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GI Final > Cirrhosis -Jenkins > Flashcards

Cirrhosis -Jenkins Flashcards

1
Q

What is cirrhosis? What does this lead to?

A
  • histologically=diffuse fibrosis and the conversion of normal liver architecture into structurally abnormal nodules
  • fibrosis: activation of hepatic stellate cells–> formation of inc amounts ofcollagenand other components of the extracellular matrix

–> dec in hepatocellular mass and function and alteration in blood flow

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2
Q

What does cirrhosis of the liver look like on ultrasound?

A

-ascities with a small nodular liver

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3
Q

Can cirrhosis be reversible?

A

In early stages, especially if it is due to HCV, it can be responsive to treatment

advanced stages =liver transplant

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4
Q

***What is the most common cause of cirrhosis in the United States?

A

Fatty liver d/t: #1 Hep C, #2 Alcoholic liver disease

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5
Q

What labs can be used for prognosis of end stage liver disease?

A
  • cholesterol ( inc INR)

- albumin (low is poor prognosis because made in liver)

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6
Q

***What can the AST and ALT be in cirrhosis? What do these labs indicate?

A

in cirrhosis, can be normal

indicate inflammation
highest AST and ALT in alcoholic hepatitis or NASH

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7
Q

What will cause a super elevated ALP?

A

biliary disease

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8
Q

What will bilirubin levels be in cirrhosis?

A

normal in well-compensated cirrhosis but will rise as cirrhosis progresses

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9
Q

***TRUE OR FALSE: Hepatitis B is the most common case of cirrhosis

A

FALSE (Hep C is, along with alcohol and fatty liver)

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10
Q

What are some complications of cirrhosis?

A
  • portal HTN –> hemorrhoids, esophageal varices, ascites, hypersplenism
  • ascites: excess fluid (lymph) in the peritoneal cavity
  • hepatorenal syndrome (renal vasoconstriction)
  • hepatopulmonary syndrome
  • hepatic encephalopathy
  • hyponatremia
  • malnutrition
  • osteoporosis
  • hypogonadism
  • fetor hepaticus (sweet, pungent breath)
  • Dupuytren’s contracture
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11
Q

What are the most common treatments for acute variceal bleeds? What procedure can be done to prevent re-bleeds?

A

band ligation and octreotide (a splanchnic vasoconstrictor)

TIPS to prevent re-bleeds if other tx fails

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12
Q

What is an important complication of TIPS?

A

a stent is placed to release portal HTN into the vena cava==> bypass the liver

–> risk of toxins (ammonia) is higher –> greater risk of hepatic encephalopathy

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13
Q

***What is the pathophysiology of ascites due to cirrhosis?

A

-vasodilation of the splanchnic system leads to dec filling in systemic system–> inc RAAS –> inc Na+ and H2O retention)
-hypoalbuminemia also causes a dec plasma oncotic P –> more leaking fluid into the peritoneal cavity –> more peripheral edema
(*Sum: increased portal pressure and low albumin)

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14
Q

What other complications can result from ascites?

A
  • resp function can be compromised –> SOB
  • malnourished
  • mm wasting
  • anorexia
  • fatigue
  • abd discomfort and pressure
  • gynecomastia
  • Spontaneous bacterial peritonitis
  • hydrothorax (pleural effusion)
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15
Q

How can you determine if someone has ascites or is just fat?

A
  • shifting dullness in percussion when pt is supine vs on side
  • fluid wave (non-specific)
  • US (can detect as little as 30 mL of fluid)
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16
Q

What is the treatment for severe ascites?

A

Paracentesis : needle into the peritoneal cavity to drain the ascitic fluid (also used for dx)

also, *diuretics (spironolactone) and sodium restriction

-should also be done when present with ascites for the 1st time to diagnose the fluid

17
Q

***What is the #2 cause of ascites?

A

cancer (ovary and liver)

cirrhosis is #1

18
Q

What are the most typical symptoms of spontaneous bacterial peritonitis? What should be the suspected cause if 2+ organisms are found in the ascitic fluid?

A

fever and abd pain

2+ organisms==> suspect a perforated viscus

19
Q

What is the 1 year survival rate of someone with massive ascites?

A

< 50%

liver transplant needed

20
Q

How does INR correspond to prognosis of cirrhosis? Why?

A

higher INR==> worse prognosis

clotting factors are created by the liver.

Vitamin K requires biliary excretion for its absorption. liver failure–> Less vitamin K –> dec 2, 7, 9, and 10 clotting factors

21
Q

What can hypersplenism lead to? What physical finding can be seen?

A

thrombocytopenia (sequestration of platelets–> low platelets)

petichiae

can also lead to DIC

22
Q

***What is pancytopenia? What is the most common cause of this?

A

pancytopenia=thrombocytopenia (low platelets), leukopenia (low WBC) and anemia (low hemoglobin)

cirrhosis (hypersplenism)

23
Q

What is the #1 cause of anemia in cirrhosis?

A

hypersplenism

24
Q

What is the reason hyponatremia is common in pts with cirrhosis and ascites?

A

inability to excrete free water because of high levels of ADH (activated by systemic vasodilation)

–> low sodium

25
Q

What is the best therapy for hepatorenal syndrome?

A

liver transplant

26
Q

What is hepatopulmonary syndrome? Is this the same as hepatic hydrothorax?

A

Triad of:

  • Liver disease
  • Increased alveolar-arterial gradient while breathing room air
  • Evidence of intrapulmonary vascular dilatations

NOT THE SAME!

27
Q

***What are the 2 main causes of death due to cirrhosis?

A

hepatic encephalopathy and GI bleeding

28
Q

***What is asterixis? Which pts will present with this?

A

bilateral but asynchronous flapping motions of outstretched dorsiflexed hands

seen in pts with hepatic encephalopathy

29
Q

What medications are used to treat hepatic encephalopathy? (3)

A
  • LACTULOSE (first line) (stimulates ammonia passage from tissues to gut lumen and inhibits ammonia production)
  • Neomycin (antibiotic)
  • other antibiotics

(3 meds==> ALL oral. if pt is comatose–> NG tube)

30
Q

What is the difference between compensated and decompensated cirrhosis? What is the median survival with both?

A

(Important for transplants)

  • compensated=no major complications
  • -> median survival is 12 years
  • decompensated=have complications (i.e. variceal bleeding, SBP, hepatocellular carcinoma, etc)
  • -> median survival is < 6 months
31
Q

What is Dupuytren’s contracture? What type of cirrhosis is this commonly seen in?

A
  • results from thickening and shortening of the palmar fascia –> flexion deformities of the fingers
  • common in alcoholic cirrhosis
32
Q

What are some other PE findings in cirrhosis?

A
  • Jaundice
  • scleral icterus
  • palmar erythema
  • Muehrcke’s nails (transverse white bands in the nails that do not indent)
  • Terry’s nails (proximal 2/3 of the nail bed is white and distal 1/3 is red)
  • clubbing
  • spider angiomata (spider telangiectasis)
33
Q

***What is the treatment for cirrhosis?

A
  • Intravascular volume is low so aldosterone level would be very high → retain sodium and water:
    1. Fluid restriction (makes aldosterone higher though)
    2. Na restriction (lowers intravascular volume → raises aldosterone)
    3. Lasix (lowers intravascular volume → raises aldosterone)
    4. Spironolactone (given to every patient b/c anti-aldosterone)
  • TIPS – decreases ascites and varices
  • La Veen shunt
  • Liver transplant – ultimate treatment

GI Final (18 decks)

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