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Advanced Pharm > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Ch.1
How to bring a prescription drug to market?

A

1-2 years to patent, send IND (investigative new drug) to FDA, Phase 1-3; if pass all 3 phases, NDA (new drug application) - takes 1 year to get [where Thalidomide got caught up]; marketing and sent to public; TOTAL = around 9 years

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2
Q

Ch.1
Monoclonal Antibodies uses in pathologic conditions?

A

cancer, autoimmune diseases

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3
Q

Part of cell that engulfs the receptor and drug together?

A

Clatherin encoated pit

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4
Q

4 Main Causes of Drug Variation?

A

Alteration (ADME, age, disease, sex, weight), Varied Concentration of Endogenous Ligand, Alteration in number or function of receptors, and Changes in Downstream Receptor (LARGEST AND MOST IMPORTANT)

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5
Q

Ch.1
Role of Drug Carriers?

A

Carry a drug across the membrane if needed (non-lipid soluble)

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6
Q

Drug Examples of Zero Elimination

A

Ethanol, phenytoin, salicylates

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7
Q

What is constant in zero order elimination?

A

ROE is constant

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8
Q

GCPRs Cascade

A

Know how to draw; G-PROTEIN activates cascade via ALPHA SUBUNIT

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9
Q

Ch.3
Volume of Distribution (Vd)

A

The space available in body to contain the drug; how much stayed in the blood vs how much went elsewhere? Shows preference to where drug will best absorb

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10
Q

Zero Order Elimination

A

ROE is constant; so much drug in body, receptors are completely saturated and you cannot get rid of the drug fast enough; Ex. Every hour, body gets rid of 150 mg of drug (ROE)

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11
Q

Ch.3
Bioavailability (F)

A
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12
Q

Ch.1
Pharmacodynamics

A

What the drug does to the body?
-Dose response

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13
Q

2 Outcomes of Desensitization within the Cell?

A

Can be recycled or a Lysosome will degrade the receptor

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14
Q

Ch.1
Toxins vs Poisons

A

Toxins - biological; puffer fish, bee, mushrooms
Poisons - non-biological; arsenic/lead

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15
Q

Ch.1
Paracelsus Quote

A

“The dose makes the poison”

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16
Q

Ch.1
Exogenous vs Endogenous

A

Ex - Outside body (norepi, epi, propanolol)
End - Inside body (norepi, epi)

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17
Q

Ch.3
Rate of Elimination (ROE)

A

The speed at which the drug is eliminated from the body

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18
Q

Ch.2
Ligand Gated Ion Channel

A

Ligand Gated - Contains ionotropic or metabotropic; ligand opens the channel, and when it leaves, the channel is shut

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19
Q

What are the 4 ways drugs get across barriers?

A

Aqueous diffusion, Lipid diffusion, Special Carriers, Exocytosis (Clatherin coated pit), Endocytosis (merge of vesicle with membrane)

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20
Q

Ch.1
Competitive Inhibitor

A

an inhibitor that competes to bind at the active site with an agonist

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21
Q

Voltage Gated Ion Channel

A

Found in excitable cells (neurons, muscle, endocrine); closed @ RMP; based on ion selectivity; 2 gates, upper and lower; When Na+ gets close to the channel, the charge opens it up to allow Na+ in. The bottom gates shuts first after, then both gates completely shut and the whole process starts over again

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22
Q

Ch.2
Desensitization Definition

A

Drug bound to receptor, but cell shuts down signaling process. Decrease effectiveness of drug; protective mechanism; if constantly being signaled, has process where cell can shut down the signals

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23
Q

Ch.1
Pharmacokinetics - ADME

A

Absoprtion
Distribution
Metabolism
Excretion

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24
Q

Ch.1
Father of Western Medicine

A

Hippocrates

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25
Q

Ch.1
Inverse Agonist

A

STRONG! Binds to same receptor as agonist, but produces opposite response: binds to inactive form of the receptor. Completely shuts down the receptor

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26
Q

Ch.1
Covalent Bond

A

Strongest; share same chemicals or ions; irreversible; Less specificity

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27
Q

Ch.1
Racemic Mixture

A

Mixture between different mirror Isomers of a drug. Ex: R-Ketamine (more toxic) and S-Ketamine (4x more potent). Done by rotating the molecules

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28
Q

How to Calculate Therapeutic Index of a Drug?

A

Td50/Ed50: Wider = safer; narrow = more toxic

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29
Q

Competitive Inhibitor vs Allosteric (non-competitive) Inhibitor

A

Competitive - Blocks @ the active site [A+B]; surmountable; Countered by increasing agonist
Allosteric - Blocks @ site other than active site [A+D]; insurmountable; irreversible

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30
Q

Ch.3
Concentration (C)

A

Sub-defined to: C in blood, C in plasma, C in H2O (unbound)

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31
Q

Ch. 1
Electrostatic Bond

A

Most common; bond based on ionic charges, hydrogen, Van der Waals

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32
Q

Ch.1
Regulation of Prescription Drugs

A

Have to have licensed provider; viewed by public as “more effective”; increased risk for toxicity

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33
Q

What is constant in 1st order elimination?

A

CL is constant

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34
Q

Ch.1
Regulation of OTC Drugs

A

Able to get freely; less risk for toxicity due to usually wider TI

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35
Q

Allosteric

A

Bind not @ active site of the receptor. Non-competitive; Insurmountable; Irreversible

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36
Q

Ch.2
Inotropic Ion Channel

A

More common; ligand binding and channel on same protein; nAch receptor in skeletal muscle; Sux binds to this receptor

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37
Q

Ch.3
4 different ways a drug gets across barriers

A

Aqueous Diffusion, Lipid Diffusion, Special Carriers, Endocytosis (Clatherin Coated Pit) and Exocytosis (merge vesicle with membrane)

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38
Q

Ch.1
Allosteric Inhibitor

A

Binds outside of Active Site on Receptor Protein

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39
Q

1st Order Elimination

A

Drug slowly leaves body; CL remains constant (Ex. Every hour, 12% leaves the body)

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40
Q

Agonist

A

Activator; bind to similar ligand endogenous in the body

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41
Q

Ch.1
Partial Agonist

A

Weaker than a full agonist; Antagonist in presence of full agonist. Lower intrinsic activity than full agonist
Ex: Epi with Partial Agonist = Decreased effect of Epi

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42
Q

Ch.2
Metabotropic Ion Channel

A

Ligand activates GCPR –> 2nd messenger opens channel (cAMP binds to channel and opens)

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43
Q

Receptor

A

Component that interacts with drug and initiates a chain of events that lead to drug observed effect

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44
Q

Ch.3
Target Concentration (TC)

A
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45
Q

Ch.3
Half-Life (T1/2)

A

The time it takes for 50% of the drug to be eliminated from the body

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46
Q

Ch.1
How can a partial agonist also be an antagonist?

A

Partial agonist, when in presence of agonist, turns into an antagonist. This is because the 2 compete, thus decreasing the desired effect of the med. The partial agonist prevents the agonist from accessing the receptor

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47
Q

Ch.1
Pharmacogenomics

A

Study of genetic profile to see how body will respond to certain drug given

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48
Q

Ch.2
The Molecular Components of Desensitization in the
GPCR

A

Betaerestin
Clatherin Coated Pit

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49
Q

Ch.2
Types of Ligands that Bind to Receptors Inside the Cell

A

Gas (NO activated within cell to dilate smooth muscle and decreased BP) and Lipid Soluble Agents (Steroids)

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50
Q

Ch.1
Role of the FDA

A

To regulate drugs and make sure they are safe and effective; reviews claims and makes recommendations

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51
Q

Ch.1
Most common drug carriers in the blood

A

Albumin - acid drug binding
A1-Acid Glycoprotein - basic drug binding
Lipoproteins - neutral drug binding

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52
Q

Elimination of the drug is based off of what?

A

Clearance of the drug

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53
Q

Metabotropic Ion Channel

A

Ligand activates GCPR; 2nd messenger opens up ion channel’ Ex. cAMP binds to ion channel to open up

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54
Q

Ch.1
Precursor to Pharmacology

A

Materia Medica

55
Q

Ch. 2
Cell signaling process

A

Signaling Molecule –> Receptor –> Signal Transduction Protein –> 2nd Messenger–> effector protein (change in the cell)

56
Q

Ch.1
First Recorded Physician

A

Imhotep

57
Q

What is Clearance (CL)?

A

The ability of the body to clear the drug; elimination is based off CL; remains constant in 1st order elimination

58
Q

4 Transmembrane Signaling Methods

A

(1) Intracellular Receptors (lipid soluble)
(2) Cell Surface Receptors: Ions, Catalytic, GCPRs

59
Q

Ch.1
Father of Toxicology

A

Paracelsus

60
Q

What does a high CL mean?

A
61
Q

What is a clatherin coated pit?

A

Part of the cell wall that engulfs the receptor/drug combo and either recycles it or lysosomes will come digest the receptor

62
Q

Stereoisomerism and Drug Effects

A

Same chemical makeup, just different arrangement of the atoms; can cause greater desired effect, but may contain more adverse effects

63
Q

Ch.2
Most Common Second Messenger (per Lecture)

A

cAMP and IP3

64
Q

Ch.1
Physiologic Antagonism

A

Drugs opposite effect @ different receptors
Ex: Epi @ B1B2 to increase HR
Acetylcholine @ M1M2 to decrease HR

65
Q

2 types of ligands that bind to receptors within the cell?

A

Gas - Shearing forces in vessel cause NO to open the vessels and lower BP
Lipid Soluble Agents - Steroid hormone binds to steroid receptor, then increases transcription and translation in nucleus

66
Q

Ch.3
Pharmacokinetic Variables (ADME)

A

Adsorption, Distribution, Metabolism, Excretion

67
Q

What does a high Vd mean?

A

Less concentration in blood, as it distributes elsewhere in the body (Hydroxychloroquine likes to spread to adipose tissues, so high Vd)

68
Q

6 Types of Antagonist Receptor Interactions

A

Competitive, Non-Competitive (Allosteric), Partial Agonist, Inverse Agonist, Opposite Charge, Physiologic Antagonism

69
Q

GDP, GTP, GPCR Definitions

A

GDP - Guanosine Diphosphate (inactive)
GTP - Guanosine Triphosphate (active)
GPCR - G-Coupled Protein Receptors

70
Q

Ch.2
Role of Second Messengers

A

Relay the message sent from the effector protein to create cellular response

71
Q

Antagonist

A

inhibitor; blocks ligand; does not activate response

72
Q

GCPR Structure and Components

A

7TM structure; A,B,Y subunits: A is most important as sends GTP over to effector protein and starts cascade, B and Y are structural

73
Q

Orthosteric

A

Bind @ active site of the receptor

74
Q

Monoclonal Antibodies and How they Are produced?

A

Drugs extracted from living organisms; taken from a single clone of a single plasma cell

Recombinant DNA technology; isolate antigen, inject into mouse, mouse makes antibodies, take plasma cells from mouse, mix plasma cell with myeloma cell to create immortal cell; inject back into mouse ( see how it responds, and now you have unlimited copies)

75
Q

Ch.1
Toxicology

A

study of undesired effects of chemicals on living systems

76
Q

Ch.3
Clearance (CL)

A

The ability of the body to clear the drug; elimination is based off clearance

77
Q

Protein that blocks OH group during desensitization

A

Betaerestin

78
Q

GPCR Signaling

A

Signaling Molecule - Receptor - Signal Transduction Protein - Secondary Messenger - Effector Protein

79
Q

What is Concentration (C)?

A

Concentration of drug in blood (Cb), plasma (Cp), or H2O/unbound (Cu)

80
Q

Phosphorylation Cascade

A

Know how to draw; RECEPTOR activates cascade

81
Q

Ch.1
Hydrophobic Bond

A

Weakest; no charge; more specificity to lock and key. Lipid soluble

82
Q

Ionotropic Ion Channel

A

Part of Ligand gated ion channels; more common; ligand binding to site and channel on same protein; Ex. nACh receptor in skeletal muscle (SUX binds to this receptor)

83
Q

What is Volume Distribution (Vd)?

A

How much drug stays in the blood vs how much goes to other parts of the body

84
Q

Ch.1
Pharmacokinetics

A

What does body do to the drug?
- 1/2 life: BBB

85
Q

Ch.1
Potency vs Efficacy

A

Potency - Amount of drug needed to produce desired effect (EC50 and Emax)
Efficacy - Drugs capacity to produce desired effect (Kd and Bmax)

86
Q

2 Types of Ligand Gated Ion Channels

A

ionotropic and metabotropic

87
Q

Receptor Site

A

Protein on cell membrane that binds with ligand

88
Q

Explain CYP450 Metabolism

A

The drug (RH) binds to CYP450. CYP450 has an Iron group attached which goes through various oxidation reactions.

89
Q

Hepatic Portal System Blood Flow

A

GI - Local Veins - Hepatic Portal Vein - Sinusoids - Hepatic Vein - Vena Cava - Systemic Circulation

90
Q

Tylenol Normal Dosage Pathway

A

Phase 2 reaction: Glucuronidation and sulfation are added to tylenol to help it be excreted easier from the body

91
Q

Hepatic Enzyme Induction

A

Some drugs enhance synthesis or inhibit degradation: If metabolism deactivates the drug, then DECREASED drug effect. If metabolism activates the drug, then INCREASED drug effect

92
Q

Most common CYP450s?

A

CYP3A4*1 (50%), CYP2D6 (20%), CYP2B6 (8%)

93
Q

What is the “Wild Type” CYP enzyme?

A

CYP3A4*1; occurs most often in the population

94
Q

Hepatic Enzyme Inhibition

A

If metabolism deactivates the drug, then INCREASED drug effect; if metabolism activates the drug, then DECREASED drug effect

95
Q

What is a Prodrug?

A

A drug that is inactive until converted by the body’s metabolic process (Plavix)

96
Q

Phase 1 Metabolic Reactions

A

Convert drug to more polar; Oxidation (CYP450), Reduction, Hydrolysis, Dehydrogenation [these turn drug lipo-hydrophilic for excretion]

97
Q

Phase 2 Metabolic Reactions

A

Adding larger molecules to a drug, making it more hydrophilic; conjugation to endogenous substrate (Glucuronidation) and (Glutathione - GSH)

98
Q

Glucuronidation (UDP Glucuronic Acid)

A

Phase 2 Reaction; Adding a glucose molecule to a drug to make it easier to excrete (makes more hydrophilic)

99
Q

Glutathione (GSH)

A

Phase 2 Reaction; binds to drug to make easier to excrete (hydrophilic)

100
Q

Hepatic Artery Blood Flow

A

Systemic Circulation - Hepatic Artery - Sinusoids - Hepatic Vein - Vena Cava - Systemic Circulation

101
Q

What is an Active Drug?

A
102
Q

What test determines kidney function?

A

Creatinine Clearance (mL/min)

103
Q

IBW for Men

A

52 + (1.9 kg x inches over 5 ft)

104
Q

IBW for Women

A

49 + (1.7 kg x inches over 5 ft)

105
Q

What is Peak? When do you draw it?

A

Highest concentration of drug in blood; 5-10 min after IV administration

106
Q

What is Trough? When do you draw it?

A

Lowest concentration of drug in blood; 30 min prior to next dose

107
Q

7 Routes of Drug Administration?

A

IV, IM, SC, PO, Rectal, Inhalation, Transdermal

108
Q

What is 1st Order Elimination?

A

Drug slowly leaves body, as CL is constant; Sigmoidal

109
Q

What is 0 Order Elimination?

A

So much drug in your body, your receptors become saturated and you cannot get rid of it fast enough. Occurs when body ability to eliminate has reached max capacity. ROE is constant, as you can only get rid of so much at a time; Linear

110
Q

What Remains Constant in 1st Order Elimination?

A

Clearance (CL)

111
Q

What Remains Constant in 0 Order Elimination?

A

Rate of Elimination (ROE)

112
Q

3 Drugs that can easily get to 0 Order Elimination?

A

ethanol, phenytoin, salicylates

113
Q

Parts of the BBB?

A

ABC Transporters, Vascular Epithelium (primary site of exclusion), Other Cells (Astrocytes and Podocytes)

114
Q

What are High Extraction Drugs?

A

Drugs that are sensitive to 1st pass metabolism; large portion are extracted in the liver

115
Q

What is a high extraction ratio? How does this compare to Blood flow and CL?

A

(0.7-1); High blood flow (Q) and High CL

116
Q

Tylenol OD pathway

A

Phase 1 Reaction; Non Lethal when CYP3A4 goes through GSH-conjugation, which adds Mercapturic Acid (swept out of the body)
Lethal - Glutathione runs out and Nucleophilic structures bind to cell macromolecules (leads to liver cell death)

117
Q

Capacity Limited Elimination

A

Think of 0 order elimination

118
Q

What are Drug Efflux Transporters?

A

Bind to drugs to send in or out of the cell; important when protecting barriers, such as BBB (prevent things from coming into BBB)

119
Q

Most Important ABC Transporters? 3

A

B1, C, G2

120
Q

ABCB1?

A

Broadest specificity, Critical to BBB (pumps drugs back into blood, instead of brain)

121
Q

ABCC?

A

Largest Class, but does not transport as much as B1

122
Q

ABCG2?

A

Breast cancer resistance, folate transport, antineoplastics

123
Q

The role of Drug Transporters in the Cell?

A

To Transport Endogenous Substances (hormones, glucose, amino acids, etc)

124
Q

Steady State 1/2 Lives?

A

4 Half-Lives to reach steady state

125
Q

What is steady state?

A

Time at which concentration of drug in the body stays consistent

126
Q

What are 2 drug interactions with ABCB1?

A

Loperamide with Quinidine (increased respiratory distress like opioid OD)
Digoxin with Cyclosporin (increases Dig levels = Dig toxicity)

127
Q

3 Drugs that might require dosage changes in specific genetic populations?

A

Warfarin, 6-mercaptopurin, Trastuzumab (Herceptin)

128
Q

What enzyme metabolizes Warfarin?

A

CYP2C9

129
Q

What enzyme metabolizes 6-Mercaptopurin?

A

TPMT

130
Q

Which variants show that a Patient needs less warfarin to avoid bleeding out?

A

CYP2C9 *2, *3

131
Q

What test is done to see if patient has Warfarin mutation?

A

Simple Trial and Error and Genetic Testing

132
Q

What test is done to see if patient has TPMT enzyme mutation?

A

Simple blood test (if deficient, give lower dose of 6-mercapto)

133
Q

Importance of Pharmacogenomics in Personalized Medicine?

A

5 rights of medication

Advanced Pharm (1 decks)

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