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GI Flashcards

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Biology 101 flashcards
1
Q

Common Infectious Causes of Esophagitis

A

Candida albicans (most common), CMV, HSV

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2
Q

Candida albicans (esophagitis)

A

Risk: immunocompromised
Diagnosis: endoscopy (whitish plaques), double contrast esophogram (discrete linear plaque-like lesions)

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3
Q

HSV-1 (Esophogitis)

A

Diagnosis: endoscopy/double contrast esophogram (multiple superficial flat ulcers w/ raised edges that look “volcano-like”)
Cytopathic effects: syncitia (multinucleated giant cells)

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4
Q

CMV (Esophagitis)

A

Risk: solid organ transplant pt’s
Diagnosis: endoscopy/double contrast esophogram showing giant/flat ulcers in upper/mid esophagus
Cytopathic effect: “owl’s eye” inclusion bodies

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5
Q

Gastritis

A

Course: acute or chronic
Causes: NSAIDs, ETOH, tobacco, B12 deficiency
Infectious causes: H. pylori, CMV, Candida, Histoplasma
(No erosion w/ H. pylori

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6
Q

Peptic Ulcer Dz (PUD)

A

Causes: H. pylori (or NDSAIDs)
Gastric ulcers: pain briefly after eating
Duodenal ulcers: pain a few hours after eating
Diagnosis: endoscopy required to differentiate btwn duodenal and gastric

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7
Q

Helicobacter pylori

A

G-ve, non spore forming
Motile: 5-6 polar flagella (assist in invasion of mucosa)
Catalase +ve
Urease +ve

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8
Q

H. pylori Pathogenesis

A

Flagella: (5-6) mobility and chemotaxis to colonize under mucosa
Urease: neutralize gastric acid and gastric mucosal injury caused by the ammonia
LPS: adhere to host cells; inflammation
Vacuolating toxin (vacA): gastric mucosal injury
Type IV secretion system: pili-like structure that injects effectors

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9
Q

H. pylori Diagnosis

A

Serology: non-invasive, most sensitive, checks for IgG Abs
Fecal ag: non-invasive, determines current infection, used to check response/efficacy of tx
Gastric biopsy: invasive, most specific
Carbon Urea breath test: expensive, based on urease activity, pt will exhale labeled CO2 if urease is active in stomach

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10
Q

Most common cause of food born illness?

A

Norovirus (Norwalk - caliciviridae family)

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11
Q

Acute Non-inflammatory Diarrhea

A 
Duration: < 2wks
Type: watery, not bloody
Mechanism: mucosal hypersecretion or decreased absorption w/o mucosal destruction 
Location: generally SI
Onset: abrupt
Cause: viral or non-invasive bacteria
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12
Q

Acute Inflammatory Diarrhea

A

Duration: < 2wks
Type: contains blood and/or pus
Mechanism: mucosal invasion resulting in inflammation
Location: usually colon
Cause: invasive bacteria, toxin-producing bacteria

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13
Q

Persistent Diarrhea

A

Duration: 2-4 weeks

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14
Q

Chronic Diarhea

A

Duration: > 4wks
Type: secretory, osmotic, steatorrheal, inflammatory, dysmotile factitial, iatrogenic
Cause: medication, non-infectious, parasites

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15
Q

Stool lactoferrin WBCs

A

Indicates inflammatory diarrhea

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16
Q

Stool Osmolar Gap

A

Indicates lactose intolerance/laxative use

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17
Q

Routine organisms to look for

A
  • Campylobacter sp.
  • E. coli
  • Shigella
  • Salmonella
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18
Q

Toxemia (Food Poisoning)

A

Consumption of food containing toxins

*shorter incubation than food-born

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19
Q

Food-born Infection

A

Consumption of food containing organism

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20
Q

Organisms requiring low infective dose?

A

Shigella - shiga toxin, invades Peyer’s Patches
EIEC - no toxin
*only about 10 organisms

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21
Q

Organisms associated with poultry exposure

A

Campylobacter - microaerophilic, curved organism, oxidase +ve, cytotoxin (shiga like), catalase +ve
Salmonella - motile, produce H2S, invades Peyer’s patches, N/V/D @ onset

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22
Q

Organisms associated with travel to Asia?

A

Salmonella - poultry, motile, H2S production, invasive (Peyer’s patches)
EIEC - low infectious dose, no toxin, invasive
Vibrio cholera - cholera toxin, “rice water” stool, oxidase +ve, S-shape colonies, non-invasive

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23
Q

Organisms invading Peyer’s Patches?

A

Shigella - shiga toxin, low infective dose

Salmonella - motile, produce H2S gas

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24
Q

Organisms producing LT enterotoxin (acting on adenylate cyclase)

A

ETEC - travel hx
Bacillus cereus - G+ve, spore forming
Vibrio cholera - halotolerant, “rice water” stool, TCBS agar

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25
Q

Organisms that produce ST enterotoxin (activating guanylate cyclase)

A

ETEC - travel hx, no fever

Yersinia - refrigerated food, cold countries, mild fever

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26
Q

Ciguatera toxin

A

Food: predatory reef fish
ROS: acute GI sx’s 3-6h after ingestion + parasthesias, puritis & hot/cold temp reversal

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27
Q

Scrombroid toxin

A

Food: tuna, mahi-mahi, marlin
ROS: burning in mouth w/ metallic taste, acute GI sx’s <1h after ingestion (+ sx’s like dizziness, paresthesias, rash)

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28
Q

Brevetoxin

A

Food: shellfish
Condition: Neurologic Shellfish Poisoning
Incubation: <1-3h
ROS: paresthesia, mouth numbness, tingling of mouth/extremities, + GI sx’s

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29
Q

Saxitoxin

A

Food: shellfish
Condition: Paralytic Shellfish Poisoning
Incubation: <2h
ROS: tingling and numbness of mouth spreading to extremities, ataxia (GI sx’s less common), muscular or respiratory paralysis possible in rare situations

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30
Q

Aflatoxin

A

Food: nuts & seeds
ROS: necrosis, cirrhosis, HCC (liver stuff)

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31
Q

Non-invasive inflammatory diarrheal diseases?

A

EAEC - include production of copious amounts of mucous

STEC - non-sorbitol fermenting, shiga toxin

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32
Q

Fecal fat

A

Malabsorption caused by chronic diarrhea (or Giardiasis bc it colonizes the upper SI and blocks small bile ducts)

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33
Q

ETEC

A

“Traveler’s Diarrhea”
Pathogenesis: LT (👆🏽cAMP), ST (👆🏽cGMP)
ROS: acute onset profuse watery diarrhea, NO fever, can have N/V and malaise
Recovery: <72h (self-limiting)

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34
Q

EPEC

A

“Infantile Diarrhea” (children <5yo)
Pathogenesis: efface surface of microvilli causing impaired absorptive properties which allows efflux of H2O/electrolytes
ROS: watery diarrhea

35
Q

Vibrio cholera

A

Halotolerant, acid sensitive, motile, S-shaped colonies
Risk: travel to developing countries (Africa, Haiti, India)
Pathogenesis: cholera toxin binds to GM1 receptor activating adenylate cyclase (👆🏽intracellular [cAMP])
ROS: abrupt onset of profuse watery diarrhea WITH vomiting, “rice water” stool (aka flecks of mucous)
Diagnosis: TCBS agar (sucrose is differentiating from other vibrios bc cholera is sucrose +ve)
*rotavirus is the only other diarrheal illness that leads to the same amt of fluid loss

36
Q

Clostridium perfringens

A

G+ve, spore forming
Acquired: meat & meat dishes (gravy)
Pathogenesis: colonization of SI w/ release of clostridium perfringens enterotoxin (CPE) which has cytotoxic activity causing pore formation in membranes
ROS: watery diarrhea + SEVERE abd pn (NO N/V)
Diagnosis: stool sample w/ CPE

37
Q

Bacillus cereus (diarrheal)

A

G+ve, spore forming
Acquired: rice
Pathogenesis: LT enterotoxin activating adenylate cyclase (👆🏽cellular [cAMP])
ROS: watery diarrhea w/ abd pn

38
Q

Rotavirus

A

Acquired: fecal-oral (poor hygiene)
Prevalence: children <5yo
Pathogenesis: shortening/blunting of microvilli decreasing surface area so they lose absorptive qualities
ROS: sudden onset watery diarrhea w/ or w/o vomiting lasting up to 6 days, excessive fluid loss like cholera
Diagnosis: latex agglutination, EIA

39
Q

Norovirus

A

Acquired: fecal-oral, food-borne (raw shellfish)
Prevalence: older children & adults
Seasonality: winter months
Pathogenesis: multiplies in SI and causes transient lesions in mucosa
ROS: 1-2d diarrhea/vomiting, abd cramps, myalgia, malaise, HA, low fever
Diagnosis: RT-PCR

40
Q

Adenovirus

A

Pathogenesis: URT is main target
ROS: watery diarrhea, + or - vomiting, URI, and conjunctivitis

41
Q

Cryptosporidium parvum/hominis

A

Acquired: recreational waters
Infectious and diagnostic stage: thick walled oocyst
ROS (healthy): watery diarrhea, N/V, abd cramps, resolves w/in 10 days
ROS (immunocompromised): severe sx’s, chronic diarrhea, up to 50 BMs/day, wt loss
Diagnosis: modified Ziel-Neelson stain

42
Q

Shigella sonnie

A

Non-motile, no lactose fermentation, low infective dose
Prevalence: <5yo (day care)
Pathogenesis: colonize LI then attach to M cells and plasmid encoded protein triggers cell to endocytose the organism, eventually induces cell apoptosis which leads to ulcers
ROS: watery diarrhea @ onset then becomes bloody, can have N/V later on

43
Q

Shigella dysenteriae

A

non-motile, no lactose fermentation
Pathogenesis: produces shiga toxin that binds to 28S subunit of 60S ribosome inhibiting protein synthesis leading to cell death, this causes blood mucous and WBCs in stool due to capillary thrombosis
ROS: bloody diarrhea with mucous, abd pn, fever

44
Q

EIEC

A

Low infectious dose
Prevalence: SE Asia and South America
Pathogenesis: invasion of LI then attachment/endocytosis in M cell by plasmid encoded protein, eventually induces cell apoptosis (NO toxins produced)
ROS: watery diarrhea progressing to bloody type (less severe than Shigellosis)

45
Q

Enterocolitis (S. typhirium)

A

Acquired: poultry (eggs, chicken)
ROS: watery diarrhea @ onset + N/V, low to mild fever
Duration: 2-5d
Diagnosis: colorless colonies on MacConkey’s bc no lactose fermentation
Stool culture: +ve soon after sx’s start

46
Q

Enteric Fever (S. typhi)

A

Incubation: 7-20d (insidious onset)
Fever: gradual w/ HIGH plateau
ROS: early constipation followed by bloody diarrhea eventually
Pathogenesis: disseminates into blood where it’s engulfed by macrophages –> transported to RES organs (liver) it colonizes the bladder and replicates and eventually reenters the SI via bile
Stool culture: +ve after 2nd wk
*vaccine: oral live attenuated and capsular polysaccharide IM

47
Q

Campylobacter jejuni

A

G-ve curved rod, microaerophilic, catalase +ve
Acquired: poultry, eggs, zoonotic
Prevalence: children <5yo
Pathogenesis: colonizes/invades LI and SI, enterotoxin (watery diarrhea) and cytotoxin (similar to shiga toxin, causes bloody diarrhea)
ROS: onset 3-5d after ingestion, profuse watery diarrhea at onset then bloody + severe abd pn
Diagnosis: colonies appear mucous and gray
Complications: GBS or reactive arthritis

48
Q

Yersinia enterolitica

A

Acquired: refrigerated foods
Prevalence: cold countries (children <7yo)
Pathogenesis: invasive, induces inflammatory response that mimics appy (messenteric adenitis) produces chromosomally encoded enterotoxin (ST) that 👆🏽[cGMP]
ROS: severe abd pn, watery diarrhea, mild fever
Complication: post-infective arthritis
Diagnosis: pinpoint colonies on MacConkey’s

49
Q

Post-infective Guillan-Barre Syndrome

A

Causative agent: campylobacter
Pathogenesis: Ab’s against the O ag in the bacterium cross-react w/ the GM1 ganglioside in the myelin sheath of peripheral nerves
ROS: demyelination causing ascending paralysis

50
Q

Vibrio parahemolyticus

A

Acquired: poorly cooked or raw seafood
Prevalence: Japan
Pathogenesis: invade epithelial cells and reaches lamina propria but doesnt go further
ROS: acute abd pn, watery diarrhea (sometimes bloody), N/V
Diagnosis: sucrose -ve

51
Q

Vibrio vulnificius

A 
Acquired: saltwater abrasions
Prevalence: coastal US
Pathogenesis: highly invasive
ROS (immunocompetent): gastroenteritis
ROS (liver dz'd pt): can be complicated, causes fluid filled blisters
52
Q

EAEC

A

NON-INVASIVE
Pathogenesis: aggregation adherence factor (AAF) are fimbriae that allow adherence to cells of LI, once bound they induce production of copious amounts of mucous which forms a biofilm
ROS: can be watery or bloody diarrhea

53
Q

STEC

A

NON-INVASIVE, no sorbitol fermentation
Prevalence: northern US
Pathogenesis: attachment in LI, produces verotoxin a cytotoxin similar to shiga toxin so it inactivates the 28S of the 60S ribosome subunit
Tx: NEVER ABX (killing the organism will just release more toxin)

54
Q

Hemorrhagic Colitis (STEC)

A

Prevalence: adults/elderly
ROS: watery diarrhea at onset w/ abd pn then becomes bloody

55
Q

Hemolytic Uremic Syndrome (STEC)

A

Prevalence: children
ROS: microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure

56
Q

Thrombotic Thrombocytopenia Purpura (STEC)

A

Prevalence: elderly
ROS: anemia, acute renal failure (HUS) + fever + neuro involvement

57
Q

Salmonella serotypes

A

Motile, produce H2S gas
Pathogenesis: colonize SI and LI, invade epithelial cells then replicate in M cells of Peyer’s patches in terminal SI –> after replication they travel through cell to BM and enter lamina propria, it can then enter lymph and then disseminates into blood via capillaries

58
Q

Staphylococcus aureus (GIT)

A

Coagulase +ve, catalase +ve
Acquired: foods requiring excessive handling
Prevalence: summer/holidays
Toxin: ST enterotoxin acts neurologically (emesis), and enteritic (diarrhea)
ROS: emesis w/in 6h of ingestion
Diagnosis: beta-hemolytic, mannitol salts, confirm w/ coagulase

58
Q

Bacillus cereus (food Intoxication)

A 
Spore forming
Acquired: contaminated rice
Pathogenesis: emetic (neurotoxin) is ST causing vomiting, shorter incubation than S. aureus
ROS: predominantly vomiting w/in 4h
Diagnosis: flat colonies on blood agar
59
Q

Giardia labmia

A

Binucleate, pear-shaped, flagellated trophozoite and cyst
Acquired: water from hiking/camping
Pathogenesis: attach to epithelial cells in SI (non-invasive)
Infective: cyst
Diagnostic: cyst/trophozoite
ROS: 3-4 wks of diarrhea
Diagnosis: 3 stools over several days

60
Q

Cystiosospora belli

A

ROS: watery diarrhea, persistent if untreated
Diagnosis: autofluorescent, multiple samples

61
Q

Entamoeba histolytica

A

Acquired: travel back from developing endemic countries
Infectious: mature cysts
Diagnostic: mature cysts/cysts and trophozoites in stool
Intestinal sx’s: watery diarrhea and bloody
Extraintestinal sx’s: liver abscess (of right lobe 1-3 mo after onset)

62
Q

Balantidium coli

A

Acquired: pig reservoir
Prevalence: developing countries
Infectious/diagnostic: cyst
ROS: intermittent diarrhea/abd pn/wt loss
Complication: Fulminant Colitis (rare) = bloody diarrhea w/ mucus

63
Q

Trichuris trichuria (whipworm)

A

Pathogenesis: ingestion of barrel shaped egg
ROS: abd pn, diarrhea, iron deficiency, finger clubbing, rectal prolapse (“coconut cake prolapse”)
Diagnosis: eggs in feces

64
Q

Enterobius vermicularis (pinworm)

A

Epidemiology: most common worm infection in US
Pathogenesis: ingest oval shaped eggs, worm matures, female worm goes to perinatal area @ night to deposit eggs then dies (causing itching)
ROS: anal itching
Dx: cellotape for eggs

65
Q

Diphyllobothrium latum

A

Fish tapeworm

ROS: diarrhea, B12 deficiency (megaloblastic anemia)

66
Q

Ascaris lumbricoides

A

*round worm
Transmission: fecal-oral
Pathogenesis: nodular eggs hatch inSI then larvae go to lungs, swallowed and back to SI
ROS: dry cough, CP, fever = Loffler Syndrome
Complication: bowel obstruction
Dx: fertilized egg in stool

67
Q

Hymenolepsis nana

A

Transmission: person-to-person
Epidemiology: most common tape worm (in US seen in institutionalized, immunocompromised, malnourished)
Dx: eggs in feces

68
Q

Necatur americanus and Ancylostoma duodenal (American dude)

A

*hook worm
Transmission: skin penetration (feet) by filariform larvae
Pathogenesis: filariform larvae to SI then lungs, swallowed and back to SI
ROS: iron deficiency anemia, abd pn (problematic in pregnant women)
Dx: eggs in feces (oval, clear-shelled), eosinophilia

69
Q

Strongyloides stercoralis (Strong guy)

A

*thread worm
Transmission: skin penetration (feet) by filariform larvae
Pathogenesis: filariform larvae to SI then lungs, swallowed and back to SI
ROS: urticaria and rashes a few days s/p skin penetration, pulmonary sx’s, diarrhea/abd pn weeks later
Dx: rhabditiform larvae in stool

70
Q

Clostridium difficile

A

G+ve bacilli
Pathogenesis: Toxin A (enterotoxin = watery diarrhea d/t fluid accumulation), Toxin B (similar to diphtheria toxin so causes decrease of protein synthesis and cell death = bloody diarrhea)
ROS: pseudomembranous colitis
Dx: toxin in stool

71
Q

Whipple’s Dz

A 
Etiology: Tropheryma whipplei 
Transmission: soil/sewage
Prevalence: farm/sewage workers
ROS: wt loss and arthralgia, then diarrhea, steatorrhea, fever, malabsorption, CNS and CVS sx's (culture -ve endocarditis)
Dx: biopsy w/ PAS+ macrophages, PCR
72
Q

HAV

A

Most common cause of acute hepatitis
Epidemiology: developing world
Transmission: undercooked shellfish (imported strawberries, green onions)
ROS: aversion to cigarette smoke
Prevention: vaccine (and virus is inactivated by bleach and UV radiation)

73
Q

HBV

A

Genome: partially circular dsDNA (Dane particle)
Transmission: blood-borne
Pathogenesis: produces decoys (HBsAg), causes CD8+ T-cells to induce apoptosis of infected cells
ROS: acute or chronic hepatitis, aversion to cigarette smoke
Prevention: vaccine (virus inactivated by 10% bleach)

74
Q

HCV

A

Transmission: blood-borne
Pathogenesis: error prone RNA-dependent RNA pol, inhibits apoptosis in the infected cell = persistent infection, inhibits IFN-α = chronic infection
ROS: chronic carrier status is common
Prevention: donor screening (since 1981 in US), no vaccine bc of ag variation

75
Q

Co-infection w/ HBV + HDV

A

Mechanism: HBV + delta ag present acutely

Better prognosis

76
Q

Fasciola hepatica/gigantica

A

Aka Sheep Liver Fluke leaf-shaped
Transmission: ingestion of infected plants (like fuggin watercress)
Pathogenesis: metacercariae ingested, larvae migrate (2-4mo), parasite matures (wks to yrs during latent)
ROS: liver sx’s, malabsorption bc no bile, etc.
Dx: eggs in feces

77
Q

Clonorchis sinensis

A

Aka Chinese Liver Fluke
Transmission: ingestion of undercooked/pickled freshwater fish containing cysts
Pathogenesis: metacercariae ingested resides in biliary tree
ROS: choly probs (fever, jaundice, diarrhea, pain, hepatomegaly); chronically can lead to adenocarcinoma of bile duct
Dx: operculated eggs in feces

78
Q

Anti-HBc IgM

A

“Window period” (no HBsAg or Anti-HBs would be present yet), could have some Anti-HBe Ig present
*about 5mo s/p initial infection

79
Q

Anti-HBc IgG

A

Chronic infection

*OR seen in full recovery (if no HBsAg present but Anti-HBs is present)

80
Q

HBeAg

A

Marks active replication so measures transmissibility/infectivity, seen in acute or chronic infection

81
Q

Anti-HAV IgG

A

Immune d/t vaccine or previous recovery from prior HAV infection

82
Q

Anti-HCV Ig

A

Tells you there was exposure to HCV whether the pt recovered or still has virus you’d have to do PCR for # of viral particles present

83
Q

Superinfection w/ HBV + HDV

A

Mechanism: chronic HBV infection then superimposed HDV infection = rapid dz progression, eventual hepatic encephalopathy
POOR prognosis

Microbiology (14 decks)

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