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Foundations 1 > Pharm > Flashcards

Pharm Flashcards

(57 cards)

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1
Q

Drug

A

Chemical capable of reacting w/ biological systems

Can be endogenous or foreign

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2
Q

Toxin

A

Chemical that produces undesirable effects

Synthesized by plants, microorganisms, animals, insects

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3
Q

Poison

A

Chemical that produces undesirable effects

Synthetic or inorganic compound

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4
Q

Pharmacodynamics

A

Drug’s effect on body

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5
Q

Pharmacokinetics

A

Body’s effect on drug

ADME

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6
Q

Imantinib

A

Anti-cancer drug that interacts w/ BCR-Abl kinase A (rearrangement of 9 and 22 that causes tyrosine kinase to be always “on”, phosphorylates a target important in cell proliferation)
Inhibits phosphorylation of activation group
Not toxic to any other cells

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7
Q

Ligand-gated transmembrane ion channel receptor

A

Activated by binding of ligand

Ex. Nicotinic receptor (ACh binds to 2 alpha subunits and opens Na+ gate)

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8
Q

Voltage-gated transmembrane ion channel receptor

A

Activated by change in transmembrane voltage gradient

Ex. tetrodotoxin in puffer fish inactivates fast Na+ channel

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9
Q

Second-messenger gated transmembrane ion channel receptor

A

Activated by binding of ligand to G protein-coupled receptor w/ cytosolic domain, which activates a second messenger
Ex. cAMP –> PKA

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10
Q

G protein-coupled receptor

A

Ligand binds to receptor –> receptor changes conformation –> alpha subunit dissociates and diffuses to nearby effector
Ex. activation of adenylyl cyclase to form cAMP –> PKA and PLC

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11
Q

Transmembrane receptors w/ catalytic intracellular domain

A 
Receptor tyrosine kinases
Receptor tyrosine phosphatases
Receptor serine/threonine kinases
Non-receptor tyrosine kinases
Receptor guanylyl cyclases
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12
Q

Cytoplasmic/nuclear receptor

A

Receptor AND/OR transcription factor

Ex. hormone receptors

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13
Q

Tachyphlaxis

A

Repeated administration of the same dose of a drug results in a reduced effect of the drug over time

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14
Q

Desensitization

A

Decreased ability of a receptor to respond to stimulation by a drug or ligand

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15
Q

Homologous desensitization

A

Decreased response at a single type of receptor

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16
Q

Heterologous desensitization

A

Decreased response at 2+ types of receptor

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17
Q

Inactivation

A

Loss of ability of a receptor to respond to stimulation by a drug or ligand

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18
Q

Refractory

A

After a receptor is stimulated, a period of time is required before the next drug-receptor interaction can produce an effect

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19
Q

Down-regulation

A

Repeated or persistent drug-receptor interaction results in removal of the receptor from sites where subsequent drug-receptor interactions could take place

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20
Q

Receptor

A

Site on cell or organism that binds w/ endogenous substance or drug that initiates a chain of biochemical events that leads to a response
Number limits response to drug

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21
Q

Inert binding sites

A

Proteins that bind and sequester drug and prevent it from performing its intended function
After withdrawn, the drug can come off and produce an effect
Ex. serum albumin

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22
Q

Agonist

A

Produces maximal response when receptors are fully occupied

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23
Q

Partial agonist

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A

Produces lower than maximal response at full receptor occupancy
Can act as antagonist if coupled w/ full agonist

24
Q

Antagonist

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A

Prevents action of agonist (doesn’t do anything on its own)

Doesn’t change binding site

25
Ligand
Molecule that binds to a receptor
26
Drug-receptor interaction (equation)
[D][R]/[DR] = k2/k1 = Kd
27
Low Kd
High affinity, very potent | Administered in small amounts
28
High Kd
Low affinity, less potent | Administered in larger amounts
29
Ligand-receptor binding curve (equation)
[DR]/[Rt] = [D]/(Kd + [D]) | Plots as rectangular hyperbola
30
Kd
Concentration of ligand at which half of the receptors are occupied
31
Occupancy-response curve (equation)
E/Emax = [D]/(Ke + [D]) Maximal effect Ke = value of DR that exhibits half-maximal response
32
Drug potency
Concentration at which the drug elicits 50% of its maximal response (EC50)
33
Drug efficacy
Maximal response produced by the drug (how strong the reaction is) (Emax) State at which receptor-mediated signaling is maximal and any additional drug will produce no additional response Comparatively, doesn't depend on how much drug you give
34
Effective Dose (ED50)
Dose at which50% of the population experiences a therapeutic effect
35
Toxic Dose (TD50)
Dose at which 50% of the population experiences a toxic effect
36
Lethal Dose (LD50)
Dose at which 50% of the population experiences a lethal effect
37
Therapeutic Index
TI = TD50/ED50 High TI- large separation between effective dose and toxic dose, drug will be very effective w/o adverse effects Low TI- small separation between effective dose and toxic dose, have to be careful!
38
Margin of Safety
MS = LD1/ED99 Compares concentration of drug that is lethal to first 1% of population to concentration that is effective in 99% of population Low MS- not safe, will cause some deaths, even at concentration that is therapeutic in most patients High MS- safe, will affect most patients in therapeutic way w/o causing death
39
Inverse agonist
Binds receptor in inactive state and reduces fraction of receptors in active state Causes opposite effect of agonist
40
Active site antagonist
Antagonist binds to same site as ligand | Can be reversible (competitive) or irreversible (noncompetitive)
41
Allosteric site antagonist
Antagonist binds to different site than ligand Can be reversible or irreversible (both noncompetitive) A "ceiling" to the effect exists (once all sites are occupied, no further effect is observed)
42
Chemical antagonist
Receptors are not involved Activity is based on chemical interactions Ex. Heparin (negatively charged) binds protamine (positively charged) to inactivate it
43
Physiologic antagonist
Opposing pathways must be activated to produce antagonism | Ex. glucagon increases blood glucose, insulin decreases blood glucose
44
Competitive antagonist effect on D-R curve
Reduces potency of agonist and increases Kd (curve shifts to right) Does NOT affect efficacy
45
Noncompetitive antagonist effect on D-R curve
Reduces efficacy of agonist and lowers response/decreases Emax (curve height decreased) Does NOT change Kd or potency
46
Spare receptors
Full response doesn't require occupancy of all receptors More receptors are present than are needed to produce Emax System is more sensitive to drugs (b/c low concentration of drug occupies same number of receptors)
47
Spare receptor effect on D-R curve
Lower concentration of drug gives half maximal effect (curve is shifted left wrt drug-receptor curve)
48
Noncompetitive antagonist effect on D-R curve in presence of spare receptor
Antagonist destroys spare receptors (curve shifts to right) | Agonist action is reduced (curve shifts down)
49
Hydroxyurea
Sickle cell anemia | Increases HbF
50
Sulfonylurea
T2DM | Increases insulin release by permanently closing K+ channel in B-cells in pancreas
51
Metformin
T2DM | Suppresses gluconeogenesis in liver
52
SGLT2 inhibitors
T2DM | Decreases reabsorption/ncreases excretion of glucose in kidneys
53
Pioglitazone
T2DM | Reduces insulin resistance/improves peripheral tissue sensitivity to insulin
54
Acarbose/miglitol
T2DM | Impairs absorption of glucose in small intestine
55
GLP-1 analogues
T2DM Slow transit of nutrients through stomach (makes you feel full longer, decreases appetite) Increases insulin Ends in "tide"
56
DPP-4 inhibitors
T2DM Inhibits enzyme that breaks down GLP-1 Ends in "liptin"
57
Insulin
Long-acting- basal insulin, lasts all day | Short-acting- bolus insulin, taken w/ meals

Foundations 1 (8 decks)

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