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Adrenergic blockers -pharmacology 2
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- 1What are sympathetic adrenergic neuronal blockers divided into?Peripherally acting and centrally sympathetic neuronal blockers
- 2What do peripherally blocking adrenergic blockers do?Decrease the availability of NE to its receptors
- 3What do centrally blocking neuronal blockers do?Stimulate α2 adrenergic receptors sites in brain to indirectly reduce neuronal traffic to vasomotor centers to peripheral cardiovascular organs
- 4What type of activity do peripheral acting adrenergic inhibitors inhibit?inhibit the activity of sympathetic nervous system
- 5How does peripheral acting blockers inhibit sympathetic NS?decreasing availability of NT, NE, to adrenergic receptors
- 6Peripherally acting reserpine decreases the uptake (VMAT2) of intraneuronal DA and NE, so how does it reduce amount of DA and NE?less DA and NE in storage vesicles so depletion of stored level eventually decreases the amount released with each nerve pulse ("silence neuron")
- 7Cost effective reserpine decreases what to reduce BP?Cardiac output and peripheral aerterial pressue
- 8What type of onset is Reserpine which makes it less associated with side effect?Slow onset; depression
- 9What are the CNS side effects associated with Reserpine? Why?Sedation and mental depression; NT depleting action
- 10what are some of the Reserpine side effects relating to peripheral depletion?Diarrhea, hypotension, bradycardia and fluid retention
- 11What are the side effects caused in response?Unopposed parasympathetic
- 12Reserpine is cleared from the circulation fast, why is its duration long?Depletion on NE vesicles is irreversible so its long lasting beyond termination of drug
- 13How are Reserpine and Guanethidine similar and different inhibition of peripheral SNA?They both block the reuptake of DA and NE into storage vesicles but Guanethidine also directly blocks NE from release at nerve endings
- 14Guanethidine is no longer used in the USA but it was once used in what capacity?To treat hypertension
- 15Guanethidine also cause postural hypotension, bradycardia, fluid retention, diarrhea and aggravation like reserpine but it does notCause CNS effects because it cannot enter the brain due its structure
- 16Why does guanethidine cause the side effects?Due to an unopposed parasympathetic activity
- 17What do tricyclic antidepressants prevent in the guanethidine to interfere with its effectivenessThey prevent uptake of the sympathetic nerve terminal by reuptake pump, a step needed to activate guanethidine
- 18What are centrally acting adrenergic neuronal inhibitors? Target? Why?α2- receptor agonists; vasomotor of the brain bc of the subtypes in the brain and not anywhere else in the brain
- 19What do centrally acting inhibitors do at the vasomotor centers?Decrease the sympathetic neuronal outflow from CNS to peripheral organs
- 20What is not affected by centrally acting inhibitors? Which helps how?certain normal rapid reflex mediated changes in SNA; fewer than expected hypotensive symptoms
- 21What is not treated with centrally acting inhibitors?Raynaud's and in exercise capacities (it makes things worse because SNA would have helped)
- 22Why is Methyldopa different from other centrally acting inhibitorsrequires metabolism to activate and has some unique autoimmune side effects
- 23What do enzymes that support norepinephrine formation from DA, convert Alpha-methyldopa into?alpha-methylnorepinphrine
- 24What type of agonist is methyldopa? What is its target and function?α2 adrenergic agonist; vasomotor neurons centers; decrease the outflow of SNA to peripheral tissues
- 25What happens as a result of methyldopa's decrease in SNARenal renin decreases; HR and CO may decrease, and arterial peripheral resistance falls
- 26What type of HTN is methyldopa used for? And why?HTN during pregnancy because it does not harm the fetus
- 27Methyldopa has similar side effects of other central α2 agonists like fluid retention, dry mouth and sedation but it particularly does what?induces autoimmune disorders
- 28What does a positive Coombs test signify in patients taking methyldopa? How is it stopped?Hemolytic anemia, reversed by not taking drug
- 29Clonidine is similar to methyldopa but it differs...not causing autoimmune disease
smaller dose requirement
absorbed through the skin - 30Clonidine can be given as a patch for transdermal absorption with smoother BP control and less severe side effects, how? Side effect?patches= slower rate so there are no spikes (peaks and troughs) but patches may cause local skin reactions
- 31Clonidine must be stopped slowly because of rebound hypertension, why does methyldopa not have that?Methyldopa's mechanism is storage of its of metabolites in vesicles at nerve endings so its clearance happens at a slower pace
- 32What other diseases does clonidine treat?ADHD, menopausal hot flashes, PTSD, Nicotine (alcohol and morphine) withdrawal and spinal cord analgesic
- 33Apraclonidine is structurally related to clonidine but can be used for IOP (unlike clonidine bc)?less systematic effects
- 34Guanabenz is similar to clonidine in terms of actions and use of HTN but it can also? It does not require?lower total serum cholesterol causes less reactive fluid retention (so that diuretic may not be needed)
- 35Guanfacine is also similar to Clonidine and has a hypertensive use but causes less?Sedation and withdrawal syndrome
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- Der Nutzer hat seine Fachbereichs-Information gelöscht. Karteikarten am Adrenergic blockers -pharmacology 2, erstellt von Gelöschter Nutzer am 21/10/2017.
- Erstellt von
- Gelöschter Nutzer · Okt 2017
- Aktualisiert
- 21 Okt 2017
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- 25
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- Erstellt von Jen Orellana · 21 Okt 2017
- Kopiert von Jen Orellana · 21 Okt 2017
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