ANS - Part 2

Question 0

The PNS targets

Answer 0

Smooth muscle
Cardiac muscle
Glands (heavily involved)

Question 1

The cranial region of the PNS includes

Answer 1

Midbrain and medulla

Question 2

What are some of the glandular effects of the PNS?

Answer 2

Salivation, lacrimation, digestion, urination, defecation, pupillary constriction, vasomotor control, bronchial control

Question 3

What is the main nerve of the PNS?

Answer 3

Vagus - it comes out of the brainstem

It is a global downregulator

Question 4

Why is the vagus nerve called the wandering nerve and what does it innervate?

Answer 4

It is called the wandering nerve because it innervates many thoracic and abdominal structures
Motor and sensory to larynx

Question 5

The vagus nerve supplies innervate on to all nerves of the larynx except the

Answer 5

Cricothyroid (super laryngeal)

Question 6

_______ to the laryngeal nerve results in midline position of vocal cords stridor, and laryngeal obstruction

Answer 6

Bilateral damage

Question 7

What three components make up acetylcholine?

Answer 7

Acetyl CoA
Choline
Acetyl transferase

Question 8

What receptors does Ach bind to?

Answer 8

Nicotine or muscarinic

Question 9

What breaks down Ach so that it can be used for synthesis again?

Answer 9

Acetylcholine esterase

Question 10

Why does anything that impact the PNS also impact the motor end plates of the NMJ?

Answer 10

Ach is the NT present at the ganglia of the PNS but it is also the NT at the NMJ.
As well as the second messenger of the SNS.

Question 11

Ach reuptake occurs by a high affinity ________ coupled to Na-K ATPase

Answer 11

Sodium-choline cotransport

Question 12

AchE inhibitors work at motor end plates but also affect the

Answer 12

PNS

Question 13

The blocking of AchE prevents the breakdown of Ach so that it can compete for receptors to reverse

Answer 13

Muscle relaxants

Question 14

Where is Ach stored?

Answer 14

Vesicles at the end terminal of nerves both in ganglia and second nerve

Question 15

Ach is released from vesicles when depolarization of the nerve terminal results in an ______ of calcium which promotes exocytosis

Answer 15

Influx

Leads to flaccid paralysis and respiratory failure

Question 16

Acetylcholine release can be blocked by toxins such as

Answer 16

Botulinum Toxin A

By binding to vesicles and preventing expcytosis

Question 17

What ways can Ach be terminated?

Answer 17

Reuptake
Hydrolysis
Diffusion

Question 18

Reuptake of ________ is more common than with active Ach

Answer 18

Its breakdown components

Question 19

Hydrolysis of acetylcholine is accelerated by ______ and occurs

Answer 19

Acetylcholinesterase

NMJ, synapses (primarily)

Question 20

Circulating hydrolysis of Ach that occurs through out the bloodstream is carried out by

Answer 20

Pseudocholinesterase (butyrlcholinesterase)

Question 21

Diffusion of Ach is _______ due to high

Answer 21

Minimal

Enzyme activity

Question 22

Cholinesterase inhibitors

Answer 22

Neostigmine
Edrophonium
Pyridostigmine
Physostigmine

Question 23

Nicotinic receptors are _______ ion channels

Answer 23

Ligand-gated (nicotine or Ach)

Question 24

Stimulation of nicotinic receptors leads to

Answer 24

Depolarization though sodium and potassium permeability

Question 25

Where are nicotinic receptors found?

Answer 25

NMJ

Autonomic ganglia

Question 26

There are at least ___ subtypes of muscarinic receptors

Answer 26

5

Question 27

M1 receptor

Answer 27

Autonomic ganglia and CNS

Question 28

M2

Answer 28

Supraventricular cardiac (para effects on the heart)

Question 29

M3

Answer 29

Smooth muscle and glands (contraction and dilation)

Question 30

What is the mechanism of muscarinic receptors?

Answer 30

They work by G protein coupled transduction
Upregulation of phospholipase C leads to increased inositol triphosphate and DAG
These act as second messengers that leads to more calcium release that lead to some sort of end response

Question 31

Why does activation of M3 cause vasoconstriction?

Answer 31

In regards to vasculature, M3 receptor activation on endothelial cells increases nitric oxide which leads to vasodilation
Without endothelial cells, Ach would lead to constriction

Question 32

NTG and nitroprusside lead to

Answer 32

Global dilation

Question 33

Nitric oxide is short lived and has _____ effects rather than systemic dilation

Answer 33

Focal

Question 34

Why doesn’t activation of muscarinic receptors increase conduction and contraction?

Answer 34

M2 receptors mediate inhibition via G proteins leading to hyper polarization and slower spontaneous depol (overall bradycardia)

Question 35

Cholinergic crisis is uncontrolled

Answer 35

Upregulation of the PNS