respiratory system Flashcards
what is the purpose of the upper respiratory tract
- ventilation
- humidification
- protection
- cilia
- goblet cells
- mast cells
what makes up the upper respiratory tract
- paranasal sinuses
- nasal cavity
- soft palate
- hard palate
- nostril
- oral cavity
- tongue
- trachea
- pharynx
- larynx
- vocal cords
what is allergic (seasonal) rhinitis
- related to genetics and activated by environmental factors
- inflammation of the membranes of eyes, nose and throat
- reversible treatment
what is the common cold
- viral
- variety of symptoms
- self-limiting, no cure
- symptom treatment
what are drugs that affect the upper respiratory tract
- antihistamines
- decongestants
- antitussives
- expectorants
- mucolytics
what are histamines and what released them
- chemical mediators of inflammation
- released from mast cells and basophil cell
what do histamines cause
- itching
- increased mucous secretion
- nasal congestion
- severe cases
- bronchoconstriction, edema, hypotension
- anaphylaxis
antihistamines 1st generation drug name
diphenhydramine (benadryl)
antihistamine 2nd generation drug name
loratadine (claritin)
antihistamines-mechanism of action
- block histamine 1 receptor sites (H1 receptor antagonist)
- suppresses mucous secretion (drying effect)
antihistamines-therapeutic uses
- allergic rhinitis
- hives
- anaphylaxis
- motion sickness
- insomnia
- pre-medicate (red man syndrome with vancomycin and mild blood transfusion reaction)
antihistamines-adverse effects
- dry mucous membranes
- sedation (do not mix with CNS depressants, paradoxical effect among children)
- side effects are decreased for 2nd generation drugs
what are the different types (2) of decongestants
- oral (systemic effects)
- pseudoephedrine (sudafed)
- nasal sprays (localized effects)
- oxymetazoline (afrin)
decongestants- mechanisms of action
- sympathomimetics-target local vasculature of the nose causing vasoconstriction
- reduces membrane inflammation (stuffiness)
decongestants-therapeutic uses
- allergic rhinitis
- common cold
decongestants-adverse effects
- systemic effects=tachycardia and agitation
- localized effects=rebound congestion if taken for more than 3-5 days
what are antitussive medications (opiates)
codeine and hydrocodone
what are antitussive medications (non-opiates)
- dextromethorphan (delsym)
- benzonatate (tessalon pearls)
antitussives-mechanism of action
- primarily depresses cough center in medulla
- treatment of NONPRODUCTIVE cough
antitussive-therapeutic uses
common cold or allergies
antitussives-adverse effects
- opiate effects
- dizziness
- drowsiness
- respiratory depression -reversal agent is naloxone
- constipation
- potential for abuse
- non-opiate effects are drowsiness
what are expectorant medications (protype)
guaifenesin (mucinex)
expectorants-mechanism of action
increasing the effective hydration of the respiratory tract, decreasing viscosity and promoting expectoration (to eject from the throat or lungs by coughing or hawking and spitting)
expectorants-therapeutic use
common cold
expectorants-adverse effects
- few significant effects (GI symptoms)
- increase fluid intake to maximize effectiveness
- limit use to 1 week max
what are mucolytic drugs (prototype)
acetylcysteine (mucomyst)
mucolytics-mechanism of action
- reacts directly with thick mucus to loosen secretions
- enhances flow of secretions
- nebulization provides direct contact of medication with secretions and also provides humidity to affected airways
mucolytics-therapeutic uses
- common cold
- antidote for acetaminophen overdose
mucolytics-adverse effects
- bronchospasms
- nausea/vomiting
- rash
- smells like sulfur (rotten eggs)
what is the purpose of the lower respiratory tract
- respiration
- alveoli
- surfactant
- medulla/CNS
- SNS/PSNS balance
what is pneumonia
- inflammation of the lungs (leads to ineffective gas exchange)
- bacterial/viral/aspiration
s/s of pneumonia
- SOB
- fatigue
- fever
- poor oxygenation
what is bronchitis
- bacterial/viral
- narrowed airway due to swelling/increased blood flow
what is asthma
- chronic inflammatory disorder of the airway
- genetic/activated by allergens/activation of mast cells
- inflammation, bronchoconstriction/spasm, mucus plugging
- breathlessness, chest tightness, wheezing, dyspnea, cough
- no treatment, eventually leads to permanent changes in the lungs
what is emphysema (COPD)
- related to smoking/pollution exposure
- bronchioles loose elasticity
- bronchioles hyperinflated
- progressive and permanent
s/s of emphysema
- increased CO2 retention
- minimal cyanosis
- purse lip breathing
- dyspnea
- hyperresonance on chest, percussion
- orthopneic
- barrel chest
- exertional dyspnea
- prolonged expiratory time
- speaks in short jerky sentences
- anxious
- use of accessory muscle to breathe
- thin appearance
what is chronic bronchitis (COPD)
- also related to smoking and pollution
- chronic cough and excessive sputum production
- progressive and permanent
- long term inflammation of the bronchi
drugs that affect the lower airway
- lung surfactants
- anti-inflammatory agents
- leukotriene modifiers
- corticosteroids
- bronchodilators
- beta2-adrenergic agonists
- anticholinergics
- methylxanthines
lung surfactant (prototype)
beractant (survanta)
lung surfactants-mechanism of action
lipoproteins that reduce the surface tension within alveoli, allowing expansion for gas exchange
lung surfactants-therapeutic use
replaces surfactant in neonates with respiratory distress
lung surfactant-adverse effects/nursing interventions
- only used in emergency in newborns
- proper placement of ET tube and direct injection into trachea
- hypotension, bradycardia, pneumothorax, sepsis
leukotriene modifiers (prototype) (anti-inflammatory agent)
montelukast (singulair)
leukotriene modifiers-mechanism of action
- prevent synthesis of or block leukotriene receptor sites
- leukotriene-inflammatory mediators that promote edema, inflammation, and bronchoconstriction
- suppresses inflammation, bronchoconstriction, airway edema, and mucous production
leukotriene modifiers-therapeutic uses
- asthma, allergic rhinitis, and prevention of exercise induced bronchospasm (EIB)
- taken orally at bedtime (peaks in a few hours and symptoms usually worse at bedtime)
leukotriene modifiers-adverse effects
- rare-agitated behavior in children/psychiatric events such as suicidialideations, hallucinations or depression
corticosteroids ( prototypes) (anti-inflammatory agent)
- nasal spray
- fluticasone (flonase)
- inhalation
- beclomethasone (qvar)
- oral
- prednisone (deltasone)
- IV
- hydrocortisone (solu-cortef)
- methylprednisone (solu-medrol)
corticosteroids-mechanism of action
- decrease synthesis and release of inflammatory mediators
- decrease infiltration and activity of inflammatory cells
- decrease edema of the airway mucosa
- prevents inflammation, suppresses airway mucus production, promotes responsiveness of beta 2 receptors
corticosteroids-therapeutic uses
- allergies, asthma, emphysema, chronic bronchitis, anaphylaxis
- “controller drug” does NOT provide immediate relief
- inhaled agents
- long term prophylaxis of asthma
- preferred tx for preventing asthma attacks
- oral and IV agents
- treatments of severe actions or acute asthma episodes
- limit therapy to less than 10 days (usually 5-7 days)
- peak effects in 1-2 weeks if used daily-short term
corticosteroids-adverse effects
- intranasal spray
- nose bleeds
- inhaler
- candidiasis
- hoarseness, dry mouth
- adrenal suppression with long-term, high-dose therapy
- some bone loss
- oral and IV
- systemic effects
- adrenal gland suppression, osteoporosis, hyperglycemia, infection, peptic ulcer, fluid retention (edema), and growth suppression in youth clients
beta2-adrenergic agonist (prototype) (bronchodilators)
albuterol (ventolin HFA)
salmeterol (serevent)
beta2-adrenergic agonists-mechanism of action
- activate the SNS, causes bronchial dilation
- do not have anti-inflammatory properties
beta2-adrenergic agonists-therapeutic use
asthma
COPD
beta2-adrenergic agonists-adverse effects/nursing intervention
- due to beta 2 adrenergic stimulation-tachycardia, agina, restlessness, hypertension, sweating, bronchospasms
- avoid caffeine
- caution use in clients with cardiac disease
beta2-adrenergic agonists-SABAs
- rapid onset of action
- best for acute asthma attacks
- “rescue drug”
- administered every 3-4 hrs prn
- albuterol (ProAir or Proventil HFA)
beta2-adrenergic agonists-LABAs
- slow onset of action
- do not take during acute asthma attack
- therapeutic effects last up to 12 hours
- Black Box warning: increased risk of asthma-related deaths
- salmeterol (serevent)
anticholinergics-bronchodilator (prototype)
- ipratropium bromide (atrovent)
anticholinergic-mechanism of action
- blocks the PSNS, causing SNS domination
- causes bronchial dilation
anticholinergic-therapeutic uses
- COPD, off label asthma
- combine with a beta2-agonist (combivent)
- alternative to SABAs and for asthma exacerbations
- can be taken every 4-6 hours
anticholinergic-adverse effects
dry mouth, cough, hoarseness from anticholinergic effects
methylxanthines-bronchodilator (prototype)
theophylline (theodur)
methylxanthines-mechanism of action
smooth muscle dilation of bronchi and blood vessels
methylxanthines-therapeutic use
- long term management of persistent asthma
- “controller drug” does not provide immediate relief
- peak effects in2 hours
methylxanthines-adverse effects
- GI distress, tachycardia, restlessness (insomnia)
- infrequently used due to safer medications
- narrow therapeutic range of 10-20 mcg/mL, toxicity includes dysrhythmias and seizures which can lead to death
- stay away from caffeine
