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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

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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
The three problem areas contributing to non H2O-soluble bilirubin
Hemeooxygenase, carrier protein, glucoronyl transferase
26
How many glucose attachments does it take to make bilirubin H2O-soluble?
1
27
2 Manners in which bile can be disposed
Bile to duodenum | Blood to kidney
28
Genetic deficiency of bilirubin UGT activity
Crigler-Najjar syndromes I and II
29
Possible reasons of Unconjugated Hyperbilirubinemia
Excess production of bilirubin Reduced hepatic uptake Impaired bilirubin conjugation
30
Possible reasons of Conjugated Hyperbilirubinemia
Decreased intrahepatic excretion of bilirubin | Extrahepatic biliary obstruction
31
Conjugated/unconjugated? Any lesion that tends to increase hemolysis
UNconjugated
32
Viral hepatitis produces what kind/s of hyperbilirubinemia?
Both UN and Conjugated
33
Normal limit of bilirubin
34
Jaundice will be grossly apparent when?
(1.2)(2) = >2-2.5mg/dL
35
Jaundice will be grossly apparent when?
(1.2)(2) = >2-2.5mg/dL
36
Where do most of our albumin come from?
Edi sa liver, kaya nga nandito tayo sa deck na 'to eh!
37
T or F: We excessively bleed when our liver experiences coagulopathy
T
38
Activation of which factor causes the liver to have excessive intravascular coagulation?
Hageman factor
39
Liver failure leads to an in/decrease of ammonia?
Increase. The liver fails to rid our body of NH3
40
Condition producing odor of rotting fruit Follow-up: This is caused by failure to metabolize which intestinal flora?
Fetor hepaticus Follow-up: mercaptans
41
Condition producing odor of rotting fruit Follow-up: This is caused by failure to metabolize which intestinal flora?
Fetor hepaticus Follow-up: mercaptans
42
Why would men be "by-products of liver metabolism"? (Dimacali, 2013)
Because the liver metabolizes estrogen and without the liver functions, estrogen levels increase :)
43
Why would men be "by-products of liver metabolism"? (Dimacali, 2013)
Because the liver metabolizes estrogen and without the liver functions, estrogen levels increase :)
44
Increased estrogen in females can manifest as?
Palmar erythemas and spider angiomatas
45
True or False: Liver failure prevents _______ neurotransmitters from being detoxified causing interference with synaptic activity
Hahaha. False T or F question! False lang sagot diyan :)
46
Hepatic encephalopathy affects parts of the brain in what order?
From intelligence centers to more vegetative centers until death
47
Deepest manifestation of hepatic encephalopathy?
Coma
48
Distal limb with flapping tremors
Asterixis (due to false neurotransmitters; the longer the nerves, the more disturbed they can be)
49
Most common cause of hepatic insult
Alcoholic liver disease
50
Mildest form of hepatic lesion caused by alcohol
Fatty change
51
Is alcoholic hepatitis reversible?
Yes
52
Cirrhotic livers have an increased risk of developing what?
Hepatocellular CA
53
Cirrhotic livers have an increased risk of developing what?
Hepatocellular CA
54
Patho of Alcohol Liver Disease (MLE): Alcohol is a direct/indirect toxin? Folow-up: It affects which structures?
Direct Microtubules, Mitochondrial fxn, membrane fluidity
55
A primary metabolite of alcohol
Acetaldehyde
56
A primary metabolite of alcohol
Acetaldehyde
57
Histologic feature unique to Hep B
Ground glass swollen hepatocyte
58
Actual serum Hepatitic
Hep C
59
How many percent mortality/morbidity is Hep C? Hep B?
Hep C: 50% | Hep B: 10%
60
New grading system for Hepatitis
Knodell Score: 1) # or density of inflammatory cells, 2) distribution, 3) extent of hepatic cell death, 4) extent of cirrhosis and other changes
61
Onset of fulminant hepatitis
2-3 weeks after onset of symptoms
62
Reye's Syndrome is aggravated by what medication?
Acetic salicylic acid. Replace meds with acetaminophen instead
63
Concave or convex? Fulminant hepatitis
Convex-Concave (kasi "shrunken" liver ay nag-dip lang sa normal level)
64
Drug-induced hepatitis may be indistinguishable from which etiology?
Viral hepatitis
65
Drugs causing microvesicular fatty exchange
Salicylates and tetracyclines
66
Drugs causing macrovesicular fatty exchange
Alcohol and methotrexate
67
Drugs causing macrovesicular fatty exchange
Alcohol and methotrexate
68
Nodular liver on gross can be classified as | Micro 0.3 ___
cm
69
2 processes happening simultaneously in a cirrhotic liver
fibrosis and regeneration
70
2 processes happening simultaneously in a cirrhotic liver
fibrosis and regeneration
71
Space between the endothelial cell of sinusoid and the hepatocyte
Space of Disse
72
guarding the Space of Disse
ITO Cell
73
Who responds to toxins and cytokines from Kupffer cells by producing collagen?
ITO Cells pa rin
74
Reticular framework is important because?
This is used by a guide for the hepatocytes. If this is damaged, hepatocytes will have a misguided attempt at fixing themselves
75
Mass of hepatocytes not arranged in the architecturally correct manner
Pseudolobule
76
Mass of hepatocytes not arranged in the architecturally correct manner
Pseudolobule
77
Inflammatory reaction due to accumulation of copper in the liver
Wilson's Disease
78
In the Philippines, what is the most common etiology of hepatitis?
Viral. 10% lang ang alcohol
79
Treatment for Neonatal hepatitis
Supportive
80
Treatment for extrahepatic biliary atresia
Surgery
81
In Biliary Atresia, which part is atretic? Proximal or distal?
Distal. That's why bile ends up accumulating in the liver
82
The Criggler-Najjar Syndrom type not compatible with life
Type 1. ABSENT AGT activity as compared to type 2 with REDUCED AGT activity
83
Rotor Syndrome (Philippine study). Three names you should remember:
Rotor, Florentin, Manahan
84
Histo presentation of Rotor Syndrome
Pumpkin-like appearance from time to time; bouts of occasional jaundice
85
Clinical presentation of Rotor
Acholic/Cement-like stools (kasi walang nakakalabas na conjugated bile)
86
Clinical presentation of Rotor
Acholic/Cement-like stools (kasi walang nakakalabas na conjugated bile)
87
Ratio of bile duct to portal area in bile duct proliferation
3:1
88
What do you do when a child presents with biliary atresia and neonatal hepa?
Treat atresia first. Hepa can be managed with meds easily
89
What do you do when a child presents with biliary atresia and neonatal hepa?
Treat atresia first. Hepa can be managed with meds easily
90
What parasite causes ascending cholangitis?
Ascaris
91
Triad of ascending cholangitis consists of
jaundice, RUQ pain, high fever
92
Synonymous to Biliary Hamartoma
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
Seconary biliary cirrhosis may be due to
malignancies/obstructions of the biliary tree or pancreatic head
94
Parasite responsible for portal v. obstruction and thrombosis (SOL)
Schistosoma
95
A drug-related lesion caused by external estrogen ingestion
Peliosishepatis
96
Syndrome that comes from Hepatic Vein Thrombosis
Buddi-Chiari; Nutmeg Liver (central pale and peripheral red)
97
Syndrome that comes from Hepatic Vein Thrombosis
Buddi-Chiari; Nutmeg Liver (central pale and peripheral red)
98
Most common malignancy in the liver
Mets
99
A low-grade malignancy pediatric tumore
Hemangiothelioma
100
Arises from the biliary tree, bile duct; seen in people who eat raw food
Cholangiocarcinoma (higher incidence of multifocality)
101
Parasite responsible for CholangioCA
Clonorchissinesis
102
Most common PRIMARY MALIGNANT tumor of the liver
Hepatocellular CA
103
Most common primary tumor
Hemangioma
104
Most famous marker of hepatocellular CA?
Alpha feto protein
105
Most famous marker of hepatocellular CA?
Alpha feto protein
106
Infective etiology for a single large abcess
Amoeba
107
Pyogenic small, multiple and diff etiologies abcess
From blood stream
108
Treatment for abcess
Surgical drainage or antibiotics

OS 214 G.I. (2 decks)

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