This document presents in a very organized and easily accessible way all the informations about diseases and pathology of the liver and gallbladder. It contains images that facilitate learning. Is has all the informations presented in Robbins and Cortan Pathologic Basis of Diseases.
ROBBINS AND COTRAN PATHOLOGIC BASIS OF DISEASE, Ninth Edition Anki flashcard
Necrosis
All for this textbook (51)
Written for
Poznan University of Medical Sciences
Pathology (PATHO)
All documents for this subject (3)
Seller
Follow
AlexandreAlChidiac
Content preview
Liver & Gallbladder
GENERAL FEATURES OF LIVER DISEASE
MECHANISMS OF INJURY & REPAIR
Reversible changes: fat accumulation and cholestasis (bilirubin accumulation)
Irreversible changes: necrosis (following hypoxia and ischemia) and apoptosis (autoimmune
diseases, viruses, drugs, and toxins)
Confluent necrosis: widespread death of hepatocytes
o Begins around the central vein bridges central veins and portal tracts
Regeneration of dead hepatocytes
o Mitotic replication of adjacent cells
o Differentiation and proliferation of stem cells in the canal of Hering (in chronic liver
diseases) ductular reactions (duct like structures formation)
Chronic injury large number of hepatocytes death and collapse of the underlying reticulin
scar formation: by the perisinusoidal hepatic stellate cells (highly fibrogenic myofibroblasts)
cirrhosis (fibrous septae formation)
LIVER FAILURE
ACUTE LIVER FAILURE
Live disease that produce hepatic encephalopathy within 6 months of the onset of jaundice
Fulminant liver failure encephalopathy within 2 weeks
Subfulminant liver failure encephalopathy within 3 months
Caused by: acetaminophen overdose, hepatitis (A, B, C, D, E, autoimmune, drug-induced, fatty
liver)
Cause massive hepatic necrosis, without scar formation (acute)
CLINICAL FEATURES
Increased serum transaminase decline dramatically (with loss of hepatocytes)
Hepatomegaly shrinkage (parenchyma destruction)
Retention of bilirubin jaundice (yellow discoloration of the skin), icterus (yellow discoloration
of the sclera), and cholestasis (decreased bile flow)
Hepatic encephalopathy: rigidity, hyperreflexia, and asterixis (nonrhythmic rapid extension-
flexion of the head and extremities flapping of the hands wen arms are extended and wrists
are dorsiflexed)
o Increased ammonia levels in blood and CNS
Coagulopathy
o Decreased production of coagulation factors bruising and bleeding
o Decreased metabolism of activated coagulation factors DIC
Intrahepatic obstruction ascites (but causes portal hypertension in chronic liver failure)
Hepatorenal syndrome (renal failure): sodium retention, impaired water excretion (decreased
urine output), decreased renal perfusion and GFR (by activation of renin-angiotensin axis and
sympathetic nervous system vasoconstriction of afferent arteriole)
, o Increase blood urea nitrogen and creatinine levels
CHRONIC LIVER FAILURE & CIRRHOSIS
Cirrhosis: associated with chronic liver failure, diffuse transformation of liver into regenerative
parenchymal nodules surrounded by fibrous bands
o Prominent ductular reactions with disease progression bad prognosis
Caused by: chronic hepatitis B and C, non-alcoholic fatty liver disease (NAFLD), and alcoholic liver
disease
Disease remission regression of fibrosis: thinner scar, fibrous septa breaks, regenerating
parenchymal nodules coalesce
Active drinker liver cirrhosis | After long-term abstinence
CLINICAL FEATURES
Asymptomatic until advanced stage
Jaundice, encephalopathy, and coagulopathy (similar to acute liver failure) with the addition of:
Chronic sever jaundice pruritus (itching): patients scratch their skin (risk of infections)
o Indication of liver transplantation
o Also seen in: cholestasis
Portal hypertension esophagogastric varices (causes by portosystemic shunts: blood flow
reversed from portal to systemic circulation) hematemesis
o Also causes congestive splenomegaly expanded red pulp increased sequestration
decreased platelets count
o In males: periumbilical caput medusae, hemorrhoids, testicular atrophy
o In females: oligomenorrhea, amenorrhea, sterility
Impaired estrogen metabolism in males hyperestrogenemia, causes
o Palmar erythema (local vasodilation) and spider angioma
o Hypogonadism (also in women) and gynecomastia
Increased risk of hepatocellular carcinoma HCC
Thin fibrous septa and large islands of regenerated parenchyma NO portal hypertension
Broad bands of fibrosis and loss of parenchyma portal hypertension and end-stage liver
disease
ACUTE-ON-CHRONIC LIVER FAILURE
Sudden signs of acute liver failure after years of stable and well-compensated chronic disease
Previous cirrhosis with vascular shunting OR liver parenchyma with borderline vascular supply
liver vulnerable of lethal insults: hepatitis D superinfection of chronic hepatitis B, resistance to
therapy of viral hepatitis, ascending bacterial cholangitis in primary sclerosing cholangitis,
development of metastatic carcinoma
INFECTIOUS DISORDERS
VIRAL HEPATITIS
, HEPATITIS A VIRUS (HAV)
(+) RNA, picornavirus (genus: hepatovirus)
Benign, self-limited infection, cleared by host immune response, NO carrier state
DOES NOT cause chronic hepatitis, rarely causes fulminant hepatitis
Incubation period: 3 – 6 weeks
Associated with poor hygiene and sanitation
Available vaccine
Symptoms: fever with jaundice, and nonspecific fatigue and loss of appetite
Transmission: oral-fecal, contaminated food (shellfish) and water
Detected in stool (2 – 3 weeks before and 1 week after jaundice), serum, and saliva
o Transient viremia NO blood-borne transmission
IgM appear at the onset of symptoms
Fecal shedding ends with IgM rise
IgM declines in months IgG persist for years
HEPATITIS B VIRUS (HBV)
Circular ds-DNA virus, hepadnaviridae
Self-limited infection without treatment, but with risk of chronic liver disease development
Incubation period: 2 – 26 weeks
Transmission: perinatal (during childbirth), spread among children through breaks in skin and
mucous membranes, sexual, IV drug users, blood transfusion (HBsAg screening in donors)
Young patients increased risk of chronic infection
Remains in blood during acute and chronic disease
DNA encodes
o HBcAg: nucleocapsid core protein antigen
o HBeAg: nucleocapsid precure and core region antigen
o HBsAg: envelope glycoprotein surface antigen
o Polymerase with both polymerase and reverse transcriptase activity (against treatment)
o HBx protein: transcription activator for viral genes
Outcomes of the disease (depends on host CD4+ and CD8+ immune response)
o Acute hepatitis with complete recovery
o Nonprogressive chronic hepatitis
o Progressive chronic disease with cirrhosis
o Fulminant hepatitis with massive necrosis
o Asymptomatic healthy carrier state
Increased risk of HCC
Serum markers:
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller AlexandreAlChidiac. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for $7.49. You're not tied to anything after your purchase.
