Respiratory
Drugs to Treat Respiratory Conditions
NSG 220
Structures of the Respiratory System
The upper respiratory tract consists of:
Nose
Paranasal sinus
Pharynx
Larynx trachea
The lower respiratory tract consists of:
Lungs
Bronchi
Bronchioles
Alveoli
This week we will review drugs that effect the respiratory system. We will discuss drugs that are used to treat upper respiratory tract illnesses and lower respiratory tract illnesses.
The upper respiratory tract consists of:
Nose
Paranasal sinus
Pharynx
Larynx trachea
The lower respiratory tract consists of:
Lungs
Bronchi
Bronchioles
Alveoli
Covering of the lungs-visceral (lining covering the organ/lung) and parietal (lining of the body cavity) layer, pleural space between the visceral and parietal layer which contains fluid eliminating friction.
We have diseases that affect the airway and as well illnesses that affect the airway such as the common cold, allergic rhinitis, sinus infections.
We know that when a person takes a breath, the thorax increases in size, pressure inside intrapleural and intrapulmonic layers(always negative) decrease, air rushes from the atmosphere all the way to the alveoli.
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Acute & Chronic Respiratory Diseases and Illnesses
Acute Respiratory Illnesses
Allergic Rhinitis
Common cold
Obstructive Airway Diseases
Asthma
Chronic Bronchitis
Emphysema
Class of Meds to discuss
Bronchodilators (inhaled)
corticosteroids (intranasal),
antihistamines (oral and intranasal), and
sympathomimetics (oral and intranasal)
*mast cell stabilizers
*Not discussed but treat asthma
Obstructive Airway- difficulty exhaling air- limitation of airflow due to partial or complete obstruction (once air is in difficult to exhale)
Restrictive- difficulty inhaling air (reduced expansion of the lung)
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Obstructive Airway Diseases
Asthma
Chronic inflammation of the airways
Caused by environmental triggers (medications, air pollution, allergens)
Smooth muscles around bronchioles spasm causing narrowing of airways
Increased mucous production
Initially reversible - long term is irreversible due to edema, fibrosis & scarring causing thickening of the “basement membrane”
COPD (group of diseases)
Emphysema
Structural changes- destruction of alveolar septa and elasticity of bronchial walls
Enlarged, weakened air spaces
Chronic Bronchitis “Inflammation of bronchial tubes”
Productive cough
3 months each year for 2 or more years
Called obstructive disease because you can get air out compared to restrictive diseases where you can’t get air in (osis- sarcoidosis)
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Bronchodilators
Albuterol- beta 2 agonist
1st given for severe attacks “only rescue inhaler”
Acts quickly, but doesn’t last long (short acting)
Give before steroid inhaler
Ipratropium- “anticholinergic effect”
Given 2nd during severe/acute attacks
Reduces mucous secretions
Methylxanthines (Theophylline)
Can be toxic due to narrow therapeutic range. Over 20 mcg/ml considered toxic
MOA
Beta 2 agonist dilates the bronchi opening up airways/ relax smooth muscles
Also works on beta- 1 which causes the heart to beat fast – will also feel jittery, anxious
Nursing Implications:
Avoid giving patient NSAIDs (worsens asthma)
Avoid Betablockers (can cause bronchospasms)- decreased response to beta-agonist
During severe respiratory attacks “A-I-M”
Use in sequence
Albuterol
Ipratropium
Methylprednisone
Beta 2 agonist- short acting (SABAs) to provide quick relief, given orally or by inhaler
Asthma can be treated with bronchodilators, which are beta-2 receptors agonists (stimulators) which causes the lungs to expand. People with heart conditions, however, are given the opposite: beta-receptor antagonists. Beta blockers block the effects of the hormone epinephrine.
**Remember the lungs are constricted during an asthma attack. Epinephrine is floating around to expand the lungs. But when a non-specific beta blocker is given, it blocks the bronchodilators which stimulates the lungs to open action. *** So avoid all beta blockers
Some betablockers are cardioselective and others are non-cardioselective meaning that they can block beta-1 (heart) or beta-2 (lung) receptors. If given to a person with asthma, it would block effects of bronchodilator (beta-2) resulting in narrowing of the airways.
AIM – Albuterol (1st fastest), Ipratropium (, Methyl-prednisone (Solumedrol)- slow steroid reduces inflammation
Anticholinergics becareful when giving to patients who are already dry, “fluid volume deficit”
Methylxanthines- can be toxic 10-20 mcg/ml therapeutic range. Over 20 mcg/ml is considered toxic so frequent blood draws must be obtained. Avoid given with beta-blockers
**Do not take with Ciprofloxacin or Cimetidine- can increase toxicity risk.
Avoid caffeine.
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Steroids & Anti-inflammatory Drugs (Beclomethasone, Fluticasone)
Methylprednisolone & Beclomethasone
Corticoid inhaler works directly on respiratory system reducing inflammation
Usually always given in the event of an asthma attack despite improvement
Mechanism of Action (MOA)
Reduce Swelling & Inflammation
Nursing implications
Onset of medication is slow –not a rescue medication
Increases blood glucose “sones”
Suppress the immune systems, slow wound healing
**Remember glucocorticosteroids (prednisone, dexamethasone, hydrocortisone) are for total body swelling, corticosteroids are respiratory specific
Leukotriene Inhibitors (Montelukast)**
MOA:
Suppresses the effects of leukotrienes (ultimately reducing inflammation)
Nursing Implications
Given in combination with steroids & albuterol
Long term management of chronic resp conditions
Takes 1-2 weeks for drug to reach therapeutic effect
** most commonly used
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Things to teach patient:
Albuterol
The only rescue inhaler to be used during an acute episode (neb or INH)
Can make the pt. feel “jittery/shaky” and heart rate usually increases during/after treatment
Ipratropium
Increase fluid intake
If pill form, make sure the patient does not swallow pills
Methylxanthines
Caffeine increases stimulation-increase chances of arrythmias
Always take in the morning due to restlessness
Antibiotics- Ciprofloxacin and Levofloxacin increase risk of toxicity “seizures”
Allergic Rhinitis
Most common allergic disorder
Inflammatory disorder of the upper airway
Symptoms: sneezing, rhinorrhea (runny nose), pruritis (itching), conjunctivitis, sinusitis, and nasal congestion (dilation and increased permeability of nasal blood vessels.
Triggers: airborne allergens
Two types:
Seasonal “hay fever” occurs during spring and fall due to outdoor allergens (fungi, pollen, grasses, trees)
Perennial (nonseasonal) triggered by indoor allergens usually in the home (dust mite and pet dander).
Drugs to Treat Upper Respiratory Symptoms
Decongestant (Sympathomimetics)
Oral: Pseudoephedrine** (Sudafed),
Nasal Sprays & drops: Phenylephrine (Neo-Synephrine), Oxymetazoline (Afrin)
Mechanism of Action: Stimulates alpha-adrenergic receptors causing vasoconstriction of the capillaries in the nasal mucosa
Adverse reactions: Palpitations, tachycardia, hypertension
Side effects: Drowsiness, GI irritation, Dry mouth**
Nursing Implications
Rebound congestion can occur with intranasal administration.
Avoid taking with other medications that act as sympathomimetics.
** Pseudoephedrine has the potential to be abused. Patients must purchase with a photo ID and maybe subjected to limited amounts to be purchased. (also counted at medical facilities)
Expectorants: Dextromethorphan, Guaifenesin
Mechanism of Action: Liquefy mucus by increasing respiratory tract secretions via oral absorption; available in oral preparations
Adverse reactions: GI irritation, Skin Rash, dizziness, irregular heart rate
Side Effects: Fatigue, constipation
Nursing Implications:
Promote increasing po fluids
Encourage coughing and deep breathing
Assess Respiratory Status
Have suction available
Tuberculosis
Caused by
Mycobacterium tuberculosis, Mycobacterium leprae, Mycobacterium avium
Slow growing requiring prolonged treatment
Spread through droplets propelled in the air
Coughing
sneezing
saliva
Caused by- because of these drug toxicities can occur and non-compliance makes it difficult to treat.
People don’t have any symptoms and don’t know they have it (90% of people) . Referred to as latent
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Tuberculosis
Populations
HIV
Foreign born
Pathogenesis
Immunity to M. Tuberculosis develops within weeks
Reactivation can occur in 5-10%
Treatment
Disease requires prolong therapy usually 3-9 months depending on treatment regimen
Protection against TB can be confirmed by inoculation with bacillus Calmette-Guérin (BCG) vaccine
Caused by- because of these drug toxicities can occur and non-compliance makes it difficult to treat.
People don’t have any symptoms and don’t know they have it (90% of people) . Referred to as latent
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Tuberculosis can be…
Latent (Inactive)
Not contagious, patient doesn’t have symptoms
Bacteria is inactive causing no symptoms
Can develop into active TB (5-10% of population with inactive TB) w/o treatment
Must be treated
Active
Contagious until the TB medications have been taken for two weeks
**Yes, you can catch TB more than once!
Person with latent TB may have a negative CXR, but a positive TB test
Reinfection is common
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Treating TB- Latent vs. Active
Active TB
Goal: Treat and prevent reactivation
Drug Treatment
Isoniazid (see Latent TB info)
Rifampin
(elevates LFTs
Urine, tears & sweat may turn orange)
Pyrazinamide (elevates LFTs)
Ethambutol
optic neuritis – inflammation causing vision impairment
Active TB always treated with 2 or more drugs
Mutation causing resistance.
Resistance to one drug only. So should treat with 2 different drugs to prevent reactivation
Latent TB
Drug Treatment
Isoniazid (INH) (active & latent)*
metabolized in the liver/excreted by the kidneys
teach patients to reduce or eliminate consumption of alcohol to reduce risk of hepatotoxicity.
Can cause liver damage- monitor liver function panel
isoniazid alone taken daily for 6 or 9 months
taken weekly for 3 months when combined with rifapentine
administered IM and PO
Rifampin (RIF) daily
for those who have isoniazid-resistant TB or cannot take isoniazid for other reasons
take for 4 months
Isoniazid plus rifapentine (3 months)
Once weekly
*primary prescribed agent
Don’t forget education….
Isoniazid can cause damage to the liver cells and cause hepatic necrosis.
Teach patients to identify
signs of hepatitis (jaundice, anorexia, malaise, fatigue, nausea) and notify provider immediately.
peripheral neuropathy (tingling, numbness, burning, or pain in the hands or feet), and instruct them to notify the prescriber if these occur. “
Can suppress the metabolism of certain drugs such as phenytoin causing toxic levels. Dosage may need to be adjusted.
Monitor labs
Monitor phenytoin levels
Monitor liver function test (i.e. AST)
Nursing Implications
Monitor Liver function test & Kidney function test
INH is metabolized in the liver and excreted by the kidneys
Hepatotoxicity
Cautioned in patients with renal impairment
Can reduce the effects of other drugs (increase metabolism- breaking down fast and not working).
Women taking birth control should use another form of oral contraceptive.
Phenytoin (Dilantin)- suppresses metabolism and can cause elevated levels
Adverse reactions:
Hepatotoxic
Dose-related peripheral neuropathy
Rifampin – red-orange tinged body fluids “harmless”
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Questions