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General Pathology > 1-Cell Adaptation, cell injury/cell death > Flashcards

1-Cell Adaptation, cell injury/cell death Flashcards

1
Q

Four major patterns of cellular adaptation

A
  • hypertrophy
  • hyperplasia
  • atrophy
  • metaplasia
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2
Q

Hypertrophy

A
  • increase in SIZE of cell, =increased organ size
  • increase in size is due to increased production of CELLULAR PROTEINS
  • may be physiologic or pathologic
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3
Q

example of physiologic hypertrophy

A

uterus in pregnancy

-heart is another common organ that hypertrophies (myocardial hypertrophy)

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4
Q

mechanisms of myocardial hypertrophy

A

-mechanical stretch (increased work load)
-agonistst (alpha adrenegic hormones, angiotensin)
-growth factors (IGF-1)
All these lead to signal transduction pathways

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5
Q

Hyperplasia

A
  • Increase in NUMBER of cells, which usually increases mass
  • may occur with hypertrophy
  • may be physiologic or pathologic
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6
Q

Types of physiologic hyperplasia

A
  • Hormonal (puberty)

- compensatory (regrowth of liver)

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7
Q

Pathologic hyperplasia

A
  • hormonal/growth factors

- eg endometrial or prostatic hyperplasia

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8
Q

mechanisms of hyperplasia

A
  • proliferation of mature cells driven by growth factors

- increased production of new cells from stem cells

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9
Q

Atrophy

A
  • decreased cell size and number, =reduced size of tissue or organ
  • may be physiologic or pathologic
  • fundamental change is a decrease in cell size and organelles; reduction in metabolic needs may permit survival
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10
Q

common causes of pathologic atrophy

A
  • decreased workload (disuse atrophy, like with an arm in a cast)
  • loss of innervation (denervation atrophy)
  • diminished blood supply
  • inadequate nutrition
  • loss of endocrine stimulation
  • pressure (like bed sores)
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11
Q

mechanisms of atrophy

A
  • decreased protein synthesis due to reduced metabolic activity
  • increased protein degradation in cells due to activation of UBIQUITIN LIGASES
  • increased autophagy
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12
Q

autophagy

A

engulfment and degradation of cell’s own components

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13
Q

Metaplasia

A
  • replacement of one differentiated cell type by another
  • often represents an adaptation to stress by substituting cells better able to withstand stress
  • either epithelial or mesenchymal cells may undergo metaplasia
  • REVERSIBLE
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14
Q

common area of metaplasia

A

lungs, caused by irritation, especially from smoking.

- the cells go from ciliated columnar to squamous cells (squamous metaplasia)

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15
Q

potential downside of metaplasia

A
  • loss of certain cell functions (like the ciliary activity in the lungs)
  • ?? predisposition to development of neoplasia (process of new growth, controversial)
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16
Q

mechanisms of metaplasia

A
  • re-programming of stem cells to differentiate along a new pathway
  • NOT a change in an already differentiated cell
  • differentiation is effected by cytokines, growth factors and extracellular matrix components that promote gene expression
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17
Q

Types of cellular adaptations:

A
  1. Hypertrophy-increase in size of cells
  2. Hyperplasia-increase in number of cells
  3. Atrophy-decrease in cell size, number
    4 Metaplasia-replacement of one differentiated cell type by another
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18
Q

chronic irritation leads to what type of cellular adaptation?

A

Metaplasia

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19
Q

in there is a decrease in nutrients or stimulation, what will the adaptation be?

A

Atrophy

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20
Q

If there is a stimulus that is Physiologic/pathologic (growth factors, hormones, increased demand) the adaptation will be?

A

Hypertrophy or hyperplasia; or both

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21
Q

intracellular accumulations

A
  • substances may be normal cellular constituents (lipids, carbohydrates, proteins) or abnormal substances (exogenous or endogenous)
  • may be transient or permanent
  • may be harmless or toxic
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22
Q

steatosis

A

fatty change of the liver

-enlarged and yellow

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23
Q

anthracosis

A

carbon pigment deposition in lung

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24
Q

Hemochromatosis

A

Iron overload, can occur in liver or pancreas

25
Q

Pathologic calcification of tissues

A
  • abnormal deposition of calcium salts (usually with smaller amounts of other mineral salts
  • Two forms:
    • Dystrophic calcification
    • Metastatic calcification
26
Q

Most common type of tissue calcification

A

Dystrophic calcification

27
Q

dystrophic calcification

A
  • typically found in areas of tissue necrosis

- initiated by cell membrane damage

28
Q

Steps of dystrophic calcification

A
  • Calcium ion binds to phospholipids
  • phosphatases generate phosphate groups
  • repeated cycles of calcium-phosphate binding
  • structural changes result in microcrystal
  • propagation with more calcium deposition
29
Q

Metastatic Calcification

A
  • occurs in normal tissues in setting of hypercalcemia

- deposition can occur widely throughout the body

30
Q

The causes of Metastatic calcification

A
  1. Increased secretion of PTH
  2. destruction of bone
  3. vitamin D-related disorders
  4. renal failure
31
Q

Causes of cell injury

A
  • Oxygen deprivation (hypoxia and ischemia)
  • physical, chemical, and infectious agents
  • genetic derangements, immunologic reactions
  • nutritional imbalances
32
Q

Hypoxia

A
  • oxygen deficiency

- interferes with AEROBIC oxidative respiration

33
Q

ischemia

A
  • loss of blood supply, or mismatch of blood supply and tissue demand due to
    • impeded arterial flow or
    • reduced venous drainage
  • the MOST COMMON cause of tissue hypoxia
34
Q

Examples of generalized hypoxia

A
  • pneumonia
  • CNS depression
  • high altitude
  • anemia of blood loss
  • CO poisoning
35
Q

examples of Ischemia

A
  • Atherosclerosis
  • thromboembolism (blood clot that gets dislodged)
  • external compression of artery by tumor
  • severe hypotension (poor blood flow)
36
Q

Which injures tissues faster, hypoxia or ischemia?

A

Ischemia

37
Q

infarction

A

irreversible injury/cell death

38
Q

What ceases during ischemia?

A

Delivery of both oxygenated blood and substrates for glycolysis

39
Q

Mechanisms of cell injury

A
  • depletion of ATP (eg ischemia)
  • damage to mitochondria
  • influx of clacium
  • accumulation of oxygen-derived free radicals (oxidative stress)
  • defects in membrane permeability
  • damage to DNA and proteins
40
Q

reversible injury

A

Changes related to reduced oxidative phosphorylation with depleted ATP
-swelling of ER and mitochondria; membrane blebs; clumping of nuclear chromatin

41
Q

two main morphologic correlates of reversible injury:

A
  • Cellular swelling due to failure of ion pumps, water influx (hydropic change, vacuolar degeneration)
  • fatty change, (usually live and myocardium)
42
Q

Is necrosis physiologic, pathologic, or both?

A

ALWAYS PATHOLOGIC

43
Q

Is apotosis physiologic, pathologic, or both?

A

-frequently physiologic, but may be pathologic

necrosis and apoptosis may occur in response to the same injury

44
Q

Necrosis: cytoplasmic changes

A
  • sever damage to cell membrane with loss of integrity
  • leakage of contents
  • digestion of cell by enzymes from cell’s lysosomes or leukocytes
  • phospholipids phagocytosed or degraded to fatty acids; calcification results in calcium soaps; sometimes necrotic cells/tissue become calcified
45
Q

necrosis: three patterns of nuclear changes

A
  • due to breakdown of DNA and chromatin
    1. Karyolysis
    2. pyknosis
    3. Karyorrhexis
46
Q

Karyolysis

A

fading of nucleus due to deoxyribonuclease activity

47
Q

Pyknosis

A

nuclear shrinkage and increased basophilia due to DNA condensation

48
Q

Karyorrhexis

A

fragmentation and eventual disappearance of pyknotic nucleus

49
Q

Types of tissue necrosis

A
  • coagulative
  • liquefactive
  • caseous
  • fat
  • fibrinoid
  • (gangrene)
50
Q

coagulative necrosis

A

“cells are mummified”

  • basic tissue architecture is preserved
  • injury denatured not only structural proteins but also enzymes; proteolysis is blocked
  • eventually necrotic cells are phagocytosed/digested by leukocytes
  • typical of ischemic infarcts (except in brain)
51
Q

Liquefactive necrosis

A
  • usually in setting of microbial infections
  • inflammatory cells release enzymes that digest (liquefy) fissue
  • associated with the formation of PUSS
  • typical of cerebral infarcts
  • “Wet gangrene”
52
Q

Gangrene

A
  • usually refers to ischemic necrosis (typically of a limb)
  • coagulative necrosis (dry gangrene)
  • if complicated by bacterial infection, also undergoes liquefactive necrosis (wet gangrene)
53
Q

Caseous necrosis

A
  • most often associated with tuberculous infection
  • cheese-like appearance
  • cells fragmented, lysed; tissue architecture not identifiable
  • usually surrounded by granuloma (special form of inflammatory response)
54
Q

Fat necrosis

A
  • focal areas of fat destruction
  • associated with acute pancreatitis, with release of lipases into pancreas and peritoneal cavity;
  • adipocyte membranes liquefied; release fatty acids which combine with calcium=fat saponification
55
Q

fibrinoid necrosis

A
  • usually seen in immune reactions involving blood vessels
  • deposition of antigen-antibody complexes in vessel wall
  • fibrin leaks out of vessel
  • BRIGHT PINK amorphous appearance
56
Q

apoptosis

A
  • cell membrane integrity is largely maintained
  • active, energy-dependent process; not associated with ATP depletion
  • characterized by nuclear dissolution, fragmentation of the cell, followed by removal of cell debris
  • irreparable damage to DNA or proteins, or with deprivation of growth factors
57
Q

causes of apoptosis

A
  • programmed cell destruction in embryogenesis
  • involution of hormone-dependent tissues
  • cell loss in proliferating cell populations
  • senescent cell loss
  • elimination of self-reactive lymphocytes
  • cell death induced by cytotoxic T lymphocytes
  • DNA damage (ie radiation)
  • accumulation of misfolded proteins
  • some infections
  • pathologic atrophy after duct obstruction
58
Q

Necrosis summary

A
  • always pathological
  • ATP depletion
  • membrane injury
  • many cells
  • cell swelling; disrupted organelles
  • inflammation
59
Q

Apoptosis summary

A
  • pathological or physiological
  • gene activation; proteolytic enzymes
  • single cells
  • intact organelles; apoptotic bodies
  • no inflammation; phagocytosis or apototic bodies

General Pathology (9 decks)

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