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ISBM > Spring Exam 1 > Flashcards

Spring Exam 1 Flashcards

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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
how is smooth muscle innervated
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+
26
smooth muscle contraction is ___ based
myosin based
27
describe the innervation of multiunit smooth muscle
dense innervation/high resistance
28
describe the innervation of unitary smooth muscle
low density of innervation/low resistance | -has cross bridges
29
IP3 is a key modulator in smooth muscle for _____
contraction
30
describe the 2 forms of smooth muscle fibers
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
31
what is unique about unphosphorylated myosin in a sustained contraction
it is still forming cross bridges and contributing to the sustained contractile force, but just much slower than phosphorylated mysoin
32
what mechanisms are responsible for maintaining intracellular free Ca levels in smooth muscle cells?
1. Receptor mediated (NT/hormone binds to Gq--> (+) PLC--> generates IP3 from PIP2--> IP3 binds to SR) 2. Voltage sensitive Ca channels (via depolarization) 2. receptor activated Ca channels (via ligand binding and phosphorylation)
33
how do we get rid of Ca in smooth muscle in order to relax
1. Na+/Ca2+ exchange pump (3Na in: 1 Ca out, depolarizing entitiy) 2. Calcium ATPase (primary transport, use ATP)
34
describe the regulation of skeletal, cardiac, and smooth muscle contractile activity
skeletal and cardiac = actin based (w/ troponin) | smooth= myosin based (phosphorylation of myosin ATPase via activated myosin kinase)
35
do gap junctions in muscle cells increase or decrease resistance to current flow?
decreases resistance, which ultimately reduces the amount of time it takes to depolarize adjacent cells
36
what is the primary site of integration of efferent ANS activity?
hypothalamus
37
parasympathetic fibers leave the CNS through what CN?
3, 7, 9, 10**
38
what is the key difference in somatic and ANS efferent axons ?
- 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)
39
what NTs are released in the somatic NS
ACh
40
what NTs are released in parasympathetic NS?
pregang- releases ACh as NT | postgang- releases NE or ACh as NT
41
what NTs are released in the sympathetic NS?
pregang- releases ACh as NT postgang- release ACh or NE as NT adrenal medulla- release Epi**, NE, or DA as NT
42
what are cholinergic receptors
- ACh binds to it - mainly used in parasympathetic effector organ - subtypes: cholinergic nicotinic receptor and cholinergic muscarinic receptor
43
describe what nicotine and muscarine are and what they cause when bound
- agonist to ACh - nicotine--> ligand gated Ca2+ opening - muscarine--> G protein 2nd messenger cascade
44
describe the differences in the muscarinic receptor subtypes
- M2: Gi linked (inhibits adenylcyclase--> decreased [cAMP]) | - M3: Gq linked (activated PLC to generate IP3 from PIP2--> IP3 binds to SR--> Ca release--> contraction)
45
what the effects of M2 binding
decreased HR, conduction velocity, and atrial force
46
what are the effects of M3 binding
smooth muscle contraction, endocrine and exocrine exocytosis
47
what NS are muscarinic-cholinergic receptors associated with
end organs in PSNS
48
describe the differences in the adrenergic receptor subtypes
-A1: Gq linked A2: Gi linked B1: Gs linked B2: Gs linked
49
what are the actions of B1
increases HR | *binds NE and epi
50
what are the actions of B2
helps breathing | -binds mainly epi
51
what are the actions of A1
vasoconstricts | -binds NE first
52
what are the actions of A2
(inhibits NT release presynaptically)
53
what do MAO and COMT do?
degrade NE and epi for reuptake - MAO- oxidizes the amine group - COMT- methylates
54
MAO and COMT inhibitors results in what?
prolonged effects of NA
55
what influences the effects that NT/hormones have upon tissues?
1. receptor distribution 2. receptor density 3. the affinity the receptor type has for its ligand
56
describe the receptor affinity for NE
greatest for Alpha 1 | really no affinity for beta2
57
describe the receptor affinity for epi
greatest for beta2 | will bind with alpha1 when beta is saturated
58
describe the receptor affinity for NE and Epi
equally bind to Beta 1
59
what happens with BP, SNS/PNS tone and HR with high doses of epi?
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
what happens with BP, SNS/PNS tone and HR with high doses of NE?
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
what are the 5 basic type of sensory receptors
1. mechanoreceptor 2. thermoreceptor 3. nociceptos 4. electromagnetic (eye) 5. chemoreceptors
62
type or quality of sensation
modality
63
strength or magnitude of the stimulus
intensity
64
what are the 4 dimensions of sensation
1. modality 2. intensity 3. duration/frequency 4. location
65
what is a receptor potential
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
describe how stretching generates an AP
stretch--> opens ion channels--> influx of Ca and Na--> depolarization/RP--> RP reaches threshold--> generate AP
67
describe the concept of SR adaptation
``` SR adapt (partially or completely) to any constant stimuli after a period of time ex. pacinian corpuscle ```
68
how do SR adapt?
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
the magnitude of the RP is a function of
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
what is frequency modulation?
the magnitude of the RP dictates the number of APs produced by a SR *increase RP magnitude = increased frequency of APs
71
what is the retina
the light sensitive portion of the eye that contains cones (responsible for color vision) and rods (detect dim light and black/white vision)
72
what is the fxn of the choroid and where is it located
helps focus light on the retina (blunt reflection of light) | -located inside the sclera
73
what does the ciliary body produce
humor
74
what is the main site of signal transduction in the eye
the retina
75
area of greatest visual acuity | - direct access to sensory transduction area of the retina
fovea
76
what is the clinical significance of the canal of schlemm
drainage site in corner of eye | - if occluded, pressure builds up and loss of vision (glaucoma)
77
area of Rods and cones that contain photopigments that react to incident light. All embedded adjacent to choroid
Outter segment
78
describe the path of light through the eye
through lens system--> vitreous humor--> ganglionic cells--> plexiform and nuclear layers (inner and outer)--> bipolar cells--> rods and cones in OS
79
what is the major functional segment of rods and cones and why
Outer segment b/c thats where rods and cones are. It also contains Rhodopsin and visual pigments
80
the fovea only contains
Cones!!
81
what are the components of rhodipsin
opsin and 11-cis-retinal
82
11-cis-retinal is derived from what vitamin
Vitamin A
83
how is rhodipsin activated
light hits rhodipsin--> 11-cis-retinal changes into all-trans-retinal--> conformational change or rhodipsin to Metarhodipsin II (now activated)
84
describe the current flow of rods in the dark
- constant OS: inward flow of Na+ IS: outward flow of K+
85
describe the current flow of rods in the light
NO inward current of Na+ (decreased permeability) - outward flow of K+ continues * results in hyperpolarizing membrane (-60--> -80)
86
hyperpolarizing membrane in the eye is a result of what
an unchanged outward current of K+ and decreased inward current of Na+
87
What are the results of parasympathetic innervation of the eye?
1. excite ciliary muscle (accommodation) | 2. excite pupillary sphincter (light reflex)
88
what does the ciliary muscle do?
controls focusing of the eye lens in accommadation
89
what are the NTs and Receptor types of PSNS innervation of the eye
NT: ACh Receptors: nicotinic or muscarinic
90
what are the NTs and receptor types of SNS innervation of the eye
NT: NE Receptors: alpha adrenergic
91
what are the results of sympathetic innervation of the eye
1. excite radial fibers or the iris (dilate pupil) | 2. Extra ocular muscles
92
where do the Parasympathetic preganglionic fibers come from and where do they synapse?
come from Edinger-westphal nucleus (CN3) and synapse in ciliary ganglion behind the eye
93
where do the sympathetic preganglionic fibers come from and where do they synapse?
come from intermediolateral horn of T1 and synapse in superior cervical ganglion in the sympathetic chain
94
what is Miosis
the response of constriction of the pupillary sphincter muscle and reduction in diameter of the pupil **Fxn of PSNS
95
what is Mydriasis
the response of constriction of the radial muscle of the iris and dilation of the pupil **Fxn of SNS
96
NT and receptor type of Miosis
NT: ACh Receptor: cholinergic **Fxn of PSNS
97
NT and receptor type of Mydriasis
NT: NE Receptor: alpha1 adrenergic (Gq linked) **Fxn of SNS
98
what medication causes pupilary dilation and why
tropicamide (musarinic blocking agent) | **antagonist of the PSNS
99
what 3 tubes make up the cochlea
1. scala vestibuli 2. scala media 3 scala tympani
100
What is Reissner's membrane?
very thin membrane that separates SV and SM. It traps K+ ions in the SM
101
What is the basilar membrane?
separates SM and ST. It increases in thickness as you move down the cochlea and it has the Organ of corti on it
102
what is the Organ of Corti
lies on the basilar membrane and it contains a series of electromechanically sensitive hair cells
103
what is the site of signal transduction in the hear
organ of corti
104
Hair cells are the manifestation of
pure mechano-reception
105
what are sterocilia
little hair projections on hair cells that touch or are embedded in the tectorial membrane
106
how are hair cells depolarized and hyperpolarized?
- 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
describe the current flow in a hair cell
-continuous inward current (due to K+ leaky channels), the inward current is greater with displacement of stereocilia toward the kinocilum
108
when the gates open due to mechanoreceptors in hair cells what way does K+ flow
into the cell (depolarization, following its Electrochemical gradient)
109
why is there a constant inward current in hair cells?
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
what is the NT released in second order neuron stimulation in hearing?
glutamate
111
how is a second order neuron stimulated with hearing?
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
force of a contraction
tension

ISBM (8 decks)

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