Cirrhosis and Complications

Question 1

Cirrhosis (suspect if …/mortality assessment …)

Answer 1

Suspect if incr ALT/AST, chronic liver dz
Assess mortality with:
1) Child Turcotte Pugh (CTP) score: encephalopathy, ascites, bilirubin, albumin, PT/INR (1-3 in each, 7 means transplant)
2) MELD (model for end-stage Liver Dz): estimates risk of 3 month mortality using lab values of bilirubin, creatinine, INR

Question 2

Cirrhosis (Labs/Diagnostics)

Answer 2

Low albumin, prolonged PT (INR>1.3), high bilirubin, low PLT
Nodular liver on imaging
Biopsy NOT necessary for diagnx OR transplant
Fibrous septation (portal tracts and central veins)

Question 3

Portal HTN (flow and resistance)

Answer 3

Incr flow, incr resistance, or both
Incr resistance: from incr fibrosis AND decreased NO (vasoconstriction) IN THE LIVER
Incr flow: from increased shear stress and increased NO (vasodilation) OUTSIDE OF LIVER

Question 4

Portal HTN (causes)

Answer 4

Pre-hep: portal or splenic vein thrombosis
Pre-sinusoidal: schistosomiasis
Sinusoidal: CIRRHOSIS (most common)
Post-sinusoidal: veno-occlusive dz
Post-hepatic: Budd-Chiari syndrome (hepatic vein thrombosis); CHF

Question 5

Portal HTN (pres)

Answer 5

varices, ascites, progression to hepatorenal syndrome

Question 6

Portal HTN (diagnx)

Answer 6

Measure hepatic venous pressure gradient (HVPG)

= Wedged HVP - Free HVP (systemic)

Question 7

Portal HTN (treat)

Answer 7

Vasoconstrictors [OCTREOTIDE!!] to decrease portal flow, USE FIRST IN EMERGENT CIRRHOTIC PATIENT
Vasodilators increse intrahepatic resistance
TIPS: transjugular intrahepatic portosystemic shunt –> connects branch of hepatic vein with portal vein (complications: liver failure and encephalopathy)

Question 8

Varices (assoc factors)

Answer 8

child score B/C cirrhosis, EtOH etiology, red wale marks on endoscopy
CAN LEAD TO VARICEAL HEMORRHAGE (size biggest predictor)

Question 9

Varices (pres/diagnx/treat)

Answer 9

Pres: tortuous, bulging vein (esophagus, rectum)
Diagnx: endoscopy
Treat: endoscopic band ligation, sclerotherapy (casue fibrosis around varices to increase wall thickness)

Question 10

Ascites (cause)

Answer 10

Extrahepatic increase in NO –> vasodilation –> decreased SVR (decreased EFFECTIVE ARTERIAL VOLUME) –> RAAS activation –> Na and H2O retention –> ascites
[ends up increasing sinusoidal pressure (increased resistance) –> cirrhosis]

Question 11

Ascites (pres/diagnx/treat)

Answer 11

Pres: large, distended abd, positive fluid wave
Diagnx: PARACENTESIS to check PMNs (infx), Amylase (pacreatitis), SAAG (serum-ascites albumin gradient)
SAAG >1.1 = ascites from cirrhosis (low protein in fluid) or CHF (hi protein)
SAAG

Question 12

Hepatorenal syndrome (cause/pres)

Answer 12

reduced GFR due to renal constriction because kidneys see decreased effective arterial volume
Pres: almost ALWAYS with ascites, can be triggered by large volume paracentesis, electrolyte imbalance
Type 1: rapidly progressive (Cr doubles in 2 weeks)
Type 2: slowly progressive

Question 13

Hepatorenal syndrome (dignx/treat)

Answer 13

Diagnx: normal appearing kidneys, urine NA low, nearly ALWAYS hyponatremic
diagnosis of exclusion (no shock, infx, nephrotoxic drugs)
Treat: LIVER TRANSPLANT, renal vasodilators & hemodialysis are NOT effective, and other tx under investigation

Question 14

Spontaneous Bacterial Peritonitis (cause/pres)

Answer 14

Infx of ascitic fluid, MOST LIKELY VIA BACTERIAL TRANSLOCATION (eg from intestinal lumen to mesenteric lymph nodes etc.) GRAM NEGATIVE ENTEOBACTERIA (70-80%, so sometimes gram positive, usually one organism)
Pres: Large, distended abd, positive lfuid wave, signs of infx, poss rebound tenderness

Question 15

Spontaneous Bacterial Peritonitis (diagnx/treat)

Answer 15

Diagnx: increased PMN (>250/mm3) on paracentesis
Treat: empiric tx: cefotaxime (AVOID aminoglycosides) for minimum of 5 days
ALBUMIN co-admin decreases renal dysfxn and short term mortality
Re-evaluate if PMN not down 25% in 2 days

Question 16

Hepatic Encephalopathy (causation)

Answer 16

From chronic liver failure OR as a complication from portosystemic shunt
Failure to metabolize neurotoxic substances: eg AMMONIA resulting in glutamine accumulation
MINIMAL HEPATIC ENCEPHALOPATHY: 30-70% of cirrhosis pts, impaired driving, attentive/cognitive defects

Question 17

Hepatic Encephalopathy (precipitants)

Answer 17

excess protein
GI bleeding
TIPS procedure
sedative/hypnotics
infx
diuretics (and other meds)

Question 18

Hepatic Encephalopathy (pres)

Answer 18

confusion, somnolence, personality changes (extreme = coma)
Number connection test
Asterixis (flapping tremor on wrist extension)

Question 19

Hepatic Encephalopathy (diagnx)
Do NOT use???

Answer 19

Do NOT use ammonia levels: NOT necessary, NOT reliabel, NOT correlated to severity
Use: SLOW DOMINANT RHYTHM on EEG
Metabolic gliosis/Alzheimer type 2 change in brain
May get cerebral edema

Question 20

Hepatic Encephalopathy (treat)

Answer 20

LACTULOSE (converted to lactic acid in bowel –> lowers pH –> decreases urease producing bacteria that also produce ammonia, also increase in excretion of toxin)
SYMBIOTICS/ABX (promote motility, decrease urease producing bacteria)
PROTEIN RESTRICTION
IDENTIFY AND TEAT PRECIPITANTS