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6. HDS GI Repro > Salivary Glands, Oral Cavity, Esophagel Disorders > Flashcards

Salivary Glands, Oral Cavity, Esophagel Disorders Flashcards

1
Q

Major Salivary Glands

A
  1. Parotid Gland
  2. Submandibular Gland
  3. Sublingual Gland
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2
Q

Parotid Gland

A
  • Largest salivary gland
  • Weighs 15-30 grams
  • Parotid duct (Stenson’s duct) opens opposite maxillary 2nd molar
  • Almost exclusively serous acini ⇒ produces amylase
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3
Q

Submandibular Gland

A
  • 2nd largest salivary gland
  • Weighs 10-15 grams
  • Submandibular duct (Wharton’s duct) opens lateral to lingual frenulum
  • Mix of serous and mucous acini
  • Serous acini ⇒ produce lysozyme ⇒ hydrolyze walls of certain bacteria
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4
Q

Sublingual Gland

A
  • Smallest major salivary gland
  • Weighs 1.5-2.5 grams
  • Located in the floor of the mouth
  • Covered only by oral mucosa
  • Posteriorly contacts the submandibular gland
  • Opens through Bartholin’s duct (which unites w/ Wharton’s duct) or directly into the mouth through Ravinus’s duct
  • Almost all mucous acini
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5
Q

Minor Salivary Glands

A
  • 500-1k of these glands
  • Not present in gingiva and anterior hard palate
  • Almost all are mucous except Ebner’s serous gland (located in the tongue)
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6
Q

Acute Sialadenitis

A

Acute salivary gland inflammation

  • Viral sialadenitis ⇒ usu. causes swelling of all glands
    • Paramyxovirus (mumps)
    • Epstein-Barr virus (herpes)
    • Coxsackie virus
    • Influenza A and Parainfluenza
  • Bacterial sialadenitis ⇒ localized swelling
    • S. aureus and Strep
    • Predisposing factors:
      • Dehydration
      • Malnutrition
      • Immunosuppression
      • Sialolithiasis
    • ± Surgical drainage
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7
Q

Chronic Sialadenitis

A
  • Chronic inflammation of the glands (lymphocytes, MΦ, plasma cells)
  • Gradual destruction w/ progressive sclerosis ⇒ “hard” gland (Kuttner’s ‘tumor’)
  • ± Surgical excision
  • In females associated w/ RA
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8
Q

Sialadenitis

Histology

A
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9
Q

Mucocele

A
  • Most common salivary gland lesion
  • D/t blockage or rupture of salivary gland duct ⇒ leakage of saliva into surrounding CT stroma
  • Most common site is lower lip
  • Usu. d/t trauma
  • Bluish, translucent, fluctuant lesion
  • Cyst-like spaces filled w/ mucin and inflammatory cells
  • Treated w/ excision, if not may recur
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10
Q

Sialolithiasis

A
  • Stones block the excretory ducts of the glands
  • Can be in the duct or within the gland
  • Submandibular gland within the Wharton’s duct ⇒ most frequent & larger (more calcium salts)
  • Treated w/ removal: surgically or w/ shock-wave lithotripsy
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11
Q

Benign Lymphoepithelial Cysts

A
  • Acquired process, not a true neoplasm
  • Occur in the parotid gland or upper cervical lymph nodes
  • Characterized by multilocular cysts
  • Lymphoid hyperplasia ⇒ ⊕ epithelial proliferation
  • Can be a manifestation of HIV disease
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12
Q

Sjogren’s Syndrome

Overview

A

Immune destruction of lacrimal and salivary glands

  • Results in:
    • Keratoconjunctivitis sicca
      • Dry eyes ⇒ blurring, burning, itching, thick secretions
    • Xerostomia
      • Dry mouth ⇒ swallowing difficulty, ↓ sense of taste, dry mucosa
  • Primary form = sicca syndrome
  • If these develop in a pt w/ another autoimmune disease (most often RA) ⇒ secondary Sjogren’s syndrome
  • Dx by lip biopsy to examine minor salivary glands
    • Periductal and perivascular inflammation and lymphoid follicles w/ germinal centers
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13
Q

Sjogren’s Syndrome

Etiology and Pathogenesis

A
  • Lymphoid infiltration of glands by activated CD4+ T cells and B cells
  • ⊕ Rh Factor (75%)
  • ⊕ ANA (50-80%)
  • ⊕ LE test (25%)
  • ⊕ Anti SS-A (Ro) and SS-B (La) (90%)
    • High titer of anti SS-A Ab ⇒ ↑ likelihood of extraglandular sx
      • Ab can also be seen in SLE pts
  • Certain HLA types predominate
  • EBV may play a role
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14
Q

Sjogren’s Syndrome

Associations

A
  • 40x higher incidence of lymphoma
    • Often B cell, marginal zone type
    • Monoclonal B cell pop. in salivary gland ⇒ precursor of lymphoma
  • Mikulicz’s syndrome
    • Lacrimal and salivary gland enlargement
    • Can be secondary to sarcoid, leukemia, lymphoma, Sjogren’s
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15
Q

Salivary Gland Neoplasms

Overview

A
  • Rare neoplasm (< 2% total)
  • Tends to occur in larger glands
    • 65-80% in Parotid gland
    • 10% in Submandibular gland
    • 10-25% in Sublingual & minor salivary glands
  • Inverse relationship b/t gland size and likelihood of malignant neoplasm
    • Parotid: 85% benign; 15% malignant
    • Submandibular: 60% benign; 40% malignant
    • Sublingual and minor glands: 50% / 50%
  • Most are single and unilateral
  • Several types tend to be bilateral and/or multicentric:
    • Warthin’s tumor
    • Pleomorphic adenoma
    • Acinic cell carcinoma
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16
Q

Benign

Salivary Gland Neoplasms

A
  • Pleomorphic Adenoma
  • Warthin’s Tumor
  • Benign Cyst
  • Oncocytoma
  • Monomorphic Adenoma
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17
Q

Pleomorphic Adenoma

Overview

A

‘Benign Mixed Tumor’

  • Most common salivary gland neoplasm
  • Women aged 30-50
  • Radiation risk factor
  • Mostly in parotid gland
    1. Superficial lobe ⇒ facial asymmetry
    2. Deep lobe ⇒ pharyngeal mass → dysphagia
  • Painless and slow growing
  • Myoepithelial or ductal reserve cell origin
  • Chromosomal rearrangements of PLAG1
    • PLAG1 overexpression ⇒ upregulation of genes involved in cell growth (ex. growth factor receptor signaling pathways)
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18
Q

Pleomorphic Adenoma

Gross Appearance

A
  • Round rubbery mass up to 6-10 cm
  • Mostly encapsulated w/ ± extensions into normal gland
    • Remove with wide margins
  • Cut surface gray white to bluish translucent areas
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19
Q

Pleiomorphic Adenoma

Histology

A

Composed of two elements:

  1. Epithelial/Myoepithelial
    • Many different patterns w/ areas of extreme cellularity forming tubules or sheets
  2. Fibromyxoid stroma
    • Can contain cartilage and bone

Fine need aspiration (cytology) ⇒ distinctive magenta-colored fibrils on diff-quik stain

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20
Q

Pleomorphic Adenoma

Treatment & Prognosis

A
  • Tx w/ superficial parotidectomy w/ preservation of facial nerve
    • Clean margins ⇒ cured
    • Postive margins ⇒ ~ 25% recurrence
      • Between 1.5-20 years
      • Can become malignant (2-3%)
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21
Q

Carcinoma ex Pleomorphic Adenoma

A

“Malignant Mixed Tumor”

  • Late complication
    • Longer presence ⇒ ↑ likelihood
  • Dual differentiation:
    • Epithelium: Carcinomatous
    • Stroma: Sarcomatous
  • Has a poor prognosis
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22
Q

Warthin’s Tumor

Overview

A

“Papillary Cystadenoma Lymphomatosum”

  • Benign, very rarely can recur (2%)
  • Males, 50-60 y/o
  • Smoking risk factor
  • Parotid gland / lower pole of superficial lobe ⇒ swelling
  • 10% are bilateral and can be multicentric
  • Rarely see lymphoma in tumor
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23
Q

Warthin’s Tumor

Appearance

A
  • Gross:
    • 2-6 cm encapsulated oval mass
    • Cut surface: single/multiple cysts filled w/ brown viscous fluid
    • Solid portions: gray-white (lymphoid component)
  • Histology:
    • Cystic spaces lined by double layer of epithelial cells in uniform rows
    • Epithelial cell cytoplasm is finely granular and eosinophilic (pink, reddish) ⇒ oncocytic
      • D/t accumulation of mitochondria
    • Dense lymphocytic infiltrate w/ ± germinal centers
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24
Q

Malignant

Salivary Gland Neoplasms

A
  • Mucoepidermoid Carcinoma (Low & High Grade)
  • Adenoid Cystic Carcinoma
  • Malignant Mixed Tumor
  • Acinic Cell Carcinoma
  • Epidermoid (Squamous) Carcinoma
  • Others
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25
Q

Mucoepidermoid Carcinoma

Overview

A
  • < 4 cm, well-circumscribed, partially encapsulated mass w/ infiltrative margins
  • Most common malignant neoplasm of salivary gland
  • Age range: 15-80 y/o
  • Overall M:F 1:2
    • Tongue & retromolar area M:F 1:7
  • 54% in major salivary gland
    • Parotid 60-70%
  • 46% in minor salivary gland
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26
Q

Mucoepidermoid Carcinoma

Cell Types

A

Four basic cell types:

  1. Squamous cell
  2. Clear cell
  3. Intermediate (basaloid) cell
  4. Mucous cell
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27
Q

Mucoepidermoid Carcinoma

Low Grade Tumors

A
  • Gross:
    • Cystic areas filled w/ clear mucus
  • Histology:
    • Large cysts lined by cuboidal and mucous cells
    • Sheets of intermediate cells and abundant mucous cells
    • No or rare squamous cells
  • Prognosis:
    • Recurrence: 10%
    • Metastasis: Rare
    • 5-year survival: 98%
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28
Q

Mucoepidermoid Carcinoma

High Grade Tumors

A
  • Gross:
    • Pinkish to yellowish areas
  • Histology:
    • No cysts
    • Sheets of intermediate cells
    • Prominent squamous cells
    • Almost no mucous cells
    • Necrosis, cellular atypia and increased mitosis
  • Prognosis:
    • Recurrence: 74%
    • Metastasis: 30% to regional LN
    • 5-year survival: 56%
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29
Q

Adenoid Cystic Carcinoma

Overview

A
  • 10% of all malignant salivary gland tumors
    • Parotid: less common than Mucoepidermoid & Acinic Cell carcinomas
    • Minor salivary gland: most common
  • Age: 50-70 years
  • M:F ratio 1:1
  • Identical to adnexal tumor of the skin called Cylindroma
  • Cribriform vs Tubular vs Solid morphology
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30
Q

Adenoid Cystic Carcinoma

Appearance

A
  • Gross:
    • Small poorly encapsulated masses within salivary glands
    • Cut surface: firm, white tumor w/o cysts or hemorrhagic areas
      • Punched-out spaces
  • Three architectural patterns:
    • Cribriform
    • Tubular
    • Solid (worst prognosis)
  • Histology:
    • Small cells w/ dark, compact nuclei and scant cytoplasm
    • PAS-⊕hyaline material (excess BM)
    • Prominent perineural invasion (“sneaky” fashion)
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31
Q

Adenoid Cystic Carcinoma

Prognosis

A

Directly related of completeness of excision at 1st surgery

  • Recurrence at 5 years:
    • 59% for tubular tumors
    • 89% for cribriform tumors
    • 100% for solid tumors
  • Metastases at 15 years: 34% overall
  • 15-year survival:
    • 39% for tubular
    • 26% for cribriform
    • 5% for solid
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32
Q

Acinic Cell Carcinoma (ACC)

Overview

A
  • 3% of all salivary gland tumors
  • Age range 20-70, peak in 3rd decade
  • M:F ratio 3:1
  • Parotid (81%), minor salivary glands (15%)
  • Can be bilateral & multicentric
  • Can arise in intra-parotid lymph nodes
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33
Q

Acinic Cell Carcinoma

Appearance

A
  • Gross:
    • Well-circumscribed mass between 3-5 cm. w/ encapsulation
    • Can have cysts
  • Histology:
    • Cells resemble normal serous cells
    • Can have several architectural patterns from solid to papillary/cystic and tubular
    • No prognostic significance
    • Usu. have a prominent lymphoid infiltrate in the stroma
    • Anaplasia of individual cells is important for prognosis
34
Q

Acinic Cell Carcinoma

Prognosis

A
  • Low grade malignancy
    • Recurrence 12%
    • Metastasis 8%
    • Death 6%
      • 5-year survival: 89%
      • 10-year survival: 68%
      • 20-year survival: 56%
  • Bad prognostic features:
    • Focal necrosis
    • Neural invasion
    • Incomplete resection
    • Involvement of deep lobe
  • Good prognostic features:
    • Location in minor salivary gland
35
Q

Oral Cavity

Precancerous Lesions

A

Leukoplakia and Erythroplakia

  • Risk factors: alcohol use, tobacco use, exposure to chronic irritants, HPV
  • 2:1 male predominance, seen in adults
  • Highest risk sites are floor of mouth, ventral surface of tongue
  • Must biopsy any lesion that doesn’t respond to avoidance of tobacco/alcohol
36
Q

Leukoplakia

A
  • White plaque on mucous membranes
  • Clinical definition: pathology can range from hyperplasia to dysplasia to carcinoma in situ
  • Cannot remove by scraping
  • Cannot classify clinically or microscopically as something else
  • 5-6% chance of transforming to carcinoma
37
Q

Erythroplakia

A
  • Red, velvety lesion of oral cavity
  • Often has associated dysplasia
  • 50% chance of malignant transformation
38
Q

Oral Cavity

Carcinoma

A
  • > 95% of these are squamous cell carcinoma
    • Often discovered late
    • 50% fatal overall
  • Risk factors: tobacco, alcohol, betel nuts
  • Sites: floor of mouth, tongue, hard palate, base of tongue
    • Best prognosis for lip
    • Worst prognosis for floor of mouth, base of tongue
  • Early: raised firm plaques w/ irregular roughening
  • Later: protruding mass w/ central necrosis forming an ulcer w/ raised borders
  • Can be superimposed on leukoplakia or erythroplakia
  • Begins as in-situ and then see range of differentiation
  • Usually see extensive local infiltration before metastases, slow growing
39
Q

Laryngeal Carcinoma

A
  • Many similarities to oral cavity carcinoma
  • Mostly squamous cell carcinoma
  • Same risk factors: tobacco, alcohol, betel nuts
  • Hyperplasia → dysplasia → carcinoma sequence
  • Generally presents as hoarseness
  • 60% are confined to larynx at presentation
  • Treat w/ surgery, radiation or combination
40
Q

Esophagus

Characteristics

A
  • Structure:
    • Muscular tube 23-25 cm in length
    • Pharynx → GE junction
  • Function:
    • Conduit for food and fluids
    • Prevention of reflux
  • Upper esophageal sphincter (UES) ⇒ anatomic structure
  • 3 cm segment formed by cricopharyngeus muscle and portions of prox. esophageal circular and inferior pharyngeal constrictor muscles
  • Lower esophageal sphincter (LES) ⇒ physiologically defined
    • 2-4 cm segment just proximal to anatomic GEJ
41
Q

Esophageal

Muscle Anatomy

A
42
Q

Esophagus

Congenital Anomalies

A
  • Agenesis: absence of formation (rare)
  • Atresia: thin non-canalized segment ⇒ obstruction
    • Usu. in association w/ TE fistula
    • Associated w/ hydramnios in 3rd trimester
  • Tracheoesophageal Fistula: communication between trachea and esophagus
    • Incidence of 1/800 live births
43
Q

Dyspepsia

A

Uncomfortable sensation which sits in the pit of your stomach or right in the epigastric region.

44
Q

Dysphagia

A

Difficulty swallowing

History is key!

  • Oropharyngeal dysphagia
    • Difficultly getting food to back of mouth
    • “Choking” or coughing when eating
    • Food getting into nose
    • Likely hx of stroke or any disease that effects striated muscle
  • Esophageal dysphagia
    • Solids alone ⇒ mechanical causes (Ex. Schatzki’s ring)
    • Solids & liquids ⇒ motility “nerve” causes (Ex. achalasia)
    • Continuous or intermittent?
      • Continuous ⇒ something “fixed or unchanging”
    • Associated GERD?
    • Weight loss?
45
Q

Functional

Esophageal Obstruction

A
  • Esophageal Dysmotility
    • Nutcracker Esophagus (distal contractions)
    • Diffuse Esophageal Spasm
    • LES Dysfunction
      • W/o reduced peristaltic contractions
        • That would be seen in Achalasia)
  • Dysmotility can lead to development of diverticuli
    • Ephiphrenic – just above the LES
    • Zenker – just above the UES
46
Q

Esophageal

Diverticulum

A

Outpouching of wall which includes all layers

  • Zenker diverticulum (pharyngo-esophageal): above the UES
    • D/t UES dysfunction (premature relaxation)
    • Pulsion diverticulum
    • Most common esophageal diverticulum
    • See regurgitation w/o dysphagia, aspiration, neck mass
  • Traction diverticulum: mid esophageal
  • Epiphrenic diverticulum: above LES
    • D/t discoordination of peristalsis and LES relaxation
47
Q

Esophageal Stenosis

A

Narrowing of the lumen

Mechanical obstruction

  • Congenital or acquired
  • Usu. d/t acquired submucosal thickening from:
    • Chronic GERD, radiation, tumor, systemic sclerosis, caustic injury or extrinsic compression
48
Q

Esophageal Web

A
  • Ledge-like protrusions of mucosa in upper esophagus
  • Mechanical obstruction
  • Plummer Vinson syndrome: iron deficiency anemia, glossitis, cheilosis (corners of the mouth become inflamed)
49
Q

Schatzki Ring

A
  • Ledge-like protrusions of mucosa in lower esophagus
  • Mechanical obstruction
  • Submucosal ring at squamo-columnar junction
    • Type A ⇒ both sides lined by squamous mucosa
    • Type B ⇒ one side by squamous and the other by columnar mucosa
  • Symptomatic when lumen ≤ 12 mm
    • Intermittent dysphagia to solids
  • Dilate with 18-20 mm dilator
50
Q

Esophagus

Neural Control

A
51
Q

Achalasia

Overview

A
  • Aperistasis of esophagus
    • Incomplete relaxation of LES w/ swallowing
    • Increased resting tone of LES
  • Pathogenesis:
    • Degeneration of inhibitory neurons (ganglion cells) in distal esophagus
      • Normally release nitric oxide and VIP ⇒ lets LES relax during swallowing

Incidence 0.4-1 in 100k; M=F

Peak age of 70 with smaller peak 20-40s

52
Q

Neural Control in Achalasia

A
53
Q

Achalasia

Etiology

A
  • Primary: unknown (most common)
    • Idiopathic? Viral? Autoimmune?
  • Secondary:
    • Western Hemisphere: Chagas disease (trypanosoma cruzi)
    • Genetic: Allgrove’s disease
    • Neoplastic: direct invasion or paraneoplastic
    • Infiltrative diseases: sarcoid
    • Neuropathies
    • Special cases: Pregnancy, obesity, Parkinson’s
54
Q

Achalasia

Clinical Manifestations

A
  • Dysphagia to solids and liquids (100% of pts)
  • Chest pain
  • Weight loss – generally only in severe cases
  • Heartburn
  • Secondary achalasia has a shorter duration of sx and greater percentage of weight loss (90%)
  • Complications:
    • Regurgitation and aspiration
    • Infection
    • ↑ Risk of Squamous cell carcinoma (2-4x)
  • Treat w/ balloon dilatation, myotomy
55
Q

Achalasia

Diagnosis

A
  • Esophageal Manometry – 100% accurate
  • Barium study
    • Dilated esophagus above the constricted area
    • Absence of myenteric plexus from the dilated wall
    • “Bird’s beak appearance
  • EGD showing Candida
56
Q

Hiatal hernia

A

Protrusion of stomach above the diaphragm so that it is in the chest

Allows reflux to freely flow back into the esophagus

Can be sliding or paraesophageal or mixed:

  • Sliding hernia (95%)
    • Upward displacement of both esophagus and stomach through esophageal hiatus
  • Paraesophageal (5%)
    • Upward displacement of stomach through hiatus alongside a fixed esophagus
    • Incidence: 1-20% adults, but only 9% are symptomatic
    • Complications: ulceration, bleeding perforation, strangulation, contributes to reflux
57
Q

Mallory-Weiss Syndrome

A
  • Longitudinal irregular linear tear of EG junction or proximal stomach, variable depth
  • Associated w/ excessive vomiting and refluxing (most common in alcoholics)
  • Accounts for 5-10% of UGI bleeding
58
Q

Boerhaave Syndrome

A

Esophageal rupture (often fatal)

59
Q

Esophageal Varices

A

Dilation of submucosal and serosal venous plexuses

  • Etiology: portal hypertension (in 90% cirrhotic pts)
  • Most common causes:
    • Cirrhosis (seen in 50% of cirrhotic pts, 25-40% w/ cirrhosis have variceal bleeding)
    • Schistosomiasis
  • Clinical presentation:
    • Varices are silent until they bleed
    • Bleeding is an emergency
  • Outcome:
    • 30% die w/ 1st bleed
    • > 50% rebleed within 1 year
    • Next episode has a similar mortality rate
60
Q

Esophagitis

Etiologies

A
  • Reflux esophagitis
  • Infection (candida, HSV, CMV, bacteria, etc.)
  • Ingestion or caustic substance (acid, alkali)
  • Treatment effect (chemotherapy, radiation, pills)
  • Mechanical (intubation)
  • Systemic, Metabolic or Skin Disease (e.g. Crohn’s disease, Uremia, Pemphigoid, Graft versus Host disease)
61
Q

Eosinophilic Esophagitis

A
  • Early age onset
  • Male predominant
  • Environmental or food allergen
  • GERD likely worsens condition
  • Intermittent dysphagia to solids
  • Clinical presentation
    • Feeding difficulties – age 2-3
    • GERD/vomiting – age 5
    • Abdominal pain – age 9
    • Dysphagia – age 11
    • Food impactions and esophageal strictures – age >12
  • Diagnosis: EGD with biopsy
62
Q

Eosinophils in the Esophagus

Differential

A
  • GERD
  • Hypereosinophilic Syndrome
  • Parasitic Diseases
  • Allergic Vasculitis
  • Esophageal Leiomyomatosis
  • Periarteritis
  • Inflammatory Bowel Disease
63
Q

Eosinophilic Esophagitis

Management

A
  • PPI therapy
  • Symptom diary
  • Allergy testing
  • Swallowed steroid
  • Allergy medication
64
Q

Esophageal Spasm

A

Intermittent motility issues

  • Can be triggered by drinking cold liquid or stress
  • ± Severe CP and difficulty swallowing solids and liquids (at the time of spasm)
  • X-ray shows a “cork-screw esophagus”
  • Tx targeted towards alleviating the pain
    • PPI if GERD is the cause
    • TCA’s at low dose to numb GI hypersensitivity
65
Q

Scleroderma

CREST Syndrome

A

Calcinosis; Raynaud’s phenomena; Sclerodactyly; Telangiectasia; Esophageal dysmotility

  • Esophageal dysmotility
    • Aperistalsis of esophagus
    • Low pressure LES
    • Scleroderma esophagus
  • Pathophysiology
    • Smooth muscle intimal fibrosis ⇒ LES being fibrosed open
    • Results in severe, unrelenting reflux
  • Treatment
    • Small non-fatty meals
    • Aggressive PPI therapy
    • Dilation if acid related strictures develop
    • Must be careful performing a fundoplication ⇒ can cause further dysphagia
66
Q

Gastroesophageal Reflux Disease (GERD)

Overview

A

Reflux of gastric contents into esophagus

Acid, bile or non-acid material

  • Most common cause of esophagitis
  • Anatomic causes
    • Defective LES barrier
      • Transient relaxation most important cause of reflux
        • Mediated by vagal pathways
        • Triggered by gastric distension by gas or food, after swallowing, or ↑ intraabdominal pressure
    • Diaphragmatic weakness
    • Crucal disruption
    • Hiatal hernia: no clear cause and effect relationship but most pts w/ severe esophagitis have HH
  • Gastric factors:
    • Loss of normal anatomic barrier allows acid to reflux up into esophagus
    • Acid/pepsin, delayed emptying
  • Dietary factors: Tomato based foods, Chocolate, Caffeine, Spicy foods, citrus, garlic, mint, onions
  • Lifestyle factors: pregnancy, obesity, eating and lying down, smoking, alcohol
67
Q

GERD

Clinical Manifestations

A
  • Typical symptoms
    • Heartburn
    • Regurgitation (can be acid or food)
    • Sour taste in mouth
  • Atypical symptoms
    • Laryngitis
    • Cough
    • Refractory asthma
68
Q

GERD

Pathology

A
  • Esophagitis
    • Eosinophils seen in GERD & motor d/o of esophagus
  • Basal zone hyperplasia ⇒ > 20% of epithelial thickness
69
Q

GERD

Treatment

A
  • Acid suppression medications
    • Proton Pump inhibitors
      • Bind to active proton pumps (predominantly in the body of stomach)
      • Irreversibly bind with regeneration of pumps every 48 hrs
      • Best effect is to take PPI 30 mins before meals
      • Immediate and delayed release forms
      • Ex: omeprazole, esomeprazole, pantoprazole, lansoprazole
    • Histamine blockers
      • Bind to the histamine receptor of the Proton Pump
      • Tachyplaxis (building up tolerance) – can develop in 2/3s
      • Better to take as needed
      • Works on demand
      • Ex: ranitidine, famotidine
  • Diet and lifestyle changes
    • Avoid certain foods
      • Tomato based, spicy, citrus, onion, garlic, mints, chocolate, caffeine
    • Don’t eat and recline for at least 2 hours
      • 4 hours if gastroparesis or slow emptying stomach
      • Wedge under mattress to elevate chest while sleeping
    • Stop tobacco
    • Weight loss
70
Q

GERD

Complications

A
  • Erosive esophagitis
    • Ulcer
    • Stricture
  • Pneumonitis
  • Barretts esophagus
  • Adenocarcinoma of the esophagus
71
Q

Esophagitis

A
  • Inflammation of the esophagus seen during endoscopy
  • Appears as “red streaks” or ulcers
  • In 10% of patients with true GERD
  • Pts w/ esophagitis usually need PPI therapy
  • Graded various ways
72
Q

Barrett’s Esophagus

A
  • Esophageal metaplasia
  • Normal esophageal columnar epithelium → intestinal epithelium with goblet cells
  • EGD: red, velvety tongue-like area of columnar mucosa w/ goblet cells
  • Incidence ↑
    • Up to 10% w/ GERD sx
    • Most common in white men 40-60
  • Higher risk for dysplasia in longer segment Barretts (> 3 cm)
    • Can lead to adenocarcinoma
    • Need surveillance to look for dysplasia and carcinoma
73
Q

Esophageal Dysplasia

A
  • Neoplastic epithelium that remains confined within the basement membrane
    • Lesion can be flat or raised (including polypoid)
    • Graded-two tiers:
      • Low grade
      • High grade
  • Precursor lesion to Adenocarcinoma
  • Presence of dysplasia @ initial clinical presentation important predictor of outcome
  • Controversial whether dysplasia regresses
  • Dysplasia & risk of adenocarcinoma does not respond to surgical or medical therapy
  • Clinical strategies:
    • Prevention of development of BE (treat GERD)
    • Biopsy surveillance of BE (unclear if improves pt survival)
    • If multifocal high-grade dysplasia, Carcinoma in situ, or invasive adenocarcinoma found ⇒ intervene
74
Q

Esophageal Stricture

A

Abnormal tightening or narrowing of the esophagus

  • Dysphagia to solids w/ strictures ≤ 12mm
  • True location of the stricture is where the patient points or below that area
  • Aim of dilation: ↑ luminal diameter to ≥ 12–14 mm
    • Results in immediate improvement/resolution of dysphagia in most
  • Methods of dilation:
    • Bougie – Exerts radial and axial forces as it traverses the stricture (proximal to distal)
    • Balloon – Exerts mainly radial forces equally throughout the stricture
75
Q

Esophageal Cancer

Overview

A
  • 1% of cancers in the US
  • 6% of cancers of the GI tract
  • Worldwide: Squamous Cell CA (SCCA) ⇒ 90% of esophageal cancers
  • In US: 50% SCCA, 50% AdenoCA
    • D/t rapid rise in AdenoCA in last 2 decades
  • Cancer types other than SCC and AdenoCa are very rare
76
Q

Esophageal Adenocarcinoma

Pathologic Features

A
  • > 75% distal esophagus
  • Histology:
    • Mucin-producing glands
    • Less often, signet ring cells
  • Gross appearance:
    • Flat patch
    • Raised patch
    • Nodular mass
    • Deep ulcerative
77
Q

Esophageal Adenocarcinoma

Clinical Features

A
  • Silent until advanced disease has developed
  • Manifests w/ difficulty/painful swallowing
  • Moves from solid to liquid foods
  • 5-year-survival overall < 25%
    • If found early w/ adenoCA only in mucosa or submucosa, can have 5-year survival of 80%
78
Q

Esophageal Squamous Cell Carcinoma (SCCA)

Epidemiology

A
  • Most pts > 45 y/o
  • Men > women (4:1 in US)
  • Blacks > Whites (6:1 in US)
  • High incidence areas:
  • Northern Iran, Central Asia, Northern China, Puerto Rico, South Africa, Eastern Europe
79
Q

Esophageal Squamous Cell Carcinoma (SCCA)

Etiology and Pathogenesis

A
  • Exposure to dietary/environmental carcinogens is causal
    • In US and Europe:
      • Alcohol and tobacco
    • In high incidence countries:
      • Fungusornitrosamine-containing foodstuffs
      • HPV may also play a role
  • Nutritional deficiencies potentiate
  • Genetic factors less important
  • Previous esophageal damage also a factor
80
Q

Esophageal Squamous Cell Carcinoma (SCCA)

Morphology

A
  • 50% in middle ⅓ of esophagus, 20% in upper ⅓
  • Squamous dysplasia → CIS
    • Exophytic ⇒ protrude into the lumen
    • Infiltrative ⇒ grow deeply into the wall
    • Can invade surrounding structures
    • Mostly moderate-well differentiated
  • When symptomatic ⇒ tumor usu. large and invasive
    • Pt moves from solid to liquid foods
81
Q

Esophageal Squamous Cell Carcinoma (SCCA)

Prognosis

A

5 yr survival:

  • 75% w/ superficial disease (rarely diagnosed at this stage)
  • 25% in pts w/ curative resection, advanced disease
  • 9% in all pts

6. HDS GI Repro (30 decks)

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