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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
name and briefly describe transmembrane signalling mechanisms
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
24
what is function of receptors
Receptors are there for normal function and cell cell communication Neurotransmitters, hormones, growth factors, cytokines All of these receptors potential targets for drugs
25
name and describe 4 types of chemical signalling
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
26
describe ion channels - general
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)
27
describe states of ion channels
3 states = closed, open and inactivated
28
describe Structure of voltage gated calcium channel
4 units Open or close
29
describe Structure of ligand gated ion channel
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
30
describe nmda receptor for glutamate
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
31
describe G protein coupled receptors
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
32
describe ex of g protein coupled receptors
Neurotransmitter binds --> Effector proteins = alpha, beta, gamma --> Alpha often dissociates --> Intracellular messages sent = Opens ion channel and ions flow across membrane
33
can you have stimulatory and inhibitory g proteins acting on same system - explain
Multiple receptors can modulate same pathway Balance between stimulatory and inhibitory agonist determines what response will be Fine control of many pathways
34
true or false - multiple receptors modulate the same pathway
TRUE
35
name parts of receptor for g proteins
receptor g protein effector
36
Describe g protein coupled receptors - family
>1000 adrenergic Dopaminergic Opioid Sensory - rhodopsin, olfactory, taste Glycoprotein hormones Lipids and other small molecules
37
Describe g protein coupled g protein - family
17 alpha subunits 7 beta subunits 12 gamma subunits
38
Describe g protein coupled effectors - family
Channels Cylases Phospholipases
39
how many possible g protein coupled receptors can we make
over 800 of them
40
what can g protein coupled receptors form
oligomers = clusters together and has specific impact
41
describe what happens to g protein coupled receptor when ligand binds
7 transmembrane receptors signal through g protein dissociation
42
what can g protein coupled receptors form
can form homo or hetero oligomers
43
name 3 types of enzyme linked receptors
Receptor tyrosine kinases Cytokine receptors Natriuretic peptide receptors
44
how do enzyme receptors work
Receptor must dimerize to signal Ligand binds first receptor then diffuses laterally to bind second receptor
45
describe Receptor tyrosine kinases
phosphorylation - leads to cellular response - only happens after dimerized
46
describe cytosine receptors - general
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
describe cytosine receptors - specific
R activation → dimer → phosphorylation of janus kinase and STAT proteins on tyrosine residues STAT proteins translocate to nucleus and activate transcription
48
describe Natriuretic peptide receptors = NPRs
Hormone binds and dimerize = activates enzyme that controls cyclic GMP cGMP controls many cellular processes
49
describe receptor turnover
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
name and briefly describe intracellular receptors
Classic hormone receptors (Estrogen receptor, Progesterone receptor, Glucocorticoid receptor) ALTER GENE TRANSCRIPTION = protein synthesis
51
describe steroid hormone receptor
Steroid hormone binds to receptor → translocation of steroid receptor complex to nucleus → binding of complex to dna regulatory site → transcription → translation (alters transcription)
52
what do intracellular receptors need
Ligand binding domain – dimer and then binds to dna and then transcription activated
53
describe enzymes
Drugs can block or stimulate enzyme Alter synthesis or breakdown Transmitters, cytokines, hormones
54
describe anticancer drugs
Very specific type of problem Antiproliferative activity
55
is the time to respond to ligand the same for all receptors
NOOO depends on receptor
56
describe response times for all receptors
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
do receptors adapt
yessssssh
58
describe how/why receptors adapt
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
what happens if receptors adapt and then suddenly stop taking drug
Must take higher amount to get same effect Cells continue to adapt Get a withdrawal reaction
60
what is allosteric modulation
can modify response to normal acting agonist Up or down
61
describe arithmetic scale
Measure to get 100% of response Need to know what is concentration that causes 50% of the maximum response
61
how do we Quantify ligand receptor interactions
Test on cells or tissues - plot concentration vs response
62
describe logarithimic scale
Easier to see where 50% of max is Get linear section almost Also understand range of doses
63
what does range of doses allow us to account for
biological variation
64
describe testing drugs for biological variation
To account = take 100 people and increase dose slowly Record minimal dose at which they respond to drug Get standard curve Few outliers
65
what to do with standard curve from testing drugs
Can convert it to log scale Plot cumulative response vs dose Work out ED50
66
what is ED50
Dose required to produce therapeutic effect in 50% of population FOUND ON DOSE RESPONSE CURVE
67
what is ed50 used for
Comparing drugs to each other, ex = pain relievers designing better drugs - for side effects studying magnitude of drug effect
68
describe studying magnitude of drug effect - single cell
Drug applied for 3 weeks = after the cells were much more sensitive to drug
69
describe studying magnitude of drug effect - tissue
Acetylcholine causes intestinal contraction - ileum look at response in tissue
70
describe studying magnitude of drug effect - individual
cns depressant, if increasing dose = may kill you but other drug = anesthesia
71
describe studying magnitude of drug effect - group
dose of alcohol, slow reaction time first ataxia (staggering) OVERLAP of slowed reaction time and ataxia coma (close to death curve)
72
what do agonists do
stimulate
73
describe threshold dose
concentration below which nothing happens
74
describe log concentration effect relationship
Mostly looking at potency and intensity of effect up to max but also, slope and variability
75
describe Magnitude of drug effect
as get bigger response = occupying more receptors with drug (receptor occupancy)
76
describe spare receptors
There are lots of spare receptors Can get max response with only fraction of receptors activated
77
what is affinity
affinity for receptor binding site (ability to bind) differs for different drugs
78
what is efficacy
ability to activate receptor (efficacy)
79
describe full vs partial agonist
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
why are partial agonists useful
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
what happens if have lower affinity or efficacy
Lower affinity (for receptor) = takes more to get max response Lower efficacy = never reach max
82
what do antagonists do
block access of the agonist - gets in the way
83
describe ex of antagonist
Ex - dopamine receptor blocker for schizophrenia Direct relationship between average dose needed and binding to dopamine receptor
84
Describe what antagonists can be
Competitive vs non competitive Reversible vs irreversible
85
describe competitive antagonist
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
describe non competitive antagonists
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
describe allosteric antagonism
Inhibition = max lowered
88
describe allosteric potentiation
= dose response curve moves to left
89
what happens if Drug agonist alone
normal curve
90
what happens if Drug agonist + allosteric activator
= increase response of drug
91
what happens if Drug agonist + competitive inhibitor
= shifts to right
92
what happens if Drug agonist + allosteric inhibitor
= very little response
93
why do not want irreversible antagonist
Sometimes do not want because of side effects
94
describe Quantifying side effects and toxicity
Look at dose and percent of people responding Therapeutic effect vs toxic effect vs lethal effect = want biggest possible separation between curves
95
what is therapeutic window
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
describe ideal therapeutic window
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
does therapeutic index only matter
no must look at slope too if therapeutic and toxic lines overlap = bad
97
describe formula for safety factor
Safety factor = TD1/ED99
98
compare therapeutic windows of warfarin vs penicillin
Warfarin = small therapeutic index, Need to be monitored properly Penicillin = large because targets specific feature of microbe and not you
99
describe formula for therapeutic index
TD50/ED50
100
describe outliers
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
what is important in evaluating toxicity
If toxicity has no threshold = no dose at which you are safe which can be bad

PHAR 300 (22 decks)

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