19 - Cirrhosis Flashcards
Liver Functions
You can NOT live w/o a functioning liver
Metabolizes / Stores nutrients
Synthesizes Molecules (such as cloting factors)
Breaks down Toxins
Participates in the immune sytem
Number 1 cause of cirrhosis?
ALCOHOL
Damages liver by causing fatty infiltrates = Steatosis
Damage varies by amount / duration of use + GENETICS
Heavy Drinking = >2drinks/day for men
Causes of CIRRHOSIS
Except for Viral and Alcoholic
NASH = Non-alcoholic Seatohepatisis
common in OBESITY
Primary Biliary Cirrhosis
immune attack on BILE DUCTS
Autoimmune Hepatitis
immune attack on hepatocytes
- *Hemochromatosis**
- *iron** overload from over-absorption
Signs & Symptoms of CIRRHOSIS
Typically well-compensated, without Signs or symptoms
Onset of complications can be insidious:
Malaise / Fatigue / poor appetite
ESLD = Decompensated Cirrhosis, involves
Jaundice / Ascites / Encephalopathy / Variceal Bleeding
ESLD: SIGNS
End stage liver disease, decompensated cirrhosis
Jaundice
Ascites
Caput medusa
snake looking things on abdomin
Spider Angioma
Palmar Erythema
red palms
Viral Causes of Cirrhosis
HEP C is MOST common cause for LIVER TRANSPLANT
20-30% will develop Cirrhosis within 20 years
Hep B is more common common in ASIANS
Characteristic LAB VALUES in ESLD
- *HIGH INR & Prolonged Prothrombin Time**
- reduced synthesis of clotting factors*
- *Thrombocytopenia**
- =low platelets, decreased thrombopoetin +* splenomegaly
- *Low ALBUMIN**
- poor synthetic function in the liver + poor nutrition*
Child Pugh Classification
GRADES WHAT?
Scoring System for ESLD, grading:
Encephalopathy (confusion)
Ascites
Bilirubin (mg/dL)
Albumin (g/dl)
Prothrombin ratio or time
Different Grades for
Child Pugh Classification
A = <6
highly survivable
B = 7-9
moderate, 81% 1 year survival , 57% 2-year
Grade C = score >9
severe disease, 45% 1 year survival
MELD** **Classification
Model for ESLD
score assess risk of death while awaiting LIVER TRANSPLANT
Exponential formula based on:
INR + Bilirubin
Serum Creatinine / Sodium
Higher the MELD score means what?
HIGHER RISK OF DEATH
ALSO
HIGHER ON THE PRIORITY LIST FOR LIVER TRANSPLANT
Portal Vein
(portal hypertention)
Collects BLOOD from GI Tract –> LIVER
vein that ENTERS the organ (liver)
FIRST PASS METABOLISM
- *25%** cardiac output is delivered to the LIVER
- *66%** of that is via the PORTAL VEIN
1-1.5 L/min
Portal HYPERtension
Caused by what TWO types of resistance?
INCREASED Resistance to flow** through **LIVER
- *Fixed Resistance** = nonreversible
- *Fibrosis** –> destroys sinusoids –> causes physical blockage
Variable Resistance = reversible
Caused by vasoconstrictors such as endothelin in liver
Portal HYPERtension
has INCREASED blood flow due to what?
INCREASED Blood Flow** through the **PORTAL VEIN
Vasodilation of splanchnic circulation
NO2 + Prostaglandins + TNF-alpha
Expanded Plasma Volume
Due to INCREASED sodium retention
How does CIRRHOSIS result in PORTAL HYPERTENSION?
INCREASED Intrahepatic RESISTANCE
INCREASED Portal blood flow
V
V
V
INCREASED PORTAL PRESSURE = Portal HYPERtension
OHMS LAW
Pressure = Resistance X Flow
How to Measure portal hypertension?
HVPG / WHVP / FHVP
HVPG = Hepatic Venous Pressure Gradient
- *HVPG = WHVP - FHVP**
- *HVPG > 5mmHG = PORTAL HYPERTENTION**
WHVP = Wedged hepatic venous pressure
= Hepatic sinusoid pressure
FHVP = Free hepatic venous pressure
= Hepatic OUTFLOW pressure
How does
PORTAL HYPERTENSION lead to VARICEAL HEMORRHAGE?
Complications of Cirrhosis
Portal HT -> DILATION of collateral vessels
giving alternate routes of systemic curculation to:
Rectal / Splenic Veins
Paraumbilical Veins -> Caput Medusa
Intrinsic veins of esophagus –> VARICES
Esophageal Varices
Portal HT –> alternate routes of circulation
–> blood to the ESOPHAGUS
= vomitting blood / tarry stools
Screening for varices for people with cirrhosis
And Prevention
Endoscopic GRADING of severity
small or large varices (increased risk for bleeding)
if we see LARGE or Tensioned varices then…..
- *PRIMARY PREVENTION** (prophylaxis)
- *Actions to prevent a FIRST EVENT**
1st line therapy for Primary Prevention of Varices
and what do these agents do?
Primary Prevention = Actions to prevent a FIRST event
- *NON-Selective Beta Blockers**
- *B2 blockages** results in:
splanchnic vasoCONSTRICTION,
which decreases portal blood flow + pressure
reduces FIRST incidence of 1st variceal bleed
by about HALF
Non-Selective Beta Blockers
Types & Use
Primary Prevention of Varices
NEED to have the Beta-2 action
Propranolol = 20mg BID
Nadolol = 40mg HS
Carvedilol = 3.125mg BID
goal is to REDUCE HVPG < 12mm HG
Propranolol Dose
for Primary Prevention of Varices
20mg BID
Non-selective beta blocker
Nadolol Dose
for Primary Prevention of Varices
40 mg at Bedtime
Non-selective Beta Blocker
Carvedilol Dose
for Primary Prevention of Varices
3.125 mg** **BID
Non-Selective Beta Blocker
Signs and SYMPTOMS of UPPER GI BLEED
Acute Variceal Bleeding
Weakness / Fatigue / Dizziness
HEMATEMESIS
blood in VOMIT
MELENA
DARK + tarry stools