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
Q

Caseous Necrosis

A

Occurs: Lungs

How: Combination of coagulative and liquefactive necrosis → granuloma

(common factor due to TB)

26
Q

Fat Necrosis

A

Where: Pancreas , Breast and other abdominal organs

How: lipases Sponificaton→ binding of FFA and Ca++

27
Q

Fibrinoid Necrosis

A

Where: Ateries

How: Antigens and Antibodies are deposited in the walls of the arteries

28
Q

Gangrenous Necrosis

  1. Result from
  2. Where
  3. types
A
  1. Result from Hypoxia
  2. Limbs not organs
  3. Dry vs Wet
29
Q

Dry Gangrenous Necrosis

A
  1. Insufficient Blood
  2. Coagulative
  3. Dry, Crusty, Black
30
Q

Wet Gangrenous Necrosis

A
  1. Infection
  2. Liguefactive Necrosis
  3. Cold, Swollen, Black
  4. Foul Odor (Pus)
31
Q

Apoptosis Regulated by

A

Internal cellular SIgnals

Helps maintain healthy tissue

32
Q

Apoptosis Morphology

A

Cell Shrinkage

Pyknosis→Condensing DNA

Apoptotic Bodies

33
Q

Causes of Apoptosis

A

Physiologic and Pathologic

34
Q

Two Mechanisms of Apoptosis are

A

Mitochondrial (Intrinsic)

Death Receptor (Extrinsic)

35
Q

All Apoptosis Mechanisms lead to activation of

A

Caspases
Nuclear fragmentation via endonuclease

Cytoplasmic blebing

Formaton of apoptotic bodies

Phagocytosis of above

36
Q

Mitochondrial (intrinsic) Apoptosis

A

Depends on mitochondria membrane Permeability

  • Controlled by inhibition of BCL-2
  • Cytochrome C (activated apoptosis)
  • Leads to caspases
37
Q

Death Receptor (Extrinsic) Apoptosis

A

Death Receptors(TNF) are activated →leads to caspases

TNF-tumor necrosis factor

38
Q

What creates pores in mitochondria (Mito apoptosis) ?

A

Bax/Bak (activation)

39
Q

Apoptosis vs. Autophagy

A

Apoptosis→destroys the whole cells

Autophagy→ lysosomal digestion of part of the cell’s own components (nutrient deprivation)

40
Q

Hypoxia

A

Oxygen deprivation →Decrease in ATP

  1. Failure of Na/K pump and Ca pump
  2. Cellular Swelling
  3. Reduced pH
41
Q

In Hypoxia where are the na/k and ca concentrations

A

na andd ca increase inside the cells, k outside causing cell to swell →cell to lyse

42
Q

Oxygen deprivation causes

A

ischemia

hypoxia

anoxia

43
Q

which causes of oxygen deprivation leads to a decrease in ATP?

A

Hypoxia

Anoxia

44
Q

Decrease in ATP leads to

A
  • Failure of ion pumps
  • cellular swelling
  • reduced pH
45
Q

when the ion pumps fail where are the concentrations of Na , K and Ca the greatest?

A

Na and Ca [high] INSIDE the cell

K [high} OUTSIDE the cell

46
Q

Anoxia

A

total lack of oxygen (embolism)

47
Q

ischemia

A

reduced blood supply ( gradual arterial obstruction )

48
Q

In oxygen deprivation most damage occurs from…

A

mitochondrial dysfunction

free radiacal production

49
Q

what is the result from damge due to mitochondal dysfunction and free radcal production

A
  • lipid peroxidation
  • alteration of proteins
  • alteration of dna
50
Q

how does a lack of oxygen effect the ETC ?

A

oxygen is the final electron exceptor

no oxygen→oxygen radicals appear

51
Q

what is a common consequence of hypoxia ?

A

mitochondrial Swelling

52
Q
A