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61 Cards in this Set
- Front
- Back
GI peptides: distinction
- endocrine - paracrine - neurocrines |
distinction is based on origin cell and route to target
- endocrine peptides travel thru the blood to target cells - paracrine peptides diffuse through the extracellular space to neighboring cells -neurocrines - synthesized in neurons and diffuse across synaptic gap |
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Gastrin
-source -releasing factors -functions |
source: mainly antrum of stomach, also in duodenum and jejunum
release stimulated by: amino acids, peptides, gastrin releasing peptide, stomach distension; release is inhibited by H+ functions: acid release |
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Acid secretion in the stomach
-where from -what stimulates it |
gastrin, histamine, and Ach activate the parietal cell which secretes gastric acid
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CCK
-source -releasing factors -functions |
source: duodenum, jejunum, illeum
stimulated by: fat in food, amino acids function: increases pancreatic enzyme secretion, bile and gastrin secretion, stomach emptying |
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Secretin
-source -releasing factors -functions |
source: duodenum, jejunum, ileum
stimulated by: low pH function: promotes HCO3 production from pancreas and bile, causes pepsin secretion (inhibits acid secretion) |
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GIP = glucose dependent insulinotropic peptide
-source -releasing factors -functions |
source: duodenum and jejunum
stimulated by: glucose, AA, FA causes: insulin secretion and inhibits gastric acid |
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motilin
-source -releasing factors -functions |
source: duodenum and jejunum
stimulated by: fasting function: causes motility |
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Enteric nervous system
-myenteric plexus -submucosal plexus |
- capable of regulating GI function in the absence of extrinsic innervation
-myenteric - btw circular and longitudinal muscle layers, controls muscularis externa (motility) -submucosal - controls glandular, endocrine, and epithelial cell secretion |
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parasympathetic innervation
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- excitatory for motility and secretion
innervation: - IX - upper esophagus - X - esophagus thru colon, pancreas, liver, GB - pelvic nerve - colon, rectum, anus |
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sympathetic innervation
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fibers from:
- celiac ganglion (esophagus thru SI) - superior mesenteric ganglion - transverse colon - inferior mesenteric ganglion/ hypogastric plexus - rest of colon, anus, rectum |
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Chewing
- 3 functions |
function:
- reduction in particle size - mixing of food with saliva ( easier to swallow, exposure to amylase and lipase) - stimulation of taste buds |
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Oral or Buccal phase of swallowing
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- voluntary control
- tongue moves food |
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muscle tone in esophagus, during rest
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- upper and lower esophageal sphincter are tonically contracted - isolating the esophagus
- esophageal muscles do not maintain contraction (flaccid) |
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Pharyngeal phase of swallowing
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- involuntary, controlled by the swallowing center in the reticular formation
- phase starts when bolus touches tonsils/ base of tongue --> afferents to swallowing center --> efferents back to sphincters/ esophageal muscles - inhibition of respiration - UES relaxes to let bolus enter esophagus and then contract more than normal to prevent reflux (ACh, enkephalin) - higher pressure |
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esophageal phase of swallowing
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- primary esophageal peristalsis/ slow peristaltic wave (initiated by the swallowing center)
- lower esophageal sphincter relaxes, then contracts (above normal level - ACh, enkephalin) - fundus and body of stomach relax (receptive relaxation) - relazation is mediated by vagal inhibition (NO, VIP) - inhibition of respiration |
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seconday peristalsis
- function - when it happens/ stimulated by |
- not preceeded by pharyngeal activity
- stimulated by distension of esophagus (stretch receptors --> vagus nerves) - clears the esophagus of retained food/ refluxed gastric contents - no sensation associated |
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4 Anti reflux mechanisms
in what situations do people rely on different mechanisms? |
- LES - high pressure
- seconday peristalsis, clearing of esophagus (important in pregnancy since other mechanisms are weaker) - pinching action of diaphragm on esophagus (important in infants) - reflexes (increased intragastric and intraabdominal pressure causes increase LES pressure) |
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Retching and Vomiting
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- peristalsis in SI towards stomach
retching - not tenough force to move contents thru the UES vomiting - additional contraction of the diaphragm and abdominal muscles & decreases in sphincter tone |
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Stomach functions
(4) |
Storage
- receptive relaxation (relaxes during swallowing) - accomadation (muscle relaxation due to distension - storage allows digestion by amylase/ gastric enzymes Mixing - antral muscle - facilitates digestion Size reduction Controlled gastric emptying |
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migrating myoelectric complexes
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during interdigestive period, sweep undigestible stuff out of the stomach and SI
-strong intermittent contractions -beginning is associated with motilin (stops w/ feeding/ gastrin) - generated when the stomach is empty -requires enteric system |
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antral systole
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- simultaneous contraction of the terminal antrum and the pylorus
- chyme and liquids first leave the stomach - systole causes retrograde mvmt of chyme back in to stomach (mixing) and reduction in particle size |
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What affects the change in gastric emptying rate?
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- increased gastric volume = faster emptying rate
- depends on what is in the stomach: ~smaller empties faster ~ liquids = faster ~carbs faster than protein faster than fat ~neutral faster than acid ~isotonic faster than hypotonic faster than hypertonic - duodenogastric reflex - distension of duodenum slows emptying - ileogastric reflex - distension of ileum decreases emptying - emotion can also affect emptying |
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interstitual cells of Cajal
- where - what they do |
- Electrical control activity/ slow wave originates here
- lies btw circular and longitudinal muscle layers within the inner dense circular muscle layer - signal is conducted via gap junctions to rest of cells |
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Electrical Control Activity = Basal electrical rhythm= slow waves
- ion flux |
= fluctuation of the resting membrane potential of muscle cells
Depolarization: Ca++ and Na+ influx plateau = Ca++/Na+ influx balanced with K+ efflux (via Ca++ gated K+ channels) repolarization – K+ efflux via Ca++ gated channels Varying size, doesn’t always lead to contraction |
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Electrical response activity (ERA)
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- at the plateau of the ECA, when depolarization is sufficient to activate voltage gated Ca++ channels
→ cause muscle contractions multiple ERAs – more Ca++ enters muscle cells causing a stronger contraction |
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ECA and ERA control with neuroendocrine agents
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- neuroendocrine agents can NOT initiate ECA, but can induce ERAs (cause more of the ECAs to have ERAs) by changing ion channel activity
- excitiatory: Ach and gastrin – indue ERAs, stronger contraction - inhibitory: norepinephrine, VIP, NO, epinephrine – reduce ERAs, weaker, shorter contractions |
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Inhibitors of the movement of chyme
-drug -reflex |
- morphine reduces chyme mvmt by causing an increase in muscle tone
- adynamic ileus – inhibition of muscle activity due to obstruction - intestino/conoic/peritoneo-intestinal reflexes – distension of intestine or colon or peritoneal area → inhibits muscle activity |
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Ileocecal sphincter
- function - reflexes |
Function:
- delay transit into colon (allowing time for reabsorption) - prevent bacterial overgrowth reflexes - distension in the lower ileum → relaxation (chyme can enter colon) - upper cecum distension → ⇑ contraction to prevent backflow |
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LI Structural modifications (3) and what they cause
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- tenia coli (3 bundles of longitudinal muscles, nonuniform shortening)
- reduced electrical coupling (less coordinated contraction) - 2 sets of pacemaker cells - allow localized contractions |
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rectophincteric reflex
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distension of rectum causes the enteric and parasympathetic nerves to relax the internal anal sphincter, mental perception of urge to defecate
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Gastroileal reflex
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- entry of food into the empty stomach results in the relaxation o
of the ileo -cecal sphincter leading to the emptying of ileum |
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Colonocolonic reflex
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distention of one part of the colon leading to relaxation ofother parts (final result: decreased resistance and increased aboral movement)
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Gastrocolicreflex/Duodenocolic
reflex |
entry of food into the empty stomach or chyme into the duodenum results in increases of aboral propulsive movement in the
colon. |
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Functions of Saliva
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- lubricate (for swallowing)
- dissolve (for taste) - protect – alkaline pH, lysozyme, lactoferrin, Ig - facilitate speech - carb and fat digestion (amylase and lipase) |
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Source of Saliva
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- parotid = serous secretions, amylase
- sublingual – mucous secretions - submaxillary – mixed - buccal glands – mucins |
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2 stage secretion model of Saliva
- what the 2 parts are -product |
1° acinus produces an isotonic secretion
2° ductile epithelial cells modify the secretion by reabsorbing Na+ and Ca++ and secreting HCO3- and K+, --> produces a hypotonic solution high in K+ and HCO3- |
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Sympathetic and Parasympathetic control of salivation
- amt of output - composition of secretions |
salivary nucleus of the medulla stimulates parasypmathetics, which cause:
o sustained increased salivation o protein poor sympathetics: o transient decreased salivation o protein rich both: if denervated – decresased secretion |
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Oxyntic component of Gastric secretion
- what it consists of - what each factor does - what stimulates it |
consists of:
H+, Cl-, intrinsic factor (parietal cells ) Stimulated by: feeding Increases greatly with increased secretory rate functions: o Acidic pH activates pepsinogen and lipase o HCL depantures proteins, stabilizes minerals, inactivates microbes o Intrinsice factor – required for B12 absorption |
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Control of Acid secretion
-phases of digestion associated with secretion -what enzymes are involved in control/ their receptors and effects |
Most acid is secreted when food is in the stomach, a lot is also secreted when food is smelled/ tasted/ chewed/ swallowed
Stimulate HCl release: o Gastrin --> CCK/ gastrin receptor and stimulates Ca++ release o Ach binds M3 receptor and also stimulates Ca++ release o Histamine bines H2 receptor an stimulates cAMP inhibitors of gastrin and cAMP, decreasing HCl: Somatostatin, secretin, GIP, prostaglandins transforming and epidermal growth factors |
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Non oxyntic component of gastric secretions
-whats included -what stimulates it/ secretion mechanisms |
includes:
mucous, Na+, HCO3- (mucous cells) pepsinogen (chief cells) HCO3- is secreted into the lumen from the epithleial cells by: o Cl-/ HCO3- exchanger which is stimulated by glucagon oHCO3- transporter stimulated by prostaglandin E Mucous secretion: Parasympathetic→ (+)neck mucus cell Mechanical/chemical irritation → (+) surface mucus cells |
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Disruption of the mucosal barrier
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- mucosal barrier is made by the non oxyntic component of gastric juice
- aspirin – acidification, inhibits prostaglandin (decreased HCO3- and mucus secretion) - NSAIDs - inhibits prostaglandin (decreased HCO3- and mucus secretion) - Ethanol – inhibits intracellular enzymes - Bile acids – solubiliza plasma membrane - H pylori – inflammation, immune response |
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Production of pancreatic secretions
- cells involved - what they produce |
- acinar cells – synthesize the enzymes and stored in zymogen granules until they need to be secreted)
- centroacinar and ductal cells – produce the initial, isotonic, aqueous component of pancreatic secretion; this aqueous secretion is then modified by the ductal epithelial cells: o Cl-/HCO3- exchanger secretes HCO3- into the pancreatic juice (which causes a net absorption of H+ into the blood) |
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2 functions of pancreatic secretions
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- HCO3- to neutralize chyme from stomach in the duodenum
- Emzymes to digest: pancreatic amylase, lipase, proteases (have to be converted to active form) |
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Control of secretion (autonomic and hormonal)
- aqueous portion - enzymatic portion |
Aqueous portion:
o H+ in the lumen of the intestine →(+) secretin secretion →(+) ductal cells o AcH and CCK also stimulate ductal cells Enzymatic portion o peptides, AA, FA → (+) secretion of CCK → (+) acinar cells o Ach stimulates acinar cells |
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bile salts
- functions |
o amphipathic
o emulsify lipids by surrounding the lipids, creating small lipid droplets in the intestinal lumen increasing the surface area for the digestive enzymes o form micelles w/ the products of lipid digestion – at the core of the micelle – lipid products, at the edges – bile salts – allows lipid products to move in the aqueous solution of the lumen |
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Gallbladder control
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- chyme reaches the SI: AA, peptides, FA→(+) CCK is secreted to stimulate the contraction of the gallbladder and relaxation of sphincter of Oddi → bile flows into the duodenum
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Recirculation of the bile salts – Enterohepatic circulation
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- bile salts are absorbed (from the ileum) into portal circulation by Na+-bile salt cotransporters
- hepatocytes extract bile salts from the portal blood, so only a small amt of bile salts have to be remade |
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Starch Breakdown (digestion)
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1st stach digested with alpha amylase in the saliva (inactivated when it reaches the stomach), stach digested with pancreatic amylase in duodenum → produces disaccharides
- THEN, disaccharides digested by brush border enzymes (alpha dextrinase, maltas, sucrase) → glucose - disaccharides in food – are digested by brush border enzymes trehalase, lactasem sucrase → glucose, galactose, fructose only glucose, galactose and fructose can be absorbed by epithelial cell |
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Absorption of monosacharrides across the apical (into ep cell) and basolateral (into blood) membranes
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- glucose and galactose: absorbed into epithelial cell by Na+ glucose cotransporter SGLT1
- Fructose is absorbed into the epithelial cell by GLUT5 transporter by facilitated diffusion (can’t be absorbed agst gradient) - Glucose, galactose, and fructose – all absorbed into blood via GLUT2 facilitated diffusion |
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Protein breakdown (digestion)
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- 1st proteins digested w/ pepsin in stomach (pepsinogen produced by chief cells and activated by ⇓pH - ⇑pH of duodenum in activates)
- 2nd proteins digested with pancreatic proteases (trypsin – which is activated by enterokinase in the brush border and then activates other enzymes: chymotrypsin, elastase, carboxypeptidase A and B) →AAs, di and tripeptides, larger peptides - 3rd brush border proteases in SI break down larger peptides -->di/tri peptides absorbable form: di and tripeptides, AAs |
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Protein absoprtion:
- products of breakdown - how their absorbed at apical and basolateral membranes |
AAs
apical/ ep cell membrane from lumen: - Na/AA cotranporters (separate transporters for neutral, acidic, etc) AAs - basolateral/ blood membrane: - transported into blood by facilitated diffusion Di/tripeptides, apical: - H+/ditripeptide cotransporter basolateral: Within the cell, di/tripeptides are either broken down to AAs or just absorbed as is. |
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Lipids
- 3 ingested forms - how each gets broken down/ enzymes used - where |
1. Triglycerides:
stomach -lingual and gastric lipases (triglycerides→ glycerol and FAs) SI - pancreatic lipase (triglycerides→monoglyceride, FAs) 2. Cholesterol ester: SI- cholesterol ester hydrolase ( →free cholesterol, FAs) 3. Phospholipid SI- phopholipase A2 (→lysolecithin and FAs) |
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Lipid absorption
-how they get absorbed into epithelial cell -what happens to get them into the bloodstream |
- solubolized in lumen as micelles
- @ epithelial cell, lipids are released from the micelle and diffuse down concentration gradient into the epithelial cell in duodenum, jejunum - inside epithelial cell – lipid digestion products are reesterified to reform original lipids - lipids are packaged with apoproteins and carried in chylomicrons which are put in vesicles and exocytosed into lymphatic capillaries → bloodstream |
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pancreatic insufficiency
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can’t breakdown triglycerides → in feces
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zollinger Ellison syndrome
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- too much acid from parietal cells- → acidic environment of the duodenum (not neutralized) → lipases can’t work (not prime pH) → triglycerides in feces
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bile salts deficiencies/ ways they get inactivated
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- deficiency of bile salts – can’t form micelles to absorb lipid products → lipid products are in feces (phospholipids, monoglycerides, FAs, cholesterol)
- bacterial overgrowth/ ⇓ pH – deactivates bile salts to bile acids (which is absorbed easily, too soon – prior to micelle formation) → lipid products in feces |
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Fat soluble vitamins
- what they are - how absorbed |
- vitamins A, D, E, K
- absorbed w/ lipids (packaged into micelles and then chylomicrons →blood) |
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Water soluble vitamins
-what they are -where they are reabsorbed |
Jejunum:
B1, B2, B3, folate; B6 (duodenum & jejunum), B7 (proximal intestine) Ileum: C, B12 (distal ileum) |
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Ca++ absorption
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dependent on D 1,25 dihydroxycholecalciferol
dietary vitamin D3 – converted in the liver, again in the kidney to finally 1,25 diydroxycholecalciferol which promotes Ca++ absorption from SI o [deficiency in Vitamin D or conversion to active form → rickets, osteomalacia] |
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Iron absorption
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- absorbed as free iron (Fe++) or heme iron (bound to Hb, once inside epithelial cells, Hb-iron is digested to release free iron)
- free iron in epithelial cell binds apoferritin which is transported into blood - in blood, iron is bound to transferrin for transport |
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Where are the following most absorbed:
-carbohydrates - proteins |
Carbohydrates: most in the duodenum, completed by mid jejunum
protein: mainly jejunum and ileum |