Quiz 4 Flashcards

(127 cards)

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
What characterizes Peutz-Jeghers syndrome?
mucocutaneous pigmentation and benign GI hamartomas
26
Where are the benign tumors of Peutz-Jeghers syndrome usually found?
small bowel 90% | could also be in stomach and large bowel
27
What is the cause of Peutz-Jeghers syndrome?
autosomal dominant disease
28
What do the lesions of P-J syndrome look like histologically?
frond-like appearance with a stromal/smooth muscle core covered by acinar glands and normal mucosa nuclear atypia is absent
29
What is the most common type of small bowel malignancy in the US?
adenocarcinoma
30
What is the appearance of small of large bowel adenocarcinomas?
geographic distribution
31
From what cells do carcinoid tumors arise from?
neuroendocrine
32
What do carcinoid tumors look like histologically?
nests endocrine appearance cells and nuclei are consistent in size and shape surrounded by cytoplasm
33
What are the three classifications of colorectal polyps? Give an example of each.
benign (hyperplastic polyp) pre-malignant (tubular adenoma) malignant (colorectal adenocarcinoma)
34
What is the most common type of polyp in the colon?
hyperplastic polyp
35
T/F. The cells of hyperplastic polyps display normal differentiation and maturation.
true | rice grain appearance
36
Why are adenomatous polyps called tubular adenomas?
due to the rounded nature of the neoplastic glands that form it.
37
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?
adenomatous polyp
38
Grossly, how does the adenomatous polyp appear?
hemorrhagic surface long, narrow stalk larger than 2 cm = high risk of malignancy
39
How are villous and adenomatous polyps different in terms of form?
villous are larger and sessile rather than pedunculated
40
What is another name for an adenomatous polyp?
tubular polyp
41
How do villous polyps appear histologically?
cauliflower like due to elongated glandular structures covered by dysplastic epithelium
42
Between villous and adenomatous polyps, which are more likely to have invasive carcinoma in them?
villous
43
What characterizes juvenile polyposis syndrome?
the appearance of multiple polyps in the GI tract, usually as a child up to young adulthood
44
What are the most common juvenile polyposis syndrome lesions like?
non-neoplastic hamartomatous self-limiting benign
45
What are those with juvenile polyposis syndrome more at risk for developing?
adenocarcinoma
46
What does juvenile polyposis syndrome look like histologically?
inflamed, edematous stroma eroded surface and cystic epithelial elements large, multi-lobulated
47
Where in the GI tract are FAP associated polyps mostly found?
epithelium of the large intestine
48
What is the combination of polyposis, osteomas, fibromas and sebaceous cysts called?
Gardner's Syndrome
49
What does adenocarcinoma look like histologically?
glands are long and frond-like (similar to villous adenoma) growth is exophytic crowded nuclei with hyperchromatism and pleomorphism
50
What differentiates leiomyoma from leiomyosarcoma histologically?
leiomyosarcomas have greater cell density (>2 mitotically active nuclei per hpf) and cells have more mitotically active nuclei both have increased cellularity
51
Large blue cells infiltrating mucosa with prominent clumped chromatin and nucleoli with occasional mitotic figures. What are you looking at?
non-Hodgkin's lymphoma
52
What is the minimum percent of liver needed to potentially regenerate.
25%
53
What are the 2 most common causes of chronic liver disease?
hepatitis C viral infection | alcohol-induced liver disease
54
What are the five general responses seen in liver disease?
``` degeneration and intracellular accumulation necrosis and apoptosis inflammation regeneration fibrosis ```
55
What does damage from toxic/immunologic insult result in?
swelling of hepatocytes
56
What do you call severe hepatocyte swelling? What does it look like?
ballooning degeneration | irregularly clumped cytoplasmic organelles and large clear spaces
57
Give three examples of toxic intracellular deposition
hemochromatosis Wilson's disease steatosis (triglycerides)
58
What cells engulf apoptotic cell fragments within hours of apoptosis of hepatocytes?
Kupffer cells and circulating monocytes
59
What does ischemic coagulative necrosis look like histologically?
liver cells are poorly stained and contain lysed nuclei
60
What are Councilman Bodies?
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
In viral hepatitis, what cells collect in the portal tracts as a reflection of inflammation?
lymphocytes
62
What is the inflammatory process of chronic active hepatitis called?
piecemeal necrosis
63
What is the certain exception to the potential for liver regeneration?
fulminant hepatic disease
64
What characterizes hepatocellular proliferation?
mitoses, thickening of hepatocyte chords | possible disorganization of parenchymal structure
65
What is being deposited in the case of fibrosis?
collagen
66
What is cirrhosis?
continued fibrosis leads to the liver being subdivided into nodules of proliferating hepatocytes surrounded by scar tissue
67
What does cirrhosis look like microscopically?
regenerative nodules of hepatocytes surrounded by fibrous connective tissues that bridges between portal tracts
68
What is the most common cause of hepatic infection?
viruses
69
Besides the hepatitis viruses, what are some other viruses that can cause hepatitis?
EBV CMV Yellow fever
70
Does HAV cause chronic hep or a carrier state?
no
71
When can HAV become more serious?
When in conjunction with HBV, HCV or ETOH damage
72
What is the incubation period for HAV?
2-6 weeks
73
What populations are at greatest risk for HAV?
those that live in countries with substandard hygiene and sanitation
74
What 4 states can HBV infection result in?
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
Can those with HBV infection become carriers?
yes
76
Where do most HBV carriers live?
Asia and Western Pacific Rim
77
What does HBV infection pose an increased risk for?
hepatocellular carcinoma
78
What is the only bodily fluid in which HBV is not found in an infected individual?
stool
79
T/F. Vertical transmission can lead to lifelong HBV carrier state
true
80
What is the most common chronic blood-borne infection in the US and the most common cause of chronic liver disease?
HCV
81
What is the most common mode HCV transmission?
IV druge use
82
Is it more common to pass HCV or HBV vertically?
HBV
83
T/F. Acute HCV infection is generally undetected clinically
true
84
Between HCV and HBV, which is most likely to become chronic?
HCV
85
What is the incubation period of HCV?
2-26 weeks
86
If a serum test reveals no anti-HCV antibodies, would that r/o acute HCV in a symptomatic individual? why/why not?
No. Abs might not emerge for 3-6 weeks.
87
In a majority of people with chronic HCV infection, what persists despite the presence of neutralizing antibodies?
HCV RNA
88
What is a characteristic clinical feature of chronic HCV infection?
periods of elevations in serum aminotransferases with intervening normal or near-normal levels
89
What is the name of the antigen that must encapsulate HDV for it to be active?
HBsAg
90
Which hep virus does HDV depend on for it's genetic information?
HBV
91
What two settings does HDV arise in?
acute HBV co-infection | following an established HBV infection
92
Where is HDV most common?
mediterranean middle east north africa
93
Who gets HDV in the US?
IV drug users | those needing multiple blood transfusions
94
How is HDV spread?
needles | sexual contact
95
When is HEV dangerous?
In pregnant women
96
What's up with HGV?
not much | it's an innocent bystander virus
97
What is the most important indicator of likelihood to progress to cirrhosis?
etiology
98
What are some non-viral causes of chronic hepatitis?
``` chronic alcoholism wilson's disease alpha a-antitrypsin deficiency drugs hepatotoxins AI disease ```
99
What are the three carrier states of chronic hepatitis?
asx with virus asx w/non-viral chronic hep according to lab/histological findings symptomatic chronic disease
100
What does chronic hep (due to HCV) look like histologically?
inflammatory cells and fibrous tissue (in bands, stained blue)
101
What is a ground glass hepatocyte? What does it indicate?
liver parenchymal cell that has characteristic hazy staining appearance to the cytoplasm (granular homogenous eosinophilic) HBV
102
Are ground glass hepatocytes seen in acute HBV?
no, just chronic HBV
103
What do we call irreversible liver damage due to the deposition of fibrous tissue?
cirrhosis
104
What is the progression of cirrhosis?
portal tracts exhibit fibrosis periportal septal fibrosis occurs linking of fibrous septa between lobules (bridging fibrosis)
105
What is fulminant hepatitis?
when hepatic insufficiency progresses from onset of sx to hepatic encephalopathy within 2-3 weeks.
106
Which virus usually results in fulminant hepatitis?
HBV
107
Which drug is principally responsible for non-viral fulminant hep?
acetomenophen
108
What are the 4 main causes of fulminant hepatitis?
HSV viruses drugs/chemicals mycotoxins unknown
109
What does fulminant hepatitis look like grossly and microscopically?
gross: necrotic, muddy red, mushy, blotchy bile staining outer capsule is wrinkly micro: complete hepatocyte destruction, collapsed reticulin framework, preserved portal tracts
110
Does the liver become enlarged or shrink with fulminant hep?
shrink
111
Do people recover from fulminant hep?
Potentially, f they can survive more than 1 week.
112
What happens when alcohol and acetaminophen are consumed together?
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
What compound does the liver not produce as well, due to alcohol, that makes it prone to oxidative injury?
Glutathione
114
What is the number one cause of acute fulminant liver failure?
acetamenophen
115
What are the three main diseases that result from chronic alcoholism?
hepatic steatosis alcoholic hepatitis cirrhosis
116
What parts of the cell are affected by alcohol?
microtubular and mitochondrial function and membrane fluidity
117
What intermediate metabolite of alcohol induces lipid peroxidation and oxidative damage?
acetaldehyde
118
In hepatic steatosis, what is happening in the liver?
lipids accumulate to the point of creating large, clear macrovesicular globules, which compress and displace the nucleus to the periphery of the hepatocyte
119
microscopically, how does hepatic steatosis look?
intracytoplasmic fat is seen as clear vacuoles and early fibrosis
120
What disease involves single/scattered foci and cells undergo swelling (ballooning) and necrosis?
alcoholic hepatitis
121
What type of cells might be develop with alcoholic hepatitis?
kupffer cells (hemosiderin deposited in hepatocytes)
122
What are Mallory Bodies?
hepatocytes with accumulated keratin and other proteins, which become visible as eosinophilic cytoplasmic inclusion
123
What are mallory bodies characteristic of?
alcoholic liver disease | Also can be seen in NASH, primary biliary cirrhosis, Wilson's disease and hepatocellular tumors
124
What types of cells does chronic alcoholic hepatitis almost always activate?
fibroblasts, causing fibrosis
125
What signals an irreversible stage of fibrosis?
fibrotic bands
126
T/F. Cirrhosis looks different when produced by HSV versus chronic alcohol use
false. They are indistinguishable
127
What does cirrhosis look like microscopically?
nodules of varying size entrapped in blue-staining fibrous tissue