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GI > Diseases and pathology of the esophagus > Flashcards

Diseases and pathology of the esophagus Flashcards

1
Q

difficulty swallowing –> nasal regurgitation, aspiration

A

dysphagia

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2
Q

neurologic etiologies of propulsive/motility oropharyngeal diseases

A

stroke, ALS, Parkinson’s, MS, Polio

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3
Q

muscular etiologies of propulsive/motility oropharyngeal diseases

A

myasthenia gravis, muscular dystrophy, muscle injury (surgery, radiation therapy)

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4
Q

Zenker’s diverticulum, crycopharyngeal bar, thyromegaly, fibrosis

A

benign structural oropharyngeal diseases

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5
Q

outpouching of esophagus –> food regurgitation or bacterial colonization (halitosis)

A

Zenker’s diverticulum

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6
Q

Malignant structural oropharyngeal diseases

A

Squamous cell carcinoma of the tongue, oropharynx, soft palate or upper larynx

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7
Q

dysphagia to BOTH solids and liquids, chest pain

excluding structural lesion

A

esophageal motility disorders

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8
Q

Etiologies of esophageal motility disorders

A

Achalasia, spastic disorders of the esophagus, weak peristalsis, scleroderma

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9
Q

diagnosis of esophageal motility disorders

A

exclude structural lesion (upper endoscopy or barium esophagram), esophageal manometry

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10
Q

idiopathic, impaired relaxation of LES

A

achalasia

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11
Q

achalasia epidemiology

A

both genders, all races, adults

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12
Q

Achalasia manometry findings

A

Type I (classic) = swallowing –> no significant change in esophageal pressurization

Type II = swallowing –> simultaneous pressurization spanning entire esophagus length

Type III (spastic) = swallowing –> abnormal, lumen obliterating contractions/spasms

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13
Q

treatment of Type II achalasia

A

botox, pneumatic dilation, surgical myotomy

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14
Q

pathophysiology of achalasia

A

loss of inhibitory neurons in myenteric plexus –> unopposed excitatory (cholinergic) neurons –> hypertensive nonrelaxed esophageal sphincter

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15
Q

Direct mechanical obstruction of LES

A

pseudoachalasia

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16
Q

Causes of pseudoachalasia

A

infiltrative submucosal invasion, paraneoplastic, Chagas disease

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17
Q

medical treatment for achalasia

A

if contraindications to dilation or surgery

nitrates, Ca channel blockers, sildenafil

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18
Q

multisystem disorder featuring obliterative small vessel vasculitis, fibroses of mutiple organs

GI = smooth muscle atrophy and gut wall fibrosis

A

scleroderma

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19
Q

peristalsis preserved

due to overactivity of excitatory nerves or overreactivity of smooth muscle response

A

spastic disorders of the esophagus

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20
Q

dysphagia to solids, and eventually liquids much later
weight loss (ominous)
heartburn (sometimes)

A

structural esophageal dysfunction

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21
Q

strictures (GERD, caustic), Schatzki’s ring, eosinophilic esophagitis, extrinsic compression

A

benign structural esophageal disorders

22
Q

Malignant structural esophageal disorders

A

Esophageal cancer (adenocarcinoma, SCC), metastasis (rare), direct invasion

23
Q

DYSPHAGIA TO SOLIDS, painless, regular/daily basis sx, weight loss

A

esophageal stricture

24
Q

treatment of benign esophageal stricture

A

endoscopic dilation using balloons or sequential commercial dilators

25
Q

infiltration of eosinophils in esophagus. food avoidance, dysphagia

A

eosinophilic esophagitis

26
Q

EoE demographics

A

white, middle aged men

associated with atopy, asthma, allergies

27
Q

EoE treatment

A

3D’s

Drugs (TOPICAL steroids), diet, dilation

28
Q

dietary treatment of EoE

A

eliminate milk, eggs, wheat, soy, seafood, nuts

29
Q

post-prandial (after meal) heartburn, regurgitation with acidic taste, relieved by antacids or anti-secretory meds

A

GERD

30
Q

Causes of GERD

A

inappropriate LES relaxation, hiatal hernia, surgery

rare: Zollinger-Ellison, Sjogren’s, Scleroderma

31
Q

Risk factors for GERD

A

obesity, tobacco, meds, pregnancy

32
Q

complications of GERD

A

erosive esophagitis, Barrett’s esophagitis

33
Q

Barrett’s esophagus

A

acid –> change in esophageal epithelium from squamous to columnar

34
Q

risk factors for Barrett’s esophagus

A

old, fat, white men

35
Q

Complications of Barrett’s esophagus

A

risk of adenocarcinoma

36
Q

Treatment of Barrett’s esophagus

A

Endoscopic ablation of Barrett’s tissue

endoscopic resection of visible lesions

37
Q

infectious etiologies of esophagitis

A

fungal (candida), viral (HSV)

38
Q

EGD –> punched out ulcers

histology –> viral inclusions

A

herpetic esophagitis

39
Q

EGD –> white plaques

histology –> long, thin eosinophilic inclusions

A

candida esophagitis

40
Q

EGD –> ringed esophagus, linear furrows

histology –> many eosinophils

A

eosinophilic esophagitis

41
Q

disorders leading to functional esophageal obstruction

A

nutcracker esophagus, diffuse esophageal spasm, hypertensive LES, achalasia

42
Q

disorders leading to structural esophageal obstruction

A

diverticula, esophageal mucosal webs/rings, congenital abnormalities, benign esophageal stenosis, tumors

43
Q

congenital anomalies resulting from failure of the foregut to divide into trachea and esophagus during the 4th week of embryonic development

A

esophageal atresia and tracheoesophageal fistula

44
Q

food regurgitation, drooling, aspiration

A

esophageal atresia and tracheoesophageal fistula

45
Q

which form of tracheoesophageal fistula is associated with repeated bouts of pneumonia?

A

H shape

46
Q

diffuse esophageal spasms

barium swallow –> corkscrew pattern

A

corkscrew esophagus

47
Q

barium swallow –> megaesophagus with “bird beak” at lower esophagus

A

achalasia

48
Q

EGD –> Mallory-Weiss tears

A

alcohol intoxication –> severe retching or vomiting

49
Q

esophageal varicies

A

cirrhosis

50
Q

Barrett’s esophagus histology –> elongated dark nuclei

A

low-grade dysplasia

51
Q

Barrett’s esophagus histology –> rounded nuclei, crowded glands

A

high-grade dysplasia –> high risk for adenocarcinoma progression

GI (19 decks)

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