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GI: Clin Med IIA > Disorders of the Esophagus > Flashcards

Disorders of the Esophagus Flashcards

not done

1
Q

Common sx that almost always indicate a primary esophageal disorder

A

Heartburn (pyrosis)
Dysphagia
Odynophagia

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2
Q

The feeling of substernal burning
Often radiates to the neck
Caused by the reflux of acidic material into the esophagus
Highly specific for GERD

what is this sx?

A

Pyrosis

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3
Q

Difficulty swallowing

what is this term?

A

dysphagia

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4
Q

Problems in transferring the food bolus from the oropharynx to the upper esophagus

what type of dysphagia

A

oropharyngeal

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5
Q

Impaired transport of the bolus through the body of the esophagus

what type of dysphagia

A

esophageal

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6
Q

The oropharyngeal phase of swallowing is a complex process:

A
  1. elevation of the tongue
  2. closure of the nasopharynx
  3. relaxation of the upper esophageal sphincter
  4. closure of the airway
  5. pharyngeal peristalsis
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7
Q

drooling or spillage of food from the mouth, inability to chew or initiate swallowing, or dry mouth

this pt with oropharyngeal dysphagia is having trouble of what phase of swallowing?

A

oral phase

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8
Q

an immediate sense of the bolus catching in the neck, the need to swallow repeatedly to clear food from the pharynx, or coughing / choking during meals

these are characterized by which type of dysphagia?

A

pharyngeal dysphagia

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9
Q

causes of Oropharyngeal Dysphagia

A
  1. Infectious disease
    Polio, diphtheria, botulism, Lyme disease, syphilis, mucositis (Candida, herpes)
  2. Structural disorders
    - Zenker diverticulum
    - Cervical osteophytes, cricopharyngeal bar, proximal esophageal webs
    - Oropharyngeal tumors
    - Postsurgical or radiation changes
    - Pill-induced injury
  3. Motility disorders
    - Upper esophageal sphincter dysfunction
  4. Neurologic disorders
    - Brainstem cerebrovascular accident, mass lesion
    - Amyotrophic lateral sclerosis, multiple sclerosis, pseudobulbar palsy, post-polio syndrome, Guillain-Barré syndrome
    - Parkinson disease, Huntington disease, dementia
    - Tardive dyskinesia
  5. Muscular and rheumatologic disorders
    - Myopathies, polymyositis
    - Oculopharyngeal dystrophy
    - Sjögren syndrome
  6. Metabolic disorders
    - Thyrotoxicosis, amyloidosis, Cushing disease, Wilson disease
    - med side effects: anticholinergics, phenothiazines
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10
Q

causes of Esophageal Dysphagia

A
  1. Mechanical Obstruction
  2. Motility Disorder
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11
Q

this type of Esophageal Dysphagia
is worse with solid foods than liquids

what is the cause of dysphagia?

A

Mechanical Obstruction

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12
Q

this type of Esophageal Dysphagia
is bad with both solids and liquids, what is the cause of the dysphagia?

A

motility disorder

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13
Q

Sharp substernal pain on swallowing that may limit oral intake

what is this term?

A

Odynophagia

Usually reflects severe erosive disease
May also be caused by corrosive injury due to caustic ingestions and by pill-induced ulcers

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13
Q

Odynophagia MC associated with infectious esophagitis due to what infections?

A

Candida, herpes viruses, or CMV
especially in immunocompromised patients

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14
Q

Two most common complaints with GERD

A

heartburn and regurgitation

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15
Q

Dysfunction of the Gastroesophageal Junction is vulnerable to what 3 MC mechanisms of reflux?

A
  1. Transient lower esophageal sphincter relaxation
  2. Anatomic disruption if GE Junction - Hiatal hernia, laxity in the diaphragm attachment
  3. Hypotensive lower esophageal sphincter
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16
Q

how does the Transient lower esophageal sphincter relaxation cause Dysfunction of the Gastroesophageal Junction

A
  1. Physiologic mechanism of belching
  2. Active, vagally mediated reflex allowing air to leave stomach
  3. A primary determinant of reflux is an increase in these relaxations that are associated with acid reflux rather than gas
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17
Q

how does a Hypotensive lower esophageal sphincter cause Dysfunction of the Gastroesophageal Junction

A
  • Factors that reduce lower esophageal sphincter pressure include gastric distention, smoking, certain foods, medications
  • An abrupt rise in intra-abdominal pressure can “blow open” and overcome the LES pressure
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18
Q

s/s of GERD

A
  1. heartburn
    - 30–60 mins after meals and upon reclining
    - relief from taking antacids
    - if dominant - highly diagnostic
  2. regurg possible
  3. Dysphagia or odynophagia possible
    - occurs in 1/3 of pts
    - d/t erosive esophagitis, abnormal esophageal peristalsis, or the development of an esophageal stricture
  4. “Atypical” or “extraesophageal” manifestations of gastroesophageal disease possible
    - Asthma, chronic cough, chronic laryngitis, sore throat, non-cardiac chest pain, and sleep disturbances
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19
Q

approach in evaluation of GERD

A
  1. PE and laboratory data are normal in uncomplicated disease
  2. Initial diagnostic studies are not warranted with typical GERD sx uncomplicated reflux disease
    - Further investigation required with sx that persist despite empiric PPI therapy
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20
Q

what are the “alarm features” that warrant further evaluation with GERD?

A
  1. New onset dyspepsia in pt age >60
  2. Evidence of upper GI bleed
  3. Iron deficiency anemia
  4. Anorexia
  5. Unexplained weight loss
  6. Severe dysphagia/odynophagia
  7. Persistent vomiting
  8. GI cancer in first degree relative
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21
Q

what special examination is used for:

  • documenting the type and extent of tissue damage in gastroesophageal reflux
  • detecting other gastroesophageal lesions that may mimic GERD
  • detecting GERD complications: esophageal stricture, Barrett metaplasia, and esophageal adenocarcinoma
A

Upper endoscopy (Esophagogastroduodenoscopy or EGD)

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22
Q

In the absence of prior PPI therapy, up to 1/3 of pts with GERD have what?

A

visible mucosal damage (known as reflux esophagitis)

if treated with a PPI prior to endoscopy, preexisting reflux esophagitis may be partially or completely healed

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23
Q

prevalence of hiatal hernia

A

1/4 of pts with nonerosive GERD
3/4 of pts with severe erosive esophagitis
Over 90% of pts with Barrett esophagus

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24
Q

Caused by movement of the LES above the diaphragm
Resulting in dysfunction of the gastroesophageal junction reflux barrier

what type of esophageal disorder?

A

hiatal hernia

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25
Q

what is sliding hiatal hernia

A
  1. Progressive disruption of Gastroesphageal Junction
  2. Widening of muscular hiatal tunnel and circumferential laxity of phrenoesophageal membrane allow a portion of gastric cardia to herniate upward
  3. phrenoesophageal membrane remains intact and hernia is contained within the posterior mediastinum
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26
Q

what type of hernia is associated with abnormal laxity of the gastrosplenic and gastrocolic ligaments, which normally prevent displacement of the stomach

As the hernia enlarges, the greater curvature of the stomach rolls up into the thorax

A

Paraesophageal Hernias
“rolling” hiatal hernia

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27
Q

Possible Causes/Risk Factors for Hiatal Hernia

A
  1. Age-related changes in your diaphragm
  2. Injury to the area, for example, after trauma or certain types of surgery
  3. Being born with an unusually large hiatus
  4. Persistent and intense pressure on the surrounding muscles, such as while coughing, vomiting, straining during a bowel movement, exercising or lifting heavy objects
    - Pregnancy
  5. MC age +50, obesity
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28
Q

presentation of pts with gastroesophageal reflux in sliding hiatal hernia?

A

higher amounts of acid reflux and delayed esophageal acid clearance
- heartburn, regurgitation, and dysphagia
- leading to more severe esophagitis and Barrett esophagus

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29
Q

can be asymptomatic or have only vague, intermittent sx
epigastric or substernal pain, postprandial fullness, nausea, and retching.
GERD sx are less prevalent

this presentation is associated with what type of hernia?

A
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30
Q

what type of epithelium of the esophagus is replaced by metaplastic columnar epithelium from the stomach in barrett’s esophagus

A

Squamous

Believed to arise from chronic reflux-induced injury to the esophageal squamous epithelium

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31
Q

On endoscopy there is presence of salmon-orange colored, gastric type epithelium that extends upward from the stomach into the distal tubular esophagus in a circumferential fashion

what is your dx?

A

Barrett’s Esophagus

bx obtained at endoscopy confirm the dx

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32
Q

f/u for barrett’s esophagus but no dysplasia

A

surveillance endoscopy every 3–5 years

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33
Q

f/u in barrett’s esophagus with low-grade dysplasia

A

Resect any areas of dysplasia, then repeat endoscopic surveillance in 6 mo to exclude any areas of dysplasia, then endoscopic surveillance should be repeated yearly until non-dysplastic Barrett’s exists

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34
Q

f/u in barrett’s esophagus with high grade dysplasia

A
  1. Resect all areas, then repeat EGD as soon as possible to exclude any other areas
    - Repeat at 3, 6, and 12 months
    - then yearly for 5 years, then every 3-5 years
35
Q

Reflux Disease tx with Mild, intermittent sx

A

(fewer than 2 episodes per week, no esophagitis)

  1. lifestyle modifications
    - eating smaller meals and elimination of acidic foods (citrus, tomatoes, coffee, spicy foods), foods that precipitate reflux (fatty foods, chocolate, peppermint, alcohol), and smoking cessation
    - wt loss should be recommended for overweight or have had recent wt gain
    - All pts - avoid lying down within 3 hrs after meals (the period of greatest reflux).
    - nocturnal sx - elevate head of bed to reduce reflux and enhance esophageal clearance.
  2. infrequent heartburn - antacids or oral H2-receptor antagonists
    - cimetidine
    - nizatidine
    - famotidine
36
Q

MOA of H2 receptor antagonists

A

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

37
Q

H2-receptor antagonists taken for active heartburn have a delay in onset of at least ?

A

30 minutes

provide heartburn relief for up to 8 hours.
Can take prior to heartburn inducing meal

38
Q

inital tx for Patients who fail BID H2RA therapy/Lifestyle

A
  1. INITIAL THERAPY
    - +2-3 episodes per week, sx that impair quality of life
  2. PPI therapy warranted
    - omeprazole
    - lansoprazole
    - dexlansoprazole,
    - pantoprazole
    - Taken 30 mins before breakfast x 4-8 wks
39
Q

MOA of PPI

A

Inhibit gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump

40
Q

which PPIs are available as OTC formulations?

A

Oral omeprazole, 20 mg, and lansoprazole, 15 mg

41
Q

long-term therapy for Troublesome sx in reflux disease

A
  1. achieved relief with empiric once-daily PPI - DC after 8–12 wks
  2. sx relapse - continuous PPIx 8 wk courses
  3. BID H2-receptor antagonists for pts without erosive esophagitis
  4. Long term therapy PPI therapy indefinitely for:
    - GERD complications: severe erosive esophagitis
    - Barrett’s esophagus
42
Q

SE and risks of PPIs

A

Uncommon

  1. HA, diarrhea, and abd pain
    - resolved with another formulation
  2. risks of long-term use of PPI:
    - Increased risk of infectious gastroenteritis (including C difficile)
    - Iron and vitamin B12 deficiency
    - Hypomagnesemia
    - Hip fractures (possibly due to impaired insoluble calcium absorption)
    - Dementia ??
43
Q

what surgical tx that is good for relief of sx and healing of esophagitis in most selected pts for reflux disease?

A

Surgical fundoplication

Can be performed laparoscopically with low complication rates in most instances

44
Q

Surgical treatment in reflux should be considered for:

A

(1) pts with extraesophageal manifestations of reflux, may be more effectively controlled with antireflux surgery;
(2) severe reflux disease unwilling to accept lifelong medical therapy
(3) large hiatal hernias and persistent regurgitation despite PPI

45
Q

instead of a fundoplication, what should be considered for obese patients with GERD?

A

gastric bypass

46
Q

passage of the gastric fundus behind the esophagus to encircle the distal 6cm of esophagus

helps to restore a physiologic equivalent to the normal LES

what is this procedure

A

Fundoplication

47
Q

what is and are the indications for LINX System?

A
  1. Flexible, elastic string of titanium beads wrapped around a magnetic core
    - Placed below diaphragm at junction
    - Magnets open with pressures generated during swallowing but remain closed during reflux events
  2. indication: hiatal hernia <3 cm
48
Q

when to refer GERD?

A
  1. sx do not resolve w/ empiric management with BID PPI
  2. Suspected extraesophageal GERD sx that do not resolve with 3 mo of BID PPI
  3. Significant dysphagia or other alarm sx for upper endoscopy.
  4. Barrett esophagus with dysplasia or early mucosal cancer.
  5. Surgical fundoplication is considered.
49
Q

The most serious complication of Barrett esophagus

A

Esophageal Carcinoma

50
Q

It is believed that most ____ of the esophagus and many such tumors of the gastric cardia arise from dysplastic epithelium in ______

A

adenocarcinomas
Barrett esophagus

51
Q

adenocarcinomas are MC than squamous carcinomas in US, where 1/2 of all cases occur in what part of the esophagus?

A

distal third of esophagus

52
Q

what two factors are strongly associated with an increased risk of SCC?

A

Chronic alcohol and tobacco use

53
Q

clinical findings for esophageal cancer?

A
  1. Most are advanced, incurable
  2. > 90% solid food dysphagia, with some odynophagia
  3. wt loss MC
  4. coughing on swallowing or pneumonia
    - Local tumor extension into tracheobronchial tree = tracheo-esophageal fistula
  5. Chest or back pain = mediastinal extension
  6. hoarseness = Recurrent laryngeal involvement
  7. PE often unrevealing
    - supraclavicular or cervical LAN or of hepatomegaly implies metastatic dz
54
Q

diagnostic work-up for esophageal cancer?

A

Endoscopy with bx

55
Q

how to classify esophageal pts into 2 general categories for tx:

A
  1. “Curable” Disease = Surgery +/- chemoradiation
  2. Incurable Disease
    - Chemotherapy or chemoradiation
    - Local therapy for esophageal obstruction

Cure may be achieved in patients with regional lymph node involvement

56
Q

Two most important predictors of poor survival in esophageal cancer are:

A

adjacent mediastinal spread
lymph node involvement

57
Q

A sac-like outpouching of the mucosa and submucosa through Killian’s triangle
An area of weakness between the transverse fibers of the cricopharyngeus muscle and the oblique fibers of the lower inferior constrictor muscles

A

Zenker’s Diverticulum

58
Q

cause of Zenker’s?

A
  1. loss of elasticity of upper esophageal sphincter, resulting in restricted opening during swallowing
  2. certain instances/disorders must generally be present:
    - Altered upper esophageal sphincter function
    - Abnormal esophageal motility
    - Esophageal shortening

Almost all have associated hiatal hernia and reflux

59
Q

Zenker’s sx

A
  • Dysphagia and regurgitation develop insidiously over years
  • Initial sx: vague oropharyngeal dysphagia + coughing/throat discomfort
  • As the diverticulum enlarges and retains food:
    halitosis, spontaneous regurgitation of undigested food, nocturnal choking, gurgling in the throat, or a protrusion in the neck
60
Q

complications with Zenker’s

A

Aspiration pneumonia
bronchiectasis
lung abscess
Ulceration and bleeding - retained meds
Fistula between diverticulum and trachea lumen formation
Focal cord paralysis - pressure from retained food

61
Q

diagnostic work-up for Zenker’s

A
  1. Should be suspected in middle age or older adults with progressive dysphagia (solids) and regurg
  2. barium swallow: clearly shows position and size of the diverticulum
62
Q

tx for Zenker’s

A
  1. Symptomatic = upper esophageal myotomy
    - to restore opening of upper esophageal sphincter
    - standard tx consists of:
    — eliminating functional obstruction at UES level (myotomy of cricopharyngeus muscle and upper 3 cm of posterior esophageal wall)
    — excision or suspension of the diverticulum
63
Q

what is an Endoscopic Zenker’s Diverticulectomy?

A

Obliterates the common wall between the esophagus and the diverticulum, creating one passage

64
Q

Results from progressive degeneration of ganglion cells in the myenteric plexus in the esophageal wall
This loss of cells leaves inflammatory cells of lymphocytes and eosinophils

what dx?

A

Achalasia

  • leads to failure of relaxation of LES
  • a loss of peristalsis in distal esophagus
  • distal narrowing of esophagus

The cause of the inflammation is not known

65
Q

s/s of Achalasia

A
  1. gradual onset of dysphagia for solid foods and liquids
  2. sx at presentation may have persisted for months to years
    - Substernal discomfort or fullness may be noted after eating
    - eat more slowly and adopt specific maneuvers - lifting the neck, throwing shoulders back to enhance esophageal emptying
    - Regurgitation of undigested food
    - Some experience substernal chest pain unrelated to meals/exercise
    - Nocturnal regurgitation can provoke coughing or aspiration
    - wt loss is common
66
Q

diagnostic work-up for achalasia

A
  1. Esophageal manometry
    - pressure sensing catheter in esophagus
    - measures LES sphincter pressure during swallowing
    - measures esophageal peristaltic contractions
  2. Chest radiographs
    - air-fluid level in enlarged, fluid-filled esophagus
67
Q

on Barium esophagography shows a smooth, symmetric “bird’s beak” tapering of the distal esophagus

what is the dx?

A

achalasia

characteristic findings, including esophageal dilation, loss of esophageal peristalsis, poor esophageal emptying, and a smooth, symmetric “bird’s beak” tapering of the distal esophagus

68
Q

tx for achalasia

A
  1. PNEUMATIC DILATION
    - Forceful Dilation with pneumatic balloon dilation of the LES weakens the LES by circumferential stretching or tearing of its muscle fibers
    - relief after 1-3 sessions
    - sx recur in up to 35% within 10 years but usually respond to repeated dilation
    - Perforations occur <3% of dilations and may require operative repair
  2. botox injection
    - Endoscopically guided directly into LES = reduction in LES pressure
    - MC to recur within 6–9 mo and in all pts within 2 yrs
    - most appropriate for comorbidities who are poor candidates for more invasive procedures
  3. SURGERY
    - Laparoscopic procedure
    - Heller myotomy: cut LES muscle fibers
69
Q

Lengthwise incision from just above the LES
Only outer muscles of the esophagus will be cut, leaving the inner mucosal layer untouched.

what is this procedure?

A

heller myotomy

will reduce the force of contracting muscles and relax the LES, thereby, allowing food to pass easily.

70
Q

heller myotomy makes it easy for stomach acid to recede into the esophagus, hence, what else must be done along with the myotomy?

A

fundoplication

71
Q

Radiographically, this dx has been characterized by tertiary contractions (simultaneous, dysfunctional esophageal contractions) or a “corkscrew esophagus” with barium swallow #1

A

Diffuse Esophageal Spasm

72
Q

uncoordinated (“spastic”) activity in the distal esophagus
spontaneous and repetitive contractions
Or, high-amplitude and prolonged contractions

what is this dx?

A

Diffuse Esophageal Spasm

73
Q

what intervention is useful to identify alternative structural and inflammatory lesions that may cause chest pain

A

Endoscopy

74
Q

pathophysof DES?

A
  1. Underlying patho not fully understood
    - Overriding Theory: consequence of impaired inhibitory innervation = premature and rapidly propagated contractions
75
Q

presentation of DES

A
  1. MC dysphagia for solids and liquids
    the dysphagia will occur in association with:
    - retrosternal, noncardiac CP
    - heartburn
    - regurgitation
76
Q

tx for DES

A
  1. CCB - Diltiazem
  2. TCA
  3. Sublingual Nitroglycerin
  4. Sildenafil
    - PDE inhibitor and vasodilator
    - smooth muscle relaxant that can lower the LES pressure and spastic contractions
  5. botox
77
Q

what is scleroderma?

A

Autoimmune disorder that can involve skin, lungs, heart, and GI tract

Hypotensive LES and absent esophageal peristalsis
Reflux disease MC only identifiable association

78
Q

pathogenesis of scleroderma?

A
  1. Infiltration and destruction of esophageal muscularis with collagen deposits and fibrosis
    - predisposes to severe GERD d/t inadequate LES barrier function + poor esophageal clearance of refluxed acid
  2. Dysphagia may also be manifest
    - generally mild and alleviated by eating in an upright position and using liquids to facilitate solid emptying
79
Q

tx for scleroderma

A
  1. tx GERD - PPI
  2. dysmotility - Metoclopramide
80
Q

Characterized by a nonpenetrating mucosal tear at the gastroesophageal junction

A

Mallory-Weiss Tear

81
Q

cause of Mallory-Weiss Tear

A
  1. events that suddenly raise transabdominal pressure
    - lifting, retching, or vomiting
  2. Alcoholism is a strong predisposing factor
82
Q

s/s of mallory-weiss tear

A
  1. Acute onset of GI bleeding with hematemesis
    - Red blood or coffee ground emesis
  2. epigastric pain or pain in the back
  3. Hx retching, vomiting, or straining is obtained in about 50% of cases
83
Q

diagnostic work-up for mallory-weiss tear?

A

upper endoscopy (EGD)

  • identification of 0.5- to 4-cm linear mucosal tear
  • usually located either at gastroesophageal junction or, MC - below junction in gastric mucosa
84
Q

Patients with what underlying condition are at higher risk for continued or recurrent bleeding in mallory-weiss tear

A

portal hypertension

85
Q

tx for mallory-weiss tear

A
  1. initially tx PRN w/ fluid resuscitation and blood transfusions
    - Most stop bleeding spontaneously and require no therapy
  2. Endoscopic hemostatic therapy for continuing active bleeding
    - Injection with EPI (1:10,000)
    - Cautery with a bipolar or heater probe coagulation device
    - Or mechanical compression of artery by application of an endoclip or band is effective 90–95%
  3. Angiographic arterial embolization or operative intervention is required who fail endoscopic therapy
  4. PPI - MC for acid suppression

GI: Clin Med IIA (12 decks)

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