Flashcards in Peripheral Nervous System Deck (226):
What are the two primary divisions of the peripheral nervous system?
somatic (sensory and motor) and autonomic (sympathetic and parasympathetic)
The somatic nervous system send motor or _______ impulses to skeletal muscle. Somatic sensory nerves carry impulses (or ________) that are perceived, such as touch, pressure, pain, and temperature.
What is the predominant neurotransmitter in the periphery?
What is the difference in preganglionic and post ganglionic nerves in the parasympathetic neurons vs the sympathetic neurons?
sympathetic preganglionic nerves tend to have short lengths and postganglionic tend to be longer; parasympathetic has the OPPOSITE--- long pre, short post
In regards to pre and post ganglionic nerves... what is different about the adrenal medulla?
the adrenal medulla does not have post ganglionic fibers... only PRE.... so there is a direct release of the hormones (EPI, NE)
What is the primary neurotransmitter found in the pre and post ganglionic neuron of the sympathetic nervous system?
What is the primary neurotransmitter in the pre and post ganglionic neuron of the parasympathetic nervous system?
Acetylcholine is the neurotransmitter released from somatic ______ nerves, ________ sympathetic nerves, ________ parasympathetic nerves, and _______ parasympathetic nerves.
Acetylcholine is the neurotransmitter released from somatic motor nerves, preganglionic sympathetic nerves, preganglionic parasympathetic nerves, and postganglionic parasympathetic nerves.
With one exception, norepinephrine is released from ALL sympathetic postganglionic nerves. The exception is _______.
sweat glands; AcH, not NE is released to sweat glands from sympathetic postganglionic nerves
What neurotransmitter released from the sympathetic neurons is responsible for triggering the release of hormones from the adrenal medulla?
acetylcholine..... BECAUSE the adrenal medulla is innervated by sympathetic PREGANGLIONIC neurons
What receptors are found on tissues innervated by the parasympathetic nervous system?
muscarinic receptors (cholinergic)
What receptors are found on tissue innervated by the sympathetic nervous system? The exception is the ______ ______.
adrenergic receptors; exception is the sweat glands.... where acetylcholine is released from the sympathetic postganglionic neuron to muscarinic receptors.
Where can nicotinic receptors be found?
found at the autonomic ganglia, on cells of the adrenal medulla, and at the motor-end plate of skeletal muscle
What receptor is responsible for possible bradycardia after the administration of succinylcholine?
muscarinic receptors on SA node
Alpha 1, alpha 2, and beta 1 are all examples of ______ receptors.
Does norepinephrine stimulate beta 2 receptors?
NO..... beta 2 is stimulated by epinephrine
Acetylcholine binds to nicotinic receptors except for the postganglionic neurons of the ________ nervous system.
parasympathetic; at the tissues of the PNS postganglionic.... but AcH still binds to nicotinic receptors in the PRE ganglionic parasympathetic neurons.
Where are nicotinic receptors found?
peripherally in the motor end plate of skeletal muscle and in cell bodies of both sympathetic and parasympathetic postganglionic neurons; nicotinic receptors respond to ACh or ACh agonists (sux) in a biphasic fashion
Nicotinic receptors respond to ACh or ACh agonists (sux) in a biphasic fashion. What does this mean in regards to dose?
in small doses, ACh stimulates nicotinic receptors of postganglionic sympathetic and parasympathetic neurons as well as nicotinic receptors of skeletal muscle end plate to cause depolarization; BUT IN HIGH DOSES or PROLONGED EXPOSURE, the nicotinic receptors become desensitized to succinylcholine and the postsynaptic membrane becomes inexcitable; this is called a PHASE II block
What are the 2 major subtypes of cholinergic receptors?
nicotinic and muscarinic
Cholinergic is the abbreviated term referring to __________.
acetylcholine; acetylcholine receptors are nicotinic and muscarinic
A substance (or ligand) is ________ if it is capable of producing, altering, or releasing acetylcholine ("indirect-acting") or mimicking its behaviour at one or more of the body's acetylcholine receptor types ("direct-acting").
List the "fiber types" in order from largest to smallest diameter.
A-alpha (largest and fastest), A-beta, A-gamma, A-delta, B, sC, dC (smallest and slowest)
What fiber types are myelinated?
ALL of the A fibers (alpha, beta, gamma, delta) & B; sC, dC are UNMYELINATED
Which fibers carry sensations of sharp, prickling pain and temperature?
Which fibers carry sensations of throbbing pain and temperature?
dC fibers (sensory afferent)..... they are smaller so you get a slow throbbing pain
What is the function of A-alpha fibers?
motor (efferent) and sensory (afferent) to skeletal muscle and joints; muscle length, muscle force, proprioception
What two fibers are responsible for proprioception?
A-alpha and A-beta sensory fibers
Sympathetic and parasympathetic (both autonomic) preganglionic neurons are _____ fibers.
Postganglionic sympathetic neurons are ____ fibers.
C fibers (sC)
________ nerves conduct action potentials at greater velocities than ______ nerves. (myelinated vs unmy.)
myelinated faster than unmyelinated
Do larger.... or smaller fibers conduct action potentials at a greater velocity?
Where do the cardiac accelerator fibers arise from?
What is another name for the sympathetic outflow?
thoracolumbar outflow; arises from segments T1-L2 or T1-L3
The _______ _______ is formed by the inferior cervical and first thoracic ganglia.
Notes: The stellate ganglion (or cervicothoracic ganglion) is a sympathetic ganglion formed by the fusion of the inferior cervical ganglion and the first thoracic ganglion, which exists in 80% of cases. Stellate ganglion is located at the level of C7 (7th cervical vertebrae), anterior to the transverse process of C7, superior to the neck of the first rib, and just below the subclavian artery.
The clinical significance of these ganglia is that they may be cut in order to decrease the symptoms exhibited by Raynaud's phenomenon and hyperhydrosis (extreme sweating) of the hands. Injection of local anesthetics near the stellate ganglion can sometimes mitigate the symptoms of sympathetically mediated pain such as complex regional pain syndrome type I (reflex sympathetic dystrophy). Injection is often given near the Chassaignac's Tubercle (anterior tubercle of transverse process of C6) due to this being an important landmark lateral to the cricoid cartilage. It is thought that anesthetic is spread along the paravertebral muscles to the stellate ganglion.
What are some s\s of Horner's syndrome? What causes this?
stellate ganglion blockade; The symptoms are: IPSILATERAL (meaning one-sided) miosis, ptosis, enophthalamos, flushing, increased skin temp, anhydrosis (no sweat), and nasal congestion.
How long does it take for the autonomic nervous system to mature in the neonate? What will you see in the place of bradycardia?
~6 mos; no bradycardia.... will see desaturation
All sympathetic preganglionic fibers pass through _______ (white or gray) rami while some, but not all, sympathetic postganglionic fibers pass through ______ (white or gray) rami.
PRE=WHITE, POST=GRAY; gray rami are distributed to ALL spinal nerves, while white rami are distributed to spinal nerves arising from T1-L2.
________ (WHITE or GRAY) rami allow coordinated, mass discharge of the sympathetic nervous system.
What happens when alpha-2 receptors are stimulated?
When presynaptic alpha-2 receptors are stimulated by norepinephrine or any other drug with alpha-2 receptor agonist activity, the SYNTHESIS and RELEASE of NOREPINEPHRINE is DECREASED==== THIS IS NEGATIVE FEEDBACK
What are some common alpha-2 agonist drugs?
clonidine (catapres), precedex (dexmetatomadine)-- 200:1
List out the synthesis of norepinephrine.
-tyrosine transported into nerve terminal from bloodstream
-tyrosine converted to dopa
-dopa converted to dopamine
-dopamine transported into presynaptic vesicle
-dopamine converted to norepinephrine
-NE stored in presynaptic vesicles (in adrenal medulla, NE is converted to epinephrine; normally in adrenal medulla, NE comprises 20% and EPI comprises 80%)
What happens to norepinephrine after it diffuses away from the receptor it attached to? (3 things)
it is removed from the synaptic cleft by:
1) reuptake (80%)
2) metabolism by MAO in the synaptic cleft
3) diffusion into the plasma where metabolism by COMT occurs (catechol-O-methyl-transferase)
How do most indirect acting sympathomimetics work? What is a common drug of this class used in the OR?
work in part by displacing NE from sympathetic nerve terminals; Ephedrine is commonly used; ephedrine also stimulates adrenergic receptors directly, so it is also a direct acting agent.
What are TWO drugs that should be AVOIDED in patients taking MAO inhibitors?
indirect acting sympathomimetics (EPHEDRINE) and one opioid, meperidine (DEMEROL); meperedine, like ephedrine, triggers release of NE; when either are administered to patients taking MAO inhibitors, the release of excess amounts of norepinephrine may cause a hypertensive crisis; generally more severe when giving meperidine than ephedrine.
What are some physiologic changes seen when the sympathetic nervous system is activated?
increased HR, CO, BP, blood glucose concentration; shunting of blood away from intestines and other viscera to better supply skeletal muscles; DILATION of bronchial tree
Where are alpha-1 receptors found and what happens when they are activated?
found peripherally in a variety of tissues (vascular smooth muscle, glands) innervated by sympathetic postganglionic neurons
excitatory response: arterial (increases SVR) and venous vasoconstriction (increases venous return, increases SV, increases CO)--> increased systemic arterial blood pressure
Where are alpha-2 receptors found and what happens when they are activated?
found on presynaptic nerve terminals of sympathetic postganglionic neurons, but also in tissues on postsynaptic membranes in the brainstem
stimulation on post-ganglionic, pre-synaptic nerve varicosities produce: inhibition of NE synthesis and release (negative feedback)
stimulation on postsynaptic alpha-2 in brainstem inhibits outflow of sympathetic nervous system
stimulation in substantia gelatinosa of spinal cord promotes analgesia (unrelated to SNS function)
Where are beta-1 receptors found and what happens when they are activated?
found in heart, kidney, and adipose tissue
stimulation is excitatory: increased HR and myocardial contractility--> increase CO--> increase arterial BP
Where are beta-2 receptors found and what happens when they are activated?
found in smooth muscle and in glandular tissue
stimulation if inhibitory: blood vessels of skeletal muscle dilate (small decrease in SVR, but overshadowed by beta-1), bronchodilation and relaxation of pregnant uterus
STIMULATES hepatocytes--> glycogenolysis and gluconeogenesis--> increasing blood glucose levels
What SNS receptors are found in the SA node, AV node, and muscle fibers?
What receptor stimulation is responsible for dilation of the pupils (mydriasis)?
What receptor is responsible for vasodilation of skeletal muscles?
What receptor is responsible for vasoconstriction of arterial and most systemic vessels?
What receptor stimulation is responsible for increased renin release in the kidneys?
What receptor stimulation is responsible for decreased renin release in the kidneys?
An increase in blood glucose by glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (formation of new glucose from non-carbohydrate sources, namely from amino acids) is the result of stimulation of what receptor?
What receptor stimulation causes an increase in insulin secretion by the pancreas? decrease?
What receptor causes a stimulation in the Na-K pump, thereby decreasing plasma K+?
______ receptor stimulation promotes hyperglycemia.
beta-2; glycogenolysis and gluconeogenesis
______ receptor stimulation promotes hypokalemia.
beta-2; stimulates Na-K pump
What are some side effects of the beta-2 agonist, ritodrine (Yutopar)?
hyperglycemia, hypokalemia, and tachycardia (tachy only because these drugs are known to have some beta-1 receptor activity)
What controls 85% of the resting blood pressure?
Where is renin released from?
the juxtaglomerular cells of the afferent arteriole
What does renin do?
converts angiotensinogen (a protein released into circulation from the liver) to angiotensin I
What is ACE and what does it do?
angiotensin converting enzyme; found on endothelial surface of pulmonary capillaries; converts angiotensin I to angiotensin II
What are the effects of angiotensin II?
promotes vasoconstriction and aldosterone release
What are the TWO important stimuli for aldosterone release?
angiotensin II and high serum K+ levels
What is the MOST potent vasoconstrictor out of angiotensin II and ADH?
ADH (also called vasopressin) is MORE POTENT
What are the effects of aldosterone?
increases K+ secretion (and excretion) and increases Na reabsorption, which promotes Na retention---> which promotes volume expansion
What causes the release of renin?
decreased renal BP (renal artery stenosis) and increased sympathetic nervous system activity
What receptors are stimulated by Phenylephrine (Neo-synephrine)?
Alpha 1; minimal Alpha-2
What receptors are stimulated by Clonidine (Catapress)?
Alpha-2; minimal Alpha-1
What receptors are stimulated by Isoproterenol (Isuprel)?
Beta 1 and Beta 2 in almost EQUAL amount
What receptors are stimulated by Dobutamine (Dobutrex)?
Beta 1 and minimal Alpha-1
What receptors are stimulated by Terbutaline (Brethine)?
Beta-2; minimal Beta-1
What receptors are stimulated by Albuterol (Ventolin, Proventil)?
Strong Beta-2; minimal Beta-1
What receptors are stimulated by Ritodrine (Yutopar)?
Beta-2; minimal Beta-1
What receptors are stimulated by Epinephrine (Adrenalin)?
Alpha-1 (+++), Alpha-2 (+), Beta-1 (++), Beta-2 (++), dopamine-1 (+)
What receptors are stimulated by Norepinephrine (Levophed)?
Alpha-1 (++++), Alpha-2 (+++), Beta-1 (++), NO beta-2
What receptors are stimulated by Dopamine (Inotropin)?
Alpha-1 (++), Alpha-2 (++), Beta-1 (++), minimal Beta-2 (+), DA-1 (++), DA-2 (++)
What receptors are stimulated by Fenoldopam?
What receptors are stimulated by Metoclopramide (Reglan)?
What receptors are stimulated by Ephedrine?
Alpha-1 (++), Alpha-2 (++), Beta-1 (+), Beta-2 (+)
What receptors are stimulated by Metarminol (Aramine)?
Alpha-1 (++), Alpha-2 (++), Beta-1 (+), Beta-2 (+); same as Ephedrine
Why is Dopamine unique is comparison to other catecholamines?
It simultaneously increases contractility, renal blood flow, GFR, sodium excretion, and urine output
What are some of the common uses for Dopamine?
to increase CO in patients with low systemic BP, increased atrial filling pressures, and in low urine output
What are some of the common uses for Dobutamine?
to increase CO in CHF, particularly if HR and SVR are increased
What is the primary use for Isoproterenol?
to treat complete heart block; chemical pacemaker; 1-5mcg/kg/min continuous infusion
Whether pertinent or not, what is a difference shown in literature of outcomes using phenylephrine vs. ephedrine in the parturient?
phenylephrine is associated with a higher umbilical artery pH and less fetal acidosis at delivery, compared to using ephedrine
What relationship can be seen when looking at the direction of diastolic arterial BP and SVR?
DBP changes in the same direction as systemic vascular resistance
When using low dose epinephrine, what is one attributable cause of decreases in DBP and possibly MAP?
beta-2 mediated vasodilation (beta-2 mediated decrease in SVR)
What are 5 beta-2 agonists that can be used in the treatment of reversible bronchospasm?
metaproterenol (metered dose INH, nebulization, oral)
terbutaline (MDI, neb, subcutaneous)
albuterol (MDI, oral)
isoetharine (MDI, neb)
salmeterol (MDI, long-lasting)
Which two beta-2 agonists can be given to STOP uterine contractions of premature labor?
Ritodrine (IV, oral)
Terbutaline (IV, oral)
What is a side effect of Ritodrine; caution for parturients?
tachycardia, hypokalemia, hyperglycemia, pulm edema; CROSSES THE PLACENTA, same effects can be seen in the fetus
The rebound hypertension that can be seen in sudden withdrawal of Clonidine (Catapress) is mediated by what 3 things?
catecholamines, renin, angiotensin II
What is the important physiologic response seen when administering an alpha-2 agonist such as clonidine?
decrease in BP; occurs in response to stimulation of BOTH peripheral pre-synaptic and central post-synaptic alpha-2 receptors; results in decrease of NE release to vascular smooth muscle
In addition to its antihypertensive actions, what other effects can be seen with clonidine use?
produces sedation, reduces anxiety, and promotes analgesia (REDUCES MAC by 15-50%)
What is phenoxybenzamine (Dibenzyline)... and what is it primarily used for?
adrenergic receptor antagonist; BLOCKS Alpha-1 (++++) and Alpha-2 (++); long-acting non-selective alpha-antagonist used to control BP in patients with pheochromocytoma
What kind of drug is Phentolamine (Regitine)?
non-selective alpha antagonist; Alpha-1 (+++), Alpha-2 (++)
What receptors are affected by Yohimbine (Yocon) and what is its primary clinical use?
selective alpha-2 antagonist; used to treat impotence
In respect to Prazosin (Minipress):
1) What type of drug is it and what receptors are effected
2) What is its use
3) What is its MOA
1) selective alpha-1 antagonist
2-3) Lowers BP without increasing release of NE from postganglionic sympathetic nerve terminals because it does not block alpha-2
Why is propranolol sometimes avoided in patients with irritable airways?
it is a non-selective beta-2 antagonist (beta-1 ++, beta-2 ++++); beta-2 blockade can induce bronchoconstriction
Why is esmolol so short acting?
esmolol is a competitive antagonist of beta-1 receptors; very short because it is metabolized in the plasma by non-selective esterases of the red blood cell
What are two of the primary intraoperative uses of esmolol?
to treat SVT and HTN; can be used to blunt reflex cardiovascular responses to intubation and to produce controlled hypotension
What is labetalol and its uses?
it is an agent that competitively antagonizes alpha-1, beta-1, beta-2 receptors; used to treat HTN emergencies or to produce controlled hypotension
What are clinical effects that can be seen after administration of labetalol?
decreased HR, myocardial contractility, and SVR
What is the alpha to beta ratio seen with labetalol?
alpha to beta is 1:7 (stronger beta than alpha)
What are some of the treatment options for excess myocardial depression induced by beta-antagonists?
-atropine in incremental doses of 7mcg/kg IV
-calcium chloride (250 to 1000mg IV)
-glucagon (1-10mg IV, followed by 5mg/hr IV)
-transvenous artificial cardiac pacer
What is the concept of down-regulation concerning exposure to an agonist?
chronic exposure to an agonist can cause the number of receptors to diminish (down regulation); seen in CHF--> high sympathetic outflow to compensate for decreased heart pump performance results in down regulation of beta-1 receptors
What is the concept of up-regulation concerning exposure to antagonists?
chronic exposure to a competitive antagonist can result in an increased number of receptors; seen in patients that are beta blocked--> beta blockade of beta-1 results in an up-regulation of beta-1 receptors--> if patient was abruptly withdrawn from their beta blockade, the response would be tachycardia and increased contractility because of the excessive number of receptors; could lead to myocardial ischemia in patients with CAD.
What cranial nerves carry parasympathetic nerves?
cranial nerves III, VII, IX, X; and sacral segments S2, S3, and S4
The ______ transmits fully three-fourths of the traffic of the parasympathetic nervous system.
What is another name for the parasympathetic outflow?
Where does cranial nerve III (oculomotor) arise from?
Where does cranial nerve VII (facial) arise from?
Where does cranial nerve IX (glossopharyngeal) and X (vagus) arise from?
What is the primary function of the parasympathetic nervous system?
to conserve energy and maintain organ function and support vegetative processes (resting and digesting)
What would happen if there was a MASSIVE parasympathetic response?
It would only prostrate the organism, leaving it helplessly salivating, wheezing, weeping, vomiting, urinating, defecating, and seizing
What response is seen with the eye with parasympathetic stimulation?
miosis (constriction of the pupil)
What response in the heart is seen with parasympathetic stimulation?
decreased HR, decreased speed of conduction through AV node, slight decrease in myocardial contractility
What happens to secretions when there is parasympathetic stimulation?
increased salivary, pharyngeal and laryngeal secretions; increased bronchial secretions; increased gastric acid secretion; increased secretion of digestive enzymes and bicarbonate from the pancreas into the small intestine; increased secretion of bile and bicarbonate from the liver into the small intestine
What happens to smooth muscle after parasympathetic stimulation?
bronchoconstriction; gall bladder contraction; increased motility and tone of the stomach and intestines; contraction of the bladder
What happens to acetylcholine metabolism when administering a cholinesterase inhibitor (edrophonium, neostigmine)?
metabolism of acetylcholine is impaired by cholinesterase inhibitors, so acetylcholine levels increase at ALL cholinergic (muscarinic and nicotinic) synapses
Are cholinesterase inhibitors a direct or indirect acting drug?
indirect; acetylcholine has the direct effect
Which antimuscarinic least crosses the blood brain barrier? Why?
glycopyrrolate, because it has a charged quaternary ammonium group
What is the cause and treatment of anticholinergic syndrome?
may develop in response to high doses of atropine or scopolamine; restlessness, shivering, mania, hallucinations, drowsiness, coma, excitation, agitation, motor incoordination; blurred vision, dry mouth, tachycardia, rash over face, flushed skin, hypotension; TREATED with cholinesterase inhibitor, physostigmine (an acetylcholinesterase inhibitor) 15-60mcg/kg IV... non-ionized and lipid soluble so it readily crosses the BBB
What is the reason for concern with reflux after giving antimuscarinics?
decreased tone of the lower esophageal sphincter may promote esophageal reflux since intragastric pressure is normally considerably higher than intraesophageal pressure
What drugs should you avoid in a patient receiving echothiophate eye drops for treatment of glaucoma?
avoid succinylcholine and other drugs like mivacurium or trimethaphan that are metabolized by plasma cholinesterase; echothiophate inhibits plasma cholinesterase and prolongs action of drugs that are metabolized by it
If your goal is to protect the patient from excess salivation and promote sedation, what is the best drug to use?
If you want to protect the patient from excess salivation and NOT produce sedation, what is the best drug to use?
Of the antisialagogues, which is LEAST effective at reducing salivation?
A 65 year old farmer was spraying insecticides when his vision became blurry and severe abdominal cramping started. He also started wheezing. He presented to the ER confused, disoriented, bradycardic, weak, and salivating.
1) What caused this?
2) What is the condition called?
3) What agents can be used to treat it?
1)organophosphate insecticides are cholinesterase inhibitors... inhibition of true cholinesterase with accumulation of excessive amounts of acetylcholine centrally and peripherally lead to this.
2)Cholinergic syndrome or cholinergic crisis
3)Atropine: competitive antagonist of acetylcholine... acts peripherally. It also acts centrally because it crosses the BBB; Pralidoxine: reactivates cholinesterase, may also be used.
A 68 year old patient was given scopolamine preop and atropine with edrophonium to reverse at end of the case. In PACU becomes restless, combative, confused, and has rash on upper body. She is also tachycardic.
1)What is the cause?
2)What is it called?
3) How to treat?
1) excessive blockade of aCh receptors by the antimuscarinics atropine and scopolamine
2) Anticholinergic syndrome
3) Physostigmine (Antilirium): a cholinesterase inhibitor that crosses the BBB; causes AcH to accumulate centrally and peripherally to overcome blockade of muscarinic receptors
A patient has a bronchospasm and you treat it first with terbutaline and then aminophylline. The patient has a modest response to the 2 drugs.
1) Terbutaline increases the concentration of what second messenger? What is the mechanism?
2) Aminophylline increases the concentration of what second messenger? What is the mechanism?
3) What other drugs could be used to treat the bronchospasm?
1) increases cyclic adenosine minophosphate (cAMP); This happens because terbutaline stimulates beta-2 adrenergic receptors of bronchial smooth muscle cell, which in turn activates adenylate cyclase; activated adenylate cyclase converts intracellular ATP to the second messenger, cAMP--> cAMP causes bronchodilation
2) increases the concentration of cAMP, but by a different mechanism; aminophylline, a phosphodiesterase inhibitor, prevents the breakdown of cAMP; so cAMP accumulates in the cell
3) antimuscarinics such as atropine or ipratropium (an antimuscarinic in inhaled form), volatile agents, or steroids may be used in an attempt to break the spasm.
Is the following somatic or autonomic: motor nerve to skeletal muscle?
Acetylcholine is released from the terminal of each of the following neurons EXCEPT:
1) sympathetic preganglionic neuron innervating the adrenal medulla
2) sympathetic postganglionic neuron innervating the GI tract
3) parasympathetic postganglionic neuron innervating the pupil of the eye
4) motor nerve innervating skeletal muscle
Answer is #1; the sympathetic preganglionic neuron that innervates the adrenal medulla releases norepinephrine
What type of post-synaptic cholinergic receptors are found in the SA node? (nicotinic or muscarinic)
muscarinic ; NOT nicotinic
Which of the following drugs would you AVOID in patients taking an MAO inhibitor?
AVOID #1: Meperidine--> It may cause HTN with patients taking MAO inhibitors secondary to indirect-acting sympathomimetic effects causing the release of norepinephrine.
Meperidine is a mu-receptor agonist that exerts its pharmacologic action on the CNS and the neural elements in the bowels; s\e may include dry mouth and blurred vision; it is effective in reducing shivering from diverse causes, including general and epidural anesthesia; eliminates visible shivering as well as accompanying increase in oxygen consumption
***Ephedrine can also cause this, but to a lesser degree
What is a simple definition for the somatic nervous system?
The somatic nervous system (SoNS Or voluntary nervous system) is the part of the peripheral nervous system associated with the voluntary control of body movements via skeletal muscles. The SoNS consists of afferent and efferent nerves. Afferent nerves are responsible for relaying sensation to the central nervous system whilst efferent nerves are responsible for stimulating muscle contraction, including all the non-sensory neurons connected with skeletal muscles and skin.
Release of neurotransmitter requires the entry of what substance into the nerve terminal?
What division (sympathetic or parasympathetic) and neurotransmitter (NE or AcH) should be paired with the sweat glands?
Does stimulation of B-2 adrenergic receptors lead to an increases release of glucagon from the pancreas?
NO!; but it does stimulate the Na-K pump, relax the pregnant uterus, and bronchodilate
Is diarrhea a possible s\e of ritrodine?
NO!; ritrodine s\e include hypokalemia, hyperglycemia, and possible tachycardia
What 2 primary actions does aldosterone promote, and where does it act in the kidney?
Na+ retention (volume increased), K+ excretion (hypokalemia)--> works on distal tubule
Why is Ephedrine a good choice for treating hypotension in the obstetric patient?
Because it does not significantly decrease uterine blood flow
Low levels of circulating epinephrine cause _______.
decrease in SVR
Is there a change in MAC when a patient is taking clonidine?
a decrease in MAC of 15-50%
How does prazosin (Minipress) work?
by blocking (antagonizing) vascular alpha-1 receptors without increasing the release of NE from sympathetic post-ganglionic nerves;
prazosin:sympatholytic drug used to treat high blood pressure and anxiety, PTSD, and panic disorder. It is an alpha-adrenergic blocker that is specific for the alpha-1 receptors. These receptors are found on vascular smooth muscle, where they are responsible for the vasoconstrictive action of norepinephrine. They are also found throughout the central nervous system
What is the difference in clonidine and prazosin?
Clonidine is an alpha 2 AGONIST; stimulates alpha 2 receptors in the brain which decrease peripheral vascular resistance thus lowering BP; it has specificity for a-2 receptors in vasomotor center of brainstem that results in decreased presynaptic calcium levels, thus inhibiting the release of NE--> decreasing sympathetic tone
Prazosin is alpha-1 ANTAGONIST that blocks alpha-1 without increasing the release of NE from sympathetic post-ganglionic nerves... since it has no effect on alpha-2
If a patient on propanolol had their last dose 2 hours before surgery, what medication would you be cautious about giving intra-op?
phenylephrine; unable to change HR to compensate for increased SVR
What drug acts on POST-synaptic alpha-2 receptors CENTRALLY and PRE-synaptic alpha-2 receptors peripherally?
Esmolol works primarily on what receptor?
Labetolol works primarily on which receptors?
alpha-1, beta-1 & 2--> works by competitive antagonism
An overdose of a beta blocker could be treated with all of the following except:
rationale for giving glucagon: Anecdotal evidence suggests a benefit of higher doses of glucagon in the treatment of overdose with beta blockers; the likely mechanism of action is the increase of cAMP in the myocardium, in effect bypassing the β-adrenergic second messenger system
Which IV and inhalational anesthetic should you MOST avoid in the beta-blocked patient?
Ketamine and Enflurane
Which second messenger promotes bronchoconstriction?
Inositol triphosphate (IP3)
Which agent produces bronchodilation because of its antimuscarinic actions?
It is an anticholinergic drug used for the treatment of chronic obstructive pulmonary disease and acute asthma. It blocks the muscarinic acetylcholine receptors in the smooth muscles of the bronchi in the lungs, opening the bronchi.
In regards to trimethaphan:
1) How is it metabolized?
2) Does it cause histamine release?
3) How does it work?
2) releases histamine
3) blocks nicotinic receptors at the autonomic ganglia
is a drug that counteracts cholinergic transmission at the ganglion type of nicotinic receptors of the autonomic ganglia and therefore blocks both the sympathetic nervous system and the parasympathetic nervous system. It acts as a non-depolarizing competitive antagonist at the nicotinic acetylcholine receptor, is short-acting, and is given intravenously.
The therapeutic uses of trimetaphan are very limited due to the competition from newer drugs that are more selective in their actions and effects produced. It is occasionally used to treat a hypertensive crisis and dissecting aortic aneurysm, to treat pulmonary edema, and to reduce bleeding during neurosurgery
What happens to the duration and intensity of non-depolarizing neuromuscular blockade if an excessive dose of a cholinesterase inhibitor is given?
duration and intensity are increased
What fibers carry proprioception?
What fibers carry pain and temperature?
A-delta and dC fibers
Another name for somatic in regards to its function is ______.
voluntary; part of the peripheral nervous system associated with voluntary movements--> skeletal muscle
Which nervous system is NOT protected by bones?
peripheral nervous system--> has two divisions--- 1) autonomic 2) somatic
** autonomic has two divisions---> 1) sympathetic 2) parasympathetic
What is the % ratio of norepinephrine vs. epinephrine released by the adrenal medulla?
80% EPI, 20% nor EPI
The predominant parasympathetic nerve is the ______ nerve. They have a ______ preganglia and ______ post-ganglia.
vagus; long pregang, short postgang
Sympathetic nerves have a _____ preganglia and a _______ postganglia.
short pre, long postganglia
Adrenergic fibers release _______ in the postganglia.
Parasympathetic or "cholinergic" fibers release _____ in the postganglia.
What type of cells are responsible for making EPI and NOREPI in the adrenal medulla?
Norepinephrine is released from all sympathetic POSTganglionic nerves, except for where? (only one exception)
sweat glands..... acetylcholine is released
What organ is innervated only by sympathetic PRE ganglionic neurons?
Adrenal medulla... hence acetylcholine is released from the sympathetic PRE ganglionic neurons elicits the release of hormones from the adrenal medulla (NORepi and EPI)
What type of neurotransmitter makes second messengers?
What type of neurotransmitter opens channels?
What are some examples of a ligand?
it binds to a receptor (which is a protein); ex- AcH, NE, NorEPI
Receptors can be described as one of two different things.... what are they?
1) ion channels
2) G-protein coupled receptors that make second messengers
What are the two subtypes of cholinergic receptors?
nicotinic (peripheral in motor end plate of skeletal muscle and on cell bodies of both sympathetic and parasympathetic post ganglionic neurons) and muscarinic (parasympathetic postganglionic in peripheral tissue)
Random: how many ml/cc are in 1 oz?
30mL; context: ~5oz of CSF fluid- 150mL
What is another name for the sympathetic nervous system?
thoracolumbar... because it arise from T1-L2
Sympathetic cardiac accelerator fibers arise from _______.
_______ is formed by the inferior cervical and first thoracic ganglia.
stellate ganglia... so T1--> so, some effect to the cardiac accelerators
What is an adverse reaction that can be seen with stellate ganglion blockade?
What are the s\s of Horner's syndrome?
ipsilateral miosis, ptosis, enophthalmos, flushing, increased skin temperature, anhydrosis, and nasal congestion
ALL preganglionic fibers pass through white rami communicans in route to the paravertebral ganglia. Name the 3 fates of preganglionic fibers:
1) some preganglionic fibers synapse in paravertebral ganglia with the sympathetic postsynaptic neuron--> these sympathetic postganglionic neurons pass through gray rami communicans to reach the spinal nerve, after which they travel to the skin where they constrict skin arterioles and stimulate sweat glands
2) some preganglionic fibers ascend or descend in the paravertebral ganglia before synapsing with postganglionic neurons
3) some preganglionic neurons pass through the paravertebral ganglia without synapsing; these fibers synapse with postganglionic neurons in the peripheral ganglia
**KEY concept--> all preganglionic fibers pass through WHITE rami, while some but NOT ALL sympathetic postganglionic fibers pass through GRAY rami
_____ rami allow coordinated, mass discharge of the sympathetic nervous system.
What happens when presynaptic alpha 2 receptors are stimulated by NE or any other drug with alpha 2 receptor agonist activity?
release of norepinephrine is DECREASED--> this is negative feedback
When Ca++ goes in... what comes out?
Explain the termination of NE.
once NE is diffused away from receptor (1st step), 80% goes back into terminal (reuptake)--> COMT and MAO metabolize the remaining 20%
What are the end products of NE?
-VMA (found in urine)--> tested for pheochromocytoma
What are the steps in the synthesis of norepinephrine?
Tyrosine from the bloodstream enters the nerve terminal--> tyrosine to l-dopa by hydroxylase--> l-dopa to dopamine by acid decarboxylase--> dopamine to norepinephrine by dopamine B-hydroxylase--> norepinephrine to epinephrine
What is required to enter the nerve terminal in order for the neurotransmitter to be released? (example: the release of norepinephrine)
Ca+; depolarization of voltage gated Ca+ channels
ex: in the case of NE: Ca+ channels open--> Ca+ unites with calmodulin, and this complex initiates a series of reactions leading to exocytosis--> NE diffuses into the synaptic cleft
What is norepinephrine?
A ligand, vasoactive substance, neurotransmitter....
What is the first step in the termination of action of most ligands?
diffusion of the ligand away from the receptor; ex) NE: 80% is reuptake into presynaptic nerve terminal
What is the most frequently used indirect acting sympathomimetic that also stimulates adrenergic receptors directly, making it also a direct acting agent?
What agents should be avoided in the patient taking an MAO inhibitor?
-indirect acting sympathomimetics (ephedrine)
-one opioid= merperidine (demerol)--> like ephedrine, triggers the release of NE--> this excess release of NE may cause a HTN crisis b\c pt taking MAO inhibitors are unable to effectively metabolize NE in the synaptic cleft
In general, what are the 6 main responses seen with activation of the sympathetic nervous system?
1) increased HR
2) increased CO
3) increased BP
4) dilate bronchial tree
5) shunt blood away from intestines and other viscera to better supply skeletal muscle
6) increase blood glucose concentration
What controls 85% of the resting blood pressure?
Renin is released from ______ cells of the _______ _______.
juxtaglomerular cells of the afferent arteriole
Renin converts ________ to ___________.
converts angiotensinogen (protein released by the liver) to angiotensin I
Angiotensin I is converted to angiotensin II by ________ found _________.
ACE (angiotensin converting enzyme); found on endothelial surface of capillaries and especially prominent in pulmonary capillaries
Angiotensin II promotes _______ and also a release of _______.
vasoconstriction and also release aldosterone
Name the 2 MOST potent and 2 LESS potent stimuli for release of aldosterone.
1) angiotensin II
2) high serum K+
1) low serum NA+
What is a more potent vasoconstrictor, ADH (vasopressin) or angiotensin II?
ADH (Vasopressin); controversial
What are the two primary effects of aldosterone?
1) increase K+ secretion (and excretion)
2) increase Na reabsorption (Na retention)--> volume expansion
What causes renin release?
1) decreased renal BP (renal artery stenosis)
2) increased SNS activity
_______ is used to treat complete heart block. (chemical pacemaker)
isoproterenol (1-5mcg/kg/min continuous infusion)
_______ occurs in response to chronic exposure to an agonist.
______ occurs in response to chronic exposure to an antagonist.
up regulation (suppress it and it finds a way)
_______ occurs when the number of receptors diminishes.
_______ occurs when the number of receptors increases.
In CHF, the high sympathetic outflow (to compensate for decreased heart pump performance) results in _________ regulation of beta 1 adrenergic receptors.
________ regulation occurs in a patient that is beta blocked. If the beta blocked person was abruptly withdrawn from their medication, the response would be _________ and __________ contractility b/c of the __________ number of beta 1 receptors.
up regulation occurs--> if abrupt withdrawal= tachycardia and increased contractility d\t excessive number of beta 1 receptors
*could lead to myocardial ischemia or infarction if the pt has CAD
What is another name for parasympathetic outflow?
Where does the parasympathetic or craniosacral outflow arise from?
cranial nerves III, VII, IX, X (3,7,9,10) and sacral segments S2, 3, 4.
CN ______ arises from the midbrain. CN ______ arises in the pons. CN _____ & _____ arise from the medulla.
III (oculomotor) from midbrain; VII (facial) from pons; IX and X (glossopharyngeal and vagus) from medulla
What are the 3 primary functions of the parasympathetic (craniosacral) nervous system?
1) conserve energy
2) maintain organ function
3) support vegetative processes (resting and digesting)
The massive discharge of this system would leave its victim helplessly salivating, wheezing, weeping, vomiting, urinating, defecating, and seizing.
What physiologic responses are seen with parasympathetic stimulation?
-pupils constrict (miosis)
-decreased conduction through the AV node
-slight decrease in myocardial contractility
-increased secretions, increased gastric acid secretion, increased digestive enzymes and HCO3 from the pancreas into the small intestine
The drug pilocarpine is used to treat narrow angle glaucoma. What kind of drug is it? What does it do?
(parasympathomimetic) muscarinic receptor agonist--> produces miosis--> facilitates drainage of aqueous humor--> so, IOP decreases
Do cholinesterase inhibitors act directly or indirectly? Why?
indirectly--> they raise concentration of AcH at synapses--> the AcH has the direct effects
What are the 5 primary responses seen with stimulation of muscarinic receptor sites?
2) enhanced gastric acid secretion
3) hyperperistalsis (stimulation of GI contractions)
4) miosis (constriction of pupils)
What should be your concern with a patient taking echothiophate? What is it used for?
used to treat glaucoma; it is a much longer acting cholinesterase inhibitor than neostigmine or edrophonium; placed on eye topically; these patients have depressed plasma cholinesterase activity--> prolonged Sux and mivacurium
What are the s\s of cholinergic syndrome?
miosis, salivation, bronchoconstriction, bradycardia (all muscarinic); weakness (nicotinic); confusion, seizures (all CNS)
What are the treatments for cholinergic syndrome?
-Atropine 35-70mcg/kg every 3-10 min until muscarinic symptoms disappear
-Pralidoxime (protopram) 15mg/kg IV every 20 min until skeletal muscle weakness is reversed (pralidoxime reactivates acetylcholinesterase)
-diazepam (for seizures)
What is the difference in an anticholinergic and antimuscarinic?
-anticholinergic: antagonize ach in CNS, autonomic ganglia, at tissues innervated by parasympathetic postganglionic nerves, and skeletal NMJ
-antimuscarinic: antagonize neural impulses at muscarinic receptor sites