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Pharmacology > Basic Principles of Pharm (Exam 1) > Flashcards

Basic Principles of Pharm (Exam 1) Flashcards

1
Q

Define Pharmacology and all that it entails (3)

A
  1. Study of chemical interactions with living systems (endogenous or exogenous)
  2. Medical: Prevent, diagnose, and treat disease
  3. *Toxicology *(posions/toxins): undesirable efffect of chemicals on living systems

toxins are biological vs poisons

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2
Q

Explain the History of Pharmacology until today

Notable times and peoples

A

Prehistoric, ancient egypt, ayurvedic, ancient greek, traditional chinese.
Materia Medica (greek): collection of text throughout history; precursor to pharmacology (botany and medicinal)
Pracelsus 1493-1541: Father of toxicology “Dose makes the poison”
Modern Pharm: Utilizes scientific principles and clinical testing
Anesthetic Pharm: 1. science of drug 2. Practical knowledge

Imhotep ancient egypt
Hippocrates father of western medicine
Dioscorides Materia Medica

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3
Q

Identify and define the branches of Pharmacology (4)

A
  1. Pharmacodynamics: what the drug does to the body
  2. Pharmokinetics: what the body does to the drug (ex: 1/2 life, breakdown, etc.)
  3. Pharmocogenetics: genetic profile response to a drug (ex. BrCx)
  4. Toxicology: undesirable efffect of chemicals on living systems
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4
Q

Define an agonist and what it does

A

a substance that ellicits a response (activator) targeting a receptor

ex. epi, NE

endogenous ligands are small molecules the body produces such as Epi
vs exogenous ligands are synthetic made outside of the body

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5
Q

Define an antagonist and what it does

A

a substance that blocks/shutdowns (inhibits) a receptor

ex. BB

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6
Q

What is a receptor and what types are there

A

Typically a protein and binding site for a drug
Endogenous: within the body
Exogenous: outside the body

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7
Q

Identify the difference between poisons and toxins

A

poisons are non-biologic and toxins are biologic

ex. of toxin: mushroom, pufferfish

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8
Q

Identify the physical nature of drugs (4)

A

Solid, liquid, or gas
organic: carb, lipid, protein
inorganic: metals
drug size 100-1000 MW or Da

drug size is important for transport

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9
Q

Identify the properties of receptor interactions

A

lock and key mechanism
dependent on size charge, shape and atomic composition

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10
Q

What are the three main bond types and relative strength and specificity

A

(strongest) covalent: (less specific)
(middle) electrostatic: charged, h-bonds, Van der Walls (medium specificity)
(weakest) hydrophobic: lipid soluble (very specific)

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11
Q

What is stereoisomerism (chirality) and its effects on drugs

A

Optical isomers (enantiomers) that mirror eachother but cannot be superimposed affect how drug fits in the receptor. can affect the metabolism of the drug

one isomer may be more portent and the other toxic

(D:L;R:S) Left and Right hand

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12
Q

What are racemic mixtures and give an example

A

Drug that contains both stereoisomers

ex. Ketamins (R) and (S)

(R) more roxic (S) more potent

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13
Q

Compare orthosteric vs alloteric interactions

A

Orthosteric binds to the active site of the receptor
Allosteric binds to another site; not the active site

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14
Q

Compare specific vs non-specific interactions

A

specific requires less drug concentration compared to non-specific to have the same maximum effect

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15
Q

What are the three drug-receptor interactions and what do they do

A

Agonist: Drug binds to receptor and response
Anatagonist: bind to receptor and no response
Allosteric non-competitive: activators and inhibitors

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16
Q

Define Bmax, Kd, EC50, Emax and explain their relationship to eachother

A

Bmax: maximum binding to receptor
Kd: drug concentrion 1/2 receptors bound
Emax: Maximum effect
EC50: 50% effect

decrease Kd= high affinity
increase Kd=low affintiy
decrease EC50= less drug concentration
increase EC 50= more drug concentration

Drug concentration response curve

EC 50 (potency) vs Kd (efficacy)

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17
Q

Explain how agonists, competitive inhibitors, allosteric activators, and allosteric inhibitors affect drug response curve

A

agonisits and allosteric: decrease dose and exponentially increase response
agonists: steady response and drug dose
agonists and competitive inhib: increase dose (EC50) to reach Emax
agonist and allosteric inhibitor: minimal response despite increased dose

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18
Q

Explain how indirect agonist/agonist mimic work

A

Agonists cause a downstream effect and goes from A->C, an enzyme can be activated to reduce the breakdown of C increasing it and its effect

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19
Q

Explain the receptor-antagonist interaction of competitive inhibitors

A

they bind and inhibit a response can be countered by increasing the amount of agonists (surmountable)
E50 increased; Emax the same

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20
Q

Explain the receptor-antagonist interaction of non-competitive inhibitors

A

non-competitive is insurmountable (irreversible) EC50 same; decreases Emax

orthosteric covalent binding is insurmountable

it forms a covalent bond and agonists cannot bind to active site

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21
Q

Explain the receptor-antagonist interaction of partial agonists

A

full response is not seen only partial (decreased Emax)
not related to affinity and can block full agonist binding acting as an antagonist

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22
Q

Name other mechanisms of antagonism (2)

A

Opposite charges
Physiologic antagonism such as fight and flight response vs rest and digest

adminster + charge drug to bind to - charge inhibiting effects

physiologic antagonism: Epi increase HR and ACh decreases HR

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23
Q

How do receptor configurations affect drug response

A

R’i equilibrium with R’a
Agonists shift the equilibrium to R’a
Anatgonists equilibrium does not change
Inverse Agonsits shift the equilibrium to R’i

i- inactive form a- active form
inverse agonists remains in inactive form making it an antagonists

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24
Q

Compare the drug response curve in relation to R’a and R’i with agonists, partial agonists, antagonist, inverse agonists

A

Full agonists: max response
Partial agonists: decreased response
Antagnoists: baseline response
Inverse agonist: no response

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25
Q

Give examples of B-1 Receptor drugs agonist (direct & indirect), parital agonist, antagonist, and inverse agonist

A

agonist(direct): Epi, NE
agonist(indirect): amphetamine, cocaine
partial agoinist: pindolol, acebutolol
antagonist: propanolol, atenolol
inverse: carvedilol, nadolol

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26
Q

Pharmacodynamics

what are the three concepts of duration of action

A
  1. how long the drug binds to the receptor
  2. long term downstream effects used up and signaling shutdowns (can be associated with the receptor or effects of the receptor) and covalent bond receptor is degraded
  3. densenitization: when the drug is bound to the receptor the cell still shutsdown/dampens the signal process ; protective (GPCR)
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27
Q

Name good receptor properties (2)

A

selectivivity: one receptor or one receptor type
altertation: conformational change the protein to enable it to interact with something inside the cell (downstream effect)

28
Q

Name bad receptor (inert/drug carrier) properties

A

bind to the drug but dont have any effect on the body; drug can be bound or free in the blood stream

29
Q

What is the function of bad receptors

A

bad receptors are function as drug carriers

30
Q

What is the most common drug carrier and what affects this?

A

Plasma proteins albumin
bound form: protein bound to a drug cannot cross barriers because its too large
free form: allowed to diffuse into tissue and bind to receptor

Higher drug dose, if primarily bound to plasma proteins to see an effect
Decreased albumin can make drugs more toxic
- malnutrition and liver damage decrease albumin

31
Q

Give an example of albumin carrying a drug and what can affect it

A

Phenytoin 10% free
carbemazepine competes with phenytoin and can displace phenytoin increasing free form concentration

malnutrition and liver damage

32
Q

How many binding sites does albumin have and what kind of drugs does it bind to

A

2 inert binding site
binds mostly to acidic drugs

33
Q

What kind of drug carriers bind to basic drugs

A

alpha-1-acid glycoprotein

34
Q

What kind of drug carrier binds to neutral drugs

A

Lipoproteins

35
Q

Differentiatite EC50 and ED50

A

EC50 concentration in the plasma to produce 50% effect
ED50 dose given to the patitent to produce 50% effect

36
Q

What is maximal efficacy and what are some consideration

A

Max response a drug can deliver
depends on interaction with the receptor
side effect and toxicity

clinical efficacy depends on maximal efficay not potency

37
Q

Idenetify which durgs are effective vs potent

A

B more potent
A,C,D efficacious
potentcy A>C>D

38
Q

Compare ED50, TD50,LD50, and theraputic index

A

ED50: 50% response of 50% people
TD50: 50% median toxic dose (toxic side effects)
LD50: median lethal dose; not used with humans
Therapeutic index is betweeen ED50 and TD50 and established the margin of safety

39
Q

How does therapeutic index relate to safety of the drug? How is it calculated?

A

Narrow: less safe very toxic- prescribed
Wide: more safe less toxic OTC drugs
Note in animal studies use LD50 and humans use TD50
LD50 or TD50 divded by ED50=TI

40
Q

Name some narrow TI drugs

A

warfarin: bleed out
theophylline: check serum levels

41
Q

Give an example of a narrow TI drug and explain

A

Digoxin for CHF
ED 50 2mg TD50 4mg
TI: 4/2=2 narrow
inducing arrythmias

42
Q

What can cause variations in drug responsiveness

A

polypharmacy: drug-drug interacations
indivdual pt response can vary dramtic or muted
- idiosyncratic
- usually due to genetic factors (pharmacogenomics)

43
Q

What are the variations to drug responsivenes (4)

A

Tolerance: need more of the drug to get the same effect leading to toxic side effects and addiction
Tachyphylaxis: quick tolerance to the drug
chemical antagonist: other drugs
physiologic antagonism: body block drugs

44
Q

What are (4) causes that can contribute to drug responsiveness

A
  1. alteration in concentration of the drug that reaches the receptor
  2. variation in concentration of endogenous receptor ligand
  3. alteration in number or function of receptors
  4. changes in components of response distal to the receptor
45
Q

With alteration in concentration of the drug that reaches the receptor, what factors affect this?

A

Pharmokinetics (ADME)
Liver failure
age
weight
sex
disease state

46
Q

What is the largest and most important cause of variation

A

change in downstream response to a receptor
post-receptor process
bodys ability to compensate

47
Q

How does the extension of therapeutic effects cause toxic effects

A

safest drug taken in excess will cause toxic effect (paracelsus)
toxic side effects can be an extension of therapeutic effects such as sedation

48
Q

How do drugs cross barriers

A

Drugs need to be uncharged to cross effectively
- Most barriers are cell membranes contain phospholipids and inner part is hydrophobic, so needs to uncharged to cross

Special carriers

49
Q

What affects the charge of a drug

A

pKa: dissociation constant
pH of environment

50
Q

What is the difference between a weak acid and weak base

A

weak acid: release H ions and when protonated is uncharged
weak base: takes H ions and when protonated is charged

51
Q

How can we tell if a drug is going to be charged and uncharged?

A

If pH < pKA favors protonated (H ion attached)

If pH >pKA favors unprotonated (H ion is not attached)one

52
Q

Aspirin (weak acid) pKa=3.5
what from is it in the stomach (pH=1.5)
form in the intestine (pH=6.5)

A

pH 1.5< 3.5, protonated, uncharged
pH 6.5> 3.5, unportonated, charged

53
Q

Morphine (weak base) pKa=7.9
form in stomach (pH=1.5)
form in blood (pH=7.40)

A

1.5< 7.9 protonated, charged
7.4< 7.9 near equillibrium so charged and uncharged

54
Q

Where are most drugs filtered?

A

Kidney: filtered in the glomerulus enter renal tubule and excreted in urine

55
Q

What is “trapping” a drug in urine mean?

A

weak acids can be excreted faster in alkaline urine (give bicarb)
weak bases scrected faster in acidic urine (sodium citrate)
Out of practice

56
Q

What are biologic drugs

A

drugs created by living organisms and can be isolated or modified in the lab
extracted from ABX, blood, transplant recipient, microbiome, fungi
Recombinant DNA tech

57
Q

Explain recombinat DNA technology

A

Take protein produced in human and put it into an animal/bacteria/fungi and produce it for us; used for monoclonal antibodys and fusion proteins

58
Q

Explain what monoclonal (MAb) antibodies are, benefits

A

produced from a single clone of a plasma cell
decrease adverse effects, antigen binding site very specific
receptors are isolated and produce MAb based on it
Antigen binding sites are critical to MAb
Can bind to receptor (cancer) and cause cell death

59
Q

What is the functions of an Antibody

A

recognize bind to a specific antigen
induce an immune response after binding
Variable region bind to specific protein
Constant region doesnt change

60
Q

Explain Conventional Hybridoma Technology

A

Isolate human protein and inject into the mouse it makes antibodies and when makes enough Ab kill mouse and get spleen cells (plasma cells).
Take plasma cells and merge/fuse with cancer cells(myeloma) to make it immortal.
Take cell that was producing the anitbody, isolate it in culture and propagate it and inject it back to animal or harvest MAb

61
Q

What kind of drugs end in -mab

A

Monoclonal Anitbodies (MAb)

62
Q

How are drugs regulated?

A

FDA grants approval and oversees development
Must be safe and effecticive
- botanicals safe not necesssarily effective
Reviews claims and makes recs
Category
- OTC v BTC (behind the counter)
- herbal supplmenrs

63
Q

What are prescription drugs (Rx)

A

tightly regulated not safe without guidance of health professional
Public view as much effective than OTC but safety does not equate to efficacy
regulated by the FDA

64
Q

What are non-prescription drugs

A

OTC
freely available to the public
low risk for harm/abuse
does not mean “safe”

65
Q

What is important about Thalidomide

A

Drug introduced and approved Europe in 1950s fro morning sickness
Teratogen: Phacomelia
FDA Dr. Kelsey refused approval
Used to treat multiple myeloma

66
Q

What is the process of clinical testing

A

Lead compund (2 years) apply for patent
animal testing (2 years)
Investigational New Drug (IND) approved go to clinical testing human studies
Phase 1: is it safe? ADME healthy (20-100)
Phase 2: have the disorder (100-200)
- 50% placebo, 50% drug typically end here
Phase 3: (1000)
- doubleblind before market
Phase 4: New Drug Application (NDA can take 1 year) market make money back
- report adverse reaction, formulation changes

Pharmacology (7 decks)

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