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7/24/2019 Physio Uhs Solved Past Papers 2nd Year
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PHYSIOLOGY UHS
PAST PAPERS
(SOLVED)2004-2012
Brought to you by:
MED-COM
GOD helps you !e "#e $he sou#%e&
Help o$he#s $o 'e$ helpe**
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SPECIAL SENSES
+ 1,h"$ %h".'es o%%u# /. eyes !he. $hese "#e
o%use o. " .e"# oe%$ 3 Epl"/. $he .e#5ous
6e%h"./s6 /.5o5le3(2007 "..u"l& 2008
"..u"l)
A.s, (9P %hp 1:;& Guy$o. %hp 4;)
Accomodation is invovled in this mechanism.
De
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e*tent.
>e#5ous 6e%h"./s6,
A+erent "ath#ay :
visual im"ulses on retina -,o"tic nerve -,o"tic
chiasma-,o"tic tract-,lateral geniculate body-,o"tic
radiation to visual corte* of occi"ital lobe
-,association bers to frontal lobe
Centre:
located in frontal lobe of cerebral corte* area / 0E+erent "ath#ay :
%:E+erent bers to ciliary muscles and s"hincter
"u"illae
from area / -,corticulonuclear bers "ass via internal
ca"sule to Edinger West"hal nucleus of 'rd cranial
nerve-,"reganglionic bers "ass to ciliary ganglion-,"ostganglionic bers via short ciliary nerves and
su""ly ciliary muscles and constrictor muscles
&:E+erent bers to medial rectus :
from frontal eye eld bers to nucleus of occulomotor
nerve -,and su""ly medial rectus
+ 2,D#"! $he Rhoops/. 5/su"l %y%le ? h"$ /s
$he ou$%o6e o V/$?A e
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A.s , Guy$o. %hp 70
Rhoops/. 5/su"l %y%le:
Diagram from guyton "age 1%%Role o V/$? A o# o#6"$/o. o Rhoops/.:
%:2it.A is "resent in cyto"lasm of rods and in the
"igment layer of the retina to form ne# 3E4$5A6 .
&:When e*cess retinal !it is converted bac( into 2it.A
and vice versa .
De
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light rays on eyes-,o"tic nerve-,o"tic chiasma-
,o"tic tract-,p#e$"%$"l .u%leus-,Edinger West"hal
nucleus-,ciliary ganglion-,short ciliary
nerve"arasym"athetic nerves0-,constrict s"hincterof iris
Co.se.su"l L/'h$ ReBe,
%:Contraction in both eyes #hen light thro#n in one
eye.
&:4he reason for Consensual light re9e* is that some
of the bers from "retactal nucleus of one side cross
to the o""osite side and end on the o""osite Edinger
West"hal nucleus.
+ 4,A :7 ye"#s ol 6". #epo#$s $o h/s phys/%/".
!/$h $he p#/.%/ple %o6pl"/.$ o >y%$"lop/"(./'h$/l..ess)?(200; "..u"l)
"?h"$ /s $he %"use o $h/s /so#e#3
2it.A deciency
?h/%h l"ye# o #e$/." e%o6es /6p"/#3
igmented layer ! as 2it.A is stored in this layer and
6ayer of rods as #ell because 2it. A involved information of retinal and rhodo"sin.
%?h"$ /s A#'yll Roe#$so. Pup/l3
$t is clinical condition in #hich the light re9e* is lost
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but the accomodation re9e* is "resent . u"il is also
very small .$t is an im"ortant diagnostic sign of C5;
disease such as ;/'h$ l/..ess3
2it. A deciency in diet.
?h"$ !/ll e $he #ole o he# $#e"$6e.$ /. $he
o#6"$/o. o Rhoops/. 3
$ntravenous inection of 2it.A can can reverse night
blindness in less than % hour because 2it.A is used inthe formation of retinal and rhodo"sin .
+ :,Ho! o eyes ""p$ $o #/'h$ l/'h$ ".
"#.ess3G/5e /$s s/'./
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&:hotochemicals in both rods and cones #ill have
been reduced to retinal and o"sins.
':Much of the retinal of both rods and cones #ill have
been converted into 2it.A .
':Because of these t#o e+ects conc. of "hotosensitive
chemicals remaining in the rods and cones are
considerably reduced and sensitivity of the eye to
light is corres"ondingly reduced .this is called light
ada"tation.
D"# A"p$"$/o.,
%:$f a "erson remains in the dar(ness for a long time !
the retinal and o"sins in the rods and cones are
converted bac( into light sensitive "igments.
&:7urthermore!2it.A is converted bac( into retinal to
increase light sensitive "igments ! the nal limit beingdetermined by the amount of o"sind in the rods and
cones to combine #ith the retinal.4his is called dar(
ada"tation.
':Dar( ada"tation curve ! guyton "age no. 1%).
O$he# 6e%h"./s6 o l/'h$ ". "# ""p$"$/o.,
%:Change in "u"illary si>e ada"tation u"to '? folds
#ithin fraction of seconds because of changes in the
amount of light allo#ed through the "u"illary o"ening0
&:5eural ada"tation! through bi"olar cells! hori>ontal
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cells!amacrine cells and ganglion cells ! signals rst
are strong then decrease ra"idly at di+erent stages of
transmission.Degree of ada"tation is only fe#folds but
occurs in fraction of seconds ! in contrast to the manyto hours re8uired for full ada"tation by the "hoto
chemicals.
S/'./
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%,h/%h le.s "#e use $o %o##e%$ $hese e##o#s3
4he light rays "assing through a concave lens
diverge.$f the refractive surfaces of the eye have too
much refractive "o#er !as in myo"ia! this e*cessive
refractive "o#er can be neutrali>ed by "lacing in front
of the eye a concave s"herical lens ! #hich #ill
diverge rays.
+ 8,h"$ /s A$$e.u"$/o. ReBe 3 h"$ /s /$ss/'./
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):$t can reduce the intensity of lo# fre8. sound
transmission by '? to )? decibles! #hich is about the
same di+erence as that b@# a loud voice and a
#his"er.
S/'./
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as a single lever!have a""ro*imately atthe border of
the tym"anic membrane.
4he articulation of the incus #ith the sta"es causes
the sta"es to "ush for#ard on the oval #indo# and on
the cochlear 9uid on the other side of #indo#.
S/'./
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e".ess ". pe#%ep$/5e e".ess3(2004
"..u"l)
A.s, (Guy$o. %hp 72)
1:Deafness caused by im"airment of cochlea ! the
auditory nerve! or the central nervous system
circuitsfrom the ear ! #hich is usually classied as
nerve deafness.
&:Deafness caused by im"airment of the "hysical
structure of the ear that conduct sound itself to thecochlea !#hich is usually called conduction deafness.
D/Fe#e.%e,
4he di+erence can be determined by di+erent tests as
follo#:
%:3innes 4est&:Webers 4est
':Audiometry
+ 12,A o6 l"s$ o%%u#s /. $he 5/%/./$y o "
house ? A !o6". p#ese.$ /. $he house /s h/$ y" p/e%e (sh"#p.el)o $he o6 o. he# #/'h$ "#6?
She "lso eels $h"$ he# he"#/.' /s "lso sl/'h$ly
/6p"/#e ?He# %o6ple$e e"6/."$/o. /.
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e6e#'e.%y #e5e"ls .o "u/$o#y "6"'e o
e
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:What are the features of u""er motor neuron
lesionive one e*am"le of the lesionAns:7eatures:
a0-aralysed muscles are rigids"astic "aralysis0
b0-Dee" re9e*es are e*agerrated=y"er-re9e*ia0
c0-Abdominal and cremasteric re9e*es are lost
d0-lantar re9e* becomes Babins(i!s sign
e0-5o #asting or little #asting of muscles
f0-3eaction of degeneration is absent
g0-6arge area of body involved
E*am"le
Cerebral alsy
-What are the functions of C;7Why is lumbar
"uncture generally "erformed belo# 6& segment of
s"inal cord
Ans:7unctions of C;7:i0-Acts as shoc( absorber
ii0-Acts as cushion bet#een soft and delicate brain and
rigid cranium
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iii0-Acts as a 9uid bu+er
iv0-Acts as a reservoir to regulate contents of cranium.
v0-medium for nutritional e*change
vi0-3emoves metabolites
vii0-4rans"orts medicine
6umbar "uncture is "erformed belo# 6& segment to
avoid inury to s"inal cord.4he s"inal cord terminates
at this level.
-5ame tactile rece"tors.Why does asterognosis
occur due to lesion of dorsal column tract
Ans:4actile 3ece"tors:
i0-7ree nerve endings
ii0-E*"anded ti" endings
iii0-Mer(el!s discsiv0-;"ray Endings
v0-3uni!s Endings
vi0-Fraus!s endings
vii0-Meissner!s Endings
Dorsal column tract is res"onsible for the sensations
of touch !t#o "oint discrimination!"ro"rioce"tion and"osition.We get an idea of the sha"e of the obect by
touching it.;o lesion of dorsal column tract results in
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astereognosis #hich is the inability to identify an
obect by touch #ithout visual in"ut.
-Write a note on Analgesia ;ytem
Ans:Analgesia ;ystem:
Brain can su"ress in"ut of "ain signals to the nervous
system by activating a "ain control system!called the
analgesia system.
Com"onents:
i0-4he "eria8ueductal and "eriventricular areas of the
mesence"halon ant u""er "ons surround the
a8ueduct of ;ylvius and "ortions of the 'rd And )th
ventricles.5eurons from these areas send signals to:
ii0-4he 3a"he Magnus 5ucleus! a thin midline nucleuslocated in the lo#er "ons and u""er medulla and the
nucleus reticularis "aragiganto cellularis.7rom these
second order signals are transmitted to:
iii0-A "ain inhibitor com"le* located in the dorsal horns
of the s"inal cord.
Areas that e*cite the "eria8ueductal gray area can
also su"ress the "ain.4hese are :
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i0-eriventricular area
ii0-Medial forebrain bundle
Main transmitter substances involved are :
En(a"halin and ;erotoninEn(a"halin is believed to cause both "resyna"tic
and "ost-syna"tic inhibiton of incoming ty"e C
and ty"e A delta bers.
Brain O"iate ;ystem: Endor"hins and En(a"halin
G$nection of the minute 8uantities of mor"hineeither into the "eriventricular nucleus around
third ventricle or into the "eria8ueductal gray
Area of the brainstem causes an e*treme degree of
analgesia
-Enemurate functions of Cerebellum.6ist ) features
of cerebellar diseases.
Ans.7unctions:
i0-lanning and ne tunning of s(eletal muscle
contraction
ii0-Maintainance of "osture and "erformance of
voluntary musclesiii0-7acilitates smooth and co-ordinated voluntary
movements
iv0-Ensures that force!contraction and e*tent of
movements are accurate.
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v0-3s"onds to vestibular stimuli from inner ear
vi0-Assists in maintaing e8uilibrium by modications in
muscle tone
) 7eatures of cerebellar diseases:
i0-Dysmetria and ata*ia
ii0-ast "ointing and dysdiadocho(inesia
iii0-Dysarthia
iv0-$ntention tumor
-Write the e+ects of sym"athetic stimulation
on thoracic and abdominal viscera
O3A5 E77EC4
=EA34 MH;C6E;
coronaries $ncreased 3ate$ncreased 7orce of
contraction
Dilatedbeta
&0!Constrictedal"ha0
6H5;
Bronchi
Blood vessels
Dilated
Mildly Constricted
H4 6HME5 Decreased "eristalsis
and tone
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;"hincters $ncreased 4one
6iver
gallbladders I bile duct
lucose released
3ela*ed
(idney Decreasd urine out"ut
and increased renin
secretion
Bladder
detrusor muscle
trigone
3ela*ed
Contracted
-E*"lain the 9e*or or #tihdra#al re9e* #ith the hel"
of a diagram
5euronal Mechanism of the 9e*or re9e*:
4he "ath#ay for eliciting the 9e*or re9e* "asses rst
into the s"inal cord interneuoron "ool of neurons and
only secondarily to the motor neurons.4he shortest
"ossible curcuit is a ' or ) neuron "ath#ay!ho#evermost of the signals of the re9e* transverse many
more neurons and invovle the follo#ing basic ty"es of
curcuits
i0-Diverging curcuits to s"read the re9e* to the
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necessary muscles for the #ithdra#al
ii0-Curcuits to inhibit the antagonist muscles
iii0-Curcuits to cause afterdischarge lasting many
fractions of a second after the stimulus is over
Within a fe# milliseconds!after a "ain nerve ber
begins to be stimulated !the 9e*or res"onse
a""ears.4hen in the ne*t fe# the 9e*or res"onse
begins to fatigue.7inallyy after the stimulus is
over!there is a "eriod of after-discharge
-What is the motor and sensory loss at and belo#
the level of hemisection of the s"inal cord.
Ans:E+ects at the level of lesion:
On the ;ame side:;ensory 6oss:
Com"lete anaesthesia to all forms of senses!because
"ost nerve root!"ost horn cells and lat and ventral
s"inothalamic tracts crossing to the o""osite side are
all lost
Motor disturbances:
aralysis of lo#er motor neuron ty"e due to
Damage to ant horn
On the o""osite side:
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;ensory 6oss:
5il or very slight
Motor 6oss:
5il or slight due to damage to small direct"yramidal bers of same side
E77EC4 BE6OW 4=E 6E2E6 O7 6E;$O5:
On the same side:
;ensory Disturbances:
G7ine touch and "ro"rioce"tion are lost due todamage to fasciculi gracilis and cuneatous #hich do
not cross
Gain!tem"erature and crude touch are not lost
because lateral and ventral s"inothalamic tracts cross
to o""osite sides belo# the level of lesion
Motor Disturbances :
aralysis of u""er motor neuron lesion ty"e
O5 OO;$4E ;$DE:
;ensory disturbances:
;ome loss of "ain sensations.
Motor disturbances:
5il or very slight.
-What are the functions of s"inocerebellum
Enemurate features of cerebellar diseases
Ans:7unctions:
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i0-lanning and ne tunning of s(eletal muscle
contraction
ii0-Maintainance of "osture and "erformance of
voluntary muscles
7eatures of cerebellar diseases:
i0-Dysmetria and ata*ia
ii0-ast "ointing and dysdiadocho(inesia
iii0-Dysarthia
iv0-$ntention tumor ;H6< &??1
-What is the nerve su""ly of the muscle s"indle=o#
is it stimulatedEnemurate its functions
5erve ;u""ly of Muscle ;"indle:
Motor $nnervation:G4he end "ortions of the intrafusal bers are
innervated by gamma bers
GE*trafusal bers are innervated by al"ha bers
;E5;O3< $55E32A4$O5:
4#o ty"es of sensory endings are found in the
Central rece"tor area of the muscle s"indle.4hese are:rimary ending:
$n the center of rece"tor area!a large sensory nerve
ber encircles the central "ortion of each intrafusal
bers!forming the so called "rimary ending or
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annulos"iral ending.4his nerve ber is ty"e $a ber.
;econdary Ending:
Hsually one but sometimes & small nerve endings of
ty"e $$ innervate the rece"tor region forming thesecndary ending
;4$MH6A4$O5:
i0-6engthening of the #hole muscle
ii0-Contraction of the end "ortions of the s"indles of
intra-fusal bers
7unctions:
i0-Muscle s"indle constituets a feedbac( device that
o"erates to maintain muscle length
ii0-;im"lest menifestation of muscle s"indle function is
stretch re9e*
iii0-Dynamic and static res"ons of muscle s"indle"erforms dam"ning function
iv0-;tabaili>es body "osition during tense motor
activity
v0-Maintains muscle tone
-5ame motor areas in the cerebral corte*.Eumerate
features of the lo#er motor neuron lesion
Ans:Motor areas of cerebral corte*:
i0-rimary motor corte*
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ii0-remotor corte*
iii0-;u""lementory motor corte*
7eatures of 6o#er motor neuron lesion:
i0-7lacid aralysisii0-Are9e*ia
iii0-Abdominal and cremasteric re9e*es are lost
iv0-lantar re9e* is normal
v0-Mar(ed #asting of muscles
vi0-3eaction of degeneration is "resent
vii0-7asciculationsviii0-;mall area of body is a+ected
-What are the functions of thalamusWhat are the
features of thalamic syndrome
Ans:7unctions:i0-4halamus is a great relay center
ii0-Center for crude sensations e.g crude touch and
"ressure
iii0-$m"ortant re9e* center for emotional reactions eg
rage is mediated through thalamus
iv0-$t (ee"s corte* alert through its connections #ith
ascending reticular formation!thereby causing generala#a(ening.
4halamic ;yndrome:
$t is a collection of sym"toms resulting from damage
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of 62 nucleus of thalamus due to occlusion of
thalamo-geniculate artery.
GE+ects occur on o""osite side of body
G6oss of ne sensationsG6oss of crude sensations
GE*aggeration of "ain sensations
G=y"tonia
GChorea and athetosis
A55HA6 &??J
-5ame the motor areas in the cerebral corte*.Whatare the functions of Broca!s areaWhat is the e+ect of
lesion in this area
Ans: Motor Areas:
i0-rimary motor corte*
ii0-;u""lementory motor corte*iii0-remotor corte*
7unctions of Broca!s Area:
Grovides neural curcuitary for #ord formation
Glans motor "atterns for e*"ressing individual
Words or even short "hrases are initiated and
e*ecutedGWor(s in association #ith Wernic(e!s area
GCauses the movement of muscles of s"eech in
tongue!li"s and laryn*.
E+ect of lesion:
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$t causes motor a"hasia.4he "erson is ca"able of
deciding #hat he #ants to say but cannot ma(e the
vocal system emit #ords
-Which neurotransmitters are released by the
sym"athetic "ostganglionic bersEnumerate /
e+ects of sym"athetic stimulation in the body
Ans:4hey secrete e"ine"hrine and nor-e"ine"hrine.
O3A5 E77EC4
=eart
Muscle
Coronaries
$ncreased 3ate
$ncreased 7orce of
contraction
Dilatedbeta
&0!Constrictedal"ha06ungs
Bronchi
Blood 2esselsDilated
Mildly Constricted
ut
6umen;"hincter Decreased "eristalsisand tone
$ncreased 4one
6iver
allbladder and bile
lucose released
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ducts 3ela*ed
Fidney Decreasd urine out"ut
and increased renin
secretion
Bladder
Detrusor
4rigone
3ela*ed
Contracted
enis Eaculation
7at cells li"olysis
-What is the motor and sensory loss at and belo#
the level of hemisection of the s"inal cord.
Ans:E+ects at the level of lesion:
On the ;ame side:
;ensory 6oss:
Com"lete anaesthesia to all forms of senses!because
"ost nerve root!"ost horn cells and lat and ventral
s"inothalamic tracts crossing to the o""osite side are
all lost
Motor disturbances:
aralysis of lo#er motor neuron ty"e due to
Damage to ant horn
On the o""osite side:
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;ensory 6oss:
5il or very slight
Motor 6oss:
5il or slight due to damage to small direct"yramidal bers of same side
E77EC4 BE6OW 4=E 6E2E6 O7 6E;$O5:
On the same side:
;ensory Disturbances:G7ine touch and "ro"rioce"tion are lost due to
damage to fasciculi gracilis and cuneatous #hich do
not cross
Gain!tem"erature and crude touch are not lost
because lateral and ventral s"inothalamic tracts cross
to o""osite sides belo# the level of lesion
Motor Disturbances :
aralysis of u""er motor neuron lesion ty"e
O5 OO;$4E ;$DE:
;ensory disturbances:
;ome loss of "ain sensations.
Motor disturbances:
5il or very slight.
A55HA6 &??/
-E*"lain the functions of
cerebrocerebellum.Enemurate / features of the
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cerebellar disease
Ans:7unctions of Cerebrocerebellum:
a0-7acilitates smooth and co-ordinated movements
b0-Ensures that force!direction and e*tent ofmovements are accurate.
/ 7eatures:
i0-Dysmetria and ata*ia
ii0-ast ointing
iii0-Dysdiadocho(inesiaiv0-Dysarthia
v0-$ntention tumor
vi0-Cerebellar 5ystagmus
vii0-=y"otonia
viii0-Asthenia
-Enumerate %& e+ects of sym"athetic stimulation inthe body.Which neurotransmitter are released from
"reganglionic and "ostganglionic sym"athetic nerve
bers
Ans:re ganglionic bers release acetylcholine
ost ganglionic bers releas E"ine"hrine and 5or-E"ine"hrine
O3A5 E77EC4
=eart
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Muscle
Coronaries
$ncreased 3ate
$ncreased 7orce of
contraction
Dilatedbeta&0!Constrictedal"ha0
6ungs
Bronchi
Blood 2esselsDilated
Mildly Constricted
ut6umen
;"hincter
Decreased "eristalsis
and tone
$ncreased 4one
6iver
allbladder and bile
ducts
lucose released
3ela*ed
Fidney Decreasd urine out"ut
and increased renin
secretion
Bladder
Detrusor
4rigone
3ela*ed
Contracted
enis Eaculation
7at cells li"olysis
Basal metabolism $ncreased u"to %??K
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Adrenal medullary
;ecretion
incresed
Mental activity incresed
iloerector muscles contraction
-A middle aged man #as hit by a motor car resulting
into fracture dislocation of vertebrae.6ater he
develo"ed e+ects indicating right sided hemisectionof the s"inal cord.Enumerate the features belo# and
at the level of hemisection.
Ans:E+ects at the level of lesion:
On the ;ame side:
;ensory 6oss:
Com"lete anaesthesia to all forms of senses!because"ost nerve root!"ost horn cells and lat and ventral
s"inothalamic tracts crossing
to the o""osite side are all lost
Motor disturbances:
aralysis of lo#er motor neuron ty"e due to
Damage to ant hornOn the o""osite side:
;ensory 6oss:
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5il or very slight
Motor 6oss:
5il or slight due to damage to small direct
"yramidal bers of same side
E77EC4 BE6OW 4=E 6E2E6 O7 6E;$O5:
On the same side:
;ensory Disturbances:
G7ine touch and "ro"rioce"tion are lost due to
damage to fasciculi gracilis and cuneatous #hich donot cross
Gain!tem"erature and crude touch are not lost
because lateral and ventral s"inothalamic tracts cross
to o""osite sides belo# the level of lesion
Motor Disturbances :
aralysis of u""er motor neuron lesion ty"eO5 OO;$4E ;$DE:
;ensory disturbances:
;ome loss of "ain sensations.
Motor disturbances:
5il or very slight.
-Mr.L of / years age #ith reting tremors of hand and
li"s consulted his family doctor.On e*amination he
#as found to have rigidity of limbs and e*"ressionless
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face.=e #as having short-ste""ed gait.
A0-7rom #hich disease Mr.L #as su+ering
B0-What is the cause and mechanism of this disease
c0-Which drugs can be used to treat this disease
a0-ar(insons!s disease
b0-Cause:
GDo"amine secreted in the caudate nucleus and
"utamen is an inhibitory transmitter!therefore the
destruction of do"aminergic neurons in the substantia
nigra of the "ar(insonian "atient #ould allo# thecaudate nucleus and "utamen to be overly e*cited
leading to rigidity
G;ome of the feedbac( curcuits might easily oscillate
leading to tremor.$t is involuntary tremor
GDo"amine secretion in the limbic system!
Es"ecially in the nucleus accumbens is oftendecreased along #ith its decrease in the basal
ganglia.it might be the cause of a(inesia.
-What is the ;"eech area in the Cerebral Corte*
What do you understand by Dysle*ia
Ans:Broca!s area is the s"eech area in the cerebral
corte*.4hese are areas )) and ).Dysle*ia:
$t is characterised by diculty in learning to read
9uently and #ith accurate com"rehension des"ite
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normal intelligence.
$t is a learning disability.$t includes reading
"roblems!s"elling "roblems!s"eech "roblems and
dysgra"hia that ma(es a "erson dicult to masterhand#riting.
-Enumerate e+ects of "arasym"athetic stimulation
in the body.5ame the neurotransmitter in this nervous
system
Ans:GChollinergic bers release acetylcholineGAdrenergic bers release nor-e"ine"hrine
O3A5 E77EC4
6ungs
BrochiBlood vessels
Constricted
Dilated
ut
6umen
;"hincter
$ncreased eristalsis
and tone
3ela*ed
6iverallbladder and bile ducts ;light glycogensynthesis
Contracted
Bladder
Detrusor
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4rigone Contracted
3ela*ed
Eye
u"il
Ciliary Muscle
Contracted
Contracted
enis erection
lands
5asal!lacrimal!"arotid!
submandibular!gastric!"an
creatic
;timulation of co"ious
secretion
Annual &??N
-Enlist / functions of the body controlled by
brainstem
Ans:7unctions
4he brain stem is its o#n master because it "rovides
many s"ecial control functions!such as:
i0-Control of res"iration
ii0-Control of cardiovascular system
iii0-artial control of gastrointestinal function
iv0-Control of many stereoty"ed movements of the
body
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v0-Control of e8uilibrium
vi0-Control of eye-movements
vii0-;erves as a #ay station for command signalsP
from higher centersviii0-rovide su""ort to the body against gravity
-A 1? year old man develo"s tremor in his hands and
ngers #hich become "ronounced as he reaches for a
glass of #ater or "oints to#ards an obect!=e has
diculty maintaining his balance
A0-Which com"onent of the nervous system isinvolved
B0-=o# are these tremors di+erent fro other tremors
due to lesion of nervous system
C0-Why this "erson has diculty in maintaining
balance
Ans:a0-Cerebellum
b0-4hese tremors di+er from other tumor because
these occur #hen a "erson tries to do so voluntary
action.4hats #hy these are callled voluntary or
intentional tumors.$n case of basal ganglia lesion
these are involuntary tremors.c0-ost ;"inocerebellar bers receive muscle oint info
from the muscle s"indles!tendon organs and oint
rece"tors of the trun( and lo#er limbs.4his info
concerning tension of muscle tendons and the
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movements of muscles and oints is used by the
cerebellum in the
Maintainance of "osture.4he ant s"inocerebellar tract
"rovides the same info from the u""er and lo#er
limbs.Cuneocerebellar tracts "rovide info of muscle
oint.$n cerebellar lesion the cerebellum cannot
com"rehend these info and resultss in loss of balance
A55HA6 &?%?
-A bo*er at the age of ) years #as diagnosed to be
su+ering from ar(inson!s disease.
A0-What are the characteristics of this disease
b0-;uggest "ossible treatments
Ans:Cause:
GDo"amine secreted in the caudate nucleus and
"utamen is an inhibitory transmitter!therefore thedestruction of do"aminergic neurons in the substantia
nigra of the "ar(insonian "atient #ould allo# the
caudate nucleus and "utamen to be overly e*cited
leading to rigidity
G;ome of the feedbac( curcuits might easily oscillate
leading to tremor.$t is involuntary tremor
GDo"amine secretion in the limbic system! Es"eciallyin the nucleus accumbens is often decreased along
#ith its decrease in the basal ganglia.it might be the
cause of a(inesia.
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B0-4reatment:
i0-6-Do"a
ii0-6-De"renyl
iii0-trans"lanted fetal do"amine cells
iv0-By Destroying "art of the feedbac( circuitry
-a0-What are the various ty"es of "ain
B0-E*"lain the mechanism of referred "ain #ith the
hel" of diagram
Ans:4y"es of "ain:
7A;4 A$5:
G2ery ;hort acting
GMostly caused by thermal and mechanical stimuli
GCarried by A delta bers via neos"inathalamic
"ath#ay
G6ocali>ation of "ain is good
G2elocityQ1-'? @sec
G5eurotransmitter is glutamate.
;lo# ain:
G6ong acting
GMostly caused by chemical stimuli
GCarried by C bers via "aleos"inothamlamic "ath#ay
G6ocali>ation of "ain is "oorG2elocityQ?. R & m@sec
G5eurotransmitter is substance
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Ans b0:Mechanism of re+ered "ain:
Branches of visceral "ain bers syna"se syna"se in
s"inal cord on the same second order neurons% and
&0 that reeceive "ain signals from s(in.When thevisceral "ain bers are stimulated!"ain signals from
the viscera are conducted through at least some of
the same neuron that conduct "ain signals from the
s(in and "erson has feeling that the sensation
originate in the s(in itself
-ive the structure and functions of muscle s"indleAns:;tructure:
Muscle s"indle is built around ' R %& tiny intrafusal
bers that are "ointed at their ends and attached to
the glycocaly* of the surrounding large e*trafusal
s(eletal muscle bers.
Each intrafusal ber is a tiny s(eletal muscleber.=o#ever!the central region of each of these
bers that is!the area mid#ay bet#een the & ends has
fe# or no actin and myosin
4herefore!this central "ortion does not contract #hen
the ends do.$nstead !it functuins as a sensory
rece"tor.4he end "ortions that do contract are e*citedby gamma motor nerve bers that originate from
small ty"e A gamma motor neurons in the ant horns
of the s"inal cord.E*trafusaled by bers are
innervated by al"ha brers
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7unctions:
i0-Muscle s"indle constituets a feedbac( device that
o"erates to maintain muscle length
ii0-;im"lest menifestation of muscle s"indle function isstretch re9e*
iii0-Dynamic and static res"ons of muscle s"indle
"erforms dam"ning function
iv0-;tabaili>es body "osition during tense motor
activity
v0-Maintains muscle tone Annual &?%&
- We e*"erience di+erent modalities of sensations
e.g "ain!touch etc0 although the nerve bers
transmitonly im"ulses.=o# is it that di+erent nerve
bers transmit di+erent modalities of sensationive
an e*am"le to e*"lain
Ans:Each of the "rinci"le ty"e of sensation that #e
can e*"erience-"ain!touch!sight!sound and so forth-is
called a modality of sensation.
Each nerve tract terminates at a s"ecic "oint in
4he central nervous system! and the ty"e of sensationfelt #hen a nerve ber is stimulated is deteremined
by the "oint in the nervous system to #hich the ber
leads.7or e*am"le!if a "ain ber is stimulated !the
"erson "erceives "ain regardless of #hat ty"e of
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stimulus e*cites the ber.4he stimulus can be
electricity!overheating of the ber!crushing of the
ber!or stimulus of the "ain nerve ending by damage
to the tissue cells.$n all these instances the "erson"erceives "ain.6i(e#ise!if a touch ber is stimulated
by electrical e*citation of a touch rece"tor or in
Other #ay!the "erson "erceives touch because touch
bers lead to s"ecic touch areas in the brain!bers
from the ear terminate in the auditory areas of the
brain!and the tem"erature bers terminate in thetem"erature areas.
4he s"ecity of nerve bers for transmitting only one
modality of sesation is called labeled line "rinci"le.
-A 1J yearsold man visits his neurologist and
com"lains that it is e*tremely dicult for him to stand
u" sitting "osition or start #al(ing from standing"osition.=e also com"lains of tremulous movements
of the ngers#huch disa""ear #hen he starts doing
something.
a0-#hat is the condtion called
B0What is the lesion@damage located
C0-What is the s"eculated cause of diculty this mane*"eriences in intitiating a movement
Ans: a0-ar(inson!s disease
b0-Basal ganglia
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4he a(inesia that occurs in ar(inson!s disease is
often much more distressing to the "atient than are
the sym"toms of muscle rigidity and tremor!because
to "erform even the sim"lest movement in severe"ar(insonism!the "erson must e*ert the highest
degree of conc.4he cause of a(inesia is still
s"eculative.=o#ever!do"amine secreted in the limbic
system!es"ecially in the nucleus accumbens!is often
decreased along #ith its decrease in the basal
ganglia.$t has been suggested this might reduce the"sychic drive
7or motor activity so greatly that a(inesia results
-A man of ) years received a gun short on hisbac(.=e develo"ed right sided hemisection of the
s"inal cord.
A0-ive the features belo#!above and at the level of
lesion
B0-What is Bro#n-;e8uard ;yndrome
Ans:E+ects at the level of lesion:
On the ;ame side:;ensory 6oss:
Com"lete anaesthesia to all forms of senses!because
"ost nerve root!"ost horn cells
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and lat and ventral s"inothalamic tracts crossing
to the o""osite side are all lost
Motor disturbances:
aralysis of lo#er motor neuron ty"e due toDamage to ant horn
On the o""osite side:
;ensory 6oss:
5il or very slight
Motor 6oss: 5il or slight due to damage to small direct
"yramidal bers of same side
E77EC4 BE6OW 4=E 6E2E6 O7 6E;$O5:
On the same side:
;ensory 6oss:
On the same side:;ensory Disturbances:
G7ine touch and "ro"rioce"tion are lost due to
damage to fasciculi gracilis and cuneatous #hich do
not cross
Gain!tem"erature and crude touch are not lost
because lateral and ventral s"inothalamic tracts cross
to o""osite sides belo# the level of lesion
Motor Disturbances :
aralysis of u""er motor neuron lesion ty"e
O5 OO;$4E ;$DE:
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;ensory disturbances:
;ome loss of "ain sensations.
Motor disturbances:
5il or very slight.
E77EC4 ABO2E 6E2E6 O7 6E;$O5:
On ;ame ;ide:
4here is a narro# >one of hy"eraesthesia or
hy"ersensitive to touch!"ain and thermal stimuli due
to irritation of u""er cut ends of damaged bers.
O""osite side:
=y"eraesthesia may be referred.
B0-$n Bro#n se8uard syndrome there is com"lete
hemisection of s"inal cord.$ts features are
G$"silateral lo#er motor neuron "aralysis in the
segment of lesion and muscular atro"hy
G$"silateral s"astic "aralysis belo# the level of lesionG$"isilateral band of cutaneous anasthesia in the
segment of lesion.
G$"silateral loss of tactile discrimination! and of
2ibratory and "ro"rioce"tive sensations belo# the
level of lesion.
GContralateral loss of "ain and tem" sensations belo#the level of lesion
GContralateral but not com"lete loss of tactile
sensation belo# the level of the lesion
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-What are the functions of s"inocerebellum
Enemurate features of cerebellar diseases
Ans:7unctions:i0-lanning and ne tunning of s(eletal muscle
contraction
ii0-Maintainance of "osture and "erformance of
voluntary muscles
7eatures of cerebellar diseases:i0-Dysmetria and ata*ia
ii0-ast "ointing and dysdiadocho(inesia
iii0-Dysarthia
iv0-$ntention tumor
PREPARED Y
AHSA> SARAR
L"ho#e 6e/%"l ". e.$"l %olle'e
G"s$#o/.$es$/."l Phys/olo'y
uestion 5o: % What do you (no# about "haryngealstage of s#allo#ing along #ith its nervous control
;u""lementary &??)0
Ans#er: Cha"ter 1' uyton0
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;WA66OW$5
&nd;tage haryngeal ;tage0
%-Bolus stimulates the e"ithelial s#allo#ing rece"torareas around o"ening of "haryn*.
&-;oft "alate is "ulled u"#ards.'-4he "alato"haryngeal folds and vocal cords are
a""ro*imated.)-E"iglottis s#ings bac(#ard over the o"ening of
laryn*.
-H"#ard movement of laryn* and o"ening of theu""er oeso"hageal s"hinchter.
1-Contraction of "haryngeal muscles and "ro"ulsion
of food by "eristalsis into oeso"hagus.
5ervous Control:
;ensory: ;ensory "ortions of trigeminal andglossoharyngeal nerves into the medulla! either into
or closely associated #ith the tractus solitaries.
Areas in the medulla and lo#er "ons are called
s#allo#ing centre.
Motor: th
!Nth
!%?th
and %&th
cranial nerves and a fe#cervical nerves.
uestion 5o: & Write a short note on :
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A0 haryngeal stage of s#allo#ingB0 Actions of cholecysto(inin Annual &??0
Ans#er:
A0 Ans#er 5o % above.B0 %- stimulates "ancreatic en>yme secretion.
&- stimulates "ancreatic bicarbonate secretion.'- causes gallbladder contraction.)- gro#th of e*ocrine "ancreas.
-inhibits gastric em"tying.
1-$nhibits a""etite.
uestion 5o: ' What events occur during the
"haryngeal stage of s#allo#ing 5ame the nerves
that control this stage Annual &??0Ans#er: Ans#er 5o % above.
uestion 5o:) =o# is gastric em"tying regulatedannual &??10Ans#er: Cha"ter no 1'guyton0astric factors that "romote em"tying:%-E+ect of gastric food volume on rate of
em"tying&-E+ect of the hormone gastrin on stomach
em"tyingDuodenal factors that inhibit stomach em"tying:
%-$nhibitory e+ect of enterogastric nervous
re9e*es from duodenum:
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&- 7actors initiating enterogastric re9e*es: Degree of distention of duodenum
resence of any irritation
Acidity and osmolality of the chyme resence of certain brea(do#n "roducts in
chyme'-=ormonal feedbac( from duodenum:
CCF
;ecretin
$ chec( the boo( for their detailed
functions0
uestion 5o: What are the movements of smallintestine su""lementary &??10
Ans#er: Cha"ter 1'guyton0
Movements:
4#o ty"es:
%-Mi*ing contractionssegmentation contractions0: Contractions cause segmentation of small
intestine Cho" the chyme &-' times "er minute
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7re8uency is determined by the electrical slo#
#aves normally it is %&@minute in duodenum
and eunum and in ileum /-N@minute.
Contractions can be bloc(ed by atro"ine&-ro"ulsive movements:
eristalsis in small intestine: velocity is ?.-
&cm@sec Control of "eristalsis by nervous and hormonal
signals%-;tretch of duodenal #all&-astroenteric re9e*'-astrin! cc(! insulin! motilin and serotonin
enhance motility.)-;ecretin and glucagon inhibit motility
uestion 5o: 1 6ist the motor functions of stomach
Wha are hunger contractions annual &??10
Ans#er: Cha"ter 1'guyton0
Motor 7unctions:
%-;torage function of somach: 2agovagal re9e* reduces the tone in the
muscular #all of body of stomach.
;tomach can store ?./ R %. litres of food.&-Mi*ing and "ro"ulsion of food- Basic electrical
rhythm of stomach #all: astric uices secreted by gastric glands
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Mi*ing #aves begin in the mid t#o u""er
"ortions of stomach and move to#ards the
antrum
4hese #aves are initiated by basic electricalrhythm
o#erful constrictor rings force the antral
contents to#ards "ylorus 3etro"ulsion
'-astric em"tying:Ans#er no ) above
=unger Contractions:G Contractions that occur #hen the stomach has
been em"ty for several hours.G Duration &-' minutes.G $ntense in young "eo"le and those having lo#
blood sugar levels.G ;ometimes causes mild "ain called hunger
"angsG Donot begin until %&-&) hours after last
ingestion.
uestion 5o: J What ty"e of movements occur
in small intestine #hen it becomes distended#ith chyme annual &??J0Ans#er: Ans#er no above.
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uestion 5o: / 5ame the stages of deglutition
Which changes #ill occur during second stage
su""lementary &??J0
Ans#er: ;tages:%-2oluntary stage of s#allo#ing&-haryngeal stage of s#allo#ing'-Oeso"hageal stage of s#allo#ing
uestion 5o: N #hat is enteric nervoussystem#hich defect in enteric nervous system leads
to oes"hageal achlasiaAns#er: cha"ter 1&guyton0Com"osed mainly of t#o "le*us:%-Myenteric or auerbachPs "le*us:
Controls .$.4 movements resent bet#een the inner circular and outer
longitudinal muscle layers&-;ubmucosal or meissnerPs "le*us:
Controls .$.4 secretions and local blood 9o#.
resent in the submucosa
Achlasia: Oes"hageal s"hinchter fails to rela* during
s#allo#ing Damage in neural net#or( of myenteric
"le*us in lo#er t#o thirds of oeso"hagus
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Myenteric "le*us loses its ability to cause
rece"tive rela*ation of oeso"hageal
s"hinchter.
uestion 5o: %? list the functions of stomach
ive factors #hich increase the rate of
em"tying of stomach annual &??/0
Ans#er: Ans#er no 1 above for functions.Ans#er no ) above for factors.
astric factors "romote stomach em"tying.
uestion no: %% Com"are the e+ects of
sym"athetic and "arasym"athetic stimulation
on .$.4 su""lementary &??/0Ans#er: cha"ter 1&guyton0Autonomic control:
arasym"athetic:
$ncreases .$.4 activity
Cranial "ortion by vagus nerve and sacral
"ortion by &nd!'rd!and )th"elvic s"lanchnic
nerves. ostganglionic neurons are located in
myenteric and submucosal "le*us. Enhances the activity of .$.4 functions.
E*tensive near to oral cavity and anus.
;ym"athetic:
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$nhibits .$.4 activity.
7ibres originate in s"inal cord bet#een
segments t-l&. ;ome bres enter
sym"athetic chains and then "ass to celiacganglion ormyenteric ganglion. Most of the "ost
ganglionic neurons are in these ganglion. $nnervates all the .$.4
;ecrete e"ine"hrine and nor e"ine"hrine
uestion no %&: give ve di+erences bet#een
obstructive and hemolytic aundiceAns#ers:Cha"ter no J?guyton0
%-=emolytic aundice is caused by hemolysis
of 3BCs #hereas obstructive aundice is
caused by obstruction of bile duct or liver
diseases.&-$n hemolytic aundice unconugated bilirubin
is increased #hereas in obstructive
conugated bilirubin is increased.'-H3obilinogen is increased in hemolytic
aundice and decreased in obstructiveaundice.
)-Hrine color is normal in hemolytic but it is
dar( in obstructive aundice due to
conugated bilirubin.
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-;tool color $s normal in hemolytic aundice
but "ale in obstructive aundice.1-;"lenomegaly is "resent in hemolytic
aundice but absent in obstructive aundice.
uestion no:%'
A0 Enumerate the factors that regulate
gastric em"tyingB0 Enumerate the factors that can e*cite
enterogastric re9e*es from duodenum
Ans#er: A0 ans#er no ) above for gastric em"tying
B07actors initiating enterogastric re9e*es:
Degree of distention of duodenum
resence of any irritation
Acidity and osmolality of the chyme
resence of certain brea(do#n "roducts inchyme
uestion no %): A "erson is diagnosed to have a
gastric ulcer on endosco"y.
a0 What is "atho"hysiology of this diseaseb0 =o# the intestine normally handles the
e*cessive acidity in chyme
Ans#er: A0 cha"ter 11guyton0
Caused by:
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Digestive action of gastric uice or uu"er small
intestine secretions $mbalance bet#een rate of secretion of gastric
uice and degree of "rotection a+orded bymucosal barrier and neutrali>ation of gastric
acid by duodenal uices. E*cessive secretion of acid and "e"sin
Bacterial infection by helicobacter "ylori
;mo(ing
Alcohol As"irin
B0al(alinity of the small intestine secretion
6arge 8uantity of sodium bicarbonate in "ancreatic
secretion neutrali>ing =C6! inactivating "e"sin and
"reventing digestion of mucosa
6arge amounts of bicarbonate ions by the secretion of
brunners glands and in bile
Acidic chyme entering duodenum inhibits gastric
secretion and "eristalsis in stomach
resence of acid in small intestine stimulates secretinsecretion #hich in turn stimulates bicarbonate
secretion.
PREPARED Y
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SALEHA RASHID JAI>U ARI
=H %olle'e o 6e/%/.e e.$/s$#y
E>DOCRI>OLOGY
+,Ho! oes %y%l/% A6p 6e/"$e ho#6o."l
"%$/o. "$ %ellul"# le5el3 !h/%h ho#6o.es oey$he %y%l/%-A6p 6e%h"./s6 3 (A>>UAL P"pe#
2004)
Ans:Adenylyl CyclaseRcAM ;econdMessenger ;ystem
Binding of the hormones #ith the rece"torallo#s cou"ling of the rece"tor to a G protein -----> "rotein stimulates the adenylyl cyclaseRcAMsystem! a membrane-bound en>yme----, s "roteinthen cataly>esthe conversion of a small amount of cyto"lasmicadenosine triphosphate A40 into cAM inside the
cell.-----, 4his then activates cAMP-dependent proteinkinase, #hich "hos"horylates s"ecic "roteins in thecell! triggering biochemical reactions that ultimatelylead to the cellPs res"onse to the hormone.
;ome =ormones 4hat Hse the Adenylyl CyclaseRcAM
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;econd Messenger ;ystem
Adrenocorticotro"ic hormone AC4=0Angiotensin $$ e"ithelial cells0
CalcitoninCatecholamines b rece"tors0Corticotro"in-releasing hormone C3=07ollicle-stimulating hormone 7;=0lucagon=uman chorionic gonadotro"in =C06uteini>ing hormone 6=0
arathyroid hormone 4=0;ecretin;omatostatin4hyroid-stimulating hormone 4;=02aso"ressin 2& rece"tor! e"ithelial cells0
+, D/Fe#e.$/"$e e$!ee. $he e$/olo'y ".
e"$u#es o D!"#eddeciency of anterior "ituitary secretion
"anhy"o"ituitarism0during childhood.
Q,all the "hysical "arts of the body develo" ina""ro"riate "ro"ortionto one another
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Q,d#arf does not "ass through "uberty
Q, mental level is normal
Q,African "ygmy and the 6Svi-6oraind#arf are its ty"es
CretinismQ,Cretinism is caused by e*treme hy"othyroidismduringfetal life! infancy or childhood
=>dis"ro"ortionate rate of gro#th!
Q,obese! stoc(y! and short a""earance.tongue becomes so that it obstructs s#allo#ing.
Q, mental retardation
Q,congenital cretinismand endemic cretinism are itstpes
+,Epl"/. 5"#/ous s$eps /.5ol5e /. $he
/osy.$hes/s o Thy#o/ ho#6o.es3(A>>UAL
P"pe# 2007 supple6e.$"#y 200:)
Ans:
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Q,7ormation and ;ecretion of 4hyroglobulin by the
4hyroid Cells
Q,O*idation of the $on
4he o*idation of iodine is "romoted by the en>ymepero!idaseand its accom"anying hdrogen pero!ide! #hich"rovide a "otent system ca"able of o*idi>ing iodides.
Q,$odination of 4yrosine and 7ormation of the 4hyroid=ormonesTUOrganicationV of 4hyroglobulin
o*idi>ed iodine is associated #ith an iodinase en>yme
iodine binds #ith about one si*th of the tyrosine
amino acids #ithin the thyroglobulin
molecule.4yrosine is rst iodi>ed to monoiodotrosine
and then to diiodotrosine#hic cou"led to form the
thyro*ine and triidotyrosin.
Q,;torage of 4hyroglobulin
+,h"$ "#e /Fe#e.$ se%o. 6esse.'e#s
6e%h"./s6s o ho#6o."l "%$/o.s3(A>>UALP"pe# 2007)
Ans:Adenylyl CyclaseRcAM ;econdMessenger ;ystem
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4he Cell Membrane hos"holi"id ;econdMessenger ;ystem
Calcium-Calmodulin ;econd
Messenger ;yste
M second messenger system
"rostaglandins
+,>"6e $he ho#6o.es se%#e$e #o6 $he
$hy#o/ 'l".? Epl"/. 6e%h"./s6 o "%$/o. o
s$e#o/ ho#6o.es3 (A>>UAL P"pe# 200:)
Ans: thro!ine andtriiodothronine! commonly called 4) and 4'!res"ectively.CalcitoninMechanism of action of steroid hormones:Q,steroid hormones! e*erts its e+ectsby rst interacting #ith intracellular rece"tors intargetcells. . Q,4hey can easily di+use through the cellmembrane. Once inside the cell!they binds #ith "rotein rece"tor in the cyto"lasm!and the hormone-rece"tor com"le* then interacts
#iths"ecic regulatory D5A se8uences! calledgl"cocorticoid or minerilocorticoidresponse elements, to induce or re"ress genetranscri"tion.
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Q,Other "roteins in the cell! called transcription#actors, are also necessary for the hormone-rece"torcom"le* to interact a""ro"riately.
+,E.u6e#"$e,
") e"$u#es o Cush/.'Ks sy.#o6e
) e"$u#es o Te$".y (supple6e.$"#y 200:)
Ans 7eatures of cushingXs syndrome:
hy"ersecretion of adrenal corte*.
-emotional disturbance
-Enlarged sella turcica
-moon face
-oteo"orosis
-cardiac hy"ertro"hy
-bu+alo hum"
-obesity
-Amenorrhea
-muscle #ea(ness
-"ur"ura
-s(in ulcers
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7eatures of tetany:
lo# EC7 calcium
-threshold for action "otential is lo#ered
-5ervous system is in more e*cited state
-gait abnormality scissor gait ! s"astic gait0
-movement disorders
-lac( of cordination
-oint loc(ing
+, A you.' 6". #epo#$e $o h/s "6/ly o%$o#
!/$h $he %o6pl"/.$s o p"lp/$"$/o.& loss o
!e/'h$ /. sp/$e o /.%#e"se "ppe$/$e ".
/.$ole#".%e $o he"$? O. e"6/."$/o. he !"s
h"5/.' pulse #"$e 1106/.& h/s eyes !e#e
p#o6/.e.$ ". $he#e !"s s!ell/.' o. $he
".$e#/o# s/e o $he .e%?
") #o6 !h/%h /se"se he !"s suFe#/.' 3
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) h/%h /.5es$/'"$/o.s !/ll you "5/se3
%)h"$ /s $he %"use o $he /se"se3 (A..u"l
p"pe# 200@)
Ans: a0=y"erthyroidism
b04he most accurate diagnostic test isdirect measurement of the concentration of UfreeVthyro*ineand sometimes triiodothyronine0 in the "lasma. othertests include%. 4he basal metabolic rate #hich #ill be high in thiscase.&. 4he concentration of 4;= in the "lasma. 4;= iscom"letely su""ressed by thelarge amounts of circulating thyro*ine andtriiodothyronine so there is almost no "lasma4;=.
'. 4he concentration of 4;$ is measured byradioimmunoassay. 4his is usually high inthyroto*icosis but lo# in thyroid adenoma.
C0=y"erthyroid "ateints have certain substances inthe blood. 4hese substancesare immunoglobulin antibodies that bind #ith thesame membrane rece"tors that bind 4;=. 4hey inducecontinual activation of the cAM system of the cells!#ith resultant develo"ment of hy"erthyroidism. 4heseantibodies are called throid-stim"latingimm"noglo$"lin
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and are designated 4;$.4hroid adenoma also leads to hy"erthyroidism.+, h"$ "#e phys/olo'/%"l "%$/o.s o %o#$/sol o.
p#o$e/.s ". %"#ohy#"$e 6e$"ol/s63E.u6e#"$e s/ e"$u#es o Cush/.'Ks sy.#o6e3
A..u"l p"pe# 200@ & 2008 ("%$/o. o. p#o$e/.s)
supple6e.$"#y 2008 ( "%$/o. o.
%"#ohy#"$es)M
Ans: E+ect on carbohydrate metabolism:
Q,increase gluconeogenesis
-Cortisol increases the en%mes re&"ired to con'ertamino acids into gl"cose in the li'er cells
-Cortisol ca"ses mo$ili%ation o# amino acids #romthe e!trahepatic tiss"es mainl #rom m"scle( as the
res"lt more amino acids are a'iala$le #or
gl"coneogenesis(
=>Decreased lucose Htili>ation by Cells.
E+ect on "rotein metabolism:
Q,3eduction in Cellular rotein.
4his is caused by bothdecreased "rotein synthesis and increased catabolismof "rotein already in the cells
Q,Cortisol $ncreases 6iver and lasma roteins.
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$t is believed that this results from a "ossible e+ect ofcortisol toenhance amino acid trans"ort into liver and to
enhance theliver en>ymes re8uired for "rotein synthesis
Q,$ncreased Blood Amino Acids! Diminished 4rans"ortof AminoAcids into E*trahe"atic Cells! and Enhanced 4rans"ortinto=e"atic Cells
+,h"$ "#e phys/olo'/%"l "%$/o.s o %o#$/sol o.
p#o$e/.s 3Ho! /s %o#$/sol se%#e$/o. #e'ul"$e 3
(A..u"l p"pe# 2008)
Ans 3egulation of cortisol secretion:
g JJ-1
Q,AC4= ;timulates Cortisol ;ecretion.
An im"ortant releasing factor controls AC4= secretion.4his is called corticotropin-releasing #actor C370. $t is secreted into the"rimary ca"illary "le*us of the hy"o"hysial "ortalsystem in the median eminence of the hy"othalamus
and then carried to the anterior "ituitary gland! #hereit induces AC4= secretion.
Q,AC4= Activates Adrenocortical Cells to roduce;teroids by
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$ncreasing Cyclic Adenosine Mono"hos"hate cAM0.4he most im"ortant of all the AC4=-stimulatedste"s for controlling adrenocortical secretion is
activationof the en>ymeprotein kinase A, #hich ca"sesinitial con'ersion o# cholesterol to pregnenolone(4hisinitial conversion is the Urate-limitingV ste" for all theadrenocortical hormones.+,A you.' e6"le %o.sul$e he# "6/ly
phys/%/". ? She %o6pl"/.e o #eNue.$ 6us%le
sp"s6s ". .u6.ess o "#6s ". le's? He#pl"s6" %"l%/u6 !"s :?76'l?
") #o6 !h/%h %o./$/o. !"s she suFe#/.' 3
) !"s he# pl"s6" %"l%/u6 .o#6"l3
%)h"$ !"s $he 6e%h"./s6 o he# #eNue.$
6us%le sp"s6s ". .u6.ess3 (A..u"l p"pe#
2008)
Ans: a0 4etany
b0 no ! her "lasma calcium level #as lo#er. normal
value is N./ to %%. mg@dl.
c0 =er neurons are over e*cited ! threshold for action
"otential is decreased ! even little sodium in9u* leads
to sudden muscle contraction muscle s"asms 0.
+, A oy o 10 ye"#s !"s #ou'h$ y h/s "$he#
$o " 6e/%"l spe%/"l/s$? The oy e%"use o
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#e$"#e '#o!$h "ppe"#e $o e o 4-7 ye"#s?
Du#/.' $"l/.' $he oy ".s!e#e $he Nues$/o.
/.$ell/'e.$ly? H/s oy p"#$s !e#e p#opo#$/o."$e
u$ o s6"lle# s/e,
") o6 !h/%h /so#e# $he oy !"s suFe#/.'3
) !h"$ !"s $he %"use o $h/s /so#e#3
%)!h"$ "#e /Fe#e.$ $ypes o $h/s /so#e#3
( supple6e.$"#y 2008)
Ans a0 D#arsim
b0 insucient gro#th hormone "roduced by the
anterior "itutiary hormone.
c0 African "ygmy ! 6Svi-6orain d#arsm .
+, ")h"$ "#e phys/olo'/%"l "%$/o.s o %o#$/sol
o. %"#ohy#"$es3
) !h"$ /s $he /Fe#e.%e e$!ee. Cush/.'Ks
sy.#o6e ". Cush/.'Ks /se"se3
( supple6e.$"#y 2008)
Ans a0 see above 8uestions
b0 =y"ersecretion by the adrenal corte* causes acom"le*cascade of hormone e+ects called C"shing)s
sndrome
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When CushingPs syndrome is secondaryto e*cess secretion of AC4= by the anterior"ituitary! this is referred to as C"shing)s disease
+,>"6e $he ho#6o.es o ".$e#/o# p/$u$/"#y
'l". 3 h"$ "#e so6"$o6e/".s3 ("..u"l
p"pe# 200;)
Ansro#th hormoneAdrenocorticotro"ic hormone4hyroid-stimulating hormoneonadotro"es 7ollicle-stimulating7;=06uteini>ing hormone 6=0"rolactinb0 ;omatomedians are insulin li(e gro#th factorsthough #hich gro#th hormone ta(es its action and
"erform di+erent functions li(e formation of "roteins.+, A 47 ye"# ol e6"le '/5e $he 6o.$h h/s$o#y
o "$/'ue & hu.'e# ". $h/#s$ "l6os$ "ll $he
$/6e ? $he#e /s /.%#e"se #eNue.%y o
6/%$u#"$/o. "s !ell ". $he %o6pl"/.$s h"5e
s$e"/ly !o#se.e o5e# $he l"s$ $!o 6o.$hs? l"
$es$s #e5e"l,")!h"$ /s $he l"y suFe#/.' #o63
) !h"$ /s $he phys/olo'/%"l #e"so. o /.%#e"se
#eNue.%y o 6/%$u#"$/o.3
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%) !hy /s she hu.'#y "ll $he $/6e 3
)!hy /s she "l!"ys $h/#s$y 3
e) !h"$ "#e /Fe#e.$ $ypes $o $h/s /so#e#3( A..u"l p"pe# 200;)
a. diabetes mellitus ty"e &0
b. increased osmotic e+ect of glucose decreases
tubular reabsor"tion
c. im"aired glucose u"ta(e by cells for energy.d. increased blood osmolarity stimulates the
hy"othalamus osmotic rece"tors
e. ty"e % and ty"e &
+,") !h"$ "#e $he e.o%#/.e u.%$/o.s o
p".%#e"se3) E.l/s$ $he "%$o#s !h/%h /.%#e"se /.sul/.
se%#e$/o.3( A..u"l p"pe# 2010)
Ans: al"ha cells glucagon
beta cells insulin
b. $ncreased blood glucoseY $ncreased blood free fatty acidsY $ncreased blood amino acidsY astrointestinal hormonesgastrin! cholecysto(inin! secretin!
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gastric inhibitory "e"tide0Y lucagon! gro#th hormone!cortisol
Y arasym"athetic stimulationacetylcholineY b-Adrenergic stimulationY $nsulin resistance obesityY ;ulfonylurea drugs glyburide!tolbutamide0
+, G/5e p"$hophys/olo'y ". e"$u#es o 4 ye"#
ol l"y !ho /s /"'.ose "s " %"se o $o/%'o/$e#3( A..u"l p"pe# 2010)
;ym"toms of =y"erthyroidism4he sym"toms of hy"erthyroidism are obvious fromthe"receding discussion of the "hysiology of the thyroid
hormones: %0 a high state of e*citability! &0intoleranceto heat! '0 increased s#eating! )0 mild to e*treme#eight loss sometimes as much as %?? "ounds0! 0varying degrees of diarrhea! 10 muscle #ea(ness! J0nervousness or other "sychic disorders! /0 e*tremefatigue but inability to slee"! and N0 tremor of thehands.
E*o"hthalmos
+,Ho! 24 hou# loo 'lu%ose /s #e'ul"$e /.
.o#6"l pe#so. 3( A..u"l p"pe# 2011)
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ro#th =ormone DecreasesCarbohydrate Htili>ationro#th hormone causes multi"le e+ects that
in9uence carbohydrate metabolism! including %0decreased glucose u"ta(e in tissues such as s(eletalmuscle and fat! &0 increased glucose "roduction bythe liver! and '0 increased insulin secretion.
lucose absor"tionluconeogenesislycogenolysis
insulin lo#ers glucagon increases
+,E.u6e#"$e $he spe%/
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the throid cells. Increased n"m$er o# throid cells "lus a changefrom cuboidal to columnar cells and much
infolding of the thyroid e"ithelium into thefollicles$n summary! 4;= increases all the (no#n secretoryactivities of the thyroid glandular cells.
3EA3ED B
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A. s"ermatocytogenesis
s"ermatogonium a to s"ermatogaonia b to "rimary
s"ermatocyte to secondary s"ermatocyte via meiosis
to s"ermatid
s"ermiogenesis
s"ermatid to s"erm
testosterone! 6h! 7sh! h! estradiol
+? epl"/. $he ph"ses o e.o6e$#/"l %y%le?
("..u"l 200:)
A. "roliferative "hase
increase in thic(ness due to estrogen
secretory "hase
"rogesterone causes secretion
menstrual "hase
estrogen and "rogesterone lo#er. 6h ncrease
+4? '/5e " su66"#y o "%$/o.s o es$#o'e.s?
(supp 200:)
thic(ens vagina
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increase e*ternal genitalia si>e
increase in uerine si>e! glands! vascularity
inhibit 6h and 7sh
secondary se*ual characteristics
+7? e.u6e#"$e u.%$/o.s o $es$os$e#o.e u#/.'
e$"l l/e? !h"$ "#e u.%$/o.s o se#$oll/ %ells?
("..u"l 20@)e*ternal genitalia and male genital organs increase in
si>e
su""reses formation of female genitalia
descent of testes
sertolli cells o+er nutririon! su""ort! s"ermatogenesis!s"ermiogenesis! mullerian inhibitory factor! estradiol!
inhibin
+:? %o6p"#e $he phys/olo'/%"l "%$/o.s o
es$#o'e.s ". p#o'es$e#o.es o. $he "? u$e#us ?#e"s$s? ("..u"l 2008)
estrogen increase uterus si>e! glands and increase
breast si>e and glandular tissue
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"rogesterone causes secretory "hase! decreases
contraction and gro#th of lobules and alveoli of breast
causing its s#elling
+@? "? !he. " "y su%les " 6o$he#s #e"s$&
ho! /s 6/l ee%$e ou$ /.$o "ys 6ou$h? ?
!hy /. 6o#e $h". 70 l"%$"$/.' !o6e.& $he
l"%$"$/.' %y%le /s /.h//$e3 (supp 2008)
baby suc(els ni""les - sensory im"ulses -hy"othalamus - o*ytocin and "rolactin - contraction of
myoe"ithelium - mil( eection n let do#n
inhibited because suc(ling - hy"othalamus -
su""reses 6hrh - su""ress 7sh 6h - ovarian cycle
su""ressed
+8? #/eBy es%#/e $he %h".'es $h"$ o%%u#
u#/.' $he %"p"%/$"$/o. o spe#6"$oo"? ("..u"l
200;)
acrosome reaction
>ona reaction
+;? !h/%h ho#6o."l "%$o#s %"use /.%#e"se
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%o.$#"%$/l/$y o u$e#/.e 6us%le "$ $he e. o
p#e'.".%y3 ("..u"l 2010)
o*ytocin! estrogen! "rostaglandins! cortisol
+10? '/5e ho#6o."l /.Bue.%e o. e6"le #e"s$s
u#/.' "oles%e.%e& p#e'.".%y ". l"%$"$/o.?
("..u"l 2011)
estrogen fr ductal system
"rogesterone fr glandular system
estrogen ! "rogesterone! h! "rolactin! cortisol! insulin
prepared by
Waqar Sharif
CMH Medical College
RENL PHYSIOLOGY
: #hat is ltration "ressure =o# does auto
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regulation of glomerular ltration rate 730 occur
Ans#er: 7iltration ressure: the net driving force#hich "ushes 9uid into tissue s"aces and out of
vascular sites the net result bet#een ca"illaryosmotic "ressure and intravascular hydrostatic"ressure. 7or e*am"le-it occurs in the (idneys forthe ltration "ur"oses and in the ca"illaries #herestarling forces act together to determine thedirection of going of 9uid either into the ca"illary orout of it.Auto regulation of glomerular ltration rate:%. 3ole of 4ubuloglomerular 7eedbac($n Auto regulation of 73: 4he 4ubuloglomerularfeedbac( mechanism has t#o com"onents that acttogether to control 73:%0 An a+erent arteriolar feedbac( mechanism and&0 an e+erent arteriolar feedbac( mechanism.4hese feedbac( mechanisms de"end on s"ecialdelivery to the macula densa in these circumstances
anatomical arrangements of the u*taglomerularcom"le*. 4he u*taglomerular com"le* consists ofmacula densa cells in the initial "ortion of the distaltubule and u*taglomerular cells in the #alls of thea+erent and e+erent arterioles. 4he macula densais a s"eciali>ed grou" of e"ithelial cells in the distaltubules that comes in close contact #ith thea+erent and e+erent arterioles. 4he macula densa
cells contain olgi a""aratus! #hich are intracellularsecretory organelles directed to#ard the arterioles!suggesting that these cells may be secreting asubstance to#ard the arterioles. 4ubuloglomerularfeedbac(Rmediated renal vasoconstriction thatoccurs in res"onse to the increased sodium chloride
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&. Myogenic Auto regulation of 3enal 73: ;tretch
Of the vascular #all allo#s increased movement of
Calcium ions from the e*tracellular 9uid into the
cells! causing them to contract. 4his contraction
"revents over distention of the vessel and at the
same time! by raising vascular resistance! hel"s
"revent e*cessive increases in renal blood 9o# and73 #hen arterial "ressure increases
'. =igh rotein $nta(e and $ncreased Blood
lucose: follo#ing: A high-"rotein meal increases
the release of amino acids into the blood! #hich are
reabsorbed in the "ro*imal tubule. Because amino
acids and sodium are reabsorbed together by the
"ro*imal tubules! increased amino acid
reabsor"tion also stimulates sodium reabsor"tion in
the "ro*imal tubules. 4his decreases sodium
delivery to the macula densa! #hich elicits a
4ubuloglomerular feedbac(Rmediated decrease
$n resistance of the a+erent arterioles. 4he
decreased a+erent arteriolar resistance then raises
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renal blood 9o# and 73. 4his increased 73 allo#s
sodium e*cretion to be maintained at a nearly
normal level #hile increasing the e*cretion of the
#aste "roducts of "rotein metabolism! such as
urea.A similar mechanism may also e*"lain the
mar(ed increases in renal blood 9o# and 73 that
occur #ith large increases in blood glucose levels in
uncontrolled diabetes mellitus. Because glucose!li(e some of the amino acids! is also reabsorbed
along #ith sodium in the "ro*imal tubule! increased
glucose delivery to the tubules causes them to
reabsorb e*cess sodium along #ith glucose. 4his! in
turn! decreases delivery of sodium chloride to the
macula densa! activating a 4ubuloglomerular
feedbac(Rmediated dilation of the a+erent
Arterioles and subse8uent increases in renal blood
7lo# and 73.
: Com"are and contrast metabolic acidosis occur
due to lesions
A: %. 6esion occur in the Adrenal Corte*: it causes
hy"o function of the adrenal corte* resulting in the
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AddisonPs disease .causing metabolic acidosis due to
decreased "roduction of Aldosterone #hich is
im"ortant for the conservation of 5a and =CO'.
&. 6esion occur in the .$.4: in diarrhea the intestine
fails to absorb bicarbonate ions in addition to other
ions causing metabolic acidosis.
'. 6esion of the renal tubules: the renal tubules
fails to save the bicarbonate ions a condition #hichis related to 7anconiPs syndrome.
. EZ6A$5 COH54E3 CH33E54 MH64$6$E3 MEC=A5$;M 7O3
CO5CE543A4$O5 O7 H3$5E
A5;WE3
4here are three ste"s
A =
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duct for e*am"le chloride ions are "assively absorbed
along #ith sodium ions$n "resence of AD= #ater is reabsorbed from collecting
duct increasing urea concentration in collecting duct so
urea di+uses from collecting duct into medullary
interstitium
B MA$54E5A5CE O7 MEDH66A3< =ed& 2asa recta functions as counter current e*change
mechanism that minimi>es the #ashout of solutes
from medullary interstitium7luid 9o#s through a H-tube so that 9uid and solutes
can e*change bet#een t#o arms as blood 9o#s do#n
the descending limb it ta(es u" solutes but as blood
9o#s u" the ascending limb givs u" solutes to
medullary interstitium
C E5=A5CEME54 O7 MEDH66A3< =
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4hese ste"s are re"eated thus enhanced the
medullary hy"erosmolality
. DE7$5E 3E5A6 C6EA3A5CE. =OW CA5 $4 BE H;ED 4O
MEA;H3E 6OME3H6A3 7$643A4$O5 3A4E A5D 3E5A6
6A;MA 76OW
A5;WE3
3enal clearance of a substance is the volume of "lasma that
is com"letely cleared of a substance by the (idney "er unittime
Cs Q Hs G 2 @ s
Cs Q clearance rate of a substance
Hs Q urine concentration of a substance
2 Q urine 9o# rate
MEA;H3EME54 O7 73
We give the "atient a constant su""ly of inuline because it is
neither reabsorbed nor secreted in tubule. 4he urine
secreted in a (no#n time is measured in volume from #hich
urine formed "er minute can be calculated. Concentration of
inuline in urine is also measured #hich gives us a
measurement of 73
73 Q Hs G 2 @ s
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Creatinine clearance is also used to measure 73 accurately
it is easier than inuline clearance because creatinine is
already "resent in body 9uids
73 Q Ccr Q Hcr G 2 @ cr
Ccr Q creatinine clearance
Hcr G 2 Q creatinine e*cretion
cr Q "lasma creatinine concentration
MEA;H3EME54 O7 3E5A6 6A;MA 76OW
A substance #hich is ltered and secreted but not
reabsorbed should be used. ;uch a substance is A3A
AM$5O=$H3$C AC$D A=. A= clearance indicates the
amount of "lasma "assed through (idneys
A (no#n amount of A= is inected into body after sometime
the concentration of A= in "lasma and urine and volume of
urine e*creted are estimated4O4A6 3E5A6 6A;MA 76OW Q A= clearance @ A= e*cretion
ratio
: Brie9y e*"lain ho# is Hrine concentrated
Ans#er: When there is a #ater decit in the
body! the (idney forms a concentrated urine by
continuing to e*crete solutes #hile increasing
#ater reabsor"tion and decreasing the volume
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of urine formed. 4he human (idney can
"roduce a ma*imal urine concentration of %&??
to %)?? mOsm@6! four to ve times the
osmolarity of "lasma.
4he basic re8uirements for forming a
concentrated urine are
%0 a high level of AD=! #hich increases the
"ermeability of the distal tubules and collectingducts to #ater! thereby allo#ing these tubular
segments to avidly reabsorb #ater! and
&0 a high osmolarity of the renal medullary
interstitial 9uid! #hich "rovides the osmotic
gradient necessary for #ater reabsor"tion to
occur in the "resence of high levels of AD=.
4he renal medullary interstitium surrounding
the collecting ducts normally is very
hy"erosmotic! so that #hen AD= levels are
high! #ater moves through the tubular
membrane by osmosis into the renal
interstitium from there it is carried a#ay by
the vasa recta bac( into the blood. 4hus! the
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urine concentrating ability is limited by the
level of AD= and by the Degree of
hy"erosmolarity of the renal medulla. We
discuss the factors that control AD= secretion
later! but for no#! #hat is the "rocess by #hich
renal medullary interstitial 9uid becomes
hy"erosmotic 4his "rocess involves the
o"eration of the countercurrent mechanism.4he countercurrent mechanism de"ends on the
s"ecial anatomical arrangement of the loo"s of
=enle and the vasa recta! the s"eciali>ed
"eritubular ca"illaries of the renal medulla. $n
the human! about & "ercent of the ne"hrons
are u*tamedullary ne"hrons! #ith loo"s of
=enle and vasa recta that go dee"ly into the
medulla before returning to the corte*. ;ome
of the loo"s of =enle di" all the #ay to the ti"s
of the renal "a"illae that "roect from the
medulla into the renal "elvis. aralleling the
long loo"s of =enle are the vasa recta! #hich
also loo" do#n into the medulla before
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returning to the renal corte*. And nally! the
collecting ducts! #hich carry urine through the
hy"erosmotic renal medulla before it is
e*creted! also "lay a critical role in the
countercurrent mechanism.
: E*"lain Micturition 3e9e*! What is Atonic
Bladder
Ans#er: 3eferring again to 7igure in uyton
and halls "age no.'?N0as the Bladder lls! many
su"erim"osed micturition contractions begin to
a""ear! as sho#n by the dashed s"i(es. 4hey
are the result of a stretch re9e* initiated by
sensory stretch rece"tors in the bladder #all!
es"ecially by the rece"tors in the "osterior
urethra #hen this area begins to ll #ith urine
at the higher bladder "ressures. ;ensory signals
from the bladder stretch rece"tors are
conducted to the sacral segments of the cord
through the "elvic nerves and then re9e*ively
bac( again to the bladder through the
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"arasym"athetic nerve bers by #ay of these
same nerves. When the bladder is only "artially
lled! these micturition contractions usually
rela* s"ontaneously after a fraction of a minute! the detrusor
muscles sto" contracting!
and "ressure falls bac( to the baseline. As the
bladder continues to ll! the micturition
re9e*es become more fre8uent and cause
greater contractions of the detrusor muscle.
Once a micturition re9e* begins! it is Uself-
regenerative V 4hat is! initial contraction of the
bladder activates the stretch rece"tors to cause
a greater increase in sensory im"ulses to the
bladder and "osterior urethra! #hich causes a
further increase in re9e* contraction of the
bladder thus! the cycle is re"eated again and
again until the bladder has reached a strong
degree of contraction. 4hen! after a fe#seconds to more than a minute! the self-
regenerative re9e* begins to fatigue and the
regenerative cycle of the micturition re9e*
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ceases! "ermitting the bladder to rela*. 4hus!
the micturition re9e* is a single com"lete cycle
of %0 "rogressive and ra"id increase of
"ressure!
&0 A "eriod of sustained "ressure! and
'0 3eturn of the "ressure to the basal tone of
the bladder. Once a micturition re9e* has
occurred but has not succeeded in em"tyingthe bladder! the nervous elements of this re9e*
usually remain in an inhibited state for a fe#
minutes to % hour or more before another
micturition re9e* occurs. As the bladder
becomes more and more lled! micturition
re9e*es occur more and more often and more
and more "o#erfully. Once the micturition
re9e* becomes "o#erful enough! it causes
another re9e*! #hich "asses through the
"udendal nerves to the e*ternal s"hincter to
inhibit it. $f this inhibition is more "otent in the
brain than the voluntary constrictor signals to
the e*ternal s"hincter! urination #ill occur. $f
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not! urination #ill not occur until the bladder
lls still further and the micturition re9e*
becomes more "o#erful. 7acilitation or
$nhibition of Micturition by the Brain .4he
micturition re9e* is a com"letely autonomic
s"inal cord re9e*! but it can be inhibited or
facilitated by centers in the brain. 4hese
centers include%0 ;trong facilitative and inhibitory centers in
the brain stem! located mainly in the "ons! and
&0 several centers located in the cerebral
corte* that are mainly inhibitory but can
become e*citatory. 4he micturition re9e* is the
basic cause of micturition! but the higher
centers normally e*ert nal control of
micturition as follo#s:
%. 4he higher centers (ee" the micturition
re9e* "artially inhibited! e*ce"t #hen
micturition is desired.
&. 4he higher centers can "revent micturition!
even if the micturition re9e* occurs! by
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continual tonic contraction of the e*ternal
bladder s"hincter until a convenient time
"resents itself.
'. When it is time to urinate! the cortical
centers can facilitate the sacral micturition
centers to hel" initiate a micturition re9e* and
at the same time inhibit the e*ternal urinary
s"hincter so that urination can occur.2oluntary urination is usually initiated in the
follo#ing #ay: 7irst! a "erson voluntarily
contracts his or her abdominal muscles! #hich
increases the "ressure
in the bladder and allo#s e*tra urine to enter
the bladder nec( and "osterior urethra under
"ressure! thus stretching their #alls. 4his
stimulates the stretch rece"tors! #hich e*cites
the micturition re9e* and simultaneously
inhibits the e*ternal urethral s"hincter.
Ordinarily! all the urine #ill be em"tied! #ith
rarely more than to %? milliliters left in the
bladder
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3eference uyton and halls te*t boo( of
medical "hysiology vol.% "age no.'?N-'%?.0
: Dene 7iltration Coecient and
7iltration. ive their normal value.
Enumerate factors #hich a+ect lomerular
7iltration 3ate
Ans: 7iltration co-ecient Ff0: $t is measure of the "roduct of
the hydraulic conductivity and surface area of theglomerular ca"illaries.
7ormula of ltration co-ecient:
FfQ73@5et ltration "ressure
7iltration: 7iltration is commonly the mechanical or
"hysical o"eration #hich is used for the se"aration of
solids from 9uids li8uids or gases0 by inter"osing a
medium through #hich only the 9uid can "ass.
5ormal values:
5ormal 73Q%&ml@min
5et 7iltration ressureQ%?mm=g
;o! 5ormal Ff is %&@%?Q%&.ml@min@mm=g
;o Ff is %&. ml@min@mm=g
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7actors #hich a+ect 73:
%. lomerular =ydrostatic "ressure: 5ormal value
1?mm=g0.if increased can cause increase in 73.And vice
versa.
&. lomerular Colloid Osmotic ressure: 5ormal
'&mm=g0.4his factor is inversely "ro"ortional to 73.
' Bo#manPs Ca"sule ressure 5ormal%/mm=g0 this
factor is also inversely "ro"ortional to the 73.) Bo#manPs Colloid Osmotic ressure it is normally
>ero.
uestion: What is role of urea in hy"erosmotic
renal medullary interstitium and concentration of
the Hrine
Ans#er: Hrea is an e*cretory "roduct of the body. But it
also "lays an im"ortant role in concentrating the renal
medullary interstitium through the recirculating "rocess
#hich "roduces concentrated urine #hen there is short
su""ly of #ater. 4he urea is absorbed and secreted in the
(idney tubules. 4he reabsor"tion ta(es "lace in the
medullary collecting tubules by the H4-% and Ht-'
trans"ortors.into the medullary interstitium. 4he urea is
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concentrated in the tubular 9uid by the reabsor"tion of
#ater in the ascending loo" of =enle! DC4!and cortical
collecting tubules. $t increases the concentration of urea
in the tubular 9uid #hich then di+uses thru the H4% and
H4' trans"orters by concentration gradient mechanism.
Ma(ing the (idney interstitium hy"erosmolar. While
some of the urea in the medullary interstitium in
secreted in the thin "art of loo" of =enle by H4&trans"orter in the tubules.so in this #ay urea is e*creted
in addition to ma(e the (idney interstitium
hy"erosmolar. 4he =ormone AD= is res"onsible for the
H4' o"ening and the reabsor"tion of #ater in from the
tubules in order to concentrate the urine so in conditions
#hen there is less availability of #ater AD= is secreted
#hich reabsorbs #ater and also ma(es (idney
interstitium more hy"erosmolar for the "ur"ose of
concentrating the urine.
3eference uyton and halls te*t boo( of medical
"hysiology vol.% "age no.'?-'%.0
: #hat are features of ME4ABO6$C AC$DO;$;
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=o# is it com"ensated
Ans#er: features of ME4ABO6$C AC$DO;$;:
Metabolic acidosis can result from several general causes
%0 7ailure of the (idneys to e*crete metabolic acids normally
formed in the body!
&0 7ormation of e*cess 8uantities of metabolic acids in the
body!
'0 Addition of metabolic acids to the body by ingestion orinfusion of acids
)0 6oss of base from the body 9uids! #hich has the same
e+ect
as adding an acid to the body 9uids.
0 3enal 4ubular Acidosis. 4his ty"e of acidosis results
from a defect in renal secretion of =[ or in reabsor"tion of
=CO' or both.
10 Diarrhea. ;evere diarrhea is "robably the most fre8uent
Cause of metabolic acidosis. 4he cause of this acidosis is the
loss of large amounts of sodium bicarbonate into the feces.J0 Diabetes Mellitus: With severe diabetes mellitus! blood
acetoacetic acid levels can rise very high! causing severe
metabolic acidosis.
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/0$ngestion of acids
N0Chronic 3enal 7ailure
5ote #rite names only if mar(s distribution is less for this
8uestion0
43EA4ME54 O7 AC$DO;$; COME5;4A$O5 O7 AC$DO;$;0:
4o neutrali>e e*cess acid! large amounts of sodium
Bicarbonate can be ingested by mouth. 4he sodium
bicarbonate
is absorbed from the gastrointestinal tract into the blood and
increases the bicarbonate "ortion of the bicarbonate bu+er
system! thereby increasing "= to#ard normal. ;odium
bicarbonate can also be infused intravenously! but because
of the
"otentially dangerous "hysiologic e+ects of such treatment!
other substances are often used instead! such as sodium
lactate
and sodium gluconate. 4he lactate and gluconate "ortions of
the
molecules are metaboli>ed in the body! leaving the sodiumin
the e*tracellular 9uid in the form of sodium bicarbonate and
thereby increasing the "= of the 9uid to#ard normal.
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: Dene renal threshold. =o# is glucose
reabsorbed in the renal tubules What is the
normal values of trans"ort ma*imum for
glucose
Ans#er: 3enal 4hreshold:
4he renal threshold is the concentration of a
substance dissolved in the blood above #hichthe (idneys begin to remove it into the urine.
When the renal threshold of a substance is
e*ceeded! reabsor"tion of the substance by the
"ro*imal renal tubuli is incom"lete
conse8uently! "art of the substance remains in
the urine. 4he rate at #hich each of these
substances is ltered is calculated as
7iltration Q lomerular ltration rate multi"ly
by0 lasma concentration
4his calculation assumes that the substance is
freely ltered and not bound to "lasma
"roteins. 7or e*am"le! if "lasma glucose
concentration is % g@6! the amount of glucose
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ltered each day is about %/? 6@day multi"ly by
% g@6! or %/? g@day. Because virtually none of
the ltered glucose is normally e*creted! the
rate of glucose reabsor"tion is also %/? g@day
lucose g@day0:
%. Amount lteredQ%/?
&. Amount 3eabsorbed Q%/?
'. Amount e*cretedQ?). K of ltered 6oad 3eabsorbedQ%??
: ive a summary of functions of Fidneys
Ans#er: Fidneys "erform a number of functions as
follo#s:
%. 3ole in e*cretion: it e*cretes urea! creatinine!
metabolites! drugs! to*ins
&. 3egulations of $ons and Hrea: (idneys absorbs as
#ell as e*cretes many ions li(e 5a! F! Ca! and O) in
its tubules.
'. Acid base balance: (idney through "hos"hate
bu+er hel"s the body to resist any change in the "=
of the body.
). ;ynthetic functions: it "roduces %! &
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dihydro*ycholecalciferol activated vitamin D0.
. =omeostasis of #ater: it conserves #ater #hen
blood #ater level is lo# and vice versa.
1. 3egulation of Blood "ressure and Blood 2olume:
(idneys have %??K gain in correcting the change in
the blood "ressure by controlling the #ater level.
J. 3enin ;ecretion. Macula Densa cells of (idney
secrete renin #hich is involved in renin angiotensinsystem in controlling of 73.
/. Erythro"oietin ;ecretion: During hy"o*ia the
(idneys secrete this erythro"oietin #hich causes
the haemo"oitic stem cells to "roduce a lot of 3BCs.
: A man drin(s about ?% liter of
#ater in %? minutes. What changes
occur in his #ater and electrolyte
balance
Ans#er: When there is a large e*cess
of #ater in the body! the (idney can
e*crete as much as &?6day of dilute
urine. With a concentration of as lo#
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as ? mOsm@6.
After the ingestion of % 6iter of #ater
the urine volume reaches u" to si*
times normal #ithin ) minutes after
the #ater has been drun(. =o#ever
the total amount of solute e*creted
remains relatively constant because
urine formed becomes very diluteand urine osmolarity decreases from
1?? to about %?? mOsm@6. 4hus! after
ingestion of e*cess #ater! the (idney
rids the body of the e*cess #ater but
does not e*crete e*cess amounts o