Respiratory Flashcards
Sarcoidosis.
Typical presentation : chronic cough. fatigue. lethargy, erythema nodosum (Lofgren’s syndrome Hilar / EN / Arthropathy), Lupus Pernio
Atypical presentation: 5% neurological complications. optic neuritis. mononeuritis multiplex. myelopathy. seizures. granulomas causing mass effect. Basal meningitis with cranial nerve palsies. bulbar palsy. neuropsychiatric manifestations
Causes of clubbing
NOT COPD
ABCDEF
abscess + asbestosis
bronchiectasis
CF
Dirty tumours - SCLC / mesothelioma / bronchogenic
Empyema
Fibrosing alveolitis / aspergillosis - any pulm fibrosis
CLUBBING AND CRACKLES = FAB
fibrosing alveolitis
Asbestosis
Bronchiectasis / bronchogenic cancers
OTHERS:
sarcoid / TB
RA
thyroid acropatchy
think cardiac / abdomen / thyroid
4 grades
1) loss of nail bed angle - SCHAMROTHs sign
2) boggy nail bed
3) Increased nail curvature
4) drumsticks
lung function tests
Include
Spirometry:
FVC = from peak of inspiration forced expiration - exhale for as long and as forcefully as possible
FEV1 = Lung volume expelled in 1 second
FEV1/FVC
<70% = obstructive = i.e obstruction to expiration
Tumour / COPD / asthma / pulmonary fibrosis
>70% = restrictive
trapped lung / lobectomy / pulmonary fibrosis / flail chest
Diffusion capacity:
Mixture of CO and helium inhaled
CO crosses alveolar membrane
helium does not
percentage of CO that is transferred across is calculated = TLCO - total lung carbon monoxide
Total lung volume is then calculated using remaining helium concentration which would be diluted by gas already present in lung on inspiration
gives KCO = gas transfer occuring per unit volume based on CO loss and helium remaining
low kCO - low transfer - emphysema / ILD
high kCO - high transfer where blood++ present - PE / SLE / Wegners / anti GBM
Total lung capacity - TLC
Measured using helium dilution again as above
i.e. increased dilution of helium means more air present or trapped at beginning of inspiraiton
Increased in COPD / asthma / emphysema / pulmonary fibrosis / hyperinflation
Decreased in restrictive lung conditions
Flow volume loops
Expiration - above x axis
inspiration - below y axis
measures TLC and gives a plotted course of air flow
1)normal flow loop
2)obstructive flow loop - expiration sharp decrease and then soft plateau to 0 due to air trapping
3)restrictive - sharp insp and exp peaks and trough with narrowed base to loop diagram as less volume moved and more rapid transition of gas in an out
4) fixed obstruction extra thoracic
shallow inspiration - stridor
normal exp loop but smaller as paints a restrictive picture - expiration clears obstruction
5)fixed upper air way stenosis - tumour / trauma
shallow inspiration and expiration flow loops
6)varibale upper airway obstruction
obstruction during expiration only so shallow expiration but sharp inspiration - i.e. inspiration clears obstruction
What is diffusion capacity
Essentially a measure of gas transfer and may indicate underlying pathology
Diffusion capacity:
Mixture of CO and helium inhaled
CO crosses alveolar membrane
helium does not
percentage of CO that is transferred across is calculated = TLCO - total lung carbon monoxide
Total lung volume is then calculated using remaining helium concentration which would be diluted by gas already present in lung on inspiration
gives KCO = gas transfer occuring per unit volume based on CO loss and helium remaining
What is total lung capacity and how is it measured
TLC is the measured total useable lung volume.
It is measured using helium and carbon monoxide.
CO crosses the lung alv membrane
Helium does not
The concentration of helium is measured on expiration as it will dilute proportionately according to the concentration of gas present at the beginning and end of inspiration
Therefore TLCO will be increased in any resp condition where air trapping or hyperinflation are present
TLCO will be reduced in any condition where lung volume is restricted
explain flow volume loops
Flow volume loops
Expiration - above x axis
inspiration - below y axis
measures TLC and gives a plotted course of air flow
1)normal flow loop
2)obstructive flow loop - expiration sharp decrease and then soft plateau to 0 due to air trapping
3)restrictive - sharp insp and exp peaks and trough with narrowed base to loop diagram as less volume moved and more rapid transition of gas in an out
4) fixed obstruction extra thoracic
shallow inspiration - stridor
normal exp loop but smaller as paints a restrictive picture - expiration clears obstruction
5)fixed upper air way stenosis - tumour / trauma
shallow inspiration and expiration flow loops
6)varibale upper airway obstruction
obstruction during expiration only so shallow expiration but sharp inspiration - i.e. inspiration clears obstruction
What is COPD
Progressive airflow obstruction which demonstrates very limited reversibility with bronchodilators
Associated with various pathologies but commonly due to a hyper responsiveness to inhaled irritants like cigarette smoke / silica / coal dust / specific allergen / other particulates
2 types
1. Chronic bronchitis - chronic productive cough for at least 3 months of the year over 2 consecutive years
- Emphysema: defined histologically or via CT demonstrating
a) alveolar wall destruction leading to permanent and fixed enlargement of air spaces distal to end bronchioles
b) bronchiectasis
What is emphysema
Emphysema is a form of COPD defined histologically or radiologically as the destruction alveoli walls leading to permanent and fixed enlargement of the airways distal to the end bronchioles.
What is bronchitis
Bronchitis is defined as a chronic productive cough lasting for 3 months successively over 2 years. It is a form of early COPD
Signs of COPD
pursed lips breathing - self peep to prevent airway collapse
cachexia - increased RR / catabolic process / malignancy
accessory muscle use
reduced cricosternal distance - <3cm
prolonged expiratory phase
expiratory wheeze
crackles - bronchiectasis
expiratory crackles - large airway collapse
barrel chest - hyperinflation
asterixis - CO2 retention flap
tar stained fingers
Hyper resonance to percussion - reduced hepatic and cardiac dullness -HYPERINFLATION
Reduced breath sounds over bullae
Focus of wheeze - infection - apex ?TB
day time somnolence CO2 retention / OSA
Grade COPD
- MRC Dyspnoea scale
- FEV1 Gold scale
- BODE index
Dyspnoea scale 1 - not troubled 2- SOB hurrying flat or slight incline 3 - own pace due to SOB or stops for breath at own pace 4- limited to 100m 5-house bound or SOB dressing
Gold Scale where FEV1/FVC <70%
- Mild FEV1>80%
- moderate FEV1 50-80%
- severe FEV1 <50%
- very severe FEV1 <30% OR <50% + T2RF
BODE BMI FEV1 6 Min walk test mrc dyspnoea scale
What is the BODE index
BODE index is a predictor of COPD outcome- admissions and mortality - which takes into account pulmnary and extrapulmonary manifestations of COPD
BMI
Obstructive manifestations - FEV1 (GOLD)
Dyspnoea (MRC)
Exercise tolerance - 6 min walk test
score = 0-10
weight loss is a predictor of poor outcome and decline
How to investigate / diagnose COPD
1. Pulmonary function tests Flow loop LIMITED REVERSIBILITY <15% CHANGE IN FEV1 FEV1/FVC <70% FEV1 - gold grading - BODE 6 minute walk test - BODE BMI - BODE MRC Dyspnoea scale - BODE 2. Signs and symptoms BRONCHITIS - CHRONIC SUPPURATIVE COUGH FOR >3 MONTHS IN 2 SUCCESSIVE YEARS barrel chest exp wheeze / prolonged exp phase / cricost <3cm weight loss SOBOE Asterixis 3. CXR 4. CT - emphysema / bullae / bronchiectasis 5. Hb - polycythaemia 6. GAS - CO2 retention 7. alpha 1 antitrypsin - EARLY ONSET COPD 8.sputum culture 9.throat swab / viral throat swab
COPD exacerbation causes
60% viral induced exacerbations or bacterial 30% unknown 10% pollution VIRAL: rhinovirus / adenovirus / influenza / coronavirus BACTERIAL: Strep Pneumoniae 1. Moraxella Caterhallis 2. Haemophilus 3. pneumococcal 4.mycobacterium - TB
Smoking Cessation
Smoking Cessation improves symptoms and FEV1 decliine slowed and return to near normal for age after 5 years
ONLY TREATMENT SHOWN TO ALTER DISEASE COURSE
5As = BTS approved or smoker? ready to stop? you should quit! Ill help! come back! 1. Ask about smoking status 2. Assess readiness to quit 3. advise to quit 4. assist in efforts to quit 5.Arrange follow-up
Therapy:
Identify quit day
group therapy / counselling
inform of abnormal lung funtion
Nicotine replacement therapy
limited evidence one form over another
better compliance with nasal inhaled NRT
also BUPROPRION - NORADRENALIN AND DOPAMINE REUPTAKE INHIBITOR
VARENICLINE
Partial agonist of NICOTINIC ACH RECEPTORS
NICOTINE REPLACEMENT THERAPY
Limited evidence to suggest one form better than another
inhaled forms may cause bronchospasm
nasal NRT show better compliance anecdotally
BUPROPRION - NA AND DOPAMINE AGONIST
VARENICLINE - NICOTINIC RECEPTOR AGONIST
5As assess smoking assess readiness to quite advise to quit advise on how arrange follow up
GROUP COUNSELLING
NRT
COPD TREATMENTS
ACUTE: infection? amox / clarith steroid 5 days and wean pesuodomonas - Tazocin 10 days GAS - retention C02 - ?NIV
Chronic Mucolytics - glycopyronnium or carbocisteine Early morning GAS - ?nocturnal NIV sputum culture chest physio Tailor sats Chronic T2RF - NIV or LTOT smoking cessation - 5As / NRT / Buproprion / Varenicline rescue pack
PULMONARY REHAB expectoration training psychological and CBT nutritional advice physical training IMPROVES EX TOLERANCE / QOL / REDUCES ADMISSION
Optimise nutrition
Vaccination
pneumococcal >65 or <65 if FEV1 <40%
influenza
ladder: STEP 1 SABA - monotherapy salbutamol SABA + SAMA salbutamol OR TURBUTALINE + atrovent (ipratropium)
STEP 2
LABA OR LAMA - monotherapy
Tiotropium or salmeterol / formeterol
TORCH study recommends Long acting if > 2 exacerbations per year
LABA + LAMA
TIOTROPIUM (UPLIFT study)+ SALMETEROL (TORCH) or Formeterol
STEP 3
LABA + ICS or LAMA + ICS (FEV1 <50% + >2 exacerbations per year)
SERETIDE / FOSTAIR / SYMBICORT + Tiotropium
STEP 4
BOTH LABA + ICS + LAMA + Theophyllin + pulm rehab
+ tiotropoium long acting anticholinergic (bronchodilation)
SERETIDE - salmeterol +fluticasone - steroid
FOSTAIR - formeterol + becolometasone
SYMBICORT = formeterol + budesonide
Add Roflumilast - PDE-4 antagonist where
- already on triple therapy
- Gold >3 FEV1<50%
- > 2 exacerbations per year
Add Theophyllin
UNCLEAR MECH OF ACTION / RELAXES SMC / improves Mucociliary clearance
Lots of interactions
difficult therapeutics esp in obese
Step 5 - FEV1 <30% MRC 4-5
LTOT
LTOT ambultatory needs to be used >15 hours per day
NON SMOKER
Pa02 <7.3 + high Hb + noct T1RF / pulm htn / core pulm
IMPROVES SURVIVAL AND QOL
Step 6 NIV improve QOL reduces admissions improves sleep quality and resp fatigeu RESETS RESP CENTRE LEADING TO IMPROVED DAY TIME T2RF
+/- rescue pack
+ smoking cessation - 5As + NRT + buproprion / varenicline
+ nutrition
+ vaccination
COPD Treatment ladder = 3 steps - describe + additional therapies
ladder: STEP 1 SABA - monotherapy salbutamol SABA + SAMA salbutamol OR TURBUTALINE + atrovent (ipratropium)
STEP 2
LABA OR LAMA - monotherapy
Tiotropium or salmeterol / formeterol
TORCH study recommends Long acting if > 2 exacerbations per year
LABA + LAMA
TIOTROPIUM (UPLIFT study)+ SALMETEROL (TORCH) or Formeterol
STEP 3
LABA + ICS or LAMA + ICS (FEV1 <50% + >2 exacerbations per year)
SERETIDE / FOSTAIR / SYMBICORT + Tiotropium
STEP 4
BOTH LABA + ICS + LAMA + Theophyllin + pulm rehab
+ tiotropoium long acting anticholinergic (bronchodilation)
SERETIDE - salmeterol +fluticasone - steroid
FOSTAIR - formeterol + becolometasone
SYMBICORT = formeterol + budesonide
Add Theophyllin
UNCLEAR MECH OF ACTION / RELAXES SMC / improves Mucociliary clearance
Lots of interactions
difficult therapeutics esp in obese
Step 5 - FEV1 <30% MRC 4-5
LTOT
LTOT ambultatory needs to be used >15 hours per day
NON SMOKER
Pa02 <7.3 + high Hb + noct T1RF / pulm htn / core pulm
IMPROVES SURVIVAL AND QOL
Step 6 NIV improve QOL reduces admissions improves sleep quality and resp fatigeu RESETS RESP CENTRE LEADING TO IMPROVED DAY TIME T2RF
\+/- rescue pack \+ smoking cessation - 5As + NRT + buproprion / varenicline \+ pulm rehab \+ nutrition \+ vaccination
SURGICAL TREATMENT COPD
LUNG REDUCTION
BULLECTOMY
TRANSPLANT
- LUNG REDUCTION THERAPY
excision of non functional lung allows for inflation of trapped / physiologically normal lung
REDUCES MORTALITY
IMPROVES QOL
REQUIREMENTS:
TLCO >20% (diffusion capacity demonstrating functional lung tissue
FEV1 >20%
paC02 <7.3 i.e minimal evidence of T2RF
2. Bullectomy excision of large bullae reduces risk of PTx restores elastic recoil reduces air resistance and air trapping increases functional residual capacity
REQUIREMENT:
PROGRESSIVE DYSPNOEA
FEV1<50% - GRADE 3 GOLD
BULLAE >1/3 HEMITHORIAX WITH PRESERVED HISTOLOGY SURROUNDING
- Lung Transplant
IMPROVES FUNCTIONAL CAPACITY
1 year survival = 78%
5 year 51%
REQUIREMENT:
BODE >5
CPAP - HOW DOES IT WORK
Continuous positive pressure airway ventilation
Recruites alveoli that have collapsed and therefore improves airway compliance
splints open upper airway
forces fluid back into pulmonary vasculature
improves oxygenation
Pneumonia Signs / symptoms
Pneumonia:
X ray evidence of collapse / consolidation within the lung parenchyma
- productive / supporative cough - new
- RR + pyrexia
- tracheal tug . IC recession. SC recession
- T1Rf
- pleuritic CP
- haemoptysis
- Increased diffusion gradient in prescence of pulmonary haemorrhage otherwise reduced
- focal crackles with dullness to percussion with increased vocal phremitis over it ?effusion
- clubbing if chronic / SCLC / bronchiectasis
- effusion / empyema - acidotic septated consolidative effusion
- bronchial breathing
- dysphagic ?MND / GBS / stroke - ASPIRATION
Erythema multiforme - target lesions - MYCOPLASMA
Erythema nodosum - nodes of erythema not dissimilar to jane way lesions (different aetiology)
bullous myringitis - lesions on tymp membrane
cold haemolytic anaemia - cold agglutinins /raised ldh / splenomeg if assoc spherocytosis
Pneumonia severity
CURB65 SCALE CORROLATES WITH 30 DAY MORTALITY
NEW CONFUSION
UREA >7
RR>30
BP <90
OVER 65
SCORE /5 0 = 0.7% - treat at home 1= 3% = home 2 = 10% = increased risk 3 = 17% = severe ITU 4 = 41% = severe ITU 5=57% = severe ITU
pneumonia investigations
Bloods panel ABG eosinophilia? CXR USS if indicated by CXR and clinical pleural tap if indicated +/- chest drain if empyema or resp compromise throat swab / cultures atypical screen pneumococall Ag Mycoplasma- erythema nodosum / mulitforme +HAEMOLYSIS - cold agglutinins + raised LDH legionella - travel AFBs - travel / severe / CXR pulm TB or miliary / immunosup HIV - severe presentation and young flu swab
Ct chest
BAL
pneumonia definition
an acute or chronic resp illness that is marked by inflammation of lung tissue accompanied by infiltration of alveoli and often bronchioles with white blood cells (such as neutrophils) and fibrinous exudate seen on CXR
common causes of CAP
Common bacterial
- strep pn up to 40% - esp splenetomy
- haemophilus influenzae - mroe in copd
- mycoplasma - erythema multiforme / marginatum + HAEMOLYSIS + bullous myringitis
- Q fever - chlamydophila
- legionella
- pneumococcal
- staph
- moraxella catarrhalis
- gram negs - aspiration
Atypical
Mycoplasma
pneumococcal - liver dysfunction
chlamydia
C.psitacci
C. burnetti
Viral
influenzae A/B
Treatment pneumonia
- Abx
amox and clarith +/- gram neg cover in aspiration - target sats and appropriate oxygen therapy
- pen Ax - teicoplanin and clarith / flouroquinolone
6 week CXR + FU
consider HIV screen based on presentation
Vaccination
HAP definition
Hospital aquired pneumonia with Sx presenting >72 hours post admission
USually gram neg org / pseudomonas
Define Bronchiectasis
Permanent splinting open and destruction of middle and large bronchioles due to
a) chronic infection or inflammation
b) poor drainage
c) airway obstruction (continued infection)
d) defective immune response
Causes bronchiectasis
Many causes!
Surgical sieve
V: vascular
NONE
I: infective/inflammatory CYSTIC FIBROSIS FIBROSING PULMONARY ALVEOLITIS - ASPERGILLOUS TB HIV
T: traumatic / mechanical - BRONCHIAL OBSTRUCTION COPD GRANULOMA - SARCOID TB CARCINOMA FOREIGN BODY LN COMPRESSION
A: autoimmune / OVERACTIVE / UNDERACTIVE
ALLERGIC ASPERGILLOSIS
A1 ANTITRYPSIN
HYPOGAMMAGLOBULINAEMIA
SCID
HIV
M: metabolic
RECURRENT ASPIRATION
I: iatrogenic/idiopathic
N: neoplastic
Bronchogenic cancer
C: CONGENITAL
CF
Ypungs Syndrome - CF without CFTR D508 - middle age
CP - aspiration
YELLOW NAIL SYNDROME - yellow nails - abn lymphatics - pleural effusion (chylothorax)
KARTAGENERS SYNDROME = PRIMARY CILIA DYSKINESIA: Dextrocardia / ciliary dyskinesia +bronchiectasis / otitis / subfertitily (similar to CF)
A1 Antitrypsin
Surgical sieve
V: vascular I: infective/inflammatory T: traumatic A: autoimmune M: metabolic I: iatrogenic/idiopathic N: neoplastic C : congenital
Bronchiectasis imaging changes
CXR
CYSTIC BRONCHIECTASIS
Cystic sac distribution
CYLINDRICAL BRONCHIECTASIS
Tramlines / Ring shadowing
Severe - see honeycombing - lots of ring shadowing showing fibroses / inflammed
HRCT - high sensitivity and specificity REID CLASSIFICATION Cylindrical - most advanced cystic SIGNET RING SIGN - bronchi 1.5x thickness of adjacent artery =Op Fluid levels in bronchi Mucus plugs - bronchocoeles
OBLITERATIVE BRONCHIOLITIS - TREE IN BUD APPEARANCE
Specific tests for bronchiectasis
HRCT - definitive
CF GENOTYPING / SWEAT TEST >60mmol CL - AUT REC
KARTAGENERS = primary ciliary dyskinesis - AUT REC
TB - Tuberculin skin test / Quantiferon
Cystic fibrosis - What is the commonest mutation and pathophysiology of the disease process
CF transmembrane conductance regulator protein (CFTR)
Transporter channel which regulates chloride ICM and ECM balance.
Inhibits voltage gated Na channel from reabsorbing Na from ECM
Therefore regulates water movement across cell membrane and therefore ECM viscosity via regulation of NaCL.
Commonest mutation is DF508 - >90%
Autosomal recessive
When defective Chloride ions fail to be pumped back into cell
eNAc not inhibited and as ECM Na > ICM - NA moves into cell
Draws water by osmosis
THEREFORE ECM becomes hyperviscos and high in CL concentration. - Frequently blocked ducts / poor clearance
Basis of chloride sweat test >60mmol
What is Kartageners Syndrome?
Primary Ciliary Dyskinesia
Presents akin to CF]]failure of clearance of any vesicle lined with cilia
results in bronchiectasis
chronic infection
poor drainage
airway obstruction
What is Pickwickian syndrome
Form of obesity related lung disease
Cluster of
- OSA
- Restrictive Pulm function tests
- Nocturnal hyerpcapnia
