Key Conditions: Resp Flashcards
ASTHMA: Definition
Defintion: Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.
ASTHMA: Aetiology and Epidemiology
Aetiology: FHx: pts showing atopy and links to genetic heterogeneity
Envi: host dust, pollen, pets, cigarette smoke, viral respiratory tract infection, occupational allergens
Epidemiology: 10% children, 5% adults, increasing prevalence, acute asthma responsible for 1000-2000 deaths/ year
ASTHMA: Recognise presenting symptoms
- Episodic history
- Wheeze
- Breathlessness
- Cough (worse in the morning and at night)
- IMPORTANT: ask about previous hospitalisation due to acute attacks
Precipitating Factors o Cold o Viral infection o Drugs (e.g. beta-blockers, NSAIDs) o Exercise o Emotions • Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)
ASTHMA: Recognise the signs on physical examination
- Tachypnoea
- Use of accessory muscles
- Prolonged expiratory phase
- Polyphonic wheeze
- Hyperinflated chest
Severe Attack o PEFR < 50% predicted o Pulse > 110/min o RR > 25/min o Inability to complete sentences
Life-Threatening Attack o PEFR < 33% predicted o Silent chest o Cyanosis o Bradycardia o Hypotension o Confusion o Coma
ASTHMA: Identify appropriate investigations
ACUTE o Peak flow o Pulse oximetry o ABG o CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax) o FBC - raised WCC if infective exacerbation o CRP o U&Es o Blood and sputum cultures
CHRONIC o Peak flow monitoring - often shows diurnal variation with a dip in the morning o Pulmonary function test o Bloods - check: • Eosinophilia • IgE level • Aspergillus antibody titres o Skin prick tests - helps identify allergens
ASTHMA: Generate a management plan for an acute asthma attack
• ABCDE • Resuscitate • High flow O2 • Salbutamol nebuliser (5mg initially continuously then 2-4 hourly) • Ipratropium bromide (0.5mg • Steroid therapy 1) 100-200mg IV hydrocortisone 2) 40mg oral prednisolone for 5-7 days 3) IV magnesium sulphate if no improvement Consider IV aminophyline infusion
N.B high pCO2 = bad. Means pt is fatiguing, they should be hyperventilating
DISCHARGE: • PEF > 75% predicted • Diurnal variation < 25% • Inhaler technique checked • Stable on discharge medication for 24 hours • Patient owns a PEF meter • Patient has steroid and bronchodilator therapy • Arrange follow-up
ASTHMA: Generate a chronic management plan
STEPWISE PLAN
1) Inhaled short acting B2 agonist PRN. If >1 step 2
2) Step 1 + regular inhaled low dose steroids (400mcg/day)
3) Step 2+ LABA. If still inadequate control with LABA, increase steroid dose (800mcg/day). If no LABA response, stop and increase steroid dose (800mcg/ day)
4) Increased inhaled steroid (2000mcg/day) + fourth drug e.g. leukotriene receptor antagonist, SR theophylline r B2- agonist tablet.
5) Add regular oral steroids. Maintain high dose inhaled steroid. Refer to specialist care.
Advice: educate on proper inhaler technique and routine PEFR monitoring. Develop individualised management plan. Avoid provoking factors
ASTHMA: Identify the possible complications
- Growth retardation
- Chest wall deformity (pigeon chest)
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death
ASTHMA: Summarise the prognosis
- Many children improve as they grow older
* Adult-onset asthma is usually chronic
COPD: Definition
A progressive disorder of the LOWER respiratory tract, characterised by airway obstruction with little or no reversibility.
EMPHYSEMA (destruction and dilation of the alveoli –> loss of elastic traction keeping small airways open in expiration)
CHRONIC BRONCHITIS
chronic cough and sputum most days for at least 3 months for 2 consecutive years (narrowing of the airways resulting from bronchial inflammation and bronchi with mucosal oedema, hyper secretion and squamous metaplasia)
COPD: Explain the aetiology and risk factors
Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke and air pollution ).
a1-antitrypsin deficiency (<1%) but should be considered in children
Overlaps and may co-present with asthma.
COPD: Summarise the epidemiology
- VERY COMMON (8% prevalence)
- More common in males
- 12% of inpatient admissions!
- Presents in middle age or later
- Cigarette smoking > 90% of cases in developed countries
- 10-20% of heavy smokers develop COPD
- Mortality from COPD inc in periods of heavy atmospheric pollution
COPD: Recognise the presenting symptoms
- Productive cough with white or clear sputum, wheeze and breathlessness
- Usually long Hx of smoker’s cough
- Symptoms worsened by cold or damp weather or atmospheric pollution
- Advanced disease: severe breathlessness (e.g. after getting dressed) systemically - hypertension, osteoporosis, depression, weight loss and reduced muscle mass with general weakness
COPD: Recognise the signs on physical examination
Mild COPD > 80% predicted FEV1
• May be no signs or just quiet wheezes throughout chest
Moderate COPD 50-80% predicted FEV1
Severe COPD 30-49% FEV1
• Tachypnoeic with prolonged expiration
• Accessory muscle use –> intercostal undraping on inspiration and pursing of lips on expiration
• Barrel shaped chest, cyanosis, dec cricosternal distance
• Poor chest expansion with hyper inflated lungs –> hyper resonant percussion with loss of normal cardiac and liver dullness
• Quiet breath sounds, prolonged expiration, wheeze, rhonchi and crepitations
sometimes present.
Very severe < 30% predicted FEV1
• Still responsive to CO2: breathless but rarely cyanosed. HF and oedema rare
• Unresponsive to CO2: oedematous and cyanosed but not breathless
• Hypercapnic patients: bounding pulse, peripheral vasodilation (warm), course flapping tremor and outstretched hands when PaCO2 > 10kPA. RHF signs in late stages (inc JVP, right ventricular heave, ankle oedema)
Severe hypercapnia –> confusion and progressive drowsiness
COPD: Identify appropriate investigations
Lung Function Test: OBSTRUCTIVE picture. FEV1: FVC ratio is reduced and PEFR is low. (ensure not reversible to distinguish from asthma)
CXR • often normal • Hyperinflation (>6 ant ribs) • Low, flattened diaphragms • Large bullae sometimes present • Elongated cardiac silhouette • Decreased peripheral lung markings
FBC: Inc HB level and PCV due to secondary polycythaemia
Blood gases: often normal but DESATURATE ON EXERCISE. Advanced cases may show resting hypercapnia and hyperaemia
Sputum and blood cultures for acute exacerbations
ECG and Echocardiogram for cor pulmonale
COPD: Generate a management plan
1) SMOKING CESSATION
2) Drugs:
• Bronchodilators; B2 agonists, Antimuscarinics (long acting tiotropium),
• Phosphodiesterase type 4 inhibitors e.g. Theophyllines
• Corticosteroids (Beclometasone, Prednisolone)
• O2 therapy
• ABXs (Co-amoxiclav)
• Antimucolytic agents (Carbocisteine)
• Diuretic therapy for oedematous pts
• Pulmonary rehabilitation
• BiPAP to improve nocturnal hypoxia
COPD: Identify possible complications
Acute respiratory failure: in the late stages of COPD. Chronic alveolar hypoxia and hypercapnia –> constriction of the pulmonary arterioles –> pulmonary hypertension. CO is normal or increased. Salt and fluid retention occur due to to renal hypoxia
Pulmonary hypertension due to pulmonary vascular remodelling: pts with advanced COPD. Fluid overload secondary to lung disease. Due to failure of Na+ and water excretion
Infections (particularly Streptococcus pneu- moniae, Haemophilus influenzae),
Pneumothorax (resulting from bullae rupture)
Secondary polycythaemia
COPD: Summarise prognosis
Risks factors for a poor prognosis:
• Age, worsening airflow limitation
Predictive index= BODE • BMI • Degree of airflow obstruction • Dyspnoea • Exercise capacity
0-2 = 4 year mortality rate of 10% compared to someone with 7-10
PNEUMONIA: Definition
Infection of distal lung parenchyma. Categorise: CAP vs HAP, aspiration pneumonia, pneumonia in the immunocompromised,
typical and atypical
PNEUMONIA: Explain the aetiology and risk factors
CAP: Streptococcus pneumoniae (70%). Others include; Haemophilus influenza, Mycoplasma pneumonia, Legionella,
Staphylococcus aureaus
HAP: Gram-negative enterobacteria; Pseudomonias, Klebsiella
Risk factors: age, smoking, alcohol, pre-existing lung disease, immunodeficiency, contact with pneumonia
PNEUMONIA: Summarise the epidemiology of pneumonia
Incidence 5–11 in 1000 (25–44 in 1000 in elderly).
Community- acquired causes >60 000 deaths/year in the UK.
PNEUMONIA: Recognise the presenting symptoms of pneumonia
Fever, rigors, sweating, malaise, cough, sputum (yellow, green or rusty in S. pneumoniae), breathlessness and pleuritic chest pain, confusion (severe cases, elderly, Legionella)
Atypical pneumonia: Headache, myalgia, diarrhoea/abdominal pain.
PNEUMONIA: Recognise the signs of pneumonia on physical examination
Pyrexia, respiratory distress, tachypnoea, tachycardia, hypotension, cyanosis.
Decreased chest expansion, dullness to percussion, Increased tactile vocal fremitus, bronchial breathing (inspiration phase lasts as long as expiration phase), coarse crepitations on affected side.
Chronic suppurative lung disease (empyema, abscess): Clubbing.
PNEUMONIA: Identify appropriate investigations
Blood: • FBC (abnormal WCC) • U&E (dec Na+ , especially with Legionella) • LFT • Urea (assess deyhydration) • blood cultures • ABG (assess pulmonary function) • blood film (RBC agglutination by Mycoplasma)
CXR:
• Lobar or patchy shadowing, may lag behind clinical signs, pleural effusion; Klebsiella often affects upper lobes, repeat 6–8 weeks (if abnormal suspect underlying pathology, e.g. lung cancer).
• May detect complications: Abscess (cavitation and air-fluid level)
Sputum/pleural fluid:
• Microscopy, culture and sensitivity, acid-fast bacilli.
Urine:
• Pneumococcus and Legionella antigens.
Atypical viral serology: Inc • Antibody titres between acute and convalescent samples
(>2 weeks post-onset).
Bronchoscopy (and bronchoalveolar lavage):
• If Pneumocystis carinii pneumonia is
suspected, or when pneumonia fails to resolve or when there is clinical progression
