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OS 214 G.I. > Exam 1: Gross and Histo Features of Hepatic Disorders > Flashcards

Exam 1: Gross and Histo Features of Hepatic Disorders Flashcards

1
Q

Normal weight of liver

A

1400-1600g

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2
Q

Key anatomic features of the liver

A

Portal Triad (hepatic a., portal v., and bile duct
Hepatocellular parenchyma
Hepatic veins

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3
Q

Blood supply and blood flow
80%:
20%

A

80% Hepatic portal v. (from intestines)

20% Hepatic a. (from aorta)

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4
Q

Macrophages that permanently reside in the sinusoidal space

A

Von Kupffer cells

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5
Q

If there is a blood-borne toxin, which zone in the acinar model will be the first to die?

A

Zone 1

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6
Q

If there are non-toxic substances present that become hepatotoxic when metabolized by the liver, where will it be found?

A

Zone 3

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7
Q

If there are non-toxic substances present that become hepatotoxic when metabolized by the liver, where will it be found?

A

Zone 3

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8
Q

T or F: The liver has a tremendous amount of regenerative ability

A

T

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9
Q

What are the 3 morphologic paterns observed in an injured liver?

A 
Coagulation necrosis (prototype of ischemic necrosis)
Councilman bodies (toxic/immunologic etiology)
Hydropic degeneration (cell swelling)
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10
Q

Types of necrosis

A

Focal (scattered or erratic cells)
Zonal (regional)
Submassive (entire lobules)
Massive (entire liver)

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11
Q

Types of necrosis observed in fulminant hepatitis

A

Submassive and massive

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12
Q

Earliest physiologic feature of hepatic damage

A

Hepatocyte swelling

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13
Q

Difference between Councilman bodies and Mallory bodies

A

Councilman: mummified hepatocytes
Mallory: cytoplasmic collections of denatured material

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14
Q

Difference between Councilman bodies and Mallory bodies

A

Councilman: mummified hepatocytes
Mallory: cytoplasmic collections of denatured material

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15
Q

Occurs in all but the most fulminant disease

A

Regeneration

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16
Q

Howe much of the hepatic capacity is lost to diagnose hepatic failure?

A

80-90%

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17
Q

Most common manifestation of hepatic failure

A

jaundice

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18
Q

How much of hemoglobin in the serum comes from senescent/dying red cells?

A

70%

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19
Q

How much of hemoglobin in the serum comes from hemoproteins?

A

30%

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20
Q

Heme metabolized by several enzymes, produces?

A

Bilirubin

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21
Q

jaundice is due to

A

The failure to metabolize bilirubin

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22
Q

Type of hyperbilirubinemia that is non-water soluble

A

UNconjugated

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23
Q

Type of hyperbilirubinemia that is water soluble

Follow-up question: What is attached to it?

A

Conjugated

Attached: glucose molecule

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24
Q

Type of hyperbilirubinemia that is water soluble

Follow-up question: What is attached to it?

A

Conjugated

Attached: glucose molecule

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25
Q

The three problem areas contributing to non H2O-soluble bilirubin

A

Hemeooxygenase, carrier protein, glucoronyl transferase

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26
Q

How many glucose attachments does it take to make bilirubin H2O-soluble?

A

1

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27
Q

2 Manners in which bile can be disposed

A

Bile to duodenum

Blood to kidney

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28
Q

Genetic deficiency of bilirubin UGT activity

A

Crigler-Najjar syndromes I and II

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29
Q

Possible reasons of Unconjugated Hyperbilirubinemia

A

Excess production of bilirubin
Reduced hepatic uptake
Impaired bilirubin conjugation

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30
Q

Possible reasons of Conjugated Hyperbilirubinemia

A

Decreased intrahepatic excretion of bilirubin

Extrahepatic biliary obstruction

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31
Q

Conjugated/unconjugated? Any lesion that tends to increase hemolysis

A

UNconjugated

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32
Q

Viral hepatitis produces what kind/s of hyperbilirubinemia?

A

Both UN and Conjugated

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33
Q

Normal limit of bilirubin

A
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34
Q

Jaundice will be grossly apparent when?

A

(1.2)(2) = >2-2.5mg/dL

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35
Q

Jaundice will be grossly apparent when?

A

(1.2)(2) = >2-2.5mg/dL

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36
Q

Where do most of our albumin come from?

A

Edi sa liver, kaya nga nandito tayo sa deck na ‘to eh!

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37
Q

T or F: We excessively bleed when our liver experiences coagulopathy

A

T

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38
Q

Activation of which factor causes the liver to have excessive intravascular coagulation?

A

Hageman factor

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39
Q

Liver failure leads to an in/decrease of ammonia?

A

Increase. The liver fails to rid our body of NH3

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40
Q

Condition producing odor of rotting fruit

Follow-up: This is caused by failure to metabolize which intestinal flora?

A

Fetor hepaticus

Follow-up: mercaptans

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41
Q

Condition producing odor of rotting fruit

Follow-up: This is caused by failure to metabolize which intestinal flora?

A

Fetor hepaticus

Follow-up: mercaptans

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42
Q

Why would men be “by-products of liver metabolism”? (Dimacali, 2013)

A

Because the liver metabolizes estrogen and without the liver functions, estrogen levels increase :)

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43
Q

Why would men be “by-products of liver metabolism”? (Dimacali, 2013)

A

Because the liver metabolizes estrogen and without the liver functions, estrogen levels increase :)

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44
Q

Increased estrogen in females can manifest as?

A

Palmar erythemas and spider angiomatas

45
Q

True or False: Liver failure prevents _______ neurotransmitters from being detoxified causing interference with synaptic activity

A

Hahaha. False T or F question! False lang sagot diyan :)

46
Q

Hepatic encephalopathy affects parts of the brain in what order?

A

From intelligence centers to more vegetative centers until death

47
Q

Deepest manifestation of hepatic encephalopathy?

A

Coma

48
Q

Distal limb with flapping tremors

A

Asterixis (due to false neurotransmitters; the longer the nerves, the more disturbed they can be)

49
Q

Most common cause of hepatic insult

A

Alcoholic liver disease

50
Q

Mildest form of hepatic lesion caused by alcohol

A

Fatty change

51
Q

Is alcoholic hepatitis reversible?

A

Yes

52
Q

Cirrhotic livers have an increased risk of developing what?

A

Hepatocellular CA

53
Q

Cirrhotic livers have an increased risk of developing what?

A

Hepatocellular CA

54
Q

Patho of Alcohol Liver Disease (MLE): Alcohol is a direct/indirect toxin?

Folow-up: It affects which structures?

A

Direct

Microtubules, Mitochondrial fxn, membrane fluidity

55
Q

A primary metabolite of alcohol

A

Acetaldehyde

56
Q

A primary metabolite of alcohol

A

Acetaldehyde

57
Q

Histologic feature unique to Hep B

A

Ground glass swollen hepatocyte

58
Q

Actual serum Hepatitic

A

Hep C

59
Q

How many percent mortality/morbidity is Hep C? Hep B?

A

Hep C: 50%

Hep B: 10%

60
Q

New grading system for Hepatitis

A

Knodell Score: 1) # or density of inflammatory cells, 2) distribution, 3) extent of hepatic cell death, 4) extent of cirrhosis and other changes

61
Q

Onset of fulminant hepatitis

A

2-3 weeks after onset of symptoms

62
Q

Reye’s Syndrome is aggravated by what medication?

A

Acetic salicylic acid. Replace meds with acetaminophen instead

63
Q

Concave or convex? Fulminant hepatitis

A

Convex-Concave (kasi “shrunken” liver ay nag-dip lang sa normal level)

64
Q

Drug-induced hepatitis may be indistinguishable from which etiology?

A

Viral hepatitis

65
Q

Drugs causing microvesicular fatty exchange

A

Salicylates and tetracyclines

66
Q

Drugs causing macrovesicular fatty exchange

A

Alcohol and methotrexate

67
Q

Drugs causing macrovesicular fatty exchange

A

Alcohol and methotrexate

68
Q

Nodular liver on gross can be classified as

Micro 0.3 ___

A

cm

69
Q

2 processes happening simultaneously in a cirrhotic liver

A

fibrosis and regeneration

70
Q

2 processes happening simultaneously in a cirrhotic liver

A

fibrosis and regeneration

71
Q

Space between the endothelial cell of sinusoid and the hepatocyte

A

Space of Disse

72
Q

guarding the Space of Disse

A

ITO Cell

73
Q

Who responds to toxins and cytokines from Kupffer cells by producing collagen?

A

ITO Cells pa rin

74
Q

Reticular framework is important because?

A

This is used by a guide for the hepatocytes. If this is damaged, hepatocytes will have a misguided attempt at fixing themselves

75
Q

Mass of hepatocytes not arranged in the architecturally correct manner

A

Pseudolobule

76
Q

Mass of hepatocytes not arranged in the architecturally correct manner

A

Pseudolobule

77
Q

Inflammatory reaction due to accumulation of copper in the liver

A

Wilson’s Disease

78
Q

In the Philippines, what is the most common etiology of hepatitis?

A

Viral. 10% lang ang alcohol

79
Q

Treatment for Neonatal hepatitis

A

Supportive

80
Q

Treatment for extrahepatic biliary atresia

A

Surgery

81
Q

In Biliary Atresia, which part is atretic? Proximal or distal?

A

Distal. That’s why bile ends up accumulating in the liver

82
Q

The Criggler-Najjar Syndrom type not compatible with life

A

Type 1. ABSENT AGT activity as compared to type 2 with REDUCED AGT activity

83
Q

Rotor Syndrome (Philippine study). Three names you should remember:

A

Rotor, Florentin, Manahan

84
Q

Histo presentation of Rotor Syndrome

A

Pumpkin-like appearance from time to time; bouts of occasional jaundice

85
Q

Clinical presentation of Rotor

A

Acholic/Cement-like stools (kasi walang nakakalabas na conjugated bile)

86
Q

Clinical presentation of Rotor

A

Acholic/Cement-like stools (kasi walang nakakalabas na conjugated bile)

87
Q

Ratio of bile duct to portal area in bile duct proliferation

A

3:1

88
Q

What do you do when a child presents with biliary atresia and neonatal hepa?

A

Treat atresia first. Hepa can be managed with meds easily

89
Q

What do you do when a child presents with biliary atresia and neonatal hepa?

A

Treat atresia first. Hepa can be managed with meds easily

90
Q

What parasite causes ascending cholangitis?

A

Ascaris

91
Q

Triad of ascending cholangitis consists of

A

jaundice, RUQ pain, high fever

92
Q

Synonymous to Biliary Hamartoma

A

Von Meyenberg Complex (Hamartoma of bile ducts; too many cells in one place even if there’s nothing wrong with them; occupies space and mistaken for a tumor)

93
Q

Seconary biliary cirrhosis may be due to

A

malignancies/obstructions of the biliary tree or pancreatic head

94
Q

Parasite responsible for portal v. obstruction and thrombosis (SOL)

A

Schistosoma

95
Q

A drug-related lesion caused by external estrogen ingestion

A

Peliosishepatis

96
Q

Syndrome that comes from Hepatic Vein Thrombosis

A

Buddi-Chiari; Nutmeg Liver (central pale and peripheral red)

97
Q

Syndrome that comes from Hepatic Vein Thrombosis

A

Buddi-Chiari; Nutmeg Liver (central pale and peripheral red)

98
Q

Most common malignancy in the liver

A

Mets

99
Q

A low-grade malignancy pediatric tumore

A

Hemangiothelioma

100
Q

Arises from the biliary tree, bile duct; seen in people who eat raw food

A

Cholangiocarcinoma (higher incidence of multifocality)

101
Q

Parasite responsible for CholangioCA

A

Clonorchissinesis

102
Q

Most common PRIMARY MALIGNANT tumor of the liver

A

Hepatocellular CA

103
Q

Most common primary tumor

A

Hemangioma

104
Q

Most famous marker of hepatocellular CA?

A

Alpha feto protein

105
Q

Most famous marker of hepatocellular CA?

A

Alpha feto protein

106
Q

Infective etiology for a single large abcess

A

Amoeba

107
Q

Pyogenic small, multiple and diff etiologies abcess

A

From blood stream

108
Q

Treatment for abcess

A

Surgical drainage or antibiotics

OS 214 G.I. (2 decks)

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