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Pharmacology 1 > intro to pharmacodynamics > Flashcards

intro to pharmacodynamics Flashcards

1
Q

pharmacology

A

study of substances that interact with living systems through chemical processes

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2
Q

general interactions between drugs and our bodies

A

do not add new processes but modify existing physiology, binding to regulatory molecules, activating/inhibiting body processes, replace endogenous substances

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3
Q

pharmacodynamics

A

what the drug does to the body, how and where it works, mechanism of action

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4
Q

pharmacokinetics

A

what the body does to the drug, movement in and out of the body and various compartments, how the drug is broken down and transported/excreted

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5
Q

where most drug excretion occurs

A

kidney or liver

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6
Q

drug

A

any substance that brings about a change in biologic function through a chemical action

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7
Q

drug mechanisms of action

A

augment or inhibit signaling molecules, inhibit or stimulate receptors, inhibit or increase enzyme activity

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8
Q

prednisone mechanism of action

A

steroid, works by binding and inhibiting regulatory molecules that cause inflammation, produces anti-inflammatory response

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9
Q

metoprolol mechanism of action

A

occupies beta receptors on the heart and prevents normal binding of catecholamines, decreases heart rate, beta blocker

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10
Q

levothyroxine mechanism of action

A

allows the body to make thyroid hormone, replaces endogenous chemicals your body should make

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11
Q

what is the goal of giving medication

A

correct imbalances in homeostatic functions, replace naturally occurring compound that are no longer made or become insensitive, inhibit bacterial, viral, fungal organisms that invade the body

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12
Q

examples of drugs that correct imbalances

A

pantoprazole turns off acid pumps for stomach ulcers, hydrochlorothiazide removes excess salt to treat high BP, doxorubicin inhibits hyperactive cells from replicating to treat cancer

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13
Q

examples of drugs that replace naturally occurring compounds

A

estrogen to treat hot flashes, insulin to treat type 1 diabetes

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14
Q

what is another name for a receptor

A

drug target

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15
Q

most receptors are made of __

A

proteins

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16
Q

most common type of receptor

A

extracellular

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17
Q

types of extracellular receptors

A

cell surface glycoproteins, transport proteins

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18
Q

types of intracellular receptors

A

nuclear receptors, transcription factors

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19
Q

ligand

A

interacts with a receptor to trigger or inhibit a physiological process, ie a drug

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20
Q

characteristics of receptor sites on enzymes

A

usually specific, usually require phosphorylation, can break things down or put things together

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21
Q

___ have a higher affinity at receptors than ___

A

drugs; naturally occurring compounds

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22
Q

how to increase affinity

A

increase covalent bonds by molecular chemistry

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23
Q

receptor affinity for drug binding determines ___

A

the concentration of a drug needed to form a complex with the receptor

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24
Q

selectivity is ___ as concentration of a drug is ___

A

reduced; increased

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25
why selectivity decreases with increasing drug concentration
drugs can become more attracted to other sites, creates more side effects due to reduced selectivity, drug outcompetes the naturally occurring compound, overwhelms the receptor
26
(selective or nonselective) drugs cause more side effects? why?
nonselective, they activate unwanted processes
27
example of a nonselective drug
ibuprofen, it inhibits COX1 and COX2
28
characteristics of receptors in relation to drug dosage
total number of receptors may limit maximal effect of drug, receptor number is dynamic and influenced by exposure to agonist/antagonist, actions of drug may take time to see clinical effects
29
ligand gated ion channels
ionotropic receptors, ligand causes hyperpolarization or depolarization, effects in milliseconds
30
g-protein couples receptors
metabotropic, ligand causes change in excitability, effects in seconds
31
kinase linked receptors
ligand causes protein phosphorylation and protein synthesis, effects in hours
32
nuclear receptors
ligand causes gene transcription and protein synthesis, effects in hours
33
most drug binding to receptors is (reversible or irreversible)
reversible, effect of drugs are concentration dependent
34
which type of drug is most likely to have an irreversible effect
usually drugs that are antagonists
35
law of mass action
when a drug combines with a receptor it does so at a rate which is dependent on the concentration of the drug and of the receptor
36
law of mass action equation
[D] + [R] [DR] arrow to left is K1, arrow to right is K2 k1 = rate of dissociation k2 = rate of association
37
Kd
concentration of ligand when the ligand is 50% bound to the receptor, helps determine drug dosage
38
agonist
outcompetes natural chemical to activate receptors, mimics physiological activation
39
epinephrine as an agonist
given to activate beta receptors in the heart --> increased HR and force of contractions, acts on SNS, binds to alpha receptors in SNS causing vasoconstriction in large arterterial smooth muscles --> increase BP (non selective)
40
antagonist
block receptors or enzymes in physiological systems, drug effects are opposite direction of normal physiological response
41
metoprolol as an antagonist
beta receptor antagonist in the SNS --> decreases HR
42
acetylcholine as an agonist
acts on the PNS (normal response is to decrease HR) --> increases HR
43
normal physiological response of GABA receptors
influx of Cl- into nerve so they cannot conduct transmission of nerve firing --> inhibit nerve firing
44
benzodiazepines as agonists
for anxiety, agonists of GABA, more neuron inhibition --> more relaxed and sleepy
45
flumazenil as antagonist
for overdoses on benzodiazepines, antagonist of GABA, more nerve firing, can cause seizures due to overprocessing of nerve firing
46
normal physiological function of angiotensin II
increases BP
47
action of ACE inhibitors
inhibit production of angiotensin II, decrease BP and improve renal blood flow
48
non competitive inhibition
ligand binds to a site other than receptor site, confirmation of enzyme changes and doesnt allow substrate to bind
49
competitive inhibition
ligand bind to receptor site so substrate cannot, ie ACE inhibitors
50
stereochemistry
all drugs that are not symmetrical have enantiomers with the mirror image configuration, only one will have the correct configuration for an enzyme
51
full vs partial agonist
partial increases response at a much slower rate with increased dose and tapers off much sooner --> doesnt give the full drug effect, full increases response quickly with increased dose but plateaus when all receptors are bound
52
which has a higher affinity for receptors (partial or full) agonists and why its useful
partial, this is why buprenorphine is used during opioid overdoses since it will bind to receptors more but have less effect
53
up regulation of receptors
sensitization, from continuous use of antagonists, develops months-years
54
down regulation of receptors
desensitization, continuous use of agonist, develops months-years
55
how upregulation occurs
drug is inhibiting response, body makes more receptors so normal process can occur, overall effect is more since there are more receptors to bind, decreases effect of antagonist
56
where upregulation usually occurs
CNS
57
how down regulation occurs
agonist increases response, body wants to decrease back to a normal level so receptor number is decreased, overall effect is less since there are less receptors to bind, decreased effect of agonists
58
types of tolerance
upregulation, down regulation
59
risk of tolerance depends on ___
drug, potency, chronicity of use, individual variability, physiological system involved
60
cross tolerance
drugs that affect similar receptors can make one another tolerant even without use, ie benzodiazepines tolerance can cause decreased effect of alcohol
61
withdrawal
abrupt cessasion of drugs to which tolerance has developed, causes symptoms that are opposite of the original effects of the drug
62
withdrawal of antagonist
normal effects can become heightened in upregulation due to more receptors
63
therapeutic effects
pharmacological effect of drugs used to treat a disease state, intended effects
64
side effects
pharmacological effects other than intended effects
65
adverse drug reactions
side effects significant enough to warrant a change in dose or discontinuation of a drug
66
solutions to tolerance
increase dose, change med to one with a different drug pathway but same effect
67
toxic effects
predictable side effects that are severe and indicative of too high a dose or concentration
68
groups of side effects
overextension of drug effect in a articular system which are dose related, non intended effects on other systems, idiosyncratic side effects
69
idiosyncratic side effects
unpredictable, non dose related, related to immune system response (rash or allergic reaction)
70
example of overextension of drug side effects and solution
antihypertensive causing hypotension, requires lowering the dose
71
example of non intended effects on other systems and solution
phenytoin (anti seizure) causes facial hair growth, if side effect is intolerable discontinue use
72
examples of idiosyncratic side effects and solution
hydralazine causing lupus, discontinue medication and document allergy
73
what determines drug use
want to optimize effects based on 50% receptor binding, balance efficacy and side effects, drugs lose selectivity at higher conc, drug acting on different sites causes unintended effects
74
how do drugs differ within the same class?
potency
75
potency
the conc of the drug to achieve the same effect, higher potency = lower drug dose
76
what influences potency
molecular chemistry and noncovalent bond formation
77
margin of safety
distance between dose-response curve for ideal effects and dose-response curve for adverse effects, determines dosage range
78
therapeutic index equation
TI= TD50/ED50 TD is conc of drug at 50% saturation on toxic effect curve, ED is conc of drug at 50% saturation on therapeutic effect curve
79
do you want a high or low TI
high, indicates are larger therapeutic window and a larger range of safe doses
80
drug drug interactions
effects of 2 drugs or more that increase or decrease the actions of one or another, can occur as pharmacokinetic or dynamic interactions
81
additive effect
two drugs increase the effect of one another, 1+1=2
82
synergistic effect
two drug exponentially increase effect of one another, 1+1=4
83
example of synergy
aminoglycosides and beta lacatams for endocarditis, improve killing power of antibiotics together; loop and thiazide diuretics for fluid overload, improved urine excretion
84
example of drugs that antagonize each other
psudophedrine increases BP even in patients that are taking BP lowering meds
85
causes of drug variability
body weight and size, age and sex, genetics, health, placebo effect
86
pharmacokinetic causes of variability of drug response
dose, formulation, route of administration; drug tolerance; drug interactions

Pharmacology 1 (4 decks)

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