Autonomics - Basics Flashcards

1
Q

What is the division between sympathetic and parasympathetic?

A

difference is anatomical in origin
sympathetic - thoracolumbar
parasympathetic - craniosacral

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2
Q

Where are the ganglia of the sympathetic NS? Length of pre vs post-ganglionic neurons?

A

Ganglia in paravertebral chains; pre ganglionic fibers tend to be short and post ganglionic long

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3
Q

Where are ganglia of parasympathetics? Length of fibers?

A

Ganglion cells distributed diffusely or in networks in walls of innervated organs. Long pre-ganglionic, short post-ganglionic

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4
Q

What NT is used in all ganglia?

A

Ach

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5
Q

What NT is used by post-ganglionic parasympathetics?

A

Ach - cholinergic

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6
Q

What NT is used by most post-ganglionic sympathetics?

A

NE - adrenergic

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7
Q

What are the three exceptions in the sympathetic nervous system?

A

sweat glands, renal vascular smooth muscle, and chromaffin cells in adrenal medulla

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8
Q

What NT is used by sympathetics going to sweat glands?

A

Ach

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9
Q

What NT is used by sympathetics going to renal vascular smooth muscle?

A

dopamine

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10
Q

What happens with sympathetics going to the adrenal medulla?

A

Pre-ganglionic releases Ach on chromaffin cells which acts as specialized post-ganglionic neurons and release epi and NE into the blood

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11
Q

Which branch of the ANS is more diffuse and which is more discrete?

A

Sympathetic - diffuse

parasympathetic - discrete

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12
Q

Where is the enteric nervous system located?

A

walls of the GI tract

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13
Q

What three things does the enteric nervous system receive input from?

A

preganglionic parasympathetics, postganglionic sympathetics, sensory input from within the wall of the gut

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14
Q

Where is the output of the enteric nervous system directed? What does it affect?

A

To smooth muscle and secretory cells to control motility and secretion

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15
Q

What’s the result of ligand binding to nicotinic receptors? How do the Nn and Nm differ?

A

differ in subunit composition (and sometimes in how many ligand binding sites);
ligand binding results in opening of Na and K channels and depolarization

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16
Q

What’s the mechanism of M2 and M4 receptors?

A

Gi; inhibit adenylate cyclase and/or activate K channels (hyper polarization)

hyperpolarization of M2 causes slowing of heart, inhibition of neurotransmitter release

17
Q

What’s the mechanism of M1, M3, and M5 receptors?

A

Gq; activate phospholipase C, increasing DAG and IP3 (therefore Ca2+)

smooth muscle contration by M3
neuroregulation by M1

18
Q

What’s the mechanism of alpha-1 receptor?

A

Gq; activate PLC, leads to smooth muscle contraction

19
Q

What’s the mechanism of alpha-2 receptors?

A

Gi; decrease cAMP, hyperpolarize via K channel; leads to inhibitions of neurotransmitter release

20
Q

What’s the mechanism of the beta receptors?

A

all Gs; activate adenylate cyclase and increase cAMP
beta-1 - increase in force and rate of heart
beta-2 - smooth muscle relaxation
beta-3 - increase lipolysis

21
Q

Autoreceptors are often used in presynaptic regulation. Are they generally excitatory or inhibitory?

A

inhibitory; inhibit further release of that NT

22
Q

What are receptors on the presynaptic terminal that respond to NT other than that released by that neuron and exert control on NT release called?

A

heteroreceptors

23
Q

What are possible sites of therapeutic opportunity?

A

NT synthesis, storage, release, termination

receptors on postsynaptic cells

24
Q

What are the steps in the synthesis of catecholamines? Note important locations where appropriate.

A

tyrosine -> L-DOPA (rate-limiting step)
L-DOPA -> dopamine
dopamine -> norepi (occurs in vesicles)
norepi -> epi (in adrenal medulla)

25
Q

Differences in norepi and epi.

A
norepi = neurotransmitter; action in synapse
epi = neurohormone; released into vasculature by adrenals to have effect
26
Q

What are the three ways that norepi effect is terminated?

A

Uptake 1 - ‘re-uptake’ neuron specific, high specificity, low capacity
Uptake 2 - extra-neuronal (ie by effector cell); non-specific, high capacity; how most drugs will be processed
Diffusion away into capillaries, etc

Uptake 1 is the primary mechanism!!! Uptake 2 is a lesser role

27
Q

What are the major metabolic enzymes for epi and norepi? Where are they located?

A

MAO - monoamine oxidase; located on mitochondria surface

COMT - catechol-O-methyl transferase; located in cytoplasm of many cells, notably liver

28
Q

Agonist (ISO, Epi, NE, DA, CLON) at adrenergic receptors.

A

beta1 - ISO>Epi>=NE>DA
beta2 - ISO>Epi»NE»DA
alpha1 - Epi>=NE>DA»ISO
alpha2 - CLON>Epi>=NE»ISO