Cellular Adaptations Flashcards
Normal cell
Homeostasis
Irreversible Injury leads to
Necrosis Apoptosis
What are some Reversible Injury?
- Cellular swelling
- Fatty change
- Decrease ATP
- Mito swelling
- Pyknosis
- Membrane alterations (blebbing)
Irreversible Cell Injury?
- Same as Reversible plus
- Increased Eosinophilia
- Greater Nuclear Changes
Necrosis
- Messy
- cell death assciated with membrane integrity and leakage of cellular contents
- creates local damage via inflammation
Apoptosis
- Clean
- Programmed cell death
- Cell activates enzymes that degrades DNA and nuclear+ cyto proteins
- Plasma membrane remains intact and the cell is targeted by phagocutosis
- No inflammaoty reaction
Which cell death creates an inflammation ?
Necrosis
What does Necrosis do to the membrane?
Loss of membrand integrity and leakage of cellular contents
What happens to the cell membrane with Apoptosis ?
Plasma membrane remains intact and cell is targeted by phagocytosis
What are the 5 steps of Necrosis?
- Damage to cell membrane
- Swelling
- membrane degradation
- inflammation
- fragmentation
What are the 4 steps of Apoptosis
- DNA fragmentation
- Reduction of cell volume
- Membrane Blebbing
- Formation of apoptotic bodies
Necrosis is generally the ….
result of a noxious stimulus
Necrosis Morphology
- Nuclear Changes
- Cytoplasmic Changes ( membrane breaks)
- Calcification
Nuclear changes of Necrosis Processes
- Pyknosis
- Kayorrhexis
- Karyolysis
Pyknosis
clumping of chromatin in the nucleus
karyorrhexis
Necrosis nuclear change #2
Fragmentation of the nucleus, becomes more opaque
karyolysis
Necrosis nuclear change #3
Nuclear dissolution and chromatin lysis
Necrosis Morphology
(Cytoplasmic Changes)
Increased Eosinophilia as they bind to denatured protiens
Necrosis Morphology
Calcification
- Dead cells can be phagocytosed or degraded into fatty acids.
- Fatty acids bind calcium, resulting in calcification.
Nectosis Calcificaiton types
-
Dystrophic calcification- can happen in any type of necrosis
- Usually in atheroma with atherosclerosis
-
Metabolic Calcification- Consequence of hypercalcemia. Can occur in any tissue
- result of altered hormones ( vit D disorder)
How can you tell if necrosis is occuring?
Gross apprearance
Fibrinoid requires histological examination
Patterns of Tissue Necrosis
(6)
- Coagulative necrosis
- Liquefactive necrosis
- Caseous necrosis
- Fat necrosis
- Fibrinoid necrosis
- Gangrenous necrosis
Coagulative Necrosis
Occurs in:
- Kidneys
- Heart
- Spleen
- Adrenal Glands
Protein denaturation →albumin becomes opaque
Liquefactive Necrosis
Occurs: Neurons and glial cells of the brain
How: Hydrolytic enymes make brain mushy
due to infection and hypoxia
Caseous Necrosis
Occurs: Lungs
How: Combination of coagulative and liquefactive necrosis → granuloma
(common factor due to TB)
Fat Necrosis
Where: Pancreas , Breast and other abdominal organs
How: lipases Sponificaton→ binding of FFA and Ca++
Fibrinoid Necrosis
Where: Ateries
How: Antigens and Antibodies are deposited in the walls of the arteries
Gangrenous Necrosis
- Result from
- Where
- types
- Result from Hypoxia
- Limbs not organs
- Dry vs Wet
Dry Gangrenous Necrosis
- Insufficient Blood
- Coagulative
- Dry, Crusty, Black
Wet Gangrenous Necrosis
- Infection
- Liguefactive Necrosis
- Cold, Swollen, Black
- Foul Odor (Pus)
Apoptosis Regulated by
Internal cellular SIgnals
Helps maintain healthy tissue
Apoptosis Morphology
Cell Shrinkage
Pyknosis→Condensing DNA
Apoptotic Bodies
Causes of Apoptosis
Physiologic and Pathologic
Two Mechanisms of Apoptosis are
Mitochondrial (Intrinsic)
Death Receptor (Extrinsic)
All Apoptosis Mechanisms lead to activation of
Caspases
Nuclear fragmentation via endonuclease
Cytoplasmic blebing
Formaton of apoptotic bodies
Phagocytosis of above
Mitochondrial (intrinsic) Apoptosis
Depends on mitochondria membrane Permeability
- Controlled by inhibition of BCL-2
- Cytochrome C (activated apoptosis)
- Leads to caspases
Death Receptor (Extrinsic) Apoptosis
Death Receptors(TNF) are activated →leads to caspases
TNF-tumor necrosis factor
What creates pores in mitochondria (Mito apoptosis) ?
Bax/Bak (activation)
Apoptosis vs. Autophagy
Apoptosis→destroys the whole cells
Autophagy→ lysosomal digestion of part of the cell’s own components (nutrient deprivation)
Hypoxia
Oxygen deprivation →Decrease in ATP
- Failure of Na/K pump and Ca pump
- Cellular Swelling
- Reduced pH
In Hypoxia where are the na/k and ca concentrations
na andd ca increase inside the cells, k outside causing cell to swell →cell to lyse
Oxygen deprivation causes
ischemia
hypoxia
anoxia
which causes of oxygen deprivation leads to a decrease in ATP?
Hypoxia
Anoxia
Decrease in ATP leads to
- Failure of ion pumps
- cellular swelling
- reduced pH
when the ion pumps fail where are the concentrations of Na , K and Ca the greatest?
Na and Ca [high] INSIDE the cell
K [high} OUTSIDE the cell
Anoxia
total lack of oxygen (embolism)
ischemia
reduced blood supply ( gradual arterial obstruction )
In oxygen deprivation most damage occurs from…
mitochondrial dysfunction
free radiacal production
what is the result from damge due to mitochondal dysfunction and free radcal production
- lipid peroxidation
- alteration of proteins
- alteration of dna
how does a lack of oxygen effect the ETC ?
oxygen is the final electron exceptor
no oxygen→oxygen radicals appear
what is a common consequence of hypoxia ?
mitochondrial Swelling
