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NURP 404 Patho > Cell Injury & Cell Death > Flashcards

Cell Injury & Cell Death Flashcards

1
Q

Necrosis

A

Cell death due to injury

-Initiated by pathologic stimuli from outside the cell and results in the dissolution or removal of that cell

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2
Q

Apoptosis

A

Cell death due to physiological turn over of cells

  • Involves activation of a coordinated internal cellular program that are mediated by defined cellular proteins
  • A specific, energy dependent, programed cell death
  • Helps to maintain homeostasis
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3
Q

Calcium Influx

A

Hallmark of irreversible cell injury or cell death

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4
Q

Morphologic Characteristics

A
  • excessive cell swelling

- dramatic changes to cellular organelles

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5
Q

Adaptation

A

Allows cells to survive in the short term

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6
Q

Homeostasis

A

(LOSS OF) forms the basis of most disease states

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7
Q

Cellular Adaptions

A
  • Hyperplasia
  • Hypertrophy
  • Metaplasia
  • Dysplasia
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8
Q

Atrophy

A

the shrinkage of tissue or organ size due to a reduction in cell size

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9
Q

Hypertrophy

A

An increase in cell size in response to stress

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10
Q

Hyperplasia

A

An increase in cell number and is distinct from hypertrophy

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11
Q

Non-dividing cells

A

(CARDIAC MYOCYTES) cannot divide, so adapt through hypertrophy

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12
Q

Dividing cells

A

(EPITHELIAL CELLS) may undergo hyperplasia as well as hypertrophy under stress

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13
Q

Metaplasia

A

The reversible process whereby one mature cell type is replaced by another less mature cell type

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14
Q

Dysplasia

A

Disordered growth and maturation of the cellular components of a tissue

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15
Q

Accumulate Substances

A

Under stress, cells tend to do this in response to metabolic derangments

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16
Q

Hallmarks of cell injury

A

-Accumulating substances leading to cell injury or cell death

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17
Q

Mechanisms of Cellular injury

A

Pathologic stimuli

  • Intrinsic (genetic) or extrinsic (acquired)
  • Provide etiology (cause) of disease
  • Elicit cellular responses - pathogenesis of disease
18
Q

Severity & Duration

A

(of pathologic stress) determine outcome of cell injury

19
Q

Causes of Necrosis

A
  • Trauma
  • Intoxication
  • Deficiency
20
Q

Mechanisms of Cellular Injury

A

-Hypoxic Cell Injury: Impaired energy production
-Free Radical Injury: Form damaging reactive oxygen species (ROS)
-Impaired Calcium Homeostasis: Compromise cell membrane
CALCIUM INFLUX=Cell death

21
Q

Reactive Oxygen Species (ROS)

A

Protection: superoxide disumtase (SOD) converts superoxide into hydrogen peroxide
-Catalase converts hydrogen peroxide into water and oxygen

22
Q

Excess ROS

A

Form when oxygen is limited

  • Damage the cell (lipids, proteins, etc.)
  • Leaking Membranes
  • Calcium Influx
  • Cell death
23
Q

Ischemia

A

Lack of blood flow (oxygen)

24
Q

Coagulative Necrosis

A
  • Basic cell outline is preserved
  • Acidosis denatures proteins
  • Protenin denaturation causes coagulation
25
Q

Liquifactive Necrosis

A
  • Results from autolysis or heterolysis
  • Involves digestion of cell remains
  • Typical abscess formation
26
Q

Caseous Necrosis

A

A combination of coagulative & liquefactive necrosis

-The necrotic debris is not digested completely by hydrolases, so tissues appear soft and granular (cheesy)

27
Q

Fat Necrosis

A

Focal areas of fat destruction.

This destruction of lipids is associated with abnormal release of pancreatic enzymes (lipase)

28
Q

Gangrene

A

Cell death resulting from severe hypoxia - most commonly caused by ischemia

29
Q

Dry Gangrene

A

Coagulative necrosis as a result of ischemia

30
Q

Wet Gangrene

A

Tissue is infected with bacteria and phagocyte cells are recruited, releasing enzymes that lead to a liquifactive process

31
Q

Gas Gangrene

A

Infection caused by Clostridium spp., anaerobic bacteria that produces toxins that damage the connective tissue and cause gas

32
Q

Apoptotic Bodies

A

Defined fragmented DNA

-formation of distinct structures

33
Q

Phagocytosis

A

Process of removing dead cells

-NO inflammatory response

34
Q

Autodigestion

A

Necrosis involves activation of enzymes that digest cellular components
-This may stimulate an inflammatory response

35
Q

Substances that Accumulate (as a consequence of ADAPTATION)

A

-Lipids: Especially heart & liver
-Glycogen: In liver and skeletal muscle
-Pigments
- Melanin: formed by melanocytes in skin
- Hemosiderin: formed by hemoglobin, iron
- Billirubin: in liver
-Lipofuscin: fine granular golden-brown pigment formed from phosphilipids & proteins derived from degenerating membranes
-Minerals: Calcium —- Calcification
Hyaline change: Non specific indicator, formed from protein

36
Q

Karyolysis

A

Irreversible cell death characterized by lysing of nucleus, due to action of DNAse and RNAse

37
Q

Karyorrhexis

A

Irreversible cell death characterized by fragmentation of the nucleus

38
Q

Pyknosis

A

Irreversible cell death characterized by condensation of the nucleus and clumping of chromatin

39
Q

Hypoxic Cell Injury

A
  • Reduction of oxygen - Ischemia
  • Impair energy production
    - body switches from aerobic to anaerobic processes
    - Anaerobic metabolism = lactic acid production =lactic acidemia
  • Loss of ability to fuel the cells and maintain the integrity of those pumps on the surface
40
Q

Oxygen Free Radicals

Reactive Oxygen Species (ROS)

A
  • Unpaired electrons on the molecular oxygen = highly reactive
  • Interact with lipids & proteins in the cell = compromised integrity of cell
  • Damage cell – leaking membranes - calcium able to enter the cell
41
Q

Superoxide Dysmutase (SOD)

A

An enzyme that maintains homeostasis within the cell in the presence of oxygen free radicals

  • A form of molecular oxygen that has been radicalized
  • Converts to hydrogen peroxide
42
Q

Catalase

A

An enzyme that takes the hydrogen peroxide created by superoxide dysmutase and converts to water and oxygen
=Happy cells

NURP 404 Patho (4 decks)

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