Asthma Flashcards
If this is your problem list; what are some possible DDx?
- Wheeze
- Difficulty breathing
- Exertional symptoms
- Night cough
- Chronic rhinitis not controlled
- Recurrent sinusitis
- Peanut allergy, possible accidental ingestion
- Asthma
- Paradoxical vocal fold motion
• Laryngeal edema/anaphylaxis
- Allergic rhinitis
- Cystic fibrosis
What tests/labs/imaging would be recommened in pt you suspect has asthma?
- PFT
- CXR
- Allergy testing
- Laryngoscopy (could be vocal cord misfolding)
- Sweat chloride test
What diseases could cuase this type of spirometry result?
Restrictive lung disease:
asthma or Cystic fibrosis
Define Restrictive lung diesease
category of extrapulmonary, pleural respiratory diseases that restrict lung expansion,[2] resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.
What do we expect to see on pt with asthma for their:
FVC
FEV1
FEV1/FVC
both FVC and FEV1 will decrease but FEV1 more so thus:
ratio often LESS then 80%
You tx pt you suspect has asthma with SABA. If they truly have asthma, what would you expect to see on repeat spriometry
FEV1 revesed >200 mL and increased by 12%
56 year old woman is evaluated for a 2 year history of episodic cough and chest tightness. Her symptoms began after a severe respiratory tract infection. Since then, she has had cough and chest discomfort after similar infections, typically lasting several weeks before resolving. She feels well between episodes. She is otherwise healthy and takes no medications. Physical examination reveals no abnormalities and spirometry is normal.
Next step?
Methacholine challenge testing
This patient’s history is consistent with, but not typical of, asthma
cough-variant asthma*** with normal testing btwn episodes, need to induce it
You give a pt you suspect has asthma the Methacholine challenge. What results would suggest asthma?
FEV1 will drop by 20%
complex clinical syndrome characterized by variable airflow obstruction, airway inflammation, bronchial hyper- responsiveness
Asthma
Pathophysciology of asthma
Persistent inflammation–> infiltration of airway by inflammatory cells–> Hypertrophy of airway smooth muscle + Thickening of basement membrane (lamina reticularis)–>
Hyperplasia and hypertrophy of submucosal glands–> Goblet cell hyperplasia and hypertrophy–> Hyperplasia of microvascular dilation–> Loss of epithelial cells
26 year old with poorly controlled asthma complains of increased cough. What would you expect to find in the sputum?
Charcot-Leyden Crystals
They consist of lysophospholipase, an enzyme synthesized by eosinophils, and are produced from the breakdown of these cells. **eosinophilic inflammation or proliferation
What are signs and symptoms of Vocal cord dysfunction?
have throat or neck discomfort, wheezing, stridor, and anxiety. The disorder can still be difficult to differentiate from asthma; however, affected patients do not respond to usual asthma therapy.
Get Laryngoscopy
Key things to determine when making asthma dx
Episodic sxs of airflow obstruction or airway hyper-responsiveness are present
Airflow obstruction is at least partially reversible
Alternative diagnoses are excluded
Methods to establish ashtma diagnosis
Detailed medical history
Exam focusing on upper respiratory tract, chest, and skin
Spirometry: assess obstruction/reversibility, > 5 yr. Reversibility: increase in FEV1 >12 % and 200 ml from baseline
Additional studies to exclude alternate diagnosis
Possible DDx for asthma in adults
COPD (e.g., chronic bronchitis or emphysema)
Congestive heart failure
Pulmonary embolism
Mechanical obstruction of the airways (benign/malignant tumors)
Pulmonary infiltration with eosinophilia
Cough secondary to drugs (angiotensin-converting enzyme (ACE)
inhibitors)
Vocal cord dysfunction
Possible DDx for asthma in infants for upper airway
Upper airway disease: Allergic rhinitis and sinusitis
Obstructions involving large airways
Foreign body in trachea
Vocal cord dysfunction
Vascular rings or laryngeal webs
Laryngotracheomalacia, tracheal stenosis, or bronchostenosis
Enlarged lymph nodes or tumo
DDx in young children or infants for asthma for small airways
Viral bronchiolitis or obliterative bronchiolitis
Cystic fibrosis
Bronchopulmonary dysplasia
Heart disease
46 yo male comes to ED; acute breathlessness, chest pain, cough. No radiation of pain, but hear high pitched sounds on expiration (family hx asthma)
PE: nasal polyps, sinus tenderness and respiratory hear bilateral rhonchi w/ prlongued expiration. Use accessory muscles.
Has increased IgE in blood. See opacity in frontal sinuses and hyperinflation on CXR
FEV1 is less then 80% of normal and no ST changes on EKG
What’s going on to cause this?
EArly allergic reaction in the airway including bronchial constriction, edema, mucous plugging: dude has asthma
is a clinical syndrome characterized by episodic reversible airway obstruction, increased bronchial reactivity, and airway inflammation. Environmental exposure in sensitized individuals may trigger the process.
Asthma
Pathophysiologically the allergic response in the airway is the result of a complex interaction of
mast cells, eosinophils, T lymphocytes, macrophages, dendritic cells, and neutrophils. Inhalation challenge studies with allergens reveal an early allergic response (EAR).
Clinically, the manifestations of the EAR in the airway include
bronchial constriction, airway edema, and mucous plugging.
***mast cell-derived mediators
Four to ten hours later after EAR, , one sees the late allergic response (LAR), which is characterized by
cellular infiltration into the airway and is most likely caused by cytokine-mediated recruitment of lymphocytes and eosinophils.
Degranulation of the mast cell also plays an important role.
Preformed mast cell mediators, such as histamine and proteases, are released, leading to
Bronchocnx: immediate and early phase reaction!
What is the pathway of the allergy response
Allergen–> to lymphoid tissue–> will produce IgE–> go and sensitize and coat a mast cell
THEN
reexposure to allergen will crosslink IgE on mast cell–> degranulation of histamine, tryptase and LTC4
What is goind on in the Immediate early reaciton
Mintues: degranulation–> relase histamine, Leukotrines, cytokines and proteins=
Bronchoconstriction (causes chemotaxis and cell influx)
What happens during late phase reaction?
Hours later–> cytokines/chemokines/Mediators cause
Inflammation
What are some asthma triggers?
Allergic, Viral respiratory infections, Excersice, aspirin, irritants, weather changes
A 15-year-old boy on the high school track team develops difficulty breathing associated with wheezing when running in the winter. What would be helpful to prevent symptoms?
- Premedication 15 minutes before exercise with a SABA is typically the first-line therapy
- Cover nose and mouth with scarf or face mask in cold weather to humidify air
*** Cooler, drier air causes release of bronchoconstrictor mediators from airway mast
cells: cysLTs (LTC4, LTD4) and histamine
If you have asthma and take aspirin, what can happen?
You will inhibit the Prostaglandin pathway that leads to bronchial dialation (PGG2 or PGH2) and push for the leukotriene pathway instead = Smooth mscl contraction adn bronchoconstriciton = wheezing!
What can be helpful to reduce ashtma symptoms in regards to humidity
Dust mite is one of the most common indoor allergens, except in locations where humidity is consistently less than 50%. When dust mite allergen is significantly reduced, patients have demonstrated improvement in allergic rhinitis symptoms and bronchial hyperresponsiveness.
