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Pulmonary Week 2 > ICL 2.1: Variable Obstructive Lung disease: Asthma > Flashcards

ICL 2.1: Variable Obstructive Lung disease: Asthma Flashcards

1
Q

how prevalent is asthma?

A

8% but increasing in developing countries

more common in african americans, obese, and in urban areas

boys > girls

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2
Q

what is the definition of asthma?

A

variable airway obstruction and hyperresponsiveness

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3
Q

how do you diagnose asthma?

A
  1. spirometry pre and post bronchodilator administration –> 12% increase in FEV1 means it’s asthma
  2. methacholine challenge –> administer methacholine and if a hyper-responsive bronchoconstriction response results in 20% reduction in FEV1 that’s asthma
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4
Q

what are the characteristics of asthma?

A
  1. episodic –> wheezing, breathlessness, chest tightness, cough
  2. worse at night and early morning
  3. triggers like allergens
  4. PFTs are normal between episodes!!
  5. completely reversible

most asthma deaths occur in the night and it’s highly correlated with extensive mucous plugging

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5
Q

how can asthma vary?

A
  1. triggers
  2. type and degree of inflammation (TH1 adult non-allergic vs. TH2 response atopic in children
  3. severity of symptoms
  4. response to treatment
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6
Q

what are some triggers of asthma?

A
  1. cold air
  2. allergens = pollens, grass, cockroaches, animal dander, dust mites, mold
  3. cigarette smoke
  4. air pollution, car exhaust
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7
Q

what is non-atopic asthma?

A

aka nonallergic, intrinsic asthma due to TH1 lymphocyte-drive inflammation

  1. adult onset
  2. associated with obesity
  3. tends to be difficult to control with more severe relapses
  4. skin prick tests are negative and no circulating IgE
  5. no familial pattern
  6. higher female prevalence
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8
Q

what is atopic asthma?

A

aka allergic or extrinsic asthma due to TH2 lymphocyte driven inflammation

  1. early onset, first two decades of life
  2. allergenic triggering
  3. positive skin prick test
  4. specific IgE
  5. familial pattern

less than 1/2 of asthma cases are this type despite contrary belief!

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9
Q

what are the genetic risk factors that contribute to the risk of asthma?

A
  1. ADAM 33
  2. HLA alleles
  3. IL4 polymorphisms
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10
Q

what are the environmental risk factors that contribute to the risk of asthma?

A
  1. allergen sesitization
  2. having few siblings
  3. excessive hygiene
  4. receipt of antibiotics in the first 2 years of life
  5. vaccination and prevention of disease
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11
Q

which cell types are involved in asthma inflammation?

A
  1. TH1 CD4 T-lymphocytes (intrinsic)

2. TH2 CD4+ T-lymphocytes (extrinsic)

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12
Q

how are TH1 CD4 T-lymphocytes involved in asthma?

A

they secrete:
1. TNF-alpha

  1. IL2
  2. INF-gamma
  3. lymphotoxin –alpha

these stimulate neutrophils

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13
Q

how are TH2 CD4 T-lymphocytes involved in asthma?

A
  1. they secrete IL4 which stimulates B-cell IgE production

IgE/allergen then stimulate mast cells and basophils that secrete histamine, leukotrienes, prostaglandins and proteases

  1. secrete IL5 which stimulates eosinophils

eosinophils secrete major basic protein, eosinophilic cationic protein, eosinophilic peroxidases and leukotrienes

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14
Q

what is major basic protein?

A

secreted by eosinophils which stimulated by IL5

they’re cytotoxic to epithelial cells

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15
Q

what is the role of leukotrienes in asthma?

A

they’re synthesized by eosinophils, mast cells, macrophages, and basophilic –> they are formed via the lipoxygenase pathway from arachidonic acid

LTC4 and LTD4 bind to cysteine leukotriene receptors and induce:
1. smooth muscle cells which leads to bronchial restriction and hyperactivity

  1. bronchial epithelial cells which leads to mucosal edema
  2. mucus hypersecretion from goblet cells

LTB4 binds to BLT1 receptors and induces neutrophil chemoattraction

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16
Q

what are the long-term consequences of asthma airway inflammation?

A
  1. airway smooth muscle hypertrophy
  2. epithelial cell shedding
  3. basement membrane thickening
  4. no alveolar disruption
  5. dendritic cells
  6. TH2 lymphocytes = eosinophils and mast cells
  7. goblet cell hypertrophy
  8. mucus plugs
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17
Q

which of the following concerning bornchoprovocation testing is most accurate?

A. exercise testing is more accurate than methacholine challenge testing for diagnosing asthma

B. a positive methacholine challenge test accurately separates asthma from COPD

C. negative methacholine challenge test has excellent negative predictive value in ruling out asthma

D. inhaled corticosteroid usage does not affect the sensitivity of the test

A

C. negative methacholine challenge test has excellent negative predictive value in ruling out asthma

it’s not specific but it’s really sensitive

so if it’s positive then that doesn’t necessarily mean you have asthma but if it’s negative, it means you definitely don’t

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18
Q

what are the initial steps of asthma management?

A
  1. diagnose
  2. asses severity
  3. initiate medication and demonstrate use
  4. develop written asthma action plan
  5. schedule follow up
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19
Q

how do you provisionally diagnose asthma?

A

asthma is episodic so the patient might not have anything wrong with them during your PE so the provisional diagnosis is based on history and physical

ask them about triggers, seasonal, nocturnal, exercise, age of onset, eczema, wheezing, increased expiratory time, use of accessory muscles

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20
Q

how do you differentiate asthma from vocal cord dysfunction?

A

wheezing loudness over the chest vs. neck

louder wheeze over the neck combined with predominant inspiratory wheeze is vocal cord dysfunction = GERD

21
Q

how do you definitively diagnose asthma?

A

documentation of variable airway obstruction OR hypersensitivity

variable airway obstruction is evaluated by :
1. peak expiratory flow (PEF) using hand-held personal peak-flow meter 2x daily for 2 weeks

  1. FEV1 before and after bronchodilator (12% increase)

if bronchodilator response is negative, evaluate the airway responsiveness through provocation test which is either the exercise challenge or the methacholine challenge

22
Q

in differentiating asthma from COPD, which statement is true about spirometry?

A. significant bronchodilator response confirms the diagnosis of asthma

B. bronchodilator response does not differentiate asthma from COPD

C. the absence of significant bronchodilator response confirms the diagnosis of COPD

D. a pst-bronchodilator FEV1/FVC less than 70% confirms the diagnosis of asthma

A

A. significant bronchodilator response confirms the diagnosis of asthma

23
Q

what is hyperresponsiveness in relation to asthma?

A

the autonomic nervous system is influenced by inflammation in the airways

it regulates airway tone, permeability and secretion

dysfunction leads to/complicates asthma!

24
Q

how do you measure airway hyperresponsiveness with asthma?

A

methacholine challenge!

you give methacholine and look at how much FEV1 decreases

the smaller the dose to reach a decrease of 20% in FEV1, the more severe the hyper-responsiveness

the methacholine challenge test is highly sensitive but not that specific so if it’s negative you CAN be confident that they don’t have asthma but if it’s positive it doesn’t necessarily mean they have asthma

25
Q

what factors classify the severity of asthma in patients who haven’t been on meds yet?

A
  1. symptom frequency
  2. nightime awakenings
  3. frequency of short acting B-agonist (SABA) use
  4. interference with normal activity
  5. lung function measured by spirometry

severity will range from mild, moderate to severe – there’s a big graph

26
Q

what are the classes of asthma medication?

A

QUICK RELIEF
1. bronchodilators –> SABAs, anticholinergics

  1. anti-inflammatories –> systemic corticosteroids (prednisone)

LONG TERM
1. bronchodilators –> long acting B2 agonists (LABAs), phosphodiesterase inhibitors

  1. anti-inflammatories –> inhaled corticosteroids*, leukotriene antagonists, mast cell stabilizers, immunomodulators
27
Q

what are corticosteroids used for in asthma treatment?

A

they’re highly effective anti-inflammatory substances and inhaled corticosteroids are the mainstay of asthma control!

systemic corticosteroids are used for temporary management of severe exacerbations because their systemic use is associated with significant side effects – so you want to minimize their use and get them on LABA and inhaled corticosteroids

28
Q

what are the 2 main LABA drugs for asthma?

A
  1. salmeterol

2. formoterol

29
Q

what are the advantages and disadvantages of LABA?

A

ADVANTAGES
1. reduce asthma exacerbations

  1. improve pulmonary function
  2. reduces airway responsiveness
  3. attenuate EIB
  4. provide brochodilation
  5. prevent nocturnal asthma

DISADVANTAGES
1. potential for reduced effect with long term treatment

  1. not recommended as monotherapy

should be combining with inhaled corticosteroids!

30
Q

what is the MOA of leukotriene inhibitors?

A
  1. inhibit lipoxygenase directly to reduce production of LTC4, LTD4, and LTE4
  2. antagonize CysLT receptor to reduce mucus secretion, bronchoconstriction, edema and eosinophilia
31
Q

which drug directly inhibit lipoxygenase?

A

zileuton

32
Q

which drugs are CysLT receptor antagonists?

A
  1. zafirlukast
  2. pranlukast
  3. montelukast
33
Q

which drugs are the biologics used for asthma management?

A

these drugs are used for when asthma/eczema is otherwise uncontrolled and the patient has become steroid dependent

  1. omalizumab = anti-IgE used when there’s high IgE levels
  2. dupilimab = blocks IL4 and IL13 actions by antagonizing IL4 receptor and is used when there’s eosinophilia
  3. mepolizumab is an anti-IL5 and is used when there’s eosinophilia
34
Q

what are the symptoms of a severe asthma attack?

A
  1. persistent SOB
  2. inability to speak full sentences
  3. breathless even lying down
  4. acrocyanosis
  5. agitation, confusion, inability to concentrate
  6. hunches shoulders and strained abdominal and neck muscles = use of accessory muscles
  7. need to sit or stand up to breath more easily
35
Q

what is status asthmatics?

A

acute severe asthma attack and that doesn’t respond to usually use of inhaled bronchodilators

associated with symptoms of potential respiratory failure

life threatening

36
Q

what is the stepwise approach for long term asthma control?

A
  1. SABA
  2. low dose inhaled corticosteroid

can add mast cell stabilizer or leukotriene inhibitor

  1. add LABA or medium doseICS
  2. high dose ICA + LABA and consider omalizumab for patients who have allergies
  3. high does ICS + LABA + oral corticosteroids and consider omalizumab for patients who have allergies
37
Q

what is the use of peak flow meter?

A
  1. establish baseline
  2. quantify increase in airway restriction at time of symptoms
  3. act according to asthma action plan based on results
38
Q

how do obesity and GERD effect asthma?

A

they increase the risk for asthma and severe asthma

association between obesity and asthma is stronger for non-atopic/intrinsic asthma

comorbid with obesity and asthma are GERD, OSA and DM which all increase the risk for aspiration! especially when lying down

39
Q

patient prone to severe asthma phenotype often have which of the following characteristics?

A. GERD as comorbid condition

B. gastroparesis from long-standing DM as a comorbid condition

C. OSA as a comorbid condition

D. all of the above

A

D. all of the above

40
Q

what is the aspirin-exacerbated respiratory disease triad?

A
  1. asthma
  2. recurrent nasal polyps
  3. sinusitis

this is caused by a sensitivity to aspirin and other NSAIDs that inhibit COX –> increased expression of LTC4 synthetase and production of cysteine-leukotrienes possibly associated with polymorphism of the cysteinyl-leukotriene synthase gene

AERD commonly develops suddenly in adulthood between 20-50 years old

41
Q

how do you treat aspirin-exacerbated respiratory disease?

A

AERD patients not desensitized shoulda avoid all NSAIDs to prevent reactions

to desensitize a patient, administer aspirin gradually increasing the dose –> the goal is long term daily aspirin therapy to decrease the regrowth of nasal polyps and reduce the need for corticosteroid medications

in the mean time give inhaled corticosteroids

give zileuton to inhibit production of leukotrienes or give montelukas/zafirlukast to block the function of the leukotrienes at the CysLT1 receptor

surgically remove nasal polyps but they reoccur often

42
Q

what is exercise induced bronchospasm?

A

bronchospasm occurring 5-10 minutes AFTER completion of exercise caused by mast cell degranulation

cough may be the only symptoms but they could also have chest pain, tightness, wheezing, SOB

it resolves spontaneously 30-45 minutes after finishing exercise

cold or dry climates or running are the worst triggers

43
Q

how do you diagnose exercise induced bronchospasm?

A

make them exercise then if there’s a 15% decrease in FEV1 that suggests EIB

44
Q

how do you treat exercise induced bronchospasm?

A
  1. pre-exercise short acting B agonist inhaler = albuterol
  2. mast cells stabilizers = cromolyn
  3. anti-leukotrienes = zileutin or montelukast
  4. encourage warm up period or mask or scarf over the mouth for cold-induced EIB
45
Q

how do you prevent exercise induced bronchospasm?

A
  1. SABAs
  2. LTRAs, cromolyn or LABAs are also protective

frequent or chronic use of LABA to prevent EIB is discouraged because it may be disguising poorly controlled persistent asthma

EIB is often a marker of inadequate asthma control and responds well to regular anti-inflammatory therapy

46
Q

32 year old woman present with symptoms of exercise induced SOB and chest tightness. she admits to nocturnal chest tightness and difficulty breathing. PE is normal. spirometry shows a normal FVC and no airflow obstruction. FEV1 is 80% predicted. you suspect asthma. if she does in fact have asthma, which of the following tests is most likely to confirm your suspicion of asthma?

A. post bronchodilator increase in FEB1 by 8%

B. methacholine inhalation challenge test 20% reduction in FEV1

C. a treadmill exercise challenge causing FEV1 to decrease 10%

D. post-bronchodilator increase in FEV1 by 100 mL

A

B. methacholine inhalation challenge test 20% reduction in FEV1

47
Q

what is the most common cause of occupational asthma?

A

isocyanate exposure (found in paint!)

48
Q

which conditions can mimic asthma?

A
  1. vocal cord dysfunction
  2. GERD
  3. strong emotions and stress
  4. irritants like tobacco
  5. exercise
  6. hyperventilation syndrome
  7. allergic bronchopulmonary aspergillosis
  8. Churg-Strauss syndrome

Pulmonary Week 2 (9 decks)

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