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GI II > Clinical Approach to the GI Patient: Dysphagia > Flashcards

Clinical Approach to the GI Patient: Dysphagia Flashcards

1
Q

what are the two types of dysphagia?

A

oral phase and esophageal phase

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2
Q

what could it mean if a patient presents with Hoarseness and dysphagia?

A

involvement of the larynx in the primary disease process, neoplastic disruption of the recurrent laryngeal nerve, or laryngitis from GERD

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3
Q

what exams should you do for dysphagia?

A

neck exam and skin exam (to see if there are any changes with association with scleroderma)

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4
Q

how can you diagnose oropharyngeal dysphagia?

A

video fluoroscopy of swallowing

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5
Q

how can you diagnose esophageal dysphagia?

A

barium swallow, EGD with biopsy, esophageal motility study (manometry)

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6
Q

what are the characteristics of oropharyngeal dysphagia?

A

difficulty initiating swallowing; food sticks at level of suprasternal notch; may have nasopharyngeal regurgitation or aspiration

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7
Q

what type of abnormality is Zenker’s diverticulum?

A

structural abnormality

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8
Q

what occurs in Zenker’s diverticula?

A

there is a false diverticula involving herniation of the mucosa and submucosa through the muscular layer of the esophagus posteriorly

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9
Q

in zenker’s diverticula, where does the herniation take place?

A

posteriorly in an area of natural weakness proximal to the cricopharyngeus known as Killian’s triangle

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10
Q

what is the result of Zenker’s diverticula?

A

there is loss of elasticity of the upper esophageal sphincter

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11
Q

how does zenker’s diverticula oropharyngeal dysphagia present?

A

progressive, intermittent then constant, solids and liquids

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12
Q

what are the symptoms associated with zenker’s diverticula?

A

gradual/insidious; vague symptoms at first–> coughing or throat discomfort; as diverticulum enlarges it will retain food leading to halitosis, spontaneous regurgitation, nocturnal choking, gurgling in the throat, protrusion in the neck, voice changes; palpable mass on the side of the patient’s neck?

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13
Q

how do you diagnose zenker’s diverticula?

A

video esophagography; barium swallow; DO BARIUM SWALLOW BEFORE EGD due to risk of perforation; EGD

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14
Q

what are the complications associated with zenker’s diverticula?

A

perforation (if EGD is done before barium swallow); weight loss; aspiration–> PNA/ lung abscess

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15
Q

what is an esophageal web?

A

a structural problem; thin, diaphragm-like membranes of squamous mucosa; congenital or acquired

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16
Q

where do esophageal webs occur?

A

proximal or mid esophagus (not the entire lumen)

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17
Q

when might you acquire esophageal webs?

A

eosinophilic esophagitis or plummer vison syndrome

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18
Q

what are the symptoms associated with esophageal webs?

A

it can cause oropharyngeal or esophageal dysphagia (if proximal–> oropharyngeal)

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19
Q

what are the characteristics of the presentation of esophageal webs?

A

dysphagia to solids, intermittent symptoms, not progressive

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20
Q

how do you diagnose esophageal web?

A

barium swallow (esophagram)–> best view; EGD can be done but it is less sensitive

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21
Q

what is the treatment/management for esophageal webs?

A

dilation (bougie dilator or pneumatic dilation); small endoscopic electrosurgical incision; persistent heartburn or need repeat dilation–> PPI long term

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22
Q

what population is at risk for plummer-vinson syndrome?

A

middle-aged, female>male

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23
Q

what is plummer-vinson syndrome?

A

combination of: symptomatic proximal esophageal webs, Koilonychia (spoon nails); angular chelitis; glossitis; iron-deficiency anemia

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24
Q

what is sjogren syndrome?

A

autoimmune/rheumatologic cause of oropharyngeal dysphagia; motility/propulsion problem; exocrine gland problem

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25
Q

what are the characteristics of the presentation of sjogren’s syndrome?

A

female> male, mid 50s, post menopausal; constant, not progressive, solids

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26
Q

what are the symptoms in sjogren’s syndrome cause by?

A

sicca symptoms (DRY)–> dry mouth, parotid or other major salivary gland enlargement; dry eyes

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27
Q

how do you diagnose sjogren syndrome?

A

minor salivary gland biopsy, salivary and tear production (Schirmer) testing, and serology: polyclonal hypergammaglobulinemia, anti Ro and anti La

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28
Q

what are the complications associated with sjogren’s syndrome?

A

increased incidence of oral infection (oral and esophageal candida); dental caries; strong association with B-cell non-Hodgkin lymphoma

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29
Q

what are the characteristics of esophageal dysphagia?

A

food sticks in the mid to lower sternal area; may have regurgitation, aspiration, or odynophagia; both solids and liquids

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30
Q

what is schatzki’s ring?

A

structural problem; smooth, circumferential, thin mucosal (band) structures, distal; GERD might be a possible etiology

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31
Q

what is schatzki’s ring associated with?

A

hiatal hernia

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32
Q

what are the characteristics of presentation of schatzki’s ring?

A

esophageal dysphagia, solids, intermittent symptoms and not progressive; reflux symptoms are common; steakhouse syndrome

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33
Q

what is steakhouse syndrome?

A

large, poorly chewed food bolus (like steak) is a typical instigator

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34
Q

how do you diagnose schatzki’s ring?

A

barium swallow (esophagram)–> best view; EGD can be done but is less sensitive

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35
Q

how do you treat schatzki’s ring?

A

dilation (bougie dilator or pneumatic dilation); small endoscopic electrosurgical incision; persistent heartburn or need repeat dilation–> PPI long term

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36
Q

what are the complications associated with schatzki’s ring?

A

food bolus impaction–> perforation or ulcer

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37
Q

what is an esophageal stricture?

A

structural problem; most common is peptic secondary to GERD, also can occur because of eosinophilic esophagitis, caustic ingestions, and radiation therapy

38
Q

where are most of the esophageal strictures located?

A

at the gastroesophageal junction

39
Q

how does an esophageal stricture present?

A

esophageal dysphagia, heartburn and potential weight loss, gradual (months-years); progressive; solids–> solids and liquids

40
Q

what happens as an esophageal stricture progresses?

A

reflux/heartburn lessens/improves because the stricture acts as a barrier to reflux

41
Q

how do you diagnose esophageal stricture?

A

barium swallow; endoscopy (EGD) with biopsy

42
Q

what is mandatory in all cases of esophageal stricture?

A

endoscopy (EGD) with biopsy- to differentiate peptic stricture from stricture by esophageal carcinoma

43
Q

what is the treatment/management of esophageal strictures?

A

pneumatic dilation at the time of endoscopy (EGD); long-term therapy with a proton pump inhibitor

44
Q

What is barrett esophagus?

A

specialized intestinal (metaplastic) columnar metaplasia that replaces the normal squamous mucosa of the distal esophagus; proximal displacement of the squamocolumnar junction

45
Q

what are the risk factors for barrett esophagus?

A

it is a complication of GERD; truncal obesity

46
Q

what can barrett esophagus progress to?

A

esophageal adenocarcinoma

47
Q

who is the group at greatest risk for barrett esophagus?

A

obese white males older than 50 who smoke

48
Q

what are the symptoms of barrett esophagus?

A

BE, in and of itself, does not provoke specific symptoms–> GERD has symptoms; so they patient may have a long history of reflux symptoms

49
Q

how do you diagnose barrett esophagus?

A

if a person has the risk factors for it, screening EGD for barrett esophagus should be considered; EGD with biopsy

50
Q

when is the EGD positive for barrett esophagus?

A

when there is a presence of orange, gastric type epithelium that extends upward from the stomach into the distal 1/3 tubular esophagus in a tongue-like or circumferential fashion

51
Q

when will a biopsy of barrett esophagus be positive?

A

if there are goblet and columnar cells

52
Q

what is the treatment/management of barrett esophagus?

A

acid reduction (PPI»H2 receptor antagonist (control reflux symptoms and may reduce the risk of cancer; but does not appear to cause regression of barrett esophagus); endoscopic ablation: high grade dysplasia or intramucosal adenocarcinoma; surgical resection (esophagectomy–> high morbidity and mortality: NOT recommended)

53
Q

how often should a surveillance endoscopy be performed for barrett esophagus?

A

every 3-5 years for those who have BE or have a high risk of CA; you are monitoring for adenocarcinoma

54
Q

what are the risk factors for adenocarcinoma?

A

chronic GERD, hiatal hernia, obesity, white race, male gender, and age older than 50

55
Q

what type of abnormality is squamous esophageal cancer?

A

structural problem

56
Q

what is the most common type of esophageal cancer in the world?

A

squamous esophageal cancer

57
Q

what are the risk factors for squamous esophageal cancer? (environmental/ habbits)

A

smoking, alcohol use (smoking+ alcohol= synergistic)

58
Q

what esophageal disorders are a risk factor for squamous esophageal cancer?

A

achalasia, HPV, plummer-vinson syndrome, tylosis

59
Q

what caustic esophageal disorders are a risk factor for squamous esophageal cancer?

A

chemical or thermal injury: caustic ingestion, hot beverages, radiation (5-10 years ago), Betel nuts

60
Q

how does squamous esophageal cancer present?

A

progressive dysphagia–> solid food and then solid and liquid food; males»females, african americans»> Caucasians; weight loss and anorexia; pyrosis, bleeding

61
Q

how do you diagnose squamous esophageal cancer?

A

EGD with biopsy: middle 1/3 of the esophagus

62
Q

what is the treatment/management for squamous esophageal cancer?

A

surgery (esophagectomy)

63
Q

what is the prognosis like for squamous esophageal cancer?

A

even when detected as a small lesion, esophageal cancer has poor survival because of the abundant lymphatics leading to regional lymph node metastases

64
Q

what type of abnormality is adenocarcinoma esophageal cancer?

A

structural problem

65
Q

what is the most common type of esophageal cancer in the USA?

A

adenocarcinoma

66
Q

what are the risk factors for adenocarcinoma esophageal cancer?

A

obesity, smoking, achalasia; GERD–> barrett metaplasia–> dysplasia–> adenocarcinoma

67
Q

what is the typical presentation for adenocarcinoma esophageal cancer?

A

progressive dysphagia (solid food–> solid and liquid); males> females, caucasians> african americans; >50 years old; weight loss, pyrosis, bleeding

68
Q

how do you diagnose adenocarcinoma esophageal cancer?

A

EGD with biopsy: distal 1/3 of esophagus

69
Q

what would the biopsy look like in a patient with adenocarcinoma esophageal cancer?

A

squamous–> columnar epithelium

70
Q

what is the treatment/management for adenocarcinoma esophageal cancer?

A

endoscopic therapy (ablation) (esophagectomy used to be, but has a high morbidity and mortality rate)

71
Q

what type of abnormality is achalasia?

A

motility abnormality–> propulsion problem

72
Q

what occurs in achalasia?

A

loss of peristalsis (distal 2/3) and failure of deglutitive lower esophageal sphincter relaxation; denervation of the esophagus resulting primarily from loss of nitric oxide-producing inhibitory neurons (ganglion cells) in the myenteric plexus

73
Q

what is the relationship between achalasia and age?

A

incidence increases with age

74
Q

who is at risk for secondary achalasia?

A

chagas disease–> patients from endemic regions (mexico, central and south america

75
Q

how does achalasia present?

A

gradual onset (months-years); progressive; solids and liquids; regurgitation of undigested foods; nocturnal regurgitation; substernal chest discomfort; they describe adaptive maneuvers (eating slowly and lifting the neck or throwing the shoulders back to enhance esophageal emptying)

76
Q

what might the physical exam show in a patient with achalasia?

A

weight loss; for secondary achalasia: swelling, romana sign, arrhythmias, and fever

77
Q

what is romana sign?

A

seen in secondary achalasia: unilateral painless swelling around the eye

78
Q

how do you diagnose achalasia?

A

labs: peripheral blood smear shows Trypsanosoma cruzi parasite (if it is secondary); barium esophagram; EGD: ALWAYS PERFORMED; biopsy; esophageal manometry: CONFIRMS DIAGNOSIS

79
Q

what does a barium esophagram show for patients with achalasia?

A

“bird’s beak” smooth, symmetric tapering of the distal esophagus; characteristic findings: esophageal dilation, loss of esophageal peristalsis, poor esophageal emptying

80
Q

why is an EGD always performed in cases of achalasia?

A

to exclude a distal stricture or a submucosal infiltrating carcinoma

81
Q

what does a biopsy of achalasia show?

A

loss of ganglion cells within the esophageal myenteric plexus

82
Q

what confirms diagnosis of achalasia?

A

esophageal manometry; it shows complete absence of normal peristalsis and incomplete lower esophageal sphincter relaxation with swallowing

83
Q

what is the treatment/management for achalasia?

A

reduce LES pressure using nitrates and calcium channel blockers or botulinum toxin injection during endoscopy; pneumatic balloon dilation (risk of perforation or bleeding); surgery; antiparasitic treatment in chagas

84
Q

what happens if you don’t treat achalasia?

A

without treatment the esophagus may become markedly dilated

85
Q

what type of abnormality is scleroderma?

A

a motility abnormality: propulsion problem

86
Q

what is scleroderma?

A

it is an autoimmune disease (smooth muscle fibrosis)

87
Q

what is the presentation of scleroderma?

A

30-60 years old, female> male, progressive, esophageal dysphagia (mainly solids but some liquids)

88
Q

what are the symptoms associated with diffuse scleroderma?

A

chronic heartburn (incompetent LES–> reflux esophagitis or stricture); malnutrition, xerostomia, dysphagia, gastroparesis, GAVE syndrome, chronic diarrhea

89
Q

what are the symptoms associated with limited scleroderma?

A

CREST syndrome: calcinosis cutis, raynaud’s, esophageal dysmotility, sclerodactylt, telangiectasias

90
Q

how do you diagnose scleroderma?

A

labs: serology: topisomerase I antibodies (Scl-70) for diffuse scleroderma; anti-centromere antibodies for limited scleroderma; barium esophagram; EGD can be done

91
Q

what is the treatment/management for scleroderma?

A

no approved disease modifying therapy; control symptoms (PPI) and slow progression to improve quality of life and prolong survival

GI II (20 decks)

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