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Pharm Semester 2, test 1 > test 1 > Flashcards

test 1 Flashcards

1
Q

agonist

A

a drug that activates a receptor by binding to that receptor

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2
Q

agonist bind

A

ionic, hydrogen, and van der waals interactions (making them reversible)…rarely covalently (irreversible)

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3
Q

When is the effect of the drug produced

A

when the receptor is bound to the agonist ligand

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4
Q

receptors are either

A

bound or unbound (binary)

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5
Q

The most drug effect occurs when

A

every receptor is bound

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6
Q

Antagonist

A

a drug that binds to the receptor without activating the receptor

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7
Q

antagonist bind

A

either ionic, hydrogen, and van der waals interactions, reversible

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8
Q

antagonist block

A

the action of the agonist by getting in the way, preventing the agonist from binding to the receptor and producing the drug effect

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9
Q

competitive antagonism

A

is present when increasing concentrations of the antagonist progressively inhibit the response to the agonist, shifts the agonist dose response curve to the right. (the more antagonist you give the more it’ll knock out the agonist, but it is irreversible)

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10
Q

noncompetitive antagonism

A

present when, after administration of an antagonist, even high concentrations of agonist can not completely overcome the antagonism. causes both a rightward shift of the dose-response relationship as well as a decreased maximum efficacy of the concentration versus response relationship

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11
Q

partial agonist

A

A drug that binds to a receptor (usually at the agonist site)_ where it activates the receptor but not as a full agonist, even at supramaximal doses

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12
Q

agonist-antagonist

A

partial agonist may have antagonist activity. Ex: when butorphanol is a modestly efficacious analgesic. given with fenanyl, it will partly reverse the fentanyl analgesia

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13
Q

inverse agonist

A

bind at the same as the agonist (and compete with it) but they produce the opposite effect of the agonist

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14
Q

receptors have many different conformations (shape or structure)

A

inactive (80%) and active (20%)

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15
Q

receptor state for an full agonist

A

100% active. conformation of the active state to be strongly favored

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16
Q

receptor state for a partial agonst

A

50% active, 50% inactive. not as effective in stabilizing the receptor in the active state

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17
Q

receptor state for antagonist

A

does not favor either state, it just gets in the way of the agonist binding

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18
Q

receptor state for inverse agonist

A

100% inactive, favors the inactive state, reversing the baseline receptor activity

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19
Q

receptor upregulating

A

(putting receptors on the cell surface) increasing the number of receptors, leading to an exaggerated response. Ex: lower motor neuron injury cause increase in the number of nicotinic acetycholine receptors in the neuromuscular junction, leading to an exaggerated response to succinylcholine.

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20
Q

receptor downregulating

A

(endocytosis of receptors, receptors going into cell). Ex: a patient with pheochromocytoma has an excess of circulating catecholamines, and there is a decrease in the number of B-adrenergic receptors on the cell membrane in an attempt to maintain homeostasis.

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21
Q

tachyphylaxis

A

in asthma pts, decrease response to same dose of B-agonist, looks like tolerance, because of the decreased in B-adrenergic receptors

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22
Q

location of most receptors for anesthetic drugs

A

in the cell membrane lipid bilayer

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23
Q

What interacts with membrane bound receptors

A

opiods, benzos, beta blockers, IV sedative hypnotics, muscle relaxants, catacholamines (most are antagonist)

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24
Q

drugs that interact with intracellular proteins

A

caffeine, insulin, steroids, theophylline, milrinone

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25
Q

circulating proteins

A

another target for drugs, Ex: coagulation cascade

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26
Q

some drugs dont bind to receptors

A

stomach acid like sodium citrate work by changing the gastric pH

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27
Q

cation

A

ion with a positive charge

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28
Q

anion

A

ion with a negative charge

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29
Q

chelating drugs

A

work by binding to divalent cation

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30
Q

iodine kills bacteria by

A

osmotic pressure (intracellular desiccation, best to let iodine dry)

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31
Q

IV sodium bicarb

A

changes plasma pH

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32
Q

define catalyze

A

start or accelerate

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33
Q

the proteins response to binding

A

of the drug is responsible for the drug effect

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34
Q

pharmacokinetics

A

study of absorption, distribution, metabolism, and excretion/elimination of injected and inhaled drugs and their metabolites, what the body does to the drug

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35
Q

pharmacodynamics

A

study of the bodys response to the drug, what the drug does to the body

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36
Q

PK determines

A

the concentration of a drug in the plasma or at the site of drug effect

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37
Q

PK variability

A

results from genetic modification in metabolism, interactions with other drugs, or diseases of the liver, kidneys, or other organs of metabolism

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38
Q

IV administered drugs

A

mix with body tissues and are immediately diluted from the concentrated injectate in the syringe to the more dilute concentration measured in the plasma or tissue

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39
Q

concentration =

A

amount (mass)/ volume

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40
Q

central volume

A

is the volume that IV injected drug initially mixes into

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41
Q

central compartment

A

the initial distribution (within 1 min) after bolus injection is considered mixing with the central compartment= composed of those elements of the body that dilute the drug within the first min

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42
Q

elements of the body that dilute within the first min

A

venous blood volume of the arm, the volume of the great vessels, the heart, the lungs, and the upper aorta, first passage through the lungs

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43
Q

drugs that may be taken up in the first passage through the lungs

A

drugs that are highly fat soluble

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44
Q

many of the volumes are fixed

A

except the lungs, likes fat soluble. when the lungs take up more drug it makes the apartment volume of the central compartment increase (bc lower concentration)

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45
Q

minutes later the drug will mix with

A

the entire blood volume, may take a long time for fully mix with all tissues bc some tissues have low perfusion

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46
Q

polar drugs are drawn to

A

water, where the polar water molecule find a low energy state by associating with the charged aspects of the molecule

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47
Q

nonpolar drugs are drawn (higher affinity) to

A

fat, where van der waals provide numerous weak binding sites

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47
Q

VD for highly fat soluble drugs

A

the molecule will have a large volume distribution bc it will be taken up by fat, diluting the concentration in the plasma

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48
Q

many anesthetic drugs are

A

highly fat soluble and poorly water soluble

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49
Q

imaginable VD

A

imaginable L in the plasma that is required to dilute the initial dose med to achieve the measured concentration

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50
Q

vessel rich group

A

brain, heart, kidneys, liver: bolus injection the drug initially goes to the tissues that receive the bulk arterial blood flow

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51
Q

for highly lipid soluble drugs

A

the capacity of the fat to hold the drug greatly exceeds the capacity of the highly perfused tissues, this offsets the drugs effect following a bolus

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52
Q

the fat is invisible at first

A

bc the blood supply is so low, the fat gradually absorbs more drug, removing it away from the highly perfused tissues

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53
Q

muscles in distribution

A

they have a blood flow that is intermediate between highly perfused tissues and fat, intermediate solubility for lipophilic drugs

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54
Q

most drugs are bound to

A

plasma proteins (mostly albumin), alpha1-acid glycoprotein, and lipoproteins

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55
Q

most acidic drugs bind to

A

albumin

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56
Q

most basic drugs bind to

A

alpha1-glycoproteins

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57
Q

protein binding effects the

A

distribution of drugs (b/c free/unbound drugs can cross cell membranes), and the apparent potency of drugs (b/c free drugs determine the concentration)

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58
Q

drugs that are hydrophobic

A

more likely to bind to proteins in the plasma and to lipids in the fat

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59
Q

binding of drugs to albumin

A

is nonselective and substances alike may compete for the same binding site Ex: sulfonamides can displace unconjugates bilirubin from binding sites on albumin causing bilirubin encephalopathy

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60
Q

what can decrease plasma protein concentration

A

age, hepatic disease, renal failure, and pregnancy

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61
Q

alterations in protein bindings sites are important for

A

highly protein bound drugs (<90%)

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62
Q

free fraction changes

A

as an inverse proportion with a change in protein concentration (increase protein less drug, decrease protein more drug)

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63
Q

an increase in free fraction of a drug

A

may increase the pharmacologic effects of the drug

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64
Q

the free drug concentration may change little d/t protein bc

A

the free drug concentration in the plasma and tissues represents the shared binding with all binding sites, not just plasma

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65
Q

metabolism

A

converts active, lipid-soluble drugs into water-soluble and usually inactive metabolites

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66
Q

prodrug

A

inactive parent compound that is metabolized to an active drug. Ex: codeine into morphine, morphine-6-glucuronide (metabolite of morphine)

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67
Q

4 basic pathways of metabolism

A

oxidation, reduction, hydrolysis, conjugation

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68
Q

phase 1 metabolism includes

A

oxidation, reduction, and hydrolysis, which increases the drugs polarity prior to phase two

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69
Q

phase 2 reactions

A

are conjugation reactions that covalently link the drug or metabolite with a highly polar molecule (carbohydrate or amino acid) that renders the conjugate more water soluble for subsequent excretion

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70
Q

what are mostly responsible for the metabolism of most drugs

A

hepatic microsomal enzymes

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71
Q

other areas of metabolism

A

plasma (Hofmann elimination, ester hydrolysis), lungs, kidneys, GI tract, placenta (tissue esterase)

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72
Q

where are hepatic microsomal enzymes located

A

hepatic smooth endoplasmic reticulum. also present in the kidneys, GI, and adrenal cortex

73
Q

microsomes

A

vesicle-like artifacts reformed from pieces of the ER bilayer sliced apart as cells are cut up

74
Q

microsomal enzymes

A

enzymes that are concentrated in these vesicle like artifacts

75
Q

enzymes responsible for phase 1 metabolism

A

CYP 450 enzymes, non-CYP 450 enzymes, and flavin-containing monooxygenase enzymes

76
Q

CYP 450 enzymes

A

large family of membrane-bound proteins containing a heme cofactor that catalyzes the metabolism of compounds, mostly hepatic microsomal enzymes, some mitochondrial P450

77
Q

CYP absorption peak

A

450nm when heme is combined with carbon monoxide

78
Q

CYP involves

A

oxidation and reduction steps. The most common reaction catalyzed by CPY is the monooxygenase reaction

79
Q

monooxygenase reaction

A

insertion of one atom of oxygen into an organic substrate while the other oxygen atom is reduced to water

80
Q

CYP family

A

share more than 40% sequence homology and designated by a number “CYP2”

81
Q

CYP subfamily

A

share more than 55% homology and designated by a letter “CYP2A”

82
Q

individual CPY enzymes

A

identified by a third number “CYP2A6”

83
Q

most abundantly expressed CYP

A

CYP3A4, most for anesthetic drugs

84
Q

CYP3A4 metabolizes

A

opioids (alfentanil, sufentanil, fentanyl), benzo, local anesthetics (lidocaine, ropivacaine), immunosuppressants (cyclosporine), and antihistamines (terfenadine)

85
Q

induction

A

increased expression of the enzymes. Ex: phenobarbital induces microsomal enzymes and thus can render drug less effective through increased metabolism

86
Q

inhibition

A

drugs directly inhibit enzymes, increasing the exposure to their substrates. Ex: grapefruit juice inhibits CYP3A4, increasing the concentration of anesthetic drugs

87
Q

oxidation reaction

A

require an electron donor in the form of reduced nicotinaminde adenine dinucleotide and molecular oxygen for their activity

88
Q

steps in oxidation

A

the oxygen molecule is split, with one atom of oxygen oxidizing each molecule of drug and the other oxygen atom being incorporated into a molecule of water

89
Q

examples of oxidative metabolism of drugs

A

hydroxylation, deamination, desulfuration, dealkylation, and dehalogenation

90
Q

hydroxylation

A

a chemical process that introduces a hydroxyl group (−OH) into an organic compound

91
Q

deamination

A

Deamination is the removal of an amino group from a molecule

92
Q

desulfuration

A

removal of sulfur from a molecule

93
Q

dealkylation

A

Alkylation is a chemical reaction that entails transfer of an alkyl group. The alkyl group may be transferred as an alkyl carbocation, a free radical, a carbanion, or a carbene

94
Q

dehalogenation

A

chemical reactions that involve the cleavage of carbon-halogen bonds, oxidation of a carbon-hydrogen bond to form an intermediate metabolite that is unstable and spontaneously loses halogen atom

95
Q

demethylation

A

chemical process resulting in the removal of a methyl group from a molecule. Ex: morphine to normorphine (example of dealkylation)

96
Q

dehalogenation of volatile anesthetics

A

leads to a release of bromine, chloride, and fluoride

97
Q

aliphatic oxidation

A

oxidation of a side chain. Ex: oxidation of the side chain of thiopental converts the highly lipid-soluble drug to the more water-soluble carboxylic acid derivative

98
Q

thiopental desuluration

A

transforms into pentobarbital

99
Q

epoxide intermediates

A

capable of forming a covalent bond with macromolecules and can be responsible for drug-inducted organ toxicity, in oxidation

100
Q

CYP reduction

A

transfer electrons directly to a substrate such as halothane rather than to oxygen, electron gain happens only when insufficient amounts of oxygen are present to compete for electrons

101
Q

conjugation with glucuronic acid

A

glucuronic acid is synthesized from glucose and added to lipid-soluble drug to render them more water-soluble=glucuronide conjugates that are excreted into bile and urine

102
Q

reduced microsomal enzymes in neonates

A

interferes with conjugation leading to neonatal hyperbilirubinemia and the risk of bilirubin encephalopathy. decreased enzyme activity leads to increase drug effect and toxicity

103
Q

hydrolysis

A

do not involve the CYP enzymes, happens at the ester bond, occurs outside of the liver, adding water to a molecule to break it down and form smaller molecules

104
Q

phase 2 enzymes

A

glucuronosyltransferases, glutathione-S-transferases, N-acetyl-transferase, sulfotransferases

105
Q

uridine diphoshate glucuronosyltransferase

A

cataylzes the covalent addition of glucuronic acid to a variety of endo/exogenous compounds making them more water-soluble

106
Q

glucuronidation

A

propofol, morphine (morphine 3 glucuronide, morphine 6 glucuronide), midazaolam (alpha 1 hydroxymidazolam)

107
Q

Glutathione s transferase enzyme

A

defensive system for dextoificatin and protection against oxidative stress

108
Q

N acetyltranferase

A

common phase 2 reaction for metabolism for hertercyclic aromatic amines (serotonin), and arylamines (isoniazid)

109
Q

the rate of metabolism

A

is proportional to drug concentration, clearance of the drug is constant

110
Q

metabolic capacity

A

metabolism is no longer proportional to drug concentration b/c the metabolic capacity of the organ has been exceeded…450s are al busy

111
Q

Q

A

liver blood flow

112
Q

rate of drug metabolism (R)

A

Q(Cin)-Q(Cout)

113
Q

R

A

difference between drug concentration flowing into the liver and the drug concentration flowing out of the liver X the rate of liver blood flow

114
Q

metabolism can be saturated

A

liver does not have an infinite amount of metabolic capacity

115
Q

equation used for metabolic saturation

A

Response= C/C50+C
C=drug concentration
R=fraction of maximal metabolic rate (0-1)

116
Q

Response 0

A

no metabolism

117
Q

Response 1

A

maximal metabolism rate

118
Q

When C=0

A

the response is 0

119
Q

if C is between 0-50

A

response=C/C50

120
Q

C50

A

it is the concentration associated with 50% response

121
Q

C=C50

A

response = 0.5

122
Q

C= greater than 50

A

response = 1

123
Q

high concentrations the response saturates at

A

1

124
Q

most common view of rate of metabolism

A

function of the concentration flowing out of the liver Coutlow

125
Q

ER equation

A

Cinflow-Coutflow/Cinflow

126
Q

Hepatic clearance

A

QXER

127
Q

Drugs with an ER nearly 1

A

propofol, a change in liver blood flow produces a nearly proportional change in clearance

128
Q

Drugs with lower ER

A

alfentanil, clearance is nearly independent of the rate of liver blood flow

129
Q

capacity-limited clearance

A

ER less than 1, clearance is limited by the capacity of the liver to take up and metabolize the drug, changes in the liver blood flow will have little influence on clearance

130
Q

flow-limited capacity

A

nearly 100% of the drug is extracted by the liver, the liver has tremendous metabolic capacity for the drug. flow of drug to the liver is what limits the metabolic rate.

131
Q

renal excretion

A

involves GFR, active tubular secretion, passive tubular reabsorption

132
Q

the amount of drug that enters the renal tubular lumen depends on

A

the fraction of drug bound to protein and the GFR

133
Q

renal reabsorption is most prominent for

A

lipid-soluble drugs that can easily cross cell membranes of renal tubular epithelial cells to enter pericapillary fluid. Ex: thiopental

134
Q

products less lipid-soluble

A

limit renal tubule reabsorption and facilitate excretion in the urine

135
Q

rate of reabsorption from renal tubules is influenced by

A

pH and urine flow in the renal tubules

136
Q

passive reabsorption of weak bases and acids is altered by

A

urine pH

137
Q

weak acids

A

excreted more rapidly in alkaline urine, alkalinization of the urine results in more ionized drug that cannot easily cross renal tubular epithelilal cells, less passive reabsorption

138
Q

renal blood flow and creatinine clearance is inversely correlated with

A

age

139
Q

creatinine clearance is closely related to

A

GFR b/c creatinine is water-soluble and not resorbed in the tubules

140
Q

cockcroft and gault creatinine clearance (ml/min) equation

A

Men: (140-age)Xwightkg/72Xserum creatinine

141
Q

zero order kinetics

A

rate of change is constant, decreased by a fixed amount with each half-life

142
Q

first-order kinetics

A

which means that each half-life decreases the concentration by 50%

143
Q

undergo ester hydrolysis in the plasma and tissues.

A

Succinylcholine, remifentanil, esmolol, and the ester local anesthetics

144
Q

most drugs are

A

weak acids or weak bases, that are present in ionized and nonionized forms

145
Q

nonionized molecules

A

usually lipid-soluble and can diffuse across cell membranes including the BBB, renal tubular epithelium, GI epithelium, placenta, and hepatocytes.

146
Q

nonionized form of the drug

A

that is pharmacologically active, undergoes reabsorption across the renal tubules, is absorbed in the GI tract, and susceptable to hepatic metabolism

147
Q

ionized molecules

A

poorly lipid-soluble and cannot penetrate lipid cell membranes easily

148
Q

ionized drugs

A

ionization impairs absorption of drugs from the GI tract, limits access to drug-metabolizing enzymes in the hepatocytes, and facilitates excretion of unchanged drugs, reabsorption is unlikely.

149
Q

pKa

A

the drugs disassociation constant, where is 50/50

150
Q

degree of ionization is a

A

function of its pKa and its pH of the surrounding fluid

151
Q

when pK and pH are identical

A

50% ionized, 50% unionized

152
Q

acidic drugs like barbiturates

A

tend to be highly ionized at an alkaline pH, usually supplied in a basic solution to make them more soluble in water

153
Q

basic drugs like opioids and local anesthetics

A

tend to be highly ionized in acidic pH, usually supplied in a acidic solution to make them more soluble in water

154
Q

ionized

A

charged, impermeable to the cell membrane

155
Q

bases are more ionized below

A

acids are more ionized above

156
Q

systemic administration of a weak. base (opioid) can result in

A

accumulation of ionized drug (ion trapping) in the acid environment of the stomach, also basic drugs cross the placenta from mother to fetus bc the fetal pH is lower than the mother pH

157
Q

ion trapping from mother to fetus

A

the lipid-soluble nonionized crosses the placenta and is converted to a poorly lipid-soluble ionized fraction in the more acidic environment of the fetus. the ionized fraction in the fetus can not easily cross the placenta to the maternal circulation

158
Q

pregnancy is a/w

A

increased creatinine clearance and a higher dose requirment

159
Q

systemic absorption of the drug depends on the drugs

A

solubility

160
Q

disadvantages or oral route

A

emesis caused by irritation of the GI mucosa by the drug, destruction of the drug by digestive enzymes or acidic gastric fluid, irregularities in absorption in the presence of food or other drugs

161
Q

oral drug onset of drug effect

A

determined by the rate and extent of absorption from the GI tract

162
Q

oral mostly absorbed in

A

small intestine d/t large surface area, small intestine is alkaline, enhances the absorption of weak bases (opioids) but even weak acids are mostly absorbed here bc of the large surface area

163
Q

pH in the GI tract that favor the drug in the nonionized form

A

lipid soluble, favor systemic absorption

164
Q

first pass hepatic metabolism

A

drugs absorbed from the GI tract enter the portal venous blood and thus pass through the liver before entering the systemic circulation for delivery to tissue receptors, this is the reason for large differences in the pharmacologic effect of oral and OV doses (lidocaine/propranolol)

165
Q

which route bypasses the liver, preventing first pass metabolist

A

sublingual or buccal , these drugs flow into the superior vena cava, nasal also bypasses

166
Q

transdermal route

A

provides sustained therapeutic plasma concentrations of the drug and decreases the likelihood of loss of therapeutic efficacy d/t peaks and valleys a/w intermittent drug injections

167
Q

transdermal high pt compliance

A

not as complex as continuous infusion techniques and low incidence of s/e

168
Q

drugs that favor transdermal absorption

A

combined lipid and water solubility, molecular weight of <1,000, pH 5-9 in a saturated aqueous solution, absence of histamine releasing effects, daily dosing requirements <10mg

169
Q

scopolamine and nitroglycerin

A

sustained plasma concentrations by the transdermal absorption results in tolerance and loss of therapeutic effect

170
Q

skin layer that deals with rate-limiting

A

diffusion across the stratum corneum, hair follicles and sweat ducts is where initial absorption occurs

171
Q

what effects skin absorption

A

skin permeability, thickness, scopolamine only works behind the ear (postauricular zone) its the thin and high temp

172
Q

day limit to transdermal patches

A

7 days b/c the stratum corneum sloughs and regenerates about 7days, also bc of contact dermatitis

173
Q

drugs administered in the promixmal rectum

A

are absorbed into the superior hemorrhodial veins and transported via the portal venous system to the liver, undergoing the first pass metabilizism

174
Q

drugs administered more distally

A

absorbed directly into the systemic circulation bypassing the liver

175
Q

systemic clearnace

A

the clearance for drugs permantely removed from the central compartment, clears drug from the entire system

176
Q

intercompartmental clearnace

A

clearances between the central compartment and the peripheral compartment

177
Q

concentration equation

A

Co=Xo/V
Xo is the amount of drug at time zero
V is the volume of that compartmenth

178
Q

how to rearrange the concentration equation for target concentration

A

Dose=CtXV

179
Q
A

Pharm Semester 2, test 1 (1 decks)

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