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PHA 511 > 1. Nervous System and Muscle Physiology > Flashcards

1. Nervous System and Muscle Physiology Flashcards

1
Q

Neuron: Regions

A

Cell body (soma)
Dendrites (impulses to cell body)
Axon hillock (initiation of AP)
Axon (impulses away from body)

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2
Q

60-40-20 Rule

A

60% of body weight is water

40% of body weight is ECF

20% of body weigh is ICF

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3
Q

ECF

A

75% interstitial fluid

25% plasma

Separated by capillary wall

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4
Q

Potassium (K)

A

Higher inside cell (ICF)

Circle K

Moves out of cell

Greatest influence on resting membrane potential

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5
Q

Sodium (Na)

A

Higher outside cell (ECF)

Moves into cell

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6
Q

Chloride (Cl)

A

Higher outside cell (ECF)

Moves into cell

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7
Q

The membrane must be more permeable to some ions and less permeable to others

A

Number and opening probabilities of ion channels are key

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8
Q

Primary Active Transport

A

Directly requires ATP

Ex: Na K ATPase

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9
Q

Secondary Active Transport

A

Utilizes ATP indirectly

Ex: Na and glucose movement into cell - relies on gradient created by Na K ATPase

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10
Q

Facilitated Diffusion

A

Passive movement of molecules across membrane with the help of a membrane protein

Ex: glucose

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11
Q

Cell Membrane Transport: Across Membrane

A

Endocytosis (pinocytosis, phagocytosis)

Exocytosis

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12
Q

Cell Membrane Transport: Through Membrane

A

Diffusion
Osmosis
Protein mediated transport (primary active, secondary active, facilitated diffusion)

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13
Q

Simple Diffusion

A

Linear

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14
Q

Protein Mediated Transport

A

Curve with a plateau - exhibits saturation

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15
Q

Membrane Ion Channels

A

Selective

Sometimes open, sometimes closed

  • Voltage operated
  • Receptor (ligand) operated
  • Stretch activated
  • Ungated (open all the time)
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16
Q

Conductance

A

The number of channels that are open in a membrane

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17
Q

Resting Membrane Potential

A

Potential difference that exists across the membrane of excitable cells

Established by diffusion potentials (K concentration gradient)

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18
Q

Diffusion Potentials

A

Depends on:

  • ions present
  • permeability (conductance) of each ion
  • electrochemical gradients of each ion
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19
Q

NaKATPase

A

Electrogenic (transfers positive charge out cell, unequal)

3 Na out, 2 K in

Necessary to create and maintain K concentration gradient - establishes resting membrane potential

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20
Q

Resting Membrane Potential: K

A

K leaves the cell (leaving being negative charge)

Negative charges build up inside membrane - establishing RMP

Inside: -70
Outside: 0

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21
Q

Ion Equilibrium Potentials

A 
Na = +65
K = -85
Cl = -90
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22
Q

Action Potential

A

Involves voltage gated channels (Na)

All or none phenomenon (has a threshold (-50))

Non decremental propagation

  • occurs along axon without decay
  • same strength at beginning and end
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23
Q

Action Potential: Phases

A
  1. upstroke: gNa&raquo_space; K
  2. repolarization: gK>gNa
  3. after hyperpolarization: gK»gNa
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24
Q

During which interval of the action potential would the O2 consumption in milliliters of O2 most exceed the resting level?

A

When the NaK pump reestablishes gradients across the membrane (return to rest) - ATP usage

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25
Q

Myelinated Fibers

A

Saltatory conduction (node to node)

Nodes contain high concentration of voltage gated Na channels

Insulation: good for conduction

Skipping

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26
Q

Unmyelinated Fibers

A

Electrotonic conduction

Low density of voltage gated Na channels spread throughout axon

Less efficient/fast

Large diameter = faster conduction

Walking one foot in front of other

27
Q

Multiple Sclerosis

A

MRI: gadolinium enhancing brain lesions

CSF: oligoclonal IgG bands (Dawson’s fingers around periventricular veins - inflammation)

Autoimmune disease
Loss of myelin from CNS axons - replaced by scar tissue (sclerosis)

  • Difficulty walking due to demyelinated axons (Loss of current at demyelinated segment - falls below threshold - no AP - weakness)
  • Deep tendon reflexes working early in disease
  • Eventual degeneration of nerves will lead to muscle atrophy and weakness
28
Q

Pre-synaptic Neuron

A

Contains NT

29
Q

Post-synaptic Neuron

A

Contains R

30
Q

Synaptic Delay

A

1-5 msec for chemical transmission to occur

No physical continuity bt pre and post synaptic neurons

31
Q

Synapse: excitatory c. inhibitory

A

Depends on type of receptor present - not the NT

32
Q

Amplification

A

Release of more neurochemical transmitter

More NT = more R bound = bigger response

33
Q

Characteristics of Neurotransmitters

A

Must meet all 4:
1. synthesized in presynaptic cell, enzymes for synthesis must be present in neuron

  1. must be released by presynaptic cell with stimulation in sufficient quantity to elicit postsynaptic response
  2. Mechanisms for removal or inactivation must exist
  3. when applied exogenously, must mimic in vivo response
34
Q

Synaptic Transmission

A
  1. AP at axon terminal
  2. voltage gated Ca channels open
  3. Ca enters cell
  4. Ca signals to vesicles
  5. Vesicles move to membrane
  6. Docked vesicles release NT - exocytosis
  7. NT diffuses across synaptic cleft - binds to receptors
35
Q

Postsynpatic Potentials

A

EPSP (depolarization)
-helps Na and K move

IPSP (hyperpolarization)
-helps Cl or K move

36
Q

Graded Potentials

A

Electrotonic conduction

Chemical gated channels

No refractory period

No threshold

Amplitude dependent on magnitude of stimulus

Exhibits decremental conduction

37
Q

Choline Esters

A

Small molecule, rapidly acting

Acetylcholine

Receptors:

  • nicotinic (excitatory)
  • muscarininc (inhibitory)
38
Q

Biogenic Amines

A

Small molecule, rapidly acting

Dopamine
Epinephrine
Histamine
Norepinephrine
Serotonin

Receptors (for epi,norepi)

  • alpha R
  • beta R
39
Q

Amino Acids

A

Small molecule, rapidly acting

y aminobutyric acid (GABA)
glutamate
glycine

40
Q

Neuropeptides

A

Larger, longer acting

Some:
ACTH
Endorphins
Oxytocin
Secreting
Vasopressin
41
Q

Synaptic Transmission at Neuromuscular Junction

A
  1. AP travels down motoneuron to presynaptic terminal
  2. Depolarization opens Ca2+ channels
  3. ACh released into synaptic cleft (exocytosis, ATP and Ca2+ requiring)
  4. ACh R binding at motor end plate
  5. Na entry, K efflux via open channel
  6. Motor end plate depolarization (EPP)
  7. ACh degradation via acetylcholineesterase, choline reuptake via Na/choline symport
42
Q

Myasthenia Gravis

A

Muscle weakness
Endrophonium (tensilon) test: positive
Plasma testing: antibodies against ACh R

Autoimmune disease

Destruction of Ach receptors on motor end plates

Normal Ach release

Failure does not occur until 70% of Ach R damaged (safety factor)

43
Q

Safety Factor

A

Measures how much larger EPP is compared to threshold

Normally, magnitude of EPP is large - guarantees depolarization to threshold

44
Q

Agents Affecting Neuromuscular Transmission

A

Botulinum toxin (prevents Ach release)

Hemicholinium (blocks Na/choline transporter)

Curare (competition for binding on motor end plate)

AChE inhibitors (prevents AChE from breaking down ACh)

45
Q

Flaccid Paralysis

A

Muscles cannot contract

Limp, flappy

Botulinum toxin

46
Q

Spastic Paralysis

A

Continuous muscle contraction

Rigid

47
Q

AP and the Sarcomere

A

AP travels inward through sarcomere through T tubules and along surface of muscle fiber

48
Q

Contraction of Skeletal Muscle

A

A band: no change
I band: shortens
H zone: shortens
Z lines: closer together

49
Q

Excitation Contraction Coupling in Skeletal Muscle

A
  1. AP in muscle membrane
  2. Depolarization of T tubules
  3. Opens SR Ca2+ release channels
  4. Increase intracellular Ca2+
  5. Ca2+ binds troponin C
  6. Tropomyosin moves - actin myosin interaction
  7. Cross bridge cycling and force generation
  8. Ca2+ reaccumulated by SR –> relaxation

Continues as long as intracellular Ca is high

50
Q

Muscle Cell At Rest

A

Cytosolic Ca2+ low

Myosin and actin dissociated

Myosin head holds ADP, Pi

Binding site on actin covered

51
Q

Muscle Cell After Increased Intracellular Ca

A

Ca2+ binds to troponin C

Myosin binding sites uncovered

Myosin heads bind to actin

Cross bridges formed

52
Q

Cross Bridging Cycle: Power Stroke

A

Force produced by myosin head pivots

ADP and Pi released

Bond bt actin and myosin stronger

Cross bridges pivot (~45 degrees)

Tension produced - “twitch”

Contractile force is proportional to number of cross bridges formed

53
Q

Cross Bridging Cycle: Myosin Release

A

ATP binds to myosin

Cross bridges break

54
Q

If ATP supply fails…

A

cross bridges are maintained – rigor mortis

55
Q

Cross Bridge Cycle: Regeneration of Activated Myosin

A

ATP hydrolyzed to ADP and Pi - stay bound

Myosin re-energized

Myosin displaced toward + end of actin

Next cross bridge cycle can occur

Cycle repeats as long as Ca is bound to troponin

56
Q

Relaxation

A

Depends on prompt Ca removal

57
Q

Drop in Cytosolic Ca Levels

A

Ca dissociates from troponin C

Tropomyosin/troponin complex to original conformation

Binding site on actin sterically blocked by tropomyosin

58
Q

Sarcomere

A

Basic contractile unit

Delineated by Z disks

Thick filaments
Thin filaments
M line
H zone
A band
I band
59
Q

Temporal Sequence of Events in Skeletal Muscle Contraction

A
  1. AP
  2. Rise in intracellular Ca
  3. Tension
60
Q

Duchenne’s Muscular Dystrophy

A

Poor muscle coordination
Weak muscles/grip strength
Hypertrophied muscles

Plasma analysis: elevated creatine kinase
Muscle biopsy

Loss of dystrophin

61
Q

Creatine Kinase

A

Elevated when muscles are damaged

62
Q

Duchenne’s Muscular Dystrophy: Dystrophin

A

Structural link bt cytoskeleton and muscle cell

Without: alters transmission of tension

  • damage to cell membrane (sarcolemma wilts/becomes unstable)
  • creatine kinase leaks out of cell
  • muscle weakness
63
Q

Pseudohypertrophy of calf muscles due to inflammatory response

A

Replacement of damaged muscle cells with scar tissue

Calves look okay but really its scar tissue

PHA 511 (7 decks)

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