Path GI I Oral Cavity/Esophagous (17)
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Ulcerative & Inflammatory Lesions of the Oral Cavity
- 1. Aphthous Ulcers (Canker Sores)
- 2. Herpesvirus Stomatitis
- 3. Oral Candidiasis (Thrush) – is Inflammatory
Aphthous Ulcers (Canker Sores)
- small, painful lesions (usually <5 mm="" dia="" rounded="" superficial="" erosions="" w="" erythematous="" rim="" gray-white="" exudate="" br="">are located on the non-keratinized oral mucosa, particularly the soft palate, buccolabial mucosa, floor of the mouth, & lateral border of the tongue
- they are self-limiting, usually heal w/o scarring, & will SPONTANEOUSLY recover but MAY recur in the same or different place
What can trigger aphthous ulcers (canker sores)?
- stress, fever, indigestion of certain foods, & activation of inflammatory bowel disease
- may be an autoimmune response in a who doesn't have a viral infection or lacks proper immunosuppression
Aphthous Ulcer (Canker Sore) Composition
- a shallow ulcer covered by a fibrinopurulent exudate w/ underlying infiltrate composed of MONONUCLEAR & POLYMORPHONUCLEAR leukocytes
- aka monocytes & neutrophils
- exudate b/c cells are involved
- fibrinopurulent: puss/fibrous material
- a common infection of the oral cavity caused by herpes simplex virus type I (HSV1) or type II (HSV2) & is spread from person to person
- the primary infection is asymptomatic but the virus persists in a dormant state within ganglia around the mouth (eg. trigeminal ganglia)
- this oral cavity infection is now frequently caused by HSV 2 (herpes genitalis)
How many people have been infected by herpes simplex virus type I (HSV1) by midlife?
3/4ths of the population
What conditions can reactivate the virus, leading to cold sores/fever blisters?
- fever, sun, cold exposure, respiratory tract infection, trauma, etc.; anything that causes STRESS
- the lesions appear alone or as a group of small (<5 mm="" dia="" vesicles="" filled="" w="" clear="" fluid="" most="" often="" on="" the="" lips="" around="" nasal="" orifices="" br="">they rupture, leaving behind shallow, painful ulcers that heal within weeks
- recurrences are VERY COMMON
Herpesvirus Stomatitis Sore Description
- vesicles, filled w/ exudate
- some infected cells show intranuclear acidophilic viral inclusions & ‘ballooning degeneration’
- multinucleated polykaryons form from fusion between adjacent cells
- [herpetic gingivostomatitis or lymphadenopathy may develop in an immunocompromised patient (more severe infection)]
**************in severe cases viremia may affect disseminated lesions************
- a histopathologic description of cells undergoing cell death
- the name is derived from the fact that the cells undergoing this form of cell death increase in size (balloon)
a microscopic examination of the vesicle fluid showing cells w/ inclusions & polykaryons
Oral Candidiasis (Thrush)
- caused by the yeast Candida albicans, part of the normal oral flora when there is some impairment in normal protective mechanisms (eg. w/ diabetes mellitus, anemia, antibiotic or glucocorticoid therapy, HIV infection, disseminated cancer, during infancy, etc.)
- also known as Pseudomembranous candidiasis or Moniliasis
Gross: Oral Candidiasis
- adherent, white, curd-like, circumscribed plaque anywhere in the oral cavity
- pseudomembrane composed of FUNGAL organisms superficially attached to the underlying granular erythematous inflammatory mucosa – can be scraped off (hence pseudo)
- ulceration ranges from mild → covering the entire mucosa
- infection may spread into the esophagus & can become life threatening if it spreads further
Preneoplastic Epithelial Lesions
- 1. Leukoplakia
- 2. Erythroplakia
Leukoplakia ("White Patch")
- a white patch or plaque that CAN'T be scraped off or classified as any other disease
- the mucosal patch or plaque is whitish, well-defined, w/ a demarcated margin, & is caused by epidermal thickening or hyperkeratosis
- usually found on the buccal mucosa, tongue, or floor of the mouth
- plaques may be single or multiple & vary from small lesions to large patches
Degree of 'Differentiation'
- lesions can vary from banal hyperkeratosis w/o underlying dysplasia → mild or severe dysplasia bordering on carcinoma in situ
- the frequency of malignant transformation to squamous cell carcinoma is 3 – 25% (majority DON'T turn malignant)
- marked epithelial thickening & HYPERKERATOSIS
What habit has a strong association with the development of Leukoplakia?
Tobacco, particularly pipe smoking & smokeless tobacco, is strongly associated with the development of Leukoplakia lesions
- the less common RED equivalent of leukoplakia
- lesions are red, velvety, often granular, circumscribed areas that may or may not be elevated, & have POORLY defined/irregular boundaries
- these lesions almost invariably have marked dysplasia
- have a malignant transformation rate of GREATER than 50%
Cancers of the Oral Cavity & Tongue
What type of head & neck cancer is responsible for ~95% of cases?
- Squamous Cell Carcinomas (HNSCCs)
- in the head & neck, they are most often found in the oral cavity (MOUTH)
- usually occurs after the age of 40
- many cases have metastasized by the time the primary lesion is detected which is why HALF result in death within 5 years of their discovery
Head & Neck Squamous Cell Carcinoma Risk Factors
- biggest risk factor: Tobacco use, especially pipe smoking & smokeless tobacco
- Leukoplakia & Erythroplakia
- HPV (16 & 18) are found in conjunction w/ 50% of oropharyngeal carcinoma
- Alcohol abuse (especially if combined w/ tobacco use)
- Betel quid & paan (↑ risk 8–9x)
- Protracted irritation weakly ↑ risk
Where are cancers of the oral cavity & tongue mainly found?
- at the vermilion border of the lateral margin of the lower lip, floor of the mouth, & the lateral borders of the mobile tongue
- vary from moderately to well differentiated keratinizing tumors
Sequence of Lesion Development
- early lesions resemble leukoplakia → progress in an exophytic fashion to readily visible & palpable nodular → eventually fungating lesions
- or they may assume an endophytic, invasive pattern w/ central necrosis to create a cancerous ulcer
Which cancers significantly spread to regional lymph nodes at the time of their initial diagnosis?
- 60% of carcinomas of the floor of the mouth have spread
- 50% of tongue carcinomas have spread
- lip carcinomas RARELY spread
- for the mouth & tongue cases there may be extensive regional spread
- a keratinized structure found in regions where abnormal squamous cells form concentric layers
- is seen w/ squamous cell carcinoma
- inflammation of a salivary gland
- can be due to Mucocele, Viral infections, Bacterial infections, or Autoimmunity (Sjögren Syndrome)
- most common lesion of the salivary gland results from blockage or rupture of a salivary gland duct causing leakage of saliva into surrounding tissues
- is often a consequence of TRAUMA
- a cyst-like space becomes lined by inflammatory granulation tissue which is filled w/ MUCIN & MACROPHAGES (+ other inflammatory cells)
- treated via excision of the cyst from the salivary gland
- [mucin = gel-like lubricating proteins]
Sialadenitis due to Viral Infection
- mumps → enlargement of all 3 major salivary glands, especially the PAROTID
- paramyxovirus causes most cases
- such an infection is self-limiting in children however in adults it can lead to PANCREATITIS, ORCHITIS, or even STERILITY
Sialadenitis due to Bacterial Infection
- salivary gland inflammation is usually secondary to ductal obstruction caused by stone formation (sialolithiasis) or retrograde entry of bacteria from the oral cavity, especially. in dehydration
- Staphylococcus aureus & Streptococcus viridans cause most cases
- inflammation may be interstitial OR there may be focal areas of suppurative necrosis & abscess
What type of patient is subject to greater risk when dealing with sialadenitis caused by a bacterial infection?
anyone w/ chronic, debilitating conditions, compromised immune function, or MEDICATIONS that contribute to oral or systemic DEHYDRATION
Sjögren Syndrome (Autoimmune Sialadenitis)
- a chronic disease characterized by dry eyes (keratoconjunctivitis) & mouth (xerostomia) caused by immunologically mediated destruction of the lacrimal & salivary glands
- as a result the lacrimal & salivary glands become compromised first by lymphocytic infiltration, then by fibrosis
- the salivary gland becomes enlarged
- there is INTENSE lymphocytic & plasma cell infiltration
- + ductal epithelial hyperplasia
What are the 2 types of salivary gland tumors he discusses?
1. Pleomorphic Adenoma: most common salivary gland tumor; benign/mixed; well demarcated/encapsulated
2. Mucoepidermoid Carcinoma: most common malignant tumor
What is the most common tumor of the salivary glands?
- Pleomorphic Adenoma
- a benign salivary gland mixed tumor
- is especially common in the SUPERFICIAL PAROTID gland
- is characterized by a mixture of epithelial & stromal cell elements
Pleomorphic Adenoma Mixed Tumor Description
- slowly growing
- encapsulated firm mass
- has a smooth surface
- tumor cells form ducts, acini, tubules, strands, or sheets of cells
- epithelial tissue intermingles w/ myxoid, mucoid, or chondroid areas (there is HETEROGENEITY, hence the 'mixed')
- is a well-demarcated tumor adjacent to normal salivary gland parenchyma
What is the fate of/how can a Pleomorphic Adenoma be treated?
- it can be surgically removed but may recur
- it has the potential to give RISE to a malignant mixed tumor, which is 1 of the most AGGRESSIVE of all salivary gland malignant neoplasms
- if malignancy arises from a benign pleomorphic adenoma, mortality rates are 30-50% after 5 years
- a malignant salivary (mainly in the parotid) gland tumor composed of a mixture of neoplastic epidermal cells, mucus-secreting cells, & epithelial cells of intermediate type
- it originates from DUCTAL epithelium
- it's degree of differentiation is variable & the clinical course & prognosis depends on the grade
- it's the most common primary MALIGNANT tumor of the salivary glands
Mucoepidermoid Carcinoma Cell Description
- grow in nests composed of squamous cells as well as clear vacuolated cells containing mucin
- (mucin = pink in picture on right)
- METAPLASIC replacement of SQUAMOUS by COLUMNAR epithelium in the lower third of the esophagus as a result of chronic gastroesophageal reflux
- happens more often in males than females & is more common in white people
Intestinal Metaplastic Epithelium
- contains well-formed goblet cells (REQUIRED for diagnosis) interspersed w/ gastric foveolar cells
- note an absence of real intestinal absorptive cells
- IF dysplasia is present, it is classified as low or high grade & increases ones risk of esophageal adenocarcinoma (30–100x greater risk)
What significance do esophageal veins have in terms of circulation?
they provide potential sites for communication between the intra-abdominal splanchnic circulation (visceral organ) & the systemic venous circulation
- extremely dilated sub-mucosal (immediately beneath the mucosa) veins in the lower third of the esophagus
- are most often a consequence of portal hypertension, commonly due to cirrhosis (present in 90% of such patients)
- are prone to rupture, especially those greater than 5mm in diameter → life-threatening hemorrhage
What is the primary cause of esophageal varices?
- Alcohol abuse
- the 2nd most common cause of varices is hepatic schistosomiasis
What percent of cancer deaths in 2009 could be attributed to esophageal cancer?
How many esophageal cancers in the US are adenocarcinomas?
HALF of U.S. esophageal cancer cases are Adenocarcinomas (50%)
What are almost ALL adenocarcinomas of the esophagus preceded by?
- 1. Barrett esophagus
- 2. long-standing GERD (Gastroesophageal reflux disease)
- risk of development is further increased by dysplasia, tobacco use, obesity, & prior radiation therapy
Adenocarcinoma of the Esophagus
- usually occurs in the DISTAL end of the esophagus
- presents w/ pain or difficulty swallowing, progressive weight loss, chest pain, vomiting, or hematemesis (vomiting blood)
- seen in caucasians, 7 males : 1 female (but the incidence, new cases, varies 60-fold world wide)
- 5 year survival rate is 85% in cases where the lesion is limited to the mucosa or submucosa but less than 25% in cases w/ tumor spread
By the time symptoms of an esophageal adenocarcinoma appear, has the tumor spread? If it has, to where?
the tumor usually HAS spread by the time symptoms are present, to the SUBMUCOSAL LYMPHATICS
What lowers a person's risk of developing an esophageal adenocarcinoma?
diets rich in fresh fruits & vegetables
What is often the first sign of squamous cell carcinoma of the esophagus?
- Dysphagia – difficulty swallowing
- however by this time most tumors are unable to be removed by surgery (unresectable)
Squamous Cell Carcinoma of the Esophagus
- begins as squamous dysplasia → progress to cancer
- usually occurs in the middle third of esophagus
- neoplastic squamous cells range from well differentiated w/ epithelial pearls, to poorly differentiated tumors that lack evidence of squamous differentiation
- in US adults over 45 yrs. of age, is found in 4 males for every 1 female (varies up to 180-folds within countries)
Where is squamous cell carcinoma of the esophagus most frequently found along the esophagus?
in the MID-esophagus, where it commonly causes STRICTURES (narrowing of the esophagus that causes swallowing difficulties)
Where is squamous cell carcinoma of the esophagus more commonly found geographically?
in rural & underdeveloped areas
Rick Factors for Esophageal Squamous Cell Carcinoma
- alcohol & tobacco use
- caustic esophageal injury (tissue destruction)
- achalasia (nerve damage → failure of smooth muscles to relax)
- previous radiation therapy
- frequent consumption of very hot beverages
Normal Damaging Forces of Gastric Injury
- 1. gastric acidity
- 2. peptic enzymes
Normal Mechanisms of Protection AGAINST Gastric Injury
- 1. mucous secretion onto gastric surface
- 2. bicarbonate secretion (into the mucus)
- 3. blood flow directed to mucosa cells
- 4. apical surface membrane trnsprt
- 5. epithelial regeneration
- 6. prostaglandin elaboration
Abnormal Forces of Gastric Injury
- 1. H. pylori infection
- 2. NSAID
- 3. Aspirin
- 4. Cigarettes
- 5. Alcohol
- 6. Gastric hyperacidity
- 7. Duodenal-gastric reflux
Abnormal Mechanisms of Protection AGAINST Gastric Injury
- 1. Ischemia
- 2. Shock
- 3. Delayed gastric emptying
- 4. Host factors
Characteristic of an Ulcer (NIGFS)
- ulcers include layers of necrosis (N), inflammation (I), & granulation tissue (G) [from most superficial to deep]
- a fibrous scar (S) might be present at the lowest layer, however it takes TIME to develop & is only present in CHRONIC lesions
Acute Erosive Gastritis
- a (usually transient) acute mucosal inflammatory process characterized by mucosal NECROSIS accompanied by an acute inflammatory response & hemorrhage
- in severe cases erosion (sloughing off of the superficial mucosal epithelium) may occur
- usually heals w/ complete restitution IF the noxious stimulus is removed
What DEFINES Acute Erosive Gastritis?
- an endoscopy that shows both mucosal cell EROSION & HEMORRHAGE
- mucosal edema & an inflammatory infiltrate of NEUTROPHILS + other chronic inflammatory cells may also be present
- regenerative replication of epithelial cells in gastric pits is usually prominent
- can be extremely localized or diffuse
- inflammation can range from superficial to transmural w/ hemorrhage & focal erosions
What is acute erosive gastritis most commonly associated with?
- the intake of aspirin, NSAID, excess alcohol, smoking, cancer chemotherapy, ischemic injury & any serious illnesses
- boils down to DRUGS (NS-NSAIDS) & STRESS
Non-selective non-steroidal anti-inflammatory drugs (NS-NSAIDS)
- block BOTH COX-1 & COX-2
- eg. aspirin, indomethacin, ibuprofen
- take care of inflammation, but also decrease physiologic amounts of prostaglandins
Selective NSAIDS (S-NSAIDS)
- specific for COX-2 & have the benefit of relieving symptoms of acute inflammation WITHOUT the undesirable side effects of gastrointestinal ulceration & potential renal damage
- eg. Rofecoxib (vioxx) & Celecoxib (celebrex)
Causes of Mucosal Damage in Acute Erosive Gastritis
- disruption of the adherent mucous layer
- stimulation of acid secretion b/c H+ back- diffuses into the superficial epithelium
- ↓ production of bicarbonate buffer by superficial epithelial cells
- ↓ mucosal blood flow (why increasing it helps to combat injury as previously mentioned)
- direct damage to the epithelium
What is present in gastric biopsy specimens of almost ALL patients with duodenal ulcers & the majority of patients with gastric ulcers or chronic gastritis?
Helicobacter pylori bacteria
What is the most common type of chronic gastritis in the US?
- H. pylori Gastritis
- the disease results from an imbalance btwn gastroduodenal mucosal defenses & damaging forces that overcome these defenses
- this leads to eventual mucosal atrophy & epithelial METAplasia (mucosal epithelium → intestinal epithelium)
H. pylori Gastritis
- bacteria are found on the surface mucus of epithelial cells & in gastric foveolae
- if chronic may extend to involve the body & fundus of the stomach & the mucosa can become atrophic
- treatment involves combinations of antibiotics & proton pump inhibitors
Cell Characteristics of H. pylori Gastritis:
- *INTRAepithelial Neutrophils
- *SUBepithelial (lamina propria) plasma cells
- neutrophils also accumulate in the lumen of gastric pits to create pit abscesses
What types of cells can be found in the superficial lamina propria of a stomach affected by H. pylori Gastritis?
- large numbers of plasma cells, often in clusters & sheets
- an increased number of lymphocytes & macrophages
- (neutrophils can also be seen in the lamina propria, not just intraepithelialy)
The inflammatory cell infiltration characteristic of H. pylori Gastritis has the potential to transform into what?
- lymphoid aggregates [MALTS, mucosa associated lymphatic tissue] have the potential to transform into lymphomas
- lymphoid aggregates w/ germinal centers & abundant subepithelial plasma cells in the superficial lamina propria are characteristic of H. pylori gastritis
What can be seen in H. pylori Gastritis?
- an antrum w/ intense lymphocytic & plasma cell infiltrate (these cells tend to migrate to the superficial portion of the lamina propria)
- the microorganisms themselves appear on a Steiner silver staining as small, curved rods on the surface of the gastric mucosa (there is no tissue invasion by bacteria)
Peptic Ulcer Disease (PUD)
- ulcers = a breach in the mucosa extending through the muscularis mucosae into the submucosa or deeper
- they usually occur on the anterior duodenal wall alone (solitary) in more than 80% of cases
- the imbalance of mucosal defenses & damaging forces that cause Chronic Gastritis are also responsible for PUD
What is Peptic Ulcer Disease most often associated with?
- H. pylori-induced hyperchlorhydric chronic gastritis
- this state is present in 85–100% of patients w/ duodenal ulcers & in 65% w/ gastric ulcers
- a state in the stomach where gastric acid levels are higher than normal (pH ~1–3)
- is usually defined as having a pH less than 2
What is the the primary underlying causes of PUD?
- H. pylori
- NSAID use
- both compromise mucosal defenses & cause mucosal damage
- other causative factors: diet, drugs, cigarette smoking, blood group antigens, excessive pepsinogen cleavage
Where are peptic ulcers more common, in the proximal duodenum or the stomach?
- they are FOUR TIMES more common in the proximal duodenum than they are in the stomach
- they mostly occur along the lesser curvature near the interface of the body & pylorus (region of the stomach that connects to the duodenum; the antrum is the 1st part)
PUD Ulcer Description
- a round/oval punched-out defect whose mucosal margin is usually level w/ the surrounding mucosa (heaped-up margins are more characteristic of CANCERS)
- base of ulcer is smooth & clean as a result of peptic digestion of exudate; blood vessels may be evident
- the base of active ulcers may have a thin layer of fibrinoid debris above a NEUTROPHILIC inflammatory infiltrate
- underneath these 2 layers lies active granulation tissue infiltrated w/ mononuclear leukocytes & fibrous or collagenous scar
- this forms the ulcer base
- vessel walls around the scarred areas are typically thickened & occasionally thrombosed
What is the chief complication of Peptic Ulcer Disease?
- it can be life-threatening
- it only happens in 5% of patients but accounts for 75% of deaths from the disease
- has characteristic sharp demarcations from the surrounding mucosa, w/ radiating gastric folds
- gray fibrin is found in the base of ulcer
What is the most common malignancy of the stomach?
- Gastric Adenocarcinoma
- it makes up over 90% of all gastric cancers
- is influenced by many environmental & dietary factors (as evidenced by the decline in incidences in some countries)
- overall 5-year survival rate is less than 30% in the US due to LATE DETECTION
What seems to be a KEY step in the development of diffuse gastric cancer?
the loss of E-cadherin function
In the Western world, what state is gastric adenocarcinoma in by the time it's detected?
in most cases it has penetrated beyond the submucosa into the muscularis propria & may extend through the serosa
Intestinal-type Gastric Adenocarcinoma
- a bulky, elevated tumor composed of glandular structures
- has heaped-up borders (unlike peptic ulcers) & central ulcerations
- tumor grows along broad cohesive fronts to form either an exophytic mass or ulcerated tumor
- neoplastic cells often contain apical mucin vacuoles & abundant MUCIN may be present in gland lumens
- develops from precursor lesions (eg. dysplasia & adenomas)
- mean age of presentation is 55 yrs in 2 males for every 1 female
What is this particular lesion indicative of?ADENOGAS PIC
Intestinal-type Gastric Adenocarcinoma: an elevated mass w/ heaped-up borders & central ulceration
- tending to grow outward beyond the surface epithelium from which it originates
- proliferating on the exterior or surface epithelium of an organ or other structure in which the growth originated
What is the most powerful prognostic indicator for gastric cancers?
the depth of invasion & the extent of nodal & distant metastasis at the time of diagnosis (staging)
Diffuse (Infiltrating) Gastric Adenocarcinoma
- NO true tumor mass is seen
- this type of cancer is usually made up of non-cohesive cells that instead of forming glands, have large MUCIN VACUOLES that expand the cytoplasm & push the nucleus to the cell's periphery
- this creates a SIGNET-RING cell morphology
- such cells permeate the mucosa & stomach wall individually or in small clusters
- can be recognized by their large cytoplasmic mucin vacuoles & peripherally displaced, crescent-shaped nuclei
What do infiltrating (diffuse) gastric adenocarcinoma tumors invoke?
- a Desmoplastic Reaction
- this is the pervasive growth of dense fibrous tissue around a tumor
- it stiffens the gastric wall & may provide a valuable diagnostic clue
- the rigid thickening of the wall of the whole stomach which leads to a water bottle appearance
- is characteristic of diffuse (infiltrating) gastric adenocarcinoma & is caused by a desmoplastic reaction instigated by tumor cells of this cancer
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