711 terms

Pharm final exam review slides

Undesirable, potentially harmful effects of medications
Adverse effects
Adverse effects can occur at both _______ and ________ doses
Both therapeutic and abnormal doses
True or false: not all prescriptions, OTCs, herbal remedies, and supplements have the potential for adverse effects.
False (all medications have the potential for adverse effects)
What is the hematologic condition of decreased erythrocyte, leukocyte, and/or thrombocyte production, caused by some drugs?
Blood dyscrasias
Predictable/anticipated (but still undesirable) effects of medications
Side effects
What distinguishes side effects from adverse effects?
Nursing teaching should include predictions of ________ side effects
Predictions of common side effects
Drug reactions that produce the opposite of the intended effects
Paradoxical reactions
Uncommon drug reactions often caused by genetic differences
Idiosyncratic reactions
What is the type of drug reaction due to stimulation of the immune system by the drug?
Hypersensitivity (allergic) reactions
Drug reaction that occurs due to patient overdose of the drug
Toxic reactions
Allergy-hypersensitivty reactions:
The body recognizes the drug as a _________
_______ and cellular ________ respond and are released by the body
The body recognizes the drug as a foreign invader
Histamine and cellular mediators respond and are release by the body
Allergy (hypersensitivity) reactions are especially dangerous when they occur in what part of the body?
(Bonus: why?)
The throat
The combined effect is greater than the sum of the individual agents (1+1>2)
Synergistic interaction
The combined effects is equal to the sum of the individual agents (1+1=2)
Additive interaction
One drug inhibits the ability of another drug to act (1+1<1)
Reducing (antagonist) interactions
What aspect of pharmacological administration (giving meds) needs to be adjusted for elderly patients?
Dosage (reduction)
What four aspects of pharmacokinetics become impaired in elderly patients?
Four stages of pharmacokinetics
Metabolism (biotransformation)
Excretion (elimination)
Drug transportation from the site of absorption (GI or bloodstream) to the site of action (body tissues)
Factors affecting distribution (5)
Blood flow to tissues (perfusion)
Tissue storage (tissue-specific storage)
Obesity (lipophilic drugs)/edema (hydrophilic drugs)
Drug-protein binding (albumin)
Barriers (blood-brain-barrier, placenta)
Drug-protein complexes cannot cross the ________ membrane to reach target tissues
Capillary membrane
In order for a drug to reach its target tissues, it must be ______ and _______ (from drug-protein complexes)
Free & unbound
What type of drugs are distributed into/accumulated in adipose tissue?
Lipophilic drugs (obesity)
Lipophilic drugs are (more/less) active at the site of action but are (quickly/slowly) released from fatty tissue
Less active at the site of action but slowly released from fatty tissue
What type of drugs are distributed into and remain in interstitial solution?
Hydrophilic drugs (edema)
Refers to the amount of a drug that reaches the site of actions
Factors affecting bioavailability:
First-pass _________ metabolism
__________ of the drug
Chemical _________
First-pass hepatic metabolism
Solubility of the drug
Chemical stability
The first-pass hepatic metabolism effects occurs much more often with (IV/oral) drugs than with (IV/oral) drugs
Occurs much more often with oral drugs than with IV drugs
Process to change activity in a drug and make it more likely to be excreted
(Bonus: what is the other name for it?)
Drug metabolism occurs primarily in what three organs?
Intestinal tract cells
What four components of drugs are changed during metabolism?
Chemical structure
What type of drug has no pharmacological activities?
Process by which drugs and their metabolites are removed from the body
What is the primary site of drug elimination in the body?
Drug elimination includes:
_______ filtration
_______ secretion
Partial _________
Glomerular filtration
Tubular secretion
Partial reabsorption
The drug elimination process must be careful considered in patients with what impairment?
(Bonus: why?)
Renal (kidney) impairment
(Drugs stay in the body longer, increasing the risk of toxicity)
How is the risk for toxicity avoided concerning drug elimination in renal-impaired patients?
Reduced drug doses are given
The therapeutic response of a drug most likely depends on _________ in the _______
Concentration in the plasma
The amount of a drug required to produce a therapeutic effect
Minimum effective concentration
The range in which a drug produces its desired effect (goal of drug administration)
Therapeutic range
The level of a drug that results in serious adverse effects
Toxic concentration
The length of time required for plasma concentration to decrease by 1/2 after administration
Plasma half-life (t1/2)
A drug has _______ concentration when it is administered at the same rate at which it is eliminated
Stable concentration
Repeated dosing (stable concentration) provides _______________
Provides plateau plasma level
Drugs have approximately ____ half-lives until excretion
Approximately 4 half-lives until excretion
Loose definition for what a specific drug does to the body
Pharmaco- = __________
-dynamics = ________
What are the two components of pharmacodynamics?
Drug mechanisms of action (MOA)
Effects of drug concentration on body response
Drug type that activates receptors to cause a response
Drug type that binds to receptors to block a response
Bacteria that render usually-successful antibiotics ineffective, due to mutation and transfer of genetic material from the antibiotic to the bacteria
How are superbugs more superior than weaker bacterial strains?
Superbugs replicate while weaker strains are killed.
Two human contributions to antibiotic resistance
Unnecessary prescriptions for viral illness (overuse)
Incomplete course of therapy (reinfection)
Common side/adverse effects of antibiotics (5)
Blood dyscrasias
How can NVD related to antibiotics be relieved? (2)
Avoid heavy meals
Prefer small, frequent meals (don't overload GI)
Antibiotic allergic reactions (5 symptoms)
Shortness of breath
Swelling of lips/tongue
Itch (r/t hypersensitivity)
Hives (r/t hypersensitivity)
Life-threatening allergic response of acute inflammation, due to rapid release of inflammatory mediators throughout the body
Laryngeal edema/bronchoconstriction decrease...
Oxygen intake
Vasodilation causes...(2)
Severe hypotension
Inadequacy of body to meet cellular/tissue/organ needs for oxygen/glucose is known as...(2)
Rash in response to direct sunlight/lack of sunscreen/lack of protective clothing, caused by antibiotics
If a patient develops a photosensitive rash while taking an antibiotic, what should the nurse instruct the patient to do? (3)
Avoid direct sunlight and/or wear sunscreen & protective clothing
Notify the nurse or prescriber of any rash
Stop taking the medication until the rash is evaluated
Bacteria (such as C. diff.) that proliferates when normal flora are killed by antibiotics
Fungal infections such as vaginal yeast infections and black, hairy tongue are examples of...
Two (2) names for bone marrow suppression (common adverse effect of drugs)
Blood dyscrasias
Three "decreases" of blood dyscrasias (with associated conditions)
Decreased erythrocytes, causing anemia (weakness, pallor)
Decreased leukocytes, causing leukopenia (infection)
Decreased thrombocytes, causing thrombocytopenia (bruising/bleeding)
If a female tells the nurse that she is using BCPs while taking an antibiotic, what situation should the nurse advise the patient concerning?
Drug-drug interaction (antibiotic cancels out BCPs-pregnancy could occur)
Prior to administering an antibiotic, a nurse should perform what on/for the patient?
An assessment
The nurse's pre-antibiotic assessment should include...
History of ______ _____________
__________ (physical exam, vital signs, lab reports, pregnancy test if needed)
_________-_________ interactions (drug history)
_________ and ___________
History of drug allergies
Drug-drug interactions
Culture and sensitivity
Aspect of initial assessment that determines causative pathogen of infection
Aspect of initial assessment that determines which antibiotics are effective against a causative pathogen
Most common drug (antibiotic) allergy
Penicillin allergy
If penicillin is given parenterally at clinics/ER, the patient should be observed _______ minutes before leaving even if the patient has received penicillin before w/o reaction.
30 minutes
Administration of antibiotics such as penicillin with acidic fruit juices results in what?
Neutralization of the antibiotic (alkaline)
Natural, inexpensive penicillin; only works on Gram-positive infections
Penicillin G
Penicillins (2) developed for Gram-positive and some Gram-negative infections; one of the more broad-spectrum prototypes
Extended-spectrum penicillin used against Psuedomonas
Antiobiotic widely prescribed for Gram-negative infections (structurally similar to penicillins)
How many generations of cephalosporins exist?
1st generation of cephalosporins:
__________ (Keflex)
Cephaxelin (Keflex)
2nd generation of cephalosporins:
__________ (Ceclor)
Cefaclor (Ceclor)
3rd generation of cephalosporins:
__________ (Rocephin)
Ceftriaxone (Rocephin)
4th generation of cephalosporins:
__________ (Maxipime)
Cefepime (Maxipime)
Cephalosporins are more effective against gram-_________ and (aerobic/anaerobic) bacteria
Cephalosporins have a broader __________, longer __________, and better permeability to _______-_________ fluid with each new generation of the antibiotic.
Broader spectrum
Longer duration
Better permeability to cerebrospinal fluid
Cephalosporins interfere w/ the bacterial ______ _______, making them bacteriocidal.
Bacterial cell wall
Cephalosporins have an antabuse-like interaction w/ _________ for up to 72 hours, causing impaired consciousness.
Alcohol (avoid alcohol intake while taking cephalosporins)
Broad-spectrum antibiotic used against both Gram-positive/Gram-negative infections
Tetracyclines inhibit bacterial __________ synthesis by binding to the _____ ribosomal unit, thereby interfering attachment of _______ to ______ and terminating growing amino acid chains.
Inhibit bacterial protein synthesis; bind to 30s ribosomal unit; interfere with attachment of tRNA to mRNA
Does tetracyclines' interference with bacterial protein synthesis render them bacteriocidal or bacteriostatic?
Tetracyclines bear a strong affinity for ________ to form insoluble complexes.
Prototype tetracyclines (2)
Broad-spectrum antibiotic that can be either bacteriostatic or bacteriocidal
Macrolides inhibit bacterial _________ synthesis.
Protein synthesis
What drug is administered when a patient expresses an allergic reaction to penicillins?
Macrolides (broad spectrum)
Macrolides are most effective against Gram-_________ infections.
When administered macrolides, patients should be encouraged to take the antibiotic (before eating/after eating).
Before eating (empty stomach)
The ______ coating of macrolides prevents GI irritation.
Enteric coating
___________-resistant strains are rather common, due to the drug's frequent use in the place of penicillin.
Macrolide-resistant strains
Prototype macrolide
Antibiotic most often used to treat tuberculosis (TB) and often administered parenterally alongside other drugs
Aminoglycosides are bacteriocidal by inhibiting bacteria _______ synthesis.
(Bonus: gram-positive or gram-negative bacteria?)
Protein synthesis
When administered aminoglycosides, patients should be warned concerning what adverse effects? (2)
Nephrotoxicity; ototoxicity (dizziness [vertigo], hearing loss, tinnitus)
Prototype aminoglycoside
When administering aminoglycosides, physicians should monitor the patient's urinalysis for urinary _______ and _____uria, as well as increased serum _____ and ___________.
Urinary casts; proteinuria; increased serum BUN; creatinine
Physicians must monitor the peak/trough levels of aminoglycosides for what reason?
The therapeutic range of aminoglycosides is very narrow (toxic level close to effective level).
Highest drug level in the blood
Peak level
At what time after administration should the peak level of the drug in the blood stream be examined?
15-30 minutes
Lowest drug level in the blood
Trough level
When should blood be drawn to monitor the trough level of a drug? Why?
No more than 30 minutes prior to the next infusion (to prevent toxicity w/next dose)
Which broad-spectrum antibiotic is traditionally used for UTIs? Why?
Sulfonamides (reach high concentrations in the kidneys)
Sulfonamides combine synergistically with __________, both of which are effective against UTIs.
Sulfonamides are bacteriostatic by inhibiting _____ _____ synthesis in bacteria.
Folic acid synthesis
Why are sulfonamides (sulfa drugs) effective against bacteria but harmless to humans?
Humans obtain enough folic acid from food to counter the disruption of folic acid synthesis by sulfa drugs.
Prototype sulfonamides (sulfa drugs):
___________ (Bactrim/Septra)
Sulfamethoxazole (Bactrim/Septra)
Widespread use of sulfa drugs against UTIs has led to what complication?
Strain resistance
Drugs for Influenza:
Best prevention
Annual vaccination
Drugs for influenza prophylaxis (prevention) (2):
__________ (Symmetrel)
__________ (Flumadine)
Amantadine (Symmetrel)
Rimantadine (Flumadine)
Influenza Drugs:
Use for ___-__________ individuals after confirmed outbreak.
"un-vaccinated" individuals
Drug for new, active influenza
Tamiflu (Oseltamivir)
How soon after onset of influenza symptoms should Tamiflu (Oseltamivir) be given?
Within 48 hours
Drugs for Hepatitis:
Best prevention via _______________.
(Bonus: for which two strains?)
(Hepatitis A & Hepatitis B)
Drug for Hepatitis:
Prevention through _________________ (antibodies) for those with personal contact for ________ months (passive immunity)
Drug for Hepatitis treatment
Interferon - "interferes" w/ virus infection (increases immune system)
HIV Infection:
HIV targets what?
The CD4 receptor on T4 (Helper) lymphocytes
T4 cells are part of what system?
Cell-mediated immune system
Loss of T4 cells due to HIV results in a vulnerability to develop _________ alongside HIV.
Develop infections (alongside HIV)
Therapeutic goals of anti-Hepatitis drugs:
Reduction of ____ in the blood
Increase _____ span
High quality of _____ (all things considered)
Reduction of HIV in the blood
Increase life span
High quality of life (all things considered)
Drugs for HIV (Antiretrovirals):
List 2 Reverse-Transcriptase Inhibitors
Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Drugs for HIV (Anti-retrovirals):
__________ inhibitors (PIs)
__________ (entry) inhibitors
Protease inhibitors (PIs)
Fusion (entry) inhibitors
Drugs for HIV (MOA):
What do Reverse Transcriptase inhibitors do? (______________ [Retrovir, AZT])
They are able to make HIV lose the ability to replicate DNA.
(Zidovudine [Retrovir, AZT])
Protease inhibitors block the final assembly of new ___ and control the spread of ____ to uninfected cells.
(_________ [Crixivan])
They block the final assembly of new HIV and control the spread of HIV to uninfected cells.
(Indinavir [Crixivan])
Fusion inhibitors block the fusion of _____ to _____
(___________ [Fuzeon])
Block the fusion of HIV to CD4
(Enfuvirtide [Fuzeon])
What is the function of HAART?
What conditions does it affect? (2)
Highly-Active Antiretroviral Therapy
Aggressive therapy with multiple drugs.
Haart: Simultaneous use of drugs from several ___________ to reduce probability of drug __________.
Several classes
Antifungal agents (2)
Nystatin (candida albicans)
Miconazole (athlete's foot, jock itch)
Two (2) reasons for ineffective antifungal drug therapy
Incomplete full course
Systemic fungal infections might be deadly in...
Immuno-compromised people
List four immuno-compromised people:
______________ syndrome
Taking ________ therapy
Taking _________________ to fight __________ rejection
Debilitated, _____________ or otherwise poor health
Immunodeficiency syndrome (AIDS)
Taking cancer therapy
Taking immunosuppressants to fight transplant rejection
Debilitated, malnourished or otherwise poor health
Systemic antifungal agents (2)
Amphotericin & Fluconazole bind to __________ in fungal cell membranes, causing __________.
Intensive and extended fungal treatment causes what side effects? (12)
_______ and chills
______tension and ______cardia
_____/______ pain & _____ache
GI issues (2)
Three types of toxicity
Fever and chills
Hypotension and tachycardia
Muscle, joint pain, headache
Nausea and vomiting
Renal, neuro- and hepatic toxicity
Protozoa - Malaria:
Female Anopheles mosquito is the carrier of several species of ____________.
Plasmodium is responsible for:
Malaria is caused by infected ___________ __________.
mosquito bites
Prototype antimalaria:
_________ (Aralen)
Chloroquine (Aralen)
Patient teaching (Antimalaria):
Don't stop until medication is ______
Watch for _______ deficits
Take with _____ to avoid GI upset
Possible __________ of symptoms
Start therapy ___ weeks before exposure and continue ___ weeks after prophylaxis
Don't stop medicine until gone
Watch for hearing deficits (ototoxicity)
Take with food to avoid GI upset
Possible recurrence of symptoms
Start therapy 2 weeks before exposure and continue 8 weeks after for prophylaxis.
Vaccines and Immune System (active):
________ immunity: body produces its own antibodies
__________: induced or immunization
________-lasting, often _______-long
Natural: body produces its own antibodies
Vaccination: induced or immunization
Long lasting, often life-long immunity
Vaccines and Immune System (passive):
Transfer __________ antibodies from one to another
_________: Mother to child via placenta
Pharmacotherapy: ___________, antivenins (venemous bites/stings), _____ (transfusion of whole blood)
(Lifelong/temporary) immunity
Transfer performed antibodies from one to another.
Natural: mother-to-child via placenta
Pharmacotherapy: Immunoglobulin, antivenins, sera
Temporary immunity
Side/adverse effects of Vaccines:
Minor anticipated side effects (2)
Localized inflammatory reactions (soreness, erythema and increased warmth at injection area)
Side/adverse effects of Vaccines:
Serious adverse reactions (uncommon) (4)
Fever > 103 F
CNS effects (convulsions, encephalitis)
Anaphylactic reactions (e.g. if vaccine made with eggs with patient's allergic history to eggs)
Nursing concerns when administering vaccines (3)
Timing (schedule established by CDC)
Route of administration
Nursing concerns when administering vaccines (Precautions and contraindications):
_______________ patients (transplants, chemo, long-term steroid users, etc)
__________ women
_________ event reporting
Immunosuppressed patients (transplanted, chemotherapy, long term steroid users etc.)
Pregnant women
Adverse event reporting
Nursing concerns when administering vaccines (Treatment of minor illnesses):
__________ to ease fever, discomfort, and localized symptoms
______ compresses to site
Acetaminophen to ease fever, discomfort and localized symptoms (never give aspirin to a child or adolescent because of possibility of developing Reye's syndrome)
Warm compresses to site (heating pad or towel in a very warm water rung dry)
Immunomodulators (2):
__________ (enhance immune system's ability to fight infection/disease)
__________ (suppress immune system's ability to fight infection/disease)
Immunostimulants (enhance immune system's ability to fight infection/disease-usually used to treat patients w/cancer)
Immunosuppressants (suppress immune system's ability to fight infection/disease-usually used to prevent transplant rejection/dampen hyperactive immune responses [Lupus, rheumatoid arthritis])
Immunosuppressant responsible for prophylaxis of transplant rejection
___________ (Sandimmune)
Cyclosporine (Sandimmune)
Immunosuppressant responsible for treating autoimmune conditions and malignancies
_____________ (Orthoclone, OTK3)
Muromonab-CD3 (Orthoclone, OTK3)
Immunosuppressant responsible for treating arthritis
3 important facts:
Decrease __________ response
Very high risk of _________
____________-decreased WBC count
Decrease immune response
Very high risk of infection
Leukopenia - deceased white blood cell count (normal WBC is 5,000-10,000)
Immunosuppressants (nursing interventions):
Careful _______-_________ techniques
Avoid ________ medical procedures
Avoid _________, ______ temperature and _______ suppositories
Frequent/meticulous _________ care
Bathe with ______________ soap
Avoid ________
____________ and ___________ should be changed daily/whenever soiled
Protect skin from _________ and _________
Wear ________
Careful hand washing techniques.
Avoid invasive medical procedures.
Avoid tampons, rectal temperature and rectal suppositories.
Frequent and meticulous mouth care.
Bath with antibacterial soap.
Avoid crowds.
Dressing and bandages should be changed daily and whenever soiled.
Protect skin from abrasions and lacerations.
Wear shoes.
Long term management of ________ _______ but significant _______ effects. (Ex. Rheumatoid arthritis, chronic lung disease)
Chronic disease
Adverse effects
Short term therapy of severe ____________ (acute exacerbations)
Traumatic injury such as ______ trauma or _______ injuries
Severe inflammation
Head trauma or spinal cord injuries
Corticosteroids (oral and parenteral agents):
__________ (Deltasone)
__________ (Decadron)
__________ (Medrol)
Prednisone (Deltasone)
Dexamethasone (Decadron)
Methylprednisolone (Medrol)
Affect many aspects of immune system (MOA):
Reduce circulating ____________
Deplete body of ___________ and ____________
Move ___________ from bone marrow to circulation
Block production of ________________ and ____________ Ls
Reduce circulating lymphocytes
Deplete body of monocytes and macrophages.
Move neutrophils from bone marrow to circulation.
Block production of prostaglandins and interleukin Ls
Corticosteroids: Contra. and precautions:
Never administer corticosteroids when patients has known ________ infections.
Fungal infections
Corticosteroids (contraindications and precautions):
Never administer corticosteroids to a patients with known ______ infection
Do not administer _____ virus (vaccines) to clients taking steroids (due to suppressed immune response).
Known fungal infection
Live virus (vaccines)
Corticosteroids (contraindications & precautions):
When given to clients with a history of tuberculosis, may _________ disease.
Corticosteroids (contraindications & precautions):
Increase pre-existing ____________
Corticosteroids (contraindications & precautions):
Worsen pre-existing _____ _____.
Peptic ulcers
Corticosteroids (contraindications & precautions):
Mask ___________.
Corticosteroids (contraindications & precautions):
Elevate ________ in diabetics.
Corticosteroids (contraindications & precautions):
Worsen _________, osteoporosis in ________, prexisting _____ infection.
Eye infection
Iatrogenic Cushing's disease (symptoms):
Round "moon" _____
Reddened ________
______ gain
______ obesity with comparatively thinner _____ and _____
______ hump
Easy _______
Round "moon" face
Reddened cheeks
Weight gain
Central obesity with comparatively thinner arms and legs.
Buffalo hump.
Easy bruising
Penicillinase-resistant penicillin
Patients allergic to penicillin may also be allergic to what other type of antibiotic?
Fluid fundamentals:
IV fluids are classified by ________ or _______
Osmolality or tonicity
Fluid fundamentals:
The osmolality of a fluid is determined by ______, _______, etc.
Sodium, dextrose, etc.
What type of IV fluid is recommended for fluid and/or electrolyte imbalance?
Lactated Ringer's solution
Types of IV fluids:
_________ (0.45% NaCl solution)
_________ (0.9% NaCl solution)
_________ (5% dextrose in 0.9 NaCl solution)
Hypotonic (0.45% NaCl solution)
Isotonic (0.9% NaCl solution)
Hypertonic (5% dextrose in 0.9 NaCl solution)
What are the two main categories of antineoplastic agents?
Cell-cycle specific (CCSs): cytotoxic during specific phases of the cancer cell reproductive cycle
Cell-cycle nonspecific (CCNs): cytotoxic in any phase of the reproductive cycle of cancerous cells
Phases of the cell cycle:
During which phase do most human cells predominantly exist?
G0 (resting phase)
Phases of the cell cycle:
During which phase are cancer cells not susceptible to the toxic effects of chemotherapy?
G0 (resting phase)
Phases of the cell cycle:
During which phase are the enzymes necessary for DNA synthesis produced?
G1 (postmitotic phase)
Phases of the cell cycle:
During which phase does DNA synthesis take place, from DNA separation to DNA replication?
S phase (DNA synthesis phase)
Phases of the cell cycle:
During which phase are RNA and specialized proteins made?
G2 (premitotic phase)
Phases of the cell cycle:
Which phase is divide up into four sub-phases: propphase, metaphase, anaphase, telophase?
M (Mitosis phase)
Chemotherapeutic agents act on (the same/different) phases of the cell cycle
(Bonus: which phases?)
Act on different phases of the cell cycle
(Mostly G1, S, G2, M)
Combining chemotherapeutic agents increases the chances of _________ cancerous cells
Increases the chances of eliminating cancerous cells
Combining chemotherapeutic agents reduces the possibility of drug _______ or _______
Reduces the possibility of drug resistance or mutation
Alkylating chemotherapy agent prototype:
___________ (Cytoxan)
Cyclophosphamide (Cytoxan)
Alkylating chemotherapy agents MOA:
Alter the shape of __________ and prevent ________
Alter the shape of DNA double helix & prevent cancer cell replication
Alkylating chemotherapy agents are (CCSs/CCNs)
Cell-cycle nonspecific (CCNs)
Alkylating chemotherapy agents are broad spectrum to what four (4) types of cancers?
Pancreatic neoplasms
Reproductive neoplasms
Alkylating chemotherapy agents (adverse effects):
________ suppression
Bone marrow (myelo-) suppression
Antimetabolite chemotherapy agent prototype:
__________ (MTX)
Methotrexate (MTX)
Antimetabolite chemotherapy agents MOA:
Disrupt __________ pathways of cancer cells and inhibit critical _______
Disrupt metabolic pathways of cancer cells and inhibit critical enzymes
Antimetabolite chemotherapeutic agents are cell cycle-specific to ___ phase
S phase
Antimetabolite chemotherapy agents are indicated for what five (5) types of cancers?
Breast cancer
Lung cancer
Antimetabolite chemotherapy agents (adverse effects):
_________ suppression
________tological side effects
_______ syndrome
Bone marrow (myelo-) suppression
Dermatological side effects
Stevens-Johnson Syndrome
Antitumor antibiotic chemotherapy agent prototype:
_________ (Adriamycin)
Doxorubicin (Adriamycin)
Antitumor antibiotic chemotherapy agents MOA:
Bind to ______
(Bonus: MOA similar to what other chemo agent?)
Bind to DNA
(SImilar to alkylating agents)
Antitumor chemotherapy agents are (CCSs/CCNs)
Cell cycle-nonspecific (CCNs)
Antitumor antibiotic chemotherapy agents are used to treat for what six (6) types of cancer?
Solid tumors (bone, bladder, breast, ovary, lung)
Antitumor antibiotic chemotherapy agents (adverse effects):
__________ suppression
Bone marrow suppression
Natural product chemotherapy agent categories:
_______ alkaloids
_______ inhibitors
Vinca alkaloids
Topoisomerase inhibitors
Natural product chemotherapy agent prototype:
_________ (Oncovin)
Vincristine (Oncovin)
Natural products chemotherapy agents MOA:
Bind to _______, which makes up the microtubules of the cells necessary for cell division
Disrupt _________ (resulting in cell death)
Bind to tubulin
Disrupt mitosis
Natural product chemotherapy agents are used as treatment for what two (2) types of cancer?
(Hint: both types are related to one system of the body)
Acute lymphocytic leukemia (ALL)
Natural product chemotherapy agents (adverse effects):
_______toxicity (may take several months to resolve)
Chemotherapy agents adverse reactions are related to what aspect of cancer development?
Rapidly-replicating cells
Myelosuppression (r/t chemotherapy) increases the risk for what three conditions?
Leukopenia: _________
Anemia: _________
Thrombocytopenia: ________
Leukopenia: risk of infection
Anemia: risk of hypoxia
Thrombocytopenia: risk of bleeding
Chemotherapy agents (adverse effects):
Rapidly-replicating __________ epithelial cells
Gastrointestinal epithelial cells
Chemotherapy agents (adverse effects):
Loss of hair from hair follicles
Chemotherapy agents (leukopenia/neutropenia):
Lowest point of WBC level
(Bonus: what does this pose the highest risk for?)
(Highest risk of infection)
Chemotherapy-induced anemia (nursing care):
Minimize __________ expenditures
Watch for signs of ________ deficit (fatigue, dizziness, SOB)
Instruct patient to select foods high in _______ & _______
Provide (large/small) meals with (maximal/minimal) chewing effort
Assist in _______, _________ or other physical activity
Optimize nursing interventions & activities to allow for more _______
Minimize energy expenditures
Watch for signs of oxygen deficit
Instruct patient to select foods high in protein & calories
Provide small meals with minimal chewing effort
Assist in turning, ambulating, or other physical activity
Optimize nursing interventions & activities to allow for more rest
Chemotherapy-induced anorexia (nursing care):
Assess for decreased _______, ________ to food, and _____ loss
Encourage ______, ______ meals with best-tolerated foods
Emphasize high-_______, high-________ foods
Avoid _______ or ______ foods
Try to find new favorite foods after ______ alteration
Cold, soft foods may be soothing in the event of _______
Assess for decreased appetite, aversion to food, and weight loss
Encourage small, frequent meals with best-tolerated foods
Emphasize high-protein, high-calorie foods
Avoid fatty or greasy foods
Try to find new favorite foods after taste alteration
Cold, soft foods may be soothing in the event of stomatitis
Chemotherapy-induced alopecia (nursing care):
Discuss alopecia with patient & family (before/after) it occurs
Encourage a very (long/short) haircut
Instruct client on attaining head ________, such as wigs or turbans
Wash hair gently with a _____-balanced shampoo
Handle hair as (much/little) as necessary
Avoid ________, hairspray, electric ______, and hot air ______/combs
Instruct patient that hair loss is (always/seldom) permanent and that it will regrow within __-__ months after the beginning of chemo treatment
Discuss alopecia with patient & family before it occurs
Encourage a very short haircut
Instruct client on attaining head covers, such as wigs or turbans
Wash hair gently with a pH-balanced shampoo
Handle hair as little as necessary
Avoid bleaches, hairspray, electric curlers, and hot air dryers/combs
Instruct patient that hair loss is seldom permanent and that it will regrow within 6-9 months after the beginning of chemo treatment
Chemotherapy (nursing concerns):
Obtain baseline _______ assessment and ________
Check prescriber's order and verify ______ and patient's _________
Monitor for ________ to chemotherapies
Verify patient's _______ and administer pre-___________
Wear ______ and _______ to protect self from contamination
Assess ________ site for sensation to pain, _________, and __________
Determine drug _______ with tissue damage
Obtain baseline physical assessment and vital signs
Check prescriber's order and verify dosage & patient's body surface area
Monitor for adverse effects to chemotherapies
Verify patient's ID and administer pre-medication
Wear gloves & gown to protect self from contamination
Assess IV infusion site for sensation to pain, burning, and stinging
Determine drug vesicant with tissue damage
Leakage of agents into tissues around IV site
Vesicants can cause permanent ______, ______, and ______ damage
Vesicants can cause permanent nerve, tendon, and muscle damage
Which category of drugs are utilized to reduce adverse effects?
Colony stimulating factors (CSFs)
CSFs regulate growth, differentiation, and function of what type of cells?
CSFs decrease the duration of what two conditions induced by chemotherapy?
Bone marrow stem cells
CSF prototypes (chemotherapy):
_________ (Epogen)
_________ (Neupogen)
Epoeitin Alpha (Epogen): stimulates RBC production
Filgrastim (Neupogen): stimulates neutrophil (WBC) production
Another name for H1-antagonists
H1-antagonists (antihistamines) are widely used to treat...
Allergic rhinitis
H1-antagonist MOA: compete w/___________ for receptor-binding sites after ___________ is released (in response to allergen stimuli)
Compete w/histamine for H1 receptor-binding sites after histamine is released (in response to allergen stimuli)
H1-antagonists are most beneficial when given (before/after) the release of histamine.
Before the release of histamine
1st generation H1-antagonist (antihistamine) prototype
Diphenhydramine (Benadryl)
Diphenhydramine MOA: acts _____ally/________ally, crosses _____-_____ __________
Acts centrally/peripherally, crosses blood-brain barrier
Diphenhydramine: significant central adverse effects (2)
Diphenhydramine: excessive anticholingeric adverse effects (2)
Dry mouth
Urine hesitancy
Downside of using H1-antagonists such as diphenhydramine
Tolerance occurs after several doses
2nd generation H1-antagonist prototypes (3): ________ (Claritin), ________ (Zyrtec), ________ (Allegra)
Loratidine (Claritin)
Cetirizine (Zyrtec)
Fexofenadine (Allegra)
2nd generation H1-antagonist MOA: act peripherally to bind ______ receptors
Do they cross the BBB?
Act peripherally to bind H1 receptors
In comparison to 1st generation H1-antagonists, 2nd gen. has (greater/less) significant central adverse effects (drowsiness, sedation)
Less significant central adverse effects
In comparison to 1st gen, 2nd gen H1-antagonists have (greater/less) anticholingeric effects (dry mouth, urine hesitancy)
Less anticholingeric side effects
Decongestant prototype
Pseudoephendrine (Sudafed)
Pseudoephendrine MOA (1/2):
Activates ______-adrenergic receptors (causing ________________ in nasal mucosa)
Activates alpha1-adrenergic receptors (causing vasodilation in nasal mucosa)
Pseudoephendrine MOA (2/2):
Stimulate _____-adrenergic receptors of respiratory tract (may result in some _____________)
Stimulate beta2-adrenergic receptors of respiratory tract (may result in some bronchodilation)
Pseudoephendrine: administration (2 types)
Intranasal spray
Antitussives: 2 types
Opiod antitussive prototype
Opiod antitussive (Codeine) MOA:
Suppress _______ reflex center in ________
Suppress cough reflex center in medulla
Non-opiod antitussive prototype
Non-opiod antitussive (dextromethorphan) MOA:
Inhibit _______ reflex in throat, ________, ________
Inhibits cough reflex in throat, trachea, lungs
Antitussives: adverse effects (4)
Abuse (CNS toxicity)
Interaction (alcohol/other CNS drugs)
Precautionary conditions associated with antitussive administration (3)
Productive cough
Pre-existing pulmonary disease
Expectorant prototype (two brand names)
Guaifenesin (Robitussin, Mucinex)
Guaifenesin MOA:
Reduce _________/_________ of bronchial secretions
Redue thickness/viscosity of bronchial secretions
While taking an expectorant, what habit should patients abstain from?
Smoking/exposure to 2nd-hand smoke
Indications for bronchodilators (4 diseases)
(Hint: obstructive conditions)
Chronic bronchitis
3 types of bronchodilators
Beta2 agonists
Mechanisms utilized for delivery of pulmonary drugs (2)
Metered-dose inhaler (MDI): less expensive, convenient
Nebulizer: costly
Beta2-adrenergic agonist prototypes (2): ________ (Proventil), _______ (Xopenex)
Albuterol (Proventil)
Levalbuterol (Xopenex)
Levalbuterol (Xopenex) (Beta2 agonist) is expensive, but it causes decreased _______ adverse effects.
Decreased cardiac adverse effects
Beta2 (adrenergic) agonists MOA:
Activate selective beta2-adrenergic agonist receptors in bronchus (results in broncho___________)
Two methods of beta2-adrenergic agonist administration
Inhalation (short-acting)
Oral (long-acting)
Beta2 agonist adverse effects (3)
Methylxiathines prototype
Theophylline (Theolair)
Methylxiathines MOA (1/2):
Increase cyclic _____________ in order to dilate bronchial ________ muscle
Increase cyclic adenosin monophosphate (cAMP)
Dilate bronchial smooth muscle
Methylxiathines MOA (2/2):
Suppress airway responsiveness to stimuli that promote _____________
Suppress airway responsiveness to stimuli that promote bronchospasm
Methylxiathines are not available for which type of administration?
Methylxiathines are at high risk for what complication?
Toxicity (monitor drug level)
Methylxiathines (adverse effects):
Increased cAMP causes...
___________ stimulation (restlessness, insomnia, dizziness)
____________ stimulation (restlessness)
___________ stimulation (palpitation, tachycardia)
___________ effect (urinary frequency)

Multiple _____-_____ interactions
Cerebral stimulation
Skeletal muscle stimulation
Cardiac stimulation
Diuretic effect

Multiple drug-drug interactions
Anticholinergic prototype: _______ (Atrovent)
Ipatropium (Atrovent)
Anticholinergic MOA:
Block ___________ receptors in bronchial ________ muscle
Reduce nasal ______________
Block cholinergic receptors in bronchial smooth muscle
Reduce nasal hypersecretion
A respiratory measurement test in which a device that clips on the finger measures the saturation of hemoglobin in the blood
Pulse oximetry
Respiratory measurement that gauges the maximum speed that air is exhaled from the lungs
Peak flow measurement
Infectious disease caused by Mycobacterium tuberculosis
Tuberculosis (TB)
Anti-TB agents MOA:
Kill/inhibit ___________ organism (often given in ___________)
Kill-inhibit Mycobacterium organism (often given in combination)
Giving TB drugs in combination decreases risk of drug ____________ due to ___________
Decreased risk of drug resistance due to mutation
Administration of anti-TB drugs is long and complex, usually lasting anywhere from __ months to __ years.
6 months-2 years
TB treatment in which healthcare provider directly observes the patient swallowing pills and provides education (everywhere, all the time)
Directly-observed therapy (DOT)
Evaluation for successful treatment of TB
Negative sputum culture/CXR
Anti-TB drug prototype
Isonizid (NIH)
Isonizid (NIH) MOA:
Inhibits synthesis of ______ _____ on cell wall
Bacteriocidal in ________-________ organisms
Bacteriostatic in ____________ mycobacteria
Inhibits synthesis of mycolic acid on cell wall
Bacteriocidal in rapidly-dividing organisms
Bacteriostatic in dormant mycobacterium
Most effective/safest anti-TB drug (1st line)
Isonizid (NIH)
Isonizid (NIH) is used as what two types of TB treatment?
Active treatment
Patients taking Isonizid (NIH) for TB must be monitored for therapeutic effectiveness in the first __-__ weeks of treatment
First 2-3 weeks of treatment
Proton pump inhibitors (PPIs): bind __-__-__ase enzymes in the stomach IRREVERSIBLY, preventing secretion of ___
Bind H+-K+-ATPase enzymes
Prevent secretion of gastric acid
PPIs prototype: _________ (Nexium)
Esomeprazole (Nexium)
PPIs are widely prescribed for treating ___ and ___
Other PPI prototypes (2):
__________ (Prevacid)
__________ (Protonix)
Lansoprazole (Prevacid)
Pantoprazole (Protonix)
PPIs pharmacokinetics:
Take __-__ minutes before (1st/2nd/3rd) meal (proton pump activated by food)
Take 20-30 minutes before first meal
H2 antagonist prototype (GI):
__________ (Zantac)
(Bonus: widely prescribed for what 2 conditions?)
Ranitidine (Zantac)
H2 antagonist (Ranitidine) MOA:
Block ____ receptors on parietal cells in the stomach to reduce acid production
Suppress ______ and _______ basal gastric acids
Block H2 receptors on parietal cells in the stomach to reduce acid production
Suppress daytime and nocturnal basal gastric acids
H2 antagonists pharmacokinetics:
Rapid absorption from _____ intestine (___ minutes onset of action)
Short half life/rapid excretion (from __-__ hours)
No known effects on _____
Rapid absorption from small intestine (30 minute onset of action)
Short half life/rapid excretion (from 1-4 hours)
No known effects on fetus
Antacids are used for treating symptoms of ________ (alkaline agents)
(Bonus: how is this achieved?)
Symptoms of heartburn
(Neutralization of stomach acid)
Four types of antacids
Prototype antacid: __________ (AlternaGel)
Aluminum hydroxide (AlternaGel)
Sodium bicarbonate antacids (2)
Baking soda
Magnesium hydroxide antacid (1)
Milk of Magnesia
Calcium carbonate antacids (2)
Aluminum hydroxide antacid (1)
Sodium bicarbonate antacids adverse effects:
______ retention
Contraindicated with ___________ ______ failure
Fluid retention
Congestive heart failure
Magnesium hydroxide antacids adverse effects:
Fatigue, _____tension, dysrhythmias, _____magenesemia in ______ disease
Hypermagnesemia in renal disease
Calcium carbonate antacid adverse effects:
Constipation, aggravated kidney _______, milk-_____ syndrome, rebound hyper______ and metabolic ________
Aggravated kidney stones
Milk-alkali syndrome
Rebound hyperacidity
Metabolic alkalosis
Aluminum hydroxide antacids adverse effects:
Constipation and ______phosphatemia
Some antacid combinations have the tendency to cause (respiratory/metabolic) (alkalosis/acidosis)
Metabolic alkalosis
Anticholinergic/antihistamine agents also given as antiemetic agents:
_________ (Antivert)
_________ (Hyoscine) patch
Meclizine (Antivert)
Scopolamine (Hyoscine) patch
Antipsychotic/antidopaminergic agents also given as antiemetics:
_____________ (Reglan)
_____________ (Phenergan)
Metoclopramide (Reglan)
Promethazine (Phenergan)
Benzodiazepine agent also given as antiemetic agent:
_________ (Ativan)
Lorazepam (Ativan)
Cannabinoids are given as antiemetic agents in the active ingredient form of _________
Corticosteroid agent also given as an antiemetic agent:
___________ (Decadron)
Dexamethasone (Decadron)
Serotonin (5-HT3) antagonist agent also given as an antiemetic agent:
_____________ (Zofran)
Ondansetron (Zofran)
Antiemetics (nursing concerns):
Assess 3 statuses (what are they?)
Place on ____-lying position with altered ____ to prevent aspiration
Withhold ____ and _____ until nausea subsides (and then start slowly)
Monitor for ___________ symptoms (EPS) in elderly, emaciated patients, and children
Instruct not to ______ or other hazardous activities
Avoid ______
Nutritional, fluid, and electrolyte status
Side-lying position with altered LOC
WIthhold foods and fluids
Monitor for Extrapyramidal symptoms
Instruct not to drive
Avoid alcohol
Agents that increase the frequency and quality of bowel movements
Bulk-forming laxative prototype:
__________ (Metamucil)
(Bonus: also given as _______/______ of constipation)
Psyllium mucilloid (Metamucil)
(Prevention/treatment of constipation)
Bulk-forming laxatives MOA:
Attracting _____ and thus increasing fecal bulk
Attracting water and thus increasing fecal bulk
Bulk-forming laxatives nursing concerns:
Take __-__ hours to work
Take with plenty of ______
Take 24-48 hours to work
Take with plenty of water
Stool softener/surfactant prototype:
_________ (Colace)
Docusate (Colace)
Stool softener/surfactant MOA:
Cause more ____ and ____ to be absorbed into stools
Cause more water and fat to be absorbed into stools
Stool softeners/surfactants are often used for __________, not treatment, of constipation (surgery, injury, and MI)
Prevention, not treatment
Stool softener/surfactant adverse effects (2)
Abdominal cramping
Stool softener/surfactant nursing concerns:
Take __-__ hours to work
24-48 hours to work
Laxatives (nursing concerns):
Complete ______ and _______
_______ movement and ___ functioning
Dietary and lifestyle _______ for optimal GI function
Avoid long-term use of laxatives to prevent _________
Determine _________ before administration
Complete history and assessment
Bowel movement and GI functioning
Dietary and lifestyle education for optimal GI function
Avoid long-term use of laxatives to prevent dependence
Determine etiology before administration
Anti-diarrheal agents prototype (opiod):
___________ (Lomotil)
Diphenoxylate with atropine (Lomotil)
Anti-diarrheal agent (Lomotil) MOA:
Act on ______ muscle cells in intestine to slow _______ (decrease cramping associated with severe diarrhea)
Act on smooth muscle cells of intestine to slow peristalsis
Anti-diarrheal agents prototype (non-opioid):
____________ (Pepto-Bismol)
Bismuth subsalicyclate (Pepto-Bismol)
Bismuth subsalicylate is given OTC as a PO agent against ________, ____ infection and diarrhea
H. pylori infection
In the stomach, bismuth subsalicylate turns to salicylic acid-users should take caution for salicylate toxicity if also using _______
ASA (aspirin)
Bismuth subsalicylate should not be administered to children with flu symptoms for what reason?
Reye's Syndrome
Which anti-diarrheal agent is more effective for control of severe diarrhea: Lomotil (opiod) or Pepto-Bismol (non-opiod)?
Lomotil (opiod)
Cardiac glycoside prototype:
___________ (Lanoxin, Lanoxicaps)
Digoxin (Lanoxin, Lanoxicaps)
Digoxin MOA:
Increases cardiac ___________ (positive inotropic)
Slows electrical ___________ (negative dromotropic)
Slows _______ rate (negative chromotropic)
Inhibits ___-___-___ase pump (compete w/potassium)
Increases cardiac contractility
Slows electrical conduction
Slows heart rate
Inhibits Na+-K+-ATPase pump
Therapeutic index of Digoxin, cardiac glycosides
Is this narrow or broad?
0.5-2.5 ng/mL (narrow)
Cardiac glycosides (adverse effects):
CV: ____ block, dysrhythmias
GI: __________ and NV
Vision: colored vision (________) and _____ vision
CV: AV block, dysrhythmias
GI: anorexia and NV
Vision: colored vision (yellow) and halo vision
With which two categories of patients should precaution be taken when administering cardiac glycosides?
Older patients
Renal-impaired patients
Nursing concerns (digoxin toxicity):
___________ digoxin (D/C)
Determine serum _______ levels and __________
Supportive therapy for _____ symptoms
Monitor and treat ___________
Digoxin immune FAB (__________) for severe overdose
Discontinue digoxin
Determine serum digoxin levels and blood electrolytes
Supportive therapy for GI symptoms
Monitor and treat arrythmias
Digoxin immune FAB (Digiband) for severe overdose
A series of large doses of digoxin, given to quickly reach therapeutic level
(Bonus: By way of what administration?)
Condition characterized by severe chest pain often radiating to left shoulder, arm, or jaw (brought on by physical exertion or emotional stress)
Angina pectoris
Angina pectoris drugs improve blood supply by dilating ______ to reduce (pre/afterload)
Lower oxygen demand by slowing _______ rate, reducing _________ and lowering ________ _______ to reduce (pre/afterload)
Blood supply:
Dilating veins to reduce preload

Slowing heart rate
Reducing contractility
Lowering blood pressure to reduce afterload
Organic nitrate prototype:
___________ (Nitrostat)
Nitroglycerin (Nitrostat)
Nitroglycerine (Nitrostat) MOA:
Forms ______ ______ to trigger the release of calcium ions
(Relaxes ________ muscle, reduces preload; relaxes _________ muscle, increases blood flow)
Form nitric oxide to trigger the release of calcium ions
(Relaxes venous muscle, reduces preload; relaxes arterial muscle, increases blood flow)
Adverse effects (organic nitrates):
______tension--reflex _____cardia
Headache, ________ vision, _________
Drug ________
Hypotension--reflex tachycardia
Headache, blurred vision, syncope
Drug tolerance
Always check ____ and ____ before administration of sublingual nitroglycerine
BP and HR
Determine chest pain _________, duration, and __________ as well as ____________ factors before administering sublingual nitroglycerine
Chest pain location, duration, and intensity
Precipitating factors
Routine administration of sublingual nitroglycerine takes places every ____-____ hours
Every 6-8 hours
Sublingual nitroglycerine is given every ____ minutes for chest pain as needed x3, but you MUST call 911 if the chest pain is not relieved
Every 5 minutes
Protect sublingual nitroglycerine tablets from light by storing them in a _______ bottle
Brown bottle
Topical nitroglycerine ointment administration:
Wear _______
Avoid ______
Wash __________ application site
Remove in the incidence of _________
Apply with _____________ to avoid overdose
Wear gloves
Avoid "hair"
Wash previous application site
Apply with "appli-ruler" to avoid overdose
____ nitroglycerine is only utilized in _________ care settings, with specialized IV _________
IV nitroglycerine
Specialized IV tubing
Administration of IV nitroglcerine involves constant _________ and _________ monitoring
Constant cardiac and hemodynamic monitoring
IV nitroglycerine is often titrated to the amount of _______ _______
Amount of chest pain
Beta adrenergic antagonist (blocker) prototype:
________ (Inderal)
Propanolol (Inderal)
Beta-blocker MOA:
Reduce ______ rate and ________, lowering _____________ oxgen demand
Reduce ___________
Protect against ____
Reduce heart rate and contractility, lowering myocardial oxygen demand
Reduce dysrhythmias
Protect against MI
Other beta-blocker prototypes (2):
_______ (Lopressor)
_______ (Tenormin)
Metoprolol (Lopressor)
Atenolol (Tenormin)
Noncardioselective beta-blockers may exacerbate...
Dihydropyridine calcium channel blocker prototypes (3):
_______ (Adalat)
_______ (Norvasc)
_______ (Cardene)
Nifedipine (Adalat)
Amlodipine (Norvasc)
Nicardipine (Cardene)
Calcium channel blockers that bind reversibly to closed-type calcium channels
Calcium channel-blockers MOA:
Selectively block calcium channels in ________ smooth muscle
Decrease amount of calcium available for __________ contraction
Selectively block calcium channel in vascular smooth muscle
Decrease amount of calcium available for muscle contraction
Dihydropyridine calcium channel blocker indications (2)
Angina pectoris
ACE inhibitors prototypes (3):
(Hint: ___-pril)
ACE inhibitors MOA:
Reduce conversion of ___________ I to ___________ II
Reduce ___________ effects
Increase effectiveness of _________
Protect _________
Reduce conversion of angiotensin I to angiotensin II
Reduce aldosterone effects
Increase effectiveness of diuretics
Protect kidneys
ACE inhibitor adverse effects:
Persistent _______
Postural _______
Persistent cough
Postural hypotension
Alpha2 agonists prototypes (2):
________ (Catapres)
________ (Aldomet)
Clonidine (Catapres)
Methyldopa (Aldomet)
Alpha2 agonists MOA:
Unknown _________-acting mechanism unrelated to ______ receptors
Reduce __________ nerve impulses
Unknown centrally-acting mechanism unrelated to alpha2 receptors
Reduce sympathetic nerve impulses
Alpha2 agonists (adverse effects):
Central (3): ________, depression, _______
Decreased _______/impotence
Positive ________ test (anemia)
Drowsiness, depression, sedation
Decreased libido/impotence
Positive Coombs test (anemia)
Alpha1 antagonists prototypes (2):
________ (Minipress)
________ (Cardura)
Prazosin (Minipress)
Doxazosin (Cardura)
Alpha1 antagonists (blockers) MOA:
Block ______ receptors
Relax _______ and _______ smooth muscle
Block alpha1 receptors
Relax arterial and venous smooth muscle
Alpha1 blockers (adverse effects):
___________ hypotension
_______ dose effect (hypotension)
Orthostatic hypotension
First dose effect (hypotension)
Direct-acting vasodilators prototype:
_________ (Apresoline)
Hydrylazine (Apresoline)
Direct-acting vasodilators MOA:
Dilate _______ smooth muscle directly (some also affect _____)
Dilate arterial smooth muscle directly (some also affect veins)
Direct-acting vasodilators (adverse effects):
Reflex _______
________ retention
Note: adverse effects can be minimized with _____ blockers and ______
Reflex tachycardia
Fluid retention
Note: adverse effects can be minimized with beta-blockers and diuretics
Indications for diuretic agents (5):
_______/______ failure
_______ failure/cirrhosis
_________ edema
Heart/kidney failure
Liver failure/cirrhosis
Pulmonary edema
Diuretic agents (adverse effects):
_________ imbalances
Electrolyte imbalances
Loop diuretic prototype
Furosemide (Lasix)
Loop diuretics MOA:
Block ____, ____, and ____ reabsorption at (ascending/descending) loop of Henle
Block Na+, K+, and Cl- reabsorption at ascending loop of Henle
Loop diuretics adverse effects:
Drug ________
Drug interactions
Thiazide prototype:
___________ (HydroDIURL, HCTZ)
Hydrochlorothiazide (HydroDIURL, HCTZ)
Most commonly prescribe thiazde
Hydrochlorothiazide (HydroDIURL, HCTZ)
Thiazdes MOA:
Block ___ reabsorption at (distal/proximal) tubule, resulting in less ____ reabsorption (remember: what follows salt?)
BLock Na+ reabsorption at distal tubule, resulting in less water reabsorption
Thiazides adverse effects (2)
Gout attacks
Blood dyscrasias
Potassium-sparing diuretics prototype:
_______ (Aldactone)
Spironolactone (Aldactone)
Potassium-sparing diuretics MOA:
Inhibit action of _______ in (distal/proximal) tubule and ______ ducts of nephron
Increase ______, chloride, and _____ excretion while ______ is retained
Inhibit action of aldosterone in distal tubule and collecting ducts of nephron
Increase sodium, chloride, and water excretion while potassium is retained
Potassium-sparing diuretics adverse effects:
Hyper_______, life-threatening cardiac ________
Life-threatening cardiac dysrhythmias
Osmotic diuretics prototype:
________ (Osmitrol)
Mannitol (Osmitrol)
Osmotic diuretics MOA (1/2):
Increase _______ of of the filtrate to pull water from __________/__________ space into ________ space
Increase osmolality of filtrate to pull water from intracellular/interstitial space into vascular space
Osmotic diuretics MOA (2/2):
Decreased _____ and ______ through filtration by glomerulus but incapable of being reabsorbed by renal ______
Decreased water and sodium through filtration by glomerulus but incapable of being reabsorbed by renal tubule
Osmotic diuretics indications:
Increased intra_____/______ pressure
______ failure
Increase intracranial/intraoccular pressure
Renal failure
Osmotic diuretics adverse effect:
Rebound increase in ____ and ______ (leakage of fluid)
Rebound increase in ICP (intracranial pressure) and extravasation
A substance to prevent or delay coagulation of the blood, or inhibit enlargement of blood clots
A substance to prevent platelet plugs from forming and benefit in defending the body against heart attacks and strokes
A substance to dissolve clots
A substance to promote coagulation
Hemostatic agent
Parenteral anticoagulant prototype
Heparin is given first as a ____ dose and then ________ infusion
First as a loading dose and then continuous infusion
Parenteral anticoagulants MOA:
Activation of _____________, which inhibits thrombin and (to lesser extent) factor Xa
Prevents new _________ formation and growth of existing _________ but does not dissolve _______)
Activation of antithrombin III, which inhibits thrombin and (to lesser extent) factor Xa
Prevents new thrombus formation and growth of existing thrombi but does not dissolve thrombus)
Pertinent lab value for administration of parenteral anticoagulants (how often?)
APTT q6hr
Antidote for parenteral anticoagulant (heparin) overdose
Protamine sulfate
Parenteral anticoagulants indication:
____ prophylaxis
DVT prophylaxis
What route and location are preferred for heparin?
Preferably into abdomen (rotate site)
What must you NEVER do when adminstering heparin?
Aspirate the syringe
Oral anticoagulant prototype
Warfarin (Coumadin)
Warfarin MOA:
Inhibits two enzymes involved in formation of activated ________
Inhibits synthesis of new ______ _______ (prevents new thrombus formation but does not dissolve the thrombus)
Formation of activated vitamin K
Inihibits synthesis of clotting factors
Pertinent oral anticoagulant (Warfarin) lab test(s) (how often before discharge? afterward?)
Every day before discharge
Weekly to biweekly afterward
Warfarin antidote
Vitamin K (Aqua-MEPHYTON)
Warfarin indication:
Used in IV _______ until therapeutic (lab test) achieved, and then Coumadin is administered only
Used in IV heparin
Anticoagulant safety concerns:
Bruising from ________
Monitor for _______ bleeding (gums, urine, stool)
Use soft ________
No ____ drugs without physician approval
No ____ or _______s
For warfarin, avoid cabbage, cauliflower, kale, _______, some ________, egg yolks, liver, and ______
Bruising from venipuncture
Monitor for subclinical bleeding (gums, urine, stool)
Use soft toothbrush
No OTC drugs w/o physician's approval
Avoid cabbage cauliflower, kale, spinach, some cheeses, egg yolks, liver, and tomatoes
Antiplatelet agents prototype
Acetylsalycylic acid (ASA)
Antiplatelet agents MOA:
Reducing platelet __________ through reversibly inhibiting platelet ______ (low-dose) and _______ (high-dose)
Reducing platelet aggregation through irreversibly inhibiting platelet COX-1 and COX-2
Antiplatelet agents indication:
Prevention of _______ and ______ (low dose, 81 mg/day), acute ___ (medium dose, 162-325 mg/day)
Prevention of heart attack and stroke
Prevention of acute MI
Antiplatelet agents safety concerns:
Subclinical bleeding such as _______ and _______
GI ________ or irritation
Subclinical bleeding such as petechiae or acchymosis
GI hemorrhage or irritation
Pinpoint, unraised, round, red spots under the skin (caused by bleeding)
Extravasation of blood underneath the skin (a bruise)
Thrombolytic agent prototype:
_______ (Activase)
Alteplase (Activase)
Altepase (Activase) MOA:
converts _______ to ______, which then dissolves _____ clots
degrades ________ factors V & VIII
lowers circulating amount of _______ and ______
Converts plasminogen to plasmin, which then dissolves fibrin clots
Degrades procoagulant factors V & VIII
Lowers circulating amount of fibrinogen and plasminogen
Altepase (Activase) indications:
generally used when life is jeoparized by presence of a(n) ___________
Presence of an intravascular clot
Thrombolytic agents (safety concerns):
Excessive ________
IV given in critical care units with close monitor of __________
Excessive bleeding
IV given in critical care units with close monitor of hemodynamics
Neutral fats stored in adipose tissue as an energy resource
Substances manufactured in the liver to make estrogen
Lipoprotein type responsible for delivery of most cholesterol to blood vessel periphery, contributing to plaque buildup
(Hint: "bad" cholesterol)
Low-density lipoproteins (LDLs)
Lipoprotein type responsible for transport of cholesterol back to the liver
High-density lipoproteins (HDLs)
Statin agent prototypes:
_________ (Mevacor)
_________ (Zocor)
_________ (Lescol)
(Hint: -statin)
Lovastatin (Mevacor)
Simvastatin (Zocor)
Fluvastatin (Lescol)
Statin agents MOA:
Inhibit _______ of cholesterol, thereby lowering cholesterol
Bonus: specific enzyme inhibited?)
Inhibit precursor of cholesterol, thereby lowering cholesterol
(HMG-CoA Reductase)
Statin agents (adverse effects):
GI effects (2)
_______lysis (deposit of myoglobin into the blood, causing kidney damage)
Statin agent interactions:
Which medication?
Which foodstuff? (Hint: fruit)
Statin agents (nursing concerns):
Administer in the _______, when cholesterol _______ is at its peak
Administer in the evening, when cholesterol synthesis is at its peak
Bile-sequestering agent prototype:
__________ (Questran)
Cholestyramine (Questran)
Bile-sequestering agents MOA:
Bind to ______
Form (soluble/insoluble) complexes containing cholesterol (excreted in _____)
Lower (HDL/LDL) cholesterol level by increasing (HDL/LDL) receptors on hepatocytes
Bind to bile acids
Form insoluble complexes containing cholesterol (excreted in feces)
Lower LDL cholesterol level by increasing LDL receptors on hepatocytes
Bile-sequestering agents interactions:
Which two medications?
Bile-sequestering agents contraindications:
Complete _______ obstruction
Complete biliary obstruction
HPT/lipid/cholesterol reducing agents (adverse effects):
Three (3) GI effects
Condition in which the body cannot absorb fat, causing a buildup of fat in the stool (loose, greasy, foul-smelling bowel movements)
HPT/lipid/cholesterol reducing agents (nursing concerns):
Increased ______, ______- and ______-intake
Monitor for ______ and ______ (low Vitamin K)
Other medications should be taken __ hour(s) before or __ hours(s) after administration
Teaching plans for nutrition of ____-soluble vitamins (3) and supplement use
Increase exercise, water- and fiber-intake
Monitor for bruising and bleeding
Other medications should be taken 1 hour before or 4 hours after administration
Teaching plans for nutrition of fat-soluble vitamins (A, E, & K) and supplement use
Nonselective adrenergic agonist prototypes:
__________ (Adrenalin)
__________ (Efedron)
(Bonus: which is an OTC bronchodilator?)
Epinephrine (Adrenalin)
Ephedrine (Efedron) (OTC bronchodilator)
Epinephrine (Adrenalin) is commonly administered during _____________ situations
Emergency situations
Epinephrine (Adrenalin) MOA:
Activates both ______/______ receptors
Activates both alpha/beta receptors
Epinephrine (Adrenalin) is used to treat:
_________ arrest
(i.e. ___________ allergic reaction)
Cardiac arrest
(i.e. anaphylactic allergic reaction)
Alpha-1 (adrenergic) agonist prototype:
_______ (Neo-Synephrine)
Phenylephrine (Neo-Synephrine)
Alpha-1 agonist MOA:
Activates _______-__________ receptors
Activates alpha-adrenergic receptors
Phenylephrine (Neo-Synephrine) is generally prescribed for nasal __________/_____tension
Nasal congestion
Phenylephrine (Neo-Synephrine) may be used to produce ___________ (________ dilation) during opthalmic exams
Mydriasis (pupil dilation)
Alpha-1 adrenergic agonist used solely for nasal congestion
(Hint: ________ [Sudafed])
Pseudoephendrine (Sudafed)
Alpha-1 adrenergic agonist used solely for ocular use (pupil dilation)
(Hint: ___________ [Murine])
Tetrahydrozoline (Murine)
Adrenergic agonists (general) prescribed for treatment of hypertension (nonautonomic mechanisms)
Alpha-2 agonists
Critical care adrenergic agonists (general) used for heart attack, heart failure, shock (powerful cardiac effects)
Beta-1 agonists
Adrenergic agonists (general) used to treat asthma
Beta-2 agonists
Beta-2 agonist (asthma) prototype:
__________ (Proventil)
Albuterol (Proventil)
Beta-2 agonist (pre-term labor) prototype & MOA:
___________ (Brethine)
Reduced pre-term labor contraction of ________
Terbutaline (Brethine)
Reduced pre-term labor contraction of uterus
General adverse effects of adrenergic agonists (10)
Pulmonary edema
Cardiac arrest
Three names for cholinergic antagonists:
________ blockers
Cholinergic blockers
Cholinergic antagonist purpose:
dilation of ________/drying of ________/increased ______ rate/_______dilation
Dilations of pupils
Drying of secretions
Increased heart rate
Cholinergic antagonists (blockers) MOA:
Block effects of acetylcholine at _______ or _______ receptors
Block effects of acetylcholine at muscarinic or nicotinic receptors
Cholinergic blockers compete with acetylcholine for binding at _______ receptors
Muscarinic receptors
Muscarinic antagonist (blocker) prototype
Muscarinic blockers MOA:
block ___________ receptors (at therapeutic doses)
May block both __________ and __________ receptors at high doses
Induce symptoms of ______-or_______ response
Block muscarinic receptors (at therapeutic doses)
May block both muscarinic and nictonic receptors at high doses
Induce symptoms of "fight-or-flight" response
Muscarinic antagonists are used to treat _____cardia/_____dose for muscarinic agonist overdose
Antidose for muscarinic agonist overdose
Muscarinic antagonist prototype used as anesthesia and to prevent motion sickness
(Hint: __________ [Transderm Scop])
Scopolamine (Transderm Scop)
Muscarinic antagonists: adverse effects:
Drying of ____/_____ mucosa
Urinary __________
Increased ________/________
Blurred _______/_______phobia
Drying of oral/nasal mucosa
Urinary retention
Increased heart rate/arrythmias
Blurred vision/photophobia
Centrally-acting agents (i.e. alpha-2 agonists)
(Used for what type of pain?)
(Mild or moderate pain)
Drugs used to treat severe pain
Drugs used to treat chronic pain with neuropathic nature
Adjuvant analgesics
NSAID prototypes (2)
Aspirin (ASA)
Ibuprofen (Motrin, Advil)
Inhibit the activity of ________ to decrease formation of prostaglandins
Cyclo-oxygenase (COX)
Have anti______, anti______, and anti____ aggregation properties
Anti-platelet aggregation
NSAIDs do not produce the same severe adverse effects as _____
NSAIDs adverse effects:
_______ due to irritated gastric mucosa, increased gastric acid secretion (due to inhibition of what?)
______ impairment
______ impairment
Peptic ulcer disease (prostaglandin inhibition)
Renal impairment
Hepatic impairment
Other NSAID prototypes:
_______ (Celebrex)
_______ (Toradol)
Celecoxib (Celebrex)
Ketorolac (Toradol)
Acetaminophen (Tylenol) MOA:
blocks transmission of ____ impulses to brain in response to inhibition of ________ synthesis
Blocks transmission of pain impulses to brain in response to inhibition of prostaglandin synthesis
Although Tylenol inhibits prostaglandin synthesis, it is not a COX inhibitor like ______
Apsirin (ASA)
Acetaminophen has anti______ properties, but no anti______ or anti______ properties
Antipyretic properties
No anti-inflammatory
No anti-platelet aggregation
Acetaminophen (overdose) adverse effects:
_______ dysfunction
____ stools
______ bruising
Hepatic dysfunction
Pale stools
Flank bruising
When taking acetaminophen, patients should avoid _______ to reduce toxic hepatic effects
Alcohol (EtOH-ethanol)
Analgesics that are interchangeable with opiods (also include heroine, marijuana, cocaine, and amphetamines)
Opiod agonists MOA:
activate ____ and _____ receptors
Activate mu and kappa receptors
Opiod agonist indications:
Relieve ______ to _____ pain which cannot be controlled by other analgesics
Relieve moderate to severe pain which cannot be controlled by other analgesics
Opiods are the highest causative analgesics for ________ depression by (kappa/mu) receptors
Respiratory depression by mu receptors
Opiod agonists provide (more/less) analgesia without respiratory depression when attached to (kappa/mu) receptors
Less analgesia
Kappa receptors
Mixed opiod ______/_______ activate on one receptor (i.e. kappa or mu) but block the effects on the other receptor
Mixed opiod agonists/antagonists
Opiod antagonists block _____ and _____ receptors
(What are they used to treat?)
Block kappa and mu receptors
(Opiod overdose)
Opiod agonist adverse effects:
____ depression
____ side effects (which 2 types?)
______ retention
______ depression
Physical dependence
CNS depression
GI side effects (constipation, NV)
Urinary retention
Respiratory depression
Physical dependence
Which two opiod agonists cause the greatest GI disturbances?
Opiod agonists have the tendency to cause drug _______. What does this mean for the dosage?
Drug tolerance
Increasingly larger doses are required to achieve pain relief
Opiod agonist tolerance is frequently seen in which type of pain?
Chronic pain
Opiod agonists produce which type of symptoms if stopped abruptly?
Withdrawal symptoms
Opiod agonist dependence produces a pattern of _________ drug use, continued _______ and use of the drug for an effect other than _________
Pattern of compulsive drug use
Continued craving
Use for effect other than pain relief
Despite their addictive qualities, less than ___% of patients become addicted to opiod agonists.
Less than 1%
Narcotic analgesics:
Endogenous opiod (produced naturally by body)
Narcotic analgesics prototype: ________ sulfate
Morphine sulfate
Narcotic analgesic (morphine sulfate) MOA:
Activate ___ and _____ receptor site in the _____ and ______ to alter release of (afferent/efferent) neurotransmitters
Activate mu and kappa receptor sites in brain and spinal cord to alter release of afferent neurotransmitters
Morphine sulfate MOA (2/3):
Alter ______ of and _______ response to pain
Alter perception of and emotional response to pain
Morphine sulfate MOA (3/3):
produce ______ and _______
Produce analgesia and euphoria
Narcotic analgesic (morphine sulfate) indications (2)
Chest pain
Congestive heart failure
Narcotics dilate _____ to reduce (preload/afterload)
Dilate veins to reduce preload
The euphoric effect of narcotics comes about by reducing the effects of ______ and the production of _________
Reducing effects of anxiety, production of chatecholamines
Narcotics nursing concerns:
Avoid _______ or ________ disease
Avoid gallbladder or pancreatic disease
(Biliary spasms)
Secondary narcotic prototype
________ __________ (Demerol)
Meperidine hydrochloride (Demerol)
The narcotic meperidine hydrochloride (Demerol) is used as a _______ sedative and also for ______ analgesia
Pre-operative sedative
Obstetric analgesia
Meperidine hydrochloride (Demerol) causes less ________ than morphine, but unfortunately it is not as strong of a pain killer.
Less biliary spasm
The narcotic codeine is used for treating _____ to ______ pain as well as acting as an ________ at lower doses
Mild-to-moderate pain
Antitussive at lower doses
Codeine indications:
post-op _______ or ______ injury
Post-op craniotomy or head injury
(Due to less CNS depression)
What does "PCA" stand for?
Patient-controlled analgesia
What type of analgesic is utilized for PCA?
The priority of PCA is to maintain a consistent _____ level of narcotics
Consistent blood level of narcotics
Good news: though first impression might seem otherwise, PCA is specifically designed to prevent ________ (hooray!)
Prevent overdose
What must be documented concerning PCA? (3 components)
# of attempts
# of deliveries
Total amount of drug given
Narcotic antagonist prototype:
_________ (Narcan)
Naloxone (Narcan)
Narcotic antagonists (Naloxone) MOA:
Compete with _____ agonists for mu and kappa receptors
Compete with OPIOD AGONISTS for mu and kappa receptors (My guess is that opiod agonists & narotic agonists are so similar, narcotic antagonists can hold both of them at bay)
Narcotic antagonists (Naloxone) antagonize all effects of what type of analgesic? Which one specifically?
Opiods (morphine)
Narcotic antagonists have the tendency to cause reverse...
__________ depression
(Well, that's awkward.)
Respiratory depression
Narcotic antagonist indications:
Suspected _______ overdose
_______/_______ depression (after what drug type?)
Suspected narcotic overdose
Cardiovascular/respiratory depression (after opiods)
In the event of narcotic overdose (eekk!!), narcotic antagonists are to be administered via ___ and may be repeated every ___ minutes
Local anesthetics cause loss of sensation in (large/small) areas of the body
Small (limited) areas of the body
Two major classes of local anesthetics
Ester-type local anesthetic:
__________ (Novocaine)
Procaine (Novocaine)
Amide-type local anesthtic:
________ (Xylocaine)
Lidocaine (Xylocaine)
Local anesthetics MOA:
blockage of _______ channels
Blockage of sodium channels
(Sodium channel-blockers...imagine that)
Which type of local anesthetic has lower incidence of adverse effects: ester-type, or amide-type?
Amide type
Ester-type local anesthetics are used as what two types of anesthesia?
Ester-type local anesthetics (spinal) are used for surgery on what three areas of the body?
Lower abdomen
Inguinal region
Lower extremities
Ester-type local anesthetics (spinal) are used for patients with what (3) types of diseases?
Respiratory disease
Hepatic disease
Kidney disease
When ester-type local anesthetics are administered, the patient should be placed in what position? Why? (i.e. to prevent what?)
(To prevent diaphragmatic paralysis, respiratory depression)
Ester-type local anesthesia (topical) is used for what type of skin/tissue pain?
Poison ivy dermatitis
Ester-type (topical) local anesthesia is also used as throat _______ and for ______/itching
Throat lozenges
Ester-type local anesthetics (topical) may be administered with what other type of drug? What does is bring about?
Why would you administer ester-type, local (topical) anesthetics with epinephrine to bring about vasoconstriction? (2)
To limit blood loss at surgical sites
To prolong anesthesia duration
Ester-type local anesthetics (topical) should NEVER be applied to what five sites? (Why?)
(To avoid possible necrosis)
Which type of anesthetics are used to treat muscle spasms and spasticity?
Skeletal muscle relaxants
Two major classes of skeletal muscle relaxants
Centrally-acting (Baclofen, Tizonidine)
Peripherally-acting (Flexeril, Dantrium, NSAIDs)
Centrally-acting skeletal muscle relaxant prototype:
Cyclobenzaprine (Flexeril)
Peripherally-acting skeletal muscle relaxant prototype:
________ (Dantrium)
Dantrolene Sodium (Dantrium)
Centrally-acting skeletal muscle reactants are believed to act on the CNS and are related to _______ effects
Related to sedative effects
Peripherally-acting skeletal muscle relaxants act (directly/indirectly) on skeletal muscle to relieve spasticity
Act directly on skeletal muscle
Involuntary contraction caused by injury or overuse of skeletal muscle
Muscle spasms
Nonpharmacological interventions for muscle spasms:
As well as nonpharmacological and pharmaceutical interventions, what other type of treatment is utilized for muscle spasms?
Herbal remedies
What type of drugs are given for mild muscle spasms?
NSAIDs (ASA, ibuprofen)
What type of drugs are given for moderate-to-severe spasms?
Centrally-acting skeletal muscle relaxants
Continuous state of contraction in certain muscle groups
Muscle spasticity
What type of diseases form the etiologies for muscle spasticity?
Neuromuscular diseases (spinal cord injury, cerebral palsy, dystonia, etc)
What interventions are applied for management of muscle spasticity? (3)
Direct-acting muscle relaxants
Physical therapy
CNS muscle relaxants
What two CNS muscle relaxants are adminstered for muscle spasticity?
"Master gland" that controls hormone secretion from ALL other glands
Pituitary gland
Pituitary hormones affect all functions and systems related to what four types of body functions?
Fluid & electrolyte balance
What is the major hormone located in/secreted from the pituitary?
Antidiuretic hormone (ADH)
(But as we learned in Patho, oxytocin is also secreted by the POSTERIOR pituitary. So there.)
Which brain structure releases and inhibits hormones that regulate the pituitary?
Prototype pituitary hormones:
________ (Pitressin)
________ (DDAVP)
Vasopressin (Pitressin)
Desmopression (DDAVP)
What are the (3) indications for administration of pituitary hormones (vasopressin, desmopression)?
Diabetes insipidus
Gastrointestinal hemorrhage
Nocturnal enuresis
Diabetes insipidus is caused by insufficient production of what pituitary hormone? By what two structures?
Antidiuretic hormone (ADH)
Pituitary gland (primary)
Hypothalamus (secondary)
Etiologies of diabetes insipidus (4)
(Hint: think about it...)
(Bonus: which etiology is most rare?)
Head injury
Brain injury
Brain tumor
Hereditary (rare)
What are the (2) characterized symptoms of DI?
Excessive thirst
Dilated veins in the wall of the lower esophagus
(Bleeding) esophageal varices
What condition brings about bleeding esophageal varices?
(Hint: condition with a comorbidity)
Chronic liver disease with portal hypertension
While it's nice to prevent nocturnal enuresis with ADH, there are sadly some contraindications and cautions. In fact, there are 4 of them. What are they?
(Hint: they are ALL cardiac-related, and think about what ADH does to your blood volume.)
Decreased cardiac output
Increased peripheral resistance (HPT)
As if contraindications/cautions of ADH weren't enough, there are side effects, too. What are they? (Hint: 3/4 are cardiac-related, and the other is indirectly cardiac-related.)
Premature atrial contraction
Heart block
Fluid overhydration (SIADH)
Before administering ADH, what two things should you always assess?
Vital signs
Serum sodium levels
What are the two thryoid hormones?
Tri-iodothyronine (T3)
Thyroxine (T4)
What do thyroid hormones contain that stimulate the metabolic rate of nearly all tissues?
(Bonus: what aspect of the metabolism specifically?)
(Basal metabolic rate)
Thyroid hormones are regulated by what two structures?
Anterior pituitary gland
T3 vs. T4: which hormone is most circulating?
T4 (Thyroxine)
T3 vs. T4: which hormone is more biologically active?
Condition of lacking thyroid hormones
Prototype thyroid hormone:
__________ (Synthyroid)
(Bonus: which of the two thyroid hormones specifically?)
Levothyroxine (Synthyroid)
(T4-just remember 'thyroxine' and you'll be golden, good buddies.)
Why do you think Heidi is being a bit sarcastic in typing these Quizlet cards?
Because there are only 5 days until the end of school. Get excited, people.
Replacement of thyroid hormones is CRITICAL for _______ rate, _______ output, ________ synthesis, and _______ utilization.
Metabolic rate
Cardiac output
Protein synthesis
Glycogen utilization
Indications for thyroid hormones:
Mild-to-severe __________
Mild-to-severe hypothyroidism
Thyroid hormones are used diagnostically in suppression tests to differentiate what two conditions?
Euthyroidism (normal thyroid function)
What two types of diseases contraindicate thyroid hormone administration?
Cardiovascular (CV) diseases
SEVERE renal diseases
What are two other names for thyroid hormone overdose?
Thyroid crisis
What is involved in thyroid crisis?
CV effects (5)
GI effects (5)
CNS effects (4)
PNS effects (1)
CV: angina, tachycardia, palpitations, hypertension, cardiac dysrhythmias
GI: nausea, vomiting, diarrhea, cramping, weight loss
CNS: insomnia, headache, nervousness, irritability, fever
PNS: tremors
Nursing concerns for thryoid hormones:
Baselines (3)
Heart test?
Lab studies? (3)
_____ rate (when?)
Assess for symptoms of ______/______
Baselines: vitals; body weight; I&O
Heart test: ECG
Labs: T3, T4, TSH
Symptoms of hyper/hypothyroidism
On what schedule should patients take thyroid hormones?
(Bonus: which meal is involved?)
At the same time each day, preferably before breakfast
Patients taking thyroid hormones should avoid foods that inhibit said hormones, such as:
Strawberries, peaches, pears, cabbage, turnips, spinach, kale, cauliflower, radishes, peas
Which two comorbid conditions accompany hyperthyroidism?
Exopthalmos (bulging eyes)
Goiter (big/nodular thyroid gland)
What is another name for hyperthyroidism?
Grave's Disease
Hyperthyroidism results in overactive _______ of all body processes
Overactive metabolism
Prototype anti-hyperthyroidism drug:
_________ (Propyl-Thyracil, PTU)
Propylthiouracil (Propyl-Thyracil, PTU)
Propylthiouracil (anti-hyperthyroidism drugs) MOA:
Inhibit ________ synthesis
Suppress peripheral conversion of ____ to ___
Inhibit thyroid hormone synthesis
Suppress peripheral conversion of T4 to T3
Anti-hyperthyroidism agent adverse effects (bummer!):
CNS: dizziness, _________, weakness, _______, fatigue, ________
CV: _________
Others: _____penia, ______suppression, (hyper/hypo)sensitivity reactions, rash
CNS: dizziness, neuritis, weakness, paresthesias, fatigue, headache
CV: bradycardia
Others: leukopenia, myelosuppresion, hypersensitivity reactions, rash
Anti-hyperthyroidism agent nursing concerns:
Baseline _____
Which heart test?
Which lab studies? (4)
Signs & symptoms of what condition?
Baseline vital signs
Heart test: ECG
Lab studies: T3, T4, TSH, CBC
Signs & symptoms of thyroid crisis
What are the two primary blood tests for diabetes mellitus?
Fasting plasma glucose (FPG)
Oral glucose tolerance test (OGTT)
What is the class triad of signs & symptoms for diabetes mellitus?
Polydipsia (excessive thirst)
Polyphagia (excessive appetite)
Polyuria (excessive urinary output)
What is the required pharmacotherapy for diabetes mellitus?
What are the three types of insulin (general names)?
Rapid-acting insulin prototype (________ R)
Novolin R
Intermediate-acting insulin prototype
Long-acting insulin prototype(s)
Which two insulin prototypes are often combined?
Intermediate-acting & short-acting insulins
Insulin MOA (1/2):
Decrease blood _____ levels by increasing cellular uptake of _______ and stimulating storage as _________
Decrease blood glucose levels by increasing cellular uptake of glucose and stimulating storage of glucose as glycogen
Insulin MOA (2/2):
Inhibit release of _______
Inhibit release of glucagon
What blood level should nurses always monitor before administering insulin?
Blood glucose level (Umm, duh?)
What must you NEVER do to insulin vials? What should you do instead?
(Bonus: Why?)
Shake vials
Roll vials
(Ensure gentle dispersion of medication w/in solution)
By which route is insulin given?
Ok, next question: By which route is insulin NOT given?
(Since we're already on the subject...WHY?)
(Enzymes are destroyed in the intestine)
IV administration of insulin involves which form of insulin ONLY?
Regular insulin
What size (gauge) needle(s) are used for sub-q insulin administration? What size in length?
25-26 gauge needles
1/2-3/4 inch needles
For what 3 conditions must insulin doses be adjusted?
Insulin should NOT be administered when blood glucose levels are less than ___ mg/dL
<70 mg/dL
What specific aspect of insulin therapy must nurses emphasize to patients?
Compliance (because life is better with a healthy pancreas...and kidneys...and, well, NOT losing your limbs...just saying.)
Insulin can be administered several times a day (q_h or q_h) or ACHS (before ____ and before ___)
q4h or q6h
Before meals and before bed
If a patient's blood glucose level is 150-180 mg/dL, the nurse (that would be you) should administer ___ units of insulin?
3 units of insulin
If a patient's blood glucose level is 180-210 mg/dL, the nurse should administer ___ units of insulin?
5 units of insulin
If a patient's blood glucose level is 210-240 mg/dL (yikes!), the nurse should administer ___ units of insulin?
7 units of insulin
Blood glucose <60 mg/dL
Loss of subcutaneous tissue at insulin injection sites (2)
Spongy swelling of tissue at insulin injection sites
Presence of circulating antibodies to inactivate insulin
(Bonus: what does this require?)
Immunogenic insulin resistance
(Higher insulin doses)
Medications used to lower blood glucose and treat type II diabetes (holla!!)
Oral hypoglycemia agents
Oral hypoglycemia agents often involve multiple drug _________
Multiple drug interactions for their synergistic actions
What are the indications for oral hypoglycemia agents? (2)
Type II diabetes (NIDDM), unresponsive to diet & exercise therapy
Used with insulin in patients who require large amounts of insulin (i.e. obese patients)
Anti-hyperthyroidism agent nursing concerns:
Teach patient for S&S of ________
How often should medications be taken? On what schedule?
Teach patient for S&S of hypothyroidism
Take medications at the same time every day, around the clock
Patients taking anti-thyroid agents must be instructed to monitor which vital sign?
Pulse rate
What is the most serious adverse effect of anti-thyroid agents?
What blood test should be taken regularly for patients taking anti-thyroid drugs?
(Bonus: what are you checking for?)
Complete blood count (CBC)
Diabetes mellitus is the complex disorder of the metabolism of what three nutrients?
What causes this disorder? (2)
(Hint: what cell dysfunction?)
Insufficient insulin synthesis by pancreatic beta cells (Type I) or insulin resistance (defect of insulin receptors) in target cells (Type II)
Diabetes mellitus is characterized by hyperglycemia (high blood glucose greater than ___ mg/dL)
>120 mg/dL
What is the body's normal serum glucose range?
(Remember: an insulin-synthesizing pancreas is a happy pancreas!)
60-100 mg/dL
(Was that joke too much? Perhaps.)
Type I diabetes (IDDM) affects __%-__% of patients
Type II diabetes (NIDDM) affects __%-__% of patients
Solfonylurea (oral diabetic drug) prototype:
_______ (Diabeta)
_______ (Glucotrol)
Glyburide (Diabeta)
Glipizide (Glucotrol)
Sulfonylureas (ODD) MOA:
Stimulate release of _______ from pancreatic beta cells
Increase sensitivity of ___________ to insulin
Stimulate release of insulin from pancreatic beta cells
Increase sensitivity of peripheral tissues to insulin
Biguanides (ODD) prototype:
__________ (Glucophage)
Metformin (Glucophage)
Metformin (Glucophage) (ODD) MOA:
Reduce blood glucose by reducing __________, thereby suppressing ______ production of glucose
Decrease __________ reabsorption of glucose and increase _______ uptake of glucose
Reduce blood glucose by reducing gluconeogenesis, thereby suppressing hepatic production of glucose
Decrease intestinal reabsorption of glucose and increase cellular uptake of glucose
Which oral diabetic drug is most commonly prescribed?
Metformin (Glucophage)
Meglitinide (ODD) prototype:
__________ (Prandin)
Repaglinide (Prandin)
Meglitinide (ODD) MOA:
Lowers glucose by stimulating insulin release from _________
Lowers glucose by stimulating insulin release from pancreatic beta cells
Thiazolidinedione (ODD) prototype:
___________ (Avandia)
(Note: if anyone knows how to properly pronounce this drug name, by all means, please share.)
Rosiglitazone (Avandia)
(This one, too. Good grief.)
Rosiglitazone (Avandia) (ODD) MOA:
Lowers blood glucose by increasing _______ sensitivity to insulin
Lowers blood glucose by increasing cellular sensitivity to insulin
Alpha-glucoside inhibitors (ODD) prototype:
__________ (Precose)
Acarbose (Precose)
Acarbose (Precose) (ODD) MOA:
Lowers glucose by interfering with ________ absorption from what organ system?
Lowers glucose by interfering with carbohydrate absorption from GI tract
New incretin agents (ODD) prototype:
__________ (Januvia)
Sitagliptin (Januvia)
Sitagliptin (Januvia) (ODD) MOA:
Inhibits dipeptidyl peptidase-IV (DPP-IV), thereby reducing destruction of ________, which increase levels of _______ hormones
Inhibits dipeptidyl peptidase-IV (DPP-IV), thereby reducing destruction of incretins, which increse levels of incretin hormones
ODD adverse affects (5)
ODD nursing concerns:
Take medications preferably ___ minutes prior to breakfast and at the same time each day
If a dose is missed, take it __________ and (do/do not) double-up if close to next dose
Teach signs & symptoms of hypoglycemia and instruct patient to consume _______ or _______ once hypoglycemia has occurred (and notify health providers)
Avoid other medications like _______ and _______
Encourage routine ______, proper _____, and proper ________
Take medications preferably 30 minutes prior to breakfast and at the same time each day
If a dose is missed, take it as soon as remembered but DO NOT double-up if close to the next dose
Teach signs & symptoms of hypoglycemia and instruct patient to consume juice or candy once hypoglycemia has occurred (and notify health providers)
Avoid other medications like aspirin and EtOH
Encourage routine follow-ups, proper diet, and proper exercise
There is a link between what two psycho/neuro conditions?
Insomnia & anxiety
What is another name for anxiety & insomnia agents?
(Note: a good way to remember 'depressants' is to remember their slang name: 'downers')
How are depressants classified if they are administered for anxiety? What about for insomnia?
Sedatives (anxiety)
Hypnotics (insomnia)
What are the three (3) categories of depressants?
Benzodiazepine prototype(s):
__________ (Ativan)
__________ (Valium)
__________ (Xanax)
__________ (Librium)
Lorazepam (Ativan)
Diazepam (Valium)
Alprazolam (Xanax)
Chlordiazepoxide (Librium)
Benzodiazepines MOA:
Potentiate ______
Depress ______ at different levels
Potentiate GABA (like anesthesia)
Depress CNS at different levels
What are the three (3) levels at which benzodiazepines depress the CNS?
Benzodiazepines indications:
Routine management of ________
Reduction of _______ prior to medical/surgical procedures
Reduction of _______ (same answer as above) in patients with what life support device?
Routine management of anxiety
Reduction of anxiety prior to surgical/medical procedures
Reduction of anxiety in patients with ventilators
What four (4) conditions can benzodiazepines also be used for besides anxiety (off-label)?
Alcohol withdrawal
Status epilepticus
Benzodiazepines adverse effects:
CNS: dizziness, ______, drowsiness, ______ vision, confusion
Blurred vision
Benzodiazepines have the tendency to cause paradoxical CNS _______
(Bonus: in what three categories of people?)
Paradoxical CNS stimulation
(Psych patients, the elderly, and patients with ADHD)
Benzodiazepines nursing concerns:
Assess baseline _______ and _______
Slow IV _____ or ______
Avoid _______ or operating ________
Warn patients about the danger of taking the medication with ______
Assess baseline vital signs and LOC
Slow IV push or infusion
Avoid driving or operating machinery
Warn patients about the danger of taking the medication with alcohol
Despite their depressing nature, benzodiazepines do not address what issues?
Pain issues
It is necessary to taper off benzodiazepines due to withdrawal causing what condition?
Status epilepticus
Barbiturate prototype:
___________ (Luminal)
Phenobarbital (Luminal)
Barbiturate MOA:
Bind _____ receptors and enhance activity
Bind GABA receptors and enhance activity
Barbiturate indications:
__________ by IV push
Short-term management of ______
Status epilepticus by IV push
Short-term management of insomnia
Barbiturate interactions:
________ and other CNS depressants
Alcohol and other CNS depressants
Barbiturate nursing concerns:
CNS: drowsiness, _______, dizziness, _______, reduced _____ sleep
GI: (3)
_____ and ______ depression
CNS: drowsiness, lethargy, dizziness, hang-over, reduced REM sleep
CV and respiratory depression
How often should patients be assessed when administered phenobarbital IV?
Patients taking barbiturates should be monitored for signs of what hematologic condition?
Blood dyscrasias
Anti-seizure agents suppress _______ discharges to prevent abnormal foci from forming or spreading
Suppress neuron discharges
Anti-seizure agents control ________ movement and ________ balance
Electrolyte movement
Neurotransmitter balance
Barbiturates are the traditional drugs for which type of seizure?
(Note: barbiturates have been replaced my newer & safer drugs)
Tonic-clonic seizures
Which drugs are important for use against status epilepticus?
Which anti-seizure agents are effective in the management of most types of seizures, but have MANY adverse effects?
Hydantoin prototype:
_________ (Dilantin)
Phenytoin (Dilantin)
Phenytoin (Dilantin) MOA:
Delays influx of _______ ions in neurons, and slows propagation and spread of abnormal _________
Does NOT elevate the ___________
Delays influx of sodium ions in neurons, and slows propagation and spread of abnormal discharges
Does NOT elevate the seizure threshold
Hydantoins adverse effects (remember, there are many):
Lethargy, _____ache, ________, dizziness
_________ (EOM), confusion, _______, coma, and paradoxical ________ (When do these specific adverse effects occur?)
Lethargy, headache, drowsiness, dizziness
Nystagmus (EOM), confusion, ataxia, coma, paradoxical seizures (at high doses)
Which drug type is the drug of choice for many tonic-clonic AND partial seizures?
(Hint: it's not barbiturates like you're thinking!)
Carbamezepine prototype:
Carbamazepine (_______)
Carbamezepine (Tegretol)
Carbamazepine MOA:
Inhibit _______ channels and block ________, _________ firing of neurons
Inhibit sodium channels and block repetitive, sustained firing of neurons
Carbamezepine (Tegretol) is used with what other drug for patients requiring polytherapy?
Unclassified anti-seizures prototype:
_________ (Depacon)
Valproic Acid (Depacon)
Valproic Acid (Depacon) MOA:
Increases concentration of ________ in the brain
Suppresses abnormal neuronal _______
Increases concentration of GABA in the brain
Suppresses abnormal neuronal discharges
Valproic Acic (Depacon) indications:
______ seizures
______ partial seizures
Absence seizures
Complex partial seizures
A progressive, neurodegenerative disorder characterized by abnormal motor movement
Parkinson Disease
Parkinson Disease is caused by abnormal amounts of _______ in the brain
(Bonus: what specific part of the brain?)
Abnormal amounts of dopamine in the brain
(Substantia nigra)
Cardinal signs of Parkinson Disease (4)
Tremors (shaking of the hands and head while at rest)
Muscle rigidity (resistance to passive movement of arms and legs, mask-like facial expression)
Bradykinesia (slowness of voluntary movement, speech)
Postural instability (stumbling, stooped over)
Which class of drugs is most effective against Parkinson Disease?
Dopaminergic agents
Dopaminergic agents prototype:
__________ (L-dopa)
Levodopa (L-dopa)
Dopaminergic agents MOA:
Metabolic ________ of dopamine
Dopamine in the brain is increased after metabolized through ___________ to dopamine
Metabolic precursor to dopamine
Dopamine in the brain is increased after metabolized through decarboxylation to dopamine
Dopaminergic agents may be given in combination with what other drug?
(Hint: _________ [Sinemet])
Carbidopa (SInemet)
Nurses should monitor ________ as a serious adverse effect of dopaminergic agents
The goal of dopaminergic administration is to achieve the _________ effective dose
Lowest effective dose
Nursing concerns for anti-Parkinson Disease agents (1/2):
Assess for ____ reponses/characteristics of __________
Inspect the oral cavity after drug administration in patients with __________
Teach patient to watch for full effects in __-__ weeks
Assess for CNS responses/characteristic of Parkinsonism
Inspect the oral cavity after drug administration in patients with dysphagia
Teach patient to watch for full effects in 1-4 weeks
Nursing concerns for anti-Parkinson agents (2/2):
Avoid terminating medication _______
Monitor for safety with ________ and ______
Caution for adverse effects, including _____ changes
Avoid terminating medication abruptly
Monitor for safety with ambulation and ADLs Caution for adverse effects, including CNS changes
Miscellaneous anti-Parkinson agent prototype:
__________ (Symmetrel)
Amantadine (Symmetrel)
Amantadine (Symmetrel) MOA:
Increases release of ________ from storage sites and blocks reuptake of _________
Rapid reduction in _________ followed by _________ effects after several months
Increases release of dopamine from storage sites and blocks reuptake of dopamine
Rapid reduction in symptoms followed by diminished effects after several months
Amantadine (Symmetrel) is also treated as a(n) __________ drug
Antiviral drug
Amantadine (Symmetrel) nursing concerns:
Administer drug early to avoid ________
Avoid _______ or other tasks requiring alertness
Avoid other _______ drugs
Administer drug early in the day to avoid insomnia
Avoid driving or other tasks requiring alertness
Avoid other OTC drugs
Which class of drugs is the mainstay for treatment of depression?
Tricyclic antidepressants
Tricyclic antidepressant prototypes:
__________ (Elavil)
__________ (Pamelor)
Amitriptyline (Elavil)
Nortriptyline (Pamelor)
Tricyclic antidepressants MOA:
Block reuptake/increase action of _________ and __________ (into which brain structure?)
Block _____ receptors
Block reuptake/increase action of norepinephrine and serotonin into presynaptic nerve terminate
Block acetylcholine receptors
There is no known antidote for overdose of tricyclic antidepressants, and an estimated __% of patients suffering overdose have died before reaching the hospital
70% of patients
Which anti-depressants are effective but seldom used?
(Bonus: why?)
Monoamine oxidase inhibitors
(Serious adverse effects)
Monoamine oxidase inhibitor prototype:
_________ (Nardil)
Phenelzine (Nardil)
Phenelzine (Nardil) MOA:
Binds irreversibly to ______
Intensifies actions of endogenous neurotransmitters (4)?
Binds irreversibly to monoamine oxidase (MAO)
Intensify actions of endogenous epinephrine, norepinephrine, serotonin, and dopamine
What is the most common side effects of MAO inhibitors?
Orthostatic hypotension
Patients taking MAO inhibitors should avoid food containing _________?
Foods containing tyramine
Class of second-generation antidepressants
Selective serotonin reuptake inhibitors (SSRIs)
Which anti-depressants are effective with low incidence of serious side effects?
SSRI prototype:
__________ (Prozac)
Fluoxetine (Prozac)
Block uptake of serotonin at (brain structure)
Enhance action of _________
Block uptake of serotonin at neuronal presynaptic membrane
Enhance action of serotonin
SSRIs adverse effects:
GI _______
_______ dysfunction
GI upset
Sexual dysfunction
The full therapeutic effects of SSRIs appear in __-__ weeks
2-6 weeks
Patients taking SSRIs should avoid foods containing ________ for interaction
Foods containing tyramine
Treatment of bipolar disorders focuses on impaired levels of all three _________ in (body system)
Impaired levels of all three neurotransmitters in the limbic system
Bipolar disorders agent prototype (conventional therapy for treatment):
_________ (Lithobid)
Lithium carbonate (Lithobid)
Lithium carbonate (Lithobid) MOA:
Likely acts by changing _________ balance in specific brain regions
Increases the synthesis of _______
Likely acts by changing neurotransmitter balance in specific brain regions
Increases the synthesis of serotonin
Lithium bicarbonate (Lithobid) is used with __________ or an antipsychotic for acute mania phase
Used with benzodiazepines
Lithium carbonate (Lithobid) is used with a(n) ____________ for the depressive phase
Used with an antidepressant
Anti-depressants nursing concerns:
Obtain baseline functions of what three (3) organs?
Take drug with ______ or ______ to reduce GI upset
Monitor serum levels every __-__ days initially and then every __-__ months thereafter (lithium toxicity)
Assess daily for weight, _____, and changes in skin ______ (signs of lithium toxicity)
Instruct patient to take __-__ glasses of fluids daily (to maintain hydration)
Warn for switching _________ brands
Obtain baseline functions of thyroid, kidney, and cardiac system
Take drug with meals or milk to reduce GI upset
Monitor serum levels every 1-3 days initially and then 2-3 months thereafter (lithium toxicity)
Assess daily for weight, edema, and changes in skin turgor (signs of lithium toxicity)
Instruct patient to take 8-12 glasses of fluids daily to maintain hydration
Warn for switching different brands
The primary goal of anti-psychotic drugs is to manage symptoms to function ______ and perform ______
Manage symptoms to function independently and perform ADLs
Management of psychotic disorders is challenging due to patients viewing their behavior as ______ as well as undesired ________
View behavior as normal
Undesired adverse effects
Two classes of antipsychotics
1st generation (phenothiazines & nonphenothiazines)
2nd generation (atypical)
Which generation of anti-psychotic drugs has serious side effects?
Phenothiazine (anti-psychotic) prototype:
______________ (dopamine agonist)
Chlorpromazine HCl
Nonphenothiazine (anti-psychotic) prototype:
__________ (Haldol) (dopamine D2 antagonist)
Haloperidol (Haldol)
Which generation of anti-psychotic drugs has fewer adverse effects, better patient adherence, and more effectiveness (due to specificity to subtype receptors)?
2nd generation (atypical)
2nd generation (atypical) anti-psychotic prototype(s):
_________ (Clozaril) (dopamine antagonist)
_________ (Risperdal) (dopamine antagonist)
_________ (Abilify) (dopamine system stabilizer)
Clozapine (Clozaril)
Risperidone (Risperdal)
Aripirazole (Abilify)
Anti-psychotic drugs often cause __________ symptoms associated with postural and automatic movements
Extrapyramidal symptoms (EPS)
EPS symptoms associated with anti-psychotic drugs:
Acute _______
Akathisia (what is it?)
Antipsychotic-induced _________
________ dyskinesia
Acute dystonia (severe muscle spasm of neck, back, and face)
Akathisia (uncontrollable need to move)
Antipsychotic-induce Parkinsonism
Tardive dyskinesia (involuntary movement of tongue & face)