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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
Q

Histology of carcinoid:

A

nests of carcinoid tumor w/endocrine appearance
collections of small, round cells
nuclei of consistent size/shape
cytoplasm stains pink to pale blue

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26
Q

Colorectal polyp classification is by:

A

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

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27
Q

T/F: Visually, hyperplastic & adenomatous polyps can be told apart readily.

A

False.

They look quite similar, and must be differentiated by bx.

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28
Q

Adenomatous polyps >2cm carry a greater risk of developing into carcinoma d/t collected mutations in:

A

APC
DCC
K-ras
p53 genes

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29
Q

Adenomatous polyp histology:

A 
irregular glands
hyperchromatic, crowded nuclei
less numerous goblet cells
well-differentiated & circumscribed
pedunculated
without invasion
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30
Q

Villous adenoma - appearance:

Histology:

A

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!

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31
Q

Histology of JPS (juvenile polyposis syndrome):

A

inflamed, edematous stroma
eroded surface
cystic epithelial elements

juvenile refers to the histological type, NOT age of onset

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32
Q

The combination of polyposis, osteomas, fibromas, & sebaceous cysts is termed:

A

Gardner’s syndrome

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33
Q

Inherited condition characterized by formation of hundreds to thousands of polyps, mainly in epithelium of the large intestine:

A

Familial adenomatous polyposis (FAP)

start out benign, malignant transformation can occur

34
Q

Histology of adenocarcinoma:

A 
glands - irregular, crowded
lumens containing bluish mucin
maintains some glandular configuration
hyperchromatism
pleomorphism
35
Q

T/F: more than 6 mitotically active nuclei per hpf is consistent with leiomyosarcoma.

A

False… more than 2! :(

also have greater cell density than leiomyoma

36
Q

Histology of GI lymphoma:

A

non-Hodgkin’s lymphoma cells
prominent clumped chromatin & nucleoli
occasional mitotic figures

37
Q

T/F: the liver is capable of regeneration.

A

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
Q

The dominant primary diseases of the liver are:

A 
viral hepatitis
non-viral hepatitis
alcoholic liver dz
NASH (non-alc steatohepatitis)
hepatocellular carcinoma
39
Q

Liver dz is generally [fast/slow] with [short/long] interval btw onset & dx.
What’s the exception?

A

Slow insidious process, with long interval btw.

Liver may be injured and heal without clinical detection.

Exception of fulminant hepatic failure.

40
Q

Over half of newly diagnosed liver dz patients have:

A

Hepatitis C infx (57%)

alcohol induced liver dz (24%)
non-alc (9%)
hep B (4%)

41
Q

5 general responses seen in liver dz:

A
  • degeneration & intracellular accumulation
  • necrosis & apoptosis
  • inflammation
  • regeneration
  • fibrosis
42
Q

What is ballooning degeneration?

A

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
Q

Give three examples of toxic intracellular deposition:

A

hemochromatosis (iron overload)
Wilson’s dz (copper overload)
steatosis (triglyceride accumulation w/in hepatocytes)

44
Q

What’s a Kayser-Fleischer ring?

A

greenish-brown ring around the iris, indicative of Wilson’s dz - copper accumulation

45
Q

What is the MC cause of steatosis:

A

ALCOHOLISM (developed nations)
kwashiorkor (children)

DM
obesity
severe GI malabsorption

46
Q

Describe the hepatocyte appearance in ischemic coagulative necrosis:

A

poorly stained

lysed nuclei

47
Q

Describe the hepatocyte appearance of apoptosis:

name given?

A

isolated hepatocytes coalesce
shrunken
intensely eosinophilic
fragmented nuclei

called Councilman bodies

48
Q

Injury to the liver assoc w/ influx of acute or chronic inflammatory cells is called:

A

hepatitis

49
Q

Fibrosis can significantly alter hepatic:

A

blood flow
perfusion

subdivides into proliferating nodules surrounded by scar tissue - resulting in cirrhosis

50
Q

The MC & notable liver infections are _____ in origin:

A

viral

51
Q

“Viral hepatitis” is infection of the liver caused by:

A

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
Q

Hep A:

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
Q

Hep B:

A

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
Q

Hep C:

A 
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
Q

Hep D:

A

requires co-infx w/Hep B
-> super-infx - worse than B alone
mediterranean, middle east, N africa

56
Q

Hep E:

A

acute hepatitis
resolves ~6 wks
except pregnant women - may lead to fulminant hepatic necrosis, 15-25% fatality

57
Q

Define chronic hepatitis:

A

symptomatic, biochemical, or serological evidence of continuing or relapsing hepatic dz for >6 mos, w/histological documentation of liver inflammation & necrosis.

58
Q

MC causes of chronic hepatitis:

A

HBV
HCV
HBV + HDV

other:
alcoholism
Wilson's dz
alpha-1-antitrypsin deficiency
drugs/hepatotoxins
autoimmune dz
59
Q

Most important indicator of cirrhosis liklihood in chronic hepatitis is:

A

etiology

60
Q

Describe 3 “carrier” states of chronic hepatitis:

A

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
Q

The classic ground glass appearance is assoc w:

A

chronic Hep B

characteristic hazy staining appearance
diffuse granular cytoplasm

62
Q

When hepatic insufficiency progresses from onset to hepatic encephalopathy w/in 2-3 wks, it is termed:

A

fulminant hepatic failure

63
Q

Drinking frequently -> inc efficiency of alcohol breakdown (phase I detox) -> also inc efficient at acetaminophen breakdown. How can this lead to acute liver failure?

A

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
Q

fulminant hepatitis - appearance:

histology:

A

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
Q

% of deaths from cirrhosis related to alcohol-induced liver dz:

A

40%

200K deaths annually
5th leading cause of death (auto related)

66
Q

3 major alcohol-related insults to liver:

A

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
Q

Major intermediate alcohol metabolite & it’s effect:

A

acetaldehyde
induces lipid peroxidation
subsequent oxidative damage

68
Q

hepatic steatosis - appearance:

histo:

A

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
Q

Hepatocytes with accumulated keratin & other proteins, visible as eosinophilic cytoplasmic inclusions:

A

Mallory bodies

seen in:
alcoholic liver dz
NASH
primary biliary cirrhosis
Wilson's dz
hepatocellular tumors
70
Q

If AST is >2x higher than ALT, think:

when might you see AST:ALT <1:

A

alcohol-related injury
[if you land on your AST]

NAFLD

71
Q

MC cause of fatty liver:

A

alcohol

72
Q

NAFLD is strongly associated with:

A 
obesity
dyslipidemia
hyperinsulinemia
insulin resistance
DM II
73
Q

liver bx of pts with NAFLD show:

A 
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
Q

Compare 1° vs. 2° hemochromatosis:

A

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
Q

How does hemochromatosis affect organs:

A

heart - CHF
pancreas - DM
joints - arthritis
skin - “bronze diabetes”

76
Q

Wilson’s dz is a disorder marked by toxic levels of _______ in many organs, principally which 3?

A

Copper

liver
brain
eyes

77
Q

Pathognomonic finding of Wilson’s dz is:

A

Kayser-Fleischer ring

brownish-green ring around the iris of the eye d/t deposition of copper

78
Q

alpha-1-antitrypsin deficiency:

A

autosomal-recessive d/o
abnormally low serum levels of protease inhibitor
particularly inhibits lung elastase
pts develop COPD & liver dz

79
Q

autoimmune dz characterized by T cell mediated destruction of bile ducts in liver:

A

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
Q

PBC - clinical findings:

A 
xanthomas
xanthelasmas
cirrhosis
jaundice
pruritis
foul-smelling stools, oily

assoc w/other AI d/o’s - RA, Sjogren’s

81
Q

Primary sclerosing cholangitis - findings:

A 
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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