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Pathology III > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Most common viral enteritis in all age groups worldwide:

A

Norovirus - the MC Norwalk “winter vomiting” virus
90% of epidemic outbreaks / 50% of foodborne

MC cause of severe diarrhea: Rotavirus

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2
Q

MC cause of severe diarrhea in infants/children:

A

Rotavirus

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3
Q

“Picnic food poisoning”:

A

Staphylococcus aureus

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4
Q

Food poisoning assoc w/ingestion of contaminated rice or meat & assoc w/Chinese food:

A

Bacillus cereus

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5
Q

Food poisoning assoc w/contaminated saltwater oysters, crab, & shrimp:

A

Vibrio (cholera & non-cholera)

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6
Q

Food poisoning assoc w/improper home canning:

A

Clostridium botulinum

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7
Q

“Antibiotic-induced” enterocolitis:

A

Clostridium difficile

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8
Q

Causes of food-borne illness in US (top 4):

A
  1. Norovirus
  2. Salmonella
  3. Colstridium perfringens
  4. Campylobacter
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9
Q

Cause of death by food poisoning in US (top 4):

A
  1. Salmonella
  2. Toxoplasma
  3. Listeria
  4. Norovirus

related more to fluid loss & not presenting to ED than virulence

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10
Q

The delay btw consuming contaminated food & appearance of symptoms:

A

Incubation period

typically ranges hours to days, but can be months/years (Listeriosis; Creutzfeldt-Jakob dz - mad cow, prion)

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11
Q

Enterotoxins:

A

chromosomally-encoded exotoxins, secreted in intestinal cells; often heat-stable, cytotoxic, change permeability of epithelial wall

entero- often used interchangeably with exotoxin

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12
Q

Endotoxin:

A

LPS envelope (gm -) toxins within the bacteria released upon cell lysis

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13
Q

Medical condition primarily seen in premature infants (& neutropenic cancer pts) where portions of bowel undergo necrosis:

A

Necrotizing enterocolitis (NEC)

no definitive cause
thought to possibly be infectious agent, perhaps pseudomonas aeruginosa

formula feeding increases risk 10-fold over breastfeeding

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14
Q

Most common area affected by NEC:

A

near the ileocecal valve

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15
Q

Pseudomembranous colitis is:

A
  • a cause of AAD (abx-assoc diarrhea)
  • often cause by C. diff, but not always
  • characterized by offensive-smelling diarrhea, fever, abd pain
  • informally called “C diff colitis”
  • can develop toxic megacolon
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16
Q

Mucosal appearance in pseudomembranous colitis:

A

hyperemic
partially covered by yellow-green exudate
no mucosal erosion!
numerous inflammatory cells - neutrophils
bacterial overgrowth 2° to abx use

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17
Q

Ischemic colitis:

A

Inflammation & injury d/t inadequate blood supply to the large intestine.

uncommon in general pop.
occurs in elderly post acute low BP or local ischemia

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18
Q

T/F: most small intestine tumors are asx until they grow large enough to obstruct the lumen.

A

True.

after which point they may cause intussusception or volvulus, bleed, or perforate.

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19
Q

Smooth muscle cell appearance in leiomyoma:

A

elongated spindle cells, cigar-shaped nuclei, no evidence of increased mitoses.

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20
Q

Characteristics of Peutz-Jeghers syndrome:

A

autosomal dominant - assoc w/mutation of LKB1 gene
mucocutaneous pigmentation
benign GI hamartomas in Sm Int (90%)
[may also present in stomach & Lg Int]

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21
Q

Histological appearance of PJS:

A

frond-like appearance
stromal/smooth muscle core
covered by acinar glands & normal mucosa
no nuclear atypia

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22
Q

T/F: Primary cancer of the small intestine is common.

A

False.

Relatively rare, accounts for 2% of all GI cancer.

MC - adenocarcinoma

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23
Q

Most common type of cancer found in the small intestine:

A

metastatic dz

common primary sites - colon, breast, ovary, pancreas, stomach, melanoma

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24
Q

Carcinoid tumors arise from _____ cells & usually secrete ______:

A

neuroendocrine / serotonin

NE cells are widespread in the body, esp in organs derived from the primitive intestine.

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25
Histology of carcinoid:
nests of carcinoid tumor w/endocrine appearance collections of small, round cells nuclei of consistent size/shape cytoplasm stains pink to pale blue
26
Colorectal polyp classification is by:
behavior (benign vs. malignant) &/or etiology (2° to IBD) benign - hyperplastic polyp pre-malignant - tubular adenoma malignant - colorectal adenocarcinoma untreated can lead to colorectal cancer
27
T/F: Visually, hyperplastic & adenomatous polyps can be told apart readily.
False. They look quite similar, and must be differentiated by bx.
28
Adenomatous polyps >2cm carry a greater risk of developing into carcinoma d/t collected mutations in:
APC DCC K-ras p53 genes
29
Adenomatous polyp histology:
``` irregular glands hyperchromatic, crowded nuclei less numerous goblet cells well-differentiated & circumscribed pedunculated without invasion ```
30
Villous adenoma - appearance: | Histology:
up to 10cm in length sessile (not pedunculated) larger than adenomatous polyps cauliflower-like appearance elongated glandular structures covered by dysplastic epithelium less common, but 40% contain carcinoma!
31
Histology of JPS (juvenile polyposis syndrome):
inflamed, edematous stroma eroded surface cystic epithelial elements juvenile refers to the histological type, NOT age of onset
32
The combination of polyposis, osteomas, fibromas, & sebaceous cysts is termed:
Gardner's syndrome
33
Inherited condition characterized by formation of hundreds to thousands of polyps, mainly in epithelium of the large intestine:
Familial adenomatous polyposis (FAP) start out benign, malignant transformation can occur
34
Histology of adenocarcinoma:
``` glands - irregular, crowded lumens containing bluish mucin maintains some glandular configuration hyperchromatism pleomorphism ```
35
T/F: more than 6 mitotically active nuclei per hpf is consistent with leiomyosarcoma.
False... more than 2! :( also have greater cell density than leiomyoma
36
Histology of GI lymphoma:
non-Hodgkin's lymphoma cells prominent clumped chromatin & nucleoli occasional mitotic figures
37
T/F: the liver is capable of regeneration.
True! the only human organ capable of significant regeneration 25% can potentially regenerate into a whole liver recent studies show reversibility of cirrhosis as well
38
The dominant primary diseases of the liver are:
``` viral hepatitis non-viral hepatitis alcoholic liver dz NASH (non-alc steatohepatitis) hepatocellular carcinoma ```
39
Liver dz is generally [fast/slow] with [short/long] interval btw onset & dx. What's the exception?
Slow insidious process, with long interval btw. Liver may be injured and heal without clinical detection. Exception of fulminant hepatic failure.
40
Over half of newly diagnosed liver dz patients have:
Hepatitis C infx (57%) alcohol induced liver dz (24%) non-alc (9%) hep B (4%)
41
5 general responses seen in liver dz:
* degeneration & intracellular accumulation * necrosis & apoptosis * inflammation * regeneration * fibrosis
42
What is ballooning degeneration?
cells that start to enlarge in size relative to supporting parenchyma d/t severe damage swollen hepatocytes irregularly clumped cytoplasmic organelles large clear spaces may not be reversible
43
Give three examples of toxic intracellular deposition:
hemochromatosis (iron overload) Wilson's dz (copper overload) steatosis (triglyceride accumulation w/in hepatocytes)
44
What's a Kayser-Fleischer ring?
greenish-brown ring around the iris, indicative of Wilson's dz - copper accumulation
45
What is the MC cause of steatosis:
ALCOHOLISM (developed nations) kwashiorkor (children) DM obesity severe GI malabsorption
46
Describe the hepatocyte appearance in ischemic coagulative necrosis:
poorly stained | lysed nuclei
47
Describe the hepatocyte appearance of apoptosis: | name given?
isolated hepatocytes coalesce shrunken intensely eosinophilic fragmented nuclei called Councilman bodies
48
Injury to the liver assoc w/ influx of acute or chronic inflammatory cells is called:
hepatitis
49
Fibrosis can significantly alter hepatic:
blood flow perfusion subdivides into proliferating nodules surrounded by scar tissue - resulting in cirrhosis
50
The MC & notable liver infections are _____ in origin:
viral
51
"Viral hepatitis" is infection of the liver caused by:
a group of "hepatotropic" viruses -> great affinity for the liver, able to replicate in hepatocytes MC - A, B, C, D, E ;) others - EBV, CMV, yellow fever
52
Hep A:
``` benign, self-limiting 2-6 wk incubation acute only rare fulminant dz (0.1% fatality) endemic in undeveloped countries 25% of clinically evident hepatitis worldwide ```
53
Hep B:
can produce: 1) acute hepatitis w/resolution 2) chronic hepatitis -> cirrhosis 3) fulminant dz w/liver necrosis 4) lead to Hep D ``` chronic pts -> always infectious 75% of chronic pts in Asia/pacific rim preventable - by vaccine 4-26 wk incubation present in ALL fluids (not stool) ```
54
Hep C:
``` MC chronic blood-borne inf in the US 1/2 the pts in US w/chronic liver dz MC route - inoculation, blood transfusion, IV drugs 15% transmission by sex majority progress to chronic dz ```
55
Hep D:
requires co-infx w/Hep B -> super-infx - worse than B alone mediterranean, middle east, N africa
56
Hep E:
acute hepatitis resolves ~6 wks except pregnant women - may lead to fulminant hepatic necrosis, 15-25% fatality
57
Define chronic hepatitis:
symptomatic, biochemical, or serological evidence of continuing or relapsing hepatic dz for >6 mos, w/histological documentation of liver inflammation & necrosis.
58
MC causes of chronic hepatitis:
HBV HCV HBV + HDV ``` other: alcoholism Wilson's dz alpha-1-antitrypsin deficiency drugs/hepatotoxins autoimmune dz ```
59
Most important indicator of cirrhosis liklihood in chronic hepatitis is:
etiology
60
Describe 3 "carrier" states of chronic hepatitis:
1) harbor one or more viruses, suffer little/no adverse clinical or histological effect 2) chronic dz by lab or histology, but asx or mild 3) clinically symptomatic chronic dz in mild forms, inflammation limited to portal tracts lymphs, macrophages, occasional plasma cells, rare neuts/eos architecture well preserved necrosis in individual cells
61
The classic ground glass appearance is assoc w:
chronic Hep B characteristic hazy staining appearance diffuse granular cytoplasm
62
When hepatic insufficiency progresses from onset to hepatic encephalopathy w/in 2-3 wks, it is termed:
fulminant hepatic failure
63
Drinking frequently -> inc efficiency of alcohol breakdown (phase I detox) -> also inc efficient at acetaminophen breakdown. How can this lead to acute liver failure?
with adequate glutathione, breakdown product NAPQI (from acetaminophen) is rapidly conjugated; if depleted, they have a buildup of the most hepatotoxic substance known, resulting in hepatocellular death & liver necrosis! as low as 4 gms can be toxic
64
fulminant hepatitis - appearance: | histology:
gross - necrotic areas have a muddy red, mushy appearance with blotchy bile staining; limp, wrinkled, w/too-large capsule micro - complete destruction of hepatocytes in contiguous lobules, collapsed reticulin framework, preserved portal tracts
65
% of deaths from cirrhosis related to alcohol-induced liver dz:
40% 200K deaths annually 5th leading cause of death (auto related)
66
3 major alcohol-related insults to liver:
hepatic steatosis alcoholic hepatitis cirrhosis collectively called Alcoholic Liver Dz [a maladaptive state in which hepatocytes respond in increasingly pathologic ways to a stimulus (alcohol) that originally was only marginally harmful]
67
Major intermediate alcohol metabolite & it's effect:
acetaldehyde induces lipid peroxidation subsequent oxidative damage
68
hepatic steatosis - appearance: | histo:
large, soft organ, yellow, greasy with consistent EtOH use, fibrous tissue develops around terminal hepatic veins, into sinusoids hepatocyte ballooning & necrosis, single or scattered foci, d/t accumulation of fat & water, mb deposition of hemosiderin in hepatocytes & Kupffer cells; neutrophils accumulate around degen cells; lymphs/macrophages in liver parenchyma; over years, shrunken, non-fatty, brown/green; prominent activation of fibroblasts => fibrotic bands (late, signifies irreversible stage)
69
Hepatocytes with accumulated keratin & other proteins, visible as eosinophilic cytoplasmic inclusions:
Mallory bodies ``` seen in: alcoholic liver dz NASH primary biliary cirrhosis Wilson's dz hepatocellular tumors ```
70
If AST is >2x higher than ALT, think: | when might you see AST:ALT <1:
alcohol-related injury [if you land on your AST] NAFLD
71
MC cause of fatty liver:
alcohol
72
NAFLD is strongly associated with:
``` obesity dyslipidemia hyperinsulinemia insulin resistance DM II ```
73
liver bx of pts with NAFLD show:
``` steatosis findings - accumulation of lg & sm vesicles of fat (most triglycerides) w/in hepatocytes multifocal parenchymal inflammation Mallory bodies hepatocyte death (ballooning, apoptosis) sinusoidal fibrosis ```
74
Compare 1° vs. 2° hemochromatosis:
1° - defect of HFE gene leading to excess iron absorption 1:200-500 in US / 1:10 of Northern European descent 2° - excess iron d/t administration (often d/t transfusion)
75
How does hemochromatosis affect organs:
heart - CHF pancreas - DM joints - arthritis skin - "bronze diabetes"
76
Wilson's dz is a disorder marked by toxic levels of _______ in many organs, principally which 3?
Copper liver brain eyes
77
Pathognomonic finding of Wilson's dz is:
Kayser-Fleischer ring brownish-green ring around the iris of the eye d/t deposition of copper
78
alpha-1-antitrypsin deficiency:
autosomal-recessive d/o abnormally low serum levels of protease inhibitor particularly inhibits lung elastase pts develop COPD & liver dz
79
autoimmune dz characterized by T cell mediated destruction of bile ducts in liver:
Primary biliary cirrhosis (PBC) bile ducts become clogged/destroyed, ending in fibrosis & degeneration of hepatocytes 1° histo finding - granulomatous destruction of medium size intrahepatic bile ducts
80
PBC - clinical findings:
``` xanthomas xanthelasmas cirrhosis jaundice pruritis foul-smelling stools, oily ``` assoc w/other AI d/o's - RA, Sjogren's
81
Primary sclerosing cholangitis - findings:
``` barium - beaded appearance segmental stricture dilatation of bile ducts high incidence of concurrent IBD [UC-70%] onion-skin fibrosis of bile ducts ``` pruritis jaundice progressive weakness inc risk of cholangiocarcinoma

Pathology III (5 decks)

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