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OSD_GI > Esophagus > Flashcards

Esophagus Flashcards

1
Q

What seems to be the most prevalent mechanism of GER in both asymptomatic patients (physiological reflux) and patients with GERD (pathological reflux)?

A

Transient LES
relaxation

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2
Q

3 complications of reflux esophagitis?

A

Bleeding
-Strictures
-Barrett’s (11%)

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3
Q

The 3 mechanisms that cause GER all require

A

a low LES pressure (relative to gastric pressure)

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4
Q

4 acid clearance mechanisms?

A

Saliva
- Gravity
- Esophageal Bicarbonate secretion
- Peristalsis

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5
Q

Complications of GERD?

A
  1. erosive esophagitis
  2. esophageal ulcer
  3. bleeding
  4. esophageal stricture
  5. intestinal metaplasia (Barrett’s epithelium)
  6. adenocarcinoma arising in Barrett’s epithelium
  7. other - cough (bronchitis), hoarseness (laryngitis), pneumonia, asthma, pulmonary fibrosis, chest pain, worsening asthma
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6
Q

80% of patients w/ _____ have an associated esophageal motility disorder

A

Scleroderma (Progressive Systemic Sclerosis)

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7
Q

Achalasia

A

Failure to relax the LES (absence of inhibitory input)
- High basal tone of LES & incomplete relaxation during swallowing
- Can lead to enlarged, dilated esophagus

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8
Q

Best diagnostic study for evaluating mucosal injury of the esophagus?

A

Endoscopy w/ biopsy

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9
Q

Causes/pathophysiology of reflux esophagitis?

Multifactorial - 4

A

Multifactorial

  • Decreased Lower Esophageal Sphincter (LES) tone (alcohol, CNS depressants, pregnancy, hypothyroidism)
  • Mechanical defect in LES (TE fistula repair)
  • Associated sliding hiatal hernia
  • Inadequate clearance of refluxed material
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10
Q 
Characteristics of malignant tumors of esophagus: Cell type?
Most common type worldwide? 
Epidemiology?
Gender? 
Race? 
Age?
A

Usually Epithelial

  • Worldwide, squamous cell carcinoma most common
  • China, Iran, South Africa, Puerto Rico
  • Men:women=2:1 (4:1 in U.S.)
  • Blacks>whites
  • Age >50 Years
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11
Q

Describe “esophageal” chest pain

A

Usually:
- “Squeezing, pressure-like sensation”
- Located substernally in the xiphoid area
- May radiate to the arm or jaw (like cardiac angina)
- Not exercise related & is relieved more slowly by
nitroglycerin (unlike cardiac angina)

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12
Q

Does Candida invade the superficial mucosa?

A

Yes

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13
Q

Esophageal Adenocarcinoma characteristics?

A

Usually moderate or well differentiated, mucin producing
- Glandular proliferation infiltrating esophageal waal (mucosa and submucosa, etc)
- Atypical low cuboidal cells with vesicular nuclei and prominent nucleoli
- Signet-ring cells

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14
Q

Esophageal Dysphagia: how to distinguish between a motility vs. structural disorder?

A

Motility- dysphagia to both solids & liquids
Structural- dysphagia to solids that may progress to include liquids

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15
Q

Esophageal obstruction:
A ring vs. B ring?

A

A ring = muscular B ring = mucosal (note: web also mucosal)

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16
Q

Esophageal Peristalsis
Initiated in Two ways:
- Primary?
- Secondary?

A
  1. Swallowing
  2. Esophageal distension
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17
Q

GERD Symptoms?

A

Heartburn
- Regurgitation
- Dysphagia
- Other
- Postprandial symptoms
- Chest pain
- Pulmonary symptoms

18
Q

Histological change in Barrett’s Esophagus?

A

Normal Esophagus: Non- keratinizing squamous cell epithelium
—>
Normal stomach: Non-ciliated columnar epithelium w/ goblet cells

19
Q

Histology components of the submucosa layer of esophagus?

A

Mucin-secreting glands
- Veins form in the submucosa and myenteric networks (varices)
- Submucosal and Myenteric Plexus of ganglia

20
Q

How do you distinguish: Oropharyngeal dysphagia vs. Esophageal dysphagia?

A

Oropharyngeal dysphagia can have presence of:
- Nasal regurgitation
- Cough during swallowing
- Aspiration of food into the lungs during the initiation phase of swallowing
(esophageal dysphagia doesn’t have any of these)

21
Q

Lower esophagus innervation?

A

Sympathetic and parasympathetic
- Synapse with ganglion cells in the submucosal and myenteric neural plexus of the esophagus
- Synapse with smooth muscles

22
Q

The Major Factors Contributing to the Prevention of GERD?

A
  1. A Competent LES and gastroesophageal junction.
    2 Effective clearance of refluxed gastroduodenal secretions.
  2. Neutralization of refluxed acid by salivary bicarbonate.
  3. An intact esophageal mucosal diffusion barrier
    (esophageal mucosal resistance)
  4. Normal Gastric Emptying
23
Q

Reflux esophagitis characteristics?

A

Inflammatory cells: eosinophils, neutrophil
- Basal cell hyperplasia
- Elongation of lamina propria papillae
- Ballooned squamous cells
- Vascular dilatation
- Multinucleated squamous epithelial giant cells

24
Q

Scleroderma pathophysiology?

A

Endothelial cell injury to small blood vessels that eventually leads to vascular obliteration with associated smooth muscle atrophy and fibrosis
(As the disease progresses, distal esophageal peristalsis and basal LES pressures diminish and may become nonexistent)

25
Q

Scleroderma- pathophysiology of dysphagia?

A

Vascular Obliteration And Fibrosis in Smooth Muscle leads to:
- Weak LES
- Poor esophageal contractility
- Delayed gastric emptying

26
Q

Somatic fibers of upper esophagus:
- Origin?
- Synapse with?

A

Originate in the brainstem, travel by vagus nerve
- Synapse with striated muscles

27
Q

Somatic innervation of the esophagus?

A

Originate in the brain stem
- Bundled in the Vagus nerve
- Synapse directly with striated muscles in the upper esophagus

28
Q

Squamous Cell Carcinoma of Esophagus usually involves what part of esophagus?

A

Usually involve upper or middle esophagus

29
Q

Squamous Cell Carcinoma of Esophagus: Predisposing factors?

A

Alcohol, tobacco, smoking
-Vitamin and trace metal deficiencies
-Achalasia
-Plummer-Vinson syndrome
-Genetic abnormalities

30
Q

T or F?
The measurement of LES pressures may reliably differentiate pathological gastroesophageal reflux (GERD) from physiological gastroesophageal reflux (GER).

A

False

31
Q

T or F?

The weak LES pressures alone do NOT account for GER in most patients with GERD.

A

True

combined w/ increased intra-abdominal pressure to produce GER

32
Q

Tumor ass’d w/ Barret’s Esophagus?
- US prevalence?
- Gender?
- Race?
- Age?

A

Adenocarcinoma
- 50% of esophageal CA in U.S.
- Males>females
- Whites>blacks
- Adults (>40 years)

33
Q

The upper esophageal sphincter (UES) consists of striated muscle fibers under the control of signals from somatic neurons of the a via the b nerve.

A

a) nucleus ambiguous
b) vagus nerve

34
Q

Venous supply of distal esophagus?

A

Veins of the distal esophagus drain into the portal venous system via the gastric coronary veins.

35
Q

Venous supply of proximal esophagus?

A

Veins of the proximal esophagus drain in a cranial direction, entering the systemic venous system via the azygos and hemiazygos veins in the mediastinum.

36
Q

What is Globus?

A

The sensation of “a lump in the throat” (suprasternal notch area). This sensation is relieved by swallowing.

37
Q

What is Odynophagia? Cause(s)?

A

Sensation of pain with swallowing

  • Caused by inflammatory disorders of the esophagus:
  • Infectious esophagitis
  • Corrosive esophagitis
  • Radiation esophagitis
38
Q

Bethanechol- MOA in GERD?

A
  • increases LES pressure
  • increases salivary secretion
  • increases esophageal contractions

(seldom used)

39
Q

Metoclopramide- MOA in GERD?

A
  • Dopamine antagonist
  • Muscarinic effect
  • Increases LES pressure
  • Improves gastric emptying

(seldom used)

40
Q

Sucralfate- MOA in GERD?

A
  • Sucrose-aluminum-sulfate
  • Enhances mucosal resistance
  • Local protective effect

(seldom used)

41
Q

Prostaglandins- MOA in GERD?

A
  • Improve mucosal resistance to injury
  • Decrease HCL acid secretion

(seldom used)

OSD_GI (13 decks)

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