Peripheral Nervous System "PNS"

Question 1

the Parasympathetic outflow is also termed what?

Answer 1

craniosacral

Question 2

The parasympathetic or craniosacral outflow arises from where?

Answer 2

cranial Nerves III (oculomotor), VII (facial), IX (glossopharyngeal), X (Vagus)
and Sacral segments S2, S3 and S4

Question 3

Where does it arise and what is it’s name?

CN III

Answer 3

Midbrain

Oculomotor

Question 4

Where does it arise and what is it’s name?

CN VII

Answer 4

Pons

Facial

Question 5

Where does it arise and what is it’s name?

CN IX

Answer 5

Medulla

Glossopharyngeal

Question 6

Where does it arise and what is it’s name?

CN X

Answer 6

Medulla

Vagus

Question 7

What is the bodies response to PNS or Craniosacral stimulation?
Eye

Answer 7

miosis (constriction)

Question 8

What is the bodies response to PNS or Craniosacral stimulation?
Heart

Answer 8

Bradycardia
Decreased conduction through AV node
Decreased contractility

Question 9

What is the bodies response to PNS or Craniosacral stimulation?
Secretions

Answer 9

Increased salivary
Increased bronchial
Increased Gastric
Increased Digestive

Question 10

What is the bodies response to PNS or Craniosacral stimulation?
Smooth muscle

Answer 10

Bronchoconstriction

increased motility of stomach and intestines

Question 11

what receptors are involved in mediating the responses to reversal agents such as neostigmine?

Answer 11

Nicotinic receptors are activated by ACh that accumulate in the NMJ when Acetylcholinesterase is inhibited by any anti cholinesterase. Muscarinic receptors are activated by the ACh that accumulate a the Parasympathetic tissues when acetylcholinesterase is inhibited.
** take home*- cholinesterase inhibitors INDIRECTLY stimulate nicotinic and muscarinic receptors

Question 12

How will excessive doses of acetylcholinesterase inhibitors affect Nondepolarizing neuromuscular blockade?

Answer 12

In excess doses they can paradoxically potentiate a NDMR blockade

Question 13

How will administration of acetylcholinesterase inhibitors affect Depolarizing neuromuscular blockade?

Answer 13

they will prolong the depolarization blockade of SCh

Question 14

Clinical Scenarios:
You want to protect the pt from excessive salivation.
A) if you also want to promote sedation what drug do you use?
B) If you want to avoid sedation what drug do you use?
C) of the available antisialagous which is least efficacious in reducing salivation?

Answer 14

A) scopolimine
B) Gylcopyrrolate
C) Atropine

Question 15

Clinical Scenarios:
The 65 year old farmer was spraying insecticides when his vision became blurred and severe abdominal cramps and wheezing commenced. Upon arrival to the ER in Des Moines, IA, the pt was bradycardia, salivating excessively, and very weak. He was also very confused and disorientated.
A) What caused his condition?
B) What is his condition called?
C) What agents might you select to treat his condition?

Answer 15

A) Organophosphate insecticides are cholinesterase inhibitors. Inhibition of true cholinesterase w/ accumulation of excessive amounts of ACh centrally and peripherally leads to the signs and symptoms exhibited
B) Cholinergic Crisis or Cholinergic Syndrome
C) Atropine (a competitive antagonist of ACh) it acts peripheral and acts centrally b/c it crosses the BBB.

Question 16

Clinical Scenarios:
The 68 yo pt was given Scopolimine preoperatively and atropine w/ edrophonium to reverse muscle paralysis. In the PACU the pt becomes restless, combative, and confused. A rash on the upper body is seen. Tachycardia is also present.
A) what is the cause of these signs and symptoms?
B) What is the Condition called?
C) What might you give to treat this condition?

Answer 16

A) Excessive blockade of ACh receptors by the antimuscarinics
B) Anticholinergic Syndrome
C) Physostigmine, A cholinesterase inhibitor that crosses the BBB.

Question 17

Clinical Scenarios:
Bronchospasm develops during a case. You give terbutaline first and then aminophylline. the pt has a modest response to the 2 drugs.
A) terbutaline increases concentration of what 2nd messenger? What is the mechanism?

B) Aminophylline increases the concentration of what 2nd messenger? What is the mechanism?

C) What other drugs might you try to break the bronchospasm?

Answer 17

A) Cyclic adenosin monophosphate (cAMP); it stimulates Beta 2 of the bronchial smooth muscle cell, which in turn activates Adenylate cyclase. Activated Adenylate cyclase converts intracellular ATP to the 2nd messenger cAMP. cAMP causes bronchodilation

B)Increases cAMP as well. it is a PDE inhibitor, and prevents the breakdown of cAMP, hence cAMP accumulates in the cell.

C) Antimuscarinics (atropine or ipratropium); VAAs; Steroids

Question 18

memory master pages

Answer 18

IA3d

IB8a-c