Samplex 2015 Flashcards
True of digoxin
A. Bioavailability is 75%
B. Half life is 40 hours
C. 2/3 is unchanged excreted in kidney
D. Inhibits NA-K ATPase pump
D
Study of the the drug effects on population.
A. Biopharmaceutics
B. Pharmacogenetics
C. Pharmacogenomics
D. Pharmacoepidemiology
D
Biopharmaceutics deals with the development of new drug delivery systems and new dosage forms.
Pharmacogenetics is a relatively new field. It deals with genetically mediated variations in drug responses.
Pharmacogenomics- the use of genetic information to guide the choice of drug therapy on an individual basis
Pharmacoepidemiology- study of drug effects at the population level. Helps in regulation of drugs.
Compared to the sigmoid curve of a full agonist in the log dose vs. response curve, the curve in the presence of a partial agonist:
A. will shift to the right
B. will shift to the left
C. Emax will be higher
D. Emax will be lower
D
The partial agonist has lower Emax than the full agonist. “The partial agonist produces a lower response at full receptor occupancy. The partial agonist’s inability to produce maximal effect, even when present at high concentrations that saturate binding to all receptors, is not due to decreased affinity for binding to receptors but indicated by the fact that partial agonist competitively inhibits the responses produced by full agonists.” (Basic and Clinical Pharmacology 11th ed. By Katzung, page 19)
Compared to the sigmoid curve of a full agonist in the log dose vs. response curve, the curve in the presence of a competitive antagonist:
A. will shift to the right
B. will shift to the left
C. Emax will be higher
D. Emax will be lower
A
Reversible competitive antagonism shifts the dose response curve to the right, causing the drug to behave as if it were less pontent. In the presence of a fixed concentration of agonist, increasing concentrations of a reversible competitive antagonist progressively inhibit the agonist response; high antagonist concentrations prevent response completely. Conversely, sufficiently high concentrations of agonist can completely surmount the effect of a given concentration of the antagonist; that is, the Emax for the agonist remains the same for any fixed concentration of antagonist (Figure 2–3A). Because the antagonism is competitive, the presence of antagonist increases the agonist concentration required for a given degree of response, and so the agonist concentration-effect curve is shifted to the right. [Katzung 10th ed]
Compared to the sigmoid curve of a full agonist in the log dose vs. response curve, the curve in the presence of a noncompetitive antagonist:
A. will shift to the right
B. will shift to the left
C. Emax will be higher
D. Emax will be lower
D
The presence of a noncompetitive antagonist at a low concentration produces a slight dextral shift in the agonist dose – response curve [looks similar to a competitive antagonist]. As more and more receptors are bound (and essentially destroyed), the agonist drug becomes incapable of eliciting a maximal effect. As more of the noncompetitive antagonist binds to the receptor, the effect is the same as that of a partial agonist. It does not produce the maximal effect. [Trans on Molecular Mechanisms of Drug Action]
Agonist binding has both affinity and efficacy, antagonist binding also has both affinity and efficacy.
A. True
B. False
B
Antagonists only exhibit affinity. They do not mimic the effects of endogenous regulatory compounds. By definition, antagonists have no efficacy. Efficacy is a function of receptor activation, and antagonist binding does not change receptor activation in any way
The presence of spare receptors will allow an agonist to achieve full efficacy even in the presence of non-competitive agonists.
A. True
B. False
T
The spare receptors are those that do not bind drug when the drug concentration is sufficient to produce maximal effect. Spare receptors are said to exist if the maximal drug response (Emax) is obtained at less than maximal occupation of the receptors (Bmax). The presence of spare receptors increases sensitivity to the agonist because the likelihood of a drug-receptor interaction increases in proportion to the number of receptors available. They allow maximal response without total receptor occupancy, increasing the sensitivity of the system.
In a system with spare receptors, the EC50 is lower than the Kd, indicating that to achieve 50% of maximal effect, less than 50% of the receptors must be activated.
The most important concept in pharmacodynamics is the
A. Therapeutic triangle B. Scatchard plot C. semi-log dose response curve D. presence of agonist/antagonist E. All of the above
C
The Scatchard plot
A. Is a graphic representation used in the analysis of binding phenomena in which concentration of bound ligand divided by that of the free ligand bound ligand is plotted against concentration of bound ligand
B. Is a straight line plot for one binding site (may also represent several binding sites) where the x axis intercept is B (bound drug) and the slope is -1/Kd (negative reciprocal of the dissociation/association constant)
C. Defines an equation for calculating the affinity constant of a ligand with a protein or receptor
D. Is a curve of B/F (bound ligand/free ligand) versus B (bound ligand)
E. All of the above
E
The three most important properties of a drug product are
A. efficacy, safety, quality B. efficacy, lack of significant toxicity and quality C. potency, safety and quality D. a and b E. a and c
D
(majority (if not all) of the class answered A, but during the feedback, the answer given was D because “safety” in A and “lack of significant toxicity” in B mean the same thing so A and B are both correct)
Factor/s that enhance/s absorption
A. Micronization of drug particles B. Mechanisms that lead to non-ionized moiety C. Organ/tissue perfusion D. A and B E. B and C
D
Solids must undergo the process of disintegration, degradation, and dissolution before absorption (drugs in aqueous solution absorbed faster than if in a solid state). Only non-ionized forms will be observed (weak acids in acidic urine, weak bases in basic urine). Organ and tissue perfusion is related to distribution, not absorption.
Factors that delay gastric emptying:
A. fasting B. vigorous exercise C. Billroth surgery D. lying on the right side E. cold meals
B
Among the hepatic cytochrome P450 enzymes, the one responsible for metabolizing the most number of drugs is:
A. CYP3A B. CYP2C C. CYP2D D. CYP1A E. CYP2E
A
True of the legal requirements for herbal medicines:
a. allowed to have active ingredients, excipients, and isolates from the same plant
b. Plant authentication for the source of the herbal medicine from FDA-recognized taxonomist
c. should abide by the limits set on heavy metals, aflatoxin, pesticide residue, etc.
d. should submit pre-clinical toxicity studies (both short and long term)
A
The RA No. 9502, the Universally Accessible Cheaper and Quality Medicines Act of 2008 defines drugs and medicines
A. as any chemical compound and biological substances other than food, intended for use in the treatment, prevention or diagnosis of disease in humans or animals
B. as any article other than food intended to affect the structure or any function of the human body or animals
C. to include herbal and/or traditional drugs which are the articles of plants or animals origin used in folk medicine which are recognized in the Philippines National Drug Formulary
D. All of the above
D
Pre-Clinical Testing of drugs and herbal products using animal
A. An Institutional Animal Research Committee should be established to ensure compliance with the ethical and technical requirements.
B. Investigators and other personnel shall be appropriately qualified and experienced for conducting procedures on living animals. The personnel should be given protection from zoonotic diseases and inappropriate exposure to hazardous chemicals and substances.
C. For surgical or other painful procedures, it is no longer needed to give anesthesia on animals paralyzed by clinical agents.
D. a and b only
D
The guidance on the Non-clinical safety studies for the conduct of human clinical trials required by the 2009 ICH of technical requirements for registration of pharmaceuticals for human use include:
A. As its specific objective, to reduce the use of animals in accordance with 3R (reduce, replace, re) principles
B. To use new in vitro alternative methods for safety evaluation
C. As its scope assessment of carcinogenicity potential for drugs that have special cause for concern
D. A and B
D
Acute toxicity studies based on ICH Technical requirements:
A. Can be derived from single dose toxicity studies from 2 mammalian species using clinical route in humans and 14 days of observation of animals even if lethality is not the intended end point
B. Can be attained from appropriately conducted dose-escalation studies/ short duration dose ranging studies that define max tolerated dose in general toxicity test species
C. Should provide info to predict the consequences of human overdose situations and should be available to support Phase II human clinical trials for which patient population are at higher risk of overdosing
D. Any of the above
D
Binding of acetylcholine to nicotinic cholinergic receptors triggers this cellular event:
A. Sodium enters cell.
B. Chloride ion enters cell.
C. Hyperpolarization of the membrane
D. G-protein is activated
A
The binding of GABA to its receptor leads to this effect
A. Opening of voltage gated sodium channel
B. Hyperpolarization of plasma membrane
C. Generation of action potential
D. Release of calcium from ER and mitochondria
B
Action of mannitol is specific for this receptor:
A. Ionotrophic
B. Metabotrophic
C. GPCR
D. None of the above
D
Mannitol is a non-receptor mediated drug.
Binding of salbutamol to beta-2 receptors trigger
A. Chloride enters the cell through channel
B. ATP is converted to cAMP
C. Expression of genes for transcription of actin and myosin
D. Activation of Tyrosine kinase
B
Salbutamol is a beta-2 adrenergic receptor agonist. It uses the cAMP pathway: G protein activated > conversion of ATP to cAMP> inc cAMP> Inc activity of protein kinase A> lowers intracellular Ca > myosin light chain kinase not activated
Binding of an agonist to the GABA receptor (e.g. gabapentin used in seizures) will result into the cellular response:
A. Opening of sodium channels
B. Hyperpolarization of the cell membrane
C. Generation of a membrane potential
D. Release of intracellular calcium
B
GABA receptor is an ionotropic receptor and ligand-gated ion channel. Its endogenous ligandis γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Upon activation, the GABAA receptor selectively conducts Cl- through its pore, resulting in hyperpolarization of the neuron.
Drugs that bind to GABA receptors such as diazepam and gabapentin are agonists that increase chloride conductance into the cell and induce hyperpolarization of the cell membrane. This eventually results into the inhibition of action potentials. (Mechanisms of Drug Action and Signaling Mechanisms SIM Trans, page 2)
Binding of beta blockers (eg. Propanolol) to beta receptors
A. Bronchodilation
B. Bronchoconstriction
C. Tachycardia
D. Positive ionotropic response
B
Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors.
Bronchoconstriction can occur, especially when non-selective beta-blockers are administered to asthmatic patients. Therefore, non-selective beta-blockers are contraindicated in patients with asthma or chronic obstructive pulmonary disease. Bronchoconstriction occurs because sympathetic nerves innervating the bronchioles normally activate β2-receptors that promote bronchodilation. Blockade of these receptors can lead to bronchoconstriction.
Because there is generally some level of sympathetic tone on the heart, beta-blockers are able to reduce sympathetic influences that normally stimulate chronotropy (heart rate), inotropy (contractility), dromotropy (electrical conduction) and lusitropy (relaxation). Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate.
