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Emphysema: Risk factors, epidemiology, causes, pathogenesis, and pathologyVersión en línea
Emphysema: Risk factors, epidemiology, causes, pathogenesis, and pathology
Emphysema
and
chronic
bronchitis
are
both
components
of
COPD
,
yet
they
exhibit
distinct
pathological
and
clinical
features
.
is
characterized
by
the
destruction
of
alveolar
walls
,
leading
to
enlarged
air
spaces
and
reduced
gas
exchange
efficiency
.
This
results
in
airflow
limitation
due
to
loss
of
elastic
recoil
.
,
on
the
other
hand
,
involves
inflammation
and
narrowing
of
the
bronchial
tubes
,
leading
to
increased
mucus
production
and
chronic
cough
.
While
both
conditions
result
in
airflow
obstruction
,
emphysema
primarily
affects
the
alveoli
,
and
chronic
bronchitis
primarily
affects
the
airways
.
Emphysema
is
a
chronic
,
progressive
lung
disease
characterized
by
the
of
airspaces
to
the
terminal
bronchioles
,
accompanied
by
the
destruction
of
without
significant
fibrosis
.
This
destruction
leads
to
a
loss
of
and
reduced
for
gas
exchange
,
primarily
causing
difficulty
in
.
It
is
a
major
component
of
(
)
.
The
primary
cause
is
chronic
exposure
to
lung
irritants
,
predominantly
,
which
triggers
an
inflammatory
response
and
an
imbalance
between
and
-
,
leading
to
tissue
destruction
.
Several
factors
contribute
to
the
development
of
emphysema
,
often
interacting
to
increase
an
individual's
susceptibility
:
:
The
most
significant
risk
factor
,
causally
linked
to
over
80%
of
COPD
cases
in
the
U
.
S
.
,
including
emphysema
.
Smoking
cessation
significantly
slows
the
decline
in
lung
function
.
Genetic
Predisposition
:
-
(
)
:
An
inherited
deficiency
in
?
1
-
,
an
anti
-
protease
enzyme
,
leads
to
earlier
onset
and
more
severe
emphysema
,
particularly
type
.
Family
history
of
lung
diseases
.
Age
:
The
prevalence
of
COPD
,
including
emphysema
,
increases
with
age
due
to
exposure
and
natural
lung
function
decline
.
Environmental
and
Occupational
Exposures
:
and
prolonged
exposure
to
pollutants
.
Occupational
exposure
to
irritants
(
e
.
g
.
,
,
dust
)
.
Secondhand
smoke
.
Biomass
fuel
exposure
and
indoor
air
pollution
,
especially
in
-
-
countries
.
History
of
Infections
:
Can
predispose
individuals
to
lung
disease
later
in
life
.
Low
(
)
:
Associated
with
emphysema
,
potentially
indicating
malnutrition
or
systemic
effects
of
the
disease
.
Emphysema
is
a
critical
component
of
COPD
,
which
carries
a
substantial
global
public
health
burden
:
Prevalence
:
COPD
is
the
leading
cause
of
death
globally
.
The
global
prevalence
of
moderate
to
severe
COPD
is
estimated
to
be
as
high
as
of
the
population
.
In
the
U
.
S
.
,
over
.
million
adults
were
diagnosed
with
COPD
as
of
May
2020
,
with
millions
more
likely
undiagnosed
.
Mortality
:
Mortality
rates
due
to
COPD
have
climbed
since
the
.
Recent
trends
show
a
shift
in
the
affected
population
,
with
mortality
rates
in
surpassing
,
possibly
due
to
smaller
lung
size
and
role
in
worsening
lung
damage
from
pollutants
.
Demographics
:
-
,
are
affected
more
than
other
ethnic
groups
.
The
prevalence
increases
with
age
due
to
chronic
and
progressive
nature
and
prolonged
exposure
to
tobacco
smoke
.
Healthcare
Impact
:
COPD
has
significant
healthcare
resource
implications
,
with
billions
spent
annually
on
treatment
in
the
U
.
S
.
.
are
at
a
higher
risk
of
COPD
compared
to
the
general
U
.
S
.
population
.
The
pathogenesis
of
emphysema
is
complex
,
involving
an
imbalance
between
protective
and
destructive
processes
in
the
lung
:
Protease
-
Antiprotease
Imbalance
:
Normally
,
anti
-
protease
enzymes
(
e
.
g
.
,
?
1
anti
-
trypsin
)
and
-
balance
enzymes
that
digest
proteins
(
e
.
g
.
,
elastase
)
,
,
and
oxidants
.
In
emphysema
,
there
is
an
imbalance
favoring
.
Cigarette
smoke
contains
abundant
reactive
oxygen
species
,
which
cause
and
inactivate
-
.
Immune
cells
,
stimulated
by
toxins
,
release
,
which
breaks
down
and
other
extracellular
matrix
components
in
the
alveolar
walls
.
Chronic
Inflammation
and
Oxidative
Stress
:
Environmental
toxins
(
e
.
g
.
,
cigarette
smoke
,
pollutants
)
stimulate
,
leading
to
the
accumulation
of
,
,
and
.
These
inflammatory
cells
release
,
,
and
,
leading
to
and
.
Oxidative
stress
further
promotes
proinflammatory
gene
expression
.
Alveolar
Destruction
and
Hyperinflation
:
The
continuous
destruction
of
elastic
wall
tissue
in
the
alveoli
leads
to
of
respiratory
bronchioles
and
alveoli
,
creating
larger
.
Loss
of
causes
difficulty
in
expiration
and
air
trapping
,
resulting
in
lung
,
which
can
manifest
as
a
"
barrel
chest
"
.
This
destruction
reduces
the
available
for
gas
exchange
,
leading
to
.
Airway
Damage
and
Structural
Changes
:
Chronic
inflammation
and
oxidative
stress
also
lead
to
airway
damage
and
structural
changes
,
such
as
of
bronchial
walls
,
contributing
to
increased
and
limitation
.
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