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87 Cards in this Set
- Front
- Back
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Cause of disease?
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Etiology
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Progression of the disease?
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Pathogenesis
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Signs and Symptoms?
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Clinical manifestations of disease
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Cell injury can either be?
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Reversible of Irreversible
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Irreversible cell injury leads to either?
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Necrosis
Apoptosis (planned) |
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Proliferative capacity of cells is variable?
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Labile
Stable Perment |
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continuously dividing cells ( epithelium, bone marrow)
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labile cells
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Quiescent (in GO stage; hepatocytes, smooth m., lymphocytes)
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Stable cells
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nondiving (neurons, skeletal and cardiac muscle)
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Permanent cells
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Cellular adaptions to
increased demand |
hyperplasia (increase #)
hypertrophy (increase size) |
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Cellular adaptions to
decreased nutrients |
atrophy
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Cellular adaptions to
Chronic Irritation |
Metaplasia
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Cellular adaptions to
Hypozia (acute,limited) |
reversible changes
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Cellular adaptions to
Hypoxia (severe) |
Death:
Necrosis or Apoptosis |
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Increase in cell SIZE w/ subsequent increase in organ size
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HYPERTROPHY
- can be physiologic or pathologic |
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Causes of hypertrophy?
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Increased functional demand
Hormonal stimulation |
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Increase in the NUMBER of cells in an organ which may then increase in size
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HYPERPLASIA
- physiologic or pathologic |
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2 examples of physiologic hyperplasia?
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1. Hormonal hyperplasia (f/m) breast at puberty and in pregnancy
2. Compensatory hyperplasia - liver regeneration after partial resection |
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2 examples of causes of PATHOLOGIC hyperplasia (increase in cell #)?
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1. Excess hormone - ENDOMETRIAL hyperplasia due to estrogens
2. Growth factors - Warts (HPV 6, 11) |
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is HYPERPLASIA a neoplastic process?
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NO
- but may be FERTILE SOIL for malignancy |
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Atypical Hyperplasia bad b/c
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in the endometrium carries an increased risk for development of endometrial adenocarcinoma (CA of the glands)
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Decrease in the SIZE of a cell or organ by loss of cell substance
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Atrophy
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Causes of atrophy?
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1. decreased workload
2. loss of innervation 3. Decreased blood supply 4. Inadequate nutrition 5. Loss of endocrine stimulation 6. Pressure |
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Protein degradation is important in atrophy - 2 key processes?
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1. lysosomes w/ hydrolytic enzymes
2. Ubiquitin-proteasome pathway |
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Incomplete development of an organ so that it fails to reach adult size
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HYPOPLASIA
(example, hypoplastic left ventricle) |
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REVERSIBLE change in which one ADULT cell type is replaced by another ADULT cell type?
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Metaplasia
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Metaplasia is usually the change in what cell type to what cell type?
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Columnar changes to squamous
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Typical causes of metaplasia?
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chronic irritation
Calculi in ducts Vitamin A deficiency Cervix Barret esophagus |
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Cervix metaplasia?
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COLUMNAR EPITHELIUM of the endocervic becomes SQUAMOUS (dysplasia and squamous CA may develop)
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Barrett esophagus
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Gastric reflux results in COLUMNAR epithelium REPLACING squamous epithelium in the ESOPHAGUS (dysplasia and adenocarcinoma may occur (cancer of the glands)
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COLUMNAR --> SQUAMOUS
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Cervix metaplasia
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SQUAMOUS --> COLUMNAR
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Barrett esophagus
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Atypical proliferative changes due to chronic irritation or inflammation?
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DYSPLASIA
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What is key to remember about DYSPLASIA as opposed to METAPLASIA?
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Dysplasia will become malignant if not Tx's (premalignant change), while Metaplasia is not malignant itself, but it may be a step in pathway
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oxygen deprivation
physical agents chemical agents and drugs infectious agents Immunologic reactions Genetic dereangements Nutritional imbalances |
Causes of Cell Injury
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Celular changes secondary to injury may be either
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Reversible
Irreversible |
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Cellular swelling
Cell membrane blebs Detached ribosomes Chromatin clumping |
Reversible cell changes secondary to injury
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Lysosomes rupture
Dense bodies in mitochondria Cell membrane rupture Karyolysis, karyorrhexis Pyknosis |
IRReversible cell changes secondary to injury
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Death of GROUPS of cells after INJURY; usually w/ INFLAMMATION
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NECROSIS
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genetically CONTROLLED, ATP and ENZYME-DEPENDENT death of INDIVIDUAL cells; usually NO INFLAMMATION
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APOPTOSIS
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Cell membrane doesn't rupture, phagocytosis occurs
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Apoptosis
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Neutrophils involved in cleaning up after cell death
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Necrosis
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the cellular response to injurious stimuli depends on
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the type of injury, its duration, and its severity
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The CONSEQUENCES of cell injury depend on th
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type, state, and adaptability of the injured cell
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Susceptibility of cells to ischemic necrosis
HIGH |
Neurons (3-4 min)
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Susceptibility of cells to ischemic necrosis
INTERMEDIATE |
Myocardium, hepatocytes, renal epithelium (30 min-2hr)
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Susceptibility of cells to ischemic necrosis
LOW |
Fibroblasts, epidermis, skeletal muscle (many hours)
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The morphologic changes of cell injury become apparent only after some critical biochemical system w/ in the cell has be deranged
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- manifestation of lethal damage tkae more time to develop than those of reversible damage
-ultrastructural alterations are visible earlier than light microscopic changes |
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Reversible injury
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Cellular swelling
Fatty change |
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Myocardial infarction markers
- 2 hours |
Cardiac specific enzymes and proteins
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Myocardial infarction markers
-4-12 hours |
Morphologic (light microscopic) changes
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What is visible in coagulation necrosis of myocardium?
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Lose nuclei first and anoxic
- 12-24 hours neutrophils come in to remove dead tissue |
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Morphologic changes in GROUPS of cells that follow the death of living tissue; cells and PMNs leak lytic enzymes
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Necrosis
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necrosis of the cytoplasm
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eosinophilia (pinker), vacuoles, calcification, myelin figures
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necrosis of the nucleus
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pyknosis (breaks apart), karyorrhexis, karyolysis
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Patterns of necrosis
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Coagulative
Liquefactive Caseous Fat Fibrinoid |
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Hypoxic death (except brain)
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Coagulative necrosis
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Bacterial infections; also hypoxic death in brain tissue (infarction)
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Liquefactive necrosis
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Tuberculosis
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caseous necrosis
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enzymic or traumatic damage to fatty tissue; eg. Pancreatitis (enzymic)
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Fat necrosis
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What can tell you how the cells have died
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the cytoplasm
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Difference between coagulative necrosis and liquefactive necrosis of the kidney
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coagulative necrosis - all cells die at the same time (no nuclei), kidney glomerulus
Liquefactive necrosis - glomeruli and tubules still present but abscess formation |
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liquefactive necrosis typically observed with
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bacterial infections
- BUT also w/ stroke in the brain will observe it too |
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Characteristic of granulomatous inflammation w/ central necrosis
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surrounded by MP's (nucleated giant cells)
Plus, also have T-cells to act as messengers |
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What causes fat necrosis of the pancreas?
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Damaged by trauma or a stone in duct --> enzymes leak out of pancras and begin to chew it up --> calcification and soap
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Fibrinoid necrosis in an artery is characterized by
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pinking ring going around blood vessel
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Mechanisms of cell injury?
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oxidative phophorylation
mitochondrial damage influx of Ca2+ Free radical formation Membrane damage DNA and protein damage |
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Depletion of ATP causes
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Na+ pump fails
Ca2+ pump fails Decreased protien synthesis (ribosomes detach) Unfolded protein response |
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What happens when
Na+ pump fails? |
Na+ and water enter and K+ is lost; glycolysis depletes glycogen and lowers pH (loss of enzymic activity)
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What happens when
Ca2+ pump fails? |
Ca2+ into cells (toxic)
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What happens when
decreaessd protein synthesis |
ribosomes detach
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Big problem when decreased ATP and energy source?
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Increased anaerobic glycolysis
decreased pH b/c of lactic acid buildup Clumping of nuclear chromatin |
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What can cause mitochondrial damage?
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Increased cytosolic Ca2+
Decreased ATP (hypoxia) |
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What is the Mitochondrial Permeability Transition? (MPT)
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pore that allows cytochrome C to escape
-apoptosis is triggered and cell death occurs |
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What is Cytochrome C
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usually associated with pro-apoptotic proteins
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What can result as a consequence of loss of Ca2+ homeostatsis
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Extracell. Ca2+ is 15X higher than cytosolic Ca2+
-Loss of ATP increases intracellular Ca2+ - Increased Ca2+ activates phospholipases, proteases, endonucleases and ATPases - incrased Ca2+ also increases mitochondrial permeability triggering apoptosis |
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What is a free radical?
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Single unpaired electron; highly reactive
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Normal metabolism produces what free radicals?
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superoxide anion
hydrogen peroxide and hydroxyl ion |
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What free radical is produced in neutrophils
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superoxide
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What can free radicals do that is bad?
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Lipid peroxidation of cell membranes
-protein fragmentation -breaks in DNA |
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What are some antioxidant enzymes
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superoxide dismutase
catalase glutathione peroxidase |
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What are some antioxidant vitamins?
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A, E, ascorbic acid, glutathione
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What are a few membrane permeabilty defects?
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plasma membrane
mitochondrial membrane Lysosomal membrane (release of RNases, DNases and proteases) - membranes of organelles |
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Deficiency of Oxygen; causes include cardiorespiratory failure, anemia, CO poisoning; cell injury and death
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Hypoxia
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loss of blood supply (OXYGEN AND NUTRIENTS)
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Ischemia
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Which more rapidly and severely injures tissues - hypoxia or ischemia?
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Ischemia (loss of both oxygen and nutrients)
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Loss of oxygen results in
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anaerobic glycolysis
-- causes decreased cellular pH and clumping of nuclear chromatin |
