T1 Solved Q Paper Full

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GHMC Physiology Question Paper Term 1 (set-I) & RE (set-II) Old Paper Pattern

Section A (Set-I)Q.1. Define cardiac cycle. Describe its various events with pressure & volume changes. Or What are heart sounds? Describe their

characters, mechanisms of formation with their significance. (15 Marks)Q.2. Describe molecular basis of muscular contraction. Enumerate properties of skeletal muscle. Or What are the types of

muscles? Describe the contractile proteins of skeletal muscle. (15 Marks)Q.3. Write any 2 out of 4 (2x10=20 Marks)

a) Properties of cardiac muscle.b) Pacemaker.

c) Staircase phenomenon.d) Neuromuscular junction

Section A (Set-II)Q.1. Define blood pressure & describe its regulation. Or What is normal heart rate? Give its physiological variation & describe how

heart rate is regulated. (15 Marks)Q.2. Describe in detail the structure & transmission physiology of neuromuscular junction along with suitable diagram. Or What are

the different types of muscles? Describe properties of skeletal muscle.(15 Marks)Q.3. Write any 2 out of 4 (2x10=20 Marks)

a) Cardiac output & factors affecting it.b) Difference between SA & AV nodes.

c) Sarcomere.d) Contractile proteins of skeletal muscle.

Section-B (Set-I)

Q.4 Name the clotting factors. Explain the mechanism of coagulation of blood. Or Describe ABO blood group. Add a note on Rhfactor.

Q.5 Describe glycolysis & give details of its energetics. Or Name essential fatty acids. Explain classification of fats and describefunctions of lipids?

Q.6 Write any 2 out 4a) Functions of blood.

b) Erythropoiesis.

c) Absorption of carbohydrates.

d) Glycogenesis.Section-B (Set-II)

Q.4 Define the blood. Describe its composition & functions. Or Define erythropoiesis. Describe its different stages with theirregulation. (15 Marks)

Q.5 Describe various steps of Krebs cycle & give details of the energetics. Or Define carbohydrate. Explain classification ocarbohydrates & add a note on chemistry of glucose. (15 Marks)

Q.6 Write any 2 out 4a) Blood group.b) Name the coagulation factors, with short

description of any five.

c) Functions of lipidsd) Glycogenesis

COMPOSITE SECTION ALAQ

Qu. 1. Define cardiac cycle. Describe its various events with pressure & volume changes.Qu. 2. What are heart sounds? Describe their characters, mechanisms of formation with their significance.

Qu. 3. Describe molecular basis of muscular contraction. Enumerate properties of skeletal muscle.Qu. 4. What are the types of muscles? Describe the contractile proteins of skeletal muscle.Qu. 5. Define blood pressure & describe its regulation.Qu. 6. What is normal heart rate? Give its physiological variation & describe how heart rate is regulated.Qu. 7. Describe in detail the structure & transmission physiology of neuromuscular junction along with suitable diagram.Qu. 8. What are the different types of muscles? Describe properties of skeletal muscle.

Short Notesi) Properties of cardiac muscle.ii) Pacemaker.iii) Staircase phenomenon.iv) Neuromuscular junction

v) Cardiac output & factors affecting it.vi) Difference between SA & AV nodes.vii) Sarcomere.viii) Contractile proteins of skeletal muscle.

COMPOSITE SECTION BLAQ

Qu. 1. Name the clotting factors. Explain the mechanism of coagulation of blood.Qu. 2. Describe ABO blood group. Add a note on Rh factor.Qu. 3. Describe glycolysis & give details of its energetics.Qu. 4. Name essential fatty acids. Explain classification of fats and describe functions of lipids?Qu. 5. Define the blood. Describe its composition & functions.Qu. 6. Define erythropoiesis. Describe its different stages with their regulation.Qu. 7. Describe various steps of Krebs cycle & give details of the energetics.Qu. 8. Define carbohydrate. Explain classification of carbohydrates & add a note on chemistry of glucose.

Short Notesi) Functions of blood.ii) Erythropoiesis.

iii) Absorption of carbohydrates.iv) Glycogenesis.

v) Blood group.vi) Name the coagulation factors, with short

description of any five.

vii) Functions of lipids


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GHMC Term 1 Question Paper (2011-12 Batch) Section A (Set I-II)

LAQ1. Define cardiac cycle. Describe its various events with pressure & volume changes.Definition - Events that occur in heart, during one heart beat are repeated in same cyclic manner in next beat. This repetition of events in heart

from beat to beat is called cardiac cycle.Division of cardiac cycle - The events of cardiac cycle are classified into two divisions, namely, systole and diastoleSubdivision and duration of cardiac cycle - When the heart beat at normal rate of 72/min, the duration of each cardiac cycle is about 0.3 sec. The

duration of systole is 0.8 sec and that of diastole is 0.5 sec. The subdivision of systole and diastole are as follows:a) Systole

o Isometric contraction = 0.05seco Rapid ejection period = 0.10 seco Slow ejection period = 0.15 sec

0.30 sec = .3 sec

b) Diastoleo Protodiastole = 0.04seco Isometric relaxation = 0.06 seco Rapid filling = 0.10 seco Slow filling = 0.20 seco Atrial filling = 0.20 sec

or 2nd

rapid filling 0.50 sec = .5 secTotal duration of cardiac cycle is = 0.3+0.5= 0.8 sec

Among the atrial events atrial systole occurs during the last phase of ventricular diastole. Atrial diastole is not considered as aseparate phase since it coincides with the ventricular systole and earlier part of ventricular diastole. The atrial systole extends for about 0.11sec and the duration of atrial diastole is about 0.69 sec.

Description of events of cardiac cycle1. Atrial systole - It is also known as second or last rapid filling phase or presystole. Its duration is 0.1 sec. During this period only a small

amount (10 % of blood) is forced from atria into ventricles. During atrial systole, the intra atrial pressure increase, Intraventricularpressure and ventricular volume also increase but slightly. After atrial systole, the ventricular systole starts, simultaneously atrialdiastole also starts.

2. Isometric contraction period - Isometric contraction or isovolumetric contraction is the first phase of ventricular systole. It lasts for 0.05sec. Immediately after atrial systole, the atrioventricular valves are closed due to increase ventricular pressure. The semilunar valvesare already close. Now the ventricles contract as closed cavities in such a way that there is no change in the volume of ventricularchambers or in length of muscle fibers. Only the tension increased in ventricular musculature. Because of increased tension inventricular musculature during isometric contraction, the pressure increases sharply inside ventricles. The pressure rise in ventriclescaused by isometric contraction is responsible for opening of semilunar valves leading to ejection of blood from the ventricles.

3. Ejection period - Due to the opening of semilunar valves and the contraction of ventricles the blood is ejected out of both the ventricles.First stage is called rapid ejection period. Immediately after the opening of semilunar valves a large amount of blood is rapidly ejectionfrom both the ventricles. Second stage is called slow ejection period. During this stage, the blood is ejected slowly with much less force.

4. Protodiastole - It is first stage of ventricular diastole. It last for 0.04 sec due to ejection of blood the pressure in aorta and pulmonaryartery increases and pressure in ventricles drops. When the intraventricular pressure becomes less than the pressure in aorta andpulmonary artery the semilunar valves close. The atrioventricular valves are already closed. Protodiastole indicates only the end ofsystole and beginning of diastole.

5. Isometric relaxation period - During isometric relaxation period once again all the valves of the heart are closed. Both the ventriclesrelax as closed cavities without any change in volume or length of the muscle fibers. The fall in pressure in the ventricles caused byisometric relaxation is responsible for the opening of atrioventricular valves, resulting in filling of ventricles.

6. Rapid filling phase - When AV valves are opened, there is sudden rush of blood from atria to ventricles occurs. So this period is called

the first rapid filling period. About 70% of filling takes place during this period.7. Slow filling phase - After sudden rush of blood, the ventricular filling becomes slow. It is also called diastasis. About 20% of filling occurs

in this phase.8. Atrial systole - After slow filling period, the atria contract, a small amount of blood enter the ventricle from atria and the cycle is

repeated. The atrial systole is also called the last rapid filling phase and about 10% of ventricle filling takes place during this period.LAQ2. What are heart sounds? Describe their character, mechanism of formation with their significance.

Introduction - Heart sound are the sound produced by the mechanical activities of the heart during each cardiac cycle. Heart sounds areproduced by movements of:

1. Blood through the chambers of the heart.2. Cardiac muscle, and3. Valves of the heart

Heart sounds - Four heart sounds are produced during each cardiac cycle. The first and second heart sounds are more prominent and resemblethe spoken words LUB or LUBB and DUBB or DUP respectively. These two sounds are heard by using the stethoscope. Thirdheart sound is a mild sound and it cannot be heard by using stethoscope in normal condition. But it can be heard by using amicrophone. The fourth heart sound is an inaudible sound. This sound is studied only by graphical registration i.e. thephonocardiogram.

Description of heart sounds1. First heart sound - The first heart sound is produced during isometric contraction period and earlier part of ejection period.

Causeo Produced mainly by sudden and synchronous closure of atrio-ventricular valves.o Rush of blood from ventricles into aorta and pulmonary artery.o Myocardial tension and the contraction of ventricular muscle during isometric contraction and the ejection period.o Vibration produced by atrial systole.

Characteristics - Long, soft and low pitched resembles the word LUBBDuration .10-.17 secFrequency 25-45 cycle/ secondRelation with ECG Coincides with peak of R waveNo. of vibrations in phonocardiogram 9-13

2. Second heart sound - Second heart sound is produced at the end of protodiastolic period and part of isometric relaxation.Cause - Closure of semilunar valvesCharacteristics - Short, sharp and high pitched. Resembles the word DUB


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GHMC Physiology Answers: Compiled by (Dr) Lalit Singh, Ed Dr S S Kochhar, HOD

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Duration - 0.10-0.14 sec.Frequency - 50 cycles / secRelation with ECG - Precedes or appears 0.09 second after peak of T waveNo. of vibrations in phonocardiogram - 4-6

3. Third heart sound - The third heart sound is a low pitched sound that is produced during rapid filling period of the cardiac cycle. It is alsocalled ventricular gallop or protodiastolic gallop as it is produced during earlier part of diastole. Usually the third heart sound is inaudible bystethoscope and it can be heard only by using microphone. It occurs during rapid filling phase.Cause - Rushing of blood into ventricle.Characteristics - Low pitchedDuration - 0.07-0.10 sec.Frequency - 1-6 cycle / secRelation with ECG - Between T wave and P wave.

No. of vibrations in phonocardiogram 1-4.4. Fourth heart sound - Normally fourth sound is an inaudible sound. It becomes audible only in pathological condition. It is studied only by

graphical recording that is by phonocardiography. This sound is produced during atrial systole. (late diastole) and it is considered as thephysiologic atrial sound. It is also called atrial gallop or presystolic gallop. It occurs during atrial systole.Cause Due is contraction of atrial musculature during atrial systole. During atrial systole, vibration is set up in atrial musculature and inthe flaps of the atrioventricular valves. Some vibrations are also set up in ventricular myocardium due to the ventricular distension duringatrial systoleCharacter Inaudible soundDuration 0.02 0.4 secFrequency 1-4 cycles / secRelation with ECG Between P wave and Q waveNo. of vibrations in phonocardiogram 1-2

Importance of heart sound - The study of heart sound has important diagnostic value in clinical practice because the alteration in the heart soundindicates cardiac diseases involving the valves of the heart. E.g., stenosis, atrial or ventricular septal defect, ventricular hypertrophy,bundle branch block etc.

LAQ3. Describe molecular basis of muscular contraction

Introduction - The molecular mechanism is responsible for formation of actomyosin complex that results in muscular contraction. It includes therestages.1. Excitation contraction coupling - Excitation contraction coupling is the process that occurs in between the excitation and contraction of

the muscle. This process involves series of activities which are responsible for the contraction of the excited muscle.Stages of excitation contraction coupling

o When the impulse passes through a motor neuron and reaches the neuromuscular junction, acetylcholine is released frommotor end plate. Acetylcholine causes opening of legend-gated sodium channels. So, sodium ions enter the neuromuscular

junction. It leads to the development of endplate potential in the fiber.o The action potential spread over sarcolemma and also into the muscle fiber through the tubules. The tubules are responsible for

the rapid spread of action potential into the muscle fiber. When the action potential reaches the cistern of L tubules, thesecisternae are excited. Now the calcium ions stored in the cistern are excited, and released into the sarcoplasm. The calcium ionfrom the sarcoplasm move toward the actin filaments to produce contraction.

2. Role of troponin and tropomyosin - Normally the head of myosin molecules has a strong tendency to get attached with active site of Factin. However in relaxed condition, the active site of F-actin is covered by the tropomyosin. Therefore, the myosin head cannotcombine with actin molecule.o Large number of calcium ions, which are released from L tubules during the excitation of muscle bind with troponin C. The

loading of troponin C with calcium ions produces some changes in the position of troponin molecules. It in turn, pulls tropomyosin

molecule away from F-actin. Due to the movement of tropomyosin, the active site of F-actin uncovered and immediately the headof myosin get attached to the actin.

3. Sliding mechanism and formation of actomyosin complex - Sliding theory explains how the actin filament slides over myosin filamentand form the actomyosin complex during muscular contraction. It is also called ratchet theory or walk along theory.o Each cross bridge from the myosin filament has got three components, namely, a hinge, an arm and a head. After binding with

active site of F-actin the myosin head is tilted towards the arm so that the actin filament is dragged along with it. This tilting ofhead is called power stroke. After tilting , the head immediately breaks away from the active site and return to the original active.

o Now it combines with a new active site on the actin molecule. And tilting movement occurs again. Thus head of cross bridge bendback and forth and pulls the actin filament towards the center of sarcomere. In this way all the actin filaments of both the ends ofsarcomere are pulled. So the actin filaments of opposite sides overlap and form actomyosin complex. Formation of actomyosincomplex results in contraction of the muscle.

Energy for muscular contraction - The energy for movement of myosin head (power stroke) is obtained by breakdown of adenosine triphosphate(ATP) into adenosine diphosphate (ADP) and inorganic phosphate (ip).

Sequence of events during muscular contraction -Stimulation of muscle fibers by impulse

Generation of action potential in muscle

Spreading of action potential through sarcolemma and T-tubules

Arrival of action potential at cisternae of L tubules

Release of calcium ions from cisternae into sarcoplasm

Binding of calcium ion to troponin C and change in position of troponin C

Exposure of active site of F-actin

Binding of myosin head with F-actin and power stroke in myosin head

Sliding of actin filament over myosin filament

Muscular contraction


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LAQ4. What are the types of muscles? Describe the contractile proteins of skeletal muscle.Introduction - Muscles are classified by three different methods based on different factors -

1. Depending upon striations - The muscles are divided into two groups on the basis of whether striations are present or not.a) Striated muscle - Striated muscle is the muscle which has a large number of cross striations (transverse line). The skeletal

muscle and cardiac muscle belong to this category.b) Non striated muscle - The muscle which does not have cross striations is called non striated muscle. It is also called smooth

muscle. It is found in the wall of the visceral organs.2. Depending upon the control The muscles are classified into two types -

a) Voluntary muscle - Voluntary muscle is the muscle that is controlled by the will. Skeletal muscles are the involuntary muscles.These muscles are innervated by somatic nerves.

b) Involuntary muscle - These muscles are not controlled by will. Cardiac muscle and smooth muscle are involuntary muscles.These muscles are innervated by autonomic nerves

3. Depending upon the location or situation - The muscles are classified into three types depending upon the situation -a) Skeletal muscle - Skeletal muscle is situated in association with bones forming the skeletal system. These muscles are voluntary

and striated and they are supplied by somatic nerves.b) Cardiac muscle - Cardiac muscles form the musculature of the heart. These muscles are striated and involuntary. Cardiac muscles

are supplied by autonomic nerve fibers.c) Smooth muscle - Smooth muscles are situated in association with viscera. It is also called visceral muscle. They are non-striated.

They are supplied by autonomic nervous system.Contractile proteins of skeletal muscle

Introduction - The myosin filaments are formed by myosin molecules. The actin filaments are formed by three types of proteins called actin,tropomyosin and troponin. These four proteins together constitute the muscle protein or the contractile element of the muscle.

a) Myosin molecule - Each myosin filament consists of about 200 myosin molecules. Myosin-II is present in sarcomere.o Myosin-II is a globulin with a molecules weight of 480,000. Each myosin molecule is made up of 6 polypeptide chains of which two

are heavy and four are light chains.o The two heavy chains twist around each other to form a double helix. At one end, the two chains remain twisted around one another

and form the tail portion. At the other end, both the chains turn away in opposite direction and form the globular head portion, toeach part of this head are attached two light chains.

o Each myosin head has two attachment sides. One site is for actin filament and the other one is for one ATP molecules.b) Actin molecule - Actin molecules are the major constituents of the thin filaments. Each actin molecule is called F-actin and it is thepolymer of a small protein known as G-actin.o There are about 300-400 actin molecules in each actin filaments. The molecular weight of actin is 42000. The actin molecules in the

actin filament also are arranged in the form of a double helix. Each F-actin molecule has an actin to which the myosin head isattached.

c) Tropomyosin - There are about 40-60 tropomyosin molecules situated along the double helix strand of actin filaments. Each tropomyosinmolecule has the molecular weight of 70.000. In relaxed condition of muscle, the tropomyosin molecules cover all the active sites of F-actin molecule.

d) Troponin - It is formed by three subunits.o Troponin-I attached to F-actino Troponin-T attached to tropomyosino Troponin-C attached to calcium ions

e) Other proteins of the muscle - In addition to contractile proteins, the sarcomere contains some more proteins such as -o Actinin - Attaches actin filament to Z line.o Desmin Binds Z line with sarcolemma.o Nebulin - Runs in close association with and parallel to actin filaments.o Titin - A large protein connecting M line with Z line.o Dystrophin A rod shaped large protein that connects actin filaments to dystroglycin.

LAQ5. Define blood pressure & describe its regulation.Definition Arterial blood pressure is defined as the lateral pressure exerted by the contained column of blood on the wall of arteries. The

pressure is exerted when the blood flows through the arteries. The term blood pressure refers to arterial blood pressure. Arterial bloodpressure is expressed in four different terms -

1) Systolic blood pressure The systolic pressure is defined as the maximum pressure exerted in the arteries during systole of the heart.The normal systolic pressure ranges between 110 and 140 mm of Hg.

2) Diastolic blood pressure Diastolic blood pressure (diastolic pressure) is defined as the minimum pressure in the arteries during diastoleof the heart. The DP ranges from 60 to 80 mm of Hg.

3) Pulse pressure Pulse pressure is the difference between the systolic pressure and diastolic pressure. It is usually 40 mm of Hg.4) Mean arterial blood pressure - It is the average pressure existing in the arteries. It is the diastolic pressure plus one-third of pulse

pressure.Regulation of arterial blood pressure

Body has four regulatory mechanisms to maintain the blood pressure within normal limits1. Nervous mechanism or short term regulatory mechanism - When the arterial blood pressure changes, it is brought to normal by the

nervous system within a few minutes. The nervous mechanism regulating the arterial blood pressure operates through the vasomotorsystem. The vasomotor system includes three components -

a) Vasomotor centerb) Vasoconstrictor fibersc) Vasodilator fibers

Mechanism Vasomotor center regulates the arterial blood pressure by causing vasoconstriction or vasodilatation. Its action dependsupon the impulse it receives from baroreceptors, chemoreceptors, higher centers and respiratory centers.

(i) Baroreceptor mechanism - Baroreceptors are receptors which give response to changes in blood pressure. They are situatedin the carotid sinus and wall of the aorta. When stimulus of increased blood pressure is received by baroreceptor, it in turnsends stimulatory impulse to nucleus of tactus solitarius (in medulla oblongata) via IX & X cranial nerves. This inhibitsvasoconstriction area and decreases vasomotor tone, resulting in decreased peripheral resistance. The stimulation ofvasodilator area increases vagal tone which in turn decreases the rate and force of contraction of heart, leading to reduction incardiac output. These two factors bring the arterial blood pressure back to normal level.

(ii) Chemoreceptor mechanism - Chemoreceptors are the receptors giving response to change in chemical constituents of blood.They are situated in carotid body and aortic body. Chemoreceptors are sensitive to lack of oxygen, excess of carbon dioxideand hydrogen ion concentration in blood. Whenever the blood pressure decreases the blood flow decreases resulting in


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decreased oxygen content and excess of carbon dioxide and hydrogen ion. These factors stimulate chemoreceptors whichsend impulse to excite the vasoconstriction center which leads to rise in blood pressure and blood flow increases.

2. Renal mechanism or long term regulation - Kidneys regulate arterial blood pressure by two ways:a) By regulation of ECF volume - When the blood pressure increases, kidneys excrete a large amount of water (pressure

diuresis) and salt, especially sodium (pressure natriuresis). Because of diuresis and natriuresis there is decrease in ECFvolume and blood volume, which in turn brings the arterial blood pressure back to normal level.

b) Through renin-angiotensin mechanism - When blood pressure and ECF volume decrease, renin secretion from kidney isincreased. It converts angiotensinogen into angiotensin-I. This is converted into angiotensin-II by ACE (angiotensin convertingenzyme). Angiotensin-II causes constriction of arterioles in the body so that peripheral resistance is increased and bloodpressure rises. It also leads to constriction of afferent arterioles in kidney so that the GFR reduces. This increases ECFvolume. The result is increase in the blood pressure, bringing it back to normal level.o Angiotensin-II stimulates the adrenal cortex to secrete aldosterone. This hormone increases reabsorption of sodium from

renal tubules, leading to water reabsorption which increases ECF volume and blood volume. It increases the bloodpressure back to normal level.

3. Hormonal mechanism - Many hormones are involved in the regulation of blood pressure.Hormones which increase the blood pressure are:

o Adrenalineo Nor adrenalineo Aldosteroneo Thyroxino Vasopressin

Hormones which decrease the blood pressure are:o VIP (Vasoactive intestinal peptide)o Prostaglandino Histamineo Acetylcholine etc.

4. Local mechanism In addition to nervous, renal and hormonal regulations some local substance also regulate the blood pressure.They regulate the pressure by vasoconstriction or vasodilatation.

Local vasoconstrictors o Vascular endothelial origin - Endothelinso Endothelins activate prostacyclin and thromboxane causes vasoconstriction.

Local vasodilators -o Metabolic origin CO2, lactate, H

+, adenosine

o Endothelial origin Nitric oxide, endothelial derived relaxing factor.LAQ6. What is normal heart rate? Give its physiological variation and describe how heart rate is regulated.

Introduction - Heart rate is maintained within normal range constantly. It varies during normal physiological conditions such as exercise, emotionetc. However, the altered heart rate is quickly brought back to normal by regulatory mechanism.

Normal heart rate - Normal heart rate ranges between 60 and 80 per minute.Physiological variation

1) Tachycardia - Increase in the heart rate above 100 per min.2) Bradycardia - Decrease in the heart rate below 60 per min.

Physiological conditions when tachycardia occurso Childhoodo Exerciseo Emotional condition such as anxiety.

Physiological conditions when bradycardia occurso Sleepo Athletic heart

Regulation of heart rate - Heart rate is regulated by the nervous mechanism. The nervous mechanism regulating heart rate consists of thefollowing components -

1. Vasomotor center - It is the same center in the brain which regulates the blood pressure. Earlier it was called the cardiac center.Vasomotor center has three areas -

a) Vasoconstrictor area - This area increases the heart rate, by sending accelerator impulses to heart through sympathetic nerve. Italso causes constriction of blood vessels.

b) Vasodilator area - It decreases the heart rate by sending inhibitory impulses to the heart through vagus nerve. It also causesdilatation of blood vessels.

c) Sensory area - This area receives sensory impulses via glossopharyngeal nerve and vagus nerve from periphery, particularlyfrom baroreceptors. In turn, this area controls the vasoconstriction and vasodilator areas.

2. Motor (efferent) nerve fibers to heart Heart receives efferent nerve fibers from both divisions of the autonomic nervous system,parasympathetic as well as sympathetic.a) Parasympathetic nerve fibers - Parasympathetic nerve fibers are the cardioinhibitory nerve fibers. They reach the heart through

cardiac branch of vagus nerve. The vagus nerve fibers are cardio inhibitory to heart.b) Sympathetic nerve fibers - Sympathetic nerve fibers supplying the heart have cardioaccelerator function. They carry

cardioaccelerator impulses from vasoconstrictor area of the heart.o Sympathetic tone or cardio accelerator tone is the continuous stream of impulses produced by the vasoconstrictor area. The

impulses pass through sympathetic nerves and accelerate the heart rate.o Under normal conditions, the vagal tone is dominant over sympathetic tone. It is generally believed that the sympathetic tone

does not play an important role in the regulation of cardiac function under resting physiological condition. However, it plays adefinite role in increasing the heart rate during emergency.

3. Sensory (afferent) nerve fibers The afferent (sensory) nerve fibers from the heart pass through the inferior cervical sympathetic nerve.These nerve fibers carry sensation of stretch and pain from the heart to brain via spinal cord.

Factors affecting vasomotor center - or regulation of vagal tone

Factors which increase vagal tone and thus decrease heart rate -o Respiratory center during expirationo Preoptic and anterior nuclei of hypothalamuso Baroreceptor - Mareys reflex


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Factors which decrease vagal tone and increase the heart rate -o Respiratory center during inspirationo Cerebral cortex area 13o Posterior and lateral nuclei of hypothalamuso Chemoreceptorso Stretch receptor in right atrium - Bainbridge reflex

LAQ7. Describe in detail the structure and transmission physiology of neuromuscular junction along with suitable diagram.Definition - Neuromuscular junction is the junction between the terminal branch of the nerve fiber and muscle fiber.Structure - Skeletal muscle fibers are innervated by the motor nerve fibers. Each nerve fiber (axon) divides into many terminal branches. Each

terminal branch innervated one muscle fiber through the neuromuscular junction.a) Axon terminal and motor end plate - Terminal branch of nerve fibers is called axon terminal. When the axon comes close to the muscle

fiber, it loses the myelin sheath. So the axis cylinder is exposed. This portion of the axis cylinder is expanded like a bulb which is calledmotor end plate.

b) Synaptic trough or gutter - The motor end plate invaginates inside the muscle fiber and forms a depression which is known as Synaptictrough or Synaptic gutter.

c) Synaptic cleft - The membrane of the nerve ending is called the pre synaptic membrane. The membrane of the muscle fiber is calledpost synaptic membrane. The space between these two is called synaptic cleft. The synaptic cleft contains basal lamina. Large quantityof an enzyme called acetyl cholinesterase is attached to the matrix of basal lamina.

d) Sub-neural cleft - The post synaptic membrane is the membrane of the muscle fiber. It is thrown into numerous fold called sub neuralcleft.

Neuromuscular transmission - Neuromuscular transmission is defined as the transfer of information from motor nerve ending to the muscle fiberthrough neuromuscular junction. It is the mechanism by which the motor nerve impulses initiate muscle contraction. The series ofevent during this process are as following -o Release of acetylcholine - When the action potential reaches the axon terminal, it increases the permeability of pre synaptic

membrane for calcium ion by opening the voltage gated calcium. Channels in the membrane of the axon terminal. Calcium ionenter the axon terminal from Extra cellular fluid. The calcium ion cause bursting of the vesicles. Now the acetylcholine is releasedfrom the vesicles and the process is called exocyotosis The acetylcholine diffuse across through the pre synaptic membrane andenter the synaptic cleft

o Action of acetylcholine - After entering the synaptic cleft, the acetylcholine molecule binds with nicotine receptors present in thepost synaptic membrane and from the acetylcholine- receptor complex. It opens the legends gated channels for sodium in the postsynaptic membrane. Now sodium ions from extracellular fluid enter the neuromuscular junction through these channels. Thesodium ion produce an electrical potential called the end plate potential.

o End plate potential - End plate is the change in the resting membrane potential when an impulse reached the neuromuscularjunction. The resting membrane potential at the neuromuscular junction is -90 mv. When sodium ions enter inside, slightdepolarization occurs up to -60 mv, which is called endplate potential.

o Miniature endplate potential - Miniature endplate potential is a weak end plate potential in neuromuscular junction that isdeveloped by the release of a small quantity of acetylcholine from axon terminal. The amplitude of this potential is only up to 0.5mv. The miniature end plate potentials are added together by each quantum of acetylcholine released and finally produce endplate potential resulting in action potential in the muscle.

o Fate of acetylcholine - Acetylcholine released into the synaptic cleft is destroyed very quickly with in one millisecond after therelease into the synaptic cleft. It is destroyed by the enzyme, acetyl cholinesterase. The rapid destruction of acetylcholine preventsthe repeated excitation of the muscle fibers and allows the muscle to relax.

(Draw diagram from GHMC physiology assignments on NMP)LAQ8. What are the different types of muscles? Describe properties of skeletal muscle.

Introduction - Muscles are classified by three different method based on different factors -

1. Depending upon striations - Depending upon the presence or absence of the cross striation. The muscles are divided into two groups -o Striated muscle - Striated muscle is the muscle which has a large number of cross striation (transverse line) Skeletal muscle and

cardiac muscle belong to this category.o Non striated muscle - The muscle which does not have cross striation is called non striated muscle. It is also called smooth

muscle. It is found in the wall of the visceral organs.2. Depending upon the control - Depending upon the control, the muscle are classified into two types -

o Voluntary muscle - Voluntary muscle is the muscle that is controlled by the will. Skeletal muscles are the involuntary muscle.These muscles are innervated by somatic nerves.

o Involuntary muscle - These muscle are not controlled by will. Cardiac muscle and smooth muscle are involuntary muscle. Thesemuscles are innervated by autonomic nerves

3. Depending upon the situation - The muscle are classified into three types depending upon the situation -o Skeletal muscle - Skeletal muscle is situated in association with bones forming the skeletal system. These muscles are voluntary

and striated and they are supplied by somatic nerves.o Cardiac muscle - Cardiac muscle forms the musculature of the heart. These muscles are striated and involuntary. Cardiac

muscles are supplied by autonomic nerve fibers.o Smooth muscle - Smooth muscles are situated are situated in association with viscera. It is also called visceral muscles. They are

non-striated. They are supplied by autonomic nervous system.Properties of Skeletal muscles1. Excitability Excitability is the reaction or response of a tissue to irritation or stimulation. It is a physiochemical changes. The muscles

can be excited by both direct stimulation and indirect stimulation i.e. through its nerve. The type of stimulus which can excite a livingtissue are as following-

a) Mechanical stimulusb) Electrical stimulus

c) Thermal stimulusd) Chemical stimulus

2. Contractility - The skeletal muscle gives response to a stimulus in the form of contraction. The contraction is defined as the intervalevent of the muscle which are manifested by change in either the length or tension of the muscle fibers.Contraction may be isotonic contraction or isometric contraction. Isotonic contraction is the type of muscular contraction in which thetension remains the same and the length of the muscle fibers is altered. Isometric contraction in which the length of muscle fibersremains the same and the tension is increased. Based on the contraction time, the skeletal muscles are classified into two types-, thered muscles and pale muscles.o Red muscles: The muscles which contain large numbers of type I fibers are called red muscles. These muscles are also called

slow muscle or slow twitch muscles. The red muscles have longer contraction time. Back muscles and gastrocnemius muscle arered muscles.


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o Pale muscles: These muscles have large number of type II fibers. These muscles are also called white muscle, fast muscles orfast twitch muscles. They have short contraction time. Ocular muscles are pale muscles.

Factors affecting force of contraction - The force of contraction of the skeletal muscle is affected by o Strength of stimuluso Number of stimulus

o Temperatureo Load

3. Refractory period - Refractory period is the period at which the muscle does not shows any response to the stimulus. It is becausealready one action potential is in progress in the muscle during this period. The muscle is unexcitable to further stimulation until it isdepolarized. Refractory period is of two types -

Absolute refractory period - Is the period during which the muscle does not show any response at all, whatever may be thestrength of stimulus.

Relative refractory period - Is the period, during which the muscle shows some response i f the strength of stimulus is increasedto maximum.

4. Muscle tone - Muscle tone is defined as continuous and partial contraction of the muscle with certain degree of vigor and tension.o Maintenance of tone in skeletal muscle is neurogenic. It is due to continuous discharge of impulse from gamma motor neuron

in anterior gray horn of spinal cord.o In cardiac muscle maintenance of tone is purely myogenic.o In smooth muscle tone is myogenic. It depends upon calcium level and number of cross bridges.

SAQ (i) Properties of cardiac muscles1. Excitability - Excitability is defined as the ability of a living tissue to give response to a stimulus. So also the cardiac muscles are capable

for excitability to a given stimulus leading to development of action potential and result in physiological action in the form of contraction.o Resting membrane potential - The resting membrane potential in single cardiac muscle fiber is -85 to -95 mv.o Action potential The approximate duration of the action potential in cardiac muscle is 250-350 m sec. Action potential in a single

cardiac muscle fiber occurs in 4 phases -a) Initial depolarization- The depolarization is very rapid and it last for about 2 msec. The amplitude of the depolarization is

about 420 mv.b) Initial repolarization - Immediately after depolarization there is an initial rapid repolarization for a short period of about 2 m

sec.

c) Plateau or final depolarization - The muscle fiber remain in the depolarized state for sometimes before furtherepolarization. It forms the plateau (stable period) It is for about 200 m sec. (0.2 sec) in atrial muscle and for 0.3 sec inventricle muscle. Due to the long plateau in action potential the contraction time is longer in cardiac muscle by about 5 15times than in skeletal muscle.

d) Final repolarization- Occurs after the plateau. It is a slow process and it last for about 0.5 -0.8 sec.2. Rhythmicity - It is the ability to produce its own impulses regularly. It is more appropriately named as autorhythmicity. It is also called self

excitation. Heart has a specialized excitatory structure from which the discharge of impulses is rapid. This specialized structure is calledpacemaker. From pacemaker the impulses spread to other parts through the specialized conductive system

3. Conductivity - Human heart has a specialized conductive system through which the impulses from SA node are transmitted to all otherparts of the heart. The Conductive system of the heart is formed by the modified cardiac muscle fibers. They are also called the junctionaltissue. The conductive system in human heart comprises:

o SA nodeo AV nodeo Bundle of Hiso Right and left bundle brancheso Purkinje fibers.

4. Contractility - Contractility is ability of the tissue to shorten in length after receiving a stimulus. Various factor affect the contractileproperties of cardiac muscle which are as follows:a) All or none law - According to all or none law, when a stimulus is applied whatever may be the strength, the whole cardiac muscle

gives maximum response or it does not give any response at all. Below the threshold level the muscle does not give response.b) Staircase phenomenon - When the stimulus is given at interval of two seconds without changing the strength the force increases

gradually for the first few contractions and then remains same. Gradual increase of force of contraction is called staircasephenomenon.

c) Summation of subliminal stimuli When a stimulus with a subliminal strength is applied. The quiescent heart does not show anyresponse. When few stimuli with same subliminal strength are applied in succession, the heart shows response by contraction.

d) Refractory period - Refractory period is the period in which the muscle does not show any response to a stimulus. It is of two types -o Absolute refractory period - Absolute refractory period is the period during which the muscle does not show any response at al

whatever may be the strength of the stimulus.o Relative refractory period - The relative refractory period is the period during which the muscle shows response if the strength o

stimulus is increased to maximum.Refractory period in cardiac muscle

o Compared to skeletal muscle, the cardiac muscle has a long refractory period. The absolute refractory period extendsthroughout contraction period of cardiac muscle. It is for 0.27 sec and relative refractory period extends during first half o

relaxation period which is about 0.26 sec. So the total refractory period is 0.53 sec.o Long refractory period in cardiac muscle has three advantage-o Summation of contraction does not occuro Fatigue does not occuro Tetanus does not occur

SAQ (ii) Pacemkaer (See Ans on SA & AV nodes)SAQ (iii) Staircase phenomenon. (See Ans on properties of cardiac muscle)SAQ (iv) Neuromuscular junction (See Ans under LAQ and make it short)SAQ (v) Cardiac output and factors affecting it.

Introduction - Cardiac output is the amount of blood pumped from each ventricle. Usually it refers to the left ventricular output through aorta. Therate of blood flow through different parts of the body depends upon the cardiac output. Usually cardiac output is expressed in threeways -

(i) Stroke volume - The stroke volume is defined as the amount of blood pumped out by each ventricle during each beat. Normally it is 60-80 mwhen the heart rate is normal.

(ii) Minute volume - Minute volume is amount of blood pumped put by each ventricle in one minute. It is product of liters/ventricle/ minute.


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(iii) Cardiac index - Cardiac Index is the minute volume expressed in relation to square meter of body surface area. It is defined as the amount oblood pumped out per ventricle/minute/square meter of the body surface area. Normally it is 2.80.3 liters/square meter of body surfacearea/minute.

Factors maintaining cardiac output -Cardiac output is maintained by four factors -1. Venous return - Venous return is the amount of blood, which is returned to the heart from different parts of the body. Increase in venous

return increase the ventricular filling and cardiac output are increased. Venous return in turn depends upon five factors.a) Respiratory pump - Respiratory pump is the respiratory activity that helps return of the blood back to heart during inspiration. It is

also called abdomino-thoracic pump. During inspiration thoracic cavity expands and makes the intrathoracic pressure morenegative. It increases the diameter of inferior vena cava resulting in increased venous return. At the same time, descent odiaphragm increases the intra-abdominal pressure which compresses abdominal vein and pushed the blood upward towards theheart and there by the venous return is increased.

b) Muscle pump - Muscle pump is the muscular activity that helps returns of the blood back to heart. During muscular activities theveins are compressed or squeezed. When the skeletal muscle contract the vein located in between the muscle is compressed.

c) Gravity - Gravitational force reduce the venous return. In standing position gravity causes pooling of blood in the legs which iscalled venous pooling. Because of venous pooling the amount of blood returning to heart decrease.

d) Venous pressure - It also affects the venous return. The pressure gradually decreases from venues to vena cava. The pressure inthe right atrium falls and zero during atrial diastole. This pressure gradient at every part of venous tree helps as a driving force fovenous return.

e) Sympathetic tone - The sympathetic tone causes constriction of venules. The venoconstriction pushes the blood towards heart.2. Force of contraction - The cardiac output is directly proportional to the force of contraction provided the other three factors remain

constant. Force of contraction depends upon diastolic period and ventricular filling. Force of contraction also depends upon preload andafter load. The force of contraction of heart and cardiac output are directly proportional to preload. The force of contraction of heart andcardiac output are inversely proportional to after load.

3. Heart rate - Cardiac output is directly proportional to heart rate provided other three factors remain constant. Moderate change in hearrate does not alter the cardiac output but marked increase in heart rate increases cardiac output.

4. Peripheral resistance - Peripheral resistance is the resistance offered to blood flow at the peripheral blood vessel. The cardiac output isinversely proportional to peripheral resistance.

SAQ (vi) Difference between SA and AV nodes -SA node -o In our heart, the SA node works as a pacemaker. It is made up of pacemaker cells or P cells. SA node is the part of heart from

which the impulses for heart beat are produced normally.o SA node is a small strip or modified cardiac muscle situated in the superior part of lateral wall of right atrium just below the opening o

superior vena cava.o The fibers of this node do not have contractile element. These fibers are continuous with fibers of atrial muscle so that impulses from

SA node spread rapidly through atria. The rate of production of impulses is more in SA node than in other parts.o The electrical potential in SA node is different from that of other cardiac muscle fibers. In SA node each impulses triggers the next

impulses. It is mainly due to the unstable resting membrane potential. The resting membrane potential in SA node has a negativity o-55 to -60 mv.

o SA node is 3 mm wide, 15 mm long and 1 mm thick. The sinus nodal fibers connected directly with the atrial muscle fibers, so thaany action potential that begins in the sinus node spread immediately into the atrial muscle wall.

AV node -o The AV node (atrio-ventricular node) is located in the posterior wall of the right atrium immediately behind the tricuspid valve.o AV node can also work as conducting system of heart if the SA node fails to do so. Usually the impulses passe from SA node to AV

node. The velocity of impulses at AV node is 0.3 meter/second.o The atrial conductive system is organized so that the cardiac impulse does not travel from the atria into the ventricle too rapidly. This

delay allows time for the atria to empty their blood into the ventricle before ventricular contraction begins. It is primarily the AV nodeand its adjacent conductive fibers that delay this transmission into the ventricles. The total delay is 0.16 second before the excitatorysignal finally reaches the contracting muscle of the ventricles.

SAQ (vii) Sarcomere -Definition - Sarcomere is the structural and functional unit of the skeletal muscle. It is called the basic contractile unit of the muscle.Extent - Each sarcomere extends between two Z lines of myofibril. Thus each myofibril contains many sarcomeres arranged in series through

its length. When the muscle is in relaxed states, the average length of each sarcomere is 2-3 micronsComponent - Each myofibril consists of alternate dark A band and light I band. In the middle of A band there is a light area called H zone. In

the middle of H zone lies the middle part of myosin filament. This is called M line. M line is formed by myosin blinding protein.Electron microscopic structure of sarcomere -

The electron microscopic studies reveal, that the sarcomere consists of many thread like structure called myofilaments. They are otwo types -a) Actin filament - Actin filaments are the thin filaments with a diameter of 20 A

0and a length of 1 . These filaments extend from eithe

side of the Z line, run across I band and enter into A band up to H zone.b) Myosin filament - Myosin filaments are thick filaments with a diameter of 115 A

0and a length of 1.5 . These filaments are situated in

A band.There are some lateral processes (cross bridges) arising from myosin filaments. These bridges have enlarged structure called myosin

heads at their tips. The myosin heads attach themselves to actin filaments. These heads pulls the actin filaments during contraction of themuscles by means of a mechanism called sliding mechanism or ratchet mechanism.

During the contraction of the muscle, the actin filaments glide down between the myosin filaments towards the center of H zone andapproach the corresponding the actin filaments from the next Z line. The Z line also approach the end of myosin filament so that the H zoneand I band are shortened during contraction of the muscle. During the relaxation of the muscle, the actin filaments and Z line come back tothe original position.

SAQ (viii) Contractile proteins of skeletal muscle. (See LAQ above)


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GHMC Term 1 Solved Question Paper (2011-12 Batch) Section B (Set I-II)

LAQ1 Name the clotting factors. Explain the mechanism of coagulation of blood.Introduction - Coagulation or clotting is defined as the process in which blood loses its fluidity and becomes a jelly like mass few minutes after it

is shed out or collected in a container.o Clot is a mesh of thin fibrils entangling the blood cells. These fibrils consist of fibrin threads. The fibrin is formed from fibrinogen.

Factors involved in blood clotting - Coagulation of blood occurs through a series of reactions due to the activation of a group of substances. Thesubstances necessary for clotting are called clotting factors. Thirteen clotting factors are identified -o Factor I - Fibrinogeno Factor II - Prothrombino Factor III - Thromboplastino Factor IV - Calcium

o Factor V- Labile factor or accelerator globulino Factor VI - Not knowno Factor VII - Stable factoro Factor VIII - Antihemophilic factor or antihemophilic globulino Factor IX - Christmas factor or AH factor Bo Factor X - Stuart-Prower factor or AH factor Co Factor XI - Plasma thromboplastin antecedento Factor XII - Hageman factoro Factor XIII - Fibrin stabilizing factor or Laki-Lorand factor

Mechanism of coagulation of bloodSequence of clotting mechanism -

o Enzyme cascade theory - Most of the clotting factors are proteins in the form of enzymes. Normally all the factors are present in theform of inactive proenzyme. These proenzymes must be activated into enzymes to enforce clot formation. It is carried out by a series ofproenzyme-enzyme conversion reaction.

Stages of blood clotting - In general blood clotting occurs in three stages 1. Formation of prothrombin activator - Blood clotting commences with the formation of a substance called prothrombin activator which

converts prothrombin into thrombin. It is formed either within the blood itself or outside the blood. This formation of prothrombinactivator occurs through two pathways, namely, the extrinsic and intrinsic pathways

(Draw diagram from GHMC physiology assignments on Blood)(A) Intrinsic pathway - In this pathway the prothrombin activator is formed within the blood i.e., by platelets.

Sequence of events -

During the injury, the blood vessel is ruptured. The endothelium is damaged and collagen beneath the endothelium isexposed.

When factor XII (Hageman factor) comes in contact with collagen, it is converted into activated factor XII in the presence ofkallikrein and high molecular weight (HMW) kinogen.

The activated factor XII converts factors XI into activated factor XI in the presence of HMW kinogen.

The activated factors XI activates factor IX in the presence of factor IV (calcium).

Activated factor IX activate factor X in the presence of factor VIII and calcium

When platelet comes in contact with collagen of damaged blood vessel, it gets activated and release phospholipids.

Now the activated factor X reacts with platelet phospholipid and factor V to form prothrombin activator in presence of Ca2+

Factor V is also activated by positive feedback effect of thrombin.(B) Extrinsic pathway - In this pathway, the prothrombin activator is formed in the tissue (outside blood). Extrinsic pathway is initiated

by tissue thromboplastin (factor III) which is formed through the injured tissue.

Sequence of events - The tissue that are damaged during injury release factor III i.e. tissue thromboplastin. The thromboplastin contains proteins,

phospholipid and glycoprotein, which act as proteolytic enzymes.

The glycoprotein and phospholipid components of thromboplastin convert factor X into activated factor X in presence offactor VIII.

The activated factor X reacts with factor V and phospholipid component of tissue thromboplastin to form prothrombinactivator. This reaction requires calcium ions.

2. Conversion of prothrombin to thrombin - Blood clotting mainly consist of thrombin formation. Once thrombin is formed it leads to clotformation.

Sequence of events -

Prothrombin activator that is formed in intrinsic and extrinsic pathway converts prothrombin into thrombin in presence ofcalcium.

Once formed thrombin initiates the formation of more thrombin molecules. The initially formed thrombin activates factor V.Factor V in turn accelerates formation of both extrinsic and intrinsic prothrombin activator which converts prothrombin intothrombin this is called positive feedback effect.

3. Conversion of fibrinogen to fibrin -The final step of blood clotting involves the conversion of fibrinogen into fibrin by thrombin.

Sequence of events - Thrombin converts fibrinogen into activated fibrinogen.

The activated fibrinogen is called fibrin monomer.

Fibrin monomer polymerizes with other monomer molecules and form loosely arranged strands of fibrin.

Later these loose strands are modified into dense and tight fibrin thread by fibrin stabilizing factor in the presence of Ca2+

. Allthe tight fibrin threads are aggregated to form a meshwork.

LAQ2 Describe ABO blood group. Add a note on Rh factor.Introduction- Blood groups are determined by the presence of antigen in RBC membrane. Determination of ABO blood group depends upon the

immunological reaction between antigen and antibody. Two antigens are present on the surface of RBCs and they are named as Aantigen and B antigen. These antigens are also called agglutinogens because of their capacity to cause agglutination of RBCs.Corresponding antibodies or agglutinins are present in the plasma and named as anti A and anti B antibody. When antigen and antibodyreacts with each other clumping of blood occurs.

Blood group system - More than 20 genetically determined blood group systems are known today. Landsteiner discovered two blood groupsystems called ABO system and Rh system.


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Enzymes catalysing the reaction1. Hexokinase (Glucokinase)2. Glucose-phosphate isomerase3. Phosphofructokinase4. Aldolase5. Triose-phosphate dehydrogenase6. Phosphoglycerate7. Phosphoglyceromutase8. Enolase9. Pyruvate kinase

10. Lactate dehydrogenaseo All the enzymes involved in glycolytic pathway are found in extra mitochondrial soluble fraction of the cell.

Sequence of events1. Glucose to glucose 6-phosphate - Glucose phosphorylation to glucose 6-phosphate is catalysed by the enzyme hexokinase

(glucokinase). ATP acts as phosphate donor in the presence of Mg2+

.2. Glucose 6-phosphate to fructose 6-phosphate - This reaction is catalysed by phosphohexose isomerase3. Fructose 6-phosphate to fructose 1,6 diphosphate - Fructose 6-phosphate is further phosphorylated to fructose 1,6 diphosphate by ATP in

the presence of Mg2+

and phosphofructokinase.4. Fructose 1,6 diphospate to fructose triose phosphate - Fructose 1,6 diphosphate splits into two triose phosphates i.e., glyceraldehydes 3-

phosphate and dihydroxyacetone 3-phosphate by aldolase. These triose phosphates are interconverted by enzymephosphotrioseiosmerase. Dihydroxyacetone phosphate links fat metabolism and glycolysis through glycerol.

5. Glyceraldehyde 3-phoshate to glyceraldehyde 1,3 diphosphoglycerate - Glyceraldehyde 3-phosphate is oxidized to 1,3 glyceraldehydediphosphoglycerate, which contains high energy phosphate bond. This dehydrogenase reaction takes place in the presence of inorganicphosphate and coenzyme NAD

+which is converted to NADH

++H

+. Under aerobic condition the reduced NAD is reoxidised through

electron transport chain of mitochondria. These extra-mitochondrial electrons enter the mitochondria through two routes called shuttles.They are

o Glycerol phosphate shuttleo Malate aspartate shuttle

Since 2 molecules of inter-convertible triose phosphate are formed per molecule of glucose, 4 ATP molecules are produced via theglycerol phosphate shuttle. Whereas, 6 ATP are formed via the malate aspartate shuttle in anaerobic glycolysis, no ATP is formed as theNADH is reoxidised during the conversion of pyruvate to lactate.

6. From 1,3 diphosphoglycerate to 3-phosphoglycerate - The high energy phosphate bond generated in the preceding step is captured asATP in the presence of ADP and Mg

2+. The reaction is catalysed by phoshoglycerate kinase and 1,3 diphosphoglycerate is converted into

3-phosphoglycerate.7. From 3-phosphoglycerate to 2-phosphoglycerate - The 3-phosphoglycerate is converted to 2-phosphoglycerate by the enzyme

phosphoglyceromutase8. From 2-phosphoglycerate to phosphoenol pyruvate The 2-phosphoglycerate undergoes dehydration and redistribution of energy within

the molecules, thereby producing phosphoenolpyruvate. The reaction is catalysed by enolase.9. Phoshoenol pyruvate to pyruvate - Phosphoenol pyruvate is irreversibly converted to pyruvate. The high energy phosphate in

phosphoenol pyruvate is transferred to ADP by pyruvate kinase in presence of Mg2+

.10. Pyruvate to lactate - Pyruvate is the normal end product of glycolysis in aerobic condition. However, in the absence of oxygen it is

reduced to lactate by NADH, in the reaction catalysed by lactate dehydrogenase.Reaction No. of ATP formed per mole of glucose

1. Glyceraldehyde 3-phosphate to1,3 diphosphoglycerate 62. 1,3 diphosphoglycerate to 3 phosphoglycerate 23. Phosphoenol pyruvate to pyruvate 2

Total 10ATP Consumed in hexokinase and phosphofructokinase reaction - 2

Net ATP formed 8Each high energy phosphate bond = 7600 caloriesTotal amount of energy = 8 multiplied by 7600 = 60,800 calories.

LAQ4 Name essential fatty acids. Explain classification of fatsIntroduction - The unsaturated fatty acids which cannot be synthesized in the body from other sources are called essential fatty acids. These are

linoleic acid, linolenic acid and arachidonic acid.Essential fatty acids -

o Linoleic acid CH3 (CH2)4 CH = CHCH2 CH=(CH4)7 COOHo Linoleic acid CH2 (CH2)4 CH = CH CH2CH = CHCH2 CH = CH(CH2)4 COOHo Arachidonic acid CH3 (CH2)4CO = CH(CH2)4 (CH2)2 COOH

o Linoleic acid, however, can synthesize the other two essential fatty acids provided it is present in the body in sufficient amount.Lipids - Lipids are a heterogeneous group of organic compounds which are relatively insoluble in water but soluble in solvent such as ether,

chloroform and benzene.Classification - Lipids can be classified as follows:

1. Simple lipidso Fats,o Waxes

2. Compound lipidso Phospholipidso Glycolipids (glycosphingo lipids)o Lipoproteins, Amino lipids, sulpholipids

3. Derived lipidso Fatly acids, glycerol, sterols, fatty aldehydes. steroids, ketone bodies, lipid soluble vitamins, hormoneso Glycerides, cholesterol are uncharged and hence termed as neutral lipids.


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Fats - Fats are esters of fatty acid with glycerol. A generalized structural formula of fat may be written as:O||

CH2OH HOOC-R1 CH2-O-C-R1

O| | | ||CHOH + HOOC-R2 CH-O-C-R2

O| | | ||

CH2OH HOOC-R3 CH2-O-C-R3Glycerol Fatty acid Triglycerides

Waxes - Waxes are esters of fatty acid with alcohol other than glycerol.Phospholipids Phospholipids or phosphatides are esters of fatty acids with glycerol containing an esterified phosphoric acid and a nitrogen

base. For example,o Lecithinso Cephalinso Phosphatidyl inositolo Plasmalogenso Sphingomyelins

Glycolipids - These are complex lipids containing and amino alcohol attached with an amide linkage to a fatty acid and glycosidically to acarbohydrate moiety. For example,

o Cerebrosideso Gangliosides

Lipoproteins - These are lipid protein complexes found mainly in plasma and all membranes. Lipid constituents of lipoproteins are mostlyesterified cholesterol and phospholipids.

Fatty acids - Fatty acids are hydrolysis products of fats and other lipids.o Saturated fatty acids Butyric, lauric, palmitic, stearic.o Unsaturated fatty acids - Palmitoleic, oleic, linoleic, linolenic, arachidonic

Steroids - Steroids are naturally occurring cyclic compounds having a common structural base of cyclopentano-perhydro-phenanthrene ring.LAQ5 Define the blood. Describe its composition and function.

Introduction - Blood is a connective tissue in fluid form. It carries oxygen from lungs to all parts of the body and carbon dioxide from all parts ofthe body to the lungs. It carries nutritive substance from the digestive system and hormone from endocrine glands to all the tissues. Itprotects the body against the disease and gets rid of the waste products and unwanted substances by transporting them to the excretoryorgan like kidney.

Composition of blood - Blood contains the blood cells which are called formed elements and the liquid portion known as plasma.o Blood cells - Three types of cells are present in the blood.

a) Red blood cells or erythrocytesb) White blood cells or leukocytes.c) Platelets or thrombocytes

o Plasma - Plasma is clear straw coloured fluid or the liquid part of blood. It contains 91-92% water and 8-9 % of solids. The solids are theorganic and inorganic substance.

Composition of plasma-1. Solids - 8-9 %

1. Organic substances(i) Plasma proteins

o Albumin o Globulin o Fibrinogen.(ii) Amino acids - Essential and non-essential amino acids.(iii) Carbohydrate - Glucose(iv) Fat

o Triglyceride o Cholesterols o Phospholipids(v) Internal secretion - Hormones(vi) Enzymes

o Amylaseo Carbonic anhydraseo Acid phosphateso Alkaline phosphates

o Lipaseo Esteraseo Proteaseo Transaminase

(vii) Non protein nitrogenous (NPN) substanceo Ammoniao Creatineo Creatinineo Xanthine

o Hypoxanthineo Ureao Uric acid

(viii) Antibodies2. Inorganic substances

o Sodiumo Bicarbonateo Irono Calcium

o Chlorideo Coppero Potassiumo Phosphate

o Magnesiumo Iodide

2. Water- 91-92 %3. Gases

o Oxygeno Carbon dioxideo Nitrogen


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Serum - Serum is the clear straw colored fluid that is left after blood has clotted. Serum has approximately the same volume of plasma (55 %). It isdifferent from plasma only by the absence of fibrinogen.

Function of blood -o Nutrient function - Nutritive substance like glucose, amino acids, lipids and vitamins derived from digested food are absorbed from

gastrointestinal tract and carried by blood to different for growth and production of energy.o Respiratory function - Transport of respiratory gases is done by the blood. It carries oxygen from alveoli of lungs to different tissues and

carbon dioxide from tissue to alveoli.o Excretory function - Waste products formed in the tissue during various metabolic. Activities are removed by blood and carried to

excretory organ like kidney, skin, liver etc for excretion.o Transport of hormones and enzymes - Hormones which are secreted by ductless (endocrines) glands are released directly in to the

blood. The blood transports these hormones to their target organs or tissues. Blood also transport enzymes.o Regulation of water balance - Water content of the blood is freely interchangeable with interstitial fluids. This help in the regulation o

water content of the body.o Regulation of acid-base balance - The plasma protein and hemoglobin act as buffer and help in regulation of acid base balance.o Regulation of body temperature - Because of high specific heat of the blood, it is responsible for maintaining the thermoregulatory

mechanism in the body i.e. the balance between heat loss and heat gain in the body.o Storage function - Water and some important substance like proteins, glucose, sodium and potassium are constantly required by the

tissue. These substances are taken from blood during the condition like starvation, fluid loss, electrolyte loss etc.o Defensive function - Blood plays important role in the deference of the body. White blood cells are responsible for this function.

Neutrophils, monocytes engulf the bacteria by phagocytosis. Lymphocytes are involved in development of immunity. Eosinophils areresponsible for detoxification, disintegration and removal of foreign protein.

LAQ6 Define erythropoiesis. Describe its different stages with their regulation.Definition - Erythropoiesis is the process of the origin, development and maturation of erythrocytes. Hemopoiesis or hematopoiesis is the process o

origin, development and maturation of all blood cells.Stages of erythropoiesis -

The various stages between CFU-E (colony forming unit-E cells and matured RBCs are, namely, proerythroblast, early normoblast

intermediate normoblast, late normoblast, reticulocyte, and finally, the mature erythrocyte.1. Proerythroblast (Megaloblast) -This is the first cell derived from CFU-E. It is very large in size with a diameter of about 20 . Its nucleus islarge and occupies the cell almost completely. The proerythroblast does not contain hemoglobin. The cytoplasm is basophilic in nature.

2. Early normoblast - It is little smaller than proerythroblast with a diameter of about 15 . In the nucleus, the nucleoli disappearCondensation of chromatin network occurs. The cytoplasm is basophilic in nature, so it is also called basophilic erythroblast.

3. Intermediate normoblast - This cell is smaller than the early normoblast with a diameter of 10 to 12 . The nucleus is still present. Buthe chromatin network shows further condensation. The hemoglobin starts appearing. Cytoplasm is already basophilic now, becauseof the presence of haemoglobin. It stains with both acidic as well as basic stains. Therefore, this cell is called polychromophilic.

4. Late normoblast - This diameter of the cell decreases further about 8 to 10 . Nucleus becomes very small with very much condensedchromatin, network and it is known as ink spot nucleus. Quantity of haemoglobin is increased, cytoplasm becomes acidophilic. Thecell is now called orthochromic erythroblast. In the final stage of late normoblast just before it passes to next stage the nucleusdisintegrates and disappears. The process by which nucleus disappears is called pyknosis.

5. Reticulocyte - It is also known as immature RBC. It is slightly larger than mature RBC. The cytoplasm contains the reticular networkwhich is formed by remnants of disintegrated organelles. Due to the reticular network, the cell is called reticulocyte. These cells entethe capillaries through the capillary membrane from source of production by diapedesis.

6. Mature erythrocyte - The reticular network disappears and the cell becomes the mature RBC and attains the biconcave shape. Thecell decreases in size to 7.2 diameter. The mature RBC is with hemoglobin and without nucleus.

Factors necessary for erythropoiesisDevelopment and maturation of erythrocytes depends on various factors that can be classified into general factors, maturation factorsand factors necessary for hemoglobin formation.o General factors - Those necessary for erythropoiesis are four, namely, erythropoietin, thyroxin, hemopoietic growth factor and

vitaminsa) Erythropoietin - It is also called hemopoietin or erythrocyte stimulating factors. Erythropoietin promotes the production o

proerythroblast from CFU-E of the bone marrow and helps in maturation and development from proerythroblast to mature RBC.b) Thyroxin - It is a general metabolic hormone and it helps in process of erythropoiesis.c) Hemopoietic growth factor - Hemopoietic growth factors or growth inducers are the interleukins and stem cell factors. Usually

they help in erythropoiesis.d) Vitamins - Vit B, Vit C, Vit D, and Vit E are necessary for erythropoiesis. The deficiency of these vitamins causes anemia

associated with other disorders.o Maturation factors -

o Vit B12 - It is essential for synthesis of DNA in RBCs. Its deficiency causes failure in maturation of the cell and reduction in thecell division.

o Intrinsic factor of Castle - It is essential for absorption of Vit B12 from intestine. Its deficiency leads to pernicious anemia.o Folic acid - This is essential for maturation. It is required for synthesis of DNA.

o Factors necessary for hemoglobin formation -o First class protein and essential amino acids are required for synthesis of protein part of hemoglobin.o Iron is required for the formation of hem part of the hemoglobin.o Copper is necessary for the absorption of iron from the gastro intestinal tract.o Cobalt & nickel are essential for the utilization of iron during hemoglobin formation.o Vit C, riboflavin, nicotinic acid and pyridoxine are also essential for formation of hemoglobin.

LAQ7 Describe various steps of Krebs cycle & give details of the energetics.Introduction - Pyruvate is oxidized to CO2 & H2O through a series of reactions under aerobic condition. Collectively these are called citric acid cycle

(tri carboxylic acid cycle) or more commonly as Krebs cycle. It is the most important metabolic pathway related to energy production.Site of enzymes - All the enzymes catalyzing various reactions in the pathway are located in mitochondria. Citric acid cycle is also known as a

common metabolic pathway because the intermediates of this cycle are also synthesized from compounds other than carbohydrates like fatsand protein.


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LI

eaction and inta) Pyruva

catalysthiamio O

ofatr

a) Oxaloais relea

b) Citrate

which ic) Isocitra

dehydrd) Oxalos

presene) -Keto

dehydrf) Succin

(GTP)succin

g) Succinwhich i

h) Fumari) Malate

comple

nzymes of the c1. Pyruva2. Citrate3. Aconit4. Isocitra5. Isocitra

nergetics of citriReacti

PyruvaIsocitraKetogl

SuccinSuccinMalate

As oneQ8 Define

ntroduction- Carderivatives

lassification of1. Mono

Monoand hrespe

rmediates -te to acetyl-Coed by a groupe pyrophosphatxidation decarbopyruvate dehycepts CoA andnsacetylase. Rcetate + acetyl-sed. This reactito isocitrate - T

s then rehydratere to oxalosuccogenase.uccinate to ketce of Mn

2+.

lutarate to sucogenase in presyl-CoA to succiin presence ofl thiokinase.

ate to fumarates converted to Fte to malate - Fto oxaloacetatetes the cycle.

ycle -te dehydrogenasynthetasesete dehydrogenate dehydrogenaic acid cycleon

te-acetyl-CoAte-oxalosuccinatarate-succinyl-

yl CoA-Succinatatefumarate

oxaloacetateotal

molecule of glucarbohydrate.

bohydrates are.arbohydrates -accharide - Taccharides are

exoses. Each otively.

- Pyruvate isof enzymes ca(TPP), lipoic a

xylation of pyrurogenase. Oxidform acetyl CoAduced lipoate isoA to citrate -n is catalyzed b

his step is catal

d to form isocitrinate - Isocitrat

glutarate - Oxa

inyl-CoA - Ketence of TPP, lipate - At this staGDP & inorgan

- Succinate unADH..umarate is hydra

- It is a dehyd

e complex

sese

ATP forph

teCoA

ose gives twoExplain classifhe best source

ese are the sigrouped accordthese can be f

oxidatively decalled pyruvate did, CoA, FAD aate - Pyruvate i

ised lipoate the. Lipoic acid isreoxidized by dcetyl-CoA comy a condensingsed by aconita

te.undergoes de

losuccinate is d

glutarate is oxiate FAD and Ne substrate lev

ic phosphate. G

ergoes dehydr

ted to form malrogenation react

ed through oxosphorylation

333

-2314

14+oles of pyruvat

ication of carbof energy for h

implest membeing to the numburther named a

HMC Physiolog

6

rboxylated to ahydrogenase cd NAD

+as coe

s decarboxylatereacts with ac

eleased in the rihydrolipoyl dehines with oxalonzyme citrate s

e and takes pla

hydrogenation t

ecarboxylated t

atively decarboD

+.

el phosphorylatiTP then transfe

genation to for

te in presenceion catalysed b

Krebs cycle

idative ATP

--

-

1--

1 =15 ATP moles total numberhydrates andman beings an

s of carbohydrr of carbon atoaldose or keto

y Answers: Co

etyl-CoA for itsomplex which inzymes.

with the help oetaldehyde-TPPeduced form. Bydrogenase andcetate to form cynthetase. It isce in two steps.

o form oxalosu

o ketoglutarate

xylated to succ

on takes place,rs the high en

m fumarate in

f fumarase.y malate dehyd

6. -ketogl7. Succinic8. Succinat9. Fumaras10. Malate d

formed by subphosphorylatio

1culesf ATP formeddd a note on cmay be define

ates which arepresent in a s

se, depending

piled by (Dr) La

entry into thencludes three d

f TPP to form aand convents ith these reactioFAD.itrate. A molecun irreversible reIn first step citr

ccinate. The re

and is catalyse

inyl-CoA. React

i.e., productionrgy bond to AT

resence of suc

rogenase in pre

tarate dehydrogthiokinasee dehydrogenaseehydrogenase

trate leveln

15x2 = 30 ATPhemistry of glud as polyhydrox

represented bugar molecule sn the presence

lit Singh, Ed Dr

citric acid cycleifferent enzyme

cetaldehyde-TPit to acetyl lipoans are catalyse

le of water is coaction.ate is dehydrate

action is cataly

d by isocitrate

ion is catalysed

f a high energyP. This reactio

cinate dehydrog

sence of NAD+.

enase complex

e

molecules.cose.yaldehydes and

y general formch as trioses, tof an aldehyde

S Kochhar, HO

. This reaction is. It also utilize

in the presencte, which in tur

by dihydrolipo

nsumed and Co

d to isoaconitas

sed by isocitrat

ihydrogenase i

by ketoglutarat

phosphate bonis catalysed b

enase and FA

. This conversio

ketone and the

ula C12 H24 O1troses, pentoseor ketone grou

ss

e

e

e

n

e

dy

n

i

sp


15/16

SSS

I

termi

2. Oligogener

3. Polysweigh

They aa)

oo

o

ob)

sote on chemistr

Glucose isGlucose is con

o Glycogo Riboseo Galacto

o GlucuroIn order tohydroxyl grouppoints to the le

The two oconfiguration agroup at the re

In glucoseo Hyaluroo Chondro Hepari

Q (i) FunctiQ (ii) ErythrQ (iii) Absor

ntroduction - Cadisaccharid

Structural and ial carbon atom i

accharide - Thal formula C12 (H

Raffinose -Sucrose, m

o So Mo L

Lactose & mccharides - Ma

t polymers of m

re further classifomopolysacchaCellulose - It hStarch - It con-1,4 glucosidiglucose molecGlycogen - It isimilar to thatDextrin - Theseteropolysacchucopolysaccha

ulphate, hepariy of glucosethe most impor

verted to other cn - For storage- For nucleic acise - For forming

nic acid - Has dclassify structuat the carbon nt it is an L sugaptical isomers,round the reducucing carbon to

solution after attnic acid containoitin sulphate cocontains glucons of blood. (poiesis (Maketion of carboh

rbohydrates arees must be hyd

someric classificin a straight chai

L-Glse are conden2O)n-1. For examrisaccharideltose, lactose -

ucrose = glucosaltose = glucosectose = galactoltose are reduci

jority of carbohynosaccharide re

ied as homopolyrides - The cellus a linear chainists of two mole

c bond betweenle in straight chthe major carb

f amylopectin.are the interme

arides - Theserides (glycosametc.

tant carbohydratarbohydrate havd synthesislactose of milk,

etoxicating functral and isomerixt to the terminr.dextrorotatory aing carbon in ththe right and

aining equilibriuN-acetylglucos

ntains N-acetylgamine, glucuronake short Ans f

short Ans fromydratesgood sources ofolysed to mono

ation divides sin molecule poin

coseation productsple:

isaccharides+ fructose

+ glucosee + glucose

ng sugars wherdrates found inpresented by th

saccharides andlose, starch, glyof D glucose recules, amylaseglucose molecin and -1,6 glhydrate reserv

diate products iare made up

inoglycans) and

e. It is absorbeding specific func

compound lipids

ions and a comform of simpleal carbon atom i

nd levorotatorye ring structure to the left.

approximatelyamine, glucuronalactosamine, idic acid, and sulrom LAQ)AQ)

energy and areaccharide befor

HMC Physiolog

7

ple sugar intos to the right, it i

D-Glucoseof two to ten si

as sucrose is anatural sources

general formul

heteropolysaccogen and dextriidues linked togand amylopectiules, where ascosidic bond atof human body

the hydrolysisof more thanoccur in com

into the bloodtion.

and glycoprotei

onent of mucopsugar, they arn a straight chai

of simple sugaof a represente

two third of sugic acid.uronic acid, andhuric acid.

mainly taken ine they can be a

y Answers: Co

D and L seriesis a D sugar and

mple sugars or

non-reducing soccurs in the foa (C6H10O5)n.

harides.in all contain gluether with a -1. Amylose is amylopectin is athe branch poin, stored mainly

f starch to monone sugar deriination with pr

stream. It is deri

in or proteoglyca

olysaccharide.divided into Din. When the mo

r are designateby an and

ars exist as the

sulphuric acid.

the form of starsorbed by intes

piled by (Dr) La

. If the hydroxylif it point to the

monosaccharid

gar.rm of polysacch

cose as repeati-4 glycosidic linktraight chain pbranched mole

s.in liver and mus

osaccharides.ative as repeateins. For exa

ived from glycog

ns.

and L series,lecule points to

d as (d) or (+) sign. The

form.

ch, lactose, sucrtinal tract.

lit Singh, Ed Dr

group at the cleft it is an L su

s. They are re

arides. These a

g unit.age.olymer similar tocule with -1,4

cles. The struct

ting unit. Theyple, hyaluroni

en during glyco

epending on tthe right, it is a

and (l) or (-)shows the proj

ose. Dietary pol

S Kochhar, HO

rbon next to thar.

presented by th

re high molecul

cellulose havinlinkage betwee

re of glycogen i

are also calleacid, chondriti

genolysis in live

e position of thD sugar and of

respectively. Thction of hydrox

saccharides an

e

e

gn

s

dn

r

ei

e

d


16/16

SI

SSS

I

F

bsorption of carinto circulaabsorptiono The pr

of gluco The tra

the bruo Na

+ha

glucoso Thus N

is follocapilla

o This aco Howev

absorpo The hi

mannoQ (iv) Glyco

ntroduction - Thlarge amou

echanism - Glphosphate.o UTP co UDPG

reactioo Glygoc

branchand trao Thus a

Q (v) BloodQ (vi) CoaguQ (vii) Functi

ntroduction - Lipchloroform

unctions1. They2. They

can b3. They

integri

4. Phos5. Phos6. Phos7. Mem8. Phos9. Phos10. Dipal11. Phos12. Esse

arachi13. Leuko

mem14. Doco15. Steroi

bohydrates - Thtion via portal veby increasing thsent concept rse and galacto

nsfer is mediatesh border mems been found tand galactose,

a+

enhances th

wed by their relies. Such a mective transport ofer, it is absorbtion of monosachest rate of a

se & xylose areenesisformation of gl

nts. On an avercogen is form

mbines with gluthen transfers itn catalysed by gen synthease a

ing enzyme amnsfers this fraghighly branched

groups(Make slation factors (ns of lipids.

ids are a heteroand benzene.

provide energy tprovide building

used for the syprovide essentiaity such as lipop

holipids form thholipids act asholipids help inrane phospholiholipids providehatidyl inositideityl lecithin acts

hatidyl inositol itial fatty acids aidonic acid by cytrienes synthesranes and increahexenoic acidds are the main

monosacchariin. A very smalle surface area.garding the abse is now believed by a specificrane of intestine

be essential fand also for Nabinding of the

lease into the chanism also facigalactose/glucod by the proceharide has beesorption is fou

absorbed much

ycogen in the bge about 108 gd from glucose

cose 1-phosphas glucose to thely

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