GI Flashcards
three upper GI disorders
peptic acid disorders
gastric cancer
esophageal cancer
three types of peptic acid disorders
benign peptic ulcers
GERD
zollinger-ellison syndrome (gastrinoma)
how common are peptic ulcers
how has the epidemiiology changed
very common (500,000 new cases yearly)
increasing numbers of gastric ulcers vs duodenal
two main types of peptic ulcers
duodenal and gastric
what type of peptic ulcer is most common
what age
what age of gastric
duodenal 4:1
35-55
55-70
four complications of peptic ulcers
pain 100% of the time
bleeding 10%
perforation 3-5%
gastric outlet obstruction 2%
differing pain in gastric ulcers
intermittent heartburn type vs chronic boring pain with deep ulcers
symptoms of the chronic vs acute bleeding
black tarry stools vs hematemesis
common etiology prior to 1981
stress
enviromment (smoking, spicy food)
alchool
glucocortioids and NSAIDs
what changed in peptic ulcer treatment after 1981
helicobacter pyloria was linked to PUD
what type of bacteria is helicobacter pylori
where is it common
if H pylori is not erradicated what is the risk
gram negative spirochet that causes gastritis
most common in places with poor santitation
85% of ulcers will recur
how has PUD disease changed
H pylori
nsaid and sterioids effect
increase acid production (smoking and stress)
inadequate mucosal effect (smoking)
describe the effect of H pylori on cancer
increaesd risk of gastric cancer, decreased risk of esophageal cancer
PUD treatment
eradicate H pylori
reduced acid secretion
neutralize acid
enhance mucosal defense
treatment of H pylori
2 week course of abx with bismuth or PPI
two methods to reduce acid production related to PUD
H2 receptor antagonist
PPI
what is the benefit of antacids
but?
the provide rapid pain relief but the effect is short lived and there is no indication that they promote healin
when are antacids contraindicated
tablets or liquid more effective
renal failure
liquid better than tablets
what are the protective effects of gastric prostaglandins
suppression of acid production
stimulates mucin production
increase HCO3
increase muscosal blood flow
how do H2 inbitors block acid production
block the binding f histamine in to receptors, stopping the production of cMAP from adenylate cyclase and reducting proton pump action
What is responsible for GERD
a disorder of the lower esophageal sphincter that allow acid to come up
where is GERD most common
develop countries 10-20%
risk factors for GERD
obesity
hiatal hernia
increased acid production
three symptoms of GERD
esophageal pain
nausea
coughing
three conditons associated with GERD
Barrett’s esophagus
Esophageal carcinoma
esophageal stricture
three options for GERD treatment
gastric acid suppression
lifestyle modification
surgery
what is the mean age of diagnosis of Gastric cancer
what is the gender bias
63, men 2:1
three risk factors for gastric cancer
chronic H pylori
smoking
diet high in nitrates but low in vitamin c
symptoms of gastric cancer
none, in the early stages
upper abdominal pain
anorexia/weight loss
blood loss anemia
diagnosis of gastric cancer
double contrast upper GI xray
esophagogastroduodenoscopy (EGD)
treatment for gastric cancer
gastrectomy (only possible for 30% of patients)
chemo
what is the prognosis of gastric cancer based on stage
1 60%
2 44%
3 20%
4 3%
what is the age and gender bias for esophageal cancer
50-70
3x more common in men to women
two types of esophageal cancer
squamous cell (most common)
adenocarcinoma
main symptoms of esophageal cancer
dysphagia
weight loss
pain
risk factors for esophageal cancer
tobacco (specifically for squamous cell)
obesity
GERD/Barrett’s esophagus
diagnossis of esophageal cancer
endoscopy, biopsy, Ct for stagin
what is the 5 year survivable prognosis for esophageal cancer
less than 20%
what is the treatment for a cure in esophageal cancer
surgery, radiation, chemo
four liver and biliary tract disorders
heptaitis
fatty liver
cirrhosis
gallbladder disorder
define hepatitis
acute inflammation of the liver that disrupts normal function and causes scarring
causes of hepatitis
medication, chemicals, parastites, viruses
what are the most common viral causes of cirrhosis
hep A, B, and C
how common is Hep A
how is it spread
what is the mortality rate
30% of americans are serologically positive for Hep A
fecal oral transmission from sanitation, shellfish
usualyl low, the disease does not lead to chronic infection or liver damage
what is the process of Hep A
incubation for 30 days
prodrome for several days
icteric phase for 2-3 weeks with worsening symptoms
convalescence
prodromal symptoms of Hep A
malaise, anorexia, fatigue, myalgia, RUQ tenderness
Which is more common, Hep A or B
hep A 5-6% positive
how is hep b spread
transfusion
exchange of bodily fluids
vertical transmission (mother to off spring)
contrast the course of illness between Hep A and B
they have similar symptoms and rarely fatal, BUT chronic infection is possible that increases risk of cirrhosis and hepatoma
where does the majority of chronic Hep B fall in the population
90% in neonates and infants
1-5% in normal adults
what is the risk of cirrhosis with chronic Hep B
40%
what makes Hep C more problematic
chronic infection is a comon complication and is the leading cause of cirrhosis
how to prevent Hep A
sanitation
hep A vaccine
antiobodies for post exposure treatment
preventing Hep B
screening to protect blood supply
Hep B vaccine for children
HBIG for exposure
prevention of transmission at bith