Cell injury, apoptosis and death II Flashcards

1
Q

what are some early functional changes as a result of cell injury

A
  • dec ATP gen
  • loss of MEMBRANE integrity
  • PROTEIN SYNTHESIS defects
  • cytoskeletal samage and DNA damage
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2
Q

what are some morphological changes as a result of reversible cell injury

A
  • cellular swelling
  • plasma membrane alterations (blebbing, blunting and microvilli distortion)
  • mitochondrial swelling
  • dilation of ER
  • nuclear alterations (disaggregation of granular and fibrillar elements)
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3
Q

when a cell is in necrosis what happens

A
  • extensive damage to ALL CELLULAR MEMBRANES
  • swelling of LYSOSOMES and VACUOLIZATION of mitochondria
  • extracellular calcium enters cell
  • intracellular calcium (from stores) is released
  • activation of enzymes (membrane catabolism, protein, ATP and nucleic acids)
  • continued loss of PROTEINS, COENZYMES, RNA from the hyperpermeable plasma membrane
  • nuclear changes: PYNKNOSIS (shrink), KARYORRHEXIS (fragmentation) and KARYOLYSIS (disintegration)
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4
Q

what is necrosis

A

pathological cellular or tissue death in a living organism, irrespective of cause
- there are MORPHOLOGICAL CHANGES that follow cell death, resulting from the PROGRESSIVE DEGRADATIVE ACTION OF ENZYMES on lethally injured cells

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5
Q

what are the different types of necrosis

A
  • coagulative necrosis
  • liquefactive necrosis
  • caseous necrosis
  • fat necrosis
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6
Q

describe coagulative necrosis

A
  • most common form of necrosis
  • characterised by HYPOXIC death
  • cell MAINTAINS ARCHITECTURE having lost
  • cytoplasm looks COAGULATED and stains pink with EOSIN
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7
Q

describe liquefactive/colliquative necrosis

A
  • characteristic of FOCAL BACTERIAL INF (accumulation of inflammatory cells)
  • HYPOXIC death of cells in CNS
  • complete digestion of dead cells causes tissue to become LIQUID VISCOUS MASS
  • material= creamy yellow dead cells due to dead WBC (pus)
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8
Q

describe caseous necrosis

A
  • most commonly in foci of TB inf
  • cheesy white gross appearance
  • obliterated tissue architecture
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9
Q

describe fat necrosis

A
  • often in ACUTE PANCREATITIS as a result of release of activated pancreatic lipases into substance of pancreas and the peritoneal cavity
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10
Q

what is apoptosis

A

programmed cell death

  • individual cell deletion
  • in physiological growth control and in disease
  • activated/prevented by a variety of stimuli
  • reduced apop causes CELL ACCUMULATION
  • inc apop causes EXCESSIVE CELL LOSS
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11
Q

what regulates apoptosis

A
  • tightly regulated by INTRACELLULAR program in which PRO-APOPTOTIC cells activate enzymes that degrade the cells own DNA and proteins
    NORMAL: eliminate unwanted/harmful cells
    PATHOLOGY (radiation, viral inf): eliminate irreversibly damaged cells esp when damage affects cell DNA
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12
Q

what are characteristics of apoptotic cells

A
  • degradataion of cytoskeletal framework
  • DNA fragmentation
  • loss of mitochondrial function
  • nucleus shrinkage (PYKNOSIS) and fragmentation (KARYORRHEXIS)
  • cell shrinks, retains INTACT PLASMA membrane, which rapidly induces PHAGOCYTOSIS
  • APOPTOTIC BODIES
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13
Q

what are some differences between apoptosis and necrosis

A

Necrosis:

  • has ENZYMATIC DIGESTION
  • has LEAKAGE OF CELLULAR CONTENTS

Apoptosis:

  • chromatin condensation and fragmentation
  • cytoplasm budding
  • APOPTOTIC bodies
  • phagocytosis of apoptotic bodies
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