Pharm Test 4 Flashcards
Acetaminophen indications and pt. teaching
I: minor pain, fever (drug of choice), fever, cancer headaches (antipyretic/analgesic) (not anti inflammatory)
PT:
Maximum dose is 3 (4 in hospital) grams /day – easy to overdose
Should be used in children instead of aspirin to prevent Reye’s syndrome
Teach to read labels, all otc’s
Interferes with the metabolism of warfarin (coumadin)
pediatric doses are weight based
Can cause liver damage
Avoid alcohol
acetylcysteine is antidote
Assessment of inflammation
○ usually self-limiting
○ histamine dilates blood vessels, capillaries become more permeable and causes congestion and swelling (pain and fever)
acute inflammation - edema of the surrounding tissue (may lead to pain, possible joint immobility);
result of an influx of neutrophils through permeable blood vessels
resolution - tissue regeneration (scar tissue)
anaphylaxis
Chronic - slow onset, may lack distinct phases.
Acute Inflammation: It is a nonspecific defense mechanism that neutralizes or destroys foreign substances and microbes. Usually self limiting, doesn’t need to intervene. 1. vasodilation (histamine), 2. vascular permeability (edema), 3. cellular infiltration (pus), 4. thrombosis (clots), 5. stimulation of nerve endings (pain). Use ice packs, RICE, and topical agents like creams, ointments, patches, suppositories, and intranasal sprays.
ASA dosing, side effects, expected outcomes
D: 1 to 2 tablets (325 mg to 650 mg) by mouth every 4 hours as needed.
should drink a full glass of water with each dose.
no more than 3900 mg in 24 hours
SE: Irritates digestive system, may cause bleeding, n/v/d bruising/bleeding
Salicylism may occur
Tinnitus, dizziness, headache, excessive perspiration, CNS depression, nausea, vomiting, hyperventilation
EO: NSAID: diminished fever, pain, inflammation.
Corticosteroids/glucocorticoids teaching, side effects, assessment
T: educate not to stop suddenly!!
s/e: serious side effects with long-term use: adrenal insufficiency, hyperglycemia, mood changes, cataracts, PUD (peptic ulcer disease), electrolyte imbalances, osteoporosis, impaired wound healing, bruising, decreased immune response (immunosuppression)
A: check for active infection (contraindication), assess length of use (dangerous long term), assess pain, monitor degree of bone-marrow suppression (thrombocytopenia and leukopenia)
Glucocorticoids: Effective in treating severe inflammation. Naturally release from adrenal cortex. Suppress histamine and prostaglandins. Can mask infection because it creates potential for existing infection to grow rapidly and undetected. Used for short term acute inflammation. If you need long term treatment, have low dose, alternate day dosing, and gradually discontinue.
S/s: Suppression of adrenal gland, fluid retention, HTN, weight gain, and thin skin/bruising. Serious adverse effects is increase of cortisol levels causing renal glands to atrophy like adrenal insufficiency, hyperglycemia, mood changes, cataracts, PUD, electrolyte imbalances, osteoporosis, impaired wound healing, bruising, peptic ulcer disease. Long term effects is Cushing syndrome is moon face, buffalo hump, and muscle wasting.
NSAIDS dosing, side effects, expected outcomes
Know 4 nonpharmacologic measure to supplement NSAID drug therapy (RICE)
D:Not to be taken long term. **
ketorolac (Toradol): common NSAID in hospital setting, works well.
can only use for 5 days
ibuprofen (Advil, Motrin)
800 mg q6h, maximum dose is 3200mg/day
ibuprofen better tolerated with food
s/e:
drugs that block cox 1 can have damage from long term such as bleeding ulcer in stomach or kideny damage r/t reduced renal blood flow
Block cox 2: high risk for MI,
EO(goals): diminished fever, pain, or inflammation.
Be free from nephrotoxicity
Have no GI bleeding
Which drugs are classified as Immunosuppressant, pt. teaching
Drugs:
Calcineurin inhibitors are preferred drugs for transplant rejection
Diminishes the activity of T cells and B cells
cyclosporine (Gengraf, Neoral)
Avoid grapefruit juice!!!, it will increase level
narrow therapeutic index=blood draws
Antimetabolites and Cytotoxic drugs
Inhibit leukocyte replication
Used to kill or suppress B cells and T cells
Prototype drug – azathioprine (Imuran)
Antibodies (immunoglobulins
proteins that help us recognise antigens
Prevent acute transplant rejection, autoimmune disorder and malignancies
Antibodies produced are specific to the antigen, made through genetic engineering
Prototype drug – basiliximab (Simulect),
monoclonal antibodies : made via cloning unique WBC’S
Corticosteroids
Widely used for immunosuppression and severe inflammation,help with transplant rejection
Affect nearly every aspect of the immune response; intervene at multiple steps in the immune response, including antigen presentation, production of cytokines and the proliferation of lymphocytes
Have significant long-term adverse effects
T:
All drugs may cause immunosuppression even stimulant or antidepressants because you modify immune system
Surveillance for infection is a priority, monitor closely due to already immunosuppressed system
Patient teaching: handwashing, avoid crowds, monitor signs of infection (fever, bleeding, bruising, etc) Myelosuppression: low RBC’s, WBC’s, and platelets
know prednisone side effects since it’s common but dangerous: TAPER!
Cyclosporin ((Gengraf, Neoral) teaching, drug classification and MOA
T:
Avoid grapefruit juice!!!, it will increase level
May have decreased urine output and HTN
Take with food and do not mix in Styrofoam (styrofoam is porous which sounds like cyclosPORin)
Avoid crowds, fresh fruits and veggies
narrow therapeutic index=blood draws
Report fever or any other signs of infection
May cause gingival hyperplasia1
C: immunosuppressant, Calcineurin inhibitor
MOA: preferred transplant drug, also treat rheumatoid arthritis and psoriasis: Diminishes the activity of helper T cells and B cells by activating calcineurin (a protein that activates T-cells) inhibitors (for transplant). Inhibits the transcription of interleukin 2
Filgrastim (Neupogen) indication and teaching
I: Tx: increase wbc’s via leukopoiesis for: (hiv/aids, immunosuppressed), chemotherapy induced neutropenia, chronic neutropenia, myeloid leukemia - low neutrophil count
T: SE: rash, fatigue, low platelets-nosebleeds, fever
do not take within 24 hours before chemo and 24 hours after
do not take if you are allergic to other meds made using E Coli
common s/e is aching bones and muscles
pain in upper left stomach could indicate enlarged spleen
report SOB and dyspnea this may indicate ARDS
Immunity types (passive, active), example drugs for passive immunity:
immunity achieved from active immune system response to develop antibodies (natural-get sick) and (passive-from direct antibodies)
passive: no immune response; antibodies from external source;
Passive immunization is very different and is the administration of preformed antibodies (immunoglobulins)
Immune system is not activated and memory cells are not produced
Provides immediate protection against a recent infection, a potential infection or a disease in progress
Immunoglobulins (given iv for immune deficiency)
Maternal Antibodies (breastfeed/placenta)
Gamma Globulins: Rogam: immunoglobulin given to Rh- preg. women with potential for baby for Rh+
monoclonal antibodies
IVIG/Immunoglobulin G: Used for immune deficiencies, acute disease (Guillain barre syndrome), Kawasaki disease, and autoimmune disease. Comes from donated plasms.
Gama Globulin: Gives antibodies so body doesn’t elicit immune response. Rhogam gives you antibodies so that it doesn’t illicit response. Rh- mom with a Rh+ kid. Ex. Hep A and Hep B.
Maternal Antibodies: Transferred through breast feeding/ placenta. Provides immediate protection against a recent infection, potential infection, or disease in progress.
Anti-infective therapy, how are they classified, basic principle definitions
Definition: Anti-Infective drugs are classified by their susceptible organisms, chemical structure and mechanism of action
To determine most effective antibiotic or to determine if bacteria is resistant need a culture and sensitivity
wide spectrum antibiotics can harm good bacteria (normal flora), narrow spectrum antibiotics are better because they have less effect on flora
To determine the amount to give MIC (Minimal Inhibitory Concentration) is determined in a petri dish to tell how much drug is needed to inhibit bacterial growth
Definitions: pathogens: Organisms that can cause disease
pathogenicity: Ability of organism to cause infection or disease
virulence: Ability of a microbe to produce disease when present in minute numbers
bactericidal: Kill bacteria
bacteriostatic: Slow growth of bacteria
Anti-infective resistance
May develop drug resistance by selection—the hardier microbes see what the drug looks like and will make little “pacmen” to eat up the antibiotic.
To determine most effective antibiotic or to determine if bacteria is resistant need a culture and sensitivity
rifampin (Rifadin) has common development of resistance
Sulfonamides have resistance
NOT CAUSED BY ANTIBIOTIC TREATMENTS - can be worsened by inappropriate antibiotic use or overuse
Gentamycin adverse effects
Aminoglycosides are effective against aerobic gram-negative bacteria.
Prototype drug – gentamicin (Garamycin)
S/e Watch for hearing loss (ototoxic), nephrotoxicity, impaired neurofunction
TB treatment, common pharmacotherapy
Tuberculosis (Tb) is a respiratory infection that is highly contagious through airborne droplets
Has active and latent-dormant stage of disease
causes tubercles (nodules) to form in lungs due to tissue death where bacteria reside.
Usually have 2 or more drugs prescribed
TB DRUGS: RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Streptomycin
rifampin (Rifadin) inhibits RNA synthesis
Prototype drug –isoniazid (INH) is the most likely drug to be used
taken long term
6-12 months
Resistant may be up to 24 months
Also used for prophylaxis (prevention
Do not drink alcohol
S/e: n/v, red-orange secretions and urine, peripheral neuritis, increased uric acid, visual problems ototoxic
take on empty stomach for best absorption
Billions of people are carriers of Tb-should be taking inh
lives in water and foods but cant cause disease without host
*immunosuppressed at hightest risk
Fungal infection treatment
Superficial fungal infections (mycoses) affect the hair, skin, nails and mucous membranes
Systemic fungal infections (mycoses) affect internal organs, typically the lungs, brain and digestive organs; can be fatal
Antifungal medications interfere with synthesis of ergosterol cell membrane
Prototype drug – nystatin (Mycostatin, Nilstat, Nystex)
mostly For superficial and sometimes systemic fungal infections
Increased risk for bleeding when taking warfarin (coumadin)
Several formulas available depending on the indication
Topical powder for skin
Lozenge for oral use, teach the client to dissolve in mouth
Oral suspension for thrush each client to swish or spit
Cream/ointment
Prototype drug – fluconazole (Diflucan)
Azoles are drugs of choice for many mycoses due to their efficacy and safety
Used to treat oropharyngeal, vulvovaginal, and esophageal candidiasis
Given IV/PO
terbinafine (Lamisil) is used to treat several types of superficial fungal infections
Oral prep is used for onychomycosis (nail fungus)
nail infections last a long time requiring taking Rx for long time=blood draws required to prevent med toxicity
Accumulates in nail beds
Active for many months and may cause hepatitis and neutropenia
Prototype drug for systemic infections – amphotericin B (Fungizone)
Important to check renal function (BUN renin creatinine test)
Fever and chills could be a hypersensitivity reaction; need to pre-medicate with acetaminophen, antihistamines, and corticosteroids
Immunostimulants nursing care
watch for infection
○ all drugs may cause immuno-suppressants
○ hand hygiene, avoid crowds, monitor s/s and temp
○ watch for bleeding/bruising (myelosuppression)
teach to avoid crowds, fresh fruit, veggies and flowers.
