RESPIRATORY - Asthma, COPD Flashcards
Functions of the respiratory system (5)
Gas exchange Homeostasis of the body Protection from inhaled pathogens Vocalisation Olfactory sense
FEV 1
Forced exp volume
Volume that has been exhaled at the end of the 1st s of forced expiration
Normal FEV1 value
> 80%
FVC
Forced vital capacity
Volume that has been exhaled after max exp, following a full insp
KCo
Diffusion capacity of lung per unit area for CO
TLco
Diffusion capacity of the total lung for CO
Obstructive pattern
Norm/Incr FVC
FEV1:FVC <0.7 (reduced)
Restrictive pattern
Reduced FVC (<80%)
What does decreased TLco/Kco indicate
Issue w/ gas exchange
hence rules out chest wall/diaphragm pathology
Def asthma
Chronic inflammatory condition of the airways, characterised by airway hypersensitivity
What % adults have asthma
5%
What % children have asthma
10%
Sx asthma (5)
Wheeze SOB Morning dipping Subjective feeling chest tightness Nocturnal cough
O/E asthma
Widespread expiratory wheeze
Pulmonary function test results asthma
Decreased FEV1
Relieved by B2 agonists
Common precipitants asthma
Enviro Viral infections Cold air Emotion Dx (NSAIDS/B blockers) Atmospheric pollution Occupational pollutants
How is occupational asthma diagnosed
Using peak flows before /after work/ at weekends
Important Hx points asthma
Known precipitants Diurnal variation Acid reflux Sx Atopy Hx Occupation Days off work/school Hx exaccerbations Did they req hospitalisation/ITU
Can asthma be diagnosed on clinical diagnosis aloone?
Yes
If B2 commenced and improvement of Sx
If poor response to bronchodilators, how is asthma diagnosed
Spirometry
FEV1:FVC < 0.7 +bronchodilator reversbility = diagnostic
What time of HS reaction is extrinsic asthma
T1HS
Clinical picture extrinsic asthma
Atopic indiv
w/ positive skin prick tests to common allergens
Clinical picture intrinsic asthma (4)
Middle aged indiv
With no causative agents ID’d
Generally > severe
+ quicker deteriorations in lung fct
Early phase of acute asthma attack
Bronchospasm b/c spasmogen production (Histamine, PG + LT)
SM contraction narrows airways
Late phase of acute asthma attack
Chemotaxins attract eosinophils +mononuclear cells
Infiltrate + mucosal oedema narrow airway
Which type of asthma is more likely to develop chronic asthma
Intrinsic astham
Changes in chronic asthma
Bronchoconstriction b/c incr responsiveness bronchial SM + hypersecretion mucus –> plugs
What 2 things ddoes the sputum contain in chronic asthma
Charcot-Leyden crystals
Curshman spirals
Effect on vascular system - chronic asthma
Pulmonary HTN
Features of life-threatening asthma attack (5)
-PEF <33% of best
-SpO2 <92%
-Silent chest, cyanosis or feeble respiratory effort
Bradycardia, hypotension or dysrhythmia
Exhaustion or confusion
ABG markers - life threatening asthma attack
Normal PaCO2 (b/c no longer hypoventilating)
Severe hypoxia <8
Low pH
What does raised PaCO2 indicate in acute asthma attack
Almost fatal
Mx life threatening asthma attack (8)
15L O2 NRB mask Salbutamol 5mg via nebs (every 15-30 mins) Ipratropium bromide 0.5mg via nebs PO prednisolone 50mg or IV HC 100mg No sedatives CXR Call ICU \+ MgSO4
What must you do prior to discharge for an acute asthma attack patient
Check inhaler technique
Step 1 Mx asthma
salbutamol prn
Step 2 Mx asthma
+ ICS 200-800microg
Step 3 Mx asthma
+ LABA
If response - continue
If no response - stop and increase dose of ICS to 800microg/day
Step 4 Mx asthma
Persistent poor control
Can incr Inhal ICS up to 2000microg /day
Add 4th Dx e.g. LTRA, Theophylline etc
Step 5 Mx asthma
Continuous or freq use of PO steroids
Maintain 2,000 microg ICS
Lowest dose daily oral steroid
Inhaler technique
1 - Remove cap and shake inhaler to ensure consistency of dose
2 - Pt - breath fully out
3 - Pt - breath in slowly and steadily press down on the inhaler device
4 - On inhalation, pt should hold breath for count of 10
5 - pt - slowly breathe out, repeat dose + replace mouthpiece cover. Clean device if necess after use
Role of Beta-agonists
Relax bronchial SM –> bronchodilation
SE Beta-agonists
TachyC (Beta 1)
Tremor, cramps, hypokalaemia (Beta 2)
How long does a SABA work for?
4-6hrs
How long does a LABA work for?
> 12hrs
SE ICS (main)
PO candidiasis
Pneumonia
Advice for ICS
Rinse mouth afterwards
SE - LTRA (3)
Thirst
GI disturbances
V rarely Churg Strauss
SE Theophyilline
Dose related b/c narrow therapeutic window headache Insomnia Nausea TachyC Arrhythmias
Def COPD
A disease of progressive airflow limitation that is not fully reversible, associated w/ an abnormal inflammatory resposne to the lungs to noxious particles of (g), predominantly inhaled cigarette smoke
Def Emphysema
Dilation of any part of respiratory acinus w/ destructive changes in the alveolar walls
What is tissue destruction caused by in emphysema?
Increased secretion + activation of extracellular proteases by inflammatory cells
(which are stim’d by noxious particules)
Centrilobar emphysema
changes Limited to central part of lobule directly around terminal bronchiole, w/ norm alveolar everywhere
What is the most common type of emphysema
Centrilobar emphysema
What is centrilobar emphysema assocated with
Smoking
What is panacinar emphysema
Destruction + distention of whole lobule
Who gets panacinar emphysema
a-1-antitripsin deficiency
What is a bullae
Dilated air space >1cm
Def chronic bronchitis
Daily cough + sputum for at least 3 months /yr for 2 years
What is the primary abnormality seen in chronic bronchitis?
Abnormal amount of mucus, which –> plugging of airway lumen
What index is used to show hypersecretion in chronic bronchitis?
Reid index
Ratio fland:wall thickness in the bronchus
(Incr in chronic bronchitis)
What is bronchiolitis?
Inflammation in airways <2mm in diameter
+ macrophage + lymphoid cell infiltration
What is the first pathological change in COPD
Bronchiolitis
RF COPD (6)
Cigarette smoke Occupational exposure to dusts A-1-antitrypsin deficiency Recurrent infections - childhood Low SE status Asthma/Atopy
PS COPD (4)
Productive morning cough
Increased frequency LRTI
Slowly progressive dyspnoea + wheezing
Resp failure
Signs COPD - severe dsiease
Tachypnoea Cyanosis + flapping Hyperinflation Intercostal recession insp Lip pursing on exp Signs resp distress Raised JVP if cor pulmonale Poor chest expansion Hyper-resonant throughout + loss cardiac/hepatic dullness Decr breath sounds Prolonged expiratory phase Polyphonic wheeze
Complications COPD (6)
Acute exacerbations Polycythaemia Resp failure Cor pulmonale Pneumothorax Lung carcinoma
What are ‘Blue bloaters’
Pt w/ sever COPD who are insensitive to CO2
Rely on hypoxic drive
How do Blue Bloaters ps
Not particularly breathless
But = cyanosed + oedematous
ABG results Blue Bloaters
T2RF
What treatment must be given with caution w/ Blue Bloaters
O2
What are ‘Pink puffers’
Pt remains sensitive to CO2
ABG features’Pink puffers’
Low CO2
Norm O2
But can –> T1RF
Appearance of ‘Pink puffer’
Uses accessory mm to increase their ventilation
Breathless
Pt v thin due to large amount of kcal used to breath
Does Pink Puffer or Blue bloater have > emphysema
Pink puffer
When can diagnosis of COPD be clinical?
If typical Sx in >35y/o in presence of RF
Ix for anyone suspected of COPD
Post-bronchodilator spirometry
CXR
FBC
Post-bronchodilator spirometry - stage 1 (mild)
FEV1 80% predicted value
Post-bronchodilator spirometry - stage 2 (mod)
FEV1 50-79% predicted
Post-bronchodilator spirometry - stage 3 (severe)
FEV1 30-49% predicted
Post-bronchodilator spirometry - stage 4 (v severe)
FEV1 <30% predicted
CXR features COPD (5)
Hyperinflation (>6ant/10post ribs) Flattened hemidiaphragm Large central pulm aa Reduced peripheral vascular markings Bullae
Further Ix COPD (4)
Sputum culture
EC
ABG
DLCO
Mx stable COPD (4)
Rx to resp specialist if any doubt on diagnosis
Pt education
Lifestyle advice
Medication
Medicine pathway COPD if FEV1 >50:
1 - SABA prn or SAMA prn
2 - LABA or LAMA
3 - LABA + ICS
4 - LAMA + LABA + ICS
Medicine pathway COPD if FEV1 <50:
1- SABA prn or SAMA prn
2 - LABA + ICS or LAMA
3 - LABA + LAMA + ICS
Specialist Tx COPD (6)
Pulmonary rehab PO aminophylline Mucolytics Nutritional supplement LTOT Surgery
Aims of pulmonary rehab in COPD
Increases exercise capacity
Decreases breathlessness
Improves QOL
How often is pulmonary rehab
3 sessions/week for 6 weeks
When is a patient w/ COPD started on aminophylline?
If still symptomatic after triple therapy
Who gets LTOT in COPD>
If SPO2 <92% OA
FEV1 <30%
Cyanosis
Cor pulmonale
Cause of acute exaccerbation COPD (2)
Virus
Bacteria
Pollutants
If a patient is having acute COPD exaccerbations frequently, what changes need to be made to their current Mx
++ rescue meds (azithromycin)
When to admit someone w/ acute exacc COPD (7)
Severe breathlessness Rapid Sx onset Acute confusion Cyanosis Low O2 sats worsenning peripheral oedema
Outpt Mx acute exacc COPD (5)
Incr SABA + spacer 30mg prednisolone 7-14 days PO ABx if purulent sputum/signs pneumonia Safety net Follow up 6w
