chronic shortness of breath Flashcards
CHRONIC Asthma:
History
Exam
Investigation
Treatment (with steps and actual names of drugs)
-
History:
- Recurrent episodes of COUGH, WHEEZE, SOB
- Variation (worst in morning & evening)
- History of atopy
- Family History
- Smoker
- Occupation
- Pets
-
Exam
- General inspection: normal - could have nasal polyposis
- Auscultation: wheeze
-
Investigation:
- Spirometry: FEV1: FVC <70% and reversible: 12% pre- and post-bronchodilator spirometry
- Peak expiratory flow rate: PEFR varies by, or increases by >20%, for >3 days/week over several weeks - diagnosis with PEFR diary
- Bloods
- Treatment:
- SABA (salbutamol)
- SABA + ICS (beclometasone or Budesonide)
- SABA + ICS + LTRA (Montelukast)
- LABA+ ICS (Symbicort) + LTRA
- LABA+ MORE ICS+ LTRA
- TRIAL - Theophylline and LMRA
- ORAL CS (prednisolone)
acute Asthma:
- Types
- Investigation
- Treatment (with steps and actual names of drugs)
-
Types:
- Moderate: PEF - 50-75%
- Acute -severe - PEF - 33-50%
- Life threatening - PEF - <33%
- Near fatal - pCO2 Raised
-
Investigation:
- Basic observations (e.g. HR, SpO2)
- Measure and record PEF
- O2 saturation and maintain SpO2 at 94-98%
- ABG*- repeat ABG if PaO2 <8kPa, unless SpO2 >92%; or initial PaCO2 is normal or raised; or if patient deteriorates
- Serum K+ and glucose
-
Treatment:
- Oxygen
- Nebulised salbutamol
- Nebulised Iprotropium Bromide (for acute severe or life threatning or poor response to salbutamol)
- Oral prednisolone (40-50mg) or IV Hydrocortisone (100mg)
- IV Magnesium sulfate (call for senior help)
- IV aminophylline
- ITU + intubation
A 17 year-old girl presents to the local A&E complaining of worsening shortness of breath, despite use of what she describes as her ‘blue inhaler’. On examination her oxygen saturations are 95%, she is afebrile and has a BP of 101/67. The attending physician takes an ABG and the results are shown below. Grade the severity of this patient’s asthma attack.
pH: 7.25
pCO2: 7.4 kPa (4.5-6.0)
pO2: 10.4 kPa (>10.5)
A.I cannot tell from the information available
B.Moderate
C.Acute severe
D.Life threatening
E.Near fatal
A.I cannot tell from the information available
B.Moderate
C.Acute severe
D.Life threatening
E.Near fatal
A 26-year-old bus driver presents to the GP complaining of a worsening shortness of breath. On examination, the patient is afebrile, has a BP of 110/85 and has a marked wheeze on auscultation. The only medications the patient is on is Salbutamol, PRN. What is the next most appropriate treatment step as per the treatment guidelines for this condition?
A.Replace the blue inhaler with a brown, low-dose inhaled corticosteroid
B.Replace the blue inhaler with a long-acting beta-agonist medication
C.Replace the blue inhaler with a long-acting muscarinic agonist medication
D.Add an inhaled low-dose corticosteroid to her medications, taken OD
E.Add oral corticosteroid tablets to her medications, taken OD
A.Replace the blue inhaler with a brown, low-dose inhaled corticosteroid
B.Replace the blue inhaler with a long-acting beta-agonist medication
C.Replace the blue inhaler with a long-acting muscarinic agonist medication
D.Add an inhaled low-dose corticosteroid to her medications, taken OD
E.Add oral corticosteroid tablets to her medications, taken OD
chronic COPD:
Classification:
History
Exam
Investigation
Treatment (with steps and actual names of drugs)
-
Classification: MUST have a post bronchodilator FEV1/FVC ratio of less than 0.7
- Mild: > 80%
- moderate: 50-79%
- severe: 30- 49%
- very severe: < 30%
-
History: SOB, Productive COUGH, some WHEEZE
- Age
- FHx
- Smoking status
- Occupation
-
Exam:
- General inspection: Tar staining, Cyanosis, barrel chest
- Palpation: reduced expansion, hyper- resonance
- Auscultation: reduced air movement, Wheezing, coarse crackles
- MIGHT have right heart failure
-
Investigation:
- Spirometry
- Bloods, ABG
- CXR
- Treatment (with steps and actual names of drugs)
- MILD - SAMA (Ipratropium bromide) or SABA (salbutamol) (Short acting muscarinic antagonist or short- acting beta agonist)
- MODERATE - add a LAMA (tiotropium) (to SAMA) or LABA (salmeterol) (SABA)
- SEVERE- USE a LABA and LAMA together OR LABA and inhaled corticosteroid (ICS) (Symbicort)
- VERY SEVERE- USE LAMA+ LABA+ ICS
OTHER METHODS OF TREATMENT:
- General management: smoking cessation, annual influenza vaccination, pneumococcal vaccination
- Improved survival: smoking cessation, Long term O2 therapy, Lung volume reduction surgery
What are the Guidelines ofr long term oxygen?
must have a pO2 of < 7.3 kPa
OR
pO2 less than 8 but with one of the following:
- Secondary polycythaemia
- nocturnal hypoxaemia
- peripheral oedema
- pulmonary hypertension
ACUTE exacerbations COPD:
Treatment (with steps and actual names of drugs)
- Oxygen WITH Blue Venturi Mask (24%)
- Nebulised salbutamol
- Nebulised Iprotropium Bromide (for acute severe or life threatning or poor response to salbutamol)
- Oral prednisolone (40-50mg) or IV Hydrocortisone (200mg)
- IV Amoxicillin
- IV aminophylline
- BiPAP
A 72-year-old man attends the GP complaining of increased shortness of breath and a cough productive of clear sputum. The GP notes the gentleman has a history of diagnosed COPD and decides to review his medications. The man hands the GP two inhalers, one a SABA and the other a LABA. After conducting spirometry, the GP calculates an FEV1 of 40% expected. What is the next most appropriate treatment step?
A.Replace the SABA with a LAMA
B.Replace the LABA with an LAMA
C.Add a LAMA
D.Add an ICS
E.I need to conduct more tests to determine what medications to review
A.Replace the SABA with a LAMA
B.Replace the LABA with an LAMA
C.Add a LAMA
D.Add an ICS
E.I need to conduct more tests to determine what medications to review
Which of the following is not a respiratory cause of clubbing?
A.Squamous cell lung cancer
B.Interstitial lung disease
C.COPD
D.Cystic fibrosis
An empyema (lung abscess
A.Squamous cell lung cancer
B.Interstitial lung disease
C.COPD
D.Cystic fibrosis
E. An empyema (lung abscess
interstial lung disease - Idiopathic Pulmonary Fibrosis
causes:
history
Examination
Investigation
- History: SOBOE, DRY COUGH, NO wheeze
- Animal/vegetable dusts
- Smoking status
- Occupation
- Drugs
- Bleomycin
- Methotrexate
- Amiodarone
- Examination:
- General inspection: clubbing
- Auscultation: Bi basal fine inspiratory crepitation
- signs of RHF
- Investigations:
- Bloods, ABG, BIOPSY
- CXR – ground-glass, reticulonodular, cor pulmonale, honeycombing
- High-resolution CT - ground-glass
- Lung function tests (restrictive pattern)
What are causes of pulmonary fibrosis?
Causes:
Idiopathic pulmonary fibrosis
Hypersensitivity Pneumonitis
Pneumoconiosis
Sarcodosis
interstial lung disease - Hypersensitivity Pneumonitis
causes:
history
Examination
Investigation
-
causes: Inhalation of antigenic organic dusts containing microbes
- Examples: Farmer’s (mouldy hay with thermophilic actinomycetes); Pigeon’s (bloom of bird feathers); Mushroom Worker’s (compost with thermophilic actinomycetes); Humidifier (water-containing bacteria); Maltworker’s (barley with aspergillus clavatus)
-
History: SOBOE, dry COUGH, Fever
- Acute ± chronic hx
- Keep pets
- Occupation
- Pick mushrooms
- Bird-keeper
- Farmer
- Plumber
- Malt-worker
-
Examination:
- General Inspection: Clubbing, mild pyrexia
- Auscultation: bibasal fine, inspiratory crepitations
-
Investigation:
- Bloods, ABG
- CXR – often normal* (ground-glass, reticulonodular, cor pulmonale, honeycombing)
- High-resolution CT - ground-glass
- Lung function tests (restrictive pattern)
- Broncho-alveolar lavage – increased cellularity
interstial lung disease - pneumoconiosis
causes:
history
Examination
Investigation
-
causes: Can get asbetsosis (from asbestos) or silicosis (silicon - coal worker)
- Inhalation of dust particles of coal dust, silica or asbestos (white/blue asbestos; latter more toxic)
- Pathophysiology: large nodules of dust particles, surrounded by collagen and dying macrophages.
- Damage by:
- Direct cytotoxicity of particles
- Particle ingestion by macrophages => free radical production
- Proinflammatory cytokines from macrophages
-
History: SOB, dry COUGH
- Occupation
- Coal-worker
- Builder
- Long latence
- Asymptomatic
-
Examination:
- General Inspection: Clubbing,
- Auscultation: bibasal fine, inspiratory crepitations, decreased breath sounds and RHF signs
-
Investigation:
- CXR:
- Simple = micro-nodular mottling
- Complicated = bilateral lower zone reticulonodular shadowing and pleural plaques (asbestosis is fibrotic changes, not just plaques)*
- CT – fibrotic changes
- Lung function tests (restrictive pattern
- CXR:
A 65-year-old man with a medical background of benign prostatic hyperplasia, presents to the GP with a 1 week history of worsening shortness of breath on exertion. He has a temperature of 38.5C, reports no weight loss but does mention some mild fatigue from his ‘pet pigeons keeping him up all night’ recently. On auscultation, the GP can determine fine, bi-basal inspiratory crackles. What is the most likely diagnosis?
A.COPD
B.Lung cancer
C.Bronchiectasis
D.Hypersensitivity pneumonitis
E.Idiopathic pulmonary fibrosis
A.COPD
B.Lung cancer
C.Bronchiectasis
D.Hypersensitivity pneumonitis
E.Idiopathic pulmonary fibrosis
Sleep Apnoea
cause
History
investigation
treatment
- Cause: “Characterised by recurrent collapse of pharyngeal airway and apnoea (cessation of airflow for >10s) during sleep; followed by arousal from sleep”
-
History: Chronic fatigue, unrefreshed sleep, snoring
- Obesity, smoker, alcohol
- Fatigue
- Truck Driver
- Enlarged tonsils, Macroglossia, Marfan’s syndrome
-
Investigation
- Sleep study
- TFTs
- Sleep study
-
Treatment:
- loose weight
- CPAP if bad
person comes in with dry cough, fever and SOBOE
What question do you want to ask about?
What do you think he has?
What does the chest X ray show?
hypersensitivity pneumonitis
Questions: Ask about occupation and pets
CXR:
- Mosaic pattern with areas of ground-glass atenuation and areas of low attenuation.
- Fibrosis and parenchymal distortion in a mid zone distribution.
