Mouth/Esophagus/Stomach Pathology Flashcards

1
Q

Salivary gland tumors are typically benign. What are the 2 most common benign tumors of the salivary gland, and where do they arise?

A

Pleomorphic Adenoma + Warthin’s Tumor

arise from PAROTID

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2
Q

What triad to know for Pleomorphic Adenoma?

A

painless + movable + high rate of occurrence

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3
Q

What diad to know for Warthin’s Tumor?

A

cystic + lymphatic cells

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4
Q

What’s the malignant salivary tumor to know, and how do we know its malignant?

A

Mucoepidermoid carcinoma

pain/paralysis of the facial nerve

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5
Q

What the hell is Behcet Syndrome and what’s the cause?

A

triad of recurrent aphthous ulcers + genital ulcers + uveitis

from immune complex vasculitis

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6
Q

Patient presents with white lesions in mouth that SCRAPE OFF EASILY. What can you assume about the patient?

A

oral Candidiasis

assume pt is immunocompromised (AIDS)

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7
Q

Patient presents with white lesions in mouth that BLEED WHEN SCRAPED OFF. What is the major concern with this lesion?

A

Leukoplakia

can become DYSPLASTIC, which can lead to Squamous cell carcinoma

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8
Q

Patient presents with white lesions on LATERAL TONGUE which are raised and shaggy in appearance. What is the causative organism, and what type of cellular mechanism is causing the lesion?

A

Oral hairy leukoplakia (from EBV infection, IC pt)

this is HYPERPLASIA

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9
Q

The dysfunctional cells of Achalasia are located where in the gut wall?

A

Myenteric plexus (Auerbach’s plexus)

found between the Outer Longitudinal and Inner Circular muscles of the MUSCULARIS EXTERNA

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10
Q

The 2 mechanical features of achalasia are?

A

failure to relax LES

decreased peristalsis

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11
Q

Achalasia exhibits _________ pressure proximal to LES, while Scleroderma exhibits _______ pressure

A

high (Bird’s beak sign)

low

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12
Q

Achalasia exhibits dysphagia when consuming _______ while obstructions exhibit dysphagia when consuming __________

A

solids AND liquids

just solids

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13
Q

What is the big complication for Achalasia?

A

increased risk for Squamous Cell CA of esophagus

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14
Q

Mallory Weiss syndrome involves esophageal lacerations due to _____________

A

severe vomiting (think EtOH and bulemics)

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15
Q

Contrast the esophageal pathologies associated with Painful and Painless hematemesis.

A

Painful = Mallory Weiss

Painless = Esophageal varices/portal HTN

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16
Q

Mallory Weiss syndrome can progress to __________ if the lacerations go transmural/full thickness

A

Boerhaave syndrome

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17
Q

Esophageal veins in the lower 1/3 will drain to the portal system via the _________

A

L gastric vein

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18
Q

Patient presents with Dysphagia, swollen tongue, and microcytic, hypochromic RBCs. Dx?

A

Plummer Vinson Syndrome

esophageal webs + beefy red tongue + Fe deficient anemia

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19
Q

While Achalasia is hypertonicity of the LES, the opposite is true of the LES in _________–

A

GERD

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20
Q

The characteristic cellular change seen in Barrett’s esophagus is ____________ (describe the specific cells too)

A

METAPLASIA

stratified nonkeratinized squamous epithelium is CHANGED to columnar epithelium + goblet cells

the ‘gastrification’ of the esophagus

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21
Q

Barrett’s esophagus complications include what 3 things?

A
  • esophagitis (duh)
  • esophageal ulcers
  • incr risk for Adenocarcinoma
22
Q

What are some risk factors that can lead to Barrett’s?

A
  • EtOH, smoking, obesity, fatty diet, caffeine

- Hiatal hernia (hourglass appearance)

23
Q

What are the 2 types of esophageal cancer, along with their big association?

A

Squamous Cell Carcinoma (irritation)

Adenocarcinoma (Barrett’s)

24
Q

Where do Adenocarcinomas of the esophagus metastasize?

A

CELIAC and GASTRIC nodes

-why? adenoCA found lower 1/3 (duh, Barrett’s), which is foregut

25
Q

Where do esophageal Squamous cell CA metastasize to?

A

upper 1/3: CERVICAL nodes

mid 1/3: MEDIASTINAL/TRACHEOBRONCHIAL

26
Q

Acute gastritis is caused by what basic imbalance?

A

either hi acid or decreased protection by mucosa

27
Q

Describe Prostaglandin’s role on the gastric mucosa and the pharmacologic implications.

A

PG1 required to keep integrity of gastric mucosa

NSAIDs: decrease PG1, cause gastritis

28
Q

Why are burns a risk for acute gastritis?

A

burn=hypovolemia = less ability to keep mucosa alive and/or carry away leaked protons in tissue

29
Q

What’s a Curling ulcer?

A

spot of gastritis from hypovolemia/burn

30
Q

Why does brain injury lead to acute gastritis?

A

brain injury/hi ICP = hi PS/vagal signals from brain = Ach stimulating parietal cell to make H+

31
Q

Contrast the causes of the 2 types of Chronic Gastritis.

A

Type A: Autoimmune

Type B: H. pylori

32
Q

In type A chronic gastritis, _______ cell levels are decreased, while there is hyperplasia of ________ cells

A

less Parietal cells (autoimmune destruction)

G cell hyperplasia (rxn to make more Gastrin)

33
Q

Why is type A chronic gastritis commonly found in the top (fundus, body) of the stomach?

A

this is where Parietal cells are, duh!

34
Q

Type B chronic gastritis pts are at higher risk for MALT lymphoma because?

A

its due to a bacterium (H pylori), so we’ll have marginal zone hyperplasia from the infection!

(hence why type A does not apply)

35
Q

Type B chronic gastritis is found commonly in the ________ of the stomach

A

antrum (bottom)

36
Q

H. pylori is a GNR that is linked to 2 types of cancer. Name em

A

gastric adenocarcinoma

MALToma (resolves with bacteria tx)

37
Q

Describe a common triple therapy for type B chronic gastritis.

A

Omeprazole (PPI)
Clarithromycin
Amoxicillin (alt is Metro)

38
Q

Gastric ulcers hurt __________ after meals, while Duodenal ulcers hurt _______ after meals

A

more (Gastric= greater)

less (Duodenal = decrease)

39
Q

Gastric ulcers have _________ risk for carcinoma, while Duodenal ulcers have _______ risk for carcinoma.

A

higher risk

no risk

40
Q

Contrast the general look of a Gastric vs Duodenal ulcer.

A
  • mucosal heaping around ulcer

- punched out lesion (clean margins)

41
Q

Ruptured duodenal ulcers can cause what 2 effects if posteriorly placed?

A

bleeding from Gastroduodenal a

pancreatitis

42
Q

Stomach cancer (adenocarcinoma) comes in 2 flavors, name em

A

Intestinal

Diffuse

43
Q

Contrast the gross morphology of the two types of gastric adenocarcinoma.

A

Intestinal: mass inside the stomach lumen

Diffuse: infiltrates into wall (thickens it)

44
Q

What are the risk factors for gastric adenocarcinoma?

A
  • chronic gastritis/ulcers
  • dietary nitrosamines (smoked foods)
  • Japanese ppl
  • type A blood
45
Q

What are the two Dermatologic presentations of stomach cancer?

A

acanthosis nigricans

Leser-Trelat sign (seborrheic keratoses)

both are DARK skin lesions

46
Q

Diffuse gastric adenocarcinoma exhibits what characteristic infiltrative cell in the wall of the stomach?

A

Signet ring cells

full of mucin, nucleus pushed to periphery

47
Q

What is the technical term for the gross appearance of diffuse gastric adenocarcinoma?

A

Linitis plastica (stiff, thick, leathery)

48
Q

Describe a female reproductive connection to diffuse gastric adenocarcinoma.

A

May mets to BILATERAL OVARIES

aka KRUKENBERG TUMOR

49
Q

Sister Mary Joseph nodule is located where and associated with what cancer?

A

-subQ, periumbilical region

mets of Intestinal gastric adenocarcinoma

50
Q

Virchow’s node is located where?

A

L supraclavicular region (gastric mets)