Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
386 Cards in this Set
- Front
- Back
|
what 2 nerves are impt in the PNS innervation of GI?
|
vagus: esophagus, stomach, small intesting, upper colon
pelvic: descending colon, sigmoid colon, rectum, anal canal |
|
|
waht is the vasovagal reflex?
|
info from R's in mucosa and smooth muscle relayed to CNS via vagus nerve AFFERENTS
this triggers a response that is carried back to GI tract via vagus nerve Efferents |
|
|
where do most SNS fibers synapse?
|
outside GI tract in prevertebral ganglia
|
|
|
postgang SNS fibers innervate what?
|
cells of enteric nervous system
|
|
|
what is the intrinsic/enteric innervation?
|
crossconnxn with Extrinsic but wil contract w/o CNS b/c it is intrinsic
networks formed by myenteric and submucosal plexuses relay info to and from gut via extrinsic system *works independently of extrinisc |
|
|
were are neurocines made and ho released?
|
syn in cell bodies of neurons
released by AP |
|
|
what cells release gastrin and when?
|
G cells in stomach
in response to a meal |
|
|
what does gastrin release stimulate?
|
HCl secretion by parietal cells of stomach in respone to peptides and amino acids from protein digestion, distention of stomach, vagal stimulation
|
|
|
waht is HCl release stimulated in response to?
|
in response to peptides and amino acids from proten digestion, distention of stomach, vagal stimulation
after being stimulated by G cells in stomah |
|
|
what inhibits the release of gastin?
|
acid in lumen of stomach (pH<3)
|
|
|
what happens to pts with gastinomas or Zollinger Ellison syndrome?
|
they hypersecrete gastric acid due to continuous release of gastrin into blood; they develop duodenal ulcers, diarrhea, and steatorrhea
|
|
|
what cells release cholecystokinin (CCK)?
|
I cells of proximal small intestine in respone to peptides, amino acids, fatty acids, monoglycerides
|
|
|
what does CCK stimualte?
|
gallbladder contraction and pancreatic enzyme secretion and potentiates pancreastic bicarb secretion stimulated by secretin
|
|
|
where is gastin released from? where is CCK released from?
|
gastrin: stomach
CCK: prox small I |
|
|
what does CCK inhibit?
|
gastric emptying-reason fatty meals empy more slowly than non fat meals
|
|
|
waht stimulates the release of CCK from small intestin?
|
fats, peptides, amino acids
|
|
|
waht does secretin stimulate?
|
bicarb and water secretion in pancrease and liver
|
|
|
what does secretin increase?
|
bile prodxn
|
|
|
what does secretin inhibit?
|
gastic acid secretion by parietal cells to avoid acid overload in small I
|
|
|
what cells release secretin?
|
S cells in prox Small I in response to acid
|
|
|
secretion of secretin by S cells is stimulted by?
|
response to acid in small I
|
|
|
what does gastrin inhibitory peptide (GIP) stimulate?
|
insulin release from pancrease
|
|
|
why is oral glucose more effective than intravenous glucose in causing insulin release?
|
b/c GIP stimualtes instulin relesae from pancrease
|
|
|
where is GIP secreted from?
|
prox small I
|
|
|
waht cuse the release of GIP?
|
fat, protein, carb
**only hormone relesed by all 3 major foodstuffs |
|
|
what is the only hormon that is reslased by all 3 major foodstuffs: fat, protein, carb?
|
GIP
|
|
|
when is motilin rleased?
|
cyclically every 90min from upper Small I during fasting
|
|
|
waht does motilin stimulate?
|
migrating myoelectric complex in stomach and small I
|
|
|
what is motilin release abolished?
|
by eating
|
|
|
what are the 2 paracrine hormones
|
somatostatin
histamine |
|
|
when is somatostatin rleased?
|
by cells throughout GI tract in response to acid in lumen
|
|
|
what does somatostatin inhibit?
|
gastric acid secretion and release of gastrin
rlease of all GI hormones |
|
|
what cells secrete histamine?
|
gastric enterochromafin like (ECL) cells found in high concentrations in acid secreting portion of stomach
|
|
|
action of histamine?
|
increases gastric acid secretion both directly and by potentiating effects of gastrin and Ach
|
|
|
what are the 3 neurocrines?
|
vasoactive intestinal peptide (VIP)
gastrin releasing peptide (GRP or bombesin) enkephalins |
|
|
VIP is released from?
|
nerves in mucosa and smooth muscle of GI tract
|
|
|
predom action of VIP?
|
relaxation of GI smooth muscle
|
|
|
what does VIP stimulate?
|
intestinal and pancreatic secretion
|
|
|
a pancreatic islet cell tumor can secrete?
|
VIP: thought to mediate pancreatic cholear/watery diarrhea syndrome
|
|
|
gastrin releasing peptide (GRP) is released from what? waht does it stimulate?
|
released from nerves in gastric mucosa by vagal stimulation
stimulates gastrin release by acting on G cells |
|
|
enkephalins stimulate what?
|
contraction of GI smooth muscle particulaly the lower esophageal, pyloric, and ileocecal sphincters
|
|
|
what doe enkepahlns inhibit?
|
intestinal secretion of fluid and electrolytes: this is why opiates are useful in treating diarrhea
|
|
|
why are opiates useful in treating diarrhea?
|
by enkaphlins stimulate contraction of GI smooth muscle
|
|
|
what relaxes GI smooth muscl?
|
VIP
|
|
|
what generates the slow waves of GI smooth muscle?
|
interstial cells of Cajal
|
|
|
what is a slow wave?
|
periodic changes in resting membrane potential of smooth muscle cells--also called basic electrical rhytm (BER)
|
|
|
are slow waves ~ AP?
|
no..slow waves are not AP, but do determine pattern of AP
|
|
|
what doe slow waves consist of ?
|
upstroke phase (depol) and plateau phase
|
|
|
waht must happen in slow waves for contraction to occur?
|
plateau phase must exceed threshold, then whn threshold is reached , vgated Ca channels open, Ca enters and APs fire
|
|
|
the greater the # of AP, the greater __?
|
the force of the contraction
|
|
|
can contractions in stomach occur in absence of AP?
|
yes, but not anywhere else in GI (need spike potentials for contrction)
|
|
|
is the freq of slow waves influenced by neural or hormonal inputs?
|
very little
but the freq of AP is greatly influenced by neural or hormonal inputs |
|
|
can you have slow waves w/o contractions?
|
yes but you can't have contractions w/o slow waves
*also can't have more contractoins than slow waves |
|
|
can you have more contractions than slow waves?
|
no, the freq of slow wavs sets max freq for contractions
|
|
|
what are spike potentials followed by?
|
a mechanical contraction of gastric smooth muscle
|
|
|
what are the 3 fxn of salivary secretion?
|
digestion: starts digestion of starches and fats
lubrication: facilitates swallowing protection: antibacterial |
|
|
what are teh 3 major glands for salivation?
|
parotid: b/n angle of jaw and ear
submaxillary/submandibular: located below angle of jaw sublingual: located below tongue |
|
|
what gland contributes the most to salvation?
|
submaxillary 70%
least: sublingual 10% |
|
|
what is the structur that secretes the initial saliva?
|
acinus
|
|
|
waht connects the acinus with striated duct?
|
intercalated duct
|
|
|
what structure modifies inorganic compostiion of saliva?
|
striated duct
|
|
|
action of myoepithelial csll?
|
contract when saliva prodxn is stimulated and eject saliva into mouth
|
|
|
what is the control of salivary secretion?
|
under total autonomic nervous system control..NO hormones
|
|
|
what nervous system increases salvation?
|
both PNS and SNS incrrease it /PNS more than SNS
|
|
|
in terms of salivary secretion, PNS stimulation does what?
|
is like the supersoaker
increases transport processes of acinar and ductal cells stimulates vasodilation of blood vssls stimulates glandular metabolism and growth |
|
|
action of SNS in terms of salivation?
|
like a water gun squirt
transiently increases prodxn of saliva and growth of salivary glands causes contrxn of myoepi cells causes constriction of blood vssls |
|
|
if you were to remove PNS nerve supply to salivary glands what would happen?
|
the glands would atrophy
one of the fxns of PNS is to stimulate glandular metabolsm and growth however removing SNS nerves has little effect |
|
|
what are the inducers of saliva prodxn?
|
food in mouth, smells, conditional reflexes, nausea
|
|
|
what are the inhibitors of saliva prodxn?
|
sleep, fatigue, dehydration, fear, anticholinergic drugs
|
|
|
normal p H of saliva?
|
5.5-6 but will increase to 7.8 during active secretion
|
|
|
what protins make up saliva?
|
alpha amylase: digests starches
lingual lipase: digests fats mucin: lubricts food and protects oral mucosa |
|
|
what are the bacteriocidal substances in saliva?
|
lysozyme (breaks down walls), lactoferrin (iron chelator)
|
|
|
how is the tonicity of saliva compared to plasma?
|
hypotonic to plasma b/c ducts are imperm to water
|
|
|
the intital fluid produced by acinus is hyper, hypo or isotonic?
|
isotonic to plasma
|
|
|
how does the ionic composition of saliva change as it moves through striated ducts?
|
reabsorb Na and Cl: lower Na than plasma
secrete K and HCO3: higher K and HCO3 than plasma more solute than water reabsorb so saliva becomes HYPOtonic |
|
|
how does flow affect the concentrations of ions in saliva?
|
at higher rates there is less time for reabsoprtion to occur so saliva is more ISOtonic (more Na and Cl)
However HCO3 incresaes with increasing flow b/c its secretion is stimulated when salivation stimulated (HCO3 channels in salivary gland) |
|
|
why does HCO3 conc increase with incresing flow but K doesn't in terms of salivating?
|
K decresae b/c doesn't have time to add but HCO3 increases bc of HCO3 channels (sme process that increase flow increases these channels)
|
|
|
how does pH change when activaly secreting saliva?
|
increases from 5.5-6
saliva becomes isotonic |
|
|
changes in ion conc in saliva as flow rate increase?
|
Na increases
Cl incrases K intitally decresas then plateaus HCO3 increases, then plateaus |
|
|
what is Xerostomia?
|
dry mouth
lack of salivary secretion most commonly caused by antidepresseants which have anticholinerc affect and can also be caused by Beta blockers and antihistamines |
|
|
what are the 5 causes of Xerostomia?
|
antidepressants
beta blockers anti histamines disease-Sjogrens radiation |
|
|
another name for swallowing?
|
deglutition
|
|
|
what are the 2 phases to swallowing?
|
oral (voluntary) phase
pharyngeal (involuntary( phase |
|
|
describe swallowing
|
oral phase: swallowing initiated by voluntary action of collecting bolus and forcing it into oropharynx by pushing up and back against hard palate
pharyngeal phase: nasopharynx closed by soft palate to prevent regurg; at same time breathing is inhibited for duration of pharyngeal phase laryngeal mm contract to close glottis and elevate larynx |
|
|
in terms of swallowing, where does paristalsis begin?
|
phayrnx to propel food towards esophagus then upper esophageal sphincter relaxes, allowing contrxn of constrictor mm in pharyxn to move material into esophagus
|
|
|
how do we propel food through the UES?
|
by contrxn of middle and lower constrictors of pharyynx and relax cricopharyngeal muslce
|
|
|
lesions in swallowing center w/n medulla result in loss of ?
|
pharyngeal phase of swallowing, may result in aspiration
|
|
|
difficulty in swallowing is called waht?
|
dysphagia
freq casused by neurological disorders, but also associated with lesions of mouth, throat or esophagus |
|
|
describe the mm componetns in esophagus
|
upper 1/3 striated
lower 1/2 smooth |
|
|
fxn of UES and what forms it?
|
formed by cricopharyngeal muscle
separates esophagus from oral cavity and **prevents entry of air relaxes to let food enter, contracts to prevent air |
|
|
fxn of LES and what forms it?
|
separates esophagus from stomach and prevents entry of gastric acid
LES is not a distinct muscle, but does have increased pressure compared to rest of esophagus |
|
|
when does UES contract and when does it relax?
|
relaxes to permit entry of food bolus into esophagus
contracts to prevent reflux of food |
|
|
wht initiates primary peristaltic contraction?
|
swallowing
|
|
|
fxn of primary peristaltic contraction when swallowing?
|
creates a zone of increased pressure behind food, initiated by swallowing
|
|
|
what happens as bolus approaches LES?
|
sphincter relaxes, allowing bolus to enter stomach; LES then contracts preventing reflux
|
|
|
what intitates the secondary peristaltic contraction?
|
presence of food in esophagus, which stretches mechanical R's cuasing another peristaltic wave unti all material is removed from esophagus
|
|
|
when do you need the secondary peristaltic contraction?
|
if primary peristaltic contraction does not remove all food from esophagus
|
|
|
during quiescent times, what is the status of LES?
|
tonically contracted
|
|
|
waht type of foods will reach stomach faster?
|
liquids and semisolid foods swallowed in upright position b/c of gravity
|
|
|
what causes GERD?
|
decreased tone of LES, which leads to reflux of stomach acid
causes heartburn and esophagitis, can lead to ulceration and stricture |
|
|
long term of exposure of esophagus to acid leads to what?
|
Barrett's esophagus
constant injury to esophagus causes continuous cell growth (metaplasia) if unTx: lead to esophageal cancer |
|
|
what surger can now be done for pts with Barrett's esophagus?
|
fundoplication: fold the top of the stomach around itself to create high P zone that fxns as LES
|
|
|
what is the neuromuscular disoder of lower 2/3 of esophagus?
|
achalasia: leading to absence of peristalsis and failure of LES to relax
|
|
|
what is the result of achalasia?
|
food accumulates in esophagus taking hors to enter stomach and causing dilation of esophagus
*neuromuscular disorder of lower 2/3 of esophagus |
|
|
what doe pts with achalasia experience?
|
dysphagia, regurg of ingested food, wt loss
food accumulates in esophagus |
|
|
what can you do to Tx achalasia?
|
botox to cause relaxation of LES
endoscopic procedures |
|
|
how would you compare the pressue of LES in achalasia with normal?
|
high resting pressure that does not relax after a swallow
|
|
|
anothr name for belching?
|
eructation
|
|
|
how does belching/eructation occur?
|
air swallowd during eating or drinking (aerophagia) or gas from heavy meal or carbonated beverages forms bubble instomach
when LES relaxes during swallow air enters esophagus and is regurg |
|
|
first symptom of pt with achalasia?
|
difficulty swallowing
|
|
|
what are the 2 fxnl regions of stomach?
|
orad (proximal)
caudad (distal) |
|
|
fxns of orad and caudad?
|
orad: responsible for receiving ingested meal
caudad: responsible for contractions that mix food and propel it into duodenoum |
|
|
how does the thickness of circular and longitudinal layers of smooth muscle change as we move distally towards the pylorus?
|
increase distally
thin layers in orad region have weak contractions and thick layers in caudad region have stronger contractions |
|
|
what are the 3 fxns of stomach?
|
storage
mixing empyting |
|
|
waht is receptive relaxation
|
process by which orad stomach relaxes to accomodate ingested meal
|
|
|
receptive relaxation is mediated by?
|
vagovagal reflex, which is intiated by distention of stomach and is abolished by vagotomy
|
|
|
presence of food stimulates caudad to what?
|
to increase contractions, which mixes food with gastric secretions and redues size of particles
when food is mixed into pasty consistency it is called chyme |
|
|
what must happen to propel food into duodenum?
|
caudad stomach contracts
|
|
|
peristatltic contractions of stomach originate in what part of stomach?
|
midstomach (near fundal-corpus border) and proceed cadally; as they move distaly toward pylorus both velocity and force of c ontract increase
|
|
|
slow waves of stomach orginate where?
|
in pacemaker loaced near border of orad and caudad areas
|
|
|
what is retropulsion?
|
waves of contraction close distal antrum and pyloric sphincter before chyme reaches theres, which causes most of the chyme to be propelled back into stomach to be mixed
|
|
|
what is the migrating myoelectric complex?
|
contracts that occur at 90min intervals during fasting
clear the stomach of any residual food abolished by eating |
|
|
waht abolishes the migrating myoelectric complex?
|
eating
|
|
|
how does the rate of gastric emptying vary?
|
depends on type of food ingested
liquids empty faster than solids carb rich food leaves faster than protein rich food protein rich food leaves faster than fat rich food order of fastset: liquids, carb, protein, fat |
|
|
how does the rate of gastric empyting change in regards to pressure in orad stomach?
|
rate inversely proportional to pressure in orad stomach , which increases slowly during digestive period
|
|
|
how is gastric empyting controlled?
|
by signals from duodenum
|
|
|
what inhibits gastric empyitng?
|
high proton concentration
fat or protein digestion products non isotonic solutions increased distention in orad stomach incresed P in prox small I decresed freq and force of peristaltic contrxns in cuadad stomach |
|
|
what is gastroparesis?
|
impaired/delayed empyting of stomach
produces symptoms of fullness, loss of appettie, nausea, vomiting |
|
|
what can cuase gastroparesis?
|
diabetes, medicatoins that slow contractions in intesting (antiAch), neurological disorders, obstriction of gastroduodenal canal by peptic ulcers or cancer
|
|
|
increased gastric empyting can cuause?
|
diarrhea b/c of increased osmotic load in small I or duodenal ulcers b/c stomach acid damages duodenum
|
|
|
what is dumping syndrome?
|
occurs when lower end of small I fills too quickly with undigested food from stomach
-occurs either durin/right after meal -predom result of stomach surger |
|
|
action of low pH on stomach?
|
inhibits gastric emptying
|
|
|
what are the 2 regions of stomach involved in gastric secretion/
|
oxyntic gland mucosa: prox 80%stomach
pyloric gland mucosa: distal 20% stomach |
|
|
actions of oxyntic gland mucosa and pyoric gland mucosa?
|
oxyntic: secrete acid, pepsinogen, intrinsic factor, mucus
pyloric: secrete gastrin, mucus and pepsiongen |
|
|
what aer the different cell types that make up the oxyntic gland?
|
surface epi cells: exntend into duct openng
mucus neck cells secrete mucus stem cells in mucus neck cell area proli into surface epi or parietal cells parietal cells secrete acd and intreince factor chief/peptic cells secrete pepsinogen |
|
|
action of parietal cells and chief cells in oxyntic gland?
|
parietal ;secrete acid and intrinsic factor
chief: secrete pepsinogen |
|
|
what compoent of gastric juice begins digestions of dietary protein?
|
HCl
|
|
|
what compenent of gastric juice converts pepsinogen to pepsin and proides optimal pH for action of enzyme?
|
HCl
|
|
|
3 actions of HCl in stomach
|
1. converts pepsinogen to pepsin
2. begins digestion of dietary protein 3. kills most bacteria that enter stomach-lack of or redxn in acid prodn leads to bactrial infxns of stomach and upper small I |
|
|
where does pepsin come from?
|
stored and secreted as inactive pepsionogen that is converted by gastric acid/HCl and by pepsin itself
|
|
|
fxn of pepsin?
|
begins digestion of protien by splitting interior peptide bonds i proteins
|
|
|
waht cuases the greatest increase in secretion of pepsin?
|
vagal stimulation
|
|
|
fxn of mucus?
|
protective coating for stomach and lubricant and barrier b/n cells and ingested material
|
|
|
what re the 2 different forms of mucus?
|
soluble form: secreted by mucus neck cells after stimulation by vagus nerve
insoluble form: secreted by surface epi cells |
|
|
when is soluble mucus not presnt?
|
in resting stomach
|
|
|
when is insoluble mucus present and soluble isn't?
|
insoluble present in resting stomach and in response to chemical or physical irritation
solbule form not present in resting stomach |
|
|
fxn of insolbule/visible form of mucus in stomach?
|
secreted as a gel forming unstirred layer over mucusa; over 1mm thick
traps dead cells from mucosa and forms protective coat HCO3 trapped in insoluble layer thus maintaining pH at surface of stomach near neutrality |
|
|
what happens to insolbule mucus on contact with acid?
|
precipitates into clumps and passes into duodenum with chyme
|
|
|
how does the suface mucosal layer alter pH
|
keeps the pH at surfae to remain near 7, wheras the pH of gastric juice in lumen is 1-2
this is the gastric mucosal barrier that prevents damage to mucosa by gastric contents |
|
|
what is intrinsic factor and what secretes it?
|
glycoprotein secreted by parietal cells of gastric mucosa that binds VitB12
necessary for absorption of vitamin in ileum |
|
|
why do we need intrinsic factor?
|
need intrinsic factor to be secreted by parietal cells in gastric mucosa to bind Vit B12
w/o IF, we wouldn't be able to absorb VitB12 in ileum |
|
|
w/o intrinisc factor what would happen?
|
pernicious anemia
total gastrectomy pts require injections of VitB12 |
|
|
how is HCl secreted from parietal cell?
|
w/n cell CO2 and water form H and HCO2
the H is expelled inot lumen of stomah via H-K antiporter ATPase Cl enters cell in active exchange for the HCO3 that is leaving into blodstram, the Cl is then secreted into lumen by channel K enters via BL Na-K pump then enters lumen via channels |
|
|
what is the alkaline tide?
|
HCO creates alkaline tide in venous blod of actively secreting stomach by rasing pH
|
|
|
how does ionic compostiion of gastric juice change with rate of secretion/
|
al low basal rates, gastic jiuic primarily NaCl from nonparietal secretion
at high stimulated rates, gastric juice primarily HCl from parietal secretion |
|
|
how are K conentrations in gastric juice compared to plasma?
|
always higher than plasma; chronic vomiting may lead to hypokalemia
|
|
|
during the prodxn of acid, H enters the lumen in exchange for waht ion?
|
K
|
|
|
during the prodxn of acid, Cl enters parietal cell in exchange for waht ion?
|
HCO3
|
|
|
a pt presents with diabetes. what syndrome would you consider?
|
gastroparesis: dabestes affects the nerves regulating stomach motility
|
|
|
dumping syndrome is seen most often in pts who?
|
had stomach surgery
|
|
|
pernicious anemia is caused by a loss of waht?
|
parietal cells which secrete IF. IF is necessary for absorption of vitB12
|
|
|
Zollinger-Ellison is caused by what?
|
tumor that hypersecretes gastrin
|
|
|
what are the 3 stimulants of acid secretion?
|
Ach
histamine gastrin "HAG" |
|
|
waht R's do the stimulants of acid secretion bind to?
|
Ach: binds muscarininc R's on parietal cell mem
histamine: binds H2 R's on parietal cell mem gastrin: binds gastrin/CCK-B R's on parietal cell mem |
|
|
what do Ach, gastrin and histamine activate for acid secretion?
|
Ach: activates PLC to catalyze the form of IP3, release Ca
gastrin: activates PLC histamine: activates adenylate cyclase to form cAMP |
|
|
what is potentiateion?
|
occurs when response to simulataneous admin of 2 stimulants is greater than sum of responses to either agent alone
|
|
|
what does histamine potentiate?
|
actions of gastrin and Ach; thus H2 R blockers effective in inhibiting acid secretion b/c they block not only action of histamine but histamines' potentiating effects on Ach and gastrin
|
|
|
what does Ach potentiate?
|
actions of histamine and gastrin
Ach release histamine from ECL cell |
|
|
what does the ECL cell have R's for?
|
R's for gastrin and Ach
gastrin stimulates relesae and syn of histamine and prolif of cells Ach stimulates relesae and syn of histamine but not as much as gastrin |
|
|
what 2 hormones stimulate syn and release of histamine?
|
gastrin and Ach by binding to R's on ECL cell
histamine then binds to parietal cell via H2 R's to stimulate acid production |
|
|
what are 2 inhibitors of acid secretion?
|
low pH in stomach
chyme in duoedenum |
|
|
describe the neg feedback mech of acid secretion after eatng meal
|
prior to meal pH is low
after meal ingested, pH of stomach rises, leading to secretion of acid once meal is digested, stomach empty, pH drops: when below 3.0, gastrin release inhibited |
|
|
when the pH is low in the stomach, waht is released?
|
somatostatin: inhibits acid secretion by parietal cells and gastrin secretion by G cells
the gastrin that is released to raise the pH also stimulates the D cell to release somatostatin |
|
|
how does chyme in duodenum inhibit acid secretion?
|
triggered by acidity, osmolarity, fat content of chyme
these inhibit gastrn relesae by G cell/and or acid secretion by parietal cell |
|
|
what 2 combos of substances can produce the highest rate of acid secretion?
|
histamine + gastrin
histamine + Ach b/c of potentiation |
|
|
what are the 4 phases of acid secretion?
|
basal secretion
cephalic phase gastric phase intestinal phase |
|
|
when does basal secretion of acid occur?
|
in absence of all gastric stimulation
shows circadian rhythms in humans-hightes output in eventing, lowest in morning; however gastrin levels relatively constant |
|
|
when does the cephalic phase occur? (acid secretion)
|
intiated by thought, sight, taste, or smell of food
|
|
|
how does the cephalic phase occur (acid secretion)?
|
mechanoR's, chemoRs, central pathways bring info from thought, sight, taste, smell of food to vagal nucleus then vagal efferent nerves carry impulses to stomach
vagus nerve then incresa aicd secretion via Ach direcly stimulating parietal cell or causes the release of GRP |
|
|
waht are the 2 ways in which vagus nerve incresae acid secretion in stomach?
|
Ach directly stimulates parietal cell
Ach cuaes release of GRP to act on G cell to release gastrin |
|
|
what initiates the gastric phase of acid secretion?
|
entry of food into stomach
this buffers acid, raising pH from 2 to 6 |
|
|
how does the gastric phase of acid secretion work?
|
food enters stomach cuasing pH to rise
rise in pH permits vagal stimulation from cephalic phase to initiate and stimule from gastric phase to maintain, gastrin releaes |
|
|
in the gastric phase of acid secretio, distention of stomach activates what?
|
mechanoR's which initiate both local and vagovagal reflexes; these stimulate gastrin release via GRP and acid secretion via Ach
|
|
|
whta is the only nutrient that stimulates gastric secretion?
|
protein, but must be broken down to peptides and amino acids; apparently cuases direct chemical release of gastrin from G cells
|
|
|
what do Ca and caffeine stimulate?
|
acid secretion
|
|
|
what inhibits gastric phase of acid secretion?
|
acid in stomach
|
|
|
what intiates intestinal phase of acid secretion?q
|
presence of protein digestion products in duodenum
then the prox duodenum secretes gastrin which stimulates acid prodxn |
|
|
what phase of acid secretion responds the most?
|
gastric phase :60%
cephalic:30% intestinal:10% |
|
|
what are the intiating stimuli for the phases of acid secretion in stomach?
|
cephalic: chewing, swallowing
gastric: distention, digested protein intestinal: distention, digested protein |
|
|
what causes gstric ulcers?
|
caused when protective barrier of stomach breaks down, leading to injury of gastric mucosa by acid and pepsin; ususally found in distal stomach
*pain relieved wth eating |
|
|
characteristics of duodenal ulcers?
|
more common than gastric ulcers
pts tend to have increased levls of acid, gastrin, pepsin |
|
|
what 2 factors can cuae peptic ulcers?
|
H, pylori infexn
NSAIDs (aspirin) alcohol as age increases, incidence increase |
|
|
how do we Tx peptic ulcers?
|
combo of antibiotics, proton pump inhibitor, bismuth
|
|
|
how can H. pylori live in stomach?
|
can produce large quantities of urease, enzyme that generates ammonia to neutralize the acid that quickly kills other bacteria
also thins the mucus layer, poisoning nearby cells with ammonia and other toxins |
|
|
def of vomiting/emesis?
|
forceful expulsion of gastric and intestinal contents through mouth
protective mxn to rid body of noxious or toxic substanes |
|
|
can you have vomiting w/o nausea?
|
yse, and nausea w/o vomiting
|
|
|
how does emesis/vomiting occur?
|
wave of reverse or anti-peristalsis begins in distal small I, moving GI contents toward stomach
general discharge of autonomic nervous system before and during emesis leads to incresaed salivation, sweating, rapid breathing, and irregular heartbeat |
|
|
waht does retching involve
|
all involuntary motions of vomiting w/o prodxn of vomitus
|
|
|
where is the vomiting center located? what activates it?
|
medulla
activated by affernet impulses triggered by tickling back of throat, distention of stomach or duo, vestibular stimulation (motion), painful injury to genitourinary system |
|
|
if you directly activate the vomiting cetner what happens?
|
vomiting w/o nausea or retching
|
|
|
how do you get retchin w/o vomiting?
|
stimulation of 2nd separate medullary area leads to retechin w/o vomiting
|
|
|
what is the chemorecptor trigger zone?
|
in 4th ventricle of brain
activated by emetics, radiation, and motion sickness *responds to humoral stimuli |
|
|
why is it believed taht morning sickness occurs?
|
protect fetus early in devlopment when toxins can cuase most damage
nausea affects 70-85% of preg women 5/1000 women have severe nausea and vomting which causes them to lose wt-Hyperemesis of pregnancy |
|
|
what outcomes can occur due to hyperemesis of preg or protracted vomiting?
|
metabolic alkalosis due to loss of gastric acid
hypokalemia due to loss of K in vomit and decr K uptake hyponatremia due to loss of Na in vomit |
|
|
how is the autonomic nervous systme involved in vomiting?
|
before and during emesis get increased salivation, sweating, rapid breathing, irregular heartbeat
|
|
|
major part of digestion occurswhere in small I?
|
duodenum and jejunum
|
|
|
what structural compoentns of small I incresae the surface area and by how much?
|
folds of Kerckring: 3x
villi: 30x microvilli: 600x |
|
|
waht projects from the Folds of Kerckring?
|
villi
lines entire mucosal surface |
|
|
what protrudes from the surface of villi intestinal cells?
|
microvilli
also called brush border |
|
|
waht project down into surface at base of each villi in small I?
|
crypts
3crypts/villus |
|
|
what are the 3 types of cells in the small I?
|
enterocytes
goblet cells crypt cells |
|
|
what are enterocytes and what is there fxn?
|
columnar epi cells in villus of small I
microvilli protrude from them fxn digestion, absorption, secretion *if at tip of villi more capable of digstion and absorption than those at base |
|
|
where are goblet cells found in small I?
|
interspersed eith enterocytes in villus
secrete mucus |
|
|
job of crypt cells of small I?
|
found in crypts at base of villus
prolif cells in intestine-form both enterocytes and goblet cells secrete fluids and electrolytes |
|
|
which of thecells of the small I divid?
|
cyrpt cells: also secrete fluids
|
|
|
fxn of small I?
|
mix chyme w/ digestive juices and bile to facilitate digestion and absroptoin
further reduce size of chyme to incresa soubility bring chyme into contact with absorptive surface of microvilli propel chyme from duo to colon |
|
|
what are the 3 types of contractions in small I?
|
segmentation
peristaltic migrating motility complex (MMC) |
|
|
waht are the most common type of intestinal contractions?
|
segmentation: only 1 segment contracts at a time
circularsmooth muscle of isolated 1-5cm segment of wall contracts, forcing chyme towards stomach and colon when muscle relaxes, chyme returns to original segment; effect is mixing of chyme with digstive juices |
|
|
in which direction is there a net movmt of chyme? why?
|
b/c of higher freq of contractions in prox int than distal, net movmt chyme towards colon
|
|
|
action of peristaltic contractions?
|
propel chyme down small I
occur only over SHORT distances-net mvmt only 1cm/min |
|
|
what is the migrating motility complex?
|
similar contraction to migrating myoelectric complex in stomach
occurs about every 90minc clears remaining chyme in small I |
|
|
how are intestinal slow wave different from those in the stomach?
|
they do not trigger contractions themselves; for contractions to occur there have to be spike potentials on top of slow waves
|
|
|
what is the strenght of insteinal contraction proportional to
|
freq of spikes generated by slow wave, which is controlled by ampilitude of slow wave--greater slow wave amp, greater freq of spkes generated adn greater strenght of contraction
|
|
|
how do the slow waves freq in intstine change?
|
decreases distally
|
|
|
motility of small I is affected by what
|
higher centers of nervous system: state of mind affects GI
|
|
|
waht is peristaltic reflex/rush?
|
contractoin that moves intestinal contents along small I
initiated by chyme in intestine which either distends wall or greatly irritates mucosa; also caused by severe cases of infectous diarrhea |
|
|
what is the intestinointestinal reflex?
|
overdistention of one segment of intestine inhibits contractile activity in rest of intestine
prevents mvmt of material into already severly distended section of bowel (ex: prevent everyone from leaving the room at one time) |
|
|
what reflex prevnts mvmt into already severely distended section of bowel
|
intestinointestinal reflex
|
|
|
what is the gastroileal reflex
|
gastric secretion and emptying triggers increased peristalsis in ileum, causing releaxation of ileocecal sphincter and mvmt of ileal contents into Large I
|
|
|
what cell types do we have in pancreas?
|
acinar cells : produce peptidases, lipases,amylases to digest
ductule cells: secrete pancreatic juice containing high conc of HCO3 which neutralizes gastric acid in duodenum and bring contents w/n pH range for optimal enzymatic digetsion of nutrients |
|
|
at all rates of secretion, pancreatic juice is hypo, hyper, or iso to plasma?
|
isotonic to plasma
|
|
|
describe the ion conc in pancreatic secretion?
|
[HCO3] higher than in plasma
[Cl] lower than in plasma [K] equ to plasma (in saliva: HCO higher, Cl lower, K lower) |
|
|
at lowest flow rates, waht is the comp of pancreatic juice?
|
Na and Cl predom
|
|
|
at highest flow rate, waht is the comp of pancreatic juice?
|
Na and HCO3
|
|
|
how do ion concentrations in pancreatic secretion change as flow rate increases?
|
Na stays same
HCO increases Cl decreases K stays same (in salvia: Na increases, Cl increases, HCO increases) |
|
|
why is venous blood from actively secreting pancrease of a lower pH than blood from nonsecreting gland?
|
b/c H is transported out of cell into blood in exchange for Na
|
|
|
how do ductule pancreatic cells modify intial pancreatic juice secreted by acinus?
|
inital juice: Na and Cl
modify: secrete HCO and absorb Cl |
|
|
in the pancreatic ductal cell, where is HCO transported out of cell?
|
on apical border for exchange for Cl; rate of secretion dependent on Cl being present in lumen
*Cl can then leave via channel back into lumen--channel mutated in CF |
|
|
where does the Na go that is pumped into cell in exchange for H in the pancreatic ductal cell?
|
right back out via Na/K to keep intracellular Na low for Na/H echange
na then follows HCO3 into lumen via paracellular route to preserve electrical neutrality |
|
|
are pancreatic ducts permeable to water?
|
yes thus water moves into lumen along osmotic gradient
|
|
|
what arethe pacreatic proteases and where are they activated?
|
trypsin and chymotrypsin
activated in small I *trypsin inhibitor secreted to protect pancreas from autodigestoin |
|
|
what happens during the cephalic and gastric phases to pancreas?
|
Ach ats on acinar cells and ductule cells
distention of stomach intitiates vasovagal reflex which stimultes secretion |
|
|
what happens during intestinal phase to pancrease?
|
acid and fat and protein digestion products in duodenum caues the release of secretin from S cells in duodenum
the secretin then acts on ductual cells to increase HCO3 secretion, which neutralizes acid fat and protein digestion produxts release CCK form I cells in duo to act on acinar cells to increase enyzme secretion |
|
|
how do CCK and Ach potentiate the action of secretin on ductal cell secretion?
|
small amts of secretin relesaed by duodenal acidifiation in presence of CCK and/or Ach produces large amts of pancreatic HcO3
|
|
|
secretin from duodenum acts where in pancrease? CCK?
|
secretin acts on ductal cells to rlease HCO3
CCK acts on ductal cells to potentiate actions of secretin and also on acinar cells to increase enyzyme secretion |
|
|
besides CCK and secretin acting on pancreatic cells what else can?
|
vasovagal reflex releases Ach on ductal and acinar cells after being intitated by acid and by fat and protein digestion products
|
|
|
how does the amt of enzymes produced by pancrease change with diet?
|
they adapt to diet
high protein, low carb: increase in prop of proteases and decrease in proprotion of amylase |
|
|
how does CCK alter expression of genes based on high protein, low carb diet? secretin and GIP?
|
CCK increses expression of genes for proteases and decreases expression for amylase
Secretin and GIP increase expresion of lipase gene |
|
|
what causes pancreatitis?
|
acute: chronic alcoholism or gallstones
chornic: repeated episodes of acute induced by alcohl abuse |
|
|
what are the symtpoms in acute and chronic pancratitis?
|
severe abdominal pain, swollen and tender abdomen, nausea, vomiting, diarrhea, fever, **serum amylase and lipase levels are greatly elevated
|
|
|
how does CF affect pancrase?
|
reduces secretion of both aqueous and enyzmatic components: cant secrete Cl therefore get concentration of pancratic juie which blocks secretion of enyzmatic component
low flow, increaed protien concn, protein plugs block secretion from pancreas |
|
|
which pancreatic ion exchanges is defective in person with CF
|
no Cl channel on apical membrane thus can't have Cl exchanging with HCO so HCO can't be reabsorbed
|
|
|
why do we need bile?
|
for digestion and absorptoin of fats and for excretion of water insoluble substances like cholesterol and bilirubin
|
|
|
who makes bile? who stores bile?
|
liver hepatocytes make bile
gallbladder stores bile during interdigestive period bile released into duodenum during digestive period after chyme has triggered release of CCK |
|
|
how do we get bile out of gallbladder?
|
chyme triggers release of CCK which produces contraction of galbladder and relaxation of sphincter of Oddi
|
|
|
what are the 4 thing that make up bile
|
1. bile acids
2, phospholipids 3. cholesterol 4. bile pigments |
|
|
where are primary bile acids made? where are they converted into secondary bile acids?
|
made in liver from cholesterol
in intestine, bacteria convert fraction of each into secondary bile acids |
|
|
where are bile acids conjugated?
|
in liver to glycine or taurine with Na to form bile salts
now they are more water soluble at intestinal pH |
|
|
what is uniqe about bile salts?
|
amphipathic: have both hydrophobic and hydrophilic portionns in aqueous soln, they orient themsleves aournd droplets of lipid and keep lipid dispersed in emulsion
|
|
|
what do bile salts form?
|
micelle with the hydrophlic compoennts of bile salts on outside
free fatty acids, monoglycerides, fat soluble vitamines and cholesterol inside micelle |
|
|
what happens to phospholipids when they are apart of micelles?
|
they are normally inosoluble to water, but are solubilized by bile salt micelles
micelles able to solubilize other lipids mre effectivley when they contain phospholipids then when they don't |
|
|
why do bile salts want phospholipids to form micelles with them?
|
micelles are able to solubilize other lipids more effectively when they contain phospholipids
|
|
|
what must happen to cholesterl before it can be secreted in bile?
|
must be solubilized by bile salt micelles bc insoluble in water
will find cholsterol in the interior of micelle |
|
|
what happens if more cholesterol is present than can be solubilized?
|
crystals form in bile..seed for gallstone formation
|
|
|
what are bile pigments?
|
principal pigment bilirubin
metabolite of hemoglobin |
|
|
is bilirubin soluble or insoluble in water?
|
insolbule but made soluble when conjugated to glucuronic acid in liver
then excreted as soluble salt bililrubin glucurnide; not found in micelles |
|
|
waht is responsbile for the golden yellow color of bile?
|
bile pigmens in bilirubin
|
|
|
explain the excretion of bile pigments?
|
metabolite of Hb from aged RBCs
unconjugated pigment is then carried tighly bound to plasma albumin to liver taken up by liver and conjugated to glucuronic acid and secreted into the bile water soluble conjugates propelled into intestine, then in the distal small bowel the pigment is acted upon by bacteria and becomes unconjugated bilirubin then pass through colon are are excreted |
|
|
what is the electrolyte composition in bile?
|
simliar to pancreatic juice: predom Na, Cl, HCO3
|
|
|
what happens in enterohepatic circulation to most of the bile salts?
|
most bile salts that enter small I actively reabsorbed in terminal ileum by active transport mxn back into portal circulation to enter liver: total pool must circulate at least 2x per meal
|
|
|
almost all bile acids in portal blood are bound to waht?
|
plasma proteins
|
|
|
how are bile acids extracted by hepatocytes?
|
bile a cids are reabsobed from teh blood by a seconary active transport mex dependent on Na gradient established by the Na/K ATPase. they then enter the bile canaliculus via facilitated diffusion pathway
water and electrolytes enter the bile through paracellular pathways along an osmotic gradient: osmotid filtration |
|
|
what happens to the small amt of bile salts lost in feces?
|
replaced by syn in liver
if fecal losses exceed rate of syn, total pool decreases in size |
|
|
what are the 2 components of biliary secretion control?
|
bile independent fraction: vol of secretion of water and electroltes
bile dependnet fraction: quantitiy of bile salts secreted by liver |
|
|
what are choleretics?
|
potent stimulators of bile secretion: bile salts and bile acids
*bile salts and acids can also inhibit new bile acid syn |
|
|
amt of bile salts secreted is directly related to what?
|
amt of bile reabsorbed by liver
|
|
|
when does the gallbladder collect bile?
|
collects bile from liver during interdigestive periods
|
|
|
how does the gallbladder concentrate bile?
|
by removing Na, Cl, HCO, water removed by osmotic gradient produced
|
|
|
major stimulus for gallbladder contrxn?
|
CCK which is released in response to fatty acids and small peptides in duodenum
|
|
|
what are the 2 actions of CCK?
|
contracts smooth muscle of gallbladder
relaxes sphincter of Oddi vagal activity during digestion also stimulates contraction |
|
|
what are the 2 diff types of gallstones?
|
cholesterol: 70-80% in Western societies
pigment stones |
|
|
what are pigment stones composed of?
|
calcium bilirubinate, unconjugated bilirubin
|
|
|
how are gallstones treated?
|
surgical removal of gallbladder-cholecystectomy
bile will empty slowly but continously into duo, fats can be digested, but high fat foods should be avoided |
|
|
job of large I?
|
absorbs most of the fluids passed into it from small I; remainder containing unabsorbed nutrients and fluids passes into feces
|
|
|
waht are Haustra?
|
sac like segments in colon
present when colon is empty dissappear during and reappear following contractions of specific segment |
|
|
what sphincter is associated with large I and what is its fxn?
|
ileocecal sphincter
when ileum distended, sphincter releaxes-contents flwo into colon when colon distended, sphincter contracts-reflux into ileium prevented |
|
|
what types of contractsion/motilty do we have in large I?
|
segmentation contractions: majority of mvmts, mix contents
peristaltic contractions: move chyme slowly along colon mass mvmt: peristaltic wave, occurs 1-3times/day, moves colonic contents long distances |
|
|
what movmt in large intestine moves colonic contents long distances into rectum?
|
mass mvmt
|
|
|
which large I conraction is partly responsible for haustra appearance?
|
segmentation contractions
|
|
|
why does fecal material mvmt move so slowly in distal colon?
|
b/c most water absorption occurs in prox colon
|
|
|
what contractions are the most predom in distal colon
|
segmentation but cause little mvmt
mass mvmts propel material inot rectum |
|
|
waht is the normal state of rectum? descrive the freq of contractions in rectum
|
normally empty
freq of conractions in rectum greater than that in sigmoid colon cuasing retrograde mvmt of fecal material into sigmoid colon |
|
|
how can we have retention and absorption of suppositories?
|
b/c freq of conractions in rectum greater than that in sigmoid colon cuasing retrograde mvmt of fecal material into sigmoid colon
|
|
|
what happens when fecal material is forced into rectum
|
rectum contracts and internal anal sphincter relaxes-rectosphincteric reflex
|
|
|
what is the rectosphincteric reflex?
|
after fecal material is forced into rectum the rectum contracts and internal anal sphincter relaxes
|
|
|
when do you feel the urge to defecate? what happens next?
|
when rectum filled 25% of capacity
defecation prevnted by external anal sphicter until you voluntarily relax it |
|
|
normal state of external anal sphincter?
|
tonically contracted: individuals lacking tonic contraction wil defecate whenever rectum fills with fecal material b/c of rectosphincteric reflex
|
|
|
what hapens when you don't defecate when you feel the urge?
|
internal anal sphincter contracts, rectum relaxes to accomodate fecal material w/n it, and urge to defecate subsides
|
|
|
what is the composition of feces?
|
relatively unaffected by variations in diet: large fraction of fecal mass nondietary in origin therefore even if starving will still defecate: inorganc material, undigested plant fibers, bacteria, water
|
|
|
what is the problem in megacolon/Hirschsprungs?
|
absence of enteric nervous system from segment of colon
normaly the enteric nervous sysem is inhibitory of contraction in the absene of enteric NS get tonic contraction, build up of material, severe constipation |
|
|
describe the differences in segmentation contractions in constipation vs diarrhea?
|
constipation: more segmentation contractions
diarrhea: lack segmentation contractions |
|
|
what can dimish freq of bowel mvmts?
|
ignoring urge to defecate
lack of exercise some medications: narcotics, antidepress old age long term use of laxatives |
|
|
what is diverticulosis?
|
developemnt of small finger like pouches through weak spots in colon wall
if they become inflamed=diverticulitis causes localized abdom pain can perforate colon wll most do not causes symtpoms |
|
|
waht is the thought of the cause of diverticulosis?
|
long term lack of fiber in diet
|
|
|
what is Crohn's disease?
|
inflammatory condition of GI Tract
if section of ileum is removed then more bile salts lost and more now need to be made in liver |
|
|
digestion and absorption of materials can only take place after the materials move through what layer to reach capillaries
|
unstirred layer the sits above microvilli
|
|
|
where are carbs, protiens, lipids, fat soluble vitamins, water soluble vitamins , Ca and Fe absorbed?
|
small I
|
|
|
where are B12 and bile acids absorbed?
|
ileum of small I
|
|
|
in order to be absorbed, what must carbs be broken down into?
|
monsachhardies: glucose, galactose, fructose
|
|
|
in order to be absorbed, what must proteins be broken down into?
|
amino acids, dipeptides, tripeptides
|
|
|
what are starches converted to and how?
|
converted to maltose, maltotrios, and alpha limit dextrans by saliveary and pancreatic alpha amylase**
|
|
|
waht enzymes break down starches?
|
salivary and pancreatic alpha amylase: start the digestion of complex carbs
|
|
|
after the starches are broken down into oligosachharides by alpha amylase, how are they broken into monosaccharides?
|
hydrolyzed to glucose by glucoamylase, maltase
sucrose cleaved by sucrase to glucose and fructose lactose digested by lactase to glucose and galactose |
|
|
what breaks down sucrose?
|
sucrase into glucose and fructose
|
|
|
what breaks down lactose?
|
lactase into glucose and galactose
|
|
|
is cellulose digested by human enyzmes?
|
no, bacteria cn braek it down
|
|
|
maltose, maltotriose and alpha limit dextrans are hydrolyzed to what?
|
glucose by glucoamylase, maltase on brush border
|
|
|
b/c the intestine will only absorb monosaccharides, how are they absobed?
|
glucose and galactse into enterocyte by common Na depend active transport with Na going down its gradient
fructose is absobed by facillitated diffusion; cannot be absobed against its conc gradient |
|
|
what happens if you take in a lot of fructose?
|
no all of it can be absorbed b/c it is exclusively absorbed by facilitated diffusion and cannot be absorbed against conc gradient thus if increase intake, gradient incresae
|
|
|
what is happening in lactose intolerance?
|
def in lactase
lactose remains in GI as unabsorbed solute decreasign water reabsorb and leading to diarrhea the undigested lactose is then metabolized by colonic bacteria |
|
|
s/s of lactose intolerance?
|
intestinal distention, borborygymi (gurgling), gas, diarrhea
w/ aging can become lactose intolerant |
|
|
who is lactose intolerance more common in?
|
adults
in infants: life threatening |
|
|
what are the 2 sources of proteins?
|
endogenous: secretory proteins and cells shed into GI tract lumen
exogenous: dietary proteins |
|
|
majority of proteins are absorbed as?
|
amino acids, dipeptides, tripeptides; larger peptides poorly absorbed if at all
|
|
|
action of endopeptidases? waht are they?
|
hydrolyze interior peptide bonds
ex: enterokinase converts inactive trypsinogen to tryspin active trypisn then autocatalyzes convertions of trypsinogen to trypsin and cymotrypsinogen to chymotrypsin |
|
|
action of enterokinase?
|
converts trypsinogen to trypsin
then trypsin autocatalyzes itselft to do the same conversion as well as convert chymotrypsinogen to chymotrypsin and proelastase to elastase |
|
|
action of exopeptidases?
|
hydrolyze one amino acid at a a time from C terminus of proteins
|
|
|
ex of exopeptidases?
|
carboxypeptidases A and B
|
|
|
action of peptiases?
|
in brush border cleave peptides produced by pancreatic proteaus to oligopeptides and amino acids
|
|
|
how are L-amino acids absorbed inot enterocytes?
|
by Na dependent secondary active transport
|
|
|
how are basic and neutral amino acids absorbed into enteroctes?
|
by facilitated diffusion unlinke L amino acids
|
|
|
transport of what is more efficent and faster than for amino acids?
|
tranpsort of di and tri peptides uses Na dept secondary active transport
|
|
|
following a meal, majority of protein is absrobed in what form?
|
di and tri peptides
most absorbed peptides then converted to amino acids by cytoplasmic peptidases |
|
|
what does cystinuria affect?
|
uptake of basic amino acids
|
|
|
waht does Hartnup diesease affect?
|
uptake of neutral amino acids
|
|
|
what does prolinura affect?
|
reabsorp of proline
|
|
|
an absence of enterokinases would decrease activity of what?
|
chymotrypsin b/c no trypsin to activate ti
|
|
|
waht percent of the iron that is eaten is absorbed?
|
amot absorbed equal to ingested
|
|
|
how is iron absorbed ?
|
as heme: bound to Hb or myoglobin fro meat or as free iron
|
|
|
what happens in enterocyte to heme iron/
|
broken down to release free iro
|
|
|
what are the 2 forms of free iron? which is more common?
|
ferrous: absorbed more readily
ferric: insoluble, most dietary iron is ferric |
|
|
how do ascobric acid and citric acid promote absorption of iron?
|
form insolulbe complexes with iron and reduce ferric to ferrous to make it more absorbable
|
|
|
what do enterocytes release in terms of iron?
|
intestinal transferrin to complex with iron in lumen and bind to receptors to be absorbed
|
|
|
what happens to absorbed transferrin-Fe complex?
|
tranpsorted to BL membrane
|
|
|
iron transported in plasma is bound to what?
|
plasma transferrin: depending on amt of Fe needed
|
|
|
why do we need ferritin?
|
b/c free iron is cytotoxic so iron in cell binds very tightly to apoferritin to form ferritin for storage
|
|
|
if you are iron deficient what do you have more/less of?
|
plasma tranferrin is increased, more iron is moved from enterocyte to plasma
|
|
|
if you have iron excess, what do you have more/less of?
|
circulating transferrin is decreased
more iron stored as ferritin iron lost when enterocytes are shed |
|
|
what is the most prevalent nutrient def?
|
iron def
most common cuase of anemia in world |
|
|
waht do you call chronic absorption of too much iron?
|
hemochromatosis:cooking food in iron pots
|
|
|
what is the most common genetic condition in US?
|
hereditary hemochromatosis
|
|
|
excess iron in liver can lead to?
|
cirrhosis and eventually liver cancer
can also damage pancreas, leading to diabetes contributes to coronary disease |
|
|
tx of hereditary hemochromatosis?
|
periodically removing blood
|
|
|
when body levels of iron are high, the formation of ferritin?
|
increases
|
|
|
how do electrolytes and water cross intestinal cells?
|
transcellular: move through cells
paracellular: more b/n cells |
|
|
what are the 4 mxns of Na transport from lumen of small I?
|
1. restricted diffusion through channels
2. Na-glucose or Na-amino acid co transport 3. Na-Cl co transport 4. Na-H exchange |
|
|
how do the mxns vary over lenght of small I for Na tranposrt?
|
duodenum/jejunum: Na absorbed mostly by Na glucose or Na-amino acid co transport and Na-H exchange
ileum: Na-Cl co transport colon: Na through channels |
|
|
in order to transport Na into enterocyte from lumen, what must occur?
|
need low intracellular [Na] therfore have Na/K ATP ase promoting transport of Na into cell
|
|
|
how is Cl transport into small I?
|
passive diffusion via paracellular route established by transport of Na
co-transport with Na and K exchange with HCO3 |
|
|
how is water absorption accomplsihed in small I?
|
active reabsorption of electroytes and nuterients creates osmotic gradient favoring passive reasborptoin of water
|
|
|
waht constitutes almost all of total dietary lipids?
|
triglycerides
|
|
|
in order to be absorbed, what must happen to lipids?
|
must be made soluble
|
|
|
what happens to lipids in stomach?
|
mixing breaks lipids into droplets to incresae total surface area availble to digestive enzymes, but low pH inhibits emulsifcation
|
|
|
waht does CCK do to allow sufficient digestion of lipids?
|
slows gastric empyting
|
|
|
how are fats emulsified in small I?
|
by actions of bile salts and lecithin, increasing surface area
|
|
|
in small I waht must combine with lipids?
|
pancreatic enzymes to hydrolyze lipids to fatty acids, monoglycrides, lysophospholipids, and cholesterol
|
|
|
what are the pancreatic enymzes that hydrolyze lipids?
|
pancratic lipase
cholesterol ester hydrolase phospholipase A2 |
|
|
action of pancratic lipiase on triglycerides?
|
cleaves them into fatty acis and monoglcerides
|
|
|
axtion of phospholipase A2?
|
cleaves phospholipids inot fatt acids and lysolecithin
|
|
|
axtion of cholesterol esterase?
|
breaks down CE to fatty acids and cholesterol
|
|
|
action of colipaes?
|
non-enzymatic protein secreted as inactive precursor by pancreas; activated in intestinal lumen by trypsin
prevents inhibition of pancreatic lipase by biles salts acts as anchor for lipase by binding enzyme to bile salts on suface droplet of emulsfied TG |
|
|
waht does colipase do?
|
hooks lipase onto bile salts to allow it to digest triglcerides
also binds micelles allowing the entry of lipid digestion produxts into micelles |
|
|
waht binds 1:1 with lipase
|
colipase
also binds bile salts micelle: keeping it close to site of hydrolysis |
|
|
how are lipids absorbed?
|
they form water soluble mixed micelles with bile
micelles then bring products of lipid digestion through unstirred water layer into contact with microvilli on surface of enterocytes |
|
|
explain how the micelle moves lipid digestion products into enterocyte
|
micells containing lipid digestion products and bile acids diffuse from the luemn into the unstirred layer where the micelle decomposes. the high conc of lipid soluble materials adjacent to the enterocyte surface allows diffusion of theese materials into the interacellular space
|
|
|
are lipids absorbed as part of intact micells?
|
no the micelle decomposes at the apical border
|
|
|
how do short and medium chain fatty acids get inot the cell? what elese gets in this way
|
b/c they are small and water soluble tehy dont need micelles so they diffiuse
glycerol is hydrophilic so it also is not contained in miceles |
|
|
waht happens to lipids in enterocytes?
|
the products of lipid digestion are reesterified to triglycerides and phosphlipids
|
|
|
what are the 2 intracellular processing pathways of lipids?
|
monoglyceriede acylation pathway
phosphatidic acid pathway |
|
|
explain the monoglyceride acylation pathway?
|
triglycerides syn from 2-monoglycerides and CoA-activated fatty acids
fatty acid binding protins then transport long chain fatty acids from membrane to smooth ER where re-esterification takes place *short and medium chain do not require resyn into TG-go straight into blood |
|
|
what is happening in the phosphatidic acid pathway?
|
2 Acyl CoA + alpha glycerophosphate beomce phospatidic acid
phsophatidic acid combines with Acyl CoA to form TG + phosphate |
|
|
both free and re-esterified cholesterol is transported in what?
|
chylomicrons
|
|
|
what forms chylomicrons?
|
resynthesized TG, cholesterol, CE and phospholipids
|
|
|
core of chylomicrons?
|
TG, esterified cholesterol, fat soluble vitamins
|
|
|
surface of chylomicrons?
|
phospholipids, apoprotein, free cholesterol
|
|
|
what do we need apoproteins for?
|
they are water soluble and are required for transporting chylomicrons out of cell
A,B,C and E w/o apoproteins can't tranport out of cell |
