Asthma II Part 1: Triggers, Comorbidities Flashcards

1
Q

Asthma Phenotypes

name 3 common ones

no strong relationships has been found between specific
pathological features and particular clinical patterns or treatment responses

A
Allergic asthma: Most easily recognized, starts in childhood. Associated with past or family history of allergic disease (atopic dermatitis, allergic rhinitis)
Inhaled corticosteroids (ICS) are helpful.

Non-allergic asthma: Not associated with allergy. Sputum may contain only a
few inflammatory cells. Less short term response to ICS

Adult onset asthma: Incidence higher in women. Asthma for the first time in adult life. Tends to be non-allergic and requires higher doses of ICS. Rule out
Work Related Asthma.

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2
Q

what are asthma triggers and what are the types?

A

things which worsen asthma symptoms
• They may or may not be easily identifiable
• Each patient with asthma will have slightly different asthma triggers

Triggers may be inflammatory or non-inflammatory
• Non-inflammatory triggers to lead to bronchoconstriction alone (no inflammatory response)

Triggers may be allergens or irritants
• Allergens cause an allergic cascade of events whereas irritants do not

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3
Q

Inflamm triggers

Aeroallergens (substances in the air)

A

Bind to IgE in sensitized individuals and ultimately activates histamine release along with other mediators, like leukotrienes

  • Once sensitized, re-exposure to these aeroallergens can trigger an exacerbation and symptoms of asthma (occurs via T-Helper 2 cell recruitment, mast cell activation through IgE, and eosinophil influx)
  • e.g., animal secretions, house dust mites, molds, cockroaches, pollens
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4
Q

Inflamm triggers

Viral (RSV, rhinovirus, influenza) or bacterial infections

A
  • Asthma exacerbations that occur in conjunction with an upper or lower respiratory tract infection may be more severe than exacerbations that occur without concomitant infection.
  • Epidemiologic studies suggest that viruses provoke asthma attacks by additive interactions with allergens or irritants such as air pollutants
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5
Q

Inflamm triggers

Air Pollutants

A

• Outbreaks of asthma exacerbations have been shown to occur in relationship to increased levels of air pollution

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6
Q

Inflamm triggers

Occupational Sensitizers

A
  • Over 300 occupational sensitizers
  • Long term exposure, causes a development of an immunological mediated response to the trigger (IgE- and cell mediated allergic reactions)
  • Occupational asthma is common in farming and agriculture work, painting, cleaning, and plastic manufacturing
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7
Q

Inflamm triggers

Tobacco and Cannabis smoke

A

• First- (smoke inhaled by smoker), second- (exhaled smoke inhaled by others, or third-hand exposure (smoke left on surfaces of objects)

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8
Q

name 5 inflamm triggers

A
Aeroallergens 
Viral (RSV, rhinovirus, influenza) or bacterial infections
Air Pollutants
Occupational Sensitizers
Tobacco and Cannabis smoke
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9
Q

non-inflamm triggers

Medications

A
  • Agents most commonly associated include ASA, NSAIDs such as ibuprofen or naproxen, and non-cardioselective β-blocker
  • Approximately 5% to 10% of adult patients with asthma will have an acute worsening of asthma symptoms after ingesting an NSAID
  • Symptoms may include: rhinorrhea, lacrimation, bronchospasm
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10
Q

non-inflamm triggers

emotions

A
  • Hyperventilation can cause airway narrowing
  • Stress, crying and laughing can trigger symptoms because breathing patterns change
  • Psychosocial
  • Inappropriate asthma self-care, a disregard for asthma symptoms
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11
Q

non-inflamm triggers

Hormonal changes

A
  • Women may experience greater symptoms during menstruation

* In pregnancy, 1/3 of asthma worsens, 1/3 improves, and1/3 stays the same

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12
Q

non-inflamm triggers

other (4)

A
  • Food additives (MSG)
  • Cold air / weather conditions
  • Physical activity (very common)
  • Strong fumes (perfumes, paints, etc.)
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13
Q

name 4 non- inflamm triggers

A

meds
emotions
hormonal changes
other (weather, food, phys activity, fumes)

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14
Q

Comorbidities

Rhinitis and sinusitis

A

• Rhinitis frequently precedes asthma and is both a risk factor for the development of asthma and is associated with increased asthma symptom severity

patients with allergic rhinitis is estimated to be 17% to 38%, and prevalence of rhinitis in patients with allergic asthma to be between 60% and 80%

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15
Q

Comorbidities

Atopic dermatitids
define atopy

A

management of atopic dermatitis may reduce severity of later asthma
• Atopy: propensity to produce specific IgE antibodies to common aeroallergens

strong association between atopic dermatitis and asthma in childhood and a similar association seen later in life.
• Association between atopic dermatitis and the development of allergic rhinitis

FYI - Approximately 40% to 60% of children with atopic dermatitis will
develop allergic rhinitis and/or asthma over time

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16
Q

Comorbidities

GERD
which drugs can make GERD worse>?

A

Relationship is not fully understood (it is unlikely in children)
- asthma - higher prev of GERD
- GERD could worsen asthma either by direct effects on airway responsiveness or via aspiration induced inflammation
- beta-agonists and methylxanthines used in the
treatment of asthma can impair function of the lower esophageal sphincter

GERD-induced cough does respond to the use of full dose PPIs in twice daily dosing, but it often takes up to three months for a response
PPI don’t help manage asthma

17
Q

Comorbidities

food allergies
see table for food additives commonly associated with allergies (extra)

A

no conclusive evidence demonstrating a change in
any dietary factor can prevent or exacerbate asthma

  • Ability of these agents to exacerbate asthma is probably minimal for most patients with asthma, and for this reason food avoidance should not be recommended until allergy confirmed
18
Q

Comorbidities

obesity
what improves asthma?

A
  • linked to asthma persistence and severity in both
    children and adults
  • effects of obesity on asthma independent of diet and physical activity, although these three factors are clearly interrelated
  • Weight reduction in obese patients with asthma has been shown to improve lung function, symptoms, morbidity, and health status
  • pt may have suboptimal response to therapy
19
Q

5 unique circumstances for asthma

A
  1. Exercise-induced bronchoconstriction (EIB)
  2. Work-related asthma (WRA)
  3. Perimenstrual asthma (PMA)
  4. Asthma in pregnancy
  5. Aspirin®-exacerbated respiratory disease (AERD)
20
Q

Exercise-Induced Bronchospasm (EIB)

what is it not called?
occurs in who?
what 2 factors most important?

A

Acute airway narrowing that occurs as the result of exercise
• Also called exercise-induced asthma (EIA), although this term is not used as often because there may not be underlying chronic asthma, nor does exercise “cause” asthma.

occurs in:

  • patients with mild, stable asthma where exercise is the only known trigger
  • thletes who don’t appear to have underlying asthma
  • olympic atheles common, more in endurance sports
  • humidity of air and level of exercise (vigour and duration) most important
21
Q

Exercise-Induced Bronchospasm (EIB)

MOA?

A

MOA unknown
- stimulus is respiratory heat loss, water loss or both, causes changes in air wall osmolality which causes mast cell degranulation, prostaglandin, leukotrienes and histamine release, and airway
hyperresponsiveness

22
Q

Exercise-Induced Bronchospasm (EIB)

Clinical presentation
FEV decrease of?

A

Chest tightness, cough, wheezing, and dyspnea
• It is defined as a transient narrowing of the airways that follows vigorous
exercise (it rarely occurs during exercise)
• There may be no increase in inflammatory cell recruitment if ppl don’t have asthma
FEV1 decrease of 15% from baseline

23
Q

Exercise-Induced Bronchospasm (EIB)

Diagnosis
how is it measured?
time it usually occurs?

A
  • wheeze, chest pain (primarily in children) or chest tightness, shortness of breath, dyspnea, excessive
    mucus production, or feeling out of shape when they are actually in good physical condition
  • minutes after vigorous activity, reaches its peak
    five to ten minutes after stopping the activity, and resolves in another
    20 to 30 minutes
  • diagnose by change in FEV1 following exercise (spir)
24
Q

Work-Related Asthma (WRA)

what are the 2 types

A
  1. Occupational asthma = asthma that is caused by work
    - 2 types
  2. Work-exacerbated asthma = asthma that pre-exists and is triggered by the workplace either by irritants or aeroallergens.
25
Q

Work-Related Asthma (WRA)

what are the 2 types of occupational asthma?

A

(a) Sensitizer-induced: Asthma induced by a specific sensitizer at work (e.g., pets in a pet store). This process is immunological and IgE mediated.
• (b) Irritant-induced: Could occur after many exposures or a single, high exposure to an irritant (e.g., chemicals). Reactive airway dysfunction syndrome (RADS) develops as a result of toxic injury from exposure.

26
Q

Work-Related Asthma (WRA)

diagnosis
what types of q may you ask
what should you never advise

A

• In every adult whose asthma begins or deteriorates while working, the possibility of work-related asthma should be considered and evaluated

key q

  • changes in work process before
  • unusal work exposure 24 h before
  • differing symptoms during time away from work
  • allergic rhinitis/conjuctivitis worse at work?

never advise a person to quit or retire until fully assessed. stress or sick leave ok

27
Q
Perimenstrual Asthma (PMA)
20-40% of women with asthma

define
diagnosis

A

Defined as a cyclical deterioration of the asthmatic condition during the premenstrual phase and/or during first few days of menstruation.

diag: self-reporting of asthma symptoms (coughing, wheezing, tightness across the chest, and breathlessness) or through a reduction of peak expiratory flow (PEF)

28
Q

Perimenstrual Asthma (PMA)

MOA

A

likely due to hormonal status but not fully elucidated:
• exaggerated inflammatory response to
asthma triggers coinciding with naturally occurring fluctuations in sex hormones.
• Other proposed mechanisms include reduced serum progesterone levels.

29
Q

Asthma in Pregnancy

what physl changes during preg can affect asthma?
read and understand

A
  • Diaphragm rises
  • Thoracic cage increases in diameter
  • Increase in oxygen consumption and metabolic rate of mom
  • Rhinitis incidence increases
  • GERD symptoms may develop
  • Hormonal changes enhance peripheral eosinophil degranulation
30
Q

Asthma in Pregnancy

does everyone get worse for asthma?
what is a signifcant risk factor?

A

1/3 of asthma may worsen, 1/3 may improve, and 1/3 will stay the same
• Smoking - asthma development in pregnancy and also exacerbates asthma.
- Also, could impact lung development in fetus predisposing them to infant wheezing and
development of asthma

31
Q

Asthma in Pregnancy

Poorly controlled asthma may have which AE?
confirm diagnosis with what? (diag is straightforward as many have history)

A
  • Low birth weight of fetus
  • Increased prematurity of fetus
  • Increased perinatal mortality
  • Maternal complications
  • Hypertensive disorders including preeclampsia
  • Hyperemesis gravidarum
  • Hemorrhage, Placenta previa

spirometry

32
Q

Aspirin®-Exacerbated Respiratory Disease (AERD)

MOA?

A

presents with a triad of rhinitis, sinusitis, and asthma
when exposed to the offending drugs

MOA
- shunting of the arachidonic acid metabolism away from the (COX) pathway toward the lipoxygenase (LO) pathway
- increased production of leukotrienes resulting in
bronchoconstriction and a decrease in prostaglandin synthesis (antiinflammatory)