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MOD > Chapter 2 (Sections 1 and 2) - Cell Responses > Flashcards

Chapter 2 (Sections 1 and 2) - Cell Responses Flashcards

1
Q

4 things in a cascade that are the disease process overview

A
  1. Etiology - cause of disease
  2. Pathogenesis - sequence of cellular events
  3. Morphologic Changes - structural alterations in cells
  4. Clinical Manifestations - signs and symptoms of disease
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2
Q

2 broad classes of causes of disease

A
  1. Genetic

2. Environmental

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3
Q

Any deviation from normal structure or function and is manifested by characteristic symptoms

A

Disease

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4
Q

A derangement or abnormality of function

A

Disorder

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5
Q

Any new or abnormal growth

A

Neoplasm

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6
Q

A set of symptoms that occur together

A

Syndrome

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7
Q

Adaptation of a cell

A

Reversible functional and structural responses to changes that allow the cell to achieve a new steady state to survive and continue functioning

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8
Q

If a cell is unable to adapt, what will occur?

A

Cell injury

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9
Q

Is a cell injury reversible?

A

Yes, up to a certain point and then it becomes an irreversible injury

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10
Q

What changes are seen in a cell with a reversible injury?

A

Swelling and fatty changes

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11
Q

If a cell suffers irreversible injury, what will occur?

A

Cell death

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12
Q

List some causes of cell injury

A

Oxygen Deprivation
Physical agents (stress)
Chemical agents - ex. drugs
Infectious agents - ex. parasite
Genetic mutations
Nutritional imbalances - ex. protein-calorie deficiency
Immunologic reactions - ex. autoimmune rxns

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13
Q

Is there a time lag between the stress applied to the cell and the morphologic changes of the cell injury?

A

Yes

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14
Q

With a cell that is undergoing necrosis, the morphologic changes may not be seen for several hours after injury. However, what can be measured much sooner and why?

A

Specific enzymes and biomarkers released from the cell due to loss of plasma membrane integrity during necrosis!!

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15
Q

What 2 phenomena characterize the point of no return for irreversible cell injury?

A
  1. Mitochondrial damage with ATP DEPLETION

2. Lysosomal and plasma membrane rupture

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16
Q

For cell death, what are the options?

A

Necrosis

Apoptosis

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17
Q

Necrosis and Apoptosis - Cell size

A 
Necrosis = Enlarged and swollen
Apoptosis = Shrinkage and chromatin condensation
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18
Q

Necrosis and Apoptosis - Plasma membrane

A 
Necrosis = DISRUPTED plasma membrane
Apoptosis = INTACT plasma membrane with blebbing
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19
Q

Necrosis and Apoptosis - Cell content release

A 
Necrosis = Digested enzymes and contents leak out disrupted plasma membrane
Apoptosis = Cellular contents can be released in apoptotic bodies
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20
Q

Necrosis and Apoptosis - Adjacent inflammation

A 
Necrosis = YES
Apoptosis = NO
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21
Q

Why is there no adjacent inflammation with apoptosis?

A

The cell is devoured by macrophages before the contents can leak out and cause an immune response

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22
Q

List 3 nucleus changes seen with Necrosis

A
  • Karyolysis
  • Pyknosis
  • Karyorrhexis
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23
Q

Karyolysis

A

Nuclear fading

- seen with necrosis

24
Q

Pyknosis

A

Nuclear shrinking

- seen with necrosis

25
Q

Karyorrhexis

A

Nuclear fragmentation

- seen with necrosis

26
Q

How do necrotic cells appear on a stain?

A

Increased cytoplasmic Eosinophilia (pink)

27
Q

Necrosis and Apoptosis - Pathologic or Physiologic?

A 
Necrosis = Pathologic
Apoptosis = Physiologic or Pathologic
28
Q

Common things that leak out of necrotic cells?

A

ATP and Uric Acid

29
Q

Coagulative Necrosis

A

Dead tissue is preserved for a few days due to proteolysis of dead cells being blocked
- Ischemia of a vessel can cause this

30
Q

Liquefactive Necrosis

A

Digestion of dead cells creates a viscous liquid (pus)

- Focal bacteria in the BRAIN may lead to this

31
Q

Gangrenous Necrosis

A

Loss of blood supply to a limb; seen in diabetes

32
Q

Caseous Necrosis

A

Yellow-white “cheesy” appearance to necrotic area

- Tuberculosis infection of the lungs can cause this

33
Q

Fat Necrosis

A

Fat destruction due to pancreatic lipases;

White chalky deposits are seen

34
Q

Fibrinoid Necrosis

A

Antigen-Antibody complexes deposited in blood vessel walls that appear more pink (eosinophilic)
- Vascular damage during immune reactions cause this

35
Q

Tightly regulated cell death; cell activates its own enzymes to degrade itself and its contents

A

Apoptosis

36
Q

Physiologic causes of Apoptosis

A

Eliminating cells no longer needed

- ex. Development, menstrual cycle

37
Q

Elimination of self reactive Lymphocytes uses what mechanism?

A

Apoptosis – Extrinsic pathway

38
Q

Pathologic causes of Apoptosis

A

Eliminating cells that are injured beyond repair

- ex. DNA damage, misfolded proteins, viral infection

39
Q

What enzymes become activated with Apoptosis?

A

Caspases

40
Q

2 pathways for Apoptosis?

A
  1. Mitochondrial pathway (intrinsic) - Most common!

2. Extrinsic pathway (Death receptor initiated)

41
Q

Job and example of Anti-Apoptotic molecules?

A

Keep the outer mitochondrial membrane IMPERMEABLE

- ex. BCL-2

42
Q

Job and examples of Pro-Apoptotic molecules?

A

Increase permeability of the outer mitochondrial membrane

- ex. Bak and Bax

43
Q

With Apoptosis, once the Pro-Apoptotic molecules increase the permeability of the outer mitochondrial membrane, what is released from there into the cytosol?

A

Cytochrome C

44
Q

For the Mitochondrial pathway of Apoptosis, what activates Caspase 9 in the cytosol?

A

Cytochrome C

45
Q

Apoptosome

A

Cytochrome C + APAF-1 in the cytosol

= Activates Caspase 9!

46
Q

For the Extrinsic pathway of Apoptosis, what receptors are activated?

A

FAS

TNF

47
Q

Once FAS and TNF receptors are activated with the Extrinsic pathway of Apoptosis, what happens next?

A
  • Activates Caspase 8 which activates Caspase 9
48
Q

What can inhibit the Extrinsic pathway of Apoptosis?

A

FLIP - binds the Pro-Caspase 8 so it cannot be cleaved and activated

49
Q

Autophagy

A

Cell eats its own contents

50
Q

When is Autophagy usually present?

A

Nutrient Deprivation

51
Q

Describe the order of events with Autophagy

A
  • Sequestration of organelles
  • Creation of an Autophagosome
  • Autophagosome fuses with lysosomes
  • Lysosomes degrade Autophagosome contents
    = Contents are recycled!
52
Q

What is an example of a disease state that dysregulation of autophagy might occur?

A

Inflammatory bowel disease, Cancer

53
Q

Pyroptosis occurs in cells that are infected with?

A

Microbes

54
Q

Pyroptosis

A

Programmed cell death; Caspase 1 activated

Caspase 1 causes IL-1 release and Fever

55
Q

Necroptosis

A

Programmed Necrosis; NO CASPASES

- Release of cellular contents and evokes inflammation

56
Q

What triggers Necroptosis by ligations?

A

TNFR1

57
Q

What form holes in the plasma membrane with Necroptosis?

A

RIPK and MLKL

MOD (68 decks)

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