DERS 02 - GIT Pathology 1 - Oral Cavity & Esophagus Flashcards

1
Q

What are the medical terms for:

  • Difficulty swallowing
  • Pain on swallowing
  • Indigestion (pain/discomfort in the upper abdomen)
  • Vomiting blood
  • Dark, sticky feces containing partially digested blood
A
  • Dysphagia
  • Odynophagia
  • Dyspepsia
  • Hematemesis
  • Melena
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2
Q

What does the presence of melena usually mean?

A

There is an upper GIT bleed

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3
Q

What is occult blood and what does it usually indicate?

A

Occult blood is blood in the feces that is not visible and only detected by lab diagnostics. It usually indicates a lower GIT bleed

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4
Q

What is oral leukoplakia?

A

A clinical term used to describe a well defined white patch or plaque in the mouth caused by epidermal thickening or hyperkeratosis. These patches/plaques cannot be removed with scraping

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5
Q

Describe the pathogenesis of oral leukoplakia

A
  1. Something causes consistent damage to the oral mucosa or tongue. Usually pipe tobacco, chewing tobacco, chronic friction (ill fitting dentures), or HPV infection
  2. Metaplasia followed by dysplasia results

Only a very small number of these plaques undergo malignant transformation

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6
Q

What is oral erythroplakia? What are its causes?

A

A poorly circumscribed red velvety eroded area in the oral mucosa. It is essentially an advanced form of leukoplakia with more marked dysplasia. Cannot be scraped off

Similar causes to leukoplakia, just more severe or longer exposure to damage

These become malignant more that 50% of the time.

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7
Q

Facts to know about Oral Hairy Leukoplakia

A
  • White, confluent, fluffy or hairy hyperkeratotic thickenings of the tongue or oral mucosa
  • Cannot be scraped off
  • Consists of layers of keratotic squames over underlying mucosal acanthosis (epidermal hyperplasia)
  • Usually caused by EBV infection in HIV patients (or other immunocompromised patients)
  • Not malignant
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8
Q

What is the most likely cause of a white patch in the mouth than can be scraped off?

A

Candidiasis

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9
Q

Facts to know about esophageal atresia

A
  • It is the non-canalization of portion of the esophagus
  • Commonly associated with:
    • Tracheo-esophageal fistula
    • Other congenital abnormalities
  • Clinical symptoms:
    • Excessive drooling
    • Aspiration pneumonia
    • Choking and cyanosis
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10
Q

Facts to know about esophageal webs and rings

A
  • They are protrutions of the esophageal mucosa into the lumen
    • Upper esophageal protrusions are called webs and are covered by squamous mucosa with a vascularized core
    • Lower esophageal protrusions are called Schatzi rings and have a columnar epithelium
  • Typically present with episodic dysphagia and infrequent pain
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11
Q

Facts to know abou plummer-vinson syndrome

A
  • AKA - Kelly Patterson Syndrome
  • The syndrome is characterized by esophageal webs, glossitis, and iron deficiency anemia (koilonychia)
  • Treatment is iron therapy and endoscopic dilation
  • These patients are high risk for squamous cell carcinoma or esophagus
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12
Q

What is achalasia? What is it AKA? What are it’s three main features?

A
  • Achalasia is the failure of smooth muscle fibers to relax, resulting in the obstruction of the GIT. The most common form is esophageal achalasia, aka cardiospasm, resulting from:
    • partial or incomplete relaxation of the lower esophageal sphincter (LES) with swallowing
    • Aperistalsis
    • Increased resting tone of the LES
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13
Q

What are the primary and secondary causes of esophageal achalasia?

A
  • Primary - loss of intrinsic inhibitory innervation of LES or loss/absence of ganglion cells in myenteric plexus
  • Secondary (pseudoachalasia)
    • Chagas disease (Trypanosoma cruzi parasite infection)
    • Diabetic autonomic neuropathy
    • Infiltrative disorders (malignancy, amyloidosis, sarcoidosis)
    • Spinal moter neuron defects
    • Down Syndrome
    • Autoimmune disease destruction of nerves
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14
Q

What are the usual clinical features of esophageal achalasia?

A
  • Dysphagia
  • Odynophagia
  • Refulx
  • Vomiting
  • Aspiration pneumonia
  • Progressive dilation of esophagus above LES
  • Squamous cell carcinoma (5% of patients)
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15
Q

Facts to know about Mallory Weiss Syndrome

A
  • It is hematemesis caused by a longitudinal mucosal or transmural tear at the eosphagogastric junction
  • Caused by inadequate relaxation of the LES during vomiting
  • Typically seen in acoholics after bouts of severe retching
  • Usually heals, but sometimes fatal
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16
Q

What is reflux esophagitis? What is it AKA? What are the primary factors causing it?

A
  • Reflux esophagitis, aka GERD, is inflammation of the esophagus caused by acid reflux
  • Largest contributing factors to GERD are:
    • Low LES tone
    • Low reparative capacity of esophagus
    • Delayed esophageal clearance
    • Increased gastric volume
17
Q

What are the primary causes of refulx esophagitis?

A
  • CNS depressants
  • Hypothyroidism
  • Pregnancy
  • Alcohol
  • Tobacco
  • Nasogastric intubation
18
Q

What is the typical presentation of reflux esophagitis? What are some associated complications?

A

Clinical Presentation

  • Dyspepsia
  • Burning sensation that increases after meals or while supine
  • Nocturnal cough

Associated Complications

  • Bleeding
  • Stricture
  • Aspiration pneumonitis
  • Barret esophagus & Adenocarcinoma
19
Q

Describe the histological and gross changes seen in reflux esophagitis.

A
  • Histology
    • Intraepithelial eosinophils
    • basal zone hyperplasia
    • Elongation of lamina propria papillae
  • Gross
    • Hyperemia

Refer to image

20
Q

Describe the typical diagnostic procedure for Barrett Esophagus

A
  1. Patient presents with similar Sx as GERD but more chronic
  2. Endoscopy reveals that the normal peraly-white esophageal squamous mucosa is replaced by a velvety pink columnar mucosa (aka - serptiginous salmon colored patch). Refer tp image
  3. Biopsy reveals columnar metaplasia with goblet cells (a change from squamous epithelium to columnar epithelium)
  4. Grading of the Barret esophagus is done based on the severity of the metaplasia/dysplasia
21
Q

How is Barrett esophagus graded and how does this inform management of it?

A
  • No dysplasia - continue screening
  • Low grade dysplasia - presence of columnar epithelium with goblet cells and elongated nuclei - more frequent screening
  • High grade dysplasia - marked disorganization of the epithelium - definitive therapy, resection, or ablation
  • Adenocarcinoma - resection

Refer to image (left is low grade and right is high grade)

22
Q

Facts to know about esophageal varices

A
  • Dilated tortuous veins in mucosa and submucosa of lower esophagus and proximal stomach
  • Overlying mucosa may appear normal, inflamed, or ulcerated
  • Heavily associated with portal hypertension, therefore:
    • Associated with alcoholism
    • Associated Liver cirrhosis
    • Associated with hepatocellular carcinoma
  • Usually asymptomatic (disregarding liver Sx) until rupture and is the cause of death of half of all cirrhosis patients
23
Q

What is and what causes eosinophilic eosphagitis? What are its clinical features? How is it distinguished from other esophagitis disorders?

A

Esophagitis caused by an allergic reaction. Usually presents with:

  • Dysphagia
  • Feeding intolerance (similar to GERD)
  • Esophageal trachealization (upon endoscopy, the esophagus appear to have rings like the trachea)
  • Atopic Disorders (symptoms often seen in hyperallergic people) - dermatitis, allergic rhinitis, asthma, etc
  • Upon histology, marked increase in intraepithelial eosinophils throughout the esophagus (not just near the stomach). See image
24
Q

Facts to know about infectious esophagitis

A
  • These infections really only occur in immunocompromised patients (usually HIV/AIDS patients)
  • Fungal
    • Candida
  • Viral
    • Herpes Simplex
      • Top image - large multinucleated cells
    • Cytomegalovirus
      • Bottom image - owl’s eye nucleus cells
25
Q

What causes esophageal squamous cell carcinoma?

A

There are many etilogies:

  • Esophageal diseases
  • Genetics - celiac disease, racial factors, etc
  • Lifestyle Choices - alcohol, tobacco, HPV
  • Diet - vitamin deficiencies, fungal contamination, etc.
26
Q

Which populations are more likely to develop esophageal squamous cell carcinoma?

A
  • Males >50yo
  • Central Asia and Northern China
  • Blacks > Whties
27
Q

Where in the esophagus does squamous cell carcinoma develop? How does is typically grow and spread?

A
  • Can occur anywhere in esophagus but the middle third is most common
  • Typically grows in a exophytic (polypoid), diffusely infiltrative, or ulcerative pattern
  • Squamous cell carcinoma can spread in several ways:
    • Direct - trachea or heart
    • Lymphatic - cervical, mediastinal, paratracheal, etc
28
Q

Describe the histological appearance of esophageal squamous cell carcinoma

A

Nests of squaous cells are seen

29
Q

Answer the following about esophageal adenocarcinoma

  • Typical population affected
  • Typical location on esophagus
  • Etiologies
  • Key histological features
A
  • Typicall occur in white men around 50yo
  • Usually occurs in the lower third of the esophagus
  • Usually the result of Barrett’s esophagus
  • Key Histological features are:
    • Infiltrative (past basement membrane)
    • Gland formation
    • Hemorrhagic
    • Occurs at gastroesophageal junction

Refer to image