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65 Cards in this Set
- Front
- Back
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Botulinum Toxin
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Inhibits Ach Release
Causes flaccid paralysis Give local or intraocular only. |
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Latrotoxin
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Increases Ach release.
Causes tetany and painful contractions. |
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Acetylcholine
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Muscarinic Agonist--> Choline Ester
Non-selective (nicotinic stimulation). Short duration...hydrolyzed too rapidly by AchE. Quaternary ammonium...charged. Does not cross the BBB. Intraocular only - glaucoma |
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Bethanechol
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Muscarinic Agonist --> Choline Ester.
Ach that has been modified. Quaternary Ammonium...does not cross the BBB. M-Selective No cardiovascular effects Long Duration due to resistance to hydrolysis by Ach. (Primarily hydrolyzed by pseudocholinesterase). Uses: Postop Gastric Distention, Vagal Atony due to bilateral vagotomy (cannot use Achesterase Inhibitor for this). Urinary and post op bladder retention, Hypotonic bladder. (NOT used with bladder or bowel obstructions.) |
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Pilocarpine
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Muscarinic Agonist --->A Natural Cholinomimetic Alkaloid - (NOT a choline ester..therefore NOT hydrolyzed by Achesterase.)
Long duration (b/c not hydrolyzed by Achesterase). Tertiary Ammonium - NOT charged..crosses BBB. CNS effects. Can cause increased glandular and gastric secretions when used systemically. Uses: ----> Xerostomia (d/t Sjogren’s syndrome, radiation therapy) ---->Intraocular (Glaucoma tx)...can cause cycloplegia |
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Muscarine
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Muscarinic Agonist - Natural Cholinomimetic Alkaloid (NOT a choline ester, NOT hydrolyzed by Achesterase).
From Amanita fungi No nicotinic effects |
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Edrophonium
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The only RAPIDLY REVERSIBLE Achesterase Inhibitor
MOA: Binds to anionic site of active AChE center, preventing Ach from binding and being hydrolyzed. No interaction with AChE esteratic site, which makes it's duration of action REVERSIBLE & BRIEF. (it's always an enzyme...there is no acetylated intermediate). Use: Tensilon test for myasthenia gravis. |
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Neostigmine
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Carbamate AchE-Inhibitor - SLOWLY REVERSIBLE
* Slowly reversible because is attracted to the anionic site by pos charge, ester bond is hydrolyzed by esteratic site & forms a “carbamylated enzyme intermediate Does not cross the BBB. Use: Treatment of MG. Reversal of NDNMB's SE: BRAdycardia, nausea |
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Neostigmine
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Carbamate AchE-Inhibitor - SLOWLY REVERSIBLE
* Slowly reversible because is attracted to the anionic site by pos charge, ester bond is hydrolyzed by esteratic site & forms a “carbamylated enzyme intermediate" that is pretty stable. This leads to it's longer duration of action than Edrophonium...but eventually the carbamate grp does dissociate and the AchE enzyme is functional again. Use: Reversal of NMB's, Tx of Myasthenia Gravis. SE: Nausea, Bradycardia, other PNS mimetric effects. (Do not treat with a muscarinic antagonist...with Myasthenia Gravis, the body will adapt to neostigmine over time and adapt to these Muscarinic effects. Also, you want to see the M-effects so that you can see when you have a neostigmine OD...so you can lower the dose.) |
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Physostigmine
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Carbamate AchE Inhibitor - SLOWLY REVERSIBLE
*Slowly reversible because interaction with esteratic grp on AchE leads to hydrolysis and a carbamaylated enzyme intermediate that is fairly stable. This gives it a LONGER DURATION OF ACTION than Edrophonium. Tertiary Amine (no charge). Crosses BBB and has CNS side effects. Use: --->Intraocular tx of Glaucoma --->To tx an OD of Antimuscarinic (atropine, scopolamine, glycopyrollate)...it crosses the BBB and counteracts the CNS effects of antimuscarinic (controversial tx due to it's own side effects). Increase in ACh outcompetes antagonist for binding sites. Controversial tx because physiostimine will have PNS mimetric effects so you have to weigh the pros and cons. SE: cycloplegia, miosis |
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Donepezil (Aricept)
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Carbamate AchE Inhibitor - SLOWLY REVERSIBLE
* Slowly reversible with a longer duration of action due to formation of a STABILE carbamylated enzyme intermediate with AChE, which deactivates the enzyme. NO CHARGE - Crosses BBB Use: Alzheimers Disease. (Alzheimer's disease is due to a loss of cholinergic neurons in the brain.) (BUT does not CURE dementia...does not stop the degeneration of neurons). |
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Carbaryl
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Carbamate AChE Inhibitor - SLOWLY REVERSIBLE.
* Slowly reversible due to formation of a STABILE carbamylated enzyme intermediate with AChE, with deactivates the enzyme and gives it a longer duration of action than Edrophonium. Use: Insecticide (Seven Dust). Has toxic effects (effect ganglionic nicotinic receptors). |
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Echothiophate
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Organophosphate AchE Inhibitor - IRREVERSIBLE
MOA: Drug is sucked into esteratic site of AChE (does not react with anionic site). Hydrolysis leads to STABILE phosphorylation of the esteratic site that is irreversible. ACh hydrolysis is no longer possible. SE: Organophosphates can cause "Ginger-Jake" Syndrome--> delayed neurotoxicity: peripheral neuropathy with demyelination that starts at the fingers and toes and moves inward. Use: Intraocular tx of glaucoma (a last resort tx when all other drugs have failed.) Used for its LONG DURATION OF ACTION. Side Effect: High risk of developing cataracts. Can also pvt pupil dilation and can cause constant accomodation (spasm of ciliary muscles). |
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Parathion
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"Pro-toxin" for an Organophosphate AchE Inhibitor - IRREVERSIBLE
MOA: Drug is sucked into esteratic site of AChE (does not react with anionic site). Hydrolysis leads to STABILE phosphorylation of the esteratic site that is irreversible. ACh hydrolysis is no longer possible. SE: Organophosphates can cause "Ginger-Jake" Syndrome--> delayed neurotoxicity: peripheral neuropathy with demyelination that starts at the fingers and toes and moves inward. Use: Insecticide. Dangerous because it is a "protoxin" that is converted in the body by cytochrome P450 enzymes to form Paraoxon. (an AChE Inhibitor). |
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Malation
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A "Protoxin" for an Organophosphate AchE Inhibitor - IRREVERSIBLE
MOA: Drug is sucked into esteratic site of AChE (does not react with anionic site). Hydrolysis leads to STABILE phosphorylation of the esteratic site that is irreversible. ACh hydrolysis is no longer possible. Use: Insecticide for head lice. Pro-toxin that is biotransformed by CYP450's in the body into this AChE Inhibitor. "Safer" than Parathion because in MAMMALS it is degraded by carboxylesterases in plasma. In INSECTS, it is NOT degraded, making it kill bugs and not people/ pets. |
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Sarin
VX Series |
Nerve Gas - Organophosphate AchE Inhibitor - IRREVERSIBLE
MOA: Drug is sucked into esteratic site of AChE (does not react with anionic site). Hydrolysis leads to STABILE phosphorylation of the esteratic site that is irreversible. ACh hydrolysis is no longer possible. SE: Organophosphates can cause "Ginger-Jake" Syndrome--> delayed neurotoxicity: peripheral neuropathy with demyelination that starts at the fingers and toes and moves inward. Aging effect is 4 hours. Eventually will die of resp fail. Can reverse with pralidoxine in less than 4 hours. |
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Pralidoxime (2-PAM)
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An irreversible AChE Inhibitor ANTIDOTE.
"Reactivator Compound" dephosphorylates the esteratic site of AChE. Phosphorylated 2-PAM is then eliminated by the kidneys. Ineffective with AGING: after a certain amt of time after taking the organophosphate, Pralidoxime will no longer work. (w/n days). DO NOT give Pralidoxime for any AChE inhibitor other than Organophosphates...could inhibit AChE even more. |
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Atropine
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Muscarinic Antagonist - Belladonna Alkaloid
* Found in the Atropa Belladonna plant and Jimson Weed *Very muscarinic Specific * Crosses BBB (but CNS effects only seen at HIGH DOSES). Use: Symptomatic Bradycardia. Used with Edrophonium to pvt bradycardia. Used with Sux in kids to pvt bradycardia. Intraocular to dilate pupils or to protect eye with an eye injury but DO NOT USE at eye doc for ex sx due to long duration of action (7-10 days), Intoxication with AChEI's (Cholinergic Crisis), Muscarinic Agonists, Some mushroom species. SE: Facial Flushing, Increased IOP, cycloplegia/photophobia...can take DAYS to recover (7-10 days) due to long duration of action, "Atropine Flush", reverses cardiac effects of muscarinic agonists and AChEI's, Acute MI, Halothane Anesthesia, Small doses impair sweat gland activity and large doses increase body temperature due to no sweating "Atropine Fever". CNS SE: These effects are caused by decreased ACh in the brain...this mimics alzheimer's disease: --->HIGH DOSES: Impaired cognition, CNS excitation, restlessness, irritability, disorientation, hallucinations, delirium --->VERY HIGH DOSES: depression, coma, medullary paralysis |
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Scopolamine
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Muscarinic Antagonist - Belladonna Alkaloid
* Found in the "Deadly Night Shade" plant and Jimson Weed * Crosses BBB - More CNS effects at lower doses than atropine. CNS effects seen at THERAPEUTIC DOSES: drowsiness, euphoria, amnesia, fatigue, dreamless sleep w/ decreased REM....used in anesthesia. Uses: Transderm Scop Patch: Anti-nausea, motion sickness (direct vestibular effects), Antisialagogue, Sedation, Protects heart from vagal responses SE: Facial Flushing, Pupil Dilation/ Cycloplegia/ Photophobia, Lack of Accomodation, Confusion/Sedation, Increased IOP, cycloplegia |
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Ipratropium Bromide
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Synthetic Muscarinic Antagonist
*Does NOT cross BBB. Use: Inhalant for asthma/ COPD tx. Intranasal tx for rhinorhea. Bronchodilator and decreases secretions. SE: |
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Glycopyrrolate
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Synthetic Muscarinic Antagonist
*Quaternary Ammonium compound. Charged, no CNS side effects! Does not cross BBB. Use: Antisialagogue, Given with Neostigmine to pvt bradycardia, reverses cardiac effects of muscarinic agonists and AChEI's, Acute MI, Halothane Anesthesia, IBS tx at HIGH DOSES (antispasmodic effects and doesn't cross BBB), overactive/ spastic bladder, Enuresis in children SE: Can induce urinary retention in male geriatric population with prostatic hyperplasia. |
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Nicotine
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Nicotinic Agonist
Binds to preganglionic and NM Junction nicotinic receptors. SNS or PNS action depending on which system is predominate at the END ORGAN. Effects are CV (SNS): Increased HR and BP due to a1 VC and increased cat release from N receptor stimulation of adrenal medulla. GI Tract (PNS): Increased tone and activity: N/V and diarrhea. Exocrine Glands(PNS then SNS): stimulate AND THEN suppress salivary and bronchial glands. CNS Stimulants: cross BBB causing tremors, convulsions, and vomiting. (REMEMBER: the tremors seen with nicotine are CNS effects and not due to stimulation at the NM Junction). Uses: Nicotine patches and nicotine gum. |
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Mecamylamine
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Ganglionic Nicotinic Antagonist
Hexamethonium compound allows it to antagonize GANGLIOINIC nicotinic receptors (as opposed to neuromuscular nicotinic receptors Decamethonium). This is a selective block. SNS or PNS effects depending on which predominates at the end organ. (Ex: postural HOTN due to block of SNS tone of vasculature and loss of baroreceptor reflex upon standing up) (Ex: lose PNS control of GI motility - constipation results Results: Postural HOTN, decreased GI motility, urinary retention, decreased glandular secretion, cycloplegia, mydriasis(lose PNS tone to eye). Decreased sweating. NOT useful therapeutically because they block all reflex responses Uses: Tourette's Syndrome. Once used to produced controlled HOTN in surgical or emergency situations. CAN BLOCK THE BARORECEPTOR REFLEXES..INCLUDING THE REFLEX DECREASE IN HR ASSOCIATED WITH a1 STIMULATION IN A MIXED RECEPTOR BETA ADRENERGIC AGONIST (B comes 1st...incr. HR, then a1 kicks in) SE: loss of ANS tone. |
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Tubocurarine
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Long-acting Non-depolarizing NMB - prototype
(curare) - Decamethonium Quaternary Ammonium compound (does not cross BBB), no CNS effects NO ORAL BIOAVALIABILITY - indians could eat curare poisoned prey and not be paralyzed. But IV, F = 100%. Bind to NM nicotinic receptors and blocks them causing flaccid paralysis. Paralysis progresses from small, rapidly moving muscles (eye and fingers) to limbs, neck, trunk, intercostals, and diaphragm. Onset: 3-5 min Duration: 60-120 min Renally excreted (Prolonged duration results from renal impairment). SE: HYPOTENSION due to histamine release, Some blockade of ganglionic nicotinic receptors, histamine release (contraindicated in asthmatics) NMB EFFECTS ENHANCED BY DECREASED Ca2+ INFLUX VIA: 1) Inhalant anesthetics 2) Local anesthetics 3) Antibiotics: Aminoglycosides, tetracycline |
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Pancuronium
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Long-acting Non-depolarizing NMB - prototype
1st generation aminosteroid derivative. DOES NOT CROSS BBB - No CNS effects Bind to NM nicotinic receptors and blocks them causing flaccid paralysis. Paralysis progresses from small, rapidly moving muscles (eye and fingers) to limbs, neck, trunk, intercostals, and diaphragm. Onset: 3-5 min Duration: 60-120 min Renally excreted (Prolonged duration results from renal impairment). SE: Blocks cardiac vagus CAUSING TACHYCARDIA, Activates SNS - effects ganglionic N receptors, NMB EFFECTS ENHANCED BY DECREASED Ca2+ INFLUX VIA: 1) Inhalant anesthetics 2) Local anesthetics 3) Antibiotics: Aminoglycosides, tetracycline |
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Atracurium
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Intermediate Acting non depolarizing NMB
DOES NOT CROSS BBB - No CNS effects Benzylquinolone Onset: 3-5 min. Duration: 30 min Metabolized by plasma esterases and hoffman elimination. (instantaneous) Metabolite is laudenosine which can cross the BBB and cause seizure activity. Has some histamine release but not as much as curare. (could cause HOTN). Contrainidcated in asthmatics. NMB EFFECTS ENHANCED BY DECREASED Ca2+ INFLUX VIA: 1) Inhalant anesthetics 2) Local anesthetics 3) Antibiotics: Aminoglycosides, tetracycline |
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Vecuronium
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Intermediate Acting non depolarizing NMB
DOES NOT CROSS BBB - No CNS effects 2nd generation aminosteroid derivative. No cardiovascular side effects Slow onset, used for longer cases Duration: 30 min. Hepatically and renally metabolized (mainly hepatic...not as much renal dependency as with long acting NMB's). NMB EFFECTS ENHANCED BY DECREASED Ca2+ INFLUX VIA: 1) Inhalant anesthetics 2) Local anesthetics 3) Antibiotics: Aminoglycosides, tetracycline |
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Rocuronium
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Intermediate Acting, Non-depolarizing NMB.
DOES NOT CROSS BBB - No CNS effects 3rd Generation Aminosteroid. Rapid onset (1 min). Duration of 20 min. Can be used for intubation. No cardiovascular side effects Hepatically and renally metabolized (mainly hepatic...not as much renal dependency as with long acting NMB's). NMB EFFECTS ENHANCED BY DECREASED Ca2+ INFLUX VIA: 1) Inhalant anesthetics 2) Local anesthetics 3) Antibiotics: Aminoglycosides, tetracycline |
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Succynylcholine
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Depolarizing NMB
DOES NOT CROSS BBB - no CNS effects Sustained depolarization (channel open) of Nicotinic receptors at NM Junction. Cannot repolarize. PHASE 1 BLOCK. Cannot be reversed by adding ACh. AChEI's will enhance the depolarization block by inhibiting AChE and PChE. Cannot be reversed by tetanic stimulation. No fade with TOF, just equally decreased amplitude. rapid onset: 30-60 sec brief duration: 3-5 min hydrolyzed by pseudocholinesterase A prolonged duration could be caused by: 1) Cholinesterase inhibition (more Ach around to bind with Sux) 2) Atypical pseudocholinesterase (can't break down Sux) 3) AChEI drug: (Example: a pt exposed to nerve gas or an insecticide would inhibit pseudocholinesterase, Myasthenia gravis pts on neostigmine, and glaucoma pts on physostigmine). (This is the opposite response than NDNMB's..increasing the dose of sux would only further increase the duration, increasing the dose of NDNMB's would shorten the duration ...out-compete ACh. ) Side effects: -->Increased potassium levels (hyperkalemia) (channel stays open) (contraindicated in burn pts or pts with hyperkalemia, muscular dystrophy...tissue damage/ muscular weakness can cause an upregulation of nicotinic receptors and increase risk of hyperkalemia). -->Increased intraocular pressure (paralyzed ciliary muscle) -->Increased intragastric pressure Bradycardia: mimics ACh at cardiac muscarinic receptors --> Can trigger malignant hyperthermia NMB EFFECTS ENHANCED BY DECREASED Ca2+ INFLUX VIA: 1) Inhalant anesthetics 2) Local anesthetics 3) Antibiotics: Aminoglycosides, tetracycline |
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Dantrolene
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Muscle Relaxant. - Neuromuscular Blocker
Blocks Ca release from intracelluar SR via Ryanodine receptors. Use: to treat malignant hyperthermia (Ryanodine receptor disfunction). |
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Metyrosine
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a-methyltyrosine: Tyrosine Kinase Inhibitor.
Blocks the synthesis of ALL catecholamines. (not widely used for this reason.) |
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Reserpine
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Blocks the synthesis of cathecholamimes.
Inhibits the enzyme that allows dopamine and NE to enter the storage vesicles. Therefore, NE can't be synthesized or taken back up, and dopamine can't be secreted. Leads to decreased levels of NE, Dopamine, and Serotonin. Use: Antihypertensive due to decreased NE. SE: Severe Depression, Increased GI and Urinary motility, Severe Sedation (crosses BBB). Not used alot due to CNS effects. Depression was the cause of the creation of MAOI's. |
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Amphetamine
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Indirect Acting Sympathomimetric (increases CNS NE)
Increases Catecholamine release (NE, DA, and Serotonin) from storage vesicles in CNS. (crosses the BBB). MOA: Taken up into the presynaptic terminals via the reuptake mechanism. Then causes the vesicles to fuse with the membrane via synaptotagmin and release their stores. Effect: CNS stimulant: Increased attention, increased mood, insomnia, euphoria & anorexia Uses: ADHD (Attention deficit hyperactivity disorder) Narcolepsy Appetite suppressant Side Effects: Even though it's a CNS drugs...it STILL release NE in the periphery so it's side effect is HTN and increased SNS tone. |
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Tyramine
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Indirect Acting Sympathomimetric (Increases NE)
Increases Catecholamine release (NE, DA, and Serotonin) from storage vesicles in CNS. (crosses the BBB). Found in cheese and red wine. Normally it is metabolized by MAO-A in the liver and it has not effect. But if you take MAOI's AND you eat tyramine rich foods then it will increase Cat release. MAOI + cheese/wine = HTN, tachycardia, CNS effects LIver disease + cheese/wine = HTN, tachycardia |
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Guanethidine
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Decreases the release of catecholamines.
Uses the reuptake system to get into the cell. Blocks release of NE from neurons and depletes NE stores (cell won't make more if it's not being released/ used, causing a decreased SNS tone. Contraindication: Pheochromocytoma: Competes with epi and NE reuptake at the reuptake site. Tumor to adrenal glands will flood system with cats...if they can't be taken back up will cause a crisis. (it's not a reuptake inhibitor because it doesn't completely block reuptake.) Use: Antihypertensive |
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Tricyclic Antidepressants
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Catecholamine reuptake inhibitor
Antidepressant...increases NE and serotonin levels in CNS. |
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Cocaine
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Catecholamine reuptake inhibitor
--> Increases NE, serotonin and dopamine in CNS CNS stimulant USES: Local anesthetic (topical) Side Effects: Cocaine’s additive centers are due to it’s ability to increase dopamine in the brain. Cocaine deaths are due to the fact that it blocks the reuptake of all cat’s include NE And Epi…so you get SNS overstimulation (HTN, MI). |
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Mono Amine Oxidase - A
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Enzyme that metabolizes catecholamines in the synapse.
Primarily found/ produced in the presynaptic mitochondria and the liver. Inactivates: NE, Epi, Serotonin, and Tyramine |
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Mono Amine Oxidase - B
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Enzyme that metabolizes catecholamines in the synpase.
Primarily found/ produced in the CNS. (B for brain) Inactivates: Dopamine |
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Catechol–O-methyl transferase (COMT)
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Enzyme that metabolizes NE and DA.
Found in the synaptic cleft on the post-synaptic side. |
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Phenelzine
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Monoamine Oxidase Inhibitor
Inhibit the degradation of NE, Epi, DA, Serotonin, and Tyramine(cat release stimulator) in the synapse. ...these then get taken back up into the presynaptic cleft. Therefore...it SUPERLOADS the presynaptic cleft with cat's. Tyramine + MAOI yields an ACUTE HYPERTENSIVE CRISIS. ...superloaded vesciles are released. |
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Tranylcypromine
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Monoamine Oxidase Inhibitor
Inhibit the degradation of NE, Epi, DA, Serotonin, and Tyramine in the synapse. ...these then get taken back up into the presynaptic cleft. Therefore...it SUPERLOADS the presynaptic cleft with cat's. Use: Antidepresssant...INCREASE levels of NE, Epi, DA, Serotonin, and Tyramine. Tyramine + MAOI yields an ACUTE HYPERTENSIVE CRISIS. ...superloaded vesciles are released. |
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Tolcapone
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Catechol–O-methyl transferase (COMT) Inhibitor.
INCREASE levels of NE and Dopamine in CNS. Use: Adjunct tx in parkinson's disease Tyramine + MAOI yields an ACUTE HYPERTENSIVE CRISIS. ...superloaded vesciles are released. |
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Norepinephrine
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MIxed receptor Adrenergic Agonist
Binds to Alpha and Beta receptors directly. (not B2) Use: to tx HOTN and cardiogenic shock SE: MI, Angina, dysrhytmias (B1), headache, palpitations, cerebral hemorrhage or pulmonary edema (a1) α1, α2 & β1 stimulation: No effects at β2 β1(first)- stimulation increases HR and SV, (increases SBP) α1 – induced vasoconstriction increases TPR & increases DBP (Reflex decreases in HR). So HR will increase initially and the reflexivly slowly decrease with alpha1 stimulation. Ocular: α1 stimulation causes mydriasis & decreased intraocular pressure (same a phenylephrine),Constricts radial muscle (dilation) Increases outflow of aqueous humor How can you block the reflexive decrease in HR associated with alpha1 stimulation of phenylephrine, NE, and dopamine???...with nicotinic ganglionic blocker--> MECAMYLAMINE The severe VC can cause a local ischemia that will lead to necrosis with subQ application. You can block this effect with an alpha 1 blocker. (prazosin) |
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Epinephrine
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Mixed Receptor Adrenergic Agonist
Binds to Alpha and Beta receptors directly. (a1, a2, B1, B2). --> causes bronchodilation, Mydriasis, decreased IOP, relaxes uterus, GI sphincters contract, Ejaculators, relaxes detrusor muscles, etc. --> Uses: hemostasis, Bronchodilation, anaphylaxis, heart block/ cardiac arrest, angioedema, increased duration of LA, Mydriasis for sx (dipivefrin-prodrug). closed angle glaucoma --> SE: Cardiovascular: hypertension, angina, cardiac arrhythmias CNS effects: fear, anxiety, restlessness (d/t stimulation of fight or flight response). Intraocular: mydriasis (without cycloplegia), stinging, hyperemia Dose dependent cardiovascular effects: Low doses: cardiovascular effects look like isoproterenol (a beta agonist) β1 stimulation: increases HR & SV, increases cardiac output, and increases SBP β2 stimulation: relaxation of vasculature decreases TPR and decreases DBP ....So HR increases Higher doses: cardiovascular effects look like NE β1 stimulation: increases HR & SV, increases cardiac output, & increases systolic BP α1 stimulation: Vasoconstriction leads to increased TPR, increased diastolic BP and reflex decreases in HR ....So HR will start out high and then reflexively slow. This can be blocked with a ganglionic nicotinic antagonist. Epinephrine Reversal: Allows you to differentiate high dose EPI from NE. Administer an α1 Antagonist (PRAZOSIN): effects of EPI go from a hypertensive (pressor) response to a hypotensive (depressor) response due to unmasked effects of B2. NE will not be as dramatic. |
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Dopamine
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Mixed Receptor Adrenergic Agonist
DOSE DEPENDENT ACTION: Beta receptors more sensitive to mixed-acting agents than Alpha receptors. Dose dependent vascular effects when α1 effects oppose β2 effects (smooth muscle contraction vs contraction). Low doses: β2 stimulation leads to vasodilation, decreased TPR and decreased DBP (reflex inc HR). And B1 inc in HR. High doses stimulate α1 receptors to increase TPR and increase DBP (reflex decrease HR) Low dose= D1 (VD in renal and mesenteric vascular beds) Moderate dose: D1, β 1 (Increase in HR, SV, and SBP) High dose: α1, β1 (Increased DBP, Reflex decrease in HR). Low doses are used to increase UO, moderate doses are used for Cardiogenic shock due to increased UO AND increased CO. |
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Phenylephrine
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Direct Acting a1 Agonist: Contracts smooth muscle
EFFECTS: --->Alpha1 contraction of vascular smooth muscle ---->Increased TPR ----->Increased diastolic BP ---->Reflex decreases in HR (baroreceptor reflex) ----> α1 contracts radial muscle of eye: mydriasis ----->α1 increase outflow of aqueous humor: Decreased IOP Uses: Nasal decongestant, tx of HOTN, Pupil Dilation for surgical procedures (has a shorter duration than atropine and no cycloplegia), glaucoma tx w/o cycloplegia SE: HTN, headache, palpitations, cerebral hemorrhage or pulmonary edema |
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Clonidine
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Direct-acting Alpha 2 Agonist
Will inhibit the release of NE, leading to decreased SNS tone systemically and in the CNS. Effect: antihypertensive. HOWEVER…the antihypertensive effect is ACTUALLY due to direct CNS effects….they effect the medullary center and actually DECREASE SNS TONE IN THE CNS to drop BP…NOT just by inhibiting NE release. |
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Methyldopa
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Direct-acting Alpha 2 Agonist in CNS
Will inhibit the release of NE, leading do decreased SNS tone systemically and in the CNS. Prodrug...converts to α-methylnorepinephrine after biotransformation. Effect: antihypertensive. HOWEVER…the antihypertensive effect is ACTUALLY due to direct CNS effects….they effect the medullary center and actually DECREASE SNS TONE IN THE CNS to drop BP…NOT just by inhibiting NE release. |
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Isoproterenol
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Direct Acting Beta Receptor Agonist
NONSELECTIVE B1 Stimulation: Increases HR and Stroke Volume (increased CO and INCREASED SYSTOLIC BP) B2 Stimulation: Bronchodilation, VD of SM vasculature (decreased TPR and DECREASED DIASTOLIC BP), relaxation of uterine smooth muscle. Isoproterenol will maintain the increase in HR because B1 will directly increase HR while B2 will stimulate the baroreceptor reflex..causing dec DBP and a reflex increase in HR. SE: risk of MI/ angina, dysrhytmias |
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Dobutamine
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Direct Acting B1 Receptor Agonist
B1 SELECTIVE Increases HR and SV (increased SBP) Use: Tx of Acute CHF SE: risk of MI/ angina, dysrhytmias |
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Albuterol
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Direct Acting B2 Receptor Agonist
B2 SELECTIVE *Bronchodilation *VD of SM beds (decreased TPR and DBP) *Increase muscle spindle activity Uses: Inhaled bronchodilator for ashthma/ COPD SE: Tremors...will increase muscle spindle firing. |
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Salmeterol
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Direct Acting B2 Receptor Agonist
B2 SELECTIVE Long Acting..used only in combination with other drugs *Bronchodilation *VD of SM beds (decreased TPR and DBP) *Increase muscle spindle activity Use: asthma/ COPD...in comb with other drugs....when used alone can mask pulmonary changes due to long duration of action. Will increase muscle spindle firing...tremors |
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Ritodrine
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Direct Acting B2 Receptor Agonist
B2 SELECTIVE *Bronchodilation *VD of SM beds (decreased TPR and DBP) *Relaxed uterine SM * Increase muscle spindle activity USE: Tocolytic...relaxes smooth muscles of uterus. Terminates preterm labor. SE: tremors...increase muscle spindle firing. |
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Selegiline
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MAO-B Inhibitor
Increases Dopamine (only) stores in the presynaptic vesicles of the CNS. Used to treat parkinson's disease. Avoid tyramine when taking. |
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Phentolamine
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Alpha 1-2 receptor COMPETITIVE antagonist - Can be overcome by adding more Alpha agonist
a1 Block Effects: Postural HOTN and decreased BP. Reflex Tachycardia. Block at smooth muscles of prostate and bladder, decreases resistance to urine flow, Miosis, Nasal congestion, Inhibits ejaculation a2 Block Effects: INcreased NE release and BP, tachycardia. Uses: Pheochromocytoma: Used in preoperative management of catecholamine secreting tumors (usually adrenal medulla). |
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Phenoxybenzamine
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Alpha 1-2 receptor NON-COMPETITIVE antagonist - cannot be overcome by adding more agonist
Long duration of action. Uses: Pheochromocytoma: Used in preoperative management of catecholamine secreting tumors (usually adrenal medulla). |
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Prazosin
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Alpha 1 antagonist
(all alpha antagonists end in -sin) Effects: Postural HOTN and decreased BP. Reflex Tachycardia. Block at smooth muscles of prostate and bladder, decreases resistance to urine flow, Miosis, Nasal congestion, Inhibits ejaculation. Not as much of a reflex tachy as with a2 blockade as well. USES: --->Antihypertensive --->Benign prostatic hyperplasia – (blocks a1 effects at bladder sphincter and at prostate gland, decreasing resistance to urine outflow.) --->Reverse vasoconstriction induced by NE Side effects --->Miosis --->Nasal congestion --->Inhibit ejaculation ---> Othostatic HOTN (When pts take these are prone to syncope with postural HOTN. Overtime…their system will adapt to the drug and they will be okay. |
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Propanolol
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Beta1-2 antagonist - Prototype
EFFECTS: --->Antagonize sympathetic stimulation of heart --->decrease BP (Lower BP by blocking activity at the heart (lowering HR) AND this effect is much greater in a HTN pt than in a healthy pt due to the effects of the disease on the body.. --->Block renin release (B1 block) --->Block production of aqueous humor in eye to decrease intraocular pressure --->CNS Effects (crosses BBB) USES: ---> Antihypertensives --->Ischemic Heart disease (Reduce episodes of angina, Decrease oxygen demand, and Improve survival after myocardial infarction) --->Cardiac Arrhythmias (decrease SA node activity and slow AV-conduction --->Hyperthyroidism: Blocks effects of sympathetic stimulation at the heart. Inhibits deiodinase activity: blocks conversion of thyroxine (T4) to triiodothyronine (T3) --->Essential familial tremor:(Block β2 activation of muscle spindle efferents) --->Prevent performance anxiety (social phobias)(Block somatic symptoms of sympathetic activation) --->Prevent Migraines (CNS effect) SE: BRONCHOCONSTRICTION - contraindicated in asthmatics/ COPD. Bronchoconstriction. Block sympathetic responses associated with hypoglycemia (contraindicated in DM), CNS effects: sedation, sleep disturbances, depression, nightmares, Chronic administration of beta receptor antagonists may shift plasma lipids (increase VLDL and decrease HDL), Rapid discontinuation of Beta blockers after chronic use is not recommended due to receptor up regulation (more beta receptors made) |
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Timolol
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Beta1-2 antagonist
EFFECTS: --->Antagonize sympathetic stimulation of heart --->decrease BP --->Block renin release (B1 block) --->Block production of aqueous humor in eye to decrease intraocular pressure WITHOUT cycloplegia or mydriasis, etc ---> CNS Effects (crosses BBB) USE: Used as topical in treatment of glaucoma (intraocular)..decreases Aqueous humor production. Side Effects: Bronchoconstriction & bradycardia due to systemic absorption. CONTRAINDICATED IN COPD OR ASTHMATICS |
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Carvedilol (coreg)
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Beta1, Beta2, alpha1 antagonist
Used as antihypertensive & in congestive heart failure Increases efficiency of heart, and decreases BP with α1 block. Effects similar to beta-adrenergic antagonists, plus decreases in BP due to α1 block Increases efficiency of heart Uses: Antihypertensive (decreased HR and SVR)… Congestive Heart Failure (increased efficiency of the heart.) SE: Chronic administration of beta receptor antagonists: may shift plasma lipids and increase LDL and decrease HDL, may cause an upregulation of B receptors and make it hard to D/C, cause bronchoconstriction, mask the signs of hypoglycemia with DM |
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Pindolol
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Partial Beta Agonist (serves as an antagonist)
Less effect on lipids (less B3 block), less Beta receptor up-regulation (because body see it as an agonist...not an antagonist....this means you can D/C it faster), Less side effects (body sees as an agonist). Increased exercise reserve due to less side effects. |
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Metoprolol
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B1 selective Antagonist
Effects: competitive antagonist at β1 receptors -->Block sympathetic stimulation of the heart -->Less bronchoconstriction than non-selective blockers -->Less influence on glycogenolysis and insulin release Uses: Antihypertensives Ischemic Heart disease Cardiac Arrhythmias SE: Some risk of developing diabetes (masks the side effects of low blood sugar). High doses still block β2. CNS EFFECTS: Sedation, Sleep disturbances (nightmares), and Depression |
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Atenolol
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B1 selective Antagonist
Effects: competitive antagonist at β1 receptors -->Block sympathetic stimulation of the heart -->Less bronchoconstriction than non-selective blockers -->Less influence on glycogenolysis and insulin release Uses: Antihypertensives Ischemic Heart disease Cardiac Arrhythmias **Less CNS effects then metoprolol**!! **Exclusive Renal excretion!!! (safe for patients with liver problems)** SE: Some risk of developing diabetes (masks the side effects of low blood sugar). High doses still block β2. |
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Carbonic Anhydrase Inhibitors
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CA is an enzyme associated with aqueous humor production
THESE DRUGS DO NOT CHANGE PUPIL DILATION AND HAVE FEW OTHER SIDE EFFECTS SO ARE VERY POPULAR. .. |
