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Intro to Pharmaceuticals > Test 5 Review > Flashcards

Test 5 Review Flashcards

0
Q

Intrapatient therapeutic variability

A

Different response in the same patient at different times

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1
Q

Interpatient therapeutic variability

A

Different response between different people

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2
Q

Pharmacokinetic variability

A

Varying of delivery, removal, efficacy, and toxicity of drug (body does to drug)
-dangerous to drugs with a narrow therapeutic index (more likely to be fatal)

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3
Q

What plays a vital role in pharmacokinetic variability?

A

Genetic effect

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4
Q

Why is body weight and composition a source of pharmacokinetic variability?

A

Obese person has a higher volume of distribution for lipophilic drugs (dissolve in fat and spread farther) so they need a smaller dose

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5
Q

How to find dose required?

A

(Avg dose/70kg) x weight in kg

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6
Q

Why is age a source of pharmacokinetic variability?

A

Very young or old people have a worse immune system and enzymes are too weak to absorb the medication correctly

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7
Q

Why are infants and children at higher risk of greater bioavailability?

A

They have increased permeability of membranes such as the BBB, they have increased water content, decreased blood flow, metabolism, and renal clearance

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8
Q

Why do the elderly have risk of greater bioavailability?

A

Decreased liver and kidney function and a higher plasma concentration (liver can’t metabolize well and kidney can’t eliminate well)

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9
Q

Why is sex a source of pharmacokinetic variability?

A

Women have higher fat content, therefore more volume of distribution for lipophilic drugs

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10
Q

Why does pregnancy and lactation affect pharmacokinetic variability?

A

Teratogenicity (drugs crossing placenta and affecting fetus) and it is unknown how some drugs will affect a pregnancy

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11
Q

Fetal Alcohol Syndrome-FAS

A

Woman either drinks during pregnancy or takes a drug that affects the child, resulting in a malformed face “teratogenic effect”

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12
Q

Why does health and disease affect pharmacokinetic variability?

A

Kidney and liver disease will affect variability, dehydration, malnutrition, etc

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13
Q

Pharmacodynamic variability

A

What the drug does to the body

-variable drug effects due to difference in structure and function of target organs or patient disease

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14
Q

Why is sex a source of pharmacodynamic variability?

A

Females are more responsive to pain medications

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15
Q

Why is idiosyncrasy a source of pharmacodynamic variability?

A

Idiosyncrasy is an unpredictable and unusual response that is undocumented, usually a genetic predisposition, so it can affect what the drug does to the body

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16
Q

Why are circadian rhythms a source of pharmacodynamic variability?

A

Because chemicals like histamine and sex hormones are highest at night, and cortisol is highest in the morning so they can affect what the drug does to the body

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17
Q

Why does drug tolerance a source of pharmacodynamic variability?

A

If someone is tolerant to a drug they need more and more, so an increased dose can affect what the drug does to the body

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18
Q

Tachyphylaxis

A

Rapidly increasing response to a drug after administering a few doses

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19
Q

Why is receptor regulation by drugs a source of pharmacodynamic variability?

A

It can result in either tolerance or a more pronounced effect, so it can influence what the drug does to the body
-receptor up and receptor down regulation

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20
Q

Receptor up regulation

A

Number of receptors increase with continuous administration of drug, resulting in too many places for the drug to attach, causing a rebound (more pronounced) drug effect

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21
Q

Receptor down regulation

A

Number of receptors decrease with continuous administration, results in not enough places for the drug to attach leading to tolerance

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22
Q

Why is drug resistance a source of pharmacodynamic variability?

A

Because 3 types of resistance lead to absorption and elimination problems, affecting what the drug does to the body

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23
Q

Intrinsic resistance

A

Resistance to causing activity when attached to a receptor, leads to decreased absorption or increased elimination, and decreased response to the drug

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24
Q

Acquired genetic resistance

A

Resistance that is acquired through a person’s genetics

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25
Q

Cross resistance

A

Resistance to one drug causes resistance to similar drugs that use the same enzyme system (multiple drug resistance)
-must change the resistant drug to find another drug

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26
Q

Drug allergy

A

Adverse side effect that can cause rashes, itchy eyes, swollen face, or anaphylactic shock

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27
Q

Mechanism of drug allergy

A

B lymphocytes activate antibodies that attach to the mast cell, and upon second exposure the mast cell releases histamine that causes the allergic reaction

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28
Q

Drug compliance

A

Willingness and ability to stick to correct doses

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29
Q

Causes of non-compliance

A

Too many medications, cost, side effects, lack of understanding
MOST COMMON CAUSE IS SIDE EFFECTS

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30
Q

FDA

A

Food and drug administration

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31
Q

What does the FDA do?

A

Regulates development of new drug products and marketing

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32
Q

What are the FDA’s functions?

A
  1. Promote and protect public health
  2. Monitor product after it is in use
  3. Regulates products (food products, tissues of transplantation, cosmetics, electronic devices that emit radiation)
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33
Q

Federal Food, Drug, and Cosmetic Act of 1938

A

Single most important act related to the FDA, gave authority to the FDA for them to regulate food, drugs, and cosmetics

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34
Q

Steps of new drug development

A
  • Select the lead compound and check for affinity, efficacy, early ADME, toxicity
  • preclinical testing (on animals, checks for efficacy, toxicology, ADME processes then move to humans)
  • investigational new drug (IND, must be approved by the IRB)
  • clinical trials on humans with the disease
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35
Q

Institutional review board

A

IRB
Reviews and approves research on a drug before it is classified as an investigational new drug and proceeds to clinical trials

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36
Q

4 Phases of Drug Trials

A
  1. Small number of healthy volunteers-safety, toxicology, and pharmacokinetics (is it safe?)
  2. Small number of people with disease-efficacy, dosing, and adverse effects (does it work?)
  3. Larger number of sick patients-compare to current treatment (is it better?)
  4. Post marker surveillance of drug’s effects-detects adverse effects (can it stay?)—can result in removal of a drug from the market and is completely voluntary, people must report side effects to the FDA
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37
Q

How long does the process take for drug research and approval?

A

It can take 10+ years

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38
Q

What happens between phases 3 and 4 of drug trials?

A

A 1-4 year period elapses between those stages where the drug is approved for sale on the market

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39
Q

polypharmacy

A

giving multiple drugs for multiple conditions, or multiple drugs to manage one condition

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40
Q

3 types of reactions

A

pharmaceutical, pharmacokinetic, and pharmacodynamic

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41
Q

pharmaceutical reactions

A

drugs reacting chemically or physically during administration or absorption, altering the variability of one or both drugs–chelation, adsorption, altering gastric pH, and incompatibilities

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42
Q

chelation

A

agents (chelating agents) bind to a drug forming an insoluble complex that is poorly absorbed
ex) tetracycline and ciprofloxacin (antibiotics)=insoluble complex

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43
Q

adsorption

A

physical binding of a drug with other solids, leading to increased absorption
ex) antacids adsorb and decrease absorption of iron

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44
Q

alteration of gastric pH

A

some drugs are used to increase pH, and may affect drugs that absorb better at a low pH
ex) omeprazole increases gastric pH, and decreases absorption of ampicilin

45
Q

incompatibilities

A

some drugs can decrease the effects of other drugs

ex) when IV fluids are mixed together they may be incompatible and decrease their effects

46
Q

what happens when meds are taken on an empty stomach?

A

the plasma concentration is very high since there is nothing else to absorb

47
Q

why should you not take meds with milk?

A

the medicine binds to the milk and forms an insoluble complex–this delays absorption and reduces effect

48
Q

what should you take medications with?

A

water

49
Q

pharmacokinetic interactions

A

changes to the ADME processes of another drug (what the body does to the drug

  • account for the most drug interactions
  • ADME processes, distribution interactions, excretion interactions, biotransformation interactions, enzyme induction and inhibition
50
Q

gastric motility and emptying time

A

low gastric emptying time-higher bioavailability, increased absorption from small intestine
high gastric emptying time-low bioavailability, decreased absorption and stays in stomach longer

51
Q

what is the normal gastric emptying time?

A

90 minutes

52
Q

intestinal flora

A

bacteria in the large intestine that help absorb drugs-if there are less bacteria, it leads to less metabolism and a high concentration b/c the medicine isn’t absorbed fast enough

53
Q

saturation of carrier mediated absorption

A

all receptor are occupied and the drugs can’t reach the target–low bioavailability and absorption

54
Q

distribution interactions

A

displaces the drug from the transporter, resulting in an increased plasma concentration and increased metabolism and excretion

55
Q

excretion interactions

A

changes urinary pH-increased urinary pH leads to decreased excretion of bases, increased excretion of acids (acids are 0-6 on scale, bases are 8-14)

56
Q

alteration of tubular secretion

A

tubular secretion is active transport with a specific transporter for acids and bases, and competition b/w these results in decreased secretion and clearance

57
Q

biotransformation interactions

A

affects metabolism of other drugs, and if a drug stays in the stomach too long it is less available for absorption

58
Q

enzyme induction

A

potentiated effect

ex) St. John’s wort induces CYP3A, and when given with other drugs it causes faster elimination

59
Q

enzyme inhibition

A

another drug is inhibited
ex) CYP3A is inhibited by grapefruit juice, increasing the bioavailability of the drug it is given with, leading to toxicity

60
Q

most important enzyme in the liver?

A

CYP3A, most often responsible for life threatening drug reactions and metabolized 55% of all drugs

61
Q

pharmacodynamic drug interactions

A

one drug changes the pharmacological effect of another (drug does to body, molecular and chem. interactions)
-additive, synergistic, and antagonistic reactions

62
Q

additive reaction

A

something is added

  • most common type of pharmacodynamic reaction
  • 1+1=2
63
Q

synergistic reaction

A

combined effect of the medications is greater than either of their individual effects
-1+1=3

64
Q

antagonistic reaction

A

results in inhibition

-classified as competitive, noncompetitive, etc

65
Q

tyramine

A

compound in cheese that causes hypertensive crisis if given with antidepressants, because it increases availability (toxicity) of the compound

66
Q

why can warfarin not be taken with greens?

A

greens have vitamin K, warfarin is an anti-vitamin K drug and an anticoagulant, so it renders warfarin ineffective

67
Q

what can replace the friendly bacteria killed by antibiotics?

A

compounds in yogurt

68
Q

why can drugs not be taken with alcohol?

A

alcohol has depressive properties and either an additive or synergistic reaction, so it leads to high blood pressure

69
Q

what happens when alcohol is taken with tylenol?

A

it produces a higher level of toxic metabolites, affecting the liver

70
Q

why is grapefruit juice bad for medications?

A

it binds to CYP3A, inhibiting it, increasing the toxicity and effect of the drug. also causes decreased metabolism

71
Q

what happens if herbal tea is taken with estrogen?

A

it leads to increased estrogen amounts

72
Q

what happens when St. John’s wort is given with the majority of medications?

A

it causes nausea, weakness, and fatigue

73
Q

what does warfarin do with some medications?

A

its effect as an anticoagulant is decreased causing increased bleeding and bruising

74
Q

pharmacogenetics

A

study of genetically determined variability in response of people to drugs
-studies specific differences

75
Q

pharmacogenomics

A

study of effect of person’s genetic inheritance on body’s response to drugs by studying multiple genes and alleles
-uses a genome wide approach, more broad than pharmacogenetics

76
Q

DNA

A

codes for producing genetic chemicals

77
Q

RNA

A

messenger, carries info through cytoplasm

78
Q

transcription

A

DNA->mRNA

takes place in the nucleus, a DNA strand untwists to form two single-strand mRNA molecules

79
Q

translation

A

mRNA->proteins
takes place in the ribosomes, the mRNA formed from transcription carries the message through the cytoplasm to the ribosomes to carry out translation

80
Q

how many chromosomes do humans have, and what are they called?

A 
46 total (23 from sperm, 23 from egg)
22 pairs are called autosomes, and 23rd pair are the sex chromosomes (XX or XY)
81
Q

gene

A

sequence of DNA that encodes a particular trait

82
Q

complementary base pairs of DNA

A

adenine-thymine

guanine-cytosine

83
Q

2 alternative forms (alleles) of genes

A

homozygous-two same alleles (SS)

heterozygous-two different alleles (Sc)

84
Q

how many known genes are in the human genome?

A

30,000

85
Q

genotype

A

how genes are arranged–genetic makeup

86
Q

phenotype

A

physical expression of the genotype

87
Q

gene expression

A

manifestation of genotype into the phenotype

88
Q

mutation

A

occurs in less than 1% of population

permanent change or structural alteration of DNA

89
Q

germline mutation or hereditary mutation

A

mutation transmitted through germ cells (sex cells) through the generations

90
Q

acquired mutation

A

acquired through exposure to toxins (radiation, smoke, etc) that occurs in a single cell after conception and it spreads to all cells that multiply from it

91
Q

polymorphism

A

mutation that occurs in over 1% of population

92
Q

most common type of polymorphism

A

single nucleotide polymorphism–one of the nucleotides in the A-T G-C base pairs is replaced

93
Q

sickle cell anemia

A

a single amino acid changes in the hemoglobin, causing a RBC to form into a sickle shape and can’t function correctly

94
Q

glucose 6 phosphate dehydrogenase deficiency (G6PD)

A

most common enzyme deficiency, certain medications cause hemolysis (rupture of RBC)
-there are no obvious signs, and it is more common in males and african americans

95
Q

monogenic disease

A

1 gene is involved

-cystic fibrosis, huntington’s, sickle cell anemia

96
Q

polygenic disease

A

more than 1 gene is involved

-asthma, heart disease, Alzheimers

97
Q

gene deletion

A

leads to enzyme deficiency, leads to slow metabolizers–toxicity

98
Q

gene amplification

A

increased gene expression, leads to more enzyme and fast metabolizers (if the drug is eliminated too fast it can cause resistance)

99
Q

hyporesponsers

A

receptors are under-responding, some may be inactive and this leads to a low availability of the drug

100
Q

hyper-responders

A

receptors are over-responding, so a small dose could cause a large response

101
Q

variation can change the availability of drug transporters

A

decreased transporters=low availability, drug doesn’t reach target so no response
increased transporters=too much drug reached the target and causes too much of a response

102
Q

those that are slow metabolizers probably have a what?

A

genetic problem

103
Q

clinical applications of pharmacogenomics

A

help identify a group that will benefit from a drug and the group that will experience toxicity, so a drug can still be marketed

104
Q

benefits of pharmacogenomics on drug therapy

A

advanced disease screenings (people know their risks so make better lifestyle choices), drugs with more specific targets, choice of drugs and dose, and more universal drugs

105
Q

genetics

A

identification of disease susceptibility in genes and gene variants by studying patients

106
Q

genomics

A

identification of genes and gene families as drug targets based on sequence similarities

107
Q

functional genomics

A

understanding function of gene and variants

108
Q

identifying drug compound

A

finding compound that interacts appropriately with the target

109
Q

compound optimization

A

alteration of compound structure to optimize pharmacokinetic(ADME) and pharmacodynamic (drug to body, chemical reactions) properties

Intro to Pharmaceuticals (10 decks)

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