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GI, Liver, GallBladder, Pancreas > P- Oral Cavity and Esophagus > Flashcards

P- Oral Cavity and Esophagus Flashcards

1
Q

List the five causes of GI bleeding in order of most frequent to least frequent.

A
  1. gastric/duodenal ulcers
  2. gastric erosion
  3. varices
  4. Mallory Weiss tears
  5. gastric cancer
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2
Q 
Describe the structure of the esophagus.
It extends from where to where?
It is made of what kind of cells?
What type of muscle is present?
What does it lack that the rest of the GI system has?
A

It extends from the cricopharyngeus (UES) to just below the diaphragmatic hiatus (LES).

It is made of stratified squamous epithelium and has a squamocolumnar junction where it meets the stomach.

The top is skeletal muscle, the middle is skeletal and smooth and the lower portion is smooth.

It lacks serosa.

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3
Q

What is the significance of the esophagus lacking serosa?

A
  1. It rips/tears more easily

2. cancers are able to metastasize more easily

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4
Q

What 5 symptoms commonly present with problems of the esophagus?

A
  1. dysphagia
  2. odynophagia
  3. regurgitation
  4. chest pain
  5. heartburn
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5
Q

Describe the 4 microscopic layers of the esophagus from innermost to outermost.
(what is the structure/function)

A
  1. non-keratinized mucosa - stratified squamous epithelial lining and lamina propria lined by muscularis mucousa (thin muscle)
  2. Submucosa- loose connective tissue and mucus glands to keep esophagus moist
  3. Muscularis Propria - Thick muscular layers to propel food down
  4. Adventitia- loose connective tissue [NO SEROSA]
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6
Q

What is achalasia?

What is a potential cause in Central/South America?

A

Inflammation of myenteric plexus of the esophagus that leads to LES failure to relax and lack of peristalsis when swallowing.

T. cruzi is a potential cause

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7
Q

A patient presents with difficulty eating, weight loss, halitosis and regurgitation of undigested food. This has been gradual for months/years before seeking treatment. What is the likely cause?

A

achalasia

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8
Q

What are treatments for achalasia?

A

You cannot restore peristalsis, but you do want to decrease LES pressure.

  1. endoscopic balloon dilations
  2. myotomy (division of sphincter muscle)
  3. temporary relief with botox
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9
Q

What is a hiatal hernia? What are the 2 major types? Which is more common?
What complications can arise?

A

It is when part of the stomach protrudes above the diaphragm into the chest cavity

  1. sliding hiatal hernia- part of the stomach protrudes in the same plane as the esophagus ** most common
  2. Paraesophageal hiatal hernia- protrusion of stomach through enlarged hiatus. It can result in torsion of the stomach cutting off blood supply (medical emergency)
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10
Q

What is Mallory-Weiss Syndrome?

What are causes?

A

Violent vomiting or retching tears the esophagus longitudinally at the GE junction.

  1. bulimia
  2. chronic alcoholism

If it contaminates the mediastinum it is called Boerhaave syndrome.

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11
Q

What are gastro-esophageal varices?

A

dilation of the esophago-gastric venous plexus due to high portal venous pressure and large portal-systemic gradient

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12
Q

When portal venous pressure is increased because of fibrosis (usually due to chronic liver disease/cirrhosis), where does the blood divert?

A

Into PRE-EXISTING vascular channels that can connect portal system to the SVC and IVC.

  1. proximal stomach/lower esophagus
  2. falciform ligament (periumbilical)
  3. hemorrhoids
  4. retroperitoneal
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13
Q

In western countries, what are the 2 leading causes of portal hypertension and gastro-esophageal varices?

In less developed countries what is a major cause of varices?

A
  1. viral (Hep C)
  2. alcoholic cirrhosis

Less developed: schistosomiasis

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14
Q

How are variceal bleeds treated?

A
  1. IV drugs to lower portal pressure (b-blocker, somatostatin, vasopressin)
  2. endoscopic ligation with banding
  3. TIPS (transjugular intrahepatic porto-systemic) for uncontrolled or recurrent bleeds (stent to connect portal and hepatic veins bypassing the sinusoids)
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15
Q

What is the general definition of esophagitis?

What are the 5 types?

A

injury of the esophageal mucosa with subsequent inflammation.

  1. GERD
  2. infectious
  3. eosinophilic esophagitis
  4. “pill” esophagitis/irritant/corrosive
  5. chemoradiation esophagitis
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16
Q

What are the 3 main types of infective esophagitis?

A
  1. HSV (usually 1)
  2. CMV
  3. Candida
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17
Q

What is the usually presentation of someone with HSV esophagitis? Who does it usually effect and what is the treatment?

A

It presents with inflammation and ulcers causing dysphagia and odynophagia.
It affects mostly immunocompromised people
It is treated with acyclovir and famcyclovir

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18
Q

What are the classic endoscopic findings of HSV? Where should you take a biopsy from for definitive diagnosis?
What cells are infected?
What part of the cells are infected?

A

There are ulcers with exudate on the lower 1/3 of the esophagus
Take the biopsy from the edge of the ulcer where viable squamous epithelial cells are.
The nucleus is affected and is:
1. multi-nucleated
2. molding
3. muddy chromatin
4. margination

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19
Q

What are the 2 main manifestations of CMV in the GI system?

A
  1. colitis (most frequently)

2. esophagitis

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20
Q

How does someone with CMV esophagitis present? Who is most likely infected? What is the treatment?

A

CMV esophagitis presents with odynophagia and dysphagia along with systemic infection (eyes, liver, colon, lungs).
HIV infected patients are most likely to be infected.
Treat with famcyclovir.

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21
Q

What are the classic endoscopic findings of CMV esophagitis?
Where do you take the biopsy from?
What cells are infected? What structure of the cells are infected?
What viral inclusions are present?

A

There will be a single shallow ulceration in the distal esophagus.
The biopsy is taken from the base of the ulcer because this is where the endothelial, macrophages and stromal cells are.
The cytoplasms AND nucleus are infected and the viral inclusions are basophilic “owl eyes”

22
Q

What is the most common infection of the esophagus? Who does it affect? What is treatment for non-severe and severe cases?

A

Candida- immunocompromised

  1. non-severe = nystatin
  2. severe = ketoconazle
23
Q

What is seen on endoscopy for Candida esophagitis?

What is seen microscopically?

A

Scattered white-yellow plaques that coalesce and ulcerate

Microscopically, there is hyperplastic, hyperkeratotic squamous cells and inflammatory cells with pseudohyphae infiltrate “spaghetti and meatballs”

24
Q

Describe the epidemiology of eosinophilic esophagitis.

A

It was first recognized in children but has been found in an increasing number of adults.

25
Q

What are the 4 most common symptoms of eosinophilic esophagitis?

A
  1. chronic dysphagia (years)
  2. recurrent esoph. food impaction
  3. heartburn (like GERD)
  4. history of atopy (dermatitis, asthma, other hypersensitivity rxns)
26
Q

What is the endoscopic appearance of someone with EE? What is believed to be the cause?

A

There is a corrugated appearance with fine concentric rings of mucosa in the esophagus.

It is believed to be due to the release of histamine from activated mast cells in the esophagus wall–>cascade resulting in Ach–>contraction of muscle fibers in muscularis mucosa–> concentric rings

The lumen is also narrowed with longitudinal furrows and dilation of strictures causing tears.

27
Q

Describe the microscopic features of EE.

A

There are “microabsesses” or clusters of eosinophils in the epithelium and underlying connective tissue in a “top heavy” distribution.

28
Q

On histopathology alone, it is difficult to distinguish between severe reflux and EE. What is the distinction dependent on?

A
  1. clinical presentation
  2. endoscopic features
  3. histology
29
Q

Most people who have GERD can be diagnosed on symptoms alone. What are the predominant symptoms of GERD?

A
  1. heart burn- mid upper abdomen to mid chest toward the mouth. Occurs after eating and is relieved by antacids like Tums. Worse when bending or lying down
  2. gastroesophageal reflux or regurgitation
  • odynophagia
  • dysphagia
  • chest pain
30
Q

What can severe and prolonged GERD lead to?

A
  1. Erosion/ulceration of squamous mucosa–> metaplasia to intestinalized mucosa (columnar–Barrett’s epithelium)–>dysplasia–> adenocarcinoma
  2. fibrosis- narrowing/shortening the esophagus
  3. dysphagia, odynophagia
  4. heartburn
  5. GI bleed leading to Fe deficiency
31
Q

What are the 6 main causes of GERD?

A
  1. decreased LES efficiency
  2. decreased peristalsis so acid is cleared slowly
  3. pregnancy/obesity- mechanical effects
  4. Hiatal hernia - traps acid above the diaphragm
  5. increased production of gastric acid
  6. smokings/alcohol/benzodiazapine decreases LES pressure
32
Q

What is the main medical and surgical treatments for GERD?

A

Medical:
-PPI to suppress acid

Surgery
- anti-reflux surgery tightens the LES

33
Q

What 3 microscopic findings suggest GERD?

A
  1. Scattered eosinophils (not clustered like EE) in the epithelium with or w/o neutrophils
  2. basal zone hyperplasia (>20%)
  3. papillae elongation(papillae with fibrovascular centers occur more than 2/3 of the way up the epithelium)
34
Q

What is Barrett’s esophagus?

A

the replacement of the normal squamous epithelium of the esophagus with metaplastic columnar epithelium (intestinal metaplasia) with Goblet Cells. **

35
Q

How does Barrett’s esophagus look endoscopically?

A

Salmon-pink tongues of mucosa extending up from the GE junction making a jagged band at the GEJ.

36
Q

If a patient with GERD is referred for endoscopy, what is the chance they have BE?
What is the chance that if they have BE it will be AdCa at the time of the first endoscopy?

A

There is a 10-20% change there is barrett’s esophagus.

There is a 5% chance that someone with BE will have adenocarcinoma on the first visit

37
Q

What patient population with BE has the highest risk for developing adenocarcinoma?

A

men with long-term reflux symptoms who smoke and drink

38
Q

Most esophageal cancers arise in the epithelium and thus are carcinomas.
What are the 2 main classes of esophageal carcinomas?
Anatomically, where is each more likely to be found?
What are the inciting factors for each?

What is the population MOST affected by each?

A
  1. SCC- upper 2/3
    - smoking
    - alcohol
    - diet (nitrosamines, aflatoxin, vit. deficiencies)

*White men >50

  1. adenocarcinoma - lower 2/3
    - GERD
    - BE

*Black men >50

39
Q

What is the microscopic appearance of SCC in the esophagus?

A
  1. desmosomes (intercellular bridging)
  2. keratin/keratin pearls
  3. hyperchromasia (very blue) with high NC ratio, apoptotic figures
40
Q

What is the microscopic appearance of adenocarcinoma?

A
  1. glandular- look for lumens
  2. cribriforming - swiss cheese
  3. papillary
  4. mucin cells nests
  5. signet rings
41
Q

How is the incidence of SCC and adenocarcinoma changing in the US?

What region of the world has the highest incidence and is thus dubbed “esophageal cancer belt”?

A
  1. SCC is going down because of the reduction of smoking and alcohol
  2. AdCa is going up because of BE

This is making the overall incidence of esophageal cancers remain relatively constant

ECB = southern/eastern Africa and Eastern Asia (almost all SCC)

42
Q

What are symptoms of esophageal carcinoma?

A
  1. dysphagia, odynophagia
  2. weight loss **
  3. chest pain radiating to the back
  4. hoarseness (if tumor affects laryngeal nerve)
  5. coughing up blood
  6. increased aspiration risk -> pneumonia
43
Q

Why is it crucial to put a person with chronic esophagitis and/or BE on close surveillance?

A

Because they can progress to adenocarcinoma.

Further, AdCa are rarely cured by surgical resection because they spread quickly to lymphatics and adjacent structures

44
Q

What is the prognosis for esophageal carcinomas?

A

Poor because people present with advanced disease (when 1/2 the lumen of the esophagus is compromised, usually)

5YSR = 15% meaning that 85% die in 5 years(most w/in the first year)

45
Q

What are the curative treatments for esophageal carcinoma?

What are palliative treatments?

A

Curative:

  1. early stage endoscopic mucosal resection
  2. late stage surgical resection
  3. radiation/chemo

Palliative

  1. stent to keep lumen open
  2. feeding tube
  3. tumor ablation/radiotherapy
46
Q

What is the most important predictor of survival for someone with esophageal carcinoma?

A

Stage of the cancer:
T- how far has the primary spread (size, depth, invasion of adjacent organs)
N- lymph nodes it has metastasized to
M-metastasis to distal organs

Staging also takes into account:

  1. type of cancer (AdCa vs. SCC)
  2. grade of cancer (well vs. not well differentiated)
47
Q

A tumor extends into the submucosa. What T stage is it in?

A

T1

48
Q

A tumor invades into the muscularis propria. What T stage is it?

A

T2

49
Q

A tumor invades into the adventitia. What stage is it?

A

T3

50
Q

A tumor invades adjacent structures/organs (like the aorta). What T stage is it in?

A

T4

GI, Liver, GallBladder, Pancreas (24 decks)

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