Asthma Flashcards

1
Q

A chronic inflammatory lung disease that results in variable episodes of airflow obstruction that’s usually reversible is defined as:

A

asthma

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2
Q

What is the curent prevalence of asthma:

A

children, boys, women

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3
Q

What ethnicity has the highest asthma morbidity and mortality:

A

African Americans

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4
Q

What are the types of episodes experienced in asthma attacks:

A

recurrent episodes of wheezing, breathlessness, chest tightness, cough all happening typically at night or early in the morning

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5
Q

What is the genetic influence in relation to asthma:

A

Atopy which is the body producing an antibody, immunoglobulin- E, that responds to common allergens

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6
Q

What can immunoglobulin E trigger in a pt:

A

allergic rhinitis, asthma, hay fever, eczema

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7
Q

How does the immune response affect asthma:

A

hygiene hypothesis suggest that baby’s need to be exposed to things that cause allergies in order to not be allergic or have asthmatic episodes

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8
Q

How do allergens affect asthma:

A

House mites, dander

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9
Q

How does exercise affect asthma:

A

Exercise induced asthma occurs AFTER vigorous activity and usually in the cold

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10
Q

How does air pollutants trigger asthma:

A

Ozone, pollution, and smoking trigger asthma

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11
Q

How does occupational factors trigger asthma:

A

agricultural workers, painters, plastic mechanics, cleaning work

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12
Q

How do respiratory infections trigger asthma:

A

VIRAL infections such as RSV (respiratory syncytial virus in children) and the rhinovirus are two major factors in the development of asthma d/t causing the bronchial system to be hyperresponsive

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13
Q

How do nose and sinus problems affect asthma:

A

Allergic rhinitis is a major predictor in adult asthma; sinusitis must be treated and nasal polyps removed for asthma to be better controlled

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14
Q

How do drugs and food additives affect asthma:

A

Pts with sinusitis and lrg nasal polyps are sensitive to specific drugs. Asthma triad (nasal polyps, asthma, and sensitivity)are sensitive to ASA and NSAIDs; Beta blockers 2 may trigger asthma d/t bronchospasm; ACE inhibitors trigger cough; Food dye tartrazine (Yellow color)

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15
Q

How does gastroesophageal reflux disease (GERD) affect asthma:

A

Typically causes nocturnal asthma (can occur in the day) by stomach acid being aspirated into the lungs triggering vagal stimulation and bronchoconstriction

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16
Q

How do psychological factors affect asthma:

A

Strong emotions (stress, laughter) can cause hyperventilation or hypocapnia which can lead to airway narrowing

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17
Q

What are the characteristics of asthma:

A

recurring variable S/S; airflow obstruction; bronchial hyper-responsiveness

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18
Q

What is the key feature of asthma:

A

inflammation which will lead to cough, chest tightness, wheeze, dyspnea

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19
Q

In the pathophysiology of asthma, what occurs, after exposure to allergens or irritants:

A

Mast cells, epithelial cells, and IgE bodies are released

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20
Q

During the inflammatory cascade response, what do the mast cells and epithelial cells produce:

A

mast cells degranulate to release leukotrienes, histamine, cytokines, PGs, and nitric oxide=vasodilation/cap permeability and cellular infiltration; epithelial cells produce cytokines too

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21
Q

What is the resulting inflammatory process result in:

A

vascular congestion, airway edema, thick tenacious mucus, bronchial muscle spasm, thickening of airway walls, increased bronchial hyper-responsiveness

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22
Q

What is the response to increased lung volume from trapped air and airflow limitation:

A

hyperventilation

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23
Q

Hyperventilation will cause:

A

decrease perfusion and ventilation of the alveoli; early hypoxemia w/decreased CO2 and increased pH (low CO2 and high ph = respiratory alkalosis)

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24
Q

What will occur if respiratory alkalosis isn’t resolved:

A

CO2 will normalize as the pt tires and then will increase to produce respiratory acidosis (an OMINOUS sign of RESPIRATORY FAILURE)

25
In the pathophysiology of asthma, what occurs after the mast cells have degranulated their contents, IGE have been activated, and epithelial cells produce their cytokins:
inflammatory mediators cause vasodilation and cellular infiltration (neutorphils, lymphocytes, eosinophils)
26
What occurs after cellular infiltration:
activation of neutrophils and eosinophils will release more chemical mediators and neuropeptides (effects nervous system) that will prolong the asthma occurrence for 24 hrs or more
27
What occurs after inflammatory mediators cause vasodilation:
increased cap permeability causing bronchospasm, vascular congestion, edema formation, mucous secretion, impaired mucociliary function, thickening of airway walls=bronchial hyper-responsiveness and airway obstruction
28
What do the sympathetic nervous system regulate in asthmatic pts:
contain beta-adrenergic receptors that mediate the bronchial dilation and diminish mucus secretion (epinephrine can relax the bronchial muscles)
29
What do the parasympathetic system regulate in asthmatic pts:
regulates airway smooth muscle tone; contain Cholinergic receptors that respond to acetylcholine (released d/t airway nerve ending stimulation) to make the muscles contract
30
Structural changes ( smooth muscles hypertrophy, mucus hypersecretion, fibrosis of epithelium) in the bronchial wall causing a progressive loss of lung function if no prevention is initiated is defined as:
remodeling
31
How can airway remodeling be prevented:
corticosteroids
32
What is caused by high-velocity flow of air through narrowed airway; is a unreliable sign in gauging severity; severe attacks may have no audible sound d/t marked airflow (ominous sign) is defined as:
wheezing
33
What are the clinical manifestations of asthma:
Wheezing, cough, dyspnea, chest tightness
34
If a pt states that they are getting tired of breathing is an indication of
respiratory arrest and emergency should be prepared
35
How does asthma affect mental status:
AAO, restless, agitated; apprehhensive, confusion, drowsy
36
How does asthma affect the integumentary:
diaphoresis, cold clammy skin, cyanosis
37
how does asthma affect cardiovascular:
tachycardia, pulsus paradoxus, HTN, hypotension
38
How does asthma affect RR:
dyspnea, prolonged expiration, nasal flaring, accessory muscle use
39
Diminished or absent BS (silent chest) is d/t:
increased work of breathing; ominous sign of RR failure
40
What type of labs would you expect to see for asthmatic pts:
ABGs, hypoxemia; pulmonary function test (PFT=decreased FEV)
41
Silent chest/tight chest; fear/anxiety of suffocation; increased accessory use of breathing; prolonged attack; confused/drowsy; less than 60 HR are all S/S of what severe life threatening attack:
status asthmaticus (mechanical ventilation may be needed
42
An essential objective measure in testing lung function that demostrates obstruction and assess reversibility in asthmatic pts is defined as:
Spirometry (essential Dx tool)
43
What are some other Dx studies of asthma:
Peak expiratroy flow rate (PEFR); CXR, allergy skin testing; ABG/pulse ox; CBC/Eosin/IGE count; sputum C &S
44
What are the four essential components in Tx asthma
Assessment/monitoring; pt education; control of factors causing asthma; pharmacological Tx
45
What is a way of avoiding triggers to asthma:
premedication before exercise
46
When the allergen cannot be avoided and drug therapy is not effective, what is done:
Immunotherapy (desensitization)
47
The goal of long-term asthma control is:
Maintain control of chronic asthma
48
The goal of quick relief asthma is:
Treat symptoms and exacerbations
49
What is the first line of choice for asthma control and how does it work:
ICS suppress the inflammatory response via decreasing hyperresponsiveness/mucous production; increases B2 receptors and responsiveness for B2 agonists; taken daily (predisone/FLOVENT)
50
Mast cell stabalizers:
Cromolyn/Nedocromil; inhibits IGE from causing mast cells to release chemical mediators; NOT USED FOR ACUTE ATACKS; prevents bronchospasms and attacks; Used BEFORE exercise
51
Leukotrine modifiers
Singulair; blocks action of leukotriene; antiinflammatory/bronchospasm; Add on therapy to REDUSE dose of ICS; PO only
52
Anti-IgE
Xolair; decreases levels of IgE; given subq 2-4 weeks if ICS is not effective for persistent asthma; High risk of anaphylaxis
53
Short acting B2 agonists (SABAs)
"buterol" used in ACUTE episodes; bronchodilates; increases mucociliary clearance; should not be used alone
54
What are Side effects of SABAs:
Heart related: tachycardia, palpations, nausea, tremors
55
Long Acting B2 agonists
"M-terols" Added to daily dose of ICS for long-term controle of moderate-severe asthma; NOT USED As !st line medications; SABAs should always be available
56
Methylxanthines
Last choice bronchodilator drug; only given if other bronchodilator drugs are not effective d/t narrow margin of safety
57
What are the side effects of methylxnthines:
Heart related: SZ, tachycardia, dysrhythmias; HA; GI S/S
58
Anticholinergic:
Atrovent; blocks parasympathetic system from bronchoconstricting; USED IN COMBINATION with other bronchodilators; side effective is DRY MOUTH
59
For the Peak Flow Zone System:
Green zone (80-100=feeling good r/personal best); yellow zone (50-80=need to use SABAs, if not better, meds need to be change); Red zone (less than 50 take SABA right away and go to ER)