MCQ No. 1971 | IMA
For UV visible spectrum electronic excitation occur in the range of
For UV visible spectrum electronic excitation occur in the range of
Anonymous Quiz
40%
200-800 mμ
43%
400-800 mμ
12%
400-700 mμ
4%
300-600 mμ
MCQ No. 1972 | IMA
Which detector is used to detect cations & anions?
Which detector is used to detect cations & anions?
Anonymous Quiz
15%
Flourometric detector
55%
Conductivity detector
25%
Amperometric detector
5%
Refractive index detector
Definitions and Concepts Central to Understanding Pharmacokinetics
• Bioactivation
Either (1) conversion of prodrug to any active drug, or (2) conversion of the active drug to a reactive, electrophilic meta- bolic intermediate.
• Bioequivalence
Generally referring to overall ‘equal’ bioavailability between two comparable drugs; usually between generic and trade name formulations of a drug.
• Biotransformation
In general, the metabolic change of a lipophilic drug to a more hydrophilic metabolite allowing renal or biliary excretion.
• Blood–brain barrier
Protective mechanism for brain neurons; due to tight junctions (and lack of intercellular pores) in brain capillaries; highly lipophilic drugs may ‘overcome’ this barrier.
• Detoxification
The metabolic conversion of a reactive, electrophilic intermediate to a more stable, usually more hydrophilic compound.
• Enteral
GI administration of a drug.
• Enterohepatic recirculation
Sequence of initial GI absorption of drug followed by hepatic excretion into bile and small bowel, followed by subsequent GI reabsorption.
• Bioactivation
Either (1) conversion of prodrug to any active drug, or (2) conversion of the active drug to a reactive, electrophilic meta- bolic intermediate.
• Bioequivalence
Generally referring to overall ‘equal’ bioavailability between two comparable drugs; usually between generic and trade name formulations of a drug.
• Biotransformation
In general, the metabolic change of a lipophilic drug to a more hydrophilic metabolite allowing renal or biliary excretion.
• Blood–brain barrier
Protective mechanism for brain neurons; due to tight junctions (and lack of intercellular pores) in brain capillaries; highly lipophilic drugs may ‘overcome’ this barrier.
• Detoxification
The metabolic conversion of a reactive, electrophilic intermediate to a more stable, usually more hydrophilic compound.
• Enteral
GI administration of a drug.
• Enterohepatic recirculation
Sequence of initial GI absorption of drug followed by hepatic excretion into bile and small bowel, followed by subsequent GI reabsorption.
• First-pass effect
Drugs which have significant metabolism in the liver, before widespread systemic distribution—occurs after GI absorption, by way of portal vein to liver.
Drugs which have significant metabolism in the liver, before widespread systemic distribution—occurs after GI absorption, by way of portal vein to liver.
• Half-life
Duration of time for 50% of the absorbed and bioavailable drug to be metabolized and excreted.
Duration of time for 50% of the absorbed and bioavailable drug to be metabolized and excreted.
• Prodrug
A pharmacologically inactive precursor of the biologically active ‘drug’.
A pharmacologically inactive precursor of the biologically active ‘drug’.
Definitions and Concepts Central to Understanding Pharmacodynamics
• Active metabolite
A drug metabolite which retains the same/similar pharmacologic properties as the parent drug.
• Affinity (binding)
A physical measurement which reflects the attraction of the drug ligand to a given receptor molecule.
• Agonist
Drug which binds to a given receptor initiating an effector mechanism → pharmacologic response.
• Antagonist
Drug which binds to a receptor, but fails to activate the effector mechanism.
• Cross tolerance
Reduced pharmacologic effect when exposed to a new, chemically related drug.
• Downregulation
Reduced receptors number/availability, presumably due to a negative feedback mechanism.
• Inverse agonist
Drug which stabilizes receptors which have some constitutive activity to an inactive conformation.
• Ligand
Any molecule (drug) which binds to the drug receptor; binding can be by hydrogen bonds, ionic forces, or covalent forces.
• Partial agonist
Drug which binds to a receptor and weakly initiates an effector mechanism and resultant response.
• Receptor
The molecule to which the drug (ligand) binds to initiate its effector response; location can be cell membrane, cytosolic, or intranuclear
• Refractoriness
(synonyms—desensitization, tachyphylaxis) Temporary lack of responsiveness to a drug, subsequent to prior drug efficacy.
• Second messenger
Biochemical mediator (commonly calcium or cyclic adenosine monophosphate) that serves to relay the signal initiated by the receptor/effector in signal transduction.
• Signal transduction
Cellular biochemical pathways which relays a second messenger ‘signal’ from the receptor to the effector mechanism
• Tachyphylaxis
A diminished pharmacologic response after repeated drug administration; can be due to down regulation or receptor seques- tration (transiently ‘unavailable’ to the drug).
•Tolerance
Diminished effect (generally adverse effect) after repeated drug administration (most common is tolerance to sedating drugs such as antihistamines).
• Active metabolite
A drug metabolite which retains the same/similar pharmacologic properties as the parent drug.
• Affinity (binding)
A physical measurement which reflects the attraction of the drug ligand to a given receptor molecule.
• Agonist
Drug which binds to a given receptor initiating an effector mechanism → pharmacologic response.
• Antagonist
Drug which binds to a receptor, but fails to activate the effector mechanism.
• Cross tolerance
Reduced pharmacologic effect when exposed to a new, chemically related drug.
• Downregulation
Reduced receptors number/availability, presumably due to a negative feedback mechanism.
• Inverse agonist
Drug which stabilizes receptors which have some constitutive activity to an inactive conformation.
• Ligand
Any molecule (drug) which binds to the drug receptor; binding can be by hydrogen bonds, ionic forces, or covalent forces.
• Partial agonist
Drug which binds to a receptor and weakly initiates an effector mechanism and resultant response.
• Receptor
The molecule to which the drug (ligand) binds to initiate its effector response; location can be cell membrane, cytosolic, or intranuclear
• Refractoriness
(synonyms—desensitization, tachyphylaxis) Temporary lack of responsiveness to a drug, subsequent to prior drug efficacy.
• Second messenger
Biochemical mediator (commonly calcium or cyclic adenosine monophosphate) that serves to relay the signal initiated by the receptor/effector in signal transduction.
• Signal transduction
Cellular biochemical pathways which relays a second messenger ‘signal’ from the receptor to the effector mechanism
• Tachyphylaxis
A diminished pharmacologic response after repeated drug administration; can be due to down regulation or receptor seques- tration (transiently ‘unavailable’ to the drug).
•Tolerance
Diminished effect (generally adverse effect) after repeated drug administration (most common is tolerance to sedating drugs such as antihistamines).
Venlafaxine is an effective antidepressant that blocks reuptake of both serotonin and norepinephrine.
A related drug, atomoxetine, which is a selective norepinephrine reuptake inhibitor, is used to treat attention-deficit/hyperactivity disorder (ADHD).
The precise mechanism of action of the tricyclic drugs is unknown. These drugs block the reuptake of biogenic amines, including norepinephrine and serotonin.
MAO inhibitors increase levels of norepinephrine, serotonin, and dopamine by inhibiting their degradation.
Bupropion is an effective antidepressant that is also approved for use (in combination with behavioral modification) in smoking-cessation programs.
Mirtazapine is an effective antidepressant that antagonizes central presynaptic α2 receptors.
Sibutramine is a norepinephrine, 5-HT and dopamine reuptake inhibitor that is used as a weight-loss agent.
LITHIUM, carbamazepine, and valproate are drugs used for the treatment of bipolar disorder.
LITHIUM has a low therapeutic index and the frequency and severity of adverse reactions is directly related to the serum levels.
Diuretics: Site of action & Mechanism
Osmotic Diuretics: =/=> water reabsorption throughout the tubules, but mostly in the proximal tubule (mannitol)
Carbonic Anhydrase Inhibitors: proximal tubule, =/=> C.A (acetazolamide, dorzolamide)
Loop Diuretics: thick ascending loop of Henle, =/=> Na+/K+/2Cl- transporter (furosemide, ethacrynic acid)
Thiazides: early distal tubule, =/=> Na+/Cl- symporter (hydrochlorothiazide, indapamide)
K+ sparing agents: distal nephron (late distal tubule + colecting ducts). Aldosterone receptor antagonist (spironolactone) or =/=> Na+/K+ exchange by =/=> of Na+ channels (amiloride, triamterene)
Osmotic Diuretics: =/=> water reabsorption throughout the tubules, but mostly in the proximal tubule (mannitol)
Carbonic Anhydrase Inhibitors: proximal tubule, =/=> C.A (acetazolamide, dorzolamide)
Loop Diuretics: thick ascending loop of Henle, =/=> Na+/K+/2Cl- transporter (furosemide, ethacrynic acid)
Thiazides: early distal tubule, =/=> Na+/Cl- symporter (hydrochlorothiazide, indapamide)
K+ sparing agents: distal nephron (late distal tubule + colecting ducts). Aldosterone receptor antagonist (spironolactone) or =/=> Na+/K+ exchange by =/=> of Na+ channels (amiloride, triamterene)