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10 Cards in this Set
- Front
- Back
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What is Neuropharmacology?
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Study of drugs that alter processes controlled by the nervous system (peripheral and central)
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What are cholinergic receptors?
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Mediate responses to acetylcholine, hence mediate responses at all junctions with acetylcholine as the transmitter
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What is acetylcholine?
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a direct-acting cholinergic neurotransmitter agent widely distributed in body tissues, with a primary function of mediating synaptic activity of the nervous system and skeletal muscles. Its half-life and duration of activity are short because it is rapidly destroyed by acetylcholinesterase. Its activity also can be blocked by atropine at junctions of nerve fibers with glands and smooth muscle tissue. It is a stimulant of the vagus and parasympathetic nervous system and functions as a vasodilator and cardiac depressant. Acetylcholine is used therapeutically as an adjunct to eye surgery and has limited benefits in certain circulatory disorders because of its short half-life.
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What are adrenergic receptors?
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Mediate responses to norepinephrine and epinephrine, hence mediate responses with ep and norep as transmitters
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What is norepinephrine?
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adrenergic hormone (catecholamine) that acts to increase blood pressure by vasoconstriction but does not affect cardiac output. It is synthesized by the adrenal medulla, the peripheral sympathetic nerves, and the central nervous system. It is available as a drug, levarterenol, which is used to maintain the blood pressure in acute hypotension secondary to trauma, heart disease, or vascular collapse.
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What is epinephrine?
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endogenous adrenal hormone and synthetic adrenergic agent. It acts as an agonist at alpha-1, alpha-2, beta-1, and beta-2 receptors. indicationsIt is prescribed to treat anaphylaxis, acute bronchial spasm, and nasal congestion and to increase the effectiveness of a local anesthetic. contraindication Known hypersensitivity to this drug prohibits its use. adverse effects Among the most serious adverse effects are arrhythmias, increases in blood pressure, rebound congestion (when it is used as a decongestant), tachycardia, and nervousness.
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What are receptor subtypes?
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Respond to the same transmitter but are found in different places in the body. EX. Receptors responding to acetylcholine are found in ganglia of autonomic nervous system, at neuromuscular joints, and on organs related to parasympathetic nervous system. These receptors are different from one another even though they are all activated by the same thing. So, they are in the same category, cholinergic, but are in different subtype groups based on their unique differences
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Discuss the concept of selective drug action and receptors.
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Selective drug action means that we can target the location of a drugs action based on receptor types. Drugs will act on certain, specific types of receptors. Since our body has several different receptors we select a drug to target the receptors we need activated or blocked and use the appropriate drug. The more different receptors in the body, the more greater the chances of producing selective drug effects. There is a great example on page 103. In the diagram, Mort has all functions activated by one receptor thus selective drug action is impossible because it will target other receptors too. Merv has all body functions activated by different receptors. It is possible to target one function for him without changing others.
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Describe the mechanism of action of neuropharmacologic drugs.
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First, here’s how neurons elicit responses from other cells: There is axonal conduction where there is conduction of an action potential down the axon of a neuron. Next there is synaptic transmission where information is carried across the gap between the neuron and the post-synaptic cell. The post-synaptic cell can be another neuron, a muscle cell, or a cell with within a secretory gland. In order for the action potential to cross the gap, the neurotransmitter molecule must be released from the axon terminal and the molecules must bind to receptors on the post-synaptic cell. When this happens, a series of events occurs in the postsynaptic cell, causing a change in its behavior. The nature of the change depends on the identity of the neurotransmitter and type of cell.
Now, here’s how neuropharmacologic drugs affect the body: most of neuropharmacologic drugs alter synaptic transmission while a few alter axonal conduction. Interfering with synaptic transmission allows drugs to be much more selective because this process is more unique to the sire whereas axonal conduction is similar in most nerves and will affect most nerves (example of axonal interruption is local anesthetic). Synapses are more unique because they employ different neurotransmitters at different sites, and there are many different receptors the body can use for those neurotransmitters. Nueropharmacologic drugs ultimately influence the receptor and there effect will be based on the ability to alter receptor activity. Synaptic transmission is a 5-part process that can be affected by drugs. Here is how each step is affected: Transmitter synthesis- increase or decrease transmitter synthesis or cause the synthesis of transmitter molecules that are more effective than the natural transmitter molecule itself (in theory they could synthesize faulty transmitter molecules however there are no meds that do this) Transmitter storage- interfere with transmitter storage and thus decrease receptor activation Transmitter release- drugs either promote or inhibit release of transmitters (thus increase or decrease activation) Receptor binding- drugs that act directly at the receptors can bind to receptors and cause activation (agonist), bind to receptors and block activation (antagonist), or bind to receptor components and enhance receptor activation by the natural transmitter at the site (agonist) Termination of transmission- drugs can block neurotransmitter reuptake or inhibit neurotransmitter degradation, both of these increase the amount of neurotransmitter in the synaptic gap to increase and receptor activation to increase *Activation is an effect on receptor function equivalent to that produced by the neurotransmitter at a particular synapse. *A decrease in receptor activation is when the drug effects are equivalent to reducing the amount of natural transmitter available for binding. |
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3. Discuss the location and response of the peripheral cholinergic and adrenergic receptor subtypes (table 13-2 and 13-3). And distinguish among the different receptors, normal responses of receptors, and how drugs affect these receptors and responses.
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Bladder anatomy:
Detrusor- smooth muscle bladder wall Trigone- base of bladder Sphincter- in neck Peripheral Cholinergic Receptor subtypes (mediate junctions with acetylcholine as transmitter) Receptor subtype Location Response to receptor activation Nicotinic N All autonomic nervous system ganglia and the adrenal medulla Stimulation of parasympathetic and sympathetic prostaglandionic nerves and release of epinephrine from the adrenal medulla Nicotinic M Neuromuscular junction Contraction of skeletal muscle Muscarinic All parasympathetic target organs: Eye Heart Lung Bladder GI tract Sweat glands Sex organs Blood vessels Contraction of ciliary muscle focuses lens for near vision, contraction of iris sphincter muscle causes miosis (decreased pupil diameter) Decreased rate Constriction of bronchi Promotes secretions Contraction of detrusor increases bladder pressure Relaxation of trigone and sphincter allows urine to leave the bladder Coordinated contraction of detrusor and relaxation of trigone and sphincter causes voiding Salivation Increased gastric secretions Increased intestinal tone and motility Defecation Generalized sweating Erection Vasodilation Functions for peripheral Adrenergic Receptor Subtypes (mediate responses with epinephrine and norepinephrine and transmitters) Receptor Subtype Location Response to Receptor Activation Therapeutic applications of activation Consequences to activation Alpha 1 Eye Arterioles Skin Viscera Mucous memb. Veins Sex organs, male Prostate capsule Bladder Contraction of radial muscle of eye causes mydriasis (increased pupil size) Constriction Constriction Ejaculation Contraction Contraction of trigone and sphincter Hemostasis Nasal decongestion Adjunct to local anesthesia (delays absorption) Prolongs absorption Allows reduction in dosage Reduces systemic effects Elevation of blood pressure Mydriasis (pupil dilation) Hypertension Necrosis with extravasation (vasoconstriction=no oxygen/death) Bradycardia Alpha 2 Presynaptic nerve terminals Inhibition of transmitter release No therapeutic effect Rarely causes adverse effects Beta 1 Heart Kidney** Book says actiation of renal beta-1 receptors is not associated with beneficial or harmful effects Increased rate Increased force of contraction Increased AV conduction velocity Rennin release Cardiac arrest (initiate contraction) Heart failure (increases force of contraction) Shock (increases heart rate and force of contraction, maintains blood flow to vital organs) Atrioventricular heart block (enhance impulses, help to overcome AV block) Elevate blood pressure?? Book says no indication for Kidneys Altered heart rate or rhythm Angina pectoris Beta 2 *only epinephrine can activate beta-2 Arterioles Heart Lung Skeletal muscle Bronchi Uterus Liver Skeletal muscle Dilation (increases blood flow) Dilation (increase oxygenation) Relaxation (prevents labor) Glycogenolysis (increase energy, glycoegn => glucose) Enhanced contraction, glycogenolysis Asthma (bronchial dilation) Delay of preterm labor (uterine relaxation) Fight-or-flight activation Hyperglycemia (glycogen=>glucose in liver to give more energy) Tremor (activation in skeletal muscles enhances contraction) Dopamine **only responds to dopamine Kidney Dilation of kidney vasculature Treats shock, enhances renal blood flow/perfusion Enhances cardiac output **Dopamine also activates beta-1 receptors in heart and enhances cardiac performance (not a consequence, just a side note) |
