Cirrhosis and Comp. of Liver D [3]

Question 1

Complications of cirrhosis

Answer 1

variceal hemorrhage
ascites
encephalopathy
jaundice

Question 2

Most common causes of cirrhosis

Answer 2

HCV

alcohol

Question 3

Which one has complications?
Compensated cirrhosis
Decompensated cirrhosis

Answer 3

Compensated Cirrhosis - no complications

Decompensated cirrhosis - complications

Question 4

Liver biopsy is not necessary to dx for pre-transplant eval if we can find what?

Answer 4

decompensated (complications) cirrhosis or CT scan diagnosing cirrhosis

PE: spider angiomata, palmar erythema

Question 5

Mechanism of portal HTN and how it leads to cirrhosis

Answer 5

portal HTN can be due to increase resistance or increase in venous inflow

↑ intrahepatic resistance → portal HTN → distortion of sinusoidal architecture of the liver → even more ↑ R

(blood has to go through different ways like esophagus to get back to heart; also blood backs up in portal veins leading to splenomegaly)
- ↑ intrahepatic resistance in cirrhosis is not only structural but also fxnal

Question 6

MELD score

Answer 6

estimates risk of 3 mo mortality
Determines priority in cirrhosis
- higher score = priority

6.4+9.8xlog(INR) + 11.2xlog(Cr) + 3.8xlog(Bili)

nL = 6

Question 7

Cirrhosis is what type of portal HTN

Answer 7

Sinusoidal

• small hepatic v are obstructed
• RUQ pain, ascites, hepatomegaly, jaundice

HVPG is increased >5

Question 8

Pre-hepatic HTN

Answer 8

Portal or splenic ven thrombosis

liver is nl, blood backs up in spleen and esophagus

Question 9

Pre-sinusoidal portal HTN

Answer 9

Shistosomiasis
- eggs are stuck b4 the sinusoids

HVPG is nl (3-5)

Question 10

Post-sinusoidal portal HTN

Answer 10

veno-occlusive disease

HVPG is increased >5

Question 11

Post-hepatic portal HTN

Answer 11

Budd-chiari syndrome
(hepatic vein thrombosis)

HVPG is nl (↑P - ↑P @ heart)
(pre and post hepatic is nl)

Question 12

In cirrhosis, NO activity is ____ and vasoconstrictors are ____

Answer 12

NO reduced
VC increased

→ increased resistance →

• structural changes (fibrosis, regenerative nodules)
• active vasoconstriction (↓No, ↑VC)

(note: ↑ NO → splanchnic vasodilation → ↑portal venous inflow → ↑portal HTN)

Question 13

NL hepatic venous pressure gradient (HVPG) is

Answer 13

3-5 mmhg

HVPG = WHVP - FHVP

Question 14

Which type of portal HTN is HVPG elevated in?

Answer 14

sinusoidal

post sinusoidal

Question 15

Predictors of variceal hemorrhage

Answer 15

variceal size (larger more likely to rupture)
red signs (risk 4 bleed)
child

Question 16

Decreasing what two things reduce risk of variceal rupture?

Answer 16

↓ portal P

↓ HVPG

Question 17

Therapies for varices

Answer 17

Vasoconstrictor - OCTREOTIDE!
- ↓ splanchnic flow → ↓portal pressure

TIPS/shunt surgery
- create comm btwn portal v and hepatic V

Question 18

Most common cause of ascites

Answer 18

cirrhosis

- US is most sensitive way to detect ascites

Question 19

How does portal HTN result in ascites?

Answer 19

Portal HTN → shear stress → ↑ NO → vasodilation → BP goes down → activation of neurohormonal systems (renin, angiotensin, aldosterone) → sodium and water retension → ASCITES

Question 20

Refractory ascites

Answer 20

acites that cannot be managed by diuretics anymore

-80%

Question 21

Serum-Ascites Albumin Gradient (SAAG):

Answer 21

. SAAG correlates with sinusoidal pressure. SAAG 1.1 nl

Most patients with CIRRHOTIC ASCITES will have serum-ascites albumin GREATER than 1.1

Peritoneal malignancy will be less than 1.1

Question 22

Hepatorenal syndrome

- what is always present?

Answer 22

renal failure in pts with:

1. cirrhosis
2. advanced liver failure
3. severe sinusoidal portal HTN

ASCITES AND HYPONATREMIA are ALWAYS PRESENT IN HRS

• no significant change in kidney
  (fxnl renal failure)

Question 23

Type I vs Type II hepatorenal syndrome

Answer 23

Type I: rapidly progressive renal failure (2 weeks)

Type II: more slowly progressive

Question 24

Spontaneous Bacterial Peritonitis (SBS)

Answer 24

bacterial translocation →
migration of viable microorganisms from intestinal lumen to mesenteric lymph nodes and other extraintestinal organs and sites →
increase conditions associated with high risk of infxn by gram (-) organisms (burn, shock, trauma) but DOES NOT increase pre-hepatic portal HTN

Question 25

Hepatic Encephalopathy

Answer 25

neuropsychiatric complication due to

1. portosystemic shunt
2. chronic liver failure

Due to failure to metabolize neurotoxic substances (hyperammonemia) → glutamine accumulation

(note: astrocytes are the only cells in the brain that can metabolize ammonia)

Question 26

tx for hepatic encephalopathy

Answer 26

lactulose

• 2-3 bowel movements/day
• less time to absorb ammonia, trap it in colon and increase movement through colon

Antibiotics to kill bacteria in gut that make ammonia