Respiratory Flashcards
Define Chronic Obstructive Pulmonary Disease (COPD)
Poorly reversible airflow limitation, usually progressive and persistent inflammatory response.
Define Asthma
Reversive obstruction of the airways.
Bronchospasm and excessive airway secretions.
Types of COPD
Types of asthma?
Blue Bloaters and Pink Puffers.
Extrinsic and intrinsic
How does COPD clinically present?
Respiratory: Chronic cough,
exertional breathlessness,
regular sputum production, wheeze.
Other: Abnormal posture (leans forward),
drowsiness/mental confusion,
underweight, ankle oedema.
How does Asthma clinically present?
Wheeze, dyspnoea, chest tightness, cough (particularly if after exercise/cold air/allergen).
Hx: FH of asthma, past hx of atopy, regular episodes.
Paroxysmal.
What does blue bloaters refer to?
Compensatory …….
Chronic bronchitis is underlying pathology.
Compensatory increase in cardiac output leads to hypoxia.
What does pink puffers refer to?
Compensatory.
Emphysema underlying pathology.
Compensatory hyperventilation prevents hypoxia.
What causes extrinsic asthma?
External factors.
What causes intrinsic asthma?
Idiopathic.
Cause of COPD
Chronic inflammation of the airways.
Usually by smoking, also occupational irritants.
This causes the mucous gland hypertrophy, and increase in neutrophils, macrophages and lymphocytes in airways
-> Increase in inflammatory mediators (recurrent cycle)
-> Breakdown of lung tissue.
Cause of Asthma
Largely unknown.
Two main categories: Atopy: IgE antibodies readily produced against common exposures.
Increased responsiveness of airways to inhaled stimuli: histamine and methacholine.
Diagnostic test for COPD
Spirometry, CXR: >6 ribs visible (hyperinflation).
Diagnostic test for Asthma
History and evidence of obstruction (PEF / Spirometry) during episodes.
Treatment of COPD
Stop smoking (slows deterioration).
1: SABA or short-acting antimuscarinic
2: +LABA / + long acting antimuscarinic
3: Inhaled glucocorticoid
4: Long-acting antimuscarinic + LABA + Inhaled steroid
5: + Long term oxygen therapy (care not to remove hypoxic drive in blue bloaters).
Treatment of Asthma
SABA
-> Corticosteroids
-> LABA
-> Increase dose of corticosteroids
-> prednisalone
-> hospital.
Complications of COPD
Respiratory failure.
Complications of Asthma
Pneumonia,
pneuomothorax.
Define Rhinitis
Sneezing attacks,
nasal discharge
or blockage for more than 1 hour most days.
Define Bronchiectasis
Permanent dilatation and thickening of the airways.
Types of Rhinitis
Seasonal.
Perennial.
How does seasonal rhinitis clinically present?
Seasonal sneezing attacks, in response to allergens.
Rhinorrhoea and nasal congestion.
Itchy eyes.
How does perennial rhinitis clinically present?
All year round sneezing attacks in response to allergens.
Rhinorrhoea and nasal congestion.
How does Bronchiectasis clinically present?
Variance: Intermittent episodes of expectoration and infection
—> persistent daily expectoration of purulent sputum.
Resp symptoms: chest pain, dyspnoea and haemoptysis.
May present as persistent asthma.
Signs: Coarse crackles, wheeze possible.
When does seasonal rhinitis occur?
Hay fever’ occurs during summer months.
When does perennial rhinitis occur?
Occurs throughout the year.
Cause of seasonal rhinitis
Allergy to grass and tree pollen
and a variety of mould spores from cultivated plants.
Cause of perennial rhinitis
Allergens include house mites or domestic pets.
Cause of Bronchiectasis
Chronic inflammation of airways: large number of causative conditions;
Asthma, post-infection, immunodeficiency.
Diagnostic test for Rhinitis
Skin prick test with extensive medical history.
Diagnostic test for Bronchiectasis
HRCT: Bronchial wall dilation.
Thickening harder to define.
CXR: Exclude other causes.
Treatment of Rhinitis
Avoidance of allergens.
If practical; anti-histamines.
Treatment of Bronchiectasis
Prevent further deterioration.
Stop smoking.
Physiotherapy: Airway clearance.
Medication: Antibiotics, bronchodilators (if airflow obstruction).
Surgery: Lung resection.
Complications of Rhinitis
Reduced quality of life.
Sinusitis.
Complications of Bronchiectasis
Repeated infection,
respiratory failure,
pneumothorax (from coughing).
Sequelae of Rhinitis
Asthma.
Define Cystic fibrosis
Mutated CFTR Cl transport
-> Dysfunction of secretions
-> multiple organ dysfunction.
Define Sarcoidosis
Multisystem chronic inflammatory condition
- formation of non-caseating epithelioid granulomata.
Types of Cystic fibrosis
Various mutations.
Most common DF508.
How does Cystic fibrosis clinically present?
Infancy: Recurrent resp infections, diarrhoea, failure to thrive,
rectal prolapse, nasal polyps, acute pancreatitis,
portal hypertension, variceal haemorrhage, steatorrhoea.
Adults: Recurrent resp infections, atypical asthma, bronchiectasis,
male infertility (congenital bilateral absence of vas deferens),
heat exhaustion, portal hypertension, steatorrhoea.
Signs: Finger clubbing, cough with purulent sputum, crackles,
wheezes, resp obstruction
How does Sarcoidosis clinically present?
50% of time, asymptomatic; incidental CXSR discovers.
Can affect any organ.
Tends towards lungs, eyes and skin.
Lung (>90% of cases): Dyspnoea, non-productive cough.
Skin: Erythema nodosum.
Eye: Granulomatous uveitis.
What is significant about cystic fibrosis?
Most common inherited condition.
What is sarcoidosis the most common cause of?
Lung granulomas.
Pathophysiology of Sarcoidosis
Non-caseating granulomata form at various sites in the body, particularly the thoracic cavity, skin and eyes.
Bilateral hilar lymphadenopathy and/or pulmonary infiltrations.
Cause of Cystic fibrosis
Autosomal recessive.
Various mutations.
Most common DF508.
Cause of Sarcoidosis
Unknown.
Diagnostic test for Cystic fibrosis
Sweat test (98% sensitive),
genetic testing,
sinus X ray (opacification of sinuses)
Diagnostic test for Sarcoidosis
CXR, High serum ACE.
Treatment of Cystic fibrosis
Resp: Chest physio 2qd, prophylactic antibiotics, bronchodilators
Nasal polyps: Steroids, poss. Polyopectomy
Endocrine: Pancreatic enzymes.
General: High protein intake, genetic counselling
Treatment of Sarcoidosis
If no pulmonary infiltration: No treatment; remits in 2/3s of cases in two years.
If pulmonary infiltration: prednisalone.
Complications of Sarcoidosis
Respiratory failure and renal damage.
10% risk of death in black people.
Sequelae of Cystic fibrosis
Osteoporosis,
psych problems.
Define Idiopathic pulmonary fibrosis
Fibrosis of lung interstitium causing restrictive respiratory defect.
Define Pulmonary hypertension
Increase in mean pulmonary arterial pressure (>20mmHg).
How does Idiopathic pulmonary fibrosis clinically present?
Breathlessness, non-productive cough.
Finger clubbing (2/3) inspiratory basal crackles.
Eventually leading to: resp failure, pulmonary hypertension, cor pulmonale.
How does Pulmonary hypertension clinically present?
Exertional dyspnoea, lethargy and fatigue (inability to ^CO with exercise).
Once Rt Vent failure develops:
Peripheral oedema and abdominal pain (hepatic congestion).
Pathophysiology of Idiopathic pulmonary fibrosis
Patchy fibrosis of interstitium,
minimal or absent inflammation,
acute fibroblastic proliferation and collagen deposition.
Pathophysiology of Pulmonary hypertension
Depends on aetiology. Increase in pulmonary vascular resistance
-> Increase in mean pulmonary arterial pressure.
If chronic, this can cause damage to vasculature and further disease.
Cause of Idiopathic pulmonary fibrosis
Idiopathic.
Cause of Pulmonary hypertension
Various causative conditions
-> Increase in pulmonary vascular resistance.
Hereditary, idiopathic, SLE, HIV, Portal hypertension.
Diagnostic test for Idiopathic pulmonary fibrosis
CXR: Ground Glass appearance => honeycomb lung.
(CT :most sensitive).
ABG: hypoxia normal CO2.
Spirometry. ANA and RF Ab in 1/3.
Diagnostic test for Pulmonary hypertension
CXR: Enlarged pulmonary arteries.
ECG: Ventricular hypertrophy.
Treatment of Idiopathic pulmonary fibrosis
High dose prednisolone (30mg).
Lung transplant.
Treatment of Pulmonary hypertension
Oxygen, warfarin and diuretics for oedema, with oral CCB for pulmonary vasodilation.
Treat underlying cause.
Complications of Pulmonary hypertension
Deteriorating Rt Heart function/failure (Cor pulmonale).
Pleural effusions.
Sudden cardiac death.
Sequelae of Idiopathic pulmonary fibrosis
Median survival 5 years without transplant.
Define pleural effusion
Pleural fluid is substantially higher volume than normal.
Types of pleural effusion
Transudate.
Exudate.
Chylothorax.
How does pleural effusion clinically present?
Asymptomatic, if small.
Otherwise dyspnoea.
Signs: Reduced chest wall movement,
dull ‘stony’ percussion,
absent breath sounds,
reduced vocal resonance.
Cause of Transudate pleural effusion
Heart failure,
cirrhosis,
hypoalbuminaemia,
peritoneal dialysis.
Cause of Exudate pleural effusion
Pneumonia,
malignancy,
pulmonary embolus with infarction.
Cause of Chylothorax pleural effusion
Neoplasm,
trauma,
TB,
sarcoidosis,
cirrhosis.
Diagnostic test for pleural effusion
CXR: Bilateral effusions indicate congestive cardiac failure.
Pleural aspiration: If clinical picture suggests transudate; avoid.
Treatment of Transudate pleural effusion
Treat underlying cause.
Small effusions;
observation.
Treatment of Exudate pleural effusion
Drained. If recurrent malignant;
possible pleurodesis following aspiration.
Treatment of Chylothorax pleural effusion
Depends on cause.
Trauma; surgical repair and drain.
Malignant; possible pleurodesis following aspiration.
Complications of Transudate pleural effusion
Depends on cause.
Unilateral heart failure
-> congestive heart failure.
Complications of pleural and chylothorax pleural effusion
If caused by malignancy; poor prognosis.
Define Pneumothorax
Collection of air in the pleural cavity
-> collapse of lung.
Types of Pneumothorax
Primary Spontaneous (PSP).
Secondary.
Tension pneumothorax.
How does PSP and Secondary pneumothroax clinically present?
Sudden onset of pain.
Shortness of breath.
How does tension pneumothorax clinically present?
Sudden onset of pain.
Shortness of breath.
Severe respiratory distress.
Pathophysiology of PSP and Secondary pneumothorax?
Pocket of air in the pleural cavity
-> Partial/complete collapse of the lung on affected side.
Pathophysiology of tension pneumothorax
Pleural tear acts as a one-way valve.
Allows air into the cavity but not out. Increasing unilateral pressure
-> Severe respiratory distress,
shock and cardio-respiratory arrest.
Cause of primary spontaneous pneumothorax
Thought to be a congenital issue
-> Rupture of the pleural bleb.
Can be trauma.
Cause of secondary pneumothorax
Depends on underlying disease.
Associated with COPD.
Can be due to trauma.
Cause of tension pneumothorax
Rare, can be iatrogenic from mechanical ventilation/chest drains.
Can be trauma.
Diagnostic test for PSP and Secondary pneumothorax
CXR.
Diagnostic test for tension pneumothorax
Skip - immediate action.
Treatment of pneumothorax
Aspiration and oxygen.
Stop smoking to prevent recurrence.
Pleurodesis.
Complications of PSP and Secondary pneumothorax
Recurrence.
Complications of tension pneumothorax
Imminent death.
Define Mesothelioma
Cancer of the mesothelial cells.
Define carcinoma of the lung
Cancer of a lung cell
(95% of the time bronchial).
Types of lung cancer -
Non-small: Squamous.
Non-small: Large cell.
Non-small: Adenocarcinoma.
Small cell.
How does mesothelioma clinically present?
Shortness of breath,
dull diffuse chest pain (occasionally pleuritic),
weight loss, lethargy.
Pleural effusion.
History of asbestos exposure, sometimes.
Potentially a palpable chest wall mass.
How does carcinoma of the lung clinically present?
Local effects: Cough, chest pain, haemoptysis and breathlessness.
Spread within chest: Involve pleura/ribs -> pain and fractures.
Spread to brachial plexus causes pain in shoulder and arm.
Spread to sympathetic ganglion -> Horner’s syndrome.
Spread to left recurrent laryngeal nerve -> hoarseness of voice.
Metastases: Bone and brain
Other: Weight loss and finger clubbing.
Mesothelioma - note
Rarely metastasises to distant sites.
Associated with asbestos.
Non-small: Adenocarcinoma (lung cancer) - note
Most common lung cancer in non-smokers.
Pathophysiology of Non-small: Squamous (lung cancer) clinically present?
Most present as obstructive lesion -> infection.
Occasionally cavitates.
Commonly has local spread.
Widespread metastases.
Cause of mesothelioma
Strong association with asbestos inhalation (80% of cases attributable).
Genetic risk.
Cause of all 3 non-small lung cancers
Smoking, urban areas and asbestos exposure.
Probably a genetic risk.
Cause of small cell lung cancer
Smoking, urban areas and asbestos exposure.
Probably a genetic risk.
Diagnostic test for mesothelioma
CXR: Pleural effusion.
Potentially rib destruction.
Pleural aspiration: Straw coloured or blood stained.
Pleural biopsy: Gold standard.
Diagnostic test for carcinoma of the lung (all types)
CXR: Round fluffy/spiking shadow
Sputum/Bronchoscope biopsy: Determine cell type.
Treatment of mesothelioma
Surgical: Ressection (pleurectomy and decortication may relieve pain and effusions)
Chemo: Improves survival of patients with unressectable mesothelioma.
Radio: Mostly for pain control if at all.
Treatment of all 3 non-small lung cancers
Surgery can be curative.
Chemo can downstage tumours to render them operable.
Radio: Large doses can help localised squamous cancers (can cause fibrosis).
Treatment of small cell lung cancer
Limited disease (single anatomical or radiation field):
Chemo- Radio- combination.
Extensive disease: Chemotherapy.
Complications of mesothelioma
Poor prognosis.
Complications of carcinomas of the lung (all types)
Local: Nerve palsy (recurrent laryngeal, Horner’s syndrome)
Metastatic: Brain; confusion, fits, neuro deficit
Bone; pain, hypercalcaemia
Liver; Hepatomegaly
Non-metastatic: Endocrine; IADHS, Cushings, hyperthyroidism.
Skeletal; clubbing.
Define Pulmonary thromboembolus and infarct
Thromboembolus blocks right ventricular outflow, pulmonary arteries, branches.
Types of Pulmonary thromboembolus and infarct
Small-medium.
Massive - (medical emergency).
How does a small-medium pulmonary thromboembolus and infarct clinically present?
Breathlessness,
pleuritic chest pain,
haemoptysis if infarction.
Tachypnoea, pleural rub, exudative pleural effusion.
How does a massive pulmonary thromboembolus and infarct clinically present?
Severe central chest pain,
shock,
pale,
sweaty,
tachypnoea,
tachycardia,
cyanosis,
^JVP, RV heave and ^2nd heart sound + gallop.
Small-medium pulmonary thromboembolus and infarct - note
Can be clinically silent.
Cause of pulmonary thromboembolus and infarct
Risk factors for DVT (see heamotology).
Long periods of immobility (usually sat down) such as a long flight or surgery.
Diagnostic test for pulmonary thromboembolus and infarct
Revised Geneva score to predict probability of PE.
CXR (decreased vascular markings, raised hemi diaphragm).
ECG may exclude differentials eg MI. D-dimers, spiral CT.
ECHO diagnostic and can be performed at bedside, good for massive.
Treatment of pulmonary thromboembolus and infarct
Initial therapy: Oxygen.
Thrombolysis, LMWH, warfarin.
High risk of recurrence: Vena cava filter.
Complications of massive pulmonary thromboembolus and infarct
Acute right heart failure,
syncope and death follow rapidly.
Define Acute coryza
Common cold - infection by rhinovirus.
Define Influenza
Infection by influenza virus.
Types of Influenza
Serotype A
Serotype B
Serotype C
How does Acute coryza clinically present?
Incubation period of 12hrs - 5 days.
Then, malaise, mild pyrexia, sore throat and watery nasal discharge.
How does Influenza clinically present?
Incubation period of 1-3 days.
Abrupt fever, aching in limbs, sore throat and dry cough.
Influenza - Serotype A - note
More frequent and cause of major outbreaks.
Further categorised by surface antigens: H (haemagglutinin) and N (neuraminidase).
Influenza - Serotype B - note
Tends to circulate with A in yearly outbreaks.
Not as severe.
Influenza - Serotype C - note
Mild/asymptomatic illness akin to the common cold.
Pathophysiology of Acute coryza
Virus binds to ICAM-1 receptors
-> releases inflammatory mediators by unknown mechanism.
Cause of Acute coryza
Infection by rhinovirus:
spread by droplets and close personal contact.
Cause of Influenza
Infection by influenzae virus.
Transmission by droplet or direct nasal or eye contact with hands carrying virus.
Diagnostic test for Influenza
Not needed.
Serology shows four fold increase in antibody titre over a 2 week period.
Treatment of Acute coryza
Symptomatic.
Nasal decongestants, ibuprofen for malaise.
Treatment of Influenza
Symptomatic.
Paracetamol, bed rest, fluids.
Complications of Influenza
Pneumonia, either viral or bacterial.
Define Pneumonia
Acute inflammation,
with intense infiltration of neutrophils in and around alveoli and terminal bronchioles.
Define Tuberculosis
Infection by Mycobacterium tuberculosis.
Types of Pneumonia
Location.
Causative agent.
Types of Tuberculosis
Primary TB.
Milliary TB.
Secondary TB.
Primary TB - note
Dormant infection within calcified caeseating granulomatous lesions.
Milliary TB - note
Initial infection is not successfully controlled by caeseating granulomas.
Secondary TB - note
Occurs when semi dormant TB is activated by impaired immune function,
as in AIDS, malnutrition or immunosuppressive therapy.
How does Pneumonia clinically present?
Vary depending on infecting agent.
Most commonly; pyrexia, cough, sputum, pleurisy, dyspnoea, pleural effusion, pleural rub.
How does Primary TB clinically present?
Asymptomatic.
How does Milliary and Secondary TB clinically present?
Fatigue, malaise, fever, weight loss, anorexia, failure to thrive, pyrexia.
Pathophysiology of TB
Initial infection: bacteria is engulfed by macrophages in the lung and stored in granulomas.
Leaves granulomatous lesions (caseating centres, surrounded by epithelial cells).
Can lay dormant around the body; moved by lymph.
Reactivated by being immunocompromised.
Cause of Pneumonia
Various causative agents; S. aureus, L. pneumophila, M. pneumoniae.
Can be iatrogenic.
Community Acquired, due to atypical pathogens, or occur in the immunocompromised.
Cause of TB
Commonly spread by inhalation of droplets.
Infection with TB.
Diagnostic test for Pneumonia
CXR: Consolidation.
FBC and sputum culture.
CURB 65.
Diagnostic test for Primary TB
Tuberculin test positive.
Normal CXR.
Diagnostic test for Milliary and Secondary TB
CXR: pleural effusion.
Typical; patchy or nodular shadow.
Microbio samples: Culture of sputum
Treatment of Primary TB
As with Active TB,
in patients identified as being at risk.
Treatment of Milliary and Secondary TB
6 month drug treatment: Isoniazid,
rifampicin (first two months; pyrazinamide and ethambutol).
Treatment of Milliary and Secondary TB
6-month drug treatment: Isoniazid,
rifampicin (first two months; pyrazinamide and ethambutol).
