This document provides an overview of interstitial lung disease (ILD), also known as diffuse parenchymal lung disease. It discusses the epidemiology, diagnostic approach, classification, and treatment of ILD. The diagnostic approach involves obtaining a thorough history, physical exam, pulmonary function tests, imaging like chest X-rays and HRCT, and tissue sampling via bronchoscopy or surgical lung biopsy. ILDs can be classified as idiopathic interstitial pneumonias, granulomatous diseases like sarcoidosis, connective tissue disease-associated, and those related to occupational or environmental exposures. Treatment depends on the underlying cause but may include immunosuppression, antifibrotic drugs, managing comorbid
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.
An approach to Interstitial Lung Disease / Diffuse Parenchymal Lung DiseaseThomas Kurian
YouTube link: https://youtu.be/gPr31qrivUc
An approach to Diffuse Parenchymal Lung disease / Interstitial Lung disease with emphasis on the idiopathic causes.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
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.
An approach to Interstitial Lung Disease / Diffuse Parenchymal Lung DiseaseThomas Kurian
YouTube link: https://youtu.be/gPr31qrivUc
An approach to Diffuse Parenchymal Lung disease / Interstitial Lung disease with emphasis on the idiopathic causes.
Interstitial lung disease is a general category that includes many different lung conditions. All interstitial lung diseases affect the interstitium, a part of the lungs' anatomic structure.
Some of the types of interstitial lung disease include:
Interstitial pneumonia: Bacteria, viruses, or fungi may infect the interstitium of the lung. A bacterium called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis : A chronic, progressive form of fibrosis (scarring) of the interstitium. Its cause is unknown.
Nonspecific interstitial pneumonitis: Interstitial lung disease that's often present with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
Practical approach to interstitial lung diseases Hamdi Turkey
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
Interstitial lung diseases (ILDs) are a group of more than 200 different disorders that cause scarring in the lungs. Scar tissue in the lungs can make it harder for you to breathe normally. In ILDs, scarring damages tissues in or around the lungs’ air sacs and airways.
Practical approach to interstitial lung diseases Hamdi Turkey
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
Do Not Forget To Visit Our Pages On Facebook on the following Links:
https://www.facebook.com/groups/569435236444761/
AND
https://www.facebook.com/groups/690331650977113/
A detailed description of sarcoidosis, pulmonary in specific but also covering the other systems. a rare entity in india or a better way to say, often an overlooked disease.
Interstitial lung diseases (ILDs) are a group of more than 200 different disorders that cause scarring in the lungs. Scar tissue in the lungs can make it harder for you to breathe normally. In ILDs, scarring damages tissues in or around the lungs’ air sacs and airways.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
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
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.
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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.
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. INTRODUCTION
• Interstitial Lung Disease refers to a broad range of conditions that
have common clinical, physiological, and radiological features.
• By strict definition Interstitial lung disease involves abnormalities of
the interstitium – “the potential space between the epithelium and
capillary endothelial basement membrane within the alveolus”.
3. • Interstitial is a misleading terminology because most of these disorders
are associated with extensive alteration of airway and alveolar
architecture in addition to changes in interstitial compartment.
• For this reason Diffuse Parenchymal Lung Disease or DPLD is the
better term
4. EPIDEMIOLOGY
• Incidence ranges from 3-26/1,00,000 per year.
• Prevalence of preclinical and undiagnosed ILD is estimated to be 10
times that of clinical recognized disease.
• IPF is the most common form representing at least 30 percent of the
incident cases.
16. • H/o wheezing- hypersensitivity pneumonitis, eosinophilic pneumonia
or sarcoidosis.
• H/o pleuritic chest pain- serositis in a patient with CTD, or
pneumothorax from LAM, LCH.
• Hemoptysis- diffuse alveolar hemorrhage
17. AGE
• IPF most commonly occurs
in patients aged >60 years
• <50 years rare
• 20-40 years
1) Sarcoidosis
2)CTD associated ILD
3)LAM
4)PLCH
GENDER
Female-premenopausal
1.LAM
2.Tuberous scelerosis
Men-
1.RA
2.IPF and occupational
related ILDs
18. Time Course of Disease Onset
Acute: [days to week]
• 1.AIP
• 2.eosinophilic pneumonia
• 3.hypersensitivity pneumonitis
Subacute : [weeks to month]
1.sarcoidosis
2.drug induced ILD
3.Alveolar hemorrhage syndrome
4.COP
Chronic: months to years
• 1.sarcoidosis
• 2.PLCH
• 3.CTD
19. PAST MEDICAL HISTORY
• Prior diagnosis of connective tissue disease
• Case of HIV disease- lymphocytic interstitial pneumonia (LIP) are
common.
• h/o acute or chronic kidney disease might suggest underlying
vasculitis, pulmonary– renal syndromes, or CTD.
• h/o liver disease could suggest sarcoidosis, primary biliary cirrhosis.
• h/oAsthma and allergic rhinitis - GPA
20. MEDICATION
HISTORY
• Nitrofurantoin
• Amiodarone
• Bleomycin
• Methotrexate
• Azathioprine
• Rituximab
FAMILY
HISTORY
• Percentage of familial pulmonary
firbrosis varies 5 to 20 %
1.non specific interstitial pneumonia
2.desquamative interstitial pneumonia
3.unusual interstitial pneumonia
28. HRCT
• More sensitive than chest radiograph
• Radiographic Characteristics of the UIP Pattern “Definite UIP”
• Peripheral, subpleural distribution
• Basilar predominance
• Reticular markings and traction bronchiectasis
• Honeycombing
• Absence of inconsistent features
29. Pulmonary Function Test
• Most forms of ILD demonstrates a restrictive ventilatory defect due to
decreased compliance and increased recoil of the lung parenchyma.
• Presence of obstruction suggests either concomitant obstructive lung
disease, or the presence of an airway-centered lung ILD such as LCH,
LAM or sarcoidosis.
30. BRONCHOSCOPY
• Useful in the diagnosis of DPLD.
• Inspection of the upper and lower airways, bronchoalveolar lavage
(BAL), and the performance of transbronchial lung biopsy.
• BAL:
1)Cell count and differential,
2) Cytology
3) Viral assays
4) Microbiologic cultures
31. • Blood lavage specimens- diffuse alveolar hemorrhage
• milky white BAL fluid- pulmonary alveolar proteinosis
• BAL eosinophilia (>25%)- acute eosinophilic pneumonia
• BAL lymphocytosis - granulomatous ILD, suggestive of
hypersensitivity pneumonitis, drug reaction, or cellular NSIP
32. • Positive lymphocyte proliferation assay in chronic beryllium disease.
• Asbestos bodies in asbestosis.
• CD1a positive cells on flow cytometry may lead to a diagnosis of
LCH.
• In the immunocompromised host, BAL fluid is highly sensitive for the
diagnosis of bacterial, viral, fungal, and mycobacterial diseases.
33. SURGICAL LUNG BIOPSY
• Despite a high yield in certain forms of lung disease, the utility of
transbronchial biopsy for most of the IIP (such as IPF, NSIP, and LIP)
is low and surgical biopsy is often required for accurate diagnosis.
• The usual technique is video-assisted thoracoscopic surgery (VATS)
that has a low morbidity and mortality in selected populations.
35. UIP or IPF
• MC of all chronic ILD
• Typical c/f presentation
• Median survival approximately 3 years,
depending on stage at presentation.
• B/L Reticular bibasilar and subpleural opacities.
minimal ground-glass and variable honeycomb
change.
• Type I pneumocytes are lost, and there is
proliferation of alveolar type II cells. "Fibroblast
foci" of actively proliferating fibroblasts and
myofibroblasts.
44. Coal worker pneumoconiosis
Rounded opacities between 1 and 5 mm (upper and
middle zones)
small irregular and linear opacities Progressive
massive fibrosis almost always starts in an upper
zone Calcification is not a feature
Cavitation of PMF can occur
Caplan's syndrome is the name given to the
combination of rheumatoid disease and several
round nodules (usually 1 to 5 cm in diameter) in the
lungs of a coal miner.
45. Silicosis
Active molucule:free silica or crytalline(quartz).
Clues to diagnosis : Micronodular pattern and crazy paving
pattern on HRCT
2 forms:a)Acute silicosis: within 2 yrs
b)Chronic silicosis:10-30yrs
Simple silicosis : Upper lobes Small multiple nodules Egg
shell calcification
Complicated : >1 cm nodules
BAL yields a PAS-positive milky white fluid
A/w- increased incidence of TUBERCULOSIS
46. Asbestosis
Clues to diagnosis X Ray: reticular interstitial
pattern pleural plaques ( lower lung field ,
cardiac border and diaphragm ) Irrregular linear
opacities first noted in lower lung fields.
HRCT : Distinct subpleural curvilinear opacities
5-10 mm length parallel to pleural surface
BAL: Asbestos bodies
Most common asbestos-related cancer-
Adenocarcinoma of Lung.
Mesotheliomas –Tumors that arise from
mesothelial cells that line the pleural cavities
47. ILD in vasculitis
Suspect if Mononeuritis mutiplex Renal involvement Skin
lesions haemoptysis
MC seen is Wegeners Granulomatosis
X ray : consolidation, typically resolving within a matter of days,
multiple abcesses
HRCT : ground-glass partial alveolar filling. Hb : anaemia ( iron
defeciency )
BAL :- frank blood-staining in sequential lavage (acute
presentation) and numerous macrophages containing iron,
identified by Perl's stain
DLCO :- may be increased in acute conditions but is chronically
low
51. Granulomatous ILD
• 1) Sarcoidosis :
• A multisystemic disoder of unknown cause having Non caseating granuloma in
lungs and other systems.
• F>M(20-40yrs)
• DIAGNOSIS-
• 1) Chest X-ray- B/L- Hilar adenopathy(Bat-wing type)
• 2)ACE level
• 3) sr Ca2+
• 4)Transbronchial Biopsy to see Non-caseating granuloma(IOC)
• Treatment:a) self resolving over 2-3 yrs b) Corticosteroids (prednisone)
c) Methotraxate
• 2) Hypersensitivity Pneumonia
60. Treatment objectives in ILD
• 1. Provide symptom-relief
• 2. Slow down disease progression
• 3. Prevent complications
• 4. Improve quality of life
• 5. Prolong survival
• 6. Prevent treatment-complications
• 7. End-of-Life care and palliative treatment
61. Treatment
• REMOVAL FROM EXPOSURES
• IMMUNOSUPPRESSIVE THERAPY
• ANTIFIBROTIC DRUGS
• TREATMENT OF COMORBIDITIES
• PALLIATIVE CARE
• LUNG TRANSPLANTATION
62. Removal From Exposures
• Drug reaction is suspected- should be discontinued
• Mold growth, removal of birds from the home, extensive cleaning of
upholstery, window coverings, and ventilation systems.
• Occupational exposures- avoided
63. Immunosuppressive Therapy
• Some forms of ILD, including COP, CTD– associated ILD, and
sarcoidosis, shows favorable response to steroids and other
immunosuppressive agents.
• When a more prolonged course of therapy is anticipated, azathioprine
or cyclophosphamide, permit low dose of steroids.
• If no clinical improvement is seen after 3 to 6 months of therapy,
discontinuation of immunosuppressive therapy should be strongly
considered.
64. Antifibrotic Drugs
• Useful in progressive fibrotic lung diseases.
• 1) Pirfenidone, a small-molecule drug which have antifibrotic
properties.
• stabilize lung function.
• 1) Nintedanib- anti PDGF
65. Lung Transplant
• Most patients with ILD referred for lung transplantation have IPF-
advanced stage.
• a severely impaired DLCO (< 39%) as well as advanced fibrosis on
HRCT predict poor survival and are considered to be triggers for
active listing.
