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115 Cards in this Set
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enterocolitis |
def- inflammation of mucous in sm and lg intestine
characteristic- diarrhea Cause- infectious, inflamm bowel disease, radiation, GvH disease |
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what organism cause dysentary
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bloody diarrhea, frequent, small volume, leukocytes in stool, abd pain
campylobacter shigella salmonella yersinia ETEC EHEC typhiod (enteric) fever **these ones invade mucoas and make exotoxins- Pg synthesis blocks fluid reabs |
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we know tht campylobacter, shigella, salmonella, yersinia, enteric (typhoid) fever, ETEC and EHEC all make dysentary. what are some NON infectious causes
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UC
chrons ischemic colitis |
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what can be the systemic effect of campylobacter (besides dysentary)
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gullian barre syndrome
autoimmune paralysis |
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the invasive bacteria that cause dysentary (campylo, shigella, salmonella, typhoid, yersinia. ETEC EHEC) have what systemic manifestations
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1. reactive arthritis (esp in HLA B27ppl)
2. erythema nodosum Reiter- yersinia, shigella hemolytic uremic- shiga toxin producing e coli |
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what is the infectious cause of hemolytic uremic syndrome
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shiga toxin made by e coli
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what organism that causes dyenstart also causes...
1. GBS 2. Reiter 3. HUS 4. Osteomylitis 5. Mesenteric lymphadenitis w/necrotizing granulomas |
1. GBS- campylobacter
2. Reiter- yersinia, shigella 3. HUS- shiga toxin from e coli 4. Osteomylitis- salmonella (esp in SS) 5. Mesenteric lymphadenitis w/necrotizing granulomas- yersinia |
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A 24 y/o man presents with a 4‐day history of
abdominal pain, fever, and anorexia • The abdomen is tender to palpation and a CT is requested (shown on following slide) • What structures are enlarged? • What are causes of this condition? • What labs are most helpful in establishing Dx? • What is the likely microscopic morphology? |
sounds like appendicitis, BUT CT shows sm intestine and mesentary
lots of granulomas, its YERSINIA. dysentary, causes reiters and necrotizing granulomas and mesenteric lymphadenitis **recall chrons also makes granulomas :) **common in ileum, and R colon/appendix |
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what pathogens cause pseudomembrance
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shigells
campylobacter c diff |
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what are the clinical and morphological features of typhoid
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human disease, US causes acquired from other areas. Fecal oral, typhoid survives gastric HCL and is taken up by M cells in sm intestine.
CLINICAL: fever, bloody diarrhea, chronic infetion with carrier state, encephalopathy, myocarditis MORPHOLOGICAL: sm intestine, LINEAR enlargement of peyers path, ulceratios, mesenteric lymphadenopathy, splenomegaly (maco infiltrate), Typhoid Nodule- macro aggregates in LIVER, BM. sepsis |
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your pt just came home from mexico where she drank the water in an animal field. She has a tender spleen, and the liver shows aggregates of macro surrounded by necrosis. She has had bloody diarrhea and a maculopapular rash on her ant trunk. What will her small intestine look like
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linear enlargement of peyers patches- TYPHOID
systemic, human only. we have vaccine fecal oral- survives HCL, taken up my M cells in sm intestine linear enlargment of peyers, ulceration--> sepsis mesenteric lymphadenopathy splenomegaly- macro infiltrate typhoid nodule in LIVER nad BL Rose spots on ant trunk can cause CNS, heart, lung, osteomylitis, gall bladder etc |
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what causes pseudomembranes
infectious and otherwise |
pseudomembrane colitis, aka AB associated colitis. c diff- enterotoxin A/B
shigella EHEC staph candida Ischemic coliis volvulus |
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AB assicated colitis
pathogensis clinical morphologic |
Pathogenesis: C dif A/B exotoxins. AB cause lysis of C dif and LOTS of toxins are released
Clinical: watery diarrhea, relapse common. fever, leukocytosis, abd pain, hypoalbiminemia Morphologic: pseudomembranes, Volcanic eruption / Mushroom cloud of mucopurulent exudate extends from superficially damaged crypts |
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what is associated with a "volcanic or mushroom cloud" release of PMN, exudate from superficially damaged intestinal cyrpts
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AB assicated colitis, C diff
its A/B toxins release in large numbers after AB are given. this releases LOTS of exudate and makes pseudomembranes abd pain and watery diarrhea |
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This patient presented with abdominal pain
and watery diarrhea of > 1L of stool/day while receiving cefazolin for aspiration pneumonia. • Abdomen was distended and mildly tender with hyporeactive bowel sounds. Colonic mucosa revealed multiple small, whitish‐yellow plaques covering a hyperemic mucosa. Changes extended to the transverse colon. What is the cause of his diarrhea? • How do you make the diagnosis? Morphology? • Lab test? • How is this disease treated? |
AB mediated colitis, pseudomembrane.
lab- look for C diff A/B exotoxin, look for mushroom cloud explosion of PMN/exudate from intestinal crypts Biopsy demonstrated focal ulcerations of colonic mucosa with mucopurulent exudate extending from superficial crypts and forming an overlying mushroom cloud. • ELISA assay confirmed the presence of Clostridium difficile toxin A. • Treatment with metronidozale led to complete resolution of clinical and endoscopic findings. treat: metradanazole |
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what is a serious complication of pseudomembrane colitis
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toxic megacolon
gets HUGE **recall AB mediated pseudomembrane colitis- mushroom cloud, watery diarrhea, low albumin. C dif exoto |
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what is bacterial overgrowth sundrome
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its assocaited with:
low gastric acid immune issues dysmotility issues- blind loop sx: malans stearorrhea osmotic diarrhea (chronic) AFTER they eat |
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tell me about the blind loop that a surgeon creates during gastric bipass?
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the fx stomach is made REALLY small
the rest of the stomach secretes things and so is needed but its cut off from anything superrior to it. it is attached to sm intestine creating a BLIND loop! bacteria can come from sm intestine into that big stomach and get bacterial overgrowth --> malabs partial gastrectomy- gastrojejunostomy- creates a duodenal blind loop. |
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what causes diarrhea that does NOT have PMN in it OR blood.
who gets it |
1. virus- norovirus, rotavirus, adenovirus
2. Cholera, C diff 3. ETEC, 4. Cryptosporidiosis- esp in AIDS pts |
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does the following create a dysentary with blood and PMN
Norovirus, adenovirus, rotavirus cholera c dif cryptosproidious |
all are WATERY no PMN, no blood
Rota- young kids Noro- ppl on crusises, most common Adeno- immunosuppressed |
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water or blood diarrhea
Cholera campylobacter shigello Salmonella Enteric thyphoid Yersinia ETEC EHEC C diff Adenovirus Norwalk Rotavirus |
Cholera: water
campylobacter: either shigello: blood Salmonella: blood Enteric thyphoid: blood Yersinia:blood ETEC: blood EHECBlood C diff:water Adeno: water Norwalk: water Rota: water |
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tell me about cholera
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preformed ENTEROtoxin causes watery Secretory diarrhea (secretory- >500, occurs during fast, Normal osmolar gap. ex cholera, EHEC, C diff)
the B subunit of enterotoxin bings GMI on enterocyte 2. adenyl cyclase released adn stim cAMP 3. cAMP opens CFTR, releases Cl-, bicarb, water, inhibits NaCL receptor --> massive watery diarrhea |
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what ist eh most common vibrio infection, how is it acquired
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vibrio parahemolyticus seafood realted enteritis
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how does the cholea toxin work to make secretory diarrhea
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1. B bubunit binds GM1 on enterocyte
2. adenyl cyclase released 3. adenyl cyclase stim cAMP release 4. cAMP opens CFTR 5. open CFTF releases Cl, NaBicarb & water into lumem 6. inhibits Na Cl reabs --> 7. secretory massive watery diarrhea |
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who gets rice water stool that can lead to hypovolumic shock
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cholera
toxin releases cAMP to NaBicarb, Cl and water in lumen. causes secretory MUCOSA remains in tact |
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A 32 y/o woman presents to the physician with
alternating bouts of diarrhea and constipation. She also has chronic abdominal pain relieved by frequent bowel movements. Her symptoms are exaggerated by stress. The patient denies fever or weight loss. She has a negative hemoccult test. Colonoscopy and endoscopy reveal no abnormalities. Which of the following is the most probable diagnosis in this patient? A) Celiac sprue B) Colorectal carcinoma C) Inflammatory bowel disease (IBD) D) Irritable bowel syndrome (IBS) E) Pseudomembranous colitis |
irritable bowel SUPER COMMON, be sure there are no red flags like blood in poo or fever, weight loss etc
NO morpholocical change |
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what is the combination of abd pain and change in bowel habits w/o another organic cause called
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irritable bowel disease, SUPER common
more than 3 days for more than 3 months: releaved by defication change in ffrequency of pooping change in stools themselves **labs/imaging/endoscope is normal *more common in females |
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what are the 3 things that come into play with irritable bowel syndrome
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1. change in bowel MOTILITY
2. Visceral hypersensitivity 3. psychososial **can follow infectious/inflammatory enterocolitis (a perm change can set this up) misdx as GB disease, pelvic pain to another cause |
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A 22 y/o man presents to the physician with a
one year history of chronic, recurrent right lower quadrant abdominal pain and diarrhea. The patient also has had low‐grade fevers and a 6.7‐kg (15‐lb) weight loss during this period. Endoscopy of his terminal ileum shows multiple erosions. Which of the following is the most likely diagnosis in this patient? A. Celiac sprue B. Collagenous colitis C. Crohn’s disease D. Irritable bowel syndrome E. Ulcerative colitis |
A. Celiac sprue: celiac, wheat intolerance
B. Collagenous colitis: C. Crohn’s disease*** D. Irritable bowel syndrome, this is periumbilical pain with change in bowel but NO fever or weight loss E. Ulcerative colitis: this is colon abviously |
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IBS
IBD |
IBS- irritable bowel, its a catch all for abd pain and poo changes that is NOT related to antoehr cause
IBD- inflammatory bowel disease. more disease like. UC or chrons |
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what is the pathogenesis of IBD
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1 genetic
2. commensal (normal) flora 3. abnormal T cells From First AID Chrons- disordered response to normal bacteria UC- autoimmine more common in female in their 20's common in whites and ashknazi jews |
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NOD2
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mutation in Chrons disease
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what are the genes involved in IBD
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CHRONS: NOD2, Th1, granuloma
UC: Th2 activation BOTH: IL23 receptor polymorphism which maintains the proinflammatory Th17 pro inflammatory response |
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tell me about the epithelial defects in chrons and UC
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1. CHRONS: tight junctions, tranepithelial transport, mucin, paneth cell granules
2. UC: defect in the ECM inhibitor of matric metalloproteases |
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whats the hygein hypothesis of IBD
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we are too clean, give our immine something to do so its not making things up to do like kill our digestive system
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A 15 y/o girl presented with weight loss,
abdominal cramps and arthralgias. She had been in good health until 2 years earlier. She suffered recurrent arthritis from age 13 with intermittent joint swelling treated by ibuprofen. • Her mother was concerned about absence of menarche and secondary sex characteristics. • She was of average size until age 13. She was now 30th percentile for height and 5th percentile for weight. Patient was a “picky” eater who now did not finish her favorite foods. She described loose bowel movements and streaks of blood in her stool. She had recent onset of abdominal cramps after eating. • PE showed mild tenderness of the abdomen with fullness in the right lower quadrant. • There were effusions of the right knee and left elbow and a skin nodule on the right shin but no joint deformities.A small bowel series showed edema and a cobblestone appearance in a 30 cm segment of terminal ileum. Colonoscopy showed scattered aphthous ulcers in the sigmoid colon and hepatic flexure. The ileocecal valve was narrowed and ulcerated. Biopsy showed superficial ulcerations; granulomas whats the dx |
chrons- ileum and colon. complicated by malabs, arthritis and erythema nodosum
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is dermatitic herpetiformis associated with celiac or chrons
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celiac
chrons gets erythema nodosum |
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what are some other names for chrons
frequency what part of GI is involved |
regional enteritis
terminal enteritis gramulomatous colitis its skip lesions seen in 15-25 and 50-60 increased in smoking ocerall is increasing can be anywhere from mouth to anus, common in terminal ileum, ilececal valve, cecum can be a combo of sm intestine only sm and large or large onle. jsut small intestine is most common |
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whats the deal with apthous ulcers and IBD
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ICM- said UC
Path said- CHrons |
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is this chrons or UC
anal fistula, fissures, paneth cell metaplasia |
chrons, also see skip lesions and apthous ulcers
transmural inflammation non caseating GRAMULOMA paneth cell metaplasia crypt abcess |
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ok so chrons involves the entire thickness of the GI in skip leasions. what does this make it look lkike
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garden hose wall with cobblestone and creeping fat
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if you see segments of bowel affected with inflammation into the muscularis and there are granulomas whats the deal
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chrons disease- IBD
can also have fissure, ulcer, cobblestone, garden hose rubbery thickness, creeping fat |
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when do you see garden hose thickening of the intestine
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chrons- its transmural inflammation
cobblestone, granuloma, creeping fat commonin terminal eleum, ileocecal valve and cecum, LINEAR ulcers |
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your pt is 20 and complains of intermitent attacks that are are ppt by stress. she has diarrhea, fever, abd pain. It look slike an acute abdomen but can be asx for weeks to months. attacks are triggered by stress, diet adn cigs
what disease, what will labs show she has a "moon facie" acne, thining hair, puffy cheeks |
chrons
LABS: WBC in poo, +occult blood, blood loss anemia, malabs--> anemia, prolonged PT, hypoalbuniemia |
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A 15 y/o girl presented with weight loss,
abdominal cramps and arthralgias. She had been in good health until 2 years earlier. She suffered recurrent arthritis from age 13 with intermittent joint swelling treated by ibuprofen. • Her mother was concerned about absence of menarche and secondary sex characteristics. • She was of average size until age 13. She was now 30th percentile for height and 5th percentile for weight. Patient was a “picky” eater who now did not finish her favorite foods. She described loose bowel movements and streaks of blood in her stool. She had recent onset of abdominal cramps after eating. • PE showed mild tenderness of the abdomen with fullness in the right lower quadrant. • There were effusions of the right knee and left elbow and a skin nodule on the right shin but no joint deformities. A small bowel series showed edema and a cobblestone appearance in a 30 cm segment of terminal ileum. Colonoscopy showed scattered aphthous ulcers in the sigmoid colon and hepatic flexure. The ileocecal valve was narrowed and ulcerated. Biopsy showed superficial ulcerations; granulomas. • Diagnosis: Crohn disease of ileum and colon, complicated by malabsorption, arthritis and erythema nodosum. Patient treated with mesalamine without improvement. Prednisone resulted in reduction in symptoms, weight gain and onset of menses. • Therapy was complicated by acne, thinning hair and puffy cheeks (“moon facies”). • Azthioprine was added. At age 20, she presented with abrupt onset of abdominal pain, distention, vomiting and absence of bowel movements. • She was hospitalized on steroids with some improvement. • Small bowel series x‐rays showed stricture of terminal ileum with inflammatory mass and fistulae between the ileum and cecum. • The affected ileum and cecum were resected and patient discharged on azathioprine. what are complications of chrons Patient did well on azothioprine and married at age 23. In anticipation of pregnancy, she discontinued medications. Four months after cessation, erythema nodusum appeared and therapy was resumed. • Pregnancy was uneventful and she delivered a healthy baby. • 6 weeks later she developed painful perirectal abscess and fistula. There were ulcers of the anal canal and rectum on proctoscopy. |
1. strictures- surgery to remove
2. fistula 3. peritoneal abcess, perianal fistula 4. terminal ileum disease- protein loosing enteropathy, hypoalbumin, edema 5. malabs- steatorrhea, B12 deficit 6. increaased colon cancer in chrons that involves the colon 7. erythema nodosum |
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what are the extraintestinal sx of chrons
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1. erythema nodosum
2. migratory polyarthritis 3. HLA B27 ankylosing spondylitis, sarcoilitius 4. uvitis 5 clubbing |
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tx for chrons
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immunosuppression, TNFa blockers
surgery only for fistula abcess |
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what is teh ulceroinflammatory disease that is limited to the colon and affects only teh mucosa or submucosa
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ulcerative colitis
lots of crypt abcesses rectum involved, only colon, no skip leions |
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what does this describe
colonic involvement with no skip leipons, crypt abcess nad, inflammation limited to mucosa nad submucosa |
UC
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if you see a colonic sample with leisons on the mucosa that expose the muscularis continusouly from rectum to some proximal area
what else |
UC
pseudopolyps- toxic megacolon- damage of neural plexus HIGH risk of getting carcinoma 10- years after onset |
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is toxic megacolon associated with UC
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ya, bc of the neural damage to colon. it dilates and gets HUGE
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tell me a little about the clinical features of UC
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relapse, ppt by stress (like chrons)
bloody mucoid diarrhea for days to months, some get sonstipation lower abd pain releived by pooping |
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20 y/o man with recent diagnosis of UC had
continuous bloody stools and weight loss. Unresponsive to immunosuppression. CT shows Swaminath A and Feingold D. N Engl J Med 2010;362:635 megacolon and free air in abdomen. Taken to surgery following transfusions. Total colectomy with ileostomy performed. Dx: |
fulminant UC.
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when is primary sclerosing cholangitis seen
what are other complications of the initial cause |
complication of UC
get migrating polyarthritis ankylosing spondolytit uveitis skin lesion- erythema nodusum, pyoderma gangrene megacolon DVT adenocarcinoma |
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are these complications of UC or Chrons
uvitis erythema nodosum pyogenic gangrene DVT arthritis cholangitiis toxic megacolon cancer |
UC
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what is the tx for UC
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1. immunosuppression
2. colectomy 3. lots of endoscopies to check for cacner |
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chrons or UC
stricture DVT megacolon recurrenct after surgery malabs thick looking wall pseudopolyps cancer |
stricture- chrons
DVT UC megacolon UC recurrence- chrons malabs- chrons thick wall- chrons pseudopolyps- both but more in UC cancer- both |
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Diversion Colitis
Collagenous Colitis Lymphocytic Colitis Graft c Host disease |
Diversion Colitis: hartmans pouch- anus, and lower rectum ends blindly with ostomy. colitis likely due to microbiota and diversion of fecal stream nurtients
Collagenous Colitis: adult women with constant water diarrhea but no weight loss. cramping abd pain, no predisose for cacner Lymphocytic Colitis: assoicated with autoimmune disease Graft c Host disease: T cells of graft kill hostcrypt cell necrosis w/o inflammatory response |
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This 62 y/o male presented 12/29 to the ER with
abdominal pain of 4 days duration starting on 12/25. Pain was diffuse and had waxed and waned. It was accompanied by anorexia and nausea. There was no bowel movement for 48 hours and in the last 12 hours he had started vomiting. He was afebrile. • He had never been seriously ill before and was taking no medications. • Abdomen was diffusely tender; distended amylase up, WBC up, Hb low, Hct X‐ray of the abdomen revealed dilated loops of small intestine in a step ladder pattern diagnostic of.... He was admitted to the hospital and taken to surgery 12‐30 where left lower quadrant and pelvic peritonitis and abscess in the region of the sigmoid colon were discovered. Segmental colectomy with colostomy was performed. Multiple diverticuli were identified with diverticulitis and perforation. |
super common
small bowel obstruction |
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ok so there are "other" kinds of colitis
which one is this 1. assoicited with blind rectum/anus, colitis due to microbiots 2. autoimmune 3. adult women, watery diarrhea not weight loss 4. cyrpt necrosis w/o inflammatory response |
1. diversion
2. lymphocytic 3. collagenous 4. G v Host |
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what does SBO look like
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step ladder pattern
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what is the "true" diverticulum
wht about acquitred whats the diff btwn them |
meckles, there was also znekers diverticulum in the neck
acquired diverticula- common in l colon adn LACKS muscularis propria |
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where are diverticuliaa from diverticular disease located
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next to tenia coli
l colon no muscularis propria mucosa herniates through the muscularis an onstructed diverticula becomes a diverticulitis |
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what sthe pathogenesis of diverticula
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focal weakness in colonic wall, increased intraluminal pressure causes exaggerated peristalsis this then can blow out portions of mucosa
related to lack of fiber in the poop |
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what are the clinical features and complications of diverticular disease
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1. clinical- not as helpful, old ppl. L colon, constipation or diarrhea. recutm always feel full
2. pathogenesis of focal weakness, no fiber and then BOOM! out they pop 3. complications: MASSIVE blood loss |
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this describes what
Focal weakness in colonic wall ‐ Sites of nerve and vessel penetration • Increased intraluminal pressure ‐ Exaggerated peristaltic contractions ‐ Spasmodic segmental sequestration ‐ Related to lack of bulk (fiber) in feces |
diverticular disease pathogensis
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A 73 y/o man c/o acute bright red bloody stools. Urgent
colonoscopy reveals profusely bleeding diverticulum. A bleeding vessel was identified a the neck of the diverticulum (arrow in panel A). Hemostasis was achieved by injection of epinephrine. he then went septic, what happened |
pericolic abcess from ruptured diverticulum
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what are complications of diverticular disease
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1. diverticulitis
2. perforation 3. pericolic abcess 4. peritonitis 5. fistula 6. stricutre 7. hemorrhage |
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what are some causes of obstruction
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1. stricture- chrons, diverticulitus
2. inguinal hernia 3. intussucpetion 4. meconium ileus- imperforate anus, CF 5. infarct/thrombus 6. volvulus 7. adhesion 8. nerve 9. megacolon 10. cancer 11. feval impaction 12. diverticulosis |
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An 83 y/o man has a lifetime of chronic
constipation. For the past 5yrs., he has complained of mild lower abdominal discomfort. On PE, bowel sounds are active; there are no masses and no tenderness. A CT is scan is shown. What does the CT show? Is he at increased risk for cancer? What important complication can occur? |
*constipation leads to increased intraluminal pressure in rectum and sigmoid colon.
1. CT- air filled circular pockets in rectum- diverticulitis 2. increased cancerL NO 3. massive bleed, diverticulitis, pericolic abcess, peritonitis, fistula, stricture, |
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what does this supply
1. celiac artery 1. SMA 3. IMA |
1. celiac, duodenum
2. SMA- proximal jejunum to prox transverse colon 3. IMA- distan transverse to midrectum - IMA gives rise to superior hemorrhoidal |
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what are the 2 types of ischemic injury of the bowel
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1. ischemic colitis:
-Mural: mucosa and submucosa -mucosal: mucosa only 2. transmural Infarct: full thickness necrosis |
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wht causes mural and mucosal ischemic colitis
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hypoperfusion, can be acute or chronic
Acute- heart failure, shock, constrictors, marathon runners Chronic: arterial comprimise **can progress to transmural |
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what exactly is marathon diarrhea
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when ppl run for so long blood is shunted from gut to legs and things
get a mucosal or mural infartc (NOT transmural) |
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what is the pathogensis of a transmural infarct
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acute/COMPLETE comprimise of A or V- major mesenteric vessel
more common in artery so if SMA is lost you loose jejunum to prox transverse colon IMA would be distal transverse colon to midrectum |
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what kinds of things can cause transmural ischemia in the bowel- causes of vascular comprimise
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1. artherosclerosis
2. aortic aneurysm 3. hypercoaguability 4. embolization 5. vasculitis 6. mechanial- adhesion 7. cancer |
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what are the 2 phases of ischemic injury
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1. Hypoxic injury- transient hypoxia can be dangerous or not
2. reperfusion injury- more damaging, free rads and PMN |
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what is a watershed area
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its near splenic flexure and rectum, its where blood supply runs out and it a common site of ischemic colitis
Splenic flexure: SMA and IMA watershed area Rectal flexure: IMA and hypogastric artery watershed area **its the far end of the blood supply, its most affected by hypoperfusion |
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what does colon that has ischemic colitis look like
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pseudomembrane
epithelial surface sloughs off/atrophy NO hemorrhage ---> can lead to FIBROSIS, can cause stricture |
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ok you are looking at a colon you see a pseudomembrane but the pt is not infectious. There is epithelial sloughing and the begining of fibrosis, whats the deal? whats a complication
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ischemic colitis
can cause stricture |
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ischemic colitis looks like what clinically
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cramps
diarrhea GI bleed, fecal occult blood, leukocytes in poo stricture, obstruction resembles enterocolitis or IBD |
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Colonoscopy:
82 y/o man with Splenic flexure of this patient: y mucosa bloody diarrhea erythematous, edematous and Sudden onset friable. Loss of normal vascular left lower abdominal pain followed by bloody di h Hi t f markings Normal diarrhea. History of atherosclerotic heart disease, hypertension. patient: note vascular ki No antibiotics. No recent hospitalization |
ischemic colitis- artherosclerosis
will have pseudomembrane, mucosal damage |
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classify the ischemic colitis
the mucosa and submucosa is sloughing off and fibrosing, the muscularis seems to be intact |
mural
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tell me more about transmural infarcts
what part of bowel affecrted a or venous, demarcation |
fullthickness involved: mucosa, submucosa, muscularis
typically involves and long segment A occlusion- sharp demarcation V occlusion- indistinct demarcation BOTH will look hemorrhagic infarct, dusky red/purple |
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complications of transmural infarct
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serositis
gangrene peritonitis **keep in mind, a sharp demarcation is A occlusion, and indistinct is venous occlusion. BOTH show a red, pupple lesion |
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This 81 y/o female was admitted from the
rehabilitation unit on 12‐28 where she was recovering from a recent CVA (stroke). What is the most common cause of CVA? • She c/o abdominal pain, nausea and vomiting. • After passage of several bloody stools, she experienced no more bowel movements. • PE on admission: diffuse tenderness to palpation and no rebound tenderness. What is this clinical condition? WBC: 23,300 (5,000‐10,000), 88% segs • Hb10.6 gm; Hct 29.5%. Platelets 168,000. • Abdominal x‐rays: dilated, gas‐filled loops of small intestine consistent with small bowel obstruction. • The pain decreased in intensity over the next day then became severe.A surgical consultation was ordered in the pm of 12‐31 and the diagnosis made of acute surgical abdomen. • Patient was taken to OR on 1‐1 and 54 cm of infarcted small intestine were removed. • Postoperatively, the patient had to be maintained on a ventilator. Acute renal failure was diagnosed. Patient succumbed the following day. What is the differential diagnosis of small bowel obstruction/acute surgical abdomen? • What is the likely etiology of her intestinal obstruction? • What do postoperative ventilator dependence and renal failure indicate? |
common cause of CVA- artherosclerosis, be thinking ischemic colitis
called ileus: distension, pain, gas decrease in pain and then severe means we had a rupture DDx: ABO, acute abdomen. Paralytic ileus, vascular, meds, curgery Hers was vascular, ischemia. bc of stroke info Vent use: ARDS, acute tubular necrosis, acute liver,---> septic shock with ARDS |
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tell me about intestinal infarct and gangrene
waht vessel is common mortality onset, sx course of disease |
SMA thrombosis
high mortality sudden onset of abd pain, tenderneaa, NV, bloody diarrhea RAPID progression to shock and dead **abd wall gets rigid and board like |
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what are some ischemic bowel things that are caused by something else (2 iscumic colitis)
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1. rradiation
2. CMV 3. necrotizing enterocolotis |
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tell me about CMV and intestinal infarct
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CMV causes infarct-
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tell me about radiation and intestinal infarct
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radiation cuauses acute injury
anorexia, cramps, malabs diarrhea, fluid, electrolyte loss, can get ulcers and strictures |
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who gets radiation enterocolitis
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its ischemia
seen in ppl who get radiation for prostate, BM, lymphoma, cervix |
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who commonly gets necrotizine enterocolitis
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premies! it leads to ischemic colitis
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Infant born prematurely at 26 wks. gestation.
• Early neonatal period complicated by hypotension, respiratory distress. A patent ductus arteriosus required surgery after failure of indomethacin therapy. • Feeding was begun on day 26. On day 52, he developed abdominal distension and frank blood in stools. X‐ray showed portal vein gas and air in wall of intestine. Died despite Tx of septic shock with DIC. Abd x ray showed air in portal vein and air in intestinal wall: |
?? is this necrotizing enterocolitis- this leads to ischemia
Release of cytokines with oral feeding leads to ischemia with necrosis, perforation • Clinical, fulminant cases: abdominal distension, ileus, bloody diarrhea • May die of septic shock |
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whats angiodysplasia of the GI tract
where is it common what are clinical features |
its NOT precancer, its tortoius dialted BV in old folks
CECUM, R colon most sommon painless bleed |
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your old pt is bleeding from the R colon, whats the deal
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angiodysplasia, dilated tortous BV, not precacner
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A 70 y/o man has an 8 mon. history of
increasing fatigue. Hb is 8 g/dL (nl 13.8‐17); MCV 71. Colonoscopy demonstrates an abnormal area shown (17.19). What do his labs indicate? What is the diagnosis of the lesion pictured? What is the pathogenesis |
anemic, GI blood loss
shows squirly worm like BV, angiodysplasia pathogenesis: mechanical occlusion of submucosal veins by normal distension |
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whats the pathogenesis of angiodysplasia
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Mechanical occlusion of submucosal veins
by normal intestinal distention leads to focal dilation • Predispositions: ‐ vascular fragility, cross‐linked proteins accumulate with aging ‐ congenital morphologic predisposition as we get old we cross link protein adn we dont stretch. the BV dont stretch, the cecum dilates and puts pressure on veins and makes then collapse, and other parts distend--> focal dilations in submucosa. they can then bleed |
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what are hemorrhoids
predisposing factors |
variceal dilation of the anal and perianal venous plexus
common in ppl over 50 ppl who strain or are constipated. fat, pregnant, PORTAL HTN |
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compare internal and external hemorrhoids
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EXTERNAL: below anorectal line, inferior hemorrhoid plexus, covered by SQUAMOUS epithelium, PAINFUL
Internal: superior hemorrhoid plexus, covered by COLONIC type mucosa, PAINLESS commononly internal and external cooccur |
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complications of hemorrhoids
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itch, burn, hurt, blood clots/thrombus
PROLAPSE--> strangulation, infarction Ulceration fissure BLEEDING |
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constipation, fat, preg, portal HTN are all risk factors for what
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hemorrhoids
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what are ALL of the causes of GI bleed
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1. esophageal varicie
2. mallory weiss tear 3. hemorrhagic gastritis- EtOH, Nsaids, ASA 4. Gastric ulcer 5. duodenal ulcer 6. Ischemic bowel disease 7. intussecption 8. meckle diverticulum 9. angiodysplasia 10colonic carcinoma 11 IBD 12 Diverticulosis 13 rectosigmoid carcinoma 14 hemorrhoids 15 anal fissure 16 infectious colotis: yersinea, e coli, shigella, |
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whats the pathogenesis MORPHOLOGY and clinical features of acute appendicitis
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1. pathogensis:
Lumen Obstruction: kids- lymphoid hyperplasia, adults fecolith 2. MORPH: PMN in muscularis propria, dull granular serosa, dilated BV. fibropurulent exudate, ulceraitions, gangrene 3. Clinical: any age, periumbilical pain that goes to RLQ, NV, fever, tenderness. leukocytosis in 50% |
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who gets appendicits from lymphoid hyperplasia what about fecolith
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kids lymphoid
adults fecolith |
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what does an infected appendix look like
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red, dilated BV, pus
follow tinea down to appendix, if it gets gangrenous it can rupture |
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A 22 y/o woman initially developed nausea
with periumbilical pain 1 day before admission; pain is now localized to her right lower quadrant and she has rebound tenderness. Her CT shows an enlarged appendix containing a fecolith. Inflammatory stranding entends into adipose tissue. What is the diagnosis? What complications can occur |
fecolith is hard gross poop, common ppt for appendicitis in adults
acute appendicitis perforation, abcess, peritonitis, pyelonephritis, hepatic abcess, bacterimia |
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whats the complcations of appendicitis
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perforation
peritonitis/abcess phylonephritis bacteremia |
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why is appendicitis more fatal in kids
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they have a small little omentum so it wont cover the appendix and prevent spread of lots of the infection
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what are the causes of sterile peritonitis
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Bile perforation
acute hemorrhagic- enzymes digest adipose Endometriosis reptured dermoid cyst |
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A 55‐year‐old man is brought to the
emergency department with abdominal pain, fever, and dyspnea. Past history includes appendectomy 8 yrs. earlier. • Abdominal radiography shows free air as well as signs of small‐bowel ileus. What is the most likely diagnosis? Why does he have dyspnea? An emergency laparotomy is performed. Intraoperatively, a lower small‐bowel perforation is identified within an ischemic segment, with evidence of peritonitis. Partial ileal resection with end‐to‐end anastomosis is performed. What are the complications of perforated viscus? Treatment with broad‐spectrum antibiotics is initiated. Septic shock with hypotension requiring vasopressor support, hypoxemia requiring mechanical ventilation, and renal dysfunction develop, with an elevated serum lactate level. What is the mortality rate for septic shock |
adhesion
can cause ileus, complication --> ischemicc infarct --> infarct -->peritonitis --> sepsis --> septic shock --> ARDS 50-90% mortality with septic shock |
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mech of peritoneal infection
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extension of bactera through wall of viscous
perforation of viscous ascending to pelvin via female genital tract |
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what are some predisposing conditions to infectious peritonitis
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Appendicitis
• Ruptured peptic ulcer • Cholecystitis, bile peritonitis, pancreatitis • Diverticulitis • Strangulation of bowel: hernia, volvulus • Acute salpingitis • Abdominal trauma • Peritoneal dialysis • Toxic megacolon; ischemia of bowel |
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whats spontaneous bacterial peritonitis
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peritonitis in the absence of an obvious source of infection
*bacteria extend through wall of intestine or are blood borne in ascites *occurs in children with nephrotic syndrome or liver cirrhosis caused by E coli or pneumococci |
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whats the clinical for peritoneal infection
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Fibrinopurulent exudate covers peritoneal
surfaces • Abscesses may form: subhepatic, omental sac • and /or subdiaphragmatic • Ileus symptoms: abdominal pain, distension • Board‐like rigidity of abdomen • Progression to septic shock • May be fatal |
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outcome of infections peritonitis
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death from sepsic shock
resolution, abcess fibrous adhesion |
