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Gastrointestinal and Liver > Lectures 1,2: Esophagus > Flashcards

Lectures 1,2: Esophagus Flashcards

1
Q

Four layers of the esophagus

A

Mucosa, muscularis mucosae (thin), submucosa, muscularis propria

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2
Q

In which esophageal layer are the salivary glands located?

A

Muscularis mucosae

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3
Q

Three components of the muscularis propria (progressing downward)

A

Smooth muscle, myenteric plexus, skeletal muscle

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4
Q

Line between esophagus and stomach

A

Z line

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5
Q

Stem cells become what kind of cells and then what kind of cells in esophageal renewal?

A

Stem cells –> basal cells –> mature cells

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6
Q

What can assess by looking at the thickness of the basal cells?

A

Esophageal surface injury

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7
Q

What is the most dangerous caustic chemical class? What happens upon exposure? Long-term consequences (2)?

A

Alkalis –> odorless/tasteless and cause rapid injury die to necrosis and saponification –> perforation and death; narrowing and squamous cell carcinoma

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8
Q

Describe pill esophagitis: definition and pathogenesis. What is symptom and the endoscopic finding?

A

Injury due to prolonged contact of pill to mucosa; esophagus collapses and secretions decrease during sleep; presents with acute chest pain and the finding is “kissing ulcers”

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9
Q

How does a bisphosphonate become corrosive? What kind of medication?

A

Dissolves in the stomach and refluxes into lower esophagus; bone-building medications

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10
Q

Describe candida esophagitis: how it presents and endoscopic finding

A

Presents as odynophagia (terrible pain on swallowing) and oral thrush; finding is whitish plaques with normal esophagus inbetween made of desquamated cells and fungi

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11
Q

CMV esophagitis is associated with what state? What does it indicate?

A

Immunocompromised; viremia

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12
Q

What kinds of cells do CMV infect? What does this cause in the esophagitis?

A

Mesenchymal cells (NOT squamous cells –> so must biosy BASE of the ulcer); ulcers

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13
Q

T/F: Herpes esophagitis can infect both immunocompetent and immunocompromised hosts

A

True

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14
Q

Herpes infect what kind of cells? What are three characteristic findings?

A

Squamous; 1. Cell-cell detachment, 2. Multinucleation; 3. “Ground glass” nuclei

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15
Q

What causes injury in reflux esophagitis?

A

Gastric acid, pepsin, and duodenal contents (trypsin, bile)

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16
Q

Describe GERD grossly and histologically

A

Erythematous; congested capillaries (suggest chemical injury)

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17
Q

What are some other manifestations of reflux esophagitis? Take-home point?

A

Edemic cells (ballooned with large intracellular spaces) and basal cell hyperplasia with eosinophils; VARIABLE reflux histology

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18
Q

Histology of reflux-associated “peptic” ulcer…

A

PUS = neutrophils, exudate

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19
Q

Three complications of reflux esophagitis

A

Ulcer –> odynophagia, hematemesis; regeneration –> Barrett esophagus (columnar); stricture –> dysphagia

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20
Q

Describe eosinophilic esophagitis: incidence, presentation, etiology, and treatment

A

Rising incidence; presents with dysphagia/food impaction; antigen driven (allergic); tx with dietary restriction and PPIs (may be potentiated by acid reflux)

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21
Q

Endoscopic findings of eosinophilic esophagitis (3) and histological findings (2)

A

Transverse rings; longitudinal furrows, tiny white mucosal plaques; eosinophil aggregates at surface (plaques) and fibrosis

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22
Q

Who usually gets EoE? Who usually gets GERD?

A

EoE = children and adults; GERD = usually adults

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23
Q

Symptoms of EoE vs GERD

A

EoE = dysphagia, impaction; GERD = heartburn

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24
Q

Pathogenesis of EoE vs GERD

A

EoE = IgE and cell mediated injury; GERD = chemical injury

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25
Q

Site of EoE vs GERD

A

EoE = Pan-esophageal; GERD = distal esophagus

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26
Q

Tx of GERD

A

Suppression of acid secretion and reflux

27
Q

Describe Barrett esophagus: definition, what type of “plasia” and symptoms

A

Columnar-lined esophagus in response to GERD; a form of metaplasia; no symptoms

28
Q

Barrett esophagus is a risk factor for…

A

Risk factor for esophageal adenocarcinoma

29
Q

About what % of chronic GERD patients get Barrett esophagus

A

10%

30
Q

What does Barrett esophagus look like grossly and histologically?

A

Salmon-colored esophagus; stomach-like columnar lining with goblet cells (necessary to be sure it was esophagus)

31
Q

Barrett esophagus malignant progression. Fast or slow?

A

Metaplasia –> increasingly dysplastic mucosa (low grade to high grade dysplasia) –> Barrett adenocarcinoma; slow (takes years)

32
Q

Management of Barrett esophagus (3)

A

Manage GERD, surveillance, ablation/surgery

33
Q

Symptoms of Barrett adenocarcinoma and 5-year survival

A

Symptoms: dysphagia and weight loss; 5-year survival = 15%

34
Q

Risk factors for squamous cell carcinomas, divided into underdeveloped and industrialized

A

Developping = dietary deficiencies, aflatoxins, indoor coal burning; Industrialized = alcohol + smoking

35
Q

Who tends to get squamous cell carcinoma in the US?

A

Older males who smoke and drink and live in urban environments, higher in African Americans

36
Q

Symptoms of squamous cell metaplasia (4)

A

Progressive dysphagia, weight loss, hemoptysis, hoarseness

37
Q

Most people who die of squamous cell carcinoma die of what kind of complication? 5-year survival?

A

Local; 5-year survival 5-10%

38
Q

Muscles of upper esophageal sphincter

A

Cricopharyngeus and lower fibers of inferior pharyngeal constrictor

39
Q

Two phases of swallowing (describe)

A

Oral (voluntary): bolus propelled backward by tongue; Pharyngeal phase: soft palate elevates to close off nasopharynx and larynx moves antero-superiorly to bring larynx away from bolus, then larynx closes and UES relaxes

40
Q

Describe pressure wave of lower esophageal sphincter

A

Starts at a resting pressure (closed), then relaxes (receptive relaxation), and finally contracts before returning to rest

41
Q

How long does it take food to get down the esophagus

A

6-7 seconds

42
Q

What is a test to examine esophageal pathology?

A

Esophageal manometry

43
Q

How does progesterone affect the LESp?

A

Lowers the LESp

44
Q

Symptoms of esophageal disorder

A

Dysphagia, heartburn, odynophagia, chest pain, regurgitation, ‘atypical’ symptoms (hoarseness, cough, wheeze)

45
Q

Esophageal disorders tests (5)

A

Barium esophagram (structural lesion), endoscopy with biopsy (visualize esophageal mucosa), endoscopic ultrasound (imaging lesions), esophageal monometry (pressures/contraction), acid reflux (pH) studies (measures pH for 24 hours)

46
Q

Can barium swallow ever demonstrate GE reflux?

A

Yes, if they reflux at that moment

47
Q

Can esophageal manometry demonstrate GE reflux?

A

Can demonstrate tendency for GE reflux

48
Q

What is the best test for reflux?

A

Acid reflux/pH studies

49
Q

Esophageal diseases (2 classes, 3 subtypes for 1 class)

A

Gastroesophageal reflux disease (GERD) and motor disorders (achalasia, scleroderma, esophageal spasm)

50
Q

GERD: define and symptoms. Is all reflux a disease?

A

Reflux of gastric contents into the esphagus; heartburn (worse with food, lying down), chest pain, etc; not a disease unless there is dammage

51
Q

Do you always see GERD macroscopically?

A

2/3 of the time, no (but may be apparent histologically)

52
Q

Pathogenesis of GERD is a balance between aggressive (acid) and defensive factors. What are the defensive factors?

A
  1. Anti-reflux barrier = most important and includes LES and crural diaphragm; 2. Esophageal acid clearance which includes saliva, peristalsis, gastric emptying, intact esophageal mucosa, lack of hiatal hernia
53
Q

Define hiatal hernia. Treatment?

A

Acid pocket within proximal stomach and loss of crural pinch; associated with increased transient LES relaxations; tx = surgical

54
Q

Two types of hiatal hernia

A

Sliding and para-esophageal (not associate with heartburn, but more pain/dysphagia)

55
Q

Consequences of GERD (4)

A

Mucosal injury, stricture, Barrett’s metaplasia, esophageal adenocarcinoma

56
Q

Structural problems are associated with…what’s on the diff dx?

A

Solid foods; progressive: carcinoma (rapid), peptic stricture (gradual w/ GERD hx), intermittent: web/ring

57
Q

Motility disorders are associated with…what’s on the diff dx?

A

Solids and liquids; progressive: achalasia (tonically shut LES, no heartburn), scleroderma (heartburn hx where SM is replaced by fibrous tissue), intermittent: spasm (with chest pain)

58
Q

Achalasia: pathogenesis, manometric findings, sx

A

Loss of inhibitory ganglion cells within myenteric plexus, LES remains tonically contracted; hypertensive LES w/ impaired relaxation and aperistaltic esophagus; sx = dysphagia, regurgitation, weight loss, chest pain

59
Q

Achalasia: barium swallow finding

A

Bird-beak w/ aperistaltic body

60
Q

Achalasia: tx

A

Botox toxin, pneumatic (balloon) dilation, most effective = heller myotomy (cut SM of esophagus to relax LES)

61
Q

Pseudo-achalasia (2 causes)

A

Chagas’ disease due to T. cruzii infection and cancer of GE junction

62
Q

Scleroderma: define and manometry findings

A

CT disorder because SM replaced by fibrotic tissue; tonically open with poor peristalsis

63
Q

Diffuse esophageal spasm: sx, X-ray finding, manometry, tx

A

Sx: chest pain, odynophagia; X-ray: corkscrew esophagus; manometry: simultaneous, repetitive contractions w/ normal LES; tx: muscle relaxants, Ca2+ channel blockers, nitrates

64
Q

Nutcracker esophagus: define and sx

A

Very high amplitude contractions (>180 mmHg) but normal peristalsis; sx = pain

Gastrointestinal and Liver (19 decks)

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