Exam 1 Pharm Flashcards

1
Q

Pharmacology

A

the study of the biological effect of drugs (chemicals) that are introduced into the body to create some sort of change

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2
Q

Pharmacokinetics

A

what happens to drugs in the body

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3
Q

Pharmacodynamics

A

mechanism of action; effects on the body

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4
Q

Chemical Name

A

long and complex name used in research

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5
Q

Generic Name

A

official name of the drug; lowercased
NEED TO KNOW FOR ALL MEDS

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6
Q

Trade Name

A

brand name that is given by the pharmaceutical company; upper cased

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7
Q

prototype

A

Typically the first drug of the group that is created that represents the whole group (class) of medication. New drugs in the class are compared to this one in effectiveness and side effects. i.e. Advil/ibuprofen represents that NSAID class and other manufacturers’ (kroger, walgreens, etc) version gets compared with the original.

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8
Q

Therapeutic Effects

A

Intended effects i.e. Tylenol given for fevers and pain

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9
Q

Side Effects

A

Unintended effects that are unavoidable i.e. Tylenol may cause upset stomach
NEED TO KNOW MOST COMMON FOR ALL MEDS

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10
Q

Toxicities

A

Harmful effects related to levels of drugs in the system

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11
Q

Adverse Effects

A

Unexpected, dangerous reaction
NEED TO KNOW MOST COMMON FOR ALL MEDS

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12
Q

Allergic Reaction

A

unexpected, sometimes dangerous immune system response

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13
Q

Classification

A

describes a group of medications that work similarly (usually based on MOA, physiologic effect or chemical structure) i.e. beta blockers, ACE inhibitors
NEED TO KNOW FOR ALL MEDS

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14
Q

Mechanism of Action

A

How the drug works in the body
NEED TO KNOW FOR ALL MEDS

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15
Q

Indications

A

Why are we giving this medication
NEED TO KNOW FOR ALL MEDS

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16
Q

Contraindications

A

reason people should not take this med i.e. liver failure pts should not take acetaminophen
NEED TO KNOW FOR ALL MEDS

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17
Q

Nursing Consideration

A

What does the nurse need to know about this med: contraindications, assessments to perform prior to admin, serious interactions with other drugs, CYP
NEED TO KNOW FOR ALL MEDS

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18
Q

How do new drugs get approved?

A

FDA approves meds; meds must undergo very strict clinical tests at different thresholds

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19
Q

Preclinical Trial

A

medication tested on lab animals for therapeutic and adverse effects

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20
Q

Phase I Studies

A

drug tested on healthy human volunteers to make sure it doesn’t hurt people

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21
Q

Phase II Studies

A

drug tested on patients who have the disease the drug is designed to treat

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22
Q

Phase III Studies

A

drug used in a vast clinical market; prescribers are informed of adverse effects and things to monitor for in their patients. If unexpected responses occur the drug may be taken off the market

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23
Q

Phase IV Studies

A

continued evaluation (post market); if severe reactions occur this may result in a blackbox warning

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24
Q

Controlled Substances

A

drugs that have potential for abuse

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25
Q

1970 Controlled substances act

A

government started regulating manufacturing and distribution of drugs that have potential for abuse; given a rating of schedule I-V

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26
Q

Schedule I

A

no approved for medical use, no therapeutic effect i.e. heroin, LSD

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27
Q

Schedule II

A
  • used medically but high potential for abuse
  • NARCOTICS (opioids) and amphetamines i.e. hydromorphone (Dilaudid), oxycodone
  • NO AUTOMATIC REFILLS
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28
Q

Schedule III

A

-potential for abuse but less so then schedule II
-non barbiturate sedatives, non amphetamines, stimulants i.e. Lortab, Vicodin

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29
Q

Schedule IV

A

-some potential for abuse
-sedatives, anti-anxiety i.e. Xanax, valium, Ambien

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30
Q

Schedule V

A

-medications with small amounts of narcotics or stimulants
-usually antitussives i.e. codeine, ephedrine

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31
Q

OTC Drugs

A

-consumer must be able to dx own condition and monitor effectiveness EASILY
-low risk for SE and abuse potential
-some meds only available behind the counter due to abuse potential i.e. sudafed (meth), narcan

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32
Q

Dietary Supplement Health Education Safety Act

A

-can only claim affect on BODY STRUCTURE or FUNCTION (not medical condition)
-i.e. St. John’s Wort affects emotional balance (not treat depression)
-est. purity standards also

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33
Q

Why do dietary/herbals matter?

A

-herbals can increase toxicity of prescription meds or decrease therapeutic effects i.e. ginkgo biloba suppresses platelet aggregation so inc. RF bleeding in pts on anti platelets or anti coags
-always ask specifically about other medications, supplements, OTC, herbals, vitamins etc.

34
Q

Teratogens

A

substances that can cause congenital malformations in developing fetus
-think alcohol, marijuana, and nicotine

35
Q

Category A

A

safe for fetus

36
Q

Category B

A

lack of studies to show benefit/risk to fetus; typically safe

37
Q

Category C

A

No studies, animals studies show possible risk - speak with OB

38
Q

Category D

A

have shown possible risk to the fetus; must show major benefits to mom - discuss risk/benefits with OB

39
Q

Category X

A

KNOWN RISK - cannot be outweighed by benefit i.e. thalidomide, chemo, isotretinoin/retin A (accutane)
- usually have to be b.c. to take

40
Q

Pharmacogenomics

A

the study of how genes affect a person’s response to drugs
- used to developed safe, effective medications with doses tailored to a person’s genetic makeup
- this gp will respond, this gp will have bad SE, this gp will be non responders bc of their genetics

41
Q

What are the 3 stages of drug action?

A

1 - pharmaceutic
2 - pharmacokinetic
3 - pharmacodynamic

41
Q

Pharmaceutic Phase (1)

A

disintegration then dissolution of the drug so it can be absorbed and used (just oral meds)

tablet - granules - smaller particles - total dissolution in GI tract

42
Q

Pharmacokinetic Phase (2)

A

what the body does to the drug
4 parts - absorption (small intestine absorbs into blood, FIRST PASS), distribution (leaves the blood across the cell membrane to the site of action where it will exert its effect) THIS IS WHERE PARENTERAL MEDS START, metabolism/biotransformation (broken down by the liver from active lipid soluble drug to water soluble metabolite to allow kidneys to excrete), excretion (mostly kidneys, sometimes by liver through bile)

43
Q

Pharmacodynamic Phase (3)

A

what the drug does to the body (MOA) to create intended effect, therapeutic action (also sometimes results in undesired effects - SE)
- drug may increase, decrease, replace, inhibit, destroy, protect or irritate to CREATE A RESPONSE

44
Q

First Pass Effect

A

metabolism of drug in the liver before systemic circulation
- affects bioavailability of PO MEDS
- bioavailability of IV is 100%

45
Q

What are the 3 routes of absorption?

A

enteral, parenteral, transdermal

46
Q

Enteral Absorption

A

GI tract (oral/gastric mucosa, small intestine, rectum)
- EC: small intestine (first pass effect)
- PO: break down in stomach, small int. abs. (first pass effect)
- SL, buccal, rectal: onsite absorption d/t highly vascularized NO FIRST PASS

47
Q

Parenteral Absorption

A

SQ, IM, IV, intrathecal (spinal canal), epidural (space around the spinal cord)
- IV is fastest
- NO FIRST PASS

48
Q

Transdermal Absorption

A

absorption of meds through application to body surfaces
- eyes, skin, ears, nose, lungs
- slower onset, prolonged interaction
- localized

49
Q

What is the major site of excretion of drugs and how does it work?

A

Kidney
- some of the drug is secreted and some is reabsorbed through renal tubules
- i.e. PCN G 90% is excreted so very little reabs. = drug need to be given more frequently to maintain steady state in the body

50
Q

What factors affect distribution?

A
  • CIRCULATION (decreased blood = decreased distribution)
  • PVD (think infection in feet)
  • Abscess (swelling and exudate decreases blood flow to the site)
  • Tumors
  • BLOOD BRAIN BARRIER = cells in the capillary wall in the brain with very tight junctions that prevent drug passage
  • drugs must have a transport system or be VERY lipid-soluble to cross BBB i.e. glucose, alcohol
  • blood brain barrier not fully developed in infants
  • PROTEIN BINDING EFFECT = temporary storage of drug molecule that allows drug to be available for a longer period of time; given in ratio of bound to unbound drug
  • only the unbound drug is available to exert an effect
  • goal is to maintain a steady state of free drug
  • amount of available albumin affects amount of free drug, dec. albumin = inc. risk for toxicity, think malnutrition and liver disease
  • i.e. warfarin/Coumadin is very protein bound (97-99%), leaves 1-3% to exert effect
  • if a person is taking two highly protein bound drugs, then they will compete for available protein and result with both medications having more free med in the body
51
Q

What affects drug metabolism?

A
  • impaired liver function = drug toxicity
  • drugs taken concurrently that use same isoenzyme for metabolism
52
Q

How are drugs metabolized in the liver?

A

Cytochrome P450, a group of isoenzymes that metabolize drugs
- about 1/2 of drugs use this system
- drug-drug interactions can occur when drugs that use the same isoenzyme are taken concurrently

53
Q

CYP450 Substrate

A

drug is using CYP450 for metabolism to concert to active form

54
Q

CYP450 Inducer

A

increases the breakdown and elimination of the drug resulting in less amount of drug in the body and less therapeutic effect

55
Q

CYP450 Inhibitor

A

decrease the breakdown and elimination of the drug, resulting in more drop in the body and increased risk for toxicity
- grapefruit juice is an inhibitor, it will stop breakdown of medication and lead to toxicity
- don’t take meds with grapefruit juice and don’t drink it for 2-4 hours after taking meds

56
Q

Serum half-life ( T 1/2)

A

time required for the serum concentration of a drug to decrease by 50%
- takes 5 half-lives for 97% to be eliminated
- informs how often the drug needs to be given
- a 1/2 life of a week = 5 wks for drug to be 97% eliminated
- goal = “steady state” which essentially means dosing that results in medication being taken in at the same rate at metabolism/excretion

57
Q

What affects drug excretion?

A
  • kidney disease or dysfunction = drugs build up and can cause toxicity
    MONITOR : BUN, creat, GFR (best measure of kidney function)
58
Q

What is GFR?

A

glomerular filtration rate
- best measure of kidney function
- calc. from creat, age, body size, age, gender
- r/t to free drug concentration in the plasma because if drug is not getting excreted from the kidneys it is building up in the blood (think toxicity)

59
Q

What is a “steady state”?

A

intake of drug = amount metabolized/excreted
- takes about 4-5 half-lives for “steady state” to occur if the patient is taking the medication
- goal is to get to a steady state think b/p meds, ATB

60
Q

What is “around the clock dosing (ATC)”?

A

maintain 50% concentration in the body
-used to treat chronic pain
i.e. morphine 10mg q 3 hr - after about 4 doses would be a “steady state” of 5 mg at all times

61
Q

What factors affects pharmacodynamics?

A

receptors = proteins located on cell surfaces that interact with drugs to produce effects, i.e. hormones, neurotransmitters
chemicals BIND with the drug = drug-receptor complex, which initiates a physiochemical rxn: agonist or antagonist

62
Q

Drug Onset

A

time it takes for drug to elicit therapeutic response (latent period)

63
Q

Drug Peak

A

time it takes for drug to reach max therapeutic effect

64
Q

Drug Duration

A

time drug concentration is sufficient to elicit therapeutic effect

65
Q

Agonist (Receptor Theory of Drug Action)

A

a drug that has the ability to stimulate/activate a desired therapeutic effect by binding to a receptor

66
Q

Antagonist (Receptor Theory of Drug Action)

A

drug that inhibits/blocks other natural substances (ligands) from binding and causing a response

67
Q

Receptor-Less Activation

A

drug acts through simple physical or chemical interactions with small molecules

68
Q

Therapeutic index

A

measure of relative safety of a drug

69
Q

Narrow Therapeutic Index (NTI)

A

ratio of a drug’s toxic level to level at which it provides therapeutic effect
- therapeutic levels checked regularly to avoid toxicity i.e. theophyllin, dig, phenobarbital, lithium, coumadin

70
Q

High Alert Meds

A

drugs most likely to cause serious harm or death
- insulin
- heparin
- opioids
- injectable KCL
- neuromuscular blocking agents
- chemo
Usually require a cosignature when administering

70
Q

Black Box Warning

A
  • required by the FDA for drugs that are especially dangerous
  • the strongest safety warning a drug can carry and remain on the market
    -black box warning must appear prominently (package insert, product label, magazine page, commercial) BUT many ppl don’t read these - SO NEED TO EDUCATE THE PATIENT
71
Q

What are processes to prevent drug errors?

A

Tall man lettering, computerized systems for med admin (barcode scanning), pt info readily accessible, standardizing and simplifying, reminders, include patient in the therapy, use leading zeros, don’t use training zeros, restrict high-alert drugs

72
Q

Types of drug interactions

A

Drug-drug, drug-food, drug-herb, drug-disease (think liver)

73
Q

What can be done to minimize drug interactions

A

Minimize # of drugs patient receives, thorough drug hx, be extra vigilant in monitoring when pts are on drugs with narrow therapeutic index

74
Q

Additive effects

A

2 drugs taken with similar MOA

75
Q

Synergism/Potentiation

A

2 drugs with DIFFERENT MOA but result in a combined drug effect greater than that of either drug alone I.e. Coumadin and ASA

76
Q

Activation

A

Decreases metabolism rate of the drug (CYP450 system)

77
Q

Displacement

A

Displacement of one drug from plasma protein binding sites by a second drug thereby increasing effect of displaced drug

78
Q

Antidote

A

Drug given to ANTAGONIZE the toxic effects of another drug

79
Q

What are drug interactions that decrease therapeutic effects?

A

Antidote
Decreased Intestinal Absorption (think PO meds and small intestine resection)
Activation of drug metabolizing enzymes increases rate of drug metabolism and gets out of system sooner

80
Q

Older Adults and Pharmacokinetic Consequences

A

Hepatic changes (drugs metabolized more slowly), GI changes (decreased absorption of PO drugs), cardiac and circulatory changes (decreased distribution of drugs), renal changes (drugs excreted less completed)