pharm test 1 Flashcards

1
Q

what is pharmacology. and what is medical pharmacology

A

study of chemical interactions with living systems. medical pharmacology is the study of substances used to prevent, diagnose, and treat diseases

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2
Q

what is toxicology and who is the father

A

component of pharmacology; undesirable effects of chemicals on living systems. not SS. Paracelsus- “The dose makes the poison”

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3
Q

difference between toxins and poisons

A

toxins- biological substances
poisons- not biological. can be agonist or antagonist

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4
Q

describe early medicine

A

prehistoric- shamanism, animism, spiritualism, divination. ayurvedic is indian medicine and then traditional chinese medicine is still going strong
in ancient Egypt Imhotep is first recorded physician

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5
Q
A

rod of Asclepius

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6
Q

Materia Medica

A

precursor to pharm textbook; first medical textbook in western world. author is Dioscorides but probs multiple authors. body of knowledge on plants and medical substances. discussed preparation and use and precursor to pharmacology

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7
Q

Modern Pharmacology

A

adherence to scientific principals and controlled drug trials to get rid of placebos. evaluation of therapeutic claims and got rid of worthless medicines. about 70 groups of drugs

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8
Q

pharmacodynamics

A

what the drug does to the body
agonist- drug binds to receptor and activates response. effect may be greater or lesser than native ligant

antagonist- bind to receptor and prevent binding of native ligand; does not elicit response

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9
Q

pharmacokinetics

A

what the body does to the drug
Absorption
Distribuition
Metabolism
Excretion

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10
Q

pharmacogenetics

A

looking at genetic profile to see how you will respond to drug

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11
Q

agonist

A

elicits response from receptor aka will have downstream response. response is usually similar to endogenous ligand of body. can be more or less effective than natural ligand

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12
Q

antagonist

A

blocks the endogenous ligand or blocks receptor from working; shuts down receptor. does not elicit response

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13
Q

organic compounds

A

C, O, or H. carbs, lipid, proteins

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14
Q

drug size

A

expressed in molecular weight usually daltons. most drugs 100-1000 MW and if >1000 then cannot diffuse easily so need to give straight into blood stream

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15
Q

receptor interactions

A

appropriate size, electrical charge(polar is full or half charge), shape, and atomic composition are all part of lock and key mechanism

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16
Q

3 main types of bonds

A

1) covalent is strongest; stronger the bond the less specificity; harder to break, share electrons
2) electrostatic- think charged molecules like ions, hydrogen bonds, and van der waals forces(water)
3) hydrophobic- lipid soluble drugs, forms with things that dont have charge, most numerous and have to be very specific

17
Q

chirality and isomers

A

asymmetry; concept of mirror images (stereoisomerism)
optical isomers are mirror images of one another with a carbon difference
example) glucose and fructose are isomers; have same formula but different shape

18
Q

racemic mixtures

A

mixture of 2 mirror images of one another; so 2 optical isomers
example) racemic ketamine is mixture of S Ketamine(4x more potent) and R Ketamine(more toxic)

19
Q

orthosteric

A

binds at active site
Emax can only go up so much bc receptor tires out

20
Q

allosteric

A

binds not at active site
activators- agonist
inhibitors- if allosteric then noncompetitive inhibitor. if given with agonist then will never overcome aka will never get maximum effect of agonist

21
Q

specific and nonspecific

A

more you give of a drug the more nonspecific binding. for specific bindings there is a max drug bound concentration bc only so much receptor. nonspecific the drug will bind also somewhere else besides active site so there is more drug bound concentration

22
Q
A

Drug Concentration Response Curve aka how much drug in blood
Right: drug effect and drug concentration
more concentration the more response. EC50 is concentration where you see 50% of the effect. single point on curve

LEFT: receptor bound drug and drug concentration
Kd is drug concentraion at which 1/2 of receptors bound. never changes but differs with each drug

23
Q

EC50 and Kd

A

EC50 = concentration where you see 50% of the effect. single point on curve

Kd= drug concentration at witch 1/2 of receptors bound. never changes but different for every drug. DOES not deal with effect of drug. inverse to affinity. if low Kd then high affinity bc does not take as long to get receptors bound

EC50 does NOT equal Kd because might not take long for 50% of receptors to be bound. but if take more drug to get 50% of receptors bound then high Kd aka low receptor affinity

24
Q
A

Response to how much drug curve

A is just agonist. has a Emax

A+B is agonist plus competitive inhibitor. the effect will be dulled at first but then the agonist will outcompete with competitive inhibitor and will reach Emax but just need more drug to reach it

A+ C is agonist plus allosteric activator(agonist) so makes drug bind better so get even higher response than just agonist

A+D is agonist plus allosteric inhibitor so noncompetitive antagonist and cant outcompete so wont get same response

25
Q

agonist mimic or indirect agonist

A

agonist has downstream effects so a agonist mimic or indirect agonist is not working at the active site nor even at the receptor site but will increase the downstream effect

26
Q

competitive antagonist

A

can be overcome by increase amount of agonist aka surmountable; bind and inhibit agonist response.

effect muted at first but if keep giving agonist will outcompete antagonist. so EC50 will be higher bc will need more agonist to have 50% of effect

27
Q

noncompetitive antagonist

A

insurmountable– no matter how much agonist will never be able to outcompete noncompetitive antagonist

irreversible if form covalent bond

28
Q

partial agonist

A

produce a lower response at full receptor occupancy; block full agonist binding

usually bc of shape

in absence of full agonist= agonist
in presence with full agonist= antagonist

29
Q
A

if both partial and full agonist given, partial agonist will outcompete full agonist but will have less effect. so here partial agonist acting like antagonist in presence of full agonist

30
Q

inverse agonist

A

-only considered agonist bc elicits response
-greater affinity for drug inactive form than stabalized form
-antagonist activity bc favors inactive form–> binds to receptor and then that receptor’s response is less than its baseline activity
-lower than competitive antagonist effect bc less than baseline

31
Q

potency and efficacy

A
32
Q

agonist vs partial vs antagonist vs inverse

A

direct agonist–> binds to active site and elicits response
indirect like cocaine ~mimic~ but dont bind and increase activity of agonist(?)

partial agonist–> if given alone then would have effect but not as strong. if given with full agonist then actually block response(baseline)

antagonist–> prevents agonist binding so just baseline response

inverse agonist–> favors inactive form so block native ligand and decrease effect of receptor; acts as an antagonist but is an agonist bc elicits response

33
Q

Bmax?

A

maximum binding to receptor

34
Q

Duration of Drug action pharmacodynamics

A

1)only as long as drug binds to receptor; bind and release; covalent bond does not bind and release

2) how long do downstream effects last until downstream effectors go away; if covalent bond then receptor degraded

3) desensitization–> cell shuts down signaling process

35
Q

good and bad receptor properties

A

GOOD
-selective aka one receptor or one receptor type bc not good if bind to many different receptors bc then many different effects
-alteration–> in order for downstream effects to occur the receptor must have conformation change when the ligand binds to it

BAD
-nonregulatory molecules that bind to drugs with no detectable change in function aka inert binding sites or drug carriers but NO EFFECT

36
Q

drug carriers

A

1) Plasma Proteins(albumin) think of albumin as bad?
-separation of free and bound–> bound is plasma protein to drug so drug cant cross barriers. unbound the drug can cross barriers and diffuse into tissues and bind to receptor and have effect. unbound form=free form; can bounce back and forth from bound to unbound and depends on drug ex) phenytoin likes albumin; so OSMOLARITY of blood
-effects on distribution, target, elimination–> super highway for drugs
-decreased levels bc of malnutrition, liver damaged–> made in liver so if any liver problems or malnutrionsist then can have effect ex) phenytoin likes albumin so if malnutrionished the more sensitive that pt will be to that drug bc more will bind to receptor

2) Displacement of drug
-if 2 drugs given together then can kick/compete for albumin site ex) phenytoin and carbazepam–> will have higher free concentration

albumin likes acidic drugs more
alpha1 glycoproteins like basic drugs more
lipoproteins like neutral drugs more

37
Q

Drug Response Curves
potency and efficacy

A

-sigmoid in nature

POTENCY
-amount in plasma
-EC50 or ED50 of a drug required to produce 50% of that drug’s maximum effect
-small amount and max effect means very potent
-clinicians like dose and pharmacists like concentration bc amount in blood stream able to interact with receptors

MAXIMUM EFFICACY
-differs on drug
-max effect drug can deliver
-depends on interaction with receptor
-must also take into account toxicity
-clinical effectiveness of drug is based on max efficacy not potency

38
Q
A

A, C, and D are equally efficacious but have different ED50s

B is more potent because reach ED50 faster but is not as effective as A, C, and D

39
Q

Median Effective Dose(ED50), Median Toxic Dose(TD50) and Median Lethal Dose(LD50)

A