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Volume 1
Peripheral Nervous System
| Question | Answer |
|---|---|
| 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 |
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