diseases of lungs

Diseases of LungsPatho-B Lab

Atelectasis with congestion

Bronchiectasis

Emphysema

Bronchial Asthma

Adenocarcinoma Lung

Pulmonary edema

Bronchopneumoniae

NEW SLIDES

Lobar Pneumoniae

Viral Pneumoniae

Lung Abscess

Tumor Emboli- Lung

Chronic Pulmonary Congestion

TB Lungs

OLD SLIDES

• Atelectasis, known as Lung Collapse, is loss of lung volume caused by inadequate expansion of air spaces.

Types of Atelectasis• Compression Atelectasis- Usually associated with accumulation of fluids/blood/air

with in the pleural cavity which mechanically collapse the adjacent lung..

– Frequently occurs with pleural effusions caused most commonly by Conjustive Heart Failure.

– Reversible

• Resorption Atelectasis- Occurs when an obstruction prevents the air from reaching distal airways.

– Most common cause of resorption atelectasis is obstruction of bronchus by a mucopurulent plug.

– Reversible

• Contraction Atelectasis- Occurs when either local or generalized fibrotic changes in the lung/pleura hamper expansion and increase elastic recoil during expiration.– Irreversible

• Diagnosis:- – Radiological examination ----X-ray

• Clinical Manifestation– Dyspnea– Productive Cough

***Significant adventitious sounds on Auscultation,dullness on percussion

• Treatment :- Treating the underlying cause.

– Bacteriological and Mycological examination of sputum( To treat the underlying cause if infectious in nature with relative intervention)

• Preventive measures for aspiration in childrens, post op surgical patients decreases the risk of Atelectasis

• Complication:- May worsen bronchial Asthma,Bronchiectasis.

Hallmark

Alveolar Collapse

LPO

**Congestion

**Anthracosis

**Alveolar collapse

Congestion Here can give A clue of the Patient suffereringFrom compressiveType of Atelectasis

HPO

• Bronchiectasis is the permanent (abnormal) dilation of bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, associated with chronic necrotizing infections.

• 2 Processes involved in Pathogenesis– Obstruction– Chronic persistent infection

• Diagnosis:-

– Sputum culture – May reveal Pseudomonas aeruginosa, fungi such as Aspergillus and various Mycobacteria

– Radiological Examination – X-ray findings not significant unless very gross... CT scan is much more sensitive for Bronchiectasis

• Clinical Manifestation

– Chronic productive cough(Foul smelling)– Fever,Malaise, aand increased cough and sputum volume.– Haemoptysis(can be slight of massive)– Halitosis is a common feature– Clubbing of fingers may develop

• Management

– In patients with airflow obstruction, bronchodilators to enhance airway patency.– Physiotherapy – to keep the dilated bronchi empty of secretions– Antibiotic therapy(Ciprofloxacin, ceftizimide 12 hourly 25—750 mg IV infusion)

Normal Bronchus

Normal Bronchioles

Dilated Bronchiolewith secretion within

LPO

LPODilated Bronchiolewith secretion within

Inflammatory changes in the wall of the bronchiole..

Necrotized smooth muscles and supporting tissue due to inflammation

HPO

Bronchioles

LPO

Dilated Bronchi LPO

Secretions within The bronchi due toAccumulation of Pus in dilated bronchi

LPO

ProminentFibrotic change and Inflammatory changeIn entire slide

Inflammatory and fibrotic Changes found in the Surrounding lung tissue

HPOBronchiectatic cavity Filled with secretions ,Lined by normal epitheliumWith some granulation tissue

Inflammatory Changes in theBronchial wall

HPO

** Inflammatory changes**Fibrotic changes**Anthracosis

LPO

** Inflammatory changes**Fibrotic changes HPO

** Inflammatory changes**Fibrotic changes

LPO

• Characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of wall without obvious fibrosis

• Most common cause – Smoking (Nicotine)

• 2 Pathogenic Mechanisms are

– Excess cellular proteases with low antiprotease activity

– Excess of oxygen species

Types of Emphysema• Centriacinar(Centrilobar) Emphysema

– Involves central of proximal acini sparring the distal alveoli.

• Panacinar(Panlobar) Emphysema– Uniform enlargement of the acini from the level of respiratory

bronchiole to terminal alveoli.

• Distal acinar(Panseptal) Emphysema– Proximal part of acini is normal but distal part is involved

• Irregular Emphysema– Irregular involved acini, almost invariably associated with scarring.– Most common form of Emphysema

• Diagnosis– Alpha1-antiprotease assay– CT is more sensitive that X-ray for Emphysema

• Clinical Manifestation– Dyspnea is usually the first symptom(Progressive)– Cough and Wheezing in patient with underlying Chronic bronchitis or Chronic

asthmatic bronchitis.– Weight loss– Barrel Chest

• Management– Smoking cessation– Oxygen Therapy– Pulmonary rehabilitation– Mucolytic therapy

Thinning And destruction of Alveolar walls LPO

Thinning And destruction of Alveolar walls

LPO

• Characterized by chronic airway inflammation and increased airway hyper-responsiveness

• Funtionally characterized by the presence of airflow obstruction which is variable over the short periods of time or is reversible with treatment

Types of Asthma• Atopic/Extrinsic Asthma – Most common type

– +ve Family History common– +ve Allergy causing Attacks (Rhinitis, urticaria, eczema)– Elevated Ig-E serum levels

• Non Atopic/ Intrinsic /Acquired Asthma– Non immune in nature– +ve Family history uncommon– No associated Allergy– Ig-E serum levels are normal

• Drug Induced Asthma– Drug like Aspirin provoke asthma– Patient with Aspirin sensitivity present with Recurrent Rhinitis,Bronchospasm,urticaria

• Occupational Asthma– Stimulated by fumes(plastics,resins), organic and chemical dusts(wood,cotton)– Attacks usually develop after repeated exposure to the inciting agents

Triad of Reversible airway obstruction

• Chronic inflammation with eosinophils

• Bronchial smooth muscle cell hypertrophy

• Hyperreactivity

Significant Morphology in Asthma• Macroscopic

– Occlusion of the bronchi and bronchioles by thick, tenacious Mucous plugs.

• Microscopic– Mucous plug contain whorls of shed epithelium(Curschmann spirals)– Numerous eosinophils and Charcot leyden crystals(collections of

crystals made of eosinophil proteins) are also present

• Diagnosis– Diagnosis is made on the basis of compatible clinical history combined with the

demonstration of the airflow obstruction– Pulmonary function tests– Measurement of allergic status( Elevated sputum or peripheral blood eosinophil

count )– Airway inflammation assessment

• Clinical Manifestation– Typically symptoms includes recurrent episodes of wheezing, chest tightness,

breathlessness and cough

• Management– Avoiding aggravating factors – Short acting inhaled beta2- Agonist (Bronchodilators) – For patients with mild

intermittent asthma(Symptoms less than once a week for 3 months and fewer than 2 nocturnal episodes)

– Long acting beta2 agonist(salmeterol,formoterol) if patient remains poorly controlled– Low/high dose steroid therapy depending on the severity of symptoms

LPO**Airway Remodelling in Asthma**

-Thickening of Basement membrane of the bronchial epithelium

-Edema and inflammatory infiltrate in walls

-Increase in the size of the glands

-Hypertrophy of the bronchial muscle walls

LPO**Airway Remodelling in Asthma**


-Edema and inflammatory infiltrates in wall



HPO**Airway Remodelling in Asthma**


-Edema and inflammatory infiltrates in wall



Classification of Lung tumors for therapeutic purposes

• Small Cell Lung Carcinomas(SCLC)– All small cell lung carcinomas have metastasized by the time they are

diagnosed hence they cannot be cured by surgery, Chemotherapy and Radiation is the only treatment for SCLC

• Non small cell lung Carcinoma(NSCLC)- poor response to chemotherapy and are better treated by surgery.

– Squamous cell– Adenocarcinoma ----- Most common of lung cancer in women and non

smoker– Large cell carcinoma

• Most common of lung cancer in women and non smoker• Precursor –Atypical adenomatous hyperplasia(AAH)• Occur as central lesions but

are more peripherally located• Many arising in relation to peripheral lung scars (scar carcinomas)

Histological types• Acinar(Gland forming)• Papillary• Solid

• In general all Adenocarcinomas grow slowly and form smaller masses than other subtypes but they tend to metastasize widely at an early stage.

• Diagnosis:-– Histologic diagnosis– Bronchoscopy– Bronchial biopsy– CT/Ultrasound

• Clinical Manifestation– Cough is common early symptom – Haemoptysis– Bronchial obstruction– Recurrent pneumonia– Lassitude and Weight loss- indicated metastatic spread– Hoarseness

• Management– Surgical resection for all Non small cell lung carcinoma-NSCLC

**Stromal invasion(Bronchial mucosa)

**Desmoplasia(growth of fibrous or connective tissue)



**Acinar typeGland formingAdenocarcinoma

**Stromal invasion


**Cytologic atypia

**Pleomorphism

• Caused due to accumulation of fluids in lungsEtiology• Cardiogenic pulmonary edema– Most common clinical problem seen frequently in left

ventricular failure.

• Noncardiogenic pulmonary edema– Renal failure– Acute Respiratory distress syndrome(ARDS)

• Signs:- JVP – increased, sweating, cool extremities, dullness and crepitation at base.

• Chest radiograph:- Cardiomegaly,pleural effusion.

• ECG- decreased left ventricular function

• Decreased PaO2

• Can lead to Acute severe dyspnea.

• Management:- – Treating the underlying cause– Usually the prognosis is poor(with survival 2-3 years) unless Heart-lung

transplantation is performed.

4 stages of lobar/Broncho Pneumonia

• Congestion– Affected lobe is heavy, red boggy,histologically vascular congestion can be seen with

scattered neutrophils in the alveoli.

• Red hepatization– Lung shows liver like consistency, the alveolar spaces are packed with neutrophils, red cells

and fibrin.

• Gray hepatization– Lung is dry,gray, and firm, because the red cells are lysed while the fibrinosuppurative

exudate persists within the alveoli

• Resolution– Follows in umcomplicated cases, as exudates within the alveoli are enzymatically digested

to produce granular, semifluid debris that is resorbed, ingested by macrophages, organized by fibroblast growing into it.

Pneumonia• Diagnosis

– Radiological- X-ray(Pleural effusions)– Microbiological- sputum direct smear– Blood culture +ve for pneumococcal pneumonia– Serology-For viral infections,mycoplasma,legionella

• Clinical Manifestation– Typically presents as acute illness– Systemic features – fever, shivering, vomiting,anorexia, headache.– Pulmonary symptoms-cough(initially dry,painful and later accompanied by expectoration of

mucopurulent sputum)

• Management– Rest, cessation of smoking– Antibiotic therapy– Oxygen to all patients with tachypnea,hypoxemia,acidosis.– Analgesic for pleural pain

• Pneumonia generally defined as any infection in the lung.

• Initial infection is in bronchi which gradually extends in adjacent alveoli.

• Patchy distribution of inflammation implies Bronchopneumonia and is usually involves more than one lobe.

Bronchiolitis

Vascular congestion

Congestion

Red Hepatization

Gray hepatization

Bronchiolitis

Congestion

Congestion

Red Hepatization

Gray hepatization

Red Hepatization

Gray hepatization

LPO Patchy Inflammation of the Interstitium and Septa

Mononuclear infiltrates in alveolar wall

Inflammatory changes only in the interstitium

LPO

Mononuclear infiltrates inThe alveolar walls

Edematous walls

HPO

Congested alveolar wall

There is fibrosis in the alveoli Along with purulent exudate (at the pointer)

HPO

Purulent exudate in High power shows presence of neutrophils

Exudates in alveoli

Bronchopneumonia

Viral pneumonia Bacterial pneumonia

Bronchopneumonia:- Infection involving bronchi initially and then alveoli

Viral pneumonia:- Interstitium involves

Bacterial pneumonia:- Alveoli filled with exudates and fluid

• Etiology:-Aspiration of Pyogenic organism most common cause of lung abscess

• Liquefactive type of necrosis.

• In lung abscess there is localized collection of pus, or a cavity lined by chronic inflammatory tissue.

• It may also be produced by infection of previously healthy lung tissue with Staph. Aureus,Klebsiella pneumonia.

• Diagnosis –– X-ray(segmental opacity with consolidation or collapse)

• Clinical Manifestation:-– High Pyrexia– Systemic upset– Clubbing(10-14 days)– Consolidation on chest examination– Pleural rub common

• Management– Oral Amoxicillin 6hourly effective in most of the patients- 2 weeks– If Anaerobic – Metronidazole 400mg 8 hourly -2weeks

Complete destruction of lung parenchymaDue to the chronic inflammation

Neoplastic cellsWithin the vessel

• Congestion is a passive process resulting from impaired venous return out of the tissue.

• It may occur systematically, as in cardiac failure or it may be local as in venous obstruction.

• Chronic Passive congestion is a long standing congestion in which the stasis of poorly oxygenated blood causes chronic hypoxia which in turn leads to the death of the parenchymal tissue.

• Productive cough associated with dyspnea is usually the first symptom

• It involves treating the underlying cause usually.

**Thickened & fibrotic septa

** Alveolar space contains numerous Hemosiderin laden Macrophages (heart failure cells)

TB-LUNGS• Caseative type of necrosis caused by Mycobacterium.

• M. Tuberculosis Spreads through inhalation of aerosolised droplet nuclei from other infected patients.

• Characterized by granulomatous inflammation.

• Diagnosis:- – Usually confirmed by direct microscopy and culture of sputum samples. – Tuberculin test– Fluid examination(pleural fluid)

• Clinical Manifestation– Chronic cough often with haemoptysis– Pyrexia – Unresolved pneumonia– Exudative pleural effusion– Weight loss

• Management– Classical 4 drug TB therapy

Reference

• Robbins -8th Ed

• Davidson’s principles and practice of Medicine

• http://www.virtualmedicalcentre.com/humanatlas1/vmc_white.asp?anid=0004

http://www.virtualmedicalcentre.com/humanatlas1/vmc_white.asp?anid=0004

http://www.virtualmedicalcentre.com/humanatlas1/vmc_white.asp?anid=0004

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diseases of lungs

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