Peripheral Nervous System "PNS" Flashcards
the Parasympathetic outflow is also termed what?
craniosacral
The parasympathetic or craniosacral outflow arises from where?
cranial Nerves III (oculomotor), VII (facial), IX (glossopharyngeal), X (Vagus)
and Sacral segments S2, S3 and S4
Where does it arise and what is it’s name?
CN III
Midbrain
Oculomotor
Where does it arise and what is it’s name?
CN VII
Pons
Facial
Where does it arise and what is it’s name?
CN IX
Medulla
Glossopharyngeal
Where does it arise and what is it’s name?
CN X
Medulla
Vagus
What is the bodies response to PNS or Craniosacral stimulation?
Eye
miosis (constriction)
What is the bodies response to PNS or Craniosacral stimulation?
Heart
Bradycardia
Decreased conduction through AV node
Decreased contractility
What is the bodies response to PNS or Craniosacral stimulation?
Secretions
Increased salivary
Increased bronchial
Increased Gastric
Increased Digestive
What is the bodies response to PNS or Craniosacral stimulation?
Smooth muscle
Bronchoconstriction
increased motility of stomach and intestines
what receptors are involved in mediating the responses to reversal agents such as neostigmine?
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
How will excessive doses of acetylcholinesterase inhibitors affect Nondepolarizing neuromuscular blockade?
In excess doses they can paradoxically potentiate a NDMR blockade
How will administration of acetylcholinesterase inhibitors affect Depolarizing neuromuscular blockade?
they will prolong the depolarization blockade of SCh
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?
A) scopolimine
B) Gylcopyrrolate
C) Atropine
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?
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.
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?
A) Excessive blockade of ACh receptors by the antimuscarinics
B) Anticholinergic Syndrome
C) Physostigmine, A cholinesterase inhibitor that crosses the BBB.
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?
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
memory master pages
IA3d
IB8a-c
