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76 Cards in this Set

  • Front
  • Back

2 primary forms of lipids in the blood

Triglycerides & Cholesterol

Are these lipids lipid or water soluble, what does this mean?

Water soluble, must bind to be active

What are apolipoproteins?

Specialized lipid-carrying cells that lipids

Where are triglycerides stored? What are they used for?

Stored in fat;used for energy

What are cholesterol used for?

Used to make steroid hormones cell membranes, & bile acids

What are lipoproteins? Where are they metabolized?

A combination of triglycerides or cholesterol with apolipoproteins used to transport lipids through the blood; metabolized in the liver

What are 3 types of lipoproteins?

Very low density lipoprotein (VLDL)



Low density lipid protein (LDL)



High density lipoprotein (HDL)

Very low density lipoprotein: how much lipid vs protein content?


Where is it produced?


What does it do?


What happens once they circulate?

Least protein, most lipid content


Produced by the liver


Transports endogenous lipids to peripheral cells


Once circulated, they become LDLs

High density lipoproteins: what is the protein vs lipid content?


What do they do?


What is it called the good lipid?

Most protein, least lipid content


Responsible for recycling cholesterol


Good lipid because its cardioprotective

What is a pt at risk for once they're cholesterol levels are >300? Why are they at risk for thrombi? How does hypercholesteremia work?

CAD


Plaque can cause thrombi & embolisms


If the liver has an excess amount of cholesterol,the number of LDL receptors on the liver decreases which results in an accumulation of LDL in the blood

What are antilipemics used for?


What is the drug type based on?


What should be done before starting a pt on antilipemics?

Antilipemics are used to lower lipid levels & as an adjunct in diet therapy.


Drug choice is based on the specific lipid profile (type of hyperlipidemia) of pt (aka phenotyping)


All non drug means if controlling cholesterol levels should be tried for atleast 6 mo. & found to fail before therapy

6 types of antilipemics

HmG-CoA reductase inhibitors (HMGs/statins)


Bile acid sequestrants


Niacin


Frolic acid derivatives


Cholesterol absorption inhibitors


Omega 3 fatty acids

HMG-CoA reductase inhibitors: family name**


MOA**


Indications


Adverse effects**


Contraindications


Interactions


Nursing care

"Statins"


Most potent LDL reducers



MOA: inhibit HMG-CoA reductase, which is an enzyme used by the liver to produce & regulate cholesterol. By doing this it slows the rate of cholesterol production.** When less cholesterol is produced, the liver increases LDL receptors so that LDL Can be recycled



Indications


1st-line drug x hypercholesteremia (most dangerous/common dyslipidemia)


Treats type IIa & IIb hyperlipidemias


Decreases LDL BY 30-40%


Decreases triglycerides by 10-30%


Increases HDL by 2-15%



Adverse effects


Mild GI disturbances


Rash


Headache


Myopathy (muscle pain)**


possibly leading to rhabdomyolysis (break down of muscles)


Elevations in ALT, clotting time, thrombocytopenia, & eosinophilia



Contraindicated


Pregnancy


Liver disease



Interactions


Oral anticoagulants


Drugs metabolized byCYP3A4:


Erythromycin,-azole antifungals, verapamil, diltiazem, HIV inhibitors, amiodarobe, & grapefruit juice (>myopathy; limit 1 qt daily)



Nursing care


Take at night


Liver panel baseline, ck q 6 mo.


Monitor creat,may increase


Monitor for muscle pain, change in urine color,fever, malaise, N/V


Teach it takes 6-8 wks to see results


Monitor for protein in urine


Simvastatin - report memory loss, confusion, hyperglycemia, & increase a1c levels

Bile acid sequestrates/iron exchanging resins


Drugs


MOA


Indications


Contraindications


Adverse effects


Nursing care

Bile acid sequestrates: drugs:


Cholestyramine (Questran), colestipol (Colestid), colesevelam (Welchol)



MOA


Prevent resorption of bile acids from small intestines so that cholesterol cannot be absorbed. Bile acid is then insoluble so it is excreted through the feces. The more the bile acids are excreted in the feces, the more the liver converts cholesterol to bile acid.


Decreases LDL by 15-30%


Increases HDL by 3-8%



Indications


2nd line of drug therapy


Type II hyperlipoproteinemia


Relief of pruritis associated with biliary obstruction (cholestyramine)


May be used along with "statins"



Contraindications


Bowel/biliary obstruction


PKU (Phenylketonuria)



Adverse effects


Constipation


H/A, nausea, belching, bloating


Adverse effects tend to disappear overtime


Toxicity can lead to obstruction



Nursing


Compliance is an issue, d/t powder form


Teach to increase fiber & water intake &admin with food to decrease GI effects


All drugs must be taken at least 1 hr before of 4-6 hr after admin d/t decreased absorption


Asses for PKU d/t inability to process aspartame appropriately


Powder form must be mixed thoroughly but not stirred & nevertaken dry; do not dilute or sprinkle on food

Niacin (Nicotinic acid)


What is it?


What dose must be used?


MOA


Indications


Adverse effects


Contraindications

Niacin


Vitamin B3 (OTC)


Lipid lowering properties require high doses than when used as a vitamin; effective, ineffective, often used in other lipid lowering drugs



MOA


Thought (unknown) to increase activity of lipase, which breaks down lipids. Decreases cholesterol/triglyceride metabolism & catabolism


Decreases triglycerides 30-70%


Increases HDL 20-30%



Indications


All phenotypes of hyperlipidemia except type I



Adverse effects


Take with meals & start on low dose & gradually increase to minimize adverse effects


Small doses of ASA/NSAIDs may be taken to minimize flushing


Flushing (d/t histamine release)


Pruritis (itchiness)


GI distress (d/t histamine release increasing GI secretions & motility)


Breaks down fibrin clots



Contraindications


PUD/GI ulcer


Hemorrhagic processes

Fibric acid derivatives/Fibrates


Drugs


MOA


Indications


adverse affects


Interactions


Contraindications


Nursing care

Fibric acid derivatives


Drugs


gemfibrozil (Lopid)


Febofibrate (Tricor)



MOA


Believed to activate lipase (which breaks down cholesterol). Also suppresses release of free fatty acid from adipose tissue, inhibits synthesis of triglycerides in the liver, & increase secretion of cholesterol in the bile


Primary affect triglycerides


Also increase plasmafibrolysis (break down of blood clots)


Decrease triglycerides and increase HDL by 25%



Indications


Hyperlipidemias type III, IV, & V



Adverse effects


Abd discomfort, diarrhea, nausea


Blurred vision, headache


Increase PT & LFTs



Interactions


Oral anticoagulants


Statins (r/f myosotis)


Decrease H&H & WBC


Increase clotting time, AST, ALT, & bilirubin (by-product of RBCs)



Contraindications


Liver, kidney, & gall bladder disease



Nursing care


Must be monitored closely if on Coumadin


Monitor LFTs & x gallstones

Cholesterol Absorption inhibitors



Drug(1)


MOA


What is it enhanced by?


Indication

Exetimibe (Zetia)


Inhibits absorption of cholesterol & related sterols from the small intestine. Results in decreased LDL & triglycerides & increased HDL


Often enhanced with Statins


Trials continue; recommended only when pt have not responded to other therapy

Cholesterol Absorption inhibitors



Drug(1)


MOA


What is it enhanced by?


Indication

Exetimibe (Zetia)


Inhibits absorption of cholesterol & related sterols from the small intestine. Results in decreased LDL & triglycerides & increased HDL


Often enhanced with Statins


Trials continue; recommended only when pt have not responded to other therapy

Herbal: omega-3 fatty acids


Adverse effects


Interaction

Fish oil products


Used to reduce cholesterol


Rash, belching, allergic reaction


Potentially interacts with anticoagulants

Cholesterol assessment

Risk Factors of hyperlipidemia


Male >45


Family hx if premature CAD (MI or death before 55 y/o in father or other male first degree relative or before 65 in first degree female relative)


Current cigarette smoking


BP >140/90/ current antihypertensive therapy


HDL <40 mg/dL


Diabetes



Assess for alcohol/recreation drug use d/t liver dysfunction



Assess LFT: AST CPK & ALT before & during therapy

Coagulation cascade

The series of steps beginning with the intrinsic & extrinsic pathways of coagulation & proceeding through the formation of a fibrin clot

Coagulation cascade

The series of steps beginning with the intrinsic & extrinsic pathways of coagulation & proceeding through the formation of a fibrin clot. Fibrin is a stringy insoluble protein produced by thrombin & fibrinogen during the clotting process. Each activated factor serves as a catalyst that amplifies the next reaction.

2 types of cascade pathways

Extrinsic pathways are activated by external penetration (bullet), factors VII & X are then activated by thromboplastin from is vessel wall



Intrinsic pathways are activated when factor XII (inactive throughout blood) comes in contact with exposed collagen on the inside of damaged vessels.

Fibrinolysis system

Once a clot is formed & fibrin is present, the fibrinolysis system is activated. This system initiates the breakdown of clots and serves to balance the clotting process. Fibrinolysis is the reverse of the clotting process. In this process, fibrin bind to plasminogen so that it can convert to plasmin. The plasmin break down the fibrin thrombus to a lesser form so that it does not become an embolus

Anticoagulants/antithrombolytics


MOA


Indications


Adverse effects

MOA


Inhibit the action or formation of clotting factors


Does not "thin" the blood, it prevents clot formation


Has no direct effect on an already formed clot


Used prophylactically to prevent thrombi/emboli



The MOA depends on the drug (where it works in the clotting cascade)



Indications


MI, unstable angina, a-fib, in dwelling devices, & major orthopedic surgeries


Warfarin prevents


Heparins, LMWHs, direct thrombin inhibitors, & factor Xa inhibitors are used to prevent AND treat



Adverse effects


Bleeding (localized or systemic)


Heparin-induced thrombocytopenia (HIT) (from decreased plat)


N/V, abdominal cramps, thrombocytopenia

Anticoagulants/antithrombolytics


MOA


Indications


Adverse effects

MOA


Inhibit the action or formation of clotting factors


Does not "thin" the blood, it prevents clot formation


Has no direct effect on an already formed clot


Used prophylactically to prevent thrombi/emboli



The MOA depends on the drug (where it works in the clotting cascade)



Indications


MI, unstable angina, a-fib, in dwelling devices, & major orthopedic surgeries


Warfarin prevents


Heparins, LMWHs, direct thrombin inhibitors, & factor Xa inhibitors are used to prevent AND treat



Adverse effects


Bleeding (localized or systemic)


Heparin-induced thrombocytopenia (HIT) (from decreased plat)


N/V, abdominal cramps, thrombocytopenia

6 types of anticoagulants

Heparin


Warfarin


Thrombin inhibitors


Antiplatelets


Methylxanthine derivatives


GP IIb/IIIa inhibitors

Heparin:


Dose, route, where/how is it given?


Onset/half-life


MOA


What is HIT treated with?


What should happen with OD?


Can it be given with pregnancy?


PTT therapeutic range

Dose is weight based


SQ (abd) or IV & cked by 2 RNs


Do not aspirated or massage site


Onset is immediate half-life is 1-2hr


MOA: binds to Antithrombin III, turns off factors II, IX, & X (thrombin is most sensitive to factor II)



HIT tx with direct thrombin inhibitors - lepirudin or argatroban



If OD occurs, may be able to just drop machine, depending on dose, if dose is intentionally larger for certain cases protamine sulfate should be admin



Can be given with pregnancy



PTT between 45-70

Heparin:


Dose, route, where/how is it given?


Onset/half-life


MOA


What is HIT treated with?


What should happen with OD?


Can it be given with pregnancy?


PTT therapeutic range

Dose is weight based


SQ (abd) or IV (preferably upper quads) & cked by 2 RNs


Do not aspirated or massage site


Onset is immediate half-life is 1-2hr


MOA: binds to Antithrombin III, turns off factors II, IX, & X (thrombin is most sensitive to factor II)



HIT tx with direct thrombin inhibitors - lepirudin or argatroban



If OD occurs, may be able to just drop machine, depending on dose, if dose is intentionally larger for certain cases protamine sulfate should be admin



Can be given with pregnancy



PTT between 45-70

Heparin: Low Molecular Weight Heparins (LMWHs)


2 drugs


Why is this drug preferred?


Admin where?


MAO


Contraindicated

Enoxparin (Lovenox) & dalteparin (Fragmin)



Preferred because it has a predictable anticoagulant response & does not require labs



Admin in abd (prefer upper quads)



Inhibits ONLY factor X



Contraindicated in in dwelling epidural catheters = hematoma

Warfarin


MOA


Adverse effects


Interactions


Antidote


Contraindications


Teaching


Therapeutic & Normal PT level

MOA


Inhibits vit K synthesis by bacterian in GI tracts which inhibit the production of clotting factors II, VII, & X (vit k-dependent clotting factors are normally synthesized in liver)



Adverse effects


Skin necrosis & "purple toes" syndrome




Drug/food interactions


Amiodorone, fluconazole, erythromycin, metronidazole, sulfonamide atbs, & cimetidine


Capsium pepper, feverfew, dong quia, garlic, ginkgo, & St. John's wort



Antidote vitamin k (phytonadione)



Contraindicated in pregnancy



Teach drug is for long term use


Takes 3 days to reach active level


Tomatoes and green leafy veggies can decrease effectiveness



PT normal - 1.5-2.5 therapeutic - 2-3

Bridge therapy

When pt is being switched from heparin/LMWH to warfarin OR vice versa, there needs to be several days overlap, during which bleeding risk increases



Warfarin has a very long half-life, when pt is having surgery, they will switch to heparin/LMWH so that it can be quickly d/c'd before surgery because heparin has a shorter half-life

Thrombin inhibitors


Drugs (5)**


Indications


How to take


Side effects & adverse effects


Teaching



Thrombin factor Xa inhibitor


drug (2)


MOA


Contraindications

Human Antithrombin III (Thrombate)


lepirudin (Refludan)


bivalirudin (Andriomax)


argatroban (Argratroban)


dabigatran (Pradaxa)**



Prophylactic for A-Fib & DVT



Oral: do not chew or crush



Side effect abdominal discomfort


Can have serious adverse effects (d/t no lab monitoring/no antidote--half life is 12-17 hrs**)



Teach to discontinue 1-2 days before surgery or dental procedure


Lapses in therapy increases stroke risk



Factor Xa inhibitors


Same effects as direct thrombin inhibitors but more selective


fondaprainus (Arixtra)


Contraindicated with a creat of <30mL/min or body wt <50kg


Stop therapy if PLAT <100,000/microliter



rivaroxaban (Xarelto)

Antiplatelet drugs


Drugs (4)


MOA


Indications

Aspirin (acetylsalic acid)


ADP inhibitors:


clopidogrel (Plavix)


prasugrel (Effient)


ticagrelor (BRILINTA)



MOA


Prevent platelet aggregation; works before the clotting process



Indications


Prevent stoke


Acute unstable angina & MI

Antiplatelets: Aspirin**



MOA


How long do effects last


Indication


Interactions


Contraindications


Teaching


Adverse effects

MOA


Prevents platelet aggregation, results in dilation if vessels & inhibition if platelet aggregation



Effects last up to the plat life (7 days)



81 mg/day to px MI



Do not take with anticoagulants



Contraindicated in children/teens with flulike symptoms because it can cause Reye's syndrome to occur



Teach to d/c 8 days before surgery or invasive procedures



Adverse effects


Drowsiness, dizziness, confusion


Flushing, N/V, GI bleed, heart burn, diarrhea (thorough GI assessment)


Bone marrow suppression (low WBC, RBCS, PLAT


Ototixicity with high doses

Antiplatelets: ADO inhibitors


3 drugs**

clopidogrel (Plavix)


prasugrel (Effient)


ticagrelor (BRILINTA)

Treatment of common cold

Antihistamines


Nasal decongestants


Antitussive


Expectorants



Treatment is symptomatic - not curative



Difficult to identify whether cause is viral or bacterial

MOA of ADP Inhibitors (Plavix)

Inhibits platelet aggregation by altering platelet membrane so that it can no longer receive the signal to aggregate



Inhibits the activation of glycoprotein receptors (GP IIb/IIIa) on a surface of the platelet

ADP Inhibitors: clopidogrel (Plavix)


Adverse effects

Adverse effects


Bone marrow suppression


Flu-like symptoms


Nose bleed

ADP Inhibitors (Plavix)**


Indications

Used to prevent CVA, TIA, & PE

Methylxanthine Deriratives


MOA


Indication (1)


Drug (1)**


Side effects

Decreases blood viscosity to improve peripheral circulation; has antiplatelet effects that make blood cells more flexible


Treats Raynauds Disease; rarely used


pentoxifylline (Trental)


CNS stimulation SE

GP IIb/IIIa Inhibitors


What is GP IIb/IIIa?


MOA


Route


Indication


3 Drugs


Adverse effects


Nursing care

GP IIb/IIIa are a component of the platelet membrane which is a potent stimulator for platelet adhesion


MOA


Blacks the receptor protein in the platelet wall membranes


Prevents thrombi formation


Route - IV


Indication - Px thrombi formation in critical situations like cardiac life support to increase perfusion


Drugs


tirofan (Aggrastat)


eptifibatide (Integrilin)


abciximad (ReoPro)



Adverse effects


Increased Risk for stroke


Bradycardia, hypotension, edema, dizziness, thrombocytopenia



NC


Continuous C/V monitoring

INR therapeutic range & control



PTT therapeutic range**

INR


therapuetic - 2-3


control - 1.5 - 2.5



PTT 45-70


Decongestants


3 main types

Adrenergic


Anticholinergic


Corticosteroids (Inhaled intranasal steroids)

Adrenergic decongestants


What does it stimulate?


Contraindications


Drug (1)


Adverse effects

Constricts/Sympathomimetic


Contricts small blood vessels of nasal sinuses via alpha receptors. Tissue shinks & nasal secretions in the swollen mucous membranes are better able to drain.



Avoid with MOAIs


phenylephrine (Neo-Synephrine)



Adverse effects


Nervousness, insomnia, palpitations, tremors, HTN, tachycardia (Caused by SNS effects caused by stimulation of heart, blood vessels, & CNS)

Anticholinergics


Popularity


What does it stimulate?


Drugs (1)

Less commonly used


Parasympathomimetics



ipratropium (Atrovent)

Common cold


Most caused by:


2 types

Most caused by viral infection


Rhinovirus


Influenza

Corticosteroids (Inhaled Intranasal steroids)



MAO


Contraindications


Drugs (5)


Adverse effects

Anti-inflammatory effect - work to turn off the immune system cells involved in the inflammatory response. Decreased inflammation = decreased congestion.



Contraindicated with nasal mucosal infection



Beconase, Rhinocort, Nasalide, Flonase, Nasacort, Omnaris



Adverse effects


Local mucosal dryness & irritation

Decongestants:


Route -- differences


Drug effects


Indications


Contraindications/Precautions


Nursing Care

Oral (Systemic)


Delayed onset, prlonged duration


Less effective d/t first pass


No rebound congestants


Exclusively adrenergics


Ex - pseudophedrine (Sudafed)



Inhaled/Topical


Fast onset - quick duration


Potent


No systemic effects


Sustrained over several days causes rebound congestion, tamper medication with oral route***



Drug Effects


Shrink engorged nasal mucous membrane


Relieve nasal stuffiness



Indications


Rhinitis


Common cold


Sinusitis


Hay fever


Allergies


Surgery/diagnostic procedures to facilitate viewign



Contraindications


Cardiovascular/CNS disorders


Narrow angle glacoma,


Diabetes


Hyeprthyroidism


Prostate disease (d/t adverse effects)


Caffeine-containing products



Caution with antihypertensive meds



Nursing care


Report sx that exceed 1 week

Coughing

In some cases, couhging can be harmful, such as after hernia repair surgery



Cough center is stimulated by stretching of bronchi alveoli, & pleura being stretched

Antitussives:


Indication


2 types


Drugs (2)


MOA of each


Adverse effects


Contraindications


Cautions


Nursing Care

Indication


For nonproductive cough & cases where cough is harmful



2 types


Opoiods


Nonopoiods



MOA of each


Opoiods


Suppresses the cough reflex by direct action on the cough center in the medulla


Ex - codeine (Robitusin A-S, Dimetant-DC), hydrocodone)


Have a drying effect on mucosa, to thicken secretions (to px runny nose)



Non-opioids


Suppress the cough reflex by numbing the stretch receptors in the respiratory tract & preventing the cough reflex from being stimulated


Ex - benzonatate (Tessalon Perles), dextromethorphan (Vicks Formula 44, Robitussin-DM--^r/f abuse*)


Benzonatate - suppresses the cough relfex by anesthetizing (numbing) the stretch receptors in the resp. tract, which prevents reflex stimulation of the medullary cough center


Dextromethorphan - contraindicated in hyperthyroidism, cardiovascular disease, HTN, glaucoma, & MAOI use



Adverse effects


Decreased CNS effects: dizziness, H/A, sedation, N/V, drowsiness, sedation, lightheadedness, constipation, respiratory depression



Contraindications


Alcohol use, MAOIs, Antihistamines, Opioid drugs



Cautions


With CNS depression, anoxia, hypercapnia, respiratory depression, COPD, & renal impairment



Nursing Care


-Perform respiratory & cough assessment


-Instruct to avoid driving/operating machinery because of CNS effects


-Don't administer with adventitious lung sounds because it needs expectorated


-Report cough that last >1wk, persistent H/A, fever, or rash


-Safety assessment r/t SE of dizziness, sedation, & drowsiness

Traditional


What makes them bettter than non-sedating?


6 drugs



Can you stop them abruptly?

Older



Work peripherally & centrally; cross blood-brain barrier (increased r/f fall)


Have anticholinergic effects, making them more effective than nonsedating drugs in some cases



diphenhydramine (Benadryl), brompheniramine, chlorpheniramine, dimenhydrinate, meclizine, promethazine



Rebound effect if stopped abruptly**

COPD: Asthma


Stepwise therapy for the management of asthma

Step Drug Class


Step 1 - Short-acting inhaled beta2, agonist PRN


Step 2 - Low- dose inhaled corticosteroid


Step 3 - Low- dose ICS & long acting beta 2 agonist or medium-dose ICS


Steph 4 - Medium dose inhaler plus LABA


Steph 5 - High-dose ICS & LABA; + omalizumab x allergies


Step 6 - High dose ICS & LABA & corticosteroid & consider omalizumad for allergies

COPD: Chronic Bronchitis

Chronic inflammation & low grade infection of the bronchi)

COPD: Emphysema

Condition of the lungs characterized by enlargement of the air spaces distal to the bronchiales

COPD


Def & Sx

Obstruction of air flow through small airways; asthma has chronic aspects & acute episodes during which there is:


Bronchospasms


Inflammation of the bronchial mucosa


Edema of bronchial mucosa


Production of viscous mucus

Bronchodilators


What do they do


2 classes

Relax Bronchial smooth muscle, which causes dilation of the bronchi & bronchiales that are narrows as a result of the disease process



Beta-adrenergic agonists


Anticholinergics

MOA of ADP Inhibitors (Plavix)

Inhibits platelet aggregation by altering platelet membrane so that it can no longer receive the signal to aggregate



Inhibits the activation of glycoprotein receptors (GP IIb/IIIa) on a surface of the platelet

Bronchodilators:


Beta-Adrenergic agonists


MOA


Indications


Contraindications


SE to report



Short-acting


Drugs (5)


Long-acting


Drugs (5)


MOA



3 types of Beta agonists


Nonselective Adrenergics


MOA


Indication


Drug (1)


Adverse Effects



Nonselective beta-adrenergics


MOA


Drug (1)


Adverse effects



Selective Beta2 adrenergics


MOA


Drug


Adverse effects


What happens if used too long


Beta-Adrenergic agonists


MOA


Activation of beta2 receptors activates a beta agonist called adenylate cyclase which makes cAMP, which relaxes smooth muscle in the airway & results in bronchial dilation & increased airflow



Indications


-Relief of bronchospasm r/t asthma, bronchitis, & other pulmonery disease; used to treat & px acute attacks


-Hypotension & shock


-Produces relaxation to px premature labor



Contraindications


HTN, dysrhythmias, CVA


Use of beta blockers or MAOIs



Caution with Dm



SE to report


Insomnia, jitteriness, restlessness, palpitations, chest pain, or any change in sx



Short-acting


Drugs


albuterol (ventolin)


levabuterol (Xonpenex)


pirbuterol (Maxair)


terbutaline (Brethine)


metaproterenol (Alupent)


Long-acting


Drugs


Arformoterol (Brovana)


formoterol (Forafil, Performist)


salmeterol (Serevent)


MOA


Stimulates adrenergic receptors in SNS



3 types of Beta agonists


Nonselective Adrenergics


MOA


stimulate alpha, beta 1 (cardiac), & beta2 (resp) receptors; emergencies only; alpha receptors cause constriction within the blood vessels which reduce the edema of the mucous membranes & limits secretions normally made


Drug (1)


epinephrine (epipen)


Adverse Effects


insomnia, restlessness, anorexia, vascular h/a, hyperglycemia, tremor, cardiac stimulation (SNS respon



Nonselective beta-adrenergics


MOA


Stimulate both beta1 & beta2 receptors


Drug


metaproterenol (Alupent)


Adverse effects


(from beta1 cardioselective receptors) Cardiac stimulation, tremor, angina pain, vascular H/A, HTN



Selective Beta2 adrenergics


MOA


Stimulates only beta2 receptors


Drug


albuterol (Proventil)


Adverse effects


(Less effects) Hypotension/Hypertension, vascular h/a, tremor



What happens if used too long?


If used to often, may lose beta2 effects & start using beta1 receptors--causing such (heart) SE


Anticholinergics


MOA


Drugs (2)


Adverse effects


Indications


Contraindications


Precautions

MOA


Causes bronchial constriction & narrowing of the airways. Anticholinergics bind to Ach (PSNS) receptors on the bronchial tree, preventing Ach from binding. Results in airway dilation, preventing bronchoconstriction



Drugs


ipratropium bromide (Atrovent)


triotropium (Spiriva)



Adverse effects


Dry mouth/throat, nasal congestion, heart palpitations, GI distress, H/A, coughing, anxiety



Indications


Used to px brochoconstriction


Chronic bronchitis or emphysema bronchospasms -- NOT used for acute symptoms - action is slow & prolonged



Contraindications


Allergy to drug (ex - atropine), or peanuts or legumes;



Caution


Narrow angle glaucoma & prostate enlargement

Xanthine derivative


2 types


MOA


Drug effects


Indications


Adverse effects


What to report


Contraindicated


Interactions

2 types


Plant Alkaloids - Caffeine, theobromine, theophylline (metabolizes to caffeine)


Only theophylline is used clinically


Synthetic Xanthines: aminophylline (metabolized to theophlline) & dyphilline



MOA


Increases levels of E-producing cAMP-=this is done by competitively inhibiting phosphodiesterase (PDE), the enzyme that breaks down cAMP. Results in decreased cAMP levels, smooth muscle relaxation, brocnhodilation, increased airflow



Drug effects


Causes bronchodilation by relaxing smooth muscle in the airways. Results in relief of bronchospasm & greater airflow into & out of the lungs. Also causes CNS stimulation (increases RR)


-Causes cardiovascular stimulation: increases force of contraction, increased HR, resulting in increased CO & increased blood flow to the kidneys/GFR (diuretic effect)--increased perfusion


-Higher intracellular levels of cAMP contribute to smooth muscle relaxation & inhibit IgE-induced release of chemical mediators that drive allergic reactions



Indications


-Dilation of airways in asthmas, chronic bronchitis, & emphysema


-Mild to moderate cases of acute asthma


-Adjunct drug in tx of COPD


-Not used as frequently because of potential for drug interactions & variables related to drug levels in the blood; more as a preventative dose than for acute tx; Usually only used with end-stage COPD



Adverse effects


Sinus tachycardia, extrasystole, palpitations, ventricular dysrhythmias, anorexia, GERD while sleeping, increased urination, hyperglycemia



What to report


N/V, restlessness, insomnia, irritability, tremors



Contraindicated


Dysrhythmias, seizure, hyperthyroid, PUD



Interactions


allopurinol, cimetidine, marcolide atb (erythromycin), Cipro, flu vaccine, oral contraceptives; smoking increases xanthine metabolism; foods: charcoal-broiled, high protein, low carb foods = low serum levels

ADP Inhibitors: clopidogrel (Plavix)

Adverse effects


Bone marrow suppression


Flu-like symptoms


Nose bleed

ADP Inhibitors (Plavix)

Used to prevent CVA, TIA, & PE

Methylxanthine Deriratives


MOA


Indication (1)


Drug (1)


Side effects

Decreases blood viscosity to improve peripheral circulation; has antiplatelet effects that make blood cells more flexible


Treats Raynauds Disease; rarely used


pentoxifylline (Trental)


CNS stimulation SE

GP IIb/IIIa Inhibitors


What is GP IIb/IIIa?


MOA


Route


Indication


3 Drugs


Adverse effects


Nursing care

GP IIb/IIIa are a component of the platelet membrane which is a potent stimulator for platelet adhesion


MOA


Blacks the receptor protein in the platelet wall membranes


Prevents thrombi formation


Route - IV


Indication - Px thrombi formation in critical situations like cardiac life support to increase perfusion


Drugs


tirofan (Aggrastat)


eptifibatide (Integrilin)


abciximad (ReoPro)



Adverse effects


Increased Risk for stroke


Bradycardia, hypotension, edema, dizziness, thrombocytopenia



NC


Continuous C/V monitoring

INR therapeutic range & control



PTT therapeutic range

INR


therapuetic - 2-3


control - 1.5 - 2.5



PTT 45-70


Types of URI

common cold, laryngitis, pharyngitis, rhinitis, sinusitis, tonsilitis

Pathophys of URI

Infection & Allergens cause inflammatory response



Histamine bind to H1 receptors on membranes & vessels



Excessive mucus production results from inflammatory response to histamine invasion



Fluid drops down the pharynx into esophagus & lower resp tract, causing cold symptoms: sore throat, cough, upset stomach



Irritation of nasal mucosa triggers:


Sneeze reflex


Release of inflammatory vasoactive substances, dilating small blood vessels in the nasal sinuses & causing nasal congestion

Non Bronchodilating Drugs (4)

Leukotiene Receptor Antagonists (LTRAs)



Inhaled Corticosteroids (glucocorticoids)



Phosphodiesterase-4 Inhibitor



Monoclonal Antibody



Antiasthmatic

Non Bronchodilating Drugs (4)

Leukotiene Receptor Antagonists (LTRAs)



Inhaled Corticosteroids (glucocorticoids)



Phosphodiesterase-4 Inhibitor



Monoclonal Antibody



Antiasthmatic

Leukotreine Receptor Antagonists (LTRAs)


2 types


3 drugs


What are leukotrienes?


MOA


Drug Effects


Indications


Adverse effects


Contraindications


Nursing care

What are leukotrienes?


Substances released when a trigger, such as car hair, starts a series of chemical reactions in the body. The leukotrienes cause an allergic reaction.



MOA


LTRAs prevent leukotrienes from attaching to receptors on cells in the lung and in circulation. Inflammation is blocked, & asthma symptoms are relieved.



Drug Effects


LTRAs are the first medication to focus on the immune response of asthma rather than treating with bronchodilators.


-Prevent smooth muscle contraction of the bronchial airways


-Decrease mucus secretion


-Prevent vascular permeability (thus decrease congestion)


-Decrease neutrophil &leukocyte mobility to the lungs preventing inflammation



Indications


Prophylaxis & treatment of asthma in pt >12 y/o


NOT meant for management of asthma attacks


Montelukast is treats allergic rhinitis



Adverse effects


H/A, nausea, dizziness, insomnia, liver dysfunction (AST/ALT*), diarrhea



Contraindications


Allergy to povidine, lactose, titanium dioxide, or cellulose; don't take with phenobarbital or rifampin



Nursing care


Effects take 1 wk


Med red for drug interactions


Liver tests before therapy


Take q night even if sx improve


Narrow therapeutic range - monitor lab values*

Non-Bronchodialating drugs:


Inhaled corticosteroids (aka glucorticoids)


Drugs (7)


MOA


What does it work as?


Routes? -- whats the difference?


Indications


Adverse effects


Contraindications


Nursing care

Drugs


beclomethasone dipropionate (Beclovent)


budesonide (Pulmicort Turbuhaler)


dexomethasone sodium phosophate (Decadron Phosphate Respihaler)


fluisolide (AeroBid)


fluticasone (Flunase)


triamcinolone acetonide (Azmacort)


ciclesonide (Omnaris)



MOA


Stabilize membranes of WBCs that release harmful bronchoconstricting substances. Increase responsiveness of bronchial mooth muscle to beta-adrenergic stimulation. Reduces inflammation & enhance beta agonist activity.



What does it work as?


Anti-inflammatory



Routes? -- whats the difference?


Oral & inhaled form - inhaled from reduces systemic effects



Indications


Persistent Asthma; often used concurrently with beta-adrenergic agonists



Adverse effects - pharyngeal irritation, coughing, dry mouth, oral fungal infection (RINSE MOUTH*), systemic effects are rare



Contraindications


Candida infection (corticosteroids suppress immune system)



Nursing care


Takes several weeks for full effect


Teach pt to monitor dx with peak-flow meter


Encourage spacer device x successful inhalation

Phosphodiesterase-4 Inhibitor


Drug (1)


Indication


Adverse effects

roflumilast (Daliresp)


Indicated to prevent coughing & excess mucus; used to decrease fatal COPD exacerbations


Adverse effects - N/V/D, H/A, insomnia, dizziness, wt loss, psychiatric symptoms

Phosphodiesterase-4 Inhibitor


Drug (1)


Indication


Adverse effects

roflumilast (Daliresp)


Indicated to prevent coughing & excess mucus; used to decrease fatal COPD exacerbations


Adverse effects - N/V/D, H/A, insomnia, dizziness, wt loss, psychiatric symptoms

Monoclonal Antibody Antiasthmatic


Drug (1)


MOA


Route (1)


Nursing care (1)

omalizumab (Xolair)


MOA


selectively binds to IgE, which in turn limits the release of mediators of the allergic response


Route - injection


NC


Potential for producing anaphylaxis - monitor closely x hypersensitivity - not given to take at home

Nursing care for drugs treating the lower respiratory tract

Encourage pt to take measures to promote generally good state of health so as to prevent, relieve, or decrease symptoms of COPD


- Avoid exposure to conditions to precipitate bronchospasms (allergens, smoking, stress, air pollutants)


- Adequate fluid intake


- Compliance with medical tx


- Avoid exercise, fatigue, heat, cold, & caffeine



Encourage prompt tx for flu & to get vaccinated against flu/pm



Perform thorough assessment before beginning therapy


-Skin color, VS, SaO2, Sputum character, Allergies, PMH, Medications



Teach use of MDIs



Monitor for therapuetic effects:


Deceased dyspnea, wheezing, restlessness, anxiety


Increased respiratory pattern, activity tolerance, & ease of breathing