Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PRIN > PRIN 9 Excitable Membranes > Flashcards

PRIN 9 Excitable Membranes Flashcards

1
Q

What is Rhabdomyolysis?

A

breakdown of muscle fibers that leads to the release of muscle fiber contents (myoglobin) into the bloodstream.

Myoglobin is harmful to the kidney and often causes kidney damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the resting potential of a typical neuron differ from that of a cardiac/skeletal muscle cell?

A

Neuron:
-60 to -70 mV

Cardiac/Skeletal:
-80 to -90 mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the role of a primary (Ia) sensory nerve fibre?

A

innervates nuclear bag and nuclear chain intrafusal muscle fibres.
Afferent - stretch reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the role of an α-motor neuron?

A

forms synapses with extrafusal muscles fibres and controls muscle contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the term applied to a weak stretch that is not powerful enough to trigger depolarize?

A

receptor / generator potential

only causes a sub threshold stimulation
***graded phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the result of deformation of a Ia sensory fibre ending by stretching?

A

opens stretch-activated channels that conduct net inward Na+ current and cause the receptor potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

During the upstroke of the Action Potential, what predominates?

A

g-Na dominates over g-K (which is delayed)

K-Voltage channels respond more slowly to membrane depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Status of voltage gated Na+ channels

A

Resting: CLOSED
Depolarizing; OPEN Conducting
Re-polarizing: OPEN - INACTIVATED
Hyperpolarizing: CLOSED - INACTIVATED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Status of voltage gated K+ channels

A

Resting: CLOSED
Depolarizing; CLOSED
Re-polarizing: OPEN CONDUCTING
Hyperpolarizing: OPEN CONDUCTING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the status of the Na+ and K+ voltage gated channels during the fall of the AP?

A

Na+ = Open Inactivated

K+ = Open Conducting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the definition of Threshold?

A

defined as the Vm at which inward Na+ current first exceeds outward K+ current.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Absolute VS Relative Refractoriness

A

ABS: impossible to re-stimulate AP

REL: we can make it fire, but it requires a bigger stimulus
threshold is higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes Absolute Refractoriness?

A

the membrane is unexcitable

  • some NaV channels are still inactivated and thus are unavailable to conduct current even if the activation gate is opened
  • Some KV channels are still open and able to oppose the depolarizing effect of any Na+ current
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is meant by electrotonus?

A

ELECTRO-TONUS:

process by which electrical events propagate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is meant by Electrotonic Decay?

A

process by which charge leaks outward, across the membrane, as current travels along the axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ra vs Rm

A

Ra = Axial Resis

Rm = Membrane Resis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Formula for Length Constant (lambda)

A

lamda = square root of (Rm/Ra)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens to Ra as the diameter or the axon is increased?

A

Ra= Axial Resistance

As the “straw” becomes wider, Ra decreases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which way with the electrical current travel when Rm>Ra?

A

If the Membrane Resistance is greater than the Axial Resistance, then it will travel DOWN the axon since this is the path of least resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which way with the electrical current travel when Ra>Rm?

A

If Axial Resistance is greater, then the current will simply leak out the membrane as there is less resistance there.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What TWO variables influence the rate of action potential propagation?

A

(1) DIAMETER OF FIBRE
Increasing Axon diameter decreases Ra

(2) AMOUNT OF MEMBRANE CAPACITANCE
Decreasing Capacitance decreases the time delay of voltage change across membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What forms the Myelin Sheath?

A

PNS: Schwann Cells

CNS: Oligodendrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where along the axon is the capacitance higher?

A

Capacitance is higher in the Nodes of Ranvier. This is where the Na+ channels are located.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Temporal Summation
VS
Spatial Sumation

A

TEMPORAL:
High frequency of a single input
(involves repetitive activation of a SINGLE synapse)

SPATIAL:
Simultaneous activation of multiple synapses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the two most common receptor subtypes that Glutamate acts on?
AMPA-gated channels: allow Na, K. NMDA-gated channels: allo Na, K and Ca
26
At RMP, what is the status of the glutamate receptors?
AMPA-gated channels dominate NMDA-gated channels blocked (don't want Ca coming in at RMP)
27
What is the effect of GABA?
allows influx of Cl- | Prevents cell from causing an AP by clamping it back down to -70mV
28
How wide is the synaptic cleft?
50 nm
29
Within the post-synaptic membrane, where are the voltage-gated Na+ channels located?
Peri-junctional membrane | "shoulders" of each fold
30
What is the site of muscle AP initiation?
Peri-junctional Zone | located in the depths of the Peri-junctional Folds
31
Describe the Nicotinic ACh receptors...
5 subunits requires 2 molecules of ACh open pore conducts Na & K
32
What is the role of Synaptogamin?
Senses a local rise of Ca2+ in the pre-synaptic bouton and triggers the exocytosis of docked vesicles
33
What are Fasciculations?
VISIBLE "twitches" Motor unit fires in response of spontaneous a-MN APs Motor unit functional
34
Fibrillation
occurs after complete denervation **Motor unit NON-functional **individual muscle fibers spontaneously contract NON-Visible
35
What has gone wrong in polio?
Virus kills cell bodies in ventral horn Death of a-MN cell body causes Paralysis as ason degenerates and NM transmission is blocked Some motor muscle mass is maintained
36
Guillan-Barre Syndrome
PNS disorder | Autoimmune Cells attack on Schwann cells degrading myelin
37
What does Botulism do?
``` Acts on PRE-synaptic mechanism Disrupts SNARE proteins, prevents ACh release Flaccid Paralysis (hangs limp) ```
38
What does the Simpson Plus Test diagnose?
Myasthenia Gravis
39
What is meant by Safety Factor
large amounts of vesicles ready to go | Ensures MUCH more ACh is released what what is actually required to trigger AP in muscle cell
40
Myasthenia Gravis
Most common post-synaptic NMJ disorder | Reduces ACh binding and EPP safety factor
41
How can muscle contraction be evoked?
(1) Volitionally (2) Tendon Tap (brief muscle stretch) (3) electrical stimulation of nerve (4) direct stimulation of muscle fibres
42
What comprises a motor unit?
a-MN and all the muscle fibres it innervates
43
EMG? EEG? ECG?
EMG = Electro-myo-graphy (electrical activity of skeletal muscles) EEG = Electro-encephalo-graphy (brain) Electrocardio-graphy (heart)
44
What is CMAP?
Compound Muscle AP CMAP is the extracellular correlate of near-synchronous AP discharge in a number of muscle fibres We used surface electrodes to detect fibrillations and fasciculations
45
What is the Hoffman Reflex?
Only H-wave is evoked Produced by using stimulation with a low intensity electric current such that only the largest Ia sensory axons are evoked
46
How can the M-wave be increased?
M-wave will increase as stimulus is turned up
47
How can propagation speed be increased?
(1) increase axon diameter (2) increase transverse resistance of the cable (myelin) (3) Decrease the capacitance of the cable
48
What is the difference between the H-reflex and the spinal stretch reflex?
H-reflex bypasses the muscle spindle
49
Orthodronic VS Antidromic
Orthodromic = Hand to Brain Antidromic = Brain to hand
50
What is CSNAP?
Ccompund Sensory-Nerve AP | *Represents the signal generated by AP discharge in a number of sensory axons
51
Normal Nerve Conduction Velocities
50-70 m/s = Normal myelinated large fibre nerve <40m/s = Damaged / demyelinated nerve
52
What are muscle spindles?
Muscle spindles are sensory receptors within the belly of a muscle detect changes in the length of this muscles and allow for coordinated movements
53
What clinical conditions affect spinal motor neurons and/or cortico-spinal neurons?
ALS | Polio
54
What is MEPP?
Motor End Plate Potential
55
Describe Actin
Each actin filament (F-actin) is composed of a helix of globular actin (G-actin) monomers. Each G-actin monomer has a binding site for myosin which, during rest, is covered by tropomyosin.
56
What is the effect of Ca2+ in muscle cell?
Toponin C binds Ca2+. This causes a conformational change such that Tropomyosin gets moved out of the way. This exposes actin's myosin binding site.
57
What is the effect of myosin head binding to the actin filament?
(1) reduces the affinity for ADP and Pi and so it gets released. (2) Myosin head rotates 45 degrees (3) ATP binds and mediates release of actin from myosin
58
What is the triad?
Sandwich of: SR lateral sac T-tubule SR lateral sac Triads are the location where translation of the action potential into an intracellular calcium transient occurs
59
What are T-tubules?
extensions of ECM, relays AP through cells ensures that the action potential is carried quickly and deeply into the muscle
60
Order of Receptors / Molecules connecting AP from T-Tubule into SR
DHPR ryr1 Triadin Calsequestrin
61
What is DHPR
Dihydro-pyridine Receptor voltage gated calcium channel located in the cell membrane (myoplasm on inside // ECM t-tubule on outside)
62
What is the role of Calsequestrin in the SR?
binds/stores 50 mol calcium/mol of protein in the lumen of the SR
63
Coupled VS Non-coupled ryr1
COUPLED ryr: only every other ryr receptor is coupled with a DHPR UN-COUPLED ryr: open in response to calcium released from the coupled receptors (get activated in response)
64
What happens to Calsequestrin during an AP?
(1) change in configuration of ryr is transmitted via triadin to calsequestrin (2) calsequestrin changes from a random coil to a more linear configuration (3) Calsequestrin then releases Ca into the lumen of the SR, (4) calcium exits into myoplasm through open ryr
65
What is summation?
Additional stimuli, delivered prior to the time at which force has returned to baseline, causes re-opening of the ryr and superposition of the next contraction on top of the declining phase of the previous contraction
66
What is Tetanus?
summed contractions caused by fast summation
67
What causes the mrapid increase in muscle mass of body builders?
the CNS has been trained to increase the firing rate to maintain tetanus maxed at about 4 weeks ... plateau
68
What is Hypercapnia?
elevated CO2
69
How do we treat hypercapnia?
Hyperventilation
70
How do we treat MH? | How do this work?
Dantrolene **blocks up RYR pore and prevents Ca@+ from escaping the SR lumen (like a cork in a bottle)
71
How do we treat Acidosis?
NaHCO3 infusion | deliver bicarbonate
72
How do we treat Hyperkalemia?
INSULIN drives K+ into cells promotes GLUT4 for glucose (irrelevant) but also stimulates Na+/K+ pumps
73
What's the problem with Hyperkalemia?
BAD for heart - cardiotoxic
74
What is the first sign of MH?
increased CO2 & HR
75
Under normal physiological conditions the equilibrium potential for Ca2+ (across the plasma membrane) is:
Positive
76
When does recovery from Na channel inactivation occur?
during the after-hyperpolarization (AHP)
77
d-tubocurarine, pancuronium and rocuronium cause skeletal muscle paralysis by:
acting as competitive antagonists of the nicotinic cholinergic receptor at the motor end-plate
78
How does Hyperkalemia affect the RMP?
Hyperkalemia causes the RMP to become LESS negative because it causes the equilibrium potential for potassium to become LESS negative.
79
Creatine vs Creatinine
``` Creatine ...broken down to... Creatinine ...taken to .... kidneys ```
80
What does Creatine Kinase do?
Catalyses the reaction that transfers a phosphate group to Creatine to make a high energy compound (skeletal muscle)
81
When is the potassium conductance (gK) of the membrane larger than then sodium conductance (gNa)?
(1) at RMP .... and | (2) during the after hyperpolarization
82
A unique and distinguishing feature of smooth muscle cells is:
dense bodies and caveolae
83
What IS the sarcolemma?
Simply the cell membrane of the a skeletal muscle cell
84
Which region within the sarcomere contains both Myosin & Actin?
A Band
85
Which region within the sarcomere contains only myosin?
H zone
86
What is the MOA of paralytic shellfish poison and other such toxins?
blocks voltage-gated Na channels in nerves. depolarization can't occur
87
Hyperkalemia VS Hypokalemia What is the effect of each on RMP?
Hyperkalemia will increases likelihood of depolarization (make RMP less negative) Hypokalemia will decrease likelihood (make RMP more negative)
88
How are non-depolarizing NMBA drugs eliminated? rocuronium, mivacurium ...
plasma cholinesterases

PRIN (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions