This document discusses diffuse interstitial (infiltrative, restrictive) lung diseases. It defines them as heterogeneous disorders characterized by diffuse chronic involvement of pulmonary connective tissue. The major categories discussed include fibrosing, granulomatous, eosinophilic, and smoking-related diseases. Specific conditions like idiopathic pulmonary fibrosis, sarcoidosis, and pneumoconiosis are examined in terms of their pathogenesis, morphology, and clinical course.
3 main groups of species that have anatomically similar respiratory tracts are; 1) cattle, sheep, and pig, 2) dog, cat monkey, rabbit and rat, 3) horse and man. These anatomical and physiological differences largely determine why some pathogens affect only some species (e.g, Pasteurella haemolytica affects cattle but not pigs) and less so in others (cats and dogs).
Alveolar walls are not solid but are perforated by numerous pores which permit the passage of bacteria and
exudate between adjacent alveoli.
3 main groups of species that have anatomically similar respiratory tracts are; 1) cattle, sheep, and pig, 2) dog, cat monkey, rabbit and rat, 3) horse and man. These anatomical and physiological differences largely determine why some pathogens affect only some species (e.g, Pasteurella haemolytica affects cattle but not pigs) and less so in others (cats and dogs).
Alveolar walls are not solid but are perforated by numerous pores which permit the passage of bacteria and
exudate between adjacent alveoli.
Unpacking the 2010 Census (2013 Updated Version) - Part 1jzur
"Unpacking the 2010 Census: The New Realities of Race, Class, and Jurisdiction" is co-sponsored by Hope in the Cities and the Virginia Center for Inclusive Communities. The program examines the dramatically changing landscape of human need and what we must do collectively to address the plight of our neighbors and to build a just and inclusive community in metropolitan Richmond, Virginia. This presentation was conceived, researched and designed by Dr. John V. Moeser, Senior Fellow at the Bonner Center for Civic Engagement at the University of Richmond. Part 1 of the "Unpacking the 2010 Census" presentation focuses on the current data and demographics in metropolitan Richmond.
Slideshow is from the University of Michigan Medical School's M2 Respiratory sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Resp
Restrictive lung diseases (interstitial lung diseases)
Histological Structure of Alveoli
The wall of the alveoli is formed by a thin sheet of tissue separating two neighbouring alveoli.
This sheet is formed by epithelial cells and intervening connective tissue.
Collagenous , reticular and elastic fibres are present.
Between the connective tissue fibres we find a dense, anastomosing network of pulmonary capillaries. The wall of the capillaries are in direct contact with the epithelial lining of the alveoli.
Neighbouring alveoli may be connected to each other by small alveolar pores (pores of Kohn).
The epithelium of the alveoli is formed by two cell types:
Alveolar type I cells (small alveolar cells or type I pneumocytes) are extremely flattened and form the bulk (95%) of the surface of the alveolar walls.
Alveolar type II cells (large alveolar cells or type II pneumocytes) are irregularly (sometimes cuboidal) shaped.
They form small bulges on the alveolar walls.
Type II alveolar cells contain are large number of granules called cytosomes (or multilamellar bodies), which consist of precursors to pulmonary surfactant (the mixture of phospholipids which keep surface tension in the alveoli low) .
Cilia are absent from the alveolar epithelium and cannot help to remove particulate matter which continuously enters the alveoli with the inspired air. Alveolar macrophages take care of this job. They migrate freely over the alveolar epithelium and ingest particulate matter.
FUNCTIONS OF PULMONARY CELLS
Type I pneumocytes
Permeable to Oxygen and CO2, do not divide
Type II pneumocytes
Reserve cells
secrete pulmonary surfactant
Serve as repair cells
Alveolar macrophages
Phagocytosis
Pores of Kohn (allow passage of Macrophages)
Interstitial Lung Diseases [ILD] Approach to ManagementArun Vasireddy
Diffuse (interstitial) lung disease includes a wide variety of relatively uncommon conditions presenting with characteristic clusters of clinical features and marked by an immune response. There are over 200 specific diffuse lung diseases, many of unknown etiology. The combined incidence is 50 per 100,000, or 1 in 2000 people. Because these conditions cause aberrant lung function, morbidity and mortality due to lung injury and fibrosis are not uncommon. Both environmental and genetic factors are believed to contribute to the development of diffuse lung disease. Antigen processing and presentation are important in the development of the immune response seen in the disease, and it is thought that the likely candidate genes predisposing patients to this category of disease are those of the major histocompatibility complex. Genes that affect the immune, inflammatory, and fibrotic processes may also influence who develops the disease. If we can identify the genes that cause diseases characterized by lung injury and fibrosis, we can eventually develop genetic interventional approaches to treatment.
About the path to the uska screenshot of the uska screenshot of the uska screenshot of the uska screenshot of the uska screenshot of the uska screenshot of the uska
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
2. Obstructive Versus Restrictive
Pulmonary Diseases
Such a classification is based on pulmonary function tests.
A critical part of the initial workup of patients.
1. obstructive disease (airway disease)- limitation of airflow.
2. restrictive disease-reduced expansion of lung parenchyma.
Obstructive disease: hallmark is a decreased expiratory flow rate (FEV1
it follows that the ratio of FEV1 to FVC ).
Diffuse restrictive diseases FVC is reduced and the expiratory flow rate
is normal or reduced proportionately (ratio of FEV1 to FVC is near
normal).
3. Focus on restrictive defect
Occurs in two general conditions
1. Chest wall disorders in the presence of normal lungs (e.g in diseases
of the pleura, Guillain-Barre syndrome.
2. Acute or chronic interstitial lung diseases (classic acute restrictive
disease is ARDS, Chronic restrictive diseases pneumoconiosis, interstitial
fibrosis of unknown aetiology, and most of the infiltrative conditions
(e.g., sarcoidosis).
THE SECOND CONDITION IS WHAT WE WILL FOCUS ON.
4. Diffuse Interstitial (Infiltrative,
Restrictive) Diseases
Heterogeneous group of disorders
characterised by diffuse usually
chronic involvement of pulmonary
connective tissue. Principally the
most peripheral and delicate
interstitium in alveolar walls
5. DEFINITION cont.…
Many of the entities are of unknown cause and pathogenesis.
Some have an intra-alveolar as well as an interstitial component.
Account for about 15% of non-infectious diseases.
Clinical and pulmonary functional changes.
Patients have dyspnoea, tachypnea, end-inspiratory crackles, and
eventual cyanosis, without wheezing.
Classic physiologic features: reductions in carbon monoxide diffusing
capacity, lung volume, and compliance.
CXR-picture and the term infiltrative.
Early stages-can often be distinguished .
Advanced forms- hard to differentiate becoz, of end-stage lung.
6. DEFINITION cont.…
Categorized either as clinicopathologic syndromes or as having
characteristic histology .
Frequency of disease: most common associations are
-Environmental diseases (approximately 25%)
-Sarcoidosis (approximately 20%)
-Idiopathic pulmonary fibrosis (approximately 15%)
-the collagen vascular diseases (approximately 10%)
more than 100 different causes and associations account for the
remaining interstitial disease.
8. Pathogenesis cont.…
Earliest common manifestation of most of the interstitial diseases is
alveolitis.
In mild and self-limited injury, resolution with restoration of normal
architecture follows.
Accumulation of leukocytes has two consequences.
-1. Distorts the normal alveolar structures .
-2. Release of mediators that can injure parenchymal cells and
stimulate fibrosis
THESE RESULT IN END STAGE LUNG
9. Pathogenesis cont.…
initial stimuli for alveolitis are as heterogeneous, ROS, directly toxic to
endothelial cells, epithelial cells etc.
Compliment and macrophage mediated accumulation of
inflammatory cells is seen I most diseases .
CMI is seen in disease like sarcoidosis with formation of granulomas .
11. Fibrosing Category
1. Idiopathic Pulmonary Fibrosis (cryptogenic fibrosing alveolitis)
Diffuse interstitial fibrosis (usual interstitial pneumonia (UIP)), which in
advanced cases results in severe hypoxemia and cyanosis.
Males are affected more often than are females.
Approx. two-thirds of patients are older than 60 years of age at
presentation.
similar pathologic findings in the lung may be noted with well-defined
entities such as asbestosis
12. Morphology
Pleural surfaces of the lung have the appearance of cobblestones .
The cut surface shows fibrosis (firm, rubbery white areas).
Patchy interstitial fibrosis.
Earliest lesions appear as fibroblastic foci .
Temporal heterogeneity.
Honeycomb fibrosis occurs.
The interstitial inflammation is usually patchy and consists of an alveolar
septal infiltrate of mostly lymphocytes .
Foci of squamous metaplasia and Intimal fibrosis and medial thickening
of pulmonary arteries often present.
14. Usual interstitial pneumonia. Fibroblastic focus with fibres running parallel to surface
and bluish myxoid extracellular matrix.
15. Clinical Course
IPF usually presents insidiously
Gradual onset of a non-productive cough and progressive dyspnoea.
O/E
"dry" or "Velcro"-like crackles during inspiration.
Cyanosis, cor pulmonale, and peripheral oedema .
Investigations: Surgical lung biopsy remains the gold standard for
diagnosing IPF .
Prognosis is poor mean survival of 3 years or less.
16. Nonspecific Interstitial Pneumonia
Unknown aetiology, affects mostly 45 to 55 year olds.
Lung biopsies fail to show diagnostic features of any of the other well-
characterized interstitial diseases.
"wastebasket" type of diagnosis, it is important to differentiate non-
specific interstitial fibrosis from UIP.
Divided into cellular and fibrosing patterns.
Fibroblastic foci are typically absent.
Clinical course : Patients present with dyspnoea and cough of several
months' duration
cellular pattern have a better outcome
17. Cryptogenic Organizing
Pneumonia
Synonymous with "bronchiolitis obliterans organizing pneumonia.
Clinical course
cough and dyspnoea .
Radiographically have subpleural or peribronchial patchy areas of
airspace consolidation
Some individuals recover spontaneously, but most require treatment
Histologically
Polypoid plugs of loose organizing connective tissue within alveolar
ducts, alveoli, and often bronchioles .
Organizing pneumonia with intra-alveolar fibrosis.
There is no interstitial fibrosis/ honeycomb
19. Pulmonary Involvement in Collagen
Vascular Diseases
systemic lupus erythematous, rheumatoid arthritis, systemic sclerosis,
and dermatomyositis-polymyositis are examples.
Histologic variants , with NSIP, UIP-pattern (similar to what is seen in IPF),
vascular sclerosis, organizing pneumonia, and bronchiolitis (small
airway disease, with or without fibrosis) being the most common.
Pulmonary involvement in these diseases is usually associated with a
poor prognosis.
20. Pneumoconiosis
Non neoplastic lungs reaction to inhalation of mineral dusts in the work
place and organic as well as inorganic particles, fumes and vapours.
21. Mineral Dust-Induced Lung Disease
Agent Disease: Exposure
Coal dust exposure: Simple coal workers' pneumoconiosis: macules and
nodules Complicated coal workers' pneumoconiosis: PMF- Coal mining
Silica exposure: Silicosis -Sandblasting, quarrying, mining, stone cutting,
foundry work, ceramics
Asbestos exposure: Asbestosis pleural effusions, pleural plaques, or diffuse
fibrosis; mesothelioma; carcinoma of the lung and larynx- Mining, milling, and
fabrication of ores and materials; installation and removal of insulation
22. Pathogenesis
Size, shape, solubility, and reactivity of the particles etc determine the
reaction of the lung to mineral dusts .
The amount which cause disease depends on the factors above.
Coal dust is relatively inert (large amounts must deposit).
Silica, asbestos, and beryllium are more reactive than coal dust (fibrotic
reactions at lower concentrations)
Macrophages accumulate and endocytose the trapped particulates
More reactive particles trigger the macrophages to release inflammatory
mediators.
Tobacco smoking worsens the effects of all inhaled mineral dusts, more so with
asbestos than with any other particle.
Larger particles resist dissolution these tend to evoke fibrosing collagenous
pneumoconiosis (characteristic of silicosis).
23. Coal Workers' Pneumoconiosis
("black lung" )
Findings range from: 1.asymptomatic anthracosis, 2.simple coal
workers' pneumoconiosis (CWP),3. complicated CWP or progressive
massive fibrosis (PMF).
Fewer than 10% of cases of simple CWP progress to PMF.
PMF is a generic term that applies to a confluent fibrosing reaction in
the lung; this can be a complication of any one of the three
pneumoconiosis discussed here.
Anthracite mining has been associated with a higher risk of CWP.
24. Morphology
Pulmonary anthracosis: innocuous coal-induced pulmonary lesion
-Inhaled carbon pigment is engulfed by alveolar or interstitial macrophages.
-Which then accumulate in the connective tissue along the lymphatics,
including the pleural lymphatics, or in lymph nodes.
Linear streaks and aggregates of anthracotic pigment are seen.
Simple CWP: coal macules and the somewhat larger coal nodule are seen.
-The upper lobes and upper zones of the lower lobes are more heavily
involved.C
-Centrilobular emphysema can occur.
Complicated CWP (PMF)
Occurs on a background of simple CWP by coalescence of coal nodules
characterized by intensely blackened scars larger than 2 cm, sometimes up to
10 cm in greatest diameter
25. Progressive massive fibrosis superimposed on coal workers' pneumoconiosis. The large
blackened scars are principally in the upper lobe. Note the extensions of scars into
surrounding parenchyma and retraction of adjacent pleura.
26. Clinical Course
Usually a benign disease that produces little decrement in lung function.
Increasing pulmonary dysfunction, pulmonary hypertension, and cor
pulmonale, seen if PMF develops.
Progression from CWP to PMF has been linked to a variety of conditions
including coal dust exposure level and total dust burden
Once smoking-related risk has been taken into account, there is no increased
frequency of bronchogenic carcinoma in coal miners.
27. Silicosis
Currently the most prevalent chronic occupational disease in the
world. Slowly progressive.
Caused by inhalation of crystalline silica.(quartz is most commonly
implicated in silicosis)
After inhalation the particles interact with epithelial cells and
macrophages.
Ingested silica particles cause activation and release of mediators by
pulmonary macrophages, including IL-1, TNF.
When mixed with other minerals, quartz has a reduced fibrogenic
effect.
28. Morphology
Silicotic nodules .
Microscopically, the silicotic nodule demonstrates concentrically
arranged hyalinized collagen fibers surrounding an amorphous center.
"whorled" appearance of the collagen fibres.
Polarized microscopy reveals weakly birefringent silica particles,
primarily in the center of the nodules.
Fibrotic lesions may occur in the hilar lymph nodes and pleura.
"eggshell" calcification .
29. Advanced silicosis seen on transection of lung. Scarring has contracted the upper lobe into a
small dark mass (arrow). Note the dense pleural thickening
31. Clinical Course
Usually detected in routine chest radiographs performed on asymptomatic
workers.(fine nodularity in the upper zones of the lung is seen)
After PMF is present the disease may be progressive, even if the person is no
longer exposed.
Many individuals with PMF develop pulmonary hypertension and cor
pulmonale,
Disease is slow to kill, but impaired pulmonary function may severely limit
activity.
Silicosis is associated with an increased susceptibility to tuberculosis.
32. Asbestosis and Asbestos-Related
Diseases
occupational exposure to asbestos is linked to :
(1) parenchymal interstitial fibrosis (asbestosis)
(2) localized fibrous plaques or, rarely, diffuse fibrosis in the pleura
(3) pleural effusion
(4) bronchogenic carcinoma.
(5) malignant pleural and peritoneal mesothelioma
(6) laryngeal carcinoma.
33. Pathogenesis
There are two distinct forms of asbestos Serpentine and amphibole.
Amphibole are more pathogenic than the serpentine chrysotile.
Asbestos causes fibrosis by interacting with lung macrophages.
Asbestos probably also functions as both a tumor initiator and a promoter.
Potentially toxic chemicals adsorbed onto the asbestos fibers undoubtedly
contribute to the pathogenicity of the fibres.
34. Morphology
Marked by diffuse pulmonary interstitial fibrosis.
Asbestos bodies distinguish it from diffuse interstitial fibrosis.
Asbestosis begins in the lower lobes and subpleurally ( In contrast to
CWP and silicosis)
Contraction of the fibrous tissue distorts the native architecture,
creating enlarged airspaces enclosed within thick fibrous
walls.(honeycombed formation).
Pulmonary hypertension and cor pulmonale may result.
Pleural plaques (well-circumscribed plaques of dense collagen often
containing calcium.)
Uncommonly, asbestos exposure induces pleural effusions, which are
usually serous but may be bloody.
35. High-power detail of an asbestos body, revealing the typical beading and
knobbed ends (arrow)
36. Asbestosis. Markedly thickened visceral pleura covers the lateral and diaphragmatic surface
of lung. Note also severe interstitial fibrosis diffusely affecting the lower lobe of the lung
37. Clinical Course
Dyspnea (exertion then at rest)
Productive cough
The disease may remain static or progress to CHF, cor pulmonale, and
death
Disease manifestations more common 20 years after exposure.
The relative risk for mesotheliomas, normally a very rare tumor , is more
than 1000-fold greater.
Concomitant cigarette smoking, has no association with increased risk
of mesothelioma.
38. Drug- and Radiation-Induced
Pulmonary Diseases
Acute and chronic alterations in respiratory structure and function can result from
drugs.e.g
Bleomycin, an anticancer agent, causes pneumonitis and interstitial fibrosis
Amiodarone, an anti-arrhythmic agent, is also associated with pneumonitis and
fibrosis
Radiation pneumonitis .
Acute radiation pneumonitis-fever, dyspnea out of proportion to the volume of
irradiated lung, pleural effusion, and pulmonary infiltrates. Progress to chronic
radiation pneumonitis may occur, associated with pulmonary fibrosis.
39. Granulomatous Diseases
Sarcoidosis -bilateral hilar lymphadenopathy or lung involvement (or
both), visible on chest radiographs, is the major presenting
manifestation .
The prevalence of sarcoidosis is higher in women than in men, BLACKS
than whites .
Sarcoidosis is one of the few pulmonary diseases with a higher
prevalence among nonsmokers.
40. Aetiology and Pathogenesis
Unknown but evidence points to the1. immune dysregulation in 2.
genetically predisposed individual 3. exposed to certain environmental
agents
Cell mediated response to unidentified antigen driven by CD4= helper T
cells. CMI. These accumulate In the Intra-alveolar and interstitial space.
IL -2 and IFN-GAMMA etc from TH-1 cells, result in T-cell expansion and
macrophage activation, respectively, this eventually lead to recruitment of
additional T cells and monocytes and contribute to the formation of
granulomas.
Polyclonal hypergammaglobulinemia and anergy to common skin test
antigens occur. (TH-cell dysregulation)
Familial and racial clustering of cases and association with certain human
leukocyte antigen (HLA) genotypes (e.g., class I HLA-A1 and HLA-B8)
Viruses, mycobacteria, Borrelia, pollen have been proposed as the inciting
agent for sarcoidosis .
41. Morphology
noncaseating epithelioid granuloma.
Central necrosis unusual
Granulomatous fibrous and hyaline with chronicity.
Schaumann bodies and Asteroid bodies are also seen (not pathognomonic of
sarcoidosis) .
The granulomas predominantly involve the interstitium rather than airspaces,
with some "lymphangitic" distribution tendency.
The bronchoalveolar lavage (BAL) contains abundant CD4+T cells.
Diffuse interstitial fibrosis resulting in a honeycomb lung in 5-15%.
hilar and paratracheal lymph nodes are enlarged in 75% to 90% of patients.
42. Morphology cont…
Skin lesions : approximately 30-50% of cases of patients.
-Erythema nodosum, the hallmark of acute sarcoidosis ( Sarcoidal granulomas are
uncommon in these lesions).
-Lupus pernio.
Involvement of the eye and lacrimal glands occurs in about one-fifth to one-half of
patients
-ocular involvement: takes the form of iritis or iridocyclitis (Corneal opacities,
glaucoma, and (less commonly) total loss of vision may then develop.
-Posterior uveal tract is also affected.
-Ocular lesions are frequently accompanied by inflammation in the lacrimal
glands sicca syndrome may occur..
Unilateral or bilateral parotitis with painful enlargement of the parotid glands in <
10%.
Mikulicz syndrome, is also seen.
43. Morphology cont…
-The spleen In about three-fourths of cases it contains granulomas, in
approximately 10% it becomes clinically enlarged.
The liver demonstrates microscopic granulomatous lesions, usually in the portal
triads.
Bone marrow is reported in as many as 40% of patients, although it rarely causes
severe manifestations. Sometimes there is hypercalcemia and hypercalciuria.
Muscle involvement : is often underdiagnosed, since it may be asymptomatic.
muscle weakness, aches, tenderness, and fatigue should prompt consideration
of occult sarcoid myositis.
Muscle biopsy could be a useful tool in the diagnosis of sarcodosis.
45. Clinical Course.
In many individuals the disease is entirely asymptomatic, discovered on routine
chest films .
bilateral hilar adenopathy or as an incidental finding at autopsy
In others, lesion to other tissues may be presenting manifestations.
In about two-thirds of symptomatic cases there is a gradual appearance of
respiratory symptoms .
Lung or lymph node biopsy are often used.
Sarcoidosis follows an unpredictable course .
65% to 70% of affected individuals recover with minimal or no residual
manifestations.
20% develop permanent lung dysfunction or visual impairment.
Of the remaining 10% to 15%, most succumb to progressive pulmonary fibrosis and
cor pulmonale.
Patients presenting with hilar lymphadenopathy alone have the best prognosis,
followed by those with adenopathy and pulmonary infiltrates.
46. Hypersensitivity Pneumonitis
An immunologically mediated inflammatory lung disease (allergic alveolitis).
Results from heightened sensitivity to inhaled antigens such as moldy hay .
Immunologically mediated injury occurs at the level of alveoli.
Occupational exposures are diverse, probably have very similar pathophysiology.
Several lines of evidence suggest that hypersensitivity pneumonitis is an
immunologically mediated disease.
Increased numbers of T lymphocytes of both CD4+ and CD8+ phenotype, also
indication of a type III hypersensitivity and type IV hypersensitivity against the
implicated antigen(s).
hypersensitivity pneumonitis is an immunologically mediated response to an
extrinsic antigen that involves both immune-complex and delayed-type
hypersensitivity reactions.
progression to serious chronic fibrotic lung disease can be prevented by removal
of the environmental agent.
48. Morphology
Patchy mononuclear cell infiltrates, demonstrated in both acute and
chronic forms of hypersensitivity pneumonitis.
Lymphocytes predominate, but plasma cells and epithelioid cells are also
present.
In acute forms of the disease, variable numbers of neutrophils also may be
seen.
Interstitial noncaseating granulomas are present in more than two-thirds of
cases.
In advanced chronic cases, diffuse interstitial fibrosis occurs.
Interstitial fibrosis and obliterative bronchiolitis (late stages)
Intra-alveolar infiltrates in over 50%
50. Clinical Course
May present either :
As a may present either as an acute reaction with fever, cough,
dyspnea, and constitutional complaints 4 to 8 hours after exposure .
As a chronic disease with insidious onset of cough, dyspnea, malaise,
and weight loss.
Temporal relationship of symptoms to exposure to the incriminating
antigen in acute rxn makes diagnosis obvious.
51. Pulmonary Eosinophilia
These diverse diseases are generally of immunologic origin but are incompletely
understood .
characterized by an infiltration and activation of eosinophils, the latter by elevated levels
of alveolar IL-5.
Pulmonary eosinophilia is divided into the following categories:
1. Acute eosinophilic pneumonia with respiratory failure.
-characterized by: rapid onset of fever, dyspnea, hypoxia, and diffuse pulmonary
infiltrates on chest radiograms.
2. Simple pulmonary eosinophilia (Löffler syndrome).
-characterized by transient pulmonary lesions, eosinophilia in the blood, and a benign
clinical course.
-The alveolar septa are thickened by an infiltrate containing eosinophils and
occasional
giant cells
52. Pulmonary Eosinophilia
3. Tropical eosinophilia
-caused by infection with microfilariae, a parasite.
4. Secondary eosinophilia,
- Seen, for example, in association with asthma, drug allergies, and certain forms of
vasculitis.
1.Idiopathic chronic eosinophilic pneumonia.
-Characterized by aggregates of lymphocytes and eosinophils within the septal walls
and the alveolar spaces, typically in the periphery of the lung fields .
-accompanied by high fever, night sweats, and dyspnea.
-Good response to corticosteroids
53. Smoking-Related Interstitial
Diseases
Desquamative interstitial pneumonia (DIP) and respiratory bronchiolitis are the two eg.
Accumulation of large numbers of macrophages with abundant cytoplasm
containing dusty brown pigment (Smoker's macrophages ) in the airspaces in DIP.
- The alveolar septa are thickened by a sparse inflammatory infiltrate (usually
lymphocytes), and interstitial fibrosis, when present, is mild.
- good prognosis with excellent response to steroid therapy and smoking cessation.
Respiratory bronchiolitis .
characterized by the presence of pigmented intraluminal macrophages akin to DIP,
but in a "bronchiolocentric" distribution (first- and second-order respiratory
bronchioles).
54. Clinical course
DIP
presents in the fourth or fifth decade of life, more common males than
females 2 : 1.
Virtually all patients are cigarette smokers.
55. Desquamative interstitial pneumonia. Medium-power detail of lung to demonstrate the
accumulation of large numbers of mononuclear cells within the alveolar spaces with only
mild fibrous thickening of the alveolar walls
56. PULMONARY ALVEOLAR
PROTEINOSIS
Pulmonary alveolar proteinosis (PAP) is a rare disease
Characterized :
-Radiologically by bilateral patchy asymmetric pulmonary opacification .
-Histologically by accumulation of acellular surfactant in the intra-alveolar and
bronchiolar spaces.
Three distinct classes of this disease. acquired, congenital, and secondary PAP.
1. Acquired PAP is of unknown etiology.
-Without any familial predisposition; it represents 90% of all cases of PAP.
-Now considered to be autoimmune disorder and can occur post double lung
transplant
2. Congenital PAP is a rare cause of immediate-onset neonatal respiratory distress.
-Cause unclear
58. Morphology.
Characterized by a peculiar homogeneous, granular precipitate
within the alveoli.
Minimal inflammatory reaction
Causing focal-to-confluent consolidation of large areas of the lungs
with minimal inflammatory reaction.
On section, turbid flud exudes from these areas.
Marked increase in the size and weight of the lung
59. Pulmonary alveolar proteinosis, histologic appearance. The alveoli are
filled with a dense, amorphous, protein-lipid granular precipitate, while the
alveolar walls are normal.