EMPHYSEMA

RESPIRATORY PATHOLOGY
Emphysema is characterized by irreversible enlargement of the airspaces distal to
the terminal bronchioles accompanied by destruction of their walls without
fibrosis.

Small airway fibrosis has also been shown to be present along with emphysema.

DEFINITION
 According to the
anatomic distribution of
BASIS FOR
CLASSIFICATI
the lobule
ON
Based on the segments
of the respiratory units
that are involved
 TYPES

01 02 03 04
Centriacinar Panacinar Paraseptal Irregular
 Most common type

Central or proximal parts of the acini are involved

CENTRIACIN
AR Alveoli are spared

EMPHYSEM Both emphysematous and normal airspaces are present within the
same acinus and lobule
A
Upper lobes – apical segments

Inflammation is seen
IN • DISTAL ACINUS MAY ALSO BE INVOLVED
• DIFFERENTIATION FROM PANACINAR MAY BECOME
CHRONIC DIFFICULT

CASES, • OCCURS PREDOMINANTLY IN CHRONIC SMOKERS

• ASSOCIATED WITH COPD
CENTRIACINAR EMPHYSEMA
Acini are uniformly From respiratory Lower zones – Severe at the bases Associated with alpha
enlarged bronchiole to anterior margins 1 antitrypsin
terminal blind alveoli deficiency

PANACINAR EMPHYSEMA
PANACINAR
EMPHYSEM
A
 Distal portion is
involved
PARASEPT
AL More striking

EMPHYSE adjacent to pleura

MA Along the ct septa

and margins of the
lobule
 Occurs adjacent to areas of fibrosis, scarring
or atelectasis
More severe in upper half of the lungs

CHARACTERIS Multiple , continuous , enlarged spaces from

TICS less than 0.5 cm to more than 2 cm in diameter
Sometimes cystlike

Probably underlies many cases of

pneumothorax in young adults
 DISTAL
ACINAR
EMPHYSEM
A
Airspace enlargement with fibrosis

Acini are irregularly involved

Associated with scarring

In most instances – insignificant small
foci.

IRREGULAR EMPHYSEMA
IRREGULAR
EMPHYSEM
A
PATHOGENES
IS
 Inhaled cigarette smoke and other
noxious stimuli

PATHOGENES Lung damage and inflammation

IS
Parenchymal destruction Airway disease

Bronchiolitis
and chronic b
ron chitis
emphysema
 FACTORS
INFLUENCING
DEVELOPMEN
T OF
EMPHYSEMA
 1. INFLAMMATORY MEDIATORS AND
LEUKOCYTES

Eg : LTB4 , IL-8 , TNF

Released by the resident epithelial cells and macrophages

Attract inflammatory cells from circulation (chemotactic
factors )
Amplify the inflammatory process (proinflammatory
cytokines )
Induce structural changes (growth factors )
2. PROTEASE
–
ANTIPROTEA
SE
IMBALANCE
 Tobacco smoke
substance Alveolar damage
s inflammatory
3.
OXIDATI
oxidants
oxidants VE
STRESS
Inflammation
Tissue damage
 GENE INVOLVEMENT
• NRF2 CODES FOR A TRANSCRIPTION FACTOR THAT SERVES AS A SENSOR FOR
OXIDANTS

Upregulate the
Intracellular Protect cells
expression of
oxidants from oxidative
multiple genes
activate NRF2 damage
that
 4. INFECTIONS
MAY EXCACERBATE ASSOCIATED INFLAMMATION AND
CHRONIC BRONCHITIS
PATHOGENESIS
REVISION OF
TYPES
 MORPHOLOGY

Upper two thirds Large alveoli

Voluminous Overlapping the
r more severely can be seen on
lungs heart
affected cut section
 GROSS
APPEARANCE
 LARGE APICAL BLEBS ARE MORE
CHARACTERISTIC OF IRREGULAR
EMPHYSEMA SECONDARY TO SCARRING
AND OF DISTAL ACINAR EMPHYSEMA
01 02 03
Abnormally large Pores of kohn are so Septa appears to be
alveoli are separated large floating
by thin septa with
only focal
centriacinar fibrosis

MICROSCOPICALLY
MICROSCOPI
C
 CONTD.

Prolonged
Decrease in capillary bed
vasoconstriction –
area
changes in PAH

Deform and compress the

Large abnormal blebs or
respiratory bronchioles
bullae
and vasculature
COMPARISO
N
CLINICAL • SYMPTOMS APPEAR ONLY IF ATLEAST 1/3RD OF THE FNAL
PARENCHYMA IS DAMAGED

COURSE • DYSPNEA – INSIDIOUS

• C/O COUGH OR WHEEZING (VARIABLE)
• WEIGHT LOSS
• BARREL CHEST
• PROLONGED EXPIRATION (IMPAIRED EXPIRATORY
OUTFLOW)
• SITS IN HUNCHED OVER POSITION
• BREATHES THROUGH PURSUED LIPS
HUNCHED OVER
POSITION
 Cough – slight

Severe overdistension
SEVERE
EMPHYSEM Low diffusion capacity
A
Blood gas values – normal at rest

Overventilate and remain well

oxygenated(pink puffers)
 PINK
PUFFERS
 COMPLICATIONS

• COR PULMONALE
• CONGESTIVE HEART FAILURE
• SECONDARY PULMONARY HYPERTENSION
• ALL ASSOCIATED WITH POOR PROGNOSIS
 DEATH DUE TO

Coronary artery Respiratory Right sided Massive

disease failure heart failure collapse of
lungs
 TREATMENT

• SMOKING CESSATION
• OXYGEN THERAPY
• LONG ACTING BRONCHODILATORS
• INHALED CORTICOSTEROIDS
• PHYSICAL THERAPY
• BULLECTOMY
 IN FEW

Lung volume reduction Lung transplant

surgery
OTHER FORMS OF EMPHYSEMA
LUNG 1. COMPENSATORY HYPERINFLATION

OVERINFLATIO 2. OBSTRUCTIVE OVERINFLATION

N OR FOCAL 3. BULLOUS EMPHYSEMA

EMPHYSEMATO 4. INTERSTITIAL EMPHYSEMA

US CHANGE