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CPR Exam 2 > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

What is the major NTM of the PSN?

Where is it found?

What does it activate?

A

ACh

found at all preganglionic autonomic fibers, all postganglionic parasympathetic fibers, and few postganglionic sympathetic fibers (sweat)

activates nicotinic and muscarinic receptors

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2
Q

What is the major NTM of the SNS?

Where is it found?

What is its classification?

A

NE

at most postganglionic sympathetic fibers

catecholamine

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3
Q

Epinephrine is made where?

How is epinephrine released?

how is it classified?

A

Adrenal medulla and a few places in the brainstem

Depolarization of the preganglionic sympathetic neuron releases Ach and it binds to its receptor on the adrenal medulla which releases Epi (and NE)

catecholamine

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4
Q

What is the precursor to NE and Epi?

What does it do?

classified as?

A

Dopamine (made in neurons)

Works on CNS and renal vascular smooth muscle

catecholamine

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5
Q

What are the cotransmitters we should know?

A

ATP

Neuropeptide Y

VIP

Substance P

others

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6
Q

Describe the synthesis of Ach

A

choline transporter takes choline from EC space into neuron

choline acetyltransferase (ChAT) catalyzes the synthesis of Ach by combining the acetyl from Acetyl CoA with choline

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7
Q

Describe the release of Ach

A

when the AP reaches the axonal terminal of the preganglionic fiber, it depolarizes it causing increase of Ca

Increase in Ca causes vesicular membrane fusion with the cell membrane and Ach is released

SNARE complex allows the fusion between the membrane and the vesicle using VAMPs and SNAPs

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8
Q

Describe the binding of Ach to cholinergic receptors

A
  • Ach diffuses across the synaptic cleft and binds to nicotinic Ach receptors of the neuronal sybtype which allows Na to enter the postganglinoic fiber or adrenal medulla
  • Na entry causes depol. and AP of the postganglionic fiber or release of Epi and NE
  • Can bind to muscarinic Ach receptors on organs and cause decrease HR, glandular secretion, Sm. M relaxation (PNS)
  • Can activate nicotinic and muscarinic presynaptic membranes as well and modify it’s own release
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9
Q

Describe the termination of Ach signaling

A

acetylcholinesterase cleaves Ach into acetate and choline

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10
Q

Ach Receptor Type: M1

Location:

Structure:

Mechanism:

A

Location: CNS, ganglia

Structure: GPCR, Gq/11

Mechanism: Activation of phospholopase C, IP3, DAG

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11
Q

Ach Receptor Type: M2

Location:

Structure:

Mechanism:

A

Location: Heart, nerves, Sm. M

Structure: GPCR, Gi/o

Mechanism: inhibtion of adenylyl cyclase, decrease cAMP, activates K channels

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12
Q

Ach receptor: M3

Location

Structure

mechanism

A

Location: Glands, SM. M, endothelium

Structure: GPCR Gq/11

Mechanism: activation of PLC, IP3, DAG

(Same as M1 but diff. location)

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13
Q

Ach Receptor: M4

Location

Structure

Mechanism

A

Location: CNS

Structure: GPCR, Gi/o

Mechanism: inhibits AC, decrease cAMP, activates K channels

(Same as M2 but in different locations)

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14
Q

Ach Receptor: M5

Location

Structure

Mechanism

A

Location: CNS

Structure: GPCR, Gq/11

Mechanism: Activates PLC, IP3, DAG

(Same as M1, same as M3 minus location)

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15
Q

Ach Receptor: Nm

location

structure

mechanism

A

location: skeletal NMJ
structure: ligand gated ion channel
mechanism: Na, L depolarizing ion channel

same as Nn receptor type except located in postganglionic cell body, dendrites, and CNS

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16
Q

Describe the synthesis of catecholamines

A

Tyrosine goes into the nerve terminal and becomes DOPA which becomes DOPAMINE which becomes NE and then Epi

the final step occurs only in the adrenal medulla and in a few epinephrine containing neuronal pathways in the brainstem

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17
Q

Describe the storage of catecholamines

A

vesicular monoamine transporter (VMAT2) tranports DA into the vesicle during de novo synthesis

VMAT2 is relatively promiscuous and tranports DA, NE, and Epi and serotonin across the vesicle membrane

Inhibited by Reserpine, causes depletion of catecholamines from sympathetic nerve endings

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18
Q

Describe the release of catecholamines

A

occurs upon AP and influx of Ca

triggering event in the adrenal medulla: release of Ach by the preganglionic fibers and it’s interaction with nAchRs on chromaffin cells to produce a localized depolarization

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19
Q

Describe the binding of catecholamines to adrenergic receptors

A

catecholamines diffuse across the synaptic cleft and bind to adrenergic alpha and beta receptors

this activates stimulatory and inhibitory G proteins

effector organ responses include contraction, glycogenolysis, gluconeogenesis, relaxation, and increased force and rate of heart contraction

20
Q

What is the major mechanism that terminate teh actions of catecholamines?

A

reuptake into the nerve terminals

NET and the DAT are primarily involved

after reuptake, catecholamines are stored in vesicles by VMAT

21
Q

What is the secondary mechanism of signal termination of catecholamines?

A

dilution out of the junctional cleft and uptake at the extraneuronal sites by the transporters ENT, OCT1, and OCT2 and subsequent metabolic tranformation

  1. MAO: metabolizes catecholamines that have been released and undergone reuptake, located on the outer surface of mitochondria
  2. COMT: metabolism of endogenous circulating and adminstered catecholamines, largely cytoplasmic
22
Q

What is the end result of a1-receptor activation?

A

Muscle contraction

(except in gut, where it relaxes)

23
Q

Activation of A2 receptors results in what?

A

vascular smooth muscle contraction

decreased insulin secretion

decreased release of NE (presynaptic a2 receptors)

24
Q

Activation of B1 receptors results in what?

A

increased force and rate of heart contraction and AV nodal conduction velocity

found in myocardium

25
Q

Activation of B2 receptors causes what?

A

vascular, bronchial, GU, and GI smooth muscle relaxation

found in Sm. M and most other places

26
Q

Activation of B3 receptors do what?

A

result in lipolysis

found on adipose

27
Q

Dopamine activates D1 receptors in renal smooth muscle which leads to what?

A

vasodilation

natriuresis and diuresis via renal vascular smooth muscle

can increase HR and vascular vasoconstriction in high concentrations on a1 and B1 receptors

28
Q

Alpha 1 receptors stimulate contraction of what?

A

all smooth muscle

Examples:

vasoconstriction is due contraction of vascular smooth muscle

mydriasis is due to contraction of irisi radial muscle

uterine contraction during pregnancy

29
Q

Beta 2 receptors stimulate relaxation of what?

A

All smooth muscle

Examples:

relax tracheal and bronchial smooth muscle

relax uterine smooth muscle

relax intestinal smooth muscle

30
Q

Muscarinic receptors stimulate contraction of all what?

A

Smooth muscle (different than a1 receptors)

Examples:

miosis due to contraction of iris sphincter muscles

contraction of bladder detrusor muscle

contraction of intestinal SM. M

stimulate decrease in HR in SA node and contractility of heart muscle

31
Q

vascular smooth muscle is only innervated by the sympathetic nervous system. Vascular relaxation happens how?

A

Ach and mAChR activate the release of Endothelium derived relaxing factor (Nitric Oxide)

32
Q

Describe the release of EDRF (NO)

A

in response to an AP, Parasymp. neurons release Ach which reach mAchRs and activates them

NO is produced by endothelial cells and diffuses to the Sm. M around the vessel and causes relaxation

33
Q

the primary controlled variable in cardiovascular function is what?

A

mean arterial pressure

34
Q

Describe the baroreceptor reflex with the example of NE

A

NE produces direct effects on vascular and cardiac muscle

a slow infusion of NE increases PVR and increases MAP

in the absence of reflex control, this rise in NE will increase heart rate and contraction force

with intact reflex control, the negative feedback response to an increase in PSN discharge occurs at the SA node

this causes a marked increase in PVR and MAP and slowing of the heart rate

This bradycardia is the opposite of the drug’s effect (which we would expect, since it’s a negative feedback loop)

35
Q

What medication can be used to treat stage fright?

A

Beta Blockers

(Nonselective beta receptor antagonist)

36
Q

what medication treats respiratory distress due to narrowing of airways (asthma, bronchitis, etc)

A

B2 receptor agonist

too much can cause tachycardia

37
Q

Overdosing on diphenhydramine can cause fever, fixed and dilated pupils, increased heart rate and delirium as well as cutaneous vasodilation.

What division of the ANS is overactive?

Which receptors are involved in the presenting sx?

Stimulating what receptor will fix this?

A

SNS

Inhibition of Muscarinic AchR (basically causing unopposed activation of the SNS by inhibiting the PNS)

mAchR agonist with an acetylcholinesterase inhibitor that cross the BBB (for the delerium)

38
Q

How do you treat someone when you want to increase the heart’s force of contraction (inotropy) and decrease the heart rate (chronotropy)

How does it work?

A

Na/K ATPase (Digoxin)

Inhibiting Na/K keeps a bunch of Na in the cell which inactivates the Na/C Exchanger which leads to increased Ca in the cell which increases force of contraction without touching the rate

39
Q

After treating someone with digoxin for a while, they may want to prescribe something to decrease both force of contraction and heart rate. How?

A

By targeting B1 receptors since they are the most specific for heart muscle

(muscarinic agonist would cause vague systemic PNS sx)

40
Q

A child having an asthma attack shows airway constriction and increased pulse and HR. What divisions of the ANS are causing these issues?

What do you use to treat?

A

Pulse and HR is SNS

Airway restriction is PNS

B2 agonist and mAChR antagonist to relax Sm.M

too much B2 can act on B1 receptors on the heart and cause tachycardia

41
Q

Giving alpha adrenergic receptor agonist causes increased mean blood pressure and decreased heart rate. Why?

How do we block the decrease in heart rate (not just speed up the heart)

A

baroreceptor mechanism says “oh the pressure is too high, we should calm things down and slow the HR” and so the HR slows down.

muscarinic Ach R antagonist

42
Q

The key receptors on the heart responsible for increasing hr and contractility are what?

A

B1 receptors

43
Q

a muscarinic antagonist released on the effector cell in the lungs (end organ) causes what?

The SNS releases what compound at the synapse between the postganglionic cell and the target organ?

Which NTM is released from the presynaptic nerve to the post synaptic nerve in the SA node in the SNS?

A

relaxation

NE (Epi if F.F)

Ach onto a nAchR

44
Q

What NTM is always released between pre- and post-synaptic nerves?

A

Ach

45
Q

Alpha 1 receptors

Muscarinic receptors

Beta 1 Receptors

Beta 2 Receptors

A

Vasoconstriction

Contracts Smooth Muscle

increases HR and contractility of heart

Relaxes Smooth Muscle and Vasodilates (often talked about in terms of the lung)

CPR Exam 2 (33 decks)

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