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605 Pharmacology > Spinella Midterm Material > Flashcards

Spinella Midterm Material Flashcards

1
Q

pharmacology

A

study of the action of chemicals on biological systems; study the drugs

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2
Q

pharmacy

A

provide info about medications; dispense the drugs safely

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3
Q

pharmacokinetics

A

what the body does to a drug - how it distributes, metabolizes, eliminates, or absorbs the drug

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4
Q

pharmacodynamics

A

what the drug does to the body - how it elicits an effect

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5
Q

3 “Steps” of Pharmacology

A

Drug Dose –> Plasma Concentration –> Effect

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6
Q

Combination of which “steps” make up pharmacokinetics?

A

drug dose and plasma concentration

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7
Q

Combination of which “steps” make pharmacodynamics?

A

plasma concentration and effect

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8
Q

What explains how to achieve target concentration - pharmacokinetics or pharmacodynamics?

A

pharmacokinetics

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9
Q

What explains the optimal target concentration - pharmacokinetics or pharmacodynamics?

A

pharmacodynamics

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10
Q

drugs

A

substances which act on biological systems, usually by binding a receptor

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11
Q

receptor

A

molecule that selectively binds a ligand (drug) and undergoes a modification

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12
Q

biologics

A

produced from a living organism

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13
Q

pharmaceuticals

A

implies that there is a manufacturing process involved

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14
Q

inactive ingredients

A

make medication into final form for administration - can include coating, fillers, binders, solubilizers and disintegrants

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15
Q

active ingredients

A

those which elicit the desired pharmacologic effects

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16
Q

How is a drug named?

A

chemical name upon discovery –> code name for development –> nonproprietary generic name –> brand name upon patent and marketing

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17
Q

Are brand and generic drugs the same?

A

yes, they are bioequivalent - same ingredients, strength, dosage form, and route of administration

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18
Q

supplement

A

supplement taken orally that contains micronutrients like vitamins, probiotics, minerals, AAs, enzymes

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19
Q

Are supplements drugs?

A

no

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20
Q

What kind of claims can supplements make - health or disease?

A

health - cannot be marketed as alleviating the effects of a disease

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21
Q

Are supplements regulated by the FDA?

A

yes, but only post-marketing

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22
Q

Does efficacy and safety have to be proven before the sale of drugs? Supplements?

A

Drugs = YES
Supplements = NO

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23
Q

nutraceuticals

A

made from food or part of a food (ex: glucosamine, chondroitin)

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24
Q

Problems with Supplements and Nutraceuticals

A

can be ineffective, make false claims, contain unlisted ingredients, interact with drugs, contain toxic contaminants, adverse effects

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25
Q

Is there scientific data behind supplements?

A

not very much if any at all

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26
Q

Examples of nutraceuticals?

A

garlic, green tea, ginseng, glucosamine, etc

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27
Q

Efficacy

A

the ability of a drug to bind to a receptor and generate an effect; how well a drug works; the MAXIMUM effect a drug can produce

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28
Q

Which drug is the most effective?

A

A

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29
Q

Potency

A

relative concentration of a drug required to produce a given effect; how STRONG is a drug

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30
Q

Which is the most potent?

A

A (EC50 is at the lowest concentration)

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31
Q

Therapeutic Index Equation

A
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32
Q

What does a small therapeutic index mean?

A

harm is more likely at therapeutic doses

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33
Q

Therapeutic Window

A

space between the minimum effective concentration and the minimum toxic concentration

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34
Q

What therapeutic index is better - larger or smaller?

A

LARGER, ideally greater than 10 but better be greater than 1

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35
Q

What is the therapeutic index of this drug?

A

10

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36
Q

What is the therapeutic index of this drug?

A

100 (95 divided by .95)

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37
Q

Margin of Safety Equation

A
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38
Q

Agonist

A

drug that binds to receptor and activates it

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39
Q

Antagonist

A

drug that binds to receptor but does not activate it and prevents activation by an agonist

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40
Q

Competitive Antagonist

A

antagonist that can be overcome by increasing the concentration of the agonist

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41
Q

Irreversible Antagonist

A

cannot be overcome no matter what the concentration of the agonist

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42
Q

Full Agonists

A

produces the same effect as the endogenous ligand

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43
Q

Can full agonists differ in potency or efficacy?

A

POTENCY (efficacy will be the same)

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44
Q

Does a competitive agonist have an effect on efficacy or potency of the endogenous ligand?

A

Potency

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45
Q

Are competitive antagonists reversible?

A

yes

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46
Q

Are non-competitive agonists reversible?

A

NO, they are irreversible

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47
Q

Does a non-competitive (irreversible) agonist have an effect on efficacy or potency of the endogenous ligand?

A

Efficacy (because fewer receptors are available for binding)

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48
Q

What kind of antagonist is at work here?

A

Competitive Antagonist (decreasing potency)

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49
Q

What kind of antagonist is at work here?

A

Non-competitive (irreversible) antagonist (decreasing efficacy)

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50
Q

What does ADME stand for? (the big 4 of pharamacokinetics)

A

Absorption
Distribution
Metabolism
Elimination

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51
Q

Goal of pharmacokinetics?

A

obtain a drug concentration in the therapeutic range for your patient

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52
Q

Absorption

A

movement of a drug from its site of administration into the bloodstream

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53
Q

Distribution

A

movement of a drug from the blood into other body fluids and tissues

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54
Q

Metabolism

A

chemical transformation of a drug within the tissues, generally to enhance elimination of the drug and its metabolites

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55
Q

Elimination

A

excretion of a drug out of the body by various pathways

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56
Q

Major excretory organ?

A

kidney

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57
Q

Does a drug have to be lipid soluble to move across a cell membrane (be absorbed)?

A

yes (non-ionized) (hydrophobic)

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58
Q

To eliminate a drug in the urine, should it be charged or uncharged?

A

charged (ionized) (hydrophilic)

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59
Q

5 Ways to Cross a Biological Membrane

A
  1. Filtration
  2. Passive Diffusion
  3. Facilitated Diffusion
  4. Active transport
  5. Endocytosis
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60
Q

The major route of entry for most drugs is what?

A

Passive Diffusion

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61
Q

pH-partition theory

A

pKa and the lipid water partition coefficient of the compound determine passage of a drug

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62
Q

Is diffusion first order or zero order?

A

first order

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63
Q

Saturable

A

carrier/receptor involved in transport

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64
Q

Which of the five transport mechanisms are saturable/selective?

A

facilitated diffusion, active transport, and endocytosis

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65
Q

Which of the five transport mechanisms require energy (ATP)?

A

active transport and endocytosis

66
Q

Which of the five transport mechanisms work with a concentration gradient?

A

passive and facilitated diffusion

67
Q

Which of the five transport mechanisms work via a pressure gradient?

A

Filtration

68
Q

Can ionized compounds enter via filtration?

A

no

69
Q

Are most pharmaceutical drugs strong or weak acids/bases?

A

weak acids and bases (so that they only partly ionize in solution)

70
Q

Henderson-Hasselbach Equation for Weak Acid

A
71
Q

Henderson-Hasselbach Equation for Weak Base

A
72
Q

In the stomach, are weak acids IONIZED or UNIONIZED?

A

unionized (think acids in an acidic solution are not charged)

73
Q

In the stomach, are weak bases IONIZED or UNIONIZED?

A

ionized

74
Q

In the intestine, are weak acids IONIZED or UNIONIZED?

A

ionized

75
Q

In the intestine, are weak bases IONIZED or UNIONIZED?

A

unionized

76
Q

How do you get rid of a basic drug in the urine?

A

acidify it (ex: with ammonium chloride)

77
Q

How do you get rid of an acidic drug in the urine?

A

alkalize it (ex: with sodium bicarbonate)

78
Q

To excrete a drug in the urine, should it be in its ionized or unionized form?

A

ionized (charged)

79
Q

First pass effect

A

the loss of a drug as it passes for the first time through the absorption process (pre-systemic circulation/elimination)

80
Q

Which drugs are susceptible to the first pass effect?

A

oral drugs

81
Q

Based on these Henderson-Hasselbach equations, would you expect to be in the stomach or the small intestine?

A

stomach

82
Q

First Order Half Life

A

eliminates a constant FRACTION of the drug per unit time

83
Q

Zero Order Half Life

A

eliminates a constant QUANTITY of the drug per unit time

84
Q

Definition of Biologic Half Life

A

the time required for the plasma drug concentration to decrease by one half

85
Q

Approximately how many half lives to reach steady state concentration?

A

5 (five)

86
Q

Factors that influence Drug Absorption

A

lipid solubility, particle size, route of administration, stability of drug, blood flow, concentration gradient, surface area, species, etc

87
Q

Bioavailability

A

the fraction of the dosed parent drug that reaches the systemic circulation unchanged

88
Q

Bioavailability of a drug administered IV?

A

100%

89
Q
A

Acidify; BH+

90
Q

Equation for Half-Life

A

T 1/2 = 0.693 x (Vd/Clp)

Vd = volume of distribution in L
Clp = plasma clearance in liters per hour

91
Q

Equation for Volume of Distribution

A

Vd = D / Co

D = dose given
Co = concentration in the plasma

92
Q

Equation for Plasma Clearance

A

Clp = Kel x Vd

Kel = elimination constant
Vd = volume of distribution

93
Q

Effect of drugs with high water solubility on Vd and Clp?

A

small Vd and high blood plasma conc.

94
Q

Effect of drugs with high lipid solubility on Vd and Clp?

A

large Vd and low blood plasma conc.

95
Q

Will a drug with a higher volume of distribution have a longer or shorter half life?

A

Longer

96
Q

Would a drug with a faster/higher plasma clearance have a longer or shorter half life?

A

shorter

97
Q

Approximately how many half-lives to reach steady state concentration?

A

5 (five)

98
Q

Process of Drug Metabolism

A

convert a lipid-soluble pharmacologically active drug into a water-soluble inactive metabolite

99
Q

2 Primary Ways Drugs are Excreted

A
  1. Renal excretion (urine)
  2. Hepatic Elimination (bile, feces)
100
Q

Less Common Pathways by which Drugs can be Eliminated

A

milk, sweat, saliva, tears, lung respiration

101
Q

pro-drug

A

the initially inactive form of a drug

102
Q

Phase 1 Metabolism

A

drugs which either add polar groups or remove non-polar groups

103
Q

Phase 2 Metabolism

A

functional group on drug or Phase 1 metabolite is combined with an endogenous substrate to get a more water soluble compound

104
Q

Major Phase 1 Metabolism Reactions (3)

A
  1. Oxidation
  2. Reduction
  3. Hydrolysis
105
Q

Major Phase 2 Metabolism [Conjugation] Reactions (6)

A
  1. Glucuronidation
  2. Acetylation
  3. Glutathione Conjugation
  4. Glycine Conjugation
  5. Sulfate Conjugation
  6. Methylation
106
Q

oxidation

A

adding oxygen or removing hydrogen from a drug

107
Q

reduction

A

adding hydrogen to the drug

108
Q

Hydrolysis

A

addition of water molecule to the drug (commonly with esters and amides)

109
Q

Main Goal of Drug Metabolism?

A

increase water solubility for drug excretion

110
Q

Enterohepatic Circulation

A

metabolite in the liver is conjugated with glucuronide, then goes from bile duct into GI tract, and some bacteria in GI tract can deconjugate and go back through portal vein back to liver –> increases drug exposure

111
Q

Most common usage of NSAIDs?

A

mild to moderate pain management and musculoskeletal disorders

112
Q

Are NSAIDs appropriate for visceral pain and broken bones?

A

NO

113
Q

Most common side effect of NSAIDs?

A

GI upset (ulceration due to the inhibition of the protective effects of prostaglandins)

114
Q

NSAID Effect on COX

A

inhibit COX activity (directly binding to active site)

115
Q

Steroid Effect on COX

A

inhibit COX levels (by preventing production)

116
Q

Are NSAIDs acids or bases?

A

weak acids

117
Q

What is the only NSAID that irreversibly inhibits COX?

A

aspirin (anti-thrombic)

MOA: it acetylates the COX enzyme

118
Q

Flunixin Meglumine

A

Banamine
NSAID used for colic in horses (anti-inflammatory, analgesic, anti-endotoxic, and antipyretic)

can also be used in other large animals

119
Q

PGE2

A

most potent prostaglandin and the principle mediator of pain/inflammation/fever

120
Q

Most COX-2 selective drug in vet med?

A

Firocoxib

121
Q

Three Main Organ Systems Most Commonly Associated with [NSAID] Toxicity

A
  1. Gastrointestinal
  2. Renal
  3. Hepatic
122
Q

If NSAIDs are weak acids, then where are they absorbed?

A

stomach

123
Q

Why are cats susceptible to acetaminophen toxicity?

A

lack enzyme for glucuronidation (glucuronyl transferase)

124
Q

Is aspirin COX1 or COX2 selective?

A

COX-1

125
Q

Can dogs use Advil, Motrin, or Aleve?

A

absolutely the fuck not

126
Q

Meloxicam

A

COX-2 preferential that is one of cats’ only approved NSAIDs (there’s only two), and ONLY as a one time injection, according to drug label

127
Q

Meloxicam Overdose in Cats?

A

acute renal failure and death

128
Q

Besides meloxicam, what’s the only other approved NSAID for cats?

A

Robenacoxib (Onsior)

administered orally (also available as an injectable), also COX-2 preferential

129
Q

Which COX produces the prostaglandins most associated with inflammation?

A

COX-2

130
Q

Do NSAIDs inhibit prostaglandin production?

A

yes

131
Q

Galliprant

A

new drug which targets the EP4 receptor (for PGE2) and does not inhibit COX

for OA in dogs

132
Q

Why is COX-2 a main target of our anti-inflammatories?

A

COX-2 isn’t really commonly produced in the body, except at sites of inflammation

133
Q

Who is the “good guy” - COX-1 or COX-2?

A

COX-1

has physiological functions GI protection, kidney function, platelet function, and regulation of blood flow

134
Q

Who is the “bad guy” - COX-1 or COX-2?

A

COX-2

causes inflammation, pain, and fever

135
Q

5 Classes of Diuretics

A
  1. Osmotic
  2. Carbonic Acid Inhibitors
  3. Loop
  4. Thiazides
  5. Potassium Sparing
136
Q

What class of diuretic will cause the most increase in urine volume?

A

loop diuretics (highest percent sodium excretion increase (25%))

137
Q

Which class of diuretics can cause hypercalciuria?

A

Loop diuretics (increases calcium excretion)

138
Q

Which class of diuretics can cause hypocalciuria?

A

Thiazide diuretics

139
Q

Hypokalemia is a risk of what two diuretic classes?

A

loop and thiazide

140
Q

Metabolic alkalosis is a risk of what two diuretic classes?

A

loop and thiazide

141
Q

Mannitol

A

osmotic diuretic

142
Q

Acetazolamide

A

carbonic acid inhibitor

143
Q

Furosemide

A

loop diuretic

144
Q

Hydrochlorothiazide

A

thiazide diuretic

145
Q

Amiloride

A

potassium sparing diuretic

146
Q

Spironolactone

A

potassium sparing diuretic

147
Q

Which class of diuretics has a potential side effect of metabolic acidosis?

A

carbonic acid inhibitors (greater increase in bicarbonate excretion)

148
Q

Enzyme that produces prostaglandins?

A

COX

149
Q

What do prostaglandins do?

A

many things, but help mediate (cause) pain, inflammation, and fever

150
Q

What drugs are more soluble in the bloodstream - ionized or unionized?

A

ionized

151
Q

Diuretic

A

a drug that increase the excretion rate of water (sodium)

152
Q

Therapeutic goal of diuretics?

A

decrease ECF (edema) and/or excess intravascular volume (hypervolemia)

153
Q

Carbonic Acid Inhibitor Site of Action

A

proximal convoluted tubule

154
Q

Osmotic Diuretic Site of Action

A

proximal convoluted tubule and descending limb of Henle

155
Q

Loop Diuretic Site of Action

A

ascending limb of Henle

156
Q

Thiazide Diuretic Site of Action

A

distal convoluted tubule

157
Q

Potassium-Sparing Diuretic Site of Action

A

distal convoluted tubule

158
Q

If mannitol was accidentally given orally, what’s the biggest side effect?

A

diarrhea

159
Q

Diuretic sometimes used for treatment of glaucoma?

A

mannitol

160
Q

Diuretic Resistance/Braking Phenomenon

A

kidney can sense high levels of sodium further down in the renal tubule and kicks in RAAS and can even add more transporters to try and compensate

161
Q

Major difference between loop and thiazide diruretics?

A

thiazides promote RESORPTION of calcium while loops promote EXCRETION of calcium

605 Pharmacology (11 decks)

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