Upper Airways
Nose
INFLAMMATIONS
Inflammatory diseases, mostly in the form of the common cold. Most of these
inflammatory conditions are viral in origin, but they are often complicated by
superimposed bacterial infections .
Infectious Rhinitis.
Infectious rhinitis is in most instances caused by one or more viruses.
(adenoviruses, echoviruses, and rhinoviruses). They cause a profuse
catarrhal discharge During the initial acute stages, the nasal mucosa is
thickened, edematous, and red; the nasal cavities are narrowed; These
changes may extend producing a pharyngotonsillitis.
Allergic Rhinitis.
Allergic rhinitis (hay fever) is initiated by sensitivity reactions to
allergens. The allergic reaction is characterized by marked mucosal
edema, redness, and mucus secretion, accompanied by a inflammatory
infiltration rich in eosinophils.
Nasal Polyps.
Recurrent attacks of rhinitis eventually lead to focal protrusions of the
mucosa, producing so-called nasal polyps, which may reach 3 to 4 cm in
length. On histologic examination, these polyps consist of edematous
loose stroma, with contain cystic mucous glands and infiltrated with a
variety of inflammatory cells.
Chronic Rhinitis.
Chronic rhinitis caused by repeated attacks of acute rhinitis, whether microbial or
allergic in origin, with the eventual development of superimposed bacterial infection.
Sinusitis
Acute sinusitis is most commonly preceded by acute or chronic rhinitis,
Impairment of drainage of the sinus by inflammatory edema of the
mucosa is an important contributor to the process . Acute sinusitis may, in
time, give rise to chronic sinusitis, particularly when there is interference
with drainage.
Nasopharynx
INFLAMMATION
Pharyngitis and tonsillitis are frequent concomitants of the usual viral
upper respiratory infections. Bacterial infections may be superimposed on
these viral involvements, or the bacteria may be primary invaders. The
most common
are the β-hemolytic streptococci, but sometimes
Staphylococcus aureus A typical appearance is of enlarged, reddened
tonsils (due to reactive lymphoid hyperplasia) with presence of exudate.
Tumors of the Nose, Sinuses, and Nasopharynx
Nasopharyngeal Angiofibroma
This is a highly vascular tumor that occurs almost exclusively in
adolescent males. Despite its benign nature, it may cause serious clinical
problems because of its tendency to bleed profusely during surgery.
Sinonasal Papillomas.
These are benign neoplasms arising from the sinonasal mucosa and are
composed of squamous or columnar epithelium. Although their etiology
is still unproven, HPV types 6 and 11 have been identified in the lesions.
Olfactory Neuroblastomas .
These are uncommon, highly malignant tumors They arise most often
superiorly and laterally in the nose from olfactory mucosa. . Olfactory
neuroblastomas tend to metastasize widely. Combinations of surgery,
radiation, and chemotherapy yield a 5-year survival rate of 50% to 70%.
Nasopharyngeal Carcinomas.
Three sets of influences apparently affect the origins of these neoplasms:
(1) heredity, (2) age, and (3) infection with EBV.
It takes one of three patterns: (1) keratinizing squamous cell carcinomas,
(2) nonkeratinizing squamous cell carcinomas, and (3) undifferentiated
carcinomas .with abundant lymphocyte infiltration
Nasopharyngeal carcinomas tend to grow silently until they have become
unresectable and have often spread to cervical nodes or distant sites.
Radiotherapy is the standard modality of treatment, yielding in most
studies about a 50% to 70% 3-year survival rate.
Larynx
INFLAMMATIONS
Laryngitis may occur as the manifestation of allergic, viral, bacterial, or
chemical insult, or the result of heavy exposure to tobacco smoke.
Although most infections are self-limited, they may at times be serious,
especially in infancy or childhood, when mucosal congestion, exudation,
or edema may cause laryngeal obstruction. The most common form of
laryngitis, encountered in heavy smokers, constitutes an important
predisposition to the development of squamous epithelial changes in the
larynx and sometimes overt carcinoma.
REACTIVE NODULES (VOCAL CORD NODULES AND POLYPS)
Reactive nodules, also called polyps, sometimes develop on the true vocal
cords, most often in heavy smokers or in individuals who impose great
strain on their vocal cords (singers' nodules). They are typically covered
by squamous epithelium . The core of the nodule is a loose vascular
connective tissue.
CARCINOMA OF THE LARYNX
Sequence of Hyperplasia-Dysplasia-Carcinoma.
]
Macroscopically, the epithelial changes range from smooth, white or
reddened focal thickenings, to irregular verrucous or ulcerated, whitepink lesions.The various changes described are most often related to
tobacco smoke, the risk being proportional to the level of exposure.
Microscopically---About 95% of laryngeal carcinomas are typical
squamous cell tumors.
Carcinoma of the larynx manifests itself clinically by persistent
hoarseness. Later, laryngeal tumors may produce pain, dysphagia, and
hemoptysis
With surgery, radiation, or combination therapy, many patients can be
cured.
SQUAMOUS PAPILLOMA
Laryngeal squamous papillomas are benign neoplasms, usually on the
true vocal cords, Papillomas are usually single in adults but are often
multiple in children . The lesions are caused by HPV types 6 and 11. do
not become malignant, but they frequently recur.
Histologically--- papillomas are made up of multiple finger-like
projections supported by central fibrovascular cores and covered by
stratified squamous epithelium.
Respiratory system
Lecture -1
Dr.Rehab Almudhafar
Introduction
function: exchange of gases between inspired air and blood. The right lung bud eventually divides
into three branches—the main bronchi—and the left into two main bronchi, thus giving rise to three
lobes on the right and two on the left. The right main stem bronchus is more vertical and more directly
in line with the trachea than is the left. Consequently, aspirated foreign material, such as vomitus,
blood, and foreign bodies, tends to enter the right lung rather than the left. The main right and left
bronchi branch giving rise to progressively smaller airways.
Progressive branching of the bronchi forms bronchioles. Further branching of bronchioles leads to the
terminal bronchioles, which are less than 2 mm in diameter. The part of the lung distal to the terminal
bronchiole is called the acinus; which composed of respiratory bronchiols, alveolar duct & alveolar
sac.
The microscopic structure of the alveolar wall composed of capillaries, interstitium of elastic &
collagen fibers & lining of flat cells (pneumocytes type I) & rounded cells (pneumocytes type II)
source of surfactant, alveolar macrophages usually lie free within the alveolar space.
From the microscopic standpoint, except for the vocal cords, which are covered by stratified squamous
epithelium, the entire respiratory tree, including the larynx, trachea, and bronchioles, is lined by
pseudostratified, tall, columnar, ciliated epithelial cells.
Atelectasis (Collapse)
Atelectasis refers either to incomplete expansion of the lungs (neonatal atelectasis) or
to the collapse of previously inflated lung, producing areas of relatively airless
pulmonary parenchyma, leading to ventilation perfusion imbalance & hypoxia.
Acquired atelectasis, encountered principally in adults, may be divided into:1. resorption (or obstruction), is the consequence of complete obstruction of an
airway which prevent air from reaching distal airways, obstruction by mucus
plug, foreign body or tumor.
2. compression, whenever the pleural cavity is partially or completely filled by
fluid , tumor, blood, or air.
3. Contraction atelectasis occurs when local or generalized fibrotic changes in
the lung or pleura prevent full expansion.
Atlectasis except for contraction type are potentially reversible.
PULMONARY EDEMA
Hemodynamic Pulmonary Edema
The most common hemodynamic mechanism of pulmonary edema is that attributable
to increased hydrostatic pressure, as occurs in left-sided congestive heart failure. the
clinical setting, pulmonary congestion and edema are characterized by heavy, wet
lungs. Fluid accumulates initially in the basal regions of the lower lobes because
hydrostatic pressure is greater in these sites (dependent edema). Histologically, the
alveolar capillaries are engorged, and an intra-alveolar granular pink precipitate is
seen. Alveolar microhemorrhages and hemosiderin-laden macrophages ("heart
failure" cells) may be present.
Edema Caused by Microvascular Injury
The second mechanism leading to pulmonary edema is injury to the capillaries of the
alveolar septa. Here the pulmonary capillary hydrostatic pressure is usually not
elevated, and hemodynamic factors play a secondary role.
ACUTE RESPIRATORY DISTRESS SYNDROME (DIFFUSE ALVEOLAR
DAMAGE)
it is a clinical syndrome caused by diffuse alveolar capillary damage. It is
characterized clinically by the rapid onset of severe life-threatening respiratory
insufficiency & may progress to extra-pulmonary multisystem organ failure.
ARDS is a well-recognized complication of numerous and diverse conditions,
including both direct injuries to the lungs and systemic disorders .
Pathogenesis.
The alveolar capillary membrane is formed by two separate barriers. In ARDS the
integrity of this barrier is compromised by either endothelial or epithelial damage
leading to increase vascular permeability & wide spread surfactant abnormality.
Recent studies suggest that in ARDS lung injury is caused by an imbalance between
pro-inflammatory & anti-inflammatory mediators shifting the balance to proinflammatory state leading to neutrophils activation.
Neutrophils are thought to have an important role in the pathogenesis of ARDS by
secreting a variety of products like oxidents & proteases that damaging the alveolar
epithelium.
Finally the balance between destructive & protective factors (endogenous
antiproteases & antioxidants) determines the severity of ARDS.
Morphology.
In the acute stage, the lungs are heavy, firm, red, and boggy. They exhibit congestion,
interstitial and intra-alveolar edema, inflammation, and fibrin deposition
Resolution is unusual; more commonly, there is organization of the fibrin exudate,
with resultant intra-alveolar fibrosis.
Obstructive Versus Restrictive Pulmonary Diseases
(1) obstructive disease (or airway disease), characterized by an increase in resistance
to airflow owing to partial or complete obstruction at any level, from the trachea and
larger bronchi to the terminal and respiratory bronchioles.
(2) restrictive disease, characterized by reduced expansion of lung parenchyma, with
decreased total lung capacity.
Obstructive Pulmonary Disease
emphysema, chronic bronchitis, asthma, and bronchiectasis . Emphysema and
chronic bronchitis are often clinically grouped together and referred to as chronic
obstructive pulmonary disease (COPD almost certainly because one extrinsic
trigger—cigarette smoking—is common to both.
TABLE 1-- Disorders Associated with Airflow Obstruction: The Spectrum of
Chronic Obstructive Pulmonary Disease
Clinical Anatomic Major Pathologic
Term
Site
Changes
Chronic
bronchitis
Bronchiectasis
Bronchus
Etiology
Signs/Symptoms
Mucous gland Tobacco smoke,
hyperplasia,
air pollutants
hypersecretion
Cough, sputum
production
Bronchus Airway dilation and
Persistent or
scarring severe infections
Cough, purulent
sputum, fever
Asthma
Bronchus
Smooth muscle
hyperplasia, excess
mucus,
inflammation
Emphysema
Acinus
Airspace
enlargement; wall
destruction
Immunologic –
Episodic
type 1 wheezing, cough,
hypersensitivity
dyspnea
reaction or
undefined causes
Tobacco smoke
Dyspnea
Small airway Bronchiole
Inflammatory Tobacco smoke,
*
disease,
scarring/obliteration
air pollutants,
bronchiolitis
miscellaneous
Cough, dyspnea
EMPHYSEMA
abnormal permanent enlargement of the airspaces distal to the terminal bronchiole,
accompanied by destruction of their walls and without obvious fibrosis.[10] In contrast,
the enlargement of airspaces unaccompanied by destruction is termed "overinflation,"
Types of Emphysema.
there are four major types: (1) centriacinar, (2) panacinar, (3) paraseptal, and (4)
irregular. (figure 2)
Figure (2)
upper lobes, particularly in the apical segments. The walls of the emphysematous
Pathogenesis
emphysema is seen to result from the destructive effect of high protease activity in
subjects with low antiprotease activity.
Figure 3
CHRONIC BRONCHITIS
persistent cough with sputum production for at least 3 months in at least 2 consecutive
years, in the absence of any other identifiable cause.
Morphology.
Grossly, there may be hyperemia, swelling, and edema of the mucous membranes, frequently
accompanied by excessive mucinous to mucopurulent . The characteristic histologic features
of chronic bronchitis are chronic inflammation of the airways (predominantly lymphocytes)
and enlargement of the mucus-secreting glands of the trachea and bronchi.
ASTHMA
Asthma is a chronic inflammatory disorder of the airways that causes recurrent
episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night
and/or in the early morning. These symptoms are usually associated with widespread
but variable bronchoconstriction and airflow limitation that is at least partly
reversible, either spontaneously or with treatment. It is thought that inflammation
causes an increase in airway responsiveness (bronchospasm) to a variety of stimuli. .
Morphology.
Grossly, the lungs are overdistended because of overinflation . The most striking
macroscopic finding is occlusion of bronchi and bronchioles by thick, tenacious
mucous plugs. Histologically
• Thickening of the basement membrane of the bronchial epithelium
• Edema and an inflammatory infiltrate in the bronchial walls, with a
prominence of eosinophils and mast cells
• An increase in size of the submucosal glands
• Hypertrophy of the bronchial wall muscle
BRONCHIECTASIS
Bronchiectasis is a disease characterized by permanent dilation of bronchi and
bronchioles caused by destruction of the muscle and elastic tissue, resulting from or
associated with chronic necrotizing infections.
Morphology.
The airways are dilated, sometimes up to four times normal size.
Characteristically, the bronchi and bronchioles are sufficiently dilated that they can be
followed, on gross examination, directly out to the pleural surfaces
The histologic findings acute and chronic inflammatory exudation within the walls
of the bronchi and bronchioles, associated with desquamation of the lining epithelium
and extensive areas of necrotizing ulceration.
Lec—3---
Diffuse Interstitial (Infiltrative, Restrictive) Diseases
Diffuse interstitial diseases are a heterogeneous group of disorders characterized
predominantly by diffuse and usually chronic involvement of the pulmonary
interstitium in the alveolar walls. These disorders account for about 15% of
noninfectious diseases seen by pulmonary physicians.
Examples---pneumoconiosis, sarcoidosis, idiopathic pulmonary fibrosis & collagen
vascular diseases.
Pathogenesis.----- the earliest common manifestation of most of the interstitial diseases
is alveolitis,[43] [44] that is, an accumulation of inflammatory cells within the alveolar
walls and spaces which results in the release of mediators that can injure parenchymal
cells and stimulate fibrosis.
Pneumoconiosis
non-neoplastic lung reaction to inhalation of mineral dusts encountered in the
workplace. Now it also includes diseases induced by organic as well as inorganic
particulates and chemical fumes and vapors.
Examples---anthracosis, silicosis & asbestosis.
GRANULOMATOUS DISEASES
Sarcoidosis
Sarcoidosis is a systemic disease of unknown cause characterized by noncaseating
granulomas involving many organs, but bilateral hilar lymphadenopathy or lung
involvement is visible on chest radiographs in 90% of cases.
Etiology and Pathogenesis.
Although the etiology of sarcoidosis remains unknown, several lines of evidence
suggest that it is a disease of disordered immune regulation in genetically predisposed
individuals exposed to certain environmental agents.
Morphology---Histologically, all involved tissues show the classic noncaseating granulomas , each
composed of an aggregate of tightly clustered epithelioid cells, often with
multinucleated giant cells. Central necrosis is unusual. With chronicity, the
granulomas surrounded by fibrous rims.
Two other microscopic features are often present in the granulomas:
(1) laminated concretions composed of calcium and proteins - Schaumann bodies
(2) stellate inclusions - asteroid bodies .
Figure 4
65% to 70% of affected patients recover with minimal or no residual manifestations.
20% have permanent loss of some lung function or some permanent visual
impairment. Of the remaining 10% to 15%, some die of cardiac or central nervous
system damage.
Diseases of Vascular Origin
PULMONARY EMBOLISM
Blood clots that occlude the large pulmonary arteries are almost always embolic in
origin. The usual source of pulmonary emboli—thrombi in the deep veins of the leg
in more than 95% of cases— . It is the major cause of death in about 10% of adults
who die acutely in hospitals.
Pulmonary embolism is a complication principally in patients who are already
suffering from some underlying disorder, such as cardiac disease or cancer, or who
are immobilized for several days or weeks, those with hip fracture being at high risk.
Hypercoagulable states, either primary or secondary (e.g., obesity, recent surgery,
cancer, oral contraceptive use, pregnancy).
PULMONARY HYPERTENSION
The pulmonary circulation is normally one of low resistance, and pulmonary blood
pressure is only about one eighth of systemic blood pressure. Pulmonary hypertension
(when mean pulmonary pressure reaches one fourth of systemic levels) is most
frequently secondary to structural cardiopulmonary conditions that increase
pulmonary blood flow or pressure (or both), pulmonary vascular resistance, or left
heart resistance to blood flow.
Pulmonary Infections
Respiratory tract infections are more frequent than infections of any other The vast
majority are upper respiratory tract infections caused by viruses (common cold,
pharyngitis) but bacterial, viral, mycoplasmal, and fungal infections of the lung
(pneumonia)
Predisposing factors---• Loss or suppression of the cough reflex, as a result of coma, anesthesia,
(This may lead to aspiration of gastric contents.)
• Injury to the mucociliary apparatusin cigarette smoke, inhalation of hot or
corrosive gases.
• Interference with the phagocytic or bactericidal action of alveolar
macrophages by alcohol, tobacco smoke.
• Pulmonary congestion and edema
• Accumulation of secretions in conditions such as bronchial obstruction
Streptococcus Pneumoniae
Streptococcus pneumoniae, or pneumococcus, is the most common cause of
community-acquired acute pneumonia. Examination of Gram-stained sputum is an
important step in the diagnosis of acute pneumonia-presence of numerous neutrophils
containing the typical Gram-positive, lancet-shaped diplococci
Pneumococcal
pneumonias respond readily to penicillin treatmen
Morphology.
Bacterial pneumonia has two gross patterns of anatomic distribution: lobular
bronchopneumonia and lobar pneumonia , Patchy consolidation of the lung is the
dominant characteristic of bronchopneumonia .
Lobar pneumonia is an acute bacterial infection resulting in fibrinosuppurative
consolidation of a large portion of a lobe or of an entire lobe.
Figure 5
In lobar pneumonia, four stages of the inflammatory response have classically been
described:
stage of congestion, the lung is heavy, nd red. It is characterized by vascular
engorgement, intra-alveolar fluid with few neutrophils, and often the presence of
numerous bacteria.
The stage of red hepatization that follows is characterized by massive confluent
exudation with red cells (congestion), neutrophils, and fibrin On gross examination,
the lobe now appears distinctly red, firm, and airless, with a liver-like consistency,
The stage of gray hepatization follows with progressive disintegration of red cells
giving the gross appearance of a grayish brown, dry surface.
the final stage of resolution.Fig. 15-35A ).
Complications of pneumonia include
(1) tissue destruction and necrosis, causing abscess .
(2) spread of infection to the pleural cavity, causing empyema;
(3) organization of the exudate, which may convert aportion of the lung into solid
tissue
(4) bacteremic dissemination to the heart valves, pericardium, brain, kidneys,
spleen, or joints, causing metastatic abscesses, endocarditis, meningitis.l
Respiratory system
Lec-4Tumors
A variety of benign and malignant tumors may arise in the lung, but the vast majority (90% to
95%) are carcinomas .
Carcinomas--Lung cancer is the most common cause of cancer mortality worldwide. This is
largely due to the carcinogenic effects of cigarette smoke.
Cancer of the lung occurs most often between ages 40 and 70 years, with a peak
incidence in the fifties or sixties. the 5-year rate for all stages only 15%.
Etiology and Pathogenesis.
1- Tobacco Smoking.
87% of lung carcinomas occur in active smokers or those who stopped recently.
smokers of cigarettes have a 10-fold greater risk of developing lung cancer than nonsmokers, and heavy smokers (more than 40 cigarettes per day for several years) have
a 60-fold greater risk.
Smoking cause epithelial changes that begin with squamous metaplasia and progress
to squamous dysplasia, carcinoma in situ, and invasive carcinoma.
2- Industrial Hazards. High-dose ionizing radiation is carcinogenic.
3-Air Pollution.Atmospheric pollutants may play some role in the increased
incidence of lung carcinoma today.
4- Genetics. Occasional familial clustering has suggested a genetic predisposition.
Classification.
• Squamous cell carcinoma (25% to 40%)
• Adenocarcinoma (25% to 40%)
• Small cell carcinoma (20% to 25%)
• Large cell carcinoma (10% to 15%)
Morphology------
Grossly--Solid whitish grey, fungating or infiltrative mass, firm consistency with foci of
hemorrhage & necrosis.
Squamous Cell Carcinoma.
Squamous cell carcinoma is most commonly found in men and is closely correlated
with a smoking history. Usually central position near or about the hilus.
Microscopic--- characterized by keratinization.
Well differentiated CA---Keratinization more prominent with keratin pearl formation.
Moderately
differentiated---less
extensive
keratinization.
Poorly differentiated ----only small focus of keratinization with increase mitosis.
Adenocarcinoma--This is a malignant epithelial tumor with glandular differentiation .
Adenocarcinoma is the most common type of lung cancer in women and nonsmokers.
As compared to squamous cell cancers, the lesions are usually more peripherally
located, tend to be smaller, & grow more slowly than squamous cell carcinomas but
tend to metastasize widely and earlier
They vary histologically from well-differentiated tumors with obvious glandular
elements to solid masses with only occasional glands. .
bronchioloalveolar carcinoma distinct type of adenocarcinoma .
Histologically, the tumor is characterized by a pure bronchioloalveolar growth pattern
with no evidence of stromal, vascular, or pleural invasion. The key feature of
bronchioloalveolar carcinomas is their growth along preexisting structures without
destruction of alveolar architecture.
Bronchioloalveolar carcinoma with characteristic growth along pre-existing alveolar septa, without
invasion.
Small Cell Carcinoma.
This highly malignant tumor has a distinctive cell type. The epithelial cells are small,
with scant cytoplasm, ill-defined cell borders. Necrosis is common and often
extensive.
Small cell carcinomas have a strong relationship to cigarette smoking; only about 1%
occur in nonsmokers. They occur both in major bronchi and in the periphery of the
lung.
Large Cell Carcinoma
This is an undifferentiated malignant epithelial tumor that lacks the cytologic features
of small cell carcinoma and glandular or squamous differentiation.
Local effect of bronchogenic carcinoma--1. Partial obstruction may cause marked focal emphysema.
2. total obstruction may lead to atelectasis.
3. The impaired drainage of the airways is a common cause for
severe suppurative bronchitis or bronchiectasis.
4. Compression or invasion of the superior vena cava can cause
venous congestion, dusky head and arm edema —the superior
vena cava syndrome.
5. Extension to the pericardial or pleural sacs may cause pericarditis
or pleuritis with effusions.
Paraneoplastic Syndrome (systemic effect)
The hormones or hormone-like factors elaborated from lung carcinoma include
• Antidiuretic hormone (ADH), inducing hyponatremia owing to
inappropriate ADH secretion
• Adrenocorticotropic hormone (ACTH), producing Cushing
syndrome
• Parathormone--- hypercalcemia.
• Calcitonin, causing hypocalcemia
• Gonadotropins, causing gynecomastia
• Serotonin and bradykinin, associated with the carcinoid
syndrome
spread & metastasis of primary lung carcinoma—
Distant spread of lung carcinoma occurs through both lymphatic and hematogenous
pathways.
No organ or tissue is spared in the spread of these tumors, but the adrenals, for
obscure reasons are involved in more than half the cases. The liver , brain , and bone
are additional favored sites of metastases.
METASTATIC TUMORS
The lung is the most common site of metastatic neoplasms. Both carcinomas and
sarcomas arising anywhere in the body may spread to the lungs via the blood or
lymphatics or by direct continuity.