Exam 2 Flashcards
phases of biliary and pancreatic secretion
- cephalic (5-10%)
- gastric (10-20%)
- intestinal (70-85%)
- STIM. BY SECRETIN AND CCK
leptin
ob gene product in adipocytes (binds to cytokine receptors); levels correlate with BMI
induces alpha-MSH in POMC neurons, reduces AGrP (anorexogenic) to supress appetite/stim. energy expenditure
high in obese people
amylin
co-secreted with insulin from β cells
slows gastric emptying and secretion, dec. pancreatic exocrine secretion and bile secretion, stimulates satiety
reduces post prandial glucose spike
B12 absorption
- B12 released in stomach by pepsin, B12 combines with R protein (saliVary gland)
- in SI R protein is degraded, B12 combines with intrinsic factor
- B12/intrinsic factor absorbed in ileum by Na cotransporters
niacin
reactions its used for, deficiency disease/cause, source
(B3) NAD and NADPH
*has the highest RDA of all B vitamins
- reactions: redox (electron acceptor/donor)
- deficiency: pellagra - dermititis, diarrhea, dementia, death - due to corn diet/isoniazid TB tx
- sources: humans can make from Trp, corn has to be treated with alkali, meat, fish, yeast
- toxicity: facial flushing/hepatitis
- use: lower TG and LDL/raise HDL
space of disse
in hepatocytes; microvilli sit in there (kind of beneath endothelial cells) - perisinusoidal
hepcidin
made by liver, for Fe absorption
IL6/high hepatocyte Fe releases hepcidin; binds to FP transporter to inhibiti release of Fe, downregulates DMT1 and inhibits release of Fe from macrophages
ascorbic acid
reactions its used for, deficiency disease/cause, source
vit C
- rxn: cofactor in collagen and catecholamine synthesis, anti-oxidant, inc. absorption of non-heme iron
- deficiency: scurvy (bad collagen cross linking), loose teeth, bruising, poor wound healing, petechiae
- sources: citrus fruits, tomatoes
- use in septic shock
law of the intestine
frequency of BER is greater in the proximal portion than distal portion of small bowel (12/min vs 8/min)
higher proximal motor activity pushes chyme distally
what is accomodation?
tension falls off in time but the muscle stays stretched due to internal rearrangement of microfibrils (because no Z lines)
pantothenic acid
reactions its used for, deficiency disease/cause, source
(B5) - coenzyme a
- reaction: carboxylation and carb energy reactions as a carrier for acyl chains, ach synthesis, adrenal hormone synthesis
- deficiency: (rare) fatigue, depression, irritability, neuropathy
- sources: unprocessed foods (meat, veggies, whole grains, microbiota)
iron deficiency symptoms
pica (ice chewing), leg cramps, fatigue, pale
pyridoxine/pyridoxal, pyridoxamine
reactions its used for, deficiency disease/cause, source
(B6) PLP
- reaction: in AA metabolism rxns (transamination and decarboxylation, glycogen phosphorylase)
- deficiency: (rare alone) poor diet/alcoholics
- symptoms:irritability, condusion, depression, stomitis
- sources: meat, starchy veggies (potatoes), non citrus fruits (bananas/avo), fortified in pasta
- toxicity: pain and numbeness
entero gastric reflex
decreases stomach emptying and increases duodenal activtiy distal to stimulus
gastroparesis
slowed gastric emptying
may be due to vagal nerve dysfunction, nNOS synthesis malfunction / loss of ICCs
where is gastrin secreted from and what does it do?
secreted by antral G cells from stretch/distension/AA
G cells release GRP
Gastrin binds to CCKB receptors to activate Gαq
(CCKA receptors inhibit gastric acid secretion)
what is an implication of loss of villus tips?
gluten enteropathy - autoimmune fur to HLA that sensitize T-cells to gluten
loss results in diarrhea and malnutrition
mechanism for secretory diarrhea
toxins increases cAMP which activates PKC, increases Cl flux by opening channels already present and makes new channels, inhibits Na H exchanger
HCO3 can’t compensate as more Cl is in enterocyte than plasma so more HCO3 into lumen to compensate for loss of anions, any excess H is removed by HCO3 combining ↑ acidosis
increases K loss in exchange for Na into enterocyte
⇒dehydration, metabolic hyperchloremia, hypokalemia acidosis
mechanisms for insulin release
- cephalic phase
- digestive phase
- absorptive phase - glucodetectors in blood and liver tell pancreas to release inulin, info travels via nucleus of the solitary tract (NST) into hypothalamus
low flow vs. high flow saliva formation
low flow: very hypotonic, low volume, low pH (6.8)
high flow: stimulated by Cl channel (basolateral) - slaiva with higher HCO3, Na, pH (8.4), low K
what does bile interfere with and how is that overcome?
bile interferes with pancreatic lipase, but is overcome by secreting co-lipase
what is ferroportin disease
mutations in ferroportin so hepcidin can’t bind ⇒ too much Fe in plasma
entero-enteric reflex
increases motor activity distal to distending/irritating stimulus, decreases proximal motor activity
(in abnormal distension/irritation, clears offending stimulus from bowel, doesn’t add material to stimulated portion)
events for defectation
- stim. of defecation reflex - contraction of distal colon, relaxation of internal anal sphinceter
- changing ano-rectal angle











