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ISBM > Spring Exam 1 > Flashcards

Spring Exam 1 Flashcards

1
Q

3 types of muscles

A
  1. Voluntary (skeletal, striated- controlled by Somatic NS)
  2. Involuntary (smooth, no striations- controlled by ANS)
  3. Cardiac (striated- modulated by ANS)
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2
Q

describe the T. Tubule system

A

it is intimate with the SR (which releases Ca) in skeletal and cardiac muscle.
- promotes rapid membrane depolarization and produces tension actively and passively

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3
Q

what is the functional unit of a muscle fiber

A

sarcomere

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4
Q

describe the parts of a sarcomere

A

A band- spans entire thick filament
I band- spans where there is only thin filament
H zone- spans where there is only thick filament

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5
Q

Describe the 3 subunits of troponin

A

troponin I: has a strong affinity for actin
troponin T: strong affinity for tropomyosin
troponin C: strong affinity for calcium ions

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6
Q

describe the position of tropomyosin while in a resting state

A

lies on the active sites of actin so attraction cannot occur between actin and myosin to cause a contraction

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7
Q

describe the thick filament

A

made of myosin

  • myosin heads possess ATPase (cleave ATP–> ADP and use the released energy for contraction)
  • myosin heads form cross bridges
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8
Q

what is the functional unit of skeletal muscle

A

a motor unit
aka a single motor neuron and each of the muscle fibers (cells)
**a single neuron may innervate multiple muscle fibers due to axonal branching

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9
Q

define a muscle twitch

A

a single stimulus followed by a single muscle contraction

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10
Q

describe the excitation-contraction coupling process

A

a stimulus–> brief delay–> muscle membrane is depolarized–>generates an AP–> muscle contraction AFTER AP/repolarization is complete due to changes in [Ca2+]

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11
Q

in basic terms, how do you get a tetanic/sustained contraction?

A

Temporal summation

-frequent triggering of muscle fiber AP by a single neuron

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12
Q

A motor unit is made up of

A

a motor neuron and the skeletal muscle fibers innervated by that axon

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13
Q

an axon terminal formed with a synaptic connection with a muscle fiber

A

neuromuscular junction

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14
Q

what are some pharmacological examples of Ca channel blockers

A

verapamil, nifedipine, magnesium, manganese

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15
Q

describe what happens when succinyl choline is used as a pharmacological agent

A

succinyl choline binds to acetyl-choline receptor–> causes an end plate potential–> muscle fiber becomes depolarized–> Na+ voltage gated channels open during AP–> Na channels stay in closed-inactive state bc succinyl choline is not broken down–> cell is inexcitable=short term paralysis

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16
Q

how do Ca channel blockers work?

A

block the voltage gated Ca++ channels on the presynaptic neuron. Therefore, there is no influx of Ca with an AP and vesicles w/ NT never use or enter synapse and muscle fiber is not excitable

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17
Q

describe the basic physiology of a muscle contraction

A

nerve AP stimulated–> acetylcholine is released–> depolarization (EPP) and increased permeability to Na+ and K+–> Ca channels in SR are activated and Ca influx and Na outflux–> muscle AP–> spread of excitation in muscle via TTS–> muscle contraction

**muscle AP proceeds ALL contractile activity

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18
Q

what proteins are responsible for affecting SR Ca release?

A

DHPR (dihydropyridine receptor)

RYR (ryanidine receptor)

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19
Q

describe the role of DHPR and RYR

A

DHPR is in the TTS. when TTS is depolarized, DHPR interacts with RYR in the cytoplasm, which results in the liberation of Ca2+ from SR to cytoplasm. Therefore there is an increase in [Ca] = increase contraction of sarcomeres

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20
Q

describe SERCA’s role

A

an ATPase that takes back Ca2+ into the SR –> leads to inactive stage of muscle contractile units

*describes why the myoplasmic concentration of Ca is transient!

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21
Q

active tension development is a function of what

A

the amount of overlap between the thick and thin filaments

Max tension= max overlap

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22
Q

what are the sources of ATP for a contraction?

A
  • *metabolically generated and stored as phosphocreatine (via direct phosphorylation)
    2. Lactate (anaerobic glycolysis)
    3. glycogen (stored in high levels in skeletal muscle) (Oxidative phosphorylation)
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23
Q

describe the composition of slow muscle fibers

A
  • extensive blood vessel system
  • increased mito (support high oxidative metabolism)
  • more myoglobin
  • slower myosin ATPase
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24
Q

describe the composition of fast muscle fibers

A
  • increased SR for rapid Ca release to initiate contraction
  • increased glycolytic enzymes for rapid release of NRG by glycolysis
  • less myoglobins
  • faster myosin ATPase
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25
Q

how is smooth muscle innervated

A

in an “en passent fashion”- the innervating neuron has multiple releasing sections along the axon.
-Also dual innervated (innervated by hormones or by NT), which results in increased free Ca2+

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26
Q

smooth muscle contraction is ___ based

A

myosin based

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27
Q

describe the innervation of multiunit smooth muscle

A

dense innervation/high resistance

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28
Q

describe the innervation of unitary smooth muscle

A

low density of innervation/low resistance

-has cross bridges

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29
Q

IP3 is a key modulator in smooth muscle for _____

A

contraction

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30
Q

describe the 2 forms of smooth muscle fibers

A
  1. multiunit= not coupled, found extensively in arteriole SmM and are very small (en passant synaptic type)
  2. Unitary= cells coupled via gap junctions and projections, less dense, found in visceral muscle and organs
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31
Q

what is unique about unphosphorylated myosin in a sustained contraction

A

it is still forming cross bridges and contributing to the sustained contractile force, but just much slower than phosphorylated mysoin

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32
Q

what mechanisms are responsible for maintaining intracellular free Ca levels in smooth muscle cells?

A
  1. Receptor mediated (NT/hormone binds to Gq–> (+) PLC–> generates IP3 from PIP2–> IP3 binds to SR)
  2. Voltage sensitive Ca channels (via depolarization)
  3. receptor activated Ca channels (via ligand binding and phosphorylation)
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33
Q

how do we get rid of Ca in smooth muscle in order to relax

A
  1. Na+/Ca2+ exchange pump (3Na in: 1 Ca out, depolarizing entitiy)
  2. Calcium ATPase (primary transport, use ATP)
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34
Q

describe the regulation of skeletal, cardiac, and smooth muscle contractile activity

A

skeletal and cardiac = actin based (w/ troponin)

smooth= myosin based (phosphorylation of myosin ATPase via activated myosin kinase)

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35
Q

do gap junctions in muscle cells increase or decrease resistance to current flow?

A

decreases resistance, which ultimately reduces the amount of time it takes to depolarize adjacent cells

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36
Q

what is the primary site of integration of efferent ANS activity?

A

hypothalamus

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37
Q

parasympathetic fibers leave the CNS through what CN?

A

3, 7, 9, 10**

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38
Q

what is the key difference in somatic and ANS efferent axons ?

A
  • somatic extend from CB in anterior horn and travel uninterrupted to synapse w/ a motor plate (a single neuron)
  • Autonomic extends from CB in CNS out the ventral root to synapse w a post-gang CB, which projects to end organ (2 neurons pre and post-gang)
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39
Q

what NTs are released in the somatic NS

A

ACh

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40
Q

what NTs are released in parasympathetic NS?

A

pregang- releases ACh as NT

postgang- releases NE or ACh as NT

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41
Q

what NTs are released in the sympathetic NS?

A

pregang- releases ACh as NT
postgang- release ACh or NE as NT
adrenal medulla- release Epi**, NE, or DA as NT

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42
Q

what are cholinergic receptors

A
  • ACh binds to it
  • mainly used in parasympathetic effector organ
  • subtypes: cholinergic nicotinic receptor and cholinergic muscarinic receptor
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43
Q

describe what nicotine and muscarine are and what they cause when bound

A
  • agonist to ACh
  • nicotine–> ligand gated Ca2+ opening
  • muscarine–> G protein 2nd messenger cascade
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44
Q

describe the differences in the muscarinic receptor subtypes

A
  • M2: Gi linked (inhibits adenylcyclase–> decreased [cAMP])

- M3: Gq linked (activated PLC to generate IP3 from PIP2–> IP3 binds to SR–> Ca release–> contraction)

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45
Q

what the effects of M2 binding

A

decreased HR, conduction velocity, and atrial force

46
Q

what are the effects of M3 binding

A

smooth muscle contraction, endocrine and exocrine exocytosis

47
Q

what NS are muscarinic-cholinergic receptors associated with

A

end organs in PSNS

48
Q

describe the differences in the adrenergic receptor subtypes

A

-A1: Gq linked
A2: Gi linked
B1: Gs linked
B2: Gs linked

49
Q

what are the actions of B1

A

increases HR

*binds NE and epi

50
Q

what are the actions of B2

A

helps breathing

-binds mainly epi

51
Q

what are the actions of A1

A

vasoconstricts

-binds NE first

52
Q

what are the actions of A2

A

(inhibits NT release presynaptically)

53
Q

what do MAO and COMT do?

A

degrade NE and epi for reuptake

  • MAO- oxidizes the amine group
  • COMT- methylates
54
Q

MAO and COMT inhibitors results in what?

A

prolonged effects of NA

55
Q

what influences the effects that NT/hormones have upon tissues?

A
  1. receptor distribution
  2. receptor density
  3. the affinity the receptor type has for its ligand
56
Q

describe the receptor affinity for NE

A

greatest for Alpha 1

really no affinity for beta2

57
Q

describe the receptor affinity for epi

A

greatest for beta2

will bind with alpha1 when beta is saturated

58
Q

describe the receptor affinity for NE and Epi

A

equally bind to Beta 1

59
Q

what happens with BP, SNS/PNS tone and HR with high doses of epi?

A

increase BP and HR, decreased SNS tone

-alpha1 binding mediates vasoconstriction, which dominates B2 vasodilation. increase BP is sensed by baroreceptors and body will try to decrease pressure. BUT since epi is a potent B2 agonist, the reflex evoked is weaker than epis direct effect on teh heart and therefore still have increased HR

60
Q

what happens with BP, SNS/PNS tone and HR with high doses of NE?

A

increase BP and PNS tone, decrease HR

-NE has strong affinity for A1R which mediates vasoconstriction, therefor increase BP. increase BP is sensed by baroreceptors and body will try to decrease pressure by increasing vagal activity (PNS) and decrease HR

61
Q

what are the 5 basic type of sensory receptors

A
  1. mechanoreceptor
  2. thermoreceptor
  3. nociceptos
  4. electromagnetic (eye)
  5. chemoreceptors
62
Q

type or quality of sensation

A

modality

63
Q

strength or magnitude of the stimulus

A

intensity

64
Q

what are the 4 dimensions of sensation

A
  1. modality
  2. intensity
  3. duration/frequency
  4. location
65
Q

what is a receptor potential

A

a graded response to a stimulus that may be depolarizing or hyperpolarizing.
-RPs have a threshold in stimulus amplitude that must be reached before a response is generated (aka an AP)

66
Q

describe how stretching generates an AP

A

stretch–> opens ion channels–> influx of Ca and Na–> depolarization/RP–> RP reaches threshold–> generate AP

67
Q

describe the concept of SR adaptation

A 
SR adapt (partially or completely) to any constant stimuli after a period of time
ex. pacinian corpuscle
68
Q

how do SR adapt?

A

SR responds to high impulses at first and generate frequent AP but then progressively slower rate until the rate of AP decreases to fewer or none

-AP on onset of stimuli and removal of stimuli but not inbetween

69
Q

the magnitude of the RP is a function of

A

the strength of the applied stimulus
- allows us to differentiate between low level of pain (pin prick) bc we can reach RP threshold with a weak stimlui and still generate AP and greater levels (stab) (differentiate less)

70
Q

what is frequency modulation?

A

the magnitude of the RP dictates the number of APs produced by a SR
*increase RP magnitude = increased frequency of APs

71
Q

what is the retina

A

the light sensitive portion of the eye that contains cones (responsible for color vision) and rods (detect dim light and black/white vision)

72
Q

what is the fxn of the choroid and where is it located

A

helps focus light on the retina (blunt reflection of light)

-located inside the sclera

73
Q

what does the ciliary body produce

A

humor

74
Q

what is the main site of signal transduction in the eye

A

the retina

75
Q

area of greatest visual acuity

- direct access to sensory transduction area of the retina

A

fovea

76
Q

what is the clinical significance of the canal of schlemm

A

drainage site in corner of eye

- if occluded, pressure builds up and loss of vision (glaucoma)

77
Q

area of Rods and cones that contain photopigments that react to incident light. All embedded adjacent to choroid

A

Outter segment

78
Q

describe the path of light through the eye

A

through lens system–> vitreous humor–> ganglionic cells–> plexiform and nuclear layers (inner and outer)–> bipolar cells–> rods and cones in OS

79
Q

what is the major functional segment of rods and cones and why

A

Outer segment b/c thats where rods and cones are. It also contains Rhodopsin and visual pigments

80
Q

the fovea only contains

A

Cones!!

81
Q

what are the components of rhodipsin

A

opsin and 11-cis-retinal

82
Q

11-cis-retinal is derived from what vitamin

A

Vitamin A

83
Q

how is rhodipsin activated

A

light hits rhodipsin–> 11-cis-retinal changes into all-trans-retinal–> conformational change or rhodipsin to Metarhodipsin II (now activated)

84
Q

describe the current flow of rods in the dark

A
  • constant
    OS: inward flow of Na+
    IS: outward flow of K+
85
Q

describe the current flow of rods in the light

A

NO inward current of Na+ (decreased permeability)

  • outward flow of K+ continues
  • results in hyperpolarizing membrane (-60–> -80)
86
Q

hyperpolarizing membrane in the eye is a result of what

A

an unchanged outward current of K+ and decreased inward current of Na+

87
Q

What are the results of parasympathetic innervation of the eye?

A
  1. excite ciliary muscle (accommodation)

2. excite pupillary sphincter (light reflex)

88
Q

what does the ciliary muscle do?

A

controls focusing of the eye lens in accommadation

89
Q

what are the NTs and Receptor types of PSNS innervation of the eye

A

NT: ACh
Receptors: nicotinic or muscarinic

90
Q

what are the NTs and receptor types of SNS innervation of the eye

A

NT: NE
Receptors: alpha adrenergic

91
Q

what are the results of sympathetic innervation of the eye

A
  1. excite radial fibers or the iris (dilate pupil)

2. Extra ocular muscles

92
Q

where do the Parasympathetic preganglionic fibers come from and where do they synapse?

A

come from Edinger-westphal nucleus (CN3) and synapse in ciliary ganglion behind the eye

93
Q

where do the sympathetic preganglionic fibers come from and where do they synapse?

A

come from intermediolateral horn of T1 and synapse in superior cervical ganglion in the sympathetic chain

94
Q

what is Miosis

A

the response of constriction of the pupillary sphincter muscle and reduction in diameter of the pupil
**Fxn of PSNS

95
Q

what is Mydriasis

A

the response of constriction of the radial muscle of the iris and dilation of the pupil
**Fxn of SNS

96
Q

NT and receptor type of Miosis

A

NT: ACh
Receptor: cholinergic
**Fxn of PSNS

97
Q

NT and receptor type of Mydriasis

A

NT: NE
Receptor: alpha1 adrenergic (Gq linked)
**Fxn of SNS

98
Q

what medication causes pupilary dilation and why

A

tropicamide (musarinic blocking agent)

**antagonist of the PSNS

99
Q

what 3 tubes make up the cochlea

A
  1. scala vestibuli
  2. scala media
    3 scala tympani
100
Q

What is Reissner’s membrane?

A

very thin membrane that separates SV and SM. It traps K+ ions in the SM

101
Q

What is the basilar membrane?

A

separates SM and ST. It increases in thickness as you move down the cochlea and it has the Organ of corti on it

102
Q

what is the Organ of Corti

A

lies on the basilar membrane and it contains a series of electromechanically sensitive hair cells

103
Q

what is the site of signal transduction in the hear

A

organ of corti

104
Q

Hair cells are the manifestation of

A

pure mechano-reception

105
Q

what are sterocilia

A

little hair projections on hair cells that touch or are embedded in the tectorial membrane

106
Q

how are hair cells depolarized and hyperpolarized?

A
  • when stereocila move TOWARD kinocilum, they open the gates (mechanoreceptors) and cause depolarization
  • when stereocilia move AWAY from kinocilum, they close the gates, and the cell hyperpolarizes
107
Q

describe the current flow in a hair cell

A

-continuous inward current (due to K+ leaky channels), the inward current is greater with displacement of stereocilia toward the kinocilum

108
Q

when the gates open due to mechanoreceptors in hair cells what way does K+ flow

A

into the cell (depolarization, following its Electrochemical gradient)

109
Q

why is there a constant inward current in hair cells?

A

K+ leaks out of hair cells to through the basolateral membrane into the sclera tympani (ST) due to leaky channels (following STRONG concentration gradient)

110
Q

what is the NT released in second order neuron stimulation in hearing?

A

glutamate

111
Q

how is a second order neuron stimulated with hearing?

A

depolarization of the hair cell opens voltage-gated Ca channels to open–> influx of intracellular Ca–> cause vesicles to release glutamate across synapse–> NT causes EPSP and depolarizes the afferent VIII fibers

112
Q

force of a contraction

A

tension

ISBM (8 decks)

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