nerve & muscle 45 qs with their answer keys by dr. roomi

8/2/2019 NERVE & MUSCLE 45 Qs With Their Answer Keys by Dr. Roomi

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NERVE & MUSCLE PHYSIOLOGY-SEQs 19.5.2010

Q.1 What is END-PLATE POTENTIAL? How is it produced?

In which disease end-plate potential is of low voltage? (2+2+1 mark)

Key:

END PLATE POTENTIAL:

It is a local potential of motor end plate, i-e., the thickened muscle membrane that issupplied by a motor-neuron, thus forming a component of neuro-muscular junction.

When impulse is transmitted from motor nerve to the muscle, the impulse arriving in the

end of the motor neuron increases the permeability of its endings to calcium ions.

Calcium ions trigger exocytosis of acetylcholine containing vesicles acetylcholinediffuses to the muscle-type nicotinic acetylcholine receptors, which are concentrated at the

tops of junctional folds of the membrane of motor end plate.

Binding of acetylcholine to these receptors increased sodium & potassium conductance

of the membrane influx of sodium depolarizing potential is produced called END

PLATE POTENTIAL

The current created by this local potential depolarizes the adjacent muscle membrane to its

firing level. Purpose of EPP is to build the threshold potential (- 65 mV).If RMP is-90 mV, then threshold is -65 mV, we need 25 mV potential change.Purpose of EPP is to reach the threshold of action potential.

So voltage of EPP is much more than required, because required is only 25 mV.

It is called SAFETY FACTOR.

This is followed by removal of acetylcholine from synaptic cleft by acetylcholinesterase,present in high concentration at NMJ. Action potentials are generated on either side of end

plate conducted away from end plate in both directions along muscle fiber.

An average human end plate contains about 15 to 40 million acetylcholine receptors. Each

nerve impulse releases about 60 acetylcholine vesicles, and each vesicle contains about

10,000 molecules of neurotransmitter. This amount is enough to activate about 10 times thenumber of acetylcholine receptors needed to produce a full end plate potential.

So a propagated response in the muscle is regularly produced, and this response hides /obscures the end plate potential. However, EPP can be seen if the tenfold safety factor is


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overcome & the potential is reduced to a size that is insufficient to fire the adjacent muscle

membrane. This can be achieved by administration of small doses of curare, a drug that

competes with acetylcholine for binding to muscle-type nicotinic acetylcholine receptors.Response is then recorded only at end plate region & decreases exponentially away from it.

Under these conditions, EPPs can be shown to undergo temporal summation.

(comparison table between EPP and Action Potential has been removed as advised &

points of EPP only from the table are mentioned below)

EPP:

Local potential recorded only at End plate region.

It varies with strength of stimulus / amount of neurotransmitter released. It can show

summation.

In Myasthenia Gravis, Miniature End Plate Potentials (MEPP = 0.5 mV) are produced.

A rare auto-immune disease.

Voltage of EPP is very low (Miniature EPP) action potential is not followed. At rest

normally, a few synaptic vesicles break to liberate Ach from synaptic vesicles smallchange in EPP (about 0.5 mV) called MEPP. Amplitude varies directly with [Ca++] and

inversely with [Mg++].

Impulse fails to transmit through NMJ Severe muscle weakness & fatigue (Extra-ocular

muscles ptosis, diplopia, difficulty in Swallowing, weakness of Respiratory and Facial

muscles)

Q.2 Draw strength duration curve. Define the units of excitability & give their clinicalapplication? What is meant by Utilization Time? (2+1+1+1 marks)

Key:


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Key:

Units of excitability are Rheobase and Chronaxie.

RHEOBASE: Voltage or strength of stimulus required just to excite the tissue, e.g., 1mV.

(0.5 mark)

CHRONAXIE: A time for which a stimulus double the rheobase, when applied, just excites

the tissue, e.g., 2 mV. It is a unit of time. (0.5 mark)

Damage to nerve fiber is determined by measuring Chronaxie. Most excitable fibers have

minimum value of Chronaxie. (1 mark)

The time for which Rheobase must be applied to excite the tissue is UTILIZATION TIME.

(1 mark)

Q.3 What is Spike Potential? Why sodium ions cannot pass through potassium channels?

Give the ionic basis of Absolute Refractory Period, After Depolarization and After

Hyperpolarization. (1+1+1+1+1 mark)

Key:


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KEY:

SPIKE POTENTIAL:

Part of action potential between threshold value and beginning of after depolarization

is called Spike potential. (1 mark)

Sodium channels have highly negative charge on inside. Hydrated form of Sodium

ions is larger. Size of Potassium channels is smaller, so Sodium cannot pass throughPotassium channels. (1 mark)

Absolute refractory period includes depolarization and first 1/3 of repolarization.

Sodium inactivation gates are still closed and will not open till potential reachesresting value. (1 mark)

During repolarization, Potassium becomes accumulated on outer side of membrane

which slows down further efflux after 70% of repolarization leading to slowrepolarization called After depolarization. (1 mark)

When potential has reached the resting value, it does not stay there and becomes more

negative and called After hyperpolarization. It is because when Potassium has reached

resting value, some Potassium channels are still open and Potassium efflux continues,resulting into more negative membrane potential. (1 mark)

Q.4 What is the mechanism of action of post-synaptic neuro-muscular transmission

blockers? Classify them with examples & give their uses. (1+3+1 mark)

KEY:

MECHANISM:

They do not interfere with release of Acetylcholine but antagonize with action of

Acetylcholine. (1 mark)

Classification: 2 types:

1. Competitive: Compete with acetylcholine to bind with acetylcholine receptors on

motor end plate as they are given in large doses

no depolarization, no E.P.P

Muscle relaxes. (0.5 mark)

Examples: (1 mark)

Snake poisons (alpha Bungaro toxin in snake venom), Synthetic (Flexidyl or Galamine used in O.T) and

Natural (Detubo-curarine).

2. Depolarizing: Resemble acetylcholine in action. They bind with receptors


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depolarization of persistent nature. Only 1 nerve impulse is transmitted initial

twitching of muscle. (0.5 mark)Examples: (1 mark)

Suxamethonium, Decamethonium and Hexamethonium.

USES: (1 mark)1. Muscle relaxant in surgery.

2. Has been used in Psychotic patients in electro-convulsive therapy.

Q. 5 Give five differentiating features between unitary & multiunit type of

smooth muscle. (5 marks)

KEY: 1 mark for each.

1. LOCATION2. TYPE OF JUNCTIONS

3. ARRANGEMENT4. CONTROL

5. ACTION POTENTIAL.

1. LOCATION:

UNITARY: Wall of GIT, ureter, bile duct, uterus and large blood vessels.

MULTIUNIT: Ciliary muscle of eye, Iris of eye and pilo-erector muscle.2. TYPE OF JUNCTION:

UNITARY: Diffuse junction. No contact with nerve fiber. Neurotransmitter is

released near the fiber.MULTIUNIT: Contact junction.One of the autonomic nerves form junction withmuscle fiber and releases neurotransmitter like nor-epinephrine.

3. ARRANGEMENT:

UNITARY: Sheaths or bundles with gap junctions in between, so act as single unit.

If one part is excited whole is excited.

MULTIUNIT: Individual muscle fibers. Each fiber has insulating outer membrane

with glycoprotein and collagen consistency. Independently each muscle fiber isexcited.

4. CONTROL:

UNITARY: Mainly non-nervous stimuli (hormonal stimuli like oxytocin and

serotonin). Show spontaneous contraction.MULTIUNIT: Mainly through nervous stimuli. Does not show spontaneous

contraction.

5. ACTION POTENTIAL:UNITARY: 3 types: Spike, Plateau and Slow wave. Rhythm due to increased or

decreased pumping of sodium.

MULTIUNIT: Not required as individual muscle fibers are too small to produceaction potential. Only localized depolarization in response to excitation.


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Q.6 Two different patients present with arterial PH of 7.6 & 7.4 respectively. In whichcase tetany may be aggravated more easily & why? (1+4 marks)

Key:

In the first case (alkalosis), tetany is aggravated. (1 mark)

Because protein molecules behave as acid in alkaline pH and can donate H andbecome anions which bind positive ions (Na, K, Ca) (1 mark)

protein bound form of Ca increases & ionic form decreases (1 mark)

decreased Ca in ECF no complete closure of activation gates of Na channels atrest. (1 mark)

Na ions leak into membrane from ECF Hypopolarization (Membrane potential

becomes less negative and near to threshold) & on slight stimulation action potential

e-g., Tetany. (1 mark)

Q.7 A 30 year old lady complained of double vision (diplopia), severe muscle weakness& fatigue. She has drooping of eyelids and an enlarged shadow of thymus on

ultrasound.

a. What can be the possible diagnosis of this disturbed physiology?

b. What is the physiological basis of this pathology?

c. What positive finding do you expect in her serum examination?d. What medicine can alleviate the ladys complaints?

(1+2+1+1 mark)

Key:a. MYASTHENIA GRAVIS (1 mark)b. A rare auto-immune disease. Irreversible damage to acetylcholine receptors at

motor end plate, though acetylcholine is normally released.

Voltage of EPP is very low (Miniature EPP) action potential is not followed. At rest

normally, a few synaptic vesicles break to liberate Ach from synaptic vesicles small

change in EPP (about 0.5 mV) called MEPP.

Impulse fails to transmit through NMJ Severe muscle weakness & fatigue (Extra-

ocular muscles ptosis, diplopia, difficulty in Swallowing, weakness of Respiratory

and Facial muscles)(2 marks)

c. AUTO-ANTIBODIES against acetylcholine gated receptor channels.

(1 mark)


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d. ANTICHOLINE ESTERASES (Neostigmine or Physostigmine).

These inhibit enzyme acetylcholine esterase acetylcholine is not hydrolyzed

more acetylcholine available for available number of receptors.

(1 mark)

Q.8 Why ATP is required for muscle relaxation in an alive person?

Compare the onset of rigidity after death incase of hot and cold environmental

temperatures. Why this rigidity disappears 24 hours after death? What is thescientific name for rigidity after death, give its forensic significance?

(1+1+1+2 marks)

KEY:

Calcium pump needs ATP to pump back calcium into terminal cisternae muscle

relaxation by detachment of cross-bridges of myosin from actin.(1 mark)

Rapid onset incase of hot weather and slow incase of cold.(1 mark)

Due to autolysis of muscle proteins, resulting from hydrolytic enzymes from

lysosomes.(1 mark)

RIGOR MORTIS.Cause of death by a weapon incase of suicide, as the weapon remains in the rigid

hand as contracture develops soon after death and lasts for 16-24 hours. It also

gives some estimate of the number of hours elapsed since death.(2 marks)

Q.9 Give a brief account of fast and slow muscle fibers. (5 marks)

Key

Every body muscle is a mixture of fast & slow muscle fibers.Also are present intermediate fibers in between them.


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Significance of fast fibers:

Muscles that react rapidly are mainly composed of fast fibers, with only few slow

muscle fibers.Significance of slow fibers:

The muscles that respond slowly & have a prolonged contraction, mainly consist of

slow fibers. (1 mark)

Fast Vs Slow

muscle fibers: Fast / Large fibers.

Great strength of contraction.

Extensive sarcoplasmicreticulum (to supply calcium forcontraction).

Less blood supply (oxidativemetabolism is of secondaryimportance)

Fewer mitochondria (onlysecondary importance ofoxidative metabolism).

White muscle due to lack ofmyoglobin.

Motor unit smaller. Richernerve supply.

Slow / Smaller fibers.

Innervated by smaller nerves.

Richer blood supply to supplyextra amount of oxygen.

Increased no. of mitochondriafor high level of oxidativemetabolism.

Increased myoglobin to storeoxygen.

Red muscle due to myoglobin.

Motor unit larger.

(4 marks)

Q. 10 Compare 3 types of muscle. (5 marks)


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From Saladin


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SMOOTHSMOOTH

MUSCLEMUSCLECARDIACCARDIAC

MUSCLEMUSCLESKELETALSKELETAL

MUSCLEMUSCLE

11. Gap.. Gap. 2.2. Contact.Contact.Gap junctionsGap junctionsNo gap junctionsNo gap junctions

11.. Visceral/ UnitaryVisceral/ Unitary::

sheaths or bundlessheaths or bundles

act as a single unit.act as a single unit.

22.. MultiMulti--unit typeunit type::

Individual muscleIndividual muscle

cell is a muscle fiber.cell is a muscle fiber.

Individual cardiacIndividual cardiac

cell is not a musclecell is not a muscle

fiber, but connectedfiber, but connected

in series to form ain series to form a

muscle fiber.muscle fiber.

Individual skeletalIndividual skeletal

muscle cell is amuscle cell is a

muscle fiber.muscle fiber.

HomogeneousHomogeneous

cytoplasm, nocytoplasm, nocrosscross--striationsstriations

CrossCross--striatedstriatedCrossCross--striatedstriated

InvoluntaryInvoluntaryInvoluntaryInvoluntaryVoluntaryVoluntary

SMOOTHSMOOTH



MUSCLEMUSCLE


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FewerFewer

mitochondria.mitochondria.

MostlyMostlyglycolyticglycolyticmetabolism.metabolism.

More mitochondriaMore mitochondria

(25% mass). Major(25% mass). Major

source of energy issource of energy isfat (60%) at rest.fat (60%) at rest.

Few mitochondria.Few mitochondria.

Major source of energyMajor source of energy

is CHO.is CHO.

GlycolysisGlycolysis Citric acidCitric acid

cycle.cycle.

In some placesIn some places

(intestine), randomly(intestine), randomly

distributed thick &distributed thick &

thin filamentsthin filaments

interdigitateinterdigitate..

Intercalated discs /Intercalated discs /

gap junctions are atgap junctions are at

the level of Zthe level of Z

membranes. (membranes. (DiadDiad))

Triad is at theTriad is at the

junction of A & Ijunction of A & I

bands.bands.

Single centralSingle central

nucleus.nucleus.Single centralSingle central

nucleus.nucleus.Multiple peripheralMultiple peripheral

nuclei.nuclei.

SMOOTHSMOOTH



MUSCLEMUSCLE

FewerFewer

mitochondria.mitochondria.

MostlyMostlyglycolyticglycolytic

metabolism.metabolism.

More mitochondriaMore mitochondria

(25% mass). Major(25% mass). Major

source of energy issource of energy is

fat (60%) at rest.fat (60%) at rest.

Few mitochondria.Few mitochondria.

Major source of energyMajor source of energy

is CHO.is CHO.

GlycolysisGlycolysis Citric acidCitric acid

cycle.cycle.

In some placesIn some places(intestine), randomly(intestine), randomly

distributed thick &distributed thick &

thin filamentsthin filaments

interdigitateinterdigitate..

Intercalated discs /Intercalated discs /gap junctions are atgap junctions are at

the level of Zthe level of Z

membranes. (membranes. (DiadDiad))

Triad is at theTriad is at thejunction of A & Ijunction of A & I

bands.bands.

Single centralSingle central

nucleus.nucleus.Single centralSingle central

nucleus.nucleus.Multiple peripheralMultiple peripheral

nuclei.nuclei.

SMOOTHSMOOTH



MUSCLEMUSCLE


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Visceral:Visceral: Refractory period isRefractory period ismore than in Skeletalmore than in Skeletal

muscle.muscle.

CanCant bet betetanizedtetanized..Longer R.P. (300Longer R.P. (300millimilli--sec)sec)

Can beCan betetanizedtetanized. Shorter. Shorterrefractory period. (2refractory period. (2--33

millisecmillisec))

Visceral:Visceral:3 types of3 types ofaction potential:action potential:

Spike, plateau & slowSpike, plateau & slowwave (rhythm due towave (rhythm due to

increased or decreasedincreased or decreased

pumping of sodium).pumping of sodium).

Slow transmission.Slow transmission.

Prolong contraction.Prolong contraction.

MultiMulti--unitunit:: localizedlocalized

depolarization. Smalldepolarization. Small

fibers,fibers,Ac.PotAc.Pot. not reqd.. not reqd.

(Up to 60 mV).(Up to 60 mV).

Action potentialAction potential

with plateau.with plateau.

(Up to +20 mV(Up to +20 mVovershoot).overshoot).

Latch mechanism.Latch mechanism.

ProlongedProlonged

contraction.contraction.

SlowSlowATPaseATPase

activity in Myosinactivity in Myosin

head.head.

Spike potential.Spike potential.

(Amplitude up to(Amplitude up to

120 mV).120 mV).

Quick transmissionQuick transmission

of impulse alongof impulse along

sarcolemmasarcolemma.. LessLess

duration ofduration of

contraction.contraction.

ATPaseATPaseactivity notactivity not

so slow.so slow.

SMOOTHSMOOTH



MUSCLEMUSCLE

Visceral:Visceral: ShowShow

spontspont.. contraccontrac..

Stress & reverseStress & reverse

stress relaxation.stress relaxation.

MultiMulti--unitunit:: Nervous.Nervous.

Not spontaneous.Not spontaneous.

Automaticity &Automaticity &

RhythmicityRhythmicity..No automaticity.No automaticity.

NoNo rhythmicityrhythmicity..

Visceral:Visceral: like Cardiaclike Cardiac

Muscle.Muscle.

MultiMulti--unitunit:: likelikeSkeletal Muscle.Skeletal Muscle.

FunctionalFunctional

syncitiumsyncitiumas aas a

whole.whole.

As a whole obeysAs a whole obeys

All or none law.All or none law.

One muscle fiber isOne muscle fiber is

aasyncitiumsyncitium..

Single fiber obeysSingle fiber obeysAll or none law.All or none law.

SMOOTHSMOOTH



MUSCLEMUSCLE


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Examples:Examples:

Visceral:Visceral:

. Wall of GIT,. Wall of GIT, ureterureter,,

bile duct, uterus,bile duct, uterus,

large Blood Vesselslarge Blood Vessels

MultiMulti--unit:unit:

CiliaryCiliarymuscle, iris,muscle, iris,

pilopilo--erector.erector.

Example:Example:

Heart muscle inHeart muscle in

thorax.thorax.

Examples:Examples:

Muscles coveringMuscles covering

the bones of limbs.the bones of limbs.

Intermediate.Intermediate.MoreMoremyoglobinmyoglobin..

More glycogen.More glycogen.More blood supply.More blood supply.

LessLessmyoglobinmyoglobin..

Less glycogen.Less glycogen.Less blood supply.Less blood supply.

SMOOTHSMOOTH



MUSCLEMUSCLE

11. Short notes:

a. Summation of synapse

b. Post tetanic facilitation. (2.5 +2.5 marks)

2 TYPES OF SUMMATION2 TYPES OF SUMMATION::

TEMPORALTEMPORAL

Impulses transmit throughImpulses transmit through11or few synaptic knobsor few synaptic knobsrepeatedlyrepeatedly effects on posteffects on post--synaptic neurons are addedsynaptic neurons are added stimulation.stimulation.

Second stimulus must fallSecond stimulus must fallwhen effect of 1when effect of 1stst one is stillone is still

there.there. JO PATHAR PAY PANIJO PATHAR PAY PANI

PARAY MUTTASIL, TOPARAY MUTTASIL, TOBAY SHUBA GHIS JAAYBAY SHUBA GHIS JAAYPATHAR KI SIL!PATHAR KI SIL!

SPATIALSPATIAL

Impulses are conductedImpulses are conductedalong aalong anumber ofnumber ofsynapses simultaneouslysynapses simultaneously effects oneffects onpostsynaptic neuron arepostsynaptic neuron are

addedadded

excitation.excitation.MOUJ HAY DARYAMOUJ HAY DARYAMEIN OR BAYROONMEIN OR BAYROONA DARYA KUCHA DARYA KUCHNAHIN!!NAHIN!!


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b. Post tetanic facilitation.

POSTPOST--TETANIC FACILITATIONTETANIC FACILITATION

OR POTENTIATIONOR POTENTIATION:: ((Rest is best for testRest is best for test!)!)

If impulses are conducted through a synapse rapidlyIf impulses are conducted through a synapse rapidlythen rest is given to synapsethen rest is given to synapse then again impulses arethen again impulses areconductedconducted response of postresponse of post--synaptic neuron issynaptic neuron isincreased.increased.

Calcium ions enter in synaptic knob in eachCalcium ions enter in synaptic knob in eachtransmission, before fatigue occurstransmission, before fatigue occurs increase no. ofincrease no. ofcalcium accumulate in knobcalcium accumulate in knobmore neurotransmittermore neurotransmitter

releasedreleased

more EPSPmore EPSP.. After fatigueAfter fatigue if rest is givenif rest is givenmore calcium ionsmore calcium ions

become availablebecome available facilitation.facilitation.

12. Write a note on Wallerian Degeneration. (5 marks)

Changes in distal stump of injured nerve: (2 marks)

Axon & myelin sheath completely degenerate (secondary / Wallerian

degeneration).

Simultaneous degeneration throughout length of nerve fiber.

Changes appear in 24 hrs & complete in 3 wks.

Continued conduction for 3 days post injury.

After 5th day all function is stopped.


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HISTOLOGICAL CHANGES IN DEGENERATION OF NERVE:

Axoplasm breaks up into short segments.

Swelling of neurofibrils become tortuous & disappear after sometime.

Within few days, space containing axoplasm shows only a little debris.

Myelin sheath disintegrates fat droplets appear (8th to 32nd day).

Lecithin molecules present in myelin sheath completely hydrolyzed to glycerol,

fatty acids, phosphoric acid & choline removed by increased number ofmacrophages (appearing as foam cells due to their high lipid content) or by bloodstream.

Endoneurium remains intact within endoneurial tubes.

Schwann cells proliferate & their increased number along with fibrous tissue

false neuroma. (True neuroma in regeneration)

(3 marks)


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Q. 13 Define REFRACTORY PERIOD and its types. What is its mechanism? Give

the normal value of ABSOLUTE REFRACTORY PERIOD of skeletal

muscle?

(2+2+1 mark)

Key: Definition: During the local response, threshold is lowered, but during the rising &

much of the falling phases of spike potential, neuron is refractory to stimulation. This is

called refractory period.

Mechanism: Ionic basis is given:

2 types:

Absolute : During depolarization & first 1/3 of repolarization. Here sodium

inactivation gates are still closed & will not open till potential reaches resting value.

Relative : From end of first 1/3 of repolarization to the beginning of after

depolarization. (here stronger stimulus can produce action potential).

Normal value of absolute refractory period of skeletal muscle: 2-3 msec.

(Normal value of absolute refractory period of ventricular muscle: 200-300 msec)

Q.14 A hyperventilating young girl of 20 years reports to her physician with a

typical position of the hand at the wrist due to spasm of muscles. An I/V

injection of a calcium salt results in remarkable improvement of the girls

condition.

a. What is the technical name given to this condition of the girl?

b. Why was calcium so effective?

c. What is the role of calcium in muscle contraction? (1+2+2 marks)

Key:

a. TROUSSEAUS SIGN: A spasm of muscles of the upper extremity thatcause flexion of the wrist & thumb with extension of fingers. It is a sign

of tetany.

b. Sign of Tetany was manifested due to hypocalcemia.Hypocalcemiaincreased excitability of nervous tissue.

Calcium (normal levels) stabilizes the membrane:

Inner side of sodium channels is highly negatively charged.Calcium ions from ECF bind with negative inner surface of sodium channels

complete closure of activation gates of these channels at rest.

Decreased calcium in ECF no complete closure of activation gates of sodium

channels at rest sodium ions leak into membrane from ECF hypo-polarization

(membrane potential becomes less negative & near to threshold) &

on slight stimulation action potential (tetany).


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c. Calcium is needed by skeletal muscle for coupling of excitation with

contraction. Action potential enters deep into muscle fiber from T-Tubulesaround which are terminal cisternae.

So depolarization spreads from T Tubules terminal cisternae.

Membrane of terminal cisternae is depolarized opening of voltagegated calcium channels calcium ions move into terminal cisternae.

When it is in sarcoplasm, calcium is utilized by troponin C to initiate muscle

contraction (excitation-contraction coupling).

4 calcium ions can bind with 1 molecule of troponin C it breaks the bond

between troponin I & Actin tropomyosin strands become loose they reach a

deeper position active sites on actin are uncovered

Muscle contraction involves power strokes.

Before contraction, a molecule of ATP becomes attached to myosin head.

It is hydrolyzed to ADP to liberate energy stored in myosin head.

When active site is uncovered myosin head binds with active site on actin. With stored energy, there is power stroke.

At hinges, myosin molecule moves & carries along actin / thin filaments

Contraction is initiated by calcium ions.

As long as calcium ion is sufficient in sarcoplasm muscle contraction continues.

Q.15 How is RMP generated? (5 marks)


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Key:

Potential difference across cell membrane at rest:

Inside negative with respect to outside.

Potential values vary:

In nerve fiber: -90 mV In skeletal muscle: -90 mV

In cardiac muscle: -85 mV

In nerve cell body: -70 mV

In smooth muscle: -55 mV to -60 mV

Mechanism of regulation of RMP:Mechanism of regulation of RMP:

INSIDEINSIDE

OUTSIDEK+

4 mEq/ L

Na+

140 mEq / L

140 mEq / L 14 mEq / L

SO K+ IS 35 TIMES > INSIDE THAN OUTSIDE

Na+ IS 10 TIMES > OUTSIDE THAN INSIDE

K+ WILL TEND TO DIFFUSE OUT & Na+ WILL TEND TO DIFFUSE IN.K+ WILL TEND TO DIFFUSE OUT & Na+ WILL TEND TO DIFFUSE IN.

INSIDE CELL MEMBRANE ARE PROTEIN CHANNELS (LEAK / VOLTAGE /INSIDE CELL MEMBRANE ARE PROTEIN CHANNELS (LEAK / VOLTAGE /

LIGAND GATED) K+ , Na+ LEAK CHANNELS ARE 100 TIMES MORE PERMEALIGAND GATED) K+ , Na+ LEAK CHANNELS ARE 100 TIMES MORE PERMEABLEBLE

TO K+ THAN TO Na+. (AT REST MORE K CHANNELS ARE OPEN THAN Na)TO K+ THAN TO Na+. (AT REST MORE K CHANNELS ARE OPEN THAN Na)

SO MAIN MOVEMENT IS K+ OUTFLUXSO MAIN MOVEMENT IS K+ OUTFLUX

WHICH CONTRIBUTES TO RMP (negative inside)WHICH CONTRIBUTES TO RMP (negative inside)


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Mechanism of regulation of RMPMechanism of regulation of RMP

(continued)(continued)

Another factor is NaAnother factor is Na++

--

KK++

pump (active all the time).pump (active all the time).

Pumps out 3 NaPumps out 3 Na++ ions &ions &

Pumps in 2 KPumps in 2 K++ ions.ions.

So more electroSo more electro--positive ions are pumped out &positive ions are pumped out &

contributes to RMP.contributes to RMP.

As membrane is more permeable to KAs membrane is more permeable to K++ at rest, & muchat rest, & much

ionic diffusion, so large amount of Kionic diffusion, so large amount of K++ should moveshould move

out, but net movement is not much. Why???out, but net movement is not much. Why???

This is because when K+ moves out, anions (non-diffusible: proteins, organic

phosphate & organic sulfate anions) attract them back.

But this movement is sufficient to cause relative electro-negativity inside themembrane.

Out of -90mV, -86mV is due to K+ outflux &

-4 mV is due to Na+ K+ pump.What is the evidence???

Evidence of major contribution to RMP by K+ ion:

If we change, [K+] in ECF RMP is disturbed.

If there is hypo-kalemia in ECF RMP will become more negative due to more

potential difference hyper-polarization (more K+ leak out than resting level

more negativity on inside).

If there is hyper-kalemia RMP becomes less negative (less K will leak out due to

less potential difference) hypo-polarization (less negativity on inside).

But changes in [Na+] in ECF no significant effect on RMP.

We can also prove this by Nernst Equation.

Nernst Equation:

EMF (mV) = +/- 61 log conc. inside / conc. outside Assume that at rest, cell membrane is highly permeable to Na+, then:

-61 log 14/140

(-)for Na+ & K+ & (+) for Cl-)= -61 log 0.1

= -61 x -1

= + 61 mV

So potential difference across cell membrane should be +61mV, which is wrong.


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Assume that at rest, cell membrane is highly permeable to K+, then:

- 61 log 140 / 4

= -61 log 35

= -61 x 1.54

= -94 mV (close to RMP)

So this assumption is correct that at rest, cell membrane is highly permeable to K+.

Goldman Hodgkin-Katz Equation:

Goldman HodgkinGoldman Hodgkin--Katz Equation:Katz Equation:

EMF (mV) =EMF (mV) =

-- 61 log61 log CC Na+Na+ii PP Na+Na+ + C+ C K+K+ ii PP K+K+ + C+ C ClCl-- oo PP ClCl--

CC Na+Na+oo PP Na+Na+ + C+ C K+K+ oo PP K+K+ + C+ C ClCl--ii PP ClCl

--

WITH GOLDMAN EQUATION SUMMATED POTENTIAL = -86 mV

(C = CONCENTRATION, P= PERMEABILITY)

K+ Na+ leak channels are highly permeable to K+ but there is some inward

movement of Na+ + 8 mV potential is generated.

-94 mV is due to K+ efflux

+ 8 mV is due to Na+ influx

-94 + 8 = -86 mV = Goldman potential

-4 mV is due to Na+ K+ pump

-86 4 = -90 mV = RMP.

Q.16 Define CHRONAXIE. How is an action potential propagated along amyelinated nerve fiber? (5 marks)

Key:

CHRONAXIE: A time for which a stimulus, double the rheobase when applied, just

excites the tissue, e.g., 2 mV. (Chronological is from time, so chronaxie is a unit of

time). (1 mark)


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Propagation of action potential along a myelinated nerve fiber: (4 marks)

Node to node conduction. Also called saltatory / jumping conduction.

All channels are present at nodes of Ranvier.

Myelin sheath is absent & only neurilemma is there at the node.


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Local circuit of saltatory conduction:

Polarized node adjacent depolarized node through axoplasm polarizednode.

C o m p a r a s o no m p a r a s o n o f ve l o c i t i e sf v e l o c i t i e si n 2 t y pe s o f f ib e r s :n 2 t y pe s o f f ib e r s : MyelinatedMyelinated

120 m/sec (fast)120 m/sec (fast)

Thicker nerve fiber =Thicker nerve fiber =

longerlonger internodeinternode ==

greater velocitygreater velocity

e.ge.gAA--alpha fibersalpha fibers

Less energy expenditure dueLess energy expenditure dueto less ionic changeto less ionic change

as internodes are not beingas internodes are not beingused, only nodes are used.used, only nodes are used.

UnmyelinatedUnmyelinated

22--5 m/sec5 m/sec


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Q.17 Draw & label the NMJ. Enumerate various events involved in neuromusculartransmission. (5 marks)

Key:

Diagram: (1 mark)


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Events:

Nerve impulse nerve terminal depolarization of membrane of nerve terminal

opening of voltage gated calcium channels in membrane.

Calcium (ECF) End foot / nerve terminal agitation of some of the synaptic

vesicles (125 -150 vesicles become agitated & fuse with membrane) break their

acetylcholine into synaptic cleft by exocytosis.

Ach (released) binds with receptors (part of protein molecules) at motor end

plate (Ach gated channels/ cholinergic receptors/ ligand gated channels) of nicotinic

type at motor end plate opening of Ach gated channels sodium influx EPP(localized potential change). It is graded (amplitude is directly proportional to

amount of Ach released). Not self propagated, so decrease with distance. Prolonged

in duration.

Because of EPP Threshold for action potential is reached (-65 mV).

If RMP is -90 mV, then threshold is -65 mV, we need 25 mV potential change.

Purpose of EPP is to reach the threshold of action potential.

So voltage of EPP is much more than required, because required is only 25 mV.

It is called SAFETY FACTOR.


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Recycling

Ach once released, remains bound with receptors only for 1 msec.

Some diffuses out to ECF & rest is hydrolyzed by enzyme acetylcholine esterase of

sub-neural cleft.

Ach (on hydrolysis) Choline + Acetate

So that new impulse can be transmitted through NMJ.

These channels have 5 sub-units:2 alpha sub-units which protrude out on surface &

3 others are beta, gamma & delta.

Ach synthesized in synaptic knob vesicle released recycled.

Mitochondria energy Ach formation from CoA & Choline synaptic knob.

Impulse reaches agitation of vesicles Ach binds with receptors Ach

esterase acetate & choline recycled.

Q.18 Draw & label Action Potential of nerve fiber. List all of its components & give theionic basis for each of these. Define After depolarization & After

hyperpolarization.

(2+1+2 marks)


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R M P-90 mV

T hresho ld-65 mV

0 mV

+35 to 40 mV

A fter H yper-polarization

(U ndershoot) / Sub-normal period (-95 mV )

[K+efflux continues, K+channels remainopen for some time after R M P is rH ere tissue is difficult to be excite

D epolarization Repolarization[K+efflux]

T ime (ms)

(O vershoot)

Peak

M embrane Voltage

(mV)

RM P-90 m

[Rapid

N a+influx]

Completeopening offast N a+ channels

SlowRepolarization/ K+accumulE xcitable/Super-normal perio

A fterD epolarization

(70% ofrepolarization/ start ofA fter-D epolarization

Spike potential

(First 1/ 3 ofrepolarization)

Relative Refractory period

A bsolute R efractory period

[N a+ inactivation gates are still

-65mV

Action potential Graph: (2 Marks)

x-axis: Time in milliseconds (0.25 mV)

y-axis: Voltage in millivolts (0.25 mV)

RMP: - 90 mV (0.25 mV)

Threshold: - 65 mV (0.25 mV)Peak: +35 to 40 mV (0.5 mV)

Phases: Depolarization (upstroke), Repolarization (downstroke), Hyperpolarization

(negative, below the baseline) (0.5 mark)

Note: If ionic basis is mentioned on the graph, then it is not needed in the text.


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STAGES & IONIC BASIS:

Resting Membrane Potential (-90 mV) is due to tendency of potassium ions to moveout of the interior of nerve fibers. At this stage conductance for potassium ions is 50-

100 times as great as conductance for sodium ions greater leakage of sodium ions

through the leak channels. (0.25 marks)

Depolarization phase starts from threshold value (-65 mV), when all the sodium

gates / channels open up sodium influx. It ends at the peak level (+35 to 40 mV).(0.25 mark)

Repolarization phase starts at the peak (+35 to 40 mV) and ends at the baseline

(RMP = - 90 mV). It is due to potassium efflux (potassium gate is open).(0.25 mark)

Absolute refractory period includes depolarization and first 1/3 of repolarization.

Sodium inactivation gates are still closed and will not open till potential reaches

resting value. (0.25 mark)

During repolarization, Potassium becomes accumulated on outer side of membranewhich slows down further efflux after 70% of repolarization leading to slow

repolarization called After depolarization. (1 mark)

When potential has reached the resting value, it does not stay there and becomes morenegative and called After hyperpolarization. It is because when Potassium has

reached resting value, some Potassium channels are still open and Potassium effluxcontinues, resulting into more negative membrane potential.(1 mark)


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Q. 19 What is LATCH PHENOMENON in a smooth muscle fiber? What is its

importance & how is it regulated? (2+1+2 marks)

key:

Smooth muscle can maintain prolong contraction with expenditure of small amount ofenergy LATCH MECHANISM.

Importance:

It can maintain prolong tonic contraction in smooth muscle for hours with little use of

energy. Little continued excitatory signal is required from nerve fibers or hormonal

sources.

Once smooth muscle has developed full contraction, the amount of continuing excitation

usually can be reduced to far less than the initial level, yet the muscle maintains its fullforce of contraction.

The energy consumed to maintain contraction may be as little as 1/300 the energy requiredfor comparable sustained skeletal muscle contraction.

Regulation:

When myosin kinase & myosin phosphatase enzymes are both strongly activated, the

cycling frequency of myosin heads & velocity of contraction are great.

As the activation of enzymes decreases, the cycling frequency decreases, but at the same

time, the deactivation of these enzymes allows the myosin heads to remain attached to theactin filament at any given time remains large. (Slow ATPase activity of myosin head).

Because of the number of heads attached to actin determines the static force of contraction,tension is maintained, or latched; yet little energy is used by the muscle, because ATP isnot degraded to ADP except on rare occasion when a head detaches.

Q.20 Define and draw a sarcomere. Enumerate changes which occur in it during

muscle contraction. (2+3 marks)

key:

SARCOMERE: The structural & functional unit of muscle. The portion of myofibril

between two successive Z lines. (0.5 mark)

Diagram: see under changes.


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Histological changes during muscleHistological changes during muscle

contraction:contraction: RELAXED MUSCLERELAXED MUSCLE ::

22--2.52.5m length ofm length ofsarcomeresarcomere..

AFTER CONTRACTIONAFTER CONTRACTION::

11--1.51.5m length ofm length ofsarcomeresarcomere..

Length of A band constant.Length of A band constant.

Length of I band (Length of I band (ActinActinfilament on either side of Zfilament on either side of Zline, not covered by Myosin)line, not covered by Myosin)decreases.decreases.

Z Membranes become closer.Z Membranes become closer.

H zone decreases / disappearH zone decreases / disappear

Sliding of thin over thickSliding of thin over thickfilaments.filaments.

Length of individualLength of individualfilaments remain the same.filaments remain the same.

(3 marks)

(1.5 marks)


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Q.21 How is action potential propagated along a myelinated nerve fiber? What are

the advantages of this propagation? (5 marks)

Q.25 What is salutatory conduction? What are its advantages? Which nerve fibers

have maximum velocity of conduction? (1+2+2 marks)

Key:Propagation (saltatory conduction): (3 marks)

See Q. 16

Advantages: (2 marks)

i. It increases velocity of conduction directly in proportion to the fiber diameter,

velocity ofA alpha fibers = 120 meters/sec.

ii. Conservation of energy- less energy expenditure.

Q. 22 Define Rheobase & Chronaxie. Show these units in Strength-duration curve.

(1.5+1.5+2 marks)

Key:

RHEOBASE: Voltage / strength of stimulus required just to excite the tissue,

e.g., 1 mV.

CHRONAXIE: A time for which a stimulus, double the rheobase when

applied, just excites the tissue, e.g., 2 mV. (Chronological is from time).


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Q.23 Draw & label NMJ. How is EPP produced? What change occurs in this

potential in Myasthenia Gravis? (2+2+1 mark)

key:

See Q.17 & Q.1

Q.24 What is Compound Action Potential? Draw & label it. (3+2 marks)

Key:

Multi-peaked action potential recorded from a nerve.

For example: Sciatic nerve has number of nerve fibers of different diameters

& different velocity of conduction.

When action potential from different nerve fibers are recorded multiplepeaks.

3 main peaks: A, B, C.

A is further divided into alpha, beta, gamma, delta. A & B types are myelinated & C type is unmyelinated.

Compound action potential is basis of physiological classification of nerve

fibers.

A alpha fibers with maximum diameter have highest velocity of conduction, up

to 120 m/sec.

Even lower most graph is enough.


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Q.26 Compare the features of Isometric & Isotonic types of skeletal muscle

contraction. (5 marks)

key:

Isotonic IsometricIsotonic Isometric

TYPES OF CONTRACTION

ISOTONIC (same tone)

Muscle lengthdecreases but muscletension constant.

Work is done in thistype of contraction.

Example: lifting ofbook from a table.

(1 mark each point =

3 marks)

ISOMETRIC

(same length)

No appreciable

change in length of

muscle but muscle

tension increases. Work is not done.

Example: heavy

weight balancing by

weight lifters and

body builders.


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IsotonicIsotonic IsometricIsometric

Muscle develops

tension but does

not shorten

No movement

Muscle shortens,

tension remains

constant

Movement

occurs


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Body movements are a mixture of isotonic and isometricBody movements are a mixture of isotonic and isometric

movements.movements.In muscleIn muscle 2 types of elements:2 types of elements:

1) Contractile elements1) Contractile elements::

((thinthin// actinactin && thickthick/ myosin filaments)/ myosin filaments)

2) Elastic elements2) Elastic elements::

((tendons &tendons & sarcolemmalsarcolemmal ends of muscle fibersends of muscle fibers

attached to tendons)attached to tendons)

Elastic component is in series with contractile component.Elastic component is in series with contractile component.

ContractileContractilecomponent undergoescomponent undergoesshorteningshortening&&

elasticelasticcomponent undergoescomponent undergoesstretchingstretching..

Muscle must shorten 3Muscle must shorten 3--5% extra to neutralize5% extra to neutralize

the stretching of elastic component.the stretching of elastic component.

In isometric exercise, only 3In isometric exercise, only 3--5% muscle5% muscle

shortening, tendons are stretching & thisshortening, tendons are stretching & this

shortening neutralizes the stretchingshortening neutralizes the stretching nono

change in length.change in length.


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Significance: Isometric contraction is used

to compare the functional characteristics

of different muscle types including Fastand Slow Muscle Fibers .

(0.5 mark)

Body movements are a mixture of

isotonic and isometric movements.

(0.5 mark)

Q.27 When sciatic nerve is electrically stimulated, which type of potential record is

obtained? Draw & explain it. (5 marks)

COMPOUND ACTION POTENTIAL is produced.

Diagram: See Q. 24

Q.28 How is impulse conducted from a nerve to muscle fiber? What is myasthenia

Gravis? (3+2 marks)

Key:

See NMJ Q.17

Myasthenia Gravis:


Voltage of EPP is very low (Miniature EPP) action potential is not followed.At rest normally, a few synaptic vesicles break to liberate Ach from synaptic

vesicles small change in EPP (about 0.5 mV) called MEPP. Amplitudevaries directly with [Ca++] and inversely with [Mg++].

Impulse fails to transmit through NMJ Severe muscle weakness & fatigue(Extra-ocular muscles ptosis, diplopia, difficulty in Swallowing, weakness ofRespiratory and Facial muscles)


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EPP Vs APEPP Vs AP

EPP:EPP:

Local potential recorded onlyLocal potential recorded only

at End plate region.at End plate region.

Voltage: 0.5Voltage: 0.5mV (MEPP)mV (MEPP)

EPP varies with strength ofEPP varies with strength of

stimulus / amount ofstimulus / amount of

neurotransmitter released.neurotransmitter released.

Can show summation.Can show summation.

AP:AP:

SelfSelf--propagated.propagated.

Voltage: 35Voltage: 35--40 mV40 mV

AP follows All or NoneAP follows All or None

Law/ requires only thresholdLaw/ requires only threshold

stimulus.stimulus.

Does not show summation.Does not show summation.


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AutoAuto--antibodiesantibodiesare producedare producedagainst Ach gatedagainst Ach gatedreceptor channelsreceptor channels& these& thesereceptors are destroyedreceptors are destroyedirreversiblyirreversibly, though Ach is present (, though Ach is present (poverty amongstpoverty amongst

plenty/ have the money, but pizza shop is closedplenty/ have the money, but pizza shop is closed/ all dressed up but no place to go!/ all dressed up but no place to go!).).

TREATMENTTREATMENT:: AnticholineAnticholineesterasesesterases((NeostigmineNeostigmine,,PhysostigminePhysostigmine))marked improvement.marked improvement.

AdrophoneumAdrophoneuminjectioninjection: (short acting anti: (short acting anti cholinecholineesterase)esterase)

Mechanism of actionMechanism of action:: anticholineanticholineesterasesesterases inhibitinhibit

enzymeenzymecholinecholineesteraseesterase Ach not hydrolyzedAch not hydrolyzedmore Ach availablemore Ach availablefor available number of receptors.for available number of receptors.


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Evidence of autoimmune disease:

Auto antibodies detected in patients blood.

In many of these cases, thymus is enlarged & thymectomy is of benefit.

If mother is myasthenic, newborn shows features of myasthenia for few weeksbecause antibodies cross the placenta.

But antibodies die in few weeks, due to limited life span. They will destroy fewreceptors, which will regenerate later.

Q.29 Differentiate between a graded potential & action potential. (5 marks)

EPP Vs APEPP Vs AP

EPP:EPP:








AP:AP:





stimulus.stimulus.



39/54

OR

the following question may be asked:

EPSP Vs Action Potential

EP PVs A TI N P TENTIAL:s :

Table 2Table 2--44MushtaqMushtaq

Na+ first, then K+Na+ first, then K+To Na+ & K+ at oneTo Na+ & K+ at one

time but Na+ influx istime but Na+ influx is

muchmuchgreategreatethan K+than K+

effluxefflux

Increased permeability toIncreased permeability to

ionsions

Absent; size is always theAbsent; size is always thesamesame

PresentPresentDecrement (decline ofDecrement (decline ofsize with distance)size with distance)

obeyedobeyedNot obeyed; size directlyNot obeyed; size directly

proportional to intensityproportional to intensity

of stimulusof stimulus

All or none lawAll or none law

presentpresentabsentabsentRefractory periodRefractory period

Self propagatingSelf propagating

22msecmsec

Nil; remains localized, 20Nil; remains localized, 20

msecmsecPropagation & DurationPropagation & Duration

HighHighLowLowMagnitudeMagnitude

Action PotentialAction PotentialEPSPEPSPPropertyProperty

Q.30 Which record is obtained when a nerve trunk is stimulated?

Draw and explain this record. (5 marks)

Key: Compound Action Potential

See Q. 24


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Q.31 How is MYELIN SHEATH formed in the peripheral and central nervous

system? What are its functions? (2+3 marks)

MyelinogenesisMyelinogenesis

Formation of myelin sheath around the axon.Formation of myelin sheath around the axon.

In peripheral nerveIn peripheral nerve, it starts at 4, it starts at 4thth I.U month.I.U month.

It is completed in 2It is completed in 2ndnd year after birth.year after birth.

Myelin sheath is produced by layers of Schwann cells.Myelin sheath is produced by layers of Schwann cells.

Outermost layer of Schwann cells remain asOutermost layer of Schwann cells remain asneurilemmaneurilemma//Sheath of Schwann.Sheath of Schwann.

Cytoplasm of Schwann cells is not deposited.Cytoplasm of Schwann cells is not deposited.

Nucleus of Schwann cells remain betweenNucleus of Schwann cells remain betweenneurilemmaneurilemma& myelin& myelin

sheath. I t is flattened & elongated.sheath. I t is flattened & elongated. 1 nucleus at each inter1 nucleus at each inter--node of axon.node of axon.

SchwaanSchwaancellscells absentabsent in CNSin CNS..

NeurilemmaNeurilemmais absent in CNS.is absent in CNS.

In CNSIn CNS OLIGODENDROGLIAOLIGODENDROGLIA MYELIN SHEATH.MYELIN SHEATH.

In PNSIn PNS SCHWANN CELLSSCHWANN CELLS MYELIN SHEATHMYELIN SHEATH..


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Functions:

FASTER CONDUCTION: Saltatory / jumping HIGH INSULATION: Prevents stimulation of neighboring fibers.

Q.32 An unidentified dead body was found in a street. The dead body was having

rigidity. It was handed over to the police. After about 24 hours, rigidity of the

dead body had disappeared.

a. Why was the dead body having rigidity and what is that condition called?

b. Why did the rigidity disappear?

(3+2 marks)

Key:

a. Several hours after deathmuscles of dead body become rigid rigor mortis.

After death ATP not available no detachment of cross-bridges of myosin

from active site of actin filaments contracture / rigidity.

b. After about 24 hrs rigor mortis disappears due to autolysis of muscle proteins(resulting from hydrolytic enzymes from lysosomes).


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Significance: (CAN BE MENTIONED)

Forensic significance:Cause of death

If suicide has been committed, the gun or dagger is locked in the hand.

Duration of deathSome idea. Within 16 hrs of death, rigor mortis remains. It disappears after 16-24 hrs of

death.

Q.33 Which types of muscle contraction predominantly occur in a body builder

during his performance and a Tennis player during his play? Compare

the features of these types of contraction. (5 marks)

Key:

Isometric contraction in body builder while weight lifting in a stationary position.

Isotonic contraction in tennis player during his play.

See Q.26

Q.34 Briefly explain the factors responsible for generation of RMP. What do you

understand by Nernst potential. How does it explain the equilibrium across

the cell membrane? (2+1+2 marks)

Key:

See Q.15

Q.35 Classify the nerve fiber according to their diameter and conduction

velocity. List the differences between EPP & Action Potential in a muscle

fiber. (3+2 marks)

key:


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Classification by sensoryClassification by sensory

physiologists:physiologists:

UnmyelinatedUnmyelinated

fibers carryingfibers carrying

pain, itch,pain, itch,

temperature &temperature &

crude touch.crude touch.

0.30.3--1.31.3m inm indiadia

ConductionConduction

Velocity:Velocity:0.50.5--

2.3 m/ sec2.3 m/ sec

Fibers carryingFibers carrying

temperature,temperature,

crude touch &crude touch &

pricking pain.pricking pain.

33mmin dia.in dia.RangeRange: 2: 2--55mm


Velocity:Velocity:1212--3030

m/ secm/ sec

Fibers fromFibers from

cutaneouscutaneoustactiletactile

receptors &receptors &

flower sprayflower spray

endings of muscleendings of muscle

spindle.spindle.

88

mm

in dia.in dia.

Range & V elocityRange & Velocity

((betabeta):):

55--1212m, 30m, 30--7070

m/ secm/ sec

Range & V elocityRange & Velocity

((gammagamma): 3): 3--66m,m,

1515--30 m/ sec30 m/ sec


golgigolgitendontendon

organs.organs.

1616mmin dia.in dia.

RangeRange: 12: 12--2020mm


velocityvelocity: 70: 70--120120

m/ secm/ sec


annulospiralannulospiral

endings ofendings of

muscle spindles.muscle spindles.

1717micronmicrondiadia

RangeRange: 12: 12--2020mm


velocityvelocity: 70: 70--120120

m/ secm/ sec

IV /IV / CCI I I /I I I /AAdeltadelta

I I /I I /A betaA beta& gamma& gamma

IbIb// AAalphaalpha

IaIa// AAalphaalpha

EPP Vs AP: See Q.29

Q.36 What is stress relaxation and reverse stress relaxation in a smooth muscle.

List the events occurring during the propagation of action potential in an

unmyelinated nerve fiber. (2+3 marks)

key:

Stress Relaxation:

Smooth muscle can increase its size to accommodate increased volume, withoutsignificant increase in pressure /tension

e.g we give massive blood transfusion to a person B.P increases but within few

hours normal due to stress relaxation.


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Smooth muscle in vessel wall undergoes stress relaxation accommodate

increased blood volume now even increased blood volume does not lead to

increased blood pressure.

Smooth muscle in stomach wall accommodate more food.

Smooth muscle of urinary bladder (detrusor) can hold increased volume of urine.

Smooth muscle of uterus can accommodate growing fetus.

REVERSE STRESS RELAXATION:

Smooth muscle contracts around the reduced volume no significant fall in

pressure.

e.g., in hemorrhage blood loss from body may cause shock but reverse

stress relaxation of smooth muscle in vessel wall can prevent shock because it

contracts around the reduced blood volume now even reduced blood volumeadequately fills vascular system.

Disparity between circulatory blood volume & capacity of vascular system is basic

factor for shock.

In neurogenic shock (vasomotor centre failure vasodilation) capacity increases

but blood volume is same. This disparity cannot be compensated by reverse stressrelaxation.

Stress and reverse stress relaxation are due to loose arrangement of myosin & actin

filaments which can adapt themselves to adopt a new size.


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Propagation of action potential in un-myelinated nerve fiber:

Point to point conduction.

Local circuit of current is formed between depolarized point & adjacent polarized point.


46/54

Current flowing out through depolarized point, activates Na+ channels at polarized point

depolarization action potential.

Then a new circuit of current is formed between this depolarized point & adjacentpolarized point.


47/54

This is point to point conduction of nerve impulse / action potential by forming local circuit

of current between depolarized point & polarized point.

In case of unmyelinated nerve fiber, velocity of conduction is slow, because it is point topoint.

Synapses only allow propagation between pre synaptic to post synaptic

neuron inside the body, but in vitro it is in both directions.

Q.37 Explain the events that occur when the motor nerve supplying a skeletal

muscle is stimulated to produce the muscle contraction. (5 marks)

key:

Depolarization wave on sarcolemma transverse tubules of sarcoplasmic

reticulum

(1 mark)

This in turn causes rapid opening of large numbers of calcium channelsrelease of calcium. (1 mark) Calcium binds with Troponin C (1 mark)

Displacement of Tropomyosin Active sites of actin are exposed. Hydrolysis of

ATP at the head of Myosin ADP & Phosphate

(1 mark)

Power stroke: Myosin cross-bridges bend at hinges drag actin over myosin

Length of sarcomere decreases contraction of skeletal muscle.

(1 mark)Also draw diagrams: Fig. 7.6 & Fig. 6.4. (Guyton)

Q.38 Write short note on:a. Rigor Mortis

b. Myasthenia Gravis

(2.5+2.5 marks)

Key a.

Several hours after deathmuscles of dead body become rigid rigor mortis.

Its onset depends on:

Temperature: increased temperature rapid onset.

Activity: Vigorous activity of muscle before death rapid onset.

Mechanism:

After death ATP not available no detachment of crossbridges of myosin from

active site of actin filaments contracture / rigidity.

After 16-24 hrs rigor mortis disappears due to autolysis of muscle proteins

(resulting from hydrolytic enzymes from lysosomes).


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Key b.


Voltage of EPP is very low (Miniature EPP) action potential is not followed. Atrest normally, a few synaptic vesicles break to liberate Ach from synaptic vesicles

small change in EPP (about 0.5 mV) called MEPP. Amplitude varies directly

with [Ca++] and inversely with [Mg++].

Impulse fails to transmit through NMJ Severe muscle weakness & fatigue

(Extra-ocular muscles ptosis, diplopia, difficulty in Swallowing, weakness ofRespiratory and Facial muscles)

EPP Vs APEPP Vs AP

EPP:EPP:








AP:AP:





stimulus.stimulus.



49/54


50/54

Auto-antibodies are produced against Ach gated receptor channels & these

receptors are destroyed irreversibly, though Ach is present (poverty amongst

plenty/ have the money, but pizza shop is closed /all dressed up but no place to

go!).

TREATMENT: Anticholine esterases (Neostigmine, Physostigmine) marked

improvement.

Adrophoneum injection: (short acting anti choline esterase)

Mechanism of action: anticholine esterases inhibit enzyme choline esterase

Ach not hydrolyzed more Ach available for available number of receptors.

Evidence of autoimmune disease:

Auto antibodies detected in patients blood.

In many of these cases, thymus is enlarged & thymectomy is of benefit.

If mother is myasthenic, newborn shows features of myasthenia for few weeks

because antibodies cross the placenta.


51/54

But antibodies die in few weeks, due to limited life span. They will destroy few

receptors, which will regenerate later.

Q.39 What is Walk-along theory & sliding filament model of skeletal musclecontraction?

(2.5 + 2.5 marks)

Walk-along mechanism: Interaction between Activated Actin Filament and Myosin Cross-bridges

Calcium ions activate actin filament.

Heads of cross bridges from myosin filaments become attracted to active sites of

actin filament contraction (walk along or ratchet theory of contraction).

When a head attaches to an active site, the attachment simultaneous profound

changes in intramolecular forces between head and arm of its cross-bridge.

New alignment of forces, causes the head to tilt towards the arm & drag actin

along with it. This tilt of head is called power-stroke.

Immediately after tilting, head automatically breaks away from the active site.

Head then returns to its extended direction. Head then combines with a new active site farther down along actin.

Head then tilts again new power stroke &

Actin moves another step.

Thus heads of cross-bridges bend back and forth and step by step walk along the

actin filament, pulling the ends of 2 successive actin filaments toward the centre of

myosin filament.


52/54

Each cross bridge is believed to workindependently, attaching & pulling in a

continuous repeated cycle.

So, greater the number of cross-bridges, in contact with actin, at any given time,greater is the force of contraction, theoretically.

Sliding filament mechanism:

\

Basic mechanism is shown in the figure of sarcomere in relaxed and contracted state.

In relaxed state: ends of actin from 2 successive Z dics, barely begin to overlap oneanother.

In contracted state: actin filaments have been pulled inward among myosin filaments

their ends overlap to maximum extent. Also Z discs have been pulled by actin filaments up

to the ends of myosin filaments muscle contracts by a sliding filament mechanism.

This inward sliding is caused by forces generated by interaction of myosin cross-bridgeswith actin filaments.

These forces are inactive at rest, but activate when action potential arrives calciumrelease from sarcoplasmic reticulum activation of forces between actin & myosin

contraction.

Energy for contraction comes from ATP ADP + energy.


53/54

Q.40 Compare the saltatory & non-saltatory conduction of nerve impulse.

(5 marks)

Key:

1. Saltatory: in myelinated nerve fibers. Non-saltatory in un-myelinated2. Saltatory is fast conduction. Slow conduction.

3. It utilizes less energy. More energy used.

4. Velocity of conduction is directly Pain / C fibers is an exampleProportional to fiber diameter.

A alpha fibers is an example.

5. Jumping conduction from one node Point to point conduction.

to the next node. Local circuit ofcurrent is completed between depol-

arized node & adjacent polarized

node. Current flowing through

polarized node, activates sodiumchannels.

Also draw diagrams for both

.


54/54

Q.41 Compare & contrast action potential / contraction of:

a) Skeletal Vs cardiac muscle

b) Skeletal Vs smooth muscle

c) Cardiac Vs smooth muscle

Key:

See Q.10

Q.42 Briefly discuss in step wise manner general mechanism of muscle

contraction. (5 marks)

key:See Q.37

Q.43 Define & explain frequency summation & multiple fiber summation of

skeletal muscle. (5 marks)

key:

Guyton pg 81

FREQUENCY SUMMATION:

Draw fig: 6.13 Guyton

At a low frequency: individual twitch contractions.

At increasing frequency: each new contraction occurs before the preceding one is

over.

second contraction is added partially to the first total strength of contraction

rises with increasing frequency.At a critical level of frequency: successive contractions become so rapid fuse

together smooth & continuous whole muscle contraction tetanization.

MULTIPLE FIBER SUMMATION:

Weak signal from CNS to contract a muscle smaller motor units of muscle may

be stimulated in preference to larger motor units.

As strength of signal increases, larger and larger motor units begin to be excited aswell, with larger motor units having 50 times the contractile force of smaller units

(SIZE PRINCIPLE). Smaller motor units are driven by small motor nerve fibers &

small motor neurons in spinal cord are more excitable than larger ones, so they are

excited first.Different motor units are driven asynchronously by spinal cord contraction

alternates among motor units one after the other, thus providing smooth contractioneven at low frequencies of nerve signals.

nerve & muscle 45 qs with their answer keys by dr. roomi

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