Quiz 4 Flashcards
Most common viral enteritis in all age groups worldwide:
Norovirus - the MC Norwalk “winter vomiting” virus
90% of epidemic outbreaks / 50% of foodborne
MC cause of severe diarrhea: Rotavirus
MC cause of severe diarrhea in infants/children:
Rotavirus
“Picnic food poisoning”:
Staphylococcus aureus
Food poisoning assoc w/ingestion of contaminated rice or meat & assoc w/Chinese food:
Bacillus cereus
Food poisoning assoc w/contaminated saltwater oysters, crab, & shrimp:
Vibrio (cholera & non-cholera)
Food poisoning assoc w/improper home canning:
Clostridium botulinum
“Antibiotic-induced” enterocolitis:
Clostridium difficile
Causes of food-borne illness in US (top 4):
- Norovirus
- Salmonella
- Colstridium perfringens
- Campylobacter
Cause of death by food poisoning in US (top 4):
- Salmonella
- Toxoplasma
- Listeria
- Norovirus
related more to fluid loss & not presenting to ED than virulence
The delay btw consuming contaminated food & appearance of symptoms:
Incubation period
typically ranges hours to days, but can be months/years (Listeriosis; Creutzfeldt-Jakob dz - mad cow, prion)
Enterotoxins:
chromosomally-encoded exotoxins, secreted in intestinal cells; often heat-stable, cytotoxic, change permeability of epithelial wall
entero- often used interchangeably with exotoxin
Endotoxin:
LPS envelope (gm -) toxins within the bacteria released upon cell lysis
Medical condition primarily seen in premature infants (& neutropenic cancer pts) where portions of bowel undergo necrosis:
Necrotizing enterocolitis (NEC)
no definitive cause
thought to possibly be infectious agent, perhaps pseudomonas aeruginosa
formula feeding increases risk 10-fold over breastfeeding
Most common area affected by NEC:
near the ileocecal valve
Pseudomembranous colitis is:
- 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
Mucosal appearance in pseudomembranous colitis:
hyperemic
partially covered by yellow-green exudate
no mucosal erosion!
numerous inflammatory cells - neutrophils
bacterial overgrowth 2° to abx use
Ischemic colitis:
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
T/F: most small intestine tumors are asx until they grow large enough to obstruct the lumen.
True.
after which point they may cause intussusception or volvulus, bleed, or perforate.
Smooth muscle cell appearance in leiomyoma:
elongated spindle cells, cigar-shaped nuclei, no evidence of increased mitoses.
Characteristics of Peutz-Jeghers syndrome:
autosomal dominant - assoc w/mutation of LKB1 gene
mucocutaneous pigmentation
benign GI hamartomas in Sm Int (90%)
[may also present in stomach & Lg Int]
Histological appearance of PJS:
frond-like appearance
stromal/smooth muscle core
covered by acinar glands & normal mucosa
no nuclear atypia
T/F: Primary cancer of the small intestine is common.
False.
Relatively rare, accounts for 2% of all GI cancer.
MC - adenocarcinoma
Most common type of cancer found in the small intestine:
metastatic dz
common primary sites - colon, breast, ovary, pancreas, stomach, melanoma
Carcinoid tumors arise from _____ cells & usually secrete ______:
neuroendocrine / serotonin
NE cells are widespread in the body, esp in organs derived from the primitive intestine.
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
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
T/F: Visually, hyperplastic & adenomatous polyps can be told apart readily.
False.
They look quite similar, and must be differentiated by bx.
Adenomatous polyps >2cm carry a greater risk of developing into carcinoma d/t collected mutations in:
APC
DCC
K-ras
p53 genes
Adenomatous polyp histology:
irregular glands hyperchromatic, crowded nuclei less numerous goblet cells well-differentiated & circumscribed pedunculated without invasion
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!
Histology of JPS (juvenile polyposis syndrome):
inflamed, edematous stroma
eroded surface
cystic epithelial elements
juvenile refers to the histological type, NOT age of onset
The combination of polyposis, osteomas, fibromas, & sebaceous cysts is termed:
Gardner’s syndrome
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
Histology of adenocarcinoma:
glands - irregular, crowded lumens containing bluish mucin maintains some glandular configuration hyperchromatism pleomorphism
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
Histology of GI lymphoma:
non-Hodgkin’s lymphoma cells
prominent clumped chromatin & nucleoli
occasional mitotic figures
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
The dominant primary diseases of the liver are:
viral hepatitis non-viral hepatitis alcoholic liver dz NASH (non-alc steatohepatitis) hepatocellular carcinoma
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.
Over half of newly diagnosed liver dz patients have:
Hepatitis C infx (57%)
alcohol induced liver dz (24%)
non-alc (9%)
hep B (4%)
5 general responses seen in liver dz:
- degeneration & intracellular accumulation
- necrosis & apoptosis
- inflammation
- regeneration
- fibrosis
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
Give three examples of toxic intracellular deposition:
hemochromatosis (iron overload)
Wilson’s dz (copper overload)
steatosis (triglyceride accumulation w/in hepatocytes)
What’s a Kayser-Fleischer ring?
greenish-brown ring around the iris, indicative of Wilson’s dz - copper accumulation
What is the MC cause of steatosis:
ALCOHOLISM (developed nations)
kwashiorkor (children)
DM
obesity
severe GI malabsorption
Describe the hepatocyte appearance in ischemic coagulative necrosis:
poorly stained
lysed nuclei
Describe the hepatocyte appearance of apoptosis:
name given?
isolated hepatocytes coalesce
shrunken
intensely eosinophilic
fragmented nuclei
called Councilman bodies
Injury to the liver assoc w/ influx of acute or chronic inflammatory cells is called:
hepatitis
Fibrosis can significantly alter hepatic:
blood flow
perfusion
subdivides into proliferating nodules surrounded by scar tissue - resulting in cirrhosis
The MC & notable liver infections are _____ in origin:
viral
“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
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
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)
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
Hep D:
requires co-infx w/Hep B
-> super-infx - worse than B alone
mediterranean, middle east, N africa
Hep E:
acute hepatitis
resolves ~6 wks
except pregnant women - may lead to fulminant hepatic necrosis, 15-25% fatality
Define chronic hepatitis:
symptomatic, biochemical, or serological evidence of continuing or relapsing hepatic dz for >6 mos, w/histological documentation of liver inflammation & necrosis.
MC causes of chronic hepatitis:
HBV
HCV
HBV + HDV
other: alcoholism Wilson's dz alpha-1-antitrypsin deficiency drugs/hepatotoxins autoimmune dz
Most important indicator of cirrhosis liklihood in chronic hepatitis is:
etiology
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
The classic ground glass appearance is assoc w:
chronic Hep B
characteristic hazy staining appearance
diffuse granular cytoplasm
When hepatic insufficiency progresses from onset to hepatic encephalopathy w/in 2-3 wks, it is termed:
fulminant hepatic failure
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
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
% of deaths from cirrhosis related to alcohol-induced liver dz:
40%
200K deaths annually
5th leading cause of death (auto related)
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]
Major intermediate alcohol metabolite & it’s effect:
acetaldehyde
induces lipid peroxidation
subsequent oxidative damage
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)
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
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
MC cause of fatty liver:
alcohol
NAFLD is strongly associated with:
obesity dyslipidemia hyperinsulinemia insulin resistance DM II
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
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)
How does hemochromatosis affect organs:
heart - CHF
pancreas - DM
joints - arthritis
skin - “bronze diabetes”
Wilson’s dz is a disorder marked by toxic levels of _______ in many organs, principally which 3?
Copper
liver
brain
eyes
Pathognomonic finding of Wilson’s dz is:
Kayser-Fleischer ring
brownish-green ring around the iris of the eye d/t deposition of copper
alpha-1-antitrypsin deficiency:
autosomal-recessive d/o
abnormally low serum levels of protease inhibitor
particularly inhibits lung elastase
pts develop COPD & liver dz
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
PBC - clinical findings:
xanthomas xanthelasmas cirrhosis jaundice pruritis foul-smelling stools, oily
assoc w/other AI d/o’s - RA, Sjogren’s
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
