Diseases of respiratory organs

Acute inflammative disease

s of the lungs
 Acute inflammative diseases of the lun
gs include:
 Acute pneumoniae (diseases with accum
ulation of exudation in the lumen of th
e alveoli)
 Acute pneumonitis (diseases with sprea
ding of inflammation onto alveolar wa
ll with secondary accumulation of exu
dation in the lumen of the alveoli)
Acute inflammative disease
s of the lungs (pneumoniae)
 Acute pneumoniae are a group of ac
ute infectious inflammative diseases
of the lungs that vary in etiology, p
athogenesis and morphologic chara
cteristics and mostly affect respira
tory areas with presence of intraal
veolar exudation
 Epidemiology

 The highest morbidity is among patient o

f the hospitals (8,5%)
 In the intensive care units - 13%
 During chemotherapy of tumors - 30%
 Etiology

 Pneumococcus (Streptococcus pneumoniae) - 90% of

all cases
 Other bacteria (clebsiella, blue pus bacillus, Pfeiffer’s b
acillum, streptococci, staphilococci, colon bacillus, pro
teus, hemophilic bacillus, iersinia, etc)
 Viruses (influenza virus, adenoviruses, respiratory-syn
citial viruses, parainfluenza virus, measles virus, etc)
 Mycoplasma
 Fungus (actinomycosis, aspergillosis)
 Rickettsies (Q-fever)
 Protozoa (pneumocysta)
 Mixed microflora
 Risk factors

 Infections of upper respiratory ways (esp

ecially viral)
 Obstruction of bronchial tree
 Immunodeficiency
 Alcohol abuse
 Smoking
 Inhalation of toxic substances and dust
 Trauma
 Injury
 Impairment of pulmonary hemodynamics
 Pathogenesis

 There are 4 known ways for the microbes

to infiltrate the lungs:
 Air-drop, with inhalated air
 Aspiration from nasopharynx and fauces
 Hematogenous way from distant foci of i
nfection
 Contagious way from adjacent infected a
rea
 Classification

 Classification of E. V. Guembitskiy (1983) is

based on seven main principles:
 etiologic
 pathogenetic
 clinicopathologic
 nosologic
 spreading of the process
 heaviness of the disease
 type of clinical course
 Classification

 Based on clinicopathologic peculiarities t

here are:
 Croupous (lobular) pneumonia
 Bronchopneumonia (focal)
 Interstitial pneumonia
 Croupous pneumonia

 There are also terms – lobular, fibrinous, pleuropneum

onia, which reflect morphologic peculiarities of affectio
n of the lungs
 Infectious-allergic disease
 Is an independent nosologic form
 Is caused by pneumococci of 1st, 2nd and 3d types, rar
ely – by clebsiella (Friedlander’s diplobacillus)
 Typical is the simultaneous affection of alveoli of the w
hole lobe, the bronchi are not affected
 Is always accompanied by fibrinous pleuritis
Stages of croupous pneumonia
 1 – stage of flood (microbe edema) ,1st d
ay: there is plethora of capillaries, in the
alveoli there is serous exudation with gre
at quantity of microbes
 2 – stage of red hepatization, 2nd day: mi
croscopically: alveoli are filled with exud
ation consisting of fibrin and erythrocyte
s; macroscopically: the affected lobe is e
nlarged, dense (hepatization) (опеченени
е), red in color, on pleura there are fibrin
ous impositions
Stages of croupous pneumonia
 3 – stage of gray hepatization, 4-6 days: micros
copically: capillaries are empty, in alveolar exu
date there are fibrin, leucocytes, macrophages,
on pleura there are fibrinous impositions; macr
oscopically: the affected lobe is enlarged, dens
e, on section it is granular, homogenous, gray i
n color
 4 – stage of resolution, 9-11 days: fusion and r
esorbtion of fibrinous exudation with the help
of neutrophils and macrophages
Croupous pneumonia w
ith consolidation of the
whole left upper lobe
There is strict differen
ce between upper lob
e and consolidated lo
wer lobe of the lung in
croupous pneumonia
Complications of croupous pne
umonia
 Pulmonary -
 Carnification (organization of exudation in lumen of alveoli)
 Abscess of the lung
 Gangrene (damp)
 Extrapulmonary -
 Appear in lymphogenous
 (purulent mediastinitis,
 pericarditis,
 peritonitis,
 purulent arthritis)
 Or hematogenous spreading of infection (acute ulcerous endocar
ditis (often of tricuspid valve),
 purulent meningitis,
 abscess of the brain)
 Causes of death

 Letality is about 3%
 Death is caused by acute cardio-pulmonary i
nsufficiency or purulent complications
 Lobar Friedlander’s pneumonia

 More often appears as intrahospital (nosoca

mial) infection
 Affects old people, newborn and alcoholics
 Typical is necrosis of alveolar walls with ofte
n formation of abscesses, foci of carnificatio
n and significant interstitial fibrosis
Bronchopneumonia (focal pneu
monia)
 Presents the most part of acute pneumonias
 Is polyetiologic, the most often pathogens are bact
eria: pneumococci, staphylococci, streptococci, bl
ue pus bacillus, etc.
 May appear as nosocamial infection in weakened p
atients, usually caused by gram-negative microorg
anisms and staphylococcus aureus
 Often appears as autoinfection. May be aspirationa
l, hypostatic, post-operational, or develop on back
ground of immunodeficiency
 Often complicates other diseases
 Morphologic manifestations

 At first the bronchi are affected. The inflammation spre

ads to the alveoli from the walls of the bronch in desce
nding way in endobronchitis or peribronchially in panb
ronchitis and destructive bronchiolitis
 Exudation may be serous, purulent, hemorrhagic, mixe
d
 By diffusion of the process there are acinar, lobular, co
nfluent, segmentary, miliar pneumonia
On section of the lung
there is typical picture
of bronchopneumonia
with areas of brown-y
ellow consolidation. O
ther parts of the lung
are dark red because
of significant pulmon
ary plethora
Bronchopneumonia. L
ighter areas, which lo
ok elevated on secion
, are areas of consolid
ation of the lung
Bronchopneumonia. Alveoli are filled with multiple neutr
ophils. Notice the dilated capillaries in the walls of alveoli
because of vasodilatation in acute inflammative process
Bronchopneumonia. In alveoli there is neuthophilic a
lveolar exudation. Clinical manifestation is productiv
e cough
Complications of bronchopneu
monia
 Carnification
 Formation of abscesses
 Pleuritis with possible development of e
mpyema of pleura
Absceding pneumonia with hemorrhages. Alveo
lar walls can’t be seen because of early formati
on of the process
Absceding pneumonia on an early stage. Alveol
ar walls are hard to discern, there are visible lay
ers of neutrophils
 Interstitial pneumonia

 Inflammation develops mostly in alveolar septa with se

condary accumulation of exudation in lumen of alveoli.
Synonyms are: alveolitis, pneumonitis
 Process can be diffuse or bordered
 Is caused by certain pathogens: viruses, fungi, mycopl
asma, chlamidiae (ornitosis), rickettsies (Q-fever-pneu
morickettsiosis), pneumocysta
 Viral pneumonia
 Most common in children
 Is often caused by viruses of influenza, parainfluenza, respiratory-
syncytial virus, adenovirus
 Typical is hyperplasia of alverolar epithelium with formation of gia
nt cells, which look differently in various diseases, possible is squ
amous metaplasia of bronchiolar epithelium
 Is often complicated by secondary bacterial infection
 The most often viral pneumoniae in immunodeficiency conditions
is cytomegalovirus pneumonia цитомегаловирусная пневмония
(opportunistic infection). For this disease typical is mostly monon
uclear infiltration of alveolar septa, hyperplasia of alveolar epitheli
um, appearance of large cells with typical intranuclear inclusions,
in lumen of alveoli there is serous liquid
Microscopic picture of viral pneumonia with int
erstitial lymphocytal infiltration. Alveolar exudat
e is absent
 Mycoplasmal pneumonia

 Also known as “atypic pneumonia”

 One of the most common forms of non-bacterial pneu
monia. Usually appears in children and teenagers
 The beginning is more unnoticeable than in bacretial p
neumonia
 Typical is inflammative lymphoplasmacytal infiltration
of alveolar septa, hyperplasia of alveolar epithelium, pr
esence of intraalveolar hyaline membranes, exudate m
ay be absent in lumen of alveoli; often it is combined w
ith changes that are typical for bronchopneumonia: ap
pearance of leucocytes in lumen of bronchiols and alv
eoli
 Pneumocystic pneumonia
 Opportunistic infection most typical for patients with HIV-infection
. Can also be found in other forms of immunodeficiency. Is cause
d by P. carinii – conditionally pathogenic microorganism
 In patients with impairments of cellular it can develop because of f
ormer presence of pneumocysts in pulmonary foci of latent infecti
on or because of fresh infection
 Typical is desquamation of cells of alveolar epithelium and filling
of the alveoli with foamy liquid, in which pneumocysts are present
, as well as plethora and lymphohistiocytal inflitration of alveolar s
epta with their possible destruction
 Typical is growing short breath on background weakly shown phy
sical and rontgenologic signs
 May proceed as a mixed-infection with joining of other flora
Lung in pneumocystal
pneumonia. Diffuse c
onsolidation of lung ti
ssue
Pneumocystal pneumonia. Microscopically each alv
eolus is filled with pink granular exudation
Chronic non-specific disease
s of lungs (CNDL)
 CNDL are a group of diseases of lungs of v
arious etiology and morphology, for whic
h typical is development of chronic cough
with excrection of phlegm and paroxysma
l or constant short breath, not connecte
d to specific diseases of lungs, especially
tuberculosis
 CNDL group includes

 Chronic bronchitis
 Bronchial asthma
 Multiple bronchiectasis
 Chronic obstructive emphysema of lungs
 Chronic abscess
 Chronic pneumonia
 In all CNDL develop hypertension of pulmo
nary circulation and cor pulmonale
 Depending on morphofunctional peculiarit
ies of impairment of air-bearing and respi
ratory areas of the lungs there are obst
ructive and restrictive CNDL
 On later stages of diseases there can be
combination of obstructive and restrictiv
e components
Obstructive diseases of the
lungs
 In the base of obstructive diseases of the
lungs lies impairment of drainage functio
n of bronchi with partial or complete obs
truction, which increases resistance of p
assing air воздуха:
 Chronic obstructive emphysema of lungs
 Chronic obstructive bronchitis
 Multiple bronchiectasis
 Bronchial asthma
 Restrictive diseases of lun
gs
 For restrictive diseases of lungs typical is decre
ase of volume of pulmonary parenchyma with dec
rease of vital capacity of the lungs. In the base
of restrictive diseases of lungs lies development
of inflammation and fibrosis in interstitium of re
spiratory areas, which is accompanied by progre
ssive respiratory insufficiency:
 Interstitial diseases of the lungs
 Mechanisms of development
 Bronchitogenous,of CNDL
based on impairment of drainag
e function of bronchi and bronchial passability –
chronic bronchitis, multiple bronchiectasis, chro
nic obstructive emphysema of lungs, bronchial a
sthma
 Pneumoniagenous, connected to acute pneumonia
and its complications (acute abscess, carnificati
on) and leading to development of chronic absce
ss and chronic pneumonia
 Pneumonitogenous mechanism determines develop
ment of chronic interstitial diseases, represente
d by various forms of fibrosing alveolitis, or pne
umonitis
 Chronic bronchitis
 Chronic bronchitis is a disease characteri
sed by excessive production of mucus by b
ronchial glands, which leads to developm
ent of productive cough for at least 3 mo
nths yearly during at least 2 years.
 Smoking – the most important etiologic fa
ctor of chronic bronchitis
 Hyperplasia of mucous glands – one of mai
n morphologic criteria of chronic bronchi
tis
Classification of chronic br
onchitis
 By spreading:
 Local (often in II, IV, VIII, IX, X segments of lungs)
 Diffuse bronchitis
 Depending on presense of bronchial obstruction:
 Obstructive
 Non-obstructive
 By type of catarrhal inflammation:
 Simple catarrhal
 Mucous-purulent
 Pathologic anatomy
 In chronic bronchitis walls of bronchi become thi
ckened, surrounded by layers of connective tissu
e, sometimes bronchi are deformed. In long course
saccular and cylindrical bronchiectasis. Micros
copic changes are caused by development of chr
onic mucous or purulent inflammation with metap
lasia of integumentary epithelium and hyperpla
sia of mucous glands and goblet-like cells in bro
nchi, during which in the bronchial wall there is c
ellular inflammative infiltration, overgrowth o
f granulation tissue, sclerosis and atrophy of m
uscular layer
Chronic bronchitis. Bronchus with increased quantit
y of cells of chronic inflammation in submucous me
mbrane
 Multiple bronchiectasis
 Multiple bronchiectasis is characterized by com
bination of typical morphologic substrate – signi
ficant bronchoectasis and certain extrapulmon
ary symptom complex, based on respiratory hypo
xia and development of hypertension in pulmonar
y circulation. Patients’ fingers look like drumsti
ck, typical are “warm” cyanosis, hypertophy of r
ed ventricle and development of cor pulmonale
 Bronchoectasis is a stable pathologic dil
atation of one or few bronchi, containing
cartilage plates and mucous glands, with
destruction of elastic and muscular laye
rs of bronchial walls
 By origin bronchoectasis may be inborn an
d acquired. Acquired bronchoectasis deve
lop on background of chronic bronchitis a
nd might be considered morphologic subst
rate of multiple bronchiectasis
 Often development of bronchiectasis is co
nnected to complicated measles and heav
y form of influenza
Morphologic characteristi
cs
 By macroscopic picture bronchiectasis may be sa
ccular (on level of proximal bronchi, including b
ronchi of 4th order) and cylindrical (on level of b
ronchi of 6th – 10th order)
 In microscopic investigation in wall of bronchiect
asis there is chronic purulent inflammation with
destruction and atrophy of structural elements
and sclerosis. In adjacent pulmonary tissue ther
e are fields of fibrosis, foci of obstructive emphy
sema
Bronchiectasis. Bronchi i
n medium lower area of t
he lung are significantly
dilated
Bronchiectasis. Notice the dilated bronch, muc
ous membrane and bronchial wall are hard to di
scern because of necrotic inflammation with de
struction.
Complications of multiple b
ronchiectasis
 Pulmonary hemorrhage
 Abscesses of the lungs (bronchiectatic a
bscesses)
 Empyema of pleura
 Chronic cardio-pulmonary insufficiency
 Secondary amyloidosis (АА-amyloidosis)
Chronic obstructive emphys
ema of the lungs
 Emphysema of the lungs is a syndrome, cha
racterized by stable dilatation of air-ca
rrying spaces, more distally from termin
al bronchioles. There are various types o
f emphysema of lungs – perifocal, vicaria
l, senile, idiopathic, interstitial, chronic o
bstructive
 Chronic obstructive emphysema of the lun
gs is a disease caused by formation of chr
onic obstruction of air-carrying ways bec
ause of chronic bronchitis and bronchiolit
is
Pathogenesis of chronic obstructi
ve emphysema of the lungs
 The disease is connected to destruction of
elastic and collagenous frames of the lu
ng because of activity of leucocytal prot
eases (elastase, collagenase) in inflamm
ation.
 Decisive pathogenetic link is genetically
conditioned deficiency of serum inhibitor o
f proteases - α1-antitrypsin. Possible is th
e role of absolute or relative acquired d
eficiency of serum α1-antitrypsin (in hepat
ic diseases) or locally synthesized by Cla
ra’s cells of terminal bronchioles (in chr
onic bronchiolitis)
 Morphologic characteristics of c
hronic obstructive emphysema of
lungs
 In chronic obstructive emphysema of lungs lumen
s of respiratory bronchi and alveoli are widened
, alveolar walls are thinned and straightened, e
lastic fibers disappear in them; capillary net is
reduced, which leads to development of capillar
y-alveolar block and impairment of gas exchang
e (pulmonary insufficiency)
 Because of sclerotic changes in pulmonary capil
laries and increased pressue in the system of pul
monary artery – cor pulmonale develops
Centrolobular emphysema of upper lung fields.
Notice the loss of lung tissue with significant bl
ack anthracosis pigmentation
Emphysema of the lung. Morphologically can b
e seen destruction of alveolar walls, surviving a
ir spaces are dilated
 Chronic abscess

 Develops from acute abscess, often is localized i

n II, VI, IX, X segments of the right lung
 Is the source of bronchogenous spreading of puru
lent inflammation in the lung
 Macroscopic picture: abscess represents a cavit
y, full of pus, surrounded by dense capsule
 Microscopic picture: outer layers of capsule are
represented by connective tissue, inner layers –
by granulation tissue and pus (pyogenous membr
ane)
Notice the abscesses
in upper and lower lob
es of the left lung
 Chronic pneumonia
 Is characterised by combination of many patholo
gic processes in the lungs: areas of carnificatio
n and fibrosis are alternating with cavities of c
hronic abscesses; in peribronchial and perivascu
lar tissue develop chronic inflammation and fibr
osis, which leads to development of emphysema, w
hich is supported by chronic bronchitis; in the ves
sells sclerotic changes are noticed.
 Each inflammation is followed by appearance of
fresh foci of inflammation with increase of affe
cted area and sclerotic changes, which leads to
pneumofibrosis and deformation of pulmonary tis
sue
Chronic interstitial diseases of t
he lungs
 Are followed by diffuse interstitial fibrosis wit
h development of honeycomb lung in the end, for
which typical is cystous transformation of termi
nal and respiratory bronchioles
 Very quickly appear block of aerohematic barri
er, secondary pulmonary hypertension and cor p
ulmonale
 Main principles of classification of interstitial d
iseases – etiology and character of productive i
nflammation in common
 By etiology interstitial diseases are divided into
diseases with established and non-established et
iology; the latter ones being more often
Chronic interstitial diseases with
estimated etiology
 Black-lung disease caused by organic and
inorganic dust
 Exogenous allergic alveolitis
 From etiologic factors of alveolitis impor
tant are bacteria, fungi, dust containing
antigenes of animal and plant origin. It is
widely spread between people who work i
n farming (“farmer’s lung”, “miller’s lung”,
etc), as well as working in textile industr
y, pharmaceutics, etc
Chronic interstitial diseases with
non-established etiology
 Idiopathic fibrosing alveolitis (acute for
ms are named disease of Hammen - Rich)
 Secondary fibrosing alveolitis in rheumat
ic diseases and HBV-infection
 Sarcoidosis
 Fibrosing alveolitis in goodPascher’s synd
rome
 Idiopathic hemosiderosis of the lungs
 Eosinophilic pneumonia
 Alverolar proteinosis, etc
 Cancer of the lung

 Among malignant tumors takes the f

irst place in morbidity and lethality
among men in majority of countries. P
rognosis is bad
 Etiology

 Not established, but there are impressive clinica

l and experimental data which confirms connecti
on of the disease with influence of cancerogens o
f the environment. Among cancerogenous agents
should be noted:
 Components of tobacco dust (asbestos, nickel, ch
rome, beryllium, carbon dust)
 Dust particles, containing radionuclids, thrown i
nto atmosphere during damage on APP
 Significant role is played by CNDL and tuberculos
is of the lungs, which are often background dise
ases
Classification of cancer of
the lung
 1. By localization:
 Central cancer, growing from trunk, lobu
lar bronchi and from proximal part of se
gmental bronchus
 Peripheral cancer, growing from bronchi
of lesser caliber, bronchioles, possibly a
lveoles
 Mixed (massive) cancer
 2. By type of growth:
 exophytic (endobronchial)
 endophytic (exo- and peribronchial)
 Classification of cancer of
the lung
 3. By macroscopic form:
 Plaque-like
 Polypous
 Endobronchial diffuse
 Nodular
 Branchy
 Nodular-branchy
 cavernous
 Pneumonia-like
 Classification of cancer of
 4. By microscopicthe lung
picture (hystogenesis):
 Squamous cell (epidermoid), variant – spindle-cel
l
 Small-cell – lymphocytelike, intermediate-cellu
lar, combined
 adenocarcinoma: acinar, papillary, bronchiolo-a
lveolar carcinoma, solid with mucus production
 Large-cell, variants – giant-cell, light-cell
 Glandular-squamous cancer
 Carcinoid tumour
 Cancer of bronchial glands: adenoid-cystous can
cer, cystous cancer, mucoepidermal cancer, etc.
 The worst prognosis is in large- and small-cell c
ancer
 Central cancer
 Develops in large bronchi
 Precancer processes – squamous cell metaplasia and
dysplasia of bronchial epithelium on background of c
hronic inflammation
 Early appear impairments of bronchial passage, whic
h leads to atelectasis and abscesses of the lung
 Main methods of diagnostics: bronchoscopy with biops
y, cytologic investigation of phlegm, x-ray investigat
ion
 Main macroscopic forms: polypous, nodular, branchy,
nodular-branchy
 Most often microscopic types: squamous and small-cel
l
Squamous cell cancer
of the lung. In central
area of the tumor ther
e is a cavity because
of insufficient blood s
upply for an overgrow
n tumor
Microscopic picture of squamous cell cancer with ne
sts of polygonal cells with pink cytoplasm and strict
cellular borders. Nuclei are hyperchromatic and ang
ular
 Peripheral cancer
 Often develops in a scar
 Main method of diagnostic – x-ray
 Main macroscopic forms – nodular, nodular-bran
chy, cavernous and pneumonia-like
 Microscopic forms are various, glandular carnin
omas prevail, often bronchiolo-alveolar cancer
is encountered
Peripheral adenocarci
noma of the lung
Glandular structures, formed in this tumor, are typic
al for medium-differentiated adenocarcinoma of the l
ung
 Metastasis of cancer of the lun
g
 First metastasis found in regionar (peribronchia
l) lymphatic nodes
 Then bifurcational, paratracheal, mediastinal
and cervical lymphatic nodes are involved, carci
nomatosis of pleura and peritoneum may develop
 Hematogenous metastasis mostly to liver, bones,
adrenal glands and the brain