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Gastrointes > 010614 esophageal disorders > Flashcards

010614 esophageal disorders Flashcards

1
Q

swallowing mechanism

A

initial phase if voluntary but as bolus is pushed backward by tongue to hypopharynx, the involuntary phase of the swallow reflex is triggered

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2
Q

antegrade transit

A

peristalsis
it’s coordinated and sequnetial contraction of the esophageal muscle

primary peristalsis occurs with appropriately timed relaxation of the upper and lower esophageal sphincters

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3
Q

esophageal peristalsis subtypes

A

primary peristalsis: triggered by swallow (pharyngeal contraction and UES relaxation)

secondary peristalsis: triggered by esophageal distension

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4
Q

peristalsis is generated by what nerves?

A

intrinsic (enteric neural plexus)

extrinsic (vagus nerve)

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5
Q

how is peristalsis generated differently in the proximal and distal esophagus?

A

proximal: striated muscle peristalsis. involves motor end plate. action potential causes Ca release mostly from SR via T tubules. sequence of peristalsis is generated by the swallowing central generator of the brainstem
distal: sm musc peristalsis. varicose nerve endings and gap jxns. Ca influx is from outside. Dual innervation (both inhibitory wave and excitatory wave). peristalsis goes in waves of inhibition and excitation.

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6
Q

dysphagia

A

difficulty eating during swallow

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7
Q

swallowing takes how long?

A

just 10 seconds, so if it’s longer, it’s not dysphagia

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8
Q

globus sensation

A

lump in the throat

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9
Q

what to ask for hx in dysphagia pt

A

what kind of food (solid, liquid)

intermittent or progressive

other symptoms? (heartburn, regurgitation, odynophagia, chest pain)

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10
Q

regurgitation

A

effortless return of gastric contents moving upward into the throat (sometimes associated with sour and bitter taste)

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11
Q

heartburn

A

burning feeling rising to the chest

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12
Q

odynophagia

A

pain during swallow and bolus transit

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13
Q

differential of dysphagia

A

esophageal (sticks or hangs up after swallow, may have chest pain)

pharyngeal (difficulting initating swallow. coughing, choking and nasal regurgitation)

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14
Q

common causes of dysphagia

A

mechanical (peptic stricture, esophageal ring, cancer)

neuromuscular (achalasia, esophageal spasm, dysmotility)

eosinophilic esophagitis can be mechanical or neuromuscular

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15
Q

if the dysphagia occurs with solid food only, what should you think of?

A

think mechanical obstruction

if it’s progressive and over 50 yrs old, think cancer

if pt has chronic heartburn, think peptic stricture

if it’s intermittent, think esophageal ring

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16
Q

if the dysphagia occurs with solid or liquid food, what should you think of?

A

NEUROMUSCULAR

if it’s progressive with heartburn/regurgitation, think scleroderma or achalasia

if it’s intermittent and there’s chest pain, think spasm

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17
Q

diagnostic approaches to esophageal disorders

A

upper GI endoscopy (to look at structure)

esophageal manometry (looks at muscle and sphincters by measuring esophageal intra luminal pressure)

radiography/esophagram (gives info on both structure and fxn)

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18
Q

what is the gold standard for diagnosis of esophageal motor disorders?

A

esophageal manometry

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19
Q

what is an esophageal spasm

A

top and bottom of esophagus are contracted at the same time

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20
Q

achalasia

A

poor relaxation of LES, increased LES tone

in the body of the esophagus, there’s lack of peristalsis (instead, there is disorganized nonperistaltic contractions of the esophageal body)

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21
Q

bird peak appearance

A

achalasia

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22
Q

pathophysiology of achalasia

A

abnormal fxn of LES is due to impaired and then loss of inhibitory NO activity

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23
Q

peak incidence of achalasia is at what age?

A

7th decade and 20-30

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24
Q

what symptoms can you see in pt with achalasia

A

DYSPHAGIA

chest pain, HEARTBURN, regurgitation, weight loss

food stasis, bacterial fermentation and acidity may result in esophagitis and heartburn

slow and stereotypical eating movements

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25
Q

sigmoid shape esophagus

A

achalasia

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26
Q

differential diagnosis or secondary achalasia for a pt with achalasia

A

malignancy
other infiltrative disorders (amyloidosis, sarcoidosis)
Chagas disease
paraneoplastic syndromes
autonomic nerve damage (diabetes, polio, surgical)

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27
Q

corkscrew radiography

A

esophageal spasm

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28
Q

how is complete aperistalsis/scleroderm esophagus different from achalasia?

A

in complete aperistalsis, it’s not a nerve problem. the muscle is unable to contract. and there’s no LES obstruction

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29
Q

pathophysiology of GERD

A

most important barrier against reflux is the constant LES tone.

incompetent LES causes reflux, which causes prolonged acid contact in esophagus, which causes esophagitis, causing decreased peristalsis and also decreased LES pressure. it’s a vicious circle.

30
Q

what increases PAF and PGE2 in the pathophysiology of GERD?

A

H2O2, which is increased with IL-6

31
Q

what do PAF and PGE2 do in the pathophysiology of GERD?

A

they reduce ACh release and LES tone

32
Q

hiatal hernia

A

separation of the diaphragmatic crura and LES, resulting in protrustion of stomach into thorax

33
Q

sliding hiatal hernia is symptomatic or asymptomatic commonly?

A

asymptomatic

34
Q

morphology of GERD

A

basal zone hyperplasia of total epithelial thickness

small number of EOSINOPHILS, followed by neutrophils

35
Q

endoscopic morphology of GERD/reflux esophagitis

A 
simple hyperemia may be only change
mucosal breaks (erosions)
36
Q

is hyperemia in endoscopy specific?

A

no

37
Q

the most common cause of esophagitis

A

reflux of gastric contents

38
Q

risk factors for reflux esophagitis

A

obesity

39
Q

classic symptoms of reflux esophagitis

A

heartburn
regurgitation (going back up in throat)

also dysphagia (but dysphagia is an alarm symptom–would want to rule out achalasia and eosionphilic esophagitis)

40
Q

how to manage GERD

A

lifestyle modifications (weight loss, elevation of bed, avoiding late meals, avoiding trigger foods)

pharmacologic therapy (anti secretory drugs for esophagitis, proton pump inhibitors)

operative management (fundoplication surgery, etc)

41
Q

complications of GERD

A

esophageal ulcer
esophageal stricture (scarring)
bleeding
Barrett’s esophagus

42
Q

esophageal stricture causes

A

narrowing of esophageal lumen

43
Q

eosinophilic esophagitis

A

epithelial infiltration by large numbers of eosinophils

44
Q

what differentiates eosinophilic esophagitis from GERD

A

in eosinophilic esophagitis, there’s an ABUNDANCE of eosinophils as opposed to a few in GERD. also, eosinophils can be found far from the gastroesophageal jxn.

45
Q

clinical presentation of eosinophilic esophagitis

A

adults: dysphagia

in children: nausea, burning and food intolerance

personal or family hx of atopia

46
Q

most common cause of food impaction

A

eosinophilic esophagitis

47
Q

diagnosis of eosinophilic esophagitis

A

histologic confirmation of more than 15 eosinohpils per higher power field in eophageal mucosa

48
Q

endoscopic features of eosinophilic esophagitis

A

it’s helpful but not required

corrugated esophagus
longitudinal furrows

findings are non specific

49
Q

tx for eosinophilic esophagitis

A

elimination diet
topical steroids
systemic steroids
endoscopic dilation

50
Q

causes of esophagitis

A 
GERD
eosinophilic
chemical 
infectious
iatrogenic
skin disorder associated
51
Q

infectious esophagitis is most frequent in whom?

A

debilitated or immunosuppressed

52
Q

how to differentiate types of viral esophagitis?

A

HSV-NUCLEAR inclusions within rim of degenerating epithelial cells at the ulcer edge

CMV-CYTOPLASMIC AND NUCLEAR inclusions within capillary endothelium and stroma

53
Q

most common cause of fungal esophagitis?

A

candida

54
Q

incidence of bacterial esophagitis

A

very rare

55
Q

what skin disorders are associated w esophagitis?

A

desquamative skin disease (bullous pemphigoid, epidermolysis bullosa)

lichen planus
Crohn’s disease

56
Q

where is the Z line?

A

at the end of the LES

57
Q

Barrett’s esophagus

A

normal esophageal sq epithelium is replaced by metaplastic columnar mucosa (especially intestinal metaplasia)

58
Q

what is the defining feature of intestinal metaplasia?

A

Goblet cells

59
Q

Barrett’s esophagus is a complication of

A

chronic GERD

60
Q

Barrett’s esophagus presents how?

A

often asymptomatic

61
Q

Barrett’s esophagus can predispose to?

A

dysplasia and adenocarcinoma

62
Q

types of esophageal tumors

A

squamous cell carcinoma

adenocarcinoma

63
Q

esophageal adenocarcinoma is typically seen in what population?

A

white middle aged male

64
Q

risk factors for esophageal adenocarcinoma

A

dysplasia in Barrett’s esophagus
tobacco use
obesity
radiation therapy

65
Q

in esophageal adenocarcinoma, what is frequently present near the tumor?

A

Barrett’s esophagus

66
Q

squamous cell carcinoma of esophagustypically occurs in whom

A

African Am male adults older than 45

67
Q

risk factors for sq cell carcinoma in esophagus

A 
alcohol, tobacco
poverty
caustic esophageal injury history
achalasia and Plummer Vinson
hot beverage consumption
previous radiation
68
Q

is dysphagia common for esophageal tumors?

A

not very. if it’s present, usually at end of disease

69
Q

symptoms of esophageal sq cell carcinoma

A 
dysphagia (at end of disease)
odynophagia
obstruction
weight loss
vomiting
70
Q

overall five yr survival rate for esophageal sq cell carcinoma

A

poor (usually it’s in advanced stage already at diagnosis)

Gastrointes (11 decks)

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