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Week 2 (Quiz 1) Flashcards

1
Q

Pharmacokinetics

A

encompasses ADME principles, everything before drug reaches site of action

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2
Q

Pharmacodynamics

A

What the drug does at the site of action; therapeutic effects/toxicities

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3
Q

Therapeutic effect

A

When effect is easily quantifiable over a range of drug concentrations

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4
Q

Plasma concentration

A

for drugs with reversible effects when effect is not easily detectible and plasma concentration accurately reflects drug concentration at site of action

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5
Q

When can you not do drug monitoring?

A

When the drug has irreversible effects (plasma concentration will not correlate to effect)

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6
Q

What is an example of ineffective drug monitoring?

A

ASA irreversibly binds platelets until platelet dies

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7
Q

What are the two ways to do drug monitoring?

A
  1. Therapeutic effect

2. Plasma concentration

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8
Q

Why can time of blood collection cause interpretation issues?

A

if drug is still in distribution phase, plasma concentration will overestimate drug at action site

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9
Q

What happens to Vd as drug in plasma decreases?

A

Increases

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10
Q

Pediatric absorption

A

highly variable dependent on state of development (rectal administration effective for neonates and infants); 1-3 years have increased intestinal glutathione that may inactivate some drugs.

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11
Q

Pediatric distribution

A

Vd changes with body composition changes and plasma protein levels

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12
Q

Pediatric metabolism (hepatic)

A

Decreased in neonates and infants, approaches adult levels after 1 year

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13
Q

Pediatric excretion (renal)

A

Decreased in neonates, approaches adult levels after 6-12 months

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14
Q

Pregnancy absorption

A

NORMAL; some alterations due to decreased GI motility

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15
Q

Pregnancy distribution

A

Increased Vd (hydrophilic drugs) due to increased intravascular volume and dilution of plasma protein

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16
Q

Which type of drugs cross the placenta?

A

Lipophilic drugs cross the placenta

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17
Q

Pregnancy metabolism

A

NORMAL

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18
Q

Pregnancy excretion

A

Increased renal blood flow and GFR results in enhanced excretion

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19
Q

Obese absorption

A

NORMAL; obesity-associated conditions may affect absorption

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20
Q

Obese distribution

A

Vd alteration is drug specific. Increased Vd for most lipophilic compounds; normal for others

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21
Q

Obese metabolism

A

NORMAL; obesite-associated conditions (NASH) may affect hepatic metabolism

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22
Q

Obese excretion

A

Normal, although the precise effect of obesity on the kidneys is unclear at present

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23
Q

Geriatric absorption

A

Normal (age-associated conditions may affect absorption; polypharmacy increases risk of drug-drug interactions

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24
Q

Geriatric distribution

A

Vd alterations due to changes in body compositions and plasma protein (increased body fat, decreased albumin as liver ages)

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25
Geriatric metabolism
Decreased phase I metabolism, normal phase 2, other conditions may contribute to declining hepatic function
26
Geriatric excretion
Decreased renal function resulting in impaired excretion
27
Differences on average between males and females
1. lower BMI 2. smaller kidney/liver, 3. smaller Vd 4. higher % body fat
28
Tolerance
decreased pharmacologic response at same effective concentration after
29
Sensitization
Increased pharmacologic effect at same effective concentration over time
30
What are examples of sensitization?
up regulation of targeted receptors with chronic administration of b-blockers
31
Tachyphylaxis
rapid development of tolerance with closely spaced successive doses of drug or poison.
32
Percent predictable extensions of drugs mechanism of action
80-85
33
Percent hypersensitivity reactions
10-15%
34
Percent unexplained
5%
35
What are pathologic absorption variables of the GI tract?
Decreased in celiac disease and Whipple's disease from inflammation/destruction of villa; vomiting = less time for absorption
36
What are gastric emptying (delayed or decreased) variables of the GI tract?
gastroparesis; atropine (parasympathetic receptor blocker decreases GI motility); DM (GI neuropathy decreases parasympathetic action)
37
Epinephrine impact on GI tract
↑ duration of local anesthetic (↓blood flow by vasoconstriction, ↓ absorption into circulation = ↑ drug at target)
38
Cholestyramine impact on GI tract
(used in hyperlipidemia) binds acetaminophen, warfarin, digoxin; in gut, prevents absorption by binding other ingested drugs
39
Tetracycline impact on the GI tract
sequestered by bivalent cations (Ca++ and Mg++ - milk and antacids)
40
Ferrous sulfate impact on the GI tract
binds D-penicillamine, thyroxine, methyldopa
41
Drug displacement example with albumin
Drug-albumin: lipid-soluble and anionic drugs have affinity for albumin (bound) --> if albumin-bound drug is displace by another drug w/ albumin affinity --> toxicity of first drug (↑bioavailable first drug in plasma)
42
Drug replacement example: sulfonamide
displaces bilirubin -->↓ bili. conjugation --> jaundice and hyper bilirubinemia
43
Drug replacement example: Phenytoin
antiepileptic that binds albumin, other drugs displace phenytoin and↑serum concentrations
44
What diseases create reduced albumin
hepatic disease, renal disease, malnutrition/dec. protein intake
45
Who has higher percent body fat?
neonates, elderly, women
46
What does increased body fat do to tissue distribution?
↓ bioavailability of lipophilic drugs,↑ bioavailability of hydrophilic drugs
47
Percent body water - calculation
utilize body surface, rather than weight to calculate
48
Percent body water - changes
↑ in neonates/children,↓with age
49
What diseases cause decreased hepatic perfusion?
↓ metabolism: heart failure, Budd-Chiari (occlusion of hepatic portal system)
50
Who has decreased enzyme?
Neonates and preemies, elderly
51
Decreased glucuronyltransferase in neonates
leads to jaundice
52
With increased pt. age, what happens with benzodiazepines metabolism?
increased side effects
53
What are the 6 ways that metabolism can be altered in hepatocytes?
1. decreased perfusion 2. hepatic pathology 3. decreased enzyme 4. increased enzyme via induction 5. competition 6. altered functionality
54
Gilbert's syndrome
Autosomal recessive - repeats in UGT1A1 ↓ function | = ↑ unconjugated bilirubin
55
Example of mutation altering hepatic functionality
Crigler-Najjar Syndrome - lack UGT1A1
56
Example of variable number tandom repeats hepatic functionality
Gilbert's syndrome
57
Excretion factors
1. Perfusion 2. Pathology 3. Drug-drug interaction
58
Probenecid and kidney function
(treats gout/hyperuricemia by inhibiting anion transporter) - inhibits renal excretion
59
Thalidomide in utero
given in 50s-60s as sedative = caused limb malformations
60
Diethylstilbestrol (DES) in utero
used in 40s-70s to prevent miscarriages = causes female children to develop clear cell vaginal/cervical adenocarcinoma at 15-20 years
61
TPMT and thiopurine drugs
thiopurine drugs [i.e. 6MP, 6TG, azathioprine] (chemotherapy) metabolized by TPMT and XO into harmless metabolite; otherwise risk bone marrow toxicity
62
Low TPMT and thiopurine drugs
low TPMT = ↑ toxicity, risk for secondary neoplasm
63
High TPMT and thiopurine drugs
high TPMT = ↓ therapeutic effect of chemotherapy
64
CYP2D6 and Tamoxifen
tamoxifen (breast cancer) pts contain CYP2D6 mutations that affect response to this anti-cancer drug
65
UGT1A1 and irinotecan
if UGT1A1 has 7 dinucleotide (TA) repeats = ↓ activity = ↑ buildup of toxic metabolite
66
EGFR inhibitor and TKR receptors
mutations found in lung adenocarcinomas that change how | carcinoma reacts to EGFR inhibitors; tumor can be super responsive or not responsive
67
BRAF
most frequently mutated gene in melanomas - BRAF inhibitors that target the mutation are new treatment with excellent response rate using Vemurafenib
68
What are the two phenotypes for CYP2 family genes
Extensive metabolizers and poor metabolizers
69
If metabolite is active/toxic in EM
risk for toxicity at lower doses of drug
70
If metabolite is inactive in EM
therapeutic dose may not | be enough to have effect
71
If metabolite is inactive in PM
pt gets no effect of drug
72
If metabolite is active in PM
pt has too | much drug/risk for toxicity

Pharm (9 decks)

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