quiz 4- bowel 2, liver 1, 2, 3 Flashcards
• What is are the terms for S/L I inflammation?
o Enteritis: small bowel inflammation
o Colitis: large bowel inflammation
o Enterocolitis: both large and small bowel involvement
• What can cause enterocolitis (coloenteritis)? Ssx?
o MC: infectious enteritis.
o Crohn’s, UC, ischemic colitis, radiation induced
o Infx: bacteria, viruses, fungi, parasites
o Ssx: freq diarrhea, w or w/o N/V, abdl pain, fever, chills, alteration of general condition.
o Dehydration
• What microorganisms can cause acute enterocolitis?
o Bacteria: Salmonella, Shigella, Escherichia coli, Campylobacter etc.
o Viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses
o Fungi: Candidiasis, esp immunosuppressed, or prolonged abx
o Parasites: Giardia
o lamblia (↑ incidence, ↓clinical manifestation), Balantidium coli, Blastocystis homnis, Cryptosporidium (diarrhea in immunosuppressed), Entamoeba histolytica (amebic dysentery, tropical)
• What are endotoxins?
o associ w some g(-) bacteria
o a structural molecule of the bacteria, recognized by immune system
o usu released after lysis
• What are Enterotoxins?
o protein toxin, released in intestine; chromosomally encoded exotoxins
o heat-stable, low molecular weight, water-soluble
o often cytotoxic, mostly pore-forming (mostly Cl- pores) → ↑Cl- permeability of apical membrane of intestinal mucosal cells. pores activated by ↑ cAMP or Ca2+ intracellularly. → Cl- into lumen, Na, water follow → secretory diarrhea in hrs
o ex: Staphylococcus aureus, E. coli.
• What are exotoxins?
o excreted by microorganism (secreted, or released on cell lysis), cause major damage, destroy cells or disrupt normal cellular metabolism
o highly potent. Most destroyed by heating. Susceptible to Abs, but mb fatal
o Some deliver thru projections (cyto-cyto)
o Local or systemic effects
o Ex: effector proteins injected by type III secretion apparatus of Yersinia into target cells
• What are some examples bacterial enterotoxins?
o Clostridium difficile
o E coli O157:H7
o Clostridium perfringens (C perfringens enterotoxin)
o Vibrio cholerae (Cholera toxin)
o Staph aureus (Staphylococcal Enterotoxin B)
o Yersinia enterocolitica
o Shigella dysenteriae (Shiga toxin)
• What are common viral causes of enterocolitis?
o Mc= Norwalk virus. Aka winter vomiting. (norovirus). 90% non-bacterial GE in world, 50% all food GE in US
o Rotavirus = single most common cause of severe diarrhea in infants, children
o Noroviruses: ssRNA, non-enveloped.
• What are common bacterial exotoxins?
o botulinum toxin of Clostridium botulinum
o Corynebacterium diphtheriae exotoxin, produced during life-threatening sxs of diphtheria.
• What are some toxigenic bacteria that cause watery, but not bloody/WBC diarrhea?
o Staphs aureus: “picnic food poisoning”
o Bacillus cereus: food poison assoc w contaminated rice or meat from Chinese restaurants
o Vibrio (cholera and non-cholera): food poison assoc w contaminated saltwater crabs and shrimp
o Clostridium botulinum: assoc w improperly prepared home canned fruits and vegetables
o Clostridium difficile: “abx induced” enterocolitis
• What are examples of enteric bacteria that commonly cause bloody diarrhea?
o Campylobacter jejunai and fetus: mc bacterial cause bloody diarrhea in US from contaminated pork, lamb, beef, milk products, water, exposure to infected household pets
o Salmonella: fecal-oral, raw milk, chicken, eggs. requires large inoculum unless immunocompromised. Mucosal invasion → exudative diarrhea. Salmonella enterotoxin → secretory diarrhea.
o Shigella: highly contagious w very small inoculum. contaminated water, milk, food supplies
o E coli: different serotypes cause diarrhea. Enteropathogenic type in nurseries up to 12 mos w fever, vomit, watery diarrhea. Enterhemorrhagic type, esp serotype 0157:H7: bovine reservoir, undercooked beef, unpasteurized milk. Comp: HUS, TTP
• What are the stats of food poisoning in US? Causes?
o in 2007, 47.8 million (16%), 127,839 hospitalized, 3,037 died
o food illness: #1 norovirus, 2 Salmonella, 3 Clostridium perfringens, 4 Campylobacter
o food death: 1 Salmonella, 2 Toxoplasma gondii, 3 Listeria, 4 Norovirus
• what is Necrotizing enterocolitis (NEC)? Etio?
o mostly in premature infants, or neutropenic CA pt 2nd to gut colonization
o portions of bowel undergo necrosis. MC=near ileocecal valve
o no definitive known cause. mb infx (cluster outbreaks in NICUs), no common organism identified
o mb Pseudomonas aeruginosa
• what puts the neonate at risk for NEC?
o Combo of intestinal flora, inherent weak immune system, empirical abx 5+ days, alterations in mesenteric blood flow, milk feeding
o almost never seen in infants before oral feedings are initiated
o Formula feeding ↑ risk 10x compared to breast fed
o breast milk protects premature infant: Igs, also dt rapid digestion
• what is xray finding in NEC? Gross?
o Pneumatosis intestinalis: gas cysts in bowel wall (not lumen)
o Gross: intestinal necrosis, pneumatosis intestinalis, perforation site
• What is pseudomembranous enterocolitis?
o Often dt Clostridium difficile (st aka C. difficile colitis)
o can cause of abx-assoc diarrhea (AAD)
o foul diarrhea, fever, abd pain
o severe: life-threatening complications can develop, such as toxic megacolon
o Broad spectrum abx or immunosuppression allows overgrowth of flora (C diff, S. aureus, Candida)
• describe gross and histo PMEC:
o G: Mucosa of colon is hyperemic, partially covered by a yellow-green exudate; mucosa not eroded
o H: Overlying pseudomembrane has numerous inflammatory cells, mainly Ns, necrotic epithelium, fibrin, mucus → overgrowth of microorganisms takes place
• How is PMEC dx?
o First line: Stool test for C diff toxin (A and B), ↑ false (-) rate
o Also, 1) stool culture for C diff (GDH Ag), if (+) → 2) PCR for toxin genes
o Colonoscopy, sigmoidoscopy → “pseudomembranes” on colon, rectum
• What is ischemic colitis? Cause? Ssx? Gross?
o Inflame, injury of LI dt inadequate blood supply
o Uncommon, but more in elderly
o Dt: change in systemic circulation (acute ↓BP dt hemorrhage) , or constriction of blood vessels, clot (local)
o Usu no specific cause identifies
o Ssx: vary, abd pain (often left), mild-mod rectal bleeding. fever N/V, diarrhea
o Pale areas, w dusky bluish appearance on colon wall (severe)
• Which arteries specifically contribute to ischemic colitis?
o Weak pts, “watershed” areas, at borders of collateral vessel from sup and inf mesenteric arteries: at splenic flexure, transverse colon
o Watershed areas are most vulnerable
o Rectum has dual blood supply (inf mes a, internal iliac a) thus rarely involved in IC
• What is radiation enteritis? Ex?
o Severe inflammation, neovascularization, ulceration
o Dt radiation tx
o Ex: 55 yo female, radiation after hysterectomy, BL salpingo-oophorectomy for endometrial carcinoma. Radiation=external beam, brachytherapy
o → rectal bleeding
o Sigmoidoscopy: extensive radiation proctitis
• What are small bowel tumors?
o benign and malignant, relatively uncommon (compared to LI CA)
o Usu asx, or large enough to obstruct lumen, cause intussception or volvulus
o May bleed, rarely perforate
• What are benign SI tumors? Types?
o well-circumscribed, smooth, small, don’t easily bleed or ulcerate, but only bx can confirm
o mb single lesions or multiple of several subtypes; rare; usu asx throughout life
o Adenocarcinoma: MC type; usu near stomach; may obstruct;
o Hyperplastic polyps
o Adenomas
o Gut stromal tumors
o Lipomas
o Hamartomas
o Hemangiomas
• What are hyperplastic polyps of SI? Ademoas?
o HP: mucosal growths, duodenum, proximal ileum. single or mult. Usu asx, no malig potential
o A: 3 types: adenomatous polyps, Brunner gland adenomas, villous adenomas (rare, duodenum, bleeding, obstruction, mb malig, esp >4cm). single or mult, sessile or pedunculated. Histo: intraluminal extensions of sub/mucosa mult acini on central fibrovascular core. Varying differentiation
• What are gut stromal tumors? Histo? Ex?
o Benign: Aka Leiomyomas & Leiomyosarcoma
o smooth muscle; usu near LI, mb in Meckel’s, spindle cells bw muscularis propria and muscularis mucosa, may form intra/extraluminal masses, transmural lesion
o focal or annular lesions, ulceration, or deeper necrosis → bleeding, marked hemorrhage (mc complications)
o malig: diff to distinguish, 2-3x less common, depends on cell size, differentiation, mitotic bodies (>2 per 10 hpf is risk)
o histo: elongated spindle cells, w cigar-shaped nuclei, no ↑mitosis
o ex: leiomyoma at ligament or treitz (suspensory mm of duodenum)
• what are lipomas of SI? Histo?
o submucosal, mesenchymal origin. usu ileum/ileocecal valve, pedunculated. sessile or ependymal. Mb big enough to cause colicky abd pain, intermittent bowel obstruction, Intussusception
o mb surface ulceration, central necrosis, hemorrhage
o Histo: mature adipose w fibrous strands
• What are SI hemangiomas? 3 types?
o vascular tumors, 3 types: capillary, cavernous (mc), mixed
o solitary or mult, up to 10% of small bowel lesions.
o GI bleeding common. chronic (long-standing occult anemia) or profound (require massive transfusion, emergent laparotomy)
o Difficult to dx and localize sx lesions
• What are SI harmartomas? Ssx? Tx?
o Assoc w Peutz-Jeghers syndrome
o Focal, resemble neoplasm of tissue of origin, not malig, grows at same rate as surrounding tissue, but disorganized
o Usu asx; Colicky abd pain, GI bleeding, obstruction (usu dt intussusception)
o St Malig (2-3%) , w other non-GI CAs
o Tx: surveillance, biannual barium upper GI series, flexible endoscopy beginning at age 10
o **harmartomas also seen in stomach and LI, outside GI
• What are common complications w benign SI tumors, usu depending on size?
o Bowel obstruction: up to 30%, leading cause of intussusception in adults.
o Volvulus: from serosal ependymal lesions
o GI bleeding: up to 38%; occult, heme-positive stool, or acute and copious (esp large vascular lesions). may require transfusion, embolization, emergency surgery
o Perforation: → peritonitis, need emergency laparotomy
• what is PJS? Incidence? 2 types? Ssx?
o AD, mucocutaneous pigmentation (face, lips, buccal mucosa, hands, feet), benign GI hamartomas (90%)
o Rare: 1:25,000-300,000 births
o Familial: STK11 gene. AD
o Sporadic: not AD, unknown gene
• What are ssx of PJS? Dx?
o Pigmentation: oval, round, brown, black macules or spots, 1–10 mm
o Intestinal polyps (hamartomas), jejunum and ileum
o Dx: avg at 23, or identified at birth by astute pediatrician
o Often 1st presentation is bowel obstruction dt intussusception → mortality
o Before puberty: mucocutaneous lesions on palms and soles
• What is histo appearance of SI hamartomas?
o distinctive frond-like appearance, stromal/smooth muscle core covered by acinar glands and normal mucosa. No Nuclear atypia
o hyperplastic mucosal epithelium, arborizing pattern of smooth muscle
• what are other risks assoc with PJS?
o ↑ CA in multiple sites
o Hamartomas small malignant potential (<2-3%)
o ↑ risk carcinomas of pancreas, liver, lungs, breast, ovaries, uterus, testicles, other organs
• What are growth patterns of benign SI tumots?
o Intralumnal: assoc secondary bowel obstruction and intussusception
o Infiltrative
o Serosal: linked to small bowel volvulus
• What theories explain the scarcity of SI tumors, and ↓ malignant transformation?
o 1) rapid intestinal transit thru SI limits contact time to mucosa.
o 2) greater fluidity of small bowel chyme may dilute luminal irritants
o 3) alkaline pH, low bacterial colony counts
o 4) ↑ benzyl peroxidase (detox potential carcinogens)
o 5) ↑ IgA, widespread gut lymphoid tissue → impede growth, transformation
• What are malignant SI tumors?
o 64% of SI tumors
o 40% are adenocarcinomas
o 1st CA of SI relatively rare, 2% of all GI CAs
o MC= Adenocarcinoma, in US
o Other: carcinoid tumors, lymphomas, sarcoma aka gastrointestinal stromal tumors (GISTs)
o Often not found until metastasize, other complications
• What are SI adenocarcinomas?
o Similar to LI adenocardinomas, but tend to be more proximal (near stomach)
o 50% duodenum (1st to be exposed to ingested chem, pancreaticobiliary secretion, bile mb carcinogenic), 30% jejunum, 20% ileum (dt crohn’s)
o tend to co-occur in same individuals, ↑ risk in survivors of colorectal CA and vice versa.
o arise from premalignant adenomas, sporadically, or w familial adenomatous polyposis.
o Adenoma → dysplastic → carcinoma in situ → invasive adenocarcinomas
o → metastasize via lymphatics, portal circulation to liver, lung, bone, brain, other
• What are GISTs of SI?
o 25-30% in distal jejunum, ileum
o all regarded as potentially malignant
o 2 main criteria for degree of agressiveness: size and mitotic count per hpf
o > 5 cm w mitotic count > 5 per 50 hpf = high-risk lesions
• What tumors commonly metastasize to SI?
o Metastatic is mc CA in SI
o Melanomas; breast, lung, cervical adenocarcinomas; ovary, pancreas, colon, stomach
o SI is most frequent site of metastatic melanoma in GI tract dt rich blood supply
o →Metastatic lesion mb found up to 21 yrs after tx of primary tumor
o Breast and lung are unclear
• What are possible sxs of SI benign tumors (non-specific)?
o Abd pain: nonspecific, dull, epigastric in location, w larger lesions
o mb constipation, N/V
o diarrhea, early satiety, anorexia, hemorrhage, melena, volvulus
o Bowel obstruction, up to 30%; → intussusception in adults.
o GI bleeding, up to 38%, occult, heme-positive stool, or acute and copious,
o perforation into peritoneal cavity, uncommon
• what is epidemiology of SI CAs? Px?
o Slightly higher in blacks than whites, mb 2x
o M>F, 1.4:1
o Avg 60
o 30-35% 5-yr survival for adenocarcinomas, 2%% for sarcomas
• What are carcinoid tumors of SI?
o 29%-40% of 1st SI cancers, incidence rising in US
o Arise from neuroendocrine cells
o Mostly ileum, within 60 cm of ileocecal valve.
o < 1 cm 15% risk metastasis at time of dx
o > 2 cm 50%.
o Metastasis targets: liver, lungs, bones.
o Carcinoid syndrome: excess 5-HT
• What is appearance of SI carcinoid tumors?
o Gross: at ileocecal valve, smooth, well circumscribed
o Mb submucosal or extend into lumen
o Histo: endocrine appearance, collections of small round cells, nuclei consistent in size and shape
• What is a colorectal polyp?
o fleshy growth in lining o benign (hyperplastic polyp), pre-malignant (tubular adenoma), malignant (colorectal adenocarcinoma) o untx: potentially develop into colorectal cancer
• what are hyperplastic colorectal polyps?
o MC colorectal polyps, usu benign, < 1/4 in
o Hyperplastic= ↑ # cells; normal differentiation and maturation
o “rice grains” on colonic mucosa
o In lower part of crypt, cells become more crowded and hyperchromatic
o Usu descending colon and rectum of elderly
o Looks like adenomatous polyp
• What arte tubular adenomas?
o aka adenomatous polyp
o rounded neoplastic glands, smooth surfaces, discreet
o common in adults
o Small ones are virtually always benign
o > 2 cm ↑ risk carcinoma, dt APC, DCC, K-ras, p53
• What is histo and gross appearance of a benign adenomatous polyp?
o On stalk; glands more irregular, crowded, rounded; darker/hyperchromatic and more crowded nuclei
o ↓ goblet cells
o Benign: well-differentiated, closely resembles normal colonic structure.
o Gross: hemorrhagic surface (mb initially detected by stool occult blood screen), long narrow stalk. If > 2 cm, ↑ risk malig
• What are the benign tumors of LI?
o adenomas, leiomyomas, fibromas, neurofibromas, lipomas, carcinoid tumors
• what are villous adenomas? Appearance?
o Less common than adenomatous polyps; more likely to have invasive carcinoma (40%)
o Gross: sessile, not pedunculated, larger than tubular adenoma
o Usu several cm in diameter, up to 10cm long
o Micro: cauliflower-like appearance, dt elongated glandular structures covered by dysplastic epithelium
• What is Juvenile polyposis syndrome?
o mult polyps in GI tract, usu child, adolescent, young adult
o “juvenile”= histological type, not age (age is variable)
o mostly non-neoplastic, hamartomatous, self-limiting, benign
o but ↑ risk adenocarcinoma (9-50% lifetime risk)
o ssx: rectal bleeding, abdominal pain, diarrhea, anemia
o colonoscopy or sigmoidoscopy: various size and shaped polyps, sessile or pedunculated
• what is micro appearance of JPS?
o characteristic inflamed, edematous stroma; eroded surface and cystic epithelial elements.
o Mb dysplasia or not, but usu large and multi-lobulated polyps should be carefully evaluated for neoplastic changes
o Epithelial surface maturation differentiates reactive/reparative change from dysplastic change.
• What is Familial adenomatous polyposis (FAP)?
o AD, hundreds to thousands of polyps in LI epithelium (early adolescence)
o Mb risk of other malignancies (duodenum, stomach)
o start benign → malignant transformation into colon adenocarcinoma if untx (100% lifetime risk)
• What are ssx of FAP? Imaging? Tx?
o ssx: mb bleed, IDA
o if malig: weight loss, altered bowel habit, or metastasic to liver, etc
o sigmoidoscopy: carpet of small adenomatous polyps.
o Tx: total colectomy, by 20
• what is garner’s syndrome? Ssx? Work-up
o AD. =FAP + combo of polyposis, osteomas/osteomata (benign bone tumors), fibromas, sebaceous cysts
o Add’l ssx: “CHRPE - congenital hypertrophy of retinal pigment epithelium”, jaw cysts, , epidermal inclusion cysts
o Need xrays; mb osteomas in long bone
o early age: subtle defects in mandible; Eye exams detect pigmented lesions of retinal fundus.
o Colonoscopy and other invasive tests to check for polyps every 1-2 yrs
• What is gross appearance of LI adenocarcinoma? Micro?
o May arise from villous adenoma
o Gross: surface is polypoid, reddish pink. mb large ulcer w tumor lesion. Hemorrhage from surface → guaiac positive stool; ulcer suggests CA; encircling mass common in descending colon
o micro: may see edge of carcinoma arising in villous adenoma. neoplastic glands are long and frond-like (like villous adenoma). primarily exophytic (outward into lumen); mb some differentiation (w irregular, crowded glands, nuclei, hyperchromatic, pleomorphic, mb no normal goblet cells), lumens w mucin
• what are ssx of LI adenocarcinoma? Staging?
o Ssx: change in stool or bowel habits mb dt mass effect of tumor o Staging (dukes): based on degree of invasion into and through wall
• what is Dukes staging system?
o For colon CA, 4 categories
o A: Tumor is only as deep as mucosa
o B1: in muscularis propria
o B2: through muscularis propria.
o C1: to muscularis propria and LNs, positive for CA
o C2: through muscularis propria and LNs, positive for CA
o D: outside intestine, mb spread to nearby organs
• What is histo appearance of a leiomyosarcoma?
o leiomyoma can be differentiated from leiomyosarcoma; both have ↑ cellularity
o leiomyosarcomas: ↑cell density, more mitotically active (> 2)
• what is histo appearance of GI lymphoma?
o large blue non-Hodgkin’s lymphoma cells, infiltrating thru mucosa
o prominent clumped chromatin and nucleoli w occasional mitotic bodies
• What is the liver?
o largest visceral gland in body (3 lbs, 1200-1600g); red-brown, smooth surface; 4 lobes → 1000s of lobules
o blood supply by hepatic a (O2) and portal v (nutrients)
o only internal organ capable of signifigant regeneration, only 25% needed to totally regenerate
o dt hepatocytes are unipotent stem cells → quiescent (G0) hepatocytes can reenter cell cycle (G1) → mitosis
o think Prometheus getting his liver eaten every day by vulture, regenerating
• What is the role of the liver?
o main detox organ of endogenous and exogenous substances
o metabolism of carbohydrates, proteins fats
o produces bile, alkaline, digestion, emulsification of lipids
o produces coagulation factors (I, II, V, VII, IX, X, XI, C, S, AT)
o storage: glucose (glycogen), vit B12, iron, copper
o RES has immunologically active cells, ‘sieve’ for Ags via portal system
• Describe the role of the fetal liver:
o 1st tri: main site of RBC production
o 32nd wk: BM almost completely takes over
• What are the major primary diseases of the liver?
o Viral hepatitis o Non-viral hepatitis o Alcoholic liver disease o Non-alcoholic fatty liver o Hepatocellular carcinoma
