Physio Uhs Solved Past Papers 2nd Year

7/24/2019 Physio Uhs Solved Past Papers 2nd Year

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PHYSIOLOGY UHS

PAST PAPERS

(SOLVED)2004-2012

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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


voluntary muscles

7eatures of cerebellar diseases:



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.


On the ;ame side:

;ensory 6oss:


"ost nerve root!"ost horn cells and lat and ventral

s"inothalamic tracts crossing to the o""osite side are

all lost

Motor disturbances:


Damage to ant horn



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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






O5 OO;$4E ;$DE:



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:


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


30/121

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


31/121

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.


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:


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





aralysis of u""er motor neuron lesion ty"eO5 OO;$4E ;$DE:



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


33/121

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


37/121

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.


38/121

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


39/121

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


40/121

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


On the ;ame side:;ensory 6oss:


"ost nerve root!"ost horn cells


43/121

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


;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






O5 OO;$4E ;$DE:


44/121



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


45/121

-What are the functions of s"inocerebellum

Enemurate features of cerebellar diseases

Ans:7unctions:i0-lanning and ne tunning of s(eletal muscle

contraction


voluntary muscles

7eatures of cerebellar diseases:i0-Dysmetria and ata*ia


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:


48/121

&- 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


49/121

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


50/121

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:


53/121

$nhibits .$.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.


54/121

-;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:


55/121

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


56/121

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


57/121

;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


58/121

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:


59/121

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


60/121

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.


61/121

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


62/121

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


63/121

) 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


64/121

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.


65/121

$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


66/121

$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


67/121

#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


69/121

%) !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!


70/121

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%/


72/121

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


73/121

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


74/121

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


75/121

"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


77/121

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


78/121

&. 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


80/121

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 =


81/121

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


84/121

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


85/121

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


86/121

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


87/121

"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*


88/121

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


89/121

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


91/121

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;$;


94/121

=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.


96/121

: 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

Documents

Physio Uhs Solved Past Papers 2nd Year