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GI Final > Esophageal and Stomach CIS > Flashcards

Esophageal and Stomach CIS Flashcards

1
Q

How do you treat GERD?

A

acid suppression and lifestyle modfication

  • Decrease alcohol and caffeine
  • small low fat meals
  • assess psychosocial situation
  • PPI usually first line compared to H2 blocker or other acid suppressing meds
  • H. Pylori eradication if indicated
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2
Q

What are some red flags that need endoscopy or Abd imaging if we see them?

A 
Weight loss
persistent vomiting
constant or severe pain
dysphagia
hematemesis 
melena
anemia
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3
Q

When else would you do and endoscopy?

A
  • failed response to 4-8 weeks of PPI

- or when frequent symptoms relapse after PPI discontinued

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4
Q

Esophageal stricture

A
  • esophageal dysphagia
  • structural problem
  • solids… progressive to liquids don’t go down
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5
Q

What is the most common type of esophageal stricture?

A

peptic secondary to GERD

-can also occur because of eosinophilic esophagitis

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6
Q

How do you Dx an esophageal stricture?

A

Barium swallow/EGD

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7
Q

How do you Tx an esophageal stricture?

A

Dilation, PPI/H2 blocker

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8
Q

Esophageal ring (Schatzki)

A

Esophageal dysphagia
-structural problem
solids
intermittent symptoms

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9
Q

What is a typical instegator of esophageal rings?

A

meat

-that’s why it is AKA “steakhouse syndrome”

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10
Q

is esophageal ring acquired or congenital?

A

acquired!

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11
Q

How do you diagnose an esophageal ring

A

barium swallow/EGD

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12
Q

How do you treat an esophageal ring?

A

Dilation

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13
Q

Barret esophagus

A

-specialized columnar metaplasia that replaces normal squamous mucosa of the distal esophagus in some persons with GERD

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14
Q

What does Barret esophagus progress to?

A

esophageal adenocarcinoma

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15
Q

How do you diagnose Barrett esophagus?

A

EGD with Bx

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16
Q

what group is at greatest risk for Barrett esophagus?

A

obese white males older than 50

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17
Q

When should screening EGD for Barrett’s be considered?

A

in pts with a chronic 10 year history of GERD symptoms

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18
Q

How do you treat Barrett’s?

A

Surveillance endoscopy
endoscopic ablation
surgical resection
PPI (better than H2-receptor antagonists)

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19
Q

esophageal cancer

A

adenocarcinoma or SCC

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20
Q

Adenocarcinoma

A
  • M>W
  • Barrett’s
  • distal 1/3 of esophagus
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21
Q

SCC

A 
>45
-M>W
-middle 1/3 
smoking
alcohol
HPV
Esophageal disorders like achalasia and plummer vinson syndrome
-radiation 5-10 years prior
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22
Q

Scleroderma

A
  • esophageal dysphagia
  • dysphagia to mainly solids but some liquids
  • motility disorder aka propulsion problem
  • absent peristoalsis combine with severe weakness of the LES
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23
Q

What is the hallmark of Scleroderma?

A

microangiopathy and fibrosis of the skin and visceral organs

-Thickening and hardening of the skin

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24
Q

How will a patient with Scleroderma present?

A

-chronic heartburn and Raynaud phenomenon

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25
Q

What is Reynaud phenomenon?

A

that change in color of the fingertips

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26
Q

What are some characteristics about Scleroderma?

A
  • ANA present in 90% speckled or centromere
  • Topisomerase I antibodies
  • Anticentromere antibodies
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27
Q

When is Topoisomerase I antibodies present in scleroderma?

A
  • 30% in diffuse disease

- ABSENT in limited disease

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28
Q

When is there ANticentromere antibodies in Sclerdoerma?

A

in limited disease

-RARE in diffuse disease

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29
Q

Diffuse Scleroderma (dcSSC)

A
  • includes proximal extremities and trunk
  • early and progressive internal organ involvement
  • worse prognosis
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30
Q

Limited Scleroderma (lcSSc)

A

-fingers, toes, face, distal extremities
-Raynaud’s commonly precedes other sxs
-CREST syndrome
-indolent course
GOOD PROGNOSIS

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31
Q

What is CREST syndrome

A 
Calcinosis cutis
raynauds
esophageal dysmotility
sclerodactylyl
telangiectasia
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32
Q

Localized Scleroderma

A
  • benign sckin conditions
  • affect children
  • discrete areas of discolored skin indruation
  • NO raynauds
  • NOT systemic
  • histologicall indistinguishable from SSc
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33
Q

What do patches mean on localized scleroderma?

A

Morphea

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34
Q

What do coalesced patches mean on localized scleroderma?

A

generalized morphea

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35
Q

Zenker’s diverticulum

A

usually in upper esophagus

  • structural abnormality
  • False diverticula involving herniation of the mucosa and submucosa through the muscular layer of the esophagus
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36
Q

between what two muscles will a zenker’s diverticulum pop out at?

A

cricopharyngeus muscle and the inferior pharyngeal constrictor muscles

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37
Q

What are the symptoms of Zenker’s diverticulum?

A

dysphagia, regurg, choking, aspiration, voice changes, Halitosis, weight loss

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38
Q

What is the name of the area where a Zenker’s diverticulum will show up?

A

area of natural weakness proximal to the cricopharyngeus known as Killian’s triangle

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39
Q

How do we dx Zenkers?

A

Barium swallow

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40
Q

Tx of Zenkers

A

Surgery

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41
Q

Sjogren’s

A 
Rheumatologic
F>M
Postmenopausal
-sicca symptoms
-keratoconjunctivitis sicca (foreign body sensation
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42
Q

What are the sicca symptoms?

A

Dry eyes, mouth… leads to oropharyngeal dysphagia

  • vaginal dryness, tracheo-bronchial dryness
  • increased incidence of oral infx (candida)
  • dental caries
  • Parotid or other major salivary gland enlargement
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43
Q

What has a strong assoction with Sjogren’s?

A

B cell non-hodgkin lymphoma

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44
Q

What were some of the parasites she talked about?

A 
Trichinella spiralis
Trypanosoma cruzi
Trypanosoma Brucei
Trypanosoma Gambiense
Toxooplasma Gondii
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45
Q

Trichinella spiralis

A

Fever , myalgia, splinter hemorrhage,

-Wild game meat

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46
Q

Trypanosoma Cruzi

A

Chagas disease

-vector is kissing bug (Reduviid)

47
Q

Trypanosoma brucei

A

African sleeping sickness

-Tsetse fly

48
Q

Trypanosoma gambiense

A

Antigenic variation
-African sleeping sickness
Tsetse fly

49
Q

Toxoplasma Gondii

A

Toxoplasmosis, Ring enhancing Lesions,

-Kitty cat

50
Q

Achalasia

A

esophageal dysphagia

  • motility disorder…. solids to liquids (progressive)
  • propulsion problem: absent peristalsis and failure of deglutitive LES relaaxtion
51
Q

What does primary Achalasia show?

A

loss of ganglion cells within the esophageal myenteric plexus

52
Q

What is secondary cause of achalasia?

A

Chagas Disease
-chronic phase develops years after infection and results fromd estructino of autonomic ganglion cells throughout the body, includeing hte heart, gut, urinary tract, and respiratory tract

53
Q

What will we see on barium esophagram for achalasia?

A

Bird-beak and sigmoid deformity of the esophagus

54
Q

How do you dx achalasia?

A

barium swallow x-ray and/or esophageal manometry (definitive)

55
Q

Tx of achalasia

A

LES pressure can be reduce by nitrates and CCB therapy, pneumatic balloon dilatation, Botox injection, or surgical myotomy

56
Q

What does manometry look like in Achalasia?

A
  • incomplete LES relaxation
  • Increased LES tone/ Elevated esophageal resting pressure
  • Loss of peristalsis (aperistalsis)
57
Q

Esophageal Web (plummer Vinson)

A
  • esophageal dysphagia
  • solids
  • structural problem
  • INTERMITTENT symptoms
  • When circumferential, similar to Schatzki rings
58
Q

How to Dx esophageal web

A

Barium swallow/ EGD

59
Q

Tx esophageal web

A

dilatation

60
Q

Plummer Vinson syndrome

A

combo of

  • symptomatic proximal esophageal webs
  • IRON DEFICIENCY anemia
  • angular chelitis
  • glossitis
  • koilonychia (spoon nails)
  • middle aged woman
61
Q

Eosinophilic Esophagitis (EOE)

A

-M>F with hx of allergies or atopic conditions

62
Q

Dx of EOE

A

lost of vascular markings (edema)

  • multiple circular esophageal rings creating a corrugated appearance
  • “feline esophagus”… looks like trachea
  • longitudinally oriented furrows, and punctate exudate
63
Q

What does Bx look like on EOE

A

squamous epithelial eosinophil-predominant inflammatio

-diagnosis requires biopsy with histologic finding of >15-20 eosinophils per high -power field

64
Q

When should we suspect EOE?

A

in a patient with dysphagia and esophageal food impactions

65
Q

What are some complications of EOE?

A

Esophageal stricture, narrow-caliber esophagus, food impaction, and ESOPHAGEAL PERFORATION

66
Q

Tx EOE

A

PPI, elimination diets, swallow topic glucorticoids, allergist referral

  • empiric elimination of common food allergies
  • esophageal dilation is very effective at relieving dysphagia in patients with fibrostenosis
67
Q

What is a risk of esophageal dilation?

A

deep esophageal mural laceration or perforation

68
Q

How does eosinophilic esophagitis present in adults?

A
  • dysphagia
  • pyrosis
  • poor medication response
  • regurgitation of undigested food
  • eosinophilia
69
Q

How does EOE present in children?

A
  • Vomiting
  • difficulty feeding
  • dysphagia
  • failure to thrive
  • eosinophilia
70
Q

What is the result of foreign bodies and food impaction?

A

complete obstruction

  • cause an inability to handle secretions
  • FOAMING AT THE MOUTH
  • SEVERE CHEST PAIN
71
Q

Esophagitis

A

dysphagia and frequently Odynaphagia

-mainly solids

72
Q

What pill is with esophagitis?

A

Doxycycline, quinidine, pheytoin

-virtually any pill has the potential to cause

73
Q

What are some causes of esophagitis?

A

infectious (candida/herpes/CMV)
eosinophilic
caustic

74
Q

How does diffuse esophageal spasm present?

A

can’t eat solids or liquids… intermittent and nonprogressive

  • CORCKSCREW ESOPHAGUS”
  • results from spastic contraction of the circular muscle in the esophageal wall…. it’s a helical array of muscle so it looks like a corkscrew
  • could also look like a ROSARY BEAD thing
75
Q

What is normal in Diffuse esophageal spasm?

A

LES function

-disordered motility restricted to the esophageal body

76
Q

Dx DES

A

Manometry, EGD

77
Q

Nutcracker esophagus

A

swallowing contractions are too powerful

-greater amplitude and duration but normal coordinated contraction

78
Q

how is the LES in nutcracker esophagus?

A

relaxes normally

-but has an elevated pressure at baseline

79
Q

If they can’t keep solid foods down more so than liquids, what’s the problem?

A

mechanical obstruction

80
Q

If they can’t do solids or liquids, then what?

A

it’s a motility disorder

81
Q

What problems could be going on if there’s issues with the oral phase of swallowing?

A 
neuro
muscular
rheumatic
metabolic
infectious
structural
motility
82
Q

esophageal perforation, what causes it?

A

trauma: instrumentation

83
Q

What syndrome can lead to spontaneous rupture at the GE junction?

A

Boerhaave’s syndrome

84
Q

How does Boerhaave’s syndrome present?

A

pleuritic retrosternal pain that can be associated with pneumomediastinum and subcutaneous emphysema

85
Q

Dx of Boerhaave’s syndrome

A

CT of the chest… detecting MEDIASTINAL air

86
Q

How is esophageal perforation confirmed?

A

by contrast swallow, usually Gastrografin followed by thin barium

87
Q

Tx of Esophageal Perforation

A

NGT suction, NPO, Parenteral antibx and surgery

88
Q

What does Mallory-Weiss Tear look like?

A

vomiting, retching, or vigorous coughing

89
Q

What is Mallory Weiss Tear?

A

nontransmural tear at the GE junction

-common cause of upper GI bleeding

90
Q

How is MWT dx

A

history, RGD

91
Q

Tx MWT

A

Bleeding usually abates spontaneously
-protracted bleeding may respond to local epinephrine or cauterization therapy, endoscopic clipping, or angiographic emobolization

92
Q

Esophageal Varices

A

Dilated submucosal veins

  • asymptomatic or hemetemesis… emergency
  • liver disease workup
93
Q

How do diagnose Esophageal varices

A

EGD

94
Q

How to Tx esophageal varices

A

banding, sclerotherapy, balloon tamponade, variceal ligation, B blocker to decrease portal HTN

95
Q

How will a hiatal hernia present?

A

more acid reflux and chest discomfort

-radiograph will have their left diaphragm up higher

96
Q

What causes peptic ulcer disease?

A

NSAID
-H. Pylori
_ETOH

97
Q

Dx of PUD

A

Esophagoduodensocopy (EGD) +/- H. Pylori

  • Can be colonized with H. pylori and not have an ulcer
  • Can have an ulcer and be (-) for H. Pylori
98
Q

Tx of PUD

A

H2 blocker and PPI

-eradicate H. Pylori

99
Q

Gastric Ulcer disease

A
  • Associated with H. Pylori 75% of the time
  • lesser curvature of the antrum
  • burning epigastric pain
  • worsens 30 min after eating (postprandial)
100
Q

What increases the risk for Gastric Ulcer disaes?

A

H. pylori and smoking

101
Q

Duodenal Ulcer

A

-95% 2ndary to H. Pylori
-presents as gnawing pain
-1 to 3 hours after eating
-anterior wall of proximal duodenum
NSAIDs/steroids fall into the other 5% for risk factor

102
Q

Helicobater pylori… what are they?

A

Curved gram negative rods that produce urease (microaerophilic spiral gram negative baccili with flagella

  • poverty, overcrowding
  • person to person fecal oral transmission most likely
103
Q

What will H. Pylori cause?

A

Chronic Gastritis

  • antrum
  • increased gastrin
  • increase in HCl production by parietal cells
  • increased risk of duodenal ulcer
104
Q

what tumor is H. pylori associated with?

A

MALToma

105
Q

What toxin is associated with disease progression and gastric cancer?

A

CagA

106
Q

How to test for H. Pylori

A

Stool antigen immunoassay
C 13 or 14 urea breath test
-these two are most sensitive and specific

107
Q

Histologic exam for H. Pylori

A

EGD with biopsy
-H and E stain or warthin starry stain
Or rapid CLO (clofazimine test)
-could be inaccurate if patient recently treated with PPI

108
Q

Serology for H. pylori

A

H. pylori antibodies, IgA

*ideally, patient should be off PPI and/or Abx for 7-14 days prior to testing

109
Q

Zollinger Ellison syndrome

A

PUD that isn’t repsponding to tx, is severe, atypical, recurrent

  • non-beta islet cell- gastrin secreting tumor: (primary gastrinoma)
  • hypertrophic gastric mucosa
110
Q

Where are the gastrin secreting tumors located in ZE syndrome?

A
  • Pancreas 25%
  • Proximal duodenum 45%
  • Lympho nodes 5-15 %
111
Q

What autosomal dominant familial syndrome is ZE associated with?

A

MEN1

112
Q

Malignancy in ZE

A

2/3 are malignant

-1/3 have already metastasized to the liver at presentation

113
Q

How to rule out MEN1

A

fasting Gastrin and other tests

GI Final (13 decks)

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