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Advanced Pharm > Exam 1 Review > Flashcards

Exam 1 Review Flashcards

1
Q

Define Pharmacology

A

The study of drugs and their effects on the body

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2
Q

CYP2D6: Drugs to Know

A

Quinidine (inhibit)

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3
Q

SLC 21 Transporters

A

OATPs; passive transport (FD)

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4
Q

Blood volumes in Body: Whole blood and plasma

A

Whole Blood - 5.6L/70 kg
Plasma - 2.8L/70Kg

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5
Q

Hepatic Blood Flow: Non-1st Pass Effect

A

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

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6
Q

FDA Regulation: How to bring a drug to market

A

In-Vitro Studies: 1-2 years
Animal Testing: 3-4 years
* Send IND to FDA
P1: 20-100 healthy individuals; is it safe?
P2: 100-200 sick individuals; placebo effect
P3: 1000+ sick individuals; marketing, double-blind
*Send NDA to FDA @ 8-9 yrs (takes 1 year for this- where Thalidomide got stuck)
New Patent- 20 years

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7
Q

Inert Receptors: Albumin

A

2 sites, drug has to be free form, decreased levels in liver and malnutrition issues

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8
Q

Describe the Tylenol Pathway: Normal and OD

A

Normal - Tylenol is metabolized by P2 reactions of Glucuronidation and Sulfation
OD - Tylenol resorts to P1 metabolism in Toxic Intermediates, then can try P2 GSH-conjugation. If this does not work, it will result in P1 Nucleophilic Macromolecule Hepatocyte death

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9
Q

Inert Receptors: 3 Types with Preference for Drug

A
  1. Albumin - Acidic drugs
  2. A1- acid glycoprotein - Basic Drugs
  3. Lipoprotein - Neutral Drugs
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10
Q

Isomer Definition

A

Same chemical formula, but different structure

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11
Q

Chiral Definition

A

Broad definition of being mirror image of itself

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12
Q

FDA: Herbals

A

Safe, not effective per say

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13
Q

MAB: Definition

A

Derived from living organisms; single clone of single cell; made of 2 light and 2 heavy chains; can bind to single cell; “umab”

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14
Q

Receptor Theory: 3 Factors

A
  1. Affinity determines dose
  2. Selectivity varies per drug
  3. Can be agonist or antagonist
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15
Q

What is most Important in Therapeutic Drug Monitoring

A

Clearance!!

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16
Q

Enantiomer Definition

A

Make up racemic mixtures; “Hand” example; mirror image

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17
Q

Metabolic Rate with Drug Dose: Rapid Metabolizer

A

Prodrug - Good, need less amount to avoid toxic
Drug - less effective, as broken down quick

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18
Q
A
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19
Q

Define T 1/2

A

The time it takes for 50% of the drug to decrease

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20
Q

ABCG2

A

Breast Cx, folate (most common in GI tract)

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21
Q

Define Vd

A

The drug concentration in blood vs how much left to other parts of the body; High Vd = drug goes to other places besides blood

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22
Q

Define Rational Dosing

A

Goal is to achieve desired beneficial effects with minimal adverse effects

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23
Q

Brussel Sprouts Question

A

Warfarin inactivated by CYP1A2, Brussel Sprouts induce CYP1A2. What happens to Warfarin? Less effective and have to give more

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24
Q

Describe Cell Signaling

A

Signal Molecule (drug, ligand) - Receptor - Transduction Protein (AC or PLC) - 2nd Messenger (IP3, DAG, cAMP) - Effector Protein (PKA)

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25
Q

Explain Phosphorylation Cascade

A

Ligand binds to the receptor - Creates Kinase (inactive) and Kinase (Active) - Kinase (A) creates Protein 1 (I) and Protein 1 (A) - Protein 1 (A) creates Protein 2 (I) and Protein 2 (A), etc..

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26
Q

BBB

A

3 parts: cells, tight junction, ABC efflux transporters
O2, CO2, ethanol, nicotine, insulin, albumin

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27
Q

Define Loading Dose

A

Bolus; after giving, slow maintenance is key to avoid toxic

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28
Q

RTK: Pathway

A

2 ligands bind to both monomers simultaneously, creating a dimer – Uses 6 ATP to phosphorylate the dimer– after this is done, activates relay protein to do function

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29
Q

RTK Structure

A

Catalytic Cell Surface Receptor; 2 monomers when bound become a dimer

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30
Q

SLC Proteins

A

Solute Carrier Proteins; 15-30% of all membrane proteins; High Specificity (Na, glucose, Acetyl-Coa, AA)

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31
Q

Hepatic Blood Flow: First-Pass Effect

A

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

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32
Q

HOP: Father of Toxicology, with quote

A

Paracelsus - “dose makes poison”

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33
Q

Drug Dosage Variation: Herceptin

A

Antibody shuts down receptor; HER2 over-expression

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34
Q

What are Sinusoids?

A

Mixed oxygen and non-oxygen blood b/c meeting of hepatic vein and hepatic artery; in Liver Lobule (hepatocytes)

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35
Q

Non-First Pass Effect Definition

A

Anything else besides PO meds; Rectal 50% bypass 1st pass

36
Q

MAB: How they are Created (Recombinant DNA)

A

Isolate Antigen – inject mouse with antigen – mouse produces antibodies – take antibodies from mouse and mix with Myeloma Cell from Spleen to make Immortal Cell – inject Immortal Cell into mouse to have infinite copies

37
Q

Define Steady State

A

The amount of drug given = amount eliminated (think normal IV med in ICU); 4 T1/2’s

38
Q

Prodrugs and Drugs: Pt.1
Drug 1 metabolized and made inactive by CYP3A4, Drug 2 induces CYP3A4. What will happen to Drug 1?

A

Drug 1 will be less effective

39
Q

What does a High CL mean

A

The body eliminates the drug faster

40
Q

What is the ABC gene family

A

Efflux transporters that have Nucleotide Binding Domains

41
Q

Define F

A

Bioavailability is the fraction of unchanged drug reaching systemic circulation (Oral may have low F; IV 100%)

42
Q

HOP: First Textbook

A

Materia Medica

43
Q

Receptor Theory: Proteins

A

Regulatory, Structural, Functional, Enzymes, Shape, Transport

44
Q

Zero Order Kinetics: Drug Examples

A

ethanol, phenytoin, Salicylate

45
Q

Define Maintenance Dosing

A

Steady State Dosing

46
Q

Prodrugs activated by CYP3A4, Drug 2 induces CYP3A4. What happens to ProDrug?

A

Prodrug will be more activated

47
Q

GPCR: Adenylyl Cyclase

A

Ligand binds to receptor, GDP converts to GTP and Gprotein via A subunit is sent over to transduction protein (Adenylyl Cyclase), AC then converts ATP to cAMP, which cAMP activates Protein Kinase C, which starts phosphorylation cascade/completes task

48
Q

Zero Order Kinetics

A

Where receptors get saturated, it saturates the elimination properties– body can only get rid of drug so fast, so CL varies on concentration of drug and ROE is constant; usually with toxic doses

49
Q

CYP450: Induction and Inhibition

A

Induction - If induced, increases what is already being done
Inhibition - If inhibited, decreases what is already being done

50
Q

Transmembrane Signaling: Intracellular and Cell Surface

A

IC - Lipid Soluble
CS - GPCR, Ion channel, Catalytic (RTK)

51
Q

What does a High Vd mean

A

The drug likes to enter other portions of the body rather than the blood

52
Q

HOP: 1st Physician

A

Imhotep

53
Q

Kd50 and BMAX

A

Kd - efficacy; this is the dotted line on the x-axis; amount of drug given to get 50% receptors bound
BMAX - 100% receptors bound; above max may lead to toxic dose

54
Q

Define Flow-Dependent Elimination and Extraction Ratio (formula)

A

The amount of blood going through the organ and the amount extracted from the organ vs how much stays in there; Formula - CL (o) = Q x (CLi - CLo)/CLi

55
Q

Racemic Mixture Definition

A

2 Enantiomers combined to create more effective, safe drug

56
Q

Ligand Gated: Ionotropic vs Metabotropic

A

Ionotropic - Ion channel; ligand binds to open up channel, and when it leaves, channel closes
Metabotropic - GPCR attached

57
Q

1st-Pass Effect Definition

A

Only for PO meds; metabolized by liver before reaching systemic circulation

58
Q

ABCB1

A

Broadest specificity; Critical in BBB; Tons of drugs and classes; Loperamine w/ Quinidine = Opiate like effects/resp. depression
Digoxin and Cyclosporine = Increased Dig toxicity

59
Q

Desensitization: Pathway

A

Ligand binds to receptor, creating phosphorylation in the OH groups (normally elicit a response) – Betaerestin comes in to block this from creating a response– then drags receptor and drug to a Clatherin Coated Pit– in pit, either recycling or Lysosome acidic degradation occurs

60
Q

Drug Dosage Variation: Warfarin

A

Metabolized by CYP2C9; if do not have CYP2C9, increased chance for toxic (may need lower dose or new drug); need genetic testing

61
Q

EC50 and EMAX

A

EC50 - Potency; amount of drug given to get 50% of desired response
EMAX - 100% desired response; has max limit

62
Q

HOP: Father of Western Medicine

A

Hippocrates

63
Q

GI-Tract

A

Most common is ABCG2; Tylenol (glucuronides from P2 hepatic metabolism)

64
Q

Desensitization: Definition

A

When the receptor gets saturated, the drug becomes less effective and the body turns off the receptor to reset the combination to work effectively next time again

65
Q

P1 Reactions

A

Oxidation (CYP450), Hydrolysis, Dehydrogenation, Reduction

66
Q

Describe the CYP450 Pathway

A

Drug binds to CYP450; goes through a bunch of oxidation reactions; Oxygen pops off to form a H2O molecule, leaving the drug as a ROH molecule, making it hydrophilic and easy to excrete; Flavoprotein reacts with CYP450 and is oxidized and recycled; similar next to that as NADPH is oxidized and recycled

67
Q

Extraction Ratio: High, Intermediate, Low

A

High: >0.7
Intermediate: 0.3-0.7
Low: <0.3

68
Q

Metabolic Rate with Drug Dose: Poor Metabolizer

A

Prodrug - less effective, as needs to be metabolized in order to elicit response
Drug - good, stays in system longer; may need less to avoid toxic

69
Q

CYP2B6: Drugs to Know

A

Phenobarb (induce), Clopidogrel (inhibit)

70
Q

Liver

A

Mostly excrete to Bile post metabolism; SLC (OATPs) and ABC’s

71
Q

Hasselbach: pH<pKa

A

protonated; acid = no charge, base = charge

72
Q

Receptor Theory: Orphan Receptor

A

We do not know endogenous ligand of this receptor

73
Q

1st Order Kinetics

A

Most drugs go through this; non-toxic dose; Blood levels of drugs decrease while CL remains constant

74
Q

4 Variations of Drug to Response

A
  1. Alteration in Physiology
  2. Alteration number/function of receptors
  3. Concentration of endogenous ligands
  4. Change to downstream effect (LARGEST AND MOST IMPORTANT)
75
Q

GPCR: Phospholipase C

A

Ligand binds to receptor, Gprotein activates transduction protein (Phospholipase C), PLC then activates IP3,DAG, IP3 and DAG go to ER and activated Ca++ channel, Ca++ is 2nd messenger and actives proteins for a cell response

76
Q

Drug Dosage Variation: 6-MP

A

Metabolized by TPMT; if deficient in TPMT, increased risk for toxicity; need blood test

77
Q

ABCC

A

Antineoplastics

78
Q

P2 Reactions

A

Glucuronidation, GSH-Conjugation

79
Q

B-CSF Barrier

A

Pia Mater and Ependymal Cells; similar to BBB, but less efflux

80
Q

FDA: OTC vs BTC

A

OTC - “less effective” by public, less chance of toxicity
BTC - “more effective” by public, need licensed Physician, increased risk of toxicity

81
Q

Hasselbach: pH>pKa

A

unprotonated; acid = charge, base = no charge

82
Q

FDA: Thalidomide

A

Med that was used for morning sickness in pregnant women; turned out to be Teratogenic (caused limb deform)

83
Q

Define CL

A

The ability of the body to eliminate the drug; elimination is based off CL; Varies based off concentration

84
Q

Low Kd = ?

A

high affinity = increased drug binding

85
Q

GPCR Structure

A

7 TM structure with Carboxyl end group; 3 subunits of A,B, gamma

86
Q

Ligands that bind within the cell: Gasses, Steroids

A

Gasses - High BP in vessels activates NO - NO diffuses to smooth muscle, dilating vessels and lowering BP
Steroids - Lipid soluble and can get into nucleus of cell

87
Q

MAB: Use

A

Cx, AI, ID

Advanced Pharm (9 decks)

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