Phamacodynamics and Pharmacokinetics

Question

What is pharmacodynamics?

Answer 1

The effects of a drug on the body.

Answer 2

What the body does to a drug.

Answer 3

The effects of a drug on the body.

Answer 4

What the body does to a drug.

Answer 5

determine the appropriate dose range for patients and compare how safe or effective different drugs are.

Answer 6

design and optimise treatment plans for individuals.

Answer 7

determine the best route and frequency of administration of a new drug.

Answer 8

Administration

Answer 9

Absorption

Answer 10

Distribution

Answer 11

Dissolving

Answer 12

Metabolism

Answer 13

Modification

Answer 14

how a drug gets from the site of administration into the blood.

Answer 15

how a drug moves from the blood to target cells.

Answer 16

how the drug elicits its effect on the body.

Answer 17

how a drug is eliminated from the body.

Answer 18

how the drug moves in the body, for example leaving the blood stream and distributing non uniformly into intracellular fluids.

Answer 19

how long the drug moves around in the blood for.

Answer 20

how the drug is inactivated by the body.

Answer 21

how the drug is eliminated from the body, for example in bile.

Answer 22

how the body inactivates the drug.

Answer 23

enzymatic modification.

Answer 24

how the drug travels through the body.

Answer 25

how the drug passes cell walls.

Answer 26

how the drug is eliminated from the body, for example in urine, bile or faeces.

Answer 27

how long the drug can stay in the body unchanged.

Answer 28

how the drug gets from the site of administration to the GI tract.

Answer 29

how the drug elicits a cellular response.

Answer 30

Completely synthetic materials.

Answer 31

Synthetic materials but using the template of a naturally occurring compound.

Answer 32

Biologics (derived from growth factors and recombinant proteins).

Answer 33

Electricity.

Answer 34

Nitrogen gas.

Answer 35

Receptors, Ion Channels, Enzymes and Carriers.

Answer 36

Hormonal Receptors, Gated Ion Channels, Metabolic Enzymes, Carriers.

Answer 37

Receptors, Ion Channels, Enzymes, Channels.

Answer 38

Ion Channels, Reception, Enzyme Inhibitors, Carriers.

Answer 39

Ion Channels, Receptors, Enzymes, Channels.

Answer 40

Charge Distribution

Answer 41

Charge Distribution

Answer 42

Van der Waals Forces, Hydrogen Bonds, Ionic Bonds, Covalent Bonds

Answer 43

Covalent Bonds, Ionic Bonds, Hydrogen Bonds, Van der Waals Forces

Answer 44

Van der Waals Forces, Ionic Bonds, Hydrogen Bonds, Covalent Bonds

Answer 45

Covalent Bonds, Hydrogen Bonds, Ionic Bonds, Van der Waals Forces

Answer 46

They do not target proteins, they simply act by virtue of their physiochemical properties.

Answer 47

They target more than one type of protein.

Answer 48

They are never metabolised by the body, they stay unchanged in the liver forever.

Answer 49

They are always available as over the counter medicines.

Answer 50

They do not have to be licensed.

Answer 51

Ion Channel

Answer 52

always activate the receptor.

Answer 53

either activate the receptor or stop something else from activating it.

Answer 54

block the receptor.

Answer 55

denature the receptor.

Answer 56

can block the channel.

Answer 57

can modulate the opening and closing of the channel.

Answer 58

can denature the channel.

Answer 59

can stimulate the production of many more channels than normal.

Answer 60

can break down the ion that normally uses the channel.

Answer 61

either inhibit the enzyme or act as a false substrate.

Answer 62

block the enzymes active site.

Answer 63

denature the enzyme.

Answer 64

cause the release of neurotransmitter.

Answer 65

activate the enzyme.

Answer 66

Neurotransmitters

Answer 67

Ion Channels

Answer 68

a drug which blocks the response to an agonist.

Answer 69

a drug that combines with a receptor to elicit a cellular response.

Answer 70

a drug that binds with an ion channel.

Answer 71

receptors.

Answer 72

ion channels.

Answer 73

ligand binding assay

Answer 74

plaque assay

Answer 75

dose/response curve

Answer 76

ligand gated

Answer 77

voltage gated

Answer 78

temperature gated

Answer 79

concentration gated

Answer 80

time centred

Answer 81

an agonist to open the channel.

Answer 82

energy (in the form of ATP) to open the channel.

Answer 83

an antagonist to open the channel.

Answer 84

They are not linked to receptors.

Answer 85

They require a change in electrical charge across a membrane in order to open and close.

Answer 86

They can be blocked by antagonist drugs.

Answer 87

There are binding sites for agonist drugs.

Answer 88

They are linked to G-protein coupled receptors.

Answer 89

They require an agonist to open the channel.

Answer 90

Ionotrophic

Answer 91

Metabotrophic

Answer 92

activate adenyl cyclase and Ca2+ channels

Answer 93

inhibit adenyl cyclase and activate K+ channels

Answer 94

activate phospholipase C

Answer 95

activate adenyl cyclase and Ca2+ channels

Answer 96

inhibit adenyl cyclase and activate K+ channels

Answer 97

activate phospholipase C

Answer 98

activate adenyl cyclase and Ca2+ channels

Answer 99

inhibit adenyl cyclase and activate K+ channels

Answer 100

activate phospholipase C

Answer 101

G-Protein linked receptor

Answer 102

Kinase linked receptor

Answer 103

Ion channel

Answer 104

ligand binding ➨ dimerisation ➨ autophosphorylation

Answer 105

dimerisation ➨ ligand binding ➨ autophosphorylation

Answer 106

ligand binding ➨ autophosphorylation ➨ dimerisation

Answer 107

change in membrane potential ➨ autophosphorylation ➨ dimerisation

Answer 108

change in membrane potential ➨ dimerisation ➨ autophosphorylation

Answer 109

are located in the cytoplasm

Answer 110

are located in the nucleus

Answer 111

form homodimers (dimers with other receptors of the same type)

Answer 112

form heterodimers

Answer 113

have endocrine ligands (steroids/hormones)

Answer 114

have lipid (fatty acid) ligands

Answer 115

have a positive feedback effect

Answer 116

they are intracellular.

Answer 117

they are extracellular.

Answer 118

they require ATP to be activated.

Answer 119

they are millions of different types of them.

Answer 120

Gene Transcription

Answer 121

Gene Translation

Answer 122

Protein Degredation

Answer 123

Orthosteric

Answer 124

Allosteric

Answer 125

Metabotrophic

Answer 126

Ionotrophic

Answer 127

house full and partial agonists, and reversible competitive antagonists.

Answer 128

bind positive and negative, non competitive antagonists.

Answer 129

house full and partial agonists, and reversible competitive antagonists.

Answer 130

bind positive and negative, non competitive antagonists.

Answer 131

a ligand that combines with receptors to elicit a cellular response.

Answer 132

a ligand that served to block the effect of other ligands which combine with receptors to elicit a cellular response.

Answer 133

X axis : [log] drug dose Y axis : % response

Answer 134

X axis : [log] agonist concentration Y axis : measure of response

Answer 135

X axis : % response Y axis : [log] drug dose

Answer 136

X axis : measure of response Y axis : [log] agonist concentration

Answer 137

the response of a particular system to a drug at varying concentrations.

Answer 138

the drug dose required to produce a specified response in each member of a population.

Answer 139

the drug dose required to produce a specified response in each member of a population.

Answer 140

the response of a particular system to varying concentrations of an agonist.

Answer 141

you can estimate Emax

Answer 142

you can estimate EC50 and ED50

Answer 143

you can compare the efficacy and potency of different drugs

Answer 144

you can calculate Emax

Answer 145

you can calculate half life

Answer 146

you can estimate clearance

Answer 147

the ability of an agonist to activate a receptor (refers to the maximum effect an agonist can produce regardless of dose).

Answer 148

the likelihood the an agonist will bind to a receptor (refers to the maximum binding of an agonist regardless of dose).

Answer 149

high efficacy (AR* is very likely)

Answer 150

low efficacy (AR* is unlikely)

Answer 151

low efficacy (AR* is less likely).

Answer 152

high efficacy (AR* is very likely)

Answer 153

drugs which block the response to an agonist.

Answer 154

the same as agonists.

Answer 155

endogenous molecules like hormones and neurotransmitters.

Answer 156

physiological

Answer 157

pharmacological

Answer 158

enterohepatic

Answer 159

active site

Answer 160

physiological

Answer 161

pharmacological

Answer 162

allosteric

Answer 163

allosteric

Answer 164

directly compete with agonists for binding at the active site.

Answer 165

block the active site permanently because they form covalent bonds with it. The receptor must be replaced before more agonist can bind.

Answer 166

reversibly bind to an allosteric site on the receptor, altering binding at the active site.

Answer 167

irreversibly bind at an allosteric site, permanently altering the active site.

Answer 168

reversibly bind to an allosteric site on the receptor, altering binding at the active site.

Answer 169

irreversibly bind at an allosteric site, permanently altering the active site.

Answer 170

block the active site permanently because they form covalent bonds with it. The receptor must be replaced before more agonist can bind.

Answer 171

directly compete with agonists for binding at the active site.

Answer 172

reversibly bind to an allosteric site on the receptor, altering binding at the active site.

Answer 173

irreversibly bind at an allosteric site, permanently altering the active site.

Answer 174

block the active site permanently because they form covalent bonds with it. The receptor must be replaced before more agonist can bind.

Answer 175

directly compete with agonists for binding at the active site.

Answer 176

reversibly bind to an allosteric site on the receptor, altering binding at the active site.

Answer 177

block the active site permanently because they form covalent bonds with it. The receptor must be replaced before more agonist can bind.

Answer 178

irreversibly bind at an allosteric site, permanently altering the active site.

Answer 179

directly compete with agonists for binding at the active site.

Answer 180

can be overcome with increased agonist concentration.

Answer 181

causes a shift to the right on the agonist response curve.

Answer 182

causes reduced maximum response on the agonist response curve.

Answer 183

reduces slope of the agonist response curve.

Answer 184

is due to covalent binding with the active site.

Answer 185

can be overcome with increased agonist concentration.

Answer 186

causes a shift to the right on the agonist response curve.

Answer 187

causes reduced maximum response on the agonist response curve.

Answer 188

is due to covalent bonding at the active site.

Answer 189

reduces slope on the agonist response curve.

Answer 190

cause reduced slope of the agonist response curve.

Answer 191

cause a shift to the right of the agonist response curve.

Answer 192

cause reduced maximum response on the agonist response curve.

Answer 193

physiochemical/pharmacokinetic properties of the drug

Answer 194

therapeutic objectives

Answer 195

patient preference

Answer 196

drugs that are poorly absorbed by or are unstable in the GI tract.

Answer 197

drugs that require rapid onset of action.

Answer 198

drugs that require slow onset of action.

Answer 199

for drugs that require a high level of control over dose.

Answer 200

bolus: all at once

Answer 201

infusion: over time

Answer 202

depot: solid/oil

Answer 203

bolus: over time

Answer 204

bolus: solid/oil

Answer 205

infusion: solid/oil

Answer 206

infusion: all at once

Answer 207

intravenous

Answer 208

intramuscular

Answer 209

subcutaneous

Answer 210

submuscular

Answer 211

Small Intestine

Answer 212

Large Intestine

Answer 213

large, highly permeable surface area

Answer 214

varies in pH along it's length

Answer 215

constant pH

Answer 216

enterocytes contain drug metabolising enzymes

Answer 217

enterocytes contain transporters in their membranes

Answer 218

tought, flat surface area

Answer 219

contains stomach acid

Answer 220

it is very short in length

Answer 221

the drug causes vomiting

Answer 222

the patient is vomiting

Answer 223

the drug is excreted in the urine

Answer 224

the patient has a low blood count

Answer 225

It bypasses first pass metabolism.

Answer 226

It bypasses 2/3 of first pass metabolism.

Answer 227

It has a rich blood supply.

Answer 228

pH can vary.

Answer 229

pH is always around 8.

Answer 230

It has very slow absorption giving a continuous slow release of drug.

Answer 231

It has very fast local absorption giving a rapid release of the drug to a small area.

Answer 232

systemic circulation

Answer 233

pulmonary circulation

Answer 234

Formulation of the drug

Answer 235

Charge on the drug

Answer 236

Blood flow to the site of absorption

Answer 237

Surface area of the site of absorption

Answer 238

Contact time at absorptive surface

Answer 239

Gastric emptying

Answer 240

Cost of drug

Answer 241

Kidney function

Answer 242

maximum concentration of a compound after administration

Answer 243

time at which Cmax is reached

Answer 244

area under the concentration/time curve

Answer 245

measure of the extent of absorption

Answer 246

absorption rate constant

Answer 247

maximum concentration of a compound after administration

Answer 248

time at which Cmax is reached

Answer 249

area under the concentration time curve (considered a measure of systemic exposure)

Answer 250

measure of the extent of absorption compared to IV

Answer 251

absorption rate constant (a measure of the speed of absorption)

Answer 252

maximum concentration of a compound after administration

Answer 253

time at which Cmax is reached

Answer 254

area under the concentration/time curve (considered a measure of systemic exposure)

Answer 255

measure of the extent of absorption compared to IV

Answer 256

absorption rate constant (a measure of the speed of absorption)

Answer 257

maximum concentration of a compound after administration

Answer 258

time at which Cmax is reached

Answer 259

area under the concentration/time curve (considered a measure of systemic exposure)

Answer 260

measure of extent of absorption compared to IV

Answer 261

absorption rate constant (a measure of the speed of absorption)

Answer 262

maximum concentration of compound after administration

Answer 263

time at which Cmax is reached

Answer 264

area under the concentration/time curve (considered a measure of systemic exposure)

Answer 265

measure of extent of absorption compared to IV

Answer 266

absorption rate constant (a measure of the speed of absorption)

Answer 267

F = (AUC oral/AUC IV) x (dose IV/dose oral)

Answer 268

F = (AUC IV/AUC oral) x (dose oral/dose IV)

Answer 269

it's ability to cross cell membranes (based on physiochemical properties)

Answer 270

the amount of blood flow to individual tissues (perfusion)

Answer 271

the extent of its plasma protein binding

Answer 272

the site of administration

Answer 273

CYP polymorphisms

Answer 274

distribute quickly into tissues and organs.

Answer 275

tend to stay in the systemic circulation rather than distribute into tissues and organs.

Answer 276

is produced by the liver

Answer 277

binds mostly acidic and some neutral drugs

Answer 278

concentration is decreased in malnutrition and cirrhosis

Answer 279

is normally present at around 3.5-5g/L

Answer 280

binds basic and some neutral drugs

Answer 281

is normally present at around 0.4-1.1mg/L

Answer 282

is a plasma protein

Answer 283

is produced by the kidneys

Answer 284

is produced by the liver

Answer 285

binds basic and some neutral drugs

Answer 286

binds acidic drugs

Answer 287

is present at around 0.4-1.1mg/L

Answer 288

is present at around 3.5-5g/L

Answer 289

is an acute phase protein which elevated in some diseases such as cancer

Answer 290

Volume of Distribution (VD)

Answer 291

Clearance (CL)

Answer 292

by exhalation

Answer 293

in the urine

Answer 294

after metabolism forming water soluble metabolites

Answer 295

often eliminated unchanged in the urine.

Answer 296

eliminated in the urine or bile after metabolism to make them more water soluble.

Answer 297

always stored in the body.

Answer 298

eliminated by exhalation.

Answer 299

typically undergo metabolism to form water soluble metabolites before elimination.

Answer 300

are eliminated unchanged.

Answer 301

are stored as starch.

Answer 302

are eliminated by a process called first pass metabolism.

Answer 303

Clearance (CL)

Answer 304

Elimination Rate Constant (Ke)

Answer 305

the volume of plasma (or blood) cleared of the compound in a given time. (e.g. L/hr)

Answer 306

how long it takes for half of the drug to be eliminated.

Answer 307

the process by which the body metabolises a drug.

Answer 308

is known as Ke.

Answer 309

is the slope of the logged concentration-time graph.

Answer 310

has units of 1/time.

Answer 311

is linked to Ka.

Answer 312

is not relevant in humans.

Answer 313

the time it takes for the concentration of active drug to reach half its current value.

Answer 314

half the time taken for all of the drug to be eliminated.

Answer 315

are a large superfamily of heme-cofactor containing enzymes.

Answer 316

metabolise thousands of endogenous and exogenous compounds.

Answer 317

are abbreviated to CYPs.

Answer 318

are mostly highly concentrated in the heart and lungs.

Answer 319

are found in the cytoplasm of cells.

Answer 320

CYPs add a reactive functional group (e.g. -OH) to the active drug compound.

Answer 321

CYPs cleave active drug compounds to make them unreactive.

Answer 322

CYPs are not involved.

Answer 323

reduced metabolism of substrate drug

Answer 324

increased metabolism of substrate drug

Answer 325

increased drug exposure

Answer 326

reduced drug exposure

Answer 327

risk of toxicity

Answer 328

risk of lacking therapeutic effect

Answer 329

increase in biosynthesis of the enzymes (due to increased gene transcription)

Answer 330

increased metabolism of substrate

Answer 331

decreased metabolism of substrate

Answer 332

increased drug exposure

Answer 333

decreased drug exposure

Answer 334

toxicity risk

Answer 335

risk of lack of therapeutic effects

Answer 336

Conjugation

Answer 337

Esterification

Answer 338

Elimination

Answer 339

sulphuric acid

Answer 340

amino acids

Answer 341

glucuronic acid

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Phamacodynamics and Pharmacokinetics

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