Deck 2 Flashcards
Define Asthma
Reversible, obstructive due to exercise/allergens/stress or idiopathic.
Key symptoms are expiratory wheeze, diurnal dyspnoea, chest tightness which VARY
Histologically, bronchial inflammation and eosinophils
Acute asthma phase vs late phase
Early is bronchospasm (histamine, PD2, leukotrienes)
Late phase has cellular infiltrates and oedema (narrows), also hyperreactive
Chronic asthma features
Bronchoconstriction, mucusal oedema, carcot leyden crystals (eosinophil granules), Curschman spirals, pulmonary HTN
Diagnosis of Asthma
If under 5, Tx based on obs/clinical judgement and objective testing ASAP
5-16, use spirometry (look for reversibility), if not then FeNO test
17+ uses spirometry, FeNO, peak flow variability. Also use airway hyperreactivity (histamine or methacholine challenge)
Tx for asthma
SABA
Add ICS
Add LRTA
LABA+ICS+SABA
MART is LABA+steroid as reliever and preventer
Moderate acute asthma
PEFR 50-75%, increasing symptoms, no acute asmtha features
Acute severe asthma
PEF 33-50%, RR>25, HR>110, inability to complete sentences in 1 breath
Life threatening asthma
SpO2 <92%, PEFR <33%, silent chest, poor respiratory effort, cyanosis, altered consciousness
COPD definition
progressive airflow obstruction but not fully reversible.
See mucus hypersecretion, ciliary dysfunction, airflow limitation, hyperinflation, impaired gas exchane and pulmonary HT (hypoxaemia induced vasoconstriction)
COPD RF
Smoking, indoor pollution, occupational toxin, genetic factor, infection, socioeconomic factors
COPD symptoms
Start as asymptomatic apart from exertion, then chronic cough, progressive dyspnoea, regular sputum, whzeeze, fatigue, weight loss, anorexia, cough syncope, depression
Haemoptysis is not common feature, so consider ddx (lung cancer, bronchiectasis, TB)
COPD examination
Hyperinflated chest, wheeze, quiet breath sounds, pursed lip breathing, accessor muscles, paradoxical movement of lower ribs, peripheral oedema, cyanoses, raised JVP, cachexia
COPD spirometry + other investigations
FEV1<80% FVC >80% (although may be reduced) FEV1/FVC <0.7 DLCA reduced in emphysema ECG may show cor pulmonale
COPD management
SABA/SAMA Add LAMA (tiotropium) Steroids can be added Mucolytics Smoking cessation Rescue Abx
Chronic bronchitis
productive sputum on most days for 3 months of at least 2 successive years.
Does not imply airway inflammation.
Caused by chronic irritation stimulating mucus (increase goblet cells).
Sputum increases infection risk.
Proximal airspace disease.
Reid index shows ratio of gland: all thickness (increased)
Typically 40s, mild or late dysponoea, copious sputum, recurrent infection, repeated resp failure and increased airway resistance. on CXR, prominent vessels and large heart
Emphysema
Distal airspace disease with increased terminal bronchiole size and reduced gas exchange.
No fibrosis.
Caused by protease/antiprotease imbalance.
Centrobular is most common (smoking association). Panaacinar is whole lobule, alpha 1 antitrypsin.
Typically 50s-75, severe early dyspnoea, scant sputum, occasional infections. Resp failure at terminal phase. Relatively normal airway resistance but low recoil. Small heart and hyperinflation on CXR.
Lung cancer symptoms
Dry cough (over 3 weeks), haemoptysis, dyspnoea (esp exertional), chest pain (radiating to shoulder?), recurrent infections, clubbing, lymphadenopathy, B symptoms, thrombocytosis, bone pain, hoarseness, fever, dysphagia
Lung cancer investigation
CXR, then staging CT
Bronchoscopy can be used for histology, but only useful up to bronchioles.
Lung cancer types (general)
Small cell (15%) and NSC (85%)
Small cell lung cancer
OAT cell.Rare. Associated with smoking. Grow quickly and metastasise early, so poor prognosis.
Can cause cavitating lesions. Comes from bronchoepithelium but differentiates neuroendocrine. Associated with paraneoplastic syndromes (SIADH, Cushings - > rarely causes MG like syndrome (Eaten Lambert, but symptoms improve with use)
Has pulmonary carcinoid rare subtype which can be benign
Squamous cell lung cancer
NSC. 50% of lung cancers. Heavy smoking association. OFten central, near carina. Tend to have obstructive symptoms and may have overlying infection. Slow growth.
Can diagnose on sputum cytology. May secrete PTH and cause hypercalcaemia
Adenocarcinoma Lung cancer
20% of lung cancers. Equal gender. Less smoking association. Typically peripheral, but can be central. Can arise at scars.
Subtype is bronchoalveolar carcinoma (comes from alveoli and T2 pneumocytes -spreads along alveolar septa. Good prognossi if no mets)
Large cell anaplastic carcinoma (lung)
10% of lung cancers. Need EM to differentiate as often has squamous or adenocarcinoid features.
Metastases to lungs
Breast, kidney, testicular and bladder cancer
Primary lung cancer complications
SVC compression/obstruction, recurrent laryngeal nerve palsy, horner syndrome, distant mets to brain, bone, liver and adrenals
Exudate: Causes Biochemistry Typical precipitating factor Associations
Alteration to formulation or absorption of pleural fluid
>30g/L (or >0.5 effusion:serum protein, effusion:serum LDH >0.6)
Seen in malignancy, infection, pulmonary embolism, pneumonia, TB, mesothelioma, RA, SLE, lymphoma
Often unilateral. If polymorphs in effusion then suggests PE, TB or asbestosis. Lymphocytes in effusion suggests malignancy or TB
Transudate Causes Protein content Typical precipitating factor Associations
Caused by hydrostatic pressure alterations, pleural permeability and oncotic pressure
protein <30g/L, lower protein and lower LDH than exudates
Seen in ‘failures (HF, liver failure, peritoneal dialysis, nephrotic syndrome, (rarely) hypothyroidism or ovarian tumour (Meig’s syndrome)
Often bilateral.
Pleural effusion investigation
CXR (will only see once >250mL),
Chest tap and broncoscopy (esp if no known cause)
Empyema
Can form from stagnant effusion, esp exudate with high protein content
Pneumonia
Pulmonary parenchyma infection plus new shadow on CXR (separate from bronchitis)
In bacterial, inflammatory exudate in alveolar spaces gives consolidation.
In viral infections, alveoli often spared and interstitium affected (pneumonitis/interstitial pneumonia)
Bronchopneumonia
Primary infection around bronchi.
Spreads around lobules and can be multiple lobes. More common at age extremes (immobility and secretion retention.
Tends to affect bases
Lobar pneumonia
Distal airspace affected. Spreads over whole lobe. More common in adults
Pneumonia exam
Fever, productive cough, dyspnoea, tachypnoea, confusion, pleuritc chest pain (may refer). Coarse crackles. Dull to percussion. Pleural rub. Bronchial breathing. Increased vocal resonance (not in effusion, pneuothorax or collapse)
Pneumonia RF
male, elderly, smoker, alcoholic, chronic disease, secondary to bronchial obstruction (e.g. cancer)
CAP Criteria RF Common organisms Atypicals
CAP is in community or within 48h of admission. Peak age is 50-70, more in winter/spring.
Increase risk in COPD, diabetes, CVD and immunosuppression.
Common pathogens: S pneumonia (most common - lobar pneumonia and rusty sputum), H influenzae (COPD, <110) and moraxella catarrhalis.
S aureus more common after viral pneumonia
Atypicals are:
mycoplasma (more common in 17-44, longer illness, extra pulmonary features (rash, hepatitis, D&V, pericarditis, meningoencephalitis), legionella (classically smokers post holiday - often SIADH, CN palsy, proteinuria, haematuria, bilateral bases)
Chlamydia (LFT derangement and hyponatraemia)
Severity is CURB 65: New confusion (MMT 8 or less) Urea >7mmol/L RR>30 BP <90 sys or <60 diastolic 65+ 0-1 is low (community, 2 is mod (?hospital), 3 -5 is hospital
HAP
LRTI +pneumonic change >48h admission or if admitted in last 7 days.
RF is increased hospital stay, poor mobility, reduced cough, over 70, underlying disease.
Most commo causes: enterobacteria, pseudomonas (60%), rest are s. pneumoniae, H influenzae and S aureus
Aspiration pneumonia
May not show on CXR
Consider if low GCS and evidence of vomiting
Add metronidazole for anaerobic cover
pneumonia stages
Congestion (24h, alveoli fill with fluid and bacteria)
Red hepatisation (airless, capillaries dilate, exudate in pleura)
Gray hepatisation (macrophages, neutrophils, fibrin)
Resolution (8-9 days without Abx)
Pneumonia complications
Sepsis, lung abscess (mrore common in s aureus), empyema (more common with strep pneumoniae), carnification (scaring from resolution failure - reduces resp function), amylodiosis (amyloid deposit)
TB infection
Drops lodge in alveoli.
80% of people eliminate, 20% have primary infection (can be asymptomatic). If elimination fails, TB in macrophages and multiplies and disseminates (more like in HIV) or cal form granulomatous lesion (heals by fibrosis, invades locally)
Can reactive during immunocompromise (RF are age, steroids, immunosuppressive drugs (esp ant TNF), diabetes, CKD, HIV.
pulmonary TB symptoms
cough, haemoptysis, fever, B symptoms. clubbing (advanced), erythema nodosum
TB investigation
Culture, sputum (AFB), histology (caseating granuloma), CXR primary: (Ghon focus, if lymphs then complex) - lobar/patchy consolidation, effusion, lymphadenopathy, miliary)
CXR latent may show nodules
CXR secondary shows necrosis, cavitation, consolidation, effusion, miliary TB
Mantoux test (>5mm is positive in immunosuppressed, prior TB or recent contact; >15 is positive in any individual)
PCR (can’t distinguish active/latent)
Culture is GSTD but takes 6 weeks on Lownstein Jensen medium
Extrapulmonary TB and symptoms
Less common. Larynx, pleura, brain, kidneys, bone. Not infectious unless larynx.
Meningitis, painless lymphadenopathy, arthritis (Pott in spine), lupus vulgaris/erythema nodosum (cutaneous TB), chest pain (pericarditis)
Bronchiectasis definition
Structural pathology (subsegmental airways dilate (bronchi/bronchioles) - decreasing surface/volume ratio and allows mucus plugging. Cole's viscious circle with initial insult causing blockage, inflammatory infiltrate and elastase mediated parenchyma damage which distorts physiology. Mucus stasis gives risk of future insult Overlap with COPD but COPD is functional/physiological and bronchiectasis is structural (see dilatation on CT)
Cylindrical bronciectasis
Most common, airways widen but structure remains
Varicose bronchiectasis
Tortuous
Cystic bronchiectasis
Rare, sever, outpouchings. Associated with CF
Bronchiectasis RF
CF, primary ciliary dyskinesia, infection, obstruction (COPD, tumour, aspergillosis, irritants), idiopathic. Can be tertiary due to primary disease (hypogammaglobulinaemia (immune deficiency) or RA)
Bronchiectasis S+S
SOB, cupfuls of sputum (often green+/- blood), fatigue, PMHx of lung insult.
Can have dry bronchiectasis with no cupfuls of sputum
Clubbing, coarse inspiratory crackles, wheeze, low body habitus due to demands
Bronchiectasis complications
Mixed obstructive/restrictive condition
Recurent pneumonia
Pleural effusion (transudate)
Larger blood vessels erode (massive haemoptysis)
Increased pulmonary resistance (RHF)
Cerebral abscess if bacteria spread
Amyloidosis (autoimmune response to chronic inflammation
Bronchiectasis investigations
FBC, U&E, coag screen, CRP, sputum microscopy (H influenzae, S pneumoniae, P aeruginosa most common - consider fungal)
CXR (pneumonia, effusion, bronchial thickening
Spirometry (obstructive) - note peek flow not appropriate)
CT scan (signet ring pattern, widening around inflammed bronchiole)
Igs, functional antibodies, aspergillus serology
Restrictive lung disease
Get reduced max lung volume (e.g. fibrosis), increase in dead space (effusion/pus)
FEV1 reduced, reduced FVC but FEV1/FVC may be normal or increased
Restrictive lung causes
Fibrosis, occupational lung disease, oedema, lobectomy, bronchiectasis, kyphoscoliosis, neuromuscular disease affecting diaphragm, obesity, pregnancy, sarcoidosis, RA, SLE
Pulmonary fibrosis symptoms and signs
ronchi, SOB, Wheeze, chest pain, fatigue, anxiety, depression, cyanosis, clubbing, fine crackles
Pulmonary fibrosis:
Focal, interstitial or replacement disease
Focal is generally occupation link and affects lymphoid tissue (can be triggered by local inflammation)
Interstitial is more diffuse (think extrinsic allergic alveolitis (T3HS)
Replacement is seen in RA, TB and CT disease where tissue damage has been
Apical fibrosis causes
Aspergillosis TB Extrinsic allergic alveolitis Ankylosing spondylitis Sarcoid Histiocytosis Occupational (beryllosis/silicosis)
Basal fibrosis causes
Drug induced (amiodarone, bleomycin, busulfan, methotrexate, vincristine, nitrofurantoin) RA CT disease Idiopathic pulmonary fibrosis Asbestosis
Extrinsic allergic alveolitis
T3HS. Tertiary fibrosis. Can be bird droppings, hay mould, hops, M avium from hot top, fungi from musical instrument
Fibrosis investigations and prognosis
ABG, CPR, ANA/Rh factor for CT disease CXR/CT (honeycomb) FEV1>80, FVC<80, FEV1/FVC>0.7 Reduced gas exchange Lung biopsy
Poor prognosis, tx is slowing progression.
Pirfenidone downregulates procollagens. Nintedanib is TK inhibitor
Alternative is lung transplant
Mesothelioma O/E
O/I
Diminished breath sounds (effusion, trapped lung, bronchial obstruction), dull to percusion
CXR (effusion, pleural thickening, reduced lung volume, calcification/fibrosis)
CT nodular thickening (but can be benign)
Effusion tap can allow differentiation of transudate and exudate, but cytology not useful.
methothelioma types and mets
Epitheloid is more favourable
Sarcoimoid and mixed are unfavourable
Often mets to contralateral lung, liver, adrenal gland, kidney, potentially bone
90% are pleural, 5-10% peritoneal, but can get pericardial and testicular
Air cannulae %
on air, 21%.
1L = 25%, 2L=28%, 3L= 32%, 4L=36%
Base excess
Amount of acid required to normalise pH.
Negative means metabolic acidosis, positive is metabolic alklaosis.
pH and oxygen binding
In acidotic blood, oxygen more tightly bound.
In alkalosis, oxygen dissociates more readily
Lung cancer referral and investigations
40+ with 2+ symptoms (or 1+ if smoker) then urgent CXR and referral
CR scan for staging (liver and neck)
PET-CT if aiming for cure (may have problems in renal impairment).
If PET CT is positive nodes, then EBUS TBNA needed
Bone scintigraphy can be used for bone mets (not needed if PET-CT negative)
CR/MRI for ?brain mets
LUL collapse
Veil sign
LLL collapse
Sail sign
RUL collapse
Reverse S sign of Golden (?mass) -see horizontal fissure displacement
RML collapse
Loss of R heart silhouette
RLL collapse
Loss of R hemidraphram silouhette. May see rib crowding due to volume loss
Superior sulcus tumour
Pancoast tumour. T3. MRI recommended (although CT may be useful)
Visceral/parietal pleural extensions
Visceral goes to 6th rib in MCL, 8th in MAL and 10th in MSL.
Parietal goes to 8th, 10th and 12
Kco vs TLCO
diffusion capacity per unit area vsDiffusion capacity for total lung
Decrease means gas exchange problem, not a chest wall deformity.
smoking cessation
NRT or bupropion if >10day
Empyema organisms
Streptococcus pneumoniae, H influenzae, Klebsiella, pseudomonas
cAN BE VIRAL (COXSACKIE, ADENOVIRUS, ECHOVIRUS)
cAN GIVE FIBROUS PLEURAL ADHESIONS AND CALCIFICATION
Causes of resp acidodis and symptoms
poor ventilation, airway obstruction, emphysema, neuromuscular obesity
Gives headache, tachycardia, bounding pulse, CO2 flap, papilledema, Kussmaul respiration, Potassium derangement (hypokalaemia, or hyperkalaemia if renal function impaired)
Causes of resp alkalosis
Can be CNS (pain/anxiety/meningitis, trauma, psychosis, fever), hypoxaemia (pneumonia, pulmonary oedema, severe anaemia, high altitude), salicates, progesterone, pregnancy, haemothorax, flail chest, PE, HF, heat exposure, septicaemia
Metabolic acidosis
Either too much acid or not enough H+ excretion. Normal anion gap then bicarb is lost (GI/renal loss), renal acidosis, potassium sparing diuretics, ACEi/NSAID, bicarbonate secreting villous adenoma
Large anion gap in increased acid (DKA, lactic, urate, ingested acid/aspirin)
Anion gap
Note that bases (cations) are positive, and acids (anions) negative.
So a large anion gap means extra acid.
Metabolic alklaosis
Can be H+ loss (vomiting) or from direct increase in bicarb (retention, alkali ingestion - Milk alkali syndrome, villous adenoma if chloride secreting, hypercalcaemia, aldosteronism, steroids, Cushings