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Pharm > Basic Principles of Pharm > Flashcards

Basic Principles of Pharm Flashcards

PPT 1

1
Q

What is Pharmacology?

A

The study of chemical interactions with living systems

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2
Q

What does Endogenous mean?

A

Chemicals inside the body
Natural Ligands
Ex) Epi released in body during fight or flight response

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3
Q

What does Exogenous mean?

A

Chemicals outside the body
Ex) giving Epi IV

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4
Q

What is Medical Pharmacology?

A

Substances used to prevent, diagnose, and treat diseases

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5
Q

What does toxicology mean?

A

Undesirable effects of chemicals on/in living systems (Not side effects)
Things that are toxic to you
Ex) Poisons

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6
Q

Who is the first recorded physician?

A

Imhotep (3000 BCE)

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7
Q

When was pharmacology first started?

A

in 3000 BCE with the first recorded physician Imhotep

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8
Q

What is traditional medicine referred to in India?

A

Ayurvedic

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9
Q

What country is Ayurvedic native to?

A

India

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10
Q

What is Hippocrates?

A

Ancient Greek Father of Western Medicine

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11
Q

Who is the “Father of Western Medicine”?

A

Hippocrates

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12
Q

Who is Asclepius?

A

Ancient Greek; God of Medicine

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13
Q

What is the Rod of Asclepius?

A

Medical symbol often confused with the Caduceus.
Has only 1 snake on rod

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14
Q

Who is the God of Medicine?

A

Asclepius

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15
Q

What is a Caduceus?

A

Rod of Hermes
Hermes is Greek Messenger God
Used for trade
Often confused as a medical symbol
Has 2 snakes on rod

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16
Q

What is the 1st medical book with pharm?

A

Materia Medica

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17
Q

Who wrote Materia Medica?

A

Greek Physician: Dioscorides (c40 BCE)

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18
Q

What was the basis of Materia Medica?

A

Pertains to using botanical substances for medicinal use

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19
Q

Who is the father of Toxicology?

A

Paracelsus (1493 - 1541)

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20
Q

What did Paracelsus, the father of Toxicology, believe?

A

“All things are poison, and nothing is without poison”
“The dose makes the poison”
This means means to me that if you give something in a large enough quantity then it will be poison

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21
Q

What is the purpose of controlled drug trials?

A

It attributes to the regulation of drugs.
Assures that medications are not a placebo effect.
Has helped to get rid of pointless medicines by evaluations of therapeutic claims.

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22
Q

About how many drug categories are there?

A

70

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23
Q

-vir

A

Antiviral

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24
Q

-cillin

A

Penicillin- Abx

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25
Q

Cef-

A

Cephem- Abx

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26
Q

-mab

A

Monoclonal antibodies

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27
Q

-ximab

A

Chimeric antibody; repsonds to multiple antigens

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28
Q

-zumab

A

humanized antibody

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29
Q

-tinib

A

Tyrosine-Kinase inhibitor

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30
Q

-vastatin

A

HMG-CoA reductase inhibitor

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31
Q

-prazole

A

Proton pump inhibitor

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32
Q

-lukast

A

Leukotriene receptor antagonists

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33
Q

-grel-

A

platelet aggregation inhibitor

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34
Q

-axine

A

Dopamine and Serotonin-norepinephrine reuptake inhibitor

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35
Q

-oxetine

A

Antidepressant related to fluoxetine

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36
Q

-sartan

A

Angiotensin receptor antagonist

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37
Q

-oxacin

A

Quinolone- Abx

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38
Q

-barb-

A

Barbiturates

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39
Q

-xaban

A

Direct Xa inhibitor

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40
Q

-afil

A

Inhibitor of PDE5 with vasodilation

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41
Q

-prost

A

Prostaglandin analogue

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42
Q

What is generic name vs trade name?

A

Generic names can be easily grouped together by stem. Trade names can change depending on company.
We will use generic names.

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43
Q

What is Phamacodynamics?

A

What a drug does to the body
Ex) Increases heart rate

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44
Q

What is Pharmacokinetics?

A

What the body does to the drug
Ex) Half life after metabolizing

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45
Q

What is Pharmacogenomics?

A

Genetic profile to determine how you will respond to a drug before administering it

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46
Q

What gene responds to Herceptin in Breast Cancer?

A

HER2

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47
Q

What is an agonist?

A

A drug that binds to receptor and elicits response.
Effects may be more or less than native ligand.

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48
Q

What is an antagonist?

A

Binds to receptor and blocks receptor reaction.
Prevents binding of native ligand

49
Q

What is the difference between an agonist and antagonist?

A

Agonists activate receptors to elicit a response; antagonist block receptors to prevent a response.

50
Q

What is a poison?

A

a nonbiological substance that has negative effects on the body.
Ex) lead

51
Q

What is a toxin?

A

biological substance that has negative effects on the body (created from living substances)
Ex) poison mushrooms

52
Q

What affects the route of administration?

A

-The state of the matter; solid, liquid, or gas
-Molecular weight

53
Q

What are the most basic organic compounds?

A

Carbohydrate, lipid, protein, nucleic acids

54
Q

What makes a compound inorganic?

A

Compounds without Hydrogen, Carbon, or oxygen.

55
Q

What are the units for molecular weight?

A

Daltons

56
Q

How does molecular size effect diffusion?

A

Most drugs weigh between 100-1000 Daltons. A weight of >1000 makes it that the drug cannot readily diffuse.

57
Q

What is Dalton equal to?

A

1g/mol

58
Q

What is a receptor?

A

Proteins: large chain of amino acids

59
Q

What is the relationship between a drug and a receptor?

A

It’s similar to a lock and key; when the key fits you get the expected response, when it doesn’t fit you don’t get the same response.

60
Q

What things affect if a drug will fit into receptor?

A

Size, electrical charge, shape, and atomic composition.

61
Q

What is a covalent bond?

A

Strongest bond d/t shared electrons; 50-150 kcal/mol

62
Q

What is an electrostatic bond?

A

Also called an ionic bond, donates electrons which form cations and anions.
5-10 kcal/mol

63
Q

What is a hydrogen bond?

A

A type of electrostatic/ionic weak bond
2-5 kcal/mol

64
Q

What is Van der Waals forces?

A

A type of electrostatic/ionic weak bond

65
Q

What is a hydrophobic bond?

A

The weakest but most numerous bond. They consist of lipid soluble drugs.
0.5-1 kcal/mol

66
Q

What does hydrophobic mean?

A

“Water hating”

67
Q

Where is a receptor in the body?

A

Mostly it is attached on the surface of a cell

68
Q

Where does an agonist or competitive antagonist bind to the receptor?

A

Active site

69
Q

What happens after an agonist binds to a receptor?

A

There is a response within the cell

70
Q

What is an isomer?

A

Same formula but different shape; they will not have the same effects.

71
Q

What are examples of isomers?

A

Fructose and Glucose
Both C6H12O6
But different shapes

72
Q

What is a Stereoisomerism?

A

Optical Isomers or mirror images.
Same formula but mirrored shapes.
They do not have the same effect.

73
Q

Why a stereoisomerism important?

A

Consists of most racemic mixtures

74
Q

What is the main difference in isomers/stereoisomers?

A

Isomer are different compounds even though they have the same chemical formula therefore you have different side effects.

75
Q

What is the difference between R-ketamine and S-ketamine?

A

R- is more toxic and S- is 4x more potent
Changes effects at the receptor

76
Q

What is Racemic ketamine?

A

R- and S- ketamine mixture

77
Q

What is the pure form of ketamine?

A

Esketamine (S-ketamine)

78
Q

Where does orthosteric bonding take place?

A

Inside the receptor active site.

79
Q

Where does allosteric bonding take place?

A

Outside the active site on a receptor.
(Non-competitive)

80
Q

What is the relationship between bond strength and bond specificity?

A

It is inversely proportional.
The stronger the bond, the less specific the bond. The weaker the bond, the more specific the bond.

81
Q

What is the difference between specific and non specific binding?

A

Specific binding is highly selective and binds to the receptor that its meant to be with; non specific binding is more generalized.

82
Q

Why would we want to give a drug that is non specific binding?

A

Specific binding has a max; we give more of the drug until all specific receptors are saturated and they have reached their max. Once we have binded to all the specific receptors we can give a non specific binding drug to increase the desired effects.

83
Q

What is an example of a drug that is non specific binding?

A

Albumin

84
Q

What is the pharmacokinetics acronym?

A

ADME
Absorption
Distribution
Metabolism
Excretion

85
Q

What is a native ligand?

A

A compound that is already in the body
Ex) Epi from fight or flight response

86
Q

Describe the Dose Response Curve.

A

It is the “Log Dose” x “Response”
It shows that if we give an increased dose then we’ll increase the response until we reach the therapeutic index (desired pain relief). But if we continue to increase the dose beyond that, the receptors will become saturated and the response will plateau. We will see more toxic side effects at that point.

87
Q

What is the therapeutic index in the Dose Response Curve?

A

The point where pain relief is established or the desired effect in present.

88
Q

What is drug concentration?

A

How much concentration is present in the blood at a specific time.

89
Q

What does the Drug Concentration Response Curve show?

A

It can either show the drug effect/response or the the receptors bound.

90
Q

What is EC(50) and E(max) in the Drug Concentration Response Curve?

A

EC(50) is a point on the horizontal axis (Drug Concentration) where you see 50% of drug effects.
E(max) is a point on the curve where you max out the drug effects right before the curve plateaus.

91
Q

What is K(d) and B(max) on the Drug Concentration Response Curve?

A

K(d) is a point on the horizontal axis where 50% of the receptors are bound.
B(max) is the point where 100% of the receptors are bound.

92
Q

What is the difference between K(d) and EC(50)?

A

K(d) is referring to 50% of receptors vs EC(50) is referring to 50% effect/response of drug.

93
Q

What is the relationship between K(d) and receptor affinity?

A

The relationship is inverse.
Low K(d) = high drug/receptor affinity; the drug binds well to the receptor.
High K(d) = low drug/receptor affinity; the drug doesn’t bind well to the receptor.

93
Q

What is another name for a competitive inhibitor?

A

Competitive antagonist

94
Q

Describe the relationship between an agonist and a competitive antagonist?

A

An agonist can outcompete a competitive antagonist by increasing the dose of the agonist. Eventually you will get the same results after increasing dose of agonist.

95
Q

Describe the relationship between an agonist and an allosteric antagonist?

A

You cannot outcompete an allosteric antagonist (non-competitive antagonist) because it’s not competing for the same receptor site.
If you keep increasing dose of agonist, you will only see a toxic effect. The results will be dramatically lower and will not increase with an increase of the dose of the agonist.

96
Q

Describe the relationship between an agonist and an allosteric activator?

A

An agonist and and allosteric activator (allosteric agonist) work together to get an increased result. An allosteric activator binds outside out of the active site.

97
Q

What are downstream inhibitors?

A

They are naturally occurring enzyme that blocks the downstream effects of agonist

98
Q

What does surmountable mean?

A

To be outcompeted

99
Q

Is a competitive antagonist surmountable?

A

Yes, if you continue to give the agonist then the competitive antagonist will be surmounted

100
Q

Which bounds are insurmountable?

A

Allosteric inhibitors and competitive antagonists with covalent bonds (Covalent bonds are basically permanent), therefore you will never outcompete.

101
Q

When would you want to give a non competitive antagonist?

A

When you want to decrease the natural ligand effects (counteract)

102
Q

What is a partial agonist?

A

It produces a lower response at the receptor than a full agonist at B(max)
Partial agonist… partial response

103
Q

What happens in the presence of an agonist and a partial agonist?

A

The partial agonist will outcompete the full agonist when given at the same time.
Acts as an antagonist.

104
Q

Why don’t partial agonists give the same response as full agonists?

A

SSEA - Shape, size, electronic charge, and atomic composition of drug. Therefore receptor doesn’t have the same reaction.

105
Q

What is another method of antagonism?

A

Oppositely charged drugs can bind to each other preventing their effects.
Has no receptor involvement
Ex) Heparin (-) and Protamine (+)

Physiological antagonism which is 2 drugs binding to 2 different receptors and having the opposite responses.
Ex) 1 drug increases HR / 2nd drug decreases HR

106
Q

What does R(a) and R(i) stand for?

A

R(a) = Receptor active
R(i) = Receptor inactive

107
Q

Example how R(a) and R(i) works as far as receptor activity.

A

Unoccupied receptors stay in a constitutive state = They are ALWAYS switching back and forth from active and inactive.

108
Q

Which types of drugs favor R(i)?

A

Inverse agonist!!!!!!
The I in Inverse means R(i) !!!!!!!

109
Q

Which types of drugs favor R(a)?

A

Agonist and competitive antagonist

110
Q

What is an inverse agonist?

A

Acts as an antagonist; has a greater affinity to R(i) and stabilizes R(i) form.
Can shut down the downstream response.
Drops BELOW the constitutive activity line (drops below agonist line)
In practice, we will refer to as antagonist.

111
Q

What does a Beta-1 Receptor do?

A

Increases contractility; Increases heart rate; Releases Renin (Helps perfuse kidneys)

112
Q

Examples of Beta-1 Agonists

A

Epinephrine
Norepinephrine

113
Q

What are indirect (mimic) agonists?

A

They bind to the downstream inhibitors, amplifying the agonist response.
Ex) Amphetamine, Cocaine

114
Q

Examples of partial Beta-1 agonists

A

Pindolol
Acebutolol

115
Q

Examples of Beta-1 antagonists

A

Propanolol
Atenolol

116
Q

Examples of Inverse Beta-1 agonist

A

Carvedilol
Nadolol

117
Q

Which has the strongest effect: Antagonist or Inverse agonist?

A

Inverse agonist; it falls below the constitutive line. The constitutive line is where an antagonist would be.

118
Q
A

Pharm (30 decks)

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