exam 1 Flashcards

1
Q

Transfer of drug from site of administration to systemic circulation

A

Absorption

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2
Q

Transfer of drug from systemic circulation

A

Distribution

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3
Q

Enzymatic alteration of a drug

A

Metabolism

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4
Q

Removal of a drug from the body

A

Excretion

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5
Q

metabolism + excretion

A

Elimination

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6
Q

Action of the drug on the body

The reason you take the drug

A

Pharmacodynamics

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7
Q

Action of the body on the drug

Fate of the drug in the body

“ADME”

A

Pharmacokinetics

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8
Q

The more _____________ the drug, the easier it is to cross the cell membrane

A

lipophilic

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9
Q

Hydrophilic

A

heads

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10
Q

lipophilic:

A

tails

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11
Q

The extent of drug absorption

A

bioavailability (F)

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12
Q

what is the primary area of absorption

A

duodenum

(dissolution + disintegration = stomach)

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13
Q

reflects loss of drug due to hepatic (and intestinal) metabolism on the way to the systemic circulation

A

first pass effect

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14
Q

what type of drug form diffuses across membrane

A

NON-ionized (lipid soluble)

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15
Q

where does the majority of metabolism occur

A

plasma or central compartment (where the kidneys and the liver reside)

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16
Q

true or false
IV (both infusion and single dose/bolus) are always 100% or 1

A

true

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17
Q

what are the 3 steps of distribution

A

1st disintegration: drug leaves the capsule; optional step (e.g., suspensions)

2nd dissolution: drug molecules dissolve in gastric fluid

3rd absorption

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18
Q

_____________ = metabolism + excretion

A

elimination

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19
Q

The more ____________ the drug, the easier it is to cross the barrier

A

lipophilic

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20
Q

the heads of the membrane are _______________

A

Hydrophilic

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21
Q

the tails of the membrane are ________________

A

Lipophilic

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22
Q

______hill Transport = Passive

A

DOWN

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23
Q

What is an example of passive diffusion

A

facilitated diffusion

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24
Q

particles that are transported by facilitated diffusion (passively) are (4):

A

o Small (monomers)
o Polar (water-soluble/hydrophilic)
o Charged ions (e.g., glucose, Ca, Cl, Na, K)
o Transport proteins (e.g., membrane transporters)

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25
Q

2 types of facilitated diffusion

A

pores/channels
carrier proteins

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26
Q

___hill Transport = Active

A

UP

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27
Q

factors that influence the GI tract

A
  • GI motility
  • Gastric emptying
  • Intestinal motility
  • Perfusion of the GI tract
  • Presence of other drugs
  • Presence or absence of food
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28
Q

second opportunity to be absorbed

A

enterohepatic recycling

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29
Q

which form is most easily absorbed

A

un-ionized form

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30
Q

Primary site for drug:
disintegration + dissolution

A

stomach

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31
Q

Primary site for oral drug:
absorption

A

duodenum

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32
Q

binding to tissue/protein components

A

ADsorption

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33
Q

water-soluble, high protein binding

A

small/low Vd

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34
Q

lipid-soluble, low protein binding

A

large/high Vd

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35
Q

> ____% protein bound = highly protein bound

this IS clinically relevant for protein binding issues

A

> 90%

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36
Q

what 3 things create DIFFICULT transport

A

tight junctions
astrocytes
pericytes

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37
Q

what 2 things create EASY transport

A

lipophilic/un-ionized
small molecular weight

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38
Q

If an efflux transporter is exposed to a drug inhibitor (preventing the efflux pump from working properly), it will ___________ the likelihood of absorption

A

ENHANCE

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39
Q

EFFLUX transporter example

A

ATP-Binding Cassette (ABC) Transporters

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40
Q

INFLUX transporter example

A

Solute Carrier Transporters (SCT)

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41
Q

Factors Impacting Drug Binding for HIGHLY Bound (>90%) Plasma Proteins

A
  • Protein concentration
  • Protein size (Da, kDa)
  • Number of protein binding sites; bound (CB)
  • Association binding constant
    o Measure of the tightness of the binding (whether the drug can detach from a protein easily)
  • Concentration of unbound drug (Cu) or free drug (Cf)
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42
Q

hydrostatic balance; keeps the blood volume intact

medium MW
large concentration

A

albumin

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43
Q

medium MW
VARIABLE concentration (goes up in times of stress; non-detectable in healthy people)

A

a1-acid glycoprotein (AAG)

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44
Q

protein carrier of fat

large MW
small concentration

A

lipoprotein

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45
Q

Factors that Decrease Albumin Concentrations

decreased protein synthesis

A

liver dx

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46
Q

Factors that Decrease Albumin Concentrations

excess elimination of protein

A

kidney dx

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47
Q

Factors that Decrease Albumin Concentrations

increased protein catabolism

A

trauma, surgery

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48
Q

Factors that Decrease Albumin Concentrations

decreased protein synthesis and increased protein catabolism

A

malnutrition

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49
Q

Factors that Decrease Albumin Concentrations

distribution of albumin into extravascular space

A

burns

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50
Q

Metabolism =

A

Biotransformation
* Enzymatic (usually) or non-enzymatic

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51
Q

what 3 things impact the liver metabolism

A

blood flow
enzyme activity
protein binding

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52
Q

the liver makes the drug more ______________, _____________ the polarity (so that the kidneys can eliminate it)

A

HYDROphilic
INCREASED polarity

so that it can be eliminated

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53
Q
  • Drugs are transported into hepatocytes by
A

o 1) Passive diffusion
o 2) Carrier-mediated transport

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54
Q

4 Major Consequence of Drug Biotransformation/Metabolism

A
  • Increase in water solubility
  • Increase in rate of elimination
  • Termination of biologic activity
  • Bioactivation (desired or undesired)
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55
Q

Something that is not pharmacologically activated until the body does something to activate it

Normally metabolized to their active form, and then can be metabolized further

A

prodrug/desired drug

codeine

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56
Q

Instead of being inactive, it is __________, and could be transformed into an active metabolite, same effect, or different effect from a drug

A

active drug

demerol (normeperidine)

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57
Q

superfamily of monooxygenases

Heme-containing enzymes, catalyze the oxidation of organic substances

A

CYP450

phase 1
of hepatic metabolism

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58
Q

o Conjugation reactions
o Glucuronide

A

phase 2
of hepatic metabolism

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59
Q

P-Glycoprotein (P-gp) or ABC-B1

A

ABC transporters
efflux

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60
Q

Proposed to predict the kinetics of drugs such as
digoxin,
cyclosporine
and fexofenadine

A

P-Glycoprotein (P-gp) or ABC-B1

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61
Q

transporters: influx

A

SLC transporters (solute carrier)

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62
Q

Located on both the basolateral/blood/plasma side and the apical/lumen/organ side

A

SLC (influx) + ABC (efflux)

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63
Q

plasma/blood
side

A

basolateral

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64
Q

lumen/organ
side

A

apical

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65
Q

most important factor for excretion

A

nephron

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66
Q

transporters actively making the drug more concentrated in the urine

A

secretion

(example: abx)

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67
Q

drug gets placed back into the plasma/blood from the urine; GIVE EXAMPLE

A

reabsorption

lithium is example

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68
Q

If clearance of a drug is LESS than < 120 ml/min, then we know the drug is filtered + net ___________________

A

reabsorption

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69
Q

If clearance of a drug is MORE than > 120 ml/min, then we know the drug is filtered + net ______________

A

secretion

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70
Q

taken back up through the portal vein into the liver

A

enterohepatic recycling

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71
Q

Excretes drug by emptying into the duodenum

A

bile

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72
Q

_______________ ____________ is why some drugs have a long half-life

A

enterohepatic recycling

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73
Q

Primary drug of
biliary extraction (intact or as metabolites)

A

diazepam

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74
Q

Primary drug of
enterohepatic circulation:

A

morphine

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75
Q

Determinants in the Selection of Drug Route

A
  • Type of desired effect
  • Physiochemical properties
  • Rapidity of effect
  • Quality of effect
  • Condition of patient
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76
Q

Pharmacokinetic Parameters:
Assessment of ________________

A

Bioavailability

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77
Q

Max concentration

A

Cmax

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78
Q

Time to max concentration

A

Tmax

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79
Q

the % of the drug available to systemic circulation

fraction absorbed from gut

The rate and extent to which an active drug ingredient or therapeutic moiety is absorbed from a drug product and becomes available at the site of action

A

Bioavailability (F)

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80
Q

rate + extent of drug exposure in the body

A

Area Under the Curve (AUC)

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81
Q

RATE of ELIMINATION, per unit of time

A

K
hr-1, min-1, sec-1

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82
Q

Rate of elimination, per unit of time (K)
o Linear vs. non-linear (____________-________)

A

Michaelis-Menten

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83
Q

VOLUME of drug eliminated per unit of time

A

clearance (Cl)
ml/hr, L/min

only ml or L!

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84
Q

hour, min, seconds

A

t 1/2 life

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85
Q

5 x t1/2 =

A

steady state

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86
Q

ml or L only

A

Vd

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87
Q

The comparison of bioavailability of different formulations, drug products, doses, or batches of the SAME drug product

Example: tablet vs solution

A

bioequivalence

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88
Q

example of drug with narrow therapeutic index/range

A

phenytoin

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89
Q

most drugs have a _______ therapeutic index

A

WIDE

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90
Q

peak (tied to _________) and a trough (tied to _________)

A

efficacy

toxicity

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91
Q

AUC:MIC

A

AUC: minimum inhibitory concentration (MIC) needed to kill off bacteria

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92
Q

amount= changes
fraction= constant

A

first order

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93
Q

most common route of elimination

follows natural log

K= h-1, sec-1, min-1

A

first order

94
Q

amount=constant
fraction=changes

example: ethanol/beer

A

zero order

95
Q

least common

K0 = amount/time (mg/h, g/h, mcg/min)

“Saturation Kinetics”

A

zero order

96
Q

1st: First-order elimination
at low amounts

2nd: Zero-order elimination at high amounts/saturation

A

Mixed order (Michaelis-Menten)

97
Q

example of mixed order

A

phenytoin

98
Q

2 phases:
1st: Alpha=distribution phase
2nd: Beta=elimination phase

A

TWO-compartment model

99
Q

Hydrophilic
Bound drug

Example: digoxin
(not in the heart right away, takes time to equilibrate between plasma and heart tissue)

A

TWO-compartment model

100
Q

Instantaneous

Lipophilic
Unbound drug

A

ONE-Compartment model

101
Q

1st: central/plasma
2nd: rapidly goes into CNS
3rd: slowly goes into fat or adipose tissue (leading to drug accumulation and side effects)

Example: general anesthetics

A

THREE-compartment model

102
Q

4 main hepatic enzymes

A
  • CYP3A4
  • CYP2C9
  • CYP2C19
  • CYP2D6
103
Q

fraction not bound to protein

A

fu

104
Q

innate ability of liver enzymes to metabolize (intrinsic clearance)

A

Cl int

105
Q

well-stirred model

A

hepatic clearance

impacted by:
1) QH: liver blood flow

2) Clint: innate ability of liver enzymes to metabolize (intrinsic clearance)

3) fu: fraction NOT bound to protein

106
Q

bioavailability provides evidence by understanding how much of a drug is metabolized*

A

first pass effect

Absolute: AUCPO x DoseIV/ AUCIV x DosePO

107
Q

Basis for determining GFR in the clinical setting

This is because it is almost exclusively filtered by the kidneys

A

Creatinine Clearance (CrCl)

108
Q

equation that utilizes serum creatinine for GFR estimation

A

Cockcroft and Gault Equation

109
Q

fraction excreted unchanged in the urine

A

fe

110
Q

Assumptions/True Statements:

Bioavailability (F) = 1 or 100% is available at time zero (0)

C0 (initial concentration), Tmax, Vd = 100% of drug delivery

Not effected by the “first pass effect”

A

IV bolus

111
Q

One Compartment Model = ___________ Compartment

A

CENTRAL

primarily hydrophilic drugs

112
Q

Assumptions/True Statements:

Vd is complete at time = 0 (Tmax)
Distribution equilibrium is instantaneous

A

IV BOLUS + ONE comparment model

113
Q

mcg/ml, mg/L, etc

A

AUC

114
Q

concentration at a given time

A

Ct

115
Q

initial concentration at time=0

A

Co

116
Q

RATE of elimination between Co and Ct

A

K

117
Q

time between Co and Ct

A

T

118
Q

Assumptions/True Statements:

Bioavailability (F) = 1 or 100%

You CANNOT assume that 100% of the drug is there at time = 0 (Co = 0)

Cmax, Tmax, Vd = 100% of drug delivery

Enters the body: zero order
Leaves the body: first order elimination

A

IV INFUSION

119
Q

C0 (initial concentration), Tmax, Vd = 100% of drug delivery

Tmax = time 0

A

bolus

120
Q

Cmax, Tmax, Vd = 100% of drug delivery

A

infusion

121
Q

true or false

amount/concentration eliminated is HIGHER at the beginning in FIRST order

A

true

122
Q

takes into account ln, NOT evenly spaced on the Y axis

A

semi-log paper (first order)

123
Q

The more the drug-to-enzyme interactions, the ____________ the binding

A

stronger

124
Q

The degree to which a drug acts on a given site relative to other sites

A

selectivity

125
Q

The dose range of a drug that provides safe and effective therapy with minimal adverse effects

A

therapeutic window

126
Q

Binds to a receptor and turns it “on”; causing activation of signaling cascades within the cell

A

agonist

127
Q

Binds to a receptor and turns it “on”; LESS EFFICACY than full agonists

A

PARTIAL agonist

128
Q

Binds to a receptor and does not activate it

A

antagonist

129
Q

Most drugs bind to ____ type of receptor

This can result in “non-discriminatory” negative effects

A

> 1

example: antipsychotics and antidepressants

130
Q

receptors are STILL THERE, by constantly stimulating it, you keep the G-proteins from interacting with the receptor (the drug binds and no response occurs)

A

desensitization

131
Q

Over time, the receptor is physically REMOVED from the membrane, it is not there anymore

A

down-regulation

132
Q

true or false

down-regulation occurs with AGONISTS

A

true
tolerance develops

albuterol, insulin

133
Q

When a constant stimulus (agonist) is applied to a receptor, the cell’s response will diminish over time

A

tolerance

134
Q

RAPID development of tolerance

To achieve the same response: must increase the dose

A

tachyphylaxis

135
Q

at the drug/receptor level:

the observed response is not the %, but rather the ___________

A

number/amount

1,000 receptors at 50% is > 10 receptors at 50%

136
Q

Over time, more receptors appear on the membrane

Antagonists: constant blockade of a receptor

Sensitivity occurs if meds abruptly stopped

A

up-regulation

“BUS”

137
Q

fastest “receptor”

A

LIGAND-gated ion channels (milliseconds)

138
Q

example of ion channels

A

o Examples: nicotinic; Ach
o Drug: Lidocaine, NMBs, Lorazepam

139
Q

2nd fastest “receptor”

A

G-protein coupled receptors (GPCRs)

140
Q

example of G-protein coupled receptors (GPCRs)

A

o Examples: muscarinic; Ach
o Drug: epi, opioids

141
Q

6 main types of “receptors”

A
  • 1) Ion channels
  • 2) G-protein coupled receptors (GPCRs)
  • 3) Transmembrane receptors
  • 4) Intracellular receptors
  • 5) Extracellular enzymes
  • 6) Cell surface adhesion receptors
142
Q

Shift the dose-response curve to the ______ (more SENSITIVE)

A

LEFT

lorazepam + GABA

143
Q

Receptor activated ion channel
example

A

Muscarinic M2 in the nodal cardiac tissue w/ vagal nerve stimulation; the channel is being altered by a receptor

144
Q

VOLTAGE Gated

Some drugs bind to the:
 Inactivated state (propafenone)
 Activated state

A

Local anesthetics

145
Q

Neuromuscular, nicotinic

A

LIGAND GATED ion channels

146
Q

comprised of abY subunits

A

heterotrimeric

147
Q

Alpha a subunit gives up ______, takes on GTP

A

GDP

GTP is activated

148
Q

How can closely related GPCRs cause completely OPPOSING cellular responses

A

TYPE of ALPHA subunit; G PROTEIN types are different

149
Q

How can UNrelated GPCRs cause a similar cellular response

A

similar G-protein pathways

150
Q

What are the 2 steps for drug-receptor binding

A

1) binding = receptor occupancy
2) activating = tissue response

151
Q

Numerator=_____________=K off

A

dissociation

152
Q

Denominator=______________= K on

A

association

153
Q

Kd

the lower the value, the _________ the affinity of the drug

A

higher

154
Q

Reflects the ligand concentration at which 50% (half) of all available receptors will be BOUND with ligand

A

Kd

155
Q

only _________ can cause a tissue response/activate a receptor

A

agonists

156
Q

lower affinity = _________ shift

A

lower=RIGHT (you need a HIGHER concentration to achieve the % bound)

157
Q

higher affinity = _________ shift

A

higher=LEFT

158
Q

receptor occupancy, % bound

A

Kd
Bmax

159
Q

tissue response, % effect

A

EC50
Emax

160
Q

effective concentration for 50% (half) of max EFFECT

A

EC50

161
Q

the response/effect elicited by a drug

A

efficacy

162
Q

efficacy is determined by 2 things

A

Related to the NUMBER of ligand-receptor complexes formed

Related to the EFFICIENCY in which the ligand-receptor complex can produce a response

163
Q

How is efficacy assessed from the dose-response graph

A

How high the Emax plateaus

  • Antagonist= 0 efficacy
  • Partial agonist= halfway
  • Full agonist= all the way at the top (100%)
164
Q

INVERSELY related to drug concentration required to produce a defined effect or response

A

potency

Potency is a comparable thing

165
Q

morphine and fentanyl have the same _________, but different potency

A

efficacy

166
Q

HIGHER EC50=*

A

requires MORE to obtain the same effect

“weaker drug”

167
Q

surmountable antagonist

A

Reversible/Surmountable/Competitive

168
Q

full agonist + reversible antagonist

would cause a ___________ shift

A

RIGHTward shift (would require additional agonists to achieve the same response)

169
Q

full agonist + IRreversible antagonist

would cause a ___________ shift

A

DOWNward shift
because you would have less max attainable effect

170
Q

example of physiologic antagonists

counteracts each other

A

glucagon and insulin

171
Q

example of chemical antagonists

interacts directly with the drug

A

protamine and heparin

172
Q

example of a
Partial Agonist + Full Agonist

A

Abilify
Schizophrenia drug (D2 partial agonist)

173
Q

Partial Agonist + Full Agonist
EXCESS dopamine

A

DOWNward shift

174
Q

Partial Agonist + Full Agonist
DEFICIENT dopamine

A

UPward shift

175
Q
  • Considered the safety factor of a drug
  • The relationship between the amount of drug that causes a specific adverse effect and the amount that causes the desired effect
A

Therapeutic Index/Range

176
Q

You want the toxic dose to be __________ than the dose that causes the desired effect*

A

higher

this causes a wide TR

177
Q

examples of mismatch between:
Drug Level and Drug Effect
(3)

A

Irreversible/pseudo-irreversible binding to a receptor

Clotting factors (half-lives of 2-3 days)

Exceptionally high therapeutic index (“very safe” drugs with high doses)

178
Q

examples of
irreversible/pseudo-irreversible binding to a receptor

A
  • Omeprazole, Plavix, Exelon

Half-life and duration do NOT match up

179
Q

true or false
Even beta1 selective drugs (like metoprolol) still have some effect on beta2 receptors (CAUTION with asthma)

A

true

180
Q
  • Once activated, they initiate a phosphorylation cascade
  • Similar to G-protein coupled receptor, but uses a different second messenger
  • Changes gene transcription, takes hours
  • Example: insulin receptor
A

Kinase Linked Receptors

181
Q

often in anesthesia; can use lower doses to achieve the same effect

A

synergistic
1+1=3

182
Q

usually the drugs act on the same site

A

additive

183
Q

effect of one drug with known effect is increased by a 2nd drug that does not have that effect
o Levodopa + carbidopa

A

potentiation

184
Q

4 types of CNS depressants that work on GABA

A

Benzos (versed)

Barbiturates (phenobarbital)

Ethanol

most IV + volatile anesthetics

185
Q

positive allosteric modulators
increase the (2)

A

FREQUENCY of the chloride channel opening
or
DURATION of chloride channel opening

186
Q

Opioids + inhaled anesthetics

Majority effect: ____________

A

analgesia

187
Q

Opioids + benzos
effect: ____________

A

Sedation

188
Q

is sweating common with PNS symptoms

A

yes

189
Q

anti-muscarinics should be cautioned with ____________

A

elderly

190
Q

6 examples of anti-muscarinics

A

Benztropine: treats Parkinson’s

Prochlorperazine: anti-emetic

Diphenhydramine: blocks histamine + muscarinic, motion sickness

Atropine: dries secretions, bradycardia

Glycopyrrolate: dries secretions, bradycardia

Scopolamine: motion sickness, N/V

191
Q

o Hyperkalemia can cause (6)

A

 Bradycardia
 Heart block
 Muscle weakness
 Flaccid paralysis
 Metabolic acidosis
 Death

192
Q

DILATE the AFferent arteriole
(Increase blood flow into glomerulus)

A

prostagladins

193
Q

CONSTRICT the EFferent arteriole
(Decreases outflow from glomerulus)

A

ATII

194
Q

NSAIDS inhibit _________________

A

prostaglandins

195
Q

ACEi/ARBs decrease production of ______

A

ATII

think “A&A”

196
Q

long-acting; opioid treatment therapy

A

naltrexone

197
Q

With naltrexone levels decreased (at the end of dosing interval), the body has upregulated the opioid receptors, leading to an ________________ response to opioids

A

exaggerated response!

198
Q

INCREASE in transporters or metabolizing enzymes

A

induction

199
Q

INHIBITION of transporters or metabolizing enzymes

A

inhibition

200
Q

with a drug that INHIBITS P-gp activity, ________ digoxin will stay in the body

A

MORE will stay

201
Q

with a drug that INDUCES P-gp activity, ________ digoxin will stay in the body

A

LESS will stay

202
Q

what are the 4 INDUCERS for CYP3A4*

A

Carbamazepine
Rifampin
Phenobarbital
Phenytoin

“CRPP”

203
Q

what are the 8 INHIBITORS for CYP3A4:

A

macrolide abx (clarithromycin)
verapamil
diltiazem
grapefruit juice
HIV protease inhibitors (ritonavir)
cyclosporines
amiodarone
azoles (antifungals)

“My sons, Vera and Dilt are grapeful to navigate their cycles amid the Azoles.”

204
Q

with INHIBITORS, it will lead to toxicity, except with ____-_______

A

pro-drugs

opposite effect (fewer active metabolites are occurring due to inhibition of metabolism; so, there is LESS therapeutic effect; example: codeine)

205
Q

major types of inhibitors

A

1) Reversible: temporary

2) Irreversible: permanent
Example: clarithromycin

206
Q

Which type of drug is more absorbed

A

non-ionized

207
Q

Chelation is a type of ____________

A

absorption

208
Q

examples of di-valent and tri-valent cations

A

minerals
Calcium, Iron, Zinc, Magnesium, Aluminum
(Antacids, dietary/vitamin supplements, dairy products)

they DECREASE absorption of some drugs when taken together

209
Q

when taking minerals, wait at least 2-4 hours for these 3 types of drugs

A
  • TetraCYCLINES (doxycycline, minocycline)
  • Quinolones (levofloxacin, moxifloxacin)
  • Osteoporosis drugs
210
Q

INHIBITION leads to

A

toxicity (except with prodrugs)

211
Q

INDUCTION leads to

A

decreased drug effects

212
Q

Any drug that is ____ protein bound can be passively filtered

A

NOT protein bound = passive

213
Q

true or false
URINE filtration is passive and does NOT use transporters

A

true
it is passive

214
Q

ligand gated*
how long?

A

milliseconds

215
Q

g-protein*
how long?

A

seconds

216
Q

kinase-linked*
how long?

A

hours

217
Q

nuclear*
how long?

A

hours

218
Q

alterations in DNA inherited from a parent and are found in the DNA of virtually all cells

A

hereditary/germline

219
Q

alterations in DNA that develop throughout a person’s life

A

acquired/somatic

220
Q

examples of pharmacoDYNAMICS

A

drug-receptor,
agonists/antagonists
therapuetic effect vs toxic effects
downregulation vs upregulation

the reason you take the drug

221
Q

examples of pharmacoKINETICS

A

ADME

first pass effect
Vd
Cmax, tmax, bioavailability

222
Q

human genome started

year

A

1990

223
Q

sequencing center

year

A

2001

224
Q

finished version of human genome sequence completed

year

A

2003

225
Q

laboratory (one illumina sequencer)

year

A

2017

226
Q

rare, single gene, several mutations, large phenotypic effect
o Example: down syndrome

A

mendelian/simple

227
Q

2 different versions/alleles

A

polymorphic

228
Q

DNA variants for which we know the location in the genome and can easily determine a person’s genotype

A

marker loci

229
Q
  • Tailoring medical prevention and treatment therapies to the characteristics of each patient, improving their quality of life and health outcome
    o “The right medicine to the right person at the right dosage at the right time”
A

precision medicine

230
Q

Example of Pharmacogenomics (gene)

A

CYP2D6: codeine

231
Q

true or false

IV infusion is F=1

A

true
anything IV, whether infusion or bolus