Digestive Tract Disease Flashcards
Ulcers: Helicobacter Pylori Gastritis
S/S + CA
S/S: most h.pylori infections are asymptomatic, belching, vomiting may occur, horrible breathe (they raise pH in stomach so digestion can’t fully occur), abdominal pain, bleeding
CA: Helicobacter Pylori (Gram NEGative curved microaerophile with polar flagella); it uses Urease to turn urea in our stomach into amonia (pH 2 to pH 5.5-6) making it more basic in the area directly around it, and it can’t survive in acid so it gets into the mucous lining to surviv
Ulcers: Helicobacter Pylori
Epidemiology + Prevention and Treatment
Epidemiology: most people in their 70s will get it at some point, not necessarily going to hurt you though; black TARY stool (black poop) is indicative, and this is because bleeding happens somewhere in the GI tract and it oxidizes on the fecal matter making it black
Prevention: No proven prevention measures LOL
Cholera
S/S + CA
S/S: classic example of severe watery diarrheal disease, has “rice water stool” appearance (cloudy gelatinous); vomiting may occur at onset, severre muscle cramps result from loss of fluids and electrolytes, severe dehydration can lead to organ failure and death
CA: Vibrio Cholerae (curved, Gram NEGative rod)
several types of O-Antigen (O1 is current serotype grouped by halotolerant, which means it can grow in alkaline conditions)
O-Antigens are used as an identifier for different strains, vibrio is normally a marine organism found int he sea and if people get it it’s from contaminated water; malnourished populations don’t eat enough nutrients because stomach acid is too basic, so it can survive
Cholera
Toxin + Epidemiology + Treatment/Prevention
Toxin: A-B mediated toxin that keeps the regulatory G protein “on” which causes cells to overproduces cAMP (signal) which causes lots of ions to rush out of the intestine, and water follows solute concentration so water rushes out of the cells as well (leads to watery diarrhea); this also means that they aren’t intracellular because the toxin binds to the outside of the cell
Epidemiology: fecal contamination of water most common source of transmission; human feces to fertilizers then you eat crop and then get cholera, person w/cholera may discharge at least 1 million bacteria per milliliter of feces)
Organism lives in a cycle so it shows up and duplicates/creates toxin, and then it leaves via fecal matter to infect other hosts
Treatment/Prevent: replacement of fluids and electrolytes decreases mortality from 30% to 1%, sanitation and safe water supplies, 2016 vaccine was introduced for endemic areas (eh might not be that great)
Shigellosis
CA + S/S + Epidemiology
S/S: classic is dysentery (watery diarrhea w/other thing in it depending on strain so blood, WBCs, cell debris); cuz it’s gram NEGative you get headache, vomiting, fever stiff neck, convulsions, and joint pain…usually fatal for infants in developing countries
CA: there are four species of shigella, but the one everyone writes papers about is S. Flexnuri
they essentially get taken in by M-cells and the WBCs on the other side are unable to kill them, and so they spread and infect other cells and when they are in those cells they bind to actin to move laterally into other cells to infect them
HUS: Hemolytic Urea Syndrome
A-B toxin stops protein synthesis, destroys liver!
Epidemiology: fecal-oral route and small infectious dose and spread because they aren’t easily killed by stomach acid, spread rapidly in populations w/poor sanitation, fecally contaminated food and water cause outbreaks, and anal intercourse can potentially lead to this
HUS: Hemolytic Urea Syndrome
(more in depth cuz he lectured more on it)
it’s a shiga toxin (A-B mediated) and it essentially stops protein synthesis
it sticks to your kidneys and kills them by sticking to blood vessels which causes inflammation –> global issue; you get frothy urine because of denatured proteins, edema (liquid going into surrounding tissues and swelling), potentially blood in urine (like dark/amber coca cola colored) because of kidney damage, kidney scarring can occur
T(x): antibiotics can alert other shigella to create more toxin because when one dies they send an SOS signal to other bacteria letting them know they’re dying and so the rest make more toxin
Escherichia Coli Gastroenteritis
S/S: depends on the strain; some cause watery diarrhea, others dysentery, one group hemolytic uremic syndrome
CA: escherichia coli; Gram NEGative rod closely related to shigella
Mentioned in class: E.Coli is common for GI tract infection and dysentery (water diarrhea plus something else), E.Coli ferments lactose, so it creates bile salts and turns pink (pos) on a MAC plate: Shigella doesn’t grow on a MAC plate, and in general these infections (E.Coli variations) are a only a huge concern because the diarrhea indicates lots of water loss, so worry about dehydration
T(x) + Prevention: most of the time it’s self-limiting (means that it will go away w/o antibiotic treatment) and usually that’s because antibiotic use can create resistance, however the outcome can worsen in patients w/STEC infections specifically; replacement of lost fluid is important, hand washing, pasteurization of drinks/food is good at prevention too
Hamburger was recalled because of O157:H7 (o-antigen type: flagella type) which is an STEC; this can occur cuz sometimes killing cows is messy and E.Coli in intestine can get into meat, and if not cooked all the way (like rare/medium rare) then you could get E.Coli from that
DAEC (diffusely adhering E.Coli)
Characteristic Features: grows a diffuse layer in a thick mucus-associated biofilm on the intestinal epithelium; produces toxins
it’s spread out individually, not in clumps
Leads to diarrhea, really not great with kids
EAEC (Enteroaggregative E.Coli)
grows in brick-like aggregations in thick mucous, they just grow in clusters together rather than separately
you get diarrhea!
ETEC (Enterotoxigenic E.Coli)
colonizes small intestine and produces toxins that are really similar to cholera; that basically means that the toxin causes movement resulting in ions and water loss, but it’s not as much loss as with cholera
EIEC (Enteroinvasive E.Coli)
invades the intestinal epithelium, causing a disease very similar to shigellosis; invasive = they get into the cells, but EIEC doesn’t have toxin, and they don’t have actin polymerization like shigella
ONLY E.Coli that’s invasive
EPEC (Enteropathogenic E.Coli)
colonizes small intestine, changes actin filaments into pedestals; pushes proteins into the host cell and causes epithelial cell to rearrange actin –> actin can change outside shape, so it makes a push pedestal; pedestal has a receptor on it so that other E.Col can stick on
Type III Secretion System (T3SS): tube cap that opens up to let proteins go from bacteria into the epithelial cell
The receptor on the pedestal is called “TIR” and it’s what allows E.Coli to stick on to the host cell
STEC (Shiga Toxin Producing E.Coli)
colonizes large intestine and releases Shiga-like toxin and basically has the same S/S as shigella which means it can lead to HUS
Clostridium Difficile Infection (CDI)
it’s a nosocomial infection (health associated) and it’s antibiotic associated; normally you wouldn’t have it but when you take antibiotics it can kill other bacteria inside of you, so CDI is free to grow like crazy in the intestine
S/S: Can form Pseudomembranous Colitis (yellow pseudomembrane), mild diarrhea, and potentially fatal inflammation of colon
CA: Clostridium Difficile, a Gram POSitive rod-shaped, endospore forming anaerobe
Pathogenesis: toxins disrupt host cell actin, causing lethal effects to the intestinal epithelium
Epidemiology: primarily occurs in hospitalized patients on antibiotic therapy
T(x) + prevention: when feasible stop antibiotics; otherwise use vanomyocin, metronidazole, or Dificid.
Norovirus Gastroenteritis
Most common cause of gastroenteritis in US
S/S: abrupt onset of nausea, vomiting (worse in older children/adults), watery diarrhea –> take a few days for symptoms to subside
CA: Norovirus are single stranded RNA viruses (viruses are infectious particles so you can’t use antibiotics, and they are very infectious via fecal and oral route)
Pathogenesis: infect epithelium of upper small intestine, causing cell death and decreased production of digestive enzymes, epithelium recovers after 2 weeks; immunity is only short term for unknown reasons
Epidemiology: transmission is via fecal-oral route, highly contagious- only 10 virions (resist destruction, stable in environment) is enough, epidemics common on cruse ships AND dormitories!! wash ur hands!
