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Pathology > Cell Injury, Death, and Adaptations > Flashcards

Cell Injury, Death, and Adaptations Flashcards

1
Q

Cell and Tissue Adaptations

A

Hyperplasia
Hypertrophy
Atrophy
Metaplasia

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2
Q

Adaptations are instigated by…

A

Growth factors, hormones, or cytokines

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3
Q

general examples of cell adaptation response

A

interacting with receptors at cell surfaces, inducing signaling pathways inside the cell, modify transcription of structural and functional proteins, cause division

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4
Q

hypertrophy

A

increase in the size of cells leading to increase in size of tissue or organ due to increased synthesis of cellular components

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5
Q

difference between hyperplasia and hypertrophy

A

hypertrophy in contrast With hyperplasia does not require a cell population to be capable of cell division but it can occur in fully mature- non dividing cells

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6
Q

Hyperplasia

A

this is an increase in number of cells and increases volume of the organ or tissue
it is ONLY in cell population capable of division
It can be physiologic or pathologic

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7
Q

hypertrophy of hepatocytes is what type

A

physiologic hypertrophy

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8
Q

hypertrophy of hepatocytes

A

due to increased endoplasmic reticulum in response to the functional demand for metabolism of ingested drugs such as phenobarbital

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9
Q

muscel hypertrophy is what type

A

physiologic hypertrophy

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10
Q

muscle hypertrophy

A

induced by ‘pumping iron’
increased size of individual skeletal muscle fibers is due to increased numbers of actin and myosin fibers and cellular organelles necessary to support increased function, most importantly mitochondria

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11
Q

myostatin

A

molecule related to TGF-beta family of growth factors- inhibiot of muscle growth
born without it- you have hypertrophy of muscle at a young age without any muscle training

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12
Q

stimulus for muscle hypertrophy

A

mechanical stretch that cell membrane transducers convert to the appropriate protein transcription signals

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13
Q

pathologic hypertrophy

A

happens in response to abnormally increased peripheral vascular resistance - like hypertension and signal transduction pathways lead to increased synthesis of functional proteins and growth factors and agents that affect peripheral vessel tone and caliber (maybe even kidney function)

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14
Q

cardiac muscle hypertrophy is an example of what type of hypertrophy

A

pathiologic hypertrophy

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15
Q

hyperplasia

A

increase in number of cells and increase in the volume of the organ or tissue
CAN ONLY BE INITIATED WHERE THERE IS A CELL POPULATION CAPABLE OF DIVISION AND PROLIFERATION. can be pathogenic or physiologic

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16
Q

lactating breast is an example of..

A

physiologic hyperplasia

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17
Q

lactating breast

A

physiologic hyperplasia- with increase in cell number and size of the breasts lobules in lactation due to stimulation from estrogen and the pituitary hormone prolactin - hormonal hyperplasia

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18
Q

post-hepactomy regeneration

A

type of physiologic hyperplasia
restoration of the volume of the liver following partial hepactomy for injury or organ donation (compensatory hypertrophy) the stimulus for this regeneration is growth factor production by the residual hepatocytes

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19
Q

follicular hyperplasia of lymph nodes

A

type of patholigic hyperplasia
could happen in neck in response to an oral infection or dental abscess
exposure to the antigens of the infectious agent leads to B-cell proliferation in the follicles of the regional lymph node

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20
Q

benign prostatic hyperplasia

A

pathologic hyperplasia
common disorder in men over 50- when testosterone metabolite (DHT) induces nodular enlargement of the gland
impinges on prostatic urethra and causes urinary distention

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21
Q

squamous hyperplasia

A

pathologic hyperplasia
response to chronic irritation, like ill-fitting denture
area of mucosa may become thickened to compensate for repeated loss of surface epithelial cells
molecular mediator is the TGF-alpha

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22
Q

when does proliferation end in both hyperplasia and hypertrophy

A

when the stimulus that induced it is removed

if failure to do this it could become neoplastic (autonomous)

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23
Q

T/F hyperplasia can often occur with hypertrophy

A

T - uterus and breasts in pregnancy and lactation is both hyperplasia and hypertrophic

24
Q

atrophy

A

shrinkage of a tissue due to loss of cell size or number

it can be pathologic or physiologic

25
Q

what drives atrophy?

A

imbalance between protein synthesis and protein degradation

26
Q

pathway responsible for accelerating proteolysis in atrophy?

A

ubiquitin-proteasome pathway

27
Q

ubiquitin-proteasome pathway

A

targeted proteins are conjugated with ubiquitin which chaperones the protein into a cytoplasmic organelle called proteasome where it is degraded

28
Q

autophagic vacuoles and what process is called

A

atrophic cells that exhibit numerous lysosomes that contain fragments of cell components such as mitochondria or endoplasmic reticulum - process is called autophagy

29
Q

residual bodies

A

atrophic cells accumulation of chrunken lysosomes that contain lipofuschin, which is the residue of hydrolytic enzyme digestion

30
Q

brown atrophy and example

A

from residual bodies - confer brown color on atrophic organs
on heart of patient with dying illness or cachecia (chronic illness and wasting of body)

31
Q

atrophy of disuse

A

something being in a cast - not using is so muscle being immobilized or OSTEOPOROSIS IN ASTRONAUTS that is induced by prolonged weightlessness during space flight

32
Q

denervation atrophy

A

interruption of the peripheral nerve supply to muscle due to trauma or disease that results in rapid atrophy and loss of denervated muscle fibers

33
Q

causes of cell injury and necrosis

A 
oxygen deprivation
physical agents
chemical agents and drugs
infectious agents
immunological reactions
genetic derangement's
nutritional imbalances
34
Q

most common epithelial metaplasia?

A

conversion of columnar to a squamous phenotype due to chronic irritation
prime example is smoking - metaplasia of the lower respiratory tract

35
Q

barrett’s esophagus

A

more susceptible squamous mucosa in lower esophagus by a more acid -resistant gastric or intestinal columnar mucosa in response to persistant acid reflux from the stomach

36
Q

adenocarcinoma

A

caused from barretts esophagus - squamous to columnar and this is a malignant tumor formed from glandular structures in epithelium

37
Q

reversible injury

A

cellular swelling

fatty change

38
Q

cellular swelling

A

a type of reversible injury
alterations in the plasma membrane energy-dependent ion pump
the cell cytoplasm and endoplasmic reticulum is distended (by water) but cell membranes are in tact
considered a hydrophic change

39
Q

hydrophic change associated with?

A

cellular swelling

40
Q

fatty change

A

a type of reversible injury
hypoxic or toxic environments - mainly in the liver
associated with obesity, diabetes, and alcoholism
excessive stress in the fat metabolism system
TRIGLYCERIDE ACCUMULATION IN SMALL AND LARGE VACUOLES IN HEPATOCYTES

41
Q

mallory body

A

hyaline - associated with the fatty deposits and change within the liver

42
Q

karyolysis

A

fading due to compelte absence of the nucleus in necrosis

43
Q

karyorrhexis

A

nuclear fragmentation of cells that are necrotic

44
Q

myelin bodies

A

whorled aggregations and distruptions/ fragmentations of cell membranes in necrotic cells - at the ultrastructural level and looking at a light microscope will give you indication as to what could have been the nectrotic factor

45
Q

coagulative necrosis

A

likely due to a ischemic injury or myocardial infarct
ghost outlines of cells are preserved due to calcium infusion and early denaturation of structural proteins and enzymes - like lysosomal enzymes
CYTOPLASM WITH INCREASED EOSINOPHILIA DUE TO LOSS OF RNA AND FIBRILS AND CROSS STRIATIONS CANNOT BE APPRECIATED
example - gangrenous necrosis - ischemic necrosis

46
Q

gangrenous necrosis

A

ischemic necrosis - black discoloration

47
Q

liquefactive necrosis

A

no ghost outlines because the dead cells have been hydrolyzed by lysosomal enzymes that were ruptured
viscous liquid and later a cavity

typically due to a bacteria infection and also infarct in the CNS

48
Q

caseous necrosis

A

aka ‘cheesy necrosis’

describes the gross appearance of necrosis seen in tuberculosis

49
Q

fat necrosis

A

faintly outlined necrotic cells produced by action of enzymes in pancreas and tissues, MAINLY FAT.
release of FA–> early formation of chalky calcium deposits (soaps)
calcium deposits likely to form in multiple types of necrosis

50
Q

the two apoptosis pathways

A

extrinsic- use of cell membrane receptor (death receptor initiated)
intrinsic - use of the mitochondrial pathway

51
Q

apoptosis is accomplished through activation of what enzymes?

A

caspases

52
Q

caspases

A

initial mechanism of apoptosis*
denature cytoplasmic proteins and fragments of the cytoskeleton of both cytoplasm and nucleus
ACTIVATE DNAases - systematically digest DNA into smaller fragments of uniform size

53
Q

extrinsic apoptosis uses

A

ligand and receptor interactions

TNF-1 and FAS –> trigger the adapter proteins –> FADD–>pro caspase -8 –> caspase cascade initiated

54
Q

intrinsic apoptosis uses

A

removal of growth hormones and factors –> mitochondrial anti apoptopic BCL-x and BCL -2 –> BAX and BAC –> cytochrome c–> increase membrane permeability –> bind to apf-1–> caspase -9 and caspase cascade

55
Q

caspase 9

A

intrinisic apoptosis mechanism

56
Q

caspase 8

A

activated in the extrinsic apoptosis mechanism

57
Q

causes of apoptosis

A

either adaptive or physiologic

pathologic

Pathology (20 decks)

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