Cellular Adaptations Flashcards

1
Q

Normal cell

A

Homeostasis

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2
Q

Irreversible Injury leads to

A

Necrosis Apoptosis

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3
Q

What are some Reversible Injury?

A
  1. Cellular swelling
  2. Fatty change
  3. Decrease ATP
  4. Mito swelling
  5. Pyknosis
  6. Membrane alterations (blebbing)
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4
Q

Irreversible Cell Injury?

A
  1. Same as Reversible plus
  2. Increased Eosinophilia
  3. Greater Nuclear Changes
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5
Q

Necrosis

A
  • Messy
  • cell death assciated with membrane integrity and leakage of cellular contents
  • creates local damage via inflammation
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6
Q

Apoptosis

A
  • 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
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7
Q

Which cell death creates an inflammation ?

A

Necrosis

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8
Q

What does Necrosis do to the membrane?

A

Loss of membrand integrity and leakage of cellular contents

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9
Q

What happens to the cell membrane with Apoptosis ?

A

Plasma membrane remains intact and cell is targeted by phagocytosis

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10
Q

What are the 5 steps of Necrosis?

A
  1. Damage to cell membrane
  2. Swelling
  3. membrane degradation
  4. inflammation
  5. fragmentation
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11
Q

What are the 4 steps of Apoptosis

A
  1. DNA fragmentation
  2. Reduction of cell volume
  3. Membrane Blebbing
  4. Formation of apoptotic bodies
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12
Q

Necrosis is generally the ….

A

result of a noxious stimulus

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13
Q

Necrosis Morphology

A
  1. Nuclear Changes
  2. Cytoplasmic Changes ( membrane breaks)
  3. Calcification
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14
Q

Nuclear changes of Necrosis Processes

A
  • Pyknosis
  • Kayorrhexis
  • Karyolysis
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15
Q

Pyknosis

A

clumping of chromatin in the nucleus

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16
Q

karyorrhexis

A

Necrosis nuclear change #2

Fragmentation of the nucleus, becomes more opaque

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17
Q

karyolysis

A

Necrosis nuclear change #3

Nuclear dissolution and chromatin lysis

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18
Q

Necrosis Morphology

(Cytoplasmic Changes)

A

Increased Eosinophilia as they bind to denatured protiens

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19
Q

Necrosis Morphology

Calcification

A
  • Dead cells can be phagocytosed or degraded into fatty acids.
  • Fatty acids bind calcium, resulting in calcification.
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20
Q

Nectosis Calcificaiton types

A
  • 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)
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21
Q

How can you tell if necrosis is occuring?

A

Gross apprearance

Fibrinoid requires histological examination

22
Q

Patterns of Tissue Necrosis

(6)

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Fat necrosis
  5. Fibrinoid necrosis
  6. Gangrenous necrosis
23
Q

Coagulative Necrosis

A

Occurs in:

  • Kidneys
  • Heart
  • Spleen
  • Adrenal Glands

Protein denaturation →albumin becomes opaque

24
Q

Liquefactive Necrosis

A

Occurs: Neurons and glial cells of the brain

How: Hydrolytic enymes make brain mushy

due to infection and hypoxia

25
Caseous Necrosis
Occurs: Lungs How: Combination of coagulative and liquefactive necrosis → granuloma (common factor due to TB)
26
Fat Necrosis
Where: **Pancreas** , Breast and other abdominal organs How: lipases Sponificaton→ binding of FFA and Ca++
27
Fibrinoid Necrosis
Where: Ateries How: Antigens and Antibodies are deposited in the walls of the arteries
28
Gangrenous Necrosis 1. Result from 2. Where 3. types
1. Result from Hypoxia 2. Limbs not organs 3. Dry vs Wet
29
Dry Gangrenous Necrosis
1. Insufficient Blood 2. Coagulative 3. Dry, Crusty, Black
30
Wet Gangrenous Necrosis
1. Infection 2. Liguefactive Necrosis 3. Cold, Swollen, Black 4. Foul Odor (Pus)
31
Apoptosis Regulated by
Internal cellular SIgnals Helps maintain healthy tissue
32
Apoptosis Morphology
Cell Shrinkage Pyknosis→Condensing DNA Apoptotic Bodies
33
Causes of Apoptosis
Physiologic and Pathologic
34
Two Mechanisms of Apoptosis are
Mitochondrial (Intrinsic) Death Receptor (Extrinsic)
35
All Apoptosis Mechanisms lead to activation of
**_Caspases_** Nuclear fragmentation via endonuclease Cytoplasmic blebing Formaton of apoptotic bodies Phagocytosis of above
36
Mitochondrial (intrinsic) Apoptosis
Depends on mitochondria membrane Permeability * Controlled by inhibition of BCL-2 * Cytochrome C (activated apoptosis) * Leads to caspases
37
Death Receptor (Extrinsic) Apoptosis
Death Receptors(TNF) are activated →leads to caspases TNF-tumor necrosis factor
38
What creates pores in mitochondria (Mito apoptosis) ?
Bax/Bak (activation)
39
Apoptosis vs. Autophagy
Apoptosis→destroys the whole cells Autophagy→ lysosomal digestion of part of the cell's own components (nutrient deprivation)
40
Hypoxia
Oxygen deprivation →Decrease in ATP 1. Failure of Na/K pump and Ca pump 2. Cellular Swelling 3. Reduced pH
41
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
42
Oxygen deprivation causes
ischemia hypoxia anoxia
43
which causes of oxygen deprivation leads to a decrease in ATP?
Hypoxia Anoxia
44
Decrease in ATP leads to
- Failure of ion pumps - cellular swelling - reduced pH
45
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
46
Anoxia
total lack of oxygen (embolism)
47
ischemia
reduced blood supply ( gradual arterial obstruction )
48
In oxygen deprivation most damage occurs from...
mitochondrial dysfunction free radiacal production
49
what is the result from damge due to mitochondal dysfunction and free radcal production
- lipid peroxidation - alteration of proteins - alteration of dna
50
how does a lack of oxygen effect the ETC ?
oxygen is the final electron exceptor no oxygen→oxygen radicals appear
51
what is a common consequence of hypoxia ?
mitochondrial Swelling
52