Module 2: GI: Oral Cancers and Esophageal Non-Cancer Pathologies Flashcards by Nicole Pritchard

First lets start off with the basics of GI. What are signs and symptoms of upper GI disease?

Dysphagia 
Epigastric pain 
Heartburn, dyspepsia, and flatulence 
Loss of appetite 
Nausea and Vomiting 
Hematemesis

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What are signs and symptoms of lower GI disease?

Colicky abdominal Pain 
Abdominal Distention 
Diarrhea 
Constipation 
Blood in Stools: Occult (Guaiac test) , Hematochezia and Melena 
Anemia

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What are signs and symptoms of upper and lower GI disease?

Epigastric tenderness/mass
Heptaomegaly
Splenomegaly 
Ascites 
Visible peristalsis 
Abdominal rigidity/guarding

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The first topic to be discussed is issues with the oral cavity. What are the two types of leukoplakia?

Oral Hairy Leukoplakia: not dysplastic
- -Associated with EBV and seen in HIV patients
- -No malignant potential
- –Histology: hyperkeratosis (epidermal thickening of the stratum corneum) with acanthosis
Oral Leukoplakia: dysplastic but BM is intact
- -Pre-malignant in 5% and cannot be scraped off
- –pre-disposing factors: tobacco use, ill-fitting dentures and HPV (slide 1a)

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What is Erythroplakia?

Erythroplakia aka erythroplasia:

–dysplastic but BM is intact
–Pre-malignant: over 50% of patients
-much higher chance of becoming malignant
-less common
-poorly circumscribed

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Next we move on to oral cancer. What are the two morphologies for oral carcinoma?

Exophytic: growing outward like a mushroom, fungating; presents early (seen in pic in lab)
Endophytic: grows inwards, more dangerous

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What does the histology for oral carcinoma look like?

Squamous cell carcinoma with well differentiated keratin pearls
—seen on excisional biopsy

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What are the top 3 locations for oral carcinoma?

Vermilion border of lower lip
Floor of the mouth
Lateral Boarder of the tongue (seen in pic 2)

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What are the predisposing factors for oral carcinoma?

Tobacco Chewing (most common) 
Alcohol
Jagged Teeth 
Ill-fitting dentures 
HPV (16 &amp; 18) 
-more common in men than women

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What is the presentation for oral carcinoma?

Asymptomatic

pain on chewing

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What would a biopsy for oral carcinoma show?

Malignant squamous cells with keratin pearls

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Oral carcinoma spreads via the lymphatics, which lympathetics?

Anterior cervical lymph nodes

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Now moving on to esophageal lesions. The first one to speak about is a congenital malformation called esophageal atresia, what is the etiology?

Disruption of elongation and separation of esophagus and trachea during embryogenesis —- leads to a tracheo-esophageal fistula.

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What is esophageal atresia associated with?

Maternal polyhydramnios, single umbilical artery (this is the one he stressed in class)

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What is the presentation of a newborn with esophageal atresia?

Choking and cyanosis after infant’s first feeding

Excessive drooling of saliva in new born

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Now moving onto the non neoplastic conditions in the esophagus. What is a hiatal hernia?

Stomach protrudes through an enlarged esophageal hiatus in the diaphragm

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What is the presentation of a hiatal hernia?

Reflux of gastric contents due to incompetence of LES

–gastric contents literally go into the esophagus

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What are the two types of hiatal hernia?

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Sliding type: epigastric pain and heart burn

2. Paraesophageal (rolling) type: volvulus, strangulation and perforation

Moving onto the next esophageal non neoplastic condition is Achalasia/Cardiospasm. What is the pathogenesis for this?

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Incomplete relaxation of the LES in response to swallowing —- functional esophageal obstruction

What are the two forms of achalasia/cardiospasm?

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Primary form: loss of intrinsic inhibitory innervation of LES and smooth muscle
- loss/absence of ganglion cells in myenteric plexus
Secondary form (pseudoachalasia): impaired function from a variety of causes: Chagas due to Trypanosoma cruzi, polio, paraneoplastic syndrome, and sarcoidosis

What are the main features of Achalasia?

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Aperistalsis
Partial/Incomplete relaxation of LES
Increased resting tone of LES

What is the presentation for Achalasia?

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Dysphagia
Odynophagia 
Reflux of contents 
Vomiting 
Aspiration Pneumonia (due to vomit entering into the resp system)

How is the best investigation for diagnosis of Achalasia?

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See lack of normal peristaltic pressure wave on Manometry

What are the complications of Achalasia?

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Progressive dilatation of esophagus above the LES
Increased risk of developing SCC (5%)
–aka preneoplastic so needs to be treated aggressively

The next non-neoplastic condition of the esophagus is Mallory Weiss Tears, what is the pathogenesis for these?

Longitudinal mucosal tears at the esophagogastric junction due to inadequate relaxation of LES during vomiting (increased pressure)

What kind of patients get Mallory Weiss Tears?

Alcoholics Bulemics --both after a bout of retching

What does the tear look like on histology?

Tear can be mucosal or transmural

What is the defining factor for Mallory Weiss tears, that distinguishes them from Esophageal Varices?

Hematemesis (Painful) --literally vomit cups full | ---usually heal if small, but can be fatal if big

Next esophageal condition to be discussed is esophageal varices, what is the etiology?

Only seen in Portal HTN --- diseases that impede this flow cause portal HTN, which leads to the development of esophageal varices - -usually following Cirrhosis which can turn into HCC (From Hep C or alcoholism) - -other causes of portal HTN: hemochromatosis, budd chiari (Hepatic vein stenosis) and right heart failure

What is the pathogenesis for esophageal varices?

``` Portal HTN (increase in pressure in the portal vein) --- induces development of collateral channels that allow portal blood to shunt into the caval system --Tortuous dilated veins lying primarily in the submucosa of the distal esophagus and proximal stomach ```

Besides, Esophageal what are the other locations for varices?

Gastric Hemorrhoids Caput Medusae

What is the presentation for esophageal varices?

See signs and symptoms of cirrhosis or underlying pathology not from the esophageal varices themselves (asymptomatic)

What are the complications of esophageal varices?

Rupture of varices --- massive painless hematemesis --- hypovolemic shock (most common cause of death) - -rupture is due to too high pressure either from the cirrhosis or HCC) - -splenomegaly and ascites are also seen with portal HTN

What is the best investigation for esophageal varices?

Upper GI endoscopy

Esophagitis is inflammation of the squamous mucosa, what are the etiologies?

``` Irritants: alcohol, acids, alkali or GERD (most common cause) Infections: HSV, CMV, Candida Allergic: eosinophilic esophagitis Uremia Anticancer therapy ```

What is seen on histology for reflux esophagitis?

Inflammation: eosinophils, lymphocytes, +/- neutrophils Elongation of the lamina propria papillae Basal Zone Hyperplasia: normally one layer gets thickened

What is the presentation for reflux esophagitis?

``` Dyspepsia Burning sensation Waterbrush (sour brash) Nocturnal Cough --symptoms increase after lying down or after a large meal ```

What investigations are done for reflux esophagitis?

Endoscopy: irregular area of hyperemia (vascular congestion) at the esophagogastric junction

What are complications of reflux esophagitis?

Bleeding Stricture Formation Aspiration Pneumonia Barrett's Esophagus --- adenocarcinoma

Therefore what are the four key components leading to reflux esophagitis?

1. Decreased LES tone (CNS depressants, hypothyroidism, pregnancy, alcohol, tobacco, nasogastric intubation) 2. Delayed esophageal clearance 3. Increased gastric volume 4. Decreased reparative capacity of esophagus

The next non-neoplastic esophageal condition to discuss is Eosinophilic Esophagitis, what is the presentation for this?

Children: feeding intolerance and GERD symptoms Adults: Food impaction and dysphagia

What is the clinicopathologic disease for eosinophilic esophagitis?

Normal pH and fail to respond to medication

What investigations are done for eosinophilic esophagitis?

Endoscopy: see trachealization of the esophagus (esophageal rings, linear furrows, and white plaques) -- greater than 15 eosinophils/HPF with microabscess and superficial layering, basal zone hyperplasia

Module 2: GI: Oral Cancers and Esophageal Non-Cancer Pathologies Flashcards

(43 cards)