Summary
Summary documents
- Module
- Respiratory (HH5607)
- Institution
- Brunel University (BU)
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Asthma Pathophysiology
o Atopic asthma: high levels of Ige and specific Ab response to Ige. Produce Ige to
common environmental allergens like dust mites, animal proteins and fungi. Ige
activates mast cells and produces a power inflammatory reaction (macrophages
in airway present antigen to helper T cells activate and secret cytokines
ige production Ige binds to mast cells degranulation of mast cells releases
histamine, proteases, neutrophils and eosinophils which prolongs allergic
response
o Non-atopic asthma: later in life, imbalance between PNS and SNS. PNS releases
Ach and causes bronchoconstriction. SNS stimulates mast cells and produces a
powerful inflammatory reaction
o Inflammatory response
o Characterised by inflammation (Mucosal oedema), bronchospasms, sputum
production, chronic inflammation and remodelling
o Chronic inflammation and remodelling: hypertrophy of smooth muscle,
hyperplasia of mucus glands, thickening of basement membrane
o Status asmaticus: unresponsive to therapy, PEFR<50%
o Brittle asmaticus: can get unprovoked attacks, carry epipen
Clinical features: SOB, wheeze, cough (if exacerbation, irritant receptors), mucus
production (usually exacerbation), decreased exercise tolerance, chest tightness,
hyperinflated, hypoventilation
Auscultation: wheeze, reduced BS
Chest xray: hyperinflated (10th or 11th rib touching diaphragm)
Other investigations:
o ABG
o Lung function tests:
FEV1/FVC <40% would be severe impairment
PEFR: breathe out as hard and as fast as they can
Medical Management
o Bronchodilators: SABA e.g. salbutamol+ventolin, LABA e.g. salmeterol+
serevent, SAMA e.g., ipratropium bromide+ Atrovent, LAMA e.g. Spiriva+
tiatropium bromide
o Steroids e.g. budesonide+ pulmicort
o flu vaccine
o O2 therapy
o Ventilation: PaO2<6.5, patient exhaustion, hypotension (systolic <90), resp. or
cardiac arrest
Physiotherapy Management
o Positioning to maximize V/Q mismatch: side lying will preferentially ventilate the
dependent lung, relieve breathlessness
o ACBT
, o IPPB (if fatigued, will passively give patient a breath)
o Relaxation techniques
o Education: exercise will release catecholamines to open airways
** a lot of smokers not likely to see GP, think they have smokers cough
**60-80% FEV1 is mild COPD, <40% FEV1 is severe COPD
COPD: Emphysema
Patho:
o A disease in alveoli with permanent enlargement of distal air spaces due to
protein breakdown of alveolar septa and destruction of elastic fibres. Formation
of bullae where alveoli join together Loss of radian traction causes airways to
become floppy and get elastic recoil of the airways which airway collapse on
expiration
o Mainly related to smoking and small percentage (2-3%) is related to alpha 1
antitrypsin deficiency which inhibits the action of elastase which destroys elastin.
Signs of genetic cause are that they usually develop it younger
o Secondary effects: airflow obstruction, increased airway resistance, increased
WOB, less surface area for gas exchange (isolates from chronic bronchitis), V/Q
mismatch
Clinical features: SOB, wheeze, cough, decreased exercise tolerance, chest tightness,
hyperinflated, hypoventilation, history of smoking, chest tightness
PT problems: reduced TV, V/Q mismatch, increased WOB, breathlessness, pursed lip
breathing, fixed ULs, use of accessory muscles, poor gas exchange
Auscultation: reduced breathe sounds, wheeze (polyphonic)
Chest xray: hyperinflated, long/thin heart, black lung fields, horizontal ribs, bullae (large
black region)
Medical management: LTOT (if <7.3), diuretics (RVF), flu vaccine
o Smoking cessation program: 4 times more likely to quit (ASK,ADVISE, ACT)
Surgical options: LVRS (remove a part of overexpanded lung) to remove bullae which
will relieve compression, reuces lung volume and allows doming (rising) of diphragm.
Reduces WOB, reduces V/Q mismatch
Risk factors: RVF due to HPVC which increases pulmonary hypertension and can cause
heart failure. Signs could be ankle oedema and raised jugular venous pressure.
PT management: education about smoking cessation, breathlessness management,
importance of exercise (pulmonary rehab), positions of ease **don’t use IPPB if bullae
with acute exacerbation: could acute on chornic: similar to respiratory acidosis w/
partial compensation
If CO2 levels rise after checking ABG following oxygen therapy, switch to NIV like a
facemask b/c increases TV and gets rid of excess CO2
COPD: Chronic Bronchitis
Pathophysiology:
, o Chronic inflammation of the airways, insidious onset with morning cough
(smoker’s cough)
o Characterized by productive cough for three months for two consecutive years
o Possible causes: environtal pollutants, smoking (Main), occupational exposure,
repeated bronchial infections
o Inhalation of pollutants (usually smoke) causes irritation of the mucosa lining
airways
o Narrowing is secondary to mucosal eodmea, smooth muscle hypertrophy and
periobronchial fibrosis. Excessive bronchial secretions due to hypertrophy and
hyperplasia of goblet cells which causes increased mucus production, reduces
function of cilia and repeated infections can occur.
Clinical features:: SOB, wheeze, productive cough, mucus production, decreased
exercise tolerance, hypoventilation, history of recurrent chest infections, history of
smoking, chest tightness
o Secondary effects: airway obstruction, increased airway resistance, increased
WOB, V/Q mismatch, impaired gas exchange
Auscultation: inspiratory crackles due to sputum, wheeze (sputum can cause wheeze)
Chest xray: consolidation if infected, patchy shadowing, increased hilar shadowing
(pulmonary hypertension), increased cardiac shadow
Pharmacology: bronchodilators (If reversibility shown), steroids, flu vaccine, antibiotics,
diuretics (RVF)
PT treatment: Education about smoking cessation, breathlessness management,
pulmonary rehabilitation, sputum clearance techniques if appropriate
Bronchiectasis
Patho:
o Bronchiectasis is chronic and permanent widening of the airways and
destruction of bronchial wall, elastic content, blood vessels, cartilage, smooth
muscle. Results in decreased Mucoiciliary clearance and retained secretions,
making patients susceptible to recurrent infections and infection cause further
damage. Some possible causes of bronchiectasis: 53% idiopathic, 29% post
infectious
Post-infection: measles, TB, whooping cough
Immune defects: hypogammaglobulinemia because it normally produced
antibody response
Allergic bronchopulmonary aspergillos: increased response to aspergillus
which is a fungi, become wheezy
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