Respiratory

Topics
28. Community-acquired pneumonia
29. Hospital-acquired pneumonia
30. Pulmonary tuberculosis
31. Extrapulmonary tuberculosis
32. Bronchial asthma – classification, therapy, and prevention
33. Acute bronchial asthma (status asthmaticus)
34. Chronic bronchitis, bronchiectasis
35. Chronic obstructive pulmonary disease (COPD) – diagnosis and therapy in a stable patient

36. Acute exacerbation of the chronic obstructive pulmonary disease

37. Idiopathic pulmonary fibrosis
38. Lung cancer
39. Pleural effusions
40. Pneumothorax
41. Acute and chronic respiratory insufficiency
28. Community-acquired pneumonia
• Streptococcus pneumoniae (commonest), Haemophilus influenzae, Moraxella catarrhalis, S. aureus. Give
amoxicillin.
• Atypicals: Mycoplasma pneumoniae, Legionella species, and Chlamydia. Could also be viral.
• Fever, rigors, malaise, anorexia, dyspnea, cough, purulent sputum, hemoptysis, and pleuritic pain.
Confusion in elderly. Cyanosis.
• High respiratory rate, high urea, low BP = severe pneumonia.
• Signs of lung consolidation (reduced expansion, dull percussion, crackles, tactile fremitus, bronchial
breathing).
• Pleural effusion.
• Check SpO2/BP because complications of pneumonia are type 1 respiratory failure, hypotension. Other
complications are empyema and lung abscess.
• Order urine for strep pneumoniae antigen.
• Order CBC, blood culture, and U&E (high urea = severe).
• Diagnose with Xray/sputum culture.
• Use CRP to guide ABx treatment.
29. Hospital-acquired pneumonia
• If the pneumonia occurs 48 hours after admission. Most commonly E.
coli or Staph aureus. Also Pseudomonas, Klebsiella, Bacteroides, and
Clostridia.
• In early onset (less than 4 days), patients still commonly get H.
Influenza, S. Pneumoniae, M. Catarrhalis.
• Aminoglycoside IV + antipseudomonal penicillin IV.
30/31. Pulmonary/extrapulmonary TB
• Active infection occurs when the immune system is compromised. It can arise from primary infection, or
re-activation of previously latent disease.

• TB can affect any organ in the body. Likes to infect lymph nodes (lymphadenitis), pleura (pleuritic), liver
(hepatitis), brain (meningitis), spine (Pott disease), and other bones (osteomyelitis), Colon (strictures,
adhesions, obstructions).
• Miliary TB is hematogenous spreading of small granulomatous tissue, with small millet seed appearance
on lung, and it can spread to whole body especially the meninges (meningitis).

• Order an xray (cavitation, pleural effusion, fibronodules, lymphadenopathy, calcification in the upper
lobes), PPD skin test, IFN-gamma test, sputum culture.
• Prevent using BCG vaccine.
• Treat: isoniazid, rifampin, pyrazinamide, ethambutol for 2 months. Then switch to just isoniazid and
rifampin for 4 months.
32/33. Bronchial asthma
• Classification: atopic (classical), non-atopic (viral), aspirin-induced,
occupational, exercise-induced.
• Signs + symptoms + diagnosis  FA p638.
- Diurnal variation: symptoms vary in severity throughout the day.
- Exercise tolerance, acid reflux, disturbed sleep.
- Hyperinflated chest (low PaO2; low PaCO2). Hyper-resonant. Low FEV1.
- Skin-prick tests may help to identify allergens.
- In acute attacks, order an ABG + xray (to exclude infection).
• Therapy  FA p649.
• Prevention.
• Status asthmaticus (acute asthma) = FA p638.
34. Chronic bronchitis, bronchiectasis
• Chronic bronchitis: productive cough for over 3 months in the span of
2 years.
- Reid index over 50%. Hypertrophy of mucosal glands.
- Patient has cyanosis, dyspnea, wheezing, crackles, CO2 retention (in ABG), and
secondary polycythemia. Can lead to cor pulmonale.
- Normal RR, unlike emphysema (which is high RR).
• Low FEV1/FVC ratio (below 70%) is hallmark of COPD.
• Main risk factor of COPD is smoking.
Cont.
• Bronchiectasis: chronic infection of bronchi/bronchioles 
permanent dilation of bronchi/bronchioles.
- Caused by cystic fibrosis, kartagener syndrome, tumor or some other
obstruction, infections (usually).
- Patient will have cough, dyspnea, and smelly sputum.
- Can lead to cor pulmonale.
- Patient can also have finger clubbing and hemoptysis.
35. (COPD) – diagnosis and therapy in a stable patient
• Diagnosis:
- Clinical (cough, dyspnea, cyanosis in chronic bronchitis, weight loss and pursed lips in emphysema).
- Spirometry.
- X-ray (emphysema bullae  pneumothorax).
- ECG (cor pulmonale).
- ABG (low O2 with high CO2, especially in chronic bronchitis).
- CBC (polycythemia in chronic bronchitis).
- CT (lung enlargement in emphysema).
• Therapy:
- Stop smoking!
- Diet/exercise.
- Mucolytics for chronic bronchitis.
- B2 agonists (both salbutamol and salmeterol).
- Anticholinergic drugs (ipratropium + tiotropium).
- Inhaled corticosteroids (budesonide) may be added.
• Therapy in acute exacerbation:
- Salbutamol and ipratropium.
- IV corticosteroids (methylprednisolone) and Abx (amoxicillin) are added mainly in acute exacerbation.
- Consider O2 therapy, especially in acute exacerbation. Try to keep it over 90%. Adjust via ABG.
- Noninvasive positive-pressure ventilation (NPPV) if there is respiratory acidosis or CO2 retention in acute exacerbation.
- Intubation and mechanical ventilation may be required if the above do not stabilize the patient.
36. Acute exacerbation of COPD
• Definition: A persistent increase in dyspnea which is triggered by infection.
• Increased sputum production and increased cough are common.
• Acute COPD exacerbation can lead to acute respiratory failure requiring hospitalization, and
possibly mechanical ventilation; potentially fatal.
• Order ABG, CBC, Xray (pneumothorax or infection), sputum culture, blood culture if fever.

• Therapy in acute exacerbation:

- Salbutamol and ipratropium.
- IV corticosteroids (methylprednisolone) and Abx (amoxicillin) are added mainly in acute
exacerbation.
- Consider O2 therapy, especially in acute exacerbation. Try to keep it over 90%. Adjust via ABG.
[Be careful in chronic bronchitis because they are insensitive to CO2 due to retention. They rely
on hypoxia for RR regulation. So if you give too much O2 to them, their RR will drop!]
- Noninvasive positive-pressure ventilation (NPPV) if there is respiratory acidosis or CO2 retention
in acute exacerbation.
- Intubation and mechanical ventilation may be required if the above do not stabilize the patient.
37. Idiopathic pulmonary fibrosis
• Repeated cycles of lung injury  wound healing (collagen deposition, and thus
fibrosis).
• Results in end-stage “honeycomb lung” and digital clubbing.
• Reason for lung injury is unknown.
• Symptoms: dry cough, fine crackles during inspiration.
• Complications: respiratory failure, lung cancer.
• Order an ABG, CRP, Anti-nuclear antibody (ANA), x-ray (lower lung volume,
honeycomb lung), CT (same as x-ray but better), spirometry (high FEV1/FVC ratio),
lung biopsy.
• Treat by supportive care: oxygen, chest rehab. In the end, lung transplant needed.
38. Lung cancer
• FA p647.
• Pathoma p95.
• Symptoms: Cough, haemoptysis, dyspnea, chest pain, weight loss, digital
clubbing.
• Spreads to adrenals, brain, bone, liver (jaundice, hepatomegaly).
• Diagnosis: x-ray (presents as nodular coin-lesion), CT scan (for staging and
revealing lymphadenopathy and further metastasis in the body).
- Could be consolidation/pleural effusion/collapse on x-ray.
- Order cytology of sputum and pleural fluid.
- Fine needle aspiration or biopsy.
- Bronchoscopy to assess histology and if its operable or not.
• Treat small cell carcinoma with chemo + radiation. Treat non-small cell carcinoma
with surgery.
39. Pleural effusions
• Excess accumulation of fluid between pleural layers  lung cannot expand fully during
inspiration. Must be pumped out with thoracentesis.
• Could be transudate, exudate, or lymphatic in nature.
- Transudate due to HF, nephrotic syndrome, or cirrhosis (microalbuminuria).
- Exudate is due to malignancy, pneumonia, trauma (vascular permeability). Must be drained, otherwise
risk of infection.
- Lymphatic (chylothorax) due to thoracic duct injury from trauma or malignancy.
• Transudate has low protein content (below 25g/L). Exudate has high protein content
(over 35g/L) and is cloudy. Lymphatic has high fat content and milky.
• Patient can be asymptomatic, or dyspnea with pleuritic chest pain.
• Order an x-ray (blunting of the costophrenic angles).
• Also order an ultrasound which will guide the drainage  check cytology for WBCs, and
check chemistry for protein, pH, glucose, LDH.
• Decreased breath sounds, dull percussion, decreased tactile fremitus, if large tracheal
deviation away from side of lesion.
40. Pneumothorax
• FA p643-644.
• Pathoma p98.
• Can cause severe deterioration of COPD in patients (different from
acute exacerbation of COPD, which is due to bacterial or viral
infection).
41. Acute and chronic respiratory insufficiency
• Respiratory failure occurs when gas exchange is inadequate, resulting in hypoxia.
• It is defined as a PaO2 less than 8kPa and subdivided into two types according to PaCO2 level (normal or low = type 1 RF;
hypercapnia = type 2 RF).
• So, in Type 2, PaO2 is below 8kPa. PaCO2 is over 6kPa.
• Alternatively, hypoxia is PaO2 below 60mmHg. Hypercapnia is PaCO2 over 50mmHg.

• Type 1 is due to V/Q mismatch (pneumonia, pulmonary edema, PE, asthma, emphysema, pulmonary fibrosis, ARDS).
• Type 2 is due to hypoventilation (asthma, COPD, sedative drugs, trauma, neuromuscular diseases, CNS tumor, trauma,
kyphoscoliosis), with or without V/Q mismatch.
• Patient will be hypoxic (cyanosis, dyspnea, confusion, polycythemia, pulmonary HTN  cor pulmonale).
• Patient might be hypercapneic (headache, peripheral vasodilation, tachycardia, bounding pulse, tremor, coma). Patient’s
blood pH will be acidic due to respiratory acidosis.
• Inability to speak in complete sentences, use of accessory muscles of respiration.
Cont.
• Order blood tests (CBC, U&E, CRP, ABG, pH). ABG and pH can show
respiratory acidosis in type 2 RF.
• Order X-ray, sputum culture, blood culture if fever, spirometry (COPD).
• Treatment:
- Type 1: treat underlying cause. Give oxygen. Assisted ventilation if
hypoxic.
- Type 2: may be insensitive to CO2 and reliant on hypoxia to influence RR,
so be careful with the oxygen therapy. Guide the oxygen therapy with
ABG. Maybe NPPV. If fails, consider intubation and ventilation.
Cont.
• Acute type 2: happens very fast in minutes to hours, so the
hypoventilation will cause respiratory acidosis. pH will be low.
• Chronic type 2: happens over days so renal compensation will start
working, so pH will not be as low and bicarbonate concentrations will
be higher.
• Cannot distinguish acute and chronic type 1 RF via ABG. The clinical
markers of chronic hypoxemia, such as polycythemia or Cor
pulmonale, suggest a chronic disease.