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neurophysiology > final exam Faruqui > Flashcards

final exam Faruqui Flashcards

1
Q

many organs of the body contain smooth muscle, such as?

A 
walls of hollow organs
GI tract
bladder
uterus
ureters
blood vessels
eye muscles
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2
Q

fiber diameter of type 1/2 muscles

A

1 small

2 large

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3
Q

twitch (rise and fall) of type 1/2 muscles

A 
1 slow (100msec)
2 fast (7.5msec)
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4
Q

mitochondrial content of type 1/2 muscles?

A

1 high

2 low

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5
Q

oxidative enzyme activity of type 1/2 muscles

A

1 high

2 low

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6
Q

glycolytic enzyme activity of type 1/2 muscles?

A

1 low

2 high

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7
Q

myoglobin content of type 1/2 muscles

A

1 high

2 low

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8
Q

SR content type 1/2 muscles?

A

1 LOW

2 high

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9
Q

Capillary density of type 1/2 muscles

A

1 high

2 low

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10
Q

fatigue resistance of type 1/2 muscles?

A

1 very high

2 low

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11
Q

Functions of smooth muscle?

A 
Produce motility (propelling chyme)
Maintain tension (diameter of blood vessels)
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12
Q

what are the types of smooth muscles?

A

unitary

multiunit

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13
Q

what type of smooth muscle has gap junctions?

A

unitary

gap junctions permits fast spread of electrical activity

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14
Q

what is the spontaneous, slow wave activity of unitary smooth muscle called?

A

pacemaker activity

GI tract during perstalsis

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15
Q

what does hypoxia in the blood vessels cause?

A

vasodilation and thus relaxation of the smooth muscle

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16
Q

what also causes vasodilation as well as increased hydrogen atoms?

A

excess CO2

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17
Q

what is the unitary smooth muscle found in the gut walll, with slow rhythmic contractions and cells showing a Calcium A.P?

A

phasic smooth muscle

voltage sensitive Ca channels

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18
Q

what is the unitary smooth muscle found in arteries and encircles their walls,e exhibits continous contractions, not electrically excitable?

A

Tonic smooth muscle

contraction and relaxation play an important role in regulating blood flow

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19
Q

what are some examples of multiunit smooth muscle?

A 
iris of the eye
ciliary muscle sof the eye lens
vas deferens
pulmonary air passages
arrector pili muscles of hair follicles
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20
Q

what type of smooth muscle has no coupling between cells and each muscle fiber behaves as a single motor unit?

A

Multiunit smooth muscle

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21
Q

multiunit smooth muscle is innervated by what?

A

autonomic nervous system

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22
Q

thick myofilaments of the smooth muscle contains what?

A

myosin

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23
Q

thin filaments of smooth muscle are composed of?

A

actin and tropomyosin only

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24
Q

smooth muscle does not have transverse tubules, as they are replaced by?

A

Caveoli

The SR is also less developed than in skeletal or cardiac muscle

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25
Q

what are varicosities?

A

bulges within motor nerve fibers of both types of smooth muscle

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26
Q

in smooth muscle, as action potential travels down the motor nerve, neurotransmitter is released from where?

A

synaptic vesicles stored in these varicosities

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27
Q

depolarization of the smooth muscle action potential opens?

A

Voltage-gated Ca2 channels in the membrane

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28
Q

how else can Ca2+ enter the cell in the smooth muscle membrane?

A

Ligand Gated channels

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29
Q

another mechanism Ca2+ can be released from the Sarcoplasmic Reticulum is? how is it opened?

A 
Inositol triphospate (IP3)-gated Ca2+ release channels
(opened by hormones and neurotransmitters)
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30
Q

a rise in intracellular Ca2+ concentration prompts binding of Ca2+ to?

A

Calmodulin protein, which can bind 4 Ca2+ ions

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31
Q

what binds to, and activates myosin-light-chain-kinase?

A

Ca2+ calmodulin complex

32
Q

how does the activation of kinase phosphorylates myosin filament happen?

A

phosphorylated myosin binds to actin to form cross bridges, producing muscular contraction and tension

33
Q

how many ATP molecules are utilized for each cross bridge of phosphorylated myosin?

34
Q

what triggers myosin to be dephosphorylated by myosin-light-chain-phosphatase?

A

when the Ca2+ concentration decreases inside the muscle cell

35
Q

Myosin and actin may not detach immediately due to?

A

latch-bridge mechanism

36
Q

what are the benefits of the latch-bridge mechanism?

A

can remain bound bound without energy (steady tonic level maintained)
-very fatigue resistant

37
Q

muscle fibers relax when the Sarcoplasmic reticulum re-accumulates Ca2+ via the?

A

Ca2+ ATPase, thus lowering the sarcoplasmic (cytoplasmic) Ca2+ concentration

38
Q

what are calcium channel blockers and their effect on the heart

A

disrupts the movement of calcium (Ca2+) through calcium channels.

  • decrease blood pressure in patients with hypertension.
  • CCBs are particularly effective against large vessel stiffness, one of the common causes of elevated systolic blood pressure in elderly patients.
  • used to alter heart rate, to prevent cerebral vasospasm, and to reduce chest pain caused by angina pectoris.
39
Q

skeletal V. smooth

resting membrane potential

A

smooth -50 to -60mV
-activated by neurotransmitters, hormones, and stretching
skeletal -70 to -90mV
-activated by neurotransmitters only

40
Q

skeletal v> smooth

cycling of cross-bridges

A 
smooth= slow
skeletal= fast
41
Q

skeletal v. smooth

onset of contraction and relaxation

A 
smooth= long
skeletal= short
42
Q

smooth v. skeletal

force of contraction?

A 
smooth= high
skeletal= low
43
Q

smooth v. skeletal

percent of shortening?

A 
smooth= high
skeletal= low
44
Q

smooth V. skeletal

latch mechanism for prolonged holding

A 
smooth= great
skeletal= less
45
Q

smooth V. skeletal

energy requirement

A 
smooth= low
skeletal= high
46
Q

incidence and cause of urinary bladder hypertrophy?

A

common in aged men

benign or cancerous enlargement of the prostate gland—> obstruction of the bladder outlet

47
Q

clinical manifestations of urinary bladder hypertrophy?

A

micturation problem
bladder distension
impaired emptying
diminished ability of bladder muscles to contract

48
Q

characteristics of atherosclerosis?

A
  • artery wall thickens due to build up of cholesterol, TGs
  • Lesions due to hypertension, diabetes,smoking—–> decrease blood/O2 to heart and brain
  • causes heart attack
49
Q

what is an ischemic stroke?

A

-decrease in blood to brain due to embolism or obstruction

50
Q

what is a hemorrhagic stroke?

A

accumulation of blood in the brain

51
Q

characteristics of cardiac muscle?

A

striated (like skeletal muscle)

-branched, connected by gap junctions va intercalated discs (unlike skeletal muscles)`

52
Q

what is the syncytium?

A

the group of cardiac cells that comprise the 2 atria and 2 ventricles that act like 1 cell

53
Q

what do the gap junctions in the cardiac muscle allow?

A

allows the action potential to spread to both atria at once, causing a simultaneous contraction

54
Q

where are the T-Tubules located in the cardiac muscle?

A

located at the Z-disc level

55
Q

in cardiac muscle Ca2+ comes from what two sources?

A

ISF

Cisternae of sarcoplasmic reticulum

56
Q

when Ca2+ comes from ISF what happens?

A

Voltage gated Ca2+/Na+ (slow) channels allow Ca2+ to diffuse into cardiac muscle cells from interstitial fluid

57
Q

when Ca2+ come from the cisternae of sarcoplasmic reticulum, where does it release to?

A

release into sarcoplasm

58
Q

what is the sustained depolarization of the cardiac cells is termed what?

A

plateau phase

59
Q

depolarization does not produce contraction, unless what enters the cell?

A

Ca2+ entering through voltage sensitive Ca2+ channels

60
Q

repolarization of the cardiac cells is caused by what?

A

outward diffusion of K+ through voltage-gated K+ channels

61
Q

relaxation of the heart muscle occurs because?

A

Ca2+ is actively transported from the sarcoplasm into both SR and the interstitial fluid

62
Q

characteristics of muscular dystrophy?

A

-muscles degenerate, lose strength, and are replaced by adipose and fibrous tissue
-Erb Duchenne
Incidence-1 in 3500 male live births ages 2-10

63
Q

symptoms of muscular dystrophy?

A
  • muscles degenerate, lose strength and are gradually replaced by adipose and fibrous tissue
  • hip, leg, abdominal muscles are affected
  • child falls frequently
  • scoliosis (muscles shorten then they atrophy)
64
Q

causes of muscular dystrophy

A

defect in production of dystrophin
- a large protein that links T-Tubules to sarcolemma
Defect in Ca channels of SR allowing Ca ions to leak uncontrollably—> activate phospholase

65
Q

incidence of the autoimmune disease myasthenia gravis?

A

usually in women ages 20 to 30

men ages 50-60

66
Q

symptoms of myasthenia gravis

A

facial muscles affected first
drooping eyelids
double vision
difficulty-swallowing, chewing, talking

67
Q

cause of myasthenia gravis?

A

antibodies attack neuromuscular junctions, bind to ACH receptors in clusters

68
Q

treatment of myasthenia Gravis?

A

cholinesterase inhibitors- make more ACH available

69
Q

incidence of Fibromyalgia?

A

15x more common in women than men

70
Q

symptoms of Fibromyalgia?

A

tender spots, pain, tenderness, stiffness of muscles, tendons and surrounding connective tissues

71
Q

cause of fibromyalgia?

A

aggravated by physical or menta stress, trauma, exposure to dampness or cold, poor sleep

72
Q

treatment of fibromyalgia?

A

gentle aerobic fitness program in beneficial

73
Q

what is a synapse?

A
  • connection where info is transferred between a nerve fiber and another
  • communication might be electrical or chemical
74
Q

describe electrical type of synapse?

A

very fast current flow through gap junctions

-facilitate simultaneous/coordinated contractions in cardiac/ visceral muscles

75
Q

describe chemical synapse?

A

tiny gap called a synaptic cleft
-chemicals are released into cleft, Action potential can only release chemicl, it has no direct impact on presynaptic cell

76
Q

what does each branch of a motor nerve fiber end in?

A

a bulbous enlargement called a synaptic knob

77
Q

the synaptic knob fits snugly in a depression on the sarcolemma of the muscle fiber called the?

A

motor end plate

neurophysiology (1 decks)

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