Cancer Drugs
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Cancer is uncontrolled rapid cellular growth
o Do not have growth control mechanisms or positive physiologic function
o Grow and invade adjacent tissues or break away and travel via blood/lymph
First signs of malignancy are fatigue, fever, weight loss (unplanned)
Chemotherapy drugs have a narrow therapeutic index, and are harmful to healthy normal cells (hair follicles, GI
tract, bone marrow)
o Dose-limiting adverse effects in GI tract, absolute neutrophil count
o Nadir is the lowest point, 10-14 days after chemo has been given
Nursing Implications
o Assess baseline blood counts prior to administering
o Use infection prevention techniques
o Watch for oral thrush, anticipate nausea/vomiting - dronabinol and megestrol to stimulate appetite
o Watch for Mg, K, Na, Ca imbalances
o Myelosuppression
 Trend CBC, CMP, uric acid
 Administer hematopoietic drugs
 Neutropenia – no fresh flowers, no sick visitors, hand hygiene
 2 readings of temp >100.5
 Report fevers ASAP
 Watch for bleeding
o Report ringing/roaring in the ears, tingling, numbness, pain, painful swollen joints, skin care, pain
management, sterility, menopausal symptoms, non-drug contraception
o Infections, bleeding, pulmonary (bleomycin) and cardiac toxicity (doxorubicin)
Cell-cycle Nonspecific: kill cells in any phase of the cell cycle
o Alkylating drugs
 Cyclophosphamide, cisplatin
 Form abnormal chemical bonds in cancer DNA
 Brain tumors, lymphomas, leukemia, breast cancer, bladder cancer
o Cytotoxic antibiotics
 Use intercalation to block DNA synthesis
 Bleomycin, doxorubicin
 Monoclonal antibodies (“-mab”) aimed at control of cancer to give more time
o Hormonal agents
 Oppose effects of hormones
 Anastrozole, tamoxifen, raloxifene
 Competes with estrogen on malignant cells
 Leuprolide (progestin, causes tumor cell regression)
 AE: Jaundice, hypercalcemia, fluid retention, NV, hot flashes, vaginal dryness
Cell-cycle Specific: Kill cells in a specific phase of the cell cycle
o More effective in tumors with high growth fraction (blood cancers like leukemia and lymphoma)
o Antimetabolites (S phase)
 Closely resemble normal metabolites, inset false substrate, resulting in defective product
 Methotrexate (folic acid), mercaptopurine (purine), fluorouracil (pyrimidine)
 Methotrexate also used to treat psoriasis, RA, sickle cell anemia
o Mitotic inhibitors
 Vinca alkaloids – vincristine
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Work during before or during mitosis, interfere with cell division
o Topoisomerase Inhibitors
 Used primarily for ovarian and colorectal cancer, SCLC
 Inhibit DNA function in the S phase, breaks down DNA strands
 Give atropine as a pre-med to prevent diarrhea
 Irinotecan, topotecan
Men's/Women's health
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Women’s Health
o Estrogen
 Responsible for development and maintenance of female reproductive, secondary sex
characteristics, and shaping of skeleton and contours
 Estradiol is principle and most active endogenous estrogen
o Estrogenic drugs
 Conjugated estrogens (Premarin) -widely used
 Bind and produce response in tissues where estrogen receptors are
 Female genitals, breasts, pituitary, hypothalamus
 Used for treatment and prevention of disorders resulting from estrogen deficiency
 Menopausal symptoms, oral contraception, uterine bleeding, osteoporosis
 The smallest dosage that works is used, same time every day, don’t skip
 Contraindicated in people with estrogen-dependent cancers, clotting disorder or history,
pregnancy
 Report unilateral calf swelling, redness, warmth, pain, SOB
 Interact with anticoagulants, rifampin, SJW, tricyclic antidepressants, smoking
 Adverse effects – thrombolytic events, nausea, chloasma (dark skin patches)
o Progestins
 Progesterone, medroxyprogesterone, megestrol
 Used for: treatment of uterine bleeding, amenorrhea, palliative for cancers, prevent conception,
prevent miscarriage, alleviation of premenstrual symptoms
 Megestrol used in cancer patients to stimulate appetite and weight gain
 Adverse effects – liver dysfunction, PE, nausea, edema, weight gain
 Contraindications similar to estrogens
o Contraceptive Drugs
 Prevent ovulation by inhibiting the release of LH & FSH, increasing uterine mucus viscosity,
improve regularity of cycle, decrease blood loss, decrease incidence of ovarian cysts and ectopic
pregnancies
 Risk of thromboembolic events, PE, MI, stroke
 Interact with antibiotics (especially penicillins, cephalosporins), barbiturates, isoniazid/rifampin
(TB)
 BBs, warfarin, TCAD, vitamins, hypnotics, anticonvulsant may be less effective if given
with oral contraceptives
o Osteoporosis
 Women older than 60 should take calcium and vitamin D for bone health
 Bisphosphonates
 Alendronate, ibandronate
 Inhibit osteoclast-mediated bone reabsorption
 Contraindicated in hypocalcemia, esophageal dysfunction, those unable to sit/stand for
30 minutes after taking
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Adverse effects – Esophageal burns if medication lodges in esophagus, take with full glass
of water and remain upright
 Selective estrogen receptor modifiers (SERMs)
 Raloxifene, tamoxifen
 Stimulate estrogen receptors on bone
 Contraindicated in pregnancy, DVT, PE, retinal vein thrombosis
 Adverse effects – Hot flashes, cramps, increase risk of VTE
 Discontinue 72 hours before prolonged immobility
 Hormones
 Calcitonin inhibits osteoclast bone reabsorption
 Teriparatide (only drug that stimulates bone formation)
o Uterine Stimulants
 Adverse effects – hypertension, headache, dizziness, leg cramps, chills
 Before giving, assess mother’s vital signs and fetal heart rate
 Need continuous monitoring of these when administering
 Oxytocin – synthetic form of the hormone (posterior pituitary)
 Used to induce labor, and enhance when labor ineffective
 Stimulates painful uterine contraction
 Can also be used to control postpartum uterine bleeding, complete abortion after
miscarriage, promote milk ejection
 Risk for hypertension and fluid retention
o Stop drug for hypertension responses or fetal decelerations, turn patient on left
side, give O2, fluids, and call MD
 Ergot alkaloids
 methylergonovine
 Increase force and frequency of uterine contraction, used to prevent postpartum atony
and hemorrhage
 Progesterone antagonist
 Mifepristone
 Stimulates uterine contractions to induce abortion
 Prostaglandins
 Dinoprostone gel, misoprostol
 Used to induce labor by softening cervix and enhancing contractions
o Uterine Relaxants
 Used to stop labor that begins before term
 Indomethacin (NSAID) - inhibits prostaglandin activity
 Nifedipine – CCB that inhibits myometrial activity
 If those are ineffective, corticosteroids are given to promote lung maturity in 24-34 week fetus
Men’s Health
o Androgens
 Stimulate growth and development of male sex organs, secondary sex characteristics, synthesis
of muscle and skeletal proteins, enhance erythropoiesis, causes inhibition of endogenous
testosterone and decreased sperm production
 Can cause fluid retention, interact with anticoagulants
 Testosterone
 Synthetic derivatives of testosterone, high first-pass effect
 Methyltestosterone
 Transdermal available (gel, patches – location specific, sprays)
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Anabolic Steroids
 Increase anabolic activity, synthesis of tissue (Schedule III)
 Oxymetholone, oxandrolone
 Approved as adjunct therapy to promote weight gain after surgery, trauma
 Adverse effects – abnormal liver function (peliosis of liver, blood filled spaces),
cardiovascular issues, DVT, PE, heart attack
Androgen inhibitors
 Block the effects of androgens by inhibiting 5-alpha reductase, prevents testosterone from being
converted to DHT (androgen responsible for stimulating prostate growth and thinning of hair)
 5-alpha reductase inhibitors
 Finasteride
 Treat BPH and male baldness, lowers DHT concentrations
 Women should wear gloves when handling
 Monitor PSA because it can cause a 50% decrease in levels
 Tales 3-6 months to see therapeutic effects
 Adverse effects – loss of libido, ED, gynecomastia, myopathy
 Alpha-1 Adrenergic Blockers
 Doxazosin, tamsulosin, terazosin
 Used for symptomatic relief of obstruction from BPH, cause smooth muscle relaxation in
prostate by blocking alpha-1 receptors
 Can cause additive hypotension when given with other BP-lowering medications
 Androgen receptor blockers
 Block the activity of androgen hormones in prostate receptors
 Treat prostate cancer in testosterone positive tumors
 Flutamide, nilutamide
 Gonadotropin-Releasing Hormone Analogs
 Inhibit pituitary gonadotropin, which leads to a decrease in testosterone
 Goserelin, leuprolide, triptorelin
Phosphodiesterase Inhibitors (for erectile dysfunction)
 Sildenafil, tadalafil (long duration)
 First oral drug for treatment of ED
 Allows for buildup of cAMP, which causes relaxation of smooth muscle and permits blood to flow
into the wiener
 Also can be used to treat pulmonary hypertension
 Contraindicated in men with cardiovascular disorders, especially if they use nitroglycerin due to
significant hypotension that doesn’t respond to treatment
 Adverse effects – abnormally prolonged erection, medical emergency!
Saw Palmetto
 Herbal product used for treatment of BPH and alopecia
 Interact with NSAIDs, hormones, immunostimulants
 Adverse effects – GI upset, headache, back pain, dysuria
Hematopoietic Drugs
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Increase hematopoiesis (all or specific blood cells) by promoting the growth or differentiation of precursor cells in
bone marrow
Mild side effects indicative of immune system stimulation (fever, ache, bone pain, flushing)
Uses:
o Decrease duration of chemo-induced anemia, allowing for larger doses of chemo
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o Reduce incidence of infection, anemia, bleeding
o Decrease bone-marrow recovery time after transplant or irradiation
Erythropoietic drugs
o Epoetin-alfa
Colony-stimulating factors
o Filgrastim
 Granulocyte colony-stimulator factor, precursor cells for white blood cells known as granulocytes
(neutrophils, eosinophils, basophils--”phils”)
Platelet-promoting drugs
o Oprelvekin
 Enhances synthesis of platelets through stimulation of megakaryocytes
Psych Drugs, Extrapyramidal Symptoms
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Anxiolytic drugs
o Benzodiazepines
 Increase the action of GABA, schedule IV
 Also used for alcohol withdrawal, insomnia, muscle spasms, seizures, anesthesia
 AE: Fatigue/sedation, overdose (flumazenil), confusion, dizziness, hypotension
 Interactions more likely in renal/hepatic compromised patients
 Alprazolam (short), diazepam (longer, status epilepticus), lorazepam (intermediate, used for
acute agitation, ETOH withdrawal)
o Buspirone
 Non-habit forming, good for long-term anxiety management
Mood-Stabilizing Drugs
o Lithium
 Used to treat acute mania and bipolar maintenance
 Narrow therapeutic range (0.6 - 1.2 mEq/L)
 >1.5 produce toxicity: GI discomfort, tremor, confusion, seizures, ataxia, death
 Cardiac dysrhythmia is more serious AE, contraindicated in dehydrated/sodium imbalance
 Interact with thiazides, ACE inhibitors, NSAIDS
o Antiepileptics
o Antipsychotics (First/Second Gen)
 First generations not good at treating negative symptoms
 Chlorpromazine, haloperidol
 Second generations good at both positive and negative symptoms
 Clozapine, risperidone, aripiprazole, ziprasidone, olanzapine, quetiapine
 Clozapine: Weekly monitoring of WBCs, avoid crowds
 Block dopamine receptors in the brain, areas associated with emotion
 Second gen block specific dopamine receptors, and serotonin receptors
 AE: Agranulocytosis, anemia, neuroleptic malignant syndrome (give dantrolene or
bromocriptine), EPS, tardive dyskinesia, increased prolactin, weight gain, metabolic syndrome
 EPS: tremors, rigidity, stopped posture, shuffling gait, akathisia, dystonia
 Treat with benztropine and trihexyphenidyl or benadryl
Antidepressants - try for six weeks before increasing dosages or changing meds, assess for SI
o First Gen (TCA, MAOI)
 TCA
 Used for depression, neuropathic pain, insomnia
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MAOI
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Amitriptyline, doxepin, imipramine
Block reuptake of S and NE
AE: Sedation, impotence, orthohypo, anticholinergic effects
Can cause death by seizure or dysrhythmia—assess for suicicidality
Give in PM
Potential hypertensive crisis when given with tyramine (cheese effect)
o Aged cheese, smoked meats, wine, pickles
 Phenelzine, selegiline
Second Gen (SSRI, SNRI, Misc)
 Take about 4-6 weeks to be effective
 Take in AM for insomnia and nervousness, weight gain, sexual dysfunction,
 Serotonin syndrome: delirium, agitation, tachycardia, sweating, muscle spasms, shivering,
tremors
 Provide supportive care and taper off medication
 SSRI – citalopram, fluoxetine, escitalopram, paroxitine, sertraline
 SNRI – duloxetine, vanlafaxine
 Buproprion – NDRI – approved for smoking cessation and depression
Atropine, Amiodarone, Adenosine
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Atropine
o Antimuscarinic
o Increases heart rate, used to treat bradycardia and ventricular asystole
o Antidote for anticholinesterase inhibitor toxicity
o Used preoperatively for GI secretions
o Contraindicated in glaucoma, renal/hepatic dysfunction, GI/GU obstruction, UC
Amiodarone
o Blocks both alpha- and beta-adrenergic receptors
o Markedly prolongs the refractory period in all cardiac tissue
o Effective for controlling supraventricular and ventricular dysrhythmias
o A/E: hyper/hypothyroidism, corneal microdeposits, photosensitivity, pulmonary toxicity
o Long half-life, many days
o Interactions with warfarin and digoxin (increases by 50%)
o Avoid if severe bradycardia or second/third degree heart block
Adenosine
o Slows electrical conduction through AV node
o Convert paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm (especially in patients with HF,
hypotension, LV dysfunction that you can’t use verapamil for)
o Half-life = 10 seconds | only a fast IV push will do
o Commonly causes asystole for several seconds
Analgesics/pain meds/muscle relaxants
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General Notes
o Pain is an individual experience and is whatever the patient says it is
o Tolerance is that amount of pain a person can endure without interfering with normal functioning (varies
from person to person, attitude, environment, culture, anxiety)
 Increasing tolerance does not increase the physical tolerance of side effects
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Gate theory is most common, tissue injury releases bradykinin, histamine, potassium, prostaglandins, and
serotonin—medications regulate the dorsal horn in the brain and prevents impulses from being
transmitted
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Step 1: Nonopioids | Step 2: Opioids with supplements | Step 3: Big opioids with supplements
Types of Analgesics
o Opioids
 MOA: Bind to opiate receptors to relieve pain, close the gate, have maximum effect of analgesics
 Mild agonists: Codeine, hydrocodone
 Strong agonists: Morphine, hydromorphone, oxycodone, meperidine, fentanyl,
methadone
 Also used for cough suppressant, diarrhea, balanced anesthesia
 Contraindications: Asthma, respiratory insufficiency, paralytic ileus, pregnancy
 Adverse: Respiratory depression, confusion, dizziness, sedation, urinary retention, constipation,
itching
 Interactions: Alcohol, antihistamines, barbiturates, benzos, MAOIs
 Fentanyl – not for opioid naïve patients (0.1mg = 10mg morphine)
 Hydromorphone (dilaudid) - 1mg = 7mg morphine
 Methadone – use for neuropathic and cancer pain, but has prolonged half-life
o Non-opioid Analgesics
 Tylenol – analgesic/antipyretic, no anti-inflammatory or sedation
 Blocks prostaglandin synthesis
 Max dose 3000mg/day, 2000mg/day for old people and liver disease
 Antidote = Acetylcysteine (mucomyst)
 NSAIDs (analgesic, antipyretic, anti-inflammatory)
 MOA: Block cyclooxygenase (COX), which synthesizes prostaglandins
o COX1 – maintaining GI mucosa and renal blood flow
o COX2 – promotes synthesis of prostaglandins
o Aspirin – reduces formation of thromboxane
 Contraindicated if vitamin K deficiency, ulcers, bleeding, renal failure
 Interactions with anticoagulants, corticosteroids, diuretics, ACE inhibitors, protein-bound
drugs
 Adverse: Heartburn and GI bleed, renal failure, MI/stroke, tinnitus
 Can give misoprostol (Cytotec) as GI protection with NSAID
 Salicylates
o Aspirin – reduces cardiac death after MI (first sign of MI)
o Contraindicated in children under 8 (Reye’s syndrome) - progressive, potentially
non-reversible neurologic damage
o Overdose: Use loop diuretics
 Enolic acid derivatives
o meloxicam
 Acetic acid derivatives
o Indomethacin – used for RA, OA, acute tendonitis, preterm labor
o Ketorolac (Toradol) - powerful painkiller, like morphine
 Short-term use (up to five days), renal impairment is AE
 Propionic acid derivatives
o Ibuprofen - most common NSAID, RA, OA, gout, dental pain
o Naproxen - Fewer drug interactions with ACE, better AEs
 COX-2 inhibitors
o Celecoxib (Celebrex) - only one
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 OA, RA, acute pain
 Adverse: headache, sinus irritation, diarrhea, fatigue
 Not for patients with sulfa allergy
Adjunct medications for pain – assist primary drugs in relieving pain, allow for smaller doses and decreased
adverse effects of opioids
 NSAIDS
 Antidepressants
 Anticonvulsants
 Corticosteroids
Anti-Seizure
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General
o Classifications
 Generalized onset seizures
 Tonic-clonic seizures, begin with contraction and then alternate contraction/relaxation
 Absence seizures are subtle/brief without a lot of movement
 Gray matter of both hemispheres
 Partial onset seizures
 Focal onset in one lobe of the brain
 Can be simple or complex
 Psychogenic/pseudo seizures
 Seizures that are happening with no electrical brain changes
o Status epilepticus
 Multiple seizures with no recovery between them, result is hypotension, hypoxia, brain damage,
and death
 Treat with diazepam and lorazepam
 True medical emergency
o Goal of therapy is to control seizures while maintaining quality of life, minimize adverse effects
 Must measure serum drug levels
 Meds are usually lifelong, start low/slow and gradually increase until therapy works
 Also used for neuropathic pain, bipolar disorder, migraines
 Black box warning for suicidality
 Take at same time every day, with meals and fluids, do not crush, do not discontinue abruptly
 Many have tetragenic effects, increased fall risk, potentially develop tolerance
 Most common side effects are drowsiness, sedation, GI upset, skin reactions
 Monitor respiratory/cardiovascular depression, aplastic anemia, agranulocytosis
o Mechanisms (most have more than one of these):
 Reduce nerve's ability to be stimulated
 Limit spread of seizure
 Decrease speed of nerve impulses
 Slow influx of calcium and sodium into neurons, antagonizes excitatory NT glutamate
 Enhanced effects of GABA
Barbiturates (no antidote)
o Phenobarbital
o Schedule IV
o Therapeutic levels of 10 to 40 mcg/mL--confusion, shortness of breath, slurred speech indicate toxicity
o Contraindications: Porphyria, liver/kidney impairment, respiratory illness
o Most common side effect is sedation
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Hydantoins
o Phenytoin
o Therapeutic levels of 10 to 20 mcg/mL, highly protein bound
o AE: gingival hyperplasia, hirsutism, acne, osteoporosis, measles-like rashes, pink to brown urine
o IV administration
 Very irritating to veins, slow IV into large vein in 20- or smaller gauge, diluted in NS only with a
filter
 Monitor for extravasation
 Fosphenytoin can be given without burning, but need to be on cardiac monitor and infuse slowly
Iminostilbenes plus valproic acid
o Carbamazepine
 Causes auto-induction of liver enzymes, stimulating its own metabolism, leading to lower than
expected blood concentrations
 Watch CBC for anemia and bone marrow suppression
 Avoid grapefruit juice
 Oxcarbazepine is a chemical analogue, but does not auto-induce
Adjunct medications
o Gabapentin
 Analogue of GABA, increases GABA concentration and inhibits brain activity
 AE: CNS and GI symptoms
 Used for seizures, but commonly seen for neuropathic pain
o Lamotrigine
 Generalized or tonic/clonic seizures, also bipolar
 Minor GI/CNS side effects, possible SJ syndrome
o Levetiracetam (keppra)
 Adjunct therapy for partial seizures, don’t know how it works
 No drug interactions, generally well tolerated
o Pregabalin (lyrica)
 Structurally related to GABA, mechanism not fully understood, adjunct for partial seizures
 Also used for fibromyalgia and neuropathic pain
 Schedule V controlled substance
Antilipemic Medications
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Properties
o Used to lower lipid levels (TGL, LDL) as adjunct to diet therapy
o Try non-drug methods for 6 months first
o Dosed once daily with meal or bedtime to correlated with diurnal rhythm of cholesterol production in the
body
o Herbals: Garlic, flax, omega-3 fatty acids
Nursing Considerations
o Contraindications: Biliary obstruction, liver dysfunction/disease (get baseline LFT)
o May need supplemental DEAK
o May take several weeks to be effective
o Report persistent GI upset, yellow skin, abnormal bleeding, constipation
o Monitor for +LFT, muscle pain, urine changes, vision changes (routine eye exams)
Statins (HMG-CoA reductase inhibitors)
o Most potent LDL reducers (first line therapy, up to 50% reduction), well tolerated
o Simvastatin, atorvastatin (“-statin”)
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o Inhibit HMG-CoA reductase, which is used by liver to produce cholesterol
o Adverse: muscle pain/change in urine (rhabdomyolysis), GI, elevation in liver enzymes, ocular events
o Interactions: Anticoagulants, drugs metabolized by CYP3A4 (diltiazem), grapefruit, amiodarone
Bile Acid Sequestrants
o Cholestyramine, colestipol (2nd line drugs)
o Bind bile and prevent reabsorption of bile acids from the small intestine (needed for cholesterol
absorption)
o Can also use for itching association with biliary obstruction
o Adverse: Constipation, heartburn, nausea, belching, bloating, take with meals, H20, fiber, may cause mild
increase in triglycerides
o All drugs must be taken 1 hour before or 4-6 hours after
o Decrease absorption of Vitamin D, E, A, K
B-Vitamin Niacin
o Much higher doses than when used as vitamin, gradually increase dose
o Increases activity of lipase, which breaks down lipids, causes histamine release
o Adverse: Flushing, Pruritis (take NSAID 30m before), GI distress
Fibric Acid Derivatives
o Gemfibrozil, fenofibrate
o Decrease TGL and increase HDL by 25%, activates lipase which breaks down cholesterol
o Contraindications: Liver/Kidney/Gallbladder disease
o Adverse: GI discomfort, diarrhea, nausea, increased risk of gallstones, prolonged PTT
o Interactions: Anticoagulant, statins, several lab test reactions (-Hgb, Hct, WBC, +PTT, bili)
Cholesterol Absorption Inhibitor
o Ezetimibe – inhibits absorption of cholesterol and sterols from small intestines
Coagulation modifiers
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General
o Intrinsic pathway activated in response to injury (internal damage to a blood vessel)
o Extrinsic pathway is activated when blood leaks out of vessel and into tissue space
o Baseline vitals and lab values
o Constantly assess for bleeding
o Educate on not increasing foods with vitamin K, avoid NSAIDS, prevent bruising
Anticoagulants
o No direct effect on blood clot that is already formed, decrease blood coagulability
o Use for MI, angina, afib, mechanical heart valves, prevention & treatment
o A/E: Bleeding, heparin-induced thrombocytopenia (acute fall in platelets, d/c heparin)
o So many interactions (ginger, gingko, garlic, SJW, feverfew)
o Heparin
 Antithrombin III
 Frequent laboratory monitoring using aPTT (1.5-2.5x control)
 LMWH (enoxaparin/Lovenox) - factor Xa
 Do not need frequent lab monitoring
 Do not expel air bubble, do not give with heparin
 Not for use with epidural catheter
 Antidote: Protamine Sulfate
o Coumarin
 Warfarin
 Do not use in pregnancy
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 Inhibits vitamin K synthesis by GI tract
 Monitor PT/INR daily (2-3 is therapeutic)
 Antidote: Vitamin K
o Direct Thrombin Inhibitors
 Bivalirudin, dabigatran
o Selective Factor Xa Inhibitors
 fondaparinux
Antiplatelets
o Aspirin, cilostazol, clopidogrel, prasugrel
o Prevent platelet adhesion before clotting cascade
o Aspirin blocks cyclooxygenase in platelets, may cause GI upset, bleeding
o Others inhibit ADP receptor which is important in activating platelets
o Use for stroke prevention, post-MI, post TIA, unstable angina
Antifibrinolytics
o Aminocaproic acid, desmopressin
o Prevent the lysis of fibrin, promoting clot formation—used to treat and prevent excessive bleeding
(hemophilia or von Willebrand’s disease)
o Rare reports of thrombotic events
Thrombolytics
o Alteplase, Tenecteplase
o Break down existing clots, re-establishing blood flow—activate the fibrinolytic system. Effects are
systemic!
o No invasive procedures, monitor for bleeding
Medication management during and after an MI
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Pain comes from accumulation of lactic acid from anaerobic metabolism
Goal is to increase blood flow or reduce oxygen demand
MI – necrosis of cardiac tissue from complete blockage
Beta blockers and calcium channel blockers for LT management, nitrates for acute treatment
Patient reports: Blurred vision, headache, dry mouth, edema, weight gain, fainting, dyspnea
Do not drink and hot tub. Orthostatic hypotension.
Keep record of anginal attacks
During MI, prep for cardiac catheterization (MONA):
o Morphine
o Oxygen
o Nitroglycerin
o Aspirin
Nitrates
o Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
o Cause vasodilation because it relaxes smooth muscle (venous more than arterial)
o Potent dilator of coronary arteries
o Prevention and treatment of angina, use special bags and tubes, titrate slow
o Large first-pass effect with oral forms, use SL for acute treatment (burning is normal), keep it fresh, goes
bad in 3 months (dark, airtight glass bottle)
o Wear patches 12-14 hours a day only to reduce tolerance development
o A/E: Headaches, orthostatic hypotension, tolerance
o Contraindicated: Hypotension, use of ED medications
o Nitroglycerine in Emergency
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Stop activity and sit down, take tablet
No relief in 5 minutes, call EMS, take second tablet
No relief in 5 minutes, take third table
Beta Blockers
o Atenolol, metoprolol,
o Use cardioselective B1 blockers preferably, they block harmful effects of catecholamines on the heart,
improving survival after MI
o -I/C/D
o Contraindicated in systolic HF, conduction disturbances, diabetes, PVD
o A/E: Bradycardia, hypotension, fatigue, impotence
Calcium Channel Blockers
o Diltiazem, verapamil, amlodipine
o Slows calcium into smooth muscle, causing vascular relaxation and prevents spasm
o Also causes peripheral arterial vasodilation
o -D, making it useful for treating dysrhythmias
 Diltiazem is first line treatment for atrial fibrillation and atrial flutter, along with PVST
o Interaction with grapefruit, can cause constipation
Thyroid
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T3, T4
o Regulate basal metabolic rate, normal growth/development, and thermoregulation
o Hypothyroidism – thickened skin, brittle hair and nails, constipation, lethargy, depression, anorexia, cold
intolerance, weight gain, tongue swelling
 Use levothyroxine or liothyronine sodium to treat
 SE: nervousness, tachycardia, weight loss, insomnia, diuresis
 Interact with anticoagulants, antacids, phenytoin
o Hyperthyroidism – diarrhea, flushing, increased appetite, muscle weakness, tachycardia, weight loss, muscle
wasting, menstrual changes, breast enlargement, intolerance to heat, exophthalmos, irritability
 Thyroid storm induced by stress or infection is severe side effect
 Use methimazole or propylthiouracil (PTU) to treat
 SE: Liver/bone marrow toxicity, nausea/vomiting, leukopenia, increased BUN & creatinine
o Take medications in AM on empty stomach, don’t switch brands, may decrease digoxin levels, increase
anticoagulants, decrease oral diabetics
o Avoid eating foods high in iodine
o Monitor WBC counts for leukopenia
Calcitonin - Maintain adequate levels of calcium in extracellular fluid
Parathyroid

Secretes parathyroid hormone
o Release of calcium by bones into the bloodstream.
o
o
Absorption of calcium from food by the intestines.
Conservation of calcium by the kidneys.
Adrenal

Adrenal cortex
o Cortisol






Anti-inflammatory
Carb, protein, fat metabolism
Stress effects, alter/suppress normal immune response
Cushing’s is excess, Addison’s is deficiency
Used for anti-inflammatory, cerebral edema, collagen diseases, dermatologic diseases, endocrine
disorders, GI disease, exacerbations of respiratory illness, hematologic disorders, ophthalmic
disorders, organ transplants, leukemia, lymphoma, nephrotic syndrome, spinal cord injury
 Glucocorticoids
 Prednisone, dexamethasone, hydrocortisone, methylprednisolone (IV)
 Contraindications: serious infections, gastritis, diabetes, organ dysfunction
 A/E: Heart failure, edema, hypertension, psychosis, hyperglycemia, ulcers, fragile/thin
skin, poor wound healing, glaucoma, weight gain, osteoporosis
 Interact: Potassium-Wasting diuretics, aspirin, NSAIDs, anticholinesterase drugs,
immunizing biologics, antidiabetics
 Must taper to discontinue
o Aldosterone
 BP control, maintenance of K+ levels and pH
 Fludrocortisone (treatment for Addison’s)
Adrenal medulla – epinephrine & norepinephrine
Insulin





Rapid-acting (“The log showed that 15 minutes felt like an hour during 3 rapid responses”)
o Insulin lispro, insulin aspart, insulin glulisine
o O: 5-15M | P: 1-2H | D: 3-5H
o SubQ injection or continuous subQ infusion pump
o Must eat a meal after injection (5-15 minutes)
o Afrezza (inhaled)
 P: 12-15M | D: 2-3H
 Admin 20 minutes before meals
 Don’t give to smokers or people with chronic lung disease, risk for acute bronchospasms
Short-acting (“Regularly short staffed nurses went from 30 patients to (2) 8 patients”)
o Regular insulin (Humulin R)
o O: 30-60M | P: 1-5H | D: 6-10H
o IV bolus, IV infusion, subQ
 May give IV for DKA, acute hyperkalemia, post-surgically
Intermediate (“Nurses play hero to (2) 8 16-year-olds")
o Insulin isophane suspension (NPH)
 Often combined with regular insulin, white/cloudy appearance
o O: 1-2H | P: 4-8H | D: 10-18H
o Can give after meals
Long-acting (“The two long nursing shifts never peaked but lasted 24 hours”)
o Insulin glargine (Lantus), insulin detemir (Levemir)
o O: 1-2H | P: none | D: 24H
o Also referred to as basal insulin, usually dosed once daily
o Maintains blood glucose regardless of meals
Disadvantage of sliding scale is that it delays treatment until hyperglycemia occurs, resulting in large swings in
blood sugars
o More beneficial is bolus dosing to keep patients at a continuous blood glucose level
Diabetic oral and injectable meds







Diagnosis: Fasting blood glucose above 126 mg/dL or HbA1C greater or equal to 6.5% (goal of treatment is <7%,
fasting blood glucose of 70 to 130 mg/dL)
o Symptoms include polyuria, polydipsia, polyphagia, glycosuria, fatigue, weight loss
o Type 1: Lack of insulin production or autoimmune destruction of beta cells
o Type 2: Caused by insulin deficiency and insulin resistance
 Associated with several comorbid conditions (obesity, CAD, HTN, collectively referred to as
metabolic syndrome)
 Long-term complications are micro- and macro-vascular
o Concerns for these patients increase during stress, infection, illness, pregnancy, steroids
Symptoms & treatment of hypoglycemia
o Headache, sweatiness, blurry vision, tinnitus, tachycardia, hunger, irritability, anxiety, weakness
o Administer 15g of carbs if conscious (D50 or IV glucagon if not)
 Wait 15 minutes, if still <70, repeat (up to three times)
Biguanides
o Metformin
o First-line treatment and most commonly used oral drug for DM2
o Mechanism:
 Decrease production of glucose by the liver
 Decrease intestinal absorption of glucose
 Improve insulin receptor sensitivity
o AE: Nausea, cramping, fullness, diarrhea, weight loss (take with meals), hypoglycemia, lactic acidosis—
discontinue if patient doing contrast studies due to renal impacts
Sulfonylureas
o Glipizide
o Mechanism:
 Binds to specific receptors on beta cells, causing release of insulin
 Decreases secretion of glucagon
o Contraindicated if patient is NPO or has hypoglycemia
o AE: hypoglycemia, weight gain, rash, fullness
o Take with food to minimize GI upset
Glinides (meglitinides)
o Repaglinide
o Mechanism:
 Similar to sulfonylureas, but must be given with each meal
o AE: Headache, hypoglycemic effects, dizziness, weight gain, URI
Thiazolidinediones
o Pioglitazone, rosiglitazone
o Mechanism:
 Decrease insulin resistance, inhibits gluconeogenesis
 Enhance sensitivity of insulin receptors
o AE: hepatic toxicity (monitor LFTs), edema, anemia, contraindicated with heart failure
Alpha-glucosidase inhibitors
o Acarbose, miglitol
o Mechanism:
 Reversibly inhibit alpha-glucosidase resulting in delayed absorption of glucose
o Take with first bite to prevent post-prandial glucose elevations
o AE: flatulence, diarrhea, abdominal pain—do not cause hypoglycemia, weight gain


Depeptidyl peptidase-IV inhibitors
o Sitagliptin
o Mechanism:
 Delay breakdown of incretin hormones (which increase insulin secretion and lower glucagon
secretion) by inhibiting DPP-IV
o AE: URI, headache, hypoglycemia (more common when combined with sulfonylureas)
Injectable
o Amylin agonist
 Pramlinitide subcut
 Slows gastric emptying, suppresses glucagon secretion, modulates appetite, use when other
drugs haven’t worked for DM1 or DM2
 AE: Nausea, vomiting, contraindicated with gastroparesis
o Incretin mimetics (GLP-1 agonists)
 Exenatide – injection pen, 1 hour before meals
 Mimics the incretin hormones (increases insulin secretion and lowers glucagon secretion)
 AE: Nausea, vomiting, weight loss, hypoglycemia, rare cases of pancreatic issues
Antifungals
-
-
-
Overall, impair cell membrane of fungus, avoid in liver failure patients
“azoles”
o Imidazoles: ketoconazole, triazole: fluconazole
o Inhibit P-450, leading to cell death
o Less toxic and as effective
o S/E: Nausea, vomiting, diarrhea, use with caution in renal/liver failure, watch for skin rashes, need
alternative birth control
Echinocandins ($$$)
o “-fungin”: caspofungin, micafungin
o Prevent the synthesis of glucans (part of cell wall)
Polyenes – bind to sterols in cell membrane, causing death
o Amphotericin B, nystatin (PO thrush, candidiasis)
o Amphotericin B: Drug of choice for severe systemic fungal infections
 Amphoterrible. Heart dysrhythmias, neurotoxicity, tingling, pain, convulsions, renal toxicity, fever,
GI upset, infiltration
 Use premedications, long infusion time, monitor VS Q15-30m
o Nystatin: Slowly/completely dissolve or swish as long as possible
Antituberculars
-
-
TB: granulomas in the lungs with clear boundaries, cheesy center
o Commonly in lungs, brain, bone, liver, kidney
o Spread via droplets, very slow-growing organism
o MDR-TB is resistant to isoniazid and rifampin
Meds reduce cough, usually within two weeks, but medication goes for at least six months and sometimes as long
as 24 months – monitor compliance!
Rifampin, isoniazid, pyrazinamide, ethambutol, streptomycin
o Rifampin
 Macrolide antibiotic, inhibits protein synthesis
 SE: hepatitis, discoloration of urine/tears (red-orange)
 Oral contraceptives become ineffective, watch LFTs
o
-
Isoniazid
 Drug of choice. Inhibits cell wall synthesis
 Contraindicated with liver disease
 May need to provide pyridoxine (B6) to combat neurological issues caused by INH
o Pyrazinamide
 SE: Hepatotoxicity, hyperuricemia
 Watch LFTs and uric acid levels
o Ethambutol
 Can cause vision loss and optic neuritis
 Monitor vision acuity
o Streptomycin
 Can cause ototoxicity and nephrotoxicity
Mantoux tests is normal test to detect exposure
BCG is vaccine given to world’s young children, can cause false positive on Mantoux test
Do not consume alcohol, assess contraindications, and wear N95/airborne precautions
Take medications at same time every day, exactly as ordered. Contagious during the early part of their illness.
Need three negative sputum cultures to be non-infectious!
Antibiotics
-
-
Most common severe reactions: difficulty breathing, rash, hives, skin reaction, severe GI intolerance
Interfere with cell wall synthesis, protein synthesis, DNA replication, disrupt chemical reactions within the
bacterial cell
Overall, take as prescribed, most common SE are NVD, take with 6-8 oz of water, use back up birth control, wash
hands, caution exposure to sunlight, do not take excessively
Sulfonamides (G+/G-)
o Often combined with other antibiotic
o Prevent synthesis of folic acid
o Don’t give if sulfa allergy
o Treat for UTI, HIV pneumonia, URI, outpatient staph infections
o Steven Johnson’s Syndrome
Beta-Lactam Antibiotics (tazobactam opens ring so penicillin can be effective)
o Penicillins (G+)
 Ampicillin, amoxicillin, piperacillin, Zosyn, Augmentin (don’t end in –cillin)
 Disrupt normal cell wall synthesis
 Inquire about known drug allergy, NVD
 Only patients with throat swelling or hives should not receive cephalosporins
 Take with water, not juice. Interactions (NSAIDs, BC, warfarin)
o Cephalosporins
 1st gen (G+) - cefazolin, cephalexin – surgical prophylaxis and cellulitis
 2nd gen (G+, some G-) - cefuroxime - only generation that can treat anaerobes!
 3rd gen (G-, some G+) - ceftazidime, cefdinir, ceftriaxone – majority IV
 4th gen (broader spectrum) - cefepime – UTI, skin infections, pneumonia
 5th gen (broadest spectrum) - ceftaroline – only one that treats MRSA
 Some may cause disulfiram reaction when taken with alcohol, monitor renal and hepatic function
o Carbapenems
 Broadest antibacterial function of any to date
 Reserved for complicated body cavity and connective tissue in acute hospital patients
 Must be infused over 60 min to prevent seizures
 Imipenem, meropenem
o
-
-
-
-
-
Monobactams
 Aztreonam
 Synthetic, used against gram negative HAIs, moderately severe systemic infections and UTIs
Macrolides
o Erythromycin, azithromycin, clarithromycin
o Considered bacteriostatic – given for strep, URI, syphilis, Lyme, gonorrhea, H. pylori
o Highly protein bound and metabolized in the liver
o Enhanced absorption when taken on an empty stomach
Quinolones (G- and some G+)
o Ciprofloxacin, levofloxacin, moxifloxacin
o Used for complicated UTI, respiratory, bone, joint, STIs, treats anthrax!
o Interact with antacids, calcium, magnesium, zinc, sucralfate
o NVD, prolonged QT interval, ruptured tendons, tendonitis, not recommended for kids under eight years
old
Aminoglycosides (G-/ some G+)
o Potent, drug for virulent infections, no oral forms
o Gentamicin, neomycin, tobramycin, streptomycin, amikacin
o Used for serious G- bacteria, resistant G+
o Ototoxicity/nephrotoxicity! Get peaks and troughs
o Gentamycin therapeutic range is 6-12mcg/mL
Tetracyclines (G+/G-)
o Doxycycline, tigecycline, tetracycline
o Wide spectrum, used for tuberculosis, leprosy, chlamydia, rickettsia
o Discoloration of teeth and enamel in <8 years old
o Do not take during pregnancy
o Avoid milk, iron, antacids, sunlight
Miscellaneous
o Flagyl
 Treat intraabdominal and gynecologic infections (C. Diff)
 Protozoal infections
 Avoid alcohol
o Vancomycin (glycopeptide)
 Treatment of choice for MRSA
 Also used for C.diff
 Monitor blood levels, may cause ototoxicity and nephrotoxicity
 Red Man Syndrome! - slow infusion, antihistamine
o Clindamycin
 Used for chronic bone, GU, intrabdominal infections
 Reserved for serious/resistant infections
 May cause c.diff infection
o Linezolid
 Used to treat VRE, MRSA, pneumonia
 May cause hypotension, serotonin syndrome if combined with SSRIs
o Nitrofurantoin
 Primarily used for UTIs because concentrates in the urine
 Use carefully if patient has renal failure
o Daptomycin
 Treats skin and soft-tissue infections caused by MRSA and VRE
 Do not use for pneumonia because inactivated by surfactant
Antivirals
-
-
-
-
-
Can be used to treat non-HIV viral infections (flu, HSV, CMV, hepatitis)
Acyclovir
o Used for HSV-1, 2, VZV
o Helps lesions dry and crust over, not a cure
o Famciclovir used for shingles, valacyclovir topical cream
Ganciclovir
o Used to treat CMV infection, CMV retinitis with implanted form
o Can cause bone marrow suppression, watch CBC
Ribavirin and sofosbuvir (treatment for hepatitis C)
o Ribavirin can be used for RSV infections in infants
o Sofosbuvir can be used for chronic hepatitis C, 90% cure rate
Amantadine
o Only active against influenza A
Oseltamivir
o Active against influenza A and B
o Reduce duration of illness by 3-5 days, PO
o Begin treatment within 2 days of influenza symptom onset
o Zanamivir - inhaled way to treat influenza A and B
HIV and AIDS Treatment
o HAART (Highly Active Antiretroviral Therapy) - Goal is to find regimen that will best control symptoms,
infection, minimize side effects, and prolong survival
o Reverse transcriptase Inhibitors (RTIs)
 Prevent production of new viral DNA
 Zidovudine
 Remain upright for 30 minutes after administration to prevent GI irritation
 SE: Bone marrow suppression, insomnia expected for 3-4 weeks
o Watch for signs of opportunistic infections, toxic to liver
o Not sure but help to manage symptoms
COPD/Asthma


General
o Asthma can be intrinsic (no history of allergies) or extrinsic (history of allergies)
o Status asthmaticus is a prolonged asthma attack and is a medical emergency
o Avoid exposure to allergens, drink fluids, comply with treatment
o Take bronchodilators first!
o Only use SABAs as rescue inhalers
o 1-2 minutes between puffs, 2-5 minutes between each medication
Bronchodilators
o Beta-2 Adrenergic Agonists
 Activate SNS, relaxing bronchial smooth muscle, causing dilation of airways
 Short Acting Beta Agonist
 Albuterol, levalbuterol, terbutaline
 If used too frequently, loses B2-specific actions and stimulates B1 as well
 Long Acting Beta Agonist
 Salmetrol
 Not for acute treatment, never give more than 2x daily
 A/E: Hypotension, or hypertension, vascular headache, tremor, palpitations
o

Anticholinergics
 Ipratropium, tiotropium, duoneb (ipratropium & albuterol)
 Prevent ACh from binding, bronchodilation, reduced secretions
 A/E: dry mouth, constipation, urinary retention, increase ocular pressure
o Xanthine derivatives
 Aminophylline, theophylline, caffeine
 Inhibit phosphodiesterase, increasing cAMP, causes CNS stimulation
 Not commonly used due to interactions and need for monitoring (<20mcg/mL)
 A/E: Sinus tachycardia, palpitations, ventricular dysrhythmias, hyperglycemia
Non-Bronchodilators
o Leukotriene Receptor Antagonists
 Montelukast
 Leukotrienes cause inflammation, bronchoconstriction, these prevent them from attaching to
receptors, blocking inflammation
 Used for prophylaxis and long-term prevention of asthma
 Don’t use if allergic to povidone, lactose, titanium dioxide, or cellulose
 Assess liver function before beginning therapy
o Corticosteroids
 Fluticasone, dexamethasone, prednisone, methylprednisolone
 Stabilize membranes of cells that will release inflammatory agents, increase responsiveness of
bronchial smooth muscle to adrenergic stimulation
 Used for chronic asthma/COPD
 IV are generally only for acute exacerbation or severe asthma
 Beware of oral fungal infections/thrush, rinse mouth after
 May increase serum glucose levels, beware with diabetics
 Use bronchodilator first!
Parkinson's Disease


General
o Chronic, progressive, degenerative disorder
o Caused by imbalance of two neurotransmitters
 Dopamine (deficiency, substantia nigra does not produce)
 Acetylcholine (excess due to dopamine depletion)
o Symptoms start when 80% of dopamine is depleted
 TRAP – Tremor, rigidity, akinesia, postural instability
 Also: drooling, pill rolling, mask expression, shuffling gait
 Chorea: irregular, spasmodic movements of limbs and face
 Dystonia: abnormal muscle tone leading to abnormal movements in head, neck, feet
o Rapid swings in response to levodopa lead to “on-off phenomenon”
o Eases symptoms but does not slow progression
o Fall risk is number one priority
o Medication timing is critical!
Indirect-acting dopaminergic drugs
o MAOI-B inhibitors
 Rasagiline, selegiline
 Break down catecholamines in the CNS, increase dopamine stimulation and preserve existing
dopamine
 Do not have the cheese effects because it’s selective for MAO-B
 Used as monotherapy or with Carbidopa-Levodopa
o

Dopamine modulators
 Amantadine
 Anti-viral, causes release of dopamine and other catecholamines from storage, blocks reuptake of
dopamine
o COMT inhibitors
 Entacapone, tolcapone
 Block COMT, the enzyme that catalyzes the breakdown of catecholamines, prolongs the duration
of levodopa
 AE: urine/sweat discoloration, GI upset, may worsen dyskinesia. Tolcapone has been associated
with severe liver failure
Direct-acting dopaminergic drugs
o Non-dopamine receptor agonists
 Bromocriptine (ergot) | also, non-ergots (pramipexole, ropinirole)
 Directly stimulate pre- or post-synaptic dopamine receptors
 Also inhibits production of prolactin
 AE: GI upset, dyskinesia, sleep disturbance, caution in patients with PVD or heart disease or those
taking adrenergic drugs (because it causes vasoconstriction)
 Non-ergots can be used to treat restless leg, are more specific for D2 receptors
o Dopamine replacement drugs
 Carbidopa-levodopa
 Levodopa is precursor to dopamine, blood-brain barrier restricts exogenous dopamine but lets it
in and then is converted
 Carbidopa is given to transport the levodopa to the brain so it doesn’t get broken down in the
periphery.
 Allows for smaller doses of levodopa to be given and reduces adverse effects
 Becomes more difficult to treat with levodopa as the disease progresses
 Contraindicated/caution with glaucoma
 AE: dysrhythmia, hypotension, chorea, muscle cramps
 Interacts: pyridoxine (B6) and dietary protein, take on empty stomach, time appropriately with
protein intake (30 minutes before or 1 hour after meals), taking with non-selected MAOIs can
lead to hypertensive crisis
o Anticholinergics
 Benztropine, trihexyphenidyl
 Block the effects of Acetylcholine
 Used to treat muscle tremors and rigidity as adjunct therapy
o Antihistamines as symptom management
 Diphenhydramine
Digestive drugs (Nausea, vomiting, diarrhea, constipation, and GERD)
-
Diarrhea
o Goal of treatment: stop frequency, alleviate cramps, replenish fluids, prevent nutritional deficiencies –
take the cause of the diarrhea into consideration when treating
o Don’t use for obstruction or colitis!
o Decrease absorption of many drugs (digoxin, quinidine, hypoglycemic drugs), increase bleeding time,
increase toxicity of methotrexate
o Absorbents
 Coat walls of GI tract, bind to toxin, which is then eliminated through stool
 Bismuth-subsalicylate (not for kids- Reye's), colestipol, cholestyramine
 Side effects – increased bleeding time, constipation, dark tongue and stool
o
-
-
Antimotility drugs
 Anticholinergics
 Decrease intestinal muscle tone and slow peristalsis, reduces secretions
 Belladonna alkaloids
 Side effects – urinary retention, impotence, headache, dry skin, flushing
 Not for patients with NEG, GI obstruction, myasthenia gravis, paralytic ileus, toxic
megacolon
 Opiates
 Decrease bowel motility and reduce pain by relieving rectal spasms
 Codeine, diphenoxylate with atropine (Lomotil), loperamide
 Side effects – drowsiness, dizziness, lethargy, N/V, respiratory depression
o Probiotics
 Replenish destroyed bacteria of the GI tract, restoring normal balance
 Lactobacillus acidophilus
Constipation
o Bulk-forming
 Act like high fiber in natural diet, absorb water to increase bulk to distend bowel
 Psyllium
 Side effects – esophageal blockage/obstruction, take with at least 8 oz water
 Only laxative okay for long-term treatment
o Emollient (stool softeners, lubricant laxatives)
 Promote more water and fat absorbed into stool to lubricate, only softens, does not cause
immediate pooping
 Docusate salts (stool softener) | mineral oil (lubricant)
o Hyperosmotic
 Increase fecal water content and increase osmotic pressure
 Polyethylene glycol – large volume, allow time to consume to prevent nausea
 Lactulose – also used to reduce serum ammonia in liver disease
 Used for chronic constipation, diagnostic preparation
 Side effects – bloating, electrolyte imbalances
o Saline
 Increase osmotic pressure, causing water and salt to enter bowel wall
 Sodium phosphate enema, magnesium hydroxide, magnesium citrate
 Used for constipation and surgical preparation
 Side effects – magnesium toxicity, cramping, electrolyte imbalance
 Contraindicated in renal disease and cardiac disease (due to sodium)
o Stimulant
 Increases peristalsis via intestinal nerve stimulation
 Most likely to cause dependence!
 Senna, bisacodyl (most common, 6-12 hour effects)
 Used for acute constipation, diagnostic preparation
 Can cause malabsorption, gastric irritation, abdominal pain
 Take on empty stomach with water, avoid other meds within an hour, no milk/antacids
o Peripherally acting opioid antagonists
 Treatment of constipation related to opioid use or bowel resection
 Block entrance of opioid into bowel, allowing bowel to continue functioning with opioid use
 Methylnaltrexone
Nausea/vomiting
o
o
o
o
o
o
o
-
o
GERD
o
o
o
Neurotransmitters involved in vomiting: Acetylcholine, dopamine, H1, prostaglandins, 5-HT3, neurokinin
1
 Many work by blocking one of the vomiting pathways, preventing the stimulus
 Majority block effects of dopamine and 5HT3 on CTZ
 Overall goals are to treat N/V, minimize F/E disturbances, minimize loss of nutritional status
 Taking them with alcohol can cause severe CNS depression
 Assess mucous membranes, capillary refill, skin turgor, electrolytes, IOs
 Many cause severe drowsiness, warn patients about driving
 Check BP prior to administration, give antiemetics 30-60 minutes before chemo
Anticholinergics
 Block ACh receptors in inner ear, dry secretions, reduce GI muscle spasm
 Scopolamine (motion sickness)
 Contraindicated with glaucoma
Antihistamines (H1 receptor blockers)
 Inhibit ACh binding to H1 receptors, antispasmodic and antisecretory
 Dimenhydrinate, diphenhydramine, meclizine (vertigo), hydroxyzine
Antidopaminergics (Phenothiazines)
 Block dopamine receptors, good for hiccups
 Prochlorperazine, promethazine
 Side effects: sedation, orthostatic hypotension, EPS, photosensitivity
Prokinetic
 Block dopamine receptors in the CTZ, stimulate peristalsis
 Used for GERD, n/v, high residuals in tube feeding
 Metoclopramide
 Side effects: hypotension, EPS—take prior to meals
Serotonin blockers
 Block serotonin receptors in the GI tract and CTZ
 Ondansetron
 Prolonged QT interval, give doses 30 minutes prior to start of chemo or before surgery is over
Tetrahydrocannaboids (THC)
 Alter mood and body perceptions of surroundings, indicated for anorexia associated with weight
loss
 Dronabinol
 Side effects: dizziness, postural hypotension
Steroids & benzodiazepines
H. pylori first line treatment includes proton pump inhibitor, clarithromycin, and
amoxicillin/metronidazole
 Or, proton pump inhibitor, bismuth subsalicylate, and tetracycline or metronidazole
Stress ulcer – give histamine receptor blocking drug or proton pump inhibitor
Antacids
 Basic compounds used to neutralize stomach acids
 Magnesium counteracts constipating effects of aluminum and calcium
 Do not give these to patients with renal failure
 May lead to kidney stones and/or gastric acid rebound
 Do not prevent acid, instead neutralize it, and promote gastric mucosal defense mechanisms
 Contraindicated in patients with electrolyte disturbances or GI obstruction
 Aluminum salts are used in patients with renal disease, given with Mg+ for constipation
 Calcium carbonate most common (Tums), may cause kidney stones, constipation


o
o
o
o
o
Sodium bicarbonate buffers HCl, may cause metabolic alkalosis, and patients with heart issues
These drugs reduce the ability of other drugs to be absorbed into the body through chelation,
increased stomach pH and increased urinary pH (quinolone absorption is reduced by 50%, for
examples)
 Administer most medications 1-2 hours after antacid
H2 Antagonists
 Reduce acid secretion by blocking H2 receptors of parietal cells (90% blocked)
 Cimetidine, nizatidine, famotidine (“-tidine”)
 Very well tolerated, can cause CNS issues in older people, cimetidine may cause impotence and
gynecomastia
 Smoking decreases the effectiveness of H2 blockers
 Cimetidine results in increased drug levels of many drugs
 Take 1-2 hours before antacids, usually diluted in NS and given over two minutes, rapidly can
cause hypotension
Proton Pump Inhibitors
 Inhibit the parietal cells from releasing H+, end in “-prazole”
 H2 blockers and antihistamines do not stop the action of this pump by binding to the H+/K+
ATPase enzyme, preventing the secretion of H+
 All gastric acid secretion is temporarily blocked (achlorhydria)
 Omeprazole, pantoprazole
 First line for GERD, esophagitis, ulcers, NSAID-induced ulcers, active GI bleed
 Generally well tolerated except for some dizziness and diarrhea
 Administer 30 minutes before eating, food may decrease absorption
 Capsule contents can be opened but do not crush/chew granules
Sucralfate
 Cytoprotective drug, used for stress ulcers and peptic ulcer disease
 Binds to the base of ulcers and erosions, coating them and forming a protective barrier
 Give other drugs at least two hours before this medication, may also cause nausea, constipation,
dry mouth
 Can be used to reduce phosphate levels in chronic renal failure
Misoprostol
 Like a prostaglandin, protects mucosa from injury, maintains blood flow
 Used for prevention of NSAID-induced gastric ulcers
 Often produce abdominal cramps and diarrhea
Simethicone
 Antiflatulent drug
 Breaks gas bubbles into smaller ones, reducing their excretion
 Avoid foods that are gas-producing
Parameters for use of digoxin and nursing considerations
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General HF Information
o Reduced ejection of blood or resistance to ventricular filling, the heart is unable to pump blood to meet
the body’s metabolic needs
o Left-sided HF: Pulmonary edema, coughing, SOB, dyspnea
o Right-sided HF: Systemic venous congestion, ascites, hepatic congestion
o Early HF treatment: ACE, ARB, BB, Loop diuretics
o Severe stages: Aldosterone antagonists (spironolactone, epleronone)
o Miscellaneous HF drugs:
 Hydralazine/isosorbide dinitrate (BiDil) is first for African Americans
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 dobutamine (B1-adrenergic, increases stroke volume)
 Nesiritide – synthetic BNP, causes vasodilation, diuresis (ICU, severe HF)
 Milrinone – phosphodiesterase inhibitor, increases cAMP, +inotropic
Parameters for Use
o Cardiac glycoside, used to control ventricular response to atrial fibrillation and HF
o MOA: Inhibits Na/K ATPase pump, resulting in more intracellular Na/Ca, also stimulates vagus nerve so
has some parasympathetic stimulating effects
 +Inotrope, -Chronotrope, -Dromotrope
 Increases SV, coronary circulation, decreases BP
 Improves symptom control, QOL, exercise tolerance
o Very narrow therapeutic window (0.5-2.0 ng/mL)
o Low potassium and magnesium increase toxicity
Nursing Considerations
o Once daily, same time every day
o Assess apical pulse for one full minute (hold for <60), heart/breath sounds, serum labs (potassium,
sodium, magnesium, calcium, renal/liver function)
o Adverse: Dysrhythmias, bradycardia or tachycardia, seeing green, yellow, purple, halo vision, flickering
lights, anorexia, nausea, vomiting, diarrhea
o Avoid giving with high-fiber foods
o Immediately report weight gain of 2+ pounds in a day or 5+ pounds in a week
o Hypokalemia and hypercalcemia increase risk of toxicity, as well as pacemaker, hypothyroid, renal
disease, rapid digitalization (loading doses)
o Antidote – digibind – forms a complex and binds, inactivating it, indicated for:
 Hyperkalemia in a digitalis-toxic patient
 Cardiac dysrhythmias
 Digoxin overdose