Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
164 Cards in this Set
- Front
- Back
|
retroperitoneal strucutres (10)
|
duodenum (2nd-4th), pancreas (except tail), kidney, ureters, adrenals, rectum, IVC, aorta, ascending colon, descending colon
|
|
|
veins involved in esophageal varices
|
L gastric (P) and esophageal (S)
|
|
|
veins involved in caput medusae
|
paraumbilical (P) and superficial and inferior epigastric veins (S)
|
|
|
veins invlved in internal hemmoroids
|
superior rectal (P) and inferior and middle rectal veins (S)
|
|
|
order in femoral triangle
|
L to M: nerve, artery, vein, empty, lymph (NAVEL)
|
|
|
artery around which hernias are either L or M
|
inferior epigastric artery
|
|
|
Brunners glands
|
only GI glands in the submucosa, located in duodenum, secrete alkaline mucus to neurtralize the acidic contents from the stomach
|
|
|
type of histamine and muscarinic receptors located on parietal cells
|
M3 and H2
|
|
|
receptor which takes up glucose and galactose into enterocytes
|
SGLT1 (Na dependent)
|
|
|
how is bilirubin made water soluble
|
its glucuronidated (conjugated) via glucuronyl transferase
|
|
|
main micro findings in Celiac
|
blunting of villi and inflammation in lamina propia, primarily in the duoden and jejun
|
|
|
incr risk of MALT lymph is associated with which dz
|
type B (H. pylori) chronic gastritis
|
|
|
Sister Mary Joseph sign
|
stomach CA mets to the umbilicus
|
|
|
congenital hypertrophy of the pigmented epithelium is associated with what
|
FAP familial adenomatous polyposis
|
|
|
what are mallory bodies composed of
|
obiquinated keratin
|
|
|
what two molecules do HCC's sometimes make
|
EPO and insulin like protein
|
|
|
Bronze diabetes
|
refers to hemochromotosis, leads to cirrhosis of the liverr, DM, and skin pigmentation
|
|
|
primary sclerosing cholangitis
|
intra and extrahepatic fibrosis of bile ducts, ERCP shows beading, "onion skin fibrosis", assoc with UC
|
|
|
primary biliary cirrhosis
|
granulomatous destruction of intrahepatic bile ducts, pruritis is usually the first and most common sign, assoc with scleroderma and CREST
|
|
|
cholangitis
|
inflammation of the ducts
|
|
|
cholecystitis
|
inflammation of the gallbladder
|
|
|
+ Murphrey's sign
|
inspitory arrest on deep palpation
|
|
|
causes of acute pancreatitis
|
gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion sting, hyperCa/lipid, drugs; kids is seatbelt trauma
|
|
|
migratory thrombophlebitis is associated with what
|
pancreatic CA, redness and tenderness on palpation
|
|
|
Courvoisier's sign
|
obstructive jaundice with palpable gallbladder, seen in pancreatic CA
|
|
|
abdominal layers from outside in (9)
|
skin, campers fascia (fat), scarpas fascia (fibrous), external oblique, internal oblique, transversus abdominus, transversalis fascia, extraperitoneal tissue, peritoneum
|
|
|
falciform ligament
|
connects liver to ant abd wall; contains ligamentum teres
|
|
|
hepatoduodenal ligament
|
part of lesser omentum, connects greater and lesser sacs, contains the portal triad structures (hepatic artery, portal vein, common bile duct)
|
|
|
gastrohepatic ligament
|
contains gastric arteries; seoarates the R greater and lesser sacs, can be cut in surgery to access the lesser sac (ex: pancreas)
|
|
|
gastrocolic ligament
|
contains the gastroepiploic arteries, part of greater omentum
|
|
|
gastrosplenic ligament
|
contains the short gastrics, separates the L greater and lesser sacs
|
|
|
splenorenal ligament
|
connects the spleen to the posterior abd wall, contains splenic arteries and veins
|
|
|
location of the Myenteric and submucisal plexi
|
submucosal (Meisners) in the submucosa, Myenteric (Auerbachs) is located in the muscularis externa inbetween the inner and outer layers of SM
|
|
|
functions of the myenteric and submucosal plexi
|
myenteric: coordinates motility, submucosal: regulates local secretions, blood flow and absorption
|
|
|
plica cicularis vs. villi
|
plica: in SI, projections of mucosa and submucosa; vill: SI, only epithelium and lamina propia of the mucosa
|
|
|
vertebral levels at which the the celiac artery, renal artery, SMA and IMA (for this one, include adj structure) come off of the aorta
|
celiac: T12; SMA: L1; renal: L2; IMA: L3 (just inferior to where the 3rd part of the duodenum crosses the midline)
|
|
|
PNS innervation to fore, mid and hindgut structures
|
forgut and midgut: vagus; hindgut: pelvics
|
|
|
most common cause of SI infarct
|
occlusion of SMA
|
|
|
structures supplied by celiac artery
|
stomach to prox duodenum, liver, gallbladder, pancreas
|
|
|
structures supplied by the SMA
|
distal duodenum, rest of SI, cecum, ascending colon, 2/3 transverse
|
|
|
structures supplied by IMA
|
distal 1/3 of transverse colon, descending colon, sigmoid colon, upper rectum
|
|
|
what part of the GI is affected if the splenic artery is blocked
|
the upper part of the greater curvature of the stomach, this is because the short gastrics have poor anastomoses
|
|
|
where would you place a stent to relieve portal HTN
|
between the splenic and left renal vein
|
|
|
what occurs above the pectinate line and what is the blood supply and drainage
|
internal hemorrhoids (not painful because they are viscerally innervated), adenocarcinoma; arterial supply from superior rectal (branch of IMA), venous is to sup rectal vein to IMV to portal system
|
|
|
what occurs below the pectinate line and what is the blood supply and drainage
|
external hemorrhoids (painfun, innervated by inferior rectal, branch of pudendal), SCC; arterial from inferior rectal (branch of pudendal); drainage to inf rectal vein to internal pudenal vein to internal iliac to IVC
|
|
|
what part of the liver contains the P450 system
|
zone III, near central vein
|
|
|
which area of the liver is most sensitive to toxic injury
|
zone III, near central vein
|
|
|
which area of the liver is most sensitive to alcoholic hep
|
zone III, around central vein
|
|
|
which area of the liver is most sensitive to viral hep
|
zone 1, around portal tract
|
|
|
which sides of the hepatocytes face the bile cannaliculi and which the sinusoids
|
apical faces cannaliculi, basolateral faces sinusoids
|
|
|
femoral sheath
|
formed few cm below inguinal ligament, contains fem A and V and lymph, but NOT the nerve
|
|
|
horizontal position of medial vs. median umbilical ligaments
|
median (only 1) is in the very center, there are 2 medial ligaments which are lateral to the median and just medial to the femoral triangle/inguinal canal
|
|
|
sliding hiatal hernia
|
most common diaphragmatic hernia, GE junction is displaced superiorly, "hourglass stomach"
|
|
|
what is the weakness in an indirect hernia
|
the transversalis fascia; often due to failure of the process vaginalis to fuse in infants
|
|
|
what layers of spermatic fascia cover indirect vs. direct hernias
|
indirect: all 3 layers(external spermatic, cremasteric, internal spermatic); direct: only external spermatic
|
|
|
which type of hernia is most likely to cause bowel incarceration
|
femoral
|
|
|
where are Peyer's patches found
|
in LP and submucosa of SI
|
|
|
salivary secretion control
|
stimulated by both symp (T1-T3 sup cerv ganglion) and para (CN 7 and 9)
|
|
|
composition of saliva at different flow rates
|
low flow rate: hypotonic, plenty of time to reabsorb NaCl; high flow rate: isotonic, less time to reabsorb NaCl; high K+ and bicarb due to active secretion
|
|
|
cephalic stage of gastric acid secretion
|
mediated by cholinergic and vagal mech, triggered by though, sight, smell and taste of food
|
|
|
gastric stage of gastric acid secretion
|
mediated by gastrin, triggered by chem stimulus of food and distension of stomach
|
|
|
intestinal stage of gastric acid secretion
|
mino, stimulated when protein containing foods enter duodenum
|
|
|
why do you not feel full in a non-fat meal
|
no CCK is release which would normally decr gastric emptying and maintain gastric distension which signals satiety
|
|
|
salivary vs. pancreatic amylases
|
salivary: hydrolyzes a-1,4 linkages to yield disaccharides; pancretic: hydrolyzes starch to oligo and disaccharides
|
|
|
oligosaccaride hydrolases
|
at brush border of intestine, produce monosaccarides (gluc, galact, fruct) which can be absorbed
|
|
|
what are bile acids conjugated to to make bile salts
|
taurine or glycine
|
|
|
urobilinogen
|
byproduct of gut bacterial modification of conjugated bili; 80% is excreted in feces, 20% reabsorbed f which 10% is excreted into urine and 10% goes back to liver
|
|
|
common causes of dysphagia for solids only vs. S and L
|
solids: obstruction like esophageal wevs, CA, etc; S and L: peristalsis problem; upper esophagus could be myasthenia gravis or stroke, lower can be achalasia, CREST
|
|
|
achalasia
|
failure of relaxation of LES due to loss of myenteric plexus (loss of VIP) which also causes uncoordinated peristalsis, "birds beak",
|
|
|
Plummer Vinson syndrome
|
due to Fe deficiency; causes dysphagia (esophageal webs), glossitis, Fe def anemia, achlorhydria, incr risk of SCC
|
|
|
locations of esophageal CA
|
upper and middle: SCC; lower: adenoCA
|
|
|
risk factors for esophageal CA
|
alcohol, achalasia, Barret's esophagus, ciagrettes, diverticuli, esophageal web, esophagitis, familial, stricture (lye)
|
|
|
how do you screen for malabsorption
|
due a Sudan stain for fat in the stool
|
|
|
where does celiac vs. tropical sprue affect the GI
|
celiac: prox SI (jejunum); tropical: prox SI usually but can infect entire SI
|
|
|
Whipple's dz
|
flat blunt villi in SI, ID tropheryma whippelii on EM; PAS+ foamy macrohphages in the intestinal lamina propia, older men; can also have fever, tender lymphadenopathy, arthralgias, etc
|
|
|
bile salt def
|
can cause malabsorption; due to decr production (cirrhosis), duct blockage, bacterial overgowth in SI, terminal ileal dz (Crohns) preventing reabsorption
|
|
|
typical micro appearence of celiac sprue
|
blunting of villi and lymphs in the lamina propia
|
|
|
pts with celiac have incr risk of what
|
T-cell lymphoma
|
|
|
what kind of gastric ulcer is produced in burn patients
|
Curling's ulcer, decr plasma volume leads to sloughing of the gastric mucosa
|
|
|
what kind of gastric ulcer is produced in brain injury
|
Cushing's ulcer, incr vagal stimulation leads to incr ACh which leads to incr H+
|
|
|
type A chronic gastritis
|
occurs in body and fundus; autoimmune against parietal cells which leads to achylorhdria and pernicious anemia; incr risk of adenoCA
|
|
|
type B chronic gastritis
|
affects the antrum (lower part of stomach); caused by H. pylori infection, have chronic inflammatory infiltrate in lamina propia, can cause metaplasia; incr risk of MALT lymphoma
|
|
|
Menetrier's dz
|
gastric hypertrophy with protein loss, parietal cell atrophy and incr mucus cells; precancerous; rugae of stomach are hypertrophied
|
|
|
risk factors for stomach CA
|
nitrosamines (Japan, smoked foods), achlorhydria, chronic gastritis, type A blood
|
|
|
common features of stomach CA (2)
|
signet cells, acanthosis nigricans
|
|
|
where in the stomach does CA occur and what do they look like
|
antrum and pylorus (lesser curvature), are usually ulcerative; this is why you must biopsy all stomach lesions!!!
|
|
|
what about H. pylori causes gastric vs. duodenal ulcers
|
gastric: destr of local mucus layer, inflammatory response; duodenal: due to incr acidity of fluid
|
|
|
layers of duodenal ulcer
|
necrotic debris, infllamtion with PMN predominance, granulation tissue, fibrosis
|
|
|
rapid urease test
|
place gastric biopsy in urea solution, look for color change indicitive of incr pH; verifies presence of H. pylori
|
|
|
which part of the GI does Crohns vs. UC affect
|
Crohns: usually terminal ileum and colon, anus, spares rectum, skip lesions; UC: always starts with the rectum and moves proximally
|
|
|
X-ray of bowel with UC and chrons
|
chrohns: string sign due to bowel wall thickening; UC: lead pipe
|
|
|
micro of UC vs. chrohns
|
UC: crypt absecess; crohns: granulomas, lmyphoid aggregates
|
|
|
intestinal manifestations of UC vs. Crohns
|
Crohns: diarrhea +/- blood, colicky pain, RLQ; UC: bloody diarrhea, recurrent L sided cramping
|
|
|
extra-GI manifestations of UC vs. Crohns
|
Crohns: migratory polyarteritis, erythema nodosum, uveitis; UC: pyoderma gangrenosum, primary sclerosis cholangitis
|
|
|
best test to diagnose diverticulitis
|
CT
|
|
|
zenkers ziverticulum
|
false diverticula formed at the junction of the pharynx and esophagus (cricopharyngeas muscle); presents with halitosis, regurg through nose, dysphagia
|
|
|
gallstone ileus
|
air in the gallbladder and colicky pain, due to fistula between the gallbaldder and SI
|
|
|
where is intussuception most likely to occur and in who
|
terminal ileum into cecum, infants (3m-6m)
|
|
|
what serves as the nidus for intussuception in adults and children
|
adults: polyps, CA; children: hyperplastic Peyer's patches
|
|
|
where in the GI does Hirschsprung's affect
|
always involves the rectum
|
|
|
angiodysplasia
|
tortuous dilation of vessels in the GI due to incr pressure, most often in cecum and ascending colon, causes bleeding
|
|
|
genes involved in colon CA and how the progression occurs
|
normal mucosa → loss of APC → polyp → loss of K-RAS → incr size → loss of p53 and DCC → CA
|
|
|
Gardner's syndrome
|
fam aden polyposis plus osseous and soft tissue tumors, retinal hyperplasia
|
|
|
Turcot's syndrome
|
fam aden polyposis plus brain involvement (glioma, medullablastoma)
|
|
|
what part of the GI is always affected in FAP
|
rectum
|
|
|
HNPCC (incl area affected and inheritence)
|
mutation in DNA mismatch repair, AD, prox colon always involved, no polyps, 80% chance of CRC, incr endometrial and ovarian CA
|
|
|
what can you give to a pt with a carcinoid tumor to prevent symptoms
|
octeotride
|
|
|
organisms which cause spontaneous peritonitis in adults and children
|
adults: E. Coli, kids: S. pneumo
|
|
|
hepatic encephalopy cause plus treatment
|
incr in aromatic AA's are converted to false NTs, also incr in serum ammonium; causes mental status changes, sleep disturbances, asterixis, coma; treat with lactulose which helps convert NH3 to NH4 to be excreted
|
|
|
causes of fatty liver in alcoholics
|
incr NADH, substrates in alcohol metab are used to make liver TGs, decr b-ox of FAs, incr mob, of FAs from adipose
|
|
|
what paraneoplastic syndromes does HCC cause
|
EPO and insulin like proteins
|
|
|
how do you know a liver CA is primary and not a met
|
if it makes bile
|
|
|
characteristic findings in Wilsons
|
asterixis, basal ganglia degeneration, cirrhosis, decr ceruloplasmin, corneal deposits, dementia, dyskinesia, dysathria, HA
|
|
|
Cu levels in Wilson
|
decr in ceruloplasmin (due to cirrhosis) causes an incr in free Cu but total Cu is decr
|
|
|
classic triad in hemochromotosis
|
cirrhosis, DM, skin pigmentation "bronze diabetes"
|
|
|
Fe studies in hemochromotosis
|
incr ferritin, incr Fe, decr TIBC, incr transferrin sat
|
|
|
primary sclerosing cholangitis
|
intra and extrahepatic; inflammation and fibrosis of bile ducts, causes alternating strictures and dilation with "beading" on ERCP; onion skinning fibrosis, assoc with UC, incr risk of cholangioCA
|
|
|
primary biliary cirrhosis
|
autoimmune disorder that occurs in women, granulomatous destruction of intrahepatic bile ducts; causes severe puritis (early finding), steatorrhea, hypercholest (xanthoma) and late onset jaundice; incr alk phos, incr IgM, auto-mito Ab's; assoc with sclerodema and CREST
|
|
|
secondary biliary cirrhosis
|
due to extrahepatic biliary obstruction, incr pressure causes injury and fibrosis, can cause bile lakes, ascending cholangitis
|
|
|
risk factors for cholelithiasis
|
female, fat, fertile, forty, flatulent
|
|
|
charcot's triad of cholangitis
|
jaundice, fever, RUQ pain (inflammation of bile duct)
|
|
|
cholangitis vs. cholecystitis
|
cholangitis: inflammation of bile duct; cholecystitis: inflammation of gallbladder
|
|
|
Murphey's sign
|
inspiratory arrest on deep palpation, + in cholelithiasis
|
|
|
cholesterol gallstones
|
cholesterol plus small amounts of Ca-bilirubinate, mostly radiolucent with areas of opacity due to Ca
|
|
|
pigment gallstones
|
radiopaque, seen in patients with chronic RBC hemolysis and biliary infection, contain Ca-bilirubin soaps
|
|
|
brown pigment stones
|
Ca soaps plus uncoj bili plus cholesterol crystals, assoc with infection of biliary tract, incr in Asia
|
|
|
what do you use to diagnose gallstones
|
US
|
|
|
causes of acute pancreatitis
|
gallstones (2), ethanol (1), steroids, mumps, autoimmune, scorption sting, hyperCa/hyperlipid, drugs (ex: sulfa); in kids, seatbelt trauma is somewhat common
|
|
|
sentinal sign of acute pancretitis
|
localized ileus causes air on x-ray in SI, due to nearby inflammation
|
|
|
how do you diagnose pancretitis
|
CT necessary because gut blocks the pancreas on US
|
|
|
common presenting signs of pancreatic CA
|
abdominal pain, weight loss, migratory thrombophlebitis (redness and pain on palpation of extremeties, Trousseua's sign), obstructive jaundice with palpable gallbladder (Courboisiers)
|
|
|
assoc mutations in pancreatic CA and assoc risks
|
K-RAS, p53; assoc with smoking (but not alcohol), chronic pancreatitis, DM, age
|
|
|
location of stem cells for SI
|
crypts of Lieberkum, located at the base of the villi
|
|
|
muscle type of esophagus
|
upper: skeletal; lower: SM
|
|
|
causes of rectal prolapse in kids <2 (3) and elderly (1)
|
kids: whooping cough, trichuriasis, CF; elderly: straining
|
|
|
most common location of anal fissure
|
posterior midline
|
|
|
unique characteristics about sinusoids
|
have gaps between endothelial cells to allow stuff to pass through, have no BM
|
|
|
incretins
|
includes GIP and glucagon-like peptide (GLP), are Gi hormones that stimulate release of insulin in response to oral glucose
|
|
|
roles of the stomach besides mechanical breakup
|
protein digestion (via HCl and pepsins), secrete IF for B12 absorption
|
|
|
mechanism of action of signal transduction with CCK8 receptors, PG's and somatostanin on gastric parietal cell
|
CCK8: binding of gastrin activates Gq (Ca++/IP3); PG's and somatostatin: activate Gi which inhibits cAMP;
|
|
|
pump located on gastric parietal cell
|
K/H ATPase (K in, H out)
|
|
|
enterokinase
|
secreted by the duodenal mucosa, activates trypsin
|
|
|
salivary gland tumor
|
generally benign, occur in parotid; include pleomorphic adenoma (most common, painless, moveable, high rate of occurence), Warthins (salivary gland tissue in a LN surrounded by lymp tissue) and mucoepidermoid CA
|
|
|
M. avium infection
|
produces a Whipple like infection in AIDS patients
|
|
|
most common cause of appendicitis is kids and adults
|
kids: infection like mumps, adenovirus, due to hyperplasia of lymph tissue here; adults: fecolith
|
|
|
2 common causes of GI fistula formation
|
Crohns and Diverticulitis (ex: pneumoturia, from fistula formation with bladder)
|
|
|
where does volvus most commonly occur
|
sigmoid, there is redundant mesentary, usually in elderly, leads to infarction
|
|
|
ischemic colitis
|
reduction in intestinal blood causes ischemia, commonly at splenic flexure in elderly
|
|
|
most common location for colon polyps
|
rectosigmoid
|
|
|
which tumor can produce pellagra
|
carcinoid: incr 5-HT synthesis → incr tryptophan use → decr niacin production → pellagra
|
|
|
duputren's contracture
|
fibrosis of the tendons in the hands, causes pulling of the digits; seen in cirrhosis
|
|
|
findings in Reye's
|
fatty liver (microvesicular), hypoglycemia, cerebral edema, convulsions, coma
|
|
|
infiltrate in alcoholic hep
|
PMN
|
|
|
ursodiol
|
primary bile acid that can be used in gallstone treatment, decreases cholesterol synthesis into bile
|
|
|
cholecystitis
|
inflammation of gallbladder, can be infectious or due to gallston complication, incr ALP if bile duct becomes involved (ascending cholangitis)
|
|
|
porcelein gallbaldder
|
calcification of gallbladder that can occur with chronic cholycysitis, can progress to CA so you should remove it
|
|
|
Grey-Turner and Cullen's signs
|
associated with hemorrhagic pancretitis; GT: flank hemorrhage; Cullens: periumbilical hemorrhage
|
|
|
receptors in the chemoreceptor trigger zone
|
D2 receptor, 5HT3, blocking then acts as antiemetic
|
|
|
colicky pain
|
pain and pain free intervals, due to total obstruction of the SI; due to intestines trying to move stool against obstruction; can eventually lead to ileus
|
|
|
differences in localization of SI vs. colon infarction
|
SI: diffuse; colon: localized
|
|
|
most common CA of upper lip
|
basal cell CA
|
|
|
high pitched "tinkly sounds" over the abdomen
|
SI obstruction
|
|
|
osmotic laxitives
|
Mg hydroxide/citrate
|
|
|
where are lipids absorbed
|
in the jejunum
|
