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Muscular system
- 1. MUSCULAR SYSTEM (MUSCLE ANDNERVE ) PRESENTED BY APARNA C LAKSHMY
- 2. On thebasis of presence or absence of striations Striated – skeletal and cardiac muscles Non-striated – smooth muscle Depending upon the control Voluntary muscle – skeletal muscle – controlled by somatic nerve Involuntary muscle – cardiac and smooth muscles – sympathetic and parasympathetic division of autonomous NS Classification of Muscle
- 3. Depending uponthe situation Skeletal muscle – attached to bone Cardiac muscle – form the musculature of heart Smooth muscle – associated with visceral organs.
- 4. COMPARATIVE STUDY OFSKELETAL ,CARDIAC AND SMOOTH MUSCLE
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- 11. PRODUCING BODYMOVEMENTS. STABILIZING BODY POSITIONS. STORING AND MOVING SUBSTANCES WITHIN THE BODY. GENERATING HEAT (THERMOGENESIS) FUNCTIONS OF MUSCULAR TISSUE
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- 20. MYOSIN MOLECULE ACTIN MOLECULE TROPOMYOSIN TROPONIN MUSCLEPROTEINS (CONTRACTILE ELEMENTS)
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- 27. EXCITABILITY CONTRACTILITY EXTENSIBILITY ELASTICITY RHYTHMICITY PROPERTIES OF MUSCLE
- 28. Excitability Stimulus 1. Mechanical 2. Electrical 3.Chemical 4. Thermal Contractility. Types 1. Isotonic 2. Isometric PROPERTIES OF MUSCLE
- 30. Based onthe contraction time Red muscle Long contraction time Myoglobin content is more (red) Sarcoplasmic reticulum is less extensive Blood vessels are more extensive Mitochondria are more in number Long latent period Contraction is less powerful Fatigue occurs slowly Contraction Time
- 31. White muscle Shorter contraction time Myoglobin content is less (pale) Sarcoplasmic reticulum is more extensive Blood vessels are less extensive Mitochondria are less in number Short latent period Contraction is more powerful Fatigue occurs quickly
- 32. Strength ofstimuli Number of Stimulus Temperature Load Factors Affecting Force of Contraction
- 33. Sub minimalor subliminal stimulus Minimal stimulus or Threshold stimulus or liminal stimulus Submaximal stimulus Maximal stimulus Supramaximal stimulus EFFECT ON STRENGTH OF STIMULUS
- 34. Effect of twostimuli 1. Beneficial Effect 2. Superposition or superimposition or incomplete summation 3. Summation EFFECT ON NO OF STIMULUS
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- 36. 1. Fatigue 2. Tetanus Effectof Multiple stimuli
- 37. Physiological tetanus When multiple stimuli are applied at a high frequency, muscle remains in a contracted state. Relaxes only after stoppage of stimulus or fatigued. Pathological tetanus Toxin of Clostridium tetani – affect NS lead to paralysis of muscle Upper jaw muscle – locking of jaws If not timely treated lead to death. TETANUS
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- 39. Heat Rigor Cold Rigor Calcium Rigor Rigor Mortis RIGOR
- 40. The failureof relaxation of muscle after contraction in death. ATPs are not available and Ca++ cannot pumped back. Develop fully up to 12 hrs and passed off when decomposition starts after 48 hrs of death. Medico legal importance Determining the time of the death (rigor mortis takes different time to set in different individuals) Can predict, whether the death is after a long Rigor Mortis
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- 42. CHANGES DURING MUSCLECONTRACTION ELECTRICAL PHYSICAL HISTOLOGICAL(MOLECULAR) CHEMICAL THERMAL
- 43. RESTING MEMBRANEPOTENTIAL ACTION POTENTIAL GRADED POTENTIAL ELECTRICAL CHANGES
- 44. Resting membranepotential is the electrical potential difference (voltage)across the cell membrane under resting condition It is also called membrane potential ,transmembrane potential,transmembrane potential difference or transmembrane potential gradient There is negativity inside and positivity outside the muscle fiber. The condition of the muscle during resting membrane potential is called polarized state RMP of skeletal muscle: -90mv Resting Membrane Potential
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- 46. The ionic imbalanceis produced mainly by 2 transport mechanisms in the cell membrane: 1.Sodium -potassium pump Sodium and potassium ions are transported by this pump, It moves 3 Na ions out of the cell and 2 potassium ions inside the cell by using energy from ATP IONIC BASIS OF RMP
- 48. 2.SELECTIVE PERMEABILITYOF CELL MEMBRANE 1. Channels for major anions(negatively charged substances )like proteins are absent or closed.so these substances remain inside the cell and maintain RMP
- 49. 1. LEAK CHANNELS Cl-Channels are mostly closed in resting conditions ,Cl -ions are retained outside the cell. In resting condition,all the k+ leak channels are opened but most of the Na + leak channels are opened.Because of this K+ which are transported actively into the cell,can diffuse back out of cell in an attempt to maintain the concentration equilibrium That is,in resting condition ,the passive k+ efflux is much greater the the passive Na+ influx
- 50. The sequentialchange of membrane potential after application of a stimulus is known as AP. After application of a stimulus Magnitude of membrane potential changes
- 51. 2 phases Depolarization Initial phase of AP in which interior of the muscle becomes positive and exterior becomes negative Repolarization It is the phase of AP when the potential inside the muscle reverse back to the RMP
- 52. During onset ofdepolarization,there is slow influx of Na+.when depolarization reaches 7- 10 Mv,the voltage gated Na+ channels start opening at a faster rate and cause overshoot But the Na+ transport is short lived.So the channels open and close quickly. At the same time,the K+ channels start opening ,this leads to efflux of K+ out of the cell causing repolarization IONIC BASIS OF AP
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- 54. GP is amild local change in the membrane potential that develops in receptors ,synapse,or neuromuscular junction when stimulated. It is also called graded membrane potential or graded depolarization. GRADED POTENTIAL
- 55. ACTION POTENTIAL GRADEDPOTENTIAL PROPAGATIVE LONG DISTANCE SIGNAL BOTH DEPOLARIZATION AND REPOLARIZATION OBEYS ALL OR NONE LAW SUMMATION IS NOT POSSIBLE HAS REFRACTORY PERIOD NON PROPAGATIVE SHORT DISTANCE SIGNAL ONLY DEPOLARIZATION OR HYPERPOLARIZATION DOESNOT OBEY ALL OR NONE LAW SUMMATION IS POSSIBLE NO REFRACTORY PERIOD
- 56. Change inlength of muscle fibers Change in the tension 2.PHYSICAL CHANGES
- 57. Stages 1. Excitation contractioncoupling 2. Role of troponin and Tropomyosin 3. Sliding Mechanism Molecular basis of muscular contraction
- 58. Meaning Process that occursin between the excitation and contraction of the muscle Excitation Contraction Coupling
- 59. Impulse reachesthe neuromuscular junction causing release of Acetylcholine(Ach) from motor endplate Ach causes opening of ligand gated Na channels Development of endplate potential causing generation of action potential in muscle fiber. Action potential spreads over sarcolemma and also into muscle fiber through T-tubules . Excitation Contraction Coupling
- 60. Causing rapidspread of action potential into the muscle fibers When action potential reaches the cisternae of L- tubules ,the cisternae are excited Ca ions stored in the cisternae are released into sarcoplasm The Ca ions from the sarcoplasm moves towards the actin filamnet to produce the contraction
- 61. Explains howthe actin filaments slide over myosin filaments and form actomyosin complex during muscular contraction It is also called ratchet or walk along theory SLIDING MECHANISM (SLIDING THEORY)
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- 64. The lengthof all sarcomeres decreased as the ‘z’ lines come close to each other. The length of the ‘I’ band decreases since the actin filament from opposite side overlap. The ‘H’zone either decreases or disappears. The length of ‘A’ band remains the same. Changes occuring in the sarcomere
- 65. Pumping ofca ions into L-tubules Release of Ca ions from troponin C Detachment of myosin head from F actin Muscular Relaxtion Relaxation of the muscle
- 66. ATP isneeded mainly for, 1. Spread of action potential into muscle 2. Liberation of Ca ions from cisternae of L-tubules inton sarcoplasm 3. Movements of mysosin head 4. Sliding mechanism Chemical Changes
- 67. Muscle fibershave 3 ways to produce ATPs 1. From creatine phosphate 2. By anaerobic cellular respiration 3. By aerobic respiration
- 68. In resting condition–Alkaline During onset of contraction-Acidic During later part of contraction-Alkaline At the end of contraction - acidic Changes in pH during muscular contration
- 69. Resting heat Initial heat 1. Heat of activation 2. Heat of shortening 3. Heat of relaxation Recovery heat Thermal changes
- 70. Stimulation ofmuscle fiber 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 EVENTS OF MUSCULAR CONTRACTION
- 71. Binding ofcalcium ions to troponin C and change in position of troponin C Exposure of active sites of F actin Binding of myosin head with F-actin and power stroke in myosin head Sliding of actin filaments over myosin filaments Muscular contraction
- 73. DEFINITION Neuromuscular junction isthe junction between the terminal branch of the nerve fiber and muscle fiber Neuromuscular junction
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- 76. Skeletal musclefibers are innervated by motor nerve fibers. Terminal branch of nerve fiber is called axon terminal. The portion of axis cylinder expanded like a bulb which is called motor endplate. The motor endplate invaginates inside the muscle fiber and forms a depression which is know as synaptic trough or synaptic gutter STRUCTURE
- 77. The membraneof the nerve ending is called the presynaptic membrane. The membrane of the muscle fiber is called postsynaptic membrane which contain receptors called nicotinic acetylcholine receptors. The space between these two is called synaptic cleft. Synaptic Cleft
- 78. The axonterminal contains mitochondria ,which is the source of energy for synthesis of acetylcholine and synaptic vesicles which contain acetylcholine,which is responsible for neurotransmission The postsynaptic membrane thrown into numerous folds called subneural clefts
- 79. Definition NMT isdefined as the transfer of information from motor nerve ending to the muscle fiber through neuro muscular junction It is the mechanism by which the motor nerve impulses initiate muscle contraction NEUROMUSCULAR TRANSMISSION
- 80. MOTOR NERVE FIBERS •ACTION POTENTIAL AXON TERMINAL • OPENING OF VOLTAGE GATED CALCIUM CHANNELS • ENERY OF CALCIUM IONS FROM EXTRA CELLULAR FLUIDS • OPENING OF VESICLES AND RELEASE OF Ach Synaptic cleft Passage of Ach NEUROMUSCULAR TRANSMISSION
- 81. Postsynaptic membrane • BINDINGOF Ach WITH RECEPTOR AND FORMATION OF Ach -RECEPTOR COMPLEX • OPENING OF LIGAND GATED SODIUM CHANNELS • ENTRY OF SODIUM IONS FROM ECF • DEVELOPMENT OF ENDPALTE POTENTIAL MUSCLE FIBER • GENERATION OF ACTION POTENTIAL • EXCITATION CONTRACTION COUPLING • MUSCULAR CONTRACTION
- 82. Neuromuscular blockers arethe drugs ,which can prevent the transmission of impulses from nerve fiber to the muscle fiber through the neuromuscular junctions NEUROMUSCULAR BLOCKERS
- 83. Curare 1. Preventstransmission by combining with acetylcholine receptors.So the Ach cannot combine with the receptors Bungarotoxin 1. It is a toxin from the venom of deadly snakes 2. It affects transmission by blocking the Ach receptors IMPORTANT NEUROMUSCULAR BLOCKERS
- 84. Succinylcholine andCarbamylcholine 1. These drugs block transmission by acting like Ach and keeping the muscle in a depolarized state. 2. These drugs are not destroyed by cholinesterase causing muscle to remain in a depolarized state. Botulinum Toxin 1. Dervied from the baccteria clostridium botulinum 2. It prevents release of Ach from axon terminal into NMJ
- 85. These drugsinactivate the enzyme,acetylcholinesterase Examples 1. Neostigmine 2. Physostigmine 3. Disopropyl fluorophosphate DRUGS STIMULATING NMJ
- 86. The singlemotor neuron,its axon terminals,and the muscle fibers innervated by it are together called motor unit. MOTOR UNIT
- 87. Muscular Dystrophy 1.Duchenne Muscular dystrophy 2. Becker’s muscular Dystrophy Disease involving muscle tone 1. Hypertonicity hypertonia 2. Hypotonia 3. Myotonia Becker type myotonia(generalised myotonia) Thomsen type myotonia Disorders of skeletal Muscles(myopathy)
- 88. Fibrillation anddenervation hypersensitivity Myasthenia Gravis Lambert -Eaten Syndrome Mc Ardle’s Disease Mitochondrial Myopathy Nemaline Myopathy
- 89. Muscular Dystrophy 1.Duchenne Muscular dystrophy It is a sex – linked recessive disorder. It is due to the absence of a gene product called dystrophin in the X chromosome. It is characterized by degeneration and necrosis of muscle fiber
- 90. 2..Becker’s muscular Dystrophy It is a sex- linked disorder It occurs due to reduction in quantity or alteration of dystrophin Common features are slow progressive weakness of legs and pelvis,pseudohypertrophy of calf muscles,fatigue and mental retardation.
- 91. Slow andweak muscular contraction because of defective neuromuscular activity Inability to maintain the prolonged contraction of skeletal muscular contractions Weakness and fatigability of arms and legs Double vision and droopy eyelids due to the weakness of ocular muscles Difficulty in swallowing due to weakness of throat muscles Difficulty in speech due to weakness of muscles of speech symptoms