GI 7 Flashcards
what is diarrhea?
-an increase in the frequency, volume and fluid content of the feces due to increased secretion, reduced absorption and increased motility
-2 million people die from every year
four types
-osmotic: H2O stays in GI and solute stays in lumen
-secretory: own immune cells or bacteria
-inflammatory: bacterial infection
-motility induced: dont know yet
what is clostridium difficile (infection of GI tract) and fecal bacteriotherapy?
the use of penicillin-based antibiotics can alter the normal bacterial flora
-remaining bacteria have reduced competition for space and nutrients
-leaves you prone to infection by C. difficile
-colitis: watery diarrhea, fever, nausea and abdominal pain
-treatments: fecal transplant through colonoscopy or poop pill
what is vomiting?
-contents of the stomach and occasionally the small intestine are forcefully expelled through the mouth
-associated with nausea (motion sickness, full stomach or certain bacterias trigger chemoreceptors)
-vomiting center in the medulla causes three primary response
what are the three responses of the vomiting center in the medulla?
- retrograde contractions in the small intestine and stomach
- contraction of abdominal and inspiratory muscles (diaphragm) increases gastric pressure
- relaxation of esophageal sphincters
what is the immune function of the GI tract?
gut-associated lymphoid tissue (GALT): 80% of lymphocytes located in the gut (immune tissue bc there is always bacteria coming through)
-M cells play a big role
what are M cells and their functions?
M cells play a big role in immune responses: sample lumen contents
-receptor mediated endocytosis
-transport antigens to macrophages, lymphocytes and dendritic cells
-release cytokines to attract more immune cells to attack invaders
-cytokines can also trigger increased Cl-secretion (diarrhea) to flush out pathogens
what is the importance of behavioral mechanisms?
-the Gi system does not regulate intake, so therefore we rely on behavioral mechanisms (hunger and satiety)
what did they discover in the brains of rats when getting burned?
not correct in humans
what parts of our brain are responsible for appetite and satiety?
ARC: arcuate nucleus
PVN: paraventricular nucleus
LH: lateral hypothalamus
NTS: nucleus tractus solitarii
what are the longterm regulations of feeding behaviour?
days weeks and months
1. Glucostatic theory: glucose metabolism in the hypothalamus regulates food intake
2. lipostatic theory: signals from the bodies fat stores regulate food intake
behavioral mechanisms function to __________________________
MAINTAIN BODY WEIGHT AT A RELATIVELY STABLE VALUE
what is the lipostatic theory?
-evidence came in the 1960s with the identification of ob/ob mice
-in 1994, the protein leptin was identified
-this gene must encode a protein that tells the brain that the fat reserves are normal
what is leptin?
-released from adipocytes and regulates body mass by acting directly on neurons of the hypothalamus that decreases appetite and increase energy expenditure
what is the response to elevated leptin?
acts on arcuate nucleus
1. inhibition of lateral feeding center
2. activation of PVN
i) increased TSH, ACTH from pituitary (increased metabolic rate throughout the body)
ii) visceromotor response: increased sympathetic output (increased body temp)
what is the response to decreased leptin?
- reduced activation of a-MSH and CART neurons
-reduced activation of PVN (decreased TSH and ACTH), decreased metabolic rate
-activation of parasympathetic output - activation of NPY and AgRP containing neurons
-stimulation of feeding center
-further inhibition PVN
what is the lipostatic summary
leptin supplementation failed to treat obesity
-likely a decreased sensitivity to leptin in obese individuals
-ex: reduced ability of leptin to cross BBB or reduced receptor expression
what is short-term regulation?
aside from social and cultural factors, short-term regulation of feeding behavior depends on how long it has been since the last meal and how much was consumed at that time
-balance between satiety signals that are generated during digestion and orexigenic signals that are generated during fasting
-Ghrelin, gastric distension, CCK, insulin: complements long term regulation
what is ghrelin?
released by cells in the stomach in response to emptying
-stimulates NPY/AGRP containing neurons in the arcuate
-ghrelin injection will stimulate food intake experimentally
-mice lacking NPY/AgRP neurons will not respond to ghrelin
what is gastric distension and CCK?
-gastric distension is sensed by mechanosensory neurons and this information in sent to the NTS which has connections to the PVN and ARC
-CCK is released by I cells in response to fats and amino acids entering the small intestine: administration inhibits meal frequency and size
-both act on the NTS to stimulate the feeling of satiety
what do insulin and blood glucose levels cause?
-during cephalic and gastric phase, increased insulin would cause a drop in blood glucose driving hunger through activation of NPY/AgPR neurons
-during the intestinal phase, the increased blood glucose and corresponding increase in insulin would act as a satiety signal through activation of aMSH/CART neurons in the arcuate nucleus
