Esophageal Diseases Flashcards
(90 cards)
1
Q
What is atresia?
A
the esophagus segment comprises a thin, noncanalized cord with a proximal blind pouch connected to pharynx and distal pouch leading to stomach
2
Q
How is it discovered after birth?
A
immediate regurgitation after feeding
3
Q
How can atresia be treated?
A
surgery
4
Q
What are the late complications?
A
- GERD - acid reflux as stomach acid or bile irritate the esophagus lining 2. esophagitis - inflammation of the stomach caused by stomach acids backing up into the esophagus, infection, some medication and allergies
5
Q
Describe what atresia looks like?
A
- associated with fistula connecting the upper or lower pouch with the trachea or a bronchus 2. most common is a blind upper segment, fistula between blind lower segment and trachea
6
Q
What is achalasia? (cardiospasm, megaesophagus)
A
Esophageal motor disorder characterized by lack of progressive peristalsis and partial/incomplete relaxation of lower esophageal sphincter (LES) preventing passage of food into stomach
7
Q
What are the causes?
A
Chagas’disease (Trypanosoma cruzi destroys myenteric plexus of esophagus - common in South America)
8
Q
What are the symptoms?
A
- progressive dilation of esophagus above LES 2. variable wall thickness 3. absent myenteric ganglia in middle of esophagus 4. non gastric regurgitation
9
Q
Condition that can potentially arise cause of achalasia?
A
5% risk of esophageal squamous cell carcinoma
10
Q
Describe achalasia on a micro level?
A
depletion/absence of ganglion cells
11
Q
What is a hiatal hernia?
A
condition involving herniation of part of the stomach through an opening in the diaphragm - separation of diaphragmatic crura and widening of space between muscular crura and esophageal wall
12
Q
Which hernia is the most common?
A
sliding hernia - 95% : protrusion of stomach above diaphragm creates bell shaped dilation
13
Q
Describe the incidence?
A
1-20% of adults + increases with age 2. only 9% with sliding hernias have heartburn or regurgitation of gastric juices into the mouth
14
Q
How is this type of hernia accentuated?
A
- bending forward 2. lying supine 3. obesity
15
Q
What are the complications of this hernia?
A
- ulceration 2. bleeding 3. perforation 4. strangulation
16
Q
What are lacerations? (Mallory-Weiss syndrome)
A
longitudinal tears at gastroesophageal junction or in proximal gastric mucosa
17
Q
What are the causes?
A
severe wretching - associated with alcoholism (vomiting and reflux with alcoholic stupor)
18
Q
Describe the tears?
A
can be mucosal or full thickness
19
Q
Consequences of lacerations?
A
cause 5-10% of upper GI bleeds but are usually limited and surgery is not necessary
20
Q
Describe the treatment?
A
- support 2. vasoconstrictors 3. transfusions 4. balloon tamponade
21
Q
What is Boerhaave syndrome?
A
full thickness tear/esophageal rupture - may be lethal
22
Q
What are varices?
A
- Dilated tortuous vessels, usually submucosal, that develop due to portal hypertension 2. Collaterals in lower esophagus divert flow from portal vein, through coronary veins of stomach, into esophageal veins, into azygous veins, into vena cava
23
Q
Describe the incidence?
A
present in 90% of cirrhotic patients - associated with alcoholism
24
Q
What are the consequences of varices?
A
may rupture and cause massive hemorrhage
25
How can you detect death by an esophageal variceal hemorrhage?
1. blood stains at death scene 2. unusual body positions of deceased
26
What are the causes of varices?
1. portal hypertension 2.hepatic schistosomiasis - a disease caused by an infection with freshwater worms
27
Describe tretament?
1. sclerotherapy (injection of thrombotic agents) 2. balloon tamponade
28
State differential diagnoses for hematemesis? (vomitting blood)
1. gastritis 2. esophageal lacertaion 3. peptic ulcer
29
What is esophagitis?
epithelial damage and inflammation of the esophagus
30
What casues it?
gastroesophageal reflux - reflux of gastric contents into lower esophagus
31
Describe the histologic changes?
1. erosion 2. ulceration 3. exudation 4. subtle
32
What is the incidence of GERD in the population?
3-4% in general population - usually mild or moderate disease
33
What are the causes of GERD?
1. pregnancy 2. hiatal hernia 3. delayed gastric emptying (increased gastric volume)
34
Describe the epidemiology of GERD?
1. in adults over age 40 -2. occasionally in children
35
What are symptoms of GERD?
1. Pain may be mistaken for myocardial infarction 2. bleeding (almost never massive) 3. stricture 4. Barrett’s esophagus with possible Barrett’s ulcer
36
What is the pathophysiology of GERD?
chronic exposure to gastric juices impairs reparative capacity of esophageal mucosa - gastric acid injury to mucosa is critical
37
How do you diagnose?
1. clinical (heartburn, regurgitation) 2. intraesophageal pH monitoring 3. endoscopic and histologic examination
38
Describe the treatment?
1. motility promoting drugs 2. H2 receptor antagonists 3. proton-pump inhibitors 4. surgery to reduce hiatal hernia
39
Describe the gross histology?
hyperemic mucosa with focal hemorrhage
40
Describe the micro histology?
1. inflammatory cells in epithelial layer (eosinophils, neutrophils) 2. basal cell hyperplasia
41
Describe the epidemiology of infectious esophagitis?
1. immunocompromised 2. patients with diabetes or on antibiotic therapy
42
Causes of infectious esophagitis?
1. Candida 2. herpes simplex virus 3. cytomegalovirus
43
Candida is ussually associated with?
1. antibiotic use in non-immunocompromised 2. CMV 3. HSV esophagitis
44
Describe what is seen during endoscopy of infectious esophagitis?
gray-white pseudomembrane or plaques in mid- to distal esophagus
45
Describe the micro histology?
densely matted pseudohyphae and budding spores
46
Cytomegalovirus is usually associated with?
immunocompromised patients
47
Describe the gross histology?
punched out mucosal ulcers similar to herpes simplex
48
Describe the micro histology?
1. virus present in endothelium and enlarged stromal cells at ulcer base 2. Inclusions are intranuclear surrounded by clear halo
49
Describe herpes simplex?
1. an opportunistic infection in immunosuppressed patients 2. Self-limited in healthy patients; may cause esophageal perforation or disseminate in immunocompromised patients 3. Must rule out HSV infection in esophageal ulcers from immunocompromised patients
50
Describe the gross histology?
shallow vesicles and ulcers - may coalesce into extensive areas of erosion
51
Describe the micro histology?
1. ulcers contain necrotic debris and exudate with neutrophils 2. viral inclusions present in multinucleated squamous cells at margin of ulcer
52
What is Barrets esophagus?
Distal squamous mucosa is replaced by metaplastic columnar epithelium with goblet cells as a response to prolonged injury - is irreversible
53
Benefits of the columnar eptithelium?
more resistant to acid, pepsin and bile
54
Consequences?
major risk factor for esophageal adenocarcinoma (relative risk: 30-50), particularly in older white men
55
Epidemiology?
mean age at diagnosis is 60+ - usually men
56
Cause?
chronic gastroesophageal reflux
57
Symptoms?
long history of heartburn and other reflux symptoms
58
Gross histology?
1. red velvety GI type mucosa between pale squamous mucosa of lower esophagus 2. may have tongues extending up from GE junction or a broad band displacing the GE junction proximally 3. may have preserved squamous islands
59
Micro histology?
squamous epithelium replaced by columnar epithelium of intestinal type with goblet cells
60
Diagnosis?
Characteristic endoscopic appearance with histologic findings - Associated with hiatal hernia, peptic ulceration, esophageal stricture
61
Treatment?
1. anti-reflux therapy 2. endoscopy every 1-2 years to detect dysplasia or early adenocarcinoma
62
Describe Barretts high grade dysplasia?
up to 50% risk of invasive adenocarcinoma - should rebiopsy immediately to exclude “missed” carcinoma
63
Describe its treatment?
esophagectomy if diagnosis confirmed
64
Describe Barretts low grade dysplasia?
may progress to high grade dysplasia or carcinoma for up to 10 years
65
Describe its treatment?
give intense antireflux therapy and intense surveillance
66
Describe the micro histology of Barretts low grade dysplasia?
1. preservation of crypt architecture with minimal distortion 2. atypical nuclei limited to basal half of the crypts
67
Describe the micro histology of Barretts high grade dysplasia?
more severe atypia and architectural complexity than low grade dysplasia
68
Describe the transition normal squamous epithelium to adenocarcimona?
squamous epithelium - Barretts esophagus - low grade dysplasia - high grade dysplasia - adenocarcinoma
69
What is a carcinoma?
cancer
70
Describe the symptoms of carcinomas?
most patients are asymptomatic during early stages, they often present with advanced or metastastic disease
71
Describe the metastases locations of carcinomas?
metastases usually to liver, lungs, pleura
72
What is an adenocarcinoma?
a type of cancer that develops in the glands that line your lungs
73
Describe the epidemiology of adenocarcinomas?
1. 30-40% of primary esophageal cancers 2. Age 40+, usually white men
74
What are the diseases associated with adenocarcinomas?
in Barrett’s esophagus patients: 1. 73% had hiatal hernia 2. 63% were smokers 3. 45% alcohol users
75
What are the symptoms of adenocarcinomas?
none or gastroesophageal reflux disease
76
What is the mortality?
5 year survival 15-25%
77
What is the most common disease associated with adenocarcinomas?
85% arise in setting of Barrett’s esophagus
78
Describe the pathophysiology of adenocarcinomas?
1. Most present with invasion through esophageal wall (60-80%), often with nodal involvement (30-60%) 2. Tend to invade via submucosal lymphatics
79
What are the prognostic factors of adenocarcinomas?
1. depth of invasion 2. lymph node metastases 3. status of resection margins
80
Describe the gross histology?
usually distal esophagus with invasion of gastric cardia - appear as flat patches to nodular masses
81
Describe the micro histology?
moderate or well differentiated, usually mucin producing (intestinal type mucosa) - usually has adjacent Barrett’s mucosa with high grade dysplasia
82
What is squamous cell carcinomas?
cancer of the squamous cells of the esophagus
83
Describe the epidemiology?
1. Highest incidence in northern Iran, northern China - due to polycyclic aromatic hydrocarbons 2. South Africa 3. increasing incidence in Subsaharan Africa – HIV associated 4. most common esophageal cancer
84
What are the causes?
1. deficiency of vitamins A, C, thiamine, B6, riboflavin or zinc, molybdenum; fungal contamination, nitrates / nitrosamines, Betel nuts, alcohol, tobacco, urban environment 2. achalasia 3. corrosive strictures 4. long standing esophagitis 5. radiation therapy 6. HPV in high risk regions
85
What are the symptoms?
1. dysphagia 2. anorexia 3. weight loss
86
What is the usual location of squamous cell carcinoma?
90% in mid/lower esophagus - Often multifocal
87
Describe the pathophysiology?
1. Most present with invasion into muscularis propria 2. In resection specimens, 30-40% have invasion of adjacent mediastinal structures that may cause fistulas; 50% have lymph node metastases 3. Distant metastases to lungs, liver, bones, adrenal glands 4. Exfoliative cytology is accurate, particularly for lesions in lower 1/3 of esophagus; cytology plus biopsy is recommended
88
What are the prognostic factors?
the stage is most important
89
What is the gross histology?
1. deep irregular ulcers with nodular margins 2. gray-white plaque-like thickenings of mucosa 3. polypoid exophytic lesion
90
What is the micro histology?
most are moderate to well differentiated
