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Adrenergic drugs
Kaplan medical
| Question | Answer |
|---|---|
| What is Epinephrine reversal? | To test if Epinephrine or NE is given If you give an α₁-blocker and then epinephrine, you get hypotension — that’s epinephrine reversal. If you give an α₁-blocker and then norepinephrine, you do not get hypotension because NE lacks β₂ activity |
| Describe the synthesis of NE | Tyrosine gets taken up (presynaptic neuron) converted to DOPA —> Dopamine —> NE Enzymes: 1) Tyrosine hydroxylase 2) DOPA decarboxylase/ L- aromatic among acid decarboxylase 3) DA beta hydroxylase |
| What is the rate limiting step in NE synthesis? | Tyrosine hydroxylase |
| When NE gets released from te presynaptic neuron it has different fates (4), what are they? | 1) Reuptake (by NaCl NE co-transporter) this is why NE has such a short half life 2) Act on the adrenergic receptors (alpha or beta) 3) broken down 4) signal a negative feedback loop via a receptor on the presynaptic neuron (alpha 2) |
| NE gets broken down by 2 enzymes, what are they? (in the synaptic space and mobile pool in presynaptic neuron) | Synaptic space: by COMT Presynaptic neuron: by MAO-A |
| Alpha 1 receptor agonists? | Phenylephrine |
| Alpha 2 agonists? | 1. Clonidine 2. Methyldopa |
| Non selective beta receptor agonists?(2) | 1. Isoproterenol ( beta 1= beta 2) iso= the same/equal 2. Dobutamine (beta 1> beta2) |
| Beta 2 selective agonists (3)? | 1. Albuterol 2. Terbutaline 3. Salmeterol |
| Beta 3 selective agonists (1)? | Mirabegron (used for overactive bladder but only oerscribes after M3 antagonist haven’t work, Oxybutynin) |
| What is the difference between NE and Epi (based on the receptor they do/donot work on)? | Beta 2 receptors (NE does not but Epi does) |
| Which adrenergic receptors are more sensitive to activators? (Alpha or Beta) | Beta receptors followed by alpha receptors |
| Dopamine works on which receptors? (Based n what) | Dopamine works on D1, B1 and A1 depending on the dose. From low to high dose follow this sequence. |
| Cathecolamines effect is first on which organ, blood vessels or cardiac muscle (heart)? | Blood vessels gets work upon first. |
| Epi can increase (alpha1) or decrease (beta 2) the BP, what determine what it will do? | The DOSE. |
| High dose Epi acts as which drug? | NE |
| Low dose Epi acts as which drug? | Isoproterenol (beta1=beta2) |
| What drugs “increase” the RELEASE of NE from the presynaptic neuron (3)? | 1. Tyramine ( this occurs when a MAO-A inhibitor is given b/c it gets to accumulate) 2. Amphetamines (increase release of DA, NE, 5HT) 3. Pseudoephedrine (not really used anymore but Phenylephrine) |
| What drugs inhibits the NE reuptake (2) ? | 1. cocaine 2. TCAs (Tricyclic antidDepressants) |
| What are the forms of MAO and where are they found? | MAO-A (anywhere) and MAO-B (brain mostly) - MAO-A metabolizes tyramine, NE, 5HT) - MAO-B metabolized DA. Agonists is Selgiline |
| Non-selective alpha blockers (2)? | 1. Phentolamine 2. Phenoxybenzamine (noncompetitive inhibitor used in Pheochromocytoma) |
| alpha 1 selective blocker? | All the “-zosin” - Prazosin - Doxazosin Terazosin Tamsulosin (treat BPH only) All of the -zosin act on alpha 1 and are good for BHP but the last one is isolated BHP) |
| Alpha 2 selective blocker? | Mirtazapine |
| Beta 1 blockers vs Non-selective beta 1 blocker? (Names | Beta 1 blockers: A-M w/ suffix -o lol Beta 1 non selective blockers: N-Z w/ suffix -o lol |
| What are the effects of glucagon on the heart? | It’s a Positive inotropic and chronotropic via its own Gs receptor (not via beta 1). That is why it is used in beta-blocker overdose. |
| What are the partial Beta blocker agonist (Intrinsic sympathomimetic activity) ? | 1. Acebutolol 2. Pindolol. Alone they acts as a agonists (not the case in the human body) but in the prescience of NE or Epithey acts as a n antagonist. |
| Which beta blocker does not enter the CNS? | Atenolol |
| what are the (2) Beta blockers w/ alpha blocker properties? | 1. Labetalol 2. Carvediol |
| Which beta blocker also has K channel blockage properties? | Sotalol |
| What is Open angle Glaucoma? | A chronic condition with increased intraocluar pressure d/t decreased reabsorption of aqueous humor. Lead to progressive, painless vision loss, if untreated. |
| What is intraocular pressure and how is it maintained. | A balance between fluid formation and its drainage from the globe. |
| Which structure makes the aqueous humore and what helps with the drainage? | -Fluid formation; Ciliary epithelial cells makes the fluid ( a beta agonist aids in this recess too that is why a beta blocker is used in glaucoma to stop this fluid formation) drainage: PGF2a aids in drainage (a prostaglandin) |
| What is a closed angle glaucoma? | Acute condition w/ increased IOP dt blockade of the canal of Schlemm. |
| Which class of drugs are contraindicated in closed angle glaucoma? | Abtimuscarinic drugs and alpha 1 agonists b/c both increase the IOP. |
| What is a PGF2a agonist and MOA? | Latanoprost. Increases aqueous humor drainage through the uveoscleral pathway |
| What other two drugs decrease aqueous humor formation? | Acetazolamide and Apraclonidine |
| What is a Dopamine agonist? | Fenoldepam |
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DVD27
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