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Volume 1

Peripheral Nervous System

QuestionAnswer
What are the two divisions of the peripheral nervous system? somatic and autonomic
The somatic nervous system sends ___ impulses to the ___. motor (efferent) to the skeletal muscle
Somatic sensory nerves carry impulses that are _____. perceived (touch, pressure, temperature, pain)
What are the two divisions of the autonomic nervous system? sympathetic and parasympathetic
Describe the length of pre and post ganglionic nerves of the sympathetic nervous system. Sympathetic Preganglionic: short; postganglionic: long
Describe the length of pre and post ganglionic nerves of the parasympathetic nervous system. Parasympathetic: Preganglionic: long; postganglionic: short
The autonomic preganglionic neurons synapse with the postganglionic neurons at the autonomic ____. ganglia
The adrenal medulla is innervated by ____ _____ neurons. sympathetic preganglionic
What is the predominant neurotransmitter of the periphery? acetylcholine
Where is acetylcholine released from? somatic motor nerves, preganglionic sympathetic nerves, preganglionic parasympathetic nerves, and postganglionic parasympathetic nerves
Where is norepinephrine released from? sympathetic postganglionic nerves
What is the exception to release of norepi from sympathetic postganglionic nerves? sweat glands
What is released from sweat gland sympathetic postganglionic nerves? acetylcholine
What is the adrenal medulla innervated by? sympathetic preganglionic neurons
Acetylcholine released from sympathetic preganglionic neurons elicits the release of ___ from the adrenal medulla. hormones
Where are muscarinic receptors found? on tissues innervated by the parasympathetic nervous system
Where are nicotinic receptors found? at the autonomic ganglia, on cells of the adrenal medulla, and at the motor end plate of skeletal muscle.
Where are adrenergic receptors found? on tissues innervated by the sympathetic nervous system ( except sweat glands)
What type of receptors are located on sweat glands? muscarinic- acetylcholine is released from the sympathetic post-ganglionic neuron to muscarinic receptors
Are nicotinic receptors found on sympathetic or parasympathetic postganglionic neurons? both
Nicotinic receptors respond to __ or __ agonists in a ___ fashion. ACh, ACh, biphasic
What effect does ACh have on nicotinic receptors in small doses? ACh stimulates nicotinic receptors of postganglionic sympathetic and parasympathetic neurons as well as nicotinic receptors of the skeletal muscle end plate to cause depolarization
What effect does ACh have on nicotinic receptors in large doses or with prolonged exposure? the nAChR becomes desensitized to succinylcholine and the postsynaptic membrane becomes non-excitable.
What is this block called when it occurs at the motor end plate of skeletal muscle? Phase II block or desensitization block
What neurons conduct action potentials faster, those with larger diameters or those with smaller diameters? neurons with larger diameters conduct action potentials at greater speeds
What is the function of A alpha fibers? efferents adjust skeletal muscle force and length
A alpha and A beta sensory fibers are responsible for _____. proprioception
dC fibers carry sensations of what? throbbing pain and temperature
A delta fibers carry sensations of what? sharp, prickling pain and temperature
Sympathetic and parasympathetic preganglionic neurons are ____ fibers. B fibers
Postganglionic sympathetic neurons are ____ fibers. C fibers
Do myelinated or unmyelinated nerves conduct action potentials at greater velocities? myelinated
The thoracolumbar outflow arises from which segments? T1-L3
The thoracolumbar outflow is also called ___. sympathetic
Where do most sympathetic preganglionic neurons synapse with postganglionic fibers? in the paravertebral ganglia
Sympathetic cardiac accelerator fibers arise from ___. T1-T4
The stellate ganglion is formed by the what two ganglia? inferior cervical and first thoracic ganglia
What are signs and symptoms of Horner's syndrome? ipsilateral miosis (constriction), ptosis (drooping eyelid), enophthalmos (no eyes), flushing, increased skin temperature, anhydrosis (no sweating), and nasal congestions
What is Horner's syndrome a result of? stellate ganglion blockade
Where do sympathetic preganglionic neurons arise? in the intermediolateral horn
All preganglionic fibers pass through the ___ ___ communicans in route to the paravertebral ganglia. white rami
What are the three fates of preganglionic fibers? 1. some synapse in the paravertebral ganglia with the sympathetic postsynaptic neuron 2. Some ascend or descend in the paravertebral ganglia before synapsing with postganglionic neurons 3. some pass through the paravertebral ganglia without synapsing
What happens to sympathetic neurons that synapse in the paravertebral ganglia at their level? the sympathetic postganglionic neurons pass through the grey rami communicans to reach the spinal nerve, after which they travel to the skin where they constrict skin arterioles and stimulate sweat glands
Preganglionic neurons that pass through the paravertebral ganglia without synapsing, where do they synapse with postganglionic neurons? in peripheral ganglia
Preganglionic white rami are distributed to which spinal nerves? those arising from T1-L2
Grey rami are distributed to which spinal nerves? all spinal nerves from the ganglia
Grey rami allow for what? coordinated, mass discharge of the sympathetic nervous system
What is the sympathetic equivalent of an ANS nerve terminal? varicosity
The varicosity is the site of what? synthesis and release of norepi
What type of receptors are present in the surface of the nerve terminal of the sympathetic post ganglionic neuron? alpha 2 receptors
When the presynaptic alpha 2 receptors are stimulated by norepi or any other drug with alpha 2 receptor agonist activity, the synthesis and release of norepi is increased or decreased? decreased
Is this positive or negative feedback? negative
The presence of postsynaptic alpha 2 receptors s explains what? the early transient hypertension seen following a dose of clonidine
In the synthesis of norepinephrine where is tyrosine transported into the nerve terminal from? bloodstream
List the cascade of catecholamine formation Tyrosine -L dopa - dopamine - norepinephrine - epinephrine
Where is norepi converted to epi? adrenal medulla
Norepi comprises __% and and epi comprises __% of the norepi/epi pool in the adrenal medulla. norepi 20% and epi 80%
Where is norepi stored? presynaptic vesicles
Describe the steps involved in the release of norepi. AP travels along axon of symp post gang neuron; depolarization opens voltage gated Ca channels, Ca diffuses through channels into nerve terminal down gradient, Ca united w/calmodulin, this complex leads to exocytosis; norepi diffuses into synaptic cleft.
Describe the response of tissue to norepi. Norepi combines with adrenergic receptors of postsynaptic membrane, norepi-receptor complex causes activation of adenylate cyclase; second messengers have tissue specific actions-> arterial smooth muscle contracts, HR increases, contractility increases
What is the first step in the termination of the actions of Norepi? diffusion of norepi (ligand) away rom receptors
How else are the actions of norepi terminated? norepi is actively transported back into the presynaptic nerve terminal; small amounts of NE are metabolized in the synaptic cleft by MAO; small amounts of NE diffuse into the bloodstream, once in the vascular compartment, NE is metabolized by COMT
How is 80% of released norepi returned to the nerve terminal? reuptake via active transport
Where is MAO found? on the surface of mitochondria, some MAO leaks from the nerve terminal into the synaptic cleft
What does MOA stand for? mono-amine-oxidase
What does COMT stand for? catechol-O-methyl transferase (COMT)
Indirect acting sympathomimetics act how? by displacing norepinephrine from sympathetic nerve terminals
What is the most frequently used indirect acting sympathomimetic? ephedrine
Why should Demerol (meperidine) be avoided when taking an MAO inhibitor? meperidine triggers the release of norepi
What happens when ephedrine or demerol are administered to a patient taking an MAO inhibitor? the release of excess amounts of norepi may cause a hypertensive crisis
Which causes a more severe reaction, ephedrine or demerol - and MAO inhibitor? demerol
In response to internal or external changes, the sympathetic nervous system acts to: increase HR, CO, and BP, dilate bronchial tree, shunt blood away from intestines and other viscera to better supply skeletal muscle, increase blood glucose concentration
The sympathetic nervous system is needed for the emergency response to stressful situations; it (is/is not) necessary for survival. is not
Where are alpha 1 adrenergic receptors found? peripherally in a variety of tissues such as (vascular smooth muscle, glands) innervated by sympathetic postganglionic neurons
What are the results of stimulation of alpha 1 receptors? excitatory response: contraction of vascular smooth muscle; arterial and venous vasoconstriction -> increased systemic vascular resistance -> increased systemic ABP; venoconstriction: inc venous return, inc SV, increased CO -> increase systemic ABP
Where are alpha 2 receptors found? on presynaptic nerve terminals of sympathetic postganglionic neurons, tissues on postsynaptic membranes in the brainstem and in the peripheral tissues
What occurs with stimulation of alpha 2 receptors on sympathetic postganglionic, presynaptic nerve varicosities? inhibition of norepinephrine synthesis and release
Is this positive or negative feedback system? negative
What occurs with stimulation of postsynaptic alpha 2 receptors in the brainstem? inhibits outflow of the sympathetic nervous system
What occurs with stimulation of alpha 2 receptors in the substantia gelatinosa of the spinal cord? promotes analgesia ( this response is unrelated to sympathetic nervous system function
Where are beta 1 receptors found? heart, kidney, and adipose tissue
Stimulation of beta 1 receptors is ___. excitatory
What effects does beta 1 stimulation produce? increase in HR, increase in myocardial contractility -> increase in CO -> increase in arterial blood pressure
Where are beta 2 receptors found? in smooth muscle and in glandular tissue
Stimulation of beta 2 receptors in smooth muscle is (stimulatory/inhibitory). inhibitory
Beta 2 adrenergic receptor stimulation causes what? skeletal muscle blood vessel dilation, small decrease in SVR, bronchodilation, and relaxation of pregnant uterus.
What does beta 2 adrenergic receptor stimulation of hepatocytes result in? stimulates glycogenolysis and gluconeogenesis, and increased blood glucose levels
What is glycogenolysis? breakdown of glycogen to glucose
What is gluconeogenesis? the formation of new glucose from non carbohydrate sources, namely amino acids
Glycogenolysis and gluconeogenesis (increase/decrease) he concentration of blood glucose and may lead to (hyper/hypo) glycemia. increase, hyperglycemia
Beta 2 receptor stimulation promotes (hyper/hypo)-glycemia. hyperglycemia
Beta 2 receptor stimulation promotes (hyper/hypo)-kalemia. hypokalemia
What are side effects of the beta 2 agonist ritodrine (yutopar)? hyperglycemia, hypokalemia, and tachycardia - because it has some beta 1 adrenergic receptor activity
85% of resting blood pressure is controlled by ____. renin
Where is renin released from? juxtaglomerular cells of the afferent arteriole
What does renin do? converts angiotensinogen to angiotensin I
Angiotensinogen is a protein released into the circulation from ___. the liver
Where is angiotensin converting enzyme found? on the endothelial surface of capillaries
ACE is especially prominent in __ ___. pulmonary capillaries
What does angiotensin II promote? vasoconstriction and aldosterone release
What are the two important stimuli for aldosterone release? angiotensin II and high serum potassium
What are two less potent stimuli for aldosterone release? low serum sodium and ACTH
Which is a more potent vasoconstrictor- angiotensin II or ADH? ADH - this is controversial: Guyton agrees with this, but Barash says angiotensin II is the most potent
Aldosterone increases potassium (reabsorption/excretion) and increases sodium (reabsorption/excretion). potassium excretion, sodium reabsorption
This promotes sodium __ and volume ___. retention and expansion
Renin release occurs in response to what? decreased renal blood pressure and/or increased sympathetic nervous system activity and Cl-
What are the uses for epinephrine? prolong the action of LA, treat life threatening allergic reactions, cardiopulmonary resuscitation (supraphysiologic doses are not necessary), increase myocardial contractility with continuous infusion
Why does epinephrine prolong the action of local anesthetics? decrease systemic absorption
What are the uses for dopamine? to increase cardiac output in pts with low systemic blood pressure, increased atrial filling pressures, and in low urine output
Dopamine increases cardiac output secondary to what? increased myocardial contractility
Dopamine is unique among catecholamines in that it simultaneously increases what? contractility, renal blood flow, glomerular filtration rate, sodium excretion, and urine output
What is isoproterenol used for? to treat complete heart block, acts as chemical pacemaker
What rate of isoproterenol is used to treat complete heart block? 1-5 mcg/kg/min
What is dobutamine used for? increase cardiac output in congestive heart failure, particularly if heart rate and systemic vascular resistance are increased
Dobutamine increases cardiac output secondary to what? secondary to increased myocardial contractility
What is ephedrine used for? to treat hypotension, to treat bronchial asthma (oral administration), and as a decongestant nasal spray
What is phenylephrine used for? hypotension, topical nasal decongestant, prolong the duration of spinal anesthesia when added to local anesthetic solutions
Why may you choose phenylephrine or ephedrine for hypotension in the parturient due to spinal or epidural anesthesia? Phenylephrine is associated with a higher umbilical artery pH and less fetal acidosis at delivery
Diastolic arterial blood pressure changes in the (same/opposite) direction as systemic vascular resistance. same
Decreases in diastolic blood pressure and possibly also mean arterial pressure with low dose epinephrine are attributable to what? beta 2-mediated vasodilation (beta 2 mediated decrease in SVR)
What class of medications would be used to treat reversible bronchospasm and stop uterine contractions of premature labor? beta 2 adrenergic agonists
What specifics drugs would be used to treat reversible bronchospasm? metaproterenol, terbutaline, albuterol, isoetharine, salmeterol
Which specific medications would be used to stop uterine contractions of premature labor? ritodrine and terbutaline
What are side effects of beta 2 adrenergic agonists? tremor, tachycardia, transient decrease in arterial oxygenation, acute metabolic responses-hyperglycemia, hypokalemia, hypomagnesemia- lactic acidosis
What are side effects of ritodrine? tachycardia, hypokalemia, hyperglycemia (ketoacidosis is a risk in insulin dependent diabetics), pulmonary edema-especially if hydration is aggressive
Does ritodrine effect the fetus? yes it crosses the placenta and the same side effects may be seen in the fetus
Name 3 centrally acting sympathomimetics. Clonidine, dexmedetomidine, and alpha-methyldopa
What are the brand names for these drugs? Clonidine: Catapres; dexmedetomidine: Precedex; alpha-methydopa: Aldomet
What is the mechanism of action of centrally acting sympathomimetics? inhibit outflow of the sympathetic nervous system by stimulating postsynaptic a-2-receptors in the brainstem. Stimulation of postsynaptic a-2 receptors in the vasomotor center of the brainstem medulla has an inhibitory action on the symp nervous system
What effects do the central action of clonidine have? analgesia, sedation, and decreased anxiety
Which two centrally acting sympathomimetics also act peripherally? clonidine and alpha-methyldopa
How do these agents work peripherally? by stimulating presynatpic alpha 2 receptors of sympathetic postganglionic neurons, thereby inhibiting the production and release of norepi from these neurons
What is the purpose of using centrally acting sympathomimetics to act peripherally? treatment of hypertension
What may occur with sudden withdraw of clonidine? rebound hypertension
What is rebound hypertension mediated by? catecholamines, renin, and angiotensin II
What class of drug is phenoxybenzamine? a long acting non-selective alpha adrenergic antagonist
What is phenoxybenzamine used for? to control blood pressure in patients with pheochromocytoma
What class of drug is phentolamine? non-selective alpha adrenergic antagonist
What class of drug is yohimbine? a selective alpha 2 adrenergic antagonist
What is yohimbine used to treat? impotence and idiopathic orthostatic hypotension
What class of drug is prazosin? selective alpha 1 adrenergic antagonist
How does the mechanism of action of prazosin differ from nonselective alpha adrenergic antagonists? lowers blood pressure without increasing the release of norepinephrine from postganglionic sympathetic nerve terminals because it dose not block alpha 2 receptors.
What class of drug is propanolol? non selective beta 2 antagonist
What patient population is propanolol avoided in? Why? irritable airways: beta 2 adrenergic receptor blockade can induce bronchoconstriction
What class of drug is esmolol? competitive antagonist of beta1 adrenergic receptors
Why is esmolol short acting? It is metabolized in the plasma by non selective esterases of the red blood cell
What is esmolol used to treat? intraop SVT and intraop hypertension; to blunt the reflex cardiovascular responses to intubation and to produce controlled hypotension
What class of drug is labetalol? competitive antagonist of alpha 1, beta 1 and beta 2 adrenergic receptors
What is labetalol used for? hypertensive emergencies or to produce controlled hypotension
Describe the cardiovascular effects of labetalol. decreases HR, myocardial contractility, and SVR
For labetalol, beta to alpha blockade is __:__. 7:1
What is phentolamine used for? treatment of acute hypertensive emergencies, local infiltration when a sympathomimetic is accidentally administered extravascularly, intraoperative management of pheochromocytoma, treatment of autonomic nervous system hyperreflexia
What is prazosin used to treat? chronic control of blood pressure in patients with pheochromocytoma
When treating hypertension with a beta adrenergic antagonist, what is the mechanism of action? blood pressure decreased secondary to decrease in cardiac output owing to decreased hr; blood pressure decreased secondary to decrease in secretion of renin
Describe the mechanism of action of beta blockers for angina pectoris. decreased myocardial oxygen requirements secondary to decreased heart rate and cardiac output; treatment of post myocardial infarction
Describe the MOA of beta blockers for suppression of cardiac dysrhythmias. Decreased sympathetic nervous system activity to the heart with a resultant decrease in the rate of spontaneous phase 4 depolarization of ectopic cardiac pacemakers (especially if due to digitalis toxicity)
Beta Blockers blunt the excess sympathetic nervous system activity associated with: direct laryngoscopy and intubation; hypertrophic obstructive cardiomyopathies, pheochromocytoma, hyperthyroidism, cyanotic episodes in pts with tetralogy of fallot, reflex baroreceptor mediated increases in hr in pts treated with vasodilators, anxiety
What are the clinical uses of labetalol? hypertensive emergency, angina pectoris, attenuation of increases in blood pressure and hr occurring during and after surgery, treatment of rebound hypertension following withdraw of clonidine
What are the side effects of beta blockers: cardiovascular bradycardia- heart block due to decreased phase 4 depolarization in nodal tissue, decreased myocardial contractility- heart failure; cold hands and feet; reflecting the peripheral vasoconstriction associated with unopposed beta 2 receptor blockade
What are the side effects of beta blockers: airway resistance bronchoconstriction: reflects beta 2 receptor blockade, especially in patients with preexisting obstructive airway disease
What are the side effects of beta blockers: metabolism decreased glycogenolysis (hypoglycemia without the warning sign of tachycardia is a risk in pts with DM); unrecognized hypoglycemia
What are the side effects of beta blockers: hyperkalemia increased plasma potassium concentration (beta 2 adrenergic receptor blockade depresses the activity of the sodium potassium pump; potassium is pumped into cells at a reduced rate, so plasma potassium concentration increases.
What are the side effects of beta blockers: interactions with anesthetics additive myocardial depression - no evidence that this depression is excessive
What are the side effects of beta blockers: nervous system fatigue and lethargy
What are the side effects of beta blockers:fetus bradycardia, hypotension, hypoglycemia
What are the treatment options for excess myocardial depression induced by beta antagonists? atropine, dobutamine, calcium chloride, glucagon, pacemaker; dopamine is NOT recommended
The normal heart functions adequately after beta adrenergic receptor blockade so long as ______ is not abnormally elevated. systemic vascular resistance
Explain why the heart cannot function if SVR is abnormally elevated. With an increase in SVR, the beta blocked heart may be unable to respond to the increased workload, and heart failure may ensue.
Accordingly, the increase in SVR produced by ___ stimulation in the patient who is beta blocked can produce heart failure. adrenergic (sympathetic)
Explain a clinical situation that this would apply to. The patient with pheochromocytoma should be alpha locked prior to instituting beta blockade. Beta receptor blockade without alpha receptor blockade in the patient with pheochromocytoma can cause heart failure.
Which anesthetic agent has the least favorable interaction with beta blockers? ketamine
Which anesthetic agent has the most favorable interaction with beta blockers? Isoflurane
Why is ketamine the least favorable drug to be used with beta blockers? Ketamine stimulates the sympathetic nervous system so it promotes an increase in SVR. this increase in SVR is not compensated by an increase in myocardial contractility bc the heart is beta blocked, so heart failure may ensue
Which produces a greater myocardial depression in the presence of a beta blocker, halothane or enflurane? enflurane
What is down regulation? in response to chronic exposure to an agonist, the number of receptors diminishes
What are clinical examples of down regulation? in a patient with congestive heart failure. The high sympathetic outflow (to compensate for decreased heart pump performance) results in down regulation of beta 1 receptors
What is up regulation? In response to chronic exposure to a competitive antagonist, receptors increase in number
What are clinical examples of up regulation? pts who are beta blocked: if the B bl pt were abruptly withdrawn from medication, the response would be tachycardia and inc contractility bc of the excessive number of B1 receptors, which could lead to myocardial ischemia or infarction if the pt has CAD
What are clinical examples of up regulation? continued any disease or injury that disrupts impulses in the motor nerve innervating the skeletal neuromuscular junction leads to up regulation of nicotinic receptors at the motor end plate as well as proliferation of extrajunctional nicotinic receptors
After injecting local anesthetic into the intrathecal space, you determine that the level of sensory block is T4. What is the anatomical landmark for the T4 sensory dermatome? the nipples
After injecting local anesthetic into the intrathecal space, you determine that the level of sensory block is T4. Do you expect that this patient will develop tachycardia during the case? No. Autonomic block (sympathetic block in this case) is 2-6 dermatomes higher than sensory block. Since symp outflow from T1 to T4 includes the cardioaccelerator fibers, blockade of this segment will prevent tachycardia. The patient may be bradycardic
Your patient has been treated with an MAO inhibitor for depression. General anesthesia is planned for a ruptured appendix. What drug will you most avoid using in this patient? What other drug might you also want to avoid using? Most: meperidine (demerol); ephedrine
Your OB patient is given ritodrine for her premature labor. What kind of dug is ritodrine? a tocolytic, meaning it relaxes the pregnant uterus. More specifically it is a beta 2 adrenergic receptor agonist.
What are three side effects of ritodrine? Hyper or hypoglycemia? Hyper or hypokalemia? Tachycardia or bradycardia? hyperglycemia, hypokalemia, tachycardia
Your OB patient becomes hypotensive and needs a vasopressor. What agent may be best in this situation? Ephedrine dose not appreciable decrease uterine blood flow, and phenylephrine dose not produce fetal acidosis
The patient will undergo surgery to remove a pheochromocytoma: If you were to both beta and alpha block, which would you do first? Alpha block first: alpha blockade causes arterial dilation, a decrease in SVR, and a decrease in afterload. These changes make it easier for the heart to eject blood after beta blockade.
What would happen if beta blockade occurred first? heart failure might result because the beta blocked heart might not be able to eject an adequate stroke volume when systemic vascular resistance and afterload become elevated as a result of increases in circulating epi and norepi
What alpha adrenergic blocker could you use to control hypertension during this case? Phentolamine (Regitine) is an alpha blocker that could be selected
The patient is beta blocked to treat hypertension. The anesthesiologist terminates the beta blocker therapy 48 hours prior to surgery. Preop the pts is tachycardia, hypertensive, and ECG signs of myocardial ischemia.
What explains the tachycardia and ECG changes of myocardial ischemia? When beta receptors are blocked by a competitive antagonis, beta receptors up regulate. When the beta blocker is withdrawn, the unblocked heart with excessive numbers of beta receptors is hypersensitive to catecholamines.
You probaly would treat this problem with what agent? esmolol (brevibloc) because it is short acting and titrating to a desirable blood pressure is fairly easy to accomplish
Should beta blocker therapy be discontinued prior to surgery? no beta blocker therapy generally shoudl not be discontinued prior to surgery.
Your patient is on a high dose beta blocker. You would avoid using what IV general anesthetic? Ketamine: stimulates the sympathetic nervous system which will constrict block vessels and increase systemic vascular resistance and afterload. The beta blocked heart may not tolerate the increased afterload and heart failure may ensure.
What is another name for the parasympathetic nervous system? craniosacral
Where does the parasympathetic nervous system outflow arise from? the midbrain, pons, and medulla of the brainstem and sacral cord (S2-S4)
Which cranial nerves are the midbrain, pons, and medulla associated with? midbrain CN III, pons CN VII, medulla CN IX and X,
Which cranial nerves carry parasympathetic nerves? CN III, VII, IX and X
The ____ transmits fully three-fourths of the traffic of the parasympathetic nervous system. vagus
What is the primary function of the parasympathetic nervous system? to conserve energy and maintain organ function and support vegetative processes
Is the parasympathetic nervous system or sympathetic nervous system more selective and localized in its effects? parasympathetic nervous system
A massive parasympathetic response would only prostrate the organism, leaving it helplessly what? salivating, wheezing, weeping, vomiting, urinating, defecating, and seizing
The parasympathetic nervous system is essential for the _____ _ __ . maintenance of life
Describe the response to the parasympathetic nervous system: eyes pupil constricts
Describe the response to the parasympathetic nervous system: heart decrease heart rate; decreased spread of conduction through atrioventricular node; decreased myocardial contractility
Describe the response to the parasympathetic nervous system: secretions inc salivary, pharyngeal, laryngeal, bronchial secretions; inc gastric acid secretion; inc secretion of digestive enzymes and HCO3 from the pancreas into the small intestine; inc secretion of bile and HCO3 from the liver into the small intestine
Describe the response to the parasympathetic nervous system: smooth muscle bronchoconstriction, gall bladder contraction, increased motility and tone of the stomach and intestines, contraction of the bladder- detruser muscle
Name 6 cholinergic agonists. methacholine, carbachol, bethanechol, pilocarpine, muscarine, arecoline
What is the mechanism of action of cholinergic agonists? these agents combine with and activate muscarinic receptors in the same fashion as ACh. They mimic activation of the parasympathetic nervous system
Describe the treatment of glaucoma. Pilocarpine is used in the treatment of narrow-angle glaucoma. Its applied topically to produce miosis. Drainage of aqueous humor is facilitated by miosis, so intraocular pressure decreases. Carbachol is also a topical treatment for narrow angle glaucoma
Describe the treatment of ileus or urinary retention. Bethanechol is used to treat adynamic ileus and also urinary retention
Name 5 cholinesterase inhibitors. edrophonium, neostigmine, pyridostigmine, physostigmine, echothiopate
What is the mechanism of action of cholinesterase inhibitors? (1) Cholinesterase inhibitors inhibit both true acetylcholinesterase and plasma cholinesterase. True acetylcholinesterase is found peripherally where muscarinic receptors are located (parasympathetically innervated tissues) and where nicotinic receptors are
What is the mechanism of action of cholinesterase inhibitors? (2) located (autonomic ganglia and skeletal neuromuscular junction). Since true cholinesterase is found postsynaptically, cholinesterase inhibitors have postsynaptic actions. Metabolism of ACh is impaired by cholinesterase inhibitors, so acetylcholine levels
What is the mechanism of action of cholinesterase inhibitors? (3) increase at all cholinergic (muscarinic and nicotinic) synapses. The therapeutic actions of edrophonium, neostigmine, and pyridostigmine occur at the skeletal neuromuscular junction, where reversal of nondepolarizing neuromuscular blockade is achieved.
What is the mechanism of action of cholinesterase inhibitors? (4) The primary mechanism of action of these agents is to inhibit true cholinesterase. REcognize that cholinesterase inhibitors act indirectly by raising the concentration of ACh at synapses. The ACh has the direct effects.
What is the mechanism of action of cholinesterase inhibitors? (5) In addition to the inhibition of acetylcholinesterase some cholinesterase inhibitors (edrophonium) may also act presynaptically to trigger the production and release of ACh from presynaptic more terminals.
What are the actions of cholinesterase inhibitors at muscarinic receptor sites? bradycardic, enhanced gastric secretion, hyperperistalsis, miosis and salivation
What are the actions of cholinesterase inhibitors at nicotinic receptors? stimulation of autonomic ganglia, stimulation of neuromuscular junction
What are cholinesterase inhibitors used for? reversal of non-depolarizing neuromuscular blockade; produce parasympathetic effect to treat glaucoma, paralytic ileus, atonic bladder; treat myasthenia gravis; treat anticholinergic syndrome; Alzheimer's, postop analgesia, postop shivering
Describe the actions of cholinesterase inhibitors on plasma cholinesterase. Cholinesterase inhibitors not only inhibit true cholinesterase, they also may inhibit pseudocholinesterase. Neostigmine and pyridostigmine, but not edrophonium, produce marked prolonged inhibition of plasma cholinesterase.
Should you administer a cholinesterase inhibitor after succinylcholine or mivacurium administration? SCh and mivacurium, both metab by plasma cholinesterase, would have their action prolonged if administered after neostig or pyridostig. SCh and mivacurium are contraindicated in pts with chronic cholinesterase inhibitor therapy such as echothiopate.
Is echothiopate longer or shorter acting than other cholinesterase inhibitors? longer acting
Is echothiopate useful for reversing nondepolarizing neuromuscular blockade? no
What is the main use of echothiopate? treatment of glaucoma
Echothiopate that is absorbed systemically inhibits ___ ____ activity. plasma cholinesterase: the actions of succinylcholine and mivacurium are prolonged
What common chemicals are also cholinesterase inhibitors? organic insecticides
Physostigmine can produce signs and symptoms of excessive ____ peripherally and in the brain (centrally). acetylcholine
The farmer who uses insecticides may fall victim to ____ syndrome. cholinergic
What are symptoms of cholinergic syndrome? muscarinic: miosis, difficulty focusing, salivation, bronchoconstriction, bradycardia, abdominal cramps; nicotinic: weakness (ranging from mild weakness to paralysis); CNS; dysphoria, confusion, ataxia, seizures, coma
What is the treatment for cholinergic syndrome? atropine, 35-70mcg/kg IV every 3-10 minutes until muscarinic symptoms disappear; pralidoxime 15 mg/kg IV every 20 minutes until skeletal muscle weakness is reversed; diazepam
Why would you give diazepam for cholinergic syndrome? seizures
How does pralidoxime work to treat cholinergic syndrome? pralidoxime reactivates acetylcholinesterase
How will excessive doses of acetylcholinesterase inhibitors affect nondepolarizing neuromuscular blockade? In excessive doses, acetylcholinesterase inhibitor can paradoxically potentiate a nondepolarizing neuromuscular blockade
How will administration of acetylcholinesterase inhibitors affect depolarizing neuromuscular blockade ? Acetylcholinesterase inhibitors prolong the depolarization block of succinylcholine.
Define anticholinergic. a drug that antagonizes transmission of neural impulses at any site where ACh is the NT; may antagonize ACh in the CNS, at the autonomic ganglia, at tissues innervated by parasympathetic postganglionic nerves, or at the skeletal neuromuscular junction
Define antimuscarinic. A drug that antagonizes the transmission of neural impulses at sites where there are muscarinic receptors; antimuscarinics competitively antagonize the actions of acetylcholine at tissues innervated by parasympathetic postganglionic nerve
Name 3 antimuscarinic agents. atropine, scopolamine, glycopyrolate
What is the mechanism of action of antimuscarinics? competitive inhibitors; they combine with muscarinic receptors and prevent ACh from interacting with the receptors
What are the sites of action of antimuscarinics? tissues innervated by parasympathetic postganglionic nerves. Blockade of postsynaptic muscarinic receptors leads to responses opposite those seen with parasympathetic nervous system stimulation.
Scopolamine and Atropine also have actions at site of ___ transmission in the CNS because they ____. cholinergic; they cross the blood brain barrier
Describe changes in parasympathetic nervous system function produced by antimuscarinic drugs. pupillary dilation, failure of accommodation, tachycardia, inc speed of condution through AV node, dec salivary and pharyngeal secretons, dec bronchial secretions, bronchodiltion, dec tone and motility of lower esoph sphincter, decreased bladder tone
Which antimuscarinic least crosses the blood brain barrier? Why? glycopyrolate, because it has a charged quarternary ammonium group
What are CNS effects of atropine and scopolamine? in clinical doses, atropine has sedative and amnesic actions. Scopolamine has a more marked and longer lasting sedative effect than atropine. scopolamine is a good amnesic. It may also produce euphoria. It is used prophylactically to treat motion sickness
What may develop in response to high doses of atropine or scopolamine? anticholinergic syndrome
How is central cholinergic syndrome characterized? by behaviors such as restlessness, shivering, mania, hallucinations, delirium, drowsiness, coma, excitation, agitation, disorientation, short term memory loss, emotional instability, and motor incoordination
These symptoms are due to what? excessive antagonism of muscarinic receptors in the brain
What are peripheral manifestations of anticholinergic syndrome? blurred vision, dry mouth, tachycardia, dry and flushed skin, rash over face, neck and upper chest, and hypotension
Which group of patients are most sensitive to antimuscarinics and are most likely to experience the anticholinergic syndrome? pediatric and geriatric patients
What is anticholinergic syndrome treated with? cholinesterase inhibitor physostigmine 15-60mcg/kg IV
Physostigmine is (ionized/nonionized), (tertiary/quarternary) ammonium, lipid (soluble/insoluble), and (does/does not) readily cross the blood brain barrier. nonionized, tertiary, lipid soluble, does
Do antimuscarinics decrease the tone of the upper or lower esophageal sphincter? lower
Explain why the probability of esophageal reflux increases when the patient is given an antimuscarinic drug? A decrease in tone of the lower esophageal sphincter may promote esophageal reflux since intragastric pr is normally much higher than intraesophageal pr. Maintaining normal lower esophageal sphincter tone is important for preventing esophageal reflux
Bronchial smooth muscle tone is under the influence of ___ second messenger systems and ___ second messengers. 3 and 4
Bronchodilation is promoted by stimulation of ____ adrenergic receptors. B2
Name non selective adrenergic agonists. epinephrine, isoproterenol, ephedrine
What receptors do epinephrine, isoproterenol, and ephedrine work on? epi: a1, a2, b1, b2; isoproterenol: b1, b2; ephedrine: a1, a2, b1, b2
Bronkosol contains isoetharine in solution for ____. nebulization
Bronkometer contains isoetharine in a _____. metered dose inhaler
Do beta 2 selective adrenergic agonists have B1 receptor adrenergic activity? yes some
Because of this, in higher doses, beta 2 agonists may have what effects? tachycardia, hypertension and palpitations
___ ____ is a common occurrence following administration of a beta 2 selective adrenergic agonist. This is particularly true for __ and ___. muscle tremor; terbutaline and albuterol
What GI effects may beta 2 agonists have? nausea and vomiting
Why may hypokalemia occur with beta 2 agonists? beta 2 agonists stimulate the sodium potassium pump driving potassium into the cell
Nonspecific inhibition of phosphodiesterase leads to an accumulation of ___ and bronchi___. cAMP and bronchodilation
____ also competeiively antagonize the adenosine receptors. xanthines
Name two drugs that are xanthines. theophylline and aminophylline.
What are CNS effects of xanthines? CNS is stimulated by xanthines, nervousness, anxiety, insomnia, and nausea and vomiting
What are respiratory of xanthines? bronchodilation, respiration is stimulated- the respiratory centers become more responsive to CO2
Aminophylline is used to treat what respiratory related issue? neonatal apnea
What are common adverse effects associated with chronic therapy with a xanthine? anorexia, nausea, vomiting, and abdominal discomfort
What occurs with serious toxicity of xanthines? seizures, arrhythmias, coma, cardiorespiratory arrest
Does aminophylline cross the placenta? yes
Describe how antimuscarinics cause bronchodilation? they antagonize ACh and consequently cause bronchodilation because less IP3 is produced in the cell, so less calcium is available to the contractile proteins
Are volatile inhaltional agents potent bronchodilators or bronchoconstrictors? bronchodilators: they have been used successfully in the treatment of status asthmaticus
What class of drug is cromolyn sodium? inhibitor of mast cell histamine release
What is cromolyn sodium to treat? prophylactic treatment with cromolyn sodium prevents histamine release and bronchoconstriction
What action do steroids have on bronchioles? glucocorticoids such as cortisol probably have multiple actions in reversing asthmatic obstruction: reduction of inflammatory mucosal swelling and edema, bronchial smooth muscle relaxation, bronchial vasoconstriction, decreased capillary permeability
What effect may steroids have on b2 receptors? steroids may restore responsiveness of asthmatic patients to beat 2 receptor stimulation
What type of drug is doxapram? respiratory stimulant
What is the action of doxapram? doxapram is a general CNS stimulant; it increases alveolar ventilation and thus can be used to reverse respiratory depression
Name three leukotriene antagonists. zileuton, montelukast, zafirlukast
What is the mechanism of action of leukotriene antagonists? zileuton impairs conversion of arachidonic acid to leukotrienes. Montelukast and Zafirlukast are leukotriene rcptr competitive antagongists. All leukotriene antagonists dec bronchospasm, vasoconstriction, and eosinophil recruitment producd by leukotrienes
Created by: valleyanesthesia