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Pharm 2024 > PPT 1 > Flashcards

PPT 1 Flashcards

Unit 1

1
Q

What is Pharmacology?

A

The study of how drugs interact with living systems, including their effects, mechanisms of action, and therapeutic uses

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2
Q

What does Endogenous mean?

A

Chemicals coming from 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

Who is the “Father of Western Medicine”?

A

Hippocrates

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10
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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11
Q

Who is the God of Medicine?

A

Asclepius

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12
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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13
Q

What is the 1st medical book with pharm?

A

Materia Medica

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14
Q

Who wrote Materia Medica?

A

Greek Physician: Dioscorides (c40 BCE)

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15
Q

What was the basis of Materia Medica?

A

Pertains to using botanical substances for medicinal use

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16
Q

Who is the father of Toxicology?

A

Paracelsus (1493 - 1541)

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17
Q

What did Paracelsus, the father of Toxicology, believe?

A

“The dose makes the poison”

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18
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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19
Q

About how many drug categories are there?

A

70

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20
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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21
Q

What is Phamacodynamics?

A

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

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22
Q

What is Pharmacokinetics?

A

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

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23
Q

What is Pharmacogenomics?

A

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

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24
Q

What gene responds to Herceptin in Breast Cancer?

A

HER2

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25
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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26
Q

What is an antagonist?

A

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

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27
Q

What is a poison?

A

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

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28
Q

What is a toxin?

A

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

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29
Q

What affects the route of administration?

A

The state of the matter; solid, liquid, or gas.

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30
Q

What are the macromolecules?

A

Carbohydrate, lipid, protein, nucleic acids

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31
Q

What makes a compound inorganic?

A

Compounds without Hydrogen, Carbon, or oxygen.

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32
Q

What are the units for molecular weight?

A

Daltons

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33
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.

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34
Q

What is Dalton equal to?

A

1g/mol

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35
Q

What is a receptor?

A

Proteins in the cell membrane that respond to a substance

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36
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.

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37
Q

What factors affect drug interaction with a receptor?

A

Size, reactivity/charge, shape, and atomic composition.

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38
Q

What is a covalent bond?

A

Strongest bond d/t shared electrons;

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39
Q

What is an electrostatic bond?

A

Also called an ionic bond, donates electrons that form cations and anions (hydrogen bonds and van der waals forces)

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40
Q

What is a hydrophobic bond?

A

The weakest but most numerous bond. They consist of lipid-soluble drugs, no charge

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41
Q

Where does the drug bind to the receptor?

A

Active site

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42
Q

What is an isomer?

A

Molecules with the same molecular formula

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43
Q

What are examples of isomers?

A

Fructose and Glucose
Both C6H12O6

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44
Q

What is a Stereoisomerism?

A

Isomers that differ in spatial arrangement of atoms, rather than order of atomic connectivity
(Optical Isomers or mirror images)

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45
Q

How do optical isomers apply to pharmacology?

A

Racemic mixtures

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46
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

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47
Q

Where does orthosteric bonding take place?

A

Binding at the primary active site on the receptor

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48
Q

Where does allosteric bonding take place?

A

Drug binds to something other than the primary active site (Non-competitive)

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49
Q

What is the relationship between 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.

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50
Q

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

A

Albumin

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51
Q

What is the pharmacokinetics acronym?

A

ADME
Absorption
Distribution
Metabolism
Excretion

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52
Q

What is an endogenous (native) ligand?

A

What the body normally produces that binds to active site
Ex) Epi from fight or flight response

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53
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 Emax (max effect). 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.

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54
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.

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55
Q

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

A

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

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56
Q

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

A

K(d) is referring to 50% of receptors bound vs EC(50) refers to 50% max effect of drug.

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57
Q

What is another name for a competitive inhibitor?

A

Competitive antagonist

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58
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 - surmountable

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59
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 - insurmountable

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60
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.

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61
Q

What are downstream inhibitors?

A

They act inside the cell by blocking an aspect of the downstream effect.

62
Q

What does surmountable mean?

A

To be outcompeted/overcome

63
Q

Is a competitive antagonist surmountable?

A

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

64
Q

Which bonds are insurmountable?

A

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

65
Q

When would you want to give a non competitive antagonist?

A

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

66
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

67
Q

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

A

The partial agonist will compete with the full agonist when given at the same time, reducing overall response
Acts as an antagonist.

68
Q

What is chemical antagonism?

A

Directly interacts with agonist chemically to neutralize it or prevent it from binding to receptor; opposite charges
Ex) Heparin (-) and Protamine (+)

69
Q

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

A

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

70
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.

71
Q

Which types of drugs favor R(i)?

A

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

72
Q

Which types of drugs favor R(a)?

A

Agonist and competitive antagonist

73
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
In practice, we will refer to as antagonist.

74
Q

What are indirect (mimic) agonists?

A

They don’t bind to the receptor but increase the levels of the endogenous ligand (natural agonist) or increase the receptor’s response to the endogenous ligand
This can result in an agonistic effect by enhancing the natural signaling pathway downstream

Ex) Amphetamine, Cocaine

75
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.

76
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.

77
Q

What is physiological antagonism?

A

Acts at a different receptor but produces an opposite physiological effect to that of the agonist
Effect: Does not compete with the agonist at the same receptor, but rather opposes its action through a different mechanism.
Example: Epinephrine (which increases heart rate) can act as a physiological antagonist to histamine (which decreases heart rate), even though they act on different receptors.

78
Q

Describe the differences between competitive vs non-competitive inhibition in a graph

A

Comp: The effect of the agonist can be overcome by increasing the concentration of the agonist
Non-comp: Reduces the maximum effect of the agonist, and this effect cannot be overcome by simply increasing the concentration of the agonist

79
Q

Describe an irreversible antagonist

A

Insurmountable because it binds and doesn’t let go (i.e. covalent bond)
- can be competitive or non-competitive depending on where it binds

80
Q

Describe a graph in which an agonist is alone, an agonist + competitive antagonist, agonist + allosteric agonist, and an agonist + allosteric inhibitor

A
81
Q

Describe a graph showing constitutive activity, full agonist, partial agonist, antagonist, and an inverse agonist

A
82
Q

What are the 4 branches of pharmacology?

A

Pharmacodynamics
pharmacokinetics, pharmacogenomics
toxicology

83
Q

List bond types from strongest to weakest

A

Covalent > electrostatic > hydrophobic

84
Q

What is a full agonist?

A

Binds to receptor and produces max possible response that the receptor can achieve (full biological effect)

85
Q

What are the 4 ways drug action can cease?

A
  1. Effects last only as long as drug binds receptor (binds and releases)
  2. Action persists after drug has dissociated (downstream effects just as important as receptor itself - phosphorylation or
    covalent bonds - until receptor is degraded)
  3. Desensitization - prevents excessive activation when agonist molecules present for extended periods of time (GPCRs)
  4. Receptor degradation (covalent bond)
86
Q

What are the 2 properties that make a receptor good?

A

Selective and alteration

87
Q

What are the bad (inert) receptors?

A

Non-regulatory molecules that bind drugs with no detectable change in function (ex. albumin) - drug carriers

88
Q

Why are inert binding sites important?

A

Affects drug distribution and determines amount of free drug in circulation

89
Q

What is the difference between a free vs bound drug carrier?

A

Bound: when plasma protein (albumin) is bound to drug, can’t cross barriers. Protein too large to cross barriers
Free (unbound): drug not bound to carrier.
- Only free drug can cross barriers and bind to receptors

90
Q

How does plasma protein binding effect how much of the drug we need to give?

A

If 90% bound to albumin and 10% free, will have to give a higher dose of drug to get the effect you want to see

91
Q

How does malnutrition effect albumin and drug dosing?

A

Malnourished patients have lower levels of albumin. More free drug available vs bound to albumin
- same dose given to malnourished patient will have much higher % of free drug (more toxicity)

92
Q

Give an example of a medication that binds to albumin

A

Phenytoin - 90% bound to albumin

93
Q

How can drug carriers cause displacement of drugs?

A

Drugs can compete for binding sites on albumin, one displacing the other; both drugs will have higher % of free drug
ex. phenytoin and carbamazepine

94
Q

What are the 3 most important protein drug carriers?

A
  • Albumin is PRIMARY drug carrier
  • a1-acid glycoprotein (AGP)
  • lipoproteins
95
Q

Why are dose response curves important?

A

They give us some idea of how much drug we have to give to get the response that we’re interested in

96
Q

What shape are all dose response curves?

A

Sigmoidal (S-shaped)

97
Q

Define potency

A

Concentration of dose needed to reach desired effect
- give small amount and get max effect - drug very potent

98
Q

EC50

A

EC50 - concentration of drug in plasma at 50% effect (pharmacologists)

99
Q

Define maximal efficacy

A

Max possible response a drug can deliver; more important than potency, determines effectiveness of drug

100
Q

What determines the clinical effectiveness of a drug?

A

Maximal efficacy

101
Q

ED50

A

ED50 - median effective dose; the dose required to achieve 50% of the desired response in 50% of the population (clinicians)

102
Q

TD50

A

Median toxic dose - where we see 50% of population with toxic side effect of the drug; used in human studies

103
Q

LD50

A

Median lethal dose - used in animal studies

104
Q

Therapeutic index

A

TI (animals) = LD50/ED50
TI (humans) = TD50/ED50

105
Q

How does therapeutic index correlate with drug safety?

A

The larger the therapeutic index the safer the drug is; est. margin of safety

106
Q

Describe efficacy vs potency in a graph

A

A reaches ED50, then C, then D
A, C, and D are equally efficacious
Potency: B > A > C > D
Drug B is most potent, but less efficacious

So c1 c2 and c3 - all three are going to have different Ed 50s, but if we look at the maximal efficacy, they all have the same maximal response

107
Q

Describe digoxin in terms of therapeutic index

A

Giving digoxin we’re inducing arrhythmias; getting therapeutic doses and still getting side effects because of narrow TI (TD50=4, ED50=2. TI= 4/2 = 2)

108
Q

What is an idiosyncratic response?

A

A strange or unusual way of behaving in reaction to drug

109
Q

What is usually the culprit of an idiosyncratic response?

A

Pharmacogenomics - genetic factors making patient hypo or hyper-reactive to drug

110
Q

What are the 4 causes that may contribute to variation in drug response?

A
  1. Alteration in concentration of drug that actually reaches the receptor
  2. Variation in concentration of endogenous receptor ligand
  3. Alteration in number or function of receptors
  4. Changes in components of response distal (downstream) to receptor
111
Q

What is the largest/most important cause of variation in drug response

A

Changes in components of response distal (downstream) to receptor - downstream proteins and body’s ability to compensate

112
Q

What patient factors can contribute to variation of drug response?

A
  • Rate of absorption/ distribution/ clearance
  • Age
  • Weight
  • Sex
  • Disease state
  • Liver and kidney function
113
Q

How would disease contribute to variation in drug response?

A

Disease process may have less cells that are active, especially liver cells

114
Q

What are extensions of therapeutic effects?

A

Toxic effects - sedative drugs can lead to coma/death in high doses

115
Q

How can drugs cause toxic effects?

A
  1. Some drugs produce both desired and adverse effects at same receptor (racemic mixtures)
  2. Other drugs bind to different classes of receptor sites (diff responses at diff receptors)
116
Q

Describe oral drug absorption

A

Oral drugs: GI → portal tract (liver) → systemic circulation → into tissues to bind to receptors

117
Q

What effects the charge of a drug?

A

pKa = dissociation constant

118
Q

What does the Henderson Hasselbach Equation relate?

A

The ionization constant (pKa) to [H+] (pH)

119
Q

What is the pKa?

A

Describes acidity, or how likely a molecule is to give up a proton

120
Q

What is the ratio of pH distance from pka?

A

Factor of 10, for every 1 point that pH gets away from pKa is a factor of 10 times
ex. if pH 2 points lower than pKa. will 100x favor the protonated form

121
Q

If pH>pKa

A

favors unprotonated form

122
Q

If pH<pKa

A

favors protonated form

123
Q

If a weak acid is protonated it is…

A

Not charged

124
Q

If a weak base is protonated it is…

A

charged

125
Q

In order to cross barriers, a compound will want to be ____

A

uncharged; more lipid soluble

126
Q

If aspirin (weak acid) has pKa = 3.5, what form does it take in the stomach (pH = 1.5)?

A

Protonated, uncharged

127
Q

If aspirin (weak acid) has pKa = 3.5, what form does it take in the intestine (pH = 6.5)?

A

Unprotonated, charged

128
Q

Where are most drugs filtered?

A

Glomerulus

129
Q

What are biologics?

A

Drugs created/extracted by living organisms (monoclonal antibodies, insulin, growth hormones)

130
Q

What suffix do monoclonal antibodies end in?

A

-mab

131
Q

How does recombinant DNA technology work?

A

take protein normally produced in human, put in animal/bacteria/fungi to produce it for us

132
Q

What makes monoclonal antibodies great for treatment?

A

Their specificity - decreased adverse effects and increased efficacy because they target a specific antigen with antigen binding site

133
Q

What are the two major functions of antibodies?

A
  • Recognize and bind (specific) antigen
  • Induce immune responses after binding
134
Q

The variable region of an antibody mediates what?

A

Binding
- Affinity and specificity for an antigen

135
Q

The constant region of an antibody mediates what?

A

Immune response

136
Q

Define monoclonal

A

Single clone of a single cell that we isolate, immortalize, and grew it up in culture and now have billions of antibodies

137
Q

FDA requires them to be safe, but doesn’t have to be effective

A

Herbal supplements/vitamins

138
Q

Prescription vs OTC drugs

A

RX: only available by recommendation of authorized health professional - viewed as more effective
OTC: freely available to general public; lower risk for harm/abuse (doesn’t = safe)

139
Q

Describe the phases of clinical testing

A
  1. Healthy volunteers; not looking at effectiveness, just safety
  2. Double-blind (one placebo, one drug); uses patients with disease process the drug is supposed to treat to determine if the drug works
  3. Involves assessing whether the new treatment is better than existing treatments
  4. Treatment is approved and available; long-term effects observed
140
Q

What medication for morning sickness was rejected by the FDA due to it causing Phocomelia?

A

Thalidomide

141
Q

Describe how monoclonal antibodies are made

A
  1. Immunization - mice are immunized with an antigen
  2. Spleen extraction - when sufficient titer is reached the mice are euthanized and spleen is removed as a source of cells for cell fusion
  3. Cell fusion - spleen cells fused with immortal myeloma cells
142
Q

Albumin want to bind to _____ drugs

A

acidic

143
Q

A1-acid glycoprotein want to bind to _____ drugs

A

basic

144
Q

Lipoproteins want to bind to _______ drugs

A

neutral

145
Q

Prior to phase 4 of drug studies it requires a

A

NDA (New Drug Application)

146
Q

Drugs approved by the FDA must be proven to be

A

Safe and effective

147
Q

The FDA regulates the way drugs can be

A

marketed (what claims can be made about the drugs)

148
Q

In Vitro studies are looking for new drugs identified as

A

Lead compound

149
Q

When a company identifies a potentially useful lead compound they will

A

apply for a patent

150
Q

Prior to drug researchers conducting human studies they must first

A

Ensure safety in animals and be approved for an IND (Investigational New Drug)

Pharm 2024 (32 decks)

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