Chapter 14 - Oral Cavity and GI Tract Flashcards
Aphthous Ulcers
Recurrent aphthous ulcerations, canker sores, most common oral mucosal pathosis, *T-cell-mediated immunologic reaction
Causes: Different causes for different people, genetic predisposition (HLA linked)
Nutritional deficiencies, hematologic abnormalities, trauma, stress
Minor Aphthous Ulcers
Nonkeratinized mucosa, prodromal symptoms, 3-100 mm, begins in childhood, females>males, healing 7-14 days, fewest recurrences
Herpetiform Aphthous Ulcers
Small lesions (1-3mm), as many as 100, tend to coalesce into larger lesions, nonkeratinized or keratinized mucosa, female>male, adult onset, greatest number of lesions and most recurrences
Major Aphthous Ulcers
Extremely painful ulcer, longest duration per episode (1-10 ulcers), deeper, larger (1-3cm in diameter), labial mucosa, soft palate, and tonsillar fauces, tongue, onset after puberty
Herpesvirus Infection: Herpes Simplex Type I
Primary infection (initial exposure) -young age, often asymptomatic, usually does not cause significant morbidity Virus taken by sensory nerves and transported to the nearest sensory or autonomic ganglia Trigeminal ganglion usually involved
Primary Herpetic Stomatitis
Acute infection: children-herpetic gingivostomatitis, adults-pharyngotonsillitis
Small vessicles on lips or nasal orifices
Rupture to form shallow, painful ulcers
Systemic manifestations- fever, malaise, cervical lymphadenopathy
Recurrent Herpetic Stomatitis
ulcers bound to bone mucosa, gingiva, hard palate, and lips
multiple causes of reactivation
Candidiasis
Candida albicans normally present in the oral cavity in 30-40% of population Predisposing factors (antibiotic therapy, corticosteroid therapy, diabetes, immunodeficiency, debilitating disease, under dentures)
Pseudomembranous Candidiasis
“Thrush”, creamy white plaques (cottage cheese), can be rubbed off, underlying mucosa appears red and burns
Buccal mucosa, tongue and palate
Humanpapilloma Viral Lesions (HPV)
May cause: squamous papilloma, Verruca Vulgaris
May be solitary or multiple
Labial mucosa, tongue, buccal mucosa, gingiva
Pink, cauliflower-like growths
Epstein Barr infection
Oral Hairy Leukoplakia
usually HIV-associated, lateral borders of tongue, vertical white patches, does not rub off, EBV virus is the cause
Fibroma/ Focal Fibrous Hyperplasia
Most common benign soft tissue tumor of connective tissue origin
Probably due to irritation, not true neoplasm
Any site, age, varies in size
Normal color, elevated, sessile or pedunculated, ulcerated or smooth
Treatment: excision
Pyogenic Granuloma
Solitary, circumscribed red sessile or pedunculated, ulcerated nodule
More common in women, with pregnancy
May bleed spontaneously
Can occur on gingiva, labial mucosa or tongue
Pathogenesis: reactive hyperplasia of vascularized granulation tissue
Treatment: excision
Leukoplakia
“A white patch that cannot be scraped off and cannot be characterized as any other disease”
Assocated w/ hyperplasia or hyperkeratosis, Idiopathic
High risk sites: floor of mouth, lateral borders of tongue, ventral tongue, soft palate
3-25% (depending on location) may develop into invasive squamous carcinoma
Erythroplakia
Red, velvety, circumscribed areas w/ well defined borders
Associated with marked squamous dysplasia/ carcinoma in situ
Transformation to squamous carcinoma is 50% or more
Squamous Cell Carcinoma
Most common cancer in the oral cavity
Tends to occur in older individuals, less likely before age 40, but can occur in children and teenagers, clinically aggressive, about 50% kill patient within 5 yrs
Dry Mouth
Etiology: salivary gland autoimmune disease, radiation therapy, commonly prescribed medications
Oral signs: dry mucosa, atrophy of papillae of the tongue w/ fissuring or ulcerations
Oral complications: increased rates of dental caries and candidiasis, difficulty in speaking and swallowing
Sialadenitis
Inflammation of salivary gland
Causes: viral (mumps, paramyxovirus), bacterial (variety of organisms, usually secondary to duct obstruction by stone - sialolithiasis), autoimmune (Sjogren’s syndrome)
Mucocele
Trauma-related, draining duct damage leads to extravasation of mucus into surrounding tissue, lower lip is the most common site
Pleomorphic Adenoma
Most common benign salivary gland neoplasm
Also called “mixed tumor of salivary gland”
Oral lesions are usually located in hard palate
Mucoepidermoid Carcinoma
Most common salivary gland malignancy
2nd-7th decade of life
Asymptomatic swelling in palate usually
Odontogenic cysts
Cyst: an epithelium lined cavity, epithelium of odontogenic origin
Developmental: dentigerous cyst; odontogenic keratocyst s inflammatory: periapical cyst
Dentigerous cysts: originates around the crown of an unerupted tooth due to degeneration of the dental follicle
Odontogenic keratocysts: aggressive lesions w/ high recurrence rate, multiple odontogenic keratocysts-seen in nevoid basal cell carcinoma syndrome
Periapical cysts: very common, occurs due to necrosis of pulpal tissue
Acute pharyngitis
rhinoviruses, coronaviruses, respiratory syncytial viruses, many other viruses, Group A streptococcus, Difficult to distinguish viral from bacterial
Vocal Cord Papiloma
Squamous epithelial lesion - similar to those in the oral mucosa
May be multiple in children - called “Juvenile laryngeal papillomatosis”
HPV 6 & 11 association
Vocal Cord Nodules
Chiefly in heavy smoker or singers
Result of chronic irritation or vocal cord overuse
Not neoplastic
Hoarseness main symptoms
Laryngeal Tumors Malignant
95% are squamous carcinomas
May be: glottic, supraglottic, subglottic
Persistent hoarseness
Smoking most important risk factor
Mechanical Obstruction of Esophagus
Agenesis: absence of esophagus
Atresia: thin noncanalized cord replaces a segment of esophagus, more common at or near tracheal bifurcation
Fistula: abnormal connection b/n upper or lower esophageal pouches to the broncus or the trachea - may result in aspiration, suffocation, pneumonia, or severe fluid or electrolyte imbalances
Stenosis: narrowing of the esophagus due to submucosal fibrosis
Function Obstruction of Esophagus
Dysmotility: interferes w/ delivery of food and fluids to the stomach due to uncoordinated wave of peristaltic contractions or spasm of muscularis - causes inc esophageal wall stress and cause small diverticula
Achalasia: characterized by failure of lower esophageal sphincter relaxation and inc tone w/ esophageal peristalsis
Histal Hernia
Sliding hernia most common
Portion of proximal stomach protrudes above diaphragm
10% are symptomatic (Reflux esophagitis, Chronic gastric acid regurgitation may damage teeth)
Mallory-Weiss Syndrome
Longitudinal tears at the esophagogastric junction (10% are purely esophageal)
Original description in chronic alcoholics, but may be seen w/ any severe vomiting
Histal hernia in 75%
Bleeding is usually self-limiting, but may be life-threatening
Symptom: hematemesis
Varices
Occur in 66% of patients w/ cirrhosis, most often alcoholic cirrhosis
Asymptomatic until rupture, then massive hematemesis
20-30% die in first episode of bleeding
Rebleeding common (70% within one year)
Cirrhosis of liver impedes portal blood flow causing portosystemic shunts
Flow diverted through coronary veins of stomach to submucosal esophageal veins
Esophageal Web Plummer-Vinson Syndrome
Anemia (iron deficiency)
Clinical features: upper esophageal web, atrophic glossitis, slightly inc risk of upper esophageal squamous carcinoma
Reflux esophagitis
in western countries
Gastroesophageal reflux disease “GERD”
Symptom: heartburn
Consequence: bleeding, strictures, Barrett esophagus
Barrett Esophagus
Replacement of normal squamous mucosa by metaplastic columnar epithelium
Consequence of chronic reflux, 4:1 male
Mostly whites
40X inc risk of adenocarcinoma of distal esophagus
Esophageal Cancer Symptoms
Insidious onset, Dysphagia & obstruction, Weight loss, anorexia, fatigue, weakness in later stages, 7:1 male predominance
Squamous Carcinoma
90% of esophageal cancers worldwide are squamous Adenocarcinoma most common in US Blacks>whites worldwide HPV-associated in high incidence areas Alcohol & tobacco 50% in mid 1/3 of esophagus
Adenocarcinoma
Almost always arises in Barrett esophagus
Almost always distal 1/3 esophagus, often at EGD, usually males, >50 yr
Prognosis not good-terrible actually
Acute Gastritis
Usually transient, epigastric pain, nausea, vomiting, may have mucosal erosion resulting in hemorrhage
Causes: NSAIDS, alcohol, smoking, chemotherapy, uremia, shock, severe physiologic stress
Chronic Gastritis
Most common form of gastritis, Chronic inflammatory changes leading to mucosal atrophy and metaplasia
Helicobacter pylori most common cause by far
H. Pylori gastritis
Gram negative rod
Mode of acquisition not clear (person-person)
May have upper abdominal pain, nausea & vomiting
Treatment w/ antibiotics leads to resolution, but can recur
Most patients w/ gastric or duodenal ulcers have H. Pylori
Mechanisms: Proinflammatory Cytokines, decreased bicarbonate production, decreased gastric mucous production, increased acid secretion
Autoimmune chronic gastritis
autoantibodies to acid producing enzyme in parietal cells leads to cellular injury, loss of acid-producting parietal cells and mucosal atrophy
Reduction in gastric acid & intrinsic factor secretion
Leads to poor absorption of vitamin B12 resulting in “pernicious anemia”
May be associated w/ other autoimmune disorders
inc. gastric cancer risk
Peptic Ulcers
Ulcers produced by action of gastric acid/pepsin (mucosal defenses breached, imbalance b/n defense mechanisms and damaging acid/pepsin)
Occur in 1st portion of duodenum and stomach - ratio of 4:1
Frequent in patients w/ alcoholic cirrhosis, chronic renal failure, hyperparathyroidism
Pathogenesis: 70% of gastric ulcers associated w/ H. pylori (most of remainder due to NSAIDS), 90% of duodenal ulcers associated w/ H. pylori, cigarette smoke causes mucosal ischemia, corticosteroids & NSAIDS inhibit prostaglandins necessary for mucosal integrity
Symptoms: gnawing, burning, or boring epigastric pain occuring 1-3 hr after meals and at night, nausea, vomiting, bloating, belching
Complications: Bleeding*, perforation of ulcer w/ peritonitis, cancer arising in benign gastric ulcers rare, cancer in duodenal ulcers virtually nonexistent
Treatment: antibiotics, acid inhibitors (histamine blockers or proton pump inhibitors)
Acute Gastric Ulceration “Stress Ulcers”
Multiple small ulcers appearing during severe physiologic stress (trauma, sepsis, extensive burns, brain trauma, combo of reduced bicarbonate secretion), significant bleeding may occur
Gastric Tumors - “Polyps”
“Polyp” - may be inflammatory, hyperplastic or neoplastic
Most arise in the setting of “chronic gastritis”
Most are hyperplastic (innocuous)
Adenomas (neoplastic, up to 40% greater than 2 cm may harbor adenocarcinoma)
Peutz-Jehgers Syndrome
Pathogenesis: autosomal dominant disorder
Pathology:
Benign Harmatomatous polyps of gastrointestinal tract, Melanotic macules on facial skin (buccal mucosa, intra-oral mucosa, hands, feet, and perineum), Increased cancer risk (18X), gastrointestinal and other sites, Hamartomatous polyps themselves are not malignant or premalignant
Gastric Cancer (Carcinoma)
90-95% are adenocarcinoma, 5-yr survival rate <20%
Proposed precursor lesions: H. pylori-induced chronic gastritis most important known etiology, autoimmune gastritis
Symptoms: usually none until advanced, abdominal discomfort and weight loss
Locally extensive disease (liver and lymph node involvement common)
Complications: bleeding, perforation, malnutrition, extension of cancer into adjacent organs, liver failure
Inflammatory Bowel Disease
Crohn disease and ulcerative colitis are collectively called IBS
Genetic predisposition, profound derangement of gastrointestinal mucosal innate immunity, autoimmune component suspected, inflammation is final common pathway for bowel injury
Crohn Disease
Systemic, granulomatous inflammatory disease w/ predominately gastrointestinal involvement
2nd & 3rd decades, mostly in women
Characteristic feature: segmental, transmural inflammation w/ scarring, granulomatous but granulomas not always found
Symptoms and Clinical Course: diarrhea, crampy abdominal pain and fever, onset abrupt an dmimic acute appendicitis, blood in stool w/ colon
about 60% - fluctuating disease w/ years of active symptoms followed by years of remission
Complications:Fistula formation, abdominal abscesses, intestinal strictures, measurably inc risk for GI cancer Extra-gastrointestinal (eye involvement; skin lesions; arthritis; liver diseases)
Ulcerative Colitis
Ulcero-inflammatory disease affecting only colon and limited to mucosa and submucosa
Begins in rectum extending proximally in a continuous fashion (polyarthritis, eye & skin involvement, liver disease)
@ initial diagnosis, 50% of patients have disease limited to rectum or rectosigmoid colon, *“skip” lesions do not occur, ulcerated mucosa bleeds easily (grossly bloody, mucoid stools common many/day) “Pseudopolyps”
Clinical course: chronic relapsing and remitting
Complications: blood & electrolyte loss from diarrhea, severe colonic dilation - “Toxic megacolon”, most feared long-term complication is development of adenocarcinoma
Meckel Diverticulum
Blind-ended protrusion of ileum w/in 2 ft of ileocecal valve resulting from persistence of omphalomesenteric duct
May contain gastric mucosa which can ulcerate producing pain simulating acute appendicitis
Hirschsprung Disease: “Congenital Megacolon”
Aganglionic segment of rectum and sigmoid colon (developmental, migration failure of neural crest cells to reach distal bowel, affected segment remain contracted)
Lack of peristalsis (obstruction, dilation, perforation w/ peritonitis)
Ischemic Small Bowel Disease
Infarction of bowel wall (Transmural- entire thickness, Mural- muscularis spared, Mucosal- only mucosa)
Causes: arterial thrombus, arterial embolus, venous thrombosis, nonocclusive ischemia
Symptoms: abdominal pain, usually sudden followed by shock and vascular collapse, peritonitis is perforation occurs, mortality rate: 90%
Hemorrhoids
Variceal dilations of anal and perianal submucosal venous plexuses:
Causes: venous stasis of pregnancy, chronic constipation w/ staining, cirrhosis of liver w/ portal hypertension
Colonic Diverticulosis
Outpouchings lined by mucosa and submucosa at areas where nerves and arterial vasa recta penetrate the muscularis
Thought to be related to low-fiber diet resulting in reduced stool bulk requiring greater pressure to defecate
Complications: inflammation, necrosis, and perforation of diverticulum, peritonitis or localized abscess, scarring and colonic obstruction
Symptoms & Treatment: usually asymptomatic (25% of patients have intermittent cramping or discomfort in left lower quadrant of abdomen, great discomfor and fever if inflamed)
High fiber diet, antibiotic if evidence of diverticulitis
Pseudomembranous Colitis (Antibiotic-associated colitis)
Caused by toxins elaborated by Clostridium difficile, gram positive
Toxins bind to colonic mucosa and damage it
Fecal-oral spread especially in hospitals and extended care facilities
Occasionally occurs w/out antibiotic treatment
Infants rarely affected, immature mucosa apparently does not bind toxins
New, more virulent strain of C. difficile emerged in about 2003
Malabsorption Syndromes
Suboptimal absorption of fats, fat-soluble & other vitamins, proteins, carbs, electrolytes, mineral and water
Most common types (Crohn disease, pancreatic insufficiency, celiac disease, lactase deficiency)
Pancreatic Insufficiency
Cystic fibrosis or chronic pancreatitis (fats and proteins not digested, loss of fat-soluble vitamins, osmotic diarrhea and steatorrhea, voluminous, foul-smelling stools)
Celia Disease (Gluten-Sensitive Enteropathy)
Reduced small intestinal surface area due to atrophy of villi (immune-mediated mucosal injury, hypersensitivity to gluten)
Sensitivity to gluten
Strong genetic susceptibility
Common - 1/300
Infancy to mid-adulthood
Symptoms: diarrhea & malnutrition
Dental Practice Implications: When seen in childhood - enamel hypoplasia
adults - aphthous ulcers, dermatitis herpetiformis
Lactose Intolerance
inherited deficiency rare
Acquired deficiency common (N. American adult, dec production of lactase by small intestinal epithelium)
Symptoms: abdominal cramping, bloating, diarrhea due to overgrowth of intestinal bacteria in presence of excess carb
Avoid milk products
Intestinal mucosa is normal
Acute appendicitis
10% of people in US
Peak in 2nd & 3rd decade
Obstruction of appendix in 50-80% of cases (Fecalith usually, less commonly tumor or ball of pinworms
Symptoms: periumbilical pain initially, then localizing in RLQ, Anorexia, nausea, vomiting, constant pain in RLQ
Differential Dx: viral mesenteric lymphadenitis, gastroenteritis, pelvic inflammatory disease, rupture of ovarian follicle at ovulation, ectopic pregnancy, Meckel diverticulitis, Crohn disease
Non-neoplastic Polyps
Hyperplastic Polyp (most common colonic polyp, 90% of colonic polyps) Most less than 5 mm in diameter Cause unknown Not considered premalignant 40% of adults harbor them
Colonic Adenoma
Neoplastic polyp (may be "sessile" [broadbased] or "pedunculated" [on a stalk]) Size important predictor of malignant potential (<1 cm - cancer rare, >4 cm - 40% contain adenocarcinoma)
Familial Adenomatous Polyposis
Uncommon
Autosomal dominant disorder
Mutations in the APC gene, a tumor suppressor gene
500-2500 colonic adenomas
100% incidence of colonic adenocarcinoma by midlife unless colon resected
Gardner Syndrome
Phenotypic variant of familial adenomatous polyposis
Colonic polyposis - colon cancer (100%)
Desmoid tumors - 20% - fibromatosis
Slightly elevated risk of duodenal and thyroid cancer
Osteomas of jaws, skull, long bones, and multiple supernumerary teeth
Epidermoid cysts of skin
Colorectal Adenocarcinoma
15% of cancer-related deaths in USA
Majority arise from adenomas
Most in 60-70 y/o
High fat, refined diet may be carcinogenic although unproven at present
Colorectal Carcinoma Distribution
Cecum and ascending colon (38%) Transverse colon (18%) Descending colon (8%) Sigmoid colon (35%) Multiple sites (1%)
Colorectal Carcinoma
Left sided cancer: annular, encircling lesions, “Napkin ring” or “Apple core lesion” by barium radiography
Right sided cancer: polypoid, fungating masses, less obstruction, grows into spacious cecum and ascending colon
Clinical Course - occult bleeding then changes in bowel habits and crampy, LLQP
Left side worse than right due to infiltrative growth of cancer
Single most important prognostic indicator is the stage of the tumor at time of diagnosis
Carcinoid Tumor
All potentially malignant, Arise from endocrine cells (those of appendix & rectum almost never metastasize, small bowel often metastasize to liver & lymph nodes)
Carcinoid syndrome occurs when metastatic to liver since serotonin is not inactivated
