PNS Meds Flashcards
Recall how peripheral nervous system is classified
somatic nervous system: you control the movement
autonomic nervous system: involuntary, SNS and PSNS
Examples of processes controlled by ANS
blood pressure
heart rate & breathing
body temperature
balance of water and electrolytes
body fluids production (saliva, sweat, tears)
digestion
urination
defecation
sexual response
You do not need to control these process!
Tell which neurotransmitter binds to cholinergic receptors
Acetylcholine
Recall what neurotransmitters trigger an adrenergic receptor
Norepinephrine
Epinephrine
Dopamine
List the 3 subtypes of cholinergic receptor subtypes
Nicotinic N
Nicotinic M
Muscarinic
Describe what happens when a nicotinic N receptor is stimulated
Nicotinic N is found in the adrenal medulla
–> release epinephrine
Describe what happens when a nicotinic M receptor is stimulated
Nicotinic M is found in neuromuscular junction –> contraction of skeletal muscle
Recall the effects of muscarinic receptor actions throughout the body
Eyes: accommodation (ciliary muscle contraction) and pupil constriction
Heart: decreased rate
Lungs: bronchial constriction
GI tract: increased secretions and intestinal motility
Urinary bladder: increased pressure
List the 3 adrenergic receptor subtypes
Alpha 1, Beta 1, and Beta 2
Recall what happens when alpha 1 receptors are stimulated
Eye: pupil dilation
Arteries and veins: constriction
Male sex organs: constriction & ejaculation
Bladder: contraction of bladder and sphincter
Identify where beta 1 receptors are located
Heart: increased rate and FOC
Kideys: renin increase
Recall what happens when beta 2 receptors are stimulated
Arterioles: dilation (deliver more blood to heart, muscle, etc.)
Bronchi: dilation
Uterus: relaxation (slow down labor!)
Skeletal: increased contraction
Liver: glycogenolysis
Recall what neurotransmitter stimulates muscarinic receptors
Acetylcholine
Compare cholinergic and anticholinergic effects
Enhance the effects of Ach, increasing the actions of PSNS
Competitively block the effects of Ach, increasing SNS activity
Recite what occurs when the muscarinic receptors are activated by the cholinergic drug bethanechol
Bethanechol activates muscarinic receptors in the bladder!
increase bladder pressure, relaxation of smooth muscles and sphincter
Allows urine to leave the bladder –> commonly used in post-partum patients and patients with neurogenic atony of bladder
In short: relief of urinary retention
What groups of patients should be cautious with bethanechol
Bethanechol could enhances muscarinic receptors in other parts of the body
–> caution for patients with asthma, cardiac problems, peptic ulcers, or intestinal obstruction
Anticholinergic drugs are also known as…
parasympatholytic drugs
antimuscarinic drugs
muscarinic blockers
**anticholinergics block the actions of Ach at muscarinic receptors
Discuss the effects of atropine on the body
Atropine is an antagonist to muscarinic receptors
Recall that muscarinic receptors are located in eyes, heart, GI tract, lungs, urinary bladder.
Thus, its parasympatholytic effects include pupil dilation (mydriasis), increased HR, decreased saliva flow, open airways, decreased urinary activity.
List 4 therapeutic indications for atropine
- bradycardia
- eye disorders
- preanesthetic
- muscarinic poisoning
Describe the mechanism of action of the neuromuscular blockers (NMBs)
Neuromuscular blockers (NMBs) prevent Ach from activating nicotinic M receptors at the skeletal neuromuscular junction
–> cause skeletal muscle paralysis!
The patient no longer has control of skeletal muscles, which include the diaphragm.
Recognize the rationale of using general anesthetics and/or analgesics with NMBs
Since NMBs do not affect CNS, the patient is fully awake and aware of pain.
–> general anesthetics and/or analgesics must also be given to the patient
Describe the four important parts of neuromuscular junction
- Axon
- Motor-end-plate
- Muscle fiber (tubular cell called a myocyte)
- Myofibril
If we take a closer look…
- presynaptic terminal
- synaptic vesicles (store NTMs)
- sarcolemma
- nicotinic M receptors
- mitochondrion (cell’s powerhouse, producing ATP)
Describe the rationale of using sedation with neuromuscular blockers (NMBs)
Sedation is ALWAYS used with NMBs to decrease the anxiety that would come from a person being totally paralyzed while still awake.
List 3 common indications when paralysis with NMBs is used
- surgery
- endotracheal intubation
- mechanical ventilation
Explain the healing benefits of paralysis with intubation
- NMBs eliminate the gag reflex when being intubated
- Patients feel uncomfortable being intubated (it makes them feel air hungry)
- When patients are critically ill, they will not waste energy they need to heal on “fighting” the mechanical ventilator
Specify the route of administration of neuromuscular blockers (NMBs)
Must be given IV
NMBs cannot cross blood brain barrier –: no impact on CNS (paralysis, not sedation)
It cannot cross placenta either, minimal effects on a fetus
Identify the pharmacologic effects of NMBs in the skeletal muscles and the central nervous system (CNS)
- leads to severe muscle relaxation (aka flaccid paralysis)
- no impact on CNS
List 2 life-threatening adverse effects of NMBs
- respiratory arrest
- cardiovascular effects (hypotension)
Recite the 2 types of NMBs
- competitive NMBs (aka non-depolarizing NMBs)
- depolarizing NMBs
What are the characteristics of competitive NMBs?
The onset of paralysis is quick, but it takes 20-45 min to reach the peak and then decline gradually. It takes 1 hour for the complete recovery.
Competitive NMBs are used for longer procedures.
What are the characteristics of depolarizing NMBs?
The onset of paralysis is quick, and its effect is ultrashort-acting. It reaches the peak after 1 min and fades after 4-10 minutes.
5 examples of competitive NMBs
Atracurium
Cisatracurium
Pancuronium
Rocuronium
Vecuronium
they end in “-ium”
Which competitive NMBs are good choice for patients with renal/hepatic dysfunction?
What is the risk factor?
Atracurium and Cisatracurium
They have the risk of hypotension due to histamine release (histamine cause peripheral vasodilation)
Atracurium: cholinesterase in plasma break it down
CIsatracurium: spontaneous degradation
Which competitive NMBs have no risk of hypotension?
Pancuronium: excreted through urine, may produce tachycardia
Rocuronium: eliminated by hepatic metabolism
Vecuronium: excreted in the bile
Example of depolarizing NMB
Succinylcholine
Describe the mechanism of action of succinylcholine
Succinylcholine binds to Ach receptors and cause a prolonged (delayed) depolarization of motor-end-plate
–> results in flaccid paralysis of skeletal muscle
Specify the indication for succinylcholine
used for muscle relaxation during intubation
What would happen when pt has low pseudocholinesterase activity and receives succs?
No rapid succinylcholine degradation
–> paralysis may last for hours!
***Pseudocholinesterase is a plasma enzyme produced in the liver that is responsible for the metabolism of the common anesthesia drugs, succinylcholine, and mivacurium, as well as ester local anesthetics
Describe postoperative myalgia due to succinylcholine
Pt may develop muscle pain in neck, shoulders, and back within 12-24 hours after surgery, due to muscle contractions
(the exact cause is unknown)
What electrolyte imbalance may happen with succinylcholine?
Hyperkalemia
Succs promote the release of K from tissues.
Identify patients in whom significant hyperkalemia is most likely to occur with succinylcholine
Hyperkalemia is rare, but could be life-threatening.
Most likely to occur in patients with major burns, multiple trauma, denervation of skeletal muscle, or upper motor neuron injury.
Recite the life-threatening adverse effect of succinylcholine
malignant hyperthermia (severe reaction to certain drugs used for anesthesia)
List 6 clinical features of malignant hyperthermia
- muscle rigidity
- elevated temperature
- cardiac dysrhythmias
- unstable blood pressure
- electrolyte imbalance
- metabolic acidosis
Describe the treatment of malignant hyperthermia
- immediately discontinue succinylcholine
- lower body temp (ice packs & cold saline infusion)
- administer IV dantrolene
Describe the mechanism of dantrolene
Dantrolene is a direct-acting skeletal muscle relaxant. It reduces the metabolic activity of skeletal muscle –> reduction of high fever and muscle rigidity
Compare pros & cons of dantrolene
- treats malignant hyperthermia & NMS and effect is reported withing minutes of administration
- has a risk of hepatotoxicity
List 2 drug classes that interact with succinylcholine
cholinesterase inhibitors (result in more intense effects)
some antibiotics (aminoglycosides, tetracyclines, etc. can intensify the succs effect)
