Respiratory Flashcards
(93 cards)
1
Q
Acute asthma definition
A
An asthma exacerbation is an acute or subacute episode of progressive worsening of symptoms of asthma, including shortness of breath, wheezing, cough and chest tightness
2
Q
How common is acute asthma
A
Roughly 9% of people (5.4million in UK)
160,000 per annum incidence
3
Q
Who does acute asthma affect
A
1 in 11 children - in early childhood it is higher in boys than girls -> in adulthood this is the other way round
160,000 per annum incidence
1 in 12 adults
4
Q
What causes acute asthma
A
Airway inflammation and hyper responsiveness - different underlying disease processes and variations in severity, clinical course and response to treatment
• Airway limitation is usually reversible, either spontaneously or with treatment
- Chronic asthma – may be irreversible as a result of wall remodelling and mucus impactation
Characterised into:
Extrinsic: allergens can be identified by +ve skin-prick reactions to common inhaled allergens, e.g. dust mite, pollen and fungi, in adults sensitisation to chemicals or biological products in the workplace may be the cause
Intrinsic: often starts in the middle age and no definite external cause can be identified, many pts do show a degree of atopy and on close questioning give a hx of respiratory symptoms consistent with childhood asthma
5
Q
Risk factors for asthma
A
- Personal or Fx of atopic disease – asthma, eczema, allergic rhinitis or allergic conjunctivitis
- Respiratory infections in infancy
- Exposure to tobacco smoke and inhaled particulates
- Obesity
- Social deprivation
- Flour dust and isocyanates from paint
6
Q
Symptoms/signs of asthma
A
- Variable symptoms
- Wheeze, cough, breathlessness and chest tightness
- Symptoms are commonly diurnal (worse at night or early morning) and/or triggered or exacerbated by exacerbated by exercise, viral infection and exposure to cold air or allergens
- In children, it can also be triggered by emotion and laughter
- In adults, it can be triggered by use of NSAIDs and B-blockers
Signs - wheeze in auscultation
7
Q
DDx for asthma
A
- Normal structures
- Skin infections
- Benign tumours
- Malignant primary tumours
- Thyroid lumps
- Salivary gland lumps
- Congenital and developmental lumps carotid body tumours
- Aneurysms
- Trauma
8
Q
Investigations for asthma
A
1st LINE: - PEAK FLOW MEASUREMENT - O2 SATS – performed immediately - SHORT-ACTING BRONCHODILATOR TRIAL – should be initiated immediately, lack of response is unsual and suggests that the condition is not caused by asthma • CONSIDER: ABG and CXR
9
Q
Management for asthma
A
• ACUTE:
- MILD EXACERBATION: 1ST LINE: inhaled short-acting beta-2-agonist, adjunct: oral corticosteroid
- MODERATE TO SEVERE EXACERBATION: 1ST LINE: oxygen and inhaled short-acting beta-2-agonist, + oral corticosterioid,
• SYMPTOM MANAGEMENT:
- OCCASIONAL SYMPTOMS: PEFR 100% predicted. Inhaled short acting β2 agonist as required
- DAILY SYMPTOMS: PEFR≤80% predicted. Add regular inhaled low dose corticosteroids up to 800µg daily
- SEVERE SYMPTOMS: PEFR 50-80% predicted. Add inhaled LABA (Long acting β agonist), if still not controlled add either LTRA (Leukotriene receptor antagonist) or oral theophylline
- SEVERE SYMPTOMS: PEFR 50-80% predicted. Increase inhaled corticosteroids up to 2000µg daily
- SEVERE SYMPTOMS DETERIORATING: PEFR≤50% predicted. Add 40mg prednisolone daily
10
Q
Prognosis and complications of asthma
A
Prognosis is dependant on cause
Drug complications e.g. salbutamol induced tremor
11
Q
Bronchial Carcinoma definition
A
Cancer that begins in the tissue that lines or covers the airways of the lungs, including small cell and non- cell lung cancer
12
Q
How common is bronchial carcinoma
A
Accounts for 9% of primary lung tumours
Most common malignant tumour in the western world
Third common cause of death after heart disease and pneumonia
13
Q
Who does bronchial carcinoma affect
A
3:1 M:F
14
Q
What causes bronchial carcinoma
A
• Non-small cell: exposure to radon, second-hand smoke, pollution etc
- Squamous (40%): most present as obstructive lesion leading to infection, occasionally cavitates, local spread common, widespread mets occur late
- Large Cell (25%): poorly differentiated tumour, mets easily
- Adenocarcinoma: most common lung cancer associated with asbestos exposure, proportionally more common in non-smokers, usually occurs peripherally, local and distant mets
• Small-cell (20-30%): arises from endocrine clls (Kulchitsky cells), secretes polypeptide hromones, early development of widespread mets, responds to chemo, poor prognosis
15
Q
Risk factors for bronchial carcinoma
A
Smoking Urban areas Passive smoking Exposure to asbestos Possibly also contact with arsenic, chromium, iron oxides and the products of coal combustion
16
Q
Symptoms of bronchial carcinoma
A
- Local effects of tumour within a bronchus: cough, chest pain, haemoptysis and breathlessness
- Spread within the chest: may directly involve the pleura and ribs, causing pain and bone fractures, spread to incolve the brachial plexus and causes pain in the shoulder and inner arm (Pancoast tumour), spread to the sympathetic ganglion (horner’s syndrome) and spread to the LRL nerve causes hoarseness and bovine cough, tumour may directly involve the oesophagus, heart or SVC
- Metastatic disease: mets are common to bone (presenting with pain and sometimes spinal cord compression) and brain (change in personality, epilepsy, focal neurological signs
- Non-metastatic manifestations: rare apart from finger clubbing, amy also be malaise, lethargy and weight loss
17
Q
Signs of bronchial carcinoma
A
• Often no physical signs, although lymphadenopathy signs of a pleural effusion, lobar collapse or unresolved pneumonia may be present
18
Q
Investigations for bronchial carcinoma
A
- Confirm the diagnosis: CXR will usually be abnormal by the time a lung cancer is causing symptoms, round shadow, the edge of which is fluffy or spikey, may be evidence of cavitation, lobar collapse, a pleural effusion or secondary pneumonia, spread through the lymphatic channels give rise to lymphangitis carinomatosis, apprearing as streaky shadowing throughout the lung, a minority of tumours may be hidden by the mediastinum, so possibly order a CT after normal CXR for a smoker with haemoptysis
- Determine the histology: sputum is examined for malignant cells, bronchoscopy is used to obtain biopsies for histological investigations and washings for cytology, transthoracic fNA under radiographic guidance is useful for obtaining tissue diagnosis from peripheral lesions
- Assess the spread of the tumour: PET CT
19
Q
Management of bronchial carcinoma
A
- Non-small-cell lung cancer: surgery can be curative in non-small-cell cancer, neo-adjuvant chemo may downstage tumours to render them operable, adjuvant post-operative chemotherapy and radiotherapy improves survival, radiotherapy in high doses can produce good results in patients with localised squamous carcinoma if surgey is declined, complications are radiation pneumonitis and fibrosis, palliative radiotherapy is useful for bone pain, haemoptysis and SVC obstruction, chemotherapy is given in advanced disease and improves median survival from 6 to 10 months
- Small cell lung cancer: limited disease (confined to a single anatomical or radiation field) is treated with combined chemo and radiotherapy with 25% survival at 5 years extensive disease is reated with chemo with a median survival of 9-13 months and a 2-year of 20%
20
Q
Prognosis and complications of bronchial carcinoma
A
Dependant on cancer and staging
21
Q
Pneumothorax definition
A
When air gains access to and accumulates in the pleural space
22
Q
How common is a pneumothorax
A
24/100,00 a year for men and 10/10,000 for women
Tends to affect young people as they tend to be fitter.
23
Q
Causes of a pneumothorax
A
- PRIMARY: primary spontaneous pneumothorax occurs without preceding trauma or precipitating event, and develops in a person without clinically apparent pulmonary disease
- SECONDARY: secondary spontaneous pneumothorax occurs as a complication of an underlying pulmonary disease, with COPD from cigarette smoking being the most common predisposing condition in the US and accounts for approx. 70% of these pneumothoraces, other predisiposing respiratory conditions include pneumocystitis jirovecuu respiratory infection, CF and TB
24
Q
Risk factors for pneumothorax
A
Cigarette smoking Family history of pneumothorax Tall and slender body build Age <40yrs Recent invasive medical procedure Chest trauma Acute severe asthma COPD TB AIDS- related pneumocystitis CF
25
Symptoms/ signs of pneumothorax
Presence of risk factors
Chest pain - occurs on the same side as the pneumothorax
Dyspnoea - degree depends on the size of the pneumothorax and presence and severity of pre existing lung disease
Hyper expanded ipsilateral hemithorax- degree depends on the size of the pneumothorax and whether a tension pneumothorax develops
Hyper- resonance on percussion of the affected side
Ipsilateral absent or finished breath sounds
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DDx of pneumothorax
```
Asthma, acute exacerbation
COPD, acute exacerbation
PE
MI
Pleural effusion
Bronchopleural fistula
Fibrosing lung disease
Oesophageal perforation
Giant Bullae
```
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Investigations of pneumothorax
* CXR – visceral pleural line typically identified, if the patient has an underlying lung disease, other abnormalities such as emphysema, lung masses and pulmonary infiltrates may be present
* CONSIDER – CT chest, chest ultrasound, bronchoscopy
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Management of pneumothorax
• TENSION PNEUMOTHORAX: 1ST LINE: immediate needle decompression + oxygen therapy + tube thoracostomy
• ACUTE:
- PRIMARY SPONTAENOUS PNEUMOTHORAX: 1ST LINE – WHEN SMALL: supplemental oxygen therapy and observation, WHEN BREATHLESS OR LARGE –supplemental oxygen therapy and percutaneous aspiration
o When aspiration fails, a chest tube or small bore cathter should be inserted
- SECONDARY SPONTANEOUS PNEUMOTHORAX/PATIENT IS >50: 1ST LINE – WHEN SMALL: hospitalisation and supplemental oxygen, WHEN MODERATE: hospitalisation and supplemental oxygen + percutaneous aspiration, WHEN LARGE: hospitalisation and supplemental oxygen + chest-tube thoracostomy
• TRAUMATIC PNEUMOTHORAX: hospitalisation and supplemental oxygen + percutaneous aspiration
• All patients not to fly for two weeks after treatment.
29
Prognosis and complications of pneumothorax
Prognosis - primary and secondary = at risk for recurrent pneumothoraces
Complications- re-expansion pulmonary oedema
- talc pleurodesis-related ARDS
30
Pleural effusion definition
* A pleural effusion results when fluid collects between the parietal and visceral pleural surfaces of the thorax
* A thin layer of fluid is always present in this space for lubrication and ease of movement of the lung during inspiration and expiration
* If the normal flow of fluid is disrupted with either too much fluid produced or not enough removed then fluid accumulates resulting in a pleural effusion
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How common is a pleural effusion
Affects 1.5 million people in the US
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Causes of pleural effusion
• Leading cause is CHF and pneumonia is second
• Excessive accumulation of fluid in the pleural space. Can be detected clinically when more than 500mL, but on X-ray more than 300mL. Massive effusions are most commonly malignant in origin.
• Pleural effusions are transudates or exudates. Transudates occur when the balance of hydrostatic forces in the chest favour the accumulation of pleural fluid; occasionally they occur due to movement of fluid from the peritoneum or retroperitoneal space. Differentiation of transudate from exudate is the key to subsequent management; treatment for a transudative effusion is that of the underlying disease while treatment of an exudate often requires specific pleural intervention.
• Transudate: Pleural fluid protein <30g/L. Heart failure. Hypoalbuminemia (e.g. nephrotic syndrome, cirrhosis). Constrictive pericarditis. Hypothyroidism. Ovarian fibroma producing right sided effusion (Meigs’ syndrome).
• Exudate: Pleural fluid protein >30g/L. Infection (empyema/Parapneumonic effusion/TB). Malignancy (primary or secondary). PE with infarction. Connective tissue disease. Rare causes: (post MI syndrome, acute pancreatitis, mesothelioma, sarcoidosis, chylothorax, drugs e.g. methotrexate, amiodarone).
• USE LIGHT CRITERIA – IF ONE OF THE LIGHT CRITERIA IS PRESENT IT IS EXUDATE:
- Effusion protein/serum protein ratio greater than 0.5
- Effusion lactate dehydrogenase (LDH)/serum LDH ratio greater than 0.6
- Effusion LDH level greater than two-thirds the upper limit of the labs reference range of serum LDH
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Risk factors for pleural effusion
CHF- most common cause of pleural effusion
Pneumonia
Malignancy
Recent coronary artery bypass graft surgery
PE
MI
RA
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Symptoms and signs of pleural effusion
Presence of risk factors
Pleuritic chest pain- commonly presents with pain that is worse with inspiration and may be exacerbated by cough and movement
Cough - productive cough may be present if effusion results from pneumonia, however fluid collection and irritation of the pleural surfaces alone causes a non- productive cough
Quieter breath sounds - over the area of effusion
Decreased or absent tactile fremitus
Dyspnoea
Stony dullness to percussion
35
DDx of pleural effusion
Pleural thickening
Pulmonary collapse and consolidation
Elevated hemidiaphragm
Pleural tumours / extrapleural fat
36
Investigations for pleural effusion
• 1st LINE:
- PA and lateral CXR - dense homogenous shadow occupying part of the hemithorax and a meniscus visible on an erect CXR
- Pleural ultrasound – more sensitive and specific than CXR
- LDH and protein in pleural fluid and serum – indicates an exudate if the ratio of pleural fluid protein to serum protein is >0.5 – absence of these findings the effusion is likely to be a transudate
- RBC count in pleural fluid
- WBC count and differential of pleural fluid
- Cytology of pleural fluid – cytology is positive is >60% of malignant pleural effusions – abnormal cells present in malignant pleural effusion
- pH of pleural fluid – needs to be measured with an ABG machine
- Glucose in pleural fluid – almost 100% of effusions due ot empyema and rheumatoid arthtirits
- FBC and CRP – infection such as pneumonia
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Management of pleural effusion
* CHF – 1ST LINE: diuretic e.g. furosemide, if large include a therapeutic thoracentesis
* INFECTIVE – 1ST LINE: empirical IV abx e.g. amoxicillin/clavulanate or vancomycin
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Prognosis and complications of pleural effusion
Prognosis is dependant on underlying condition
| Complications include atelectasis/ lobar collapse, pleural fibrosis, trapped lung
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Community acquired pneumonia definition
* Pneumonia acquired outside hospital or healthare facilities
* Clinical diagnosis is based on a group of signs and symptoms related to LRTI – presence of fever >38, cough, expectoration, chest pain, dyspnoea and signs of invasion of the alveolar space
40
How common is Community acquired pneumonia and who does it affect
24.8 cases per 100,000
| Affects mainly adults
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Causes of Community acquired pneumonia
* Streptococcus pneumoniae is the bacteria that is most often responsible for CAP in adults
* Some other common bacteria that cause CAP are H. influenzae
42
Risk factors for Community acquired pneumonia
```
• Age >65
• Residence in a healthcare setting
• COPD
• Exposure to cigarette smoke
• Alchol abuse
• Poor oral hygiene
• Use of acid-reducing drugs
• Contact with children
Weak: diabetes, chronic renal disease, chronic liver disease, use of opioids
```
43
Symptoms and signs of community acquired pneumonia
* Presence of risk factors
* Cough with increasing sputum production – less common in older patients
* Fever or chills – less common in older patients
* Dyspnoea
* Pleuritic chest pain
* Abnormal auscultation findings – asymmetric breath sounds, pleural rubs, ageophony (increased resonance of voice sounds heard on auscultation) and increased fremitus may be heard
* Dullness to percussion – suggests consolidations and/or pleural effusion
* Myalgia and arthralgia
44
DDx of community acquired pneumonia
* Acute bronchitis
* CHF
* COPD
* Asthma
* Bronchiectasis
* TB
* Lung cancer or lung metastases
* Empyema
45
Investigations of community acquired pneumonia
• 1st LINE:
- CXR – new infiltrate provides definitive diagnosis of pnuemonia
- FBC - leukocytosis
- Serum electrolytes, urea – usually normal
- Blood glucose – may be elevated
- ABG – may reveal low arterial oxygen saturation
• CONSIDER: blood culture, sputum, LFTs, CRP, procalcitonin
46
Investigations of community acquired pneumonia
• 1st LINE:
- CXR – new infiltrate provides definitive diagnosis of pnuemonia
- FBC - leukocytosis
- Serum electrolytes, urea – usually normal
- Blood glucose – may be elevated
- ABG – may reveal low arterial oxygen saturation
• CONSIDER: blood culture, sputum, LFTs, CRP, procalcitonin
47
Management of community acquired pneumonia
• ACUTE:
- PREVIOUSLY HEALTHY: 1st LINE – amoxicillin first line, if allergic to penicillin macrolide or tetracycline therapy e.g. azithromycin
- CO-MORBIDITES: 1ST LINE - fluoroquinolone or combination therapy e.g. levofloxacin
• INPATIENT:
- 1ST LINE: fluoroquinolone or combination therapy e.g. azithromycin AND amipicillin
• If it is a MRSA infection ADD – vancoymycin or linezolid
48
Prognosis and complications of community acquired pneumonia
Prognosis is dependant on age, general state of health and the setting where antibiotic treatment is given
Complications include pleural effusion, septic shock, ARDS, Antibiotic associated c.diff colitis
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Hospital acquired pneumonia definition
• An acute LRTI that is acquired after at least 48hrs of admission to hospital and is not incubating at the time of admission
50
How common is Hospital acquired pneumonia
Common presentation in infection and in malignancy
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Causes of Hospital acquired pneumonia
• Most causes are caused by bacteria, especially aerobic gram-negative bacilli, such as Pseudomonas aeruginosa, e. coli, klebsiella pneumoniae and Acinetobacter species
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Risk factors of hospital acquired pneumonia
* Poor infection control/hand hygiene
* Intubation and mechanical ventilation
* H2 antagonist and antacid use
* Poor oral hygiene
* Reintubation
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Symptoms/ signs of hospital acquired pneumonia
* Presence of risk factors
* Dyspnoea
* Productive cough – thick yellow or green sputum
* Fever
* Chest pain
* Asymmetrical expansion of the chest
* Diminished resonance – may be diminished on the side of pneumonia
* Egophony – localsing sign auscultated over the affected area of the lung – change in the sound of a patients voice i.e. ‘eee’ ‘aaa’
* Whipser pectoriloquy – referred to when a whisper is heard clearly and loudly while auscultating over the affected part of lung
* Crackles
* Tachycardia
A diagnosis of HAP must require positive imagine plus 2 or 3 clinics, features: fever >38, leucocytosis or leukopenia
54
DDx of Hospital Acquired Pneumonia
```
Cardiogenic pulmonary oedema
ARDS
Pleural effusion
Atelectasis
Pulmonary haemorrhage
Lung cancer
```
55
Investigations for hospital acquired pneumonia
CXR
WBC count with differential - elevated decreased WBC count
Culture of LRT sample
Pulse oximetry
CONSIDER: ABG, diagnostic thoracentesis, CT chest, CRP, Procalcitonin
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Management of hospital acquired pneumonia
* BEFORE CULTURE RESULTS: 1st LINE: empirical antibiotic monotherapy e.g. cefepime IV
* AFTER CULTURE: dependent on results
57
Complications and prognosis of hospital acquired pneumonia
Prognosis is dependant on cause
| Complications include Empyema, PE/pulmonary infarction, c. difficile colitis due to broad-spectrum antibiotic use
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atypical pneumonia definition
Atypical bacterial pneumonia is caused by atypical organisms that are not detectable on gram stain and cannot be cultured using standard methods e.g. mycoplasma pneumoniae, chlamydiphila pneumoniae and legionella penumophila
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how common is atypical pneumonia
incidence of atypical pathogens in community acquired pneumonia is approximately 22% globally
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who does atypical pneumonia affect
mycoplasma pneumonia, chlamydia pneumonia and legionella pneumophila
61
risk factors for atypical pneumonia
- close community settings
- immunosuppression
- WEAK: cigs, chronic lung disease, travel, male, immunomodulating drugs
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symptoms/ signs of atypical pneumonia
- presence of risk factors
- age <50years
- persistent cough
- long duration of symptoms
- dry cough
- recent community exposure
- throat involvement - due to to m pnumoniae and coxiella burnetti pneumonia, pharyngitis and hoarseness will be present as well
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Ddx of atypical pneumonia
* Typical bacterial pneumonia
* Viral pneumonia
* TB
* Fungal pneumonia
* Pneumocystis jirovecii pneumonia
* PE
* Anthra
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investigations for atypical pneumonia
* CXR – may show more extensive abnormalities than physical examination would suggest
* WBC count – may be slightly elevated, may see relative lymphocytosis if infection is viral
* Haemoglobin – may show anaemia – may accompany mycoplasma pneumoniae
* LFTs – elevated enzyme levels – suggests m. pneumoniae or legionella pneumophila
* Oxygen saturation in air – may be low (<90%)
* Urea – elevation i urea suggests more severe disease favouring hospitalisation
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management of atypical pneumonia
* NON-PREGNANT AND PREGNANT ADULT – macrolide e.g. azithromycin
* WHEN IT IS LESS COMMON ZOONOTIC ATYPICAL PATHOGENS – chlamydophila psittaci and coxiella burnetti (Q fever) – doxyclcline is 1st line
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prognosis and complications of atypical pneumonia
prognosis - predicted according to the initial severity of illness
complications - rash, pericarditis, atherosclerosis, neurologi cal complications, pleural/parapneumonic effusion
67
PE definition
* Consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities
* Thrombus formation in the venous system occurs as a result of venous stasis, trauma and hypercoagulability (virchows triad)
68
how common is PE
300/100,000
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Causes of PE
• Life threatening condition resulting from dislodged thrombi occluding the pulmonary vasculature; right heart failure and cardiac arresr may ensue if not aggressively treated
70
risk factors of PE
- increasing age
- DVT
- Surgery within the last 2 months
- bed rest >5 days
- Fx of VTE
- active malignancy
- recent trauma or fracture
- pregnancy/postnatal period
- paralysis of the lower extremities
- Protein C and S deficiency
- contraceptive pill
- long haul flight
71
symptoms/signs of PE
- presence of risk factors
- chest pain: pleuritic in nature
- dyspnoea
- tachypnoea
- presyncope/syncope
- hypotension (systolic BP <90mmHg)
- feeling of apprehension
- cough
- tachycardia
- fever
- unilateral swelling/tenderness of calf
- haemoptysis
- elevated JVP
- sternal heave
- accentuated pulmonary component of S2
72
Ddx of PE
- Angina
- MI
- Pneumonia
- Bronchitis
- COPD
- Asthma
- CHF
- Pericarditis
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Investigations for PE
• WELLS CRITERIA/GENERVA SCORE:
- Clinical signs and symptoms of DVT
- PE is number 1 diagnosis
- Heart rate >100
- Immobilisation at least 3 days OR surgery in the previous 4 weeks
- Previous, objectively diagnosed PE or DVT
- Haemoptysis
- Malignancy with treatment within 6 motnhs or palliative
* PERC RULE: rules out PE if not criteria are present and pre-test probability is <15%: age>50, HR>100, O2 sat on room air <95%, unilateral leg swelling, haemoptysis, recent surgery or trauma
* 1st LINE: Multiple-detector computed tomographic pulmonary angiography – has the best diagnostic accuracy of all advanced non-invasive imaging methods, diagnosis is confirmed by direct visualisation of thrombus in a pulmonary artery, appears as a partial or complet intraluminal filling defect, need to have an eGFR over 30 to conduct this if not give IV fluids before and after
* Ventilation-perfusion (V/Q) scan – area of ventilation is not perfused, negative V/Q excludes PE
* Coagulation studies - need baseline for noacs and LMWH
* Urea and creatinine – need baseline for noacs and LMWH
* D-dimer test – elevated
* CONSIDER: CXR, MRI, pulmonary angiography, electrocardiography, ABG, thrombophilia screen, ultrasonography
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prognosis and complications of PE
prognosis - 1% risk of mortality
complications - acute bleeding during treatment, recurrent venous thromboembolic event, pulmonary infarction, cardiac arrest/ death
75
idiopathic pulmonary fibrosis definition
- Rare form of fibrotic lung disease with no known aetiology that progress over the course of several years and is characterised by the formation of scar tissue with the lungs and progressive dyspnoea
76
how common is idiopathic pulmonary fibrosis
• More common in males and usually presents in the late 60s
77
causes of idiopathic pulmonary fibrosis
* Cause is unknown
| * Associated with cigarette smoke, organic or metal dust, GORD, diabetes, and infection
78
risk factors for idiopathic pulmonary fibrosis
* Advanced age
* Male
* Fx
* Cigarette smoking
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symptoms for idiopathic pulmonary fibrosis
* Presence of risk factors
* Dyspnoea – on exertion
* Cough – typically non-prodctive
* Crackles – end-expiratory, basilar crackles are almost universally present on lung exam, typically dry and Velcro in quality
80
signs for idiopathic pulmonary fibrosis
* Clubbing
* Fine End inspiratory crackles
* Weight loss
81
DDx for idiopathic pulmonary fibrosis
* Non-speciic interstitial pneumonia
* Cryptogenic organising pneumonia
* AIP
* Asbestosis
* Connective tissue disease-associated interstitial lung disease
82
investigations for idiopathic pulmonary fibrosis
• 1st LINE:
- CXR: basilar, peripheral, bilateral, asymmetrical, reticular opacities – most prominent in lower lung zones
- HIGH-RESOLUTION CT: basilar and subpleural predominant areas of increased reticulation, honeycombing and possible traction bronchiectasis or bronchiolectasis
- ANTI-NUCLEAR ANTIBODIES: normal or mildy elevated
- RHEUMATOID FACTOR: normal or mildy elevated
- ANTI-CYCLIC CITRULLINATED PEPTIDE: normal
- MYOSITIS PANEL: normal
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management of idiopathic pulmonary fibrosis
• 1st LINE:
| - ADMISSION TO HOSPITAL + HIGH-DOSE CORTICOSTEROID: prednisolone 30mg daily
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prognosis snd complications of idiopathic pulmonary fibrosis
prognosis - Pts with IPF experience progressive dyspnoea and functional decline over time
complications - • GORD, pulmonary hypertension, pulmonary infection
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how common is COPD
3 million in UK (roughly 5%) but with 2 million of those undiagnosed.
86
who does COPD affect
Generally, people over 50, but it has a very insidious onset. More common in men but has recently reached a plateau.
87
causes of COPD
Airway narrowing as a result of hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree, bronchial wall inflammation and mucosal oedema. The epithelial cell layer may ulcerate an, when ulcers heal, squamous epithelium may replace columnar epithelium (squamous metaplasia). Emphysema is defined pathologically as dilation and destruction of the lung tissue distal to the terminal bronchioles.
90% due to cigarette smoking. Respiratory infections can precipitate an acute exacerbation. See other causes below.
88
risk factors for COPD
Tobacco smoking. Pipe, cigar, water pipe, and marijuana smokers are also at increased risk of COPD. Passive smoking.
Occupational exposure: Exposure to dust, chemicals, noxious gases, and particles. About 20% of diagnosed cases of COPD can be attributed to occupational exposure.
Air pollution: indoor and outdoor, such as wood or coal burning stoves.
Genetics: Homozygous α1 antitrypsin deficiency accounts for less than 1% of COPD cases, but it is still the best-documented genetic risk factor. Progression of COPD is still accelerated by smoking.
89
symptoms of COPD
Cough + production of sputum
wheeze and breathlessness following many years of a smoker’s cough.
Frequent infective exacerbations occur, giving purulent sputum
90
signs of COPD
Polyphonic wheeze. Breathless at rest, with prolonged expiration, chest expansion is poor and the lungs are hyper-inflated (barrel chest). Thin with loss of muscle mass. Pursed-lip breathing. Increased work of breathing: leaning forward, accessory muscles of respiration, tracheal tub, nasal flare, paradoxical abdominal movement, indrawing of intercostal muscles.
Pink puffers: breathlessness is the predominant problem; they are not cyanosed.
Blue bloaters: hypoventilation; they are cyanosed, may be oedematous and have features of CO2 retention.
91
investigations for COPD
Lung function tests (spirometry), show progressive airflow limitation with increasing disease severity and breathlessness. Some patients have partially reversible airflow limitation with an increase in FEV1 (but usually <15%) following inhalation of a β2 agonist.
Chest x-ray may be normal or show signs of hyper inflated lungs indicated by low, flattened diaphragms and a long narrow heart shadow.
ABGs may be normal or show hypoxia ± hypercapnia in advanced cases
92
Treatment for COPD
Cessation of smoking. Bronchodilators. A stepwise approach to drug therapy is used similar to that used in asthma. Inhaled tiotropium bromide, a long-acting once-daily antimuscarinic agent, is used as an initial maintenance therapy with a rescue short acting β2-agonist to prevent or reduce symptoms. A long acting β2 agonist is added in patients with persistent dyspnoea. Corticosteroids: Assessment of reversibility is made with a 2-week course of oral prednisolone (30mg daily), with measurement of lung function before and after treatment. Prevention of infection: vaccine’s. Oxygen: PaO2 < 7.3 kPa when breathing room air. PaO2 < 8.0kPa with secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or evidence of pulmonary hypertension.
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Ddx for COPD
Asthma and probably the same differentials as for asthma (but ofc the ones for older age people)
