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Medicine year 4 CDM > Block 3: asthma, COPD, PE > Flashcards

Block 3: asthma, COPD, PE Flashcards

1
Q

Asthma definition

A

Asthma is a chronicrespiratorycondition characterized by recurrent episodes of airflow obstruction, bronchial hyperresponsiveness, and underlying inflammation.

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2
Q

Asthma pathophysiology

A
  • Driven by Th2 inflammation (eosinophils, lymphocytes and mast cells)
  • 1/4 of asthma is non-eosinophilic and driven by neutrophils. Less steroid responsive and harder to treat
  • Airway obstruction develops through smooth muscle constriction, mucosal infiltration and mucous hyper-secretion
  • Eventually remodelling can develop causing loss of reversibility in chronic asthma
  • Eczema, seasonal allergic rhinitis and nasal polyps are often associated with high IgE and asthma
  • Sinusitis, reflux and obstructive sleep apnoea can all worsen asthma control
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3
Q

Asthma risk factors

A
  • Genetics
  • Environmental: allergens (pollen, dust), respiratory infection, tobacco smoke and air pollution
  • Immunological factors: imbalance in immune response particularly type 2 helper cells
  • personal or family history ofatopy
  • antenatal factors: maternal smoking, viral infection during pregnancy (especially RSV)
  • low birth weight
  • not being breastfed
  • maternal smoking around child
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4
Q

Atopy and occupational asthma

A

Atopy: IgE mediated conditions i.e. atopic dermatitis (eczema) and allergic rhinitis (hay fever)

Occupational asthmais usually diagnosed by observing reduced peak flows during the working week with normal readings when not at work. Examples of common occupational allergens include isocyanates and flour. Ask if their symptoms are better on holiday or at the weekend

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5
Q

Asthma physical changes

A
  • A chronic inflammatory of the airways secondary to type 1 hypersensitivity
  • Causes reversible bronchospasm resulting in airway obstruction
  • Airway inflammation: causes oedema, mucus production and bronchoconstriction
  • Bronchoconstriction: contraction of airway smooth muscle due to histamine and leukotrienes
  • Airway hyperresponsiveness: narrowing in response to allergens, irritants and cold air
  • Mucus production and airway remodelling: changes include subepithelial fibrosis, increased smooth muscle mass, mucus gland hypertrophy, and angiogenesis. Airway remodelling can cause irreversible airflow obstruction and progressive decline in lung function, may not be entirely reversible
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6
Q

Asthma: clinical features

A
  • Wheeze: high pitched whistling sound that occurs in expiration
  • Cough: worse at night/early morning
  • Chest tightness
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7
Q

Asthma testing patients >= 17 years

A
  • patients should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma
  • all patients should have spirometry with a bronchodilator reversibility (BDR) test
  • all patients should have a FeNO test
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8
Q

Asthma testing children 5-16 years and <5 years

A
  • all children should have spirometry with a bronchodilator reversibility (BDR) test
  • a FeNO test should be requested if there is normal spirometry or[obstructive spirometry]with a negative bronchodilator reversibility (BDR) test

<5 years: on clinical judgement, cant be confirmed till >5

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9
Q

Tests available for asthma: FeNO and spirometry

A
  • FeNO= in adults level of >= 40 parts per billion (ppb) is considered positive. In children a level of >= 35 parts per billion (ppb) is considered positive
  • Spirometry= FEV1/FVC ratio less than 70% (or below the lower limit of normal if this value is available) is considered obstructive
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10
Q

Testing available for asthma: reversibility and peak flow monitoring

A
  • Reversibility testing in response to nebulised salbutamol (spirometry)= in adults, a positive test is indicated by an improvement in FEV1 of 12% or more and increase in volume of 200 ml or more. In children, a positive test is indicated by an improvement in FEV1 of 12% or more
  • Peak flow monitoring (2-4 weeks can be useful), variability in peak flow of 20% suggests asthma
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11
Q

Asthma treatment in adults

A
  1. Newly diagnosed asthma: SABA (salbutamol)
  2. SABA + low dose ICS (400mg) (beclometasone)
  3. SABA + low dose ICS + leukotriene receptor antagonist (LTRA) (montelukast)
  4. SABA + low dose ICS + LABA (salmeterol). Continue LTRA depending on patients response
  5. SABA +/- LTRA. Switch ICS/LABA for a maintenance and reliever therapy (MART) that includes a low dose ICS
  6. SABA +/- LTRA + medium dose ICS MART. OR consider changing to fixed dose of moderate ICS and a separate LABA
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12
Q

Asthma: maintenance and reliever therapy (MART)

A
  • a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
  • MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)
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13
Q

Asthma: dosage of ICS

A
  • <= 400 micrograms budesonide or equivalent = low dose
  • 400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
  • > 800 micrograms budesonide or equivalent= high dose.
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14
Q

Moderate acute asthma exacerbation

A
  • Increasing symptoms.
  • PEFR >50-75% of the patient’s best or predicted score.
  • No features of acute severe asthma.
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15
Q

Acute severe asthma exacerbation

A
  • PEFR 33-50% of the patient’s best or predicted score.
  • Respiratory rate (RR) ≥ 25 breaths per minute.
  • Heart rate (HR) ≥ 110 beats per minute.
  • Inability to complete sentences in one breath.
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16
Q

Life threatening asthma exacerbation

A
  • PEFR <33% of the patient’s best or predicted score.
  • SpO₂ <92%, PaCO2 is normal
  • PaO₂ <8kPa.
  • Absence of audible breath sounds over the chest (silent chest).
  • Cyanosis (usually of the lips), hypotension
  • Reduced respiratory effort, exhaustion
  • New-onset arrhythmia.
  • Reduced Glasgow coma score (GCS).
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17
Q

Near fatal asthma exacerbation

A

Raised PaCO₂ (>6kPa) and/or need for mechanical ventilation.

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18
Q

Acute asthma exacerbation

A
  • Can be unprovoked or provoked by viruses, bacteria, allergens like mould or tobacco smoke
  • Tend to develop in less than 6 hours with worsening of breathlessness, cough, wheeze and chest tightness
  • Things that suggest increased severity: tachypnoea, tachycardia, inability to speak in full sentences, silent chest
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19
Q

Acute asthma exacerbation: investigations

A
  • PEFR and FEV1 assess severity, PEFR is expressed as a percentage of the patients best or predicted score
  • SpO2: drop to <92% suggests its life threatening
  • Arterial blood gas (ABG): indicated if the patient’s SpO₂ is <92% or PEFR is ≤30% of best or predicted. Hypercapnia (PaCO₂ >6kPa) suggests that a patient’s attack is near-fatal. Most patients will have respiratory alkalosis in severe cases with hypercapnia they have metabolic acidosis
  • Venous blood gas: less useful
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20
Q

Management of acute asthma exacerbation: initial

A
  • Initial treatment: high dose SABA, if life threatening/ near fatal give by standard pressurised metered-dose inhaler (pMDI) or by an oxygen-driven nebulizer.
    -Prednisolone PO daily 40-50mg,continue for at least 5 days or when the patient recovers. Continue normal medication
21
Q

Management of severe/life threatening acute asthma exacerbation

A
  • Admit to hospital
  • Oxygen: if acutely unwell use 15L non re-breathe, nasal canulae or venturi can be used. Maintain SpO2 at 94-98%
  • IV magnesium sulphate and IV aminophylline
  • Nebulised ipatropium bromide (SAMA), given 0.5mg 4-6 hourly
  • Mechanical ventilation, only after talking to seniors
22
Q

Follow up asthma exacerbation

A
  • Any possible triggers for the attack.
  • Inhaler use and technique.
  • Optimisation of treatment and a plan for preventing further exacerbations.
23
Q

Acute asthma exacerbation- chest x-ray is not routinely recommended for patients except for

A
  • Suspected pneumomediastinum or pneumothorax
  • Suspected consolidation
  • Life threatening asthma
  • Failure to respond to treatment satisfactorily
  • Requirement for ventilation
24
Q

Summary of management for acute asthma exacerbation

A
  • A to E structure
  • Controlled oxygen therapy (94-98%)
  • Salbutamol nebulisers, can be given back to back if there is a poor response to the initial dose
  • Hydrocortisone (IV) or Prednisolone (PO)
  • Ipratropium nebulisers- in severe or life threatening cases or where there is an inadequate response to initial treatment
  • Magnesium sulphate (IV) or Theophylline (as aminophylline infusion IV) can be considered under specialist guidelines
  • Incubation and ventilation may also be required
25
Q

Understanding the severity of asthma

A
  • have you had difficulty sleeping because of your asthma symptoms (including cough)?
  • have you had your usual asthma symptoms during the day (cough, wheeze, chest tightness, or breathlessness)?
  • has your asthma interfered with your usual activities (e.g. housework, work/school, etc)?
26
Q

Poorly controlled asthma is:

A
  • 3 or more days a week with symptomsor
  • 3 or more days a week with required use of a SABA for symptomatic reliefor
  • 1 or more nights a week with awakening due to asthma.
27
Q

Risk factors for asthma mortality and what else to ask

A
  • It’s also important to know how many exacerbations requiring oral steroids, ED attendance or admission the patient has had in the last 6-12 months- and whether they have ever been admitted to ITU and/or ventilated for asthma.
  • Risk factors for asthma mortality include: poor adherence to preventer medication, high use of reliever medication, hospital attendance for asthma in the last year, previous near-fatal asthma, and smoking.
28
Q

Specialised asthma medication

A
  • Long acting muscarinic, theophylline, new biological therapy and oral steroids
  • Omalizumab is a subcutaneous anti-IgE monoclonal antibody which has been used for some years to treat poorly controlled patients with atopy and high IgE
  • Newer subcutaneous monoclonal antibody treatments include Mepolizumab and Benralizumab which target eosinophils.
29
Q

COPD

A

Umbrella term encompassing chronic bronchitis and emphysema. Mostly due to smoking

Chronic bronchitis- a productive cough that lasts at least three months of two consecuative years

Emphysema- the abnormal, permanent enlargement of the air spaces due to the breakdown of alveoli.

29
Q

Risk factors/ CXR for COPD

A

Risk factors: Smoking, pollution and exposure to dust, Alpha 1 antitrypsin deficiency

chest x-ray:
- Useful to exclude other causes like malignancy
- In COPD you will see Hyperextended lungs, Flattened Hemidiaphragm, Bullae

29
Q

Clinical signs of COPD include

A

Barrel chest, Cyanosis, Flapping tremor, Pursed lip breathing, Use of accessory muscles, wheeze. Will be breathless at normal oxygen saturations due to emphysema causing destruction of alveoli and reduced gas transfer.

29
Q

COPD: spirometry

A
  • FEV1/FVC ratio <70% (below)
  • Scalloping of flow/volume curve
29
Q

Consider COPD when they present with

A
  • Are over 35 with a risk factor i.e. smoking
  • Exertional breathlessness
  • Chronic cough
  • Regular sputum production
  • Wheeze
  • Frequent winter ‘bronchitis’
29
Q

COPD management conservative

A
  • Smoking cessation
  • Pneumococcal vaccination and annual influenza vaccine
  • Pulmonary rehab- combines physical therapy with disease education and nutritional, psychological and behavioural intervention. Programme is done in groups and lasts 6-8 weeks
30
Q

Management of acute exacerbation of COPD

A
  • A to E assessment
  • Controlled oxygen therapy- should be monitored with ABG’s to ensure they are not hypercapnic
  • Steroids (PO)
  • Salbutamol nebulisers (bronchodilator)
  • Ipratropium nebulisers (bronchodilator)
  • Consider antibiotics- if symptoms are severe or there are changes to the sputum
  • Non invasive ventilation- if there is hypercapnia and acidaemia
  • Intubation and ventilation can be considered in patients with severe exacerbations who don’t respond to treatment
30
Q

COPD medication

A
  • Short acting bronchodilator i.e. salbutamol. They will initially be offered either a SABA or a Short Acting Muscarinic antagonist
  • Combination therapy: Long acting beta agonist (LABA) or Long Acting Muscarinic Antagonist (LAMA) or a Long Acting Beta Agonist or Inhaled Corticosteroid (ICS). The second option is normally for patients with asthmatic features
  • Triple therapy- for patients who still have day to day symptoms which affect the quality of their life or they have one severe or two moderate exacerbations within a year. LABA + LAMA + ICS
30
Q

COPD: further management steps

A
  • May need long term oxygen therapy, home nebulisers, prophylactic antibiotics and mucolytics. Some patients may need lung volume reduction surgery
  • You go from short acting, to combination therapy, to triple therapy if symptoms are not controlled.
31
Q

COPD: acute exacerbation

A

Sustained worsening of the patients symptoms from their usual stable state which is beyond normal day to day variations and is acute in onset

31
Q

Investigations for acute exacerbation of COPD

A
  • Blood tests- including FBC, urea and electrolytes, C reactive protein
  • Cultures- blood cultures, sputum cultures. Will show if there is a source of infection
  • Arterial blood gas- is there evidence of hypercapnia, acidosis. Is oxygen appropriate
  • Chest x-ray: to exclude pneumonia/ other pathology
32
Q

PE: clinical features

A
  • Pleuritic chest pain
  • SOB
  • Cough and haemoptysis
  • Tachycardia, hypoxia
  • Elevated JVP
  • Gallop rhythm: widely split second heart sound
  • Tricuspid regurgitant murmur, pleural rub
  • Fever
  • Hypotension
  • Dizziness and syncope
  • Evidence of DVT- leg swelling, pain, warmth
33
Q

PE investigations

A
  • Bedside: Obs, ECG
  • Bloods: FBC, U&E, CRP, glucose, lipids
  • Calculate 2 level Wells Score: If>4, immediate CTPA (CT pulmonary angiogram). If<=4, D Dimer test
  • CXR: loss of vascular markings and wedge shaped peripheral infarcts- not sensitive or specific
34
Q

PE management

A
  • Medical: anticoagulated- LMWHs or fondaparinux or apixaban/rivaroxaban
  • Apixaban or rivaroxaban are first line, start when diagnosis is suspected and continue when confirmed
  • LMWH is used in antiphospholipid syndrome and renal impairment
  • Admission for patients who are haemodynamically unstable, have CT or echo evidence of right heart strain, require supplemental oxygen
  • PE which was provoked should be treated for 3 months. if its unprovoked 6 months
  • If high bleeding risk and low oral absorption; continuous unfractioned heparin infusion

Surgical: IVC filters to trap fragmented thromboembolism

35
Q

CTPA alternatives

A
  • Not contraindicated in pregnancy as radiation is low, but can use:
  • Lower limb venous ultrasound to identify a DVT
  • V/Q scans can be used in PE as avoids radiation to maternal breast tissue. Not useful if abnormal CXR or pre-existing lung disease
36
Q

PE: pathology

A
  • area of reduced perfusion although the lung is still ventilated- V/Q mismatch.
  • Resulting hypoxia can cause breathlessness.
  • If PE large can cause right sided heart failure causing breathlessness and hypoxia
  • Main cause of death: right ventricular overload causing left ventricular dysfunction i.e. not hypoxia
  • Symptoms: chest pain, haemoptysis, cardiac syncope
37
Q

Pulmonary hypertesnion

A
  • Raised pressure in the pulmonary circulation can develop chronically as a result of repeated or undiagnosed clots, idiopathic pulmonary arterial remodelling, high left heart pressures from cardiac disease, or pulmonary vascular remodelling from any lung disease (cor pulmonale).
  • Breathlessness and hypoxia can develop due to V/Q mismatch and reduced oxygen diffusion across the alveolar membrane, can be exacerbated by cardiac dysfunction
37
Q

Pulmonary hypertension: findings

A
  • More pronounced on exercise, may have normal resting saturations which drop quickly on exercise
  • The TLCO (diffusing capacity) and KCO will both drop in the presence of preserved lung volumes and spirometry.
37
Q

Risk factors for PE

A
  • Major: DVT, previous VTE, active cancer, surgery within the last 2 months, Immobility >5 days, lower limb trauma/fracture, pregnancy, postpartum
  • Less significant: Increasing age >60, COCP, HRT, BMI >30, airplanes, varicose veins, superficial venous thrombosis
37
Q

Acute PE

A
  • Main cause of death in acute PE is cardiac shock: causing right ventricular failure and haemodynamic instability
  • Haemodynamic instability is defined as a systolic BP <90mmHg or a sustained (>15min) drop of > 40mmHg, or evidence of end-organ hypoperfusion, or cardiac arrest.
  • Consider for thrombolysis with IV alteplase- can cause bleed f haemodynamically unstable
38
Q

PE: interim treatment

A

Interim therapeutic anticoagulation to be given if unable to access immediate diagnostic procedures:

  • apixaban or rivaroxaban first line, and if these are not suitable, low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban,
    or
  • LMWH concurrently with a vitamin K antagonists for at least 5 days.
  • Bloods (don’t delay treatment): FBC, LFT, U&E, PT and APPT

Medicine year 4 CDM (41 decks)

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