11 GI

q123456's version from 2016-06-01 19:53


Question Answer
Hepatic encephalopathyincreased ammonia
decreaed BUN
In liver desease, ammonia is not efficiently converted to urea.
cholestasisreduction in bile flow>>>intestinal malabsorption of the fat soluble vitamins>>>vitamin A, E and K deficiency
vitamin D deficiency: osteomalacia
vitamin A deficiency: collisions while driving at night+dry skin
Intrahepatic Cholestasis

1) Primary biliary cirrhosis KA32-12
acholic stools and bone pain "a woman itches at night"
granulomatous destruction of interlobular bile ducts
increased serum cholesterol

2) Primary sclerosing cholangitis
prolonged pruritus and fatigue
Young male
Ulcerative colitis
hepatobiliary diseaseliver function(PT, bilirubin, albumin and cholesterol),
liver structural integrity and cellular intactness (transaminases)
the biliary tract (alkaline phosphatase and r-glutamyl transferase)
alkaline phosphatasebone and biliary tract
osteoblasts:alkaline phosphatase
osteoclasts:acid phosphatase, urinary hydroxyproline excretion and urinary deoxypyridinoline excretion
hepatic abscessS aureus
HemochromatosisAutosomal recessive, chromosome 6, HFE gene
basolateral surface of epithelial cells of the small intestine crypt
skin pigmentation and diabetes mellitus
cholecystectomyno effect on the secretion and absorption of the bile acid, but less able to tolerate large fatty meals
Bilirubinuptake by liver: passive process no ATP
secretion:active transport ATP
once in the bile, the conjugated bilirubin can enter the intestine >>>urobilinogen (by bacteria)>>>feces and urine

if can not be excreted into the biliary system>>> diffusion, hyperbilirubinemia, loosely bound to albumin>>>excreted in urine (not urobilinogen) KA31-39 KA35-25
Dubin-Johnson syndrome (Black liver)
Rotor's syndrome
UDP glucuronyl transferase:
Gilbert's (reduced activity)
Crigler Najjar (no acitivity, fatal in the neonatal period )

Fibrate >>>suppression of cholesterol 7a-hydroxylase activity>>>increased cholesterol

WOMEN, pregnancy and usage of oral contraceptive pills
estrogen>>>increase hepatic HMG-CoA>>>biosynthesis of cholesterol
progesterone>>>gallbladder hypomotility

Cholesterol stones:light yellow to dark green or brown
Bilirubin stones: pigment, dark, black
infection E COLI, Ascaris, liver fluke
B-glucuronidase>>>bilirubin glucuronides->unconjugated bilirubin >>>brown stones

Gallstone ileus: Abdominal pain, nausea and vomiting
A >2.5 cm cholesterol mass (gallstone) erodes into the interstinal lumen through a cholescystoenteric fistula>>>obstrucint the ileocecal valve>>>air in the bilary tree
Wilson diseaseLiver involvement
The slit-lamp examination
Parkinsonian like tremor and ataxia
deposition of copper of the cornea (Descemet’s membrane).
in liver, copper+a2-globulin=ceruloplasmin--->plasma, excess copper>>>bile>>>stool
Diffuse gallbladder calcificationHigh risk of gallbladder cancer
needs Cholecystectomy
***acute calculous cholecystitis:
HIDA scan: failed gallbladder visualization >>> obstruction
cirrhosisstellate cells are activated to produce a dense layer of matrix material that is deposited in the perisinusoidal space.

Collagen deposition blocks the endothelial fenestrations and prevents the free exchange of materials from the blood.

Kuppfer cells also are activated and produce cytokines that are involved in fibrosis

1 Hyperestrinism in males: liver cannot degrade androstenedione>>>Androstenedione is aromatized into estrogen in the adipose cells.
1) Gynecomastia
2) Spider telangiectasia
3) Decreases libido, erectile dysfunction

2 Reversible renal failure without renal parenchymal disease
3 Portal hypertension>>>splenomegaly, esophageal varices, hemorrhoids, periumbilical venous collarterals
4 inability to synthesize coagulation factors>>>bleeding
5 decreased synthesis of protein C/S>>>hypercoagulable
6 ascites: hypoalbuminemia and secondary hyperaldosteronism
7 increase in serum ammonia NOT UREA!!>>>hepatic encephalopathy

Portal hypertension

1 Hepatic portal vein
2 Splenic vein
3 Superior mesenteric vein
4 Inferior mesenteric vein>>>superior rectal vein (<<>>the middle and inferior hemorrhoidal veins)
Acute hepatitisp53
Fever and dark urine
Fever, fatigue, joint pain and skin rash
mononuclear cell infiltrates, hepatocyte swelling and apoptosis
Ballooning degeneration

hepatocellar cytoplasm become filled with the spheres and tubules of HBsAg>>>Granular eosinophilic appearance

T cell mediated immunity: HBV infection (not HBV induced hepatocellular carcinoma)
Hepatitis B virus does not have a cytotoxic effect itself: HBsAg/HBcAg on the cell surface stimulate the host's cytotoxic CD8+ >>>Destory infected hepatocytes
hepatocelluar carcinomaalpha-fetoprotein+liver mass
p53 mutation>>> High levels of dietary aflatoxin exposure>>>
Drug indced hepatotoxicityAminotransferase elevation/prolong PT/Liver atrophy
surgical anesthetic indced hepatotoxicity: After sugury, sudden nausea, fatigues and anorexic
Biliary sludgeA viscous mixture of small particles derived from bile. These sediments consist of cholesterol crystals, calcium salts, calcium bilirubinate, mucin, and other materials.
reye syndromehepatic failure and acute encephalopathy
children with febrile illness treated with Aspirin
mitochondrial dysfunction
Steatosis (no necrosis and inflammation)
EM shows decreased mitochondria and glycogen depletion>>>hepatic dysfunction>>>Hyperammonemia on the CNS>>>cerebral edema
Total Parenteral Nutrition (feeding IV)absent enteral stimulation>>>decreased cholecystokinin release>>>biliary staiss//// disturbance of bile acid circulation>>>cholesterol supersaturation of hepatic bile>>>gallstones


Question Answer
lactose intoleranceosmotic diarrhea

bacterial fermentation of lactose produces fatty acids and hydrogen>>>acidifies the stool, lower its pH

lactase deficiency:normal intestinal mucosa

lactose tolerance test: oral administration of 50g of lactose, with blood levels measured at 0, 60 and 120 min, blood glucose increases<20mg/dL and abdominal pain/bloating/diarrhea>>>lactose intolerance
M cells within a Peyer's patch ileal mucosaShegella
GlycoproteinThe periodic acid schiff reaction
flat plain x-raytoxic megacolon
Crohn's disease KA36-21granulomas
skip lesions
Linear ulcerations

Fistulas, strictures

bile acids are not reabsorbed by the mucosa of the terminal ileum

kidney oxalate stone
the excess lipids +calcium>>>making calcium unavailable for complexing with oxalate>>>oxalate stone

Th1 helper cells, IL-2. IFN-r
increased activity of the NF-kB protein

erythema nodosum,
pyoderma gangrenosum
ankylosing spondylitis
ulcerative colitisrectum
treatment: sulfasalazine
SE bone marrow suppression

mesalamine (5-aminosalicylic acid, 5-ASA)
olsalazine (a dimer of 5-ASA)
Celiac sprueincreased intraepithelial lymphocytes
crypt hyperplasia
blunted interstinal villi
celiac disease>>>GI inflamed and atrophic>>>vitamin D deficiency: bone pain and weakness, osteomalacia>>>Low Ca, PO4, High PTH
celiac trunkL gastric A
Splenic A-->Short gastrics and L gastroepiploic A.
Common hepatic A--->Hepatic A, Gastroduodenal A and R gastric A

a thrombus causes occlusion of the proximal part of the gastroduodenal artery. in the absence of other arterial pathology, the stomach has no infarction. Why? gastroduodenal A>>>R gastroepiploic A<->L gastroepiploic A.
distal greater curvature: R gastroepiploic A<->L gastroepiploic A.
hirschsprung diseasePresent at birth, it causes difficulty passing stool.

Aganglionic segment in large bowel (distal sigmoid and rectum)

neural crest cells to migrate to the intestinal wall
Meissner: submucosal plexi of the bowel wall
Auerbach: myenteric plexi of the bowel wall
colon cancerProgression from normal mucosa to a small polyp: APC
Increase the size of the polyp: Kras
Malignant transformation of adenoma into carcinoma: P53 and DCC
Increased activity of COX-2 Colon adenocarcinoma>>>aspirin
CEAA sensitive indicator of colorectal cancer recurrence
Energy production1 g of protein yield 4 cal of energy
1 g of carbohydrate produces 4 cal of energy
1 g of fat produces 9 cal of energy
lipidjejunum: main site of lipid absorption
duodenum:main site of digestion of dietary lipids
90% fissures occur at?the posterior midline of the anal verge
lower anal canal: inferior rectal artery/inferior rectal vein
adenomatous polypsdysplasia, villous >4 cm >>>adenocarcinoma
rectal carcinomato liver metastasis via superior rectal v (>>>IMV>>>portal V)


Question Answer
H pylorilowers somatostatin cells in the antral mucosa>>>the lack of inhibition by somatostatin >>> excessive release of gastrin >>>causes gastric acidity>>>duodenal ulcer:

causes gstric acid secretion but is protected by urease
non invasive
pyloric antrum
treatment for ulcerssucralfate: aluminum sucrose sulfate, polymerizes in the acidic environment of the stomach.
misoprostol: PGE1 agonist decreases gastric acid secretion and promotes bicarbonate and mucus production
omeprazole: inhibits the H+/K+ pump on parietal cells
cimetidine: H2 antagonist
Epigastric pain after meal+no abnormalities in GIatherosclerosis involves intestnal arteries>>>intestinal hypoperfusion
gastric carcinomaIntestinal type
metaplasia (H. pylori), Ménétrier disease(CMV, H Pylori)

Diffuse type
infiltrative growth with the stomach wall
Signet ring cells: spread hematogenously to both ovaries.

a) tingling sensation in feets or hands (pernicious anemia),
b) Metastasis to left supraclavicular node (Virchow node) / umbilicus (Sister Mary Joseph nodule)
c) Acanthosis nigricans: pigmented/axilla
d) seborrheic keratosis: Benign pigmented epidermal tumor/pseudo horn cyst formation
total gastrectomylifelong supplementation of vitamin B12
zollinger ellison syndromehypersecretion of gastrin by a pancreatic tumor
Rugal thickening with acid hypersecretion
hyperplasia of the grastric gland secondary to increased gastrin secretion from a gastrinoma (pancreatic tumor)
gastric secretionchief cells:pepsinogen, deeper lamina propria
parietal cell:hydrochloric acid and intrinsic factor, superficial lamina propria


Question Answer
GERD symptomsCouching
(systemic sclerosis)
diffuse: anti-DNA topoisomerase (anti-Scl 70)
CREST=limited scleroderma: anti-centromere

Tight, hardened skin
Raynaud's phenomenon: vessel spasms-->cold, turns white, numb
telangiectasias: red spots or lines on skin
calcium deposits under the skin
swallowing difficulties: fibrous replacement of esophageal muscles>>>dilated>>>Heartburn/Reflux>>>barrett esophagus and adenocarcinoma
Mallory Weiss syndromealcoholism
hematemesis: rapid increase of intraabdominal and intraluminal gastric pressure (vomiting)
periodic non-peristaltic contractions of a large amplitude and long durationdiffuse esophageal spasm (chest pain dysphagia not associated with exertion and is not relieved by rest, mimic unstable angina)
diverticulumzenker: cricopharyngeal muscle weakness or fibrosis, dysphagia, food aspiration>>>pneumonia

a. Vitelline (omphalomesenteric) duct remnant
(1) True diverticulum (all layers)
(2) 2 inches long, 2 feet from ileocecal valve, 2% of population, 2% symptomatic
b. Contains pancreatic/gastric mucosa
c. Clinical findings
(1) Newborn finding: Fecal material in umbilical area due to persistence of vitelline duct
(2) painless lower GI Bleeding and iron deficiency in newborns and young children

Clinically impossible to distinguish Meckel diverticulitis from appendicitis
Diagnosis: 99mTc nuclear scan identifies parietal cells in ectopic gastric mucosa

Treatment is surgery.

Colonic diverticula: mucosa and submucosa, pulsion by mechanism, false by structure
plummer vinson syndromeatrophic glossitis, esophageal webs and iron deficiency anemia>>>proximal 1/3 of esophagus>>>squamous cell carcinoma


Question Answer
vasoactive interstinal peptide VIPsecretion of water and electrolytes
relaxation of SM in GI
Lower HCl

vasoactive interstinal peptide VIPoma
pancreatic islet cell tumor
non pancreatic beta cells
watery diarrhea+achlorhydria (absence of hydrochloric acid in the gastric secretions)
pancratitisPancreatic pseudocyst.:
The cyst lacks a true epithelial lining
lined by fibrin and granulation tissue, with typical changes of chronic inflammation.
abdominal pain and vomiting after drinking, abdominal mass after several weeks

Acute pancratitis: Triglyceride levels rise to >1000 mg/dL
duodenum hormonesCCK:
I cells KA34-48
stimulated by the protein and fat,
1)increases pancreatic enzyme secretion
2)gallbladder contraction (allow more bile to enter the duodenum)
3)inhibit gastric emptying KA34-11

Secretin: S Cells. increases bicarbonate secretion from pancreas and enhances bicarbonate concentration in duodenal
pancreatectomypancreatic amylases deficiency>>>polysaccharides can not be absorbed by the intestinal mucosa, monosaccharide can e.g D-xylose (glucose and galactose)

peptsin: stomach
trypsin: pancreas
peptidases: small intestine

salivary amylase: salivary gland
pancreatic amylase: pancreas
maltase: small intestine

fat: lipase: pancreas
Octreotidemimics natural somatostatin, used for carcinoid tumor
carcinoid tumorserotonin, bradykinin, histamine, and prostaglandins
secrete serotonin>>>diarrhea, flushing, wheezing
GI, lungs
carcinoid tumors that originate in the digestive tract generally do not produce symptoms unless the tumors have spread to the liver because the liver can destroy the substances
The outflow of serotonin can cause a depletion of tryptophan leading to niacin deficiency.

5-hydroxy-indoleacetic acid

fibrous intimal thickening with endocardial plaques limited to the right heart

e.g. KA25-33,recurrent episodic diarrhea, turns red, starts wheezing, left upper lobe lung mass
Integration of viral DNA into the cellular genome of the hostactivates the IGF/receptors>>>cell proliferation


Question Answer
Prostate specific antigenProstate
Human chorioic gonadotropinGestational trophoblastic disease