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Bronchial Asthma and COPD

Risk Factors
a. Endogenous Factors
- Genetic predisposition polmorphism
- Atop
- Air!a hperresponsi"eness
- Gender
- Ethnicit#
$. En"ironmental Factors
- %ndoor allergens
- Outdoor allergens
- Occupational sensiti&ers
- Passi"e smoking
- Respirator in'ections
- O$esit#
- Earl "iral in'ection
- Diet "itde'
(riggers o' asthma
- allergens
- )R(% "iral
- E*ercise and hper"entilation +uid snthesis
- Cold air change in osmolalit in +uid lining
- ,ulphur dio*ide
- Drugs -$-$lockers - $ronchoconstrict. aspirin acetlsaliclic acid
$lock ccloo*genase/
- ,tress
- %rritants
Pathophysiology of asthma
Genetic predisposition -0 air!a in+ammation-.
1gienic hpothesis (h2 "s (h3
- (h2 protecti"e immunit in ctokine $alance
o Presence o' older si$lings
o Earl e*posure to da care
o (B. measles hep a
o Rural en"ironment
- (h3 more prone to BA
o ,ensiti&ation to dust mites. etc4..
5ost Common in+ammator cells in Asthma Eosinophils!
Air!a in+ammation in asthma
- Epithelial damage
- Bm thickening
- Air!a remodelling
1istopatholog o' small air!a in 'atal asthma
- 5ucus plug !ith trapped in+ammator celss
- Go$let cell metaplasia
Air!a 1perresponsi"eness
- E*cessi"e $ronchoconstriction response to multiple inhaled triggers
that !ould ha"e no e6ects in normal air!as
- 7inked to 're8uenc o' asthma smptoms
- Direct $ronchoconstrictors
- %ndirect $ronchoconstrictor
o Allergens
o %rritant
o ,ulphur o*ide
A. ,creening ,trategies
2. 1*
o Cough !9c !orsens at night
o Recurrent !hee&es
o Recurrent DOB
o Recurrent chest tightness
3. PE
o PE ma $e normal
o :hee&es are characteristic ;ndings $ut not "er speci;c
'or asthma -produced !hen air!as are constricted/
B. ,trategies 'or Con;rmation
2. ,pirometr
o (o doc air+o! o$struction
o Dec FE<2. FE<29F<C. PEF
o A 23= -3>> m7/ impro"ement in FE<2 either
spontaneousl or a'ter inhalation o' B3 agonist is
considered signi;cant
3. Peak E*pirator Flo! Rate -PEFR/
o Correlates closel !9 FE<2? used as an ad@unct and not a
su$stitute 'or spirometr
o Better suited 'or monitoring rather than d*
o PEF increases 3>= a'ter 2A-3> minutes4
B. Air!a hperresponsi"eness
o 5ethacholine or histamine inhalation challenge
o 3>= 'all in FE<2 'rom $aseline
- )suall normal $ut ma sho! hperin+ated lungs
,kin Prick test
- -D/ - allergic asthma
- --/ intrinsic asthma -non-atopic tpe. adult-onset/
Di6 D*
- <ocal cord paresis
- 7arngeal ca
- (racheal ca
- Bronchial ca
- Foreign $odies
- Bronchopulmonar dsplasia
- O$literati"e $ronchiolitis
- Cstic ;$rosis
Classi!ation of Asthma
- Asthma Cont"ol
o REFER (O EC(EE( to !9c mani'estation o' asthma ha"e
$een reduced or remo"ed $ t*
- Asthma se"erit
o $ased on the intensit o' t*. to achie"e good control
Chronic Asthma
%ntermittent Persistent
Datime s* monthl !eekl dail
Eocturna a!akening less than mo mo-!kl nightl
Rescue B3 use less than !eekl !kl to dail se"eral times a da
PEF or FE<2 0F>= o' predicted G2-F= o' predicted HG>=
Asthma Control
G%EA 3>>F and PCRAD5 3>>I
Datime s*. limitations o' acti"ities. nocturnal s*. need 'or rescue9relie"er
t*. lung '*n
)ncontrolled i' B or more o' partl controlled is present
ControlledJ none o' the 6
Partl controlledJ an
2. 5inimal or no s*
3. 5inimal attacks episodes or attack
B. Eo emergenc "isits
K. 5inimal need 'or relie"er
A. Eo limits on phsical acti"ities and e*ercise
G. Eearl normal lung '*n
L. 5inimal or no side e6ects 'rom meds
D"#gs #s$% to t& Asthma
A' Cont"oll$"s
- Corticosteroids most impt inhaled or sstemic
- 7ong-acting $ronchodilator
- (heophlline
- Anti-leukotrienes
- Eon-steroidal anti-in+ammator
o ,odium cromoglcate -cromoln/
o Eedocromil sodium
- Anti-allergic agents
o Metoti'en
B. Relie"ers
- ,hort acting $ronchodilator
%nhaled ,ABA
Oral Beta3 agonsit
,hort acting theophlline
- Anti-cholinergic agents
o %nhaled ipratropium $romide
,hort-acting B3 agonist
- (* o' choice 'or acute e*acer$ation and pret* o' e*ercise-induced
Rela* air!a muscle
Enhance mucociliar clearance
Dec "ascular permea$ilit
5oduclate mediator release 'rom mast cell and $asophils
Anti-cholinergic agents
- Block post-ganglionic e6erent "agal paths
- Block re+e* $ronchocronstriction caused $ inhaled irritants
- ,lo! action G>-I> min $e'ore peak $ronchodilation is achie"ed
- ,hould ont $e used as 2
line therap
- %nhi$its phosphodiesterase in ,5Cs
- )sed 'or nocturnal asthma -,R preparation/
- E*hi$its anti-in+ammator e6ects -atopic/
%nhaled Corticosteroids
- 5ainsta therap 'or persistent asthma
- 5ost e6ecti"e anti-in+ammator agent in asthma
- Reduces air!a in+ammation and impro"es air!a
- Reduces s* and e*acer$ation
- %mpro"es lung '*n
- Decreases need 'or $ronchodilator rescue
,stemic Corticosteroids
- A $urst o' oral steroids -A-2> das/ ma$e used as a ma*imum therap
to achie"e control o' asthma
- Reser"ed 'or t* o' acute se"ere asthma
- 5a AEs
Com$ined 7ABA and %nhaled Corticosteroids
- Greater impro"ement in the control o' s* and lung '*n among p*s !9
persistent asthma
- Addtl clinical $ene;t results 'rom steroid-induced transcription o' B3
adrenoreceptor gene !9 resultant inc snthesis o' the B3 receptor
protein inc eNcienc o' $oth drugs
- Block leukotriene snthesis $ en&me inhi$ition or inter'ere !9
leukotriene $inding receptors
- 5a$e gi"en as controller drug 'or mild persistent asthma !herein
inhaled corticosteroids are not in used
- )sed as add-on therap 'or moderate to se"ere persistent asthma
- %nh the %gE-mediated release 'rom mast cells and a cell-selecti"e
and mediator-slecti"e suppressi"e e6ect on other in+ammator
- 7ittle $ene;t in long term-control
,teroid-spacing therapies
- Anti-%gE -Omali&uma$/
o Block A$ that neutrali&es circulating %gE !9out $inding to
cell-$ound %gE
- %mmunotherap
o Eot recommended in most asthma t* guidelines
(lo)al initiati*$ on asthma +(INA, Philippin$ !ons$ns#s "$po"t on
asthma an% %& of mgt
A!#t$ S$*$"$ Asthma
- %nc chest tightness. !hee&ing and dspnea. o'ten not or poorl relie"ed
$ their usual relie"er drug
Re'ractor asthma
- DiNcult to control despite ma*imal inhaled therap
- Anti-leukotrienes
- CausesJ
o E*posure to high am$ient le"els o' allergens
o )nidenti;ed occupational agents
o ,e"ere rhinosinusitis
Corticosteroid resistant asthma
- Failure to respond to a high dose o' oral prednisone -K>mg9kg 'or 3
- Anti-%gE
-pre"enta$le and treata$le dse characteri&ed $ air+o! limitation that is
not 'ull re"ersi$le
- air+o! limitation is usuall progressi"e-asthmaJ episodic/ and associated
!9 a$normal in+ammator response o' the lung to no*ious particles and
- commonl $ut "aria$l assoc !9 dse !9 other organ sstem that can
contri$ute to the c* 'eature in indi"idual p*s
--- emphsema. chronic $ronchitis. small air!a dse start
- K
leading cause o' death in ),
- A
leading cause o' the death !orld!ide and !ill $e the B
cause in 3>3> -:1O/
Risk 'actorsJ
- Cigarette smoking
- Occupational dusts and chemicals
- %ndoor air pollution 'rom $iomass 'uel
- Outdoor air pollution
- Passi"e or second hand smoke
- Genetic suscepti$ilit
%n+ammator 5echanisms in COPD
Cigarette acti"ate al"eolar macrophages CCC chmeokines -%7F. GRO-
a. 7(F/ neutro neutrophil elastasecathepsins. matri* metalloproteins -
proteases - emphsema and mucus hpersecretion
CDF lmphoctes per'orins. gran&mes proteases
-O*idati"e stress in COPD/
Eo*ious particles and gases --host 'actors/ lung in+ammation
- %m$alance in antiproteinases
- O*idati"e stress
- Elastase antielastase hpothesis 5C mechanism in pathophsio
- %n+ammation and e*tracelluar matri* proteolsis
- Cell death
- %ne6ecti"e repair
- (pical ;ndings
Air+o! o$struction
o Persistent reduction in FE< most tpical ;nding
o Reduced FE< 2. sho!s no signi;cant response to inhaled
$ronchiodilator -23 = reductionin FE<2/
o FE<29F<C red
o Air trapping inc R< and R<9(7C
o Progressi"e hperin+ation
%nc (7C
,een in late dse
1elps to compensate 'or air!a o$struction
Can push the diaphragm into a +attened position
Gas e*change impairment
o PaO3 usu remain near normal until FE<2 is dec to A>=
o Ele"ation o' PaCO3 is not e*pected until FE< is H or O 3A=
o Pulmo 1PE is usu mild
o Eon-uni'orm "entilation due to regional di6erences and
air!a resistance
o <entilatio9per'usion mismatching accounts 'or dec in
PaO3 5C cause o' hpo*emia in COPD
Pathologic Changes
- -hpo*emia/ Remodelling o' "essel !all. prominent intimal
thickening pulmonar hpertension
7ung Parenchma
- Centrilo$ular 'orm o' emphsema more 're8uentl in upper lung
region in mild cases -in smokers/
- Primar mechanism im$alance o' endogenous 4
- 5ucus hpersecretion
- Ciliards'*n
- Air+o! limitation
- Pulmonar hperin+ation
- Gas e*change a$normalit
- Pulmonar hpertension
- Corpulmonale -in R sided heart 'ailure 3ndar to a long-standing
lung dse/
%rre"ersi$le - Fi$rosis and
narro!ing o'
- 7oss o' elastic
recoil due to al"
- Destruction o'
al"eolar support
that maintains
patenc o' small
Re"ersi$le - Accumulation o'
cells. mucus. and
plasma e*udate in
- ,5 contraction in
peripheral air!as
- 4
Syst$mi! E-$!ts
- ,stemic O*idati"e stress
o Atherosclerosis
o 1percoagula$ilit
- A$normal o' circulator ctokines
o (EF !t loss
o %7 G hpercoagula$ilit. inc ;$rinogen le"els
o Renin-angiotensin alteration polcthemia
o G5-C,F "ascular permea$ilit
- Chronic cough. sputum production. dspnea on e*ertion-to
di6erentiate in p*s !9 heart dse/
- 7arge $arrel chest
- Prominent accessor muscles o' respiration
- 7o!. +at diaphragm
- Diminished $reath sounds and distant heart sounds
- Prolonged e*piration !9 generali&ed !hee&ing
A. Detecti"e strateg
,uspect COPD in p*s !9J
- 0K> rs
- 1* o' e*posure
- 4
B. Con;rmation
- ,pirometr J FE<29F<C HL>=
Post$ronchodilator responseJ FE< dec $ 23= -#/
C. Addtl.
- EmphsemaJ hperin+ation !idened %C and retrosternal spaces?
+attened diaphragm. inc AP dm
- Chronic $ronchitisJ tram line -"ascular markings/
- Pulmo 1PEJ prominent large "essels
- C( scan
- Anti-trpsin de;cienc screening
-Grading o' COPD ,e"erit/
Di- D&
Asthma. C1F.
Asthma -sensiti&ing agent/ COPD -no*ious agents/
Eos neutro.and macrophages
CdK (lmpho CDF
Completel re"ersi$le completel irre"ersi$le
- Pre"ent dse progression
- Relie"e s*
- %mpro"e e*ercise capacit
- %mpro"e PO7
- Pre"ent and t* complication
- Pre"ent and treat e*acer$ation
- Reduce mortalit
- ,moking cessationJ single most e6ecti"e and cost-e6ecti"e !a to
reduce risk o' de"eloping COPD and delaing its progression
- B"on!ho%ilato"s
- 5ainsta o' t*
- Pre"ent or reduce persistent s*
- E*J B3 agonists and anticholinergics 2
- 5eth*anthine
- Com$ination therap
- Regular t* !9 inhaled gluco is onl 'or !ith an FE<2 HA>=
- Chronic use o' oral steroids in not recommended
- %n+uen&a "accines reduce illness and e*acer$ation in FK-FA= and
pre"ents death in COPD p*s $ L>= -once a ear. $est time to
administer during rain season/
- Pneumococcal "accine is recommended 'or COPD GA rs and older
and in ounger COPD p*s !9 FE< HK>= -once e"er A ears/
- Recommended onl 'or t* o' in'ectious e*acer$ations and other
$acterial in'ections
- O"erall $ene;ts are "er small
- Regular use is not ad"isa$le
%mmunomodulator and her$al meds
- Eot recommended
O*gen (herap in COPD
- GOA7J to inc the $aseline PaO3 to at least G> mm1g and to
produce arterial O3 saturation o' at least FF-I>=
%ndications 'or long term therap
- PsO3 HAA mm1G or ,aO3 HFF= !9 or !9out hpercapnea
- PaO3 AA>G> mm1G or ,aO3 0FI= $ut !ith e"idence o' pulmo
1PE. polcthemia -1c(0AA=/. or peripheral edema suggesting
Eon-pharmacologic mgt
- P*mgt
- Pulmo reha$ilitation
- Eutrition
- ,urger
o Bullectom
o 7ung "olume reduction
o 7ung transplant
Pharmacologic (*
5ildJ "accine. !hen s*J short acting $ronchodilator
5odJ D regularl long acting $ronchodilator. i' "er s* do reha$
,e"ereJ D glucocosteroids. check i' candidates 'or O3 therap or surger
-$ullectom. lung transplant/
Acute e*acer$ations
- :orsening o' sta$le condtion
o %nc in cough and sputum
o %nc purulence o' sputum
o %nc in $reathlessness !9 or !9out !hee&e
o %nc hpo*emia
- %nhaled $ronchodilator
- ABCs
- ,stemic glucocorticoids
- O3
- 5echanical "entilator support
o %n"asi"e
o Eon-in"asi"e
- Pneumothora*. corpulmonale. pneumonia. sleep a$normalities.
giant $ullae. acute respirator 'ailure