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Pharmacology 3001 > MIDTERM 1 > Flashcards

MIDTERM 1 Flashcards

1
Q

Drug

A

any substance that causes an change in cellular/biological effect

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2
Q

Therapeutic agent

A

-drug used to TREAT disease/condition

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3
Q

Prophylactic agent

A

-drug used to PREVENT disease/condition

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4
Q

Pharmacy

A

the art of PREPARING, COMPOUNDING and DISPENSING chemicals for medicinal use

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5
Q

Pharmacology

A

the study of drugs and their effects

  • what they are, how they work, what they do
  • divided into PD and PK
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6
Q

Pharmacodynamics (PD)

A
  • what drugs do to the body

- studying the relationship between concentration of drug + effect

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7
Q

Pharmacokinetics (PK)

A

-what the body does to drugs

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8
Q

Pharmacogentics/ Genomics

A

-variations in drug response due to genetics

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9
Q

Toxicology

A
  • study of undesirable effects of chemicals on living systems
  • poisons, antidotes, unwanted side effects
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10
Q

FDA Pregnancy categories

A

Category A: drug is safe for pregnancy
-penicillin, anti-histamine

Category B/C: drug MAY cause harm

Category D: drug LIKELY to cause harm

Category X: drug shown to cause harm, DO NOT USE
-interfere with pathways of fetal development

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11
Q

Examples of category X drugs

A
  • Ace inhibitors: fetal renal and CV damage
  • Anti-epilileptic drugs: neural tube defects, CV damage
  • Warfarin: anatomical malformations, CNS and CV damage
  • Valproic acid: neural tube defects, anatomical malformations, CNS, CV damage
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12
Q

Drug development time line

A

1) In-vitro studies
- 2 years
- chemical synthesis

2) Animal testing
- from year 2-4
- at end –> IND (Investigational New Drug)
- successful on animals, can begin testing on humans

3) Clinical trials
PHASE 1: is it safe?
-healthy volunteers, young males
-determine pharmacokinetics (what body does to drugs) and toxicity

PHASE 2: does it work in people?

  • people with the condition of interest
  • determine drug efficacy and dosing

PHASE 3: does it work double blind?

  • large scale trials
  • confirm safety and efficacy
  • results determine if drug goes to market
  • –> at 8-9 mark –> NDA/ New drug application

4) Marketing

PHASE 4: post marketing surveillance

  • after drug approval
  • withdrawn if significant problems
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13
Q

Exceptions to the drug development timeline

A
  • many drugs for life-threatening conditions (HIV, cancer, AIDS) skip steps to get drugs to patients faster
  • may result in less info being known about a drug
  • higher frequencies of adverse effects
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14
Q

DIN

A
  • drug identification #

- required by law in Canada

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15
Q

NPN

A
  • natural product number

- ex: multivitamins

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16
Q

Numbers for drugs

A
  • allows for tracking
  • recalls
  • adverse rxns
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17
Q

Serendipitous discovery

A
  • drug found by accident or when trying to dine something else
    ex: penicillin
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18
Q

Intelligent (or rational) drug design

A
  • identify a target, design a drug to modulate this target

ex: reverse transcriptase inhibitors (HIV therapy)

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19
Q

High throughput screening

A

test large libraries of compounds to determine “hits”

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20
Q

“Me too” drugs

A
  • related drugs produced after the 1st/OG discovery

- mostly just improvements, nothing new

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21
Q

Canadian drug advertising regulations

A

Food and drugs Act
-prevents false advertising

Food and drug regulations
-cannot advertise benefits and or/therapeutic use

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22
Q

Chemical name of a drug

A

IUPAC

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23
Q

Generic name

A
  • USUALLY a universal name of a drug product
  • ex: ibuprofen
  • acetaminophen/paracetamol
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24
Q

Brand name/trade name

A
  • determined by manufacturer
  • different across the world

ex: over 100 diff brands of ibuprofen
- Advil
- Motrin

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25
Q

Pharmacodynamics

A
  • what drugs do to the body
  • studying the relationship between concentration of drug + effect

L + R ⇌ LR (ligand-receptor complex)

L= ligand

  • binds to specific receptors
  • drugs, endogenous molecules (NTs and hormones)

ASSUME: biological effect is proportional to amount of LR
-more drugs bound to receptor, the greater the effect

26
Q

How do drugs elicit their effects?

A

by mimicking to blocking the actions of hormones + NTs (endogenous molecules)

27
Q

Major classes of receptors targeted by drugs

A

1) Ligand-gated ion channels
- ligand binds, change in concentration of intracellular ions, leads to cellular effect
ex: Nicotinic acetylcholine receptor (milliseconds)

2) Enzyme-linked receptors
- ligand binds, protein phosphorylation, cellular effect
ex: insulin receptor (seconds- minutes)

3) G-protein coupled receptors (GPCRs)
- ligand binds, activates G protein, intracellular 2nd messengers, cellular effect
ex: B-adrenergic receptor (seconds to minutes)

4) Ligand activated transcription factors
- located inside the cell
- ligand binds, activates transcription factor, regulates gene expression
ex: estrogen receptor (hours)

28
Q

Ligand receptor binding

A
  • reversible
  • non covalent forces:

Decreasing strength:
Ionic –> H bonds –> Hydrophobic –> Van de waals

29
Q

Strength and number of bonds determines

A
  • Affinity of ligand for receptor

- functional effect of ligand on receptor

30
Q

Lock and key model of ligand-receptor activation

A

Endogenous ligand= hormone or NT = key
Receptor= lock
*hormone/NT acts as a key, binds to the receptor, “unlocks it” –> induces a biological effect

Agonist= mimics NT/ hormones

  • binds to their receptors, elicits the same response as endogenous ligand
  • ex: bobby pin
  • “picks the lock”

Antagonist

  • binds to receptor
  • BLOCKS NT’s and hormones from binding
  • inhibits receptor activation by agonists

ex: jamming a stick in the lock, other shit can’t bind

31
Q

Relationship between ligand concentration and receptor binding

A
  • ligand binding to receptor: hyperbolic
  • can also undergo semi-log transformation, same shit

Bmax= max amount of receptors bound
-all receptors are bound by ligand

B= fraction of receptors bound

kd= dissociation constant, concentration of the ligand at 1/2 Bmax, measure of affinity of receptor-ligand interaction

B= Bmax * [L] / [L] + kd

32
Q

Graded dose response curve

A
  • responses that have an infinite number of intermediate states
  • ex: vessel dilation, blood pressure change, HR change
33
Q

Emax

A

maximum effect/response achieved by the ligand

34
Q

ED50

A
  • ligand dose at which 50% of E max is achieved

- POTENCY

35
Q

Quantal phenomena

A
  • all or none: 2 states (ex: death, pregnancy, cure, pain relief)
  • useful to describe population rather than individual responses to drugs
  • based on plotting cumulative frequency distribution of responders vs. log dose
36
Q

Potency

A
  • the amount of agent needed to produce a given effect
  • ED50
  • smaller ED50= higher potency
37
Q

Efficacy

A
  • the MAXIMUM effect that can be achieved with an agonist
  • the functional impact on a receptor
  • Emax (max % effect)

higher Emax= higher efficacy

38
Q

Types of agonists

A
  • Full agonists and partial agonists
  • POTENCY DOESN’T FACTOR INTO WHETHER IT IS PARTIAL OR FULL
  • ONLY EFFICACY: the functional outcome
39
Q

Full agonist

A

ANYTHING WITH MAX EFFICACY

  • high potency + max efficacy
  • low potency + max efficacy
40
Q

Partial agonist

A

ANYTHING WITH REDUCED EFFICACY

  • high potency + reduced efficacy
  • low potency + reduced efficacy
41
Q

Failure of partial agonists to produce a maximal response

A
  • not due to decreased affinity: kd can be identical for partial and full
  • partial agonists have a lower functional impact on the receptor
42
Q

Constitutive receptor activation

A

-going from inactive –> active via agonist or spontaneously

agonist: binding induces conformational change in the receptor from inactive –> active
- may also stabalize the active state

43
Q

Agonist (experiment to measure constitutive receptor activation)

A
  • has an independent effect on receptor activity: ACTIVATES
  • caused vasodilation
  • HAVE EFFICACY: functional impact on a receptor
44
Q

Antagonist

A
  • by itself, will bind to the receptor and block it
  • but doesn’t matter if agonist is not present
  • impacts receptor activity only in the presence of agonist
  • HAVE POTENCY, LACKS EFFICACY
45
Q

Inverse agonist

A
  • stabilizes the inactive state
  • destabilizes the active state

-REDUCES CONSITITIVE RECEPTOR ACTIVATION

has an independent impact on receptor activity
produces effect opposite to agonist
-INACTIVATES THE receptor

46
Q

Types of antagonism

A

chemical antagonism, physiological antagonism, pharmacological antagonism

47
Q

Chemical antagonism

A

DIRECT interaction of two chemicals/substances
-effect of one or both is lost

ex: acidic + basic= loss of activity of both drugs

48
Q

Physiological antagonism

A
  • INDIRECT interaction of two substances with opposing physiological actions
    ex: Histamine decreases bp through vasodilation, epinephrine increases bp through vasoconstriction
49
Q

Pharmacological antagonism

A

-blocking substances from interacting with its receptor by another substance

  • bind to receptors, but do not activate signalling
  • the decreased biological effect is the result from agonists being unable to bind the receptor
50
Q

Types of pharmacological antagonists

A

1) Competitive antagonist
- REVERSIBLY binds receptor
- inhibition can be overcome by increasing the concentration of the agonist
- affects potency/ED50
* does not decrease the # of receptors available for activation*

2) Non-competitive antagonist
- IRREVERSIBLY (covalently) binds to receptor
- or irreversibly binds to allosteric site
- inhibition can’t be overcome by increasing concentration of agonist
- decreases efficacy/ Emax
* DO DECREASE THE # OF RECEPTORS AVAILABLE FOR ACTIVATION*

51
Q

ID50/ IC50

A
  • inhibitory dose/ inhibitory concentration
  • concentration dose at 1/2 Emax
  • AKA POTENCY FOR ANTAGONIST
52
Q

Emax (antagonist)

A

max biological effect achieved by antagonist

-NOT A MEASURE OF EFFICACY, only agonists have efficacy

53
Q

Drug desensitization

A

AKA: resistance, refractoriness, tolerance, tachyphylaxis
-diminished effect of drug due to continuous exposure

two types, receptor mediated and non-receptor mediated

54
Q

Receptor mediated desensitization

A

1) Loss of receptor function
- receptor stops working (change in conformation)
- rapid desensitization/ decreased response
- due to feedback of agonist
ex: phosphorylation of a.a in GPCRs block coupling to G proteins

2) Reduction of receptor #
- decrease in # of receptors
- slower, long term
- due to feedback of agonist
ex: phosphorylation of a.a in GPCRs causes removal from cell surface

55
Q

Non-receptor mediated desensitization

A

1) Decreased receptor coupled signalling components
- decrease in signalling molecules required for response
- prolonged GPCR stimulation, decreases 2nd messengers

2) Increased metabolic degradation
- increased metabolism + increased elimination of drug
ex: barbiturates induce metabolic enzymes that degrade the drugs

3) Physiologic adaptation
- decrease in drug effects due to homeostatic responses

56
Q

Adverse drug effects

A

side effects, toxic reaction, allergic reaction

57
Q

Side effect

A
  • action of drug at OTHER SITES to produce undesirable effects
  • depends on does
  • not directly related to the desired effect of drug
58
Q

Toxic reaction

A
  • excessive action of drug at intended target site
  • depends on dose
  • directly related to the desired effect of drug
59
Q

Allergic reaction

A
  • immune response to drug
  • does not depend on dose
  • not related to desired effect of drug
60
Q

Discuss the adverse effects of cyclosporine

A

Benefits: promotes survival of transplanted organs
-dose dependent, result of immunosuppression (so that organs don’t get rejected)

ADVERSE EFFECTS

Side effect

  • kidney damage
  • not related to intended pharmacological activity
  • magnitude of effect is dose dependent

Toxic effect

  • increased risk of infection due to immunosuppression
  • consequence of intended pharmacological action (immunosuppression)

Allergic effect

  • rash, hives, itching, breathing difficulties
  • not related to intended pharmacological activity
  • not dose dependent
61
Q

Therapeutic index (TI)

A

TI= Toxic ED50/ Beneficial ED50

  • relative measure, not absolute
  • if outcome = death, need large TI
  • if outcome = headache, can have a lower TI
62
Q

Therapeutic window

A

-RELATIONSHIP TO DOSE

the range of DOSAGES of a drug
-associated with: adverse effects, therapeutic benefit, lack of effect in a population

Pharmacology 3001 (4 decks)

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