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119 Cards in this Set
- Front
- Back
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Triglycerides |
neutral fats which account for 90% of total lipids in the body. |
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Phospholipids |
essential to building plasma membranes |
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Steroids |
A diverse group of substances having a common chemical structure called sterol nucleus, or ring structure *cholesterol most widely known *contribute to atherosclorosis |
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Apoproteins |
A protein carrier 3 types HDL, LDL, VLDL |
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How lipids transported in plasma |
Lipid molecules are not soluble in plasma, they must be specially packaged for transport through the blood. |
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LDL (Lousy) |
Transports cholesterol from the liver to tissue and organs. Carries the highest amount of cholesterol (bad cholesterol) known to contribute to plaque deposit & CAD 100mg/DL |
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HDL (good) |
Good cholesterol, it's thick and helps remove other types of lipids -Reverses cholesterol transport, assists in moving it away from the tissue & back to the liver -40mg/DL |
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VLDL |
Primary carrier of triglycerides in the blood. VLDL in the body will become LDL which is the transporter of cholesterol |
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1st line agent for treating lipid disorders |
Statins: Drops LDL, lower triglycerides, lower VLDL and Rise HDL *best to reduce blood lipid levels |
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lipid disorder |
check labs (lipid profile), LDL, HDL, VLDL, accurate h&p, pt height and weight, dietary summary, assess LFT's
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HMG-CoA reductase lower cholesterol and LDL |
The cholesterol pathway gets blocked. Less cholesterol made liver makes more HDL receptor on the surface of liver cells and the greater and number of receptors the greater uptake of LDL. |
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Why would someone take atorvostatin (Lipitor) QHS. |
Blood levels of both LDL and cholesterol are reduced ultimately this will reduce the risk of MI and stroke *give at night when cholesterol being produced |
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How does bile acid resin cholesystramine (Questran) lower cholesterol |
Questran binds with the bile acids containing cholesterol in an insoluble complex the is excreted in the feces. Cholesterol levels decline due to fecal loss. -used in combo with statins, decrease cholesterol, decrease LDL & increase HDL |
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Risks and Benefits for taking nicotinic acid (Niacin) |
Risk- Flushing, hot flushing, nausea, gas, diarrhea and possible gout. Not good for diabetic pt (raises blood glucose levels) Benefits- Decreases VLDL levels which lowers triglycerides and increase in HDL..eventually lowering cholesterol |
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How cholesterol absorption inhibitors, such as ezatimibe (Zetia) reduces cholesterol |
It inhibits the absorption of cholesterol. Cholesterol is absorbed by the intestinal lumen by cells in the jejunum and the small intestine. Zetia blocks up to 50% of this absorption and the body responses by producing more cholesterol. |
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atorvastatin (Lipitor) |
inhibits HMG-CoA Use: reduces serum lipid levels Adverse: Rhabdomyolysis *check LFT's & report muscle pain |
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cholestyramine (Qestran) |
Bile acid sequestrant Use: In combination with statins Adverse: Can bind other drugs, increasing potential for drug-drug interactions. |
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Gemfibrozil (Lopid) |
Fibric acid agent (fibrate) Use: Reduces LDL levels Adverse: GI related, dyspepsia, diarrhea, nausea, and cramping. |
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Clotting Cascade |
Intrinsic or extrinsic pathways lead to formation of fibrin clot. When collagen is exposed at the site of injury, damaged cells initiate a series of complex reactions called coagulation cascade. |
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fibrinolysis
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clot removal starts within 24-48 hours of clot formation
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Anticoagulants differ from thrombolytics |
Anticoagulants will prevent the formation of clots and will keep an existing clot from getting larger. Thrombolytic are dangerous drugs and they are used to dissolve life-threatening clots. Problem is they also dissolve the clots that we need. |
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Heparin & Warfarin |
Mechanisms: inhibit specific clotting factors Reversal agents: Oral or parenteral administration of vitamin K |
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Heparin and Warfarin used simultaneously? |
Warfarin acts by inhibiting the hepatic synthesis of coagulation. Pt. begin anticoagulation therapy with heparin and are switched to warfarin when their condition stabilizers. Transitioning the two drugs are administered concurrently for 2-3 days because warfarin takes several days to achieve optimum effect. |
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Heparin sodium/low molecular weight heparin PTT |
Use: Can decrease the ability of the blood to clot Lab: Activated partial Thromboplastic time (aPTT) and platelet count Values: 25-35 seconds Adverse: high values indicate risk for bleeding Tx OD: Antagonist protamine sulfate |
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Warfarin (Coumadin) PT |
Use: Treat and prevent blood clots Lab: Prothrombin time (PT) and Platelet count & PTT/INR Values: INR 2-3 Platelet 150,000-350,00 Adverse: high values indicate risk for bleeding, platelets below 20,000 indicate thrombocytopenia Tx OD: Vitamin K |
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Aspirin (Bayer) |
Use: Prevent blood clots (Antiplatelet) Lab: Platelet count Values: 150,000-350,000 Adverse: below 20,000 indicate thrombocytopenia |
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Monitoring patients on aspirin |
All vitals and monitor hepatic function |
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Abciximab (Reopro) |
Use: prevents blood clots during procedure to block blood vessels. Lab: Platelet count Adverse: below 20,000 indicate thromboytopenia |
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Clopidogrel (Plavix) |
Use: prevent thromboemboytopenia (thrombi formation after stroke or MI) MAO: alter plasma membrane platelets so they can't aggregate Lab: Bleeding time Adverse: long bleeding time indicates a low platelet count or anticoagulant therapy. Tx OD: platelet transfusions |
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Use for thrombolytics |
To break down fibrin and restore blood flow
*used to treat acute MI, DVT, CVA, PE, arterial thrombosis & to clear IV catheters *dangerous drugs, used for emg. |
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Monitoring patients on thrombolytics |
BP, PR, I and O neurological status and monitor changes in lab values. |
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Indications for hemostatics |
They stop bleeding by preventing fibrin from dissolving and shorten bleeding time--> promote formation of clots adverse: hypercoagulation w/ estrogen & oral contraceptive do not take aspirin on this drug |
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Compare and contrast angina vs MI |
Acute chest pain due to insufficient O2 to myocardium. Causes increase myocardial O2 demand. MI occurs when a coronary artery becomes completely occluded. |
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Atherosclerosis contributes to angina and MI |
Atherosclerosis is the presence of fatty fibrous material within the walls of the coronary arteries. Plaque develops progressively over time, producing varying degrees of intravascular narrowing, that limits the free flow of blood through the vessels. |
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Stable Angina |
angina occurrences are fairly predictable as to frequency, intensity and duration -relieved by rest |
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Unstable Angina |
Episodes of angina arise more frequently, become more intense, or occur during periods of rest. *throbus is causing the pain = vessel NOT completely occluded |
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Vasospastic or Prinzmetal's Angina |
Occurs when the decreased myocardial blood flow is caused by spasms of the coronary arteries. |
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Silent Angina |
Form of a disease that occurs in the absence of chest pain. One or more coronary arteries are occluded, but the pt. remains asymptomatic. |
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Unstable Angina |
Gives the same extreme chest pain, as MI. The thrombus causing the pain however, has not completely occluded the coronary artery. |
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MI |
Occurs when a coronary artery becomes completely occluded. Deprived of its O supply, the affected are of myocardium becomes ischemic and myocytes begin to die in about 20 min unless the block supply is quickly restored. |
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Nitroglycerin (Nitrostat) |
Mechanism: Taken while an acute angina episode is in progress or just prior to physical activity. Reversal agents: Hypotension may be reversed with administration of IV normal saline. |
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Atenolol (Tenormin) |
Mechanism: Blocks beta1-adrenergic receptors in the heart, which slows the HR and reduces contractility. Reversal agents: Atropine or isoproterenol may be used to reverse bradycardia. *first line for angina pain |
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Diltiazem (Cardizem, Cartia XT, Dilacor XR) |
Mechanism: Inhibits the transport of calcium into myocardial cells relaxing the arterial smooth muscle. Reversal agents: Atropine or isoproterenol may be used to reverse bradycardia caused |
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Reteplase (Retavase) |
Mechanisms: Converts plasminogen to plasmin Reversal agents: no Tx for overdose |
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BMONA |
Beta Blockers (LOL) Morphine Oxygen Nitroglycerin Aspirin |
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When and how thrombolytic agents be used to treat MI |
Should be used in cases of acute MI, it's used to restore circulation to myocardium -->dissolving the clot Used if we cannot get the pt. to a cardiac lab within 90 mins will give thrombolytic. |
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Monitor patients taking morphine sulfate |
All vital esp. respiratory since morphine slows breathing. |
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monitor patients taking organic Nitrates |
BP sitting and standing to watch for hypotension |
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Heart Failure |
Inability for the ventricles to pump enough blood to meet the body's metabolic demands. L=lungs R=body |
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Preload |
The volume of blood in a ventricle at the end of diastole. All preload is determined by venous return. |
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Afterload |
The resistance that the heart muscle must overcome to eject blood up and out; afterload is the resistance against a ventricle; effects cardiac output |
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Inotropic |
The change in contractility of the heart |
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Positive inotrope |
drugs that increase contractility |
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Negative inotrope |
drugs that decrease contractility |
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Chronotropic |
positive chronotrope increase HR negative chronotrope decrease HR |
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Dromotropic |
effects electricity throughout the heart increase or decrease electricity |
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diuretics |
*first drug given in treatment of HTN -increases urine output, reducing blood volume & cardiac workload -reduce edema & pulmonary congestion -used for mild to moderate HTN -adverse: monitor I&O,electrolyte imbalances, especially HYPOkalemia, orthostatic hypotension -monitor & assess BP & HR before giving Prototypes: spironolactone, furosemide(Lasix) |
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Ace Inhibitors agngiotension 2 *end in PRIL |
enalapril (Vasotex) MAO: block the affect of angiotension 2, lowering PVR & decrease blood volume. Reduction in pre-load & vasoconstriction -good for diabetic pt; protects kidneys -can cause HYPERkalemia -can cause nagging cough -known to cause ANGIOEDEMIA in AA -does NOT affect HR |
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ARB angiotension2 receptor blocker *end in SARTAN |
losartan (Cozaar) MAO: block angiotension receptors in smooth muscle -reduction in vasoconstriction & blood volume -switch to ARB if nagging cough with ACE |
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Calcium Channel Blockers (CCB) |
nifedipine MAO: blocks calcium channels causing vasodilation & reducing BP -reduces muscle contraction, relaxes smooth muscle= reducing PVR -reduction in pulse -good for AA; IC intracellular calcium ** AVOID GRAPEFRUIT JUICE= may enhance absorption! -monitor HR & BP, ECG prior to & during therapy -signs of HF & tachycardia |
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Beta blockers *end in LOL |
metoprolol (Lopressor) MAO: block beta 1; inhibit secretion of renin -first line agents in treatment of hypertension -work against SNS stimulation -DON'T use for ASTHMA/COPD (bronchospasm) or DIABETIC pt (masks the signs of hypoglycemia) -negative inotropic effect -asses BP & HR, monitor blood glucose |
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alpha1-adrenergic antagonists -NOT first line |
doxazosin (Cardura) MAO: blocks sympathetic receptors in arterioles leading to vasodilation -used in combination with other drugs,usually diuretics |
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alpha2- adrenergic agonist |
MAO: decrease outflow of sympathetic nerve impulses from CNS to heart & arterioles Adverse: sedation, dizziness drugs: clonadine (Catapress) & methydopa (Aldomet) |
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Direct Vasodilators *dangerous |
MAO: vasodilation by direct relaxation of arterial smooth muscle -ONLY for severe HTN or hypertensive crisis Adverse effects: reflex tachycardia, fluid & na retention -vasodilate= august afterload Drug: Nitropress; monitor for cyanide toxicity, monitor pt, can lower BP instantly |
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What lab value should be closely monitored for clients taking loop diuretics? |
Serum Potassium levels should be monitored |
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What effects do loop diuretics on preload |
Decrease Preload. Effective in removing fluid from the body; decreasing blood volume by urinating it out and in turn reduces cardiac workload |
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What drugs have the potential to worsen HF? |
Beta blockers but they have become standard therapy for many pt. with HF disorder |
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How do beta blockers benefit HF clients? |
Beta blockers block the cardiac actions of the sympathetic NS Slower HR and reducing BP= decreasing workload of the heart |
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How do monotherapy benefit HF clients? |
They ae rarely used but when they are in use they are paired with ace inhibitors |
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How do negative inotropes benefit HF clients? |
Used for earlier HF pt. that still have some inotrope in their heart. |
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MOA for heart failure |
Use: lower BP used for clients that cannot take ACE inhibitors Adverse reactions: reflex tachycardia and orthostatic hypotension |
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How do cardiac glycosides treat HF? |
increase force of heart beat, slowering HR Use: advanced stages of HF *second line treatment for HF *ck apical pulse for full 1 min.before administering resp 60bpm. |
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digoxin (Lanoxin)
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MAO: cause more forceful heatbeat, slower HR Use: to increase contractility or strength of myocardial contraction Adverse: Toxicity digoxin serum blood between 0.5-2 ..1.8 theraputic level Early signs: N&V,overdose= IV infusion of Ca to cause muscle contractions |
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Normal electrical flow throughout the myocardium |
SA node is the primary generator of the heart, set to pace the heart between 60-100bpm |
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Atrial or Ventricular tachycardia |
Rapid heartbeat greater than 100 bpm in adults |
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Heart Block |
Blockage in the electrical conduction system of the heart may be partial or complete |
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Premature Atrial or Premature Ventricular Contractions (PVC) |
An extra beat often originating from a source other than the SA node; only considered serious if it occurs in high frequency; may be precursor of more serious dysrhythmias |
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Sinus Bradycardia |
Slow heartbeat less than 60 bpm, originating the SA node; may require a pacemaker |
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refractory period |
period in conduction cycle when myocardial cells cannot produce another action |
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Equipment used to monitor dysrhythmias? |
ECG measure the wave of electrical activity in the heart |
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Cardiac meds. being discontinued? |
NEVER should they be abruptly stopped. *can cause rebound hypertension |
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Use of adenosine in the termination of paroxysmal supraventricular tachycardia |
Adenosine is a natural occurring nucleoside. When given as a 1-2 second bolus IV injection, adenosine terminates serious atrial tachycardia by slowing conduction through the AV node and decreasing automaticity of the SA node. |
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(Dysrhythmias) Sodium Channel blocker (Class I) Procainomide |
Mechanism: to block sodium ion channels which slows rate of impulse conduction across the heart (HR D/C) Use: to correct atrial and ventricular dysrhythmias Adverse: Can create new dysrhythmias or worsen existing ones. Put pt on monitor *high dose can produce CNS effects |
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(Dysrhythmias) Beta-Adrenergic Blockers (Class II) Propranolol |
Mechanism: Block beta-receptors, which reduces automaticity and slows conduction velocity across the myocardium. Use: treat atrial dysrhythmias assoc. with HF Adverse: Bradycardia, hypotension with dizziness and fainting bronchospasm. |
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(Dysrhythmias) Potassium Channel Blockers (Class III) amiodarone (Cordarone, Pacerone) |
Mechanism: block potassium ion channels in myocardial cells, which prolongs refractory period of the heart. Use: to treat resistant ventricular tachycardia, atrial dysrhythmias with HF use limited due to adverse. Adverse effects: potentially fatal pneumonia-like syndrome elevated liver enzymes, thyroid dysfunction, skin discoloration, bradycardia, and hypotension. |
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(Dysrhythmias) Calcium Channel Blockers (Class IV) verapamil (Calan) |
Mechanism: block calcium ion channels which reduces automaticity and slows myocardial AV conduction velocity. Use: treat supraventricular dysrhythmias Adverse: Bradycardia, hypotension, headache |
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(Dysrhythmias) adenosine (Adenocard) |
Mechanism: decrease automaticity of SA node and slow conduction through AV node but not act by blocking ion channels. supraventricular tachycardia=SVT *facial flushing, dyspnea, 6,12,12 need cart and continues ECG-> pt will vomit, hold arm up |
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(Dysrhythmias) digoxin (Lanoxin) |
Mechanism: decrease automaticity of SA node and slow conduction through AV node but not act by blocking ion channels. Use: certain types of atrial dysrhythmias Adverse: Creates new dysrhythmias or worsens existing ones. Vomiting, headache, visual disturbance. |
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Allergic rhinitis |
inflammation of the nasal mucosa due to exposure to allergens--> causes histamine release |
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histamine
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chemical mediator of inflammatory response (allergic response) -histamine 1=smooth muscle of vascular system causes symptoms of allergic rhinitis -histamine 2=found in stomach responsible for peptic ulcers |
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h1 receptor antagonists (antihistamine) |
diphenydramine (Benadryl) -short acting MAO: H1 recepter blocker Use: treat minor symptoms of allergy & cold Adverse: dry mouth & urinary retention, tachycardia, mild hypotension |
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H1 receptor antagonists assist in tx in cough |
Benadryl & Allegra Used to tx minor symptoms of allergy and the common cold such as sneezing, runny nose, and tearing of the eyes. Diphenhydramine is often combined with analgesic decongestant or expectorant in OTC cold and flu. *Lethargy and could use as sleeping pill |
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intranasal coricosteriods
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*used prophalictically, must be administered 2-3 weeks prior to allergen exposure -cause mild vasoconstriction -vascular--> possible to spread systemically Prototype: cromolyn (NasalCrom) |
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fluticasone (Flonase) |
MAO: decreases local inflammation in nasal passages, thus reducing nasal stiffness
Use: treatment of seasonal allergies
Adverse: nasal irritation |
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Intranasal & oral sympathomimetics |
use: decongestants *use for only 3-5 days due to rebound congestion! *local action within minutes -few systemic effects |
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Dangers of using sympathomimetics with resp. disorders |
Causes the fight or flight we see dilated pupils, vasoconstriction, bronchodilation, gluconeogenesis, decreased in blood flow to the gut and diaphoresis. |
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oxymetazoline (Afrin)
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MAO: stimulates alpha-adrenergic receptors in sympathetic nervous system causing arterioles in nasal passages to constrict Use: treat nasal decongestion adverse: rebound congestion |
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Opioids and nonopioids with tx of cough |
opioids are used to inhibit a severe cough but they have an abusive potential and they decrease the CNS and decrease respiration. nonopioids are used to inhibit a mild or moderate cough (dextroethorphan). It is a derivative of an opioid but doesn't possessive any opioid characteristics. |
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Mucolytics |
Directly break down the mucous molecule. It liquefies your mucus. Be careful giving this to pt. who have trouble coughing or they can drown on their own mucous. Have suction set up! *Acetylcysteine(treat tylenol OD) |
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Expectorants |
promotes mucus secretion by making the mucus thinner making it easier to remove by coughing *Guaifenesin (Robitussin DM) |
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antitussive
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inhibit cough *best way to stop cough |
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dextromerthorphan (Delsym)
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*orphan of opioids MAO: acts in medulla to inhibit cough reflex Use: component in most OTC severe cold & flu preparations Adverse: dizziness, drowsiness, upset GI benzonate (Tessalon) other drug |
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ventilation
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moves air into and out of lungs
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perfusion |
flow of blood through lungs
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respiration
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exchange of gas *need adequite blood flow |
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Asthma |
Chronic disease and has components of inflammation and bronchospasms. Will develop when pt. comes into contract with a trigger. Can go into asthmaticus (prolonged attack) resistant to drug therapy |
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Albuterol |
Bronchodilators used to tx asthma. Short moderate acting beta2 adrenergic agonist and it is the only drug used as a rescue agent with asthma. Adverse: shakiness, tachycardia, and jitters |
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Levalbuterol |
similar to albuterol but the side effects are minimal |
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Salmeterol |
Works by binding to beta2adrenergic receptors in bronchial smooth muscle to cause bronchodilation Report chest pain ASAP |
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Inhalation |
Common route administration for pulmonary drugs. Rapid and efficient, rich blood supply allows for quick absorption and onset of action.
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Aerosol therapy |
Suspension of droplets or particles in a gas. Onset of action almost immediate, immediate relief of bronchospasm loosens thick mucus.
*Need to rinse mouth |
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Montelukast (Singulair) *Leukotriene Modifiers |
prevents airway edema and inflammation by blocking leukotriene receptors in airways *headache, nausea, diarrhea |
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Cromolyn (Intal) Nedocromil (Tilade) *Mast cells stabilizers |
Inhibit mast cells from releasing histamine and other chemical mediators of inflammation *less effective than inhaled corticosteroids *ineffective at relieving acute bronchospasm |
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Theophylline *Methylxanthines |
Group of bronchodilators related to caffeine Narrows margin of safety, interacts with numerous drugs *dangerous drugs, can cause seizures, Remove all caffeine from pt. *Prophylactically |
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Beclomethasone (Qvar) *Corticosteroids |
Acts by reducing inflammation most potent anti-inflammatory *Drug of choice for long-term prophylaxis of asthma not used to terminate acute attacks! *Limit use under 10 days *Watch for thrush |
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Albuterol (Proventil, Ventolin, VoSpire) *Beta2Adrenergic Agonists |
To terminate acute bronchospasms in progress and to reduce the frequency of asthma attacks *can be used acutely or prophylactically *should always have albuterol inhaler on you if you have asthma |
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Ipratropuim (Atrovent) *Anticholinergics |
Block the parasympathetic NS with bronchodilators effects. *Bronchodilators Inhaler form *used as alternative to beta agonists in asthma therapy; think drying *nasal drying |
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Drug of choice for treating Acute bronchospasm |
Albuterol (Proventil, Ventolin, VoSpire) Beta 2Adrenergic Agonist |
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how to stimulate SNS if no MDI
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CAFFEINE!! will stimulate SNS & cause bronchodilation if no inhaler
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