Mamalian Physiology Exam 3 Study Guide
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Transcript of Mamalian Physiology Exam 3 Study Guide
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Exam 3 Study Questions
Respiratory System
Introduction
1. Distinguish between organismal and cellular respiration.
Cellular (internal) intracellular metabolic processes that generate ATP and produce CO2
o Anaerobic in the ctosol! strictl glcolsis! without O2
o Aerobic in matri" o# mitochondria! with O2
Organismal (e"ternal) entire se$uence o# e%ents in%ol%ed in the e"change o# O2 and CO2
betweeno Air mo%ed in and out o# lungs (allows e"change o# air between e"ternal en%ironment
and al%eoli) %ia breathing&%entilationo '"change o# CO2 and O2 (between air in al%eoli and blood in the pulmonar
capillaries) %is di##usion (CO2 and O2 mo%e down concentration gradients acrosspulmonar capillaries)
o
Transport Co2 and O2 (between lung and tissues in circulator sstem) %ia bloodo '"change o# Co2 and O2 (between blood and tissues %ia sstemic capillaries) %ia
di##usion
2. hat are the general #unctions o# the respirator sstem
*acilitates water loss and heat elimination
+umidi#ies and warms inspired air en route to the lungs
,aintains phsiological p+ b regulation o# CO2 that is e"haled
-ncreases %enous return (respirator pump)
De#ends against inhaled #oreign matter (lie bacteria)
/emo%e0 inacti%ate0 or acti%ate %arious materials passing through pulmonar circulation
%ocaliation
. Describe the sstem o# 3conducting structures3 in the respirator tract. 4tate their #unctions ande"plain how each is accomplished.
4tructures5
o Trachea di%ides (26 le%els o# branching #rom trachea to smallest bronchioles) into /
and 7 bronchus and each continues to di%ide into smaller0 more numerousbronchioles
o Trachea and bronchi5 rigid0 cartilaginous walls0 rings to help eep shape
o 8ronchioles5 contain a laer o# smooth muscle (82 adrinergic /s! 'P- 9 dilation)
*unctions5
o Conduct air between atmosphere and e"change sur#ace
o arm incoming air to : C (impro%es blood;s abilit to transport CO2 and O2)
o +umidi# incoming air (air reaching al%eoli is saturated with water)
o *ilter incoming air %ia straining (nasal hairs remo%e an particles
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that assists in lung e"pansion b reducing water sur#ace tension inthe hdrated air
,acrophages5 present in al%eolar lumen! #ight in#ection and digest
damaged tissue
Pores o# @ohn5 holes in the walls o# adacent al%eoli! allow
contralateral %entilation 'ach al%eolus is surrounded b a bed o# capillaries
o Al%eolocapillar membrane5 al%eolar membrane and capillar membrane together!
#orm the respirator e"change sur#ace 8lood and air DO BOT ,-usuall %er close0 so e"change occurs b
di##usion *ic;s law5 di##usion is ma"imal with increased sur#ace area and short
di##usion distance (both o# these #actors optimied with AC membrane) Drawbacs5
4hort distance #or in%ading organisms to enter circulation
Can become easil dehdrated since each is onl 1 laer thic thin
membrane re$uires constant hdration
*unctions5
o 4ites across which gas e"change between the air and blood occurs
6. Describe how the lungs are situated in the thoracic ca%it. Discuss the structure and #unction o# thepleural sac.
7ungs tae up much o# the thoracic ca%it (rest is heart0 esophagus0 thmus0 some ner%es0
and all associated blood %essels)
7ungs and heart are protected in the #ront& sides b the ribs&sternum0 bacbones in the bac0
and the diaphragm0 which #orms the #loor o# the thoracic ca%it
Diaphragm5 large0 domeshaped sheet o# seletal muscle that completel separates the
thoracic and abdominal ca%ities
Pleural sac5 separates each lung #rom the thoracic wall and other surrounding structures
o -nside 9 pleural ca%it
o 2 laers5 parietal pleura adheres to thoracic wall0 and %isceral pleura adheres to lungo 4ur#aces o# the pleura secrete intrapleural #luid which lubricates the pleural sur#aces
as the slide past each other during respirator mo%ements
Pulmonary Ventilation
1. '"plain the mechanisms underling the tendenc o# the lungs to collapse.
'lastic properties o# the lungs contribute to the tendenc o# the lungs to collapse
7ungs are rich is elastin
4ur#ace tension5 due to air&water inter#ace in the al%eoli! water molecules more strongl
attracted to other water molecules than to the air in the al%eoli
2. hat is sur#actant0 what produces it0 and what are its #unctions 8e sure to de#ine and e"plain lungcompliance.
4ur#actant5 a comple" mi"ture o# lipids and proteins secreted b Tpe -- Al%eolar calls!
reduces sur#ace tension o# humidi#ied area to reduce pull! eeps the water molecules #romgetting to close together and collapsing the lung since the lipids and proteins are nonpolar
Compliance5 change in lung %olume resulting #rom a change in the pressure gradient
. h don;t the lungs collapse in %i%o
4ur#actantproteins are nonpolar and pre%ent the water molecules #rom getting close
enough together to shrin the al%eoli
7aw o# 7aPlace5 inward collecti%e pressure (P) is directl proportional to sur#ace tension (T)
and in%ersel proportional to al%eolar radius (r)o P92T&r
?. '"plain0 stepbstep0 the series o# e%ents that underlies inspiration and e"piration. 8e sure to
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discuss the changes which occur in intrapulmonar pressure0 intrapleural pressure0 and lung %olumeduring a respirator ccle.
8ole;s 7aw5
6. 7ist the muscles o# inspiration and e"piration0 and e"plain the role o# each in pulmonar %entilation.
-nspirator muscles
o Euiet breathing5 8e#ore inspiration5 all inspirator muscles rela"ed
Onset o# inspiration5 acti%ation o# phrenic ner%e9 contraction o# diaphragm!
contraction o# e"ternal intercostals (outer laer o# muscle between ribs) 9e"pands&stretches ribs 9 increased sie o# thoracic ca%it
o 7abored& Deeper 8reathing
-ncreased contraction o# both diaphragm and e"ternal intercostals
Contraction o# accessor inspirator muscles (in nec)
Pulls&li#ts upper ribs
Attached to sternum helps raise upper part o# thoracic ca%it
'"pirator muscles5
o Euiet breathing5
'"piration is passi%e! diaphragm rela"es *orced e"piration (during deeper breathing)
Contraction o# abdominals (shrins thoracic ca%it)
Contraction o# internal intercostals (brings ribs together0 shrining
thoracic ca%it)
F. De#ine tidal %olume0 inspirator reser%e %olume0 e"pirator reser%e %olume0 residual %olume0#unctional residual capacit0 %ital capacit0 total lung capacit and #orced e"pirator %olume.
Tidal %olume5 the %olume o# air entering or lea%ing the lungs during a single breath (at rest
usuall about 6== m7)
-nspirator reser%e %olume5 the e"tra %olume o# air that can be ma"imall inspired o%er and
abo%e the tpical resting tidal %olume! accomplished b ma"imal contraction o# the
diaphragm0 e"ternal intercostals0 and accessor inspirator muscles (a%erage 9 === m7) '"pirator reser%e %olume5 the e"tra %olume o# air that can be acti%el e"peried b ma"imall
contracting the e"pirator muscles beond that normall passi%el e"pired at the end o# atpical resting tidal %olume (a%erage 9 1=== m7)
/esidual %olume5 the minimum %olume o# air remaining in the lungs e%en a#ter a ma"imal
e"piration (a%erage 9 12== m7)
*unctional residual capacit5 the %olume o# air in the lungs at the end o# a normal passi%e
e"piration! */C 9 '/> G /> (a%erage 9 22== m7)
>ital capacit5 the ma"imum %olume o# air that can be mo%ed out during a single breath
#ollowing a ma"imal inspiration! #irst inspires ma"imall0 then e"pires ma"imall (>C 9 -/> GT> G '/>) ! represents the ma"imum %olume change possible within the lungs (a%erage 99?6== m7)
Total lung capacit5 the ma"imum %olume o# air that the lungs can hold (T7C 9 >C G />)(a%erage 9 6:== m7)
*orced e"pirator %olume5 the %olume o# air that can be e"pired during the #irst seconds o#
inspiration in a >C determination! usuall *'>1 is about H=I o# >C
:. De#ine minute %olume and al%eolar %entilation. Describe and e"plain the in#luence o# al%eolar%entilation on the al%eolar and sstemic arterial partial pressures o# o"gen and carbon dio"ide.
,inute %entilation5 %olume o# air e"pired each minute
o >'o 9 # (resp. rate) " >t (tidal %olume)
o At rest5 9 12 br&min " 6== m7&br 9 F 7&min
o '"ercise (world class) 9 F= br&min " === m7&br 9 1H= 7&min
Al%eolar >entilation5 %olume o# air mo%ed in and out o# al%eoli per unit o# time
o >oA9 # (respirator rate) " >A(>tidal>D)
o T+' #actor that determines PCO2 and PO2 in al%eoli0 and ultimatel sstemic
circulation
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o -ncreased al%eolar %entilation 9 increased O2 in sstemic circulation and decreases
CO2 in sstemic circulation
Ventilation-Perfusion Matching
1. hat is %entilationper#usion matching and wh is it important
Air#low and blood #low at a particular al%eolar inter#ace usuall matched as much as possibleb local controls to accomplish e##icient e"change o# O2and CO2.
8ecause o# gra%itational e##ects0 some regional di##erences in %entilation and per#usion e"ist
#rom the top to the bottom o# the lung.o Person standing upright5 %entilation and per#usion are both less at the top o# the lung
and greater at the bottom o# the lung0 but gra%it e"erts a more mared e##ect onblood #low than on air#low.
o >entilationper#usion ratio (the rate o# air#low compared to the rate o# blood #low)
decreases #rom the top to the bottom o# the lungo Top o# the lung recei%es less air and blood than the bottom o# the lung0 but it recei%es
relati%el more air than blood!o 8ottom o# the lung recei%es more air and blood than the top o# the lung0 but it
recei%es relati%el less air than blood.2. '"plain0 stepbstep0 the mechanisms b which %entilation and per#usion o# al%eoli are balancedwith one another.
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as a partial pressure gradient
Partial pressure gradients e"ist between the al%eolar air and pulmonar capillar blood and
between sstemic capillar blood and surrounding tissues
Kas alwas di##uses down its partial pressure gradient #rom the area o# higher partial pressure
to the area o# lower partial pressure
. hat are the partial pressures o# o"gen and carbon dio"ide in the atmosphere0 conductingstructures (inspiration %s. e"piration)0 al%eoli0 sstemic arterial blood0 and sstemic %enous blood'"plain all di##erences.
"lood !as #ransport
1. '"plain how O2is transported in the blood.
Phsicall dissol%ed5 2I O2 transported lie this (O2 not %er soluble in blood)
o =.2 m7 O2& 7 blood a%g. CO 9 6 7&min1.6 m7 O2 transported&min
8ound to hemoglobin (+g8)5 LHI bound to +g8
o About 1== m7 O2 transported %ia +g8&min
o O2 bound to +g8 does not contribute to PO2 in blood
o 8inding o# )2 to +g8 increases the a##init o# +g8 #or ne"t O2 because it changes the
structure o# the heme group0 a##ecting other heme groups0 increasing the a##init o#
the other heme groups #or the ne"t O2
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2. Draw the o"genhemoglobin dissociation cur%e0 e"plain the basis #or its sigmoidicit0 and e"plainits signi#icance.
/eaction pushed le#t or right depending on partial pressure o# O2 high pushes right0 low
pushed right
Plateau region5 as long as PO2 in arteries&al%eoli < F=:= mm+g0 +g8 about L=Isaturated
and most normal metabolic needs can be met 4teep region5 as demand #or O2 increases due to metabolic need0 +g8 releases more O2
o As much as H6I O2 ma be released #rom +g8 during e"ercise
. Describe the in#luence o# temperature0 p+ and PCO2on the a##init o# hemoglobin #or o"gen.
Temperature5 as temperature increases0 a##init #or O2 decreases (downward&rightward shi#t)
p+5 as p+ decreases0 a##init #or O2 decreases (downward&rightward shi#t)
PCO25 as PCO2 increases0 a##init #or O2 decreases
-,PO/TABC'5 these shi#ts are important because the allow more O2 to be released to meet
metabolic need during times o# e"ercise&internal respiration
?. '"plain hemoglobin;s role in coupling o"gen deli%er to tissue metabolic demand.
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6. Describe how CO2is transported in the blood. '"plain the roles o# hemoglobin in this process.
Dissol%ed5 CO2 more soluble in blood than O20 so about 1=I o# all CO2 carried in blood is
dissol%ed (1&2 in plasma0 M in /8C)
8icarbonate -on5 (F=I)
Carbamino compound5 (=I) CO2 G +g8 +g8CO2 (binds to globin0 not heme part)
hen increased PCO2 or NCO2 in blood0 both reactions shi#t right
Another reaction5 +GG+g8h+g8acts as a bu##er to reabsorb the increased N+G in
blood #rom increased NCO2
F. /econstruct the #igure on slide 1 in our handout and e"plain the shi#ts in the chemical reactionsas blood #lows through the sstemic capillaries and the pulmonar capillaries.
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:. '"plain the mechanism underling the increase in CO2carring capacit o# blood in response todecreased saturation o# hemoglobin with o"gen.
H. '"plain the role o# hemoglobin in coupling CO 2remo%al to tissue metabolic demand.
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L. De#ine and e"plain the basis #or the 8ohr and +aldane e##ects.
8ohr e##ect5 As more CO2is released to the blood0 more carbonic acid is #ormed! carbonic
acid dissociates to +Gand +COions0 the +Gions bind to +b0 reducing it (++b) and
stabiliing the low a##init structure o# +b
The +aldane '##ect5 encourages CO2e"change in the lungs and tissues5 when plasma partial
pressure o# o"gen and o"gen saturation o# hemoglobin decrease0 more CO2can be carriedin the blood. This is due to the increased abilit o# +b to bind CO 2directl0 #ormingcarbaminohemoglogin (+bCO2)! deo"genated blood can carr more CO2 at an gi%en PCO2than o"genated blood
"lood-#issue !as Exchange
1. '"plain the mechanism b which o"gen and carbon dio"ide are e"changed between the blood andcells.
8oth tra%el down their concentration gradients %ia passi%e di##usion
Regulation of Respiration
1. Describe the pattern o# action potentials tpicall recorded in motor neurons o# the phrenic ner%e.
Aps onl seen during inspiration
'"piration is passi%e when at rest
-ncrease in AP acti%it as inspiration approaches end (signal to stop or recruit increased
motor units)
2. Describe the roles o# the medullar dorsal and %entral respirator groups0 pneumota"ic center0apneustic center and pre8otinger comple" in the regulation o# respiration.
,edullar respirator center5 source o# basic rhthmicit! without this0 inspiration ceases 9
deathneuronal controlo Dorsal respirator group5 all neurons dri%e inspiration during resting breathing
(controls e"ternal intercostals and diaphragm)o >entral respirator group5 contains neurons that acti%ate inspirator and e"pirator
muscles during labored breathing (e"ercise)o Pre8otinger comple"5 thought to be the pacemaer center #or the respirator center
(lie 4A node in the heart)
Pneumota"ic center5 important #or inhibiting&limiting inspiration
Apneustic center5 stimulates inspiration
. '"plain the role o# o"gen in the regulation o# al%eolar %entilation. '"plain the mechanism b whichit alters al%eolar %entilation.
Changes in arterial PO2 detected b peripheral chemoreceptors (which measure dissol%ed
NO20 not what;s bound)
-# PO2 decreases #rom 1== mm+g (normal) to F= mm +g5 little to no e##ect on al%eolar
%entilation because there;s still a high I o# +g8 saturation (big reser%e) -# PO2 drops below F= mm+g0 now there;s a big increase in al%eolar %entilation (re#le"i%e)
Conclusion5 moment to moment respiration BOT regulated b sstemic PO2 ou;d ha%e to
be almost dead (PO2 9 2=) be#ore ou see a big increase in %entilation rate our brainwould be #ried
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?. '"plain the role o# carbon dio"ide in the regulation o# al%eolar %entilation. '"plain the mechanismb which it alters al%eolar %entilation. 8e sure to discuss the bloodbrain barrier.
Changes in arterial PCO2 detected b central chemoreceptors (#ound on %entrolateral
sur#aces o# medulla which are bathed in C4*) Chemoreceptors5 BOT CO2 receptorsthe;re N+G receptorsmonitor p+ changes in
C4*
Capillaries in C4* BOT highl permeable (87OOD 8/A-B 8A//-'/) +G can;t di##use #rom
capillaries into C4*
CO2 can di##use #rom capillaries into C4*0 where it combines with +2O and #orms carbonic
acid then bicarbonate ion and a proton (this is the proton that bonds to the chemoreceptor)
CO2 indirectl in#luences respiration rate
6. Draw the negati%e #eedbac loop that regulates sstemic arterial PCO 2. '"plain0 stepbstep0 how
the loop responds to an increase or decrease in PCO2.
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F. '"plain the role o# +Gin the regulation o# al%eolar %entilation. '"plain the mechanism b which italters al%eolar %entilation.
+Gcan;t easil di##use #rom capillaries into C4*
Peripheral chemoreceptors ha%e poor sensiti%it to arterial CO2 and are weal responsi%e to
arterial arterial O2 until F= mm+g
+owe%er0 peripheral chemoreceptors are highl responsi%e to slight changes in N+G
p+ ma change despite normal PCO2 (reasons other than respirator)
increased N+Gdecreased p+increased %entilation
decreased N+Gincreased p+decreased %entilation
Renal Physiology
Anatomy
1. 4ummarie the #unctions o# the idnes.
,aintaining +2O balance in the bod
,aintain proper osmolarit o# bod #luids0 primaril through regulating +2O balance (important
to pre%ent osmotic #lu"es into or out o# the cells0 which could lead to detrimental swelling orshrining o# the cells)
/egulating the $uantit and concentration o# most 'C* ions
,aintaining proper plasma %olume (important in longterm regulation o# arterial blood
pressure)
+elping maintain proper acidbase balance o# the bod (b adusting urinar output o# +G and
+CO)
'"creting (eliminating) the end products (wastes) o# bodil metabolism (i# allowed to
accumulate0 man o# the wastes are to"ic0 especiall to the brain) '"creting man #oreign compounds that ha%e entered the bod
Producing erthropoietin0 a hormone that stimulates red blood cell production
Producing renin0 an enmatic hormone that triggers a chain reaction important to salt
conser%ation b the idnes
Con%erting %itamin D into its acti%e #orm
2. Describe the gross anatom o# the urinar sstem including that o# the idnes.
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. Draw a nephron and identi# its parts.
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?. Describe the specialied %asculature o# the nephron.
6. Distinguish anatomicall and #unctionall between u"tamedullar and cortical nephrons.
Cortical nephron5
o H=I o# all nephrons
o Klomerulus and maor tubular components mostl in corte"
o Collecting duct passes through medulla
Qu"tamedullar nephron5
o 2=I o# all nephrons
o 7oop o# henle digs deepl into the medulla
7o+ o# u"tamedullar nephrons generates medullar osmotic gradient (#"n5
#orm concentrated urine)o /est o# nephron is in the corte"
o Collecting duct passes through medullao +as special capillaries called %asa recta
F. Describe the structure o# the u"taglomerular apparatus.
A close conunction o# distal con%oluted tube and a##erent arteriole
cell tpes5
o ,esangial cells5 holds clomerular capillaries together
o ,acula densa (tubular component)5 in walls o# DCT
o Kranular cells (%ascular component)5 in walls o# a##erent arteriole
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!lomerulus
1. Describe the structure o# the glomerular membrane.
Klomerular membrane5 plasma entering the glomerulus must pass through the glomerular
membrane to enter 8owman;s capsul! it has laers
o Klomerular capillar wall5 4ingle laer o# endothelial cells! similar to other capillaries
'ndothelial cells contain large pores (#enestrations)
Capillar membrane in glomerulus about 1==" more permeable to +2= than
other solutes -mpermeable to large plasma proteins0 but permeable to albumin
o 8asement ,embrane (acellular)
Kelatinous laer o# collagen and glcoprotein
Collagen pro%ides structural strength
Klcoprotein5 negati%el chargedrepels negati%el charged proteins0
especiall albumin (1I albumin actuall enters 8owman;s capsul) All o# albumin that enters 8owman;s capsul is reabsorbed in pro"imal tubule
(urine normall protein #ree)o -nner laer o# 8owman;s capsul
+as podoctes cells with multiple e"tensionsinterloc with others
#orming #iltration slits (can contract& rela" to open&close them)
2. rite and e"plain the %ersion o# the 4tarling7andis hpothesis that summaries the #actors thatdetermine glomerular #iltration rate.
4tarling7andis hpothesis5 the #luid mo%ement due to #iltration across the wall o# a capillar is
dependent on the balance between the hdrostatic pressure gradient and the oncoticpressure gradient across the capillar
Klomerular capillar blood pressure #a%ors #iltration
o Determined b5
Contractile #orce generated b %entricles (,AP)
/esistance to #low in a##erent and e##erent arterioles
o 66 mm+ghigher than in other capillaries because diameter o# a##erent arteriole
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Plasmacolloid osmotic pressureopposes #iltration
o Nproteins in glomerulus (plasma) '
Podoctes5 contraction o# podoctes closes gaps on the membrane between capillar and
8owman;s capsul0 decreasing K*/ (decreases how much can pass into 8owman;s capsul)
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o
?. '"plain0 stepbstep0 how K*/ is regulated intrinsicall.
ithout this5 e%er -ncrease&decrease in ,AP would increase&decrease renal blood #low and
increase&decrease K*/
,ogenic mechanism5
o -ncreased stretching o# a##erent arterioles (due to increased ,AP) a##erentarterioles constrict to decrease blood #low into glomerulusdecrease K*/
o Decreased ,AP 9 a##erent arteriole dilates&rela"es to increase renal blood #low and
increase K*/
Tuboglomerular #eedbac5 in%ol%es u"taglomerular apparatus
o -ncreased ,APincreased glomerular blood #lowincreased K*/increased
tubular #iltration #lowtubular components stretchdetected b macula densecells,DCs release ATP and adenosine constriction o# a##erent arterioles decreased glomerular blood #lowdecreased glomerular capillar blood pressure decreased net #iltration pressuredecreased K*/
o ,acula densa also releases BO0 stopping %asoconstriction mediated b ATP and
adenosine
6. '"plain the mechanisms b which smpathetic stimulation o# the idnes changes K*/.
-ncreased smpathetic tone to a##erent arterioles 9 shortterm regulation o# 8P
Parasmpathetic ner%ous sstem has no e##ect on arterioles& idnes
-ncreased smpathetic out#low acti%ated mesingial cells0 and the contractresult5
decreased #iltration sur#ace area in glomerulus decreased glomerular #iltration
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Proximal *onoluted #u+ule
1. '"plain the mechanism (standing gradient theor o# isoosmotic reabsorption) b which Ba G0 @G0 Cland +2O are reabsorbed #rom the pro"imal con%oluted tubule. 8e sure to detail the structure o# thetubular wall.
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8asolateral membrane ne"t to lateral space BaG&@G atpase pumppumps BaG out o#
tubular cell and into lateral space0 there#ore NBaG in ctoplasm o# tubular cell is low comparedto NBaG in tubular #iltrate
7uminal membrane permeable to BaG BaG mo%es down its concentration gradient #rom
lumen into tubular cells (passi%e)
A$uaporin channels in both membranes permeable to +2O0 so +2O #ollows BaG into lateral
space Cl channels in both luminal and 87 membranes as +2) lea%es0 concentration gradient #or
Cl to #ollow NCl lumen increasesCl #ollows +2O into lateral space
BaG0 Cl0 and +2= accumulate in lateral space pressure increases0 so it starts to mo%e
towards the peritubular capillaro Capillar hdrostatic pressure is >'/S low (blood had to pass through 2 arterioles to
get here)o Plasma colloid osmotic pressure is high (should be no proteins interstitial more N
in plasma)o *iltration pressure in peritubular capillaries is negati%e (net reabsorption)
o There#ore0 *P 9 neg throughout peritubular capillaries P.C.s reabsorb
solute&sol%ent throughout nephron
all o# this starts with the acti%it o# BaG&@G atpase pump i# that stops0 none o# this canhappenU
2. '"plain the mechanism b which glucose0 amino acids and %itamins are reabsorbed b thepro"imal con%oluted tubule.
Klucose5 normall 1==I o# A77 #iltered glucose (glucose that enters 8owman;s capsule) is
reabsorbed in the pro"imal tubule
8ecause o# BaG&@G atpase pump0 NBaGctoplasm is low 4K7T on luminal membraneBaG mo%es down its concentration gradient and energ is
utilied to mo%e glucose up its concentration gradient Nglucose in ctosol o# tubular cell ishigh
Klucose di##uses down its concentration gradient out o# tubular cells and into the lateral space
Klucose carried to the peritubular capillaries b #luid mo%ement and glucose di##uses into the
peritubular capillaries
. '"plain the relationships between plasma glucose le%el and the rates o# glucose #iltration0reabsorption and e"cretion b the idnes.
Klucose is #reel #iltered #rom glomerulus into 8owman;s capsule high plasma Nglucose 9
high Nglomerular #iltrate
*iltered load5 $uantit o# an substance #iltered per minute 4stem e"hibits a ma" rate o# reabsorption (tubular ma"imum0 T,)about :6 mg
glucose&min
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o Acti%e reabsorption 9 through proteintaes time and #inite number o# 4K7T2 in
membraneonce the;re all #ull&saturated0 e%er other molecule o# glucose eepsgoing (this is the onl place is can be reabsorbed)
o Conse$uentl0 glucose can be lost in urine! when rat #iltration < rate reabsorption0
e"cess glucose e"creted in urine! at a normal K*/ 126 ml&min0 a clucoseconcentration o# == mg&1== ml 9 T,o# :6 mg&min
*iltration rate 9 plasma concentration " K*/ '"cretion rate 9 #iltration rate reabsorption rate
o Bormal plasma glucose concentration5
1== mg&1== m7well below renal threshold at normal Nglucose
Klucose reabsorption not regulated in idnes all o# it gets reabsorbed
unless our glucose le%el is super higho Pro"imal tubule5 normall reabsorbs 1==I o# glucose0 AAs0 %itamins0 and potassium
o DO'4 BOT depend on glucose needs o# organism
?. '"plain how unwanted metabolic wastes are concentrated in the pro"imal con%oluted tubule.
'%erthing that;s le#t behind in the tubular #iltrate concentrates because e%erthing else that
was diluting its concentration is gone& has been reabsorbed
Rric acid0 creatinine0 and phenols le#t o%er
6. Compare the composition o# the tubular #luid e"iting the pro"imal tubule with the glomerular #iltrate.
,oop of enle
1. hat is the medullar osmotic gradient and wh is it important
-n the interstitial #luid o# the renal medulla
Allows e"cretion o# urine o# %aring osmolarities (1== mOsm&7 to 12== mOsm&7)
DO'4 depend on hdration status o# organism
2. '"plain0 stepbstep0 the mechanism b which the loop o# +enle creates the medullar osmoticgradient. 8e sure to summarie the rele%ant permeabilit and transport properties o# each segment o#the loop o# +enle0 distal con%oluted tubule and collecting duct.
4tarting with thic ascending limb5
o *luid in TA75 primar solutes are BaG0 Cl0 and urea (R)
o TA7Ba&Cl atpase (acti%e transport)BaG and Cl into interstitium
o TA7 not permeable to +2O#iltrate lea%ing TA7 is %er dilute (1== mOsm&7)
o Thic A7 not permeable to urea
-t concentrates
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.istal conoluted #u+ule and *ollecting .uct
1. De#ine and e"plain the importance o# water and mineral balance.
2. h is it important that N@G'C* be regulated
plas a e role in the membrane electrical acti%it o# e"citable tissues
increases and decreases in the plasma ('C*) @ concentration can alter the intracellularto
e"tracellular @ concentration gradient0 which in turn can change the resting membranepotential.
@G e"cess and @G de#icienc result in decreased cardiac e"citabilit
o rise in 'C* @ concentration reduces resting potential (maes it less negati%e)0 which
decreases the e"citabilit o# neurons0 seletal muscle cells0 and0 most importantl0cardiac muscle cells0 b eeping the %oltagegated Ba channels responsible #or therising phase o# the cardiac action potential in their inacti%e (closed and not capable o#opening) state
cell membrane unable to repolarie completel a#ter depolariation to return
the channel to its closed and capable o# opening con#ormation. 4ome Ba channels are more sensiti%e than others to the depolariing e## ect.
As more and more Ba channels are inacti%ated b rising @ le%els0 cardiace"citabilit progressi%el decreases.
o A #all in 'C* @ concentration results in hperpolariation o# ner%e and muscle cell
membranes0 which also reduces their e"citabilit. A greater depolariation thannormal is needed to bring the membrane to threshold potential.
mani#estations o# 'C* @ depletion are seletal muscle weaness0 diarrhea
and abdominal distension caused b smooth muscle ds#unction0 andabnormalities in cardiac rhthm and impulse conduction.
. 4ummarie how @Gis handled b each segment o# the nephron. -n particular0 e"plain themechanism b which @Gis secreted b the distal con%oluted tubule.
Potassium ion is selecti%el mo%ed in opposite directions in di##erent parts o# the tubule
acti%el reabsorbed in the pro"imal tubule and acti%el secreted b principal cells in the distal
and collecting tubules
one tpe o# intercalated cell acti%el secretes @ and another tpe acti%el reabsorbs @ in the
distal and collecting tubules in conunction with +G transport
'arl in the tubule @ is reabsorbed in a constant0 unregulated #ashion0 whereas @ secretion
later in the tubule b the principal cells is %ariable and subect to regulation.
8ecause the #iltered @ is almost completel reabsorbed in the pro"imal tubule0 most @ in the
urine is deri%ed #rom controlled @ secretion in the distal parts o# the nephron rather than #rom
#iltration During @ depletion0 @ secretion in the distal parts o# the nephron is reduced to a minimum0 so
onl the small percentage o# #iltered @ that escapes reabsorption in the pro"imal tubule is
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e"creted in the urine@ that normall would ha%e been lost in urine is conser%ed #or thebod0
hen plasma @ le%els are ele%ated0 @ secretion is adusted so that ust enough @ is added to
the #iltrate #or elimination to reduce the plasma @ concentration to normal
@ secretion0 not the #iltration or reabsorption o# @0 is %aried in a controlled #ashion to regulate
the rate o# @ e"cretion and maintain the desired plasma @ concentration.
?. '"plain0 stepb step0 the mechanism b which N@G'C*is regulated.
Potassium ion secretion o# distal and collecting tubules coupled to Ba reabsorption b the
energdependent basolateral Ba@ pumppump mo%es Ba out o# the cell into the lateralspace and also transports @ #rom the lateral space into the tubular cells
resulting high intracellular @ concentration #a%ors net mo%ement o# @ #rom the cells into the
tubular lumen
,o%ement across the luminal membrane occurs passi%el through the large number o# @ lea
channels in this barrier in the distal and collecting tubules
8 eeping the interstitial #luid concentration o# @ low as it transports @ into the tubular cells
#rom the surrounding interstitial #luid0 the basolateral pump encourages passi%e mo%ement o#@ out o# the peritubular capillar plasma into the interstitial #luid. A potassium ion lea%ing the
plasma in this manner is later pumped into the cells0 #rom which it passi%el mo%es into thelumen.
basolateral pump acti%el induces the net secretion o# @ #rom the peritubular capillar plasma
into the tubular lumen in the distal parts o# the nephron
-n the distal and collecting tubules0 the @ channels are concentrated in the luminal membrane0
pro%iding a route #or @ pumped into the cell to e"it into the lumen0 thus being secreted. -n theother tubular segments0 the @ lea channels are located primaril in the basolateralmembrane. As a result0 @ pumped into the cell #rom the lateral space b the Ba@ pumpsimpl mo%es bac out into the lateral space through these channels
@ reccling permits the ongoing operation o# the Ba@ pump to accomplish Ba reabsorption
with no local net e##ect on @
6. h is it important that 'C* osmolarit be regulated
F. 4ummarie how water is handled b each segment o# the nephron. -n particular0 e"plain themechanism b which water is reabsorbed b the late distal con%oluted tubule and collecting duct. 8esure to discuss the role o# the medullar osmotic gradient.
H=I reabsorbed b PCT and 7O+ regardless o# hdration status o# the animal! 2=I
reabsorbed b DCT and CD adusting according to the hdration status o# the organism
+2O absorption in DCT and CD occur %ia osmosis re$uires that the walls o# DCT and CD
permeable to +2Oo Permeabilit o# walls regulated b AD+antidiuretic hormoneincreases
permeabilit o# walls o# DCT and CD to +2O
:. '"plain0 stepb step0 the mechanism b which 'C* osmolarit is regulated.
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/eason out5
o 'C* mOsm < ==5 increased AD+o 'C* mOsm ==5 decreased AD+
AD+ 9 antidiuretic hormoneincreases
H. '"plain wh a rise (or #all) in BaGintae results in a rise (or #all) in 'C*>. '"plain wh a rise (or #all)in 'C*> results in a rise (or #all) in arterial blood pressure.
V BaG 9 V 'C* Os, 9 V AD+ release 9 V +2O reabsorption 9 V 'C*> 9 V 8> 9 V >/ 9 V
preload 9 V %ent. Pressure generated 9 V 4> 9 V CO 9 V,AP
*all in BaG would be all the opposite
L. 4ummarie how BaGis handled b each segment o# the nephron0 -n particular0 e"plain themechanism b which it is reabsorbed b the distal con%oluted tubule and earl collecting duct.
H= I o# BaG reabsorbed in pro"imal tubule and ascending 7O+ without regard to sodium loado# the organism
/eabsorption o# BaG Cl in DCT and CD regulated b aldosterone
o +igh aldosterone5 increased BaG reabsorption in DCT and CD 9 decreased BaG in
urine! opposite #or low aldosteroneo ,echanism5
-ncrease BaG&@G atpase pumps in basolateral membrane (increased BaG
out and @G in) -ncreased BaG channels in luminal membrane
-ncreased BaG reabsorption #rom DCT and CD
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1=. '"plain the relationship between K*/0 tubular #luid reabsorption and urine #low.
4mall changes in either K*/ or reabsorption rate 9 large changing in urine #low rate0
ultimatel changing blood %olume0 >/0 4>0 CO0 and ,AP
11. '"plain the mechanism b which a rise (or #all) in arterial blood pressure results in a rise (or #all) inK*/.
1=. '"plain the mechanism b which a rise (or #all) in arterial blood pressure results in a #all (or rise) inthe rate o# tubular #luid reabsorption b the nephron. 8e sure to e"plain0 in detail0 the role o# the renninangiotensin sstem.
Qu"taglomerular apparatus5 DCT comes in close pro"imit with a##erent arterioleo Kranular cells5 detect decrease in a##erent arteriole pressure 9 release o# renin
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o ,acula densa cells5 detect decrease in BaC7 in tubular #iltrate 9 stimiluates granular
cells to release renino 4mpathetic ner%ous sstem5 decreases ,APincreases smpathetic tone
increases renin release
Angiotensin5
o 4nthesied and released b li%er
o Present in blood stream in high concentrationso -nacti%e b itsel#con%erted to angiotensin - b renin
Angiotensin -5
o -nacti%econ%erted to Angiotensin -- b Angiotensin con%erting enme (AC')
which is present in epithelial cells o# pulmonar capillaries
Angiotensin --5
o 4timulates release o# aldosterone b adrenal corte"
-ncreased BaG&Cl reabsorption in DCT and CD +2O #ollowsincreases
'C*>o 4timulates hpothalamus
-ncreases thirstincreases 'C*>increase >/W
-ncreases AD+ releaseincreased +2O reabsorption in DCT and CD
decreased urine %olumeincreased 'C*>o Arteriolar %asoconstriction
-ncreased TP/increased ,AP
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11. '"plain how e"tracellular #luid %olume0 arterial blood pressure0 sodium balance and water balanceare interdependent and coordinatel controlled. 8e sure to discuss the reninangiotensin sstem.
4'' A8O>'
Micturition
1. '"plain the neural circuit that underlies the micturition re#le". 8e sure to discuss the internal ande"ternal urethral sphincters.
2. '"plain the role o# higher centers in the control o# urination.
4ee abo%e