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Pharmacology > Intro to pharm > Flashcards

Intro to pharm Flashcards

1
Q

pharmacology

A

-Study of how drugs interact with body to produce therapeutic effects
-Effect of drugs on living systems
-Complex science that requires
knowledge of biochem,
physio, orgo and molecular bio

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2
Q

drug

A

-Anything used to treat, dx or prevent disease
-What’s in a name? (Ex – Tylenol):
-Chemical name: N-acetyl-p-aminophenol
-Generic: acetaminophen
-Brand (commercial): Tylenol
-Abbreviation: APAP

-Classification of drugs:
-May be based on structure, mechanism of action or the effects it produces

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3
Q

drug control and development

A

-1906 – Pure Food and Drug Act
-1938 – Food, Drug and Cosmetic
Act
-New drug Application (NDA) – must be
submitted to FDA before drug can be
marketed
-1962 – Efficacy data required

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4
Q

clinical testing of drugs

A

-phase 1 – clinical pharmacology
-Phase II – clinical investigations
-Phase III – clinical trials
-Phase IV – post marketing studies

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5
Q

drug measurement

A

-metric system
-apothecary system
-avoirdupois system

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6
Q

metric equivalents

A

-1 gram = 1000 mg
-1mg = 1000 mcg
-1 mL = 1cc
-kg, g, mg, mcg
-L, mL, cc

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7
Q

apothecary system

A

-1 ounce = 30cc = 30 mL = 30g
-1 dram = 4 mL
-1 grain = 60 mg
-grain= gr
-dram = dr
-nitroglycerin 1/150 gr = 400 mcg or 0.4 mg
-ferrous sulfate 5 gr = 300 mg

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8
Q

household measurement

A

-1 cup (C) = 240 cc = 8 oz
-1 tsp = 5 cc * = 5 ml
-1 tbsp = 15cc * = 15 ml
-drop = gtt

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9
Q

pharmacodynamics

A

-Biochemical & physiological effects
of drugs and mechanisms of action
(MOA)
-*** What a drug does to the body –
how they work
-dose response curve- action increases as concentration increases- S curve

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10
Q

pharmacokinetics

A

-Study of how the body absorbs,
distributes, metabolizes and
excretes drugs
-Pharmacokinetics is what the body
does to the drug
-95% of drugs are systemically
distributed
-pharmacokinetics can change based on dose, race -> genetic testing when nothing works

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11
Q

pharmacotherapeutics

A

-Prevention and treatment of
disease
-Risk-benefit ratio* -> how safe is a drug:
-Used to describe adverse effects
of drug in relation to its beneficial
effects
-Acceptability of ratio depends on severity of disease being
treated

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12
Q

toxicology

A

-study of poisons (recognition,
treatment, prevention)
-Drugs:
-Adverse drug reactions (ADRs) or side
effects (SEs) at therapeutic doses
-Toxicity at higher doses

-Chemicals –> not used in therapy
(household, industrial, environmental,
drugs of abuse)

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13
Q

teratology

A

-study of monsters
-how drugs taken during pregnancy can cause fetal morphology
-ex. retinols (accutane) category x
-category A, B, C, D, X (worst) -> some drugs can change category based on trimester

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14
Q

therapeutic index (TI)

A

-TI – margin of safety
-ED- effective dose- lowest dose with effect
-you want a large range -> antibiotics
-In animals LD50/ED50 -> lethal dose / effective dose
-In humans TD1/ED1 -> Minimum toxic dose/minimum therapeutic dose
-Drugs with a high TI are “safe”
-Drugs with a low TI are “not safe” –
usually require therapeutic blood level
monitoring
-ex: digoxin, lithium, AMG, vanco,
phenytoin, carbamazipine, warfarin

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15
Q

how do drugs work

A

-site of action for drug is receptors
-Receptor may be: membrane,
membrane protein, cytoplasmic or
extracellular enzyme
-Drug binding site: proteins,
glycoproteins or lipoproteins
-Specificity – receptor must be able to
recognize a drug for it to work
-Lock & Key - drug-receptor complex
-Drug-receptor complex – produce a biochemical or physiological response

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16
Q

effects of drug binding

A

-Release of neurotransmitter
-Release of hormone
-Release endogenous chemicals
-Change electrical potential
-Changes membrane permeability
-Cause cascade effect

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17
Q

duration of action

A

-one a day- long duration of action
-4 times a day- short duration of action -> low affinity to receptor

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18
Q

agonists

A

-drugs that combine with a receptor and activates that receptor
-produces the same response as an
endogenous chemical
-stimulates the release of an endogenous chemical
-Has affinity for a receptor and efficacy
(intrinsic activity)
-ex. epinephrine – adrenergic agonist

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19
Q

antagonist

A

-Drug that combines with receptor
used by an endogenous chemical and
BLOCKS or diminishes the response of the endogenous agent
-Drug that combines with a receptor and INHIBITS the release of an endogenous compound.
-Drug that INTERCEPTS the signal
generated by an endogenous agent.
-ex. atropine – cholinergic
antagonist

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20
Q

agonist/antagonist (both)

A

-Partial agonist –> has affinity but low
efficacy
-butorphenol (Stadol) u & k activity
-Competitive Antagonism – agonist and antagonist compete for the same
receptor site
-Non-competitive antagonism – agonist and antagonist bind at different sites on the same receptor
-low doses it works -> high doses it loses effects
-often pain pills

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21
Q

potency vs efficacy

A

-Potency: If the dose of drug A is
less than drug B to achieve the
same response –> Drug A is more
potent (1mg vs. 100mg)
-high dose drugs are not potent
-Efficacy: The magnitude of the
maximum effect (predefined) -> relative to a person -> maximal effect in a person

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22
Q

tolerance-what changes?

A

-Reduced response to the same
dose or increased dose needed for
the same response
-Change in receptor sensitivity
-Change in pharmacokinetics of
drug
-Usually happens slowly, depends
on the drug, some do and some
don’t.
-ex: Narcotics, Nitroglycerin

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23
Q

dependence

A

-Don’t confuse tolerance with
dependence or addiction
-Need for the drug- psychological or physiological

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24
Q

placebo effect

A

-psychological response
-well designed clinical trial will contain a placebo group

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25
Q

allergy (hypersensitivity)

A

-An adverse immune reaction that
results from a previous exposure to a
particular chemical or one that is
structurally similar
-ACID- anaphylaxis (IgE), circulatory, immune complexes, delayed
-Divided into 4 categories:
-Type I
-Type II
-Type III
-Type IV

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26
Q

allergy type 1

A

-anaphylactic* reactions mediated by IgE antibodies
-red
-Symptoms include: urticaria, rash, vasodilation, hypotension, edema, inflammation, rhinitis, asthma, tachycardia, etc.
-symptoms are result of release of histamine, prostaglandins
and leukotrienes
-ex. Penicillin

27
Q

allergy type 2

A

-cytolytic* reactions mediated by IgG and IgM antibodies that affect the cells of the circulatory* system.
-Symptoms include hemolytic anemia,
thrombocytopenia, granulocytopenia.
-usually subside within several months
after drug discontinuation
-ex. quinidine, methyldopa

28
Q

allergy type 3

A

-Arthus reactions are IgG mediated where immune complexes* are deposited in vascular endothelium -> destructive inflammatory response called serum sickness occurs here
-general malaise
-Symptoms include erythema
multiforme, arthritis, nephritis, CNS
abnormalities and myocarditis, SLE (lupus)
and Steven-Johnson Syndrome
-ex. sulfonamide antibiotics

29
Q

allergy type 4

A

-delayed* hypersensitivity reactions mediated by T-lymphocytes and macrophages* (not immunoglobulin)
-When sensitized cells come in
contact with the antigen ->
lymphokines cause inflammatory reaction
-ex. poison ivy, antibiotics,
benzocaine

30
Q

idiosyncratic rxns

A

-unusual response to drug
-usually caused by genetic difference in metabolism or immunologic mechanisms

31
Q

reactivity

A

-Hyperreactive- intensity of a given
dose of drug is greater than
anticipated
-Hyporeactive- intensity of a given
dose of drug is less than expected

32
Q

when is reactivity a concern

A

-Therapeutic effect not observable
-important with low TI meds
-underdosing – can be as lethal as
overdosing
-What can you do?? ->
-Blood levels
-Plasma levels

33
Q

pharmacokinetics 4 aspects

A

-absorption
-distribution
-metabolism
-excretion

34
Q

what is a membrane

A

-lipid bilayer
-made of phospholipids and cholesterol
-drugs with higher lipid solubility cross membranes more readily
-cross via:
-passive diffusion
-Facilitated diffusion- passes with gradient but requires carrier protein.
-Active transport- against gradient and requires energy (requires ATP)
-Pinocytosis- formation and movement of vesicles (packages) across membranes -> requires energy

35
Q

passive diffusion

A

-MC
-Most drugs pass through membranes by this mechanism
-Diffuse down the concentration
gradient (from high to low)
-For non-electrolytes it is proportional
to lipid solubility
-For electrolytes it is related to pH

36
Q

absorption & factors that affect it

A

-rate at which a drug leaves its site
of administration and the extent to
which it occurs
-Bioavailability
-First Pass Effect
-Other factors that modify absorption:
-Drug solubility
-Drug concentration
-Circulation at site
-Absorbing surface area
-Transport proteins (P-glycoprotein

37
Q

bioavailability

A

-extent (%) to which a drug reaches its
site of action or a biological fluid that has access to that site
-i.e. the oral bioavailability of acetaminophen is 90%).
-may be due to the way an oral
dosage form is formulated (i.e. very hard tablets don’t dissolve)
-Bioavailability = (Qty Drug reaching Circ) / (Qty Drug Administered)
-IV bioavailability is 100%

38
Q

first pass effect

A

-Drugs that are well absorbed from
the G.I. tract and are metabolized
in the liver, have decreased
bioavailability as a result of the
First-Pass Effect
-liver takes remaining not absorbed

39
Q

factors that modify absorption

A

-Factors that modify absorption:
-drug solubility (solutions > suspensions > capsules> tablets)
-circulation at site
-absorbing surface area
-gastric emptying time -> faster gastric time -> less bioavailability (younger)
-slower gastric time -> higher bioavailability (older)
-intestinal motility
-food

40
Q

routes of administration: enteral

A

-oral (PO)- safest, cheapest, easiest
-absorption of PO drugs occurs in first third of SI BUT some drugs cant be absorbed -> too irritating, destroyed by acids or enzymes in GI, altered by foods or chemicals

-sublingual (SL)- used for very highly lipid soluble or potent drugs

-rectal (PR)- only useful when oral is not possible
-elderly, pediatric, when pt is unconscious or has nausea or vomiting
-most drugs are irritating to rectal mucosa and their absorption is unpredictable and variable

41
Q

routes of administration: Parenteral

A

-fastest to slowest
-IV- no absorption phase -> accurate, immediate, irreversible, must be aqueous
-IM- onset is slower and duration is longer than IV -> absorption is delayed and is related to vascularity
-SQ, SC- onset is slower and duration is longer than IM bc fat is less vascular than muscle

42
Q

routes of administration: miscellaneous

A

-topical- local drug effect -> creams, lotions etc.
-transdermal- unique delivery system -> drug crosses skin and enter circulation for systemic effect
-aerosol- very rapid onset -> extremely large SA for absorption and good blood supply -> used mostly for local effect

43
Q

distribution

A

-Distribution is the delivery of drug
from circulation to tissues
-Volume of Distribution
-Movement of drug through compartments
-each time it moves to new compartment -> must cross a membrane
-partition between 2 compartments is dependent on lipid and protein content, pH, osmotic pressure, and blood supply
-younger more fluid, older less fluid
-increased permeability increase distribution
-perfusion rate
-protein bound drugs
-pH
-40L in body
-2 important compartments:
-BBB
-Placental barrier

44
Q

distribution: protein

A

-protein binding affects drug distribution
-protein binding sites are sometimes referred to as reservoirs*
-binding of drug to protein may
significantly affect its bioavailability.
-DRUGS THAT ARE BOUND TO ANYTHING (other than a receptor) ARE INACTIVE***
-Drugs must be free or unbound to be
active

45
Q

blood brain barrier

A

-membranes separating the blood
from CSF and brain is more restrictive than any other membrane
-brain is highly lipophilic
-some drugs will concentrate in the brain (CNS depressants) and other may be completely excluded (many antibiotics)
-increase inflammation -> increase permeability -> water solubles might be able to cross then (meningitis)

46
Q

placental barrier

A

-membranes separating the
blood from the placenta are less
restrictive than most other
membranes.
-As a result, drugs pass quite easily
to the developing fetus.
-Assume all drugs will cross

47
Q

biotransformation / metabolism

A

-Body tries to convert any chemical
into one that is inactive and water
soluble, so that it can be excreted (pee and poo)
-Most, but not all, biotransformations occur in the liver
-classification*:
-1. phase 1- non-synthetic- oxidation (cyt P450 mixed fxn oxidases) reduction, hydrolysis
-2. phase 2- synthetic- conjugation (glucuronidation, sulfonation)
-both are enzymatic
-drug oxidizes and becomes another -> converted at a diff part of body -> more effective
-occur primarily in liver but may occur in GI tract, lung, skin or kidneys

48
Q

cytochrome P450 (CYP450) enzymes

A

-main phase I enzyme system involved
in the oxidative metabolism of drugs,
chemicals and some endogenous
substances
-Comprised of many isoforms, each with its own substrate specificity:
-CYP3A4 – predominant isoform: 50% of CYP-mediated metabolism **
-CYP2D6 – second most common isoform: 30% of CYP-mediated metabolism,
-CYP2C9 – third most common isoform: 10%

49
Q

CYP isoforms and their substrates

A

-CYP3A4: benzos, HIV drugs, calcium channel blockers
-CYP2D6:psychotropics, codeine, beta-blockers
-CYP2C9: phenytoin, warfarin, NSAIDs

50
Q

Regulation of the CYP450 system

A

-Enzyme Inhibitors: slow down metabolism of other drugs metabolized by CYP450
-Enzyme Inducers: speed up metabolism of other drugs metabolized by CYP450

51
Q

pharmacogenetics and pharmacogenomics

A

-terms may be used interchangeably
-Pharmacogenomics - general study of all of the many different genes that determine drug behavior.
-Pharmacogenetics - study of inherited differences (variation) in drug metabolism and response
-applications of pharmogenomics:
-study genes which encode for drug-
metabolizing enzymes
-Study genes which encode for defective structural proteins that may result in increased susceptibility to disease

52
Q

single nucleotide polymorphisms (SNPs)

A

-variations in the human genome
-a response to a drug is often linked to these DNA variations
-susceptibility to certain diseases is also influenced by DNA variations

53
Q

CYP2D6

A

-most studied genetic polymorphism
-Affects metabolism of psychotropics,
codeine, beta-blockers and antiarrhythmics
-7% of caucasians and 1-3% of African
Americans and Asians have defects

54
Q

CYP2C9

A

Affects phenytoin and warfarin metabolism

55
Q

pharmacogenomics and ethnicity

A

-Alcohol and aldehyde dehydrogenase in Asians is decreased -> increase in
cancer in upper respiratory tract
-G6PD deficiency in 14% African
Americans -> RBC hemolysis with sulfa
drugs
-N-acetyltransferse -> “slow acetylators” more common in middle east population, therefore increase risk of INH (Isoniazid) induced ADRs -> drug levels are higher in these pts bc they arnt metabolizing it -> adverse reactions

56
Q

advantages of pharmacogenomic research

A

-Determine the genetic basis of drug
response in individuals
-Develop individualized drug therapies for treating disease
-Provide tailored drug therapy based
on genetically determined
effectiveness and ADRs

57
Q

miscellaneous polymorphisms

A

-Transport proteins (P-glycoprotein)
-Drug-receptor alterations

58
Q

excretion

A

-Drugs are eliminated from the body either unchanged or as metabolites
-clearance- rate at which drug is eliminated from body
-steady state- when rate of administration = clearance -> as you take more meds you will get closer to steady state -> eventually you will excrete the same amount you take in
-concentration affects steady state
-Most important routes in humans are:
-Kidney
-Feces - either unabsorbed drug or via biliary excretion
-breast milk

-the control of excretion via the kidney is pH related:
-more alkaline urine increases the excretion of weak acid
-more acid urine increases the excretion of weak base

59
Q

half life

A

-(t1/2)
-time it takes for concentration of drug to be reduced by hald
-plasma half life
-elimination half life

60
Q

factors affecting pharmacokinetics and pharmacodynamics

A

-patient factors can modify a drug’s
effect and dosage:
-Age, weight, gender, genetics,
underlying disease, immune status,
psychological or placebo effect
-drug-drug and drug-food
interactions

61
Q

mechanisms of drug interactions

A

-synergism- combined effect is greater than the sum -> Ex. augmentin
-potentiation - an inactive drug increases the effect of another
-Induction - one drug increases the drug-metabolizing enzyme activity of another
-Inhibition - metabolism or excretion of one drug is blocked by another
-Unbinding - one drug displaces another from a protein binding site. (More unbound drug = more activity)

62
Q

drug safety in pregnancy*

A

-Category A
-Category B
-Category C
-Category D
-Category X

63
Q

article to read

A

-genomics
-what pas needs to understand and why

Pharmacology (16 decks)

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