RESPIRATORY HISTOLOGY

Respiratory Conduction Portion Ciliated Seromucinous secretion

System pseudostratified
columnar
epithelium
Two Functional From the nasal cavity to Goblet cells secrete
Components: the bronchi→ Ciliated seromucinous which
1. A conduction pseudostratified provides consistency to
portion for Columnar epithelium the cilia in the movement
transport of inspired (rich in goblet cells). of secretory products in an
air and expired upward direction towards
gases between the the nose.
atmosphere and Asyou go down, the It aids in the elimination of
circulatory system. height of the epithelium inhaled particles and other
decreases to: a environmental debris.
2. The respiratory ciliated simple It absorbs and detoxifies
portion where the columnar and then soluble gases—First line
actual exchange of to →cuboidal of defense against
gases occur in the epithelium invasive pathogens.
alveoli.

The connective tissue

beneath the epithelium
(lamina propria) is rich
in lymphoid cells-
produce IgA---
transported across the Simple cuboidal Goblet cells with a
epithelium and is epithelium seromucinous secretion
effective in killing
bacteria and viruses.
Nasal Cavity Larynx Pharynx Trachea Bronchi
It contains the The larynx is a hollow, 1.The Nasopharynx:-- It branches out in Primary bronchi→gives
ciliated bilaterally symmetric structure ciliated psudostratified to two primary rise to secondary and
pseudostratified framed by plates of hyaline columnar epithelium bronchi tertiary bronchi.
epithelium with cartilage and muscle.
one to each lung.
numerous goblet -The mucosa is wear and tear, Secondary bronchi
2.Oropharynx:
cells supported by a the epithelium is stratified supplies the lobes of each
Stratified squamous
richly vascular squamous epithelium. The cartilage of the lungs.
epithelium and pure
lamina propria becomes less regular
containing serous mucous glands in the ends of the
and mucous glands. primary bronchi. Tertiary bronchi supplies
the segments of each lobe.
Abundant goblet cells, It then turns into
a submucosa of loose smaller airways called
connective tissue bronchioles.
containing
seromucinous glands, Secondary and tertiary:
and the adventitia, Possess discontinuous
which contains the U- cartilaginous plates in their
shaped cartilage, C.T. adventitia (less rigidity)
and smooth muscle.

T
Transition of PS
Columnar to Stratified
squamous

Bronchioles Terminal Bronchiole The Lungs

The last order of Cilia may still be present, but The connective tissue Elastic recoil plays a major
tertiary bronchi goblet cells gradually within the lungs is role in contraction of the
gives rise to several disappear. rich in elastic fibers lung during expiration.
orders of bronchioles and smooth
muscle, which A primary bronchus and
Elastic fibers increase in
The diameter allows the lungs to the pulmonary vessels
number in the lamina propria.
decreases –the expand when the enter each lung at the
submucosal glands negative intrathoracic hilus. The right lung has
These features are particularly
disappear so what is pressure is increased three lobes and the left
prominent in the last
left is essentially during inspiration. lung has two, and each
generation of bronchioles, the
mucosa lobe receives a branch of
Terminal Bronchioles, which Bronchiole with
There epithelium is the primary bronchus.
give rise to the respiratory Prominent Smooth
simple columnar
portion of the bronchial tree. Muscle Layer
to cuboidal. Each lobe is subdivided
into bronchopulmonary
segments and finally into
lobules of pyramidal
shape, the base facing the
surface of the lungs.
The pulmonary Pulmonary artery with Pulmonary artery The last generation of
artery enters the bronchus breaks up into the bronchioles gives rise to
hilus with the alveolar capillaries Terminal Bronchioles,
primary bronchus which gives rise to two
and follows the The venous return orders of Respiratory
precise branching follows a separate Bronchioles.
pattern. course in that the
alveolar capillaries
The respiratory bronchioles
The pulmonary coalesce into small
give rise to several alveolar
artery and its veins in the intralobar
ducts. It is here where the
branches are thin- septae and join other
walls are filled with
walled, as compared branches in the
alveolar outpouchings
to arteries of similar interlobar septae
called the Alveolar Sacs
caliber in the
systemic circulation,
Alveolar Sacs: contain
due to the
reticular and elastic fibers
pulmonary blood
but no smooth muscle.
pressure being much
lower than that of
the systemic
circulation.

Alveoli Surfactant
These are delicate, A single wall, the The alveoli are lined It is secreted and spreads
cup-shaped intraalveolar septum is by two cell types along the epithelial surface
structures that are formed between adjacent that are continuous where it reduces surface
lined by an extremely alveoli with one another: tension at the air-filled
attenuated simple interface, stabilizing
squamous epithelium The septum is composed of Type I alveolar diameters, thus
lining cells of adjacent Pneumocytes: are preventing collapse
alveoli and has connective squamousepithelial during expiration.
Macrophages(histio tissue consisting of reticular cells that make up the
cytes) are present in and elastic fibers with an barrier thru which
the septae or inside anastomosing network of Alveoli with capillaries gases pass in the
the alveoli--play an capillaries. exchange between
important role in the blood and air.
phagocytosis and Alveoli with macrophages
disposal of Type II
particulate matter Pneumocytes:
that reaches the cuboidal epithelial
distal passages cells that contain an
and alveoli organelle called a
multilaminar body
or cytosome, which
contains a surface-
active phospholipid
called Surfactant.
PNEUMONIAS
Pneumonia Alveolar pneumonia
1.Alveolar a. Focal Patchy
Pneumonia: (bronchopneumonia) bronchopneumonia
-May be limited to the
intraalveolar
alveoli or may involve the
inflammation usually
alveoli and the bronchi.
caused by a bacteria:
-Patchy distribution
Intra-Alveolar pneumonia involving one or more Interstitial pneumonia
A.BRONCHOPNEUM
lobes
ONIA
b. Diffuse: (lobar
B. LOBAR pneumonia) limited to a
PNEUMONIA segment bronchi and Lobar pneumonia
surrounding parenchyma.
-it may include the
2. Interstitial Interstitial pneumonia
pneumonia: Interstitial pneumonia
Involves alveolar whole lobe. w/mononuclear cells.
septae including
viral pneumonia

-Usually caused
by viruses---if
poorly treated can
become chronic
 Etiologies of
pneumonias
Can be caused by:
Bacteria, viruses and
less commonly by
fungi, protozoa and
other parasites and
aspiration.
-Bacteria accounts for
75%.
If aspirated into the lower
respiratory tract—can
cause pneumonia.
Hepatization
Pathogens Routes of Bronchopneumonia
pathogenesis
-Streptococcus 1.Inhalation in air It begins with
droplets (TB) bacterial invasion of
-Staphylococcus
2. Aspiration from the bronchial or
-Hemophilus influenza upper respiratory tract bronchiolar mucosa.
(strep and staph)
-Followed by
3.Aspiration of infected
Legionella or T.B., exudation of PMN’s
CMV pneumonia with particles—often caused
fungia, viruses—not into the lumen of the
inclusions by anaerobic bacteria.
present in airways.
-comonin unconscious
nasopharyngeal flora people, with neuro
may cause pneumonia. Inflammation may be
deficits,
limited to small number
4.Hematogenous
Legionella—acquired of lobules or may
spread: Bacteria may be
from inhalation of spread. (lobar
transported to the lungs
bacteria from pneumonia
by the blood.
humidifiers or AC.
Aspiration pneumonia
Viral pneumonias—by with acute inflammation
close contact with an and bacterial colonies
infected person.
-Herpes and CMV may
be latent in the human
body and become
reactivated.
Interstitial Complications
pneumonia
As the intra alveolar Hepatization of lower -Usually diffuse and Bacterial pneumonia
exudates accumulate – bilateral
-May occur rapidly
air is replaced and the -Inflammation affects the
progressing cases
lung parenchyma is alveolar septae
caused by virulent
consolidated.
pathogens
-This process is known -Mycoplasma
as hepatization pneumoniae is the Purulent pulmonary
1. Pleuritis-extension of
most common empyema
-it becomes denser in x- inflammation can lead to
rays pleural effusion.
lobe -Does not result in a. Pyothorax: Pus fills
Patchy consolidations exudation of PMNinto the pleural cavity
(infiltrates) alveolar lumen (like b. Empyema: Pockets
alveolar pneumonia) of pus encapsulated by
fibrous tissue—it occurs
more commonly.
-Viruses invade the
septae and cause
necrosis along with
mononuclear cell
infiltration.

Most resolve with minor

alveolar damage.

Complications Contd. Clinical Features Diagnosis

2. Abscesses: Affect children <5 years 1.Confirmed with CXR-
associated with virulent old and people >70 pulmonary infiltrates
organisms such as years old.
staph—it causes 2.Bacteriologic studies of
destruction of the lung 1.Primary or sputum
parenchyma and community acquired -can yield proof of
suppuration. Honeycomb-lung due to infection
fibrosis -affect healthy people
Pus causes destruction of 3. Peripheral blood
2.Secondary
the bronchi walls and smears
Pneumonias
permanent dilation Pulmonary abscess— -confirmed by
(nosocomial)
(bronchiectasis) staph leukocytosis
-in persons with existing (neutrophilia)
3. Chronic lung illnesses
disease: caused by 4. Blood gas analysis
Pneumonia with
unresponsiveness to Signs and symptoms -may detect hypoxia and
interstitial fibrosis
treatment. -High fever, chills, even respiratory
-Destruction of the lung coughing, SOB, dypsnea, acidosis.
parenchyma with tachypnea
concomitant fibrosis
Inflammatory exudates
transform the lung
Abscess formation cause tissue destruction
into
and bleeding giving rise
honeycomb like to mucopurulent, blood-
structure. tinged, “rust-colored
sputum”.

Staph on gram stain

-
Pneumococcal Pneumonia
Infection with St. 4 pathological Gray hepatization
pneumonia sequential phases: 3. Gray Hepatization: (wbc and fibrin)
>50% of all bacterial By 3-8 days, the lungs
1.Engorgement: serous
pneumonias become grayins as the
exudates pours into the
WBC’s and the fibrin
-usually affect the lower alveoli from dilated leaky
consolidate in the alveoli
lobes due to gravity. blood vessels.
4. Resolution: By 7-11
days exudates is lysed
2. Red hepatization Bronchopneumonia vs
and reabsorbed by
(within 48hrs) RBC’s, normal
macrophage restoring
fibrin, and PMN fill the
tissue.
alveoli
lobar pneumonia

Clinical features Staph aureus Gram negative bacteria Atypical pneumonia

pneumonia
Sudden with chills Staph aureus tends to Pseudomonas Klebsiella pneumoniae Mycoplasma
Fever, produce multiple Most common infection occurs in pneumonia—bacterial
Pleuritic chest pain, abscesses. hospital-acquired middle-aged, alcoholic -like organism that
cough and rust-colored -Mortality rate is over pneumonia. males. A thick current- causes an interstitial
sputum. 50% red jelly sputum is pneumonia
Characterized by characteristic
The vaccine for vascular lesions that
pneumococcus is 80-90% cause infarcts and
effective against most necrosis of the lung
serotypes and is usually parenchyma
given to high-risk
patients The most common
-Clinical sx’s are
causes of lung
milder, the fever is less
Staph aureus abscesses infections in Cystic
pronounced.usually no
Fibrosis pt’s Gram negative bacteria chills.

-The cough is mild and

does not produce bloody
or mucopurulent
 sputum.

-No signs of septicemia,

leukocytosis, or
abscesses
Legionella pneumophila Pathogenesis Clinical presentation
Legionnaires’ disease
Causes Legionnaires -This organism is Organism, a facultative Severe pneumonia--
Disease. ubiquitous in natural intracellular organism, high Fevers-- Fever
-community and in and man-made water settles in the lower greater than 40°C
hospitalized immuno- environments respiratory tract and is (range, 38.8-40.5°C)
compromised engulfed by
-Aerosolized
patients macrophages
contaminated water is -Mental confusion,
-Gram negative rod
inhaled, resulting in - Proteinuria Legionnaires’
-Famous for causing an
infection -Microscopic hematuria Disease-Lobar
outbreak of pneumonia -It inhibits
-Outbreaks have even Infiltrate
at an American Legion phagocytosis,
been found associated Cough is a prominent
convention survives and
with growth in shower symptom, although the
replicates inside the
heads sputum is frequently
macrophage
-No person to person scanty and nonpurulent
transmission has been
identified. -People who smoke, Should be suspected
drink alcohol (a lot) in patients who
are>50 and smokers
-Pts with AIDS, cancer, Alveoli with foamy
or if the sputum gram
renal transplants are macrophages
stains reveals
predisposed to infection
neutrophils and very few
organisms

Fungal pneumonias Histoplasmosis Cryptococcus

neoformans
Diagnosis -Usually develop from -Caused by Histoplasma -Causes Cryptococcosis,
inhaled spores causing capsulatum a systemic, opportunistic
Legionella antigens by
granuloma formation, mycosis, which affects
using fluorescent
scarring, calcification, - Usually a self-limited the meninges and the
antibody staining
and cavity formation lungs
mycosis, but can lead to
a systemic
granulomatous
Calcified Granuloma of It has a world-wide
- Histoplasma, infection in the
Histoplasma distribution, and the
immunosuppressed
Aspergillus, main reservoir is
(AIDS)
Cryptococcus, pigeon droppings in
Coccidioidiomycosis, the soil, but the birds
Candida, and are not affected.
Pneumocystis. - It grows in soil
Histoplasma Pneumonia
heavily contaminated
Organisms within - It occurs almost
with bird or bat
Macrophages exclusively in persons
droppings (bat guano)
with impaired cell-
mediated immunity
Aspergillus fumigatus Clinical findings
-Causes Aspergillosis, -It can colonize and also
caused by an environ- invade abraded skin,
mental fungi that wounds, burns, cornea,
produces lung infections or paranasal sinuses

- It has a characteristic - Immunocompromised

appearance, having patients are susceptible
septate hyphae that
Mucicarmine Stain for forms V-shaped
Cryptococcal Pneumonia
the Capsules of branches
with Mucoid (clear)
Cryptococcus
Capsules

“Soap bubble”
Aspergillus pneumonia

Aspergillus Fungal Ball

Coccidioides immitis- Pathogenesis Granuloma
Pneu.
-In soil, it forms hyphae -The Arthrospores
- Coccidioidomycosis with Arthrospores that form Spherules (in the
are very light and can be lungs)--large vacuoles
A chronic, necrotizing carried by the wind to be with a thick wall that are
infection that resembles inhaled. filled with Endospores
Tuberculosis, and is
endemic to arid regions
of Southwestern U.S. and - the endospores form
Latin America new spherules which
-“Valley fever” spread forming
(CENCAL) caseating granulomas,
similar to T.B.
Clinical presentation Candida Pneumocystis carinii
-Initially asymptomatic An important cause
pneumonitis, of diffuse interstitial
-limited to the lungs and pneumonia in
regional lymph nodes, immunocompromised
but can disseminate to patients
granulomatous lesions.

Ruptured spherules - Transmission occurs

Spherule of
Coccidioides with by inhalation that
Candida albicans produces no disease in
Endospores
 Pneumonia with healthy patients, but
Pseudohyphae causes pneumonia in
AIDS patients

Pathogenesis Clinical
-The presence of the cup -There are bilateral rales
or boat-shaped cysts in and rhonchi and the
the alveoli induces an CXR reveals a diffuse
inflammatory response, interstitial pneumonia
resulting in a frothy,
eosinophilic, edema -Cough fever, dyspnea
fluid that blocks oxygen
exchange Diagnosis is made by Pneumocystis carinii
microscopic examination Pneumonia
of lung tissue obtained Silver Stain (GMS) for
by bronchoscopy, BAL, or Cyst Organisms
Pneumocystis carinii open lung biopsy
Pneumonia
Pink, Foamy Exudate
within
Tuberculosis Pathogenesis
-A chronic, bacterial -The encapsulated The inhaled organisms
infectious disease caused bacteria elicits multiply in the alveoli
by Mycobacterium formation of because alveolar
tuberculosis granulomascomposed macrophages cannot
of stimulated readily kill the bacteria.
macrophages
-It is transmitted from →multinucleated giant Grossly, the healed,
person to person by cells. Forms a Ghon Primary TB with Ghon
subpleural Ghonnodule
respiratory aerosols complex:peripheral Complex
is well circumscribed
parenchyma with central necrosis. In
-Infection is not marked granuloma + infected later stages, the
-It is an obligate aerobe, by acute purulent hilar node. lesion is fibrotic and
whose cell wall lesions. calcified.
→characteristic of
contains Mycolic acid,
primary TB -calcification that can be
a complex lipid.
Primary Ghon seen on CXR. (coin
-Doesn’t attract PMNs
Complex of Tuberculosis lesion)
-Not marked by purulent The initial infection -casseous necrosis
lesions usually occurs in the
 lower lobes and
consists of a Ghon
Complex.
Progressive Primary Secondary infection TB
TB
Primary TB tends to -Represents a
spread to other parts of reactivation of a
the lungs in children and dormant primary
immunosuppresed— infection (Ghon
progressive primary complex)
TB.The initial lesion
Cavitation
enlarges rapidly and -The bacteria typically
Multi-nucleated giant there is erosion of spreads to the apex of
Tuberculosis with
cells bronchi or bronchioles by the lungs.
Caseous
Necrosis central liquefaction. Involvement of hilar nodes
is common as well.

Causing a granulomatous Secondary TB—cavities

pneumonia where
confluent granulomas tend
to produce cavities—
AFB Stain for
common sources of
Tuberculosis
Granuloma hemoptysis

-Cavities can cause

erosions into both
bronchial tubes and
pulmonary blood vessels
Complications of Complications of Clinical features of TB
Secondary TB spread
Miliary Spread: -Contra-lateral -Fever, fatigue, night
pneumonia, pleuritis, sweats, and weight loss.
It seeds in distal organs
with effusion and pleural
with innumerable small
millet seed-like lesions. granulomas, TB -Primary TB remains
-Presence of small laryngitis, intestinal clinically unrecognized in
tuberculous granulomas tuberculosis, due to 95% of cases
swallowing of
-GI tract if swallowed, or tuberculous material. -The symptoms of
spread to the kidneys, Miliary spread TB -lymphatic spread to the secondary TB includes a Acid Fast Stain of
brain or bones, if
disseminated via the hilar lymph nodes with non-productive, dry Sputum
eroded bloodstream). infection to the neck cough, low-grade fever, Initial test for
area (called Scrofula), as loss of appetite, with minor diagnosis.
well as TB Meningitis hemoptysis from early
and Osteoarthritis. cavitary lesions.
Sarcoidosis Pathogenesis
A multisystemic The cause and - The lungs are infiltrated -These non-caseating
granulomatous pathogenesis are with CD-4 positive T- granulomasmay involve
disease of unknown unknown. helper lymphocytes, as any organs in the body.
etiology, presumably It has a are the lymph nodes -The lungs, lymph
mediated by cell- predilection for the -Non-caseating nodes of the thorax and
mediated immunity lungs and mediastinal granulomas neck, and the liver are
(hilar) lymph nodes. most often involved. non-caseating
granulomas

Granulomas Node involvement

-Asteroid Bodies (star- The nodes are
shaped crystals) characteristically
-Schaumann Bodies enlarged and
(calcified lamellar sometimes calcified.
structures) may be seen When present in the hilar
in granulomas. area the matted nodes are Potato nodes
Non-caseating called “Potato Nodes”,
-The granulomas are seen on chest X-ray
Sarcoidosis of the lungs
distributed around
bronchi, bronchioles and
blood vessels
granulomas
Sarcoidosis with
pulmonary fibrosis

Sarcoidosis in the lymp

node
Skin involvement Clinical features
The spleen is affected - Lesions may also -Most symptomatic
(75%) (splenomegaly) appear on the mucous patients have a low-
Seen as granulomas in membranes of the oral grade fever, feel tired
the parenchyma. cavity, larynx, and URT. and anorexic
Involvement of the
-Granulomas in the both lacrimal and salivary -Dyspnea, cough,
the portal triads glands, causing an iritis wheezing
and possible loss of
vision. -Peripheral
Sarcoidosis of the skin lymphadenopathy,
-Erythematous cutaneous lesions, eye
plaques similar to lupus. involvement,
splenomegaly, or
hepatomegaly
-60% of patients have
elevated serum levels
of Angiotensin-
Converting Enzyme
(ACE), which is released
from macrophages in
granuloma.

Hilar lymphadenopathy Sarcoidosis with end-

stage progressive
pulmonary fibrosis.

COPD
COPD Bronchial Asthma Pathogenesis Histopathology of
Asthma
Lung diseases Characterized by attacks lymphocytes, Bronchi show:
characterized by chronic marked by wheezing macrophages, 1. chronic 1.Mucus in the lumen
airway obstruction. during expiration, cough eosinophils, basinophils inflamamation and 2.Inflammation and
and dyspnea. and plasma cells 2. Overabundance of basement membrane
Asthma
produce a variety of mucus in the lumen. thickening
Chronic bronchitis chemical mediators. – If mucus 3.Enlarged mucosa
In more than 50% of the
contains whorls glands
cases, the disease -act in response to
 begins in childhood. an of shed epithelial 4.Smooth muscle
Two types: cells then are hyperplasia
Allergen and do two
1. Extrinsic: called:
things:
mediated by type Curshmann
1 hypersensitivity Spirals.
response.
– Begins in 1. Increase
childhood permeability of
2. Intrinsic: blood vessels
Precipitated by 2. Stimulate the
non-immune contraction of
Thick mucus in lumen
response and smooth muscle
and basement
includes physical cells.
membrane thickening
factors (heat or
cold), exercise,
psychological -These mediators include
stress, chemical histamine, bradykinins
irritants, air and PG’s
pollution and
bronchial
infection.
-Usually begins
in adult life.
Asthma with
eosinophils

Asthma
The lungs are pink, and
touch in the midline.

-overabundance of
mucus plugs in the
lumen→forming casts

Asthma with Thickened

Asthma with Goblet Cell Mucus Plug in Bronchial
Basement Membrane Bronchial Asthma with
Hyperplasia, and Smooth Asthma
and Smooth Muscle Enlarged Mucus Glands
Muscle Hyperplasia
Hypertrophy and Inflammation
Clinical Features Chronic Bronchitis Pathology
Extrinsic asthma begins Defined as a chronic 1.Fibrous thickening of
before the age of 10. cough and production of the walls of the bronchi
sputum for a minimum of and bronchiole.
three months a year for
-Lumens filled with
Disease is characterized at least two consecutive
mucus.
by attacks of cough years.
wheezing, and dyspnea.
ETIOLOGY Chronic Bronchitis With
-Hypertrophy of mucous
Hyperplasia of Mucus
-smoking is the main glands
Cells
cause of chronic
bronchitis (90%) -Oversecretion of
-air pollution, toxic mucus
fumes and pneumonias -Hyperplasia of goblet
as well. cells

-Because of this
there is infiltration of Chronic Bronchitis with Chronic Bronchitis with
lymphocytes, Increased Goblet Cells Chronic Inflammatory
macrophages and Cells in Submucosa
plasma ells.
Over production of Complications
mucus
With time surface Due to the increased Peribronchial fibrosis
epithelium may show production of mucus by may affect the
ulcerations or submucosal glands, it vasculature resuling in
metaplasia of may lead to cyanosis. pulmonary hypertension
columnar epithelium and chronic Cor
into stratified The hypoxia may be so Pulmonale.
squamous epithelim. pronounced during
coughing that it causes
Squamous Metaplasia of
cyanosis
Bronchial Epithelium
-blue-bloaters

Emphysema—due to
smoking.
Enlargement of the
airspaces distal to the
terminal bronchioles with
destruction of the
alveolar walls
Emphysema due
toAlpha-1-Antitrypsin
Deficiency
It is a genetic deficiency,
an autosomal recessive
disorder, results in 1% of
cases of Emphysema
-Alpha-1-antrypsin: It is
essential in protection
against naturally
occurring proteases.
COPD
Most affected Pathogenesis
-It affects smokers: Proteolytic enzymes Elastases in the lungs
released from the probably account for
It is hypothesized that
leukocytes destroy the the loss of elastin fibers
the irritants in smoke
alveolar walls, causing in the alveolar walls.
provoke an influx of
abnormal enlargement of
inflammatory cells into
the alveolar spaces,
the alveoli.
characteristic of
Emphysema
The proteases Bullae
The proteases are The deterioration of 1.Centriacinar
produced by bacteria, the elastic and (centrilobular) emphysema
PMN’s, monocytes, and reticular→“Bullae”
-widening of the airspaces
macrophages during the formation.
in the center of the lobule
phagocytic process, and
and
are capable of destroying
elastin and reticular
-involves predominantly
fibers in the lung.
the respiratory
bronchioles, with sparing
of the alveoli, and
primarily seen in the
upper lobes
-Bullae are parenchymal -Most common form of
air-filled spaces greater Emphysema and is
than 1 cm in diameter. typically found in cigarette
smokers
2.Panacinar emphysema -Blebs, are subpleural air- Clinical Features
filled spaces formed by
-Involves all the -The chest is over-
rupture alveoli which can
airspaces distal to the expanded and “Barrel-
rupture into the pleural
terminal bronchioles. Shaped
cavity, causing a
- involves the alveoli.
pneumothorax. -Tachypnea

-The Chest X-Rays show

clear lung fields with over
inflation

Cystic Fibrosis
The defect in the obstruction of the fetal
transport of chloride intestines and
across the cell pancreatic ducts
membrane results in a cause:
lack of NaCl in the
→meconium ileus with
glandular secretions
peritonitis
of all the exocrine
glands, most importantly -dehydrated muconium
the pancreas, intestines (fetal intestinal contents)
and the bronchi. may cause intestinal
rupture and dissipation
of intestinal contents.

-Bronchial mucous
transforms into viscous
plugs that prevents
normal respiration

-Predisposing the
Hard, Chronic Cystic Fibrosis
individual to recurrent
Pancreatitis Involvement of Pancreas -incurable disease, and
 bacterial infections most affected
individuals die in their
twenties or thirties as a
-These individuals often result of pulmonary
have chronic bronchitis infections.
and bouts of recurrent
pneumonia, often
leading to bronchiectasis Cystic Fibrosis Lung with
Bronchiectasis

Bronchiectasis
. The abnormally dilated
bronchi and bronchioles
are filled with
mucopurulentmaterial
which stagnates and
therefore cannot be
cleared by coughing. Bronchiectasis with Dilated
Bronchus, Necrotizing
A permanent dilatation
-Infection results and Inflammation and Mucosal
of the bronchi which is
spreads into adjacent Destruction
the most common
complication of alveoli and recurrent
chronic bronchitis pneumonias are common
with hematogenic spread
of infection to other
organs