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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
What is LD 50?
Dose at which 50% of patients will experience a lethal effect
26
What is the therapeutic window described as?
Efficacy without unacceptable toxicity
27
TI=
TD 50/ED 50
28
What do high and low TI indicate in respect to a drug's therapeutic window?
High TI drugs: wide therapeutic window (desirable/safer) | Low TI drugs: small/narrow therapeutic window
29
4 ways drugs traverse the cellular membrane:
1. Passive diffusion (small/hydrophobic) 2. Facilitated diffusion- energy independent 3. Active transport- energy dependent 4. Endocytosis
30
Most drugs are: ______ acids or ______ bases in solution
Weak
31
What does pKa represent?
The pH at which 50% of the drug is ionized
32
What is pH trapping determined by?
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
How do drugs penetrate the CNS/BBB?(4)
1. Small and hydrophobic 2. Active transport 3. Facilitated transport 4. Intrathecal (bypass BBB)
34
ASA is an example of a ______ acidic drug.
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
What are the ADME of Pharmacokinetics?
Absorption Distribution Metabolism Excretion
36
What is the bioavailability of a drug?
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
What are some factors that affect absorption of a drug? (4)
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
What are some advantages to oral administration of a drug?
``` Safe Convenient Economical Painless Systemic infection less likely ```
39
What are some disadvantages to oral administration?
``` Absorption challenges (GI environment harsh, passage across GI epithelium, slow delivery, first-pass metabolism) ```
40
Where are weak acids and weak bases absorbed?
Weak acids: Stomach | Weak bases: Small intestine
41
What are disadvantages of rectal administration of drugs?
Erratic absorption Irritation Could be affected by first pass metabolism (~50% bypasses liver)
42
Which types of drug administration are not affected by first pass metabolism?
Parenteral Mucous Membrane Transdermal
43
Transdermal administration requires drugs with:
high lipophilicity
44
Where does distribution of drugs occur?
Plasma | Target tissue
45
What is the volume of distribution?
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
Distinguish between low and high Vd:
Low Vd= retained within vascular compartment (not distributed well to target) High Vd= highly distributed into non-vascular compartments
47
What is a prodrug?
An inactive form of a drug that will more easily absorb across the GI tract and once metabolized by the liver becomes active
48
What can an active drug be metabolized into?
Inactive drug Active metabolite Toxic metabolite
49
In order for a drug to be metabolized it must be ______ in plasma.
Unbound
50
Biotransformation reactions include two phases:
Phase I: oxidation/reduction | Phase II: conjugation/hydrolysis
51
Enzymes that catalyze oxidative reactions: (Phase I)
1. CYP 450***(95% of all reactions, 75% of all drugs) 2. Alcohol dehydrogenase 3. MAO (monoamine oxidase)
52
What can cause CYP450 induction?
- Increased transcription or translation (upreg. of enzymes) - Decreased degradation (prevent degradation of enzymes) - Induction by another drug or autoinduction
53
What can cause CYP 450 inhibition?
- Incidental or deliberate - Competitive inhibition - Irreversible inhibition
54
Factors that affect drug metabolism?
- Genetics - Race and ethnicity - Age and gender - Diet (grapefruit juice, inhibit CYP450 3A4) - Disease states
55
Two forms drugs can be excreted in:
Unchanged | Metabolites
56
Excretory organs: (3)
Lungs (elimination of polar compounds, anesthesia drugs) Renal (GFR, active tubular secretion) Feces (mainly unabsorbed orally administered drugs or drugs excreted via bile)
57
Non-ionized lipophilic drugs are favored for ______ absorption.
Oral
58
Drugs must be _____ (______) in order to reach its its site of action and be metabolized and eliminated.
free (non-protein bound)
59
What is true of drugs with a low Vd?
They may be highly protein bound and more likely to remain in the plasma compartment.
60
What is the fundamental hypothesis of Clinical Pharamacokinetics?
Pharmacologic or toxic response to a drug is related to the accessible concentration of the drug
61
What are the three most important parameters related to the fundamental hypothesis of clinical pharmacokinetics?
Clearance Volume of distribution Bioavailability
62
Clearance measures the body's ability to:
Eliminate drug. Includes metabolism and excretion. CL= (Metabolism=Excretion)/ [Drug in plasma]
63
What is first-order kinetics?
1:1 | Increase in plasma concentration = matched increased in clearance
64
What is zero-order kinetics?
Increase in plasma concentration with no increase in clearance -->Saturation kinetics
65
What is the half-life of a drug?
Time it takes for the plasma concentration to be reduced by 50%
66
Factors that affect half-life include:
Changes in Vd | Changed in clearance
67
How is potency different that efficacy?
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
How many half lives usually are needed for a drug to have been cleared from the body?
About 5.
69
Describe on-target adverse effects in intended tissue.
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
Describe off-target adverse effects in intended tissue .
Incorrect receptor is activated or inhibited in the intended tissue
71
Describe on-target adverse effects in unintended tissue.
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
Describe off-target adverse effects in unintended tissue
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
Type I or immediate-type hypersensivity (humoral):
Antigen- binding IgE on mast cells Histamine and serotonin mediated Hives, uticaria PCN Anaphylaxis (not usually first exposure)
74
Type II or Ab dependent cellular cytotoxicity (humoral):
IgG and IgM complement-binding cell bound antigen Neutrophils, macrophages, and NK cells Hemolysis Cefotetan Cytoxic
75
Type III or immune complex (humoral):
IgG and IgM complement binding soluble antigen Neutrophils, macrophages, NK cells, reactive oxygen species and chemokines Cutaneous vasculitis Mitomycin C Ex-lupus
76
Type IV or delayed-type hypersensitivity (cell-mediated):
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
Pharmcokinetic drug-drug interactions describe:
Drugs inhibit metabolism of another drug, causing increased drug levels/ concentration
78
Pharmacodynamic drug-drug interactions describe:
Drugs causing another drug to work on a receptor (not effecting concentration of drug)
79
What is true of drugs with a HIGH Vd?
Drugs with a HIGH Vd may have low protein affinity and therefore high tissue perfusion.

Pharmacology (48 decks)

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