PULMONARY OS 213

BLOCK B
Trans 26 |
PRECEPTORS Exam 2

OUTLINE The figure shows a marked inflammation of

the bronchi and bronchiolar walls. The inflammatory
I. CASE 1: BRONCHIECTASIS cells are seen as dark blue nuclei under the mucosal
II. CASE 2: CHRONIC BRONCHITIS lining. The right portion of this bronchiole shows
III. CASE 3: DIFFUSE ALVEOLAR epithelial erosion. There is exudate in the lumen.
DAMAGE Acute inflammatory cells, especially PMNs, are also
present, although evidence of chronic inflammation is
also likely to be present.

QUESTIONS
CASE 1: BRONCHIECTASIS
1. What are the underlying conditions associated with
A case of a 20 year old patient who bronchiectasis?
presented with recurrent fever and productive cough.
Sputum gradually became copious, foul and purulent. Bronchiectasis is caused by conditions that
Initial PE includes bronchial breath sounds on the predispose to chronic necrotizing infections and
peripheral lung fields; and bibasal crackles. consequent destruction of muscle and elastic support
tissue of bronchi and bronchioles. The most common
conditions are:
a. Bronchial obstruction (tumors; foreign
bodies), diffuse obstructive airway
diseases (atopic asthma; chronic
bronchitis)
b. Congenital or hereditary conditions
(congenital bronchiectasis; cystic
fibrosis)
c. Necrotizing or suppurative pneumonias.

2. What processes are necessary for the

development of bronchiectasis?

a. Persistent obstruction
b. Superimposed infection
Figure 1. Cut section of the left lung 3. What type of inflammatory cells are present?
Compare with asthma.
Bronchiectasis is the permanent dilation of
bronchi and bronchioles and is secondary to cycles of • Acute inflammatory cells, especially
obstruction and infection. Note the inflamed left main PMNs, are present, although evidence of
stem bronchus in figure 1. It gives rise to branches in chronic inflammation is also likely to be
the left lower lobe that has been opened to present.
demonstrate that they extend nearly to the pleural • By comparison, in asthma, the
surface in this specimen. The diameters of the two inflammatory cells are composed of
opened bronchial branches in the lower lobe are CD4+ lymphocytes, eosinophils, mast
each greater than the diameter of the bronchus from cells, and a few neutrophils.
which they originate, indicating the severity of
bronchial dilation.

CASE 2: CHRONIC BRONCHITIS

A case of a 62 year old chain-smoker who
presented with persistent cough with daily sputum
production for almost 10 months each year since
1999. Occasionally, patient spat blood-tinged sputum,
but no consult was done until patient had dyspnea,
fever, and palpitations. Initial PE revealed cyanosis,
dynamic precordium and diffuse crackles on both
lungs.

Figure 2. Section from a bronchiole.

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 PULMONARY
PRECEPTORS
Figure 3. Trachea and the main bronchi
The figure shows that the trachea in the mid-
upper field is hyperemic, and the bifurcation and main
stem bronchi contain mucopurulent exudate. The
underlying epithelium is also inflamed. This picture
may occur in chronic bronchitis and a superimposed
infection. However, one may also see this picture as
part of an acute inflammatory process in a patient
dying of acute pneumonia. Remember that chronic
bronchitis is a clinical term.
Figure 4. Section of the bronchial wall.
The histological section reveals that there are
changes typical of chronic bronchitis. The bronchial
epithelium is partially denuded in some regions but
squamous metaplasia is present in others. The
basement membrane is thickened and the mucosal
vessels are engorged and dilated. A moderate
number of plasmacytes and lymphocytes are present
in the submucosa and the gland layer which is
markedly enlarged and composes almost half of the
wall thickness of the bronchus. Majority of the galnds
are mucous in character. The glands and ducts are
dilated and filled with mucinous secretion containing
desquamated cells and inflammatory cells.
QUESTIONS
1. What is your diagnosis? Bases?
The diagnosis is chronic bronchitis. It is a
clinical term referring to a persistent cough with
sputum production for at least three months in two
consecutive years.
Characteristic features supporting this
diagnosis are hypersecretion of mucous in the large
August 3, 2006 Rrrr…
OS 213
BLOCK B
Trans 26 |
Exam 2
airways, chronic inflammation of the airways
(predominantly lymphocytes) and hypertrophy of the
submucosal glands in the trachea and bronchi.
2. How does the mucous gland hyperplasia in
chronic bronchitis differ from that in a typical case of
asthma?
In typical allergic asthma, which also has
mucous gland hyperplasia, the bronchial wall has an
inflammatory infiltrate in which eosinophils are
prominent. There is also hypertrophy and hyperplasia
of smooth muscle cells in asthma.
3. What is the Reid Index?
It is the ratio of the thickness of the mucous
gland layer to the thickness of the wall between the
epithelium and the cartilage. The normal ratio is 0.4.
It is increased in chronic bronchitis.
CASE 3: DIFFUSE ALVEOLAR DAMAGE
A case of a 52 year old diabetic, with a
history of cerebral infarct and with left-sided
residuals, who was diagnosed to have community
acquired pneumonia on admission. Patient was
admitted for 6 days and was apparently improved on
discharge. At home, patient developed high grade
fever, body malaise and recurrence of productive
cough. Home medications were continued and
consult was done only 5 days later. Patient already
presented with difficulty of breathing and was
subsequently re-admitted. At the wards, patient was
hypotensive, tachypneic and febrile. Intubation was
done due to sudden respiratory distress and
cyanosis. Chest x-ray showed diffuse bilateral
alveolar infiltration. Despite resuscitative efforts,
patient demised on the 2nd hospital day.
Figure 5. Lung section, scanning view.
The figure shows diffused infiltration by
inflammatory cells with loss of alveolar architecture.
There are areas revealing collection of pink
amorphous material and hyalinized deposits. Most
areas have necrotic debris with admixed neutrophils.
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 PULMONARY
PRECEPTORS
Figure 6. Lung section, HPO.
The figure show damaged alveolar wall with
fibrin rich hyaline material lining it.
QUESTIONS
1. What is your histologic diagnosis?
Diffuse alveolar damage, representing the
usual underlying pathologic change of the clinically
defined Adult Respiratory Distress Syndrome.
2. Can the exact etiology be determined by the
microscopic findings alone?
No. The morphologic changes are non-
specific. DAD is best viewed as the pathologic end-
result of acute alveolar injury caused by a variety of
insults and initiated by different mechanisms.
3. What is the likely cause in this case? What other
conditions can cause these findings?
Sepsis, diffuse pulmonary infections, gastric
aspiration, and mechanical trauma are responsible
for more than 50% of cases of ARDS. Other possible
causes include:
• Injuries: (pulmonary contusion;
near drowning; fat embolism; burns;
ionizing radiation)
• Inhaled irritants: (oxygen toxicity;
smoke; irritant gasses and
chemicals)
• Chemical injury: (heroin or
methadone overdose;
aspirin; barbiturate
overdose; paraquat)
• Hematologic conditions: (multiple
transfusions; DIC)
• Pancreatitis
• Uremia
• Cardiopulmonary bypass
• Hypersensitivity reactions:
organic solvents, drugs
August 3, 2006 Rrrr…
OS 213
BLOCK B
Trans 26 |
Exam 2
3. Enumerate the composition of the hyaline
membrane seen in the histologic sections.
The waxy hyaline membranes lining the
alveolar walls consist of fibrin-rich edema fluid mixed
with the cytoplasmic and lipid remnants of necrotic
epithelial cells.
4. What pathologic finding is central to the
development of ARDS?
Diffuse damage to the alveolar capillary
walls. Neutrophils are thought to play an important
role in the pathogenesis of acute lung injury and
ARDS. In contrast, the respiratory distress in
newborns is initiated by deficiency in pulmonary
surfactant.
GREETINGS
Dave: Oh my God, I have already reached the
saturation point, shet, when it comes to writing
greetings. I can’t feel any excitement anymore. This
is so weird for it’s the only thing that I look forward to
during transcribing but I think, this probable pathology
is just secondary to the toxicity inflicted by the shet
thing called “pulmo”. Shet. Shet. Shet. Nevertheless,
I have to occupy the remaining space. Sayang
naman. JOJO, we love you still. Pulmo lang ang shet,
youre still gorgeous and “the best. Thanks Joguel for
lending us your flash. Salamat talaga. Hi BioDil
people. Jorel, happy birthday uli, hope nagustuhan
mo ang mga flowers and butterflies na pinaghirapan
nmin ni JOJO. Bea, babayaran na kita, sorry, antagal
kasi ni Vince magbayad. Orm, bagay pala kayo ni
Bea, hehe. Chelle, salamat sa copy nung samplex
and SGD thingy. John, congrats! Unit 2B people,
magtipid na daw tayo sa kuryente sabi ni Rikka,
hehe. Sorry, madami ako kasalanan in connection
with the high kuryente natin. Sandee, ate mahal
talaga kita. Kathy, minsan shet ka no, hehe, pero
girl….shet ka talaga, hehe, love you Kathy. Tara,
mahirap talagang gumamit ng laptop mo, hitech shet.
Mel R, miss na kita, din a tayo nakakapagusap. Atrio,
I salute you, buti ka pa, napagod na sa CLOSET,
yung iba, kahit hypoxemic at cyanotic na, CLOSETA,
pa din…Kakapagod nun, but I respect them, echoz!
HeHe. Val, uy girl, salamat sa pagtanggap ng work,
mahal talaga kita. Dala ka ng car sa med mission ha.
Pasakay Please! Maqi, Mai, and Mia, thanks sa mga
conversations hehe, Maqi, dakila ka talagang
negastar. Iaia and Glai, sorry medyo maingay ako ha.
Binky, hay ang boobs talagang nagpupumiglas hehe.
Go lang ng Go girl. Kris, salamat sa pagpapainvade
ng unit nyo. Siena, ang sarap ng pulvoron mo. Sa
mga BOYs na nagbigay ng flower kay JOrella, thank
you. Pinasaya nyo ang bading. HehE. Geno and
Odessa, basta.Hehe.
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