Term
| WHAT IS PHARMACODYNAMICS? |
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Definition
| WHAT THE DRUG DOES TO THE BODY. |
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Term
| WHAT DOES PHARMACODYNAMICS ADDRESS? 3 ANSWERS |
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Definition
| THE MECHANISM OF ACTION (MOA), RECEPTOR INTERACTIONS, AND DRUG EFFECTS |
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Term
| FOR A PHYSIOLOGIC RESPONSE TO OCCUR, DRUGS MUST HAVE INTERACTION WITH WHAT? |
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Definition
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Term
| WHAT FORMS CAN THE DRUGS BE? 5 ANSWERS |
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Definition
| EXOGENOUS SUBSTANCE THAT WE ADMINISTER, HORMONE, ENZYME, NEUROTRANSMITTER, OR OTHER ENDOGENOUS COMPOUND...THESE ARE CALLED LIGANDS |
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Term
| WHAT ARE THE 2 VARIABLES RELATED TO ED50? WHAT DO THEY MEAN? |
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Definition
| DEPENDS ON WHETHER THE MEASUREMENT IS GRADED OR QUANTAL. GRADED RELATIONSHIPS ARE CONTINUOUS (PAIN SCALE 0-10). QUANTAL RELATIONSHIPS ARE ALL-OR-NONE (DID IT WORK OR NOT?) |
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Term
| WHAT IS THE DEFINITION FOR GRADED ED50? |
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Definition
| DOSE REQUIRED TO PRODUCE 50% OF THE MAXIMAL EFFECT. |
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Term
| WHAT IS THE DEFINITION FOR QUANTAL ED50? |
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Definition
| DOSE THAT PRODUCED THE DESIRED OUTCOME IN 50% OF THE PATIENTS. |
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Term
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Definition
| THE DOSE REQUIRED TO PRODUCE A TOXIC EFFECT FOR 50% OF THE POPULATION. MAY HAVE A DIFFERENT NUMBER ATTACHED LIKE ED50, ED95 |
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Term
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Definition
| THE LETHAL DOSE FOR 50% OF THE POPULATION (MAY BE THE SAME AS THE TOXIC DOSE). MAY HAVE A DIFFERENT NUMBER ATTACHED LIKE ED90, ED95 |
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Term
| WHAT IS A THERAPEUTIC INDEX? WHAT IS THE EQUATION? |
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Definition
| THE RATIO OF THERAPEUTIC (EFFECTIVE) TO TOXIC DOSE. TI=TD50/ED50 |
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Term
| WHAT DOES IT MEAN IF YOU HAVE A WIDE THERAPEUTIC INDEX? |
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Definition
| YOU HAVE A WIDE MARGIN OF SAFETY |
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Term
| WHAT DOES IT MEAN IF YOU HAVE A NARROW THERAPEUTIC INDEX? |
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Definition
| YOU HAVE A NARROW MARGIN OF SAFETY. |
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Term
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Definition
| HOW MUCH DRUG DOES IT TAKE TO ELICIT A RESPONSE. |
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Term
| WHAT DOES POTENCY BETWEEN DRUGS MEAN? |
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Definition
| IT IS MEASURED BY THE DOSE IT TAKES TO ELICIT THE SAME RESPONSE. EX DILAUDID IS MORE POTENT THAN MORPHONE BECAUSE IT TAKES 1MG OF DILAUDID TO ELICIT THE SAME RESPONSE AS 10MG OF MORPHONE. |
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Term
| IF YOU HAVE 2 DRUGS WITH CERTAIN ED50, WHICH ONE WHOULD BE MORE POTENT? |
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Definition
| THE DRUG WITH THE LOWER ED50. |
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Term
| WHAT IS AFFINITY? GIVE SOME EXAMPLES. |
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Definition
| HOW MUCH A DRUG/CHEMICAL "LIKES" ITS RECEPTOR. A DRUG WITH A HIGH AFFINITY FOR IT'S RECEPTOR BINDS EASILY, AND A LOWER CONCENTRATION OF A DRUG MAY BIND ENOUGH RECEPTORS TO ELICIT A RESPONSE. |
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Term
| IN REPONSE TO AFFINITY, TYPICALLY WHAT IS THE PHYSIOLOGIC RESPONSE FROM? |
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Definition
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Term
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Definition
| IT IS THE EFFECTIVENESS. IS IT THE MAXIMAL RESPONSE PRODUCED BY A DRUG. |
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Term
| WHAT ARE QUESTIONS TO ASK ABOUT EFFICACY? |
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Definition
| CAN THE DRUG PRODUCE AN EFFECT? MORE SPECIFICALLY, IS THE DRUG CAPABLE OF PRODUCING THE MAXIMAL EFFECT? |
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Term
| HOW DOES AGONISTS, PARTIAL AGONISTS, AND ANTAGONISTS DISPLAY EFICACY? |
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Definition
| AGONISTS DISPLAY MAXIMAL EFFICACY, PARTIAL AGONISTS HAVE LESS THAN MAXIMAL EFFICACY, AND ANTAGONISTS HAVE NO EFFICACY. |
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Term
| WHAT IS EFFICACY ALSO KNOWN AS? |
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Definition
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Term
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Definition
| IT IS THE SITE OF ACTION OF A DRUG |
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Term
| WHAT CAN RECEPTORS BE? 4 ANSWERS |
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Definition
| RECEPTORS CAN BE A PROTEIN, CYTOPLASMIC OR EXTRACELLULAR ENZYME, OR A NUCLEIC ACID |
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Term
| WHAT IS A DEFINITION AND EXAMPLE OF A GENERALIZED RECEPTOR? |
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Definition
| GENERALIZED RECEPTORS ARE THOSE THAT HAVE FUNCTIONS ESSENTIAL TO A CELL'S NORMAL PHYSIOLOGIC FUNCTION. EX. DNA, PROTON PUMPS OF THE STOMACH, ETC.. |
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Term
| WHAT IS A SPECIALIZED RECEPTOR AND GIVE AN EXAMPLE? |
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Definition
| SPECIALIZED RECEPTORS ARE MOLECULES THAT HAVE EVOLVED SPECIFICALLY TO REACT TO ENDOGENOUS OR EXOGENOUS CHEMICAL COMPOUNDS. EX. ALPHA AND BETA ADRENERGIC RECEPTORS, CHLORIDE ION CHANNELS, ETC.. |
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Term
| WHAT MODEL DEPICTS HOW DRUGS BIND TO THE RECEPTOR? |
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Definition
| THE LOCK AND KEY THEORY. THE DRUG MUST FIT THE RECEPTOR AND BE ABLE TO ACTIVATE IT. |
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Term
| WHAT DETERMINES HOW LONG THE DRUG'S EFFECT WILL LAST, AND WHEATHER OR NOT THE BOND IS REVERSIBLE? |
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Definition
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Term
| WHAT ARE THE DIFFERENT TYPES OF CHEMICAL BONDS? 5 ANSWERS |
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Definition
| COVALENT BONDS, IONIC BONDS, HYDROGEN BONDS, HYDROPHOBIC BONDS, AND VAN DER WAALS BONDS |
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Term
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Definition
| STRONG BONDS WHICH NEED ENERGY TO BREAK (ERREVERSIBLE DRUG-RECEPTOR BINDING) |
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Term
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Definition
| STRONG BONDS THAT MAY BE REVERSED OR BROKEN BY A CHANGE IN pH. |
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Term
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Definition
| MODERATELY STRONG BONDS AMONG H,N,F, AND O. |
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Term
| WHAT IS A HYDROPHOBIC BOND? |
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Definition
| IT IS MORE OF A WEAK FORCE. WHEN A PROTEIN STRUCTURE WHICH ARE REPELLED BY AQUEOUS SOLUTIONS TOWARD EACH OTHER. |
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Term
| WHAT IS A VAN DER WAALS BOND? |
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Definition
| VERY WEAK BONDS THAT ARE EASILY BROKEN |
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Term
| WHAT DOES MOST DRUG - RECEPTOR BONDS CONSIST OF? |
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Definition
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Term
| WHAT IS A SIGNAL TRANSDUCTION? |
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Definition
| ONCE THE DRUG AND RECEPTOR BIND, A CONFORMATIONAL CHAGNE OCCURS IN THE RECEPTOR AND A SIGNALING PATHWAY IS ACTIVATED WHICH IS CALLED A SIGNAL TRANSDUCTION. |
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Term
| THE TYPE OF ______ DETERMINES WHAT "SIGNAL" IS SENT, AND THE PHYSIOLOGIC EFFECT. |
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Definition
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Term
| WHAT ARE THE TYPES OF RECEPTORS? 4 ANSWERS |
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Definition
| G-PROTEIN COUPLED RECEPTORS, LIGAND-GATED ION CHANNELS, TYROSINE KINASE RECEPTORS, AND NUCLEAR HORMONE RECEPTORS. |
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Term
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Definition
| A HUGE FAMILY OF RECEPTORS THAT IS RESPONSIBLE FOR A LARGE RANGE OF FUNCTIONS INCLUDING SMELL AND SIGHT, IMMUNE FUNCTIONS, BEHAVIOR AND MOOD, AND ANS FUNCTIONS. |
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Term
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Definition
| OPIOID, ADRENERGIC, HISTAMINE, ETC.. MOST OF OUR DRUGS ACT ON GPCRs. |
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Term
| HOW MANY TIMES DOES GPCR SPAN THE CELL MEMBRANE? |
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Definition
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Term
| INTRACELLULAR HOW MANY SUBUNITS ARE THERE? |
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Definition
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Term
| DESCRIBE THE SUBUNITS A,B,Y. |
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Definition
| THE B AND Y SUBUNITS ARE SO TIGHTLY BOUND THAT THEY DO NOT SEPARATE. THE A SUBUNIT IS THE MORE ACTIVE UNIT. |
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Term
| WHAT IS BOUND TO THE A SUBUNIT IN THE INACTIVATED STATE OF THE RECEPTOR? |
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Definition
| GDP (GUANASINE DIPHOSPHATE) |
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Term
| WHAT HAPPENS WHEN A LIGAND BINDS TO THE EXTRACELLULAR PORTION OF THE RECEPTOR? |
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Definition
| 1) A CONFOMATIONAL CHANGE OCCURS IN THE RECEPTOR. 2) THE GDP ON THE A SUBUNIT IS REPLACED WITH GTP. 3) THIS CAUSES THE B/Y SUBUNITS TO DISSOCIATE FROM THE A SUBUNIT. 4) THE (NOW ACTIVATED) A SUBUNIT IS AVAILABLE TO ACTIVATE THE ADENYLY CYCLASE IN THE CELL. 5) THE ADENYLY CYCLASE STIMULATES THE CONVERSION OF ATP TO cAMP. 6) cAMP ACTIVATES PROTEINS (PROTEIN KINASE A), WHICH HAVE VERY TISSUE SPECIFIC EFFECTS |
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Term
| THE A SUBUNIT CAN BE ONE OF SEVERAL TYPES. WHAT ARE THEY? |
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Definition
| s (STIMULATING)- INCREASES ADENYLY CYCLASE AND THEREFORE INCREASES THE PRODUCTION OF cAMP. I (INHIBITORY)- DECREASES ADENYLYL CYCLASE ACTIVITY AND THEREFORE REDUCES THE PRODUCTION OF cAMP. q ACTIVATES PHOSPHOLIPASE C WHICH FORM INOSITOL TRIPHOSPHATE (IP3) AND DIACYLGLYCEROL (DAG) FROM THE MEMBRANE PHOSPHOLIPIDS |
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Term
| WHAT DOES IP3 AND DAG DO WHICH IS FORMED BY PHOSPHOLIPASE C THAT IS ACTIVATED BY q? |
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Definition
| IP3 AND DAG CAUSE AN INCREASE IN INTRACELLULAR CALCIUM WHICH IS IMPORTANT IN MUSCLE CONTRACTION AND NEUROTRANSMITTER RELEASE, AMONG OTHER THINGS. |
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Term
| WHAT ARE THE 4 SECOND MESSENGERS AND WHAT DO THEY DO? |
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Definition
| cAMP, IP3, DAG, AND CALCIUM ARE CALLED SECOND MESSENGERS BECAUSE THEY CAUSE CERTAIN ENZYMATIC REACTIONS IN TARGET CELLS THAT EVENTUALLY LEAD TO A PHYSIOLOGIC EFFECT. |
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Term
| WHAT IS cAMP DEGRADED TO by what? |
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Definition
| 5'-AMP by phosphodiesterase |
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Term
| DESCRIBE A LIGAND-GATED ION CHANNEL. |
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Definition
| LIGAND GATED= A LIGAND HAS TO OPEN THE GATE (ION CHANNEL) |
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Term
| A LIGAND IS A PROTEIN WITH HOW MANY SUBUNITS ATTACHED? |
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Definition
| 4-5 (TETRAMETRIC OR PENTAMETRIC) |
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Term
| WHAT IS UNIQUE ABOUT THE SUBUNITS? |
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Definition
| THE SUBUNITS ARE SPECIFIC TO DIFFERENT TISSUES. EX. THE NICOTINIC RECEPTOR IN THE AND IS DIFFERENT THEN THE NICOTONIC RECEPTOR IN THE NEUROMUSCULAR JUNCTION...SO EVEN THOUGH IT IS THE SAME RECEPTOR AND BOTH REPOND TO ACH, THEY HAVE DIFFERENT EFFECTS AND DIFFERENT DRUGS THAT BIND |
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Term
| WHAT HAPPENS HAVE THE RECEPTOR IS ACTIVATED BY A LIGAND? |
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Definition
| ONCE ACTIVATED BY A LIGAND, THE ION CHANNEL IS OPENED AND THE RECEPTOR SPECIFIC ION (NA, CL, ETCC.) ((ELECTROSPECIFIC ION)) RUSHES IN AND CAUSES A CHANGE IN THE MEMBRANE POTENTIAL, WHICH *ACTIVATED* OR *INHIBITS* SOME CELLULAR FUNCTION. |
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Term
| ARE THERE ANY SECOND MESSENGERS IN ION CHANNEL (LIGAND CHANNEL) RECEPTOR ACTIVATION? |
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Definition
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Term
| WHAT IS TYROSINE KINASE RECEPTORS ALSO KNOWN AS? |
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Definition
| TRANSMEMBRANE ENZYME LINKED RECEPTORS |
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Term
| TYROSINE KINASE RECEPTORS ARE BEING RECOGNIZED WITH GROWING IMPORTANCE WHERE/HOW? 3 ANSWERS |
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Definition
| HUMAN GENOMIC MAKEUP AND ARE RESPONSIBLE FOR COUNTLESS CELLULAR PROCESSES, INCLUDING PROLIFERATION OF CANCER CELLS. |
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Term
| HOW DOES TYROSINE KINASE RECEPTORS FUNCTION AS? |
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Definition
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Term
| WHAT HAPPENS TO A TYROSINE KINASE RECEPTOR IF A MUTATION RENDERS THE RECEPTOR IN THE STUCK POSITION? |
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Definition
| THE MUTATED CELL PROLIFERATES UNCONTROLLED (CANCER CELLS, SO THESE RECEPTORS ARE A LARGE TARGET FOR MANY ANTI-NEOPLASTIC DRUGS |
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Term
| THE TYROSINE KINASE RECEPTORS, ALTHOUGH DOESN'T INTERACT WITH ANESTHETIC DRUGS OFTEN, INTERACT WITH WHAT? |
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Definition
| RECEPTORS OF INSULIN, HUMAN GROWTH FACTOR, VASCULAR ENDOTHELIAL GROWTH FACTOR, AND MANY OTHER IMMUNOLOGICAL AND HORMONAL RECEPTORS. |
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Term
| ON A TYROSINE KINASE RECEPTOR WHERE DOES THE LIGAND BIND AND WHERE DOES THE TYROSINE KINASE POSITIONED AT? |
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Definition
| THE LIGANDS BIND AT THE CELL SURFACE AND THERE IS AN INTRACELLULAR COMPONENT WHICH CONTAINS THE TYROSINE KINASE |
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Term
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Definition
| A KINASE IS AN ENZYME THAT TRANSFERS PHOSPHOROUS FROM ATP TO SPECIFIC TARGETS...THIS IS CALLED PHOSPHORYLATION. |
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Term
| TYROSINE KINASES SPECIFICALLY PHOSPHORYLATE WHAT? |
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Definition
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Term
| WHAT HAPPENS TO A TYROSINE KINASE RECEPTOR ONCE THE LIGAND BINDS TO THE RECEPTOR? |
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Definition
| THE RECEPTOR DIMERIZES (2 STRUCTURES JOIN TOGETHER) |
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Term
| WHAT HAPPENS AFTER A TYROSINE KINASE RECEPTOR DIMERIZES? |
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Definition
| PHOSPHORYLATION OCCURS WHICH ACTIVATED A NUMBER OF SECOND MESSENGER SIGNAL TRANSDUCION MECHANISMS. THESE IN TURN CAUSE A PHYSIOLOGIC EFFECT SPECEFIC TO THE LIGAND AND SECOND MESSENGER SYSTEM. |
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Term
| WHERE ARE NUCLEAR HORMONE RECEPTORS LOCATED? |
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Definition
| IN THE CYTOPLASM OF THE CELL |
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Term
| LIGANDS TYPICALLY EXIST IN WHAT FORM? HYDROPHOBIC, HYDROPHILIC, ETC.. |
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Definition
| HYDROPHOBIC (LIPOPHILIC) BECAUSE THEY HAVE TO CROSS THE MEMBRANE |
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Term
| NAME 4 EXAMPLES OF HYDROPHOBIC LIGANDS. |
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Definition
| SEX HORMONES, GLUCOCORTICOIDS, MINERALCORTICOIDS, AND THYROID HORMONES |
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Term
| ONCE THE HYDROPHOBIC LIGANDS ATTACHE TO THE NUCLEAR HORMONE RECEPTORS IN THE CYTOPLASM OF THE CELL WHAT HAPPENS? |
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Definition
| THE HORMONE BINDS TO A RECEPTOR IN THE CYTOPLASM WHICH TRAVELS TO THE NUCLEUS IN THE CELL. IN THE NUCLEUS THE RECEPTOR COMPLEX BINDS TO SPECIFIC DNA SEQUENCES AND ALTERS GENE TRANSCRIPTION. |
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Term
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Definition
| LIGANDS THAT ACTIVATE A RECEPTOR AND PRODUCE A PHYSIOLOGIC RESPONSE (THE KEY FITS, AND IT TURNS THE LOCK) |
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Term
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Definition
| ARE LIGANDS THAT BIND TO A RECEPTOR, BUT DO NOT ACTIVATE IT (THE KET FITS, BUT IT WON'T TURN THE LOCK...BUT NOW YOU CAN'T PUT ANOTHER KEY IN) |
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Term
| WHAT DO ANTAGONISTS PREVENT FROM BINDING TO THE RECEPTOR? |
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Definition
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Term
| WHERE CAN AN ANTAGONIST BIND TO? |
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Definition
| ANTAGONISTS MAY BIND TO THE ACTIVE BINDING SITE ON THE RECEPTOR OR TO AN ALLOSTERIC SITE. AN ALLOSTERIC AGONISTS MAY ALSO ALTER THE EFFECT OF AN ACTIVE AGONIST. |
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Term
| WHAT HAPPENS IF AN ANTAGONISTS BINDS TO A ALLOSTERIC SITE? |
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Definition
| BINDING AT AN ALLOSTERIC SITE DOES NOT PREVENT AN AGONIST FROM BINDING, BUT IT PREVENTS RECEPTOR ACTIVATION. |
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Term
| WHAT IS COMPETITIVE ANTAGONISTS? |
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Definition
| COMPETITIVE ANTAGONISTS COMPETE FOR THE SAME ACTIVE SITE ON A RECEPTOR AS THE AGONIST. |
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Term
| ARE COMPETITIVE ANTAGONISTS REVERSIBLE? |
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Definition
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Term
| COMPETITIVE ANTAGONISTS CAN BE OVERCOME BY WHAT? |
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Definition
| ANTAGONISTS CAN BE OVERCOME BY AN AGONIST IF THE CONCENTRATION OF THE AGONIST AND ITS AFFINITY FOR THE RECEPTOR IS ADEQUATE. |
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Term
| WHAT DOES THE COMPETITIVE ANTAGONISTS DO TO THE AGONISTS? |
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Definition
| THE POTENCY OF THE AGONISTS IS REDUCED (YOU'LL NEED MORE IN ORDER TO ACHIEVE THE SAME RESPONSE). |
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Term
| WHAT DOES COMPETITIVE ANTAGONISTS DO TO THE LIGANDS? |
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Definition
| THEY DIFFUSE OFF OF THE RECEPTOR AND ARE ELIMINATED |
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Term
| WHAT IS A NONCOMPETITIVE ANTAGONISTS? |
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Definition
| A NONCOMPETITIVE ANTAGONISTS BIND TO THE RECEPTOR WITHA COVALENT BOND, LEAVING THE RECEPTOR UNAVAILABLE FOR AGONIST BINDING OR BIND (REVERSIBLY OR IRREVERSIBLY) TO AN ALLOSTERIC SITE. ONCE ENOUGH OF THE RECEPTORS ARE BOUND BY NONCOMPETITIVE ANTAGONISTS, IT MAY BE IMPOSSIBLE FOR AN AGONIST TO ILLICT A MAXIMAL RESPONSE. THEREFORE THE EFFICACY OF THE AGONIST IS DIMINISHED. |
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Term
| WHAT MUST BE FORMED IF BOND IS IRREVERSIBLE RELATED TO NONCOMPETITIVE ANTAGONISTS? |
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Definition
| NEW RECEPTORS. EX. ASA BIND IRREVERSIBLY TO INACTIVATE PLT AGGREGATION..THE EFFECT LASTS APROX. 7-10 DAYS UNTIL NEW PLTS ARE FORMED. |
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Term
| WHAT IS ANOTHER NAME FOR PARTIAL AGONISTS? |
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Definition
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Term
| WHAT IS A PARTIAL AGONISTS? |
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Definition
| DRUGS THAT ARE UNABLE TO CAUSE A FULL CONFORMATIONAL CHANGE TO A RECEPTOR. |
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Term
| WHAT HAPPENS IF A PARTIAL AGONIST IS BOUND AND A FULL AGONISTS BINDS AS WELL? |
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Definition
| THE RESPONSE TO A FULL AGONIST WILL BE PARTIALLY INHIBITED. SAID TO HAVE SOME AGONIST AND SOME ANTAGONIST EFFECTS |
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Term
| WHAT DOES A CHEMICAL ANTAGONIST DO? |
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Definition
| SOME MEDICATIONS DO NOT BIND TO A RECEPTOR TO CAUSE THEIR EFFECT, BUT RATHER INTERCEPT ANOTHER CHEMICAL OR DRUG BEFORE IT HAS THE OPPORTUNITY TO ACT. EX. PROTAMINE IS GIVEN TO COUNTERACT THE EFFECTS OF HEPARIN. IT WORKS BY FORMING AN IONIC BOND WITH HEPARIN (HEPARIN IN NEGATIVELY CHARGED COMPOUND WHEREAS PROTAMINE IS A POSITVELY CHARGED) |
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Term
| IN RELATION TO DOSE RESPONSE CURVES WHAT IS THE X AND Y AXIS? |
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Definition
| THE X AXIS IS THE DOSE OR CONCENTRATION OF DRUG (TYPICALLY IN LOGARITHMIC FORM). THE Y AXIS IS THE EFFECT OR RESPONSE. |
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Term
| HOW DOES THE SHAPE OF THE CURVE EFFECT MARGIN OF SAFETY. |
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Definition
| STEEP CURVES REPRESENT DRUGS WITH A NARROW MARGIN OF SAFETY (SMALL CHANGES IN THE DOSE CAUSE LARGE CHANGES IN THE RESPONSE). WIDE CURVES REPRESENT DRUGS WITH A WIDE MARGIN OF SAFETY. |
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Term
| WHAT HAPPENS WITH THE DIFFERENT SHIFTS WITH DOSE RESPONSE CURVES? |
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Definition
| A RIGHT SHIFT IS LESS POTENT (YOU NEED MORE DRUG TO GET A RESPONSE). A LEFT SHIFT IS MORE POTENT (LESS DRUG TO GET A RESPONE). UPWARD SHIFT IS MORE EFFICACIOUS (ABLE TO REACH MAXIMAL EFFECT). DOWNWARD SHIFT IS LESS EFFICACIOUS (UNABLE TO REACH A MAXIMAL EFFECT). IF THE CURVE MOVES ALONG THE DOSE AXIS (X), IT DEALS WITH POTENCY; IF IT MOVES ALONG WITH RESPONSE AXIS, IT DEALS WITH EFFICACY. |
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Term
| RECEPTOR CONCENTRATION CAN CHANGE IN RESPONSE TO WHAT? |
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Definition
| RECEPTOR CONCENTRATION CAN CHANGE (SOMETIMES RAPIDLY) IN RESPONSE TO REPEATED EXPOSURE TO AN AGONIST OR ANTAGONIST. THIS CAN BE RESPONSIBLE FOR A DIMINISHED OR EXAGGERATED RESPONSE TO A DRUG. |
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Term
| WHAT DOES UPREGULATION OF RECEPTORS MEAN? |
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Definition
| UP-REGULATION OF RECEPTORS OCCURS WHEN REPEATED EXPOSURE TO AN ANTAGONIST OCCURS, AND THE TISSUE IS ATTEMPTING TO RESTORE AN EQUILIBRIUM BETWEEN AGONIST AND RECEPTOR. EX. CHRONIC B-BLOCKADE WILL RESULT IN AN UPREGULATIONB OF B RECEPTORS. IF THE B-BLOCKER IT WITHDRAWN, CATECHOLAMINES (ENDOGENOUS OR EXOGENOUS) WILL BEIND TO THOSE RECEPTORS AND CAUSE AN EXAGGERATED, OR REBOUND AUTONOMIC EFFECT. |
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Term
| WHAT IS DOWN REGULATION MEAN? |
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Definition
| DOWN-REGULATION OF RECEPTORS OCCURS WHEN THERE IS REPEATED EXPOSURE TO AN AGONIST, AND THE TISSUE RESPONSE BY TRYING TO REDUCE THE AVAILABLE BINDING SITES. EX. REPEATED ADMINISTRATION OF ALBUTEROL IN AN ASTHMATIC PATIENT CAUSES DOWN REGULATION OF THE B2 RECEPTORS IN THE LUNGS, LEADING TO AN INABILITY OF THE DRUG TO CAUSE BRONCHODILATION |
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Term
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Definition
| THE ACUTE PHENOMENON OF DESENSITIZATION OR DOWN-REGULATION OF RECEPTORS TO THE POINT OF DECREASED DRUG FUNCTION. |
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Term
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Definition
| TOLERANCE IS THE EFFECT OF DOWN-REGULATION SEEN OVER A PERIOD OF TIME WITH CONTINUED ADMINISTRATION OF A DRUG. INCREASING DOSES ARE REQUIRED TO PRODUCE THE SAME EFFECT. |
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