Neuro Phys Part 2 Flashcards

(70 cards)

1
Q

How does the preganglionic communicate with the postganglionic for the SNS and PaNS?

A

acetylcholine (ACH) act on cholinergic receptors

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2
Q

what are the cholinergic receptors that acetylcholine acts on from preganglionic to postganglionic for SNS and PaNS?

A

N-receptors (nicotinic)

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3
Q

How does the postganglionic communicate with the target in the PaNS?

A

acetylcholine (ACH) act on cholinergic receptors

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4
Q

what are the cholinergic receptors that acetylcholine acts on from postganglionic to target for PaNS?

A

either N-receptors (nicotinic) or M-receptors (muscarinic)

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5
Q

How does the postganglionic communicate with the target in the SNS?

A

Norepinephrine (NE)/ noradrenalin to act on adrenergic receptors and sometimes acetylcholine (ACH) to act on cholinergic receptors

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6
Q

what are the adrenergic receptors that norepinephrine acts on from postganglionic to target for SNS?

A

alpha or beta receptors

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7
Q

what are the two exceptions to sympathetic neurotransmitter releases?

A
  1. adrenal medulla releases mostly epinephrine directly into blood stream
  2. ACH is released by sympathetic nerves in skin to regulate sweat glands
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8
Q

what is a specialized sympathetic ganglion that releases mostly Epinephrine (some NE) directly into blood stream to reach all tissues

A

adrenal medulla

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9
Q

Norepinephrine and epinephrine are stored in ? until a depolarization causes release via exocytosis

A

vesicles

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10
Q

Norepinephrine and epinephrine are known as ?

A

catecholamines

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11
Q

what is the starting component to synthesize catecholamines?

A

tyrosine

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12
Q

explain catecholamine synthesis

A

tyrosine get hydroxyl group added to become L-Dopa then gets a decarboxylzed to get dopamine. Then it gets transported into the vesicle and hydroxylate and become norepinephrine

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13
Q

what is the enzyme that converts tyrosine into L-DOPA?

A

tyrosine hydroxylase

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14
Q

what is the enzyme the converts L-DOPA into dopamine?

A

DOPA decarboxylase

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15
Q

what transports the dopamine into the vesicle?

A

vesicular monoamine transporter (VMAT)

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16
Q

what is the enzyme that converts dopamine into norepinephrine?

A

dopamine B-hydroxylase

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17
Q

for adrenal medulla, what converts norepinephrine into epinephrine?

A

phenlethanolamine-N-Methyltransferase

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18
Q

what would transport the epinephrine back into the vesicle?

A

vesicular monoamine transport (VMAT)

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19
Q

for catecholamine degradation, 50-80% of secreted norepinephrine is taken up again into the ?

A

presynaptic terminal for degradation

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20
Q

what are the two enzyme that can degrade norepinephrine?

A
  • monoamine oxidase
  • catechol-O-methyl-transferase
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21
Q

what are the 3 options for NE degradation?

A
  1. be transported back into the presynaptic terminal for reuptake into a vesicle for degradation by MAO
  2. transported into the postsynaptic terminal for degradation by COMT
  3. act on a pre-synaptic alpha2 receptor to turn off further release
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22
Q

acetylecholine is synthesized in presynaptic nerve terminals then stored in ? prior to release

A

vesicles

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23
Q

what are the components that make up acetylcholine?

A

acetyl-CoA + Choline

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24
Q

what is the enzyme that makes acetylcholine

A

choline acetyltransferase

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25
how is acetylcholine degraded
After secretion into synapse, ACH is degraded to acetate and choline
26
what is the enzyme that degrades acetylcholine
acetylcholinesterase
27
what is take back up into the presynaptic terminal for reuse after acetylcholine degradation?
choline
28
What is the typical cardiovascular response during a sympathetic ("fight or flight") situation?
Increased heart rate and contractility (fast, pounding heart).
29
How does parasympathetic input differ from sympathetic input on heart function?
Parasympathetic input decreases heart rate but has little effect on contractility.
30
What happens to the bronchioles during a sympathetic response?
They relax to allow maximum air entry (gasping for air).
31
What happens to GI tract motility and sphincters during a sympathetic response?
GI motility decreases, and sphincters contract (you’re not digesting food in fight/flight).
32
How are the salivary glands affected by sympathetic stimulation?
Digestive secretions are minimal; salivary glands are mainly under parasympathetic control.
33
What happens to blood flow to the GI tract during sympathetic stimulation?
It is minimized; blood is redirected to more vital areas (like muscles).
34
What happens to the bladder during a sympathetic response?
The detrusor muscle relaxes, and the internal sphincter contracts (you hold your urine).
35
What metabolic processes are activated during sympathetic activation for energy?
- glycogenolysis (breaking down glycogen) - lipolysis (breaking down fat)
36
What causes "goosebumps" or hair standing up during fear?
Arrector pili muscles contract – sympathetic innervation only.
37
What happens to the pupils during a sympathetic response?
Pupils dilate to allow more light in ("wide with fear").
38
What type of autonomic fibers innervate sweat glands?
Sympathetic cholinergic fibers (sympathetic only, but release ACh).
39
Where are alpha and beta receptors located, and how do they affect blood vessels?
Alpha receptors: skin/vasculature → vasoconstriction Beta receptors: skeletal muscle, heart, liver → vasodilation
40
NE and E have similar actions at their targets. However, based on its receptor selectivity, NE or E is more likely to cause reflex bradycardia?
NE is more likely than E
41
what is reflex bradycardia?
a sudden large increase in blood pressure can cause the heart to reflexively slow down in an effort to decrease blood pressure again
42
NE causes ? by activating ? which causes increased blood pressure. it also binds to ? but have no significant dilation effect
vasoconstriction alpha 1 adrenergic receptors beta 2 adrenergic receptors
43
What is a direct-acting pharmaceutical?
A drug that acts at the receptor.
44
What is an indirect-acting pharmaceutical?
A drug that acts outside the receptor (e.g., affecting neurotransmitter availability or degradation).
45
Define agonist.
A molecule that binds and activates a receptor or enzyme.
46
Define antagonist.
A molecule that binds and inactivates a receptor or enzyme.
47
What are adrenergics (sympathomimetics)?
Drugs that increase adrenergic (sympathetic) responses.
48
What are antiadrenergics?
Drugs that inhibit adrenergic (sympathetic) responses.
49
How can sympathetic drugs be classified?
As direct (agonist/antagonist) or indirect; and as adrenergic or antiadrenergic.
50
What is a non-selective beta agonist?
A drug that activates both beta-1 and beta-2 receptors with minimal alpha activity.
51
What does a selective beta-1 agonist do?
It primarily activates beta-1 receptors (heart), with minimal action on beta-2 or alpha receptors.
52
What happens if you block VMAT (vesicle storage of NT)?
Decreased catecholamine transmission.
53
What happens if you cause NT “leakage” outside the vesicle?
Increased catecholamine transmission.
54
What is the effect of inhibiting reuptake of catecholamines?
Increases catecholamine transmission.
55
What is the effect of inhibiting catecholamine degradation?
Increases catecholamine transmission.
56
What happens when auto-receptors inhibit NT release?
Catecholamine transmission decreases.
57
What are cholinergics (cholinomimetics)?
Drugs that increase cholinergic (parasympathetic) responses.
58
What are anticholinergics?
Drugs that inhibit cholinergic (parasympathetic) responses.
59
What is botulinum toxin (BoTox®), and how does it work?
An indirect anticholinergic; it blocks ACh release at NMJ → reduced muscle contraction.
60
What are 3 clinical uses of BoTox®?
- reduce wrinkles - reduce muscle spasticity - prevent migraines
61
What happens in myasthenia gravis (MG)?
Autoantibodies block nicotinic receptors at NMJ, leading to muscle weakness/paralysis.
62
What type of drug is used to treat MG?
Anticholinesterase (inhibits the cholinesterase enzyme, increasing ACh at the NMJ).
63
Is an anticholinesterase the same as an anticholinergic?
No, anticholinesterases are cholinergic (increase ACh), while anticholinergics block ACh.
64
In anaphylactic shock, what causes the drop in blood pressure?
Vasodilation; treated by activating alpha-1 receptors (causing vasoconstriction).
65
What receptor activation helps treat bronchoconstriction in anaphylaxis?
Beta-2 receptor activation (causes bronchodilation).
66
What kind of agonist treats both vasodilation and bronchoconstriction?
Alpha-1 and beta-2 agonist (e.g., epinephrine).
67
What NT binds to nicotinic receptors?
Acetylcholine (ACh).
68
What NT binds to alpha-1 and alpha-2 receptors?
Norepinephrine slightly more than epinephrine.
69
What NT binds to beta-1 receptors?
Epinephrine slightly more than norepinephrine.
70
What NT binds to muscarinic (M) receptors?
Acetylcholine.