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GI2 E1 > esophagus > Flashcards

esophagus Flashcards

robbins

1
Q

what is the purpose of manometry

A

differentiate between the different types of esophageal dysmotility by checking LES tone and peristalsis

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2
Q

what are the three types of esophageal dysmotility

A
  1. nutcracker syndrome= high amplitude contractions of distal esophagus with loss of normal coordination
  2. diffuse esophageal spasm with repetitive, simultaneous contractions of the distal sm m.
  3. hypertensive lower esophageal sphincter- LES high resting pressure/incomplete relaxation
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3
Q

because wall stress is increased, esophageal dysmotility may result in development of ______, primarily the ___ ____

A

small diverticulae

epiphrenic diverticulum

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4
Q

spasm of the ____ M after swallowing can result in increased P within the ____ ____ and thus the development of ___ ____, which is located directly above the __ ____ ____

A

cricopharyngeus

distal pharynx

Zenker diverticulum

upper esophageal sphincter

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5
Q

what population is zenker diverticulum most likely to present in

A

age > 50 y.o

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6
Q

Sx of Zenker’s Diverticulum

A

regurge and halitosis because food gets stuck in the diverticulum

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7
Q

mechanical esophageal obstruction, such as _____, starts with inability to ______ and progress to _______

A

strictures of CA

swallow solids

liquids

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8
Q

describe benign esophageal stenosis

A

narrowing of the lumen due to fibrous thickening of the submucosa, associated with atrophy of the muscularis propria and secondary epithelial damage

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9
Q

benign esophageal strictures often maintain their ___ and ___, while malignant strictures are often associated with ______

A

appetite, weight

weightloss

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10
Q

what are esophageal mucosal webs

A

idiopathic, ledge-like protrusions of the mucosa that may cause obstruction

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11
Q

in what population are you most likely going to see esophageal mucosal webs

A

women older than the age of 40, associated with GERD, graft-vs-host ds

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12
Q

upper esophagus webs may be accompanied by what other conditions

A

iron deficiency anemia, glossitis, cheilosis =Plummer-Vinson syndrome

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13
Q

in esophagus, semi-circumferential lesions that protrude less than 5 mm, made of fibrovascular CT and overlying epithelium

A

esophageal webs

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14
Q

what is the clinical presentation of esophageal webs

A

nonprogressive dysphagia associated with incompletely chewed food

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15
Q

in esophagus, circumferential, thicker than 2-4 mm, includes mucosa, submucosa, and sometimes hypertrophic muscularis propria

A

schatzki rings

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16
Q

schatzki rings: differentiate between A rings and B rings

A

A rings= above the gastroesophageal junction in the distal esophagus, covered by squamous mucosa

B rings= at the squamocolumnar junction of the lower esophagus, with gastric cardia-type mucosa

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17
Q

achalasia is characterized by this triad

A

incomplete LES relaxation

increased LES tone

aperistalsis of the esophagus

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18
Q

What are the sx of achalasia?

A

dysphagia for solids and liquids, difficulty in belching, and CP

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19
Q

what is the etiology of achalasia

A

distal esophageal inhibitory neuronal (ganglion cell) degeneration

x vagus N/ dorsal motor nucleus of vagus

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20
Q

what is the etiology of secondary achalasia

A

happens in Chagas Ds (trypanosoma cruzi infection–> destruction of myentric plexus, failure of peristalsis, and esophageal dilation)

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21
Q

association of achalasia with these three etiologies suggests that achalasia may be driven by immune-mediated destruction of esophageal neurons

A

HSV1 infection
sjögren syndrome
autoimmune thyroid disease

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22
Q

what is the treatment of achalasia

A

laproscopic myotomy, pneumatic balloon dilatation, botox injection

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23
Q

longitudinal esophageal tears near the gastroesophageal junction, most often associated with sever retching or vomiting secondary to acute alcohol intoxication

A

mallory-weiss tears

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24
Q

describe the etiology of mallory weiss teras

A

esophageal relaxation fails during prolonged vomiting.. gastric contents overwhelm the gastric inlet and cause the esophageal wall to stretch and tear

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25
Q

transmural tearing and rupture of the distal esophagus

A

boerhaave syndrome

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26
Q

describe the prognosis and treatment of boerhaave syndrome

A

=an emergency that results in severe mediastinitis and requires surgical intervention

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27
Q

what is the clinical presentation of boerhaave syndrome

A

CP, tachycardia, shock

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28
Q

common irritants of the mucosa of the esophagus

A

alcohol, corrosive acids or alkalis, hot fluids, heavy smoking

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29
Q

describe the presentation of esophageal chemical injury

A

in children, due to accidental ingestion of household cleaning

in adults, often after attempted suicide

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30
Q

esophageal infections in otherwise healthy people are uncommon and often due to ____. infections in immunosuppressed patients is more common and can be caused by ___

A

herpes simplex virus

herpes simplex virus, CMV, fungal organisms, candidiasis

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31
Q

what is the most common fungal infection of the esophagus

A

candida

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32
Q

pill induced esophagitis frequently occurs at the site of ____. ulceration, when present, is accompanied by ________ and eventually _____

A

strictures

superficial necrosis with granulation

fibrosis

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33
Q

nonpathogenic oral bacteria are frequently found in _________, which pathogenic organisms may invade the ___ ____ and cause _____ or overlying mucosa

A

ulcer beds

lamina propria, necrosis

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34
Q

_____ virus usually causes punched-out ulcers (in esophagus)

A

herpes

35
Q

_______ causes shallower ulcerations and characteristic nuclear and cytoplasmic inclusions within capillary endothelium (in esophagus)

A

CMV

36
Q

submucosal glands in the ___ and ____ esophagus secrete ____ and _____

A

proximal and distal

mucin and bicarb

37
Q

what is the most frequent cause of esophagitis

A

reflux of gastric contents into the lower esophagus, most commonly caused by transient LES relaxation

38
Q

what is the most common outpatient GI complaint in the US

A

esophagitis

39
Q

what factors and conditions can cause LES relaxation and gastric reflux

A

normally mediated by vagus N

can be triggered by gastric distension, gas or food, mild pharyngeal stimulation, stress,

swallow-induced relaxation of LES

abrupt increase in intra-abdominal P

alc and tobacco use, obesity, CNS depressants, pregnancy, hiatal hernia, delayed gastric emptying, increased gastric volume

40
Q

(esophagus) basal zone hyperplasia exceeding 20% of total epithelial thickness and elongation of lamina propria papillae extending into the upper third

A

extensive GERD

41
Q

in what population is GERD most common

A

older than 40, infants and children

42
Q

describe the clinical presentation of GERD

A

heartburn, dysphagia, regurge of sour-tasting gastric contents

in chronic GERD–> attacks of severe CP

43
Q

what is the treatment for GERD and what are some complications of reflux esophagitis

A

PPIs for symptomatic relief

complications–> ulceration, hematemesis, melena, stricture development, Barrett esophagus

44
Q

“separation of diaphragmatic crura and protrusion of the stomach into the thorax through the resulting gap”

A

hiatal hernia

45
Q

what is the clinical presentation of hiatal hernia

A

heartburn and regurge

46
Q

in what population will you see hiatal hernia

A

can have congenital in infants and children

mostly acquired later in life

47
Q

what are the sx of eosinophilic esophagitis

A

food impaction and dysphagia in adults and feeding intolerance in children

majority of patients are atopic- atopic dermatitis, allergic rhinitis, asthma, modest peripheral eosinophils

48
Q

(esophagus) large number of intraepithelial eosinophils, particularly superficially

A

eosinophilic esophagitis

49
Q

differentiate the sx and trx of GERD vs eosinophilic esophagitis

A

unlike GERD, acid reflux is not prominent in eosinophilic esophagitis and high doses of PPIs usually do not provide relief

in e.e., give dietary restrictions (no milk or soy), and topical or systemic corticosteroids for atopic sx

50
Q

“tortuous dilated veins lying primary within the submucosa of the distal esophagus and proximal stomach”

A

esophageal varices

51
Q

what are the two most common causes of esophageal varices (the portal HTN that precedes them)

A

first- alcoholic cirrhosis

second- hepatic schistosomiasiss

52
Q

what is the risk of untreated varices

A

rupture–> hemorrhage into the lumen of the esophageal wall–> overlying mucosa appears ulcerated and necrotc

53
Q

(esophagus) squamous cells with nuclear inclusions = __

- seen in the setting of ___

A

HSV, immunocompromised (infectious esophagitis)

54
Q

what two viral infectious should come to mind with infectious esophagitis

A

HSV-1 and CMV

55
Q

vascular ectasia- what is he?

A

in the antrum of the stomach
=watermelon stomach-

= ectatic mucosal vessels producing stripes of edematous erythematous mucosa alternating with less severely injured paler mucosa

associated with cirrhosis and systemic sclerosis

56
Q

what does H. Pylori infection look on endoscopy

A

nodular lesions in the antrum

57
Q

what population is associated with adenocarcinoma

A

white men

58
Q

what is the treatment for esophageal variceal hemorrhage

A

an emergency

can be treated by inducing splanchnic vasoconstriction 
 endoscopically by sclerotherapy
balloon tamponade
variceal ligation (banding is semi-permanent)

patient’s with high risk for hemorrhage are treated prophylactically with B blockers to reduce portal blood flow and with endoscopic variceal ligation

59
Q

what is the prognosis of esophageal varices hemorrhage

A

30% die from hypovolemic shock, hepatic coma, etc.

50% of those who survive will have a recurrent hemorrhage within 1 year

60
Q

complication of GERD that is characterized by intestinal metaplasia within the squamous mucosa of the esophagus

A

barrett esophagus

61
Q

in what population is Barrett esophagus most common

A

white males between 40-60

62
Q

the greatest concern in Barrett esophagus is that it confers an increased risk of ___ ______

A

esophageal adenocarcinoma

63
Q

“one or several tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction” “metaplasic mucosa alternates with residual smooth, pale squamous mucosa”

A

barrett esophagus

64
Q

Barrett esophagus can only be identified through ___ and ___, which are usually prompted by _______

A

endoscopy and biopsy,

GERD sx

65
Q

what is the trx for Barrett esophagus

A

surgical resection, esophagectomy, photodynamic therapy, laser ablation, and endoscopic mucosectomy

66
Q

the most common esophageal CA

A

squamous cell carcinoma

67
Q

most esophageal adenocarcinomas arise from ___ ____

A

Barrett esophagus

68
Q

risk factors for adenocarcinoma

A 
obesity-related GERD
barrett esophagus
tobacco
radiation
H.
69
Q

protective factors against adenocarcinoma of the esophagus

A

a diet full of fruit and vegetables

H. pylori (decreased acid secretion secondary to gastric atropy)

70
Q

in what population is adenocarcinoma most common

A

Caucasian, men in the US/UK/Australia/Netherlands

71
Q

describe the genetic and epigenetic changes that cause the progression from Barrett’s to adenocarcinoma

A

first mutation of TP53 and downregulation of CDKN2A, aka p16/NK4a

later progression= amplification of EGFR, ERGBB2, MET, cyclin D1, and cyclin E

72
Q

esophageal adenocarcinoma usually occurs in the ___ ____ of the esophagus and may invade the ___ ___ ____

A

distal third

adjacent gastric cardia

73
Q

esophageal adenocarcinomas most commonly produce ___ and form ___, with intestinal-type morphology

A

mucin

glands

74
Q

describe the prognosis of adenocarcinomas

A

by the time they present, its usually already spread to the submucosal lymphatic vessels

5 year survival less than 25%

in the few patients where it is limited to the mucosa or submucosa, the 5 year survival is about 80%

75
Q

in what population are you most likely to see squamous cell carcinoma

A

adults older than 45, males, AAs

also in patients in western kenya under 30 who consume traditional fermented milk

76
Q

what are risk factors for squamous cell carcinoma

A

alcohol and tobacco use, poverty, caustic esophageal injury, achalasia, tylosis, plummer-vinson syndrome, diets without fruits or vegetables, previous radiation to the mediastinum

77
Q

describe alcohol as a risk factor for squamous cell carcinoma

A

not a risk factor on its own, but is synergistically risky with tobacco use

78
Q

what genetic abnormalities are associated with squamous cell carcinoma of the esophagys

A

amplification of SOX2, over-expression of cyclin D1 (cell cycle regulator), loss of function of TP53, E-cadherin, and NOTCH1

79
Q

where in the esophagus are squamous cell carcinoma commonly found

A

middle third of the esophagus

80
Q

describe the morphology of squamous cell carcinoma in the esophagus

A

begins as an in situ lesion called squamous dysplasia

early lesions appear as small, gray-white, plaque-like thickenings

81
Q

metastasis from the upper third of the esophagus will go to ____, from the middle third will go to ________,and from the lower third will go to the _________

A
  1. cervical lymph nodes
  2. mediastinal, paratracheal, and tracheobronchial nodes
  3. gastric and celiac nodes
82
Q

what is the clinical presentation associated with squamous cell carcinoma

A

dysphagia, odynophagia, obstruction causing to switch to liquid foods
prominent weight loss, debilitation
hemorrage and sepsis with tumor ulceration, iron deficiency

sometimes the first sx are aspiration of food via a tracheoesophageal fistula

83
Q

what is the prognosis of squamous cell carcinoma

A

5 year survival= 75% if superficial

overall= 20%, and varies by stage, age, race and gender

GI2 E1 (19 decks)

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