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UM - Pharmacology > Pharmacology Basics > Flashcards

Pharmacology Basics Flashcards

Basic Principles of Pharmocology, Pharmacokinetics, and Drug Receptors

1
Q

List the 3 different ways to name medications

A

Chemical
Generic
Trade

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2
Q

Explain the differences between generic and brand name medications

A

Generic: Less expensive, same bioavailability, different inactive ingredients

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3
Q

List the steps in the drug approval process

A
  1. In Vitro
  2. In animals
  3. Humans
    a. Phase I: Healthy adults
    b. Phase II: Small target pop
    c. Phase III: Larger target pop
  4. Marketing
    a. Phase IV: Postmarketing surveillance
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4
Q

Describe Scheduled medications and implications of patient use

A

There are 5 schedules of medications that the FDA classifies and regulates with V being the least potential for abuse and I being the most potential of abuse

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5
Q

Potency vs maximum efficacy

A

Potency is how much medication needs to be given to produce a specific effect whereas maximum efficacy is how large of an effect can be created (the ceiling effect)

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6
Q

Connect therapeutic index to drug safety and adverse effects

A

Therapeutic index is the toxic dose divided by the effective dose –> the higher it is, the greater its safety

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7
Q

Which name is the official name of a drug?

A

Generic name

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8
Q

Which schedule of medication cannot be used for treatment or research?

A

Schedule 1

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9
Q

median effective dose vs median toxic dose

A

The median effective dose is the amount where 50% of the population starts seeing some benefit from the drug whereas the median toxic dose is the amount where 50% of the population exhibits adverse effects

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10
Q

What do dose-response curves tell you?

A

They show the threshold dose and the ceiling effect for a given medication in a log scale

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11
Q

Sites of drug storage in the body

A
  • adipose: primary site because many medications are lipid soluble
  • bone: toxic agents
  • muscle
  • organs: liver and kidney
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12
Q

primary site of drug elimination in the body

A

Liver

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13
Q

What are the routes of administration?

A
  1. Enteral
    a. oral
    b. Sublingual and bucc
    c. Rectal
  2. Parental
    a. Inhalation
    b. Injection
    c. Topical
    d. Transdermal
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14
Q

Advantages of Oral Administration

A
  • easiest
  • self- administer
  • controlled manner of entry
  • small intestine absorption
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15
Q

Disadvantages of Oral Administration

A
  • need to have high degree of lipid solubility
  • may irritate stomach
  • first pass effect
  • eventual amount and rate of drug reaching target is less predictable
  • acidic environment of the sromach
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16
Q

What is the first pass effect

A
  • after absorption via small intestine, drug sent to liver and may be metabolized there before reaching target tissue, causing less of a dose at the target tissue
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17
Q

Advantages of sublingual and bucal administration

A
  • avoid first pass effect (transmucosal absorption in mouth)
  • good if pt had swallowing difficulty
  • faster effect than swallowing
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18
Q

Disadvantages of sublingual and bucal administration

A
  • drug must be able to easily pass into venous system

- amount taken is limited

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19
Q

Advantages of Rectal Administration

A
  • if vomiting prevents drug from being given orally
  • do not have to swallow it (pt unconscious)
  • local effect on recital tissue (hemorrhoids, constipation, etc)
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20
Q

Disadvantages of rectal administration

A
  • drug absorbed poorly or incompletely

- irritation of rectal mucosa

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21
Q

Advantages of Inhalation for administration

A
  • large alveolar SA promotes diffusion into pulmonary circulation (ex. Anesthesia medications)
  • direct delivery to bronchial and alveolar tissue for pulmonary diseases
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22
Q

Disadvantages of inhalation

A
  • irritate alveoli

- drug particles can get trapped by cilia and mucous making it difficult to predict the exact amount of drug delivered

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23
Q

List the types of injection

A 
Intravenous 
Intra-arterial
Subcutaneous 
Intramuscular 
Intrathecal
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24
Q

What is the risk for all types of injection

A

Infection

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25
Q

Advantages of IV Injection

A
  • accurate and known quantity of a drug entering bloodstream
  • reaches target tissue rapidly (good for emergent situations)
  • 100% bioavailable
  • steady infusion overtime to prevent large fluctuations in plasma concentrations
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26
Q

Disadvantages of IV Inju

A

Difficult to counter side effects if full dose injected

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27
Q

Advantages of IA Injection

A

Large dose of medication can reach target tissue (chemo & radiopaque dyes)

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28
Q

Disadvantages of IA Injection

A

Difficult and dangerous procedure

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29
Q

Advantages of Subcutaneous Injections (SQ or SC)

A
  • slower, more prolonged release into systemic circulation (hormonal contraceptives)
  • easy for pt to learn to self-administer (insulin)
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30
Q

Disadvantages of SQ/SC Injection

A
  • can only deliver small amount of medication
  • could irritate subcutaneous tissue
  • Bruising
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31
Q

Advantages of intramuscular injections

A
  • to treat a problem directly in injected muscle (Botox)
  • Steady prolonged release of drug into systemic circulation (vaccines, antipsychotics)
  • plasma concentrations achieved rapidly (a few minutes)
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32
Q

Disadvantages of intramuscular injections

A

Cause a significant amount of pain and muscle soreness

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33
Q

Advantages of intrathecal injections

A
  • better access to spinal cord
  • bypass the blood brain barrier
  • directly administered to area
34
Q

Disadvantages of intrathecal injections

A

Very technical

35
Q

Advantages of topical administration

A
  • primarily to treat skin conditions (absorbs poorly through the upper dermis into the systemic circulation - wound healing products and steroids for inflammation)
  • Application to mucous membrane can lead to systemic absorption (eye drops and ear drops)
36
Q

Disadvantages of topical administration

A
  • applying the correct amount can be difficult

- only effective in treating outer layers of the skin

37
Q

Advantages of transdermal administration

A
  • introduces drug into body without breaking the skin

- Can provide steady prolonged delivery via medicated patches

38
Q

Disadvantages of transdermal administration

A
  • Drug must be able to pass through dermal layers intact
39
Q

What are the two type of transdermal medication’s physical therapist can use

A

Iontophoresis and phonophoresis via estim (ionto) and ultrasound (phono) to subcutaneous tissue

40
Q

Define bioavailability

A

The extent to which the drug reaches the systemic circulation

41
Q

IV vs Oral administration and plasma concentrations

A

IV administration has a higher and faster plasma concentration whereas oral is slower and has a lower peak

42
Q

Which routes have a highly variable bioavailability

A

Oral and Inhaltion: 5 to <100%

Rectal: 30 to <100%

43
Q

Which four routes have a 75 to less than or equal to 100% bioavailability

A

Sublingual/buccal
IM
SQ
Transdermal

44
Q

List the movement across cell membrane barriers & state:

  1. Cost E?
  2. Low—> high or high —> low
A
  1. Passive: No E, H->L
  2. Active: E, L->H
  3. Facilitated diffusion: No E, L->H
  4. Endocytosis and exocytosis: allows for large non-lipid soluble molecules to enter and exit
45
Q

List the factors affecting distribution

A
  • Tissue permeability
  • blood flow (high perfusion —> reaches tissue faster)
  • Binding to plasma proteins (only free drugs can exert pharmacological effect)
  • Binding to subcellar components (if bound in a cell, cannot be distributed to other compartments)
46
Q

What is the volume of distribution and why do we care

A

Amount of drug administered divided by concentration of drug and plasma. It tells us how well the drug is distributed through the body and can impact elimination.

47
Q

Interpret:
Vd = 42 L
Vd < 42 L
Vd > 42 L

A
  • drug is distributed uniformly throughout body fluids
  • Drug is retained in the bloodstream
  • Drug is being concentrated in the tissue
48
Q

List the adverse consequences of drug storage

A
  • high concentration of drug/drug metabolites/toxic compounds can cause damage to the tissues they are stored in (lead poisoning )
  • High concentrations of therapeutic drugs (can become toxic and cause damage)
  • Can soak up the drug preventing it from reaching target tissue
  • can lead to redistribution of drugs after desired effects
49
Q

What is oxidation

A
  • Oxygen added or hydrogen removed from the OG compound.

- predominant method of drug transformation in the body

50
Q

List some of the methods of bio transformation in the body

A
  • oxidation (predominant)
  • reduction
  • hydrolysis
  • conjugation
51
Q

Where does biotransformation (metabolism) occur for most drugs

A

In the liver

52
Q

How does tolerance develop

A

Prolonged use of drugs alters enzymes:

  1. More metabolizing enzymes are being produced
  2. Fewer metabolizing enzymes are being broken down
53
Q

Where is the primary site for drug excretion

A

The kidneys

54
Q

What happens when:

  1. Administration > elimination
  2. Elimination > administration
A
  1. Drug accumulation/toxicity

2. Drug concentration is too low

55
Q

What is clearance

A

The measure of a single organ or tissue’s ability to eliminate a drug

56
Q

What contributes to an organ being able to eliminate a drug

A
  • blood flow to the organ (perfusion)

- how much of the drug is extracted (organ function)

57
Q

What is half-life

A

The amount of time required for 50% of the drug remaining in the body to be eliminated
- impacted by Volume distribution and clearance changes

58
Q

List some things that can cause variations in drug response and metabolism

A
  • genetics
  • disease
  • drug interactions
  • age
  • diet
  • sex
59
Q

What is affinity

A

The amount of attraction between a drug and receptor.

  • high affinity = easily able to bind to open receptors
  • low affinity = need more of the drug in order to fill up receptors
60
Q

Agonist vs Antagonist

A

An agonist binds to a receptor to imitate a change in cell function, has affinity, and has efficacy whereas an antagonist will bind and not create a change in cell function (lacks efficacy), even though it has affinity for a receptor.

61
Q

Define receptor desensitization

A

Brief and transient decrease in receptor responsiveness

62
Q

What are drug receptors

A

A component on or within a cell that a substance can bind to

- most commonly located on the surface

63
Q

Mechanism for surface receptors linked directly to ion channels

A

The receptors act as an ion pore changing the membrane permeability (to open or close channel)

64
Q

Mechanism of action for surface receptors linked directly to enzymes

A

The receptor spans the whole membrane, w/molecule attaching on the surface, that then triggers an enzymatic reaction (activation or inactivation) on the other side of the cell membrane

65
Q

Mechanism of action for surface receptors linked to regulatory (G) proteins and the role of the second messenger

A

Membrane receptor affects cell function by linking to an intermediate regulatory protein located on the inner surface of the cell (creates a cascade effect)

66
Q

List the 2 types of G proteins

A

Stimulatory (increase response of cell)

Inhibitory (decrease cell activity)

67
Q

Process for drug that influences a second messenger

A
  1. Drug as first messenger -> binds outside and causes biochemical change inside the cell
  2. Substance produced inside the cell from the biochemical change is what then mediates the change in cell function
68
Q

What are intracellular receptors

A

Located within the cell so the drug has to diffuse through the bilateral
- steroids

69
Q

What is drug selectivity

A

When a drug only influences one type of cell or tissue and produces a specific response (relative)

70
Q

Differentiate concepts of affinity and selectivity

A

Affinity is how well the drug is able to bind to the receptors and selectivity delineates which receptors the drug will bind to

71
Q

What is efficacy

A

How much of a change a drug causes

72
Q

Competitive vs Noncompetitive Antagonists

A

In competitive antagonists, whichever of the two drugs has the higher concentration will win & bind whereas noncompetitive antagonists form strong, permanent bonds to receptor and will lock it down until the receptor expires.

73
Q

What is a partial agonist

A

Drug that does not produce a maximal response compared to a strong agonist, even if all available receptors are occupied

74
Q

What is the hierarchy of efficacy

A
  • strong agonist
  • partial agonist
  • strong noncompetitive antagonist
75
Q

What is a mixed agonist-antagonist

A
  • stimulate certain receptor subtypes AND block the effects of endogenous substances or other receptor subtypes (do both simultaneously)
76
Q

What is an inverse agonist and what is its goal

A
  • Drugs that bind to the same receptor as the agonist but have the opposite effect of the agonist on cellular function
  • decreased activity in situations where the receptor is too active or overstimulated
77
Q

Define receptor downregulation

A

Decrease in number of receptors available (slower and prolonged process; few days)

78
Q

What is receptor supersensitivity

A

Prolonged decrease in stimulation of receptors results in an increase in receptor sensitive to substances
Ex - more sensitive to caffeine since they haven’t had it in a while

79
Q

What is receptor upregulation

A

Increase in number of receptors, resulting in an increase in function
(Instead of having 100% of receptors, 150% receptors)

80
Q

True or false: all drugs act on receptors

A

False - some drugs change DNA or create a chemical reaction or other

UM - Pharmacology (4 decks)

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