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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
Explain Phosphorylation Cascade
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..
26
BBB
3 parts: cells, tight junction, ABC efflux transporters O2, CO2, ethanol, nicotine, insulin, albumin
27
Define Loading Dose
Bolus; after giving, slow maintenance is key to avoid toxic
28
RTK: Pathway
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
29
RTK Structure
Catalytic Cell Surface Receptor; 2 monomers when bound become a dimer
30
SLC Proteins
Solute Carrier Proteins; 15-30% of all membrane proteins; High Specificity (Na, glucose, Acetyl-Coa, AA)
31
Hepatic Blood Flow: First-Pass Effect
GI -- Local Veins -- Hepatic Portal Vein -- Sinusoids - Hepatic Vein - Vena Cava - Systemic Circulation
32
HOP: Father of Toxicology, with quote
Paracelsus - "dose makes poison"
33
Drug Dosage Variation: Herceptin
Antibody shuts down receptor; HER2 over-expression
34
What are Sinusoids?
Mixed oxygen and non-oxygen blood b/c meeting of hepatic vein and hepatic artery; in Liver Lobule (hepatocytes)
35
Non-First Pass Effect Definition
Anything else besides PO meds; Rectal 50% bypass 1st pass
36
MAB: How they are Created (Recombinant DNA)
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
Define Steady State
The amount of drug given = amount eliminated (think normal IV med in ICU); 4 T1/2's
38
Prodrugs and Drugs: Pt.1 Drug 1 metabolized and made inactive by CYP3A4, Drug 2 induces CYP3A4. What will happen to Drug 1?
Drug 1 will be less effective
39
What does a High CL mean
The body eliminates the drug faster
40
What is the ABC gene family
Efflux transporters that have Nucleotide Binding Domains
41
Define F
Bioavailability is the fraction of unchanged drug reaching systemic circulation (Oral may have low F; IV 100%)
42
HOP: First Textbook
Materia Medica
43
Receptor Theory: Proteins
Regulatory, Structural, Functional, Enzymes, Shape, Transport
44
Zero Order Kinetics: Drug Examples
ethanol, phenytoin, Salicylate
45
Define Maintenance Dosing
Steady State Dosing
46
Prodrugs activated by CYP3A4, Drug 2 induces CYP3A4. What happens to ProDrug?
Prodrug will be more activated
47
GPCR: Adenylyl Cyclase
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
Zero Order Kinetics
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
CYP450: Induction and Inhibition
Induction - If induced, increases what is already being done Inhibition - If inhibited, decreases what is already being done
50
Transmembrane Signaling: Intracellular and Cell Surface
IC - Lipid Soluble CS - GPCR, Ion channel, Catalytic (RTK)
51
What does a High Vd mean
The drug likes to enter other portions of the body rather than the blood
52
HOP: 1st Physician
Imhotep
53
Kd50 and BMAX
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
Define Flow-Dependent Elimination and Extraction Ratio (formula)
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
Racemic Mixture Definition
2 Enantiomers combined to create more effective, safe drug
56
Ligand Gated: Ionotropic vs Metabotropic
Ionotropic - Ion channel; ligand binds to open up channel, and when it leaves, channel closes Metabotropic - GPCR attached
57
1st-Pass Effect Definition
Only for PO meds; metabolized by liver before reaching systemic circulation
58
ABCB1
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
Desensitization: Pathway
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
Drug Dosage Variation: Warfarin
Metabolized by CYP2C9; if do not have CYP2C9, increased chance for toxic (may need lower dose or new drug); need genetic testing
61
EC50 and EMAX
EC50 - Potency; amount of drug given to get 50% of desired response EMAX - 100% desired response; has max limit
62
HOP: Father of Western Medicine
Hippocrates
63
GI-Tract
Most common is ABCG2; Tylenol (glucuronides from P2 hepatic metabolism)
64
Desensitization: Definition
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
P1 Reactions
Oxidation (CYP450), Hydrolysis, Dehydrogenation, Reduction
66
Describe the CYP450 Pathway
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
Extraction Ratio: High, Intermediate, Low
High: >0.7 Intermediate: 0.3-0.7 Low: <0.3
68
Metabolic Rate with Drug Dose: Poor Metabolizer
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
CYP2B6: Drugs to Know
Phenobarb (induce), Clopidogrel (inhibit)
70
Liver
Mostly excrete to Bile post metabolism; SLC (OATPs) and ABC's
71
Hasselbach: pH
protonated; acid = no charge, base = charge
72
Receptor Theory: Orphan Receptor
We do not know endogenous ligand of this receptor
73
1st Order Kinetics
Most drugs go through this; non-toxic dose; Blood levels of drugs decrease while CL remains constant
74
4 Variations of Drug to Response
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
GPCR: Phospholipase C
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
Drug Dosage Variation: 6-MP
Metabolized by TPMT; if deficient in TPMT, increased risk for toxicity; need blood test
77
ABCC
Antineoplastics
78
P2 Reactions
Glucuronidation, GSH-Conjugation
79
B-CSF Barrier
Pia Mater and Ependymal Cells; similar to BBB, but less efflux
80
FDA: OTC vs BTC
OTC - "less effective" by public, less chance of toxicity BTC - "more effective" by public, need licensed Physician, increased risk of toxicity
81
Hasselbach: pH>pKa
unprotonated; acid = charge, base = no charge
82
FDA: Thalidomide
Med that was used for morning sickness in pregnant women; turned out to be Teratogenic (caused limb deform)
83
Define CL
The ability of the body to eliminate the drug; elimination is based off CL; Varies based off concentration
84
Low Kd = ?
high affinity = increased drug binding
85
GPCR Structure
7 TM structure with Carboxyl end group; 3 subunits of A,B, gamma
86
Ligands that bind within the cell: Gasses, Steroids
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
MAB: Use
Cx, AI, ID

Advanced Pharm (9 decks)

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