Cough +/- wheeze Flashcards
sLO: identify common/important differential diagnoses for cough +/- wheeze (including asthma and COPD) & have an understanding of the demographics and RF’s associated with each cause
What are the common causes of Cough +/_ wheeze?
(Chronic not acute)
All chronic cough begins as subacute - differentials include all causes of subacute cough –> post infectious = most common and self limiting.
Cough exceeding 8 weeks –> chronic cough
Common: in non smoking adults (norm CXR/NO ACEi)
- Post nasal drip (upper airway cough syndrome) - 34%
- Asthma - 25%
- GORD - 20%
- Non asthmatic eosinophilic bronchitis - 13%
Others:
- ACEi - dry cough, tickling/scratching sensation in throat
- Post infectious cough
- COPD - Chronic Bronchitis –> considered when hx of chronic productive cough > 3 months or the year and for 2 consecutive years
- Bordetella pertussis - (whooping cough) - when local infection rates high test
Less common: Consider causes that stimulate the airway mechanical/ chemical receptors via feeding into the vagus nerve including nerves in the chest wall, diaphragm, oesophagus, abdominal wall and external auditory meatus
- disorder of airway - Bronchiectasis
- disorder of lung parenchyma - interstitial lung disease - e.g. hypersensitivity pneumonitis / occupational or environmental exposure, autoimmune SLE (stimulates afferent nerves)
- Irritation of external ear canal - infection/wax/hearing aids may produce cough via reflex mediated by Arnold’s nerve (ear- cough reflex = mechanical stimulaion of external auditory meatus activates auricular branch of vagus nerve inducing cough)
LO: identify common/important differential diagnoses for cough +/- wheeze (including asthma and COPD) & have an understanding of the demographics and RF’s associated with each cause
What are some of the important differentials for cough +/- wheeze?
Important dx:
-
Lung carcinoma –> most common sx lung cancer
- often accompanied by sx of weight loss, haemoptysis, chest pain, dysponea, hoarseness, fatigue and anorexia
-
Asthma -->
- chronic cough PLUS dysponea/ wheezing/ chest tightness worsens at night/on exposure to allergens
-
Pneumonia –>
- change in character of cough
- appearance of sputum purulence
- fever
-
COVID 19
- cause - severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
- fever/ cough/dysponea/ fatigue
-
Tuberculosis
- Chronic cough
- accompanied by night sweats and weight loss
- Inreased risk - HIV infected/immunosuppressants/recent immigration or refugee status
-
Bordella pertussis infection
- B pertussis infection - paroxysmal cough
- inspiratory whooping
- vomiting post cough - post tussive vomiting
-
Intersitial pulmonary fibrosis
- cough with progressive dysponea - dry crackels and clubbing
What is the definition of cough?
What is an acute cough vs chronic cough?
Cough - short explosive expulsion of air, reflex forced expiration against a closed glottis
Acute cough = cough lasting less than 3 weeks
Chronic cough = cough lasting greater than 8 weeks
(subacute inbetween stage)
Revision: (in order to understand cough reflex)
Airway histology - what lines the trachea and bronchi?
What innervation is there?
Where does this information go?
- Physiology of the airway (bronchis and L/R main bronchi)
- Top layer = mucosa –> formed of psuedostratified columnar epithelium + goblet cells
- lie on top of basement membrane, below is the smooth muscle
- below this is the smooth muscle –> contains immune cells –> mast cells (Defence and allergic response)
- cartilage –> making up the trachea
- Innervation –> both rapidly adapting and slowly adapting, C fibres –>mechanoreceptors
- All part of the vagus nerve –> medulla
- –> Brings back to NTS = nucleus tractus solitarus
What factors may trigger cough?
Once the afferent information is received in the medullar what is the efferent part?
Where does this go and what does it stimulate?
- Chemical factors
- Cytokines
- histamine
- Mechanical factors
- foreign body or cancer
- Trigger the sensory nerve fibres –> travel via vagus nerve to NTS in medulla
- Synapses with other neurones to trigger cough reflex
- Efferent nerve fibres:
- Phrenic
- spinomotor
- recurrent laryngeal
- Goes to effector muscles -> respiratory muscles, laryngeal muscles and bronchial smooth muscles
- Initiates cough reflex
Cough reflex phases
- Inspiratory phase
- deep breath in –> stretch expiratory muscles –> increase pressure within lungs
- Compression phase
- Glottis closes –> respiratory muscles contract
- increased pressure within lungs
- expiratory phase
- glottis opens
- air expelled out –> due to high pressure in lungs
LO: Identify key features of the history - particularly social and occupational history - which help differentiate between common causes of this presentation
Overview of a respiratory history - key components
-
PC:
- SQITAS
- onset of the cough, when does it come on, has it changed over time?
- how would they describe the cough - productive or dry/ tickling/scratching/ whooping
- associated symptoms - fever/ SOB/ fatigue/weight loss
- alleviating factors - salbutamol, rest etc
- worsening factors - allergies/ cold air
- severity - can patient speak in full sentences?
- SQITAS
-
Sytemic enquiry - Key respiratory questions:
- SOB - pneumonia/asthma/COPD
- cough - productive = pneumonia/COPD/bronchiectasis or dry = pulm fibrosis, ACEi
- haemoptysis - lung CA/PE
- wheeze- ashtma/COPD
- chest pain - worse on inspiration = pleuritic (PE or pleurisy)
- Systemic symptoms - fatigue, fever or night sweats, weight loss, ankle swelling
-
PMH:
- Asthma or COPD - admissions to hospitals/ exacerbations
- other: PE/pulmonary fibrosis/TB/Motor neurone disease/ CHF/ cystic fibrosis/ alpha1 antitrypsin deficiency
- Current treatment - DHX - is it well controlled
- DHx: ACEi (Dry cough), methotrexate and amiodarone - (induce pulmonary fibrosis), BB and NSAIDS (bronchoconstriction)
- OTC medication
- surgeries - lobectomy/ bronchscopy
- Allergies
-
FH:
- atopy: ashtma, eczema, allergic rhinitis
- alpha 1 antitrypsin?
-
SH:
- Smoking - Primary cause of preventable resp illness and death
- what do they smoke> marijuana assocaited w emphysema
- Establish duration of smoking, quantity smoked
- pack years = [number of years smoked] x [average number of packs smoked per day]
- 1 pack = 20 cigarettes
- Occupation - allergen exposure (farmers) + mesothelioma & asbestos exposure (shipyards/construction/plubing)
-
Travel history:
- infective causes -TB (africa/south asia/ russia/china/southamerica)
Red flag symptoms for Respiratory history?
- Cough > 3 weeks
- change in character of chronic cough
- Persistent cough in a smoker
- haemoptysis (lung CA/TB)
- persistent hoarseness > 3 weeks or sore throat
- persistent palpable neck lumps or unilateral enlarged tonsil
- dysponea - difficulty completing sentences (asthma/COPD/CHF decompensation or exacerbation)
- unexplained weight loss (TB/Lung CA)
- night sweats (TB)
- fever (TB or pneumonia)
- Severe thoracic pain or pleurisy - (penumonia/TB/PE)
LO: Identify features on examination to differentiate between common causes
General resp exam signs
1) stridor - what is it, causes?
2) wheeze - what is it, causes?
3) cough descriptions
- Stridor
- Inspiratory sound due to obstructed air flow through narrowed airway
- obstruction in lumen (tumour/foreign body/vocal cord palsy), within walls (oedema and anaphylaxis/ laryngospasm) or extrinsic (goitre/ lymphadenopathy)
- Wheeze
- expiratory sound - high pitched whistling sound made by obstructed air flow through narrowed airways
- allergies/anaphylaxis/asthma/bronchiectasis/bronchitis/COPD/pneumonia
- Coughs:
- Loud, brassy cough –> implies pressure on trachea
- hollow “bovine” coughing –> reccurent laryngeal nerve palsy
- barking cough - occurs in croup (URTI in young children)
Common causes:
Asthma - define
What are the two types of asthma?
Asthma –> recurrent and reversible airways obstruction characterised by wheeze/SOB and nocturnal cough.
3 key features:
- Reversible airways obstruction
- Bronchial hyperresponsiveness
- Airways inflammation
Two types:
1) Atopic/ extrinsic = Typical onset in childhood, associated with atopy –> genetic predisposition to amount an exaggerated inappropriate immune response to an allergen –> associated with hayfever and eczema.
2) Non-atopic/ intrinsic = Typical onset middle age, often after upper RTI, no Hx of. atopy
Common causes: Asthma
Pathophysiology?
Early stage?
Late?
Remodelling?
- Two phases of development : early hypersensitisation of airways and initial exposure to allergen (reversible), later phase chronic remodelling (irreversible)
-
Early:
-
Exposure to allergen –> presentation of allergen by APC to Th2 cell –> secretes inflammatory cytokines (IL3/5):
- Chemotaxis of inflammatory cells –> particularly eosinophils
- Eosinophils release toxic granule proteins –> damage to resp epithelium and exposure of nerve fibre endings –> airway hyperresponsiveness
- B plasma cells –> make and release IgE
- mast cells –> express IgE receptors
- Next exposure to allergen/trigger –> IgE crosslinking, degranulation of mast cells
- mast cells release leukotrienes and histamine –> potent bronchoconstrictors.
-
Exposure to allergen –> presentation of allergen by APC to Th2 cell –> secretes inflammatory cytokines (IL3/5):
-
Late phase:
- Progressive inflammatory reaction –> continued infiltration of Th2 cells and eosinophils
- Eosinophils –> release leukotrienes and toxic granular proteins –> damage to resp epithelium/exposure of sensory and cholinergic fibres
- Sensory and cholingergic fibres activated by inflammatory mediators –> cholinergic reflex –> SMC contraction = bronchial hyperesponsiveness
-
Chronic remodelling:
- GF release from inflammatory cells –> SMC hypertrophy and hyperplasia
- increase in Goblet cells –> submucosal gland hyperplasia + ↑ mucus production –> mucus plug & BM thickening
- rexpsoure of allergen -> IgE crosslinking –> histamine/leukiotriene release -> bronchoconstriction
- PLUS increased vascular permeability –> oedema
Demographics of asthma?
Risk factors?
- 10-15% childhood/ adolescents affected
- Typically starts 3-5 yrs - worsens or improves during adolescence
Risk factors:
- Genetics - family hx or PMH of eczema or atopy (allergic rhinitis)
- Acute triggers: dust/mould/pollen/pet hair
- environmental factors: cold air/ exercise/ emotion/ drugs/ viral infection/ atmospheric pollution/ occupational sensitisers
- medication - NSAIDS/ BB blockers - bronchoconstriction
Asthma:
Key symptoms on history?
- Cough
- wheeze - expiratory
- chest tightness
- SOB/ dysponea - often worse at night
- diurnal variation
- marked morning dipping of peak flow, improvement throughout the day
- disturbed sleep
- FH of atopic disease or PMH of atopy - hayfever/ eczema/allergic rhinitis
- occuptional exposure
Asthma: Examination signs?
- Wheeze/cough/sob
- expiratory wheeze
- polyphonic wheeze –> both insp/exp (more severe)
- Tachypnoea (moderate- severe episode) (> 25)
- Tachycardia (moderate-severe) (>110bpm)
- Accessory muscle use (Moderate-severe)
- In children –> supraclavicular and intercostal retraction + nasal flaring (resp distress), abdominal breathing, tracheal tug? (moderate-severe)
- reduced breath sounds when severe
- difficulty completing sentences in 1 breath
- hyperinflated chest
- percussion can be hyperresonant
- Decreased FEV1 and PEFR
Skin manifestations –> atopic dematitis or ecezma
Asthma: Signs of life- threatening attack?
- Silent chest
- exhausation
- cyanosis (o2 sats , 92 %)
- confusion
- PEF < 33%, Pa02 under 8kPa, PaCO2 normal (4-6kPa) due to hyperventilation driven by hypoxia, leads to more CO2 being blown off despite overall reduction in ventilation, as this becomes more severe PaCO2 rises above 6kPa.
- bradycardia
Asthma: Investigations
In children
-
Bedside: PEFR:
- In children not diagnostic but lower than age/height predicted - airway obstruction
- ABG and pulse oximetry
-
Spirometry –> shows obstructive pattern of the flow volume loop
- decreased FEV1/FVC ratio (less than 0.7) - due to decrease in FEV1 by osbtructed airways, FEV1 reduces more than FVC).
- Challenge testing –> decrease in FEV ~15% in response to histamine or exercise (depending on history)
- Then bronchodilator response - 12% improvement in FEV1/FVC - significant inresponse to either B2 agonist/corticosteroid
-
Bloods:
- FBC –> eosinophilia?
-
CXR –>
- May show hyperinflation
-
Special tests:
- sweat test –> CF –> sweat chloride > 60mmol/L
Asthma: investigations in adults?
- FEV1 / FVC ratio –> primary diagnostic test –> in asthma < than 80% of predicted
- bronchodilator reversibility test - improvement of FEV1 by 12% from baseline
- challenge tests –> direct challenge (bronchoconstrictor e.g. histamine) or indirect (exercise or saline)
- PEFR –> long term daily considered for patients w moderate-severe asthma, allows us to monitor and response to therapy
- CXR –> exclude other pathology, may show infection in acute exacerbation, may show hyperinflation
- FBC –> raised eosinophils and/or neutrophilia
- special –> can do immunoassay for allergen specific IgE and skin prick testing
Management of asthma:
Severe acute asthma treatment?
OSHIT
- Oxygen - 94-98% maintain
- Salbutamol (B2 adrenoreceptor agonists)
- high dose inhaled is first line- nebulised (6L/min)
- IV only
- relax bronchial smooth muscle - increase CAMP
- Hydrocortisone (Glucocorticoid) (IV infusion)
- reduce bronchial inflammation
- then daily prednisilone - oral
- Ipratroprium (anticholinergic) - nebulised
- when poor initial response to bronchodilators, achieves greater bronchodilation than B2 agonist alone
- Theophylline IV (methylxanthine)
- inhibits phosphodiesterase enzymes to reduce bronchoconstriction by increasing CAMP levels
PLUS Magnesium sulphate: Single dose IV with poor response to inhaled bronchodilator therapy
Management of asthma: Chronic management?
- Assess baseline asthma status - PEF/spirometry, advice on avoiding triggers/ weight loss/smoking cessation, explain inhaler technique
- SABA - Short acting B2 agonist - reliever
- Inhaled corticosteroid - preventer therapy
- if person using SABA more than 3x / week/ symptoms often or waking at night
- Then add on therapy:
- Leukotriene receptor antagonists (oral therapy)
- if still uncontrolled –> low dose ICS + Leukotriene antagonist add long acting beta 2 agonist (LABA)
- If still uncontrolled –> ICS + fast acting LABA
- then increase ICS to moderate dose
- then consider adding methyxanthine
COPD:
define
Definition = COPD disease characterised by airflow limitation that is not fully reversible- encompasses both emphysema and chronic bronchitis.
Chronic inflammation affects central airways/ peripheral airways/ lung parenchyma/ alveoli and pulmonary vasculature.
Main components = narrowing and remodelling of airways, ↑goblet cells and enlargement of mucus secreting glands in central airways, vascular bed changes and pulmonary HTN.
Airflow limitiation = progressive, associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
FEV1 < 80% of predicted, FEV1/FVC < 0.7
Main forms of COPD
-
Chronic bronchitis: Blue bloaters
- Larger airways - bronchi and bronchioles
- mucus gland hyperplasia and hypertrophy
- hypersecretion of mucus –> ciliary dysfunction
- mucus overproduction/ less removal leads to
- chronic cough with sputum production on most days for 3 months of 2 consecutive years
- Chronic asthma
-
Emphysema: Pink puffers
- small airways (smaller bronchioles, alveoli)
- Inflammatory response –> neutrophil invasion –> elastin breakdown –> loss of alveolar integrity
- air space enlargement
- distal to the terminal bronchioles
- alveolar wall destruction
Risk factors for COPD?
- smoking - 95% cases + cannabis smoking (liked to emphysema)
- genetics - alpha 1 anti trypsin deficiency (cannot control neutrophil elastase which destroys alveoli, abnormal alpha 1 antitrypsin can also accumulate in liver).
- recurrent lung infections
- air pollution or occupational exposure
- low birth weight
- low SE status
Pathophysiology of emphysema?
Both in airway
and of pink puffer?
Airway:
- Exposure of cigarette smoke/air pollutants
- activates macrophages –> normally reside in alveolus
- macrophages release proinflammatory cytokines –> recruits neutrophils from pulm circulation to alveolus
- Neutrophils –> release proteases –> elastase –> breaks down elastin
- loss of elastic recoil –> leads to air trapping and hypoventiliation
- leads to hypoxaemia and hypercapnia
- oxidative stress –> release of oxygen free radicals by inflammatory cells
- leads to apoptosis of alveolar pneumocytes –> destruction of alveolar walls and pulmonary capillaries
- reduction in both ventilation and perfusion –> matched V/Q deficit
Pink puffer:
- alveolar destruction/ pulmonary capillary destruction –> air trapping + hyperinflation (barrel chest), reduced perfusion (matched V/Q deficit)
- leads to hypoventilation –> hypercapnia and hypoxia
- hyperinflation –> ↑ effort to breathe –> cachexia, dysponea, use of accessory muscles
COPD pathophysiology:
Chronic bronchitis -
pathophysiological changes to airway?
Pathophysiology of the blue bloater?
- Exposure to cigarette smoke/ pollutants leads to irritation of the bronchial airway lining
- activation of immune response- innate and adaptive
- infiltration of bronchial respiratory epithelium by Neutrophils, macrophages and T lymphocytes (Th1 and Th2)
- Release of proinflammatory cytokines –> leads to oxidative stress –> vasodilation and oedema
- stimulation of mucosal gland hypertrophy and hyperplasia & ↑ in goblet cells
- hypersecretion of mucus and plug formation -–> mucus overproduction
- Both oedema and mucus hypersecretion reduces cilia motility –> reduced clearance of mucus –> increased susceptibility to infection
- bronchi become clogged –> recurrent infection and chronic inflammation
- bronchoconstriction and airway obstruction
Leads to hypoventilation of alveoli –> reduced PAO2 and increased PACO2 –> therefore increased PaCO2 and decreased PaO2. (hypercapnia and hypoxia)
Hypoxia –> leads to polycythemia (increased Hb) –> cyanosis –> blue
hypoxaemia –> hypoxic pulmonary vasoconstriction –> ↑ pulmonary vascular resistance –> R sided hypertrophy (cor pulmonale) and heart failure
Reduced venous return to L side of heart –> reduced LV output –> activates RAAS -> fluid retention + oedema = BLOATER
