Inflammation Lecture 1 Dr Ejaz Waris
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The document discusses inflammation and its key aspects. It defines inflammation as the body's protective response to injury that involves vascular changes like increased blood flow and permeability. This allows immune cells and fluid to reach the injured tissue. The cardinal signs of inflammation are heat, redness, swelling, pain, and loss of function. Acute inflammation is driven by chemical mediators and involves leukocyte migration from blood vessels to tissue through adhesion molecules and selectins.
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This document provides 200 important points and definitions related to general pathology. It covers topics such as inflammation, necrosis, apoptosis, hypersensitivity reactions, immune responses, and characteristics of different types of tumors and cancers. The points define processes like hypertrophy, atrophy, metaplasia, chemotaxis, and the roles of cytokines, chemokines, and other mediators in the inflammatory response. Cancer-related topics include oncogenes, tumor markers, types of hypersensitivity reactions, and characteristics of squamous cell carcinoma and adenocarcinoma.
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1. Inflammation is the complex response of blood vessels and leukocytes to harmful stimuli, and is designed to remove the stimuli and heal damage.
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3. Chronic inflammation lasts weeks or months, with ongoing attempts to repair damage alongside continued inflammation and injury. It features mononuclear cells and may form granulomas.
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The document summarizes inflammation and its processes. It describes the sequence of events in acute inflammation, from vasodilation to resolution. It lists chemical mediators involved like histamine, cytokines, and eicosanoids. Acute inflammation can resolve completely, form scar tissue, or progress to chronic inflammation. Chronic inflammation involves lymphocytes, macrophages and plasma cells and can be caused by persistent infection, prolonged insult, or autoimmunity.
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Cell injury can result in irreversible cell death through necrosis or apoptosis. Necrosis is unprogrammed cell death resulting from external factors like hypoxia or toxins. It is characterized by cellular swelling and membrane rupture. Apoptosis is programmed cell death that plays an important role in development and homeostasis. During apoptosis, the cell shrinks and breaks into membrane-bound fragments that are phagocytosed. Following cell death, tissues can develop gangrene due to bacterial invasion or calcification when calcium salts deposit in dead or degenerated tissues. Cells attempt to adapt to injury through processes like atrophy, hypertrophy, hyperplasia, and metaplasia.
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This document discusses several types of metaplasia and dysplasia:
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1. Inflammation is the complex response of blood vessels and leukocytes to harmful stimuli, and is designed to remove the stimuli and heal damage.
2. Acute inflammation occurs rapidly via increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate the cause and lasts hours to days.
3. Chronic inflammation lasts weeks or months, with ongoing attempts to repair damage alongside continued inflammation and injury. It features mononuclear cells and may form granulomas.
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This document discusses several types of metaplasia and dysplasia:
- Metaplasia is the replacement of one type of epithelium with another, such as squamous metaplasia in the lungs of smokers. Dysplasia refers to abnormal cell growth.
- Examples of metaplasia include intestinal metaplasia of the stomach and Barrett's esophagus. Squamous metaplasia can occur in the lungs, bladder, and breasts.
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The document discusses various types of intracellular accumulations and pathologic calcification. It defines three categories of intracellular accumulations: (1) a normal cellular constituent accumulated in excess, (2) an abnormal substance that is either exogenous or endogenous, and (3) a pigment. It then describes specific examples of accumulations including lipids, cholesterol, proteins, glycogen, pigments, and minerals. It also discusses two types of pathologic calcification: dystrophic calcification which occurs in areas of necrosis and metastatic calcification which may occur in normal tissues with hypercalcemia.
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1) Biopsy is the use of diseased tissue or cells for diagnostic purposes, including different types of tissue and cell biopsies.
2) Growth disorders include increased growth like hypertrophy and hyperplasia, decreased growth like atrophy, and abnormal cell differentiation like metaplasia and dysplasia. Cell injury can be reversible or irreversible and cause cell death through necrosis or apoptosis.
3) Inflammation is characterized by redness, heat, pain, swelling, and loss of function, and involves processes like increased blood flow and the migration
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Adaptation of cellular growth & differentiation
This document discusses the adaptation of cellular growth and differentiation in response to environmental stressors. It describes several mechanisms of adaptation, including altered cell surface receptor binding and protein synthesis. Adaptive disorders that can occur include atrophy (shrinkage), hypertrophy (enlargement), hyperplasia (increased cell number), metaplasia (cell type transformation), and dysplasia (abnormal cell development). Metaplasia can be epithelial or mesenchymal, and dysplasia can progress to carcinoma if the stimulus is not removed. Overall, the document outlines how cells can adapt their size, number, and type in response to physiological or pathological stimuli.
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Cell Adaptation
Homeostasis refers to the steady state that cells exist in normally, with an equilibrium between the cells and their environment to allow for adequate functioning. When this balance is disturbed, it can predispose cells to pathology. Cells can adapt to changes through processes along a spectrum, including helpful adaptations like hypertrophy (increase in cell size) and hyperplasia (increase in cell number), or more harmful adaptations that can lead to cell injury or death if the stress cannot be adapted to. Adaptations may involve changes in cell size or number, or changes to a different cell type through metaplasia. Dysplasia refers to some loss of cellular control, as seen in conditions like cervical dysplasia, and can progress
Metaplasia
Hyperplasia is an increase in the number of cells in an organ or tissue. It can be physiologic, such as during pregnancy, or pathologic, such as with excessive hormone stimulation. Hypertrophy is an increase in cell size within an organ or tissue, often due to increased functional demands. Atrophy is a decrease in cell and organ size due to loss of cell substance from factors like disuse or inadequate nutrition. Metaplasia is a reversible change where one adult cell type replaces another, such as squamous replacing columnar epithelium from chronic irritation. These changes can sometimes progress to cancer if the predisposing stimuli persist long-term.
Cell injury: CELL ADAPTATIONS
This document discusses various cellular adaptations and injury. It defines atrophy, hypertrophy, hyperplasia, and metaplasia. Atrophy is a decrease in cell size and number. Hypertrophy is an increase in cell size. Hyperplasia is an increase in cell number. Metaplasia is the replacement of one cell type with another. Examples of each type of adaptation are given, including how squamous cell metaplasia in smokers replaces normal trachea and bronchial cells, and how warts represent skin hyperplasia.
Cell injury inflammation and repair
Cell injury, death, inflammation and repair involves complex biological processes in the body. Acute inflammation is characterized by increased blood flow, swelling, heat and pain as the body responds to injury. This involves vascular changes that allow fluid and immune cells to enter injured tissues. Chronic inflammation is a prolonged response involving lymphocytes and macrophages that can lead to tissue destruction and fibrosis. The body aims to resolve acute inflammation and repair damage, but chronic inflammation can persist long-term from infections, toxins or autoimmune conditions.
Metaplasia (1)
Metaplasia is a reversible change where one adult cell type replaces another in response to stress. For example, in smokers the ciliated trachea cells are often replaced with squamous cells. This change arises from the reprogramming of stem cells due to signals from cytokines, growth factors and the extracellular matrix. If the stress persists, metaplasia can predispose the tissue to malignant transformation.
Necrosis,gangrene and apoptosis
This document summarizes different types of cell death including autolysis, necrosis, gangrene, and apoptosis. It describes the morphology, causes, and characteristics of coagulative, liquefactive, caseous, fatty, fibrinoid, and gangrenous necrosis. The key differences between dry, wet, and gas gangrene are highlighted. The document also provides details on the initiation and execution phases of apoptosis, the role of caspases, and morphological and biochemical changes in apoptosis.
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The document provides an overview of the immune system and inflammation. It discusses the inflammatory response process, including the vascular and cellular stages. It describes the signs of inflammation (rubor, tumor, calor, dolor, functio laesa) and cells involved in inflammation like neutrophils, eosinophils, basophils, and monocytes. It also discusses mediators of inflammation like kinins, complement system, histamine, serotonin, arachidonic acid metabolites, platelet activating factor, cytokines, and nitric oxide. Finally, it covers acute phase response, types of inflammation (acute vs chronic), and factors that influence wound healing.
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Cell injury and death can occur through two main processes: necrosis and apoptosis. Necrosis is unprogrammed cell death that results from external factors disrupting cellular homeostasis, leading to membrane damage and cellular contents leaking into surrounding tissues. The cell loses its normal structure. Apoptosis is programmed cell death that occurs as part of normal development or in response to cellular damage, and involves nuclear fragmentation and formation of apoptotic bodies that are phagocytosed without inducing inflammation. Necrosis can take various forms depending on the cause and extent of injury, such as coagulative, liquefactive, caseous or gangrenous necrosis. Cell injury precedes cell death and involves disruption of ATP production, calcium homeostasis and cellular
Healing and repair
Healing after injury can occur through regeneration, which restores normal tissue structure, or repair via scar formation. The healing process involves inflammation, angiogenesis, fibroblast proliferation, and connective tissue remodeling. Cutaneous wound healing occurs in three phases - inflammation, proliferation, and maturation. Factors like nutrition, infection, circulation, and hormones can influence healing. Fracture healing typically involves procallus formation, osseous callus formation, and remodeling to restore bone structure and strength.
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This document provides definitions for various pathological terms starting with letters A through M. Some of the terms defined include abscess, acute, amyloidosis, anaphylaxis, aneurysm, angiogenesis, apoptosis, atrophy, benign, biopsy, carcinoma in situ, chronic, congestion, cyst, degenerative, differentiation, edema, effusion, empyema, fibrosis, gangrene, granuloma, hemorrhage, hemostasis, hyperemia, hyperplasia, hypertrophy, ischemia, malignant, and metastasis. The document defines these medical terms concisely in a glossary format.
Necrosis & gangrene pathology calcification
This document defines and describes various pathological processes including degeneration, necrosis, apoptosis, gangrene, and calcification. It discusses four main types of degenerative cell changes: cellular swelling, fatty change, hyaline change, and mucoid change. It also describes five types of necrosis: coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Apoptosis is defined as a genetically programmed form of cell death. Gangrene is described as necrosis with superadded putrefaction. Pathologic calcification can be either dystrophic or metastatic.
Necrosis
Necrosis is the morphologic changes that follow cell death in living tissues. It can be caused by ischemia, physical agents, chemical agents, or immunological injury. The main types of necrosis include coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis, and fibrinoid necrosis. Coagulative necrosis preserves tissue architecture with denatured proteins and enzymatic digestion of cells. Liquefactive necrosis results in a liquid viscous mass. Caseous necrosis is a type of coagulative necrosis seen in tuberculosis that leaves cheesy white tissue.
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Pathology is the scientific study of disease through examination of tissues and cells. Key terms include:
- Pathology examines structural and functional changes in disease (pathophysiology examines disordered function).
- Disease is a condition causing discomfort, while illness is one's reaction to disease through symptoms and signs.
- Syndromes describe combinations of symptoms from altered physiology. Important tissues include lesions in patients and pathologic changes seen macroscopically and microscopically. Etiology examines causal factors and pathogenesis examines how lesions are produced.
Cell injury l2 medical sept. 2018
This document provides an overview of cell injury, specifically necrosis and apoptosis. It discusses several types of necrosis including coagulative, liquefactive, caseous, gangrenous, fibrinoid, and fat necrosis. Apoptosis is defined as programmed cell death that is regulated by death pathway genes and involves cell shrinkage, chromatin condensation, blebbing, and phagocytosis without inflammation. Key differences between necrosis and apoptosis are highlighted, such as necrosis resulting from irreversible injury and inflammation, while apoptosis is a regulated process without inflammation.
(1,2) introduction of pathophysiology+ cell injury copy
This document provides an overview of pathophysiology concepts including biopsy, growth disorders, cell injury, and inflammation. It can be summarized as:
1) Biopsy is the use of diseased tissue or cells for diagnostic purposes, including different types of tissue and cell biopsies.
2) Growth disorders include increased growth like hypertrophy and hyperplasia, decreased growth like atrophy, and abnormal cell differentiation like metaplasia and dysplasia. Cell injury can be reversible or irreversible and cause cell death through necrosis or apoptosis.
3) Inflammation is characterized by redness, heat, pain, swelling, and loss of function, and involves processes like increased blood flow and the migration
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(1,2) introduction of pathophysiology+ cell injury copy
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Similar to Inflammation Lecture 1 Dr Ejaz Waris
Inflammation acute + chronic
Inflammation is the body's protective response to injury or infection that involves increased blood flow, swelling, heat, pain, and loss of function. The document outlines the general considerations of inflammation including its definition, causes, and cardinal signs. It then discusses the major events of acute inflammation including vascular changes, exudation of fluid, and recruitment and activation of leukocytes. Finally, it classifies inflammation into acute and chronic types and further classifies acute inflammation based on the type of exudate produced (serous, fibrinous, suppurative, hemorrhagic).
Inflammation
Acute inflammation is characterized by two major components: vascular changes and cellular events. The vascular changes include vasodilation, increased vascular permeability, and slowing of blood flow. This allows plasma proteins and leukocytes to leave the bloodstream and enter the injured tissues. The cellular events involve the migration of phagocytes such as neutrophils from the bloodstream into the injured tissues by the processes of margination, pavementing, emigration, and chemotaxis. The phagocytes then recognize, attach to, engulf, and destroy pathogens and cellular debris through phagocytosis, resolving the inflammatory response.
INFLAMMATION.pptx
Inflammation is the body's immune response to injury or infection. It involves vascular changes like increased blood flow and permeability, as well as cellular events like leukocyte migration and phagocytosis. The classic signs are redness, swelling, heat, pain, and loss of function. Acute inflammation follows two main phases - vascular events that alter blood vessels, and cellular events where leukocytes migrate to the site and phagocytose pathogens. This process aims to destroy infectious agents and initiate healing.
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Inflammation is the protective response of tissues to injury. The key events of acute inflammation are vasodilation, increased vascular permeability, and leukocyte emigration. Increased permeability allows plasma proteins and cells to exit vessels and accumulate at sites of injury. This leads to edema, which can be an exudate or transudate depending on protein content. Exudates have high protein levels from significant vessel changes, while transudates have low protein from hydrostatic/osmotic imbalance without major vessel changes. The mechanisms driving permeability involve histamine and other mediators causing both immediate and delayed responses from the endothelium.
inflammation lecture cmlt.pptx
Inflammation is the protective response of tissues to injury. The key events of acute inflammation are vasodilation, increased vascular permeability, and leukocyte emigration. Increased permeability allows plasma proteins and cells to exit vessels and accumulate at sites of injury. This leads to edema, which can be an exudate or transudate depending on protein content. Exudates have high protein levels from significant vessel changes, while transudates have low protein from hydrostatic/osmotic imbalance without major vessel changes. The mechanisms driving permeability involve histamine and other mediators causing both immediate and delayed responses from the endothelium.
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Inflammation is the body's response to injury or infection that is characterized by redness, swelling, heat, pain, and loss of function. The cardinal signs of inflammation are caused by increased blood flow, increased vascular permeability, and leukocyte infiltration at the site of injury or infection. Acute inflammation typically involves neutrophils and resolves within 48 hours, while chronic inflammation involves mononuclear cells and persists for longer than 48 hours. Inflammation can lead to abscess formation, progression to chronic inflammation, resolution, or repair through scarring or fibrosis.
Inflammation part 1 by
- Inflammation is the body's protective response to injury or infection that involves increased blood flow, immune cell activity, and release of chemical mediators. It has both acute and chronic forms.
- The cardinal signs of inflammation are redness, heat, swelling, pain, and loss of function. It involves vascular changes like increased permeability and leukocyte emigration from blood vessels.
- Leukocytes like neutrophils, macrophages, and lymphocytes are involved. Chemical mediators regulate the inflammatory response. Acute inflammation typically resolves in a few days while chronic inflammation persists long-term.
Inflammation Lect
1. Inflammation is the body's response to infection, irritation, or injury, characterized by redness, swelling, heat, and pain. It involves the immune system and blood vessels.
2. Acute inflammation is a short-term response to recent injury or infection, marked by increased blood flow, blood vessel permeability, and migration of white blood cells. Chronic inflammation is a long-term response involving lymphocytes, macrophages, and fibrosis.
3. Inflammation can resolve, lead to abscess or fibrosis, and is mediated by chemical signals like histamine, bradykinin, prostaglandins, and cytokines. Different cell types and patterns characterize specific inflammatory diseases.
acute inflammation
Inflammation is the body's protective response to injury or infection that is characterized by heat, swelling, redness, pain, and loss of function. The cardinal signs of inflammation are caused by increased blood flow, increased vascular permeability, and leukocyte infiltration at the site of injury or infection. Acute inflammation typically lasts less than 48 hours and is characterized by neutrophil infiltration, while chronic inflammation lasts longer than 48 hours and is characterized by mononuclear cell infiltration. Inflammation can result in abscess formation, progression to chronic inflammation, resolution to normal tissue, or repair through scarring or fibrosis.
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The document defines inflammation and describes the key aspects of acute and chronic inflammation. It discusses the cardinal signs of acute inflammation, potential causes, and the main events in the inflammatory response, including vascular changes, exudation of fluid and cells, and cellular events like leukocyte extravasation and phagocytosis. Acute inflammation is a rapid local response lasting days, while chronic inflammation persists for weeks to months with simultaneous tissue destruction and healing.
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Inflammation is the body's response to eliminate injurious agents and damaged tissue. The four cardinal signs of inflammation are redness, swelling, heat, and pain. Inflammation can be classified as acute, chronic, or subacute based on its duration and the host's defense capacity. Acute inflammation involves fluid accumulation, platelet activation, and neutrophil infiltration within 2 weeks to repair tissue. Chronic inflammation lasts a long time and involves lymphocytes, plasma cells, and macrophages with granulation tissue formation. The inflammatory response involves vascular changes like vasodilation, increased permeability and leukocyte migration, as well as cellular events like phagocytosis to remove pathogens and debris.
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Acute inflammation is defined as the rapid host response to infection or tissue injury that lasts less than 48 hours. It is characterized by increased blood flow, vascular permeability, and leukocyte infiltration at the site of injury. The cardinal signs of acute inflammation are redness, warmth, swelling, pain, and loss of function. The major components are alterations in vascular caliber, changes in microvascular structure, and leukocyte emigration and activation. Acute inflammation can lead to resolution of the problem, or progression to chronic inflammation, abscess, or ulcer formation depending on the severity and type of injury or pathogen.
Inflammation
Acute inflammation is the early response of tissues to injury and involves vascular and cellular events. The vascular events include vasodilation, increased vascular permeability allowing plasma proteins to leave circulation, and accumulation of leukocytes from the blood vessels into tissues. The principal leukocytes in acute inflammation are neutrophils. The cellular events in acute inflammation help destroy, dilute or isolate injurious agents. Mediators of acute inflammation include histamine, prostaglandins, nitric oxide, complement factors and cytokines. Acute inflammation is rapid in onset, relatively short in duration and aims to return tissues to normal function.
Inflamggvggffgggggggggggmation lecture.ppt
Inflammation is the body's protective response to eliminate the initial cause of cell injury and promote tissue repair. The classical signs of acute inflammation are heat, redness, swelling, pain, and loss of function. Acute inflammation is short-lived and involves increased blood flow, vascular permeability, and recruitment of immune cells like neutrophils to the injured site. Chronic inflammation lasts longer and is characterized by lymphocytes, plasma cells and macrophages, tissue destruction, and fibrosis. The outcome of acute inflammation is typically resolution and healing of the damaged tissues.
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Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, and pain. It can be acute, occurring rapidly with a short duration, or chronic, with a longer, insidious onset. Acute inflammation is driven by increased blood flow and vascular permeability, allowing fluid, proteins, and immune cells like neutrophils to enter tissues. This causes swelling and activates immune responses like phagocytosis of pathogens. Chronic inflammation is prolonged, features mononuclear immune cell infiltration, and can cause simultaneous tissue destruction and healing over weeks to years. Macrophages play a key role by releasing enzymes and radicals that damage tissues but also promote healing through proliferation of new blood vessels and connective tissue.
1. inflammation introduction-dr. sinhasan- mdzah
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It is a protective process that helps destroy and remove harmful substances from the body and prevents minor infections from becoming overwhelming. The inflammatory response involves vascular changes like increased blood flow, exudation of fluid and proteins from blood vessels, and emigration of white blood cells. It can be either acute, resolving on its own, or chronic, persisting long-term and potentially causing tissue damage. Historically, the five cardinal signs of inflammation were identified and chemical mediators were found to play a key role. Stimuli that can cause inflammation include infections, trauma, toxins, and immune reactions
Inflammation
aetiology of inflammation; types of inflammation; how inflammation occur; cells involve in inflammation; role of wbc in inflammation; outcome of inflammation; how inflammation associated with immunity, clotting system, complementary system kinin system, how inflammation is associated with oral cavity; disease associated with inflammatory system
INFLAMMATION AND REPAIR.pptx
This document provides an overview of inflammation and repair. It begins with the historical context of inflammation and defines the cardinal signs. It then discusses the types of inflammation as acute or chronic, depending on duration. Acute inflammation involves vascular and cellular events like increased permeability and leukocyte migration. Mediators of inflammation include cytokines, the clotting system, kinin system, and complement system. Chronic inflammation is characterized by mononuclear cell infiltration and long-term tissue destruction. Healing and repair occurs through regeneration of tissues or repair via granulation tissue formation and wound contraction.
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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.
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Olfactory Genes:
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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.
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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:
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Some toxic substances are odorless at lethal concentrations.
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Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
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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 lead (limb II)
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5. Enlist some common indications for obtaining an ECG
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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
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Inflammation Lecture 1 Dr Ejaz Waris
- 1. "Opportunities are usually disguised by hard work, so most people don't recognize them." - Ann Landers
- 2. INFLAMMATI0N Dr. EJAZ WARIS , FCPS Assistant Professor Histopathology,FMHC
- 6. Laryngitis:
- 8. Pneumonia
- 10. The 5 Cardinal Signs of Heat Redness Swelling Pain Loss Of Func.
- 27. Acute Inflammation - Mechanism 1.Alterations in vascular calibre leading to increased blood flow 2.Microvasculature structural changes 3.Leukocyte emigration
- 41. Vascular changes
- 43. "Each time you are honest and conduct yourself with honesty, a success force will drive you toward greater success. Each time you lie, even with a little white lie, there are strong forces pushing you toward failure."