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NURP 404 Patho > Cell Injury & Cell Death > Flashcards

Cell Injury & Cell Death Flashcards

(42 cards)

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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

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A

Pathologic stimuli

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

Severity & Duration

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A

(of pathologic stress) determine outcome of cell injury

19
Q

Causes of Necrosis

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A
  • Trauma
  • Intoxication
  • Deficiency
20
Q

Mechanisms of Cellular Injury

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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)

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A

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

22
Q

Excess ROS

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A

Form when oxygen is limited

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

Ischemia

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A

Lack of blood flow (oxygen)

24
Q

Coagulative Necrosis

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A
  • Basic cell outline is preserved
  • Acidosis denatures proteins
  • Protenin denaturation causes coagulation
25
Liquifactive Necrosis
- Results from autolysis or heterolysis - Involves digestion of cell remains - Typical abscess formation
26
Caseous Necrosis
A combination of coagulative & liquefactive necrosis | -The necrotic debris is not digested completely by hydrolases, so tissues appear soft and granular (cheesy)
27
Fat Necrosis
Focal areas of fat destruction. | This destruction of lipids is associated with abnormal release of pancreatic enzymes (lipase)
28
Gangrene
Cell death resulting from severe hypoxia - most commonly caused by ischemia
29
Dry Gangrene
Coagulative necrosis as a result of ischemia
30
Wet Gangrene
Tissue is infected with bacteria and phagocyte cells are recruited, releasing enzymes that lead to a liquifactive process
31
Gas Gangrene
Infection caused by Clostridium spp., anaerobic bacteria that produces toxins that damage the connective tissue and cause gas
32
Apoptotic Bodies
Defined fragmented DNA | -formation of distinct structures
33
Phagocytosis
Process of removing dead cells | -NO inflammatory response
34
Autodigestion
Necrosis involves activation of enzymes that digest cellular components -This may stimulate an inflammatory response
35
Substances that Accumulate (as a consequence of ADAPTATION)
-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
Karyolysis
Irreversible cell death characterized by lysing of nucleus, due to action of DNAse and RNAse
37
Karyorrhexis
Irreversible cell death characterized by fragmentation of the nucleus
38
Pyknosis
Irreversible cell death characterized by condensation of the nucleus and clumping of chromatin
39
Hypoxic Cell Injury
- 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
Oxygen Free Radicals | Reactive Oxygen Species (ROS)
- 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
Superoxide Dysmutase (SOD)
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
Catalase
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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