Patho chapter 14 - GI

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• Superficial mucosal ulcers of unknown origin. Common first two decades of life. Painful & recurrent. M: Solitary/multiple, shallow, hyperemic, Covered by thin exudate & rim of erythema. Resolves within 7-10 days Aphtous ulcers
• Primary infection occurs at age 2-4, then stay latent until activated by e.gtrauma, allergies, UV-light, extreme temperatures etc. M: group of small vesicles on lips, nasal orifices, buccal mucosa, gingiva, hard palate, can fuse with eachother to form a polykaryon. HSV 1
• Most common fungal infection of oral cavity. Caused by C. albicans. Disease occurs b.c.o immunosupression, diabetes. 3 kinds: pseudomembranous, erythematous, hyperplastic Oral candidiasis
• Submucosal nodular fibrous tissue masses. Formed when chronic irritation results in reactive CT hyperplasia. often Located in buccal mucosa. No malignancy! Fibroma (fibrous proliferative lesion of oral cavity)
• Pedunculated masses in children, young adults & pregnant. Caused b dense proliferation of immature vessels (like in granulation tissue). Can regress, mature into dense fibrous masses or develop into peripheral ossifying fibroma. Often located in gingiva of younger. M: richly vascularized, ulcerated, red/purple, rapid growing Pyogenic granulomas (fibrous proliferative lesion of oral cavity)
• A white patch or plaque that cannot be scraped off or characterized as any other disease. Precancerous & of unknown origin. M: White raised patch, smooth with well demarcated borders & minimal elevation. Has dysplasia, nuclear & cellular pleumorphism, loss of normal maturation, hyperkeratosis. Leukoplakia
• Red, velvety eroded area that is flat/slightly depressed. Associated with greater risk of malignancy than leukoplkia. Has high dysplastic & anaplastic changes, inflammatory cell infiltrates of lymphocytes & macrophages. At risk: Male, 40-70 years, tobacco smoker Erythroplakia
• Sixth most common neoplasm in the world. Often diagnosed at advanced stage. Caused by tobacco (causes mutation of TP53, p63 & notchi genes). Occurs in tonsillar crypts or base of tongue often. Develops from dysplastic lesions and worsened by hot bevarages. M: raised, firm plaques (early), elarged lesions, ulcerated, protruding, irrregular, indurated or rolled borders (later), well differentiated, keratanizing, anaplastic & sometimes invade vessles. Squamous cell carcinoma of oral cavity
• Dry mouth caused by medications e.g antidepressant. Major feature of sjögren syndrome. M: dry mouth, atrophic tongue papillae, fissuring, ulcers, inflammatory enlargement. Can lead to caries & difficulties speaking & swallowing. Xerostomia
• Dehydration, medication, virus (mumps), bacteria, trauma (mucocele, most common) – causes decr. flow & incr. deposits on wall of ducts. Causes formation of microsialolithiasis (stones) which form larges sialolithiasis. Leads to inflammation! Sialadenitis
• Benign, most common tumor of salivary glands. 60 % of tumors in parotid. Caused by overexpression of PLAG1. M: rounded, well-demarcated, don't exceed 6 cm, encapsulated, has epyhelial & mesenchymal differentiation (myoepothelial & ductal cells) in acimi, ducts, irregular strands, or sheets. Has islands of chondroid & foci of bone. No evident dysplasia or mothoch. activity. Pleumoprhic adenoma of salivary gland
• Malignant, not common tumor. Mostly in parotid. Composed of mixtures of squamous cells, mucous secreting cells & intermediate cells. Caused by rearrangement of MAML 2 gene. M: large, circumscribed, lack well-defined capsules, infiltrative. Has a cut surface of pale gray-white small, mucinous cysts. Contain cords, sheets, cýsts lined by squamous, mucous or intermediate cells. Mucoepidermoid carcinoma
• Complex gr. of lesions with diverse & course behaviors. Caused by differentitation of odontogenic epithelium or ectomesenchyme or both. Most common types are ameloblastoma ( indolent course, slow-growing, locally invasive, no chondroid or osseus differentiation) and odontoma (most common, arise fr. epithelium, has alot of deposots of enamel & dentin) Odontogenic tumors
• 1. Incomplete LES relaxation 2. incr. LES tone 3. Esophageal aperistalsis Achalasia
• Portal hypertension causes shunting of blood away from portal system (portosystemic shunt) to esophagus which leads to bleeding esophageal varices
• Severe retching & vomitting leads to increased pressure in esopagus and leads to a superficial longitudinal tear in mucosa layer. mallory Weiss laceration
• Transmural tear of esophagus & mediastinitis. Rare & serious and leads to hematemesis & mackler's triad of symptoms. Boerhaave syndrome
• Gastroesophageal reflux disiease affecting 40+ mostly. Mucosal barrier is impeded by: Alcohol, tobacco, obesity, pregnancy, CNS depressants, hiatal hernias, decreased gastric emptying & gastric volume. GERD
• GERD has a characteristic morphology of hyperemia, eosinophilia followed by neutrophilia & basal zone hyperplasia
• What does GERD lead to? Barret's esophagus
• Barret's esophagus is characterized by intestinal metaplasia in the mucosa & dysplasia and is seen as tongues or patches of red, velvety mucosa extending upwards.
• What kind of mucosa is found n Barret's esophagus? Smooth pale sq. mucosa (prox), light brown columnar (distal) with goblet cells
• 20-30% of esophageal cancers. Usually begins in cells lining the inside of esophagus & middle portion & in male. Linked to long term acid reflux & tobacco. Occurs at the G-E junction. Adenocarcinoma of esophagus
• Most common esophageal tumor. Alcohol, hot bevarages, injury, tobacco, radiation therapy. Located in middle third of esophagus as an in situ lesion in the form of sq. dysplasia. Spread via esophageal wall. Can be ulcerated or infiltrative. Squamous cells carcinoma of esophagus
• Most commonly affecting critically ill pateints with schock, sepsis or severe trauma Stress ulcers of stomach
• Occuring in proximal duodenum and associated withs evere burns or trauma Curling ulcers of stomach
• Arising in stomach, duodenum or esophagus of person with intracranial disease, have a high incidence of perforation Cush ulcers of stomach
• Whar are acute peptic ulcers caused by? NSAID
• What is chronic gastritis caused by? H. pylori infection
• Asymptomatic, transient inflammation of mucosa of stomach. Seen as a lamina propria with edema & congestion, the surface epithelium is intact, neutrophils are found, blood loss, active inflammation, hematemesis, ulcers, erosion, Acute gastritis
• Test shows H. pylori bacteria, hypogastrinemia, neutrophils in the L. propria & BM, Plasma cells, lymphocytes, macrophages, thickened rugal fold, intestinal metaplasia, goblet cells, antral inflammation Chronic gastritis
• Antibodies formed & attack parietal cells (thus also intrinsic factor & acid). Decr. acid leads to production of gastrin which results in hypergastrinemia & hyperplasia of G -cells (intestinal metaplasia) & pernicious anemia. Autoimmune gatsritis
• NSAID, H. pylori and corticosteroids cause imbalance of mucosal defences. Mostly in proximal duodenum, shallow, solitary, smooth base, rund/oval, hemorrhagic, perforation. Located near interface of body & antrum. Peptic ulcer disease
• What are gatsric polyps? Nodules/masses projecting above mucosa cause by epith/stromal hyperplasia
• 75% of all polyps, 50-60 year olds at risk. Caused by chronic gastritis, reactive hyperplasia or bacteria. M: ovoid, smooth surface, irregular, custically dilated, elongated, acute or chronic inflammation present. Surface erosion & dysplasia seen. Precancerous. Inflammator & hyperplastic polyps
• Found sporadically in familial adenomatous polyposis. No neoplastic potential & usually asymptomatic. Caused by use of proton pump inhibitor. Cause by incr. gatsrin release ( by reduced acidity) & glandular hyperplasia. Fundic gland polyps
• Most common malignancy in japanese male of 50 years. Caused by diet, genetics (CDH1, APC, B -catenin, TP53) & incr. prod of proinflammatory mediators & EBV. Types: intestinal & diffuse Gastric adenocarcinoma
• Morphology of tumor: Most common & seen in elderly. Bulky, glandular, look- like esophageal & colonic adenocarcinomas, grow along broad cohesive fronts --> form exophytic mass or ulcers. Has abundant mucin. The tumor is Intestinal type of gastric Adenocarcinoma
• Morphology of tumor: worst prognosis of the two, seen in younger. Has infiltrative growth pattern, desmoplastic reaction 6 Linitis plastica. Composed of discohesive cells & large mucin vacuoles expanding the cytoplasm & pushing the nucleus peripherally (SIGENT RING CELLS). The tumor is diffuse type of of gastric adenocarcinoma
• A reaction that is associated with some tumors and is characterized by the pervasive growth of dense fibrous tissue around the tumor. The formation of scar tissue (adhesion) within the abdomen after abdominal surgery is another type Desmoplastic reaction
• "leather bottle" appearance found in gastric adenocarcinoma Linitis Plastica
• Tumors named after the cell type theymostly resemble e.g leiomyoma, leiomyosarcoma, schwannoma, glomus tumor. Arises from ectomesenchyme in stomach. Caused by mutation in C-kit gene or PDGFRA gene. M: spindle cells, epitheloid cells, ucnommon spread outside of abdomen, solitary, well-circumscribed, fleshy, submucosal mass Gatrointestinal stromal tumor
• tumor that can arise in any tissue. Organ transplant recipient & stem cell replacement are mostly at risk because those are the frequent sites of EBV positive B cells. M: destruction of crypts. Lymphoma of stomach
• Tumors arising from neuroendocrine organs (e.g. endo pancreas) or neuroendocrine-differentiated GI epithelia (e.g. G cells). Slower growing than carcinoma. Has intense desmoplastic reaction. Symptoms depend on hormones produces & prognosis depend on location of tumor. 60 + at most risk. carcinoids
• Failure of migration of neural crest cells. Absence of meissner or auberbach plexus. No contratction of rectum & colon - remains dilated. Male predominance, female more severe. Hirschprung disease
• Reduced blood supply to intestine because of injury, mucosal infarction (nonocclusive), atherosclerosis (transmural infarction), CF, systemic vasculitices. Leads to production of reactive O2 species, reperfusion injury, inflammation, ischemic injury, bowel edema. Ischemic bowel disease
• Gluten (glutadin) in foods triggers immune cells to attack cells (TH2, MHCII, IgA) in small intestine. Seen as atrophic villi, crypts hyperplasia, incr. CD4+ & CD8+, eosinophils, plasma cells, mast cells, dermatitis Celiac disease
• What role does the MHC play in celiac disease? When macrophages engulf the deaminated gliadin, the MHC presents it.
• what gene is MHC IIin celiac disease encoded by? HLA-DQ & HLADQ1
• Puch formin in hollow of intestine is known as sigmoid diverticula and can either be true (of all layers) or pseudo (few layers).
• What are the causes of diverticula formation? Low fiber diet, high fatty foods, red meat, marfan syndrome & Ehler-danlos syndrome
• Morphology of diverticulas? small, flask-like, surrounded by epiploic appendices, thin wall of atrophic mucosa, compressed submucosa & attenuated muscularis propria
• A chronic condition resulting from inappropriate mucosal immune activation. Composed of Crohn's disease & ulcerative colitis. Inflammatory bowel disease
• Inappropriate mucosal immune activation occuring in any area (but regional) and TRANSMURAL. Female predominace & younger adults/adolescents. M: skip leasions, aphtous ulcers, cobblestone appearance, creeping fat, neutrophilia, crypt abscess, dissortian of mucosal architecture, paneth cells metaplasia, noncaseating granuloma, thick wall. Crohn's disease
• inappropriate mucosal activation in colon and rectum . Involves MUCOSA & SUBMUCOSA. Seen in entire small intestine/bowel (pancolitis). Female predominance & younger adults/adolescents. Pdeudopolyps, mucosal atrophy is seen. Ulcerative colitis
• Something inbwteen crohn's disease & ulcerative colitis. Can't really be diagnosed as either. You call it –– Intermediate colitis
• (1) 8-10 years of disease (2) pancolitis (3) active inflammation Risks of dysplasia and neoplasm formation in Inflammatory bowel disease
• inflammatory, hamartomatous, hyperplastic Classification of poplyps in intestine
• Rare, autosomal dominat poplypoid syndrome. Familial, located in small intestien mostly. Cause by loss of function mutation in LKB1/STkll genes. M: Multiple, mucoucutaneus hyperpigmentation, large, pedunculated (w/ stalk), lobulated contour, has network of CT, smooth m, lamina propria & gland Peutz-Jeghers syndrome
• Hyperplastic polyps do not have dysplasia.
• Adenomas of intestine do have hyperplasia.
• Tubular, tubulovillous, villous sessile serrated types of adenomas in the intestine
• Which of the colon polyps has malignant potential? adenoma
• characterized by the presence of multiple polyps in the colon together with osteomas of the skull, thyroid cancer, epidermoid cysts and fibromas Gardner Syndrome
• It often occurs in the first few months of life and is characterized by non-bile stained and projectile vomiting, poor feeding and weight loss. What is the name of this disease? pylorostenosis
• gastrointestinal stromal tumor. It is the most common primary mesenchymal tumor of GI tract. Derives from Cajal cells, characterized by mutation of the gene encoding tyrosine kinase. Prognosis is correlated with tumor size. most common gene mutation in GISTs? c-KIT
• characterized by the presence of multiple polyps in the colon together with tumors of the central nervous system Turcot Syndrome
• mostly in parotid, ductal or myoepithelial cells are arranged in ducts, acini, irregular tubules, strands, or even sheets. pleomorphic adenoma
• Which of the following is the most common cause of micronodular cirrhosis of the liver? hemochromatosis, alcoholism
• The risk for cancer transformation in colon polyps depend on their histologic structure and size. Which polyps show the highest risk for cancer transformation? Villous adenomas

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