Pathology 2

Key Concepts of Cell Injury (Hücre Yaralanmasının Temel Kavramları)

• Healthy Cell (Sağlıklı Hücre)

  • Homeostasis: The stable equilibrium state of a healthy cell is crucial for its survival and function, maintained through various physiological processes such as cellular signaling, nutrient transport, and waste management. Disruptions in homeostasis can result in cell injury.

  • Injurious Stimulus: Any external or internal factor (e.g., toxins, pathogens, hypoxia, or mechanical injury) that disrupts homeostasis can lead to cellular dysfunction. Examples include exposure to heavy metals, UV radiation, infections, and ischemia, which may trigger a cascade of biochemical and molecular events leading to cell injury.

Types of Cell Injury (Hücre Yaralanma Türleri)

• Reversible Injury: (Geri Dönüşümlü Yaralanma)

  • This occurs in situations where the injurious stimulus is mild and transient. Cells can recover their normal structure and function if the injurious stimuli are promptly removed. For instance, slight hypoxia may lead to cellular swelling, but if oxygen supply is restored quickly, the cell can revert to its normal state.

• Irreversible Injury: (Geri Dönüşümsüz Yaralanma)

  • Severe, progressive damage that overwhelms the cell's ability to repair itself leads to cell death. This can occur due to prolonged exposure to harmful stimuli, resulting in irreversible changes in the cell structure and function, such as loss of membrane integrity and mitochondrial dysfunction.

Outcomes of Irreversible Injury (Geri Dönüşümsüz Yaralanmanın Sonuçları)

• Necrosis: (Nekroz)

  • An uncontrolled and chaotic process of cell death characterized by the breakdown of cellular components and the subsequent release of intracellular substances into the extracellular space, often leading to inflammatory responses. Types of necrosis include coagulative, liquefactive, gangrenous, caseous, fat, and fibrinoid necrosis, each with distinct characteristics and causes.

• Apoptosis: (Apoptoz)

  • A highly regulated and organized process of programmed cell death that serves as a mechanism to eliminate damaged or unwanted cells without inflammation, essential for maintaining tissue homeostasis and development. It can occur under both physiological processes, such as embryonic development, and pathological conditions, such as DNA damage or cellular stress.

Irreversible Cell Injury (Geri Dönüşümsüz Hücre Yaralanması)

Morphological Changes (Morfolojik Değişiklikler)

• Plasma Membrane Blebs: (Plazma Zarı Kabarcıkları)

  • Characterized by the formation of bubble-like protrusions in the plasma membrane, indicating cell stress and impending cell death.

• Increased Intracellular Volume: (Artmış İntraselüler Hacim)

  • This occurs primarily due to the influx of water resulting from ion imbalances, leading to cellular swelling. This change often signifies early stages of cell injury.

• Mitochondrial Changes: (Mitochondrial Değişiklikler)

  • Visible swelling of mitochondria can occur alongside morphological changes such as calcification, indicating disrupted energy production and cellular metabolism.

• Disaggregated Ribosomes: (Dağılmış Ribozomlar)

  • These free-floating ribosomes in the cytoplasm exhibit changes in protein synthesis capacity, further indicating cellular distress.

• Dilated Endoplasmic Reticulum: (Şişmiş Endoplazmik Retikulum)

  • Characterized by swelling and vesicular transformations, signifying disruption of normal protein processing and secretion functions.

Nuclear Changes (Nükleer Değişiklikler)

• Condensed Chromatin: (Kondanse Kromatin)

  • A hallmark of nuclear degeneration; indicates loss of normal nuclear architecture and function, often observed in irreversibly injured cells.

• Shriveled Membrane: (Büzülmüş Zat)

  • A significant shrinkage and damage of the nuclear membrane indicates critical cellular distress.

Characteristics of Irreversibility (Geri Dönüşsüzlük Özellikleri)

• Mitochondrial Dysfunction: (Mitochondrial Fonksiyon Bozukluğu)

  • A critical indicator of irreversible injury, leading to loss of ATP production and initiating cell death pathways.

• Structural DNA Integrity Loss: (Yapısal DNA Bütünlüğü Kaybı)

  • Damage to the DNA structure results in failure of genetic repair mechanisms, marking the transition to irreversible cellular changes.

• Membrane Function Disturbances: (Zar Fonksiyonu Bozuklukları)

  • Profound disruptions in membrane functions, leading to loss of selective permeability and eventual cell lysis.

Reversible Injury Indicators (Geri Dönüşümlü Yaralanma Göstergeleri)

Early Signs of Recovery (Kurtarma İçin Erken İşaretler)

• Increased Cell Size: (Artmış Hücre Boyutu)

  • The process of cellular hypertrophy emerges as the cell works to restore its normal physiological functions.

• Clumping of Chromatin: (Kromatin Toparlanması)

  • Indicates a disorganization of chromatin structure, signaling early cellular stress.

• Swelling: (Şişme)

  • Particularly noted in the endoplasmic reticulum (ER) and mitochondria; serves as a critical indicator of cellular injury.

• Membrane Blebs: (Zar Kabarcıkları)

  • Small blister formations on the cell membrane that suggest early stages of injury.

• Myelin Figures: (Miyelin Figürleri)

  • Degraded lipid components of cells, indicating phospholipid damage and cellular compromise.

Additional Signs (Ek Göstergeler)

• Vacuolation: (Vakuolizasyon)

  • The formation of vacuoles within the cell, often associated with cellular swelling and necrosis.

• Inflammatory Response: (İnflamatuar Yanıt)

  • Necrosis typically triggers a potent inflammatory response, mobilizing immune cells and promoting tissue repair.

Necrosis Overview (Nekroz Genel Bakış)

Definition (Tanım)

• Accidental cell death characterized by a disruption of membrane integrity and associated inflammatory response. Often results from severe injury or lack of blood supply.

Features of Necrosis (Nekrozun Özellikleri)

• Cellular Content Leakage: (Hücresel İçerik Sızıntısı)

  • Resulting from membrane disruption, allowing cellular contents to spill, leading to inflammation and damage to surrounding tissues.

• Inflammatory Response: (İnflamatuar Yanıt)

  • A localized response from surrounding tissues triggered by necrotic cell death.

Necrosis Morphology (Nekroz Morfolojisi)

Light Microscopy Findings (Işık Mikroskobu Bulguları)

• Increased Eosinophilia: (Artmış Eozinofili)

  • Observed due to loss of RNA and alterations in protein binding, indicating necrotic changes.

• Glassy Appearance: (Cam Görünüm)

  • Microscopic appearance indicating loss of normal structural integrity, typically signifying necrotic cells.

• Vacuolation: (Vakuolizasyon)

  • Presence of bubbles indicative of underlying necrotic processes, often observed microscopically.

Nuclear Changes in Necrosis (Nekrozda Nükleer Değişiklikler)

• Pyknosis: (Piknoz)

  • Cellular shrinkage associated with a dense nuclear stain, indicating irreversible injury.

• Karyorrhexis: (Karyoreksis)

  • Fragmentation and dissolution of the nucleus, signifying severe cellular damage.

• Karyolysis: (Karyolizis)

  • Fading or dissolution of chromatin basophilia, suggesting loss of nuclear integrity.

Tissue Necrosis Patterns (Doku Nekrozu Desenleri)

Types of Necrosis (Nekroz Türleri)

• Coagulative Necrosis: (Koagülatif Nekroz)

  • Characterized by preservation of tissue architecture despite cell death, typically seen in cases of ischemia.

• Liquefactive Necrosis: (Sıvılaşmış Nekroz)

  • Results in the formation of pus-like liquid due to the transformation of necrotic tissue into a liquid viscous mass, prevalent in brain infarcts.

• Gangrenous Necrosis: (Gangrenöz Nekroz)

  • Results from the complete loss of blood supply to a region, often leading to tissue death and potential systemic complications.

• Caseous Necrosis: (Kazeöz Nekroz)

  • Associated commonly with tuberculosis infections, characterized by cheese-like (caseous) necrotic tissue.

• Fat Necrosis: (Yağ Nekrozu)

  • Occurs due to trauma or inflammation of adipose tissue, leading to lipolysis and release of inflammatory mediators.

• Fibrinoid Necrosis: (Fibrinoid Nekroz)

  • Results from immune complex deposition in blood vessel walls, leading to vascular damage and inflammation.

Coagulative Necrosis (Koagülatif Nekroz)

• Description: (Tanım)

  • Maintains structural integrity despite cell death, often seen in myocardial infarctions where necrosis occurs without immediate loss of tissue architecture.

Liquefactive Necrosis (Sıvılaşmış Nekroz)

• Characteristics: (Özellikler)

  • Characterized by the transformation of the tissue into a viscous liquid mass filled with pus due to local bacterial infection or prolonged ischemia.

• Examples: (Örnekler)

  • Commonly observed as a result of cerebral infarcts and bacterial infections.

Caseous Necrosis (Kazeöz Nekroz)

• Description: (Tanım)

  • Results in a granulomatous formation filled with necrotic debris, commonly associated with mycobacterial infections such as tuberculosis.

Fat Necrosis (Yağ Nekrozu)

• Causes: (Nedenler)

  • Often arises from trauma or damage to adipose tissue, resulting in lipolysis and inflammatory response in the surrounding area.

Fibrinoid Necrosis (Fibrinoid Nekroz)

• Context: (Bağlam)

  • Mainly associated with immune-mediated vascular damage, leading to necrotic changes in the walls of blood vessels.