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Pharm2 intro
| Question | Answer |
|---|---|
| What does the somatic motor neuron release and what type of receptor does it bind to? | ACh, Nm |
| What are 4 pathways of NE once it has been released from the post synaptic neuron? | 1.Binds to Alpha2 receptors causing inhibition of further NE release (always). 2.Bind to effector cell receptor. 3.Diffuse out of synapse. 4.Re-uptake into pre-snaptic neuron cleft/terminal bouton via NET (either reused or degraded by MAO). |
| What is the main mechanism of NE inactivation? | Re-uptake by NET (NE Transporter) and degraded in the post-ganglionic pre-synaptic nerve terminal by Monoamine oxidase (MAO). |
| Phenylethanolamine-N-methyltransferase (PNMT) | Enzyme in the adrenal medulla that converts NE to Epi. **this explains the 9:1 Epi:NE ratio. |
| Greater affinity to NE: Alpha1 or Alpha2s? | SAME AFFINITY |
| Greater affinity to NE: Beta1 or Beta2s? | Beta1 have a much greater affinity. |
| Greater affinity to Epi: Alpha1 or Alpha2s? | SAME AFFINITY |
| Greater affinity to EPI: Beta1 or Beta2s? | SAME AFFINITY |
| Enzyme responsible for ACh breakdown in the synaptic cleft? | AChE |
| if ACh diffuses out of the synaptic cleft and enters into the BL, what is it converted into? | 1.Choline. 2.Acetate. |
| Locations of Nicotinic Receptors? | 1.Parasymp ganglion. 2.Sympathetic ganglion. 3.Skeletal muscle (need the fast response N receptors, not the slower responding M receptors). |
| Which ACh receptor is a fast response Na+/K+ ligand gated channel? | Nicotinic: 1.Nn: Neuron (firing). 2.Nm: Muscle (contraction). **Na+ influx causes depolarization |
| Which ACh receptor is a slower response G-protein receptor? | Muscarinic |
| What mechanism is used by all adrenergic receptors? | G-protein coupled receptors. |
| G-proteins: Gs | Activates adenylyl cyclase (Inc cAMP and PKA). See with: 1.Beta1 (Heart & Kidney). 2.Beta2 (Smooth muscle & liver). 3.Beta3 (adipose) |
| G-proteins: Gq | activates phospholipase CB (Inc [Ca+] and PKC). See in: 1.Alpha 1 (smooth muscle, secretory glands). 2.M3 (smooth muscle, secretory glands) |
| What would an increase in intracellular [Ca+] as a result of Gq? | 1.Smooth muscle contraction. 2.Inc secretion |
| G-proteins: Gi | Inhibits adenylyl cyclase (Dec cAMP, Inc K+ permeability). See in: 1.Alpha2 (Pre-synaptic symp clefts, inhibits further NE release). 2.M2 (Dec HR in Heart) |
| B1 affect on heart & Kidney (juxtaglomerular cells) | 1.Heart: Inc HR and contractility. 2.Kidney: Renin release. **Gs |
| B2 affect on smooth muscle and liver? | 1.Smooth muscle: relaxation. 2.Liver: glycogenolysis, gluconeogenesis.. **Gs |
| B3 affect on adipose | Lipolysis. **Gs |
| How many molecules of ACh are required to open Nicotinic ligand-gated Na+/K+ channels? | 2 |
| What happens if you activate an Gi in the SA node? | Inc K+ permeability, causes hyperpolarization (via GIRK channels) which will prolong the diastolic depolarization phase. |
| Chronic exposure to an Antagonist? | Receptor Up-regulation. |
| Chronic exposure to an Agonist? | Receptor Down-regulaiton. |
Created by:
WeeG
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