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A-Patho/pharm 2 > respiratory system > Flashcards

respiratory system Flashcards

1
Q

what is the purpose of the upper respiratory tract

A
  • ventilation
  • humidification
  • protection
    • cilia
    • goblet cells
    • mast cells
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2
Q

what makes up the upper respiratory tract

A
  • paranasal sinuses
  • nasal cavity
  • soft palate
  • hard palate
  • nostril
  • oral cavity
  • tongue
  • trachea
  • pharynx
  • larynx
  • vocal cords
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3
Q

what is allergic (seasonal) rhinitis

A
  • related to genetics and activated by environmental factors
  • inflammation of the membranes of eyes, nose and throat
  • reversible treatment
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4
Q

what is the common cold

A
  • viral
  • variety of symptoms
  • self-limiting, no cure
  • symptom treatment
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5
Q

what are drugs that affect the upper respiratory tract

A
  • antihistamines
  • decongestants
  • antitussives
  • expectorants
  • mucolytics
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6
Q

what are histamines and what released them

A
  • chemical mediators of inflammation
  • released from mast cells and basophil cell
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7
Q

what do histamines cause

A
  • itching
  • increased mucous secretion
  • nasal congestion
  • severe cases
    • bronchoconstriction, edema, hypotension
    • anaphylaxis
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8
Q

antihistamines 1st generation drug name

A

diphenhydramine (benadryl)

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9
Q

antihistamine 2nd generation drug name

A

loratadine (claritin)

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10
Q

antihistamines-mechanism of action

A
  • block histamine 1 receptor sites (H1 receptor antagonist)
  • suppresses mucous secretion (drying effect)
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11
Q

antihistamines-therapeutic uses

A
  • allergic rhinitis
  • hives
  • anaphylaxis
  • motion sickness
  • insomnia
  • pre-medicate (red man syndrome with vancomycin and mild blood transfusion reaction)
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12
Q

antihistamines-adverse effects

A
  • dry mucous membranes
  • sedation (do not mix with CNS depressants, paradoxical effect among children)
  • side effects are decreased for 2nd generation drugs
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13
Q

what are the different types (2) of decongestants

A
  • oral (systemic effects)
    • pseudoephedrine (sudafed)
  • nasal sprays (localized effects)
    • oxymetazoline (afrin)
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14
Q

decongestants- mechanisms of action

A
  • sympathomimetics-target local vasculature of the nose causing vasoconstriction
  • reduces membrane inflammation (stuffiness)
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15
Q

decongestants-therapeutic uses

A
  • allergic rhinitis
  • common cold
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16
Q

decongestants-adverse effects

A
  • systemic effects=tachycardia and agitation
  • localized effects=rebound congestion if taken for more than 3-5 days
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17
Q

what are antitussive medications (opiates)

A

codeine and hydrocodone

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18
Q

what are antitussive medications (non-opiates)

A
  • dextromethorphan (delsym)
  • benzonatate (tessalon pearls)
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19
Q

antitussives-mechanism of action

A
  • primarily depresses cough center in medulla
  • treatment of NONPRODUCTIVE cough
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20
Q

antitussive-therapeutic uses

A

common cold or allergies

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21
Q

antitussives-adverse effects

A
  • opiate effects
    • dizziness
    • drowsiness
    • respiratory depression -reversal agent is naloxone
    • constipation
    • potential for abuse
  • non-opiate effects are drowsiness
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22
Q

what are expectorant medications (protype)

A

guaifenesin (mucinex)

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23
Q

expectorants-mechanism of action

A

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)

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24
Q

expectorants-therapeutic use

A

common cold

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25
Q

expectorants-adverse effects

A
  • few significant effects (GI symptoms)
  • increase fluid intake to maximize effectiveness
  • limit use to 1 week max
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26
Q

what are mucolytic drugs (prototype)

A

acetylcysteine (mucomyst)

27
Q

mucolytics-mechanism of action

A
  • 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
28
Q

mucolytics-therapeutic uses

A
  • common cold
  • antidote for acetaminophen overdose
29
Q

mucolytics-adverse effects

A
  • bronchospasms
  • nausea/vomiting
  • rash
  • smells like sulfur (rotten eggs)
30
Q

what is the purpose of the lower respiratory tract

A
  • respiration
    • alveoli
    • surfactant
  • medulla/CNS
  • SNS/PSNS balance
31
Q

what is pneumonia

A
  • inflammation of the lungs (leads to ineffective gas exchange)
  • bacterial/viral/aspiration
32
Q

s/s of pneumonia

A
  • SOB
  • fatigue
  • fever
  • poor oxygenation
33
Q

what is bronchitis

A
  • bacterial/viral
  • narrowed airway due to swelling/increased blood flow
34
Q

what is asthma

A
  • 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
35
Q

what is emphysema (COPD)

A
  • related to smoking/pollution exposure
  • bronchioles loose elasticity
  • bronchioles hyperinflated
  • progressive and permanent
36
Q

s/s of emphysema

A
  • 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
37
Q

what is chronic bronchitis (COPD)

A
  • also related to smoking and pollution
  • chronic cough and excessive sputum production
  • progressive and permanent
  • long term inflammation of the bronchi
38
Q

drugs that affect the lower airway

A
  • lung surfactants
  • anti-inflammatory agents
    • leukotriene modifiers
    • corticosteroids
  • bronchodilators
    • beta2-adrenergic agonists
    • anticholinergics
    • methylxanthines
39
Q

lung surfactant (prototype)

A

beractant (survanta)

40
Q

lung surfactants-mechanism of action

A

lipoproteins that reduce the surface tension within alveoli, allowing expansion for gas exchange

41
Q

lung surfactants-therapeutic use

A

replaces surfactant in neonates with respiratory distress

42
Q

lung surfactant-adverse effects/nursing interventions

A
  • only used in emergency in newborns
  • proper placement of ET tube and direct injection into trachea
  • hypotension, bradycardia, pneumothorax, sepsis
43
Q

leukotriene modifiers (prototype) (anti-inflammatory agent)

A

montelukast (singulair)

44
Q

leukotriene modifiers-mechanism of action

A
  • 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
45
Q

leukotriene modifiers-therapeutic uses

A
  • 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)
46
Q

leukotriene modifiers-adverse effects

A
  • rare-agitated behavior in children/psychiatric events such as suicidialideations, hallucinations or depression
47
Q

corticosteroids ( prototypes) (anti-inflammatory agent)

A
  • nasal spray
    • fluticasone (flonase)
  • inhalation
    • beclomethasone (qvar)
  • oral
    • prednisone (deltasone)
  • IV
    • hydrocortisone (solu-cortef)
    • methylprednisone (solu-medrol)
48
Q

corticosteroids-mechanism of action

A
  • 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
49
Q

corticosteroids-therapeutic uses

A
  • 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
50
Q

corticosteroids-adverse effects

A
  • 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
51
Q

beta2-adrenergic agonist (prototype) (bronchodilators)

A

albuterol (ventolin HFA)

salmeterol (serevent)

52
Q

beta2-adrenergic agonists-mechanism of action

A
  • activate the SNS, causes bronchial dilation
  • do not have anti-inflammatory properties
53
Q

beta2-adrenergic agonists-therapeutic use

A

asthma

COPD

54
Q

beta2-adrenergic agonists-adverse effects/nursing intervention

A
  • due to beta 2 adrenergic stimulation-tachycardia, agina, restlessness, hypertension, sweating, bronchospasms
  • avoid caffeine
  • caution use in clients with cardiac disease
55
Q

beta2-adrenergic agonists-SABAs

A
  • rapid onset of action
  • best for acute asthma attacks
  • “rescue drug”
  • administered every 3-4 hrs prn
  • albuterol (ProAir or Proventil HFA)
56
Q

beta2-adrenergic agonists-LABAs

A
  • 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)
57
Q

anticholinergics-bronchodilator (prototype)

A
  • ipratropium bromide (atrovent)
58
Q

anticholinergic-mechanism of action

A
  • blocks the PSNS, causing SNS domination
  • causes bronchial dilation
59
Q

anticholinergic-therapeutic uses

A
  • COPD, off label asthma
  • combine with a beta2-agonist (combivent)
  • alternative to SABAs and for asthma exacerbations
  • can be taken every 4-6 hours
60
Q

anticholinergic-adverse effects

A

dry mouth, cough, hoarseness from anticholinergic effects

61
Q

methylxanthines-bronchodilator (prototype)

A

theophylline (theodur)

62
Q

methylxanthines-mechanism of action

A

smooth muscle dilation of bronchi and blood vessels

63
Q

methylxanthines-therapeutic use

A
  • long term management of persistent asthma
  • “controller drug” does not provide immediate relief
  • peak effects in2 hours
64
Q

methylxanthines-adverse effects

A
  • 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

A-Patho/pharm 2 (3 decks)

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