Flashcards in Module 2: GI: Oral Cancers and Esophageal Non-Cancer Pathologies Deck (43):
First lets start off with the basics of GI. What are signs and symptoms of upper GI disease?
Heartburn, dyspepsia, and flatulence
Loss of appetite
Nausea and Vomiting
What are signs and symptoms of lower GI disease?
Colicky abdominal Pain
Blood in Stools: Occult (Guaiac test) , Hematochezia and Melena
What are signs and symptoms of upper and lower GI disease?
The first topic to be discussed is issues with the oral cavity. What are the two types of leukoplakia?
1. 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
2. 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)
What is Erythroplakia?
Erythroplakia aka erythroplasia:
---dysplastic but BM is intact
---Pre-malignant: over 50% of patients
--much higher chance of becoming malignant
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
What does the histology for oral carcinoma look like?
Squamous cell carcinoma with well differentiated keratin pearls
---seen on excisional biopsy
What are the top 3 locations for oral carcinoma?
1. Vermilion border of lower lip
2. Floor of the mouth
3. Lateral Boarder of the tongue (seen in pic 2)
What are the predisposing factors for oral carcinoma?
Tobacco Chewing (most common)
HPV (16 & 18)
-more common in men than women
What is the presentation for oral carcinoma?
pain on chewing
What would a biopsy for oral carcinoma show?
Malignant squamous cells with keratin pearls
Oral carcinoma spreads via the lymphatics, which lympathetics?
Anterior cervical lymph nodes
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.
What is esophageal atresia associated with?
Maternal polyhydramnios, single umbilical artery (this is the one he stressed in class)
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
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
What is the presentation of a hiatal hernia?
Reflux of gastric contents due to incompetence of LES
--gastric contents literally go into the esophagus
What are the two types of hiatal hernia?
1. 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?
Incomplete relaxation of the LES in response to swallowing ---- functional esophageal obstruction
What are the two forms of achalasia/cardiospasm?
1. Primary form: loss of intrinsic inhibitory innervation of LES and smooth muscle
-loss/absence of ganglion cells in myenteric plexus
2. 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?
Partial/Incomplete relaxation of LES
Increased resting tone of LES
What is the presentation for Achalasia?
Reflux of contents
Aspiration Pneumonia (due to vomit entering into the resp system)
How is the best investigation for diagnosis of Achalasia?
See lack of normal peristaltic pressure wave on Manometry
What are the complications of Achalasia?
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?
--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?
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
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?
Waterbrush (sour brash)
--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?
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