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71 Cards in this Set
- Front
- Back
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normal mucosa of SI
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Mucosa – Epithelial cells – simple columnar
With micro vili Mucus secreting cells – goblet cells Small nucleus Lymphocytes – in small number (IEL) normal 10 per 100 epithelial cells villi prominent Increase surface area Crypts – deepest portion of mucosa Glands |
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SI division of submucosa
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SI division
Submucosa Duodenum – brunner’s glands Submocusa ileum – peyer’s patches |
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celiac disease risk factors and clinical onset
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(1)Celiac Disease
Immune mediated disorder in genetically susceptible hosts with damage to SI mucosa and malabsorption Occurs mostly in Northern European whites Clinical onset from infancy to late adulthood Abdominal pain, diarrhea, steatorrhea, dermatitis herpetiformis, fatigue |
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celiac pathogenesis
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Pathogenesis:
Genes: Class 1 HLA-B8 and Class II DR3 or DQW2 Exposure to gliadin in gluten stimulates immune system to damage intestines Lymphocytes invade and damage epithelium CD4 CD8 and Antibody mediated Possible link to adenovirus exposure |
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clinical findings in celiac
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Findings:
Atrophy or blunting or flattening of villi Glands are longer than normal Crypt hypertrophy Mitotic figures and lymphocytes increase/invasion |
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refractory sprue
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(2)Refractory Sprue
Absent or incomplete clinical response to gluten free diet Pathogenesis: Abnormalities in T cells in many patients Patients with loss of CD4, CD8 and monoclonal TCR rearrangement Possible early stage T cell lymphoma |
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Giardiasis
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Most common intestinal parasite in US
More common in children Etiology: G. lamblia infects via ingestion of water or food contaminated by cysts Abrupt or gradual onset of diarrhea More severe and protracted with underlying immunodeficiency or malnutrition Biopsy: triangular shaped objects attached to mucosa surface Prevents absorption – get diarrhea |
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crohn's disease risk factors
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(4)Crohn’s Disease
Idiopathic chronic inflammatory disorder involving any part of the GIT Chronic disorder More common in developed nations of world Incidence rising in the US Genetic predisposition Presentation: most common in young adults/adolescents |
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Crohn's Disease gross pathology
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Gross pathology:
Thickened wall with firm, stiff consistency due to fibrosis, muscular hypertrophy, and fat wrapping Scarring in the submucosa Strictures from thickened walls Mucosa – shows spectrum of ulcers Aphthous ulcers – shallow Progresses to fissures – deep, longitudinal ulcers through wall of intestine Can invade into adjacent structures Cobble stoning from fibrosis and edema Skip areas – portion of small intestine involved, but intervening is normal |
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crohn's disease histology
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Histology
Transmural chronic inflammation with lymphoid nodules String of beads Fibrosis – particularly submuocsa Muscular and neuronal hypertrophy Basilar plasmacytosis PMNs in LP and epithelium (cryptitis) Ulcers (and fissures) Psuedopyloric metaplasia Non-necrotizing granulomas Vasculitis Marked variability |
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Small intestine structure
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Structure – dramatic surface area
Circular folds Have villi Cells have microvilli Mucosal surface under trophic influences that can be manipulated to increase surface/absorption of a particular ion Move villi helps stir chime and absorb more nutrients Microvilli can be extended in response to food increasing surface area |
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Functional organization of villi
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Functional organization of villi
Columnar cell with central lacteal that feeds lymphatics Arteriole supply and venous drainage Most shunted of blood supply to mucosa Can increase blood supply in response to food |
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cell types in villi
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Cell types of Villi
Enterocyte – ones at tip primarily absorb Express hydrolases, absorb water/ions In crypts – primarily secrete Endocrine Goblet Paneth |
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relative absorption in jejunum vs colon
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Jejunum – does most water absorption
Absorbs about 5.5L Colon – most efficient 1.3L absorbed – but this is most of what it sees |
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cellular mechanism of absorption
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Cellular Mechanism
Water is passive and dependent on ions (Na) and solutes (sugars, AA) Movement is transcellular or paracellular (through cell or through tight junctions) Bidirectional – follows osmolarity Permeability of gut – decreases from jejunum to colon Small molecules move better paracellular in jejunum than colon Can more easily move ions and solutes in jejunum Sodium is actively absorbed K is passively absorbed in small intestine Can be secreted in colon when luminal contents are low (follows concentration gradient) CL is absorbed HCO3 is absorbed in jejunum, but secreted ileum and colon |
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absorption in the jejunum
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Tight junctions are leaky
Na is absorbed actively (1)dependent nutrient co-transporters Glucose/Na cotransporter, AA/Na cotransporter (2)Na/H exchanger (3)Na/K ATPase – moves from cell, basolaterally Water follows concentration gradient out of lumen Water movement, creates a K gradient from lumen to cells K follows water CL follows charge gradient…follows K out of lumen paracellularly Na/H exchanger acidifies the lumen and reacts with HCO3 to release CO2 and water CO2 diffuses across the epithelial cell barrier into the blood Intracellular HCO3 crosses basolateral surface Net: NaCl, KCL, and NaHCO3 absorption |
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absorption in the ileum
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Ileum Function:
Tight junctions are less leaky Net rate of Na absorption is smaller Larger electrochemical gradient Less solute absorption CL is absorbed via CL/HCO3 exchanger Exist through CL channel protein HCO3 is secreted via CL/HCO3 exchanger Direction secretion in crypt cells by CFTR Net: NaCL and KCL absorption, HCO3 secretion |
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absorption in the colon
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Colon Function:
Tight junctions are very tight Na is moved against a large electrochemical gradient Little Na/solute cotransport Exception – short chain fatty acids Na is absorbed by Na channels – electrogenic Na absorption (ENaC) Stimulated by aldosterone Na moved across basolateral membrane by Na/K-ATPase K moves down electrochemical gradient into the lumen via channel Can also be absorbed by the apical H/K-ATPase Really moves passively as it follows water – can be lost during diarrhea CL is absorbed via CL/HCO3 exchange and exits through CL channel protein CL absorbed paracellularly too HCO3 is secreted via the CL/HCO3 exchanger Net: NaCl absorption, KHCO3 secretion |
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basic causes of diarrhea
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Basic causes:
(1)osmotic diarrhea – presence of osmotically active, non-absorbable contents in lumen Pull water into lumen (2)exudative diarrhea – loss of epithelial cells or disruption of tight junctions allows water and electrolytes to accumulate in the lumen. Drugs, bugs, celiac (3)diarrhea associated with motility disturbances – increase and decrease Increased – thryotoxicities, opiate withdrawal Decreased – large diverticula, smooth muscle damage associated with scleroderma, muscular dystrophy, diabetes, bacterial overgrowth (4)secretory diarrhea – excess water secretion into intestine Infection, cholera, endocrine tumors, drugs |
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secretory vs osmotic diarrhea
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In broad terms: Secretory vs Osmotic
Osmotic – poorly absorbed, low molecular weight solutes create an osmotic force Lactase deficiency, foods and supplements Secretory – over stimulation of intestinal secretory capacity or blocked ion absorption Over stimulation – most often CL Blocked – most often Na Bacterial enterotoxins, neuroendocrine tumors, inflammatory mediators, bile acids, drugs Complex – most common clinically |
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determining secretory vs osmotic diarrhea
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Determine differences:
Look at stool electrolytes Osmotic diarrhea – greater than 50mOsm Secretory diarrhea – less than 50mOsm |
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cholera and diarrhea
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Cholera:
Cholera Toxin A irreverisbily activates adenylate cyclase, increases cAMP Activates CL secretion via CFTR Na passively follows CL Water follows CL and Na flux Cholera toxin also inhibits non-nutrient Na and CL absorption at villus tip Cholera patient may produce 20L per day Tx. With oral rehydration Adminster solution of glucose and salt – increases driving force for water absorption by Na/glucose co-transporter |
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Acute stress Ulcers
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Rapidly developing, usually superficial, multiple ulcers
Associated with shock, severe trauma, serious burns, increased intracranial pressure Circular, sharply delineated defects, usually <1cm Dark red-brown base No scar Shallow, seen in association with hypotension |
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Classification of Chronic Gastritis
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Nonatrophic
Most common H. pylori Multifocal atrophic Autoimmune |
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H pylori
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G- spiral rod
Strong affinity for gastric surface epithelium Congregates near tight junctions and in mucus Produces urease, ammonia, acetaldehyde, Most common in developing countries High prevalence in children – early infection Prevalence declining in the US |
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H. pylori associated gastric disorders
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Nonatrophic gastritis – most commonly associated
Adenocarcinoma Gastric lymphoma |
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pathology of gastritis
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Lymphoid follicles/nodule
Expansion of LP by plasma cells Neutrophils in LP and epithelium of surface and pits erosions |
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multifocal atrophic gastritis
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Multiple areas of chronic gastritis with marked glandular atrophy and intestinal metaplasia in fundus and antrum
Damage to goblet cells Metaplasia precursor to adenocarcinoma of stomach H pylori infection acquired early in life |
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Autoimmune gastritis
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Corpus restricted atrophic gastritis
Predominantly in the body Circulating antibodies to IF and parietal cells Iron deficiency common Risk factors – adenomas, adenocarcinoma, endocrine tumors Metaplasia |
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autoimmune gastritis pathology
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Pathology:
Early – diffuse or multifocal dense mononuclear infiltrates of fundus mucosa Florid: predominant atrophy of fundic glands, diffuse mononuclear infiltrates invading glands, pit hyperplasia, possible reduced mucosal thickness, intestinal metaplasia End stage: marked or complete loss of fundic glands, pit hyperplasia, microcystic change, thin mucosa, intestinal metaplasia Thin mucosa, loss of structures |
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peptic ulcers
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Chronic – usually solitary, ulcer anywhere exposed to gastric secretions
Most common – in duodenum in 1st segment M>F H. pylori In stomach – distal proportion Gastric – antral or on lesser curvature Duodenal – 1st segment and anterior wall Round, sharply punched out, straight walls, clean base Usually solitary lesion Usually fibrosis, causes puckering of mucosa so it appears to radiate from ulcer |
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complications of peptic ulcers
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Complications – bleeding
Penetration of adjacent structures |
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Gastric adenocarcinoma
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Overall incidence and mortality rates declined significantly worldwide
Marked decline in intestinal and distal cancers Increased incidence in cardiac cancers Better living conditions has caused decrease |
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risk factors for gastric adenocarcinoma
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Risk factors
H pylori gastritis Dietary nitrates Salted and smoked foods Partial gastrectomy Adenomas |
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gastric adenocarcinoma types
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intestinal
diffuse |
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intestinal gastric adenocarcinoma
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(a) Intestinal
Mean age 55 M>>F H. pylori associated Gross – polypoid Histology – gland forming |
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diffuse gastric adenocarcinoma
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(b)Diffuse
Mean age 45 M=F Not associated with H. pylori Gross – infiltrative Histology – signet ring cells More aggressive Signet ring form Rounded cells Crescent shape nucleus because huge accumulation of mucin in cytoplasm Hyperchromatic nuclei |
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early gastric carcinoma
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Early Gastric carcinoma
Cancer confined to mucosa or submucosa More common in Japan Depth invasion + lymph node involvement tell you prognosis |
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gastrointestinal lymphomas
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GIT most common site for extra nodal non-hodgkin lymphoma
Stomach most common site Predisposing factor: H. pylori Small intestine – celiac Large intestine – ulcerative colitis or crohns People with immune deficiency Small Bowel – The cancers tend to be lymphoma Gastric lymphomas DLBC Marginal Zone lymphoma Arise in MALT Associated with H. pylori Begin as low grade, but left untreated become aggressive and can become DLBC Musical folds are more prominent = “cerebreform” |
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Gastric MALTomas
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Gastric MALTomas
Nearly all associated with H. pylori infection Composed of small to medium sized tumor cells with slightly irregular nuclei and clear cytoplasm Usually confined to mucosa and submucosa as diffuse infiltrate Lymphoepithelial lesions Increased number of plasma cells Prognosis – better |
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GI stromal Tumors
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GI stromal Tumors
Most commonly in stomach but can be else where (small bowel, then large) M=F Adults No known risk factors Interstitial cells of cajal – thought to be cell of origin Cant tell benign vs malignant under microscopic |
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GI stromal Tumors tx and predictors of malignancy
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Tx with gleevec because of c-kit mutation
Compsod of spindled or epithelioid tumor cells or mixed Predictors of malignant behavior Size >5cm MF count >5/50 hpf Invasion of LP Tumor cell necrosis Dense cellularity |
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Salivary glands
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Exocrine glands and ducts
Glands – parotid Parachymal or epithelial cells Basophil, granular cytoplasm Secrete amylase Submandibular Lined with mucinous cells and basophilic granular cells (mixed) Minor Lined with mucinous cells |
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parotid glands
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Parotid gland – small columnar cells, basophilic cytoplasm, centrally located nuclei, arranged in ducts
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submandibular glands
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Submandibular gland:
Top center, top half of the circle, duct clearly shows the basophilic granular cells But in the right side, basophilic nuclei and abundant clear cytoplasm |
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minor glands
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Minor glands:
Most of cells are mucous secreting cells |
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benign vs malignant tumors of the salivary glands
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Most benign – mobile on palpation
Malignant – grow rapidly Infiltrate superficial and deep tissues Fixed masses on palpation Can invade nerves, producing pain, paresthesias, and VII paralysis Site of tumor: Parotid gland – most benign Submandibular – most benign but increased risk of malignant Minor – 50% malignant Smaller glands are more likely to have malignant, but total proportion of tumors still benign |
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benign salivary gland tumors
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(1) pleomorphic adenoma
(2)warthin's tumor |
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pleomorphic salivary gland tumors
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(1)pleomorphic adenoma (benign mixed tumor)
Most common Sharp circumscription Linear pink structure – collagen that surrounds tumor Not very dark – lots of extracellular matrix Epithelial cells: make this section of the tumor Small pale cells, with even spaced chromatin Absence of nucleoli Little cytoplasm Myopepithelial cells make this proportion of the tumor: This field is predominantly myopepithelial Produce extracellular matrix Pale chromatin and no mitiotic figures Production of duct-like system from tumor epithelium, filled with myoepithelial cells and their products Dx by fine needle aspiration biopsy |
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warthins salivary gland tumors
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(2)warthin’s tumor
Almost exclusive in the parotid Most common in elderly men Most commonly bilateral Warthin’s Tumor: Gross – cavitation Softer on palpation Thin collagen capsule Epithelium – is the cancerous cell type Tall columnar, recapitulating the ducts Lymphocytes – the darker blue cells Reactive Non-neoplastic but associated with epithelium Lymphocytes in the top Cavitary stuff in the left, debris Rods = cholesterol crystals from where cells die |
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malignant salivary gland neoplasms
types |
(1)mucoepidermoid carcinoma
mucus/glandular cells squamous cells =combination of adenoma and squamous cells (2)adenoid cystic carcinoma - most often in submandibular and minor |
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mucoepidermoid carcinoma of salivary glands
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Mucoepidermoid carcinoma
Mucus/glandular cells Squamous cells =combination of adenoma and squamous cells Mucoepidermoid CA Dense cytoplasm Keratin being produced on the left On the right – mucous being produced Mixed cell type |
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adenoid cystic carcinoma of salivary glands
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Formed by small to large nests of neoplastic malignant cells
Scant cytoplasm Homogenous nucleus High N/C ratio Form “holes” with pink basement membrane |
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sjorgen's syndrome
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Bilateral salivary gland enlargement because lymphocyte infiltration
90% in middle to older women Dx from minor salivary gland biopsy Periductal and perivascular lymphocytic infiltrates T cells attacking and damaging epithelium |
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anatomy of esophagus
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Tubular msucualr organ in mediastinum from oropharynx to infradiphragmactic stomach
Mucosa – nonkeratinizing stratified squamous epithelium, glandular distal 1-2cm Muscularis: upper 1/3 = striated Lower 2/3 = smooth muscle LES stratified squamous cells, make more cytoplasm as they mature |
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candida esophagitis
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White plaques and pseudomembranes
Mucosa is nodular, friable, and ulcerated Ulcers usually shallow Microscopic – neutrophils in epithelium Erosions or ulcers Mesh of fibrin, PMNs, debris Degenerative changes Yeast or/and pseudohyphae |
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herpes esophagitis
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Gross: clusters of well delineated shallow ulcers with raised borders
Serpinginous erosions Extensive denudation Unremarkable nonulcerated mucosa Microscopic: Erosion or ulcer Mixed inflammatory exudates Small vessel necrosis Enlarged squamous cells with round eosionphillic inclusions with halo Enlarged nuclei Multinucleated giant cells with “ground glass” |
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GERD
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GERD:
Pathology is nonspecific Acute changes - Intraepithelial segmented WBCs Basal cell hyperplasia Papillomatosis – elongated papillae Erosions Chronic changes: Fibrosis – structuring Barrett’s esophagus |
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barrett's esophagus
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Acquired condition secondary to GERD
2 components: Endoscopic – columnar epithelium proximal to GEJ into tubular esophagus Histologic – intestinal metaplasia – goblet cells Glandular dysplasia and adenocarcinoma May give rise to adenocarinoma |
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eosinophilic esophagitis
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Idiopathic immune-mediated disorder of children and adults
Possibly related to food Other allergic conditions like asthma Pathology: >20 eosinophilis/HPF in mucosa Rx. Corticosteroids, specific food elimination |
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carcinoma of esophagus
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SCC most common internationally
Highest in china and iran USA – adenocarcinoma more common Prognosis: Stage and depth of invasion Risk Factors: SCC – food and water rich in nitrates and nitrosamines, alcohol, tobacco, vitamin deficiencies, achalasia, HPV, black men Adenocarcinoma – Barrets Esophagus, white men |
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glandular dysplasia in BE
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Glandular Dysplasia in BE
Indefinitie/low grade and high grade basd on architectural and cytologic features Problem of inflammation 5 year risk of adenocarcinoma Increases with increased dysplasia If High grade, 50% have adenomcarcinoma elsewhere in esophagus |
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Ulcerative colitis
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recurrent acute or chronic inflammatory disorder with extensive ulcers of colon and involvement of extracolonic sites
M=F Gross – starts at rectum (right sided), extends conintually ulcers can coalesce, progressive mucosal sloughing Loss of mucosa can create islands of remnant mucosa = psuedopolyps Histology: acutely cryptitis and crypt abscesses that coalesce under mucosa Marked goblet cell depletion regeneration Neutrophils invade mucosa – cryptitis Neutrophils into lumen – crypt abscess Chronically – branched irregular glands, increased plasma cells and eosinophils Basilar plasmacytosis |
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granulomatous colitis
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Granulomatous Colitis = Crohn’s Diseaes
Can involve colon in 40% of cass Gross: segmental – skip lesions Predominantly right sided Rectal sparing in 50% Cobble stoned mucosa from fibrosis and edema Histology: minimal mucosal atrophy and regeneration with preserved mucin Transmural lymphoid aggregates, non caseating granulomas, edema, Can get fissures |
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diverticular disease
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Diverticular Disease:
Hypertrophy of taenia coli and circular muscle with flask shaped sacs of mucosa and submucosa protruding Sigmoid involved 99% Benign most often Complications – inflammation, pericolic abscess, hemorrhage |
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hyperplastic polyp
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Hyperplastic Polyp
Usually asymptomatic Usually multiple Gross: sessile – no stalk On mucosal fold Histology: elongated glands with papillary infolding Small basal nuclei and abdundant mucin No atypia Small nuclei to cytoplasm ratio Glands are long and irregular curvature Small tuft protruding into lumen |
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juvenile polyp
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Juvenile Polyp
More common in children Single or multiple lesions Rectum is most common site Gross: pedunculated (stalked) Head is ulcerated and rounded Numerous cysts filled with mucin Histology: dilated crypts embedded in excess of lamina propria with inflammation |
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colonic adenomas
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Colonic Adenomas:
Sharply circumscribed elevations of dysplastic epithelium Gross: pedunculated or sessile Histology: Can be tubular Vilious Mix Dysplastic epithelium with reduced mucus, increased nucleus to cytoplasm ration, hyperchromasia, high mitotic rate stratification of nuclei (not located at basal |
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adenoma carcinoma sequence
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Adenoma Carcinoma Sequence
Adenocarcinomas arise from adenomas Risk factors for being cancerous Size >2cm Histology Tubular less likely Villous more likely Degree of dysplasia |
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colonic carcinoma
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Colonic Carcinoma
More likely in elderly (60s and up) Gross: (1) left side – circumferential napkin ring constriction Obstruction (2)right side – exophytic growth and anemia Histology: variants – classic glandular (b) colloid – worse prognosis |
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familial adenomatosis polypsos
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Familial Adenomatosis Polypsos
Auto dominant Appears in 2 or 3 decade Develop series of adenomas that become cancerous Tx – prophylactic colectomy |
