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Pathology Post Midterm > Module 2: GI: Oral Cancers and Esophageal Non-Cancer Pathologies > Flashcards

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

1
Q

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

A 
Dysphagia 
Epigastric pain 
Heartburn, dyspepsia, and flatulence 
Loss of appetite 
Nausea and Vomiting 
Hematemesis
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2
Q

What are signs and symptoms of lower GI disease?

A 
Colicky abdominal Pain 
Abdominal Distention 
Diarrhea 
Constipation 
Blood in Stools: Occult (Guaiac test) , Hematochezia and Melena 
Anemia
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3
Q

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

A 
Epigastric tenderness/mass
Heptaomegaly
Splenomegaly 
Ascites 
Visible peristalsis 
Abdominal rigidity/guarding
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4
Q

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

A
  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)
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5
Q

What is Erythroplakia?

A

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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6
Q

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

A

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

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7
Q

What does the histology for oral carcinoma look like?

A

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

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8
Q

What are the top 3 locations for oral carcinoma?

A
  1. Vermilion border of lower lip
  2. Floor of the mouth
  3. Lateral Boarder of the tongue (seen in pic 2)
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9
Q

What are the predisposing factors for oral carcinoma?

A 
Tobacco Chewing (most common) 
Alcohol
Jagged Teeth 
Ill-fitting dentures 
HPV (16 & 18) 
-more common in men than women
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10
Q

What is the presentation for oral carcinoma?

A

Asymptomatic

pain on chewing

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11
Q

What would a biopsy for oral carcinoma show?

A

Malignant squamous cells with keratin pearls

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12
Q

Oral carcinoma spreads via the lymphatics, which lympathetics?

A

Anterior cervical lymph nodes

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13
Q

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

A

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

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14
Q

What is esophageal atresia associated with?

A

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

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15
Q

What is the presentation of a newborn with esophageal atresia?

A

Choking and cyanosis after infant’s first feeding

Excessive drooling of saliva in new born

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16
Q

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

A

Stomach protrudes through an enlarged esophageal hiatus in the diaphragm

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17
Q

What is the presentation of a hiatal hernia?

A

Reflux of gastric contents due to incompetence of LES

–gastric contents literally go into the esophagus

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18
Q

What are the two types of hiatal hernia?

A
  1. Sliding type: epigastric pain and heart burn

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

19
Q

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

A

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

20
Q

What are the two forms of achalasia/cardiospasm?

A
  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
21
Q

What are the main features of Achalasia?

A

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

22
Q

What is the presentation for Achalasia?

A 
Dysphagia
Odynophagia 
Reflux of contents 
Vomiting 
Aspiration Pneumonia (due to vomit entering into the resp system)
23
Q

How is the best investigation for diagnosis of Achalasia?

A

See lack of normal peristaltic pressure wave on Manometry

24
Q

What are the complications of Achalasia?

A

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

25
Q

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

A

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

26
Q

What kind of patients get Mallory Weiss Tears?

A

Alcoholics
Bulemics
–both after a bout of retching

27
Q

What does the tear look like on histology?

A

Tear can be mucosal or transmural

28
Q

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

A

Hematemesis (Painful) –literally vomit cups full

—usually heal if small, but can be fatal if big

29
Q

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

A

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
30
Q

What is the pathogenesis for esophageal varices?

A 
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
31
Q

Besides, Esophageal what are the other locations for varices?

A

Gastric
Hemorrhoids
Caput Medusae

32
Q

What is the presentation for esophageal varices?

A

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

33
Q

What are the complications of esophageal varices?

A

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
34
Q

What is the best investigation for esophageal varices?

A

Upper GI endoscopy

35
Q

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

A 
Irritants: alcohol, acids, alkali or GERD (most common cause)
Infections: HSV, CMV, Candida 
Allergic: eosinophilic esophagitis 
Uremia
Anticancer therapy
36
Q

What is seen on histology for reflux esophagitis?

A

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

37
Q

What is the presentation for reflux esophagitis?

A 
Dyspepsia
Burning sensation 
Waterbrush (sour brash) 
Nocturnal Cough 
--symptoms increase after lying down or after a large meal
38
Q

What investigations are done for reflux esophagitis?

A

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

39
Q

What are complications of reflux esophagitis?

A

Bleeding
Stricture Formation
Aspiration Pneumonia
Barrett’s Esophagus — adenocarcinoma

40
Q

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

A
  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
41
Q

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

A

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

42
Q

What is the clinicopathologic disease for eosinophilic esophagitis?

A

Normal pH and fail to respond to medication

43
Q

What investigations are done for eosinophilic esophagitis?

A

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

Pathology Post Midterm (50 decks)

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