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Pharmacology I > unit 1- concepts > Flashcards

unit 1- concepts Flashcards

1
Q

drug

A

•any chemical that can affect living processes

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2
Q

pharmacology

A
  • study of drugs and their interactions with living systems
  • physical/chemical properties
  • physiologic/biochemical effects
  • knowledge of history, sources, uses
  • knowledge of absorption, distribution, metabolism, excretion
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3
Q

clinical pharmacology

A

•study of drug interactions in humans

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4
Q

therapeutics

A
  • use of drugs to dx, prevent, tx disease or to prevent preggo
  • medical use of drugs
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5
Q

Factors influencing intensity of drug responses

A
  1. ) administration- dose, route, time
  2. ) pharmacokinetics
  3. ) pharmacodynamics
  4. ) individual pt variation
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6
Q

pharmacodynamics

A

•processes that, once the drug reaches site of action, determine nature and intensity of response

  1. ) receptor interaction
  2. ) pt functional state
  3. ) placebo effects
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7
Q

how do you classify propofol (Diprivan)

A
  • general anesthetic
  • CNS sedative
  • suppresses respiratory system
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8
Q

pharmacokinetics

A

•movement of drugs within the body

  1. ) absorption
  2. ) distribution
  3. ) metabolism
  4. ) excretion
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9
Q

many penicillins have to be given on an empty stomach b/c…

A

•presence of food in stomach can interfere with absorption

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10
Q

aspirin absorption

A
  • acidic molecule
  • remains nonionized in stomach -> absorbed
  • ionizes in intestine -> little absorbed
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11
Q

absorption

A
  • drug movement from site of administration into blood

* amount absorbed determines intensity of effects

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12
Q

factors affecting drug absorption

A
  • rate of dissolution (faster)
  • surface area (high)
  • blood flow (high b/c [] gradient)
  • lipid solubility (lipid soluble faster)
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13
Q

enteral administration

A

•via gastrointestinal tract

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14
Q

parenteral administration

A
  • injection
  • outside GI tract
  • IV
  • subQ
  • IM
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15
Q

Intravenous administration

A
  • no barriers to absorption
  • instantaneous and complete absorption
  • rapid onset of action
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16
Q

advantages IV administration

A
  • allows for precise control
  • large fluid volumes
  • use of irritant drugs (diluted in blood)
  • eliminates need for absorption
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17
Q

disadvantages IV administration

A
  • high cost
  • irreversible
  • risk for fluid overload
  • risk for infection
  • risk for embolism
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18
Q

advantages IM route

A
  • ideal for poorly soluble drugs

* ideal for depot preps (drugs absorbed slowly over time)

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19
Q

disadvantages IM route

A
  • discomfort/inconvenience

* bleeding risks, so not ideal for pt on anticoagulant therapy

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20
Q

oral (PO) administration

A
  • drugs absorbed through stomach, intestine, or both
  • barriers of cells lining GI tract and capillary wall
  • absorption determined by solubility/stability, pH, gastric emptying, food, coadministration, drug coating
  • drugs must go through liver before general circulation
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21
Q

advantage PO route

A
  • easy, convenient, cheap
  • safer than injection
  • reversible and able to be sped up
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22
Q

disadvantages PO route

A
  • effectiveness variability among pts
  • potential for enzymatic inactivation
  • requires pt cooperation
  • risk for local irritation
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23
Q

what occurs first when an oral drug is absorbed

A

•drugs molecules move from small intestine into portal venous system

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24
Q

distribution

A

•drug moment form blood to interstitial space of tissues and into cells
•determined by:
1.) blood flow to tissues
2.) ability of drugs to exit vascular system
3.) ability of drugs to enter cells

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25
Q

abscesses

A
  • impedes blood flow at tissue

* lack blood supply, so drugs can’t get to bacteria within

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26
Q

solid tumor

A
  • impedes blood flow at tissue

* limited blood supply, esp. at core, which makes them resistant to drug therapy

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27
Q

how drugs exit vascular system

A
  1. ) capillary beds
  2. ) blood brain barrier
  3. ) placental transfer
  4. ) protein binding
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28
Q

drug exit via capillary bed

A
  • through pores in wall

* BETWEEN cells

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29
Q

blood brain barrier (BBB)

A
  • tight junction caps. in CNS
  • drugs must pass THRU and must be lipid soluble or have transporter
  • protects, but also limits drug access
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30
Q

membranes of placenta

A

•separate maternal circulation from fetal
•do NOT constitute absolute barrier to drugs
•lipid soluble pass thru
•non-ionized, polar, or protein bound don’t pass
*best to assume that ALL drugs pass thru

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31
Q

protein binding of drugs

A
  • many drugs travel thru bloodstream by binding to albumin
  • % active and able to perform, be metabolized/excreted is % not bound to protein
  • bound drug may act as a reservoir from which drug is slowly released as unbound form (maintaining equilibrium when previous unbound metabolized)
  • albumin most abundant and important b/c never leave bloodstream (large/no transporter)
  • percentage of drug binding determined by binding attraction
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32
Q

free drugs

A
  • unable to bind to saturated protein

* go to target tissue

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33
Q

multiple drug therapy

A
  • compete with each other on albumin binding sites
  • on drug can displace another, causing [free] to rise
  • more free drug increases intensity of drug responses and may lead to toxicity
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34
Q

which drug is most likely to increase metabolism of other drugs

A

•barbiturates (ex: phenobarbital) b/c known to increase NZ activity in liver
•stimulates induction
•important b/c other drugs are metabolized faster in liver, so decreased therapeutic effect of the other drugs
*barbiturates are used for seizures

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35
Q

metabolite

A
  • metabolized drug
  • can be active or inactive
  • Ex: Demerol converted into active metabolite, which results in adverse affects
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36
Q

metabolism (biotransformation)

A
  • enzymatically mediated alteration of drug structure
  • most occurs in liver
  • performed by hepatic microsomal NZ system (P450 system)
  • includes breakdown and synthesis
  • nutritional status plays a key role
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37
Q

P450 system

A
  • performs drug metabolism

* hepatic NZ that are capable of catalyzing rxns using drug substrates

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38
Q

therapeutic consequences of drug metabolism

A
  1. ) accelerated renal excretion
  2. ) drug inactivation (most common)
  3. ) increased therapeutic action
  4. ) activation of prodrugs (inactive -> active)
  5. ) increased/decreased toxicity
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39
Q

factors that affect metabolism

A
  1. ) age
  2. ) induction of drug-metabolizing NZ
  3. ) first-pass effect
  4. ) nutritional status
  5. ) competition b/t drugs
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40
Q

first pass effect

A
  • rapid inactivation of certain oral drugs, resulting in no therapeutic effects
  • drugs at risk are administered parenterally to bypass liver temporarily
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41
Q

excretion

A
  • movement of drugs and their metabolites out of the body
  • kidney most important organ (urine)
  • also excrete via bile, sweat, saliva, breast milk, expired air
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42
Q

factors that modify excretion

A
  • urinary pH- ionized at pH of urine, remain in tubule and excreted
  • competition for tubular transport sites
  • age
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43
Q

plasma drug levels

A
  • concentration of drug in blood
  • measured to regulate drug responses in regards to dosing/timing
  • remain higher for longer period of time in children
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44
Q

minimum effective concentration (MEC)

A
  • plasma drug level below which therapeutic effects will not occur
  • effective drugs must be at or above MEC
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45
Q

toxic concentration

A

•plasma level at which toxic effects begin

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46
Q

therapeutic range

A
  • range of plasma drug levels between MEC and toxic concentration
  • enough drug to be effective, but not so much to be toxic
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47
Q

drug half-life

A

•time required for amount of the drug in the body to decrease by 50%
•half life may increase in certain protein bound drugs, which have a slow release based on metabolism of previously unbound drugs
*drugs peak at 4 t/12s

48
Q

therapeutic index

A

•difference between the effective dose (ED) in 50% of people/animals and the lethal dose (LD) in 50% of people/animals
TI = LD(.5)/ED(.5)
*narrower TI -> greater degree of toxicity

49
Q

agonist vs. partial agonist

A
  • agonist binds to a receptor, initiating biological response
  • partial agonist binds to receptor, but doesn’t fully activate it
  • when administered together agonist competes w/ partial agonists, which essentially acts as an antagonist at a given receptor
50
Q

FDA drug standards

A
  • purity
  • bioavailability
  • potency
  • efficacy
  • safety/toxicity
51
Q

3 most important characteristic of ideal drug

A
  1. ) effectiveness
  2. ) safety
  3. ) selectivity
52
Q

effectiveness

A

•drug elicits response for which it was given

53
Q

safety

A
  • drug that cannot produce harmful effects (even in high dose)
  • no drugs are actually safe, but measures can be taken to reduce adverse effects
54
Q

selectivity

A
  • drug that elicits only the response for which it is given

* no side effects- impossible to actually achieve

55
Q

other properties of ideal drug

A
  • reversible
  • predictability
  • low cost
  • ease of administration
  • freedom from drug interactions
  • chemical stability
  • possession of simple generic name
56
Q

randomized controlled trial

A
  • most reliable way to objectively assess drug therapies
  • used to evaluate all new drugs
  • involves use of controls, randomization, and blinding
57
Q

labeled drug

A

•only used for indication determined in clinical trials

58
Q

off-labeled drug

A

•used for non-FDA approved indication

59
Q

limitations of new drug development

A
  • limited testing in women/children

* failure to detect all adverse effects

60
Q

why all adverse effects cannot be detected in trials

A
  • small # pts given drug
  • short time on drug
  • pt dont’ represent ALL individuals
61
Q

chemical name

A
  • description of drug using nomenclature of chemistry

* Ex: N-acetyl-para-aminophenol (acetaminophen)

62
Q

generic (non-proprietary) name

A
  • noncommercial name assigned to a drug by US adopted names
  • each drug has only ONE
  • syllables at end indicate class
  • Ex: acetaminophen
63
Q

trade (proprietary/brand) name

A
  • name under which drug is marketed
  • simpler than generic name
  • FDA approved
  • Ex: Tylenol
64
Q

problems with trade names

A
  1. ) single drug can have multiple trade names

2. ) same trade name may have different ingredients

65
Q

Over-the-counter drugs

A

•drugs that can be purchased w/o Rx

66
Q

1970 Controlled Substances Act

A
  • rules for manufacture and distribution of drugs with abuse potential
  • creation of drug “schedules”
  • directions for prescribing, dispensing, administering, and record keeping
67
Q

drug scheduling

A
  • classifies drugs with abuse potential
  • schedule 1 worst potential for abuse
  • schedule V very low potential for abuse
68
Q

objective of drug therapy

A

•provide maximum benefit w/ minimum harm

69
Q

what amendment was created secondary to the thalidomide tragedy?

A

•Harris-Kefauver Amendments
•sought to strengthen all aspects of drug regulation
•required that drugs be proved effective before marketing
•required that all drugs that had been introduced between 1932 and 1962 undergo testing for effectiveness; any drug that failed to prove useful would be withdrawn
•established rigorous procedures for testing
new drugs

70
Q

6 rights of medication administration

A
  1. right patient
  2. right drug
  3. right dose
  4. right route
  5. right time
  6. right documentation
71
Q

uncontrolled substances

A
  • Rx medication that requires monitoring by provider,but doesn’t pose risk of abuse/addiction
  • Ex: antibiotics
72
Q

controlled substances

A
  • Rx medications that have potential for abuse /dependence
  • scheduled drugs
  • schedule II-V approved
73
Q

nurses role in med admin

A
  • minimize adverse effects/interactions
  • make PRN decisions
  • manage adverse effects/toxicity
  • pt education
  • assess
  • knowledge
74
Q

medication contraindications

A
  • pt conditions that make it unsafe or potentially harmful to administer certain meds
  • Ex: allergies, dz, hx of rxn
75
Q

medication interactions

A
  • when given with another drug/food, medications have the potential to interact
  • can have increasing or decreasing therapeutic effects
  • agonist-antagonist- counteract
  • actions at separate receptor sites
  • same toxicities
76
Q

what happens if pt takes morphine and lorazepam (Ativan)

A
  • they can lead to respiratory distress

* one will increase the effect of the other (resp. depression)

77
Q

vitamin K and drug interactions

A

•decreases therapeutic effects of warfarin and puts pt at risk for clots

78
Q

grapefruit juice and drug interactions

A
  • inhibits med metabolism in small bowel, increasing amt of med available for absorption
  • puts pt at risk for increased therapeutic/adverse rxns
79
Q

tyramines and drug interactions

A
  • causes hypertensive crisis in pts taking MAOIs (antidepressant)
  • pt should avoid processed meat and cheese
80
Q

caffeine and drug interactions

A

•speeds everything up

81
Q

side effect

A
  • expected and inevitable effects when a medication is given
  • occur when medication given at therapeutic dose
  • discontinuation of med not ideal
82
Q

adverse effect

A
  • undesired, inadvertent, and unexpected dangerous effects of medication
  • side effects, toxicity, allergy, idiosyncratic (genetic), iatrogenic, physical, carcinogenic, teratogenic
  • influenced by age, illness, multiple drug therapy, genetics, route, etc
83
Q

iatrogenic adverse effect/rxn

A
  • disease produced by drugs
  • similar to idiopathic (naturally occurring) dzs
  • Ex: pt taking antipsychotic has sx similar to Parkinson’s
84
Q

physical dependence

A

•body has adapted to drug exposure in such way that an abstinence syndrome will result if drug discontinued

85
Q

QT drug

A
  • interval drugs
  • have the ability to prolong the QT interval (time required for ventricles to repolarize)
  • can lead to torsades pointes- fatal ventricular fibrillation
86
Q

Pharmacogenomics

A
  • genetic makeup of individual in relation to drug responses
  • alterations in drug metabolism
  • alteration in drug receptors/targets
  • alteration in immune response/hypersensitivity
87
Q

pharmacodynamic tolerance

A
  • reduced responsiveness to med administered over time

* Ex: morphine

88
Q

metabolic tolerance

A

•metabolism of med increases over time and effectiveness is reduced

89
Q

cross-tolerance

A

•pt demonstrates tolerance to drug with chemically similar composition to another drug that is already tolerated

90
Q

accumulation

A
  • med concentration in body increased by the inability to metabolize or excrete it rapidly enough
  • results in toxic med effect
  • decreased renal fxn key player in med accumulation
91
Q

placebo effect

A

•positive medication effects influenced by psychological factors

92
Q

medication errors

A
  • mistake involving 6 rights
  • Overdose/Underdose
  • Extra dose/Omitted dose
  • Wrong dosage form
  • Wrong diluent
  • Wrong strength/concentration
  • Wrong infusion rate
  • Wrong technique (includes inappropriate crushing of tablets)
  • Deteriorated drug error (dispensing a drug after its expiration date)
  • Wrong duration
93
Q

reporting medication errors

A
  • via Medication Errors Reporting (MER) program

* objective not to blame, but to improve safety

94
Q

medication reconciliation

A
  • process of comparing list of all meds that pt is currently taking with list of new meds about to be provided
  • conducted whenever pt undergoes transition in care (admission, discharge, step down, etc)
95
Q

pregnancy and pharmacokinetics

A
  • physiologic changes in kidney, liver, and GI tract
  • increased GFR (increase dosage)
  • hepatic metabolism of some drugs increases (increase dosage)
  • bowel tone/motility decrease means longer time for absorption (reduce dosage)
96
Q

teratogenesis

A
  • congenital malformations and dysfunctions produced in embryo or fetus as a result of harmful drug exposure
  • birth defects including cleft palate, clubbed foot, hydrocephalus, neurobehavioral, and metabolic
97
Q

assessing teratogenic potential

A
  • stage of pregnancy and amount of drug administered
  • first trimester -> gross malformation
  • second/third trimester -> fxn abnormalities
98
Q

category A-D drugs

A

•category A pose little to no risk for fetus
•category D pose fetal risk
*drugs should only be used if benefits outweigh risks

99
Q

category X drugs

A
  • positive evidence of human fetal risk

* the risks involved in use of the drug in pregnant women clearly outweigh potential benefits

100
Q

category N drugs

A

•not classified by FDA

101
Q

lactation and medication

A
  • most meds secreted in breast milk, so must exercise caution when taking meds that are harmful to infants
  • most at risk drugs are those w/ extended half life
  • “safe” drugs should be taken immediately after breastfeeding to minimize concentration exposed to infant
102
Q

pediatric dosages

A
  • based on body weight or body surface area
  • some based on age due to risks of growth/development
  • great individual variation
  • high risk for adverse rxn
103
Q

neonate/infant increased sensitivity to drugs

A

•immature liver, kidney, gastric, and BBB
•due to immature pharmacokinetic processes:
-absorption
-renal excretion
-hepatic metabolism
-BBB
-protein binding

104
Q

how to determine pediatric dosage

A

(BSA x adult dose)/ 1.73 m²

105
Q

pharmacokinetics in children 1 y/o and older

A
  • drug sensitivity similar to that of adults

* metabolize drugs faster than adults (may require higher dose or less time b/t)

106
Q

drug therapy in geriatrics

A
  • more adverse drug rxns
  • mor drug-drug interactions
  • more sensitive b/c of altered pharmacokinetics
107
Q

Beer’s list

A

•list of drugs to avoid in older adults

  1. NSAIDS
  2. digoxin
  3. certain diabetes drugs
  4. muscle relaxants
  5. anxiety/sleeping pills
  6. demerol
  7. certain OTCs
  8. antipsychotics
  9. estrogen
  10. anti-cholinergic
108
Q

polypharmacy

A
  • taking several medications simultaneously (Rx and/or OTC)

* if done with diminished bodily fxns toxicity can occur

109
Q

type 1 diabetes

A
  • insulin-dependent

* pancreatic beta cells destroyed and insulin synthesis/release impaired

110
Q

type 2 diabetes

A
  • non-insulin dependent

* insulin resistance and impaired insulin secretion

111
Q

ketoacidosis (DKA)

A
  • cells w/o enough glucose burn fat and produce ketones
  • can develop w/ hyperglycemia if not enough insulin to bring glucose to cells
  • occurs w/ hypoglycemia if not enough glucose for cells
  • rare in type 2
112
Q

hyperosmolar hyperglycemic nonketotic syndrome (HHNS)

A
  • type 1 or 2 (more in 2)
  • blood sugars rise and body tries to get rid of excess sugar thru urine
  • urinate a lot first, then become concentrated
  • leads to dehydration, seizures, and coma
113
Q

gestational diabetes

A

•diabetes that appears during preggo and subsides rapidly after delivery

114
Q

hypothyroidism

A
  • deficiency in thyroid hormone
  • severe: myxedema
  • infants: cretinism
  • slow mind/body, reflexes, HR
  • hair thin
  • cold, dry skin
115
Q

hyperthyroidism

A
  • excessive thyroid hormone secretion
  • Graves dz or toxic nodular goiter dz
  • fine hair
  • finger clubbing
  • tremors
  • flushing/tachy
  • edema
  • bulging eyes
  • warm, moist skin

Pharmacology I (9 decks)

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