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462 Cards in this Set
- Front
- Back
retroperitoneal structures
|
duodenum (except 1st part), desc colon, asc colon, kidney and ureter, pancreas (except tail), aorta, ivc, adrenal gland, rectum
|
|
pain from retroperitoneal structures referred to
|
back
|
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which zone of liver partcipates in phase 2 biotransformation
|
3
|
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which zone of liver is most hypoxic
|
3
|
|
function of space of disse
|
lymphatic drainage
|
|
zone of liver affected first by viral hepatitis
|
1
|
|
presence of focal abdominal pain signifies
|
muscle tear or malingering
|
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what does falciform connect and contain
|
liver to ant wall, ligamentum teres
|
|
what does hepatoduodenal connect
|
liver to duodenum, portal triad (can be compressed in omental foramen of winslow)
|
|
what does gastrohepatic connect
|
ls stomach to liver, gastric a (seperates greater and lesser sac)
|
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what does gastrocolic connect and contain
|
gr stomach to transverse, gastroepiploic a
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what does gastrosplenic connect and contain
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gr stomach to spleen, short gastrics
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layers of gut wall
|
mucosa (contains epithelium, lamina, muscularis mucosa), submucusa (meissner), muscularis externa (auerbach=myenteric), serosa/adventitia
|
|
activity of meissner
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secretions
|
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activity of muscularis externa - inner vs outer
|
inner = circular, outer = long
|
|
where is lymphoma most likely to arise from in GI
|
maltoma (pylori), peyers patches
|
|
which part of GI has most goblet cells
|
jejunum
|
|
which part of gi has brunner's glands
|
duodenum
|
|
which part of colon has villi
|
small intestine
|
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what does crypts of lieberkuhn do
|
make enzymes, form new epithelium
|
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vertebral level of celiac, sma, ima, bifurcation
|
t12, l1, l3, l4
|
|
draw out the branches of the celiac trunk
|
p311
|
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where is sma relative to duodenum
|
behind 3rd part
|
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where is celiac relative to duodenum
|
gastroduodenal a goes behind 1st part of duodenum
|
|
collateral circulalation: internal thoracic
|
goes to sup epigastric and then inferior epigastric (which came from ext iliac)
|
|
collateral circulalation: superior pancreaticoduodenal (from celiac)
|
inferior pancreaticoduodenal (sma)
|
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collateral circulation: middle colic (sma)
|
left colic (ima)
|
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portal collateral: esophageal varices
|
left gastric w/ esophageal
|
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portal collateral: umbilical varices
|
paraumbilical w/ superficial and inferior epigastric
|
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portal collateral: rectum
|
sup rectal w/ sup and inf rectal
|
|
where is TIPS used
|
portal v and hepatic v
|
|
2 surgical therapies for portal htn
|
1. shunt b/w splenic vein and l renal v. (thought to lead to fewer complications) 2. shunt b/w hepatic vein and portal vein
|
|
above pectinate line: cancer, artery, vein
|
adenocarcinoma, superior rectal artery, superior rectal vein
|
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below pectinate line: cancer, artery, vein
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SCC, inf rectal art (from int pudendal), inf rectal
|
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innervation of anal canal
|
below pectinate line = inf rectal n from pudendal n (painful)
|
|
where does common bile duct empty into
|
duudoenum pt 2
|
|
organization of neurovasculature in femoral region
|
naval (lat to med)
|
|
what is femoral triangle
|
van
|
|
what is femoral sheath
|
just the femoral v,a,and canal (lymph nodes) no nerve
|
|
what does indirect hernia protrude through
|
deep ring
|
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where does direct hernia protrude through
|
abdominal wall
|
|
what goes inside spermatic cord
|
tunica vag, lymphatic, pampeniform, deferential a, cremaster a, testicular a, cremaster n, testicular n
|
|
discuss differences b/w above and below arcuate lie
|
above, ant = ext + int oblique, below, ant = ext + int + transverse abdominis
|
|
usual cause of diagphragmatic hernia in infants
|
defective pleuroperitoneal membrane
|
|
sx of diapgragmtic hernia
|
acid reflux, bowel sounds at left lung base
|
|
which one is the GE junction displaced
|
sliding vs paraesophageal
|
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which diagprgamtic hernia has risk of strangulation
|
paraesophageal
|
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which hernia is common in children
|
indirect
|
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which hernia is common in older men
|
direct
|
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which hernia is common in women
|
femoral
|
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where is inf epigastric relative to indirect hernia
|
medial
|
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where is inf epigastric relative to direct hernia
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lateral
|
|
components of hasselback triangle
|
rectus, inguinal lig, inf epigastric
|
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inguinal lig rel to femoral hernia
|
superior
|
|
pubic tubercle rel to femoral hernia
|
medial
|
|
what aa's stimulate gastrin
|
phe, trp
|
|
how does vagus stimulate gastrin release
|
release of grp
|
|
which gi hormone can promote growth of gastric mucosa
|
gastrin
|
|
which gi hormones are stimulated by distention
|
gastrin, vip
|
|
which gi hormones are INFLUENCED by vagal stimulation
|
gastrin, vip, SS (downregulated), pepsin
|
|
how does CCK cause pancreatic secretion
|
acting on neural muscarinic pathways
|
|
what cells secrete cck
|
I cells
|
|
what organs does secretin act on
|
pancreas (bicarb), stomach (decrease acid), and liver (bile)
|
|
which gi hormones promote acid secretion. Which ones are against acid secretion
|
gastrin & histamine. SS, GIP, secretin, prostaglandins
|
|
which gi hormones promote gastric mobility? Against?
|
gastrin, motillin. Cck
|
|
which gi hormones promote insulin release? Against?
|
gip. Ss
|
|
where are I cells located
|
duodenum and jejunum
|
|
where are k cells, what do they secrete
|
duodenum and jejunum. GIP = glucose dep insulinotropic peptide, gastric inhib peptide
|
|
which GI hormone is inhibited by adrenergic input
|
vip
|
|
which GI hormone is decreased in achalasia
|
NO
|
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which GI hormone produces migrating motor complexes
|
motilin
|
|
what GI hormone do macrolides stimulate
|
motilin
|
|
what GI hromones are secreted from parasympathetic ganglia
|
vip and enkelphin
|
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effect of enkelphin
|
inhibit secretions and contract smooth mm
|
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who makes intrinsci factor
|
parietal cells
|
|
who makes bicarb in gi tract
|
stomach (same cells that secrete mucus), duodenum (brunner), saliva, pancreas
|
|
which salivary secretion is the moust viscous
|
sublingual
|
|
is salivary secretion by sympathetic or parasympathetic
|
both, but sympathetic stimulates sublingual more, parasymp for parotid
|
|
effect of flow rate on saliva
|
high flow rate = isotonic.
|
|
concentration of potassium in saliva
|
higher
|
|
what can decrease salivary secretion
|
sleep & dehydration
|
|
what hormone can act on salivary secretion
|
aldosterone can increase k+ secretion and na+ reabsorption, means more cl absorpbed too
|
|
enterochromaffin cells - aka, function
|
kulchitsky cells that line gi tract and make 5ht that regulates motility and nausea
|
|
can atropine block acid secretion? Gastrin secretion?
|
yes, no
|
|
which GI hormones are regulated by acid levels
|
gastrin, secretin, ss
|
|
what enzyme activates trypsinogen
|
enterokinase
|
|
tonicity of pancreatic fluid
|
isotonic
|
|
rate limiting step in carbohydrate digestion
|
oligosaccharide hydrolase
|
|
what does pancreatic amylase digest
|
starch to oligosacchardie and disaccharide
|
|
what kind of linkage does salivary amylase digest
|
alpha-1,4
|
|
what transports glucose and galactose
|
sglt1 (na dep)
|
|
what transports fructuse
|
glut5
|
|
where is iron absorbed
|
duodenum
|
|
what are R binder
|
synthesized in salivary gland to bind b12, degraded by stomach
|
|
where is folate absopbed
|
jejunum
|
|
where is b12 absorbed
|
ileum
|
|
where are bile acids absorbed
|
ileum
|
|
where are M cells located, what is their functigon
|
payere's patches, take up antigen
|
|
bile salts vs bile acids
|
bile acid conj to glycine or taurine = acid
|
|
how is cholesterol excreted from the body
|
bile
|
|
what is the rate limiting step in bile synthesis
|
7alpha hydroxylase
|
|
what happens to concentration of na, hco3, cl, k as flow rate increases
|
na, k stay the same. Cl declines, hco3 increases
|
|
what happens if cl transport is borken in pancreas
|
cl=cftr, no cl transport into lumen means no sodium and water folow it, means less fluid
|
|
what is direct biliribuin converted to
|
urobilinogen in gut by bacteria
|
|
what percent of urobilinogen is excreted
|
80
|
|
where does ezetimibe act in the cholesterol cycle
|
blocks uptake of cholesterol from brush border
|
|
is bilirubin that is oxidized by phototherapy conjugated? Where is it excreted
|
no, it's excreted in bile
|
|
what are normal levels of direct bilirubin in blood
|
0, to see in blood must have pathology that pushes it back to liver and bloodstream
|
|
what is main risk factor for salivary gland tumors
|
smoking
|
|
which salivary gland tumors tend to be malignant
|
ones that occur in minor salivary glands
|
|
characteristics of pleomorphic adenoma (aka mixed tumor)
|
painless, movable, oft angle of jaw, high recurrence, benign
|
|
characteristics of warthin's tumor
|
benign, salivary gland tissue trapped in lymph node, males
|
|
characteristics of mucoepidermoid carcinoma
|
malignant
|
|
on mediastinal xray, how to tell b/w esophagus and trachea
|
trachea will be lucent (dark) cuz of air
|
|
pathology of solid dysphagia
|
obstruction from stricture, malignancy, LES
|
|
pathology of solid & liquid dysphagia
|
improper peristalsis from neuromuscular (myasthenia), achalasia, crest, spasm
|
|
birds beak on barium
|
achalasia
|
|
pathology of achalasia
|
loss of myenteric plexus, can be congenital or chagas
|
|
vomiting up foods at night
|
achalasia
|
|
decreased NO producing neurons
|
achalasia
|
|
decreased VIP producing neurons
|
achalasia
|
|
risk factors for gerd
|
pregnancy, overweight
|
|
which one has painless bleeding: esophageal varices or mallory weiss
|
varices
|
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where does bleeding occur in esophageal varices
|
lower 1/3 of esopagus
|
|
what is esophagitis associated with
|
gerd, infection (hsv, candida, cmv), chemicals
|
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who is mallory weiss seen in usually
|
alcoholics and bulimics
|
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what causes esophageal strictures
|
gerd, lye ingestion
|
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what is hammmonds crunch and who is it seen in
|
air and secretions can be released into anterior mediastinum from esophageal tear in boerhaave
|
|
what is transmural esophageal rupture, what is it caused by
|
boearhave, violent retching
|
|
triad of plummer vinson
|
esophageal web, glossitis, anemia
|
|
what is diffuse esophageal spasm
|
periodic nonperistaltic contraction of esophagus. Pain is like angina. Not accoc/ w/ exertion, not releived by rest, crampy
|
|
what causes barrett's
|
gerd, esophagitis, esophageal ulcer
|
|
risk factors for esophageal cancer
|
alcohol/achalasia, barrett, cigarett, diverticuli, esophageal web & esophagitis, family hx, gerd, hot dots (ie. Nitrosamines)
|
|
met of esophageal cancer
|
local node, then liver/lungs
|
|
prelvaence of esophageal adenocarcinoma vs scc
|
adenocarciona more common in us, wcc worldwide
|
|
how to dx malabsoprtion
|
fat in stool, secreased serum beta carotene, d-xylose will be absorbed in pancreatic malabsoprtion but not bowel insufficiency or bacterial overgrowth
|
|
histology of whipple's dz
|
t whipplii organism w/ pas+ macrophage in lamina prop and mesenteric nodes
|
|
what other organism can mimic whipples dz
|
mac in hiv+, also has pas+
|
|
sx of whipples
|
arthralgia, cardiac, neurologic in older men
|
|
what area of bowel does celiac affect
|
jejunum
|
|
histology of lactase def
|
normal appearing villi
|
|
stool osmotic gap in lactase def
|
increased (osmotic diarrhea)
|
|
what three things are needed for proper fat absorption
|
functioning lipase, bile salts, villi in small intestine
|
|
what dzz can cause lowered lipase
|
pancreatic dz, increased gastrin (eg gastrinoma) which increases acid which inhibits lipase
|
|
name pathology in bile saltes
|
bacterial overgrowth and liver dz
|
|
how can abetalipoproteinemia cause malabsoprtion
|
can't make apoB, cant make CMs
|
|
histology of abetaliporoteoinmia
|
fat in enterocytes
|
|
Dx of pancreatic insufficiency
|
secretin test, bentiromide (causes secretion of chymotrypsin)
|
|
tx of secretory diarrhea
|
fluid replacement that has glucose (glucose/na transport)
|
|
baby diarrhea vs adult
|
baby diarrhea usually hypotonic
|
|
what other dzz is celiac assoc/ w/
|
dermatitis herpetiformis, downs
|
|
celiac is allergy against what
|
gliadin
|
|
which malabsorption has risk of malignancy
|
celiac sprue, you see increased lymphocytes in lamina propria, similar to hashimotos
|
|
what antibodies are elevated in celiac
|
tissue transglutaminase, gliadin, anti=endomysial
|
|
physiologic role of tissue transglutaminase
|
deaminates absorbed gluten and enhances antigenicity
|
|
which gastritis is erosive: acute or chronic
|
acute
|
|
causes of accute gastritis
|
disrution of mucal barrier from stress, nsaid, alcohol, uremia, burns, brain injury (increased vagal tone)
|
|
types of chronic gastritis
|
type a = fundus = pernicious. B = pylori = antrum
|
|
characteristics of menetrier dz
|
gastric hypertrophy, parietal atrophy (achlorydia), and more mucous cell. Precancer
|
|
stomach cancer met
|
local spread, then liver/node met - virchow node, krukenburg, sister mary joseph
|
|
presence of more than 100 seborrheic keratosis on body could indicate
|
gastric cancer
|
|
risk factors for stomach cancer (4)
|
nitrosamine (smoked foods), acloryhida, chronic gastritis, type A blood
|
|
characteristics of stomach cancer
|
signet ring cell, acanthosis nigricans
|
|
linitis plastica -- association wi/ h pylor
|
none
|
|
what is linitins plastica
|
diffuse form of stomach cnacer where stomach becomes thickened and hard like a leather bottle
|
|
where are most stomach cancers located
|
lesser curv and antrum
|
|
where is stomach cancer most common
|
japan - smoked meats
|
|
gastrin levels in person w/ achloryhydria
|
elevated
|
|
pain with meals - gastric vs duodenal ulcer
|
increases in gastric, decreases w/ duodenal
|
|
who is likely to be more obese duodenal or gastric ulc
|
duodenal ulcer
|
|
which ulcer more assoc/ w/ h pylori
|
both are, except duodenal almost always
|
|
hypertrophy of brunners glands
|
duodenal ulcer
|
|
which ulcer due to mucosal protection, gastric acid secretion
|
duodenal = both, gastric = mucosal protection
|
|
which ulcer (pud) can be malig
|
duodenal never malig, gastric sometimes
|
|
lesions of pud vs cancer
|
ulcer has clean punched out margin. Carcinoma is irregular
|
|
where can ulcer penetrate
|
pancreas, gastroduodenal
|
|
erosion vs ulcer penetration
|
erotion doesn't penetrate muscularis mucosa
|
|
which ibd is thought to be disordered response to intestinal bacteria
|
crohns
|
|
which ibd has skip lesions
|
crohns
|
|
which ibd always has rectal involvement
|
uc
|
|
which ibd has rectal sparing
|
crohns
|
|
which part of gi does crohns tend to affect
|
terminal ileum and colon
|
|
morphology of crohns
|
transmural, cobblestone mucosa, creeping fat, thickened wall, fistula, ulcer
|
|
which dz has loss of haustra
|
uc
|
|
what ibd has pseudopolyps
|
uc, comes from islands of remaining mucosa
|
|
which ibd does not have granulomas
|
uc
|
|
which ibd has lymphoid aggregats
|
crohns
|
|
complications of crohns
|
stricture, fistula, malabsoprtion
|
|
complications of uc
|
malnutrition, toxic megacolon, colorectal carcinoma
|
|
risk of colorectal carcinoma: uc vs crohn
|
uc is higer
|
|
what is associated with toxic megacolon
|
uc
|
|
which ibd is associated with bloody diarrhea
|
uc
|
|
for each of the following, name association: erythema nodosum, ankylosing spondylitis, uveitis
|
all are crohns
|
|
for each of the following, name association: pyoderma gangrenomsum, cholsterol stones, migratory polyarthritis
|
all crohns, except pyoderma gangrenosum
|
|
what is associated with 1* sclerosing cholangitis
|
uc
|
|
which ibd assoc /w nod2
|
crohns
|
|
sx of ibs
|
pain improves with defecation, change in stool freq, change in appearance of stool
|
|
what is ibs assoc w/
|
childhood sex abuse, domestic abuse, psych
|
|
what is appendicitis caused by
|
obstruction CAUSES fecalith (bacterial infection)
|
|
what is main differential for appendicitis
|
diverticulitis, ectopic preg, gastroenteritis, ruptured follicuar cyst, mesnteric lymphadenitis, meckel
|
|
histology of appendicitis
|
lymphoid hyperplasia after viral infection in kids.
|
|
progression of appendicitis
|
diffuse periumbilical pain that becomes localized at mcbuenrye
|
|
where are most diverticula located
|
sigmoid colon
|
|
histology of diverticula
|
weak muscularis externa
|
|
diverticulosis vs diverticulitis
|
osis = many diverticula, itis = inflammation. Osis can bleed, but itis usually doesn't due to scarring
|
|
risk factor for diverticulosis
|
age, low fiber
|
|
does diverticulosis have painful bleeding
|
painless (mcc rectal bleeding)
|
|
LLQ pain
|
diverticulitis w/ pain and fever
|
|
complications of diverticulitis
|
perforation leading to peritonitis, abscess, bowel stenosis, fistula formation (esp w/ bladder)
|
|
where is zenker located
|
jcn of pharynx and esophagus
|
|
which msucle is weak in zenker
|
criopharyngeus
|
|
where is traction diverticula located
|
midpoint of esophagus
|
|
where is epiphrenic diverticula located
|
esophageal diverticula located above les
|
|
what persists in mecleks
|
vitelline duct
|
|
what is rule of 2's for meckel
|
2 in, 2 ft, 2%, 2 yrs, 2 tissues
|
|
where is meckel located
|
ileum
|
|
dx for mechek
|
pertechnetate
|
|
what is omphalomesenteric cyst
|
cystic dilation of vitelline duct
|
|
what is intussception in adults assoc/ w/
|
intraluminal mass or tumor
|
|
Dance sign
|
intussception - sausage mass in RUQ
|
|
where does volvulus usually occur
|
cecum, sigmoid colon
|
|
cause of intuscception in children
|
adenovirus, meckel
|
|
what is missing in hirschsprung
|
no auerbach or meissner (both of them)
|
|
what gene is often mut in hirschsprung
|
ret
|
|
what part of gi will be abnormal in hirshsprung
|
constricted part, which is aganglionic
|
|
duodenal atresia - vomiting
|
bilious
|
|
xr of duodenal atresia
|
double bubble,
|
|
duodenal atresia assoc w/ what
|
downs
|
|
sx of ischemic colitis
|
pain after eating (just like gastric ulcer!)
|
|
where does ischemic colitis occur
|
splenic colitis (watershed) and distal colon
|
|
where is angiodysplasia usually found
|
cecum, terminal ileum, asc colon
|
|
what is the main cause of intestinal infarction
|
entrap due to adnesion , or indirect inginal hernia
|
|
characteristic finding in gallstone ileus
|
air in biliary tree
|
|
what kind of polyps are precancerous
|
villous>tubulouvulous> tubular adenomatous polyp
|
|
what can villous polyps secrete
|
protein, K+, lead to loss of those bings from blood
|
|
where are colon polyps usually found
|
rectum, sigmoid
|
|
juvenile polyps vs juvelie polyposis syndrome
|
syndrome has risk of crc
|
|
peutz jeghers syndrome
|
AD, multiple hamartoms throughout gi, w/ hyperpig mouth, lips, hands, genetialia
|
|
UC associated crc vs normal
|
arise earlier, occur at mult sites, tend to be dysplasia first rather than polyp, uniformly distributed (usually crc is left)
|
|
what region always infolved in fap
|
rectum
|
|
gardners syndrome
|
fap + osseous/soft tissue tumor + retinal hyperplasia
|
|
turcot syndrom
|
fap + cns tumor
|
|
what is messed up in hnpcc
|
dna mismatch repair
|
|
risk factors for crc
|
adenomatous polyps, ibd, s bovis, tobacco, juvenile polyp syndrome, peutz jegher, high fat low fiber diet
|
|
distal vs proximal crc
|
distal = obstruction, colicky pain, hematochezia and stoool shape change. Prox = dull pain, anemia, occult blood, these are usually bulkier
|
|
stool occult blood - why is it not specific
|
can't distinguish b/w hemoglobin from myoglobin
|
|
apple core lesion on xr
|
crc
|
|
nsaids relationship to crc
|
less incidence of polyps
|
|
where do crc met to
|
liver, lungs, bone brain
|
|
crampy vs colicky pain
|
colicky pain is intermittent pain w/ areas of pain free interval. Produced when peristalsing against obstruction
|
|
most common cause of obstruction
|
ABC - adhesion, bulge (hernia), cancer
|
|
what is order of gene mutation in chromosomal instability crc
|
apc (decreased cell adhesion and increased prolif), kras (signal transduction), loss of p53 (increased tumor)
|
|
where is carcinoid tumor usually located
|
appendix, ileum, rectum
|
|
where are carcinoid tumors usually likely to be malig
|
small intestine
|
|
dense core body on EM
|
carcinoid
|
|
sx of carcionoid syndrome
|
BFDR - brochospasm, flushing, diarrhea, right heart (tips)
|
|
dx of carcinoid syndrome
|
5-hiaa in urine
|
|
causes of cirrhosis
|
alcohol, postviral, autoimmune, autoimmune, metabolic dz (iron, wilson, antitryp, galactosemia)
|
|
alt>ast
|
viral hep
|
|
ast>alt
|
alcohol
|
|
lfts in lever disase
|
increased estrogen, increase pt/inr, decrease lipids, platelets
|
|
when is ggt increased
|
liver dz, heavy alcohol consumption
|
|
when is alp increased in gi dz
|
obstructive liver dz
|
|
mumps can elevate what gi enzyme
|
amylase
|
|
findings on reye's syndrome
|
fatty liver, mitochondrial change, leads to hypoglycemia and comma
|
|
which viral infection assoc w/ reyes
|
vzv, flu b
|
|
how does aspirin cause hypoglycemia
|
inhbits atp synthase in etc, which kills beta oxidation
|
|
things which can cause hepatic steatosis
|
alcohol, non alcoholic (i.e. metabolic syndrome), didanosine, stavudine, reyes
|
|
histology of alcoholic hepatitis
|
necrotic hepatocytes w/ neutrophils, mallory bodies (intracytoplasmic eosinophilic)
|
|
what is pathology of mallory bodies
|
alcohol ubiquitinates intermediate filaments
|
|
which zone is sclerosed in alcoholic liver dz
|
zone 3
|
|
paraneoplastic secretions of hcc
|
epo, insulin-like, pth-like
|
|
how does hcc spread
|
hematogenous
|
|
what carcinogen can cause hcc
|
aflatoxin
|
|
why do you see hypoglycemia in hcc
|
insulin like factor
|
|
why do you see polycythemia in hcc
|
epo
|
|
histologic findings in hcc
|
bile in neoplastic cells
|
|
what is cardiac cirrhosis
|
chf that results in congestion and necrosis in liver
|
|
what type of pathology causes councilman bodies
|
they are swelled. Toxic or viral hepatitis
|
|
causes of budd chiari
|
hypercoagulable state, polycythemia, preg, hcc
|
|
jvd is seen in budd chiar
|
no
|
|
type of congestion seen in budd chiari
|
centrilobular
|
|
where does alpha1 antitrypsin accumulate in deficiency
|
hepatocellar er
|
|
what type of empysema in a1at def
|
panacinar
|
|
histology of a1at def
|
pas+
|
|
inheritance of a1at
|
codominant
|
|
mcc of cirrohosis in childre
|
a1at
|
|
what allele is normal and which allelel is dz in a1at
|
M, Z/S
|
|
what enzyme is difficient in neonates
|
udp glucuronyl transferase
|
|
how will the following change hyperbilirubinemia, urine bilirubin, urine urobilinogen (hepatocellular, obstructive, hemolytic)
|
p332
|
|
how does light convert unconjugated bilirubin to soluble form
|
uvb light converts to dipyrrole
|
|
mechanisms of conjugated hyperbilirubinemia
|
extrahepatic obstruction, biliary epithelial dmg, intrahepatic obstruction, impaired transport across hepatocyte
|
|
mechanisms of unconjugated hyperbilirubinemia
|
increased production, increased uptake and storage, decreased conjugation
|
|
compare the following disease: gilbert, crigler najjar 1&2, dubin johnson, rotor
|
gilbert and crigler najjar are unconjugated. Crigler has absent udp glucuronyl transferase, but type 2 is less severe. Dubin johnson and rotor is conjugated. Dubin has a black liver. In dum and rotor will see epinephrine products in lysosomes
|
|
which hereditary hyperbilirubinemia is tx w/ phenobarb, how does it work
|
crig najjar 2, which increases liver enzyme synthesis (cyp inducer)
|
|
pathophys of wilsons disease
|
liver can't excrete copper, and copper can't enter circulation as ceruloplasmin
|
|
sx of wilsons
|
asterixis, basal ganglia degen, ceruloplasmin decrease, cirrhosis, corneal deposit, carcinoma (hcc), chorea, dementia
|
|
tx for wilsons
|
penicillamine
|
|
what mineral can decrease copper absorption
|
zinc
|
|
what gene is often mutated in hemochromatosis? which chromosome?
|
hfe, chromomosome 6
|
|
triad of hemochromatosis
|
bronze diabetes + micronodular cirrhosis
|
|
micronodular vs macronodular cirrhosis
|
micronodular due to metabolic issue whereas macronodular due to necrosis from postinfectious or drug induced
|
|
can hemachromatosis set off metal detector
|
yes
|
|
tx of hereditary hemochromotosis
|
phlebotomy, deforoxamine
|
|
what hla type is associated with hemochromatosis
|
hla a3
|
|
what type of cardiomyopathy accoc/ with hemochromatosis
|
restrictive, dilated
|
|
risk factors for hcc
|
hepatitis b&c, wilson, hemochromatosis, a1at, alcoholic cirrhosis, carcinogen(afalotoxin)
|
|
ferritin levels during inflammation
|
increased, cuz it is app
|
|
primary sclerosing cholangitis - gender, histology, presentation, labs
|
histology: onion skinning and fibrosis of intra and extrahepatic bile ducts with NO GRANULOMA (1* biliary cirrhosis has granuloma)
dx - seen with ercp ('beading" of extra and intrahepatic ducts), increased igm, panca+ sx - pruritis, jaundice, dark urine and light stools, association with UC, males, risk for cholangiosarcoma |
|
how to distinguish b/w extrahepatic and intrahepatic biliary obstruction
|
us
|
|
primary biliary cirrhosis - pathophys, presentation, labs, extra
|
autoimmune reaction that results in lymphocytic infiltration (no fibrosis like psc), increased antimitochondrial, granulomas, get pruritis BEFORE JAUNDICE cuz pruritis not from bile salts, assoc/ w/ other autoimmune, increased conj bilirubin, alp
|
|
secondary biliary cirrhosis - pathophys, presentation, labs
|
extrahepatic obstruction that leads to injury of intrahepatic ducts. Pruritis jaundice, dark urine, light stools, increased direct bili, increased alp
|
|
risk factor for gallstones
|
female, fat, fertile, forty
|
|
triad for cholangitis
|
jaundice, fever, ruq pain, htn, altered mental status
|
|
risk factors for cholesterol gallstones
|
obesity, crohns, cystic fibrosis, age, fibrates, estrogen, multiparity, rapid weight loss, native american
|
|
risk factors for pigment stones
|
hemolysis, alcohol cirrhosis, age, biliary infection
|
|
brown stones
|
cbd infection, asian
|
|
complications of gallstones
|
cholecystitis, ascending cholangitis, acute pancreatitis
|
|
in what population is biliary colic painless
|
diabetes
|
|
what is seen on imaging for gallstone ileus
|
air in biliary tree
|
|
dx of gallstone
|
us
|
|
how to dx cholecystitis
|
radionucleotide (hida) scan = cholescintigraphy
|
|
risk factors for acute pancreatitis
|
gallstone, ethanol, trauma, steroids, mumps, autoimmune, scoropion, hypercalc/hyperlipid, ercp, drugs (didanosine, zalcitabine, stavudine, ritonovir)
|
|
what is sentinal sx in acute pancreatitis
|
localized ileus in duodenum accumulates air
|
|
will someone with acute pancreatitis be hungry? Nauseus?
|
no, yes
|
|
complications of acute pancreatitis
|
dic, ards, hypocalcemia, diffuse fat necrosis, pseudocyst, hemorrhage, infection
|
|
why can pancreatitis cause hemorrhage
|
can't absorb vit k
|
|
why can pancreatitis cause ards
|
activation of phospholipase a2 in lung
|
|
alcohol effect on pancreas
|
thickens ductal secretions and injurs acini
|
|
dx of pancreatic dzz
|
ct, not us
|
|
sentinel sign in gi dz
|
inflammation causes ileus in proximal segment of gi tract, which collects air
|
|
where are most pancreatic tumors located and what does that cuase
|
head, obstructive jaundice
|
|
groups at risk for pancreatic cancer
|
jewish, afam
|
|
markers for pancreatic cancer
|
cea, ca199
|
|
is pancreatic cancer assoc/ w/ etoh
|
no
|
|
risk factors for pancreatic adenocarcinoma
|
cigarettes, chronic pancreatitis
|
|
common presentation for pancreatic cancer
|
weight loss, migratory throbophlebitis, obstructive jaundice w/ palpable gallbladder (courviouser)
|
|
painless jaundice in elderly gentleman
|
pancreatic cancer
|
|
met to virchows node or paraumbilical node
|
can see in stomach cancer or pancreatic
|
|
5 side effects of cimetidine
|
antiandrogen, cyp inhibit, crosses bbb, cross placenta, increase creatinine
|
|
what other h2 block besides cimetidine can icnrease cretinine
|
ranitidne
|
|
best tx for ze syndrome
|
ppi
|
|
best tx for acute variceal bleed
|
octeotide
|
|
triple therapy for h pylori
|
metro, amox/tetra, bismuth
|
|
ci to use of misoprostol
|
pregnant (abort)
|
|
which drug that is used to treat nsaid ulcer can also induce labor
|
misoprostol
|
|
what type of medication is pirenzepine, propantheline
|
muscarinic ag. blocks M1 on ECL cells and M3 on parietal cells.
|
|
mechanism of action of muscarinic ag
|
block m1 on ecl, block m3 on parietal
|
|
conditions treatable with ss
|
varices, acromegaly, vipoma, carcinoid
|
|
which andacid can cause diarrhea
|
mg hydroxide
|
|
which antacid can be used for ckd pts to reduce phosphate
|
al hydroxide
|
|
which antacids can cause hypokalemia
|
al oh, mg oh, ca co3
|
|
which antacid can cause rebound acid secretion
|
calcium (stim of g cells)
|
|
toxicity of infleximab
|
tb reactivation or respiratory infection
|
|
what nsaid can cause oligospermia
|
sulfasalazine
|
|
what is sulfasalazine used for
|
ibd
|
|
what medicine used to treat ibd can trigger sulfa allergy
|
sulfaslazine
|
|
mechansim of odansetron
|
5ht3 ag
|
|
which antiemetic can cause headache and why
|
odancetron cuz it antagonizes serotonin and opens blood vessels (opposite of triptan)
|
|
which antiemetic can cause parkinsonian sx
|
metoclopramide, prochlorperazine
|
|
mechanism of promethazine
|
first gen h1 ag (like diphenylhydramine, meclizine, hydroxyzine, doxylamine)
|
|
toxicity of first gen antihist
|
they act on muscarine so get antimuscarinic sx
|
|
which antiemetic can interact with digoxin and diabetic agents
|
metoclorpamide
|
|
which antiemetic is CI in pts with small bowel obstruction? Why?
|
metaclopramide, this antiemetic is also a prokinetic
|
|
does metoclorpamide affect colon transport time?
|
no
|
|
which prokinetics act on ach
|
bethanechol, achei
|
|
which prokinetics act on serotonin
|
metachlorpromide
|
|
which prokinetic acts on motillin
|
macrolide
|
|
what are slow waves in gi
|
oscillating membrane potentials (NOT AP's) that start in cajal cells that lead to Aps. Although these waves are not influenced by neurohormonal, aps are
|
|
what controls swallowing, what cns are involved
|
medulla, 9-10
|
|
what controls opening of les
|
vagal n (using vip)
|
|
what is receptive relaxation and what does it involve
|
when food enters stomach, vasovagal inputs and cck is involved to relax the stomach
|
|
how does the stomach mix food
|
contraction of proximal stomach causes contraction of distal stomach
|
|
what factors regulate stomach emptying
|
isotonicity of chyme increases emptying. Fat, cck, and acid in duodenum slow it
|
|
describe the gastroileal reflex
|
food in stomach increases peristalsis in ileum and relaxation of ileocelcal sphnicnet
|
|
purpose of haustra in large intestine
|
segmentation contraction
|
|
describe whether the following occurs in medullary vomiting center or chemoreceptor trigger zone: gag, gastric distention, innerear, emetics, radiation
|
gag and gastric distention occur in medullary vomiting center. Inner ear involves both. emetics and radiation are ctz
|
|
what gene regulates amount of transferrin in blood
|
hfe, chromomosome 6
|
|
where are carbohydrates absorbed
|
mostly duodenum
|
|
where are amino acids absorbed
|
mostly duodenum
|
|
where are lipids absorbed
|
mostly jejunum
|
|
where are fat vitamins absorbed
|
mostly jejunum
|
|
how is sodium absorbed in colon
|
passive defusion (there is a na/k pump that generates the gradient)
|
|
how is chloride absorbed in gut
|
mostly cl/hco3 exchange, but passive, na/cl also
|
|
how is k+ absorbed in gut
|
passive diffusion
|
|
what can regulate k+ absorption in gut
|
aldosterone can increase k+ excreiton
|
|
mechanism of osmotic diarrhea in cholera infection
|
camp dependent insertion of cftr, secretion of cl
|
|
what is herpangina and what causes it
|
cox, multiple lesions on palate and pharynx surrounded by erythema
|
|
most common cause of exudative tonsilits
|
viral
|
|
when is cervicofacial actinomycosis seen
|
draining sinus tract, usually after tooth extraction
|
|
signs of peritonsillar abscess? What usually cause it
|
pyogenes. Uvula deviation, foul breath, "hot potato" voice
|
|
what is sialadenitis, caused by what
|
inflammation of major salivary gland, saureus
|
|
oral findings of congential syphilis
|
mulberry molar, hutchinson's teeth (blunted incisor)
|
|
pathogenesis of dental caries
|
strep mutans makes H+ from sucrose
|
|
vesicles and bullae with targetoid appearance that involves mouth
|
sjs
|
|
melanin on lips and oral
|
peutz jeghers
|
|
causes of tooth discoloration
|
tetracycline, flouride, congenital erythropoietic porphyria
|
|
what is leukoplakia, causes
|
squamous hyperplasia, smoking, alcohol, hpv
|
|
dentigenous cyst
|
3rd molar, ameloblastoma
|
|
ameloblastoma - where is it, xray
|
mandible, soap bubble on sray
|
|
foods that decrease les tone
|
coffee, caffeine, ccbs
|
|
osmotic gap in secretory diarrhea
|
decreased
|
|
why might a diarrhea come from large intestine
|
infection, laxative, ibd
|
|
will small bowel obstruction present with rebound tenderness
|
no , no peritonitis
|
|
causes of mesenteric vein thrombosis
|
pv, antiphospholipid, rcc into ivc
|
|
distinguish ischemia from sbo
|
sbo will have colicky pain. Ischemia will have diffuse abdominal pain, bloody diarrhea, and no bowel sounds
|
|
what is angiodysplasia assoc/ w/
|
vwd, calcific aortic stenosis
|
|
where are anal carcinoma usually located
|
above dental line
|
|
where is anal fissure usallly located
|
b/w dentate line and anal verge
|
|
hla assoc/ of autoimmune hepatitis
|
dr3/4
|
|
could autoimmune hepatits possibly be fulminant
|
eys
|
|
labs for autoimmune hepatitis
|
serum ana, anti smooth mm
|
|
acute fatty liver of pregnancy
|
can't beta oxidate, fatal to both mother and child
|
|
effect of preeclampsia on liver
|
portal triad necrosis, hellp syndrome (lft)
|
|
what causes fulminant liver failure
|
viral hep, drugs (acetominophen), reye
|
|
mcc of ascending cholangitis
|
e cloi
|
|
causes of spontaneous peritonitis
|
e coli in adult, s pneumo in children
|
|
what organism can cause portal hypertension
|
schistomiosis
|
|
what could cause a liver infarct
|
PAN, transplant rejection
|
|
*** WHAT CAN CAUSE LIVER FIBROSIS
|
mtx, amniodarone, retinoic acid
|
|
what drugs can cause acute hepatitis
|
inh, halothane, methyldopa, acetominophen
|
|
what drug can cause cholestasis
|
ocp, steroid
|
|
peritoneal fluid analysis -- saag gradient
|
increased in liver origin, decreased in peritonitis (1.1 = cutoff)
|
|
what is hepatorenal syndrome
|
renal fialure w/o renal dz. Need liver transplant
|
|
focal nodular hyperplasia
|
benign tumor of liver, central stellate scar w/ radiating fibrous septae
|
|
complicationof cavernous hemangioma
|
most common benign of liver, potential hemororage
|
|
what can cuase development of liver adenoma
|
ocp, steroid, von gierke
|
|
caroli dz
|
segmental dilation of intrahepatic bile ducts assoc/ w/ arpkd
|
|
causes of cholangiosarcoma
|
1* sclerosing cholangitis, chlorchis sinensis, thorotrast, cystic dz. Usually in ampulla or cbd
|
|
where is pain likely to radiate to with gallstone dz
|
rt shoulder
|
|
what pain medicine can be used for gallstone
|
NOT morphine, use mepiridine
|
|
what is dystropic calcification of gallbladder assoc w/
|
gb adenocarcinoma
|
|
complciation of annular pancreas
|
small bowel obstruction
|
|
why can pancreatitis cause hypoxemia
|
destruction of surfactant by circulating pancreatic enzymes
|
|
pancreatic pseudocyst - vs nor mal cyst
|
no epithelial lining
|
|
what activates capillary lpl
|
apoc2. levels are increased byinsulin
|
|
What is a good tg level
|
<150
|
|
what type of familial hypercholesterolemia likely to see decreased apoE and palmar erythema
|
3
|
|
how to calculate ldl
|
cholsetrol - hdl -tg/5 (need to fast to get good tg lvl)
|
|
what is increased in type v famiali hypercholsrol
|
cm, vldl
|
|
ineffective copper absorption that leads to hyperpig + course brittle gray hair
|
menke's syndrome
|
|
proteins must be broken down into what before they are absorbed
|
only aa's, di and tripeptides can be absorbed. Aa's are transported by na cotransport. Di and tri are transported by h+ cotransport
|
|
how far must carbs be digested before they can be absorbed
|
to monosaccharides
|
|
how are bile acids absorbed in terminal ileum
|
na cotransport
|
|
what can cause spontaneous bacterial peritonitis
|
ascites (i.e. from cirrhosis or nephrotic syndrome). If cirrhosis, then e coli. If nephrotic, then s pneumoniae.
|
|
pain after eating that causes weight loss in elderly
|
ischemic colitis
|
|
dilation of sinusoids due to anabolic steroids, b henselae
|
peliosis hepatitis
|
|
review notes on small and large bowel path i.e. SBO vs ischemia, etc
|
end chapter notes
|
|
what is budd chiari
|
thrombosis of IVC or hepatic veins
|
|
3 causes of cholecystitis
|
1. gallstone/obstruction (most common) 2. ischemia 3. infection -- HOWEVER, ischemia and infection is involved in pathogenesis of gallstone-related dz
|
|
effect of surgery tx on crohns
|
has tendency to spread
|
|
why are there increased renal stones in crohns
|
cuz exposed fasts on intestial mucosa bind calcium which increase oxalate absorption
|
|
another name for meissner plexus? where is it located?
|
submucosal nerve plexus, submucosa
|
|
another name for auerbach plexus? where is it located?
|
myenteric nerve plexus. muscularis externa
|
|
atrophic testes + high glucose + tan skin + malabsorption
|
hemochromatosis
|
|
apthous ulcers + chronic diarrhea + perineal abscesses
|
crohns dz
|
|
uc vs crohns: which one is autoimmune. which one is disordered response to bacteria
|
uc = autoimmune. crohns is disordered response
|
|
what type of hernia goes through both the external and internal inguinal ring? which type goes through just the external?
|
indirect hernia toes through both into the scrotum, so it is covered by all 3 layers of fascia. direct hernia goes through just the external. direct hernia is next to the rectus, and indirect is lateral to the inf epigastrics
|
|
what dzz have centrilobular hemorrhage and necrosis in liver
|
things which cause CHRONIC congestion -- budd chiari, chronic RHF, etc
|
|
where are kayser fleischer rings located in wilsons
|
cornea, not iris
|
|
where are hamartomas in NF1
|
iris, not cornea
|
|
is jejunum proximal or distal small bowel
|
considered proximal
|