GI Flashcards

Question

gastritis

Answer 1

-ACUTE -CHRONIC -AUTOIMMUNE -OTHER: -EOSINOPHILIC -ALLERGIC -LYMPHOCYTIC -GRANULOMATOUS -GVH

Answer 2

-hemorrhagic -(NSAIDs), particularly aspirin -Excessive alcohol consumption -Heavy smoking -CHEMO -Uremia -Salmonella, CMV -Severe stress (e.g., trauma, burns, surgery) -Ischemia and shock -Suicidal attempts, as with acids and alkali -Gastric irradiation or freezing -Mechanical (e.g., nasogastric intubation) -Distal gastrectomy -histology- erosions, hemorrage -neutrophils !!!!!!!!!!!!

Answer 3

-NO EROSIONS, NO HEMORRHAGE -Chronic infection by H PYLORI!!!! -Immunologic (autoimmune), e.g., PA -Toxic, as with alcohol and cigarette smoking -Postsurgical, reflux of bile -Motor and mechanical, including obstruction, bezoars (luminal concretions), and gastric atony -Radiation -Granulomatous conditions (e.g., Crohn disease) -GVH, uremia -Few neutrophils -Lymphocytes, lymphoid follicles -REGENERATIVE CHANGES: -METAPLASIA, intestinal -ATROPHY, mucosal hypoplasia, “thinning” -DYSPLASIA

Answer 4

-10% -ANTIBODIES AGAINST-> : -acid producing enzyme H+ -K+ -ATPase -gastrin receptor -intrinsic factor -> pernicious anemia -> low B12

Answer 5

-EOSINOPHILIC, middle aged women -ALLERGIC, children (also eosinophils) -LYMPHOCYTIC, T-Cells, body, DIFFUSE -GRANULOMATOUS, Crohn’s, other granulomas -GVH, in bone marrow transplants

Answer 6

-Ulcer on lining of stomach or duodenum -“PEPTIC” implies acid cause/aggravation -ULCER (all layers are compromised) vs. EROSION (muscularis mucosa intact) -MUC -> SUBMUC -> MUSCULARIS -> SEROSA -Chronic, solitary (usually), adults -Most caused by H. pylori -NSAIDS -“STRESS” -Gnawing, burning, aching pain, epigastric -Fe deficiency anemia -Acute hemorrhage -Penetration, perforation: -Pain in BACK -Pain in CHEST -Pain in LUQ -Not felt to develop into malignancy

Answer 7

-Bleeding: -Occurs in 15% to 20% of patients -Most frequent complication -May be life-threatening -Accounts for 25% of ulcer deaths -May be the first indication of an ulcer -Perforation: -Occurs in about 5% of patients -Accounts for two thirds of ulcer deaths -Rarely, is the first indication of an ulcer -Obstruction from edema or scarring: -Occurs in about 2% of patients -Most often due to pyloric channel ulcers -May also occur with duodenal ulcers -Causes incapacitating, crampy abdominal pain -Rarely, may lead to total obstruction with intractable vomiting

Answer 8

-!!!!!!!!!!!low grade lymphoma, chronic gastritis, adenocarcinoma !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! -Responsible for majority of peptic ulcers, as well as chronic gastritis and potentially gastric cancer/lymphoma -Present in about 20 percent of people < 40 years old and half of those over 60 years; most infected people do not develop ulcers; unknown why -H. pylori weakens protective mucous coating of stomach and duodenum, allowing acid to reach mucosa; acid and bacteria irritate mucosa, cause ulcer -H. pylori able to survive in stomach acid because it secretes enzymes that neutralize the acid -Causes 80% of gastric peptic ulcers -Causes almost all duodenal peptic ulcers -Causes chronic gastritis -Causes gastric adenocarcinomas -Causes MALT lymphomas

Answer 9

-NSAIDS -“STRESS” ULCERS -ENDOGENOUS STEROIDS: -SHOCK -BURNS -MASSIVE TRAUMA -Intracranial trauma, Intracranial surgery -SEPSIS -EXOGENOUS STEROIDS -CUSHING ULCER -usually small (<1cm), superficial, multiple

Answer 10

-RUGAL PROMINENCE (cerebriform) -NO INFLAMMATION -HYPERPLASIA of MUCOSA -dont focus on diseases: -Ménétrier disease, resulting from profound hyperplasia of the surface mucous cells with accompanying glandular atrophy, ass. w. CMV, H. Pylori, ↑TGF-α -Hypertrophic-hypersecretory gastropathy, associated with hyperplasia of the parietal and chief cells within gastric glands (NORMAL gastrin) -Gastric gland hyperplasia secondary to EXCESSIVE gastrin secretion, in the setting of a gastrinoma (Zollinger-Ellison syndrome)

Answer 11

-BENIGN: -“POLYPS” (HYPERPLASTIC vs. ADENOMATOUS) -LEIOMYOMAS (Same gross and micro as smooth muscle) -LIPOMAS (Same gross and micro as adipose tissue) -MALIGNANT -ADENOCarcinoma -LYMPHOMA -POTENTIALLY MALIGNANT -G.I.S.T. (Gastro-Intestinal “Stromal” Tumor) -CARCINOID (NEUROENDOCRINE)

Answer 12

-MC malignant tumor of stomach -H. pylori associated -Japan, Chile, Costa Rica, Colombia, China, Portugal, Russia, and Bulgaria -M>>F -Socioeconomically related -RISK FACTORS: -H. pylori -Nitrites, smoked meats, pickled, salted, chili peppers, socioeconomic, tobacco -Chronic gastritis, Barrett’s, adenomas -Family history

Answer 13

-adenocarcinoma of stomach -grows diffusely through all layers of stomach -thickened wall -leather bottle appearance -poor prognosis -SIGNET RING CELLS

Answer 14

-Lymphoid origin; 6th decade of life -Grossly indistinguishable from adenocarcinoma -5% of gastric malignancies are primary lymphomas -Most common is B Cell Type (MALTomas, diffuse large B-cell lymphoma) -!MALTomas (lymphomas of mucosa-associated lymphoid tissue) are the majority (extranodal marginal B-cell lymphomas) -MALT Tx: H. Pylori eradication (antibiotics) -> basically puts pt into remission

Answer 15

-Solitary, circumscribed, fleshy mass, whorled cut surface – may be ulcerated -can be up to 30 cm -Mesenchymal neoplasms - arise from interstitial cells of Cajal (innervated network of intestinal pacemaker cells for gut peristalsis), located in muscularis propria (“spindle” cells) -Rare; > 1/2 arise in stomach (can happen anywhere) -not common < 40 years -!!! IHC for c-KIT (aka CD117) usually positive, useful diagnostic marker -Prognosis depends on size, mitotic index, and location – gastric GISTs somewhat less aggressive than those in small intestine -Recurrence or metastasis rare if < 5 cm; common if > 10 cm -GISTs with mutations in KIT or PDGFRA respond to imatinib, a tyrosine kinase inhibitor, especially used in patients with unresectable, recurrent or metastastic disease

Answer 16

-NORMAL: Anat., Vasc., Mucosa, Endocr., Immune, Neuromuscular -PATHOLOGY: -CONGENITAL -ENTEROCOLITIS: DIARRHEA, INFECTIOUS, OTHER -MALABSORPTION: INTRALUMINAL, CELL SURFACE, INTRACELL. -(I)IBD: CROHN DISEASE and ULCERATIVE COLITIS -VASCULAR: ISCHEMIC, ANGIODYSPLASIA, HEMORRHAGIC -DIVERTICULOSIS/-ITIS -OBSTRUCTION: MECHANICAL, PARALYTIC (ILEUS) (PSEUDO) -TUMORS: BENIGN, MALIGNANT, EPITHELIAL, STROMAL

Answer 17

-DUPLICATION -MALROTATION -OMPHALOCELE- abdominal wall defect: intestines, liver, and occasionally other organs remain outside of abdomen in a sac because of a defect in the development of muscles of abdominal wall -GASTROSCHISIS-birth defect: infant's intestines protrude out of the body through a defect on one side of the umbilical cord. -ATRESIA/STENOSIS SPECTRUM -MECKEL -AGANGLIONIC MEGACOLON (HIRSCHSPRUNG DISEASE) - cant defecate

Answer 18

-meckel (terminal ileum, “vitelline” duct) diverticulum -Most common true diverticulum, most common congenital anomaly of GI tract, occurs in ileum due to failed involution of vitelline duct (connects lumen of developing gut to yolk sac) -Solitary diverticulum extends from the antimesenteric side of the bowel -“rule of 2's”: Occurs in approximately 2% of the population, generally present within 2 feet (60 cm) of ileocecal valve, approximately 2 inches (5 cm) long, twice as common in males, most often symptomatic by age 2 (only approximately 4% symptomatic)

Answer 19

-HIRSCHSPRUNG DISEASE -absence of ganglion cells in a segment of the bowel in an infant; leads to aperistalsis -Failure to pass a first stool for 24-48 hours is suggestive of HS -> meconium -distention -aperistalsis -Infants with HS often have abdominal distention, abdominal pain, and vomiting; constipation, poor weight gain, and slow growth

Answer 20

-Small intestine, duodenal bx -also called SPRUE or NON-tropical sprue -Also called GLUTEN-SENSITIVE ENTEROPATHY: -Sensitivity to GLUTEN, a wheat protein, gliadin -Immobilizes T-cells -Also in oat, barley, rye -Progressive mucosal “atrophy”, i.e. villous flattening! -Relieved by gluten withdrawal -bloating -chronic diarrhea -flatulence, greasy, bulky, and bad--smelling stools -nausea or vomiting abdominal -pain -Increased risk of malignancy; most common cancer is enteropathy-associated T-cell lymphoma, an aggressive lymphoma of intraepithelial T lymphocytes

Answer 21

-Prevalent in tropical regions of the Caribbean, India, South Africa, and Southeast Asia -Affected patients often suffer from malabsorption, malnutrition, and stunted growth -Epidemic forms -NOT related to gluten -Exact cause not known; acquired disorder, may be related to environmental and nutritional factors, or related to an infectious organism (viral or bacterial), dietary toxin, parasitic infestation, or nutritional deficiency -Tropical Sprue causes damage to mucosal lining of the intestine resulting in impaired absorption of food, minerals, and water

Answer 22

-Rare, multi-orgam chronic disease caused by Tropheryma whipplei -Bacteria-laden macrophages accumulate within small intestinal lamina propria and mesenteric lymph nodes, causing lymphatic obstruction (malabsorptive diarrhea of Whipple disease due to impaired lymph drainage) -Bacteria-laden macrophages can accumulate within mesenteric lymph nodes, synovial membranes, cardiac valves, brain, and other sites -Most common in Caucasian men, particularly farmers and others with occupational exposure to soil or animals; genetic risk factors may exist -Triad of diarrhea, weight loss, and arthralgia -Extraintestinal symptoms may precede malabsorption by months or years and include arthritis; arthralgia; fever; lymphadenopathy; and neurologic, cardiac, or pulmonary disease -a rare, systemic infectious disease caused by the bacterium Tropheryma whipplei

Answer 23

-DEFINITION of diarrhea: INCREASE in MASS, FLUIDITY, and/or FREQUENCY -DIARRHEA is a SYMPTOM: 1) SECRETORY, 2) OSMOTIC, 3) EXUDATIVE, 4) MALABSORPTION, 5) MOTILITY -INFECTIOUS (Viral, Bacterial, Parasitic) -NECROTIZING -COLLAGENOUS -LYMPHOCYTIC -AIDS -DRUG INDUCED -RADIATION -“SOLITARY” RECTAL ULCER

Answer 24

-Secretory: -Viral damage to mucosal epithelium -Entero-toxins, bacterial -Tumors secreting GI hormones -Excessive laxatives -Osmotic -Disaccharidase deficiencies -Bowel preps -Antacids, e.g., MgSO4 -“osmotic” diarrhea means there are too many solutes in the lumen and therefore absorption is impaired -Exudative -BACTERIAL DAMAGE to GI MUCOSA; increased damage to intestinal mucosa epithelium can result in exudate from mucosa into lumen – usually caused by gram positive gut flora -Inflammatory bowel disease -Malabsorption - -characterized by defective absorption of fats, fat- and water-soluble vitamins, proteins, carbohydrates, electrolytes and minerals, and water; excessive loss of nonabsorbed substances in stool -Steatorrhea: excessive (large volumes) fecal fat and bulky, frothy, greasy, yellow or clay-colored stools -chronic malabsorptive disorders most common in US are pancreatic insufficiency, celiac disease, and Crohn disease

Answer 25

-VIRAL -Rotavirus (69%), Calciviruses, Norwalk-like, Sapporo-like, Enteric adenoviruses, Astroviruses -BACTERIAL -E. coli, Salmonella, Shigella, Campylobacter, Yersinia, Vibrio, Clostridium difficile, Clostridium perfringens, TB -Bacterial “overgrowth” -PARASITIC -Ascaris, Strongyloides, Necator, Enterobius, Tricuris -Diphyllobothrium, Taenia, Hymenolepsis -Amebiasis (Entamoeba histolytica) -Giardia

Answer 26

-Rotavirus most common -Selectively infects and destroys mature enterocytes in the small intestine -Crypts spared -Most have a 3-5 day course -Person to person, food, water

Answer 27

-Ingestion of bacterial toxins -Staph -Vibrio -Clostridium -Ingestion of bacteria which produce toxins -Traveller’s diarrhea, E.coli -Infection by enteroinvasive bacteria -Enteroinvasive E. coli (EIEC) -Shigella -Clostridium difficile -E. coli: -Toxin, invasion, many subtypes -Food, water, person-to-person -Usually watery, some hemorrhagic -INFANTS often -SALMONELA - food, non-hermorrhagic -SHIGELLA - person-to-person, invasive, often bloody diarrhea -CAMPYLOBACTER – Toxins, invasion, food spread -VIBRIO cholera - Water, fish, person-to-person; epidemics, no invasion (watery diarrhea), enterotoxin

Answer 28

-CYTOTOXIN (lab test readily available) -NOSOCOMIAL -PSEUDOMEMBRANOUS (ANTIBIOTIC ASSOCIATED) COLITIS

Answer 29

-NEMATODES (ROUNDWORMS) -Ascaris, Strongyloides, Hookworms (Necator & Anklyostoma), Enterobius, Trichuris -CESTODES (TAPEWORMS) -FISH (DIPHYLLOBOTHRIUM latum) -PORK (TAENIA solium) -DWARF (HYMENOLEPSIS nana) -PROTOZOANS: AMOEBA (ENTAMOEBA histolytica), Giardia lamblia- Giardiasis in humans - caused by infection of small intestine by the CYST of a single-celled organism Giardia lamblia; occurs worldwide with prevalence of 20–30% in developing countries

Answer 30

-NECROTIZING ENTEROCOLITIS (neonate) (Cause unclear) -COLLAGENOUS (Cause unclear) -LYMPHOCYTIC (Cause unclear) -AIDS -GVHD after BMT, as in stomach -DRUGS (NSAIDS, etc., etc., etc.) -RADIATION, CHEMO -NEUTROPENIC (TYPHLITIS), (cecal, caecitis) -“DIVERSION” (like overgrowth) -“SOLITARY” RECTAL ULCER (anterior, motor dysfunction)

Answer 31

-LACTASE by far MOST COMMON -ACQUIRED, NOT CONGENITAL -LACTOSE -> GLUCOSE + GALACTOSE -OSMOTIC DIARRHEA

Answer 32

-CROHN DISEASE (granulomatous colitis) -ULCERATIVE COLITIS -COMMON FEATURES -IDIOPATHIC -DEVELOPED COUNTRIES -COLONIC INFLAMMATION -SIMILAR Rx -BOTH have CANCER RISK UC>CD

Answer 33

-TRANSMURAL, THICK WALL -NOT LIMITED to COLON -GRANULOMAS -FISTULAE COMMON -TERMINAL ILEUM OFTEN -SKIP AREAS -“CRYPT” ABSCESSES NOT COMMON -NO PSEUDOPOLYPS -MALABSORPTION

Answer 34

-MUCOSAL, THICK MUCOSA -LIMITED to COLON -NO GRANULOMAS -FISTULAE RARE -TERMINAL ILEUM NEVER -NO SKIP AREAS -“CRYPT” ABSCESSES COMMON -PSEUDOPOLYPS -NO MALABSORPTION -granulomas are NOT found -mucosal pseudopolyps are found

Answer 35

-ISCHEMIA/INFARCTION -ANGIODYSPLASIA – not true dysplasia -HEMORRHOIDS

Answer 36

-HEMORRHAGE is the main HALLMARK of ischemic bowel disease -ARTERIAL THROMBUS -ARTERIAL EMBOLISM -VENOUS THROMBUS -CHF, SHOCK -INFILTRATIVE, MECHANICAL -MUCOSAL -> TRANSMURAL -Especially seen in elderly with cardiovascular problems -Severe pain, rigid abdomen

Answer 37

-not really dysplasia -NOT neoplastic -twisted, dilated submucosal vessels, can rupture

Answer 38

-INCREASED INTRABDOMINAL PRESSURE -i.e., VALSALVA -INTERNAL vs. EXTERNAL -Like varices, ultimate cause is chronically elevated increased submucosal venous pressure, either from portal hypertension (much less likely), or ANYTHING which commonly causes chronically increased abdominal pressure

Answer 39

-FULL THICKNESS BOWEL OUTPOCKETING -Assoc. w.: -INCREASED LUMINAL PRESSURE, ↑transit time -AGE -L -> R (decreased liquidity) -Decreased dietary FIBER -Weakening of wall -IMPACTION -INFLAMMATION -PERFORATION -> Peritonitis, local, diffuse -BLEED, silently, even fatally -OBSTRUCT -COMMON -NOT assoc. w. neoplasm, but may mimic carcinomas clinically, radiologically, surgically, and grossly -Diverticuli resemble hernias of the colonic wall in that they occur @ sites of entry of mucosal arteries as they pass through the muscularis – represents weak spot that leads to a diverticulum if the individual generates high colonic intraluminal pressure (low fiber diet) -True v. Pseudo diverticulum

Answer 40

-ADHESIONS (post-surgical) -IMPACTION -HERNIAS -VOLVULUS -INTUSSUSCEPTION -TUMORS -INFLAMMATION, such as IBD (Crohn) or divertics -STRICTURES/ATRESIAS -STONES, FECALITHS, FOREIGN BODIES -CONGENITAL BANDS, MECOMIUM, INPERF. ANUS -ILEUS, esp. postsurgical -INFARCTION -MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE

Answer 41

-disruption of normal propulsive gastrointestinal motor activity from NON-mechanical mechanisms -Motility disorders that result from structural abnormalities are termed mechanical bowel obstruction

Answer 42

-NON-NEOPLASTIC (POLYPS) -EPITHELIAL -MESENCHYMAL (STROMAL) -LYMPHOID -BENIGN -MALIGNANT

Answer 43

-HYPERPLASTIC (NON-NEOPLASTIC) -ADENOMATOUS (TRUE NEOPLASM, and regarded by many as PRE-MALIGNANT) -SESSILE vs. PEDUNCULATED -TUBULAR vs. VILLOUS -Villous adenomas behave more aggressively than tubular adenomas; HIGHER rate of developing into adenocarcinomas than the “tubular” patterns.

Answer 44

-1) POLYPOSIS (NON-NEOPLASTIC, hamartomatous) -2) POLYPOSIS (NEOPLASTIC, i.e., cancer risk) -3) HNPCC: (Hereditary Non Polyposis Colorectal Cancer)

Answer 45

-Loss of APC gene -Mutation of K-RAS -Loss of SMADs (regulate transcription) SMADs are intracellular proteins that transduce extracellular signals from TGF beta ligands to the nucleus where they activate downstream TGF-ß gene transcription -Loss of p53 -Activation of TELOMERASE -cancer risk factors: -Family history -Age (rare <50) -LOW fiber, HIGH meat, LONG transit time, refined carbs

Answer 46

-From existing ADENOMATOUS POLYPS -DE-NOVO -DYSPLASIA -> INFILTRATION -> METASTASIS

Answer 47

-POLYPOID -ANNULAR, CONSTRICTING -DIFFUSE

Answer 48

-CARCINOID, with or without syndrome -LYMPHOMA (MALTOMAS, B-Cell) -LEIOMYOMA/-SARCOMA -LIPOMA/-SARCOMA

Answer 49

-MORE LIKELY TO BE SQUAMOUS, or “basaloid” -WORSE IN PROGNOSIS -HPV RELATED

Answer 50

-Junction of 3 tenia coli, variable in location -All 4 layers, true serosa -Thickest layer is submucosal lymphoid tissue -APPENDICITIS (ACUTE) -MUCOCELE -MUCUS CYSTADENOMA -MUCUS CYSTADENOCARCINOMA

Answer 51

-GENERALLY, a disease of YOUNGER people -OBSTRUCTION by FECALITH the classic cause but fecaliths present only about half the time -EARLY APPENDICITIS: NEUTROPHILSMucosa, submucosa -NEED NEUTROPHILS in the MUSCULARIS to confirm the DIAGNOSIS -25% normal rate, usually -Perforation -> peritonitis the rule, if no surgery

Answer 52

-Mucocele (common) - CYST on APPENDIX filled with MUCIN; Can RUPTURE to become: -PSEUDOMYXOMA PERITONEII -Mucinous Cystadenoma (rare) -Mucinous Cystadenocarcinoma (rare)