Asthma Flashcards
what is asthma
reversible episodes of airway obstruction d/t:
- muscle hyperactivity (in airways–contraciton/relaxation in excess)
- Inflm (exudate & swelling compromising airway)
what is atopy
genetically induced hypersensitivty some predisposition there
asthma as ______ and ______ forms
extrinsic(atopic) & Intrinsic (non-atopic) factors
what is the etiology(cause of asthma)?
- complex
- genetic & environmental factors
- hypersensitivity to stimuli (such as allergens, strong odours, a/w irritants, exercise)
- T cell differnetaiton toward T2H (T1 helper cells propageted in defense to microbes, bacteria, virus, cytokine. T2 helper cells in defense of antigens)
patho of asthma
- stimulus
- hypersenstivity
- 2 phased response
there are _____ and _____ triggers of asthma
non atopic tiggers: infection, drugs, cold air
atopic triggers: allergens
when do the early and late phases of asthma happen
early phase: begins right away only lasts about an hour(not an absolute number could differ)
late phase: peaks a 6 hrs, can last hours or days
what are the manifestations of asthma?
- wheezing (drawing & expelling air forcefully through narrowed airways)
- dyspnea
- increased resp effort (pursed lip breathing) (nasal flaring)
- alt resp statues & ABGS (changes in abgs)
diagnosing asthma
- hx, px
- pulm function tests (spirometery)
- labs
- inhalation challenge tests (testing for hyperresponsivness to inhlaed allergens)
treatment of asthma
- control with decreased meds (chronic control use as little meds as possible)
- preventative measures: no smoking &avoid allergens & irritants
- 4 step of drugs
what is the 4 steps of drugs to treat asthma?
step 1: short acting bronchodilators (inhaled prn)
step 2: add an inhaled steroid (inhaling so delivering locally into respiratory tract so decreases systemic effects (bad side effects)
step 3: add long acting bronchodilator to steroid
step 4: -short course steroid (ORAL)
-add 3rd drug leukotrine receptor antagonist(blocks inflm, leukotrine mediates allergic response, blocking from happening) or theophyline (potent bronchodilator)
early phase of asthma (simple)
- allergen enters (mast cell already sensitized to allergen)
- Mast cells–release histamine, leukotrines, interleukings & prostaglandins causing:
- bronchospasm and
- infiltration of inflammatory cells with causes release of cytokines, interleukins, & other inflammatory mediator causing airway inflammation
late phase of asthma (simple)
airway inflammation which causes edema, impaired mucociliary function, & epithelial injury, causing airflow limitation this can also lead to increased airway responsivness
Acute phase response
- happens right away 5-10 min
- prior sensitization to allergen (type 1 hypersensitivity)
- subsequent exposure–allergen binds to igE on mast cells causing mediator release cause inflm
- mediators open intracellular junctions and allergen enters submucosa
- increased permeabliity and increasd mucus secretion causes edema of airway
- bronchospasm via parasympathetic ns)
- dyspnea & wheezing
- a/w constriction
- can last up to one hour
Late phase response
- peaks 4-8 hrs post exposure
- can last days to wks
- influx of inflm cells (via chemotaxis)–causing epithelial damage(which will not be reversible)–decrease in mucociliary function (prone to recurrent infections) and hyperesponsiver airways (new triggers-stimuli that were not triggers become triggers, frequent severe episodes)
