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GI II Exam 1 > Chapter 17: Congenital Disorders and Neoplasms of the ESO > Flashcards

Chapter 17: Congenital Disorders and Neoplasms of the ESO Flashcards

1
Q

What are the 4 types of congenital abnormalities of the esophagus?

A
  1. Obstruction
  2. Achalasia
  3. Esophagitis
  4. Neoplasms
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2
Q

The GI tract is a common site of developmental abnormalities. In these cases, defects of what other organ should be considered?

A

defects of other organs that develop in the same embryonic period should be sought

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3
Q

__________ are structural developmental anomalies that disrupt normal GI transit and typically present early in life.

A

Atresia and fistulae

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4
Q

Intestinal atresias are _____ common than esophageal atresias but often involve the _____.

A

less

duodenum

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5
Q

____________ is the most common form of congenital intestinal atresia, while the

__________ is the most common site of fistulization.

A
  • Imperforate anus
  • Esophagus
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6
Q

Imperforate anus is a result of what embryologically?

A

Cloacal diaphragm does not involute

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7
Q

When are atresia, fistula and duplications of the esophagus discovered?

Treated?

A
  • Shortly after birth, due to regurg when eating.
  • W/o surgery, cannot live.
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8
Q

What is esophageal atresia?

A
  • Incomplete development of the esophagus.
  • Thin, non-canalized cord replaces part of esophagus and causes mechanical obstruction.
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9
Q

What is the most common form of esophageal atresia?

A

Atresia with associated fistula at/near birfurcation of trachea

  • Upper segment of esophagus is blind
  • Fistula b/w lower segment and trachea, most commonly at or near bifurcation of trachea

*Figure B is most common

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10
Q

Are a fistula & atresia always present together?

A

No (C) is just a fistula

(A) is just atresia.

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11
Q

Fistulas of the esophagus can lead to what sxs?

A
  1. Aspiration
  2. Suffocation
  3. Pneumonia
  4. Severe fluid/electrolyte imbalances
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12
Q

_____________ an incomplete form of atresia where lumen is narrow d/t fibrous

thickening of the wall, causing partial or complete obstruction.

Most often involves what parts of the GI tract?

A

Stenosis

-ESO and SI

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13
Q

Developmental abnormalities of the the esophagus are associated with what other defects?

A
    • Congenital heart defects
    • GU malformation
    • Neurologic disease
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14
Q

When congenital GI disorders are present, what other associations should we consider?

A

VACTERL associations

  • Vertebral
  • Anal anomalies
  • Cardiac
  • TE fistula
  • Renal anomalies
  • Limb anomalies
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15
Q

Diaphragmatic hernia occurs when?

If severe, what happens?

A
  • Incomplete formation of the diaphragm allows the abdominal viscera to herniate into the thoracic cavity.
  • When severe, can cause pulmonary hypoplasia => incompatible with life
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16
Q

Difference between omphalocele and gastroschisis?

A
  • Omphalocele: abdominal musculature does not close completely, abdominal viscera herniates outside of abdomen into ventral membranous sac.
  • Gastroschisis is similar, but involves ALL layers of abdominal wall (peritoneum => skin) = all organs exposed
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17
Q

What is the most frequent site of ectopic gastric mucosa and what is it referred to here?

May result in what problems?

A
  • Upper 1/3 of esophagus (Inlet patch)
  • Dysphagia, esophagitis, Barrett esophagus, or rarely, adenocarcinoma
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18
Q

What are examples of ectopia seen within the GI tract?

A
  • Ectopic pancreatic tissue: in stomach or esophagus
  • Gastric heterotropia: patches of ectopic gastric mucosa in the small bowel or colon
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19
Q

Gastric heterotropia may present with what signs/symptoms?

A

Occult blood loss due to peptic ulceration of adjancent mucosa

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20
Q

What is the most common true diverticulum and where does it occur?

A
  • Meckel diverticulum
  • Ileum
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21
Q

Cause of Meckel Diverticulum?

A

Failed involution of vitelline duct

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22
Q

What is the rule of 2’s in regards to Meckel Diverticulum?

A
  • 2% of population
  • 2x more common in males
  • Symptomatic by age 2 (only 4% are ever symptomatic!)
  • Present within 2 ft of ileocecal valve
  • 2 in. long
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23
Q

What may be present in a Meckel Diverticulum that causes symptoms and what are these symptoms?

A
  • Mucosal lining of Meckel diverticula can resemble the NL SI.
  • However, ectopic pancreatic and gastric tissue can be present, which will secrete acid and cause peptic ulceration of adjancent SI tissue –> occult bleeding or abdominal pain resembling appendicitis or obstruction.
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24
Q

Which sex is most commonly affected by congenital hypertrophic pyloric stenosis?

A

M (3-5x more likely)

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25
Q

Which genetic disorders are associated with an increased risk of Pyloric Stenosis?

A
  1. Turner syndrome
  2. Trisomy 18
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26
Q

Which enviornmental factors have been linked to an increased risk of developing pyloric stenosis?

A

Erythromycin or azithromycin exposure, orally or via mother’s milk in first 2 weeks of life

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27
Q

When and how does congenital hypertrophic pyloric stenosis typically present?

A
  • Between 3rd - 6th weeks of life
  • New onset regurgitation w/ projectile, NON-bilious vomiting after eating w/ frequent demands of re-feeding
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28
Q

What is found on PE with a congenital hypertrophic pyloric stenosis?

What is tx?

A
  • Firm, ovoid, 1-2 cm abdominal mass
  • Tx = myotomy (splitting of muscle) is curative
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29
Q

What is Hirschsprungs disease (megacolon)?

A
  • Absence of ganglion cells, derived from NC, in the colon that begins at the rectum => extends proximal, causing
    • proximal dilation
    • functional obstruction of the bowel
    • loss of coordinated peristatlic contractions.
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30
Q
  • What causes the absence of ganglion cells in Hirschsprungs disease (congenital megacolon)?
  • Affects proximal and distal intestinal segment how?
A
    • Migration of NCC from cecum to rectum is arrested prematurely
    • OR when ganglion cells undergo premature death
    • Proximal segment: dilated
  • - Distal segment: lack both the Meissner submucosal and Auerbach myenteric plexus
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31
Q

Which genetic abnormality can account for the majority of familial cases of Hirschsprung disease?

A

LOF mutation of RET (receptor tyrosine kinase)

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32
Q

How does Hirschsprung disease typically present?

A
  1. Failure to pass meconium in the immediate postnatal period.
  2. => Obstruction or constipation
  3. => Abdominal distension and bilous vomitting
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33
Q

What are the major threats to life in regards to Hirschsprung disease?

A
  1. Enterocolitis
  2. Fluid/electrolye imbalance
  3. Perforation
  4. Peritonitis
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34
Q

Diagnosis of Hirschsprung disease requires what?

Which stain can be used?

A
  • Documenting absence of ganglion cells within affected segment
  • Immunohistochemical stains for acetylcholinesterase for ganglion cells
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35
Q

Which part of the colon is ALWAYS affected in Hirschsprung Disease?

A

Rectum

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36
Q

What are some causes of acquired megacolon?

Which is associated with loss of ganglion cells and which aren’t?

A
  • Chagas disease —> Trypanosoma cruzi (Reduviid bug) = loss of ganglion cells
  • Other causes that are NOT associated w loss of ganglion cells
    • ulcerative colitis
    • inflammatory stricture
    • obstruction by neoplasm
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37
Q
  • Esophagus is a tube that delivers digested food and fluids to the stomach.
    • Structural (mechanical) obstruction or functional obstruction can prevent this. How functional obstruction prevent delivery of food & fluids to stomach?
A

Discruption of coordinated peristaltic contractions that occur after we swallow.

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38
Q

__________ allows us to categorize 3 types of esophageal dysmotility.

What are they?

A
  1. Nutcracker esophagus
  2. Diffuse esophageal spasm
  3. Hypertensive lower esophageal sphincter (LES)
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39
Q

What is nutcracker esophagus?

A

Long, high amplitude contractions in the distal esophagus that are cause some loss of NL coordination (NL coordination in proximal).

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40
Q

What is diffuse esophageal spasm?

A
  • Diffuse, uncoordinated contractions (repetitive and simultantous) of the esophagus (corkscrew)
    • On manometry: no high pressure
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41
Q

On Barium swallow, which esophageal obstruction looks like a corkscrew?

A

Diffuse esophageal spasm

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42
Q

What do the following show on Esophageal manometry?

    • Nutcracker ESO
    • Diffuse esophageal spasm
    • Hypertensive LES
A
  • Nutcracker ESO: high pressure at baseline, but relaxes normally
  • Diffuse esophageal spasm: LES function is NL
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43
Q

What is hypertensive lower esophageal sphincter?

A
  1. High resting pressure of LES
  2. Incomplete relaxation

W/O alterations in the patterns of esophageal contraction.

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44
Q

How can hypertensive LES be differentiated from achalasia?

A

Achalasia: ↓ esophgeal peristaltic contractions

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45
Q

Esophageal dysmotility causes ___________, which can result in the formation of ___________.

A
  • ↑ wall stress
  • small diverticulae, primarily the epiphrenic divertiulum, located above the LES.
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46
Q

What can form a Zenker diverticulum?

A

Impaired relaxation and spasm of the cricopharyngeaus muscle after swallowing => increased pressure in distal pharynx => Zenkers diverticulum.

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47
Q

Where does Zenkers diverticulum (_________ diverticulum) form?

A
  • Pharyngoesophageal diverticulum
  • RIGHT above the upper esophageal sphincter
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48
Q

When do Zenker Diverticulae most commonly develop (age)?

What symptoms do they cause when small vs large?

A
  • 50s
  • Small (asymptomatic); large (accumulate food and cause regurg and halitosis)
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49
Q

What are causes of mechanical obstruction of the esophagus?

How does it present?

A
  • Strictures/stenosis or cancer
  • Progressive dysphagia that begins with inability to swallow solids => liquids. However, because it happens slowly, patients may subconsciously change their diet to favor soft foods and not notice it until obstruction is almost complete.
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50
Q

Fibrous thickening of the submucosa, causing lumen of esophagus to narrow most often due to inflamation/scarring due to GERD, irradiation or caustic injury.

  • Muscularis propia begins to atrophy and there is secondary epithelial damage.
A

Esophageal stenosis (benign)

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51
Q

How can we differentiate functional obstruction/ benign strictures vs. malignant strictures?

A
  • Functional obstruction/ benign strictures: can maintain weight and appetitie
  • Malignant strictures: WL
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52
Q

How are esophageal mucosal webs and esophageal rings (Schatzki rings) different?

A
  • Esophageal mucosal webs are ledge-like semi-circumferential protrusions of fibrovascular CT and overlying epithelium.
    • MC: proximal or mid ESO
  • Schatzki rings are circumferential, thicker and include [mucosa, submucosa and hypertrophic muscularis propria].
    • MC: distal ESO
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53
Q

Esophageal mucosal webs most often occur in whom?

Associated with what other diseases?

A
  • Woman >40 yo
  • GERD, chronic GVHD, or blistering skin diseases
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54
Q

What are the characteristic findings in Plummer-Vinson syndrome?

A
  • Esophageal mucosal webs in the upper esophagus
  • Iron-deficiency anemia
  • Glossitis (beefy red tongue)
  • Cheilosis (cracking of corners of mouth)
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55
Q

Esophageal rings located _____________ are called A rings; whereas those located ________________ are called B rings.

A
  • A rings = above GE junction
  • B rings = at the squamocolumnar junction
56
Q

What type of mucosa are A and B Schatzki rings covered by?

A
  • A rings = squamous mucosa
  • B rings = gastric cardia type of mucosa
57
Q

Esophageal webs causes ___________ dysphagia.

A

Non-progressive dysphagia associated w/ incompletely chewed food

58
Q

When we swallow, what normally allows LES to relax?

A
  1. Inhibitory neurons release NO and vasoactive intestinal polypeptides
  2. Normal cholinergic signaling is interrupted.
59
Q

What is the triad of Achalasia?

A
    1. Incomplete LES relaxation
    1. Increased LES tone
    1. Aperistalsis of esophagus
60
Q

Achalasia causes _______ dysphagia and…

A
  1. Progressive/gradual dysphagia for solids + liquids
  2. Hard time burping
  3. Chest pain
61
Q

Primary achalasia is the result of what?

What nerve/nucleus may be affected?

A
  • Degeneration of the inhibitory neuronal (ganglion cells) in distal esophagus
  • Extraesophageal vagus n. and dorsal motor nucleus may also undergo degenerative changes
62
Q

Secondary achalasia may arise in relation to infection by what bug?

What are the characteristics of this type of achalasia?

A

Chagas disease (Trypanosoma cruzi), causing

  1. Destruction of myenteric plexus (duodenal, colonic and uteric)
  2. Failure of peristalsis
  3. Esophageal dilation
63
Q

Linkage of achalsia to which immune disorders suggest that achalasia may also be driven by immune-mediated destruction of inhibitory esophageal neurons?

A
  1. HSV1 infection
  2. Immunoregulatory gene polymorphisms
  3. Sjorgen syndrome
  4. Autoimmune thyroid disease
64
Q

What are 3 treatment options for both primary and secondary achalasia?

A

1) Surgery (Laparoscopic myotomy)
2) Pneumatic balloon dilation
3) ↓ LES pressure (BOTOX injection, to inhibit LES cholinergic neurons)

65
Q
  1. Complete absence of NL peristalsis
  2. Incomplete LES relaxation w swallowing.
A

Achalasia

66
Q

_________ can result from chemical or infectious mucosal injury.

Infection is most common in _____________.

A
  • Esophagitis
  • Immunocompromised
67
Q

What are the 2 main sx related to pathology of GI tract?

A
  1. Abdominal pain
  2. GI hemorrhage
68
Q

_____ blood loss of the GI tract is a medical MRGC.

A

Acute blood loss

69
Q

Which are more common: UGI bleeds or LGI bleeds?

A

UGIB

70
Q

ID the source of bleeding based on the character of blood:

Vomiting bright red blood (hememesis)

A

If GI, most likely proximal to the ligament of Trietz.

71
Q

ID the source of bleeding based on the character of blood:

Black, tarry stool (melena)

A

Upper GI bleed

72
Q

ID the source of bleeding based on the character of blood:

Bright, red blood in rectum (hematochezia)

A

Lower GI bleed (or very rapid UGI bleed)

73
Q

Esophageal causes of vomitting of bright red blood (hematemesis)

A
74
Q

Mallory-Weiss tears are what?

A
  • Longitudinal, incomplete mucosal tears (only mucosa and submucosa) on the gasdtric side of the GE junction, which may extend to the distal ESO.
75
Q

Mallory-Weiss tears are most commonly associated/caused by what?

A
  1. Severe retching (i.e., bulimia)
  2. Vomiting secondary to acute alcohol intoxication
76
Q

What is Boerhaave syndrome and how does it compare to Mallory-Weiss tears?

A
  • Much less common, but MORE severe
  • Transmural tearing and rupture of the distal esophagus
77
Q

What occurs in patients suffering from Boerhaave Syndrome and how do they present?

The pt presentation often includes what other differential dx?

A
  • Severe mediastinitis (air in mediastinum 2’ to perf. Esophagus)
  • Severe chest pain, tachypnea, and shock**
  • Subcutaneous emphysema
  • Initial diff dx usually includes an MI
78
Q

Which is considered a catastrophic event: Mallory-Weiss syndrome or Boerhaaves syndrome?

What do we hear on ausculatation?

A
  • Boerhaaves syndrome
  • Hamman’s signs: crunching sound due to pneumomediastinum
79
Q

Chemical or infectious esophagitis can cause what symptoms?

A

Range from: Odynophagia => hemorrhage, stricture or perforation.

80
Q

What are causes of chemical esophagitis in kids vs adults?

A
  • Kids: ingestion of household cleaning products
  • Adults: attempted suicide, causing severe damage
  • Other: pills, alkalis, acids
81
Q

What is pill-induced esophagitis?

A

Less severe chemical injury to the esophageal mucosa that occurs when pills lodge and dissolve, instead of going into stomach.

82
Q

Infectious esophagitis in healthy individuals in UNCOMMON and most often due to ___________.

A

HSV

83
Q

Viral esophagitis caused by Herpes virus is distinguished by what morphological characteristics?

A
  • Punched-out ulcers
  • Nuclear viral inclusions
84
Q

Infectious esophagitis in debilitated/immunospressed is MORE common and caused by what?

A
  1. HSV
  2. CMV
  3. Fungus
85
Q

Viral esophagitis caused by CMV is distinguished by what morphological characteristics?

A
  • Shallow ulcers
  • Nuclear and cytoplasmic inclusions (characteristic)
86
Q

Which fungi are the most common causes of esophagitis?

A
    • Candidiasis (most common)
    • Mucormycosis
    • Aspergillosis
87
Q

Esophagitis caused by what organism is characterized morphologically by gray-white, pseudomembranes composed of densely matted fungal hyphae and inflammatory cells covering the esophageal mucosa?

A

Candidiasis

88
Q

What is the most common viral cause of esophagitis?

A

Herpes simplex

89
Q

Pt presents with apoptosis of basal epithelial cells, atrophy of mucosa and fibrosis of submucosa of esophagus WITHOUT signifiant acute inflammatory infiltrates on histology. What is this?

A

Esophageal GVHD

90
Q

What are causes of LES relaxation?

A
  • 1. Vagal mediated pathways
  • 2. ↑ intra-abdominal pressure
  • 3. Obesity
  • 4. Hiatal hernia
  • 5. Delayed gastric emptying (gastroparesis)
  • 6. Idiopathic.
91
Q

What is the most common cause of esophagitis and the most common outpatient GI diagnosis?

A

Reflux esophagitis into the lower esophagus. (GERD)

92
Q

What is the most common cause of gastroesophageal reflux?

A

Transient relaxation of lower esophageal sphincter

93
Q

Recruitment of which immune cells are often seen morphologically with more severe injury as a result of GERD?

A
  • Eosinophils recruited into squamous mucosa
  • Followed by neutrophils
94
Q

What is pathogenic of reflux esophatitis d/t GERD

A

1. Eosinophils and neutrols in the squamous mucosa

2. Elongation of papilla in the lamina propria that ends to the upper 1/3

3. Basal zone hyperplasia

95
Q

What are some of the complications that may result from reflux esophagitis?

A
    • Ulceration
    • Hematemesis
    • Melena (dark sticky feces)
    • Stricture development (ulcer -> loss of mucosal layer –> fibrosis)
    • Barrett esophagus
96
Q

What are the symptoms of Eosinophilic Esophagitis in both adults and children?

A
  • Adults - food impaction and dysphagia
  • Children - feeding intolerance and GERD-like sx’s
97
Q

What is the cardinal histological feature of eosinophilic esophagitis?

i.e., large #’s of which cells and where

A

Large #’s of intraepithelial eosinophils, particularly superficially

98
Q

How is eosinophilic esophagitis different from GERD?

A
  • Acid reflux is NOT prominent
  • PPI’s usually do NOT provide relief
99
Q

The majority of patients with eosinophilic esophagitis are also what?

Many have what underlying disorders?

A

Atopic: genetic tendency to develop allergic diseases such as

  • Atopic dermatitis
  • Allergic rhinitis
  • Asthma
  • Modest peripheral eosinophilia
100
Q

What are 2 major causes of Esophageal Varices?

Normal route of blood flow?

A

1) Portal HTN (cirrhosis - alcoholic liver disease): collateral channels form where portal and caval systems communicated–> congested subepithelial and submucosal venous plexi in distal esophagus and prox. stomach
* - Left gastric vein —> Portal V.
2) Hepatic schistosomiasis - parasitic disease -> flukes (trematodes)

101
Q

Variceal hemorrhage is a medical emergency that can be treated how?

A
    • Inducing splanchnic vasoCONSTRICTION
    • Endoscopic sclerotherapy (inject thrombotic agents)
    • Balloon tamponade
    • Variceal ligation
102
Q

What are the signs/symptoms of esophaeal varices?

A
    • Esophageal bleeding
    • PAINLESS hematemesis
103
Q

In people with esophageal varices, ______ die initially and _____ recurr within a year.

A

30%;

50%

104
Q

Diseases that impede what flow cause the formation of esophageal varices, an important cause of esophageal bleeding.

A

Venous blood from the GI tract goes through the liver via the portal vein, before going to the heart => systemic circulation.

105
Q

What are symptoms of hiatal hernia?

A
  • Heartburn
  • Regurg of gastric juices
106
Q

What is a complication of chronic GERD?

A

Barrett esophagus:

  • Metaplasia of lower esophageal mucosa (stratified squamous epi —> nonciliated columnar epithelium w/ goblet cells)
107
Q

The greatest concern in Barrett esophagus is that it confers an increased risk of developing?

A

Esophageal adenocarcinoma

108
Q

Even though a vast majority of esophageal adenocarcinomas are associated with Barrett’s esophagus, what is important to remember?

A

Most individuals with BE do not develop esophageal tumors.

(0.2-2% have dysplasia)

109
Q

How is Barrets esophagus diagnosed?

A

Endoscopy and biospy, showing evidence of metaplastic columnar mucosa above GE junction.

110
Q

What does BE esophagus look like?

A

Patches of red, velvety mucosa the extend up from GE junction: pale squamous esophageal mucosa alternates with light brown gastric mucosa distally.

111
Q

When [Barretts esophagus + dysplasia], what do we see?

A
  1. Atypical mitosis
  2. Nuclear hyperchromasia
  3. Irregularly clumped chromatin
  4. ↑ nuclear-to-cytoplasm ratio
  5. Failure to epithelial cells to mature as they migrate to the esophageal surface
112
Q
  • BE w/o dysplasia
  • BE w/ low-grade dysplasia
  • BE w/ high-grade dysplasia

What are the chances of becoming adenocarcinoma?

A
  • 0.5%
  • 10%
  • 40%
113
Q

Which type of esophageal cancer is most common worldwide; which is becoming more prevalent?

A
  • Squamous cell carcinoma = more common worldwide
  • Adenocarcinoma is becoming more prevalent in the US and Western society
114
Q

Benign tumors of the esophagus are usually __________.

A

Mesenchymal

115
Q

Most esophageal adenocarcinomas arise from ____________.

A

Barretts esophagus

116
Q

What is the most likely factor contributing to the ↑ rates of esophageal adenocarcinoma, especially in the US?

A

Increased incidence of obesity-related GERD and Barrett Esophagus.

117
Q

What is associated w/ ↓ risk of esophageal adenocarcinoma?

A
  • Some types of H. pylori
  • Cause gastric atrophy –> ⇩ acid secretion and reflux
118
Q

Which ethnicity and sex is most commonly affected by esophageal adenocarcinoma?

Recent increased incidence in which populations?

A
  1. Caucasians
  2. Men 7x more likely
  3. Recent ↑ rates in: Hispanic men and White women
119
Q

Progression from Barrett Esophagus => Adenocarcinoma occurs over a period of time in a stepwise acquisition of genetic changes, which are seen early on and later in this progression?

A
  • Early: mutations of TP53 and downregulation of CDKN2A
  • Later: amplification of EGFR, ERBB2, MET, cyclin D1 and cyclin E
120
Q

Where in the esophagus does adenocarcinoma typically occur and where may it invade?

Major morphological characteristics?

A
  • Distal 1/3 of esophagus and may invade adjacent gastric cardia
  • Initially flat/raised patches —> large masses >5cm
  • Tumor produces mucin and forms glands
121
Q

How does a patient with an esophageal adenocarcinoma typically present (signs/symptoms)?

A
  1. Pain or difficulty swallowing
  2. Progressive weight loss
  3. Hematemesis
  4. Chest pain
  5. Vomiting
122
Q

By the time a patient presents with symptoms of esophageal adenocarcinoma, what has the cancer likely done?

How does this affect prognosis?

A
  • Spread to submucosal lymphatic vessels
  • Overall 5-year survival is <25%
    • If cancer is limited to the mucosa or submucosa the 5-year survival is closer to 80%
123
Q

Which gender has the greatest risk for esophageal SqCC of the esophagus and what is the typical age?

Which race of people are at the greatest risk?

A
  • >45 yo
  • Males 4x more
  • African Americans 8x more affected!!!
124
Q

Which part of the esophagus do the majority of squamous cell carcinomas begin?

A

Middle 1/3 of the esophagus

125
Q

Esophageal squamous cell carcinoma risk factors

A

- Alcohol and Tobacco use (major factor)

  • Achalasia –> rotting food –> irritation
  • Tylosis = thickening of palms and soles + white patches in mouth
  • Plummer-Vinson syndrome –> rotting food on ledge of web
  • Frequent consumption of hot beverages
  • Hx of Radiation to Mediastinum
  • HPV infection –> p16 + E6 + E7
126
Q

SqCC of the esophagus has a very high incidence in which 5 geographic locations?

A
  • - Iran
  • -China
  • - Hong Kong
    • Brazil
    • South Africa
127
Q

How does esophageal SCC begin?

Early appearane?

Late appearance?

A
  • Begins as in situ lesion (squamous dysplasia)
  • Early: small grey-white plaque thickenings
  • Late: exophytic tumor masses –> obstruct lumen
128
Q

Which genetic mutations play a role in the development of squamous cell carcinoma of the esophagus?

A
  • Amplification of SOX2
  • Over-expression of cyclin D1
  • Loss-of-function mutations in TP53, E-cadherin, and NOTCH1
129
Q

Which 3 structures surrounding the esophagus do SCC’s sometimes invade and what does this lead to in each?

A

1) Respiratory tree –> pneumonia
2) Aorta –> catastrophic exsanguination
3) Mediastinum/Pericardium

130
Q

Differentiate the esophageal cancer on the top from that on the bottom; what are the distinguishing morphological features?

A
  • Top: adenocarcinoma; often organized w/ glands
  • Bottom: SCC of the esophagus; moderately to well-differentiated w/o presence of glands
131
Q

HY: Cancers in the upper, middle, and lower 1/3 of the esophagus will have different sites of metastasis, what are they?

A
  • Upper 1/3: cervical LN’s
  • Middle 1/3: mediastinal/paratracheal/tracheobronchial LN’s
  • Lower 1/3: gastric and celiac nodes
132
Q

What are the common signs and symptoms of someone presenting with SCC of the esophagus?

What is seen if the tumor ulcerates?

A
  1. Progressive dysphagia (solids –> liquids)
  2. Odynophagia (painful swallowing)
  3. Pt’s alter diet so have impaired nutrition and prominent wt. loss
  • If tumor ulcerates => hemorrhage or sepsis w/ sx’s of iron deficiency anemia
133
Q

What is the association of TE fistula and SCC of the esophagus?

A

Often, the 1st sx’s of SCC are caused by aspiration of food via a TE fistula

134
Q

How has endoscopic screening impacted the prognosis of esophageal SCC?

What is the overall prognosis in the US?

A
  • 5-year survival of 75% if caught early while still superficial
  • Overall in the US 5-year survival remains <20%
135
Q

Tylosis (dry hands and feet), a risk factor for esophageal SCC, is a mutation in __________ and causes _________

A
  • RHBDF2 mutation
  • Howel-evans syndrome
136
Q
A

GI II Exam 1 (19 decks)

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