Pathologies In ViVa format Flashcards
Bronchiectasis
Pathology
Cause
Symptoms
ODPAAR
Bronchiectasis
• Chronic dilation of one or more bronchi
• Bronchi- airway. Ectasis = widening
Pathophysiology
• Permanent abnormal dilation
• Destruction of:
• Bronchial wall
• Cartilage
• Elastic tissue
• Smooth muscle components
• Blood vessels
• Results in impaired mucociliary clearance.
Causes
• Post-infective – TB, measles, whooping cough
• Cystic fibrosis, primary ciliary dyskinesia
• Immune defects -hypogammaglobulinaemia
• Allergic bronchopulmonary aspergillosis
• Gastro-oesophageal reflux
• Localized bronchial obstruction – foreign body, tumor
Clinical Features PHB DFC – Paul Has Bronchiectasis, David Fakes Concern.
• Persistent, productive cough
• Haemoptysis
• Breathlessness
• Decreased exercise tolerance
• Finger clubbing
• Chest pain (infective exacerbation)
Spirometry
Airway collapse – obstructive.
Hyperinflation. Reduced FEV1/FVC %
Increased RV, TLC, VC.
Decreased IRV.
Medical management – BTS Guidelines Bronchiectasis – No reduction in exacerbations was identified for inhaled corticosteroid use in a 2009 meta-analysis. • Bronchodilators – • Steroids • Surgery (lobectomy, single/double lung transplant) • Antibiotics • Flu vaccine • Ig therapy Physiotherapy • Education • Daily airway clearance regimen for life • Breathlessness management • Increase exercise tolerance
Oxygen – Yes. Possible hypercapnia (COPD like presentation)
Drugs – Antibiotics, flu vaccine, Ig therapy, steroids, bronchodilators (same as asthma0
SABA – salbuterol, terbutaline – LABA – salmeterol. SAMA – tiotropium. LAMA – tiotropium bromide.
Corticosteroids - BTS guidelines for bronchiectasis found no evidence of improving exacerbations from long term use of corticosteroids.
Antibiotics Flu vaccine Positioning – Gravity assisted positioning. Drain. ACBT? – Yes. All. NO MT. Adjuncts – IPPB or Acapella.
Refer? Pulmonary rehab.
Cystic Fibrosis Cause Pathology Symptoms TESTS ODPAAR
PBVS
Pathology:
Genetic - autosomal recessive defect on chromosome 7. Mutation in the CFTR gene, affecting chlorine channels.
This leads to thick, dehydrated intraluminal mucus.
Dx:
Sweat test
Meconium ileus
Symptoms; Productive cough Haemoptysis. Breathlessness Decreased exercise tolerance Hyperinflation Increased WOB Cor pulmonale. Recurrent chest infections Pneumothorax Wheeze
TESTS
Auscultation
Coarse crackles
CXR
Consolidation - white patches.
Oxygen? Drugs Bronchodilators Steroids Pancreatic enzymes (creon) Diuretics Antiobiotics (nebulized or portocaths) LTOT
Pre-physiotherapy: • DNase - mucolytic • Inhaled bronchodilator • Hypertonic saline / mannitol Post-physiotherapy: • Inhaled steroid • Inhaled antibiotic
Positioning -GAP.
ACBT
Adjuncts
IPPB or Acapella. McIlwaine 2013 - Better than HFCWO during LTEE.
MT - Vibration, shakes, percussion.
NICE guidelines for cystic fibrosis management - Do not offer high frequency vibrations to pt unless authorised by a clinical specialist.
Refer
Dietician
Diabetes management
Pulmonary Rehab.
IPF
Idiopathic Pulmonary Fibrosis
• Chronic progressive fibrotic lung disorder
• Average survival time @ Dx = 2.5-3.5 years
Pathophysiology
• Abnormal and excessive deposition of fibrotic tissue in the pulmonary interstitium with minimal associated inflammation
• Clusters of fibroclasts form characteristic fibrogenic foci located in the injured lung
Symptoms: • Gradual onset • Dyspnea • Non-productive cough • Finger clubbing
Tests Lung Function Test (LFT) shows restrictive defect - Decreased FVC / VC. - Normal FEV1 - Increased FEV/FVC ratio
Auscultation
• Inspiratory crackles on auscultation
CXR
Bilateral fibrotic dark patches.
ODPAAR Oxygen - 60% Venturi for breathlessness. Drugs - LTOT. Positioning - Ease ACBT - BC Adjunct - ? Refer: Lung transplant Pulmonary rehab
COPD - Causes Pathology Symptoms Long term hypoxia symptoms
Tests (auscultation, CXR, functional testing)
ODPAAR
COPD
Causes- Smoking
Mutation in alpha 1 antitrypsin (emphysema)
Pathology Chronic bronchitis: Reduced ciliary function V/Q sputum shunt Bacterial colonisation occurs
The -itis part of bronchitis Smooth muscle hypertrophy Bronchial secretions Mucosal oedema Peribronchial fibrosis (BBMP)
Emphysema:
Protein breakdown leading to erosion of the alveolar septa, dilating the distal air spaces and destroying capillary beds.
Leads to formation of emphysemous bullae.
Reduces radial traction of airways, causing them to become floppy.
Symptoms Productive cough Hyperinflated Wheeze Decreased exercise tolerance History of chest infections History of smoking
Increased WoB: Accessory muscle recruitment Active expiration Prolonged Expiration Pursed lip breathing Fixing upper limbs Speech difficulty Soft tissue recession Hoover's sign
Long term hypoxia symptoms:
1. Polycythaemia
RBC’s increase in production increase the hematocrit of the blood.
Red, rosy appearance
2. Cor pulmonale
Chronic HPVC from V/Q mismatch leads to increased load on right ventricle (supplies pulmonary arteries). Increases jugular venous pressure and swelling at the ankles.
Tests: Auscultation: Inspiratory crackles (CB) Reduced breath sounds (Emphysema) Wheeze
CXR: Patchy shadowing Hilar shadowing Hyperinflation (more in emphysema) Bullae (emphysema)
Functional Testing: Hyperinflation results in: Increased RV, FRC, TLC Decreased FEV1, FEV1/FVC ratio Decreased IRV.
O:
Oxygen - Yes. Potentially hypercapnic - use 24% Venturi looking at sat range 88-92%. Wait 30 minutes.
If improvement, 28%. If no, non-invasive ventilation.
D: Drugs Bronchodilators SABA - salbutomol SAMA - tiotropium (Atrovent) LAMA - Spiriva - Iatropium bromide Xanthiine Aminophyll
Disease modifiers Corticosteroids - Prednisone - Liquid Pred Monkelukast - cytokine inhibitor. Diuretics Antibiotics Flu vaccine LTOT if PaO2 < 7.3 kPa Oxygen card!
Positioning
POE- High side lying
ACBT - Whole
Adjunct -
Refer
Pulmonary rehab.
Describe the physiotherapy management of a patient with DMD who has developed a respiratory tract infection. They are hypoxic, have retained secretions, and are showing signs of fatigue.
Hypoxic- Need oxygen
Fixed flow venturi mask @ 60%. Position of ease - high side lying.
Retained secretions:
1. Manually assisted coughs.
Can be done in supine (anterior push) or sitting
2. Mechanical insufflation / exsufflation.
Positive and negative pressure machine that increases inspiratory capacity and assists cough reflex, respectively, allowing clearing of secretions.
3. . Cough assist machine
4. GAP for drainage
Antibiotics / antivirals.
Mucolytic - mannitol or DNAse `
• Describe the pathophysiology of
pneumonia relating it to the presenting
symptoms (10)
The pathophysiology of pneumonia – An inflammatory response of the lungs secondary to infection by bacteria or viruses. This causes a vascular response – leading to vasodilation and increased capillary permeability – causing capillary leak into the alveoli, as well as the negation of the HPVC
Charlie Chaplin Farts Have Really Serious Weight.
- Cough – lung inflammation and sputum production
- Chest pain – inflammation of the pleura
- Fever and rigor – infection
- Haemoptysis – Capillary leak
- Rapid shallow breathing – poor V/Q
- Sputum production – only when consolidation is cleared
- Weight loss – sign of infection.
• Describe the criteria necessary for gas
exchange (2.5) How may these be
disrupted in pneumonia (7.5)
Gas exchange criteria
1) Concentration/pressure gradient.
• Lack of airflow to the alveoli causes a decreases in alveolar partial pressure, reducing the effectiveness of gas exchange
2) Gas Solubility
O2 is less soluble than CO2. During respiratory disease, lack of partial alveolar pressure (and other factors) that negatively affect gas exchange will lead to hypoxia.
3) Thickness
Diffusion for gas exchange is inversely proportional to distance of the tissue. Increased effusion in the alveoli and interstitial tissues secondary to inflammation from pneumonia reduce the rate of diffusion .
4) Surface area
Alveoli blocked from consolidation do not participate in gas exchange, reducing the total surface area for gas to diffuse across
5) V/Q mismatch
Shunt – loss of ventilation causes a lack of gas exchange. The body normally compensates by HPVC (hypoxic pulmonary vasoconstriction) to redirect blood flow to areas of good perfusion, but inflammatory cytokines cause local vasodilation, negating this compensatory affect.
This is the largest contributor to reduced gas exchange from pneumonia.
• Describe the physiotherapy management
for a patient with a consolidated right
middle lobe pneumonia (10)
Positioning for optimal V/Q Position of ease. Left side lying - likely breathless - high side lying w/no head tilt.
High flow O2 therapy - Venturi 60% Analgesics for pain Antibiotics/fungals/virals for infection Airway clearance if productive of sputum - ACBT Fluid replacement(maintain BP) Ventilatory support
