PHYSIOLOGY FOR NURSES ESPECIALLY FOR FIRST YEAR NURSING STUDENTS BASED ON INC SYLLABUS

1. MUSCULAR SYSTEM
(MUSCLE AND NERVE )
PRESENTED BY
APARNA C LAKSHMY

2.  On the basis 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 upon the situation
Skeletal muscle – attached to bone
Cardiac muscle – form the
musculature of heart
Smooth muscle – associated with
visceral organs.

4. COMPARATIVE STUDY OF SKELETAL
,CARDIAC AND SMOOTH MUSCLE

5. SKELETAL MUSCLE

6. CARDIAC MUSCLE

7. SMOOTH MUSCLE

11.  PRODUCING BODY MOVEMENTS.
 STABILIZING BODY POSITIONS.
 STORING AND MOVING SUBSTANCES
WITHIN THE BODY.
 GENERATING HEAT (THERMOGENESIS)
FUNCTIONS OF MUSCULAR TISSUE

12. STRUCTURE OF
SKELETAL MUSCLE

15. MUSCLE CELL(FIBER)

17. SARCOMERE

19. MYOSIN FILAMENT

20. MYOSIN MOLECULE
ACTIN MOLECULE
TROPOMYOSIN
TROPONIN
MUSCLE PROTEINS
(CONTRACTILE ELEMENTS)

21.  OTHER PROTEINS
ACTININ
DESMIN
NEBULIN
TITIN
DYSTROPHIN

22. Myosin Molecule

23. ACTIN FILAMENT

25. SARCOTUBULAR SYSTEM

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 on the 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 of stimuli
 Number of Stimulus
 Temperature
 Load
Factors Affecting Force of
Contraction

33.  Sub minimal or subliminal stimulus
 Minimal stimulus or Threshold stimulus
or liminal stimulus
 Submaximal stimulus
 Maximal stimulus
 Supramaximal stimulus
EFFECT ON STRENGTH OF
STIMULUS

34. Effect of two stimuli
1. Beneficial Effect
2. Superposition or superimposition
or incomplete summation
3. Summation
EFFECT ON NO OF STIMULUS

35. Graphical representation

36. 1. Fatigue
2. Tetanus
Effect of 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

38. Pathological tetanus

39.  Heat Rigor
 Cold Rigor
 Calcium Rigor
 Rigor Mortis
RIGOR

40.  The failure of 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

41. Physiology of muscle
contraction

42. CHANGES DURING MUSCLE CONTRACTION
 ELECTRICAL
 PHYSICAL
 HISTOLOGICAL(MOLECULAR)
 CHEMICAL
 THERMAL

43.  RESTING MEMBRANE POTENTIAL
 ACTION POTENTIAL
 GRADED POTENTIAL
ELECTRICAL CHANGES

44.  Resting membrane potential 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

45. IONIC BASIS OF RMP

46. The ionic imbalance is 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 PERMEABILITY OF 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 sequential change 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 of depolarization,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

53. ACTION POTENTIAL CURVE

54. GP is a mild 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 GRADED POTENTIAL
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 in length of muscle fibers
 Change in the tension
2.PHYSICAL CHANGES

57. Stages
1. Excitation contraction coupling
2. Role of troponin and Tropomyosin
3. Sliding Mechanism
Molecular basis of muscular
contraction

58. Meaning
Process that occurs in between the
excitation and contraction of the
muscle
Excitation Contraction Coupling

59.  Impulse reaches the 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 rapid spread 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 how the 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)

62. SLIDING MECHANISM

64.  The length of 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 of ca 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 is needed 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 fibers have 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 of muscle 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 of calcium 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 is the
junction between the terminal
branch of the nerve fiber and
muscle fiber
Neuromuscular junction

74. Neuromuscular junction

76.  Skeletal muscle fibers 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 membrane of 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 axon terminal 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 is defined 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
• BINDING OF 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 are the
drugs ,which can prevent the
transmission of impulses from nerve
fiber to the muscle fiber through the
neuromuscular junctions
NEUROMUSCULAR BLOCKERS

83.  Curare
1. Prevents transmission 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 and Carbamylcholine
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 drugs inactivate the enzyme,acetylcholinesterase
Examples
1. Neostigmine
2. Physostigmine
3. Disopropyl fluorophosphate
DRUGS STIMULATING NMJ

86.  The single motor 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 and denervation 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 and weak 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