Liver Disorders Flashcards by Richard Froude

Physiologic liver functions

lipid, carb, protein metab
clotting factor production
detox
storage of vitamins and glycogen
bile processing and secretion

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Liver composition and role

Composed of hepatocytes, bile ducts, blood vessels
Central organ of metabolic homeostasis
Large functional reserve and regenerative capacity

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Causes of chronic liver dz

Hep C, EtOH Induced, Non-EtOH fatty liver dz, Hep B

Also, blood flow abnormalities, usually INTRAHEPATIC lfow probs (from cirrhosis occlusion)

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Grade and Stage

grade = amount of infl and injury
Stage = amount of fibrous tissue deposition (on liver biopsy)

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Liver Failure (info/cause/3 types)

Caused by acute or chronic failure via cirrhosis
NEED TO HAVE 80-90% loss of function before you see sx
1) massive necrosis, 2) cirrhosis (scarred liver) 3) dysfunction +/- cirrhosis or necrosis

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Liver Failure (pres)

Ascites, jaundice, scleral icterus
Spider angioma, palmar erythema, gynecomastia
Coagulopathy, encephalopathy, renal failure

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Cirrhosis (info/cause/pres)

Scarred liver, common end point to many chronic liver dz
Result of recurring death of hepatocytes and deposition of ECM
Pres with 1) PORTAL HTN (splenomegaly, eso varcies, ascties, periumbilical medusae, encephalotphay
2) JAUNDICE (bilirubin production > clearance)
3) CHOLESTASIS (impaired bile flow)

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Cirrhosis (diagnx)

Diffuse fibrous septation that divides the liver parenchyma in NODULES

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Hepatitis (Acute)

Causes and Infl cell profiles

New onset (

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Hepatitis (def)

Inflammatory dz of hepatocytes (liver) and characterized by presence of inflammatory cells in the tissue of the liver

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Hepatitis (Chronic)

Causes and accumulations

Sx dz for >6 mos
Common causes CHRONIC VIRAL (moslty C, B, D), autoimmune, drug injury
SPOTTY injury (looks less severe than acute)
Grade: amount of infl
Stage: amount of fibrosis
Cytoplasmic accumulations: fat (steatosis), bile (cholestasis), iron (hemosiderosis), Copper (Wilson), Viral (viral hepatitis GROUND GLASS HISTOL)

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VIRAL HEPATITIS
Hep C (info)

Major cause of liver dz in US
Genetically unstable (many genotypes and subtypes)A
Anti-HCV Ab are made BUT are not neutralizing so NO VACCINE
Risks: IV drugs, multiple partners, surgery, needle injury, multiple HCV contacts

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VIRAL HEPATITIS
Hep C (pres/diagx/treat)

85% acute to chronic dz, often asymptomatic if acute
Diagnx: Lymphoid aggregates (see chronic hep)
Treat: GOAL: remain HCV RNA neg for 12 WEEKS AFTER STOPPING TX
Genotype 1: SVR 40-70% (PegIFN, Ribavarin, protease inhib)
Genotype 2 & 3: PegIFN, Ribavarin

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Hepatotropic viruses

hepatocyte is primary target

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SVR? (for Hep)

Sustained Virological Response = Cure

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VIRAL HEPATITIS
Hep B (cause/diagnx/treat)

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Major cause of liver dz WORLDWIDE
dsDNA virus (can integrate into genome)
Transmitted via blood, VACCINE EXISTS
Diagnx: GROUND GLASS HEPATOCYTES, SANDED NUCLEUS
Treat: IFN for 1 yr (flu-like side fx), nucleoside/tide (Tenofovir)
IF: HBsAg > 6 mos, HBV DNA > 10^5, persistent or intermittent high ALT and AST (cirrhosis)

VIRAL HEPATITIS
Hep B (pres MARKERS)

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Most ADULTS recover (5% progress to chronic) - more children do
HBsAg (surface antigen): ACTIVE INFX
HBsAb: IMMUNITY to HepB
HBcAb: ACTIVE or PRIOR infx
HbeAg: ('e' antigen) HIGH VIRAL LOAD
HBeAb: LOW VIRAL LOAD
HBV DNA: ACTIVE VIRAL REPLICATION

VIRAL HEPATITIS

Hep D

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cannot replicate, COMPLETELY DEPENDENT ON HEP B COINFECTION, potentiates effects of Hep B, parenteral transmission
Pres: increased risk of fulminant Hep, + activity and faster progress to end-stage liver dz
Diagnx: may show increased plasma cells

VIRAL HEPATITIS

Hep A

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Oral/fecal transmission (and bad strawberries)
VACCINE available
Does NOT progress to chronic
Diagnx: IgM Ab in serum

VIRAL HEPATITIS

Hep E

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Oral/fecal trans
HIGHER MORTALITY in PREGNANT WOMEN
Acute
Diagnx: Igm/IgG Ab in serum

AUTOIMMUNE

Autoimmune Hep

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Immune attack of hepatocytes, 78% women, usually with autoimmune dz
Pres: variable
Diagnx: serology: AutoAb (ANA, ASMA, Anti-LKMB) & elevated IgG but PLASMA CELL RICH
Treat: Immune suppression (steroids, Azathioprine), treat for a few years after normal to prevent relapse

AUTOIMMUNE
Primary Biliary Cirrhosis
(info/pres)

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Bad name: not necessarily cirrhosis
Immune attack of INTRAHEPATIC ONLY small caliber bile ducts
nearly ALWAYS middle aged women
Pres: INSIDIOUS ONSET WITH PRURITUS BEFORE JAUNDICE

AUTOIMMUNE
Primary Biliary Cirrhosis (PBC)
(diagnx/treat)

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Elevated ALP, IgM (GGT, bilirubin)
AMA in 90%
Granulotamous lympocytic cholangitis, florid duct lesion, eventual ductopenia
Treat: URSODEOXYCHOLIC ACID (aka ursodiol, slows prog)
Fair prognosis (25% with liver failure at 10 yrs)

AUTOIMMUNE
Primary Sclerosing Cholangitis
(info/pres/treat)

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Immune attack of INTRA- AND EXTRAHEPATIC bile ducts (usually larger caliber)
M>F, 70% have UC, increased risk for cholangiocarcinoma
Asymptomatic (elevated ALP) –> progresses to fatigure, pruritus, jaundice
Treat: no good tx, manage progression

AUTOIMMUNE Primary Sclerosing Cholangitis (Diagnx)

Persistent ALP elevation and IgM Diagnx with cholangiography (ALTERNATING BILIARY STRICTURES AND DILATION) No specific serology PERIDUCTAL "ONION SKIN" FIBROSIS --> progresses to fibrous obliteration of bile ducts

DRUG INDUCED (general)

common cause with many patterns of injury Intrinsic: all affected in dose related way Idiosyncratic: only certain people have bad reaction Treat: discontinue drug

DRUG INDUCED | Acetaminophen

Intrinsic (all affected), often in suicide attempts Major casue of ACUTE liver failure Injury in ZONE 3 (cnetral vein), CONFLUENT CENTRILOBULAR COAGULATIVE NECROSIS Treat: Remove drug (lavage, charcoal), N-acetylcysteine

METABOLIC LIVER DZ (here adults, but more common in kids) EtOH related Steatohepatitis vs Non EtOH

EtOH: blocks lipid clearance (beta-oxidation of lipids into CO2 and ketones) and stimulates lipogenesis Non-EtOH (NASH): assoc with metabolic syndrome (obesity, DM) fatty liver --> decreased lipolysis

METABOLIC LIVER DZ | EtOH/non-EtOH Steatohepatitis (pres/diagnx/treat)

Steatosis = lipid production>clearance (may progress to steatohepatitis) Diagnx: ballooned degeneration, PMN infiltrates pericentral/perilobar fibrosis EtOH: Mallory Bodies (AST AT LEAST 2s ALT) Treat: life modification

METABOLIC LIVER DZ Hereditary Hemochromatosis (cause/pres)

Iron overload (genetic), AR, HFE mutation [*C282Y* and H63D], M>F Pres: 44% with joint stiffness Hyperpigmentation, Diabetes, Hypothyroidism Hypogonadism, Cardiomyopathy, Cirrhosis

METABOLIC LIVER DZ Hereditary Hemochromatosis (diagnx/treat)

``` Iron stain (prussian blue), Fe in HEPATOCYTES, NOT Kupffer cells (would be hemosiderosis) HPE gene testing, + ferrtin, + transferrin sat., + Fe sat. TREAT: Tx phlebotomy, endpoint: serum ferritin at 50ng/ml - Fe intake, genetic counseling, if anemic: chelation ```

METABOLIC LIVER DZ | Wilson Dz

Copper overload (genetic), AR, ATP7B mutation (transporter for bile excretion of Cu) Pres: Liver dz and neuropsych dz Diagnx: Copper stain (Rhodamine) Treat: chelators (D-penacillinamince, tirentine, then transition to oral zinc

METABOLIC LIVER DZ | Alpha-1-anti-trypsin

Dec produciton of A1AT (protease inhib), AR, PiZZ dz genotype (PiMZ heterozygote is normal) Pres: assoc with emphysema (10% have liver dz) Diagnx: PAS-positive, diastase resistant pink globules of A1AT in hepatocytes

``` LIVER MASSES Hepatocellular Carcinoma (malignant) ```

Most common malignant liver tumor Almost always in pts with chronic liver dz (eg Hep B, C, EtOH), dismal long term survival Diagnx: THICKENED HEPATIC PLATES (trabeculae), UNPAIRED ARTERIOLES (neovasculatization), ELEVATED AFP Treat: resect/transplant and if not: trans-arterial chemoembolization

LIVER MASSES | Malignant Cholangiocarcinoma

Neoplasm of bile ducts (intra- or extrahepatic), PSC is major risk factor, dismal long tern survival (25% at one year) Diagnx: GLAND FORMING WITH DESMOPLASIA

LIVER MASSES | Metastases

Common place for metastases, well circumscribed, most tumors in liver are metastatic of other cancers

LIVER MASSES | Hemangioma (Benign)

MOST COMMON OF ALL HEPATIC TUMORS F>M, 4:1 Pres: usually small and asymptomatic, vague RUQ pain, early satiety, nausea, vomiting Diagnx: spongy appearance, dilated thin walled vascular spaces Treat: resect for larger ones

LIVER MASSES | Focal Nodular Hyperplasia (Benign)

F>M, 4:1, arise due to local vascular flow anomaly, hepatocyte mass Pres: usually small and asymptomatic, vague RUQ pain, early satiety, nausea, vomiting Looks cirrhotic but focal, CENTRAL STELLATE SCAR, ENLARGED ABNORMAL ARTERIOLES

``` LIVER MASSES Hepatocellular Adenoma (Benign) ```

Women of childbearing age, ORAL CONTRACEPTIVE USE, LOW RISK OF MALIGNANCY, no chronic liver dz Pres: asymptomatic or RUQ pain, risk of rupture/hemorrhage into abd (if v large) Diagnx: hepatocyte proliferation (looks like hepatocellular carcinoma)

Liver Disorders Flashcards

(39 cards)