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73 Cards in this Set
- Front
- Back
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What is another name for the parasympathetic nervous system?
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craniosacral
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What is another name for the sympathetic nervous system?
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thoracolumbar
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What do all preganglionic fibers release?
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acetylcholine (acts on nicotinic receptors)
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What is the length of preganglionic parasympathetic fibers?
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long
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What is the length of the postganglionic parasympathetic fibers?
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short
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What do postganglionic parasympathetics release?
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acetylcholine (act on muscarinic receptors)
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Where are the cell bodies of the preganglionic sympathetic nerve fibers?
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lateral horn of the gray matter of the thoracic and lumbar spinal cord
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Where do the preganglionic sympathetic neurons terminate?
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- paravertebral chains (postganglionic release NE)
- prevertebral ganglia (postganglionic release NE) - adrenal medulla (release epi right into blood stream) - postganglionics to sweat glands release acetylcholine - those innervating the renal vasculature release dopamine |
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What does the myenteric plexus (Auerbach's plexus) do?
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controls contraction and relaxation
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What does the submucosal plexus (Meissner's) do?
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controls secretions, absorption, and blood flow
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What effect does seratonin have on the GI tract?
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it is the major intrinsic transmitter and is excitatory
IT increases GI activity and stimulates peristalsis through various receptors |
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What effect does nitric oxide have on the GI tract?
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it is the major inhibitory transmitter an
although VIP, ATP and pituitary adenylate cyclase-activating peptide also inhibit GI activity |
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What do Substance P and Neurokinin A do ?
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released in combo with Ach and contribute to excitation, as does ATP acting on P2X purinergic receptors
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What is vesamicol?
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a compound that blocks the transport of Ach into the vesicles
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What can block the release of Ach?
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botulinum toxin - it interferes with the fusion proteins by digesting them
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What is the lifespan of Ach?
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milliseconds
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What is hemicholinium?
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a compound that can block the transporter that takes choline back up into the nerve terminals
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What is reserpine?
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a drug that inhibits catecholamines' uptake into vesicles by VMAT
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What is the main mechanism for termination of the action of NE in the synaptic cleft?
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Reuptake into the terminal by the norepinephrine transporter (NET aka Reuptake 1)
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Where is MAO located? What does it do?
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on the outer surface of mitochondria in the nerve terminal. It breaks down free NE in the mobile pool in the nerve terminal
(it is also found in the liver and GI tract where it contributes to breakdown of circulating NE and Epi) |
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Where is COMT located? What does it do?
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found throughout the body, especially in the liver and breaks down circulating NE and epinephrine
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What does MAO do in relation to food?
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Breaks down tyramine that is ingested in food, preventing it from being absorbed.
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What does Dopamine form when broken down?
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Homovanillic acid (HVA)
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How are levels of NE and Epi metabolism measured?
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concentrations of 3-methoxy-4-hydroxy-mandelic acid
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Blood vessels receive primarily what kind of innervation?
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sympathetic
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Sweat glands receive primarily what kind of innervation?
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sympathetic
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Which nervous system has been referred to as trophotrophic? What does that mean?
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Parasympathetic system
"leading to growth" |
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Which nervous system has been called ergotropic? What does it mean?
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sympathetic nervous system
leading to energy expenditure |
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Where are nicotinic receptors located?
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on autonomic ganglia
in the brain on skeletal muscle |
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What are nicotinic receptors?
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fast acting receptors linked to sodium channels, which are opened to produce depolarization
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Are cholinesterase inhibitors direct acting or indirect acting?
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indirect acting
they do not stimulate the receptor, but instead amplify the effects of ACh and increases its effectiveness at both nicotinic and muscarinic receptors |
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What attributes to nicotine's addictive properties?
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It causes a release of dopamine in the nucleus accumbens and prefrontal cortex
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What are some symptoms of nicotine poisoning?
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Vomiting
Convulsions (from CNS stimulation) followed by coma and respiratory arrest Muscle contractions due to NMJ stimulation Hypertension and cardiac arrhythmias followed by hypotension |
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How do we treat nicotine poisoning?
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atropine to block muscarinic receptors
with anticonvulsants to decrease seizures with mechanical respiration until nm blockade is reversed |
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Why are cholinesterase inhibitors used in myasthenia gravis?
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to prolong the action of ACh in the synaptic cleft
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What is SLUDGE?
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The muscarinic manifestations of Salivation
Lacrimation Urination Defecation Gastric distress Emesis often seen in organophosphate toxicity |
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If exposure to organophosphates is by inhalation what symptoms will manifest first?
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symptoms of respiration and in the eye will occur first
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If oral administration of organophophates occurs, what are the symptoms to observe first?
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GI symptoms
decreased BP with a compensatory increase in sympathetic tone |
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What will cause death in patients with organophosphate toxicity?
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from respiratory paralysis - 5 minutes to 24 hours after, depending on severity of exposure and agent used
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What are the treatments for organophosphate toxicity?
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atropine
2-PAM maintenance of respiration |
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In who would tachycardia as a result of atropine be most noticeable?
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healthy young adult with high vagal tone
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Would a cholinergic antagonist have an effect on the ventricles? Why/Why not?
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No! they don't receive parasympathetic innervation
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What is the "saying" to remember the effects of atropine poisoning?
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Dry as a bone, blind as a bat, mad as a hatter, red as a beet
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When do we know we have injected enough atropine to counteract cholinesterase inhibitor poisoning?
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inject until dry mouth and mydriasis appear, which indicates that the muscarinic receptors are being effectively treated
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What is the backbone structure of all neuromuscular blocking agents?
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2 molecules of ACh
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How are the non-depolarizing neuromuscular blockers administered?
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must be injected IV due to their highly ionized state. (also why they don't cross BBB and don't cause CNS effects)
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What is the sequelae of neuromuscular blocking agents' effects?
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Small muscles (eye, jaw, larynx) are generally affected first, followed by larger muscles (limbs and trunk). The intercostal muscles of the diaphragm are the last to be paralyzed and the first to be recovered.
*Recovery occurs in the reverse order of paralysis! |
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In reference to the "train of four" or the "double burst" how do nondepolarizing agents effect twitch height?
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causes a "fade" represented by decrease in twitch height
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In reference to the "train of four" or the "double burst" how do depolarizing blockade (succinylcholine) effect twitch height?
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the size of each twitch is reduced but there is no fade in the twitch height
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What is post-tetanic potentiation?
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Tetanic stimulation releases a large amount of Ach. Because nondepolarizing blockers are competitive antagonists, the increased Ach following tetanus will result in transient relief of the block. Therefore, the response following a period of tetanus will be larger than normal.
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What is Dibucaine number?
What is normal/abnormal? |
genetic differences in ability to metabolize succinylcholine are expressed in terms of Dibucaine number
80% is normal 20% is abnormal |
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What is Dibucaine?
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a local anesthetic that causes inhibition of AChE
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What may occur in succinylcholine administration to people with burns, nerve degeneration, head trauma, infection, kidney disease, etc.?
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May cause a pronounced release of potassium in the blood. If the rise is high enough, cardiac arrest may occur. This is a life-threatening situation especially in patients with CHF.
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What may happen in heavily muscled patients when given succinylcholine?
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may increase intragastric pressure and cause regurgitation and aspiration
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What antibiotics enhance neuromuscular blockade? How?
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Aminoglycoside antibiotics (streptomycin) by decreasing ACh release through blockade of prejunctional Ca2+ chanels
Tetracylcines may also enhance neuromuscular blockade through Ca2+ chelation |
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How are the effects of the non-depolarizing neuromuscular blockers reversed?
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administration of cholinesterase inhibitors (usually neostigmine or purridostigmine) which increase ACh both by inhibiting AChE and increasing ACh release
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What is the optimum distance between the quaternary ammonium groups for the muscle receptor?
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10
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What is the optimum distance between the quaternary ammonium groups for the ganglionic receptor?
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6
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What abolishes the effect of indirectly acting adrenergic drugs?
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denervation or depletion of NE stores with the drug Reserpine
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In people with atherosclerosis, what is the concern with treating them with alpha agonists?
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The baroreceptor response may be repaired, and the effects of alpha agonists on blood pressure may be magnified
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What is the specific effect of alpha agonists on the eye?
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they cause mydriasis without affecting accommodation
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What effect do alpha agonists have on intraocular pressure? What is the mechanism?
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Alpha receptors decrease the production and increase removal of aqueous humor, decreasing intraocular pressure.
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What happens when both alpha 1 and alpha 2 receptors are blocked?
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Since stimulation of alpha2 receptors normally modulates (decreases) NE release, removing this modulation will enhance the release of NE and beta receptor stimulation will become more pronounced
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Where are alpha1A receptor subtype prominent?
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in the prostate
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Where are Alpha 1B receptor subtypes prominent/important?
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blood vessels
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How do beta blockers reduce intraocular pressure?
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by decreasing production of aqueous humor
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What is the problem with administering beta blockers to diabetics?
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Glucagon response become impaired in DM-I and inhibiton of glycogenolysis and decreased release of glucose from the liver due to beta blockade may impair the ability of diabetics to recover from hypoglycemia
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What will overdose of beta blockers cause?
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Hypotension and bradycardia, with longer AV conductin time and a widened QRS complex
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What are the first choice drugs for treatment of open angle glaucoma?
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prostaglandin analogues
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What are the second choice drugs for treatment of open angle glaucoma?
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beta blockers
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What are the third choice drugs for treatment of open angle glaucoma?
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the selective alpha 2 agonists (apraclonidine and brimonidine)
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How do carbonic anhydrase inhibitors work?
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they work in the epithelium of the ciliary body to decrease formation of bicarb ions, decreasing fluid production and intraocular pressure
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What is the relationship between alpha 2 receptors and NE?
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blocking a2 receptors causes an increase of NE release
on the other hand - a2 agonists block the release of NE |
