Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

KMMS > Intro to Pharmacology > Flashcards

Intro to Pharmacology Flashcards

1
Q

A molecule on the surface of the cell (or inside it) that receives an external signal and produces some type of cellular response is known as a ________-__________ interaction.

A

drug-receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A protein recognition molecule for a chemical mediator

A

Receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

“Ligand-binding theory” describes how the right molecule binds to the receptor, which leads to a conformational change in the ________, leading to cellular changes.

A

protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Drugs can change the ________ and _________ of body functions

A

amplitutde and speed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

___________ prevent the binding of endogenous compounds.

A

Antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The site on a receptor where a non-competitive antagonist binds is called an

A

allosteric binding site or allosteric effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name some examples of competitive reversible antagonists

A

Beta blockers, atropine, naloxone, and Prazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drugs that have opposing physiological actions at different receptors

A

Functional or physiological antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The effect of adrenaline on histamine produced in anaphylaxis is what type of antagonism?

A

Functional or physiological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a chemical antagonist?

A

A substance that binds to and inactivates the agonist itself (as opposed to something that binds to an inactivates a receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

This describes how tightly a ligand binds to a receptor

A

Affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The probability that a drug molecule will bind to an available receptor at any given instant in time is expressed numerically as the _______ ________ (__)

A

dissociation constant (Kd)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The dissociation constant is the concentration of ________ required to occupy ____% of the available receptors.

A

agonist, 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The lower the dissociation constant (Kd), the _________ the affinity.

A

higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The ability of an agonist to produce a biological effect

A

Drug efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Drug efficacy is expressed numerically as

A

R Max (maximum response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What numerical expression is used to compare whether one drug is as effective as another?

A

R Max

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

A measure of drug activity expressed in terms of the amount required to produce an effect of given intensity

A

Drug potency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Drug potency depends on both _______ and ________.

A

affinity, efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

One measure used to look at drug potency is _____

A

EC 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Half maximal effective concentration is represented as .

A

EC 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

This is the concentration of a drug, anitbody, or toxicant which induces a response halfway between the baseline and maximum after a specified exposure time

A

EC 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The ________ the EC50, the _________ the potency.

A

lower, higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can drugs be classified? (List 3 ways)

A
  1. Site or mode of action
  2. Therapeutic use
  3. Chemical structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

“What the body does to the drug”

A

Pharmacokinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

“What the drug does to the body”

A

Pharmacodynamics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List the four main phases of pharmakokinetics (ADME)

A

Absorption
Distribution
Metabolism
Excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

This is the process of transfer of the drug from the site of administration into the general/systemic circulation.

A

Absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How much of the drug, if taken orally, reaches the systemic circulation after first-pass metabolism?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

The process by which a compound is transferred from the general circulation to other parts of the body and into the tissues is known as

A

Distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

The process by which a drug is chemically altered in a way that facilitates its action or enhances its elimination from the body

A

Metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

The main site of drug metabolism in the body

A

the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name the sites of drug metabolism in the body

A 
Liver
Kidneys
GI tract
Lungs
Skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

The superfamily of enzymes that metabolise >75% of drugs used in medicine

A

Cytochrome p450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the effect on the drug in the body with enzymatic induction?

A

Faster clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the effect on the drug in the body in cases of enzymatic inhibition?

A

Accumulation of drug in the system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

The process by which drugs or their metabolites are removed from the body

A

Excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are routes of drug excretion?

A

Renal, biliary, respiratory, dermal, faecal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Pharmacodynamics mainly has to do with the interaction of the drug with rthe body’s _______

A

proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What occurs when the drug interacts with the same type of receptor at different sites around the body, and/or interacts with more than 1 type of receptor?

A

Side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

True or false: No drug is free of side effects

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Individual drug response can be influenced by

A 
Age
Gender
Genetics
Previous exposure
Disease
Interactions
Body composition
Variability in PK and PD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Briefly list the key stages of drug development

A 
Non-clinical testing
Phase I, II, and III clinical studies
Registration with MHRA
Launch phase
Post-launch research and development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is “2 species toxicology” in the non-clinical testing phase?

A

Testing on 1 rodent species and 1 non-rodent species for a minimum of 14 days to determine PK and ADME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does the non-clinical testing phase look for?

A 
Effects on:
Pharmacokinetics
ADME
Pharmacodynamics
Local tolerance/phototoxicity/immunotoxicity
Genotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

This phase of clinical trials tests a new drug on a small group of humans- usually multiples of 10, in healthy volunteers or patients affected with the particular disease.

A

Phase I clinical trials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Phase I trials look for:

A 
*SAFETY/TOLERABILITY*
Data on PK/PD
Guide to therapeutic dose
Drug/food interactions
Drug/Drug interactions
QT prolongation potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why would ECG’s be performed on volunteers in Phase I clinical trials?

A

To look for QT prolongation- abnormal heart rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How long do Phase I trials typically last?

A

1-4 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Distribution of phase I clinical trials?

A

Single centre, one country

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

This phase of clinical trials involves several hundred partipants (multiples of 100) who are living with the condition the new medication is meant to treat.

A

Phase II clinical trial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

These are randomised clinical trials to show that the candidate drug results in a biological and/or clinical change associated with the disease or mechanism of action.

A

Phase II clinical trial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

This phase of clinical trial enables dose selection (most effecacious dose) for the next phase

A

Phase II clinical trial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How long do phase II clinical trials typically last?

A

3-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

This phase of clinical trials is known as the “therapeutic exploratory” phase

A

Phase II

56
Q

This phase of clinical trials usually involves multiples of 1000 patients who have the condition that the new medication is meant to treat

A

Phase III

57
Q

Trials in phase III can last for __________

A

several years

58
Q

The main purpose of this phase of clinical trials is to evaluate how the new medication works in comparison to existing medications for the same condition.

A

Phase III

59
Q

How many randomised controlled trials take place in Phase III?

A

At least two

60
Q

What are the end points of Phase III clinical trials?

A

Safety is essential!
Regulatory acceptance
Patient reported outcomes for QOL

61
Q

In phase III clinical trials, the safety and efficacy of the new drug is compared to

A

the current standard of care

62
Q

Distribution of phase III clinical trials?

A

> 10 centres, multinational

63
Q

This is the phase where further scientific data is collected on efficacy or safety objectives. Can look for new disease indications.

A

Phase IIIb or phase IV

64
Q

Prior to the invention of antibiotics, _________ __________ were the leading cause of death.

A

infectious diseases

65
Q

What are the three ideal characteristics of antiobiotic therapies?

A
  1. Selective toxicity
  2. Slow emergence of resistance
  3. No interference with other drugs
66
Q

Name some of the PATIENT FACTORS to consider that might affect either the PK or the patient response to treatment

A

Decreased liver or kidney function

Whether they are immunocompromised

67
Q

List the six principal mechanisms of antiobiotic actions

A
  1. Cell wall
  2. DNA replication
  3. RNA synthesis
  4. Antimetabolites
  5. Protein synthesis against Rb 50
  6. Protein synthesis against Rb 30
68
Q

What is the mneumonic for remembering protein synthesis ihibitors?

A

Ma life AT cell

Macrolides- Lincosamides (clindamycin)- Aminoglycoside, Tetracyclines- Clindamycin, Erythromycin

50s 30s 50s

69
Q

NITu MET SULtan in CEPtember with a FLUid PEN and a CAR

A 
Nitrofurans = DNA synthesis inhibitor
Metronidazole= DNA replication inhibitor
Sulfonamides = Antimetabolites
Cephalosporin = cell wall inhibition
Fluoroquinolone = DNA replication
Penicillin= cell wall inhibition
Carbapenem= cell wall inhibition
70
Q

Name the two types of drugs affecting the bacterial cell wall

A
  1. Beta lactams

2. Glycopeptides

71
Q

Beta lactams bind bacterial _____________

A

transpeptidases

72
Q

What are the enzymes that are essential for peptidoglycan synthesis?

A

Transpeptidases

73
Q

Beta lactams prevent the cross-linking peptides from binding to the

A

tetrapeptide side chains

74
Q

Are beta lactam drugs bactericidal or bacteristatic?

A

Bactericidal

75
Q

The two main classes of beta lactams commonly used in practice include:

A
  1. Penicillins

2. Cephalosporins (Cephalexin, Cefuroxime)

76
Q

The beta lactam drugs generally reserved for difficult to treat infections include

A

Carbapenems and monobactams

77
Q

Vancomycin, Teicoplanin, and Telavancin are in what type pf drug class?

A

Glycopeptides (inhibit cell wall synthesis)

78
Q

When are glycopeptides used?

A

Only for Gram + bacteria, in serious infections where bacteria is producing beta-lactamase. Generally administered IV.

79
Q

What is the treatment for C.Difficile infection?

A

Oral Vancomycin

80
Q

What is the main adverse effect associated with glycopeptides?

A

Nephrotoxicity

81
Q

Ciprofloxacin, Nalidixic acid, Norfloxacin, and Ofloxacin are what class of drugs?

A

Quinolones

82
Q

Mechanism of action for this drug class: Inhibits DNA gyrases needed for DNA supercoiling, replication and separation

A

Quinolones

83
Q

What types of infections are quinolones used for?

A

UTI (not first line), pseudomonal infection, GI infections, STI’s

Gram negative, Gram positive, anaerobes, mycoplasma, chlamydia

84
Q

Metronidazole is a pro-drug. This means that only _________ organisms can metabolise it into its active form. Metabolites that are produced are toxic to the DNA.

A

anaerobic

85
Q

List some of the potential adverse effects associated with extended use of metronidazole

A

Mutagenic, carcinogenic, teratogenic

86
Q

Drug that inhibits RNA synthesis

A

Rifampicin

87
Q

Which drug is bactericidal in mycobacteria?

A

Rifampicin

88
Q

How does Rifampicin inhibit mRNA synthesis?

A

By binding to RNA polymerase

89
Q

Rifampicin is a strong inducer of which enzyme?

A

Cytochrome p450

90
Q

Which drug produces an unusual side effect of orange-coloured saliva, tears, sweat, and urine?

A

Rifampicin

91
Q

Trimethoprim and sulfonamides are what type of drugs? (MOA?)

A

Anti-metabolites

92
Q

Trimethoprim and sulfonamides-

bacteriocidal or bacteriostatic?

A

Bacteriostatic

93
Q

Co-trimoxazole (Trimethoprim combibned with sulfamethoxazole)- Bacteriocidal or bacteriostatic?

A

Bacteriocidal

94
Q

Which group of drugs work by inhibiting synthesis of tetrahydrofolate?

A

Anti-metabolites:

Trimethoprim & sulfonamides

95
Q

What are the classes of drugs that inhibit the 30s subunit of the bacterial ribosome?

A

AT

Aminoglycosides
Tetracyclines

96
Q

What is the class of drugs that inhibit the 50s subunit of the bacterial ribosome?

A

Macrolides

97
Q

What type of drug is gentamycin?

A

Aminoglycoside

98
Q

Aminoglycosides like gentamycin- bactericidal or bacteristatic?

A

Bactericidal

99
Q

Side effects associated with gentamycin (aminoglycosides)?

A

Nephrotoxicity and ototoxicity

100
Q

Are Tetracyclines bactericidal or bacteriostatic?

A

Bacteriostatic

101
Q

Which type of drug has the following side effects: Phototoxicity, chelation of metal ions leading to discolouration of teeth, bone growth inhibition?

A

Tetracyclines

102
Q

Erythromycin, Azithromycin, and Clarithromycin belong to which drug class?

A

Macrolides

103
Q

What is the MOA of macrolide antibiotics?

A

Inhibit protein synthesis at the 50s subunit of bacterial ribosomes (70s)

104
Q

Which class of broad-spectrum antibiotic is often prescribed in cases of penicillin allergy

A

Macrolides

105
Q

What types of bacteria are macrolides effective against?

A

Both gram positive and gram negative- broad spectrum

106
Q

The ability of bacteria and other microorganisms to resist the effects of an antibiotic to which they were once sensitve.

A

Antiobiotic resistance

107
Q

Bacteria produce _____ _____________ which catalyse the hyrolysis of the beta lactam ring, inactivating beta lactam antibiotics.

A

beta lactamases

108
Q

Describe the ways in which bacteria can develop resistance to antibiotics

A 
Mutations in cell genes
Gene transfer (vertical or horizontal)
Inactivation or modification of the antibiotic
Alteration of microbial enzymes
Alteration of the target
Reduced uptake of the antibiotic
Development of alternative pathways
109
Q

Drug class of amoxicillin

A

Beta lactam (chemically modified penicillin)

110
Q

MOA of Amoxicillin

A

Inhibition of cell wall synthesis

111
Q

Activty of Amoxicillin

A

Broad spectrum. Used to treat sore throat, skin infections, respiratory infections, UTI’s

112
Q

Half life of Amoxicillin

A

One hour

113
Q

Excretion of Amoxicillin

A

Urine

114
Q

Interactions with Amoxicillin

A

Can increase levels of other protein-bound drugs

115
Q

Adverse effects of Amoxicillin

A

ALLERGY.

Damage to commensal microflora (GI disturbance, thrush)

116
Q

Clarithromycin drug class

A

Macrolide

117
Q

Clarithromycin MOA

A

Inhibition of protein synthesis in the 50s subunit of bacterial ribosome

118
Q

Activity of Clarithromycin

A

Broad spectrum. Similar to penicillin. Used in cases of Penicillin allergy

119
Q

Clinical uses of Clarithromycin

A

Similar to amoxicillin (sore throat, skin infections, resp infections, UTI) also used in CHLAMYDIA

120
Q

Protein binding of Clarithromycin

A

High

121
Q

Metabolism of Clarithromycin

A

Hepatic

122
Q

Half life of Clarithromycin

A

1-6 hours

123
Q

Excretion of Clarithromycin

A

Metabolites in bile

124
Q

Adverse effects of Clarithromycin

A

Nausea and diarrhea. May alter cardiac conduction (arrythmias)

125
Q

Vancomycin drug class

A

Glycopeptide

126
Q

MOA of Vancomycin

A

Inhibition of cell wall (peptidoglycans)

127
Q

Activity of Vancomycin

A

ONLY GRAM POSITIVE BACTERIA

128
Q

Vancomycin has a ___________ therapeutic window.

A

narrow

129
Q

GI absorption of Vancomycin

A

Very low

130
Q

Protein binding of Vancomycin

A

50%

131
Q

Metabolism of Vancomycin

A

None

132
Q

Half life of Vancomycin

A

4-8 hours

133
Q

Excretion of Vancomycin

A

Urine

134
Q

Major adverse effects of Vancomycin

A

Nephrotoxicity and ototoxicity

135
Q

Interactions of Vancomycin

A

Other ototoxic or nephrotoxic drugs

KMMS (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions