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Flashcards in Cirrhosis Deck (36)
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1
Q

Which types of hepatitis can cause acute liver failure but not cirrhosis?

A

Hepatitis A and Hepatitis E

2
Q

What are some exam findings associated with Cirrhosis?

A
  • Cachexia (muscle wasting)
  • Jaundice
  • Ascites
  • Spider Angioma
  • Duputyren’s contractures
  • Edema
  • Breast development
  • Palmar erythema
3
Q

Where are spider angiomas found and how do they appear?

A

Often present above level of the belly button - small arterial/venous dilations on the skin

4
Q

What hormone leads to palmar erythema? How is this associated with liver disease?

A

Estrogen

The liver decreases estrogen levels so its dysfunction leads to increased estrogen

5
Q

What is a consequence of the narrowing of tendons in cirrhosis?

A

Duputren’s contractures

6
Q

How does cirrhosis lead to caput medussa?

A

Varicose veins dilate on the abdominal wall due the need for blood to bypass the liver

7
Q

How does cirrhosis lead to edema?

A

The liver cannot produce as much protein and this decreases the oncotic pressure intravascularly which leads to edema

8
Q

What makes up the dark rim around the liver in this image?

A

Fluid - leading to ascites

9
Q

How does hepatic fibrosis involve stellate cells?

A

Stellate cells are overactivated and lay down collagen in the space of disse

10
Q

What abnormalities add 1 point to the Child Pugh scoring criteria?

Albumin:

Bilirubin:

INR:

Ascites:

Encephalopathy:

A

Albumin: >3.5 g/dL

Bilirubin: <2 mg/dL

INR: <1.70 seconds

Ascites: None

Encephalopathy None

11
Q

What abnormalities add 2 points to the Child Pugh scoring criteria?

Albumin:

Bilirubin:

INR:

Ascites:

Encephalopathy:

A

Albumin: 2.8-3.5 g/dL

Bilirubin: 2-3 mg/dL

INR: 1.71-2.20 seconds

Ascites: Easily controlled with diuretics

Encephalopathy: Easily controlled with lactulose

12
Q

What abnormalities add 3 points to the Child Pugh scoring criteria?

Albumin:

Bilirubin:

INR:

Ascites:

Encephalopathy:

A

Albumin: <2.8 g/dL

Bilirubin: >3 mg/dL

INR: >2.20 seconds

Ascites: Poorly controlled with diuretics

Encephalopathy: Poorly controlled with lactulose

13
Q

Child Pugh class

  • A score of 5-6 is considered ______
  • A score of 7-9 is considered ______
  • A score of >9 is considered ______
A

A score of 5-6 is considered compensated
A score of 7-9 is considered decompensated
A score of >9 is considered decompensated

14
Q

What 4 factors make up the MELD score (model for end-stage liver disease)?

A
  • INR
  • Bilirubin
  • Creatanine
  • Dialysis at least twice in the past week
15
Q

What are the three types of portal hypertension?

Which type is associated with cirrhosis?

A
  1. Pre-hepatic (Portal vein thrombosis)
  2. Intra-hepatic (associated with cirrhosis)
  3. Post-hepatic (enlargement of sinusoids)
16
Q

How does the hepatic artery attempt to compensate for an increase in portal vein pressure?

A

The hepatic artery dilates (to compensate for decreased blood flow to the liver)

17
Q

What are some complications of Cirrhosis?

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

How does cirrhosis lead to leukopenia and thrombocytopenia?

A
  • Blood is shunted into the spleen with increased pressure in the liver
  • Increaed blood flow to spleen causes splenomegaly
  • Splenomegaly causes the spleen to sequester platelets and WBCs leading to leukopenia and thrombocytopenia
19
Q

What medications are used to reduce risk of rupture and bleeding in esophageal varices? (not for actively bleeding patients)

A
  • Non-selective B-blockers (propanalol and nadolol)
    • Decrease cardiac output by blocking B-1 receptors
    • Produce splanchnic vasoconstriction by B2 blockade
20
Q

How are active variceal hemorrhages treated?

What other treatment can prevent futue bleeding episodes?

A

Octreotide (Somatostatin analog) - decreases amount of blood flow through portal vein

Varceal Band Ligation - For patients who cannot tolerate beta blockers

21
Q

Describe the pathophysiology of ascites from cirrhosis (10 steps)

A

Cirrhosis → Increased resistance to portal flow → Portal hypertension → Splanchnic arterial vasodilation → Decreased effective circulating volume → Activation of vasoconstrictor and antinatriuretic factors → Sodium and water retention → Plasma volume expansion → ascites

22
Q

How does cirrhosis lead to hyponatremia?

A
  • Decreased effective circulating volume leads to increased vasopressin and renin-angiotensin/aldosterone
  • This leads to increased water and sodium retention
  • Eventually water retention is greater than sodium retention leading to hyponatremia
23
Q

How is ascites managed?

A
  • 2000mg sodium restricted diet
  • Diuretics
    • Spironolactone - inhibits aldosterone (thiazide diuretic)
    • Furosemide - lowers potassium (loop diuretic)
24
Q

What are the top two symptoms in patients with SBP (spontaneous bacterial peritonitis)?

A

Abdominal pain (80%) and fever (70%)

25
Q

What are the top two bacterial pathogens in SBP?

A

Mostly gram negatives

  • E. Coli
  • Streptococci
26
Q

Describe hepatorenal syndrome

A

Progressive renal failure associated with advanced cirrhosis and ascites

27
Q

What are three differential diagnoses of renal failure in cirrhosis? What urine sodium level is associated with each?

A
  • Acute tubular necrosis (>20 mEq/L sodium)
  • Pre-Renal (<10)
  • Hepatorenal syndrome (<10)
28
Q

Hepatopulmonary syndrome causes _____ of vasculature

A

dilation (due to backup)

29
Q

How can the decrease in blood flow to the lungs be improved in hepatopulmonary syndrome?

A

Increase oxygen intake

30
Q

How does cirrhosis lead to mental status changes (Hepatic Encephalopathy)?

A

Gut-derived neurotoxins → Hepatic Insufficiency/Hepatic Bypass → Crossing of BBB → CNS changes

31
Q

What neuromuscular disorder is also associated with Hepatitc encephalopathy?

A

Asterixis - impaired communication with brain stem leads to involuntary wrist movement

32
Q

What metnal status changes are associated with the different levels of hepatic encephalopathy?

  • Grade 0:
  • Grade 1:
  • Grade 2:
  • Grade 3:
  • Grade 4:
A
  • Grade 0: no alteration in consciousness, intellectual function, or behavior
  • Grade 1: Trivial lack of awareness, euphoria or anxiety, short attention span
  • Grade 2: Lethargy, disorientation, personality change, inapproptiate behavior
  • Grade 3: Somnolence to semistupor, confusion, response to noxious stimuli
  • Grade 4: Coma, no response to noxious stimuli
33
Q

What are three mechanisms in hepatic encephalopathy treatment with lactulose?

A
  • Lactulose is cathartic - keeps colon clean
  • Lactulose lowers pH (increases lactic acid)
  • Lactulose causes protonation of NH3 → NH4+
34
Q

How does Lactulose compare with Rifaximin in HE treatment?

A

Lactulose is less effective at decreasing asterixis but is also less expensive compared to Rifaximin

35
Q

What is the most common origin of acute liver failure in the the USA

A

Acetaminophin

36
Q

What are the components of fulminant liver failure?

A
  • Acute liver failure
    • hepatocyte necrosis
  • Cerebral edema (most likely cause of death)
    • Inability of liver to metabolize ammonia
    • Astrocyte swelling and cerebral herniation