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GIGU2 Exam 2 > Liver, Gallbladder, Pancreas - Dr. Dobson > Flashcards

Liver, Gallbladder, Pancreas - Dr. Dobson Flashcards

1
Q

alimentary canal

A

GI tract

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2
Q

accessory digestive structures

A
  1. teeth
  2. tongue
  3. salivary glands
  4. liver
  5. pancreas
  6. gallbladder
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3
Q

portal triad

A
  1. Hepatic Artery
  2. Portal Vein
  3. Bile Duct (flowing opposite way)
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4
Q

Canals of Hering

A

connect to bile ductules and into terminal bile ducts

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5
Q

Space of Disse contains what

A

= scattered Kupffer cells
= hepatocyte microville
= Hepatic stellate cells

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6
Q

normal indirect bilirubin level

normal direct bilirubin level

A
  1. 0.2-0.9

2. 0.1 - 0.3

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7
Q

Abnormalities in labs showing liver disease

A
  1. GGT (98% chance of lver disease if not normal level)

2. AST/ALT levels

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8
Q

AST > 3000U/L

A

severe HTN episode causing centrilobular necrosis (seen in acetaminophen overdose + acute viral hepatitis)

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9
Q

AST = 100 -300 U/L

A

alcoholic liver disease , chronic liver diseases, chronic viral hepatitis

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10
Q

AST : ALT = 2:1

A

alcoholic hepatitis

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11
Q

high ALP

A

bone disease or liver disease

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12
Q

high ALP + high GGT =

A

cholestatic liver disease

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13
Q

how to assess liver function

A
  1. PT : acute liver function changes (since it makes coag factors)
  2. Albumin : chronic liver function changes
  3. gamma-globulin levels (only elevated in chronic liver function decline)
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14
Q

acute hepatitis pattern

A

elevated AST/ALP, other things are variable levels

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15
Q

cirrhosis pattern

A

elevated gamma-globulin (with B-g bridging pn serum electrophoresis), elevated PT, LOW albumin

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16
Q

chronic hepatits pattern

A

combination of acute hepatitis and cirrhosis patterns

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17
Q

Obstructive liver disease pattern

A

cholestasis : elevated ALP and elevated bilirubin

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18
Q

histologic changes that are reversible

A
  1. fat steatosis
  2. bilirubin cholestasis
  3. ballooning (cell swelling)
  4. Mallory Hyaline filaments
  5. cytoplasmic clearing
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19
Q

coagulative necrosis

A

SEEN : acute toxic or ischemic injuries or severe viral or autoimmune hepatitis
HISTOLOGY : confluent, bridging, pan-acinar

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20
Q

how do apoptotic cells look like

A

round / oval mass of intensely eosinophilic cytoplasm + dense nuclear chromatin fragments (seen in HCV)

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21
Q

Mechanism of liver repair

A

scar (hepatic stellate cells)and regression and regeneration (hepatocytes are like stem cells)

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22
Q

Hepatic stellate cells

A

normal : lipid Vitamine A storing cells

acute of chronic injury conditions : fibrogenic myofibroblasts causing scarring

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23
Q

what activates hepatic stellate cells

A

TNF-a

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24
Q

Areas that fibrose and scar

A

link 2 portal triads and then continue and cause cirrhosis (nodules are the surviving cells trying to replicate)

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25
Q

liver failure happens when how much of the liver isn’t functioning and survivor rate

A

80%-90%

80% mortality unless liver transplant is done

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26
Q

acute liver failure most common cause and definition of it

A
  1. Acetominophen overdose = massive necrosis
  2. liver disease with encephalopathy and coagulopathy within 26 weeks of initial injury in the absence of pre-existing liver disease
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27
Q

other causes of Acute liver failure

A
  1. fatty liver of pregnancy (steatosis) no necrosis

2. virus infection

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28
Q

acute liver failure sx

A

V, N, icterus, jaundice, itching, HIGH LFTs
= life threatening coag abnormalities*
= hepatic encephalopathy
= can lead to multi-organ failure if not tx

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29
Q

Chronic Liver failure is associated mostly with and most common cause of it

A
  1. cirrhosis happens from this

2. chronic HBV, chronic HCV, NAFLD, AFLD cause this

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30
Q

CTP score of :

  1. 5-6
  2. 7-9
  3. 10-15
A
  1. class A, 15-50 years
  2. class B, transplant candidate
  3. class C, 1-3 months
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31
Q

chronic liver failure sx

A 
40% asymptomatic until advanced stage*
WL, weakness, Portal HTN** , jaundice**
1. palmar erythma*
2. Spider angiomata*
3. Hypogonadism*
4. Gynecomastia *
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32
Q

portal HTN from cirrhosis can cause

A
  1. ascites (85%)
  2. varices, hemorrhoids, abd wall vessle dilations
  3. splenomegally —-> thrombocytopenia, panocytopenia
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33
Q

what organisma can involve the biliary tree and liver as local infections or systemic infections

A
  1. bacteria,
  2. fungi
  3. halminths : schistomsomaisis, strongyloidiasis
  4. protozoa : malaria, cryptosporidium
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34
Q

HAV :
TR
Dx
chronic liver disease y/n

A

ssRNA

  1. fecal oral, water contaminated
  2. Serum IgM ABs
  3. no
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35
Q

HBV :
TR
Dx
chronic liver disease y/n

A

partially dsDNA

  1. parenteral, sexual, perinatal
  2. HBsAg, HBcAg, , PCR HBV DNA
  3. 5%-10% of times yes
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36
Q

HCV :
TR
Dx
chronic liver disease y/n

A

ssRNA

  1. Parenteral , Intranasal cocaine use
  2. ELISA for HCV AB, PRC HCV RNA
  3. more then 80% yes
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37
Q

HDV :
TR
Dx
chronic liver disease y/n

A

ssRNA circular

  1. parenteral
  2. serum IgM and IgG, PCR for HDV RNA
  3. 10% (co-infection), 90%-100% (Superinfection) yes
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38
Q

HEV :
TR
Dx
chronic liver disease y/n

A 
ssRNA
1. Fecal oral
2. Serum IgM and IgG, PCR for HEV RNA
3. only if immunocompromised yes
= no vaccine
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39
Q

HAV risk of acute hepatic failure

A

0.2% , its a benign self limited disease, poor hygiene and sanitation

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40
Q

HAV sx and complications

A
  1. jaundice, fatigue, recover in 3mos

2. cholestasis, Extrahepatic : rash, arthralgia, vasculitis

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41
Q

HBV 4 different disease pathways

A
  1. acute hep —-> recovery + clearance
  2. acute hepatic failure + massive liver necrosis
  3. chronic hep that can —-> cirrhosis
  4. asymptomatic healthy carrier
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42
Q

high HBV prevealence places most common TR

A

childbirth (90% cases + 40% of the infants)

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43
Q

main determinant to outcome of HBV infection

A

the hosts immune response, strong can resolve the acute infection

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44
Q

protien formed in HBV that is associated with HCC

A

HBx

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45
Q

HBeAB means what

A

ACUTE : infection has peaked and on wane

CHRONIC : not made or at late course of disease

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46
Q

HBV and rate of getting liver failure and chance of being chronic

A
  1. 0.3% its self limited

2. 5%-10% especially if from childbirth then also high chance of getting HCC

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47
Q

chronic HBV TX

A

INF-g and Antiviral reverse transcriptase inhibitors (tenofovir) = slow detrimental effects

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48
Q

most common cause of chronic hepatits

A

HCV

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49
Q

HCV sx

A

asymptomatic during acute phase(85%)
= persistent infection and chronic hepatitis **
= cirrhosis can lead to HCC

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50
Q

reason its hard for immune system to resolve HCV

A

many variants formed

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51
Q

co-infection of HDV and superinfection of HDV

A
  1. acute HBV + HDV

2. chronic HBV + HDV

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52
Q

HEV TR and prevalence location, risk of becoming chronic and death risk

A

water-borne and fecal oral, young middle aged, 30% of acute hepatitis in India
= no chronic liver disease unless immunosuppressed
= 20% in pregnant women

53
Q

chronic hepatitis hallmark

progressive chronic liver damage hallmark

A
  1. increased portal lymphocytic chronic inflammation + fibrosis (also seen in autoimmune hep and steatohepatitis)
  2. scarring
54
Q

HBV chronic infection histology

A

ground-glass hepatocytes from accumulatino of hep B surface Ag (HBsAg)

55
Q

HCV chronic infection histology

A

portal tract expansion by a lymphoid follicle

56
Q

toxins that can injure the liver and wherein liver the injury occurs

A

drugs, herbals, supplements, poisons, household products, shampoo, pestacides, perfumes)
= ZONE 3 (perivenular hepatoctes) injury in the central zone of the nodule where CYP450 is

57
Q

2 ways the liver injury from a toxin can happen

A
  1. direct toxicity : liver converts it to XENOBIOTIC

2. immune mechanism : toxin acts as a hapten to convert a cellular protein to an Ig

58
Q

most common type of drugs causing liver injury

A

AB, cardiovascular drugs, CNS, antineoplastic, NSAIDs

59
Q

2 reversible things that can happen to liver when drinking a lot of alcohol

A
  1. Steatosis : fatty change, periventricular fibrosis
  2. Hepatitis : liver cell necrosis, inflammation, mallory bodies, fatty changes
    = both can lead to cirrhosis if not reversed (fibrosis + hyperplastic nodules)
60
Q

alcohol is metabolized by what CYP

A

CYP2E1

61
Q

% of alcoholics that get cirrhosis

A

10%-15%

62
Q

3 types of alcohol producing liver diseases

A
  1. steatosis
  2. steatohepatitis
  3. steatofibrosis / cirrhosis
63
Q

steatosis sx and labs

A
  1. hepatomegaly, minimal sx

2. high bilirubin and alk phosphate

64
Q

Steatohepatitis sx and labs

A
  1. tender hepatomegaly, can have cholestasis

2. high bilirubin, AST : ALP = 2:1 **, elevated alk phosphate

65
Q

Steatofibrosis / cirrhosis sx and labs

A
  1. hepatic dysfunction, coagulation abnormalities

2. hypoproteinemia (low albumin and factors for clotting)

66
Q

acute vs chronic alcoholism

A
  1. effects CNS (and can GI and liver) only and is reversible

2. chronic : liver stomach, GI, pancreas, CNS, and all other organs, high morbidity

67
Q

most common causing chronic liver disease

A

is NAFLD : hepatic steatosis not from alcohol

common in metabolic syndrome

68
Q

metabolic syndrome

A
  1. DM / glucose or insulin intolorance / high fasting glucose
  2. BP over 140/90
  3. dyslipidemia, central obesity, pr microalbuminuria
69
Q

steatosis is when how much of the liver cells are involved

A

5%

70
Q

where does fibrosis start in adults and children with NAFLD

A

adults : around central vein as fine spider web and then expands
children : portal fibrosis

71
Q

NAFLD dx and what you see on imaging

A
  1. fat accumulation and biopsy needed to dx fibrosis
72
Q

NAFLD labs/sx seen show what and can lead to what

A
  1. elevated LFTs and RUQ pain or fullness, malaise

2. cardiac death CAD, HCC

73
Q

Iron amounts is controlled by what

A

intake + absorption in SI

not by excretion

74
Q

hereditary hemochromatosis does what to what organ and also sx after how much is stored

A

liver stores 98% Fe so hepatomegaly + cirrhosis

= sx after 20g stored

75
Q

hereditary hemochromatosis mutation in what

A

Ferroportin (HEF gene mutation , C–> T called C282Y) = common in caucasians

76
Q

main regulator of Fe absorption in normal person

A

Hepcidin (HAMP gene)

77
Q

hereditary hemochromatosis sx

A

hepatomegaly**, hypogonadism *, amenorrhea *, abd pain, skin pigmentations (sun exposed areas), DM, cardiac dysfunction

78
Q

hereditary hemochromatosis DX how

A

high serum ferritin and Fe, liver biopsy only not needed anymore with genetic testing

79
Q

hereditary hemochromatosis histology in biopsy

A

Prussian blue stain, = hepatocytes with iron stained blue

80
Q

hereditary hemochromatosis can lead to what complications

A

cirrhosis, HCC or cardiac problem

81
Q

hereditary hemochromatosis tx effect on HCC

A

no effect since genetics are still mutated even if you remove the Fe overload

82
Q

Wilsons disease mutation and cause

A

ATP7B mutation causing X excretion of Cu into bile and ceruloplasmin

83
Q

Cu accumulates where in wilsons disease

A
  1. liver
  2. brain : tremor, chorea, rigid dystonia
  3. eye :
  4. kidney, bones, parathyroid glands)
    5, RBCs : hemolytic anemia
84
Q

Wilsons disease SX presenting with

A

acute or chronic liver disease

85
Q

Wilsons disease DX

A

low celuluplasmin , high hepatic Cu or high Cu in urine

86
Q

a1 - Antitrypsin deficiency (a1AT) mutation and cause

A

PiZ / PiZZ mutation*
= X a1AT* which inhibits proteases (esp N elastase, protease released at inflammation)
= proteases always on

87
Q

a1 - Antitrypsin deficiency (a1AT) SX leads to what conditions

A
  1. pulmonary emphysema,
  2. liver disease from accumulation on misfolded proteins a1AT : “toxin gain of function mutation “
  3. jaundice, hepatitis
88
Q

most common inherited hepatic disorder

A

a1 - Antitrypsin deficiency (a1AT)

89
Q

Piz mutation is what

A

point mutation Glu –> Lys = a1AT-Z

90
Q

cholestasis hallmark seen in histology

A

green-brown plugs of bile in hepatocytes + dilated canaliculi

91
Q

liver conjugates bilirubin with what

A

glucuronic acid

92
Q

when can you see jaundice at what level of bilirubin

A

2mg/dL to 2.5mg/dL

93
Q

3 causes of unconjugated bilirubin

A
  1. hemolytic anemia
  2. ineffective erythropoiesis
  3. defective conjugation with glucuronic acid
94
Q

high unconjugated bilirubin causes what

A

accumulation in tissues esp neurologic (kernicterus) , when all albumin is saturated

95
Q

conjugated bilirubin 3 most common causes

A
  1. Hepatocellular disease
  2. bile duct injury
  3. biliary obstruction
96
Q

common thing to see in conjugated bilirubin

A

easily excreted in urine so you see it there

97
Q

common sx besides jaundice from elevated bilirubin

A
  1. pruritus
  2. skin xanthomas (cholesterol accumulation)
  3. malabsorption
98
Q

cholestatic disease shows what

A
  1. high alk phosphate + high GGT

2. enzymes at apical (canalicular) membrane of hepatocytes and bile duct cells

99
Q

what causes jaundice in babies

what is the tx and what can make it worse

A
  1. LOW UGT1A1 : glucuronidation conjugator

2. blue light therapy, breast milk can make more bilirubin accumulate

100
Q

hallmark histology in Dubin-Johnson syndrome

A

black-brown melanin-like pigment in hepatocytes

101
Q

Crigler- Najjar Syndrome type 1 and type 2 :

mutation and sx and what type of bilirubin

A

type 1 : X UGT1A1 activity, fatal at neonatal
type 2 : low UGT1A1 activity , mild, occasional kernicterus
= unconjugated

102
Q

Gilbert syndrome : mutation and sx and what type of bilirubin

A

low UGT1A1 activity : not serious

= unconjugated

103
Q

Dubin- Johnson syndrome : mutation and sx and what type of bilirubin

A

MRP2 (canalicular multidrug resistant protein) mutation = X biliary excretion of bilirubin glucuronides , Black liver , not harmful
= conjugated
= cant secrete conjugate bilirubin

104
Q

Rotors syndrome : mutation and sx and what type of bilirubin

A

low hepatic uptake , storage, excretion , not harmful

= cant store conjugated bilirubin

105
Q

cholestasis come from an obstruction in the large bile duct, what happens if its not corrected + TRIAD of one of those causes

A
  1. bilirary cirrhosis from fibrosis happening

2. ascending cholangitis : —–> fever, ABD pain, jaundice* = TRIAD, can lead to abscess and sepsis

106
Q

obstructive and not obstructive causes of neonatal cholestasis

A

OBSTRUCTIVE : Biliary atresia

NON-OBSTRUCTIVE : paucity of bile duct (Alegielle syndrome), infection, genetic transporter defect

107
Q

biliary atresia is what

A

complete or partial obstruction of the extrahepatic biliary tree (1st 3mo of life)

108
Q

biliary atresia tx and prevalence

A

surgery

= most common cause of death from liver disease in childhood

109
Q

splitting liver

A

larger portion given to adult, smaller given to child = saves 2 lives when transplanted

110
Q

Kasai procedure

A
  1. remove biliary tree and gallbladder
  2. connect SI to liver to drain bile
  3. duodenum attached to the SI you attached to the Liver
111
Q

autoimmune hepatits is what type

A

type 1 (adults, LMK-1 ABs) and 2 (children)

112
Q

2 types of autoimmune cholangiopathies

A
  1. Primary sclerosing cholangitis

2. primary biliary cirrhosis

113
Q

gene associated with autoimmune hepatitis in caucasians, japanese, south americans

A

HLA ** all

  1. DR3
  2. DR4
  3. DRB1
114
Q

DX autoimmune hepatitis + prevalence in sex

A

female

  1. exclude viral hep and drug hep and other causes
  2. AutoABs
  3. elevated serum IgG
  4. liver biopsy
115
Q

staining of autoABs :

  1. homogenous staining in cell
  2. centromere stain in cell
  3. speckled stain in cell
A
  1. SLE
  2. Sjögrens syndrome
  3. ag against RNPs and Sm
116
Q

TX of autoimmune hepatitis

A

prednisone + azathioprine at times

117
Q

Autoimmune Hepatitis sx

A

high AST/ALP
= looks like viral or drug induced hep, abd pain, N/V
= fibrosis or cirrhosis on biopsy

118
Q

Primary Biliary Cholangitis (PBC) :

  1. age
  2. gender
  3. associated SX
  4. serology
  5. radiology
  6. duct lesions
A
  1. 50yo
  2. female
  3. Sjögrens syndrome, thyroid disease, scleroderma, Celiac D, RA
  4. AMA+ (95%), ANA+ (45%)
  5. none
  6. florid duct lesions, loose small ducts
119
Q

Primary Scerlosing Cholangitis :

  1. age
  2. gender
  3. associated SX
  4. serology
  5. radiology
  6. duct lesions
A
  1. 30yo
  2. male
  3. IBD (UC)
  4. ANCA+, AMA-, ANA-/+
  5. Strictures and beading or large bile duct, pruning smaller ducts
  6. inflammatory destructioin of extrahepatic and large hepatic ducts, fibrotic obliteration of medium and small intrahepatic ducts
120
Q

Primary Biliary Cholangitis (PBC) : what happens

A

autoimmune disease of inflammation to small to medium intrahepatic bile ducts

121
Q

Primary Biliary Cholangitis (PBC) :sx and labs seen

A
  1. pruritus and fatigue increasing slowly, splenomegaly, jaundice, hyperpigmentation, vit D malabsorption, steatorrhea, hypercholesteremia
  2. high ALK Phosphatase, ABs against PDH complex in Mitochondria**
122
Q

Primary Biliary Cholangitis (PBC) : TX

A

oral ursodeoxycholic acid (natural bile), liver transplant

increased risk of HCC

123
Q

Primary Scerlosing Cholangitis : is what

A

inflammation and obliterative fibrosis of extrahepatic and large intrahepatic bile ducts and dilation of preserved segments

124
Q

Primary Scerlosing Cholangitis : AB t-cell AND histology

A
  1. HLA -B8

2. “onion skin concentric scar”

125
Q

Primary Scerlosing Cholangitis : huge association to what

A

UC (T-cells travel from GI to liver)

126
Q

Primary Scerlosing Cholangitis : sx

A
  1. high ALK Phosphatase
  2. jaundice, pruritus, fatigue
  3. chronic pancreatitis, chronic cholecystitis
  4. Ascending cholecystitis**
127
Q

Primary Scerlosing Cholangitis : eventually becomes

A

hepatic fibrosis and cirrhosis, cholangiocarcinoma

128
Q

Primary Scerlosing Cholangitis : gold stanard to dx and TX

A
  1. “beading”in large intrahepatic duct and extrahepatic ducts by ERCP**
  2. medical anti-inflammatory MX, liver transplant (all end stage liver diseases need to tx with Liver transplant**)

GIGU2 Exam 2 (4 decks)

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