8. Nguyeân nhaân
Daøy vaùch lieân tieåu thuøy(Baïch huyeát ,TM,teá
baøo),vaùch PN, moâ keõ do:
+Dòch:NöôùcPhuø phoåi; Chaát protein Daõn
baïch huyeát
+Vieâm nhieãm:
Nhieãm truøng:Vi ruùt, u haït(lao,naám),PCP(carini)
Töï phaùt:
Beänh maïch maùu colagen:RA,xô cöùng bì,AS.
Taùc nhaân ngoaïi lai:Buïi phoåi,thuoác.
U: lan theo baïch huyeát, moâ keõ (u haït ö axít), taïo
xô tö phaûn öùng cuûa u.
May 30, 2012 8
9. Caùc bieåu hieän beänh moâ
keõ i :
1. M ô ø ñ ö ô ø n g - l ö ô ù
D aøy thaønh lieân tieåu thuøy vaø xô.
2 . M ô ø n o á t lö ô ù i:
V ieâm moâ keû quanh maïch maùu-pheá quaûn.
3 .N o á t.
4 . M ô ø k ín h ñ u ïc :
Giai ñoaïn caáp, daøy moâ keû quanh pheá nang.
M aïch maùu thaáy trong ñaùm nhu moâ phoåi “lôø môø”
5 . T o å o n g : Giai ñoaïn cuoái beänh lyù ,daïng voøng
2-10mm.
May 30, 2012 9
10. Vuøng chi phoái
+Thuyø treân:
AS,buïi phoåi,sarcoid,u haït öa axit, lao,
nang xô (khoâng phaûi beänh moâ
keõ)..
+Thuøy döôùi:
Hít,thuoác,DIP,asbestosis,xô bì,beânh
mm collagen.daûnPQ(Khoâng phoåi
moâ keõ)
May 30, 2012 10
11. Sö phaùt trieãn
C aáp:
Vieâm PN dò öùng (taêng maãn
caûm),phuø ,taêng saûn baïch huyeát,
viruùt..
M a ïn :
Lan traøn u trong baïch huyeát,vieâm
nhieãm ,xô phuø.
May 30, 2012 11
12. Theå tích phoåi
T a ê n g t h e å t íc h :
U haït öu axit(traøn khí maøng phoåi 20%)
Lymphagioleiomyomatosis (traøn khí maøng
phoåi)
Nang xô(keát hôïp nhöng khoâng phaûi
beânh moâ keõ).
G ia û m t h e å t íc h :
IFF,xô cöùng bì
May 30, 2012 12
13. B e ä n h m a ø n g p h o å i:
Maûng maøng phoåi:Abestosis
Dòch maøng phoåi:CHF,di caên baïch
huyeát,RA
N o á t ly m p h o :
Lôùn:Haïch aùc tính,lao,naám,sarcoid
Voâi hoaù;Nhieãm buïi
May 30, 2012 13
14. Moâ keõ
-Moâ keõ bình thöôøng treân HRCT khoâng
thaáy ñöôïc, nhöng khi beänh lyù thì bieåu
hieän roõ treân HRCT
-Nhöõng ngaên moâ keõ cuûa phoåi.
+Q uanh boù P Q -maïch maùu.
+T rung taâm tieåu thuyø(Ñ oaïn xa cuûa boù P Q -
mmaùu).
+M oâ keõ vaùch lieân tieåu thuøy(T höôøng thaáy
ñöôøng vuoâng goùc maøng phoåi).
+M oâ keõ döôùi maøng phoåi.
+M oâ keõ vaùch P N
May 30, 2012 14
15. Daøy vaùch lieân tieåu thuøy.
-Do phuø, u, xô.
-Thöôøng ôû ngoaïi bieân ñöôøng vuoâng
goùc maøng phoåi.Trung taâm hình ña giaùc.
-Phuø phoåi hoaëc di caên theo baïch huyeát
Daøy saéc neùt .Xô thì söï daøy khoâng
ñoàng nhaát vaø caáu truùc cuûa phaân
thuøy bò roái loaïn.
-Daøy saéc neùt trong di caên u baïch huyeát
coù xu theá goø geà hoaëc daïng noát.
May 30, 2012 15
102. P u lm o n a r y
L y m p h a n g io le io m y o
m a t o s is L A M
May 30, 2012 102
103. P u lm o n a r y
H is t io c y t o s is X
( E o s in o p h ilic
G r a n u lo m a )
H ig h r e s o lu t io n
C T u s u a lly
d e mo ns tra te s a
c o m b in a t io n o f
c ys ts a n d
n o d u le s e v e n
w he n the
r a d io g r a p h
s h o w s a r e t ic u lo -
n o d u la r p a t t e r n .
T h e c o m b in a t io n
o f n o d u le s a n d
t h i n -w a l l e d c y s t s
is h ig h ly
s u g g e s t iv e o f H X
in t h e p r o p e r
c lin ic a l s e t t in g .
May 30, 2012 103
109. • S e p t a l L in e s :
• Lymphatic spread of tumor
• Pulmonary edema
• Ir r e g u la r L in e a r P a t t e r n :
• Idiopathic pulmonary fibrosis
• Asbestosis
• Sarcoidosis
May 30, 2012 109
110. • C y s t ic P a t t e r n :
• Idiopathic pulmonary fibrosis
• Lymphangioleiomyomatosis
• Pulmonary histiocytosis X
• N o d u la r P a t t e r n :
• Sarcoidosis
• Silicosis
• Coalworker's pneumoconiosis
• Extrinsic allergic alveolitis
• Pulmonary histiocytosis X
May 30, 2012 110
111. N o á t lô ù n v a ø n h o û t r o n g n u m o â
v a ø k e á t h ô ïp t h a ø n h ñ a ù m q u a n h
b o ù P Q -M M .
K e á h ô ïp n o á t n h o û v a ø d a ïn g
ñöôøng .
• M i d d l e : Combination of small nodules and linear
opacities.
• R i g h t : Large indistinct opacities of "alveolar
sarcoidosis" (A).
May 30, 2012 111
• L e f t L o w e r : Honeycombing in the periphery in a
126. Noát trung taâm tieåu thuøy
-ÔÛ trung taâm tieåu thuøy.
-Kích thöôùc gioáng nhau.
-Khoaûng caùch caùc noát khoaûng 1-2.5cm.
-Caùch maøng phoåi khoaûng 5-10mm.
-Thöôøng keát quaû caáp hoaëc maïn do vieân
tieåu PQ.
-HRCT trong vieâm tieåu PQ vaø PQ:Noát
trung taâm giôùi haïn roõ hoaëc môø, daïng
“Tree-in-bud”, daøy thaønh PQ
May 30, 2012 126
127. Noát töï do
-Moâ taû noát phaân boá lung tung trong phoåi doïc
theo maøng phoåi, raõnh lieân thuøy vaø coù
trong trung taâm tieåu thuyø (nhöng noù ñôn
ñoäc).
-Trong boù PQ-mm thì ôû ñoaïn cuoái ÑM nhoû coøn
noát trong di caên baïch huyeát vaø sarcoid thì ôû
trung taâm boù PQ-mm
-Noát naøy phaân boá raõi raùc hai beân vaø khoâng
coù vò trí öu theá
(Noát töï do Raõi raùc coøn noát trung taâm thì
May 30, 2012 127
ñoàng ñeàu)
128. D ia g n o s is : M ilia r y m e t a s t a s is f r o m
T h y r o id c a n c e r
C T of c as e 3 0
Papillary Carcinoma of thyroid is occured in 60% (20%
follicular, 15% anaplastic, 1-5% medullary carcinoma) of
all thyroid carcinomas, metastasize to regional lymph
nodes in 40%, hematogenous to lung in 4%(early spread
to lung and bone in follicular carcinoma). In papillary
carcinoma, tumor usually concentrates radioiodine, but in
follicular carcinoma, tumor usually concentrates
pertechnetate.
Of 731 patients with papillary thyroid cancer, 91 had
metastases outside regional lymph nodes. The most
common site was intrathoracic, occurring in 73 of the 91
patients. Miliary, micronodular pulmonary metastases,
with iodine 131 (I-131) uptake and "curable" by I-131
treatment were encountered in 7 patients. (Hoie J, et. al.
Cancer;1988(61)1-6 )
R e tu rn to C a s e 3 0
May 30, 2012 128
129. D ia g n o s is : P u lm o n a r y L y m p h a n g it ic C a r c in o m a t o s is
HRCT findings in Pulmonary Lymphangitic Carcinomatosis
1. smooth or nodular peribronchovascular interstitial thickening ("peribronchial cuffing")
2. Smooth or nodular interlobular septal thickening
3. Smooth or nodular thickening of fissures
4. Normal lung architecture
5. Prominence of centrilobular structures
6. Diffuse, patchy, or unilateral distribution
7. Lymph node enlargement
8. Pleural effusion
Although, peribronchovascular interstitial thickening and smooth septal thickening, as are
often seen in patients with pulmonary lymphangitic carcinomatosis (PLC), can also be
seen in association with pulmonary edema, the differentiation of these entities can usually
be made on clinical grounds. Nodular or beaded interstitial thickening is characteristic of
PLC, but not pulmonary edema. In the study by Ren et al, nodular septal thickening was
not noted in any pathologic specimens of patients with pulmonary edema, fibrosis, or in
normal lungs. However, it is clear that the presence of nodular septal thickening is a
nonspecific finding that reflects a perilymphatic distribution of abnormalities, also
commonly seen in patients with sarcoidosis and coal worker's pneumoconiosis or silicosis.
In sarcoidosis and coal worker's pneumoconiosis, although nodules are commonly seen,
the septal thickening is usually less extensive than that seen in a patients with lymphatic
spread of tumor. Moreover, in sarcoidosis and coal worker's pneumoconiosis, distortion of
lung architecture and secondary pulmonary lobular anatomy is common, particularly if
septal thickening is present; this distortion is not seen in patients with PLC. On the other
hand, the presence of pleural effusion would be more in keeping with PLC than
sarcoidosis or silicosis. In pulmonary fibrosis, nodular septal thickening is uncommon and
May 30, 2012 of the thickened interlobular septa are irregular. Distortion of the lung
the margins 129
architecture and lung destruction (honeycombing) are common in patients with fibrosis.
130. Diagnosis: Primary lung cancer (adenocarcinoma) in
RLL
with miliary metastasis and pericardial seeding
Radiologic Findings
Chest PA shows innumerable multiple tiny nodules
uniformly distributed throughout both lungs.
Chest lateral shows suspicious ovoid opacity in lower
lung zone.
HRCT shows numerous miliary nodules in diffuse and
random distribution in both lungs.
Some linear densities are noted in peripheral portion
suggesting interlobular and intralobular septal thickening.
Irregular spiculated ovoid mass is noted in RLL.
Moderate amount of pericardial effusion is noted.
May 30, 2012 130
131. DMLD (diffuse micronodular lung disease), each nodule being < 3mm in diameter and
occupying more than two-thirds of lung volume on chest radiograph, can be
differentiated by its distribution.
Centrilobular distribution is seen in DPB (diffuse panbronchiolitis), infectious
bronchiolitis, H. influenza, bronchogenic disseminated tuberculosis, pneumoconiosis,
primary lymphoma, and foreign body-induced necrotizing vasculitis.
Perilymphatic distribution is noted in pneumoconiosis, sarcoidosis, amyloidosis.
Random distribution is found in miliary tuberculosis and pulmonary metastasis.
The nodules in pulmonary metastatic disease appeared to be slightly larger and are
more variable in size than those in miliary tuberculosis. They show relatively well
defined margins.
Miliary metastases are most likely to be due to thyroid, renal carcinoma, bone
sarcoma, trophoblastic disease, or melanoma.
May 30, 2012 131
132. Cystic fibrosis (CF) is a hereditary disease of autosomal recessive transmission. The
basic abnormality consists of abnormal secretions from variable exocrine glands
including the salivary, sweat glands, pancreas (90%), large bowel and tracheobronchial
tree. Infants who died of CF shows normal lung, by contrast, older patients who die of
the disease invariably shows pulmonary changes, including airway mucus plugging,
pneumonia, bronchiolitis obliterans, bronchiectasis, atelectasis and overinflation (1).
The incidence is as high as 1 per 500 in Scotland, 1 per 2000-3500 in whites, 1 per
90,000 in Asian. Asians who have CF may have a more severe clinical course than
whate controls (1). As a result of improved medical care, life expectancy has increased.
Whereas the survival rate older than 17 years used to be about 5 % by the 1970s, for
infants born today in the UK, the predicted mean life expectancy is 40 years.
Chest radiography reveals extensive obstruction of medium-sized and small airways
of the lungs, hyperinflation, cylindrical and cystic bronchiectasis, nodular and fingerlike
shadows of mucoid impaction. CT can reveal pathologic changes not visible on
conventional chest radiograms, particularly mucoid impaction, detailed scoring of
bronchiectasis, peribronchial thickening, mucous plugging, atelectasis, consolidation,
cysts, bullae and emphysematous change. Paranasal sinus opacification due to chronic
sinusitis and polyposis is almost universal in patients with CF (1).
The most common organisms of combined lung infection are P. aeruginosa, S
aureus, H. influenza, B. cepacia. Allergic bronchopulmonary aspergillosis occurs in 5-10
% (serum precipitins against A. Fumigatus detected 51 % of patients) (1).
May 30, 2012 132
