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Advanced Pharmacology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Pharmacology

A

Study of chemical interactions with living systems

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2
Q

Toxicology

A

Undesirable effects of chemicals on living systems. NOT SIDE EFFECTS

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3
Q

Early Medicine: Prehistoric

A

Shamanism, animism, spiritualism, divination

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4
Q

Early Medicine: Ancient Egypt
Imhotep

A

First recorded physician
“architect of the pyramids”

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5
Q

Early Medicine: Ayurvedic

A

Ancient Indian Medicine

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6
Q

Early Medicine: Ancient Greek
Hippocrates

A

Father of modern western medicine

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7
Q

Early Medicine: Traditional Chinese Medicine

A

Still prevalent today, utilizes plant derivatives

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8
Q

What is the most ACCURATE symbol of medicine?

A

Rod of Asclepius
God of Medicine

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9
Q

Rod of Caduceus

A

Modern Medicine Symbol
Staff of Hermes (messenger of the gods).

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10
Q

Materia Medica

A

First western medical textbook. Attributed to Dioscorides. Collections of works throughout history about botany/medicinal substances. Precursor to pharmacology

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11
Q

Paracelsus

A

Father of Toxicology
“The dose makes the poison”

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12
Q

Pharmacodynamics

A

What the drug does to the body

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13
Q

Pharmacokinetics

A

What the body does to the drug; half-life, crossing barriers

A-Absorption: How it crosses barriers
D-Distribution: Where does it go
M-Metabolism: Active or Inactive when given
E-Elimination/Excretion: Exits body

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14
Q

Pharmacogenomics

A

Response to drug based on genetics. Sometimes will do DNA testing prior to administration of drug.
Ex: HER2 for Breast Cancer

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15
Q

Toxicology

A

Study of toxins and poisons and negative effects on the body

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16
Q

Agonist

A

Illicit response when drug binds to receptor

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17
Q

Antagonist

A

Blocks drug/endogenous ligand from binding to receptor

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18
Q

Poisons

A

Non-biologic
Ex: arsenic, lead, cadmium

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19
Q

Toxins

A

From living organisms
Ex: mushrooms, puffer fish

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20
Q

Allosteric

A

Binding site outside of the active site

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21
Q

Orthosteric

A

Active Site

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22
Q

Physical Nature of Drugs: Different Types of Drugs

A

-Solid/Liquid/Gas
-Organic Compounds: carbohydrate, lipid, protein, nucleic acids
-Inorganic Compounds: lithium, Fe. DON’T have C, O, H in makeup

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23
Q

Drug size is expressed in:

A

Molecular Weight (Daltons)
Most drugs 100-1000MW
>1000 MW cannot diffuse readily across barriers

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24
Q

Receptor Interactions

A

-Appropriate Size
-Electrical Charge
-Shape
-Atomic Composition

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25
Q

Covalent Bond

A

Shares electrons. STRONGEST bond, LOWEST specificity

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26
Q

Electrostatic Bonds

A

Charged (Ionic) Molecules, Hydrogen Bonds, Van der Waals forces (water)
Moderate strength & Specificity

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27
Q

Hydrophobic-lipid soluble drugs

A

Forms between a drug and receptor that BOTH don’t have a charge. MOST numerous. WEAKEST bond. HIGHEST specificity

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28
Q

Relationship between Bond Strength and Specificity

A

Inversely Proportional

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29
Q

Stereoisomerism

A

Mirror Images/Optical Isomers (D:L; R:S)

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30
Q

Racemic Mixtures

A

A combination of optical isomers
Ex: Racemic (R,S)-Ketamine (most common form)

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31
Q

What makes an amino acid

A

Carbon, Carboxyl Group, R Group, Hydrogen

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32
Q

S-ketamine

A

4x more potent. Purified Form

33
Q

R-Ketamine

A

More toxic

34
Q

Receptor

A

A protein made up of tens of thousands of amino acids to which a ligand/drug binds

35
Q

Receptor Site

A

The active site where the ligand/drug will bind

36
Q

Therapeutic Index

A

Threshold between max effect of drug and toxic response. Saturation of receptors demonstrates plateau phase. Difference between ED50 and LD50 (or TD50) on graph

37
Q

Bmax

A

Maximum Receptors Bound

38
Q

Kd

A

Drug concentration at which 1/2 of receptors are bound

39
Q

Emax

A

Maximum effect of drug

40
Q

EC50

A

Drug concentration at which you have 50% of effect

41
Q

Explain these graphs

A

Drug Response Curves

42
Q

Why does Kd not equal EC50?

A

Max effect does not require 100% of receptors to be bound

43
Q

Competitive Inhibitor

A

Binds to active site to inhibit agonist response. Can be countered by increasing amounts of agonist

44
Q

Surmountable

A

Able to outcompete competitive inhibitor by increasing amounts of agonist

45
Q

What line represents Competitive Inhibition

A

A+B

46
Q

What line represents an Allosteric ACTIVATOR

A

A+C

47
Q

What line represents an Allosteric INHIBITOR

A

A+D

48
Q

Non-Competitive Inhibitor

A

Does not compete for active site. Can bind to other sites on receptor. Insurmountable

49
Q

Insurmountable

A

Agonist cannot outcompete inhibitor. Irreversible

50
Q

Physiologic Antagonism

A

Drugs act at different receptors to squelch effect of other drugs
Ex: epinephrine binds to beta receptor and increases heart rate

51
Q

Partial Agonist

A

Binds with less affinity, more muted response. Can act as an ANTAGONIST in the presence of a full agonist

52
Q

Full Agonist

A

Induces conformation change in receptor for maximal effect

53
Q

Inverse Agonist

A

Antagonist on Steroids. Greater affinity for Ri form. Greater shutdown of downstream effect

54
Q

Ri vs Ra

A

Ri=Inactive Receptor form
Ra=Active Receptor form

55
Q

Potency

A

small amount, maximum effect

56
Q

Efficacy

A

More important than potency. Greatest possible response a drug can deliver. Depends on interaction with receptor

57
Q

Potency vs Efficacy

A

The clinical effectiveness of a drug depends on its maximal efficacy, not potency

58
Q

Drug Carriers

A

“drug super highway. Carries drug throughout body”
Ex: Albumin

59
Q

Inert Binding Sites

A

Binds to drug but does not cause a response

60
Q

Albumin

A

Primary carrier. Binds mostly to acidic drugs

61
Q

A1-acid glycoprotein

A

binds mostly to basic drugs

62
Q

Lipoproteins

A

Binds mostly to neutral drugs

63
Q

Therapeutic Index Formula

A

LD50/ED50 (in animals)
TD50/ED50 (in humans)

The safer the drug, the wider the therapeutic index

64
Q

Causes of Variation

A
  1. Alteration in concentration of drug that actually reaches the receptor
  2. Variation in concentration of endogenous receptor ligand
  3. Alteration in number and function of receptors
  4. Changes in components of downstream response
65
Q

pH < pKA in weak acid

A

protonated and uncharged

66
Q

pH < pKA in weak base

A

protonated and charged

67
Q

pH > pKA in weak acid

A

unprotonated and charged

68
Q

pH > pKA in weak base

A

unprotonated and uncharged

69
Q

Henderson Hasselbach Equation

A

pKA is the pH at which ionized and un-ionized concentrations are equal

70
Q

What are MAb’s

A

Monoclonal Antibodies. Produced by clones of a single parent cell. Targeted therapy approach for various diseases. Targets various receptors or growth factors on the cell surface and modulates their vital functions

71
Q

Antigen Binding Site

A

Critical part of MAb. Only binds to one particular target in the body

72
Q

How are MAb’s produced

A
  1. Targeted antigen is isolated and removed.
  2. Antigen is then introduced into a mouse/host organism
  3. Mouse will then produce its own antibodies against the antigen.
  4. Mouse is euthanized and spleen removed to obtain antibodies
  5. Antibodies fused with immortal myeloma cells (immortalization)
  6. New cells grown in culture
73
Q

Basic Structure of MAb

A

Antigen Binding Site, Constant domain

74
Q

Use of MAb’s in pathology

A

Asthma, migraines, cancer

75
Q

Role of the FDA

A
  1. Oversees development process in US
  2. Grants approval for marketing
  3. Reviews all claims/makes recommendation
  4. Ensures safety & efficacy
76
Q

OTC (non-prescription)

A

Freely available to public, low risk for harm/abuse. DOES NOT EQUATE TO SAFE

77
Q

Prescription Drugs

A

-Only available by recommendation of authorized health professional
-Viewed as “more effective” by the public
-Drug misuse has higher potential for harm
-Regulated by the FDA

78
Q

Thalidomide

A

Introduced in the 50’s in Europe for morning sickness. Teratogenic. MD Kelsey blocked approval in US. Presently used for multiple myeloma as immune suppressor.

Advanced Pharmacology (2 decks)

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