GI tract infections Flashcards
C. difficile colitis
-epidemiology (risk factors, transmission)
Risk Factors: recent antibiotic use, recent hospitalization, long-term care facilities, older age, proton pump inhibitors
Transmission: fecal-oral
C. difficile colitis
-pathophysiology
Ab kill normal flora, C. diff overgrows, releases toxin A and B, mucosal injury and inflammation.
Pseudomembranes are formed
Ab most likely to lead to C. diff colitis
Clindamycin
Fluoroquinolones
But ALL can lead to it.
C. difficile colitis
-clinical presentation
- usually within 2 weeks of Ab therapy
- watery diarrhea
- elevated WBCs
- low grade fever
- in severe cases, fulminant colitis
C. difficile management
- Mild/moderate: metronidazole
- Severe: vancomycin (PO)
If neither gets better in 4-6 days, add the other.
Traveller’s diarrhea
-likely etiology for acute onset, gradual onset/chronic, dysentery, one brief episode
Acute onset:
80-90% Bacteria
-ETEC and EAEC most common
10-20% Viral
Gradual onset/Chronic
-Giardia or Entameoba histolytica
Dysentery
-Salmonella, campylobacter, shigella
Brief episode
-preformed toxin food poisoning
Stool samples cansnd cannots
Can: shigella, campylobacter, salmonella, O&P
Cannot: distinguish ETEC/EAEC from normal E. coli, identify viral causes
Management of travellers diarrhea
1) identify the pathogen if symptoms are severe and persist >72hr
2) Rehydration fluid
3) Ab only for severe symptoms: fluoroquinolones, azithromycin
3) Don’t use anti-motility agents unless you are using an Ab
Rotavirus
-epidemiology (infectivity, demographics)
- highly infectious (lots of virions passed, only need a few to infect)
- 6-24 months weaning, developing world because they don’t use vaccine
Rotavirus
-pathophysiology
- The virus infects and replicates in cells at the tip of villi in the small intestine.
- These cells die/are damaged
- Reduced absorptive capacity
- Intensely dehydrating
Rotavirus
-management
- Oral rehydration solution
- Zinc
- In some countries can give the ROTARIX vaccine to prevent the episode in the first place, but if you get it you have immunity usually
Hepatic abscess
-etiology
Amoebic liver abscess
- travel or from endemic area
- negative blood cultures
- anchovy paste aspirate
Bacterial liver abscess
- developed world
- biliary tract obstruction
- polymicrobial
- purulent aspirate
- postive blood cultures
Management of hepatic abscesses
Amoebic
- don’t have to drain usually
- Metronidazole
Bacterial
- always drain
- Ab that cover G(-) bacilii, enterococci and anaerobes
Helicobacter pylori
-pathophysiology
- swims through mucus of stomch
- can neutralize stomach acid (urease)
- adheres to epithelial cells
- causes inflammation –> gastric or duodenal ulcer
- USUALLY ASYMPTOMATIC until ulcer or gastric cancer
Gastric ulcers
-etiology
70-80% H. pylori