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PAS 506 > Exam 2 (Pharm) > Flashcards

Exam 2 (Pharm) Flashcards

1
Q

Pharmacology

A

Study of substances interacting with living systems through chemical process

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2
Q

Pharmacodynamics

A

Action of drug on body.
Used to determine drug group class and appropriateness for treatment.

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3
Q

Pharmacokinetics

A

Actions of body on drug.
ADME.
Absorption
Distribution
Metabolism
Excretion

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4
Q

Drug

A

Chemical or substance that causes physiologic effect when introduced to the body.
Cause a change in biological function through chemical actions

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5
Q

Medication

A

Specific chemical preparation of one or more drugs for therapeutic effect

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6
Q

Medical Pharmacology

A

Study of substances designed to prevent, diagnose, and treat diseases

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7
Q

Toxicology

A

Study of unwanted effects of chemicals on living systems

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8
Q

Receptor

A

Target of drug.
Responds to specific signaling molecules

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9
Q

Ligand

A

Signaling molecule that binds to receptor

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10
Q

Flycosides

A

Carbohydrate portion of plant with one or more sugar combined with hydroxy compound. Used as natural drug

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11
Q

Where do essential oils come from

A

Leaves, root, bark

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12
Q

Where are fixed oils and mineral oils from

A

Seeds

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13
Q

Protamine Sulfate

A

Heparin antidote from fish sperm

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14
Q

Heparin

A

Anticoagulant from pig intestine

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15
Q

Premarin

A

Estrogen replacement from horse urine

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16
Q

What are minerals often used for

A

Homeostasis

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17
Q

Where all can natural drugs come from

A

Plants
Animals
Marine
Minerals
Microorganisms

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18
Q

Pros of natural drugs

A

Natural affinity
Specific to binding targets

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19
Q

Disadvantages of natural drugs

A

Costly
Less sustainable
May work differently than expected

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20
Q

Semi-synthetic drugs

A

Naturally occurring substances that have been chemically altered (ex. paclitaxel from yew needles)

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21
Q

Synthetic drugs

A

Fully man made drugs.
Majority of drugs are made this way

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22
Q

Example of recombinant DNA being used to make drugs

A

Plasmid DNA of bacterium taken out and a section is cut out and replaced with part of human genome (ex. insulin).

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23
Q

Covalent

A

Strong bonds.
Usually not reversible

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24
Q

Electrostatic (ionic) bonds

A

More common than covalent bonds.
Vary in strength

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25
Q

Hydroohobic bonds

A

Very week.
Important in interactions of highly lipid soluble drugs with receptors

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26
Q

Phase 1 of drug development

A

Safety.
Small number of healthy volunteers

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27
Q

Phase 2 of drug development

A

Efficacy.
hundreds of pts with disease used.
Single blind studies

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28
Q

Phase 3 of drug development

A

Efficacy.
More controlled studies in thousands of pts.
Double blind and cross over
Apply for NDA

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29
Q

Phase 4 of drug development

A

Post-marketing surveillance AFTER drug goes to market

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30
Q

Translational research

A

Moving drug from science lab to clinic for screening and testing

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31
Q

Me too analog of a drug

A

tweaking a molecule to make it work better or have less side effects

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32
Q

Composition of matter patent

A

Filed for ef]ffective novel compound

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33
Q

Use patent

A

Filed for new and nonobvious use for a previously known chemical

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34
Q

Lifetime of a patent

A

20 years

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35
Q

Trademark

A

Drugs proprietary (brand) name

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36
Q

No-effect dose

A

max dose at which toxicity is not seen

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37
Q

Minimum lethal dose

A

smallest dose observed to kill any experimental animal

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38
Q

Median lethal dose (LD50)

A

dose that kills 50% of animals in test group

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39
Q

How long do clinical trials take

A

4-6 years

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40
Q

Crossover experiment design

A

Alternates periods of administration of test drug, placebo preparation, and standard treatment in each individual patient to minimize cofounding factors.

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41
Q

What factors of patients might effect study results

A

Presence of other diseases.
Lifestyle of subjects.

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42
Q

How soon do adverse drug rxns need to be reported

A

Reported within 15 days to the FDA through MedWatch

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43
Q

FD&C Act of 1938

A

Required new drugs to be safe and pure.
Labes should containd directions.
Mandated premarket approval by FDA.
Did NOT require proof of efficacy

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44
Q

Kefauver-Harris Amendment (1962)

A

Required proof of efficacy

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45
Q

FDA Amendments Act of 2007

A

Granted FDA greater authority.
Required post-approval studies.
Made clinical trial operations more visible to the public.

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46
Q

FDA Safety and Innovation Act of 2012

A

Gave FDA authority to accelerate approval of urgently needed drugs.

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47
Q

Therapeutic drugs

A

Based on usefulness in treating disease.
ex. Antihypertensives, antidepressants, antihyperlipidemics.

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48
Q

Pharmacologic Drugs

A

Based upon mechanisms of action.
ex. ACEI, ARBs, Beta-blockers

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49
Q

Schedule I drugs

A

-High potential for abuse
-No current accepted med use
-No safety for use

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50
Q

Schedule II drugs

A

-High potential for abuse
-can’t be refilled
-Some accepted medical use with severe restrictions.
-Potential for severe physical and/or psychological dependence

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51
Q

Schedule III drugs

A

-Less potential for abuse than schedule I or II.
-can be refilled up to 5 times (6 month supply)
-Some medical use accepted.
-Potential for low or moderate physical dependence and/or high psychological dependence

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52
Q

Schedule IV

A

-Low potential for abuse relative to schedule III.
-Current accepted medical use
-Limited dependence to schedule III when abused

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52
Q

Schedule V drugs

A

-Low potential for abuse
-Current accepted med use
-Less potential for producing psychological or physical dependence

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53
Q

Pregnancy drug category A

A

Controlled studies show no risk (safe)

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54
Q

Pregnancy drug category B

A

No evidence of risk in humans, but animal research finds risk.

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55
Q

Pregnancy drug category C

A

Risk cannot be ruled out. Human studies are lacking and animal studies are lacking or show risk.

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56
Q

Pregnancy drug category D

A

Positive evidence of risk, but benefits might outweigh the risk.

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57
Q

Pregnancy drug category X

A

NEVER give to pregnant

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58
Q

Active receptor

A

Constitutive (continuous) activity without ligand.

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59
Q

Inactive receptor

A

Dormant until ligand binds turning it on

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60
Q

Factors that affect activation of receptors

A

Specificity.
Selectivity.
Affinity.

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61
Q

Specificity

A

Capacity of drug to cause action by binding to receptor.
If high, drug has only one intended effect.
If low, lots of side effects.
Making a certain thing happen when you open the door.

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62
Q

Selectivity

A

Ability of drug to discriminate between target receptors.
If high, less side effects bc not binding with similar receptors.
If low, lots of side effects
Like using the right key to open the right door.

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63
Q

Affinity

A

Strength of attraction between drug and receptor.
High affinity has low dissociation constant and is associated with lower dose requirement

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64
Q

Dissociation constant (Kd)

A

Concentration of drug that occupies 50% of available receptors

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65
Q

Agonist

A

Binds to and activates receptor.
Causes a change in conformation of receptor or incorporation of machinery.
Can be direct or indirect effect

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66
Q

Full agonist

A

Activates receptor-effector systems to max.

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67
Q

Partial agonist

A

Binds and activates receptor with less effect.
Acts as agonist in absence of full agonist.
Acts as antagonist in presence of full agonist.
Useful in withdrawal patients to relieve withdrawals without giving them a high

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68
Q

Inverse agonist

A

Binds to receptor with constitutive (constant) activity and turns off or significantly decreases activity.

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69
Q

Antagonist

A

Binds to receptor but no complication.
Can be competitive or noncompetitive inhibition.
Can be reversible or irreversible.

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70
Q

Allosteric Binding

A

Molecule binds at site other than active site and either inhibits or enhances enzyme.

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71
Q

When is it most common for duration of drug action to be over

A

Well after drug has dissociated (Not as soon as the drug leaves the receptor)

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72
Q

Four families of receptor

A

Ion channels (voltage and ligand gated)
GPCR
Enzyme linked
Intracellular

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73
Q

Ligand Gated Ion Channel

A

Extracellular portion has binding site.
When ligand binds, pore is open.

74
Q

Voltage-gated ion channels

A

Controlled by membrane potential.
Depolarization opens the channel
Two parts: volatge sensor and pore

75
Q

GPCR

A

Ligand binds to extracellular protein on extracellular portion changing shape of G protein.
Alpha subunit binds GTP and moves away from receptors.
Second messengers then activated.

76
Q

Gs receptor

A

Leads to Adenylyl cylcase which leads to cAMP that starts ac ascade that alters protein activity and increases HR

77
Q

Gq receptor

A

Leads to phospholipase C that leads to IP3 and DG that trigger release of Ca and activates protein kinase C

78
Q

Gt receptor

A

Leads to increase in guanylyly phosphatase that leads to
decrease in cGMP.
Uses Guanalyl Cyclades and cgmp?
Then regulates physiologic processes and has inflammatory effect and glucagon release

79
Q

Gi receptor

A

Lowers adenylyl cyclase lowering cAMP.
Opening K channels lowering HR

80
Q

Enzyme linked receptors

A

When ligand binds to receptor, tyrosine kinases phosphorylate the receptor.
Activated receptor then catalyzes phosphorylation of tyrosine residues on different target signaling proteins leading to cascade

81
Q

Cytokine receptor

A

Require an intermediary (JAK) to phosphorylate tyrosine kinases.
Ligand binds causing cytokine receptors to dimerize.
JAKs activated and phosphorylate tyrosine residues.
Tyrosine residues initiate signaling through STATs.
STATs dimerize and dissociate from receptor to travel to nucleus and regulate transcription of specific genes.

82
Q

Intracellular receptors

A

Ligands must be lipophilic.
Bind to specific DNA seq near the gene to be altered in transcription or translation.

83
Q

Consequences of intracellular ligand-receptor binding

A

Lag period of 30 min to several hours.
Effects can persist for hours or days after concentration has reached zero.

84
Q

Receptor desensitization

A

Receptors get overstimulated and quit responding as intensely for a period of time.

85
Q

Down regulation of receptors

A

Receptors need finite time to rest after stimualtion.
Receptors internalize into cell.

86
Q

Upregulation of receptor

A

Repeated exposure of receptor to antagonist results of up-regulation of receptors.

87
Q

Enteral

A

Oral, sublingual, or buccal

88
Q

Parenteral

A

Drug bypasses digestive system.
IV, IM, SQ, ID
More rapid and predictable absorption.
Can damage tissue or lead to infections

89
Q

Topical

A

Medication is put on affected area

90
Q

Oral

A

By mouth (passes through GI)
Most common
Must be able to withstand acidity of stomach.

91
Q

SL/buccal

A

Rapid absorption through capillaries.
Bypasses GI

92
Q

IV

A

Rapid effect and max control

93
Q

IM

A

Aqueous solution.
Sustained dose over extended interval.

94
Q

SQ

A

Simple diffusion
Not for drugs that irritate tissue

95
Q

ID

A

Used for diagnostics (like TB skin test)

96
Q

Intrathecal

A

Directly into CSF.
Local rapid effects

97
Q

Inhalation/Intranasal

A

Rapid deliver.
Almost as rapid as IV.

98
Q

Rectal

A

Bypasses 50% of portal circulation minimizing breakdown in liver.
Useful for vomiting pts or children.
Absorption is unreliable

99
Q

Transdermal

A

Patch.
Drug seeps out at steady rate.

100
Q

Aqueous passive diffusion

A

Drug moves through aqueous channels in intracellular junctions.
Drug moves down concentration gradient.
Does not involve a carrier

101
Q

Lipid passive diffusion

A

Drug moves through lipid bilayer with no help.
Drug moves from high to low concentration

102
Q

Facilitated diffusion

A

Uses transport proteins to move drug across membrane.
Faster than passive diffusion.
Drug moves down concentration gradient.
No energy

103
Q

Special Carrier transport

A

Active transport.
Drug moves from low to high concentration

104
Q

What factors influence absorption

A

pH
Blood flow
Total surface area
Contact time
Expression of P-gp

105
Q

How does pH affect absorption

A

Weak acid absorbed best at acidic pH
Weak base absorbed best at alkaline pH

106
Q

How does pH affect secretion

A

Weak acid excreted faster in alkaline urine
Weak base excreted faster in acidic urine

107
Q

How does blood flow affect absorption

A

Increased bloodflow increases absorption

108
Q

How does surface area affect absorption

A

More surface area in organ (small intestine) means faster absorption of drug

109
Q

P-gp

A

Pumps drug out of the cell.
If expressed, the rate of absorption of the drug in that cell will be decreased.
Bacteria and cancer cells use this pump to their advantage

110
Q

Bioavailability

A

Fraction of unchanged drug that reaches systemic circulation

111
Q

IV drug bioavailability

A

100% (bc it goes straight into circulation)

112
Q

IV dose vs PO dose size

A

PO dose would likely be bigger bc liver could inactivate significant amount of drug before it reaches systemic circulation.

113
Q

Distribution

A

Drug reversibly leaves bloodstream and enters extracellular fluids and tissues.
IV drugs do this rapidly.

114
Q

Factors that influence drug distribution

A

Lipophilicity
Cardiac output and local blood flow
Capillary permeability
Binding of drugs to plasma proteins and tissues
Volume of distribution

115
Q

How does lipophilicity affect drug distribution

A

The more lipophilic a drug is the easier it can get out of the blood and into tissues.
It can be slowly released from fatty tissues.
Lipophillic molecules can also cross BBB unlike polar molecules.

116
Q

How does blood flow affect drug distribution

A

The greater the blood flow to tissues, the greater the distribution.
There is greater blood flow in brain, liver, heart, and kidney.
Less blood flow in adipose tissue, skin, vescera

117
Q

Slit junction

A

large, protein bound molecules can get through.
Present in liver and spleen.

118
Q

Tight junction

A

Prevent large, protein bound molecules from getting through.
Hydrophilic drugs can easily get through.
Present in brain

119
Q

Spleen and liver capillaries

A

Slit junctions.
Large portion of capillary membrane exposed for exchange with blood and tissues

120
Q

Brain capillaries

A

NO split junctions.
Capillary structure is continuous.
Drugs must go through CNS capillaries or active transport to enter.

121
Q

Free drug

A

Unbound.
Only way drug can bind to target.

122
Q

Volume of distribution

A

Ratio between amount of drug in body vs amount of drug in plasma.

123
Q

What does a high volume of distribution mean

A

It will leave blood plasma and go everywhere, so higher dose is needed to get desired effect.

124
Q

High MW drugs Vd

A

Low. can’t easily get out of bloodstream

125
Q

Low MW drugs Vd

A

High. Can more easily get out of bloodstream

126
Q

Hydrophilic drugs Vd

A

Low. Can’t easily get out of blood stream

127
Q

Lipophilic drugs Vd

A

Higher. Can easily get out of bloodstream and be absorbed into tissues.

128
Q

If drug has High Vd how is it’s duration of action

A

Longer

129
Q

Ideal properties of drug to be excreted

A

Hydrophilic bc if lipophilic it will be reabsorbed in the kidney

130
Q

Metabolism

A

Biotransformation to make a drug able to be excreted.
Usually makes the drug more hydrophilic and inactivates it

131
Q

Prodrug

A

Transformed into it’s more active form through metabolism.

132
Q

Main organism of metabolism

A

Liver.
Drug is absorbed in small intesine and go to liver through hepatic portal vein. Liver begins metabolizes drug and drug enters systemic circulation

133
Q

First pass effect

A

Biotransformation (metabolism) of drug before reaching systemic circulation (usually in liver sometimes in GI tract).
Seen in oral and rectal drugs but not with parenteral or SL/buccal

134
Q

Phase I metabolism rxn

A

Introduces or unmasks hydroxyl on molecule
Often use CYP450.
Primarily in liver

135
Q

CYP450 Enzymes

A

CYP1A2
CYP2A6
CYP2B6
CYP2C9
CYP2D6
CYP2E1
CYP3A4
Uses reduction, oxidation rxns or hydrolyzes drug to add hydroxyl molecule to make it more hydrophilic

136
Q

Most important CYP450 enzyme

A

CYP3A4

137
Q

CYP2D6

A

Used to metabolize codeine into its active form morphine.

138
Q

What happens if CYP450 is inhibited

A

Drug concentration in the plasma would increase bc CYP450 would not be able to break it down as efficiently

139
Q

Phases II metabolic rxn

A

Polar group is conjugated (attached) to drug to make it more hydrophilic.
UGT (a transferase) is most common enzyme used

140
Q

First order kinetics

A

Rate of drug metabolism is proportional to concentration of free drug (% stays same).
Drug has specific half life.
Linear kinetics (but is curved on a graph)
MOST DRUGS

141
Q

Zero Order Kinetics

A

Rate of metabolism remains constant over time.
Drug concentration does not affect rate of metabolism.
nonlinear kinetics (but is a line on graph)
ex. aspirin and phenytoin

142
Q

Most important organ for excretion

A

Kidneys

143
Q

Elimination

A

Inactivation or excretion of drug.

144
Q

Clearance

A

Volume of plasma cleared over time (mL/min).
Does not tell amount of drug cleared from body.
Can’t be directly measured.
Represents body’s ability to eliminate drug and predict rate to decide right dosage.

145
Q

Systemic clearance

A

Sum of clearance at each organ

146
Q

What happens to person’s clearance as they get older

A

Decreases

147
Q

Liver role in excretion

A

Excrete unchanged drug into bile

148
Q

What all processes does a drug pass through in the kidney

A

Glomerular filtration
Active tubular secretion (proximal)
Passive tubular reabsorption (distal)

149
Q

Glomerular filtratino

A

Afferent arterioles carry drug to nephron.
Hydrostatic pressure pushes free drug into bowmans capsule.
Low GFR causes drug to not be pushed out so its stuck in blood.
High protein binding makes it hard for drug to go through filter.
Lipid solubility and pH NOT a factor.

150
Q

Proximal tubular (PCT) secretion

A

Drugs secreted from efferent arteriole into PCT through ACTIVE transport with anion and cation transporters with low specificity

151
Q

Distal tubular (DCT) reabsorption

A

Passive.
Nonpolar drug diffuses out of lumen back into circulatoin.
Changes lumen pH

152
Q

First order elimination kinetics

A

Depends on blood flow of drug to elimination organ.

153
Q

Zero order elimination kinetics

A

Same amount eliminated over time.
Blood flow doesnt matter.

154
Q

Half life

A

amount of time needed for plasma concentration to decrease 50% after drug is discontinued.

155
Q

Accumulation

A

Takes 4-5 half lives after drug is first administered to achieve steady state

156
Q

How long does it take to get rid of 95% of drug

A

4-5 half lives

157
Q

Steady state

A

Rate of drug elimination equals rate of drug adminstration

158
Q

Loading dose

A

First dose of medication given is larger dose to get to desired effect more quickly. However, can be dangerous with regards to toxicity and plasma concentration could take longer to decrease.

159
Q

Should IV meds be given fast or slow

A

Slow

160
Q

What method can be used to prevent the highs and lows of the effect of the drug

A

Smaller doses at shorter intervals

160
Q

What happens to steady state when clearance is incresased

A

Steady state will decrease, Inverse relationship.

161
Q

Vd in elderly

A

Vd is lower
Less body mass, so less tissue for drug to escape to

162
Q

Vd in obese

A

Vd is higher.
More tissue for drug to escape to

163
Q

When does absorption typically occur

A

2 hours after administration of the drug.
But some drugs take longer

164
Q

When is the best time to take samples to test concentration once steady state has been reached

A

At midpoint of dosing interval.

165
Q

Potency

A

Concentration of drug producing 50% of max effect.\
Depends on Kd of receptors and efficiency of drug-receptor interaction

166
Q

Efficacy

A

Measure of Magnitude of response.

167
Q

Intrinsic activity of antagonist

A

0

168
Q

Intrinsic activity of full agonist

A

1

169
Q

Intrinsic activity of partial agonist

A

Between 0 and 1

170
Q

Intrinsic activity of inverse agonist

A

less than 0

171
Q

Intrinsic activity

A

Drug’s ability to fully activate receptor

172
Q

Therapeutic index

A

Ratio of drug dose that produces toxicity in halg population devided by the dose that produces a desired or effective response in half the population
TI=TD50/ED50.
High TI values needed for must drugs bc it shows it takes much higher dosage to become toxic than the dosage to get desired effect.

173
Q

WHO

A

The degree to which the person’s behavior corresponds to the agreed recommendations from health care provider.

174
Q

Adherence

A

Pt and provider collaborate to find the best way to get care.

175
Q

Primary non-adherence

A

non-fulfillment.
Can’t afford meds.
Didn’t get sent to pharmacy.
Pharmacy is out.
Pt never picked up from pharmacy.

176
Q

Secondary non-adherence

A

non-persistence.
Pt stops taking dose without instruction or consultation with provider.

177
Q

Tertiary non-adherence

A

non-conforming.
Skipping doses
Taking at wrong time (ex. with/without food)
Taking more/less than perscribed.

178
Q

non adherence rate

A

10-92%
average of 50%.
half of those are intentional

179
Q

Does chronic or acute have better adherence

A

acute

180
Q

What often causes non-adherence in elderly

A

Have to remember to take lots of drugs.

181
Q

How quickly should you follow up after changing meds

A

Month

PAS 506 (9 decks)

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