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Medications Prototypes: Non-Prototypes:

IndicationsDosing/Medication formsMOA Background info:

ContraindicationsDrug interactionsTherapeutic outcomesAdverse effectsToxicity Treatment during ToxicityNursing interventions Patient Teaching

Information in this study guide was taken from the source below:

LILLEY, LINDA LANE. RAINFORTH COLLINS, SHELLY. SNYDER, JULIE S. PHARMACOLOGY AND THE NURSING PROCESS, 8th Edition. MOSBY, 2017.

Autonomic Nervous system

Drugs

Direct acting Cholinergic (muscarinic) agonistMedications Prototypes:

Bethanachol (Urecholine)Non-Prototypes:Dry mouth—-cevilimine (Evoxac)- Pilocarpine (Salagan)

Glaucoma—-eye drops

Indications -post-op urinary retention-post-op colon atony (paralytic ileus)

Increase parasympathetic system activity-increase urination-decrease intra-ocular pressure-increase saliva production

Dosing/Medication formsMOA Direct acting muscarinic agonist (parasympathomimetic)—

-agonist binds to muscarinic receptors-Mimics the action of ACH***Does NOT cross BBB can’t be used as an antidote for cholinergic antagonist toxicity

Background info:

Contraindications -Gastric ulcers-obstructions or weaknesses of bladder/bowel-low cardiac output-hyperthyroidism

Hyperthyroidism + bethanacholhypotensionbaro receptors release norepinephrineincrease in BPtachycardia (dysrhythmia) People with hyperthyroidism are very sensitive to norepinephrine and epinephrine.

-History of asthma or COPDDrug interactionsTherapeutic outcomes -increase urination

-increase BMsAdverse effects Severe:

-Hypotension-bradycardia-bronchospasm

Rare:-seizures

Toxicity Caused by: wild mushrooms, Organophosphates (insecticides), Nerve Gas (chemical warfare—EX: Sarin Gas-SLUDGE: Salivation, Lacrimation, Urination, Defacation, GI upset, Emesis

**DUMBELLS: Diarrhea (defection), Urination, Miosis, Bradycardia, Bronchorrhea, Bronchoconstriction, Emesis, Lacrimation, Lethargy, Salivation

**Remember: Bradycardia/bronchospasms/bronchial secretions can ALL lead to tachycardia because they are stressful eventsSNS takes over

Treatment during ToxicityAtropine—anti cholinergic agent-EX: (mark 1 auto injectors given to US soldiers)

Nursing interventions -Asses for patient conditions affecting Heart Lungs GI Tract Urinary Tract

-Assess presence of multiple meds with cholinergic activity-Prevent injury/complications

Have bedpan/urinal available Provide night light in room Monitor patient for blurred vision

Monitor patient for altered mental status if elderly

Patient Teaching

Indirect acting cholinergic (muscarinic) agonistMedications Prototypes:

Physotigmine (Antilirium)Non-Prototypes:Alzheimer’s DiseaseDonezepil (Aricept)

Myesthenia Gravis-Neostigmine-Pyridostigmine ambenonium

Indications -Myasthenia Gravis Myesthenia Gravis diagnosed using: Edrophonium (Tensilon)

-Tricyclic antidepressant overdose-Exposure to chemical warfare agents-Alzheimers dementia-physostigmine = antidote for cholinergic antagonist toxicity

Altered mental status***Crosses the BBB which is why it’s used when patients show signs of altered mental status

Signs of anticholinergic toxicityMOA: physostigmine transiently reverses anticholinergic effects and aids diagnosis in unclear cases

Dosing/Medication formsMOA Indirect acting cholinergic agonist—

-binds to acetyl cholinesteraseinhibits destruction of acetylcholineincreasing ACH availabilityprolongs action of ACH at muscarinic (cholinergic) receptor sites-Phyostigmine binds reversibly to active site on ACH

Background info:

Contraindications Contraindicated in: Bradycardia AV block Uncontrolled ashma/wheezing seizures

Drug interactionsTherapeutic outcomes -increase strength of muscle contraction

-cholinergic effect in GI tract and urinary tract

Adverse effects -Severe confusion-tachycardia

Toxicity Caused by: wild mushrooms, Organophosphates (insecticides), Nerve Gas (chemical warfare—EX: Sarin Gas-SLUDGE: Salivation, Lacrimation, Urination, Defacation, GI upset, Emesis

**DUMBELLS: Diarrhea (defection), Urination, Miosis, Bradycardia, Bronchorrhea, Bronchoconstriction, Emesis, Lacrimation, Lethargy, Salivation

**Remember: Bradycardia/bronchospasms/bronchial secretions can ALL lead to tachycardia because they are stressful eventsSNS takes over

Treatment during ToxicityAtropine—anti cholinergic agent-EX: (mark 1 auto injectors given to US soldiers)

Nursing interventions -Asses for patient conditions affecting Heart Lungs GI Tract Urinary Tract

-Assess presence of multiple meds with cholinergic activity-Prevent injury/complications

Have bedpan/urinal available Provide night light in room Monitor patient for blurred vision

Monitor patient for altered mental status if elderly

Patient Teaching

Cholinergic AntagonistsMedications Prototypes:

AtropineNon-Prototypes:-COPD—Itratropium (Atrovent)-Urinary incontinence—Oxybutinin (Ditropan)**Many OTC and prescription drugs have anticholinergic effects-scopolomine—used for motion sickness and to dry up excess secretions in dying patients-hycosamine

-antihistamines-Tricyclic antidepressants-incapacitating agents-ingested items—jimson weed amanita muscaria mushrooms-parasympatholytic medications

Indications -Antidote for cholinergic toxicity-symptomatic bradycardia (meaning abnormal for the person)-Dilation of pupils-Dry secretions before surgery-Sine diarrhea medications contain atropine

Dosing/Medication formsMOA Cholinergic Antagonist

Direct Muscarinic Antagonist (parasymptholytic)Competitively binds to muscarinic receptorsblocks effect of ACH

Background info:

ContraindicationsDrug interactionsTherapeutic outcomes -Increase HR

-Dries Secretions-Decreases GI motility-dilates puils-decrease urinary incontinence-dilate small airways

Adverse effects -Tachycardia-Dry Mouth-Blurred vision-photophobia-increased intra-ocular pressure-urinary retention-constipation-CNS excitation/psychosis

-hot dry flushed feeling-dry mucus membranes in respiratory tract-bronchodilation in medium/small airways-Decreased GI motility and secretions-decreased bladder contraction-Urinary retention-decreased sweatingoverheating

Toxicity Single drug taken in excess, multiple anticholinergic drugs taken simultaneously, intentional overdose, unintentional ingestion, medical noncompliance, geriatric polypharmacy-Tachycardia (often the first sign—can approach 150 bpm)-dry mouth-Midriasis w/ Blurred Vision, photophobia, increased intra-occular pressure-urinary retention-constipation + decreased bowel sounds-CNS excitation/psychosis

Altered level of consciousness—soft spoken, mumbling, word salad, hallucination, delirium, coma

Seizures-hot dry skin—hyperthermia (low grade fever) + no sweating-Flushed color

Red as a beat (atropine), Dry as a bone (atropine; scopolamine), hot as a hare (atropine), blind as a bat (atropine), mad as a hatter, full as a flask (oxybutynin (Ditropan))

Treatment during Toxicity-Mild symptoms

Dim room Fluids ativan

-physostigmine = antidote when the following occur:

Altered mental status + severe CNS effects + tachycardia

***Crosses the BBB which is why it is used when patients show altered mental status. Needs to get to the brain

Signs of anticholinergic toxicity MOA: physostigmine transiently

reverses anticholinergic effects and aids diagnosis in unclear cases

o Contraindicated in: Bradycardia AV block Uncontrolled

ashma/wheezing seizures

Nursing interventions -Good oral hygiene for dry mouth (xerostomia)-Fluids and fiber for decreased GI secretions and peristalsis-Dim lights in room for midriasis-Monitor HR and BP for tachycardia—control HTN-Monitory elderly especially for:

CNS signs—agitation, confusion, hallucination, psychosis Undiagnosed glaucoma Memory impairment

-Treat mental agitation-physical constraints-Mental restraints--Benzos-Look for anticholinergic effects from common OTC/prescription drugs

Cold remedies Antihistamines Antipsychotics

Tricyclic antidepressants

Patient Teaching

Adrenergic Agonists (Sympathomimetic drugs)Alpha 1, Beta 1, Beta 2 agonists

Medications Prototypes: Epinephrine—Low specificity/High AffinityAlpha 1 agonists-Orthostatic hypotension Midodrine (ProAmatine)**Prodrug (active metabolites is what does the work. Has to be

converted)o Give 3-4 times daily to stimulate peripheral vasoconstrictionBP stays up so

patient doesn’t fall when standing-Opthalmic conjunctival congestion: Visine-Topical nasal Decongestants Afrin-Oral Decongestant Pseudoephedrine (Sudafed)-Profound hypotension Levophed IV (norepinephrine) “leave em dead”

o Stimulates alpha 1 and some beta 1…NO beta 2o Given to very sick patients in ICU with extremely low hypotension (SHOCK)o Metabolized by dopamine

Phenylephrine (Neo-synephrine) IV

Beta agonistsDobutrex (dobutamine)—Beta 1 more than beta 2Inotropin (dopamine)—Beta 1-Naturally occurring catecholamine neurotransmitter-potent dopaminergic as well as alph1 + beta 1 activity depending on dose

Alpha 1—low dosesdilate blood vessels in brain, heart, kidneys, and mesenteryincreases blood flow to those areas

Beta 2—higher dosesincreases cardiac contractility and output

Felodopam (corlopam)-reduce BP in hypertensive crisis -improves blood flow to the kidney-dopamine 1 receptor agonistvasodilates arterioles

Indications Cardiovascular uses Cardiac arrest Anaphylaxis

-Manage simple open-angle glaucoma-used during eye surgery to control bleeding-used adjunct with local anesthesia (lidocaine)decreases circulation to the area-inhaled in acute episodes of severe asthma when patient is unresponsive to usual measures (albuterol)

Dosing/Medication formsMOA Alpha 1 agonistperipheral vasoconstrictionincreases BP

Beta 1 agonists (stimulants—primary use and in low doses)increases HR and force of contraction (inotropy)Beta 2 agonistrelaxes bronchiolar smooth muscle (broncodilationCan be administered via IV, subcutaneously, or endotracheal tube if no IV available

Background info:

ContraindicationsDrug interactionsTherapeutic outcomes -Increased HR

-Midriasis-Easier breathing (bronchodilation)Alpha 1 receptors-increase BP-activates alpha receptors to constrict arterioles of bronchioles + inhibits histamine release

Heart B1 Receptors-Increased HR (chronotropy)-Increased cardiac contraction (inotropy)-Increased cardiac conduction (dromotropy)

Kidney B1 Receptors-increased renin secretion

Beta 2 Receptors-dilate smooth muscle of bronchi

Adverse effects -Arteriols in skin, viscera, and mucus membranes— vasoconstriction-Male Sex organs—ejaculation-Uterus—Contraction-Muscle of iris (pupil)—Midriasis-GI muscles—decreased motility (decreased peristalsis and secretions)-Bladder sphincter—constriction (inhibit bladder contraction—less peeing)-Dry mouth

-sweating-restlessness tremor-Adrenal secretion of epinephrine/norepinephrine-Glycogenolysis/Gluconeogenisis/inhibit insulin secretions-Increased HR/Increased conduction/vasodilation in the HEART-Bronchodilation

Toxicity Treatment during Toxicity

Nursing interventions Patient Teaching

Alpha 1 Antagonist (Blocker)Medications Prototypes:

Doxazosin (Cardura) Tamsulosin (Flomax)Phentolamine (Regitine)

Non-Prototypes:Prazosin (Minipress)Terazosin (Hytrin)

-can be used for frost biteIndications -HTN

-Used for vasodilationreduction in preload Counteract excessive injection of epinephrine/norepinephrine Prevent tissue necrosis after epi/norepi infusion extravasation

-Doxazosin (Cardura) Hypertension BPH

-Tamulosin (Flomax) Used for BPH ONLY Approved for kidney stones too (check this to make

sure) Alpha 1 receptors in bladder and prostate alpha

blockers relax smooth muscle of bladder neck and urethral prostate

Phentolamine (Regitine)—used for severe HTN caused by pheochromacytoma (tumor on adrenal gland tissue)

Venous and arterial dilationreduction of preload/afterload in severe hypertension (pheochromocytoma)

Dosing/Medication forms

MOA Alpha 1 antagonists-Dilate arteries and veins-Decreases peripheral vascular resistance-Decreases systemic and pulmonary venous pressure-Increase cardiac ouput

Background info:

Contraindications -Hypersensitivity to: Drug Drug class Components in the drug

-Hepatic impairment-Hypotension

Caution in elderly patients-Pregnancy—this is a category c drug

Drug interactions

Therapeutic outcomes

Adverse effects -Hypotension-Tachycardia-Palpitations-Chest pains-Dysrhythmias-Peripheral edema-Headaches/drowsiness/anxiety-depression-weakness-fatigue (until tolerance builds)-N/V-diarrhea-constipation-Abdominal pain-Incontinence-Dry mouth-ejaculatory function



Alpha 2 AgonistsMedications Prototypes:

-Clonidine-Also Methyldopa (aldomet)

Non-Prototypes:

Indications -HTN-Chronic Pain-Opioid withdrawl


MOA Alpha 2 agonist-Inhibits release of norepinephrine from the presynaptic neuron in the CNSprevents SNS activation by norepinephrine in the PERIPHERY-Located in presynaptic-sympathetic nerve terminal

Inhibit outflow of norepinephrine from CNS Acting like a feedback loop to assist decreasing BP

-Reduce activity of renin in the kidneys

Background info:

Contraindications

Drug interactions


Adverse effects


Nursing interventions Patient Teaching-do not stop abpruptly especially if on a beta blocker as well-causes rebound HTNstroke/MI-call dr if you want to stop

Short acting Beta 2 Agonist (SABA)**More info in COPD/Asthma Section

Medications Prototypes:Albuterol

Non-Prototypes:

Indications -Asthma attack


MOA Beta 2 Agonists (stimulants) Background info:

Contraindications

Drug interactions

Therapeutic outcomes -Dilate bronchial smooth muscle (bronchodilation)-Liver—glycogenolysis-Uterus—relaxation-GI—decreased motility-Skeletal muscle—peripheral vasodilation

Adverse effects



Beta receptor antagonists—Beta BlockersMedications Prototypes:

Propranolol (Inderal) Atenolol (Tenormin)

Non-Prototypes:Metoprolol (Lopressor)—B1 selective (less lipid soluble than propranolol)Bisoprolol (zebeta)—B1 selectiveLabetolol (normodyne)—used for extreme HTN emergencies—Ex: 220/115 less lipid soluble than propranolol)

Drugs that block Alpha and Beta receptors—vasodilate as well as slowing the HR and decreasing contractility-Labetolol (normodyne)-Carvedilol

Indications -HTN-Angina pectoris (chest pain)

Decreases myocardial contractilityreducing O2 demand 1ST CHOICE FOR ANGINA PREVENTION Decreased adverse cardiovascular events in patients with angina and silent ischemia (diabetics)

-Myocardial infarction Required after MI Reduce circulating catecholamines (NE/E and dopamine)decreases post MI mortality

-Heart Failure (HF)—specific drug used for this Early and mild HF

-Dysrhythmias-Migraine headaches—used if they cross the BBB-Anxiety—EX: stage fright-Glaucoma—eye drops used (think reducing pressure in the eye just like you reduce blood pressure in HTN)


MOA Compete with the endogenous catecholamines Epinephrine Norepinephrine

Background info:

Prototype PropranololBeta receptor AntagonistLipid soluble—crosses the BBB and more likely to cause the fatigue/lethargy/nightmares/depression/sexual dysfunctionExcreted primarily via hepatic metabolismNot cardio selectiveinhibits/blocks B1 and B2 receptors

Atenolol (Tenormin)Beta receptor antagonistWater soluble—doesn’t cross the BBB shouldn’t cause the same fatigue that propranolol causes (less CNS side effects)Eliminated by the kidneysCardio selectiveonly blocks beta 1

Contraindications -uncompensated HF-shock-heart block-Not as effective in black patients unless used in conjunction with a diuretic

Thought to be low renin-hypertensives-check to see if patients getting allergy tested are on beta blockersbeta blockers will prevent epinephrine from working if patient goes into anaphylaxis-Check to see if patients doing cardio stress testing are on beta blockersbeta blockers will prevent epinephrine working if the patient goes into cardiac arrest

Prototype PropranololDo not give to patients with COPD or severe asthma because of Beta 2 antagonismbronchoconstriction

Atenolol (Tenormin)No Broncho constrictioncan give to patients with COPD or severe asthma

Drug interactions -Alpha 2 agonists (clonidine)—all vasodilate causing a synergistic effectpharmacodynamic effectAV block/bradycardia/hypotension

Also cant acutely end clonidine or clonidine with a beta blocker. Same side effects as beta blocker Clonidine withdrawal: Increased BP, hypertensive crisis, hypertensive encephalopathy, strokes, fatalities MOA: increased catecholamine release after clonidine withdrawalvasoconstriction **higher risk for patients who are taking a non-cardio selective beta blocker with clonidine

-Calcium channel blockers-ACE inhibitors/ARBs-Cimetidine (Tagamet)—CYP450 inhibitor)-NSAIDs—cause fluid retentionincreased preload-Insulin and sulphonylureas—mask the symptoms of hypoglycemia

Therapeutic outcomes Prototype Propranolol-bronchoconstriction-decrease HR-Decrease AV conduction-Decrease contractility

Atenolol (Tenormin)-decrease HR-Decrease AV conduction-Decrease contractility

Adverse effects -Bradycardia—can lead to heart block if too much used-Orthostatic HypotensiondizzinessCold extremities-bronchoconstriction (if not cardio selective)-Drowsiness/fatigue-Masks symptoms of hypoglycemia (coming back to this in ENDO section)-Impotence (inability to go to the restroom) in GU-Agranulocytosis (acute condition involving severe and dangerous leukopenia—usually neutrophils are low—neutropenia)

Severe Side Effects (caused by acute withdrawal) -CHF/MI-exacerbation of angina and HTN (rebound HTN)-Severe Bradycardia-Heart Block-Dysrhythmias-Bronchospasm (non-cardio selective beta blockers)-Hypersensitivity reaction

Toxicity -CYP 450 inhibitorsdecreased enzymes created by the liverhigher level of free drug (beta blocker) in the bloodtoxicity

Climetidine (Tagemet) Nifedipine (Procardia) Hldol Paroxitine (Paxil) Quinidine Lithium

Amiodarone

Treatment during Toxicity

Nursing interventions Asses:-HR & BP-Cardiac rhythms-lung sounds

Patient Teaching-Do not stop abruptlyrebound HTNstroke or MI-Check sugar levels since hypoglycemia may be masked

Catecholamines promote glycogenolysis and mobilize glucose in response to hypoglycemia

Because they’re being blocked—sugar levels need to be checked in diabetics on insulin-Track GU function because of incontinence -Teach patients to assess HR & BP

Cardiovascular Disease Drugs for

Hypertension

Goals in interventions in Cardiovascular DiseaseDecrease preload-Dietary Modification

Limit Sodium intake and retention

-Diuresis

Decrease HR and Contractility-Beta blockers

Decrease Afterload and improve coronary blood flow-Vasodilation

Alpha blockers and alpha 2 agonists

ACE Inhibitors and ARBs Calcium Channel Blockers Nitrates

Slow HR and increase force of Contraction-Digoxin

Calcium channel BlockersMedications Prototypes:

-Nifedipine (Procardia)—Dihydropyridine-Verapamil (Calan, Isoptin) & Diltiazem (Cardizem)—Non Dihydropyridines

Non-Prototypes:

Indications -HTN-Can help with anginaNifedipine (Procardia)Dihydropyridine-Given for HTN—they are NOT given to slow the HR

Varapamil (Calan) & Diltiazem (Cardizem)Non-Dihydropyridine-given to slow HR**still some vasodilation occurs


MOA Decrease cardiac muscle contractilityreduces myocardial O2 demand Background info:

Nifedipine (Procardia)Dihydropyridinesvasodilate

Varapamil (Calan) & Diltiazem (Cardizem)Non-DihydropyridineEffect the nodes (i.e. affect the electrical impulses of the heart. In this case they slow the heart rate down) + vasodilate

Contraindications -People with severe Hypotension-Cardiac dysrhythmias -CHF-Dysfunction-Hypersensitivity to the drug/drug class/components of the drug-Bradycardia or heart blocks-Renal impairment-Hepatic impairment-Acute MI

Drug interactions


Adverse effects All-constipation-dizziness-facial flushing-headache-peripheral edema-bradycardia heart block-CHF-Gingival Hyperplasia-Eczema like rash in elderly

Especially with Verapamil:-Constipation-Gingival Hyperplasia


Nursing interventions Patient Teaching-Tell people to floss/brush their teeth if they have gingival issues

ACE InhibitorsMedications Prototypes:

LisinoprilNon-Prototypes:

Indications


MOA ACE InhibitorsPrevent the breakdown of bradykininprevents conversion of angiotensin I to angiotensin IIVasodilation

BLOCK THE FORMATION OF ANGIOTENSIN II-prevent sodium and water retention by inhibiting aldosterone secretionDiuresisdecreased preload/left ventricular end diastolic volume (LVEDV)decrease the workload of the heart

Background info:

Contraindications -Make sure the patient is not pregnant (ok in the 1st trimester but contraindicated in 2nd and 3rd)-Bilateral renal artery stenosis-Severe allergy-Children-High potassium-Interactions-K sparing Diuretics-Potassium supplements-allergy to an ARB?

Drug interactions


Adverse effects -Dry cough (caused by the build up of bradykinin)-Orthostatic hypotensiondizziness/fatigue-hyperkalemiamusculoskeltal pain-Photosensitivity-Angioedema (more often in women than men—more often in black people in general)-Stevens-Johnson Syndrom-Liver toxicity-Fetal harm

Toxicity -Angioedema in this case = drug induced angioedema 40% of people who develop hives (uticaria) from a drug will also have swelling of

deeper sub dermis which is manifested as swelling of the face/tounge/lips and may even involve the throat. ***This is an IgE Mediated reaction

-SJS—toxic when mucus membranes are involved



ARBs—Angiotensin II receptor BlockersMedications Prototypes:

LosartanNon-Prototypes:

Indications


MOA -prevent angiotensin II’s mediated vasoconstriction of aldosterone BLOCK THE ACTION OF ANGIOTENSIN II

-Decrease SVR-Decrease Afterload

Background info:

Contraindications -Make sure the patient is not pregnant (ok in the 1st trimester but contraindicated in 2nd and 3rd)-Less effective in Black people (low renin hypertensive)-Have they ever had an angioedema reaction on an ACE inhibitor? If so…DO NOT GIVE AND ARB

Sometimes hard to tell if the drug caused the angioedema or if the patient had a familial propensity for angioedema-Bilateral renal artery stenosis-Severe allergy-Children-High potassium-Interactions-K sparing Diuretics-Potassium supplements

Drug interactions


Adverse effects -Hyperkalemia-Angioedema (more often in women than men—more often in black people in general)-Anaphylaxis-Hypotension-Stevens-Johnson Syndrome-Liver toxicity-Fetal harm

Toxicity -Angioedema in this case = drug induced angioedema 40% of people who develop hives (uticaria) from a drug will also have swelling of

deeper sub dermis which is manifested as swelling of the face/tounge/lips and may even involve the throat. ***This is an IgE Mediated reaction

-SJS—toxic when mucus membranes are involved



Diuretics

Thiazide Diuretics—Gentler diuretic than loop diureticsMedications Prototypes:

Hydrochlorothiazide (HCTZ)Non-Prototypes:

Indications -HTN (low doses used alone or used in conjunction with another anti-HTN med if two are needed)-CHF (because it decreases preload)


MOA Inhibits reabsorption of sodium, potassium, chloride in distal convoluted tubule of the nephronosmotic diuresis (decreasing preload)dilate small arterioles (decrease afterload)

Background info:

Contraindications -patients with renal failure—can’t take this because it reduces blood supply to the afferent arteriole-drug allergies-hepatic coma-severe renal failure-Drug interactionsto the right

Drug interactions Check the drugs the patient is on! Lots of drug interaction can happen here:

1. Anti-diabetic drugs Antagonismincreased blood glucose2. Corticosteroidsadditive effecthypokalemia3. DigoxinHypokalemiadigoxin toxicity4. Lithiumdecreased lithium clearanceLithium toxicity


Adverse effects -Hypokalemia-hyperglycemia-hyperuricemia—high uric acid in bloodgout-hypersensitivity—anaphylaxis-skin rash-photosensitivity



Loop diuretics—VERY POTENT DIURETICSMedications Prototypes:

Furosemide (Lasix)Non-Prototypes:-Bumetanide (Bumex)-Torsemid (Demedex)-Ethacrynic acid (Edecrin)

Indications


MOA -Work in the thick ascending limb of the loop of Henleinhibit reabsorption of chloride secondarily inhibit the reabsorption of sodium-activate renal prostaglandinsvasodilate vessels in kidney/lungs/and rest of body-Reduce preload and afterload

Background info:

Contraindications

Drug interactions


Adverse effects -Hypotension (because of volume depletion)-Hypokalemiaanorexia/nausea, muscle weakness, hypotension, confusion-ototoxicity (6-7%) with rapid IV administrationcan cause deafness-Stevens Johnson Syndrom (blistering rash—if affects mucus membranes patients have to be admitted into burn unit of ICU)take patient off IMMEDIATELY-Thrombocytopenia (rare)-Tinnitus (usually temporary and reversible)—if given in high rapid dose can cause permanent damage

**This is a sulphonamide but Patients with sulpha allergies usually DO NOT have allergic reactions to loop diuretics

Side effects of Potassium replacement-DO NOT give IV push of potassium to people in cardiac arrest-avoid extravasationthrombophlebitis-Hyperkalemia**check creatinine—should be >1.5


Nursing interventions Give K+ if necessary PO or IV Potassium-if the gut works…USE IT!! (PO)-IV 40 mEq/L at 10 mls/Hr (on an IV pump) with peripheral (IV)—This can be painful-usually given in a central IV line to assure good dilution by the rapid flow in the blood vessels

**IF you see low K+check Mg+ as well. Often times, have to replete Mg+ in order to get K+ up

Patient Teaching-Teach patients to maintain good nutrition—potassium containing foods (unless they are also taking a potassium sparing diuretic)-Suggest patients to change positions slowly--<avoid orthostatic hypotension and possible falls-do not add potassium to your diet (because this is a potassium sparing diuretic)-take diuretics in the morning to avoid nocturia and potential falls

Potassium sparing diuretics— Fairly weak diureticsMedications Prototypes: Non-Prototypes:

Triamterene (Dyrenium)-acts directly on the distal tubule and collecting ductinhibits Na+ and water reabsorption**This is different from spironolactone because spironolactone competitively binds the aldosterone receptors-Side effects

Thrombocytopenia (rare) Decrease in folic acid (megaloblastic anemia) Kidney stones

Indications -ascites (caused by cirrhosis)-hyperaldosteronism

Adrenal origin CHF Post MI (spironolactone = cardioprotective)

-HTN-In combination with thiazide or loop diuretic to counteract potassium loss

Dosing/Medication formsMOA -Blocks Aldosterone in the distal tuble of the nephron

-competitively binds the aldosterone receptorsinhibits reabsorption of Na+ and water (usually induced by aldosterone)-has cardio-protective effects (will be discussed during CHF lecture)

Background info:

ContraindicationsDrug interactionsTherapeutic outcomesAdverse effects

-Normal potassium levels – 3.5-5.0 mEq/L

-Hypokalemia symptoms: Anorexia, nausea, muscle weakness, hypotension, confusion

ALL Potassium sparing Diuretics-Headache-drowsiness-confusion-ataxia-GI upsets and diarrhea-HyperkalemiaSpecific to Spironolactone (caused by the antiandrogen effects that produce estrogen-like effects)-Gynecomastia in men-Amenorrhea or irregular menses-Post menopausal bleeding-Renal failure-Agranulocytosis (rare)-Stevens-Johnson syndrome (when TEN below also involves the mucus membranes)-Toxic epidermal necrolysis (rare but serious skin problem)

Toxicity Treatment during ToxicityNursing interventions -Monitor the patients’ vital signs and pertinent lab values

-Be aware of potential food/drug interactions-prevent falls!!

Patient Teaching-Teach patients to maintain good nutrition—potassium containing foods (unless they are also taking a potassium sparing diuretic)

DO NOT ADD POTASSIUM TO DIET WITH SPIRONALACTONE BECAUSE THIS IS POTASSIUM SPARING

-Suggest patients to change positions slowly--<avoid orthostatic hypotension and possible falls-take diuretics in the morning to avoid nocturia and potential falls

Cardiovascular Disease Drugs for

Angina/MI

Types of AnginaTherapeutic goal—

Increase blood flow to the heart muscle Decrease myocardial oxygen demand

Goals of therapy Minimize the frequency of attacks and decrease the duration/intensity of angina pain Improve the patient’s functional capacity with as few adverse effects as possible Delay or prevent an MI

Treating angina if 911 called (ANOM) Aspirin—prevents platelet aggregation Nitrates—dilate coronary and other arteries Oxygen—increases O2 supply Morphine—relieves pain and vasodilates

Chronic Stable Angina Atypical Angina Unstable anginaOther names Classic Angina

Effort AnginaPrinzmetal’s AnginaVasospastic Angina

Pre-infarction anginaCrescendo angina

Occurs when? With activity -at rest-Same time of day-Often at night

-increases in frequency/severity/duration of attacks

Related to? Coronary artery narrowing/occlusion (myocardial ischemia)-can be relieved by nitroglycerin

-coronary artery spasm May be a prodromal of an MI in progress

NitratesMedications Prototypes:

NitroglycerinNon-Prototypes:Isorbide dinitrate (Imdur, Monoket, Ismo)-oral agents used for prophylaxis in situations that may provoke angina-longterm prophylaxis of angina-provide continuous levels of nitroglycerin

Indications -angina (ischemic heart pain)

IV Nitrates used for:-Severe HTN-Ischemic pain (unstable angina or MI)-Pulmonary edema associated with MI

Dosing/Medication forms How to take Nitroglycerin for chest pain1. Stop activity2. Sit/lie down3. Take sublingual nitro (can repeat every 5 minutes for a total of 3 nitros)4. If no relief after 1 nitrocall 911

**NOT DRIVE TO THE HOSPITALRapid acting:-Treats acute angina attack-Sublingual tablets (most common), translingual spray, IV infusion, buccal (placed between gum and cheek), chewable forms

Intermediate acting forms-Nitrobid paste-used in hospital and works quickly-can be removed quickly if the BP drops too fast-paste squeezed out onto piece of paper w/ markings in ¼ inches (ch. 9 for pic)-ordered in fractions of an inch (EX: apply ½ inch nitrobid paste to clean, dry skin every 12 hrs)-patients can be sent home with it if they can’t afford other forms of nitrates

Long acting forms-prevent angina episodes-pills, paste, or transdermal patch

MOA -cause dilation because of effect on vascular smooth muscle-potent dilating effect on coronary arteries-Used to prevent/treat angina

**Works just like naturally occurring nitric oxide (endothelial derived relaxing factor)Nitroglycerin (prodrug)converted to Nitric oxide by sulph-hydryl groupsredistributes blood supply to the myocardium

1. Low dosesvenous dilation2. High dosesarterial dilationrisk for orthostatic HTN

Background info:

Contraindications -Severa Anemia-Closed angle glaucoma-Hypotension-make sure patient is not on drugs for erectile dysfunction (Viagra, Cialis, levitra)—powerful vasodilators; can cause synergistic effect with nitro

Wait 24 hrs if on short acting drug Wait 48 hours if on long acting drug

Drug interactions


Adverse effects -orthostatic HTN-headaches (will likely happen on first time—usually diminish in frequency and intensity with continued use)-Tachycardia (caused by low BP—body’s compensatory response)-Tolerance my develop:

Drugs become ineffective if 8-12 hr drug free interval is not providednecessary to allow the body to regenerate the sulph-hydryl groups needed to convert nitroglycerin into nitric oxide


Nursing interventions Preventing Side effects: Patient Teaching

-Monitor patients BP to make sure it doesn’t get too low-If nitroglycerin is ordered as needed (prn) Nurse does the following

Check vital signs before giving the drug Give the drug (if vital signs permit) Give drug again 5 mins after first sublingual nitro If patient is still having chest pain, Systolic pressure must be 90 mmHg or greater to

safely administer the second nitro If systolic blood pressure is less than 90 mmHgMAP will be too low to adequately

perfuse the brain/coronaries/kidneys-applying nitroglycerin paste

Wear gloves Squeeze prescribed amount onto the measuring paper Make sure old patch removed Apply paste/paper to clean, dry skin and secure paper with tape Do not rub in Rotate sites to prevent skin irritation

-applying transdermal patches with adhesive backing Apply to clean, dry skin (upper chest or arm) Make sure old patch is removed first

Remind patient about need to remove patch for the 8-12 hr drug free interval

ANOM (emergency personnel if ambulance called, or nurses—MAKE SURE TO ASK IF PATIENT IS ALLERGIC TO ASPIRIN FIRST!)

1. Aspirin—inhibits platelet aggregation (WE DO NOT WANT PLATELETS CLUMPING AROUND THE RUPTURED PLAQUE)

2. Nitroglycerin—powerful vasodilator (Tablet given under the tonguegets into circulation in about 1 min)**Someone will also be starting an IV bag and hooking patient up to heart monitor

3. Oxygen4. Morphine

You want to prevent complete occlusion of the coronary arterylimits the heart muscle damage

-These are potent dilators of large and small coronary arteries—stand slowly-Tolerance may develop

Avoid by removing patch 8-12 hours (when you go to bedreplace in the am) Don’t dose pills after 5 pm (Ex: may be prescribed to take twice daily)

-Sit/lie down before taking because of orthostatic HTN risk-change positions slowly-teach patients how to properly apply ointment

Remove old ointment Wear gloves to apply Rotate site Don’t rub in

-Teach patients how to use transdermal forms Rotate site Take off for 8 hours at night Remove old patch and replace with new

-Nitroglycerin tablets Do not chew/crush sublingual form Burning sensation felt with the sublingual form indicates the drug is still potent

(potency lost after 3 months once bottle is opened)Store in airtight dark glass bottle w/ metal cap and no cotton filler—cannot be plastic bottle

Cardiac GlycosidesMedications Prototypes:

DigoxinNon-Prototypes:

Indications -uncompensated HF Other medications to treat HF

o Na restrictiono Diuretics (loop diuretics and K supplements; potassium sparing diuretics—spironolactone is cardio protective)o Oxygeno Morphine

-Atrial fibrillation (controls ventricular rate)-Atrial Flutter (controls ventricular rate)


MOA -Slows the HR (negative Chronotrope)-Increases the force of contraction (positive inotrope)—may also increase myocardial oxygen consumption-Slows the number of impulses getting through the AV node and decreases conduction (negative dromotrope)

Background info:

Contraindications -People who have a sensitivity to it-Cardiac dysrhythmias-Ventricular tachycardia-Ventricular fibrillation-Acute MI-Cardiomyopathy-heart blocks-hypokalemia-Renal impairmentreduced clearance

Conditions that predispose to digoxin toxicity-Hypokalemia-hepatic dysfunction-hypercalcemia-Hyperthyroidism-Renal disease-Advanced age (>80)—independent risk factor for morbidity and mortality

Drug interactions

Therapeutic outcomes -Increase Stroke volume (SV)-Decrease venous blood pressure and venous engorgement-Increase coronary circulation-promotes diuresis because of improved cardiac output-relies exertional + paroxysmal nocturnal dyspnea, cough, and cyanosis

Adverse effects -Gi—EARLY SIGN OF TOXICITY Anorexia Nausea Vomiting

CNS—LATE SIGN OR TOXICITY Headache Fatigue Confusion Convulsions

Cardiac—LATE SIGNE OF TOXICITY Dysrhythmias—bradycardia, heart block, tachycardia

Eye—colored vision (seeing green, yellow, purple)—LATE SIGN OF TOXICITY

Toxicity Potassium and digoxin compete for the atp-ase pump binding sitesin hypokalemic states, Treatment during Toxicity

-very narrow therapeutic index

Drug level must be monitored (.5-2.0 ng/ml)

-Low potassium levels increase toxicity

Monitor electrolyte levels

Elderly at higher risk

more digoxin is allowed to bind heremore digoxin in cardiac cells + release of stored calciumincreased drug effecttoxicity

If digoxin toxicity already present + atp-ase binding sites are full of digoxinpotassium will not be able to get back t=into the cardiac cellshyperkalemia

GI (anorexia, nausea, vomiting)—EARLY SIGNEye (colored vision—green, yellow, purple), CNS changes, Colored vision –LATE SIGNS

Life threatening serum evels of digoxin>10 ng/mLin adults>4 ng/mL in kids

Mild—GI symptoms-provider may hold drug until levels come down-resume treatment at a lower dose

Sever—Eye, Heart, Vision symptoms-Hyperkalemia K>5.0 mEq/L-Life threatening dysrhythmias-Life threatening digoxin overdoseUse digoxin immune Fab (Digibind or Digifab)Antibody that recognizes digoxin and forms a complex with itinactivates digoxin

Nursing interventions - Drug level must be monitored (.5-2.0 ng/ml)-monitor electrolyte levels

Normal levels of potassium = 3.0-5.0 mEq/L-elderly at higher risk-Monitor for signs of toxicity

Nausea/vomiting/diarrhea Visual disturbances Altered mental status Apical HR less than 60 bpm—YOU MUST LISTEN FOR ENTIRE MINUTE BECAUSE

THERE MY BE ARRYTHMIAS. MUST BE HR AND NOT PULSE—NOT ALL PULSES WILL GO THROUGH

-check dosage forms carefully and follow directions for giving-don’t give digoxin with high fiber foods (it’s also a plant—fiber will bind to digoxin inhibiting absorption)-Assess drug allergies and contraindications-Asses clinical parameters

BP Apical HR one full minute—if HR <60 hold dose and call prescriber) Daily weight—report increases in weight ECG Labs—K+ Ca2+ liver functions (AST/ALT), kidney functions (creatinine clearance)

-monitor for therapeutic effects Increased urinary output (UO) Decreased: edema, SOB, dyspnea, crackles, fatigue Resolution of paroxysmal nocturnal dyspnea

Improved peripheral pulses, skin color, and temperature (should notice these with decreased edema)-Hold the dose and notify prescriber if patient shows signs of toxicity

Patient Teaching-Teach patients to check their own HR and let—should check carotid pulse at the angle of the jaw-patients should weigh everyday and record their weight. Report if:

Daily gain of 1kg a week Weekly increase of 5lbs = 2kg = 2L fluid

Antilipemic Drugs

Statins—AntilipemicsMedications Prototypes:

Atorvastatin (Lipitor)Non-Prototypes:-Rosuvastatin (Crestor)-Lovostatin (mevacor)-Pravastatin (prevachol)

-Simvastatin (Zocor)Fluvastatin (Lescol)-Pitavastatin (Livalo)

Indications First line drug therapy for hypercholesterolemia—one of the most commonly used drugs in this class-patients with known cardiovascular disease-patient with LDL cholesterol > 190 mg/dl-patient with no evidence of CVD but LDL level between 70-189 mg/dl and a 10 year risk of ≥7.5% (of what??)-Diabetics 40-75 years w/ LDL levels 70-89 mg/dl + no evidence of CVD

Dosing/Medication formsMOA Inhibit HMG-CoA reductaselowers the rate of cholesterol production

Used by the liver to produce cholesterol-reduce LDL levels up to 50%-Increase HDL levels by 2-15%-Reduce triglycerides by 10-30%

Background info:

Contraindications -Check drugs/diet Grapefruit juice—Cyp450 inhibitortoxic levels of statin in the bloodstatin toxicity Oral anticoagulants

-check drug reference for drug interactions-Biliary obstruction-Liver dysfunction

-Liver disease-Pregnancy-Scheduled surgery-OTC medications-Other drugs that need Cyp 450 enzymes to metabolize them

Drug interactions -Grapefruit juice—Cyp450 inhibitortoxic levels of statin in the bloodstatin toxicity-Oral anticoagulants

Therapeutic outcomesAdverse effects -mild transient GI disturbances

-Rash-Headache-Elevations in liver enzymes (AST/ALT)-Liver disease-Myopathy (muscle pain)

Toxicity -Myopathy can lead to rhabdomyolysis (very dangerous—can lead to death) Breakdown of muscle proteins Myoglobinuria (muscle proteins in the urine)urinary elimination of myoglobin Can lead to acute renal failure

-changes in urine color


Nursing interventions -For antilipemic drug therapy in general Obtain thorogh health and medication history Assess diatary patterns, exercise level, weight, height, vital signs, tobacco, and

alcohol use, and family history Assess for contraindications Assess for conditions that require cautious use and drug interactions

o Liver diseaseo Pregnancyo Scheduled surgeryo OTC medicationso Other drugs that need Cyp 450 enzymes to metabolize them

Obtain baseline liver function studies Patients on long term therapy may need supplemental fat-soluble vitamins (ADK and

E) Refer to guidelines regarding administration times and meals Counsel patient concerning diet and nutrition on ongoing basis Instruct patient on proper procedure for taking the medications

To minimize adverse effects of niacin, start on low initial dose and gradually increase it—take with meals; take aspirin (or other NSAID) 30 mins before the dose to decrease flushing

Patient Teaching-Instruct the patient to IMMEDIATELY report any signs of toxicity

Muscle soreness Changes in urine color

-Dosed once daily-usually take w/ evening meal or at bed timecorrelates with diurnal rhythm (??Look up)

Diurnal rhythm—cholesterol production-if the patient can’t take at night—there is no harm in taking in the morning. Just make sure you take it once a day.

Bile Acid Sequestrants

Medications Prototypes:Cholestyramine (Questran)

Non-Prototypes:

Indications -Relief of pruritus associated with partial biliary obstruction (cholescystitis) -can be used along with statins


MOA -prevent absorption of bile acids from the small intestineno cholesterol absorbed Bile acids are necessary for absorption of cholesterol

Background info:

Contraindications -Known hypersensitivity-phenylketonuria (genetic disorder—look up)-pregnancy-lactating women-caution when administering dry powder-Liver disease

-Scheduled surgery-OTC medications-Other drugs that need Cyp 450 enzymes to metabolize them-Biliary obstruction-Liver dysfunction-Active liver disease

Drug interactions -ALL drugs must be taken at least 1 hour before OR 4-6 hours after the administration of bile acid sequestrants-High doses of bile acid sequestrants decrease the absorption of fat soluble vitamins (ADEK)


Adverse effects -constipation Can use this knowledge to treat the loos bowel movements that occur after rectal resection

-heartburn-nausea-belching-bloating-mild increases in triglyceride levels**possibility. Not always


Nursing interventions -prevent esophageal/bowel obstructions Bile acid sequestrants can’t be absorbed Drug must be dissolved in 8 oz of water Must be immediately administered after dissolving in water

Treatment for esophogeal/bowel obstructions-restore gut motility

Bethanochol fluids

-For antilipemic drug therapy in general Obtain thorogh health and medication history Assess diatary patterns, exercise level, weight, height, vital signs, tobacco, and




E) Refer to guidelines regarding administration times and meals Counsel patient concerning diet and nutrition on ongoing basis Instruct patient on proper procedure for taking the medications Powder forms must be taken with a liquid, mixed thoroughly but not stirred—never

dry! Other meds should be taken 1 hour before or 4-6 hours after meals to avoid

interference with absorption

Patient Teaching-ALL drugs must be taken at least 1 hour before OR 4-6 hours after the administration of bile acid sequestrants-mix thoroughly in the 8 oz of water but don’t stir

Vitamins/minerals for hypercholesteremia

Medications Prototypes:Niacin (Nicotinic Acid)—Vitamin B3

Non-Prototypes:

Indications -lower triglycerides, total serum cholesterol, and LDL levels-Increase HDL

Dosing/Medication formsMOA -Increase activity of lipaseincreased lipid breakdown

Lipase breaks down lipids-Reduces the metabolism (catabolism) of cholesterol and triglycerides

-lipid-lowering properties (high doses—higher than when used as vitamin supplements)-effective, inexpensive, often used with other lipid-lowering drugs

Background info:

Contraindications -liver disease-peptic ulcer disease-gout-HTN-active bleeding-Biliary obstruction-Liver dysfunction-Pregnancy-Scheduled surgery-OTC medications

Drug interactions


Adverse effects -Flushing (caused by histamine release)-Pruritis-GI distress


Nursing interventions Preventing flushing/pruritis-start with low initial dose and increase gradually-take an aspirin or other NSAID 30 mins before the dose, to avoid flushing-take with meals-For antilipemic drug therapy in general

Obtain thorogh health and medication history Assess diatary patterns, exercise level, weight, height, vital signs, tobacco, and



Contraindicationso Biliary obstructiono Liver dysfunctiono Active liver disease


E) Refer to guidelines regarding administration times and meals Counsel patient concerning diet and nutrition on ongoing basis

Instruct patient on proper procedure for taking the medications

Patient TeachingTo prevent side effects like pruritus and flushing-take an aspirin or other NSAID 30 mins before the dose, to avoid flushing-take with meals-provide teaching regarding us of NSAIDs and aspirin-Let patients know these drugs may take several weeks to show effectiveness

Miscellaneous Antilipemics

Medications Prototypes:Ezetimibe (Zetia)

Non-Prototypes:

Indications -Lower cholesterol, LDL, and triglyceride levels-Increase HDL levels-can be used with statin drugs or monodrug


MOA -inhibits absorption of cholesterol and related sterols from the small intestinereduced cholesterol, LDL, and triglyceride levelsincreased HDL levels

Background info:

Contraindications -Biliary obstruction-Liver dysfunction-Active liver disease-Pregnancy-Scheduled surgery-OTC medications

Drug interactions


Adverse effects






E) Refer to guidelines regarding administration times and meals Counsel patient concerning diet and nutrition on ongoing basis

Instruct patient on proper procedure for taking the medications

Patient Teaching

Herbal products for hypercholesteremia

Medications Prototypes:Garlic

Non-Prototypes:

Indications -Antispasmodic-Antihypertensive-antiplatelet-lipid reducer


MOA Background info:

Contraindications -Possible drug interactions with Warfarin Diazepam NSAIDs—may enhance bleeding when taken with these

-Someone who is about to have surgery-HIV-Diabetes

Drug interactions


Adverse effects -dermatitis-vomiting-diarrhea-flatulence-anti-platelet activity



alcohol use, and family history Assess for contraindications

Patient Teaching-Can’t take before a surgery because of anti-platelet activity

Usually need to stop about 2 weeks prior to surgery

Oils for hypercholesteremia

Medications Prototypes:Flax (Seed and Oil)

Non-Prototypes:

Indications -Atherosclerosis-Hypercholesterolemia-GI distress-Menopausal symptoms



Contraindications -Drug interactions

Drug interactions -Anti-diabetic drugs-Anticoagulant drugs


Adverse effects -Diarrhea (if you start too much too quickly because of fiber increase)-Allergic reactions (gluten)



alcohol use, and family history Assess for contraindications

Patient Teaching

Drugs to Modify Coagulation

Antiplatelet drugsMedications Prototypes:

Aspirin Non-Prototypes:Enolic acid derivatives

Meloxicam (Mobic)Indications Dose: 81 mg – 325 mg (thrombo-prevention)

-should be administered at the first site of an MI-If not given before arriving in the emergency dept.—aspirin is one of the first drugs given if there are no contraindications-given to prevent future clots

-Reduce the risk of fatal and non-fatal strokes-Acute coronary syndromes (ACS)

Unstable angina Myocardial infarction

-prevent further strokes/MI**if a stent is put in the artery—continue Plavix + aspirin for 1 year

Higher doses: (EX: 650 mg)-Analgesic-anti-inflammatory-antipyretic-Headache/Neuralgia/myalgia/arthralgia-Pain syndromes resulting from inflammation:

Arthritis, pleurisy, pericarditis-Systemic lupus erythematosus—has anti-rheumatic effects

Dosing/Medication forms ANOM for MI:AspirinNitroglycerinOxygenMorphine

MOA Irreversibly inhibits the production of enzyme: Cyclooxygenase in the plateletplatelet cannot regenerate cyclooxygenasereduction in thromboxane synthesis in platelets and prostacyclin in vascular endothelial cellsplatelets cannot aggregate and form a clot-changes the balance between prostacyclin (inhibits platelet aggregation) + Thromboxane A2 (promotes platelet aggregation)-vascular endothelium recovers and can synthesize more prostacyclin-thromboxane A2 synthesis can only recover after new platelets are formed-the life of a platelet in the blood stream is 7-8 daysas long as the patient continues to take asprin, platelets will not be able to aggregate**important in preventing MI and strokes

Background info:

Contraindications -renal dysfunction-Known drug allergy

Patients w/ known aspirin allergy are NOT allowed to have NSAIDs-Thrombocytopenia-Active bleeding-Recent trauma-stroke (see page 422)-known drug allergy-Age > 2 (kids under 2 at risk for Reye’s syndrome)-Do not give to children/teenagers recovering from chickenpox or flu-like symptomsReye’s syndrome-surgery coming upshould stop aspirin 7-8 days before to prevent hemorrhage

-Conditions that place the patient at risk for bleeding Vitamin K deficiency PUD Renal dysfunction Concurrent use of antiplatelet/anticoagulant drugs

Drug interactions -Anticoagulants-Antiplatelet drugs-Aspirin-Corticosteroids + other ulcerogenic drugs-Protein bound drugs (competition)-Diuretics + ACE inhibitors (NSAIDs cause fluid retention)


Adverse effects -GI: Heartburn/Severe GI bleeding (can be caused by blocking COX-1)/Hepatotoxicity

-Renal (nephrotoxic): Decreased creatinine clearanceAcute renal failure

-Blood: Altered hemostasis—risk of bleeding Do not use with antiplatelet drugs or steroidsbleeding

-Skin eruption-Sensitivity reaction (SJ syndrome)

Caused by COX 2 inhibitors in particular-Neuro:

Tinnituso May be first sign of aspirin toxicity

Hearing lossToxicity Salicyism -Metabolic Treatment during Toxicity

-Neuro: Tinnitus w/ possible hearing loss/ Dimness of

vision/Headache/ Dizziness/ Mental confusion/ Drowsiness-GI

Nausea/Vomiting/Diarrhea-CV

Increased HR-Respiratory

Hyperventilation/Hypoglycemia/Hyperglycemia/Sweating/Thirst

-Hepatotoxicity-renal toxicity

NSAIDs block prostaglandin functionprecipitates acute/chronic renal failure

Can compromise existing renal function Renal toxicity can occur in patients with

dehydration, HF, liver dysfunction, or use of diuretics or ACE inhibitors

-Reye’s syndrome in children (especially post viral attack) Acute encephalitis Coma Liver damage

Possible permanent neurological damage

-Discontinue drug-supportive care-Dialysis given if:

pH < 7 renal dysfunction/renal failure pulmonary edema CNS symptoms progressing to coma

o Early symptoms = tinnitus + nausea

Nursing interventions Patient Teaching-patients with renal failure need to let ALL healthcare providers know-surgery coming upshould stop aspirin 7-8 days before to prevent hemorrhage

Antiplatelet drug***COME BACK!!!Medications Prototypes:

Clopidogrel (Plavix)Non-Prototypes:

Indications Antithrombotic effects (prevent clotting)-Reduce the risk of fatal and non-fatal strokes-Acute coronary syndromes (ACS)

Unstable angina Myocardial infarction

-prevent further strokes and MI**if a stent is put in the artery—continue Plavix + aspirin for 1 year

Dosing/Medication formsMOA -Prevents the release of ADP from the platelet + inactivates the IIb/IIIa receptor on the

membrane of the platelet-Alters the platelet membrane so it cannot receive the signal to aggregate and form a clot

Background info:

Contraindications -Thrombocytopenia-Active bleeding-Recent trauma-stroke (see page 422)-known drug allergy-Age > 2 (kids under 2 at risk for Reye’s syndrome)-Do not give to children/teenagers recovering from chickenpox or flu-like symptomsReye’s syndrome-surgery coming upshould stop aspirin 7-8 days before to prevent hemorrhage

Drug interactionsTherapeutic outcomesAdverse effectsToxicity Treatment during ToxicityNursing interventions Patient Teaching

-surgery coming upshould stop aspirin 7-8 days before to prevent hemorrhage

AnticoagulantsMedications Prototypes:

Heparin (unfractionated)Non-Prototypes:Fondaparinux (arixtra)—inhibits factor Xa

Indications -Used as prophylactics to prevent thrombosis MI Unstable angina Atrial Fibrillation

-20% chance of stroke if patients with atrial fibrillation are not anticoagulated-Blood gets sluggishpools in left ventricleclot forms in atriumstroke

Indwelling devices such as mechanical heart valves Major surgery (especially orthopedic surgery)

-treatment of thrombosis to prevent more clots from forming/prevent embolus from forming once a patient has a thrombus

DVT Pulmonary embolus Stroke

**DOES NOT DISSOLVE ALREADY FORMED THROMBUS

Dosing/Medication forms Injectable Anticoagulant Drug (parenteral administration—IV infusion)-Parenteral administration: IV infusion

Administered parenterally because it is a large polar molecule ***CAN NOT BE GIVEN ORALLY

-weight based protocol-Dosed in units not mg-Loading dose w/ maintenance infusion-Lab test monitoring—partial thromboplastin time (PTT)-Short half-life—1-2 hours

In pregnancy:-IV drip during labor-Given to women who have predisposition for clotting (possible on lovenox during pregnancy)

MOA -Binds to antithrombin IIIturns off Xa and thrombin (factor IIa)-Turns off coagulation factors and prevent clot prevention

Background info:

Contraindications -Notify the physician if you notice rapid drop in platelet countDoctor will:

Order a sample of blood to check for heparin associated antiplatelet antibodies are present If present—diagnosis of HIT is made

-Discontinue all Heparin immediately-Give Argatroban by IV infusion

Drug interactionsTherapeutic outcomesAdverse effects -Nausea

-vomiting-abdominal cramps-thrombocytopenia-HIT below

Signs of excessive bleeding (localized or systemic): bleeding from gums when brushing teeth unexplained nosebleeds heavy menstrual bleeding bloody/tarry stools (hematochezia) blood in urine/sputum abdominal pain

Toxicity Heparin Induced Thrombocytopenia (HIT)—Happens in about 5% of patients on unfractionated HeparinDiagnosis:

Hx of exposure to Heparin + Rapid decline (50%) in platelet count Remember the platelets may still be in the normal range

Paradoxically (Contradictory) acute thrombotic events**Patient still has the over-clotting issue so you go lower in the clotting cascade:

Argatroban by IV infusion Direct thrombin inhibitor—lower in the clotting cascade

Antidote: Protamine Sulphate—1mg neutralizes 100 units of unfractionated Heparin

Treatment during ToxicityAntidote: Protamine Sulphate—1mg neutralizes 100 units of unfractionated Heparin

Nursing interventions -Make sure to check the IV doses with another nurse (high alert drug)-Use weight based protocol for IV infusion-Different loading doses and initial infusion rates for the standard and modified protocols-Monitor PTT per the protocol-Maintenance infusion rate based on the PTT result-Monitor CBC and PT/INR-Monitor the patient for the conditions listed in the protocol and inform the physician of complicaions

Patient Teaching-Signs of abnormal bleeding/skin changes-measures to prevent bruising, bleeding, or tissue injury-wear a medic alert bracelet-consult health care provider before taking other medications, OTC drugs, and herbal supplements


Enoxaparin (Lovenox)—Low weight HeparinNon-Prototypes:

Indications -Used as prophylactics to prevent thrombosi MI Unstable angina Atrial Fibrillation



-treatment of thrombosis to prevent more clots from forming/prevent embolus from forming once a patient has a thrombus DVT Pulmonary embolus Stroke

-Pregnant women with predisposition for clotting

**DOES NOT DISSOLVE ALREADY FORMED THROMBUSDosing/Medication forms -More predictable anticoagulant response

-Immediate anticoagulant effect-Fixed weight based dosing-Does not require lab monitoring-Given SubQ-Q12 hours (treatment) or daily (prevention—t1/2 12 hours) ???-More expensive than unfractionated Heparin, but can be given at home by self injection—Low

Dosing in pregnancy:-40 mg per day throughout the pregnancy-switched to heparin IV during labor (shorter half life)

MOA -Prevent/treat venous clotting and arterial clotting-Inhibit clotting factors + ultimately prevent the formation of a fibrin stabilized clot

Background info:

Contraindications

Drug interactions

Therapeutic outcomesAdverse effects -Nausea

-vomiting-abdominal cramps-thrombocytopenia-HIT (below)

Signs of excessive bleeding (localized or systemic): bleeding from gums when brushing teeth unexplained nosebleeds heavy menstrual bleeding bloody/tarry stools (hematochezia) blood in urine/sputum abdominal pain

Toxicity Heparin Induced Thrombocytopenia (HIT)—Happens in about .5-1% of patients on LMWHDiagnosis:

Hx of exposure to Heparin + Rapid decline (50%) in platelet count Remember the platelets may still be in the normal range

Paradoxically (Contradictory) acute thrombotic events**Patient still has the over-clotting issue so you go lower in the clotting cascade:

Argatroban by IV infusionDirect thrombin inhibitor—lower in the clotting cascade


Nursing interventions Patient Teaching-Signs of abnormal bleeding/skin changes-measures to prevent bruising, bleeding, or tissue injury-wear a medic alert bracelet-consult health care provider before taking other medications, OTC drugs, and herbal supplements


Fondiparinux (Atrixtra)Non-Prototypes:

Indications -Used as prophylactics to prevent thrombosis MI Unstable angina Atrial Fibrillation



-treatment of thrombosis to prevent more clots from forming/prevent embolus from forming once a patient has a thrombus DVT Pulmonary embolus Stroke

**DOES NOT DISSOLVE ALREADY FORMED THROMBUSDosing/Medication forms -Injectable—Sub Q

-Once daily dosing (t1/2 23 hrs)-no lab monitoring-Can be given at home-More expensive

MOA -Synthetic Xa inhibitor Background info:

Contraindications

Drug interactions


Adverse effects -Nausea-vomiting-abdominal cramps-thrombocytopeniaSigns of excessive bleeding (localized or systemic):

bleeding from gums when brushing teeth unexplained nosebleeds heavy menstrual bleeding bloody/tarry stools (hematochezia) blood in urine/sputum abdominal pain


Nursing interventions **Same nursing precautions as lovenox?? Patient Teaching-Signs of abnormal bleeding/skin changes-measures to prevent bruising, bleeding, or tissue injury-wear a medic alert bracelet-consult health care provider before taking other medications, OTC drugs, and herbal supplements

Oral AnticoagulantsMedications Prototypes:

Warfarin (Coumadin)Non-Prototypes:-New Oral Anti Coags

Oral Xa inhibitors Apixaban (Eliquis) Rivaroxaban (Xaralto)

-Oral Direct Thrombin Inhibitors Dabigatran Etexilate (Pradaxa)

***No routine monitoring needed BUT—There are NO antidotes for these drugs!

IndicationsDosing/Medication forms -Given orally

-Inhibits Vitamin K dependent clotting factors-Patient with first clotting episode (Ex: DVT) should be anticoagulated for 3 months

Lovenox is expensive so you don’t put them on this for 3 months but it is more immediate Start with Lovenox and Warfarin at same time until INR = 2-3 (reach steady state on warfarin in 8 days) Take patient off of Lovenox and they continue the warfarin for the remaining time

**Remember these drugs don’t lyse the clot…they only prevent new clots from forming + prevent them from breaking off into the lungs and producing a Pulmonary Embolus

MOA Inhibits the formation of vitamin K depending clotting factors: II VII IX X Background info:

Contraindications -Patients > 60Drug interactions Drug interactions:

-Capsicum pepper-garlic-ginger-ginko-ginseng-feverfew**These supplements must be stopped before surgery because they increase bleeding effect

Therapeutic outcomesAdverse effects

Major Side Effects-Risk increased with: Increased dosesPatients > 60

-Excessive bleeding (localized or systemic): bleeding from gums when brushing teeth unexplained nosebleeds heavy menstrual bleeding bloody/tarry stools (hematochezia) blood in urine/sputum abdominal pain vomiting blood (hematemesis)

Have patient come to clinic or go to ER (will stop Coumadin and/or given vitamin k)-Nausea-vomiting-abdominal cramps-thrombocytopenia

Toxicity Liver takes 48-72 hours to regenerate the vitamin dependent clotting factors Treatment during Toxicity-Antidote: Vitamin K—given for excess anticoagulation

Sub Q (1-2 mg) Orally (5-10 mg) Can NOT be given via IV

-Can give fresh frozen plasma if you need rapid reversal of Coumadin EX: if a patient needs an invasive surgery

Nursing interventions -Monitor by Prothrombin Time + International Normalized Ration PT/INR Test

-May be started while patient is still on Heparin until PT/INR indicates adequate anticoagulation Therapeutic range warfarin INR = 2-3 EX: if a patient needs to be put on anticoags—you put them on lovenox and Warfarin

at the same time until INR = 2-3then lovenox can be stopped-T1/2 48 hrs—steady state can take about 8 days to be reached-Monitor PT/INR regularly (weekly until stable—then monthly for maintenance)-Monitor for signs of excessive bleedinghave patient come in to office or go to ER

Patient Teaching-Importance of lab testing PT/INR-Signs of abnormal bleeding/skin changes-measures to prevent bruising, bleeding, or tissue injury-wear a medic alert bracelet-consistent dietary intake of vitamin k containing foods-consult health care provider before taking other medications, OTC drugs, and herbal supplements

Thrombolytic Drugs (clot busters)Medications Prototypes:

Alteplase (t-PA, Activase)Non-Prototypes:

Indications -Acute MI Have to be w/in 6 hour window After receiving t-PA in hospital they are sent home on low dose aspirin + beta blocker

-Arterial thrombus-DVTOcclusion of shunts or vascular catheters-Pulmonary Embolus-Acute Ischemic stroke

Dosing/Medication formsMOA Background info:

Contraindications Absolute:-Active Internal bleeding-Suspected aortic dissection-Known intracranial brain tumor-Previous intracranial hemorrhagic stroke at any time-Other strokes or cerebral events w/in 1 year-head trauma-Pregnancy-Recent non compressible vascular pncture-uncontrolled HTN (>180/110)

Relative:-Severe HTN-Cerebrovascular disease-Recent Surgery (w/in 2 weeks)-Cardiopulmonary resuscitation

Drug interactions


Adverse effects -Bleeding Internal Intracranial Superficial

-Nausea-Vomiting-Hypotension-anaphylactoid reactions-cardiac dysrhythmias (can be dangerous)

Toxicity Treatment during ToxicityNursing interventions -Monitor overnight after receiving t-PA

-Perform neuro checks for: States of consciousness Pupil reactions Ability to speak Ability to move all extremeties

-Monitor IV sites for bleeding, redness, and pain-Monitor for bleeding from:

Gums Nose Mucous membranes Injection sites

-Observe for signs of internal bleeding Decreased BP Increased pulse Restlessness

-Monitor for cardiac dysrhythmias-perform neuro checks hourly for 24 hrs

Patient Teaching

Anti-Fibrinolytic Drugs—FYI not prototypes

Medications Prototypes: Non-Prototypes:Aminocaproic acid (Amicar)Tranexamic acid Desmopressin

Indications


MOA -STOP bleeding-Varies by drug but ALL prevent the lysis of fibrin

Aminocaproic acid (Amicar)—prevents breakdown of fibrin clot Tranexamic acid—coompetitively inhibits the activation of plasminogen to plasmin Desmopressin—causes a dose dependent increase in plasma factor VIII

(vonWillebrand factor)

Background info:

Contraindications

Drug interactions


Adverse effects



Diabetic Medications

InsulinMedications Prototypes: Non-Prototypes:

-Apidra (insulin glulisine) = rapid acting-Glargine (Lantus) = Basal-Long acting (gives coverage for between meals and overnight)

24 hr insulin Only given once per day Highly effective insulin for in/outpatient care—no peaks/valleys in blood sugar levels

-Levemir (Detemir) = Basal-long actingIndications Diabetes

Dosing/Medication forms -Regularly scheduled (basal bolus or basal prandial) = nutritional Insulin Mealtime coverage (prandial)short/rapid acting insulin Between meal coverageintermediate or long-acting

-Sliding scale (correctional/supplemental coverage) Coverage when you need it Regular, lispro, or aspart Sliding scale Finger stick blood glucose test multiple times a day—number of units given are based

on the recorded blood sugar (insulin dose increases as sugar level increases) Typically used for hospitalized diabetic patients or those on TPN or enteral tube

feedings Disadvantage: delays insulin administration until hyperglycemia occurslarge swings

in glucose control (poor glycemic control because not physiologic)-Combination of a regularly scheduled and sliding scale treatment

Common Regimens:-Basal insulin only

Glargine Levemir

-Basal-bolus therapy (basal-prandial) Regular and NPH Regular and Glargine (Lantus) or levemir (detimir) Lispro and glargine/levemir Lispro and NPH Apidra and lantus (glargine)

**Lantus can NOT be mixed with other insulins using the “RN” method. If lantus is prescribed in a combohave to be done with separate syringes.**Lispro and aspart should NEVER be mixed with regular insulin

-Measured in units—each mL = 100 units (doses are very small) 50 unit or 100 unit syringes

o If administering a dose smaller than 50 unitsuse a .5mL insulin syringe Insulin Pens (used for inpatients and outpatients—you dial the amount prescribed and

inject using special needle on the end of the pen) Devices Pumps

-Subcutaneously (usually insulin is given this way)

-IV (can only be regular insulin)— this would be in the case of DKA Small bag of IV fluid mixed w/ insulin + administered by infusion pump to deliver

hourly IV dose of regular insulin (finger sticks taken hourly in this case)

-Patients who take insulin at home take it 1-4 times a day***hybrid mixtures (70/30 and 50/50) are only given if specifically ordered by the physician—never home brewed

Humulin -R = regular (fast/short acting) = meal time insulin-N = NPH (neutral protamine hagedorn) = intermediate acting

Cloudy (suspension) Protamine = large protein molecule that takes longer to ender bloodstream

-Humalog (lispro) = rapid acting = meal time insulin Onset of action = 15 minutes

-Ultralente-70/30 (NPH 70% and regular insulin 30%)-50/50 (NPH 50% and Regular insulin 50%)

Novolin -R = regular (fast/short acting) = meal time insulin-N = NPH (neutral protamine hagedorn) = intermediate acting

Cloudy (suspension) Protamine = large protein molecule that takes longer to ender bloodstream

-Novolog (aspart) = rapid acting = meal time insulin-Ultralente-70/30 (70% Aspart protamine and 30% insulin aspart)

MOA -Binds to Insulin receptorsallows glucose to be actively transported into the cell Background info:HgA1C—normal > 7%

Contraindications -hypoglycemia-excess insulinshock/coma/death

NPO patients-scheduled nutritional insulin should be held-basal insulin can be continued at a lower dose + sliding scale (correction insulin)-EX: preoperative patients

No nutritional insulin Give basal/supplemental insulin (dose should be clarified with prescriber)

**sliding scale only should be medical history…but we will definitely be given sliding scale ordersDrug interactions Drugs that can increased blood glucose

-Steroids Corticosteroids

-Diuretics

Thiazides Loop diuretics

-estrogenTherapeutic outcomes -tight glucose controlReduce incidence of long term complications of diabetes

-Tight blood pressure control-Cholesterol control-Triglycerides control

Adverse effects Hypoglycemia (usually occurs when too much insulin is given)Primary symptoms:-hunger-nausea-tachycardia-feel weak/faintSecondary symptoms-anxiety-tremor-sweating-headache

-double visionTertiary Symptoms (brain not getting enough sugar)-confusion-agitation-combativeness-always consider hypoglycemia for any patient who has sudden change in LOC-common errors with insulin

Dose omission Overdose/underdose

-know types of insulins (can’t just say clear or cloudy)-carful with LASA insulins

Continuous occurrences of Hypoglycemia Organic Brain syndrome (OBS)-chronic confusion-psychosis-cognitive dysfunction

**Brain being deprived of glucose for too long. Usually happens to elderly patients

This is why we usually allow these patients blood sugar levels to get a little higher than normal

Toxicity -Insulin coma-Considered a high alert drug: incorrect doses could be fatal

Treatment during ToxicityTreatment during Hypoglycemia (Conscious):-4 oz OJincreases blood sugar in 5 minutes-8 oz milk if patient can’t/won’t drink OJ-glucose tablets/gels can be bought at the pharmacy

Treatment during Hypoglycemia (Unconscious):-IM or IV treatment-Dextrose 50% in water (D50%)given via IV and elevates blood sugar immediately-Glucagon (IM)—especially patients in a nursing home or at home and can’t get an IV line

Takes appx 15 minutes to work Family can be trained on how to inject

Still call 911Nursing interventions Preventing Side effects:

-Make sure you have food in patient w/in 15 minutes of giving rapid acting insulin (aspart/lispro/Apidra)-Make sure you have food in patient w/in 30 minutes of giving regular insulin-Plan snacks about 7-8 hours after taking NPH insulin (midday)—because blood sugar will drop around then-If you don’t have an order for 70/30 and a patient takes both regular/NPH insulin together, draw up the Regular (clear) first and the NPH (Cloudy—suspension) second—you will be an RN when you graduate-Don’t shake insulin (will denature protein)—roll between hands instead-check blood glucose level before giving insulin (make sure the patient has a meter and shows they know how to use it)-Ensure correct storage of insulin vials

1. Never Freeze2. Don’t expose to direct heat/light3. Never use past expiration date4. Inspect before use. Don’t use if particles or clumps are

visible5. If unopened/not in usestore in fridge

a. Glargine and Levemir don’t require refrigeration

6. Opened/in usestore at room temp <86 degrees7. Store prefilled syringes with needle tip up

-ONLY use insulin syringes, calibrated in units to measure/give insulin-ensure correct timing of insulin dose with meals

Patient Teaching-Make sure patients know correct dosing (high alert drug)-Make sure patients check their blood sugar w/ glucometer before taking insulin (have to be able to show they know how before leaving the hospital)-Patients must know how insulin is measured (in units)-must be shown how to draw up/mix insulin from vials if they can’t afford an insulin pen-need to be shown where to inject (subQ tissue)-inject subQ @ 90 degree angle-do NOT aspirate once the needle is in-NEVER massage the injection site

Preventing/treating hypoglycemia-teach how foods/exercise affect their glucose-should be taught how to monitor their blood sugar level (capillary blood sugar monitor)-sometimes DR orders twice a day once at home; In hospital sometimes 4 times a day—before each meal (AC) and before bedtime (HS)-patients should carry glucose tablets/gels at all times

Oral anti-Diabetic drugsMedications Prototypes:

Biguanide: Metformin (Glucophage)Non-Prototypes:-DPP4 Inhibitors sitagliptin (Januvia)-GLP1 agonist liraglutide (victoza)-Glitazones piaglitizone (Actos)-SGLT2 Inhibitor empagliflozin (jardiance)SulfonylureasGlipizide (Glucotrol)-Stimulate secretion of insulin-Type II diabetes only-Highly protein bound-Major side effect = hypoglycemia-Do not have to hold in patients with sulfa allergy

Combination drugs (most contain metformin)-Avandamet-Metaglip-Janumet-Liraglutide (Victoza)

Indications Only used for Type II

Dosing/Medication forms -found in multiple combination drugs-twice daily-can use alone-can use with another oral diabetes drug—ex: sulfonylureas-can use with non-insulin injection like liraglutide (victoza) or insulin-use as prophylactic for someone w/ prediabetesprevents full blown diabetes

MOA -works in the liver and gut-decrease glucose production and increase ability of cell to use glucose-reduces GI absorption-No hypoglycemia

Background info:

Contraindications -Pregnancy (can only use insulin)-creatinine levels

If >1.5 should not be given to patient-renal impairment-alcoholics-liver disease

-severe deyhydration-HF-Age greater then 80-IV contrast

Discontinue (D/C) prior day of IV dye Must wait 48 hours to continue after IV dye

Drug interactionsTherapeutic outcomesAdverse effects

-Risk increased with: Age > 80 Renal

insufficiency**Patients with creatinine levels >1.5 should NOT take metformin

-diarrhea (most common)-nausea-anorexia-weight loss-vitamin b12 deficiency anemia (pernicious anemia)—i

mpaired absorption of B12 numbness tingling

-Lactic acidosis High risk patients Rare but serious

-hypoglycemia (drug works on cell and liver—no increase in insulin)Toxicity Lactic acidosis

Hyperventilation (attempt to blow off acid) Hypotension Extreme weakness (due to acid buildup)


Nursing interventions Patient Teaching-Diet: protein up; CHO down, Fat down-Weight loss: even 10% improves glycemic control-Exercise: improves insulin activity-Smoking cessation-Oral anti-diabetic drugs may not be effective unless the patient also makes behavioral/lifestyle changes

Adrenergic Drugs

GlucocorticoidsMedications Prototypes:

Prednisone (Deltasone)Non-Prototypes:Systemic Corticosteroids-Solu-Cortef IV and Cortef po (hydrocortisone)—have mineralocorticpid properties-Decadronoral or IV dexamethasone—stronger than prednisone-Deltasone (prednisone) oral

Category C in pregnancy Intermediate acting

-Dexamethasone (Decadron)-Methylpridnisolone (Medrol dosepak)-Methylprenisolone (Depot Medrol)—Long acting steroid for joint injection

-Solu-medrol (methylprednisone) IV Most commonly used IV steroid used in anti-

inflammatory and immunosuppressant drugs Pregnancy category C Contains benzyl alcohol as preservative Cant be given to children younger than 28 days 4mg solumedrol = 20mg solucortefsolumedrol 5X

stronger than solucortef

Indications -Adrenocortical insufficiency (Addison’s disease)-Cerebral edema-Spinal cord injufy-Collagen diseases-Dermatologic diseases-GI diseases-Thrombocytopenia—increase platelet production-overactive immune system activity + inflammation in:

Organ and bone marrow transplants Collagen diseases—rheumatoid arthritis Dermatologic diseases

-lymphona-Gi diseases-inflammation—Asthma + COPD

Addison’s Disease S&S:-low sodium-low glucose-increased potassium-dehydration-weight loss

Dosing/Medication forms Low doses = physiologic dose (what replacing normal levels most people make on their own) Replacement therapy For someone with hyposecretion of adrenocortical steroids (Addison’s disease)

High Doses = pharmacologic dose Larger dose than what the body would normally produce Anti-inflammatory properties

o Stabilize the cell membranes of inflammatory intracellular organelles—lysosomes

o Decrease the permeability of capillarieso Decrease the migration of WBCs into already inflamed areas

Suppress the normal immune responseWould be given if a person who receives replacement therapy is also going through a stressful event like surgery

Local Methods of administration (not absorbed into blood stream)-Inhalation—Maxaair, Vaceril, Flovent, or Pulmicort

For bronchospastic states Prevent asthma on a daily basis Decrease the inflammation response in the lungs

-Nasally—Flonaise (Fluticasone) or Rhinocort (budesonide) For allergic rhinitis and to prevent the recurrence of polyps after surgical removal

-Topically For inflammation of the eye, ear, and skin

-Intraarticular (into a joint)Systemic methods of administration-IV-IM-orally

MOA -Reduce inflammation by stabilizing cell membranes of inflammatory cells called lysosomes-Lower fever by reducing the release of interleukin-1 from WBCsBackground info:Natural:

Cortisol Cortisone

-Increase B receptors formation in heart and lungs-Responsible for carbohydrate, protein, fat metabolism-Promote breakdown of protein, production of glycogen in the liver, and redistribution of fat from peripheral to central areas of the body-Increase blood glucose level-Increased secretion in the stress response –fight or flight-Synthesized from cholesterolreleased and stimulated by ACTH under negative feedback control (diurnal rhythm)-Peak levels are secreted early in the moring (6-8am)decrease during the daylower peak in late afternoon (4-6pm)

-vital to survival-these are synthesized when needed—NOT stored

Effects: Ability to stabilize lysosomal membranes + reduce capillary permeability Anti-inflammatory Fever reduction (inhibit release of interleukin 1 from WBCs + stimulate erythropoiesis) Carbohydrate and protein metabolism Fat metabolism Maintenance of normal BP Stress effect

Contraindications

Drug interactions


Adverse effects Acute:-Immunosuppressant effect-Hyperglycemia

Glucocorticoids cause the cells to become insulin resistant Less likely to happen with someone who has normal pancreatic function and who does

not already have diabetes Sometimes steroids “unmask” a person’s diabetes

-Hypertension (hydrocortisone) More likely with hydrocortisone because it increases cortisol + aldosterone Aldosterone causes sodium retention

-Mood swings Depression Mania Euphoria Hallucination Usually patients experience these symptoms early—especially if on high doses People with history of mental illness are not necessarily at risk

-Peptic ulcer disease (PUD) Caused by medication induced prostaglandin suppression.-->protective prostiglandins

don’t form mucous layer in stomach liningless blood goes to the stomach + glucocorticoids stimulate production of more HClacid ruins stomach lining + duodenum

Can also decrease gastric painpatient can perforate an ulcer in their stomach/duodenum without knowing

-Vertebral compression fractures Occurs acutely in patients who already have osteoperosis

-Weight gain Caused by increase food intake Proteins/carbs/fats being broken down quickerbody is depleted and needs

morehunger

-Cardiac dysrhythmias (due to hypokalemia caused by hydrocortisone)

Chronic (any patient using glucocorticoids for 2 months + is at risk)Cushing’s syndrome—increased secretion of adrenocortical hormones/excess exogenous intake-redistribution of body fat from arms and legs to face, shoulders, trunk and abdomen

Moon face Buffalo hump Pot bellypurple striae

-Na and water retention-potassium loss-muscle weekend-Osteoperosis

can lead to osteoporotic fractures—most common in ribs and vertebrae Increase osteoclastic activity and decrease osteoblastic activity Decrease intestinal absorption of calciumPTH is increasedpulls calium from bone

into the bloodmore calcium lossin bones-myopathy

Caused by muscle breakdownthin arms and legs Also thin skin

-inhibited protein synthesis-Euphoria or mania (may lead patients to ask for more)-Physical dependence

Over time, your adrenal glands atrophy and shut downgland can no longer produce adrenal hormones on demand in times of stresspatients need increased doses of steroids to get them through stressful events (trauma/surgery)

May take adrenal glands days/monts/a full year to get back to normal-Growth retardation in kids

Toxicity Treatment during ToxicityNursing interventions -Look for S&S of infection

Caused by immunosuppressant effect Remember: steroids given for Addison’s are replacement steroids, but steroids given

for inflammation/joint pain will increase the potential for infection TB can occur more easily in these patients Most likely with systemic administration

-Anti ulcer drugs should be taken to prevent ulcers/perforated ulcers Proton Pump Inhibitors (PPI) H2 blockers

-Measure height + weight regularly in kids on steroids

Patient Teaching-patients can’t abruptly stop taking steroids

Leads to an acute adrenal crisisThe only way to treat this is with steroids

MineralocorticoidsMedications Prototypes:

FludrocortisoneNon-Prototypes:

Indications Need for chronic mineralocorticoid replacement-Adrenocortical insufficiency (Addison’s disease)-Cerebral edema-Spinal cord injufy-Collagen diseases-Dermatologic diseases-GI diseases-Thrombocytopenia—increase platelet production-overactive immune system activity + inflammation in:





MOA -conserve sodium in the body + affect fluid/electrolyte balance

Natural: Aldosterone

-Na, K, and fluid balance Blood pressure control Maintenance of serum potassium

levels Maintenance of pH levels in the

bloodSodium and water resorption

Background info:

Contraindications

Drug interactions


Adverse effects



CNS Depressants/ Stimulants

Benzodiazepines--Alcohol Withdrawal treatment + AnxiolyticCNS Depressant—Relieve anxiety, irritability, and tension

Medications Prototypes:Lorazepam (Ativan)

Non-Prototypes:-Diazepam (Valium)-Chlordiazepoxide (Librium)-Xanax (alprazolam)-Versed (midazolam)-Restoril (Temazepam)

Other CNS Depressants:-Alcohol-Benzodiazepines-Barbituates-Marijuana (schedule I)-Opioids (Schedule II/III)—AKA Narcotics-Pure opium/heroin (Schedule I)

Vicodin (hydrocodone + acetaminophen) = schedule II

Dangerous thing about heroin—on the streets it is often cut with fentanyl which is 80-100 times more powerfulleads to deaths

Indications Alcohol withdrawal (Delerium tremens—DTs = severe)-Insomnia-tremors-Temp > 101 (38 degrees Celsius)-Tachycardia HR > 140-HTN BP > 200/140-Agitation-Psychotic behavior-Cardiac Arrest—dysrhythmias

Often due to hypomagnesemia

-Acute anxiety-procedural comfort-muscle spasms-with anesthesia-alcohol withdrawal

-Usued as initial treatment for seizures to arrest (Stop) a seizure Duration of action = 72 hours

Has replaced diazepam (valium) as the drug of choice, but BOTH work

Dosing/Medication forms -Dosage + frequency depend on severity-Should be used in lowest doses/frequencies because of habit forming potential-IV administration

Need to be careful if given IV or with other CNS depressants Look for respiratory + cardiac depression

-POUsually don’t cause the cardiac + respiratory depression unless taken with other CNS depressants + alcohol

MOA -increase the action of GABA (gamma aminobutyric acid) in the CNSGABA is a neuro-inhibitory neuro-hormone that quiets the brainCNS depressants

Background info:

Contraindications -Pregnancy—category D-difficulty breathing (COPD or Asthma)

Drug interactions -other sedatives-alcohol


Adverse effects -Sedation-Drowsiness-Confusion-Groggy when waking up

Patients given during surgery Patients who take them for sleep

-Cardiac and respiratory depression

-Hypotension-Loss of coordination-headache-nausea/vomiting-Dry mouth (anti cholinergic effect)-Constipation (anti cholinergic effect)

Toxicity -dangerous when taken with other sedatives and alcohol Treatment during Toxicity-symptomatic-supportive-weaned slowly

Especially for chronic users of Xanax (alprazolam)

Antidote—flumazenil (Romazicon)-reverses effect of benzodiazepines

-can cause seizures + cardiac dysrhythmias if used on chronic user (complete reversal)-does not antagonize the CNS effects of other drugs affecting GABA

Alcohol Barbiturates General anesthesia

-Give with EXTREME caution (because of seizures)

Nursing interventions -If the admitting physician does not prescribe a benzodiazepine to prevent the agitation related to alcohol withdrawal—call and ask!-Patients may be monitored in the ICU if the withdrawal is severe

Cardiac monitor incase of cardiac arrest Cardiac arrest due to electrolyte imbalance

-Replacement may be needed of the following: Thiamine (B1) Hydration Magnesium

-Because of sedation/confusion—patients are a fall risk Older patients may not clear benzos normally because of decreased renal

functionthey will become more sedatedmore risk of fall/injury-Patients cannot stop suddenly if they take benzos chronicallyleads to seizures-If given IV :

Monitor cardiac and respiratory rateo Cardiac monitoro Pulse oximeter (measures oxygen saturation)

Follow hospital policy if given for conscious sedation-Check for signs of addiction

Check last date of prescription + count how many pills should be left. If there are less available than there should beconsider addiction

-Side rails up—prevent falls-Administer slowly IV—prevent hypotension-Monitor mental status—especially in older adults-Teach patients to avoid driving when sleepy-Know suicide status—ask questions compassionately and encourage patients to get help

Patient Teaching-do not stop cold turkey if chronic user—will lead to seizures

Drugs to maintain abstinence from alcoholMedications Prototypes:

Disulphram (Antabuse)Non-Prototypes:-Naltrexone (Trexan)

Decreases cravings Reduces relapses

-Acamprosate (Campral) Decreases cravings

Reduces relapsesIndications


MOA -alters the metabolism of alcohol in the body-for people who are serious about wanting to stop drinking alcohol-no clear evidence that it decreases cravings or reduces relapse rates-not given often in the US

Background info:

Contraindications

Drug interactions


Adverse effects -Acetaldehyde syndrome (occurs if someone on antabuse has even 1 drink) Severe nausea Vomiting Thirst Hypotension Chest pain Difficulty breathing Pulsating headache Blurred vision Vertigo confusion


Nursing interventions -Do not allow patients to have ANY alcohol Patient Teaching-Patients cannot have even one drink—they will get acetaldehyde syndrome if they do

Amphetamines (stimulants)Medications Prototypes:

Methylphenidate (Ritalin)Non-Prototypes:-Provigil—narcolepsy-Triptans (Imitrex)—Migraine headaches

Structurally similar to stiumlants Stimulate serotonin in the arteries

of the brainvasoconstiriction

Stimulants of abuse:-Methylphenidate (Ritalin) + other ADHD drugs-Cocaine

Highly addictive VasoconstrictorCan produce

MI/Stroke Erosion in nasal septum

-Methamphetamine More potent than cocaine

-Methylenedioxymethamphetamine (MDMA—ecstasy)-Other designer drugs

Indications -ADHD-Keep pilots/soldiers alert during war time-Narcolepsy-Obesity (limited due to tolerance—usually combined with other drugs for weight loss)-Neonatal apnea

25% of premiesImmaturity of respiratory center and lungs



Contraindications

Drug interactions

Therapeutic outcomes Patients with ADHD-Focus thoughts-Ignore distractions-Mood elevation-Reduced fatigue-Sense of increased alertness

Adverse effects -decreased appetite-weight loss-headache-jitteriness

Toxicity -Convulsions-Coma-Cerebral hemorrhage-MI/stroke-Death


Nursing interventions -changing the medication dosage-adjusting the schedule of medication-using a different medication

Patient Teaching

Antiepileptic Medications

Tonic-clonic Seizures (AKA Grand mal Seizures)— Immediate loss of consciousness Tonic phase of muscle contraction followed by jerking muscle movements (may start in one area and spread) Patient may bite tongue or be injured as they fall Urinary incontinence is common

Status epilepticus (general—THIS IS WHAT WE REFERENCE IN THIS CLASS) Convulsive type-generalized tonic-clonic seizures that occur repeatedly with almost no time from one seizure to the next Series of seizures that persist for 20-30 mins+ MEDICAL EMERGENCY 20% mortality Permanent neurological damage if lasts longer than 20 mins Treatment needs to start w/in 5 mins of onset CNS changes

o Loss of consciousnesso Loss of bladder control

SNS effectso Tachycardiao Hyperthermiao Elevated bp

Metabolic effectso Hypoglycemiao Acidosiso These are because of the muscles using up all of their available glucosebody goes into anaerobic metabolismbuildup of lactic acidacidosis

TYPES OF STATUS EPILEPTICUS SEIZURES:Absence seizures

Brief but repetitive periods of lack of attention Spasmodic eye blinking for up to 30 seconds Ex: teacher complains Johnny continues to “not pay attention” in class and always looking out the window Rare after age 14

Atonic Seizures Seizures (drop attacks) Sudden loss of muscle control + syncope

Myoclonic seizures— Brief localized muscular jerking

Febrile seizures Usually in children ages 6m-5 years High fever + virus Usually generalized tonic-clonic seizures Short duration Treated symptomatically with Tylenol and tepid sponge bath Usually no long lasting damage/epilepsy

Non Drug therapy options Neurosurgery

Vagus nerve stiumulation

Traditional Anti-Epileptic DrugMedications Prototypes:

Phenytoin (Dilantin)Non-Prototypes:**Cerebyx = Dilantin prodrugmetabolized into Dilantin + can be givin IM or IV but dosing is not equivelant

Indications -Prevention/control of seizure activity-Long term maintenance therapy for chronic recurrent seizures (epilepsy)-Acute treatment—status epilepticus

**First line choice for maintenance of a seizure free stateDosing/Medication forms -Narrow therapeutic index (10-20mcg/ml)

Variable absorption of different products Varies among patients Half-life varies with dose (8-60 hours)

o Half-life is short initially (8 hours)extended release taken 3 times a day (every 8 hours)

o Once steady state is reachedpatients take once a day at bedtime Keep blood levels below 20 mcg/ml

-Given IV first and then PO

-Serum drug concentrations must be measured to identify: Initial dose Patient compliance Reason for loss of seizure control Reason for toxicity

-Discontinuance Must be discontinued VERY slowly

Must be seizure free 1-2 years (not guarantee the Dr. will take you off)MOA -Suppress Sodium influx into neurons

-Suppress calcium influx into axon terminals-hepatic enzyme inducerwill prevent effectiveness of other drugs

Background info:

Contraindications -Pregnancy-Known drug allergies-Cardiovascular disorders

Heart block Bradycardia

-Drugs that increase Dilantin levels (CYP 450 inibitors)

Diazepam (Valium) Isoniazid (TB drug) Cimetidine (Tagamet) Grapefruit

-Competitors for protein binding sites Valproic acid

Drug interactionsTherapeutic outcomesAdverse effects -Mild sedation

At therapeutic doses (10-20 mcg/ml) Early complaint until tolerance develops

-hypotension—especially when given for Cardiac dysrhythmias Status epilepticus Remember to give very slowly

-Suicidal thoughts/behavior-Decrease the effects of

Warfarin

Birth control (oral contraceptives) Corticosteroids

-Bradycardia/heart block-Gingival hyperplasia-Interferes with Vitamin D absorption

Rickets in children Osteoporosis in adults

-Hirsutism-Dilantin Facies (increased thickening of subcutaneous facial tissue)-Liver damage (rare—most likely a drug allergy)

Toxicity >20mcg/ml-Nystagmus-Double vision-Ataxia-Confusion/dizziness/drowsiness

-Nausea-Rash

TEN—Toxic Epidermal Necrolysis Steven’s Johnson’s syndrome (if mucous

membranes are involvedpatient must go to ICU burn unit)


Nursing interventions -IV forms given slowly No more than 50 mg/min

-Monitor vital signs-Avoid extravasation

This means make sure the IV does not get pulled out of the site

The pH of Dilantin is 12 (very basic) will irritate subcutaneous tissues (veins and soft tissue)

Stabilized with propylene glycol (antifreeze)-Can only be used with normal saline during IV admin

Does the patient want to drive? Have to get special permission to drive Each state has different rules Have to be seizure free for X amount of time Compliant with meds Not sleepy No alcohol use or other drugs DPS makes decision

Patient Teaching

Traditional Anti-Epileptic Drug

Medications Prototypes:Carbamazepine (Tegretol)

Non-Prototypes:

Indications -Prevention/control of seizure activity-Long term maintenance therapy for chronic recurrent seizures (epilepsy)-Patients who do not tolerate Dilantin well-Mood stabilization (refractory to lithium)-Bipolar disorder (refractory to lithium)**First line of defense for partial and tonic-clonic seizures

Dosing/Medication forms -Therapeutic range 4-12 mcg/ml-Hepatic enzyme inducer

can increase its own metabolism as wellHalf-life decreases over time (40-15 hours)

MOA -Suppress Sodium influx into neurons Background info:

Contraindications -NOT used in status epilepticus-NOT used in acute management of generalized tonic-clonic seizures-NOT used in Myoclonic/absence/atonic seizuresmay worsen them-Pregnancy-Heart failure

Drug interactions -Phenytoin (Dilantin) + Phenobarbital = hepatic inducers Increase carbamazepine metabolismdecrease free-drug availability

-Grapefruit Increase peak and trough levels of carbamazepine by 40%!!!


Adverse effects Early:-Nystagmus-Blurred Vision-Diplopia-Ataxia-Vertigo-Headache

Long-term:-Osteoperosis-hypoosmolor state (caused by increasing the secretion of ADH)-Mild rash

Treat with prednisone-Photosensitivity-Hematologic effects:

Bone marrow suppressionanemia/ thrombocytopenia/Leukopenia Anemia/thrombocytopenia respond to discontinuation

Leukopenia usually improves even with continued use—stop drug if WBC < 3000/mm3

Toxicity -Fatal aplastic anemia (very rare)-TEN/Steven’s Johnson Syndrome—STOP DRUG (SJS patients need to be in burn unit)


Nursing interventions -Run CBC before the start of therapy + periodically-Teach patients about hematological manifestations

Fever Sore throat Pallor Weakness Infection Easy bruising

Patient TeachingTeach patients about hematological manifestations

Fever Sore throat Pallor Weakness Infection

Easy bruising

Traditional Anti-Epileptic DrugMedications Prototypes: Non-Prototypes:

Valproic Acid (Depakene)

Indications -Prevention/control of seizure activity-Absence + Myoclonic seziures-Long term maintenance therapy for chronic recurrent seizures (epilepsy)-Mood stabilization-Bipolar disorder


MOA -Suppress Sodium influx into neurons-Suppress calcium influx into axon terminals

Background info:

Contraindications -NOT used in status epilepticus-Not approved for children < 2

Drug interactions


Adverse effects -GI upset-Weight gain-Hair thinning-Ankle edema

Toxicity -Hepatotoxicity-Pancreatitis



New Anti-epileptic DrugsMedications Prototypes:

Pregabalin (Lyrica)Gabapentin(Neurontin)

Non-Prototypes:

Indications -Prevention/control of seizure activity-Long term maintenance therapy for chronic recurrent seizures (epilepsy)-Acute treatment—staus epilepticus-Neuropathic pain (pain arising from nerve damage)Fibromyalgia—overactive nerves causing musculoskeletal pain


MOA -augment GABA (primary inhibitory CNS neurotransmitter) This is how Benzodiazepines and Barbiturates work

Background info:

Contraindications

Drug interactions


Adverse effects



Thyroid Medications

Thyroid replacement therapyMedications Prototypes:

Levothyroxine (Synthroid)Non-Prototypes:

Indications -Thyroid disease (Hashimoto’s Thyroiditis)-Hypothyroidism caused by medical treatment-Surgical removal of thyroid-After radioactive iodine to treat cancer-Hypothyroidism of pregnancy (examine dosage every 4 weeks…try to keep mom on lower end of normal TSH levels)-Diagnosis of suspected Hyperthyroidism

TSH suppression test—if you have Hyperthyroidism and you are given LevothyroxineTSH becomes suppressed. -Prevention or treatment of various types of goiters

**Most commonly prescribed thyroid replacement


MOA -Replaces thyroid hormones (T4) the thyroid can’t produceNormal thyroid levels = euthyroid

Background info:

Contraindications

Drug interactions

Therapeutic outcomes -Decreased symptoms of hypothyroidism-improved energy levels-improved mental and physical stamina

Adverse effects -Cardiac dysrhythmia Most significant side effect

-Tachycardia-Palpations-Angina-HTN-Insomnia-Tremmors-Headache-Anxiety-Nausea/Diarrhea/weight loss/anorexia-Menstrual irregularities-Sweating/heat intolerance/fever


Nursing interventions -Keep doses in normal range to prevent side effects Taking too much will cause tachycardia, palpations, anxiety Taking too late in the day will cause insomnia

o Advise patients to take in the morning-Monitor patients for return of hypothyroidism symptoms

This would indicate an inadequate dosebubble up to provider so dose can be increased

-Teach patients to report anxiety, palpitations, and insomnia-OTC medications or herbal supplements need primary care provider approval-Teach patients that therapeutic effects may take several weeks to occur

Levothyroxine has a 7 day half-lifeabout 28 days until steady state-Monitor for therapeutic response-Monitor for adverse effects

Patient Teaching-Advise patients to take in the morning to prevent insomnia-Teach patients to report anxiety, palpitations, and insomnia-OTC medications or herbal supplements need primary care provider approval-Teach patients that therapeutic effects may take several weeks to occur

Levothyroxine has a 7 day half-lifeabout 28 days until steady state-Take on an empty stomach

30 min – 1 hour before breakfast Enhances absorption orally Maintains constant hormone levels Helps prevent insomnia (taking in the am)

-Do NOT abruptly discontinue—lifelong therapy is usually the norm-Take at the same time everyday-Do not switch brands w/o PCP approval (different half lives etc)-Alert other healthcare providers if you are taking thyroid drugs to avoid drug interractions

May increase activity of anticoagulants Patients with diabetes may need increased dosages of hypoglycemic medications

May decrease serum digoxin levels

Antithyroid DrugsMedications Prototypes:

Propylthiouracil (PPU) Methimazole (Tapazole)

Non-Prototypes:-Surgery to remove all or part of the thyroid gland

Lifelong thyroid replacement needed-radioactive iodine (iodine 131) to treat:

Grave’s disease Cancer

-Potassium iodineGiven after iodizing radiation exposure

Indications



Contraindications PPU-Pregnancy

Category D in first trimester = only given if absolutely necessary for the mother in 1st trimester

Methimazole (Tapazole)-Pregnancy

Category D in 2nd/3rd trimester = only given if absolutely necessary for the mother in 2nd/3rd trimester

Drug interactions

Therapeutic outcomes -No evidence of hyperthyroidism

Adverse effects -Leukopenia which manifests as Fever Sore throat Lesions

Toxicity -Agranulocsytosis—Bone marrow toxicity-Liver dysfunction—liver toxicity


Nursing interventions -Better tolerated when given with food-Give at same time of day to maintain consistent blood levels-never stop medication abruptly-Avoid eating foods high in iodine

Seafood Soy sauce Tofu Iodized salt

-Monitor for therapeutic response-Monitor for adverse effects

Patient Teaching-Better tolerated when given with food-Give at same time of day to maintain consistent blood levels-never stop medication abruptly-Avoid eating foods high in iodine

Seafood Soy sauce Tofu Iodized salt

Opioid/ Non-Opioid Analgesics

Opioid AnalgesicsMedications Prototypes:

Morphine SulphateNon-Prototypes:-Codeine

Metabolized into morphine (prodrug) Someone who has fast metabolism of this drug may experience respiratory depression

because they convert it to morphine too quickly-Hydromorphone (Dilaudid)

7 X more powerful than morphine—given to people who don’t tolerate morphine well Causes significant urinary retention because of powerful anticholinergic effects Give bethanechol with this

-Vicodin (hydrocodone + acetaminophen) Combined with acetaminophen to reduce the narcotic need + utilize central and

peripheral pain pathways Schedule II

-Meperidine (Demerol) Metabolized into toxic metabolite (nor-meperidine) Can cause tremors, seizures, and death in patients with renal dysfunction Increases serotonin levelsrisk of serious drug interactions w/ antidepressants Re-read on this from earlier notes!!!

-Oxycodone (hillbilly heroin) Synthetic schedule II opioid Immediate release form = oxycodone Extended release form = oxycontin For major pain relief only—major source of rx drug abuse

-Fantanyl 80-100X more powerful than morphine IV (anesthesia), nasal spray (field military use), lolly pop (Actiq), buccal form (Fentora),

and transdermal patch (Duragesic) Doses are in micrograms NOT miligrams Used extensively in hospice

-Methadone Not only for drug addicts

Inexpensive, very effective pill for severe/chronic pain—often used in hospice-Imodium—anti diarrheal medicine

Some morphine addicts may take 32 to get a high—will cause concrete poop-Tramadol (Ultram/Ultracet)

Novel drug given for moderate-severe pain Opioid agonist (mu receptors) Weak serotonin/norepinephrine reuptake inhibitor (SNRI) Used for post-op pain + fibromyalgia Schedule IV—low abuse potential, but still take caution (especially patients with

history of addiction) Manageable side effects

Indications -Severe pain (used alone)-cough

Phenergan + codeine for patients with dry hacking cough who can’t sleep at night-diarrhea (Imodium)-anesthesia

-Moderate pain (low dose used w/ non opioid—combination drugs)-reduce anxiety and dyspnea

Helps patients who are anxious about not being able to get their breath-Reduce preload (vasodilation)-Balanced ansasthesia

Dosing/Medication forms -IV push-IV pump—continuous infusion-Intermittently by patient control (PCA)-orally

Immediate release (MSIR) Extended release (MSER) Generic trade name = MSCONTIN

Anything ending in CONTIN = extended release/long acting

Equianalgesia-Ability to provide equivelant pain relief by calculating dosages of different drugs/routs of administration that provide comparable analgesiaEx:

Hydromorphone (Dilaudid) = 7 X Morphine 10 mg morphine given + 1 mg hydromorphone 4 hours later = 17 mg morphine w/in 4

hour period

MOA Three types of opioid analgesics-Agonist

Bind to opioid pain mu receptors in the brain/spinal cord and GI tract

Cause analgesic response (reduction of pain sensation)

-Partial agonist (aka mixed agonist) Cause weaker neurologic response

than full agonist No mood elevation

Ceiling effect (reach maximum analgesic effect—eventually analgesia does not improve—not even with higher doses

-Antagonist Competitively Bind to mu pain receptors to

block response of opioids Completely or partially reverses the CNS

depression caused by opioids Do not relieve pain Given if patient needs to be taken off opioids

Complete reversal will lead to withdrawal in an opioid dependent patient

Background info:Receptor type mu:

Morphine supraspinal analgesia, respiratory depression, euphoria, sedation

(moderate) Located in CNS tissues and the gut

Receptor type kappa: Ketocyclazocine spinal analgesia, sedation (2x the level as mu receptors), miosis

Receptor type delta: Enkephalins

analgesia

Contraindications -Known drug allergy

-Respiratory insufficiency Severe asthma or COPD Morbid obesity Sleep apnea

-Elevated intracranial pressure Vasodilation causes increase in ICP

-Paralytic ileus Because opioids already cause constipation

Drug interactions -Alcohol-Antihistamines-Barbituates-Benzodiazepines-Monoamine oxidase inhibitors-Marijuana-Sleeping pills

Therapeutic outcomes -decreased complaints of pain-Decreased severity of pain-increased periods of comfort-improved activities of daily living, appetite, and sense of well-being-decreased fever-Decreased evidence of inflammation

Swelling, pain, stiffness, tenderness of joint/muscle

Adverse effects -Respiratory depression (caused by CNS depression) Give Nalaxone (Narcan) if respiratory rate becomes too low Buprenorphine + naloxone = suboxone also used Used for complete or partial reversal of opioid induced respiratory depression Must be given regardless of if patient experiences withdrawal symptoms

-Nausea/vomiting-diaphoresis + flushing-miosis-constipation-Drowsiness-Euphoria-tranquility-Other mood alterations-depress cough reflex-Skin itching (Caused by histamine release)-GI—anticholinergic effects (dry mouth, constipation)

Bind to opioid receptors (Mu) in the gut—this can constipation or relieve diarrhea-Urinary retention-Physical dependence

Withdrawal will happen if a patient has to be taken off abruptly for any reason

Withdrawal:Withdrawal symptoms: (occurs if the drug is abruptly stopped)-peak period = 1-3 days-Duration = 5-7 daysSigns:

Drug seeking Mydriasis Diaphoresis Rhinorrhea Lacrimation Diarrhea Elevated BP + pulse

Symptoms: Intense desire for drug Muscle cramps Arthralgia Anxiety Nausea Vomiting Diarrhea Rhinorrhea Malaise

Withdrawal treatment:-Clonidine (alpha 2 agonist that prevents the release of norepinephrine in the brainrelieving SNS symptoms-Methadone

For patients who can’t quit—they go to methadone clinics where they receive one dose a day

Can also be used for pain control When patients are on expensive

drugs like oxycontin or MScontin—they can take methadone instead to save money


Nursing interventions -assess for: Allergies

Patient Teaching-advise patients to change positions slowlyprevents orthostatic hypotension

Current medications (including alcohol and illicit drug us) Medical history Potential contraindications + drug interactions

-Obtain baseline vital sinds + L&O ???-Assess pain

Location Type of ain Pain level—using pain scale

-contact physician immediately if: Vital signs change Patient condition declines Pain continues

-Monitor for adverse effects Respiratory rate < 10 breaths/min Dyspnea Diminished breath sounds Shallow breathing

-advise patients to change positions slowlyprevents orthostatic hypotension-give oral forms w/ food to minimize gastric upset-prevent constipation

Adequate fluid Fiber Laxatives

-Manage pain (pharm and non-pharm approaches) Medicate patients before pain becomes severe (provides adequate analgesia + pain

control Massage Application of ice/heat Acupuncture Distraction Medicate patient before doing painful procedure

-advise patients to follow directions for administration carfully-keep record of pain experiences + response to treatments-do not take other OTC meds/herbal supplements w/o consulting physician-notify physician if signs of allergy/adverse effects-required to evaluate pain relief w/in 20-30 mins of drug administration

-give oral forms w/ food to minimize gastric upset-remind patients to take short acting pain meds before pain becomes severe-advise patients to follow directions for administration carfully-keep record of pain experiences + response to treatments-do not take other OTC meds/herbal supplements w/o consulting physician-notify physician if signs of allergy/adverse effects

Non-Opiod AnalgesicsMedications Prototypes:

TylenolNon-Prototypes:

Indications -Pain (mild to moderate)-Fever (mild to moderate)-alternative for those allergic to aspirin

Dosing/Medication forms -OTC (oral)-Combo medications with opiods-IV

Rapid onset No first pass effect Can be given before + during surgery Switch to oral when patient can take fluid Pregnancy Category C Approved for nursing mothers

-Maximum daily dosing: Healthy adults = 3000 mg/day Elderly/adults with liver disease = 2000 mg/day

-IV form dosing is by age, weight, frequencyStill same max dosing restrictions

MOA -Reduction of pain chemicals at site of injury-Blocks pain impulses by inhibiting prostaglandin synthesis in CNS + peripherally blocks pain impulse transmission-Stimulates serotinergic + cannabinoid receptors in CNSaugments analgesic effects-No tolerance or physical dependence—Ceiling effect-Antipyretic + Analgesic effect-No anti-inflammatory effects

Background info:

Contraindications -Drug allergy-Liver dysfunction-Possible liver failure-G6PD deficiency

Drug interactions -Alcohol-hepatotoxic drugs


Adverse effects

Toxicity -hepatic necrosisliver failure More than 2.6g in 24 hoursrisk for mild liver failure 10g = Deliberate OD 15g = death Amount ingested is usually inaccuratebest if acetaminophen levels can be resulted

in first 4 hourso If you can’t documentconsidered as an OD

Treatment during ToxicityAntidote: N-acetylcysteine (Mucomyst)-Prevents the hepatotoxic metabolite of acetaminophen from forming-Most effective given w/in first 10 hours of OD-Can be given max w/in 3 days after OD-Used to be given orally (foul smelling given through nasogastric tube)-Now given via IV

Acetadote 50 mg/kg and 100 mg/kg over 21 hour period—Total 150 mg/Kg

Nursing interventions Adjuvant drugs: Assist primary drugs in relieving pain Antidepressants—(Amitriptyline) Anticonvulsants—Gabapentin or Pregabalin

-Lidoderm patch Applied patch containing lidocaine Not to be worn > 12 hours prevent systemic absorption Often times given for severe shingles pain after sores have gone (post-herpetic

neuralgia) Cannot give on open sores/wounds

May be used with other analgesic modalities

Patient Teaching

Anti-Inflammatories

(Steroids, NSAIDs, Gout)

GlucocorticoidsMedications Prototypes:

Prednisone (Deltasone)Non-Prototypes:Systemic Corticosteroids-Solu-Cortef IV and Cortef po (hydrocortisone)—have mineralocorticpid properties-Decadronoral or IV dexamethasone—stronger than prednisone-Deltasone (prednisone) oral

Category C in pregnancy Intermediate acting

-Dexamethasone (Decadron)-Methylpridnisolone (Medrol dosepak)-Methylprenisolone (Depot Medrol)—Long acting steroid for joint injection

-Solu-medrol (methylprednisone) IV Most commonly used IV steroid used in anti-

inflammatory and immunosuppressant drugs Pregnancy category C Contains benzyl alcohol as preservative Cant be given to children younger than 28 days 4mg solumedrol = 20mg solucortefsolumedrol 5X

stronger than solucortef

Indications -Adrenocortical insufficiency (Addison’s disease)-Cerebral edema-Spinal cord injufy-Collagen diseases-Dermatologic diseases-GI diseases-Thrombocytopenia—increase platelet production-overactive immune system activity + inflammation in:




Dosing/Medication forms Low doses = physiologic dose (what replacing normal levels most people make on their own) Replacement therapy For someone with hyposecretion of adrenocortical steroids (Addison’s disease)

High Doses = pharmacologic dose Larger dose than what the body would normally produce Anti-inflammatory properties

o Stabilize the cell membranes of inflammatory intracellular organelles—lysosomes

o Decrease the permeability of capillarieso Decrease the migration of WBCs into already inflamed areas

Suppress the normal immune responseWould be given if a person who receives replacement therapy is also going through a stressful event like surgery

Local Methods of administration (not absorbed into blood stream)-Inhalation—Maxaair, Vaceril, Flovent, or Pulmicort

For bronchospastic states Prevent asthma on a daily basis Decrease the inflammation response in the lungs

-Nasally—Flonaise (Fluticasone) or Rhinocort (budesonide) For allergic rhinitis and to prevent the recurrence of polyps after surgical removal

-Topically For inflammation of the eye, ear, and skin

-Intraarticular (into a joint)Systemic methods of administration-IV-IM-orally

MOA -Reduce inflammation by stabilizing cell membranes of inflammatory cells called lysosomes-Lower fever by reducing the release of interleukin-1 from WBCsBackground info:Natural:

Cortisol Cortisone

-Increase B receptors formation in heart and lungs-Responsible for carbohydrate, protein, fat metabolism-Promote breakdown of protein, production of glycogen in the liver, and redistribution of fat from peripheral to central areas of the body-Increase blood glucose level-Increased secretion in the stress response –fight or flight-Synthesized from cholesterolreleased and stimulated by ACTH under negative feedback control (diurnal rhythm)-Peak levels are secreted early in the moring (6-8am)decrease during the daylower peak in late afternoon (4-6pm)

-vital to survival-these are synthesized when needed—NOT stored

Effects: Ability to stabilize lysosomal membranes + reduce capillary permeability Anti-inflammatory Fever reduction (inhibit release of interleukin 1 from WBCs + stimulate erythropoiesis) Carbohydrate and protein metabolism Fat metabolism Maintenance of normal BP Stress effect

Contraindications

Drug interactions


Adverse effects Acute:-Immunosuppressant effect-Hyperglycemia

Glucocorticoids cause the cells to become insulin resistant Less likely to happen with someone who has normal pancreatic function and who does

not already have diabetes Sometimes steroids “unmask” a person’s diabetes

-Hypertension (hydrocortisone) More likely with hydrocortisone because it increases cortisol + aldosterone Aldosterone causes sodium retention

-Mood swings Depression Mania Euphoria Hallucination Usually patients experience these symptoms early—especially if on high doses People with history of mental illness are not necessarily at risk

-Peptic ulcer disease (PUD) Caused by medication induced prostaglandin suppression.-->protective prostiglandins

don’t form mucous layer in stomach liningless blood goes to the stomach + glucocorticoids stimulate production of more HClacid ruins stomach lining + duodenum

Can also decrease gastric painpatient can perforate an ulcer in their stomach/duodenum without knowing

-Vertebral compression fractures Occurs acutely in patients who already have osteoperosis

-Weight gain Caused by increase food intake Proteins/carbs/fats being broken down quickerbody is depleted and needs

morehunger

-Cardiac dysrhythmias (due to hypokalemia caused by hydrocortisone)

Chronic (any patient using glucocorticoids for 2 months + is at risk)Cushing’s syndrome—increased secretion of adrenocortical hormones/excess exogenous intake-redistribution of body fat from arms and legs to face, shoulders, trunk and abdomen

Moon face Buffalo hump Pot bellypurple striae

-Na and water retention-potassium loss-muscle weekend-Osteoperosis

can lead to osteoporotic fractures—most common in ribs and vertebrae Increase osteoclastic activity and decrease osteoblastic activity Decrease intestinal absorption of calciumPTH is increasedpulls calium from bone

into the bloodmore calcium lossin bones-myopathy

Caused by muscle breakdownthin arms and legs Also thin skin

-inhibited protein synthesis-Euphoria or mania (may lead patients to ask for more)-Physical dependence

Over time, your adrenal glands atrophy and shut downgland can no longer produce adrenal hormones on demand in times of stresspatients need increased doses of steroids to get them through stressful events (trauma/surgery)

May take adrenal glands days/monts/a full year to get back to normal-Growth retardation in kids

Toxicity Treatment during ToxicityNursing interventions -Look for S&S of infection

Caused by immunosuppressant effect Remember: steroids given for Addison’s are replacement steroids, but steroids given

for inflammation/joint pain will increase the potential for infection TB can occur more easily in these patients Most likely with systemic administration

-Anti ulcer drugs should be taken to prevent ulcers/perforated ulcers Proton Pump Inhibitors (PPI) H2 blockers

-Measure height + weight regularly in kids on steroids

Patient Teaching-patients can’t abruptly stop taking steroids

Leads to an acute adrenal crisisThe only way to treat this is with steroids

MineralocorticoidsMedications Prototypes:

FludrocortisoneNon-Prototypes:

Indications Need for chronic mineralocorticoid replacement-Adrenocortical insufficiency (Addison’s disease)-Cerebral edema-Spinal cord injufy-Collagen diseases-Dermatologic diseases-GI diseases-Thrombocytopenia—increase platelet production-overactive immune system activity + inflammation in:




Dosing/Medication formsMOA -conserve sodium in the body + affect

fluid/electrolyte balanceNatural:

Aldosterone-Na, K, and fluid balance

Blood pressure control Maintenance of serum potassium

levels Maintenance of pH levels in the

bloodSodium and water resorption

Background info:

ContraindicationsDrug interactionsTherapeutic outcomesAdverse effectsToxicity Treatment during ToxicityNursing interventions Patient Teaching

NSAIDs Medications Prototypes:

Aspirin Non-Prototypes:Enolic acid derivatives

Meloxicam (Mobic)Indications Dose: 81 mg – 325 mg (thrombo-prevention)

-should be administered at the first site of an MI-If not given before arriving in the emergency dept.—aspirin is one of the first drugs given if there are no contraindications-given to prevent future clots

Higher doses: (EX: 650 mg)-Analgesic-anti-inflammatory-antipyretic-Headache/Neuralgia/myalgia/arthralgia-Pain syndromes resulting from inflammation:

Arthritis, pleurisy, pericarditis-Systemic lupus erythematosus—has anti-rheumatic effects

Dosing/Medication forms ANOM for MI:AspirinNitroglycerinOxygenMorphine

MOA -Irriversible inhibitor of COX-1 receptors w/in the platelets themselves-Reduced formation of thromboxane A2

A2 normally promotes platelet aggregationOther NSAIDs do NOT have this antiplatelet effect

Background info:


Patients w/ known aspirin allergy are NOT allowed to have NSAIDs

-Conditions that place the patient at risk for bleeding Vitamin K deficiency PUD Renal dysfunction Concurrent use of antiplatelet/anticoagulant drugs


Therapeutic outcomesAdverse effects -GI:

Heartburn/Severe GI bleeding (can be caused by blocking COX-1)/Hepatotoxicity-Renal (nephrotoxic):

Decreased creatinine clearanceAcute renal failure-Blood:

Altered hemostasis Do not use with antiplatelet drugs or steroidsbleeding

-Skin eruption-Sensitivity reaction (SJ syndrome)

Caused by COX 2 inhibitors in particular-Neuro:

Tinnituso May be first sign of aspirin toxicity

Hearing lossToxicity Salicyism

-Neuro: Tinnitus w/ possible hearing loss/ Dimness of

vision/Headache/ Dizziness/ Mental confusion/ Drowsiness-GI

Nausea/Vomiting/Diarrhea-CV

Increased HR-Respiratory

Hyperventilation/Hypoglycemia/Hyperglycemia/Sweating/Thirst

-Metabolic-Hepatotoxicity-renal toxicity

NSAIDs block prostaglandin functionprecipitates acute/chronic renal failure

Can compromise existing renal function Renal toxicity can occur in patients with

dehydration, HF, liver dysfunction, or use of diuretics or ACE inhibitors

-Reye’s syndrome in children (especially post viral attack) Acute encephalitis Coma Liver damage

Possible permanent neurological damage

Treatment during Toxicity-Discontinue drug-supportive care-Dialysis given if:

pH < 7 renal dysfunction/renal failure pulmonary edema CNS symptoms progressing to coma

o Early symptoms = tinnitus + nausea

Nursing interventions Patient Teaching-patients with renal failure need to let ALL healthcare providers know

Acetic Acid Derivatives

NSAIDsMedications Prototypes:

Ketorolac (Toradol)Non-Prototypes:Acetic acid derivatives

Indomethacin (Indocin) Analgesic, anti-inflammatory, anti-rheumatic, and antipyretic properties Used for: RA, OA, acute bursitis or tendonitis, ankylosing spondylitis, acute gouty

arthritis, PDA, preterm labor Oral, recta, IV use Powerful NSAID—limited to 2-3 days to prevent renal/GI adverse effects

Enolic acid derivatives Meloxicam (Mobic)

Indications -moderate to severe acute pain Up to 5 days of use Use limitations due to the potential adverse effects on the kidneys and GI tract

Dosing/Medication forms -PO-IV-IM

MOA -Analgesic effects comparable to narcotic drugs like morphine Background info:


Patients w/ known aspirin allergy are NOT allowed to have NSAIDs-Conditions that place the patient at risk for bleeding

Vitamin K deficiency PUD Renal dysfunction

Concurrent use of antiplatelet/anticoagulant drugs


Therapeutic outcomesAdverse effects -Renal impairment

-edema-GI pain-Dyspepsia-nausea

Toxicity -hepatotoxicity-renal toxicity

NSAIDs block prostaglandin functionprecipitates acute/chronic renal failure Can compromise existing renal function

Renal toxicity can occur in patients with dehydration, HF, liver dysfunction, or use of diuretics or ACE inhibitors


Nursing interventions Patient Teaching-patients with renal failure need to let ALL healthcare providers know

Propionic Acid DeriviativesNSAIDs

Medications Prototypes:-Ibuprofen (Motrin, Advil)—MOST COMMONLY PRESCRIBED NSAID-Naproxen (Aleve)—Second most commonly prescribed NSAID

Non-Prototypes:

Indications -Analgesic anti-inflammatory effects-Initial treatment for mild to moderate pain-RA-OA

-Primary dysmenorrhea-gout-dental pain

-musculoskeletal disorders-antipyretic actions-fever

Dosing/Medication forms Ibu ProfenOTC strength = 200 mgPrescription strength = 400, 600, 800 mgMax daily dose = 2400 mg—regardless of OTC strength or prescription strength

Doses may be higher for patients with RA and OARA = systemic disease—patients need to be on disease modifying drugs early in treatment

Naproxen Sodium (Aleve)OTC strength = 220 mg every 12 hoursPrescription strengthn = 500 mg every 8-12 hoursLimited to 2-3 doses per day because of risk of renal dysfunction-somewhat better adverse effect profile than ibuprofen-fewer drug interactions w/ ACE inhibitors given for HTN

MOA -Block COX 1 and/or COX 2 (cyclooxygenase) COX 1 = good cox—maintains GI mucosa COX 2 = bad cox—present at sites of inflammation

-Antipyretic effect Blog prostaglandin E2 in hypothalamus

-Properties analgesic Anti-inflammatory

Background info:


Patients w/ known aspirin allergy are NOT allowed to have NSAIDs-Conditions that place the patient at risk for bleeding

Vitamin K deficiency PUD Renal dysfunction

-Concurrent use of antiplatelet/anticoagulant drugsDrug interactions -Anticoagulants

-Antiplatelet drugs-Aspirin

-Corticosteroids + other ulcerogenic drugs-Protein bound drugs (competition)-Diuretics + ACE inhibitors (NSAIDs cause fluid retention)


Adverse effects -GI: Heartburn Severe GI bleeding (can be caused by blocking COX-

1) Hepatotoxicity

-Renal (nephrotoxic): Decreased creatinine clearance Acute renal failure

-CV: Increased risk of MI + stroke (all except aspirin) Because NSAIDs do not have anti-platelet effects

(only aspirin) NSAIDs can counteract the cardio protective

properties of aspirin-Neuro:

Tinnituso May be first sign of aspirin toxicityo Hearing loss

-Blood: Altered hemostasis Do not use with antiplatelet drugs or

steroidsbleeding-Skin eruption-Sensitivity reaction (SJ syndrome)

Caused by COX 2 inhibitors in particular


NSAIDs block prostaglandin functionprecipitates acute/chronic renal failure Can compromise existing renal function Renal toxicity can occur in patients with dehydration, HF, liver dysfunction, or use of

diuretics or ACE inhibitors


Nursing interventions -Remind patients that Ibuprofen and Aleve are NOT interchangeable Very different chemicals Very different dosing cycles

Patient Teaching-patients with renal failure need to let ALL healthcare providers know

COX-2 Inhibitor-**First and ONLY COX-2 inhibitor on the market

NSAIDsMedications Prototypes:

Celecoxib (Celebrex)Non-Prototypes:

Indications -OA/RA-Acute pain symptoms-ankylosing spondylitis-primary dysmenorrhea

Dosing/Medication formsMOA -Block COX 1 and/or COX 2 (cyclooxygenase)

COX 1 = good cox—maintains GI mucosa COX 2 = bad cox—present at sites of inflammation

-Antipyretic effectBlog prostaglandin E2 in hypothalamus-Properties

analgesic Anti-inflammatory

Background info:

Contraindications -CAN NOT be used on patients with known sulpha allergySimilar drug structure to sulpha antibiotics


Therapeutic outcomesAdverse effects -Sensitivity reaction (SJ syndrome)

Caused by COX 2 inhibitors in particular-Headache-Sinus irritation-Diarrhea-Fatigue-Dizziness-Lower extremity edema-HTN


NSAIDs block prostaglandin functionprecipitates acute/chronic renal failure Can compromise existing renal function Renal toxicity can occur in patients with dehydration, HF, liver dysfunction, or use of

diuretics or ACE inhibitors


Nursing interventions -Remind patients that Ibuprofen and Aleve are NOT interchangeable Very different chemicals Very different dosing cycles

Patient Teaching-patients with renal failure need to let ALL healthcare providers know

Anti-Gout DrugsMedications Prototypes:

Allopurinol (Zyloprim)Non-Prototypes:-Febuxostat (Uloric)

Non-purine selective inhibitor of xanthine oxidase More selective for xanthine oxidase than allopurinol may pose greater risk of cardiovascular events than allopurinol

-Colchicine (Colcyrs) used to be the drug of choice but causes significant adverse effects reduces inflammatory response to the deposits of urate crystals in joint tissue used for short-term management or prevention of gout may cause short-term leukopenia + bleeding into GI and urinary tracts

-Probenecid (Benemid) inhibits reabsorption of uric acid in the kidneys increases the excretion of uric acid

not used as much now because of newer drugs availableIndications -Prevent uric acid production

-prevent acute tumor lysis syndrome



Contraindications

Drug interactions


Adverse effects -exfoliative dermatitis-Toxic epidermal necrolysis -SJS



Herbal products for inflammation/painMedications Prototypes:

Glucosamine + ChondroitinNon-Prototypes:

Indications -Pain of OA



Contraindications

Drug interactions -Enhance effects of warfarin-May increase insulin resistance (glucosamine)


Adverse effects -GI discomfort-Headache-Skin reactions (glucosamine)



Psychotherapeutic Medications

Tricyclic Antidepressants**Second line choice for pain—Adjuvant analgesics

Medications

Tyramine containing foods Smoked salmon

+ meats Pepperoni,

bologna, salami Aged cheeses Figs Avocados

Prototypes:Amitriptyline (Elavil)Non-Prototypes:-Monamine Oxidase Inhibitors (MAOIs)

Considered the third line in refractory depression if patient not responsive to SSRIs or TCAs

Can be lifesaving in atypical depression Disadvantages:

o Potential to cause hypertensive crisis when taken with tyramine containing foods

o Tyramine is an amino acid that is a precursor to NEmore tyramine consumed leads to more NE madetoxic levels of NE and spill into the peripheryhypertensive crisis

Drug-food interactions are more likely than an OD (cheese reaction)

o Rapid onset of 15-90 mins after ingestiono Most symptoms resolve w/in 6 hours

Fatalities have been reported due to the hypertensive crsisAtypical depression—excessive sleeping and increased appetiteMAOI overdose:-symptoms can be delayed for hours after ingestion-HTN, tachycardia, tremors, seizures, hyperthermia

-Treatment = protect the brain + heart by eliminating the toxin Gastric lavage (if early enough 1-2 hours) Supportive care Hemodialysis

-usually drug-food interaction-drug-drug interactions possibleMeperidine (Demerol), dextromethorphan. SSRIs, St Jon’s wort, Triptans for migrains, Linezolid (antibiotic to treat MRSA), methylene blue

Indications -refractory depression Largely replaced by newer antidepressants (SSRIs and SNRIs) for depression Side effects can be deadly in overdose situations

-Current uses (very low doses): Chronic pain

o Neuropathic paino Diabetic peripheral neuropathyo migraines

InsomniaDosing/Medication formsMOA -Block the reuptake of:

Norepinephrine Serotonin

-More NE + serotonin molecules accumulate in the synapsegreater + more prolonged binding to the post synaptic neuron-correct the balance of neurotransmitter concentrations in the CNSincreasing the concentrations of themcorrects abnormality that causes depression

Background info:-Major Neurotransmitters involved in depression:

serotonin dopamine norepinephrine People with depression have low levels of these hormones

Reuptake—when the neurotransmitter is taken back up from the synapse into the terminal portion of the pre-synaptic neuron

ContraindicationsDrug interactionsTherapeutic outcomesAdverse effects -Powerful anticholinergic effects (block muscarinic receptors)

Tachycardia Dry mouth Constipation Urinary retention

-Antihistamine effects (block histamine) Sedation

-Block alpha 1 receptors Vasodilation

Orthostatic HTNToxicity -Overdose is lethal!—70=80% die before making it to the hospital

-CNS + respiratory systems are mainly affected-death results from seizures or cardiac dysrhythmias

Immediate danger: Tachycardia + abnormal heart rhythm Patients w/ preexisting heart disease or cardiac dysrhythmias are at increased risk

Very rare for cardiac toxicity to occur in absence of an overdose

Treatment during Toxicity-No specific antidote-manage seizures + dysrhythmias-basic life support measures

Nursing interventions -if a patient comes in with possible overdose—YOU MUST MONITOR THEM FOR AT LEAST 6-12 HOURS

It may take this long for toxicity symptoms to present Should be on a monitored bed in ICU

-Patients on EKG before therapy initiated to make sure they don’t have dysrhythmias

Patient Teaching

SSRIsAntidepressants—NEWER **First line choice

Medications Prototypes:Fluoxetine (Prozac)

Non-Prototypes:-Celexa (citalopram)-Luvox (Fluvoxamine)-Paxil (paroxetine HCL)**-Zoloft (Sertraline)**-Lexapro (escitalopram)-Pexeva (paroxetine mesylate)

**Highly protein bound

-Buproprion (Wellbutrin) Helps with smoking cessation

(Zyban) Have to have a diagnosis of

depression in order for insurance to pay for it

Can’t be used if patient has a history of seizures—lowers the seizure threshold

Fewer sexual side effects than SSRIsIndications -Depression

-Bipolar disorder (in depressive state)-Eating disorders-OCD-Panic disorder-Social anxiety disorder-Chronic anxiety-PTSD

Dosing/Medication formsMOA -highly protein bound

-Selective Serotonin reuptake inhibitorsserotonin is left available in the synapse for useBackground info:

Contraindications -Check to see if patient is on an anticoagulantDrug interactions -Anticoagulants

Causes increased risk of bleedingTherapeutic outcomes -Takes 4-6 weeks for maximum effect (can take as little as 2 weeks or longer than 6 weeks)Adverse effects Caused by increased circulating serotonin

Weight gain Nausea—may go away after a few weeks Headache—may go away after a few weeks Tremor

-Sexual dysfunction Most common—70% May get WORSE over time Major reason for non-compliance with these drugs Happens in both men and women Often leads to change in medication—like switching to wellbutrin (below_

-Increased risk of bleeding—in combination with anticoagulantsInhibit serotonin in platelets + decrease the ability of platelet to aggregate

Toxicity -Serotonin syndrome (too much) Serotonin Shake and bake Fever + tremors + confusion (including hallucinations) + hyperflexia Indicator of toxicity Symptoms can show as early as 2 hours after combining drugs or as late as 72 hours

later Can lead to death

-Withdrawal syndrome (too little) Happens when patients decide to take themselves off because they don’t like the

side effects More common than toxicity Symptoms occur 7-10 days after stopping the drug Accronym FLUSH F—Flu like symptoms (aches and pains, tired, not themselves) L—Lightheadedness (most common symptom) U—Uneasiness (anxious) S—Shakiness + sleepiness

H--Headache

Treatment during Toxicity-Hold medication-symptoms with gradually resolve

Withdrawal:-symptoms can last up to 14 days-to prevent—patients should be weaned off


SNRIs

**First line choice for depression—NEWEST AntidepressantMedications Prototypes:

Venlafaxine (Effexor)Non-Prototypes:Duloxetine (Cymbalta)

Indications -Depression-PainEffexor

can be used in patients who don’t benefit from SSRIs Works quickly because of short half life

Patients feel better faster and return to work faster

Cymbalta: 4 FDA approvals—

o Depressiono Diabetic neuropathyo Chronic musculoskeletal pain

Pain of fibromyalgiaDosing/Medication forms

MOA -highly protein bound-Serotonin Norepinephrine reuptake inhibitorsboth are left available in the synapse for use

Background info:

Contraindications -Liver functions-Heavy drinking

Defined as: 3+ drinks a day for males-Severe HTN

Drug interactions


Adverse effects

-Less adverse effects than MAOIs and TCAs

-Cymbalta: Weight gain

and sexual dysfunction are less than the others

-Hypertension

Similar side effects as SSRIs:-Caused by increased circulating serotonin

Weight gain Nausea—may go away after a few weeks Headache—may go away after a few weeks Tremor

-Sexual dysfunction Most common—70% May get WORSE over time Major reason for non-compliance with these drugs Happens in both men and women Often leads to change in medication—like switching to wellbutrin (below_

-Increased risk of bleeding—in combination with anticoagulantsInhibit serotonin in platelets + decrease the ability of platelet to aggregate

Toxicity -Hepatotoxicity (caution) Treatment during Toxicity

Nursing interventions **BLACK BOX WARNING:Suicidal thoughts + behaviors (children-adulthood)

Monitor patients for suicide risk Teach family for signs

Teach family to contact providers immediately

Patient Teaching-Teach family for signs of depression-Teach family to contact providers immediately

Mood stabilizers (antimanic drugs)Medications Prototypes:

Lithium (Lithium carbonate)Non-Prototypes:

Indications -Bipolar disorder Controls mania Prevents recurrent mania/depression

DRUG OF CHOICE**Antiepileptic drugs are also used

Dosing/Medication forms -Given 2-3 times daily-Has to be given in divided doses

Therepeutic range: .6 – 1.2 mEq/Lshort half life—rapid renal excretion

MOA -Stabilize Ca and Serotonin-Excellent bioavailabilty

Background info:

Contraindications -Pregnancy This drug is teratogenic and should not be used during pregnancy Category D 11% risk of cardiac deformities in developing fetus If continued through 1st trimester

-Patients with renal impairment-Dehydration-Renal dysfunction-Cardiac Dysfunction-Known sodium imbalance-patients on diuretics

Drug interactions -diuretics

Therapeutic outcomes -reduces euphoria + hyperactivity-does NOT cause sedation at therapeutic levels-Antimanic effects take 5-7 days-Full effect not seen for 3 weeks

Adverse effects -Nausea-Excess thirst-polyuria-tremor (even at therapeutic doses)

**Get better once tolerance developsToxicity -Considered a salt (on periodic table between sodium + potassium)rapidly excreted via the kidneys

-levels about 1.5 mEq/L considered toxicTreatment during Toxicity

Mild:-Nausea/vomiting/diarrhea-Thirst-polyuria-weakness-slurred speech

Severe-GI upset-Course tremors-confusion-EKG changes-Sedation-Ataxia

-Blurred vision-Tinnitus-Coma-Seizure-Renal failure-Death

Nursing interventions -Monitor sodium levels If kidney perceives low Na+ levelsholds

on to lithiumtoxicity-Encourage normal sodium intake-caution w/ diuretics-Na+ loss from diarrhea can also cause toxicity-Encourage patient to drink lots of water

-Assess for signs of toxicity before administering a new dose-monitor lithium levels-Monitor creatinine levels-Monitor intake/output-Give with food if nausea occurs-If lithium is high or sodium is low—contact the provider

Patient Teaching-Take with food to prevent nausea—bioavailability with not change-encourage salt intake + adequate water intake to prevent toxicity-Encourage patients to have blood levels drawn as prescribed

Conventional AntipsychoticsMedications Prototypes:

-Chloropomazine (Thorazine) -Haloperidol (Haldol)

Non-Prototypes:

Indications -Depressive and drug induced psychosis-Schizophrenia-Bipolar disorder-Autism-Movement disorders—Tourette’s Syndrome-Severe Nausea (Haldol)-Intractable hiccups (Thorazine)

Dosing/Medication formsMOA -Block dopamine receptors in the brain

Block dopamine receptors in the limbic system + basal ganglia (areas involved in emotional response, cognitive function, motor function)

Background info:

Contraindications -Patients with known seizure disorders because conventional antipsychotics increase the potential for seizures

Drug interactionsTherapeutic outcomes Decrease positive symptoms in schizophrenia

Hallucinations Delusions Conceptual disorganization

Do not help negative symptoms Social withdrawal Blunted affect Poverty of speech catatonia

Adverse effects -Movement disorders –EPS (Extrapyramidal system side effects) Caused by imbalance of dopamine + ACH Give patients Cogentin to restore balance Benadryl is also a strong anticholinergic drug Ex:

o Acute dystonia (spasms)— Laryngospasm—airway closure. Usually happens early in treatment Most life threatening Can also result in spasms of face, neck, tongue, and back muscles

o Parkinsonism— Bradykinesia, tremors, rigidity

o Tardive dyskinesia— Occurs late in treatment Irreversible Occurs in up to 20% of patients treated w/ conventional antipsychotics Worm-like twisting and writhing movements of the tongue and face—usually first

indication Lip smacking and tong protrusion

-Seizures-low libido-neuroendocrine side effects:

Gynecomastia in men Menstrual irregularities in women

Toxicity Treatment during ToxicityNursing interventions -Cogentin + Benadryl

given IV or PO reduce levels of Ach in the brain to restore

balance of Ach and Dopamine prevents acute dystonia, parkinsonism’s, and

Tardive dyskinesia-Use the nursing process

Assessment: vital signs (baseline) + emotional state (risk of harm to self or others)

Diagnosis: identify the problem Planning/patient education Intervention: use the 9 rights

Evaluation: appropriate lab monitoring-have patients wear sunscreen-Have patients on MAOIs avoid tyramine containing foods-avoid antacids w/in 1 hour of taking antipsycotics-Check the mouth for cheeking—to make sure patient actually swallowed the medicine-Monitor lab studies as appropriate

CBC blood glucose liver function Serum creatinine

Drug levels

Patient Teaching-Provide simple explanations

side effects interactions

-Emphasize benefits of combined drug therapy and psychotherapy-Advise patient that simultaneous use of alcohol + other CNS depressants can be fata-Monitor for therapeutic effects

Improved mood/cognition Improved appetite/sleep paturn Participation in activities of daily living Decreased psychotic symptoms—less mania w/bipolar disorder

Monitor for self injury during the period until maximal effect of the drug + improvement of symptoms

Atypical Antipsychotic medications – NEW Medications Prototypes:

-Clozapine (Clozaril)-Olanzepine (Zyprexa)-Risperidone (Risperdal)

Non-Prototypes:

Indications


MOA -Block specific dopamine receptors: Dopamine-2 (D2) Treats positive symptoms: delusions + hallucinations

-Block specific Serotonin receptors Serotonin-2 (5HT 2) This is responsible for their improved efficacy profiles Treats negative symptoms: cognitive impairment, depression, self-care decline

-Also block: histamine, ACH, alpha 1 receptors

Background info:

Contraindications

Drug interactions

Therapeutic outcomes -Treatment of positive symptoms: delusions + hallucinations-Treatment of negative symptoms: cognitive impairment, depression, self-care decline, cognitive dysfunction (often seen in schizophrenics) This is what makes them superior to conventional antipsychotics

Adverse effects Caused by blocking histamine, ACH, and alpa 1 receptors-Sedation-Anticholinergic symptoms

Dry mouth, constipation, blurred vision, urinary retention, etc-Orthostatic HTN

Caused by serotonin blockade-significant weight gain—

some patients as much as 30-50 pounds major problem with drug Zyprexa (olanzapine) and risperidone (Risperdal)

-Rare for these drugs to cause EPS



Antiparkinson’s Medications

Dopamine ModulatorsAnti-Parkinson’s Drugs

Medications Prototypes:Amantadine (Symmetrel)

Non-Prototypes:

Indications -Parkinson’s disease Specifically used to treat dyskinesia associated w/ carbidopa-levodopa

-used early in treatment-usually effective for 6-12 months-also a drug for influenza

Symptoms occur when about 80% of the dopamine stored in the substantia nigra of the basal ganglia is depletedSymptoms can be partially controlled as long as there are functioning nerve terminals that can take up dopamine

TRAP Tremor

o Pill rollingo Presenting sign in 70% of caseso Also tremor of hands and extremities

Rigidityo Cogwheel rigidity—resistance to passive movement

Akinesiao Absence of psychomotor activity resulting in mask-like facial expression

Postural instabilityo Unsteadiness o Associated w/ bradykinesia and rigidty)

Bradykinesia—slowness of movemento Leads to danger of falling, leaning to one side, even when sitting

Dosing/Medication formsMOA -Cause release of dopamine + other catecholamines from their storage sites in basal ganglia that

have not been destroyed yet-Blocks reuptake of dopamine in the presynaptic nerve fibers-Results in higher levels of dopamine in the synapses between nerves + improved dopamine neurotransmission between neurons

Background info:

Contraindications -are they on anticholinergics?

Drug interactions -Increased anticholinergic adverse effects when given with anticholinergic drugsTherapeutic outcomes -May take 3-4 weeks for therapeutic outcome

-usually effective for 6-12 months-Improved sense of well-being + mental status-increased appetite-increased ability to perform ADLs, concentrate, think clearly

-Less intense parkinsonian manifestations Tremor Shuffling gait Muscle rigidity

Involuntary movements (dyskinesia)Adverse effects -relatively mild

-Dizziness-insomnia-nausea

Toxicity Treatment during ToxicityNursing interventions -perform a thorough assessment, nursing history, and medication history

-Include questions about patient’s CNS GI/GU tracts Psychologic + emotional status

-Assess for signs + symptoms of PD Masklike expression Speech problems Dysphagia Rigidity of arms, legs, and neck

-Assess for conditions that may be contraindications-Assist patient w/ walking because of dizziness-Administer oral doses w/ food to minimize GI upset-Encourage patient to force fluids

At least 3000 mL/day (unless contraindicated)-Provide patient education regarding PD and the medication therapy-Inform patient not to take other medications w/ PD drugs w/o checking w/ physician first-Do not discontinue anti-PD drugs suddenly-Teach patient about expectd therapeutic + adverse effects with anti PD drug therapy

Patient Teaching-avoid alcohol-do not quit medications abruptly-must be taken at dosage/time prescribed

Inability to do this may lead to exacerbation of symptoms + development of complications

Missing a dose of even 30 minutes may lead to an “off period” that can last for hours-warn patients about adverse effects

Dopamine Replacement Drugs

Anti-Parkinson’s DrugsMedications Prototypes:

Carbidopa-Levodopa (Sinemet)Non-Prototypes:

Indications -Parkinson’s disease-works will with patients with early PD who still have functioning nerve terminals-Usually only effective for 5-10 years

As PD progresses it becomes more difficult to control it with levodopaEventually levodopa no longer controls PD and patient is seriously debilitated

Dosing/Medication forms -Large doses of levodopa needed to get dopamine to the brain cause adverse effects-administered PO

MOA Levodopa-biological precursor to dopamine—crosses the BBB and converted to dopamine-taken up by the dopaminergic terminalconverted to dopaminereleased as needed-works presynaptically to increase brain levels of dopamine**dopamine can’t cross the BBB like levodopa can—which is why you have to take levodopa instead

Carbidopa (Lodosyn)-reduces dose of levodopa needed-does not cross BBB-prevents levodopa breakdown in the peripherymore levodopa crosses the BBBlevodopa can be converted to dopamine

Background info:

Contraindications -closed angle glaucomaUsed cautiously in patients with open angle glaucoma

Drug interactions -Tricyclic anti-depressants (TCA)-antipsychotics-benzodiazepines-pyridoxine (vitamin B6)-Levodopa + MAOIs – A may result in hypertensive crisis “cheese effect”

Therapeutic outcomes -May take 3-4 weeks for therapeutic outcome-Improved sense of well-being + mental status-increased appetite-increased ability to perform ADLs, concentrate, think clearly

-Less intense parkinsonian manifestations Tremor Shuffling gait Muscle rigidity

Involuntary movements (dyskinesia)Adverse effects -Confusion

-involuntary movements (dyskinesia)-Muscle cramps-depression-urinary retention

-GI distress-Hypotension-cardiac dysrhythmias-“Off-On” phenomenon—patients who use levodopa long term experience times when their symptoms are under control and other times when symptoms are not well controlled

Toxicity Treatment during ToxicityNursing interventions -best taken on an empty stomach

Can be taken with food to minimize GI side effects Carbidopa (Lodosyn)—taken adjunct to treat

nausea associated w/ sinemet-may continue eating protein-rich foods

Portions of meat—about the size of a deck of cards Take medicine 30 min before eating protein meal or

1 hour after-Best given several hours before bedtime to prevent insomnia-perform a thorough assessment, nursing history, and medication history-Include questions about patient’s

CNS GI/GU tracts Psychologic + emotional status

-Assess for signs + symptoms of PD

Masklike expression Speech problems Dysphagia Rigidity of arms, legs, and neck


At least 3000 mL/day (unless contraindicated)

-Provide patient education regarding PD and the medication therapy-Inform patient not to take other medications w/ PD drugs w/o checking w/ physician first



Missing a dose of even 30 minutes may lead to an “off period” that can last for hours

-warn patients about adverse effects

MAO – B Inhibitor (Monoamine oxidase – B inhibitors)

Anti-Parkinson’s DrugsMedications Prototypes: Non-Prototypes:

Indications -Parkinson’s disease

Dosing/Medication forms -Can be used alone-Can be used as adjunct w/ levodopa

MOA MAOI – B (Selective)-Indirect-acting dopaminergic receptor agonists-Increase available dopamine in CNS

MAOI – A (Non-selective)-increase levels of norepinephrine

Background info:

Contraindications -Known drug allergy-Concurrent use w/ meperidine (Demerol)

Drug interactions MAOI – B (Selective)-No “cheese” effective

MAOI – A (Non-selective) –used to treat depression-Interact with tyramine containing foods

Cheese Red wine Smoked meets Beer

-Tyramine is a precursor of norepinephrineMAOI – A + tyramine increases norepinephrine levelshypertensive crisis = cheese effect

Therapeutic outcomes - May take 3-4 weeks for therapeutic outcome-Improved sense of well-being + mental status-increased appetite-increased ability to perform ADLs, concentrate, think clearly-Less intense parkinsonian manifestations

Tremor Shuffling gait Muscle rigidity

Involuntary movements (dyskinesia)Adverse effects -Headache

-Confusion-insomnia-dizziness-hypotension-nausea

Toxicity Treatment during ToxicityNursing interventions -Oral disintergrating dose

should be placed on the tongue + not swallowed until it is completely melted

take w/o liquid take in the morning before breakfast foods/fluids not to be taken 5 mins

before or after-patient should move slowly to prevent orthostatic hypotension-perform a thorough assessment, nursing history, and medication history-Include questions about patient’s


-Assess for signs + symptoms of PD Masklike expression

Speech problems Dysphagia Rigidity of arms, legs, and neck


At least 3000 mL/day (unless contraindicated)

-Provide patient education regarding PD and the medication therapy-Inform patient not to take other medications w/ PD drugs w/o checking w/ physician first-Do not discontinue anti-PD drugs suddenly-Teach patient about expectd therapeutic + adverse effects with anti PD drug therapy



Missing a dose of even 30 minutes may lead to an “off period” that can last for hours

-warn patients about adverse effects-Oral disintergrating dose

should be placed on the tongue + not swallowed until it is completely melted take w/o liquid take in the morning before breakfast foods/fluids not to be taken 5 mins before or after

-patient should move slowly to prevent orthostatic hypotension

Catechol Ortho-Methyltransferase (COMT) InhibitorsAnti-Parkinson’s Drugs

Medications Prototypes:Entacapone (Comtan)

Non-Prototypes:

Indications -Parkinson’s disease


MOA -Indirect acting dopamine receptor agonists-Block COMT-Prolong the duration of action of levodopa + reduce the wearing-off phenomenon

Background info:COMT—-enzyme that catalyzes the breakdown of the body’s catecholamines

Contraindications

Drug interactions

Therapeutic outcomes -may be noticed w/in a few days As opposed to other drugs that may take weeks

-Improved sense of well-being + mental status-increased appetite-increased ability to perform ADLs, concentrate, think clearly-Less intense parkinsonian manifestations


Involuntary movements (dyskinesia)Adverse effects -GI upset

-urine discoloration-sweat discoloration-worsen dyskinesia that is already present


Nursing interventions -perform a thorough assessment, nursing history, and medication history-Include questions about patient’s




At least 3000 mL/day (unless contraindicated)-Provide patient education regarding PD and the medication therapy-Inform patient not to take other medications w/ PD drugs w/o checking w/ physician first-Do not discontinue anti-PD drugs suddenly-Teach patient about expectd therapeutic + adverse effects with anti PD drug therapy




Anticholinergic TherapyAnti-Parkinson’s Drugs

Medications Prototypes:Benzotropine (Cogentin) – pure anticholinergic drugDiphenydramine (Benadryl) – antihistamines

Non-Prototypes:

Indications -Parkinson’s disease Muscle tremors + rigidty associated with PD These two symptoms are caused by the excessive cholinergic activity

-EPS symptoms from conventional antipsychotic medicines-Does NOT relieve bradykinesia

Dosing/Medication formsMOA -Block the effects of ACh Background info:

Contraindications

Drug interactions -Alcohol

Therapeutic outcomes -May take 3-4 weeks for therapeutic outcomes-Improved sense of well-being + mental status-increased appetite-increased ability to perform ADLs, concentrate, think clearly-Less intense parkinsonian manifestations


Involuntary movements (dyskinesia)Adverse effects -Hyperthermia (during hot weather or exercise)

-Tachycardia-Confusion-Disorientation-toxic psychosis-urinary retention-dry throat-constipation (decreased GI motility)

-nausea-vomiting-decreased salivation-mydriasis-smooth muscle relaxation

Red as a beat (atropine), Dry as a bone (atropine; scopolamine), hot as a hare (atropine), blind as a bat (atropine), mad as a hatter, full as a flask


Nursing interventions -perform a thorough assessment, nursing history, and medication history-Include questions about patient’s




At least 3000 mL/day (unless contraindicated)-Provide patient education regarding PD and the medication therapy-Inform patient not to take other medications w/ PD drugs w/o checking w/ physician first-Do not discontinue anti-PD drugs suddenly-Teach patient about expectd therapeutic + adverse effects with anti PD drug therapy-Monitor for response to drug therapy




Dry mouth: Can use artificial saliva drops, gum, frequent mouth care, fluid, sugarless gum/hard candy may be helpful

-Do not take with other medications-Take at bedtime

Anti-Allergy/ Cold/ Cough Medications

H1 Receptor antagonists/blockers1st Generation antihistamines**First line of defense for mild allergies; Second line defense for anaphylaxis

Medications Prototypes:-Diphenhydramine (Benadryl)

Non-Prototypes:-Chlorpheniramine (Coricidin HBP)

Good for patients with HTN or BPH Causes less anticholinergic effects:

o Urinary retentiono Sedationo Elevated BP/HR

-Dramamine—anticholinergic used for motion sicknessIndications -Allergies (Mild and severe)

Environmental allergens (hay fever, mold, pollens) Anaphylaxis—

o Epinephrine SQo IV steroidso H1 + H2 blockers (not first line defense)

Symptoms of allergies: nasal congestion/runny nose/coughing/sneezing, itchy eyes, itchy skin/hives (urticarial), scratchy throat, anaphylaxis, bronchoconstriction

-Non-allergic uses Insomnia—1st generation antihistamines (Benadryl) Common cold Motion sickness (Dramamine) Chemo therapy induced nausea Parkinson’s disease (because of anticholinergic effects) Mild transfusion reactions

**Used in addition to epinephrine, steroids, and H2 blockers in anaphylaxisDosing/Medication formsMOA -Bind selectively to H1 receptorsblock effect of histamine

-Bind to muscarinic receptorsanticholinergic effects Sedation drying of secretions

**DO NOT block the release of histamine

Background info:H1 histamine receptors:

Mediate smooth muscle contraction + dilation of capillaries Capillaries become more permeable (leaky)leads to bronchoconstriction in lungs +

edema of airways Play bigger role in allergic rhinitis than H2 receptors

H2 histamine receptors:Mediate the accelerations of HR and gastric acid secretions

Contraindications -Antihistamine products shouldn’t be given to young children in generalDrug interactions -Other CNS depressants

Alcohol Opioids Benzodiazepines

-Other anticholinergics Agents to prevent incontinence (can’t hold pee) Psychiatric medications (antipsychotics) Nausea medications Cogentin (benzotropine)—Used to treat EPS reactions in patients on antipsychotics (can be caused by both types but usually traditional like Thorazine and Haldol)—balances dopamine and

acetylcoholine.Therapeutic outcomes -Antihistaminic effects:

reduce local flushing reduce edema (urticarial) Reduce itching/pain

-Anticholinergic effects: Reduce salivary/gastric/lacrimal/bronchial secretions Urinary retention Induce sleep (if used for insomnia)

Restores balance between dopamine/acetylcholine (if used for parkinson’s)Adverse effects -Drowsiness/sedation

-Dry mouth-Urinary retention

Paradoxical effect:-excitation usually happening in children and elderly

Toxicity Treatment during ToxicityNursing interventions -prevent falls Patient Teaching

-Take at bedtime-avoid driving-avoid alcohol

H1 receptor antagonists/blockers2nd generation Antihistamines**First line of defense for mild allergies; Second line defense for anaphylaxis

Medications Prototypes:-Claritin (Loratidine)-Allegra (fexofenadine)-Zyrtec (cetirizine)-Clarinex (Desloratidine

Non-Prototypes:

Indications -Allergies (Mild and severe) Environmental allergens (hay fever, mold, pollens) Anaphylaxis—

o Epinephrine SQo IV steroidso H1 + H2 blockers (not first line defense)

Symptoms of allergies: nasal congestion/runny nose/coughing/sneezing, itchy eyes, itchy skin/hives (urticarial), scratchy throat, anaphylaxis, bronchoconstrictionDosing/Medication formsMOA 2nd generation in particular

-Peripherally acting antihistaminesdo not cross BBBless CNS effects that first gen antihistamines have

minimal to no sedationminimal to no anticholinergic effects

Antihistamines in general:-Bind selectively to H1 receptorsblock effect of histamine-Bind to muscarinic receptorsanticholinergic effects

sedation drying of secretions

**DO NOT block the release of histamine

Background info:H1 histamine receptors:

Mediate smooth muscle contraction + dilation of capillaries Capillaries become more permeable (leaky)leads to bronchoconstriction in lungs +

edema of airways Play bigger role in allergic rhinitis than H2 receptors

H2 histamine receptors:Mediate the accelerations of HR and gastric acid secretions

Contraindications Antihistamine products shouldn’t be given to young children in general

Drug interactions -Other CNS depressants Alcohol Opioids Benzodiazepines

-Other anticholinergics Agents to prevent incontinence (can’t hold pee) Psychiatric medications (antipsychotics) Nausea medications Cogentin (benzotropine)—Used to treat EPS reactions in patients on antipsychotics (can be caused by both types but usually traditional like Thorazine and Haldol)—balances dopamine and

acetylcoholine.Therapeutic outcomes -Antihistaminic effects:

reduce local flushing reduce edema (urticarial) Reduce itching/pain

-Anticholinergic effects (less w/ these second generation): Reduce salivary/gastric/lacrimal/bronchial secretions

Adverse effects NO DROWSINESS W/ THESEToxicity Treatment during Toxicity


Nasal Corticosteroids

Medications Prototypes:-Rhinocort-Nasonex-Flonase (OTC)-Omnaris-NasoCort (OTC)

Non-Prototypes:

Indications -seasonal allergies and perennial allergic rhinitis-allergy induced asthma


MOA -Stabilize capillary cell membranes + prevent release of pro-inflammatory proteinsWork locally to reduce inflammation in nasal cavities + sinuses**More effective than antihistamines alone

Background info:

Contraindications

Drug interactions


Adverse effects -Nasal irritation-Nasal burning with first few doses


Nursing interventions Patient Teaching-Make sure patients head is down (nose to toes)—you do NOT want this running down patients throat

Nasal spray DecongestantsAlpha 1 agonists

Medications Prototypes:-Phenylephrine (Neo-Synephrine)-Oxymetazoline (Afrin)

Non-Prototypes:

Indications


MOA -Alpha 1 agonist (Sympathomimetic ) Work immediately Local effects Short duration of action

Background info:

Contraindications

Drug interactions


Adverse effects Afrin: Causes rebound congestion (rhinitis medicamentosa) DO NOT use more than 3 days


Nursing interventions Patient Teaching-Do not use Afrin for more than 3 days-Look at your toes when spraying your nose-Wait 10 minutes before blowing your nose

Oral DecongestantsAlpha 1 agonists

Medications Prototypes:-Pseudoephedrine (Sudafed)

Non-Prototypes:

Indications


MOA -Alpha 1 agonist (Sympathomimetic) Less powerful than intranasal decongestants Longer acting Less potent effects than nasal No rebound congestion

Background info:

Contraindications -Patients with HTN Check with provider first

-Narrow angle glaucoma (dilated pupil can worsen angle narrowing)-Uncontrolled cardiovascular disease-hyperhtyroidism—

Increases sympathetic effect Patients w/ hyperthyroidism are sensitive to catecholamines

-History of BPH or urninary obstruction (remember the alpha receptors at the base of the male bladder/prostate) -Sales limited to prevent methamphetamine production

Drug interactions


Adverse effects -Tachycardia (palpitations)-HTN-Agitation-Insomnia


Nursing interventions -assess for drug allergies Patient Teaching

Opioid Antitussives (Cough medicine)Medications Prototypes:

Phenergan (Promethazine) + Codeine cough syrupNon-Prototypes:-hydrocodone and other opioids usually taken for pain-codeine (Robitussin A-C, Dimetane-DC)

Indications -Nonproductive cough: Dry cough May keep patients up at night Can be severe enough to cause syncope or broken rib

-May be used when coughing is harmful After brain surgery

Dosing/Medication forms -available only by perscription

MOA Suppress cough reflex by direct action on cough center in the medulla Background info:

Contraindications -Productive cough Thick sputum expelled from lower airways by cough DO NOT GIVE antitussives to these patients—they NEED to get the gunk out of lungs

-Children under 4 Dosing errors and accidental ingestions are the leading causes of rare adverse events in young children Can cause sedation if too much given Antihistamine products shouldn’t be given to young children in general

Drug interactions -DO NOT TAKE WITH ALCOHOL—causes sedation

Therapeutic outcomes -reduce cough

Adverse effects -antihistamine properties like Benadryl—Phenergan acts as antihistamine/anticholinergic Sedation Nausea Vomiting Lightheadedness constipation

**can be seriousToxicity -Respiratory depression

-Hypotension-Sedation


Nursing interventions -Report any of the following symptoms to caregiver: Cough that lasts more than a couple weeks Persistent headache w/ cough Productive cough and fever

-For nonproductive coughs only!-monitor for therapeutic effects

Patient Teaching

Non-Opioid antitussives (cough medicine)

Medications Prototypes:-Dextromethorphan**most common ingredient in OTC cough suppressants (EX: Vicks formula 44, Robitussin DM)- Benzonatate (Tessolon pearls)

Non-Prototypes:

Indications


MOA -suppress the cough reflex by numbing the stretch receptors in the respiratory tractpreventing the cough reflex from being stimulated

Background info:

Contraindications -careful with abuse in teens

Drug interactions


Adverse effects Dextromethorphan:-dizziness-drowsiness-nausea

Benzonatate: (usually stronger side effects than with DM)-dizziness-headache-sedation-nausea-others—people sometimes don’t like this drug


Nursing interventions -Report any of the following symptoms to caregiver: Cough that lasts more than a couple weeks Persistent headache w/ cough Productive cough and fever

-For nonproductive coughs only!-monitor for therapeutic effects

Patient Teaching

ExpectorantsMedications Prototypes: Non-Prototypes:

Indications -Mucus buildup-Productive cough


MOA -breakdown thin secretionsallowing expectoration of sputum Background info:

Contraindications

Drug interactions


Adverse effects -nausea—rare


Nursing interventions -use with caution in patients w/ Elderly Asthma Respiratory insufficiency

-patients should receive more fluids if permitted to help loosen up/liquefy secretions-monitor for therapeutic effects-report symptoms below lasting > 3 weeks—viral URTI may cause cough that lasts > 3 weeks)

Fever Cough

Other symptoms

Patient Teaching-increase fluid intake (if permitted—ex: not with someone with HF)

Increased fluid intake is what really helps with thick secretions + humidificaiton

-Be careful taking with other meds because: common in OTC cough/cold products Often combined with dextromethrophan

Asthma/COPD Medications

SABA (Short Acting Beta2 Agonist)—Sympathetic agonistsMedications Prototypes:

-Albuterol (Proventil/Ventolin)-ipratropium bromide (Atrovent)

COPD medication- Combivent (MDI w/ albuterol + Atrovent)

COPD Combination drug w/ albuterol

Non-Prototypes:-Xopenex (levalbuterol)

Often used in the hospital Available for home nebulizers but more expensive than albuterol

Indications -asthma symptoms (SABA) Quick relief Rescue inhaler exercise induced bronchospasm

Taken just before exercise-COPD exacerbations

In COPD the SABA may or may not be combined with a anticholinergic drug as wello Prototype: ipratropium bromide (Atrovent)o FYI: Spriviao Cause bronchodilation in small/medium sized airways and reduce excess bronchial secretions

Combination drug = Combivent (MDI w/ albuterol + Atrovent)Dosing/Medication forms -Inhaled

MDI (multi dose inhaler)o Need some coordination to inhale; get about 10% of drug delivery to lungso Some have spacers which allow more effective delivery of the medication particleso Help patients overcome difficulties in coordinating the timing of the inhaler actuation and when to inhaleo Slow down the speed of delivery of the aerosol into the mouthless of the drug impacts the throat

Nebulizero Medication is in solution form and is hooked up to a compressor that usually supplies air/oxygen along w/ the drugo Compressed oxygen then mixes with the drug installed in the nebulizer capdelivered as an aerosol via the mouthpiece to the patient as the patient inhales

-Oral syrups for pediatricsMOA Beta 2 Agonists (stimulants) Background info:

Asthma—inflammation of airwaysbronchoconstriction + mucus production Symptoms: wheezing, dyspnea Allergic (extrinsic) Idiopathic (Intrinsic) Exercise induced Drug induced

Status asthmaticus Prolonged asthma attack that does NOT respond to typical drug therapy May last several minutes to hours Medical emergency

Requires aggressive managementContraindications

Drug interactions

Therapeutic outcomes -Dilate bronchial smooth muscle (bronchodilation)Adverse effects Inhaled:

MinimalSerial Nebulizers:-frequent treatments cause loss of beta 2 specificity-tremors-nervousness

Oral syrups (pediatrics):-Tremors-Excess dosesangina, tachycardia, cardiac dysrhythmias


Nursing interventions Patient Teaching-keep track of the number of doses in the canister + how often they use the MDI-Mark the MDI w/ the date it will be emptyget a refill at least a few days before that date-Clean nebulizers once a week

Oral/IV CorticosteroidsShort-term control of inflammation—Asthma

Medications Prototypes:-Solumedrol-Prednisone

Non-Prototypes:

Indications -Quick/rapid relief of inflammation ONLY (Acute asthma symptoms)-COPD

Moderate symptoms

Dosing/Medication forms -IV for severe exacerbations (in ER or hospital) Methylprednisolone (Solumedrol If severe attack—1-3 times per day then taper down)

-PO for acute exacerbation (if patient is stable enough to be treated in the office Prednisone (deltasone) Start w/ higher daily dose then taper down

MOA -stabilize membranes of mast cells and eosinophils that release harmful bronchoconstricting substances-increase responsiveness of bronchial smooth muscle to beta-adrenergic stimulation

Background info:Asthma—inflammation of airwaysbronchoconstriction + mucus production

Symptoms: wheezing, dyspnea Allergic (extrinsic) Idiopathic (Intrinsic) Exercise induced Drug induced


Requires aggressive managementContraindications

Drug interactions


Adverse effects



Inhaled CorticosteroidsLong-term control of inflammation—Asthma

Medications Prototypes:Pulmocort (budesonide)

***Hydrofluoroalkalinesbcx—Propellant that disperses the drug is HFA

Non-Prototypes:-Flovent (fluticasone)-Azmacort (triamcinolone)-Vanceril, Beclovent (beclomethasone)-Aerobid (flunisolide)- Hydrofluoroalkalinesbcx—Propellant that disperses the drug is HFA

Indications -long acting prevention of asthma attacks-NOT taken for acute attacks

Dosing/Medication forms -inhaled-used EVERYDAY via MDI

Twice a day W/ or w/o long acting beta agonist—inhaled twice daily until the asthma is under control; always used with a steroid, never alone

MOA -Stabilize cell membranes-decrease production and release of leukotrienes

Background info:Asthma—inflammation of airwaysbronchoconstriction + mucus production

Symptoms: wheezing, dyspnea Allergic (extrinsic) Idiopathic (Intrinsic) Exercise induced Drug induced


Requires aggressive managementContraindications -Fungal infections

-Aids-TB

Drug interactions


Adverse effects Inhaled:-fungal infections


Nursing interventions Patient Teaching-gargle/rinse mouth with warm water after last inhalation

Prevent oral fungal infections Dysphonia (hoarseness) may be a sign of fungal infections

-not taken for acute attacks

Long Acting Beta 2 Agonists (LABA)Second line therapy after corticosteroids

Medications Prototypes:Salmeterol

Non-Prototypes:

Indications -prevention of asthma attacks-second line therapy after corticosteroids-COPD exacerbation prevention

Dosing/Medication forms -inhaled twice daily until asthma is under control

MOA -stimulate beta 2 receptors + relax bronchial smooth muscle-effects begin slowly but persist up to 12 hours

Background info:

Contraindications

Drug interactions


Adverse effects


Nursing interventions -Never used alone—higher risk of asthma death Patient Teaching

Leukotriene inhibitorsMedications Prototypes:

Singulair (montelukast)Non-Prototypes:

Indications -prevention of asthma exacerbation-severe allergic rhinits

Dosing/Medication forms -PO

MOA -Blocks the formation of leukotrienespreventing airway stimulation Prevent LTs from attaching to receptors located on both circulating immune cells and

those in the lungsalleviating asthma symptoms by reducing inflammation

Background info:Leukotrienes are a part of the inflammatory response

Contraindications

Drug interactions


Adverse effects -Minimal side effects Headache Nausea diarrhea insomnia



Combination Drugs for Asthma—Dry Powder Inhalers (DPIs)Medications Prototypes:

-Advair (Fluticasone + Solumedrol)-Symbicort (Budesonide + formeterol)

**Combination of LABA + Inhaled corticosteroid

Non-Prototypes:

Indications -Long acting care of asthma-DO NOT take for acute symptoms

Dosing/Medication forms DPIs-Deliver a specific amount of dry micronized powder with each inhaled breath-Don’t require as much coordination as MDIs-No propellantsless environmental concerns-Deliver about 20% of the drug directly to the lungs

MOA combines long acting beta 2 agonist w/ corticosteroid Background info:

Contraindications -NOT for acute asthma symptoms

Drug interactions


Adverse effects


Nursing interventions Patient Teaching-Rinse mouth after use-Take everyday

Xanthines—For Asthma and COPDMedications Prototypes:

Theophylline Non-Prototypes:

Indications -Maintenance therapy in asthma-Great for nocturnal asthma- serious asthma exacerbations or status asthmaticus

aminophylline (prodrug converted to theophylline)-COPD

Given in dr office for long term bronchodilation after moderate symptoms

Dosing/Medication forms -Oral (Theodur) for maintenance therapy-IV for serious asthma exacerbations or status asthmaticus-Sustained release or non-sustained release-Half-life dependent on form-metabolized by the liver-Narrow therapeutic index-Therapeutic level 5-15 mcg/ml

MOA -Blocks adenosine receptors-increase cAMPblocking bronchial smooth muscle contstriction-metabolized to caffeine

Background info:

Contraindications

Drug interactions -Smoking increases theophylline clearance CYP450 inducertheophylline metabolism is increaseddecreased therapeutic level of the drug Increase the dose if a patient smokes to maintain the drug levels in the therapeutic range

-caffeine—CYP450 inhibitor increases theophylline’s effect increase level of drug and contribute to toxicity


Adverse effects

Toxicity Toxicity:>20 mcg/ml-N/V/D-Restlessness-agitation-Insomnia-Tremor

Serious Toxicity:>30 mcg/ml-EKG changes-seizures-Hypotension and angina



Anticholinergics for COPD

Medications Prototypes:Ipratropium Bromide (Atrovent)

Non-Prototypes:Spiriva HandiHaler (inhalation dry powder)-Inhibits Ach-mediated bronchoconstriction + decreases mucus production-Used for treatment of COPD (not acute attacks)-better for small airway disease

Indications -Prevent bronchoconstriction-May be combined with SABA (Combivent)

Combivent (MDI w/ albuterol + Atrovent) COPD Combination drug w/ albuterol

-NOT used for acute asthma/COPD exacerbationsDosing/Medication forms Atrovent alone:

-Can be given for prevention using anticholinergicCombivent (Albuterol + Atrovent)-acute exacerbation

MOA Slow and prolonged action Background info:

Contraindications

Drug interactions


Adverse effects -oral dryness-cough-heart palpitations (sensations of chest fluttering and racing heart rate)



Drugs for Anemia

Erythropoiesis-Stimulating AgentsMedications Prototypes:

Epoetin alpha (Procrit)Non-Prototypes:Darbepoetin (Aranesp)

Longer acting form Given to patients on dialysis SQ or IV injection

Indications -Anemia associated w/: end stage renal disease chemo-therapy induced anemia zidovudine therapy for AIDS

Dosing/Medication formsMOA Biosynthetic forms of the natural hormone erythropoietin Background info:

Erythropoietin:-Produced by the kidney and stimulates RBC production in the bone marrow

Common causes of RBC cytoplasmic maturation defects Low iron ingestion Low iron absorption Low iron transport from body storage sites Genetic disorders (ex: thalassemia genotype)

Iron = essential mineral in the body that carries oxygen in hemoglobin and myoglobin Stored in the liver, spleen, and bone marrow Iron deficiency results in microcytic anemia

Contraindications -Uncontrolled HTN Ex: if patient comes in with BP 150/90 and hasn’t taken their BP medicationsend them home, tell them to take their meds, and come back tomorrow

-Hemoglobin levels > 10 g/dL (cancer patients)—don’t give

o Can only be used for cancer patients for whom cure is not the goal >11g/dL for (renal patients)—Don’t give

-Risk of thrombosis-Drug allergy

Drug interactions


Adverse effects -Fever-Headache-Pruritus-rash-nausea-vomiting-arthralgia-injection site reactions

Toxicity -Hypertension-Thromboembolic events (MI/Stroke)


Nursing interventions -Most patients receiving epoetin alfa (Procrit) need to also receive an oral or IV iron preparation-Procrit is ineffective w/out adequate amounts of iron and proper bone marrow functions

Check bone marrow function Check iron stores

Patient Teaching

Oral Iron Preparations

Medications Prototypes:Ferrous Sulfate (FeSO4)

Non-Prototypes:-Ferrous Fumarate (Femiron)-Ferrous gluconate

Indications -prevention and treatment of iron-deficiency syndromes-Alleviates the symptoms of iron-deficiency anemia but the underlying causes need to be corrected

Dosing/Medication forms -given as single drug or part of a multi-vitamin preparation containing iron-Iron in prenatal vitamins prevents iron deficiency in the mother because the baby will take what it needs from her

MOA Background info:Common causes of RBC cytoplasmic maturation defects

Low iron ingestion Low iron absorption Low iron transport from body

storage sites

Genetic disorders (ex: thalassemia genotype)

Iron = essential mineral in the body that carries oxygen in hemoglobin and myoglobin

Stored in the liver, spleen, and bone marrow

Iron deficiency results in microcytic anemiaContraindications -Ulcerative colitis

-PUD-Other GI disorders-KEEP AWAY FROM CHILDRENtoxicity

Most common cause of pediatric poisoning deathsDrug interactions Foods that enhance iron absorption:

-orange juice-veal-Fish-Ascorbic Acid (vitamin C)

Foods that impair iron absorption:-Eggs-Corn-Beans-Cereal products containing phytates**Eggs and beans are common dietary sources of iron

Therapeutic outcomes -Improved nutritional status-Increased weight, activity tolerance, well being-Absence of fatigue

Adverse effects -Nausea-Vomiting-Diarrhea-Constipation

-Stomach cramps/pain-Black/tarry stools-may stain teeth (liquid forms)

Toxicity -Coma-Shock-Seizures

Treatment during Toxicity-Symptomatic and supportive measures

Suction and maintenance of the airway

Correction of acidosis Control shock/dehydration w/ IV

fluids, blood, oxygen, and/or vasopressors

Severe symptoms:-Chelation therapy w/ Deferoxamine

Used for iron overlaod—2g IV x1 for 1 unit PRBCs

-Deferasirox (Exjade) Oral mixed with apple juice

Taken daily for patients w/ iron overload from frequent transufsions

Nursing interventions -Assess patient history and medication history including drug allergies-Assess for potential contraindications-Assess baseline lab values

Hemoglobin Hematocrit Iron studies

-Obtain nutritional assessment-Patients should remain upright for 15-30 mins after dose to avoid esophageal corrosion

-Encourage patients to eat foods high in iron and folic acid-Take liquid preparations with a straw—can stain teeth-Do not administer w/ any other products-Do not shake the vial-monitor blood pressure-give B12 supplements as prescribed-give with plenty of fluids but not with antacids or milk-Food may prevent absorption—but due to side effects, prescribers may tell patients to give with food and take more frequently

Patient Teaching

Parenteral Iron PreparationsMedications Prototypes: Non-Prototypes:

-Iron Dextran (INFeD)-Iron Sucrose (Venofer)—preferred by doctors

Ferric gluconate (Ferrlecit, Nulecit)

Indications -when patients can’t take iron PO-when patients can’t absorb iron in the GI tract-rapid replenishment of depleted iron stores from acute or chronic blood loss

Dosing/Medication formsMOA Background info:

Common causes of RBC cytoplasmic maturation defects Low iron ingestion Low iron absorption Low iron transport from body storage sites Genetic disorders (ex: thalassemia genotype)

Iron = essential mineral in the body that carries oxygen in hemoglobin and myoglobin Stored in the liver, spleen, and bone marrow

Iron deficiency results in microcytic anemiaContraindications All anemias other than iron deficiency anemiasDrug interactions Foods that enhance iron absorption:

-orange juice-veal-Fish-Ascorbic Acid (vitamin C)

Foods that impair iron absorption:-Eggs-Corn-Beans-Cereal products containing phytates

**Eggs and beans are common dietary sources of ironTherapeutic outcomes -Improved nutritional status

-Increased weight, activity tolerance, well being-Absence of fatigue

Adverse effects Iron Dextran-may cause anaphylactic reactions

Major orthostatic hypotension Fatal anaphylaxis

Iron Sucrose:-much lower risk of anaphylaxis-most common adverse effect = hypotension

Related to infusion rate Most likely in low weight, older adults

Toxicity -Coma-Shock-Seizures

Treatment during Toxicity-Symptomatic and supportive measures

Suction and maintenance of the airway

Correction of acidosis Control shock/dehydration w/ IV

fluids, blood, oxygen, and/or vasopressors

Severe symptoms:-Chelation therapy w/ Deferoxamine

Used for iron overlaod—2g IV x1 for 1 unit PRBCs

-Deferasirox (Exjade) Oral mixed with apple juice

Taken daily for patients w/ iron overload from frequent transufsions

Nursing interventions Iron Dextran-Test dose of 25 mg iron dextran administered before injection of the full dose

To prevent anaphylactic reaction Remaining dose given w/in 1 hour

-IV doses: Give carefully according to manufacturer’s instructions-Have resuscitative equipment available in case of anaphylaxis-Must flush IV line w/ 10 mL of normal saline

Iron sucrose:-No need for test dose-large doses infused over 2.5-3.5 hours

Iron preparations in general:-Assess patient history and medication history including drug allergies-Assess for potential contraindications-Assess baseline lab values

Hemoglobin Hematocrit Iron studies

-Obtain nutritional assessment-premedicate patient w/ diphenhydramine, acetaminophen, and/or IV hydrocortisone-patient should remain incumbent for 30 mins because hypotension can occur-encourage patient to move slowly/purposefully

Patient Teaching

Megaloblastic Anemia Treatments

Medications Prototypes:-Cyanocobalamin (B12)-Folic acid

Non-Prototypes:

Indications

RBC nuclear maturation defects

Cyanocobalamin (B12)Pernicious anemia (B12 deficiency)-Inability to absorb B12 in the terminal illium

Alcoholics Aging Bariatric surgery Drug induced--Metformin

Folic acid-Folic acid Anemia caused by malabsorption:

Alcoholics Drug induced—Dilantin Drug induced—Methotrexate (used in RA and some cancer therapies)

-During pregnancy to prevent neural tube defects Should start 1 month before pregnancy and continue throughout pregnancy

-Do NOT use until actual cause of anemia is determined

Dosing/Medication forms Cyanocobalamin (B12)-Administered orally or intranasally-administered by deep intramuscular injection

Folic acid-water soluble, B-complex vitamin—essential for erythropoiesis-Can be given IV and added to total parenteral nutrition solutions


Contraindications -Check whether anemia is due to folic acid deficiency or vitamin b12 deficiency Treating a folic acid deficiency before eval of B12 levels will mask the B12 deficiency Untreated pernicious anemia leads to neurologic damage

Drug interactions

Therapeutic outcomes -Improved nutritional status-Increased weight, activity tolerance, well being-Absence of fatigue

Adverse effects


Nursing interventions -Determine cause of anemia before administering folic acid-administer oral folic acid w/ food-Monitor for therapeutic responses-Monitor for adverse effects

Patient Teaching

ABX/ Anti-Virals/ Anti-fungals

PenicillinMedications Prototypes:

-Penicillin G repository forms IM—Benzathine and Procaine Thick paste—Bicillin or Wicillin

o Slow release

Non-Prototypes:Penicillin-beta lactamase inhibitor combination drugs:-Widely used in the hospital and outpatient settings

Amoxicillin + clavulanic acid = Augmentin-For serious in-hospital infections like pseudomonas (bad gram negative bug); given IV for serious infections

Ampicillin + sulbactam = Unasyn Ticarcillin + Calculanic acid = Timentin Piperacillin + tazobactam = Zosyn

*Used for gram negative and resistant infections**Be aware of these trade names…a lot of people don’t know they’re penicillins***Carbenicillin, pipericillin, ticarcillin—high amounts of sodium in these drugs

Watch for increased fluid volume Can worsen CHF

Indications -MOST Gram positive bacteria Ex: Streptococcus

-SOME gram negative bacteria N. gonorrhea N. meningitidis

-Spirochetes Treponema pallidum (Syphilis)

Dosing/Medication forms -Usually Given IV or IM-Repository PCN

Given IM in smallsmall amounts of PCN are released over a period of weeks Used for Syphilis and Gonorrhea

Penicillin G Only 30% absorbed when given PO—not usually recommended PO because very acid

labile IM—Benzathine and Procaine Thick paste—Nicillin and Wycillin

o Thick paste for slow release IV—Penicillin G potassium salt parenteral

Given aqueous IV only

Penicillin V Oral—Pen-Vee K More absorbed then G but less potent

Used a lot for strep throat

MOA Beta-Lactam abx Background info:

Contraindications -Penicillin allergy People allergic to PCNs are 4-6X more likely to be allergic to other beta-lactam abx

-Patients on cephalosporins Cross reactivity btwn PCNs and cephalosporins is between 1%-4%

Drug interactions LOTS OF DRUG INTERACTIONS-NSAIDs—compete for protein binding-Oral Contraceptives—PCN may decrease efficacy of BCPs-Warfarin—reduced vitamin K produced in gutPT/INR goes Up-Pen VK contains potassium

may increase hyperkalemia associated w/ supplements, ACE inhibitors, ARBS, or potassium sparing diuretics

Therapeutic outcomes -Decrease in specific S&S of infection are noted

**Subtherapeutic response: When S&S of infection do NOT improve

Fever down WBC down

o Neutrophils decreaseo Monocytes and basophils go up

Redness + inflammation down Drainage down Pain down

Adverse effects -Allergic reactions .7%-4% of all cases Urticaria Pruritus Angioedema Anaphylaxis

-N/V/D Most common with all abx


Nursing interventions -When first ordered by provider: Check serum creatinine Check Baseline WBC Check Baseline neutrophil count Assess for allergies Obtain cultures Hold patient for 30 min if they’re outpatient

o After IM injection to monitor for reaction Advise patient to take oral doses with water NOT juice

-Assess for allergies Some patients may have been told in the past that they are allergic to penicillins

when infact they may have just had an adverse reaction-Medication reconciliation—LOTS OF DRUG INTERACTIONS

Patient Teaching-All oral abx are absorbed better if taken w/ at least 6-8 oz of water

CephalosporinsBROAD SPECTRUM ABXMost commonly used abx in the hospital setting

Medications Prototypes:1st generation:

Cephalexin PO (Keflex) Cefazolin IM/IV (Anacef)

3rd generation: Ceftriaxone (Rocephin) Ceftazadime (Fortaz)

Non-Prototypes:-2nd gen

No CSF Less gram + more Gram – Ceclor (Cefaclor) Cefoxitin (Mefoxin IM/IV)

-4th gen Excellent CSF Excellent gram – coverage Maxipime (Cefepime)

-5th gen Cefaroline (Teflaro) ONLY CEPHALOSPORIN TO TREAT

MRSA

Indications -Gram positive and gram negative infections Pneumonia Otitis media Meningitis Wounds Staphylococcus aureus but NOT MRSA

-Most used abx in the hospital setting

1ST Generation— Cephalexin (Keflex) PO Ancef IV treatment Treat gram + Skin and soft tissue infections—kill strep and staph Active against staph except MRSA No anaerobic coverage Poor gram – coverage Used for surgical prophylaxis + susceptible staph

infections Do NOT penetrate CSF

NOT resistant to Beta-lactamase

3rd Generation— Ceftriaxone (Rocephin) Much reduced gram + activity Gram –

o Salmonellao Enterobactero N. gonorrheao H. influenzao Anaerobes

Enters CSF—especially Rocephin Most are resistant to Beta-Lactamase Major uses: Klebsiella, surgical prophylaxis, gram –

meningitisCeftriaxone (Rocephin) does not require dose reduction in renal dysfunction

Dosing/Medication forms Ceftriaxone (Rocephin):-IV and IM injection-Long half-life-dosed 1X a day-elimination is primarily hepatic-Easily passes meninges and diffused into CSF to treat CNS infections and STDs

MOA -Beta-lactam abx-Bactericidal action

Inhibit cell wall synthesis-Divided into groups according to their antimicrobial activity-Semisynthetic derivatives

Background info:

Contraindications -PCN allergies People allergic to PCNs are 4-6X more likely to be allergic to other beta-lactam abx 10% chance of severe reaction if severely allergic to PCN

Drug interactions


Subtherapeutic response: When S&S of infection do NOT improve

-Decrease in specific S&S of infection are noted Fever down WBC down

o Neutrophils decreaseo Monocytes and basophils go up

Redness + inflammation down Drainage down Pain down

Adverse effects -Fewer allergic reactions than PCN

-GI upset-Super infections

AAPC? AAD? And Candida (yeast) infections-Nephrotoxicity-Thrombophlebitis

Given by slow IV piggy backDilute drug (50-100 mL IV solution)


Nursing interventions -When first ordered: Assess for allergies

o The extent of PCN allergies is important Check creatinine clearance Check baseline WBC count Check baseline neutrophil count

-During therapy Ongoing renal status assessments

o Creatinine levels Monitor IV site closely if given via IV

-Remember Rocephin does not have to be dose-reduced in renal insufficiency-Give oral forms w/ food

-Each class of abx has a specific adverse effects and drug interactions that must be carefully assessed and monitored-the most common adverse effects of abx are N/V/D-All oral abx are absorbed better if taken w/ at least 6-8 oz of water

Patient Teaching

SulfonamidesMedications Prototypes:

-Sulfamethoxazole/trimethoprim (Bactrim)-Septra

Non-Prototypes:Silvadene-topical formulation-Thick white cream-applied to burned skin for prevention/treatment of infection

Indications -Effective against both gram + and gram – bacteria-Skin infections

Ex: Staph-UTIs

E. coli-URTI—many different organisms-prophylaxis

Pneumocystis Jirovecii pneumonia (PJP) Occurs in patients with AIDS


MOA Bacteriostatic—prevent folic acid synthesisinterfere with growth and replication**Trimethoprim is the minor drug in Bactrim; Both parts of the drug inhibit different steps of folic acid synthesis

Penetrates tissues well Breast milk, bile, prostatic fluid, vaginal fluids Highly protein bound

High potential for drug interactions

Background info:

Contraindications -Infants less than 2 months old Sulfa is highly protein boundit can displace bilirubin from albuminthe bilirubin is free to circulate and enters the braincauses condition called kernicteruscan result in

permanent brain damage

Drug interactions Other highly protein bound drugs-aspirin-loop diuretics-warfarin-sulfonylureas for diabetes


Adverse effects -mild/moderate skin reactions in the sun-Anemia-Toxic epidermal Necorlysis or SJS

Toxicity -Steven’s Johnson syndrome—if allergic Treatment during ToxicityPatients go to burn unit

Nursing interventions -Monitor patients closely if on other highly protein bound drugs listed below-Assess for allergy to sulfonamides-assess the skin-make sure patients take in at least 2000 mL of fluid per day

Prevents crystaluria Monitor intake and output

-monitor RBCs because of risk of anemia

Patient Teaching-protect against sunlight-immediately report blisters/sores in the mouth or around the eyes-make sure patients take in at least 2000 mL of fluid per day

Unless contraindicated because of pre-existing condition like HF

MacrolidesMedications Prototypes:

Clarithromycin (Biaxin)Azithromycin (Zithromax)—

Z pack, or Tri-Pak PO or IV

Non-Prototypes:Erythromycin-Older macrolide-Assess for GI affects-Can be hepatotoxic-Potent CYP 450 inhibitor—increases levels of

Theophylline Carbamazepine warfarin

Fidaxomicin (Dificid)-newest macrolide-used for C. diff unresponsive to PO or IV vancomycin

Indications Clarithromycin (Biaxin)-Bronchitis-Pneumonia

Azithromycin (Zithromax)-Atypical pneumonia-Legionaire’s-Chlamydia-prevention of AIDs related pneumonias

Mycobacterium avium complex Pneumocystis carinii pneumonia (PCP)

-Useful in patients w/ beta-lactam abx allergy-Pregnancy category B

Dosing/Medication forms -ZithromaxGive on empty stomachLong action drug—dosed once daily


Contraindications -pregnancy category B

Drug interactions Biaxin-can elevate digoxin levels by 50%


Adverse effects -GI upset when given PO version


Nursing interventions -give PO doses with light snack Biaxin erythromycin

-Monitor for digoxin toxicity if administering Biaxin-Assess for GI upset-Assess for drug interactions-Explain long action of Zithromax-Monitor IV site-monitor for digoxin toxicity

if patient is on biaxin

Patient Teaching-take PO doses with light snack

TetracyclinesBROAD SPECTRUM ABX

Medications Prototypes:Doxycycline (Vibramycin)

Non-Prototypes:-Tetracycline

Not very solubleIndications -chlamydial infections

-other STIs-Helicobacter pylori (GI infection causing ulcers)-Acne (low doses)-Skin infections-Anthrax


MOA -Bacteriostatic—Inhibits protein synthesis-Doxycycline is more lipid soluble than tetracycline

Background info:

Contraindications -pregnant women May retard fetal skeletal development

-lactating women

Drug interactions


Adverse effects - Super infections Diarrhea Candida (throat, vagina, bowl)

-Irreversible stain teeth in children ages (4 months – 8 years) This is when kids are getting new teeth/losing teeth

-photosensitivity


Nursing interventions -Do not give with the below because they reduce the oral absorption of the tetracycline (bind to trivalent and divalent metallic ions and form insoluble complexes)

Milk Antacids Iron salts (iron, calcium, magnesium)

-give with 6-8 oz of fluid (preferably water)

Patient Teaching-do not take if pregnant or breastfeeding-avoid sunlight and tanning beds-take with 6-8 oz of fluid (preferably water)-DO NOT TAKE WITH

Milk Antacids Iron salts (iron, calcium, magnesium)

Resistant infections

MRSA (Methicillin Resistant Staph. Aureus) Daptomycin (Cubicin)Linezolid (Zyvox)Cefaroline (Teflaro)—MRSA only

VRE (Vancomycin Resistant Enterococcus) Daptomycin (Cubicin)Linezolid (Zyvox)

ESBL CRE (Extended Spectrum Beta-Lactamase Carbapenem Resistant Enterobactracea) Coly-MycinTuburculosis (MDR—multi drug resistant)C. diff Fidaxomicin (Dificid—5th generation macrolide)

AminoglycosidesNARRO SPECTRUM ABX

Medications Prototypes:Gentamycin (Garamycin)

Non-Prototypes:

Indications IV Forms-Gram negative (mostly) and some gram positive bacteria-Serious life threatening infections-Sepsis

Can be used alone or with other abx—synergistic effects for certain gram + bacteria that are resistant to other abx

Topical form-skin infections-ear infections-eye infections

Dosing/Medication forms -IV and topical forms ONLY—poor oral absorption-Narrow therapeutic index

Margin of safe blood levels is small-Long half life-excreted renally

MOA -Bactericidal Inhibit protein synthesis

o Bacteria Make abnormal proteins which affect the cell wall

Background info:

ContraindicationsDrug interactions -Synergistic reactions w/

PCN and Cephalosporin-Ototoxic drugs

Loop diuretics Vancomycin

-Nephrotoxic drugs PCN Cephalosporin Vancomycin

Therapeutic outcomesAdverse effects Block ACH in skeletal muscle

Potential for paralysis of diaphragm because of ACH block-super infections-fever-rash

Toxicity -Inner ear (ototoxicity)—can be cochlear (auditory—due to damage of outer hair cells in the inner ear) and vestibular—MAY BE IRREVERSIBLE

Tinnitus Hearing loss—deafness or high

frequency hearing loss Headache Dizziness Vertigo ataxia

-Renal tubes (nephrotoxicity)--REVERSIBLE related to the rapid uptake of the

drug by proximal tubular cellsproximal tubular cells ar then killed

-Respiratory depression (neurotoxicity) Headache Weakness Paralysis

Paralysis/weakness—due to blocking of ACH. Especially after anesthesia or paralysis on a ventilator


Nursing interventions -Monitor renal function Peak drug levels—measure adequacy of dose Trough drug levels—measure if drug levels are elevatedtoxicity

o Patient is not clearing the drugo Ask Dr. about reducing the dose or changing drugs

-assess hearing + vestibular function Do this on admission so you can tell if changes happen after the medication Older adults may already have hearing loss/gait changes—we need a baseline If patient is too ill, ask the family

-monitor closely after anesthesia-How to mix and administer

Do not mix in syringe w/ other drugs Do not mix in same line with PCNs

Patient Teaching

Fluoroquinolones “Quinolones”

Medications Prototypes:Ciproflaxacin (Cipro)

Non-Prototypes:-Levoflaxacin (Levaquin)-Moxifloxacin (Avelox)

Indications

**Because they are prescribed for so many things there is a potential for overuse

-Gram negative organisms Pseudomonas

-Some gram positive organisms-Respiratory infections-Bone and Joint infections-GI infections-Skin infections-STDs-Anthrax

Dosing/Medication forms -IV form-PO form

Excellent oral absorption Same blood level as if given IV

MOA -Bactericidal-Alter DNA of bacteria causing death-Do NOT affect human DNA

Background info:

Contraindications -People who already have tendon issues-Kids/teens < 18

Drug interactions -CYP450 inhibitors (Look up…is cipro a cyp 450 inhibitor or does it interact badly w. them?)-Antacids

Reduce absorption of floruquinalones


Adverse effects -CNS Headache Dizziness Fatigue Depression Restlessness Insomnia

-GI N/V/D Constipation Thrush Increased liver function studies Others

-Cardiac Prolonged QT interval

-Integumentary Rash Pruritus Urticarial Flushing Photosensitivity

-Others Fever Chills Blurred vision Tinnitus

-BLACK BOX WARNING: increased risk of tendonitis and tendon rupture


Nursing interventions -Make sure this type of abx is necessary before prescribing Long list of side effects Potential for overuse

BLACK BOX WARNING—check for tendon issues

Patient Teaching

Miscellaneous abxMedications Prototypes: Non-Prototypes:

Metronidazole (Flagyl) -Clindamycin Good for anaerobic organisms Bone, GU, intra-abdominal infections Adverse effects: AA pseudomembranous colitis Neuromuscular blocking effects

Nitrofuranatoin (Macrodantin)Indications

Dosing/Medication forms -Protozoal infections Trichomonas

o If a patient has this, their partner needs to be treated as well Ameobiasis Giardiasis

-Anaerobic infections C. Diff—has been used in the past but is NOT FDA approved for this Gardnerella Bacteroides Heliocobacter Other GI infections Intraabdominal infections


Contraindications

Drug interactions -Alcohol


Adverse effects

Toxicity -Do NOT drink alcohol w/ this medication for 48 hours afterward Patients will have a disulfram (Antabuse)-like reaction



Glycopeptide abx (term not used by teacher—just for own knowledge)NARROW SPECTRUM ABX

Medications Prototypes:Vancomycin

Non-Prototypes:

Indications -Staph + strep-Gram POSITIVE bacteria ONLY-MRSA infections + other gram positive infections-Penicillin allergic patients for streptococcal endocarditis-Antibiotic Associated Colitis (AACP) caused by C. Diff

ONLY reason to give PO because the abx need to come in contact with the bacteria Given IV if the patient is NPO

Dosing/Medication forms -Given IV unless for c.diff

MOA -Bactericidal-Interferes w/ cell wall synthesis

Background info:

Contraindications

Drug interactions -Additive w/ other ototoxic + nephrotoxic drugsTherapeutic outcomes

Adverse effects -“Red man” syndrome—of head, face, neck, and upper trunk area When given IV, it must be given over 60-90 minutes Hypotension due to vasodilation from histamine release Flushing Itching THIS IS NOT AN ALLERGIC REACTION—Because nurse gave too fast

-VREToxicity -Nephrotoxicity

-OtotoxiciyTreatment during Toxicity

Nursing interventions -Must be given on a need basis because of VRE potential Need positive MRSA culture report

- Nephrotoxicy:-monitor drug levels peak and trough after 3rd and 4th dose

the pharmacist will usually take over the monitoring after this trough levels are repeated ever 3-5 days

-Monitor creatinine levels before starting the treatment + every 3-5 days afterwards-Ensure adequate hydration—as long as it’s not contraindicated

-Monitor patients who: are receiving higher than normal doses for better penetration to the site of inctions

o Ex: meningitis Altered volumes of distribution

o Burn patientso Trauma patients

Patients whose treatment is failing Rapidly changing renal function who are NOT receiving peritoneal or hemodialysis Normal renal function requiring long-term therapy

o 4-6 weekS-Antihistamines may be ordered in the event of “red mans” syndrome-Monitor IV site carefully (central line)

Patient Teaching

Anti-tubercular medicationsMedications Prototypes:

4 drug regimen to overcome resistence Isoniazin (INH) Pyrazinamide (PZA) Rifampin Ethambutol

Non-Prototypes:

Indications


MOA Background info:-Tuberculosis is caused by bacterial species called mycobacterium -Most commonly affects the lungs-Frequently drug resistant

Contraindications

Drug interactions


Adverse effects -Pyridoxine—Vitamin B6 deficiency-Liver toxicity



Antiviral DrugsMedications Prototypes:

Acyclovir (Zovirax)Non-Prototypes:-Valcyclovir (Valtrex)

PO only Prodrug that is converted to

acyclovir in the liver-Famcyclovir (Famvir)

PO only Herpes simplex 1 Herpes simplex 2 Herpes zoster (shingles)

Other Anti-virals not part of acyclovir family:-Prep (Truvada)

HIV prevention-Gancyclovir (Cytovene)

Cytomegalovirus (CMV)-Ribavirin (Virazole)

Respiratory Syncytial Virus (RSV)

Indications -Herpes infections Herpes 2: needs to be treated w/ an outbreak and suppressed between outbreaks

-Herpes zoster Patients can also get vaccinated—usually patients > 65 at risk

-IV form of acyclovir Type A & B influenza Oseltamivir (Tamiflu)

Dosing/Medication forms -PO-IV-Topical-Doses and frequency of administration vary w/ type of herpes infection being treated


Contraindications -Severe drug allergy-Major renal or hepatic dysfunction-chronic alcohol use-optic neuritis

Drug interactions


Adverse effects



AntifungalsMedications Prototypes:

-Nystatin (Mycostatin)-Amphotericin B- Oral difulcan (Fluconazole)

Non-Prototypes:-Caspofungin (Aspergillus)

IV form Severe invasive diseases

Indications -Oral candida (Candidia albicans—thrush) Nystatin (Mycostatin) Swish and swallow or swish and spit Can be given in lozenges—Mycelex troches

-Vaginal infections Vaginal inserts Mycostatin cream Mycelex troches Oral difulcan (Fluconazole)—150 mg x 1 dose

-Amphotericin B Drug of choice for severe systemic fungal infections

Dosing/Medication forms -Topical-IV-PO

MOA Background info:Fungal infections caused by:-Yeasts-Molds-An infection caused by a fungus called mycosis-may be mild—annoying

Ex: athletes foot Oral candidiasis Vaginal infections may occur as superinfections after abx therapy or in

immunocompromised patients-Can be systemic—life threateningOften in the case of immunocompromised patients

Contraindications

Drug interactions


Adverse effects -Amphotericin B—if administered too fast Fever Chills Nausea hypokalemia


Nursing interventions Amphotericin B-premedicate with Tylenol to reduce fever and chills-premedicate with antiemetic to prevent nausea-monitor potassium levels

Patient Teaching

Antacids/ Acid Reducing

Medications

AntacidsMedications Prototypes:

-TUMS—calcium carbonate-Amphogel—Aluminum hydroxide-Mylanta—Magnesium hydroxide

Non-Prototypes:

Indications

Dosing/Medication forms -Liquid and tablet form

MOA -Neutralize acid that is already present in the stomach-Work in minutes-DO NOT prevent formation of acid

Background info:

Contraindications -Severe renal failure—poor clearance-Electrolyte imbalance-GI obstruction-Known drug allergy

Drug interactions


Adverse effects -Calcium containing—TUMS Rebound hyperacidity Kidney stones Systemic alkalosis Hypercalcemia

o Normal calcium levels = 8-10.4o Remember patients with bone cancer

may develop hypercalcemia because their body’s are not able to absorb the calcium in their bones

o S&S: headache, constipation, anorexia, nausea

-Aluminum containing—Amphogel Constipation

-Magnesium containing—Mylanta Diarrhea



Histamine 2 (H2) blockers (antagonists)Medications Prototypes:

Famotidine (Pepcid)Ranitidine (Zantac)Cimetidine (Tagamet)

Non-Prototypes:

Indications -Reduce acid-adjunct w/ H1 blockers for allergy treatment-safe when used short term


MOA -Block acid production by inhibiting the enzyme cAMP cAMP provides the intracellular energy to drive the proton pump of the parietal cells

Background info:

Contraindications

Drug interactions -Cimetidine is a STRONG cyp450 inhibitor Zantac and Pepcid are weaker cyp450 inhibitors (Pepcid is the weakest of the 3)


Adverse effects -CV—hypertension + dysrhythmias especially when given rapid IV

-CNS—headache-Pulmonary—pneumonia

remember acids in stomach help digest food AND kill bacteria. There’s more chance bacteria can get aspirated into the lungs if H2 receptors are blocked -Endocrine—Gynecomastia (men) + galactorrhea (women)

Cimetidine binds to androgen receptors causing androgen blockadegynecomastia + impotence Cimetidine is an antagonist for dihydrotestosterone which leads to exaggerated estrogen effectwomen may get galactorrhea and men may get gynecomastia

-GI—Nausea, Diarrhea, abdominal cramps-Hematologic—neutropenia, thrombocytopenia (rare)

Thrombocytopenia w. Tagamet and Zantac—less so with Pepcid-Skin—rash, urticarial, sweating, flushing-GU/Renal—Impotence, increased BUN/creatinine



PPIs (Proton Pump Inhibitors)Medications Prototypes:

Prilosec OTCNon-Prototypes:

Indications -short term acid relief Will heal a duodenal ulcer in 4 weeks Will heal a gastric ulcer in 8 weeks May take several days for PPI to ease ulcer pain

-GERD Reflux of the stomach acid up in the esophagus Occurs w/ relaxation of the lower esophageal sphincter

Dosing/Medication forms Examples of drug coctails for GERD, Ulcers, Etc.Example 1 GERD:

1. Sucralfate (Carafate)a. Not a PPI or H2 blockerb. Forms a gel over the ulcer bedc. Not absorbed systemicallyd. Protects the ulcer while it’shealing—like a BANDAID

2. PPI—PrilosecExample 2 GASTRIC ULCER:

3. Clarithromycin (Biaxin)—antiobiotica. Kill bacteria

4. Omeprazole (Prilosec)—PPIa. Prevent acid secretion

5. Bismuth subsalicylate (PeptoBismol)a. Prevents bacterium from adhering to the GI mucosa and speeds its exit from the body

6. Amoxicillin (antibiotic)a. Kill bacteria

Example 3 Patient with cancer spread to the bones and hypercalcemia1. Nutritional changes2. H2 blocker or PPI

Example 4 flatulance1. Simethicone (Gas EX)

b. Alters the elasticity of the mucus-coated gas bubbles which cause them to break into smaller ones

MOA -Block the H+ and K+ ATPase pump in the parietal cell Prevent acid formation

-More powerful than H2 blockers-works in about 1 hour and blocks 50-100% of acid production by 24 hours

Inhibition lasts 72 hours due to prolonged binding at the H+ and K+ ATPase enzymeAfter discontinuance—acid secretion returns gradually over 3-5 days

Background info:

Contraindications

Drug interactions


Adverse effects



Anti-Diarrheal/ Anti-Constipation

Medications

AdsorbentsAnti-Diarrheal Medications

Medications Prototypes:Aluminum hydroxide (Ampogel)Bismuth subsalicylate (PeptoBismol)Cholystyramine (Questran)

Non-Prototypes:-New drug for IBS-D = eluxodoline (Viberzi)

Indications -diarrhea Goal of Diarrhea treatment: Treat the underlying cause

o Acute diarrhea Sudden onset in a previously healthy person Lasts from 3 days—2 weeks Self-limiting Responds to treatment Resolves w/o sequelae Caused by: bacteria, viruses, drugs/medicine, nutritional factors,

protozoao Chronic diarrhea

Lasts for more than 3-4 weeks Associated w/ recurring passage of diarrheal stools +/- fever Loss of appetite Nausea/vomiting Weight loss Chronic weakness Caused by: tumors, diabetes mellitus, addison’s disease,

hyperthyroidism, irritable bowel syndrome, AIDS Stop the stool frequency Alleviate the abdominal cramps Replenish fluids and electrolytes

Prevent weight loss and nutritional deficits from malabsorptionDosing/Medication forms Examples of drug cocktails for patients with diarrhea

Example 1—46 year old mom w/ stressful lifestyle diagnosed w/ IBS (no intermittent constipation)1. Lifestyle + dietary modifications

a. Diet journal to see what is the cause: is she drinking a lot of wine at night to deal with stress?b. Is she on medication like metformin that can cause diarrheac. Is she on an anti-depressant like Prozac that can cause gas + diarrhea?

2. Anti-diarrheal medicationsa. Immodium OTCb. If immodium doesn’t workDr will prescribe lomotil

3. Bulk forming agentsa. May be advised to take an adsorbant like cholystyramine (questran)

i. Start w/ ¼ package and work your way upNew drug for IBS-D = eluxodoline (Viberzi)

MOA -coat the walls of the GI tractBind to the causative bacteria/toxinthen eliminated through the stool- Cholystyramine (Questran)

In small amounts: soak up excess fluids and bulk up the stools

Background info:

Contraindications Children (babies and toddlers) Medication may not be necessary or safe Pedialyte and/or clear liquids Avoid sugary juices + milk products BRATY diet—Bananas, Rice, Applesauce, Toast, yogurt

Drug interactions


Adverse effects -Aluminum hydroxide (Ampogel) Can lead to constipationsometimes used for patients who have diarrhea


Nursing interventions Oral rehydration protocol (Ex: IV fluid shortage due to hurricane Maria in PR)-Drink 500-1000 mL fluids in ER and continue at home-Method: take two large sips (3o mL) every 3-5 minutes (track intake on paper)-Wait 20 minutes after vvomiting before trying again-give analgesics, antipyretics, anti-emetics, and encouragement as needed-Can use the following liquids

Pedialyte: contains the correct balance of glucose and salt (oral electrolyte solution) Water dilute juice dilute sports drinks can make your own solution too (home brew)

Patient Teaching

Anti-cholinergicsAnti-Diarrheal Medications

Medications Prototypes:-Atropine-opioids-codeine-paregoric-hycosamine

Non-Prototypes:Lomotil

Combination of opioid (diphenoxylate) + atropine (schedule V)Immodium OTC

Structural analogue to opioid meperidine (Demerol) Suppresses bowel motility Poorly absorbed and does NOT cross the VVV Heroin addicts take up to 32 if they can’t get their heroin fixconcrete in bowels

Paragoric Camphorated tincture of opion

Contains morphine .4mg/mlIndications -diarrhea

Dosing/Medication forms Examples for drug coctails for diarrheaExample 1 infectious diarrhea from drinking water in a stream

1. Stool studiesa. Check for ova and parasites and other markers to guide appropriate

treatment2. Oral hydration

a. Clear fluids containing electrolytes like pedialyteb. Gatorade has too much sugarc. If limited because you’re in a different countrydrink tea made with

boiled water or bottled soda3. Abx: Ciprofloxacin (Cipro) or Metronidazole (Flagyl)

a. Sometimes doctors may pre-prescribe abx like Cipro if they know a patient is going out of the country

4. No drugs to slow peristalsis for 24 hoursthen take immodium

Example 2—55 year old man complaining of 4-5 watery stools a day. Receiving chemo therapy drug for colon cancer known to cause diarrhea

1. .25 mg of Atropine IVImmodium—up to 8 a day

2. If immodium alone doesn’t slow it downalternate immodium w/ lomotil (prescription)

3. Narcotic (opioid) pain medicineExample 3—46 year old mom w/ stressful lifestyle diagnosed w/ IBS (no intermittent constipation)

1. Lifestyle + dietary modificationsa. Diet journal to see what is the cause: is she drinking a lot of wine at night

to deal with stress?b. Is she on medication like metformin that can cause diarrheac. Is she on an anti-depressant like Prozac that can cause gas + diarrhea?

2. Anti-diarrheal medicationsa. Immodium OTCb. If immodium doesn’t workDr will prescribe lomotil

3. Bulk forming agentsa. May be advised to take an adsorbant like cholystyramine (questran)

i. Start w/ ¼ package and work your way upNew drug for IBS-D = eluxodoline (Viberzi)

MOA -slow diarrhea Background info:Contraindications Children (babies + toddlers)

Medication may not be necessary or safe Pedialyte and/or clear liquids Avoid sugary juices + milk products

BRATY diet—Bananas, Rice, Applesauce, Toast, yogurtDrug interactions


Adverse effects Oral rehydration protocol (Ex: IV fluid shortage due to hurricane Maria in PR)-Drink 500-1000 mL fluids in ER and continue at home-Method: take two large sips (3o mL) every 3-5 minutes (track intake on paper)-Wait 20 minutes after vvomiting before trying again-give analgesics, antipyretics, anti-emetics, and encouragement as needed-Can use the following liquids

Pedialyte: contains the correct balance of glucose and salt (oral electrolyte solution) Water

dilute juice dilute sports drinks can make your own solution too (home brew)

o 32 oz watero 6 teaspoons sugaro ½ teaspoon salt

-Do NOT give to babies + toddlers



Constipation medicationsMedications Prototypes:

-Bulk forming agents—Methylcellulose (Metamucil/Citucel) Pull water into the bowel and add bulk to fecal mass Preferred for prevention + treatment of chronic constipation

-Stool softeners—AKA Emolients; Ducosate (Colace) Cause more water and fat to be absorbed into the stool Given in the hospital post-op

-Stiumulatns—Bisacodyl (Dulcolax) and Herbal Senna (Sennokot) Promote peristalsis by irritiating the bowel mucosa Should not be taken long term Bisacodyl (Dulcolax)—PO or Suppository

o Works by stimulating the nerve endings in the walls of the large intestine (colon) and rectum

o Causes the muscle in the intestinal wall to contract more often + with increased force

o Increased peristalsis moves the contents of the intestine through the colon to the rectum so that the bowel can be emptied

o Occasional constipationo Be careful for overuse in the elderly

-Hyper-osmotics—Su Prep, GoLytly, Miralax, fleets enemas Used for rapid bowel cleansing for colonoscopy prep Miralax is polyethylene glycol 3350—

o draws water into the stoolo Used for occasional constipationo Can be used daily in small amounts for people on constipating drugs

-Saline cathartics and osmotics Not absorbed Pull water into the stool Cause rapid and complete bowel cleansing Used as bowel preps before colonoscopy

-Magnesium tablets + antacids containing magnesium—Milk of magnesium Loosens stools Gentle laxative frequently prescribed as need for constipation in the hospital

-Miscellaneous—lactulose (Enulose) Man made sugar Powerful laxative—for more difficult to treat constipation (fecal impaction) Also given to patients w/ liver failure to help clear the elevated ammonia levels that

cause encephalopathyIndications -Analgesics—especially opioids

Any patient on an opioid needs to be on a bowel program: fluids, fiber, stool softeners, laxatives-Poor diet—no fiber

Recommended amount: 32 g per day Adds bulk, increases feeling of fullness (good for weight loss), helps bind cholesterol in the gut, improves the number of bowel movements Have to start slow—don’t start with 32 grams a day off the batt

-physical inactivity Lack of activity decreases peristalsis This is one of the reasons we get patients out of bed after surgery to walk them Early ambulation gets the bowel moving + prevents DVTs

-Psychological Factors (anxiety, stress, hypochondria)-Diabetes, hyperthyroidism, pregnancy, hypercalcemia, hypokalemia-Neuromuscular diseasesMyasthenia gravis, multiple sclerosis, spinal cord injuries

Dosing/Medication forms Examples of Drug coctails for constipationExample 1—Man w/ severe constipation over 4 days, abdominal cramping, morphine for cancer in bones and low fluid intake

1. check calcium levelsa. risk for hypercalcemia because of bone cancerb. constipation is a sign of hypercalcemia

2. IV fluid if dehydrated3. Abdominal x-ray + listen to bowel sounds— to make sure no bowel obstruction4. Laxative like lactulose (Enulose)

a. 45 cc POb. repeat q1-2 hours until patient has BM

5. Daily miralax in addition to daily stool softeners, laxatives, and increased fluids6. Increase fluids at home7. If he gets stopped up again, he can take another dose of lectulose


Contraindications -bowel obstruction Must rule out before giving oral laxatives Give suppository if this hasn’t been ruled out yet

Drug interactionsTherapeutic outcomesAdverse effectsToxicity Treatment during ToxicityNursing interventions -Occasional constipation should first be addressed by adding more fluids and fiber to the die Patient Teaching

Anti-Nausea/ Anti-Vomiting Medications

NK1 Inhibitors (FYI)Antiemetic Medications

Medications Prototypes: Non-Prototypes:

Indications -Nausea Unpleasant feeling that often precedes vomiting Immediate (up to 24 hours): related to illness, anesthesia, drugs—especially some chemotherapy drugs Delayed (48-72 hours after treatment) Anticipatory: occurs as a result of a memory of a treatment that caused nausea. Occurs in anticipation of the next treatment

-Vomiting (Emesis) Forcible emptying of gastric contents Occasionally intestinal contents—if there’s a bowel obstruction

-Give for use around chemo

Dosing/Medication forms Can be given w/ or w/o steroids—1 hour before chemo Dexamethasone (Decadron)

o If given for chemo-induced nausea—give after (days 2,3,4) w/ Emendo Treats the delayed nausea

MOA unclear—calms all systems down Used for prevention of chemotherapy induced and post-operative nausea

MOA -Block NK1 receptors in the CTZ and gut-Most work by blocking several different receptorsblocking the stimulus that induces vomiting-relieve nausea + vomiting

Background info:Neurokinins are part of the family of tachykinins derived from supstance-P

Contraindications

Drug interactions


Adverse effects


Nursing interventions -Assessment to plan for antiemetic therapy-Assess complete nausea and vomiting history including precipitating factors

Young women Red heads History of motion sickness History of morning sickness (pregnancy)

-Assess current medications-Assess for contraindications and potential drug interactions-Many of these drugs cause severe drowsinesswarn patients about driving or performing any hazardous tasks

Patient Teaching

BenzodiazepinesAntiemetic Medications

Medications Prototypes:-Lorazepam (Ativan)

Non-Prototypes:

Indications -very useful for anticipatory nausea


MOA -Blocks impulses from the higher cerebral centers to the vomiting center In the medulla Background info:

Contraindications

Drug interactions


Adverse effects When given with rapid IV infusion:-Sedation-orthostatic hypotension





Patient Teaching-Do not take w/ alcohol—may cause severe CNS depression-change positions slowly to prevent orthostatic hypotension and dizziness

Antihistamines + AnticholinergicsMedications Prototypes:

Benadryl + ScopolamineNon-Prototypes:

Indications Histamine antagonists (antihistamines):-Motion sickness—

Dramamine + Diphenhydramine (Benadryl) and Scoalmine

Muscarinic antagonists (Anticholinergics): Pre-operatively Motion sickness Scopolamine—Transdermal patch behind ear


MOA Histamine antagonists (antihistamines) Block histamine and ACH receptors from the labyrinth

Muscarinic antagonists (Anticholinergics)

Background info:

Contraindications

Drug interactions


Adverse effects






Cannabinoids—antiemetic medicationsMedications Prototypes:

Dronabinol (Marinol) Non-Prototypes:

Indications -chemotherapy related nausea and vomiting


MOA -Inhibitory effects on reticular formation, thalamus, and cerebral cortex Background info:

Contraindications

Drug interactions


Adverse effects -alter mood and body’s perception of its surroundings **Not necesarrily ideal because of this side effect

-stimulates appetite and weight gain-may cause orthostatic hypotension






Serotonin Blockers (5HT3)Medications Prototypes:

Ondansetron (Zofran)Non-Prototypes:Palonosetron (Aloxi)—

long acting-Dolasetron (Anzemet)-Granisetron (Kytril)

Indications -Nausea/vomiting patients receiving chemo postoperative patients pregnancy

Dosing/Medication forms -Pill-Orally disintegrated tablet (ODT)

Take PRN q8 Alternate with Phenergan—especially if she needs to be alert at work

-IV

-Routine post-op N/V—Give low dose-Pre-chemo—Give High dose

Example of nausea treatment for patient getting chemo:1. Emend—NK1 inhibitor used w/ decadron

a. Take day 1 1 hour before chemob. Days 2, 3 after chemo

2. IV Zofran or Aloxi + IV Decadron + IV Benadryl a. 30 mins before chemo treatment

3. Decadrona. Treats delayed nausea that occurs after highly emetogenic chemob. Day 4

4. Zofran ODT q8 hours and alternate w/ Phenergana. Especially alternate if she needs to be alert at work or look after kids

5. Phenergan gela. Applied to the wrist q6-8 hoursb. Use when sedation is not an issue, like at nightc. Alternate w/ Zofran if you need to be alert

MOA -Block serotonin receptors in the GI tract, CTZ, and VC CTZ = Chemoreceptor trigger zone

o Area of medulla oblongata that communicates with other structures in the vomit center to induce vomiting

VC = vomit center-Do NOT make patients sleepy like Compazine and Phenergan

Background info:

Contraindications

Drug interactions


Adverse effects -headache






Antidopaminergic drugs—antiemetic medicationsMedications Prototypes:

-Prochlorperazine (Compazine)-Promethazine (Phenergan)

Non-Prototypes:-Haloperidol (Haldol)

For nausea in patients w/o Terminal illness on hospice care who can no longer take oral medications

Mixed in a capsule suppository w/ Ativan + Benadrylo Combination known as ABH

Indications

Dosing/Medication forms -PRN Gel applied q 6-8 hours prn

o Applied to inside of the wristo This is if sedation is not a problem

PO can be given alternating with Zofran—if you need to stay alerto Zofran doesn’t cause drowsiness

Example of nausea treatment for patient getting chemo:1. Emend—NK1 inhibitor used w/ decadron

a. Take day 1 1 hour before chemob. Days 2, 3 after chemo

2. IV Zofran or Aloxi + IV Decadron + IV Benadryl a. 30 mins before chemo treatment

3. Decadrona. Treats delayed nausea that occurs after highly emetogenic chemob. Day 4

4. Zofran ODT q8 hours and alternate w/ Phenergana. Especially alternate if she needs to be alert at work or look after kids

5. Phenergan gela. Applied to the wrist q6-8 hoursb. Use when sedation is not an issue, like at night

Alternate w/ Zofran if you need to be alertMOA Prochlorperazine (Compazine)

-Class of Antipsychotic medication called phenothiazines

Same class as the conventional antipsychotics--Thorazine

-blocks the dopamine receptors on the CTZ

Promethazine (Phenergan)-Derivative of of the phenothiazine class-Has 1st generation anti-histamine properties—-Blocks histamine receptors + dopamine receptors on the CTZ

Background info:

Contraindications

Drug interactions


Adverse effects






Prokinetic Drugs—Antiemetic drugsMedications Prototypes:

Metoclopramide (Reglan)Non-Prototypes:

Indications -Nausea/Vomiting Can also be used for GERD delayed gastric emptying


MOA -Block dopamine in the CTZcause CTZ to be desensitized to impulses it received from the GI tract-Stimulate peristalsis in GI tractenhances emptying of stomach

Background info:

Contraindications

Drug interactions


Adverse effects -Long term use may cause tardive dyskinesia—EPS Remember this is irreversible—have to give anticholinergics??


Nursing interventions -Assess for EPS side effects

Antemetics in general:-Assessment to plan for antiemetic therapy-Assess complete nausea and vomiting history including precipitating factors




Herbal products—antiemetics Medications Prototypes:

GingerNon-Prototypes:

Indications -Nausea/vomiting caused by Chemotherapy Morning sickness Motion sickness



Contraindications

Drug interactions -May increase absorption of oral medications-increase bleeding risk w/ anticoagulants


Adverse effects -anorexia-Nausea-vomiting-skin reactions






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