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GI > 14. Cirrhosis > Flashcards

14. Cirrhosis Flashcards

1
Q

What will be present on exam in a patient with cirrhosis?

A 
Cachexia
Jaundice
Ascities 
Spider angioma
Duputren's contractures 
Edema
Breast development
Testicular atrophy
Palmar erythemia
Hair loss
Encephalopathy
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2
Q

What lab findings will there be with cirrhosis?

A 
Elevated transaminases, bilirubin, ALP, PT/INR
Decreased albumin
Thrombocytopenia
Leukopenia
Renal insufficiency
Hyponatremia
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3
Q

Where is cachexia from cirrhosis especially prominent?

A

Temporal wasting

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4
Q

What are spider angioma?

A

Dilated arterioles in the distribution of the SVC (chest up)

Blanches from the center out with pressure

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5
Q

What causes palmar erythemia with cirrhosis?

A

Increased estrogen levels leads to increased blood flow in the periphery
**VASODILATION

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6
Q

Dupuytren’s contractures are more common in patients with ___ cirrhosis

A

Alcoholic

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7
Q

What is caput medussae?

A

Visible abdominal wall collateral veins due to recanalization of the umbilical vein

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8
Q

What cell is causing the fibrosis in hepatic fibrosis?

A

Stellate

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9
Q

What criteria does the Child-Pugh Scoring Criteria take into account?

A 
Albumin
Bilirubin
INR/PT
Ascities 
Encephalopathy
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10
Q

What are the three classes of Child-Pugh

A

A: 5-6 70-75% 5yr survival
B: 7-9 40-45%
C: >9 10-15%
**transplant survival is around 70%, so don’t transplant person with A class

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11
Q

What scoring system is used to rank transplant patients?

A

MELD model: based on the INR, bilirubin, creatinine, dialysis

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12
Q

What is the normal pressure difference between the portal vein and hepatic vein?

A

4-5 mmHg

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13
Q

What causes pre-hepatic portal HTN?

A

Portal vein thrombosis

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14
Q

What is the key cause of intra-hepatic portal HTN?

A

Cirrhosis

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15
Q

What are three key causes of post hepatic portal HTN?

A
  1. Hepatic vein thrombosis (Budd-Chiari Syndrome)
  2. Right heart failure
  3. Valvular heart disease
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16
Q

What are the 6 key complications of cirrhosis?

A
  1. Variceal bleeding
  2. Ascites
  3. Spontaneous bacterial peritonitis (SBP)
  4. Hepatorenal syndrome
  5. Hepatopulmonary syndrome
  6. Hepatic encephalopathy
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17
Q

What is the risk associated with varices

A

Thin walled–rupture, hard to stop bleeding due to low levels of coagulation factors and sequestration of platelets in the spleen

18
Q

What drugs are used for varices (non active)?

A

Beta blockers: decrease the risk of first bleeding, rebleeding, and increased survival

19
Q

What are the two ways by which beta blockers treat varices?

A

Decrease CO by blocking beta1

Produce sphanchnic vasoconstriction by blocking beta2

20
Q

What tx is used for active variceal hemorrhage?

A

Octreotide: somatostatin analog, decreases intestinal blood flow
Band ligation may also be used

21
Q

What is the pathophysiology of ascites with cirrhosis?

A 
Increased resistance to portal flow
Portal HTN
Splanchnic arterial vasodilation
Decreased effective circulating volume
Activation of vasoconstrictor/antinatriuretic factors (renin, angiotensin, aldo, vasopressin)
Sodium and water retention
Plasma volume expansion
Ascites
22
Q

Is water retention or sodium retention greater with cirrhosis?

A

Water retention from increased vasopressin–leads to hyponatremia

23
Q

What are the components of management of ascities?

A
  1. 2000 mg sodium restricted diet

2. Diuretics- spironolactone (aldo inhibitor) and furosemide

24
Q

What are the two key sx of patients with SBP (spontaneous bacterial peritonitis)

A

Abdominal pain 80%

Fever 70%

25
Q

What are pathogens commonly involved in spontaneous bacterial peritonitis?

A 
E.coli 45%
Streptococi 30%
Klebsiella 10%
G- bacilli 8%
Anaerobes 1%
**60-70% gram - because that is what is found in the GI tract
26
Q

What is hepatorenal syndrome?

A

Progressive renal failure associated with advanced cirrhosis and ascities

27
Q

What type of renal failure presents with urine sodium over 20 and cell debris in the urine?

A

Acute tubular necrosis

28
Q

What happens to the urine sodium in hepatorenal syndrome?

A

<10; kidneys sense that they are not being perfused because there is so much blood flow in the GI tract
Retain sodium

29
Q

Why does the PaO2 drop in hepatopulmonary syndrome?

A

Vasodilation leads to the inability of the alveoli to effectively oxygenate all the passing blood
*100% oxygen will correct

30
Q

What is the pathophysiology behind hepatic encephalopathy?

A

Gut derived neurotoxins are not cleared due to hepatic insufficiency and bypass of the liver by collaterals
Toxins cross the BBB and lead to CNS changes

31
Q

What is a specific sx seen with hepatic encephalopathy?

A

Asterixis with the “stop traffic” movement

32
Q

What is the grading scale for hepatic encephalopathy?

A

Grade 0: No alteration in conciousness, intellectual function, or behavior
Grade 1: Trivial lack of awareness, euphoria or anxiety, short attention span
Grade 2: Lethary, disorientation, personality change, inappropriate behavior
Grade 3: Somnolence to semistupor, confusion, response to noxious stimuli
Grade 4: Coma, no response to noxious stimuli

33
Q

What grade of hepatic encephalopathy warrents hospital admission?

A

Grade 2: lethargy, disorienation, personality change, inappropriate behaviour

34
Q

What grade of hepatic encephalopathy warrents ICU?

A

Grade 3: somnolence to semistupor, confusion

Gade 4: coma, no response

35
Q

What drug should be administered for hepatic encephlopathy?

A

Lactulose: nonabsorbable dissacharide. Lactic acid lowers the pH in the colon, conversion of ammonia to ammonium, which can be removed in the feces

36
Q

What is an alternative to lactulose for hepatic encephalopathy?

A

Rifaximen

37
Q

What are the components of treatment for hepatic encepathlopathy

A

Fluids
NO sleep meds
Look for infection
Give lactulose or rifaximin

38
Q

What is the MC of acute liver failure in the US?

A

Acetaminophen

39
Q

What is fulminant liver failure?

A

Acute liver failure with coagulopathy and encephalopathy

40
Q

What is the main risk in fulminant liver failure?

A

Cerebral edema: cerebral herniation is the major cause of death

41
Q

What causes cerebral edema in fulminant liver failure?

A

Inability of the liver to metabolize ammonia
Ammonia and glutamate converted by the action of glutamine synthetase into glutamine by brain astrocytes
Astrocyte swelling leads to cerebral edema

GI (28 decks)

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