Respiratory medicine Flashcards

1
Q

Definition of COPD

A

A disease state characterised by airflow limitation that is not full reversible, is progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases

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2
Q

Definition of emphysema

A

Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles with destruction of alveolar walls without fibrosis

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3
Q

Definition of chronic bronchitis

A

Persistent cough with sputum production for at least 3 months in at least 2 consecutive years

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4
Q

Pathophysiology of COPD

A

Smoking - inc. neutrophils - elastases and proteases released - emphysema (breakdown of alveolar wall etc.)

a1-antitrypsin inactivated by cigarette smoke - imbalance between protease and antiprotease activity

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5
Q

Emphysema classifications

A

According to site of damage:
CENTRI-ACINAR emphysema:
- destruction concentrated around respiratory bronchioles
- distal alveolar ducts and alveoli tend to be preserved
- extremely common form, not always associated with disability

PAN-ACINAR emphysema:

  • less common
  • distension and destruction of WHOLE acinus (area supplied by terminal bronchiole)
  • associated with a1-antitrypsin deficiency

IRREGULAR emphsema:
- patchy scarring and damage of lung parenchyma

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6
Q

Cause of airflow limitation in COPD

A

Reduced elasticity due to emphysema - red. recoil - collapse of airway during expiration
Inflammation and scarring - narrow airway
Mucus plugging of smaller airways

ALL CAUSE V/Q MISMATCH

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7
Q

Clinical features of COPD

A
Productive cough
Wheeze
SOB
Frequent infective exacerbations
If severe:
- cyanosis
- pursed lip breathing, accessory muscles
- tachypnoea with prolonged expiration
- intercostal recession
- hyperinflated chest
- reduced chest expansion
- loss of normal cardiac and liver dullness to percussion
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8
Q

Investigations in COPD

A
FEV1:FVC less than 0.8
Reduced PEF
May be partly reversible (less than 12%)
CXR:
- often normal
- overinflation of lungs, low flattened diaphragms
- sometimes large bullae
- large proximal blood vessels, relatively little blood visible in peripheries
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9
Q

Management of COPD

A
COPD-X guidelines:
C: confirm diagnosis and severity
O: optimise function
P: prevent deterioration
D: Develop support (therapeutic relationship, MultiD care, action plans, support group)
X: manage exacerbations
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10
Q

Assessing severity in COPD

A
FEV1/FVC less than 70% in all, class according to % predicted 
Mild: over 80% predicted
Moderate: less than 80% predicted
Severe: less than 50% predicted
Very severe: less than 30% predicted

(Mod: breathlessness on walking, cough and sputum, Severe: SOB on minimal exertion, daily activities severely curtailed, chronic cough)

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11
Q

Optimising function in COPD

A

Goals: active therapy v palliative v terminal
Relievers: SABA, SAMA (ipratropium bromide)

Preventers: LAMA (tiotropium) LABA (indacterol - OD, salmeterol - BD)

ICS: consider if mod-sev and frequent exacerbations

Non-pharm: physical activity, pulmonary rehab, chest physio, smoking cessation, nutrition
Management of co-morbidities

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12
Q

Preventing deterioration in COPD

A

Smoking cessation
Immunisations: annual influenza, pneumococcal
+/- Mucolytic agents (N-acetylsysteine)
Oxygen therapy if hyopxaemia

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13
Q

Management of COPD exacerbations

A

Early diagnosis
Inhaled bronchodilators
Systemic corticosteroids
Antibiotic therapy (if clinical signs of infection)
Controlled O2 delivery
NIPPV for acute hypercapnie venitlator failure

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14
Q

Complications of COPD

A

Respiratory failure
Cor pulmonale (Pulmonary HTN)
Fluid retention and peripheral oedema secondary to renal hypoxia

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15
Q

Definition of asthma

A

A chronic inflammatory condition of the airways characterised by reversible airflow limitation, airway hyper-responsiveness to a wide range of stimuli and bronchial inflammation

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16
Q

Epidemiology of asthma

A

Peak age of 1st presentation = 3y
M:F 2:1 in childhood, 1:1 by adulthood
affects up to 15% children, 10% adults
More common in developed countries

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17
Q

Assessing severity of asthma

A

Intermittent:

  • less than weekly daytime sx
  • less than 2 night-time sx per month
  • infrequent, brief exacerbations
  • FEV1 80% predicted, variability less than 20%

Mild persistent:

  • more than weekly, not daily daytime sx
  • less than weekly night-tin sx
  • occasional exacerbations, may affect activity or sleep
  • FEV1 80% predicted, 20-30% variability

Moderate persistent:

  • daily symptoms
  • night-time sx weekly or more
  • occassional exacerbations may affect sleep or activity
  • FEV1 60-80% predicted, variability over 30%

Severe persistent:

  • daily symptoms, restricting physical activity
  • frequent night-time symptoms
  • frequent exacerbations
  • FEV1 60% predicted or less, variability over 30%
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18
Q

Conditions suggestive of CF in adults

A
BRANIAC
Bronchiectasis
Recurrent pancreatitis
Allergic bronchopulmonary mycosis
Infertility (Male)
Nasal polyposis
Infection with non-tuberculous mycobacterium
Adult (there isn't' actually another A) - could be osteoporosis
Chronic sinusitis
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19
Q

Definition of bronchiectasis

A

The congenital or acquired irreversible abnormal dilation and destruction of bronchial walls

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20
Q

Types of bronchiectasis

A

Cylindrical:

  • dilated bronchi with straight, regular outlines
  • tram-track lines (parallel to each other)
  • Signet ring

Saccular/cystic:

  • most severe form
  • ballooned appearance of bronchi +/- air-fluid levels
  • large, cystic areas with honeycomb appearance
  • thicker bullae of emphysema

Varicose:
- bronchi with dilated segments and other areas of constriction - “string of pearls”

Follicular:
- extensive lymphoid nodules in bronchial walls

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21
Q

Clinical features of bronchiectasis

A
Chronic cough w purulent sputum
Haemoptysis
dyspnoea and wheezing
Chest pain
Postnasal drip
Chronic fatigue
Bilateral basal crackles
Wheeze
Ronchi
Clubbing (in long-standing, severe bronchiectasis)
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22
Q

Investigations in bronchiectasis

A

High resolution CT:

  • signet ring (end-on dilated bronchi are larger than accompanying pulmonary artery)
  • Tramlines (non-tapering bronchi)
  • cysts with air-fluid levels
  • mucus plugging of dilated bronchi (flame and blob sign/tree-in-bud pattern)
Sweat chloride test
Electron microscopic evaluation of ciliary structure (primary ciliary dyskinesia)
Genetic tests (CFTR, a1 antitrypisin genotypes)
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23
Q

Management of bronchiectasis

A

Prolonged Abx for infective exacerbations (10-14d Augmentin)
Bronchodilators - if airflow obstruction
Inhaled corticosteroids

Pulmonary rehab
Bronchial hygiene therapy (inc. removal of secretions)
Surgery (if obstructing tumour, removal of severely damaged segments etc.)

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24
Q

CXR findings in PE

A

Often normal in small/medium PE
May show small effusion (blunting of costophrenic angle)

Massive PE:

  • oligaemic lung fields
  • dilation of pulmonary arthery in hilum
  • is often normal
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25
Q

ECG findings in PE

A

Sinus tachycardia
Sometimes AF

In massive:
Peaked P waves lead II (RA dilatation)
R axis deviation (RV dilatation)
RBBB, T wave inversion on R precordial leads

Classic S1Q3T3 is rare

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26
Q

Wells criteria for PE

A
Clinical sx of DVT = 3
PE more likely than other diagnoses = 3
Prior DVT/PR = 1.5
Tachycardia = 1.5
Immobilised 3d or surgery in last 4w = 1.5
Haemoptysis = 1
Malignancy = 1

5 or more, likely - perform CTPA
If less than 5, low risk, perform D-dimer to exclude

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27
Q

Management of PE

A
Parenteral anticoagulant
- LMWH is agent of choice for initial treatment (unfractionated if significant renal disease)
Oral warfarin or rivaroxaban
Target INR 2-3
Minimum 3 months anticoagulation

Thrombolytics are indicated in patients with haemodynamic instability (systolic BP under 90)
+/- patients with poor prognostic markers (inc. troponin, RV dilatation)

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28
Q

Assessing severity of pneumonia

A
SMART-COP
Systolic BP less than 90 = 2
Multilobar involvement on CXR = 1
Albumin less than 35 = 1
Respiratory rate over 25 (30 if 50 or older) = 1
Tachycardia over 125 = 1
Confusion = 1
Oxygen low (93%, 90% if 50) = 2
pH - acidaemic = 2

Severe if over 5 points - high risk of needing intensive respiratory or vasopressor support

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29
Q

Management of community acquired pneumonia

A

Mild CAP:

  • oral amoxicillin
  • augmentin if suspect haemophilus
  • doxy or clariithromycin if atypical
  • oral clarithromycin if penicillin allergic

Moderate: inpatient treatment

  • IV benzylpenicillin + oral doxy or clarithromycin
    • gentamicin if gram -ve organism identified in sputum or blood
  • IV ceftriaxone if allergic to penicillin

Severe:
IV antibiotics + IV azithromycin

30
Q

Definition of tuberculosis

A

A multi-systemic infection that most commonly affects the pulmonary system and is caused by mycobacterium tuberculosis

31
Q

Areas highly endemic for TB

A

Sub-Saharan Africa

Russia

32
Q

Diagnosis of TB:

A

CXR:

  • Primary: Ghon foci in midzones
  • Secondary: cavitation in upper zone

Tissue or fluid MC&S -don’t swab

  • Acid fast bacilli test (Ziehl-Neelsen or auramine)
  • NAAT e.g. PCR

+/- tracheal aspirates
+/- bronchoscopy specimens (e.g. alveolar lavage)

33
Q

Management of TB

A

NOTIFIABLE DISEASE

6 months antibiotic therapy (12m minimum if CNS TB)
For fully susceptible TB:
- 2 months RIPE: rifampicin, isoniazid, pyrazinamide, ethambutamol
- following 4: isoniazid + rifampicin

+ supplemental pyridoxine (VitB6)

+ adjunct corticosteroids in CNS and pericardial disease (reduce long-term complications)

34
Q

Symptoms of TB

A

Pulmonary:

  • productive cough +/- haemoptysis
  • weight loss
  • fevers - low-grade, late afternoon
  • night sweats
  • larynx involvement (hoarse voice, severe cough)
  • pleura involvement (pleuritic chest pain)

LN:

  • enlarged cervical or supraclavicular
  • +/- indurated overlying skin
  • +/- sinus tract formation with purulent d/c

GI:

  • abdominal pain
  • diarrhoea +/- blood

Spinal (Pott’s) articular TB:

  • monoarticular arthritis
  • weight bearing joints

Miliary TB:

  • Includes CNS in 20%
  • respiratory symptoms
  • cholestasis
  • GI symptoms

CNS:

  • HIV +ve patients mainly
  • tuberculous meningitis
35
Q

Latent TB infection

A

Initial containment of infection within granuloman (Ghon focus)

  • Negative sputum therefore not infectious to others
  • Tuberculin skin test usually +ve
  • May visualise small calcified Ghon focus on CXR
36
Q

What is a Ghon focus

A

The initial focus of disease in TB
On CXR: small calcified nodules

Ghon complex = Ghon focus + regional LN caseation
Primary complex of Ranke = Ghon focus within regional draining LN

37
Q

Tuberculin (Mantoux) skin test

A

+ve 2-4 weeks after infection

+ve test = visible AND palpable induration peaking 48-72h following intracutaenous injection of purified protein derivative of M tuberculosis

(+ve reflects T-cell mediated immunity to mycobacterial antigens, does not differentiate between infection, active disease or vaccination)

38
Q

Epidemiology of primary lung cancer

A
  • Most common cause of malignancy-related death in developed countries
  • 5th most frequently diagnosed cancer in australia
  • Avg age of diagnosis 40-70y
  • 1y survival 40%
  • 5y survival 15%
    Cigarette smoking accounts for over 90%
39
Q

Most common forms of primary lung cancer

A

Squamous cell carcinoma (25-40%)

  • closely related to smoking
  • usually central and close to carina
  • relatively slow-growing
  • 60% resectable at time of diagnosis
  • firm, grey-white, may be ulcerated
  • highly variable microscopic appearance

Adenocarcinoma (25-40%)

  • bronchial derived or bronchioalveolar types
  • not as closely linked to smoking as SCC
  • most common type in women
  • peripherally located (small bronchi and bronchioles) THEREFORE DON’T PRESENT WITH FEATURES OF OBSTRUCTION

Small cell carcinoma (20-25%)

  • highly malignant, mets early
  • strong link to smoking
  • most common type linked with ectopic hormone production
  • derived from neuroendocrine cells of broncial epithelium
  • most often in hilar/central regions
  • virtually incurable by surgery

Large cell carcinoma (10-15%)

  • central or peripheral
  • poor prognosis
  • microscopically: large polygonal cells with pleomorphic nuclei
40
Q

Metastasis sites of primary lung cancer

A
LABB
Liver
Adrenals
Brain 
Bone
41
Q

Paraneoplastic syndromes associated with lung canceer

A
Mostly seen in small cell carcinomas
ADH - SIADH
ACTH - Cushing's syndrome
PTHrP - hypercalcaemia
Calcitonin - hypocalcaemia
42
Q

Stages of non-small cell lung cancer

A

I: only in lung, no nodal spread
II: Lung + local nodal involvement
III: lung and LN in middle of chest, IIIa = only ipsilateral LN involved, IIIb = contralateral or cervical LN involvement
IV: both lungs, pleural space or distant metastasis

43
Q

Stages of small cell cancer

A

Limited: cancer only in one area of lung +/- local ipsilateral LN

Extensive: spread to contralateral lung, other areas of chest or distant organs

44
Q

Management of non-small cell lung cancer

A

Stage I-II: Surgical resection (RTx, CTx, or observation if not suitable for surgery)

Stage IIIa: Induction chemotherapy - surgical resection + mediastinal RTx
OR Radical combination chemoradiotherapy

Stage IIIb: radical combination chemoradiotherapy

Stage IV: Chemotherapy + palliative radiotherapy for specific sites (brain, bone pain)

45
Q

Management of small cell lung cancer

A

Limited disease:
Platinum based CTx + thoracic radiotherapy

Extensive disease:
- Combination CTx

46
Q

Genetic mutation associated with squamous cell cancer of the lung

A

DDR2 in 4%

sensitive to treatment by dasatinib (kinase inhibitor)

47
Q

Definition of pulmonary hypertension

A

A haemodynamic state in which the pressure in the pulmonary artery is elevated above a mean of 25mmHg

pulmonary ARTERIAL hypertension = pulmonary artery pressure over 25 with left heart filling pressure less than 15

48
Q

Classifications of pulmonary hypertension

A

Group 1: pulmonary arterial HTN
- idiopathic, heritable, CTD, HIV, congenital heart disease etc.

Group 2: HTN secondary to LH failure

Group 3: Pulmonary HTN secondary to lung disease and/or hypoxia (COPD, ILD)

Group 4: Chronic thromboembolic pulmonary hypertension

Group 5: Pulmonary HTN with unclear multifactorial mechanisms (myeloproliferative neoplasms, splenectomy, sarcoid, vasculitis, thyroid disorders etc.)

49
Q

signs of pulmonary HTN

A
Loud P2
Parasternal lift (hypertrophied RV)
Pansystolic murmur (TR)
RV S4
Other signs of RHF (hepatomegaly, oedema, ascited, raised JVP etc.)
50
Q

Management of pulmonary HTN

A

General (for all groups of pulmonary HTN):

  • diuretics
  • O2 therapy
  • Anticoagulation (warfarin)
  • Digoxin (inc. RVEF)
  • Exercise
  • Vaccinations
51
Q

Definition of interstitial lung disease

A

Chronic, non-malignant, non-infectious disease of the lower respiratory tract characterised by inflammation and derangement of the alveolar walls and damage to the lung parenchyma by inflammation and fibrosis

52
Q

Causes of ILD

A

Acute ILD:

  • idiopathic
  • allergy (penicillin, fungi, helminths)
  • toxins (amiodarone, sulfasalazine, MTX, immunosuppresants, chlorine)
  • Vasculitis (Goodpastur syndrome)

Chronic ILD:

  • idiopathic
  • inorganic dusts (asbestosis, siderosis[iron], silicosis, granulomatous)
  • organic dusts (bacteria or animal protein [bird fancier’s lung])

Systemic diseases:

  • collagen vascular disease (RA, AS, SLE, Sjogren syndrome)
  • Neoplastic (lymphoma)
  • sarcoidosis
  • IBD
  • amyloidosis
  • HIV-associated
53
Q

Clinical features of interstitial lung disease

A

Progressive SOBOE
Persistent non-productive cough
Fever
Haemoptysis (alveolar haemorrhage syndromes e.g. Goodpastures)
Symptoms of collage vascular disease etc.

Clubbing (esp in idiopathic)
End-expiratory fine crackles (like velcro) THAT DO NOT SHIFT WITH COUGHING
Signs of Pulm HTN
- loud P2
- Pansystolic murmur (TR)
- raised JVP
- R sided heave and S3
Extrapulmonary signs of collagen vascular disease
54
Q

CXR in interstitial lung disease

A

May help to narrow differentials for cause

  • Patterns (upper v lower lobe)
  • Ground-glass attenuation
  • Kerly B lines
  • Hilar/mediastinal lymphadenopathy
55
Q

Management of interstitial lung disease

A

General measures:

  • oxygen therapy
  • pulmonary rehabilitation
  • smoking cessation
  • vaccinations

Idiopathic:

  • N-acetylcysteine (mucolytic)
  • Lung transplantation
  • trial prednisolone 6-12w

Collage vascular disease related:

  • Treat underlying cause
  • mycophenolate mofetil

Wegener Granulomatosis:
- Cyclophosphamide + prednisolone

Goodpasture syndrome:

  • Plasmapheresis (eliminate anti-GBM antibodies)
  • Cyclophosphamide OR prednisolone
56
Q

Definition of sarcoidosis

A

A chronic multisystem granulomatous disease of unknown cause, characterised by the presence of non-specific, non-caseating granulomas
Over 90% have respiratory tract involvement

57
Q

Common symptoms in symptomatic individuals with sarcoidosis

A
Fatigue
Night sweats
Weight loss
Dry cough
Dyspnoea
Skin disease (e.g. erythema nodosum)
Eye disease
Cardiac disease (arrhythmias)
Neurosarcoidosis (CNeuropathies, myelopathy, seizures)
MSK (arthritis in 35%)

LOCALISED WHEEZING +/- crackles

58
Q

CXR in sarcoidosis

A

Bilateral hilar adenopathy
R paratracheal adenopathy
Parenchymal infiltration
Fibrosis: honeycombing, cysts, bullae, traction bronchiectasis

59
Q

CT chest in sarcoidosis

A
Nodules
Ground-glass opacities
Bronchiectasis
Cysts
Thickening of pleural surface
60
Q

Management for respiratory sarcoidosis

A

Prednisolone 20-40mg/day if SOB or reduced FVC

Inhaled corticosteroid for wheezing

61
Q

Definition of respiratory failure

A

Syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination

62
Q

Classifications of respiratory failure

A

Type I/Hypoxaemic:
Arterial oxygen pressure less than 60 with normal or low arterial CO2 pressure
i.e hypoxaemia WITHOUT hypercapnia

Type II/Hypercapnic:
PaCO2 over 50 (patients are often hypoxaemic as well)

63
Q

Causes of type I respiratory failure

A

Pretty much any acute lung disease, generally involving fluid filling or alveolar collapse

  • COPD
  • Pneumonia
  • Pulmonary oedema
  • Pulmonary fibrosis
  • Asthma
  • Pneumothorax
  • Pulmonary embolism
  • Pulmonary arterial hypertension
  • Acute respiratory distress syndrome
64
Q

Causes of type II respiratory failure

A
COPD
Severe asthma
Drug overdose/poisoning
Neuromuscular disease
Chest wall abnormalities
65
Q

Management of respiratory failure

A
Reverse/prevent tissue hypoxia
- ICU admission if acute
- secure airway
- Supplemental O2 (intubation and ventilation may be required in severe hypoxaemia)
Treatment of underlying cause
66
Q

Management of pneumothorax

A

Small (less than 20%)
- observe at 2-weekly intervals until air reabsorbed
Medium pneumothorax (20-50%)
- aspirate air, if no recurrence treat as above
Large pneumothorax (over 50%):
- aspirate air, if no recurrence treat as above
- if recurrence - intercostal drainage tube with underwater seal for 2-3 days

If recurrent (more than twice) consider surgery or if contraindicated, peurodesis (adhesion of visceral and parietal pleura with talc, bleomycin or tetracycline)

67
Q

Causes of pleural effusion

A

Transudates (often larger on R side)

  • Heart failure
  • Hypoproteinaemia (e.g. nephrotic syndrome)
  • constrictive pericarditis
  • Hypothyroidism
  • Ovarian tumours (Meigs’ syndrome)

Exudates:

  • Bacterial pneumonia (common)
  • Carcinoma of the bronchus and pulmonary infarction (common)
  • Tuberculosis
  • Autoimmune rheumatic disease
  • RARE: post-MI syndrome, acute pancreatitis
68
Q

At what point can a pleural effusion be detected

A

Radiologically at 300mL

Clinically at 500mL

69
Q

Biochemistry of transudate v exudate

A

Transudate:
Protein under 30
Lactic dehydrogenase under 200
Fluid:serum LDH ratio less than 0.6

Exudate:
protein over 30
LDH over 200

70
Q

Clinical features of pleural effusion

A
Reduced chest expansion on affected side
Mediastinal shift away from lesion
Stony dull percussion 
Reduced or absent vesicular breath sounds
Reduced vocal resonance
Nil adventitious sounds
71
Q

Spirometry in obstructive v restrictive pictures

A

Obstructive:

  • FEV1 reduced
  • FVC reduced or normal
  • FEV1/FVC reduced

Restrictive:

  • FEV1 reduced OR normal
  • FVC reduced
  • FEV1/FVC Normal or increased

Mixed: reduced FEV1, FVC and FEV1/FVC

Asthma - over 12% (or 200mL) improvement in FEV1 (or FVC) post bronchodilator