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MBBS - Year 1 > Physiology - Soft Tissue > Flashcards

Physiology - Soft Tissue Flashcards

1
Q

What does the PNS consists of

A

All axons and ganglia outside CNS
Autonomic and somatic system
Cranial nerves (except II)

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2
Q

Divisions of autonomic nervsous system

A

Parasympathetic

Sympathetic

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3
Q

Motor nerves in somatic nervous system

A

Efferent

Afferent

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4
Q

Effernet motor nerves

A

Run from CNS to periphery

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5
Q

Afferent. motor nerves

A

Run from periphery to CNS

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6
Q

Motor unit

A

Motor nerve axon

All the muscle fibres it innervates

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7
Q

What determines the size of motor unit recruited

A

Type of task and force

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8
Q

Te reusing potential of the cell membrane

A

BIG differences between the electrical potential inside the cell compared to the outside (-70 to -90 mv)
Big differences between intracellular and extracellular ionic conc. Na is low inside and high outside and K is high inside and low conc

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9
Q

Sodium ATPase pump

A

Na-K ATPase pump moves 2K+ molecules into the cell in exchange for 3Na+ molecules moved out
Maintains conc gradient of Na and K
Small direct effect on membrane potential

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10
Q

Initiation of AP

A

Sensory receptors transducer energy to change potential of axon
Threshold is reached and VgNa channels open, starting the ap

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11
Q

Steps of the action potential

A

Depolarisation
Repolarisation
Hyperpolarisation

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12
Q

Depolarisation

A

The inside of the cell becomes less negative with respect to the outside. VgNa channels are open (Na+ moves in) and VgK channels are closed.

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13
Q

Repolarisation

A

The cell is trying to restore balance and bring the potential difference of the cell more -ve than the outside. VgNa channels are closed and VgK channels open (K+ moves down the electrochemical gradient)

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14
Q

Hyperpolarisation

A

The eflux of K+ causes the inside of the axon to become TOO negative so the resting potential is restored using the Na-K ATPase pump

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15
Q

Refractory period

A

The duration before another AP can be generated, regardless of stimuli

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16
Q

Propagation of AP

A

Slight excess of +ve charge inside the axon hillock and excess of -ve charge outside so a potential difference builds up between the diff regions of the axon. This causes local circuit currents, opening VgNa channels so the action potential can advance

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17
Q

Increasing nerve conduction velocity

A

Larger diameter

Insulation

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18
Q

What is muscle

A

Bundle of fibres that can contract to produce movement; this can be voluntary or involuntary

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19
Q

Types of muscle

A

Striated (skeletal) muscle – locomotion and posture
Smooth muscle – peristalsis
Cardiac muscle – heart contraction

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20
Q

Contraction

A

Shortening

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21
Q

Elasticity

A

Returning to resting state

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22
Q

Hypertrophy

A

Increase in size

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23
Q

Hyperplasia

A

Increase in number (usually muscle cells)

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24
Q

Structure of skeletal muscle

A

Tendon attaches to bone
Epimysium – muscle
Perimysium – fascicle
Endomysium – fibre

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25
What are muscle fibres filled with
Myofibrils
26
Sarcolemma
Plasma membrane of muscle fibre
27
Sarcoplasm
Cytoplasm inside muscle fibre
28
Sarcolasmic reticulum
Smooth endoplasmic reticulum acts as a storage organelle for Ca2+
29
Transverse tubular system (TT)
Invaginations of sarcolemma
30
Triad
Terminal cisternae of 2 SR and TT in close proximity
31
Sarcomere
Unit of contraction of the myofibril
32
Z line
Either ends of the sarcomere; thin filaments insertion
33
M line
Origin of thick filaments, middle of sarcomere
34
A band
Overlap of thick and thin filaments
35
I band
Only thin filaments
36
What does the myosin head bind to and what features allow this
Actin 2 alkali light chains help stabilise myosin head Hinge region allows movement of myosin head
37
What is the myosin tail formed of
2 intertwined heavy chains
38
What allows ATPase activity on myosin
2 regulatory light chains
39
Actin
Binding site for myosin | Thin filaments
40
What does tropmyosin do
Block myosin receptors
41
What does troponin do
Control tropomyosin position
42
What happens to the sarcomere during contraction
All bands and H-zone gets smaller
43
Excitation-contraction coupling
AP motor nerve end plate propagates along membrane and down TT Opens Vg L-type Ca2+ channels on TT Coupling between DHP receptor and Ca2+ release channels, releases the Ca2+ from the SR Ca2+ released into myofibril activating troponin C and cross-bridge cycling
44
Initiation of cross-bridge cycling
Tropomyosin blocks myosin binding site When Ca2+ binds to the high affinity sites on troponin C a conformational change takes place in the troponin complex Troponin I moves away from the actin filament Troponin T pushes tropomyosin away from myosin binding site on actin Myosin head binds to actin
45
How does calcium modulate contraction
Through regulatory proteins rather than direct interaction w/ actin and myosin
46
Types of troponin
C: binds Ca2+ I: anchors complex to actin T: binds to tropomyosin
47
Cross-bridge cycle in skeletal muscle
``` Initially myosin head attached to actin filament after ‘power stroke’ from previous cycle – can remain in this state for indefinitely longer period, as occurs in rigor mortis Step 1 – ATP binding Step 2 – ATP hydrolysis Step 3 – cross-bridge formation Step 4 – release of Pi from myosin Step 5 - ADP release ```
48
Terminating muscle contraction
Ca must be removed from cytoplasm Na-Ca exchanger Ca pump at plasma membrane Ca reuptake into SR and binds to calsequestrin
49
How can muscle force be determined
By no. individual muscle fibres stimulated at a given time
50
What does amount of muscle force generated depend on
``` No. active muscle fibres Cross-sectional area of muscle Initial resting length of muscle Rate at which muscle shortens Frequency of stimulation ```
51
Isometric contraction
Muscle length fixed, stimulation of muscle will cause increase in tension but no shortening
52
Analogy for isometric contraction
Similar to holding a weight in your hand w/ your arm outstretched, you will feel that the muscle is working w/out changing length
53
Isotonic contraction
Muscle length not fixed | Stimulation of muscle will cause muscle shortening provided tension generated is stronger than opposing load
54
Analogy for isotonic contraction
Similar to holding a weight in your hand and lifting and lowering your hand, bending at the elbow
55
Passive tension
Tension measured before muscle contraction
56
Length tension rship
At any fixed length if muscle is contracted an addn. active tension develops due to cross-bridge formation Length-tension relationship is direct result of the anatomy of the thick and thin filaments overlapping within individual sarcomeres
57
Force-length rship
As velocity increases, force decreases | At maximum power is generated at approx. 1/3 shortening velocity
58
Summation in single muscle fibres
One AP will lead to single skeletal muscle twitch | As muscle twitch far exceeds duration of AP it is possible to generate a 2nd AP before 1st contraction has subsided
59
Tetanus state
Twitches – AP generated faster than muscles can react
60
Types of muscle fibres
Red White Intermediate
61
Red muscle fibres
Slow twitch and fast twitch, requires oxygen and glycogen
62
White muscle fibres
Fast twitch, glycogen is main energy store, gets fatigued quickly
63
Fast twitch (2b) muscle fibres
Fatiguable White Glycolytic metabolism High levels of glycogen
64
Slow twitch muscle fibres
Resistant to fatigue Red (myoglobin) Oxidative metabolism Low levels of glycogen
65
What determines strength of skeletal muscle
Size
66
What is the cross sectional area of muscle fibres proportional to
The strength that can be generated
67
What are long muscle fibres good for
Rapid movement
68
What are shirt muscle fibres good for
Large forces
69
Fast twitch (2a) muscle fibres
Red Either endurance or rapid force Quickly fatigue
70
Concentric isotonic contraction
Length of muscle changes in direction of contraction
71
Eccentric isotonic contraction
Length of muscle changes opposite to direction of contraction
72
Effects of endurance exercise training
Increased mitochondrial function --> increased O2 Hypoxia inducible factors (HIFs) involved in gene control of red muscle cell production and regulation of glycolytic enzymes Increased [Hb]
73
Individual variation in proportion of diff fibre types
Training does not significantly change proportions of fibre types Athletes find the sport that fits their abilities
74
Respiratory substrates in intense short-term exercise - 10-15s
Creatine phosphate
75
Respiratory substrates in intense short-term exercise -up to 2 mins
Glycogen to glucose-6-phiosphate
76
Respiration inintense short-term exercise - several min
Lactic acid build up Oxygen debt About 2L of oxygen required to replenish ATP and creatine phosphate
77
Respiration in longer, less intense exercise
Glycogen from circulation Glucose from plasma Hepatic glucose production increases
78
What happens when hepatic glucose increases
Short term glycogenesis | Longer term gluconeogenesis – muscle proteolysis, glucagon and insulin, fatty acid release
79
VO2 max
Oxygen usage under maximal aerobic activity
80
EPOC
Excess post exercise oxygen consumption
81
Fast component of recovery phase
Resting levels of ATP and CP restored
82
Slow component of recovery phase
Lactic acid converted to glucose in liver | Lactic acid converted to pyruvic acid
83
How is the increased oxygen demand met during exercise
Increase in ventilation rate | Increase in tidal volume
84
Tidal volume
Volume of air displaced during respiration
85
Changes in blood gases during exercise
Arterial O2 and venous CO2 do not change significantly during exercise Respiratory system can provide adequate aeration
86
Oxygen consumption during exercise
Oxygen consumption increases Similar rate for first few seconds reaches steady state where lactate acid accumulation is minimal Other factors like fuel availability limit exercise VO2max when steady state oxygen consumption doesn’t increase w/ work intensity
87
Changes in alveolar diffusion during exercise
Oxygen and carbon dioxide diffusion capacity increases w/ exercise Related to increase in perfusion more than ventilation
88
Redistibutrion of blood flow during exercise
As exercise continues, blood flow to the muscles increase substantially
89
Cardiac changes in exercise
Increased cardiac output by increased stroke volume and increased heart rate
90
Stroke volume
How much blood pumped out with each cycle
91
Control of cardiac output
Increase in activity of sympathetic nerves --> increases stroke volume, ventricular myocardium decrease ion parasympathetic nerves --> increases hr, SA node These both increase cardiac output
92
Control of stroke volume
Decreased venous return --> increases end-diastolic volume Increased sympathetic activity/ epinephrine --> increases contractibility of ventricle Arterial pressure also decrease These increase stake volume
93
What does change in central venous pressure change
Diastolic filling pressure, more blood available to fill heart
94
What does total peripheral resistance change
Ability to expel blood into arterial system
95
Starlings Law
The fuller the heart is, the harder it will contract increasing the stroke volume (ventricular performance)
96
Benefits of exercise and reducing cardiovascular disease risk
Reduced blood pressure Increased circulating HDL and reduced Triglycerides Changes in arterial wall homeostasis reducing atherosclerotic disease Improved aortic valve function and reduction in calcification Increased ventricular chamber wall thickness Increased red cells (to a point) Changes in cardiac vasculature to increase oxygen availability
97
Exercise and depression
Moderate clinical effect in a decline in depression Long term follow up on mood found in favor of exercise No more effective than psychological or pharmacological treatments Important for those who do not want pharmacological treatment

MBBS - Year 1 (93 decks)

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