COPD IS A TERM USED FOR A GROUP OF LUNG/AIRWAY DISEASES
THAT ARE NOT FULLY REVERSIBLE
OBSTRUCTED DUE TO CHRONIC BRONCHITIS,
EMPHYSEMA OR BOTH
ACCOUNTS FOR LARGE RATES OF MORBIDITY AND
MORTALITY: EXPECTED TO BE LEADING CAUSE OF DEALTH
BY 2030
SYMPTOMS
DYSPNOEA
CHRONIC
COUGH
REGULAR SPUTUM
PRODUCTION
RISK FACTORS
SMOKING
HAS MANY ADVERSE EFFECTS: PRODUCTION OF DESTRUCTIVE PROTEOLYTIC ENZYMES RELEASED FROM
INFLAMMATORY CELLS IN THE LUNGS, OXIDATIVE STRESS AND THE INACTIVATION OF ALPHA-1 ANTI-TRYPSIN
ESTIMATED THAT 15-20% SMOKERS DEVELOP COPD
SERINE PROTEASE INHIBITOR THAT BALANCES
THE ACTION OF NEUTROPHIL-PROTEASE
ENZYMES IN THE LUNGS
CHEMICALS
ORGANIC AND INORGANIC DUSTS, CHEMICALS AND FUMES
EXPOSURE CAN CAUSE COPD DEPENDING ON LUNG
IMPAIRMENT, INTENSITY AND DURATION OF EXPOSURE
ACCOUNTS FOR 10-20% OF COPD CASES
INDOOR AIR
POLLUTION
OPEN FIRES OF WOOD, ANIMAL DUNG, COAL AND AGRICULTURAL RESIDUES CAN LEAD TO HIGH LEVELS OF
INDOOR AIR POLLUTION ESP IN POORLY ENTILATED AREAS
ACCOUNTS FOR 10-20% OF COPD CASES
GENETICS
GENE THAT IS RECESSIVE AND HEREDITARY: DEFICIENCY OF THE ALPHA 1 ANTI-TRYPSIN GENE
PATHOPHYSIOLOGY
EMPHYSEMA
PROGRESSIVE AND DESTRUCTIVE ENLARGEMENT OF THE BRONCHIOLES AND ALVEOLAR
SACS
LEADS TO LOSS OF SURFACE AREA FOR GAS EXCHANGE & LOSS OF ELASTIC RECOIL FOR
EXPIRATION- CAN RESULT IN AIRWAY COLLAPSE ESP DURING EXPIRATION & HYPERVENTILATION
PANACINAR
LESS COMMON & OCCURS AS A RESULT OF AN ALPHA-1 ANTI-TRYPSIN GENE
DEFICIENCY
STUDIES SHOW THIS TYPE IS LESS COMMON IN FEMALES AS OESTROGEN
INCREASES THE EXPRESSION OF PROTEASE INHIBITORS INCLUDING ALPHA-1
TRYPSIN
CENTRILOBULAR
DESTRUCTION OF BRONCHIOLES,
ALVEOLAR DUCTS AND ALVEOLI,
COMMON IN
SMOKERS/WORKING IN
POLLUTED AREAS
CHRONIC BRONCHITIS
PRESENCE OF A COUGH AND SPUTUM PRODUCTION FOR ATLEAST 3 MONTHS IN 2 CONSECUTIVE YEARS
AN INFLAMMATORY RESPONSE TO INHALED IRRITANTS (USUALLY DUE TO CIGARETTE SMOKING)
RESULTS IN THE ACCUMULATION AND HYPER-SECRETION OF MUCUS-SECRETING GLANDS IN THE BRONCHIAL TREE
CAN INCREASE RISK OF BACKTERIAL OR VIRAL INFECTIONS AND THUS WORSEN SYMPTOMS
OTHER CHANGES
IMPAIRMENT OF GAS
EXHANGE RESUKTING IN
HYPOXAEMIA AND
HYPERCAPNIA, PULMONARY
HYPERTENSION AND
VASCULAR REMODELLING
VR INCREASES RIGHT VENTRICULAR PRESSURE AND CAN LEAD TO VENTRICULAR HEART FAILURE KNOWN AS COR PULMONALE
PHARMACOLOGY
BRONCHODILATORS
BETA-2-AGONISTS
SHORT ACTING (SABA)
SALBUTAMOL & TERBUTALINE
ORAL,
INHALATION
TABS / CAPS, MDI / DPI
LONG ACTING (LABA)
SALMETEROL & FORMOTEROL
INHALATION
ONLY
MDI / DPI
STIMULATE BETA-2 ADRENORECEPTORS IN BRONCHIAL SMOOTH
MUSCLE, INCREASE cAMP LEVELS AND PKA ACTIVITY, CAUSING
BRONCHODILATION
CAN ALSO INHIBIT MEDIATOR RELEASE FROM MAST CELLS AND
TNF-ALPHA RELEASE FROM THE MONOCYTES AND INCREASES
MUCUS CLEARANCE FROM CILIATED CELLS
CORTICOSTEROID
THERAPY
INHALED CORTICOSTEROIDS
BECLOMETASONE
INHALATION
MDI / DPI
HIGH POTENCY INHALED CORTICOSTEROIDS
BUDESOMIDE
INHALATION
MDI /
DPI
LIPOPHILIC THEREFORE CAN ENTER CELL EASILY, BIND TO INTRACELLULAR
RECEPTORS WHICH DIMERISE AND MIGRATE TO THE NUCLEUS, COMPLEX AFFECTS
TRANSCRIPTION OF mRNA OF SPECIFIC PROTEINS.
INCREASE SYNTHESIS OF ANTI-INFLAMMATORY PROTEINS VIA
TRANSACTIVATION. REDUCE THE SYNTHESIS OF
PRE-INFLAMMATORY PROTEINS VIA TRANSREPRESSION
INCREASE SYNTHESIS OF ANNEXIN-1 = A NATURAL
INHIBITOR OF PHOSPHOLIPIDASE 2
THEREFORE LESS ARACHADONIC ACID
AVAILABLE TO BE METABOLISED BY COX-1 LOX
ENXYMES AND HENCE LESS PGs AND LTs
SYNTHESISED
THEY ALSO DECREASE THE SYNTHESIS OF
PRO-INFLAMMATORY PROTEINS (COX-2 & NOS-2)
AND INHIBIT NUCLEAR FACTOR K (INVOLVED WITH
THE INFLAMMATORY CYTOKINE PRODUCTION)
MUSURINIC
ANTAGONISTS
SHORT ACTING (SAMA)
IPRATROPIUM
INHALATION
DPI / MDI /
NEB
BLOCK ACH RELEASE FROM
THE VAGUS NERVE
LONG ACTING (LAMA)
TIOTROPIUM
INHALATION
DPI /
pMDI
BLOCK M3 RECEPTORS ON SMOOTH MUSCLE THUS ANTAGONISING THE
EFFECTS OF ACH ON THE SNOOTH MUSCLE, REDUCING INTRACELLULAR CONC
OF cGMP AND CAUSING BRONCHIAL SMOOTH MUCLE RELAXATION AND
BRONCHODILATION
METHYLXANTHINES
THEOPHYLLINE, AMINOPHYLLINE (PRODRUG)
ORAL
MR TABS / CAPS
NON-SELECTIVE PHOSPHODIESTERASE INHIBITOR AND INCREASES cAMP OR cGMP
RESULTS IN RELAXATION OF THE AIRWAY SMOOTH MUSCLE
HIGHER DOSES OF THIS DRUG EXHIBITS BRONCHODILATORY EFFECTS & INCREASE
DIAPHRAGMATIC STRENGTH & AID MUCUS CLEARANCE BY CILIATED CELLS
PHARMACEUTICS
pMDIs
PORTABLE,
CHEAP,
DISPOSABLE,
REPRODUCIBLE
DOSE
COLD FREON EFFECT,
REQUIRES INHALER
TECHNIQUE,
PROPELLANT (CFCs),
HIGH ORAL DEPOSITION,
MAX DOSE 5mg
USE OF SPACER:
OVERCOME
INHALATION/ACTUATION
COORDINATION ISSUES &
COLD FREON EFFECT
DPIs
COMPACT, PORTABLE,
UNOBTRUSIVE,
PROPELLANT FREE,
BREATH ACTUATED,
NO TECHNIQUE
REQUIRED, DELIVER
LARGER DOSES
COMPARED TO MDI,
NO COLD FREON
EFFECT
DEPENDS ON PT INSPIRATION FLOW
RATE, HUMIDITY MAY CAUSE
PARTICLES TO AGGREGATE AND
CAPSULES TO SOFTEN, DOSE IS
LOST IF PT EXPIRES INTO DPI,
LACTOSE
LIMITING FOR COPD PT
NEBULISER
NON-SPECIFIC
INHALATION
TECHNIQUE, DELIVERS
LARGE DOSES, SIMPLE
FORMULATION
INHALATION IS TIME
CONSUMING, BULKY
DEVICE, CONTENTS
EASILY
CONTAMINATED,
EXPENSIVE, POOR
DELIVERY EFFICACY &
VARYING
PERFORMANCE
PATIENT AND CLINICAL MONITORING
SPIROMETRY
MRC
DYSPOEA
SCALE
GRADE 1
GRADE 2
GRADE 3
GRADE 4
GRADE 5
TOO BREATHLESS TO LEAVE THE HOUSE/ BREATHLESS WHEN DRESSING/ UNDRESSING
STOPS FOR BREATH AFTER WALKING ~100M OF AFTER A FEW MINS ON LEVEL GROUND
WALKS SLOWER THAN CONTEMPORARIES ON LEVEL GROUND B/C OF
BRETHLESSNESS/ HAS TO STOP FOR BREATH WHEN WALKING AT OWN PACE
SOB WHEN HURRYING OR WALKING UP A HILL
NOT TROUBLED BY BREATHLESSNESS EXCEPT ON STRENUOUS EXERCISE
PERFORMED
AT TIME OF
DIAGNOSIS
TO RECONSIDER
DIAGNOSIS IF PTS
SHOW EXCEPTIONAL
RESPONSE TO
TREATMENT
MEASURE
POST-BRONCHODILATOR
SPIROMETRY
TO
CONFIRM
COPD
DSIAGNOSIS
CONSIDER ALTERNATIVE DIAGNOSIS OR INVESTIGATIONS IN:
OLDER PEOPLE
WITHOUT TYPICAL
SYMPTOMS OF
COPD WHERE
FEV1/FVC RATIO:
>0.7
YOUNGER PEOPLE
WITH SYMPTOMS
OF COPD WHERE
FEV1/FVC RATIO:
=>0.7
FEV1 VALUE
(PREDICTED)
>80% = STAGE 1
(MILD)
COPD SHOULD ONLY
BE DIAGNOSED IF
RESP SYMPTOMS
PRESENT
50 - 79% = STAGE 2
(MODERATE)
POST-BROCHODILATOR FEV1 / FVC = <0.7
30 - 49% = STAGE 3
(SEVERE)
<30% = STAGE 4
(VERY SEVERE)
AIRFLOW OBSTRUCTION DEFINED AS REDUCED FEV1/FVC RATIO (<0.7)
SPIROMETRY SHOULD BE PERFORMED IN PTS >35, CURRENT OR EX-SMOKERS, AND HAVE A CHRONIC COUGH
SPIROMETRY SHOULD BE CONSIDERED IN PTS WITH CHRONIC BRONCHITIS
A SIG. NO. OF THESE
WILL GO ON TO
DEVELOP AIRFLOW
LIMITATION
FURTHER
INVESTIGATIONS
AT THE TIME OF THEIR INITIAL DIAGNOSIS, PRECAUTIONS MUST BE TAKEN
CHEST RADIOGRAPH
TO EXCLUDE OTHER PATHOLOGIES
FULL BLOOD COUNT
TO IDENTIFY ANAEMIA OR POLYCYTHAEMIA
BODY MASS INDEX (BMI)
ADDITIONAL INVESTIGATIONS SHOULD BE PERFORMED TO AID MANAGEMENT IN SOME CASES
SERIAL DOMICILLIARY PEAK
FLOW MEASUREMENTS
TO EXCLUDE ASTHMA IF DIAGNOSTIC DOUBT REMAINS
CT SCAN OF
THORAX
TO INVESTIGATE SYMPTOMS THAT SEEM DISPROPORTIONATE TO SPIROMETRIC IMPAIRMENT,
TO INVESTIGATE ABNORMALITIES SEEN ON CHEST RADIOGRAPH, TO ASSESS SUITABILITY FOR
SURGERY
ALPHA-1
ANTITRYPSIN
IF EARLY ONSET, MINIMAL SMOKING OR FAMILY HISTORY
TRANSFER FACTOR FOR
CO (TLCO)
TO INVESTIGATE SYMPTOMS THAT SEEM
DISPROPORTIONATE TO THE SPIROMETRIC IMPAIRMENT
ECG
TO ASSESS CARDIAC STATE IF FEATURES OF COR PULMONALE
SPUTUM
CULTURE
TO IDENTIFY ORGANISMS IF SPUTUM IS PERSISTENTLY PRESENT AND PURULENT
PULSE
OXIMETRY
TO ASSESS NEED FOR OXYGEN THERAPY, IF CYANOSIS OR COR
PULMONALE PRESENT OR IF FEV1 <50% PREDICTED
ASSESSMENT OF
SEVERITY AND
PROGNOSTIC
FACTORS
COPD IS HETEROGENEOUS SO
NO SINGLY MEASUREMENT
CAN GIVE ,ADEQUATE
ASSESSMENT OF SEVERITY,
SEVERITY IS IMPORTANT TO
MEASURE AS IT GIVES A
PROGNOSTIC OUTLOOK
FEV1 IS A POOR
REFLECTION OF
DISABILITY,
FEV, BMI, TLCO, MRC
SCALE, paO2 AND
COR PULMONAE
MUST BE ASSESSED
CLINICAL
FEATURE
SMOKER/EX-SMOKER
NEARLY ALL
POSSIBLY
COPD
ASTHMA
SYMPTOMS <35 YEARS
RARE
OFTEN
CHRONIC PRODUCTIVE COUGH
COMMON
UNCOMMON
BREATHLESSNESS
VARIABLE
PERSISTENT &
PROGRESSIVE
NIGHT TIME WAKING W/
BREATHLESSNESS / WHEEZING
COMMON
UNCOMMON
SIGNIFICANT DIURNAL / DAY-TO-DAY
VARIABILITY OF SYMPTOMS
COMMON
UNCOMMON
MANAGEMENT
SMOKING CESSATION
UP TO DATE SMOKING HISTORY
INCLUDING PACK YEARS SMOKED
SHOULD BE DOCUMENTED FOR
EVERYONE WITH COPD
ALL COPD PTS, REGARDLESS OF AGE,
SHOULD BE ENCOURAGED TO STOP
SMOKING, AND OFFERED HELP AT
EVERY OPPORTUNITY TO DO SO
UNLESS CONTRAINDICATED,
OFFER NRT, VARENICLINE OR
BUPROPION WITH APPROPRIATE
SUPPORT PROGRAM TO OPTIMISE
RESULTS
TREATMENT
INFECTION CAN COMPLICATE COPD AND CAN BE PREVENTED BY VACCINATION
PERSISTENT DYPNOEA /
EXACERBATIONS DESPITE
SABA/SAMA USE
FEV1 ≥ 50% PREDICTED: OFFER OD LAMA (INSTEAD OF QDS SAMA) OR LABA
FEV1 < 50% PREDICTED: EITHER ICS WITH LABA IN COMBINATION INHALER, OR LAMA
FEV1 ≥ 50% PTS WITH
PERSISTING DYSPNOEA /
EXACERBATIONS DESPITE LABA
MAINTENANCE THERAPY
CONSIDER LAMA + ICS IN COMBINATION INHALER
CONSIDER LAMA IN ADDITION TO LABA WHERE ICS IS NOT TOLERATED OR DECLINED
INITIAL COURSE FOR
ALLEVIATION OF DYSPNOEA AND
EXERCISE LIMITATION
SABA OR SAMA INHALERS TO BE PRESCRIBED
PTS WITH PERSISTENT DYSPNOEA AND
EXACERBATIONS DESPITE LABA + ICS
COMBINATION MAINTENANCE THERAPY
OFFER LAMA IN ADDITION, IRRESPECTIVE OF FEV1
VICE VERSA
MAINTENANCE USE OF
ORAL CS THERAPY IS
NOT NORMALLY
RECOMMENDED
SO,ME PTS WITH ADVANCED
COPD MAY REQUIRE
MAINTENANCE ORAL CS WHEN
THEY CANNOT BE WITHDRAWN
FOLLOWING AN EXACERBATION
IN SUCH CASES,
KEEP DOSE AS LOW
AS POSSIBLE
PTS TREATED WITH
LONG-TERM ORAL CS
SHOULD BE MONITORED FOR
DEVELOPMENT OF
OSTEOPEROSIS & GIVEN
APPROPRIATE PROPHYLAXIS
PTS OVER 65 SHOULD BE
GIVEN PROPHYLAXIS
WITHOUT MONITORING
THEOPHYLLINE
SHOULD ONLY BE GIVEN AFTER
TRIAL OF SHORT-ACTING AND
LONG-ACTING
BRONCHODILATORS, OR IN PTS
UNABLE TO USE INHALERS
REQUIRES (TDM)
MONITORING DUE TO
INTERACTIONS/TOXICITY
EXTRA CAUTION WITH ELDERLY
DUE TO ALTERED
PHARMACOKINETICS & LIKELY
CO-MORBIDITIES/POLYPHARMACY
EFFECTIVENESS TO BE
ASSESSED BY SYMPTOM
IMPROVEMENT, DAILY
ACTIVITY, EXERCISE CAPACITY
& LUNG FUNCTION
DOSE TO BE REDUCED AT
TIME OF EXACERBATION IF
MACROLIDE OR
FLUROQUINOLONE IS
PRESCRIBED
MUCOLYTIC THERAPY: ONLY TO BE USED WHEN
PTS HAVE A CHRONIC COUGH WITH SPUTUM
PRODUCTION & CONTINUED IF SYMPTOMATIC
RELIEF IS OBSERVED UPON USE
KEEP IT
SIMPLE
SMOKING
INHALER TECHNIQUE
MONITORING
PREVENT DISEASE PROGRESSION
SYMPTOM CONTROL
MEDICINES REVIEW
COPD PATIENTS
ARE ELIGIBLE
FOR
TARGETTEDMUR
AND NMS
PHARMACOTHERAPY
LIFESTYLE
AEROBIC EXERCISE TOLERANCE
DIET
BREATHING EXERCISES
PSYCHOLOGICAL SUPPORT
SHARED DECISION MAKING
PATIENT BELIEFS & EXPERIENCES
EDUCATION
PURPOSE OF DRUG
S/E OF INHALED CS
SIGNS OF TOXICITY
COUNSELLING
SIGNS OF TOXICITY
ENCOURAGE CONCORDANCE
TO ENSURE ADHERENCE
INTEGRATED
APPROACH TO CARE
MULTIDISCIPLINARY TEAM
RESPIRATORY
NURSE
SPECIALIST
GP
PHYSIOTHERAPIST
DIETICIANS
OCCUPATIONAL
THERAPISTS
SOCIAL
WORKER
MULTIDISCIPLINARY
PALLIATIVE CARE
TEAM
HOSPITAL AT
HOME SCHEMES
CLINICAL &
COMMUNITY
PHARMACISTS
THE NHS
COPD OBJECTIVES
1
2
3
4
TO ENHANCE QUALITY OF LIFE FOR PEOPLE WITH COPD ACROSS ALL
GROUPS, WITH A POSITIVE, ENABLING EXPERIENCE OF CARE AND SUPPORT
UNTIL THE END OF LIFE
TO REDUCE THE NO. OF PEOPLE WITH COPD WHO DIE PREMATURELY THROUGH
EARLY IDENTIFICATION, DIAGNOSIS & INTERVENTION, WITH PROACTIVE CARE AND
MANAGEMENT OF ALL STAGES OF COPD, WITH PARTICULAR FOCUS ON
DISADVANTAGED GROUPS AND AREAS OF HIGH PREVALENCE
TO REDUCE THE NO. OF PEOPLE WHO DEVELOP COPD BY ENSURING
THE PUBLIC IS EDUCATED ABOUT THE IMPORTANCE OF LUNG HEALTH, WITH
RISK FACTORS ADDRESSED, REDUCED OR AVOIDED & PROACTIVELY
ADDRESS HEALTH INEQUALITIES
TO IMPROVE RESPIRATORY HEALTH AND WELL-BEING OF
ALL COMMUNITIES AND REDUCE INEQUALITIES
5
TO ENSURE PEOPLE WITH COPD ACROSS ALL SOCIAL GROUPS RECEIVE SAFE
AND EFFECTIVE CARE WHICH MINIMIZES PROGRESSION, ENHANCES RECOVERY
AND PROMOTES INDEPENDENCE