Tissue Injury and Response

Question 1

agents of stress

Answer 1

hypoxia
physical agents (heat,cold,radiation,trauma)
chemical agents and drugs
infectious agents
genetic derangements
nutritional imbalances
immunological reactions

Question 2

direct cellular responses to stressors: cellular adaptations (chronic exposures)

Answer 2

hypertrophy, atrophy, hyperplasia, metaplasia, neoplasia

Question 3

direct cellular responses to stressors: cell injury (acute exposures)

Answer 3

reversible injury, cell death (necrosis, apoptosis)

Question 4

direct cellular responses to stressors: degeneration (chronic exposures)

Answer 4

subcellular alterations and cell inclusions
intracellular accumulations
pathologic calcification

Question 5

hypertrophy

Answer 5

increase of cells in a tissue

little or no increase in size of nucleus just the cytoplasm

Question 6

factors inducding hypertrophy are

Answer 6

• ischemia
• increased functional demand and or endocrine stimulation
• increased cardiac demand due to: increased peripheral resistance will cause hypertrophy of the cardiomyocyte
• loss of part of an organ

Question 7

hyperplasia

Answer 7

an increase in the number of cells in a tissue
this is a non-neoplastic increase in cell number
some cells lack significant replicative ability to handle increased load, others are able to divide rapidly
EX: prostatic hyperplasia

Question 8

metaplasia

Answer 8

reversible replacement of one cell type for another
the new cell type may be better adapted/protected against the injurious agent
this is generally consider an undesirable change

Question 9

metaplastic responses

Answer 9

most common example of adaptive metaplasia is: the replacement of respiratory epithelium with squamous epithelium due to chronic irritation (chronic smokers will show this response)
vitamin A deficiency will also induce this change

Question 10

Neoplasia

Answer 10

the abnormal proliferation of cells, resulting in a structure known as neoplasm
an abnormal mass of issue, the growth which exceeds and is uncoordinated with that of normal tissues and persists in the same excessive manner after cessation of the stimulus which evoke the change
- they might be benign, pre-malignant or malignant
generally the result of genetic alterations although epigenetic changes may also be involved

Question 11

atrophy

Answer 11

an acquired decrease in the size of an organ that was once of normal proportions

Question 12

atrophy is in contrast to

Answer 12

aplasia-defective development or congenital absence of an organ/tissue

hypoplasia: incomplete development of a tissue
agenesis: the complete absence of a tissue or organ

Question 13

features of atrophy: decrease in number of cells

Answer 13

many times results in replacement of lost cells with fat or CT
atrophy of parenchymal cells will result in the accumulation of lipofuscin (a granular yellowish/brown pigment)

Question 14

features of atrophy: decrease in cell

Answer 14

volume

Question 15

cause of atrophy

Answer 15

• decreased workload (skeletal muscle following inactivation)
• loss of innervation (loss of n input lead to reduction in muscle size)
• diminished blood supply
• inadequate nutrition
• loss of endocrine stimulation (reduction of breast/uterine tissue during menopause)
• aging

Question 16

testicular atrophy

Answer 16

can come from injury (focal atrophy)

or steroid use (gross appearance)

Question 17

Reversible cell injury (degeneration)

Answer 17

-depending on dose and chronicity of toxicant exposure, cell possess defensive mechanisms to protect against direct toxic injury
sometimes results in cell swelling or fatty changes

Question 18

Irreversible cell injury: necrosis

Answer 18

represents a process of events leading to destruction of the cell

• necrotic cells have characteristics of condensation of nucleus and enhance basophilic staining
• this type of cell death invokes an inflammatory response, fibrotic outcome

Question 19

coagulative necrosis

Answer 19

commonly produced by cutting off blood supply (infarction)

characterized by loss of cellular detail while maintaining overall tissue architectural features

Question 20

liquefactive necrosis

Answer 20

the dead tissue softens and eventually liquefies
seen in the CNS
can also be applied to the pus seen in abcesses

Question 21

caseous necrosis

Answer 21

gets its name from the “cheesy” macroscopic appearance of the tissue, particularly striking example is necrotic tissue due to tuberculosis infection
architectural appearance of the tissue is totally lost

Question 22

mechanism of necrosis: loss of cell viability

Answer 22

dysregulation of calcium metabolism
alteration in actin/focal adhesionite proteins
cell shape changes (blebbing)
activation of calcium-dependent proteases
disruption of cell membranes

Question 23

Response to necrotic tissue damage

Answer 23

if a tissue undergoes necrotic damage the host repair or regeneration system will be activated

Question 24

regeneration

Answer 24

the replacement of damaged tissue with an exact replicate of the original structure

Question 25

repair

Answer 25

the process used to replace damaged tissue with scar, following an injury that compromises the vascular tree

Question 26

component process of the repair or scarring process: acute inflammation

Answer 26

inflammation is the norma and beneficial response to all cellular injury it only becomes a problem when the magnitude of the injury response exceeds that required to deal with the initial cellular or tissue insult without some inflammation the healing response is blunted: coagulation, neutrophil influx, monocyte/macrophage activation

Question 27

component process of the repair or scarring process: chronic inflammation

Answer 27

inflammation of prolonged duration (weeks or months) in which active inflammation tissue destruction and attempts at healing are proceeding simultaneously sometimes chronic inflammation may follow acute inflammation when acute inflammation cannot be resolved

Question 28

other component process of the repair or scarring process

Answer 28

- neovascularization - CT deposition - contraction - remolding

Question 29

Irreversible cell injury: apoptosis

Answer 29

an ordered physiologic process that allows for the selective elimination of a cell population

Question 30

Intrinsic apoptotic pathway

Answer 30

results from cellular damage due to radiation, redox injury and drugs that produce direct DNA change mitochondria central to the pathway, with cell injury resulting in leakage of cytochrome C from the mitochondria: this results in activation of the caspases, activated caspases degrade cytoskeletal and nuclear proteins

Question 31

Extrinsic apoptosis pathway

Answer 31

involves binding of ligand to cell surface death receptors central to physiological cell death regulation in the immune system and to prevent cancer the receptors (dimerize/trimerize) upon ligand binding, with adaptor proteins binding to the cytoplasmic tails - leading got the activation of caspases, activated caspases degrade cytoskeletal and nuclear proteins

Question 32

apoptosis results in

Answer 32

degenerative effects | cell death

Question 33

direct action of apoptosis

Answer 33

direct binding to critical molecule or cellular organelles

Question 34

conversion to reactive metaoblite apoptosis

Answer 34

formation of reactive free radical ssubsequent lipid peroxidation