Pharmacology Cumulative
1. BBW: FDAs most stringent warning for drugs and medical devices on the market, alert public or health care
providers of serious side effects (injury or death), required by FDA
2. REMS: risk, evaluation, mitigation, strategy. A drug safety program that the FDA can require for certain meds with
serious safety concerns; helps ensure the benefits of the meds outweigh the risk; requires clinicians/health care setting to
become certified before prescribing
REMS is a subset of BBW
3. Drug: a substance, other than food or water, either artificial or natural, that affects the function of the body
4. Pharmacology: the science of drugs, including their origin, composition, phar- macokinetics, therapeutic use and
toxicology (what drugs are, what they do, and how they work)
5. MOA: specific biochemical interaction through which a drug substance produces its pharmacological effect. Usually
includes the specific molecular targets to which the drug bonds
6. Receptor:
Agonist
Antagonist
Agonist-antagonist: Agonist: binds to and activates a receptor Full agonist: binds to and
activates a receptor complex
Partial agonist: binds to a component of a receptor complex
Antagonist: binds to and blocks activation of a receptor
Agonist-antagonist: binds to a component of a receptor complex and blocks the activation of a second component of
the receptor complex
7. enzyme inhibitors: a drug which inhibits metabolic activity, stops processes
8. enzyme inducers: type of drug which binds to an enzyme and increases meta- bolic activity (revs up system) — less
of the drug effect
9. pharmacokinetics: discipline that describes the absorption, distribution, metabo- lism and eliminations of drugs; how
drug concentration changes as it moves through different compartments of the body (what the body does to the dug)
10.pharmacodynamics: what the drug does to the body
11.pharmacokinetics: metabolism: how the drug is processed and broken down (primary site: liver, kidney, GI tract)
Another word for metabolism: biotransformation. The irreversible transformation of parent compounds into daughter
compounds (usually done by enzymes). Most of this the time happens in the liver (also GI tract, kidneys, lungs, blood)
, Pharmacology Cumulative
12.Drug metabolism outcomes: Active > broken down to an inactive form, in- cludes most drugs
Inactive > activated into an active form. Inactive form is a prodrug Lipid > something added to
make it more polar (more water soluble) Lipid bc it allows med to get to where it needs
13.Why do we metabolize drugs?: To convert from a lipid soluble for to a water soluble form for excretion
14.Pharmacological phenotypes: HOW someone clears a drug. Pharmacokinetics: plasma
drug concentration, clearance. Metabolism: ultra rapid, rapid, normal, intermediate, poor.
Pharmacodynamics: responder, non responders; normal function, no function
15.Decreased drug metabolism:
Genetic variants and pharmacokinetic impact: decreases enzyme activity, de- creased affinity for substrates, inactive
(non functional) enzymes. [the enzyme is not able to properly breakdown drug]
Potential impact on clinical pharmacokinetic parameters: decreased clearance, in- creased half life [stays in body longer]
16.Increased drug metabolism:
Genetic variants and pharmacokinetic impact: increased enzyme activity, in- creased amount of metabolizing enzyme
Potential impact on clinical PK parameters: increased clearance, decreased half life [drug leaves body faster]
17.Prodrugs must be metabolized to which are then metabolized into
and metabolites: active drugs active and
inactive metabolites
18.Prodrug is in order to get past the gut and not get de- graded. Prodrugs are
usually . must be modified to become a drug:
Prodrug is encapsulated/coated
Prodrugs are usually inactive
Prodrugs must be modified to become a drug
19.poor metabolizers: increased active parent drug leads to more inactive metabolite (increased effect
and/or toxicity)
20.ultra rapid metabolizer: parent drug leads to more inactive metabolite and decreased effect bc everything
went through metabolism
Too much inactive metabolite can build up toxicity
21.CYP450
metabolism predominately uses CYP450 responsible for most
drug reactions
superfamily of : Phase I metabolism predominantly uses CYP 450
, Pharmacology Cumulative
responsible for most drug metabolism oxidation reactions Superfamily of enzymes
22.If an active drug which is poorly metabolized receives CYP sub- strates...what do you see?: increased
pharmacologic effect and increased toxicity
23.If an active drug which is ultra rapidly metabolized receives CYP sub- strates...what do you see?:
decreased pharmacologic effect
Because it's broken down so fast
24.If a prodrug which is poorly metabolized receives a CYP substrate...what do you see?: decreased
pharmacologic effect and no toxicity since the drug has no effect
25.Codeine metabolism: A small percent of codeine is turned into active drug morphine. With an ultra rapid
metabolizer, the formation of morphine is increased leading to an increased risk of toxicity. With a poor metabolizer,
the codeine is not changed into morphine leading to insufficient pain relief/decreased pharmacologic effect
26.Oral administration pros/cons: Advantages: convenient, easily packaged and stored, compliance/adherence
enhanced
Disadvantages: must have oral access/capabilities, low solubility, low permeability, irregular absorption, degradation by G
tract, first pass effect, food interactions
27.buccal/sublingual pros/cons: Pros: avoids GI tract, avoids first pass effect Cons: high probability of
swallowing, can only give as small doses
28.IV administration pros/cons: Advantages: 100% bioavailable, rapid response, bypass first pass metabolism
Disadvantages: invasive, requires IV access, sterility requires, trained personnel, institutional use, rapid toxicity possible
29.Sub Q pros/cons: Advantages: 100% bioavailable, rapid response, bypass first pass metabolism
Disadvantages: invasive, requires IV access, sterility requires, trained personnel, institutional use, rapid toxicity possible
30.IM pros/cons: Advantages: complete absorption, larger volume than SQ, self administration possible
Disadvantages: invasive, irritating/inflammation, patients don't like needles, limited by volume (max dose 5mL)
Higher dose than SubQ
31.inhaler pros/cons: Advantages: bypass first pass metabolism, gasses are rapidly absorbed, limits systemic
circulation
Disadvantages: irritating, bronchospasm, technique must be precise but is often variable
, Pharmacology Cumulative
32.Rectal pros/cons: Advantages: absorption faster than oral, bypass first pass metabolism, useful for children and
patients with no oral or IV access Disadvantages: degradation by bacterial flora, involuntary expulsion, can be difficult
for self administration, uncomfortable
33.Transdermal pros/cons: Advantage: less invasive, avoids first pass metabo- lism, fewer side effects, delivers
steady infusion over a prolonged period of time, improves patient adherence
Disadvantages: low permeability across the skin, requires educated patient (when to place another), lack of adhesion to
the body, storage/disposal requirements
34.Topical pros/cons: Advantages: may eliminate need for systemic treatment, enhance systemic treatment, decreased
risk of systemic adverse reaction, decrease risk of drug interactions, ease of administration, smaller amount of medication
needed
Disadvantages: local irritation/allergic reaction, decreased penetration, potential systemic absorption and adverse effects,
poor compliance/adherence, administra- tion errors, large area to cover, severity of condition, may be transferred to other
people, unintended drug absorption
35.indications topical corticosteroids: Indications: immunosuppressive proper- ties, relief of inflammation and
pruritis associated with steroid responsive der- matoses
Highly responsive: psoriasis, atopic dermatitis
Less responsive: insect bites, allergic contact dermatitis. Lupus erythematous
36.topical corticosteroids ADE: Metabolic syndrome effects - hyperglycemia and cushings
Amount of adrenal suppression is related to:
Steroid potency
Factors that increase absorption: occlusion, use on large skin areas, inflamed areas, high concentrations
Local side effects: burning, itching, irritation, erythema, dryness, skin thinning/ atrophy (decreased thinning, keratinocyte
fibroblasts, stratum corneum changes, related to higher potency steroids)
37.Topical retinoids
indications
ADE: Topical retinoids: (adapalene, tretinoin, tazarotene) Indications: acne
ADE: erythema, irritation, dryness, skin peeling, photosensitivity
38.Topical antimicrobials: (topical erythromycin and clindamycin) Indications
ADE: indication: acne
1. BBW: FDAs most stringent warning for drugs and medical devices on the market, alert public or health care
providers of serious side effects (injury or death), required by FDA
2. REMS: risk, evaluation, mitigation, strategy. A drug safety program that the FDA can require for certain meds with
serious safety concerns; helps ensure the benefits of the meds outweigh the risk; requires clinicians/health care setting to
become certified before prescribing
REMS is a subset of BBW
3. Drug: a substance, other than food or water, either artificial or natural, that affects the function of the body
4. Pharmacology: the science of drugs, including their origin, composition, phar- macokinetics, therapeutic use and
toxicology (what drugs are, what they do, and how they work)
5. MOA: specific biochemical interaction through which a drug substance produces its pharmacological effect. Usually
includes the specific molecular targets to which the drug bonds
6. Receptor:
Agonist
Antagonist
Agonist-antagonist: Agonist: binds to and activates a receptor Full agonist: binds to and
activates a receptor complex
Partial agonist: binds to a component of a receptor complex
Antagonist: binds to and blocks activation of a receptor
Agonist-antagonist: binds to a component of a receptor complex and blocks the activation of a second component of
the receptor complex
7. enzyme inhibitors: a drug which inhibits metabolic activity, stops processes
8. enzyme inducers: type of drug which binds to an enzyme and increases meta- bolic activity (revs up system) — less
of the drug effect
9. pharmacokinetics: discipline that describes the absorption, distribution, metabo- lism and eliminations of drugs; how
drug concentration changes as it moves through different compartments of the body (what the body does to the dug)
10.pharmacodynamics: what the drug does to the body
11.pharmacokinetics: metabolism: how the drug is processed and broken down (primary site: liver, kidney, GI tract)
Another word for metabolism: biotransformation. The irreversible transformation of parent compounds into daughter
compounds (usually done by enzymes). Most of this the time happens in the liver (also GI tract, kidneys, lungs, blood)
, Pharmacology Cumulative
12.Drug metabolism outcomes: Active > broken down to an inactive form, in- cludes most drugs
Inactive > activated into an active form. Inactive form is a prodrug Lipid > something added to
make it more polar (more water soluble) Lipid bc it allows med to get to where it needs
13.Why do we metabolize drugs?: To convert from a lipid soluble for to a water soluble form for excretion
14.Pharmacological phenotypes: HOW someone clears a drug. Pharmacokinetics: plasma
drug concentration, clearance. Metabolism: ultra rapid, rapid, normal, intermediate, poor.
Pharmacodynamics: responder, non responders; normal function, no function
15.Decreased drug metabolism:
Genetic variants and pharmacokinetic impact: decreases enzyme activity, de- creased affinity for substrates, inactive
(non functional) enzymes. [the enzyme is not able to properly breakdown drug]
Potential impact on clinical pharmacokinetic parameters: decreased clearance, in- creased half life [stays in body longer]
16.Increased drug metabolism:
Genetic variants and pharmacokinetic impact: increased enzyme activity, in- creased amount of metabolizing enzyme
Potential impact on clinical PK parameters: increased clearance, decreased half life [drug leaves body faster]
17.Prodrugs must be metabolized to which are then metabolized into
and metabolites: active drugs active and
inactive metabolites
18.Prodrug is in order to get past the gut and not get de- graded. Prodrugs are
usually . must be modified to become a drug:
Prodrug is encapsulated/coated
Prodrugs are usually inactive
Prodrugs must be modified to become a drug
19.poor metabolizers: increased active parent drug leads to more inactive metabolite (increased effect
and/or toxicity)
20.ultra rapid metabolizer: parent drug leads to more inactive metabolite and decreased effect bc everything
went through metabolism
Too much inactive metabolite can build up toxicity
21.CYP450
metabolism predominately uses CYP450 responsible for most
drug reactions
superfamily of : Phase I metabolism predominantly uses CYP 450
, Pharmacology Cumulative
responsible for most drug metabolism oxidation reactions Superfamily of enzymes
22.If an active drug which is poorly metabolized receives CYP sub- strates...what do you see?: increased
pharmacologic effect and increased toxicity
23.If an active drug which is ultra rapidly metabolized receives CYP sub- strates...what do you see?:
decreased pharmacologic effect
Because it's broken down so fast
24.If a prodrug which is poorly metabolized receives a CYP substrate...what do you see?: decreased
pharmacologic effect and no toxicity since the drug has no effect
25.Codeine metabolism: A small percent of codeine is turned into active drug morphine. With an ultra rapid
metabolizer, the formation of morphine is increased leading to an increased risk of toxicity. With a poor metabolizer,
the codeine is not changed into morphine leading to insufficient pain relief/decreased pharmacologic effect
26.Oral administration pros/cons: Advantages: convenient, easily packaged and stored, compliance/adherence
enhanced
Disadvantages: must have oral access/capabilities, low solubility, low permeability, irregular absorption, degradation by G
tract, first pass effect, food interactions
27.buccal/sublingual pros/cons: Pros: avoids GI tract, avoids first pass effect Cons: high probability of
swallowing, can only give as small doses
28.IV administration pros/cons: Advantages: 100% bioavailable, rapid response, bypass first pass metabolism
Disadvantages: invasive, requires IV access, sterility requires, trained personnel, institutional use, rapid toxicity possible
29.Sub Q pros/cons: Advantages: 100% bioavailable, rapid response, bypass first pass metabolism
Disadvantages: invasive, requires IV access, sterility requires, trained personnel, institutional use, rapid toxicity possible
30.IM pros/cons: Advantages: complete absorption, larger volume than SQ, self administration possible
Disadvantages: invasive, irritating/inflammation, patients don't like needles, limited by volume (max dose 5mL)
Higher dose than SubQ
31.inhaler pros/cons: Advantages: bypass first pass metabolism, gasses are rapidly absorbed, limits systemic
circulation
Disadvantages: irritating, bronchospasm, technique must be precise but is often variable
, Pharmacology Cumulative
32.Rectal pros/cons: Advantages: absorption faster than oral, bypass first pass metabolism, useful for children and
patients with no oral or IV access Disadvantages: degradation by bacterial flora, involuntary expulsion, can be difficult
for self administration, uncomfortable
33.Transdermal pros/cons: Advantage: less invasive, avoids first pass metabo- lism, fewer side effects, delivers
steady infusion over a prolonged period of time, improves patient adherence
Disadvantages: low permeability across the skin, requires educated patient (when to place another), lack of adhesion to
the body, storage/disposal requirements
34.Topical pros/cons: Advantages: may eliminate need for systemic treatment, enhance systemic treatment, decreased
risk of systemic adverse reaction, decrease risk of drug interactions, ease of administration, smaller amount of medication
needed
Disadvantages: local irritation/allergic reaction, decreased penetration, potential systemic absorption and adverse effects,
poor compliance/adherence, administra- tion errors, large area to cover, severity of condition, may be transferred to other
people, unintended drug absorption
35.indications topical corticosteroids: Indications: immunosuppressive proper- ties, relief of inflammation and
pruritis associated with steroid responsive der- matoses
Highly responsive: psoriasis, atopic dermatitis
Less responsive: insect bites, allergic contact dermatitis. Lupus erythematous
36.topical corticosteroids ADE: Metabolic syndrome effects - hyperglycemia and cushings
Amount of adrenal suppression is related to:
Steroid potency
Factors that increase absorption: occlusion, use on large skin areas, inflamed areas, high concentrations
Local side effects: burning, itching, irritation, erythema, dryness, skin thinning/ atrophy (decreased thinning, keratinocyte
fibroblasts, stratum corneum changes, related to higher potency steroids)
37.Topical retinoids
indications
ADE: Topical retinoids: (adapalene, tretinoin, tazarotene) Indications: acne
ADE: erythema, irritation, dryness, skin peeling, photosensitivity
38.Topical antimicrobials: (topical erythromycin and clindamycin) Indications
ADE: indication: acne
