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Pharmacology > General Principles of Pharmacology > Flashcards

General Principles of Pharmacology Flashcards

1
Q

What is the mechanism of van der Waals bonding and degree of bond strength?

A

Shifting of electron density in areas of a molecule, or in a molecule as a whole, results in the generation of transient positive or negative charges. These areas interact with transient areas of opposite charge on other molecules
Bond Strength: + (weakest)

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2
Q

What is the mechanism of Hydrogen bonding and degree of bond strength?

A

Hydrogen atoms bound to nitrogen or oxygen become more positively polarized, allowing them to bond to more negative polarized atoms such as oxygen, nitrogen, or sulfur
Bond Strength: ++

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3
Q

What is the mechanism of Ionic bonding and degree of bond strength?

A

Atoms with an excess of electrons (imparting an overall negative charge on the atom) are attracted to atoms with a deficiency of electrons (imparting an overall positive charge on the atom)
Bond strength: +++

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4
Q

What is the mechanism of Covalent bonding and degree of bond strength?

A

Two bonding atoms share electrons. Often irreversible

Bond strength: ++++ (strongest)

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5
Q

What is pharmacodynamics (PD)?

A

What the drug does to the body

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6
Q

What is pharmacokinetics (PK)?

A

What the body does to the drug

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7
Q

What are some characteristics of hydrophillic drugs? (5)

A
  1. Water-loving/water-soluble
  2. Polar, usually ionized
  3. Renally excreted
  4. Requires transport mechanism to cross cell membrane and BBB
  5. Form H+ bonds
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8
Q

What are some characteristics of hyrophobic drugs? (4)

A
  1. Lipophillic
  2. Fat-loving/water insoluble
  3. Passively diffuses across cell membranes and BBB
  4. Non-polar, usually not ionized
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9
Q

What is an enantiomer?

A

Mirror images of drug

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10
Q

What are four transmembrane drug-receptor interactions?

A
  1. Ion channels
  2. G protein channels
  3. Enzyme w/in cytosolic domain
  4. Passive
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11
Q

What type of drugs passively move through the cellular membrane?

A

Hydrophobic drugs move through the hydrophillic outer membrane towards the hydrophobic inner membrane

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12
Q

How is DR different from DR*?

A

DR is the binding of the drug and the receptor with no effect, DR* is the binding and the elicitation of an effect (usually the conformation change in a receptor)

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13
Q

What is true of full Agonists?

A
  • The elicit the maximal response

- Stabilizes DR* (causes full effect)

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14
Q

What is true of Partial or Mixed Agonist-Antagonists?

A
  • Activates receptor but not with maximal efficacy

- Stabilizes DR (no effect) and DR*(effect) =mixed

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15
Q

What is true of Inverse Agonists?

A
  • Inactivates free receptors
  • Stabilizes DR in the case of R*

(R* being a freely active receptor, once the drug binds it creates DR= inactive)

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16
Q

What are Antagonists?

A

Inhibition of agonist activity

Stabilize DR, prevent DR*

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17
Q

What is true of Competitive Antagonists?

A
  • Reversible binding blocks agonist at active site

- Stabilizes DR, prevents DR*

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18
Q

What is true of Noncompetitive Antagonists?

A
  • Irreversible binding blocks agonist at active or allosteric site (binds to alternate site, not active site and prevents agonist from binding or eliciting a response)
  • Stabilizes DR, prevents DR*
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19
Q

_______ antagonists bind reversibly to the active site and __________ antagonists bind irreversibly to the active or allosteric site.

A

Competitive and Noncompetitive

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20
Q

What is a competitive antagonist’s effect on potency and efficacy?

A

Potency: Effected
Efficacy: Not effected

(Binds reversibly to the active site of the receptor, competes with agonists binding to the site)

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21
Q

What is a noncompetitive active site antagonist’s effect on potency and efficacy?

A

Potency: Not effected
Efficacy: Effected

(Bind irreversibly to the active site of receptor, prevents agonist binding to this site)

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22
Q

What is a noncompetitive allosteric antagonist’s effect on potency and efficacy?

A

Potency: Not effected
Efficacy: Effected

(Binds reversibly or irreversibly to site other than active site of receptor, prevents conformational change required for receptor activation by agonist)

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23
Q

What is ED 50?

A

Dose at which 50% of patients will experience a therapeutic effect

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24
Q

What is TD 50?

A

Dose at which 50% of patients will experience a toxic effect

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25
Q

What is LD 50?

A

Dose at which 50% of patients will experience a lethal effect

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26
Q

What is the therapeutic window described as?

A

Efficacy without unacceptable toxicity

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27
Q

TI=

A

TD 50/ED 50

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28
Q

What do high and low TI indicate in respect to a drug’s therapeutic window?

A

High TI drugs: wide therapeutic window (desirable/safer)

Low TI drugs: small/narrow therapeutic window

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29
Q

4 ways drugs traverse the cellular membrane:

A
  1. Passive diffusion (small/hydrophobic)
  2. Facilitated diffusion- energy independent
  3. Active transport- energy dependent
  4. Endocytosis
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30
Q

Most drugs are: ______ acids or ______ bases in solution

A

Weak

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31
Q

What does pKa represent?

A

The pH at which 50% of the drug is ionized

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32
Q

What is pH trapping determined by?

A

pKa and pH gradient across the membrane. Nonionized molecules that move across mucosal barriers and become ionized will not likely move back to where they were ( ex ASA->stomach->plasma)

33
Q

How do drugs penetrate the CNS/BBB?(4)

A
  1. Small and hydrophobic
  2. Active transport
  3. Facilitated transport
  4. Intrathecal (bypass BBB)
34
Q

ASA is an example of a ______ acidic drug.

A

Weakly

Protonated in the stomach (nonionized, not charged= can pass through the gastric mucosa membrane)
Deprotonated in the plasma (ionized, charged= will most likely not go back-pH trapping )

35
Q

What are the ADME of Pharmacokinetics?

A

Absorption
Distribution
Metabolism
Excretion

36
Q

What is the bioavailability of a drug?

A

The extent to which a drug reaches systemic circulation/fraction absorbed

Ex- 100% bioavailability means 100% of the drug is absorbed into the systemic circulation

37
Q

What are some factors that affect absorption of a drug? (4)

A
  1. Concentration (higher=greater absorption)
  2. Circulation at site of absorption
  3. Drug solubility (extent and rate of dissolution)
  4. Surface area (pulm, intestine, skin)
38
Q

What are some advantages to oral administration of a drug?

A 
Safe
Convenient
Economical 
Painless
Systemic infection less likely
39
Q

What are some disadvantages to oral administration?

A 
Absorption challenges 
(GI environment harsh, passage across GI epithelium, slow delivery, first-pass metabolism)
40
Q

Where are weak acids and weak bases absorbed?

A

Weak acids: Stomach

Weak bases: Small intestine

41
Q

What are disadvantages of rectal administration of drugs?

A

Erratic absorption
Irritation
Could be affected by first pass metabolism (~50% bypasses liver)

42
Q

Which types of drug administration are not affected by first pass metabolism?

A

Parenteral
Mucous Membrane
Transdermal

43
Q

Transdermal administration requires drugs with:

A

high lipophilicity

44
Q

Where does distribution of drugs occur?

A

Plasma

Target tissue

45
Q

What is the volume of distribution?

A

Volume of fluid required to contain the total amount of drug absorbed in the body at uniform concentrations equal to that in the plasma steady state

46
Q

Distinguish between low and high Vd:

A

Low Vd= retained within vascular compartment (not distributed well to target)
High Vd= highly distributed into non-vascular compartments

47
Q

What is a prodrug?

A

An inactive form of a drug that will more easily absorb across the GI tract and once metabolized by the liver becomes active

48
Q

What can an active drug be metabolized into?

A

Inactive drug
Active metabolite
Toxic metabolite

49
Q

In order for a drug to be metabolized it must be ______ in plasma.

A

Unbound

50
Q

Biotransformation reactions include two phases:

A

Phase I: oxidation/reduction

Phase II: conjugation/hydrolysis

51
Q

Enzymes that catalyze oxidative reactions: (Phase I)

A
  1. CYP 450***(95% of all reactions, 75% of all drugs)
  2. Alcohol dehydrogenase
  3. MAO (monoamine oxidase)
52
Q

What can cause CYP450 induction?

A
  • Increased transcription or translation (upreg. of enzymes)
  • Decreased degradation (prevent degradation of enzymes)
  • Induction by another drug or autoinduction
53
Q

What can cause CYP 450 inhibition?

A
  • Incidental or deliberate
  • Competitive inhibition
  • Irreversible inhibition
54
Q

Factors that affect drug metabolism?

A
  • Genetics
  • Race and ethnicity
  • Age and gender
  • Diet (grapefruit juice, inhibit CYP450 3A4)
  • Disease states
55
Q

Two forms drugs can be excreted in:

A

Unchanged

Metabolites

56
Q

Excretory organs: (3)

A

Lungs (elimination of polar compounds, anesthesia drugs)
Renal (GFR, active tubular secretion)
Feces (mainly unabsorbed orally administered drugs or drugs excreted via bile)

57
Q

Non-ionized lipophilic drugs are favored for ______ absorption.

A

Oral

58
Q

Drugs must be _____ (______) in order to reach its its site of action and be metabolized and eliminated.

A

free (non-protein bound)

59
Q

What is true of drugs with a low Vd?

A

They may be highly protein bound and more likely to remain in the plasma compartment.

60
Q

What is the fundamental hypothesis of Clinical Pharamacokinetics?

A

Pharmacologic or toxic response to a drug is related to the accessible concentration of the drug

61
Q

What are the three most important parameters related to the fundamental hypothesis of clinical pharmacokinetics?

A

Clearance
Volume of distribution
Bioavailability

62
Q

Clearance measures the body’s ability to:

A

Eliminate drug. Includes metabolism and excretion.

CL= (Metabolism=Excretion)/ [Drug in plasma]

63
Q

What is first-order kinetics?

A

1:1

Increase in plasma concentration = matched increased in clearance

64
Q

What is zero-order kinetics?

A

Increase in plasma concentration with no increase in clearance
–>Saturation kinetics

65
Q

What is the half-life of a drug?

A

Time it takes for the plasma concentration to be reduced by 50%

66
Q

Factors that affect half-life include:

A

Changes in Vd

Changed in clearance

67
Q

How is potency different that efficacy?

A

Potency describes a lower dose of one drug being needed vs. another to produce a desired response; efficacy of the drugs do not change if they are dosed correctly.

Ex- 10mg of Aorvastatin and 20mg of Simvastatin have the same efficacy but Atorvastatin is a more potent drug.

68
Q

How many half lives usually are needed for a drug to have been cleared from the body?

A

About 5.

69
Q

Describe on-target adverse effects in intended tissue.

A

Dose too high
Chronic activation or inhibition of effects

Ex- SSRI’s act on the CNS to increase serotonin at synapse which increases mood by may also causes sexual dysfunction

70
Q

Describe off-target adverse effects in intended tissue .

A

Incorrect receptor is activated or inhibited in the intended tissue

71
Q

Describe on-target adverse effects in unintended tissue.

A

Correct receptor, but incorrect tissue
Dose too high
Chronic activation or inhibition effects

Ex- Benadryl attaches to histamine receptors to treat allergy and crosses BBB to attach to histamine receptors there (wrong tissue)= sedative effect

72
Q

Describe off-target adverse effects in unintended tissue

A

Incorrect receptor is activated or inhibited.

Ex-Beta blocker, beta-1 antagonist to reduce HR and contractility, may also inhibit (antagonize) beta 2 receptors in the respiratory tract causing bronchoconstriction.

73
Q

Type I or immediate-type hypersensivity (humoral):

A

Antigen- binding IgE on mast cells
Histamine and serotonin mediated
Hives, uticaria
PCN

Anaphylaxis (not usually first exposure)

74
Q

Type II or Ab dependent cellular cytotoxicity (humoral):

A

IgG and IgM complement-binding cell bound antigen
Neutrophils, macrophages, and NK cells
Hemolysis
Cefotetan

Cytoxic

75
Q

Type III or immune complex (humoral):

A

IgG and IgM complement binding soluble antigen
Neutrophils, macrophages, NK cells, reactive oxygen species and chemokines
Cutaneous vasculitis
Mitomycin C

Ex-lupus

76
Q

Type IV or delayed-type hypersensitivity (cell-mediated):

A

Antigen in association with MHC protein on the surface of antigen presenting cells
Cytotoxic T lymphocytes, macrophages, and cytokines
Macular rashes and organ failure
Sulfamethoxazole

Ex- PPD, takes ~48hrs

77
Q

Pharmcokinetic drug-drug interactions describe:

A

Drugs inhibit metabolism of another drug, causing increased drug levels/ concentration

78
Q

Pharmacodynamic drug-drug interactions describe:

A

Drugs causing another drug to work on a receptor (not effecting concentration of drug)

79
Q

What is true of drugs with a HIGH Vd?

A

Drugs with a HIGH Vd may have low protein affinity and therefore high tissue perfusion.

Pharmacology (48 decks)

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