Cough +/- wheeze Flashcards

1
Q

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)

A

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)
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2
Q

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?

A

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
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3
Q

What is the definition of cough?

What is an acute cough vs chronic cough?

A

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)

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4
Q

Revision: (in order to understand cough reflex)

Airway histology - what lines the trachea and bronchi?

What innervation is there?

Where does this information go?

A
  • 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
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5
Q

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?

A
  • 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
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6
Q

Cough reflex phases

A
  1. Inspiratory phase
    • deep breath in –> stretch expiratory muscles –> increase pressure within lungs
  2. Compression phase
    • Glottis closes –> respiratory muscles contract
    • increased pressure within lungs
  3. expiratory phase
    • glottis opens
    • air expelled out –> due to high pressure in lungs
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7
Q

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

A
  • 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?
  • 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)
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8
Q

Red flag symptoms for Respiratory history?

A
  • 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)
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9
Q

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

A
  1. 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)
  2. Wheeze
    • expiratory sound - high pitched whistling sound made by obstructed air flow through narrowed airways
    • allergies/anaphylaxis/asthma/bronchiectasis/bronchitis/COPD/pneumonia
  3. Coughs:
    • Loud, brassy cough –> implies pressure on trachea
    • hollow “bovine” coughing –> reccurent laryngeal nerve palsy
    • barking cough - occurs in croup (URTI in young children)
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10
Q

Common causes:

Asthma - define

What are the two types of asthma?

A

Asthma –> recurrent and reversible airways obstruction characterised by wheeze/SOB and nocturnal cough.

3 key features:

  1. Reversible airways obstruction
  2. Bronchial hyperresponsiveness
  3. 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

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11
Q

Common causes: Asthma

Pathophysiology?

Early stage?

Late?

Remodelling?

A
  • 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.
  • 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
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12
Q

Demographics of asthma?

Risk factors?

A
  • 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
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13
Q

Asthma:

Key symptoms on history?

A
  • 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
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14
Q

Asthma: Examination signs?

A
  • 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

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15
Q

Asthma: Signs of life- threatening attack?

A
  • 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
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16
Q

Asthma: Investigations

In children

A
  • 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
17
Q

Asthma: investigations in adults?

A
  • 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
18
Q

Management of asthma:

Severe acute asthma treatment?

A

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

19
Q

Management of asthma: Chronic management?

A
  • 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
20
Q

COPD:

define

A

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

21
Q

Main forms of COPD

A
  • 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
22
Q

Risk factors for COPD?

A
  • 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
23
Q

Pathophysiology of emphysema?

Both in airway

and of pink puffer?

A

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
24
Q

COPD pathophysiology:

Chronic bronchitis -

pathophysiological changes to airway?

Pathophysiology of the blue bloater?

A
  • 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

25
Q

History: symptoms of COPD?

A
  • RF’s –> smoking/ advancing age (40 yrs and above)
  • SOB/dysponea (chronic)
  • Chronic cough - sputum production
  • Frequent infective exacerbations w purulent sputum
    • fever
    • severe sob
    • chest pain
  • Resp failure signs - hypoxia and hypercapnia
  • wheezing/ chest tightness (less commmon)
  • fatigue
  • weight loss
  • exercise intolerance
  • ankle oedema
26
Q

COPD: Examination signs

A
  • Tachypnoea
  • clubbing, peripheral cyanosis, flap (hypercapnia)
  • resp distress - use of accessory muscle, intercostal recession, pursed lips
  • barrel chest - hyperesonance on percussion
  • ausculation - wheeze, poor air movement, coarse crackles
  • R sided HF signs –>
    • distended neck veins
    • hepatomegaly
    • JVP > 5cm from sternal angle
    • peripheral oedema
27
Q

COPD: investigation

A
  • Spirometry:
    • 1st line
    • reduced FEV1 (< 80% of predicted)
    • reduced FEV1/FVC ratio –> less than 0.7 as obstructive disease
      • FEV1 reduces more than FVC due to airway obstruction
    • Severity classified by patient’s FEV1
  • Bedside
    • pulse oximetry (low)
    • ABG
      • PaO2 –> decreased below 8kPa
      • paCO2 –> increased 6.7kPa
      • Type 2 resp failure
    • ECG
      • ​RVH signs/ ischaemia
  • Bloods:
    • FBC –> assess severity, may show polycythemia (↑haematocrit), anaemia and ↑WBC in exacerbation
  • Imaging:
    • CXR –> flattened diaphragm, increased intercostal spaces, hyperinflation. Check for exacerbation (pneumonia and pneumothorax).
    • CT –> bullae
  • Special tests:
    • DLCO –> diffusing capacity of lung for carbon monoxide –> if decreased supports emphysema > chronic bronchitis
28
Q

COPD: long term management?

A
  • patient education and self management: exercise
  • Smoking cessation
  • pneumoccoal (Streptococcus pneumonia) and annual influenza vaccination

Stepwise drug therapy:

Bronchodilation –>

SABA–> salbutamol

Then

LABA –> formoterol/ salmeterol

Then

Combination of anticholinergic (ipratroprium/ tiotroprium ) PLUS SABA/LABA

Then

consider PDE inhibitors - theophylline / aminophylline

Then inhaled corticosteroids PLUS LABA

Failure of medical management –> Pulmonary rehabilitation (physical exercise and self management)

Oxygen therapy:

  • Minimise pulmonary HTN/ improves exercise tolerance /QOL
  • patients w PaO2 < 7.3 kPa or SaO2 < 88% (with or without hypercapnia)

Surgical:

  • bullectomy - surgical removal of bulla (dilated air space > 1cm)
  • lung volume reduction surgery or lung transplant last step

Palliative care –> advanced end stage COPD –> low dose opiod analgesic/ BZD

29
Q

COPD: acute exacerbation management?

A
  • SABA - salbutamol - eother metered dose inhaler or nebulised in moderate/severe
  • Add short acting muscarinic antagonist (ipratroprium) - nebulised
  • Kepp on LABA if already on this
  • oral or IV corticosteroid - 5 days post exacerbation - prednisilone oral daily or hydrocortisone IV
  • oxygen - check pulse oximetery/ ABG
    • deliver via venturi - 24-28% oxygen - aim for 88-92% sats
    • repeat ABG
  • ABX –> amoxicillin/ doxycycline/ clarithromycin
  • Hypercapnic Type2 2 resp failure –> Non invasive ventilation