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Pharmacodynamics: What is an LDR curve? What is the difference between quantal and graded LDR curves? Potency If the maximal response to a new medication is a 50mmHg decline in SBP, what is the ED50 on a graded LDR curve? If the desired response for a new medication is a decrease in SBP to < 130 mmHg, what is the ED50 ona quantal LDR curve? Efficacy Compare each drug's potency and efficacy What degree of effect a dose change will have (slight change on a steep curve will NSG 531 Advanced Pharmacology Exam 2 What does the steepness of anLDR ilicitilargeletfectsy bigiehangelonla curve indicate? Stereoisomer Enantiomers Racemic mixture Ka Kd NSG 531 Advanced Pharmacology Exam 2 The concentration of drug in the plasma when 50% of the target receptors are occupied Partial agonist Why would we give a partial agonist? Competitive antagonism What will the LDR curve of an agonist combined with a fixed dose of a competitive antagonist look like? A drug that binds to a receptor and stimulates an effect that has both lower potency (curve is shifted right of the full agonist) and efficacy (curve is shorter in height). To prevent undesirable side effects of the full agonist, or because the full agonist isn't necessary. Ex: greater pain relief and psychotropic effects from methadone, but less respiratory depression from buprenorphine. Reversible; effects depend on the relative concentration of the agonist and antagonists (which also occupy receptor sites) Parallel to the agonist curve, but shifted to the right. Effects of the antagonist can be overcome with an increased dose of the agonist. always overcome it by giving a higher dose of agonist. Receptors are considered when the maximal response is elicited by an agonist at a concentration that doesn't produce full occupancy of the available receptors. We can demonstrate that spare receptors exist if an agonist's EC50 is than its Kd. A drug with an EC50 of 1 mole/liter and a Kd of 2 moles/liter tells us that: Signal transduction Spare; curve could continue to be shifted right and parallel, even with irreversible, noncompetitive antagonists, until all spare receptors are in use and the antagonist concentration is high enough. lower; the drug is eliciting maximum effects in 50% of the population while occupying less than 50% of the receptors (spare receptors exist to be recruited in the event that an antagonist is given) EC50 < Kd, meaning that the drug doesn't need to occupy all the receptors to elicit a maximum effect. There are more receptors available that will be occupied if an antagonist drug is given. The conversion of an extracellular chemical signal (ligand, drug, etc.) True or false: signal transduction pathways amplify the signal so that only a few extracellular molecules are needed to evoke a response. What are the four major receptor sites in tissues that act as targets for drugs? What is the next step after a ligand binds to a complementary G protein- coupled receptor? NSG 531 Advanced Pharmacology Exam 2 into a cellular response (action potential, etc.). True; the reason why we can get maximal respones to a drug without full receptor occupancy. 1) G protein-coupled receptors (mostcommon) 2) enzyme-linked receptors 3)ligand-gated ion channels 4) intracellularreceptors The ligand sends a signal to the G protein (composed of alpha, beta, and gamma subunit). The alpha subunit breaks off to be phosphorylated and becomes activated alpha-GTP, which proceeds to True or false: phosphorylation of intracellular proteins is a major mechanism of action for many of our drugs. Describe the effects after activation of a tyrosine kinase (enzyme)-linked receptor. Ligand-gated ion channels S17 NSG 531 Advanced Pharmacology Exam 2 True After the ligand binds, signals are sent to the intracellular tyrosine kinase domain of the receptor and a conformational change, or allosteric activation, occurs (tyrosine kinase domains swivel to face, and autophosphorylate, each other). Afterwards, other cellular proteins are also susceptible to being phosphorylated by the activated enzymes. Channel composed of simple proteins that act like a gate. When a ligand binds to the receptor, the channel opens and a specific ion moves in or out of the cell according to its concentration gradient. Those ions may potentiate or inhibit an action potential. Intracellular receptors Describe the mechanism by which activation of intracellular receptors produce new proteins. True or false: after ligand binding, the response from a ligand-gated ion Expressed only within the cytoplasm, such that any binding ligand must be lipid soluble and diffuse according to its concentration gradient (often a steroid). Has 3 components - a drug binding site, heat shock protein, and underlying DNA-binding domain. The ligand (steroid) binds to the receptor, which stimulates release of the heat shock protein and exposes the underlying DNA-binding domain. The receptor then translocates into the nucleus of the cell and activates a gene, transcribes mRNA, translocates ribosomes, and produces new proteins. True; intracellular receptors involve the longer process of synthesizing new proteins. channels open and K+ rushes out (repolarization). Cell becomes hyperpolarized to -90mV and K+ channels close, then resting membrane potential is restored to - 70mvV. What is the stimulus that ends depolarization after Na+ rushes into the cell through a voltage-gated ion channel? Absolute refractory period Relative refractory period Channel-inactivating segment blocks the channel and Na+ is prevented from entering the cell. Triggers repolarization. The period from the initiation of an action potential to just after the peak of depolarization, lasting 1-2 ms. All Na+ channels are blocked by the channel-inactivating segment and cannot reopen, no matter how strong the stimulus. When enough Na+ channels have reverted back to their resting state (without the channel-inactivating True or false: refractory periods prevent hyperreactivity, which is important for homeostasis. What are the 2 divisions, and 3 principal functions of the autonomic nervous system? Functions of the parasympathetic nervous system (PNS): Functions of the sympathetic nervous system (SNS): In the sympathetic nervous system, the preganglionic fibers segment) that they could respond to a strong stimulus. True Parasympathetic and sympathetic; regulates heart, smooth muscles, and secretions. Rest and digest: slows heart rate, increases gastric secretions, empties bladder and bowel, focuses eye for near vision, constricts pupil, constricts bronchi. Fight or flight: increases heart rate, increases BP, shunts blood from skin and viscera to skeletal muscles, dilates bronchi, and mobilizes energy stores. short; thoracic and lumbar region of the spinal cord; long How is acetylcholine synthesized and released from pre- and postganglionic fibers? What happens to ACh after it's released into the synapse? How is norepinephrine synthesized and released from post-ganglionic fibers in the ANS? The nutrient choline enters the cell via a symporter (with Na+). An enzyme strips acetyl coenzyme A of its acetyl group and gives it to choline, making it acetylcholine. ACh is packaged into vesicles and stored. An action potential triggers the opening of voltage-gated Ca2+ channels. Flood of Ca2+ causes the vesicles to move to the end of the axon, fuse with the cell membrane, and mediate exocytosis. ACh can 1) bind to its muscarinic or nicotinic receptors 2) be degraded by acetylcholinesterase into acetate and choline, or 3) bind to the presynaptic receptor to inhibit further release of ACh. The precursor tyrosine is brought into the cell via a symporter (with Na+). Tyrosine is converted into dopa, which is converted into 8/17 NSG 531 Advanced Pharmacology Exam 2 voltage-gated Ca2+ channels. Flood of Ca2+ causes the vesicles to move to the end of the axon, fuse with the cell membrane, and mediate exocytosis. What happens to norepinephrine once it's released into the synapse? dopamine. Dopamine is stored in vesicles, and inside the vesicles it's converted to norepinephrine. An action potential triggers the opening of Norepinephrine can 1) bind to alpha or beta receptors expressed on the surface of the target cell, 2) be degraded into inactive metabolites by the enzyme COMT to be excreted in urine, or 3) bind to a presynaptic receptor to inhibit further release. Bethanechol Pilocarpine 9/17 NSG 531 Advanced Pharmacology Exam 2 Muscarinic receptor agonist that contracts ciliary muscles of the eye to allow Selective M3 receptor agonist that causes bladder muscle contraction and sphincter relaxation...indicated for urinary retention. Adverse effects: salivation, lacrimation, bronchospasm, diarrhea, and bradycardia. for aqueous humor outflow...indicated for glaucoma. Atropine Nonselective competitive (against ACh) muscarinic antagonist. Indicated for bradycardia, Gl hypermotility, and to induce pupil dilation (mydriasis) for eye exams. Adverse effects: dry mouth, blurred Epinephrine is released from , and binds to Norepinephrine is released from , and binds to Alpha 1 adrenoceptors are what type of receptor? Where are alpha 1 receptors located? What effects does ligand binding have at each site? vision, urinary retention, constipation, anhidrosis (inability to sweat). the adrenal medulla; all four adrenoceptors (with a greater affinity for beta receptors) post-ganglionic fibers; alpha 1, alpha 2, and beta 1 receptors (greater affinity for alpha receptors). G protein-coupled receptors, linked to the phospholipase C beta pathway. Binding of norepinephrine will increase IP3 and lead to smooth muscle contraction. Eyes (mydriasis), blood vessels in skin, viscera, gut, kidney, and brain (vasoconstriction), genitourinary (prostate contraction and ejaculation, smooth muscle contraction of internal urethral sphincter). 
