The document discusses the processes of wound healing through regeneration and repair. Regeneration involves the proliferation of parenchymal cells to restore original tissues, while repair involves proliferation of connective tissue elements and fibrosis. Repair was described as occurring through granulation tissue formation and wound contraction. The phases of wound healing were explained as inflammation, clearance and ingrowth of granulation tissue. Primary and secondary wound healing were also summarized.
may start early after tissue damage
regeneration
by parenchymal cells of the same type
reparation
replacement by connective tissue (fibrosis)
result - scar
may start early after tissue damage
regeneration
by parenchymal cells of the same type
reparation
replacement by connective tissue (fibrosis)
result - scar
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Dentist in pune.(BDS. MDS) - Dr. Amit T. Suryawanshi. Wound healing in Dentis...All Good Things
entist in pune. (BDS. MDS) - Dr. Amit T. Suryawanshi. Seminar- Wound healing in dentistry.
Email ID- amitsuryawanshi999@gmail.com
Contact -Ph no.-9405622455
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BONE CHANGES AFTER TOOTH EXTRACTION /orthodontic courses by Indian dental aca...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The variety of wounds present challenges to the physician to select the most appropriate management to facilitate healing.
A complete wound history along with knowledge of the healing potential of the wound, as it relates to the specific medical and environmental considerations for each patient, provides the basis of decision making for wound management.
It is essential to consider each wound individually in order to create the optimal conditions for wound healing.
Understanding of wound healing is as important as knowing the pathogenesis of disease, because satisfactory wound healing is the ultimate goal of treatment.
If we are able to understand the mechanism of wound healing, we can design treatment approaches that maximize favorable conditions for wound healing to occur.
Wound healing refers to a living organism's replacement of destroyed or damaged tissue by newly produced tissue. In undamaged skin, the epidermis and dermis form a protective barrier against the external environment
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
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.
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.
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
- 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
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. The body response to injury in an attempt to
restore normal structure and function.
Involves 2 distinct processes:
◦ Regeneration: healing takes place by proliferation
of parenchymal cells and usually results in complete
restoration of the original tissues.
◦ Repair: healing takes place by proliferation of
connective tissue elements resulting in fibrosis and
scarring.
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3. Repair is the replacement
of injured tissue by
fibrous tissue.
Two processes are
involved in repair:
◦ Granulation tissue
formation;
◦ Contraction of wounds.
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4. Th3 phases are observed in the formation of
granulation tissue
PHASE OF INFLAMMATION
PHASE OF CLEARANCE
◦ Combination of proteolytic enzymes liberated from
neutrophils, autolytic enzymes from dead tissues
cells
◦ phagocytic activity of macrophages clear off the
necrotic tissue, debris and red blood cells.
PHASE OF INGROWTH OF GRANULATION
TISSUE
◦ 2 main processes: angiogenesis or
neovascularisation, and fibrogenesis
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5. Wound starts contracting after 2-3 days and
the process is completed by the 14th day.
Reduced by approximately 80% of its original
size
This process aids in rapid healing – lesser
surface area of the injured tissue has to be
replaced
It takes place in following step : Dehydration
and formation of myofibroblast (intermediate
between fibroblast and muscle cells.
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7. Healing of skin wounds -
classical example of
combination of
regeneration and repair
It can be accomplished in
one of the following
two ways:
◦ Healing by First intention
(primary union)
◦ Healing by Second intention
(secondary union)
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8. Healing of a wound which has the following
characteristics:
◦ clean and uninfected;
◦ surgically incised;
◦ without much loss of cells and tissue; and
◦ edges of wound are approximated by surgical sutures
• The incision causes only focal disruption of
epithelial basement membrane continuity and
death of a relatively few epithelial and
connective tissue cells.
• As a result, epithelial regeneration
predominates over fibrosis.
• A small scar is formed, but there is minimal
wound contraction
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9. Within 24 hours,
◦ neutrophils are seen at the incision margin, migrating
toward the fibrin clot.
◦ Basal cells at the cut edge of the epidermis begin to
show increased mitotic activity.
Within 24 to 48 hours
◦ epithelial cells from both edges have begun to migrate
and proliferate along the dermis, depositing basement
membrane components as they progress.
◦ The cells meet in the midline beneath the surface scab,
yielding a thin but continuous epithelial layer
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10. Neutrophils have been largely replaced by
macrophages,
Granulation tissue progressively invades the
incision space.
Collagen fibers are now evident at the
incision margins, but these are vertically
oriented and do not bridge the incision.
Epithelial cell proliferation continues, yielding
a thickened epidermal covering layer.
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11. neovascularization reaches its peak as
granulation tissue fills the incisional space.
Collagen fibrils become more abundant and
begin to bridge the incision.
The epidermis recovers its normal thickness
as differentiation of surface cells yields a
mature epidermal architecture with surface
keratinization.
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12. There is continued collagen accumulation and
fibroblast proliferation.
The leukocyte infiltrate, edema, and
increased vascularity are substantially
diminished.
The long process of "blanching" begins,
accomplished by increasing collagen
deposition within the incisional scar and the
regression of vascular channels.
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A, The incised wound as well as suture track on either side are filled with
blood clot and there is inflammatory response from the margins.
B, Spurs of epidermal cells migrate along the incised margin on either side as
well as around the suture track. Formation of granulation tissue also begins
from below.
C, Removal of suture at around 7th day results in scar tissue at the sites of
incision
14. Healing of a wound having the following characteristics:
◦ open with a large tissue defect, at times infected;
◦ having extensive loss of cells and tissues;
◦ the wound is not approximated by surgical sutures but is left
open.
• The basic events in secondary union are similar
to
primary union
• Differ in having a larger tissue defect which has
to be bridged.
• Hence healing takes place from the base
upwards as well as from the margins inwards
• Results in a large and sometimes ugly scar
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16. Initial haemorrhage.
◦ As a result of injury, the wound space is filled with blood and
fibrin clot which dries.
Inflammatory phase
◦ initial acute inflammatory response
◦ followed by appearance of macrophages which clear off the debris
as in primary union.
Epithelial changes.
◦ As in primary healing, the epidermal cells from both the margins
of wound proliferate and migrate
◦ into the wound in the form of epithelial spurs till they meet in the
middle and re-epithelialise the gap completely.
◦ However, the proliferating epithelial cells do not cover the
surface fully until granulation tissue from base has started
filling the wound space
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17. • Granulation tissue
Main bulk of secondary healing is by granulations.
Granulation tissue is formed by proliferation of
fibroblasts and neovascularisation from the adjoining
viable elements.
Its deep red, granular and very fragile.
With time, the scar on maturation becomes pale and
white due to increase in collagen and decrease in
vascularity.
Specialised structures of the skin like hair follicles and
sweat glands are not replaced unless their viable
residues remain which may regenerate.
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18. • Wound contraction.
Its an important feature of secondary healing, not seen in
primary healing.
Due to the action of myofibroblasts present in granulation
tissue, the wound contracts to one-third to one-fourth of
its original size.
Wound contraction occurs at a time when active
granulation tissue is being formed.
• Presence of infection
Bacterial infection may delays the process of healing due
to release of bacterial toxins
These provoke necrosis, suppuration and thrombosis.
Debridement: Surgical removal of dead and necrosed
tissue, helps in preventing the bacterial infection of open
wounds.
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A, The open wound is filled with blood clot and there is inflammatory
response at the junction of viable tissue.
B, Epithelial spurs from the margins of wound meet in the middle to cover
the gap and separate the underlying viable tissue from necrotic tissue at the
surface forming scab.
C, After contraction of the wound, a scar smaller than the original wound is
left.
22. Infection
Implantation : epidermal cyst
Pigmentation: rust-like colour due to staining with
haemosiderin.
Deficient scar formation: inadequate formation of
granulation tissue
Incisional hernia
Hypertrophied scars and keloid formation: Excessive
formation of collagen in healing
Excessive contraction: Dupuytren’s (palmar) contracture,
plantar contracture and Peyronie’s disease (contraction of
the cavernous tissues of penis).
Neoplasia. Rare, e.g. squamous cell carcinoma in Marjolin’s
ulcer i.e. a scar following burns on the skin
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KELOID EPIDERMAL CYST
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Pigmentation of Wound Dupuytren’s (palmar) contractur
27. Fracture results in well defined tissue response to
remove the debris and to re-establish vascular
supply and to produce a new skeletal matrix.
The timing and histology of process of healing is
dependent on location of fracture and local and
systemic factors.
Depending on this factors healing take place in
either of two ways, i.e.:
◦ Primary Bone healing
◦ Secondary bone healing
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28. It take place when in following condition
◦ Excellent anatomic reduction
◦ Minimal or no mobility
◦ Good vascular supply at fracture site
• It occurs in two different ways i.e.:
Gap Healing
Contact Healing
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29. Even with excellent rigid
fixation, a perfect
anatomic reduction rarely
exist due to deforming
forces like muscle pull
and function
In such cases blood
vessels from periosteum,
endosteum and haversian
canal invade the gap,
bridging mesenchymal
osteoblastic precussors.
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30. Bone is directly deposited on the fracture
fragmenst without resorption and cartilage
formation.
Gap = < 0.3 mm – lamellar bone forms
directly.
Gap = 0.3 – 1mm woven bone forms first
followed by lamellar bone
Healing takes place over 6 weeks.
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31. When there is adequate contact, essentially a
zero gap, then healing take place through
contact heatling.
◦ There is Osteoclastic activity at the fracture ends which
results in bone resorption and finally remodelling by
Bone metabolising unit (BMU), Bone repair unit (BRU),
and bone remodelling unit (BRU).
• There is formation of osteon which forms
the bone again between gap created in
remodelled bone.
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32. It take place in fracture without surgical
intervention and after semi-rigid fixation.
It takes place in four stages:
◦ Intermediate reaction
◦ Procallus formation
◦ Osseous callus formation
◦ Remodelling
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A, Haematoma formation and local inflammatory response at the fracture site.
B, Ingrowth of granulation tissue with formation of soft tissue callus.
C, Formation of procallus composed of woven bone and cartilage with its
characteristic fusiform appearance and having 3 arbitrary components —
external, intermediate and internal callus.
D, Formation of osseous callus composed of lamellar bone following clearance
of woven bone and cartilage.
E, Remodelled bone ends; the external callus cleared away. Intermediate callus
converted into lamellar bone and internal callus developing bone marrow cavity
34. Robbinson's basic pathology 8 ed
Harsh Mohan - Textbook of Pathology 6th Ed.
Color atlas of pathology
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