6. Cirrhosis Flashcards
LO1: Dx Cirrhosis based on PE (10)
1) Scleral icterus
2) Jaundice
3) Spider angioma
4) Caput medusae
5) Umbilical hernia
6) Enlarged left lobe of liver
7) Gynecomastia
8) Splenomegaly
9) ascites
10) Dupuytren’s contractures-ring finger tendon
LO1: Dx Cirrhosis based on labs: Liver insuffiency (3), Portal HTN (1)
Liver Insufficiency 1) Low albumin (<3.8 g/dL) 2) INR > 1.3 3) Bili >1.5 mg/dL Portal HTN 1) Low Plt <150,00
LO1: Dx Cirrhosis based on rad -CT/US/MRI (6)
1) Nodular Liver
2) Caudate hypertrophy
3) Ascites
4) Splenomegaly
5) Venous Collaterals
6) Hepatocellular carcinoma
LO2: Portal HTN in Cirrhosis -> varices (5)
1) Cirrhosis->
2) Increased resistance to portal flow ->
3) Increased portal pressure ->
4) Varices ->
5) Variceal growth
LO3: Dx ascites due to portal HTN
Routine (4), Optional (7)
1) US- most sensitive Routine 2) albumin Protein 3) PMN cell count 4) Bx cultures Optional 1) Glucose 2) LDH 3) Amylase 4) RBC 5) TB smear 6) cytology 7) TG
LO3: Dx ascites due to bx peritonitis (2)
1) Ascitic fluid w/ PMN count > 250/mm^2
2) Tx only indicated when culture is positive
LO4: Mechanism for developing hepatic encephalopathy (5)
1) Increased Ammonia crosses BBB
2) Increase astrocytic peripheral benzodiazepine -R
3) Neurosteroid production
4) Modulation of GABAa-R -> cortical depression
5) Hepatic Encephalopathy
LO4: Risk factors for worsening hepatic encephalopathy (5)
1) Excess protein
2) TIPS
3) gI bleed
4) Sedatives/hypnotics
5) Diuretics -> decrease Serum K -> Plasma volume down-> azotemia
LO5: Components of MELD score (3)
1) INR
2) Serum Cr
3) Serum total bili
- estimates 3 month mortality
LO5: MELD score use in ranking Transplant Pts (4)
1) Fulminant hepatic failure - highest priority
2) Same blood -highest MELD determines priority
3) Wait time used to break ties of = MELD
4) MELD updated at regular intervals
Mechanisms of portal HTN in cirrhosis (sinusoidal) (1ab, 2a)
1) Increased intrahepatic resistance (initial)
a) Structural -fibrosis, regenerative nodules
b) Active vasoconstrict - decrease NO, increase vasoconstrictors
2) Increased portal venous inflow
a) splanchnic vasodilation -increased NO
Sinusoidal obstructive syndrome (3)
1) Small hepatic veins obstructed
2) Complication of myeloablative regimens for bone marrow transplant
3) RUQ pn, ascites, HM, jaundice
Budd-Chiari Syndrome (3)
1) Obstruction of hepatic veins -small, large, IVC
2) Often from thrombosis due to hypercoagulability
3) Abd pn, ascites, edema
LO2: Portal HTN in Cirrhosis -> Ascites (7)
1) Portal HTN ->
2) Shear stress ->
3) Increased NO
4) Vasodilation-decrease SVR ->
5) Activate RAAS ->
6) Na and H20 retention ->
7) Ascites
Portal Pressure Measurement (2)
1) Definitive for dx portal HTN
2) HVPG (NL 3-5 mmHg) -hepatic venous pressure gradient
HVPG in DDx of portal HTN (2)
1) NL - pre-hepatic, pre-sinusoidal, and post-hepatic
2) Elevated - sinusoidal and post-sinusoidal
HVPG formula
HVPG = Wedged hepatic venous pressure (WHVP) - free hepatic venous pressure (FHVP)
FHVP - internal 0 to correct for extravascular pressure increase
TIPS?
Transjugular intrahepatic Portosystemic shunt
Variceal Tx (5)
1) Vasoconstrictors (octreotide)
2) venodilators
3) Vasoconstrict + venodilate
4) Endoscopic tx
5) TIPS
Ascites Tx (1, 2b, 3b)
1) Portal HTN no ascites-consider Na retention
2) Uncomplicated ascites
a) Na restriction + diuretics
b) Large volume paracentesis (LVP) w/ tense ascites
3) Refractory Ascites
a) LVP + albumin
b) TIPS
Refractory Ascites Types (2)
1) Diuretic -intractable ascites (80%) - therapeutic doses not possible due to diuretic complications
2) Diuretic-resistant ascites - No response to maximal spironolactone and furosemide
Hepatorenal Syndrome (4)
1) Renal failure in pts w cirrhosis
2) absence of significant histo changes -fxnl renal failure
3) marked arteriolar vasodilation in extra-renal circulation
4) Marked renal vasoconstriction leading to reduced GFR
Dx hepatorenal syndrome (6)
1) advanced hepatic failure and portal HTN
2) Cr> 1.5 or Crcl < 40
3) Absence of shock, bx infxn or nephrotoxic drug
4) Absence of excessive GI or renal loss
5) No renal fxn improvement after plasma volume expansion
6) Urinary protein < 500 and nl renal US
What is always present in HRS? (2)
AScites
Hyponatremia (almost universal)
Mechanism to ascites, hepatorenal syndrome, and hyponatremia (3)
Cirrhosis -> Activate RAAS->
1) Sodium retention =ascites
2) renal vasoconstriction = hepatorenal syndrome
3) water retention = hyponatremia
HRS management (1, 2)
1) Liver Transplant -proven
Under investigation
1) Vasoconstrictor + albumin
2) TIPS
Ascites Clinical Picture (6)
1) Fever
2) Jaundice
3) abd pn
4) AMS
5) abd tenderness
6) Hypotension
Spontaneous Bacterial Peritonitis (2)
1) Mostly occurs by bacterial translocation
2) Microorganisms from gut lumen to mesenteric LN and extraintestinal organs
SBP Tx (3)
1) empiric antibx avoid AG
2) 5 days minimum
3) reevaluate if PMN has not decreased by 25%
Hepatic Encephaopathy? (5)
1) Neuropsych complication fo cirrhosis
2) Results from
a) Portosystemic shunt
b) Chronic liver failure
3) Failure to metabolize neurotoxins
4) Astrocyte morphology and fxn alteration
5) Clinical Dx
Hepatic encephaopathy Tx (3)
1) Identify cause
2) Lactulose
3) Protein restriction, short term
Serum albumin gradient (SAAG)
Serum-Ascites Albumin Gradient. Serum Albumin - Ascites Albumin
