0107101230 - Mfm Ii - Cell Injury And Death (Bassett)

Front 1

What are the three phases that a cell goes through relative to stress?

Back 1

1) adaptation
2) injury (reversible or irreversible)
3) death through necrosis or apoptosis

Front 2

Atrophy

Back 2

an adaptation response to a cell where the size of the cell is decreased. causes: decreased workload, ischemia, lack of hormonal or neural stimulation, malnutrition

Front 3

Hypertrophy

Back 3

an adaptation response to a cell where the size of the cell is increased. causes: increasd workload, increased hormonal stimulation

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Hyperplasia

Back 4

an adaptation response to a cell where the number of cells increases.

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hormonal hyperplasia

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increases functional capacity of tissue like breast hyperplasia during puberty

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compensatory hyperplasia

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increases tissue mass after damage or resection, like regeneration of liver or kidney after partial removal

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pathologic hyperplasia

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usually caused by excessive hormonal stimulation and will regress when hormonal stimulation is stopped.

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example of pathologic hyperplasia

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thyroid hyperplasia in Graves Disease

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Hypoplasia

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underdeveloped organ because of deficient number of cells, commonly caused by congenital condition

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Aplasia

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complete lack of development of organ

Front 11

Examples of hypoplasia

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testes in Klinefelter's, pulmonary hypoplasia in newborns with oligohydramnios

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Examples of aplasia

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thymus in DiGeorge, cutis aplasia, anemia

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metaplasia

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reversible change in which one type of cell is replaced by another. usually caused by stress that causes a change and can be problematic when stressor does not desist. eg epithelial metaplasia in smokers

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dysplasia

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"disordered growth"

Front 15

hypoxia

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cell injury caused by decreased oxygen to tissue usually because of decreased blood flow

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physical agents that can cause cell injury

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trauma, temperature extremes, radiation, electrical shock

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chemical agents that can cause cell injury

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hypertonic glucose, salt, poison, pesticides, alcohol, drugs, oxygen in high concentrations

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infectious agents that can cause cell injury

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viruses, bacteria, fungi, parasites

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immunologic reactions that can cause cell injury

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anaphylaxis, autoimmune disease

Front 20

genetic derangements that can cause cell injury

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enzyme defects, chromosomal abnormalities

Front 21

four sites of cell injury

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1) \/ ATP
2) Membrane
3) /\ intracellular Ca
4) ROS

Front 22

what are the effects of \/ ATP?

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1) ER swelling, cellular swelling because of Na/K pump cannot be regulated;
2) \/ glycogen, /\ lactic acid because now using glycolysis;
3) lipid deposition

Front 23

what are the effects of /\ Ca+

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ATPase activity increases
phospholipases break down membranes
proteases break down proteins
endoluceases make acid
increases mitochondrial permeability -> apoptosis

Front 24

mitochrondrial damage -> ?

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\/ ATP, /\ Ca+

Front 25

list ROS that could be problematic for cell damage?

Back 25

O2-, H2O2, OH-

Front 26

why are ROS problematic?

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disrupt lipid membranes, oxidative modification of proteins, DNA damage

Front 27

how can one defend against ROS damage?

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1) antioxidants (vit A, C, E, glutathione)
2) storage and transport proteins (cerulupolasmin and transferrin) bind Fe and Cu to stop formation of ROS
3) intracellular enzymes (superoxide dismutase, catalase, glutathione peroxidase) convert ROS to O2 and H2O

Front 28

What are the 2 types of cell death?

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necrosis and apoptosis

Front 29

What is significant about necrosis?

Back 29

always pathologic and does not just refer to cell death, but also the spectrum of morphological changes that follow cell death in living tissue

Front 30

what cytoplasmic changes occur with necrosis?

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1) eosinophilia - eosin binds to cytoplasmic proteins and causes brilliant deep pink staining
2) hyalinization - glycogen loss causes a homogenous cytoplasm instead of granulated
3) vacuolization - enzymatic digestion of organelles leaves vacuoles
4) calcification

Front 31

what nuclear changes occur with necrosis?

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1) karyolysis - nucleus is very pale blue
2) pyknosis - nucleus shrinks and becomes darker
3) karyorrhexis - nucleus is fragmented

Front 32

what are the three microscopic and gross patterns of necrotic tissue?

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1) coagulative
2) liquefactive
3) caseous

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coagulative necrosis

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tissue pattern of necrosis that is most common. nuclei absent, but cell outlines still exist. common in ischemic death of heart, liver, and kidney tissue.

Front 34

liquefactive necrosis

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tissue pattern of necrosis where cells liquefy and dissapear microscropically and grossly (gross holes in tissue), common with bacterial and fungal infections because of hypoxic death in CNS in brain infarcts, pancreas, abscesses

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caseous necrosis

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combination of liquefactive and coagulative, presents grossly as a cheesy appearance, microscopically as necrotic focus surrounded by granulomatous inflammation, common in TB

Front 36

what are the other lesser discussed catagories of necrosis

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fat necrosis, fibrinoid necrosis, wet or dry gangrenous necrosis

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apoptosis

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programmed cell death can be physiologic or pathologic, caused by fragmentation of INDIVIDUAL cell nuclei and cytoplasm; never elicits inflammation due to rapid phagocytosis

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mophological quality of apoptosis

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1) involves single cells
2) nuclear chromatin condenses against nuclear membrane
3) blebbing (pooching of cell membrane) into extravessicles to be phagocytized
4) does not elicit inflammation

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normal lysosomal catabolism

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molecule is endocytized by cell, lysosome internally endocytizes the foreign body, catbolises the foreign body, binds and excises the bits of the foreign body outside the cell and then lysosome restores itself to take care of another foreign body

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abnormal lysosomal cataolism

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for whatever reason, lysosomes fail and there is intracellular accumulation that leads to apoptosis

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lipid accumulations

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intracellular accumulations of lipids that can be pathologic. fatty liver can develop and can be visualized by Oil Red O Staining

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other intracellular lipid accumulations

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atherosclerosis, xanthomas, inflammatory foci, cholesterolosis, Neimann-Pick disease

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intracellular protein accumulation

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presents as rounded eosinophilic droplets or aggregates in cytoplasm,

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exogenous pigments

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common with carbon or coal dust, tattoos

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endogenous pigments

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melanin, lipofuchsin (yellow or brown "aging pigment" or bruising pigment, hemosiderin (derived from hemoglobin, yellow brown bruising pigment), bilirubin (from bile, leads to jaundic)

Front 46

what are the two types of calcification?

Back 46

1) dystrophic - very comon, Ca deposits in damaged tissue (heart valves in elderly)
2) metastatic - uncommon calcium deposits in normal tissues