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Pharmacology Test 1 > Theory > Flashcards

Theory Flashcards

1
Q

drug scheduling

A
  • I: no medical use, high likelihood of abuse (ie. heroin, LSD)
  • II-V: all have medical uses
    • but abuse potential is less as we move from class II to class V
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2
Q

chemical name

A

uses chemical nomenclature

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3
Q

generic name

A
  • final syllable can indicate drug class
  • has to be approved by US Adopted Names Council
  • each drug has only one generic name
  • facilitates communication and promotes safe and effective drug use
  • more specific than the brand names
  • can be more complicated than the trade name
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4
Q

trade name

A
  • brand name
  • a drug can have many of these
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5
Q

name the 4 processes of pharmacokinetics

A
  • absorption
  • distribution
  • metabolism
  • excretion
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6
Q

passage of drugs across membranes

A
  • membranes are close, so drugs must often pass thru cells not between
    • the barrier is the cytoplasmic membrane
  • 3 ways to cross:
    • channels and pores: only allows small ions thru like Na and K
    • transport systems: can be active or passive
      • all are selective
    • direct penetration of membrane: which requires a drug be lipid soluble
      • polar mcs and ions are not lipid soluble, so can’t penetrate, so they would have to be carried across with a protein b/w cells
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7
Q

P-glycoprotein

A
  • multi-drug transporter protein
    • transports many drugs out of cell
    • found in liver, kidney, placenta, intestine, capillaries, brain
      • helps get drugs eliminated, away from fetus, or out of the brain
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8
Q

what are polar mcs?

A
  • compounds that have an uneven charge, but NO net charge
  • dissolve in polar solvents, like water
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9
Q

what are ions?

A
  • have a net charge
    • unable to cross membrane
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10
Q

weak acids and bases

A
  • may be charged or not depending on the medium they are in
    • acids ionize in basic media: so they give up a proton and become negatively charged
    • bases ionize in acidic media: so they accept a proton and become positively charged
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11
Q

explain ion trapping/pH partitioning

A
  • pH differs on each side of membrane, so mcs accumulate where pH favors ionization
    • acidic drugs accumulate on basic side of the membrane
    • basic drugs accumulate on acidic side of the membrane
  • absorption is enhanced when difference b/w pH of the blood and that of the site of administration is such that a drug will be ionized in the blood
    • acidic drugs ionize in basic media, so they will accumulate on the basic side, so if blood is more basic than site of administration, then absorption occurs
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12
Q

what are the 5 factors affecting absorption?

A
  • rate of dissolution
    • dissolve before can be absorbed
  • surface area: large SA, higher absorption rate
    • orally administrated drugs often absorbed from small intestine b/c of the microvilli, so the SA is larger
  • blood flow: high blood flow, high absorption rate
    • maintains gradient that is higher b/w drug outside the blood and drug inside the blood
  • lipid solubility: if lipid soluble, they can directly cross the membrane
  • pH partitioning/ion trapping
    • absorption inc when difference b/w pH of blood and pH at the site of administation is such that drug mcs will have tendency to become ionized in the blood
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13
Q

what are the 2 groups of routes that drugs may be administered?

A
  • enteral: via GI, oral (PO)
  • parenteral: intravenous (IV), subcutaneous, intramuscular (IM)
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14
Q

IV: barriers to absorption

A
  • none: absorption is bypassed b/c drugs injected directly into blood
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15
Q

IV: absorption pattern

A
  • instantaneous and complete
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16
Q

IV: advantages

A
  • rapid onset
    • good for emergency
  • control over drug levels
  • can use large fluid volumes
  • can use irritant drugs b/c diluted in blood
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17
Q

IV: disadvantages

A
  • irreversible
    • administer over 1 min or more to help dilute
  • expensive
  • inconvenient
  • difficult, so not good for self administration
  • risk of fluid overload, infection, embolism
  • drug must be water soluble
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18
Q

IM and subQ: barriers to absorption

A
  • capillary wall, but easy to pass b/c large spaces b/w cells
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19
Q

IM and subQ: absorption pattern

A
  • rapid: water soluble drugs
  • slow: poorly soluble drugs
  • rapid: where high blood flow
  • slow: where poor blood flow
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20
Q

IM and subQ: advantages

A
  • permits use of poorly soluble drugs
  • permits use of depot preparations:
    • drug absorbed slowly over a period of time
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21
Q

IM and subQ: disadvantages

A
  • possible discomfort
  • invonvenient
  • potential for injury
  • cannot be used if receiving anticoagulant therapy
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22
Q

oral: barriers to absorption

A
  • epithelial lining of GI tract
    • drugs must pass thru the cells rather than between b/c tightly packed, so lipid soluble more likely to go across unless there is some kind of transport protein for a water soluble drug
    • P glycoprotein is a transporter that pumps some drugs out of epithelial cells and back into the intestinal lumen
  • capillary wall
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23
Q

oral: absorption pattern

A
  • slow and variable
  • depends on:
    • solubility/stability
    • gastric/intestinal pH
    • gastric emptying time
    • food in gut
    • coadministration of other drugs
    • special coatings on drugs
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24
Q

oral: advantages

A
  • easy
  • convenient
  • inexpensive
  • ideal for self medicating
  • potentially reversible: so safer than parenteral
    • if given incorrectly, can correct with activated charcoal while still in the GI tract
    • also with PO, no risk of fluid overload, infection, or embolism
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25
Q

oral: disadvantages

A
  • variability of absorption
  • inactivation of some by gastric acid and enzymes b/c of first pass effects or digestive enzymes destroying the drug in the stomch
  • possible nausea/vomiting from local irritation
  • pt must be conscious and cooperative and must be able and willing to swallow
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26
Q

movement of drugs following GI absorption

A
  • starts in GI tract and gets absorbed thru the wall of the GI tract into the blood
  • then first goes to the portal V–>liver where it either
    • is made to be more polar, more water soluble
    • is glucuronidated: so a glucose derivative is added to the lipid soluble drug
  • then the drug can either go:
    • out to the IVC–>heart–>general circulation–>eventually excreted in the kidney
    • (for glucuronidated drugs) go out into bile–>back into the GI tract where it is broken back down into the drug and the glucose–>can either be:
      • excreted in the feces
      • be reabsorbed further down the GI tract into the blood–>portal vein–>liver
  • this is a cycle called entero hepatic cycling
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27
Q

oral administration preparations

A
  • drug preparations are chemically equivalent if they have the same amount of the identical drug
  • preparations are equal in bioavailability if drug they contain is absorbed at the same rate to the same extent
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28
Q

oral preparation: tablets

A
  • drug plus binders/fillers compressed together
    • if made by different company, can differ in disintegration and dissolution have have differing bioavailability
      • SO, can differ in onset and intensity
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29
Q

oral preparation: enteric coated preparations

A
  • drug covered in material that will dissolve in intestine but not stomach, it is a coating that must have more basic environment to dissolve
  • use to:
    • protect drug from acid/pepsin in the stomach
    • protect stomach from drugs that cause gastric discomfort
  • absorption very variable b/c variations in gastric emptying
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30
Q

oral preparations: sustained release

A
  • capsules w/ tiny spheres containing drug that dissolves at variable rates
    • permit reduction of daily doses
    • produce steady drug levels over time
    • high cost and potential for variable absorption
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31
Q

3 factors affecting distribution

A
  • blood flow to tissues: rate at which blood flows determines rate at which drug is delivered to target organ
  • exiting vascular system via capillary beds
    • in capillaries, drugs can pass b/w and not thru cells so no resistance
    • BBB: tight junctions b/w cells which prevent drug passage
      • only lipid soluble drugs or those with transport systems can cross
      • P glycoprotein protects CNS
    • placental drug transfer
    • protein binding to plasma albumin
  • entering cells: determined by lipid solubility and transport systems
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32
Q

which 2 factors can affect blood flow distribution of drugs?

A
  • abscesses: no internal blood vessels so drugs can’t reach bacteria within
  • tumors: limited blood supply toward core
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33
Q

explain how placental drug transfer affects distribution

A
  • lipid soluble and non-ionized drugs can pass across placenta to fetus
  • ionized, highly polar, protein bound, or substrates of P glycoprotein cannot get to fetus
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34
Q

explain how protein binding to plasma albumin can affect drug distribution

A
  • drugs can reversibly bind to protein
    • plasma albumin: always in bloodstream b/c so large
      • drugs bound to albumin can’t leave blood, only free mcs can leave blood
    • can be a source of drug interaction b/c drugs competing for sites on albumin
      • if displace a drug, the free conc of the displaced drug can inc, so that drug’s response is increased
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35
Q

metabolism of drugs

A
  • mostly done in the liver
    • done by the P-450 enzyme system
  • irreversible transformation of parent cpds into daughter cpds then disbursed thru the body
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36
Q

what are the therapeutic consequences of drug metabolism?

A
  • accelerated renal excretion of drug
    • kidneys can’t excrete lipid soluble drugs, so
        1. convert to H2O soluble to increase excretion by inc polarity or
        1. glucuronidation (glucose derivative is attached to drug)–pushed out into bile
  • drug inactivation
  • increased therapeutic action: metabolism inc effectiveness
  • activation of prodrugs: inactive when administered, then made active
  • inc/dec in toxicity
    • dec if make drug inactive
    • inc if convert to more toxic form
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37
Q

metabolism and age

A
  • infants have limited ability to metabolize
    • drugs are not tested on very young b/c their kidneys and liver and immature
  • older adults have a decreased ability
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38
Q

drug metabolizing enzymes

A
  • some drugs metabolized by P-450 b/c they are substrates of P-450 enzyme system
  • inducers: act on liver to increase rate of drug metabolism
    • as metabolism inc, drug plasma levels decrease, and kidney function inc (so creatinine decreases)
    • 2 consequences:
      • if also substrate, can mandate inc dosage to maintain effects
      • can accelerate metabolism of other drugs and mandate an increase in their dosage
  • inhibitors: decrease rate of metabolism of drugs
    • as drug metabolism dec, blood plasma rates increase, and kidney function dec (so creatinine levels inc)
      • can cause inc toxicity and bad S/E
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39
Q

explain the first pass effect

A
  • rapid hepatic inactivation of certain oral drugs
    • sometimes, drug b/c goes from GI–>portal V–>liver can be inactivated when first going thru liver, so have to be administered parenterally
    • if liver capacity to metabolize drug is high, then it can ianctivate the drug on the first pass thru the liver
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40
Q

drug metabolism and nutrition

A
  • P450 enzymes require co-factors to function
  • if malnourished, then not getting enough protein to maintain muscle mass, and water is stored in muscle
    • if wasting of muscle occurs, then drugs that are water soluble have too much drug in blood stream following subsequent doses so can become toxic
    • especially occurs in the elderly
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41
Q

competition b/c drugs and their metabolism

A
  • if 2 drugs metabolized by the same pathway, can decrease rate at which one is metabolized and may build up
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42
Q

steps in renal excretion of drugs

A
  • glomerular filtration
    • blood w/ drugs comes in capillaries where forced thru pores, but blood cells and bound drugs stay behind in the capillaries b/c too large
  • passive tubular reabsorption
    • lower concentration of drug in blood than urine drives lipid soluble drugs back to blood, so have to convert lipid soluble drugs to more polar form to excrete, so that it will stay in the urine
    • if not lipid soluble, then continues on in urine
  • active tubular secretion
    • pump drugs from blood to kidney lumen
      • one pump for each organic acids, organic bases, and P glycoprotein
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43
Q

factors that modify renal excretion of drugs

A
  • pH dependent ionization
    • by manipulating urine pH to promote ionization of the drug, you can dec passive reabsorption of drug back to the blood
      • so if we have an acidic drug and make the urine basic, the drug will more likely be ionized, so it will not be carried back to the blood by passive tubular reabsorption
  • competition for active tubular transport can delay renal excretion and prolong drug effects
    • can only carry so much at once, so if drug doesn’t go back to urine, then effects are pro-longed
  • age
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44
Q

routes of non-renal excretion

A
  • breast milk: lipid soluble drugs can be passes to infant in breast milk
  • bile: excreted to small intestine–>feces
  • lungs: excrete volatile anesthetics
  • sweat and saliva
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45
Q

Grapefruit Juice and Cytochrome P-450

A
  • Grapefruit juice: many medications interact with grapefruit juice
    • More a pt drinks, the more inhibition of CYP3A4 that occurs
    • Dec first pass metabolism of drugs, so inc the bioavailabilty of the drug
  • CYP3A4 is found both in the liver and the intestinal wall
    • with grapefruit juice, that on the intestinal wall is inhibited more, which decreases the intestinal metabolism of many drugs, so the amount available for absorption inc–>inc levels of the drug in the blood–>more intense drug effects
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46
Q

define polymorphism

A

genetic variability in how a person may respond to a particular drug class

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47
Q

what changes to the body does pregnancy bring about as it relates to pharmacokinetics?

A
  • Pregnancy brings about changes in the kidney, liver, GI tract, so change in dosage may need to occur
    • 3rd trimester, the renal blood flow is doubled, so inc in glomerular filtration rate, so the drugs eliminated by glomerular filtration experience inc clearance
    • Hepatic metabolism inc
    • GI motility and tone decrease, so there is prolonged time for drugs to be absorbed or reabsorbed in enterohepatic circulation
      • Inc levels of drugs whose absorption is usually poor
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48
Q

adverse rxns in pregnancy

A
  • biggest issue is teratogenesis
49
Q

what does the effect of a teratogen depend on?

A
  • dependent on which stage of pregnancy drug is given
    • preimplantation (conception-week 2)
      • if dose of drug is high, death will occur to baby
    • embryonic (weeks 3-8)
      • exposure to teratogens causes gross malformation
    • fetal (weeks 9-term)
      • teratogen exposure disrupts function rather than structure
50
Q

why are pediatric pts sensitive to drugs?

A

organ system immaturity

51
Q

what kind of effects do you see with drugs in neonates?

A
  • drugs have intense and prolonged effects
    • levels remain above MEC longer than in adult, so effects are prolonged
    • with a subQ injection, levels remain above MEC longer and levels rise higher, so effects more intense and prolonged
52
Q

why do we have inc drug sensitivity in pediatric pts?

A
  • immaturity of 5 processes:
    • drug reabsorption
    • protein binding
    • exclusion of drugs from CNS by BBB
    • hepatic drug metabolism
    • renal drug excretion
53
Q

absorption orally for pts under 1 yo

A
  • if drug absorbed in stomach, then longer gastric emptying time, so inc absorption
  • if drug absorbed in intestine, then delay in effects of drugs b/c of longer gastric emptying times
54
Q

absorption intramuscularly for pt under 1 yo

A
  • absorption is slow and erratic
    • slow b/c low blood flow to muscles
    • but, by early infancy, absorption is more rapid than in adults
55
Q

absorption transdermally for pts under 1 yo

A
  • more rapid and complete
    • stratum corneum is thin and blood flow to skin is higher
    • inc risk of toxicity from topical drugs
56
Q

distribution in pts under 1 yo

A
  • protein binding
    • limited b/c of low levels of albumin and endogenous cpds compete with drugs for the limited amt of binding sites
      • so more free medication in infants, which intensifies results, so dosages should be reduced
  • BBB
    • not fully developed so drugs have easy access to CNS
      • so give in smaller doses
57
Q

hepatic metabolism in pts under 1 yo

A
  • metabolism is low in newborns
    • sensitive to drugs that are eliminated by hepatic metabolism
    • adult levels reached by age 1
58
Q

renal excretion in pts under 1 yo

A
  • reduced at birth
    • renal blood flow, glomerular filtration, and tubular secretion are all low
    • if drug eliminated by renal excretion then need reduced dose or at longer intervals
  • adult levels reached by 1 yo
59
Q

PK for children 1 YO and older

A
  • similar to adults
  • BUT metabolize drugs faster than adults until 6 yo
    • so may need inc in dosage or reduction in dosing intervals for drugs eliminated by hepatic metabolism
60
Q

why do geriatric pts have more adverse rxns and more drug drug rxns?

A
  • altered pharmacokinetics secondary to organ system degeneration
  • multiple and severe illnesses
  • multi drug therapy
    • polypharmacy
  • poor adherence
61
Q

changes in absorption in geriatric pts

A
  • GI absorption:
    • percent of oral dose that becomes absorbed does not change
    • rate of absorption may be slowed b/c of delayed gastric emptying so drug responses may be delayed
62
Q

changes in distribution in geriatric pts

A
  • inc body fat: provides storage for lipid soluble drugs so plasma levels of these are reduced and there is less of a response
  • dec lean body mass and total body water
    • water soluble drugs become distributed in smaller volume, so the concentration is inc and the effects may be more intense
  • reduced conc of albumin
    • inc levels of free drug so effects may be more intense
63
Q

changes in metabolism in geriatric pts

A
  • rates of hepatic metabolism decline due to:
    • reduced hepatic blood flow
    • reduced liver mass
    • dec activity of liver enzymes
      • all lead to prolonged exposure of certain drugs
  • Depending on the way drug is metabolized during first pass effect, there is usually a first phase and a second phase, but they lose the first phase, so only have second phase which include glucuronidation, acetylation, and sulfuration (all old folks have GAS), so many times drugs that need a lot of metabolism should not be given to the elderly
64
Q

changes in excretion in geriatric pts

A
  • renal fcn declines
    • drug accumulation secondary to reduced renal excretion is most important cause of severe adverse rxns in older adults
    • all due to reduced renal blood flow, glomerular filtration rate, tubular secretion, and number of nephrons
  • should check creatinine clearance
65
Q

why would parenteral injections be preferred to oral preparations?

A
  • emergencies if need rapid medication onset
  • situtations where plasma drug levels need to be tightly controlled
  • drugs that would be destroyed by gastric acid, GI enzymes, or hepatic enzymes
66
Q

parenteral routes: speed of absorption

A
  • IV>IM>subQ
    • subQ slowest b/c relies on capillaries to distribute
67
Q

drug distribution in malnourished pts

A
  • malnourished pts:
    • albumin levels can be reduced so drugs can have less albumin to bind to, so free levels of drugs inc and toxicity
68
Q

gender differences in drug responses

A
  • do not know how a lot of medications will react in women b/c more studies conducted on men
  • Pregnant pt:
    • A: okay to give
    • X: don’t give b/c high risk
  • Can affect sperm quality or quantity for men
69
Q

explain an agonist

A
  • drug binds to its receptor and mimics actions of body’s own regulatory compounds
    • drug that is an agonist works in the same way as a desired chemical in the body
    • have affinity and high intrinsic activity
70
Q

explain an antagonist

A
  • block the agonists (whether endogenous or exogenous) from stimulating the receptors
    • prevents normal rxn from occurring
    • has affinity for receptor by no intrinsic activity, so prevents R activation and normal processes from occurring
  • act by preventing receptor activation
    • so, if no agonist is present, administration has no observable effect
71
Q

explain the 2 categories of antagonists

A
  • noncompetitive: bind irreversibly to R, so effect is like reducing total number of receptors available for activation by an agonist
    • reduce maximal response an agonist can cause, since it is irreversible even by adding more agonist, since the Rs are blocked, the effects will not increase
  • competitive: binds reversibly
    • if agonist and competitive antagonist have equal affinity, then receptor will be occupied by whichever is in highest concentration
72
Q

explain a partial agonist

A
  • agonist with only moderate intrinsic activity
  • maximal effect that it can produce is less than that of a full agonist
  • can act as an agonist or antagonist
    • will act as an antagonist if pt already on a full acting agonist, so will produce a smaller effect than an agonist alone would produce (so blocks some of the power of the full agonist)
73
Q

what happens if the receptors of a cell are continually exposed to an agonist?

A
  • cell becomes less responsive
    • it is said to be “desensitized”
    • could occur by down regulation meaning the cell actually breaks down some of the receptors that normally responded to the agonist
74
Q

what happens if the receptors of a cell are continually exposed to an antagonist?

A
  • the cell becomes hypersensitized
    • up regulation occurs by more receptors being created to respond to the antagonist
75
Q

explain an allergic rxn

A
  • it is an immune response caused by an Ag
  • will present as anaphylaxis: bronchospasm, laryngeal edema, hypotension
    • need to use epinephrine which will cause:
      • bronchodilation
      • vasoconstriction to return BP to normal
        • works by activating beta 1 receptors in the heart and beta 2 in the lungs
76
Q

which drugs cause most allergic rxns?

A
  • penicillins: most common
  • NSAIDs
  • sulfonamides: diuretics, antibiotics
77
Q

explain the general mechanism of antihistamines

A
  • find a receptor on a mast cell and prevent histamines from attaching to the cells and causing symptoms of an allergic rxn like bronchospasm and edema
    • antihistamines help reduce histamine release
  • histamine is released in response to injury, allergy, and inflammatory rxns
78
Q

properties of first and second generation antihistamines

A
  • both used for symptoms of allergy, reduces itching, and pain
  • histamine binds receptors and causes vasodilation, hypotension, flushing, headache, bronchoconstriction
  • H1RA will help the effects and cause more vasoconstriction, bronchodilation
  • 1st generation (diphenhydramine) are more sedating than second generation (loratidine)
    • 1st gen are very lipid soluble so can cross BBB and bind to the H1 receptors there
      • 2nd generation are not lipid soluble so do not cross BBB
    • pts should avoid alcohol and pther CNS depressants b/c these intensify the depressant effects of first generation H1 Receptor antagonists
  • No antidote available for antihistamines
79
Q

explain therapeutic range

A
  • when drug levels are high enough to be effective (so above MEC), but not high enough to be toxic
    • so falls b/w MEC and toxic concentration
    • it is the range where the drug concentration will cause therapeutic effects in the majority of patients, and adverse rxns in the minority of patients
  • narrow therapeutic range is more dangerous and harder to dose safely, b/c very narrow range from MEC to toxic level
80
Q

what is the minimum effective concentration?

A
  • lowest possible level in which a drug would give any therapeutic effects
81
Q

when are peak and trough levels in drug serum concentration?

A
  • peak level is 30 minutes after a drug is given
  • trough level is 30 minutes before the next dose of a drug is given
82
Q

what is the loading dose?

A
  • higher dose is used to increase drug levels in the body quickly
    • once give, the drug level will be closer to the therapeutic dose and a normal dose can be given
83
Q

what determines the duration of action of a drug?

A
  • metabolism
  • excretion
84
Q

what makes a drug dangerous and harder to dose safely?

A
  • a narrow therapeutic range, so small range b/w MEC and toxic dose level
85
Q

explain half life

A
  • how rapidly amount of drug declines in the body by half based on metabolism and excretion
    • time for amount of drug in body to decrease by 50%
  • determines the dosing interval
    • so the shorter the half life of the drug, the shorter the dosing interval to maintain therapeutic effects
86
Q

explain the process of repeated dosing to reach a plateau

A
  • Drug accumulates in body until it reaches plateau (steady level)
    • Amt of drug eliminated b/w doses equals the dose administered
      • Average drug levels will remain constant and plateau
      • Typically takes 4 half lives
      • Not dependent on dosage size
87
Q

epi-pen considerations

A
  • Epinephrine: adrenergic drug
    • Inc Cardiac outpuut–>elevates BP
    • Suppresses glottal edema
    • Counteracts bronchoconstriction
    • Single use, spring activated needle, IM injection in outer thigh (can give thru clothing) for 10 sec, massage for 10 sec following injection
    • After use: call 911, go to ER
      • Effects start to fade in 10-20 min
      • Enzymes broken down so drug will metabolize quickly
      • After calling 911, you need to administer a second dose if the symptoms don’t go away
      • Then after you give epi, you need to give just a regular steroid to continue to decrease allergic symptoms
  • Can be used with lidocaine/novocaine b/c it causes it to work longer
88
Q

explain the dose response relationship

A
  • relationship b/w size of an administered dose and the intensity of the response
    • determines minimal amount needed to produce a response
    • determines maximum response a drug can elicit
    • as dose inc, the response becomes larger–so the drug responses are graded
      • so we can adjust tx to a particular pt by lowering or raising dosage until response of desired intensity it achieve
      • **but at some point as dose increases, the increase in dose is unable to elicit a further inc in response
89
Q

what is maximal efficacy?

A
  • largest effect a drug can produce
    • ie. if drug A can produce more pain relief than drug B no matter how large the dose of drug B is, we can say drug A has greater maximal efficacy
90
Q

what is potency?

A
  • amount of drug we must give to elicit an effect
    • ie. for any specific degree of pain relief, the required dose needed to reach that degree of pain relief is greater for drug B than drug A, so because drug A produces pain relief at a lower dose than B, er would say that drug A has greater potency than B
91
Q

what are the 4 types of receptors that an agonist or antagonist can bind to?

A
  • cell membrane embedded enzymes
    • binding domain outside, catalytic site inside
    • agonist drug activates the R and increases the activity
    • response occurs within seconds
  • ligand gates ion channels
    • regulate flow of ions and is specific for a particular ion
    • when drug (agonist) binds, channel opens and ions flow in or out based on the concentration gradient
    • response within milliseconds
  • G protein coupled receptors
    • agonist activates receptor–>activates G protein–>activates effector
    • quick response
  • transcription factors
    • found w/in the cell on DNA in nucleus to regulate protein synthesis
    • responses are delayed
    • only activated by lipid soluble mcs b/c inside cell
92
Q

drug selectivity

A
  • selectivity of a drug is possible b/c they act on specific receptors
    • you want the drug to be selective, so it will cause fewer side effects
    • if drug selective for a receptor that regulates a few processes, drug that works on that receptor will also have effects on all of the processes even if not intended use
93
Q

explain affinity

A
  • strength of attraction between drug and its receptor
    • high affinity means that the drug is strongly attractd to its receptor
    • reflected by its potency: if strongly attracted to a receptor, drugs with high affinity can bind to receptors when in low concentrations, so drugs with high affinity are effective in low doses
      • drugs with high affinity are potent
94
Q

explain intrinsic activity

A
  • ability of a drug to activate a receptor following the binding of the drug to the receptor
    • high intrinsic activity causes intense receptor activation
    • reflected by the maximal efficacy, so drugs with high intrinsic activity have high maximal efficacy
      • causing intense receptor activation, they are able to cause intense responses
95
Q

explain the average effective dose

A
  • called ED50
  • dose that is required to produce a defined therapeutic response in 50% of the population
    • described as the “standard dose”: often start here when trying to figure out the best dose to give to a particular patient
96
Q

explain the therapeutic index

A
  • ratio of a drug’s LD50 to ED50
    • LD50: average lethal dose, so lethal to 50% of animals in the studies
    • large therapeutic index indicates drug is relatively safe
97
Q

what does potentiating mean?

A
  • when a patient is taking 2 medications, one drug may intensify or potentiate the effects of the other
    • this is a potentiative interaction
  • these types of interactions can be:
    • beneficial: can cause increased therapeutic effects
    • detrimental: can cause an increased risk for adverse effects (ie. aspirin and warfarin)
98
Q

what is synergy?

A
  • When the interaction causes an increase in the effects of one or both of the drugs the interaction is called a synergistic effect.
99
Q

what does 1 oz equal?

A

=2 tbsp=6 tsp=30 mL

100
Q

define pharmacokinetics

A
  • what the body does to drug
101
Q

define pharmacodynamics

A
  • what the drug does to the body
102
Q

which medication PO is the fastest absorbed?

A

liquid medication

103
Q

which populations are at the highest risk for ADRs?

A

very young and the very old

104
Q

what are the types of allergic rxns and how do you treat each?

A
  • mild rash: contact dermatitis
    • _​_tx: diphenhydramine
  • rash that is more broadly spread over the body
    • tx: larger dose of diphenhydramine or a steroid
  • hives and difficulty breathing: anaphylaxis
    • _​_tx: epinephrine
105
Q

if the pt’s liver is impaired, what happens with water soluble drugs?

A
  • they stay in the body longer, so their effects last longer
    • if another dose is given, this could lead to build and possible toxicity
106
Q

what to do as the nurse when there is a narrow therapeutic range?

A
  • Need to monitor blood serum levels and monitor target organs that are known to harmed by toxic levels of the blood
    • Check the liver by looking at hepatic panel and checking transaminases
      • Want to check baselines and throughout therapy
      • How to check when not able to do labs? Look for jaundice and watch urine to go from yellow–>tea colored–>dark brown
    • How to monitor kidneys?
      • BUN and creatinine as well as glomerular filtration rate
      • How to check when not able to do labs
        • Low output
        • Normal colored urine in normal amounts–>really high volume of crystal clear urine: indicates diuretic phase of renal damage
107
Q

Who would we want to be careful of recommending NSAIDS to?

A

those with renal problems

108
Q

What population should we limit high dose steroids over an extended period of time?

A
  • Someone who already has a fungal infection b/c this will kill them due to the glucocorticoids inhibiting the immune system, and the only thing that stops the fungi from killing us is the immune system
  • Diabetics b/c steroids cause hyperglycemia, so they would just have more problems controlling diabetes
109
Q

How do glucocorticoids impact cellular metabolism in the body?

A
  • They are lipid soluble, so they go to their target inside the cell membrane
    • They suppress the immune system, so the components they slow down/stop is protein synthesis–>this means their interleukins and Ab will be decreased if they are taking this glucocorticoid
    • So you would want them on a high protein diet
    • In elderly ppl who take a lot of steroids: muscle loss, bone loss (Bone fractures)
110
Q

what would you suggest to a female patient who is taking glucocorticoid for a long period of time and she is still in period that she is depositing mineral for bones?

A
  • suggest that she do weight bearing exercise, b/c glucocorticoids can cause osteoporosis
111
Q

what is first peak effect?

A
  • especially for HTN, you want to watch these, b/c the first one can cause you to have hypotension
  • So with first meds, you need to monitor the first dose
112
Q

7 Rights of Med Administration

A
  • right patient
  • right medication
  • right route
  • right dose
  • right time
  • right indication
  • right documentation
113
Q

which NSAID has the biggest chance of causing bleeding?

A

Aspirin

114
Q

what are the effects of glucocorticoids on carbohydrates?

A
  • increase glucose availability by:
    • stimulation of gluconeogenesis: making of glucose from AAs
    • reduction of peripheral glucose utilization
    • inhibition of glucose uptake by muscle and adipose tissue
    • promotion of glucose storage in the form of glycogen
115
Q

what are the effects of glucocorticoids on proteins?

A
  • promote protein breakdown
    • this provides AAs for glucose synthesis (gluconeogenesis)
  • leads to muscle wasting, thinning of skin
116
Q

what are the effects of glucocorticoids on fats?

A
  • promotes lipolysis (fat breakdown)
  • causes fat redistribution if glucocorticoids present for long periods of time
    • “potbelly, moon face, buffalo hump”
117
Q

how long will grapefruit juice stay in your system?

A

2 days or more

118
Q

what is therapeutic objective?

A

to provide maximum benefit with minimal harm

119
Q

what are the phases of clinical drug development?

A
  • Phase 1: healthy volunteers
  • Phase 2 & 3: Patients
  • Phase 4: General Population

Pharmacology Test 1 (3 decks)

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