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Pharmacology > Drug Variability and Harmful effects > Flashcards

Drug Variability and Harmful effects Flashcards

1
Q

Most often quantitative as a drug produces a “larger”
or “smaller” effect and/or lasts for a longer or shorter
period of time….while qualitatively exerting the
same effect.
-can result from a different drug
concentration at sites of drug action OR by different
responses to the same drug concentration.

A

Variation

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2
Q

Different response

to the same concentration

A

Variation:

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3
Q

Phase ___ metabolism decreases with age:

Reduction, Oxidation and hydrolysis

A

Phase 1 metabolism

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4
Q

Phase ____ metabolism does not decrease with age

A

Phase 2 metabolism

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5
Q 
Implications of \_\_\_\_\_\_\_\_
• Clinical Impact – “response” vs. “toxicity”
• Lack of efficacy 
• Side effects and drug toxicity
• Including unexpected side effects
A

Variation

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6
Q

– time it takes for serum concentrations to reduce by half in the elimination phase (it takes 4.5 to 5 half-lives to
reach steady-state)

A

Half-life

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7
Q

– ability to cross into fatty tissue, may increase Volume of Distribution
• Examples: (diazepam [Valium™], carbamazepine [Tegretol ™], trazodone [Desyrel ™])

A

Lipophilicity

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8
Q

– alternative sequences at a locus within a DNA strand (alleles) that persist in a population

A

Polymorphisms

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9
Q

– DNA sequence variations occur when a single nucleotide in the genome
sequence is altered (substitute one nucleotide for another, e.g. C for T)

A

Single nucleotide polymorphisms (SNPs)

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10
Q

(e.g. 7% of Caucasians are deficient of 2C9, 20% of Japanese and Chinese are deficient of
2C19, 8% of Caucasians are deficient of 2D6, and 3% of African-Americans are deficient of 2D6)

A

Genetic polymorphisms

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11
Q 
Results when the drug produces a larger or smaller effect, acts longer or 
shorter in duration, while from a qualitative standpoint still demonstrating the 
same effect (receptor level).
A

Quantitative variation

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12
Q

• In african americans, Hydralazine and Nitrates offer better or worse mortality
benefit in heart failure vs. Caucasian

A

Better mortailty benefit

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13
Q

• In african americans ACE inhibitors (enalapril [Vasotec ™ ])do or do not work
as well because of lower renin concentrations

A

Do not

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14
Q

• Chinese do or Don’t metabolize alcohol as well, results in
increase plasma concentration of acetaldehyde

A

Don’t

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15
Q

• Chinese display Increased or decreased sensitivity to the beta-blocker
propranolol (Inderal ™) even though metabolized
faster

A

Increased

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16
Q

Is excretion more or less efficient in newborns and over age of 65?

A

Less efficient

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17
Q

Age ____ total body water and _____ lipid distribution with age

A

Decreased body water; increased lipid distribution

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18
Q

Pregnancy considerations

______ maternal plasma albumin

A

• Reduced

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19
Q

Pregnancy considerations

_____ cardiac output

A

• Increased

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20
Q

Pregnancy considerations

______ renal blood flow and GFR

A

• Increased

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21
Q

Pregnancy considerations

_______ transfer of lipophilic drugs

A

• Increased

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22
Q

___ drugs are slow to get to fetus

A

Hydrophilic drugs

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23
Q

____ drugs are quickly gotten to fetus despite slow clearance

A

Lipophilic

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24
Q 
\_\_\_\_\_ Reactions
•Typically harmful
•Do not require large drug doses
•Genetic connection
•Immunological factors
A

Idiosyncratic

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25
Q

– agents like propranolol (Inderal™) reduce effectiveness of Beta agonists used for asthma treatment (e.g. albuterol [Ventolin™], salmeterol [Serevent™])

A

Beta Blockers

26
Q

– agents that decrease K+ (e.g. hydrochlorothiazide) predispose to digoxin toxicity

A

Diuretics

27
Q

– inhibit the breakdown of “pressor” agents (e.g. tyramine)

A

MAOIs

28
Q

– increased bleeding

A

ASA/Warfarin

29
Q

– increase the risk of hypertension by inhibiting prostaglandin

A

NSAIDs

30
Q

– additive sedative effects

A

Antihistamines, Opiates, ETOH

31
Q

– e.g. valproic acid (Depakote ™) inhibits platelet formation

A

Anticonvulsants

32
Q

– impacted by dopamine agonists (e.g. levodopa/carbidopa [Sinemet™])

A

Dopamine Blockers

33
Q

– Cogentin may decrease the effectiveness of AChE Inhibitors (e.g. donepezil [Aricept ™])

A

Anticholinergics

34
Q

GI absorption ____ by meds that inhibit gastric emptying

e.g. atropine, anticholinergics, opiates

A

slowed

35
Q

GI absorption ______ by meds that increase gastric

emptying (e.g. metoclopramide [Reglan™])

A

increased

36
Q
  • Competition for protein binding sites
  • Alterations in “free” drug concentrations
  • Impact secondarily on elimination
A

Distribution

37
Q
  • Tubular secretion

* Altered urine flow and urine pH

A

Excretion

38
Q
  • Use of multiple medications by a patient

* ≥ 5 medications

A

Polypharmacy

39
Q 
• Result from main pharmacological action and can 
reasonably be expected
• Often addressed with dose reduction
• Usually reversible
• Some events more discrete
A

Adverse effects

40
Q 
Adverse effects
• Can be \_\_\_\_\_ when dose is excessive
• Aspirin and tinnitus 
• Clozapine (Clozaril ™ ) and seizures
• Bupropion (Wellbutrin ™) and seizures
A

predictable

41
Q

Adverse effects
______ idiosyncratic reactions
• Penicillin and anaphylaxis
• Clozapine and aplastic anemia

A

Unpredictable

42
Q

• Animal testing
• Doses significantly above therapeutic range
• Identify organ toxicity
• “acceptable” toxicity differences dependent upon
targeted disease state

A

Drug toxicity testing

43
Q

•__________ Interactions
Lipid peroxidation – peroxidation of unsaturated lipids, hydroperoxides
(ROOH) are formed and break down lipid membranes
Reactive oxygen species – formation of hydrogen peroxide and are
excitotoxic, cytotoxic, and neurodegenerative
Depletion of glutathione – disrupts normal cellular defense
Modification of sulfhydryl groups – result in cell death from acute calcium
overload and activation of degrading enzymes

A

Non-Covalent

44
Q

What are the 4 non covalent interactions that induce cell damage via toxins?

A

Lipid peroxidation
ROS
Depletion of glutathione
Modification of sulfhydryl groups

45
Q

What are the 2 covalent interactions that cause cell damage?

A

Hepatotoxicity

Nephrotoxicity

46
Q

_______ Interactions – targets DNA, proteins,
peptides, lipids, and carbohydrates
Hepatotoxicity
Nephrotoxicity

A

Covalent

47
Q

– results from covalent modification of

DNA

A

Mutagenesis

48
Q

– sequence codes for proteins that

regulate cell growth

A

Alteration of DNA

49
Q

– chemical substances that cause

cancer

A

Carcinogens

50
Q

– result is gross structural
malformations during fetal development and is
different than other forms of fetal damage (e.g.
growth retardation)

A

Teratogenesis

51
Q

What are the 3 mechanisms of teratogenicity?

A

Blastocyte formation – cell division occurring
Organogenesis – structural formation
Histogenesis and maturation of function – nutrient supply

52
Q

( known teratogens)

– sedative/hypnotic – shortened long bone development

A

Thalidomide

53
Q

( known teratogens)

– tretinoin and isotretinoin: facial issues

A

Vitamin A Derivatives

54
Q

( known teratogens)

– cyclophosphamide causing neural tube defects

A

• Alkylating agents and antimetabolites

55
Q
  • May be immediate or delayed following exposure
  • Dose doesn’t matter
  • Not related to primary drug MOA
  • Incidence < 25%
  • Skin reactions most common
A

Allergic reactions

56
Q

Are most meds immunogenic on their own and low or high molecular weight?

A

No immunogenic on own; low molecular weight

57
Q

_______ – release of histamine and leukotrienes (sudden onset)
• Penicillins
• Adrenocorticotropin
• Heparin

A

Anaphylactic shock

58
Q

What drug causes hemolytic anemia as a hematological rxn?

A

Sulfonamides

59
Q

Which 3 drugs cause agranulocytosis as a hematological rxn?

A

Clozapine
Sulfonamides
Thiazide diuretics

60
Q

____ drugs cause thrombocytopenia as a hematological rxn?

A

Valproic acid

61
Q 
• Swelling of mouth, face, neck, 
or tongue
• Red skin, rash, hives
• Difficulty breathing
• Wheezing
• Rapid Pulse
- Wheel and flare
A

Anaphylaxis

Pharmacology (12 decks)

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