patoloji-ders-notlari

Yara İyileşmesi ve Tamir

Serdar Balcı

Yara İyileşmesi ve Tamir

Dr. Serdar BALCI

Tamir (İyileşme)

Hasar sonrası doku mimarisinin ve aktivitesinin restorasyonu

Hasarlı dokunun rejenerasyonu

Bağ dokuda skar oluşumu

Rejenerasyon

Skar oluşumu (Nedbeleşme)

Rejenerasyon kapasitesi olmayan dokularda

Dokudaki destek yapılarda zarar görümüştür

Tamir fibröz doku oluşumu ile sonuçlanır → skar oluşumu

Kayıp parankimal hücrelerin fonksiyonu yerine getirilemez

Yapısal sağlamlık elde edilmeye çalışılır, böylece rezidü hücreler aktivitelerini yerine getirebilir

Organizasyon

Organize pnömoni

İnflamatuar eksuda ile dolu bir boşlukta gelişen fibrozis

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins Basic Pathology

Hücre ve doku rejenerasyonu

Hücre ve doku rejenerasyonundaki faktörler

Hücre proliferasyonu

Büyüme Faktörleri

Ekstaselüler Matriks

Hücre çoğalmasının kontrolü

Dokuların çoğalma kapasiteleri

Robbins Basic Pathology

Kök Hücreler

Robbins Basic Pathology

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins Basic Pathology

Robbins and Cotran’s Pathological Basis of Diseases

Büyüme Faktörleri

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins Basic Pathology

Robbins Basic Pathology

Ekstraselüler matriks

Robbins Basic Pathology

Ekstraselüler matriksin fonksiyonları

Skar oluşumu

Ciddi, kronik hasar

Bölünemeyen hücreler hasara uğradığında

Tamir bağ doku ile olur

Rejenerasyon gösteren hücreler ve skar birlikte olabilir

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Tamir başlangıcı hasardan sonra ilk 24 saat içinde başlar

Fibroblastların göçü

Fibroblast ve endotel hücre proliferasyonu

Robbins Basic Pathology

Granülasyon dokusu

Çok miktarda damar

Arada lökositler

Makroskopik olarak pembe granüler görünüm

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Anjiogenez

Robbins Basic Pathology

Robbins Basic Pathology

Fibroblastların aktivasyonu ve Bağ doku birikimi

Fibroblastlar hasar bölgesine göç eder ve çoğalır

Bu hücrelerce üretilen ESM proteinleri birikir

Transforming growth factor-β (TGF-β)

Platelet-derived growth factor (PDGF)

Sitokinler

Bağ dokunun yeniden biçimlendirilmesi

Doku tamirini etkileyen faktörler

Robbins Basic Pathology

Robbins Basic Pathology

Cilt yaralanmalarının iyileşmesi

Robbins Basic Pathology

Primer iyileşme

Temiz, enfekte olmayan cerrahi kesi

Cerrahi sütürlerle yaklaştırılmış

Epitelyal bazal membran devamlılığında fokal bozulma

Görece az epitelyal ve konnektif doku ölümü

Tamirin temelinde epitelyal rejenerasyon var

Küçük bir skar oluşur

Minimal yara kontraksiyonu olur

İnsizyon bölgesi öncelikle fibrin pıhtısı ile dolar

Granülasyon dokusu hızlıca gelişir

Yeni epitelle kapatılır

İlk 24 saat

İnsizyon sahasındaki fibrin içine nötrofiller ilerler

Epidermiste kesilen yerlere komşu bazal hücrelerde mitotik aktivite artar

Robbins Basic Pathology

24-48 saat

Her iki uçtaki epite

Epithelial cells from both edges have begun to migrate and proliferate along the dermis

Deposite basement membrane components as they progress

The cells meet in the midline beneath the surface scab

A thin but continuous epithelial layer.

Robbins Basic Pathology

Healing by First Intention

By day 3

Neutrophils replaced by macrophages

Granulation tissue progressively invades the incision space

Collagen fibers are evident at the incision margins, but these are vertically oriented and do not bridge the incision

Epithelial cell proliferation continues, yielding a thickened epidermal covering layer

Robbins Basic Pathology

By day 5

Neovascularization reaches its peak

Granulation tissue fills the incisional space

Collagen fibrils become more abundant and begin to bridge the incision

The epidermis recovers its normal thickness

Differentiation of surface cells yields a mature epidermal architecture with surface keratinization

Robbins Basic Pathology

Second week

Continued collagen accumulation and fibroblast proliferation

The leukocyte infiltrate, edema, and increased vascularity are substantially diminished

Increasing collagen deposition within the incisional scar

Regression of vascular channels

Robbins Basic Pathology

By the end of the first month

Scar consists of a cellular connective tissue

No inflammatory cells

Covered by a normal epidermis

Dermal appendages destroyed in the line of the incision are permanently lost The tensile strength of the wound increases with time

Robbins Basic Pathology

Healing by Second Intention

Robbins Basic Pathology

Healing by Second Intention (secondary union)

Inflammatory reaction is more intense

Abundant granulation tissue

Robbins Basic Pathology

Healing by Second Intention

Accumulation of ECM and formation of a large scar

Followed by wound contraction by myofibroblasts

Robbins Basic Pathology

Healing of Skin Wounds

Wound strength

70% to 80% of normal by 3 months

Usually does not improve

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Fibrosis in Parenchymal Organs

Excessive deposition of collagen and other ECM components in a tissue

Deposition of collagen in chronic diseases.

The basic mechanisms of fibrosis are the same as those of scar formation during tissue repair

Tissue repair occurs after a short-lived injurious stimulus, follows an orderly sequence of steps

**Fibrosis is induced by persistent injurious stimuli **

Responsible for organ dysfunction and even organ failure

Yara İyileşmesi ve Tamir

Dr. Serdar BALCI

Tamir (İyileşme)

Hasar sonrası doku mimarisinin ve aktivitesinin restorasyonu

Hasarlı dokunun rejenerasyonu

Bağ dokuda skar oluşumu

Rejenerasyon

Skar oluşumu (Nedbeleşme)

Rejenerasyon kapasitesi olmayan dokularda

Dokudaki destek yapılarda zarar görümüştür

Tamir fibröz doku oluşumu ile sonuçlanır → skar oluşumu

Kayıp parankimal hücrelerin fonksiyonu yerine getirilemez

Yapısal sağlamlık elde edilmeye çalışılır, böylece rezidü hücreler aktivitelerini yerine getirebilir

Organizasyon

Organize pnömoni

İnflamatuar eksuda ile dolu bir boşlukta gelişen fibrozis

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins Basic Pathology

Hücre ve doku rejenerasyonu

Hücre ve doku rejenerasyonundaki faktörler

Hücre proliferasyonu

Büyüme Faktörleri

Ekstaselüler Matriks

Hücre çoğalmasının kontrolü

Dokuların çoğalma kapasiteleri

Robbins Basic Pathology

Kök Hücreler

Robbins Basic Pathology

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins Basic Pathology

Robbins and Cotran’s Pathological Basis of Diseases

Büyüme Faktörleri

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins and Cotran’s Pathological Basis of Diseases

Robbins Basic Pathology

Robbins Basic Pathology

Ekstraselüler matriks

Robbins Basic Pathology

Ekstraselüler matriksin fonksiyonları

Skar oluşumu

Ciddi, kronik hasar

Bölünemeyen hücreler hasara uğradığında

Tamir bağ doku ile olur

Rejenerasyon gösteren hücreler ve skar birlikte olabilir

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Tamir başlangıcı hasardan sonra ilk 24 saat içinde başlar

Fibroblastların göçü

Fibroblast ve endotel hücre proliferasyonu

Robbins Basic Pathology

Granülasyon dokusu

Çok miktarda damar

Arada lökositler

Makroskopik olarak pembe granüler görünüm

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Anjiogenez

Robbins Basic Pathology

Robbins Basic Pathology

Fibroblastların aktivasyonu ve Bağ doku birikimi

Fibroblastlar hasar bölgesine göç eder ve çoğalır

Bu hücrelerce üretilen ESM proteinleri birikir

Transforming growth factor-β (TGF-β)

Platelet-derived growth factor (PDGF)

Sitokinler

Bağ dokunun yeniden biçimlendirilmesi

Doku tamirini etkileyen faktörler

Robbins Basic Pathology

Robbins Basic Pathology

Cilt yaralanmalarının iyileşmesi

Robbins Basic Pathology

Primer iyileşme

Temiz, enfekte olmayan cerrahi kesi

Cerrahi sütürlerle yaklaştırılmış

Epitelyal bazal membran devamlılığında fokal bozulma

Görece az epitelyal ve konnektif doku ölümü

Tamirin temelinde epitelyal rejenerasyon var

Küçük bir skar oluşur

Minimal yara kontraksiyonu olur

İnsizyon bölgesi öncelikle fibrin pıhtısı ile dolar

Granülasyon dokusu hızlıca gelişir

Yeni epitelle kapatılır

İlk 24 saat

İnsizyon sahasındaki fibrin içine nötrofiller ilerler

Epidermiste kesilen yerlere komşu bazal hücrelerde mitotik aktivite artar

Robbins Basic Pathology

24-48 saat

Her iki uçtaki epite

Epithelial cells from both edges have begun to migrate and proliferate along the dermis

Deposite basement membrane components as they progress

The cells meet in the midline beneath the surface scab

A thin but continuous epithelial layer.

Robbins Basic Pathology

Healing by First Intention

By day 3

Neutrophils replaced by macrophages

Granulation tissue progressively invades the incision space

Collagen fibers are evident at the incision margins, but these are vertically oriented and do not bridge the incision

Epithelial cell proliferation continues, yielding a thickened epidermal covering layer

Robbins Basic Pathology

By day 5

Neovascularization reaches its peak

Granulation tissue fills the incisional space

Collagen fibrils become more abundant and begin to bridge the incision

The epidermis recovers its normal thickness

Differentiation of surface cells yields a mature epidermal architecture with surface keratinization

Robbins Basic Pathology

Second week

Continued collagen accumulation and fibroblast proliferation

The leukocyte infiltrate, edema, and increased vascularity are substantially diminished

Increasing collagen deposition within the incisional scar

Regression of vascular channels

Robbins Basic Pathology

By the end of the first month

Scar consists of a cellular connective tissue

No inflammatory cells

Covered by a normal epidermis

Dermal appendages destroyed in the line of the incision are permanently lost The tensile strength of the wound increases with time

Robbins Basic Pathology

Healing by Second Intention

Robbins Basic Pathology

Healing by Second Intention (secondary union)

Inflammatory reaction is more intense

Abundant granulation tissue

Robbins Basic Pathology

Healing by Second Intention

Accumulation of ECM and formation of a large scar

Followed by wound contraction by myofibroblasts

Robbins Basic Pathology

Healing of Skin Wounds

Wound strength

70% to 80% of normal by 3 months

Usually does not improve

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Robbins Basic Pathology

Fibrosis in Parenchymal Organs

Excessive deposition of collagen and other ECM components in a tissue

Deposition of collagen in chronic diseases.

The basic mechanisms of fibrosis are the same as those of scar formation during tissue repair

Tissue repair occurs after a short-lived injurious stimulus, follows an orderly sequence of steps

**Fibrosis is induced by persistent injurious stimuli **

Responsible for organ dysfunction and even organ failure