B4.032 - Big Case Asthma Flashcards
Type 1 HS - allergic asthma
what is a T1 HS reaction
Immediate hypersensitivity reaction
Involve IgE mediated relaesae of histamine and other mediators from mast cells and basophils
what are type 2 HS reactions
Cytotoxic hypersensitivity
Involve IgG or IgM antibodies bound to cell surface antigens, with subsequent complement fixation
what is a T3 HS reaction
immune complexc reactions
involve circulating antigen-antibody immune complexes tha teposit in post ca;illary venules, with subsequent complement fixation
what is a T4 HS reaction
delayed
cell mediated immunity
mediated by T cells rather than by antibodies
what is an arthrus reaction
type 3 immune complex mediate dHS that occurs following the intrdermal injection of antigen in the presence of a high level of circulating antibody. Within 4-12 hours the area becomes red and oedematous
which cell line is increased in patient with an acute asthma exacerbation, severe asthama or smokers with asthma?
in acute setting neutrophils are the major component
what is the 2007 definiton of asthma
Chronic inflammatory disorder of airway in whihc many cells an cellular elements play a role : mast cells, eosinophils, neutorphils, T lymphocyetes, macrophages, epithelial celsls. In susceptible indiviiduals this inflammation causes recurrent episodes of coughing (particularly at night or early in the morning), wheezing, breathlessness and chest tightness.
when do asthmatics wheeze
on expiration
describe the cause of inflammation in asthma
- inhaled antigen activates mast cells/Th2 cells in airway
- inflammatory mediators/cytokines
- bone marrow activation
- eosinophils migrate ot area of allergic inflammation
- eosinophils release inflammatory mediators
In pt with acute episode of asthma
Airway remodeling
why? hes 31, hopefully hes recieved treatment and had controlled asthma so he wouldnt have remodeling
what causes airway remodeling
chronic asthmatic episodes that are poorly controlled
the smooth muscle constricts during an asthmatic episode, if you have chronic constriction due to failure to control constant asthma then this smooth muscle hypertrophies
asthma pathogenesis
- airways infiltrated wiht eosinophils and mononuclear cells
- vasodilation and mocrovascular leakage
- airway smooth muscle hypertrophy
- new vessel formation
- increased numbrs of epithelial goblet cells
- deposition of interstitial collagens beneath epithelium
will giving bronchodilators help with airway remodeling
not if its already formed
All can play a role
A. gender is key here
describe gender and asthma prevalence
before puberty boys higher prevalence
after puberty girls higher
what factors initiate inflammation/asthma?
what factors favor Th1 phenotype
Presence of older siblings
Early exposure to daycare
TB, measles, hepA
Rural environment
what factors favor Th2 phenotype
widespread use of antibiotics
western lifestyle
Urban evironment
diet
sensitization to house-dust mites and cockroaches
What does the Th1 phenotype lead to
protective immunity
what does the Th2 phenotype lead to
Allergic diseases including asthma
A. currently available therapies (ICS) for asthma control symptoms, but do not modify disease severity
AKA if you give a beta agonist once they go off the medicine they will still have symptomes
ENT consultation
Classic - woman with PTSD –> vocal chords spasm
once you bypass obstruction with probe the symptoms should dissapate
Answer is A. Fibrotic stricture is going to result in flattening of both the inspiratory and expiratory flow-volume loop. The other three answers are extrathoracic issues that would result in flattening of the inspiratory limb like we see on the above loop. See next couple slides.
what is vocal cord dysfunction, what does it mimic, epidemiology
an abnormal adduction of vocal cords durign respiratory cycle
Often mimics persistent asthma
more common in young females with psychiatric illnesses
localization of airflow obstruction to laryngela pharynx is an important clinical discriminatory feature wiht VCD
what type of lesion causes this
Fixed lesion
* neoplams of central airway
* vocal cord paralysis with fixed stenosis
* fibrotic stricture
what type of lesion causes this
variable extrathoracic lesions
* vocal chord paralysis
* subglottic stenosis
* neoplasm
* goiter
what type of lesion can cause this
variable intrathoracic lesion
* Tumor of lower trachea
* thracheomalacia
* strictures
* wegners granulomatosis or relapsing plychondrosis
Everything essentially
key indicators for considering diagnosis of asthma
what is spirometry looking for
airflow obstruction
reversibility
is there one single test to diagnose asthma?
no
what is reversibility
when the patient blows the FEV1 is low, but when you give a bronchodilator in the clinic the FEV1 should open up
whats methocholine challenge testing
Given to bronchocontrict and if it doesnt work think something else
C - allay the spasm during the paroxysm
B
why does avoidance improve asthma symptoms?
decreased exposure means decreased reaction
what is the best appraoch to asthma treatment
mutlifaceted. single steps are generally ineffective
A. yes
D. medium dose ICS
what is mild intermittent asthma
* symptoms = 2 days / week
* Breif exacerbations
* SABA use <2x/month
* nighttime symptoms <2x / week
* asymptomatic with normal lung function between exacerbations
* FEV1 and PEF >/= 80% predicted
*PEF variablility
what mediaction do you give someone with mild intermittent asthma
albuterol
what is mild persistent asthma and how do you treat
inhaled cortico steroid (ICS) is the gold standard
*symptoms >2 d / wk but not daily
* minor limitations
* SABA >2d/week but not daily, not more than 1x /day
*nighttime asthma symptoms 3-4x/month
* FEV1 and PEF >/= 80% predicted
* PEF variability 20-30%
how do you treat mild persistent asthma
ICS
what is moderate persistent asthma
* daily symptoms
* exacerbations >2x/week
* affects activity
* nighttime symptoms >1x / week but not nightly
* daily use of short activng beta agonist
* FEV1 adn PEF > 60% and <80% predicted
* FEV1/FVC reduced 5%
*PEF variability
what is severe persistent asthma
* continuous symptoms
* frequent exacerbations
* frequent nighttime symptoms
* limited activity
*FEV1 and PEF <60
* PEF variability >30%
Answer is E. IV steroids are important but will not help in the acute exacerbation phase. They take 12 to 24 hours to work.
what is the expert panel conclusion on sever asthma exacerbations in the ED
Ipratropium bromide (atrovent) , administered in multiple doses along with SABA provides additive benfit
D. his LABA use
you need to have ICS with LABA always!!! Never just LABA
why do patients start taking LABAs instead of ICS
because ICS dont make you feel good but dont bronchodilate, LABA makes you feel better sooner so patients tend to just use those
what is bronchothermoplasty
burn airways/scar muscle layer so the muscle cant constrict
You are taking care of Mr. Smith, a 35 yo veteran, who reports intermittent compliance issues with is asthma meds. You should be most concerned about what?
A. his dose of ICS
B. allergen avoidacen strategies
C. his occupational exposure risk
D. his LABA use
E. his inhaler technique
Answer is D. We don’t want asthmatics to use LABA’s alone. Need to be on inhaled steroid as well.
Mrs. P. is a 35 yo female with moderate compliance with her asthma. Which of the following statements is correct in regards to her management of acute asthma exacerbations?
A. A peak-flow-based plan may be particularly useful for patients who have difficulty perceiving airflow obstruction and worsening asthma (Evidence D).
B. Appropriate intensification of therapy by increasing inhaled short-acting beta2-agonist (SABA) and, in some cases, adding a short course of oral systemic corticosteroids (Evidence C).
C. Recognition of early signs of worsening asthma and taking prompt action (Evidence B).
D. Patient education, including a written asthma action plan to guide patient self-management of exacerbations at home, especially for patients who have moderate or severe persistent asthma and any patient who has a history of severe exacerbations
(Evidence D).
Answer D: This slide speaks to the importance of pt education and providing an asthma action plan so pt’s can initiate a therapy plan from home if and when they start to develop an exacerbation. These plans often direct them to contact their physician if they are not improving with specified therapy.
Mrs. P. does not recognize her asthma has worsened and ends up being admitted to unit 66 for an acute asthma exacerbation. She reports dyspnea, cough, and wheeze and believes her trigger is the humidity. Which therapy below has not been shown to have significant benefit for the hospitalized asthma patient?
A. Oxygen to keep sats>92%
B. Prednisone 60mg po
C. Levaquin 500mg qd
D. SABA
E. Atrovent
E. Atrovent
Remember, this has been shown to be beneficial on arrival to the ER during an exacerbation. If the pt does not improve and is admitted then albuterol is the drug of choice for bronchodilation but not both.
You return to check on Mrs. P after admitting 2 other patients from the ER. She appears less tachypnic than before, but is still using her accessory muscles to breath. She appears mildly confused and is having a difficult time speaking. Her oxygen levels are stable on 2 liters. The most important next step in her care is?
A. Check an ABG
B. Intubate the patient
C. Start heliox stat
D. Add magnesium infusion to her management
E. Call a rapid response
A. check ABG
Answer is A. This pt is showing signs of respiratory fatigue. Don’t be fooled by less tachypnea. As an asthmatic pt. fatigues they start to become more hypercapnic (retain CO2). This is likely contributing to her confusion. You need and ABG to assess her acid-base status and to see if she is developing a respiratory acidosis. If she is then you would call a rapid response, move her to the ICU and provide her with NIV or intubation. Additional magnesium is used for bronchodilation. Heliox is used for worsening hypercapnia when you are trying to clear CO2. Changes gas flow dynamics in the airway.
Mrs. P. just can’t catch a break and gets intubated. You are asked by the respiratory therapist for ventilator settings. Your recommended ventilator strategy will be which of the following?
A. Active hyperventilation to remove C02.
B. Shortened expiratory phase to improve ventilation
C. Moderate tidal volume ventilation to maintain plateau pressures below 40.
D. Controlled hypoventilation
E. Permissive hypocapnia
Answer is D. We ventilate pt’s with asthma at low lung volumes, slow rates (hypoventilation) and prolonged expiratory times. Remember, when they are obstructed with severe bronchial constriction during status asthmaticus they struggle to get the air out of their lungs. They are at increased risk of stacking breaths and air-trapping which will make the pressure in their thorax go up. This can result in hemodynamic compromise and shock. You don’t want them to hyperventilate, we always want to maintain plateau pressures below 30 to protect against ventilator-induced lung injury. We allow for permissive hypercapnia. Allow their PCO2 to run a little on the high side (pH of 7.20 to 7.25) until their bronchoconstriction improves with therapy.
what is step one of treatment for asthma patients
SABA PRN
what is step 2 for persistent asthma
Low dose ICS
alternative:
Cromoly, LTRA, Nedocromil, theophyline
what is step 3 in treatment for persistent asthma patients
ICS + LABA
OR
Medium dose ICS
Alternative:
Low dose ICS
and LTRA, theophylline or zileutron
what is step 4 in treatment for persistent asthma
medium dose ICS + LABA
alternative:
medium dose ICS, adn LTEA, theophylline or zileuton
what is step 5 in treatment for persistent asthma
High dose ICS + LABA
AND
consider omalizumab for patients with allergies
what is step 6 for treatment of persistent asthma
High dose ICS + LABA + oral corticosteroid
AND
consider Omalizumab for patients who have allergies
what should you check before stepping up asthma treatments
adherance, environmental control, comorbid conditions
when can you step down mediactions
when asthma is well controlled at least 3 months
