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235 Cards in this Set
- Front
- Back
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Layers of GI tract internal to external?
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Mucosa (epith/basal lamina, lam prop, muscularis muc)
Submucosa Musc Externa (inner long, outer circ) Serosa |
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Location in esophagus of squam cell carcinoma vs. adenocarcinoma?
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Squam cell = middle 1/3 (upper 2/3)
Adenocarcinoma = LOWER 1/3 (Barrett's change to goblet) |
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4 espoh contrictions?
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UES
aortic arch left primary bronchus espoh hiatus in diaph (T10) |
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What is ZENKER'S DIVERTICULUM?
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Point of weakness between thyropharyngeous and cricopharyngeous that allows buldge/diverticulum
MOSTLY ON L (CONVEX) "Killian's Triangle" |
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Would you litigate the inf thyroid artery distal or proximal to esoph branch during a thyroidectomy?
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DISTAL, maintains perfusion through espoh branch of inf thyroid artery
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What is Achalasia?
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Loss of neurons in myenteric plexus or dorsal PS/Vagal nerve so GI segement CONSTRICTED
"Bird's Beak" |
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Where do lymphatics drain for upper 2/3 esoph and lower 1/3?
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upper 2/3 = INTERNAL JUGULAR
lower 1/3 = CELIAC |
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What is the reason for pyloric antrum removal?
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to decrease G cells
less gastrin stim on parietal so less acid! less ulcer! |
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What is Zollinger-Ellison syndrome?
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a common triangle for GASTRIN prod TUMOR outside of stomach: mainly DOUDENUM and PANCREAS
common hep/cystic ducts jxn 2nd and 3rd part of duodenum jxn head and neck of pancreas |
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What arteriers are divided to increase strength of the LES?
If celiac occluded to stomach, what would be collateral flow? |
short gastric off splenic artery
SMA would provide INF PANCDUOD |
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What nerves would be cut in a highly selective vagotomy to reduce parietal cells/HCL in fundus and body?
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Nerves of Larajet (except ant) and CRIMINAL NERVE OF GRASSI)
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Why would gastric cancer likely cause obstructed pancreatic ducts?
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Cancer metast to pancreas by lymphatics or directly spread to pancreas
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What structurs increase SA of sm intestine, and by how much?
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plicae circ = 3x
intest villi = 10x MICROVILLI = 20X! |
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what are the frouf histological changes in celiac sprue?
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Disarrayed Enterocytes
Villus atrophy crypt hyperplasia inflamm of lamina propria |
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Primary site for duodenal ulcers and significance of ligament of TREITZ?
Also, what two arteries cause vasc compression on the duod? |
90% ulcers in post wall of superior/1st part (may affect liver/gall)
lig of Treitz attaches to duodjej flex, contains skel of diaph and smooth of duod, contract to facil move. ****for DX OF INCOMPLETE MALROTATION OF SM INTEST SMA and aorta |
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What is most common place for intussusception and significance?
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ILEOCOLIC, b/c proximal segment is smaller than distal
cancer is #1 cause of decreased motility and intusseption in adults |
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What are true and pseudo diverticula?
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True = congential, all layers
False = acquired, mucosa/sub SIGMOID COLON/DESC COLON (DISTAL AND LEFT ALMOST ALWAYS INVOLVED) points of weakness between tenia coli and where blood vessels penetrate wall |
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Where would colon cancer most likely lead to obstruction?
What part of lg intest likely to be ischemic? Where would you cut IMA to repair an AAA? |
LEFT bc smaller and viscous
SPLENIC FLEX (watershed btwn midd colic/SMA and left colic/IMA) "critical point of griffiths" cut IMA PROXIMAL to Arch of Riolan to can still supply lg intest |
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How do gallstones cause pancreatitis?
How does a pancr tumor cause ascites/jaundice? |
occludes amp, enz accum and digest (lipase) cause necr, edema, isch
tumor puts pressure on portal vein/bile duct = accum fluid and retain bile |
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Where to anorectal absesses originate?
What is most common fistula? |
infection of anal glands = perianal abscess (least likely = supralev)
INTERSPHINCTERIC (45%) |
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What cells are the culprit for fibrotic changes in a cirrotic liver?
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perisinusoidal cells (aka hepatic stellate and cells of ito) b/c decrease enz secr
*note arterioles are better gage of necr than acinus (only see necr at apical of hep lobule) |
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What is the triangle of CALOT?
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CYSTIC ART
CYSTIC DUCT COMMON HEP DUCT *used in surgery, must divide cystic art distal to the branch that supplies the liver if the branch supplies the liver (gall remove) |
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What is the GI tube mainly lined with?
What is CT/sm musc made of? Procto & Stomodeum? |
ENDODERM
mesoderm ectoderm |
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Divisions of foregut, midgut, hindgut, and vasc supply?
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fore = esoph-prox duod (CELIAC)
mid = distal duod - prox colon (SMA) hind = distal transv - sup anal (IMA) |
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When/how does the esophagus develop?
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4th week
tracheoespoh septum divides foregut into laryngtrach and esoph tubes epith (endoderm) becomes SSNK RECANAL AT END OF 8TH |
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Common malformations and associations of esophagus?
WHERE does esoph stenosis occur? |
Atresia = 83% also have fistula!!
(fail to recanal) MID TO DISTAL ESOPH STEN! -contain respir tiss -fibr hypertroph (my plex damage) -mucosal diaph bc no recanal |
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When/how does the stomach develop?
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dilation of caudal foregut, mid 4th week
dorsal grows faster than ventral so straight hand (thumb L twd you) LARP LEFT BECOMES ANTERIOR RIGHT BECOMES POSTERIOR (ventral/lesser moves right, dorsal/greater moves left) |
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Common malformation of stomach?
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Infantile hypertrophic pyloric stenosis
Projectile vomitting so do myotomy/NO |
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When/how does the duodenum develop?
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early 4th week to 6th
*distal to ampulla bile & cys ducts is divide for fore/midguts |
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Three stages of midgut rotation
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HERNIATION: C shaped vertical loop, rotates 90 counterclock
REDUCTION: horiz loop convolutes on CN end and moves back first to right side around 10th week, Cd end follows and ends up on left FIXATION: ADDITIONAL ROTATION OF 180 DEGREES COUNTERCLOCK total rotation = 270 |
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What is the most common cause of jejenal and ileal stenosis?
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VASCULAR ACCIDENT
not fail to recanal |
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What is double bubble sign?
Will vomit have bile? |
Duodenal obstruction (dilated proximal segment due to incomplete recanal, annular pancreas, gene mut) AND distended stomach
if distal to Ampulla of Vater, vomit will have bile *atresia always bile |
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Does the ascending colon form by descent of cecum?
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Probably not, because no room for cecum to return to the RUQ in the first place, just MOVES RIGHT INTO RLQ
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Malformations of the midgut?
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Omphalocele = intest don't return in 10th week, incomplete closure lat folds
Umbilical Hernia = intest return and herniate pre/post natal (un/covered) NonRotation = LEFT sided colon, asymptomatic Mixed Rotation/VOLVULUS = peritoneal bands cause duod obst, LADD's BANDS push duod on post wall (dbl bubble-DEAD bowel) "Corkscrew Sign" & "Whirlpool" Reversed Rotation = 270 clock, duodenum is ant to SMA, transverse is post to SMA Meckel's Diverticulum = TRUE, CONG, 40-50 cm from ILEALcecal jxn (sometimes fibrous cord, fistula, gastric tissue/HCL) |
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Development of the hindgut?
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Cloacal membrane (endo/cloaca and ecto/procto) partitioned by URORECTAL SEPTUM (fuse 7th wk)
-dorsal = rectum/cranial anal (rup 8th) -ventral = urogentical sinus |
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Components of the anal canal?
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-Upper 2/3 cranial anal = HINDGUT
IMA-superior rectal Autonomic Inf mesenteric nodes -Lower 1/3 anal = PROCTO/ECTO Int Iliac-Int pudendal-Inferior Rectal Inf Rectal N superficial inguinal nodes Pectinate line divedes endo/procto WHITE LINE OF HILTON = intersphincteric jxn (above line is SSNK, below line is SSK) |
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Malformation of hindgut?
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Congenital Megacolon (fail of myenteric plex, constriction bc agonglionic)
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Development of Liver/Biliary?
Malformation? |
Ventral outgrowth from caudal foregut @ 4th week
Hepatic Diverticulum = lg cranail forms liever, sm caudal forms gall/cystic ALAGILLE SYNDROME: low number of bile ducts in portal spaces --> Familial interhep Cholestasis (notch mut) = less bile and absorp of fat |
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Development of the Pancreas?
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endo cells of caudal foregut, form dorsal/LARGER and ventral buds
as duod rotates, ventral/sm post and dorsal front and FUSE(& ducts) MAIN DUCT = ventral bud & Distal Dorsal Accessory = PROXIMAL DORSAL |
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Malformations of the pancreas?
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Annular = bifid ventral, obstructs duod
pancreas divisum = 10% most common panc cong, ducts DON'T fuse *chronic pancreatitis bc most panc through SMALL DUCT on top, not vater/main |
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What are three functions of HCL in the stomach?
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1) kills microbes
2) denatures proteins for digestion 3) Activates PEPSINOGEN (zymogen/inactive precursor to PEPSIN) |
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What do submaxillary glands, serous foliate papillae, serious alveoli, and mucous alveoli produce in the mouth?
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submax = 90% saliva
serous foliate papilla = lingual lipase* serous alveoli = alpha amylase mucous alveoli = mucin (lube/imm) |
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Is pepsin essential?
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NO! people have gastric bypass
Also HDGC (mut in CDH1, cadherin) and have elective stomach removal |
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What does pancreas do?
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Makes ENZ! in zymogen form
-amylase -lipases -peptidases -also NaCl/NAHCO3 to neutralize PANCREATIC ALPHA AMYLASE IS SECRETED IN ACTIVE FORM! |
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Function of Liver/Gall?
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Make bile acids in liver and store in gall for digestion of lipids
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Digestion of Starch?
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a-amylase (ENDO ENZ) in mouth randomly breaks 1,4 bonds/nonterminal of amylose & apectin (NOT suc/lac) into diff sizes
Continues in INTESTINE (disach/oligo cleave into MONO from NON-REDUCING end by membrance bound glycosidases *sucrase/lactase/etc |
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Why can't humans digest cellulose?
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We don't have B1,4 ENDOglucosidases!
lactase can break other B1,4 if recognize galactose on end |
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Further digestion of oligo (sucrose/lactose) takes place where/with what?
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at luminal surface of SM INTEST
membrane bound GLYCOSIDASES |
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Which transporter works by secondary active transport?(maintained by Na+/K+ ATPase)
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GLUT 1
Na+ in/Glucose in syntranporter secondary transport Na out/ K in |
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Which transporters work by facilitated diffusion? AND WHERE DO THEY BRING CARBS?
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GLUT 5 = FRUCTOSE INTO CELL
GLUT 2 = GLUCOSE/GALACTOSE/FRUCTOSE INTO PORTAL VEIN (from cell) **Fanconi-Bickel*** |
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Lactose Intolerance?
lactose can break B1,4 if recognize galactose |
Asian/African, 1/2 world
can't break lactose into galac/gluc bact break down lactose in lg int gases prod osmol increase = D, dehydrate and H2 breath test* |
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What is Fanconi-Bickel Syndrome?
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mut in GLUT 2, AR
hepatorenal glycogen accum, renal tube dysfxn, impaired use gluc/galac Sxs: fever, vomit, growth fail, rickets (3-10mo) |
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What kind of enzyme is Pepsinogen? Where is it secreted?
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Endoprotease
Produced by chief cells (STOMACH) converted to active pepsin by acidic conditions and AUTO-ACTIVATION |
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What enzymes are secreted by the pancreas? Which one is exoprotease?
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Chymotrypsin, trypsinogen, procarboxypep (EXO), proelastase are all zymogens
TRYPSIN (active trypsinogen) IS A KEY TO ACTIVATION CASCADE!!! This enzyme activ most enzymes! *****enteropeptidase activates trpsin |
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What enzymes are secreted by the intestine? And what is the importance of the first?
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ENTEROPEPTIDASE (activates trysinogen to make trypsin)
also aminopeptidase (cleaves off single aa's from amino term of peptide) |
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What are the two most common causes of pancreatitis? *
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Gall stones lodge in ampulla of Vader
Alcohol abuse (abnorm sphincter oddi) (zymogens build up and are activated) |
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Clinical importance of Cystic Fibrosis?
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decrase NaHCO3 = thick pancr juice
Decrease panc ENZ in 80% "PANCREATIC INSUFFICIENCY" (and 10% develop pancreatitis) |
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Overlap in transporter selectivity can compensate for single non-fxnal mutations in tranporters. BUT WHAT DEFECT CAUSES CYSTINURIA?
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SLC3A1 (heavy 45%)
SLC7A9 (light 53%) tranporter defect that can no longer catalyze the re-uptake of aa in the KIDNEY -->cysteine is not water sol so failure to resorb leads to precip and STONES |
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What are the majority of dietary lipids and how are the majority of lipids digested?
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TAG's (90%) into free FA & glycerol
PANCREATIC LIPASE 1:1 w/ colipase (zymogen active by acid) to prevent denature by bile acids (also lingual and gastric lipases) Bile Acides disperse lipids into micelles for enz to digest bc they are not water sol, pancreas also secretes choles ester hydrolase and PhosphoL A2 |
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How are lipids absorbed?
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micelles approach UNSTIRRED WATER LAYER next to brush border membrance and are DIRECTLY absorbed (insde to ER to re-syth lip)
TAG's re-ester, pkg into CHYLOMIC contains apolipoprot B48 to stabiliz |
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Causes of steatorrhea?
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lipid malabsorption due to eating -indigestible fats (olestra)
-bile acid delivery prob to sm intest -low pancrease fxn -defect mucosal cells (bact/parasite) |
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Where are the following maily located?
Tcells, Bcells, macros? Lymphos & plasma cells? *2 sites Are mucosal or serum antibody responses shorter? |
GI lymphoid tissue
epith/lamina propria (spleen/nodes) MUCOSAL (mo-yr) vs (serum decades) |
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What is the difference between primary, secondary, and tertiary lymphoid sites?
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1 = make lymphos (bone m, thymus)
2 = reside (nodes, peyers, spleen) 3 = path elim/battle! (GI*, skin, lungs) |
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What is GALT?
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Gut Assoc Lymph Tissue
-Peyer's, appendix, lg intest aggreg, cells in lamina propria most have B cell follic and T cell areas w/APC's |
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What are "M cells" (microfold) and where are they found?
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in Peyer's Patch, transfer Ag from gut lumen to lymph tiss where APC's present to T cells, which activ B cells to make a GERMINAL CENTER so prolif B cells make Abs
**Peyers imp for Ab (IgA) and CTL responses ***Some PATHs bind M and use as ENTRY SITE (salm, yers, shig) |
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What are IEL mainly comprised of?
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T LYMPHOCYTES!! (1 IEL : 5 epith)
-alpha/beta: std, T help/CTL -gamma/delta: atypic, higher in dis *some IEL's are CD8 to kill viruses *cells in lam prop mainly CD4 |
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What path does a B cell take in an immune response of the GI tract?
What plays a major role in this? |
LONG PATH! stim B from peyer travels lymph capill to blood then back to lamina propria in GI
USES ADDRESSINS for "homing" |
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What is the significance of the POLY-IG RECEPTOR?
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(plasma cells produce) IgA in lam prop
binds POLY-Ig receptors tranported to mucosal side (bind bact, viruses, and toxins) **Receptor piece still connected is the SECRETORY PEICE that must be attached to RESIST PROTEASES same for CTL's but just bind, don't actually secrete IgA antibodies |
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What is the significance of IgA?
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Most abundant Ab in the body
*mucosal sites* -->2 monomers (dimeric) IgA1=cleaved by bact IgA2=NOT destroyed, want both IgA: opson (phago) & eosin degran (parasites) |
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How can you diagnose obstructive jaundice?
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High serum IgA!
back up blood, hepatic cells can't transport IgA into bile (can't excrete) |
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Why are gamma delta T cells rule breakers? Considered adaptive like the rest?
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They recognize ag-nonspecific entities (heat shock proteins, nucleotides, phospholipids) *****
They don't have to recognize MHC! INNATE not adaptive like normal |
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What can mast cells respond to?
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Food allergens!
bind mast lining the cut coated w/IgE (normally against parasites also) |
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What can be upregulated on intestinal epithelial cells with inflammatory cytokines such as IL8???
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ICAM 1 increased!! important for transport of cells across the muc epith
Increase immune response! |
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The role of high and low dose oral antigens on oral tolerance (unresponsiveness of immune)?
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HIGH dose: "clonal delection of T" lots of Ag will destroy T lymphos specific to recognizing it
LOW dose: "clonal anergy" viable but cant respond to Ag, PLUS reg T cells downreg immune |
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What is the most common immunodeficiency and why don't you typically have any problems?
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Selective IgA deficiency**
IgM can compensate!! greater risk for autoimmune dis if absorb macromolec that mimic self |
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How can food hypersensitivities lead to hypoalbuminemia and massive protein losing enteropathy?
(fatal anaphylactic rxns) |
IgE mediated hypersensitvity
vasoactive amines (hist) cause vasc permeability!! |
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What is mechanism of gluten-sensitive enteropathy? (Celiac Sprue)
What on IEL's is increased 10-15X? |
villous atrophy SM INTEST (malabsorp)
GLIADIN (gluten) not broken down to aa, so immune response to whole molecule GAMMA DELTA TCR INCREASED!! Must stay away from gluten for life or may increase GI lymphomas & carcinomas! |
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Major inflamm immune disorders?
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UC: superficial, lg intest, uclers, granuloCYTE inflamm cells (lots of neutrophils) need total colectomy!
CD: Ileum and asc colong, granolumatous lesions!, macros won't die by apop, TNF-alpha and INFLIXIMAB (if resect, will recur) |
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Pernicious Anemia is caused by autoimmune antibodies against?
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Intrinsic Factor & Parietal Cells
B12 can't be transported into blood, likely need suppl = magaloblast anemia + neuropathy |
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How can you tell Bacterial vs. Viral cause of Gastroenteritis?
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VIRAL = freq VOMIT early
BACT = FEVER, abd pain, blood and mucous in stool (absent vomit) *get stool culture* shig/salm HIGH WBC shig left shift |
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What is BOTULISM?
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Clost Botulium (an, +, spore, club)
TOXIN MED (activated by prot cleav) A degrades NT vess release protein = FLACID PARALYSIS (flop baby) and respiratory failure!!!! no fever bc no bact inflamm exotoxin resist dig till intest/high pH Tx: antitoxin (serum sick) and recover slow |
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What is Antibiotic Assoc PSUEDO MEMBRANOUS COLITIS?
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Clost Difficile (an, +, spore, rod)
#1 cause nocosom D, Abx (Clind) -2nd/3rd gen cephalosporins/Chemo Exotoxins A/B glycosylate a Gprot for actin fil polym = lose cytoskel and enterocytes plaques form, test toxin in stool, and give METRONIDAZOLE, fluids |
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What is SHIGELLOSIS?
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Shig dysenteriae ( --, rods, NON LACTOSE FERM, NO H2S, No motile)
SHIGA enterotoxin-A stops prot syn low inf dose-water & Bloody/Pus D invade mucosa, not bloodstream* S.dysten = SEVERE, travel D S. Sonnei = domestic D Tx: fluids and if severe, flouroquin (cipro) BUT tendon damage! DO NOT USE ANTI-PERISTAL!!! |
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What is SALMONELLOSIS?
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Salmon typhimyrium/enteritis/typhi
(--, non lactose ferm, H2S!, MOTILE) and invade bloodstream *Eneterocolitis: typhimurium & enteritis, invade lam prop (*tums lowers inf dose, also PPIs careful) *Septicemia: typhimurium & typhi *TYPHOID: typhi**, mult peyer and spread to GALL and spleen, bacteremia induced fever (LPS) ----->slower, ROSE SPOTS, nonbloody D, liver fxn! notify CDC NO TX (sxs), deathy in young/old Abx prolong shedding, if severe or risk septicemia use cipro or azith |
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What is E.coli gastroenteritis?
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E.coli (--, rod, LACTOSE FERM! norm)
Ag: O wall, H flag, K cap Traveler's D "Monetzuma" |
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ETEC? (EnteroToxigenic E.coli)
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Toxin (2) and Traveler's D
ADHERES to mucosa SM intest, nausea, vomit, cramp MASSIVE water D = DEHYDRATE |
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EIEC? (EnteroInvasive E.coli)
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INVADE mucosa
(blood pus, like shigella) Inflamm/Lg intest fever, cramps, blood/pus (dysentery) |
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EPEC? (EnterPathogenic E.coli)
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PEDS PATHOLOGY/dev countries
plasmid dep adhesions cause LOSS OF MICROVILLI at site attach (pedastal actin fibril under bact) |
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EHEC? (EnterHemmorrhagic E.coli)
*why can't you give Abx??? |
Hemolytic Uremic Syndrome (2-7%)
no penetrate but "shiga toxin SLT 1 & 2" cause HUS (lyse RBC, kid fail) Lg intest, Bloody D w/o pus, fever **Abx? NO! rapid lysis EHEC's = high release shigalike toxins = HUS |
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Characteristics of CHOLERA?
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Vibrio cholerae (--, rod, likes salt/pH)
Exo(cholera)TOXIN, heat killed A activ aden cyclase, high CAMP! this increases Cl- secr/H2O out Severe watery D "rice H2O stool" NO PMN's in stool! only activ secr Tx: fluid/electro only, no human fert! |
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What does CAMPYLOBACTER JEJUNI cause?
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#1 CAUSE D IN U.S.! fatal AIDS/old
(motile, --, MICROAEROPHILLIC)*** penetrate intest, inflam, dysent 1/2 POULTRY 90%, check stool self-limit, but severe(eryth/cipro(R*)) |
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Major cause of GASTRITIS?
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H.PYLORI (--, microaero, polar flag)
**UREASE enz create alk to survive in stomach and convert urea to ammonia *Dx: urea breath test (ingest - CO2) ***Tx: 2 ABx & PPI (tetra/clar,ompr) 20% infect (80% over 75yrs), families, low SES, and fecal oral |
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What are the three narrowings and three muscle types of the esophagus?
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Cricoid, bifurcation trachea, diaphragm
upper 1/3 STRIATED middle 1/3 MIX lower 1/3 SMOOTH (SSNK mucosa) |
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Most common esoph anamoly?
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ATRESIA: noncanal, incomplete
80-90% also w/FISTULAS! **regurg after feed, assoc w/other cong agenesis (no espoh) is very rare |
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Two types of Hiatal Hernias
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(stom into thoracic, aquired, asymp)
-SLIDING TYPE (90%): stomach above diaph, bell dilation in thorax -PARAESOPH TYPE: sep/side part up ALONG esoph, blood cut off |
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Three types of diverticula (from dysmotility and increased pressure)?
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-Zenker (PharyngEsoph): above UES
-Traction: middle esoph -Epinephric:above LES all accum food and can regurgitate |
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What is Plummer-Vinson Syndrome?
Name 4 characteristics |
MUCOSAL WEB (ledge protrude of mucosa into lumen)
*UP ESOPH, Iron def ANEMIA, ATROPHIC GLOTTIS, CHEILOSIS uncommon, postmenop women * |
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What are two types of esoph rings?
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circ, thicker than webs! dist esoph
(muc + sbmuc + hypertr musc prop) -A RING: above squamcolum jxn -SCHATZKI RING: @ sqcol jxn! (schantz meet in the midd w/rings) Both rings/webs show episodic dysphagia! |
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What can stenosis be caused by?
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"incomplete atresia" fibrous thicken
-Acquired after severe INJURY/SCAR: GERD, Radiation, Scleroderma, other caustic/chem injury PROGESSIVE DYSPHAGIA |
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Major features of ACHALASIA?
MOST COMMON CAUSE?* |
fxn obstruct, bird's beak
**incomplete relax LES & increased LES resting tone = Aperistalsis **SECONDARY CAUSE: CHAGAS (affects myenteric plexus) |
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What is M allory W eiss syndrome?
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Esoph lacerations/tears at gastroesoph jxn
VOMIT AGAINST PRESSURE *alcoholics, heal on own |
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Most important complication of esoph varices?
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RUPTURE (50% deaths adv cirrhosis)
increased press in esoph plex bc portal ven impeded and forms coll bypass *alcoholic cirrhosis) Dilated veins in SUBMUCOSA! |
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Four causes of Extrinsic Esophagitis?
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Ingest chemical
Infection (VIRAL HSV/CMV)** Trauma Iatrogenic (pill-Fe, radiation) |
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WHAT ARE THE THREE M's of HERPES ESOPHAGITIS???????
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MULTINUCLEATION more nuc #
MOLDING stick MARGINATION chromatin pushed to sides from nucleus increase |
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Two causes of intrinsic espohagitis and most common one (w/3 histol characteristics)?
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REFLUX more common-->Barrett
*increased inflam, eosin also *basal zone hyperplasia *up extend of lam prop in papillae Eosin esophagitis *ENTIRE ESOPH so bx mid/dist** (more eosin than reflux, tx steroids) |
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How much does risk of adenocarcinoma increase with Barrett's Esophagus?
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30x!!!!! (precursor is dysplasia)
-no polar, darker, strat, high glands replace squam w/gastric & intest STEM CELLS INDUCE RE-EPTHELIALIZATION bc high acid forms irreg jxn pink squam and white columnar DX: GOBLET where don't belong must survey/protocol! low grade = 1 yr (high grade 3mo) |
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Benign vs. Malignant Tumors?
What is sad about them? |
Benign: Leiomyoma (sm musc)
Malig: adenocarcinoma & squam cell DISPROPORTIONATE MORTALITY bc sxs develop too late (5yr = 9%) and easy for lymph spread |
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Who gets Squam Cell Carcinoma and why?
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AA males, over 45 yrs in underdev
Middle 1/3 esophagus!!! environ + lifestyle (alc/tobacco) -achalasia, plummer-vinson? hyperplasia, LG nuc/nests, keratin** |
|
|
Who gets Adenocarcinoma and why?
|
white males, western (50%) gerd <1/2
barretts w/dysplasia and accum mut*** (diet & h.py help) DISTAL 1/3, glands prod mucin and push nuc to side: SIGNET RING |
|
|
How does medicare control your diagnoses?
|
can get 80% from just Hx
ONLY GET 5 w/Medicare must justify tests (ABD PAIN) sed rate? cholecystits vs metastatic lipase elev longer, checks pancrtits K+ if anticipate surgery BUN/creatinine if anticipate imaging! |
|
|
What is an ERCP?
|
Endoscopic Retrograde Cholangio Pancreatography
case shows stone @ sphinct Odi, blocks biliary and pancreas = PANCREATITIS & CHOLECYSTITIS **if pancreatits = NPO!! don't wantC stim release of pancr enz |
|
|
What are the cells of the fundus, body, and antrum of stomach?
|
FUNDUS/BODY: Parietal (HCL) and Chief (pepsin)-->pinker, round
ANTRUM: Mucus* |
|
|
Who gets pyloric stenosis and why?
|
2-3 wk male infants, palp olive mass Hyperplasia of pyloric musc propria
-persistent PROJECTILE non-bile VOMIT |
|
|
Who gets Diaph Hernias and why?
|
IN UTERO, incomplete form of diaph!
abd visc into thoracic = PULMONARY HYPOPLASIA |
|
|
TWO causes of Chronic Gastritis?
|
A*Autoimmune: autoAb to parietal/IF
B*Environment: infect H.pylori****** also caffeine, alcohol Cx: ulcer, cancer (2-4%) Bx: chronic inflam (lymph/plasma) and NEUTROPH if ACTIVE** |
|
|
Causes of Acute Gastritis?
|
Not as Common! NSAIDS, alc, tob
acute inflamm = NEUTROPHILS -punctate hemorr, slough superfic epith, erythem and vasc edema LP |
|
|
Two types of acute gastric ulcer?
mult, discrete, shallow, <1cm brwn base and adj muc normal |
-CURLING: burns or trauma duod ulcer
-CUSHING: high cran pressure, stime vagal, hypersecr HCL *focal muc defect during STRESS -nsaids inhib COX, low PG = injure -hypoxia and splanchnic vasoC |
|
|
What percentage of DUOD ULCERS are CAUSED by H.PYLORI**?
|
85-100% DUOD! (65% gastric)
even though lives in STOMACH has tighter relationship w/DUOD ULCERS! role in chronic gastritis (antrum), PUD, gastric lymphoma, gastric adenocarcinoma |
|
|
Autoimmune Gastritis can lead to what?********
|
VIT B12 DEF! (pernic/meg anem) F
neurolog not helped w/B12 replace, dis assoc w/other AI problems (10% chron gastritis (2nd common) autoAB to par/IF = gland ATROPHY low acid stim Gcell gastrin release: hyperplasia and carcinoid tumors!! |
|
|
What type of gastropathy shows FOVEOLAR HYPERPLASIA (CORKSCREW)?
|
REACTIVE (CHEM)
-muc edema, vasc congest bile reflux (pyl bypass), NSAIDS |
|
|
What causes WATERMELON STOMACH?
|
GAVE (Gastric Antral Vasc Ectasia)
long stripes of eryth mucosa, alt less injured mucosa micro: sim to reactive BUT **dilated capill w/ fibrin thrombi** |
|
|
Define PUD?
|
Peptic Ulcer Dis (submuc/deeper)
duod*/men, worse pm (w/in 3hr eat) epigastric pain! hemorr in 1/4 -exposure to acid juices punched out, superfic fibrin, gran tiss, try to regen, scar at base |
|
|
Three progressive Cx of Chronic Gastritis?
|
1) Intest Metaplasia (AI H.pylori)
2) dysplasia: dark nuc, larger, but DO NOT MATURE at SURFACE :( 3) adenocarcinoma |
|
|
Two examples of Hypertrophic Gastropathies (giant cerebriform LG gastric RUGAL folds)?
|
1) MENETRIER DISEASE
(excessive secr TGF-a) -diffuse hyperpl surf fov-corkskrw -cystic dilation -antrum NOT affected -HYPOPROTeinemia - RISK adenoC 2) ZOLL-ELL SYNDROME: (gastrinoma, secr GASTRIN) -fundic gland hyperplasia** -5x increase par, thic muc***** -pancreas/sm bowel |
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|
What are two bezoars?
|
"bizarre" indigestible ingested
-phytobezoar: plant -TRICHOBEZOAR; HAIRBALL |
|
|
Benign, in between, and malignant gastric tumor examples?
DYSPLASIA IS FINAL COMM PATH for CARCINOMA* |
Benign: polyp
-hyperplastic: 3/4, fov gland, gross* -fundic gland: dilate gland -neoplastic/adenoma: dark 10%, prog C 2/5, dysplastic, chronic gast or FAP In Btwn: neuroendocrine, GI stromal Malig: 95% carcinoma, lymphoma high mortality incidence is decreasing chronic gast, h.py, diet pylrus/antrm (60%) less curv |
|
|
Intest type gastric carcinoma?
linitis plastica? diffuse type gastric carcinoma? |
-gland form column epith, metapl w/goblet cells (glands have lumen debris-mucin)
-diffuse expand thickness of stomach = leather bottle stomach! -signet ring in submuc! |
|
|
4 types of less common gastric tumors?
|
1) lipoma: benign fatty
2) lymphoma* most, extranodal marg zone B cell MALT! (h.pyl/infl) 3) neuroendocrine/carcinoid 4) GI Stromal Tumor (GIST) **Interst cells of CAHAL (CKIT MUT) cont activ tyrosine kin path, stop apoptosis so high prolif (tx w/tyr kin inhib) tumor spindle cell arrange |
|
|
What is the difference between omphalocele and gastroschisis?
Note what heterotopia is... |
Omphalocele is abdom muscular herniation (40% other cong defects)
Gastroschisis: muscle + ALL LAYERS OF ABD WALL involved, organs exposed to environ, no mem hetertopia is ectopic tissue->ulcers |
|
|
What are the five rules of two's for MECKEL'S DIVERTICULUM? (true)
(congenital) |
-2% pop
-2 yr olds symp -2x males -2 ft from ileocecal -2 types ectopic epith (gastric/pancr) *also complic = intuss, incarc, perf |
|
|
Common findings in HIRSCHPRUNG?
|
Males, 1:5000 births, assoc Down's
no pass mecon & distend neonate distal seg lack ganglion cells/narrow (prox = dilated = gang present!) RECTUM ALWAYS, fxn obstruct risk perforation! |
|
|
Most common site of mechanical obstruction? And four obstructs that make up 80% of cases?
|
SMALL BOWEL (bc narrow lumen)
-adhesions -hernias -volvulus (sigmoids, obstruct/infarct) -intussusception (tumor adults) |
|
|
Difference between mucosal and transmural infarts and the most common site for ischemic bowel disease?
|
-mucosal: only muc hypoperfusion
-transmural: acute obstruct major vess, more common *SB** less collateral supply! dep mesen supp (1-4perf) *SPLENIC FLEXURE common bc watershed SMA/IMA |
|
|
How will patient present if have total infartion of isch bowel disease? Incomplete infarction?
|
Total: SHOCK, mortality >50%, severe pain w/blood D and melena, bloat
Incomplete: NONSPEC abd complain Chronic Isch: inflam muc, fib, patch (can be segmental bc art supply!) |
|
|
What is considered isch injury to the colon and sm bowel, typically in premature infants?
|
NEC (Necrotizing EnteroColitis)
-immature gut, intiate feed get edema, hemorr, and necrosis -may require massive bowel resection |
|
|
What is characteristic finding of MALABSORPTION SYNDROMES?
|
STEATORRHEA
sxs: D, gas, abd pain, wt loss, vit def!! -caused by celiac, panc insuff, CD |
|
|
What are the HLA 2 classes for CELIAC DISEASE?
What AB do B cells produce? Most sensitive and most specific? |
DQ2, DQ8
Anti-gliadin anti-endomysium **specific anti-tTG ***sensitive (to test serum bc ab to glut/gliad) *Remember T cells, high lymphos! |
|
|
What is most important characteristic finding in CELIAC?
|
INTRAEPITH LYMPHOCYTES!! (IEL)
-villous blunt, crypt hyperplasia -N.euro, AI -silent (pos blood/atroph, no sxs) -latent (pos blood, NO atroph/sxs) |
|
|
Associated findings, tx, and cx of celiac?
|
-dermatitis herpetiformis blister 10%, lympho gastritis, lympho col
-tx: gluten free diet -cx: IRON/VIT DEF, LYMPHOMA! |
|
|
four main categories of D? And two that persist w/fasting?
(dystentery! pain, blood, sm vol D) |
-Secretory: STAY FAST, secr ions or isotonic stool
-Osmotic: lactose intol, unabsorb luminal soluts -Malabsorptive: nut decrease absorp, steatorrhea -Exudative: STAY FAST, due to inflam, see pus blood |
|
|
Which causative agent of bacterial enterocolitis has a specific finding?
|
YERSINIA: necr GRANULOMAS ilieum peyer's appendix, colong mes nodes, and SYSTEMIC SPREAD
*also salm/typhoid, shig, camp |
|
|
Defining features of Abx=assoc colitis?
|
-D after Abx
-patchy green PSEUDOMEMB -fibrin, PMN's, mucin -C.diff in stool (overgrow) **Volcano explode (mucin) crypts** |
|
|
What is whipple disease caused by? What finding is generally absent?
*hint = abx help |
Tropheryma whippelii, +, actinomycete (white females, 30s)
-sm intest muc have distend/foamy MACROPHAGES in LP and rod bac -INFLAMM IS ABSENT! |
|
|
What should you know about inflam bowel disease?
|
-inapprop muc immune activ, 20 yr old white females
-UC: colon/RECTUM, muc/sub only, crypts branched -CD: any area, transmural, GRANUL* |
|
|
Which IBD is continuous, mucosal, involves rectum, and may have ulcers and pseudopolyps?
|
UC! gross specimen
|
|
|
Which IBD is patchy, shows cobblestone mucosa, involves the term ilieus and anus, and may have FISTULAS, fat wrapping, and thick, fibrotic, stenotic bowel wall?
|
CD! gross specimen
*may have bearclaw ulcer (linear fibr) |
|
|
Which IBD will show lymphoid aggregates*, scar,**transmural inflam, and non-necr granulomas on histol?
|
CD
*both CD/UC show crypt abscesses |
|
|
Which IBD has higher risk for malignancy, especially after 10 years? Also toxic megacolon?
Which has higher recurrance after surgery |
UC! UC
CD! |
|
|
What is microscopic colitis?
2 types? |
infalmm only seen microscopically, but chronic, nonbloody, watery D
-Lymphocytic: HIGH IEL's, norm subepith coll layer, assoc celiac/AI -Collagenous: DENSE coll layer, middle aged female, high IEL, mixed inflam in LP |
|
|
What is the difference btwn diverticulosis and diverticulitis?
|
-osis: lots of diverticula
-itis: +1 divertic become inflam/pain! ACQUIRED, 50% over 60, W diet due to focal wkness in bowel wall Mucosa through musc propria *pseudo = no musc involvement |
|
|
What are harmartomatous polyps?
|
tumor like growths of mature, NOMRAL tissues
sporadic of part of syndrome |
|
|
Describe Juvenile polyps?
|
focal malform 5 YRS, rectal bleed and mostly COLON (colectomy if hemr)
-pulm avm and HIGH RISK COLON ADENOCA (dysplagia) -round 1-3 cm, smth, pedun(stalk), cystic spaces w/debris, LP inflam |
|
|
What mutation causes Peutz-Jeghers Syndrome and what are the clincial findings?
-why so scary? |
LKB1/STK11 (lose tumor supp mut)
AD, mucocut pigment of buccal INCREASE RISK OF C ALL KINDS!!! -most common sm intest -ABORIZING sm muscle -GI cancers arise away from polyps - |
|
|
What mutation causes Cowden syndrome?
-three characteristics? -strange thing about cancer risk? |
PTEN (loss fxn in tumor supp)
-Macrocephaly, GI harm polyps, benign skin tumors -INCREASE C RISK BREAST, FOLLIC THYROID, ENDOMET (NOT GI!!!) |
|
|
Difference between Bannayan-Ruvalcaba-Riley Syncrome and Cowden?
|
BRR ONLY: MENTAL/DEV DEFICIENCY, AND lower neoplasia
(both harm polyp, lipomas, macroceph, hemangiomas, pig mac penis) |
|
|
What syndrome is NONhereditary, nonspecific, non-polyploid mucosa, but has harm polyps similar to juv?
|
Cronkhite-Cananda Syndrome
*nail atrophy, split hair (50% fatal) -round dil cystic w/inflam |
|
|
Where are hyperplastic polyps most common?
|
L colon, SERRATED (branch crypt)
starfish shaped just decreased turnover = pile up of non malignat (distinguish from SSA) >50% after 60yrs |
|
|
Most common neoplastic polyp and precursor to coloretal cancer?
%pop? |
ADENOMAS 50% by 50 yrs (Wdiet)
most in colon, low grad dysplasia** *colonoscopy! most silent (low protein, K+ bc villi can secr) |
|
|
distinguish btwn villous and tubulovillous adenomas?
|
villour larger (up to 10cm colon muc) and finger like project
tubvil = intermed, mix tub/vill |
|
|
Why doesn't intramucosal carcinoma have malig potential?
-best correl w/risk malig? |
bc you don't have vessels until submucosa! so no spread (invasive = beyond musc mucosae)
-POLYP SIZE! high grade dysplasia |
|
|
Which adenocarcinoma (malig potential) has crypt dilation and lateral growth, but no low grade dysplasia?
|
SESSILE SERRATED ADENOMA
-serrated through full length of glands ***distinguish from hyperplastic poylp |
|
|
Mut/characteristics of FAP?
Two types? |
AD mut in APC gene, risk adenoma 100% in 30 years, poor teens, prophylactic colectomy
-Gardner Syndrome: osteomas, epiderm cysts, tumors, dental -Turcot Syndrome: CNS TUMORS 2/3 have APC mut, medulloblast 1/3 have other, glioblastoma |
|
|
What should you remember for APC/B-catenin pathway for FAP, 80% sporadic CRC)?
|
Adenoma --> Carcinoma
LOSS 1 APC** (tum supp), lose #2 Accum mutations! proto-onco mut = KRAS!!*** lost more tum sup = P53*** |
|
|
Gene mut and characteristics for HNPCC/Lynch?
-microsatellite intab path? |
MLH1, MLH2 (mismatch repair)
error accum -OLDER than FAP (45-50), but younger than sporadic colon C -defect MMR: MLH1/2 & BRAF*** can test w/immunocytoche, if brown gene IS being expressed |
|
|
Etiology of bowel tumors: sm vs lg intest?
|
sm: 75% length but rare tumors
lg: most common malig GI and 2nd cause cancer deaths behind lung! mostly affect males, dev, W diet -cecum, trans, des, rect/sig |
|
|
Where are you likely to see polypoid, exophytic mass?
Where would you see annular napkin ring "apple core" constricts? PROGNOSIS COLORECTAL ADENOCARCINOMA?********* |
-prox colon
-distal colon Px: depth of invasion and LN metast most tall colum, some mucin/signet |
|
|
What characterizes a tumor with more pink/gran cytoplasm, SALT/PEPPER NUCLEI that aren't as dark, and monotonous uniform cells?
|
CARCINOID/NEUROENDOCRINE
-produce bioactive prod (zoll-ellison) -good survival 90% if not hep spread -yllw tan submuc masses (sm bowel, stomach or colon are aggressive -not rectum!) |
|
|
Most common site for GI LYPHOMA?
Describe Celiac Sprue-assocc lymphoma? |
-STOMACH! 60%
********younger (30s), T cell lymphoma, poor prognosis :( |
|
|
Cells and mut of GI Stromal Tumors?
|
-Interstitial cells of CAJAL
-CD117 (c-kit pos) mut *malig depends on location(sm/lg intest), size, mit activ |
|
|
Where would a basaloid carcinoma occur in the anal canal?
Where would a sqam cell carcinoma occur? |
--Basaloid = transitional middle 1/3
-Sqam cell = lower 1/3 *HPV, warts |
|
|
How does one get melanosis coli?
|
Chronic laxative use
accum macros in LP w/pigment see on colonoscopy |
|
|
Two major causes of Hemorrhoids?
|
due to elev ven press from
-Constipation (strain) -Pregnancy (venous stasis) external must be below anorect line 5% pop |
|
|
What do you find w/acute appendicitis?
|
brown/yllw discolor
necr, thick walls LOTS OF NEUTROPHILS! |
|
|
What is the Rome 3 criteria for IBS diagnosis? (10-20% ppl)
|
recurrent abd pain/discomfort at least 3 days/month during last 3 months...
+ 2 assoc sxs (change freq, form, passage, mucus, bloat, distention) |
|
|
What are the four bowel patterns of IBS? What percentage of patients change subtypes/in 1 yr? Switch to?
|
-IBS D
-IBS C -IBS mixed same day -IBS alt D & C diff days *75% change (1/3 from C --> D) |
|
|
What age does IBS affect? What might you think if they are not this age?
|
-YOUNGER, before 35 yrs
-if older, flag up for inflam, cancer |
|
|
What are ALARM SXS (that you should NOT HAVE) w/IBS?
To prove there is no organic disease before dx a pt w/IBS.... |
-no major wt loss
-no blood! in stool -no fat -no nocturnal D or pain -no gluten/lactose intol -no fever, sweat, chills (inflam) *ask change/duration bowels, onset or stressors in life, and age! |
|
|
11 differential diagnoses for IBS! Must rule out...
|
IBD, Celiac, GERD, PUD, Adhesions, Endometriosis, sm bowel Cancer, mesenteric Ischemia, bact overgrowth, pancreatitis, bact induced colitis/enter
|
|
|
What are common SXS assoc with IBS?
|
postprandial urgency
diffuse pain w/o radiate (LLQ) abdom distention* lower thresh? alternating habits eating = worse, pooping = better |
|
|
Interesting findings on PMH, PSH, SOC, FAM?
|
-fibromyalgia, depress, endomet
-surgeries/adhesions -celiac (10%), IBD, colonC *do pelvic and rectal exam! |
|
|
Treatment plan for IBS
|
-placebo 50%, but can give anti-spasmodics, anti-depress, and fiber/cathartics for constipation
-RIFAXIMIM (tx for IBS w/o contipation) for sm/lg intest flora suppression, not absorbed system (so alt gut flora --> IBS????) |
|
|
Two examples to treat D in IBS? efficacy of probiotics? what else (simple) might help?
|
-loperamide, serotonin antag (alestron)
-probiotics help 50/50 -REASSURE pts, don't ignore new |
|
|
Four summary points from IBS lecture?
|
-Key to dx IBS = Hx and PE!
-IBS Dx = NO ALARM SXS -diagnostic studies often unhelpful -Tx? 50% placebo and improve SXS |
|
|
What do underdeveloped countries with high incidence of intestinal parasites have lower prevalence of IBD:UC/CD?
|
indiv exposed to pathogenic environments more likely to immune tolerance (less change IBD)
*INCIDENCE has increased in U.S. from 1/100,000 to 8/100,000 (plat) |
|
|
What two age groups are most affected by IBD?
|
-15-35 years
-second peak in 50s females slightly more (smoke CD assoc but helps UC!) (breast C/OCP UC) |
|
|
What are the four etiologic hypotheses of IBD?????
|
**all involve microbes (alt muc gut)
-Persist Infect (mycobact, H.pyl) -Dysbiosis (less protective bact) -Defective muc integrity (alt mucus, more perm, cell starv, impair restit) -Dysreg Immune: loss toler, agg cell activ, defective apop |
|
|
3 pathogenesis theories of IBD and examples of each?
|
1) Genetic Influence: familial occur, 40 UC gene suscept and 70 in crohns
-NOD 2 def in CROHNS 2) Environmental Triggers: abx/diet alter flora & infect, NSAIDS, stress, smoke alter muc barrier 3) Luminal Antigens |
|
|
What is the role of bacteria in IBD?
What T cell pathway is involved w/dev of IBD? |
Won't have immune activation w/o bacteria! (stim TH1, macro and others)
TH17! --> through IL 23 and IL 17 |
|
|
What has been the most important blocking antibody drug to treat inflammatory IBD cascade?
|
INFLIXIMAB! most prominent TNF-alpha antagonist!
(also can target IL 12, 23, TGF-B, and intercell adhesion molecules) |
|
|
Which IBD syndrome will you see "granular" fine sandpaper like texture and obscured vasc pattern?
|
UC
* most freqent manifestation of dis = Rectal Bleeding!!!! *Collar Button Ulcers ALSO * Toxic colitis is rare complication, but also UC |
|
|
Again, distinguish CROHN's from UC?
|
ileum/colon, rectum spared, bleed less, perianal dis, segmental, fistulae, granulomas, asym involve, presents like acute appendicitis (RLQ), obstruct cramp/distend, STRING SIGN!!!
*apthae punched out ulcers, canker sore of intest *do serol tests *if CD/UC for 7+ yrs, screen and biopsy for dysplasia every year |
|
|
EXTRAINTESTINAL MANIFESTATIONS OF IBD?! (6)
And half pop has..? |
-Arthritis
-Episcleritis, uveitis -Apthous stomatitis -Erytherma nodosum = CD** -Pyoderma gangrenosum = UC** -vasc complications *OSTEOPENIA |
|
|
What is one of the dreaded complication of IBD?
|
Sclerosing Cholangitits = UC
risk for cholangio carcinoma, only cure is LIVER TRANSPLANT |
|
|
What are the four goals of IBD therapy?
|
1: induce clinical remission (corticosteroids)
2: MAINTAIN remission (avoid long steroid tx) 3: enhance qual of life 4: avoid long-term toxicity |
|
|
Tx for IBD is like a pyramid, start w/least toxic and move up. What are the different categories?
|
1) supportive (anti D, bile seq, bulk, antidep, pain manage, anti-spas)
2) AMINOSALICYLATES**: Mod sulfasalazine, mesasalamine (proc) ABX** :metron, quinol 3) CORTICOSTEROIDS: severe prednisone, budesone, ACTH 4) IMMUNOMODULATORS: fail! **6MP, **azathiprine, methotrexate, cyclosporine*ill and no surgery!, anti-TNF (infliximab) |
|
|
Remission induction vs maintenance for UC?
|
Induction: aminosalic, cortico, 6mp/azath, cyclosporine
Maintain: aminosalic, 6mp/azath |
|
|
Remission induction vs. maintenance for CD?
|
Induction: aminosalic, ABX cortico, IMMUNE MOD, DIET
Maintain: IMM MOD aminosalic, ABX |
|
|
Importance of sulfasalazine in IBD?
|
sulfapyridine linked to 5ASA
intest bact cleave di azo bond and release 5ASA discovered in pt w/RA, tx D and blood also ***can't take if sulfa allergy!!! |
|
|
Use of oral aminosalicylate in IBD tx? (Delivery methods)
|
different deliveries: pH dep, time release, bact cleavage
TX MILD TO MOD CASES IBD |
|
|
Sulfa and 5ASA toxcities?
|
Sulfa: male infert, hemolytic anemia, agranulocytosis
*>> ASA: rash, fever, HA, etc ASA: nephritis BOTH: alveolitis, pancreatitis |
|
|
Antibiotics such as metronidazole tx mainly what disease in IBD?
|
CROHNS
-perineal -post op CD dis prevention -Pouchitis* adverse: nausea, metallic furry taste, candidiasis, periph neuropathy is dose dep |
|
|
Difference in steroids to treat IBD?
|
-Budesonide: rapid metab 90% first pass, less systemic absorb
-Prednisone poorly absorbed oral UC or CD mod/severe -Hydrocortisone partial absorb** affect hypoth-pit axis if cont use parenteral: sever UC or CD |
|
|
Highest morbidity and mortality assoc with tx for CD/UC?
|
STEROIDS and narcotics!
-osteopor, myopathy -hyperglyc, depress, anxiety -cataract, glaucoma, growth fail -increased infect |
|
|
Azathioprine and 6MP and adverse effects
|
-aza prodrug converted to 6mp
anti metab stop nuc acid synth WBC **pancreatitis, fever, rash, hep, opp infects, bone marr suppress, min risk lymphoma NOT LIKE STEROID if no improve: methotrexate = CD |
|
|
Infliximab is indicated in what conditions?
WHY SO IMPORTANT FOR MAINTENANCE? |
CHIMERIC MONOCLON AB to TNF alpha (3/4 hum, 1/4 mice)
**Only way to tx long w/o steroids 40% of time close fistulas :) :) ;) used to tx: peds crohns, CD, ankylosing spondylitis, UC |
|
|
What is new surgical technique for UC that saves the anal sphincter?
|
IPAA = ileal pouch anal anastomosis
(vs brooke ileostomy w/fecal incont) -->half will dev pouchitis, 5% bag *30% UC will have surgey <10 yrs |
|
|
Prevalence of surgery in CD and recurrence?
|
80% will require an operation
w/in a year 3/4 will have visible lesions |
|
|
Surgical and Medical tx for CD perineal CX?
|
surgical: incision/drain, fistotomy, setons, divert ostomy flaps
medical: abx, anti-tnf, 6mp/aza, methotrex, cycosporine |
|
|
PUD, who gets it?
|
10% chance in lifetime, male 2:1 but becoming equal bc female smoke rate and use of NSAIDS
avg age: 70 years |
|
|
What are 3 stimulants of gastric secr?
Inhibitor? |
Histamine (mast in LP), Gastrin (fundus/antrum and duod), and ACH (near par by vagal stim)
SOMATOSTATIN released from antral D cells |
|
|
What are the 3 main phases of digestion?
|
Cephalic: vagal/ach, thought/senses
Gastric: food in stomach and distention causes GASTRIN rel Intestinal: SOMATOSTATIN rel to stop acid secr when food in duod |
|
|
What are the 2 DIRECT causes of PUD?
What are the assoc risk factors? |
H.PYLORI & NSAIDS
smoke, stress, alcohol, famhx, steroids chronic, trauma, zoll-ell |
|
|
Is H.pylori more likely to cause duodenal ulcers or gastric ulcers?
|
90% duodenal! (75% gastric)
breaks down urea to ammonia/HCO3 -NH4 attracks inflam -HCO3 allows growth in acidic area (3x damage = inj/inflam/gastrin rel) **bug can infect other sites but must be GASTRIC TISS (barrets) |
|
|
How does H.pylori increase gastrin levels in the stomach?
|
by decreasing the amount of D cells in the antrum! Less inhib (somatostatin on parietal) = MORE ACID!
|
|
|
High risk of ulcer and NSAIDS (#2 cause PUD) depends on what?
|
DOSE AND STRENGTH OF DRUG
**usually affects STOMACH **Just LOCAL ulcer (not diffuse infl) *tend to have MI/CVA pts with ulcers bc taking aspirin every day Bleeding/perforation more common |
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Most common site for GASTRIC ulcers?
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INCISURA ANGULARIS (60%)
TYPE 1 -not assoc w/increased acid secxr -alc, smoke, steroids, infect |
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Will you have an increase in acid secretion with a duodenal ulcer?
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NO! 70% normal
Just imbalance of protective, and acid don't use acid level to DX ulcers! |
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Will eating make gastric ulcers better or worse?
Will eating make duodenal uclers better or worse? |
-WORSE! more acid in stomach
-BETTER! HCO3 secr in duodenum |
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What is the gold standard for diagnosing duodenal or gastric PUD?
Method of choice to document H.pylori eradication? Eradication method? |
ENDOSCOPIC GASTRO-DUODENOSCOPY (EGD) invasive?
-try antacids, H2 antag, PPIs UREA BREATH TEST after TWO ABXS and ONE PPI ***never H2 blockers!!******* |
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How often does PUD need surgery?
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8-20%
if perforated/Cx, prevent recurrence, rule out malignancy (Reed: perf, bleed, obstruct) Also do surgery for manage/cure: truncal, parietal, vagotomy, antrect |
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What is the most common symptomatic, malig, neuroendocrine tumor of the pancreas? What is the clinical trial associated?
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ZOLLINGER-ELLISON
1) Gastric acid hypersecr********* 2) PUD 3) Non-beta islet cell of pancreas 1/4 assoc MEN(mult endoc neo) |
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What are the borders of Passaro's Triangle? (Common site of gastrinomas and zoll-ell)********
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1) common/cystic duct jxn
2) 2nd/3rd duoc 3) neck/body pancreas zoll-ell = PUD and high gastrin |
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Zoll-Ell dx and tx?
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dx: somatostatin rec scintigraphy, CT
tx: gastrectomy, PPI, resect, RFA px: good (80% survival if no metast) 40% if metast WORST: lg tumor outside passaro with liver metast |
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What layer of the colon is perforated by nutrient arteries and creates a weakness in the wall?
main cause of diverticula? |
MUSCULARIS LAYER
hard stools from low fiber diets (and trying to push too hard to move it makes muscularis hypertrophy) |
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Diverticula can occur anywhere along the colon, but what is the most common place?
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SIGMOID COLON (narrowest lumen and stool has least amount of water)
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What is the most common cause of a painless lower GI bleed?
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*Diverticular bleed*
nurtirent artery can stretch and erode >60 yrs, mostly self-limited |
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How can you DX and TX (if won't go away) diverticula?
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Dx: BRBPR rectum, SOB, Tachy, dizzy/syncope, mental change (typically no abd pain) MUST rule out UPPER GI/fast bleed w/scope
Tx: IVF/Blood (don't drop Hmglob below 7, transfuse w/packed RBC) **Surgery if >6units PRBC in 24 hr ---->colon resection, high fiber |
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If patient presents with LLQ PAIN, FEVER-Lshift, tachy/normal BP, what would you expect?
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Inflam and perforation of diverticulum:
fecalith obstructs diverticulum, get bact growth, microperf, and abscess in abd cavity (case 2 by sigmoid) *No correl w/nuts, seeds, popcorn |
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How to confirm diverticulitis and what should you avoid?
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-H&P!, abdom xray r/o free air, CBC
*CT (RADIOLOGY) best=confirm dx **NO enemas/colonscopies in acute setting bc may force more bact out! |
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How would you treat uncomplicated diverticulitis?
Why do you need to do a colonoscopy in 4-6 weeks? |
no abscess so outpt, ABX, LOW FIBER* (rest), IV ABX if pain/inflam
-30% chance of recurrence -colonoscopy in 4-6 weeks r/o C (present in same way) |
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How would you treat complicted diverticulitis (abscess or inflamm)?
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admit, IV ABX, Bowel rest, IV fluids
-through skin abscess drain -peritonitis: ER or HARTMANS |
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What is Hartman's procedure? Why can't you just sew the colon together?
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Take out sigmoid and bring desc colon to colostomy.
If tried to sew rectum and desc, inflam may cause sutures to fall apart = feces in peritoneal cav |
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Complications of diverticulitis?
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FISTULAS: most common colon to bladder, but do cytoscopy to r/o bladder C (where bladd erodes colon)
OBSTRUCTION: from musc hyper, scar from recurr (rest bowel/NPO) |
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What is recurrence of diverticulitis?
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1/3 will have 2nd time-->1/3 those 3rd
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When would you do an elective resection (sigmoidectomy) for diverticulitis? Who is offered?
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Elective = NO INFLAM (ER there is)
-chronic? abx to decrease inflam Offered after 2nd complicated (traditionally 1st), or 4th uncomplicated case Do LOW fiber diet for few weeks so stool is liquid/low P, then switch to HIGH fiber to prevent divertic again |
