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129 Cards in this Set
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What to do if BP is too high or too low
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If it's too high, we can use:
- Angiotensin-Converting Enzyme (ACE) Inhibitors - Angiotensin II Receptor Blockers (or Inhibitors) - Beta Blockers - Calcium Channel Blockers - Diuretics If it's too low, we can: - Have blood pressure medications or diuretics adjusted, changed, or stopped by the doctor if they are causing low blood pressure symptoms. - Improve postural hypotension by making changes in diet such as increasing water and salt intake, increasing intake of caffeinated beverages (because caffeine constricts blood vessels), using compression stockings to compress the leg veins and reduce the pooling of blood in the leg veins. - Treat dehydration with fluids and minerals (electrolytes). |
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Some chronic medical conditions help direct which antihypertensive agent is used or not used: Peripheral-acting Alpha Adrenergic Blocker
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Bening Prostetic Hyperplasia (relaxes bladder's sphincter & patients are able to urinate)
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Some chronic medical conditions help direct which antihypertensive agent is used or not used: DIURETICS
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Thiazides: Indicated for treatment of HYPOcalcemia.
Thiazides: Contraindicated for renal disease, gout, diabetes, hyperlipidemia (Elevate uric acid and lipids) Mannitol: Should not be used with Renal or cardiac dysfunction! Furosemide: Can be used with patients with low GFR! Spironolactone: Prevention and treatment of hypokalemia, edema especially in liver failure and adrenal disease issues. Decreases effects of anticoagulants Patients who use Digoxin (which Tx Atrial fib, Atrial flutter, or HF) should NOT use Diuretics. |
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Some chronic medical conditions help direct which antihypertensive agent is used or not used: BETA BLOCKERS
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If the patient has allergies and uses epinephrine to treat them, the BB will interfere with epinephrine's efficacy.
Also, OTC ephedrine might cause uncontrolled alpha constrtiction and lead HTN due to baroreceptor reflex. |
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Some chronic medical conditions help direct which antihypertensive agent is used or not used: CALCIUM CHANNEL BLOCKERS
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CCB can make renal & heart failure worse.
Patients with renal or hepatic dysfunction may have a reduced clearance of the drugs |
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Some chronic medical conditions help direct which antihypertensive agent is used or not used: Angiotension Converting Enzyme (ACE) Inhibitors
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Treats essential HTN with normal renal function
However, ACE-I are renal protective in diabetics! They are used even if diabetics don't have HTN to protect renal function. For HF patients it can be used with Digoxin (which Tx Atrial fib, Atrial flutter, or HF) and diuretics! |
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Some chronic medical conditions help direct which antihypertensive agent is used or not used: Angiotensin II Receptor Blockers (ARBs)
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Direct Renin Inhibitors are the drugs of choice for patients who are allergic to ACE-I and have developed angioedemas or coughs.
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Patient education for HTN drugs: DIURETICS
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Postural hypotension & hypovolemia for ALL OF THEM!
DIURETICS: -Urine will increase for a few weeks but the drug is still needed. Patients may stop or self-increase the dose. - Voiding at inopportune times: tailor schedule to lifestyle, don’t take late in the day - Diet: Low or controlled salt intake. More likely to need K supplements. Must drink water! - Adherence: Symptomless, feel cured, perceive SE as worse than HTN - SE: Hypovolemia, Fall risk! |
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Patient education for HTN drugs
ACE-I |
ACE-I:
– Full effects not seen for several weeks – Taste impairment disappears in 2-3 weeks – Cough not indicative of lung disease – Do not use in renal artery stenosis – Do not use K supplements or susbstances containing large amounts of K (i.e., saltsubstitutes, low-sodium milk) – Do not use with pregnancy (no blood to fetus) |
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Patient Education for HTN drugs. CALCIUM CHANNEL BLOCKERS
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CALCIUM CHANNEL BLOCKERS:
–If extended release form do not chew or crush –Take HR before dose, must be at least 45 –Can make heart failure worse –Support hose/elevation of legs |
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Patient Education for HTN drugs. BETA BLOCKERS
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BETA BLOCKERS:
–Don’t alter the drug regimen. DON'T STOP MED: Rebound HTN! -–Check pulse: if < 45, don’t give |
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How can you tell if a med is working or toxic: DIURETICS
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Signs of hypovolemia: Dizziness, confusion, insatiable thirst, salt
craving Signs of hypokalemia: Thirst, muscle weakness, lethargy, depression, muscle cramping, vomiting Furesomide: HEARING LOSS! |
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How can you tell if a med is working or toxic: Cardiac Glycoside (Digoxin)
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– early toxicity: n/v, vision changes
– late toxicity: dysrhythmias due to progressive heart block |
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How can you tell if a med is working or toxic: Anti-Dysrhythmics
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All antidysrhythmics have the potential to worsen the dysrhythmia or create a new one. Thus, EKG is the only way to assess if the drug is effective. It is also important to monitor all body systems, not just the CV system. Patients taking antidysrhythmics should take their HR for 1 full minute before dose.
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What labs need to be watched with different meds? ( HTN, anticoags, diuretics, lipids etc)
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- Diuretics: Monitor potassium levels!
- Glycosides (Digoxin): Monitor drug & potassium levesl! Low K, increases dig binding! Resulting in ↑HR. Hypokalemia and hypomagnesemia increase risk of toxicity, whereas hyperkalemia and hypercalcemia may produce dysrhythmias - Anti-dysrhythmics: EKG is the only way to make sure drug is working. - Anti-lipid Therapy: Conduct Liver Function Tests (LFT) to prevent liver damage from statins. Also do CK tests to measure muscle breakdown with these same drugs. - Anticoagulants: When using Heparin, monitor activated partial thromboplastin time (aPTT) frequently! When using Warfarin, monitor prothrombin/International Normalized Ratio (PT/INR) monthly! If dosage is changed, then weekly. |
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Concepts of antirhythmic drug care and nursing implications
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Antiarrhythmic medicines slow the electrical impulses in the heart so that it can resume its normal rhythm and conduction patterns. The four different ways these medicines work are:
• Class I antiarrhythmic medicines are sodium channel blockers, which slow electrical conduction in the heart. • Class II antiarrhythmic medicines are beta blockers, which block the impulses that may cause the irregular rhythm and interfere with hormonal influences (such as adrenaline) on the heart's cells. This type of antiarrhythmic also reduces blood pressure and heart rate. • Class III antiarrhythmic medicines are potassium channel blockers, which slow the electrical impulses in the heart. • Class IV antiarrhythmic medicines are calcium channel blockers, which work like class II medicines. Because each kind of antiarrhythmic medicine works in a slightly different way, no one medicine is used to treat every kind of arrhythmia. An antiarrhythmic medicine can sometimes cause more arrhythmias or make an arrhythmia worse (called proarrhythmia). A patient and his or her doctor must work closely together with good communication to try out the different kinds of antiarrhythmic medicines and determine which medicine works best for that patient. This process may include additional monitoring or testing |
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Anti-lipid therapy and patient education
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The primary safety concern with statins is an uncommon condition called myopathy, in which a patient may experience muscle pains and certain lab tests may be elevated. A specific myopathy, called rhabdomyolysis, can lead to kidney failure, but fortunately its occurrence is very rare. The risk for myopathy/rhabdomyolysis is highest at higher doses and in older people (over 65 years), those with hyperthyroidism, and those with renal insufficiency (kidney disease).
In general, all statin therapy should start at a lower dose and be raised incrementally until healthy cholesterol levels are maintained. Patients should immediately tell their doctor about any unusual muscle discomfort or weakness, fever, nausea or vomiting, or darkening of urine color. Statins can also affect the liver, particularly at higher doses, so patients should have periodic liver function tests. Anyone with liver problems and women who are pregnant or breastfeeding should not use statins. |
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Anginal meds use and precautions, patient education
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There are currently four types of medicines used to treat stable angina:
Nitrates Beta blockers Calcium channel blockers Ranolazine Nitrates or beta blockers are usually preferred for initial treatment of angina, and calcium channel blockers may be added if needed. The number and type of medicines used are often tailored to how frequently angina occurs in an average week. One or fewer — People who have one or fewer angina episodes per week are usually advised to take sublingual (under the tongue) nitroglycerin when an episode of angina occurs and immediately before activities that could cause angina. Two or more — People who have two or more angina episodes per week are usually advised to take longer-acting antianginal medicines. This may include a long-acting nitrate or a beta blocker. Treatment with added medicines — If angina persists while taking one medicine, a second medicine may be added. Combined treatment may relieve angina more effectively than a single medicine. If angina persists on two medicines, a third medicine or coronary angiography may be recommended. Angiography can help determine how severe coronary artery disease is and if a stent or bypass surgery is needed. |
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So which drug works where in the heart to do what?
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1. Improve Cardiac Contractability
- glycosides & ace inhibitors 2. Decrease Preload - diuretics 3. Decrease Afterload - vasodilators 4. Ventricular Restructuring and Rate Control - BB |
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How DIURETICS work
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•Major site of action is the kidney nephron
•All interfere with reabsorption in the tubules of the kidney. •Because Na is so prevalent in dietary intake, Potassium is the electrolyte of greatest fluctuation that we must monitor •Also affect Ca, glucose, and uric acid. •Those that block reabsorption of Na from the tubules produce the greatest amount of water loss: Proximal & loop drugs more powerful than distal drugs in reducing fluid |
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DIURETICS TX
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HTN
CHF (edema) Cirrhosis Cerebral & Pulmonary Edema |
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DIURETICS SE
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Hypovolemia
Hypokalemia/Hyperkalemia Hypoclacemia/Hypercalcemia Hyperlipididemia Hyperglycemia in DB OD: Hypotension r/t hypovolemia Potassium imbalances can lead to cardiac dysfunction |
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Four types of Diuretics
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–Osmotic (mannitol)
–Loop (furosemide) –Thiazide (hydrochlorothiazide) –Potassium sparing (spironolactone, triamterene) |
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Mannitol
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Osmotic
Tx: IV agents for cerebral edema (intracranial pressure) Wks: Pharmacologically inert 6 carbon sugar molecule that keeps H2O in the tubule. SE: Edema (drug can leave all capillaries, except in the brain). Can increase intracranial bleeding. To consider: Crystallizes. Heat 1st. Needs a filter. Nursing: Always measure urine output. Empty foley 1st then administer. |
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Furosemide (Lasix)
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Loop
Tx: Significant edema (CHF, cirrhosis, renal disease), HTN Stronger than thiazides Note: Ok for pts w/renal failure! Less effect on lipids! SE: Postural and general hypotension, OTOXICITY! D-D: No DIGOXIN (dysrhythmias!), No NSAIDs (Interfere w/drug) RN: No SULFA allergies! (anaphylaxis!) If allergy is not severe, can use in ER. |
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Hydrochlorothiazide (HCTZ)
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Thiazide
Tx: HTN, Edema, hypocalcemia Note: Less powerful than loop Wks: Inhibits Na and Cl reabsorption in early distal tubule SE: Same for all Diuretics Consider: Not good for pts w/renal insufficiency! RN: No SULFA allergies! (anaphylaxis!) If allergy is not severe, can use in ER. |
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Sumatriptan
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Sumatriptan is a triptan sulfa drug containing a sulfonamide group. It is used for the treatment of migraine headaches.
Please note that Hydrochlorothiazide is a sulfonamide with a similar molecular structure to this drug. These drugs should not be given to patients w/severe sulfa allergies. |
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Spironolactone (Aldactone)
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Potassium-sparing
Note: Low potency. Modest urine output so used in conjunction w/other Diuretics Tx: Hypokalcemia, HTN, liver disease r/t aldosterone blockage Wks: Antagonist of aldosterone. Gets rid of Na and keeps K. Pump reversal. SE: Like Diuretics. Gynecomastia, menstrual irr, impotence. D-D: ACEi, Salt subs, K supplements & rich foods, decrease anticoagulant effects |
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Clonidine (Catapres)
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Central-acting Sympatholytics stop SNS stimulation in the brain & subsequent outflow to periphery. Block of alpha 2 receptors inhibits NE release.
Tx:Moderate hypertension SE: Same as general ones plus high risk for rebound HTN if drug abruptly withdrawn. This is the reason, clonidine is a SECOND LINE AGENT. It produces ortho hypotension (↓BP, ↑HR). Also, psychiatric disturbances OD: Toxic dose stimulates alpha 1 & produced HTN! D-D: Unknown mechanism induced HTN with Beta Blocker! |
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Peripheral-acting Alpha Adrenergic Blocker
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Wks: Blocks alpha1 receptors (alpha1 stimulation =
vasoconstriction), result is vasodilation and ↓ peripheral vascular resistance. Less cardiac effects because no beta action. Tx: hyperlipidemia, and BPH (relaxes bladder's sphincter & pt's are able to urinate). Step II HTN drug because of SE (ortho hypot). RN: Drug causes ortho hypotension with the first dose! Instruct to take at night, before bed. |
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Prazosin
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Wks: Selective alpha 1 adrenergic antagonist/blocker. Dilates arterioles and veins and relxes smoth muscle in the neck bladder and prostatic capsule.
Tx: Approved only for HTN, but benefits men with Benign Prostatic Hyperplasia (BHP) SE: Orthostatic Hypotension, Reflex tachycardia RN: Patients can faint with first dose or experience hypotension. Start with small doses! |
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Angiotension Converting Enzyme (ACE) Inhibitors. How they work.
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–Completely blocks the angiotensin I converting enzyme
–Prevents the production of angiotensin II which is a powerful vasoconstrictor –Decreases vascular tone –Absence of aldosterone release leads to excretion of fluid –Renal protective in diabetics |
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Angiotension Converting Enzyme (ACE) Inhibitors. TREAT
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–Essential HTN with normal renal function
–Often used with a thiazide or loop diuretic •counteracts K retention of ACE –HF: used with digoxin and diuretics. STOPS Heart remodeling after initial damage! –Diabetes •For renal protection even without HTN |
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Angiotension Converting Enzyme (ACE) Inhibitors. SE
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– Hyperkalemia (Can elevate K!)
– Dry cough (occurs in about 1/3 of patients) – Angioedema!!!! (if pt develops, he cannot ever be on ACE-I's!) |
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Angiotension Converting Enzyme (ACE) Inhibitors. Education
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– Full effects not seen for several weeks
– Taste impairment disappears in 2-3 weeks – Cough not indicative of lung disease – Do not use in renal artery stenosis – Do not use K supplements or susbstances containing large amounts of K (i.e., salt substitutes, low-sodium milk) – Do not use with pregnancy (no blood to fetus) |
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Beta Blockers. How they work
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• Receptors
– Beta1—referred to as cardioselective because they block receptors in the heart – Beta2—primarily in smooth muscle & lungs • Action (blockade of beta1) – Decreases HR, conduction, contractility, and cardiac output – Inhibits renin release by the kidney – Reduces myocardial oxygen demand – Decreases peripheral vascular resistance which lowers BP • Action (blockade of beta2) – Bronchoconstriction • Patients with asthma, CHF, emphysema at risk – Should use cardioselective agent – Masks symptoms of acute hypoglycemia and hyperthyroidism |
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Propranolol (Inderal)
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Selective Beta Blocker: (-olol)
Wks: Decreases cardiac contractility (negative inotropic effect) which drops arterial pressure and inhibits renin release Tx: – HTN – Chronic angina (balances O2 supply and demand) – Treat cardiac dysrhythmias – **Prevent a second MI (Decreases O2 demand) – Treat vascular HA – Tremors – Anxiety/Stage fright: ↓HR |
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Beta Blockers. SE
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–Negative chronotrope
–Negative inotrope –Negative dromotrope Bradycardia, fatigue, drowsiness, anxiety, difficulty breathing, GI sx, impotence, cold hands and feet, depression |
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Beta Blockers. D-D
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Blocks action of sympathomimetics (epi)
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Beta Blockers. Education
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•Education
–Don’t alter the drug regimen •consistently take with food or without food –No OTC decongestants and cough and cold meds with pseudoephedrine/phenylprine –How to avoid orthostatic hypotension –Weight and diet management –Check pulse: if < 45,don’t give –Monitor for signs of depression –Should be on one post MI! |
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Beta Blockers. RN Considerations
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•Rebound hypertension
•When body has HTN meds on board and they are suddenly stopped –Massive sympathetic “rescue” causes rapid HR and high BP |
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Digoxin (Lanoxin)
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Digitalis (Cardiac Glucosides)
Wks: As a positive inotrope, negative chronotrope and negative dromotrope Tx: HF, dysrhytmia (Atrial fib or Supraventricular d.) SE: –cardiac: bradycardia, AV block, other rhythm disturbances –GI: n/v, anorexia –vision: green/ yellow tint to white objects, HALOS around lights (usually not tiltoxic) RN: Low therap. range. Long T1/2! Take Apical Pulse, if less than 40 bpm, hold drug! Digitalization: Higher doses at first; then typical doses D-D: – drugs that reduce absorption or decrease fxn • antacids, laxatives, cholesterol-lowering agents, ACE/ARB – drugs that depress cardiac function • beta blockers, calcium channel blockers – hypokalemia: Diuretics! Low K increases dig binding = ↑HR • the most common cause of dig overdose • even therapeutic levels may be too high if K is low |
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Immune Fab (Digibind)
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If DIGOXIN Toxicity develops, DIGIBIND is the antidote:
Immune Fab ( Digibind) binds with molecule and then is excreted by kidney. As more tissue molecules are released into the bloodstream (diffusion), more binding takes place |
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Nitroglycerin (NTG)
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Organic Nitrate Vasodilator for short & long Tx
Wks: -Vasodilates vessels in the periphery and decreases workload of the heart –Dilates coronary arteries improving blood flow (does not dilate plaque covered, damaged vessels) Tx: Angina SE: HA, HYPOTENSION, Reflex tachycardia RN: Nitro will bind to IV tubing during an emergent MI or severe angina. Must use special tubing & glass bottle. Run through pump! Monitor BP! High fall risk! Also, wear gloves if using ointment! D-D: all antihypertensives & sympathomimetics, sildenafil (VIAGRA) |
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Anginal meds use and precautions, patient education
NITRO |
For Emergent Chest Pain: Sublingual tablet, wait 5 min; if pain continues, can repeat with second and third dose. If CP continues after second dose, call 911 (used to be 3 doses)
Allow to dissolve slowly, don’t eat, drink, or smoke. Patient should feel tingling sensation under tongue, if not present the drug may have lost its potency. Drug needs to be airtight light resistant. Once opened, expires in 6 mos. Temperature sensitive. HA & ortho hypotension expected |
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Propanolol
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Non-selective Beta Blocker. Affinity for all beta receptors
Tx: Angina, for PROPHYLAXIS only, not short term tx. If MI, reduce infarct size and short term mortality RN: Worsens vasospastic angina! Don’t stop drug abruptly! |
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Calcium Channel Blockers
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Tx: Prevention of Vasospastic angina (more common in females)
•Action –decreases myocardial contractile force (negative inotropic effect) –decreases HR (chronotropic effect) –decreases automaticity (dromotropic effect) –decreases VASOCONSTRICTION in coronary and systemic circulations, which explains why CCBs are effective in vasospastic angina |
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If you have MI, HA or HTN you should be on...
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Either a CCB or a BB!
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Beta Blockers - Dysrhytmias
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Tx:
-Ventricular dysrhythmias (shown to be particularly effective with post-MI dysrhythmias) -HTN -Hyperanxiety (stage fright) -hyperthyroid (racing heart) |
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Concepts of antirhythmic drug care and nursing implications: Types of drugs.
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Group I: fast sodium channel blockers
Group II: β blockers Group III: potassium channel blockers Group IV: calcium antagonists |
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Concepts of antirhythmic drug care and nursing implications: Sodium channel blockers
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Quinidine & Lidocaine
Wks: slow depolarization and repolarization in the atria, ventricles, and His-Purkinje system. Stabilizes cell membrane, prevents influx of sodium, result is depression of conduction velocity thru SA and AV nodes. Tx: Long-term prophylaxis of supraventricular rhythms, often used after atrial flutter or atrial fibrillation RN: Low Margin of safety (narrow window). Measure width of QRS! Stop drug if increases by 50%. Increases risk of Digoxin toxicity: Monitor for heart block! SE: tremors, twitching, blurred vision, tinnitus |
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Concepts of antirhythmic drug care and nursing implications: Beta Blockers
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Beta Blockers
Tx: -Ventricular dysrhythmias (shown to be particularly effective with post-MI dysrhythmias) -HTN -Hyperanxiety (stage fright) -Also hyperthyroid (racing heart) |
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Concepts of antirhythmic drug care and nursing implications: Potassium Channel Blockers
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Delay Repolarization
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Amiodarone (Cordarone)
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Potassium Channel Blockers
Wks: Prolongs action potential, increases the refractory period in all cardiac tissues resulting in decreased automaticity, prolonged AV conduction, blocks sodium, potassium, and calcium channels. Tx: Life-threatening ventricular dysrhythmias. Use for resuscitation and supraventricular d. SE: Pulmonary fibrosis, thyrotocixosis. BLUE-GRAY skin color. |
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Concepts of antirhythmic drug care and nursing implications: Calcium Channel Blockers
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Tx:
-SupraVentricularTachycardia -HTN SE: HA, nausea, dizzy, flushing, edema, tachy. Flushy & edema due to the vasodilation. |
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Concepts of antirhythmic drug care and nursing implications: Other drugs
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Adenoside (Adenocard)
Atropine Digoxin |
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Adenoside (Adenocard)
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Adenosine is a natural constituent of muscle tissue.
Wks: Slows AV node conduction. It actually stops the heart briefly! Resets the heart! Tx: PSVT (paraoxsysmal supraventricular tachycardia) SE: Chest pain RN: Short t1/2 - 6 s so you must infuse fast (under 3 s). Use 2 injections in central line: one w/saline, one w/drug: Helps push medication fast & close to the heart |
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Atropine
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Wks: Action is anticholinergic effect, blocks vagal stimulation and increases HR (increases conduction thru the AV node)
Tx: Bradycardia |
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Digoxin
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Wks: Action is to slow HR and improve conduction and increase contractility
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What are the 2 main Anti-lipemic Agents?
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1.Bile acid sequestrants
2.Cholesterol synthesis inhibitors: HMG-CoA inhibitors (STATINS) |
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Cholestyramine (Questran)
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Bile acid sequestrant
Tx: Hyperlipidimia, ↑LDL Wks: Binds with bile (made by liver to help digest fats) so it cannot be reabsorbed and is excreted in feces. Body responds by making more cholesterol and bile than before. However, loss is greater than gain so decreases cholesterol. SE: Constipation, No fat sol. vitamin abs., farts, n/v, abd pain: Brown Baby! It also tastes BAD. D-D: Binds with other meds! Affects their abs. Binds with Dig! Thus, helps w/Dig OD! |
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LovaSTATIN
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Most effective drugs to lower LDL!
Wks: Inhibits critical enzyme in formation of cholesterol thus decreasing total cholesterol, LDL, and triglycerides while also increasing HDL Tx: Primary hyperlipidemia which does not respond to diet alone SE: HA, GI disturbances, myalgia (can progress to MUSCLE DAMAGE, as well as drug induced LIVER DYSFUNCTION (use with care in presence of liver disease or chronic alcoholism) D-D: GRAPEFRUIT RN: Due to possible liver & mm damage, start at low dose! Also, all statins are in pregnancy category X |
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Differences between Lovastatin & Pravastatin?
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Lovastatin's absorption increases when taken with food, whereas absorption of pravastatin decreases when taken with food.
Also, all statins are extensively bound to plasma proteins with the exception of pravastatin, which is about 50% bound to plasma proteins, making it less likely to displace albumin-bound drugs, such as warfarin. All statins are subject to extensive first-pass metabolism with the exception of pravastatin. Pravastatin does not undergo extensive CYP450 metabolism, which can increase a drug's likelihood of producing muscle toxicity due to drug interactions. Lipophilic statins (lovastatin) undergo hepatic and enteric metabolism via the cytochrome P450 (CYP450) system Water soluble statins (pravastatin) are excreted largely unchanged these statins are minimally metabolized by the cytochrome P450 enzyme system before elimination. Pravastatin has therefore been not shown to participate in any clinically relevant drug-drug interactions with CYP450 agents Pravastatin is eliminated primarily in the feces, whereas lovastatin is eliminated in the bile. |
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Anti-lipid therapy and patient education
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Muscle degeneration can result from statin therapy. Therefore, patients should be instructed to inform provider about unaccounted mm pain.
The muscle breakdown into components can block the renal glomerulus and lead to renal failure and possible death. Meds should not be taken if unaccountable muscle aches or pains are present. Also, statins mixed with other anti-lipemics are more likely to have issues since the stronger the statin the more risks. |
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Anticoagulants
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Therapy is primarily prophylactic to prevent fibrin deposits, extension of a thrombus, or thromboembolic complications.
Its action is to decrease blood coagulability. Two forms are available: injectable--rapid acting, temporary or oral--long-term therapy |
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Anticoagulant types (5)
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1. Platelet aggregation—ASA, clopidogrel
2. Interruption of coagulation pathway--heparin 3. Indirectly by decreasing formation of several clotting factors--warfarin 4. Dissolve clot after formation—streptokinase 5. Inhibition of thrombin- dabigatran |
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Aspirin
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Aspirin besides being an analgesic, anti-pyretic, and anti-inflammatory also has an antiplatelet effect by inhibiting the production of thromboxane, which under normal circumstances binds platelet molecules together to create a patch over damaged walls of blood vessels. Because the platelet patch can become too large and also block blood flow, locally and downstream, aspirin is also used long-term, at low doses, to help prevent heart attacks, strokes, and blood clot formation in people at high risk of developing blood clots. It has also been established that low doses of aspirin may be given immediately after a heart attack to reduce the risk of another heart attack or of the death of cardiac tissue.
Tx: Prophylaxis for MI in patients with angina or history of MI and Transient Ischemic Attack (TIAs) or Cerebro-Vascular Accident (CVA) One 325 mg tablet can double bleeding time for up to 7 days--it takes that long to make new platelets! Note: Anti-platelet agents are best for prevention of ARTERIAL CLOTS. |
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What are the contraindications for anticoagulants?
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Active hemorrhage
Recent hemorrhagic stroke Recent surgery Hemophilia Pregnancy (although Heparin can be used by pregnant pts!) Recent abortion/miscarriage |
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Heparin (UFH = Unfractionated Heparin)
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Parenteral Anticoagulants (administered SC or IV)
NOTE: It does not dissolve clots. It only prevents them! Wks: Direct blocking of intrinsic pathway clotting cascade, helps antithrombin inactivate factor Xa and thrombin. Tx: Prophylactic anticoagulation--low dose for high risk patients undergoing procedures with a high degree of blood loss; Full dose anticoagulation--for DIC, embolism or thrombus management. SE: Bleeding--GI, GU; allergic reactions to animal product; & Heparin induced thrombocytopenia (HIT) = Body generates Abs against drug. Pt's can lose their digits! D-D: Agents that increase bleeding, mainly ASA RN: Monitor aPTT frequently! Heparin effect starts quick & stops just as quickly! Therefore, observe RN protocol to determine whether to continue current dose, hold for a period or increase the drip/titration rate. Note: Heparin is measured in unit not ml/hr! |
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Protamine Sulfate
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If Heparin Toxicity develops:
The aPTT will be too prolonged leading to pt bleeding to death. Stop administering and give antidote: protamine sulfate (has a strong positive charge which binds with heparin’s negative charge) |
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Low-molecular-weight Heparin
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Wks: Inactivates factor Xa
Tx: Prevention of Deep Venous Thrombosis (DVT) post-op (hip, abd, knee); treatment of established DVT; and unstable angina SE: Local erythema, pain, hematoma at injection site |
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Differences between low and unfractionated heparins and warfarin; how and when they are used and precautions
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With UFH, the loading dose is followed by frequent aPTT labs. This is not the case with low-mw-heparin, which does not require blood monitoring. Also, UFH is given through IV or SC (parenterally only) for faster acting, whereas low-mw-heparin is longer acting (24 hrs). The pt can be taught to self-inject w/preloaded syringes (although not IM as hematomas can develop w/either heparin). Even though Low-mw-heparin is more expensive, UFH saves in lab work, hospitalization and less RN care.
Warfarin is longer acting than Heparin. Therefore, heparin is usually used to start therapy in conjunction w/warfarin. Heparin's effects are seen earlier. Warfarin doses are based on monitoring of PT/INR. Heparin's are based on aPTT. The INR can be checked once a week for Warfarin if there has been a change of dose, if not in 1-6 mos. This is because Warfarin is long acting (2-5 days) and changes are not seen as fast as with Heparin (<4 hrs). Also heparin is given parenterally, whereas Warfarin is given orally. Heparin's antidote is Protamine Sulfate. Warfarin's is Vitamin K. Finally, heparin influences the intrinsic system in the clotting cascade, whereas warfarin influences the extrinsic system. |
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What are Heparin's bleeding precautions?
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-Pt should consider having an Electric Razors
-Gums will bleed when brushing teeth -Small bump can be BIG trouble -Pain in joint can bleed -Longer than normal for hemostasis for injections and venipunctures |
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Warfarin (Coumadin)
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Oral Anticoagulant
Wks: does not work in the blood but in the liver to inhibit synthesis of vitamin K dependent clotting factors (VII, IX, X, and prothrombin) Tx: Long-term prophylaxis and treatment of venous and arterial thrombosis or pulmonary embolism, adjunctive tx for prevention of MI or Transient Ischemic Attack (TIA) recurrence SE: Bleeding; decreased dietary Vit K intensifies effect, increased Vit K decreases effect. D-D: Anticoagulants react with EVERYTHING! RN: -Long t1/2 (36 hrs). -Increased bleeding, can usually control by omitting one or two doses of the drug, don’t stop abruptly! -Antidote is Vitamin K! Not K+ = potassium! |
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Why are Heparin & Coumadin often used together?
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Coumadin takes days to have any effect. Therefore, Heparin is almost immediate (1.5 hours).
If on heparin drip, expect to start Coumadin at the same time. Heparin inhibits thrombin; Coumadin inhibits synthesis of Vit K dependent clotting factors They are not substitutes for each other! |
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Thrombolytic Therapy
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Thrombolytics are CLOT BUSTERS, unlike heparin or warfarin.
The prototype is streptokinase (Streptase), which comes from beta hemolytic strep. Wks: Reacts with plasminogen found in clots and converts it to plasmin which dissolves the clot Tx: Pulmonary or systemic emboli or thrombi; acute MI; Unblocks central IV lines! SE: Allergic rxn, hypotension D-D: ASA (Relative contraind), NSAIDs, and anticoagulants RN: -Only parenterally, destroyed in GI. -Monitor for subtle bleeding (tarry stools/pink urine, joints swelling). If notice change of LOC, STOP drug! LOC = Cranial bleeding! -Insert tubes 1st, then administer. Otherwise, BLEEDING! -Anticipate hemorrhages! |
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Oral iron supplements
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Note: Iron sulfate is the most common. Only 60% of iron is absorbed w/supplements.
Tx: Anemia SE: Upset stomach and constipation. If gastritis from another source (ulcers, ETOH) can worsen it; rheumatoid arthritis worsens OD: Toxic for children! Too much iron, has anemia S/S: Fatigue, aches RN: For better absorption: Take with OJ. Better taken on empty stomach, but this increases gastritis risk |
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Antacids and Iron
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The exact mechanism by which antacids decrease iron absorption is unknown. Some antacids may bind to iron, preventing its absorption. Alterations in gastric pH by antacids may also play a role.
Iron supplements should not be taken within 1 hour before or 2 hours after antacids. |
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Epoetin alfa (Epogen or Procrit)
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RBC production
Wks: Mimics natural hormone from the kidney & needs Iron, folic acid, & B12 to work. Tx: Anemia of Chronic renal failure; Chemotherapy induced anemia (IF NOT involving the bone marrow) SE: • Hypertension • If Hg exceeds 12 increases risk of MI, CVA and heart failure • Increases risks of blood clots |
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Step therapy for Asthma
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• Step 1 (Mild)
– SABA, if used more than 2x/wk consider step 2. • Step 2 (Mild persistent) – Low-dose steroid inhaler daily. An LT antagonist or methylxanthine are alternatives for pts over 12 years of age. SABA inhaler for acute symptom control. • Step 3 (Moderate) – Intermediate-dose ICS or low dose ICS with LABA. SABA inhaler for acute symptom control. • Step 4 (Moderate) – Medium dose ICS+ LABA inhaler. SABA inhaler for acute symptom control. • Step 5 – High dose ICS and LABA • Step 6 – Addition of an oral steroid (2 mg/kg/day not to exceed 60 mg/day) used daily. |
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Concept of rescue inhalers:
Dry powder inhalers (DPI)/diskus |
Dry powder inhalers (DPI)/diskus
•~20% of drug to lungs •No propellant •Breath activated/micropowderdirectly inhaled |
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Concept of rescue inhalers: Metered-dose inhalers (MDI)
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Metered-dose inhalers (MDI)
•1-2 puffs of an aerosol solution, inhaled •Required respiration/hand coordination •Only ~10% reaches lungs; 80% to oropharynx •Propellants: Hydrofluoroalkane(HFA) |
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Aids for rescue inhalers:
Nebulizers |
Nebulizer Inhalation Delivery
–Fine mist –Requires machine –Best option: high doses of medication possible •Given slower, as airways open, greater penetration and more medication dose received |
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Spacers
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Spacers are aerosol-holding chambers, add-on devices and spacing devices, spacers are long tubes that slow the delivery of medication from pressurized MDIs. Spacers should always be used with MDIs that deliver inhaled corticosteroids. Spacers can make it easier for medication to reach the lungs, and also mean less medication gets deposited in the mouth and throat, where it can lead to irritation and mild infections.
Note that 21% of medication gets to the lungs with a spacer. Only 9% without the device. |
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How to use a spacer
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1. Shake the inhaler well before use (3-4 shakes)
2. Remove the cap from your inhaler, and from your spacer, if it has one 3. Put the inhaler into the spacer 4.Breathe out, away from the spacer 5. Bring the spacer to your mouth, put the mouthpiece between your teeth and close your lips around it 6. Press the top of your inhaler once 7. Breathe in very slowly until you have taken a full breath. If you hear a whistle sound, you are breathing in too fast. Slowly breath in. 8. Hold your breath for about ten seconds, then breath out. |
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Regulation of Bronchial Smooth Muscle
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•Parasympathetic NS: Acetylcholine
–Major controller of sympathetic tone –Primary control of smooth muscle tone –Vagusnerve →Ach receptors →bronchoconstriction •Sympathetic NS: Epinephrine “Fight or Flight” –Beta 2 adrenergic receptors on smooth muscles –Epieffects all adrenergic receptors –Bronchodilation |
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Which receptors are asthmatics more sensitive to?
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Asthmatics have an abnormal reaction to alpha stimulation and an exaggerated response to muscarinic agonists.
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Histamine
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Histamine produces bronchoconstriction. Histamine is in mast cells and is released in response to allergens and some drugs (e.g., morphine)
Histamine binds to H1, H2 receptors • H1 stimulation – Vasodilation of venules/arterioles (i.e., face) – ↑ capillary permeability secondary to capillary endothelial contraction – Bronchoconstriction – Other: itching and pain d/t sensory receptors, secretion of mucus • H2 Stimulation – Secretion of gastric acid • Type I hypersensitivity/Anaphalyxis reactions – Allergen + IgE →crossbridges→mast cell/basophil degranulation →release of histamine – Anaphylaxis – Angioedema – Urticaria (hives) – Rhinitis • Inflammation of nasal mucosa/swelling/congestion • Sneezing, itching and watery eyes • Seasonal or perennial, allergens |
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CV considerations of respiratory meds
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For asthma:
-Albuterol can cause cardiac symptoms (angina, dystrhythmias) - Methylxanthines can cause ventricular dysrhythmias - Antihistamines can provoke tachycardia/palpitations. Because of their anti-cholinergic side effects, they should be used with caution in patients with hyperthyroidism (tachycardia), HTN or BPH/urinary retention For non-allergic rhinitis: - When using Pseudoephederine use caution with HTN/CVD due to alpha-1 and beta 1 agonist effects |
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Diphenhydramine(Benadryl)
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1st Generation Antihistamine
Wks: H1 Antagonist receptor. Block action of histamine (Not the release of histamine, only its effects!). They also bind to bind to muscarinic Ach receptors (causing: dry mouth, urinary retention, blurred vision, tachycardia) Tx: Blocks flushing; ↓permeability, ↓edema; Reduces itching and pain; Antitussive; Antiemetic; Blocks mucus secretion (except in asthmatics: It thickens secretions!) SE: SEDATION! RN: –Caution: Anti-cholinergic side effects, use with caution in patients with glaucoma, hyperthyroidism (tachycardia), HTN or BPH/urinary retention –Sedation: do not take with ETOH, no driving –No H2 (gastric) actions –Not useful for non-allergic rhinitis –Not useful for asthma |
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What do Beta 2 Agonists do on the lungs?
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Wks: Relaxes bronchiolar smooth muscle
ADME: Inhaled/Oral SE: Usually no systemic effects. Warning: if dose too high, loses selectivity and can cause systemic effects RN: -Fast relief, also used for long-term maintenance -Maintenance drug ONLY. |
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Salmeterol
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Bronchodilator
Tx: • Long-term control of reversible airway obstruction due to asthma and for maintenance treatment of asthma and prevention of bronchospasm • Prevention of exercise-induced asthma • Maintenance treatment to prevent bronchospasm in COPD including chronic bronchitis and emphysema |
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Albuterol
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• Beta 2 Agonist
– Onset of action: 5-30 minutes – No anti-inflammatory capabilities • Adverse effects – Hyperglycemia: Patients with DM only • B2 receptors in liver → glycogen → glucose – Tremor/nervousness/possible cardiac dysrhythmias • Long-acting: Not first line agent. May ↑ risk of asthma-related death if not used properly. • Oral: Can cause cardiac symptoms (angina, dystrhythmias) – Use with caution – Used for long term maintenance only |
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What's the difference between Salmeterol and Albuterol?
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For many patients with asthma, both anti-inflammatory drugs and beta, agonists are necessary to control breakthrough symptoms. However, current beta, agonists such as albuterol have a short duration of action. Salmeterol is a new [beta.sub.2]-adrenergic receptor agonist with a bronchodilator effect 10 times that of albuterol. In addition, studies indicate that it prevents bronchoconstriction induced by various causes (methacholine, histamine, allergens, hyperventilation of cold air, and exercise) for up to 12 hours.
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Glucocorticoids
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Glucocorticoids (GC) are a class of steroid hormones that bind to the glucocorticoid receptor. The name glucocorticoid (glucose + cortex + steroid) derives from their role in the regulation of the metabolism of glucose, their synthesis in the adrenal cortex, and their steroidal structure. GCs are part of the feedback mechanism in the immune system that turns immune activity (inflammation) down. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis.
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Beclomethosone/Flovent
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Glucocorticoid Drug
Wks: Suppression of Inflammation • ↓secretion of inflammatory mediators •↓infiltration of inflammatory cells •↓edema of airway mucosa –Prophalyxis, give on fixed schedule –First line agents for maintenance SE: Adrenal suppression, bone loss, Oral candidiasis Administration: –Use spacer –Gargle/rinse afterwards –Best if used with B2 agonist: B2 opens airways, better penetration of glucocorticoid |
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Isoniazid (INH)
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Tx: TB
Wks: Causes cell wall disruption, bactericidal SE: GI distress, hepatitis D-D: Daily use of ETOH increases risk of liver toxicity RN: MONITOR: –AST and ALT monthly –Sputum cultures periodically –Need ophthalmologic exam if vision changes |
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Rifampin (RIF)
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TURNS EVERY SECRETION ORANGE (Yes, even your contacts become orange!)
Tx: TB Wks: Broad-spectrum bactericidal, blocks RNA SE: GI distress, flu-like symptoms D-D: –Daily use of ETOH increases hepatotoxicity risk –Causes subtherapeuticlevels of HIV protease inhibitors - EVERY ANTIBIOTIC DECREASES BIRTH CONTROL EFFECTIVENESS. This is how many babies are made. RN: NO ALCOHOL! |
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Pyrazinamide (PZA)
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Tx: TB
Wks: Bacteriostatic or bactericidal depending on dose SE: Arthralgia r/t hyperuricemia, jaundice |
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Ethambutol
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Tx: TB
Wks: Bacteriostatic, effective only against actively dividing mycobacteria SE: Optic and peripheral neuritis, decreased ability to see red and green, elevated uric acid levels |
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Where are Isoniazid, Rifampin, Pyrazinamide, & Ethambutol metabolized in the body?
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LIVER! DO NOT DRINK ALCOHOL WHILE UNDERGOING TB TREATMENT!
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Can Isoniazid, Rifampin and Pyrazinamide be used together?
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YES, they can & they should!
• Isoniazid and Rifampin—Rifamate • Isoniazid with Rifampin and Pyrazinamide— Rifater |
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TB Treatment Regimen
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• Usual regimen for active disease is four-drug therapy daily for 8 weeks
–Isoniazid(INH) 300 mg –Rifampin(RIF) 600 mg –Pyrazinamide(PZA) 2 g –Ethambutol(EMB) 15-25 mg/kg •Then –INH and RIF 2-3 times a week for 18 weeks, or 12 months in HIV patients –Drug resistance requires 24 months of treatment |
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Monitoring TB Meds
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•Monitor:
–alanine aminotransferase (AST) and alanine aminotransferase (ALT) monthly (which is the ratio of serum AST to ALT; elevated serum levels of both enzymes characterize hepatic disease) –Sputum cultures periodically –Need ophthalmologic exam if vision changes |
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TB med education
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Patient should understand that TB treatment is long, needs strict adherence (to avoid multi-resistant strains), requires not drinking ANY alcohol (as well as monthly monitoring of liver enzymes), and involves 4 medications. The standard "short" course treatment for TB is isoniazid, rifampin, pyrazinamide, and ethambutol for two months, then isoniazid and rifampicin alone for a further four months. The patient is considered cured at six months (although there is still a relapse rate of 2 to 3%). For latent tuberculosis, the standard treatment is six to nine months of isoniazid alone. If the patient exhibits drug resistance, 24 months of treatment are required.
Medication should be taken on an empty stomach w/full glass of water. Rifampin will stain everything orange. Female pt should consider other birth control besides the pill. Patient should be educated to report any changes in vision. |
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What are the 2 Adrenal hormone classes?
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– Corticosteroids with a) Glucocorticoids that act on glucose AND b) Mineralcorticoids that act on mineral salts
– Androgens |
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Glucocorticoids
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–Functionally identical to the steroids produced in the adrenal cortex
•Physiologic effect = regulation of glucose metabolism •Pharmacologic effect = anti-inflammatory effects •Functionally, the glucocorticoids all do the same thing: the difference between the agents has more to do with the onset, duration of action, and side effect profile |
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Implications of drugs both short & long term: STEROIDS
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•Always taper the patient off of glucocorticoids IF they have been on medication for more than one week
–After high levels of drug therapy, adrenal suppression results –Abrupt cessation of drug means there is insufficient time for HPA axis to return to normal –Withdrawal symptoms = hypotension, hypoglycemia, myalgia, arthralgia, and fatigue… this can be life-threatening! Also, patients should know that long term use can redistribute adipose tissue, resulting in a potbelly and moon face |
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What is aldosterone?
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Aldosterone is the principal of a group of mineralocorticoids. It helps regulate levels of sodium and potassium in the body–i.e. it helps retain needed salt, which in turn helps control blood pressure, the distribution of fluids in the body, and the balance of electrolytes in the blood.
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S/S of aldosterone imbalances: High aldosterone
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When aldosterone gets too high, blood pressure also gets too high and potassium levels become too low. Patients will experience muscle cramps, muscle weakness, and numbness or tingling in their extremities.
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S/S of aldosterone imbalances: Low aldosterone
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This is a cortisol deficiency (like Addison disease). Kidneys will excrete too much salt, leading to low blood pressure; low blood volume; a high pulse and/or palpitations, dizziness and or lightheadedness; fatigue; and a craving for salt. Symptoms of low aldosterone can also include frequent urination, sweating, a slightly higher body temperature, and a feeling of thirst, besides the craving of salt. Potassium can fall, as well.
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Steroids Lab Monitoring
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For Mineralcorticoids meds monitor lytes, especially K+
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Thyroid replacement therapy
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• Thyroid physiology, the formation of thyroxine
– The synthetic analogues to T3 and T4 look and act exactly like the endogenous compound • T3 = liothyronine T4 = levothyroxine • These hormones have three principal actions – Stimulation of energy production, setting the basal metabolic rate, setting oxygen consumption and heat production – Stimulation of the heart and inotropic/chronotropic parameters which will influence cardiac output and oxygen consumption – Promotion of growth and development of the brain and other nervous system components, and the development of skeletal muscle Please note that it takes about 1 month to reach a steady state |
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Implications of drugs both short & long term: Thyroid replacement therapy
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Drug treatment is for life. Stopping treatment will result in a return of hypothyroidism symptoms
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Thyroid Replacement Therapy Labs
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Monitor Thyroid Stimulating Hormone (TSH)! Dose is increased or decreased until TSH is within normal limits.
Also, for treatment of hyperthyroidism with Propylthiouracil/PTU: Check CBC frequently! Stop drug if depressed WBC count! |
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Iodine 131 Thyroid Ablation Therapy
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Radioactive iodine (I-131), an isotope of iodine that emits radiation. When a small dose of I-131 is swallowed, it is absorbed into the bloodstream in the gastrointestinal tract and concentrated from the blood by the thyroid gland, where it begins destroying the gland's cells.
Patients who undergo this treatment should know that not all of the gland is destroyed. Also, that there is a risk that too much gland may be eliminated and that they are at a risk of developing hypothyroidism. This treatment is not for children or pregnant patients. Only adults over the age of 30 are authorized to get this treatment. |
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Precautions with I-131 Thyroid Ablation Therapy
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The treatment involves radioactive material entering the patient’s body. Thus, the patient should observe the following:
• Use private toilet facilities, if possible, and flush twice after each use. • Bathe daily and wash hands frequently. • Drink a normal amount of fluids. • Use disposable eating utensils or wash your utensils separately from others. • Sleep alone and avoid prolonged intimate contact for three or four days. Brief periods of close contact, such as handshaking and hugging, are permitted. • Launder your linens, towels, and clothes daily at home, separately. No special cleaning of the washing machine is required between loads. • Do not prepare food for others that requires prolonged handling with bare hands. • If you are breast-feeding, you must stop. • You should avoid becoming pregnant from six months to one year after treatment. • You must be sure you are not pregnant before receiving I-131. |
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What's vasopressin?
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Antidiuretic Hormone (ADH) ontrols the reabsorption of molecules in the tubules of the kidneys by affecting the tissue's permeability. Without this hormone stored & released by the posterior pitutary, patients void excessive urine volume!
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Desmopressin acetate (DDAVP)
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Posterior Pituitary Replacement
Wks: As a synthetic vasopressin (ADH) analog; enables kidneys to concentrate urine if problem is with pituitary; can also stop bleeding in hemophilia (as it increases release of Factor VIII) Tx: Neurogenic Diabetes Insipidus (DI) (NOT effective in DI with renal cause), bedwetting. SE: HTN, flushing, water retention, rhinitis, nausea RN: Monitor fluid balance and watch for overload |
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Vitamin C
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Vitamin C or L-ascorbic acid or L-ascorbate is an essential nutrient. Ascorbate acts as an antioxidant by protecting the body against oxidative stress. It is also a cofactor in at least eight enzymatic reactions including several collagen synthesis reactions that, when dysfunctional, cause the most severe symptoms of scurvy.
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St John's Wort
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Tx: Mild depression
RN: -Takes 3 months for real effect cannot take with RX forms of anti-depressants -Should not be taken during pregnancy |
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Regulations and Labels of Herbals
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-Not under the FDA
-Not regulated like Prescription Drugs -The FTC has oversight responsibility. They monitor advertising and reports of SE. Can stop sale of product. |
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How & when to take supplements. Also, with what type of education.
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The most important thing to do is educate yourself about supplements and warn patients about experimenting, as well as the risk of SE if mixing with prescription meds.
Encourage patients to purchase standardized products from a single company and to follow recommended doses. Elderly, pregnant women, and children have an increased risk of interactions and SE from supplements. Some herbs are unsafe during pregnancy |
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Some Herbs That May Increase Clotting Times or Interact with Anticoagulants
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Garlic
Ginger Ginkgo biloba Ginseng Green tea |
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Some Herbs That Should Not be Taken Internally
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Liver toxicity:
-Life root -Kava Induce cranial bleeding/CVA? -Ginko -Ginseng Life-threatening ifexercising and possibly dehydrated: -Ephedra |
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Some Herbs That Should Not be Taken During Pregnancy
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Ephedra
Ginger Ginkgo biloba Ginseng Green tea Horseradish Kava kava Licorice Milk thistle Red clover Rhubarb St. John’s wort |
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Herbs with positive Research Base
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-St. John’s Wort for mild depression
-CQ10: helps resupply enzymes used up faster when on statins -Glucosamine Chondroitin for joint pain and stiffness |
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Water Soluble Supplements
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Chemical which dissolve in the serum and fluids of the cells
Not easily stored in the body Needs more frequent replacement |
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Fat Soluble Supplements
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Stored and metabolized in lipid tissues
Highest risk for toxicit |
