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59 Cards in this Set
- Front
- Back
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Esophagitis. Defined. Prevalence. Types.
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Defined: inflammation of esohageal mucosa
Prevalence: 5% of US population Types: (1) Reflux Esophagitis (GERD) (2) Infectous Esophagitis (3) Barrett Esophagus (4) Other - radiation or chemical |
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Reflux Esophagitis - gastric contents reflux back into esophagus. *most important cause of esophagitis
Etiology? |
(1) Decreased lower esophageal sphincter (LES) tone
(2) Hiatal Hernia (3) Increased Intra-abdominal pressure |
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Causes of decrease in tone of lower esophageal sphincter?
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(1) fatty meals
(2) Alcohol (3) Smoking (4) Presence of Nasogastric tube (5) Pregnancy (progesterone) |
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Causes of increased luminal pessure in abdomin?
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(1) Large meals
(2) Obesity (3) Pregnancy (mass effect) (4) Bending at the waist |
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What is the pathogenesis of reflux esophagitis?
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- gastric fluid (very acidic) causes esophageal mucosal damage (squamous, not made to withstand damage)
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What are morphological changes in reflux esophagitis?
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- inflammatory cells in esophageal squamous epithelium (lymphocytes, eosinophils, neutrophils)
- basal zone hyperplasia - elongation of lamina propria papilla because it is generating quickly - spongiosis - intracellular edema, fluid between the cells |
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What are the clinical findings in reflux esophagiits?
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- dysphagia
- heart burn/chest pain - hematemesis |
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What are the consequences/complication in reflux esophagitis?
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- bleeding
- ulceration - stricture: deep ulcers can heal with scaring leadng to narrowing of the esophageal lume - Barrett esophagus |
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What is the etiology of infectious esophagits?
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fungal - candidiasis and viral (herpes and CMV)
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What is the pathogeneisis of infectious esophagitis?
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- inflammation and resulting tissue damage in response to infectious viral or fungal agent
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What are some morphologic changes of infectious esophagitis candida?
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- gross - white/grey adherent pseudomembranes
- micro- yeast and psuedohyphae |
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What are some morphologic changes of infectious esophagiti herpesvirus?
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- gross - punched out ulcers
- micro - HSV and CMV have characteristic viral cytopathic effect - multinucleated squamous epithelial cells - margination of normal chromatin forming a peripheral rim - virus infecting nucleus, pushing all host chromatin to the side wth central ground glass appearance - nuclear moulding |
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What are the morphologic changes of infectious esophagitis CMV?
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- enlarged cells
- large inclusion (allie inclusion) - infects stomal cells and endothelium |
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What are the clinical findings associated with infectious esophagitis?
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- immunosuppressed patients - transplant, AIDS, ect
- Dysphagia - pain |
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What is the etiology of barrett esophagus?
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- caused b acid reflux, cells change over time.
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In Barrett Esophagus, the distal esophageal squamous epithelium is replaced by?
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etaplastic COLUMNAR epithelium (with intestinal type goblet cells)
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What are the two diagnostic criteria for barrett esophagus?
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(1) Endoscopic findigs - (red, velvety mucosa), see slamon colors stripes up, need to see goblet cells
(2) Histologic - findings of columnar mucosa with goblet cells in biopsy material from specified location |
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What are some risk factors of Barrett esophagus?
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- age >40
- Caucasian - Male - any underlying cause for long standng reflux esophagitis |
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What are some complications of Barrett's esophagus?
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- Dysplasia
- adenocarcinoma |
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Which two esophageal tumors are present? These are uncommon (6% of all cancer in the GI tract) and usually asymptomatic with a low survival rate
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- adenocarcinoma
- Squamous Cell Carcinoma |
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Gastritis is defined as the inflammation of the gastric mucosa, histologic definition. What is the etiology?
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NUMEROUS
- NSAID/ASA use - ETOH and smoking - infection (Helicobacter pylori) - Autoimmune (chronic) |
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What is the pathogenesis of Gastritis?
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- mucosal damage
- incresed H+ secretion with back diffusion - Decreased bicarb buffer - reduced blood flow - Alteration to adherent mucus layer - direct epithelial damage |
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What are the morphologic findings of Gastritis?
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- Gross: acute and chronic are variable - congestion, ulceration, atrophy, irritated stomach, hmorrhage
- Micro: acute/active: neutrophils in lamina propria and in the epithelim Chronic: lymphocytes nd plasma cells in lamina propria and in epithelium (non neutrophils), +/- mucosal atrophy with intestinal metaplasia |
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What type f gastritis is the most common chronic type of gastritis in the U?. It als has the greater risk of carcinoma, lmphoma and 90% of patiens with chronic gastritis have H. pylori present. It is also a major etiologic facor in peptic ulcers.
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H. Pylori Chronic Gastritis.
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What are some pathogenic virulence factors associated with H. Pylori Chronic Gastritis?
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- motility (flagella)
- urease - releases ammonia, causes cell injury and buffers gastric acid - Protease - degrades protective mucus barrier - Exotoxin - damages epithelial cells. |
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What are morphologic findings associated with H. Pylor Chronic Gastritis?
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- Early: acute/active gastritis and nuetrophils and microorganisms
- Late: chronic and lymphocytes and microorganisms |
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Define Ulcer.
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An ulcer is the dirsuption of the mucosa that extends through the muscularis mucosa. A peptic ulcer is a disruption of the mucosa tha extends through the muscularis mucosa in region of GI tract exposed to acid secretions (stomach and duodenum).
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What is the etioloy of peptic ulcer disease?
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- decreased mucosal defenses
- increased mucosal damage |
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What are the gross morphologic changes?
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- anterior wall first part of duodenum
- less curvature of stomach - sharply punched out mucosal defect |
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What are the micro morphologic changes?
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Four characteritic zones:
(1) Fibrinopurulent exudate - lots of neutrophils (2) Necrotic Tissue (3) Granulation tissue- firovscular network with lose strma (4) Fibrotic tissue - depending on amount of time |
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What are clincal findings associated with peptic ulcer disease?
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- epigastric pain
- iron deficiency anemia if they bleed too much - hemorrhange - perforation -free air in abdomen |
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Gastric adenocarcinoma has irreglar areas that affects many layers of the lining and can be deeply invasive. What are some risk factors?
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- dietary - benzopyrene and ntrosamines (smoked, grilled, frid foods)
- low socioeconomic status - Helicobacter infection (antral/body tumors) - smoking - other - atrophic gastritis, pernicious anemia, subtotal gastrectomy, gastric adenomatous polyps |
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T/F: In the pathogenesis of Gastric Adenocarcinoma there are multiple genetic alterations.
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- p53 mutations
- E-cadherin expression alterations - TGFBRII - BAX - IGFRII |
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In gastric adenocarcinoma, there are two morphological subtypes,what are they?
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(1) Intestinal - very disordered appearance
(2) Diffuse - infiltrating poorly diferentiated single cells - the whole wall is replced with malignant cells |
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Celiac disease is an immune mediated disease characterized by...
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(1) Malabsorption
(2) Small intestine mucosal flattening (3) Symptomatic response to removal of gluten from diet. |
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What is gluten?
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Gluten is a protein component (gliadin) found in wheat, oat, barley, and rye.
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What is the etiology of Celiac Disease?
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- gluten sensitivity with tissue damage
- different HLA difference |
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What is the pathogenesis of celiac disease?
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- enterocyte damage
- failure of crypt zone cells to regenerate |
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What is the gross pathology of celiac disease?
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- flat mucosa with loss of ridges and convultions (scalloped appearance is key description)
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What are the microscopic findings associated with celiac disease?
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- shortening in vllous height
- elongation of crypts - increased lymphopasmacytic infiltrate in lamina propria - histologic changes are patchy - Surface epithelium in celiac disease with cubo-columnar epithelium and numerous intraepithelial lymphocytes - fusion of microvilli (it looks flat) |
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What are the clinical findings associted with celiac disease?
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- usually presents in childhood
- disease more severe in distal duodenum and uper jejunum, always involves proximal - decreases distally and may be minimal in distal ileum - severity of malabsorption dependent on length of small bowel involvement and correlates with variability in clinical presentation. |
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What is acute appendicitis?
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An inflammatory disease of the wall of the appendix.
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What is the pathogenesis of acute appendicitis?
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- obstruction of the appendiceal orifice (fecalith, parasites), the opening
- distention of the lumen and bacterial invasion |
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What are the gross and microscopic findings of acute appendicitis?
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- Gross: congestion wit ha fibrinopurlent exudate on teh serosal surface
- Microscopic: mucosal ulceration with nutrophils infiltrating the wall of the appendix. - If not removed can result in transmural perforation and perforation. |
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T/F: Inflammatory Bowel Disease (IBD) is idiopathic, that is the etiology is not well understood.
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True.
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IBD is dividied into two types. What are they?
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(1) Crohn disease
(2) Ulcerative Colitis |
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What does the dx of IBD require?
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(1) Chronicity
and (2) Exclusion of other etiologies (particularly infectious) The mucosa presents abnormally because the crypts may not reach the muscularis mucosae and are irregular. This is unlike normal mucosa where the crypts go all the way down. |
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What is the gross pathology of Chrons disease?
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- Discontinuous involvment of GI (can affect stomach, small intestine,and large intestine, intervening normal tissue, skip lesions, it can effect some areas and not others)
- Transmural inflammation - leads to thickening of wall - neutrophils all the way through - "creeping fat" - mesenteric fat wraps around affected area, cirrhossis of the outside - fistulas - mucosal ulceration and "cobblestone" appearance |
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what is the microscopic pathology of Chron's disease?
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- "Active" inflammation and chronic (cryptitis and crypt abscess)
- features of chronicity- crypt branching/ drop out - mucosal ulceration - transmural lymphoid aggregates - non-caseating granulomas - refers to lack of necrotic debris in the center of the granulomas (difference between it and ulcerative colitis) - healing with fibrosis |
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What are the local complications of Chron's disease
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- small bowel obstruction (common) - continuing fibrosis
- iron deficiency - perforation - fissuring and fistulation can lead to intra-abdominal abscess formation - malabsorption |
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What is the gross pathology of ulcerative collitis?
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- continuous involvement: dista rectum to variable length proximal
- involves colon and rectum only - inflammation limited to mucosa - psedopolyps- islands o intact, regenerative mucosa surrounded by adjacent ulcerated/inflammed mucosa (cobblestone effect) |
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What i the microscopic pathology of ulcerative collitis?
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- "Active" inflammation: (1) cryptitis - intraepithelial neutrophils and (2) crypt abscess 0 neutrophils in crypt lumens
- features of chroicity: crypt branching/drop out - mucosal ulceration |
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What is diverticular disase?
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Protrusions of the mcosa htorugh the muscle wall. It is common in western socieity where there is a lack of fiber in the diet.
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In diverticular disease, what is the gross pathology?
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- range in number (few to many)
- arranged in parallel rows( usually sigmoid colon) - may contain impacted and calcified stool (fecalith) corn! |
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Both UC and CD are asosociated with an increased risk of developing colon cancer.
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True
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What are the microscopic findings associated with diverticular disease?
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- flask-like outpouchin of mucosa and submucosua thoriugh muscularis
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What are complications associated with diverticular disease?
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- Asymptomatic in 80% of affected individuals
- inflammation (diverticulitis) resulting in: (1) perfration an pericolonic abscess (2) Hemorrhage - erosion into major blood vessels present in the connective |
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What are adenomatous polyps?
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- Benign gland forming, epithelial neoplass of colonic mucosa, disordered cell growth.
- Adenomatous polyps are the precursor lesions of the vast majority of colorectal cancers. - though not all will will result in cancer. |
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What are some characteristics of adenomatous colonic epithelium?
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- pleomorphic, hyperchromatic nuclei
- nuclear psudostratification - loss of cytoplasmic mucin |
