ANS - Part 2 Flashcards
The PNS targets
Smooth muscle
Cardiac muscle
Glands (heavily involved)
The cranial region of the PNS includes
Midbrain and medulla
What are some of the glandular effects of the PNS?
Salivation, lacrimation, digestion, urination, defecation, pupillary constriction, vasomotor control, bronchial control
What is the main nerve of the PNS?
Vagus - it comes out of the brainstem
It is a global downregulator
Why is the vagus nerve called the wandering nerve and what does it innervate?
It is called the wandering nerve because it innervates many thoracic and abdominal structures
Motor and sensory to larynx
The vagus nerve supplies innervate on to all nerves of the larynx except the
Cricothyroid (super laryngeal)
_______ to the laryngeal nerve results in midline position of vocal cords stridor, and laryngeal obstruction
Bilateral damage
What three components make up acetylcholine?
Acetyl CoA
Choline
Acetyl transferase
What receptors does Ach bind to?
Nicotine or muscarinic
What breaks down Ach so that it can be used for synthesis again?
Acetylcholine esterase
Why does anything that impact the PNS also impact the motor end plates of the NMJ?
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.
Ach reuptake occurs by a high affinity ________ coupled to Na-K ATPase
Sodium-choline cotransport
AchE inhibitors work at motor end plates but also affect the
PNS
The blocking of AchE prevents the breakdown of Ach so that it can compete for receptors to reverse
Muscle relaxants
Where is Ach stored?
Vesicles at the end terminal of nerves both in ganglia and second nerve
Ach is released from vesicles when depolarization of the nerve terminal results in an ______ of calcium which promotes exocytosis
Influx
Leads to flaccid paralysis and respiratory failure
Acetylcholine release can be blocked by toxins such as
Botulinum Toxin A
By binding to vesicles and preventing expcytosis
What ways can Ach be terminated?
Reuptake
Hydrolysis
Diffusion
Reuptake of ________ is more common than with active Ach
Its breakdown components
Hydrolysis of acetylcholine is accelerated by ______ and occurs
Acetylcholinesterase
NMJ, synapses (primarily)
Circulating hydrolysis of Ach that occurs through out the bloodstream is carried out by
Pseudocholinesterase (butyrlcholinesterase)
Diffusion of Ach is _______ due to high
Minimal
Enzyme activity
Cholinesterase inhibitors
Neostigmine
Edrophonium
Pyridostigmine
Physostigmine
Nicotinic receptors are _______ ion channels
Ligand-gated (nicotine or Ach)
Stimulation of nicotinic receptors leads to
Depolarization though sodium and potassium permeability
Where are nicotinic receptors found?
NMJ
Autonomic ganglia
There are at least ___ subtypes of muscarinic receptors
5
M1 receptor
Autonomic ganglia and CNS
M2
Supraventricular cardiac (para effects on the heart)
M3
Smooth muscle and glands (contraction and dilation)
What is the mechanism of muscarinic receptors?
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
Why does activation of M3 cause vasoconstriction?
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
NTG and nitroprusside lead to
Global dilation
Nitric oxide is short lived and has _____ effects rather than systemic dilation
Focal
Why doesn’t activation of muscarinic receptors increase conduction and contraction?
M2 receptors mediate inhibition via G proteins leading to hyper polarization and slower spontaneous depol (overall bradycardia)
Cholinergic crisis is uncontrolled
Upregulation of the PNS
