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Pharmacology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

How are drugs classified

A

therapeutic: based on how they are used to treat a disorder; pharmacologic or structural: mechanism of action and the physiologic effects

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2
Q

How to name a drug

A

chemical: physical and chemical properties; generic: always lowercase; trade: marketed name

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3
Q

What is the drug approval process

A

preclinical lab and animal studies; phase 1: smaller number of patients looking for an optimal dosage range, pharmacokinetics, and safety; phase 2: patients have the disease testing for, looking for effectiveness and side effects; phase 3: larger group of patients looking for effectiveness and side effects; phase 4: refining understandings of medication and testing it against others

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4
Q

What are controlled substances?

A

drugs with a high frequency of abuse and high potential for addiction or physical dependence

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5
Q

How are controlled substances ranked

A

there’re 5 classes ranking from highest to least potential for addiction

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6
Q

What is the nursing process

A

assessment, nursing diagnosis/human needs statement/problem, SMART goal planning, implementation, evaluation

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7
Q

What are the rights of medication administration (5,3,2,1)

A

know institutional policies; five basic rights: right drug, right dose, right time, right form/route, right patient; three drug checks: check when taking out, when preparing, before administering to patient; two patient identifiers; one documentation done after administration

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8
Q

What is a medication error?

A

a preventable event that may cause or lead to inappropriate medication use or patient harm

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9
Q

How do you report a medication error?

A

confirm patient safety, report to prescriber and nursing management, document error per policy and procedure

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10
Q

What is medication reconciliation?

A

the process of tracking a patient’s medications as they proceed from one health care provider to another

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11
Q

What is polypharmacy?

A

patients receiving multiple prescriptions that may have conflicting pharmacologic actions

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12
Q

What are the routes of drug adminisration?

A

enteral: by mouth tablets or capsules can be buccal (cheek) or sublingual (under tongue), parenteral: intradermal, subcutaneous, intramuscular, intravenous, and topical: including patches, ophthalamic, otic, nasal, rectally, and vaginally

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13
Q

What is the first pass effect?

A

when the drug is filtered through the liver which can transform or inactivate the medication thus changing the bioavailability; only the oral route (with the exception of sublingual) undergo the first pass effect

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14
Q

What is pharmacokinetics?

A

how the drug works in the body; ADME: absorption, distribution, metabolism, excretion

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15
Q

What is ADME?

A

absorption: movement of drug from where administered into tissues; distribution: unbound drug transported by the bloodstream to its site of action; metabolism: takes place mainly in the liver; excretion: takes place mainly in the kidneys

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16
Q

What is albumin?

A

the most common blood protein that carries the majority of a protein-bound drug molecules, the longer the drug is bound the longer the half life

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17
Q

How many half lives need to undergo for a drug to be considered effectively removed from the body?

A

approximately five

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18
Q

What are some considerations for those who are pregnant?

A

the fetus is at greatest risk during the 1st trimester when the organs are being developed, drug transfer to the fetus is more likely to happen in the third trimester

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19
Q

What are the consideration categories of drugs for pregnant people?

A

A: no risk to fetus
B: no data on risk to fetus
C: adverse effects found in animal fetuses, case by case basis
D: possible fetal risk reported
X: fetal abnormalities found, not to be used in pregnant people

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20
Q

What are some considerations for those who are breastfeeding?

A

although drug levels in breast milk are usually lower than in the circulation of the person breastfeeding breastfed infants at risk for exposure to drug consumed by person breastfeeding

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21
Q

What is the conversion of 1 kg to lbs?

A

2.2 lbs per 1 kg

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22
Q

What is the conversion of 1 in to cm?

A

2.54 cm per 1 in

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23
Q

What are some pharmacokinetic considerations of neonatal and pediatric patients?

A

absorption: gastric pH is less acidic, gastric emptying is slowed, intramuscular absorption is faster and irregular; distribution: greater total body water meaning lower fat content, decreased level of protein binding, immature blood-brain barrier; metabolism: liver is immature and does not produce enough microsomal enzymes; excretion: kidney immaturity effects glomerular filtration rate and tubular secretion

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24
Q

What are some pharmacokinetic considerations for older adults?

A

most likely to result in adverse effects and toxicity; absorption: gastric pH is lower, gastric emptying is slowed, movement through GI is slow due to decreased muscle tone and activity, blood flow to GI is reduced, absorptive surfaces in GI reduced; distribution: lower total body water and increased fat content, decreased production of proteins by liver resulting in decreased protein binding of drugs; metabolism: fewer microsomal enzymes and reduced blood flow to liver; excretion: decreased glomerular filtration rate and number of nephrons

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25
Q

What is inflammation?

A

localized protective response that is stimulated when there is injury to the tissues, the response serves to destroy and dilute, or even wall-off both injurious agent as well as injured tissue

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26
Q

What are the endogenous components of inflammation?

A

histamine, serotonin, bradykinin, leukotrienes, prostaglandins

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27
Q

What is cyclooxygenase?

A

produce prostaglandins that promote inflammation and fever; COX-1 and COX-2, only COX-1 produce prostaglandins that activate platelets and protect the stomach and intestinal lining

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28
Q

What are NSAIDS?

A

nonsteroidal anti-inflammatory drugs, they are a large and chemically diverse group of drugs with the following properties: analgesic, anti-inflammatory, and antipyretic

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29
Q

What is the mechanism of aspirin?

A

inhibits platelet aggregation by binding to COX-1 and -2

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30
Q

What is aspirin used for? What is it’s dosage? What are its side effects?

A

shown to reduce cardiac death at the first sign and after a myocardial infarction, it can be used for headache, pain from inflammation such as arthritis, and system lupus erythematosus; dosage is 81-324 mg; side effects include GI bleeding, nausea, vomiting, diarrhea, tachycardia, tinnitus, diminished vision, confusion

31
Q

What are some examples of NSAIDS that are propionic acid derivatives? What are their maximum dosages?

A

ibuprophen (used commonly due to least amount of side effects): max dosage 1200 mg, ketoprofen: max dosage 200 mg, naproxen: max dosage 500 mg

32
Q

filler card

A

filler

33
Q

What are some side effects for NSAIDS that inhibit COX-1 and -2

A

nausea, vomiting, GI bleeding, renal impairment

34
Q

What are some examples of COX-2 inhibitors? What are their benefits and cons?

A

rofecoxib, valdecoxib, celecoxib; avoided most GI side effects because they avoided inhibiting prostaglandin production in the stomach but they do increase incidence of MI, stroke, and death

35
Q

What is ketorolac? It’s route? It’s side effects?

A

an NSAID with strong analgesic effect, a good choice for patients with opioid addictions; route of oral, IM, and IV; used short term due to side effects of kidney impairment, edema, GI pain, and nausea

36
Q

What are corticosteroids? Examples and routes? Side effects?

A

suppress inflammation and normal immune response; dexamethasone, methylprednisone via IV, prednisone via PO, natural hormones in the body including glucocorticoids, mineralcorticoids, and sex hormones; side effects include: mood changes, hyperglycemia, osteroporosis, immunosuppression

37
Q

Can corticosteroids be immediately stopped?

A

No, especially when used long term because when used the body stops making their own natural hormones

38
Q

How are antineoplastic drugs identified and categorized?

A

identified by protocol names; divided into cell cycle-specific, cell cycle-nonspecific, and some who have characteristics of both

39
Q

What are some examples of cell cycle-specific drugs? How do they work? Side effects/what are they used for?

A

prevent cellular growth by blocking compounds necessary for reproduction; folate antagonist: blocks conversion of folic acid to its active form folate ex/ methotrexate with leucovorin (to give healthy cells folate), can lead to myelosuppression. purine antagonist: blocks synthesis of DNA and RNA ex/ cladribine. pyrimidine antagonist: blocks synthesis of DNA and RNA ex/ cytarabine for leukemia and non-hodgkin leukemia

40
Q

What are some examples of cell cycle-nonspecific drugs? How do they work? What are they used for? Side effects?

A

alkylating drugs, cyclophosphamide; alter DNA; variety of cancers; causes nausea and vomiting

41
Q

What is extravasation and why is it bad for antineoplastics?

A

leakage of IV medications; if antineoplastics become extravasated they can damage veins and tissues around the site of infusion

42
Q

How do hormonal antineoplastics work? Examples? Side effects?

A

block sex hormone receptors or block the sex hormone; tamoxifen: block estrogen receptors on some types of breast cancer, bicalutamide: antiandrogen; side effects include hypertension, hot flashes, and depression

43
Q

Considerations for antineoplastics?

A

drugs have a narrow therapeutic index (effects cancer cells and normal cells), combination of drugs are usually more effective, drug resistance, nearly all drugs cause adverse effects

44
Q

What are some examples of adverse effects of antineoplastics and their signs?

A

myelosuppression through anemia (pale and fatigue), leukopenia (fever and chills), neutropenia, and thrombocytopenia; alopecia, nausea and vomiting, stomatitis, nadir (lowest wbc count)

45
Q

What are the types of tests to diagnosis bacteria?

A

culture test: to see what’s growing; sensitivity test: to see what can kill it

46
Q

What are the types of antibiotic therapies?

A

empiric: treatment of an infection before specific culture information has been specific culture; definitive: tailored to treat organism identified with cultures; prophylactic: done to prevent infections

47
Q

What are some considerations of antibiotics?

A

superinfection (caused by the death of normal bacterial fauna), resistance, food and drug interactions, host factors, allergies

48
Q

What are the actions of antibiotics? mechanisms of action?

A

bactericidal: kill bacteria and bacteriostatic: inhibits growth eventually leading to bacterial death; blocking cell wall synthesis, dna replication, rna synthesis, and protein synthesis

49
Q

What are the classes of antibiotics?

A 
"Antibiotics Can Terminate Protein Synthesis For Microbes" 
Aminoglycosides
Cephalosporins
tetracyclines
Penicillins 
Sulfanomides
(Floro)quinolones
Macrolides
50
Q

What are sulfonamides mechanism? What type of bacteria are they effective against? Examples?

A

bacteriostatic: prevents folic acid synthesis; effective against gram positive and negative; often used in combination with antibiotics (ex/ sulfamethoxazole/trimethoprim);

51
Q

What are some nursing considerations for sulfonamides?

A

increase fluid intake, interactions with: phenytonin (seizure medication) could reach toxicity levels, warfarin causes blood to become too thin, birth control lowers effectability

52
Q

What are some side effects of sulfonamides?

A

delayed skin reactions, photosensitivity, agranulocytosis and aplastic or acute hemolytic anemia

53
Q

How do beta-lactam antibiotics work? What are the antibiotic classes in this group? How is bacterial resistance shown?

A

a beta-lactam ring inhibits cell wall formation; penicillins, cephalosporins, carbapenems, and monobactams; bacteria create beta-lactamase

54
Q

How do penicillins work? What are the groups? Side effects? Interactions?

A

bactericidal by disrupting cell wall synthesis; penicillinase-resistant penicillins, aminopenicillin: broad spectrum effective against gram negative (ex/ amoxicillin used for ear, nose, and throat), extended-spectrum: used for more serious infections, combination agents: penicillin used with beta-lactamase inhibitors (unasyn, augmentin, timentin, zosyn, avycaz); typical GI side effects; birth control and warfarin

55
Q

What are the combination agents?

A

Unasyn (ampicillin/sulfactam), augmentin (amoxicillin/clavulanic acid), timentin (ticarcillin/clavulanic acid), Zosyn (piperacillin/tazobactum), Avycaz (cefazdime/ avibactam)

56
Q

How do cephalosporins work? How are they categorized?

A

semi-synthetic antibiotics that are bactericidal by disrupting the cell wall; categorized by antimicrobial activity against gram positive and gram negative from one to five, as the generation increases their effectiveness against gram positive bacteria decrease while their effectiveness against gram negative increases

57
Q

What are some special cases of cephalosporins?

A

ceftriaxone (3rd generation) can pass through the blood-brain barrier, ceftaroline (5th generation) can work against MRSA, ceftolozane/tazobactum has a beta-lactamase inhibitor and is good for severe UTIs

58
Q

What are some nursing considerations for cephalosporins?

A

GI issues, pruritus, redness, edema, avoid alcohol, birth control interactions

59
Q

How do carbapenems work? and how are they given? What is their suffix?

A

bactericidal by disrupting cell wall, broadest antibacterial action; only given by IV over 60 minutes as it may cause seizures; “-penem”

60
Q

How do macrolides work? What are some examples? What are they used for?

A

bacteriostatic by preventing protein synthesis by binding to 50s unit of ribosomes; FACE: Fidaxomicin (treats c.diff), Azithromycin, Clarithromycin, Erythromycin; strep infections, mild to moderate upper and lower respiratory tract infections, spirochetal infections such as syphilis and lyme disease, gonorrhea, chlamydia, and mycoplasm

61
Q

What are the side effects of macrolides?

A

GI effects: primarily with erythromycin, birth control interactions

62
Q

How do tetracyclines work? What is their suffix? What are some nursing considerations?

A

bacteriostatic by preventing protein synthesis by binding to 30s unit of ribosome, broad spectrum; “-cycline”; interactions with antacids and Ca, Mg, and Al supplements by binding with them and forming insoluble comples, diary products decrease absorption, tooth discoloration and skeletal development and therefore should not be used in children younger than 8 years or pregnant or lactating people, photosensitivity

63
Q

What are some MDR?

A

MRSA, VRE, ESBL, CRE

64
Q

How do aminoglycosides work? Some examples and suffixes? Route of entry?

A

bacteriocidal by preventing protein syntehsis by binding to 30s unit of ribosome; GNT: gentamicin, neomycin, tobramycin “-micin” and “-mycin”; poor oral absorption most are given IV (except for neomycin)

65
Q

What are some nursing considerations for aminoglycosides?

A

serum and kidney monitoring is key due to severe toxicities: nephrotoxicity, ototoxicity

66
Q

What is minimum inhibitory concentration?

A

lowest concentration of medication needed to kill a certain level of bacteria

67
Q

How do quinolones work? Route of entry? Suffix? Nursing considerations?

A

broad spectrum bactericidal by altering bacterial DNA; excellent oral absorption; “-floxacin”; interactions with antacids, Ca, Mg, fe, Zn will reduce oral absorption and increased for tendon rupture (typically seen in older adults)

68
Q

How do vancomycin work? What are they used for? Nursing consideration?

A

bacteriocidal by binding to cell wall; treatment of choice for MRSA and c.diff; ototoxic and nephrotoxic, red man syndrome

69
Q

What are the portal of entries for viruses?

A

inhalation, ingestion, inoculation, via placenta

70
Q

What are immunoglobulins?

A

high concentration of antibodies who kill viruses

71
Q

What are the characteristics of herpes virus family? What are the types? What are some treatments?

A

very contagious with no cure and can lay dormant in the nervous system; HSV-1: oral herpes seen as cold sores but can effect oral, eyes, and genitals . HSV-2: genital herpes but can also be seen orally, this and -1 can be transmitted at birth. HSV-3: varicella seen as chickenpox and shingles. HSV-4: epstein-barr. HSV-5: cytomegalovirus; acyclovir and valacyclovir for 1 and 2 (will reduce symptoms) and varicell and zoster for 3

72
Q

What are neuroaminidase inhibitors? What is an example? Side effects?

A

used for influenza A and B and will help prevent new viruses from leaving the cell to infect other cells therefore decreasing the time of infection; osteltamivir; taken 48 hours of onset of symptoms; nausea and vomiting

73
Q

What are some examples of fungal infections?

A

oral candidiasis: thrush, aspergillosis: systemic lung (seen with transplant patients)

74
Q

What are some examples of antifungals and their nursing considerations?

A

amphoterian B: binds to cell membrane, may premedicate to lower side effects caution for kidney disease and bone marrow suppression; azoles: “-azole” used as systemic and topical to disrupt fungal cell membrane; nystatin for tinea cruvis (fungal infection of groin) and thrush

Pharmacology (6 decks)

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