Gastrointestinal Disorders Flashcards
What is cause of peptic ulcer disease?
90% of the time H. pylori is detected if duodenal ulcers, 75% it is detected with gastric ulcers
what are risk factors for peptic ulcer disease?
chronic use of NSAIDs, aspirin, glucocorticoids
smokers > 1/2 PPD
high stress
what are signs of acute abdomen? (perforation from various causes such as ulcer perforation)
severe pain, board like abdomen, quiet bowel sounds, rigidity
what is standard outpatient management of peptic ulcer disease?
H2 receptor blockers/ antagonists- famotidine daily
or
PPI- pantoprazole, omeprazole, lansoprazole- 30 minutes before meals
what is black box warning for PPIs?
increase osteoporosis with long term PPI use- not recommended
what is standard outpatient treatment for H. pylori erradication?
Quadruple therapy: 2 antibiotics + PPI +/- bismuth (pepo bismol) for 10-14 days.
Antibiotic considerations:
Triple therapy (first treatment regimen, however contraindicated if PCN allergy or previous exposure to macrolide, because of antibiotic resistance) PPI + clarithromycin + amoxicillin
Latest quadruple therapy: PPI + bismuth + metronidazole and tetracycline
What is effect of bismuth subsalicylate (pepto-bismol) on H. pylori?
direct antibacterial action against H. pylori
promotes prostaglandin production/ stimulates gastric bicarbonate
What are anti-ulcer pharmacotherapeutic recommendations? mucusal protective therapy?
PPI- can be given for several weeks, but not recommended for longterm use H2 blockers 6-8 weeks Sucralfate (Carafate) - requires acidic environment, so avoid antacids and H2 blockers- associated with decreases in nosocomial pneumonia Bismuth subsalicylate (pepto bismol)- antibacterial against H. pylori, promotes prostaglandin production/ stimualtes gastric bicarbonate (antacid effect) Antacids (maalox)- do no reduce the amount of gastric acidity- neutralizes but not treating problem of too much gastric acid- that's what PPI does
how to detect GI ulcers bleeding/ perforated? what is treatment?
upright films shows free air most cases- air under diaphragm
tx: NG tube for lavage. bleeding stops spontaneously in 80% of cases
IV H2 blocker (famotidine)
Hepatitis A
oral-fecal transmission
Outbreaks: contaminated water and food, sexual contact
infectious blood/ stool for 2-6 week incubation period
acute illness, low mortality rate
hepatitis B
blood borne DNA virus- serum, saliva, semen and vaginal secretion transmission-
blood transfusions, sexual activity, mother-fetus
hepatitis C
blood borne RNA virus
blood transfusion, and 50% of cases r/t IV drug use
s/s fatigue, anorexia, n/v,
icteric involvement: weight loss, jaundice, RUQ pain, clay colored stool, dark urine, fever, hepatosplenomegaly.
hepatitis C diagnostics
ua: proteinuria, bilirubinuria
elevated LFTs: AST/ ALT
slightly elevated: LDH, bilirubin, alk phos, PT
Hepatitis A serology
** presence of antibody: Anti-HAV + immunoglobulins to indicated time frame of infection
acute illness: 1-3 months: anti-HAV (antibody) and IgM
chronic/ immunity: IgG and anti-HAV- exposed, immune,
hepatitis B serology
active Hep B: HBsAg (surface antigen), HBeAg (protein from core), Anti-HBc (antibody to core antigen), IgM
Chronic Hep B: HBsAg, Anti-HBc (antibody to core), Anti-HBe (antibody to protein), IgM, IgG (chronic)
Recovered: Anti-HBc (antibody to core), Anti-HBs (surface antibody indicates recovery)