The document discusses wounds and the wound healing process. It defines a wound as a break in the skin or tissue integrity caused by injury. Wounds are classified based on various factors like cleanliness, depth, and type. The healing process involves three phases - inflammatory, proliferative, and remodeling. The inflammatory phase prepares the wound for healing. In proliferation, new tissue is formed through granulation. Remodeling provides increased strength over months. Healing occurs through regeneration or repair, with the former restoring original tissue and the latter resulting in scar tissue. Growth factors play important roles in the complex cellular cascade of wound healing.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Localised protective response elicited by injury or destruction of tissues which serves to destroy , dilute or wall off (sequester) both injurious agent and the injured tissues (Dorlands medical dictionary). Cardinal signs of inflammation
Celsus 1st century AD
Rubor – redness
Tumor -swelling
Calor -heat
Dolor -pain
Virchow
“function laesa”- loss of function
Jbhzj gccycgccychcvycyxfthvyc4dygih8h me feel so special daughter is in the given questions and answers in love you so much to do but I have to be with me and my friends and my friends are not at
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Localised protective response elicited by injury or destruction of tissues which serves to destroy , dilute or wall off (sequester) both injurious agent and the injured tissues (Dorlands medical dictionary). Cardinal signs of inflammation
Celsus 1st century AD
Rubor – redness
Tumor -swelling
Calor -heat
Dolor -pain
Virchow
“function laesa”- loss of function
Jbhzj gccycgccychcvycyxfthvyc4dygih8h me feel so special daughter is in the given questions and answers in love you so much to do but I have to be with me and my friends and my friends are not at
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
Subscribe our channel on youtube - Copy and paste this URL. https://www.youtube.com/channel/UC_gylEXTrjmEbbOTSXjuZ4Q/videos?view_as=public
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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.
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.
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
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
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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.
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
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.
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.
3. WOUND
It is a circumscribed injury which is caused by external
force & it can involve any tissue & organ
A wound is a break in the skin integrity or tissues often
which may be associated with disruption of the
structure & function
A cut or break in the skin continuity of any tissue,
caused by injury or operation
6. CLASSIFICATION BASED ON THE TYPE OF
WOUND
Clean incised wound
Lacerated wound
Bruising or contusion
Hematoma
Puncture wound
Abrasion
Crush injury
Injuries to bone & joint (open/ closed)
Injuries to nerve (clean cut or crush)
Injuries to arteries & veins
Penetrating wounds
7.
8.
9.
10.
11.
12.
13. CLASSIFICATION BASED ON THICKNESS OF
WOUND
Superficial wound
Partial thickness
Full thickness
Deep wounds
Complicated wounds
Penetrating wounds
18. HEALING
Healing is the body’s response to injury in an attempt to
restore normal structure & function.
The process of healing involves 2 distinct processes:
Regeneration
Repair
19. REGENERATION
Is when healing takes place by proliferation of
parenchymal cells & usually results in complete
restoration of the original tissues.
The goal of all surgical procedures should be
regeneration which returns the tissues to their normal
microstructure & function.
20. REPAIR
It is a healing outcome in which tissues do not return
to their normal architecture & function.
Repair typically results in the formation of scar tissue.
21. During healing, a complex cascade of cellular events
occur to achieve resurfacing, reconstitution and
restoration of tensile strength of injured tissue
Wound healing occurs in 3 phases
1. Inflammatory phase
2. Proliferative phase
3. Remodeling phase
22. INFLAMMATORY PHASE
A. Immediate to 2-5 days
B. Hemostasis
✓ Vasoconstriction – damaged blood vessels constrict
✓ Hemostasis is achieved by formation of platelet plug &
activation of extrinsic & intrinsic clotting pathways.
✓ Formation of a provisional fibrin matrix
C. Recruitment of inflammatory cells into the wound by
potent chemoattractants
23. EARLY EVENTS IN INFLAMMATION
Fibrin and fibronectin form a lattice that provides scaffold
for migration of inflammatory, endothelial, and
mesenchymal cells.
Neutrophilic infiltrate appears: removes dead tissue &
prevent infection.
Monocytes/macrophages follow neutrophils: orchestrated
production of growth factors & phagocytosis.
24. LATE EVENTS IN INFLAMMATION
Entry of lymphocytes.
Appearance of mast cell
25. PROLIFERATIVE PHASE
2 days to 3 weeks
Granulation tissue formation (composed of
fibroblasts,macrophages and endothelial cell)
Angiogenesis
Contraction: Wound edges pull together to reduce the
defect
Epithelialization
Epithelial cells migrate across the new tissue to form a
barrier between the wound and the environment
26. MESENCHYMAL CELL PROLIFERATION
Fibroblasts are the major mesenchymal cells involved in
wound healing, although smooth muscle cells are also
involved.
Macrophage products are chemotactic for fibroblasts.
PDGF, EGF, TGF, IL-1, lymphocytes are as well.
Replacement of provisional fibrin matrix with type III
collagen.
27. ANGIOGENESIS
Angiogenesis reconstructs vasculature in areas
damaged by wounding, stimulated by high lactate
levels, acidic pH, decreased O2 tension in tissues.
Recruitment & assembly of bone marrow derived
progenitor cells by cytokines is the central theme.
EGF-1 is most potent angiogenic stimulant identified.
Heparin is also an important as cofactor, TGF- alpha,
beta, prostaglandins also stimulate.
28. EPITHELIALIZATION
Basal cell layer thickening, elongation, detachment &
migration via interaction with ECM proteins via
integrin mediators.
Generation of a provisional BM which includes
fibronectin, collagens type 1 and 3
Epithelial cells proliferation contributes new cells to the
monolayer. Contact inhibition when edges come
together.
29. REMODELING PHASE
3 weeks to 2 years
New collagen forms which increases the tensile strength
of the wound
19 types identified. Type 1(80-90%) most common, found
in all tissue. The primary collagen in a healed wound.
Type 3(10-20%) seen in early phases of wound healing.
Type V smooth muscle, Types 2,11 cartilage, Type 4 in
BM.
30. REMODELLING
The number of intra and intermolecular crosslinks
between collagen fibers increases dramatically.
A major contributor to the increase in wound breaking
strength
Quantity of Type 3 collagen decreases replaced by Type 1
collagen
Remodeling continues for 12 months, so scar revision
should not be done prematurely.
31. WOUND CONTRACTION
Begins approximately 4-5 days after wounding by action
of myofibroblasts.
Generally occurs in large surface wounds.
Represents centripetal movement of the wound edge
towards the centre of the wound.
Maximal contraction occurs for 12-15 days, although it
will continue longer if wound remains open.
32. WOUND CONTRACTION
The wound edges move toward each other at an average
rate of 0.6 to .75 mm/day.
Wound contraction depends on laxity of tissues, so a
wound on the soft area will contract faster than a wound
on the scalp or pretibial area.
Wound shape also a factor, square is faster than circular.
33. WOUND STRENGTH
Skin wounds
At the end of first week, wound strength is approximately
10% of unwounded skin
Wound strength increases rapidly over next 4 weeks and
then slows down at approximately at third month,
reaches a plateau at about 70- 80% of the tensile strength
of unwounded skin
Scar tissue is never as strong as the original tissue
34. IMPORTANT GROWTH FACTORS
RESPONSIBLE FOR WOUND HEALING
Platelet derived growth factor:
Promotes migration and proliferation of fibroblasts
Is chemotactic for monocytes
Epidermal growth factor
Promotes growth of endothelial, epithelial cells and
fibroblasts
35. GROWTH FACTORS IN WOUND HEALING
Fibroblast growth factor:
✓ Promotes synthesis of ECM proteins including
fibronectin.
✓ Chemotactic for fibroblasts and endothelial cells
✓ Promotes angiogenesis
Vascular Endothelial Growth Factor (VEGF)
✓ Angiogenesis
Macrophage derived growth factors
✓ IL-1 and TNF
✓ Promote proliferation of fibroblasts and endothelial cells.
36. WOUND HEALING
Wound healing is accomplished in one of the following
two ways:
➢ Healing by first intention (primary union)
➢ Healing by second intention (secondary union)
37. HEALING BY FIRST INTENTION (PRIMARY
UNION)
❑ Occurs in clean, incised wounds with good apposition
of the edges – particularly planned surgical incisions
(clean wounds – no infections or foreign bodies)
❑ 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
38. SEQUENCE OF EVENTS
Immediate:
❖ The narrow incisional space rapidly fills with fibrin
clotted blood
❖ Dehydration at the surface produces a scab to cover and
protect the healing repair site
Within 24 hrs
❖ Movement and proliferation of epithelial cells across the
wound resulting in a thin, but continuous epithelial layer
❖ Early inflammation close to the edges (neutrophils)
39. SEQUENCE OF EVENTS CONT…
2-3 days
❖ Neutrophils replaced by macrophages
❖ Macrophages remove the blood clot
❖ Proliferation of epithelial cells
❖ Fibroblastic activity
40. SEQUENCE OF EVENTS CONT…
10-14 days
❖ Scab loose (aka dry clot)
❖ Epithelial covering complete
❖ Fibrous union of edges
❖ Wound still weak
❖ vascularization
41. BY THE END OF THE FIRST MONTH
❖ Scar comprises of a cellular connective tissue devoid of
inflammatory infiltrate, covered by intact epidermis
❖ Dermal appendages destroyed in the line of incision are
permanently lost
❖ Tensile strength of the wound increases and
42. HEALING BY SECOND INTENTION
(SECONDARY UNION)
This occurs in open wounds, particularly when there has
been significant loss of tissue, necrosis or large wounds
with irregular margins
Regeneration of parenchymal cells cannot completely
reconstitute the original architecture
Abundant granulation tissue grows in from the margin to
complete the repair
Granulation tissues consists of:
✓ ECM fibroblasts
✓ Macrophages, neutrophils
✓ New blood vessels
43. SEQUENCE OF EVENTS
Early
➢ Cavity fills with blood & fibrin clot.
➢ Acute inflammation commences at junction of living tissue.
A few days
➢ Scab dries out
➢ A single sheet of epithelial cells is being pushed between
the surface debris & the underlying living tissue.
➢ New capillary loops bring macrophages, neutrophills &
fibroblasts
47. LOCAL FACTORS THAT DELAY/RETARD
WOUND HEALING
➢ Infection : Most important cause of delayed wound healing,
Persistent injury and inflammation
➢ Mechanical factors: Motion early in healing
➢ Foreign material - like suture material and foreign bodies
➢ Size, location & type of wound: wounds in ↑ vascularized
areas (face) heal faster than in poorly vasc areas (tendon,
feet)
➢ Small wounds heal faster than larger: incisions faster than
blunt trauma (contusions)
48. COMPLICATIONS OF WOUND HEALING
Deficient scar formation:
Can lead to two types of complications:
A. Wound Dehiscence (rupture of wound): Most common
after abdominal surgery (coughing, vomiting)
B. Ulceration - Defect in the continuity
49. WOUND DEHISCENCE
➢ Rupture of wound
EXCESSIVE FORMATION OF REPAIR
COMPONENTS
➢ Keloid / hypertrophic scar (excess collagen)
➢ Exuberant granulation or proud flesh (excessive
granulation tissue that protrudes above the level of the
surrounding skin and impairs the growth of epithelium)
51. KELOID / HYPERTROPHIC SCAR
➢ Raised scars due to accumulation of excess amounts of
collagen ( type III – type I)
➢ Hypertrophic scars do not grow beyond the boundaries
of the original wound
➢ Keloids grow beyond the boundaries of the original
wound (more serious)
55. EXAGGERATED CONTRACTION
➢ Deformation of surrounding tissue or wound
➢ Can compromise the movement of joints
➢ Most common on palms, soles, anterior thorax
following severe burns