Golan Vocabulary

Medicine Smd 535 with Koles at Wright State University

About this deck

By: Elizabeth Markus
Textbook:

Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access (Robbins Pathology)
Created: 2011-08-16
Size: 71 flashcards
Views: 5

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Adrenergic Neurotransmission

Adrenergic nerves release the neurotransmitters: Norepinephrine (NE), epinephrine, EP, and dopamine DA. The synthesis of the neurotransmitters DA and NE and EP and the hormones NE and EP takes place by a pathway that involves 5 enzymes. Tyrosine is generally considered the starting point. There are at least two adrenergic receptor sites (alpha or beta). Stimulation of alpha receptors is associated with constriction of small blood vessels in the bronchial mucosa and relaxation of smooth muscles of the intestinal tract. Beta receptor activation relaxes bronchial smooth muscles which cause the bronchi of the lungs to dilate.

Cholinergic Neurotransmission

Based on ACh. Receptors divided into two broad classes, Muscarinic cholinergic receptors (G protein linked, at all parasympathetic post ganglionic fibers) and Nicotinic cholinergic receptors (ligand gated). Transmission involves neuromuscular junction.

Agonist

Molecule that, upon binding to its target, causes a change in the activity of those targets.

Antagonist

Inhibit the ability of their targets to be activated (or inactivated) by physiologic or pharmacologic agonists

Alkylating agent

Cytotoxic agent: Interfere with DNA replication and gene expression by conjugating alkyl groups to DNA

Alpha Adrenoreceptors

Type of adrenergic receptor, selective for norepinephrine and epinephrine. There is a1 and a2.

Beta adrenoreceptors

Three subclasses. All three activate Gs, a stimulatory G protein. Gs activates adenylyl cyclase, leading to increase in intracellular cAMP.

Anaphylaxis

Also known as a Type 1 hypersensitivity response or immediate hypersensitivity. Results from production of IgE after exposure to an antigen.

Antimetabolite

A class of cytotoxic agents that are structural analogues of endogenous (natural) metabolites like folates, purines, and pyrimidines, and that function as inhibitors of the enzymes of nucleotide synthesis

Afferent Neuron

Neurons that transmit information toward the brain

Efferent Neuron

“Motor” neuron, carries nerve impulses away from the CNS to effectors like muscles and glands

Antiplatelet Agent

Agents that inhibit platelet function (to inhibit thrombosis) as a prophylactic and therapeutic strategy against myocardial infarction and stroke

Anticoagulant agent

Target various factors in the coagulation cascade, therby interrupting the cascade and preventing the formation of a stable fibrin meshwork (secondary plug)

Autoimmunity

Results when the organism’s immune system attacks its own cells

Autoreceptor

Class of receptors on the presynaptic membrane. Regulate neurotransmitter release.

Bioavailability

Fraction of administered drug that reaches the systemic circulation.

Catecholamine

Norepinephrine, epinephrine, and dopamine.

Chelator

Multidentate structure with multiple binding sites. Binds metal so that these metals can be reduced in the body through metal-ligand complexes.

Chemotherapeutic agent

Interfere with cell proliferation and rely on rapid cell cycling and/or promotion of apoptosis for their relative selectivity against cancer cells—used as treatment for cancer.

Combination Antineoplastic Therapy

Used in the treatment of cancer. Include agents that act of different molecular targets, at different phases of the cell cycle, and with different dose-limiting toxicities

Competitive (reversible) antagonist

Binds reversibly to the active site of a receptor.

Noncompetitive (irreversible) active site antagonist

Binds active site of a receptor either covalently or with very high affinity—in either case, it is effectively irreversible

(Competitive antagonists reduce agonist potency, whereas noncompetitive antagonists reduce agonist efficacy)

*acts by preventing the receptor from being

Dose-response relationships

Pharmacodynamics of a drug can be quantified by the relationship between the dose of the drug and the patient’s response to the drug

Down-regulation of receptor

Prolonged receptor stimulation by ligand induces the cell to endocytose and sequester receptors in endocytic vesicles. This prevents the receptors from coming into contact with ligands, resulting in cellular desensitization. Way to alter receptor number.

Drug Clearance

Rate of elimination of the drug from the body relative to the concentration of the drug in plasma OR rate at which plasma would have to be cleared of the drug to account for the observed kinetics of change of the total amount of drug in the body

Drug-drug interactions

Pharmacokinetic interactions arise when one drug changes the absorption, distribution, metabolism, or excretion of another drug, thereby altering the concentration of active drug in the body. Pharmocodynamic interactions arise when one drug changes response of target or nontarget tissues to another drug.

Drug metabolism or biotransformation

A number of organs (especially liver) are capable of metabolizing drugs. Hepatic enzymes chemically modify a variety of substituents on drug molecules, thereby either rendering the drugs inactive or facilitating their elimination. These modifications are known as biotransformation

Elimination half-life

The amount of time over which the drug concentration in the plasma decreases to one half of its original value

Enteral drug administration

Administration of drug by mouth. Simplest of drug routes. Exploits existing weaknesses in human barrier defenses, but it exposes the drug to harsh acidic (stomach) and basic (duodenum) environments that could limit its absorption

Parenteral drug administration

Drug is introduced directly into systemic circulation, cerebrospinal fluid, vascularized tissue, or some other tissue space. Immediately overcomes barriers that can limit effectiveness of orally administered drugs (rapid, controlled drug delivery, used to cross bbb) but disadvantages include infection, toxcicity.

Enzyme induction and inhibition

Can be incidental (side effect of drug) or deliberate (desired effect of therapy). If increase P450 enzyme induction (increase transcription): a drug can increase its own metabolism, a drug can increase the metabolism of a co-administered drug.

First order kinetics

Majority of drugs demonstrate first-order kinetics when used in standard therapeutic doses. Amount of drug that is metabolized or excreted in a given unit of time is directly proportional to the concentration of drugs in the systemic circulation at the time

Zero order kinetics

Once saturation occurs, the clearance rate fails to increase with increasing plasma drug concentrations

First pass effect

Liver is the main organ of drug metabolism. Orally administed drugs are often absorbed in the GI tract and transported directly to the liver via portal circulation. Thus liver has opportunity to metabolize drugs before they reach systemic circulation and therefore before they reach their target organs. Liver gets “first pass”.

Graded dose-response curve

Describe effect of various doses of a drug on an individual. Effect of a drug as a function of its concentration.

Quantal dose-response curve

Plots the fraction of the population that responds to a given dose of drug as a function of the drug dose. Describe the concentrations of a drug that produce a given effect in a population.

Hyperreactivity

Describes an exaggerated response at normal levels of stimuli (ie: airways of asthmatics respond too vigorously)

Hypersensitivity

Describes a normal response at abnormally low levels of stimuli (ie: airways of asthmatics construct to stimuli that do not produce a response in normal people)

Immunosuppression

Suppressing immune system, either deliberately (for organ transplants for example) or pathogenic.

Ionotropic Receptors

Receptor on the post-synaptic membrane. Binding of neutotransmitter to ligand-gated these opens channels that mediate ion flux across the postsynaptic membrane. Ion flux leads to excitatory or inhibitory potentials.

Metabotropic Receptors

Receptor on post-synaptic membrane. Binding of neurotransmitter to these G protein coupled receptors causes activation of intracellular second messenger signaling cascades

Loading Dose

Initial doses of drug, often administered to compensate for drug distribution into tissues (may be higher than would be required if the drug were retained in the vascular compartment)

Maintenance Dose

Once steady state drug concentrations are achieved in plasma and tissues, subsequent doses need to replace only the amount of drug that is lost through metabolism and excretion. This is maintenance dose, and is dependent on drug clearance (rate in = rate out at steady state)

Median Effective Dose (ED50)

Dose at which 50% of subjects exhibit a therapeutic response to the drug. A type of response that can be examined using the quantal dose-response relationship.

Median Lethal Dose (LD50)

Dose at which 50% of subjects die: A type of response that can be examined using the quantal dose-response relationship.

Multiple drug resistance (MDR) transporters

Many potentially toxic lipophilic compounds can be excluded from the brain by these class of proteins. These transporters pump hydrophobic compounds out of the brain and back into the blood vessel lumen

Muscarinic Cholinergic Receptors

G protein linked and expressed at the terminal synapses of all parasympathetic postganglionic fibers and a few sympathetic postganglionc fibers, at autonomic ganglia, and in the CNS

Nicotinic Cholinergic Receptors

Ligand gated ion channels that are concentrated postsynaptically at many excitatory autonomic synapses and presynaptically in the CNS

Partial agonist

Molecule that binds to a receptor at its active site but produces only a partial response, even when all of the receptors are occupied (bound) by the agonist.

pH trapping

Net diffusion of acidic and basic drugs across lipid bilayer membranes can be effected by this charge-based phenomenon which depends on the drug’s acid dissociation constant (pKa) and the pH gradient across the membrane

Pharmacodynamic Tolerance

Caused by neuronal adaptations resulting in reduced response to the same concentration of drug at its site of action in the nervous system

Pharmacokinetic Tolerance

Develops when the capacity to metabolize or excrete the drug increases as a result of drug exposure

Physical (physiologic) Dependence

Emergence of withdrawal syndrome upon drug discontinuation or administration of a specific antagonist

Psychological Dependence

Continued craving for drug and proclivity to return to out-of-control opioid use even after acute withdrawal symptoms have abated

Potency (EC50)

Potency of a drug is the concentration at which the drug elicits 50% of its maximal response

Efficacy (Emax)

Maximal response produced by the drug

Prodrug

Administered as inactive form of a drug

Selective Agonist vs. nonselective agonist

Agonist selective for one certain type of receptor (will effect one but not others of a type) vs. one that is generalized

Selective Antagonist vs. nonselective antagonist

Antagonist selective for one certain type of receptor vs. one that is generalized

Spare receptors

If a maximal response could be achieved with less than 100% receptors occupancy, then extra receptors are spare receptors.

Steady-state drug concentration

Reached when Kin (drug entry) and Kout (elimination) are equal

Sympathomimetic Drug

In the short term, the agent can increase the net release of catecholamine from the synaptic terminal, and thus mimic sympathetic stimulation

Sympatholytic Drug

Over a longer period, however, agent depletes the pool of available catecholamine and thus as an inhibitor of sympathetic activity

Tachyphylaxis

Drugs showing diminishing effects over time

Therapeutic Index

Therapeutic window (range of doses of a drug that elicits a therapeutic response without toxicity in a population of patients) can be quantified by the TI:

Thrombolytic Agent

Used to lyse already formed closts and thereby restore the patency of an obstructed vessel before the distal tissue necrosis occurs

Xenobiotic

Foreign substances that are not naturally found in the body

About this deck

By: Elizabeth Markus
Textbook:

Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access (Robbins Pathology)
Created: 2011-08-16
Size: 71 flashcards
Views: 5

About StudyBlue

“I have been getting MUCH better grades on all my tests for school. Flash cards, notes, and quizzes are great on here. Thanks!”
Kathy