Respiratory Pathology Flashcards
asthma dx
clinical: *episodic *wheezing SOB (potentially hard to talk, accessory muscle use --> EMERGENCY) cough mucus chest tightness/chest pain
may use sx journals to identify causes of exacerbations
further testing rarely done, but if it were:
- spirometry: only abnormal during exacerbation, reduced FEV1 (FEV1/FVC <70%)
- peak flow: PEV (peak expiratory volume) and PEFR (peak expiratory flow rate) both reduced
- bronchoprovocation studies show sx exacerbation with certain irritants
- FeNO (fractional exhaled nitric oxide) elevated (note that this is more often used to monitor tx response)
- sputum analysis: curschmann’s spirals (casts from small bronchi that cause mucus plugs, may obstruct to extent that no air or meds can pass), charcot-leydan crystals (needle-shaped shards from eosinophil breakdown)
FeNO
fractional exhaled nitric oxide
NO is a marker of inflammation
i.e., indicates airway inflammation
most often used in measuring tx response to asthma
sometimes for dx asthma
elevated in asthma, especially during exacerbation
elevated in COPD exacerbation only
normal to low in stable or chronic COPD
extrinsic vs intrinsic asthma
extrinsic (allergic):
allergen –> DC –> Th2 –> eosinophil recruitment
– IL4 antagonists will be more effective in this population
intrinsic (nonallergic):
irritant/stimulus/hormonal signalling –> mast cells –> neutrophils and eosinophils
– leukotriene antagonists will be more effective in this population
- both involve both pathways, but skewed significantly toward one or the other
- both result in eosinophil activation
- both result in bronchospasm, bronchial edema, and bronchial hyperreactivity
- both treated with beta-adrenergic agonists (albuterol; bronchodilator) and steroids (fluticasone, budensonide; broad-spectrum anti-inflammatory)
- both can be treated with TSLP antagonists and eosinophil antagonists: IL5, IL13, IgE (antagonists)
episodic wheezing and dyspnea with “seasonal allergies”
extrinsic asthma
tx bronchodilators, steroids, potentially IL4 and TSLP antagonists, IL5, IL13, IgE antagonists
episodic wheezing and dyspnea “but only when I exercise”
intrinsic asthma
tx bronchodilators, steroids, potentially leukotriene and TSLP antagonists, IL5, IL13, IgE antagonists
r/o deconditioning
episodic wheezing and dyspnea d/t “smoke from the wildfires”
intrinsic asthma
tx bronchodilators, steroids, potentially leukotriene and TSLP antagonists, IL5, IL13, IgE antagonists
episodic wheezing and dyspnea d/t “smog”
intrinsic asthma
tx bronchodilators, steroids, potentially leukotriene and TSLP antagonists, IL5, IL13, IgE antagonists
episodic wheezing and dyspnea d/t “hay fever”
extrinsic asthma
tx bronchodilators, steroids, potentially IL4 and TSLP antagonists, IL5, IL13, IgE antagonists
episodic wheezing and dyspnea d/t “stress”
intrinsic asthma
tx bronchodilators, steroids, potentially leukotriene and TSLP antagonists, IL5, IL13, IgE antagonists
r/o anxiety/panic attacks
asthma complications
short term: asthma attacks –> life threatening
long term –> chronic infections, fibrosis
curschmann’s spirals
casts from small bronchi that cause mucus plugs, may obstruct to extent that no air or meds can pass
seen in asthma sputum analysis
Charcot-laydan crystals
needle-shaped shards from eosinophil breakdown
seen in asthma sputum analysis
asthma severity classification
intermittent, mild persistent, moderate persistent, severe persistent
consider:
- sx frequency
- sx timing (early morning, late night)
- frequency of rescue inhaler use
- FEV1, PEV, PEFR
potential asthma triggers
extrinsic/allergic:
- seasonal, pollen, hay fever, etc
- dust, dust mites
- mold
- cockroaches
- pets
- etc.
intrinsic/nonallergic:
- tobacco and other inhaled drugs
- viral infections
- environmental smoke
- smog, car fumes
- exercise
- stress
either/drug-induced:
- beta blockers
- NSAIDs (especially aspirin/COX1)
preferred asthma treatment track (GINA 2021 track 1)
step 0: identify and eliminate triggers, where possible
step 1-2: sx < 4-5 days/wk
- ICS-formoterol as needed
step 3: sx most days or waking 1+ night/wk, or uncontrolled on step 1-2
- low-dose maintenance ICS-LABA
- ICS-formoterol as needed
step 4: sx every day or waking 1+ night/wk, AND low lung function, or uncontrolled on step 3
- medium-dose maintenance ICS-LABA
- ICS-formoterol as needed
- short-course oral corticosteroids during severe attacks or persistent phases
step 5: sx daily, waking 1+ night/wk, and low lung function, or uncontrolled on step 4
- all of step 4 PLUS:
- LAMA
- refer for phenotypic assessment, based on results:
- – anti-IgE
- – anti-IL5/5R
- – anti-IL4R
- consider high-dose ICS-LABA
- ICS: inhaled corticosteroid, e.g. fluticasone, budesonide
- LABA (should not be used w/o ICS): long-acting beta AGonist, e.g. albuterol SULFATE, formoterol, salmetrol
- ICS-LABA: combined formulations e.g. budenoside-formoterol (Symbicort), fluticasone-salmeterol (Advair)
- note that formoterol onset is fast enough to be used as a rescue inhaler; LABAs otherwise must me combined with a SABA rescue inhaler
- LAMA: long-acting muscarinic ANTagonist, e.g. tiotropium bromide; may be used in place of LABA if other LABAs cannot be used
- SABA: short-acting beta AGonist, e.g. albuterol
pt with asthma less than 4-5 days a week should be started on ____
ICS-formoterol (preferred) prn
or
(< 2x/month) SABA (e.g., albuterol) + ICS whenever albuterol is needed
(> 2x/month) low-dose maintenance ICS + prn SABA
pt with asthma most days, waking 1+ night/wk, or uncontrolled on prn-only should be started on ____
ICS-formoterol low dose daily and prn (preferred)
or low-dose maintenance ICS and prn SABA
pt with asthma daily, waking 1+ night/wk, and reduced lung function, or uncontrolled on low-dose + prn should be started on ____
ICS-formoterol med-dose daily and prn (preferred)
or medium-dose maintenance ICS-LABA and prn SABA
and oral corticosteroids in severe attacks or persistent phases
pt with asthma daily, waking 1+ night/wk, and reduced lung function, or uncontrolled on med-dose + prn should be started on ___
med to high dose ICS-formoterol (preferred; or ICS-LABA + prn SABA)
+ LAMA
+ refer for phenotyping (–> IgE, IL4, IL5, etc. biologics based on results)
indications for LABA vs SABA
COST: $30-40 without insurance for SABA + ICS only versus $200-300 without insurance for ICS-formoterol, both with coupon
AGE: ICS-formoterol is approved as first-line for ages 12+ or second-line for ages 6+, i.e., children <6 must use SABA + ICS, and children 6-12 must use SABA + ICS as first-line tx
CONTRAINDICATIONS: ICS-formoterol is contraindicated in diabetes, htn, heart problems, liver problems, hypO-K, immunocompromised, certain infections, and others; albuterol alone is safe in many of these conditions, adding ICS makes it more difficult. Albuterol hypersensitivity is more common.
asthma pt talking in phrases, prefers sitting, not agitated, no accessory muscle use, rr 20-30, hr 100-120, O2 sat 90-95
mild to moderate exacerbation
tx:
- SABA 4-10 puffs via spacer + metered dose inhaler
- oral corticosteroids (prednisolone) 40-50 mg or 1-2 mg/kg up to 40 mg in children
- oxygen, nasal canula OK in adults, mask in children
transfer to acute care if worsening
else assess response at 1 hour
d/c and f/u after asthma exacerbation
d/c if O2 sat >94, not using SABA, PEF improving
on d/c start or step up ICS, continue reliever, check adherence and technique, OCS for 5-7 days (adults) or 3-5 days (children)
f/u at 1-2 days (children), 2-7 days (adult)
cont OCS if needed for 1 wk up to 3 mo, check modifiable risk factors, check inhaler adherence and technique
refer to pulm if >1-2 exacerbations/year
asthma pt drowsy or confused, silent chest
LIFE THREATENING
transfer to acute care
m/w and at ED, high-dose SABA via nebulizer, ipratropium bromide, O2, systemic corticosteroid, HF-NRB O2
consider Mg++ IV
rescue breathing if unresponsive
intubate as soon as feasible, ideally prior to respiratory arrest
asthma pt talking in words only, tripoding or hunched, accessory muscle use, rr >30, hr >120, O2 sat <90%, PEV <50% of pt’s best
severe attack
transfer to acute care
m/w and at ED, med-to-high dose SABA via nebulizer, ipratropium bromide, O2, systemic corticosteroid, HF-NRB O2
consider Mg++ IV
monitor for signs of life-threatening attack or arrest:
increase doses
rescue breathing if unresponsive
intubate as soon as feasible, ideally prior to respiratory arrest
emphysema pathophysiology
- irritants activate neutrophil elastases, lead to progressive breakdown of elastin in bronchiolar walls
- becomes more compliant and loses recoil (becomes less like a balloon and more like a plastic bag)
- air becomes trapped in alveoli, leading alveoli to “burst”
- burst alveoli can’t hold air, and “mega alveoli” created from multiple alveoli bursting and fusing together have less surface area to exchange gas
- can lead to increased inflammation and fibrosis over time
- often accompanies chronic bronchitis as both are caused by similar irritants
emphysema dx
clinical: SOB esp w/ exertion tachypnea *hypOcapnic *pursed lip breathing + red cheeks + lack of cyanosis = "pink puffers" *barrel chest minimal cough w/ small amounts of mucus, unless +chronic bronchitis reduced breath sounds hypER-resonant
spirometry req’d for dx:
- FEV1, FVC, and FEV1/FVC ratio all decreased (FEV1 decreases more than FVC)
- because harder to expel air
- progressive worsening over time
imaging: CT preferred, XR also can see many changes
*hyperinflation, flattened hemidiaphragms
increased, irregular radiolucency (more white)
— most common type, centrolobular (termed based on the part of the alveolus it affects) is primarily seen in the upper part of all lobes, patchy distribution
— panlobular (again, named based on effect on alveolus) is associated with alpha-1-antitrypsin deficiency and affects lower lobes
diaphragmatic tenting
fewer blood vessels, distorted
note that emphysema dx is based mostly on structural changes while chronic bronchitis dx is based mostly on clinical presentation
copd and heart failure
- lungs have natural response to vasoconstrict to damaged or blocked alveoli, to shunt to functioning alveoli
- too many damaged or blocked alveoli –> too much vasoconstriction (pulmonary hypertension)
- increased afterload to right ventricle –> RVHF
alpha-1-antitrypsin deficiency
an inherited form of emphysema d/t lack of enzyme that breaks down proteases that break down elastin (overall result is elastin breakdown)
clinical suggestions:
- usually onset b/f age 30
- little to no exposure history
- familial
- distribution in lower lobes
main causes of emphysema
*cigarette smoke (1st or 2nd hand) indoor open-flame/coal stoves (developing countries) environmental/smog occupational (asbestos, coal, ...) genetic (alpha-1-antitrypsin deficiency)
ventilation-perfusion mismatching
lot of air
not a lot of gas exchange
happens in emphysema due to air trapping that results in breakdown of alveoli
chronic bronchitis pathophysiology
- inflammation of bronchial walls (neutrophils and lymphocytes)
- smooth muscle cell proliferation and reactivity –> bronchospasms, cough, wheezing
- goblet cell proliferation and hypertrophy –> too much mucus (blocks airways)
- squamous metaplasia (structural changes) –> cilia not as effective at clearing mucus –> too much mucus (blocks airways)
