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exam 1 Flashcards

1
Q

sources of medication

A
  • plants
  • animals
  • minerals
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2
Q

medications made in labs

A

they are more standardized and consistent, they include synthetic, semi-synthetic, and biotechnology

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3
Q

drugs are classified according to

A
  • effect on body system (cardiac, CNS, GI)
  • therapuetic use (antiemetics, antihypertensives, antidepressants)
  • chemical characteristics (adrenergic, benzodiazepine)
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4
Q

medication may fit into more than one category… example

A

morphine is a CNS depressant, narcotic pain reliever, and an opiod

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5
Q

prototypes

A

the first drug developed in a class of category

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6
Q

examples of prototypes

A

morphine and penicillin

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7
Q

patent of new drugs

A

the manufacturer decide the trade name and no other company can use that name until the patent expires

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8
Q

expiration of the patent

A

other companies may produce the drug under a different trade name but with the same chemical makeup

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9
Q

generic name reflects

A

chemical makeup/composition

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10
Q

trade names/ brand names are usually

A
  • more expensive
  • uppercase letters (Tylenol)
  • may have a copay
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11
Q

generic names are usually

A
  • less expensive
  • lowercase letters (acetaminophen)
  • usually covered by health insurance
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12
Q

prescription

A

written by a HCP

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13
Q

OTC

A

does not require prescription

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14
Q

food and drug and cosmetic act (FDA)

A
  • regulates the manufacturing, distribution, advertising and labeling of official USP drugs
  • require companies to meet standards of purity and strength determined by analysis
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15
Q

controlled substance act

A
  • regulates manufacturing and distribution of narcotics, stimulants, depressants, hallucinogens, and anabolic steroids
  • requires pharmaceutical industry to maintain physical security ands strict record keepin
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16
Q

drug enforcement agency (DEA)

A
  • enforces CSA
  • secures storage and accurate records to drugs
  • prescribers have a DEA# that is associated with all prescribed controlled substances
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17
Q

nurse’s role with controlled substances

A
  • keep them locked
  • admin only to pt’s with valid order/prescription
  • maintain accurate record of each dose given in narcotic record and medication admin record
  • keep accurate inventory and report discrepancies
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18
Q

drug schedule classifies drugs based on

A
  • abuse potential
  • accepted medical applications in US
  • safety and potential for addiction
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19
Q

schedule I

A
  • drug has high potential for abuse
  • not currently accepted for medical use
  • lack of safety under medical supervision
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20
Q

example of schedule I drugs

A

heroin, LSD, marijuana, ecstasy, metaqualone

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21
Q

schedule II/IIN

A
  • substances have high potential for abuse
  • accepted medical use in US or use with severe restrictions
  • abuse of drug may lead to psycholigical and physical independence
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22
Q

schedule II/IIN examples

A

hydromorphone (dilaudid), methadone (dolophine), meperidine (Demerol), oxycodone (OxyContin, Percocet), fentanyl, morphine, opium, codeine, hydrocodone

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23
Q

IIN

A
  • amphetamine (adderall)
  • methamphetamin (Desoxyn)
  • methylphenidate (ritalin)
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24
Q

schedule III

A
  • potential for abuse less than drugs in schedules I and II
  • substance is accepted for medical use
  • abuse may lead to moderate to low potential for physical dependence but high psychological dependence
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25
Q

schedule III examples

A

> 90mg of codeine/dosage unit (tylenol w/ codeine), buprenorphine (suboxone)

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26
Q

schedule IV

A
  • low potential for abuse and low risk of dependence
  • currently accepted in medical use
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27
Q

schedule IV examples

A
  • alprazolam (xanax), carisoprodol (soma), clonazepam (klonopin), diazepam (Valium), lorazepam (ativan), midazolam (Versed)
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28
Q

schedule V

A
  • low potential for abuse
  • accepted for medical use
  • limited quantity of narcoticcs
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29
Q

schedule V examples

A
  • cough preparations containing no more than 200mg of codeine/100mL or 100 grams (robitussin AC with codeine
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30
Q

medication rights

A

right…
- person
- route
- med
- time
- indication
- documentation

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31
Q

principles of drug administration

A
  • drug rights
  • drug information including use, adverse effects, contraindications, therpuetic effects, drug specifics
  • order accuracy
  • read back
  • right concentration
  • abbreviations
  • dose calc
  • dose measurement
  • technique
  • correlation to pt diagnosis
  • triple pt verification
  • omit delay of dose
  • high risk pt’s
  • report ADEs
  • knowledge and skills
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32
Q

legal responsibilities of nurse

A
  • lisenced under NPA to administer meds by HCP, NP, PAs, and dentists
  • safe and accurate med administration
  • recognizing and questioning errors
  • regusing to admin unsafe meds
  • delegating in compliance with law
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33
Q

harm

A

impairment of physical, emotional, or psychological function or structure of body and/or pain resulting therefrom

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34
Q

monitoring

A

to observe or record relevant physiological or psychological signs

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35
Q

intervention

A

change in therapy or active medical/surgical treatment

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36
Q

intervention neccessary to sustain life

A

cardiovascular and respiratory support

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37
Q

category A

A

events that have capacity to cause error

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38
Q

category C

A

error that reached the pt but didn’t cause harm

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39
Q

category E

A

error that contributed to harm and required intervention

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40
Q

category G

A

error that contributed to permanent pt harm

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41
Q

category I

A

error that contributed to pt death

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42
Q

orders must include

A
  • pt full name
  • name of medication
  • dose
  • route
  • frequency
  • date
  • time
  • HCP signature
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43
Q

verbal and telephone orders have to be

A

signed by HCP and transcriber

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44
Q

prevention of med errors

A
  • CPOE
  • bar coding
  • limiting use of abbreviations
  • med reconciliation
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45
Q

controlled release

A
  • enteric coated to prevent stomach upset
  • maintains more consistent serum drug levels
  • allows less frequent admin
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46
Q

tablets/capsules

A
  • contain high amount of drug
  • intended to be absorbed slowly over long period of time
  • should NOT be broken, open, crushed, or chewed
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47
Q

med delivery systems

A
  • tablets
  • controlled release
  • systemic absorption through skin (fentanyl path, nitroglycerin)
  • external or implanted (insulin, opioids, anticancer)
  • solutions
  • creams
  • suppositories
  • local treatment
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48
Q

herbal and dietary supplement concerns

A
  • can affect absorption, metabolism, and distribution
  • unknown active ingredients
  • may prevent person from seeking HCP
  • can cause interactions
  • lack of evidence
  • lack of transparency to provider
  • nurses need adequate knowledge
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49
Q

pharmaco

A

study of drugs

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50
Q

kinetics

A

movement through the body

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51
Q

pharmacokinetics

A

the study of how drugs move throughout the body

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52
Q

pharmachodynamics

A

how do drugs get into body cells?
what impact do the cells have?
what drug does to the body?

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53
Q

drug transport through cell membranes

A
  • lipid soluble drugs dissolve in the lipid layer of the cell membrane and diffuse into or out of the cell
  • gated channels regulate the movement of ions
  • carrier proteins attach to drug molecules and move them across cell membranes
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54
Q

steps of pharmacokinetics

A
  1. absorption
  2. distribution
  3. metabolism
  4. excretion
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55
Q

absorption

A
  • oral drug is swallowed and enters stomach
  • drug moves into small intestine
  • drug crosses cell membranes into the bloodstream
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56
Q

what slow or speeds absorption

A
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57
Q

oral is the

A

slowest route of entry

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58
Q

inhalation is a

A

fast route to the brain

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59
Q

injections take effect

A

within seconds

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60
Q

transdermal

A

released into bloodstream over several hours

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61
Q

intramuscular

A

epipens or vaccines

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62
Q

bioavailability

A
  • drugs taken orally are broken down by liver during the first pass
  • some of the dose becomes inactive (made water soluble for excretion)
  • only some of the drug is distributed to the rest of the body in unchanged form (BIOAVAILABLE)
  • IF a drug has a high first pass effect… it has low bioavailability if given orally
  • IV drugs are 100% bioavailable (it bypasses the intestine/liver)
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63
Q

protein binding

A

plasma proteins (mainly albumin) act as carriers for drug molecules within the blood stream so when they bind the drugs stay inactive but the free molecules are able to leave the blood stream and act on the body’s cells

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64
Q

metabolism

A

cytochrome P450 (CYP) enzymes in liver metabolize most drugs
CYP1,2 and 3 metabolize drugs

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65
Q

genetic variability in CYP enzymes result in

A

variable pt responses to drugs even when given at same dose

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66
Q

cyp450 enzyme inducers

A

phenytoin, carbamazepine, rifampin, alcohol (chronic), barbiturates, st john’s wort

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67
Q

chronic admin of CYP450 inducers cause

A

larger amounts of enzymes which speeds up metabolism causing an increased dose for the drug to have therapuetic effects, it also impacts other drugs that CYP450 metabolize

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68
Q

CYP450 inhibitors

A
  • grapefruit, protease inhibitors, azole antifungals, cimitedine, macrolides (except azithromycin), amiodarone, non-DHP CCBs (diltiazem, verapamil)
  • compete for enzymes
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69
Q

excretion involves

A

the kidneys, feces, liver, and other parts of the body like lungs or sweat

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70
Q

minimum effective concentration

A

refers to the minimum amount of a drug needed to reach impact on the patient

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71
Q

therapuetic concentration

A

where the drug takes effect

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72
Q

toxic concentration

A

high dose of drug within the blood

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73
Q

drug half life

A

time for concentration of a drug to be reduced by 50% (determined by metabolism and excretion)

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74
Q

agonist drug simple terms

A

attaches to a receptor site and enhances cellular activity

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75
Q

antagonist drug in simple terms

A

attaches to a receptor site and blocks cellular activity

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76
Q

receptor theory of drug action: drugs chemically bind with receptor sites causing

A
  • activation, inactivation, or alteration of intracellular enzymes
  • changes in the permeability of cell membranes to one or more ions (e.g., Na+, Ca+)
  • modification of the synthesis, release or inactivation of neurohormone
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77
Q

agonist

A

drugs that produce effects similar to naturally occuring neurotransmitters and hormones
accelerates or slows normal cell process

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78
Q

antagonist

A

blocks a response by occupying receptor sites

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79
Q

non receptor drugs

A
  • antacids
  • osmotic diuretics
  • anticancer drugs
  • metal chelating agents
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80
Q

variables impacting drug action

A
  • dose
  • route
  • drug-diet
  • drug-drug
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81
Q

individual variables impacting drug actions

A
  • age, body comp
  • pharmacogenomics (genetics, ethnicity, sex)
  • preexisting conditions
  • psychological considerations
  • tolerance and cross-tolerance
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82
Q

peak drug level

A

highest plasma concentration of drug at a specific time, indicates the rate of absorption

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83
Q

when should peak blood level be drawn

A

at proposed peak time according to route of admin

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84
Q

through drug level

A

lowest plasma concentration of a drug, measures the rate at which the drug is eliminated

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85
Q

when are trough drug levels drawn

A

immediately before the next dose of a drug is given regardless of route of administration

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86
Q

adverse effects of drugs

A
  • any undesired responses to medication administration
  • all drugs can produce adverse effects
  • can occur with usual therapuetic dosing
  • more likely to occur or be more severe with high dosing or IV dosing
  • especially likely to occur with high alert drugs and in neonates, infants or older adults or in people who take multiple drugs (polypharmacy)
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87
Q

black box warnings

A

FDAs warning about serious side effects of a drug

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88
Q

interactions that increase therapeutic or adverse drug effects

A
  • additive effects or synergism
  • interference with metabolism
  • displacement
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89
Q

interactions that decrease drug effects

A
  • antidote medication (antagonizes toxic effect of another drug)
  • decreased intestinal absorption of drugs
  • increased metabolism rate of drugs
  • compete for same receptors
  • drug and diet (warfarin and vitamin K)
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90
Q

toxicology: drug overdose

A
  • results from excess amounts of medication
  • may damage body tissues
  • may result from single large dose or prolonged ingestion of smaller doses
  • may involve alcohol, prescription, OTC, or illicit drugs
  • can be a medical emergency
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91
Q

main goals of treatment for a drug overdose

A
  • starting treatment soon after ingestion
  • supporting and stabilizing vital function
  • role of posion control
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92
Q

prevent further damage of drug overdose by

A
  • reducing absorption
  • increasing elimination
  • administering antidotes whenever possible (ex. activated charcoal)
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93
Q

antidote to acetaminphen

A

acetylcystine

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94
Q

antidote to calcium channel blockers

A

calcium gluconate

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95
Q

antidote to heparin

A

protamine sulfate

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96
Q

antidote to warfarin

A

vitamin K

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97
Q

antidote to opioids

A

naloxone

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98
Q

antidote to beta blockers

A

glucagon

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99
Q

inflammation

A
  • triggered by cell or tissue damage or dead cells/noxious stimuli like bacteria
  • vascular stage and cellular stage inducing clotting, swelling, pain, s/s of inflammation
  • inflammatory mediators released at same time (histamines, cytokines, bradykinin, complement, etc.)
  • leukocytes (wbc>10), C reactive protein, ESR increases
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100
Q

vascular stage of inflammation

A

vasodilation bringing blood to the site causing redness, swelling, heat, pain, loss of function, and clotting

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101
Q

cellular stage of inflammation

A

leukocytes move to area of injury into tissue and engulf bacteria/cellular debris during phagocytosis, products are exudates (swelling, pain)

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102
Q

stages of inflammation

A
  1. histamine and prostaglandins are released
  2. capillaries dilate and clotting begins
  3. chemotactic facotrs attract phagocytic cells
  4. phagocytes consume pathogen and cell debris
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103
Q

histamine

A
  • highly concentrated in mast cells, basophils, platelets
  • cause vasodilation
  • increases capillary and venule permeability - stimulates nerve endings to cause pain
  • stimulates movement of eosinophils into injured tissue
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104
Q

bradykinin

A
  • becomes activated with tissue injury
  • WBCs ingest damaged cell in injured tissue and release enzymes that ACTIVATE kinins
  • activated kinins prolong the vasodilation and vascular permeability cause by histamines (erythema, heat, pain)
  • stimulate pain in nerve endings
  • increase mucous secretion
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105
Q

complement

A

group of plasma proteins that destroy cell membranes of pathogens causing
- vasodilation
- vascular permeability
- promoting movement of WBCs into area (chemotaxis)

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106
Q

cytokines

A
  • interferons and intterleukins
  • act locally and systemically
  • chemotaxis of WBCs
  • inflammatory response
  • fever
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107
Q

prostaglandins

A
  • found in most body tissue
  • if a cell is injured, arachidonic acid is produced differentiating into COX-1 and 2 enzymes
  • COX1 enzymes are prostaglandins that protect GI tract, platelets, kidneys and smooth muscle
  • COX2 enzymes are prostaglandins that increase inflammation (vasodilation, edema, fever, pain)
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108
Q

why treat inflammation if it is productive

A
  • can be too much
  • can damage nearby healthy tissue
  • goal is to minimize damage to nearby tissue and promote rapid healing
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109
Q

osteoarthritis

A
  • degradation of articular cartilage, bone, and synovium
  • primary osteoarthritis - no hx injury
  • secondary osteoarthritis - due to previous injury or inflammatory condition
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110
Q

clinical manifestations of osteoarthritis

A
  • pain
  • stiffness (early morning - decreases with activity)
  • joint instability
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111
Q

pathophysiology of rheumatoid arthritis

A
  • inflammation of synovium causing swelling and joint damage
  • endothelium activates chemotactic factors and attract leukocytes ot joint spaces causing an exaggerated immune response in genetically susceptible hosts
  • antibody-antigen complexes form, activate complement, T cells and an unregulated immune response
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112
Q

nurses role in drug therapy

A
  • know why the drug is being given and mechanism of action
  • know contraindications, cautions, and interactions
  • know nursing implications and actions (admin right dose, evaluate outcomes, monitor for adverse effects, provide education to enhance self and family care using teachback)
113
Q

drugs used for pain, fever, and inflammation

A

acetaminophen
aspirin
nsaids

114
Q

salicylates

A

acetylsalycilic acid (ASA)
salsalate

115
Q

example of slicylates

A

asprin

116
Q

asprin mechanism of action

A
  • acts both centrally and peripherally to block transmission of pain impulses
  • reduces fever by acting on the hypothalamus
  • diminishes inflammation (OA, RA)
  • low doses suppress platelet aggregation
  • pregnany persons are at risk for preeclampsia
  • low dose indicated to manage ischemic stroke, transient ischemic attack, angina, and acute MI
  • overall inhibits prostaglandin synthesis
117
Q

contraindication of asprin

A
  • low dose aspirin (75-81mg up to 325 mg) is given to reduce risk of MI, TIA, and stroke in patients with prior MI or TIA
  • non-enteric coated tablet 160 mg - 325 mg chewed or crushed as soon as acute MI is suspected
  • antipyretic; ADULTS ONLY
  • children and adolescents should not take this med with reye’s syndrome or an allergy to tartrazine (cross-allergy)
  • high potential for toxicity in older adults; monitor for bruising and bleedin
  • epigastric distress, GI s/s common, increased risk of GI bleed/ulcer
118
Q

signs of salicylate overdose/poisoning

A
  • tinnitus/difficulty hearing
  • headache, confusion, drowsiness, vertigo, sweating
  • early: respiratory alkalosis due to hyperventialation
  • later: respiratory depression and acidosis
  • fluid and electrolyte imablance
  • nausea vomiting fever
119
Q

acetaminophen class

A

nonnarcotic analgesic and an antipyretic

120
Q

acetaminophen

A
  • does not cause n/v, or GI bleed
  • doesn’t interfere with clotting
  • equal to ASA in analgesic and antipyretic effects (lacks anti-inflammatory activity)
  • metabolized in liver; small amount reamins in body as toxic metabolite (inactivated by glutathione except in larger doses)
  • acute or chronic overdose can result in liver damage or fatal liver necrosis
  • usual therapuetic doses may cause/increase liver damage in those who abuse alcohol
  • available in tablet, liquid, and rectal suppositories, IV
121
Q

trade name of acetaminophen

A

tylenol

122
Q

use of acetaminophen

A

mild pain and/or fever

123
Q

acetaminophen mechanism of action

A
  • may relieve fever through central action in the hypothalamic heat-regulating center
  • may inhibit pain sensitizers at pain receptors in the periphery
124
Q

contraindications to acetaminophen

A
  • liver failure
  • use of other OTCs containing acetaminophen
125
Q

caution with acetaminophen

A
  • liver disease
  • G6PD deficiency
  • chronic malnutrition
  • long-term alcoholuse
  • severe hypovolemia
  • severe renal impairment
126
Q

maximum dose of acetaminophen

A

4000 mg/24 hrs

127
Q

adults and children >12 dosage of acetaminophen

A

325mg - 650 mg orally q4-6hrs
may give without food

128
Q

special considerations for admin of acetaminophen

A
  • children <12 dosed on BW
  • adults with GFR 10-50mL/min need less frequent dosing
  • do not crush extended release forms
  • use liquid for children or those with hard time swallowing
  • shake liquid forms before using
  • use correct measuring device for liquid (not household spoon)
129
Q

WARNING (Acetaminophen)

A

if pt is taking acetaminophen around the clock and also taking a combination product, they are OVERDOSING

130
Q

acetaminophen toxicity

A
  • max is 4000 mg/4g from all sources
  • overdose causes hepatotoxicity
  • s/s are nonspecific so check plasma levels
  • later manifestation include jaundice, vomiting, CNS stimulation with excitement, and delirum followed by coma and death
  • gastric lavage and activated charcoal (if overdose detected within 4 hrs after ingestion)
  • antidote (acetylcystine, oral or IV, most beneficial given within 8-10 hours but does not reverse damage already sustained
131
Q

evaluation of acetaminophen

A
  • assess temp and fever relief
  • assess quality and intensity of pain
132
Q

patient education w/ acetaminophen

A
  • many OTC products contain acetaminophen so avoid exceeding daily dose
  • excess alcohol use can cause liver damage (limit to 2g/day max if alcohol use problem)
  • contact HCP if s/s of liver damage (jaundice, poor appetite, weakness)
  • contact HCP if skin rash or reaction
  • correct measuring device and amount
  • check for drug-drug interactions (carbamazepine, phenytoin, rifampin)
133
Q

NSAIDS classification

A

analgesic
antipyretic
anti-inflammatory

134
Q

first generation NSAIDs

A
  • ibuprofen (motrin, advil), naproxen, (aleve, naprosyn)
  • indomethacin (indocin, ketorolac, toradol)
  • meloxicam (mobic), piroxicam, feldene
135
Q

first generation NSAIDs inhibit

A

COX-1 and 2

136
Q

second generation

A

celecoxib (celebrex)

137
Q

second generations inhibits

A

primarily COX-2

138
Q

NSAIDs mechanism of action

A
  • inhibit prostaglandin synthesis in CNS and PNS
  • inhibit COX-1 and 2 enzymes require for prostaglandin production
  • relieve pain by acting centrally and peripherally to block pain impulse transmission
139
Q

propionic acid derivaties

A

ibuprofen
inhibits prostaglandin synthesis in both central and peripheral nervous systems

140
Q

oxicam derivative

A

meloxicam

141
Q

acetic acid derviative

A

indomethacin
strong anti-inflammatory effects and more severe adverse effects than the propionic acid derivatives

142
Q

selective COX-2 inhibitors

A

celecoxib
selectively block production of prostaglandings associated with pain and inflammation without blocking those associated with protective effects on gastric mucosa, renal function, and platelet aggregation

143
Q

ibuprofen (propionic acid derivative) use

A
  • osteoarthritis
  • RA
  • dysmenorrhea
  • fever
  • headache
144
Q

mechanism of action of ibuprofen (propionic acid derivative)

A

inhibits formation and release of prostaglandin by inhibiting COX enzymes and suppresses inflammation

145
Q

contraindications of ibuprofen (propionic acid derivative)

A

GI uclers or bleeds
post CABG
pregnany women >20 wks gestation (fetal harm)

146
Q

black box warning of ibuprofen (propionic acid derivative)

A

may increase risk of MI or stroke (more risk with higher dose)

147
Q

caution of ibuprofen (propionic acid derivative)

A

renal insufficiency

148
Q

interactions of ibuprofen (propionic acid derivative)

A

anticoagulants
codeine/oxycodone
corticosteroids

149
Q

ibuprofen adult dose

A
  • mild to moderate pain = 400 mg PO q4-6 hrs
  • arthritis pain = 300-600 mg PO 3-4x/day
150
Q

max dose of ibuprofen/day

A

3200 mg/day

151
Q

special consideration of administration ibuprofen (propionic acid derivative)

A

children 6mo+ have dosage based on weight

152
Q

adverse effects of ibuprofen

A
  • GI upset, anorexia, nausea, vomiting, indigestion
  • GI bleed, ulcer
  • acute renal failure
153
Q

education with ibuprofen (propionic acid derivative)

A
  • take w/ meals or milk to reduce GI upset
  • do not exceed 3.2g or 3200 mg /day
  • caution with aspirin, steroids, and alcohol
  • report s/s of GI bleed (blood in vomit, stool, or urine; coffee ground vomit, black or tarry stools)
  • seek medical attention if chest pain, dyspnea, weakness in one side of body or slurred speech
154
Q

meloxicam (oxicam derivative)

A
  • respiratory and hematologic adverse effects
  • caution w/ ACE inhibitors, diuretics, aspirin, and anticoags
  • caution with lithium (can cause toxicity)
155
Q

gout pathophysiology

A
  • uric acid crystallizes in blood or body fluidss and the precipitate accumulates in connective tissue
  • crystals trigger an immune response where neutrophils secrete lysosomes for phagocytosis, which increase immune resopnse and damage tissue
156
Q

gout diet

A
  1. avoid beer and alcohol
  2. avoid organs and game meats
  3. avoid sardines, anchovies, scallops
  4. avoid asparagus, spinach, and peas
157
Q

gout

A

overproduction of uric acid or inability to excrete uric acid which accumulates in synovial joints become enlarged from infiltration of WBCs

158
Q

colchicine (mitotic agent)

A
  • used for treatment and prevention of gout
  • inhibits migration of WBCs into body tissues containing urate crystals; decreases the inflammatory reaction to the urate crystals deposited in tissues
159
Q

allopurinol (uricosuric agents)

A

used to reduce serum uric acid levels

160
Q

colchicine administration

A
  • adults: 1.2 mg at first sign of flare and 0.6 mg 1hr after
  • give w/ food
  • dose adjustment if reduced creatinine clearance
  • if used w/ allopurinol, colchicine should be started first to prevent acute gouty attack
161
Q

evaluation of colchicine

A

reduction in gouty arthritis attacks

162
Q

adverse effects of colchicine

A
  • GI; nausea, vomiting, diarrhea, abdominal pain
  • Heme: aplastic anemia, bone marrow depression causing risk of bleeding, and fatigue
163
Q

education of colchicine

A
  • avoid grapefruit juice
  • keep out of reach of children
  • report muscle pain or weakness
  • report tingling in toes and fingers
  • report unusal bleeding or bruising, weakness, or tiredness
164
Q

allopurinol admin

A
  • adults 200-300 mg/day
  • give w/ food
165
Q

max dose of allopurinol

A

800 mg/day

166
Q

evalutation of allopurinol

A

uric acid levels (normal is 3-7 mg/dL)

167
Q

adverse effects of allopurinol

A
  • CNS: drowsiness, veritgo
  • GI: N,V,D, abdominal pain
  • GU: hepatotoxicity, renal impairment
  • skin: rash
168
Q

education w/ allopurinol

A
  • drink fluids (but avoid alcohol) to prevent kidney stones
  • take w/ or immediately after meals
  • do not drive or perform difficult tasks requiring mental alterness
  • report rashes to HCP
  • inducer for warfarin
  • rash with - cillins
169
Q

characteristics of bronchoconstrictive disorders

A
  • airway inflammation
  • bronchoconstriction
  • airway hyperresponsiveness
  • mucosal edema
  • excessive mucous production
170
Q

cause of asthma

A

real cause is unknown but is associated with a genetics and environmental exposures

171
Q

characteristics of asthma

A

bronchoconstriction and inflammation
hyperactivity to stimuli

172
Q

symptoms of asthma

A
  • dyspnea
  • wheezing
  • chest tightness
  • cough
  • sputum production
173
Q

when does asthma start

A

usually at younger age

174
Q

what areas have higher prevalence of asthma

A

urban areas
places where wildfires are common
high pollution areas (NYC, Chicago, etc)

175
Q

with asthma wheezing is observed mostly with

A

expiration

176
Q

pathophysiology of asthma

A

irritants/allergens are inhaled causing IgE to get released leading to the release of inflammatory mediators from mast cells

177
Q

inflammatory mediators

A
  • prostaglandins
  • leukotrienes
  • histamines
178
Q

3 hallmark issues with asthma

A
  1. airway inflammation or swelling
  2. extra production of mucous clogging the airway
  3. tightening of muscles around airways (bronchoconstriction)
179
Q

relationship between GERD and asthma

A

studies show that GERD can develop from asthma and asthma can worsen GERD
microaspritations can cause asthma attacks

180
Q

bronchoconstrition narrows airways…

A

so the sphincter action can completely occlude airway which is aggraveted by inflammation, mucosal edema, and excessive mucous causing mast cells to release inflammatory mediators causing bronchoconstriction and inflammation

181
Q

intermittent asthma

A
  • exercise induced
  • reversible
  • avoidance of triggers will cause relief
182
Q

mild asthma

A

recurrent
has reversible changes
need medications

183
Q

moderate asthma

A

slightly worse than mild asthma

184
Q

severe asthma

A
  • not reversible
  • airway remodeling which is caused by chronic inflammation causing fibrosis/hardening of cells and airways causing enlargement of smooth muscleand mucous cells
185
Q

status asthmaticus you might see

A
  • breathlessness
  • chest tightness
  • agitated or anxiety
  • difficult concentration / LOC
  • may need epinephrine because it is an agonist that will increase HR and give adrenaline
186
Q

relivers of asthma

A

short acting beta2-adrenergic agonists (salbutamol, fenoterol)

187
Q

controllers of asthma

A

long acting beta2-adrenergic agonists
(fomoterol)

188
Q

preventers of asthma

A

inhaled corticosteroids
(ciclesonide, beclomethasone, budesonide)

189
Q

bronchodilators prevent and treat

A

bronchoconstriction
composed of:
1. adrenergics (short and long acting)
2. anticholinergics
3. xanthine’s

190
Q

anti-inflammatory agents

A
  • prevent and treat inflammation of airways
  • decrease mucosal edema
  • decrease mucous secretions that narrow airways
    composed of:
    1. corticosteroids
    2. leukotriene modifiers
    3. immunosuppressant monoclonal antibodies
    4. mast cell stabilizers
191
Q

adrenergic drugs are effective in acute asthma attacks because they act as

A

ADRENELINE

192
Q

short acting bronchodilators (adrenergics)

A

albuterol (SABA)

193
Q

long acting bronchodilators (adrenergics)

A

salmeterol (LABA)

194
Q

albuterol drug class

A

adrenergic shortacting beta 2-agonist and bronchodilator

195
Q

use of albuterol

A

drug of choice for acute asthma exacerbations to treat or prevent bronchospasm for asthma or other reversible obstructive airway disease (exercise induced treatment)
rescue inhaler
3-4 hrs

196
Q

patho of abuterol

A

stimulates beta2-adrenergic receptors in smooth muscle of bronchi and bronchioles and stimulates enzymes to produce cyclic AMP to dilate bronchioles

197
Q

adverse effects of albuterol

A
  • most common: muscle tremor
  • major: cardiac and CNS sitmulation (angina, tachycardia, palpitation, agitation, anxiety, insomnia, seizures)
198
Q

contraindications of albuterol

A
  • hypersensitivity
  • cardiac dysrhythmias (any A-fib or prone to going into SVT do NOT give because it will increase HR)
  • severe CAD
199
Q

salmeterol drug class

A

long acting beta 2 adrenergic agonist

200
Q

salmeterol use

A

used to achieve and maintain prophylactic control of persistent asthma
long term control

201
Q

pathophysiology of salmeterol

A

maintenance inhalant medication for long term control of persistent asthma

202
Q

adverse effects of salmeterol

A
  • urticaria (hives)/rash
  • angioedema (swelling, mainly around face)
  • bronchospasm
  • headache
  • cough w/ mucous
  • chest tightness
  • CNS issues with overdose
203
Q

contraindication of salmeterol

A

hypersensitivity

204
Q

where are beta2 receptors found

A

on smooth muscle of lungs

205
Q

stimulated beta2 receptors causes

A

smooth muscle relaxation aka bronchodilation

206
Q

dosing of bronchodilators

A

MDI: 90mcg in 2 puffs q4-6h
nebulizer: 2.5mg 3-4x/day or q20minx3

207
Q

evaluation of bronchodilators

A
  • breath sounds
  • vs
  • work of breathing
208
Q

pt teaching of bronchodilators

A
  • supply at home
  • expiration
  • adverse effects
209
Q

what medications are adrenergics to treat asthma?

A

albuterol (SABA)
salmeterol (LABA)

210
Q

anticholinergics

A
  1. ipratropium
  2. tiotropium
211
Q

anticholinergics relationship w/ bronchodilators

A

synergistic effects so they work better together

212
Q

ipatropium drug class

A
  • anticholinergic
  • bronchodilator
  • short acting
213
Q

use of ipratropium

A

useful in long-term management of asthma and other conditions causing bronchoconstriction and act synergistcally with bronchodilators
NOT EFFECTIVE FOR ACUTE BROCHOSPASMS

214
Q

patho of ipratropium

A

blocks the action of acetylcholine in bronchial smooth muscle inhibiting bronchoconstriction and mucous secretions
takes effect in 5-15 minutes and lasts about 2-5 hrs

215
Q

adverse effects of ipratropium

A
  • cough
  • nervousness
  • nausea
  • GI upset
  • headache
  • dizziness
216
Q

contraindications for ipratropium

A
  • hypersensitivity to drug or atropine
  • narrow angle glaucoma
  • BPH
  • bladder neck obstruction
217
Q

black box warning on salmeterol

A

not effective in acute asthma

218
Q

tiotropium class

A

anticholinergic bronchodilator
long acting muscarinic antagonist (LAMA)

219
Q

use of tiotropium

A

maintenance therapy of bronchoconstriction associated with chronic bronchitis and emphysema
NOT EFFECTIVE IN RELIEVING ACUTE ATTACKS (Black box warning)

220
Q

patho of tiotropium

A

reduce bronchospasm, COPD exacerbation, maintenance therapy for bronchitis and emphysema
intake 1 caosue (18mday) inhaled 2x/daya

221
Q

adverse effects of tiotropium

A
  • dry mouth
  • headache
  • dizziness
  • abdominal pain
  • constipation
  • diarrhea
  • flulike symptoms
  • chest pain
222
Q

contraindications of tiotropium

A
  • hypersensitivity
  • narrow angle glaucoma
  • DO NOT take w/ ipratropium
223
Q

xanthines

A

short acting theophylline and long acting theophylline

224
Q

short acting theophylline class

A

alkaloid bronchodilator

225
Q

use of s.a. theophylline

A

treat symtpoms of asthma as a second line agent for severe disease or those unable to be controlled by first line drugs
taken q6-8hrs
black box; not used for acute asthma

226
Q

patho of s.a. theophylline

A

relaxes bronchial smooth muscle promoting bronchodilation

227
Q

adverse effects of s.a. theophylline

A
  • monitor serum drug levels due to high accumulation in blood
  • tachycardia
  • dysrythmias
  • palpitations
  • restlessness
  • agitation
  • insomnia
  • nausea
  • vomiting
  • convulsions
  • causes cardiac and CNS stimulation
228
Q

contrindications for s.a. theophylline

A
  • acute gastritis and PUD
  • caution in pt’s w/ seizures and CV disorders
229
Q

L.A theophylline class

A

alkaloid bronchodilator

230
Q

use of L.A theophylline

A

treat symptoms of asthma as a second line agent for severe disease or those unable to be controlled by first line drugs
taken q12hrs
black box: not for acute asthma

231
Q

patho of L.A theophylline

A

relaxes smooth muscle of bronchioles promoting bronchodilation

232
Q

adverse effects of L.A theophylline

A
  • monitor serum drug levels as there is a narrow therapuetic window w/ very small differences from being completely ineffective to being toxic
  • tachycardia
  • dysrythmias
  • restlessness
  • agitation
  • insomnia
  • n/v
  • convulsions
  • cardiac and CNS stimulus
233
Q

contraindications for L.A theophylline

A
  • acute gastritis and/or PUD
  • caution in pt’s with seizures and CV disorders
234
Q

short acting bronchodilators

A
  1. albuterol (adrenergic bronchodialtor)
  2. ipratropium (anticholinergic)
  3. short acting theophylline (xanthine)
235
Q

long acting bronchodilators

A
  1. salmeterol (adrenergic bronchodilator)
  2. tiotropium (anticholinergic)
  3. long acting theophylline (xanthine)
236
Q

anti-inflammatory agents

A
  • prevent and treat inflammation of airways
  • decrease mucosal edema
  • decrease mucous secretions that narrow airways
237
Q

corticosteroids

A

beclomethasone

238
Q

leukotriene modifiers

A

montelukast

239
Q

mast cell stabilizers

A

cromolyn

240
Q

immunosuppressant monoclonal antibodies

A

omalizumab

241
Q

beclmoethasone drug class

A

corticosteroid

242
Q

use of beclomethasone

A

prophylactic management of asthma, recommended to be used w/ short-acting beta2-adrenergic agonist (rescue inhaler/albuterol)

rinse and spit after use

243
Q

patho of beclomethasone

A

suppress airway inflammation, decreases mucous and edema and repairs damaged epithelium

244
Q

adverse effects of beclomethasone

A
  • headache
  • pharyngitis
  • cough
  • dry mouth
  • hoarseness
  • candididis/thrush (fungal infection)
  • nausea
245
Q

contraindications of beclomethasone

A
  • allergy
  • recent nasal surgery
  • injury or ulcers
  • can interfere with healing
246
Q

steroids can be

A

dangerous to immunity

247
Q

montelukast drug class

A

leukotriene modifier

248
Q

use of monetelukast

A

long term treatment of asthma, management of exercise induced asthma and allergic rhinitis

249
Q

black box warning of montelukast

A
  • neuropsychiatic events - agitation, aggressive, heavier anxiety, depression, disorientation, attention distuurbance, hallucinations, insomnia, irritability, suicidal ideation, tremor
250
Q

patho of montelukast

A
  • prevents leukotrienes from binding to receptors reducing bronchostriction and inflammation caused by leukotrienes
251
Q

adverse effects of montelukast

A
  • headache
  • n/v
  • diarrhea
  • hyperkinesia
  • infection
252
Q

contraindications of montelukast

A
  • hypersensitivity
  • previous psychological issues
253
Q

montelukast is

A

antagonist

254
Q

omalizumab class

A

immunosuppressant monoclonal antibody

255
Q

omalizumab use

A

adjunctive therapy for moderate to severe persistent allergic asthma that is not well controlled with corticosteroids and long acting beta2-agonists given subq

256
Q

omalizumab patho

A

limits activation and release of mediators in the allergic response

257
Q

adverse effects of omalizumab

A
  • headache
  • nausea
  • fatigue
  • anaphylaxis
  • injection site rxn
258
Q

contraindications to omalizumab

A

hypersensitivity or allergic rxn

259
Q

cromolyn class

A

mast cell stabilizer

260
Q

cromolyn use

A

alternative for prophylaxis for acute asthma in pt’s with mild persistent asthma
administered through inhalation

261
Q

cromolyn patho

A

prevents the release of bronchoconstrictive and inflammatory substances

262
Q

adverse effects of cromolyn

A
  • dysrythmias
  • hypotension
  • chest pain
  • restlessness
  • dizziness
  • convulsion
  • CNS depression
  • anorexia
  • n/v
263
Q

black box warning of omalizumab

A

anaphylaxis

264
Q

contraindications of cromolyn

A

hypersensitivity

265
Q

fluticasone/sameterol class

A

combination regimene with smaller doses of each agent to decrease adverse effects

266
Q

use of fluticasone/salmeterol

A

smaller doses to decrease adverse effects and increased with exacerbation
rinse and spit after use

267
Q

fluticasone/salmeterol patho

A

combination drug to treat both inflammation and bronchoconstriction

268
Q

adverse effects of fluticasone/salmeterol

A
  • headache
  • nausea
  • hoarseness
  • oral thrush
  • may raise BP
269
Q

contraindications of fluticasone/salmeterol

A

hypersensitivity

270
Q

getting ready for inhaler

A
  • if not used in a while prime it by pumping it 3-4x
  • take cap off and look to see if anything is inside
  • shake inhaler hard 10-15x before use
  • exhale to the end of normal breath
271
Q

how to use inhaler

A
  • inhaler must be upright when placed in mouth with sealed lips
  • press down and breathe for 3-5 seconds
  • hold breath to 10
  • pucker lips and breathe out slowly through mouth
  • wait 1 minute between inhalations
  • put cap back on and rinse mouth with water and spit
272
Q

COPD

A

made of chronic bronchitis and emphysema which usually develop as a result of long-standing exposure to airway irritants such as cigarette smoke

273
Q

COPD is

A

more constant and less reversible

274
Q

chronic bronchitis

A

defind as frequent cough with sputum production for 3 months for 2 consecutive years

275
Q

pathophysiology of COPD Chronic Bronchitis

A

increase in numbre of goblet cells and mucous glands of the airway which leads to increased mucous in the airways causing the airways to narrow leading to a cough with sputum

276
Q

emphysema pathophysiology

A

enlargement and destruction of the alveoli distal to the terminal bronchioles from long-term lung damage and inflammation

the changes to alveolar walls decreases the surface area available for gas exchange as well as decreased lung elasticity

destruction of capillaries feeding the alveoli the small airways that collapse during expiration cause trapping of CO2 and stimulate reduction of O2 exchange at the alveoli

277
Q

nursing process implementation process for COPD

A
  • use measure to prevent or relieve bronchoconstriction when possible
  • include prevention of respiratory disease and promoting adequate airway
  • specific monitoring should be in place like a peak flow meter
  • remove excess secretion
  • encourage coughing, deep breathing, percussion, and postural drainage
  • help pt ID and avoid irritants
  • assist pts w/ asthma to ID early signs of difficulty
  • reduce anxiety
  • smoking cessation
278
Q
A

path/pharm (4 decks)

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