PHYSIOLOGY UHS PAST PAPERS (SOLVED) 2004-2012

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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 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

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.

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? 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 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. 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 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 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. 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: 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 , 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? (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? 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 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 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 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: 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 HEART MUSCLES coronaries Increased Rate Increased Force of contraction Dilated(beta 2),Constricted(alpha) LUNGS Bronchi Blood vessels GUT LUMEN Sphincters Dilated Mildly Constricted Decreased peristalsis and tone Increased Tone EFFECT

Liver gallbladders & bile duct kidney Bladder detrusor muscle trigone

Glucose released Relaxed Decreasd urine output and increased renin secretion

Relaxed 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 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 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: i)-Planning and fine tunning of skeletal muscle contraction ii)-Maintainance of posture and performance of voluntary muscles Features of cerebellar diseases: i)-Dysmetria and ataxia ii)-Past pointing and dysdiadochokinesia 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 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 intrafusal 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 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

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

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 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 Heart Muscle Coronaries

EFFECT Increased Rate Increased Force of contraction Dilated(beta 2),Constricted(alpha)

Lungs Bronchi Blood Vessels Gut Lumen Sphincter Liver Gallbladder and bile ducts Decreased peristalsis and tone Increased Tone Glucose released Relaxed Dilated Mildly Constricted

Kidney Bladder Detrusor Trigone Penis Fat cells

Decreasd urine output and increased renin secretion Relaxed Contracted Ejaculation lipolysis

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 spinothalamic tracts 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 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. 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: i)-Dysmetria and ataxia ii)-Past Pointing iii)-Dysdiadochokinesia iv)-Dysarthia v)-Intention tumor 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 Heart Muscle Coronaries Increased Rate Increased Force of contraction Dilated(beta 2),Constricted(alpha) Lungs Bronchi Blood Vessels Gut Lumen Sphincter Liver Gallbladder and bile ducts Decreased peristalsis and tone Increased Tone Glucose released Relaxed Dilated Mildly Constricted EFFECT

Kidney Bladder Detrusor Trigone Penis Fat cells Basal metabolism

Decreasd urine output and increased renin secretion Relaxed Contracted Ejaculation lipolysis Increased upto 100%

Adrenal medullary Secretion incresed Mental activity Piloerector muscles incresed contraction

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. 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 spinothalamic tracts 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 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-Mr.J of 58 years age with reting tremors of hand and lips consulted his family doctor.On examination he was found to 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 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 Lungs Brochi Blood vessels Gut Lumen Sphincter Liver Gallbladder and bile ducts Bladder Detrusor Trigone

EFFECT

Constricted Dilated Increased Peristalsis and tone Relaxed Slight glycogen synthesis Contracted

Contracted Relaxed

Eye Pupil Ciliary Muscle Penis Glands Nasal,lacrimal,parotid, submandibular,gastric,pancreatic

Contracted Contracted erection Stimulation of copious secretion

Annual 2009 Q-Enlist 8 functions of the body controlled by brainstem? Ans:Functions 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? 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? 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: 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 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 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 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? 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? 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 spinothalamic tracts 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 of same side EFFECT BELOW THE LEVEL OF LESION: On the same side: Sensory Loss: 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. 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 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: i)-Planning and fine tunning of skeletal muscle contraction ii)-Maintainance of posture and performance of voluntary muscles Features of cerebellar diseases: i)-Dysmetria and ataxia ii)-Past pointing and dysdiadochokinesia 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. 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. 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  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 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 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) 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 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. 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.  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

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) 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 =>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 =>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 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 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 -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 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)} 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 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 corticotropinreleasing 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 ? 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. 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. 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 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) 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 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
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 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

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

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

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 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 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 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.

Q. EXPLAIN COUNTER CURRENT CONCENTRATION OF URINE? ANSWER There are three steps

MULTIPLIER

MECHANISM

FOR

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 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 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

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. 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 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 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 greater contractions of the detrusor muscle. Once a micturition reflex begins, it is “selfregenerative ” 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 selfregenerative 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 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 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 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 (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 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 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 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 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, 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 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: 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 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 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 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 hypertonicabout 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 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 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 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 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.

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 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 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 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. 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.

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 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 CONCENTRATION? ANSWER

EXTRACELLULAR

FLUID

HYDROGEN

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. Kidneys regulate extracellular fluid H+ concentration through three fundamental mechanisms 1. Secretion of H+ 2. Reabsorption of filtered HCO33. Production of new HCO3Hydrogen 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? ANSWER The tubulogromerular feedback mechanism has two components that act together to control GFR 1. An afferent arteriolar feedback mechanism Little flow of glomerular filtrate causes decreased sodium and chloride concentratin at macula densa. This causes afferent arteriolar dilatation this allows increase blood flow which increases glomerular pressure and increases the GFR back towards normal 2. An efferent arteriolar feedback mechanism Low GFR causes excess reabsorption of sodium and chloride ion in ascending limb, reducing ion concentration at macula densa this causes juxtaglomerular cells to release rennin and formed angiotensin 2 this causes constriction of efferent arterioles which causes increase pressure in glomerulus to rises GFR. Figure 26-19 Q. DEFINE GLOMERULAR FILTERATION RATE GFR.

ANSWER Quantity of glomerular filtrate formed each minute in all nephrons of both kidneys is called glomerular filtration rate. GFR = Filtration pressure * Filtration co-efficient 125ml/min or 180 lt/day Q. ENLIST THE DETERMINENTS OF GFR. ANSWER It is determined by 1. Hydrostatic and colloid osmotic forces across glomerular membrane 2. Glomerular capillary filtration co-efficient GFR = Kf * Net filtration pressure Net filtration pressure represents the sum of hydrostatic and colloid osmotic forces. 1. Glomerular hydrostatic pressure Pg which promotes filtration 2. Hydrostatic pressure in bowman’s capsule Pb outside capillary which opposes filtration 3. Colloid osmotic pressure of glomerular capillary plasma proteins which opposes filtration 4. Colloid osmotic pressure of proteins in bowman’s capsule which promotes filtration GFR = Kf * (Pg – Pb – Forces Favoring Filtration (mmhg)

Glomerular hydrostatic pressure Bowman’s capsule colloid osmotic pressure Forces Opposing Filtration (mmhg) Bowman’s capsule hydrostatic pressure

60 0

18

Glomerular capillary colloid osmotic pressure 32 Net filtration pressure = 60-18-32 = +10 mmhg INCREASING FACTORS 1. 2. 3. 4. Increase renal blood flow Increase glomerular pressure Increase blood pressure Efferent arteriolar constriction

DECREASING FACTORS 1. 2. 3. 4. Increase plasma colloid osmotic pressure Increase bowman’s capsule pressure Afferent arteriolar constriction Sympathetic stimulation

Q. DRAW CYSTOMETROGRAM. ANSWER Figure 26-8 Page 309 Reference by medical physiology GUYTON and HALL

Q. ENLIST THE ABNORMALITIES OF MICTURATION WITH A REASON FOR EACH. ANSWER 1. ATONIC BLADDER Micturation reflex can not occur if the sensory nerve fibers from the bladder to spinal cord are destroyed, preventing the transmittion of stretch signals from bladder common cause of atonic bladder is crush injury to the sacral region of spinal cord.

2. AUTOMATIC BLADDER If the spinal cord is damaged above the sacral region but the spinal cord segments are still intact, typical micturatuon reflex can not occur

3. UNINHIBITED NEUROGENIC BLADDER It is also called as spastic neurogenic bladder or hyperactive neurogenic bladder. This condition derives from partial damage in the spinal cord or the brain stem that interrupts most of the inhibitory signals

4. NOCTURNAL MICTURATION It is the involuntary voiding of urine during night it is also known as enuresis or bed wetting. It occurs due to the absence of voluntary control of micturation.

Q. DEFINE a) FILTRATION FRACTION Fraction of renal plasma flow that is filtered. It is calculated as follow FILTRATION FRACTION = GFR/ RENAL PLASMA FLOW It is about 20% of the plasma flowing through the kidney. b) FILTRATION CO-EFFICIENT GFR in both kidneys per mmhg of filtration pressure is called filtration coefficient. FILTRATION CO-EFFICIENT = GFR / FILTRATION PRESSURE It is 12.5 ml / min / mmhg c) WHAT IC MICTURATION REFLEX? Micturation is a process by which the urinary bladder empties when it becomes filled As the bladder fills many superimposed micturation contractions begin to appear these are the result of stretch reflex initiated by sensory stretch receptors in the bladder wall especially by the receptors in posterior urethra. Steps of micturation reflex are Filling of urinary bladder ↓ Stimulation of stretch receptors ↓

Afferent impulses via pelvic nerve ↓ Sacral segment of spinal cord ↓ Efferent impulses via pelvic nerve ↓ Contraction of detrusor muscle and relaxation of internal sphincter ↓ Flow of urine into urethra and stimulation of stretch receptors ↓ Afferent impulses via pelvic nerve ↓ Inhibition of pudendal nerve ↓ Relaxation of external sphincter ↓ Voiding of urine Once a micturation reflex begins it is self regenerative. This cycle repeats itself again and again until the bladder has reached a strong degree of contraction then after a few seconds to more than a minute the reflex

begins to fatigue and the regenerative cycle of micturation reflex ceases allowing rapid reduction in bladder contractions.

Q. DEFINE METABOLIC ACIDOSIS Acidosis resulting from excess accumulation of metabolic or fixed acids is called metabolic acidosis. It causes a decrease in the ratio ofHCO3 to H+ in renal tubular fluid.

Q. WHAT IS THE ROLE OF ANTIDIURETIC HARMONE ADH IN MECHANISM OF CONCENTRATED URINE FORMATION? ANSWER In presence of ADH, late distal tubule, cortical collecting tubule and collecting duct become permeable to water. So water is reabsorbed by osmosis from these tubules into madullaryinterstitium due to its hyper osmolality . Thus urine contains less water and becomes concentrated. Q. WHAT ARE THE VARIOUS BUFFER SYSTEMS IN BLOOD? 1) Bicarbonate buffer system 2) Phosphate buffer system 3) Proteins buffer system

Q. A MAN OF 40 YEARS HAS SPINAL CORD DAMAGE ABOVE SACRSL REGION

A) WHICH TYPE OF ABNORMALITY OF MICTURATION THE MAN IS LIKELY TO HAVE Automatic bladder B) WHAT ARE THE FEATURES OF THIS ABNORMALITY? Durin the first stage after the damage to spinal cord because the state of spinal shock micturation reflexes are suppressed caused by sudden loss of facilitative impulses from the brain stem and cerebrum Urinary bladder loses the tone and becomes atonic resulting in overflow incontinence During the second stage after shock period micturation reflex returns however the voluntary control is lacking There is hypertrophy of detrusor muscle so that capacity of bladder reduces Some patients develop hyperactivemicturation reflex. Q. GIVE INNERVATION OF URINARY BLADDER. Principal nerve supply of bladder is by PELVIC NERVES which connects the spinal cord through sacral plexus. Pelvic nerves are both Sensory nerve fibers Motor nerve fibers Sensory nerve fibers detect the degree of stretch in bladder wall

Motor nerves transmitted in pelvic nerves are parasympathetic fibers these terminate on ganglion cells located in wall of bladder short postganglionic nerves then innervate the detrusor muscle. Skeletal motor fibers transmitted through the pudendal nerve to external bladder sphincter Bladder receives sympathetic innervations from the sympathetic chain through the HYPOGASTRIC NERVES connecting mainly with the L2 segment of spinal cord. These sympathetic fibers stimulate mainly the blood vessels.

PREPARED BY: IMRAN ASHRAF (AIMC) AREEZA RANA (FMHC)

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