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Path 3 > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

What is enterocolitis?

A

inflammation of the colon and small intestine

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2
Q

What is the most common cause of enterocolitis?

A

infectious enteritis

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3
Q

What is the most common cause of viral enteritis?

A

Norwalk virus

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4
Q

What is the most common cause of diarrhea in infants and young children?

A

Rotavirus

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5
Q

What type of bacteria are endotoxins associated with?

A

gram negative that are released after lysis of the bacteria

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6
Q

What exotoxin is produced by the organism that causes diphtheria?

A

Corynebacterium diphtheriae exotoxin

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7
Q

What exotoxin is produced by Clostridium botulinum?

A

botulinum exotoxin

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8
Q

What is the mechanism by which enterotoxins disrupt functioning of the intestines?

A

they kill cells by altering the apical membrane permeability of the mucosal cells of the intestinal wall

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9
Q

With food poisoning, is the stool usually bloody with leukocytes?

A

No. Just good ol’ watery diarrhea.

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10
Q

What bacteria is common associated with contaminated rice and meat from chinese restaurants?

A

Bacillus cereus

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11
Q

What pathogen is associated with contaminated salt water crabs and shrimp?

A

Vibrio (cholera and non-cholera)

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12
Q

What population is most associated with necrotizing enterocolitis (NEC)?

A

premature infants

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13
Q

T/F. NEC has no definite cause.

A

True. An infectious agent, such as Pseudomonas aerunginosa, is suspected.

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14
Q

What bacterium often causes Pseudomembranous colitis?

A

Clostridium difficile

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15
Q

What is one result of Pseudomembranous colitis?

A

antibiotic-associated diarrhea (AAD)

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16
Q

What characterizes C. difficile colitis?

A

smelly diarrhea, fever, abdominal pain

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17
Q

What complication can result from an infection with c. diff?

A

toxic megacolon

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18
Q

Histology report shows numerous inflammatory cells, mainly neutrophils, along with necrotic epithelium and mucus. What disease is characterized by this description?

A

Pseudomembranous enterocolitis

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19
Q

What disease process is occurring in ischemic colitis?

A

Inadequate blood suppy from acute low BP after hemorrhage, constricted blood vessels, or a clot, cause inflammation and injury of the large intestine.

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20
Q

What population is most affected by ischemic colitis?

A

elderly

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21
Q

What do pale areas along with a dusky, almost bluish appearance to the wall of the bowel reflect?

A

sever bowel ischemia

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22
Q

T/F. Tumors of the small bowel are more common than of the large bowel.

A

False

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23
Q

When might small bowel tumors become symptomatic?

A

if the tumor becomes large enough to obstruct the lumen or if they cause intussesception or volvulus

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24
Q

What do leiomyomas looks like histologically?

A

elongated spindle cells containing cigar-shaped nuclei

no increased mitotic activity

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25
Q

What characterizes Peutz-Jeghers syndrome?

A

mucocutaneous pigmentation and benign GI hamartomas

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26
Q

Where are the benign tumors of Peutz-Jeghers syndrome usually found?

A

small bowel 90%

could also be in stomach and large bowel

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27
Q

What is the cause of Peutz-Jeghers syndrome?

A

autosomal dominant disease

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28
Q

What do the lesions of P-J syndrome look like histologically?

A

frond-like appearance with a stromal/smooth muscle core
covered by acinar glands and normal mucosa
nuclear atypia is absent

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29
Q

What is the most common type of small bowel malignancy in the US?

A

adenocarcinoma

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30
Q

What is the appearance of small of large bowel adenocarcinomas?

A

geographic distribution

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31
Q

From what cells do carcinoid tumors arise from?

A

neuroendocrine

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32
Q

What do carcinoid tumors look like histologically?

A

nests
endocrine appearance
cells and nuclei are consistent in size and shape
surrounded by cytoplasm

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33
Q

What are the three classifications of colorectal polyps? Give an example of each.

A

benign (hyperplastic polyp)
pre-malignant (tubular adenoma)
malignant (colorectal adenocarcinoma)

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34
Q

What is the most common type of polyp in the colon?

A

hyperplastic polyp

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35
Q

T/F. The cells of hyperplastic polyps display normal differentiation and maturation.

A

true

rice grain appearance

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36
Q

Why are adenomatous polyps called tubular adenomas?

A

due to the rounded nature of the neoplastic glands that form it.

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37
Q

Under the microscope, you see irregular glads with darker and more crowded nuclei. This neoplasm is benign and well differentiated. What are you looking at?

A

adenomatous polyp

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38
Q

Grossly, how does the adenomatous polyp appear?

A

hemorrhagic surface
long, narrow stalk
larger than 2 cm = high risk of malignancy

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39
Q

How are villous and adenomatous polyps different in terms of form?

A

villous are larger and sessile rather than pedunculated

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40
Q

What is another name for an adenomatous polyp?

A

tubular polyp

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41
Q

How do villous polyps appear histologically?

A

cauliflower like due to elongated glandular structures covered by dysplastic epithelium

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42
Q

Between villous and adenomatous polyps, which are more likely to have invasive carcinoma in them?

A

villous

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43
Q

What characterizes juvenile polyposis syndrome?

A

the appearance of multiple polyps in the GI tract, usually as a child up to young adulthood

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44
Q

What are the most common juvenile polyposis syndrome lesions like?

A

non-neoplastic
hamartomatous
self-limiting
benign

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45
Q

What are those with juvenile polyposis syndrome more at risk for developing?

A

adenocarcinoma

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46
Q

What does juvenile polyposis syndrome look like histologically?

A

inflamed, edematous stroma
eroded surface and cystic epithelial elements
large, multi-lobulated

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47
Q

Where in the GI tract are FAP associated polyps mostly found?

A

epithelium of the large intestine

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48
Q

What is the combination of polyposis, osteomas, fibromas and sebaceous cysts called?

A

Gardner’s Syndrome

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49
Q

What does adenocarcinoma look like histologically?

A

glands are long and frond-like (similar to villous adenoma)
growth is exophytic
crowded nuclei with hyperchromatism and pleomorphism

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50
Q

What differentiates leiomyoma from leiomyosarcoma histologically?

A

leiomyosarcomas have greater cell density (>2 mitotically active nuclei per hpf) and cells have more mitotically active nuclei
both have increased cellularity

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51
Q

Large blue cells infiltrating mucosa with prominent clumped chromatin and nucleoli with occasional mitotic figures. What are you looking at?

A

non-Hodgkin’s lymphoma

52
Q

What is the minimum percent of liver needed to potentially regenerate.

A

25%

53
Q

What are the 2 most common causes of chronic liver disease?

A

hepatitis C viral infection

alcohol-induced liver disease

54
Q

What are the five general responses seen in liver disease?

A 
degeneration and intracellular accumulation
necrosis and apoptosis
inflammation
regeneration
fibrosis
55
Q

What does damage from toxic/immunologic insult result in?

A

swelling of hepatocytes

56
Q

What do you call severe hepatocyte swelling? What does it look like?

A

ballooning degeneration

irregularly clumped cytoplasmic organelles and large clear spaces

57
Q

Give three examples of toxic intracellular deposition

A

hemochromatosis
Wilson’s disease
steatosis (triglycerides)

58
Q

What cells engulf apoptotic cell fragments within hours of apoptosis of hepatocytes?

A

Kupffer cells and circulating monocytes

59
Q

What does ischemic coagulative necrosis look like histologically?

A

liver cells are poorly stained and contain lysed nuclei

60
Q

What are Councilman Bodies?

A

the result of apoptotic death of a single liver cell
look like eosinophilic globules
surrounded by normal liver parenchyma of those suffering from viral Hepatitis, yellow fever, or other viral syndromes

61
Q

In viral hepatitis, what cells collect in the portal tracts as a reflection of inflammation?

A

lymphocytes

62
Q

What is the inflammatory process of chronic active hepatitis called?

A

piecemeal necrosis

63
Q

What is the certain exception to the potential for liver regeneration?

A

fulminant hepatic disease

64
Q

What characterizes hepatocellular proliferation?

A

mitoses, thickening of hepatocyte chords

possible disorganization of parenchymal structure

65
Q

What is being deposited in the case of fibrosis?

A

collagen

66
Q

What is cirrhosis?

A

continued fibrosis leads to the liver being subdivided into nodules of proliferating hepatocytes surrounded by scar tissue

67
Q

What does cirrhosis look like microscopically?

A

regenerative nodules of hepatocytes surrounded by fibrous connective tissues that bridges between portal tracts

68
Q

What is the most common cause of hepatic infection?

A

viruses

69
Q

Besides the hepatitis viruses, what are some other viruses that can cause hepatitis?

A

EBV
CMV
Yellow fever

70
Q

Does HAV cause chronic hep or a carrier state?

A

no

71
Q

When can HAV become more serious?

A

When in conjunction with HBV, HCV or ETOH damage

72
Q

What is the incubation period for HAV?

A

2-6 weeks

73
Q

What populations are at greatest risk for HAV?

A

those that live in countries with substandard hygiene and sanitation

74
Q

What 4 states can HBV infection result in?

A
  1. actue hep with resolution
  2. chronic hep, which may become cirrhosis
  3. fulminant hep with massive liver necrosis
  4. the backdrop for HDV infection
75
Q

Can those with HBV infection become carriers?

A

yes

76
Q

Where do most HBV carriers live?

A

Asia and Western Pacific Rim

77
Q

What does HBV infection pose an increased risk for?

A

hepatocellular carcinoma

78
Q

What is the only bodily fluid in which HBV is not found in an infected individual?

A

stool

79
Q

T/F. Vertical transmission can lead to lifelong HBV carrier state

A

true

80
Q

What is the most common chronic blood-borne infection in the US and the most common cause of chronic liver disease?

A

HCV

81
Q

What is the most common mode HCV transmission?

A

IV druge use

82
Q

Is it more common to pass HCV or HBV vertically?

A

HBV

83
Q

T/F. Acute HCV infection is generally undetected clinically

A

true

84
Q

Between HCV and HBV, which is most likely to become chronic?

A

HCV

85
Q

What is the incubation period of HCV?

A

2-26 weeks

86
Q

If a serum test reveals no anti-HCV antibodies, would that r/o acute HCV in a symptomatic individual? why/why not?

A

No. Abs might not emerge for 3-6 weeks.

87
Q

In a majority of people with chronic HCV infection, what persists despite the presence of neutralizing antibodies?

A

HCV RNA

88
Q

What is a characteristic clinical feature of chronic HCV infection?

A

periods of elevations in serum aminotransferases with intervening normal or near-normal levels

89
Q

What is the name of the antigen that must encapsulate HDV for it to be active?

A

HBsAg

90
Q

Which hep virus does HDV depend on for it’s genetic information?

A

HBV

91
Q

What two settings does HDV arise in?

A

acute HBV co-infection

following an established HBV infection

92
Q

Where is HDV most common?

A

mediterranean
middle east
north africa

93
Q

Who gets HDV in the US?

A

IV drug users

those needing multiple blood transfusions

94
Q

How is HDV spread?

A

needles

sexual contact

95
Q

When is HEV dangerous?

A

In pregnant women

96
Q

What’s up with HGV?

A

not much

it’s an innocent bystander virus

97
Q

What is the most important indicator of likelihood to progress to cirrhosis?

A

etiology

98
Q

What are some non-viral causes of chronic hepatitis?

A 
chronic alcoholism
wilson's disease
alpha a-antitrypsin deficiency
drugs
hepatotoxins 
AI disease
99
Q

What are the three carrier states of chronic hepatitis?

A

asx with virus
asx w/non-viral chronic hep according to lab/histological findings
symptomatic chronic disease

100
Q

What does chronic hep (due to HCV) look like histologically?

A

inflammatory cells and fibrous tissue (in bands, stained blue)

101
Q

What is a ground glass hepatocyte? What does it indicate?

A

liver parenchymal cell that has characteristic hazy staining appearance to the cytoplasm (granular homogenous eosinophilic)
HBV

102
Q

Are ground glass hepatocytes seen in acute HBV?

A

no, just chronic HBV

103
Q

What do we call irreversible liver damage due to the deposition of fibrous tissue?

A

cirrhosis

104
Q

What is the progression of cirrhosis?

A

portal tracts exhibit fibrosis
periportal septal fibrosis occurs
linking of fibrous septa between lobules (bridging fibrosis)

105
Q

What is fulminant hepatitis?

A

when hepatic insufficiency progresses from onset of sx to hepatic encephalopathy within 2-3 weeks.

106
Q

Which virus usually results in fulminant hepatitis?

A

HBV

107
Q

Which drug is principally responsible for non-viral fulminant hep?

A

acetomenophen

108
Q

What are the 4 main causes of fulminant hepatitis?

A

HSV viruses
drugs/chemicals
mycotoxins
unknown

109
Q

What does fulminant hepatitis look like grossly and microscopically?

A

gross: necrotic, muddy red, mushy, blotchy bile staining
outer capsule is wrinkly

micro: complete hepatocyte destruction, collapsed reticulin framework, preserved portal tracts

110
Q

Does the liver become enlarged or shrink with fulminant hep?

A

shrink

111
Q

Do people recover from fulminant hep?

A

Potentially, f they can survive more than 1 week.

112
Q

What happens when alcohol and acetaminophen are consumed together?

A

Alcohol upregulates phase 1 of ETOH, meaning they are better at breaking ETOH down
This means they will also break down acetamenophen down better too and NADPQI is one of the byproducts of this breakdown.
NADPQI is the very hepatotoxic because it binds to vital proteins and the hepatocyte membrane

113
Q

What compound does the liver not produce as well, due to alcohol, that makes it prone to oxidative injury?

A

Glutathione

114
Q

What is the number one cause of acute fulminant liver failure?

A

acetamenophen

115
Q

What are the three main diseases that result from chronic alcoholism?

A

hepatic steatosis
alcoholic hepatitis
cirrhosis

116
Q

What parts of the cell are affected by alcohol?

A

microtubular and mitochondrial function and membrane fluidity

117
Q

What intermediate metabolite of alcohol induces lipid peroxidation and oxidative damage?

A

acetaldehyde

118
Q

In hepatic steatosis, what is happening in the liver?

A

lipids accumulate to the point of creating large, clear macrovesicular globules, which compress and displace the nucleus to the periphery of the hepatocyte

119
Q

microscopically, how does hepatic steatosis look?

A

intracytoplasmic fat is seen as clear vacuoles and early fibrosis

120
Q

What disease involves single/scattered foci and cells undergo swelling (ballooning) and necrosis?

A

alcoholic hepatitis

121
Q

What type of cells might be develop with alcoholic hepatitis?

A

kupffer cells (hemosiderin deposited in hepatocytes)

122
Q

What are Mallory Bodies?

A

hepatocytes with accumulated keratin and other proteins, which become visible as eosinophilic cytoplasmic inclusion

123
Q

What are mallory bodies characteristic of?

A

alcoholic liver disease

Also can be seen in NASH, primary biliary cirrhosis, Wilson’s disease and hepatocellular tumors

124
Q

What types of cells does chronic alcoholic hepatitis almost always activate?

A

fibroblasts, causing fibrosis

125
Q

What signals an irreversible stage of fibrosis?

A

fibrotic bands

126
Q

T/F. Cirrhosis looks different when produced by HSV versus chronic alcohol use

A

false. They are indistinguishable

127
Q

What does cirrhosis look like microscopically?

A

nodules of varying size entrapped in blue-staining fibrous tissue

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