Asthma to Pleural Effusion Flashcards
Is hypersensitivity the same as hyper-reactivity? Hyperactivity?
No - important to diferentiate these apparently
What occurs in asthma?
What is common in individuals with asthma?
- Complex condition - is chronic w acute episodes
reversible episodes of a/w obstr d/t inflam + muscle hyperactivity (spasm)
Chronic inflm of a/w d/t having hyper-responsive a/w (when already inflamed is esp sensitive to stimuli like cold) + recurrent, reversible bronchospasm
Most often individual has other allergies eg: hay fever
What is the “true” etiology of asthma?
Other factors?
True = complex trait (genetic + enviro factors)
- Have hypersensitivity to stimuli:
alergens, a/w irriants, exercise, strong odours, cold air
etiology only happens once → once genetic factors and stimuli are in place, the disease has occurred….the rest are TRIGGers only
Patho of asthma?
Outline acute phase response
SEE FIG 29-5 + 6 p. 682/3
Trigger –> excessive hypersensitivity –> 2 phase response:
ACUTE PHASE RESPONSE
- Prior sensitization to allergen (Type 1 H) –> acute/early phase occurs after initial sensitization has already occured
- Subsequent exposure –> allergen binds to IgE coated mast cells –> mediator release (leukotrienes, interleukins, prosta, hist) –> inflm response
- Intracellular junctions open –> allergens enter submucosa (mast cells here…more mediator release)
- Inc perm + inc mucus sec –> edema of airways
- PNS stimulated bronchospasm (Mediators also bring about bronchospasm)
- Dyspnea + wheezing
- Lasts up to 1 hour
During acute phase, what is the body’s attempt at compensation?
Further constriction as attends to limit inhalation of irritant
Outline LATE PHASE RESPONSE in asthma
Peaks 4-8hrs
Is possible for person to go straight to this phase (begins like early phase but just persists)
- Mnfsts of acute phase persist
- Self-sustaining cycle of exacerbation
- Can last days to weeks
- Influx of inflm cells (as attracted to mediators…then release even more) –> epithelial damage, dec mucociliary fx (with accum of mucous) + hyperresponsive airway (now responding to even more triggers, causing frequent and severe episodes)
• Bronchospasm even worse!
Do you consider the frequent and recurrent asthma episodes as “exacerbations and remissions”?
Ahmed says no!
What receptors mediate bronchoconstriction + dilation? What mediates this?
How does this connect to possible cause of asthma?
Bronchoconstriction via alpha adrenergic receptors
Bronchodilation via Beta adrenergic receptors
- cAMP mediates (= second messenger… this is physiologic)
- Possible lack of Beta receptor stimulation in asthma (can’t stimulate dilation)
Difference between adrenergic and cholinergic?
Adrenergic = referring to adrenaline Cholinergic = ACh
Does a person with asthma have normal resp function between attacks?
• Independent of asthmatic attack, individual with asthma already has compromised respiratory status normally (more than others) but then also separate set of manifestations during an attack
???????
Manifestations of asthma
- Dyspnea
- Wheezing
- Immobiliation? (in extreme cases, if can’t breath won’t move)
- Bronchospasm + coughing
- Inc resp effort
- Ventilatory compromise (alt resp status and ABG’s) - will show hypoxemia, etc
Others include nasal flaring, propping body to facilitate breathing
Dx of asthma
Hx, px
labs
pulm fx tests (won’t differentiate from COPD)
Inhalation challenge tests (inhale allergens to see if response…this differentiates from COPD)
Tx of asthma
- Control with minimal meds
- Preventative: avoid allergens, no smoking
- DRugs (in steps)
1) Inhaled short acting bronchodilators PRN
2) add inhaled steroid
3) add long acting bronchodilator or steroid
4) Short acting steroid po, add 3rd drug = leuiotriene receptor agonist or theophylline (bronchodilator) po - this step refers to some occassions in which per can undergo acute attack that lasts days or weeks (goes directly to late phase) – will give short course of oral steroids (for a couple of weeks) and add leukotriene receptor antagonsist of theophylline (bronchodilator, some minimal anti-inflm property as well)
Atelectasis =
3 kinds?
Collapse of part of lung - impedes filling
- affected part non-fx
1) Obstructive/resorptive
2) compression
3) contraction
SEE FIG 29-4 p. 679
1) Obstructive/resorptive atelectasis?
A/w obstruction (eg: by mucus) –> air trapped (in a/w + alveoli) –> air absorbed into caps –> local collapse
Compression atelectasis?
Extensive pression on lungs (eg: by tumour)
Contraction atelectasis?
Scar tissue contraction –> a/w collapse
* Has trauma to lung, scar tissue forms to fill gap, pulls damaged tissues together, which causes the collapse
Manifestations of atelectasis?
- Dyspnea
- Tachypnea
- Dec Chest expansion
- Tachycardia
Dx of atelectasis?
Tx?
Px
CXR
CT
Bronchoscopy
Tx = cause
Pleural effusion aka
What is it?
Hydrothorax
Accum of fluid in plural space
d/t abnormal seepage +/or drainage
What are the different possible fluids that accum in pleural effusion and what is the appropriate term for each? What does this tell you?
Exudate: inflm fluid, high protein content
Transudate: non-inflm fluid, low protein content
Empyema: purulent (d/t bacterial infection)
Hemothorax: blood
Chylothorax: lymph fluid
• What fluid has built up tells you the cause:
Et of pleural effusion?
1) Usually CHF (most likely left sided but could be either)
2) Infection (causes inflm)
3) CA (tumour causes injury, inflm + exudate formation)
4) Pulm infarction (ischemia….EXPLAIN THIS)
Patho of pleural effusion
first describe what occurs normally
- Fluids enters via parietal caps
- Drains into parietal lymphatics
- Fluids entra exceeds drainage –> pleural effusion
External p prevents proper expansion of lungs (like cardiac taponade)
• Has very big effect on transcapillary exchange
o If have too much fluid flowing in and not enough moving out, will move from the tissues in to the spaces in the membranes
Manifestations of pleural effusion?
- based on cause + vol
- Dyspnea
- Pleuritic pain
- Lung compression
Dx and tx of pleural effusion?
Dx:
xray (won’t show smaller vol)
US, CT (see smaller vol)
Tx:
- Cause
- Thoracentesis (+ fluid analysis –> blood, pus, tumour cells?)
- Chest tube? (if can’t be fixed properly, need continued drainage
…want to collect fluid before it solidifies!
• If frequent problem, will introduce sclerosing agent (causes sclerosis – inflm, will cause membranes to be brought together)
Why aren’t diuretics used as tx for pleural effusion?
Take too long! Need to restore vital fx asap
