The presentation is for the use of Physiotherapy students. It covers a brief introduction, classification, clinical features and general principles of management.
Fracture Healing,Introduction,Pathology&Stages,Factors influencing osteogenesis,differences in healing of fractured bone by conservative&operative management.
The presentation is for the use of Physiotherapy students. It covers a brief introduction, classification, clinical features and general principles of management.
Fracture Healing,Introduction,Pathology&Stages,Factors influencing osteogenesis,differences in healing of fractured bone by conservative&operative management.
Can read freely here
https://sethiortho.blogspot.com/
Fracture Healing and
Mechanical stability
Perren`s strain theory
Fracture healing
Indirect Healing
Direct healing
Fixation techniques and stability
Nonunion and Management
Fracture healing
Biological environment
Age
Nutritional status
Blood supply
Metabolic
Mechanical stability
Absolute
Relative
Surgical procedure
Alters biological environment
Selection of fixation
Alters mechanical environment
Mechanical Stability
Parren's strain theory
Strain
Relative deformation of a material when a given force is applied
Relative changes in the fracture gap divided by original fracture gap = L / L
Stability determines the Strain at the fracture site
Stable fixation – less strain
Unstable fixation – high strain
Large gap fracture – less strain
Cross section of the fracture-
Fracture gap strain VS cells response
The degree of inter fragmentary strain appears to govern the cellular response.
Each of these tissues is able to tolerate a different amount of strain:
Perren's strain theory….
When the inter fragmentary strain is <2% bone repair occurs by direct healing
While for intermediate amount of IFS (5–10%) the fracture heals by indirect healing.
Stain theory of healing –Indirect healing
Indirect Healing
Indirect Healing…
Hard callus formation
Indirect Healing
Remodeling Stage
Months to years
Conversion of woven bone into lamellar bone
Formation of Medullary cavity
Return of biomechanical property
Influenced by wolf law – Remodeling based on stress
Stain theory of healing…pseudo arthrosis
Complete instability
Callus is unable to form because the strain is too much for it to tolerate.
The more strain-tolerant fibrous tissue forms
Bone ends are sealed over with cortical bone
Formation of false joint with synovial fluid in the gap
Hypertrophic nonunion
Unstable fracture
Excess callus formation unable to reduce the IFS
Creates a hypertrophic non union
Direct Healing
Anatomically reduced rigid fixed fractures
Formation of cutting cones
>100,000 remodeling units work at time
Direct osteonal remodeling
Without callous
Activation
resorption by osteoclasts
osteoid formation by osteoclasts
Primary osteons
Mineralization
Direct Healing….
Fixation techniques and stability
Relative stability
Intramedullary nailing
Load sharing device
Inter fragmentary micro motion
Fracture gap strain is usually 2-10%
Body responds by forming more soft callus to try and decrease the strain
Fixation of diaphyseal fractures – strength and less duration
Relative stability
Absolute stability
Absolute stability
TBW
Lag screw fixation
Interfragmentary strain,
Nonunion and Management
Nonunion ….
Fracture is fixed rigidly but a gap is present
Direct healing may not be able to bridge the gap
The lack of strain may inhibit callus formation and secondary healing
Predispose to non-union
Management –
Stages of Bone healing and madalities to enhance bone healing Surya Vijay Singh
Bone healing, direct bone healing, indirect bone healing, primary and secondary bone healing, stages of bone healing, substitute of bone healing, autografting and allograft, fracture healing
everytime i listen to a lecture, i wonder...shall i teach someone about ignoring, or how to ignore something...this concept was actually started with a though, how to ignore a teacher...Phylosophical presentation...
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
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
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
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.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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3. Fracture
A disruption or break in
the continuity of the
structure of bone
Traumatic injuries
account for the majority
of fractures
4. How does a fracture occur?
Results from
Injury
Direct (soft tissue injury is common)
Indirect
Twisting
Compression
Bending
tension
Repetitive stress
Abnormal weakening
5. Classification of fracture
On the basis of etiology
On the basis of displacement
On the basis of communication with external
environment
On the basis of site of fracture
On the basis of fracture morphology
On the basis of stability
6. ‘
On the basis of
etiology
Traumatic
Atraumatic
Pathological
Stress
fracture
Insufficiency
fracture
Stress Fracture
Pathological Fracture
Insufficiency Fracture
Traumatic Fracture
7. Un-displaced Fracture
On the basis of displacement
Un-displaced
Displaced
Translation
Angulation
Rotation
Length
Displaced Fracture
8. On the basis of communication with external
environment
Closed Fracture
Open Fracture
9. On the basis of site of fracture
Epiphyseal fracture
Metaphyseal
Diaphyseal
Upper third
Middle third
Lower third
Junctional
10. On the basis of fracture morphology
Transverse
Spiral
Oblique
Comminuted
Impacted
Segmental
Avulsion
11. On the basis of stability
Stable
Occur when a piece of the
periosteum is intact across
the fracture
Unstable
Grossly displaced
Periosteum completely torn
14. Fracture Healing
Proliferative physiological
state
Restores the tissue to its
original physical and
mechanical properties
Influenced by a variety of
systemic and local factors
16. Primary Healing
Osteonal Healing
Involves direct attempt by the cortex
to reestablish itself
Gaps in reduction heal by vessel
ingrowth-mesenchymal cells-
osteoblasts-osteoclast cutting cones
Direct contact areas heal by cutting
cones allowing passage of vessels
Resembles normal remodelling
Occurs only with anatomic reduction &
rigid fixation
17. Secondary healing
Enchondral Healing
Response of periosteum/ external soft tissues
Recapitulation of embryonic intramembranous
ossification and endochondral ossification
Intramembraneous= peripheral to fracture
Endochondral= adjacent to fracture
Motion enhances periosteal response
External soft tissue forms bridging callus
(Periosteal bridging callus)
18. STAGES OF FRACTURE HEALING
Cortical bone(FROST 1989)
Inflammation phase
Stage of Hematoma Formation 1-
2 Days
Stage of Inflammation 2-7 Days
Stage of Granulation
Reparative phase
Stage of Soft Callus Formation 1-
3 Weeks
Stage of Hard Callus Formation 3-
6 Weeks
Remodelling Phase >8. Weeks
Stage of Remodelling stage
(Consolidation)
Stage of Modelling stage
(Remodelling)
20. Reparative phase
Primary callus response (2 weeks)
Inflammation triggers cell division and angiogenesis
Chondrocytes secrete collagen and proteoglycans
Creates fibrocartilage
Bone formation
Soft callus turns to hard callus (lamellar bone)
21. Re-modelling phase
Begins during the middle of the repair phase
Continues up to years
Allows the bone to assume its normal configuration
Wolff’s law
The stresses on the bone is directly proportional to
remodelling
22. Growth Factors
Bone Morphogenic Protein
Osteoinductive
Mesenchymal cells to osteoblasts
Transforming growth factor beta
Induces mesenchymal cells and osteoblast to produce
type II collagen
Regulates cartilage and bone formation in fracture callus
23. Insulin like growth factor II
Promote cell proliferation and matrix synthesis by
chondrocytes and osteoblasts
Responsible for formation of fracture callus
Platelet derived growth factor
Stimulate osteoblast or osteoprogenitor cell activity
Promote bone formation
25. Stability and fracture Healing
Stability determines strain
Stain
Strain is defined as change in fracture gap divided by the fracture gap (ΔL/L)
Highest fracture site strain is seen in a simple fracture
Stability
Absolute stability
Relative stability
Strain determines type of healing
Strain less than 2% results in primary bone healing (endosteal healing).
Strain 2% to 10% results in secondary bone healing (enchondral ossi cation).
Strain greater than 10% does not permit bone formation.