Cell Adaptation, Injury, and Death Flashcards Preview

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Flashcards in Cell Adaptation, Injury, and Death Deck (25):
1

Loss of Normal Cell Functions

Hypoxia, physical agents, chemical agents and drugs, infectious agents, genetic derangments,
aging, immunologic reactions, nutritional imbalancements

2

Cells failing to adapt lead to:

Necrosis, apoptosis

3

Atrophy

Caused by poor blood supply, aging, loss of neuronal/endocrine stimulation

4

hypertrophy

Normally an increase capactity for the tissue

Ex: increase in heart and muscle size

5

hyperplasia

Inc in cell number. Usually functional gain

Ex: increase in breast size during preganancy, tumor

6

metaplasia

One shape of a cell type to another. Functional loss

Ex: smokers

7

Necrosis

Degradation of protiens and enzyme degranulation. Exhaustion of O2 and nutrients
Depletion of ATP in the cell (Na/K pump)
Lysis of membrane
Inflammation
Phagocytosis of cellular debris (neutrophils)

8

Coagulative necrosis

Cell death w/in tissue. Looks fine on outside, dead inside.

Pro denaturation dominates over hetero and autolysis.
Cell die, explode and lysosomes touch each other

9

Gangrenous necrosis

Loss of BF

10

Liquefactive necrosis

Differs from necrosis because:
Autolysis and heterolysis dominates over pro denaturation

11

Caseous necrosis

Bacteria enters tissue. There are no cells to get rid of it, so immune system builds wall around it. Inside dies only. Characteristic of tuberoculosis

12

Fat necrosis

Necrosis in adipose tissue. Fatty acids + Ca = soap. Common in fatty areas.
Ex: pancreas, GI system

13

Apoptosis

Programmed cell death
Intracellular signaling
Degranulates into vesicles
Phagocytosis
No inflammation
Initiated by extrinisc and intrinsic pathways

14

Apoptosis

Programmed cell death
Intracellular signaling
Degranulates into vesicles
Phagocytosis
No inflammation
Initiated by extrinisc and intrinsic pathways

15

Extrinsic pathway (death receptor inititated pathway)

Initiates apoptosis.
TNF and FAS bind to their receptors
Eventual initiator of caspases

16

Intrinsic pathway (mitochondrial pathway)

Initiates apoptosis
1. Activation of BCL2 and TP53 lead to alterations in mitochondria within cell.
2. Releases cytochrom C
3. Caspases (enzymes envolved with programmed cell death)

17

Caspases

Pro-enzymes in intracellular proteolytic degredation

Leads to cell shrinkage, chromatin condensation and fragmentation (apoptotic bodies)

Plasma membrane alterations allow cell to be phagocytized by macrophages

18

Mechanisms of cell injury
- depletion of ATP
- mitochondrial damage
- calcium
- oxidative stress

- Shuts down many machinery that relies on ATP
- Leakage of cytochrome C (apoptosis)
- Influx of Ca leads to: phospholipases, ATPase, endonucleases which breaks down ATP, lipids, pro
- ROS, damages lipids, pros, nucliec acids

19

Cellular accumulations
- Lipofusin (pig)
- Melanin (p)
- Hemosiderin (p)
- Metastatic calcification C

Happen because of abnormal metabolism, defect in pro.
Result of dmg. Occur as a result of intrinsic abnormality

20

lipofusin (pigment)

Accumulation
Wear and tear pro composed of complex lipids
Inc age = Inc lipofusin
In brain or n. system

21

Melanin (pigment)

Accumulation
Brown/black pigment from tyrosine in melanocytes.
UV radiation produces more pigments

22

Hemosiderin (pigment)

Accumulation
Iron derived from hemoglobin. Yellow brown microscopic granules. (diabetes)

23

Metastatic Calcification

Accumulation
Occurs in viable tissue in presence of hypercalcemia

24

Dystrophic calcification

Accumulation
Occurs in non viable tissue in presence of normal calcium serum levels (can lead to heart disease)

25

Mechanisms Mediating Cellular death (4)

DNA dmg
Dec cellular replication
Reduction in stem cell capacity
Accumulation of metabolic dmg