Pneumoconiosis refers to chronic lung diseases caused by inhaling certain particles. The pathogenesis depends on factors like particle size, shape, solubility and exposure amount. Small particles can cause acute lung injury while large particles induce fibrosis. Common forms include silicosis from silica exposure seen in miners, asbestosis from asbestos exposure historically seen in insulators, and coal workers' pneumoconiosis from coal dust exposure in miners which can lead to emphysema. Diseases are characterized by nodular lesions and fibrosis. Complications can include tuberculosis infection and increased lung cancer risk.
Pneumoconiosis- dust with size and different types of occupational pneumoconic diseases, clinical features, diagnosis and prevention of pneumoconiosis.
Pneumoconiosis- dust with size and different types of occupational pneumoconic diseases, clinical features, diagnosis and prevention of pneumoconiosis.
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/
Complexities of occupational and environmental lung diseases, exploring their causes, symptoms, diagnosis, and prevention measures. For more information please contact us: 9779030507.
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)
Asbestos - Environmental Health - What to know?.pptxMuhammad Mozaik
This was an assignment in the second semester of Public Health school, that we had been given to talk about toxic materials and their effects on Health.
I chose the color Blue in these slides, to match it with Blue Asbestos.
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/
Complexities of occupational and environmental lung diseases, exploring their causes, symptoms, diagnosis, and prevention measures. For more information please contact us: 9779030507.
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)
Asbestos - Environmental Health - What to know?.pptxMuhammad Mozaik
This was an assignment in the second semester of Public Health school, that we had been given to talk about toxic materials and their effects on Health.
I chose the color Blue in these slides, to match it with Blue Asbestos.
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
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.
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
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
2. Pneumoconiosis-
• Pneumoconioses encompass a group of chronic fibrosing diseases of
the lung resulting from exposure to organic and inorganic
particulates, most commonly mineral dust
3.
4. • Pathogenesis-
(1) amount of dust
(2) size, shape, and buoyancy of the particles
o small particles,1 to 5 μm –acute lung injury
o Large particle-evoke fibrosing collagenous pneumoconioses
(3) particle solubility and physiochemical reactivity-small particles composed of
injurious substances of high solubility
(4) additional effects of other irritants
5. • particles stimulate resident innate immune cells in the lung
• invokes systemic response
• a genetic predisposition
8. Silicosis
• Silicosis is the most common pneumoconiosis in the world, and
crystalline silica (e.g., quartz) is the usual culprit
• caused by inhalation of proinflammatory crystalline silicon dioxide
9. Pathogenesis-
crystalline and amorphous forms
• crystalline forms (including quartz, cristobalite, and tridymite)- much more
fibrogenic
• Phagocytosed silica crystals activate the inflammasome, leading to the release of
inflammatory mediators, particularly IL-1 and IL-18
10. • disease may continue to worsen even if the patient is no longer
exposed
• It is associated with an increased susceptibility to tuberculosis
• Patients with silicosis have double the risk for developing lung cancer
11. SIMPLE NODULAR SILICOSIS: most common form of silicosis
PROGRESSIVE MASSIVE FIBROSIS: nodular masses greater than 2 cm
in diameter, in a background of simple silicosis
• bilateral
• 5–10 cm
• Central cavitation
12. ACUTE SILICOSIS:
• heavy exposure to finely particulate silica during sandblasting or boiler scaling
• it is associated with diffuse fibrosis of the lung
• Silicotic nodules are not found
• Microscopically,Dense eosinophilic material accumulates in alveolar spaces
16. Coal Workers’ Pneumoconiosis
• caused by inhalation of coal particles and other admixed forms of
dust
• Contaminating silica in the coal dust favour progressive disease
• develop emphysema and chronic bronchitis independent of smoking
17. MORPHOLOGY
• Anthracosis is the most innocuous coal-induced pulmonary lesion in coal miners
coal macules (1 to 2 mm in diameter) and somewhat larger coal nodules
• Coal macules consist of carbon-laden macrophages
• Complication- centrilobular emphysema
Complicated coal workers’ pneumoconiosis (progressive massive fibrosis)
• intensely blackened multiple scars 1 cm or larger
• Microscopy- dense collagen, pigment ,+/- necrosis
18. • Caplan syndrome- combination of rheumatoid arthritis (RA) and pneumoconiosis
that manifests as intrapulmonary nodules, which appear homogenous and well-
defined on chest X-ray.
• Nodular lesions are large (1–10 cm), multiple, bilateral
• Caplan nodule- combination of silicotic and rheumatoid nodule
19.
20. Asbestos-Related Diseases
• Asbestos (Greek, “unquenchable”) includes a group of fibrous silicate minerals
that occur as thin fibers
Chrysotile accounts for the bulk of commercially used asbestos
The amphiboles include amosite, crocidolite, tremolite, actinolite and
anthophyllite.
21. • ASBESTOSIS: Asbestosis is diffuse interstitial fibrosis resulting from
inhalation of asbestos fibers
• historically seen in asbestos miners, millers and insulators
22. ETIOLOGIC FACTORS:
• Asbestos fibers may be long (up to 100 μm) but thin (0.5–1 μm), so
their aerodynamic particle diameter is small
• They deposit in distal airways and alveoli, particularly at bifurcations
of alveolar ducts
• first lesion is an alveolitis
23. PATHOLOGY:
• bilateral, diffuse interstitial fibrosis
• asbestos bodies in the lung In early stages, fibrosis
• end-stage or “honeycomb” lung
27. • BENIGN PLEURAL EFFUSION
• PLEURAL PLAQUES-
most common manifestation of asbestos
well-circumscribed plaques of dense collagen often calcified
• DIFFUSE PLEURAL FIBROSIS
• ROUNDED ATELECTASIS
• MESOTHELIOMA
• CARCINOMA OF THE LUNG
28. Berylliosis
• pulmonary disease that follows the inhalation of beryllium
• materials in aerospace, industrial ceramics and nuclear industries
29. Pathology
• Acute chemical pneumonitis or a chronic pneumoconiosis
• 10% progress to chronic disease, Chronic berylliosis
• Exposure may be minimal and brief
• Microscopically, Multiple noncaseating granulomas are distributed
along the pleura, septa and bronchovascular bundles
30. • may progress to end-stage fibrosis and honeycomb lung
• associated with an increased risk of lung cancer
32. Talcosis
• Prolonged and Heavy Exposure to Talc Dust
• magnesium silicates
• lubricants, and in cosmetics and pharmaceuticals
• Associated minerals such as silica may contribute to the fibrotic
changes
• Tiny nodules to severe fibrosis
• Foreign body granulomas associated with birefringent plate-like talc
particles
Mineral dust is mainly constituted of the oxides (SiO2, Al2O3, FeO, Fe2O3, CaO, and others) and carbonates (CaCO3, MgCO3) that constitute the Earth's crust.
1-cigarette smoking,
that impairs mucociliary clearance significantly increases
the accumulation of dust in the lungs.
Il 1il18 prion inflammasome is a multiprotein intracellular complex that activates the highly pro-inflammatory cytokines interleukin-1b (IL-1b) and IL-18.
because crystalline silica inhibits the ability of pulmonary macrophages to kill phagocytosed mycobacteria
Advanced silicosis. Scarring has contracted the upper lobe into a small dark mass (arrow). Note the dense pleural thickening.
large area of dense fibrosis containing entrapped carbon particles.
Microscopy-central area of whorled collagen fibers with a more peripheral zone of dust-laden macrophages
Progressive massive fibrosis superimposed on coal workers’ pneumoconiosis. The large, blackened scars are located principally in the upper lobe. Note the extensions of scars into surrounding parenchyma and
retraction of adjacent pleura
The lung shows patchy, dense, interstitial fibrosis.
These ferruginous bodies are golden brown and beaded, with a central, colorless, nonbirefringent core fiber. Asbestos bodies are encrusted with protein and iron.
The dome of the diaphragm is covered by a pearly white, nodular plaque.
. A noncaseating granuloma consists of anodular collection of epithelioid macrophages and multinucleated giantcells.