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TT BL and DD Exam1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the 5 key elements in pharmacotherapeutics?

A
  1. drug
  2. dose
  3. route
  4. frequency
  5. duration
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2
Q

What pharmacologic principle are drug and dose based on?

A

Pharmacodynamics -

disease targets and drugregulation

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3
Q

What pharmacologic principle are route and frequency based on?

A

Pharmacokinetics

route - AD
frequency - ME

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4
Q

What pharmacologic principle is duration based on?

A

Disease pathophysiology

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5
Q

What are 4 basic drug categories?

A
  1. prescriptions
  2. controlled substances
  3. OTC
  4. Dietary supplements
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6
Q

What phase is clinical testing starts comparing drugs to placebos or existing treatments?

A

Phase II

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7
Q

What phase of clinical testing do most drugs fail?

A

Phase III

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8
Q

What phase of clinical testing do you monitor “does it work?”

A

Phase II and III

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9
Q

If you have a drug similar to one that is already approved, what application do you use to bypass testing trials?

A

abbreviated new drug application (ANDA)

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10
Q

Do structure/function claims require FDA approval?

A

No, but needs a disclaimer.

only health claims do require FDA approval

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11
Q

What are the 3 different FDA categories of drug equivalency?

A
  1. pharmaceutical equivalents
  2. bioequivalent
  3. therapeutic equivalent
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12
Q

What does signa or “sig” indicate on a prescription pad?

A

drug directions to pts.

aka dosage regimen

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13
Q

Manufacturer distribution of depressants and stimulants are divided into 5 ______

A

schedules

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14
Q

The 5 schedules I-V are in order from (lower to higher) abuse potential or (higher to lower) abuse potential

A

higher to lower abuse potential

Schedule I - no medical use, high abuse potential

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15
Q

How many mg make 1 grain?

A

65 mg = 1 grain

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16
Q

How many grams make 1 ounce?

A

28.4g = 1 oz

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17
Q

how many grams in 1 lb?

A

454g = 1 lb

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18
Q

how many ml make 1 tsp?

A

5 ml = 1 tsp

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19
Q

how many ml make 1 tablespoon?

A

15ml = 1 tablespoon

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20
Q

how many ml make 1 oz?

A

30ml = 1 oz

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21
Q

What does od* and os stand for?

A

right eye, left eye

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22
Q

What is the relationship between Cp and Vd?

A

inverse

more drug in plasma = less being distributed

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23
Q

Higher volume of distribution = more/less lipid soluble drug?

A

more lipid soluble

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24
Q

drug formulations must be more hydrophilic/hydrophobic to dissolve and release molecule?

A

hydrophilic

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25
Q

drug molecule must be more lipophilic/lipophobic to cross membrane?

A

lipophilic

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26
Q

after drug gets metabolized by liver it becomes more/less water soluble?

A

more water soluble

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27
Q

The more unionized a drug, the more/less lipid soluble it is.

A

More

More unionized = more lipid soluble

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28
Q

P-glycoproteins move drugs from the _______ space to the ______ space

A

intracellular, extracellular

Inside-> out

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29
Q

Bioavailability is termined by comparing AUC following single/multiple dose of a drug following IV route?

A

single

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30
Q

What is another word for extravascular?

A

Interstitial

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31
Q

High Vd indicates drugs are mostly located where?

Low Vd?

A

High Vd = outside plasma

low vd = inthe plasma or ECF

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32
Q

What is the term for the route of drugs that are taken into the body other than through the digestive tract?

A

Parenteral

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33
Q

If Vd is 3L, where are the drugs mostly located?

A

restricted to plasma

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34
Q

Extracellular water is ~12ml. What two compartments make up that volume?

A 
plasma = 3L
Interstitial = 9L

(highly bound to plasma proteins)

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35
Q

If Vd is 12 L, where are the drugs mostly located?

A

In the extracellular compartment (plasma and interstitial)

enters cells poorly

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36
Q

If Vd is 41L, where are drugs mainly located?

A

Total body water

freely enter cells

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37
Q

If Vd >? 50L, where are drugs mainly located?

A

sequestered in CNS, fat

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38
Q

When weak acids are protonated, it is ionized/unionized.

This means it can/cannot cross biological membranes.

A

unionized

can - absorbed

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39
Q

Acids become nonionized in acid/base medium.

A

acid

lots of H, so it holds onto proton

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40
Q

When weak bases are protonated, it is ionized/unionized.

This means it can/cannot cross biological membranes.

A

ionized (ie: NH3+)

cannot (ion trapped)

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41
Q

Ion trapped means what?

A

Drug has been ionized and can no longer cross membrane.

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42
Q

What is the henderson hasselbach equation?

A

pH-pKa = log [non-protonated/protonated]

or 10^(pH-pKa)

n before p

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43
Q

What does it mean when pH of biologic compartment is < pKa of drug?

A

more protons are present,

there will be more protonated forms of both acid and base.

44
Q

When pH>pKa, what does it mean?

A

fewer protons present

there will be more unprotonated forms of acid and base

45
Q

greater [ ] of drug is greater on side where ionization is greater/lesser?

A

greater

				* Acidic drugs are trapped in the more basic solutions
				* Basic drugs are trapped in the more acidic solutions
46
Q

3 types of membrane compartments that act as special barriers?

A
  1. GI mucosa
    • negligible absorption of drug into blood
  2. BBB
  3. Renal tubules
47
Q

Binding of drugs to plasma proteins prolongs/reduces drug action

A

prolongs -

hinders metabolic degredation, and reduce rate of excretion.

48
Q

How are plasma proteins a potential source of DDI?

A

They are important in drugs with narrow therapeutic index.

49
Q

What is biotransformation?

A

drug metabolism

enzyme catalyzed chemical structure transormation via liver

50
Q

What is the most frequent pathway of biotransformation (drug metabolism)?

A

oxidation

51
Q

The liver makes _____ compounds converted to _____ compounds to be more readily excreted.

A

lipid soluble, –> water soluble

52
Q

Phase I reactions include:

A

oxidation
reduction
hydrolysis

53
Q

2 types of Phase I oxidation reactions

A
  1. cytochrome p450 dependent

2. cytochrome p450 independent

54
Q

Cyt p450 dependent oxidation

  1. found where?
  2. involves enzymes or cofactors?
A
  1. rich in liver

2. cofactors

55
Q

Cyt p450 independent oxidation

-what enzymes are involved?

A
  1. amine oxidases

2. dehydrogenases

56
Q

In phase I hydrolysis, what enzymes are involved?

A

esterases, amidases

57
Q

Which phase reactions are more prone to:

  1. inhibition of drug metabolism?
  2. DDI?
  3. age related changes?
A

all Phase I

58
Q

What phase reaction are more prone to saturation?

A

phase II

59
Q

Inducers do what?

A

increases drug metabolism via cyt p450 system

60
Q

What do inhibitors do?

A

decreases drug metabolism and causing decrease drug clearance

61
Q

Name some inducers

A
  1. phenobarbitol
  2. phenotoin
  3. rifampin
  4. ethanol
  5. carbamazepine
  6. st. John’s wort
62
Q

Name some inhibitors

A
  1. cimetidine
  2. grapefruitjuice
  3. HIV protease inhibitors
  4. erythromycin
  5. ketoconazole
  6. fluoxetine
63
Q

How does the kidney work in drug excretion?

A

via filtration, secretion, reabsorption

64
Q

How fast is drug clearance in:

  • filtration
  • active tubular secretion
  • tubular reabsorption
A

120 ml/min

120-600ml/min

1ml/min

65
Q

Kidney filtration or secretion is highly affected by plasma protein binding and requires free, unbound drugs?

A

filtration

66
Q

Kidney tubular secretion process/movement

A

drugs are transported directly from blood into urine.

67
Q

Kidney tubule reabsorption

A

reabsorption of lipid-soluble drugs (via passive diffusion of the proximal and distal tubes)

(water soluble metabolite less likely to be reabsorbed. Remember that the liver makes drugs MORE water soluble to be excreted)

68
Q

Describe the enterohepatic cycle

A

Drugs are excreted via bile –> bile duct –> SI –> reabsorbed into blood –> liver

69
Q

First order kinetics rate of elimination vs Zero order

A

First order: rate of elimination is proportional to [ ] of drug in plasma Cp

Zero order: rate of elimination is constant and independent of amt of drug in body

70
Q

When is first order kinetics used to eliminate drugs vs zero order?

A

Most drugs eliminated via first order kinetics

  • drugs will be removed due to zero order kinetics when hepatic metabolic enzyme systems are saturated
71
Q

Two types of receptors? examples

A
  1. generalized receptors
    • biological molecules
  2. specialized receptors
    • membrane proteins, ion channels
72
Q

Signal transduction and amplification can activate what 3 things?

A
  1. ligand-gated ion channel
  2. GPCR
  3. Kinase-linked
    receptor/hormone (nuclear) receptor
73
Q

What is response [E] of a drug proportional to?

A

receptors[R] occupied by drug [D]

74
Q

Explain what a dose response curve indicate?

A

hyperbolic

  • at low doses, drug response increases proportionally to dose
  • curve levels off bc there is a limit to response achieved
75
Q

Explain what a log dose-response curve indicate

A

sigmoid

can compare different drugs (and wide range of doses)
- straight line corresponds to therapeutic range

76
Q

What is potency?

A

EC50 or ED50

concentration or dose required to produce 50% of drugs maximal effect

-more potent, takes less to bring about EC50 or ED50

77
Q

What is efficacy?

A

ability to initiate response

-most important determinant of clinical usefulness

78
Q

Competitive reversible antagonist affects potency/efficacy

A

it decreases potency

doesnt affect# of receptors available to contribute to response

79
Q

Non competitive “reversible” antagonists affects potency/efficacy

A

It decreases efficacy (Emax goes down)

80
Q

Two types of noncompetitive antagonist

A
  1. binds to active site

2. binds to allosteric site

81
Q

Two types of noncompetitive active site antagonist?

A
  1. irreversible

2. pseudoirreversible

82
Q

What are reversible antagonists that bind to the active site of the same receptor?

A

competitive “reversible” antagonist

83
Q

Two types of noncompetitive allosteric site antagonist?

A
  1. reversible

2. irreversible

84
Q

What is ED50 for graded dose-response curve?

A

dose that produces 50% of maximal response possible

85
Q

What is ED50 for population dose-response curve?

A

effective dose that initiates target response in 50% of pop

86
Q

Higher therapeutic index indicates what?

A

safer drug

usual clinical drugs between 10-20

87
Q

FDA categories for Drug use in pregnancy: description of -

A

A

shows no risk

88
Q

FDA categories for Drug use in pregnancy: description of -

B

A

no evidence of risk

89
Q

FDA categories for Drug use in pregnancy: description of -

C

A

risk cannot be rule out

90
Q

FDA categories for Drug use in pregnancy: description of -

D

A

positibe evidence of human fetal risk

91
Q

FDA categories for Drug use in pregnancy: description of -

X

A

contraindicated in pregnancy

DO NOT USE

92
Q

What are the 4 pharmacokinetic interventions preventing drug overdoses and poisoning?

A
  1. Prevent absorption of toxin
  2. Inhibit toxication
  3. Enhance metabolism
  4. Increase elimination of toxin
93
Q

4 ways to prevent absorption of toxin

A
  1. Emesis
  2. Gastic lavage
  3. Chemical adsorption
  4. osmotic cathartics
94
Q

Important drugs for emesis

A
  1. Ipecac

2. Apomorphine

95
Q

Contraindications for ipecac or apomorphine

A

§ Patient comatose / stuporous (lack of gag reflex à risk of aspiration)

§ Ingestion of corrosive poisons (i.e., strong acids or alkalis)

§ Ingestion of CNS stimulant such as strychnine (risk of seizures)

§ Ingestion of petroleum distillate (risk of pneumonitis)

§ Pregnancy Category C: (weigh benefit vs risk, unknown if drug can cause harm)

96
Q

What is chemical adsorption

A

an emesis intervention used to prevent absorption of toxin:

binds drug in gut - limits adsorption

97
Q

What is osmotic cathartics?

A

an emesis intervention used to prevent absorption:

decreases time of toxin in GI tract if ingestion is >60

98
Q

Recommended drugs for osmotic cathartics?

A

sorbitol,
Mg citrate or sulfate
polyethylene glycol

99
Q

3 methods used to inhibit toxication (pharmacokinetic interventions)

A
  1. inhibit rate limiting enzyme
  2. hemodialysis
  3. sodium bicarb (corrects metabolic acidosis)
100
Q

4 methods used to increase elimination of toxin

A
  1. extracorporeal removal
  2. enhanced metabolism
  3. enhanced renal excretion
  4. chelation of heavy metals
101
Q

how is 70-80% of Acetaminophen (AC) metabolized?

A

conjugated with glucuronic acid or sulfate (phase II)

102
Q

5-10% of acetaminophen is metabolized how? describe

A

5-10% of AC proceeds through cytochrome P450 oxidation (phase I)

AC → becomes chemically reactive NAPQI (Ac*)
→ becomes detoxified by phase II GSH
transferase
→ excreted as mercapturate

103
Q

Describe mechanism of acetaminophen overdose toxicity

A

= hepatocellular injury due to saturation

  • Saturation of Phase II conjugation pathways ←glucuronide + sulfate→
  • This leads to excessive formation of Ac* by phase I pathway
  • Glutathione (GSH?) gets depleted
  • Ac* builds up
104
Q

Describe acetaminophen treatment.

A

N- acetylcysteine (mucomyst)

-glutathione synthesis

105
Q

What is methanol (CH3OH) metabolized to?

poisoning leads to what?

A

formic acid

○ Visual disturbance (snowstorm) soon after acidosis → cant breath → die

106
Q

What is ethylene glycol (HOCH2CH2OH) metabolized to?

Leads to what?

A

oxalic acid

○ Acute renal failure

107
Q

What is the rate limiting enzyme in methanol and ethylene glucol metabolism?

-how can you inhibit it?

A

alcohol dehydrogenase

ihibit with fomepizole

TT BL and DD Exam1 (23 decks)

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