ANS Flashcards

1
Q

What is the anatomical classification of the ANS (2) ?

A

preganglionic origin

parasympathetic nervous system cranial and sacral

sympathetic nervous system thoracic and lumbar

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2
Q

What is the physiological classification of ANS (2)?

A

Transmitter released from the nerve terminal.

cholinergic releasing acetylcholine (Ach)

adrenergic releasing Norepinephrine (NE) or Epinephrine (E)

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3
Q

What are the types of cholinoceptors (2)?

A

Nicotinic or muscarinic (both activated by Ach)

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4
Q

What are nicotinic receptors (2)?

A

muscle nicotinic (Nm) - activates (@ nm junction of somatic nerves)

Neuronal nicotininc (Nn) - activates autonomic ganglia (PSNS or SNS).

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5
Q

What are muscarinic receptors?

A

Present in effector organs innervated by postganglionic PSNS nerves.

Activated by muscarine (or bethanechol) or Ach

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6
Q

What are they types of adrenoreceptors and what activates them?

A

Alpha (α1 or α2) and Beta (β1, β2)

All activated by EP

NE activates all except β2.

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7
Q

What do parasympathetic and sympathetic nerves do (2) ?

A

PSNS –> Ach

SNS –> NE

(adrenal medulla - SNS postganglionic cell releases 85% E and 15 % NE)

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8
Q

What’s the deal with somatic nerves?

A

They don’t have ganglion and release ACH at neuromuscular junction (synapse bw nerve and skeletal muscle).

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9
Q

Where is Ach synthesized and stored?

A

ACh is synthesized in cholinergic nerve terminal and transported and stored in vesicles.

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10
Q

How is ACh released?

A

An action potential along nerve fiber causes Ca++ influx, fusion of vesicular and cell membrane, and release of ACh (exocytosis).

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11
Q

What is needed for SNS activation?

A

NE, E postganglionic VIA sympathetic nerves and/or adrenal medulla with the presence of selective adrenoceptors at target tissue.

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12
Q

What is needed for PSNS activation?

A

Ach at cholinergic nerve terminals and presence of PSNS nerves, release of Ach, and receptors (nicotinic and muscarinic).

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13
Q

Describe the mechanism of PSNS?

A

Ach released from PSNS nerves can activate M receptors

on SA and AV nodes of heart (reduce HR),
to narrow airway
increase GI tract.

Does not affect vascular tone because muscarinic receptors are present in blood vessels but not innervated with PSNS. But Ach injected in IV can dilate blood vessels and reduce blood pressure, which leads to release of nitric oxide NO cause vasodilation.

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14
Q

What are the directly acting cholinoceptor agonists (4)?

A

NON-SELECTIVE, poor lipid solubility, not used often clinically

1) ACh (nicotinic and muscarinic),

2) nicotinic receptor agonists (nicotine)

3) muscarinic receptor agonist muscarine (an alkaloid)

4) bethanechol (a synthetic agent) - increase muscle tone in urinary retention and gastrointestinal hypotonia after surgery

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15
Q

What are indirectly cholinoceptor agonists (2) ?

A

Anticholinesterase/ Cholinesterase inhibitors - inhibit cholinesterase, therefore amplify ACh.

Clinically used cholinesterase inhibitors include reversible:

1) neostigmine, a hydrophilic compound which is poorly absorbed, and does not penetrate the CNS and

2) physostigmine, which is lipophilic and well absorbed from all sites.

Both drugs can be used to increase the tone of the GI tract (in GI hypotonia) and urinary bladder (in urinary retention).

In contrast, Sarin (chemical weapon) and Malathion (insecticide) are
“irreversible” cholinesterase inhibitors which form strong covalent bonds with cholinesterase.

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16
Q

What can cholinergic blockers block (3)?

A

1) muscarinic (M atropine (reversable blockade of M receptors) & scopolamine (prevent motion sickness))

2) neuronal nicotinic (Nn, hexamethonium)

3) muscle nicotinic (Nm; curare, d-Tubocuranine) receptors.

17
Q

What are the clinical uses of antimuscarinics (6)?

A

Block actions of acetylcholine (ACh) on muscarinic (M) receptors (think blocking rest and digest)

1.Motion sickness (block ACh stimulation of M receptors in inner ear).

2.Eye: over constricted (miosis) (block ACh-induced miosis/pupil constriction).

3.Asthma (block ACh-induced bronchoconstriction).

4.Irritable bowel (inhibit ACh stimulation of bowel movement).

5.Urinary urgency (block ACh stimulation in overactive bladder).

6.Anticholinesterase poisoning (block CNS and peripheral muscarinic effects of ACh).

18
Q

What are the clinical uses of the antinicotinics?

A

AKA Nicotinic receptor antagonists

1) Ganglionic blockers (Nn) - inhibit SNS/PSNS rarely used except in emergency hyptertension

2) Neuromuscular blockers (Nm) are used to relax skeletal muscles in preperation of surgery (ex. Tubocurarine)

19
Q

Where is NE synthesized and stored?

A

Synthesized from dopamine in the adrenergic nerve terminal and is transported to storage vesicle.

19
Q

How is NE released?

A

Propagation of action potential along nerve causes Ca++ influx, fusion of vesicular and cell membrane, and release of NE or dopamine (exocytosis).

20
Q

What happens to dopamine and NE when released (3)?

A

1) Released dopamine can activate dopamine receptors

1) NE can activate adrenoceptors (alpha or beta) at effector organs to make response.

2) Released NE is primarily terminated by the NET (NE transporter) which uptakes NE and/or dopamine back into the nerve terminals.

3) NE that diffuses away from the nerve terminal can be degraded enzymatically at the postsynaptic cell or in organs.

21
Q

What are the adrenoreceptor agonists? (5)

A

Phenylephrine (α1) can cause mydriasis (contraction of radial muscle of the iris), vasoconstriction (constriction of arterioles and veins), and constriction of gastrointestinal (GI) and urinary sphincters. (selective)

Salbutamol (or terbutaline) can activate β2–adrenoceptors [bronchodilation, vasodilation of arterioles, relax uterus, increase glucose output, decrease GI and genitourinary (GU) activity]. (selective)

Isoproterenol can activate β1 (increase cardiac rate and contractility) and β2 (see above) adrenoceptors. (selective)

Epinephrine can activate all α1, α2, β1 and β2. (non selective)

NE all except β2. (Less selective)

22
Q

What adrenergic neuron blockers reduce SNS activity (2)?

A

Clonidine and α-Methyl-dopa (hypertension in preg)

23
Q

Give an overview of ACh/NE release and it’s pathway (4)?

A

1) ACh released from somatic nerve activate Nm in sketelal muscle.
2) Ach relaesed fome SNS/PSNS preganglionic nerve to activate Nn recoptors in ganglion - activates postganglionic nerve.
3) Ach relased from PSNS postganglionic nerve to tissue (heart, smooth muscle) to activate M
4) NE released from SNS postganglionic nerve to activate alpha or beta adrenoceptors.

24
Q

bethanechol

A

synthetic cholinoceptor agonist - increase urinary muscle tone and GI hypotnia post-surgery

25
Q

neostigmine

A

Indirect cholinoceptor agonist -doesn’t peneterate CNS -increase urinary muscle tone and GI hypotnia post-surgery

26
Q

physostigmine

A

Indirect cholinoceptor agonist -lipophilic/well asborbed
increase urinary muscle tone and GI hypotnia post-surgery

27
Q

atropine

A

M blocker

28
Q

scopolamine

A

M blocker - prevents motion sickness

29
Q

hexamethonium

A

Nn blocker

30
Q

d-Tubocuranine

A

Nm blocker

31
Q

Phenylephrine

A

adrenoreceptor alpha 1 agonist (think SNS symptoms)

32
Q

Salbutamol

A

adrenoreceptor beta 2 agonist- think SNS symptoms + relax utureus, increase glucose output

33
Q

Isoproterenol

A

adrenoreceptor agonist
Beta 1 - increase heart rate
Beta 2

34
Q

A1 adrenoreceptor agonists

A

contraction (blood vessels)

35
Q

A2 adrenoreceptor agonists

A

decrease SNS (decrease NE/E)

36
Q

B1 adrenoreceptor agonists

A

increase cardiac (heart rate and contractility);

37
Q

B2 adrenoreceptor agonists

A

relaxation (e.g., uterus, bronchial, blood vessels);

38
Q

Clonidine and α-Methyl-dopa

A

Adrengic neuron blockers used for hypertension in preg