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E'Pharmacology Test 1 Fall '24 > 08/21 Intro To Pharm Lecture 1 > Flashcards

08/21 Intro To Pharm Lecture 1 Flashcards

1
Q

What are exogenous chemicals?

A

Chemicals that originate outside of the body

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2
Q

What is medical Pharmacology

A

Substances used to prevent, diagnose and treat diseases

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3
Q

Define Toxicology

A

Study of Undesirable effects of chemicals on living systems. (Toxins and poisons and how they affect the body– not side effects)

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4
Q

Four practices of prehistoric Medicine

A

Shamanism, Animism, Spiritualism and Divination

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5
Q

Who was Imhotep? Where was he from? What year?

A

First recorded physician; Ancient Egypt; 3000 BCE

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6
Q

Who was the father of western/Modern medicine? Where was he from?

A

Hippocrates; Ancient Greece

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7
Q

Ayurvedic is from what country? How mays years has it been practiced?

A

Indian Subcontinent; 1000s of years.

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8
Q

God of Medicine?

A

Scapulus. Not Caduces. One snake instead of 2 around a rod.

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9
Q

First ever medical book? Who wrote it? Year? What it entails

A

Materia Medica; Dioscorides; (c40 BCE); Collection of works throughout history. Body of knowledge on botany and medical substances.

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10
Q

What are endogenous chemicals?

A

Chemicals that originate inside of the body.

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11
Q

Who coined the phrase “The dose makes the poison” ?

A

Paracelsus (1493-1541)

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12
Q

Why is the phrase “the dose makes the poison” important?

A

any drug, even one typically used for “good”, can be harmful (poisonous) when the dose is too high.

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13
Q

There are several thousands of drugs out there. How many groups are there?

A
  1. (just know prototypical drugs - others are just variations of prototype)
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14
Q

What is Pharmacodynamics?

A

the study of what the drug does to the body
I.e. You give a drug and see the HR go down.

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15
Q

What is Pharmacokinetics?

A

The study of what the body does to the drug.
I.e. what is the half life of the drug d/t the liver being able to break it down, Can the BBB stop the drug from entering the brain.

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16
Q

What is Pharmacogenomics?

A

The study of a person’s genetics to predict how well the person will respond to a certain drug or drugs (e.g cancer HER2)

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17
Q

What is an Agonist?

A

A drug that elicits a response from the receptor when it is bound to that receptor.

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18
Q

What is a ligand?

A

A molecule or atom that binds to a receptor causing changes in the cell signaling.
I.e. endogenous or exogenous drugs

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19
Q

Difference between poisons and toxins
Both can ________ or ___________ receptors

A

Poisons are inorganic (lead, arsenic). Toxins are organic (puffer fish toxins, snake venom). Both can also bind or block receptors.

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20
Q

What response do exogenous agonists typically elicit?

A

The same response you would expect from an endogenous agonist.
I.e. Endogenous Epinephrine vs exogenous epinephrine.

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21
Q

What does an antagonist do?

A

It blocks the endogenous ligand from binding to the receptor, or it blocks that receptor from functioning. It essentially shuts down the receptor- blocks it.

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22
Q

What are the categories of organic compounds?

A

Carbohydrates, lipids, proteins, nucleic acids (P-Li-Na-C)

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23
Q

Drug sizes are expressed in ___________

A

Daltons.

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24
Q

What are the characteristics that determine receptor interactions?

A

Size
Atomic composition
electrical Charge
Shape
(SACS)

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25
Q

What size of daltons cannot readily diffuse readily?; and how are they given?

A

> 1000 MW; They are given straight in the bloodstream.

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26
Q

1 Dalton = _________ (g/mol)

A

1

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27
Q

Daltons are expressed in ___________;Most drugs weigh ______ to ______;

A

Molecular weight; 100-1000 MW

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28
Q

Rank Types of Bonds from strongest to weakest and energy required to break them down

A

Covalent - 50-150 kcal/mol
Electrostatic (ionic) 5-10 kcal/mol
Hydrogen 2-5 kcal/mol
Hydrophobic 0.5-1 kcal/mol

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29
Q

What is the strongest bond in the biological system?

A

Covalent bond

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30
Q

what is an electrostatic bond?

A

A bond that is created from charges (Negative to positive) (middle weakest)

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31
Q

What is a covalent bond?

A

A bond created from 2 molecules sharing electrons (strongest)

32
Q

What is a hydrophobic bond?

A

A bond created between a non-polar (no charge) drug and a non-polar receptor site. these drugs are water-fearing and are soluble in lipids. (weakest)

33
Q

What is the relationship between bond strength and specificity?

A

Inverse
The stronger the bond the less specific (Covalent), The weaker the bond, the more specific.
(Hydrophobic-weakest)

34
Q

What are most Receptors made of?

A

Proteins

35
Q

What is an isomer?

A

Molecules that have the same chemical equation, but a different arrangement of atoms (a different shape)
I.e. fructose and glucose have the same c6h1206 but a different shape, and therefore have different effects on the body.

36
Q

Chirality meaning

A

When an object does not mirror. (An object or a system is chiral if it is distinguishable from its mirror image)

37
Q

What is an optical isomer? Will they have the same effects?

A

A mirror image of isomers. 2 molecules that have the same chemical equation but different physical structure.
*Think gloves;

No. When mirrored, the object will not lie in the right slot.

38
Q

What is a racemic mixture?

A

A 50:50 mixture of two optical isomers.
I.e. R ketamine (more toxic) and S ketamine (4x More Potent).

39
Q

What is an active site on a receptor?

A

The site on a receptor where, typically, the native ligand would bind. Orthosteric.

40
Q

Allosteric site ligands might elicit a response by_______

A

closing the active site or make active site more available.

41
Q

Are there other binding sites on a receptor besides the active site, and what do they do?

A

Yes, they act in different ways. Some close the active site where a ligand cannot bind. Some may enhance the active site in a way that makes a ligand bind better.

42
Q

What are the drugs that bind to sites on a receptor called that are NOT the active site?

A

Allosteric

43
Q

What is the classification of ligand that binds to an active site on a receptor?

A

Orthosteric

44
Q

What does ADME stand for?

A

Absorption
Distribution (where does it go? blood, muscle, tissues? gut?)
Metabolism (active form?, inactive form?)
Excretion (kidneys?

45
Q

Plateau in the Concentration/effect graph means that;

A

Receptors are saturated and response is locked out. More drugs given, toxic effects seen.

46
Q

Therapeutic index means________

A

difference between maximum dose response of a drug and toxic response

47
Q

What is the EC 50?

A

Concentration where we see 50% effect of the drug. (dose is not same as concentration)

48
Q

Bmax vs Emax

A

Bmax is the maximum binding to receptor. Emax is maximum effect of medicine (right before it plateaus)

49
Q

What is the Kd 50?

A

Concentration where 50% of receptors are bound. (Kd never changes— changes based on drug)

50
Q

Why does the Kd not equal the EC50?

A

Because a drug can bind to 25% of the receptors and elicit a 50% effect. The amount of receptors bound does not directly correlate to the same percentage of effect. (10% Kd can elicit a 50% response with some drugs)

51
Q

What does a high or low Kd on a graph mean in terms of receptor affinity?

A

Low Kd= high drug/receptor affinity
High Kd= low drug/receptor affinity

52
Q

What does an allosteric activator do? (Pic of all 4: agonist, competitive inhibitor, allosteric activator, allosteric inhibitor)

A

It is a drug that binds somewhere outside of the active site and elicits a response in the active site to bind more easily to the agonist.

53
Q

What does giving an increasing dose of an agonist + an allosteric activator do?

A

It shifts your graph to the left. It elicits an even greater response than the normal agonist, increasing the maximum effect of the agonist drug.

54
Q

What is a competitive inhibitor?

A

A subtype of antagonist that competes for the active site on the receptor.

55
Q

What does giving an increasing dose of an agonist + a competitive inhibitor antagonist do?

A

It shifts your graph to the right, meaning you will need more and more agonist drug to overcome the antagonist and eventually see the same response as an agonist drug by itself.

56
Q

What is an allosteric inhibitor?

A

An Antagonist that binds outside of the active site and is NONcompetative. (Because it binds outside of the active site)

57
Q

Can an allosteric inhibitor be surmounted?

A

No, because it binds outside of the active site and therefore can never be overtaken by the orthosteric agonist.

58
Q

What does giving an increasing dose of an agonist + an allosteric inhibitor do?

A

It shifts the graph WAY to the right, never reaching the normal agonist limits. Meaning it blocks the effects of the agonist.

59
Q

What is an agonist mimic or indirect agonist? (downstream inhibitors) (pic)

A

A drug that works down the cascade of events to increase the effects of an agonist.

60
Q

Associate competitive with

A

Surmountable. You can give more agonist and eventually outcompete the antagonist.

61
Q

Associate non-competitive with

A

Insurmountable. No matter how much agonist you give, the agonist will never win.

62
Q

What is an example of a orthosteric insurmountable antagonist?

A

An antagonist that binds at the orthosteric space and creates a covalent bond.

63
Q

A Partial agonist acts as an ______ in the presence of a full agonist

A

Antagonist

64
Q

Partial agonists bind with less affinity as they _______

A

Produce a lower response at full receptor occupancy.

65
Q

What are 2 other mechanisms of antagonism

A

Administrating the opposite charge. I.e. overdose one negatively charged heparin you counteract with positively charge Protamine. Nothing to do with a receptor.

Physiologic- squelching the effect of drug 1. I.e. Epinephrine vs. aceytlcholine. Epi binds to beta receptors to speed up HR but acetylcholine works on muscarinic receptors to slow HR down.

66
Q

What is an inverse agonist?

A

A drug that favors the inactive form of the receptor. Acting like an antagonist because is shuts the receptor down so no cascade effect can happen.

67
Q

Briefly describe the history of Pharmacology.

A

Early medicine-Imhotep first physician
Mysteria Medica- a composition of botany and how effects the body
Paracelsus- Father of toxicity
Drug trials and Clinical testing

68
Q

What is the difference between toxins and poisons?

A

Poisons are NON-biological. Toxins come from living organisms.

69
Q

Define Stereoisomerism

A

It’s a form of isomerism in which molecules have the same molecular formula and sequence of bonded atoms, but different spatial orientation.

70
Q

What is the Emax?

A

The maximum effect a drug can have when the drug is concentrated in the blood.

71
Q

What is Bmax?

A

The highest point on the graph when 100% of the receptors are bound to the drug.

72
Q

What is current receptor theory

A

Most receptors exist in equilibrium in active and inactive states. Agonists favor the active form and vise versa.
Most receptors exist in equilibrium

73
Q

Inverse Agonist has greater affinity for _______

A

Ri (Inactive form of receptor). Stabilizes the Inactive form, thus providing antagonistic activity.

74
Q

In theory, Inverse agonist are_________
In practice, inverse agonists are_______

A

Agonists as they are eliciting a response
Antagonists

75
Q

Difference between Full agonist, Patial agonist, Antagonist and Inverse agonist

A

Full agonist: We see the full response. Raises that activity Favors active form
Partial agonist: Partial response
Antagonist: Antagonistic to both-so we dont see any effect–straight line (also keeps constituitive activity)
Inverse: favors the inactive form

76
Q

How does cocaine and amphetamines actually work

A

They dont actually bind, they make the epi more available.

E'Pharmacology Test 1 Fall '24 (5 decks)

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