Cell Injury Flashcards
Causes of cell injury
Oxygen deprivation
•Physical agents
•Chemical agents and drugs
•Infectious diseases
•Immunologic reactions
•Nutritional imbalance
•Genetic derangements
Hypoxia
It refers to inadequate oxygenation of tissue. It is the most common cause of cell injury.
•Causes of hypoxia:
••• Decreased blood flow is called ischemia. It may be due to thrombosis, embolism, atherosclerosis or external compression of vessel.
Inadequate oxygenation of the blood (hypoxemia)
•–– Due to pulmonary disease
•–– Decreased perfusion of tissues: e.g. cardiac failure, hypotension shock
•–– Decreased oxygen-carrying capacity of the blood: e.g. anemia
•–– Severe blood loss.
Immunological reactions
Autoimmunity: Immune reactions to endogenous self-antigens are responsible for
autoimmune diseases.
••• Hypersensitivity reactions and other immune reactions: Heightened immune reactions to many external agents (e.g. microbes and environmental agents).
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Cellular response to injury depends on
Cellular response to injury depends on:
•1) type of injury,
•2) duration of injury and
•3) severity of injury.
Consequences of injury depends on
type of cell involved
• 2) adaptability of cell
•3) status of cell and
•4) genetic makeup of the cell.
Target and biochemical mechanisms of cell injury
1) mitochondrial damage/dysfunction
• 2) disturbance of calcium homeostasis
• 3) damage to cellular membranes and
• 4) damage to DNA and misfolding of proteins.
Reversible cell injury
A. Decreased synthesis of ATP by oxidative phosphorylation
•B. Decreased function of Na+ K+ ATPase membrane pumps:
•-Influx of Na+ and water
•-Effux of K+
•- Cellular swelling (hydropic swelling)
•-Swelling of endoplasmic reticulum
C. Switch to glycolysis
• - Depletion of cytoplasmic glycogen
•- Increased lactic acid production
•- Decreased intracellular pH
•D. Decreased protein synthesis:
•- Detachment of ribosomes from the rough endoplasmic reticulum
•E. Plasma-membrane blebs and intracytoplasmic myelin figures may be seen.
Ischemic repercussion injury
Ischaemic-Reperfusion Injury
•This is a process by which reperfused tissues sustain loss of cells in addition to the cells that are irreversibly damaged at the end of ischemia.
•It’s clinically important because it contributes to tissue damage during myocardial and cerebral infarction and following therapies to restore blood flow
•Ischaemic-reperfusion injury occur due to the new damaging processes that are set in motion during reperfusion, causing the death of cells that might have recovered
Necrosis
Morphological changes indicative of cell death in a living tissue following harmful injury.
•The necrotic cells bring out acute inflammatory reaction in the surrounding tissue.
Morphology of necrosis
Cytoplasmic changes: Increased eosinophilia.
••• Nuclear changes: These may take up one of three patterns.
•–– Pyknosis: Shrinkage of nucleus which appears shrunken and deeply basophilic (similar to ink drop).
•–– Karyolysis: Progressive fading of basophilic staining of the nuclei and leads to ghost nuclei.
•–– Karyorrhexis: Nucleus breaks up into many smaller fragments
Morphological patterns of necrosis
➢Coagulative
➢Liquefactive
➢Caseous
➢Gangrenous
➢Fat
➢Fibrinoid
Infarct
An area of localized coagulating necrosis
Coagulative necrosis
Common type, outline of dead tissues is preserved (at least for few days). Infarct is a localized area of coagulative necrosis.
••• Causes: Ischemia caused by obstruction in a vessel.
••• Mechanism: Ischemia denatures and coagulates structural proteins and enzymes.
Gross:
•–– Organs affected: All organs except the brain. More frequent in heart, kidney, spleen and limb (dry gangrene).
•–– Appearance: Involved region appear dry, pale, yellow and firm. It is wedge shaped in organs like kidney and spleen.
••• Microscopy : Indistinct outline of dead tissue. Nucleus may be either absent or show karyolysis.
Liquefactive necrosis
Dead tissue rapidly undergoes softening and transforms into a liquid viscous mass.
••• Causes:
•–– Ischemic injury to central nervous system (CNS)
•–– Suppurative infections: Infections by bacteria which stimulate the accumulation of leukocytes.
••• Mechanism: Liquefaction is due to digestive action of the hydrolytic enzymes released from
•dead cells (autolysis) and leukocytes (heterolysis).
••• Gross: Organs affected are:
•–– Brain: Necrotic area is soft and center show liquefaction
•–– Abscess anywhere: Localized collection of pus.
•–– It is also seen in wet gangrene and pancreatic necrosis
••• Microscopy: Pus consists of liquefied necrotic cell debris, dead leukocytes and macrophages (scavenger cells).
