Key cellular events after an injury
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1) Tissue damage occurs following an injury, with cellular membranes damaged and contents spilling out, leading to cell death. Blood vessels break and nerves are injured, forming a hematoma of blood and debris. 2) Chemical mediators like histamine and bradykinin signal the injury and mobilize responses, increasing blood flow and allowing leukocytes like neutrophils to reach the site. 3) Neutrophils begin cleaning debris but can also cause collateral damage, then calling macrophages for continued cleanup through phagocytosis and removal via the lymph system. Secondary injury may occur due to reduced blood flow and oxygen delivery.
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Fibrosis and scarring
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healing and tissue repair
Tissue repair occurs through either regeneration or scar formation. Regeneration involves the proliferation of residual cells to completely restore lost tissue, while scar formation deposits connective tissue when regeneration is not possible. The key stages of wound healing are inflammation, proliferation, granulation tissue formation, wound contraction, and strength acquisition. Factors like nutrition, infection, and location can influence healing. Complications include deficient or excessive scarring, contractures, and exuberant granulation. Stem cells also contribute to tissue repair through self-renewal and generation of new cells.
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Tissue repair
1. Tissue repair occurs through regeneration or healing. Regeneration replaces dead cells with the same cell type, while healing replaces tissue with fibrous scar tissue.
2. The regenerative capacity of tissues depends on their ability to proliferate. Labile tissues continuously divide, stable tissues stop dividing after birth but can proliferate in response to injury, and permanent tissues stop dividing early in life.
3. Growth factors, the extracellular matrix, and cellular proliferation play important roles in tissue repair by stimulating cell growth, promoting cell survival, and providing a scaffold for cells.
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cellular adaptation presentation (2)
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
wound healing PPT
Wound healing involves three phases: inflammatory, proliferative, and maturational. Primary healing occurs when wound edges are in direct contact while secondary healing involves granulation tissue formation. Many factors can affect wound healing including infection, nutrition, steroids, ischemia, and diabetes. Growth factors are important for different stages of healing. Stem cells can help regenerate damaged tissue. Aberrations like keloids and hypertrophic scarring exist. New treatments include skin substitutes, dressings, growth factors, and therapies like hyperbaric oxygen and offloading casts.
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Cellular adaptations
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Tissue repair
The document discusses tissue repair and the body's response to injury. When tissue is injured, it stimulates an inflammatory response to remove harmful agents and restore the tissue. The immune response also aids in this process by attacking specific invaders. Tissue repair involves inflammation, organization to restore blood supply, and regeneration or fibrosis for permanent repair. Different tissues have varying regenerative capacities. Platelets play a key role in stopping bleeding by sticking to injuries and initiating the clotting cascade through coagulation factors to form a clot and seal the wound.
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Acute inflammation is characterized by a rapid onset and short duration, while chronic inflammation persists over a longer period of time. The major differences between acute and chronic inflammation include the onset and duration of symptoms as well as the type of inflammatory cells involved. Acute inflammation is driven by neutrophils in the early stages, while chronic inflammation involves lymphocytes and macrophages. Vascular changes like increased blood flow, vascular permeability and exudation are also hallmarks of acute inflammation but are generally less pronounced in chronic inflammation.
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This document summarizes tissue growth, repair, and aging. It discusses the body's physical and immune defenses at the tissue level. When tissue is injured, the healing process begins through inflammation and regeneration or fibrosis. The type of tissue damaged and severity of injury determine whether regeneration or scar tissue formation occurs. After injury, capillaries become permeable and granulation tissue forms to allow healing as the surface epithelium regenerates. Over time, tissues experience changes due to aging, including thinning epithelia, weakened bones and connective tissue, and muscle and nervous tissue atrophy.
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cellular adaptation presentation (2)
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
wound healing PPT
Wound healing involves three phases: inflammatory, proliferative, and maturational. Primary healing occurs when wound edges are in direct contact while secondary healing involves granulation tissue formation. Many factors can affect wound healing including infection, nutrition, steroids, ischemia, and diabetes. Growth factors are important for different stages of healing. Stem cells can help regenerate damaged tissue. Aberrations like keloids and hypertrophic scarring exist. New treatments include skin substitutes, dressings, growth factors, and therapies like hyperbaric oxygen and offloading casts.
Lect 6-wound healing
The document discusses wound healing and regeneration. It describes the three phases of wound healing as the inflammatory phase, proliferative phase, and remodeling phase. The inflammatory phase involves hemostasis, inflammation, and vasodilation. The proliferative phase involves granulation, angiogenesis, contraction, and epithelialization. Finally, the remodeling phase can last up to two years as new collagen is formed and wound strength increases.
Cellular adaptations
There are four main types of cellular adaptations: hypertrophy, hyperplasia, atrophy, and metaplasia. Hypertrophy refers to an increase in the size of cells resulting in an increased organ size without new cells being produced. Cells that can divide may undergo both hypertrophy and hyperplasia in response to stress. Hypertrophy can be physiological, such as muscle growth from exercise or uterine growth in pregnancy, or pathological like heart muscle growth from hypertension. The mechanisms of hypertrophy involve cells enlarging in response to increased functional demands or stimulation by hormones and growth factors.
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Cellular or Cell adaptation !! pathology - Harsh mohan !! cell injury
Cellular or Cell adaptation !! pathology - Harsh mohan !! cell injury
Similar to Key cellular events after an injury
Tissue repair
The document discusses tissue repair and the body's response to injury. When tissue is injured, it stimulates an inflammatory response to remove harmful agents and restore the tissue. The immune response also aids in this process by attacking specific invaders. Tissue repair involves inflammation, organization to restore blood supply, and regeneration or fibrosis for permanent repair. Different tissues have varying regenerative capacities. Platelets play a key role in stopping bleeding by sticking to injuries and initiating the clotting cascade through coagulation factors to form a clot and seal the wound.
Topic: Acute and chronic inflammation
Lecture 1 (S1-S5)-introduction
Lecture 2(S 6- S11)-mechanism & sequences of acute inflammation-vascular changes
Lecture 3(S12-S20 (15-2-22)cellular changes in acute inflammation)
Lecture 4(S21-S32)concept of scaring, healing fibrosis
Lecture 5(S33-LAST) chemical mediators of inflammation
Blood
Basic information about blood and it contents and functions.
Reference: https://schoolbag.info/biology/humans/14.html
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Hemostasis is the prevention of blood loss from ruptured blood vessels. It involves three key events: 1) vascular constriction to reduce blood flow, 2) formation of a platelet plug to seal the rupture, and 3) formation of a blood clot through coagulation to reinforce the seal. Platelets adhere to collagen at the rupture site and aggregate, releasing chemicals to recruit more platelets until the plug is formed. Meanwhile, coagulation factors in the blood activate in a cascade, ultimately converting fibrinogen to fibrin fibers that strengthen the platelet plug and form a clot. The clot or plug then either organizes into fibrous tissue to permanently close the rupture or dissolves if no longer needed.
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When blood vessels
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