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Block 1 Week 7 > ANS Harvey Part 4 > Flashcards

ANS Harvey Part 4 Flashcards

1
Q

(balnk) is the only endogenous neurotransmitter acting at cholinergic receptors.

A

Acetylcholine (ACh)

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2
Q

(blank) are exogenous compounds that imitate functional responses associated with parasympathetic stimulation.

A

parasympathomimetics

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3
Q

(blank) are exogenous compounds that imitate functional responses produced by acetylcholine (ACh) at cholinergic receptors.

A

Cholinomimetics

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4
Q

(blank) are compounds that block cholinergic transmission at involving muscarinic receptors (antimuscarinics), neuronal nicotinic receptors (ganglionic blockers) or the neuromuscular junction (neuromuscular blockers).

A

Cholinergic Antagonists

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5
Q

To know what kinds of cholinomimetics responses you can get you must know what?

A

what type of receptor is involved
what type of cell/tissue is involved
the signaling pathway activated by receptor
whether effect is direct or indirect

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6
Q

Odd number receptors of cholinergic receptors are what kind of G proteins?

A

Gq

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7
Q

even number receptors of cholinergic receptors are what kind of G proteins?

A

Gi/o

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8
Q

How does Muscarine receptors 1/3/5 work?

A

by PLC, IP3->Ca2+ which creates smooth muscle contraction and vascular relaxation, and exocrine gland secretion

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9
Q

How does muscarine receptors 2/4 work?

A

by inhibiting AC and increasing potassium and creating relaxation, slow heart rate

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10
Q

What are the ways to get excitation?

A

Na+ in, little K/Cl out

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11
Q

HO do you get a nictoninc muscle receptor to work>

A

you increase Na+ and get skeletal muscle and nerve excitation

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12
Q

What kind of receptor is pentameric?

A

nicotinic receptors

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13
Q

What kind of receptor is this?
Ligand-gated ion channels

Exist as pentamers containing one or more of 5 different subunits (α β γ δ ε).

There are 9 α subunit isoforms (α1- α9) and 5 β subunit isoforms (β1- β5).

has at least two α subunits, where ACh binds.

A

nicotinic receptor

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14
Q

What are the 2 subtypes of nicotinic receptors?

A

Nm and Nn

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15
Q

What kind of receptor is this?
location – skeletal muscle

signaling mechanism – ligand gated ion channel

each channel composed of 4 different subunits: α1 β1 δ (γ or ε)
adult – (α1)2 β1 δ ε
neonatal - (α1)2 β1 δ γ

response – muscle contraction

A

nicotinic muscle receptor

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16
Q

Nm receptors increase (blank) so that you get muscle contraction.

A

sodium

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17
Q

What kind of receptor is this?
location – all sympathetic and parasympathetic ganglia, adrenal medulla, CNS

signaling mechanism – ligand gated ion channel

each channel composed of different α (8 isoforms, α2- α9) and β (4 isoforms, β2- β5) subunits in various ratios

response – neuronal excitation

A

Nn Nicotinic neuroganglionic receptors

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18
Q

What are the four receptor types of Nicotinic receptors?

A

muscle type, ganglion type, heteromeric type and honomeric type.
(They differ by subunit combinations)

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19
Q

Where are the muscle type nictonic receptors found?

A

neuromuscular junctions

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20
Q

Where are nicotinic ganglian cells found?

A

autonomic ganglia

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21
Q

Where are heteromeric and homomeric type nicotinic receptors found?

A

brain

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22
Q

What do all the types of nictonic receptors except for homomeric type have in common?

A

excited by increased Na and K permiability

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23
Q

How many muscarinic subtypes are there?

A

5

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24
Q

What receptors does this describe:

location – smooth muscle (blood vessels, airways,
eye, gut, bladder)
-endothelial cells (blood vessels)
-exocrine glands (salivary glands, sweat
glands, airways, gut)
-CNS

signaling mechanism – Gq activation of phospholipase C

response- stimulate smooth muscle contraction

      - relax blood vessels 
      - stimulate secretion
A

Muscarinic M1,M3,M5 receptors

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25
Q

What is the pathway that the muscarinic receptors use?

A

PLC+ PIP2-> IP3 +DAG-> Ca2+

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26
Q

How come muscarinic receptors 1,3,5 can constrict smooth muscle YET dilate blood vessesls?

A

Some blood vessels have parasympathetic innervation. In these blood vessels muscarinic receptors are there. The pathway for muscarinic receptors create NO which can diffuse from endothelial cell to vascular smooth muscle->cGMP-> inhibits contractions in the blood vessles ONLY via ENDOTHELIAL CELLS!

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27
Q

Can you get ACh relexation in the vascular smooth muscle if you rub of endothelial cells?

A

no

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28
Q

What receptors does this describe:
Low doses of (exogenous) ACh cause systemic vasodilation and hypotension due to activation of muscarinic receptors on vascular endothelial cells.

High doses of (exogenous) ACh cause systemic vasoconstriction and hypertension due to activation of muscarinic receptors on vascular smooth muscle cells.

A

M1,M3,M5 receptors

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29
Q

What does this describe:
location – smooth muscle (blood vessels, airways, eye, gut, bladder)
endothelial cells (blood vessels)
exocrine glands (salivary glands, sweat glands, airways, gut)
CNS

signaling mechanism – Gq activation of phospholipase C

response – stimulate smooth muscle contraction
relax blood vessels
stimulate secretion

A

M1, M3, and M5 receptors

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30
Q

Which muscarine receptors stimulate fluid secretion, gastic secretion, vesicular release of mucus and proteins (enzymes)?

A

M1,M3,M5

31
Q

What muscarine receptors does this describe?
location – cardiac muscle, CNS

signaling mechanism –Gi inhibition of adenylyl cyclase, Gi/o activation of K+ channels

response –decreases heart rate (SA node),
slows cardiac action potential propagation (AV node),decreases contractility (atria and ventricles*)

A

M2 and M4

cardiac M2) (CNS M4

32
Q

How does M2 receptors affect the SA node of heart? (remember muscarine receptors are only parasympathetic, besides sweat glands)

A

Parasympathetic stimulation produces a negative chronotropic effect by two mechanisms

  • By inhibiting cAMP production, M2 receptor activation reduces the stimulatory effect that cAMP has on pacemaker and other channels.
  • By activating K+ channels, M2 receptor activation hyperpolarizes the membrane potential of pacemaker cells, decreasing excitability
33
Q

How does M2 receptors affect the SA node of heart? (remember muscarine receptors are only parasympathetic, besides sweat glands)

A

Parasympathetic stimulation produces a negative chronotropic effect by two mechanisms

  • By inhibiting cAMP production, M2 receptor activation reduces the stimulatory effect that cAMP has on pacemaker and other channels.
  • By activating K+ channels, M2 receptor activation hyperpolarizes the membrane potential of pacemaker cells, decreasing excitability
34
Q

How does M2 receptors affect Ventricular monocytes?

A

In the presence of sympathetic tone, parasympathetic activation can inhibit ventricular contractility.

35
Q

Compounds that mimic the responses produced by cholinergic

stimulation can be divided into two different categories:

A

Direct and Indirect

36
Q

What are the 2 categories of direct-acting drugs?

A

alkaloids and choline esters

37
Q

What are two important direct acting choline esters?

A

acetylcholine and bethanechol

38
Q

Methyl substitution on β carbon (orange) of methacholine and bethanecol
reduces potency at nicotinic receptors and
limits hydrolysis by (blank).
The carbamic acid ester group (green) of carbachol and bethanecol limits hydrolysis by (blank)

A

cholinesterases.

39
Q

(blank) has longer half-life than ach (less susceptible to cholinesterases) and does not activated nicotonic receptors.

A

bethanechol

40
Q

Why does bethanechol have a less affect on the heart?

A

because it is works on odd muscarine receptors which arent common in the heart

41
Q

(blank) cholinomimetics work by inhibitin cholinesterase breakdown of endogenos ACh.

A

Indirect acting

42
Q

AChE contains two important sites at catalytic center, what are they?

A

Anionic site – interacts nitrogen and methyl groups of ACh

Esteratic or esteric site – serine + carboxyl residue of the acetyl group of ACh (ester linkage)

43
Q

AChE contains two important sites at catalytic center, what are they?

A

Anionic site – interacts nitrogen and methyl groups of ACh

Esteratic or esteric site – serine + carboxyl residue of the acetyl group of ACh

44
Q

What are the key steps in hydrolysis of ACh

A

Binding of ACh to anionic site
Cleavage of ACh at the ester linkage releasing choline
Reaction with water yielding acetic acid

45
Q

Cholinesterase inhibitors block ACh hydrolysis by:

A

Interfering with anionic site, or

Interfering with esteratic site

46
Q

What are these effects of:

  • Low levels – increase skeletal muscle activity (fasciculations)
  • High levels – neuromuscular blockade
  • Increased ganglionic transmission
  • Complex cardiovascular responses
  • CNS effects
A

cholinesterase inhibitors

47
Q

Compounds that mimic the responses produced by cholinergic stimulation can be divided into two different categories:

A

Direct and Indirect

48
Q

What category are these a part of:

  • Mono- or bis-quaternary amines – edrophonium
  • Carbamates – neostigmine, physostigmine
A

cholinesterase inhibitors (REVERSIBLE)

49
Q

What category are these a part of:

Mono- or bis-quaternary amines – edrophonium

Carbamates – neostigmine, physostigmine

A

cholinesterase inhibitors

50
Q 
What category are these a part of:
Organophosphates 
    -echothiophate – used clinically
    -parathion, malathion, diazinon used as insecticides
    -sarin, soman used as “nerve gases”
A

Cholinesterase inhibitors (IRREVERSIBLE)

51
Q

Can anything overcome organophospates?

A

2-PAM or pralidoxime if applied immediately, if some time passes (i.e. aging) organophosphates will be completely irreversible

52
Q

Can anything overcome organophospates?

A

2-PAM or pralidoxime if applied immediately, if some time passes, organophosphates will be completely irreversible

53
Q

What is an important direct acting choline ester?

A

bethanechol

54
Q

What is the therapeutic use of direct acting choline esters?

A

postoperative and neurogenic ileus

postoperative urinary retention

55
Q

What are the effects of direct acting choline esters(bethanechol)?

A

causes smooth muscle contraction (GI and urinary tract)

56
Q

What is the mechanism of action for direct acting choline esters?

A

muscarinic agonist – activates M1 and M3 receptors

negligible effect at nicotinic receptors

57
Q

What is an example of a direct acting alkaloid?

A

pilocarpine

58
Q

Was it the therapeutic use of direct acting alkaloids?

A

Glaucoma

Sjögren’s syndrome, xerostomia

59
Q

Was is the effect of direct acting alkaloids?

A

contracts sphincter and ciliary muscles of the eye facilitating aqueous humor outflow (glaucoma)
stimulates salivary gland and tear duct secretions (Sjögren’s)

60
Q

What is the mechanism of action for direct acting alkaloids?

A

muscarinic agonist (primarily M3 receptor)

61
Q

What is an example of a direct acting nicotinic agonist?

A

Nicotine : )

62
Q

What are the therapeutic uses of direct acting nicotinic agonists?

A

medical – smoking cessation

non-medical – smoking, insecticides

63
Q

What are the effects of direct acting nicotinic agonists?

A

activates NN receptors in central nervous system
activates NN receptors on postganglionic sympathetic and parasympathetic neurons
activates NM receptors at the neuromuscular junction

64
Q

What is the mechanism of action for direct acting nicotinic agonists?

A

agonist at Nm and Nn receptors

65
Q

What is an example of a cholinesterase inhibitor?

A

neostigmine

66
Q

What are the therapeutic uses of cholinesterase inhibitor?

A

treatment of myasthenia gravis
postoperative and neurogenic ileus
postoperative and neurogenic urinary retention

67
Q

What is the mechanism of action for cholinesterase inhibitor?

A

reversible cholinesterase inhibitor

68
Q

What is the effect of cholinesterase inhibitors?

A

generalized parasympathetic stimulation

69
Q

(blank) is when you lose control of muscle contraction.

A

myasthenia

70
Q

What can cure myasthenia graves?

A

neostigmine by competitvely inhibiting the antibodies so you can get contraction

71
Q

In cholinergic toxicity from direct acting nicotinic agonists, what are the predictable symptoms?

A

acute toxicity

CNS effects: convulsions, coma, respiratory arrest
neuromuscular effects: respiratory paralysis
cardiovascular effects (via CNS): hypertension, cardiac arrhythmias

chronic toxicity

CNS effects responsible for addictive properties of smoking
increased incidence of peptic ulcers

72
Q

In cholinergic toxicity from direct acting nicotinic agonists, what are the predictable symptoms?

A

acute toxicity

CNS effects: convulsions, coma, respiratory arrest
neuromuscular effects: respiratory paralysis
cardiovascular effects (via CNS): hypertension, cardiac arrhythmias

chronic toxicity

CNS effects responsible for addictive properties of smoking
increased incidence of peptic ulcers

73
Q

What does this describe?

  • carbamate cholinesterase inhibitors and organophosphates are commonly found in insecticides
  • also found in chemical warfare agents (nerve gases)

initial signs same as for muscarinic agonist intoxication

CNS effects: confusion, ataxia, convulsions, coma, respiratory arrest, cardiovascular collapse

Neuromuscular effects: weakness, fasciculations, paralysis

Treatment: atropine, 2-PAM

Prevention: pyridostigmine

A

toxicity from indirect acting compounds

Block 1 Week 7 (10 decks)

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