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
preventing Hep C
screening to protect blood supply
no HCIG
no vaccine
is Hep C commonly spread to babies through breast feeding
not commonly
should patients with hep C us protection
its not necessary
what is the effect of Hep D and B infection
a significantly more severe disease than Hep B alone
who is Hep E most dangerous in
pregnany women and immunosuppressed patients
treating viral hepatitis
infereron
antivirals to reduce the risk of liver failure
there is a cure
fatty liver disease
steatosis (fatty deposits) in the liver common in obese adult that distorts the normal structure of the liver
how is fatty liver detected
liver function test
US
CT
FLD causes and management
chronic alcohol use
obestiy
metabolic disease
drug toxicity
methods to manage FLD
stop using alcohol
lose weight with bariatric surgery if necessary
Cirrhosis
irreversible inflamatory disease that disrupts the liver function and structure
what is the result of build up of nodular and fibrotic tissue from cirrhosis
obstruction of the biliary channels and portal hypertension
three types of liver failure
alcoholic
biliary
infectious (post necrotic)
five main functions of the liver
bilirubin elimination
blood filtering
synthesis of important substances
drug detoxificaiton
mineral and vitamin storage
what types of substances are synthesized in the liver
clotting factors
albumin
CHO
bile
symptoms of cirrhosis
chronic RUQ pain
jaundice
edema
portal hypertension
reduced coagulation
reduced drug metabolism
how much does liver failure incrase the risk of liver cancer
3-5% per year
symptomatic treatment of cirrhosis
paracentesis of ascities
shunts to reduce portal hypertension
correction of coagulopathy and hypoalbumemia
direct treatment of cirrhosis
anti viral drugs for hepatitis
anti-inflammatory and immunosuppresive drugs in the case of an autoimmune disorder
liver transplant
what is the prognosis of cirrhosis
severe cirrhosis 6 month survival at 50%
moderate 5-10 yrs
what is the gender bias of cholelithaisis
women over men, 8.6% to 5.5%
what are the risk factors for gall stones
gender
old age
obesity
child bearing
diet
explain the saying “female, forty, fat, and fertile”
delineates the risk factors for gall stones
what is one medication that increases the risk of gall stones
one that decreases
cephalosporin
aspirin
what kind of diet will lower the risk of galll stones
low carb high fiber
T/F gallstones are usually symptomatic
false
what percent of people will develop episodic biliary pain related to gallstones
what are the symptoms
10-25%
RUQ pain, often at night
pain related to a high fat meal
lasts from 30 minute to hours
what is the percent break down of gallstone composition
choleterol (80-85%)
calcium bilirubinate (<20%)
what is the method of imaging a gall stone
ultrasound
what is the treatment for gallstones
laproscopy
stone dissolution with bile salts
five symptoms of acute cholecystitis
biliary pain
nausea/vomiting
fever
leukocytosis
jaudice
what is the most common cause of cholecystitis
distal occulsion of the bile duct by a gallstone
what is the risk of untreated cholecystitis
ischemia leading to perforation/rupture, followed by abcess, peritonitis, and death
signs and symptoms of acute cholecysitis
RUQ, nausea, fever
what are the laboratory signs of cholecystitis
leukocytosis, elevated bilirubin, elevated liver enzymes
what are the physical exam findings present with cholecystitis
murphy’s sign
conservative treatment of cholecystitis
NPO w/ IV fluids
analgesics
IV antibiotics
what is the surgical treatment for acute cholecystitis
laproscopy after the swelling has gone down unless there is sign of peritonitis
two types of pancreatic disorders
pancreatitis
pancreatic cancer
pancreatitis
acute or chronic inflammation of exocrine pancreas
5 risk factors for pancreatitis
alcohol abuse
smoking
female gender
biliary disease
medicaion
signs of pancreatitis
acute epigastric pain
N/V
fever
abdominal tenderness and distention
though the exact pathogenesis of pancreatitis is unknow, what are two suspected causes
edema/obstruction of the ampulla of vater
direct injury to secretory cells
two characteristics of acute epigastric pain associated with pancreatitis
abrupt onset of severe, boring pain that often radiates to the lower bac
diagnostic factors of pancreatitis
elevation of pancreatic enzymes
fever and leukocytosis
Ct imaging
what levels of lipase and amylase wuld indicate pancratitis
3x the normal limit
treatment of mild pancreatitis
bed rest with NPO
analgesia
Iv fluids
treatment of severe pancreatitis
intensive care
aggressive fluid and electrolyte replacement
possibly antibiotic use
what is the mortality for acute pancreatitis
5-25% depending on severity
what are the main risks for chronic pancreatitis
alcoholism, smoking, biliary tract disease
potential complications of chronic pancreatitis
opiod addiction
DM
malabsorption from enzyme deficiencies
pancreatic cancer
incidence and prognosis of pancreatic cancer
>30,000 increasing over the last 2 decades
overall very poor
risk factors for pancreatic cancer
smoking
chronic pancreatitis
obestity
long term diabetes
T/F its common to have severe symptoms in the early stages of pancreatic cancer
false, it is commonly asymptomatic
symptoms of pancreatic cancer
gnawing visceral midabdominal pain
weight loss
jaundice from biliary obstruction
diagnosis of pancreatic cancer
CT/Pet scan
laparotomy with biopsy or resection
treatment of pancreatic cancer
surgical resection
chemo
radation
three lower GI disorders
acute appendicitis
colorectal cancer
IBS
what is the most common abdominal surgical emergency
appendicitis
four pathologies of appedicitis
obstruction form feces, foreign body, inflammation, neoplasm
signs of appendicitis
abdominal pain
nauseaa
low fever, leukocytosis
dscribe the abdominal pain associated with appendicitis
periumbilical and epigastric, migrating to the right lowe quadrand
PE findings for appedicitis
RLQ, pain, guarding, rebound, positive psoas or obturator
diagnostic factors for pancreatitis
PE findings
CT
US
what is the treatment for appendicitis
non surgical
laparoscopy/laparotomy
Ice, iv, transport
complications of appendectomy
perforation leading to peritonitis or pelvic abcess
death from septicemia
risk fastors for colorectal cancer
dietarty fcators
HPV
IBS (crohns or UC
dietary factors associated with colorectal cancer
high fat and meat, low fiber
four ways to reduce risk of colorectal cancer
screening
low dose aspirin
high fiber, low fat diets
hormone replacement in women
what is the purpose of screening procedures for colorectal cancer
the identification and removal of adenimoatous polyps
screening procedures for colorectal cancer
fecal occult blood testing
fecal immunochemistry screening
colonoscopy
who should be screened for colorectal cancer
low risk patients every 10 years at 50
high risk earlier and more often
treatment of colorectal cancer
surgical resection for all patients
chemo
immunotherapy
two main types of IBD
Ulcerative colitis or crohns
what demographic has the highest instance of IBD
ashkenazi jews
two possible pathophysiolgies of IBD
abnormailites of intestinal microflora
possible auto immune mechanisms
symptoms of UC
diarrhea, cramping, rectal bleeding, passage of mucus
symptoms of crohns
recurrent episodes of RLQ pain
malabsorption
steatorrhea
bowel obstruction
how is IBD diagnosed
diagnostic imaging
endoscopy
treatment of crohns
symptomatic
diet
antibiotics
corticosteroids
resecetion of the terminal ileum or other segments
treatment of UC
aminosalicylates
glucocorticoids
surgery
how does the IBD increase the risk of colon cancer based on duration
after 10 yrs 2%
after 20 8%
after 30 18%
