Unit 7 Review Flashcards
what is the source of H2O and electrolytes that are secreted in digestive secretions?
Enterocytes in the crypts of Lieberkuhn
What is the function of H2O and electrolytes secreted in digestive secretions?
serves as a vehicle for absorption for the chime as it comes in contact with villi
three major GI hormones
Ach, gastrin, histamine
what does Ach, gastrine and histamine do in GI tract
stimulate the release of acid
gastrin stimulates ( ) to secrete ( ) to promote ____ and ___
gastric gland ……. hydrochloric acid
growth of gastric mucosa and promote gastric motility
homone that increases GI motility
motilin
stimulated by chime in the duodenum, stimulates gall bladder to eject bile and pancreas to secrete alkaline fluid, slows gastric emptying
Cholecystokinin
hydrolysis: hydrogen and hydroxyl ions removed/added, splitting up food into basic parts
digestion
monosaccarides are broken down from what
carbs
fats are broken down into
fatty acids and glycerol
proteins are broken down into
amino acids
the transport of particles through and to the cells, active transport, diffusion or solvent
absorption
what bacteria is involved in the development of chronic gastritis and peptic ulcers
helicobacter pylori
H pylori cause ( ) with release of ________ ________ and reactive O2 metabolites that damage mucosal epithelial cells and cause loss of protective mucosal barrier
inflammation
inflammatory cytokines
what are methods for diagnosing H. pylori
cultures, histological staining, mucosal biopsy
urea breath tests, serum antibodies, stool and serum antigen, and gastric biopsy
protect stomach lining–stimulate the secretion of mucus and bicarbonate and by inhibiting secretion of acid
prostaglandins
destructive effect on prostaglandin synthesis
ASA and NSAIDS
Gram negative infectious agent
H. Pylori
treatment for H. pylori
bismuth, combination of abx w/vit. C to prevent relapse
peptic ulcers r/t increased gastrin: a gastrinoma (gastrin secreting neruoendocrine tumor) of the pancreas or duodenum stimulates proliferation of gastric parietal cells and chronic secretions
Zollinger-Ellison syndrome
2 out of 3 symptoms x3 months: change in bowel habits, abdominal pain, bloated feeling, mucus in stool, gas, diarrhea or constipation
IBS
inflammation anywhere in digestive tract, RLQ pain, colon thickened rocky appearance, ulcers deep and may extend into all layers of bowel wall, rectal bleeding not common
Crohn’s Diseases
colon is affected site, inflammation is continuous, not patchy, pain in LLQ, colon wall is thinner and shows inflammation, ulcers only on inner lining of intestinal walls, bleeding during BMs
ulcerative cholitis
tests for colon CA
colonoscopy, sigmoidoscopy, fecal occult blood testing CT,double contrast barium enema
bring O2 rich but nutrient poor blood to liver
hepatic arteries
bring nutrient rich but O2 poor blood to liver
hepatic veins
vessel in abdominal cavity formed by union of superior mesenteric and splenic veins that channels blood from the GI tract and spleen to capillary beds in the liver
hepatic portal vein
system of veins comprising the hepatic portal vein and its tributaries
hepatic portal system
substances absorbed in the ______ ________ travel to the liver for processing before continuing to the ( ) and on to __________ ______
small intestine
heart
general circulation
blood flows through ______ vein through _______. Blood also flows from branches of the __________ _______ and mixes in the sinusoids. The _________ _____ then drains deoxygenated blood into the ________ ______ _______.
portal vein……… sinusoids
hepatic artery
hepatic vein
inferior vena cava
role of the liver in terms of carbohydrates, protein and fat metabolism
glycogen storage, plasma protein synthesis, & bile production for digestion of lipids, synthesis of albumin-protein that helps balance body fluids
Can we survive without a liver?
No. No way to compensate for the absence of liver long term
causes of jaundice
infection, Hepatitis, parasite, drugs, poisons, birth defects, excess bilirubin, or bilirubin can’t be broken down, liver damage, gall stones, gallbladder disorder, blood disorder, pancreatitis, pancreatic CA, bile build-up r/t pregnancy–pressure in abdomen
hepato-toxic drugs
APAP, NSAIDS, amiodarone, anabolic steroids, erythromycin, OCPs, sulfonamide, phenytoin, carbamazapine, to name a few
most common drug-induced liver cell necrosis, injury largely confined to certain area or liver lobule
zonal necrosis
hepatocellular necrosis with infiltration of inflammatory cells
hepatitis
liver injury leads to impairment of bile flow and causes inflammation (or sometimes no inflammation), itching and jaundice
cholestasis
hepatoxicity manifested as triglyceride accumulation: fatty liver
steatosis
drug induced, associated with other tissue granulomas
granuloma
injury to the vascular endothelium
vascular lesions
hepatocellular CA, angiosarcoma, liver adomas
neoplasms
Hep A - source of infxn, incubation, chronic vs. acute
oral/fecal, 15-50 days, no chronic, only acute
Hep B - source, incubation, chronic vs. acute
blood and bodily fluids, 45-160 days, acute to chronic
Hep C - source, incubation, chronic vs. acute
blood and bodily fluids, 14-180 days, acute - rare, chronic can lead to cirrhosis
Hep D - source, incubation, chronic vs. acute
blood and bodily fluids, needs HBV to survive, 3-7 weeks, acute leads to chronic, difficult to treat with HepB
Hep E - source, incubation, chronic vs. acute
oral/fecal, 3-8 wks, acute unless immunocompromised
bile contains too much cholesterol and not enough bile salts, infrequent emptying and contracting of gall bladder & proteins in liver and bile that promote or inhibit cholesterol crystallization
causes of formation of gall stones
risk factors for pancreatitis
ETOH, smoking, gallstones, ERCP, abdominal trauma, carcinoma, drugs, penetrating ulcers, infections, mumps, hepatitis
sudden inflammation and edema of the pancreas, leading to necrosis and secondary injury to extrapancreatic organs
pancreatitis
treatment of pancreatitis
NPO, rest pancreas, surgery - remove gall bladder or stones,aggressive fluid rehydration, ICU, surgery
gall bladder disease is usually treated by…
removing gall bladder
deadly CA–abdominal or back pain, jaundice, wt loss, light colored stools, dark urine,
pancreatic CA
reasons canc of the panc is so deadly…
rarely detected early, spreads very quickly, (easy access to nearby organs), recurrence is likely, relatively resistant to chemotherapy
diverticular disease occurs in the…
large intestine.