Cirrhosis: DR Akhondei
Cirrhosis: DR Akhondei
Cirrhosis: DR Akhondei
Dr akhondei
cirrhosis
Normal liver
Variceal bleeding
New onset of ascites
Hepatomegaly and/or
splenomegaly
CIRRHOSIS
Marked fibrosis
Destruction of vascular & biliary elements
Regeneration
Nodule formation
Cirrhosis: Pathophysiology
Cirrhosis: Pathophysiology
Cirrhosis: Pathophysiology
Causes of Cirrhosis
Alcohol
Viral hepatitis
Biliary obstruction
Veno-occlusive disease
Hemochromatosis
Wilsons disease
Autommune
Drugs and toxins
Metabolic diseases
Idiopathic
Classification of Cirrhosis
Micronodular
Macronodular
Mixed
Micronodular Cirrhosis
Cirrhosis - Alcohol
Cirrhosis - Alcohol
NAFLD/NASH
Viral Hepatitis
DIAGNOSIS
DIAGNOSIS
Manifestations of Cirrhosis
Hepatorenal syndrome
Hepatic encephalopathy
Portal hypertension
Water retention
Hematologic
Hepatocellular carcinoma
Pathophysiology of PH
Pathophysiology of PH
Etiology of PH
Pre-hepatic
2.
Intra-hepatic
3.
Post-hepatic
Pre-hepatic PH
Post-hepatic
Budd-Chiari Syndrome
Budd-Chiari Syndrome
Budd-Chiari Syndrome
Complications of PH
Varices
Prevention of Varices
Prevention of Varices
Beta blockade: Beta blockade (Nadolol,
Propranolol)
Nitrates:Organic nitrates
Surgery: No longer performed *
Endoscopy: Sclerotherapy (no longer
used*) and variceal ligation
* Refers to primary prophylaxis
Treatment of Varices
Initial Management:
1.
2.
3.
4.
5.
6.
Airway control
Hemodynamic monitoring
Placement of large bore IV lines
Full lab investigation (Hct, Coags, LFTs,)
Administration of blood products
ICU monitoring
Pharmacologic Treatment of
Varices
Balloon Tamponade
Sengstaken-Blakemore tube
Minnesota tube
Alternative therapy for pts. who fail
pharmacologic or endoscopic therapy
Complications: aspiration, perforation,
necrosis
Limited to 24 hrs; works in 70-80%
TIPS
Surgical Intervention
Devascularization
Severe complications
response
The same cell type produce hepatic
fibrosis regardless of the underling
cause.
hepatic fibrosis follows chronic,but not
self-limited,injury.
Fibrosis occurs earliest in regions where
injury is most severe.
Antifibrotic therapies :
Rationale and specific
Agent
The
paradigm of satellite cell activation
4.Neutralize the
proliferative,fibrogenic,contractile,and
proinflammatory responses of stellate
cells.
5.Stimulate apoptosis of stellate cells.
6.Increase the degradation of scar
martix,either by stimulating cells that
produce matrix proteases,down-regulating
their inhibitors ,or directly administering
matrix proteases.
DIAGNOSTIC APPROACH
DIAGNOSTIC APPROACH
DIAGNOSTIC APPROACH
Resolution
Short-term
Infection
Resolution
Long-term
Hepatitis
Long-term
Carrier
Silent
Cirrhosis
Cirrhosis
Cirrhosis
30 - 50 Years
Liver
Cancer
Death
Death
Hepatocellular
carcinoma
Turner Lisle
Cirrhosis
End result of anything that causes
hepatocellular
injury
Hepatocellular necrosis
Fibrosis
Nodular regeneration
Hepatic failure
Portal hypertension - variceal bleeding
Anatomy
Hepatic arterial
Portal venous
Hepatic artery
>1/2 of O2
Portal Hypertension
Prehepatic
Intrahepatic
Presinusoidal
Schistosomiasis
Nonalcoholic cirrhosis
Sinusoidal
EtOH
EtOH
Budd-Chiari syndrome (hepatic vein thrombosis)
Constrictive pericarditis
Heart failure
Portal Hypertension
Collateralization
Physical Exam
Jaundice
Ascites
Caput medusae
Asterixis
Spider angiomas
Palmer erythema
Testicular atrophy
Gynecomastia
+/- Palpable spleen
(portal HTN)
Lab tests
Anemia
Thrombocytopenia
Coagulopathy
Hypoalbuminemia
AST/ALT
Bili
Alk Phos
GGT
Hepatitis serologies
-fetoprotein
Liver biopsy
Cause of cirrhosis
Activity of liver disease
Approaches
Encephalopathy grade
Amount of ascites
Bilirubin
Albumin
PT (INR)
Operative mortality
A (5%)
B (10-15%)
C (25%)
Subjective
MELD
Bilirubin
INR
Creatinine
Cr Max = 4.0 mg/dL
On dialysis calculate
with CR = 4.0 mg/dL
MELD 5-20
1% increase in mortality with each integer rise in
MELD score
MELD >20
Additional 2% increase in mortality with each integer
rise in MELD score
Diagnosis of bleeding
Variceal Hemmorrhage
Multifactorial
Portal pressure >12mmHg
Treatment
Resuscitation first
Endoscopy
Pharmacotherapy
Successful in >85%
Vasopressin +/- NTG
Somatostatin/Octreotide (fewer complications)
Endoscopic treatment
Esophageal ulceration
Perforation
Worsening hemorrhage
Aspiration
Sengstaken-Blakemore tube
TIPS
Transjugular Intrahepatic Portosystemic Shunt
Emergency surgery
Indications
Prevention of recurrent
hemorrhage
Likelihood of repeat episodes >70%
Goals
Options
Portosystemic shunts
Encephalopathy
Accelerated hepatic failure
Types
Nonshunt procedures
Objectives
Ablation of varices
Extensive interruption of collateral vessels
Options
Ascites
Ascites treatment
Dietary restriction
Dietary restriction + Diuretics
SBP
Encephalopathy
Variety of manifestations
Pathogenesis - circulating cerebral toxins
Ammonia
Mercaptans
-aminobutyric acid
Shunts, hemorrhage, excessive diuresis, azotemia,
infection, increased dietary protein, sedatives
Management
Questions