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CP2 > Pharmacology ANS DSA > Flashcards

Pharmacology ANS DSA Flashcards

1
Q

What is the basis of the Somatic nervous system?

ANS?

A

Consciously controlled actions –> movement, respiration, posture

unconscious actions –> CO, blood flow to various organs, digestion

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2
Q

ANS subdivisions and where its located?

A

Sympathetic = fight or flight / thoracolumbar

parasympathetic = craniosacral, rest and digest

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3
Q

What is the primary neurotransmitter in the parasympathetic system? What does it activate?

same for sympathetic

A

Ach –> nAChR, mAChR

NE > Epi (DA); Ach –> alpha, beta receptors, dopamine receptors, nAChr, mAChr

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4
Q

What is found at all levels of the preganglionic autonomic fibers regardless of sympathetic / parasympathetic?

A

Ach that acts on nAChr

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5
Q

What is the major neurotransmitter of the SNS?

A

NE

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6
Q

Epinephrine is only really occurring where?

A

the synthesis of this only in the adrenal medulla and a few epinephrine-containing neuronal pathways in the brainstem

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7
Q

What is dopamine and where does it act on?

A

precursor to NE and Epi

acts on the CNS and renal vascular smooth muscle

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8
Q

What two AchRs are we talking about for neuronal and peripheral subtypes?

what are these also called?

where are they found / function with each location?

What are their agonists?

A

nAchr –> inotropic

Autonomic ganglia (excitatory) + adrenal medula (release epinephrine)

agonists are Ach and Nicotine

========

mAChR –> metabotropic

CNS, Autonomic ganglia, effector organs (excitatory and inhibitory) + sweat glands (sweat secretion)

ACh + Muscarine

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9
Q

What are the two sympathetic processes that we talked about that are kind of strange?

A

Adrenal Medulla

Sweat glands

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10
Q

What are the two subtypes of Nicotinic receptors?

A

Nm = skeletal muscle neuromuscular junction ligand gated channel

Nn = postganglionic cell body, dendrites, CNS –> ligand gated channel

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11
Q

What are different types of muscarinic receptors?

what’s their broad classification?

A

M1 - M5

GPCR

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12
Q

Which muscarinic receptors are coupled to GQ? what does this cause?

A

1,3,5

activation of phospholipase C (PLC) –> makes IP3 / DAG cascade

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13
Q

What muscarinic receptors are coupled to Gi/o? What does this cause?

A

2,4

inhibition of adenylyl cyclase (AC) –> cAMP production is lowered, which activates K+ channels

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14
Q

What are the muscarinic receptors that are part of the organs?

which one for the heart?

which one for the smooth muscle for the rest of the body?

A

M2 + M3

M2

M3

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15
Q

What is the difference between acetylcholine production and adrenergic production?

A

instead of destruction at the end this is mostly reuptake back into the cytoplasm

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16
Q

Explain the process of Tyrosine –> effector functions

A

Tyrosine in –> made into Dopamine –> shuttled into the vesicle through VMAT2 –> made into NE –> AP causes membrane fusion and NE spills out –> activates alpha and beta receptors on another cell

17
Q

Where does the conversion of norepinephrine to epinephrine happen?

where does tyrosine become dopamine?

Dopamine to Norepinephrine?

A

mostly in the adrenal medulla

in the nerve cytoplasm

in the vesicle

18
Q

How does Tyrosine get into the cell?

What gets dopamine into the vesicle? what’s to note about this?

after the release, what gets NE back into the nerve terminal and DA back into the terminal?

A

Sodium dependent tyrosine transporter

VMAT2 –> it’s promiscuous so it doesn’t allow only dopamine. also NE, epi, serotonin

NET and DAT (transporters)

19
Q

What does Reserpine do?

Cocaine?

A

block VMAT 2

NET, increasing the concentration of NE in the synapse

20
Q

What is the termination of catecholamine signaling?

second most common?

A

reuptake into nerve terminals is the most common (NET or DAT then stored into vesicles by VMAT2)

metabolism –> by Monoamine oxidase (MAO) and Catechol-O-methyltransferase (COMT)

21
Q

What is the final product of catecholamine metabolism?

A

VMA

22
Q

What are the two main adrenergic receptors?

what are they both?

subsets of each?

what’s the 3rd not really main adrenergic receptor?

A

Alpha and beta

GPCR

alpha 1,2
beta 1,2,3

Dopamine receptor (D1-D5)

23
Q

What is Alpha 1 coupled to?

what does it respond to?

A

Gq

respond equally to epinephrine and norepinephrine

24
Q

What is alpha 2 coupled to?

what does it respond to?

A

Gi,Go

responds equally to epinephrine and norepinephrine

25
Q

What do all beta receptors couple to? what does this do?

what activates B1? B2? B3?

what’s the only beta receptor that we don’t have drugs against?

A

Gs –> increases adenylyl cyclase which increases cyclic amp leading to L-type Ca2+ channel opening

B1 = Epi = NE
B2 = Epi >> NE
B3 = NE > Epi

B3

26
Q

What do Alpha 1 receptors generally do?

A

Stimulate contraction of all smooth muscle, if it’s vascular smooth muscle it’s causing vasoconstriction

27
Q

If we block alpha 1 receptors, what are we doing? what if it’s in the heart?

A

blocking smooth muscle contraction, we have smooth muscle relaxation.

we lead to vasodilation

28
Q

What do Beta-2 receptors generally do?

what about in the heart? lungs?

A

Relax smooth muscle –> vasodilation if that smooth muscle was in the vasculature.

lung tissue? relaxation and allow air to enter the lungs.

29
Q

What do muscarinic receptors generally do?

A

contract smooth muscle

30
Q

In the heart, what happens when we activate B1 receptors (sympathetic)?

what about parasympathetic activity? what molecule deals with this?

A

increase heart rate, increase contractility

M2 decreases heart rate and decreases contractility

31
Q

What happens in the blood vessels with regards to sympathetic activity?

parasympathetic?

A

A1 causes blood vessels –> constriction via smooth muscle

NO PARASYMPATHETICS

32
Q

how is the lack of parasympathetics of the blood vessels dealt with?

A

activation of NO synthase in the endothelium by M3 receptors

this causes vasodilation

33
Q

What causes sympathetic response for the lung?

what about parasympathetic?

glands?

A

B2 –> relaxation

M2 or M3 –> contraction

increase in secretion by M3 in the PNS, decrease by alpha 1 + b2

34
Q

How is NO released?

A

it needs an intact epithelium

Acetylcholine activates mAChR which increases calcium levels which results in the production of NO. NO then is the key component that causes vasodilation

35
Q

What happens in the adrenal medulla?

what is the release?

A

ACh from the preganglionic fibers triggers the release of EPI and NE by binding to the Nn AChRs and produces a local depolarization

80% Epi
20% NE

36
Q

What is the baroreceptor reflex?

A

Alpha 1 receptor agonist. causes constriction –> vasoconstriction –> increases blood pressure

the baroreceptor recognizes the increase in pressure and increases parasympathetic nervous system tone and decreases SNS tone.

histamine –> causes decrease in blood pressure

baroreceptor does the opposite

37
Q

What are cholinomimetic agents?

cholinoceptor-blocking drugs?

Sympathomimetic drugs?

Adrenoceptor-blocking drugs

A

AChR agonists / Acetylcholinesterase inhibitors

AChR antagonists

mimic or enhance alpha and beta receptor stimulation (agonists) (enhance release or block reuptake)

alpha and beta antagonists

CP2 (8 decks)

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