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CP Exam 2 > DSA: Autonomic Pharmocology > Flashcards

DSA: Autonomic Pharmocology Flashcards

1
Q

NS can be separated into a somatic NS (consciously controlled actions) and ANS (unconscious actions), such as CO, blood flow, digestion.

ANS can then be divided into sympathetic (thoracolumbar; fight or flight) or parasympathetic (craniosacral; rest and digest).

The actions of these subdivisions generally __________.

A

Oppose each other.

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2
Q

ANS actions

A

CO

Blood flow

Digestion

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3
Q

Parasympathetic NS

NT: _____

Receptors: _____ and _____

A

NT: ACh

Receptors: nAChR and mAChR

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4
Q

Sympathetic NS

NT: _________

Receptors: _________

A

NT: ACh, NE*, EPI, DA,

Receptors: Adrenergic (alpha and beta), DA, nAChR and mAChR

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5
Q

What is the primary mediator of all ganglionic NSs?

A

ACh

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6
Q

What is the major NT of the PNS?

Do post-ganglionic NT sympathetic fibers release them?

A

ACh

Released by a few post-ganglionic sympathetic fibers onto sweat glands.

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7
Q

_________ is the major NT of the sympathetic NS.

A

NE

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8
Q

________ is released by a vast majority of the post-ganglionic sympathetic fibers.

A

NE

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9
Q

Where is EPI made?

A
  1. Adrenal medulla
  2. Few pathways of the brainstem
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10
Q

DA is the precursor to what?

What does it act on.

A

EPI and NE

Acts on CNS and renal vascular muscle

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11
Q

nAChR (ionotropic receptors)

  1. Found in:
  2. Fx:
  3. Agonists:
A
  1. Found in: CNS, autonomic ganglia, adrenal medulla
  2. Fx: Excitatory and causes the release of catecholamines from the adrenal medulla via the sympathetic NS
  3. Agonists: ACh and nicotine
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12
Q

mAChR (metabotropic receptors)

  1. Found in:
  2. Fx:
  3. Agonists:
A

mAChR (metabotropic receptors)

  1. Found in: CNS, autonomic ganglia, effector organs such as cardiac, smooth muscle, glands), sweat glands
  2. Fx: Excitatory and inhibitory; causes sweat secretion from sweat glands
  3. Agonists: ACh and muscarine
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13
Q

M1 receptors

Located:

Structure:

Fx:

A

M1 receptors

Located: CNS and ganglia

Structure: Gq/11 GCPR

Fx: + PLC –> + IP3 and DAG

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14
Q

M2 receptors

Located:

Structure:

Fx:

A

Located: heart, nerves, smooth muscle

Structure: Gi GCPR

(-) AC–> (-) cAMP production–> activates K+ channels

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15
Q

M3 receptors

Located:

Structure:

Fx:

A

M3

Located: Glands, smooth muscle, endothelium

Structure: Gq GCPR

+PLC–> + IP3 and DAG

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16
Q

M4 receptors

Located:

Structure:

Fx:

A

Located: CNS

Stucture Gi/o GCPR

(-) AC–> (-) cAMP production–> activates K+ channels

17
Q

M5 receptors

Located:

Structure:

Fx:

A

Located: CNS

Structure: Gq GCPR

+PLC–> + IP3 and DAG

18
Q

Primary M receptors in the parasympathetic NS?

A

M2 and M3

19
Q

How is NE made in the nerve terminal?

A
  1. Tyrosine enters nerve cytoplasm via Na+ dependent tyrosine transporter:
  2. Tyrosine–> DOPA–> Dopamine
  3. Dompamine–> vesicle via VMAT-2, where it is converted to NE.

VMAT-2 is promiscuous; it can transport NE, EPI, DA and 5HT into vesicles

If in the adrenal medulla, NE–> EPI

20
Q

How is NE released from vesicle?

A

AP and influx of Ca2+

21
Q

Termination of catecholamines?

A
  • Reuptake: occurs via NET and DAT. Catecholamines are then stored in vesicles via VMAT-2
  • Metabolism via MAO and COMT (catechol-O-methyltransferase).
  • *Catecholamines are not broken down by degradative enzymes
22
Q

Reserpine

A

blocks VMAT-2; prevents DA from getting into vesicles.

23
Q

Cocaine

A

blocks NET; increases NE in synapses

24
Q

Catecholamines activate 2 subsets of adrenergic receptors; what are they?

A

Alpha (1 and 2) and beta1, 2 and 3, which are GCPRs

25
Q

Binding onto alpha-1 receptors causes what?

A

Binding causes:

  1. Contraction of all smooth muscle
  2. If vascular–> vasoconstriction
26
Q

Binding onto beta-2 receptors causes what?

A

Relax smooth muscle–> vasodilation

27
Q

Binding to muscarinic receptors causes?

A

Contraction of muscle

28
Q

Primary receptors in the heart: B1 receptors

Sympathetic activation of B1 receptors–> ____________

Parasympathetic activation of M2 receptors–> _________

A

Sympathetic activation of B1 receptors: increase HR, contraction, conduction velocity

Parasympathetic activation (primary receptor is M2): opposite

29
Q

What receptors do we bind to on blood vessels to cause vasoconstriction?

How do we vasodilate the BV?

A

A1

Parasympathetics do not innervate smooth vessels on blood vessels. Thus, mAchR receptors and nAchR are not found on the smooth muscle of the BV. However, blood vessels can relax in response to parasympathetic release of ACh as long as the endothelium is intact.

-Activation of mAChR on endothelial cells causes the production of endothelium-derived relaxing factor (EDRF), also known as Nom in response to ACh release from intact endothelium.

30
Q

Lungs

Sympathetic activation of B2–> __________

Parasympathetic activation of M2/M3–> __________

A

Lungs

Sympathetic activation of B2–> bronchodilation

Parasympathetic activation of M2/M3–> contraction

31
Q

Bronchial glands

Sympathetic activation of alpha-1–> ________

Sympathetic activation of beta-2–> _________

Paraympathetic activation of M2 and M3–> _______

A

Bronchial glands

Sympathetic activation of alpha-1–> decrease secretion

Sympathetic activation of beta-2–> increase secretion

Paraympathetic activation of M2 and M3–> stimulation

32
Q

Pheylephrine

A

A1 receptor agonist.

Increases BP via baroreceptor; increasing parasympathetic NS and decreasing sympathetic NS

33
Q

Histamine causes a decrease in blood pressure via baroreceptor reflex, which leads to?

A

a decrease in para NS activation and increase in sympathetic NS activation

34
Q

What are cholinomimetic agents?

A

drugs that mimic ACh (AChR agonists or AChE inhibitors.

35
Q

What are cholinoceptor-blocking drugs?

A

AChR antagonists

36
Q

What are sympathomimetic agents?

A

drugs that mimic or enhance a/b receptor stimulation

37
Q

What are adrenoceptor blocking drugs?

A

a/b receptor antagonists

CP Exam 2 (27 decks)

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