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PATHO > cellular adaptation, injury and death > Flashcards

cellular adaptation, injury and death Flashcards

1
Q

reversible functional and structural responses to
changes in physiologic states and some pathologic
stimuli

A

CELLULAR ADAPTATION

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2
Q

new but altered steady states are achieved,
allowing the cell to survive and continue to
function

A

CELLULAR ADAPTATION

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3
Q

refers to an increase in the size of cells, that results in an increase in
the size of the affected organ

A

HYPERTROPHY

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4
Q

result of increased production of cellular proteins

A

HYPERTROPHY

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5
Q

increase in the number of cells in an organ or tissue in response to a
stimulus.

A

HYPERPLASIA

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6
Q

result of growth factor-driven proliferation of mature cells and, in some
cases, by increased output of new cells from tissue stem cells

A

HYPERPLASIA

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7
Q

PATHOLOGIC HYPERPLASIA

A

Due to the action of hormones or growth factors occurs in several circumstances

need to increase functional capacity of hormone sensitive organs

need for compensatory increase after damage or resection

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8
Q

PHYSIOLOGIC HYPERPLASIA

A
  • caused by excessive or inappropriate actions of hormones or growth factors acting
    on target cells.
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9
Q

___ atrophy is common during normal development

A

Physiologic atrophy

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10
Q

___ atrophy has several causes and it can be local or generalized

A

Pathologic atrophy

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11
Q

COMMON CAUSES OF ATROPHY:

A

Decreased workload

Loss of innervation

Diminished blood supply

Inadequate nutrition

Loss of endocrine
stimulation

Pressure

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12
Q
  • change in phenotype of differentiated cells, often in response to chronic
    irritation, that makes cells better able to withstand the stress

-usually induced by altered differentiation pathway of tissue stem cells

  • may result in reduced functions or increased propensity for malignant
    transformation
A

METAPLASIA

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13
Q

appears whenever cells are incapable of maintaining ionic and
fluid homeostasis and is the result of failure of energy-
dependent ion pumps in the plasma membrane.

A

Cellular swelling

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14
Q

-occurs in hypoxic injury and various forms of toxic or metabolic
injury.

-manifested by the appearance of lipid vacuoles in the
cytoplasm.

A

Fatty change

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15
Q
  • First manifestation of most injuries

- Swelling of cells is reversible

A

CELLULAR SWELLING

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16
Q

due to inability to maintain ionic and fluid homeostasis

A

HYDROPHIC CHANGE

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17
Q
  • abnormal accumulation of triglyceride within parenchymal cells
  • Often seen in the liver major organ involved in fat metabolism
A

FATTY CHANGE

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18
Q

Endogenous pigments

A

ACCUMULATION OF PIGMENTS

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19
Q

MORPHOLOGICAL CELL CHANGES

A

CELLULAR SWELLING

HYDROPHIC CHANGE

FATTY CHANGE

ACCUMULATION OF PIGMENTS

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20
Q

yellowish pigment

A

BILIRUBIN

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21
Q

brownish black pigment

A

MELANIN

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22
Q

iron containing pigment

A

HEMOSIDERIN

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23
Q

black pigment in alkaptonuria

A

HEMOGENTISIC ACID

24
Q

fine yellow-brown granules

A

LIPOFUSCIN

25
Q

results when cells are stressed so severely that

they are no longer able to adapt

A

CELL INJURY

26
Q
  • the inability to reverse mitochondrial dysfunction

- profound disturbances in membrane function

A

IRREVERSIBLE CELL INJURY

27
Q

morphologic appearance of necrosis is the result of _____ of
____ and enzymatic digestion of the lethally injured
cell

A 
denaturation ( 1st blank)
intracellular proteins                  ( 2nd blank)
28
Q

Restoration of blood flow to ischemic tissues can promote
recovery of cells if they are reversibly injured, but can also
paradoxically exacerbate the injury and cause cell death.

A

ISCHEMIA-REPERFUSION INJURY

29
Q

Reperfusion occurs in several mechanisms:

A

Oxidative stress.

Intracellular calcium overload.

Inflammation.

Activation of the complement system

30
Q

pathway of cell death that is induced by a tightly regulated suicide program in
which cells destined to die activate intrinsic enzymes that degrade the cells’
own nuclear DNA and nuclear and cytoplasmic proteins

A

APOPTOSIS

31
Q

Causes of Apoptosis in Physiologic Situations

A

The destruction of cells during embryogenesis

Involution of hormone-dependent tissues upon hormone withdrawal

Cell loss in proliferating cell populations

Elimination of potentially harmful self-reactive lymphocytes

Death of host cells that have served their useful purpose

32
Q

Causes of Apoptosis in Pathologic Situations

A

DNA damage

Accumulation of misfolded proteins

Cell death in certain infections

Pathologic atrophy in parenchymal organs after duct obstruction

33
Q

major mechanism of apoptosis in all mammalian cells

A 
The Intrinsic (Mitochondrial) Pathway of
Apoptosis
34
Q

results from increased permeability of the mitochondrial

outer membrane

A 
The Intrinsic (Mitochondrial) Pathway of
Apoptosis
35
Q

The release of mitochondrial pro-apoptotic proteins is

tightly controlled by the ___ family of proteins

A

BCL2

The Intrinsic (Mitochondrial) Pathway of
Apoptosis
36
Q

is initiated by engagement of plasma membrane death

receptors on a variety of cells

A 
The Extrinsic (Death Receptor-Initiated)
Pathway of Apoptosis
37
Q

Death receptors are members of the TNF receptor family

that contain a cytoplasmic domain

A 
The Extrinsic (Death Receptor-Initiated)
Pathway of Apoptosis
38
Q

Examples of Apoptosis

A

1 Growth Factor Deprivation.

2 DNA Damage.

3 Protein Misfolding.

4 Apoptosis Induced by the TF Receptor Family.

5 Cytotoxic T Lymphocyte-Mediated Apoptosis.

39
Q

form of cell death is a hybrid that shares aspects

of both necrosis and apoptosis

A

NECROPTOSIS

40
Q

process in which a cell eats its own con- tents (Greek: auto, self; phagy,
eating)

A

AUTOPHAGY

41
Q

involves the delivery of cytoplasmic materials to the lysosome for
degradation.

A

AUTOPHAGY

42
Q

result of a progressive decline in cellular function and viability caused by
genetic abnormalities and the accumulation of cellular and molecular
damage due to the effects of exposure to exogenous influences

A

CELLULAR AGING

43
Q

Form of necrosis in which the architecture of dead tissues is
preserved at for a span of at least some days

A

COAGULATIVE NECROSIS

44
Q

___ necrosis of the supplied tissue in all organs except the

brain

A

COAGULATIVE NECROSIS

45
Q

digestion of the dead cells, resulting in transformation of the
tissue into a liquid viscous mass

A

LIQUEFACTIVE NECROSIS

46
Q

seen in focal bacterial or, occasionally, fungal infections

snecific nattern of cell death

A

LIQUEFACTIVE NECROSIS

47
Q

not a specific pattern of cell death

A

GANGRENOUS NECROSIS

48
Q

Usually applied to a limb, generally the lower leg, that has lost its
blood supply and has undergone necrosis involving multiple tissue
planes

A

GANGRENOUS NECROSIS

49
Q

encountered most often in foci of tuberculous infection

A

CASEOUS NECROSIS

50
Q

refers to focal areas of fat destruction, typically resulting from
release of activated pancreatic lipase into the substance of the
pancreas and the peritoneal cavity

A

FAT NECROSIS

51
Q

special form of necrosis usually seen in immune reactions

involving blood vessels

A

FIBRINOID NECROSIS

52
Q

typically occurs when complexes of antigens and anti- bodies are
deposited in the walls of arteries

A

FIBRINOID NECROSIS

53
Q

NUCLEAR CHANGES IN NECROSIS:

The basophilia of the chromatin may fade

A

karyolysis

54
Q

Nuclear shrinkage and increased basophilia

A

pyknosis

55
Q

Pyknotic nucleus undergoes fragmentation

A

karyorrhexis

PATHO (8 decks)

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