RESPIRATORY HISTOLOGYRespiratory System Conduction Portion Ciliated pseudostratified

columnar epitheliumSeromucinous secretion

Two Functional Components:1. A conduction portion for transport of inspired air and expired gases between the atmosphere and circulatory system.

2. The respiratory portion where the actual exchange of gases occur in the alveoli.

From the nasal cavity to the bronchi→ Ciliated pseudostratified Columnar epithelium (rich in goblet cells).

As you go down, the height of the epithelium decreases to: a ciliated simple columnar and then to →cuboidal epithelium

The connective tissue beneath the epithelium (lamina propria) is rich in lymphoid cells-produce IgA--- transported across the epithelium and is effective in killing bacteria and viruses.

Goblet cells secrete seromucinous which provides consistency to the cilia in the movement of secretory products in an upward direction towards the nose.It aids in the elimination of inhaled particles and other environmental debris.It absorbs and detoxifies soluble gases—First line of defense against invasive pathogens.

Simple cuboidal epithelium Goblet

cells with a seromucinous secretion

Nasal Cavity Larynx Pharynx Trachea BronchiIt contains the ciliated pseudostratified epithelium with numerous goblet cells supported by a richly vascular lamina propria containing serous and mucous glands.

The larynx is a hollow, bilaterally symmetric structure framed by plates of hyaline cartilage and muscle.-The mucosa is wear and tear, the epithelium is stratified squamous epithelium.

1.The Nasopharynx:--ciliated psudostratified columnar epithelium

2.Oropharynx: Stratified squamous epithelium and pure mucous glands

It branches out in to two primary bronchione to each lung.

The cartilage becomes less regular in the ends of the primary bronchi.

Abundant goblet cells, a submucosa of loose connective tissue containing seromucinous glands, and the adventitia, which contains the U-shaped cartilage, C.T. and smooth muscle.

Primary bronchi→gives rise to secondary and tertiary bronchi.

Secondary bronchi supplies the lobes of each of the lungs.

Tertiary bronchi supplies the segments of each lobe. It then turns into smaller airways called bronchioles.

Secondary and tertiary: Possess discontinuous cartilaginous plates in their adventitia (less rigidity)

T

Transition of PS Columnar to Stratified squamous

Bronchioles Terminal Bronchiole The Lungs

The last order of tertiary bronchi gives rise to several orders of bronchioles

The diameter decreases –the submucosal glands disappear so what is left is essentially mucosaThere epithelium is simple columnar to cuboidal.

Cilia may still be present, but goblet cells gradually disappear.

Elastic fibers increase in number in the lamina propria.

These features are particularly prominent in the last generation of bronchioles, the Terminal Bronchioles, which give rise to the respiratory portion of the bronchial tree.

The connective tissue within the lungs is rich in elastic fibers and smooth muscle, which allows the lungs to expand when the negative intrathoracic pressure is increased during inspiration.

Elastic recoil plays a major role in contraction of the lung during expiration.

A primary bronchus and the pulmonary vessels enter each lung at the hilus. The right lung has three lobes and the left lung has two, and each lobe receives a branch of the primary bronchus.

Each lobe is subdivided into bronchopulmonary segments and finally into lobules of pyramidal shape, the base facing the surface of the lungs.

Bronchiole with Prominent Smooth Muscle Layer

The pulmonary artery enters the hilus with the primary bronchus and follows the precise branching pattern.

The pulmonary artery and its branches are thin-walled, as compared to arteries of similar caliber in the systemic circulation, due to the pulmonary blood pressure being much lower than that of the systemic circulation.

Pulmonary artery with bronchus

Pulmonary artery breaks up into the alveolar capillaries

The venous return follows a separate course in that the alveolar capillaries coalesce into small veins in the intralobar septae and join other branches in the interlobar septae

The last generation of bronchioles gives rise to Terminal Bronchioles, which gives rise to two orders of Respiratory Bronchioles.

The respiratory bronchioles give rise to several alveolar ducts. It is here where the walls are filled with alveolar outpouchings called the Alveolar Sacs

Alveolar Sacs: contain reticular and elastic fibers but no smooth muscle.

Alveoli SurfactantThese are delicate, cup-shaped structures that are lined by an extremely attenuated simple squamous epithelium

Macrophages(histiocytes) are present in the septae or inside the alveoli--play an important role in phagocytosis and disposal of particulate matter that reaches the distal passages and alveoli

A single wall, the intraalveolar septum is formed between adjacent alveoli

The septum is composed of lining cells of adjacent alveoli and has connective tissue consisting of reticular and elastic fibers with an anastomosing network of capillaries.

Alveoli with macrophages Alveoli with capillaries

The alveoli are lined by two cell types that are continuous with one another:

Type I Pneumocytes: are squamous epithelial cells that make up the barrier thru which gases pass in the exchange between the blood and air.

Type II Pneumocytes: cuboidal epithelial cells that contain an organelle called a multilaminar body or cytosome, which contains a surface-active phospholipid called Surfactant.

It is secreted and spreads along the epithelial surface where it reduces surface tension at the air-filled interface, stabilizing alveolar diameters, thus preventing collapse during expiration.

PNEUMONIASPneumonia Alveolar pneumonia

1.Alveolar Pneumonia:intraalveolar inflammation usually caused by a bacteria:

A.BRONCHOPNEUMONIA B. LOBAR PNEUMONIA

2. Interstitial pneumonia:Involves alveolar septae including viral pneumonia -Usually caused by viruses---if poorly treated can become chronic

Intra-Alveolar pneumonia

a. Focal (bronchopneumonia)-May be limited to the alveoli or may involve the alveoli and the bronchi. -Patchy distribution involving one or more lobesb. Diffuse: (lobar pneumonia) limited to a segment bronchi and surrounding parenchyma. -it may include the whole

lobe.

Patchy bronchopneumonia

Lobar pneumonia

Interstitial pneumonia

Interstitial pneumonia w/mononuclear cells.

Interstitial pneumonia

Etiologies of pneumonias Pathogens Routes of pathogenesis BronchopneumoniaCan 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.

-Streptococcus -Staphylococcus-Hemophilus influenza

Legionella or T.B., fungia, viruses—not present in nasopharyngeal flora may cause pneumonia.

Legionella—acquired from inhalation of bacteria from humidifiers or AC.

Viral pneumonias—by close contact with an infected person. -Herpes and CMV may be latent in the human body and become reactivated.

CMV pneumonia with inclusions

Aspiration pneumonia with acute inflammation and bacterial colonies

1.Inhalation in air droplets (TB)2. Aspiration from upper respiratory tract (strep and staph)3.Aspiration of infected particles—often caused by anaerobic bacteria. -comon in unconscious people, with neuro deficits,4.Hematogenous spread: Bacteria may be transported to the lungs by the blood.

It begins with bacterial invasion of the bronchial or bronchiolar mucosa. -Followed by exudation of PMN’s into the lumen of the airways.

Inflammation may be limited to small number of lobules or may spread. (lobar pneumonia

Hepatization Interstitial pneumonia Complications As the intra alveolar exudates accumulate –air is replaced and the lung parenchyma is consolidated. -This process is known as hepatization-it becomes denser in x-rays

Hepatization of lower lobe

Patchy consolidations (infiltrates)

-Usually diffuse and bilateral-Inflammation affects the alveolar septae

-Mycoplasma pneumoniae is the most common

-Does not result in exudation of PMN into alveolar lumen (like alveolar pneumonia)

-Viruses invade the septae and cause necrosis along with

Bacterial pneumonia -May occur rapidly progressing cases caused by virulent pathogens

1. Pleuritis-extension of inflammation can lead to pleural effusion. a. Pyothorax: Pus fills the pleural cavity b. Empyema: Pockets of pus encapsulated by fibrous tissue—it occurs more commonly.

Purulent pulmonary empyema

mononuclear cell infiltration.

Most resolve with minor alveolar damage.

Complications Contd. Clinical Features Diagnosis2. Abscesses: associated with virulent organisms such as staph—it causes destruction of the lung parenchyma and suppuration.

Pus causes destruction of the bronchi walls and permanent dilation (bronchiectasis)

3. Chronic lung disease: caused by unresponsiveness to treatment. -Destruction of the lung parenchyma with concomitant fibrosis transform the lung into honeycomb like structure.

Pulmonary abscess—staph

Abscess formation

Honeycomb-lung due to fibrosis

Pneumonia with interstitial fibrosis

Affect children <5 years old and people >70 years old.

1.Primary or community acquired-affect healthy people

2.Secondary Pneumonias (nosocomial) -in persons with existing illnesses

Signs and symptoms-High fever, chills, coughing, SOB, dypsnea, tachypnea

Inflammatory exudates cause tissue destruction and bleeding giving rise to mucopurulent, blood-tinged, “rust-colored sputum”.

-

1.Confirmed with CXR-pulmonary infiltrates

2.Bacteriologic studies of sputum-can yield proof of infection

3. Peripheral blood smears-confirmed by leukocytosis (neutrophilia)

4. Blood gas analysis-may detect hypoxia and even respiratory acidosis.

Staph on gram stain

Pneumococcal Pneumonia

Infection with St. pneumonia>50% of all bacterial pneumonias-usually affect the lower lobes due to gravity.

4 pathological sequential phases:1.Engorgement: serous exudates pours into the alveoli from dilated leaky blood vessels.

2. Red hepatization (within 48hrs) RBC’s, fibrin, and PMN fill the alveoli

3. Gray Hepatization: By 3-8 days, the lungs become grayins as the WBC’s and the fibrin consolidate in the alveoli4. Resolution: By 7-11 days exudates is lysed and reabsorbed by macrophage restoring tissue.

Gray hepatization (wbc and fibrin)

Bronchopneumonia vs normal

lobar pneumonia

Clinical features Staph aureus pneumonia Gram negative bacteria Atypical pneumoniaSudden with chillsFever, Pleuritic chest pain, cough and rust-colored sputum.

The vaccine for pneumococcus is 80-90% effective against most serotypes and is usually given to high-risk patients

Staph aureus tends to produce multiple abscesses. -Mortality rate is over 50%

Staph aureus abscesses

Pseudomonas Most common hospital-acquired pneumonia.

Characterized by vascular lesions that cause infarcts and necrosis of the lung parenchyma

The most common causes of lung infections in Cystic Fibrosis pt’s

Klebsiella pneumoniae infection occurs in middle-aged, alcoholic males. A thick current-red jelly sputum is characteristic

Gram negative bacteria

Mycoplasma pneumonia—bacterial -like organism that causes an interstitial pneumonia

-Clinical sx’s are milder, the fever is less pronounced. usually no 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 Disease. -community and in hospitalized immuno- compromised patients-Gram negative rod

-This organism is ubiquitous in natural and man-made water environments-Aerosolized contaminated water is inhaled, resulting in infection

Organism, a facultative intracellular organism, settles in the lower respiratory tract and is engulfed by macrophages

Severe pneumonia-- high Fevers-- Fever greater than 40°C (range, 38.8-40.5°C)

-Mental confusion,- Proteinuria

Legionnaires’ Disease-Lobar

-Famous for causing an outbreak of pneumonia at an American Legion convention

-Outbreaks have even been found associated with growth in shower heads-No person to person transmission has been identified.

-It inhibits phagocytosis, survives and replicates inside the macrophage

-People who smoke, drink alcohol (a lot)

-Pts with AIDS, cancer, renal transplants are predisposed to infection

-Microscopic hematuria

Cough is a prominent symptom, although the sputum is frequently scanty and nonpurulent

Should be suspected in patients who are>50 and smokers or if the sputum gram stains reveals neutrophils and very few organisms

Infiltrate

Alveoli with foamy macrophages

Fungal pneumonias Histoplasmosis Cryptococcus neoformansDiagnosisLegionella antigens by using fluorescent antibody staining

-Usually develop from inhaled spores causing granuloma formation, scarring, calcification, and cavity formation

- Histoplasma, Aspergillus, Cryptococcus, Coccidioidiomycosis, Candida, and Pneumocystis.

-Caused by Histoplasma capsulatum- Usually a self-limited mycosis, but can lead to a systemic granulomatous infection in the immunosuppressed (AIDS)

- It grows in soil heavily contaminated with bird or bat droppings (bat guano)

Calcified Granuloma of Histoplasma

Histoplasma PneumoniaOrganisms within Macrophages

-Causes Cryptococcosis, a systemic, opportunistic mycosis, which affects the meninges and the lungs

It has a world-wide distribution, and the main reservoir is pigeon droppings in the soil, but the birds are not affected.

- It occurs almost exclusively in persons with impaired cell-mediated immunity

Aspergillus fumigatus Clinical findings

Cryptococcal Pneumonia with Mucoid (clear) Capsules

Mucicarmine Stain for the Capsules of Cryptococcus

-Causes Aspergillosis, caused by an environ-mental fungi that produces lung infections

- It has a characteristic appearance, having septate hyphae that forms V-shaped branches

-It can colonize and also invade abraded skin, wounds, burns, cornea, or paranasal sinuses

- Immunocompromised patients are susceptible

“Soap bubble”

Aspergillus Fungal Ball Aspergillus pneumoniaCoccidioides immitis-Pneu. Pathogenesis Granuloma- Coccidioidomycosis A chronic, necrotizing infection that resembles Tuberculosis, and is endemic to arid regions of Southwestern U.S. and Latin America-“Valley fever” (CENCAL)

-In soil, it forms hyphae with Arthrospores that are very light and can be carried by the wind to be inhaled.

-The Arthrospores form Spherules (in the lungs)--large vacuoles with a thick wall that are filled with Endospores- the endospores form new spherules which spread forming caseating granulomas, similar to T.B.

Clinical presentation Candida Pneumocystis carinii

Spherule of Coccidioides with Endospores

Ruptured spherules

-Initially asymptomatic pneumonitis, -limited to the lungs and regional lymph nodes, but can disseminate to granulomatous lesions.

Candida albicans Pneumonia with Pseudohyphae

An important cause of diffuse interstitial pneumonia in immunocompromised patients

- Transmission occurs by inhalation that produces no disease in healthy patients, but causes pneumonia in AIDS patients

Pathogenesis Clinical

Pneumocystis carinii Pneumonia

-The presence of the cup or boat-shaped cysts in the alveoli induces an inflammatory response, resulting in a frothy, eosinophilic, edema fluid that blocks oxygen exchange

-There are bilateral rales and rhonchi and the CXR reveals a diffuse interstitial pneumonia

-Cough fever, dyspnea

Diagnosis is made by microscopic examination of lung tissue obtained by bronchoscopy, BAL, or open

Pneumocystis carinii PneumoniaSilver Stain (GMS) for Cyst Organisms

Pink, Foamy Exudate within lung biopsyTuberculosis Pathogenesis-A chronic, bacterial infectious disease caused by Mycobacterium tuberculosis

-It is transmitted from person to person by respiratory aerosols

-It is an obligate aerobe, whose cell wall contains Mycolic acid, a complex lipid.

-The encapsulated bacteria elicits formation of granulomas composed of stimulated macrophages →multinucleated giant cells.

-Infection is not marked by acute purulent lesions.

-Doesn’t attract PMNs-Not marked by purulent lesions

The inhaled organisms multiply in the alveoli because alveolar macrophages cannot readily kill the bacteria.

Forms a Ghon complex:peripheral parenchyma granuloma + infected hilar node.→characteristic of primary TB

The initial infection usually occurs in the lower lobes and consists of a Ghon Complex.

Primary TB with Ghon Complex

Primary Ghon Complex of Tuberculosis

Grossly, the healed, subpleural Ghon nodule is well circumscribed with central necrosis. In later stages, the lesion is fibrotic and calcified.-calcification that can be seen on CXR. (coin lesion)-casseous necrosis

Progressive Primary TB Secondary infection TB

Tuberculosis with Caseous Necrosis

Granuloma

Multi-nucleated giant cells

AFB Stain for Tuberculosis

Primary TB tends to spread to other parts of the lungs in children and immunosuppresed—progressive primary TB.The initial lesion enlarges rapidly and there is erosion of bronchi or bronchioles by central liquefaction.

-Represents a reactivation of a dormant primary infection (Ghon complex)

-The bacteria typically spreads to the apex of the lungs.Involvement of hilar nodes is common as well.

Causing a granulomatous pneumonia where confluent granulomas tend to produce cavities—common sources of hemoptysis

-Cavities can cause erosions into both bronchial tubes and pulmonary blood vessels

Cavitation

Secondary TB—cavities

Complications of Secondary TB Complications of spread Clinical features of TB

Miliary Spread:It seeds in distal organs with innumerable small millet seed-like lesions. -Presence of small tuberculous granulomas

-GI tract if swallowed, or spread to the kidneys, brain or bones, if disseminated via the eroded bloodstream).

Miliary spread TB

-Contra-lateral pneumonia, pleuritis, with effusion and pleural granulomas, TB laryngitis, intestinal tuberculosis, due to swallowing of tuberculous material.-lymphatic spread to the hilar lymph nodes with infection to the neck area (called Scrofula), as well as TB Meningitis and Osteoarthritis.

-Fever, fatigue, night sweats, and weight loss.

-Primary TB remains clinically unrecognized in 95% of cases

-The symptoms of secondary TB includes a non-productive, dry cough, low-grade fever, loss of appetite, with minor hemoptysis from early cavitary lesions.

Acid Fast Stain of SputumInitial test for diagnosis.

Sarcoidosis PathogenesisA multisystemic granulomatous disease of unknown etiology, presumably mediated by cell-mediated immunity

The cause and pathogenesis are unknown. It has a predilection for the lungs and mediastinal (hilar) lymph nodes.

- The lungs are infiltrated with CD-4 positive T-helper lymphocytes, as are the lymph nodes-Non-caseating granulomas

-These non-caseating granulomas may involve any organs in the body. -The lungs, lymph nodes of the thorax and neck, and the liver are most often involved. non-caseating granulomas

Granulomas Node involvement-Asteroid Bodies (star-shaped crystals)-Schaumann Bodies (calcified lamellar structures) may be seen in granulomas.

-The granulomas are distributed around bronchi, bronchioles and blood vessels

Sarcoidosis of the lungs

Non-caseating granulomas

Sarcoidosis with pulmonary fibrosis

The nodes are characteristically enlarged and sometimes calcified. When present in the hilar area the matted nodes are called “Potato Nodes”, seen on chest X-ray

Potato nodes

Sarcoidosis in the lymp nodeSkin involvement Clinical features

The spleen is affected (75%) (splenomegaly) Seen as granulomas in the parenchyma.

-Granulomas in the both the portal triads

- Lesions may also appear on the mucous membranes of the oral cavity, larynx, and URT. Involvement of the lacrimal and salivary glands, causing an iritis and possible loss of vision.

-Erythematous plaques similar to lupus.

Sarcoidosis of the skin

-Most symptomatic patients have a low-grade fever, feel tired and anorexic

-Dyspnea, cough, wheezing

-Peripheral lymphadenopathy, cutaneous lesions, eye involvement, splenomegaly, or hepatomegaly

Hilar lymphadenopathy

-60% of patients have elevated serum levels of Angiotensin-Converting Enzyme (ACE), which is released from macrophages in granuloma.

Sarcoidosis with end-stage progressive pulmonary fibrosis.

COPDCOPD Bronchial Asthma Pathogenesis Histopathology of Asthma

Lung diseases characterized by chronic airway obstruction.AsthmaChronic bronchitis

Characterized by attacks marked by wheezing during

expiration, cough and dyspnea.

In more than 50% of the cases, the disease begins in childhood.Two types:

1. Extrinsic: mediated by type 1 hypersensitivity response.- Begins in childhood

2. Intrinsic: Precipitated by non-immune response and includes

lymphocytes, macrophages, eosinophils, basinophils and plasma cells produce a variety of chemical mediators. -act in response to an Allergen and do two things:

1. Increase permeability of blood vessels

2. Stimulate the contraction of smooth muscle cells.

-These mediators include histamine, bradykinins and

Bronchi show:1. chronic inflamamation

and 2. Overabundance of mucus

in the lumen.- If mucus contains

whorls of shed epithelial cells then are called: Curshmann Spirals.

1.Mucus in the lumen2.Inflammation and basement membrane thickening3.Enlarged mucosa glands4.Smooth muscle hyperplasia

physical factors (heat or cold), exercise, psychological stress, chemical irritants, air pollution and bronchial infection.-Usually begins in adult life.

PG’s Thick mucus in lumen and basement membrane thickening

Asthma with eosinophilsAsthma

The lungs are pink, and touch in the midline.-overabundance of mucus plugs in the lumen→forming casts

Asthma with Thickened Basement Membrane and Smooth Muscle Hypertrophy

Asthma with Goblet Cell Hyperplasia, and Smooth Muscle Hyperplasia

Bronchial Asthma with Enlarged Mucus Glands and Inflammation

Mucus Plug in Bronchial Asthma

Clinical Features Chronic Bronchitis PathologyExtrinsic asthma begins before the age of 10.

Disease is characterized by attacks of cough wheezing, and dyspnea.

Defined as a chronic cough and production of sputum for a minimum of three months a year for at least two consecutive years.

ETIOLOGY-smoking is the main cause of chronic bronchitis (90%) -air pollution, toxic fumes and pneumonias as well.

1.Fibrous thickening of the walls of the bronchi and bronchiole.

-Lumens filled with mucus.

-Hypertrophy of mucous glands -Oversecretion of mucus-Hyperplasia of goblet cells -Because of this there is infiltration of lymphocytes, macrophages and plasma ells.

Chronic Bronchitis With Hyperplasia of Mucus Cells

Chronic Bronchitis with Increased Goblet Cells

Chronic Bronchitis with Chronic Inflammatory Cells in Submucosa

Over production of mucus ComplicationsWith time surface epithelium may show ulcerations or metaplasia of columnar epithelium into stratified squamous epithelim.

Due to the increased production of mucus by submucosal glands, it may lead to cyanosis.

The hypoxia may be so pronounced during coughing that it causes cyanosis -blue-bloaters

Peribronchial fibrosis may affect the vasculature resuling in pulmonary hypertension and chronic Cor Pulmonale.

Squamous Metaplasia of Bronchial Epithelium

COPDEmphysema—due to smoking. Most affected PathogenesisEnlargement of the airspaces distal to the terminal bronchioles with destruction of the alveolar walls

-It affects smokers: It is hypothesized that the irritants in smoke provoke an influx of inflammatory cells into the alveoli.

Proteolytic enzymes released from the leukocytes destroy the alveolar walls, causing abnormal enlargement of the alveolar spaces, characteristic of Emphysema

Elastases in the lungs probably account for the loss of elastin fibers in the alveolar walls.

Emphysema due toAlpha-1-Antitrypsin Deficiency

The proteases Bullae

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.

The proteases are produced by bacteria, PMN’s, monocytes, and macrophages during the phagocytic process, and are capable of destroying elastin and reticular fibers in the lung.

The deterioration of the elastic and reticular→“Bullae” formation.

1.Centriacinar (centrilobular) emphysema-widening of the airspaces in the center of the lobule and

-involves predominantly the respiratory bronchioles, with sparing of the alveoli, and primarily seen in the upper lobes-Most common form of

- Bullae are parenchymal air-filled spaces greater than 1 cm in diameter.

Emphysema and is typically found in cigarette smokers

2.Panacinar emphysema-Involves all the airspaces distal to the terminal bronchioles.- involves the alveoli.

-Blebs, are subpleural air-filled spaces formed by rupture alveoli which can rupture into the pleural cavity, causing a pneumothorax.

Clinical Features-The chest is over-expanded and “Barrel-Shaped-Tachypnea-The Chest X-Rays show clear lung fields with over inflation

Cystic FibrosisThe defect in the transport of chloride across the cell membrane results in a lack of NaCl in the glandular secretions of all the exocrine glands, most importantly the pancreas, intestines and the bronchi.

obstruction of the fetal intestines and pancreatic ducts cause:→meconium ileus with peritonitis -dehydrated muconium (fetal intestinal contents) may cause intestinal rupture and dissipation of intestinal contents.

Hard, Chronic Pancreatitis Cystic Fibrosis Involvement of Pancreas

-Bronchial mucous transforms into viscous plugs that prevents normal respiration

-Predisposing the individual to recurrent bacterial infections

-These individuals often have chronic bronchitis and bouts of recurrent pneumonia, often

-incurable disease, and most affected individuals die in their twenties or thirties as a

leading to bronchiectasis

Cystic Fibrosis Lung with Bronchiectasis

result of pulmonary infections.

Bronchiectasis

A permanent dilatation of the bronchi which is the most common complication of chronic bronchitis

. The abnormally dilated bronchi and bronchioles are filled with mucopurulent material which stagnates and therefore cannot be cleared by coughing.

-Infection results and spreads into adjacent alveoli and recurrent pneumonias are common with hematogenic spread of infection to other organs

Bronchiectasis with Dilated Bronchus, Necrotizing Inflammation and Mucosal Destruction