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Flashcards in SM02 Mini2 Deck (471):

general functions of the digestive system

  1. ingest food
  2. digest food
  3. absorb nutrients
  4. defecate waste


how is the rate of delivery of luminal contents coordinated in the GI tract?

  • intrinsic nerves: enteric nervous system
  • extrinsic nerves: ANS (sympathetic & parasympathetic)
  • neurocrine signaling
  • paracrine signaling
  • endocrine hormones
  • solinocrine peptide hormones: secreted into GI lumen before affecting target


functions of digestive secretions

  • provide liquid in which solid components are digested
  • provide most digestive enzymes 
  • provides pH balance to intestinal contents
  • increases solubility & surface area of lipids to maximize digestibility
  • provides lubrication for mass movements in colon
  • protection of mucus membranes


what are the components of saliva & their functions?

  • serous fluid: moisten food & mucous memebrane
  • lysozyme: kill bacteria
  • salivary amylase: startch digestion
  • mucus: lubricate food; protect GI tract from digesting itself


what is the function of HCl in gastric secretions?

  • nonspecific digestion of food
  • activate pepsinogen to pepsin


what is the function of pepsin?

digests protein into smaller peptide chains in stomach

secreted by parietal cells as pepsinogen

activated by low pH in stomach lumen


what is the function of bile?

aka bile salts

  • emulsify fats, making them available to intestinal lipases
  • help make end products soluble & available for absoprtion by the intestinal mucosa
  • aid perstalsis


what are the pancreatic digestive secretions?

  • trypsin
  • chymotrypsin
  • carboxypeptidase
  • pancreatic amylase
  • pancreatic lipase
  • ribonuclease
  • deoxyribonuclease
  • cholesterol esterase
  • bicarbonate ions


what are the small intestine digestive secretions?

  • mucus
  • aminopeptidase
  • peptidase
  • enterokinase
  • amylase
  • lipase


what is the function of mucus throughout the GI tract?

  • protect mucosa from stomach acid, gastric enzymes, & intestinal enzymes
  • provides adhesion for fecal matter
  • protect intestinal wall from bacterial action & acid produced in feces


what is the function of trypsin?

digest proteins

breaks polypeptide chains at Arg or Lys residues


what is the function of chymotrypsin?

digests proteins

cleaves carboxyl links of hydrophobic amino acids


what is the function of carboxypeptidase?

digests proteins

removes amino acids from the carboxyl end of peptide chains


what is the function of pancreatic amylase?

digests carbohydrates

hydrolyzes startches & glycogen to form maltose & isomaltose


what is the function of pancreatic lipase?

digests fats

hydrolyzes fats (mostly triacylglycerols) into glycerol & fatty acids


what is the function of ribonuclease?

to digest ribonucleic acid


what is the function of deoxyribonuclease?

to digest deoxyribonucleic acids

hydrolyzes phosphodiester bonds


what is the function of cholesterol esterase?

hydrolyzes cholesterol esters to for cholesterol & free fatty acids


what is the function of bicaronate ions in the GI lumen?

provide appropriate pH for pancreatic enzymes


what is the function of aminopeptidase?

splits polypeptides into amino acids

from amino end of polypeptide chain


what is the function of peptidase?

spolits amino acids from poly peptide chains


what is the function of enterokinase?

activates trypsin from trypsinogen


where is mechanical digestion accomplished?

mouth via mastication 

stomach contractions

segmental contraction of intestines


where do the products go following absorption?

water soluble particles travel thru the blood to the liver via portal circulation

fat soluble particles are packaged as micelles & sent in to the lymphatic system via lacteals


where are carbohydrates digested?

  • oral cavity via salivary amylase in basic pH into poly- & disaccharides
  • duodenum via pancreatic amylase  in basic pH in to disaccharides
  • lining of small intestine @ brush boarder→​ monosaccharides​
    • lactase
    • sucrase
    • maltase
    • isomaltase


where are proteins digested?

  • gastrin lumen via pepsin→ poly- & dipeptides
  • duodenum 
    • trypsin
    • chymotrypsin
    • carboxypeptidase
  • brush border of small intestine
    • aminopeptidase
    • peptidase
  • **last 2→ amino acids, dipeptides, & tripeptides


where are fats digested?

  • stomach 
    • lingual lipase
    • gastric lipase
  • duodenum w/bile assistance
    • lipase
    • esterase
  • brush border of small intestine
    • lipase

**absorbed asa glycerol & fatty acids**


what are 2 substances absorbed in the oral cavity?

nitroglycerin & nictotine


where is skeletal muscle found along the digestive tract?

extreme oral & anal segments

allows for voluntary control at either end


how does the enteric nervous system work?

  1. stretch is sensed in one section of GI tract
  2. motor signals behind it & around it stimulate contraction of circular smooth muscle & relaxation of longitiudinal smooth muscle→ contraction of lumen
  3. motor signal ahead of stretch stimulate relaxation fo circular smooth muscle & contraction of longitudinal smooth muscle→ dilation/expansion of lumen


what is the function of the submucosal plexus?

aka Meissner's plexus

sensory & motor control of gastric secretions


what is the function of the myenteric plexus?

aka Auerbach's plexus

sensory & motor control of gastrointestinal motility


how do the myenteric & submucosal pexuses communicate w/each other?

via teriary plexus continuous w/myenteric plexus

deep muscular & mucosal plexuses

coordinate response between 2 major plexuses


what processes are controlled by the enteric nervous system?

  • GI tract motility
  • constriction of blood vessels
  • exocrine & endocrine secretions


describe intrinsic reflex of the circular muscle.


  • stretch reception
  • ACh & sibtance P from enteric motor neuron→ promote smooth muscle contraction oral to stimulus
  • different enteric motor neurons on aboral side release NO & vasoactive intestinal peptide (VIP)→ relax circular muscle
  • pressure gradient moves bolus in aboral direction


how does longitudinal muscle respond to stimulus, compared to the circular muscle?

opposite effect, same motor neurotransmitters

  • oral: NO & VIP→ relax
  • aboral: ACh & Subtance P→ contraction


how does serotonin affect the ENS?

from enteroendocrine cells

released by luminal stimuli

  • acts in a paracrine fashion to stimulate ENS interneurons activating the peristalic reflex


ACh effects in digestive system

acetylcholine: parasympathetic & enteric neurotransmitter

  • increases motility
  • closes sphincters
  • increases secretions



substance P effects in digestive system

parasympathetic & enteric neurotransmitter

  • increases motility


NO effects in digestive system

aka nitric oxide

parasympethetic & enteric neurotransmitter

  • muscle relaxation


NE effects in digestive system

aka norepinephrine

sympathetic neurotransmitter (extrinsic control)

  • decreases motility
  • decreases blood flow
  • decreases secretions


Neuropeptide Y effects on digestive system

sympathetic & enteric neurotransmitter

  • decreases motility
  • decreases secretion


VIP effects in digestive system

aka vasoactive intestinal polypeptide

enteric neurotransmitter

  • induces muscle relaxation
  • increases secretions


opoid effect on digestive system

ex. Met & Leu enkephalins

  • act indirectly on plexuses to inhibit motility & secretion


GABA effect on digestive system

aka gamma-amino butyric acid

widely expressed in END nerves

  • inhibits effects on motility & secretion


epinephrine effect on digestive system

sympathetic neurotransmitter

  • inhibits motility indirectly by acting on interneurons of ENS


how does parasympathetic stimulation affect GI function?

  • activates motility
  • inhibits sphincter tone (relaxes)- allows for more motility
  • increases secretions
  • no effect on vascular resistance


how does sympathetic stimulation affect GI function?

  • decreases motility
  • increases sphincter tone→ slows release of food/chyme
  • decreases secretions
    • except in salivary glands
  • increases vascular tone→ vasoconstriction→ decreases blood flow→ less motility


what GI hormones are produced in the stomach?

gastrin & somatostatin


how does cholecystokinin affect GI motility?

increases contractility of gallbladder smooth muscle


how does secretin affect GI motility?

increases movement of gastric juices into the duodenum


what GI hormones are produces in the small intestine?

duodenum or jejunum

secretin, cholecystokinin, motilin, glucose-dependent insulinotropic polypeptide, & somatostatin


what GI hormones are produced by the pancreatic islet cells?

insulin, glucagon, & somatostatin


what GI hormones are made in the colon?

ileum or colon

enteroglucagon & somatostatin


where is ghrelin secreted from?

fundus/upper stomach


where is gastrin secreted from?

antrum of stomach & decreasing incrementally thru to the jejunum


where is cholecystokinin secreted from?

duodenum & jejunum & less so in the ileum


where is secretin secreted from?

duodenum & jejunum & less so in the ileum


where is GIP secreted from?

aka glucose-dependent insulinotropic polypeptide

duodenum & jejunum


where is motilin secreted?

duodenum & jejunum


what signals induce the release of gastrin?

  • proteins & amino acids
  • stomach distension
  • parasympathetic nerve activity


what signal reduce or inhibit gastrin release?

decreased lunimal pH


what signals increase or induce the release of cholecystokinin?

  • proteins & amino acids
  • fatty acids
  • increased parasympathetic nerve activity


what signals increase or induce the release of motilin?

increased parasympathetic nerve activity


what signals decreased or inhibit the release of motilin?

  • proteins & amino acids
  • carbohydrates
  • fatty acids


what signals induce or increase the release of GIP?

aka glucose-dependent insulinotropic polypeptide

  • carbohydrates
  • fatty acids


what signals induce or increase the release of secretin?

  • fatty acids
  • decrease in luminal pH


actions of gastrin

act via CCKB receptors

  • increases gastric acid secretion
  • increases gastric motility
  • increases gastric mucosal growth
  • decreases gastric emptying
  • maximizes stomch churning


actions of secretin

  • increases pancreatic & biliary bicarbonate secretion
  • decreases gastric acid secretion


actions of cholecystokinin

  • increases pancreatic enzyme secretions via CCKA
  • increases gallbladder contraction via CCKA
  • decreases sphincter of Oddi tone indirectly
  • decreases gatric emptying via CCKB


actions of GIP

aka glucose-dependent insulinotropic polypeptide

  • increases pancreatic insulin secretion
  • decreases gastric acid secretion
  • decreases gastric emptying


actions of Motilin

increases gastric & intestinal motility


actions of Ghrelin

  • increases growth hormone secretion 
  • increases feeeding
  • increases weight gain


define ingestion

voluntary intake of food into the oral cavity


what important function is performed by the lips & taste buds?

sense food's temperature & composition


why is absorption limited in the oral cavity?

  • materials don't stay in there very long
  • very small surface area
  • substrates must be absorbable, but most need to undergo digestion into monomers first


what is the composition of saliva?

  • watery hypotonic fluid
  • ions: Na+, HCO3- (pH balance), Cl-, K+
  • mucus
  • digestive enzymes: salivary alpha-amylase & ligual lipase
  • lysozyme
  • peroxidases
  • antibodies



what are the functions of saliva?

  • maintenance of oral hygiene
  • lubrication for speaking
  • swallowing
  • digstive function: amylase & lipase
  • salivation to taste food & to moisten dry foods


what are the functions of mucus?

  • traps bacteria
  • creates "unstirred layer" to protect epithelial cell from acid and/or digestive enzymes in lumen
  • lubricant


what component of mucus give its gel-like characteristic?



how does saliva differ at its origin in the secretory endpieces?

isotonic serious fluid in endpieces

NaCl is removed & K+ and HCO3- are added along ducts

produces hypotonic saliva


how can salivary blood flow be increased?

  • kallikrein: paracrine enzyme from acinar cells
  • parasympathetic ACh & VIP vasodilators
  • local vasodilators


why do methanphetamine addicts experience severe tooth decay?

dry mouth

no protective properties of saliva


what are the major effects of adrenergic stimulation on salivary secretion & the receptor types involved?

  • norepinephrine released from sympathetic nerve terminals
  • alpha-adrenergic:
    • 2nd messenger: inctracellular calcium
    • greater fluid over protein secretion
  • beta-adrenergic:
    • 2nd messenger: cAMP
    • greater protein over fluid secretion


what effects does the parasympathetic nervous system have on salivary secretion?

  • ACh
    • receptor: M3
    • 2nd messenger: calcium
    • response: greater fluid over protein secretion
  • substance P 
    • receptor: tachykinin NK-1
    • 2nd messenger: calcium
    • response: greater fluid over protein production


why is it okay that reabsorption efficiency is lost through the salivary ducts during faster salivary flow?

becuase when flow is fast, swallowing is likely

thus NaCl will be reabsorbed elsewhere instead of lost


what hormones stimulate sodium reabsorption?

aldosterone & anti-diuretic hormone (ADH)


how does flow rate of saliva affect is composition?

  • at high flow, Na+ & Cl- reabsorption is decreased
  • at high flow, HCO3- & K+ secretion is increased
    • HCO3- greatly
    • K+ just keeps up for normal concentration

low flow: [Na+ & Cl-] < [HCO3- & K+]

high flow: increased [Na+ & Cl- & HCO3-]


which gland secretes salivary alpha-amylase?

acinar cells of parotid & submandibular glands


which gland secretes lingual lipase?

acinar cells of sublingual gland


which gland secretes kallikrein?

acinar (and maybe ductal) cells of parotid, sublingual, & submandibular glands


where is lingual lipase active?

secreted in the mouth

but optimal pH= 4.5-5.4, similar to a food-filled stomach


what is kallikrein?

serine protease

secreted by acinar cells in all three major salivary glands

paracrine function to increase bradykinin production at salivary arterioles→ increases blood flow to glands→ increased salivary flow rate


what is xerostomia & its cause?

dry mouth 

common w/increasing age

can be caused by pharmaceutical agents (tricyclics & sympathomimetics)

can cause difficulty swallowing & speaking


What is Sjogren syndrome?

autoimmune disorder

attaches salivary & lacrimal glands

leads to obstructed ducts

symptoms: dry mouth, superficial oral ulcerations, poor dentition, & dry eyes


what is sialolithiasis?

formation of Ca2+ stones in salivary glands

most frequently found in submandibular gland

frequently associated w/chronic infection of the glands, dehydration, Sjogren's syndrome, &/or increased local levels of Ca2+


what is the function of the pharynx?

transfer of food to esophagus


what is the function of the upper esophageal sphincter?

allow entry of food into esophagus

protects airway from swallowed material

protects airway from gastric reflux


what is the function of the esophagus?

transport bolus form pharynx to stomach

clear material refluxed from stomach


what is the function of the lower esophageal sphincter?

alloes entry of food into stomach

protects esophagus from gastric reflux


what controls the swallowing process beyond the oral stage?

swallowing center in medulla & lower pons

stimulated by touch receptors in oropharynx


what are the stages of swallowing?

  1. oral phase: tongue moves bolus into place
  2. pharyngeal: soft palate covers nasopharynx & tongue forces food up & back then down
  3. UES relaxes: epiglottis desciends to cover larynx & trachea
  4. peristalsis wave intiated


why is the pressure in the UES higher than atmospheric?

rests at 40mmHg

b/c it is usually closed as breathing is repressed when it is open

skeletal muscle subjected to enough motor tone to keep it closed

relaxes to just below atmospheric during late pharyngeal stage to allow bolus in 

after bolus passes, pressure rises above resting to propel food down esophagus


how does the LES compare to the UES?

LES is smooth muscle instead of skeletal

tonic pressure of 20mmHg

pressure drops to 0mmHg as food approaches from oral direction

stays at 0mmHg for several seconds


what controls the opening of the LES?

vagal inhibitory fibers via vasoactive intestinal peptide (VIP) & NO neurotransmitters


how does the LES remain closed?

constant ACh & substance P release from vagal excitatory fibers (VEF)


how does rabies affect the digestive system?

  • extreme excitability of swallowing center in CNS→ pharyngeal contracture at thought of swallowing→ hydrophobia
  • hypersalivation


what causes heartburn?

transient relaxations of the LES

allowing stomach acid to enter the esophagus

some chemical agents can reduce esophageal barrier function and/or prolong duration of relaxation


this manometer trace is...



this manometer trace is...



signs & symptoms of achalasia

regurgitating undigested food at night

difficulty swallowing solids & liquids

"fullness"in chest

often confused w/angina

may lose weight


cause of achalasia

idiopathic destruction of nitrergic neurons of myenteric plexus→ functional narrowing of lower esophagus & peristaltis failure

dilated esophagus proximal to narrowed gastroesophageal junction

failure of LES to relax or impaired peristalsis in distal esophagus


what are the types of dysphagia & their causes?

  • oropharyngeal: abnormalities of muscles, nerves, or structure of oral cavity, pharynx, or UES
  • esophageal: mechanical or motility problem of body of esophagus, LES, or cardia of stomach


what controls gastic motility in general?

autonomic & hormonal control


how is chyme moved into the duodenum?

pressure gradient


what allows for stomach expansion?

rugae on the inner surface of the stomach


where is the orad?

first 2/3 of stomach body


where is the caudad?

last 1/3 of body + antrum of stomach


where is the pacemaker zone of the stomach?

on greater curvature near border of fundus & orad

3-4 slow waves/min


where is the greatest capacity for expansion in the stomach?

the fundus


what controls pyloric openign & closing?

stomach factors open it & duodenal factors close it

doesn't open more than 1-2mm during gastric emptying


what is receptive relaxation?

the amount of material the stomach can accomodate w/o significant pressure changes

typically 1.5L


what are the methods for bariatric sx?

elastic band at cardiac region

vertical sleeve


gastric bypass


what are the physiological effects of bariatric sx?

reduced capacity for stomach acid secretion

reduced gastric hormone secretion


how does gastric peristaltic waves change w/& w/o food?

fed: every 15-20 econds or 3-4 waves/minute

fasting: inactive 75-90 minutes, then 5-10 minutes of intense motility

empty 12-24 hours: hunger contractions begin & peak in intensity at 3-4 days then weaken


 in what order do food types enter the duodenum from the stomach?




lipids (b/c they float to the top in the stomach)


what is antral systole?

rhythmic contractions of antrum (distal stomach)


what is retropulsion?

when food particle are forced against the resistant pyloric sphincter & reflected back into the stomach

mechanically breaks down food



suspension of partially dissolved particles

enter duodenum via pyloric sphincter 2-4mL at a time


what are the intrinsic regulatory mechanisms of gastric emptying?

  • gastric stretching→ relaxation of pyloric sphincter
  • duodenal stretching→ constrict the pyloric sphincter


what are the extrinsic regulatory mechanisms of gastric emptying?

  • Parasympathetic inceases gastric empyting
    • ACh increases gastric motility & thus pressure
    • VIP relaxes pylorus 
    • gastrin-releasing peptide causes endocrine secretion of gastrin
  • sympathetic decreases gastric emptying
    • via stimulating pyloric contraction


what is the ileal brake?

nutrients in terminal ileum & cecum

lead to peptide endocrine hormones that slow gastric emptying

peptide YY & glucagon-like peptides are thought to be involved


what duodenal factors can decrease gastric emptying?

  • duodenal distension
  • presence of nutrients (especially fats)
    • need time to be enzymatically digested
  • acidity/increased [H+] in duodenum
    • releases enterogastrones that inhibit gastric emptying & secretion of gastric acid


define enterogastrone.

any substance released from duodenum that inhibits movement of chyme towards anus

ex. secretin (pH response) & CCK (nutrient response)


what is the primary mechanism to optimize nutrient digestion & absorption?

ileal brake


fucntions of gastric secretions

  • digestion of peptides & lipids
  • protection of stomach epithelium
  • absorption of vitamin B12
  • destroy bacteria & other microorganisms


what is normal stomach pH



what protects gastric epithelium?

mucus & bicarbonate

  • secretion of alkaline fluid (bicarbonate) by surface epithelia
  • secretion of mucus 
  • prostaglandins: decrease acid secretion, increase mucosal flow, & increase HCO3- & mucus secretion
  • adequate blood flow
  • growth factors ensure replacement of damaged cells


what pharmalogical agents inhibit mucosal secretions?

NSAIDS & alcohol


how does gastric juice composition vary with flow rate?

[H+] starts low & increases exponentially

[Cl-] starts high & increases gradually

[Na+] starts high & decreases rapidly

[K+] starts very low & increases slightly


how do parietal cells secrete HCl?

via the tubulovesicular system

  • proton pumps & Cl- channels are internalized in cytosolic tubulovesicles
  • increases in cAMP & Ca2+ promote trafficking of Cl- & tubulovesicle fusion w/apical cell surface
  • creates pattern of secretory tubules extending w/in cell


why is it important that chief cell are located deeper in gastric pits than parietal cells?

they usually secrete at the same time

non-acidic cheif cell secretions provide pressure gradient to drive acid from parietal cells into main gastric lumen


what signals stimulate parietal cell acid secretion?

ACh via M3 receptor

Gastrin via CCKB receptor

Histamine via H2 receptor

*all act directly thru calcium & cAMP-dependent signaling pathways*

also: protein, smoking, caffeine, stress, alcohol, tobacco


what signals inhibit acid secretion by parietal cells?

somatostatin via SSRT1 receptor

prostaglandins (mostly PGE2 & i2) via EP3 receptors

also: stomach acid (negative feedback) & sleep


what are the phases of acid secretion & their driving factors?

  1. cephalic: before food enters stomach (30%)
    • sight, smell, thought or taste of food 
    • greater appetite, greater stimulation
  2. gastric: triggered by stomach distension (60%)
    • food entry decrease luminal [H+]
    • distension stimulate gastrin which stimulates acid secretion
  3. intestinal: duodenal G cell release of gastrin (10%)
    • due to duodenal distention


actions of Guanylin & where it is secreted

from colon

released upon eating a salt load

promotes sodium loss from kidneys


actions of uroguanylin & where it is secreted

from duodenum & proximal jejunum

released upon eating a salt load

promotes sodium loss from kidneys


actions of pancreatic polypeptide & where it is secreted

released from F cells in pancreas upon ingestion of a meal

inhibits pancreatic secretion of enzymes & bicarbonate

**role undefined**


actions of peptide YY & where it is secreted

released from distal ileum in response to a meal

decreases GI motility

decreases gastric & intestinal secretions


actions of GLP & where it is secreted

aka glucagon-like peptide or enteroglucagon

released from mucosal L cells in terminal ileum & colon

in response to luminal sugars

enhances GIP release & inhibits glucagon release


what factors influence gastric lipase secretion?

stimulates: gastrin

inhibits: glucagon-like peptide 1 & cholecystokinin


when are preduodenal lipases important?

  • as neonates b/c pancreatic lipases don't work well on milk fats
  • pts w/pancreatic insufficiency


what substaces are absorbed in the stomach?



short to medium chain fatty acids


what are the causes of vomiting?

gastric irritation

vestibular function/stimuli (motion sickness)

gastric outlet constriction


function of vomiting

means by which the upper GI tract rids itself of its contents when any part becomes excessively irritated, over distended, or over excitable

especially from the duodenum


vomiting reflex

controlled by vomiting center in medulla

coordinated w/medullary respiratory centers to prevent choking on vomit

  1. pyloric sphincter & stomach relax to receive intestinal contents
  2. sudden increase in intraabdominal pressure drives gastric contents into esophagus 
  3. in retching, UES doesn't open
  4. if UES opens, then vomitus is projected into oral cavity
    • epiglottis is tightly closed


main functions of the large intestine

fluid absorption & storage and elimination of fecal waste

most water absorbed in cecum, ascending colon, & first portion of transverse colon


what occurs to dietary fiber in the large intestine?

some but not all undergoes fermentation by gut flora (bacteria)

products are short chain fatty acids (acetate, propionate and butyrate) & get absorbed

fatty acids create more acidic colonic fluids that prevent bacterial overgrowth


what are the main components in feces?

non-startch polysaccharides like cellulose (dietary fiber)


inorganic material

in a small volume of K+-rich fluid


what are the motility patterns in the gastrointestinal tract?

  • fasting: migrating motor complex
  • digestive: stationary mixing & perstaltic
  • mucosal folding: alters surface of mucosal layer


what is the purpose of mucosal folding suring digestion?

mucosal folding is altered by the muscularis mucosae smooth muscle layer of the mucosa

alters the surface layer of mucosa for luminal exposure

movements also pump lacteals empty


describe the migrating motor complex

electrical control driving strong rhythmic contractions of stomach & small intestine during fasting state

very strong form of perstalsis

typically occurs at intervals of 90-120 minutes

  • prolonged quiescent period
  • increasing action potential frequency & contractility
  • peak electrical & mechanical activity

clears small intestine of residual content


what is the purpose of the migrating motor complex?

clear small intestine of residual contents, including: undigested food, bacteria (or it would overgrow), desquamated cells, intestinal & pancreatic biliary secretions


what is the underlying electrical mechanism behind the migrating motor complex?

slow waves of electrical impulse from the pacemaker region of the stomach travels through the small intestine

only slow waves that produce a spike produce muscle tension

typically 12 slow waves/min in duodenum & 8-9 slow waves/min in the ileum


what are ICCs?

interstitial cells of Cajal

specialized interstitial multipolar cells associated w/all regions of the gut from which slow waves are recorded

branched processes connect ICCs to each other & form a network aroudn the myenteric plexus

also communiate w/smooth muscle cells via gap junctions

direct interaction w/smooth muscle cells 


what is the purpose of segmentation?

  • acid & bicarbonate can interact w/carbonic anhydrase to create proper pH for enzymatic activity
  • enzymes & substrates can interact
  • residual multimolecule particles are torn apart
  • other materials (bile salts & colipases) can interact w/enzymes & substrates
  • materials in luminal center can become lodged in unstirred layer near intestinal wall for final digestion & absorption


what is the rate of peristalsis in the fed state?

1cm/min in the small intestine


what is the gastro-enteric reflex?

filling of the stomach induces increased motility of teh intestines downstream

requires ANS in distal locations like the ileum


what is the gastro-ileal reflex?

specific effect on the ileum

promotes emptying of ileum into cecum via ileocecal sphincter

requires ANS stimulation


what is the gastro-colic reflex?

promotes mass movements or defecation after a meal

requires ANS input


what is the duodeno-gastric reflex?

decreases motility proximally in stomach


what is the ileogastric reflex?

decreases motility proximally in stomach

requires ANS signalling


what is the colonogastric reflex?

extreme distension in one part of the small intestine promotes relaxation of the rest of the intestine & movement

overall motility is increased


what is the recto-sphincteric reflex?

relaxes internal anal sphincter

required for defecation


what hormones increase small intestinal motility?

gastrin, cholecystokinin, & serotonin


what hormones decrease small intestinal motility?

secretin & glucagon


what are the roles of the ileocecal valve?

regulates chyme flow into the colon from the ileum

protection against movement of bacteria from colon into the small intestine


how is chyme movement into the cecum regulated?

via the ileocecal valve

one-way flutter valve controlled by smooth muscle ring

cecal contraction colonic distension increases its tone (closes)

increased ileal contraction & distension causes sphincter relaxation

mediated by ENS


 what is the functional purpose to haustrations?

to facilitate concentration of a liquid chyme into semi-solid mass


how do haustrations in the colon differ from segmentations in the small intestine?

longitudinal muscle organization

both controlled by slow waves

haustrations induced by longer more intense but less frequent slow waves (3-7/min)

haustrations also promoted by ACh from PNS (vagal & sacral)


how does the sympathetic nervous system affect colonic motility?

inhibits motility via mesenteric & hypogastric plexuses


what is the speed of peristalsis in the the colon?



describe the mechanism behind mass movements

mass movements occur in sigmoid thru rectum

1-3 times/day

  • constrictive ring appears in response to distended or irritated section of colon
  • area 20cm distal loose haustrations
  • longitudinal muscle constricts
  • forces mass of material in distal direction
  • if enter rectum, feel desire to defecate


what controls defecation?

relaxation of internal anal sphincter, secretion of lubricating mucus into rectum & anal canal, and mass movement are all controlled parasympathetically

BUT relaxation of the external anal spincter & increasing abdominopelvic pressure are voluntary muscle controls


Hirschsprung's Dz

ENS excititory & inihibitory neurons from myenteric & submucosal plexuses are absent from a egment of distal colon

segment is narrowed due to tonic contraction

feces accumulate proximally & megacolon is formed from distension


measurements of ...

normal colon


measurements of...

Hirschsprung's dz colon


how much intestinal secretion are there per day?



what are the types of intestinal secretions?

  1. NaHCO3
    • duodenum, mostly
    • neutralizes stomach acid
    • secreted from Brunner's glands & enterocytes
  2. NaCl
    • via CFTR channel protein in enterocytes
    • trhoughout small intestine
    • osmotic equilibration of gut contents
    • flush pathogens from gut


net fluid movement across the gut & its driving forces

Jnet = Jabs - Jsec

movement can occur via trans- or paracellular routes

secretion is driven by secretion of Cl- & HCO3-

absorption is driven by Na+-dependent nutrient absorption


what factors increase intestinal secretions?

  • submucosal release of ACh & VIP
  • local reflexes (distension)
  • parasympathetic input thru the ENS promotes secretion of electrolytes & water


what factors inhibit intestinal secretion?

submucosal release of neuropeptide Y

sympathetic input thru the ENS


how does controling the CFTR receptor control all secretions?

CFTR controls rate of Cl- secretion

Na+ secretion is driven by Cl-

H2O secretion is driven by Na+


the aqueous component of colonic secretions is rich in...

K+ & HCO3-


why is bicarbonate needed to protect colonic mucosa?

like elsewhere to protect from low pH

low pH in colon is caused by bacterial metabolism


why is cholera life threatening?

secretes 2 toxins

one increases cAMP→ activates CFTR→ increased Cl- secretion→ increases Nasecretion→ increases H2O secretion

another makes tight junctions leakier→ increases Na+ & H2O secretion

diarrhea can reach 1L/hr→ hypovolemic shock, hypokalemia, loss of bicarbonate (causes non-respiratory acidosis)



what is the function of pancreatic ducts?

transport of pancreatic enzymes

secretion of HCO3- & water


how do the concentrations of ions in pancreatic secretions vary with flow rate?

Na+ is stable at a high concentration & K+ is stable at a low concentration

Cl- concentration decreases with increasing flow

HCO3- concentrations increase w/increasing flow


mechanism of pancreatic secretion

  1. acini produce isotonic fluid w/enzymes
  2. ductal system secretions HCO3- & absorb Cl-


what are the mechanisms of secretory control in the pancreatic acinar cells?

  • zymogen are stored in granules at apical pole
  • exocytosed upon activation of cAMP or Ca2+-dependent pathways triggered by hormones & neurocrine agents
    • fluid secretion stilumated by ACh, secretin, VIP
    • protein secretion by CCK & ACh


what receptors activate the Ca2+-dependent pathway?

muscarinic M3 & CCKA


what receptors activate the cAMP-dependent pathway?

SCTR (secretin) & VPAC2 receptor (VIP)



secretin acts mostly on the acini or the ducts?



what hormone preferentially stimulates pancreatic ducts?



how is exocrine pancreatic secretions controlled during different phases of digestion?

  • cephalic: sight, smell, taste of food→ vagal & eNS stimulation of acinar & ductal cells
  • gastric: distentsion of stomach→ vagovagal & gastropancreatic reflexes stimulate acinar & duct cells
  • intestinal:
    • acid in duodenum→ secretin stimulates ductal cells (HCO3-)
    • amino acids, fatty acids, & Ca2+→ CCK stimulates afferent arm of vagovagal reflexes to acinar & ductal cells
    • distension of duodenum or hypertonicity in duodenum→ enterohepatic reflex stimulate acinar & ductal cells
    • mediated by ACh, CCK, & VIP


when is CCK secreted?

when free fatty acids and certain amino acids are present in the lumen

secreted by I cells


how do CCK-RP & MP differ?

CCK-RP= cholecystokinin-releasing peptide

MP= monitor peptide

CCK-RP requires nutrients to stimulate its release, but MP does not


where is monitor peptide secreted from?

solinocrine secretion from the pancreatic acinar cells into pancreatic juice


where is CCK-RP secreted from?

CCK-RP= cholecytokinin-releasing peptide

solinocrine factor released from enterocytes in presence of free fatty acids


where is pancreatic alpha-amylase active?

lumen of small intestine


what are the carbohydrate digestive enzymes found in the brush border?

hydrolases: sucrase-isomaltase complex, glucoamylase (maltase), lactase


what limits monosaccharide uptake?

availability of specific membrane transporters


how are the monosaccharides (glucose, galactose, & fructose) absorbed?

Fuctose→ GLUT-5 (facilitated diffusion)

glucose & galactose→ Na+-linked symporter SGLT (all 3 together)- secondary active transporter


how do the monosaccharides enter the blood?

transport via GLUT2 in basolateral enterocyte membrane


how are the majority of amino acids absorbed?

via Na+-dependent cotransport of single amino acids OR SLC solute carriers that transport a subset of amino acids


how are di- & tripeptides absorbed?



peptide transporter 1

symporter driven by H+gradient

most important for Gly & Pro b/c proteins rich in these amino acids are slow to digest

**digested by intracellular peptidases**


what is the "kinetic advantage" of amino acids?

PepT1 allows for a faster rate of amino acid entry into the blood since they are being absorbed faster than one at a time


Hartnup's dz

autosomal recessive dz

small intestine & renal tubule abnormalities in absorption of neutral amino acids

PepT1 compensates for amino acid absorption→ amino acid absorption is normal



autosomal recessive dz

small intestine & renal tubule abnormalities in absorption of basic amino acids

PepT1 compensates for amino acid absorption→ amino acid absorption is normal


lysinuric protein intolerance

autosomal recessive disorder

impaired cationic amino acids transport across basolateral membrane

Arg, Lys, ornithine

SLC7A7 gene mutation


how can colonic water absorption be increased?


increases absorption of Na+ too

accomplished via increasing ENaC expression in the colon



why is the apical ENaC & basolateral Na+/K+ ATPase pump system important in the colon?

ENaC= eletrogenic sodium channel

creates electrical gradient that drives paracellular absorption of Cl-

this is what drives water absorption


what does the proximal colon use for energy?

short-chain fatty acids (acetate, propionate, & butyrate)

from bacterial metabolism

uptake by Na+-dependent symport: driven by low intracellular Na+


what is K+ status in the colon?

contrasting the passively absorption of the rest of the gut

Kis secreted via K+-selective channels


how does vitamin D affect divalent ion absorption?

hormone cholecalciferol, which is made from vitamin D, increases production & translocation of calcium ion channels to the apical membrane

Mg2+ uses the same ion channel

# of channels is rate-limiting for their absorption


what is the mechanism of action for milk of magnesia?

excessive magnesium has limited absorption

increased chemical gradient to luminal side

water retained in feces

thus it acts as a stool softener


what happens to Fe3+ stored in the enterocytes?

if unused, aka transported into the blood, then it will go back into the lumen when the enterocyst sloughs off in a number of days


where is ascorbic acid absorbed?



where is biotin absorbed?

duodenum & jejunum


where is choline absorbed?

small intestine


where is folate absorbed?



whre is inositol absorbed?

small intestine


where is nicotinic acid absorbed?



where is pantothenic acid absorbed?

small intestine


where are the B vitamins absorbed?

  • B1 (thiamine): jejunum
  • B2 (riboflavin): duodenum & jejunum
  • B6 (pyridoxine): duodenum & jejunum
  • B12 (cobalamin): distal ileum


what is meconium ileus?

obstruction of small intestine in newborn caused by impaction of thick, dry meconium

insufficient fluid secretion & lack of functional trypsin

cardinal sign of cystic fibrosis 

90% of cases are due to cystic fibrosis

abd distension, vomiting, failure to pass meconium w/in 24-48hrs after birth, & rapid dehydration w/assoc. electrolyte imbalance


what materials are stored in the liver?

  • protein
  • glycogen
  • vitamin A
  • vitamin D
  • vitamin B12
  • folic acid
  • iron


what is produced in the liver?

  • plasma proteins
  • glycogen
  • phospholipids
  • heparin
  • bile acids
  • bile pigments 


what metabolic functions are performed by the liver?

  • carbohydrates
    • glyconeogenesis, glycogenesis, & glycogenolysis
  • proteins
    • synthesis
    • deamination & transaminations
    • urea formation from nitrogen
  • fats
    • synthesis of: triglycerides, phospholipids, & ketone bodies


what detoxification is performed by the liver?

  • excretion of heavy metals
  • excretion of cholesterol
  • excretion of bile pigments
  • excretion of drugs
  • excretion of hormones
  • detoxification of toxic substances & conjugation


function of bile

make lipid digestion more efficient

emulsify lipids

allows for excretion of heavy metals, fat-soluble drugs, cholesterol, etc.


why are there two types of bile? compare & contrast them.

  • yellow bile comes directly form the liver
    • serous→ greater volume
  • green bile comes from the gallbladder
    • osmotically equivalent
    • fewer Na+ & Cl-
    • more bile acids
  • both work equally well
  • water concentration is equal, but volume is greatly reduced from gallbladder


composition of bile

  • bile salts
  • bile pigments (ex. bilirubin)
  • cholesterol
  • lecithin (phosphatidylcholine)
  • HCO3-
  • Ca2+
  • Na+
  • K+
  • Cl-
  • water



how much bile is excreted daily?

typically 500mL, but up to 1L


what are the types of bile acids?

  • all derived from cholesterol
  • each modification makes them more water-soluble
  • primary: made in liver
  • secondary: modified by intestinal & colonic bacteria
  • tertiary: modified by hepatocytes after recycling via enterohepatic circulation


describe the cellular mechanism of bile-dependent formation.

  1. Na+/K+-ATPase in basolateral membrane maintains gradient for Na+-dependent uptake of bile salts across sinusoidal membrane
  2. bile salts conjugated w/glycine or taurine in sER
  3. secreted into biliary canaliculus 
    • mostly by ATP-dependent transporters
  4. Na+ passes paracellularly thru tight junction from basolateral side into canaliculus
  5. water follows Na+


describe the cellular mechanism of bile-independent formation.

water flows into canaliculus due to accumulation of other osmotically active solutes (HCO3-) which exits hepatocyte via transporter in canalicular membrane


what dilutes canalicular bile & why?

water & bicarbonate

bicarbonate makes bile more alkaline

thus reducing risk of Ca2+ precipitation


what hormone affect the cholangiocyte secretions?

cholangiocyte= bile ductular cells

secretin & VIP increase secretions

somatostatin decreases secretions


what controls bile release into the duodenum?

  • ACh from ENS during cephalin phase→ mild rhythmic contractions of gallbladder
  • entry of chyme into duodenum→ CCK release from I cells→ powerful contraction of gallblader smooth muscle & indirectly relaxes sphincter of Oddi
  • intestinal phase, secretin release→ stimulated pancreas & cholangiocyte secretion of HCO3-
  • sphincter of Oddi relaxed via NO & VIP released from ENS after CCK stimulation


how much bile salts are recycled?

95% of secreted bile is returned to the liver per pass

20% of bile acid pool is replaced thru new synthesis daily


how are bile salts/acids recovered?

reabsorbed in terminal ileum

  1. carrier-mediated absorption in terminal ileum
  2. deconjugation to primary bile acid before being absorbed passively or actively
  3. conversion of primary bile acid to secondary bile acid w/subsequent absorption of deoxycholic acid
  4. passive diffusion along small intestine


why are tertiary bile acids not reabsorbed?

because they are more water soluble than fat-soluble

thus they are excreted

they are also potentially cytotoxic


what are chylomicrons?

triglycerides, cholesterol, & phospholipids aggregated together in enterocytes

transported to lacteal for lymph transport



pale, malodorous stool

caused by high concentration of fats in feces

early warning sign of cystic fibrosis


where does renal filtration occur?



what are the main functions of the kidney?

  1. clearance of blood waste products
    • urea, uric acid, creatin, drugs
  2. regulation of H2O & eletrolytes
  3. hormone secretion
    • erythropoietin & renin
  4. activation of vitamin D


inlets & outlets of kidney

inlet: renal artery

outlets: renal vein & renal pelvis/ureter


what is the functional unit in the kidney?



parts of nephron from from afferent arteriole

  1. Bowman's capsule
    • glomerular capillary
    • Bowman's space
  2. proximal convoluted tubule
  3. proximal straight tubule
  4. thin descending limb of the loop of Henle
  5. thin ascending limb of the loop of Henle 
  6. thick ascending limb of the loop of Henle
    • macula densa
  7. distal convoluted tubule
  8. connecting tubule
  9. late distal tubule
  10. late distal tubule
    • initial collecting tubule
    • cortical collecting tubule
  11. medullary collecting tubule
    • outer & inner


why does the nephron have two capillary beds?

  • glomerular capillary
    • arterial
    • filtration only
    • afferent arteriole to efferent arteriole
  • peritubular capillary bed
    • absorption, secretion, & reabsorption
    • efferent arteriole to renal vein
  • more thorough cleaning system
    • throw it all away and recollect whats needed


how much blood is sent to the kidneys?

20% of CO

normally 1L/min


where is water absorbed in the nephron?

2/3 in proximal tubule & 1/3 in distal tubule


in normal healthy circumstances, how much blood is filtered by the kidneys/min? /day?

120mL/min & 180L/day

  • 20% of CO= 1L/min
  • only plasma is filtered
    • blood is 55% plasma=600mL
  • only 20% of plasma that travels thru glomerulus is filtered= 120mL/min
  • 120mL/min * 60min/hr *24hr/day * 1L/1000mL= 180L/day


where does fine regulation of water & electrolytes take place in the nephron?

late distal tubule  & collecting tubule


where do hormone exert most of their effects on the nephron?

late distal tubule & collecting duct


where is the nephron impermeable to water?

ascending limb of loop of Henle & early distal tubule


what does facultively permeable mean?

permeable when facilitated

discretionarily permeable (ie hormonal or neuronal actions)



what controls urine volume?

not GFR

reabsorption process in distal tubule



renal plasma flow

RPFa= renal plasma flow entering kidney

RPFv= renal plasma flow leaving kidney

RPFa=RPFv in healthy kidneys b/c 99% is reabsorbed


how is the amount of substance in the unrine calculated?

urine flow (Vdot) /min * concentration of substance in urine (U)

also known as the excreted amount


how is the cleared amount calculated?

cleared is plasma cleared of substance

RPF (Pa - Pv) = Vdot * U

where Pa= arterial concentration of substance & Pv= venous concentration of substance


define clearance

volume of plasma that is cleared of a substance in a unit of time


how is clearance calculated?

C = (Vdot * U) / Pa

units are mL/min


how can clearance be measured?

measure urine excretion in a certain time frame, concentration of substance in urine & plasma

but this is dependent on plasma concentration being constant during the entire collection time period, ex. equilibrium or infusion of substance over a long period



glomerular flow rate

flow rate of fluid thru the kidney


what is the filtered load?

GFR * Pa

substance must be freely filtered



amount of substance secreted from perilobular capillary into kidney tubule

per time unit



amount of substance reaborbed from kidney tubule to perilobular capillary

per time unit


how is the excreted amount of a substance calculated?

Vdot * U = GFR * Pa + (Msdot -Mrdot)

but when a substance is neither secreted or reabsorbed GFR=C= (Vdot * U)/Pa


what is the clearance of inulin?

C= 120mL/min= GFR

b/c no excretion or absorption b/b it doesn't penetrate cell membranes


for what substances does GFR= C?

inulin and approximately creatinine


how can creatinine clearance be estimated?

from plasma concentration b/c very little is secreted or absorbed


when does C=RPF?

RPF= renal plasma flow

when substance is totally secreted

C= 600mL/min (all plasma to kidney/min)

ex. para-amino hippuric acid


excreted amount is a sum of?

filtrated substance + secreted substance


why does the secretion curve plateau?

b/c substance transport mechanism has been maximized

aka transport proteins have been saturated


why does the secretion curve curve instead of make a sharp angle at the point of plateau?

because it is graphed for the kidneys, summation of all 2 million nephrons instead of a single nephron


why is C=0 for glucose in healthy individuals?

because it is all reabsorbed


when is C >0 for glucose?

when reabsorption is maximized at 375mg/mL


what does fractional excretion tell us?

whether a substance is reabsorbed or secreted independent of the underlying mechanism

<1→ net reabsorption

>1→ net secretion


how is fractional excretion calculated?

Cx/Cinulin ≈ Cx/GFR


how is filtration fraction calculated?


healthy kidneys FF= 120mL/min / 600mL/min = 20%


what is the kidney capsule made of?

outer layer is fibroblasts & collagen

inner layer is myofibroblasts


what forms the renal medulla?

8-12 conical renal pyramids


what separates the renal pyramids from each other?

renal columns

extensions from renal cortex


what is a renal lobe?

medullar renal pyramid w/it's surrounding cortical tissue at base & sides

can be seen w/o a microscope


what is a kidney lobule?

group of nephrons around a single medullary ray & all drain into a single collecting duct

not visible w/o a microscope


renal papilla

tip of each renal pyramid that projects into a minor calyx


renal pelvis

considered expanded part of ureter

branches to form major & minor calyces


what is the funtional unit of the kidney?

uriniferous tubule = nephron + collecting duct


what separates uriniferous tubules?

loose connective tissue of the basal lamina


what are the different types of nephrons and how can they be differentiated?

majority are cortical nephrons, mostly located in the cortex (tip of loop of Henle & collecting duct enter medulla)

1:7 are juxtamedullary nephrons: long loops of Henle that extend into medulla→ crucial for production of concentrated urine


where are vasa recta found in the kidneys?

only around the juxtamedullary nephrons


function of vasa recta

participate in countercurrent exchange

production of concentrated urine


what is the blood flow pathway through the kidneys?

  • renal artery
  • segmental artery
  • interlobar artery
  • arcuate artery
  • interlobular artery
  • afferet arteriole
  • glomerulus
  • efferent arteriole
  • peritubular capillaries/vasa recta
  • interlobular vein
  • arcuate vein
  • interlobar vein
  • renal vein


what forms the renal corpuscle?

glomerulus: 10-20 capillary loops

surrounded by Bowman's capsule: double-layered epithelial cup


what cell type forms the visceral layer of Bowman's capsule?


they wrap around glomerular capillaries


what is a pedicel?

foot-like process of a podocyte that wraps around glomerular capillaries


function of nephrin

protein between pedicels of podocytes

forms slit diaphragm that allows filtration of water & sugar, but not proteins


where are mesangial cells found?

between capillaries in glomerulus


function of mesangial cells

  • physical support: cover capillary surfaces not covered by podocytes
  • contraction: respond to vasoactive substances to help maintain hydrostatic pressure for optimal flow rate
  • secretion: synthesize & secrete cytokines, prostaglandins, etc. for immune defense
  • phagocytosis: of protein aggregates that adhere to glomerular filter


what are lacis cells?

extraglomerular mesangial cells


function of the juxtaglomerular apparatus

feedback mechanism for autoregulation of renal blood flow to keep GFR relatively constant


components of juxtaglomerular apparatus

macula densa

juxtaglomerular cells

lacis cells


macula densa

columnar cells in juxtaglomerular apparatus

specialized part of distal convoluted tubule

nuclei tend to be more crowded together


juxtaglomerular cells

modified smooth muscle in wall of adjacent afferent arteriole

senses blood pressure via stretch receptors

secretes renin


mechanism of proteinuria

  • dz in glomerulus
  • increased quantity of proteins in serum (overflow proteinuria)
  • Fanconi syndrome: low rabsorption at proximal tubule


why is proteinuria common in patients w/glomerelonephritis & diabetes?

b/c they lead to increased permeability of teh glomerular filter


proteinuria is the first indicator of...

renal dz


function of proximal convoluted tubule

reabsorb water, ions, nutrients, vitamins, & small plasma proteins


how can the proximal convoluted tubule & thick descending limb of the loop of Henle be differentiated?

both simple cuboidal epithelium

PCT has microvilli with glycocalyx on apical surface & margins between cells are indistinct b/c they have a well developed interlocking system of lateral cell processes for polarized transport

thick limb appears to have clear lumen


what cells secrete erythropoeitin?

fibroblastic interstitial cells of kidnery cortex


where is simple squamous epithelim found in the nephron?

thin descending limb of loop of Henle

loop of Henle

ascending limb of loop of Henle


what cell type forms the distal convoluted tubule?

small simple cuboidal cells w/sparse microvilli


how is net filtration pressure at the glomerular capillaries calculated when given cpillary & Bowman's capsule hydrostatic & oncotic pressures?

Peffective = (PC - PBS) - (πC - πBS)

P= hydrostatic pressure

π= oncotic pressure

πBS= 0 b/c protein does not enter Bowman's space


what properties determine if a substance is filtered thru the golmerulus?

size & charge


what size particles can be filtered by the glomerular filter?

<42 angstroms

<18 angstroms are freely filtered

18-42 angstroms are partially filtered & dependent on charge



how does charge effect glomerular filtration?

18-42 angstroms→ + filter at higher rate due to - charge of pores

<18 angstroms→ - filter at higher rate


nephrotic dz affects which cell type?

glomerular epithelial cells

aka podocytes

thus affecting composition of filtrate


nephritic dz affects which cell type?

capillary endothelial cell integrity & diameter

thus affecting magnitude of GFR


what is the total area of the glomerular capillaries?



what is the total pore area of the glomerular capillaries?




what percentage of sodium is reabsorbed?



what percentage of chloride is reabsorbed?



what percentage of potassium reabsorbed?



what percentage of bicarbonate is reabsorbed?



what percentage of water is reaborbed?



how does capillary oncotic pressure change over a systemic capillarty?

increases due to concentration of proteins as they do not pass thru  the endothelium, but treated as 0

because systemic capillaries receive 5000L/day, but onlly filter 20L/day or 0.4%


how does capillary oncotic pressure change across a glomerular capillary?


but not equal to 0 like systemic

because 20% of plasma is being filtered compared to the 0.4% seen in systemic circulation


how does πand πBS compare?

similar; they both do not change

but πBS=0, because protein is not freely filtered in the glomerulus


how does PC compare in systemic v. glomerular systems?

systemic PC drops along length of capillary= driving force for reabsorption

glomerular PC is constant due to low resistance/wider radius (theoretically decreases but negligible amt)


what is PBS?

the hydrostatic pressure within the Bowman's space


b/c fluid flows thru tubular system before pressure is exerted


how does increased renal plasma flow influence GFR?

PC & PBS are constant

πBS is 0

πC decreased

therefore GFR increases


why does the πC curve less steeply with increased renal plasma flow?

concentration of proteins reduces more slowly relative to length of glomerular capillaries 

→takes longer for πC=PC

→more fluid is filtered aka increased GFR


how does isolated increased afferent arteriolar resistance influence GFR?

decreases GFR proportionately via:

  • decreased renal plasma flow
  • decreases PC



how is flow calculated?


flow= change in pressure/resistance


if efferent arteriolar resistance is higher than afferent arteriolar resistance, what effect is seen in GFR?

GFR is increased


how does isolated increased efferent arteriolar resistance affect GFR and why?

decreases GFR by reducing renal plasma flow

increases GFR by enhancing PC

overall: moderate increase in efferent arteriolar resistance increases GFR, while severe constriction reduces GFR


how does increased hydrostatic pressure in Bowman's space influence GFR?

decreases GFR

(congestion in urinary system- stone in collecting duct?)


how does dehydration influence GFR?

dehydration increases glomerular capillary oncotic pressure

→decreases GFR


how does hunger influence GFR?

during fasting/starvation plasma proteins are decreased

→decreasing glomerular capillary oncotic pressure

→increasing GFR


where is the greatest pressure change found along renal vessels?

afferent arterioles esp. in HTN pts as the glomerular pressure is kept relatively constant


over what systemic blood pressure range can the RPF/GFR be held constant by autoregulation?

100-200 systolic


how is renal blood perfusion autoregulated?

  1. myogen mehanical stretch reflex receptors in smooth muscle of arterioles
  2. tubulo-glomerular feedback via juxtaglomerular apparatus


how does sympathetic nervous activity influence GFR?

minor→ only affects efferent arterioles→ no change in GFR

strong activity: dominant effect on afferent arterioles→ greatly reduce GFR (kidney shock)


how does atrial natriuretic peptide influence GFR?

dilates afferent arterioles

→increases RPF

→ increases GFR


how do prostaglandins influence GFR?

dilate arterioles

→ increase RPF

→ increase GFR


how does NO influence GFR?

dilates arterioles

→increases RPF

→increases GFR


how does the juxtaglomerular appartus regulate GFR?

  • increased GFR
  • increases NaCl delivery to macula densea in distal convoluted tubule
  • enhanced NaCl uptake in macula densa via Na+/K+/2Cl- symporter
  • increase ATP & adenosine (ADO) concentrations
  • ATP binds P2X receptor & ADO binds A1 receptor on plasma membrane of smooth muscle of afferent glomerular arteriole
  • increases intracellular Ca2+
  • induces vasoconstriction 
  • returns GFR to normal


what inhibits renin secretion by granular cells in the afferent arteriole?

ATP & ADO induced increase in intracellular Ca2+

which is electrically coupled to 


what happens NaCl delivery to the macula densa falls?

caused by reduced GFR

  • ATP & ADO release decreases
  • decreases intracellular Ca2+ in arteriolar smooth muscle
  • stimulates granular cells to release renin
  • macula densa also produces PGE2 that stimluates granular cell secretion of renin


effect of angiotensin II

enhances NaCl retention

which enhances the retention of water


what is the driving force for transcellular reabsorption?

tubular fluid starts out more negative than interstitial fluid

b/c small - ions filter faster than + ones

-3mV compared to interstitial 0mV & intracelluar -70mV


what is the driving force for the reabsorption of organic solutes in the first half of the proximal tubule?

sodium electrochemical gradient

maintained by basolateral Na+/K+ ATPase pump

organic solutes: glucose, lactate, amino acids, phosphate (all -)


what drives the reabsorption of water in the first half of the proximal tubule?

Na+, HCO3-, & organic solute reabosption→ increases interstitial osmolarity (293osM compared to 287osM in tubular fluid→ drving force for water aborption

water move both paracellularly & transcellularly


what transporters are found in the apical membrane in te first have of the proximal tubule?

Na+/organic solute symporter (glucose, phosphate, lactate, amino acids)

Na+/H+ antiporter


what transporters are found in the basolateral membrane of the first half of the proximal tubule?

Na+/K+ ATPase antiporter

K+ leak channel

organic solute transporters

HCO3- transporter



where are most organic solutes absorbed in the tubular system?

first half of the proximal tubule


in the first half of the proximal tubule, concentration of what ion increases in tubular fluid?



HCO3- is freely filtered in the glomerulus, but how is it reaborbed?

usually as CO2 via passive diffusion into the cell

H+ pumped out of the cell reacts w/HCO3- in tubular fluid to form H2O & CO2

reacts with carbonic anhydrase w/in the cell to recycle H+ & HCO3- is transported into interstitium/blood


what transporters are found in the apical membrane in te second half of the proximal tubule?

Na+/H+ antiporter

anion-/Cl- antiporter

H & anion bind & enter cell via passive diffusion→ recycled


what transporters are found in the basolateral membrane in te second half of the proximal tubule?

Na/K ATPase antiporter

K/Cl symporter: against Cl electrogradient, but driven by K going down its electrochemical gradient


what is mainly reabsorbed in the second half of the proximal tubule?


water follows


why is Cl- reabsorbed paracellularly in the second half of the proximal tubule?

because a gradient between tubular fluid & interstitium has been created


what is the consequence of paracellular Cl reabsorption in the second half of the proximal tubule?

tubular fluid becomes + compared to blood

causes paracellular Na reabsorption

water is reabsorbed as well

1/3 of NaCl reabsorption occurs this way


what solvents are dragged with paracellular water reabsorption?

K+, Ca++, Mg++


what happens to proteins that are filtered by the glomerulus?

very small amt/day

undergo endocytosis or are partially degraded by enzymes on the apical surface of the proximal tubule

broken down w/in cell

returned to blood as individual amino acids

**very easily saturated**


orgainc anions secreted in proximal tubule

cAMP, bile, hippurate, oxalate, prostaglandins, urate


organic cations secreted in proximal tubule

creatinine, dopamine, epinephrine, norepinephrine


how are organic anions & cations secreted into the proximal tubule?

non-specific transporters


what is the concentration of solutes in tubular fluid at the end of the proximal tubule v. plasma?

Na+ unchanged from ultrafilatrate

HCO3- decreased

Cl- increased

inulin increased by 3 fold

isotonic to plasma


what is reabsorbed in the thin descending limb of the loop of Henle?

water via aquaporin 1

no NaCl


what is the tonicity of tubular fluid compared to plasma at the end of the loop of Henle?



what transporters are found in the apical membrane in the thick ascending limb of the loop of Henle?

Na/K/2Cl symporter

K leak channel

Na/H antiporter


what transporters are found in the basolateral membrane in the thick ascending limb of the loop of Henle?

K/Cl symporter

Na/K ATPase antiporter

HCO3- transporter


why is the apical K+ channel in the thick ascending limb of the loop of Henle so important? 

K+ is required for Na/K/2Cl symporter

also creates + charge in tubular fluid that drives paracellular absorption of Mg2+, Ca2+, K+, Na+


what segments of the tubular system are impermeable to water?

thick ascending limb of loop of Henle

early distal tubule


why is tubular fluid hypoosmolar at the end of the thick ascending limb of the loop of Henle?

because it reaborbs NaCl but is impermeable to water


what is absorbed in the early distal tubule?


via apical symporter

basolaterally by Na/K ATPase antiporter & Cl- channel


where are principal cells located?

late distal tubule & collecting duct


where are intercalated cells found?

late distal tubule & collecting duct


what exchange occurs in principal cells & what is its driving force?

NaCl & water reabsorption & K secretions

Na absorbed by apical Na channel & basolateral Na/K ATPase antiporter (maintained by basolateral K channel)

K secretion occurs via apical K channel

Cl absorbed paracellularly driven by - luminal voltage created by Na reabsorption

water via aquaporin 2 on apical surface & 3 and 4 on basolateral surface


what reabsorption in teh late distal tubule and collecting duct is dependen on what?

presence of ADH (anti diuretic hormone)


what exchange occurs in intercalated cells & what is its driving force?

H+ secretion via ATPase pump in apical membrane

absorb K via K+/H+ ATPase antiport pump in apical membrane

HCO3- crosses basolateral membrane


how much water is reabsorbed in the late distal tubule & collecting duct?

variable 8-20% as this is the area of fine regulation


what type of hormone is aldosterone?

non-polar mineralcorticoid

thus it can passively diffusion thru the plasma membrane & has an intracellular receptor


what are the effects of aldosterone in the late distal tubule & collecting duct?

  • increased expression of Na channels in apical membrane
  • increased activity/permeability of Na channels in apical membrane
  • increased amount of Na/K ATPase antiporters in basolateral membrane
    • stimulates synthesis of ATP

overall enhancement of Na reabsorption→ increases paracellular Cl reabsorption & K secretion across apical membrane


what cells are influenced by aldosterone?

principal cells of the late distal tubule & collecting duct


where does angiotensin II influence NaCl reabsorption?

in the proximal tubule


how does aldosterone cause alkalosis?

increased Na+ reabsorption→ increases K+ secretion by principal cells→ increased H+ secretion by intercalated cells→ increased HCO3- in blood→ increases pH


what activates the RAA system?

RAA= renin-angiotensin-aldosterone

decrease in extracellular fluid volume 


why does increased [K+]plasma instead of changes in [Na+]plasma trigger aldosterone release?

Nernst equation

because ECF/plasma levels of Na+ are high 140mM so small changes are unnoticeable

but ECF/plasma levels of K+ are normally 4mM so small movement of ions cause relatively large fluxuations


what is the function of 11beta hydroxy steroid dehydrogenase (HSD)?

breaks down cortisol in principal cells to cortisone (an inactive metabolite)

b/c cortisol is a glucocorticoid & glucocorticoid & mineralocorticoid receptors poorly distinguish between their substrates

thus w/o this enzyme the high levels of cortisol found in the blood would cause mineralocorticoid effects of Na+ retention


what inhibits HSD?

glycyrrhetinic acid in licorice

and carbenoxolone


what are the effects of hyperaldosteronism and why?

  • Na+ retention
    • hypervolemia
    • hypertension
    • edema
  • hypokalemia
    • muscle weakness
    • constipation
    • ECG changes
  • alkalosis
    • tetany, cramps
      • less H+ bound to albumin→ free plasma Ca2+ binds albumin→ decreased [Ca2+]plasma → increased neuronal activation


what effect does increased K+ excretion have on urine flow rate?

increases it

linear relationship


how does K+ reabsorption/secretion vary with K+ intake?

low K+ intake→ 3% reaabsorbed in distal tubule & 6% in collecting duct

normal-high K+ intake→ 10-100% secreted in distal tubule & 5-50% secreted in collecting duct


what is the normal range for plasma K+?



how is H+ excreted in tubular fluid?

usually as H2PO4- but limited by low [HPO42-] 40mmol/day

so also as NH4+ w/much higher capacity: ammonia (NH3) is from glutamine transamination to alpha-ketoglutarate


what effect does parathyroid hormone have on the kidneys?

increases Ca2+ reabsorption strongly in loop of Henle & distal tubule


what effect does vitamin D have on the kidneys?

aka calcitrol

increases Ca2+ reabsorption indistal tubule


what effect does calitonin have on the kidneys?

(from C cells of thyroid)

inhibits Ca2+ reabsorption in loop of Henle & distal tubule


where is the majority of Mg2+ reabsorbed?

thick ascending limb of the loop of Henle


where is Ca2+ reabsorbed in the tubular system?

65-70% in proximal tubule via apical Ca2+ channel & basolaterally by Ca2+/2H+ ATPase antiporter & 3Na+/2Ca2+ antiporter 

29-34% in loop of Henle & distal tubule in parallel with Na+


how does plasma pH influence Ca2+ absorption?

alkalosis increases Ca2+ reabsorption in distal tubule

acidosis decreases Ca2+ reabsorption in distal tubule


how does plasma [PO43-] affect Ca2+ reabsorption?

induces PTH→ increases Ca2+ reabsorption


how does extracellular volume influence Ca2+ reabsorption?

reduced extracellular volume increases Ca2+ reabsorption

increased extracellular volume decreases Ca2+ reabsorption


how much fluid would be lost if urine is not concentrated?

if urine is isotonic (300mM) & 1200mmol/day of substances excreted→ 4L water lost


why is a it necessary to build a hypertonic interstitium?

to create a driving force for water reabsorption

and thus concentrate urine


how does the ascending limb of the loop of Henle produce high medullary interstitial OsM?

it pumps out salt, but is impermeable to water

therefore OsM of interstitium increases & tubular fluid decreases


how does the collecting duct contribute to concentrating of urine?

aquaporins in collecting duct allow for reabsorption of water from tubular fluid

driving force is OsM gradient produced in loop of Henle


what is the role of the vasa recta in concentrating urine?

to absorb & wash away excess water in the medullary interstitium

helps maintain hyperosmolar interstitium in countercurrent multiplier


how does tubular flow rate influence urine concentration?

slower tubular flow→ increased concentration

vice versa

linear relationship


how does the blood flow rate in the vasa recta affect urine concentration?

increase blood flow will absorb less interstitial water

decreasing OsM of interstitium

decreasing driving force for water reabsorption

decreasing urine concentration


how does ADH influence kidneys in concentrating urine?

controls water permeability in late distal tubule & collecting duct

can concentrate up to 400x

if present, water will be reabsorbed in late distal tubule & collecting duct→ concentrated/hyperosmolar urine

if not, opposite


what is pressure natriuresis?

the excretion of Na+ in response to increasing blood pressure→ leads to water loss→ reducing blood volume

most important mechanism for blood volume control

  • mechanisms:
    • increased bp→ increased blood flow to vasa recta→washes out medullary solutes→ reduces hypertonicity in medulla
    • increase in arterial pressure→rapid decreases in # of apical Na+/H+ exchangers in proximal tubule


what is the effect of aldosterone on Na+ reabsorption?

increases NaCl reabsorption only, not water in thick ascending limb of the loop of Henle

increases NaCl & water reabsorption in distal tubule & collecting duct


what is the effect of angiotensin II on Na+ reabsorption?

increased NaCl & water reabsorption in the proximal tubule


what is the effect of arterial pressure on Na+ reabsorption?

increased atrial pressure decreases Na+ reabsorption


what is the effect of atrial natriuretic peptide on Na+ reabsorption?

decreases NaCl & water reabsorption in teh distal tubule & collecting duct


what is the effect of prostaglandins on Na+ reabsorption?

decrease the reabsorption of NaCl & water in the distal tubule & collecting duct


what is the effect of sympathetic nervous activity on Na+ reabsorption?

increases NaCl & water reabsorption throughout the nephron

stimulated by decreased ECF


how much can ADH affect GFR?

by 20%


how & where is urea exchanged in the tubular system?

reabsorbed via solvent drag in water in proximal tubule

secreted into tubular fluid by UT2 transports via facilitated diffusion on apical & basolateral membranes in the loop of Henle

reabsorbed in collecting duct by UT1 apically & UT4 basalaterally via facilitated diffusion


what is the relative permeability of urea throughout the nephron?

increased in medullary regions

majority in medullary collecting duct

also in medullary portion of loop of Henle



condition of restricted water intake

ex. kidney failure


what is the minimun urine flow?

0.3mL/min caused by extreme dehydration


what is the maximal urine flow?


exhibited by extreme water intake


how can water reabsorption be measured?




how is ADH release controled?

  • osmoreceptors sense increased interstitial osmolality
    • usually caused by increased Na+ & - associates
  • osmoreceptor stimluation provokes synthesis & release of ADH in hypothalamic-hypophysial system
  • ADH enhances water reabsorption in late distal tubule & collecting duct
  • dilution of ECF


where is the ADH receptor located?

basolateral plasma membrane of late distal tubule & collecting duct


what is the second messenger of ADH?



ADH is also known as .....? why?


b/c it causes systemic vasoconstriction


how do osmoreceptors sense change in ECF environment?

they are very permeable to water soe they shrink when ECF is hypertonic & swell when ECF is hypotonic


what neurons communicate with osmoreceptors & baroreceptors to coordinate ADH release?

nucleus paraventricularis & nucleus supraopticus in the hypothalamus

signal posterior pituitary/hypophysis


what factors display a linear relationship with increasing ADH release?

increasing ECF osmolality above 280mOsm/kg H2O

decreasing blood volume starting at a 10% loss of blood volume (or change in blood pressure by 10%)


where is ADH stored?

neurohypophysis (aka posterior pituitary)


what dz state is caused by ADH deficiency?

diabetes insipidus


how does the thirst mechanism work?

intracellular dehydration causing an increase of OsM by more that 4mOsm/L

stimulates thirst center in hypothalamus

drinking water will dilutes ICF & reduce OsM to normal


what causes salt hunger?

decrease in Na+ in ECF

causes decrease in blood volume

stimulates hypothalamus

takes several hours or days 


the absence of aldosterone is seen in what dz state?

Addison's dz


edems is present when ECF volume exceeds?



what relationship is normally seen between blood volume & ECF volume?

linear up to 7L of blood then plateau as increasing ECF creates edema


what is the most important mechanism for control of blood volume?

pressure diuresis

increase of Na+ excretion w/increased arterial pressure


what is the second messenger of ANP/BNP?



where is BNP made?

ventricles of the brain


why is urodilatin more potent that ANP?

ANP=atrial natriuretic peptide

b/c some ANP in the kidneys is broken dow by endopeptidase that does not affect urodilatin



  • secreted by: distal tubule & collecting duct
  • stimulated by: rise in blood pressure & increased ECF volume
  • function: inhibit NaCl & water reabsorption across medullary portion of collecting duct


what is an acid?

H+ dissociates from it


what is a base?

a H+ binds to it


what is a buffer?

an acid/base pair in which the pH does not vary greatly with the addition of loss of H+


Henderon-Hasselbalch equation

pH = pK + log ([A-]/[HA])


HA= acid 

pK = log{ ([H+][A-]) / [HA] }


criteria for a good buffer

pKa within 1 pH unit

high enough concentration w/in system


what is the difference between closed & open system buffers?

in a closed system, [acid] + [base] must be constant

but in an open system, [acid] + [base] can be variable


how is buffering capacity measured?

beta (buffering capacity) = delta[base] / deltapH

steeper slope of pH v. base concentration⇒ high buffering capacity

flat = no buffering capacity


why is lactate a poor biological buffer?

high enough concentration in ECF, but pH is too low (pKa= 3.1) so it can only buffer pH 2.1-4.1 and body fluids are 6.8-7.4


why is phosphate a poor biological buffer?

pKa= 6.8 thus can buffer pH 5.8-7.8

but not found in high enough concentrations in ECF (only 2mM)


why is bicarbonate a good biological buffer when it's pKa is 6.1?

0.9-1.3 pH units off of biological 6.8-7.4

is found in adequate concentrations (27mM ECF/10mM ICF)

**b/c it is the only buffer system that is OPEN in the body via the lungs as CO2 leaves it changes the equilbrium**


which amino acid are good buffers at normal biological pH?

His, Cys, & terminal NH2


why are proteins not a good biological buffer?

with a mix of amino acids, nearly any pH can be buffered by a protein

but they are relatively absent from ECF & plasma