appendicitis
visceral pain - due to luminal distention –> stretching of smooth muscle
- for the appendix - afferent pain fibers enter superior mesenteric plexus at level of T10 –> vague, referred pain at umbilicus
somatic pain - well-localized
psoas, obturator and Rovsing signs - if ruptured
colon cancer
right-sided = exophytic mass
left-sided = infiltrate intestinal wall
rectosigmoid cancer - hematochezia
- rectal adenocarcinoma - painful defecation and small caliber stools
CEA - also elevated in pancreatic, gastric, and breast cancers, IBD, COPD, cirrhosis, higher levels in smokers
node-positive colorectal adenocarcinoma - surgery + oxaliplatin adjuvant
UC and Crohns
both are associated with MSK abnormalities - AL, sacroilitis, migratory polyarthritis, erythema nodosum
UC - low-grade fevers
Crohns
IBS - relief with defecation
CRC is the most common malignancy in these pts - esp in UC pts. Unique features:
Compare to sporadic CRC - often arise from a polyp
malabsorption
many causes -… bacterial overgrowth (GI surgery, abnormal motility)
fats are the earliest and most severely affected in generalized malabsorption
- test for fat in stool with Sudan 3 satin
cholestasis
erythromycin, OCPs can cause cholestasis
Fe regulation
hepicidin = regulator of Fe homestasis
ferroportin - BL surface of enterocytes, transports Fe into blood
- binds hepcidin –> is internalized and degraded
transferrin - circulating, shuttles Fe from macrophages to bone marrow
- transferrin receptors are on all cells
ferritin in macrophages (which degrade RBCs) and enterocytes
- ferroportin on macrophage surface
renal tubular cells - secrete lactoferrin, binds Fe in urine
gallbladder
cystic duct + common hepatic –> common bile duct
bile - cholesterol, bile salts, PC, bilirubin
choledocal cyst - congenital dilation of common bile duct, presents will recurrent abdominal pain and jaundice during childhood
primary biliary cirrhosis - autoimmune
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cholecystitis - E coli, Enterococcus, Kleb, Enterobacter
- ouflow obstruction –> damage to protective mucosal layer (lecithin hydrolysis) –> chemical irritation (bile salts, which are bile acids plus glycine or taurine) –> inflammation and gall bladder hypomotility –> increased pressure and ischemia
porcelain gallbladder = thickened gallbladder with rim of calcification
- occurs due to chronic cholecystitis
- increased risk of adenocarcinoma of the gallbladder
alternatively - chronic cholecystitis can also lead to a shrunken, fibrotic gallbladder
acute ascending cholangitis - gram-negative infection after biliary duct obstruction
acalculous cholecystitis - occurs in critically ill (sepsis, immunosuppressed)
- secondary to gallbladder stasis and ischemia –> inflammation and injury
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pigment gallstones
- black - UCB (hemolytic anemia, Crohns disease due to increased enterohepatic cycling of bilirubin)
- brown - with biliary tract infections (microbes produce b-glucuronidase)
gallbladder hypomotility - slow emptying of gallbladder following CCK stim
- biliary sludge (gallbladder absorbs water from bile)
gallstone ileus - cholesterol-containing mass at ileocecal valve
- cholecystoenteric fistula (base of gallbladder adheres to SI) - can also get pneumobilia (air from the intestine that enters the gallbladder)
Whipple disease
distended macrophages in LP
malabsorptive diarrhea, weight loss, joint pain
pancreatic beta cells
glucose enters via GLUT2
1) first enzyme is glucokinase…enters TCA –> ATP
2) high ATP closes K channel (which normally causes K to leave the cell) –> depolarization –> Ca2 channel opens
3) Ca and cAMP (from GLP-1 receptor) cause insulin to exocytose
glucokinase has a lower glucose affinity than other hexokinases - glucose sensor in b-cells
- mutations cause a decrease in beta cell glucose metabolism and decreased insulin release
= MODY
- homozygous mutations lead to fatal growth retardation and severe hyperglycemia at birth
side note: glycolytic enzymes will present with hemolytic anemia
- aldolase A, enolase, PFK, PK
Wilsons disease
AR - reduced formation and secretion of ceruloplasmin
- and decreasing hepatic secretion of copper into the biliary system
Kayser-Fleischer ring - deposition of copper in the cornea
Cu deposits in the basal ganglia –> atrophy
treat with d-penicillamine trientine
cholesterol gallstones
cholesterol:
1) thiolase condenses two molecules of acetyl-coA
2) acetoacetyl-coA + acetyl-coA –> HMG-coA
3) RLS = HMG coA reductase turns HMG-coA into mevalonate
4) mevalonate –> cholesterol
cholesterol stones
bile acids
b-glucuronidase - deconjugates bilirubin
Campy
curved gram negative rod - moves in a corkscrew fashion
acquired from
inflammatory diarrhea - initially watery, later bloody
VS
S. aureus - ingest a preformed exotoxin, mayonnaise, vomiting
B. cereus - heat stable enterotoxin
Shigella - fomites (not animals)
V. parahemolyticus - shellfish
ulcer v.s. erosion
mucosa - muscularis mucosa - submucosa - muscularis propria - serosa
- gastric glands are located in the LP
erosion- through submucosa
ulcer - through submucosa
hemachromatosis
AR
HFE mutation - HFE normally interacts with the transferrin receptor, on BL membrane –> sensor of Fe stores
bronze diabetes (but exocrine pancreatic function is preserved)
hepatitis
acute viral hepatitis - pt presents with low-grade fever, anorexia/nausea, dark colored urine, RUQ pain
B (DNA virus, incorporates into genome) = sexual
C (RNA virus, no RT, will not integrate into host genome)= drug use, infection is most often asymptomatic
- chronic infection - lymphoid aggregates in portal tracts and focal macrovesicular steatosis
v.s. alcoholic hepatic steatosis - can see Mallory bodies (clumped, eosinophilic intracytoplasmic inclusions - made up of tangled IFs)
pancreatitis
acute interstitial pancreatitis
inflammatory process can continue –> acute necrotic pancreas
chronic alcoholic pancreatitis
chronic pancreatitis with dystrophic calcification
mu opioids (morphine) - cause contraction of the smooth muscle cells in the sphincter of Oddi –> increase in common bile duct pressures –> pts can develop severe RUQ, cramping, and biliary colic
diverticuli
true - Meckel, appendix
false - mucosa - submucosa - serosa (no muscle layer)
Meckel diverticulum - due to failure of vitelline duct (connects midgut to yolk sac) to involute completely (now if infant is passing meconium, then duct has not involuted at all)
stomach
vessels
gastrochisis - abdominal folds fail to merge
omphalocele - herniation of bowel into umbilical cord, normally happens but a 90deg rotation (around SMA) pulls bowels back into body
body:
1) parietal cells (Gq, eosinophlic) - secrete HCl and IF
- gastrin, Gq- stimulates HCl secretion and has a trophic effect on parietal cells
- histamine and Ach stimulate gastric acid secretion
- potentiation - Ach and gastrin act on ECL cells to increase histamine release
- HCl secretion phase - cephalic (vagus nerve - Ach, GRP), gastric phase, intestinal phase
- HCL inhibition - decreased pH, somatostatin, PGs, GIP, secretin
2) chief cells - pepsin, cephalic and gastric phases, local acid
in a gastric pit - mucous cells near top - parietal cells - chief cells
antrum:
G cells
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Gastritis:
acute (erosive) - due to increased acid burden (ex Cushing ulcer - increased ICP –> increased vagal stimulation)
chronic
PUD
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adenocarcinoma - general prognosis depends on depth + nodes (Virchow, periumbilical)
- signet ring carcinoma, diffuse type - leather bottle stomach (linitis plastica)
- loss of E-cadherin
- intestinal- type adenocarcinoma - glandular
- grow as nodular, polypoid, well-demarcated masses that rapidly expand in the gastric lumen
- often ulcerate/bleed (in antrum) - have to be differentiated from gastric ulcers by biopsy
- risk factors - chronic gastritis, nitrosamines, blood type A
ZE syndrome - rugal thickening and acid hypersecretion
Menetrier disease - associated with overproduction of TGFa
erythromycin
motilin receptor agonist - used for gastroparesis
neuropeptide Y
role in appetite and pain perception
- antagonist have been investigated as potential anti-obesity drugs
poliomyelitis
ORAL live attenuated vaccines
serum antibodies increase with both forms of the vaccine
nutrient absorption
stomach - pepsin is activated by HCl
enteropeptidase - brush border enzyme that activates trypsin
- trypsin activates other pancreatic enzymes (that are responsible for lipid and protein metabolism)
secretin - secreted by S cells of the duodenum
- stimulates the secretion of bicarb from pancreas and inhibits gastric acid secretion in stomach
EHEC O157:H7
EHEC O157:H7
ETEC (and Yersinia) - toxin increase cGMP