T1 Solved Q Paper Full

GHMC Physiology Question Paper Term 1 (set-I) & RE (set-II) Old Paper Pattern Section A (Set-I) 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) 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) Write any 2 out of 4 (2x10=20 Marks) a) Properties of cardiac muscle. c) Staircase phenomenon. b) Pacemaker. d) Neuromuscular junction Section A (Set-II) Define blood pressure & describe its regulation. Or What is normal heart rate? Give its physiological variation & describe how heart rate is regulated. (15 Marks) 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) Write any 2 out of 4 (2x10=20 Marks) a) Cardiac output & factors affecting it. c) Sarcomere. b) Difference between SA & AV nodes. d) Contractile proteins of skeletal muscle. Section-B (Set-I) Name the clotting factors. Explain the mechanism of coagulation of blood. Or Describe ABO blood group. Add a note on Rh factor. Describe glycolysis & give details of its energetics. Or Name essential fatty acids. Explain classification of fats and describe functions of lipids? Write any 2 out 4 a) Functions of blood. c) Absorption of carbohydrates. b) Erythropoiesis. d) Glycogenesis. Section-B (Set-II) Define the blood. Describe its composition & functions. Or Define erythropoiesis. Describe its different stages with their regulation. (15 Marks) Describe various steps of Krebs cycle & give details of the energetics. Or Define carbohydrate. Explain classification of carbohydrates & add a note on chemistry of glucose. (15 Marks) Write any 2 out 4 a) Blood group. c) Functions of lipids b) Name the coagulation factors, with short d) Glycogenesis description of any five. COMPOSITE SECTION A LAQ Qu. 1. Qu. 2. Qu. 3. Qu. 4. Qu. 5. Qu. 6. Qu. 7. Qu. 8. Short Notes Define cardiac cycle. Describe its various events with pressure & volume changes. What are heart sounds? Describe their characters, mechanisms of formation with their significance. Describe molecular basis of muscular contraction. Enumerate properties of skeletal muscle. What are the types of muscles? Describe the contractile proteins of skeletal muscle. Define blood pressure & describe its regulation. What is normal heart rate? Give its physiological variation & describe how heart rate is regulated. Describe in detail the structure & transmission physiology of neuromuscular junction along with suitable diagram. What are the different types of muscles? Describe properties of skeletal muscle. i) ii) iii) iv) LAQ Qu. 1. Qu. 2. Qu. 3. Qu. 4. Qu. 5. Qu. 6. Qu. 7. Qu. 8. Short Notes Name the clotting factors. Explain the mechanism of coagulation of blood. Describe ABO blood group. Add a note on Rh factor. Describe glycolysis & give details of its energetics. Name essential fatty acids. Explain classification of fats and describe functions of lipids? Define the blood. Describe its composition & functions. Define erythropoiesis. Describe its different stages with their regulation. Describe various steps of Krebs cycle & give details of the energetics. Define carbohydrate. Explain classification of carbohydrates & add a note on chemistry of glucose. i) ii) v) vi) Functions of blood. Erythropoiesis. Blood group. Name the coagulation factors, with short description of any five. iii) iv) vii) Absorption of carbohydrates. Glycogenesis. Functions of lipids Properties of cardiac muscle. Pacemaker. Staircase phenomenon. Neuromuscular junction COMPOSITE SECTION B v) vi) vii) viii) Cardiac output & factors affecting it. Difference between SA & AV nodes. Sarcomere. Contractile proteins of skeletal muscle.
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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 diastole Subdivision 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 = 0.05sec o Rapid ejection period = 0.10 sec o Slow ejection period = 0.15 sec 0.30 sec = .3 sec b) Diastole o Protodiastole = 0.04sec o Isometric relaxation = 0.06 sec o Rapid filling = 0.10 sec o Slow filling = 0.20 sec o Atrial filling = 0.20 sec nd or 2 rapid filling 0.50 sec = .5 sec Total 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 a separate phase since it coincides with the ventricular systole and earlier part of ventricular diastole. The atrial systole extends for about 0.11 sec and the duration of atrial diastole is about 0.69 sec. Description of events of cardiac cycle 1. 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, Intraventricular pressure and ventricular volume also increase but slightly. After atrial systole, the ventricular systole starts, simultaneously atrial diastole also starts. 2. Isometric contraction period - Isometric contraction or isovolumetric contraction is the first phase of ventricular systole. It lasts for 0.05 sec. Immediately after atrial systole, the atrioventricular valves are closed due to increase ventricular pressure. The semilunar valves are already close. Now the ventricles contract as closed cavities in such a way that there is no change in the volume of ventricular chambers or in length of muscle fibers. Only the tension increased in ventricular musculature. Because of increased tension in ventricular musculature during isometric contraction, the pressure increases sharply inside ventricles. The pressure rise in ventricles caused 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 ejection from 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 pulmonary artery increases and pressure in ventricles drops. When the intraventricular pressure becomes less than the pressure in aorta and pulmonary artery the semilunar valves close. The atrioventricular valves are already closed. Protodiastole indicates only the end of systole and beginning of diastole. 5. Isometric relaxation period - During isometric relaxation period once again all the valves of the heart are closed. Both the ventricles relax as closed cavities without any change in volume or length of the muscle fibers. The fall in pressure in the ventricles caused by isometric 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 are produced by movements of: 1. Blood through the chambers of the heart. 2. Cardiac muscle, and 3. 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 resemble the spoken words LUB or LUBB and DUBB or DUP respectively. These two sounds are heard by using the stethoscope. Third heart sound is a mild sound and it cannot be heard by using stethoscope in normal condition. But it can be heard by using a microphone. The fourth heart sound is an inaudible sound. This sound is studied only by graphical registration i.e. the phonocardiogram. Description of heart sounds 1. First heart sound - The first heart sound is produced during isometric contraction period and earlier part of ejection period. Cause o 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 LUBB Duration .10-.17 sec Frequency 25-45 cycle/ second Relation with ECG Coincides with peak of R wave No. 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 valves Characteristics - Short, sharp and high pitched. Resembles the word DUB
GHMC Physiology Answers: Compiled by (Dr) Lalit Singh, Ed Dr S S Kochhar, HOD

Duration - 0.10-0.14 sec. Frequency - 50 cycles / sec Relation with ECG - Precedes or appears 0.09 second after peak of T wave No. 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 also called ventricular gallop or protodiastolic gallop as it is produced during earlier part of diastole. Usually the third heart sound is inaudible by stethoscope and it can be heard only by using microphone. It occurs during rapid filling phase. Cause - Rushing of blood into ventricle. Characteristics - Low pitched Duration - 0.07-0.10 sec. Frequency - 1-6 cycle / sec Relation 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 the physiologic 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 in the flaps of the atrioventricular valves. Some vibrations are also set up in ventricular myocardium due to the ventricular distension during atrial systole Character Inaudible sound Duration 0.02 0.4 sec Frequency 1-4 cycles / sec Relation with ECG Between P wave and Q wave No. 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 sound indicates 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 there stages. 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 from motor 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, these cisternae are excited. Now the calcium ions stored in the cistern are excited, and released into the sarcoplasm. The calcium ion from 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 F actin. However in relaxed condition, the active site of F-actin is covered by the tropomyosin. Therefore, the myosin head cannot combine 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 head of myosin get attached to the actin. 3. Sliding mechanism and formation of actomyosin complex - Sliding theory explains how the actin filament slides over myosin filament and 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 of head 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 bend back and forth and pulls the actin filament towards the center of sarcomere. In this way all the actin filaments of both the ends of sarcomere are pulled. So the actin filaments of opposite sides overlap and form actomyosin complex. Formation of actomyosin complex 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

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, to each 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 the polymer 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 is attached. c) Tropomyosin - There are about 40-60 tropomyosin molecules situated along the double helix strand of actin filaments. Each tropomyosin molecule has the molecular weight of 70.000. In relaxed condition of muscle, the tropomyosin molecules cover all the active sites of Factin molecule. d) Troponin - It is formed by three subunits. o Troponin-I attached to F-actin o Troponin-T attached to tropomyosin o 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 blood pressure 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 diastole of 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 limits 1. 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 vasomotor system. The vasomotor system includes three components a) Vasomotor center b) Vasoconstrictor fibers c) Vasodilator fibers Mechanism Vasomotor center regulates the arterial blood pressure by causing vasoconstriction or vasodilatation. Its action depends upon 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 situated in the carotid sinus and wall of the aorta. When stimulus of increased blood pressure is received by baroreceptor, it in turn sends stimulatory impulse to nucleus of tactus solitarius (in medulla oblongata) via IX & X cranial nerves. This inhibits vasoconstriction area and decreases vasomotor tone, resulting in decreased peripheral resistance. The stimulation of vasodilator area increases vagal tone which in turn decreases the rate and force of contraction of heart, leading to reduction in cardiac 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 dioxide and hydrogen ion concentration in blood. Whenever the blood pressure decreases the blood flow decreases resulting in

decreased oxygen content and excess of carbon dioxide and hydrogen ion. These factors stimulate chemoreceptors which send 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 ECF volume 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 is increased. It converts angiotensinogen into angiotensin-I. This is converted into angiotensin-II by ACE (angiotensin converting enzyme). Angiotensin-II causes constriction of arterioles in the body so that peripheral resistance is increased and blood pressure rises. It also leads to constriction of afferent arterioles in kidney so that the GFR reduces. This increases ECF volume. 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 blood pressure 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 Adrenaline o Nor adrenaline o Aldosterone o Thyroxin o Vasopressin Hormones which decrease the blood pressure are: o VIP (Vasoactive intestinal peptide) o Prostaglandin o Histamine o 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 - Endothelins o 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, emotion etc. 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 occurs o Childhood o Exercise o Emotional condition such as anxiety. Physiological conditions when bradycardia occurs o Sleep o Athletic heart Regulation of heart rate - Heart rate is regulated by the nervous mechanism. The nervous mechanism regulating heart rate consists of the following 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. It also 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 causes dilatation of blood vessels. c) Sensory area - This area receives sensory impulses via glossopharyngeal nerve and vagus nerve from periphery, particularly from 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 a definite 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 expiration o Preoptic and anterior nuclei of hypothalamus o Baroreceptor - Mareys reflex

Factors which decrease vagal tone and increase the heart rate o Respiratory center during inspiration o Cerebral cortex area 13 o Posterior and lateral nuclei of hypothalamus o Chemoreceptors o 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 called motor end plate. b) Synaptic trough or gutter - The motor end plate invaginates inside the muscle fiber and forms a depression which is known as Synaptic trough 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 called post synaptic membrane. The space between these two is called synaptic cleft. The synaptic cleft contains basal lamina. Large quantity of 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 neural cleft. Neuromuscular transmission - Neuromuscular transmission is defined as the transfer of information from motor nerve ending to the muscle fiber through neuromuscular junction. It is the mechanism by which the motor nerve impulses initiate muscle contraction. The series of event 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 ion enter the axon terminal from Extra cellular fluid. The calcium ion cause bursting of the vesicles. Now the acetylcholine is released from the vesicles and the process is called exocyotosis The acetylcholine diffuse across through the pre synaptic membrane and enter the synaptic cleft o Action of acetylcholine - After entering the synaptic cleft, the acetylcholine molecule binds with nicotine receptors present in the post synaptic membrane and from the acetylcholine- receptor complex. It opens the legends gated channels for sodium in the post synaptic membrane. Now sodium ions from extracellular fluid enter the neuromuscular junction through these channels. The sodium 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 neuromuscular junction. The resting membrane potential at the neuromuscular junction is -90 mv. When sodium ions enter inside, slight depolarization 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 is developed by the release of a small quantity of acetylcholine from axon terminal. The amplitude of this potential is only up to 0.5 mv. The miniature end plate potentials are added together by each quantum of acetylcholine released and finally produce end plate 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 the release into the synaptic cleft. It is destroyed by the enzyme, acetyl cholinesterase. The rapid destruction of acetylcholine prevents the 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. These muscles 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 muscles 1. 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 living tissue are as followinga) Mechanical stimulus c) Thermal stimulus b) Electrical stimulus d) Chemical stimulus 2. Contractility - The skeletal muscle gives response to a stimulus in the form of contraction. The contraction is defined as the interval event 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 the tension remains the same and the length of the muscle fibers is altered. Isometric contraction in which the length of muscle fibers remains the same and the tension is increased. Based on the contraction time, the skeletal muscles are classified into two types-, the red 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 are red muscles.

Pale muscles: These muscles have large number of type II fibers. These muscles are also called white muscle, fast muscles or fast 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 stimulus o Temperature o Number of stimulus o Load 3. Refractory period - Refractory period is the period at which the muscle does not shows any response to the stimulus. It is because already one action potential is in progress in the muscle during this period. The muscle is unexcitable to further stimulation until it is depolarized. 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 the strength of stimulus. Relative refractory period - Is the period, during which the muscle shows some response if the strength of stimulus is increased to 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 muscles 1. 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 further repolarization. It forms the plateau (stable period) It is for about 200 m sec. (0.2 sec) in atrial muscle and for 0.3 sec in ventricle muscle. Due to the long plateau in action potential the contraction time is longer in cardiac muscle by about 5 15 times 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 selfexcitation. Heart has a specialized excitatory structure from which the discharge of impulses is rapid. This specialized structure is called pacemaker. 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 other parts of the heart. The Conductive system of the heart is formed by the modified cardiac muscle fibers. They are also called the junctional tissue. The conductive system in human heart comprises: o SA node o AV node o Bundle of His o Right and left bundle branches o Purkinje fibers. 4. Contractility - Contractility is ability of the tissue to shorten in length after receiving a stimulus. Various factor affect the contractile properties 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 staircase phenomenon. c) Summation of subliminal stimuli When a stimulus with a subliminal strength is applied. The quiescent heart does not show any response. 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 all 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 of 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 extends throughout contraction period of cardiac muscle. It is for 0.27 sec and relative refractory period extends during first half of 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 advantageo Summation of contraction does not occur o Fatigue does not occur o 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. The rate of blood flow through different parts of the body depends upon the cardiac output. Usually cardiac output is expressed in three ways (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 ml when 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. o

(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 of blood pumped out per ventricle/minute/square meter of the body surface area. Normally it is 2.80.3 liters/square meter of body surface area/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 more negative. It increases the diameter of inferior vena cava resulting in increased venous return. At the same time, descent of diaphragm increases the intra-abdominal pressure which compresses abdominal vein and pushed the blood upward towards the heart 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 the veins 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 is called 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 in the right atrium falls and zero during atrial diastole. This pressure gradient at every part of venous tree helps as a driving force for venous 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 and after load. The force of contraction of heart and cardiac output are directly proportional to preload. The force of contraction of heart and cardiac 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 heart rate 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 is inversely 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 of 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 of -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 that any 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 node and its adjacent conductive fibers that delay this transmission into the ventricles. The total delay is 0.16 second before the excitatory signal 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 microns Component - 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 of two types 0 a) Actin filament - Actin filaments are the thin filaments with a diameter of 20 A and a length of 1 . These filaments extend from either side of the Z line, run across I band and enter into A band up to H zone. 0 b) Myosin filament - Myosin filaments are thick filaments with a diameter of 115 A and 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 the muscles 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 and approach the corresponding the actin filaments from the next Z line. The Z line also approach the end of myosin filament so that the H zone and I band are shortened during contraction of the muscle. During the relaxation of the muscle, the actin filaments and Z line come back to the original position. SAQ (viii) Contractile proteins of skeletal muscle. (See LAQ above)
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. The substances necessary for clotting are called clotting factors. Thirteen clotting factors are identified o Factor I Fibrinogen o Factor II Prothrombin o Factor III Thromboplastin o Factor IV Calcium o Factor VLabile factor or accelerator globulin o Factor VI Not known o Factor VII Stable factor o Factor VIII Antihemophilic factor or antihemophilic globulin o Factor IX Christmas factor or AH factor B o Factor X Stuart-Prower factor or AH factor C o Factor XI Plasma thromboplastin antecedent o Factor XII Hageman factor o Factor XIII Fibrin stabilizing factor or Laki-Lorand factor Mechanism of coagulation of blood Sequence 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 the form of inactive proenzyme. These proenzymes must be activated into enzymes to enforce clot formation. It is carried out by a series of proenzyme-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 prothrombin activator 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 is exposed. When factor XII (Hageman factor) comes in contact with collagen, it is converted into activated factor XII in the presence of kallikrein 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. 2+ Now the activated factor X reacts with platelet phospholipid and factor V to form prothrombin activator in presence of Ca 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 of factor VIII. The activated factor X reacts with factor V and phospholipid component of tissue thromboplastin to form prothrombin activator. 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 clot formation. Sequence of events Prothrombin activator that is formed in intrinsic and extrinsic pathway converts prothrombin into thrombin in presence of calcium. 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 into thrombin 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. 2+ Later these loose strands are modified into dense and tight fibrin thread by fibrin stabilizing factor in the presence of Ca . All the 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 A antigen 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 antibody reacts 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 group systems called ABO system and Rh system.
GHM Physiology A MC Answers: Compil by (Dr) Lalit Singh, Ed Dr S S Kochhar, HOD led
A ABO system - It is based on the presence or absence of antigen A and antigen B blood is divided in four groups, namely, A group, B group, AB i p d group and O group. The blo group having antigen A is ca ood g alled A group. Th is group has a antibodies in the serum. The bloo with antigen od ntibody is called B group. If both the antigens are present the blo group is calle AB group and serum of this g e ood ed d group does not B and an contain any antibody. If both antigens are absent the blood group is called O group and bot and antibo y g O th odies are present in the serum. t Im mportance of blo group ood 1. In blood transfusion - Du uring transfusion only compatible blood must be used. While tran e nsfusing the bloo antigen of the donor and the od antibody of recipient are considered.RB of O group ha no antigen so agglutination d y e BC as o does not occur w any blood g with group of blood. Person of this group called universal do onors. Plasma of AB group has no antibody. Th person with this group are c f hus called universal ts. recipient 2. Matching and cross matc ching - Blood typ ping (matching) determines the b lood group of a p d person. Cross m matching is neede during blood ed transfusion procedure. Cross matching always done befo blood transfu sion. C a ore ly nsplant. 3. Medicall it is important during tissue tran 4. Knowled dge of blood gro oups helps to pr revent the comp plication due to Rh incompatibil ity and save the child from the disorders like e e erythrob blastosis fetalis. 5. Helpful in medicolegal ca i ases to sort out paternity disputes. p O Other blood groups o Lewis blood group b p o Kell group o MNS blood group o Duffy grou up an o I group o Luthera group o Auberg group ger o Bombay g roup o P grou up p o Kidd group o Diego group g o Sulter Xg g group R factor - Rh fac is an antigen present in RBC It was first disc Rh ctor n C. covered in rhesu monkey. Ther are many Rh a us re antigens but only the D is more y antigenic in human. n o The pe ersons having D antigen are calle Rh positive an those without D antigen are ca a ed nd alled Rh negative The antigen D does not have e. corresp ponding natural antibody (anti D) However if Rh positive blood is transfused to a Rh negative pe a ). s erson for the first time then anti t D is for rmed in that pers son. Inheritance of Rh antigen - Rhesus factor is an inherited dom o R a minant factor. It m be homozyg may gous Rhesus positive with DD or heterozygous r Rhesus posit tive with Dd. Im mportance of Rh factor h 1. Transfus sion reaction due to Rh incompa e atibility - Delayed transfusion rea ction occurs whe an Rh negativ person receiv Rh positive d en ve ves blood fo the first time. He is not affecte much since the reaction do n occurs imme or ed not ediately. The Rh antibodies deve elop within one month. Antibodies devel A loped in the recipient remain in the body for eve When this per t er. h rson receives Rh positive blood for the second time. Th donor RBCs are agglutinated and severe trans he a a sfusion reaction o occurs immediate ely. 2. Hemolyt disease of fet and newborn - Erythroblastos fetalis is a dis tic tus sis sorder in fetus ch haracterized by the presence of e erythroblasts in blood. Haemolysis occurs due to Rh inco H ompatibility i.e., the difference be t etween the Rh b lood group of the mother and baby. Haemolytic e disease leads to erythro oblastosis fetalis. It occurs when mother is Rh n negative and fetu is Rh positive (the Rh factor being inherited us e e from the father) o f es ion sive hemolysis c can cause sever complication re Usually the first child escape the complicati of Rh incom patibility. Excess such as seve anemia, hydro fetalis & kern ere ops nicterus. LA AQ3 Describe glycolysis and give details of its energetics. In ntroduction - The conversion of glucose to pyruvate and lactate is known as glyc e g colysis or Embde en-Meyerhof path hway. Lactate is produced from pyruvate on when oxygen supply to tissue is insufficient. Under aerobic c nly n e condition pyruvat enters the TCA cycle through acetyl-CoA for te further oxid dation of glucose.
EM pa athway (Glycoly ysis)

Enzymes catalysing the reaction 1. Hexokinase (Glucokinase) 2. Glucose-phosphate isomerase 3. Phosphofructokinase 4. Aldolase 5. Triose-phosphate dehydrogenase 6. Phosphoglycerate 7. Phosphoglyceromutase 8. Enolase 9. Pyruvate kinase 10. Lactate dehydrogenase o All the enzymes involved in glycolytic pathway are found in extra mitochondrial soluble fraction of the cell. Sequence of events 1. Glucose to glucose 6-phosphate - Glucose phosphorylation to glucose 6-phosphate is catalysed by the enzyme hexokinase 2+ (glucokinase). ATP acts as phosphate donor in the presence of Mg . 2. Glucose 6-phosphate to fructose 6-phosphate - This reaction is catalysed by phosphohexose isomerase 3. Fructose 6-phosphate to fructose 1,6 diphosphate - Fructose 6-phosphate is further phosphorylated to fructose 1,6 diphosphate by ATP in 2+ the presence of Mg and phosphofructokinase. 4. Fructose 1,6 diphospate to fructose triose phosphate - Fructose 1,6 diphosphate splits into two triose phosphates i.e., glyceraldehydes 3phosphate and dihydroxyacetone 3-phosphate by aldolase. These triose phosphates are interconverted by enzyme phosphotrioseiosmerase. 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 glyceraldehyde diphosphoglycerate, which contains high energy phosphate bond. This dehydrogenase reaction takes place in the presence of inorganic + + + phosphate 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 shuttle o Malate aspartate shuttle Since 2 molecules of inter-convertible triose phosphate are formed per molecule of glucose, 4 ATP molecules are produced via the glycerol phosphate shuttle. Whereas, 6 ATP are formed via the malate aspartate shuttle in anaerobic glycolysis, no ATP is formed as the NADH 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 as 2+ ATP in the presence of ADP and Mg . 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 phosphoglyceromutase 8. 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 2+ phosphoenol pyruvate is transferred to ADP by pyruvate kinase in presence of Mg . 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 6 2. 1,3 diphosphoglycerate to 3 phosphoglycerate 2 3. Phosphoenol pyruvate to pyruvate 2 Total 10 ATP Consumed in hexokinase and phosphofructokinase reaction -2 Net ATP formed 8 Each high energy phosphate bond = 7600 calories Total amount of energy = 8 multiplied by 7600 = 60,800 calories. LAQ4 Name essential fatty acids. Explain classification of fats Introduction - 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 COOH o Linoleic acid CH2 (CH2)4 CH = CH CH2CH = CHCH2 CH = CH(CH2)4 COOH o 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 lipids o Fats, o Waxes 2. Compound lipids o Phospholipids o Glycolipids (glycosphingo lipids) o Lipoproteins, Amino lipids, sulpholipids 3. Derived lipids o Fatly acids, glycerol, sterols, fatty aldehydes. steroids, ketone bodies, lipid soluble vitamins, hormones o Glycerides, cholesterol are uncharged and hence termed as neutral lipids.

Fats - Fats are esters of fatty acid with glycerol. A generalized structural formula of fat may be written as: O || HOOC-R1 CH2-O-C-R1 CH2OH | CHOH | CH2OH Glycerol | HOOC-R2 | HOOC-R3 Fatty acid | CH-O-C-R2 | CH2-O-C-R3 Triglycerides O || O ||
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 Lecithins o Cephalins o Phosphatidyl inositol o Plasmalogens o Sphingomyelins Glycolipids - These are complex lipids containing and amino alcohol attached with an amide linkage to a fatty acid and glycosidically to a carbohydrate moiety. For example, o Cerebrosides o Gangliosides Lipoproteins - These are lipid protein complexes found mainly in plasma and all membranes. Lipid constituents of lipoproteins are mostly esterified 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 of the body to the lungs. It carries nutritive substance from the digestive system and hormone from endocrine glands to all the tissues. It protects the body against the disease and gets rid of the waste products and unwanted substances by transporting them to the excretory organ 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 erythrocytes b) 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 the organic and inorganic substance. Composition of plasma1. 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 Amylase o Lipase o Carbonic anhydrase o Esterase o Acid phosphates o Protease o Alkaline phosphates o Transaminase (vii) Non protein nitrogenous (NPN) substance o Ammonia o Hypoxanthine o Creatine o Urea o Creatinine o Uric acid o Xanthine (viii) Antibodies 2. Inorganic substances o Sodium o Chloride o Magnesium o Bicarbonate o Copper o Iodide o Iron o Potassium o Calcium o Phosphate 2. Water- 91-92 % 3. Gases o Oxygen o Carbon dioxide o Nitrogen

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 is different 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 of 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 are responsible 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 of 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 is large 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 disappear. Condensation 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. But the chromatin network shows further condensation. The hemoglobin starts appearing. Cytoplasm is already basophilic now, because of 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 condensed chromatin, network and it is known as ink spot nucleus. Quantity of haemoglobin is increased, cytoplasm becomes acidophilic. The cell is now called orthochromic erythroblast. In the final stage of late normoblast just before it passes to next stage the nucleus disintegrates 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 network which is formed by remnants of disintegrated organelles. Due to the reticular network, the cell is called reticulocyte. These cells enter the 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. The cell decreases in size to 7.2 diameter. The mature RBC is with hemoglobin and without nucleus. Factors necessary for erythropoiesis Development and maturation of erythrocytes depends on various factors that can be classified into general factors, maturation factors and factors necessary for hemoglobin formation. o General factors - Those necessary for erythropoiesis are four, namely, erythropoietin, thyroxin, hemopoietic growth factor and vitamins a) Erythropoietin - It is also called hemopoietin or erythrocyte stimulating factors. Erythropoietin promotes the production of 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 the cell 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 fats and protein.
GHMC Physiolog Answers: Com G gy mpiled by (Dr) Lalit Singh, Ed Dr S S Kochhar, HOD D
R Reaction and inte ermediates a) Pyruva to acetyl-CoA - Pyruvate is oxidatively deca ate A arboxylated to ac cetyl-CoA for its entry into the citric acid cycle. This reaction is s catalys sed by a group of enzymes called pyruvate de ehydrogenase c complex which in ncludes three different enzymes. It also utilizes + thiamin pyrophosphate (TPP), lipoic ac CoA, FAD an NAD as coen ne e cid, nd nzymes. o Ox xidation decarbo oxylation of pyruv vate - Pyruvate is decarboxylated with the help o TPP to form acetaldehyde-TPP in the presence d of P of pyruvate dehyd f drogenase. Oxidised lipoate then reacts with ac n cetaldehyde-TPP and convents i to acetyl lipoa P it ate, which in turn n, ac ccepts CoA and form acetyl CoA Lipoic acid is released in the r A. r reduced form. Bo these reactio are catalysed by dihydrolipoy oth ons d yl tra ansacetylase. Re educed lipoate is reoxidized by dihydrolipoyl deh s hydrogenase and FAD. d a) Oxaloa acetate + acetyl-C CoA to citrate - Acetyl-CoA comb A bines with oxaloa acetate to form c citrate. A molecule of water is consumed and CoA A is relea ased. This reactio is catalyzed by a condensing enzyme citrate s on b e synthetase. It is a irreversible reaction. an b) Citrate to isocitrate - Th step is cataly his ysed by aconitas and takes pla in two steps. In first step citrate is dehydrate to isoaconitase se ace ed which is then rehydrate to form isocitra ed ate. are cinate - Isocitrate undergoes de e ehydrogenation t form oxalosuc to ccinate. The re eaction is cataly ysed by isocitrate c) Isocitra to oxalosucc dehydr rogenase. d) Oxalos succinate to keto oglutarate - Oxa alosuccinate is decarboxylated t ketoglutarate and is catalyse by isocitrate d d to ed dihydrogenase in 2+ presence of Mn . glutarate to succ cinyl-CoA - Keto oglutarate is oxid datively decarbo oxylated to succ cinyl-CoA. Reaction is catalysed by ketoglutarate e) -Ketog + dehydr rogenase in presence of TPP, lipo oate FAD and NA . AD f) Succiny yl-CoA to succin nate - At this stag substrate level phosphorylatio takes place, i.e., production o a high energy phosphate bond ge on of y (GTP) in presence of GDP & inorganic phosphate. GTP then transfe the high ene G ers ergy bond to AT This reaction is catalysed by TP. n yl succiny thiokinase. g) Succinate to fumarate - Succinate und dergoes dehydro ogenation to for fumarate in p rm presence of suc ccinate dehydrog genase and FAD D, which is converted to FADH.. ate ated to form mala in presence o fumarase. ate of h) Fumara to malate - Fumarate is hydra i) Malate to oxaloacetate - It is a dehydrogenation react e tion catalysed by malate dehydr rogenase in presence of NAD+. This conversion . y comple etes the cycle.
Krebs cycle E Enzymes of the cycle c 1. Pyruva dehydrogenas complex ate se 6. -ketoglu utarate dehydrog genase complex 2. Citrate synthetase 7. Succinic thiokinase ase 3. Aconita 8. Succinate dehydrogenase e 4. Isocitra dehydrogenase ate 9. Fumaras se 5. Isocitra dehydrogenase ate 10. Malate de ehydrogenase E Energetics of citri acid cycle ic Reaction med xidative ATP formed by subs strate level ATP form through ox phosphorylation p phosphorylatio n ate-acetyl-CoA 3 Pyruva Isocitra ate-oxalosuccinate 3 Ketoglu utarate-succinyl-CoA 3 Succiny CoA-Succinate yl e 1 Succinatefumarate 2 oxaloacetate Malate 3 Total T 14 1 ecules 14+ 1 =15 ATP mole As one molecule of gluc e cose gives two moles of pyruvate total number o ATP formed = 15x2 = 30 ATP molecules. m es of P LA AQ8 Define carbohydrate. Explain classif fication of carbo ohydrates and a add a note on c hemistry of glucose. In ntroduction- Carbohydrates are the best source of energy for hu t uman beings and may be define as polyhydrox d ed xyaldehydes and ketone and their derivatives. C Classification of carbohydrates c 1. Monos saccharide - Th hese are the si implest member of carbohydr rs rates which are represented b general formula C12 H24 O12. e by 2 Monos saccharides are grouped according to the numbe of carbon atom present in a su er m ugar molecule su as trioses, te uch etroses, pentoses and hexoses. Each of these can be further named as aldose or keto f f s ose, depending o the presence of an aldehyde or ketone group on e e ctively. respec
Structural and is someric classific cation divides sim mple sugar into D and L series . If the hydroxyl group at the ca arbon next to the termin carbon atom in a straight chain molecule point to the right, it iis a D sugar and if it point to the left it is an L sug nal i ts gar.
L-Glu ucose D-Glucose e Oligos saccharide - The are condens ese sation products of two to ten si mple sugars or monosaccharide They are represented by the es. general formula C12 (H2O)n-1. For exam H mple: o Raffinose - trisaccharide t o Sucrose, ma altose, lactose - disaccharides d o Su ucrose = glucose + fructose e o Maltose = glucose + glucose e o La actose = galactos + glucose se Lactose & ma altose are reduci sugars where sucrose is a non-reducing su ing eas ugar. 3. Polysa accharides - Maj jority of carbohydrates found in natural sources occurs in the fo rm of polysaccharides. These ar high molecula re ar weight polymers of mo onosaccharide re epresented by the general formul a (C6H10O5)n. e fied as homopoly ysaccharides and heteropolysacc d charides. They are further classif H arides - The cellu ulose, starch, glyc cogen and dextriin all contain glu cose as repeatin unit. ng a) Homopolysaccha o Cellulose - It ha a linear chain of D glucose res as sidues linked tog gether with a -1- glycosidic link -4 kage. sists of two mole ecules, amylase and amylopectin Amylose is a s n. straight chain po o o Starch - It cons olymer similar to cellulose having -1,4 glucosidic bond between glucose molecu n ules, where as a amylopectin is a branched mole ecule with -1,4 linkage between ule ucosidic bond at the branch point ts. glucose molecu in straight chain and -1,6 glu s ohydrate reserve of human body stored mainly in liver and muscles. The structu of glycogen is e y, ure o Glycogen - It is the major carbo similar to that of amylopectin. o e ediate products in the hydrolysis o starch to mono n of osaccharides. o Dextrin - These are the interme H arides - These are made up of more than o one sugar deriv vative as repea ating unit. They are also called b) Heteropolysaccha mucopolysaccharides (glycosaminoglycans) and occur in comb m d bination with pro oteins. For exam mple, hyaluronic acid, chondritin c sulphate, heparin etc. s n N Note on chemistr of glucose ry Glucose is the most import tant carbohydrat It is absorbed into the blood s te. d stream. It is deriived from glycog during glycogenolysis in liver. gen Glucose is conv verted to other carbohydrate hav c ving specific func ction. o Glycoge - For storage en e o Ribose - For nucleic acid synthesis ose s ans. o Galacto - For forming lactose of milk, compound lipids and glycoproteiin or proteoglyca o Glucuro onic acid - Has de etoxicating funct tions and a comp ponent of mucopo olysaccharide. In order to classify structu o ural and isomeric form of simple sugar, they are divided into D and L series, d c e e depending on th position of the he hydroxyl group at the carbon ne to the terminal carbon atom in a straight chaiin. When the mo ext olecule points to the right, it is a D sugar and of it ft ar. points to the lef it is an L suga The two optical isomers, dextrorotatory and levorotatory of simple suga are designate as (d) or (+) and (l) or (-) r o a ar ed ) respectively. The configuration around the reduc a cing carbon in the ring structure of a represented by an and sign. The shows the proje d ection of hydroxy yl group at the red ducing carbon to the right and to the left. o 2.
ars In glucose solution after att taining equilibrium approximately two third of suga exist as the form. m y onic acid contains N-acetylglucos s samine, glucuronic acid. o Hyaluro o Chondr roitin sulphate co ontains N-acetylg galactosamine, id duronic acid, and sulphuric acid. d o Heparin contains glucos n samine, glucuron acid, and sulp nic phuric acid. SA (i) AQ Functions of blood. (M Make short Ans from LAQ) f SA (ii) AQ Erythro opoiesis (Make short Ans from LAQ) L SA (iii) Absorp AQ ption of carbohy ydrates In ntroduction - Car rbohydrates are good sources of energy and are mainly taken in the form of starc lactose, sucr f ch, rose. Dietary poly ysaccharides and disaccharid must be hydr des rolysed to monos saccharide befor they can be ab re bsorbed by intest tinal tract.
A Absorption of car rbohydrates - The monosaccharid resulting from digestion, are easily absorbed into the mucosa cells of small in e des m al ntestine and pass into circulat tion via portal ve A very small amount may also be absorbed b the lymph. Th microvilli lining the mucosal ce greatly help in ein. by he g ells absorption by increasing the surface area. e esent concept re egarding the abs sorption of monosaccharide rules out the involve s ement of glucose phosphorylation The absorption e n. o The pre of gluco and galactos is now believe to take place by an active tran ose se ed b nsport rather than by simple diffus n sion. o The tra ansfer is mediate by a specific macromolecule of protein nature called carrier pr ed m o rotein, which is p present on the ex xternal surface of o the brush border memb brane of intestine e. + o Na ha been found to be essential fo accomplishing such an active transport. The carrier bears th specific bindi as o or g e e he ing sites for both + glucose and galactose, and also for Na . e + o Thus Na enhances the binding of the monosaccharide to the carrier for their transporta N e m r ation across the b brush border cell membrane. This is follow wed by their rel lease into the cy ytoplasm of the mucosal cells. From the cytop plasm, glucose/ galactose diffus into the blood se + capillar ries. Such a mec chanism also faci ilitates the transp of Na . port o This ac ctive transport of galactose/glucose requires ener provided by h rgy hydrolysis of ATP P. o However, it is absorbe by the proce of simple dif ed ess ffusion believed to be facilitated again by some carrier molecu d ules. The rate of o absorption of monosacc charide has been found to be ind n dependent of bloo sugar concen od ntration. ghest rate of ab bsorption is foun in case of ga nd alactose and glu ucose. Whereas fructose is abs s sorbed at about half of this rate e, o The hig mannose & xylose are absorbed much more slowly. SA (iv) Glycog AQ genesis In ntroduction - The formation of glycogen in the bo is called glyc e ody cogenesis. It tak place mainly in liver and mus kes y scles where glyc cogen is stored in large amou unts. On an avera about 108 g of glycogen are stored in liver an about 245 g in muscles. age nd n M Mechanism - Gly ycogen is forme from glucose Glucose is ph ed e. hosphorylated to glucose 6- p phosphate which isomerizes to from glucose 1h phosphate. . o UTP co ombines with glucose 1-phosphate to from uridine diphosphogluco (UDPG) by U e ose UDP-glucose pyrophosphorylase e. o UDPG then transfers it glucose to the non-reducing end of a pre-exis ts e e sting polysaccha ride primer forming an-1-4 gluc cosidic bond, in a ase. The UDP re eleased in this rea reaction catalysed by glycogen syntheta action can be re converted to UTP by ATP. cen ction thus results in the formatio of a linear cha of glucose m s on ain molecule linked th hrough 1,4 glu ucosidic bonds. A o Glygoc synthease ac branching enzyme amy (1,4- 1,6) tran ylo nsglycorylase the catalyses the cleavage of an 1,4 linkage n en e n near the growing end of the chain g ansfers this fragm ment to from an 1,6 linked bran point on the llinear chain. nch and tra o Thus a highly branched molecule of glycogen in formed. d
SA (v) AQ Blood groups (Make short Ans from LA s AQ) SA (vi) Coagulation factors (M AQ Make short Ans from LAQ) f SA (vii) Functions of lipids. AQ In ntroduction - Lipids are a heterog geneous group of organic compo o ounds which are relatively insolu ble in water but soluble in solven such as ether, nts chloroform and benzene. F Functions 1. They provide energy to the body, insulate the body and protect various internal organs. p o d s . 2. They provide building blocks for differ rent high molecu weight subst ular tances e.g., acet acid, a break down product o fatty acids, and tic k of e ynthesis of severa complex molecules, like choles al sterol and certain hormones. can be used for the sy n 3. They provide essentia fatty acids, wh al hich are not synthesized by hum an body. They f form substances essential for ma aintaining cellula ar integri such as lipopr ity rotein and glycolipid, in combinat tion with proteins and carbohydra s ates respectively y. 4. Phosp pholipids form the structure of me e embranes, matrix of cell wall, mye sheath, micr x elin rosome and mitochondria. 5. Phosp pholipids act as carrier of inorgan ions across th membranes ne c nic he ecessary for sec cretion of enzyme hormones, an mucins. es, nd 6. Phosp pholipids help in blood coagulatio act as prosthe group of cert on, etic tain enzymes. 7. Memb brane phospholip pids serve as sou urce of arachidon acid, which is utilized for synth nic s hesis of prostaglandins and leuko otriene. 8. Phosp pholipids provide insulation aroun nerve fibers, they work as cofa nd actor for lipoprote lipase and triglycerol lipase. ein 9. Phosp phatidyl inositide metabolite has a role to play in calcium ion dep s s n pendent hormone action. e 10. Dipalm lecithin acts as a surface acting substance and prevents adh mityl s a herence of the inn surface of lungs. ner 11. Phosp phatidyl inositol is found in good amount in brain, liver and heart tiissue. s a 12. Essen ntial fatty acids are structural elements of many tissues, and gon a t nads, they help iin synthesis of p prostaglandins, p prostacyclins from m arachi idonic acid by cy yclooxygenase en nzyme system. 13. Leuko otrienes synthes sise from archid donic acid by li ipooxygenase s system in leuco ocytes, and mai intain structure of mitochondria al memb branes and increa fibrinolytic ac ase ctivity. 14. Docos sahexenoic acid formed from diet tary linolenic acid has role in visio (present in p hotoreceptor me d on. embrane) 15. Steroids are the main constituents of sterols, bile acids sex hormones, adrenal corticoi ds and vitamin D s s, , D.

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