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Pathology > Necrosis, Apoptosis, and Postmortem Changes > Flashcards

Necrosis, Apoptosis, and Postmortem Changes Flashcards

1
Q

Liver

A

Normal liver sinks, diseased liver with hepatic lipidosis floats

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2
Q

Necrosis

A
  • Death by swelling of the cell with eventual rupture of cell membranes
  • Common usage - cell death + degradative changes
  • -Typically involves groups or zones of cells and elicits an inflammatory response
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3
Q

Apoptosis

A
  • In contrast to necrosis, is directed by cellular signaling cascades and typically affects individual cells
  • Process of condensation and shrinkage of the cell and its organelles with eventual fragmentation of the cell
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4
Q

Autophagy

A

-A possible third mechanism of cell death

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5
Q

Autolysis

A

=”Self-digestion”

  • Degradative changes in a cell due to action of endogenous enzymes, primarily from lysosomes
  • Changes are amplified and accelerated by bacterial decomposition from bacteria
  • Putrefaction
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6
Q

Putrefaction

A

=Postmortem bacterial metabolism and dissolution of host tissues result in the production of color and texture changes, gas production, and odors

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7
Q

Fixation

A
  • Rapid killing of cells by denaturing proteins to prevent autolysis and preserve architecture
  • Commonly use 10% neutral buffered formalin
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8
Q

Morphologic alterations in cell injury

A
  • Reversible injury

- Irreversible injury

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9
Q

Reversible injury

A
  • Generalized cell swelling and swelling of its organelles, blebbing of the plasma membrane, detachment of ribosomes from the ER and clumping of nuclear chromatin
  • Within limits, the cell can repair these derangements
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10
Q

Irreversible injury

A
  • Persisent or excessive injury causes cells to pass the “point of no return” into irreversible injury and cell death
  • Different injurious stimuli may induce death by necrosis or apoptosis
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11
Q

Morphologic changes associated with necrosis

A
  • Color change
  • -Pallor diffuse or patchy
  • -Dark red, brown or black
  • Loss of strength
  • Odor
  • -Foul odor if putrefactive bacteria present
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12
Q

Histologic features of single cell necrosis

A
  • Necrotic cells unable to maintain membrane integrity - contents often leak out, inciting inflammation
  • Histologically:
  • -Increased eosinophilia in HE stained slides due to decreased RNA
  • -Glassy homogeneous appearance due to loss of glycogen particles
  • -Vacuolated (moth-eaten) cytoplasm due to enzymes digesting organelles
  • -Three nuclear patterns, all due to breakdown of DNA:
  • –Karyolysis
  • –Pyknosis
  • –Karyorrhexis
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13
Q

Irreversible cell injury morphology

A
  • Karyolysis
  • Pyknosis
  • Karyorrhexis
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14
Q

Karyolysis

A

=Basophilia of the chromatin fades due to loss of DNA

–Chromatin dissolution due to action of DNAases and RNAases

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15
Q

Pyknosis

A

=Nuclear shrinkage and increased basophilia

–Also seen in apoptotic cell death

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16
Q

Karyorrhexis

A

=Pyknotic nucleus undergoes fragmentation

17
Q

Morphologic changes in reversible cell injury and necrosis

A
  • Normal kidney tubules with viable epithelial cells
  • Early (reversible) ischemic injury showing surface blebs, increased eosinophilia of cytoplasm, and swelling of occasional cells
  • Necrosis (irreversible injury) of epithelial cells, with loss of nuclei, fragmentation of cells, and leakage of contents
18
Q

Advanced cellular changes

A
  • Loss of cell outline
  • Loss of differential staining
  • Absence of cells
19
Q

Possible sequelae to necrosis

A
  • Death
  • Inflammation
  • Liquefaction (loses structure)
  • Encapsulation (collagen capsule formation)
  • Sequestration (sequestrum = fragment of dead, isolated tissue)
  • Sloughing (ulcer = surface excavation due to sloughing of necrotic tissue; tissue extends below the basal layer of epithelium)
  • Mineralization
  • Healing: outcome depends on the type of tissue and extent of injury
20
Q

Apoptosis

A
  • Pathway of cell death that is tightly regulated by intrinsic enzymes (degrade own DNA)
  • Apoptotic bodies: portions of the cytoplasm and nucleus of the apoptotic cell
  • -Plasma membrane remains intact, but its structure is altered so that phagocytosis is stimulated quickly
  • -Cell fragments are rapidly devoured before the contents have leaked out - no inflammation
21
Q

Apoptosis physiological situations

A
  • Embryogenesis
  • Involution of hormone-dependent tissues
  • Elimination of potentially harmful self-reactive lymphocytes
  • Death of host cells that have served their useful purpose (ex: neutrophils)
22
Q

Apoptosis pathologic conditions

A
  • DNA damage (radiation, cytotoxic cancer drugs)
  • Accumulation of misfolded proteins (degenerative diseases of the CNS)
  • Cell death in certain infections (simian immunodeficiency virus - SIV)
  • Pathologic atrophy in parenchymal organs after duct obstruction (pancreas, parotid gland, kidney)
23
Q

Apoptosis morphology

A
  • Cell shrinkage
  • Chromatin condensation (aggregates peripherally, under the nuclear membrane)
  • Cytoplasmic blebs and apoptotic bodies
  • Phagocytosis of apoptotic bodies, usually by macrophages
24
Q

Mechanisms of apoptosis

A

-Activated caspases

25
Q

Caspases

A

Proteases that exist as inactive proenzymes (zymogens) in the cytoplasm

26
Q

Two distinct pathways of apoptosis that converge on caspase activation

A
  1. Intrinsic mitochondrial pathway
  2. Extrinsic death receptor pathway

-Differ in induction and regulation of apoptosis

27
Q

Intrinsic mitochondrial pathway

A
  • Can be triggered by a variety of cell stressors
  • Mitochondrial outer membrane permeability (MOMP) is increased due to signaling from BCL2 family proteins
  • Cytochrome-c and other pro-apoptotic proteins leak out of the mitochondrial intermembrane space and into the cytosol
  • Cytochrome-c promotes the assembly of the apoptosome
  • Apoptosome activates caspases
  • Note: MOMP is the lethal permeabilization that initiates intrinsic apoptosis, NOT mitochondrial permeability transition pore
28
Q

Extrinsic death receptor pathway

A
  • Plasma membrane receptors are activated
  • Lead to the assembly of adaptor proteins into a “death inducing signaling complex” which activates caspases
  • Death receptors: Fas-receptor (TNF family of receptors)
29
Q

Postmortem change

A

“Decomposition”
=Degradative changes seen in cells, tissues, and organs after death of the animal
–These changes are due to the action of lysosomal enzymes

30
Q

Postmortem change microscopic alterations

A
  • Uniform loss of differential staining in a tissue section
  • Bacilli in blood vessels and tissues without inflammation
  • Gas bubbles - from putrefactive bacteria
  • Hemolysis of red blood cells - appear faint pink or orange, with indistinct margins
  • Desquamation of endothelium and epithelium (usually with normal morphology)
31
Q

Postmortem change gross alterations

A
  • Postmortem tymapnities (“bloat”)
  • -Distension of GIT; prolapsed rectum or vagina
  • Postmortem emphysema
  • -Gas pockets in tissues
  • -Due to gas-producing, PM bacilli
  • Epithelial desquamation - esp. in rumen
  • Rigor mortis
  • Algor mortis
  • Liver mortis
  • Postmortem clotting
  • Hemoglobin imbibition
  • Bile imbibition
  • Pseudomelanosis
32
Q

Rigor mortis

A
  • Stiffening of muscles after death
  • Due to release of Ca2+ and decreased ATP –> muscle contraction
  • 1-6 hours after death
33
Q

Algor mortis

A

-Cooling of body after death

34
Q

Liver mortis

A
  • Hypostatic congestion
  • Dark discoloration of dependent tissues
  • Due to gravitation of blood
35
Q

Postmortem clotting

A
  • Clotting of heart and vessels usually occurs within several hours
  • Before the clot forms, erythrocytes may settle resulting in a clot having two separate portions
  • -A red and yellow clot –> chicken fat clot
  • Separation depends on the erythrocyte sedimentation rate (ESR) and is normally high in horses
  • PM clots: unattached and tend to be shiny and wet and form a perfect cast of vessel lumen
  • AM clots: attached to vessel walls, tend to be dry and dull, and are laminated with a tail extending downstream from the point of attachment
36
Q

Hemoglobin imbibition

A

-Postmortem hemolysis –> diffusion of hemoglobin into intima and surrounding tissues –> pink or red discoloration

37
Q

Bile imbibition

A

-Yellow-green discoloration

38
Q

Pseudomelanosis

A

-Hydrogen sulfide produced by intestinal bacteria + iron from hemolyzed RBC –> iron-sulfide

Pathology (6 decks)

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