Cirrhosis - causes, symptoms, diagnosis, treatment, pathology

Question 1

usually dead tissue becomes fibrotic: thickened with heaps of protein and forms scar tissue

Answer 1

When cells injured/damaged and die off,

Question 2

constantly processing alcohol or subject to viral attack for long time (Hep B/C), other thing that causes long-term/chronic state of liver cell/hepatocyte destruction and inflammation - becomes seriously scarred and damaged - no longer reversible: becomes fibrotic: cirrhosis: irreversible

Answer 2

Liver -

Question 3

ESLD

Answer 3

Cirrhosis:

Question 4

colonies living liver cells - classic signs cirrhosis making liver more bumpy; in between nodules fibrotic tissue and collagen

Answer 4

When liver cells injuried come together and form regenerative nodules -

Question 5

Fibrosis - mediated by stellate cells between sinusoid and hepatocyte: perisinusoidal space
Hepatic artery and portal vein combine ino sinusoid then going into central vein which lined with hepatocytes - along have bile duct and those 3 constitute portal triad (vein, artery, duct)
perisinusoidal space and stellate cells - health tissue: store vitamin A and considered dormant; key role in wound-healing process
Hepatocytes injured: secrete paracrine factors: activates and change stellate cells: causing stellate cells to lose vit A, proliferate, secreteting growth factor beta1 (TGF-beta) causing them to produce collagen - main ingredient in extra-cellular matrix, fibrosis, scar tissue
As fibrotic tissue grows, compresses central veins and sinusoids; stellate cells - constantly active - producing collage and factors leading to fibrosis

Answer 5

Formation fibrotic tissue and collagen

Question 6

Central veins and sinusoids compressed and push on fluid inside, pressure increase leading to portal HTN - means fluid in blood vessels more likely get pushed out into tissue and across tissues into large open spaces (peritoneal cavity) - LEADS TO ASCITES
Congestive splenomegal and hypersplenism - spleen enlarged because fluid and blood cannot get into liver and backs up into the spleen
Circ sys diverts blood away from liver because high liver pressure - portosystemic shunt - following least resistance - towards systemic sys circulation; trigger renal vasoconstriction - increased resistance in renal circ decreasing blood flow through the kidneys leading to decreased filtration and hepatorenal failure - kidney failure follows liver failure
Fibrotic tissue, pressure build up, blood diversion from liver reduces number functional sinusional veins and number functional portal triads - leading to decrease liver function and functional units - cannot do detoxification: toxins get into brain leading to hepatic encephalopathy: ammonia; may develop asterixis; can go into a coma
Liver metabolises estrogen into inactive metabolites - removed from blood and excreted can experience: gynecomastia, spider angiomata, palmar erythmea
Liver usually conjugates bilirubin - now increased unconjugated bilirubin in blood - jaundice
Albumin produced normally - so decreased now: hypoalbuminemia
Makes clotting factor - decreases clotting factor - coag issues

Answer 6

Comps result

Question 7

Some fibrosis - compensated cirrhosis - still do lot jobs
Asymptomatic
Non-specific symp: weight loss, weakness, fatigue

Answer 7

Early on: - Symp

Question 8

Extensive fibrosis - decompenseated cirrhosis - not function properly
Jaundice, pruiritis (itchy skin)
Ascites
Hepatic encephalopathy - leading to confusion
Easy bruising

Answer 8

Later - Symp

Question 9

Liver biopsy - gold standard
Lab

Answer 9

Diagnosis

Question 10

Elevated bilirubin
Elevated enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT); AST more elevated than ALT; alkaline phsopatase (ALP); gamma glutamyl transpeptidase (GGT)
Thrombocytopenia

Answer 10

Lab

Question 11

Scarring and cirrhosis - irreversible
Prevent further damage
Treat underlying cause - stop alcohol or antiviral for Hep C/B
Adv cirrhosis with stopped liver fun: liver transplant

Answer 11

Treatment