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GI > 6/7. Esophageal Disorders > Flashcards

6/7. Esophageal Disorders Flashcards

1
Q

Triad of issues seen in Achalasia

A

Impaired relaxation of LES, Increased LES tone and loss of peristalsis in body of esophagus

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2
Q
A
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3
Q

Pathophysiology of Achalasia:

Abnormal function of the lower esophageal sphincter in achalasia is due to

A

impaired and then loss of inhibitory (NO) activity

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4
Q

Histopathologic examination of myotomy specimens with Achalasia has shown
– Degeneration of _______ in myenteric plexus
– Inflammatory______ infiltration

A

ganglion cells

lymphocytic

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5
Q

Clincal presentation of Achalasia:

peak age

Predominant symptoms

A

7th decade

dysphagia in up to >90% pts; first solids then liquids

Chest pain, heartburn, regurgitation and weight loss occur in up to 60% patients

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6
Q

Why does achalasia sometimes have subtle symptom devo?

A

slow progression and accommodative behavior is common:
– Slow and stereotypical eating movements
– Avoiding social events with meals

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7
Q

How do we Dx achalasia?

A

Two or three modalities are generally needed
(manometry, radiography and endoscopy)
• Barium esophagram or manometry have a number
of different appearances

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8
Q

DDx or Secondary Achalasia

A
  • Malignancy: Direct infiltration is usually caused by adenocarcinoma
  • Other Infiltrative disorders: Amyloidosis, sarcoidosis
  • Chagas disease: Trypanosoma cruzi, diffuse enteric myenteric destruction
  • Para-neoplastic syndromes: Small cell carcinoma of the lung
  • Autonomic nerve damage: Diabetes, polio, or surgical damage
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9
Q

Tx for Achalasia

A

focus mainly on disruption of LE

  1. Pharmacotherapy– Nitric oxide donors or Anticholinergic Agents
  2. Endoscopic therapy – Botolinum toxin injection (inhibits release of
    acetylcholine) or Pneumatic dilation
  3. Operative Therapy
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10
Q

characterized by dis-coordinated contraction of the muscularis layer and interferes with efficient delivery of food and fluids to the stomach.

A
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11
Q

The______ epithelium of the esophagus
is resistant to abrasion from foods but is sensitive to acid.

A

stratified squamous

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12
Q

The sub-mucosal glands of the proximal and distal esophagus contribute to mucosal protection by secreting

A

mucin and bicarbonate

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13
Q

Protection from acid in stomach

A 
hydrogen ions (H+) must cross the mucus–unstirred water layer–
bicarbonate barrier before contact can be made with the surface of the epithelium. Diffusion of pepsin, but not H+, is blocked by mucus; however, H+ can **be neutralized by bicarbonate ions (HCO3-)** residing in the unstirred water layer
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14
Q

Why does teh esophagus suck at mucus protection?

A

the preepithelial defense in the esophagus is poorly developed, having a limited mucus–HCO3- barrier to buffer back diffusing H+

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15
Q

Epithelial defence includes apical cell membrane and intercellular junctional complex.
Functional components include intracellular buffering by ________ and ______ and H+ extrusion processes (Na+/H+ exchange and Na+-dependent Cl-/HCO3- exchange)

A

negatively charged proteins and bicarbonate ion (HCO3-)

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16
Q

The most important barrier against reflux is:

A

is the constant LES tone
• LES prevents reflux of acidic gastric contents, which are under constant positive abdominal pressure

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17
Q

The lower esophageal sphincter and the crural
diaphragm constitute the intrinsic and extrinsic
sphincters, respectively. The two sphincters are
anatomically superimposed and are anchored to
each other by the_______ ligament.

A

phrenoesophageal

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18
Q

Reflux of gastric juices is central to the
development of mucosal injury in_____
• Duodenal bile reflux may exacerbate the damage

A

GERD

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19
Q

Inflammation from reflux induces production of ______ which incresaes ______ in the muscle

A

IL-6 which increases H2O2

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20
Q

The H2O2 from IL-6 appears to be the main cause of increase
in

A

platelet-activating factor (PAF) and PGE2

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21
Q

PAF and PGE2 (which are a reusult of H2O2) reduce

A

ACh release and LES tone–> leading to reflux

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22
Q 
Gastroesophageal junction (GEJ) barrier is defective and allows injurious contact
between esophageal epithelium and gastric contents
A

Incompetent LES

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23
Q

Most common type of imcompotent LES cause?

A

Spontaneous, transient LES relaxation which then leads to reflux and drop of pH in the eosphagus

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24
Q

Esophageal peristalsis and relaxation of the lower esophageal sphincter induced by
swallowing result from the excitation of receptors in the pharynx. The afferent stimulus travels to the sensory nucleus, the_________ (small
inset). A programmed set of events from the dorsal vagal nucleus and the nucleus ambiguus mediates esophageal peristalsis and sphincter relaxation

A

nucleus solitarius

25
Q

In esophageal peristalsis, The vagal efferent fibers
communicate with myenteric neurons that
mediate relaxation (large inset). The
postganglionic transmitters are

A 
nitric oxide (NO)
and vasoactive intestinal peptide (VIP).
26
Q

Transient LES relaxation (most common cause of LES incompetency) uses same path as eosphageal peristalsis and signals originate in:

A

pharynx, larynx or stomach

27
Q

characterized by separation of the diaphragmatic crura and LES that results in protrusion of the stomach into the thorax through the gap

A

Hiatal hernia

++ sliding is more common than para-esophageal and asymptomatic 90% time

28
Q

What changes do we see in the morphology of the esophagus as a result of refulx?

A

Basal zone hyperplasia exceeding 20% of the
total epithelial thickness and elongation of lamina propria papillae

29
Q

What different cell types do we see in the esophagus in reflux?

A

Small number of eosinophils are recruited into the squamous mucosa, followed by neutrophils, which usually are associated with more severe injury

30
Q

Whats the difference between erythemia/hyperemia and erosion ?

A

Simple hyperemia (redness)

erosion is a mucosal break and may have exudate on it

31
Q

most frequent cause of esophagitis and the most common outpatient gastrointestinal
diagnosis in the United States (10-20% population)

A

Reflux esophagitis

32
Q

Clinical symptoms seen with reflux esophagitis

A

– Heartburn: Burning or sharp epigastric/substernal discomfort radiating retrosternally
– Regurgitation: Feeling sour contents of stomach in throat – Dysphagia
• Atypical chest pain, chronic cough, hoarseness
(posterior laryngitis) also may be seen

33
Q

risk factor of reflux esophatis

A

adults over 40

obesity

34
Q

Dx of reflux esophagits

A
  1. Endoscopy
  2. Ambulatory reflux monitoring
  3. Radiography
    • Symptoms do not necessarily correlate with degree of mucosal damage
    • EGD is 90% specific in GERD diagnosis but is not sensitive (50%)
    • Ambulatory reflux monitoring has slightly better sensitivity of 70%
35
Q

When would I want to perform a biopsy with endoscopy in pt with GERD?

A

– Dysphagia
– Anemia
– Weight loss
– Abdominal mass
– Vomiting

36
Q

TX options for reflux esophatis

A

Lifestyle: wt loss, elevated bed, avoid triggers

PPI or H2 antagonits

Operative: Fundoplication (complete and partial)

37
Q

Complications of GERD

A
  • Esophageal ulcer
  • Esophageal stricture
  • Bleeding
  • Barrett’s esophagus
38
Q

Stricture most often is due to inflammation and
scarring, which may be caused by

A
  1. Chronic gastroesophageal reflux
  2. Radiation
  3. Caustic injury
39
Q

Stenosis-associated dysphagia usually is

A

progressive

40
Q

In esophageal strictures, pt have trouble with _____ long before _____

A

solids long before liquids

41
Q

Cause of narrowing in esophageal stricture

A

– Fibrous thickening of the submucosa
– Atrophy of the muscularis propria
– Secondary epithelial damage

42
Q

epithelial infiltration by large numbers
of eosinophils, particularly superficially and far from GEJ

A

Eosinophilic esophagitis

43
Q

What is the most common cuase of food impaction in adults?

A

eosinophilic esophagitis

44
Q

Common presentation of eosinopilic esophagitis in adults and children

A

food impaction in adults

nausea, burning and food intolerance in children

45
Q

What are 2 clues that could lead you down the path of eosinophilic dysphagia?

A
  • Failure of the acid suppressive treatment treatment and the absence of acid reflux
  • Personal or family history of atopia (atopic dermatitis or rhinitis or asthma)
46
Q

• EoE pathogenesis entails an allergic immune reactions to ingested/inhaled allergens that
involves _____hypersensitivity

A

T-cell–mediated

47
Q

What cytokines are released as a result of eosinophils from eosinophilc esophagits?

A

The deposition of major basic protein and
increased expression of interleukin-5 (IL-5), IL-
13, within the affected esophageal epithelium

48
Q

What do we see on histology and endoscope in pts with Eosinophilic esophagiits?

A

>15 eosinophils per field

corrucated or ringed eosophagus or one with longitudinal furrows and white abcesses

49
Q

Tx for Eosinophilic Esophagitis

A
  1. Elimination Diet (1-seafood, 2-wheat, 3-soy,
    4-nuts, 5-milk and 6-egg)
  2. Topical steroids
  3. Systemic steroids
  4. Endoscopic dilation
50
Q

What are some cuases of chemical esophagitis

A

– Corrosive acid
– Corrosive alkali (Lye ingestion)
– Alcohol
– Excessively hot fluids
– Heavy smoking
• Medicinal pills

51
Q

IG is chemical esophagitis a big concern?

A

usually self limited, pt have odynophagia or pain with swallowing

52
Q

Cuases of infectious esophagitis and who do we usually see it in?

A

– Viral organisms
– Fungal organisms
– Bacterial esophagiti

in immunocomprommised

53
Q

Your attending says the patient has viral esophagitis but wants you to identify the agent. You see punched out ulcers through the endoscope. Whats the agent and what would you expect to see histologically

A

Herpes simplex virus (punched out)

nuclear inclusions within a rim of degenerating epithelial cells at the ulcer edge

54
Q

You are looking through the endoscope and see shallow ulcerations on the surface of the esophagus. You hear a doctor mention the cuase is viral. What is the agent adn what would you expect to see on histology?

A

CMV; shallow ulcers; cytoplasmic and nuclear
inclusions within capillary endothelium and stroma

55
Q

Most common fungal esophagitis

A

Candidiasis ; presents by adherent, gray/white pseudo-membranes
(densely matted fungal hyphae and
inflammatory cells)

56
Q

Esophagitis with morphologic changes are non-specific
with ulceration and accumulation of neutrophils.

A
57
Q

Iaotrogenic esophagitis

A
58
Q

Causes of iotragenic esophagiits

A

Cytotoxic chemotherapy
– Graft versus host disease
– Radiation

GI (14 decks)

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