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;
325 Cards in this Set
- Front
- Back
|
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
|
chron's
|
|
|
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
|
|
|
celiac trunk pic.p.263
|
1)celiac trunk
2)common hepatic aa 3) L gastric aa 4) spelenic aa 5) hepatic aa proper 6) L hepatic aa 7)R hepatic aa 8)cystic aa 9)R gastric aa 10) gastroduodenal aa 11) R gastroepiploic aa 12) L gastroepiploic aa |
|
|
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
|
|
|
portal-systemic anastomoses [pic.p.264
|
--
|
|
|
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 |
|
|
Abdominal layers [pic.p.265]
|
--
|
|
|
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
|
|
|
billiary sxs [pic.p.266]
|
1)right hepatic duct
2)left hepatic duct 3)cystic duct 4)gallbladder 5)common hepatic duct 6)common duct 7) pancreatic duct 8)duodenum |
|
|
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 |
|
|
inguinal canal [pic.p.267]
|
--
|
|
|
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
|
|
|
Hemochromatosis-image 26
|
-
|
|
|
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
|
|
|
Bilirubin [pic.p.272
|
--
|
|
|
liver anatomy [pic.p.271]
|
--
|
|
|
apical surface of hepatocyts face ________
basolateral surface face ________ |
bile canaliculi
sinusoids |
|
|
Regulation of gastric acid secretion [pic.p.270]
|
--
|
|
|
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
|
