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G.I & Nutrition > Esophageal Pathophysiology > Flashcards

Esophageal Pathophysiology Flashcards

1
Q

3 functions of esophagus

A

propel swallowed food into stomach, prevent gastroesophageal reflux/clear refluxed material back into stomach, vomiting and belching

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2
Q

What does the upper esophageal sphincter separate?

A

pharynx from esophagus –> high pressure zone

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3
Q

3 muscles of esophageal sphincter

A

inferior pharyngeal sphincter, cricopharyngeus, cervical/proximal esophagus

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4
Q

Is the esophageal sphincter smooth or striated?

A

striated muscle

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5
Q

Functions of upper esophageal sphincter

A

barrier between pharynx and esophagus, prevents air entry into GI tract, and prevents reflux of gastric contents into pharynx

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6
Q

What structure anchors the gastroesophageal junction?

A

phreno-esophageal ligament

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7
Q

2 sphincters of the gastroesophageal junction

A

lower esophageal sphincter, diaphragm

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8
Q

Barrier between esophagus and stomach

A

gastroesophageal junction and its two sphincters

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9
Q

Is the lower esophageal sphincter smooth or striated?

A

smooth

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10
Q

Expansion of the chest by contraction of the diaphragm leads to increase/decrease in pressure on the LES?

A

increase

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11
Q

In what condition does LES pressure not depend on diaphragmatic contraction?

A

hiatal hernia

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12
Q

What condition is the most common cause of compromise of the phrenoesophageal ligament?

A

obesity

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13
Q

What kind of epithelial lining is there in the esophagus?

A

squamous epithelia

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14
Q

Does the esophagus have a serosal layer?

A

no, just an adventitia

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15
Q

What anatomic feature of the esophagus makes esophageal cancer so bad?

A

lymphatics in the esophagus come up to the surface epithelium –> easy cancer spread

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16
Q

Voluntary component of swallowing

A

voluntary bolus movement into pharynx –> everything past upper esophageal sphincter is involuntary

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17
Q

What is the initiator of involuntary esophageal activity?

A

act of swallowing voluntarily

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18
Q

What brain area controls voluntary component of swallowing?

A

cortex

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19
Q

What afferent nerve pathway brings information from the esophagus to the brain?

A

nucleus tractus solitarius (NTS)

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20
Q

Which brain nucleus controls the skeletal muscle of the upper esophagus and the diaphragm?

A

nucleus ambiguus

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21
Q

Which brain nucleus controls the smooth muscle of the esophagus?

A

dorsal motor nucleus

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22
Q

What is the functional difference in innervation of esophageal smooth vs striated muscle?

A

smooth muscle has an intermediate connection in the myenteric plexi before connecting with tracts; striated muscle has a direct neural connection

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23
Q

What 2 kinds of neural pathways originate in the dorsal motor nucleus?

A

caudal inhibitory and rostral excitatory pathways

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24
Q

Which neural pathway from the dorsal motor nucleus is activated first upon swallowing?

A

inhibitor pathways –> simultaneous inhibition of the entire smooth muscle esophagus (distal > upper)

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25
Which neural pathway from the dorsal motor nucleus is activated second upon swallowing?
sequential activation of excitatory pathways --> variable inhibition of the esophagus means that the proximal part of the esophagus will start contracting when excited before the distal esophagus --> peristalsis
26
Are there more noncholinergic nerves in the distal esophagus or the proximal esophagus?
More noncholinergic in the distal esophagus to ensure more inhibition in the first phase of swallowing
27
Is the lower esophageal sphincter open or closed at rest?
tonically closed at rest
28
After swallowing, does pressure on the LES increase or decrease?
pressure falls within 1.5-2.5 seconds of swallowing --> stays low for 5-6 seconds until bolus arrives
29
What molecule mediates the inhibitory pathways in the esophageal smooth muscle?
NO
30
What molecule mediates the excitatory pathways in the esophageal smooth muscle?
ACh
31
What are the three mechanisms involved in regulation of LES tone?
1. basal tone of the muscle, 2. NO inhibition, 3. ACh excitation
32
Relaxation of the lower esophageal sphincter in response to gastric distension, lasting for 10 to 30 seconds and resulting in gastroesophageal reflux or belching.
Transient LES relaxation
33
What is the trigger for TLESR?
distension of the stomach leads to vagal afferent stimulation which results in transient esophageal sphincter relaxation
34
Perception that there is an impediment to the normal passage of swallowed material.
dysphagia
35
Sensation of pain on swallowing.
odynophagia
36
Sensation of an object in esophagus when there is non.
globus
37
Is globus associated with difficulty swallowing?
no
38
Effortless return of gastric contents into chest or mouth.
regurgitation
39
Burning feeling rising from stomach or lower chest up towards neck.
heartburn
40
Classic barium xray sign of achalasia.
bird's beak
41
What does manometry on achalasia look like?
LES contraction but no contraction along rest of esophagus or gastroesophageal junction
42
Pathogenesis of achalasia
decrease in myenteric neurons in distal esophagus, especially NO releasing neurons --> no initial inhibition of esophagus
43
2 pathologic features of achalasia on histology
inflammation of myenteric nerves and ganglion, scarring of nerve with minimal residual inflammation
44
Gender preference for achalasia
none --> both M/F
45
Peak age group for achalasia
30-60
46
Incidence of achalsia
1/100,000
47
Etiology of achalasia
unclear --> maybe viral, autoimmune, neurodegenerative
48
Pseudoachalasia
looks like achalasia but due to primary GEJ cancer, metastases of lung, breast, pancreatic cancer, or benign mesenchymal tumors, pseudocysts, or amyloid
49
Are medications effective in achalsia?
no
50
What are the endoscopic/surgical treatments for achalasia and are they effective?
botulinum, pneumatic dilation, Heller myotomy, POEM --> temporary fixes with drop in success during years after surgery
51
What is a Heller myotomy?
basically a fundoplication of the LES to resolve achalasia
52
What is POEM?
In this procedure, performed in the operating room under general anesthesia, a flexible endoscope is passed into the esophagus, a mucosal flap and a submucosal tunnel is created. This tunnel extends onto the stomach. The inner circular muscle layer of the lower esophagus and sphincter (LES) is identified and a myotomy is started 3-4cm distal to the mucosal flap and carried all the way onto the stomach. --> basically separate the two muscle layers to keep the GEJ open
53
A condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications.
GERD: Gastroesophageal reflux disease
54
Criteria for GERD (2)
>=2 heartburn episodes/week and adversely affecting individual's well being
55
Elements of body that protect against GERD
saliva in esophagus, diaphragm, LES, peristalsis
56
Pathogenesis of GERD
Loss of "defense": any compromise of the elements that protect against GERD --> reduced saliva, decreased resting LES tone, peristalsis inhibition, impaired esophageal clearance, impaired tissue resistance or Increased "offense": hernia, increased distension of stomach and TLESR, delayed gastric emptying, bile reflux
57
In absence of hiatal hernia, what is the primary etiology of GERD?
transient LES relaxation (TLESR) > low LES pressure > strain + low LES pressure (e.g. bending over with weakened LES)
58
2 mechanistic links between obesity and GERD
1. increased pressure in abdomen | 2. separation of diaphragm from GEJ
59
What does GERD look like under endoscopy?
looks like a normal esophagus most of the time but can have mucosal breaks, scarring, Barrett's segment
60
Tx for GERD
lifestyle measures (most effective), antisecretory therapy (H2 blockers or PPIs), antireflux surgery
61
The major precursor to Barrett's esophagus
GERD
62
What is the key histologic feature of Barrett's esophagus?
metaplasia of esophageal lining from squamous to columnar
63
Risk factors for Barrett's
Males, Caucasians, increasing age, GERD, smoking, central obesity
64
Pathophysiology of Barrett's
Increased permeability of esophagus due to toxicity from reflux contents results in dilated intercellular spaces --> contact of noxious substances with the basal cells induces metaplasia (unclear whether it is trans-differentiation of existing cells, change in stem cells, or other etiology)
65
What transcription factors are suspected to be the key modulators of Barrett's metaplasia?
basal cell CDX and BMP4
66
How does Barrett's turn into cancer?
the usual way --> inflammation, lots of proliferation, oxidative stress --> DNA damage --> cancer
67
Can esophageal cancer be resolved via endoscopic surgery?
if early stage --> endoscopic mucosal resection +/- radiotherapy ablation of mucosa is effective
68
Endoscopic signs of eosinophilic esophagitis
rings, linear furrows, food obstruction, white exudate/eosinophilic pus
69
Diagnostic criteria for eosinophilic esophagitis
esophageal and/or upper GI symptoms with >= 15 eosinophils/hpf in >=1 biopsy specimen in the absence of GERD (failure to respond to PPI or normal pH monitoring)
70
Risk factors for eosinophilic esophagitis
Males, average age either 9 or 38
71
Clinical presentation of eosinophilic esophagitis in adults
dysphagia, food impaction, heartburn/regurgitation, chest pain, abdominal pain, odynophagia
72
Etiology of eosinophilic esophagitis
Th2 mediated allergic response to inhaled or consumed allergens --> IL4, 5, 13 --> production of eotaxin3 --> signals eosinophils and mast cells to esophagus
73
What kind of cell type is implicated in eosinophilic esophagitis?
Th2 cells
74
Main complication of eosinophilic esophagitis
fibrosis and scarring of esophagus
75
What is the primary signaling protein implicated in eosinophilic esophagitis?
eotaxin 3
76
Tx of eosinophilic esophagitis
dietary (get rid of allergen foods like milk, gluten), dilation, PPI, topical steroids,

G.I & Nutrition (43 decks)

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