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CMPP > Stomach (Part 2) > Flashcards

Stomach (Part 2) Flashcards

1
Q

how are hiatal hernias most frequently detected?

A

on xray, CT, etc.. INCIDENTALLY

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2
Q

how does the esophagus connect to the diaphragm?

A

it passes through the diaphragmatic hiatus and is anchored to the membrane there.

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3
Q

why do hiatal hernias happen? what happens to the membrane?

A

it becomes worn out, thin, and ineffective

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4
Q

what is the most common form of hiatal hernias?

A

type 1: sliding hernia (95%)

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5
Q

why do type 1 hiatal hernias occur?

A

widening of the hiatal tunnel and circumferential laxity of the phrenoesophageal membrane

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6
Q

what cavity is the hernia contained in?

A

posterior mediastinum.

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7
Q

what is the test of choice for a hiatal hernia type 1?

A

barium swallow

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8
Q

how big do hiatal hernias have to be in order to be seen on barium swallow or endoscopy?

A

> 2cm

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9
Q

how do you detect smaller hernias?

A

manometry

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10
Q

are symptoms of hiatal hernias type 1 related to the size of the hernia?

A

yes, increases with size.

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11
Q

what kind of symptoms do hiatal hernias type 1 cause?

A

GERD symptoms

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12
Q

what kind of treatment do you give for asymptomatic type 1 hiatal hernias?

A

none

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13
Q

what kind of treatment do you give for symptomatic type 1 hiatal hernias.

A

medical or surgical control of reflux –> general surgeon.

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14
Q

what types are the paraesophageal hernias?

A

type 2,3, and 4 (3 and 4 are variants of type 2)

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15
Q

how common are paraesophageal hernias?

A

not very! <5%

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16
Q

paraesophageal hernias can be a complication after…

A

anti-reflux procedures
partial gastrectomy
esophagomyotomy

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17
Q

two ligaments that anchor the stomach in place

A

gastrosplenic ligament

gastrocolic ligament

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18
Q

course of hiatal type 2’s are what?

A

progressive!

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19
Q

test of choice for type 2 hiatal hernia?

A

barium swallow

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20
Q

symptoms of hiatal hernia type 2?

A

many are asymptomatic or have vague intermittent symptoms

epigastric or substernal pain
postprandial fullness
substernal fullness
nausea and retching

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21
Q

do type 2 hiatal hernias need intervention?

A

yes! they will not resolve on their own

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22
Q

what are we preventing in treating a type 2 hiatal hernia?

A

the stomach becoming an intrathoracic organ

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23
Q

5 most common causes of Upper GI Bleeding

A 
H. Pylori
NSAIDS
Mallory Weiss Tear
Stress
Gastric Acid
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24
Q

what do upper GI bleeds commonly present with?

A

hematemesis and/or melena

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25
Q

initial evaluation should focus on

A

hemodynamic instability
diagnosis studies to determine cause
treatment of the specific disorder

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26
Q

hematemesis means bleeding from where?

A

GI tract proximal to ligamnet of Treitz

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27
Q

frankly bloody emesis suggests

A

moderate to severe bleeding

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28
Q

coffee ground emesis suggests

A

more limited or slow bleeding (digested before vomited up)

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29
Q

majority of melena occurs from

A

proximal to the ligament of treitz (90%)

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30
Q

hematochezia comes from

A

a lower GI bleed

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31
Q

important PMH to upper GI bleeds

A 
prior episodes (60%)
liver disease or alcohol abuse history
     suggest esophageal varices or portal hypertension
AAA (abdominal aortic aneurysm)
aorto-enteric fistula
peptic ulcer
malignancy
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32
Q

important medication history for upper GI bleeds

A 
asprin
NSAIDs
pill esopagitis medications (tetracycline, clindamycin, doxycycline, bisphosphonates, vitamin C, iron,...)
anticoagulants
bismuth/iron
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33
Q

if an upper GI bleed presents with epigastric pain or RUQ pain

A

peptic ulcer

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34
Q

if an upper GI bleed presents with Odynophagia, GERD, dyspepsia

A

esophageal ulcer

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35
Q

if an upper GI bleed presents with emesis, cough or retching prior to episode

A

mallory weiss tear

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36
Q

if an upper GI bleed presents with jaundice, weakness, fatigue, abdominal distension

A

liver or variceal etiology

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37
Q

physical exam clues of Upper GI bleeds

A

hypovolemia (low BP, resting tachycardia)
abdominal pain
inflammation of peritoneal cavity

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38
Q

define orthostatic hypotension

A

decrease in SBP of more than 20mmHg or a rise in HR from laying to standing more than 20 bpm

blood loss of atleast 15% in upper GI bleeds

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39
Q

supine hypotension

A

blood loss of atleast 40% in upper GI bleeds

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40
Q

rebound tenderness

A

palpating the abdomen and pain starts when you remove the hand

upper GI bleeds

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41
Q

guarding

A

firm palpation of the abdomen because patient anticipates pain

upper GI bleed

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42
Q

Labs to order for an upper GI bleed

A

CBC
coagulation studies: is it caused by a low INR?
liver function

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43
Q

when should you start treatment for upper GI bleeds?

A

ASAP, do not wait until you figure out the cause

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44
Q

what is the initial treatment for upper GI bleeds and why?

A

IV PPI

reduces rate of bleeding
decreases length of stay
decreases re-bleed rate
decreases need for blood transfusions

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45
Q

which IV PPI to use with upper GI bleeds?

A

omeprazole or pantoprazole

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46
Q

how do we administer IV PPIs for patients with upper GI bleeds?

A

as a bolus then a drip

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47
Q

adjunctive therapy for GI bleeds and why?

A

erythromycin: promotes gastric emptying by acting as an agonist of motilin receptors therefor increasing gastric motility

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48
Q

when should we use erythromycin in upper GI bleeds?

A

when it’s a large GI bleed and we need to do endoscopy

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49
Q

why can’t we use laxatives for clearing of the stomach to improve visualization?

A

they don’t work on the stomach, they work on the intestine and colon

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50
Q

what results from the fact that blood sitting in the GI tract?

A

illeus (no contractions) because it is caustic

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51
Q

what is the test of choice for upper GI bleeds?

A

endoscopy

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52
Q

what is contraindicated for upper GI bleeds and why?

A

Barium swallow because the barium will interfere with the future endoscopy, angiograms, and surgery

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53
Q

types of ulcers that classify as PUD

A

gastric and duodenal

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54
Q

ulcers are defined as

A

a break in the mucosa >5mm in size with a depth to the submucosa

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55
Q

two causes of PUD

A

H. Pylori

NSAIDs

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56
Q

is H. pylori gram + or -

A

negative

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57
Q

where does H. pylori live?

A

under the mucous gel that lines the stomach

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58
Q

describe the shape of H. pylori

A

many flagella

can change shape from S-shape to cocci

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59
Q

does H. pylori invade the cells?

A

no

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60
Q

what exposes H. pylori and causes a problem?

A

break to the gastric mucosa

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61
Q

transmission of H. pylori is by

A

fecal-oral root

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62
Q

predisposing factors of H. pylori

A 
low socioeconomic status
less education
birth or residence in developing country
domestic crowding
unsanitary living condition
unclean water/ food
exposure to gastric contents of an affected individual
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63
Q

H. pylori is almost always associated with

A

chronic active gastritis

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64
Q

how often does H. pylori cause ulcerative disease

A

10-15%

65
Q

what diseases can H. Pylori cause?

A

MALT lymphoma

gastric cancer

66
Q

what are the role of prostalandins in the GI tract?

A

to regulate release of bicarbonate and mucus
inhibit parietal cell secretion
maintain mucosal blood flow

67
Q

role of cytooxygenase (COX)

A

control prostaglandin synthesis

68
Q

what does COX-1 do?

A

expressed in a lot of tissues, but mostly GI and Kidney

it’s role is to maintain renal function, platelet aggregation function, and GI mucosal integrity

69
Q

what does COX-2 do?

A

expressed by most cells
expressed by macrophages and leukocytes when inflammation is present
helps block anti-inflammatory

70
Q

what is the therapy for preventing ulcers?

A

PPI + COX1 or COX2 inhibitors

DO NOT DO THIS IF THEY ALREADY HAVE AN ULCER!

71
Q

risk factors for PUD

A 
prior history of ulcer disease
duration of NSAID use
over the age of 75 because of gastric atrophy and gastro-mucosal health
underlying cardiovascular disease
drugs that are bad to mix with NSAIDS
72
Q

drugs that are bad to mix with NSAIDS

A 
steroids
anticoagulants
SSRIs
alendronate (biphosphonates)
clopidogrel (plavix)
73
Q

where do duodenal ulcers occr?

A

first portion of the duodenum

74
Q

how big are duodenal ulcers?

A

<1 cm in diameter

well demarcated but can be very deep

75
Q

do duodenal ulcers progress to cancer?

A

rarely

76
Q

what relieves duodenal ulcers?

A

antacids

eating

77
Q

when does the pain from duodenal ulcers occur?

A

between midnight and 3am (wakes pt up)

90 minutes to 3 hours after a meal

78
Q

gastric ulcers present with

A

pain precipitated by eating
Nausea, weight loss
older patients (60s)

79
Q

do gastric ulcers progress to cancer?

A

yes, always biopsy on discovery

80
Q

what is more common gastric or duodenal ulcers?

A

duodenal

81
Q

where does the pain occur with gastric ulcers?

A

epigastric (burning or gnawing vague, aching, hunger pain)
constant, unrelievable dyspepsia
sudden and severe abd pain –> perforation

82
Q

what would you check in a physical exam to look for duodenal ulcers?

A

epigastric tenderness
GI bleed
hemodynamically stable

83
Q

most common complication of PUD pts

A

GI bleeds

84
Q

mortality rate of GI bleeds from PUD

A

10%

85
Q

how often do patients bleed without a warning or preceeding symptom with PUD?

A

20%

86
Q

second most complication of PUD?

A

perforation

87
Q

form of perforation where the ulcer tunnels to an adjacent organ

A

penetration

88
Q

where do duodenal ulcers penetrate to?

A

pancreas

89
Q

where do gastric ulcers penetrate to?

A

left hepatic lobe

90
Q

least common complication of PUD

A

gastric outlet obstruction causing inflammation spreading to neighbor tissues

91
Q

symptoms of gastric outlet obstruction

A

early satiety
N/V
increased postprandial abd pain
weight loss

92
Q

diagnostic test of choice for PUD

A

endoscopy

93
Q

what does a benign PUD endoscopy look like?

A

smooth, regular rounded edges, flat, filled with exudate

94
Q

what does a malignant PUD endoscopy look like?

A

ulcerated mass protruding into the lumen, folds surrounding the ulcer that are nodular, fused, or thickened/ irregular

95
Q

does the size of the ulcer affect the chance of malignancy?

A

yes, increases

96
Q

what test should you do upon finding an ulcer?

A

urease testing for H. pylori

97
Q

what will cause a false negative of a peptic ulcer?

A 
bleeding
PPI therapy
H2 blockers
antibiotics
peptobismol
98
Q

what should you do if the urease test comes back negative for H. pylori?

A

stool antigen test or breath test or serology

99
Q

how does the urease test work?

A 
take a biopsy from the antrum during EGD
do CLOtest (urease)
100
Q

is the CLO test reliable for diagnosing PUD?

A

yes!

101
Q

how does the urea breath test work?

A

urea + h.pylori produce CO2 and ammonia
CO2 is detected in breath samples
must take off PPIs and Abx for 2 wks before testing

102
Q

what does serology test for?

A

IgG antibody for H.pylori

103
Q

what restrictions do we have for stool antigen testing regarding PUD?

A

must be off PPIs and Abx for 2 wks

104
Q

indications for noninvasive testing for PUD

A

test of cure (recommend urea breath test)

repeat 4-6 weeks after completeion of treatment

105
Q

three theories of treating H.pylori

A

triple therapy
quadruple therapy
sequential therapy

106
Q

when should we use triple therapy to treat H.pylori?

A

when there is a low resistance to clarithromycin

107
Q

4 meds of quadruple therapy (PUD)

A

PPI
bismuth
metronidazole
tetracyclin (sumisin)

108
Q

how should the PPI be dosed for PUD

A

BID!

109
Q

MOA of bismuth?

A

Coats ulcers and erosions
Provides a protective barrier against acid and pepsin
Has antimicrobial properties against H.pylori

110
Q

Side effect of bismuth?

A

Harmless black stools

111
Q

For what population shouldn’t you use Bismuth?

A

Children because there are trace amounts of asprin which cause Reye’s syndrome

112
Q

Antiparasitic used for quad therapy for H.pylori?

A

Metronidazole (Flagyl)

113
Q

Metronidazole’s MOA

A

Selectively absorbed by anaerobic bacteria and sensitive protozoa
After absorption it is broken down by the bacteria to release a toxin which will kill the bacteria

114
Q

Side effects of Flagyl

A

Severe nausea and vomiting if taken with alcohol (antibuse effect)
Metallic taste

115
Q

How long after flagyl therapy is completed until you can drink alcohol?

A

72 hours

116
Q

Antibiotic used to treat H. Pylori

A

Tetracycline (sumycin)

117
Q

MOA of tetracycline?

A

Broad spectrum bacteriostatic antibiotic that inhibits protein synthesis
Covers +,-,anaerobes

118
Q

When should you take tetracycline

A

On an empty stomach to improve absorption

No food, dairy, or antiacids

119
Q

Side effects of H.pylori

A

Photosensitivity

120
Q

Severe peptic ulcer disease secondary to a gastrin secreting tumor (gastrinoma)

A

Zollinger-Ellison Syndrome (ZES)

121
Q

where do most gastrinomas originate from?

A

pancreas

122
Q

ZES tumors can be grouped as

A

multiple endocrine neoplams (type 1)

123
Q

ZES gender predominence

A

men

124
Q

age group for ZES

A

30-50

125
Q

blood abmormality in ZES

A

hypergastrinemia

126
Q

80% of ZES ulcers are where?

A

gastrinoma triangle
common bile duct
2-3 portion of the duodenum
neck and body of pancreas

127
Q

are many of the ZES tumors considered malignant

A

yes, 1/2 will have mets upon presentation

128
Q

% patients with a presentation of PUD with ZES

A

90%

129
Q

suspect ZES if

A 
second part of duodenum and behind
refractory to medical therapy
recurrence after fundiplication
complications like bleeding or perforation
diarrhea
130
Q

why do patients get diarrhea in ZES

A

malapsorption and digestion

131
Q

two tests needed to diagnose ZES

A

fastin grastrin level (serum)

secretin stimulation test

132
Q

what will throw off ZES creating a false positive?

A

H. pylori pts will have increased serum but not nearly as high as ZES

133
Q

test which helps differentiate gastrinomas from other causes of hypergastrinemia?

A

secretin stimulation test

134
Q

MOA of secretin stimulation test

A

secretin when given, prompts the release of gastrin from the tumor cells, but not in normal uneffected people

135
Q

options for ZES to locate the location of the tumor

A 
esophageal ultrasound (pancreatic tumors)
somatostatin uptake testing (radioactive tag)
abdominal CT vs MRI
136
Q

treatment goals for ZES

A

address the overproduction of gastrin

resect neoplasm and control metastatic disease

137
Q

treatment of choice for ZES

A

PPIs (dosing higher than GERD or PUD)

138
Q

treatment inhibiting gastrin secretion is

A

somatostatin analouge , octrotide (Sandostatin)

139
Q

serious reactions to octrotide, sandostatin

A

pancreatitits
cholecystitis
cholestatic hepatitis

140
Q

how is the prognosis of gastric cancer>

A

deadly

141
Q

why have rates of gastric cancer gone down?

A

refridgeration
less salting of foods
h. pylori decrease

142
Q

ethnicities most prone to gastric cancer?

A

world:asian and south americanus: asian and pactific islanders

143
Q

gender and age predominance in gastric cancer

A

male

male: 70, women 74

144
Q

symptoms

A

early: none
late: n/v, dsyspagia, postprandial fullness, melena, anorexia

145
Q

hallmarks sign of gastric cancer

A

meriumbilical met, sister mary joseph nodule
virchows nodes: left supraclavicular
blumers shelf: peritoneal cul de sac palpable
leser-trelat: senporheic keratosis

146
Q

risk factors for gastric cancer

A 
chronic h.pylori infection (strongest)
pickled veggies
salted fish
smoked meats
smoking
previous gastric cancer
genetics
pernicious anemia
147
Q

diagnostic method for gastric cancer

A

EGD

staging done with CT and esophageal ultrasound

148
Q

two main types of gastric cancer

A

adenocarcinoma (95%)

MALT

149
Q

two types of adenocarcinoma gastric cancer

A

diffuse and intestinal

150
Q

no cell adhesion, thickening of the stomach wall, occus in younger patients,leather bottle appearance, poorer prognosis

A

diffuse type of ZES

151
Q

forms cohesive group of cancer cells from little tube like masdes

A

intestinal type adenocarcinoma

152
Q

treatment for adenocarcinoma

A

total gastrectomy

153
Q

what does a total gastrectomy use

A

tumor removal in no populariopn

154
Q

most frequent extra nodal site of lymphoma

A

gastric cancer (stomach)

155
Q

how does lymphoma present

A

same as adenocarcinoma

156
Q

is lymphoma treatmble

A

much more so

157
Q

are MALT lymphoma patients chronic?

A

no, resolves itself with h.pylori

158
Q

maintenence of lymphoma

A

surveillance EGD done periodically
questions
we might have to retreat pylori

CMPP (17 decks)

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