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PHAR 300 > Pharmacodynamics 1 > Flashcards

Pharmacodynamics 1 Flashcards

1
Q

what types of names can drugs have

A

chemical name
generic name
trade name

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2
Q

describe chemical name of drug

A

One
Documents chemical formula and molecular structure

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3
Q

describe generic name of drug

A

One
Universal name assigned by USAN (united states adopted name) council and by WHO international nonproprietary names (INN) program

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4
Q

describe trade name of drug

A

Unlimited
Proprietary name
Registered trademark, use restricted to owner of patent - usually manufacturer

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5
Q

which drug name do we actually use

A

GENERIC NAME

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6
Q

describe how drugs are made

A

has prefix and stem most of time
ex = clone, vir, mab as stems
ex = tu (targets tumour) and li (acts on immune system) as prefix

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7
Q

where does word drug come from

A

greek pharmakon

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8
Q

describe therapeutics

A

what you use drug for clinically

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9
Q

name ways which drugs are used in therapeutics

A

Indications = what you use drug for
Contraindications = what you wouldn’t use drug for (Another problem or Drug that interacts)

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10
Q

describe pharmacokinetics

A

what body does with drug
Absorb, distribute it, break it down (metabolism) and get rid of it (excretion)

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11
Q

describe pharmacodynamics

A

what drug is doing to you
Biological effects
how/where it acts
Effect on receptors, ion channels, enzymes and immune system

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12
Q

how do we follow drug action through body

A

Organ system → tissue → cell → subcellular target (where drug acts)

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13
Q

describe specific drugs

A

Some very specific = designed to go into active site of specific enzyme in virus - might have no effect on human who is taking it
has One target = viral enzyme- Antiviral drugs

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14
Q

describe general drugs

A

Analgesic drugs = multiple targets and more potential side effects
Opioids
Act all over the place
Will affect many organ systems

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15
Q

describe family of antihypertensive drugs generally

A

Antihypertensive drugs = blood pressure controlled in 4 different ways in body
Brain, heart, kidneys, blood vessels
Many families of drugs acting on each of these systems
Some people will respond different
Many types of drugs to use

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16
Q

describe brain target of blood pressure

A

central acting agents –> central attack –> brain

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16
Q

describe kidney target of blood pressure

A

RAAS inhibitor, diuretics, beta blocker –> increased fluid excretion –> kidneys

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17
Q

describe blood vessel target of blood pressure

A

vasodilators, calcium antagonists, RAAS inhibitors, alpha blocker –> vasodilation –> blood vessels

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17
Q

describe heart target of blood pressure

A

calcium antagonist, beta blocker –> reduction of frequency and power –> heart

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18
Q

describe example of selectivity vs generalized effect

A

Selective = radioactive iodine targets thyroid mainly
Generalized = epinephrine - many effects on organ systems (Used if blood pressure too low)

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19
Q

where are receptor sites

A

on or within cell

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20
Q

define drug receptors

A

macromolecular protein target to which endogenous ligand or exogenous agonist/antagonist bind to → cellular response
In cell membrane or inside cell
Receptors there for normally physiological function but can be acted on by drugs

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21
Q

what are drug receptors linked with

A

Receptor must be linked to cellular response elements = ion channels, enzymes, second messengers, etc

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22
Q

how do we know things about receptors

A

Know a lot about structure of receptors -
Identified by radio ligand binding/isolated, sequenced

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23
Q

name and briefly describe transmembrane signalling mechanisms

A

Some intracellular but not many =
Drug transported inside cell to be active
Most on plasma membrane
Enzymes = One directly activated by receptor or tyrosine kinase process here, Tyrosine kinase = 2 receptors that couple together and starts signalling cascade
R activated Ion channels
G protein coupled= Generates second messengers that affect cell, links R to enzyme

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24
Q

what is function of receptors

A

Receptors are there for normal function and cell cell communication
Neurotransmitters, hormones, growth factors, cytokines
All of these receptors potential targets for drugs

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25
Q

name and describe 4 types of chemical signalling

A

1 = Autocrine = cell targets itself
2 = Juxtacrine = signalling across gap junctions, cell targets cell connected by gap junctions - next door neighbour
3 = Paracrine = cell targets nearby cell - little bit away
4 = Endocrine = cell targets a distant cell through bloodstream - released into circulation

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26
Q

describe ion channels - general

A

Transmembrane spanning proteins that open to allow passage of specific ions
Voltage or receptor controlled (Voltage = like axons in nervous system
Receptor controlled = big targets for drugs)

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27
Q

describe states of ion channels

A

3 states = closed, open and inactivated

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28
Q

describe Structure of voltage gated calcium channel

A

4 units
Open or close

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29
Q

describe Structure of ligand gated ion channel

A

Nicotinic receptor - ach or nicotine
5 units
Open or closes
(Ach or nicotine binds to 2 sites on receptor = now open)
needs to bind to both sites to be able to open

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30
Q

describe nmda receptor for glutamate

A

NDMA receptor for glutamate
Binding site for glutamate and others
Drugs can bind to same site as natural agonist to stimulate or block it
Has binding site for drug
Or can bind to different site
Interesting combinations
Some receptors have multiple sites for drugs to bind to

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31
Q

describe G protein coupled receptors

A

7 different units that span membrane
Encircle active site
GTP replaces GDP on alpha unit activity now
many hormones and neurotransmitters work here
second messengers - cyclic amp for glucose release

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32
Q

describe ex of g protein coupled receptors

A

Neurotransmitter binds –> Effector proteins = alpha, beta, gamma –>
Alpha often dissociates
–> Intracellular messages sent = Opens ion channel and ions flow across membrane

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33
Q

can you have stimulatory and inhibitory g proteins acting on same system
- explain

A

Multiple receptors can modulate same pathway
Balance between stimulatory and inhibitory agonist determines what response will be
Fine control of many pathways

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34
Q

true or false - multiple receptors modulate the same pathway

A

TRUE

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35
Q

name parts of receptor for g proteins

A

receptor
g protein
effector

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36
Q

Describe g protein coupled receptors - family

A

> 1000 adrenergic
Dopaminergic
Opioid
Sensory - rhodopsin, olfactory, taste
Glycoprotein hormones
Lipids and other small molecules

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37
Q

Describe g protein coupled g protein - family

A

17 alpha subunits
7 beta subunits
12 gamma subunits

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38
Q

Describe g protein coupled effectors - family

A

Channels
Cylases
Phospholipases

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39
Q

how many possible g protein coupled receptors can we make

A

over 800 of them

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40
Q

what can g protein coupled receptors form

A

oligomers = clusters together and has specific impact

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41
Q

describe what happens to g protein coupled receptor when ligand binds

A

7 transmembrane receptors signal through g protein dissociation

42
Q

what can g protein coupled receptors form

A

can form homo or hetero oligomers

43
Q

name 3 types of enzyme linked receptors

A

Receptor tyrosine kinases
Cytokine receptors
Natriuretic peptide receptors

44
Q

how do enzyme receptors work

A

Receptor must dimerize to signal
Ligand binds first receptor then diffuses laterally to bind second receptor

45
Q

describe Receptor tyrosine kinases

A

phosphorylation - leads to cellular response - only happens after dimerized

46
Q

describe cytosine receptors - general

A

Ligand binds and dimerizes
Phosphorylation - activation of STAT (signal transducers and activators of transcription)
Proteins move into nucleus and activate transcription
Cytokine receptors control transcription of various factors within cell

47
Q

describe cytosine receptors - specific

A

R activation → dimer → phosphorylation of janus kinase and STAT proteins on tyrosine residues
STAT proteins translocate to nucleus and activate transcription

48
Q

describe Natriuretic peptide receptors = NPRs

A

Hormone binds and dimerize = activates enzyme that controls cyclic GMP
cGMP controls many cellular processes

49
Q

describe receptor turnover

A

Cells continually turning over receptors
Recycle them, pull them in from membrane
Continually recycled
If long lasting blocking drug = receptor may be recycled = that is how it is inactivated

50
Q

name and briefly describe intracellular receptors

A

Classic hormone receptors (Estrogen receptor, Progesterone receptor, Glucocorticoid receptor)
ALTER GENE TRANSCRIPTION = protein synthesis

51
Q

describe steroid hormone receptor

A

Steroid hormone binds to receptor → translocation of steroid receptor complex to nucleus → binding of complex to dna regulatory site → transcription → translation (alters transcription)

52
Q

what do intracellular receptors need

A

Ligand binding domain – dimer and then binds to dna and then transcription activated

53
Q

describe enzymes

A

Drugs can block or stimulate enzyme
Alter synthesis or breakdown
Transmitters, cytokines, hormones

54
Q

describe anticancer drugs

A

Very specific type of problem
Antiproliferative activity

55
Q

is the time to respond to ligand the same for all receptors

A

NOOO
depends on receptor

56
Q

describe response times for all receptors

A

Ion channel = milliseconds, very fast
G protein = seconds, pretty fast
Enzyme = minutes - longer
Dna linked = hours (Slower procedure, Has to get into nucleus, transcription, gets into cell and alters cell function)

57
Q

do receptors adapt

A

yessssssh

58
Q

describe how/why receptors adapt

A

Take drug repeatedly = body will want to maintain equilibrium
So will alter number of receptors in response to effect of drug
Chronic agonist = receptors down regulated
Chronic antagonist = receptors upregulated
Counteracts
Common issue for chronic use = trouble if suddenly stop

59
Q

what happens if receptors adapt and then suddenly stop taking drug

A

Must take higher amount to get same effect
Cells continue to adapt
Get a withdrawal reaction

60
Q

what is allosteric modulation

A

can modify response to normal acting agonist
Up or down

61
Q

describe arithmetic scale

A

Measure to get 100% of response
Need to know what is concentration that causes 50% of the maximum response

61
Q

how do we Quantify ligand receptor interactions

A

Test on cells or tissues - plot concentration vs response

62
Q

describe logarithimic scale

A

Easier to see where 50% of max is
Get linear section almost
Also understand range of doses

63
Q

what does range of doses allow us to account for

A

biological variation

64
Q

describe testing drugs for biological variation

A

To account = take 100 people and increase dose slowly
Record minimal dose at which they respond to drug
Get standard curve
Few outliers

65
Q

what to do with standard curve from testing drugs

A

Can convert it to log scale
Plot cumulative response vs dose
Work out ED50

66
Q

what is ED50

A

Dose required to produce therapeutic effect in 50% of population
FOUND ON DOSE RESPONSE CURVE

67
Q

what is ed50 used for

A

Comparing drugs to each other, ex = pain relievers
designing better drugs - for side effects
studying magnitude of drug effect

68
Q

describe studying magnitude of drug effect - single cell

A

Drug applied for 3 weeks = after the cells were much more sensitive to drug

69
Q

describe studying magnitude of drug effect - tissue

A

Acetylcholine causes intestinal contraction - ileum
look at response in tissue

70
Q

describe studying magnitude of drug effect - individual

A

cns depressant, if increasing dose = may kill you but other drug = anesthesia

71
Q

describe studying magnitude of drug effect - group

A

dose of alcohol, slow reaction time first
ataxia (staggering)
OVERLAP of slowed reaction time and ataxia
coma (close to death curve)

72
Q

what do agonists do

A

stimulate

73
Q

describe threshold dose

A

concentration below which nothing happens

74
Q

describe log concentration effect relationship

A

Mostly looking at potency and intensity of effect up to max
but also, slope and variability

75
Q

describe Magnitude of drug effect

A

as get bigger response = occupying more receptors with drug (receptor occupancy)

76
Q

describe spare receptors

A

There are lots of spare receptors
Can get max response with only fraction of receptors activated

77
Q

what is affinity

A

affinity for receptor binding site (ability to bind)
differs for different drugs

78
Q

what is efficacy

A

ability to activate receptor (efficacy)

79
Q

describe full vs partial agonist

A

Full agonist = completely activates receptor
Partial agonist = not stimulated to max response but does act on receptor enough, Less efficacy, Will never reach max response - lower max

80
Q

why are partial agonists useful

A

Can be useful for less side effects or could be safer
Partial agonist = occupies many receptors but response is small
But almost all the receptors can be occupied
Also can block access of full agonist=
can block other drug with much bigger effect
ex= drug addicts

81
Q

what happens if have lower affinity or efficacy

A

Lower affinity (for receptor) = takes more to get max response
Lower efficacy = never reach max

82
Q

what do antagonists do

A

block access of the agonist - gets in the way

83
Q

describe ex of antagonist

A

Ex - dopamine receptor blocker for schizophrenia
Direct relationship between average dose needed and binding to dopamine receptor

84
Q

Describe what antagonists can be

A

Competitive vs non competitive
Reversible vs irreversible

85
Q

describe competitive antagonist

A

competes at same site and blocks response
If get enough = wipes out effect of ligand, blocks so many receptors = no signal
Shifts dose response curve to right
Have to flood with agonist to get response, if give more of agonist = can still get max because of the spare receptors around
If give huge doses = can affect maximum, Lower doses have no effect on max

86
Q

describe non competitive antagonists

A

Noncompetitive antagonist = different site
Decreases response of agonist but will not wipe it out
Maximum lowered
Allosteric = can be positive or negative, Increase response to ligand or decrease

87
Q

describe allosteric antagonism

A

Inhibition = max lowered

88
Q

describe allosteric potentiation

A

= dose response curve moves to left

89
Q

what happens if Drug agonist alone

A

normal curve

90
Q

what happens if Drug agonist + allosteric activator

A

= increase response of drug

91
Q

what happens if Drug agonist + competitive inhibitor

A

= shifts to right

92
Q

what happens if Drug agonist + allosteric inhibitor

A

= very little response

93
Q

why do not want irreversible antagonist

A

Sometimes do not want because of side effects

94
Q

describe Quantifying side effects and toxicity

A

Look at dose and percent of people responding
Therapeutic effect vs toxic effect vs lethal effect = want biggest possible separation between curves

95
Q

what is therapeutic window

A

range between minimal effect of dose and dose that causes maximal effect in most people
(LD50/ED50) - in rats, now use LD10
now use ED50 vs TD50

96
Q

describe ideal therapeutic window

A

Ideal therapeutic window = level that causes toxicity in 50% of population much higher than level causing effectiveness in 50%
Also that level causing any toxicity in anyone is higher than doses that cause desired effect

97
Q

does therapeutic index only matter

A

no must look at slope too
if therapeutic and toxic lines overlap = bad

97
Q

describe formula for safety factor

A

Safety factor = TD1/ED99

98
Q

compare therapeutic windows of warfarin vs penicillin

A

Warfarin = small therapeutic index, Need to be monitored properly
Penicillin = large because targets specific feature of microbe and not you

99
Q

describe formula for therapeutic index

A

TD50/ED50

100
Q

describe outliers

A

can have very different response
Can be like 1 in 1000
Worst problem = toxic effect at very low dose
Other = give normal dose and do not respond - must give a lot of the drug

101
Q

what is important in evaluating toxicity

A

If toxicity has no threshold = no dose at which you are safe which can be bad

PHAR 300 (22 decks)

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