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GI2 E1 > infectious small intestine and colon > Flashcards

infectious small intestine and colon Flashcards

robbins

1
Q

generic clinical presentation that suggests infectious enterocolitis

A

diarrhea, abd pain, urgency, perianal discomfort, incontinence, hemorrhage

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2
Q

with what population is infectious enter-colitis associated

A

children before 5

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3
Q

pediatric infectious diarrhea is associated with what kind of organism

A

enteric virsus

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4
Q

shape+type - cholera

A

comma shaped with flagella, gram (-), anaerobe, toxin producing

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5
Q

describe the virulence of cholera, and its activity within the GI tract

A

noninvasive, remain in intestinal lumen

have flagella, use to colonize

I A subunit, 5 B subunits
cholera toxin’s B subunits will bind the GM1 ganglioside on the membrane of the epithelial cell–> A subunit goes in–> Gs–> cAMP–> Cl- release via CFTR gene –> osmotic driving force that causes diarrhea

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6
Q

transmission, clinical presentation, complications of cholera

A

fecal-oral route, water, shellfish

endemic/epidemic or sporadic: asx or mild diarrhea OR abrupt RICE WATER profuse diarrhea may smell like fish

dehydration and electrolyte imbalances, LOC, death within 24 hours. if survive, last 1 week

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7
Q

what organisms will affect the small intestine specifically

A 
cholera
salmonellosis
typhoid fever
ETEC
EPEC
whipple ds
mycobacterial infection
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8
Q

what organism will act in the ileum, appendix, and right colon

A

yersinia

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9
Q

what organisms specifically affect the colon

A 
campylobacter
salmonellosis
EHEC
EIEC
EAEC
C Dif
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10
Q

what organisms affects the L colon and the ileum

A

shigellosis

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11
Q

transmission, clinical presentation, complications of campylobacter

A

poulty, milk, other foods, wild birds

children and travelers: watery or bloody diarrhea (dysentery)

reactive arthritis, guillain-barre, syndrome, enteric fever

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12
Q

transmission, clinical presentation, complications of shigellosis

A

fecal-oral, food, water

children, migrant workers, travelers, nursing home
(watery–>bloody+pus) diarrhea, fever, abd pain
SELF LIMITED= 1 week of sx, up to a month of constitutional sx
subacute presentation in adults: several weeks of waxing and waning
can be confused for UC

reactive arthritis, urethritis, conjunctivitis, HUS, toxic megacolon

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13
Q

transmission, clinical presentation, complications of salmonellosis

A

meat, poultry, eggs, milk

in children and older adults, watery or bloody diarrhea,
anywhere from loose stools to cholera like profuse diarrhea

sepsis, abscess

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14
Q

transmission, clinical presentation, complications of typhoid tumor

A

fecal-oral route

children, adolescents, travelers
bloody diarrhea (can persist for a week), fever (resolves within 2 days), anorexia, bloating, short asx phase that gives way to bacteremia and fever like flu sx
LLQ abd pain, rose spots on chest and abd

chronic infection, carrier state, encephalopathy, myocarditis, intestinal perforation

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15
Q

transmission, clinical presentation, complications of yersinia

A

pork, milk, water

clusters of people: abd pain, fever, bloodydiarrhea,
can mimic appendicitis

reactive arthritis, erythema nodosum

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16
Q

transmission, clinical presentation, complications of ETEC

A

food or fecal-oral,

infants, adolescents, travelers: severe watery diarrhea

dehydration, electrolyte imbalance

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17
Q

transmission, clinical presentation, complications of EPEC

A

fecal-oral route

infants: watery diarrhea

dehydration, electrolyte imbalance

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18
Q

transmission, clinical presentation, complications of EHEC

A

beef, milk produce

sporadic/epidemic: bloody diarrhea

HUS

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19
Q

transmission, clinical presentation, complications of EIEC

A

cheese, deli meats, water

young children, bloody diarrhea

–

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20
Q

transmission, clinical presentation, complications of EAEC

A

unknown

children, adults, travelers: non-bloody diarrhea, afebrile

–

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21
Q

transmission, clinical presentation, complications of C. Dif

A

us of abx in hospitals,

old, immunosuppressed, prolonged use of abx: watery diarrhea, fever, leukocytosis, cramps, dehydration, hypoalbuminemia

relapse, toxic megacolon

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22
Q

transmission, clinical presentation, complications of whipple ds

A

–

caucasian men, farmers and others working with exposure to soil/animals
rare: malabsorptive diarrhea, weight loss, arthralgia

arthritis, CNS disease

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23
Q

transmission, clinical presentation, complications of mycobacterial infection

A

immunosuppressed, endemic: malabsorption

pneumonia, infection at other sites

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24
Q

trx for cholera

A

timely fluid replacement, oral rehydration

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25
Q

most common enteric pathogen in developed countries, traveler’s diarrhea

A

campylobacter jejuni

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26
Q

virulence factors of campylobacter

A

flagella, cholera toxin-like enterotoxin

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27
Q

what patients are especially likely to develop reactive arthritis with a campylobacter infection

A

those with an HLA-B27

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28
Q

describe the etiology of Guillain-Barre w campylobacter

A

molecular mimicry as Ab against C. jejuni lipopolysaccharide cross react with PNS and CNS gangliosides

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29
Q

shape+type - campylobacter

A

comma shaped, flagellated, G(-)

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30
Q

how do you diagnose campylobacter

A

stool culture, showing increased neutrophil infiltrates, cryptitis+crypt abscesses with crypt architecture is preserved

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31
Q

shape+type - shigella

A

G(-), unencapsulated, nonmotile, FACULTATIVE ANAEROBE

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32
Q

most shigella infections and death occur in ___

A

children under 5

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33
Q

outline the etiology of a shigella infection

A

resistant to the harsh acidic environment of the stomach so can get through into the stomach, get to the intestine where it will be taken up by M cells, phagocytosed by Mø at which point they cause apoptosis

ensuing inflammation–> shigella now has access to an invasion route

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34
Q

shigella has a tropism for what cell

A

M cells (lymphoid cells)

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35
Q

with shigella infection, while duration is much shorter in ___ than ___, severity is often much ____

A

children than adults

greater

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36
Q

what complication triad presents with Shigella, and which population is most likely to develop this

A

reactive arthritis, urethritis, conjunctivitis

HLA-B27 (+) men between 20 and 40

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37
Q

what syndrome can develop post shigella or shiga-like toxin (EHEC/S. dysenteria) infection

A

HUS

38
Q

describe treatment methods for shigella

A

abx treatment shortens the clinical course and reduces the duration of organism shedding in stools

ampcillin or flouroquinolone

ANTIDIARRHEAL MEDS ARE CONTRAINDICATED

39
Q

shape+type - salmonella

A

enterobacteriaceae family of G(-) bacilli

40
Q

causative agent of typhoid/enteric fever

A

salmonella typhi

41
Q

causative agent of salmonellosis

A

nontyphoid salmonella

42
Q

when is salmonella incidence highest

A

summer and fall

43
Q

salmonella virulence

A

type 3 secretion system, transferring bacterial proteins into M cells and enterocytes, through peyer’s patches

trigger actin rearrangement via Rho GTPase and bacterial endocytosis

flagellin –> TLR5 –> increase local inflammatory response

some prevent TLR4 activation

44
Q

what population is at a high risk of disseminated salmonellosis

A

genetic defects in Th17 immunity, immunosuppression

45
Q

____ can prolong the carrier state or cause relapse of salmonella infection and doesn’t help with shortening diarrheal duration

A

abx

46
Q

what populations are at a high risk of severe illness due to salmonella

A 
malignancies
immunosuppressed
alcoholics
CV dysfunction 
sickle cell
hemolytic anemia
47
Q

gallbladder colonization w S. typhi/paratyphi can be associated with..

A

gallstones

chronic carrier state

48
Q

describe the path of S. typhi in the body

A

survive through the stomach, once in the small intestine are taken up by and invade M cells

disseminate via lymphatic and blood vessels

49
Q

what histologic changes can be seen with salmonella infection

A

peyers patches in the terminal ileum enlarge and plateau-like elevate

draining mesenteric LNs are also enlarged

large oval ulcers

small and scattered perenchymal necrosis

typhoid nodules= in the BM, LN, hepatocytes replaced by Mø (phagocyte hyperplasia)

50
Q

during the febrile phase of typhoid fever, almost all ____ are positive and ____ can prevent further disease progression, and the phase can last up to ___

A

blood cultures
abx
2 weeks

51
Q

what are some complications of typhoid fever

A

encephalopathy, meningitis, seizures, endocarditis, myocarditis, pneumonia, cholecystitis

52
Q

what population is particularly susceptible to salmonella osteomyelitis

A

sickle cell disease

53
Q

agent for pulmonic and bubonic plague

A

Y. pestis

54
Q

when are yersinia infections most common

A

winter

55
Q

what does yersinia do in the body

A

invade M cell, use adhesins to bind to host B integrins–> increase iron import to stimulate systemic dissemination

56
Q

what populations are more likely to develop sepsis and death from a yersinia infection

A

chronic anemics or hemochromatosis

too much iron in body

57
Q

where does yersinia preferentially infect

A

ileum, appendix, right colon

58
Q

histologic changes w yersinia infection

A

regional LN and peyer patch hyperplasia, bowel thickening

59
Q

enteritis and colitis secondary to yersinia is common in what population

A

younger children

60
Q

extraintestinal sx of yersinia

A

pharyngitis, arthralgia, erythema nodosum

61
Q

how do you detect yersinia

A

stool culture and yersinia selective agar

LN/blood cultures

fecal leukocytes (+)

[clinically indistinguishable from salmonella + shigella)

62
Q

what are post infectious complications of yersinia infection

A

reactive arthritis with urethritis and conjunctivitis, myocarditis, erythema nodosum, and kidney ds

63
Q

shape+type - E Coli

A

G-

64
Q

what is the main type of EHEC

A

E Coli O157:H7

65
Q

predisposing factor for C Dif

A

immunosuppression + PPI use

66
Q

etiology of C. Dif infection

A

toxins released lead to disruption of epithelial cytoskeleton, tight junction barrier loss, cytokine release, apoptosis

67
Q

histologic changes seen w C Dif

A

pseudomembranes

dense infiltrates of neutrophils and occasional fibrin thrombi within capillaries
distended crypts w abscesses, volcanic like disruptions IS PATHOGNOMONIC

68
Q

trx for C Dif

A

metronidazole

vancomycin

69
Q

complications with C. Dif

A

recurrent infections

70
Q

pathogenesis of Whipple

A

malabsorption (–>malabsorptive diarrhea), lymphadenopathy, arthritis

71
Q

histologic changes with whipple

A

foamy Mø, large numbers of argyrophilic rods in the LNs

sx appear when organism laden Mø accumulate within the small intestine and mesenteric LNs–> lymphatic obstruction

white-yellow plaques

HALLMARK: dense accumulation of foamy macrophages in the small intestine

72
Q

what stains can be done for whipple disease

A

PAS +

acid fast stain to differentiate from TB

73
Q

whipple ds, you can find bacteria laden Mø built up in

A

mesenteric LN, synovial membranes of effected joints, cardiac valves, brain

74
Q

family+type - norovirus

A

single stranded DNA

caiciviridae gamily

75
Q

most common cause of acute gastroenteritis requiring medical attention

A

norovirus

76
Q

top to causes of severe diarrhea in infants and young children

A
  1. rotavirus

2. norovirus

77
Q

ASCARIS LUMBRICOIDES

method of invasion+ morphology
clinical presentation + epidemiology
diagnostic feature

A

nematode=roundworm
fecal oral: ingested eggs hatch in intestine and penetrate the intestinal mucosa–> splanchnic Vs–> systemic circulation–> grow in alveoli–> swallow and mature in intestine

physical obstruction of the intestine or biliary tree
can form hepatic abscess
ascaris pneumonitis

diagnosis with eggs in stool

78
Q

STRONGYLOIDES

method of invasion+ morphology

complications

A

=roundworm
larvae live in fecally contaminated tropical ground soil, can penetrate through unbroken skin–> migrate through lungs–> mature in intestine–> hatch and release larvae that penetrate the mucosa–> autoinfection

can persist for life, immunosuppressed can developing overwhelming autoinfection

induce peripheral eosinophilia

79
Q

NECATOR+ANCYLOSTOMA DUODENALE

method of invasion+ morphology
clinical presentation + epidemiology
test

A

hookworms
larval penetration through skin–>lungs–>trachea–>swallowed–> in duodenum will suck blood and reproduce

cause significant morbidity
multiple superficial erosions, focal hemorrhage, inflammatory infiltrates, irone deficiency anemia

diagnose by finding eggs in fecal smears

80
Q

ENTEROBIUS VERMICULARIS

method of invasion+ morphology
clinical presentation + epidemiology

test

A

pinworms
fecal oral route–> from intestine migrate to the anal orifice at night and cause intense irritation

rarely cause serious illness
rectal and perineal pruritis, contamination of the fingers

diagnosis with cellophane tape on the perianal skin

81
Q

TRICHURIS TRICHIURA

clinical presentation + epidemiology
diagnostic feature

A

whipworms infect young children

does not penetrate intestinal mucosa, so doesn’t cause serious disease
blood diarrhea and rectal prolapse with heavy infection

82
Q

SCHISTOSOMIASIS

method of invasion+ morphology
clinical presentation + epidemiology

A

in the intestines, adult worms reside within the mesenteric Vs

one version bone in the portal V–> esophageal varices

sx present when eggs are trapped within the mucosa and submucosa, granulomatous immune reaction can cause bleeding and/or obstruction

83
Q

intestinal cestodes

method of invasion+ morphology
clinical presentation + epidemiology
diagnostic feature

A

tapeworms
three types: fish, pork, and dwarf tapeworms
ingestion of raw/under-cooked meat and fish
attached to intestinal mucosa, gets its nutrients from the food stream and enlarges into a proglottids
adult worms can grow up to METERS

abd pain, diarrhea, nausea
(via tiniea d. ) B12 deficiency–> megaloblastic anemia
(t solium) –> cystacercosis= seizures and eye ds

dx by finding proglottids and eggs in stool

84
Q

ENTAMOEBA HISTOLYTICA

method of invasion+ morphology
clinical presentation + epidemiology
diagnostic feature
complication
prognosis
trx
A

protozoan that causes amebiasis
spread the fecal oral route
reside in cysts= chitin wall and four nuclei, resistant to gastric acid so can get to small intestine
colonize the epithelial surface of the colon and release trophozites–> reproduce anaerobically

seen in india, mexico, and columbia,
causes dysentery and liver abscess, abd pain, weight loss
most common cause of dysentery worldwide

create FLASK SHAPED ulcers with a narrow neck and broad base

can penetrate the splanchnic vessels and embolize to the liver, persisting after the infection has passed
go on to lung, heart, kidneys, brain
huge abscess, persist after the acute illness has passed
necrotizing colitis and megacolon

significant mortality

metronidazole

85
Q

where do E. histolytica most often effect

A

cecum and ascending colon

86
Q

GIARDIA

method of invasion+ morphology
clinical presentation + epidemiology
diagnostic feature
complication

A

fecal-oral route
resistant to chlorine
cause decreased expression of brush border enzymes, microvillous damage, apoptosis of small intestine epithelium

found in rural streams, campers–>swallowed while swimming
villous blunting with increased intraepithelial lymphocytes
chronic diarrhea, malabsorption, weight loss

characteristic pear shaped, two nuclei

despite oral antimicrobial therapy, recurrence is common

87
Q

most common parasitic pathogen in humans

A

giardia

88
Q

what elements are responsible and necessary for clearance of giardia

A

secretory IgA and mucosal IL-6

89
Q

at risk populations for giardia

A

immunosuppressed
agammaglobulinemic
malnourished

90
Q

classic clinical presentation with cryptosporidium

A

chronic diarrhea in AIDS

is acute and self-limited in the immunologically normal host

91
Q

cryptosporidium

method of invasion+ morphology
clinical presentation + epidemiology
diagnostic feature

A

resistant to chlorine so is present in unfiltered water
ingested oocyte will release sporozoites upon activation–> enterocyte will engulf the parasite

–> Na malabsorption, chloride secretion, increased tight junction permeability

watery diarrhea in children and the immunosuppressed

causes villous atrophy, crypt hyperplasia, inflammatory infiltrates

92
Q

intestinal TB has a similar infiltrate as __. how do you differentiate between the two?

A

Whipple

W= no acid fast, TB= acid fast

GI2 E1 (19 decks)

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