This document summarizes the key aspects of acute inflammation. It describes the classical signs of inflammation including heat, redness, swelling, pain, and loss of function. The acute inflammatory response involves increased blood flow, vascular permeability, and leukocyte migration. Neutrophils are generally the first responders and help remove pathogens and dead cells through phagocytosis and release of inflammatory mediators that can also cause tissue damage. The response is normally self-limiting as mediators have short half-lives and active termination mechanisms resolve the inflammation.
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
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
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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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.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Inflammation is the body's immediate response to damage to its tissues and cells by pathogens, noxious stimuli such as chemicals, or physical injury. Acute inflammation is a short-term response that usually results in healing: leukocytes infiltrate the damaged region, removing the stimulus and repairing the tissue. Chronic inflammation, by contrast, is a prolonged, dysregulated and maladaptive response that involves active inflammation, tissue destruction and attempts at tissue repair. Such persistent inflammation is associated with many chronic human conditions and diseases, including allergy, atherosclerosis, cancer, arthritis and autoimmune diseases.
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Inflammation is the body's immediate response to damage to its tissues and cells by pathogens, noxious stimuli such as chemicals, or physical injury. Acute inflammation is a short-term response that usually results in healing: leukocytes infiltrate the damaged region, removing the stimulus and repairing the tissue. Chronic inflammation, by contrast, is a prolonged, dysregulated and maladaptive response that involves active inflammation, tissue destruction and attempts at tissue repair. Such persistent inflammation is associated with many chronic human conditions and diseases, including allergy, atherosclerosis, cancer, arthritis and autoimmune diseases.
CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdfSachin Sharma
Pediatric nurses play a vital role in the health and well-being of children. Their responsibilities are wide-ranging, and their objectives can be categorized into several key areas:
1. Direct Patient Care:
Objective: Provide comprehensive and compassionate care to infants, children, and adolescents in various healthcare settings (hospitals, clinics, etc.).
This includes tasks like:
Monitoring vital signs and physical condition.
Administering medications and treatments.
Performing procedures as directed by doctors.
Assisting with daily living activities (bathing, feeding).
Providing emotional support and pain management.
2. Health Promotion and Education:
Objective: Promote healthy behaviors and educate children, families, and communities about preventive healthcare.
This includes tasks like:
Administering vaccinations.
Providing education on nutrition, hygiene, and development.
Offering breastfeeding and childbirth support.
Counseling families on safety and injury prevention.
3. Collaboration and Advocacy:
Objective: Collaborate effectively with doctors, social workers, therapists, and other healthcare professionals to ensure coordinated care for children.
Objective: Advocate for the rights and best interests of their patients, especially when children cannot speak for themselves.
This includes tasks like:
Communicating effectively with healthcare teams.
Identifying and addressing potential risks to child welfare.
Educating families about their child's condition and treatment options.
4. Professional Development and Research:
Objective: Stay up-to-date on the latest advancements in pediatric healthcare through continuing education and research.
Objective: Contribute to improving the quality of care for children by participating in research initiatives.
This includes tasks like:
Attending workshops and conferences on pediatric nursing.
Participating in clinical trials related to child health.
Implementing evidence-based practices into their daily routines.
By fulfilling these objectives, pediatric nurses play a crucial role in ensuring the optimal health and well-being of children throughout all stages of their development.
Deep Leg Vein Thrombosis (DVT): Meaning, Causes, Symptoms, Treatment, and Mor...The Lifesciences Magazine
Deep Leg Vein Thrombosis occurs when a blood clot forms in one or more of the deep veins in the legs. These clots can impede blood flow, leading to severe complications.
Leading the Way in Nephrology: Dr. David Greene's Work with Stem Cells for Ki...Dr. David Greene Arizona
As we watch Dr. Greene's continued efforts and research in Arizona, it's clear that stem cell therapy holds a promising key to unlocking new doors in the treatment of kidney disease. With each study and trial, we step closer to a world where kidney disease is no longer a life sentence but a treatable condition, thanks to pioneers like Dr. David Greene.
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
The Importance of Community Nursing Care.pdfAD Healthcare
NDIS and Community 24/7 Nursing Care is a specific type of support that may be provided under the NDIS for individuals with complex medical needs who require ongoing nursing care in a community setting, such as their home or a supported accommodation facility.
CHAPTER 1 SEMESTER V PREVENTIVE-PEDIATRICS.pdfSachin Sharma
This content provides an overview of preventive pediatrics. It defines preventive pediatrics as preventing disease and promoting children's physical, mental, and social well-being to achieve positive health. It discusses antenatal, postnatal, and social preventive pediatrics. It also covers various child health programs like immunization, breastfeeding, ICDS, and the roles of organizations like WHO, UNICEF, and nurses in preventive pediatrics.
Global launch of the Healthy Ageing and Prevention Index 2nd wave – alongside...ILC- UK
The Healthy Ageing and Prevention Index is an online tool created by ILC that ranks countries on six metrics including, life span, health span, work span, income, environmental performance, and happiness. The Index helps us understand how well countries have adapted to longevity and inform decision makers on what must be done to maximise the economic benefits that comes with living well for longer.
Alongside the 77th World Health Assembly in Geneva on 28 May 2024, we launched the second version of our Index, allowing us to track progress and give new insights into what needs to be done to keep populations healthier for longer.
The speakers included:
Professor Orazio Schillaci, Minister of Health, Italy
Dr Hans Groth, Chairman of the Board, World Demographic & Ageing Forum
Professor Ilona Kickbusch, Founder and Chair, Global Health Centre, Geneva Graduate Institute and co-chair, World Health Summit Council
Dr Natasha Azzopardi Muscat, Director, Country Health Policies and Systems Division, World Health Organisation EURO
Dr Marta Lomazzi, Executive Manager, World Federation of Public Health Associations
Dr Shyam Bishen, Head, Centre for Health and Healthcare and Member of the Executive Committee, World Economic Forum
Dr Karin Tegmark Wisell, Director General, Public Health Agency of Sweden
Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
In 1996, John McGowan and Dale Gerding first applied the term antimicrobial stewardship, where they suggested a causal association between antimicrobial agent use and resistance. They also focused on the urgency of large-scale controlled trials of antimicrobial-use regulation employing sophisticated epidemiologic methods, molecular typing, and precise resistance mechanism analysis.
Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
According to the 2019 report, in the US, more than 2.8 million antibiotic-resistant infections occur each year, and more than 35000 people die. In addition to this, it also mentioned that 223,900 cases of Clostridoides difficile occurred in 2017, of which 12800 people died. The report did not include viruses or parasites
VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
India Clinical Trials Market: Industry Size and Growth Trends [2030] Analyzed...Kumar Satyam
According to TechSci Research report, "India Clinical Trials Market- By Region, Competition, Forecast & Opportunities, 2030F," the India Clinical Trials Market was valued at USD 2.05 billion in 2024 and is projected to grow at a compound annual growth rate (CAGR) of 8.64% through 2030. The market is driven by a variety of factors, making India an attractive destination for pharmaceutical companies and researchers. India's vast and diverse patient population, cost-effective operational environment, and a large pool of skilled medical professionals contribute significantly to the market's growth. Additionally, increasing government support in streamlining regulations and the growing prevalence of lifestyle diseases further propel the clinical trials market.
Growing Prevalence of Lifestyle Diseases
The rising incidence of lifestyle diseases such as diabetes, cardiovascular diseases, and cancer is a major trend driving the clinical trials market in India. These conditions necessitate the development and testing of new treatment methods, creating a robust demand for clinical trials. The increasing burden of these diseases highlights the need for innovative therapies and underscores the importance of India as a key player in global clinical research.
3. Inflammation is war
• Coordinated response to eliminate the
cause and consequence of injury or
infection (noxious agent)
• Involves immune and vascular systems
• Acute inflammation is a stereotyped
response to recent or ongoing injury
• Chronic inflammation is a response to
prolonged problems, orchestrated by T-
helper lymphocytes
4. Inflammatory process
• Immunity inflammation
• Purpose is 3 d’s:
Destroy
Dilute
Dam-off
• Desired result is healing
Regeneration (hyperplasia)
Fibrosis (scarring)
• Collateral damage may occur
5. Classical description
• Ancient Roman, Celsus, described inflammation
• Calor—heat
• Rubor—redness
• Tumor—swelling
• Dolor—pain
• Hunter described inflammation as good in 1790s
• Virchow added a fifth clinical sign in 1800s
• Functio laesa—loss of function
• Metchnikoff discovered phagocytes 1883
• Ehrlich discovered mast cells, granulocytes 1878
as well as complement in 1899
Metchnikoff and Ehrlich shared Nobel Prize 1908
6. Inflammatory stimuli
• Physical injury
Cutaneous laceration, osseous fracture, sunburn,
toxin
• Necrosis
Resolution of regions of dead cells
• Infection
Innate response followed by adaptive response to
microbial invader
• Immunological errors
Allergies—response to environmental substances
Autoimmunity—response to self
7. Acute vascular changes
• Transient arteriolar constriction (seconds)
• Nerve reflex, endothelin
• Like the immediate first step of hemostasis
• Vasodilation of arterioles (until resolution)
• Histamine, bradykinin mediate rapid response
• Sustained by prostaglandins and NO
• Hyperemia, erythema
• Transudation increases blood viscosity, slows flow
• Stasis and congestion in venules allows cells to contact
endothelium
• Vascular leakage (minutes to hours to days)
• Histamine, bradykinin mediate rapid response
• Sustained by C3a, C5a, PAF, leukotrienes
• Exudation results in local edema
8. Increased vascular permeability
• Contraction of vascular endothelium—rounding
of cells and widening of intercellular spaces
Immediate, transient response (15-30 min)
• Stimulated by histamine, bradykinin, substance P
• venules of 20 – 60 um diameter respond
Delayed prolonged leakage (radiation burns)
• begins after 2 – 12 h delay, lasts hours – days
• stimulated by cytokines and apoptotsis of injured skin cells
• venules and capillaries respond
Immediate, sustained response (days)
• caused by direct damage to vasular endothelium
• venules, capillaries, arterioles respond
• ended by hemostasis, thrombosis, regeneration
Neutrophil-induced damage (days)
• caused when neutrophils adhere and emigrate
9. Leukocyte extravasation
• Margination, rolling
• Decreased flow rate and volume push WBCs
toward vascular walls
• Intermittent binding of selectins with glycoproteins
causes rolling
• Adhesion, pavementing
• mediated by integrins on leukocytes, activated by
cytokines
• integrin ligands VCAM-1, ICAM-1 on endothelial
cells induced by TNF and IL-1
• Transmigration or diapedesis
• chemokines stimulate adherent leukocytes to
migrate through interendothelial spaces
10.
11. Selectins and Lewis X receptors
• lectins are oligosaccharide binding proteins
• selectins are a lectin-resembling class of
glycoprotein receptors
• selectin ligands contain an oligosaccharide
called Lewis X and a sialic acid moiety
Complementary binding pairs
Endothelial surface Lymphocyte surface
P-selectin Lewis-X
E-selectin Lewis-X
CD34 L-selectin
12. Regulation of expression of
endothelial and leukocyte
adhesion molecules
A, Redistribution of P-selectin from
intracellular stores to the cell
surface.
B, Increased surface expression of
selectins and ligands for integrins
upon cytokine activation of
endothelium.
C, Increased binding avidity of
integrins induced by chemokines.
Clustering of integrins contributes to
their increased binding avidity (not
shown).
IL-1, interleukin-1; TNF, tumor
necrosis factor.
13. Adhesion molecules
• Integrins are ligands for CAMs
integrins are protein heterodimers
expressed on leukocytes
• CD11/CD18,aka lymphocyte function-associated antigen 1
(LFA-1) binds ICAM
• a4b1 binds VCAM
• CAMs bind integrins
CAMs belong to the immunoglobulin superfamily
• Intercellular CAM (ICAM)
• Vascular CAM (VCAM)
Constitutively expressed by leukocytes
• Made sticky by chemokines
14. Leukocyte transmigration
• Extension of leukocyte pseupodia between
endothelial cells
• Binding to PECAM (CD31) expressed in
endothelial junctions
• Focal digestion of basement membrane
with elastase, collagenase and
metalloproteinases from neutrophils
• Migration of leukocytes towards
chemotactic gradient
• Adhere to ECM with integrins and CD44
15. Chemotaxis of leukocytes
• Locomotion oriented along a gradient of
Bacterial products
• N-formyl peptides, lipoproteins,
lipopolysaccharides
CXC chemokines
• IL-8, aka CXCL8 or granulocyte chemotactic
protein 1
Complement proteins
• Especially C5a
arachidonic acid (AA) metabolites
• Leukotriene B4
16. Chemotactic receptors
• Specific GPCRs
activation of second messengers
increase cytosolic calcium
activate Rac/Rho/cdc42 family GTPases
• Result in movement
polymerization of actin
• increased amounts of polymerized actin at the
leading edge
• localization of myosin filaments at the back
17. Which types of leukocytes respond
• Neutrophils are generally the first types of leukocytes to
respond in acute (non-viral) inflammation or to necrosis
• Lymphocytes are usually the first cells to respond to viral
infections or autoimmune diseases
lymphocytes and plasma cells also participate in most chronic
inflammation, regardless of the inciting cause
• Macrophages begin to appear a few days after the onset
of inflammation from almost any cause, and increase in
numbers over time
activated macrophages may develop abundant cytoplasm, called
epitheloid macrophage
macrophages merge to create giant cells with multiple nuclei
• Eosinophilic inflammation is highly suggestive of a
response to helminths, arthropods, or allergens
19. Acute inflammation
• Immediate, early response
Vasodilation
Vascular permeability
Emigration of leukocytes into tissues
• Reactions of leukocytes in inflammation
Recognition of microbes and dead tissues
Removal of the offending agents
Macrophage activation
Leukocyte-mediated tissue injury
20. Receptors
• Recognition of the offending agents
Toll-like receptors
• lipopolysaccharide (LPS, or endotoxin), other bacterial
proteoglycans and lipids, unmethylated CpG nucleotides
GPCRs
• N-formyl peptides, complement (C5a), platelet activating
factor, prostaglandins, and leukotrienes
Receptors for opsonins
• IgG Fc, type 1 complement receptor (CR1)
Receptors for cytokines
• IFN-γ is the major macrophage-activating cytokine
• Activation the leukocytes
Increases in cytosolic Ca++
Activation of protein kinase C and phospholipase A2
21.
22. Activation of neutrophils
• Stimulated by chemokines such as IL-8 and
chemical mediators such as LTB4
conformational change of integrin (LFA-1) to increase
avidity for receptor (ICAM-1)
activation of Arachidonic Acid metabolic cascades
• produces vasoactive prostaglandins and leukotrienes
activation of the oxidative burst to produce reactive
oxygen species
• NADPH oxidase enzyme system produces superoxide anion
radical, which is converted to H2O2, which leads to
production of hydroxyl radical
• myeloperoxidase produces HOCl, which halogenates
microbes
secretion of lysosomal enzymes (degranulation)
23. Actions of activated neutrophils
• Phagocytosis has three steps
recognition and attachment of the particle to
be ingested
engulfment, with subsequent formation of a
phagocytic vacuole
killing or degradation of the ingested material
• Initiation of repair
stimulate the proliferation of endothelial cells
and fibroblasts
stimulate synthesis of collagen and enzymes
that remodel connective tissues
24. Phagocytosis—Recognition
• Mannose receptor
binds terminal mannose and fucose residues
of glycoproteins and glycolipids (bacterial and
fungal)
• Scavenger receptors
oxidized or acetylated low-density lipoprotein
(exogenous and endogenous lipid toxins)
• High-affinity opsonin receptors
IgG antibodies—Fc receptor
C3b breakdown product of complement—C1R
mannan-binding lectin—C1R, CD14
25. Phagocytosis—Engulfment
• Extensions of the cytoplasm (pseudopods) flow
around bound receptors
• Plasma membrane pinches off creating
phagosome
• Phagosome then fuses with a lysosomal granule
• During this process the phagocyte may also
release granule contents into the extracellular
space
• Engulfment is dependent on polymerization of
actin filaments
26. Phagocytosis—Oxygen dependent killing
• ROS generation is due to the rapid assembly and
activation of NADPH oxidase (phagocyte oxidase),
which reduces oxygen to superoxide anion
At least seven protein subunits located in the plasma
membrane and the cytoplasm of resting neutrophils
translocate to the phagosomal membrane to form the
functional enzyme complex
Respiratory burst of G6PDH activity generates NADPH
Superoxide is converted to hydrogen peroxide (H2O2),
mostly by spontaneous dismutation
Myeloperoxidase (MPO) from azurophilic granules
converts H2O2 to hypochlorite (OCl•) with Cl-
• NO generated by inducible nitric oxide synthase
iNOS, aka NOS2
NO reacts with superoxide to generate the highly reactive
free radical peroxynitrite (ONOO•)
27. Phagocytosis—Oxygen independent killing
• proteases, such as elastase and collagenase
• defensins, cationic arginine-rich granule
peptides that are toxic to microbes
• lysozyme, which hydrolyzes the muramic acid–
N-acetylglucosamine bond, found in the
glycopeptide coat of bacteria
• cathelicidins, antimicrobial proteins
• lactoferrin, an iron-binding protein
• major basic protein, a cationic protein of
eosinophils, which is cytotoxic to many parasites
• bactericidal/permeability increasing protein,
which binds bacterial endotoxin
29. Damaging effects of phagocytes
• Tissue damage occurs from
digestion of basement membranes during
transmigration; caused by elastase and
metalloproteinases
• counteracted by a1-antitrypsin, C-reactive protein, and other
circulating antiproteases
lysosomal leakage during phagocytosis (regurgitation
or frustrated phagocytosis)
• leaks acid hydrolases, free radicals, and hypochlorous acid
inflammatory mediators produced by phagocytes,
such as prostaglandins and leukotrienes
necrosis of phagocytes in situ
30. Termination of acute response
• Inflammation declines spontaneously
Mediators of inflammation are produced in rapid bursts only
while the stimulus persists
Mediators have short half-lives and are degraded after their
release.
Neutrophils also have short half-lives in tissues and die by
apoptosis within a few hours after leaving the blood
• Active termination mechanisms include
Switch from pro-inflammatory leukotrienes to anti-inflammatory
lipoxins
Release of anti-inflammatory cytokines, including transforming
growth factor-β (TGF-β) and IL-10, from macrophages
production of anti-inflammatory lipid mediators, called resolvins
and protectins, derived from polyunsaturated fatty acids
neural impulses (cholinergic discharge) that inhibit the
production of TNF in macrophages