Term
| neurotransmitter of preganglionic autonomic neurons |
|
Definition
|
|
Term
| Receptor type present in all postganglionic neurons |
|
Definition
| nicotinic cholinergic (N) receptors |
|
|
Term
| neurotransmitter of parasypmathetic post-ganglionic nerves |
|
Definition
|
|
Term
| Basic type of receptor on parasympathetic target organs |
|
Definition
| muscarinic (M) cholinergic receptors (M1-5) |
|
|
Term
| Neurotransmitter of sympathetic post-ganglionic nerves |
|
Definition
|
|
Term
| basic type of receptor on sympathetic target organs |
|
Definition
| adrenergic receptors (alpha and beta) |
|
|
Term
| this is organized for local regulation of innervated target organs |
|
Definition
| parasympathetic division of ANS |
|
|
Term
| This is organized for coordinated activation of all innervated target organs |
|
Definition
| Sympathetic division of ANS |
|
|
Term
| ------- cells in adrenal medulla release -----when stimulated by ------ |
|
Definition
| Chromaffin cells, epinepherine, ACh from the sympathetic divison |
|
|
Term
| Three methods of neurotransmitter metabolism |
|
Definition
| uptake, degredation, diffusion |
|
|
Term
| Main method of ACh metabolism |
|
Definition
| degradation by the enzyme acetylcholinesterase |
|
|
Term
| Three types of catecholamines used in signalling |
|
Definition
| epinepherine, norepinepherine, dopamine |
|
|
Term
| Main method of catecholamine inactivation |
|
Definition
| re-uptake into pre-synaptic neuron |
|
|
Term
| What is the basic method by which nicotinic cholinergic receptors work? |
|
Definition
| They are a ionotropic ligand-gated cation channel, so they allow for flow of ions (i.e. sodium) |
|
|
Term
| How many Muscarinic cholinergic receptors are we aware of? |
|
Definition
|
|
Term
| How many adrenergic alpha receptors are we aware of? |
|
Definition
|
|
Term
| How many adrenergic beta receptors are we aware of? |
|
Definition
| 3---B1, B2, (B3--not as important) |
|
|
Term
| Name the subunits of G-protein receptors |
|
Definition
|
|
Term
| What type of nucleotides do G-protein receptors bind? |
|
Definition
| Guanosine nucleotides (GTP and GDP) |
|
|
Term
| Which subunit of G-protein receptors is most important in determining what its effect will be? |
|
Definition
|
|
Term
| cAMP (cyclic adenosine monophosphate) is increased/decreased by Gas |
|
Definition
|
|
Term
| cAMP (cyclic adenosine monophosphate) is increased/decreased by Gai |
|
Definition
|
|
Term
| DAG (diacylglycerol) is increased/decreased by Gaq/11? |
|
Definition
|
|
Term
| IP3 (inositol triphosphate) is increased/decreased by Gaq/11? |
|
Definition
|
|
Term
| After dissociation from Gby, Ga subunits perform this function |
|
Definition
| increase or decrease quantity of second messenger molecules (cAMP, DAG, IP3) |
|
|
Term
| After dissociation from Ga, Gby subunits perform the following actions |
|
Definition
| increase or decrease quantity of secondary messengers, modulate the function of ion channels |
|
|
Term
| Muscarinic cholinergeic receptors (G-protein receptors) use the following Ga subunit types |
|
Definition
Gaq/11 (M1, 3, 5)
Gai (M2,4)
Gby |
|
|
Term
| adrenergic alpha receptors use the following type of G-protein subunits |
|
Definition
Gaq/11 (alpha 1)
Gai (alpha 2) |
|
|
Term
| Adrenergic beta receptors use the following type of G-protein subunit |
|
Definition
|
|
Term
| cAMP performs this action in the cell |
|
Definition
| activates protein kinase A (PKA) |
|
|
Term
| DAG performs this function in the cell |
|
Definition
| Activates protein kinase C (PKC) |
|
|
Term
| IP3 performs this function in the cell |
|
Definition
| activates protein kinase C (PKC) |
|
|
Term
| What is the basic function of presynaptic receptors? |
|
Definition
| Negative feedback to limit NT release |
|
|
Term
|
Definition
| a presynaptic receptor that is activated by the same NT that neuron is releasing (self-feedback) |
|
|
Term
| What is a heteroreceptor? |
|
Definition
| a presynaptic receptor that is activated by a different NT than that neuron produces (allows "cross-talk") |
|
|
Term
| What type of Ga subunit is present in presynaptic receptors (both cholinergic and adrenergic), and what is its function? |
|
Definition
| Gai, decreases cAMP, decreases NT release |
|
|
Term
| What does NANC transmission stand for? |
|
Definition
| Non-adrenergic, non-cholingergic transmission (use different NT or NT-like substance) |
|
|
Term
| Where does NANC transmission occur? |
|
Definition
| smooth muscle innervated by ANS |
|
|
Term
| What are the primary effects of NANC transmission? |
|
Definition
|
|
Term
| What type of receptors are present in NANC purinergic neurotransmission? |
|
Definition
| adenosine receptors and ATP receptors |
|
|
Term
| This is an endothelium-derived relaxation factor that is a type of NANC transmission |
|
Definition
|
|
Term
| Effect of increased sympathetic tone in the heart? |
|
Definition
| increased heart rate, increased conduction velocity, increased contraction, increased automaticity |
|
|
Term
| Type of cholinergic muscarinic receptor present in heart? |
|
Definition
|
|
Term
| Effect of increased parasympathetic tone in heart? |
|
Definition
| decreased heart rate, decreased conduction, decreased contraction |
|
|
Term
| type of adrenergic receptor present in the heart? |
|
Definition
|
|
Term
| Effect of sypmathetic NS on blood vessels? |
|
Definition
| Constriction of some, dilation of others. overall directs flow to skeletal muscle |
|
|
Term
| Effect of parasympathetic NS on blood vessels? |
|
Definition
| Doesn't really innervate blood vessels, but does effect endothelial production of NO |
|
|
Term
| Effect of sympathetic NS on lungs? Receptor used? |
|
Definition
| bronchodilation. Adrenergic B2 |
|
|
Term
| Effect of parasympathetic NS on lungs? Receptor used? |
|
Definition
| bronchoconstriction, increased secretion. M3 and M2 |
|
|
Term
| Effect of sympathetic NS on GI system. |
|
Definition
|
|
Term
| Effect of parasympathetic NS on GI activity? receptors used? |
|
Definition
| increase activity. M3 and M2 |
|
|
Term
| Effect of sympathetic NS on urinary bladder? |
|
Definition
|
|
Term
| effect of parasympathetic NS on urinary bladder? Receptors used? |
|
Definition
|
|
Term
| Effect of sympathetic NS on eye? receptors used? |
|
Definition
| Enhance vision. (dialate pupil, mydriasis, increase aqueous humor). a1 and B2 |
|
|
Term
| Effect of parasympathetic NS on eye? receptors used? |
|
Definition
| limit vision (pin-point pupil, miosis, lacrimal gland secretion). M3 and M2 |
|
|
Term
| Effect of sympathetic NS on salivary glands? |
|
Definition
|
|
Term
| effect of parasympathetic NS on salivary glands? receptors used? |
|
Definition
| increase secretion. M3 and M2 |
|
|
Term
| Effect of both sympathetic and parasympathetic on autonomic nerve endings? |
|
Definition
| decrease release of NT through negative feedback (autoreceptors and heteroreceptors) |
|
|
Term
| true or false: drugs can potentially target any component of autonomic transmission (NT synthesis,transport, release, receptors, breakdown/uptake) |
|
Definition
|
|
Term
| What, in general, do cholinergic agonists do? |
|
Definition
| mimic/enhance the effect of the parasympathetic system |
|
|
Term
| What is the effect of a cholinergic agonist on the heart? |
|
Definition
| decreased cardiac output (bradycardia, decreased conduction, decreased contractility) |
|
|
Term
| Effect of cholinergic agonists on lungs |
|
Definition
| causes bronchoconstriction and increased secretions |
|
|
Term
| Effect of cholinergic agonists on blood vessels? |
|
Definition
| increase production of NO by endothelial cells, smooth muscle relaxation and dilation |
|
|
Term
| Effect of cholinergic agonists on the GI |
|
Definition
| increased motility, secretions |
|
|
Term
| Effect of cholinergic agonists on the urinary bladder |
|
Definition
|
|
Term
| Effect of cholinergic agonists on the eye |
|
Definition
| miosis, lacrimation, loss of far vision |
|
|
Term
| What is the main muscarinic receptor on the heart? |
|
Definition
|
|
Term
| What is the main muscarinic receptor on the bladder? |
|
Definition
|
|
Term
| What is the acronym for the general effects of cholinergic agonists? |
|
Definition
|
|
Term
| What does SLUDGE stand for? |
|
Definition
| salivation, lacrimation, urination, defecation, GI symptoms, emesis |
|
|
Term
| What is the acronym for EXCESSIVE cholinergic stimulation? |
|
Definition
|
|
Term
| What does DUMBELS stand for? |
|
Definition
| Diarrhea/diaphoresis, urination, miosis, bronchorrhea/bronchospasm/bradycardia, emesis, lacrimation, salivation |
|
|
Term
| What is an direct acting muscarinic agonist? |
|
Definition
| a compound that directly stimulates the muscarinic receptor |
|
|
Term
| What is an indirect acting muscarinic agonist? |
|
Definition
| a compound that increases the muscarinic receptor activity by inhibiting acetylcholinesterase |
|
|
Term
| When the term "cholinergic" is used, does it generally refer to muscarinic or nicotinic receptors? |
|
Definition
|
|
Term
| This is an endogenous cholinergic rarely used clinically. |
|
Definition
|
|
Term
| What are the two direct acting cholinergic groups? |
|
Definition
| Cholinomimetic alkaloids and synthetic choline esters |
|
|
Term
| What are cholinomimetic alkaloids? |
|
Definition
| naturally occurring chemical compounds containing basic nitrogen atoms |
|
|
Term
| Classification and use of Bethanechol |
|
Definition
a choline ester sympathetic agonist that stimulates muscarinic receptors (some M3 selectivity)
basic function: promotes urinary voiding |
|
|
Term
|
Definition
| a cholinomimetic alkaloid that stimulates muscarine receptors. contributes to mushroom poisoning. See general DUMBELS signs |
|
|
Term
| Classification and use of Pilocarpine |
|
Definition
| a cholinomimetic alkaloid sympathetic agonist used to induce pupil constriction and decrease intraocular pressure during glaucoma |
|
|
Term
| General function of AChE inhibitors |
|
Definition
| are indirect cholingergic agonists. prevent hydrolysis of ACh by acetylcholinesterase and cause accumulation of ACh at sites of release |
|
|
Term
| What, generally, would be affected by AChE inhibitors |
|
Definition
| Everywhere that uses the NT ACh. autonomic effector organs and ganglia, skeletal muscle, cholinergic synapses in the CNS |
|
|
Term
| What would be the effect of AChE inhibitors on autonomic ganglia? |
|
Definition
| Stimulation, and then depression (via nicotinic receptors) |
|
|
Term
| What would be the effect of AChE inhibitors on the CNS? |
|
Definition
| Stimulation, and then depression |
|
|
Term
| What are the three general types of AChE inhibitors? |
|
Definition
Non-covelant inhibitors,
"reversible" covalent inhibitors,
"irreversible" covalent inhibitors |
|
|
Term
| What are two important AChE "reversible" covalent inhibitor drugs? |
|
Definition
| physostigmine and neostigmine |
|
|
Term
| Name some clinical uses of "reversible" covalent AChE inhibitors. |
|
Definition
| smoothe muscle atony, glaucoma, reversal of neuromuscular blocking agents, myasthenia gravis, counter CNS anticholinergic intoxication (physostigmine) |
|
|
Term
| This is a reversible AChE inhibitor that crosses the blood brain barrier |
|
Definition
|
|
Term
| What drug would you use to counter CNS symptoms of anticholinergic intoxication? |
|
Definition
|
|
Term
| This cholinergic agonist is used to empty the urinary bladder |
|
Definition
|
|
Term
| this cholingergic agonist is used to induce miosis in the eye |
|
Definition
|
|
Term
| This is used to reverse NMJ blockade. |
|
Definition
|
|
Term
| This drug is used to stimulate visceral smooth muscle |
|
Definition
|
|
Term
| This drug is used to counter anticholinergic toxicity |
|
Definition
|
|
Term
| What drug category do organophosphates fall under? |
|
Definition
| Irreversible covelant AChE inhibitors |
|
|
Term
| Name 3 varieties of irreversible covalent AChE inhibitors |
|
Definition
| organophophates, insecticides, and nerve gasses |
|
|
Term
| Poisoning with this class of compounds cause many symptoms attributable to excess muscarinic stimulation |
|
Definition
|
|
Term
| What do you use to treat organophosphate toxicity? |
|
Definition
| cholinesterase "reactivators." (pralidoxime, 2-PAM) or anticholinergics |
|
|
Term
| What receptor type do cholinergic antagonists act at? |
|
Definition
| muscarinic receptors (little effect at nicotinic) |
|
|
Term
| True or false: most cholinergic antagonists competitively block stimulation of muscarinic receptors by ACh |
|
Definition
|
|
Term
| Name the two groups of cholinergic antagonists |
|
Definition
natural anticholinergic alkaloids
semi-synthetic and synthetic alkaloid derivatives |
|
|
Term
| Name the two main natural anticholinergic alkaloids |
|
Definition
|
|
Term
| Name the 4 most common semisynthetic/synthetic cholinergic antagonists |
|
Definition
| tropicamide, ipratropium, glycopyrrolate, propantheline |
|
|
Term
| Effects of cholinergic antagonists on the heart |
|
Definition
| increased cardiac output (tachycardia, increased conduction, etc) |
|
|
Term
| Effects of cholinergic antagonists on vasculature |
|
Definition
| little effect, no innervation by Parasympathetic |
|
|
Term
| effects of cholinergic antagonists on lungs |
|
Definition
| bronchdilation, decreased secretions |
|
|
Term
| effects of cholinergic antagonists on GI |
|
Definition
| decreased motility, decreased secretion, (dry mouth) |
|
|
Term
| effects of cholinergic antagonists on urinary bladder |
|
Definition
|
|
Term
| effects of cholinergic antagonists on the eye |
|
Definition
| decreased lacrimation, mydriasis, cycloplegtia |
|
|
Term
| general effects of cholinergic antagonists |
|
Definition
|
|
Term
| True/False: Salivary glands are generally insensitive to cholingergic antagonists |
|
Definition
| false, salivary glands are one of the most sensitive organs to anticholinergics |
|
|
Term
| True or false: the effect of anticholinergics depend on the amount of parasympathetic tone present in the first place |
|
Definition
| True..the greater the amount of parasympathetic tone the larger an effect a anticholinergic drug will have |
|
|
Term
| Classification and action of atropine |
|
Definition
| a cholinergic antagonist (natural alkaloid) that competitively inhibits binding and stimulation of M receptors by ACh. Enters the CNS. |
|
|
Term
| What are the primary concerns with the use of atropine |
|
Definition
| tachyarrhythmia, prolonged GI stasis, urine retention |
|
|
Term
| What is atropine used for? |
|
Definition
| a adjunct during general anesthesia to decrease salivary and airway secretions. Also to releive symptoms of AChE poisoning |
|
|
Term
| How might atropine cause increased salivation? |
|
Definition
| although the action is supposed to decrease salivation, when it somehow ends up in the mouth it will increase it (due to being very bitter). |
|
|
Term
| Classification and action of scopolamine |
|
Definition
| cholinergic antagonist (natural alkaloid). Enters CNS. Low dose=slight sedation. High dose=excitement. similar to atropine but usually not the drug of choice |
|
|
Term
| Classification and action of glycopyrrolate |
|
Definition
| a synthetic cholinergic antagonist. similar to atropine but is quaternary so few CNS effects. Used as adjunct to general anesthesia (cecreases salivary and airway secretions) |
|
|
Term
| Classification and use of tropicamide |
|
Definition
| synthetic cholinergic antagonist. used in the eye to produce mydriasis and cycloplegia. Shorter duration of action than atropine |
|
|
Term
| Classification and use of Ipratropium |
|
Definition
| Cholinergic antagonist. Use to decrease bronchoconstriction and airway secretions. Quaternary, restrict distribution by using as an inhalant. Used for animals in chronic respiratory distress. |
|
|
Term
| Classification and use of Propantheline |
|
Definition
| Cholinergic antagonist. used to promote urine retention. decreased detrusor contraction and increased trigone and sphincter contraction. |
|
|
Term
| 2 cholinergic antagonists used to decrease secretions |
|
Definition
|
|
Term
| chlolinergic antagonist used to prevent bradycardia |
|
Definition
|
|
Term
| cholinergic antagonist used to promote bronchodialation |
|
Definition
|
|
Term
| cholinergic antagonist used to induce mydriasis and cycloplegia |
|
Definition
|
|
Term
| Cholinergic antagonist used to promote urine retention |
|
Definition
|
|
Term
| Function of ganglionic blockers |
|
Definition
| decrease autonomic regulation of target organs (both sympathetic and parasympathetic) |
|
|
Term
| What is the affect of administering nicotine? |
|
Definition
| initial stimulation of nicotinic receptors (increased ANS activity), then inhibition of nicotinic receptors (decreased ANS activity) |
|
|
Term
| How do synthetic competitive ganglionic blockers compare with nicotine? |
|
Definition
| they cause inhibition without the initial stimulation. Blocks all ANS activity |
|
|
Term
| Why aren't ganglionic blockers commonly used clinically? |
|
Definition
| Since they are decreasing all the the ANS, the effects are widespread and difficult to predict. |
|
|
Term
| What is the basic function of NMJ blocking agents? |
|
Definition
| to relax skeletal muscle with no sedative effects. |
|
|
Term
| Why would we use NMJ blockers as an adjunct to normal anesthesia? |
|
Definition
| to prevent movement during surgery |
|
|
Term
| How do the nicotinic structures of neuronal synapses and NMJ's differ? |
|
Definition
| Neuronal contain only alpha and beta subunits, NMJ contain alpha, beta, delta, and epsilon. this means that they can be targeted via differential pharmacology. |
|
|
Term
| Why are spare receptors problematic when using NMJ blockers? |
|
Definition
| must block more receptors than expected, and have lost safety factor of important muscles (diaphragm) |
|
|
Term
| How do competitive NMJ blockers work? |
|
Definition
| They block motor end plate depolarization, causing a flaccid paralysis |
|
|
Term
| This is a long-acting competitive NMJ blocker |
|
Definition
|
|
Term
| This is an intermediate-length acting competitive NMJ blocker |
|
Definition
|
|
Term
| This is a short acting competitive NMJ blocker |
|
Definition
|
|
Term
| This NMJ-blocking drug has a long duration of action, renally eliminated, and blocks muscarinic receptors (tachycardia) |
|
Definition
|
|
Term
| This NMJ blocker has an intermediate duration of action, and the half-life is not increased with renal disease. It also promotes histamine release. |
|
Definition
|
|
Term
| What can cause increased half-life of atracurium? |
|
Definition
| hypothermia and acidosis (degeneration is temperature and pH dependent) |
|
|
Term
| This NMJ blocker has a short duration of action and is rapidly hydrolysed by plasma enzymes. It also promotes histamine release. |
|
Definition
|
|
Term
| What 2 competitive NMJ blockers promote histamine release? |
|
Definition
| Atracurium and Mivacurium |
|
|
Term
| What can you do to reverse the effects of competitive NMJ blockers? |
|
Definition
| Give AChE inhibitors to increase concentration of ACh to outcompete the antagonist. |
|
|
Term
| How do depolarizing NMJ blockers work? |
|
Definition
| Cause prolonged motor end plate depolarization by stimulation of nicotinic receptors. initial fasciculation followed by relaxation |
|
|
Term
| What is the only depolarizing NMJ used clinically? |
|
Definition
|
|
Term
| Is succinylcholine pharmacologically reversible? |
|
Definition
| No. Although it is 2 ACh molecules linked together, it is resistant to AChE, and is a non-competitive antagonist |
|
|
Term
| Explain what is happening during early (phase 1) depolarizing NMJ blocker use |
|
Definition
| the drug causes persistant stimulation of the nicotinic receptors (muscle fasiciculations) until they are incapable of transmitting further impulses |
|
|
Term
| What are the potential side effects of succinylcholine use? |
|
Definition
| Histamine release and hyperkalemia (release of K from skeletal muscles) |
|
|
Term
| How do you monitor effectivness of a NMJ blockade? |
|
Definition
| Stimulate peripheral nerves (train of four) |
|
|
Term
| Problem with using NMJ blockers during anesthesia |
|
Definition
| Normal ways of monitoring patient (reflexes, muscle tone) are lost. |
|
|
Term
| What are the biggest dangers of using NMJ blockers during anesthesia? |
|
Definition
| Respiratory paralysis and malignant hyperthermia |
|
|
Term
| These antagonize ACh at NMJ nicotinic receptors |
|
Definition
|
|
Term
| These mimic ACh at the NMJ, are non-reversible, and cause fasiculations followed by flaccid paralysis |
|
Definition
| non-competitive depolarizing NMJ blockers (aka succinylcholine) |
|
|
Term
| What are sympathomimetics? |
|
Definition
| drugs that mimic the effect of endogenous sympathetic catecholamine neurotransmitters. AKA adrenergic agonists |
|
|
Term
| Name three endogenous catecholamines. |
|
Definition
| Epinepherine, norepinepherine, dopamine |
|
|
Term
| What are the pre-junctional actions (a2 receptors) of adrenergic agonists? |
|
Definition
| decrease NT release, decrease sympathetic outflow, CNS depression |
|
|
Term
| What set of drugs induce a general catabolic state? |
|
Definition
|
|
Term
| Direct acting adrenergic antagonists work on what specific part of signal transduction? |
|
Definition
|
|
Term
| What drugs work as direct acting agonists? |
|
Definition
| The endogenous catecholamines: dopamine, norepinepherine, epinepherine |
|
|
Term
| name an indirect acting adrenergic agonist. |
|
Definition
|
|
Term
| Name a mixed acting adrenergic agonist |
|
Definition
|
|
Term
| Classification and action of epinepherine. |
|
Definition
a direct acting adrenergic agonist
potent a and b agonist
most important for cardiovascular effects (increase rate, conduction, contraction). Also affects arterial blood flow. |
|
|
Term
| What receptor does epinepherine act on in the heart? |
|
Definition
|
|
Term
| What receptor does epinepherine work on in the central arteries? What does it do? |
|
Definition
| a1 receptors. stimulate smooth muscle, vasoconstriction. |
|
|
Term
| What receptor does epinepherine work on in arteries supplying skeletal muscle? |
|
Definition
| B2 receptor. inhibits smooth muscle, vasodilation |
|
|
Term
| What is the effect of a low dose of epinepherine on blood pressure? |
|
Definition
| decreases bp slightly due to B2 dominance |
|
|
Term
| What is the effect of a large dose of epinepherine on blood pressure? |
|
Definition
| increases blood pressure due to A1 receptors causing vasoconstriction |
|
|
Term
| Would a large dose of epinepherine increase/decrease flow to the renal artery |
|
Definition
| Decrease. stimulation of A1 receptors causes constriction on central arteries |
|
|
Term
| What is the effect of epinepherine on the lungs? |
|
Definition
| Strong bronchodialator through B2 receptor |
|
|
Term
| What is the general metabolic effects of epinepherine? |
|
Definition
| Increased glucose and free fatty acids |
|
|
Term
| What are the effects of epinepherine on the eye? |
|
Definition
| mydriasis (pupil dilation) and relaxation of the ciliary muscle (for distance vision) |
|
|
Term
| Name 4 clinical uses of epinepherine |
|
Definition
| relief of hypersensitivity rxns (cardio support and bronchodilation (B1 and B2)), restoring cardiac rhythm, topical hemostatic agent (constrict vessels,a1) adjunct with local anesthetics (limit spread, a1) |
|
|
Term
| Possible side effects of epinepherine? |
|
Definition
| cardiac arrhythmias, hypertension, cerebral hemorrhage, restlessness |
|
|
Term
| This is the major NT released by post-ganglionic sympathetic nerves |
|
Definition
|
|
Term
| What is the main difference in using epinepherine vs norepinepherine? |
|
Definition
| Epinepherine is much more potent on B2 receptors. Norepinepherine will not cause bronchodilation |
|
|
Term
| What is the effect of norepinepherine on blood pressure? |
|
Definition
| intense vasoconstriction causes increase in blood pressure (no B2 effect for dialation of peripheral vessels) |
|
|
Term
| Why does the HR tend to slow when using norepinepherine? |
|
Definition
| norepinepherine causes such an increase in BP that the vagal reflex is triggered, slowing heart rate. |
|
|
Term
| What is the effect on cardiac output when using norepinepherine? |
|
Definition
| Doesn't change much. Have increased BP but decreased rate. |
|
|
Term
| What is the main clinical use of norepinepherine? |
|
Definition
| to maintain BP during a cardiovascular crisis (shock) |
|
|
Term
| This adrenergic agonist has a positive inotropic effect |
|
Definition
|
|
Term
| This adrenergic agonist is used in low doses, has a short half-life |
|
Definition
|
|
Term
| What is the effect of low-dose dopamine on kidneys? |
|
Definition
| increases blood flow and sodium excretion |
|
|
Term
| This drug is used to treat congestive heart failure with compromised renal function. |
|
Definition
| dopamine (low dose only, high dose decreases blood flow to kidneys) |
|
|
Term
| Name a clinically-used, non-selective B adrenergic agonist |
|
Definition
|
|
Term
| What receptor does dobutamine work best on? |
|
Definition
| B1 (explain to me how this is a non-selective agonist????) |
|
|
Term
| What are the most important effects of dobutamine? |
|
Definition
| effect on the heart through stimulation of B1 receptors. increased contractility but not heart rate or blood pressure. |
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|
Term
| What are selective B2 agonists used for clinically? |
|
Definition
|
|
Term
| What are the benefits of using a selective B2 agonist as a bronchodilator? |
|
Definition
| Fewer cardiovascular effects (no stimulation of B2 receptors) |
|
|
Term
| Are synthetic B2 agonists short acting or long acting? |
|
Definition
| Many are resistant to metabolism and have a long duration of action. |
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|
Term
| What selective B2 adrenergic agonist is most commonly used for bronchospasms? |
|
Definition
|
|
Term
| What selective B2 adrenergic agonist is most commonly used for recurrent airway obstruction? |
|
Definition
|
|
Term
| What is the problem with long-term administration of B2 adrenergic agonists? |
|
Definition
| B receptor down-regulation can occur, leading to loss of efficacy. Can minimize with proper dose and dosing schedule |
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|
Term
| What is the benefit of B2 adrenergic agonists in livestock? |
|
Definition
| partition energy towards muscle mass. |
|
|
Term
| What is the primary effect of an A1 adrenergic agonist? |
|
Definition
| vasoconstriction and increased blood pressure |
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|
Term
| Classification and use of Phenylephrine |
|
Definition
| A selective A1 adrenergic agonist. used as a decongestant and vasopressor |
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|
Term
| What is the main function of selective A2 adrenergic agonists? |
|
Definition
| pre-synaptic inhibition of sympathetic neurons and decreased sympathetic outflow from the brain. Causes sedation, analgesia |
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|
Term
| Classification and use of (Dex)medetomaidine |
|
Definition
| a selective A2 adrenergic agonist. Used as an adjunct in sedation/anesthesia. inhibits sympathetic outflow. |
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|
Term
| What is the main selective adrenergic agonist used for vasoconstriction? (classification and name) |
|
Definition
| phenylephrine, a selective A1 adrenergic agonist |
|
|
Term
| What is the main adrenergic agonist used as a sedative? |
|
Definition
| (dex)(medetomidine, a selective A2 adrenergic agonist. decreases sympathetic outflow |
|
|
Term
| These 3 adrenergic drugs cause vasoconstriction |
|
Definition
| EPI, NE and phenylephrine |
|
|
Term
| This adrenergic drug causes presynaptic inhibition |
|
Definition
|
|
Term
| These 4 adrenergic drugs increase heart rate and contractile force. |
|
Definition
| Epi, NE, dopamine, dobutamine |
|
|
Term
| These three adrenergic drugs cause bronchodilation |
|
Definition
| Epi, albuterol, clenbuterol |
|
|
Term
| What is another term for adrenergic antagonists? |
|
Definition
|
|
Term
| What is the main pharmaceutical function of adrenergic antagonists? |
|
Definition
| block the effect of endogenous sympathetic catecholamine neurotransmitters |
|
|
Term
| What does the effect of sympatholytics depend on? |
|
Definition
| the sympathetic tone (high have more effect) |
|
|
Term
| What is the action of a direct-acting competitive adrenergic antagonist? |
|
Definition
| reversibly blocks the stimulation of A and B receptors by endogenous NT's |
|
|
Term
| What classification do most adrenergic agonists fall under? |
|
Definition
| direct acting competitive antagonists |
|
|
Term
| What is the action of a non-competitive adrenergic antagonist? |
|
Definition
| irreversibly blocks A1 and A2 receptors |
|
|
Term
| What is an example of a direct acting non-competitive adrenergic antagonist? |
|
Definition
|
|
Term
| What is a direct acting competitive antagonist that reversibly blocks A1 and A2 receptors? |
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Definition
|
|
Term
| Clinical use of both phenoxybenzamine and phentolamine? |
|
Definition
| both are non-selective A antagonists. used to reduce urethral sphincter tone to manage urethral blockages |
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|
Term
| Effect of A1 adrenergic antagonists |
|
Definition
| block stimulation of arterial smooth muscle. cause fall in blood pressure from decreased total peripheral resistance. |
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|
Term
| Classification and use of Prazosin |
|
Definition
| a selective A1 antagonist. used to relax both arterial and venous smooth muscle. Decrease in total peripheral resistance and venous return. Used in hypertension and congestive heart failure. |
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|
Term
| Function of selective A2 adrenergic antagonists |
|
Definition
| prevent central and pre-synaptic inhibition. increase sympathetic flow. |
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|
Term
| Classification and use of Atipamezole |
|
Definition
| a selective A2 adrenergic antagonist. prevents pre-synaptic and central sympathetic inhibition. used to reverse sedative and analgesic effects of medetomidine (a A2 agonist) |
|
|
Term
| Why is atipamezole an excellent drug to counteract medetomidine? |
|
Definition
| There is little chance of a relapse into sedation because the half-life of atipamezole is 2x that of medetomidine |
|
|
Term
| This is a A1 adrenergic antagonist used for vasodilation |
|
Definition
|
|
Term
| This is a A2 adrenergic antagonist used to reverse medetomidine |
|
Definition
|
|
Term
| This is a non-selective competitive A adrenergic angatonist (reversible) |
|
Definition
|
|
Term
| This is a non-selective non-competitive A adrenergic antagonist (irreversible) |
|
Definition
|
|
Term
| Effect of using a B1 adrenergic antagonist |
|
Definition
| block sympathetic innervation of the heart. Decreased heart rate and contractility |
|
|
Term
| True or false: B1 adrenergic antagonists decrease blood pressure. |
|
Definition
| True. Because they decrease cardiac output and BP=CO x PR, BP is decreased |
|
|
Term
| What dangerous side effect can excessive sympathetic innervation cause regarding the heart? |
|
Definition
| cardiac arrhythmias. Use a B1 adrenergic antagonist to decrease innervation. |
|
|
Term
| What is the primary effect of B2 adrenergic antagonists? |
|
Definition
| cause bronchoconstriction. (blocking sympathetic input to bronchiolar SM) |
|
|
Term
| What is the major clinical limitation of non-selective B antagonists? |
|
Definition
| Will effect the heart (usual goal) but will also cause bronchoconstiction |
|
|
Term
| This is a prototypical B antagonist with equal affinity for both B1 and B2 receptors |
|
Definition
|
|
Term
| Classification and use of Propranolol |
|
Definition
| a non-selective B adrenergic antagonist that is used for a antiarrhythmia. limited use because of effect on lungs (bronchoconstriction) |
|
|
Term
| A nonselective B adrenergic antagonist used for glaucoma |
|
Definition
|
|
Term
| Classification and use of timolol |
|
Definition
| A non-selective B adrenergic antagonist used to decrease aqueous humor production during glaucoma (ocular application) |
|
|
Term
| Why is it safer to use a selective B1 antagonist than a non-selective B antagonist? |
|
Definition
| Can effect B1 receptors in heart without affecting SM in lungs |
|
|
Term
| This selective B1 antagonist is used to decrease heart rate and counteract anticholinergic tachycardia |
|
Definition
|
|
Term
| Classification and use of atenolol |
|
Definition
| a selective B1 adrenergic antagonist used to decrease heart rate and counteract anticholinertgic tachycardia |
|
|
Term
| Name this drug. Adrenergic agonist, endogenous, stimulates A1, B1, B2 |
|
Definition
|
|
Term
| Name this drug: Adrenergic agonist, endogenous, stimulates A1 and B1 |
|
Definition
|
|
Term
| name this drug: Adrenergic agonist, endogenous, stimulates D1 and B1 (little bit of A1) |
|
Definition
|
|
Term
| Name this drug: a adrenergic agonist, selective for B1 |
|
Definition
|
|
Term
| Name these 2 drugs: adrenergic agonists selective for B2 |
|
Definition
| albuterol and clenbuterol |
|
|
Term
| Name this drug: an adrenergic agonist selective for A1 |
|
Definition
|
|
Term
| Name this drug: a adrenergic agonist selective for A2 |
|
Definition
|
|
Term
| Name this drug: a adrenergic antagonist, non-competitive, blocks A1 and A2 |
|
Definition
|
|
Term
| Name this drug: a adrenergic antagonist, competitive, blocks A1 and A2 |
|
Definition
|
|
Term
| Name this drug: a adrenergic antagonist specific for A1 |
|
Definition
|
|
Term
| name this drug: a adrenergic antagonist specific for A2 |
|
Definition
|
|
Term
| Name this drug: a adrenergic antagonist, non-selective B, systemic use |
|
Definition
|
|
Term
| Name this drug: adrenergic antagonist, non-selective B, ocular use |
|
Definition
|
|
Term
| Name this drug: adrenergic antagonist, selective for B1 |
|
Definition
|
|
Term
| In case of shock, which branch of the ANS needs to be stimulated? |
|
Definition
| Symptathetic. Increase cardiac output, increase peripheral resistance, increase blood pressure. |
|
|
Term
| Why might Ne be preferred over EPI in shock associated with vasodilation? |
|
Definition
| NE can achieve a greater BP increase than Epi....and something about arrhymmias.....not sure. |
|
|
Term
| Primary therapy for anaphylactic shock? |
|
Definition
|
|
Term
| Elevated intraocular pressure in the absence of signs of concurrent ocular disease |
|
Definition
|
|
Term
| eleveated intraocular pressure associated with concurrent ocular disease |
|
Definition
|
|
Term
| What breed tends to have open angle glaucoma? |
|
Definition
|
|
Term
| usual cause of primary glaucoma |
|
Definition
| narrow angle results in obstruction of aqueous outflow |
|
|
Term
| These 2 drugs are often used in combination to treat emergency glaucoma |
|
Definition
| timolol (beta antagonist, decrease aqueous humor production) and pilocarpine (cholinergic agonist, miotic agent than can open closed angle) |
|
|
Term
| The heart works ........ and in a ........manner |
|
Definition
| sequentially, synchronized |
|
|
Term
| The spread of electrical excitation in the heart is both ...... and ...... |
|
Definition
|
|
Term
| Where does cardiac electrical activity originate? |
|
Definition
| in the SA node (sinoatrial) |
|
|
Term
| Describe the spread of electrial excitation through the heart |
|
Definition
| starts in the SA node, spreads rapidly through atria, moves slowly through AV node, spreads rapidly through ventricles via the His-Purkinje system |
|
|
Term
| How does electrical current spread from one cardiac cell to another? |
|
Definition
|
|
Term
| Why do the action potential waveforms in the ventricles and the SA node appear different? |
|
Definition
| different populations of ion channels |
|
|
Term
| What is the resting trans-membrane electrical gradient of a cardiac cell? |
|
Definition
|
|
Term
| What are the three major ions associated with cardiac cell electrical activity? |
|
Definition
| Sodium, Potassium, Calcium |
|
|
Term
| What is the point to which an ion will drive the cell membrane potential if it is allowed to move freely in or out of the cell? |
|
Definition
| reversal potential (the point at which that ion is in equilibrium across the membrane) |
|
|
Term
| The reversal potential of which ion determines resting membrane potential? |
|
Definition
| Potassium (only ion channels that are open at this point) |
|
|
Term
| The resting membrane potential of sodium is +50 mV. Why is this important? |
|
Definition
| Sodium will attempt to drive the membrane potential up to +50 mV when it can move freely into the cell |
|
|
Term
| How are sodium channels in cardiac cells activated? |
|
Definition
|
|
Term
| What are the 3 functional states of ion channels? |
|
Definition
| closed, open, and inactivated |
|
|
Term
| What is the threshold for activation of voltage gated sodium channels? |
|
Definition
| -60 mV (resting potential is -90 mV) |
|
|
Term
| True or false: the entire cell must reach -60 mV to activate threshold |
|
Definition
| False: a change along the membrane is sufficient |
|
|
Term
| Explain phase 0 of the ventricular action potential. |
|
Definition
| Depolarization. Na+ channels open and sodium floods into the cell. |
|
|
Term
| Explain phase 2 of the ventricular action potential |
|
Definition
| Ca++ enters the cell. initiation of contraction. K+ begins to exit the cell. |
|
|
Term
| Explain phase 3 of the ventricular action potential |
|
Definition
| K+ still exiting the cell. repolarization. |
|
|
Term
| In comparison to sodium channels, are calcium channels slower or faster? |
|
Definition
| Much slower. They open and inactivate more slowly than sodium channels. allow for substantial calcium influx to trigger and sustain contraction. |
|
|
Term
| Why doesn't the inward movement of calcium in phase 2 cause an rise in a cell's positive charge? |
|
Definition
| Because K+ is moving out of the cell at the same time, keeping it relatively balanced. |
|
|
Term
| Which node is usually the pacemaker? |
|
Definition
|
|
Term
| What outside forces cause depolarization of the SA node? |
|
Definition
| trick question---spontaneous depolarization |
|
|
Term
| What ions are important in SA node action potentials? |
|
Definition
| Calcium and potassium (no sodium channels) |
|
|
Term
| Why don't SA node cells need a phase 2 (plateau)?? |
|
Definition
| They are not contracting. |
|
|
Term
| What ion is important for depolarization of pacemaker cells? |
|
Definition
|
|
Term
| What channels do pacemaker cells use to depolarize? |
|
Definition
| slow opening voltage gated calcium channels (threshold=-40 mV) |
|
|
Term
| What does phase 3 consist of in SA nodal cells? |
|
Definition
| repolarization through K+ channels (same as ventricular) |
|
|
Term
| What is phase 4 of pacemaker action potential? |
|
Definition
| a continuous slow depolarization (funny current) |
|
|
Term
| How is the "funny" current activated in pacemaker cells? |
|
Definition
| by hyperpolarization (such as in phase 0 of action potential). slowly depolarize towards threshold. |
|
|
Term
| Influx of what ion trigger contraction in cardiac muscle cells? |
|
Definition
|
|
Term
| How does the influx of calcium induce contraction in cardiac cells? |
|
Definition
| calcium-induced calcium release. |
|
|
Term
| What are 2 ways calcium is removed from the cytoplasm to stop cardiac contraction? |
|
Definition
pumped back into the SR by Ca++ ATPase
shunted out of cell by Na+/Ca++ exchanger |
|
|
Term
| What ion triggers contraction of cardiac muscle? |
|
Definition
|
|
Term
| What is an electrocardiograph? |
|
Definition
| electrical activity of the heart recorded through the skin |
|
|
Term
| What does the P wave in an electrocardiograph signify? |
|
Definition
|
|
Term
| What does the QRS complex in an electrocardiograph signify? |
|
Definition
| ventricular depolarization |
|
|
Term
| What does the QRS complex in an electrocardiograph signify? |
|
Definition
| ventricular depolarization |
|
|
Term
| What does the T wave signify in an electrocardiograph? |
|
Definition
| ventricular repolarization |
|
|
Term
|
Definition
| a problem with the electrial activity of the heart. Can result from disorders of impulse formation, conduction, or both. |
|
|
Term
| A change in the normal pace maker or the developement of a new ectopic pacemaker would be a disorder of...... |
|
Definition
|
|
Term
| True or false: a ectopic pacemaker is always in the ventricles. |
|
Definition
| False, it can form anywhere in the heart. |
|
|
Term
| Why is the SA node typically the pacemaker? |
|
Definition
| it has the highest depolarization frequency |
|
|
Term
| Name two situations in which a new pacemaker might become dominant. |
|
Definition
| The firing of the SA node slows abnormally, or there is an abnormal acceleration of the ectopic pacemaker. |
|
|
Term
| True or false: ectopic pacemaker activity will usually cause abnormal depolarization. |
|
Definition
|
|
Term
| Give an example of how disorders of impulse conduction can cause bradycardia. |
|
Definition
| AV nodal block, conduction not getting through normally to ventricles, slows ventricular contraction rate. |
|
|
Term
| Give an example of how a disorder of impulse conduction can cause tachycardia |
|
Definition
| A reenterent circuit can be self-perpetuating and become a pacemaker, cause abnormal impulse conduction and contraction. |
|
|
Term
| What are the realistic goals of antiarrhythmic drugs? |
|
Definition
| to minimize cardiac pump dysfunction and prevent less serious arrhythmias from becoming more serious |
|
|
Term
| What is the problem with all anti-arrhythmic drugs? |
|
Definition
| they can all induce arrthymias. |
|
|
Term
| under traditional classification of antiarrhythmic drugs, what is the function of Class 1? |
|
Definition
|
|
Term
Class 1 antiarrhythmic drugs
(sodium channel blockers) have 3 sub categories. What are they? (name and function) |
|
Definition
Class 1A:moderate conduction slowing, prolongs refractory period
Class 1B: little conduction slowing, shortens refractory period
Class 1C: profound conduction slowing, little change in refractory period |
|
|
Term
| do sodium channel blockers have any effect on the SA node? |
|
Definition
| no, the SA node has no sodium channels |
|
|
Term
| What is the effective refractory period? |
|
Definition
| The time before a cell can fire a subsequent action potential (is related to action potential duration) |
|
|
Term
| Name a Class 1A antiarrhythmic drug |
|
Definition
|
|
Term
| What is the effect of procainamide on heart cells? |
|
Definition
| A class 1A antiarrhythmic, procainamide slows conduction velocity and prolongs the refractory period. |
|
|
Term
| What situation would procainamide be useful in relieving? |
|
Definition
| reentrant supraventricular tachycardia....slows conduction velocity and breaks the cycle. |
|
|
Term
| Explain how the class 1B drug lidocaine will effect cardiac cells |
|
Definition
| lidocaine binds to inactivated sodium channels (including "late" sodium channels, which shortens the refractory period) and keeps them in the in activated state. With fewer active sodium channels, automaticity decreases, and eccentric pacemakers can be slowed down. |
|
|
Term
| What type of cells does lidocaine tend to affect? |
|
Definition
| damaged depolarized cardiac cells (why good for treating ectopic pacemaker |
|
|
Term
| Name a Class 1C antiarrhymatic |
|
Definition
|
|
Term
| What is the clinical use of flecainide |
|
Definition
| for use in emergency situations to decrease conduction velocity (ventricular fibrillation) |
|
|
Term
| In the traditional classification of antiarrhythmic drugs, what do Class II drugs do? |
|
Definition
|
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