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Physiology > Test 1, Deck 1 > Flashcards

Test 1, Deck 1 Flashcards

1
Q

which action potential has the longest duration?

A

cardiac ventricle (200 ms, 10x longer)

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2
Q

which action potential beings and ends at -90mV?

A

skeletal muscle

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3
Q

what is a space constant

A

how easily an axon can conduct electrical activity

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4
Q

small axon = ___ membrane resistance= ___ internal resistance = ___ space constant = ___ conduction

A

small axon = higher membrane resistance (but overcome by the ->) = higher internal resistance= small space constant= slow conduction

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5
Q

at the depolarized region, there is a ___ in membrane polarity, which causes ___ to flow

A

reversal, current

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6
Q

depolarization is caused by

A

opening of of h & m** gates of sodium channels- rapid increase in Na+ channel conductance

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7
Q

repolarization is caused by

A
  • delayed increase in K+ channel conductance;

- inactivation of Na+ channels (closing of h gate)

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8
Q

K+ channels deactivate by

A

repolarization of membrane potential

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9
Q

Na+ channels deactivate by

A

positive voltage of cell (one of few positive feedback loops)

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10
Q

channel properties (M & H)

A

resting- M closed, H open
activated- m open, h open
inactivated- m open, h closed

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11
Q

important difference between Na and K channels

A

K+ channels don’t have H gate, are inactivated by membrane repolarization

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12
Q

how does a more positive resting membrane potential affect the gating of Na channels?

A

H-gates begin to close as membrane becomes more positive; results in slow conduction & muscle weakness

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13
Q

absolute vs. relative refractory periods; what channel do they depend on

A
  • absolute- h-gate is closed
  • relative- hyperpolarization, where voltage difference is too great for another AP
    NA CHANNELS!
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14
Q

how does calcium modulate sodium channel activity?

A

Ca binds to proteins surrounding Na channel, makes environment more positive, h-gate closes, less APs

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15
Q

hyperCalCemia

A

increased plasma Ca+, Na+ channels become inactive (less available), conduction slows
signs: weak reflexes

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16
Q

hyperventilation

A

blow off CO2, get less H+ in blood, get less binding of Ca2+ because of increased pH, increase membrane excitability
signs: agitation

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17
Q

hyperKalemia

A

increased plasma K+, less K+ leaks out of neuron, inside of the cell becomes more positive, h-gates close and get less APs
symptoms: slow mentation, muscle weakness

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18
Q

large differences in the diameter of unmyelinated axons do/don’t change conduction velocity

A

don’t

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19
Q

schwann cells increase the ______ by increasing _____

A

space constant; membrane resistance

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20
Q

where is the only place you see action potentials

A

nodes of ranvier

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21
Q

In MS, the space constant is

A

reduced

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22
Q

steps of synaptic transmission

A
  • depolarization
  • calcium enters
  • synaptic vesicles fuse via SNARE
  • transmitter released into synaptic cleft
  • NTs bind or diffuse (NO)
  • NTs cleared away
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23
Q

two types of post-synaptic events

A

ionotropic- quick- opening of ion channels

metabotropic- slow- GPCRs

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24
Q

BoTX mechanisms, symptoms

A
  • cleaves SNAREs (synaptobrevin, SNAP-25, and syntaxin); prevents fusion of vesicles
  • affects peripheral cholinergic fibers
  • flaccid paralysis & autonomic symptoms
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25
Q

TeTX mechanisms, symptoms

A
  • cleaves SNAREs (synaptobrevin); prevents fusion of vesicles
  • taken up by inhibitory neurons in spinal cord
  • spastic paralysis & death
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26
Q

types of cholinergic fibers

A
  • all preganglionics
  • postganglionics of parasympathetic NS
  • basal forebrain
  • brainstem
  • NMJs
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27
Q

two types of Ach receptors

A

nicotinic- fast- ionotropic

muscarinic- slow- metabotropic

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28
Q

opening of ion channels (PSC) results in

A

PSP- postsynaptic potential (NOT AP)

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29
Q

types of excitatory NTs

A

Ach, glutamate

- inward Na, outward K= EPSC

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30
Q

what is an EPSP

A

cation movement which depolarizes the cell to around ~0mv, ** increasing the probability that an action potential will be fired

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31
Q

inhibitory NTs; act on which channels

A

glycine, GABA; changes permeability to Cl, moves more towards -65mV and LOCKS- will always prevent AP

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32
Q

what does the ANS control

A

MOTOR SYSTEM- cardiac muscle, smooth muscle, glands

- has motor efferents and visceral afferents

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33
Q

function of ANS

A

homeostasis, respond to external stimuli

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34
Q

major autonomic neurotransmitters

A

** Ach and norepinephrine (NE)**

epinephrine is central NT, but in ANS is mainly hormone

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35
Q

differences between neuron-neuron (and neuron-SKM) and neuron-viscera (ANS)

A
  • well defined vs en passant
  • little vs. great distance
  • ionotropic vs metabotropic
  • direct effect vs. direct&neuromodulatory effect
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36
Q

effects of nerve gas (sarin)

A

inhibits Ache, prevent Ach degredation; have too much Ach in cholinergic synapse, overstimulate muscarinic receptors causing convulsions & paralysis

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37
Q

treatment of WMD gases

A
  • diazepam: seizures
  • atropine: blocks Ach receptors
  • 2PAM (pralidoxime)- recover Ache function
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38
Q

NT for adrenergic neurotransmission; how its terminated; where degrading enzymes exist

A

NE synthesized in vesicles from DOPA; MAO and COMT; degrading enzymes in cytosol, mitochondria, circulation

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39
Q

location of pre-ganglionic cell bodies of sympathethic NS

A

C8
lateral horn of thoracics
upper lumbar

40
Q

what do preganglionic sympathetic neurons secrete

A

Ach

- acts on nicotinic receptors- ionotropic, fast acting

41
Q

location of post-ganglionic cell bodies of sympathethic NS

A
  • para-vertebral (sympathetic trunk)

- pre-vertebral ganglia (abdomen)

42
Q

sympathetic pre-ganglionic fibers are shorter/longer than parasympathetic preganglionic fibers

A

shorter

43
Q

preganglionic neurons are mostly ipsilateral/contralateral except for ___, which are bilateral

A

ipsilateral; pelvic viscera/intestines

44
Q

why is the adrenal medulla an exception

A

preganglionic neruons PASS THROUGH splanchnic; have NO post ganglionic neuron

  • is nicotinic
  • causes bolus release of NE/E into blood
45
Q

why are sweat glands an exception

A

they’re sympathetic, but activated by Ach NOT NE

46
Q

sympathetic post ganglionic fibers normally secrete

A

norepinephrine

47
Q

autonomic centers in brain

A

pons (breathing)
medulla (blood vessels)
hypothalamus (master)

48
Q

similarities between skeletal, smooth and cardiac muscle

A

all use Ca2+
all require actin & myosin
chemical energy comes from ATP

49
Q

smallest to largest muscle components

A

myofilament -> sarcomere -> myofibril -> myofiber

50
Q

what happens to the I, A, and H bands during contraction

A 
A band (myosin) stays the same
I band (actin) shrinks
H band (between actins) shrinks
51
Q

steps in EC coupling

A
  • action potential goes down t-tubule
  • depolarization activates DHPR
  • DHPR activates ryanodine receptors
  • ca2+ is released from SR
  • ca2+ initiates muscle contraction
  • SERCA pumps Ca2+ back into SR lumen
52
Q

ways to regulate muscle contraction

A

fire successive APs (summate)
turn more/fewer fibers on
build bigger fibers
change resting length of fibers

53
Q

sarcomeres in parallel add _____, but in series add _____

A

parallel/force

series/shortening

54
Q

describe length-tension diagram

A

lots of stress-too short- sterics

no stress- too long- no overlap

55
Q

isotonic contraction

A

muscle contracts and shortens- (includes concentric and eccentric contractions)- tension remains constant despite a change in muscle weights (bicep curls)

load < tension

56
Q

isometric contraction

A

muscle contracts but does not shorten; muscle actively held at a fixed length, like when you flex to show your biceps, grip an object

load = tension

57
Q

what counts for 50-70% of all ATP consumed? where is the rest used up?

A
  • actomyosin ATPase (crossbridging)
  • SERCA CA2+ ATPase
  • Na/K ATPase
58
Q

sources of ATP for muscle metabolism

A
  • creatine phosphate- 1st used and depleated
  • oxidative phosphorlation
  • glycolysis (anerobic exercise)
59
Q

types of muscle fibers

A

type 1- slow- oxidative phosphorylation- postural muscles- lots of blood vessels/mitochondria

type 2- fast- glycolysis- fast & forceful

60
Q

difference in E-C coupling between skeletal muscle and cardiac muscle

A

DHPR

physical coupling vs Ca2+ induced Ca2+ release

61
Q

weight training increases

A

the number of myofibrils

62
Q

endurance increases

A

the number of mitochondria

63
Q

relationship between alpha and beta adrenergic receptors and smooth muscle activation

A
  • alpha decreases cAMP and beta increases it

- cAMP stimulates PKA to phosphorylate MLCK, resulting in RELAXATION

64
Q

relationship between nitric oxide and smooth muscle contraction

A

vagal stimulation increases Ach in blood, which binds to endothelial cells, causing them to release NO; NO increases cGMP which stimulates the MLCP, resulting in de-phosphorylation of the light chain and relaxation of blood vessels

65
Q

sequence of electical activity

A 
SA
AV
His
Bundle branches
Purkinje
66
Q

two reasons for deviation of membrane potential from Nernst equation

A

1) small sodium influx

2) decrease in potassium permeability (inward rectification)

67
Q

two causes of inward rectification

A

1) chemical- decrease in extracellular K+

2) electrical- depolarization of the membrane

68
Q

channels during fast action potential

A

0- fast Na channels let Na in
1- transient Ito channels let K+ out
2- slow calcium channels let calcium in, transient channels close, trapping K+ in
3- delayed potassium channels open, letting K+ out
4- K+ equilibrates (IK1’s are open)

69
Q

how hypokalemia affects resting membrane potential

A

get no net change in voltage

70
Q

how hyperkalemia affects membrane potential

A

membrane potential becomes more positive

71
Q

channels during slow AP

A

4- funny channels let more Na in than K+ out
2- voltage Ca2+ channels open, and Ca2+ goes in
3- K+ channels open, K+ leaves, get repolarization

72
Q

slow vs fast AP in heart

A

slow- pace maker (e.g. SA cells)

fast- contractile cells

73
Q

what does TTX do?

A

block fast Na+ channels, turns contractile cells to slow conduction

74
Q

3 types of junctions found at intercalated disks

A

fascia adherins
macular adherins
gap junctions (connexons)

75
Q

what are gap junctions sensitive to

A

Ca2+ and H+

76
Q

properties of pacemaker cells

A

function: pace make
small diameter
few gap junctions
few myofibrils

77
Q

properties of atrial and ventricular muscle cells

A

function: contraction
medium diameter
abundant gap junctions
abundant myofibrils

78
Q

properties of His/bundle branches/Purkinjes

A

function: rapid conduction
large diameter
abundant gap junctions
few myofibrils

79
Q

2 factors that determine cardiac conduction

A

1) space constant ((Rm/Ri)^1/2)

2) rate of rise and amplitude of action potential

80
Q

membrane resistance is ___ related to K+ permeability

A

inversely

81
Q

internal resistance is ____ related to number of gap junction connections and ______ related to cell diameter

A

inversely related

82
Q

conduction is strictly related to which part of the action potential?

A

upstroke- sodium channels

83
Q

conditions that can change RMP

A

hyperkalemia
premature excitation
ischemia - build of of K+ in tissue

84
Q

P-R interval

A

conduction time from atrial muscle-AV node-his-purkinje- 200 ms

85
Q

QRS interval

A

conduction time from endocardial to epicardial surface- 100 ms

86
Q

AV nodal conduction abnormalities- type 1

A

abnormal prolongation in P-R interval (1:1 conduction)

87
Q

AV nodal conduction abnormalities- type 2

A

some atrial impulses fail to activate ventricles; not all P waves followed by QRS (e.g. 2:1 conudction)

88
Q

AV nodal conduction abnormalities- type 3

A

complete AV block; no consistent P-R interval

89
Q

sympathetic innervation to the heart

A
  • NE
  • acts on beta adrenergic receptors
  • increases speed of all things in the heart
  • increases cAMP and inward calcium
90
Q

parasympathetic innervation to the heart

A
  • Ach (vagal)
  • acts on muscarinic receptors
  • acts on everything up to AV node
  • increases K+ permeability
91
Q

supraventricular tachycardia

A
  • narrow QRS
  • normal sequence, just rapid
  • CO not affected
  • filling time decreased
92
Q

ventricular tachycardia

A
  • QRS is abnormally prolonged
  • impulse originates in ventricle and skips His-Purkinje; goes in circular pattern
  • conduction is slow
  • CO compromised
93
Q

atrial fibrillation

A
  • absence of P-waves (like static where they should be), R-R are irregular
  • non leathal
94
Q

ventricular fibrillation

A

lots of random electrical activity; is probably the end

95
Q

how to spot AV conduction abnormalities on EKG

A

look for how QRS follows p-wave

96
Q

what does digitalis inhibit and what can it cause

A
  • inhibits Na/K pump, reverses Na/Ca2+ pump

- DADs by abnormally increasing intracellular Ca2+

Physiology (22 decks)

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