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GI > SM_151b: Pathology of Metabolic Liver Disease, Viral Hepatitis, and Cirrhosis > Flashcards

SM_151b: Pathology of Metabolic Liver Disease, Viral Hepatitis, and Cirrhosis Flashcards

1
Q

Hemochromatosis is ___

A

Hemochromatosis is excess iron deposited in the tissues

  • Body iron content can be 40-80 g in hemochromatosis
  • Hemosiderin deposits in: liver, pancreas, myocardium, adrenal / thyroid / parathyroid glands, or skin
  • Primary or secondary
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2
Q

This is ___ deposition

A

This is hemosiderin deposition

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3
Q

____ mutation ____ increasing iron uptake is responsible for hereditary hemochromatosis

A

HFE mutation C282Y mutation increasing iron uptake is responsible for hereditary hemochromatosis

  • HFE gene encodes HFE protein -> regulates intestinal absorption of iron
  • Cysteine-to-thyrosine substitution at amino acid 282
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4
Q

Hemochromatosis involves _____

A

Hemochromatosis involves lifelong iron accumulation and slow and progressive injury

  • No metabolic pathway to excrete iron
  • Only way to get rid of iron is by removing dead cells with iron
  • Need 20-40 g for clinical disease
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5
Q

Hepcidin is ____ and is involved in the pathogenesis of ____

A

Hepcidin is the main regulator of iron absorption and is involved in the pathogenesis of hemochromatosis

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6
Q

Iron overload presents as ____, ____, and ____

A

Iron overload presents as cirrhosis, bronze skin, and diabetes

  • Liver -> lysosomal damage -> leakage of enzymes -> damage -> cirrhosis
  • Skin -> bronze skin
  • Pancreas -> diabetes
  • Heart -> congestive heart failure
  • Pituitary, adrenal, thyroid, and parathyroid glands -> endocrine organ malfunction
  • Joints -> pseudogout
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7
Q

Excess hemosiderin causes ____

A

Excess hemosiderin causes hemochromatosis

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8
Q

Describe clinical workup for hemochromatosis

A

Clinical workup for hemochromatosis

  1. Blood tests: serum ion, transferrin, ferritin
  2. Liver biopsy: iron stain, iron location (Kupffer cells vs hepatocytes)
  3. Therapeutic measures: phlebotomy
  4. Genetic testing to confirm HFE mutation
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9
Q

Alpha1-antitrypsin is a ___

A

Alpha-1-antitrypsin is a protease inhibitor

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10
Q

The ___ variant of alpha-1-antitrypsin is associated with severe reduction in alpha-1-antitrypsin and high risk for clinical disease

A

The PiZZ variant of alpha-1-antitrypsin is associated with severe reduction in alpha-1-antitrypsin and high risk for clinical disease

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11
Q

Alpha-1-antitrypsin variants: PiMM is ____, PiSS is ____, and PiZZ is ____

A

Alpha-1-antitrypsin variants: PiMM is wild type, PiSS is moderate reduction and no clinical symptoms, and PiZZ is severe reduction and high risk for clinical disease

  • Codominant: PiMZ -> intermediate level of alpha-1-antitrypsin
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12
Q

Describe pathogenesis of alpha-1-antitrypsin deficiency

A

Pathogenesis of alpha-1-antitrypsin deficiency

  1. Mutant alpha-1-antitrypsin not secreted
  2. Leukocyte elastase not inhibited
  3. Elastase-mediated alveolar destruction
  4. Emphysema
  5. Liver damage
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13
Q

Mutated protein in round inclusions is ____

A

Mutated protein in round inclusions is alpha-1-antitrypsin deficiency

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14
Q

Alpha-1-antitrypsin deficiency involves ____ and ____

A

Alpha-1-antitrypsin deficiency involves prominent antitrypsin deposits and cirrhotic scars

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15
Q

Alpha-1-antitrypsin deficiency is treated with ____

A

Alpha-1-antitrypsin deficiency is treated with liver transplantation

  • Hults lung disease
  • Donor liver secretes functional alpha-1-antitrypsin
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16
Q

ATP7B gene encodes ____

A

ATP7B gene encodes copper-transporting ATPase

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17
Q

Wilson disease involves a mutated ____ gene that causes ____ and ____ leading to ____

A

Wilson disease involves a mutated ATP7B gene that causes impaired excretion of copper into bile and failure to incorporate copper into ceruloplasmin leading to accumulation of toxic levels of copper in liver, brain, and eye

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18
Q

Mutant ATP7B gene leads to ____ and ____

A

Mutant ATP7B gene leads to copper overload in hepatocytes and unbound copper ions into the circulation

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19
Q

This is ___

A

This is Wilson’s disease

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20
Q

Wilson’s disease physical exam involves ____ and ____

A

Wilson’s disease physical exam involves neurologic exam and slit-lamp for Kayser-Fleischer rings

  • Diagnosis in the pre-cirrhotic phase is key
  • Once cirrhotic, treat with transplant
  • Treatment is chelation therapy
  • Treatment can prevent neurologic damage
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21
Q

This is ____ seen in ____

A

This is Kayser-Fleischer ring seen in Wilson’s disease

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22
Q

___ is inflammation of the liver

A

Hepatitis is inflammation of the liver

  • Caused by infection, fatty liver disease, autoimmune hepatitis, drug injury, cholestatic liver diseases, and metabolic liver diseases
23
Q

Liver inflammation can be located in the ____ or ____

A

Liver inflammation can be located in the hepatocytes and biliary tree

24
Q

Inflammation of hepatocytes correlates with ____ and ____ elevation

A

Inflammation of hepatocytes correlates with ALT and AST elevation

  • Hepatitis B and C
  • Autoimmune hepatitis
  • Many drug reactions
  • Steatohepatitis
25
Q

Inflammation of the biliary tree correlates with ____ and ____ elevations

A

Inflammation of the biliary tree correlates with Alk-P and GGT elevations elevations

26
Q

Viral hepatitis results from ____ and ____ viruses

A

Viral hepatitis results from hepatotropic and non-hepatotropic viruses

  • Hepatotropic: infect only or primarily the liver
  • Non-hepatotropic viruses: infect many organ systems including the liver
27
Q

Non-hepatotropic viruses occur primarily in ____, are members of the ____ family, and present as ____ or ____

A

Non-hepatotropic viruses occur primarily in immunosuppressed patients, are members of the Herpesvirus family, and present as fulminant hepatitis or acute hepatitis

28
Q

Non-hepatotropic viral hepatitis pathology includes ____, ____, and ____ and are detected by ____

A

Non-hepatotropic viral hepatitis pathology includes mixed inflammatory infiltrate, no fibrosis, and viral inclusions and are detected by immunohistochemical stains

29
Q

Only a subgroup of hepatotropic viruses lead to ___

A

Only a subgroup of hepatotropic viruses lead to chronic hepatitis

  • No non-hepatotropic viruses lead to chronic infection of the liver
30
Q

Hepatitis ___ and ___ are transmitted via fecal oral route

A

Hepatitis A and E are transmitted via fecal oral route

31
Q

Hepatitis ___, ___, and ___ are transmitted via parenteral / blood sex

A

Hepatitis B, C, and D are transmitted via parenteral / blood sex

32
Q

Hepatitis ___ is the only dsDNA hepatitis virus

A

Hepatitis B is the only dsDNA hepatitis virus

(all others ssRNA)

33
Q

Describe Hepatitis A

A

Hepatitis A

  • Does NOT cause chronic hepatitis
  • ssRNA
  • Fecal oral transmission
34
Q

Describe Hepatitis E

A

Hepatitis E

  • Causes chronic hepatitis in immunosuppressedpatients
  • ssRNA
  • Fecal oral transmission
35
Q

Describe Hepatitis B

A

Hepatitis B

  • dsDNA
  • Responsible for hepatocellular carcinoma
  • Vertical transmission in childbirth
  • Horizontal transmission: blood products, sex, IVDU
  • Vaccine available
36
Q

Describe HBV infection outcomes

A

HBV infection outcomes

  • Acute hepatitis with complete viral clearance and recovery
  • Fulminant hepatitis with massive necrosis
  • Non-progressive chronic hepatitis: persistence of HBsAg
  • Progressive chronic hepatitis ending in cirrhosis: risk factor for hepatocellular carcinoma b/c integrates into host DNA
  • Carrier state: asymptomatic
37
Q

Describe Hepatitis C

A

Hepatitis C

  • Most common blood-borne infection
  • Majority have progression to chronic liver disease
  • Risk factors: IV drug abuse, multiple sex partners, needle sticks, multiple contacts with an HCV infected person, employment in medical or dental field, unknown
38
Q

Acute viral hepatitis histology involves ____, ____, and ____

A

Acute viral hepatitis histology involves necrosis in the lobules, bridging necrosis (severe cases), and massive necrosis

  • Necrosis in the lobules: ballooning degeneration, apoptotic bodies, necroinflammatory foci, inflammation (lymphoplasmacytic)
  • Bridging necrosis (severe cases): centra-central necrosis, portal-portal necrosis
  • Massive necrosis
39
Q

These are ___ and ___ in ___

A

These are necroinflammatory foci and lymphocytic infiltrate in acute hepatitis

40
Q

This is ___ in ___

A

This is massive necrosis in acute viral hepatitis

41
Q

Chronic viral hepatitis includes ____ and ____

A

Chronic viral hepatitis includes mononuclear portal infiltration and interface hepatitis

  • Mononuclear portal infiltration: defining feature
  • Interface hepatitis: hepatocytes surrounding portal tracts are inflammed
  • Ground-glass hepatocytes: hepatitis B
  • Focal fatty change: hepatitis C
  • Fibrosis
42
Q

This is ____ in chronic viral hepatitis

A

This is chronic portal inflammation in chronic viral hepatitis

  • Composed mainly of lymphocytes
43
Q

This is ____

A

This is NO interface hepatitis

44
Q

These are ____ in chronic ____

A

These are ground-glass hepatocytes in chronic HBV

45
Q

____ in chronic HBV represent accumulation of HBV core antigen

A

Ground glass nuclei in chronic HBV represent accumulation of HBV core antigen

46
Q

This is ____ in the liver

A

This is HBcAg in the liver

47
Q

This is ____ in ____

A

This is interface hepatitis in chronic hepatitis

48
Q

____, ____, and ____ occur in chronic HCV

A

Lymphoid aggregates, portal to portal bridging fibrosis, and steatosis occur in chronic HCV

49
Q

This is ____ with ____

A

This is cirrhosis with hepatocellular carcinoma

50
Q

Causes of cirrhosis are ____ or ____

A

Causes of cirrhosis are intrahepatic or extrahepatic

  • Intrahepatic: all causes of chronic hepatitis
  • Extrahepatic: biliary tract diseases, post-hepatic causes
51
Q

Describe pathophysiology of cirrhosis

A

Pathophysiology of cirrhosis

53
Q

Micronodular cirrhosis is ____ and often occurs due to ____

A

Micronodular cirrhosis is regenerative nodules with size < 3 mm and often occurs due to alcoholism

54
Q

Macronodular cirrhosis involves ____

A

Macronodular cirrhosis involves nodules that vary in size > 3-10 mm

  • Viral hepatitis (HBV or HCV) most common cause
  • Wilson’s disease and alpha-1-antitrypsin deficiency can also cause

GI (40 decks)

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