Resp Flashcards
Define Asthma
reversible, obstructive. CO2 retention. Can be response to exercise, allergens, stress or idiopathic.
Atopic features
Expiration wheeze, dyspnoea (diurnal)
Variable
Chronic sputum, dizziness, chest pain and inspiratory wheeze make asthma less likely
Specific asthma triggers vs non specific
Only affect some patients (pets, pollen)
Non specific triggers (viral infection, cigarette smoke, pollution, cold weather, emotion, exercise) affect some patients
Atopy
Allergic rhinitis, eczema and asthma
Asthma diagnosis in under 5
Treat symptoms based on obs/clinical judgement. Review regularly and get objective testing ASAP
Asthma diagnosis in 5-16
Spirometry (reversibility is key - if not reversible then FeNO test (NO raised in asthma)
Asthma diagnosis in 17+
Spirometry for reversible obstruction (if not, then FeNO) and variable Peak Flow. Can also to histamine/methalcholine challenge - specialist test
Asthma Tx
SABA
Add ICS
Add LRTA
LABA+ICS+SABA
MART has LABA as ICS as reliever and preventer
Moderate Acute Asthma
Increasing symptoms
PEFR >50-75% predicted
No acute severe asthma features
Acute Severe Asthma
One of: PEF 33-50% predicted RR>25 HR>110 Inability to complete sentences in 1 breath
Life threatening Asthma
Any one of: PEF<33% pred. SpO2 <92% PO2 <8kPa Normal CO2 (4.6-6) Silent chest Cyanosis Poor resp effort Arrythmia Exhaustion Hypotension
Emergency Asthma management
Salbutamol neb (children can use inhalor). Can add ipratropium if no response. give oxygen if hypoxic. Steroids, IV mag sulphate .
COPD Definition
Progressive non fully reversible airflow obstruction.
Get mucus hypersecretion, ciliary disfunction, airflow limitation and hyperinflation. Impaired gas exchange and pulmonary HT (V/Q mismatch
COPD RF
Smoking, indoor air pollution, occupational toxins, outdoor pollution, genetic factors, infections, socioeconomic factors, asthma
COPD features and examination
Often asymptomatic until exertion. Chronic cough, chronic progressive dyspnoea, regular sputum, wheeze, chest tightness. Can lead to weight loss, anorexia, cough syncope and depression.
O/E: hyperinflated chest, wheeze, quiet breath sounds, pursed lip breathing, accessory muscle use, paradoxical movement of lower ribs, peripheral oedema, cyanosis, raised JVP, cachexia.
Difference between pink puffer and blue bloater
Pink puffer is more emphasematous presentation. Tends to be thin, pursed lip breathing, maintains co2 level.
blue bloater is more chronic bronchitis, larger, prone to hypercapnia
COPD investigations
CXR, FBC, BMI, spirometry, peak flow, alpha 1 anti-trypsin, CO transfer factor, oxygen sats, CT thorax, ECG, echo, ABGs, sputum culture.
COPD management
Empirical with SABA/SAMA
Can add LAMA (tiotropium) an can use LABA/LAMA combos
For frequent (2+/12 months) and steroid sensitivity features then ICS + LABA
If severe then ICS+LAMA+LABA combo
Mucolytics adjunct
ABx in acute exacerbation
Smoking cessation
Chronic Bronchitis definition
Cough productive of sputum on most says for 3 months of at least 2 successive years.
Due to chronic irritation leading to defensive increase in mucus (through goblet hyperplasia). Increased sputum production increases infection risk. This process is not necessarily inflammatory. Mucus hypersecretion occurs in the proximal airspaces
Emphysema definition
Distal airspace disease where terminal bronchiole airspace is increased through balance between proteases and antiproteases is disturbed. Macrophages and neutrophils recruited. Alveoli dilated. Occurs without fibrosis.
Comparison of chronic bronchitis and emphysema
Bronchitis onset is often 40-45, emphysema is 50-75
Dyspnoea is milder and later in bronchitis
Infections are more common in bronchitis
Respiratory failure and cor pulmonale is more common throughout bronchitis, but terminal in emphysema
Airway resistance increased in bronchitis, but normal or slight increase in emphysema
Elastic recoil normal in bronchitis, low in emphysema
On CXR, bronchitis is prominent vessels and large heart. Emphysema is hyperinflation and small heart
Comparison of COPD and asthma
COPD nearly always smoker or ex smoker
COPD is rare under 35
Chronic productive cough is common in COPD but uncommon in asthma
Dyspnoea is persistent and progressive in COPD, variable in asthma
Night time waking dyspnoea is rare in COPD but common in asthma
Asthma shows diurenal/day-to-day variation
Main haemoptysis differentials
Lung cancer, TB, bronchiectasis. Not a common COPD feature
Lung cancer RF
Smoking, age (75+), air pollution, occuputation risk, FHx of asbestos exposure
Emphysema is bigger risk factor than chronic bronchitis
Lung cancer Symptoms
Dry cough 3 weeks + Haemoptysis Chest pain (esp radiating to shoulder, pain on coughing) Recurrent chest infection Cervical lymphadenopathy Exertional dyspnoea Fatigue Weight loss Thrombocytosis Bone pain Hoarseness Fever Dysphagia
SCLC
Rare
Associated with smoking
Grows quick, mets early
Very poor prognosis, often metastasised by diagnosis
Can cause cavitating lesions and paraneoplastic syndromes.
Generally centrally located.
Squamous cell
Non small cell. 50% of lung cancers. Often Central and close to carina. Gives obstructive symptoms Relatively slow growing and may be resectable Associated with smoking Can cause cavitating lesions
Adenocarcinoma
20% of lung cancers. Equal gender distribution.
Less association with smoking.
Can rise at existing lung scarring (scar cancerS). If no mets then can have good prognosis.
Superior sulcus tumour
Occurs in lung apex (e.g. pancoast tumour).
T3 tumour.
Hilar mass
Common presentation of squamous cell and small cell carinomas (but can also be due to nodal mets).
Tumous can compress/narrow broncus (tapered bronchus is specific for lung cancer)
How does tobacco smoke damage lungs?
Benzoayrine damages DNA at cancer protecting parts,
Chromium allows other harmful chemicals to bind to DNA, increasing their toxicity
Alcohol and tobacco give synergistic effect by reducing CYP450 effectiveness and exposure to more toxins
Lung cancer genetics
Loss of Rb, P53 and P3 is common. RAS proteins mutated in 1/5 of NSCLC and carry poorer prognosis.
EGF overexpression common
Transudate causes
Think FAILURE!
Heart failure, liver failure , but can also occur in nephrotic syndrome, peritoneal dialysis and hypothyoidism
Exudate causes
Occur due to increased permeability of microcirculation, or alteration to pleural drainage to lymph nodes.
Examples are cancers, PE, pneumonia, TB, mesothelioma, Rheumatoid arthritis, sLE, lymphoma
Differentiating transuldate and exudate
Transudates have lower LDH and protein than exudates.
Lights criteria is:
- Effusion protein: serum protein >0.5,
-LDH effusion: serum >0.6
- Effusion LDH is greater than 2/3 of lab upper reference for serum LDH
If any of these is true then it is an exudate.
Transudates tend to be bilateral
Effusion diagnosis
Signs include dullness to percussion and quieter breath sounds
on CXR can see indications once >250mL (initialy costophrenic angle blunting).
If larger then see fluid in hosizonal and oblique fissures
If massive effusion then meniscus sign with mediastinal shift
Chest tap can be performed, but Hx might indicate cause and resolution.
If no known Hc then chest tap and broncoscopy
Bronchiectasis definition and pathophysiology
Airway widening.
Diagnosis of structural pathology
Permanent dilation of subsegmental airways (bronchi and bronchioles) - causes surface/volume ratio decrease and also causes gaps that fill with thick mucus (limits gas exchange - widened anatomical and physiological space)
Cole’s viscious cycle hypothesis: initial insult causes blockage, neutrophils infiltrate and elastases damage parenchyma. Mucus stasis leads to opportunistic colonisation.
RF:
Congenital (CF, primary ciliary dyskinesias), infective, fungal, obstruction, irritants, idiopathic, tertiary due to primary diseases like hypogammaglobulinaemia, RA.
Cylindrical bronchiectasis
More common, airways widen but structure remains.
Varicose bronchiectasis
Tortuous airways
Cystic bronchiectasis
Outpouchings, less common but most severe. Associated with CF.
Distinction between COPD and bronchiectasis
COPD is functional/physiological diagnosis (poorly reversible airflow obstruction) while bronchiectasis is structural (see airway dilatation on CT) - although bronchiectasis progresses to obstructive and restrictive pitcure
Bronciectasis S+S+ examination
SOB, fatigue, cupfuls of sputum (generally green, may have blood), recurrent pneumonias.
Can get pneumothorax through lung lining damage.
Can het massive haemoptysis if larger blood vessels eroded
Amyloidosis can occur (autoimmune response to chronic inflammation causes protein deposits)
Cor pulmonale can occur
Rarely, bacteria get into blood and brain (cerebral abscess)
Can also get dry bronchiectasis (no sputum) and idopathic (no PMHx of lung disease)
O/E: Ronchi, loud expiratory wheeze, mid inspiratory squeak, coarse crackles, clubbing, right heart failure.
Bronchiectasis investigations
FBC
U&E
CRP
Coagulation screen (bleeding risk factors)
Sputum (causative/propagating organisms: H. influenzae, S. pneumoniae and P. aeruginosa are common but can get mycobacterium). If culture negative, consider fungal cause. Bronchoscopy can be done if culture is negative or no sputum. Broncho alveolar lavage can also be used if no sputu,.
CXR: pneumonia, effusion, bronchial thickening
Spirometry: obstructive
Peak flow is not appropriate
High Res CT shows Signet Ring Pattern (widening around inflamed bronchiole)
May also want to test immunoglobulins, functional antibodies and aspergillus serology
Pneumonia symptoms
Fever, productive cough, SOB, hypoxia, tachypnoea, confusion
CAP definition and assessment
LRTI+ new pneumonic changes on CXR in community or within 48h of admission. Peak age is 50-70, more in winter/early spring
Commonly Strep pneumonia, H influenzae, and moraxella catarrhalis.
MRSA more common after viral pneumonia
Can also get group A strep
Atypical causes: mycoplasma, legionella, chlamydia.
Can ID pathogen by sputum or urinary antigens. CURB 65: Confusion (new onset) Urea >7mmol/L Resp rate >30 BP <90 sys <60dias 65 years +
Low risk is 0-1
Mod is 2 (?hospital)
3-5 is hospital with IV abx
HAP
LRTI symptoms +pneumonic changes on CXR after 48h admission or within 7 days of previous stay.
Risk increases with longer stay, poor mobility, reduced cough, over 70 and severe underlying disease
Common causes: enteric gram negatives (enterobacteria, pseudomonas) but can be S. pneumoniae, H, influenzae and S aureus
Aspiration pneumonia
May not show on CXR
Consider if low GCS, evidence of vomiting, stroke survivor.
If suspected then add metronidazole to cover for anaerobics
Pneumonia complications
1) sepsis/septic shock (can show as AKI, new confusion, hypoxia, high RR, deranged clotting, deranged LFT. Septic shock is sepsis plus regractory hypotension and raised lactate
2) Lung abscess (more common with S aureus, can cause pus in parenchyma) - suspect if swinging pyrexia and rising CRP
3) empyema (parapneumonic effusion stasis, more common with streptococcus pneumoniea)
Factors determining TB transmission probability
Susceptility (immune status of exposed person)
Infectiousness (number of tubercle bacilli expelled into air)
Environment (enclosed spaces, away from UV light)
Exposure (proximity, frequency and duration of exposure)
Extrapulmonary TB
Less common. Sites include larynx, pleura, brain, kidneys and bone. Generally not infectious unless also have pulmonary TB or if in larynx/pharynx.
In miliary TB, disseminates into blood stream
TB exposure pathway
80% eliminate with no infection
20% don’t eliminate and get primary disease. Often asymptomatic. Macrophages take up TB droplets but fail to kill them. TB multiplies inside macrophages (which can then spread TB around body or to lymph nodes). HIV+ patients more likely to disseminate
TB inside macrophages causes granulomatous lesion in lungs - either heals by fibrosis, invades locally or disseminates.
2-6 weeks for adaptive response, T cells involved and allow granuloma formation.
Granuloma can contain TB for life or can be reactivated
TB investigation
Culture and test for AFB(sputum , or extrapulmonary site if needed)
Histology (caseating granuloma)
Imaging: CXR can show caseating granulomas (calcifies to Ghon focus, if lymphadenopathy then Ghon complex). May see lobar/patchy consolidation, effusions, lymphadenopathy, miliary TB. May see necrosis and cavitation (esp in apex).
Latent TB CXR should be normal.
Mantoux test shows TB exposure, but FP with BCG and FN in HIV
Can do IGRA test to comfirm (don’t get FP with BCG and don’t get FN with HIV)
Management of TB
Quadrupole therapy: RIPE Rifampicin (R) Isoniazid (H) (with pyroxidine to prevent peripheral neuropathy) Pyrazinamide (Z) Ethambutol (E) R and H for 6/12, Z and E 2/12
Definition of restrictive lung disease
physical reduction in potential max lung volume.
Restrictive lung disease causes
Compliance issues (e.g. fibrosis), increase in dead space (effusion/pus)
Occupational lung disease
lobectomy
obesity
pregnancy
neuromuscular disease (affecting diaphragm)
Kyphoscoliosis
S+S of restrictive lung disease
SOB, cough, wheeze, chest pain, fatigue, anxiety, depression, Ronchie, wheeze, cyanosis, clubbing, right side heart failure
Coarse crackles in fibrosis
Fine crackles in fluid pathology
Spirometry shows FEV1 <80%, FVC <80%, but FEV1/FVC >0.7
Spirometry contrast between restrictive and obstructive
Obstructive: FEV1<80%, FVC >80%, FEV1/FVC <0.7
Restrictive FEV1<80%, FVC <80%, FEV1/FVC <0.7
Classification of restrictive lung disease
E.g. focal, interstitial, replacement.
Focal is generally occupational lung disease (affects lymphoid tissue, inflammation derived fibrosis)
Interstitial is diffuse, affects parenchyma (seen in extrinsic allrgeric alveolitis as type 3 H/S)
Replacement is sequalae of RA, TB, CT disease
Basal or Apical Fibrosis
Apical: Allergic bronchopulmonary Aspergillosis TB Extrinsic allergic alveolitis Ankylosing spondylitis Sarcoid Histiocytosis Occucational (berylliosis/silicosis)
Basal: Drug induced (amiodarone, bleomycin, methotrexate, vincristine, nitrofurantoin) RA CT disease Idiopathic pulmonary fibrosis Asbestosis
However, occupational causes (asbestosis, silicosis, berylliosis) can affect upper or lower, and RA and anklyosing spondylosis can affect both.
Drugs tend to affect the lower lobes.
Extrinsic allergic alveolitis (tertiary fibrosis)
Bird droppings Hay mou dHop mould M avium from hot tub mist Mixed fungi from uncleaned musical instruments
Pulmonary fibrosis investigations
ABG (t2Resp failure), CRP (superimposed infection), special tests (Antinuclear antibody, Rheumatoid factor)
Imaging: honeycomb on CT
Lung biopsy if doubt exists
Pulmonary fibrosis investigations
Slow progression
Pirfenidone (downregs procollagens 1 and II)
Nintedanib (TK inhibitor, anti fibrotic)
Lung transplant
Differentials for dyspnoea with wheeze
Asthma, COPD, heart failure, anaphylaxis
Dyspnoea with stridor
Upper airway obstruction.
Foreign body, tumour, acute epiglottitis, anaphylaxis
Dyspnoea with creps
Heart failure, pneumonia, bronchiectasis, fibrosis
Dyspnoea with clear chest
PE, hyperventilation, anaemia, DKA, drugs (e.g. aspirin), central cause
Dyspnoea with dullness
pneumonia, consolidation, collapse, pleural effusion, haemothorax(Stony)
Dysnpnoea with increased resonance
Pneumothorax
Phases of lobal pneumonia
1) Congestion (24h, alveoli fill with fluid/bacteria)
2) Red hepatisation (airless. Alveolar capillaries dilate. Fibrin strands extend between alveoli. Neutrophils infiltrate. Exudate in pleura)
3) Gray hepatisation (less hyperaemia. Macrophages, neutrophils and fibrin)
4) Resolution (lysis of fibrin, removal by sputum/lymphatics. Starts at 8-9 days without Abx)
Bronchopneumonia
More affects infants, young children, elderly and often secondary to other conditions (influenza/measles) or aspiration pneumonia, bronchus obstruction, inhalation of gaseous irritants, major surgery or chronic illness.
Shows diffuse opacity on CXR as inflammation of bronchioles (and more proximal)