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M2 Pulm > 12/6 Asthma - Martin > Flashcards

12/6 Asthma - Martin Flashcards

1
Q

types of lung disease & examples

A
  1. obstructive lung disease: diseases of airflow/airway resistance
  • asthma
  • COPD
  • bronchiectasis
  • *asthma-COPD overlap syndrome
  1. restrictive lung disease
  • fibrosis
  • interstitial diseases
  1. vascular lung disease
  • pulmonary HTN
  • pulmonary thromboembolism
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2
Q

asthma

key features

A

heterogeneous disease, usually characterized by chronic airway infl, defined by

  • hx of resp sx (wheeze, SOB, chest tightness and cough) varying in time/intensity
  • variable expiratory airflow limitation

reiteration: 3 key features

  1. presence of airway infl
  2. variable airway obstruction
  3. symptoms vary over time
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3
Q

pathogenesis of asthma

2 key features

cellular players, mediators of fx

A
  1. inflammation
  2. airway obstruction

cells:

  • smooth muscle
    • hypertrophy and contraction → airway narrowing, airflow obstruction
  • eosinophils
  • lymphocytes
  • mast cells
  • autonomic nerves

mediators:

  • histamine
  • leukotrienes
  • IgE
  • IL5
  • acetylcholine
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4
Q

role of:

airway smooth muscle

what happens?

innervation?

mediators

A

airway smooth muscle hypertrophy and contraction → episodic airway narrowing

innervation:

  • beta2 adrenergic receptors → relaxation
  • PSNS muscarinic ACh receptors → constriction

mediators:

  • histamine
  • leukotrienes
  • acetylcholine
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5
Q

pathology of asthma

A
  • epithelial desquamation (even in mild cases)
  • smooth muscle hypertrophy
  • mucus plugging
  • inflammatory infiltration: eosinophilic
    • (neutrophils more prominent in COPD)
  • basement membrane thickening
  • no destruction of alveoli or fibrosis
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6
Q

T Helper cell subsets

A

diff T helper subsets differ in triggers, cytokine production, target pops, and types of immunity elicited

asthma inflammation is Th2 mediated

Th1 : triggered by IL2, IL12

  • produce mainly IFNgamma
  • act on macrophages
  • elicit cell-mediated immunity

_Th2_ : triggered by IL4

  • produce IL4, IL5, IL9, IL10, IL13
  • act primarily on eosinophils, basophils, mast cells, and B cells
  • elicit humoral immunity
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7
Q

graphic of asthmatic rxn

A
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8
Q

chronic inflammation

A

can be result of exposure to irritants/pollution, infection , external allergens, auto-immune mechs

results in…

  • incr capillary permeability
  • mucosal edema
  • excess mucus production
  • epithelial damage leading to luminal cellular debris
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9
Q

asthma triggers

A

infection

allergy

  • pollen
  • cats
  • meds
  • house dust mites
  • cockroach feces

cold air

GERD

emotion

exercise

aspirin

irritants

  • nitrous oxide
  • ozone
  • particulates and aerosols
  • smoke
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10
Q

airway mucosal disease and mucus characteristics

A
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11
Q

asthma: labs

A
  • possible eosinophilia (sputum, blood) and high IgE levels
  • spirometry (variable, may be normal)
    • decr FEV1/FVC: defines obstruction
    • normal/decr FEV1
    • normal/decr FVC
    • incr TLC, RV, FRC signify air trapping
  • gas exchange → hypoxemia and hypercapnea during exacerbations
    • VQ mismatch
    • hypoventilation
  • incr exhale nitric oxide (marker of Th2 eosinophil mediated infl)
  • CXR: possibly hyperinflation
  • chest CT: occasionally rules out other disease
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12
Q

flow volume chart:

obstructive disease

A

“scooping” present

flow preferentially affected at low lung volumes

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13
Q

goal response to bronchodilators

A

12% incr in FVC or FEV1

and

absolute increase > 200cc

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14
Q

provacative testing for asthma

A

demonstrable decr in FEV1 in response to:

  1. methacholine (20%)
    * tested w increasing conc; measure PCO2
  2. exercise (10%)
  • can be delayed (1, 3, 5, 10, 15, 20 min after exercise)
  • false negs occur with too little, too much exercise
  1. occupational exposure
  2. cold air
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15
Q

causes of hyperinflation

A

1. dynamic

  • decr expiratory flow and increased respiratory rate = not enough time to exhale

2. static (in emphysema, not asthma)

  • equilibrium between chest wall expansion and lung contraction is upset in favor of higher resting volume
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16
Q

risk factors for exacerbations of asthma:

A
  • ever intubated for asthma
  • uncontrolled asthma sx
  • having 1+ exacerbation in last 12mo
  • law FEV1 (measure lung fx at start of treatment, at 3-6mo, periodically after)
  • incorrect inhaler tecnhique and/or poor adherence
  • smoking
  • obesity, pregnancy, blood eosinophilia
17
Q

asthma tx

A
  • smoking cessation
  • education (trigger avoidance, proper inhaler technique)
  • medications
  • bronchial thermoplasty (bronchoscopy procedure - warming to 140F makes smooth muscle regress)
18
Q

asthma medications:

2 broad categories

A
  1. controllers
  • anti-inflammatory
    • inhaled corticosteroids (ICS)
  • long acting bronchodilators
    • long acting beta2 agonists
    • anti-leukotrienes
    • anti-muscarinics (tiotropium)
    • methylxanthines (theophylline)
  1. relievers
  • short acting beta2 agonists
  • systemic steroids for severe exacerbations
19
Q

steps in asthma treatment

A

“step up therapy”

  1. as-needed inhaled short-acting beta2 agonist
  2. add low dose ICS
  3. low dose ICS/long acting beta2 agonist
  4. med/hi ICS/LABA
  5. refer for add-on treatment (anti-IgE, anti-IL5, thermoplasty)
20
Q

exacerbations

A

acute or subacute worsening of symptoms and lung fx compared with pt’s usual status

21
Q

ventilatory failure

A
22
Q

acute respiratory failure in severe asthma

A

gas exchange abnormalities

  • VQ mismatch → hypoxemia
  • decr ventilation → hypercapnea

high lactate levels due to severe resp muscle fatigue

mental status changes due to hypercapnea and/or fatigue (BAD)

23
Q

HYPOXEMIA:

5x physiological basis (what you’ll see in each case)

A

R → L shunt (does not current w O2)

VQ mismatch (DOES correct with O2)

hypoventilation (see normal Aa gradient)

low PiO2

diffusion issue

24
Q

evolution of hypercapneic respiratory failiure

A
  1. hi pH, lo PCO2: pt feels bad, but has reserve
  2. NORMAL PH, NORMAL PCO2
  3. lo pH, hi PCO2
    key: normal blood gas in a distressed pt…sign of impending resp failure!
25
Q

effect of oxygen

A

takeaway: pulse oximeter gives you info about ease of oxygenation

DOESN’T TELL YOU WHETHER ADEQUATE VENTILATION IS OCCURING!

hyperoxygenation can impair VQ matching → makes ventilation less efficient

  • increases alveolar wasted ventilation/dead space

→→ can lead to CO2 retention in pt with limited reserve → can’t increase total ventilation to make up for cecrease in effective alv ventilation

Haldane effect: actually displaces CO2 bound to Hb

26
Q
A

M2 Pulm (15 decks)

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