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Autonomic physiology > Final > Flashcards

Final Flashcards

1
Q

Routes of administration and characterization of each route

A

Oral (metabolism); intravenous (nonlipid, fast onset); intramuscular (lipid, slow, long release); inhalation (gas, lipid (gas exchange), Topical (lipid, slow, long release); subcutaneous (like IM); Intraperitoneal (rat stomach), intracranial (spinal cord)

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2
Q

phenomenon by which concentration of administered drug is greatly reduced before reaching circulation via _____

A

First pass effect, metabolism

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3
Q

how do orally administered drugs cross PPB of cell membranes?

A

achieve neutrality after metabolism

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4
Q

places drug can go from bloodstream

A

tissue reservoirs, proteins, tissues, metabolism and elimination

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5
Q

“bi-functional role of receptor” meaning and who?

A

Langley, “binding and transduction”

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6
Q

lock and key metaphor, who?

A

Ehrlich

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7
Q

Gs (short)

A

stimulates adenylyl cylase

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8
Q

Gi (short)

A

inhibits adenylyl cyclase

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9
Q

Gq (short)

A

stimulates PLC

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10
Q

Go (short)

A

couples directly to ion channels

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11
Q

Gs/Gi (whole sequence)

A

ligand binds, alpha subunit disconnects, activating adenylyl cyclase, converts ATP to cAMP, cAMP goes on to rearrange regulatory subunits and release catabolic subunits of PKA

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12
Q

Gq

A

ligand couples to receptor, stimulates PLC to phosphorylate PIP2 into DAG and IP3. DAG activates PKC and IP3 stimulates calcium calmodulin action

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13
Q

Go

A

ligand couples, receptor opens K+ pathways and they exocytose, leading to inhibition?

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14
Q

affinity

A

ability of drug to bind receptor

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15
Q

Kd

A

(affinity constant) concentration of drug at which 50% receptors are bound. (looks logarythmic, the one that is sharper slope is more effective (less concentration) (drug concentration vs %maximal binding)

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16
Q

IC50

A

(Competitor) concentration at which 50% of binding sites have now been taken over (like a backwards S, negative slope)

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17
Q

Efficacy

A

ability of a ligand to activate a receptor (full, partial, antagonistic)

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18
Q

Full agonist

A

intrinsic efficacy of 1

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19
Q

partial agonist

A

efficacy between 0 and 1

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20
Q

antagonist

A

bonds to receptor, intrinsic efficacy of 0

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21
Q

EC50

A

concentration of drug at which 50% of population exhibits response over certain time period (survey “has pain been relieved) (forwards s, sharper slope and smaller EC50 means better drug)

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22
Q

mechanisms of tolerance:

A

desensitization and downregulation

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23
Q

desensitization

A

when sudden, high concentrations of agonist and receptor become phosphorylated, inactivated, and internalized

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24
Q

Downregulation

A

when chronic levels of agonist, receptors become phosphorylated multiple times, inactivated, and internalized for degradation (may be way diabetes works with insulin detection / release?) not sure

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25
Q

what molecule flags for degradation?

A

B-arrestin

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26
Q

TD50

A

concentration of drug at which 50% of the population shows toxicity (S shape)

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27
Q

TD50-Ed50=______; (Larger = _____)

A

Therapeutic window; (larger=safer)

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28
Q

Metabolism types (4)

A

Oxidation, reduction, hydrolysis, conjugation

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29
Q

oxidation

A

R-CH2-CH3 —ctochrome P450)—> R-CH(OH)-CH3

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30
Q

reduction

A

R-NO2 —–> R-NH2

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31
Q

hydrolysis

A

R-CO2R’ —esterases—-> R-CO2H + R’OH

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32
Q

conjugation

A

R-OH + R’ —–> R-O-R’

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33
Q

example of the way enzymes responsible for metabolism are inhibited

A

Grapefruit juice contains furanocoumarins that inhibit cytochrome P450, leading to increased levels of circulating drug

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34
Q

Regulation of Choline Acetyltransferase amounts in the synapse (3)

A

End product inhibition
Neuronal Stimulation
Mass Action

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35
Q

negative feedback loop used to regulate production of a given molecule; prevents excess buildup of end-product

A

end-product inhibition

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36
Q

if a neuron is stimulated by depolarization from action potential, ACh will be released/used up, so choline acetyltransferase will become activated to produce more ACh and compensate for its use

A

Neuronal stimulation

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37
Q

principle on the equilibrium of a process (hypothetical)

A

mass action

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38
Q

terminates the action of acetylcholine action by breaking ACh into acetate and choline

A

Acetylcholinesterase

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39
Q

Two parts of acetylcholinesterase

A

anionic(bonding) site, (catabolic) esteratic site with serine as the “separator/transformer”

40
Q

receptor type present in NMJ, allows fast, stimulatory influx of Na+

A

Nicotinic receptors

41
Q

The types of muscarinic receptors that are stimulatory, and couple to Gq

A

M1 M3 M5

42
Q

The types of muscarinic receptors that are inhibitory, and couple to Gi/o

A

M2, M4

43
Q

scopolamine

A

Muscarinic drug that is M1 receptor antagonist that blocks input to brainstem vomition center (medulla?)

44
Q

vesicare

A

muscarinic drug that is M3 receptor antagonist that decreases contractility of bladder smooth muscle

45
Q

Axon of motor junction (presynaptic terminal) > NMJ > muscle fiber (postsynaptic membrane)

A

NMJ

46
Q

Voluntary Muscle Contraction (5 steps)

A

• Depolarization causes release of ACh from pre-synaptic
motor neuron
• ACh binds nicotinic receptors on the muscle cell
membrane to depolarize the cell
• Depolarization causes the opening of voltage-gated Ca2+
channels and diffusion of Ca2+ ions out from the SR
• Calcium binds troponin which allows movement of
tropomyosin to reveal myosin binding sites
• Myosin globular heads can attach to actin filaments and
pull, causing contraction and shortening of the sarcomere

47
Q

• Reversible = edrophonium chloride
• forms salt bridge in anionic site of enzyme but cannot be
hydrolyzed
• Slowly reacting substrates = physostigmine
• fits in the enzyme binding site and will be hydrolyzed
• Irreversible inhibitors = organophosphates
• Will form permanent bond with AChE causing total inactivation of
the enzyme within certain time frame

A

Acetylcholinesterase Inhibitors

48
Q

reversible Ach Inhibitor

A

edrophonium chloride

49
Q

physostigmine

A

slowly reacting substrate that blocks AChE

50
Q

irreversible AChE inhibitor that forms permanent bond with AChE causing total inactivation of enzyme within certain time-frame

A

organophosphates

51
Q

You might use AChE inhibtor clinically if (2)

A

Curare poisoning, myasthenia gravis

52
Q

• Antagonistic blockade of nicotinic receptors at neuromuscular
junction causes paralysis

A

• Curare poisoning

53
Q

• Antibodies to nicotinic receptors causes downregulation

A

• Myasthenia Gravis

54
Q

Inhibition of AChE increases____

A

neurotransmissions at the

cholinergic synapse

55
Q

Dopamine Synthesis

A

Tyrosine &raquo_space;»»Tyrosine hydroxylase»»» DOPA &raquo_space;»>amino acid decarboxylase»»> Dopamine (DA)

56
Q

adrenergic receptor that couples to Gq = stimulatory action

• Expressed in blood vessels to mediate constriction

A

α1

57
Q

adrenergic receptor that couples to Gi
/Go = inhibitory action
• Expressed primarily is pre-synaptic autoreceptor

A

α2

58
Q

adrenergic that all couple to Gs = stimulatory action

A

β1, β2, β3
β1 expressed in heart to mediate increased HR
• β2 expressed in bronchial tubes to mediate relaxation

59
Q

• In sympathetic response, contraction or relaxation of
smooth muscles occurs based on the ________
expressed in the muscle

A

types of receptors

60
Q

smooth muscle contraction sequence

A

Smooth muscle is found mainly in walls of
hollow organs and vasculature
q Made up of thick and thin myofilaments
n Actin and myosin
q Not organized into distinct bands
q Does not contain troponin
n Contains calmodulin
q Calcium-calmodulin complex allows activation of myosin
q Contractions are elicited by a number of stimuli
n All result in increase in intracellular calcium

n Increased calcium in the smooth muscle cell
causes contraction
q Calcium may come from extracellular or
intracellular stores
n Calcium binds calmodulin
q Calcium activates calmodulin to allow it to
stimulate myosin light chain kinase (MLCK)

n MLCK phosphorylates myosin light chains
(MLC)
q Phosphorylation leads to cross-bridge formation
with actin filaments
q Causes
contraction
Smooth Muscle Physiology
n MLCK phosphorylates myosin light chains
(MLC)
q Phosphorylation leads to cross-bridge formation
with actin filaments
q Causes contraction
n Contraction is terminated after calcium is
removed from cytoplasm
q Calcium pumps may transport intracellular calcium
into sarcoplasmic reticulum or outside of cell

61
Q

(simple) involuntary muscle contraction

A

Contraction continues until calcium removed

Phosphorylation promotes cross-bridge formation

MLCK phosphorylates myosin light chains

Calcium-calmodulin complex stimulates MLCK

Calcium binds to calmodulin

Increase in Ca2+ in smooth muscle cell

62
Q

Serotonin synthesis

A

Tryptophan > Tryptophan
Hydroxylase>
5-HTP >Amino Acid
Decarboxylase> Serotonin

63
Q

ANS neuron characteristic: 2 neuron pathway

A

preganglionic neuron with cell body in CNS –> postganglionic neuron with cell body in ganglion

64
Q

Postganglionic axons are myelinated or unmyelinated?

A

unmyelinated. Pre are myelinated, I think

65
Q

sympathetic activation targets

A 
Preganglionic fibers exit
through spinal cord
ventral root
Fibers pass through
white ramus to reach
ganglia
Synapse in sympathetic
chain ganglia with
postganglionic cell body
Spinal nerve route:
synapse in chain on
same level
Sympathetic chain
route: travel up/down
chain before a synapse
Travel through
sympathetic ganglia, but
no synapse until reaching
collateral ganglia
Travel through
sympathetic ganglia, but
no synapse; release ACh
directly on adrenal
medulla
66
Q

Sympathetic activation characteristics: 3 things that cause widespread activation

A

sympathetic chain ganglia - connectivity
NE and Epi release from adrenal medulla
• Postganglionic terminal varicosities

67
Q

only sympathetic response that affects posganglionic ACh

A

sweat glands

68
Q

3 differences between SNS and PNS activation

A 
• Spinal nerves: Lumbar and
thoracic versus cranial and sacral
• Ganglia location: Close to spinal cord versus close
to effector
• Neurotransmitter ACh and NE
versus ACh and ACh
69
Q

a-1 pathway mediates

A 
Constriction of vasculature
• Constriction of internal
sphincter in bladder and
colorectal pathway
• Contraction of radial eye
muscle for dilation
• Release of glucagon from
alpha cells of the pancreas
70
Q

a-2 pathway mediates

A

Inhibition of NE release at
SNS terminals
• Inhibition of insulin release
from pancreas beta cells

71
Q

β1 pathway mediates

A

Increased strength of
heart contraction
• Increased heart rate

72
Q

β2 pathway mediates

A

Dilation of the bronchioles
• Dilation of blood vessels
that lead to heart and
skeletal muscles

73
Q

_________ activation characteristics:
• ALL postganglionic parasympathetic neurons release ACh
• 75% of parasympathetic outflow through vagus nerve
• Effects at target tissue mediated by muscarinic receptors

A

parasympathetic

74
Q

M3 pathway mediates

A 
Constriction of bronchial
tubes and the trachea
• Contraction of detrusor
muscle of bladder
• Contraction of circular eye
muscle for pupil
constriction
75
Q

M2 pathway mediates

A

• Decrease in heart rate
through action at SA and
AV nodes

76
Q

How do SNS and PNS coordinate through synaptic level control?

A

presynaptic a2 receptor in sympathetic terminal. presynaptic m2 receptor in parasympathetic terminal

77
Q 
Sensory Receptor
-->
Sensory Neuron
-->
CNS (spinal cord)
-->
Preganglionic neuron
-->
Postganglionic neuron
-->
Effector Tissue
A

autonomic reflex arc

78
Q

How do SNS and PNS coordinate through spinal level control?

A

autonomic reflex arc

79
Q

3 locations of function of pancreas

A

beta cells, effector cells, and alpha cells

80
Q

Function of pancreas: beta cells

A

inc blood glucose, inc ATP production, inhibit outward K+
channels, depolarization opens v-gated Ca2+, exocytosis of
insulin

81
Q

Function of pancreas: effector cells

A

• insulin binds tyrosine kinase receptor, activates signal pathway, GLUT4 transporters translocate to cell surface

82
Q

Function of pancreas: alpha cells

A

• dec blood glucose, release of glucagon

83
Q

SNS synergistic activity at pancreas to increase blood glucose

A 
NE binds α1 on
alpha cells
• Stimulates IP3
pathway
• Increase Ca2+
promotes
glucagon
exocytosis 
• NE binds β2 on
alpha cells
• Activates Gs,
increase cAMP
• PKA opens
Ca2+ channels 
NE binds α2 on
beta cells
• Simulates outward
K+ current
• Slow
hyperpolarization
inhibits insulin
exocytosis
84
Q

urinary bladder reflex on detrusor

A

Stretch receptors sense filling of bladder

  • Sensory neuron projects to spinal cord
  • Synapse on preganglionic neuron&raquo_space;synapse on postganglionic neuron
  • Release of ACh onto M3 receptors in detrusor
  • Smooth muscle contraction via Gq pathway
85
Q

Micturition (other than detrusor) (parasympathetic)

A 
Relaxation of internal
sphincter
• Output from micturition
center inhibits SNS
smooth muscle
activation α1
• Relaxation of external
sphincter
• Output from micturition
center inhibits voluntary
motor neuron activation
86
Q

Bladder filling (sympathetic)

A 
Relaxation of detrusor
muscle
• NE binds β3 to inhibit smooth
muscle contraction
• SNS inhibits PNS input
• Constriction of internal
sphincter
• NE binds α1 to mediate
smooth muscle contraction
• Constriction of external
sphincter
• SNS output enhances
voluntary motor neuron
activity
87
Q

Control of blood pressure

A 
• Regulate cardiac output through:
• Changes in heart rate
• Changes in stroke volume
• Regulate total peripheral resistance through:
Changes in vasoconstriction
• Regulate blood volume through (next section of the
course):
• Changes in RAS system
• Release of aldosterone
88
Q

how blood pressure decreases heart rate

A 
• Increase in blood pressure
• Firing frequency of baroreceptors
increases
• Activates NTS neurons that project
to vagus nerve
• Increase ACh release at SA node
• M2 receptors cause
hyperpolarization through K+ efflux
• Decrease in heart rate
89
Q

increase in heart rate

A 
• Decrease in blood pressure
• Firing frequency of baroreceptors
decreases
• Activates NTS neurons that project
to RVLM
• Increase NE release at SA node
• β1 receptors cause depolarization
through decreased K+ efflux
• Increase in heart rate
90
Q

increase in contractility

A 
• Decrease in blood pressure
• Firing frequency of baroreceptors
decreases
• Activates NTS neurons that project
to RVLM
• Increase NE release at SA node
• β1 receptors cause depolarization
through decreased K+ efflux
• Increase in heart rate
91
Q

vasoconstriction to increase TPR

A

NE binds a1 and etc happens

92
Q

3 respiratory groups that regulate breathing

A

Venral, pontine, dorsal

93
Q

• 1) Inhalation: Inspiratory neurons fire à project to diaphragm and
intercostal muscles
• 2) Exhalation: Expiratory neurons fire à inhibit inspiratory neurons

A

ventral respiratory group

94
Q

• Inhibits inspiratory neurons à causes shorter respiration cycles,
increases respiration rate
• Important during breathing/exercising

A

pontine respiratory group

95
Q
  • Respond to activity of chemosensors:
  • Central – most sensitive to H+
  • Peripheral – most sensitive to changes in O2 and CO2
A

dorsal respiratory group

96
Q

Peripheral chemosensation

A 
• O2 level decreases
• O2-sensitive K+
channels close
• Depolarization and
activation of fibers to
DRG 
• CO2 level increases
• Intracellular acidity
increases
• Inhibition of K+ channels
• Depolarization and
activation of fibers to DRG
97
Q

chemosensation arc

A

Chemosensors&raquo_space;» DRG&raquo_space;» VRG &raquo_space;»>
Diaphragm/
InercostalMuscles

Autonomic physiology (2 decks)

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