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Medical Conditions 1 > Introduction to Pharmacology > Flashcards

Introduction to Pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

Pharmacology

A

the study of medications and their effects on living systems

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2
Q

Pharmacotherapeutics

A

use of medications for therapeutic reasons

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3
Q

Pharmacodynamics

A

how the drug affects the system

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4
Q

Pharmacokinetics

A

how the body affects the drug
- absorption
- distribution
- elimination

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5
Q

Toxicology

A

study of the adverse affects from medications

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6
Q

Adverse Drug Reactions (ADRs)

A

severe side effects of drugs

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7
Q

Specificity of drugs/receptors

A

only effects specific receptors

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8
Q

Endogenous ligand

A
  • a substance that is naturally occuring in the body and can be effected by a drug/a drug can mimic the affect of the substance
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9
Q

Downregulation of receptors

A

decrease in available number of receptors

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10
Q

upregulation of receptors

A

increase in available number of receptors

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11
Q

Receptor principles
- quantitative relationship
- drug selectivity
- activation/inhibition

A
  1. quantitative relationship between dose/concentration and the effects
  2. drug selectivity: based on the shape and type of receptors (alpha/beta) that they stimulate
  3. activation/inhibition of receptor causes different clinical effects
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12
Q

Types of graded dose response of drugs

A
  • Linear relationships between concentration and effect that produce a hyperbolic curve
  • logarithmic relationships between the concentration and effect gives a sigmoidal curve
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13
Q

Emax in a graded dose response of drugs

A
  • max effect where doses greater do not produce added benefit
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14
Q

minimal effective dose

A
  • concentration below which there are not any clinical benefits
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15
Q

What is a quantal dose response

A
  • when the minimium dose required to produce an intended magnitude of response is evaluated for a population
  • can give a therapeutic index which can measure how safe a drug it
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16
Q

Therapeutic window

A
  • is the dosage range between the minimum effective dose and the minimum toxic dose
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17
Q

Therapeutic index

A
  • calculated by median toxic dose or median lethal dose by the median effective dose
  • generally the larger the range the more safe the drug is
  • (have a very high toxic dose but a small effective dose)
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18
Q

What doses can be found from a quantal dose response curve

A
  • median effective dose: needed to obtain a response
  • median toxic dose: dose at which it is toxic to the biological system
  • median lethal dose: where it is lethal to the system
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19
Q

Drug potency

A
  • the amount of drug needed to produce a desired effect
  • a drug is more potent if you need to take less amount to get desired response
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20
Q

durg efficacy

A
  • the drugs ability to reach the max effect/ a measureable response
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21
Q

Full agonist

A
  • a drug or endogenous ligand that is capable of fully activating the effector system upon binding to the receptor
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22
Q

Partial agonist

A
  • a drug or endogenous ligand that binds to the receptor but achieves a lower maximal effect when with full occupancy due to lower maximal efficacy
  • in the presence of a full agonist the partial agonist can act as inhibitor
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23
Q

Allosteric response

A

does not bind directly to the receptor’s active site but influences the affinity of the receptor
- can be an activator or inhibitor

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24
Q

Competitive antagonist

A
  • a drug that binds to or very close to an agonist receptor site in a reversible way but does not activate the effector system
  • with a competitive agonist the ED (effective dose) shifts to higher doses
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25
Q

noncompetitive antagonist

A
  • causes a downward shift of the maximum response with no shift on the dose axis
  • binds to the receptor site
  • their binding is nearly irreversible or irreversible
    -effects of a noncompetitive antagonist can not be over come with increase in dose
26
Q

What are the trans membrane signalling mechanisms

A
  • transmembrane diffusion
  • transmembrane enzyme receptors
  • transmembrane receptor
  • transmembrane channels
  • g protein-coupled receptors
27
Q

transmembrane diffusion/intracellular recepotr

A
  • diffuse into the cell and bind to an intracellular receptor
  • bind to lipid soluble agonists
28
Q

transmembrane enzyme receptors/transmembrane receptor

A
  • binds outside and causes an effect inside
  • or activates cytoplasmic tyrosine kinase molecules
  • have enzymatic activity on the inside
29
Q

transmembrane channels

A
  • when the agonist or ligand binds it will open the channel to allow ions/substances to flow into the cell
  • drugs that mimic these will help to regulate the flow into the cell
30
Q

g protein-coupled receptors

A
  • increase intracellular concentrations of secondary messengers such as cAMP
  • 3 components
    1. extracellular ligand binds to specific surface receptor
    2. receptor binding triggers activation of G protein located in the cytoplasmic face of plasma membrane
    3. activated G protein then changes activity of an element usually an enzyme of ion channel
31
Q

What are factors that influence concentration of a drug

A
  • rate of absorption
  • distribution to the tissues
  • elimination from the body
  • parameters: volume of distribution and clearance
  • bioavailability: how much is actually available after being broken down
32
Q

What affects the rate of absorption of a drug

A
  • physical and chemical properties of the drug
  • route of administration
33
Q

What are the routes of administration

A
  • enteral
  • parenteral
34
Q

Enteral administration

A

going through the GI tract
- oral, sublingual, buccal, rectal
- 1st pass effect: loss of potency due to being metabolized by the liver and GI system
- no do much with sublingual and buccal since there is some direct absorption

35
Q

Parenteral administration

A
  • vascular (intravenous= direct/dangerous and intra-arterial= targets a specific organ)
  • intramuscular
  • subcutaneous
  • inhalation
  • transdermal
36
Q

distribution of a drug

A
  • permeation: movement between biological compartments
  • volume of distribution = distribution is no homogeneous throughout the body it can be sequestered into different tissues/physical compartments
37
Q

Elimination

A
  • removes biological active compounds through metabolism and excretion
  • expressed as clearance: rate of drug elimination/plasmaconcentration
  • major clearn organs: kidney, lung, liver, and GI tract
38
Q

Elimination kinetics 1st order

A
  • rate of elimination is proportional to concentration
  • ex more concentration = clearance is faster
  • constant clearance and half life
39
Q

Elimination kinetics: zero order

A
  • same amount is eliminated each time
40
Q

half life

A
  • determined by drugs volume of distribution and clearnace
  • how long does it take for 1/2 of the concentration to be gone
41
Q

half life

A
  • determined by drugs volume of distribution and clearance
  • how long does it take for 1/2 of the concentration to be gone
42
Q

What is the aim of a dosing regimen

A

results in the achievement of therapeutic levels of the drug in the blood while staying within the therapeutic window

43
Q

Loading dose
maintenance dose

A
  1. loading dose = (Vd x desired plasma concentration)/bioavailability
  2. maintenance: the goal is to keep the concentrations within the therapeutic window
44
Q

how does half life affect steady state

A
  • patients who take medications for a period of time will respond better If the medication remains at a therapeutic dose
  • this dose can be achieved by continuous administration or small frequent doses
  • can be achieved to some degree of using half life
45
Q

How can you use half life to determine dosage

A
  • to achieve steady state, want to minimize fluctuations between peak plasma levels and lowest level before the next dose
  • can dose at the half life of the drug
  • after about 5 half lives the drug should ready steady state
46
Q

Drug elimination (how long does it take to be eliminated)

A
  • usually takes 5 half lives for a drug to be completely eliminated from the body
  • drug interactions should be considered when switching meds
47
Q

What are factors that can affect half-life

A
  • drug metabolism, elimination and storage
  • drug interactions
  • pharmacogenomics
  • these all change/increase the risk of adverse drug reactions
48
Q

describe the metabolism of drugs

A
  • primarily occurs in the liver – more medications means the liver must work harder which can lead to damage
  • some metabolism can occur in the heart and kidneys which can affect the organ especially If they have an issue with that organ
  • biotransformation: most common is conversion into water soluble compounds by microsomal enzymes in the liver and allows for excretion by the kidney
    (transforms the drug to help with elimination from the body)
49
Q

Describe elimination by the kidneys

A
  • glomerular filtration: the drug is taken out of the bloodstream
  • tubular secretion
  • reabsorption of some drugs: goes back into the bloodstream
    (consider how much will be excreted/reabsorbed when making a drug)
50
Q

What are problems that can arise with drugs and kidney dysfunction

A
  • reduced elimination of drugs affects the 1/2 life
  • increased risk of adverse effects
  • more likely to have drug interactions
  • ex: people with kidney disease and older adults (systems slows down)
51
Q

What are some other ways of elimination

A

kidneys are the main one others include
- lungs
- feces
- sweat
- salvia
- breast milk

52
Q

Other factors that can affect metabolism and excretion

A
  • disease
  • age
  • gender
  • diet
  • activity
53
Q

Medication storage in adipose tissue

A
  • can store lipid soluble drugs
  • most of the drug is eliminated
  • if more of the drug is stored in tissue:
    ~ slower release
    ~ decreased bioavailability (ability to be used for the rest of the body)
  • some can be stored for a long period of time
  • more adipose tissue = more medication can be stored
54
Q

What are other tissues that store medications

A
  • bone: lead which can affect cognitive development
  • muscle: antimalarial drugs
  • organs (liver, kidney, heart): can cause damage in the organ
    (some antibiotics are stored in the kidney)
55
Q

what does drug interactions mean

A
  • metabolism of one drug, food, or substance can promote, enhance, or reduce the metabolism of another drug
56
Q

Drug interactions that reduce metabolism

A

increase the risk of adverse effects
- ex: grapefruit and statins for cholesterol causes risk of statin myopathy due to the grapefruit having an enzyme that does not allow the breakdown of statin

57
Q

drug interactions that increase metabolism

A

decreases the effectiveness
- the drug will move through the system too quickly
- alcohol and acetaminophen

58
Q

Describe pharmacogenomics

A
  • genetic differrneces may affect pharmacokinetics
  • variations in cytochrome expression can increase or decrease drug metabolism
  • overtime differences can occur such as epigenetic changes

EX: codeine, placid, warfarin
- rapid conversion of codeine to morphine
- increased or decreased platelet aggregation
- decreased clotting

59
Q

Drug tolerance

A
  • related to enzyme induction: can produce more or the enzymes stay active longer
  • body adjusts to drug and breaks it down more quickly
  • more enzymes are produced
  • enzymes are degraded slower
60
Q

What does off label uses mean

A
  • used for a function other than what it was FDA-approved for
  • EX:
    1. Neurontin: seizure medication that is also used for nerve pain
    2. fluoxetine (prozac): depression but also used for bulimia and premature ejaculation
61
Q

Other risk factors for adverse drug reaction

A
  • age
  • dose
  • prolonged use of medication
  • multiple medications

Medical Conditions 1 (16 decks)

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