OBJ - Adaptation Flashcards
4 Common cellular inclusions
1) Abnormal metabolism (Fat/Protein)
i. e. Fats/lipid vacuoles in liver
2) Mutations causing alteration in protein folding
3) Deficiency in critical enzymes (leads to accumulation of endogenous materials)
i. e. glycogen stored in diabetics
4) Ingestion of indigestible materials (leads to accumulation of exogenous materials)
- carbon
- lipofuscin - wear & tear pigment (orange)
- melanin
- hemosiderin - yellow/green/brown (heme deposits from RBC) - use Prussian Blue stain (DARK blue)
Calcium - saponification/FA which are not phagocyted become calcified
- Dystrophic - normal Ca levels -> deposits on path tissue
- Metastic - due to hypercalcemia; Ca deposits on normal tissues
Myelin Figures - whorled phospholipid masses from damaged cell membranes
Aging Process of Cells
1) Aging results from accumulation of cellular damage by FR
2) Reduced capacity to divide (telomere shortening)
3) Reduced ability to repair damaged DNA
Germ cells - don’t lose telomere length
Stem cells - lose very little
Somatic cells - telomeres shorten with each division
some cancer cells can increase their telomere length
Werner Syndrome - very rapid aging process
Necrosis Vs Apoptosis
Necrosis:
- Larger cell size (swelling)
- Nucleus: Pyknosis, karyorrhexis, karyolysis
- Disrupted plasma membrane
- Enzymatic leakage
- INFLAMMATION
- generally pathological
Apoptosis: “falling off”/cellular suicide
- Smaller cell size
- Fragmented nucleus
- Intact plasma membrane
- intact cellular components
- NO INFLAMMATION
- generally physiologic programed cell death, can be pathologic
PICTURE
Differences between:
Pyknosis, karyorrhexis, karyolysis
Pyknosis: nuclear shrinkage (pin point/tiny)
Karyorrhexis: nuclear fragmentation (break into pieces)
Karyolysis: nuclear dissolution
Hypertrophy
increase in cell size
Phys: weight lifting
Path: BPH/ big LV
Hyperplasia
Increase in cell number
Phys:
Path: BPH
Atrophy
Decrease in number AND/OR size
Phys: bedrest/inactivity
Path:
Metaplasia
change in cell type; reversible & protective
Path: lungs -> columnar with goblet cells to stratified squamous for protection
Neoplasia
abnormal growth
6 Types of Necrosis
1) Coagulative (heart)
2) Liquefactive (brain)
3) Gangrenous (wet or dry)
4) Caseous
5) Fat (pancreatic enzymes)
6) Fibrinoid
Coagulatvie Necrosis
preservation of tissue architecture but dead cells/scar tissue
Eosinophillic - birght pink
Anucleate
Days-weeks
i.e. MI
Liquefactive Necrosis
complete digestion of tissue transforming it into a liquid mass
characteristic of CNS/bacterial infections
Gangrenous Necrosis
generally in an extremity
Coagulative necrosis of several layers of tissue
“Wet Gangrene” if infection with it as well (combo of Coag/Liqueficative)
DC Ulcer
Caseous Necrosis
“cheese-like” - swiss - with holes
granular/chalky appearance
HALLMARK of TB
Fat necrosis
peripancreatic tissue death from pancreatic lipase/enzyme leakage combine with Ca to produce chalky areas of fat saponification
Fibrinoid Necrosis
**special form seen with Immune responses
THINK AUTOIMMUNE
Antigens/antibodies are deposited in vessels around/throughout organ organ
Autophagy vs Heterophagy
Autophagy: cell digests its own organelle (i.e. nutrient deprivation)
Heterophage: cell digests substances outside the cell (i.e. macrophages)
Principle of Cellular Injury
Cellular response to injury depends on:
- type
- duration
- severity of the injury
Consequence of injury depends on:
- type
- status
- adaptability
- genetic make up of the cell (hepatocyte vs neuron)
Mechanism of Cell Injury
1) Mitochondrial damage (Depletion of ATP/increase in ROS)
- ATP deletion -> failure of energy dependent functions (Na/K pump)
- accumulation of ROS
2) Entry of Ca++ into the cell
- activates enzymes that damage cellular components/trigger apoptosis
3) Membrane Damage
- affect lysosomal, mitochondrial, plasma membranes
4) Protein misfolding/DNA damage
- accumulation triggers apoptosis
Cellular responses to stress
Adaptations (hypertrophy, hyperplasia, metaplasia, atrophy)
-are reversible
Cell injury (can be reversible or irreversible -> necrosis/apoptosis)
Mechanisms of Apoptosis
1) Mitochondrial Pathway (intrinsic) Bcl2 deactivated (anti-apoptotic)/activates BAK/BAX (pro-apoptotic) which forms channels for Cytochrome C to leak out of Mito; activating initiator caspase -> executioner caspase -> triggering apoptosis
2) Death receptor Pathway (extrinsic)
FAS ligand/TNF receptor bind to “death domain” whcih recruit/activate initiator caspase -> executioner caspase -> triggering apoptosis
