GI USMLE Flashcards
baby vomits milk when fed and has a gastric air bubble. What kind of fistula is present?
blind esophagus w/ lower segment of esophagus attached to trachea
After a stressful life event, 30 y/o female has diarrhea and blood per rectum; intestinal bx shows transmural inflammation. what is thedx
crohn’s dz
young man presents w/ mental deterioration and tremors. he has brown pigmentation in a ring around the periphery of his cornea and altered LFTs. What tx should he receive?
penicillamine for wilson’s dz
20y/o male presents w/ idiopathic hyprbilirubinemia. what is the most common cause?
Gilberts dz
Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
Foregut
Celiac aa
stomach to prox duodenum, liver, gallbladder, pancreas
Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
midgut
SMA
distal duodenum to prox 2/3 of transverse colon
Given the embrionic gut region, give the aa that supplies it and the sxs supplied:
hndgut
IMA
distal 1/3 of transvere colon to upper portion of the rectum
Stoach recieves main blood supply from branches of this ________
celiac trunk
because of portal-systemic anastomoses blockage of 1 vv can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.
L gastric →azygous
What is this a common complication with?
esophageal varicies
Portal HTN
mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension
because of portal-systemic anastomoses blockage of 1 aa can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.
Superior →inferior rectal
What is this a common complication with?
external hemorrhoids
mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension
because of portal-systemic anastomoses blockage of 1 vv can result in congestion of blood in an alternate route. Given the backup what type of pathology would you see.
Paraumbilical →inferior epigastric
What is this a common complication with?
caput medusae at naval
mneu: varices of GUT, BUTT, and CAPUT are commonly seen with portal hypertension
because of portal-systemic anastomoses blockage of 1 artery can result in congestion of blood in an alternate route. What two places do the the retroperitonal vv usually back up to?
renal and paravertebral vv
layers of gut wall (inside to outside)[pic.p.264]
1) mucosa
2) submucosa
3) muscularis externa
4) serosa/adventita
mucosal layer consists of these three layers (give fxs as well)
epithelium (absorption) lamina propria (support) muscularis mucosa (mucosal motility
Submucosa includes this nerve plexus that controls these fxs
Submucosal (Meissner’s)
controls Secretions, blood flow, and absorption
Muscularis externa includes this nerve plexus that controls these fxs
Myenteric nerve plexis (Auerbach’s)
controls mobility
Muscularis externa has these two layers of mm
outer longitudinal layer
inner circular layer
This enteric nerve plexus coordinates MOTILITY along the entire gut wall. It contains cell bbodies of some parasympathetic terminal effector neurons. It is located between inner and outer layers (longitudinal and circular) smooth mm in the GI tract wall
Myenteric (Auerbach’s) plexus
This enteric nerve plexus regulates local SECRETIONS, blood flow, and absorption. It contains cell bodies of some parasympathetc terminal effector neurons. It is located between the mucosal and inner layer of smooth mm in the GI tract wall.
Submucosal (Meissner’s) plexus
These glands secrete alkaline mucus to neutrolize acid contents entering the duodenum from the stomach. They are located in the duodenal submucosa.
brunners glands
these are the only GI submucosal glands
brunner’s glands
hypertrophy of Brunner’s glands is seen in what dz
Peptic Ulcer dz
Unencapsulated lymphoid tissue found in lamina propria and submucosa of the small intestine
Peyer’s patch
Peyer’s patches are covered by a single layer of cuboidal enterocytes with specialized _____ cells intersperced.
M cells
Are their goblet cells in peyer’s patches
no
______ take up antigen.
M cells.
Stimulated _____ leave Peyer’s patch and travel through lyph and blood to lamina propria of the intestine, where they differentiate into __________.
M cells
IgA-secreting plasma cells
_____ receives protective secretory component and is then transported across epithelium to gut to deal with intraluminal Ag
IgA
Irregular “capillaries” with fenestrated endothelium (pores 100-200 nm in diameter). No basement membrane. Allows macromolecules of plasma full access to basal surface of hepatocytes through perisinusoidal space (space of Disse)
Sinusoids of liver
line formed where hindgut meets ectoderm
pectinate line
Above pectinate line or below pectinate line:
internal hemorrhoids (not painful)
above pectinate line
Above pectinate line or below pectinate line:
external hemorrhoids (painful)
below pectinate line
Above pectinate line gets _________ innervation (visceral or somatic innervation)
Viscral
internal hemorrhoids receive ________ innervation
visceral
arterial supply of above the pectinate line is from the _________
superior rectal artery (branch of IMA)
venous drainage of above the pectinate line is to the _________ to the IMV to the portal system
supierior rectal vein
cancer associated with above pectinate line is _________
adenocarcinoma
Below pectinate line is innervated via ________ innervation
somatic
external hemorrhoids recieve _______ innervation and are therefore quite painful
somatic
cancer associated with below pectinate line
squamous cell carcinoma
arterial supply to below pectinate line
inferior rectal aa (branch of internal pudendal aa)
venous drainage of below pectinate line is to _______ to internal pudendal vv to internal iliac vv to IVC
inferior rectal vv
lateral to medial in the femoral triangle
which of these sxs lie inside the femoral sheath
femoral nn, aa, vv, empty space and lymphatics (deep inguinal LNs
all except femoral nn lie in the sheath
mneu: N-(AVEL)
what sxs make up the femoral triangle
1) sartorius mm
2) inguinal ligament
3) adductor longus mm
this drug class consists of Cimetidine, rantidine, famotidine, nizatidine
H2 blockers
these drugs reversibly block histamine H2 receptors leading to decreased H+ secretion by parietal cells
H2 blockers (tidines)
these drugs are used for peptic ulcer, gastritis, mild esophageal reflux
H2 blockers (tidines)
This drug is a potent inhibitor of P-450; it also has an antiadrogenic effect and decreased renal excretion of cratinine. Other H2 blockers are relatively free fo these effects
Cimetidine
these drugs include omeprazole, lansoprazole
protone pump inhibitors (prazoles)
these drugs work by irreversibly inhibiting H+/K+ATPase in stomach parietal cells
protone pump inhibitors (prazoles)
These drugs are used for peptic ulcers, gastritis, esophageal reflux, and zollinger-ellison syndrome
protone pump inhibitors (prazoles)
these drugs work by binding to the ulcer base, providing physical protection, and allowing HCO3- secretion to reestablish pH gradient to the mucus layer
Bismuth, sucralfate
these drugs are used to help in ulcer healing and traveler’s diarrhea
Bismuth, sucralfate
triple therapy of H. pylori ucers includes
1) metronidazole
2) bismuth
3) amoxicillin (or tetracycline)
this drug is a PGE1 analog that increases production and secretion of gastric mucous barrier, and decreases acid production
misoprostol
this drug is used clinically to prevent NSAID-induced peptic ulcers, maintain a patent ductus arteriosus, and to induce labor
misoprostol
toxicity of this drug includes diarrhea. It is contraindicated in women of childbearing potential (abortifacient)
misoprostol
drugs of these this class includes pirenzepine & propantheline
muscarinic antagonist
these drugs act by blocking M1 receptors on Enterochromaffin-like (ECL) cells (decreasing histamine secretion) and M3 receptors on parietal cells (decreased H+ secertion)
Muscarinic antagoinists
these drugs are clinically indicated only for peptic ulcer
muscarinic antagonist
these drugs toxicieite include bradycardia, dry mouth, difficulty focusing eyes
muscarinic antagonist
this drug is a monoclonal antibody to TNF-alpha, a proinflammatory cytokine
infliximab
this drug is used for Crohn’s dz & rheumatoid arthritis
infliximab
this drug for crohns dz and arthritis has toxicities that include respiratory infection, fever, hypotension
infliximab
These drugs act with a combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory) which is activated by colonic bacteria.
sulfasalazine
this drug is used clinically for ulcerative colitis & crohn’s dz
sulfasalazine
the toxicities of this drug include malaise, nausea, sulfonamide toxicity, reversible oligospermia
sulfasalazine
This drug is a 5-HT3 antagonist.
Ondansetron
this drug is used to control vomiting postoperatively and in patients undergoing cancer chemotherapy
ondansetron
you will not vomit with ONDANSetron, so you can go ON DANCing.
toxicities of this antiemetic include headache and constipation
ondansetron
overuse of these drugs can affect absorption, bioavaiability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
antacid
Antacids:
Primary SEs of Aluminum hydroxide
constipation and hypophosphetemia
mneu: aluMINIMUM amount of feces
Antacids:
Primary SEs of magnesium hydroxide
diarrhea
mneu: Mg- Must Go to the bathroom
Antacids:
Primary SEs of calcium carbonate
hypercalcemia and rebound acid increase
all antacids can cause _______
hypokalemia
This is a very aggressive CA, prognosis averages 6 mo. or less, usually already metastasized at presentation.
panceratic adenocarcinoma
pancreatic adenocarcinomas are more common in the pancreatic ______(head or tail)
head–obstuctive jaundice
this often presents with:
1) abd pain radiating to back
2) weight loss (due to malabsorption & anorexia)
3) migratory thrombophlebitis (trousseau’s syndrome)
4) obstructive jaundice w/ palpable gallbladder (courvoisier’s sign)
pancreatic adenocarcinoma
this is caused by activation of pancreatic enzymes leading to autodigestion
acute pancreatitis
causes of acute pancreatitis
Gallstones Ethanol Trauma Steroids Mumps Auutoimmune dz Scorpion sting Hypercalcemia/Hyperlipidemai Drugs (e.g., sufla drugs)
mneu: GET SMASHeD
this can cause fatal pancreatitis
ddI (videx)
what is the clinical presentaton of acute pancreatitis
pt presents w/ epigastric abdominal pain raiating to back with anerexia and nausia
what 2 labs will be elevated in acute pancratitis
amylase, lipase
amylase and lipase which has the higher specificity
lipase
acute pancreatitis can lead to (give 3)
DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation, hemorrhage, and infection
chronic calcifying pancreatitis is strongly associated with _______
alcoholism
chronic obstructive pancreatitis is stongly associated with ______
gallstones
these form when solubizing bile acids and lecithin are overwhelmed by increased cholesterol and/or bilirubin
gallstones
risk factors for gallstones
1) fat
2) female
3) fertile
4) forty
3 types of gallstones
1) cholesterol stones
2) mixed stones
3) pigment stones
these stones are radioluscent with 10-20% opacity due to calcifications. They are associated with obesity, Crohn’s dz, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss, and Native American origin
Cholesterol stones
these stones are the most common type. They are radioluscent and they have both cholesterol and pigment components.
mixed stones
these stones are radiopaque. They are seen in pts w/ chronic RBC hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.
pigment stones
how do you dx gallstones
US
how do you tx gallstones
cholecystectomy
rare, often fatal childhood hepatoencephalopathy. Findings include fatty liver (microvesicular fatty change), hypoglycemia, and coma. It is associated with viral infection (especially VZV and infuenza B) and salysylates; thus, aspirin is no longer recommended for children (use acetaminophen, with caution)
Reye’s syndrome
Most common primary malignant tumor of the liver in adults.
hepatocellular carcinoma (hepatoma)
this CA is associated with hepatitis B & C, Wilson’s dz, hemochromatosis, alpha 1 antitripsin deficiency, alcoholic cirrhosis, and carcinogins (e.g., aflatoxin B1)
hepatocellular carcinoma.
this CA can present with tender hepatomegaly, ascites, polycythemia, and hypoglycemia
hepatocellular carcinoma
hepatocellular carcinoma, like renal cell carcinoma, is commonly spread via this method of dissemination
hematogenous
HCC shows elevated serum _________ level
alpha fetaprotien
HCC may lead to this syndrome ______.
Budd-Chiari syndrome
intrahepatic, autoimmune disorder characterized by severe obstructive jaundice, statorrhea, pruritis, hypercholesterolemia (xanthoma).
labs show: ↑alk phos, ↑ serum mitochondrial Ab
primary billiary cirrhosis
this disorder is due to extrahepatic biliary obstruction. Increased pressure in intrahepatic ducts leading to injury/fibrosis. Often complicated by ascending cholangitis (bacterial infection), bile statis, and “bile lakes.”
labs show: ↑alk phos & ↑conjugated bilirubin
secondary biliary cirrhosis
both intra- and extrahepatic. Inflamation and fibrosis of bile ducts leads to alternating strictures and dilation with “beading” on ERCP.
Primary sclerosing cholangitis
Primary sclerosing cholangitis us assiciated with ________
ulcerative colitis
Primary sclerosing cholangitis can lead to _______
secondary biliary cirrhosis
charcot’s triad of cholangitis
1) jaundice
2) fever
3) RUQ pain
mildly ↓ UDP-glucuronyl transferase. Asymptomatic but unconjugated bilirubin is elevated without overt hemolysis. Associated with stress
Gilbert syndrome
Absent UDP-glucuronyl transferase. Presents early in life; pts die within a few years.
Crigler-Najjar syndrome, type I
Findings include: juandice, kernicterus (bilirubin deposition in brain), ↑ unconjugated bilirubin.
Crigler-Najjar syndrome, type I
treatment of Crigler-Najjar syndrome, type I
plasmapheresis and phototherapy
Crigler-Najjar type I is a severe dz. Type II is less severe and responds to _______
phenobarbital
this d/o is due to conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.
Dubin-Johnson syndrome.
this syndrome is similar to Dubin-Johnson syndrome but even milder and does not cause black liver.
Rotor’s syndrome
normally, liver cells convert unconjugated (indirect) bilirubin into _________ bilirubin
conjugated (direct)
_______ is water soluble and can be excreted into urine
Direct bilirubin
The liver converts some of the direct bilirubin into bile to be converted by gut bacteria to ________
urobilogen
Some urobilogen is _______
reabsorbed.
Some urobilinogen is also formed directly from ________
heme metabolism
Give the jaundice type:
conjugated/unconjucated hyperbilirubinemia
↑ urine bilirubin
nml/↓ urine urobilinogen
hepatocellular jaundice
Give the jaundice type:
conjugated hyperbilirubinemia
↑ urine bilirubin
↓ urine urobilinogen
obstructive jaundice
Give the jaundice type:
unconjucated hyperbilirubinemia
no urine bilirubin
↑ urine urobilinogen
hemolytic jaundice
deposition of hemosiderin (iron)
hemosiderosis
dz caused by iron deposition
hemochromatosis
classic triad of hemochromatosis
1) micronodular cirrhosis
2) pancreatic fibrosis
3) skin pitmentation
hemochromatosis can lead to this autoimmune dz
“bronze” dbts
hemochromatosis results in this heart condition
CHF
increased risk of this CA with hemochromatosis
HCC
primary hemochromatosis follows this inheritance pattern
autosomal recessive
secondary hemochromatosis is due to this
chronic transfusion therapy
Labs for this dz show ↑ ferritin, ↑ iron, ↓ TIBC which results in ↑ transferrin saturation
hemochromatosis
tx hemochromatosis w/
phlebotomy, defoeroxamine
this dz is due to inadequate hepatic copper excretion and failure of copper to enter circulation as ceruplasmin. It leads to copper acccumulation, especially in liver, brain, cornea, kidneys, joints. Itis also known as hepatolenticular degenration
Wilson’s dz
what is the inherritance pattern of Wilson’s dz
autosoma-recessive
how do you tx Wilson’s dz
penicillamine
Wilsons dz is characterized by:
ABCD
Asterixis
Basal ganglia degeneration (parkinsonian symptoms
↓Ceruplasmin, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular, Choreiform movements
Dementia
this syndrome is due to occlusion of IVC or hepatic veins with centrilobular congestion & necrosis, leading to congestive liver dz (hepatomegaly, ascites, abdoinal pain, and eventual liver failure). It is associated with polycythemia vera, pregnancy, hepatocellular carcinoma
Budd-Chiari syndrome
This dz shows swollen and necrotic hepatocytes, neutorphil infiltration, mallory bodies, fatty change, and sclerosis around the central vein. SGOT (AST) to SGPT (ALT) ratio is usually >1.5
alcoholic hepatitis
mneu: A Scotch and Tonic: AST elevated (>ALT) w/ alcoholic hepatitis
ALT> AST in viral hepatitis
Cirrho (greek) =
tawny yellow
in portal hypertension esophageal verices can lead to these 2 things
hematemesis and melana
in portal hypertension peptic ulcers can lead to
melana
splenomegly, caput medusae, ascites, hemorrhoids, esophageal veraces, melana are all symptoms of
portal hypertension
coma, scleral icterus, fetor hepaticus (bad breath), spider nevi, gynomastia, jaundice, loss of sexual hair, asterixis (coarse hand tremor), increased PTT, anemia, ankle edema, are effects of this
effects of liver cell failure
in cirrhosis there is diffuse _____ of liver, which destoys normal architecture
fibrosis
in cirrhosis there is nodular regeneration. Micronodular nodules (<3mm) tend to be due to _______
metabolic insult (e.g.,e alcohol, hematochromatosis, Wilson’s dz)
in cirrhosis there is nodular regeneration. Macronodular nodules (>3mm) tend to be due to _______
post infectious or drug induced hepatitis
these nodules represent an increased risk for what CA?
HCC
A portacaval shunt between these 2 vv may relieve portal hypertension
splenic vv & L renal vv
this is the 3rd most common CA. Risk factors include: colorectal villous adenomas, chronic inflammatory bowel dz, high fat and low fiber diets, increaed age, familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal CA (HNPCC), DCC gene deletion, & + family hx.
colorectal CA
What is Peutz-Jeghers? Is it a risk factor for colorectal CA?
a benign polyposis syndrome
not a risk factor
who and how do you screen for colorectal CA
pts >50 w/ stool guiac, and colonoscopy
this is visualized on barium swallow x-ray as “apple core” lesion”
colorectal CA
this is a nonspecific tumor marker for colorectal CA
CEA
this is a congenital megacolon characterized by lack of enteric nervous plexus in a segment (Auerbach’s and Meissner’s plexuses) due to failure of neural crest and cell migration It presenta as chronic constipation early in life.
Hirschsprung’s dz
mneu: think of a giant spring that has SPRUNG in the colon
in hirschrung’s dz the dialated porion of the colon proximal to the aganglionic segment is called ________
transition zone
pts w/ this syndrome are at increased risk for hirschrung’s dz
downs syndrome
“telescoping” of 1 bowel segment into distal segment; can compromise the blood supply. Often due to intraluminal mass
Intussuption
twisting of portion of bowel around its mesentery; can lead to obstruction and infection. May occur at sigmoid colon, where there is redundant mesentery
Volvulus
blind pouch leading off the alimentary tract, lined by mucosa, muscularis, and serosa, that communicates with the lumen of the gut
diverticulum
this type of diverticulum consists of an outpouching of all 3 gut wall layers
true diverticulum
In this type of diverticulum, only the mucosa and submucosa outpouch
false diverticulum
this type type of diverticulum occurs especially where vasa recta perforate the muscularis externa
false diverticulum
Most diverticula are aquired are termed “false” in that they lack what
muscularis externa
most false diverticula exist where?
sigmoid colon
many diverticula is refered to as ________
diverticulosis
prevelence of diverticulosis in pts >60 is ~ ________.
50%
this condition is caused by increased intraluminal pressure and focal weakness in the colonic wall
diverticulosis
diverticulosis most frequently involves what part of the GI tract?
sigmoid colon
diverticulosis is associated with what type of diet?
low fiber
give common presenting symptoms of diverticulosis
asymptomatic or associated with vague discomfort and/or rectal bleeding
this is an inflammation of diverticula classically causing LLQ pain. It may lead to perforation, peritonitis, abscess fromation, or bowel stenosis.
diverticulitis
pt presents w/ initial diffuse periumbilical pain that then becomes localized to pain at McBurney’s point. Nausea and fever may accompany.
appendicitis
while this occurs in all age groups it is the most common indication for emergent abdominal surgery in children
appendicitis
appendicitis may perferate and become what?
peritonitis
important d/d of appendicitis in the elderly
divrticulitis
important d/d of appendicitis in women of childbering age
ectopic pregnancy
women of childbering age presents w/ pain that may be appendicitis or may be ectopic pregnancy–what is you’re next step.
order B-hCG to r/o ectopic
two most common types of inflammatory bowel dz
crohn’s dz, ulcerative colitis
possible etiology of crohn’s
infectious
possible etiology of ulcerative colitis
autoimmune
location of crohn’s
may involve any portion of GI, usually involves the TERMINAL ILIUM and colon. SKIP LESIONS. RECTAL SPARING
mneu: For CHROHN’S,think of a FAT GRANny and an old CRONE SKIPPING down a COBBLESONE road away from the WRECK (rectal sparing)
location of UC
COLITIS=colon inflamation. CONTINUOUS. ALWAYS RECTAL INVOLVEMENT.
Gross morphology of this IBD includes transmural inflammation. COBBLESTONE mucosa, creeping FAT, bowel wall thickening (“string sign” on barium swallow x-ray), linear ulcers, fissures, fistulas
CD
mneu: For CHROHN’S,think of a FAT GRANny and an old CRONE SKIPPING down a COBBLESONE road away from the WRECK (rectal sparing)
Gross morphology of this IBD includes mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentery
UC
Microscopic morphology of this IBD includes noncaseating GRANulomas and lymphoid aggregates.
CD
mneu: For CHROHN’S,think of a FAT GRANny and an old CRONE SKIPPING down a COBBLESONE road away from the WRECK (rectal sparing)
on mircroscopic morphology this IBD, shows crypt absesses and ulcers, bleeding, no granulomas
UC
complications of this IBD includes strictures, fistulas, perianal dz, malabsorption, nutritional depletion
CD
complications of this IBD includes severe stenosis, toxic megacolon, COLORECTAL CARCINOMA
UC
extraintestinal manifestations of this IBD includes migratory polyartheritis, erythema nodosum, ankylosing spondylitis, uveitis, immunologic disorders
CD
extraintestinal manifestations of this IBD includes pyoderma gangrenosum. Primary sclerosing cholangitis
UC
this type of CA is associated w/ dietary nitrosamines, achlorhydria, and chronic gastritis.
stomach CA
stomach CA is almost always this type of CA
adenocarcinoma
Stomach CA has early aggressive local spread to to the LN & this location.
liver
Stomach CA is turmed this when it is diffusely infiltrative w/ a thickened, rigid appearance.
linitis plastica
what is Virchow’s node
mets from stomach to supraclavicular node
what is Krukenberg’s tumor
bilateral mets to ovaries
Krukenberg’s tumor is characterized by abundant mucus and these type of cells
“signet ring” cells.
in Gastric ulcers pain is ________(greater or lesser) with meals
Greater - often results in weight loss
in Duodenal ulcers pain is ________(greater or lesser) with meals
lesser-often results in weight gain
H pylori is _____% in gastric ulcers and ______% in duodenal ulcers
G-70%
D-~100%
this type of ulcer is due to DECREASED MUCOSAL PROTECTION against gastric acid
Gastric ulcer
this type of ulcer is due to INCREASED GASTRIC SECRETION OR DECREASED MUCOSAL PROTECTION
Duodenal ulcer
associated with hypertrophy of Brunner’s glands
duodenal ulcer
tend to have clean, “punched-out” margins unlike the raises/irregular margins of carcinoma.
duodenal ulcers
give 2 potential complications of duodenal ulcers (2)
bleeding, penetration, perforation, and obstruction.
“triple therapy” for H pylori.
metronidazole, bismuth salicylate, and either amoxicillinn or tetracycline with or without a PPI.
incidence of peptic ulcer is 2ce in this group of people
smokers
disruption of mucosal barriers leads to inflammation
acute gastritis
acute gastritis is ______ (erosive or nonerosive)
erosive
chronic gastritis is ______ (erosive or nonerosive)
nonerosive
give 3 causes of acute gastritis
stress, NSAIDs, etoh, uricemia, burns, and brain injury
this type of ulcer is caused by burns
Curling’s ulcer
this type of ulcer is caused by brain injuury
cushing’s ulcer
what are the 2 types of chronic gastritis
type A -fundal
type B- antral
this type of chronic gastritis is caused by an autoimmune d/o characterized by autoantibodies to parietal cells, pernicious anemia, and Achlorhydria
type A-fundal
mneu: type A=4As
this type of chronic gastritis is caused by H. pylori infection
type B-antral
mneu: Type B= a Bug, H. pylori
Both types of chronic gastritis carry an increased risk of this
gastric carcinoma
this results from glandular (columnar epithelial) metaplasia–replacement of nonkeratinized squamous epithelium with gastric (columnar) epithelium in the distal esophagus. Due to chonic acid reflex.
Barrett’s esophagus
mneu: BARRett’s = Becomes Adenocarcinoma, Results from Reflux
give the common dx from the labs:
ALT>AST
viral hepatitis
give the common dx from the labs:
ALT<AST
alcoholic hepatitis
give the common dx from the labs:
AST only
MI
this is elevated in various liver dz
GGT (gamma glutamyl transpeptidase)
give the common dx from the labs:
elevated alk phos
obstructive liver dz (HCC)
bone dz
give the common dx from the labs:
increased Amylase
acute pancreatitis, mumps
give the common dx from the labs:
increased Lipase
Acute pancreatitis
decreased Ceruloplasmin
Wilson’s dz
Most common congenital anomaly of the GI tract. persistence of the vitelline duct or yolk stalk
merkel’s diverticulum
cystic dilation of vitelline duct
omphalomesenteric cyst
this may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue
merkel’s diverticulum
Give the 5 2s of Merkel’s diverticulum
2 in. long 2 feet from ileocecal valve 2% of population presents 2st 2 yrs of life may have 2 types of epithelia
failure of relaxation of lower esophageal sphincter due to loss of myenteric (Auerbach’s plexus
Achalasia
Causes progessive dysphagia. Barium swallow shows dilated esophagus w/ an area of distel stenosis.(“Bird Beak” on barium swallow.)
Achalasia
A-chalasia means
absense of relaxation
achalasia is associated with an increased risk of this.
esophageal carcinoma
Secondary achalasia may arise from this dz
Chagas’ dz
protrusions of peritoneum through an opening, usually sites of weakness
abdominal hernia
in this type of hernia abdominal sx enter the thorax. it may occur in infants as a result of defective development of pleuroperitoneal membrane
diaphragmatic hernia
this is the most common diaphragmatic hernia, in which the stomach herniates upward through the esophageal hiatus of the diaphram
hiatal hernia
This type of hernia goes through the INternal (deep) inguinal ring and external (superficial) inguinal ring and INto the scrotum.
Indirect inguinal hernia
This type of hernia bulges directly throgh the abdominal wall medial to inferior epigastric artery.
direct
MDs don’t LIe:
Medial to inferior epigastric artery=Direct hernia
Lateral to inferior epigastric artery=Indirect hernia
This type of hernia enters the inguinal ring lateral to inferior epigastric artery.
indirect
MDs don’t LIe:
Medial to inferior epigastric artery=Direct hernia
Lateral to inferior epigastric artery=Indirect hernia
Indirect hernias occur in ______ owing to failure of processus vaginalis to close. They are much more common in males
infants
this type of hernia protrudes through the inguinal (Hesselbach’s)triange. It goes through the external (superficial inguinal ring only. It often occurs in older men.
direct inguinal hernia
abdominal hernias [pic.p.273]
1) inferior epigastric vessels
2) rectus abdominus mm
3) inguinal (Poupart’s ligament)
4) direct inguinal hernia (through hesselbach’s triangle)
5) indirect inguinal hernia
hesselbach’s triangle includes:
1) inferior epigastric aa
2) lateral border of rectus abdominis
3) inguinal ligamnent
what is bile composed of (6)
bile salts cholesterol phospholipids bilirubin water ions
what are bile salts
bile acids conjugated to glycene or taurine to make them water soluable
this is a product of heme metabolism
bilirubin
bilirubin is actively taken up by these cells
hepatocytes
this type of bilirubin has been conjugated with glucuronic acid and is water soluble
direct bilirubin
this type of bilirubin is water insoluble
unconjugated
this describes yellowign of the skin and sclera as a result of elevated bilirubin levels
jaundice
apical surface of hepatocyts face ________
basolateral surface face ________
bile canaliculi
sinusoids
in carbohydrate digestion only this type of molecule is absorbed
monosaccaride (glucose, fructose, galactose)
this amylase starts digestion, it hydrolyzes alpha-1-4 linkages to yield disaccharides (maltose, maltotriose, and alpha-limit dextrans).
salivary amylase
this amylase is in highest concentration in duodenal lumen, it hydrolyzes starch to oligosaccharides and disaccarides
pancratic amylase
this amylase is at the brush border of intestines. It is the rate-limiting step in carbohydrate digestion. It produces monosaccarides from oligo-and disaccharides
oligosaccharide hydrolases
name the portion of the GI tract where the following substances would be absorbed:
etoh
stomach
name the portion of the GI tract where the following substances would be absorbed:
glucose via Na+cotransporter vit A & D Fatty acids Iron Ca++
duodenum
name the portion of the GI tract where the following substances would be absorbed:
glucose, galactose, monosaccharides, disaccharides, vit A & D
Fatty acids,
PROTIENS and AMINO ACIDS
proximal Jejunum
name the portion of the GI tract where the following substances would be absorbed:
WATER SOLUBLE VITAMENS
disaccharides
fatty acids
proteins and amino acids
terminal jejunum
name the portion of the GI tract where the following substances would be absorbed:
protiens and amino acids
VIT B12
BILE SALTS
*acts as a reserve can absorb additonal nutrents if required
Ileum
name the portion of the GI tract where the following substances would be absorbed:
H2O
K+
NaCl
Short chain fatty acids
Colon
Give the 4 glands that secrete saliva
parotid, submandibular, submaxillary, and sublingual
this component of saliva begins starch digestion. It is inactivated by low pH upon reaching the stomach
alpha-amylase (ptalin)
this component of saliva neutralizes oral bacterial acids and maintains dental health
bicarbonate
this component of saliva lubricates food
mucins (glycoproteins)
salivary secretion is stimulated by what?
autonomics-sympathetic & parasympathetic
sympathetic secretion of saliva occurs via this ganglion?
Superior cervical ganglion (T1-T3)
parasympathetic secretion of saliva occurs via these nerves?
facial & glossopharyngeal
with a low flow rate of saliva(sympathetic)expect this type of saliva
hypotonic
with a high flow rate of saliva(parasympathetic)expect this type of saliva
isotonic
intrinsic factor comes from these cells in what part of the GI
parietal cells of the stomach
the action of this GI secretory product is to function as a vit B12 binding protien which is required for B12 uptake in terminal ileum
intrinsic factor
autoimmune destruction of parietal cells results in what 2 conditions
chronic gastritis and pernicious anemia
gastric acid comes from what cells in what part of the GI tract
parietal cells of the stomach
what is the action of gastric acid
lower stomach pH
histimine, ACh, and gastrin act to ____ secretion of gastric acid
increase
somastatin, GIP, prostaglandin, secretin act to ___secretion of gastric acid
decrease
Pepsin is secreted by what cells in what part of the GI tract
chief cells of the stomach
pepsin functions how
protien digestin
what pH is the optimal fx of pepsin
1-3
pepsin production is ___ by vagal stimulation and local acid
increased
inactive pepsinogen is convertid to pepsin by _____
H+
HCO3- is produced by these cells in these 2 parts of the GI tract
mucosal cells in the stomach and duodenum
the fx of this GI secretory product is to neutrolize acid and prevent autodigestion
HCO3-
HCO3 release is stimulated by this?
secretin
gastrin is produced by these cells in this part of the stomach
G cells
antrum
this GI secretory product acts to increase gastric H+ secretion, increae growth of gastric mucosa, and increase gastric motility
gastrin
gastrin release is ____ by stomach distension, amino acids, peptides, vagal stimulation
increased
gastrin release is ____ by H+ secretion and stomach acid pH<1.5
decreased
gastrin release is increased in this CA
Zollinger-Ellison syndrome
phenylalanine and tryptophan are potent stimulators of this hormone
gastrin
Where is Cholescystokinin released from? Give cells and GI location.
I cells
duodenum
jejunum
this GI secretory product acts to increase pancreatic secretion, increase gallbladder contraction; decrease gastric emptying, increase growth of exocrine pancrease and gallbladder
Cholescystokinin (CKK)
cholecystokinin is ___ by secretin ans stomach pH <1.5
decreased
cholecystokinin is ___ by fatty acids and amino acids
increased
In cholelthiasis, pain worsens after fatty food ingestion due to this
increased CCK
What cells and GI location is secretin from
S cells
duodenum
what is the action of secretin
increased pancreatic HCO3- secretion and decreased gastric acid secretion
secretin is ___ by acid, and fatty acids in the lumen of the duodenum
inceased
increased HCO3- neutralizes gastric acid in the duodenum, allowing these enzymes to function
pancreatic
where does somatostatin come from? give the cell and the GI location
D cells in the pancreatic islets and GI mucosa
this GI secretory product acts to decrease gastric acid and pepsinogen secretion, decrease pancreatic and small indestine fluid secretion. decrease gallbladder contraction. decrease insulin and glucagon release
somatostatin
somatostatin is ____ by acid ____ by vagal stimulation
increased
decreased
this hormone is considered an inhibitory hormone with antigrowth effects (digestion and absorption of substances are needed for growth)
somatostatin
Where is gastric inhibitory peptide released from. Give the cell and the location in the GI.
K cells
duodenum and jejunum
what is the exocrine fx of of GIP
decrease gastric acid secretion
what is the endocrine fx of of GIP
increase insulin release
GIP is ____ by fatty acids, amino acids, & oral glucose.
increaed
this is the only GI hromone stimulated by all three nutrient glasses (amino acids, & oral glucose)
GIP
why is an oral glucose load used more rapidly than the equivalent given by IV
GIP
cholecystokinin is ___ by secretin ans stomach pH <1.5
decreased
cholecystokinin is ___ by fatty acids and amino acids
increased
In cholelthiasis, pain worsens after fatty food ingestion due to this
increased CCK
