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pas 753 (molecular pathophysiology) > GI > Flashcards

GI Flashcards

1
Q

three upper GI disorders

A

peptic acid disorders

gastric cancer

esophageal cancer

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2
Q

three types of peptic acid disorders

A

benign peptic ulcers

GERD

zollinger-ellison syndrome (gastrinoma)

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3
Q

how common are peptic ulcers

how has the epidemiiology changed

A

very common (500,000 new cases yearly)

increasing numbers of gastric ulcers vs duodenal

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4
Q

two main types of peptic ulcers

A

duodenal and gastric

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5
Q

what type of peptic ulcer is most common

what age

what age of gastric

A

duodenal 4:1

35-55

55-70

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6
Q

four complications of peptic ulcers

A

pain 100% of the time

bleeding 10%

perforation 3-5%

gastric outlet obstruction 2%

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7
Q

differing pain in gastric ulcers

A

intermittent heartburn type vs chronic boring pain with deep ulcers

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8
Q

symptoms of the chronic vs acute bleeding

A

black tarry stools vs hematemesis

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9
Q

common etiology prior to 1981

A

stress

enviromment (smoking, spicy food)

alchool

glucocortioids and NSAIDs

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10
Q

what changed in peptic ulcer treatment after 1981

A

helicobacter pyloria was linked to PUD

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11
Q

what type of bacteria is helicobacter pylori

where is it common

if H pylori is not erradicated what is the risk

A

gram negative spirochet that causes gastritis

most common in places with poor santitation

85% of ulcers will recur

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12
Q

how has PUD disease changed

A

H pylori

nsaid and sterioids effect

increase acid production (smoking and stress)

inadequate mucosal effect (smoking)

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13
Q

describe the effect of H pylori on cancer

A

increaesd risk of gastric cancer, decreased risk of esophageal cancer

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14
Q

PUD treatment

A

eradicate H pylori

reduced acid secretion

neutralize acid

enhance mucosal defense

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15
Q

treatment of H pylori

A

2 week course of abx with bismuth or PPI

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16
Q

two methods to reduce acid production related to PUD

A

H2 receptor antagonist

PPI

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17
Q

what is the benefit of antacids

but?

A

the provide rapid pain relief but the effect is short lived and there is no indication that they promote healin

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18
Q

when are antacids contraindicated

tablets or liquid more effective

A

renal failure

liquid better than tablets

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19
Q

what are the protective effects of gastric prostaglandins

A

suppression of acid production

stimulates mucin production

increase HCO3

increase muscosal blood flow

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20
Q

how do H2 inbitors block acid production

A

block the binding f histamine in to receptors, stopping the production of cMAP from adenylate cyclase and reducting proton pump action

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21
Q

What is responsible for GERD

A

a disorder of the lower esophageal sphincter that allow acid to come up

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22
Q

where is GERD most common

A

develop countries 10-20%

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23
Q

risk factors for GERD

A

obesity

hiatal hernia

increased acid production

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24
Q

three symptoms of GERD

A

esophageal pain

nausea

coughing

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25
Q

three conditons associated with GERD

A

Barrett’s esophagus

Esophageal carcinoma

esophageal stricture

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26
Q

three options for GERD treatment

A

gastric acid suppression

lifestyle modification

surgery

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27
Q

what is the mean age of diagnosis of Gastric cancer

what is the gender bias

A

63, men 2:1

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28
Q

three risk factors for gastric cancer

A

chronic H pylori

smoking

diet high in nitrates but low in vitamin c

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29
Q

symptoms of gastric cancer

A

none, in the early stages

upper abdominal pain

anorexia/weight loss

blood loss anemia

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30
Q

diagnosis of gastric cancer

A

double contrast upper GI xray

esophagogastroduodenoscopy (EGD)

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31
Q

treatment for gastric cancer

A

gastrectomy (only possible for 30% of patients)

chemo

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32
Q

what is the prognosis of gastric cancer based on stage

A

1 60%

2 44%

3 20%

4 3%

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33
Q

what is the age and gender bias for esophageal cancer

A

50-70

3x more common in men to women

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34
Q

two types of esophageal cancer

A

squamous cell (most common)

adenocarcinoma

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35
Q

main symptoms of esophageal cancer

A

dysphagia

weight loss

pain

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36
Q

risk factors for esophageal cancer

A

tobacco (specifically for squamous cell)

obesity

GERD/Barrett’s esophagus

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37
Q

diagnossis of esophageal cancer

A

endoscopy, biopsy, Ct for stagin

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38
Q

what is the 5 year survivable prognosis for esophageal cancer

A

less than 20%

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39
Q

what is the treatment for a cure in esophageal cancer

A

surgery, radiation, chemo

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40
Q

four liver and biliary tract disorders

A

heptaitis

fatty liver

cirrhosis

gallbladder disorder

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41
Q

define hepatitis

A

acute inflammation of the liver that disrupts normal function and causes scarring

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42
Q

causes of hepatitis

A

medication, chemicals, parastites, viruses

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43
Q

what are the most common viral causes of cirrhosis

A

hep A, B, and C

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44
Q

how common is Hep A

how is it spread

what is the mortality rate

A

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

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45
Q

what is the process of Hep A

A

incubation for 30 days

prodrome for several days

icteric phase for 2-3 weeks with worsening symptoms

convalescence

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46
Q

prodromal symptoms of Hep A

A

malaise, anorexia, fatigue, myalgia, RUQ tenderness

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47
Q

Which is more common, Hep A or B

A

hep A 5-6% positive

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48
Q

how is hep b spread

A

transfusion

exchange of bodily fluids

vertical transmission (mother to off spring)

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49
Q

contrast the course of illness between Hep A and B

A

they have similar symptoms and rarely fatal, BUT chronic infection is possible that increases risk of cirrhosis and hepatoma

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50
Q

where does the majority of chronic Hep B fall in the population

A

90% in neonates and infants

1-5% in normal adults

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51
Q

what is the risk of cirrhosis with chronic Hep B

A

40%

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52
Q

what makes Hep C more problematic

A

chronic infection is a comon complication and is the leading cause of cirrhosis

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53
Q

how to prevent Hep A

A

sanitation

hep A vaccine

antiobodies for post exposure treatment

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54
Q

preventing Hep B

A

screening to protect blood supply

Hep B vaccine for children

HBIG for exposure

prevention of transmission at bith

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55
Q

preventing Hep C

A

screening to protect blood supply

no HCIG

no vaccine

56
Q

is Hep C commonly spread to babies through breast feeding

A

not commonly

57
Q

should patients with hep C us protection

A

its not necessary

58
Q

what is the effect of Hep D and B infection

A

a significantly more severe disease than Hep B alone

59
Q

who is Hep E most dangerous in

A

pregnany women and immunosuppressed patients

60
Q

treating viral hepatitis

A

infereron

antivirals to reduce the risk of liver failure

there is a cure

61
Q

fatty liver disease

A

steatosis (fatty deposits) in the liver common in obese adult that distorts the normal structure of the liver

62
Q

how is fatty liver detected

A

liver function test

US

CT

63
Q

FLD causes and management

A

chronic alcohol use

obestiy

metabolic disease

drug toxicity

64
Q

methods to manage FLD

A

stop using alcohol

lose weight with bariatric surgery if necessary

65
Q

Cirrhosis

A

irreversible inflamatory disease that disrupts the liver function and structure

66
Q

what is the result of build up of nodular and fibrotic tissue from cirrhosis

A

obstruction of the biliary channels and portal hypertension

67
Q

three types of liver failure

A

alcoholic

biliary

infectious (post necrotic)

68
Q

five main functions of the liver

A

bilirubin elimination

blood filtering

synthesis of important substances

drug detoxificaiton

mineral and vitamin storage

69
Q

what types of substances are synthesized in the liver

A

clotting factors

albumin

CHO

bile

70
Q

symptoms of cirrhosis

A

chronic RUQ pain

jaundice

edema

portal hypertension

reduced coagulation

reduced drug metabolism

71
Q

how much does liver failure incrase the risk of liver cancer

A

3-5% per year

72
Q

symptomatic treatment of cirrhosis

A

paracentesis of ascities

shunts to reduce portal hypertension

correction of coagulopathy and hypoalbumemia

73
Q

direct treatment of cirrhosis

A

anti viral drugs for hepatitis

anti-inflammatory and immunosuppresive drugs in the case of an autoimmune disorder

liver transplant

74
Q

what is the prognosis of cirrhosis

A

severe cirrhosis 6 month survival at 50%

moderate 5-10 yrs

75
Q

what is the gender bias of cholelithaisis

A

women over men, 8.6% to 5.5%

76
Q

what are the risk factors for gall stones

A

gender

old age

obesity

child bearing

diet

77
Q

explain the saying “female, forty, fat, and fertile”

A

delineates the risk factors for gall stones

78
Q

what is one medication that increases the risk of gall stones

one that decreases

A

cephalosporin

aspirin

79
Q

what kind of diet will lower the risk of galll stones

A

low carb high fiber

80
Q

T/F gallstones are usually symptomatic

A

false

81
Q

what percent of people will develop episodic biliary pain related to gallstones

what are the symptoms

A

10-25%

RUQ pain, often at night

pain related to a high fat meal

lasts from 30 minute to hours

82
Q

what is the percent break down of gallstone composition

A

choleterol (80-85%)

calcium bilirubinate (<20%)

83
Q

what is the method of imaging a gall stone

A

ultrasound

84
Q

what is the treatment for gallstones

A

laproscopy

stone dissolution with bile salts

85
Q

five symptoms of acute cholecystitis

A

biliary pain

nausea/vomiting

fever

leukocytosis

jaudice

86
Q

what is the most common cause of cholecystitis

A

distal occulsion of the bile duct by a gallstone

87
Q

what is the risk of untreated cholecystitis

A

ischemia leading to perforation/rupture, followed by abcess, peritonitis, and death

88
Q

signs and symptoms of acute cholecysitis

A

RUQ, nausea, fever

89
Q

what are the laboratory signs of cholecystitis

A

leukocytosis, elevated bilirubin, elevated liver enzymes

90
Q

what are the physical exam findings present with cholecystitis

A

murphy’s sign

91
Q

conservative treatment of cholecystitis

A

NPO w/ IV fluids

analgesics

IV antibiotics

92
Q

what is the surgical treatment for acute cholecystitis

A

laproscopy after the swelling has gone down unless there is sign of peritonitis

93
Q

two types of pancreatic disorders

A

pancreatitis

pancreatic cancer

94
Q

pancreatitis

A

acute or chronic inflammation of exocrine pancreas

95
Q

5 risk factors for pancreatitis

A

alcohol abuse

smoking

female gender

biliary disease

medicaion

96
Q

signs of pancreatitis

A

acute epigastric pain

N/V

fever

abdominal tenderness and distention

97
Q

though the exact pathogenesis of pancreatitis is unknow, what are two suspected causes

A

edema/obstruction of the ampulla of vater

direct injury to secretory cells

98
Q

two characteristics of acute epigastric pain associated with pancreatitis

A

abrupt onset of severe, boring pain that often radiates to the lower bac

99
Q

diagnostic factors of pancreatitis

A

elevation of pancreatic enzymes

fever and leukocytosis

Ct imaging

100
Q

what levels of lipase and amylase wuld indicate pancratitis

A

3x the normal limit

101
Q

treatment of mild pancreatitis

A

bed rest with NPO

analgesia

Iv fluids

102
Q

treatment of severe pancreatitis

A

intensive care

aggressive fluid and electrolyte replacement

possibly antibiotic use

103
Q

what is the mortality for acute pancreatitis

A

5-25% depending on severity

104
Q

what are the main risks for chronic pancreatitis

A

alcoholism, smoking, biliary tract disease

105
Q

potential complications of chronic pancreatitis

A

opiod addiction

DM

malabsorption from enzyme deficiencies

pancreatic cancer

106
Q

incidence and prognosis of pancreatic cancer

A

>30,000 increasing over the last 2 decades

overall very poor

107
Q

risk factors for pancreatic cancer

A

smoking

chronic pancreatitis

obestity

long term diabetes

108
Q

T/F its common to have severe symptoms in the early stages of pancreatic cancer

A

false, it is commonly asymptomatic

109
Q

symptoms of pancreatic cancer

A

gnawing visceral midabdominal pain

weight loss

jaundice from biliary obstruction

110
Q

diagnosis of pancreatic cancer

A

CT/Pet scan

laparotomy with biopsy or resection

111
Q

treatment of pancreatic cancer

A

surgical resection

chemo

radation

112
Q

three lower GI disorders

A

acute appendicitis

colorectal cancer

IBS

113
Q

what is the most common abdominal surgical emergency

A

appendicitis

114
Q

four pathologies of appedicitis

A

obstruction form feces, foreign body, inflammation, neoplasm

115
Q

signs of appendicitis

A

abdominal pain

nauseaa

low fever, leukocytosis

116
Q

dscribe the abdominal pain associated with appendicitis

A

periumbilical and epigastric, migrating to the right lowe quadrand

117
Q

PE findings for appedicitis

A

RLQ, pain, guarding, rebound, positive psoas or obturator

118
Q

diagnostic factors for pancreatitis

A

PE findings

CT

US

119
Q

what is the treatment for appendicitis

non surgical

A

laparoscopy/laparotomy

Ice, iv, transport

120
Q

complications of appendectomy

A

perforation leading to peritonitis or pelvic abcess

death from septicemia

121
Q

risk fastors for colorectal cancer

A

dietarty fcators

HPV

IBS (crohns or UC

122
Q

dietary factors associated with colorectal cancer

A

high fat and meat, low fiber

123
Q

four ways to reduce risk of colorectal cancer

A

screening

low dose aspirin

high fiber, low fat diets

hormone replacement in women

124
Q

what is the purpose of screening procedures for colorectal cancer

A

the identification and removal of adenimoatous polyps

125
Q

screening procedures for colorectal cancer

A

fecal occult blood testing

fecal immunochemistry screening

colonoscopy

126
Q

who should be screened for colorectal cancer

A

low risk patients every 10 years at 50

high risk earlier and more often

127
Q

treatment of colorectal cancer

A

surgical resection for all patients

chemo

immunotherapy

128
Q

two main types of IBD

A

Ulcerative colitis or crohns

129
Q

what demographic has the highest instance of IBD

A

ashkenazi jews

130
Q

two possible pathophysiolgies of IBD

A

abnormailites of intestinal microflora

possible auto immune mechanisms

131
Q

symptoms of UC

A

diarrhea, cramping, rectal bleeding, passage of mucus

132
Q

symptoms of crohns

A

recurrent episodes of RLQ pain

malabsorption

steatorrhea

bowel obstruction

133
Q

how is IBD diagnosed

A

diagnostic imaging

endoscopy

134
Q

treatment of crohns

A

symptomatic

diet

antibiotics

corticosteroids

resecetion of the terminal ileum or other segments

135
Q

treatment of UC

A

aminosalicylates

glucocorticoids

surgery

136
Q

how does the IBD increase the risk of colon cancer based on duration

A

after 10 yrs 2%

after 20 8%

after 30 18%

pas 753 (molecular pathophysiology) (17 decks)

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