151 terms

Pharm Exam 3

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Preload
The pressure that stretches the heart to its maximal capacity at the end of diastolic period.
Affected by venous blood pressure and blood return (volume and venous tone).
Increased by fluid overload.
Decreased by hemorrhage, dehydration, standing, atrial fibrillation, tachycardia, MVS/TVS, vasodilation from drug or anaphylaxis.
Afterload
The pressure that the heart must overcome to pump the blood into the aorta.
Affected by arterial blood pressure measured by SVR or PVR.
Increased by dilated heart, HTN, AVS/AVR, pH
Decreased by hypertrophied left ventricle, MVR
HTN management
For 50+ pts, ↑SBP is better indicator of CV risk than ↑DBP.
Normal BP: SBP < 120 mmHg, DBP < 80 mmHg
Pts w/ prehypertension (120-139/80-90): lifestyle modification (LM)
Pts + compelling indications (HF, prior MI, high CHD risk, DM, CKD, stroke): LM + drugs
BP control target
General population: <140/90
pts w/ DM and renal diseases: <130/80
Thiazide diuretics should be initial drug therapy for most patients with uncomplicated hypertension
Routine tests for HTN management
ECG - MI, ischemia, LVH (left ventricular hypertrophy)
Urinalysis - proteinuria
BG (70-110) - Diabetes, anemia, polycythemia
Potassium (3.5-5.5)
Na (135-145)
Creatinine/BUN (1.0/<20)
INR (1.0)
BNP (<100)
MOA of diuretics
Decrease preload
Reduce the blood pressure by removing the body of salt and water via urination (decrease volume and preload).
Each diuretic works on different areas of the Kidneys by making your kidneys put more Na into your urine. The Na takes water with it from your blood.
That decreases the amount of fluid flowing through your blood vessels, which reduces pressure on the walls of your arteries.
Types of diuretics
Loop diuretics: (Lasix, Bumex) are more powerful and are often used when people have CHF and are especially useful in emergencies (NOT 1st choice).
Thiazide diuretics: #1 choice to treat HTN
Potassium-sparing diuretics: (Aldactone) help your body retain potassium and are used more often in CHF. (but NOT 1st choice).
Osmotic diurtetics
Loop diuretics
Drug Names: furosemide (Lasix), Bumetanide (Bumex), Torsemide (Demadex)
MOA: Work in the ascending limb of loop of Henle to block reabsorption of sodium and chloride and to prevent reabsorption of water
Uses: Pulmonary edema (emergent) caused by HF
Not responding to other diuretics
Hypercalcemia
DDI: other antihpertensive drugs, lithium
Loop (sulfa) SE/ADE
Hypokalemia, hypomagnesemia, hyponatremia, hypovolemia or dehydration, low CL+, low Ca++, hyperuricemia, hypotension, hyperglycemia
Metabolic alkalosis
Ototoxicity (dose-related hearing loss)
Diarrhea
Thiazide diuretics
Drug Names: hydrochlorothiazide (HydroDIURIL), metolazone (Zaroxolyn), Indapamide (Lozol),
MOA: Work in the early distal convoluted tubule to block the reabsorption of NaCL, and prevent the reabsorption of water.
Uses: first choice for essential hypertension
Edema caused by HF and kidney disease
DDI: other antihpertensive drugs, lithium
Thiazide SE/ADE
Hypokalemia, hyponatremia, hypovolemia or dehydration, hyperuricemia (gout), hypotension, hypercalcemia (kidney stone), hyperglycemia (insulin resistance), hyperlipidemia
Metabolic alkalosis
Hypersensitivity (fever, rash, anaphylaxis), intersitial nephritis
Potassium-sparing diuretics
Drug Names: triamterene (Dyrenium), amiloride (Midamor), Eplerenone (Inspra), spironolactone (Aldactone)
MOA: block the action of aldosterone (sodium and water retention), leading to potassium retention and the secretion of sodium and water.
Uses: Adjunct diuretics for HTN
CHF, NOT 1st Choice
Primary hyper-aldosteronism
Potassium-sparing SE/ADE
Metabolic acidosis, peptic ulcer
Spironolactone: hyperkalemia, gynecomastia, hirsutism, menstrual irregularities, testicular atrophy (with prolonged use), impotence
Amiloride: hyperkalemia, glucose intolerance
Triamterne: hyperkalemia, megaloblastic anemia in pts with liver cirrhosis
Osmotic diuretics
Drug Names: mannitol (Osmitrol)
MOA: reduce intracranial pressure (ICP) and intraocular pressure (IOP) by raising serum osmolality and drawing fluid back into the vascular and extravascular space.
Uses:
hypovolemic shock and severe hypotension to prevent RF
Reduce ICP and IOP
promote Na+ retention and water excretion in clients with hyponatremia and fluid volume excess.
SE/ADE: HF, pulmonary edema, renal failure, fluid/electrolyte imbalance
DDI: loop diuretics
Only used in hospital because it is very dangerous.
Nursing Implications and Patient Education for diuretics
Assess/monitor VSs, I/O, wt, electrolytes, BS, UA
Monitor and report s/s of dehydration, thrombosis/embolism and cardiac status
Start low and go slow
Instruct to manage postural hypotension: changing position slowly, dangle before standing.
Avoid use with other ototoxic medications, such as gentamicin.
Teach high-potassium diet and/or supplement
Avoid to give the meds late in the day to prevent nocturia (before 1400)
Angiotensin-Converting Enzyme (ACE) Inhibitors drug names/MOA
Drug Names: Lisinopril (Prinivil), Ramipril (Altace), Enalapril (Vasotec), captopril (Capoten)
MOA: Reduce BP by blocking the production of angiotensin II, leading to:
Reduce SNS activity -> reduce cardiac workload
Vasodilation (arteriole) (↓afterload)
↑ renal excretion of Na+ and water, and retention of K+ directly and indirectly via ALD reduction (↓ preload)
↑ renal water excretion via ADH reduction (↓preload)
ACE inhibitors uses/SE/ADE
Uses: HTN, CHF, chronic kidney disease , prevention of MI, stroke or cardiac death
SE/ADE:
N/V dysgeusia (lack of taste), dyspepsia, nasal congestion, fatigue, back pain
Dry, hacking cough, scratchy throat ( feel like feather in the throat) due to accumulation of bradykinin
Hyperkalemia
↓glomerular filtration rate (GFR) -> acute renal dysfunction (↑Cr and ↑ BUN)
Orthostatic hypotension: dizziness, lightheaded, HA
Photosensitivity
Angioedema
Neutropenia
ACE inhibitors DDI/pt education
DDI:
Diuretics + ACEI/ARB -> OH
Additive hypotensive effect when concurrently using w/ other BP-lower drugs
ACEI/ARB + K-sparing diutretics -> hyperkalemia
ACEI increase lithium level
Counteracting with NSAIDs
Nursing Implications and Patient Educations
Monitor VSs, electrolytes (K+), CBC,
Start low and go slow
Instruct changing positions slowly and dangle at bedside before standing
Notify provider if dry cough and discontinue ACEI
Avoid potassium-containing substance.
Monitor s/s of infection
ACEI/ARB should be cautiously used in pts w/ renal impairment.
Angiotensin II Receptor Blockers (ARBs) Drug names/MOA/uses/SE/ADE/DDI
Drug Names: losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), Candesartan (Atacand), olmesartan (Benicar), telmisartan (Micardis)
MOA: block angiotensin II receptor, leading to reduced cardiac workload, vasodilation, Na+ and water excretion.
Uses: HTN, CHF, chronic kidney disease , prevention of death after MI, stroke
SE/ADE: same as ACEIs, but more symptomatic hypotension, less cough and angioedema, as well as lower rate of discontinuation
DDI: additive effect when using with other BP drugs
ARB Nursing Implications and Patient Educations
Monitor VSs, electrolytes (K+), CBC,
Start low and go slow
ACEI/ARB should be cautiously used in pts w/ renal impairment.
If the patient has dry cough from ACEI, switch to ARB
If the patient has elvated Cr/BUN, or hyperkalemia or angioedema from ACEI,
Instruct pt to monitor s/s angioedema symptoms (skin wheals, swelling of tongue), stop the drug and call 911 immediately.
Instruct changing positions slowly and dangle at bedside before standing
Avoid potassium-containing substance.
Calcium Channel Blockers (CCBs) Drug names/MOA/uses/SE/ADE/DDI
Drug Names: Nifedipine (Procardia), Amlodipine, Felodipine (Plendil), Nicardipine (Cardene), Verapamil (Calan), Diltiazem (Cardizem)
MOA: Prevent Ca++ from entering the cells of heart and blood vessels walls , leading to vasodilation.
Uses: HTN, Angina, cardiac dysrhythmias
SE/ADE: rapid or slow HR, peripheral edema, OH, transient constipation and HA, dysrhythmias.
DDI: additive effect when using with other BP drugs
Non-Dihydropyridines drug names/MOA/SE/ADE/DDI/uses/Cl
Diltiazem (Cardizem), Verapamil (Calan)
MOA: block SA and AV node conduction -> decreased cardiac workload (-inotropic, -chronotropic and -dromotropic).
Arterial vasodialtion -> decreased BP and afterload.
SE/ADE: Bradycardia
DDI: Digoxin, BB
Use: Angina, HTN, Afib, tachyarrythmia
Cl: bradyarrhythmia, LVHF, heart block, hypotension
Dihydropyridines drug names/MOA/SE/ADE/DDI/uses/Cl
-dipine
MOA: arterial vasodilation -> decreased BP, afterload but reflex fast HR
SE/ADE: Tachycardia
DDI: BB -> slow HR
Use: HTN, vasospastic angina
Cl: non-vasospastic angina, hypotension
Nursing Implications and Patient Educations for CCB
Monitor VSs, wt, baseline and f/u EKG
Co-adm BB & -dipine CCB to manage reflex tachycardia
Instruct to avoid grapefruit products (liver enzyme inhibitor), prolonging DOA and increasing drug effects (SE/ADE).
Instruct pt to wear stockings (TED hose) to reduce lower leg and feet swelling, esp. in summer.
Edema can also be controlled by diuretics if stockings not effective.
Instruct changing positions slowly and dangle at bedside before standing
Instruct high fiber diet, stool softener or laxatives if constipated from CCB
Central Acting Alpha2 Agonists drug names/MOA/uses/SE/ADE
Drug names: clonidine (Catapres)
MOA: acting in CNS to ↓ NE release -> ↓stimulation of both α and βadrenergic receptors in heart (bradycardia and low cardiac output or CO) and the peripheral vascular system (A and V vasodilation->↓BP )
Use: not primary drug to treat HTN, pain, hot flashes, substances (alcohol, opiods, etc) withdrawal, ADHD and Tourette syndrome
SE/ADE: CNS depression (drowsiness and sedation), dry mouth, rebound HTN, constipation, impotence, Gynecomastia
Central Acting Alpha2 Agonists DDI/pt education
DDI:
Additive effect when using with antihypertensive drugs
Counteraction when using with MAOIs, TCA
Additive CNS depression when using with other CNS depressants (alcohol)
Patient Educations:
Instruct pts to change positions slowly.
Don't use concurrently with MAOIs and TCAs
Change transdermal patches q7 days.
Instruct pts to avoid driving and operating machine
Taper off over 2-4 days
Beta Adrenergic Blockers (Sympatholytics) drug names/MOA/types/uses/Cl
Drug Names: -olol or -lol
MOA: Block beta1-adrenergic receptors from binding to NE and Epi mainly in the heart to ↓HR, ↓cardiac contraction force, ↓conduction rate (negative CID).
Types: β1Blockers, Nonselective β Blockers, and Combined α1 and β blockers
Uses: HTN, Angina, tachydysrhythmias, MI and post MI, HF, hyperthyroidism, migraine headache, stage anxiety, pheochromocytoma, and glaucoma.
CI: AV block, sinus bradycardia, HF, DM, and depression.
Medications for Hypertensive Crisis
Hypertensive crisis: rapidly and severely ↑↑↑ BP Goal: early Dx and Tx to reduce morbidity and mortality
Types: hypertensive urgency and emergency.
HU or severe asymptomatic HTN: SBP ≥ 180 mmHg OR DBP ≥ 120 mmHg, w/o organ damage, S/S: severe HA, SOB, nosebleeds (epistaxis), and severe anxiety, no need IP care
HE or malignant hypertension: SBP ≥ 180 mmHg OR DBP ≥ 110 mmHg, w/ organ damage, S/S: CP, SOB, back pain, numbness/weakness, change in vision, difficulty speaking, IP care needed.
HU
It is harmful and unnecessary to reduce BP rapidly
Does not require hospital admission
Provide a quiet room and monitor BPs
For untreated pts: start short-actiing drugs (furosemide, clonidine, captopril) to reduce BP over hrs -> prescribe long-acting BB, ACEI/ARB or CCBs
For pts treated w/ BP meds: adjust/add drugs
F/U in two days and educate low Na diet
HE
Use IV drugs that directly dilate both arteries and veins (reduce both pre and afterload) to reduce BP rapidly.
Reduce DBP to 100-105 mmHg over 2-6 hrs
Require hospital admission.
Medications used in HE
Nitroprusside (Nipride) vasodilator
ADE: N/V, muscle twitching, sweating, hot flash, hypotension, cyanide toxicity
Nicardipine (Cardene) CCB
ADE: tachycardia, HA, flushing, local phlebitis
Clevidipine CCB
ADE: short-acting di CCB, hypotension
Labetalol BB
ADE: A1 and beta blocker, excessive hypotension
Common substances associated with hypertension
Rx: steroids, OCs (estrogen component), NSAIDs, anticonvulsants, antidepressants (e.g., MAOI)
Street and OTC drugs: Cocaine, Nicotine, and St. John's Wort
Food: Na, ethanol, Licorice, tyramine food, and heavy metals (e.g., lead, mercury, lithium)
Pathophysiology: Systolic heart failure (Left sided heart failure)
What is: pump failure, the heart muscle can't pump enough blood out to supply the whole body-> ↓ tissue perfusion and ↑pulmonary and systemic congestion
How to measure:
Stroke Volume (SV) = End Diastolic Volume - End-Systolic Volume = EDV- ESV
Ejection Fraction (EF) = (SV / EDV) × 100% (60%)
Cardiac Output (Q) = SV × HR
BNP: <100
Goal of treatment: the heart's able to pump out the blood to aorta.
How to treat: decrease preload and afterload
ACEI: Decrease Preload and afterload
Inhibit the Renin-angiotensin-aldosterone system (RAAS), block conversion of angiotensin I to II
Reduce angiotensin II production,
Dilate arterial blood vessels (decrease afterload),
Increase the water and salt removal from kidney, reduce the blood volume (preload)
The heart will not work so hard with reduce preload and afterload.
**Start at lowest possible dose and titrate up FOR ALL THE HEART MEDS
ARBs: Decrease both pre and afterload
Remember Angiotensin II is a very potent chemical that causes muscles around blood vessel to contract - thereby increasing BP
Angiotensin II receptor blockers (ARBs) are medications that block the action of angiotensin II by preventing angiotensin II from binding to angiotensin II receptors on blood vessels
Can be used in patients intolerant to ACEIs due to dry cough NOT increased Cr/BUN or angioedma
start with lowest dose and titrate up as needed.
Beta-Blockers: Decrease afterload
MOA: Decrease afterload by reducing heart rate, the force of contraction and heart conduction. (negative CID)
Use: Only for newly diagnosed HF, start low dose beta blocker and titrate up.
Monitor electrolytes
Avoid abrupt cessation
Taper dose gradually over weeks to DC
Could cause angina exacerbation, MI, Ventricular arrhythmias
Diuretics: decrease preload
Loop diuretics: rid sodium/water and reduce congestion to restore to "euvolemic" state
Drug names: Furosemide (Lasix), Metolazone (Zaroxolyn)
Give Zaroxolyn ½ hr before Lasix for weight gain >5 lb/week;
Avoid long term (secondary to electrolyte abn/volume depletion
Aldosterone Antagonists: decrease preload
Spironolactone (Aldactone), Eplerenone (Inspra)
Use/indication:
HF patients with NYHA IV with low EF in addition to standard medical therapy (BB, ACE-I and diuretics)
Patients after MI with clinical HF, low EF, and symptoms or history of DM
Contraindicated when Creatinine >2.5 or K > 5.0
Cardiac Glycosides: Digoxin MOA/uses/Cl/EE/SE
MOA:
Postive inotropic: increase force of myocardial contraction-> increase pump efficiency by improving SV and CO
Negtive chronotropic: slow heart rate -> allow ventribles more time to fill with blood and increase SV and CO
Use: treat symptomatic HF w/ ↓EF, control ventricle response to atrial fibrillation in HF patients
CI: pts w/ ventricular dysrhythmia, heart block, hypokalemia, advanced HF and renal dysfunction
Expected effect - increased contractility and cardiac output, decreased heart rate
SE: GI upset (anorexia/N/V/abd pain), bradycardia (<60 BPM), CNS effects (fatigue, weakness, vision change)
Cardiac Glycosides: Digoxin ADE/DDI
ADE: digoxin toxicity
Symptoms: hypersalivation, fatigue, nausea/vomiting/diarrhea/anorexia, Dysrhythmias, Bradycardia, visual disturbances (yellow or green halos around objects), confusion, dizziness, nightmares, agitation, and/or depression
Treatment: If signs of toxicity, hold drug and draw blood level for digoxin, give digoxin immune Fab (Digibind, DigiFab).
DDIs:
Concurrent use of thiazide and loop diuretics -> hypokalemia -> digi toxicity
ACEIs -> hyperkalemia -> reduce digoxin effect
Additive positive inotropic effect with sympathomimetic
Counteraction with non-di CCBs (verapamil)
Cardiac Glycosides: Digoxin pt education/nursing implications
Monitor VSs, EKG, K+level, digi level (0.8-2 ng/ml)
Monitor conditions increasing risk of digoxin toxicity: hypokalemia, increased serum digoxin levels, and heart disease.
Digoxin has very narrow therapeutic range (0.8 to 2 ng/mL)
Instruct pts to monitor s/s digi toxicity (anorexia, vision change)
Instruct pts to monitor s/s of hypokalemia (N/V/general weakness).
Use potassium supplements if concurrently taking a diuretic.
Antianginals patho
Angina Pectoris
Chest pain that occurs when the level of oxygen and nutrients in the blood is insufficient to meet the demands of the heart.
Usually occurs when the coronary arteries are narrowed.
Decreased oxygen supply can precipitate or aggravate angina (e.g., severe anemia or hypoxia).
Supply and Demand imbalance of O2 to myocardium.
Antianginals treatment goals
Decrease demand (reduce work load);
Increase supply;
Prevent myocardial ischemia, infarction and death, as well as the pain.
Nitrates drug names/MOA/uses/SE/ADE/DDI/Cl
Drug Names: Nitroglycerin, isosorbide
MOA:
Potent smooth muscle relaxant (reduce coronary artery spasm) and vasodilator (dilate coronary arteries) increase supply.
Dilates all blood vessels, primarily venous circulation (decrease preload) reduce cardiac demand.
Uses: Treat and prevent angina.
SE/ADE: HA, OH, Hypotension, reflex tachycardia, tolerance/dependence, ↑ICP
DDIs: concurrent use of alchol, BB, CCBs, diuretics and phosphodiesterase inhibitor hypotension
CIs: TBI, inadequate cerebral perfusion, Hypotension (line, VS q2-5min)tachy, Severe anemia
Pregnancy Category C
Nitroglycerin (Nitrates)
Sublingual route:
Rapid onset (2-3 minutes), short duration
Store the tablets in tightly capped dark container
Used in the symptomatic treatment of ischemic heart conditions (ex. Angina).
the College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend contacting EMS if chest pain or discomfort is unimproved or worsening five minutes after one nitroglycerin dose has been taken
Transdermal route
Use an intermittent dosing schedule NOT around the clock to prevent tolerance
Nitrate free period each day: 8-12 hrs/day
Remove patch , wipe off ointment and cleanse skin
Nitroglycerin (Nitrates) pt education
Monitor VSs, EKG
Instruct pts to use ASA or typlenol for HA
Instruct pts to change position slowly
Concurrent use Nitrates and BB to prevent reflex tachycardia
Start low and go slow, maximum of 3 doses (0.4mg x 3) in 15 minutes
Educate pts that tolerance is caused by repeated dosing of transdermal nitroglycerin patch or chronic use. Pts should use on-off cycles or intermittent therapy to allow adequate nitrate-free interval and prevent tolerance.
Nitroglycerin should be stored in a tightly capped dark bottle in the refrig no longer than 12 mos
Beta Blockers
MOA = Decrease heart rate and contractility by binding to and blocking the beta-adrenergic receptors in the myocardium and conduction system. Causes decreased workload of the heart.
Decreased HR = coronary arteries have more time to fill with O2 and Nutrient rich blood during diastole, increase supply
Calcium Channel Blockers
MOA:
Inhibits calcium ion influx into vascular smooth muscle and myocardium.
Increase myocardial O2 supply by relaxing smooth muscle that surround coronary arteries causing them to dilate = increased blood flow to the heart.
Dilatation of arteries throughout the body results in decreased SVR and afterload = decreased myocardial O2 demand.
* CCB's are especially useful if hypertension or coronary spasm is present.
Antiarrhythmics
Arrhythmia: "No rhythm", more common name
Dysrhythmia: Any deviation from the normal sinus rhythm of the heart
Normal Sinus Rhythm = 60-100 bpm
Bradycardia = < 60 bpm
Tachycardia = > 100 bpm
Goal of Antiarrhythmics medications:
correct heart rhythm abnormalities
Antidysrhythmia
Cardiac Conduction System:
Sinoatrial Node (SA Node)
Pacemaker
Intrinsic rate 60-100 bpm
Located in the top of the right atrium, generates an electrical impulse that travels through the atria, causing atria to contract
Atrioventricular Node (AV Node)
40-60 bpm
Impulse received by AV node in the bottom of the right atrium, slows the impulse to allow the ventricles to fill
Antiarrhythmics (bundle of HIS and purkinje fibers)
Bundle of HIS
Electrical impulse travels into the Bundle of His, located between R and L ventricles and distributes the impulse to both ventricles via right and left bundle branches
Purkinje Fibers
<40 bpm
Bundle branches end in purkinje fibers, stimulation of Purkinje fibers causes ventricular contraction.
Class III Antiarrhythmics: Amiodarone MOA/SE/ADE
Amiodarone (Cordarone and Pacerone): One of the most effective antiarrhythmic meds for controlling supraventricular and ventricular tachyarrhythmias
Side Effects
Corneal deposits, GI upset (N/V/A), photosensitivity
Adverse Events
Stiff lung due to pulmonary toxicity;
Sinus bradycardia, AV block ,hypotension-> HF
Skin damage from sun
Thyroid dysfunction
Liver damage
Blindness
Class III Antiarrhythmics: Amiodarone Cl/DDI/pt education
CI: bradycardia, heart block, liver/thyroid/pulmonary dysfunction, HF
DDIs: multiple interactions, given alone
Nursing Implication and Pt Education:
Baseline and F/U monitoring on EKG, PFTs, CXR, Thyroid labs, LFTs, and eye exam
LONG HALF LIFE (Amiodarone T1/2= 58 days), can take 2-3 months for SE/ADEs to resolve.
Monitor S/S pulmonary toxicity, HF
Overview of Coagulation Modifiers
MOA: prevent clot formation or break apart an already formed clot by either altering the clotting cascade, preventing platelet aggregation, or dissolve a clot.
Goal: increase circulation and perfusion, decrease pain and prevent further tissue damage.
Types: oral and parenteral anticoagulants, antiplatelet medications, and thrombolytic agents.
Parenteral Anticoagulants drug names/MOA/uses
Drug Names:
Heparin
Low molecular weight heparins (LMWH): enoxaparin (Lovenox), dalteparin (Fragmin), tinzaparin (Innohep)
Activated factor X (Xa) inhibitor: fondaparinux sodium (Arixtra)
MOA: prevent bleeding by inactivating clotting factors (Xa) and thrombin formation inhibit fibrin formation.
Use:
Heparin Uses:
Prophylaxis and treatment deep venous thrombosis , PE, AMI, stroke
Post operative DVT prophlyaxis
Indwelling IV catheters (heparin flush)
Can be used in pregnancy with DVT and DIC (disseminated intravascular coagulation)
Parenteral Anticoagulants uses/SE/ADE/DDI
Use:
LMWH and XaI Uses: DVT and PE prophylaxis and treatment, unstable angina, acute coronary syndrome (ACS), Coumadin bridging.
IV or SubQ, IV dose based on Partial thromboplastin time (PTT, 24-36 seconds)
SE/ADE:
Heparin and LMWH: hemorrhage, hematoma, Heparin-induced thrombocytopenia (HIT), and toxicity/overdose
XaI: hemorrhage, thrombocytopenia, epidural and spinal hematoma
DDI: additive bleeding when using with aspirin, NSAIDs, and other anticoagulants.
Parenteral Anticoagulants pt education
Monitor VSs, CBC, PLT count (>100,000/mm3), activated partial thromboplastin time (aPTT) and keep at 1.5 to 2 times the baseline.
Give protamine (antidote for heparin) in case of heparin overdose, may need to re-dose in 2 hrs
Administer SQ injection in the abdomen, 2 inch from umbilicus, NO aspiration, rotate sits
Instruct pts to monitor s/s of bleeding.
Instruct pts not to take OTC NSAIDs, aspirin and other "blood thinner" meds
Instruct pts to use electric razor and soft toothbrush
Oral Anticoagulants drug name/MOA/uses/SE/ADE/DDI
Drug Name: warfarin (coumadin)
MOA: Inhibits vitamin K-dependent coagulation factor synthesis (VII, IX , X, prothrombin or II, protein C and S) prevention of clot formation. No direct effect on a clot that has already formed.
Uses:
Prophylaxis and Treatment Deep venous thrombosis (DVT), Pulmonary embolism (PE)
Prevent clot or thrombus formation in pts with atrial fibrillation (stroke prevention)or prosthetic heart valves
Prevent extension of a previously existing clot in recurrent MI and TIAs
SE/ADE: Bleeding/hemorrhage and toxicity, preg X
DDIs: MULTIPLE Given alone
Oral anticoagulants pt education
Monitor VSs, CBC, PT/INR (1.0)
Take the medication same time everyday alone
Take several days to reach therapeutic effects. Heparin or lovenox are usually initiated at hospital to bridge the anticoagulant effect
Treating Warfarin overdose
Rapid reversal: Phytonadione (Vitamin K),
Emergent situations: fresh frozen plasma (FFP) or Factor IX or whole blood
Instruct pts to monitor s/s of bleeding. Use electric razor and soft toothbrush
Avoid other OTC drugs, ASA, NSAIDs
Avoid prolonged sitting, tight clothing
Instruct pts to maintain a consistency intake of Vit K intake . Same amount of vegetables daily.
Antiplatelets drug names/MOA/uses
Drug Name: Aspirin, abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat), clopidogrel (Plavix), ticlopidine (Ticlid), pentoxifylline (Trental), dipyridamole (Persantine), cilostazol (Pletal)
MOA: Prevent platelet from clumping together or aggregation, AKA, "blood slicker"
Uses: Prevent Unstable angina (chest pain), AMI, recurrent MI, CVA, claudication, prevention of post stent thrombosis
Antiplatelets SE/ADE/Cl/DDI
SE/ADEs:
Aspirin: GI upset (N/V/dyspepsia), hemorrhagic stroke and bleeding, thrombocytopenia, tinnitus
Plavix: Bleeding , thrombotic thrombocytopenic purpura (TTP), neutropenia, agranulocytosis, SJS
CI: not preg women in 3rd trimester and chilren w/ vial infection (ASA), not in pts w/ bleeding disorder, PUD, active hemorrhage, and renal/hepatic disorders
DDIs: additive bleeding if concurrent use of Plavix, NSAIDs, ASA, warfarin, heparin and other bleeding-inducing drugs.
Antiplatelets pt education
Monitor VSs, CBC, plt, hearing
Aspirin's antiplatelet effects last 7 days because the lifespan of platelets is 7 days,
Off aspirin for 1 week before any invasive procedure (surgery, dental, scopes, catheter, etc)
Instruct pts to take enteric-coated ASA or w/food, or use PPI
Instruct pts to monitor s/s bleeding
Instruct pts to avoid concurrent use of antiplatelets, anticoagulants and NSAIDS
Use electric razor and soft toothbrush
Thrombolytic Medications drug names/MOA/uses/SE/ADE
Drug Names: streptokinase (Streptase), Alteplase (Activase, tPA), Tenecteplase (TNKase), Reteplase (Retavase)
MOA: dissolve clots that have already formed by converting plasminogen to plasmin that destroys fibrinogen and other clotting factors
Uses: AMI, DVT, Massive PE, ischemic stroke
SE/ADE: bleeding, hypotension, Allergy
Selection of Antibacterial
Identification of the causative agent:
Collect the potential causal agent: body fluids (e.g., blood, urine, sputum, or wound drainage) to determine the micro-organism causing the infection.
Gram stain:
Gram-positive
Gram-negative
harder to kill or control
Coated with protective capsule, and hard to penetrate
Selection of Antimicrobials
Culture and Sensitivity (C & S):
Culture should be obtained prior to administration of antibacterial drugs
Aseptic techniques Fluid for culture should be carefully collected to prevent contamination and unnecessary antimicrobial treatment.
Sensitivity test to determine the antibiotics to which the bacteria is susceptible.
Selection of Antibacterial
Susceptible host
Immune system
Site of the infection: meningitis, endocarditis, abscesses
Age of the host: very young/old, preg/nursing women
Individual reactions
Selection of Antibacterial
Principles of therapy
Mono-therapy vs. combo therapy
Severity of infections
Types of causative agent (s)
Balance between benefits vs. risks
Prophylactic use
Selection of antibacterial
Classification of antibacterial drugs
Category by MOA
*Bactericidal: kill bacteria
*Bacteriostatic: stop reproduction and growth
Category by Spectrum of efficacy
Narrow-spectrum: against one type bacteria
Broad-spectrum: against G+ and G-
Selection of Antibacterial
Nursing interventions
Promote primary prevention (up to date immunization and hand hygiene)
Minimize and monitor invasive procedures
Teach pts to take the full course of antibiotics prescribed to prevent medication resistance and recurrence of infection.
Use infection control procedures to break chain of infection
General Issues in Antibacterial Therapy EE/SE/ADE
Expected effects: no signs and symptoms (s/s) of infection
No fever;
WBC : 5000-10000
No local infectious signs caused by bacteria (red, swell, draining, warm, tender, dysfunction)
Side effects
GI disturbance (loose BM severe diarrhea)
thrush, vaginal yeast infections
Adverse effects:
Allergic reactions (rash)anaphylaxis,
Pseudomembranous colitis (aka, AAC): C. difficile
Super infection
Liver/kidney dysfunction
General Issues in Antibacterial Therapy cause/prevention
Cause of *Pseudomembranous colitis and superinfection
Normal flora in gut prevents C. difficile and yeast growth
Antibacterial kills gut flora overgrowth of C. difficile and fungi. Pseudomembranous colitis and yeast infection
How to prevent?
*Probiotics: live microorganisms (Lactic acid bacteria, yeasts and bacilli)
General Issues in Antibacterial Therapy MOA/Contraindication/product names
MOA of probiotics:
Reduce antibiotic-associated colitis by restoring the imbalanced GI tract and stopping the overgrowth of pathogenic organisms (C.difficile).
Contraindication: Immunocompromised individuals
Product Names:
Activia (yogurt, soy yogurt, or as dietary supplements.
Culturelle (one tablet, po, tid)
General Issues in Antibacterial Therapy Monitoring
Monitoring
Pre: Hx allergies, C &S, WBCs, VS (temp), mental status,
Post:
EE (fever, WBCs, s/s)
SE/AE (BM, skin, yeast infection, )
IV site
Monitor vital organs (ears, liver, kidneys)
General Issues in Antibacterial Therapy pt education
Patient Education:
Take drugs exactly as prescribed (10-14 Ds):
Prevent recurrence of infection;
Prevent the development of resistant bacteria
Check SE/AE (allergy, yeast infection)
Good Hygiene (teeth-brushing, hand-washing, perineum care)
Take probiotics when taking antibacterial drugs
Increase fluid intake if permits
Types of Antibacterial Drugs
Cell wall synthesis inhibitors (CWSI)
Protein synthesis inhibitors (PSI)
DNA synthesis inhibitors (DSI)
Metabolism inhibitors (MI)
Cell Wall Synthesis Inhibitors MOA
MOA: Prevent bacteria from forming cell walls -> bacterial cell death
Bind to cell wall proteins (bricks) to prevent them being placed into cell walls
Inhibit the bacterial enzyme (glue) that cross-link the cell wall protein, make the walls loose;
Activate autolysins to eat holes in the wall, making them leaky
Cell Wall Synthesis Inhibitors Penicillins (B-lactam) EE/indication/Cl
Penicillins (β-lactam)
Common drugs: -cillin PCN, amoxicillin (Amoxil)
Expected effect: Bacterialcidal,
Indication:
Broad spectrum (most G+, some G-)
1st choice for most infections
Drug of choice for Syphilis
Prophylactic use
CI: Pts w/ hx of severe allergies, cross allergies, renal dysfunction
Cell Wall Synthesis Inhibitors Combo Penicillins
Combo Penicillins ( penicillin + beta-lactamase inhibitors) (β-lactam)
Examples:
Amoxicillin-clavulanate (Augmentin): given orally, combination intensifies effect of amoxicillin
Piperacillin-tazabactam (Zosyn)
Ticarcillin-clavulanate (Timentin)
Ampicillin-sulbactam (Unasyn)
Cell Wall Synthesis Inhibitors SE/ADE/lifespan/AB resistance
Side effects (fewer SE): mild allergic reactions, GI upset (best take 1hr before meals and 2 hrs after meals)
Adverse effects - least toxic, bleeding, kidney damage, most common cause of anaphylaxis, SJS, and supra-infection.
Lifespan considerations: Safest antibacterial agent used in pregnancy
AB Resistance: (bug -> drug)
Bacterial develop β-lactamase enzyme to destroy Penicillin.
Cell Wall Synthesis Inhibitors Cephalosporins
Cephalosporins (β-lactam): -cef-, -ceph-, kef-
4 generations: (from 1 to 4)
More effective against Gram negative and anaerobes
Increasing resistance to β-lactamase
Increasing ability to reach CNS (SE)
Indications (uses): given parenterally over 30 min
Surgical prophylaxis (1st generation)
G-, anaerobics (2nd generation)
G -, anaerobic meningitis, *gonorrhea (3rd generation)
G +/- (4th generation)
Alternative in patients with mild allergy to penicillin
CI: Not for pts/ hx sever allg to PCN or cephalosporins. Cautions in pts w/ renal impairment and risk of bleeding
Cell Wall Synthesis Inhibitors EE/SE/ADE/AB resistance
EE: most broad, bactericidal, high TI (↓ s/s of infection)
SE/AE: low toxicity, GI upset, hypersensitivity (cross-reaction with penicillin), allergy, bleeding, thrombophlebitis with IV infusion, kidneys, SJS, and suprainfection
AB resistance: Inactivated by β-lactamase like Penicillins
Cell Wall Synthesis Inhibitors Carbapenems
Carbapenems:(β-lactam)
Drug names: -enem
rtapenem (Invanz)
Imipenem/cilastatin (Primaxin)
Meropenem (Merrem)
Very broad spectrum, bactericidal
Use for mixed infections (G+/G-, aerobic/anaerobic)
Resist to β-lactamase and other MDR organisms
Given parenterally, 2nd line drugs
CI: caution in pts w/ renal impairment
SE/AE: GI upset, suprainfection, CNS changes (confusion, seizures), kidney damage, SJS, cross hypersensitivity w/PCN
Cell Wall Synthesis Inhibitors Monobactams or vancomycin
Monobactams or Vancomycin: (non β-lactam)
resistance to β-lactamase , bactericidal
Use: serious G+ infections (bone, skin, LRT)
MRSA: Methicillin-resistant Staphylococcus aureus or Staphylococcus epidermidis
CDAD (clostridium difficile associated disease): oral dose used when metronidazole not working (2nd line)
SE: GI upset (N/V/D/A)
AE: Allergy, ototoxicity (hearing loss), "red man" syndrome (Give it SLOWLY), nephrotoxicity, Thrombophlebitis, cardiac (AF), Vancomycin-resistant Enterococcus (VRE)
Monitor peak and trough blood level, IV site, VS(BP), Skin
Cell Wall Synthesis Inhibitors nursing implications
Nursing Implication
Assess hx of allergy and instruct pts to wear an allergy ID bracelet.
Observe clients for 15-30 min following administration of parenteral penicillin.
Monitor renal function (I/O, Cr, BUN)
Monitor s/s bleeding, prothrombin time, and give parenteral vitamin K for Cephalosporins
Monitor for diarrhea, skin condition and fluid status.
Ask/check seizure when giving Invanz (carbapenem)
Give Vancomycin SLOWLY, monitor its level and hearing acuity
Monitor cross-reactions between 3 β-lactam ABXs
Cell Wall Synthesis Inhibitors pt education
Patient teaching:
Advise pts to complete the entire course of therapy regardless of presence of symptoms.
Instruct pts to report any signs of an allergic response
*Highly encoraged to take the drugs at least 1 hr before or 2 hrs after antacid and food (pharmacokinetics, absorption)
Liquid form : keep tightly closed, refrig?, shake well
Life Span Considerations for Cell Wall Synthesis Inhibitors
Pediatric: anaphylaxis
Pregnancy and breastfeeding:
Penicillins, most cephalosporins - category B
Others and vancomycin - category C
Excreted in breast milk (stop breast feeding)
Older adults:
Ototoxicity (tinnitus, ringing ear)
nephrotoxicity (kidney)
urine out put, I/O,
Creatinine (Cr): < 1.2
Blood urea nitrogen (BUN): <20-29
Protein Synthesis Inhibitors subtype/MOA
Subtype:
Aminoglycosides,
Tetracyclines,
Macrolides,
Bacteriostatic or bactericidal
MOA: Slows protein production, and stop bacteria from being able to live or reproduce.
* Without making the protein, the bacteria will either die (bactericidal) or not grow (bacteriostatic)
Protein Synthesis Inhibitors Aminoglycosides drug names/indications
Aminoglycosides
Common drugs: -micin or -mycin
Gentamicin (Gentacidin)
Streptomycin (Tx of tuberculosis)
Tobramycin (Nebcin)
Bactericidal
Narrow spectrum: aerobic G -
Indications:
Aerobic infections (oxygen-dependent bacteria)
Not for anaerobic bacteria
Sepsis caused by G- enteric bacteria
Tapeworm infection
Pre-op GI prep: suppress normal flora
Don't mix aminoglycoside and penicillin in the same IV solution!!!!!!
Protein Synthesis Inhibitors Tetracycline drug names/indications/Cl
Tetracycline
Common drugs: -cycline
Doxycycline (Vibramycin), Tetracycline (Achromycin),
*Bacteriostatic
broad spectrum (G+/G-)
Indications:
Only for patients with healthy immune system
Peptic ulcer caused by H. pylori
Acne
Allergic to penicillins or cephalosporins
Chlamydia (Doxycycline 100mg , bid x 7 Ds), gonorrhea (Adjunct)
Anthrax
CI: Not for preg or young children, caution in pts w/ liver and renal diseases
Protein Synthesis Inhibitors Macrolides drug names/indications
Macrolides:
Common drugs: -mycin
Oral and IV: Azithromycin (Zithromax)
Oral: clarithromycin (Biaxin), Erythromycin (E-Mycin)
Bactericidal or bacteriostatic: depend on blood level of drug and bacteria type
broad spectrum: (G+/G-)
Indications:
Whooping cough, Strep throat caused by grp A Strep.
Mycoplasma pneumonia (atypical pneumonia) & CAP
Not for anaerobic bacteria
Allergic to penicillins or cephalosporins
Chlamydia (Zithromax, 1g), gonorrhea (Adjunct)
Other Protein Synthesis Inhibitors Clindamycin use
Clindamycin (Cleocin)
Bacteriostatic or bactericidal with high doses (G+)
Use: acne (topical), pneumonia, peritonitis, cellulitis caused by G+ (Staph. aureus), for severe anaerobic infections w/ aminoglycosides for GI wounds
Linezolid (Zyvox)
Use: reserved for severe or life-threatening infections not responding to other AB drugs (G+)
VRE: vancomycin-resistan enteroccus
MRSA: methicillin-resistant staphylococcus aureus
Diabetic foot ulcers
Common Side Effects of PSI
Aminoglycosides (e.g., gentamicin)
Nausea, vomiting, rash, fever, lethargy
Macrolides (e.g., azithromycin)
N/V/D, loss of appetite, abdominal pain photosensitivity
Tetracyclines (e.g., doxycycline)
N/V/D, tooth discoloration and hypoplasia, rash, photosensitivity, yeast infections
Clindamycin: GI upset, site irritation, thrombophlebitis
Zyvox: N/D, HA, Hypertension (vasoconstriction)
Adverse Effects of PSI
Aminoglycosides (e.g., gentamicin): Ototoxicity, nephrotoxicity, ↑neuromuscular blockade effect, neurologic disorders caused by streptomycin
Macrolides(e.g., azithromycin): ototoxicity, hepatotoxicity, metabolism of other drugs (e.g., Digoxin, warfarin), long QT (cardiac death)
Tetracyclines (e.g., doxycycline): Increased intracranial pressure (CNS toxic), kidney and liver toxicity and suprainfection
Clindamycin: ↓ liver function, ↓ white blood cell counts, give slowly by IV (shock, cardiac arrest)
Linezolid (Zyvox): ↓ blood cell counts, damage to optic nerve, HTN
Administering Protein Synthesis Inhibitors
Monitoring:
Aminoglycosides: hearing, temperature, I&O, BUN, Cr, peak and trough for Gentamicin, monitor RR and O2SAT in pts taking NMB or skeletal muscle relaxants
Tetracyclines : Monitor GI, I/O, kidney and liver functioning, bleeding.
Macrolides : check med list for high risk drugs, EKG for QT baseline, liver function
linezolid (Zyvox): monitor blood pressure, restrice Tyramine -rich foods
Patient Teaching for PSI
Instruct pts to complete the full course of therapy even w/ absence of symptoms.
Aminoglycosides: instruct pts to report neurologic s/s
Macrolides
Take with food to decrease GI side effects (but antacids delay its absorption)
Avoid sun exposure
Not take with other drugs same time
Tetracyclines
Avoid sun exposure and/or sun protective wear
Take 1 hr before or 2 hrs after meal, antacids, laxatives, dairy products, Ca+2/Fe+2/Mg+2 supplement to avoid mal-absorption
Advise client to use an alternative form of birth control.
Good oral hygiene
Linezolid (Zyvox) -no tyramine food, not MAOI.
Life Span Considerations for PSI
Pediatric:
Aminoglycosides : severe resp. depression and kidney damage
Tetracycline : not for children <8 years (discoloration of permanent teeth)
Pregnancy and breastfeeding:
Avoid amino- and tetra-, both are category D (exception: anthrax exposure)
Most macrolides are category B
Pass into breast milk (colic and diarrhea)
Older adults:
Amino-: hearing (ototoxicity,), kidney (nephrotoxicity)
Macrolides: ototoxicity when taking with loop diuretics
DNA Synthesis Inhibitors Fluoroquinolones drug names/MOA/use
Fluoroquinolones
Drug names: -floxacin
*ciprofloxacin (cipro), levofloxacin (Levaquin), moxifloxacin (Avelox), ofloxacin (Floxin)
MOA: Inhibit production of DNA, preventing bacterial reproduction
Broad-spectrum, G+ and G-
Bactericidal
Use: Skin infections, UTI, RTI, GI infection, and gonorrhea. Prevent and treat anthrax.
DNA Synthesis Inhibitors Fluoroquinolones SE/ADE
Side effects:
Rash, N/V, headache, abdominal pain, dizziness, changes in taste, burning urination (perineal area), changed blood glucose level
Adverse effects
Serious heart dysrhythmias (esp. hypokalemia),
neurotoxicity, peripheral neuropathy
Stevens-Johnson syndrome, photosensitivity
tendon rupture
Suprainfection (thrush, vaginal yeast infection)
DNA Synthesis Inhibitors Fluoroquinolones DDI/nursing
DDI:
Antacids, Fe, milk and dairy reduce the absorption of fluoroquinolones
Fluoroquinolone increase theophylline and warfarin levels
Nursing implications
Assess medicaiton hx of warfarin and theophylline
Monitor suprainfection (thrush, vaginal yeast infection)
Administering DNA Synthesis Inhibitors pt education
Patient teaching:
Increase fluid intakes to prevent concentrated urine
Take meds 2 hr before or 4 hrs after taking iron, vitamins, antacids
Patients taking warfarin (Coumadin) check INR level (<1.0)
Avoid sunburn
Instruct pts to observe s/s of pain, swelling, and redness at Achilles tendon site.
Instruct pts to observe s/s yeast infection (cottage cheese/curd-like lesions on the mouth and genital area)
DNA synthesis inhibitors lifespan
Pediatric:
Not for those < 18 years (tendon rupture)
Pregnancy and breastfeeding:
Category C
Avoid use in pregnant and breastfeeding women
Increased risk for bone, joint, tendon defects
Older adults:
Tendon rupture more common when the drug is taken up to 1 month after the drug stopped
CNS change
DNA Synthesis Inhibitors Metronidazole uses/SE/ADE/DDI/pt education
Metronidazole (Flagyl)
Uses:
pelvic inflammatory disease
Anaerobic bactericidal
Pseudomembranous colitis caused by Clostridium difficile (1st line)
vaginitis caused by trichomonas vaginalis (STD)
SE: GI discomfort (n/v/d), metallic taste in the mouth.
AE: leukopenia, neutropenia, peripheral neuropathy, CNS toxicity, bone marrow suppression
DDI: "Disulfiram reaction" with alcohol
Patient education: taken with a large glass of water and with food.
Metabolism Inhibitors drug names/MOA/use/Cl
Drug name: sulfamethoxazole /trimethoprim (SMX-TMP, Bactrim, Septra), Silver sulfadiazine (silvadene),
MOA: Stop bacteria making folic acid, which is essential for production of DNA, RNA and protein. Bacteriostatic (bactericidal for UTI),
Use:
broad spectrum (G+/G-)
Treat some nonbacterial infections
UTI, Otitis media, respiratory infections (e.g. pneumonia), and diarrhea caused by bacteria
CI: Not for pts w/ folate deficiency, sulfa allergy, preg/nursing women, renal/liver dysfunction.
Metabolism Inhibitors SE/ADE
SE: Headache, fever, skin rash, photosensitivity, N/V, itchiness
AE:
Crystalluria: form crystals in Kidneys and cause kidney stones and failure
Bone marrow suppression or blood dyscrasias (anemia and agranulocytosis)
Stevens-Johnson syndrome
Hepatitis
Metabolism inhibitors nursing implications
Nursing Implications:
"Sulfa" allergies
Glucose-6-phosphate dehydrogenase (G6PD) deficiency: Blood disorders (in black or Mediterranean males), RBC breakdown
Liver/renal function test, skin (Jaundice, bruises, blisters)
Monitor baseline and follow up CBC w/diff,
Monitor DDI: ↑bleeding (+ warfarin), hypoglycemia (+ hypoglycemic agents), ↓absorption (+ antacids)
Metabolism inhibitors pt education
Patient teaching:
Complete the full course of therapy regardless of the presence of symptoms.
Increase fluid intake as tolerated to prevent crystalluria
Instruct pts to monitor s/s liver dysfunction (abdominal pain, anorexia, yellowing skin).
Instruct pats to monitor s/s infection, anemia, and bleeding.
Instruct pts to avoid prolonged sun exposure and use sunscreen, and wear appropriate protective clothing.
Metabolism inhibitors lifespan
Pediatric:
Not give to Infants younger than 2 months (Kernicterus jaundice, increased bilirubinbrain damage)
Pregnancy and breastfeeding:
Category C
Avoid during last trimester of pregnancy and during breastfeeding
Older adults:
Take with thiazide diuretics, increase the risk for anemia and bleeding.
Antibacterial Drug Resistance etiology
Etiology:
Caused by overused, overprescribed, improperly taken antibacterial drugs
Bacteria are more likely to develop resistance to broad than narrow spectrum antibacterial drugs.
Multi-drug-resistant (MDR) organisms (AKA, "superbugs")
Methicillin-resistant Staphylococcus aureus (MRSA)
Streptococcus pneumoniae (menigitis, pneunonia)
Vancomycin-resistant Enterococcus (VRE)
Antibacterial Drug Resistance MRSA
MRSA: Hospital-acquired infections (HA-MRSA),
50% ICU patients,
Skin contact w/ drainage, indwelling catheter, IV line, ET
Pneumonia, abscesses, sepsis, death
Vancomycin (Vancocin), linezolid (zyvox)
Community-acquired MRSA (CA-MRSA)
Direct contact (warm, moist);
Treatment with cipro, clindamycin, gentamicin
Common Virus
Cell parasite:
Live inside cell;
Depend the cell to reproduce;
Utilize the cell's resources, energy, and machinery to multiply new viruses:
More easily enter the human body than bacterium and fungus;
Two types:
Common virus (non-retrovirus): treated by antiviral drugs
Retrovirus: treated by antiretroviral drugs
Antiviral Therapy (common virus)
Virustatic, not killer but suppressor, retard viral growth by preventing reproduction or replication.
Expected effects:
Shorten the duration or intensity of infection;
Prevent reactivation of a dormant viral infection
Prevent a viral infection from multiplying to the point of disease
SE/ADEs:
Allergic reactions
Teaching: take exactly as prescribed to prevent recurrence and resistance
Valacyclovir (Valtrex) and Acyclovir (Zovirax) MOA/use/SE/ADE
Name: -vir-
MOA: Slow viral reproduction by stopping viral DNA production.
Use: Epstein-Barr virus, cytomegalovirus, herpes simplex virus 1 and 2, varicella-zoster virus
Side effects - headache, dizziness, GI upset (N/V/A), malaise (not feeling well)
Adverse effects - Nephrotoxicity, leading to kidney damage and failure, Bone marrow suppression (red, white, purple), phlebitis
Valacyclovir (Valtrex) and Acyclovir (Zovirax) nursing implications/pt education
Nursing implications:
Assess medication history, allergies.
IV form: infuse slowly over 60 minutes
Adequate hydration during and 2 hrs after infusion to minimize nephrotoxicity or increasing oral fluid intake as prescribed.
Rotate IV injection sites and monitor swelling and redness.
Baseline and follow up CBC w/diff and platelet count.
Patient teaching:
Finish the full course of therapy, even though symptoms resolve.
Inform clients to expect symptom relief but not cure.
Emphasize importance of increasing fluid intake
Valacyclovir (Valtrex) and Acyclovir (Zovirax) life span
Pediatric:
Oral dosages for children older than 2 years are similar to adult dosages
Pregnancy and breastfeeding:
Category B
Excreted in breast milk
Older adults:
Dizziness, agitation, confusion
Frequently monitor kidney function
No driving or operating machinery until the drug's effects are known
Amantadine and Rimantadine MOA/use/SE/ADE
MOA: Stop viral reproduction by inhibiting the release of virus into respiratory epithelial cells to multiply
Use: influenza A viral infection
Side effects - dizziness, blurred vision, dry mouth, constipation, orthostatic hypotension,(anticholinergic SE/ADEs)
Adverse effects (amantadine) - CNS sedation, tachycardia, may worsen glaucoma, urinary retention, and depression,
*Rimantadine has fewer nervous system SE, safer
Amantadine and Rimantadine monitor/pt teaching
Pre-Monitor:
Presence of glaucoma, urinary retention, enlarged prostate gland, psychiatric problems (esp. depression with suicidal ideation)
Allergies
Patient teaching:
Dangle and rise slow to prevent dizziness and the risk for falls
Report to prescriber any worsening of depression or thoughts of suicide
Life Span Considerations for Amantadine and Rimantadine
Pregnancy and breastfeeding:
Category C (not for 1st trimester)
Excreted in breast milk (not for nursing women)
Older adults:
Reduce dosage for patients older than 65 years
Can worsen heart failure and increase edema
Weigh daily; report gain of >3 pounds in 2 days
Measure pulse at least once daily; report if irregular or hard to find
Ribavirin MOA/uses/SE/ADE
Suppresses viral action and reproduction
Uses
Refractory viral infections
hepatitis A and C, West Nile virus
Combine with interferon to treat respiratory syncytial virus (RSV) in children with chronic hepatitis C.
Side effects:
GI: N/V/D, Flu-like symptoms, injection site pain or irritation
Adverse effects:
Teratogenic (birth defects), bone marrow suppression
Damaging liver, kidneys, heart, ears, even cancer.
Administering Ribavirin
Pre-Monitor:
Hearing; cardiac, respiratory, kidney, liver functioning
Blood counts and vital signs
Post-Monitor:
Liver, kidney function test, CBC, hearing test
Patient teaching:
Take 1 hr before or 2 hr after antacids
Report allergy or other adverse effects
Life Span Considerations for Ribavirin
Pregnancy and breastfeeding:
Category X
Two forms of contraception
Pregnant nurse should no touch the drug
Older adults:
Increase the risk of liver, kidney dysfunction;
Start lower dosage
Assess for anemia, liver and kidney test
Oseltamivir (Tamiflu) and Zanamivir (Relenza) MOA/uses/SE/ADE/pt teaching
MOA: Stop spreading virus in the respiratory tract by inhibiting the enzyme neuraminidase (neuraminidase inhibitor)
Use: treat and prevent influenza A and B, H1N1flu
Side effects - N/V/D, dizziness, HA, hyperglycemic and liver dysfunction (Oseltamivir)
Adverse effects - breathing problems, confusion and seizures (Zanamivir)
Patient teaching:
*The treatment should be initiated within 48 hr of onset of known or suspected influenza.
*The recommended duration of treatment is 5 days
Flu Vaccination
Nasal-Spray Flu Vaccine:
Live Attenuated Influenza Vaccine (LAIV) should not be given within 2 wks before or 48hrs after Tamiflu
Approved for healthy people 2-49 yrs of age who are not pregnant
Flu shot:
Injected influenza vaccines, or trivalent inactivated (killed) influenza virus vaccines (TIV)
can be given anytime with Tamiflu
Approved for people older than 6 months
**Annual flu vaccine can ↓ risk of flu by 70-90% if well matched
Retroviruses
Always use RNA as its genetic material
Has high efficiency of cellular infection
Human immune deficiency virus (HIV)
Attack human immune system (CD 4+, helper/inducer T-cell)
Most severe case: acquired immune deficiency syndrome (AIDS) CD4+ ≤ 200 (normal: 600-1000)
AIDS patients have HIV infection
HIV infected people not always have AIDS
Opportunistic infections,
Six Classes of Antiretroviral Drugs
Entry inhibitors
Fusion inhibitors
Nucleoside analog reverse transcriptase inhibitors (NRTIs) (RNA DNA)
Non-nucleoside analog reverse transcriptase inhibitors (NNRTIs) (RNA DNA)
Integrase inhibitor
Protease inhibitors (PIs)
Antiretroviral Therapy
Virustatic, not killer but suppressor
Given in "cocktails" (multidrug regimens)
Highly active antiretroviral therapy (HAART) drugs: combo tablets
Reduce # of drug patients have to take daily -> less SE/ADE
Prevent drug resistance
Avoid Tx failure
Be alert to allergic reactions
Post-exposure prophylaxis consists of 4 weeks of antiretroviral therapy.
Antiretroviral Therapy EE/ADE
Expected effects - suppression of viral reproduction
Reduce viral load (# of blood virtual level).
Improve immune function (increase CD4+ count; increase ratio of CD4+/CD8+ ).
fewer episodes of opportunistic infections.
Adverse effects:
Allergic reaction (rash -> anaphylaxis)
Liver toxicity
Hyperglycemia.
Interact with many drugs and food.
Antiretroviral Therapy monitor/pt education
Monitor:
LFT, blood glucose level, CBC
Skin (jaundice, rash, blisters, and itching), blood glucose
Patient education:
Take the drugs exactly as prescribed to prevent recurrence and drug resistance.
No cure, but reduce viral load ;
Many D-D interactions, serious AE.
Call doctor if having yellow skin, dark urine, or light stool (liver toxicity)
Antiretroviral Therapy lifespan
Lifespan Consideration:
Two forms of birth control to prevent an unplanned pregnancy.
Most antiretroviral drugs for HAART are recommended for HIV positive pregnant women
Antiretroviral drugs can cross the placenta to reduce the chances of fetal infection.
HIV positive women should not breastfeed
Entry Inhibitors MOA/uses/SE/ADE/pt teaching
MOA: Decreases and limits the spread of HIV by blocking HIV from binding to the CCR5 receptor on CD4+ T-cells
Uses: treat HIV that is unresponsive to other anti-retroviral drugs
Side effects - flu-like symptoms (fever, chills, muscle aches and pains), rash, GI upset, dizziness, trouble sleeping
Adverse effects - hypotension, liver toxicity,
Patient teaching:
Practice safety regarding low blood pressure (dangle, rise slow)
Monitor and report reactions
Entry inhibitors lifespan
Pediatric:
Not approved for use in children younger than 16 years
Pregnancy and breastfeeding:
Category B
Start in second trimester
Older adults:
Orthostatic hypotension
No driving or operating machinery until the drug's effects are known
Fusion Inhibitors MOA/SE/ADE/pt teaching
MOA: Block viral docking protein from fusing with host cell
Side effects - injection site reaction, constipation, trouble sleeping, depression, muscle aches
Adverse effects - peripheral neuropathy, increased respiratory infections (including bacteria pneumonia), liver toxicity
Patient teaching:
How to do self-injection (SQ, bid)
Signs and symptoms of respiratory infection
Monitor and report respiratory s/s
Life Span Considerations for Fusion Inhibitors
Pediatric:
Drug dosages for children 6 years and older based on weight
Dosages for children younger than 6 years not established
Pregnancy and breastfeeding:
Category B
Start in second trimester
Older adults:
Vision or mobility affect self-injection (involve family members)
Nucleoside Reverse Transcriptase Inhibitors: NRTIs MOA/uses/SE/ADE/pt teaching
Drug name: -vir-, -dine
Oral: Abacavir (ziagen), zidovudine (AZT)
MOA: Reduce viral replication/reproduction by inhibiting reverse transcriptase , lowering viral DNA production, slowing viral reproduction
Uses: HIV infection
Side effects - headache, GI upset with fatty or fried foods
Adverse effects - hepatotoxicity, lactic acidosis, BMS, (red, white, purple), peripheral neuropathy with long-term use
Patient teaching:
Avoid fatty foods and fried foods (pancreatitis)
Loss of sensation increases risk for injury
Stop abacavir if flu-like symptoms develop
Life Span Considerations for NRTIs
Pediatric:
All children w/ HIV-positive should take NRTIs as part of HAART
Dosages for small children usually based on weight
Pregnancy and breastfeeding:
Increased risk for lactic acidosis in pregnancy (muscle ache, tired, lethargic, abd pain, Hypotension, slow irregular heartbeat)
Older adults:
Peripheral neuropathy develops more quickly
Teach tips to prevent injury and falls
Non-Nucleoside Reverse Transcriptase Inhibitors: NNRTIs MOA/uses/SE/ADE/pt teaching
Drug name: -vir-
MOA: Reduce HIV reproduction by inhibiting the reverse transcriptase from converting viral RNA to DNA, lowering viral DNA production.
Uses: HIV infection
Side effects - rash, GI upset, headache, difficulty sleeping, flu-like symptoms (fever, chills, aches)
Adverse effects - anemia, liver toxicity, rash, SJS
Patient teaching:
Notify prescriber of adverse reactions
Take at least 1 hr before or 2 hr after antacids
Keep all medical appointments for blood work (CBC, LFT)
Life Span Considerations for NNRTIs
Pediatric:
All children w/ HIV-positive should take NNRTIs as part of HAART
Anemia more likely
Pregnancy and breastfeeding: B and C
Older adults:
D-D interactions more likely; report all drugs to prescriber
Teach how to take pulse and assess for/report irregularities
Integrase Inhibitors MOA/use/SE/ADE/pt teaching
MOA: Inhibit the enzyme integrase (insert viral DNA into human DNA)
Use: for HIV patients who are on HAART begin to have increased viral load.
Side effects -diarrhea
Adverse effects - anemia, hyperglycemia, rhabdomyolysis (muscle break down)
Patient teaching:
take with food to decrease GI side effects
Report muscle pain and weakness to prescriber
Report symptoms of anemia (pale, fatigue, ↑HR, SOB)
Lifespan considerations for Integrase Inhibitors
Pediatric:
Not approved for use in children younger than 16 years
Pregnancy and breastfeeding:
Category C
Older adults:
More likely to take "-statin" type of lipid-lowering drugs (muscle weakness, falls)
Protease inhibitors (PIs) MOA/use/SE/ADE/pt teaching
MOA: Prevent viral replication and release of viral particles
Uses: used with other antiretroviral medication to reduce medication resistance
Side effects - headache, GI upset, difficulty sleeping, and weight gain
Adverse effects:
Liver toxicity, increased lipid and glucose levels
Uncontrolled bleeding in patients with hemophilia
Some impair electrical conduction (heart block)
Some contain sulfa
BMS and depression
Patient teaching:
Check pulse twice daily for a full minute
Life Span Considerations for PIs
Pediatric:
HIV-positive children older than age 6 years take PIs as part of HAART
Dosages for older children are nearly the same as for adults
Optimal dosages are unknown for infants and children younger than age 6 years
Older adults:
Drug interactions more likely; report all drugs to prescriber (cardiac drugs, lipid-lowering drugs)
Teach how to take pulse and assess for/report irregularities
Who is at Risk TB?
Constant, frequent contact with a person w/ TB
Immuno-compromised (HIV, AIDs, CA/chemo)
Living in crowded areas (long-term care facilities, prisons, mental health facilities)
Older adults
Abusers of injection drugs or alcohol
Lower socioeconomic groups (no insurance or limited finances, homeless )
Foreign immigrants (esp. from Mexico, Philippines, Vietnam)
Tuberculosis (TB)
How to Dx?
Active TB is diagnosed by chest x-ray, blood assay to test for the TB organism, and sputum culture (When?)
Challenges to Treat TB:
Highly communicable disease because spread by aerosol transmission (droplets)
Impermeable cell
Very slow-growing, requiring long-term and combo-therapy
Living in macrophages (intracellular bacteria)
Antitubercular Drug Therapy
First-line antitubercular drugs (different combinations and schedules) Primarily bacteriostatic
Rifampin (RIF): RNA synthesis inhibitor
Isoniazid (INH): cell wall synthesis inhibitor
Pyrazinamide (PZA)
Ethambutol (EMB): cell wall synthesis inhibitor
Streptomycin: PSI-Aminoglycoside
Antitubercular Drugs EE/SE
Expected effects: Improved s/s (cough, sputum, fatigue, breath sounds, night sweats and afternoon fever), negative sputum culture
Side effects: GI upset (N/V/A/abd discomfort)
Rifampin: reddish-orange urine/tears, urinary retention
Isoniazid: enlarged breast in men , difficulty concentrating, sore throat
Pyrazinamide: acne, photosensitivity
Pyrazinamide and ethambutol: ↑uric acid (gout)
Antitubercular Drugs ADE/nursing implications
Adverse Effects:
Rifampin: liver enzyme inducer (DDI), hepatotoxicity
Isoniazid: Peripheral neuropathy (B6) , hepatotoxicity, CNS toxicity
Pyrazinamide: Hepatotoxicity
Ethambutol: Optic neuritis (high doses), red/green color blind
Streptomycin: ototoxicity and nephrotoxicity
Nursing Implications:
Compliance issues: watches pt swallow the pills (DOT)
Vital signs (when giving IV)
Monitor mental status, renal /liver functions, vision and hearing, PN
Administering Anti-tubercular Drugs pt teaching
Patient teaching:
Keep supply of prescribed drugs on hand at all times
Continue taking drugs for at least 6 months exactly as prescribed!
Take Vit B6 when taking Isoniazid
Not to take Rifampin with other drugs TOGETHER
No OTC drugs, including herbal supplements, unless approved by prescriber
Drink adequate fluid to prevent gout
Monitor s/s liver dysfunction, have liver /kidney function checked periodically
Regular eye and hearing exam
INH is the drug of choice for the family member of TB patients
Life Span Considerations for Anti-tubercular Drugs
Pediatric:
All infants and children who have active TB should take first-line anti-TB drugs (except ethambutol)
Dosages for larger children nearly the same as for adults
Pregnancy and breastfeeding:
First-line anti-TB drugs approved for treatment of active TB , but not prevention,
Secreted in breast milk (avoid breastfeeding)
The risk for liver toxicity is higher when taking anti-TB drugs during pregnancy
Pregnant women need higher doses of a B-complex vitamin supplement when taking INH.
Older adults:
Higher risk for liver toxicity; monitor for jaundice, dark urine and light stools
Higher risk for drug interactions
Gout more common (PZA and EMB);
Drugs that interact with TB drugs include anti-hypertensives, cardiac drugs, and lipid-lowering drugs.
Fungus and its Infection
Challenges to treat fungal infections
Share similar cell structure as human cells
Tough and thick cell walls
Survive easily on human body surfaces
Most are normal flora (not causing problems unless overgrowing or entering the body)
Drugs have more SE/ADEs than antibacterial drugs
Two types of fungal infections:
Superficial : skin, mucous membranes, caused by overgrowth of Candida (e.g., thrush in mouth, yeast infection on skin and vagina)
Deep: systemic, internal organs are affected
Antifungal Drugs types/MOA
Types by action:
Fungicidal
Fungistatic
MOA: Antifungal drugs damage cell membranes and cell walls to prevent the fungus reproduce or kill it.
Azoles, polyenes, allylamines: damage cell membrane
Antimetabolites: block protein production;
Echinocandins: glucan synthesis inhibitor
Antifungal Therapy SE/ADE
SE/ADEs:
Infusion reactions: "shake and bake"
Taste changes, GI upset
Hair loss
"azoles" have photosensitivity
Bone marrow suppression (red, white, purple )
hypokalemia
Hepatotoxicity
Nephrotoxicity
Stevens-Johnson syndrome (SJS)
Dysrhythmias (azoles) prolonged QT interval
Peripheral neuropathy
Thrombophlebitis
Nursing Implication and Patient Education for Antifungal Therapy
Implications:
Assess: VSs, s/s cardiac, liver and renal dysfunction
Cardiac monitor and lab work (CBC w/diff, CMP, LFT, Cr, BUN)
Administer IV forms SLOWLY and monitor IV sites
Patient teaching:
Complete the full course of therapy even though symptoms resolve .
avoid crowds and people who are ill.
Report rashes, blisters.
Use sunscreen with "azoles"
Vaginal suppository or cream is used to treat superficial vaginal candidiasis.
Life Span Considerations for Antifungal Drugs
Pediatric:
Safety and effectiveness not established
Pregnancy and breastfeeding:
Not recommended
Older adults:
More likely to have renal insufficiency
Higher risk for liver toxicity; monitor for jaundice
Higher risk for drug interactions
Higher risk for deep vein thrombosis