Physiology MBBS part 2 solved paper uhs

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PHYSIOLOGY UHS
PAST PAPERS
(SOLVED)
2004-2012
Nishtar ken Page 1 of 128

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SPECIAL SENSES
Q 1:What changes occur in eyes when these are focused
on a near object ? Explain the nervous mechanism
invovled?(2005 annual, 2008 annual)
Ans: (JP chp 169, Guyton chp 49)
Accomodation is invovled in this mechanism.
Definition : When eyes are focused on a near object
accomodation occurs ,the process by which light rays from
near objects or distant objects are brought to a focus on the
sensitive part of retina .It is achieved by various adjustments
made in the eyeball.
Mechanism:
1:contraction of cilliary muscles ,release ligament tension on
lens
2:lens assumes a spherical shape
3:suspensry ligaments are slackened
4:convergance of eyeballs

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all the changes during accomodationovvurs simultaneously ,it
can be controlled by will power to a extent.
Nervous mechanism:
Afferent pathway :
visual impulses on retina ->optic nerve ->optic chiasma-
>optic tract->lateral geniculate body->optic radiation to
visual cortex of occipital lobe ->association fibers to frontal
lobe
Centre:
located in frontal lobe of cerebral cortex (area 8 )
Efferent pathway :
1:Efferent fibers to ciliary muscles and sphincter pupillae
from area 8 ->corticulonuclear fibers pass via internal capsule
to EdingerWestphal nucleus of 3rd cranial nerve-
>preganglionic fibers pass to ciliary ganglion -
>postganglionic fibers via short ciliary nerves and supply
ciliary muscles and constrictor muscles
2:Efferent fibers to medial rectus :
from frontal eye field fibers to nucleus of occulomotor nerve -
>and supply medial rectus

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Q 2:Draw the Rhodopsin visual cycle . What is the
outcome of Vit.Adeficiency ?(2006 annual ,2007 annual )
Ans : Guyton chp 50
Rhodopsin visual cycle :
Diagram from guyton page 611
Role of Vit. A for formation of Rhodopsin :
1:Vit.A is present in cytoplasm of rods and in the pigment
layer of the retina to form new RETINAL .
2:When excess retinal ,it is converted back into Vit.A and vice
versa .
Deficiency of Vit.A :
1:Outcome of Vit.A deficiency is Night blindness.
2:Retinal and rhodopsin formation is severly depressed.
3:For night blindness to occur person must remain on Vit.A
deficient diet for at least 3 months because large quantities of
it are mostly stored in liver.
4:It can be reversed in less than 1 hour by intravenous
injection of Vit. A.

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Q 3:Draw pathway for light reflex . What is consensual
light reflex ?(2006 supplementry)
Ans : (Guyton chp 51, JP chp 169 )
Light Reflex pathway:
light rays on eyes->optic nerve->optic chiasma->optic tract-
>pretactal nucleus->EdingerWestphal nucleus->ciliary
ganglion->short ciliary nerve(parasympathetic nerves)-
>constrict sphincter of iris
Consensual Light Reflex:
1:Contraction in both eyes when light thrown in one eye.
2:The reason for Consensual light reflex is that some of the
fibers from pretactal nucleus of one side cross to the opposite
side and end on the opposite EdingerWestphal nucleus.
Q 4:A 65 years old man reports to his physician with the
principle complaint of Nyctalopia (nightbilndness).(2009
annual)
a.What is the cause of this disorder?

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Vit.A deficiency
b.Which layer of retina becomes impair?
Pigmented layer , as Vit.A is stored in this layer and Layer of
rods as well because Vit. A involved in formation of retinal and
rhodopsin.
c.What is Argyll Robertson Pupil?
It is clinical condition in which the light reflex is lost but the
accomodation reflex is present . Pupil is also very small .It is
an important diagnostic sign of CNS disease such as SYPHILIS.
Q 5:Miss R is very selective in her diet . From last few
months she is complaining of difficulty to see at night ,
she is diagnosed to be suffering from Night Blindness
.(2010 annual)
a.What is the cause of Night Blindness?
Vit.A deficiency in diet.
b.What will be the role of her treatment in the formation
of Rhodopsin ?
Intravenous injection of Vit.A can can reverse night blindness

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in less than 1 hour because Vit.A is used in the formation of
retinal and rhodopsin .
Q 6:How do eyes adapt to bright light and darkness?Give
its significance . (2008 supplementry)
Ans: (Guyton chp 50)
Light Adaptation:
1:Process in which eyes get adapted to increased illumination.
2:Photochemicals in both rods and cones will have been
reduced to retinal and opsins.
3:Much of the retinal of both rods and cones will have been
converted into Vit.A .
3:Because of these two effects conc. of photosensitive
chemicals remaining in the rods and cones are considerably
reduced and sensitivity of the eye to light is correspondingly
reduced .this is called light adaptation.
Dark Adaptation:
1:If a person remains in the darkness for a long time , the
retinal and opsins in the rods and cones are converted back
into light sensitive pigments.

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2:Furthermore,Vit.A is converted back into retinal to increase
light sensitive pigments , the final limit being determined by
the amount of opsind in the rods and cones to combine with
the retinal.This is called dark adaptation.
3:Dark adaptation curve , guyton page no. 614.
Other mechanism of light and dark adaptation:
1:Change in pupillary size (adaptation upto 30 folds within
fraction of seconds because of changes in the amount of light
allowed through the pupillary opening)
2:Neural adaptation, through bipolar cells, horizontal
cells,amacrine cells and ganglion cells , signals first are strong
then decrease rapidly at different stages of
transmission.Degree of adaptation is only fewfolds but occurs
in fraction of seconds , in contrast to the many to hours
required for full adaptation by the photo chemicals.
Significance:
Person is able to see in the illumination as well as in the dim
light .
Q 7:A student of 5th class feels difficulty in reading from

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the blackboard while sitting in back benches of the
class?(2008 annual BDS )(Ans: Guyton chp 49)
a:From which refrective error , the student is most likely
to be suffering?
MYOPIA
b:What is the cause of this error?
In myopia, when ciliary muscle is completely relaxed , the light
rays coming from distant objects are focused in front of the
retina .This is usually due to too long as eyeball ,but it can
result from too much refrective power in the lens system of
eye.Myopic person has no mechanism by which to focus
distant objects sharply on the retina.
c:Which lens are used to correct these errors?
The light rays passing through a concave lens diverge.If the
refractive surfaces of the eye have too much refractive power
,as in myopia, this excessive refractive power can be
neutralized by placing in front of the eye a concave spherical
lens , which will diverge rays.
Q 8:What is Attenuation Reflex ? What is its

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significance?(2006 supplementry, 2005 annual)
Ans:(Guyton chp 52 )
1:This reflex is characterized by involuntary contraction of
tensor tympani and stapedius muscles in respose to loud
noise.
2:Its latent period is 40 to 80 miliseconds .
3:The tensor tympani muscle pulls the handle of malleus
inward while the stapediusmusle pulls the stapes outward.
3:These two oppose each other and thereby cause the entire
ossiculay system to develope increased rigidity , thus greatly
reducing the ossicular conduction of low frequency sound ,
mainly frequencies below 1000 cycles per second.
4:It can reduce the intensity of low freq. sound transmission
by 30 to 40 decibles, which is about the same difference as
that b/w a loud voice and a whisper.
Significance:
1:To protect the cochlea from damaging vibrations caused by
excessive loud sound.
2:To mask low freq. sound in loud environments.

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3:Decrease a person´s hearing sensitivity to his or her own
speech.
Q 9:Howossicular system in middle ear transmit sound
waves ? What is its significance ?(2010 annual)
Ans:(Guyton chp 52)
Attached to tympanic membrane is handle of malleus, this
point is pulled by tensor tympani which keeps the membrane
pulled.
This allows the sound vibrations on any portion of the
tympanic membrane to be transmitted to the ossicles.
Ossicles of middle ear are suspended by ligament in such a
way that the combined malleus and inscusact as a single
lever,have approximately atthe border of the tympanic
membrane.
The articulation of the incus with the stapes causes the stapes
to push forward on the oval window and on the cochlear fluid
on the other side of window.
Significance:

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Main significance of ossicular system is impedance matching.
Q 10: What is place principle for determining of pitch of
sound?(2006 annual)
Ans:(Guyton chp 52)
1: It is apparent that low freq.sounds cause maximal activation
of the basilar membrane near the apex of the cochlea, and
high freq.sounds activate the basilar membrane near the base
of the cochlea.
2:Therefore, the major method used by the nervous system to
detect different sound freq is to determine the positions
along the basilar membrane that are most stimulated.This is
called place principle.
Q 11:How can you differentiate b/w conductive deafness
and perceptive deafness?(2004 annual)
Ans: (Guyton chp 52)
1:Deafness caused by impairment of cochlea , the auditory
nerve, or the central nervous system circuitsfrom the ear ,

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which is usually classified as nerve deafness.
2:Deafness caused by impairment of the physical structure of
the ear that conduct sound itself to the cochlea ,which is
usually called conduction deafness.
Difference:
The difference can be determined by different tests as follow:
1:Rinne´s Test
2:Weber´s Test
3:Audiometry
Q 12:A bomb blast occurs in the vicinity of a house . A
woman present in the house is hit by a piece (sharpnel)of
the bomb on her right arm. She also feels that her hearing
is also slightly impaired .Her complete examination in
emergency reveals no auditory damage of deficit . Few
minutes later she has no complaint of hearing loss.
a: What is mechanism which protects the ear from
damage due to loud sound?
b:Whar are the benefits/function of this mechanism?

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(2012 annual)
Ans:Same as that of question no.8
Prepared by :
Ayesha Arshad and ArshiaAnjum
FMH College Of Medicine and Dentistry
Lahore.
NEUROPHYSIOLOGY
Q:What are the features of upper motor neuron lesion?Give
one example of the lesion?

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Ans:Features:
a)-Paralysed muscles are rigid(spastic paralysis)
b)-Deep reflexes are exagerrated(Hyper-reflexia)
c)-Abdominal and cremasteric reflexes are lost
d)-Plantar reflex becomes Babinski,s sign
e)-No wasting or little wasting of muscles
f)-Reaction of degeneration is absent
g)-Large area of body involved
Example
Cerebral Palsy
Q-What are the functions of CSF?Why is lumbar puncture
generally performed below L2 segment of spinal cord?
Ans:Functions of CSF:
i)-Acts as shock absorber
ii)-Acts as cushion between soft and delicate brain and rigid
cranium

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iii)-Acts as a fluid buffer
iv)-Acts as a reservoir to regulate contents of cranium.
v)-medium for nutritional exchange
vi)-Removes metabolites
vii)-Transports medicine
Lumbar puncture is performed below L2 segment to avoid
injury to spinal cord.The spinal cord terminates at this level.
Q-Name tactile receptors.Why does asterognosis occur due to
lesion of dorsal column tract?
Ans:Tactile Receptors:
i)-Free nerve endings
ii)-Expanded tip endings
iii)-Merkel,s discs
iv)-Spray Endings
v)-Ruffini,s Endings
vi)-Kraus,s endings
vii)-Meissner,s Endings
Dorsal column tract is responsible for the sensations of touch
,two point discrimination,proprioception and position.We get

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an idea of the shape of the object by touching it.So lesion of
dorsal column tract results in astereognosis which is the
inability to identify an object by touch without visual input.
Q-Write a note on Analgesia Sytem?
Ans:Analgesia System:
Brain can supress input of pain signals to the nervous system
by activating a pain control system,called the analgesia
system.
Components:
i)-The periaqueductal and periventricular areas of the
mesencephalon ant upper pons surround the aqueduct of
Sylvius and portions of the 3rd And 4th ventricles.Neurons
from these areas send signals to:
ii)-The Raphe Magnus Nucleus, a thin midline nucleus located
in the lower pons and upper medulla and the nucleus
reticularisparagigantocellularis.From these second order
signals are transmitted to:
iii)-A pain inhibitor complex located in the dorsal horns of the

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spinal cord.
Areas that excite the periaqueductal gray area can also
supress the pain.Theseare :
i)-Periventricular area
ii)-Medial forebrain bundle
Main transmitter substances involved are :
Enkaphalin and Serotonin
Enkaphalin is believed to cause both presynaptic
and post-synaptic inhibiton of incoming type C
and type A delta fibers.
Brain Opiate System: Endorphins and Enkaphalin
*Injection of the minute quantities of morphine
either into the periventricular nucleus around
third ventricle or into the periaqueductal gray
Area of the brainstem causes an extreme degree of analgesia
Q-Enemurate functions of Cerebellum.List 4 features of
cerebellar diseases.
Ans.Functions:

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i)-Planning and fine tunning of skeletal muscle contraction
ii)-Maintainance of posture and performance of voluntary
muscles
iii)-Facilitates smooth and co-ordinated voluntary movements
iv)-Ensures that force,contraction and extent of movements
are accurate.
v)-Rsponds to vestibular stimuli from inner ear
vi)-Assists in maintaing equilibrium by modifications in muscle
tone
4 Features of cerebellar diseases:
i)-Dysmetria and ataxia
ii)-Past pointing and dysdiadochokinesia
iii)-Dysarthia
iv)-Intention tumor
Q-Write the effects of sympathetic stimulation
on thoracic and abdominal viscera?
ORGAN EFFECT

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HEART MUSCLES
coronaries
Increased Rate
Increased Force of
contraction
Dilated(beta
2),Constricted(alpha)
LUNGS
Bronchi
Blood vessels
Dilated
Mildly Constricted
GUT LUMEN
Sphincters
Decreased peristalsis and
tone
Increased Tone
Liver
gallbladders & bile duct
Glucose released
Relaxed
kidney Decreasd urine output and
increased renin secretion
Bladder
detrusor muscle
Relaxed

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trigone Contracted
Q-Explain the flexor or wtihdrawal reflex with the help
of a diagram?
Neuronal Mechanism of the flexor reflex:
The pathway for eliciting the flexor reflex passes first into the
spinal cord interneuoron pool of neurons and only
secondarily to the motor neurons.The shortest possible
curcuit is a 3 or 4 neuron pathway,however most of the
signals of the reflex transverse many more neurons and
invovle the following basic types of curcuits
i)-Diverging curcuits to spread the reflex to the necessary
muscles for the withdrawal
ii)-Curcuits to inhibit the antagonist muscles
iii)-Curcuits to cause afterdischarge lasting many fractions of a
second after the stimulus is over
Within a few milliseconds,after a pain nerve fiber begins to be

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stimulated ,the flexor response appears.Then in the next few
the flexor response begins to fatigue.Finallyy after the
stimulus is over,there is a period of after-discharge
Q-What is the motor and sensory loss at and below the level
of hemisection of the spinal cord.
Ans:Effects at the level of lesion:
On the Same side:
Sensory Loss:
Complete anaesthesia to all forms of senses,because post
nerve root,post horn cells and lat and ventral
spinothalamictracts crossing to the opposite side are all lost
Motor disturbances:
Paralysis of lower motor neuron type due to
Damage to ant horn
On the opposite side:
Sensory Loss:
Nil or very slight
Motor Loss:
Nil or slight due to damage to small direct pyramidal fibers

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of same side
EFFECT BELOW THE LEVEL OF LESION:
On the same side:
Sensory Disturbances:
*Fine touch and proprioception are lost due to damage to
fasciculi gracilis and cuneatous which do not cross
*Pain,temperature and crude touch are not lost because
lateral and ventral spinothalamic tracts cross to opposite sides
below the level of lesion
Motor Disturbances :
Paralysis of upper motor neuron lesion type
ON OPPOSITE SIDE:
Sensory disturbances:
Some loss of pain sensations.
Motor disturbances:
Nil or very slight.
Q-What are the functions of spinocerebellum?Enemurate
features of cerebellar diseases?
Ans:Functions:

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muscles
Features of cerebellar diseases:
iii)-Dysarthia
iv)-Intention tumor
SUPPLY 2006
Q-What is the nerve supply of the muscle spindle?How is it
stimulated?Enemurate its functions?
Nerve Supply of Muscle Spindle:
Motor Innervation:
*The end portions of the intrafusal fibers are innervated by
gamma fibers
*Extrafusal fibers are innervated by alpha fibers
SENSORY INNERVATION:
Two types of sensory endings are found in the

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Central receptor area of the muscle spindle.These are:
Primary ending:
In the center of receptor area,a large sensory nerve fiber
encircles the central portion of each intrafusalfibers,forming
the so called primary ending or annulospiralending.This nerve
fiber is type Ia fiber.
Secondary Ending:
Usually one but sometimes 2 small nerve endings of type II
innervate the receptor region forming the secndary ending
STIMULATION:
i)-Lengthening of the whole muscle
ii)-Contraction of the end portions of the spindles of intra-fusal
fibers
Functions:
i)-Muscle spindle constituets a feedback device that operates
to maintain muscle length
ii)-Simplest menifestation of muscle spindle function is stretch
reflex
iii)-Dynamic and static respons of muscle spindle performs
dampning function

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iv)-Stabailizes body position during tense motor activity
v)-Maintains muscle tone
Q-Name motor areas in the cerebral cortex.Eumerate features
of the lower motor neuron lesion?
Ans:Motor areas of cerebral cortex:
i)-Primary motor cortex
ii)-Premotor cortex
iii)-Supplementory motor cortex
Features of Lower motor neuron lesion:
i)-Flacid Paralysis
ii)-Areflexia
iii)-Abdominal and cremasteric reflexes are lost
iv)-Plantar reflex is normal
v)-Marked wasting of muscles
vi)-Reaction of degeneration is present
vii)-Fasciculations
viii)-Small area of body is affected

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Q-What are the functions of thalamus?What are the features
of thalamic syndrome?
Ans:Functions:
i)-Thalamus is a great relay center
ii)-Center for crude sensations e.g crude touch and pressure
iii)-Important reflex center for emotional reactions eg rage is
mediated through thalamus
iv)-It keeps cortex alert through its connections with
ascending reticular formation,thereby causing general
awakening.
Thalamic Syndrome:
It is a collection of symptoms resulting from damage of PLV
nucleus of thalamus due to occlusion of thalamo-geniculate
artery.
*Effects occur on opposite side of body
*Loss of fine sensations
*Loss of crude sensations
*Exaggeration of pain sensations
*Hyptonia
*Chorea and athetosis

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ANNUAL 2007
Q-Name the motor areas in the cerebral cortex.What are the
functions of Broca,sarea?What is the effect of lesion in this
area?
Ans: Motor Areas:
i)-Primary motor cortex
ii)-Supplementory motor cortex
iii)-Premotor cortex
Functions of Broca,s Area:
*Provides neural curcuitary for word formation
*Plans motor patterns for expressing individual
Words or even short phrases are initiated and executed
*Works in association with Wernicke,s area
*Causes the movement of muscles of speech in tongue,lips
and larynx.
Effect of lesion:
It causes motor aphasia.The person is capable of
deciding what he wants to say but cannot make the vocal
system emit words

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Q-Which neurotransmitters are released by the sympathetic
postganglionic fibers?Enumerate 8 effects of sympathetic
stimulation in the body?
Ans:They secrete epinephrine and nor-epinephrine.
ORGAN EFFECT
Heart
Muscle
Coronaries
Increased Rate
Increased Force of
contraction
Dilated(beta
Lungs
Bronchi
Blood Vessels
Dilated
Mildly Constricted
Gut
Lumen
Sphincter
tone
Increased Tone

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Liver
Gallbladder and bile ducts
Glucose released
Relaxed
Kidney Decreasd urine output and
Bladder
Detrusor
Trigone
Relaxed
Contracted
Penis Ejaculation
Fat cells lipolysis
Q-What is the motor and sensory loss at and below the level
of hemisection of the spinal cord.
On the Same side:
Sensory Loss:
nerve root,post horn cells and lat and ventral spinothalamic
tracts crossing to the opposite side are all lost

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Motor disturbances:
Damage to ant horn
Sensory Loss:
Nil or very slight
Motor Loss:
of same side
On the same side:

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ON OPPOSITE SIDE:
Motor disturbances:
Nil or very slight.
ANNUAL 2008
Q-Explain the functions of cerebrocerebellum.Enemurate 8
features of the cerebellar disease?
Ans:Functions of Cerebrocerebellum:
a)-Facilitates smooth and co-ordinated movements
b)-Ensures that force,direction and extent of movements are
accurate.
8 Features:
ii)-Past Pointing
iii)-Dysdiadochokinesia
iv)-Dysarthia
v)-Intention tumor

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vi)-Cerebellar Nystagmus
vii)-Hypotonia
viii)-Asthenia
Q-Enumerate 12 effects of sympathetic stimulation in the
body.Which neurotransmitter are released from preganglionic
and postganglionic sympathetic nerve fibers?
Ans:Pre ganglionic fibers release acetylcholine
Post ganglionic fibers releas Epinephrine and Nor-Epinephrine
ORGAN EFFECT
Heart
Muscle
Coronaries
Increased Rate
Increased Force of
contraction
Dilated(beta
Lungs
Bronchi
Blood Vessels
Dilated
Mildly Constricted

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Gut
Lumen
Sphincter
tone
Increased Tone
Liver
Glucose released
Relaxed
Kidney Decreasd urine output and
Bladder
Detrusor
Trigone
Relaxed
Contracted
Penis Ejaculation
Fat cells lipolysis
Basal metabolism Increased upto 100%
Adrenal medullary Secretion incresed
Mental activity incresed
Piloerector muscles contraction

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Q-A middle aged man was hit by a motor car resulting into
fracture dislocation of vertebrae.Later he developed effects
indicating right sided hemisection of the spinal
cord.Enumerate the features below and at the level of
hemisection.
On the Same side:
Sensory Loss:
nerve root,post horn cells and lat and ventral spinothalamic
tracts crossing
to the opposite side are all lost
Motor disturbances:
Damage to ant horn
Sensory Loss:
Nil or very slight
Motor Loss:

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of same side
On the same side:
ON OPPOSITE SIDE:
Motor disturbances:
Nil or very slight.
Q-Mr.J of 58 years age with reting tremors of hand and lips
consulted his family doctor.On examination he was found to

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have rigidity of limbs and expressionless face.He was having
short-stepped gait.
A)-From which disease Mr.J was suffering?
B)-What is the cause and mechanism of this disease
c)-Which drugs can be used to treat this disease?
a)-Parkinsons,s disease
b)-Cause:
*Dopamine secreted in the caudate nucleus and putamen is
an inhibitory transmitter,therefore the destruction of
dopaminergic neurons in the substantianigra of the
parkinsonian patient would allow the caudate nucleus and
putamen to be overly excited leading to rigidity
*Some of the feedback curcuits might easily oscillate leading
to tremor.It is involuntary tremor
*Dopamine secretion in the limbic system,
Especially in the nucleus accumbens is often decreased along
with its decrease in the basal ganglia.it might be the cause of
akinesia.
Q-What is the Speech area in the Cerebral Cortex?What do
you understand by Dyslexia?
Ans:Broca,s area is the speech area in the cerebral

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cortex.These are areas 44 and 45.
Dyslexia:
It is characterised by difficulty in learning to read fluently
and with accurate comprehension despite normal intelligence.
It is a learning disability.It includes reading
problems,spellingproblems,speech problems and dysgraphia
that makes a person difficult to master handwriting.
Q-Enumerate effects of parasympathetic stimulation in the
body.Name the neurotransmitter in this nervous system?
Ans:*Chollinergic fibers release acetylcholine
*Adrenergic fibers release nor-epinephrine
ORGAN EFFECT
Lungs
Brochi
Blood vessels
Constricted
Dilated
Gut
Lumen
Increased Peristalsis and
tone

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Sphincter Relaxed
Liver
Slight glycogen synthesis
Contracted
Bladder
Detrusor
Trigone
Contracted
Relaxed
Eye
Pupil
Ciliary Muscle
Contracted
Contracted
Penis erection
Glands
Nasal,lacrimal,parotid,
submandibular,gastric,pancreatic
Stimulation of copious
secretion
Annual 2009
Q-Enlist 8 functions of the body controlled by brainstem?
Ans:Functions

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The brain stem is its own master because it provides many
special control functions,such as:
i)-Control of respiration
ii)-Control of cardiovascular system
iii)-Partial control of gastrointestinal function
iv)-Control of many stereotyped movements of the body
v)-Control of equilibrium
vi)-Control of eye-movements
vii)-Serves as a way station for ‘command signals’ from higher
centers
viii)-Provide support to the body against gravity
Q-A 60 year old man develops tremor in his hands and fingers
which become pronounced as he reaches for a glass of water
or points towards an object,He has difficulty maintaining his
balance?
A)-Which component of the nervous system is involved?
B)-How are these tremors different fro other tremors due to
lesion of nervous system?
C)-Why this person has difficulty in maintaining
balance?

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Ans:
a)-Cerebellum
b)-These tremors differ from other tumor because these occur
when a person tries to do so voluntary action.Thats why these
are callled voluntary or intentional tumors.In case of basal
ganglia lesion these are involuntary tremors.
c)-Post Spinocerebellar fibers receive muscle joint info from
the muscle spindles,tendon organs and joint receptors of the
trunk and lower limbs.This info concerning tension of muscle
tendons and the movements of muscles and joints is used by
the cerebellum in the
Maintainance of posture.The ant spinocerebellar tract
provides the same info from the upper and lower
limbs.Cuneocerebellar tracts provide info of muscle joint.In
cerebellar lesion the cerebellum cannot comprehend these
info and resultss in loss of balance
ANNUAL 2010
Q-A boxer at the age of 45 years was diagnosed to be
suffering from Parkinson,s disease.
A)-What are the characteristics of this disease?

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b)-Suggest possible treatments?
Ans:Cause:
*Dopamine secreted in the caudate nucleus and putamen is
an inhibitory transmitter,therefore the destruction of
dopaminergic neurons in the substantianigra of the
parkinsonian patient would allow the caudate nucleus and
putamen to be overly excited leading to rigidity
*Some of the feedback curcuits might easily oscillate leading
to tremor.It is involuntary tremor
*Dopamine secretion in the limbic system, Especially in the
nucleus accumbens is often decreased along with its decrease
in the basal ganglia.it might be the cause of akinesia.
B)-Treatment:
i)-L-Dopa
ii)-L-Deprenyl
iii)-transplanted fetal dopamine cells
iv)-By Destroying part of the feedback circuitry
Q-a)-What are the various types of pain?
B)-Explain the mechanism of referred pain with the help of
diagram?
Ans:Types of pain:

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FAST PAIN:
*Very Short acting
*Mostly caused by thermal and mechanical stimuli
*Carried by A delta fibers via neospinathalamic pathway
*Localization of pain is good
*Velocity=6-30 /sec
*Neurotransmitter is glutamate.
Slow Pain:
*Long acting
*Mostly caused by chemical stimuli
*Carried by C fibers via paleospinothamlamic pathway
*Localization of pain is poor
*Velocity=0.5 – 2 m/sec
*Neurotransmitter is substance P
Ans b):Mechanism of reffered pain:
Branches of visceral pain fibers synapse synapse in spinal cord
on the same second order neurons(1 and 2) that reeceive pain
signals from skin.When the visceral pain fibers are
stimulated,pain signals from the viscera are conducted
through at least some of the same neuron that conduct pain

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signals from the skin and person has feeling that the
sensation originate in the skin itself
Q-Give the structure and functions of muscle spindle?
Ans:Structure:
Muscle spindle is built around 3 – 12 tiny intrafusal fibers that
are pointed at their ends and attached to the glycocalyx of
the surrounding large extrafusal skeletal muscle fibers.
Each intrafusal fiber is a tiny skeletal muscle
fiber.However,the central region of each of these fibers that
is,the area midway between the 2 ends has few or no actin
and myosin
Therefore,this central portion does not contract when the
ends do.Instead ,it functuins as a sensory receptor.The end
portions that do contract are excited by gamma motor nerve
fibers that originate from small type A gamma motor neurons
in the ant horns of the spinal cord.Extrafusaled by fibers are
innervated by alpha fibrers
Functions:
i)-Muscle spindle constituets a feedback device that operates
to maintain muscle length
ii)-Simplest menifestation of muscle spindle function is stretch

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reflex
iii)-Dynamic and static respons of muscle spindle performs
dampning function
iv)-Stabailizes body position during tense motor activity
v)-Maintains muscle tone
Annual 2012
Q- We experience different modalities of sensations
(e.gpain,touchetc) although the nerve fibers
transmitonlyimpulses.How is it that different nerve fibers
transmit different modalities of sensation?Give an example to
explain?
Ans:Each of the principle type of sensation that we can
experience-pain,touch,sight,sound and so forth-is called a
modality of sensation.
Each nerve tract terminates at a specific point in
The central nervous system, and the type of sensation felt
when a nerve fiber is stimulated is deteremined by the point
in the nervous system to which the fiber leads.Forexample,if a
pain fiber is stimulated ,the person perceives pain regardless
of what type of stimulus excites the fiber.The stimulus can be

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electricity,overheating of the fiber,crushing of the fiber,or
stimulus of the pain nerve ending by damage to the tissue
cells.In all these instances the person perceives pain.Likewise,if
a touch fiber is stimulated by electrical excitation of a touch
receptor or in
Other way,the person perceives touch because touch fibers
lead to specific touch areas in the brain,fibers from the ear
terminate in the auditory areas of the brain,and the
temperature fibers terminate in the temperature areas.
The specifity of nerve fibers for transmitting only one
modality of sesation is called labeled line principle.
Q-A 67 yearsold man visits his neurologist and complains that
it is extremely difficult for him to stand up sitting position or
start walking from standing position.He also complains of
tremulous movements of the fingerswhuch disappear when
he starts doing something.
a)-what is the condtion called?
B)What is the lesion/damage located?
C)-What is the speculated cause of difficulty this man
experiences in intitiating a movement?

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Ans: a)-Parkinson,s disease
b)-Basal ganglia
The akinesia that occurs in Parkinson,s disease is often much
more distressing to the patient than are the symptoms of
muscle rigidity and tremor,because to perform even the
simplest movement in severe parkinsonism,the person must
exert the highest degree of conc.The cause of akinesia is still
speculative.However,dopamine secreted in the limbic
system,especially in the nucleus accumbens,is often decreased
along with its decrease in the basal ganglia.It has been
suggested this might reduce the psychic drive
For motor activity so greatly that akinesia results
Q-A man of 45 years received a gun short on his back.He
developed right sided hemisection of the spinal cord.
A)-Give the features below,above and at the level of lesion?
B)-What is Brown-Sequard Syndrome?
On the Same side:

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Sensory Loss:
nerve root,post horn cells
and lat and ventral spinothalamic tracts crossing
to the opposite side are all lost
Motor disturbances:
Damage to ant horn
Sensory Loss:
Nil or very slight
Motor Loss:
of same side
On the same side:
Sensory Loss:
On the same side:

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ON OPPOSITE SIDE:
Motor disturbances:
Nil or very slight.
EFFECT ABOVE LEVEL OF LESION:
On Same Side:
There is a narrow zone of hyperaesthesia or hypersensitive to
touch,pain and thermal stimuli due to irritation of upper cut
ends of damaged fibers.
Opposite side:
Hyperaesthesia may be referred.
B)-In Brown sequard syndrome there is complete hemisection
of spinal cord.Its features are
*Ipsilateral lower motor neuron paralysis in the segment of

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lesion and muscular atrophy
*Ipsilateral spastic paralysis below the level of lesion
*Ipisilateral band of cutaneous anasthesia in the segment of
lesion.
*Ipsilateral loss of tactile discrimination, and of
Vibratory and proprioceptive sensations below the level of
lesion.
*Contralateral loss of pain and temp sensations below the
level of lesion
*Contralateral but not complete loss of tactile sensation below
the level of the lesion
Q-What are the functions of spinocerebellum?Enemurate
features of cerebellar diseases?
Ans:Functions:
muscles
Features of cerebellar diseases:

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iii)-Dysarthia
iv)-Intention tumor
PREPARED BY
AHSAN SARWAR
Lahore medical and dental college
Gastrointestinal Physiology
Question No: 1 What do you know about pharyngeal stage of
swallowing along with its nervous control? (Supplementary 2004)
Answer: Chapter 63 (Guyton)
SWALLOWING
2nd Stage (Pharyngeal Stage)
1- Bolus stimulates the epithelial swallowing receptor areas
around opening of pharynx.
2- Soft palate is pulled upwards.
3- The palatopharyngeal folds and vocal cords are approximated.
4- Epiglottis swings backward over the opening of larynx.

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5- Upward movement of larynx and opening of the upper
oesophagealsphinchter.
6- Contraction of pharyngeal muscles and propulsion of food by
peristalsis into oesophagus.
Nervous Control:
Sensory: Sensory portions of trigeminal and glossoharyngeal nerves
into the medulla, either into or closely associated with the tractus
solitaries.
Areas in the medulla and lower pons are called swallowing centre.
Motor: 5th,9th,10th and 12th cranial nerves and a few cervical nerves.
Question No: 2 Write a short note on :
A) Pharyngeal stage of swallowing
B) Actions of cholecystokinin (Annual 2005)
Answer:
A) Answer No 1 above.
B) 1- stimulates pancreatic enzyme secretion.
2- stimulates pancreatic bicarbonate secretion.
3- causes gallbladder contraction.
4- growth of exocrine pancreas.

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5- inhibits gastric emptying.
6- Inhibits appetite.
Question No: 3 What events occur during the pharyngeal
stage of swallowing? Name the nerves that control this stage?
(Annual 2005)
Answer: Answer No 1 above.
Question No:4 How is gastric emptying regulated? (annual
2006)
Answer: Chapter no 63(guyton)
Gastric factors that promote emptying:
1- Effect of gastric food volume on rate of emptying
2- Effect of the hormone gastrin on stomach emptying
Duodenal factors that inhibit stomach emptying:
1- Inhibitory effect of enterogastric nervous reflexes from
duodenum:
2- Factors initiating enterogastric reflexes:
 Degree of distention of duodenum
 Presence of any irritation
 Acidity and osmolality of the chyme
 Presence of certain breakdown products in chyme
3- Hormonal feedback from duodenum:
 CCK

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 Secretin
 GIP (check the book for their detailed functions)
Question No: 5 What are the movements of small intestine?
(supplementary 2006)
Answer: Chapter 63(guyton)
Movements:
Two types:
1- Mixing contractions(segmentation contractions):
 Contractions cause segmentation of small intestine
 Chop the chyme 2-3 times per minute
 Frequency is determined by the electrical slow waves
normally it is 12/minute in duodenum and jejunum and
in ileum 8-9/minute.
 Contractions can be blocked by atropine
2- Propulsive movements:
 Peristalsis in small intestine: velocity is 0.5-2cm/sec
 Control of peristalsis by nervous and hormonal signals
1- Stretch of duodenal wall

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2- Gastroenteric reflex
3- Gastrin, cck, insulin, motilin and serotonin enhance
motility.
4- Secretin and glucagon inhibit motility
Question No: 6 List the motor functions of stomach? Wha are
hunger contractions? (annual 2006)
Answer: Chapter 63(guyton)
Motor Functions:
1- Storage function of somach:
 Vagovagal reflex reduces the tone in the muscular wall of
body of stomach.
 Stomach can store 0.8 – 1.5 litres of food.
2- Mixing and propulsion of food- Basic electrical rhythm of
stomach wall:
 Gastric juices secreted by gastric glands
 Mixing waves begin in the mid two upper portions of
stomach and move towards the antrum
 These waves are initiated by basic electrical rhythm
 Powerful constrictor rings force the antral contents
towards pylorus
 Retropulsion
3- Gastric emptying:
Answer no 4 above

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Hunger Contractions:
* Contractions that occur when the stomach has been
empty for several hours.
* Duration 2-3 minutes.
* Intense in young people and those having low blood sugar
levels.
* Sometimes causes mild pain called hunger pangs
* Donotbegin until 12-24 hours after last ingestion.
Question No: 7 What type of movements occur in small
intestine when it becomes distended with chyme? (annual
2007)
Answer: Answer no 5 above.
Question No: 8 Name the stages of deglutition? Which
changes will occur during second stage? (supplementary
2007)
Answer: Stages:
1- Voluntary stage of swallowing
2- Pharyngeal stage of swallowing
3- Oesophageal stage of swallowing

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Question No: 9 what is enteric nervous system?
which defect in enteric nervous system leads to
oesphagealachlasia?
Answer: chapter 62(guyton)
Composed mainly of two plexus:
1- Myenteric or auerbach’s plexus:
 Controls G.I.T movements
 Present between the inner circular and outer longitudinal
muscle layers
2- Submucosal or meissner’s plexus:
 Controls G.I.T secretions and local blood flow.
 Present in the submucosa
Achlasia:
 Oesphagealsphinchter fails to relax during swallowing
 Damage in neural network of myenteric plexus in lower
two thirds of oesophagus
 Myenteric plexus loses its ability to cause receptive
relaxation of oesophagealsphinchter.
Question No: 10 list the functions of stomach? Give
factors which increase the rate of emptying of stomach?
(annual 2008)

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Answer: Answer no 6 above for functions.
Answer no 4 above for factors.
Gastric factors promote stomach emptying.
Question no: 11 Compare the effects of sympathetic and
parasympathetic stimulation on G.I.T (supplementary
2008)
Answer: chapter 62(guyton)
Autonomic control:
Parasympathetic:
 Increases G.I.T activity
 Cranial portion by vagus nerve and sacral portion by
2nd,3rd,and 4th pelvic splanchnic nerves. Postganglionic
neurons are located in myenteric and submucosal plexus.
 Enhances the activity of G.I.T functions.
 Extensive near to oral cavity and anus.
Sympathetic:
 Inhibits G.I.T activity.
 Fibres originate in spinal cord between segments t5-l2.
Some fibres enter sympathetic chains and then pass to
celiac ganglion or

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myenteric ganglion. Most of the post ganglionic neurons
are in these ganglion.
 Innervates all the G.I.T
 Secrete epinephrine and nor epinephrine
Question no 12: give five differences between
obstructive and hemolytic jaundice?
Answers:
Chapter no 70(guyton)
1- Hemolytic jaundice is caused by hemolysis of RBCs
whereas obstructive jaundice is caused by obstruction
of bile duct or liver diseases.
2- In hemolytic jaundice unconjugated bilirubin is
increased whereas in obstructive conjugated bilirubin
is increased.
3- URobilinogen is increased in hemolytic jaundice and
decreased in obstructive jaundice.
4- Urine color is normal in hemolytic but it is dark in
obstructive jaundice due to conjugated bilirubin.
5- Stool color Is normal in hemolytic jaundice but pale in
obstructive jaundice.
6- Splenomegaly is present in hemolytic jaundice but
absent in obstructive jaundice.

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Question no:13
A) Enumerate the factors that regulate gastric emptying?
B) Enumerate the factors that can excite enterogastric
reflexes from duodenum?
Answer: A) answer no 4 above for gastric emptying
B)Factors initiating enterogastric reflexes:
 Degree of distention of duodenum
 Presence of any irritation
 Acidity and osmolality of the chyme
 Presence of certain breakdown products in chyme
Question no 14: A person is diagnosed to have a gastric ulcer on
endoscopy.
a) What is pathophysiology of this disease?
b) How the intestine normally handles the excessive acidity in
chyme?
Answer: A) chapter 66(guyton)
Caused by:
 Digestive action of gastric juice or uuper small intestine
secretions
 Imbalance between rate of secretion of gastric juice and
degree of protection afforded by mucosal barrier and
neutralization of gastric acid by duodenal juices.

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 Excessive secretion of acid and pepsin
 Bacterial infection by helicobacter pylori
 Smoking
 Alcohol
 Aspirin
B)alkalinity of the small intestine secretion
Large quantity of sodium bicarbonate in pancreatic secretion
neutralizing HCL, inactivating pepsin and preventing digestion of
mucosa
Large amounts of bicarbonate ions by the secretion of brunners
glands and in bile
Acidic chyme entering duodenum inhibits gastric secretion and
peristalsis in stomach
Presence of acid in small intestine stimulates secretin secretion
which in turn stimulates bicarbonate secretion.
PREPARED BY
SALEHA RASHID & ZAINUB ARIF
FMH college of medicine & dentistry

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ENDOCRINOLOGY
Q:How does cyclic Amp mediate hormonal action at cellular level?
which hormones obey the cyclic-Amp mechanism ? (ANNUAL
Paper 2004)
Ans:
Adenylyl Cyclase–cAMP Second
Messenger System
Binding of the hormones with the receptor
allows coupling of the receptor to a G protein ----->
G protein stimulates the adenylyl cyclase–cAMP
system, a membrane-bound enzyme---->Gs protein then catalyzes
the conversion of a small amount of cytoplasmic
adenosine triphosphate (ATP) into cAMP inside the
cell.-----> This then activates cAMP-dependent protein
kinase, which phosphorylates specific proteins in the
cell, triggering biochemical reactions that ultimately
lead to the cell’s response to the hormone.
Some Hormones That Use the Adenylyl Cyclase–cAMP
Second Messenger System
Adrenocorticotropic hormone (ACTH)

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Angiotensin II (epithelial cells)
Calcitonin
Catecholamines (b receptors)
Corticotropin-releasing hormone (CRH)
Follicle-stimulating hormone (FSH)
Glucagon
Human chorionic gonadotropin (HCG)
Luteinizing hormone (LH)
Parathyroid hormone (PTH)
Secretin
Somatostatin
Thyroid-stimulating hormone (TSH)
Vasopressin (V2 receptor, epithelial cells)
Q: Differentiate between the etiology and features of Dwarfism
and cretinism ? (ANNUAL Paper 2004 & 2006)
Ans: Dwarfism
=>dwarfism result from generalized
deficiency of anterior pituitary secretion (panhypopituitarism)
during childhood.
=>all the physical parts of the body develop in appropriate
proportion
to one another
=>dwarf does not pass through puberty

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=>mental level is normal
=>African pygmy and the Lévi-Lorain
dwarf are its types
Cretinism
=>Cretinism is caused by extreme hypothyroidism during
fetal life, infancy or childhood
=>disproportionate rate of growth,
=>obese, stocky, and short appearance.
tongue becomes so that it obstructs swallowing.
=>mental retardation
=>congenital cretinism and endemic cretinism are its types
Q:Explain various steps involved in the biosynthesis of Thyroid
hormones?(ANNUAL Paper 2005 & supplementary 2006)
Ans:
=>Formation and Secretion of Thyroglobulin by the Thyroid Cells

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=>Oxidation of the Ion
The oxidation of iodine is promoted by the enzyme peroxidase
and its accompanying hydrogen peroxide, which
provide a potent system capable of oxidizing iodides.
=>Iodination of Tyrosine and Formation of the Thyroid Hormones—
“Organification” of Thyroglobulin
oxidized iodine is associated with an iodinaseenzyme iodine binds
with about one sixth of the tyrosine amino acids within the
thyroglobulin molecule.Tyrosine is first iodized to
monoiodotyrosineand then to diiodotyrosinewhic coupled to form
the thyroxine and triidotyrosin.
=>Storage of Thyroglobulin
Q:What are different second messengers mechanisms of
hormonal actions?(ANNUAL Paper 2005)
Ans:AdenylylCyclase–cAMP Second
Messenger System
The Cell Membrane Phospholipid Second
Messenger System
Calcium-Calmodulin Second
Messenger Syste

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GMP second messenger system
prostaglandins
Q:Name the hormones secreted from the thyroid gland. Explain
mechanism of action of steroid hormones? (ANNUAL Paper 2006)
Ans: thyroxineand
triiodothyronine, commonly called T4 and T3, respectively.
Calcitonin
Mechanism of action of steroid hormones:
=>steroid hormones, exerts its effects
by first interacting with intracellular receptors in target
cells.
. =>They can easily diffuse through the cell membrane. Once inside
the cell,
they binds with protein receptor in the cytoplasm,
and the hormone-receptor complex then interacts with
specific regulatory DNA sequences, called glucocorticoid or
minerilocorticoid
response elements, to induce or repress gene transcription.
=>Other proteins in the cell, called transcription
factors, are also necessary for the hormone-receptor
complex to interact appropriately.
Q:Enumerate:
a) Features of Cushing's syndrome

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b) Features of Tetany (supplementary 2006)
Ans; Features of cushing's syndrome:
hypersecretion of adrenal cortex.
-emotional disturbance
-Enlarged sellaturcica
-moon face
-oteoporosis
-cardiac hypertrophy
-buffalo hump
-obesity
-Amenorrhea
-muscle weakness
-purpura
-skin ulcers
Features of tetany:
low ECF calcium
-threshold for action potential is lowered

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-Nervous system is in more excited state
-gait abnormality (scissor gait , spastic gait)
-movement disorders
-lack of cordination
-joint locking
Q: A young man reported to his family doctor with the complaints
of palpitation, loss of weight in spite of increased appetite and
intolerance to heat. On examination he was having pulse rate
110/min, his eyes were prominent and there was swelling on the
anterior side of the neck.
a) From which disease he was suffering ?
b) Which investigations will you advise?
c)What is the cause of the disease? (Annual paper 2007)
Ans: a)Hyperthyroidism

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b)The most accurate diagnostic test is
direct measurement of the concentration of “free” thyroxine
(and sometimes triiodothyronine) in the plasma. other tests
include
1. The basal metabolic rate which will be high in this case.
2. The concentration of TSH in the plasma. TSH is completely
suppressed by the
large amounts of circulating thyroxine and
triiodothyronine so there is almost no plasma
TSH.
3. The concentration of TSI is measured by
radioimmunoassay. This is usually high in
thyrotoxicosis but low in thyroid adenoma
.
C)Hyperthyroidpateints have certain substances in the blood.
These substances
are immunoglobulin antibodies that bind with the
same membrane receptors that bind TSH. They induce
continual activation of the cAMP system of the cells,
with resultant development of hyperthyroidism. These
antibodies are called thyroid-stimulating immunoglobulin
and are designated TSI.
Throid adenoma also leads to hyperthyroidism.
Q: What are physiological actions of cortisol on proteins and
carbohydrate metabolism? Enumerate six features of Cushing's
syndrome? {Annual paper 2007 , 2008 (action on proteins) &
supplementary 2008 ( action on carbohydrates)}

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Ans: Effect on carbohydrate metabolism:
=>increase gluconeogenesis
-Cortisol increases the enzymes required to convert
amino acids into glucose in the liver cells
-Cortisol causes mobilization of amino acids from
theextrahepatic tissues mainly from muscle. as the result more
amino acids are avialable for gluconeogenesis.
=>Decreased Glucose Utilization by Cells.
Effect on protein metabolism:
=>Reduction in Cellular Protein.
This is caused by both
decreased protein synthesis and increased catabolism
of protein already in the cells
=>Cortisol Increases Liver and Plasma Proteins.
It is believed that this results from a possible effect of cortisol to
enhance amino acid transport into liver and to enhance the
liver enzymes required for protein synthesis
=>Increased Blood Amino Acids, Diminished Transport of Amino
Acids into Extrahepatic Cells, and Enhanced Transport into
Hepatic Cells
Q:What are physiological actions of cortisol on proteins ?How is

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cortisol secretion regulated ? (Annual paper 2008)
Ans; Regulation of cortisol secretion:
fig 77-6
=>ACTH Stimulates Cortisol Secretion.
An important releasing factor controls ACTH secretion. This is
called corticotropin-releasing
factor (CRF). It is secreted into the
primary capillary plexus of the hypophysial portal
system in the median eminence of the hypothalamus
and then carried to the anterior pituitary gland, where
it induces ACTH secretion.
=>ACTH Activates Adrenocortical Cells to Produce Steroids by
Increasing Cyclic Adenosine Monophosphate (cAMP).
The most important of all the ACTH-stimulated
steps for controlling adrenocortical secretion is activation
of the enzyme protein kinase A, which causes
initial conversion of cholesterol to pregnenolone. This
initial conversion is the “rate-limiting” step for all the
adrenocortical hormones.
Q:A young female consulted her family physician . She
complained of frequent muscle spasms and numbness of arms
and legs. Her plasma calcium was 6.5mg/dl.
a) From which condition was she suffering ?

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b) was her plasma calcium normal?
c)What was the mechanism of her frequent muscle spasms and
numbness? (Annual paper 2008)
Ans: a) Tetany
b) no , her plasma calcium level was lower. normal value is 9.8 to
11.5 mg/dl.
c) Her neurons are over excited , threshold for action potential is
decreased , even little sodium influx leads to sudden muscle
contraction ( muscle spasms ).
Q: A boy of 10 years was brought by his father to a medical
specialist. The boy because of retarded growth appeared to be of
4-5 years. During talking the boy answered the question
intelligently. His body parts were proportionate but of smaller
size:
a) Fom which disorder the boy was suffering?
b) what was the cause of this disorder?
c)what are different types of this disorder? ( supplementary 2008)
Ans; a) Dwarfisim
b) insufficient growth hormone produced by the anterior pitutiary
hormone.

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c) African pygmy ,Lévi-Lorain dwarfism .
Q: a)What are physiological actions of cortisol on carbohydrates?
b) what is the difference between Cushing's syndrome and
Cushing's disease?( supplementary 2008)
Ans; a) see above questions
b) Hypersecretion by the adrenal cortex causes a complex
cascade of hormone effects called Cushing’s syndrome
When Cushing’s syndrome is secondary
to excess secretion of ACTH by the anterior
pituitary, this is referred to as Cushing’s disease
Q:Name the hormones of anterior pitutiary gland ? What are
somatomedians? (annual paper 2009)
Ans;Growth hormone
Adrenocorticotropic hormone
Thyroid-stimulating hormone
Gonadotropes Follicle-stimulating
(FSH)
Luteinizing hormone (LH)
prolactin
b) Somatomedians are insulin like growth factors though which
growth hormone takes its action and perform different functions
like formation of proteins.

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Q: A 45 year old female give the month history of fatigue , hunger
and thirst almost all the time . there is increased frequency of
micturation as well and the complaints have steadily worsened
over the last two months. lab tests reveal:
a)what is the lady suffering from?
b) what is the physiological reason of increased frequency of
micturation?
c) why is she hungry all the time ?
d)why is she always thirsty ?
e) what are different types to this disorder? ( Annual paper 2009)
a. diabetes mellitus (type 2)
b. increased osmotic effect of glucose decreases tubular
reabsorption
c. impaired glucose uptake by cells for energy.
d. increased blood osmolarity stimulates the hypothalamus
osmotic receptors
e. type 1 and type 2
Q:a) what are the endocrine functions of pancrease?
b) Enlist the factors which increase insulin secretion?( Annual

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paper 2010)
Ans: alpha cells glucagon
beta cells insulin
b. Increased blood glucose
• Increased blood free fatty acids
• Increased blood amino acids
• Gastrointestinal hormones
(gastrin, cholecystokinin, secretin,
gastric inhibitory peptide)
• Glucagon, growth hormone,
cortisol
• Parasympathetic stimulation;
acetylcholine
• b-Adrenergic stimulation
• Insulin resistance; obesity
• Sulfonylurea drugs (glyburide,
tolbutamide)
Q: Give pathophysiology and features of 43 year old lady who is
diagnosed as a case of toxic goiter?( Annual paper 2010)
Symptoms of Hyperthyroidism
The symptoms of hyperthyroidism are obvious from the
preceding discussion of the physiology of the thyroid
hormones: (1) a high state of excitability, (2) intolerance
to heat, (3) increased sweating, (4) mild to extreme
weight loss (sometimes as much as 100 pounds), (5)

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varying degrees of diarrhea, (6) muscle weakness, (7)
nervousness or other psychic disorders, (8) extreme
fatigue but inability to sleep, and (9) tremor of the
hands.
Exophthalmos
Q:How 24 hour blood glucose is regulated in normal person ?(
Annual paper 2011)
Growth Hormone Decreases
Carbohydrate Utilization
Growth hormone causes multiple effects that
influence carbohydrate metabolism, including (1)
decreased glucose uptake in tissues such as skeletal
muscle and fat, (2) increased glucose production by
the liver, and (3) increased insulin secretion.
Glucose absorption
Gluconeogenesis
Glycogenolysis
insulin lowers glucagon increases
Q:Enumerate the specific effects of thyroid stimulating hormone
(TSH) on thyroid gland?( Annual paper 2011)
Increased proteolysis of the thyroglobulin that
has already been stored in the follicles, with
resultant release of the thyroid hormones into
the circulating blood and diminishment of the

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follicular substance itself
2. Increased activity of the iodide pump, which
increases the rate of “iodide trapping” in the
glandular cells, sometimes increasing the ratio of
intracellular to extracellular iodide concentration
in the glandular substance to as much as eight
times normal
3. Increased iodination of tyrosine to form the
thyroid hormones
4. Increased size and increased secretory activity of
the thyroid cells
5. Increased number of thyroid cells plus a change
from cuboidal to columnar cells and much
infolding of the thyroid epithelium into the
follicles
In summary, TSH increases all the known secretory
activities of the thyroid glandular cells.
PREPARED BY:
Waqar Sharif
CMH Medical College
REPRODUCTION

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Q1. enumerate hormones that take part in lactation. explain the
action of prolactin. (annual 2004)
A. prolactin, oxytocin, estrogen and progesterone.production of
milk in breasts and breast enlargement
Q2. what are stages of spermatogenesis? name the hormones
which control sperm formation. (annual 2005)
A. spermatocytogenesis
spermatogonium a to spermatogaonia b to primary spermatocyte
to secondary spermatocyte via meiosis to spermatid
spermiogenesis
spermatid to sperm
testosterone, Lh, Fsh, Gh, estradiol
Q3. explain the phases of endometrial cycle. (annual 2006)
A. proliferative phase
increase in thickness due to estrogen
secretory phase
progesterone causes secretion

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menstrual phase
estrogen and progesterone lower. Lhncrease
Q4. give a summary of actions of estrogens. (supp 2006)
thickens vagina
increase external genitalia size
increase in uerine size, glands, vascularity
inhibitLh and Fsh
secondary sexual characteristics
Q5. enumerate functions of testosterone during fetal life.
whatare functions of sertolli cells. (annual 207)
external genitalia and male genital organs increase in size
suppreses formation of female genitalia
descent of testes
sertolli cells offer nutririon, support, spermatogenesis,
spermiogenesis, mullerian inhibitory factor, estradiol, inhibin

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Q6. compare the physiological actions of estrogens and
progesterones on the a. uterus b. breasts. (annual 2008)
estrogen increase uterus size, glands and increase breast size and
glandular tissue
progesterone causes secretory phase, decreases contraction and
growth of lobules and alveoli of breast causing its swelling
Q7. a. when a baby suckles a mothers breast, how is milk ejected
out into babys mouth. b. why in more than 50 % lactating women,
the lactating cycle is inhibited? (supp 2008)
babysuckels nipples - sensory impulses - hypothalamus - oxytocin
and prolactin - contraction of myoepithelium - milk ejection n let
down
inhibited because suckling - hypothalamus - suppresesLhrh -
suppress FshLh - ovarian cycle suppressed
Q8. briefly describe the changes that occur during the
capacitation of spermatozoa. (annual 2009)
acrosome reaction
zona reaction

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Q9. which hormonal factors cause increase contractility of uterine
muscle at the end of pregnancy? (annual 2010)
oxytocin, estrogen, prostaglandins, cortisol
Q10. give hormonal influence on female breasts during
adolescence, pregnancy and lactation. (annual 2011)
estrogenfr ductal system
progesteronefr glandular system
estrogen , progesterone, Gh, prolactin, cortisol, insulin
prepared by
Waqar Sharif
CMH Medical College

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RENAL PHYSIOLOGY
Q: what is filtration pressure? How does auto
regulation of glomerular filtration rate (GFR) occur?
Answer: Filtration Pressure: the net driving force
which pushes fluid into tissue spaces and out of
vascular sites; the net result between capillary
osmotic pressure and intravascular hydrostatic
pressure. For example-it occurs in the kidneys for
the filtration purposes and in the capillaries where
starling forces act together to determine the
direction of going of fluid either into the capillary or
out of it.
Auto regulation of glomerular filtration rate:
1. Role of Tubuloglomerular Feedback
In Auto regulation of GFR: The Tubuloglomerular
feedback mechanism has two components that act
together to control GFR:
(1) An afferent arteriolar feedback mechanism and
(2) an efferent arteriolar feedback mechanism.
These feedback mechanisms depend on special
delivery to the macula densa in these circumstances
anatomical arrangements of the juxtaglomerular
complex. The juxtaglomerular complex consists of
maculadensa cells in the initial portion of the distal
tubule and juxtaglomerular cells in the walls of the
afferent and efferent arterioles. The macula densa
is a specialized group of epithelial cells in the distal

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tubules that comes in close contact with the
afferent and efferent arterioles. The macula densa
cells contain Golgi apparatus, which are intracellular
secretory organelles directed toward the arterioles,
suggesting that these cells may be secreting a
substance toward the arterioles. Tubuloglomerular
feedback–mediated renal vasoconstriction that
occurs in response to the increased sodium chloride
2. Myogenic Auto regulation of Renal GFR: Stretch
Of the vascular wall allows increased movement of
Calcium ions from the extracellular fluid into the
cells, causing them to contract. This contraction
prevents over distention of the vessel and at the
same time, by raising vascular resistance, helps
prevent excessive increases in renal blood flow and
GFR when arterial pressure increases
3. High Protein Intake and Increased Blood
Glucose: following: A high-protein meal increases
the release of amino acids into the blood, which are
reabsorbed in the proximal tubule. Because amino
acids and sodium are reabsorbed together by the

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proximal tubules, increased amino acid
reabsorption also stimulates sodium reabsorption in
the proximal tubules. This decreases sodium
delivery to the macula densa, which elicits a
Tubuloglomerular feedback–mediated decrease
In resistance of the afferent arterioles. The
decreased afferent arteriolar resistance then raises
renal blood flow and GFR. This increased GFR allows
sodium excretion to be maintained at a nearly
normal level while increasing the excretion of the
waste products of protein metabolism, such as
urea.A similar mechanism may also explain the
marked increases in renal blood flow and GFR that
occur with large increases in blood glucose levels in
uncontrolled diabetes mellitus. Because glucose,
like some of the amino acids, is also reabsorbed
along with sodium in the proximal tubule, increased
glucose delivery to the tubules causes them to
reabsorb excess sodium along with glucose. This, in

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turn, decreases delivery of sodium chloride to the
maculadensa, activating a Tubuloglomerular
feedback–mediated dilation of the afferent
Arterioles and subsequent increases in renal blood
Flow and GFR.
Q: Compare and contrast metabolic acidosis occur
due to lesions?
A:1. Lesion occur in the Adrenal Cortex: it causes
hypo function of the adrenal cortex resulting in the
Addison’s disease .causing metabolic acidosis due to
decreased production of Aldosterone which is
important for the conservation of Na and HCO3.
2. Lesion occur in the G.I.T: in diarrhea the intestine
fails to absorb bicarbonate ions in addition to other
ions causing metabolic acidosis.
3. Lesion of the renal tubules: the renal tubules
fails to save the bicarbonate ions a condition which
is related to Fanconi’s syndrome.

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Q. EXPLAIN COUNTER CURRENT MULTIPLIER MECHANISM FOR
CONCENTRATION OF URINE?
ANSWER
There are three steps
A. HYPEROSMOLALITY OF THE MADULLARY INTRSTITIAL FLUID
This is achieved by following mechanisms
First the principle cause of greatly increased medullary osmolality is
active transport of Na+ and Cl- into medullary interstitium from thick
portion of ascending limb of loop of henle.
Second smaller quantities of ions are also transported into the
medullary interstitial fluid from the collecting duct for example
chloride ions are passively absorbed along with sodium ions
In presence of ADH water is reabsorbed from collecting duct
increasing urea concentration in collecting duct so urea diffuses from
collecting duct into medullary interstitium
B. MAINTENANCE OF MEDULLARY HYPEROSMOLALITY
It is maintained because of two factors
1. Medullary blood flow is very sluggish therefore removal of solutes
from medullary intrstitium by blood is minimized
2. Vasa recta functions as counter current exchange mechanism that
minimizes the washout of solutes from medullary interstitium
Fluid flows through a U-tube so that fluid and solutes can exchange
between two arms as blood flows down the descending limb it
takes up solutes but as blood flows up the ascending limb givs up
solutes to medullary interstitium

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C. ENHANCEMENT OF MEDULLARY HYPEROSMOLALITY
1. Na+ and Cl- from thick ascending limb diffuse into medullary
interstitium
2. From medullary interstitium Na+ and Cl- diffuses into thin
descending limb into the tip of papilla
3. Much of the Na+ and Cl- from tips of papilla diffuses into papillary
interstitium
4. Remaining of Na+ and Cl- is carried again back up the ascending
limb of loop of henle where the thick ascending segment
retransports this sodium chloride once again into the papillary
interstitium
These steps are repeated thus enhanced the medullary
hyperosmolality
Q. DEFINE RENAL CLEARANCE. HOW CAN IT BE USED TO MEASURE
GLOMERULAR FILTRATION RATE AND RENAL PLASMA FLOW?
ANSWER
Renal clearance of a substance is the volume of plasma that is completely
cleared of a substance by the kidney per unit time
Cs = Us * V / Ps
Cs = clearance rate of a substance
Us = urine concentration of a substance
V = urine flow rate

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MEASUREMENT OF GFR
We give the patient a constant supply of inuline because it is neither
reabsorbed nor secreted in tubule. The urine secreted in a known time is
measured in volume from which urine formed per minute can be
calculated. Concentration of inuline in urine is also measured which gives us
a measurement of GFR
GFR = Us * V / Ps
Creatinine clearance is also used to measure GFR accurately it is easier than
inuline clearance because creatinine is already present in body fluids
GFR = Ccr = Ucr * V / Pcr
Ccr = creatinine clearance
Ucr * V = creatinine excretion
Pcr = plasma creatinine concentration
MEASUREMENT OF RENAL PLASMA FLOW
A substance which is filtered and secreted but not reabsorbed should be
used. Such a substance is PARA AMINOHIPPURIC ACID PAH. PAH clearance
indicates the amount of plasma passed through kidneys
A known amount of PAH is injected into body after sometime the
concentration of PAH in plasma and urine and volume of urine excreted are
estimated
TOTAL RENAL PLASMA FLOW = PAH clearance / PAH excretion ratio

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Q: Briefly explain how is Urine concentrated?
Answer: When there is a water deficit in the
body, the kidney forms a concentrated urine by
continuing to excrete solutes while increasing
water reabsorption and decreasing the volume
of urine formed. The human kidney can
produce a maximal urine concentration of 1200
to 1400 mOsm/L, four to five times the
osmolarity of plasma.
The basic requirements for forming a
concentrated urine are
(1) a high level of ADH, which increases the
permeability of the distal tubules and collecting
ducts to water, thereby allowing these tubular
segments to avidly reabsorb water, and
(2) a high osmolarity of the renal medullary
interstitial fluid, which provides the osmotic
gradient necessary for water reabsorption to
occur in the presence of high levels of ADH.

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The renal medullary interstitium surrounding
the collecting ducts normally is very
hyperosmotic, so that when ADH levels are
high, water moves through the tubular
membrane by osmosis into the renal
interstitium; from there it is carried away by
the vasa recta back into the blood. Thus, the
urine concentrating ability is limited by the
level of ADH and by the Degree of
hyperosmolarity of the renal medulla. We
discuss the factors that control ADH secretion
later, but for now, what is the process by which
renal medullary interstitial fluid becomes
hyperosmotic? This process involves the
operation of the countercurrent mechanism.
The countercurrent mechanism depends on the
special anatomical arrangement of the loops of
Henle and the vasa recta, the specialized
peritubular capillaries of the renal medulla. In

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the human, about 25 percent of the nephrons
arejuxtamedullary nephrons, with loops of
Henle and vasa recta that go deeply into the
medulla before returning to the cortex. Some
of the loops of Henle dip all the way to the tips
of the renal papillae that project from the
medulla into the renal pelvis. Paralleling the
long loops of Henle are the vasa recta, which
also loop down into the medulla before
returning to the renal cortex. And finally, the
collecting ducts, which carry urine through the
hyperosmotic renal medulla before it is
excreted, also play a critical role in the
countercurrent mechanism.
Q: Explain Micturition Reflex, What is Atonic
Bladder?
Answer: (Referring again to Figure in Guyton
and halls page no.309)as the Bladder fills, many

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superimposed micturition contractions begin to
appear, as shown by the dashed spikes. They
are the result of a stretch reflex initiated by
sensory stretch receptors in the bladder wall,
especially by the receptors in the posterior
urethra when this area begins to fill with urine
at the higher bladder pressures. Sensory signals
from the bladder stretch receptors are
conducted to the sacral segments of the cord
through the pelvic nerves and then reflexively
back again to the bladder through the
parasympathetic nerve fibers by way of these
same nerves. When the bladder is only partially
filled, these micturition contractions usually
relax spontaneously after a fraction of a minute, the detrusor muscles stop
contracting,
and pressure falls back to the baseline. As the
bladder continues to fill, the micturition
reflexes become more frequent and cause

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greater contractions of the detrusor muscle.
Once a micturition reflex begins, it is “self-regenerative
” That is, initial contraction of the
bladder activates the stretch receptors to cause
a greater increase in sensory impulses to the
bladder and posterior urethra, which causes a
further increase in reflex contraction of the
bladder; thus, the cycle is repeated again and
again until the bladder has reached a strong
degree of contraction. Then, after a few
seconds to more than a minute, the self-regenerative
reflex begins to fatigue and the
regenerative cycle of the micturition reflex
ceases, permitting the bladder to relax. Thus,
the micturition reflex is a single complete cycle
of (1) progressive and rapid increase of
pressure,
(2) A period of sustained pressure, and
(3) Return of the pressure to the basal tone of

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the bladder. Once a micturition reflex has
occurred but has not succeeded in emptying
the bladder, the nervous elements of this reflex
usually remain in an inhibited state for a few
minutes to 1 hour or more before another
micturition reflex occurs. As the bladder
becomes more and more filled, micturition
reflexes occur more and more often and more
and more powerfully. Once the micturition
reflex becomes powerful enough, it causes
another reflex, which passes through the
pudendal nerves to the external sphincter to
inhibit it. If this inhibition is more potent in the
brain than the voluntary constrictor signals to
the external sphincter, urination will occur. If
not, urination will not occur until the bladder
fills still further and the micturition reflex
becomes more powerful. Facilitation or
Inhibition of Micturition by the Brain .The

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micturition reflex is a completely autonomic
spinal cord reflex, but it can be inhibited or
facilitated by centers in the brain. These
centers include
(1) Strong facilitative and inhibitory centers in
the brain stem, located mainly in the pons, and
(2) several centers located in the cerebral
cortex that are mainly inhibitory but can
become excitatory. The micturition reflex is the
basic cause of micturition, but the higher
centers normally exert final control of
micturition as follows:
1. The higher centers keep the micturition
reflex partially inhibited, except when
micturition is desired.
2. The higher centers can prevent micturition,
even if the micturition reflex occurs, by
continual tonic contraction of the external
bladder sphincter until a convenient time

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presents itself.
3. When it is time to urinate, the cortical
centers can facilitate the sacral micturition
centers to help initiate a micturition reflex and
at the same time inhibit the external urinary
sphincter so that urination can occur.
Voluntary urination is usually initiated in the
following way: First, a person voluntarily
contracts his or her abdominal muscles, which
increases the pressure
in the bladder and allows extra urine to enter
the bladder neck and posterior urethra under
pressure, thus stretching their walls. This
stimulates the stretch receptors, which excites
the micturition reflex and simultaneously
inhibits the external urethral sphincter.
Ordinarily, all the urine will be emptied, with
rarely more than 5 to 10 milliliters left in the
bladder

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(Reference Guyton and halls text book of
medical physiology vol.1 page no.309-310.)
Q: Define Filtration Coefficient and
Filtration. Give their normal value.
Enumerate factors which affect Glomerular
Filtration Rate?
Ans:Filtration co-efficient (Kf): It is measure of the product of
the hydraulic conductivity and surface area of the
glomerular capillaries.
Formula of filtration co-efficient:
Kf=GFR/Net filtration pressure
Filtration: Filtration is commonly the mechanical or
physical operation which is used for the separation of
solids from fluids (liquids or gases) by interposing a
medium through which only the fluid can pass.
Normal values:
Normal GFR=125ml/min
Net Filtration Pressure=10mmHg

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So, Normal Kf is 125/10=12.5ml/min/mmHg
So Kf is 12.5 ml/min/mmHg
Factors which affect GFR:
1. Glomerular Hydrostatic pressure: (Normal value
60mmHg).if increased can cause increase in GFR.And vice
versa.
2. Glomerular Colloid Osmotic Pressure: (Normal
32mmHg).This factor is inversely proportional to GFR.
3 Bowman’s Capsule Pressure (Normal18mmHg) this
factor is also inversely proportional to the GFR.
4 Bowman’s Colloid Osmotic Pressure it is normally
zero.
Question: What is role of urea in hyperosmotic
renal medullary interstitium and concentration of
the Urine?
Answer: Urea is an excretory product of the body. But it
also plays an important role in concentrating the renal
medullaryinterstitium through the recirculating process
which produces concentrated urine when there is short

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supply of water. The urea is absorbed and secreted in the
kidney tubules. The reabsorption takes place in the
medullary collecting tubules by the UT-1 and Ut-3
transportors.into the medullary interstitium. The urea is
concentrated in the tubular fluid by the reabsorption of
water in the ascending loop of Henle, DCT,and cortical
collecting tubules. It increases the concentration of urea
in the tubular fluid which then diffuses thru the UT1 and
UT3 transporters by concentration gradient mechanism.
Making the kidney interstitium hyperosmolar. While
some of the urea in the medullary interstitium in
secreted in the thin part of loop of Henle by UT2
transporter in the tubules.so in this way urea is excreted
in addition to make the kidney interstitium
hyperosmolar. The Hormone ADH is responsible for the
UT3 opening and the reabsorption of water in from the
tubules in order to concentrate the urine so in conditions
when there is less availability of water ADH is secreted
which reabsorbs water and also makes kidney

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interstitium more hyperosmolar for the purpose of
concentrating the urine.
(Reference Guyton and halls text book of medical
physiology vol.1 page no.350-351.)
Q: what are features of METABOLIC ACIDOSIS?
How is it compensated?
Answer: features of METABOLIC ACIDOSIS:
Metabolic acidosis can result from several general causes
(1) Failure of the kidneys to excrete metabolic acids normally
formed in the body,
(2) Formation of excess quantities of metabolic acids in the
body,
(3) Addition of metabolic acids to the body by ingestion or
infusion of acids
(4) Loss of base from the body fluids, which has the same effect
as adding an acid to the body fluids.
(5) Renal Tubular Acidosis. This type of acidosis results
from a defect in renal secretion of H+ or in reabsorption of

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HCO3 or both.
(6) Diarrhea. Severe diarrhea is probably the most frequent
Cause of metabolic acidosis. The cause of this acidosis is the
loss of large amounts of sodium bicarbonate into the feces.
(7) Diabetes Mellitus: With severe diabetes mellitus, blood
acetoacetic acid levels can rise very high, causing severe
metabolic acidosis.
(8)Ingestion of acids
(9)Chronic Renal Failure
Note (write names only if marks distribution is less for this
question)
TREATMENT OF ACIDOSIS (COMPENSTAION OF ACIDOSIS):
To neutralize excess acid, large amounts of sodium
Bicarbonate can be ingested by mouth. The sodium bicarbonate
is absorbed from the gastrointestinal tract into the blood and
increases the bicarbonate portion of the bicarbonate buffer
system, thereby increasing pH toward normal. Sodium
bicarbonate can also be infused intravenously, but because of the
potentially dangerous physiologic effects of such treatment,

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other substances are often used instead, such as sodium lactate
and sodium gluconate. The lactate and gluconate portions of the
molecules are metabolized in the body, leaving the sodium in
the extracellular fluid in the form of sodium bicarbonate and
thereby increasing the pH of the fluid toward normal.
Q: Define renal threshold. How is glucose
reabsorbed in the renal tubules? What is the
normal values of transport maximum for
glucose?
Answer: Renal Threshold:
The renal threshold is the concentration of a
substance dissolved in the blood above which
the kidneys begin to remove it into the urine.
When the renal threshold of a substance is
exceeded, reabsorption of the substance by the
proximal renal tubuli is incomplete;
consequently, part of the substance remains in
the urine. The rate at which each of these

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substances is filtered is calculated as
Filtration = Glomerular filtration rate (multiply
by) Plasma concentration
This calculation assumes that the substance is
freely filtered and not bound to plasma
proteins. For example, if plasma glucose
concentration is 1 g/L, the amount of glucose
filtered each day is about 180 L/day multiply by
1 g/L, or 180 g/day. Because virtually none of
the filtered glucose is normally excreted, the
rate of glucose reabsorption is also 180 g/day
Glucose (g/day):
1. Amount filtered=180
2. Amount Reabsorbed =180
3. Amount excreted=0
4. % of filtered Load Reabsorbed=100
Q: Give a summary of functions of Kidneys?
Answer: Kidneys perform a number of functions as
follows:

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1. Role in excretion: it excretes urea, creatinine,
metabolites, drugs, toxins
2. Regulations of Ions and Urea: kidneys absorbs as
well as excretes many ions like Na, K, Ca, and PO4 in
its tubules.
3. Acid base balance: kidney through phosphate
buffer helps the body to resist any change in the pH
of the body.
4. Synthetic functions: it produces 1, 25
dihydroxycholecalciferol (activated vitamin D).
5. Homeostasis of water: it conserves water when
blood water level is low and vice versa.
6. Regulation of Blood pressure and Blood Volume:
kidneys have 100% gain in correcting the change in
the blood pressure by controlling the water level.
7. Renin Secretion. Macula Densa cells of kidney
secrete renin which is involved in renin angiotensin
system in controlling of GFR.
8. Erythropoietin Secretion: During hypoxia the

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kidneys secrete this erythropoietin which causes
thehaemopoitic stem cells to produce a lot of RBCs.
Q: A man drinks about 01 liter of
water in 10 minutes. What changes
occur in his water and electrolyte
balance?
Answer: When there is a large excess
of water in the body, the kidney can
excrete as much as 20Lday of dilute
urine. With a concentration of as low
as 50 mOsm/L.
After the ingestion of 1 Liter of water
the urine volume reaches up to six
times normal within 45 minutes after
the water has been drunk. However
the total amount of solute excreted
remains relatively constant because
urine formed becomes very dilute

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and urine osmolarity decreases from
600 to about 100 mOsm/L. Thus, after
ingestion of excess water, the kidney
rids the body of the excess water but
does not excrete excess amounts of
solutes. When the glomerular filtrate is
initially formed, its osmolarity is about
the same as that of plasma (300
mOsm/L). To excrete excess water, it is
necessary to dilute the filtrate as it
passes along the tubule. This is
achieved by reabsorbing solutes to a
greater extent than water.
Tubular Fluid Remains Isosmotic in the
Proximal Tubule:
As fluid flows through the proximal
tubule, solutes and water are
reabsorbed in equal proportions, so little
change in osmolarity occurs; thus, the

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proximal tubule fluid remains isosmotic
to the plasma, with an osmolarity of
about 300 mOsm/L. As fluid passes
down the descending loop of Henle,
water is reabsorbed by osmosis and the
tubular fluid reaches equilibrium with
the surrounding interstitial fluid of the
renal medulla, which is very hypertonic-about
two to four times the osmolarity
of the original glomerular filtrate.
Therefore, the tubular fluid becomes
more concentrated as it flows into the
inner medulla.
Tubular Fluid Is Diluted in the Ascending
Loop of Henle:
In the ascending limb of the loop of
Henle, especially in the thick segment,
sodium, potassium, and chloride are
avidly reabsorbed. However, this portion

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of the tubular segment is impermeable
to water, even in the presence of large
amounts of ADH. Therefore, the tubular
fluid becomes more dilute as it flows up
the ascending loop of Henle into the
early distal tubule, with the osmolarity
decreasing progressively to about 100
mOsm/L by the time the fluid enters the
early distal tubular segment. Thus,
regardless of whether ADH is present or
absent, fluid leaving the early distal
tubular segment is hypo-osmotic, with
anosmolarity of only about one-third
theosmolarity of plasma.
Tubular Fluid in Distal and Collecting
Tubules Is Further Diluted in the Absence
of ADH:
As the dilute fluid in the early distal
tubule passes into the late distal

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convoluted tubule, cortical collecting
duct, and collecting duct, there is
additional reabsorption of sodium
chloride. In the absence of ADH, this
portion of the tubule is also
impermeable to water and the
additional reabsorption of solutes
causes the tubular fluid to become
even more dilute, decreasing its
osmolarity to as low as 50 mOsm/L. The
failure to reabsorb water and the
continued reabsorption of solutes lead
to a large volume of dilute urine.
To summarize, the mechanism for
forming dilute urine is to continue
reabsorbing solutes from the distal
segments of the tubular system while
failing to reabsorb water. In healthy
kidneys, fluid leaving the ascending

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loop of Henle and early distal tubule is
always dilute, regardless of the level of
ADH. In the absence of ADH, the urine is
further diluted in the late distal tubule
and collecting ducts and a large
volume of dilute urine is excreted.
(Reference Guyton and halls text book
of medical physiology vol.1 page
no.345-346.)
Q: Give a summary of functions of Kidneys?
Answer: Kidneys perform a number of
functions as follows:
1. Role in excretion: it excretes urea,
creatinine, metabolites, drugs, toxins
2. Regulations of Ions and Urea: kidneys
absorbs as well as excretes many ions like
Na, K, Ca, and PO4 in its tubules.
3. Acid base balance: kidney through
phosphate buffer helps the body to resist

[Type here]
any change in the pH of the body.
4. Synthetic functions: it produces 1, 25
dihydroxycholecalciferol (activated vitamin
D).
5. Homeostasis of water: it conserves water
when blood water level is low and vice
versa.
6. Regulation of Blood pressure and Blood
Volume: kidneys have 100% gain in
correcting the change in the blood
pressure by controlling the water level.
7. Renin Secretion. Macula Densa cells of
kidney secrete renin which is involved in
renin angiotensin system in controlling of
GFR.
8. Erythropoietin Secretion: During hypoxia
the kidneys secrete this erythropoietin
which causes the haemopoitic stem cells to
produce a lot of RBCs.

[Type here]
Q: Define Filtration Coefficient and
Filtration. Give their normal value.
Enumerate factors which affect
Glomerular Filtration Rate?
Answer:
Filtration co-efficient (Kf): It is measure of
the product of the hydraulic conductivity
and surface area of the glomerular
capillaries.
Formula of filtration co-efficient:
Kf=GFR/Net filtration pressure
Normal GFR=125ml/min
Net Filtration Pressure=10mmHg
So, Normal Kf is 125/10=12.5ml/min/mmHg
So Kf is 12.5 ml/min/mmHg
Filtration: Filtration is commonly the mechanical or
physical operation which is used for the separation of

[Type here]
solids from fluids (liquids or gases) by interposing a
medium through which only the fluid can pass.
Factors which affect GFR:
1. Glomerular Hydrostatic pressure: (Normal
value 60mmHg).if increased can cause
increase in GFR.And vice versa.
2. Glomerular Colloid Osmotic Pressure:
(Normal 32mmHg).This factor is inversely
proportional to GFR.
3. Bowman’s Capsule Pressure:
(Normal18mmHg) this factor is also inversely
proportional to the GFR.
4. Bowman’s Colloid Osmotic Pressure: it is
normally zero.
Question: What is role of urea in
hyperosmotic renal medullary interstitium
and concentration of the Urine?
Answer: Urea is an excretory product of the
body. But it also plays an important role in

[Type here]
concentrating the renal medullary
interstitium through the recirculating
process which produces concentrated
urine when there is short supply of water.
The urea is absorbed and secreted in the
kidney tubules. The reabsorption takes
place in the medullary collecting tubules by
the UT-1 and Ut-3 transportors.into the
medullaryinterstitium. The urea is
concentrated in the tubular fluid by the
reabsorption of water in the ascending
loop of Henle, DCT,and cortical collecting
tubules. It increases the concentration of
urea in the tubular fluid which then diffuses
thru the UT1 and UT3 transporters by
concentration gradient mechanism.
Making the kidney interstitium
hyperosmolar. While some of the urea in
the medullary interstitium in secreted in the

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thin part of loop of Henle by UT2 transporter
in the tubules.so in this way urea is excreted
in addition to make the kidney interstitium
hyperosmolar. The Hormone ADH is
responsible for the UT3 opening and the
reabsorption of water in from the tubules in
order to concentrate the urine so in
conditions when there is less availability of
water ADH is secreted which reabsorbs
water and also makes kidney interstitium
more hyperosmolar for the purpose of
concentrating the urine.
(Reference Guyton and halls text book of
medical physiology vol.1 page no.350-351.)
Q. NAME FOUR ENDOCRINE FUNCTIONS OF KIDNEY. WHAT IS THE ROLE OF
KIDNEY IN CALCIUM ION HOMEOSTASIS?
ANSWER
1. Kidney secreted erythropoietin which stimulates the production of red
blood cells by hematopoietic stem cells in bone marrow.

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2. The kidneys produce active form of vitamin D, 1, 25-dihydroxyvitamin
D3 (calcitriol) this is essential for normal calcium deposition in bone.
3. Kidneys secreted thrombopoietin, a glycoprotein, stimulates
production of platelets.
4. Kidneys secreted prostaglandins PGA2 and PGE2 that decreases blood
pressure.
CALCIUM ION HOMEOSTASIS
Calcium is both filtered and reabsorbed in kidneys but not secreted
Renal calcium excretion = Calcium filtered – Calcium reabsorbed
When calcium ion concentration falls below normal parathyroid glands are
stimulated to promote increase secretion of PTH it regulates plasma
calcium concentration by stimulating activation of vitamin D.
50% of plasma calcium can be filtered and 99% of it is reabsorbed by
tubules
PROXIMAL TUBULAR CALCIUM REABSORPTION
Most of calcium reabsorption in proximal tubules through paracellular
pathway only 20% of calcium reabsorption through transcellular pathway
FIG 29-12 Page 368
LOOP OF HENLE AND DISTAL TUBULE CALCIUM REABSORPTION
It is restricted to thick ascending limb. 50% through the paracellular route
and remaining 50% through transcellular pathway. In distal tubule it is
entirely by active transport through the cell membrane.

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q. A 60 YEAR MALE WHO IS KNOWN CASE OF DIABETES AND
HYPERTENSION FOR A LONG TIME PRESENTS WITH GENERALIZED OEDEMA,
NAUSEA, VOMITING, MENTAL DETERIORATION, CONFUSION AND SUDDEN
COLLAPSE PASSING ON TO DEEP COMA, LAB INVESTIGATION REVAEL:
BUN(BLOOD UREA NITROGEN) = high, SERUM CREATININE= high PH= high
7.2
A) WHAT IS THE MOST LIKELY DIAGNOSIS OF THIS ALMOST TERMINAL
CONDITION OF THE PATIENT?
Chronic renal failure
B) HOW HAS THE PHYSIOLOGY BEEN CHANGED BY THIS DISORDER?
Generalized edema due to water and salt retention because of
hypertension.
Uremia that is increase in urea and other non proteinnitrogens such
as creatinine these are the end products of protein metabolism must
be removed by the body but the concentration rises due to reduction
in functional nephrons so the typical symptoms of uremia nausea ,
vomiting , mental deterioration confusion.
Kidney fails to function , acids accumulate in body fluids the buffers of
body fluids can normally buffer 500 to 1000 millimoles of acids and

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phosphate compounds in bones can buffer additional few thousand
millimoles of acids when this buffering power used up blood ph falls
and patient will become comatose and die if ph falls below about 6.8.
QWHAT ARE THREE LINES OF DEFENCE AGAINST CHANGES IN H+ ION
CONCENTRATION OF BODY FLUIDS?
ANSWER
1. Acid base buffer system
2. Respiratory system
3. Renal system
HOW KIDNEYS REGULATE EXTRACELLULAR FLUID HYDROGEN
CONCENTRATION?
ANSWER
Kidneys control extracellular fluid hydrogen ion concentration by excreting
either an acidic urine or basic urine. Large number of HCO3- are filtered
continuously into tubules if they are excreted into urine this removes base
from blood. Large number of H+ are also secreted into tubular luman by
tubular epithelial cells thus removing acid from blood.
If more H+ are secreted than HCO3- is filtered there will be a loss of acid
from extracellular fluid if more HCO3- is filtered than H+ secreted there will
be a net loss of base.

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Kidneys regulate extracellular fluid H+ concentration through three
fundamental mechanisms
1. Secretion of H+
2. Reabsorption of filtered HCO3-
3. Production of new HCO3-
Hydrogen ion secretion and HCO3- reabsorption occur in all parts except
descending and ascending thin limbs of loop of henle
H+ is secreted by secondary active transport in early tubular segments.
Fig 30-5
Filtered HCO3- cannot be reabsorbed directly it is reabsorbed by a
process in which it first combines with H+ to form H2CO3 which
eventually become CO2 and H2O fig 30-5
Excretion of excess H+ and generation of new HCO3- by ammonia buffer
system fig 30-9
Reference by GUYTON and HALL
Q. DRAW AND LABLE JUXTAGLOMERULAR APPARATUS.
ANSWER
Figure 26-18 page 320
Reference by medical physiology guyton and hall
Q. HOW MACULA DENSA FEEDBACK MECHANISMS HELP AUTOREGULATE
GFR DURING DECREASED ARTERIAL PRESSURE?

Physiology MBBS part 2 solved paper uhs

Physiology MBBS part 2 solved paper uhs

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