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GI > Lecture 3: Disorders of the Esophagus > Flashcards

Lecture 3: Disorders of the Esophagus Flashcards

1
Q

What are the common symptoms of an esophageal disorder?

A
  • Heartburn (pyrosis)
  • Dysphagia
  • Odynophagia
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2
Q

What are the two types of dysphagia?

A
  • Oropharyngeal dysphagia: oropharynx to upper esophagus
  • Esophageal dysphagia: transport of bolus to body of esophagus
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3
Q

What are the 5 components of oropharyngeal swallowing?

A
  • Elevate tongue
  • Close nasopharynx
  • Relax UES
  • Close airway
  • Pharyngeal peristalsis
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4
Q

What is the characteristic description of oropharyngeal dysphagia?

A
  • Immediate sense of food catching in the neck
  • Need to swallow repeatedly to clear food
  • Coughing/choking during meals
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5
Q

What are the two causes of esophageal dysphagia?

A
  1. Mechanical obstruction
  2. Motility disorder
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6
Q

What is odynophagia characterized by?

A

Sharp, substernal pain on swallowing that may limit oral intake

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7
Q

What condition is most commonly associated with odynophagia?

A

Infectious esophagitis (Candida, herpes, CMV)

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8
Q

What are the two characteristic symptoms of GERD?

A
  • Heartburn
  • Regurgitation
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9
Q

What is the complication we are worried about with untreated GERD?

A

Barrett’s esophagus

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10
Q

What are the 3 main GE dysfunctions that can malfunction and result in GERD?

A
  • Transient LES relaxation
  • Anatomic disruption of the GE junction (hiatal hernia)
  • Hypotensive LES
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11
Q

What is the characteristic symptom of GERD?

A

Heartburn

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12
Q

Is severity correlated with tissue damage in GERD?

A

No

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13
Q

What are the extraesophageal/atypical S/S of GERD?

A
  • Asthma
  • Cough
  • Chronic laryngitis
  • Sore throat
  • Non-cardiac chest pain
  • Sleep disturbances
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14
Q

What are the alarm features of GERD?

A
  • New onset dyspepsia in pt > 60
  • Evidence of upper GI bleed
  • Iron deficiency anemia
  • Anorexia
  • Unexplained weight loss
  • Severe dysphagia/odynophagia
  • Persistent vomiting
  • GI cancer in first degree relatie
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15
Q

What would prompt us to investigate GERD further?

A
  • Failure of empiric PPI therapy
  • Alarm features
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16
Q

What is the diagnostic study of choice for GERD exams?

A

EGD

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17
Q

What is the mechanism that occurs and results in a hiatal hernia?

A
  • Movement of the LES above the diaphragm
  • Dysfunction of the GE junction reflux barrier
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18
Q

What is a sliding hiatal hernia?

A
  • Herniation of the gastric cardia upwards
  • Slides back and forth
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19
Q

What is a paraesophageal hernia?

A
  • Laxity of the gastrosplenic and gastrocolic ligaments
  • Stomach displacement
  • Greater curvature of the stomach will roll upwards
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20
Q

What are the most common risk factors for hiatal hernias?

A
  • Age 50 or older
  • Obesity
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21
Q

How does a sliding hiatal hernia typically present?

A
  • Worse GERD
  • Severe esophagitis
  • Barrett’s
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22
Q

How does a paraesophageal hernia present?

A
  • Vague, intermittent symptoms
  • Epigastric/substernal pain
  • Postprandial fullness
  • N/V

Less prevalent GERD symptoms

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23
Q

What is Barrett’s esophagus?

A

Metaplastic columnar epithelium replaces the usual squamous epithelium of the esophagus

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24
Q

What endoscopic finding suggests Barrett’s esophagus?

A
  • Salmon-orange colored, gastric type epithelium
  • Biopsy will confirm diagnosis
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25
Q

What is the management for a Barrett’s patient with low-grade dysplasia?

A
  1. Resect any areas of dysplasia
  2. Repeat endoscopy in 6 months
  3. Annual endoscopy until non-dysplastic
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26
Q

What is the management for a Barrett’s patient with high-grade dysplasia?

A
  1. Resect all areas
  2. Repeat EGD ASAP
  3. Repeat at 3, 6, 12 months
  4. Yearly for 5 years, then every 3-5 years
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27
Q

For patients with mild, intermittent GERD symptoms, what is the recommended treatment?

Mild, intermittent: < 2 episodes weekly, no esophagitis

A
  • Lifestyle modifications
  • Eat smaller meals
  • Eliminate acidic foods
  • Wt loss
  • Avoid lying down within 3 hours of eating
  • Antacids or oral H2 antagonists for heartburn
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28
Q

What is the MOA of a H2 receptor antagonist?

A

Decrease gastric acid secretion by reversibly binding to histamine H2 receptors on parietal gastric cells.

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29
Q

What are the H2 receptor antagonists?

A
  • Cimetidine
  • Nizatidine
  • Famotidine
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30
Q

When are PPIs indicated for GERD?

A
  • Failed BID H2RA/lifestyle
  • Frequent symptoms
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31
Q

What is the MOA of a PPI?

A

Inhibit gastric acid secretion by irreversibly binding and inhibiting the hydrogen-K ATPase pump.

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32
Q

How do we decide what PPI to use?

A

Cost

They all have similar efficacy?

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33
Q

For long-term therapy regarding troublesome GERD, what are the mainstays?

A
  • PPIs for 8-12 weeks and then a pause
  • BID H2RAs for those without esophagitis
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34
Q

When is PPI therapy implemented indefinitely?

A
  • GERD w/ severe erosive esophagitis
  • Barrett’s esophagus
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35
Q

What are the main concerns of PPI use?

A
  • Increased risk of infectious gastroenteritis
  • Iron and B12 deficiency
  • Hypomagnesemia
  • Hip Fx
  • Dementia
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36
Q

What is surgical fundoplication?

A

Laparoscopic surgery that can provide very good relief for esophagitis in 85% of patients

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37
Q

Who can undergo surgical fundoplication?

A
  • Patients with extraesophageal reflux
  • Severe reflux and unwilling to accept lifelong medical therapy
  • Large hiatal hernias and persistent regurg despite PPI therapy
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38
Q

When is gastric bypass recommended over fundoplication for GERD?

A

Obese patients with GERD

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39
Q

What is a LINX system?

A

Magnetic, artificial sphincter for people with hiatal hernias < 3cm

small hiatal hernias only

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40
Q

When should we consult GI regarding GERD?

A
  • Failure of empiric PPIs
  • Suspected extraesophageal symptoms that do not resolve with PPIs within 3 months
  • Significant dysphagia or alarm symptoms for EGD
  • Barrett’s
  • Surgical fundoplication consult
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41
Q

What is the epithelium type of Barrett’s and where does it occur?

A

Adenocarcinomas, most commonly in the distal 3rd of the esophagus.

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42
Q

What are the primary modifiable risk factors for squamous cell carcinoma in the esophagus?

A
  • Chronic alcohol use
  • Tobacco use
43
Q

What is the most common symptom in esophageal cancer?

A

Significant weight loss

44
Q

What PE findings suggest metastatic esophageal cancer?

A
  • Supraclavicular LAN
  • Cervical LAN
  • Hepatomegaly
45
Q

How do we diagnose esophageal cancer?

A

Endoscopy with biopsy

46
Q

How do we treat esophageal cancer?

A
  • “Curable”: surgery w/ or w/o chemoradiation
  • “Incurable”: Chemo or chemoradiation. Local therapy for obstructions

Incurable would be node spread beyond the chest.

47
Q

What are the two important predictors of poor survival in esophageal cancer?

A
  • Adjacent mediastinal spread
  • Lymph node involvement

AKA if it spreads, poor prognosis

48
Q

What kind of involvement is considered metastatic in regards to esophageal cancer?

A

Involvement of nodes outside of the chest

Suggests incurable

49
Q

What is Zenker’s diverticulum?

A

Sac-like outpouching of mucosa and submucosa through Killian’s triangle

50
Q

What is the suspected cause of Zenker’s diverticulum?

A
  • Loss of elasticity of UES, restricting the opening during swallowing
  • Altered UES function
  • Abnormal esophageal motility
  • Esophageal shortening
51
Q

How does Zenker’s typically present?

A
  • Insidious development of dysphagia and regurg
  • Halitosis (bad breath)
  • Spontaneous regurg of undigested food
  • Nocturnal choking
  • Neck protrusion
52
Q

What are the main complications with Zenker’s?

A
  • Aspiration PNA
  • Bronchiecstasis
  • Lung abscess
53
Q

What diagnostic study would help with Zenker’s?

A

Barium swallow to identify size and location

54
Q

Who should we suspect Zenker’s in?

A

Middle/older adults with progressive dysphagia

55
Q

How do we treat Zenker’s?

A

Upper esophageal myotomy to restore the opening of the UES.

Eliminates the functional obstruction at the UES.

56
Q

What is achalasia?

A
  1. Progressive degeneration of ganglion cells in the myenteric plexus in the esophageal wall. (inflammation will occur)
  2. Failure of relaxation of the LES
  3. Loss of peristalsis in distal esophagus
  4. Distal narrowing of esophagus
57
Q

What are the S/S of achalasia?

A
  • Gradual onset of dysphagia
  • Patients may adapt their eating habits to eat properly
58
Q

What is the primary way to diagnose achalasia?

A

Esophageal manometry to measure LES pressure during swallowing.

59
Q

What CXR finding may be seen in achalasia?

A

Air-fluid level in the enlarged, fluid-filled esophagus.

60
Q

What is the hallmark sign of achalasia on barium esophagography?

A

Smooth, symmetric bird’s beak tapering of the distal esophagus

61
Q

What is the primary treatment for achalasia?

A

Pneumatic dilation

62
Q

What are the additional treatment options for achalasia?

A
  • Botox injection (poor surgical candidates)
  • Surgery via Heller myotomy (cutting outer esophageal muscles)

Heller myotomy often is accompanied by a fundoplication to prevent GERD.

63
Q

What characterizes diffuse esophageal spasm?

A
  • Corkscrew esophagus seen on barium swallow
  • Esophageal manometry showing spastic activity, spontaneous & repetitive contractions, or high-amplitude & prolonged contractions
64
Q

What S/S are seen in diffuse esophageal spasm?

A
  • Dysphagia
  • Retrosternal chest pain
  • Heartburn
  • Regurg
65
Q

How do we treat DES?

A
  • CCBs (Dilt)
  • TCAs
  • SL NTG
  • Sildenafil
  • Botox

the weird esophageal disorder

Similar treatment to prinzmetal’s, which is also a spasm-related disorder

66
Q

What is scleroderma?

A

Autoimmune condition that affects skin, lungs, heart and GI tract.

67
Q

How does scleroderma esophagus typically present?

A
  • Hypotensive LES and absent esophageal peristalsis
  • Reflux is often the only identifiable association
68
Q

How does someone with scleroderma esophagus compensate for their dysphagia?

A
  • Eat upright
  • Use liquids to help swallow
69
Q

How do we treat scleroderma esophagus?

A
  • PPI for GERD
  • Metoclopramide for dysmotility

meto makes you move

Sclerodermaesophagus = GERD + poor motility of esophagus

70
Q

What is a mallory-weiss tear?

A

Non-penetrating mucosal tear at GE junction.

71
Q

What are the risk factors for mallory-weiss tears?

A
  • Alcoholics
  • Lifting, retching, or vomiting
72
Q

What are the S/S of a mallory-weiss tear?

A
  • Acute onset of GI bleeding with hematesis or coffee ground emesis.
  • Epigastric pain or LBP
  • Hx of retching, vomiting, or straining
73
Q

What is the primary diagnostic method and finding for mallory-weiss tears?

A

EGD identifying a 0.4cm-0.5cm linear tear

74
Q

What kind of HTN may predispose someone to keep bleeding from mallory-weiss tears?

A

Portal HTN

75
Q

What is the initial management for a mallory-weiss tear?

A

Fluids and transfusions

76
Q

How do we provide hemostatic therapy for mallory-weiss tears?

A
  • Injection with epi
  • Cautery
  • Mechanical compression
77
Q

What is last-resort for mallory-weiss tear treatment?

A

Angiographic arterial embolization

78
Q

What med is often given in mallory-weiss tears?

A

PPIs

79
Q

What are esophageal webs and where do they commonly occur?

A

Thin, diaphragm-like membranes of squamous membrane found in the mid or upper esophagus.

Narrows the esophagus

80
Q

What are schatzki rings and where do they occur?

A

Smooth, circumferential rings in the lower/distal esophagus

S comes after E, so schatzki is lower than esophageal webs.

81
Q

How do webs and rings typically present?

A
  • Intermittent dysphagia
  • Large food boluses most likely to cause symptoms
82
Q

How do we treat webs and rings?

A
  • Dilators
  • Electrosurgical incision
  • PPIs if persistent dilators are used.
83
Q

What are esophageal varices?

A

Dilated submucosal veins due to underlying portal HTN.

Veins are attempting to decompress the portal vein by taking on the pressure.

84
Q

What is the main concern with esophageal varices?

A

Distal bleeding of the esophagus that is very serious

85
Q

What is the MCC of portal HTN?

A

Cirrhosis

86
Q

What are the 4 bleeding risk factors for esophageal varices?

A
  • Large varices > 5 cm
  • Red whale markings on endoscopy
  • Severity of liver disease (high Child’s score)
  • Active alcohol abuse
87
Q

How does variceal bleeding typically present?

A
  • Hematesis
  • Melena
  • Hypovolemia with shock symptoms

Life-threatening

88
Q

What is the initial management for variceal bleeding?

A

Acute resuscitation w/ ABX and vasoactive drugs

ABX: rocephin
Vasoactive drug: Octreotide

89
Q

What are the medications given to someone with active variceal bleeding?

A
  • IV rocephin for a week
  • Octreotide to reduce hepatic blood flow
  • Vit K for cirrhotic patient with abnormal PTT
  • Lactulose (absorb and prevent ammonia buildup)
90
Q

Once a patient is hemodynamically stable from variceal bleeding, what is the next step?

A

Emergent endoscopy to locate the varices for banding.

Keep repeating every 2-4 weeks until the varices all become necrotic.

91
Q

How do we prevent rebleeding of varices?

A

Combo BBs and variceal band ligation

92
Q

How do we prevent the first episode of bleeding from varices?

A

Anyone with cirrhosis should have an endoscopy and go on BBs if varices are present.

93
Q

What are the last resorts for variceal bleeding treatment?

A
  • Balloon tamponade (can’t use more than 24h)
  • Transvenous intrahepatic portosystemic shunts (TIPS)

Can’t use for a long-time

94
Q

Who is infective esophagitis MC in?

A

Immunosuppressed patients

95
Q

What are the MCC organisms that cause infective esophagitis?

A
  • C. albicans
  • HSV (can affect normal ppl)
  • CMV
96
Q

What are the S/S of infective esophagitis?

A
  • Odynophagia and dysphagia
  • Substernal chest pain
  • Esophageal CMV may have colon or retinal smyptoms
  • Oral ulcers with HSV1
97
Q

How do we diagnose infective esophagitis?

A

Endoscopy with biopsy and brushings.

98
Q

How do we treat candidal esophagitis?

A

Systemic fluconazole

Fungi

99
Q

How do we treat CMV esophagitis?

A

Antiretroviral if HIV is present

100
Q

How do we treat herpetic esophagitis?

A

Oral acyclovir

101
Q

What is EGD best for?

A

Examining upper GI mucosa and getting samples

102
Q

What is barium swallow good for looking at?

A

Pharynx and esophagus

103
Q

What does esophageal manometry measure?

A
  • Motility testing to check esophageal motility.
  • Pressure of contractility during swallowing
104
Q

What is ambulatory esophageal pH monitoring used for?

A

Amount of reflux and correlation of symptoms to reflux.

Catheter or wireless

GI (17 decks)

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