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Pathology Robbins > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is Etiology?

A

Why disease arises

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2
Q

What is pathogenesis

A

How disease develops

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3
Q

In **reversible **cell injury, what changes you can see? And why?

A

Become Swollen because water gets inside as a result of the failure of energy-dependent pumps

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4
Q

What are the two main morphological changes in REVERSIBLE cell injury?

A

Cellular Swelling and Fatty Change

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5
Q

Repercussions of multiple cell swelling or the whole organ? [Macroscopic]

A

Pallor (as a result of compression in capillaries), Turgor and Weight increase.

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6
Q

Repercussions of multiple cell swelling or the whole organ? [Microoscopic]

A

Small clear Vacuoles within Cytoplasm. (Distended segments of the ER)

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7
Q

Non-Lethal Injury caused of cellular swelling is named…?

A

Hydropic Change or Vacular Degeneration

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8
Q

In reversible cell injury, Fatty Change is manifested by?

A

The appearance of Triglyceride-Containing lipid vacuoles in the Cytoplasm (typically in the liver).

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9
Q

Name of the red stain that appears in injury cells?

A

Eosinophilic

by H&E

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10
Q

Intracellular changes associated with cell injury include…?

Inflated and broken furry red balloon

A
  1. Redder
  2. Blebbing
  3. Distortion of microvilli
  4. Loosening of intracellular attachments
  5. Mitochondrial swelling
  6. Dilation of ER
  7. Detachment of ribosomes in ER.
  8. Nuclear alterations (chromatin clumping)
  9. Myelin Figures
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11
Q

Although there are no definite morphological correlations of Irreversibility, how is characterized?

A

-Inability to restore mitochondrial function (OP and ATP prod.)
-Loss of structure and functions of intracellular and plasma membrane.
-Loss of DNA and chromatin structural integrity.

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12
Q

The injury of lysosomal membranes result in…?

A

Enzymatic dissolution of the injured cell, which is the culmination of NECROSIS

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13
Q

Commonly types of injuries (or causes) in Necrosis

A

-Ischemia
-Toxins
-Various infections
-Trauma
(To severe to be repaired)

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14
Q

Features of A) Necrosis and B) Apoptosis in [ Cell size ]

A

A) Enlarged (Swelling)
B) Reduces (shrinkage)

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15
Q

Features of A) Necrosis and B) Apoptosis in [ Nucleus ]

A

A) Pyknosis-> Karyorrhexis->Karyolisis

B) Fragmentation in very small fragments

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16
Q

Features of A) Necrosis and B) Apoptosis in [** Plasma Membrane** ]

A

A) Disrupted
B) Intact; Altered structure. (Especially orientation of lipids)

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17
Q

Features of A) Necrosis and B) Apoptosis in [ Cellular Contents]

A

A) Enzymatic Digestion; may leak out of the cell
B) Intact; (released in apoptotic bodies)

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18
Q

Features of A) Necrosis and B) Apoptosis in [** Adjacent Inflammation**]

A

A) Frequent
B) No

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19
Q

Features of A) Necrosis and B) Apoptosis in [ Physiologic or pathologic role]

A

A) Invariably pathologic
B) Often physiological (elimination of unwanted cells) or maybe pathologic after some types of injury

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20
Q

What is Apoptosis?

A

Is a process that eliminates cells with abnormalities and promotes clearance of the fragments of the dead cells without eliciting an inflammatory reaction.

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21
Q

Apoptosis or Necrosis?

Occurs in healthy tissues. It serves to eliminate unwanted cells during normal development and to maintain constant cell numbers, so it is not necessarily associated with pathologic cell injury.

A

Apoptosis

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22
Q

Myocardial cells become noncontractile after how many minutes of ischemia?

A

1 to 2 minutes

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23
Q

Myocardial cells die until how many minutes?

A

20 to 30 minutes of
ischemia

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24
Q

Morphologic features indicative of the death of ischemic myocytes appear by electron microscopy within…?

A

2 or 3 hours after the death of the cells

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25
Q

Morphologic features indicative of the death of ischemic myocytes appear by light Microscope in how many hours?

A

6 to 12 hours

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26
Q

What is Necrosis?

A

is a form of cell death in which cellular membranes fall apart,
and cellular enzymes leak out and digest the cell. Also inflammation

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27
Q

Morphological Necrotic Cytoplasm changes?

A
  • increased eosinophilia (red)
  • glassy homogeneous appearance
    -vacuolated and appears “moth-eaten” (polilla)
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28
Q

Morphologic Nuclear changes by: Pyknosis

A

Nuclear shrinkage and increased basophilia; the DNA condenses into a dark shrunken mass

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29
Q

Morphologic Nuclear changes by: Karyorrhexis

A

The pyknotic nucleus can undergo fragmentation

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30
Q

Morphologic Nuclear changes by: Karyolysis

A

The basophilia fades because of the digestion of DNA by DNase activity.

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31
Q

After Karyolysis, in how many days does the nucleus disappear in the dead cell?

A

1-2 days

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32
Q

Process of dead cell calcification?

A

Dead cells-> Myeline Figures-> degraded to Fatty Acids -> Bind to Ca Salts

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33
Q

Fibrinoid necrosis is detected ONLY by?

A

Histologic examination

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34
Q

Morphologic Patterns of Tissue Necrosis for: Coagulative necrosis ?

A

The underlying tissue architecture is preserved for at least several days after death of cells in the tissue. Eosinophilic and anucleated cells may persist for days or weeks

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35
Q

Type of Necrosis that is typicall in infarcts in solid organs (Except for the brain)

A

Coagulative necrosis

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36
Q

Morphologic Patterns of Tissue Necrosis for: Liquefactive necrosis ?

A

It is seen in focal bacterial and,occasionally, fungal infections because they stimulate rapid accumulation of inflammatory cells, and the enzymes of leukocytes digest (“liquefy”) the tissue. Cells are completely digested,transforming the tissue into
a viscous liquid creamy yellow and is called pus

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37
Q

Hypoxic death of cells within the central nervous system often evokes…? (Type of necrosis)

A

Liquefactive necrosis

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38
Q

Morphologic Patterns of Tissue Necrosis for: Gangrenous necrosis ?

Not an official pattern (only in clinical practice)

A

Condition of a limb that has lost its blood supply and has undergone coagulative necrosis and liquefactive necrosis involving multiple tissue layers

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39
Q

What is known as “wet Gangrene”

A

After by liquefactive necrosis + Coagulative necrosis. The Pus generated by the destructive contents of the bacteria and the attracted leukocytes

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40
Q

Morphologic Patterns of Tissue Necrosis for: Caseous necrosis ?

A

Most often encountered in foci of tuberculous infection. Caseous means “cheeselike,” referring to the friable yellow-white appearance of the area of necrosis on gross examination. In H&E are granulomas

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41
Q

Morphologic Patterns of Tissue Necrosis for: Fat necrosis ?

A

Focal areas of fat destruction, typically resulting from the release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity (Acutepancreatitis)

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42
Q

The released fatty acids combine with calcium to produce grossly visible chalky white areas (fat saponification) are characteristics of..?

A

Fat necrosis

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43
Q

Morphologic Patterns of Tissue Necrosis for: **Fibrinoid necrosis ** ?

A

It usually occurs in immune reactions in which complexes of antigens + antibodies are deposited in the walls of blood vessels, but it also may occur in severe hypertension.

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44
Q

Deposited immune complexes and plasma proteins that leak into the wall of damaged vessels produce a bright pink, amorphous appearance on H&E called fibrinoid (fibrinlike)

A

Fibrinoid necrosis ((e.g., polyarteritis nodosa))

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45
Q

Irreversible injury and cell death in these tissues elevate the serum levels of these proteins in Cardiac muscle

A

A unique isoform of the enzyme Creatine kinase (CK) and contractile protein Troponin

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46
Q

Irreversible injury and cell death in these tissues elevate the serum levels of these proteins in Hepatic
bile duct epithelium

A

Alkaline phosphatase (ALP)

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47
Q

Damage in these tissues elevate the serum levels of these proteins in Hepatic Cells

A

**ALT and AST **(Alanine transaminase and Aspartate transaminase)

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48
Q

Pathway of cell death in which cells activate enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins

A

Apoptosis

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49
Q

During normal development of an
organism, some cells die and are replaced by new ones

A

Physiologic apoptosis

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50
Q

Mechanism of Apoptosis for a Physiologic condition during: [Embryogenesis]

A

Loss of growth factor signaling

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51
Q

Mechanism of Apoptosis for a Physiologic condition during: [Turnover of proliferative tissues
(e.g., intestinal epithelium,
lymphocytes in bone marrow,
and thymus)]

A

Loss of growth factor signaling

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52
Q

Mechanism of Apoptosis for a Physiologic condition during: [Involution of hormonedependent tissues (e.g., endometrium)]

A

Decreased hormone levels lead
to reduced survival signals

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53
Q

Mechanism of Apoptosis for a Physiologic condition during: [Decline of leukocyte numbers at the end of immune and inflammatory responses]

A

Loss of survival signals as stimulus for leukocyte activation is eliminated

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54
Q

Mechanism of Apoptosis for a Physiologic condition during: [Elimination of potentially harmful self-reactive lymphocytes]

A

Strong recognition of self antigens induces apoptosis by both the mitochondrial and
death receptor pathways

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55
Q

Mechanism of Apoptosis for a Pathologic condition during: [DNA damage]

A

Activation of proapoptotic
proteins by BH3-only sensors

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56
Q

Mechanism of Apoptosis for a Pathologic condition during: [Accumulation of misfolded proteins]

A

Activation of proapoptotic proteins by BH3-only sensors, possibly direct activation of
caspases

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57
Q

Mechanism of Apoptosis for a Pathologic condition during: [Infections, especially certain viral infections]

A

Activation of the mitochondrial pathway by viral proteins Killing of infected cells by
cytotoxic T lymphocytes, which activate caspases

58
Q

Caspases are activated by…?

A

Apoptosis

59
Q

Which pathway is more common for caspase (and apoptosis) activation

A

Mitocondrial (Intrinsic) pathway

60
Q

Explain step by step Miochondrial (intrinsic) pathway

A

->Cell injury
->Activate BH3 prt Sensors -> Bak and Bax dimerize
-> Form channels in mitocondria
-> Cytochrome c and other prt escape
->Caspase Activation
->Nuclear fragmentation (by endonucleases) and apoptotic bodies

61
Q

Explain step by step Death Receptor (extrinsic) Pathway

A

->Receptor-Ligand interaction ( Fas CD95, TNF receptor)
-> Death domain binding
->Caspase activation
->Nuclear fragmentation (by endonucleases) and apoptotic bodies

62
Q

How Macrophages recognize a apoptotic cell?

A

Phosphatidylserine is inverted opposite to cytoplasm and also cells secret soluble factors for recruiting phagocytes

63
Q

Explain Necroptosis

A

Initiated by TNF receptors but Kinases called rceptor-interactin Protein (RIP) are activated for dissolution of the cell like Necrosis.

64
Q

Explain Pyroptosis

A

Assosiated with activation of Inflammasomes for activation of Caspases for some infected cells.
Apoptosis + Fever

65
Q

Autophagy is?

A

Lysosomal digestion of the cell own components.
Starved cells can live by eating its own contens and recycling them for nutrients and energy.

66
Q

Pathway of Autophagy

A

-> Straving
->Autophagy genes activation
->Formation of autophagy vacuole (with cytosolic ocntent inside)
->Fusion of vacuole with lysosomes
->Enzyme digestion
->Use them as a source of nutrients

67
Q

How much time do striated skeletal muscle cells resist with complete ischemia without irreversible injury?

A

2 to 3 hours

68
Q

Hoy many Kg of ATP does a heathy human burn every day?

A

50-75 Kg/day

69
Q

What is HIF-1?

A

Hypoxia Inducible Factor 1 (A family of transcription factors)

70
Q

Function of HIF-1

Hypoxia inducible factor 1

A

Stimulates the synthesis of several proteins that help the cell to survive with low oxygen such as VEGF for angiogenesis to increase blood flow. Also stimulates the uptake of glucose and glycolysis.

Vascular Endothelial Growth Factor

71
Q

What is the result of the reduced activity of plasma membrane ATP-dependent sodium Pumps?

A

Intracellular acumulation of Na and efflux of K. Gain of solutes is accompanied by isoosmotic gain of water causing swelling and ER dilatation

72
Q

Consecuence of prolonged anaerobic glycolysis?

A

Lactic Acid accumulation, decreased intracellular pH, and cellular enzymes.

73
Q

Hypoxia increase ROS?

A

Probably, but it is not been fully understanded

74
Q

Ischemia-Reperfusion Injury increased injury? why?

A

Sometimes, New damage may be initiated by ROS and also the leukocytes produce it. Complement and antibodies are also activated more inflammation

75
Q

Oxidative stress refers to…?

A

Cellular abnormalities that are
induced by ROS

76
Q

Causes of ROS in cell Injury

Free Radical-mediated injury

A

->Chemical and Radiation injury
-> Hypoxia,
-> Cellular aging
-> Tissue injury caused by inflammatory cells
-> Ischemia-reperfusion injury.

77
Q

What are Free Radicals

A

Are chemical species with a single unpaired electron in an outer orbit

78
Q

Why are Free Radicals are dangerous?

A

their chemical states are extremely
unstable, and readily react with inorganic and organic molecules; when generated in cells, they avidly
attack nucleic acids as well as cellular proteins and lipids. Also initiate reactions in which molecules that react with the free radicals are themselves converted into other types of free radicals, thereby propagating the chain of damage.

79
Q

What is Respiratory Burst

or Oxidative Burst

A

The ROS generated in the Phagolysosomeand phagosomes by the leukocytes. They also produce Hypoclorite, peroxynitrite and others…

80
Q

How cells remove ROS?

A

->Some by itself spontaneously
-> By the action of Superoxide dismutase (SOD) (Removes Superoxide)
->Glutathione Peroxidases (GSH) (Degrade peroxide and Hydroxyl radical)
->Catalases (degrade peroxide)
->Other enzymes in the cytosol remove peroxynitrite
->Endogenous and exogenous **anti-oxidants ** (e.g., vitamins E, A, and C and β-carotene)

81
Q

ROS causes cell injury by damaging multiple components of cells, which ones?

A

->Lipid peroxidation of membranes. (Damage to plasma membranes as well as mitochondrial and lysosomal membranes)
-> Crosslinking and other changes in proteins (resulting in enhanced degradation or loss of enzymatic activity)
->DNA damage (reactions with thymine residues in nuclear and mitochondrial DNA produce singlestrand breaks)

82
Q

Define what happens when there’s Endoplasmic Reticulum Stress

A

The accumulation of misfolded proteins in a cell can stress compensatory pathways in the ER and lead to cell death by apoptosis.

If unfolded or misfolded proteins accumulate in the ER, they first induce a protective cellular response that is called the unfolded protein response

83
Q

What happens in the unfolded protein response?

A

This adaptive response activates signaling
pathways that increase the production of chaperones and decrease protein translation, thus reducing the levels of
misfolded proteins in the cell.

84
Q

What happen when a large amount of misfolded protein accumulates and cannot be handled by the adaptive response “unfolded protein response”?

A

the signals that are generated result in
activation of proapoptotic sensors of the BH3-only family as well as direct activation of caspases, leading to apoptosis by the mitochondrial (intrinsic) pathway

85
Q

What could cause the accumulation of misfolded proteins?

A

-Mutations
-Aging
-Infections (specially viral)
-Ischemia
Hypoxia

86
Q

Damage of DNA lead to the accumulation of which sentinel protein?

A

p53

87
Q

What p53 protein does?

A

-> Arrest cell cycle G1 (allows the DNA be repaired before mitosis)
-> Triggers apoptosis (if the damage can’t be repaired) (Stimulating BH3-only

88
Q

Repercussions of a mutation in p53

A

**Cancer **(can’t undergo to apoptosis)

89
Q

What causes the mitochondrial permeability transition pore?

A

Damage to mitochondria lead the formation of a** high-conductance channel** in the membrane this leads to the loss of mitochondrial membrane potential and pH changes, further compromising oxidative phosphorylation.

90
Q

Increased permeability of the plasma membrane and lysosomal membranes is a feature of apoptosis?

A

ABSOLUTELY NOT

91
Q

What is Hypertrophy?

A

Increase in size of cells (Resulting in an increase in the size of the organ) by the increased amoints of structural proteins and organells

NO NEW CELLS, JUST BIGGER CELLS

92
Q

What is Hyperplasia?

A

Hyperplasia is an increase in the number of cells in an organ that stems from increased proliferation, either of differentiated cells or, in some instances, less differentiated progenitor cells.

Increase in Cell Number

93
Q

Adaptive response in cells capable of replication that increase cell number

A

Hyperplasia

94
Q

Adaptive response in cells with limited capacity of replication that increase their size.

A

Hypertrophy

95
Q

During pregnancy, there is Estrogen stimulated smooth muscle _______?
a) Hypertrophy
b) Hyperplasia
c) both

A

C)

96
Q

In response to increased workload, the striated muscle cells in both the **skeletal muscle and the heart** undergo only?
a) Hypertrophy
b) Hyperplasia
c) both

A

Hypertrophy

Because adult muscle cells have a limited capacity to divide

97
Q

Cardiac enlargement that occurs with hypertension or aortic valve disease is an example of?
a) Pathologic Hypertrophy
b) Pathologic Hyperplasia
c) both

A

A)

Is for generate a higher contractil force

98
Q

Mechanisms driving cardiac hypertrophy

A

Mechanical triggers, such as stretch, and soluble mediators that stimulate cell growth, such as growth factors and adrenergic hormones.

The outcome is the induction of genes for the synthesis of more proteins and myofilaments per cell, which increases
the force generated with each contraction, enabling the cell to meet increased work demands

99
Q

An adaptation to stress such as hypertrophy can progress to functionally significant cell injury if the stress is
not relieved?
True or False?

A

True

100
Q

When mycardial fibers get a lot of hypertrphy (fragmentation and loss of myofibrillar contractile elements) what happens?

Not fully understand

A

There may be finite limits on the abilities of the **vasculature **to adequately supply the enlarged fibers, the mitochondria to supply ATP, or the biosynthetic machinery to provide sufficient contractile proteins or other cytoskeletal elements. The net result of these degenerative changes is ventricular dilation and ultimately cardiac failure.

101
Q

The proliferation of the glandular epithelium of the female breast at puberty
and during pregnancy

a) Hypertrophy
b) Hyperplasia
c) both

A

Hyperplasia

(hormonal)

102
Q

The residual tissue grows after removal or loss of part of an organ is?:

a) Hypertrophy
b) Hyperplasia
c) both

A

Hyperplasia

compensatory hyperplasia

103
Q

When part of a liver is resected, mitotic activity in the remaining cells begins as early as 12 hours later, eventually restoring the liver toits normal size, is?

a) Hypertrophy
b) Hyperplasia
c) both

A

Hyperplasia

compensatory hyperplasia

104
Q

When part of a liver is resected and for restoring the liver to its normal size, The stimuli for hyperplasia in this setting are?

A

Polypeptide growth factors produced by uninjured hepatocytes as well as nonparenchymal cells in the liver.

105
Q

Endometrial hyperplasia, which is a common cause of abnormal menstrual bleeding is caused because?

A

Pathologic hyperplasia caused by
excessive hormonal or growth factor stimulation.

106
Q

Most forms of pathologic hyperplasia are caused by?

A

Excessive hormonal or growth factor stimulation.

107
Q

Benign prostatic hyperplasia is another common example of?

A

** Pathologic hyperplasia ** (induced in
responses to hormonal stimulation by androgens)

108
Q

Papillomaviruses cause skin warts and mucosal lesions that are composed of masses of?

A

Hyperplastic epithelium. Here the growth factors may be encoded by viral genes or by the genes of the infected host cells

109
Q

Pathologic Hyperplasia could cause Cancer?

A

ABSOLUTELY YES

110
Q

Which disease is related to the growth control mechanisms become permanently dysregulated or ineffective in hyperplasia

A

Cancer

111
Q

What is Atrophy?

A

Atrophy is shrinkage in the size of cells by the loss of cell substance. Although atrophic cells may have diminished function, they are not dead

112
Q

Causes of Atrophy

A

->Decreased workload (e.g., immobilization of a limb to permit healing of a fracture)
->Loss of innervation
->Diminished blood supply
->Inadequate nutrition
->Loss of endocrine stimulation
->**Aging **(senile atrophy).

113
Q

Atrophy means cell dying?

A

Survival is still possible; a **new equilibrium is achieved **between cell size and diminished blood supply, nutrition, or trophic stimulation.

114
Q

Results from a combination of decreased protein synthesis and increased protein degradation.

A

Cellular Atrophy

115
Q

Atrophy also is associated with
autophagy?

A

Yes! with resulting increases in the number of autophagic vacuoles.

116
Q

What is Metaplasia

A

is a change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type. A cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment. Metaplasia is thought to arise by the** reprogramming of stem cells**

117
Q

Name of the change that occurs in the respiratory epithelium of habitual cigarette
smokers, in whom the normal ciliated columnar epithelial cells of the trachea and bronchi often are replaced by stratified squamous epithelial cells

A

Epithelial Metaplasia

118
Q

chronic gastric reflux, the normal stratified squamous epithelium of the lower esophagus may undergo __________ to gastric or intestinal-type columnar epithelium

A

Metaplasia or Metaplastic transformation

119
Q

The influences that induce metaplastic change in an epithelium, if persistent, may predispose to?

A

**Malignant Transformation **

Cancer

120
Q

Under some circumstances, cells may accumulate abnormal amounts of various substances, which may be harmless or may cause varying degrees of injury. The substance may be located in the

INTRACELLULAR ACCUMULATIONS

A

In the cytoplasm, within organelles
(typically lysosomes), or in the nucleus, and it may be synthesized by the affected cells or it may be produced
elsewhere.

LYSOSOMEEEEEEES

121
Q

How is the IntracellularAccumulation of: Fatty Change?

A

Fatty change, also called steatosis, refers to any accumulation of triglycerides within parenchymal cells. It is most often seen in the liver, since this is the major
organ involved in fat metabolism, but also may occur in heart, skeletal muscle, kidney, and other organs.

122
Q

Causes of Statosis

A

toxins (like alcohol), protein malnutrition, diabetes mellitus, obesity, or anoxia.

Loss of oxygenation of brain tissue is called anoxia or hypoxia.

123
Q

How is the IntracellularAccumulation of: Cholesterol and Cholesteryl Esters

A

Phagocytic cells may become overloaded with lipid (triglycerides, cholesterol, and cholesteryl esters) in several different pathologic processes, mostly characterized by increased intake or decreased catabolism of lipids. Of these, atherosclerosis is the most important

124
Q

How is the IntracellularAccumulation of: Proteins

A

**Occur when excesses are presented to the cells or if the cells synthesize excessive amount. **
i.e. Nephrotic Syndrome with heavy
protein leakage across the glomerular filter much more of the protein is reabsorbed, and vesicles containing this protein accumulate, giving the histologic appearance of pink, hyaline cytoplasmic droplets

125
Q

How is the IntracellularAccumulation of: Glycogen

A

Excessive intracellular deposits of glycogen are associated with abnormalities in the metabolism of either glucose or glycogen. In** poorly controlled diabetes mellitus**, the prime example of abnormal glucose metabolism, glycogen accumulates in renal tubular epithelium, cardiac myocytes, and β cells of the islets of Langerhans.

126
Q

How is the IntracellularAccumulation of: Pigments

A

Pigments are colored substances that are either exogenous, coming from outside the body, such as carbon, or are endogenous, synthesized within the body itself, such as lipofuscin, melanin, and certain derivatives of hemoglobin.

The most common exogenous pigment is carbon, a ubiquitous air pollutant of urban life. When inhaled, it is phagocytosed by alveolar macrophages and transported through lymphatic channels to the regional tracheobronchial lymph nodes

127
Q

How is the IntracellularAccumulation of: Pigment: Lipofuscin

A

is an insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues (particularly the heart, liver, and brain) with aging or atrophy. It is not injurious to the cell but is** a marker of past free radical injury**

complexes of lipid and proteins

128
Q

How is the IntracellularAccumulation of: Pigment: Melanin

A

Is an endogenous, brown-black pigment that is synthesized by melanocytes located in the epidermis. Although melanocytes are the only source of melanin, adjacent basal keratinocytes in the skin can accumulate the pigment (e.g., in freckles), as can dermal macrophages

129
Q

How is the IntracellularAccumulation of: Pigment: Hemosiderin

A

Is a hemoglobin-derived granular pigment that is golden yellow to brown and **accumulates in tissues **when there is a local or systemic excess of iron. The iron can be unambiguously identifiedby the Prussian blue histochemical reaction.

130
Q

What is Pathologic Calcification

A

Is a common process in a wide
variety of disease states, is the result of an abnormal deposition of calcium salts, together with smaller amounts
of iron, magnesium, and other minerals.

131
Q

Which ways can undergo in the process of Pathologic Calcification?

A

Dystrophic calcification and Metastatic calcification.

132
Q

Define Dystrophic calcification

PATHOLOGIC CALCIFICATION

A

It deposits ininjured or dead tissue, such as areas of necrosis ofany type. It is virtually ubiquitous in the arterial lesions of advanced atherosclerosis. Although dystrophic calcification may be
an incidental finding indicating insignificant past cell injury, it also may be a cause of organ dysfunction. For example, calcification can develop in aging or damaged heart valves, resulting in severely compromised valve motion.

133
Q

Define Metastatic Calcification and Causes of it

PATHOLOGIC CALCIFICATION

A

This form is associated with hypercalcemia and can occur in normal tissues. Major caises are:

1) Increased secretion of parathyroid hormone.
2) destruction of bone
3) vitamin D–related
disorders including vitamin D intoxication and sarcoidosis
4) renal failure, in which phosphate retention leads
to secondary hyperparathyroidism.

134
Q

How dystrophic calcification is initiated?

Pathologic Calcification

A

Is initiated by the extracellular deposition of crystalline calcium phosphate in membrane-bound vesicles, which may be derived from injured cells, or the intracellular deposition of calcium in the mitochondria of dying cells. It is thought that the extracellular calcium is concentrated in vesicles by its affinity for membrane phospholipids, whereas phosphates accumulate as a result of the action of membranebound phosphatases. The crystals are then propagated, forming larger deposits.

135
Q

Causes of Metastatic calcification by bone destruction:

A

Due to the effects of accelerated turnover (e.g., Paget disease), immobilization, or tumors (increased bone catabolism associated with multiple myeloma, leukemia, or diffuse skeletal metastases).

Turnover ~Rotation

136
Q

Abnormalities that contribute to cell aging.

A
  • Accummulation of mutations in DNA
  • Decreased Cellular Replication
    -Decreased Protein synthesis and damaged proteins
137
Q

What is Replicative Senescence?

A

All cells (other than stem cells) have a limited replication capacity and divisions. So in this process they become arrested in a terminally nondividing state

138
Q

Why the replicative senescence happens?

A

Progressive shortening of telomeres that results in cell cycle arrest.

139
Q

What does the telomerase does?

A

Is a specialized RNA-protein complex that uses its own RNA as a template for adding nucleotides to the ends of chromosomes. Telomerase is
expressed in germ cells and is present at low levels in stem cells, but absent in most somatic cells.

Telomere
shortening also decrease capacity of stem c. contributing aging

140
Q

Cancer cells can reactivate telomerases?

A

Yes

141
Q

Calorie restriction and exercise could reduce aging?

A

Yes, in many ways but principally by reducing chronic inflammation and probably by reducin IGF-1 Signaling that leads to lower rates of cell growth and metabolism.

Pathology Robbins (4 decks)

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