Respiratory Flashcards
what are the classic features of Asthma
wheezing and episodic SOB, worse at night/on exercise, cough/nocturnal cough, tight chest, decreased FEV1 relieve by B2 agonist
what factors should be specificall asked about in Asthma history taking
Precipitants (cold air, exercise, emotion, allergens, infection, drugs), diurnal variation in symptoms and peak flow (morning dip of peak flow common), exercise tolerance, acid reflux (known association with asthma), other atopic disease/family hx atopy, home (pets/carpet, feathered furnishings), occupation, days per week off school/work, how often waking up at night (sign of serious asthma)
what are the typical features of occupational asthma?
something at work triggering, better at weekends/holidays, not necessarily getting better in evenings as can last hours after trigger
what are some of the most common precipitants of an asthma attack?
environmental allergens (house dust mite, grass pollen, pets), cold air, emotion, viruses (rhinovirus, parsinfuenza, RSV), atmospheric pollution (sulphur dioxide, ozone, particulate matter), drugs (NSAIDS, B-Blockers), dusts/vapour and fumes (eg perfumes, cigarette smoke)
what are the differences between extrinsic and intrinsic asathma
extrinsic, mostly early onset, most frequent in atopic individuals. Can develop late onset, especially from causes such as occupational agents, aspirin intolerence or B2-adrenoreceptor agonists for hypertension/angina)
Intrinsic, usually late onset, often middle age, no causitive agent can be identified but cold exposure and exertion may trigger
what are the typical features of an acute severe asthma attack
RR >25 breaths/minute, tachycardia, PEF < 50% of predicted normal/best, widespread expiratory wheeze, inability to complete sentence in one breath, pulsus paradoxus
what are the typical features of a life-threatening asthma attack
silent chest, cyanosis, feeble respiratory effort, exhaustion, confusion, coma, bradycardia/hypotension, PEF <30% normal/best or 150L/min
what might the ABG findings of a severe asthma attack be?
High PaCO2 >6kPa, severe hypoxaemia (PaO2 < 8kpa despite O2 therapy, low and falling arterial pH
what is pulsus paradoxus
abnormal fall in bp on inspiration. Normally SBP and pulse pressure (SBP-DBP) fall during inspiration due to increased pulmonary intravascular volume but not more than 10mmHg
what conditions may pulsus paradoxus be present
respiratory, pulmonary embolism
tension pneumothorax
asthma
chronic obstructive pulmonary disease
cardiac Peridcardial effusion, cardiac tamponade
constrictive pericarditis
pericardial effusion
cardiogenic shock
explain the cellular mechanisms involved in asthma
T1 hypersensitivity, mast cells release histamine, T cells (particularly Th2) in the mucosal cellular infiltrate release IL-4 and IL-13, eosinophiles migrate in response to chemotactic factors releasing leukotrienes (LTC4 and LTD4), these constrict airways and likely are responsible for remodelling bronchii. Stimulation of afferent nerves, release of local neuropeptides which mediate odema and mucus hypersecretion, inflammation of bronchial wall causing airflow restriction by depletion of surfactant in small airways making opening difficult.
what will be the physiological features of lungs with chronic asthma
bronchoconstriction (increased responsiveness of bronchial smooth muscle), hypersecretion of mucus and mucus plugging, mucosal odema (narrowing of airway lumen), infiltration of bronchial mucosa by eosinophils, mast cells, lymphoid cells and macrophages, focal necrosis of airway epithelium, collagen deposition beneath bronchial epithelium in long standing cases, sputum containing charcot-leyden crystals from eosinophil granules and curshman spirals (mucus plugs from small airways(
Early phase asthma is characterised by …..
Early phase asthma is characterised by production of spasmogens (histamine, prostaglandin D2, leukotrienes C4 and D4 leading to bronchospasm
… is characterised by production of spasmogens (histamine, prostaglandin D2, leukotrienes C4 and D4 leading to bronchospasm
Early phase asthma is characterised by production of spasmogens (histamine, prostaglandin D2, leukotrienes C4 and D4 leading to bronchospasm
Late phase asthma is characterised by ……
Late phase asthma is characterised by production of chemotaxins (LB4, PAF) which attract leukocytes, especially eosinophils and mononuclear cells leading to inflammation of airway and hyperreactivity
…… is characterised by production of chemotaxins (LB4, PAF) which attract leukocytes, especially eosinophils and mononuclear cells leading to inflammation of airway and hyperreactivity
Late phase asthma is characterised by production of chemotaxins (LB4, PAF) which attract leukocytes, especially eosinophils and mononuclear cells leading to inflammation of airway and hyperreactivity
what is the definition of COPD?
Airflow limitation that is not fully reversible, usually progressive and associated with abnormal inflammatory response of lungs to noxious particles
What are the 3 main pathologies contributing to COPD
emphysema (destruction of air spaces and loss of elastic recoil), chronic bronchitis (mucus hypersecretion and luminal narrowing of airways) and bronchiolitis (narrowing of small airways by inflammation/scarring)
how would emphysema be defined
permanent dilation of any part of the respiratory acinus (distal to terminal bronchiole) with destruction of tissue in the absence of scarring
what are the pathalogical features of emphysema
parenchymal destruction by extracellular proteases due to reduction of normal defensive protease inhibitors, loss of elastic recoil as connective tissue in alveolar walls is destroyed, reduction in area available for gas exchange. Reduced O2 uptake despite increased ventilation. Maintain O2 blood level but become breathless on slightest exertion and become hypoxic (T1 resp failure). Large, voluminous lungs with large, dilated air spaces
What are the 2 main forms of emphysema? what are their characteristics?
Centriacinar, most common, most cases smoking related, most often in upper lobes, dilation of respiratory bronchioles at centre of respiratory acinus, dilated air spaces surrounded by normal alveoli
Panacinar, involves whole respiratory acinus, first affecting terminal alveoli and alveolar ducts, associated with smoking but more with a1 trypsinase deficiency, affects both upper and lower lobes
how is chronic bronchitis defined?
productive cough on most days for 3 months of year for at least 2 succesive years
what is the pathogenesis of chronic bronchitis
secretion of abnormal amounts of mucus causing plugging and narrowing of airway lumen, hypertrophy and hyperplasia of bronchial mucus glands, inflammation typically not present although may occur from repeated RTI, can lead to squamous metaplasia in pts with repeated infections. This leads to alveolar hypoventilation, hypoxaemia and hypercapnia (T2 RF). Individuals will typically be cyanosed but not usually having distressing dyspnoea. Hypoxic pulmonary vasoconstriction may cause hypertension and RHF (cor pulmonale)
hereditary a1 antitrypsin deficiency accounts for around … of emphysema cases
2%
what proportion of pts with COPD smoke(d)?
90%
what are the risk factors for COPD
Cigarette smoke Age older than 40 years Exposure to occupational dust and chemicals Exposure to indoor air pollution Alpha-1 antitrypsin deficiency
what features differentiate COPD from asthma
age >35, smoking, dyspnoea is constant, no marked diurnal/day to day variation, sputum production
what are the typical symptoms of somebody with COPD?
Cough, sputum production, wheeze, breathlessness, frequent chest infections, worsened by cold/foggy weather/pollution, severe breatlessness even with mild exercise
what will be the clinical findings in somebody with COPD
wheeze throughout chest, tachypnoeic with prolonged expiration, use of accesory muscles, intercostal indrawing on inspiration and pursing of lips on expiration, hyperinflated lungs, hyperresonance on percussion of liver and heart, barrel shaped chest, tracheal tug
With hypercapnia, peripheral vasodilation, bounding pulse, CO2 flap
what will be the clinical findings in somebody with Asthma
audiable, widespread polyphonic wheeze, hyper-inflated chest
what should be the ABG findings in a patient suffering an acute asthma attack?
normal/slightly reduce PaO2 and reduced PaCO2. If PaCO2 is raised transfer to HDU/ITU for ventilation
what will a chest xray be used for in asthma
exclude pneumothorax/infection
what will be the clinical features of a pt with bronchiectasis
copious amounts of purulent (bad smelling discoloured) sputum, recurrent cough and infections, intermittent haemoptysis
what may be the clinical findings of a patient with bronchiectasis
clubbing, course inspiratory crackles over infected areas, wheeze
what investigations may be performed on a pt with bronchiecstasis
sputum culture, CXR, HRCT chest, spirometry (showing obstructive pattern), bronchoscopy to locate site of haemoptysis and exclude obstruction, CF sweat test, serum immunoglobulins
what are some of the common causes of bronchiecstasis
Congenital (young’s syndrome, Kartagener’s syndrome, post infective (measles, TB, pneumonia, sarcoidosis, immunological post-lung transplant and allergic bronchopulmonaryaspergillosis, immune deficiencies (primary and IgA and IgG2)
symptoms of pneumonia
Fever/rigor, dyspnoea, malaise, nausea, productive cough, haemoptysis, pleuritic chest pain
what will be the signs of pneumonia on examination of the chest
diminished expansion, dull percussion, increased tactile vocal fremitus/resonance, bronchial breathing, pleural rub
explain the CURB65 criteria for assessing severity of Pneumonia
Confusion,
Urea > 7 mmol/l
RR >30
BP65
0 or 1 likely suitable for home treatment and oabx
2, hospital treatment
> 3 assess for ICU
what organisms commonly cause CAP
Strep pneumonaie most common, then H.Influenzae (spcially in elderly with comorbidities eg COPD), mycoplasma pneumoniae, staph aureus, legionella (specially if foreign travel), Moraxella catarhallis and chlamydia. chlamydia and myc oplasma common in young rare in elderly. Rarely gram -ve/anaerobes rare, viruses in about 15%
what organisms commonly cause HAP
most commonly g-ve enterobacteria and staph aureus, less commonly E.Coli, klebsiella, pseudomonas, bacteriodes and clostridia
What abx would be chosen for pt with CAP
mild, oral amoxicillin AND eryth or fluoroquinalone. Ampicillin/eryth if IVI req
severe; IV co-amox or cephalosporin eg cefuroxime and eryth
what abx would be chosen for HAP
aminoglyclaside (eg gent) AND antipseudomonal penicillin IV or 3rd gen cephalosporin
what factors predispose to pneumonia
viral infection with influenza/parainfluenza(staph aureus), hospitalised, smoking, alcohol excess, bronchiectasis, bronchial obstruction, immunosuppression, IV drugs, oesophageal obstruction, pets, travel
what is the typical presentation of pneumothorax
possibly nothing if small, sudden onset pleuritic pain, progressively increasing breathlessness, sudden deterioration COPD/Asthma
What might be the signs in somebody with pneumothorax
Pallor, tachy, reduced expansion on affected side, reduced/absent breath sounds, increased resonance on percussion, decreased/absent vocal resonance, tracheal deviation away from affected side in tension pneumothorax.
what are the typical risk factors of pneumothorax
asthma, COPD, TB, pneumonia, lung abscess, carcinoma, CF, lung fibrosis, ehlers-danlos, marfans, trauma,
what are the main histological types of lunc carcinoma and their incidence
squamous cell (50%), adenocarcinoma inc bronchoalveolar (20%), small cell/oat cell anaplastic (20%), large cell anaplastic (10%)
Clinically generally separated into small cell and none-small cell due to prognosis/treatment differences
what is the mean survival rate in pts with none small cell LC
50% 2 year survival without spread, 10% with
what is the mean survival rate in pts with SCLC
median survival less than 3 months if untreated, 1-1.5 years treated
What are the causes of SOB
Lungs -airways (Asthma/COPD/Tumours/Bronchiectasis)
- Parenchyma (atypical pneumonia/TB, fibrosis (pneumoconiosis/asbestos/all alveolitis), inflammatory (sarcoid/RA/Lupus)
- Circulation (PE/vasculitis)
- Pleural (pneumothorax/Pleural effusion/asbestos)
Cardiac (Failure, myopathy, mitral valve disease, constrictive pericarditis)
Neuromuscular (G.Barre, M.Gravis)
Structural (kyphoscoliosis)
What are the criteria of CURB65 score. How do they relate to severity?
Confusion (AMT 7, resp >30, BP 65
score of 5, risk of death 27.8%, 0.6%
0-1, treat as OP, oral amoxy/clarith
2-3, consider hospital
4-5, hospital plus consider ITU
Mild oral amoxy/macrolide (claryth), sever but won’t go to hospital offer both, severe in hospital plus IV B-lacamase (co-amox) plus macrolide
what are the commonest causes of bronchiectasis
childhood infections (whooping cough, measles, pneumonia), CF, allergic bronchopulmonary aspergillosus often associated with Asthma)
features of churg strauss
Asthma, eosinophilia, mono/polyneuropathy, spots/lesions on CXR, sinus probs, WBC outside blood vessel (from tissue sample) Any 2 of above. Antibodies blood test can also be done
What are the criteria for Churg-Strauss syndrome
Any 2/3 of Asthma, eosinophilia, mono/polyneuropathy, spots/lesions on CXR, WBC outside blood vessels (from biopsy). Anbody blood test can also be done
What is the treatment regime for TB
Rifampicin, isoniazid (6/12), 2 additional pyrazinamide and ethambutol daily 2/12
Extrapulmonary TB may be longer and steroids eg brain
How can somebody with TB expect to recover
Usually not infectious after about 2/52, may be weeks/months before feeling better and important to take course as directed as resistance will mean longer course of druges. Rare to return if treatment taken as advised
When should latent TB be treated
<35, HIV, healthcare worker, scars on CXR
What advice should be given regarding side effects/interactions of TB medication
Rifampicin interacts with COCP, use other protection
May rarely damage liver, LFTs before starting and monitor. Ethambutol can cause eye damage. Contact if being sick, yellow skin/eyes, tingling hands/feet, rash, blurred/altered vision, unexplained fever
