survival is 40-45%

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11
Q

What does it mean if pt is given a score of >9 for Child Pugh Score

A

Pt has elevated albumin and INR, poorly decompensated, ascites not controlled with diuretics and encephalopty not much better with lactulose

survival 10-15% 5 yrs

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12
Q

New model for End stage liver disease and why its better

A 
MODEL FOR END-STAGE
LIVER DISEASE (MELD)

*only uses the INR, bilirubin, creatine

–ascites and encephalopty are subjective

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13
Q

At what MELD score does 3 month survival go down?

A

starts to go down at 15 then big drop around 25

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14
Q

What happens in pre-hepatic portal hypertension? What vein is involved?

A

involves the portal vein before entering liver; puts at risk for portal vein thrombosis bc pressure will increase. Liver fnx normally bc still getting blood from hepatic artery

== pre-hepatic portal hypertension

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15
Q

What happens when we have portal hypertension that is Intra-hepatic?

A

Leads to Cirrhosis; this creates pressure issue across the sinusoids of portal and hepatic veins

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16
Q

What do we worry about with post-hepatic portal hypertension?

A
  • Post-hepatic; blood cant drain out of liver; get big increase in pressure!
  • Hepatic vein thrombosis (Budd-Chiari Syndrome) if you have coag issues
  • Right heart failure
  • Valvular heart disease
17
Q

COMPLICATIONS OF CIRRHOSIS

A
  • Variceal bleeding
  • Ascites
  • Spontaneous bacterial peritonitis (SBP)
  • Hepatorenal Syndrome
  • Hepatopulmonary Syndrome
  • Hepatic encephalopathy
18
Q

What is the reason we see varices in intra-hepatic portal HTN?

A

Increase pressure in liver may be d/t of scarring of sinusoids from cirrhosis, this creates high pressure for blood. Blood choices low pressure path instead of liver like the esophageal varies or other accessory veins that can rupture with high blood traffic

19
Q

What happens to spleen in cirrhosis?

A

Spleen increases in size because of high pressure in the liver and gets redirected to spleen or backed up.

see more sequestering of platelets; thrombocytopenia and leukopenia

20
Q

What do you use on esophageal varices to prevent bleeding?

A

• Use non-selective B-blockers (propanolol, nadolol)
 Decrease cardiac output by blocking B-1 receptors
 Produce splanchnic vasoconstriction by B-2 blockade

Decreases risk of first bleed, rebleeding
and increases survival

21
Q

• Use non-selective B-blockers (propanolol, nadolol)
 Decrease cardiac output by blocking ___receptors
 Produce splanchnic vasoconstriction by___ blockade

A

B-1

B-2

22
Q
A
23
Q

What do you use to treat ACTIVE variceal hemorrhage?

A

Somatostatin analogues: Octreotide!!!

vasopressin and terlipressin work as well

~ do rubberbanding as well for those that havent ruptured

24
Q

What causes asictes in cirrhotic pt?

A

Increases R to portal flow–> portal HTN–> Splanchnic Arterial VasoD

– > Decreases effective circulation volume –>

Activates vasoconstriction and Anti-naturatetic peptide = water +Na retention

Causes volume expansion==> Ascites

25
Q

What factors are released in response to decreased circulating blood volume?

A

RAAS, vasopressin, ANaturtetic peptide

26
Q

Cirrhosis leads to decreased circulating volume causing releases of:

Vasopressin causing:

Renin-angiotensin Aldosterone:

Together both cause:

A

Vasopressin: water retention

renin-angiotensin/aldosterone: Na retention

Ultimately more Water retention > Na retention = Hyponatremia

27
Q

Recommended Tx for Ascites

A

• 2000 mg sodium restricted diet
• Diuretics
 spironolactone (aldactone), inhibits aldosterone~~ acts distal convoluted tuble
 furosemide (lasix)~~ asceniding tubule

28
Q

How do patients with Spontaneous Bacterial peritonitis present and what agents cause this?

A

Mostly with abdominal pain and fever

When gram (-); E.coli, Streptococci, Klebsiella ~ bugs from GI flora

29
Q

What happens in Hepatorenal Syndrome from cirrhosis?

A

Over time urine output decreases and serum creatinine increases

kidney biopsy will be normal, the kidney is just underperfused and responding normally.

30
Q

In Acute tubular necrosis:

Urine sodium:

Urine micro:

CVP:

A

urine sodium: >20

Urine micro: Cell debris

CVP: Normal

31
Q

Pre-Renal

Urine Na:

Urine Micro:

CVP:

A

Urine Na: <10

Urine micro: normal

CVP: Low

32
Q

Hepatorenal syndrome

Urine Sodium:

Urine Micro:

CVP:

A

Urine Na: <10

Urine micro: normal

CVP: low

33
Q

What is going on in hepatopulmonary syndrome?

A

Dilation of alveoli; have decreased pressure in lung meaning less driving pressure

34
Q

Pathophysiology of hepatic encephalopathy

A

Gut derived neurotoxins–> Hepatic insufficiency OR Hepatic bypass –>

Crosses BBB–>

CNS changes

35
Q

Symptoms of hepatitis encephalopthy

A

Asterixisis, change consiousness, behavior change

36
Q

What is used as a Tx for hepatic encephalopthy?

A

Lactulose: decreases the pH to make bacteria unfavorable environment and increase cathartic effect

Rifaximin also used, Lactulose prescribed 1st and this added if lactulose doesn’t help

***takes up to 2 weeks to get better

37
Q

What two things result from Fulminant liver failure?

A

Acute liver fail: hepatocyte necrosis; coagulopathy + encephalopathy

Cerebral edema; liver cant metabolize ammonia

38
Q

What is the mechanism of cerebral edema seen in fuminant liver failure?

A

ammonia and glutamate converted by action of
glutamine synthetase into glutamine by brain astrocytes
o astrocyte swelling leads to cerebral edema
o cerebral herniation is leading cause of death

GI 2 (12 decks)

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