Cell Injury, Death, and Adaptations

Question 1

Cell and Tissue Adaptations

Answer 1

Hyperplasia
Hypertrophy
Atrophy
Metaplasia

Question 2

Adaptations are instigated by…

Answer 2

Growth factors, hormones, or cytokines

Question 3

general examples of cell adaptation response

Answer 3

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

Question 4

hypertrophy

Answer 4

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

Question 5

difference between hyperplasia and hypertrophy

Answer 5

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

Question 6

Hyperplasia

Answer 6

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

Question 7

hypertrophy of hepatocytes is what type

Answer 7

physiologic hypertrophy

Question 8

hypertrophy of hepatocytes

Answer 8

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

Question 9

muscel hypertrophy is what type

Answer 9

physiologic hypertrophy

Question 10

muscle hypertrophy

Answer 10

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

Question 11

myostatin

Answer 11

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

Question 12

stimulus for muscle hypertrophy

Answer 12

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

Question 13

pathologic hypertrophy

Answer 13

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)

Question 14

cardiac muscle hypertrophy is an example of what type of hypertrophy

Answer 14

pathiologic hypertrophy

Question 15

hyperplasia

Answer 15

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

Question 16

lactating breast is an example of..

Answer 16

physiologic hyperplasia

Question 17

lactating breast

Answer 17

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

Question 18

post-hepactomy regeneration

Answer 18

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

Question 19

follicular hyperplasia of lymph nodes

Answer 19

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

Question 20

benign prostatic hyperplasia

Answer 20

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

Question 21

squamous hyperplasia

Answer 21

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

Question 22

when does proliferation end in both hyperplasia and hypertrophy

Answer 22

when the stimulus that induced it is removed

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

Question 23

T/F hyperplasia can often occur with hypertrophy

Answer 23

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

Question 24

atrophy

Answer 24

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

it can be pathologic or physiologic

Question 25

what drives atrophy?

Answer 25

imbalance between protein synthesis and protein degradation

Question 26

pathway responsible for accelerating proteolysis in atrophy?

Answer 26

ubiquitin-proteasome pathway

Question 27

ubiquitin-proteasome pathway

Answer 27

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

Question 28

autophagic vacuoles and what process is called

Answer 28

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

Question 29

residual bodies

Answer 29

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

Question 30

brown atrophy and example

Answer 30

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

Question 31

atrophy of disuse

Answer 31

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

Question 32

denervation atrophy

Answer 32

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

Question 33

causes of cell injury and necrosis

Answer 33

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

Question 34

most common epithelial metaplasia?

Answer 34

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

Question 35

barrett's esophagus

Answer 35

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

Question 36

adenocarcinoma

Answer 36

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

Question 37

reversible injury

Answer 37

cellular swelling | fatty change

Question 38

cellular swelling

Answer 38

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

Question 39

hydrophic change associated with?

Answer 39

cellular swelling

Question 40

fatty change

Answer 40

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

Question 41

mallory body

Answer 41

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

Question 42

karyolysis

Answer 42

fading due to compelte absence of the nucleus in necrosis

Question 43

karyorrhexis

Answer 43

nuclear fragmentation of cells that are necrotic

Question 44

myelin bodies

Answer 44

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

Question 45

coagulative necrosis

Answer 45

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

Question 46

gangrenous necrosis

Answer 46

ischemic necrosis - black discoloration

Question 47

liquefactive necrosis

Answer 47

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

Question 48

caseous necrosis

Answer 48

aka 'cheesy necrosis' | describes the gross appearance of necrosis seen in tuberculosis

Question 49

fat necrosis

Answer 49

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

Question 50

the two apoptosis pathways

Answer 50

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

Question 51

apoptosis is accomplished through activation of what enzymes?

Answer 51

caspases

Question 52

caspases

Answer 52

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

Question 53

extrinsic apoptosis uses

Answer 53

ligand and receptor interactions | TNF-1 and FAS --> trigger the adapter proteins --> FADD-->pro caspase -8 --> caspase cascade initiated

Question 54

intrinsic apoptosis uses

Answer 54

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

Question 55

caspase 9

Answer 55

intrinisic apoptosis mechanism

Question 56

caspase 8

Answer 56

activated in the extrinsic apoptosis mechanism

Question 57

causes of apoptosis

Answer 57

either adaptive or physiologic | pathologic