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liver disease Flashcards

1
Q

what are the hepatic intracellular enzymes?

A

Transaminase ( AST/ALT) aka SGOT/SGPT

+

LDH

primarily indicative of hepatocyte damage ( intra-cellular )

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2
Q

what are the membrane enzymes of the liver?

A

alkaline phosphatase ( Alkphos )

Gamma GTP

5’N

Indicate bile stasis/obstruction

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3
Q

describe hepatocellular damage?

A

Its intracellular

Caused by :

Hepatitis, fatty liver disease , ischemia

enzymes invovled: ALT, AST, LDH

Management : Treat underlying cause —> antiviral therapy for hepatitis and lifestyle for liver)

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4
Q

describe obstructive damage of liver?

A

Bile flow block

Enzyme involved = ALP / GGT/ 5N

Causes : Gallstones ,bile duct strictures , tumors, primary biliary cholangitis

Management : May require surgery or endoscopic procedures

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5
Q

describe bilirubin processing ?

A

1- bilirubin is transported into the cell by carrier’s at the sinusoidal membrane

2- Binds to cytosolic binding protein and gets delivered to endoplasmic reticulum

3- Gets conjugated with 1-2 molecules of glucuronic acid by bilirubin uridine diphosphate glucuronosyltransferase ( converts bilirubin into water soluble non toxic form )

4- Conjugated bilirubin then is excreted into bile

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6
Q

what is the other name of conjugated and unconjugated bilirubin?

A

Conjugated –> direct bilirubin

Un-conjugated —> indirect bilirubin

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7
Q

what is jaundice?

A

yellow discoloration of skin , sclera

occurs when theres systemic retention of bilirubin

when serum lvl is above 2 mg ( normal lvl is below 1.2 )

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8
Q

what happens to bilirubin in normal adults?

A

Rate of systemic bilirubin production is equal to :

Rate of hepatic uptakes

Rate of conjugation

Rate of biliary excretion

so when produced is excreted

Jaundice occurs when the equilibrium between bilirubin production and clearance is changed

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9
Q

describe pre-hepatic jaundice ?

A

excessive amount of bilirubin is presented to the liver due to excessive hemolysis

leading to elevated unconjugated bilirubin in serum

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10
Q

describe hepatic jaundice?

A

Impaired :

Cellular uptake

Defective conjugation

Abnormal secretion

of bilirubin by the liver cell

Leading elevated both conjugated and unconjugated bilirubin serum

example : Hepatitis , cirrhosis , alcoholic liver disease , drug induced

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11
Q

describe post hepatic jaundice?

A

Obstructive

Impaired excretion due to mechanical obstruction to bile flow

leads to elevated conjugated bilirubin in serum

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12
Q

describe neonatal jaundice?

A

Most common type of jaundice

hepatic machinery for conjugating and excretion bilirubin does not fully mature until about 2 weeks of age (immature liver function)

almost every newborn develops tansient and mild unconjugated hyperbilirubinemia

aka neonatal jaundice / physiological jaundice

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13
Q

what are the genetic causes of abnormal neonatal jaundice?

A

Gilbert syndrome

Dubin johson syndrome

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14
Q

Describe gilbert syndrome?

A

7% of population –> common

Benign

inherited condition manifest as mid fluctuating bilirubin

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15
Q

what type of bilirubin is high in gilbert syndrome ?

A

Unconjugated hyperbilirubinemia

NO MORBIDITY —> no excessive damage

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16
Q

what causes gilbert syndrome?

A

Decreased hepatic level of glucuronsyltransferase due to mutation

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17
Q

describe dubin johnson syndrome?

A

autosomal recessive

DARKLY PIGMENTED LIVER

HEPATOMEGALY WITHOUT FUNCTIONAL PROBLEMS

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18
Q

what causes dubin johnson syndrome?

A

Defect in the transportprotein

responsible for hepatocellular excretion of bilirubin glucuronides

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19
Q

what type of bilirubin is high in dubin johnson syndrome?

A

conjugated hyperbilirubinemia

cuz its defect in excretion

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20
Q

what are the non genetic causes of abnormal neonatal jaundice?

A

massive differential diagnosis

many cuases

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21
Q

what are the types of viral hepatitis ?

A

A B C D E

they all look the same

ranging from few extra portal triad lymphocytes to FULLIMANT hepatitis

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22
Q

what is viral hipatitis associated with ?

A

1- Usually fully recovered

2- Chronic progression over years leading to cirrhosis ( not rare )

3- Risk of hepatoma ( uncommon )

4- death ( Uncommon )

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23
Q

how is hepatitis virus transmitted?

A

A—> Fecal /oral

B—-> Blood/sexual

C—-> Blood/Needle

D—-> Blood ( only in ppl with Hepatits B)

E —> Fecal/oral

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24
Q

what are the sign and symptoms/presentation of hepatitis ?

A

Jaundice

Urine dark

Stool chalky

Upper respiratory infection

All have multiple antigen ( virus ) and antibody ( serology ) serum tests

Councilman —-> bodies on biopsy ( apoptotic virus infected hepatocyte )

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25
what is the pattern of viral hepatitis ?
1- Carrier state/asymptomatic c phase 2- Acute hepatitis 3- Chronic hepatitis -Chronic persistent hepatitis (CPH ) - Chronic active hepatitis ( CAH ) 4- Fulminant hepatitis 5- Cirrhosis 6- Hepatocellular carcinoma
26
what is the distinction between acute and chronic hepatitis ?
Pattern of cell injury And Severity of inflammation acute hepatitis = showing less inflammation and MORE hepatocyte death Chronic hepatitis = More inflammation and less hepatocyte death + Fibrosis development
27
whats predominant in all phases?
Mononuclear infiltrate predominate in all phases of most hepatic disease cuz they all invoke the T cell mediated immunity MAIN CELLS THAT CAN BE SEEN IN VIRAL HEPATITIS
28
what do you see in acute hepatitis?
BASH CARS ---> Cars = quick/sudden B---> ballooning degeneration (swelling damaged hepatocyte ) A ----> apoptotic bodies ( scattered ) S ----> Spotty necrosis H ----> hyperplasia of kupffer cells C---> Canalicular cholestasis A---> Acute lobular disarray --> VERY CHARACTERISTTICS R ----> Regeneration of hepatocyte --> big evidence S ----> Scant mononuclear infiltrate
29
what do you see in chronic hepatitis ?
FBI MAP --> FBI takes long time = chronic F---> Fibrosis ( portal fibrosis )--> MOST CHARACTERISTCS --> main site of inflam B----> Bridge necrosis ( in acute was spotty ) --> most characteristics I ----> Infiltrate ( dense mononuclear infiltrate ) in acute was scant M--> Macrophage aggregate A---> apoptosis ( less than acute ) P ---> persistent inflammation
30
what is apoptotic bodies in acute hepatitis ?
Aka councilman bodies acidophilic ( Eosinophilic / pink staining on H&E) globule of cells that represent a dying hepatocyte often surrounded by normal parenchyma
31
what are the 2 types of chronic hepatitis ?
Chronic persistent hepatitis Chronic active hepatitis
32
compare persistent chronic hepatitis and chronic active hepatitis ?
Persistent : Limited periportal inflammation Mild periportal fibrosis No hepatocyte necrosis Liver function test is normal or mild change Late cirrhosis Active chronic hepatitis : Extensive inflammation More fibrosis Necrosis of hepatocytes Abnormal liver function test Early cirrhosis and other complicaitons
33
quick points about transmission of hepatitis viruses ?
A and E -----> feca/oral via food/water B and C and D----> blood born ( b is std As well ) C-----> most likely to cause chronic liver disease and progress to cirrhosis and liver caner
34
describe hepatitis A virus?
benign self limited disease incubation period of 2 to 6 weeks DOESNT cause chronic hepatitis or carrier state
35
why doesnt hepatitis A cause chronic hepatitis?
Cuz its viremia transient ( blood borne transmission occurs only rarely ) its mainly fecal/oral route
36
what can hepatitis A cause ?
Spontanenous remission in more than 8 cases Prolonged cholstasis Relapsing hepatitis Fulminant hepatitis
37
describe hepatitis B virus?
virus B can cause various clinical syndromes : 1- Acute hepatitis with recovery and clearance of the virus 2-Fulminant hepatitis with massive liver necrosis 3-Nonprogressive chronic hepatitis ( doesnt worsen overtime ) 4- Progressive chronic disease sometimes ending in cirrhosis 5- Asymptomatic carrier state
38
how do we determine the phase of infection of Hepatitis B?
Surface antigen ( HBsAg ) ----> indicate active infection either acute or chronic Core antigen ( HBcAg ) ---> confirm infection status
39
what do you see in active phase infection of Hepatitis B?
Surface antigen (HBsAg ) ---> positive Anti-HBc IgM --> positive indicates recent infection
40
what do you see in window phase infection of hepatitis B?
Here its a temporary period where HBsAg disappear before antibodies appear Surface ---> HBsAg ---> disappear so negative Anti-HBcI gM ---> positive ---> Key marker in this phase Anti body without Antigen
41
what do you see in the chronic phase of Hepatitis B infection ?
Surface HBsAg---> Positive for more than 6 month Anti HBc ig G (not M )- ---> positive = indicates ongoing chronic infection
42
describe hepatitis C?
C = worst in chronicity Major cause of liver disease Worldwide carrier rate is estimated at 175 m = 3% prevalence Major route of transmission is through blood inoculation ( B,C,D = blood )
43
compare B and C?
Less dangerous than B in acute phase More likely to go chronic than B More closely linked with HCC than B
44
what can cause non viral hepatitis ?
Staph aureus --> toxic shock Gram negative ---> cholangitis Parasitic --> Malaria , schistosomes , liver flukes Ameba --> abscesses Autoimmune --> chronic disorder associated with histologic features that may be indistringuishable from chronic viral hepatitis ALCOHOLIC HEPATITIS
45
what liver diseases can result from drugs/toxins ?
Steatosis --> by ETOH Centrolobular necrosis --> BY tylenol/acetaminophen toxicity is one of the leading causes of acute failure leading to liver transplantation Diffuse massive necrosis Hepatitis Fibrosis --> by ETOH Cirrhosis ---> ETOH Granulomas Cholestasis---> steroids
46
what are some metabolic liver diseases ?
Hemochromatosis Hemosiderosis
47
Whats the difference between hemochromatosis and Hemosiderosis ?
Hemochromatosis (Iron overload ) : Excessive accumulation of iron in the liver ( Mainly ) , PANCREAS, heart Hemosiderosis : Liver, spleen , bone marrow
48
what is the cause of hemochromatosis ?
Primary iron production : Genetic disorder Autosomal recessive disease of adult onset caused by : Usually HFE gene mutuation lead to significant damage = FIBROSIS/ CIRRHOSIS
49
what causes hemosiderosis ?
Secondary iron overload due to external factors like : Chronic blood transfusions ( Example in thalasemia ) Hemolytic anemia Excessive iron intake LESS severe ---> cell damage only occur if iron overload becomes significant
50
what happens if iron build up in pancreas?
Damage the islets of langerhan cells --> responsible for producing insulin = diabetes
51
what happens if iron buildup in skin?
Bronze or grayish appearance
52
what is the clinical presentation hemochromatosis ?
Late adults Hemochromatosis will lead to : Tissue obstruction Cirrhosis Diabetes mellitus ( due to damage to langerhan cells ) Skin bronzing Arrhythmias Gonadal dysfunction Dilated and restrictive cardiomyopathy
53
what is wilson disease?
excessive accumulation of copper ( Cu)
54
what causes wilson disease ?
Mutation in the ATP7B gene responsible for regulation of excretion of copper through bile when disturbed = copper build up in many organs : liver, brain, eyes If eye ==> kayser fleischer rings = copper deposits
55
what are the lab tests done and seen in hemochromatosis ?
Increased ferritin ---> loads of Fe to be stored DECREASED TIBC ---> total iron binding capacity --> measures capacity to bind iron using transferrin ( due to overload so no capacity left ) Increased Serum Fe---> so much it leaks into blood Increased sautration
56
what do you see in the biopsy of hemochromatosis ?
Liver Brown pigment in hepatocytes IRON IS SEEN BLUE BY PRUSSAIN BLUE STAIN --> used to differentiate between lipofuscin and iron both are brown but under prussain stain iron becomes blue
57
describe alpha 1 antitrypsin deficiency ?
autosomal recessive disorder marked by abnormally low serum of alpha 1 antitrypsin
58
what is the function of alpha 1 antitrypsin ?
inhibits proteases to protect tissue like lung and liver
59
what happens when theres a deficiency ?
emphysema / liver damage accumulation of mutant alpha 1 antitrypsin in liver cells ----> HEPATITIS, CIRRHOSIS
60
how is alpha 1 antirypsin def diagnosed ?
PAS positive inclusions ( mutant AAT build up) Treatment = aat augmentation therapy
61
what is cholestasis ?
Condition resulted from impaired bile flow and cause by : Extrahepatic or Intrahepatic obstruction of bile channels OR Defects in hepatocyte bile secretions
62
what is the primary cause of cholestasis ?
Obstruction
63
what is cholestasis associated with ?
Membrane enzyme elevation : Alkaline phophatase ( AP ) Gamma glutamyltransferase ( GGTP ) 5 Nucleotidsase ( 5 N)
64
what causes extrahepatic blockage?
Blockage in bile ducts ---> Tumor or stones obstructions Can be treated by surgical intervention affected membrane bound enzymes ( AP, GGTP, 5N ---> high in biliary obstruction )
65
what causes intrahepatic blockage?
damage to liver cells or bile canaliculi ---> disease /drug CANNOT BE TREATED SURGICAL so we need to pharmacological High intra-cellular enzymes lvls = AST, ALT,LDH
66
what is the clinical manifestation of cholestasis ?
Jaundice Pruritus -> itching Skin xanthomas (cholesterol under skin ) Fat-soluble vitamin malabsorption (A,D,E,K deficiencies )---> due to reduces bile flow so : A--> night blindless D---> bone pain K--> coagulation problems
67
what are the lab findings of cholestasis ?
Elevated serum alkaline phosphatase ( AP )--> enzyme present in bile duct epithelium n hepatocyte Impaired bile flow --> elevated bilirubin -Low vitamins due to intestinal malabsorption ( absorption of fat soluble require bile )
68
what are the benign liver tumors?
Hemangioma Focal nodular hyperplasia Adenoma Liver cyst
69
what are malignant liver tumors?
Primary liver cancers : Hepatocellular carcinoma Firbolamellar carcinoma Hepatoblastoma Metastases ---> MOST OF THE CASES
70
what are the characteristics of gross hepatic adenoma ?
Well circumscribed neoplasm Rounded Surrounded by a capsule remain in the liver pale yellow brown cuz of chronic alcoholism
71
what are the microscopic features of hepatic adenoma?
Hepatic adenoma is composed of cells that closely resemble normal hepatocyte but THE NEOPLASTIC LIVER TISSUE is disorganized hepatocyte cords and does not contain normal lobular architecture DOESNT HAVE HEXAGONAL SHAPE THAT WE NORMALLY SEE
72
describe malignant liver tumors?
99% of them are metastatic ( secondary ) Js about every malignancy will wind up eventually in the liver , like the lungs
73
describe primary liver malignancies?
like hepatomas aka hepatocellular carcinomas arise in the background of already very serious liver disease chronic hepatitis / cirrhosis Are slow groving and do not metastasize readily Hemorrhage and necrosis are key features that indicate malignancy in liver tumors
74
describe cholangiocarcinomas ?
malignancies in the intra hepatic bile ducts and look much more like adenocarcinomas than do hepatomas
75
what are the grossly features of hepatomas/ hepatocellular carcinomas ?
Unifocal --> usually massive tumor Multifocal ---> tumor made of nodules of variable sizes Diffusely infiltrative cancer ---> sometimes involves the entire liver Greenish cast because it contain bile
76
describe histological features of hepatocellular carcinomas ?
range from well differentiated lesions that reproduce hepatocyte arranged in CORDS or Glandular patterns To Poorly differentiated lesions often composed of large , multinucleate anaplastic giant cells Acini like or pseudo acinar structures and rosette like patterns suggesting disorganized arrangement Surrounding bile duct accumulation maybe observed due to bile duct proliferation and obstruction caused by tumor presences
77
what are the signs of liver metastasis ?
multiple focal area in large number Some small and large ( irregular ) Different color for example : tan white masses , multiple and irregularly sized like many large metastatic lesions
78
what are the features of cholangiocarcinoma ?
adenocarcinomas that arise from : Cholangiocytes lining the intrahepatic and extrahepatic biliary ducts Asymptomatic until they reach advances stage Prognosis is poor and most patients unresectable tumors --> palliative and chemotherapy
79
what are the histological features of cholangiocarcinoma ?
Tumor cells forming glandular structures surrounded by : Dense sclerotic stroma

PATHOLOGYY2S2 (12 decks)

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