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Respiratory Flashcards

1
Q

What are the 3 mechanisms behind asthma

A
  1. Increased thickness of airway wall due to Th2 eosinophilic inflammation & Structural change (remodelling)
  2. Increased mucus due to activation of large submucosal glands and more goblet cells
  3. Increased constriction of airway smooth muscle induced by raft of released mediators
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2
Q

What does intrinsic and extrinsic asthma mean and when are they both likely ot be diagnosed?

A

Allergic (extrinsic) asthma usually develops during childhood and is triggered by allergens such as pollen, dust mites, and certain foods. Non-allergic asthma (environmental or intrinsic) asthma usually develops in patients over the age of 40 and can have various triggers such as cold air and medications.

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3
Q

Symptoms of asthma

A
  • SOB
  • Wheezing
  • Cough (often nocturnal)
  • Chest tightness

Particularly if these are worse at night and in the early morning; occur in response to exercise, allergen exposure or cold air; occur after taking aspirin or beta-blockers

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4
Q

Examination findings in a person with asthma

A
  • Widespread expiratory wheeze
  • Increased RR, HR
  • Respiratory distress
  • Cyanosis
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5
Q

Investigations to consider for asthma

A
  1. Spirometry – obstructive lung disease – FEV1/FVC decreases
  2. Methacholine Challenge Testing – evidence of bronchial hyper responsiveness after inhalation of methacholine
  3. CXR- normal in mild cases, signs of pulmonary hyperinflation in cases of severe asthma
  4. Pulse oximetry and blood gas analysis
  5. In allergic asthma – antibody testing, total IgE, skin allergy tests
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6
Q

Management of acute attack of asthma

A
  1. Administer high doses of inhaled SABA via pressurised metered dose inhaler (pMDI) with spacer or via nebuliser
    * Salbutamol 100mcg, 12 separate actuations (6 is <6yo) by inhalation via pMDI with spacer. Repeat every 20 seconds OR 2.5mg by nebuliser
  2. If not responding to salbutamol, consider ipratropium via pMDI with spacer every 20 minutes (max 3 doses in first hour)
  • <5yo - Ipratropium 21mcg x 4 actuations via pMDI 0r 250mcg neb
  • 6+ - Ipratropium 21 mcg x 8 actuations via pMDI or 500mcg neb
  1. Oxygen if SpO2 < 95% - nasal prongs
  2. Corticosteroid – oral preferred
  • Try avoid in <5 yo
  • 6yo+ oral - prednisolone 2mg/kg (up to 50mg)
  • 6yo+ IV - hydrocortisone 4mg/kg (up to 100mg) every 6 hours for 24 hours
  1. Add on treatments
  • IV magnesium sulfate
  • IV salbutamol
  • IV aminophylline
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7
Q

Maintenance treatment for asthma

A
  1. Symptom relief
    * Salbutamol 100mcg, 1 to 2 actuations by inhalation via pmDI with spacer, as needed
  2. Preventive therapy
  3. First line – Inhaled Corticosteroids
  • Beclomethasone (pMDI) à 50-100mcg BD
  • Budesonide (DPI) à 100-200mcg BD
  1. Then Add Montelukast or cromone
  • 2-5yo à Montelukast 4mg orally, at night
  • 6-14 à Montelukast 5mg orally, at night
  1. Then add LABA
  • Do not add in < 5yo
  • Fixed dose comination inhaler has both ICS + LABA
  • Fluticasone propionate + salmeterol 50 + 25 mcg, 2 actuations by inhalation via pMDI with spaced, BD

*For adults just go straight to LABA, dont bother with Montelukast

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8
Q

What is the mechanism of action of the following drugs:

  • Salbutamol
  • Salmeterol
  • Montelukast
A

Salbutamol - Short acting B2-adrenoceptor agonist

Salmeterol - Long acting B2 adrenoceptor agonist

Montelukast - Leukotriene receptor antagonist - LTs bind CysLT1 receptors which induce airway narrowing

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9
Q
A
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10
Q

The Two Types of COPD

A
  1. Airflow limitations - Emphysema (or airway narrowing)

Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by alveolar wall destruction without obvious fibrosis.

  1. Centriacinar – involves primarily the upper lobes. Loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli. This pattern is most typical for smokers.
  2. Panacinar – involve all lung fields, particularly the bases. Loss of all portions of the acinus from the respiratory bronchiole to the alveoli
  3. Distal acinar – least common form
  4. Irregular – associated with scaring
  5. Bullous – subpleural cyst-like-air-filled spaces
  6. Chronic Bronchitis

Presence of a chronic productive cough on most days for 3 months for at least 2 consecutive years (other causes excluded)

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11
Q

Causes of COPD

A
  • Tobacco smoking (By far main risk factor)
  • Air pollution
  • Occupational exposure
  • Alpha-1-antitrypsin deficiency
  • CT disorders
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12
Q

Signs and Symptoms of COPD

A

Symptoms

  • Cough (frequently morning, usually productive, and sputum quality may change with exacerbations)
  • Shortness of breath (initially with exercise but may progress to at rest)
  • Wheezing on auscultation
  • Reduced exercise capacity
  • Recurrent chest infections

Signs

  • Barrel chest (hyperinflation)
  • Pursed lips and tripod
  • Reduced breath sounds on auscultation
  • Wheezing on auscultation
  • Early inspiratory crepitations on auscultation
  • Hyperresonance on percussion
  • Asterixis - hypercapnia
  • Distended neck veins - secondary to cor pulmonale and increased intrathoracic pressure
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13
Q

Investigations in COPD

A
  1. Spirometry – Airflow limitation is classified as a FEV1/FVC ratio < 0.70
  • To diagnose COPD need a post-bronchodilator FEV1/FVC < 0.7
  • Increased residual volume
  • Decreased diffusing capacity of CO
  1. Pulse oximetry - Low oxygen saturation. If below <92% à ABG
  2. ABG
  • pH decreased, pO2 decreased, CO2 increased, HCO3 normal or high
    1. CXR
  • Useful for ruling out other pathologies
  • Increased anteroposterior ratio, flattened diaphragm, increased intercostal spaces, and hyperlucent lungs may be seen, long narrow heart shadow, floating heart syndrome, bullous
  1. Sputum culture
  2. FBC – assess severity of an exacerbation and may show raised haematocrit, possible WCC increase in infection

COPD Assessment Test (CAT) recommended for comprehensive assessment of symptoms

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14
Q

Treatment of COPD

A

1) Conservative

  • Smoking Cessation
  • Immunisations
  • Physiotherapy
  • Physical activity

2) Home oxygen
* If PaO2 < 55
3) Medications
a) Symptomatic

  • SABA - Salbutamol 100mcg, 2 actuations inhaled by pMDI
  • Ipratropium (Anticholinergic) - 21mcg, 2 actuations by inhalation via pMDI

b) Long acting bronchodilation

Moderate to severe COPD with people experiencing frequent dyspnoea

  • LABA - Eformoterol 12mcg, BD
  • LAMA - aclidinium 322mcg, BD

c) Inhaled corticosteroids

Recommended as add on therapy for patients with both FEV1 < 50% and >= 2 exacerbations requiring treatment with antibiotics or oral corticosteroids

  • Use in combination with LABA - Budosenide + eformoterol - 400mcg + 12mcg, BD
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15
Q

Complications of COPD

A
  1. cor pulmonale
  2. CO2 retention
  3. recurrent pneumonia
  4. pulmonary hypertension
  5. respiratory failure
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16
Q

Pathogens causing community acquired pneumonia

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Moraxella catarrhalis
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17
Q

Atypical community acquired pneumonia causes

A
  1. Mycoplasma pneumoniae
  2. Chlamydophila pneumoniae
  3. Legionella pneumophila
  4. Coxiella burnettis (Q fever - dust, animals)
  5. Burkholderia pseudomallae
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18
Q

Healthcare associated pneumonia pathogens

A
  1. CAP causes
  2. MRSA
  3. Pseudomonas aeruginosa
  4. Extended spectrum beta-lactamases
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19
Q

Chronic pneumonia pathogens

A
  1. Mycobacterium tuberculosis and non-tuberculosis mycobacteria
  2. Nocardia species
  3. Fungi - Pneumocystitis jivoreci, cryptococcus neoformans
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20
Q

Clinical signs of pneumonia

A
  • Elevated RR, tachycardia, reduced oxygen saturation
  • Percussion dull
  • Increased vocal resonance
  • Bronchial breathing
  • Course crackles
  • Pleural rub
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21
Q

Investigations for pneumonia

A
  1. Oxygen saturation (ABG if puse oximetry < 92%)
  2. Blood tests
    FBC - leukocystosis, CRP, LFT, UEC
  3. CXR - lobar or multi-lobar infiltrates
  4. Sputum MC+S
  5. Urine sample - legionella/ pneumococcal antigens
  6. Viral serology
  7. Pleural fluid culture
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22
Q

Assessing the severity of Pneumonia

(CURB-65, SMARTCOP, Pneumonia Severity Index)

A

CURB-65

  • Confusion (MSQ < 8/10)
  • Urea > 7mMol/L
  • RR > 30 bpm
  • sBP < 90 or dBP < 60mmHg
  • Age > 65yo

SMART-COP

  • SBP < 90mmHg
  • Multilobar CXR involvement
  • Albumin < 35g/L
  • RR > 25 bpm
  • Tachycardia > 125 bpm
  • Confusion
  • Oxygen saturation 93% or less
  • pH < 7.35

PSI

  • Demographic - Nursing home resident
  • Comorbidities - Neoplasm, liver disease, HF, stroke, renal failure
  • Physical examination - altered mental status, RR > 30, sBP < 90, Temp > 40 or < 35, HR > 125bpm
  • Lab and radiography - pH < 7.35, blood urea nitrogen > 30mg/ dL, Sodium < 130mmol/L, glucose > 250mg/dL, haematocrit < 30%, SpO2 < 60mmHg, pleural effusion
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23
Q

Treatment of CAP

A
  • Mild –> Amoxicillin 1g orally, 8 hourly, 5-7 days
  • Moderate –> Benzylpenicillin 1.2g IV, 6 hourly + doxycycline 100mg orally, 12 hourly, 7 days
  • Severe –> Ceftriaxone 1g IV, daily
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24
Q

The types of respiratory failure

A

Type 1 - Hypoxaemia

  • Characterised by an arterial oxygen tension (PaO2) < 60mmHg with a normal or low arterial CO2 tension. Most common form of respiratory failure.
  • Associated with acute respiratory disease e.g. APO, pneumonia, pulmonary haemorrhages

Type 2 - Hypoxaemia + Hypercapnia

  • Characterised by PaCO2 higher than 50mmHg
  • Causes include drug overdose, neuromuscular disease, chest wall abnormalities, asthma, COPD
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25
Q

Whats the difference between acute and chronic respiratory failure

A

Acute develops within minutes or hours, without renal compensation; therefore pH is less than 7.3. Chronic develops over days or longer and allows time for renal compensation and increase bicarbonate concentration; hence pH slightly decreased.

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26
Q

Causes of respiratory failure

Respiratory

  • Exacerbation of asthma
  • Pulmonary embolism
  • Pulmonary oedema
  • Acute respiratory distress syndrome
  • Pneumonia
  • Acute epiglottitis
  • Inhalation injury (toxins, CO, smoke)
  • Upper airway obstruction
  • Pneumothorax
  • Bronchiectasis
  • Alveolar abnormalities (emphysema)
  • Chest wall abnormalities
  • Malignancy
  • Decompensated CCF

Non-respiratory

  • Hypovolaemia
  • shock
  • severe anaemia
  • drug overdose
  • neuromuscular disorders
  • toxins
  • trauma - blood loss, spinal injury
A
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27
Q

Investigations for respiratory failure

A
  1. Pulse oximetry - SpO2 < 80%
  2. ABG - reduced pH, hypoxaemia, hypocapnia
  3. Serum bicarbonate - elevated in chronic
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28
Q

Clinical features of respiratory failure

A
  • dyspnoea
  • confusion
  • tachypnoea
  • stridor
  • cyanosis
  • asterixis
  • headache
  • hypoventilation
  • accessory muscle use
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29
Q

Treatment of respiratory failure

A
  1. Clear airways
  2. Supplement oxygen - nasal prongs, hudson mask, non-rebreather, venturi mask, continuous positive airway pressure
  3. Treat underlying cause

*People with Type II resp failure become desensitiesed to CO2 and hypoxia drives respiration. So for hypercapnic patients or ones with chronic lung disease (COPD) aim for SpO2 of 88-92%. For normocapnic patients e.g. acute asthma aim for 94-96%.

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30
Q

Classification of lung cancer

A
  1. Small Cell Lung Cancer (15%)
  2. Non-Small Cell Lung Cancer
    i) Adenocarcinoma (40%)
    ii) SCC (20-25%)
    iii) Large cell carcinoma (5-10%)
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31
Q

Symptoms of lung cancer

A

Pulmonary symptoms

  • Cough
  • Haemoptysis
  • Progressive dyspnoea
  • Chest pain

Recurring common colds in patients > 40 should always raise suspicion of lung cancer

Extrapulmonary symptoms

  • Constitutional symptoms (Weight loss, fever, weakness)
  • Clubbing of the fingers and toes
  • Signs of symptoms of tumour infiltration or compression of neighbouring structures
  • SVC –> dyspnoea, feeling of fullness in head, oedema of face and upper extremities, prominent venous pattern on the chest, face, upper extremities
  • Paralysis of the recurrent laryngeal nerve –> hoarseness
  • Paralysis of the phrenic nerve: results in diaphragmatic elevation and dyspnoea
  • Malignant pleural effusion: dullness on percussion, reduced breath sounds on the affected side
  • Dysphagia
  • Postobstructive pneumonia

Paraneoplastic Syndromes

  • Cachexia, increased risk of thrombosis (and lung embolism)
  • Dermatomyositis
  • Acanthosis nigricans

SCLC

  • Endocrine
  • Cushing syndrome (Hypercortisolism)
  • SIADH
  • Neurological
  • Lambert-Eaton syndrome
  • Paraneoplastic cerebellar degeneration
  • Peripheral neuropathy

NSCLC

  • Endocrine
  • Hypercalcaemia of malignancy (SCC)
  • Gynaecomastia (large cell carcinoma)
  • Other
  • Hypertrophic osteoarthropathy
  • Clubbing of the fingers and toes
  • Swelling and pain in joints and long bones
  • Hypercoagulability and thrombophlebitis migrans (adenocarcinoma)
  • Nonbacterial verrucous endocarditis (adenocarcinoma)

Symptoms of metastasis

  • Brain –> headaches, behavioural changes, seizures, focal motoric deficits
  • Liver –> nausea, jaundice, ascites
  • Adrenal gland: usually asymptomatic
  • Bones –> bone pain
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32
Q

Symptoms of a pancoast tumour

A

A peripheral lung carcinoma (usually NSCLC) that is located in the nerve superior sulcus of the lung; often involves the cervical sympathetic nerves and brachial plexus

Symptoms:

  • Severe, localised pain in the axilla and shoulder
  • Horner syndrome –> miosis, ptosis and anhydrosis
  • Atrophy of arm and hand muscles
  • Oedema of the arm, facial swelling, morning headaches
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33
Q

Invetigations for lung cancer

A
  1. CXR - solitary nodule, pleural effusion, mediastinam widening, atelactesis
  2. CT imaging
  3. PET scan
  4. Bronchoscopy and biopsy

Staging

  1. CT
  2. FBC, Calcium, LFTs, UEC
34
Q

Risk factors for PE

A
  • Immobility
  • Recent surgery
  • inherited hypercoaguability disorders e.g. Factor V leiden, Protein S/C def.
  • Pregnancy
  • HRT/ oral contraceptive
  • Malignany
  • Previous PE
  • Fat emolism –> major surgery, trauma - broken femur
  • Air embolism, amniotic fluid embolism
35
Q

Symptoms of a PE

A
  • Acute Dyspnoea
  • Pleuritic chest pain
  • haemoptysis and cough
  • dizziness
  • syncope
36
Q

Signs of PE

A
  • pyrexia
  • cyanosis
  • tachypnoea
  • tachycardia
  • Raised JVP
  • pleural rub
  • pleural effusion
  • decreased breath sounds
  • DVT symptoms - unilateral painful leg
37
Q

Invetigations for PE

A

Bloods

  • D-dimer
  • FBC - thrombocytopenia ?
  • U&E - anticoagulant doses
  • ABG - decreased PaO2 and PaCO2

Imaging

  • V/Q scan
  • CTPA, CXR
  • Doppler U/S
38
Q

Treatment for PE

A

Acute setting - Haemodynamically unstable

  1. Systemic fibrinolytic therapy
    Alteplase –> 10mg IV bolus, followed by 1.5mg/kg (up to 90mg) by IV infusion
  2. Surgical embolectomy or percutaneous transcatheter embolectomy

Haemodynamically stable

  1. NOAC - Apixiban 10mg orally, BD for 2 days, then 5mg BD
  2. LMWH - debigatran (need parenteral anticoagulation)
  3. Unfractioned heparin (in renal failure)
  4. Warfarin (INR 2-3 and give parenteral anticoagulation e.g. dalteparin or enoxaparin)
39
Q

Prevention of PE

A
  1. Compression stockings
  2. Early mobilisation post-surgery
  3. Stop HRT or contraceptive pill
  4. Anticoagulation e.g. LMWH (Dalteparin) or NOAC after knee/hip replacement
40
Q

Aetiology of bronchiolitis

A
  • RSV (Respiratory Syncytial Virus)
  • Parainfluenza virus, influenza virus
  • Adenovirus, Rhinovirus, Coronavirus
41
Q

Risk factors for severe disease in bronchiolitis

A
  • Premature
  • Congenital heart or lung disease
  • Neurological disease
  • Immunodeficiency
42
Q

Clinical features of bronchiolitis

A
  • Initially presents with URTI symptoms - rhinorrhoea
  • Fever
  • Cough
  • Respiratory distress - cyanosis, tachypnoea, nasal flaring, intercostal recession
  • Poor feeding in breastfed infants
  • Auscultatory findings - wheeze, crackles
43
Q

Treatment for bronchiolitis

A

Supportive

  • Hydration
  • Suppplemental oxygen
  • Relief of nasal congestion - humidifier, phenylephrine

Severe –> rivavirin

Prevention in infants risk of severe disease –> palivizumab

44
Q

Hospitalisation indications for a child with bronchiolitis/ respiratory problem

A
  • hypoxaemia
  • tachypnoea
  • impeding oral feeding or hydration
  • Respiratory distress
  • impending respiratory failure
45
Q

Causes of Intestitial lung disease

A
  1. Idiopathic
  2. Pneumoconioses - asbestosis, silicosis
  3. Radiation pneumonitis
  4. Pharmacological - Amiodarone, methotrexate, bleomycin, nitrofurantoin, adalimumab
  5. Connective tissue disease - SLE, RA, Sarcoidosis, Scleoderma, Sjogrens
  6. Tuberculosis
  7. Legionellosis
  8. Granulomatous ILD - sarcoidosis, granulomatosis with polyangitis, eosinophilic granulomatosis
  9. Bronchoalveolar carcinoma
46
Q

Signs and smyptoms of interstitial lung disease

A

Signs

  • fine crackles
  • reduced chest expansion
  • cyanosis
  • clubbing
  • dull percussion
  • signs of CT disorder

Symptoms

  • fatigue
  • weight loss
  • progressive dyspnoea
  • non-productive cough
  • arthralgia and myalgia
47
Q

Investigations for interstitial fibrosis

A
  1. Pulmonary function tests - restrictive lung disease (FEV1/FVC above 0.7)
  2. CXR - reticular opacities
  3. CT - irregular thickening, honeycombing
  4. Bronchoscopy
  5. Investigate causes e.g. ANA for SLE
48
Q

Treatment fo Interstitial lung disease

A
  • Limit exposure to toxic substance (cease drug therapy causing it)
  • Antibiotics for infections
  • Lung transplant in end stage
  • oxygen for symptomatic relief
49
Q

Classification of aspiration

A
  1. Aspiration pneumonitis - chemical injury after aspiration of gastric contents
  2. Aspiration pneumonia - infecious process secondary to aspiration of pro-gastric contents colonised with bacteria
50
Q

Treatment of aspiration

A
  1. immediate positional drainage - place semiprone and tilted to a 30 degree head down position
  2. oropharyngeal suctioning
  3. endotracheal intubation + nasogastric tube (to empty stomach)
  4. bronchoscopy and endotracheal suctioning
  5. Antibiotics e.g. levofloxacin 500mg IV or ceftriaxon 1-2g
  6. Positive-pressure ventilation
51
Q

Pathophysiology of a tension pneumothorax

A

Tension pneumothorax develops when there is a disruption of the visceral or parietal pleura or tracheobronchial tree. Injured tissue forms a one-way valve allowing air inflow with inhalation into the pleural space & prohibiting outflow. The volume of air in the pleural space increases with each inspiration. Pressure rises in the affected hemithorax causing:

  • Ipsilateral lung collapse & hypoxia
  • Contralateral mediastinal shift
  • Collapsed lung compresses the unaffected side further compromising gas exchange
  • Kinking of the IVC & compression of the thin atrium walls
  • ↓ venous return & impaired venous return to the right atrium
52
Q

Causes of pneumothorax

A
  • Spontaneous - primary or seconary to pulmonary disease
  • Trauma
  • Iatrogenic e.g. needle aspiration
  • CT disorder - Marfans, Elhers-Danlos
  • Carcinoma
53
Q

Signs of pneumothroax

A
  • Asymmetric lung expansion
  • Tracheal deviation to contralateral side
  • Absent breath sounds
  • Decreased vocal fremitus
  • Hyper-resonance to percussion
  • Hypotenion, tachypnoea
  • pulsus paradoxus
54
Q

Treatment of pneumothorax

A
  1. For simply pneumothorax
    * (Small < 3 cm between lung and chest wall) – usually resolves spontaneously
    * (Larger or small and symptomatic) – oxygen supplementation, supine positioning, tube thoracostomy
  2. Open pneumothorax
    * Partially occlusive dressings followed by thoracostomy
  3. Tension pneumothorax
    * Emergency chest decompression via chest tube placement or needle thoracotomy followed by chest tube placement

Triangle of saftey for insertion of chest drain à nipple line, axilla, anterior latissimus dorsi, alteral pectoralis major

55
Q

Causes of Obstructive Sleep Apnoea

A
  • Obesity, especially around the neck
  • Alcohol
  • Intake of sedatives or Beta-blockers before sleep
  • Structural abnormalities that impair respiratory flow
  • Smoking
  • Family history
  • Hypothyroidism
56
Q

Symptoms of OSA

A
  • Restless sleep with waking, gasping or chocking
  • Loud, irregular snoring with apnoeic episodes
  • excessive daytime sleepiness
  • impaired cognitive function (impaired concentration, memory loss)
  • Depression, decreased libido
57
Q

Diagnostics tests in OSA

A

Sleep Studies

  1. Polysomnography (first line)
  • Apnoea and hypopnoea events
  • Oxygen desaturation
  • Arousal events on ECG
  • Bradycardia
  • Fragmentation of sleep with pathological reduction of REM-sleep phases and slow-wave sleep
  1. Home sleep apnoea testing (less sensitive) – ambulatory screening method based on the use of a device for monitoring cardiorespiratory parameters during the night

Lab tests not usually needed but can do

  1. FBC
    * Polycythemia à this occurs because hypoxia induces EPO secretion by the kidneys, which stimulate the blood marrow, leading to increased RBC production
  2. TSH
    * May be considered in patients with possible hypothyroidism
58
Q

Treatment of OSA

A

Simple things to do:

  1. Weight reduction
  2. Avoidance of alcohol and drugs that affect sleep
  3. Increased time in bed
  4. Positional therapy – sleeping on the side can improve nocturnal sleep and lessen daytime dysfunction
  5. Reduced nasal resistance – with smoking cessation and using intranasal corticosteroid spray

Escalating therapy:

  1. Continuous positive airway pressure
    Indications –> Severe OSA, moderate with symptoms of daytime dysfuncitoning or hypertension and CVD
59
Q

Causes of Bronchiectasis

A

Bronchiectasis is the permanent dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall. It is often caused as a consequence of recurrent and/or severe infections secondary to an underlying disorder.

  1. Pulmonary infections
    * Chronic infections e.g. TB
  2. Bronchial narrowing or other forms of obstruction
  • COPD
  • Aspiration
  • Tumours
  1. Disorders of secretion clearance or mucous plugging
  • Cystic fibrosis
  • Primary ciliary dyskinesia
  • Allergic bronchopulmonary aspergillosis
  1. Immunodeficiency
  2. Chronic inflammatory disease
  • RA
  • Crohn’s disease

Sjogren syndrome

60
Q

Symptoms and signs of bronchiectasis

A

Symptoms

  • Chronic productive cough with copious mucropurulent sputum
  • Rhinosinusitis
  • Dyspnoea
  • Haemoptysis
  • faigue, weight loss, pallor

Signs

  • Clubbing
  • Low pitched course inspiratory crepitations
  • Wheeze
  • Cor pulmonale
61
Q

Investigations for bronchiectasis

A
  1. CXR – inflammation and fibrosis of bronchial walls lead to the appearance of parallel lines
  2. CT – dilated bronchi with thickened walls, cysts
  3. Sputum culture and smear – to determine infectious cause
  4. FBC – anaemia of chronic disease, increased WBCs
  5. HIV testing, genetic testing for CF
  6. Pulmonary function test – obstructive pulmonary disease–> Lung diseases associated with increased resistance to airflow (e.g., COPD, bronchial asthma, bronchiectasis). Patients with obstructive lung disease have decreased FEV1, an FEV1:FVC ratio < 0.7, decreased vital capacity, increased residual volume (due to air trapping), and normal or increased total lung capacity.
  7. Bronchoscopy – visualise tumours, foreign bodies, other lesions
62
Q

Treatment for bronchiectasis

A

Bronchiectasis is a permanent anatomical malformation and therefore cannot be cured. However, symptoms and advancement of the disease can be controlled. The treatment of any underlying cause is also very important.

Conservative:

  1. Smoking cessation
  2. Antibiotic therapy of exacerbation
  3. Bronchopulmonary hygiene and chest physiotherapy
  4. Vaccinations
  5. Bronchodilators, corticosteroids and nebulized hypertonic saline are not routinely used but can be considered

Invasive

  1. Surgical resection of bronchiectasis lung or lobectomy: indicated in pulmonary haemorrhage, inviability of bronchus, and substantial sputum production in unilateral bronchiectasis
  2. Pulmonaryy artery embolization – indicated in pulmonary haemorrhage
  3. Lung transplant in severe disease
63
Q

Difference between pneumonia and acute bronchitis

A

Bronchitis refers specifically to infections causing inflammation in the bronchial airways, whereas pneumonia denotes infection in the lung parenchyma resulting in consolidation of the affected segment or lobe.

64
Q

Causes of acute bronchitis

A

Usually follows a preceding URTI

>90% are from viral infection

  • influenza A and B, RSV, rhinovirus, coronavirus, adenovirus, parainfluenza

Bacterial

  • M. pneumoniae, S. pneumoniae, H. influenzae, Pertussis, Chlamydia Pneumoniae
65
Q

Symptoms of acute bronchitis

A

Clinical diagnosis - MacFarlane criteria:

  • Acute illness of <21 days
  • Cough as predominant symptom
  • At least one other LRT symptom such as sputum production, wheezing, chest pain

No other alternative explanation

66
Q

What are the two types of fluid that can accumulate in the pleural cavity (Pleural effusion) and what causes each

A
  1. Transudate

Too much fluid leaves capillaries due to decreased oncotic pressure or increased hydrostatic pressure in the pulmonary capillaries

  1. Increased hydrostatic pressure – Heart failure –> increase pressure in pulmonary circulation –> fluid forced out of capillaries into pleural space
  2. Decreased oncotic pressure – Cirrhosis (less albumin) OR Nephrotic syndrome (proteins lost in urine) –> decreased OP in fluid from blood vessels –> pleural space
  3. Exudate

Alteration in local lung factors. Inflammation of the pulmonary capillaries –> leaky capillaries, fluid –> immune cells and proteins leak out and into the pleural space

e.g. infection, trauma, malignancy, inflammatory conditions

67
Q

Signs and symptoms of pleural effusion

A

Signs

  • Stony Dullness to percussion
  • Decreased breath sounds
  • decreaced vocal fremitus
  • Diminished chest expansion
  • Contralateral tracheal deviation
  • pleural friction rub
68
Q

Investigations for pleural effusion

A
  1. Imaging
  • CXR – blunting of costophrenic angle, homogenous density with meniscal-shaped margin
  • U/S – very sensitive, can detect amounts as low as 20mL
  • CT – most sensitive
  1. Thoracentesis
    * Removal of fluid from the pleural space for diagnostic (transudate vs exudate) and/ or therapeutic process
69
Q

Lights criteria

A

Exudate if at least 1 of the following:

  1. Fluid protein: serum protein ratio >0.5
  2. Fluid LDH: Serum LDH > 0.6
  3. Fluid LDH > 2/3 normal upper limit of serum LDH

Transudate = clear, Exudate = cloudy, Lymph = milk coloured

70
Q

Treatment of pleural effusion

A
  1. Treat underlying condition e.g. loop diuretic for acute LHF or antibiotics for pneumonia or empyema drainage
  2. Symptomatic Tx
  3. Tube thoracostomy – for recurrent pleural effusions
  4. Video-assisted thoracoscopic surgery
  5. Pleurodesis – for malignant effusions or ones that don’t respond to drugs
71
Q

Who does croup affect and what causes it

A

6 months - 3 years

Cause –> Parainfluenza virus (75%), RSV, adenovirus, influenza

72
Q

Symptoms of croup

A

Prodromal phase, 1-2 days duration of:

  • Rhinitis with nasal discharge and congestion
  • Low-grade fever
  • Possible erythematous pharynx

Laryngotracheal inflammation phase, 2-7 days duration of:

  • Symptoms occur during the evening/ night

Mild

  • Barking cough
  • Hoarseness
  • Mild inspiratory stridor due to subglottic narrowing

Moderate

  • Dyspnoea at rest
  • Pronounced thoracic retractions
  • Pallor
  • Tachycardia > 160bpm

Severe

  • Severe tachydyspnoea at rest with increasing respiratory failure
  • Cyanosis
  • Hypoxaemia
  • Bradycardia
  • Altered mental status
  • May result in pulsus paradoxus secondary to upper airway obstruction
73
Q

Treatment for croup

A

Mild

  1. Cool mist inhalation
  2. Placing infant to sleep in an upright position
  3. Breathing cool air at night
  4. Dexamethasone
  • Reduces airway swelling within 6 hours
  • Dexamethasone 0.15 mg/kg orally, as a single dose

Moderate to severe

  1. Hospitalized – if presence of stridor at rest à ICU
  2. Inhaled racemic epinephrine
  • Reduces airway swelling, faster onset than dexamethasone
  • Adrenaline 0.1% solution 5mL by inhalation via nebuliser Plus dexamethasone
  1. Humidified air or oxygen if necessary
  2. IV fluids to prevent hydration
  3. Intubation is indicated when the airway compromise is imminent
74
Q

Treatment for cystic fibrosis Add

A

Respiratory

  • Hypertonic saline nebulization
  • Improves lung function, reduces acute infective exacerbations and is safe
  • Bronchodilator therapy e.g. albuterol
  • Chest physiotherapy
  • Mucolytics (e.g. N-acetylcysteine)
  • Domase alfa 2.5mg by inhalation via nebuliser OD – reduced viscosity of CF sputum
  • In chronic rhinosinusitis à intranasal glucocorticoids
  • In chronic respiratory insufficiency
  • Long-term oxygen inhalation therapy
  • Lung transplant

Diet

  • Additional sodium chloride intake
  • High-energy diet to compensate for increased demand
  • Pancreatic enzyme supplements
  • Oral supplements – ADEK vitamins

Treatment of pneumonia

  • Infants à Staph aureus – IV vancomycin
  • Adults à pseudomonas aeruginosa – Inhaled tobramycin

Preventative measures

  • Annual flu vaccine
  • Pneumococcal vaccine
  • Palivizumab – antibody against RSV for infants < 2 years
75
Q

Pathophysiology of cystic fibrosis

A

Mutated CFTR gene –> defective chloride channel –> inability to transport intracellular chloride ions across the membrane –> exocrine glands (Sweat, mammary, salivary glands) produce hyperviscous secretions –> accumulation of secretions and blockage of exocrine glands –> chronic inflammation –> organ damage

76
Q

Investigations for cystic fibrosis

A
  1. Neonatal screening
  2. ­ Immunorective trypsinogen (IRT)
    * detects elevated levels of IRT on heel-prick blood
  3. DNA assay
    * Identify common CFTR mutation
  4. Lab tests
  5. Quantitative pilocarpine iontophoresis (sweat test) is gold standard
    * Chloride levels > 60 mmol/L on two or more occasions
  6. DNA analysis
  • Prenatal – if both parents carry use chronic villous sampling or amniocentesis
  • Postnatal/ adult – if sweat test negative in patient with suspected CF

Supportive tests

  1. Hypochloremic alkalosis may occur (due to NaCl wasting)
  2. Stool: decrease in chymotrypsin and pancreatic elastase
  3. CXR/ CT –> hyperinflation
  4. Pulmonary function test –> decrease in FEV1/FVC
  5. U/S –> fatty liver
77
Q

Clinical features of cystic fibrosis

A

GI symptoms - present frequently at infancy

  • Meconium ileus
  • failure to thrive
  • pancreatic disease - steatorrhoea, malabsorption, abdominal distention, ADEK def.
  • liver cirrhosis, biliary cirrhosis, chololithiasis
  • Intestinal obstruction

Respiratory symptoms - frequent in adulthood

  • Obstructive lung disease with bronchiectasis
  • chronic sinusitis
  • recurrent or productive cough and pulmonary infections

Sweat glands –> salty tasting sweat

MSK –> Kyphoscoliosis,osteopenia

Urinary –> UTIs, nephrolithiasis

Genital

  • Undescended testicle, vas deferens may be absent
  • amenorrhoea, viscous cervical mucus
78
Q

Cause of laryngomalacia and tracheomalacia

A

Laryngomalacia –> congenital

Tracheomalacia –> congenital, long-term intubation, recurring inflammation and infection

79
Q

Clinical features of laryngomalacia

A
  • Usually happy and thriving infants
  • inspiratory stridor - worsens in supine position, during crying, URTI, agitation and feeding
  • reflux may be present
  • failure to thrive

Omega shaped epiglottis on flexible laryngoscopy

80
Q

Drugs causing apnoea

A

CNS depressants

  • narcotic analgesics
  • benzodiazepines
  • barbituates

Respiratory muscle dysfunction

  • neuromuscular blockers
  • aminoglycoside antibiotics

Myopathy

  • corticosteroids
  • diuretics
81
Q

Drug induced causes of pulmonary oedema

A
  1. Cardiogenic Pulmonary oedema
  • Excessive IV fluids
  • Blood and plasma transfusion
  • Corticosteroids
  1. Non-cardiogenic pulmonary oedema
    * Narcotic analgesics (IV heroin)
82
Q

Why can a beta-blocker be hazardous to a person with asthma

A

B2 antagonism causes bronchoconstriciton

Medicine (11 decks)

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