The Pulmonary Table

RESPIRATORY HISTOLOGY Respiratory System

Conduction Portion

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

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

Larynx 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.

The connective tissue beneath the epithelium (lamina propria) is rich in lymphoid cellsproduce IgA--transported across the epithelium and is effective in killing bacteria and viruses. Pharynx 1.The Nasopharynx:-ciliated psudostratified columnar epithelium

Simple cuboidal epithelium

Goblet cells with a seromucinous secretion

Trachea It branches out in to two primary bronchi

Bronchi Primary bronchi→gives rise to secondary and tertiary bronchi.

one to each lung. 2.Oropharynx: Stratified squamous epithelium and pure

Seromucinous secretion

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.

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

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

Nasal Cavity It contains the ciliated pseudostratified epithelium with numerous goblet cells supported by a richly vascular lamina propria

Ciliated pseudostratified columnar epithelium

The cartilage becomes less regular

Secondary bronchi supplies the lobes of each of the lungs.

containing serous and mucous glands.

mucous glands

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 Ushaped cartilage, C.T. and smooth muscle.

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 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 mucosa There epithelium is simple columnar to cuboidal.

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

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 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 Lungs

Bronchiole with Prominent Smooth Muscle Layer

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.

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

Pulmonary artery with bronchus

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 pulmonary artery and its branches are thinwalled, 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.

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

Macrophages(histio cytes) are present in

Pulmonary artery breaks up into the alveolar capillaries

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

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

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

Type I Pneumocytes: are squamousepithelial cells that make up the barrier thru which

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.

the septae or inside the alveoli--play an important role in phagocytosis and disposal of particulate matter that reaches the distal passages and alveoli

anastomosing network of capillaries.

Alveoli with capillaries

gases pass in the exchange between the blood and air.

Alveoli with macrophages Type II Pneumocytes: cuboidal epithelial cells that contain an organelle called a multilaminar body or cytosome, which contains a surfaceactive phospholipid called Surfactant.

PNEUMONIAS Pneumonia 1.Alveolar Pneumonia: intraalveolar inflammation usually caused by a bacteria: A.BRONCHOPNEUM ONIA

Intra-Alveolar pneumonia

B. LOBAR PNEUMONIA

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

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 lobes b. Diffuse: (lobar pneumonia) limited to a segment bronchi and surrounding parenchyma. -it may include the

Patchy bronchopneumonia

Interstitial pneumonia

Lobar pneumonia

Interstitial pneumonia whole lobe.

Interstitial pneumonia w/mononuclear cells.

Etiologies of pneumonias Can 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.

Pathogens -Streptococcus -Staphylococcus -Hemophilus influenza Legionella or T.B., fungia, viruses—not present in nasopharyngeal flora may cause pneumonia.

CMV pneumonia with inclusions

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.

Routes of pathogenesis 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. -comonin unconscious people, with neuro deficits, 4.Hematogenous spread: Bacteria may be transported to the lungs by the blood.

Aspiration pneumonia with acute inflammation and bacterial colonies

Hepatization

Interstitial Complications pneumonia

Bronchopneumonia 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

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 xrays

Hepatization of lower

-Usually diffuse and bilateral -Inflammation affects the alveolar septae -Mycoplasma pneumoniae is the most common

lobe Patchy consolidations (infiltrates)

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

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

-Viruses invade the septae and cause necrosis along with mononuclear cell infiltration.

Most resolve with minor alveolar damage.

Complications Contd.

Clinical Features

Diagnosis

2. 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)

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

Honeycomb-lung due to fibrosis

-affect healthy people 2.Secondary Pneumonias (nosocomial)

Pulmonary abscess— staph

-in persons with existing illnesses

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

1.Primary or community acquired

Pneumonia with interstitial fibrosis

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

1.Confirmed with CXRpulmonary 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.

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

Abscess formation

honeycomb like structure.

Pneumococcal Pneumonia

Staph on gram stain

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 alveoli 4. 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 Sudden with chills Fever, Pleuritic chest pain, cough and rust-colored sputum.

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

Gram negative bacteria Pseudomonas Most common hospital-acquired pneumonia. Characterized by vascular lesions that cause infarcts and necrosis of the lung parenchyma

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

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

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

Gram negative bacteria

Atypical pneumonia 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 Causes Legionnaires Disease. -community and in hospitalized immunocompromised patients -Gram negative rod -Famous for causing an outbreak of pneumonia at an American Legion convention

-This organism is ubiquitous in natural and man-made water environments -Aerosolized contaminated water is inhaled, resulting in infection -Outbreaks have even been found associated with growth in shower heads -No person to person transmission has been identified.

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

-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

Fungal pneumonias

Histoplasmosis

Clinical presentation Legionnaires’ disease Severe pneumonia-high Fevers-- Fever greater than 40°C (range, 38.8-40.5°C) -Mental confusion, - Proteinuria -Microscopic hematuria Cough is a prominent symptom, although the sputum is frequently scanty and nonpurulent

Legionnaires’ Disease-Lobar Infiltrate

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

Alveoli with foamy macrophages

Cryptococcus neoformans

Diagnosis Legionella 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)

Mucicarmine Stain for the Capsules of Cryptococcus

Calcified Granuloma of Histoplasma

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

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

Cryptococcal Pneumonia with Mucoid (clear) Capsules

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

Histoplasma Pneumonia Organisms within Macrophages

- It occurs almost

Aspergillus fumigatus -Causes Aspergillosis, caused by an environmental fungi that produces lung infections

exclusively in persons with impaired cellmediated immunity Clinical findings -It can colonize and also invade abraded skin, wounds, burns, cornea, or paranasal sinuses

- It has a characteristic

-

appearance, having septate hyphae that forms V-shaped branches

patients are susceptible

Immunocompromised

“Soap bubble”

Aspergillus pneumonia Aspergillus Fungal Ball

Coccidioides immitisPneu. - Coccidioidomycosis A chronic, necrotizing infection that resembles Tuberculosis, and is endemic to arid regions of Southwestern U.S. and Latin America -“Valley fever” (CENCAL)

Spherule of Coccidioides with Endospores

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

Granuloma

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

Candida

Pneumocystis carinii An important cause of diffuse interstitial pneumonia in immunocompromised patients

- Transmission occurs

Ruptured spherules Candida albicans

by inhalation that produces no disease in

Pneumonia with Pseudohyphae

Pathogenesis -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

Pneumocystis carinii Pneumonia Pink, Foamy Exudate within Tuberculosis -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.

Pathogenesis -The encapsulated bacteria elicits formation of granulomascomposed of stimulated macrophages →multinucleated giant cells.

-Infection is not marked by acute purulent lesions.

Clinical -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 lung biopsy

Pneumocystis carinii Pneumonia Silver Stain (GMS) for Cyst Organisms

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.

Primary TB with Ghon Complex

→characteristic of primary TB Primary Ghon Complex of Tuberculosis

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

healthy patients, but causes pneumonia in AIDS patients

The initial infection usually occurs in the

Grossly, the healed, subpleural Ghonnodule 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

Tuberculosis with Caseous Necrosis

Granuloma

Multi-nucleated giant cells

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

Miliary spread TB

Secondary infection TB -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

AFB Stain for Tuberculosis

Complications of Secondary TB Miliary Spread:

-GI tract if swallowed, or spread to the kidneys, brain or bones, if

lower lobes and consists of a Ghon Complex. Progressive Primary TB 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.

Complications of spread -Contra-lateral pneumonia, pleuritis, with effusion and pleural granulomas, TB laryngitis, intestinal tuberculosis, due to swallowing of tuberculous material. -lymphatic spread to the

Cavitation

Secondary TB—cavities

-Cavities can cause erosions into both bronchial tubes and pulmonary blood vessels Clinical features of TB -Fever, fatigue, night sweats, and weight loss. -Primary TB remains clinically unrecognized in 95% of cases -The symptoms of secondary TB includes a

Acid Fast Stain of

disseminated via the eroded bloodstream).

Sarcoidosis A multisystemic granulomatous disease of unknown etiology, presumably mediated by cellmediated immunity

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

hilar lymph nodes with infection to the neck area (called Scrofula), as well as TB Meningitis and Osteoarthritis.

non-productive, dry Sputum cough, low-grade fever, Initial test for loss of appetite, with minor diagnosis. hemoptysis from early cavitary lesions.

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

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

Granulomas -Asteroid Bodies (starshaped crystals) -Schaumann Bodies (calcified lamellar structures) may be seen in granulomas. Non-caseating -The granulomas are distributed around bronchi, bronchioles and blood vessels

Sarcoidosis of the lungs

Node involvement 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

non-caseating granulomas

Potato nodes

granulomas Sarcoidosis with pulmonary fibrosis

Skin involvement

Sarcoidosis in the lymp node 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.

-Most symptomatic patients have a lowgrade fever, feel tired and anorexic -Dyspnea, cough, wheezing

Sarcoidosis of the skin

-Erythematous plaques similar to lupus.

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

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

Sarcoidosis with endstage progressive pulmonary fibrosis.

Hilar lymphadenopathy

COPD COPD

Bronchial Asthma

Lung diseases characterized by chronic airway obstruction.

Characterized by attacks marked by wheezing during expiration, cough and dyspnea.

Asthma Chronic bronchitis

In more than 50% of the cases, the disease

Pathogenesis lymphocytes, macrophages, eosinophils, basinophils and plasma cells produce a variety of chemical mediators. -act in response to

Histopathology of Asthma Bronchi show: 1. chronic inflamamation and 2. Overabundance of mucus in the lumen. – If mucus contains whorls

1.Mucus in the lumen 2.Inflammation and basement membrane thickening 3.Enlarged mucosa glands

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

an Allergen and do two things:

of shed epithelial cells then are called: Curshmann Spirals.

1. Increase permeability of blood vessels 2. Stimulate the contraction of smooth muscle cells.

4.Smooth muscle hyperplasia

Thick mucus in lumen and basement membrane thickening

-These mediators include histamine, bradykinins and PG’s

Asthma with eosinophils

Asthma 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 Extrinsic asthma begins before the age of 10.

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

Chronic Bronchitis 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.

With time surface epithelium may show ulcerations or metaplasia of columnar epithelium into stratified squamous epithelim.

Over production of mucus 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

Pathology 1.Fibrous thickening of the walls of the bronchi and bronchiole. -Lumens filled with mucus. Chronic Bronchitis With Hyperplasia of Mucus Cells

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

Chronic Bronchitis with Increased Goblet Cells

Peribronchial fibrosis may affect the vasculature resuling in pulmonary hypertension and chronic Cor Pulmonale. Squamous Metaplasia of Bronchial Epithelium

Chronic Bronchitis with Chronic Inflammatory Cells in Submucosa

COPD Emphysema—due to smoking. Enlargement of the airspaces distal to the terminal bronchioles with destruction of the alveolar walls

Emphysema due toAlpha-1-Antitrypsin Deficiency 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.

Most affected

Pathogenesis

-It affects smokers:

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

It is hypothesized that the irritants in smoke provoke an influx of inflammatory cells into the alveoli. The proteases

Bullae

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

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

-Most common form of Emphysema and is typically found in cigarette smokers

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

2.Panacinar emphysema

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

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

Clinical Features -The chest is overexpanded and “BarrelShaped -Tachypnea -The Chest X-Rays show clear lung fields with over inflation

Cystic Fibrosis The 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. -Bronchial mucous transforms into viscous plugs that prevents normal respiration

Hard, Chronic Pancreatitis

Cystic Fibrosis Involvement of Pancreas

-Predisposing the individual to recurrent

-incurable disease, and

bacterial infections

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

most affected individuals die in their twenties or thirties as a result of pulmonary infections.

Cystic Fibrosis Lung with Bronchiectasis

Bronchiectasis . The abnormally dilated bronchi and bronchioles are filled with mucopurulentmaterial which stagnates and therefore cannot be cleared by coughing. A permanent dilatation of the bronchi which is the most common complication of chronic bronchitis

-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