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Pathology > Accessory GI > Flashcards

Accessory GI Flashcards

1
Q

Describe the difference between the classic hepatic lobule and the hepatic acinus

A
  • Hepatic lobule
    • Hexagonal
    • Central vein in center
    • 6 portal tracts at periphery
  • Hepatic acinus
    • Triangle
    • 2 portal tracts at periphery extending towards central vein
    • Describes zones of blood supply
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2
Q

Describe the zones of blood supply in the hepatic acinus version of organization

A
  • Zone 1: Periportal hepatocytes
    • closest to blood supply
    • doing most of the work
    • First to be damaged by toxin in the blood
  • Zone 2: Midzoneal
  • Zone 3: Centrilobular hepatocytes
    • around central vein
    • Farthest from blood supply
    • Recruited when needed
    • First to be damaged by ischemia or lack of blood flow
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3
Q

What is the role of the following cells:

  • Kupfer cells
  • Stellate cells
A
  • Kupfer cells
    • phagocyte
  • Stellate cells
    • Myofibroblasts
      • role in liver fibrosis
    • Store Vit A
    • Located in Space of Disse
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4
Q

Ballooning degeneration of hepatocytes is found in what types of liver damage?

A

Ischemic / hypoxic injury

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5
Q

Feathery degeneration of hepatocytes is found in what types of liver damage?

A

Cells have foamy cytoplasm

  • cholestatic injury
  • Bile accumulation
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6
Q

What macromolecule is accumulated in hepatocytes with steatosis?

A

Triglyceride accumulation

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7
Q

Microvesicular steatosis is found in what types of liver damage?

A

Fatty liver of pregnancy

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8
Q

Macrovesicular steatosis is found in what types of liver damage?

A
  • Obesity
  • Diabetes
  • Hep C
  • Found with microvesicles in Alcohol fatty liver
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9
Q

Mallory bodies are most likely associated with which liver disease?

A

Alcoholic hepatitis

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10
Q

How much liver function must be lost to have Liver Failure?

A

80-90%

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11
Q

What are the features of Hepatic Failure?

A
  • Portal HTN
    • ascites
    • Congestive splenomegaly / hypersplenism
      • ingests more RBCs and platelets
    • Portosystemic shunts
      • Esophageal varicies, hemorrhoids, caput medusae
    • Secondary renal failure
  • Decreased detox
    • Increased ammonia
      • Mental status changes
    • Hyperestrinism
      • gynecomastia, spider angiomata
    • Jaundice
  • Decreased protein synthesis
    • Hypoalbuminemia
      • edema
    • Decreased clotting factors
      • Increased PT
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12
Q

What is the size difference between micronodular and macronodular cirrhosis?

A
  • Micro: <3mm
  • Macro: >3mm
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13
Q

What are the histologic changes that occur in Cirrhosis?

A
  • Deposition of collagen I and III in space of Disse
    • Normally only small amout of type II and IV
  • Loss of fenestrations in sinusoid endothelial cells
    • obliterates biliary channels
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14
Q

What is the main cell responsible for cellular architecture found in cirrosis?

A

Cell of ido (forms a myofibroblast when activated

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15
Q

Where are the regenerative cells of the liver located?

A

Bile ductules

May cause regeneration of cells and regain function following cirrhosis

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16
Q

What outcomes are associated with acute HBV infxn?

A
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17
Q

HBV Ag and significance

A
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18
Q

What is the first serologic marker to rise in HBV?

A

HBsAg (surface Ag)

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19
Q

Which HBV markers indicate acute stage?

A
  • HBsAg = surface Ag
    • first to rise
  • HBeAg / HBV DNA
  • HBcAb = Core Ab
    • IgM
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20
Q

Which HBV markers indicate chronic stage?

A
  • HBsAg (surface Ag)
    • Presence > 6 months
  • HBeAg and HBV DNA
    • may or may not be present
  • HBcAb (Core Ab)
    • IgG
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21
Q

What markers indicate infectivity in HBV?

A
  • HBV DNA
  • HBeAg (Envelope)
    • Need an envelope to mail a letter
    • (mail = transfer to another person)
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22
Q

Which HBV marker indicates immunization or resolution of disease?

A

HBsAb IgG

(Surface Ab)

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23
Q

What is the most common cause of chronic liver disease?

A

HCV

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24
Q

What is the most common indication for liver transplant?

A

HCV

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25
Q

Whic HCV is associated with metabolic syndrome?

A

Genotype 3

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26
Q

What is the serology confirmation of coinfection of HBV and HDV?

A
  • IgM anti-HDAg
    • new infxn HDV
  • IgM anti-HBcAg
    • new infxn HBV
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27
Q

What is the serology confirmation of HBV/HDV superinfection?

A
  • IgG or IgM anti-HDV
  • BHsAg present
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28
Q

Outcomes of HDV/HBV Coinfection

A

Nearly all: Recovery with immunity

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29
Q

Outcomes of HDV/HBV Superinfection

A

Most become chronic => cirrhosis

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30
Q

Characteristics Hepatitis viruses

(HOV’s chart)

A
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31
Q

Hepatitis diagnosis chart

(HOV’s chart)

A
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32
Q

What are the characteristics of Acute Asymptomatic infxn with Recovery?

A
  • Minimally elevated serum transaminases
  • Anti-HAV or anti-HBV Abs
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33
Q

What are in characteristics of each stage of Acute Symptomatic Infxn with Recovery (Hepatitis)?

  • Incubation
  • Preicteric
  • Icteric
  • Convalescence
A
  • Incubation
    • Infectivity in last days
  • Preicteric
    • non-specific symptoms
    • Serum sickness-like syndrome
      • immune complex-mediated
      • Urticaria, arthritis, glomerulonephritis
  • Icteric
    • Conjugated Hyperbilirubinemia
      • Nearly all HAV
      • 1/2 HBV
      • Absent in HCV
  • Convalescence
    • Strong immune response
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34
Q

Acute Hepatitis Morph. Changes

A

Chronic Hepatitis

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35
Q

Ground glass cytoplasm is most characteristic of which type of Hepatitis?

A

HBV

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36
Q

What is the most common cause of Chronic Hepatitis?

A
  1. HCV
  2. HBV
    • determined by age of exposure
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37
Q

Steatosis is most characteristic of which type of hepatitis?

A

HCV

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38
Q

What would be found in a serumtest of an inactive Hepatitis carrier?

A
  • (+) HBsAg
  • (-) HBeAg
    • b/c can’t transmit
  • (+) anti-HBe
  • Normal transaminase
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39
Q

What are the most common causes of Fulminant Hepatitis globally?

A
  • HAV
  • HEV
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40
Q

Fulminant Hepatitis

  • Histo
  • Symptoms
A
  • Histo
    • Loss of hepatocytes
    • Collapsed reticulin framework
  • Symptoms
    • Jaundice
    • Coagulopathy
    • Hepatic encephalopathy
    • Sepsis
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41
Q

The rosettes pictured below are characteristically associated with which form of hepatitis?

A

Autoimmune Hepatitis

  • Should also have prominent plasma cells
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42
Q

The eosinophilic inclusions in hepatocytes are characteristically associated with which type of hepatitis? What are they called?

A

Mallory Bodies

Alcoholic Hepatitis

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43
Q

What comorbidities are associated with progression of Alcoholic Hepatitis to cirrhosis (or more severe forms)?

A
  1. Iron overload
  2. HBV infxn
  3. HCV infxn
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44
Q

What is the physiopathology associated with hepatic steatosis and the formation of vesicular inclusions?

A
  • Hepatocytes shunt normal substrates to lipid biosynthesis
    • (increased lipid)
  • Impaired production of lipoproteins
    • (can’t get rid of them)
  • Increased peripheral fat catabolism
    • Increased FAs
    • Go to liver
    • Increased lipid
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45
Q

What is the most common presentation of Hepatic steatosis?

A
  • Hepatomegaly
  • Mild elevation of
    • bilirubin
    • alkaline phosphatase
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46
Q

What are the physiological changesthat lead to Hepatic Steatosis?

A
  1. Shunting of normal stubstrates to lipid biosynthesis in hepatocytes
  2. Impaired assembly of lipoproteins
  3. Increased peripheral fat catabolism
    • Releases FFA
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47
Q

What is the mechanism of hepatic injury in Alcoholic Hepatitis?

A
  • Acetaldehyde disrupts cytoskeleton
  • Generation of P450
  • Decreased glutathione
    • more susceptible to oxidative injury
  • Release of bacterial endotoxins
    • activates NF-kß
  • Release of endothelins
    • contraction of stellate cells
48
Q

What is the limit of alcohol consumption for Nonalcoholic Fatty Liver Disease / Steatohepatitis?

A

less than 20gm/wk

49
Q

What is the two hit model for NAFLD / NASH?

A
  • Insulin resistance causes accumulation of fat in liver
  • Formation of lipid peroxides and ROS
  • Oxidative damage
50
Q

What is the difference in Morphology between NAFLD and NASH?

A
  • Nonalcoholic Fatty Liver Disease
    • Macro / micro vesicular steatosis
    • No inflammation
  • NA Steatohepatitis
    • Macro / micro vesicular steatosis
    • Inflammation
    • Mallory bodies
    • Fibrosis of:
      • portal tract
      • central vein
      • sinusoids
51
Q

What disease process is pictured below?

A

Nonalcoholic Steatohepatitis

52
Q

What disease process is pictured below?

A

Nonalcoholic Fatty Liver Disease

53
Q

What gene is mutated in Hereditary Hemochromatosis? What is the most common mutation in the US?

A
  • Gene
    • HFE
    • Regulates hepcidin => reg. iron absorption
  • Mutation
    • C282 more common in US (european origin)
      • Poorer outcome
    • H63D
      • Mild accumulation
54
Q

What disease process is pictured below?

A

Secondary hemochromatosis

  • Iron primarily in Kupfer cells
  • Accumulation not as great as in primary disease
55
Q

What disease process is pictured below?

A

Primary Hemochromatosis

  • Greater accumulation of iron
  • Accumulates toward the center of hepatocytes
56
Q

Where is copper normally absorbed? How is it stored? What happens to the excess?

A
  • Absorbed in the duodenum
  • Stored in ceruloplasmin
  • Excess is secreted into bile

***ceruloplasmin and secretion into bile is decreased in Wilson disease

57
Q

What accumulates in cells in Wilson’s disease? What stain is used to visualize this accumulation in cells?

A

Copper

Rhodamine Stain

58
Q

What enzyme conjugates bilirubin? Where does this occur?

A
  • Enzyme:
    • UDP-glucuronosyl transferase
    • adds glucuronic acid
  • Location:
    • Liver ER
59
Q

Is unconjugated bilirubin soluble? Conjugated bilirubin?

A
  • Unconjugated: NO
    • bound to albumin before arriving to the liver
  • Conjugated: Yes
    • excreted in bile into the gut
60
Q

What does bilirubin become once it is metabolized in the gut? What is responsible for metabolism?

A
  • Metabolism
    • Gut bacteria glucuronidases deconjugate bilirubin
  • Becomes Urobilinogen
    • 80% to feces
    • 20% reabsorbed by bloodstream and enters urine
61
Q

From what molecule is bilirubin derived originally?

A

Heme

62
Q

What is the role of bile acids? What are they composed of?

A
  • function
    • detergents: solubilize wate-insoluble lipids
  • composition
    • cholesterol
    • taurine or glycine
63
Q

Which form of bilirubin is referred to as Delta or Indirect Bilirubin?

A

Unconjugated

(More abundant than conjugated)

64
Q

Which form of bilirubin is referred to as Direct Bilirubin?

A

conjugated bilirubin

65
Q

In intrahepatic and extrahepatic obstruction of bilirubin release:

  • How do enzyme levels change?
A
  • How do enzyme levels change?
    • Increased Alkaline phosphatase
      • greater for extrahepatic
    • Increased ALT
    • Increased GGT
    • Increased AST
      • greater for intrahepatic
66
Q

In intrahepatic and extrahepatic obstruction of bilirubin release:

  • How is digestion affected?
A
  • Decreased bile
    • Malabsorption of fat-soluble vitamins
      • Decreased Vit K:
        • Increased PT and PTT
    • Decreased urobilinogen
      • Acholic (light) stools
67
Q

What disease process is pictured below?

A

Cholestasis

Bile lake formation from cell degeneration

68
Q

What disease process is pictured below?

A

Cholestasis

  • Front: bile plugs
  • Back: ductular proliferation
    • tries to accomodate bile
69
Q

What are the causes and symptoms of cholestasis?

A
  • Causes:
    • Intrahepatic obstruction
    • Extrahepatic obst.
  • Symptoms
    • Jaundice
    • Pruritis
    • Xanthomas
    • Dark urine possible
      • elevated conjugated bilirubin
      • water soluble
70
Q

Neonatal Cholestasis

  • Unique histologic features
  • Symptoms
A
  • Histo
    • Lobular disarray
      • focal hepatocyte apoptosis
    • Rosettes
      • multinuclear giant cells
    • Extramedullary hematopoiesis
  • Symptoms
    • Jaundice
    • Dark Urine
    • Light stools
    • Hepatomegaly
71
Q

What histologic changes are associated with primary biliary cirrhosis?

A
  • Lymphocytic infiltrate in portal tracts
  • Noncaseating granulomatous destruction of intrahepatic bile ducts
  • Fibrosis
  • Cirrhosis
  • Increased hepatocellular cancer
72
Q

What disease process is pictured below?

A

Primary Sclerosing Cholangitis

  • Front: onion-skin around bile duct
  • Back: beading sign on radiography
73
Q

In secondary biliary cirrhosis, what important findings occur before cirrhosis?

A
  • Bile stasis
  • Ductular proliferation
    • neutrophil infiltrate
  • Portal Tract Edema
74
Q

In primary biliary cirrhosis, what important findings occur before cirrhosis?

A
  • Dense lymphocytic PT infiltrate
  • Granulomatous destruction of bile ducts
75
Q

In primary sclerosing cholangitis, what important findings occur before cirrhosis?

A
  • Periductal PT onion-skin fibrosis
  • Pattern of stenosis then beading of intra- and extra-hepatic ducts
76
Q

What are von Meyenburg Complexes? What symptoms occur?

A
  • Small clusters of dilated bile ducts
    • detached from biliary tree
    • located in portal tract
  • Symptoms:
    • clinically insignificant
77
Q

What causes Polycystic Liver Disease? With what other disease is it associated?

A
  • Cause
    • Inherited
    • AD
  • Disease
    • Strong association with polycystic kidney disease
78
Q

Congenital Hepatic Fibrosis

  • Appearance
  • Cause
  • Associated with what other disease?
A
  • Appearance
    • PT enlargement
    • abnormal bile ducts in CT
      • continuous with biliary tree
    • Develops portal HTN
  • Cause
    • Inherited
    • AR
  • Associated with what other disease?
    • Polycystic Kidney Disease
79
Q

Caroli Syndrome

  • Appearance
  • Cause
  • Associated with what other disease?
  • What complications can occur?
A
  • Appearance
    • Dilated bile ducts
  • Cause
    • Inherited
    • AR
  • Associated with what other disease?
    • Risk of cholangiocarcinoma
80
Q

What complications arise from cysts in the liver?

A
  • Intrahepatic cholelithiasis
  • Cholangitis
  • Hepatic abscess
  • Portal HTN
81
Q

Manifestations of problems in Hepatic Blood Flow

A
82
Q

What complication can occur with acute portal vein obstruction?

A

Congestion of liver and bowel infarction

83
Q

What is the most common intrahepatic obstruction to blood flow?

A

Cirrhosis

84
Q

Peliosis Hepatis

  • Histology
  • Associated conditions
  • Severe outcomes
A
  • Histology
    • Dilation of Sinusoids
    • Due to apoptosis
  • Associated conditions
    • Cancer
    • TB
    • HIV
    • Anabolic Steroids
  • Severe outcomes
    • Intra-abdominal hemorrhage
    • Hepatic Failure
85
Q

What symptoms are associated with Hepatic Vein Outflow Obstruction syndromes?

A
  • Tender hepatomegaly
  • Ascites
  • Jaundice
86
Q

What type of liver damage is caused by Right sided vs Left sided Heart Failure?

A
  • Right sided
    • Sinusoidal congestion
    • Blood backs up due to lack of pumping
  • Left sided
    • Ischemic necrosis
    • Lack of pumping causes reduced systemic blood pressure
87
Q

What effect can chronic CHF have on the liver?

A

Centrilobular fibrosis

88
Q

What potentially life-threatening pathology of the liver can occur during eclampsia?

A

Hepatic hematoma

Can rupture if under the Glisson capsule

89
Q

Intrahepatic cholestasis of pregnancy

  • Symptoms
  • Complications
A
  • Symptoms
    • Jaundice
      • conjugated bilirubin
    • Dark urine
    • Light stools
    • elevated transaminases
  • Complications
    • Gallstones
    • Small risk of fetal distress
90
Q

What disease process is pictured below?

A

Acute Fatty Liver of Pregnancy

Microsteatosis

91
Q

What symptoms of acute bone marrow transplant graft vs host disease occur in the liver?

A
  • Donor lymphocytes attack liver
  • Hepatitis
92
Q

What symptoms of chronic bone marrow transplant graft vs host disease occur in the liver?

A

Selective bile duct destruction

93
Q

What symptoms occur in chronic liver allograft rejection?

A

Vanishing Bile Duct Syndrome

Obliterative arteritis => loss of blood flow to bile duct (w/ immune response) => disappears

94
Q

Nodular Regenerative Hyperplasia of the Liver

  • Definition
  • Common cause of what hepatic condition?
A
  • Definition
    • cirrhosis like nodules
    • no fibrosis present
  • Cause
    • decreased intrahepatic blood flow
  • Condition
    • non-cirrhotic portal HTN
95
Q

Focal Nodular Hyperplasia

  • Population
  • Cause
  • Appearance
A
  • Population
    • Women
    • 20-40
  • Cause
    • Exogenous estrogens
  • Appearance
    • White, central, stellate scar
96
Q

What is the most common benign liver tumor?

A

Cavernous Hemangioma

97
Q

What genes are associated with Hepatocellular Carcinoma?

A
  • p53
    • Inactivation
  • WNT/beta catenin pathway
    • Activation
  • IL6/JAK/STAT pathway
98
Q

What is the difference in prognosis between large cell and small cell dysplastic change of the liver?

A
  • Large cell
    • Marker forincreased surveillance
  • Small cell
    • Directly premalignant
99
Q

What are the differences between a low grade and high grade dysplastic nodules?

A
  • Low
    • No atypia
    • PT present
  • High
    • Small cell change
    • Atypia
    • Few PT
    • Subnodules w/i nodules
100
Q

What disease process is pictured below?

A

Fibrolamellar variant of SCC of liver

101
Q

What congenital anomaly is pictured below?

A

Phrygian cap

Folded fundus

102
Q

What causes Acute Acalculous Cholecystitis?

A

Ischemia most common

Cystic artery

103
Q

What causes Chronic Cholecystitis? What bugs may initiate an attack?

A
  • Cause
    • Unknown
    • Important: Supersaturation of bile
  • Bugs
    • E. coli
    • Enterococci
104
Q

Rokitansky-Aschoff sinuses occur in what pathology of the gallbladder?

A

Chronic Cholecystitis

(due to reactie proliferation of buried crypts)

105
Q

What disease process is pictured below?

A

Porcelain gallbladder

Dystrophic calcification

(increased risk cancer)

occurs w/ Chronic Cholecystitis

106
Q

What disease process is pictured below?

A

Xanthogranulomatous cholecystitis

Due to Chronic Cholecystitis

107
Q

What disease process is pictured below?

A

Hydropic Gallbladder

Due to Chronic cholecystitis

108
Q

What are the clinical features of chronic Cholecystitis?

A

Recurrent attacks

Nausea / vomiting

***Intolerance to fatty food***

109
Q

What is the most common form of Carcinoma of the Gallbladder?

A

Adenocarcinoma

110
Q

Carcinoma of the Gallbladder is more common in which population?

A
  • Females
  • Countries
    • Chili
    • Bolivia
    • N India
111
Q

Which form of CA of the Gallbladder has the best prognosis?

A

Papillary

112
Q

What mutation can result in Pancreas agenesis?

A

PDX1

(homozygous loss of function)

113
Q

What is the pathology and treatment of autoimmune pancreatitis?

A

Lymphoplasmacytic sclerosing pancreatitis

  • Path:
    • IgG4 secreting plasma cells in the pancreas
  • Treatment:
    • responds to steroid therapy
114
Q

What genes are important in the progression to Pancreatic Carcinoma?

A
  • K-RAS
  • p16
  • p53
  • SMAD4
115
Q
A

Pathology (27 decks)

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