Cell adaptations

Question 1

cell interaction

Answer 1

through extracellular matrix, vascular elements through reception of soluble and insoluble signals-> received by molecules on cell surface.

Question 2

types of soluble diffusible signals

Answer 2

1. ) environmental monitoring: metabolic state, nutrition, electrolytes, waste products, O2/Co2, ion [ ], pH
2. ) soluble hormones: growth factor, interleukins, autocrine, paracrine, endocrine.
3. ) pharmacological agents

Question 3

types of insoluble signals

Answer 3

cell to cell or extracellular matrix
1.) anchoring to stromal elements, to other parenchymal cells and tissue, migrating cells, provide signaling as well as anchorage.

Question 4

physical signaling

Answer 4

stretch, cold heat

Question 5

Example of physical signaling: systemic hypertension

Answer 5

increased ventricular pressures-> increased stretch of myocardial cells-> increased protein synthesis (actin myosin) with increased size of fibers (hypertrophy)

Question 6

cell activation: resting state

Answer 6

homeostasis, unactivated, set signal then induces to activated state-> change cell function

Question 7

cellular signaling

Answer 7

activation of cell surface receptor-> transduction of signal-> cascade of intracellular mediators-> change in gene transcription

• new enzyme activity
• secretion
• cell movement
• change in cell surface receptors

Question 8

example of cell signaling

Answer 8

growth factor + intracellular oncogene-> PI3K-> PIP2-> PIP3 + binding factors -> cell migration, death, metabolism, cell proliferation

Question 9

Physiological response

Answer 9

response to physiological signals to alter the state of homeostasis

Question 10

pathological response

Answer 10

cell injury or adaptive response that results in alteration of physiological function, cell injury that progresses to cell death

Question 11

Labile cells

Answer 11

cells that divide continuously: skin, GI, respiratory epithelial cells, stem cells

Question 12

quiescent or stable cells

Answer 12

cells that divide only in situations of stress of repair: most glandular tissue, liver, stromal, smooth muscle, endothelial cells, renal tubular epithelium

Question 13

cells that DO NOT divide

Answer 13

cardiac muscle, skeletal muscle, nerve cells

Question 14

what does an adaptive response promote?

Answer 14

promote a return back to homeostasis or establish a new physiological state

• reversible changes
• happen in tissue that result from cellular responses to environmental signals

Question 15

Positive trophic responses

Answer 15

hypertrophy, hyperplasia, regeneration

Question 16

hypertrophy

Answer 16

increase in SIZE of cells, resulting in increase in size of organ
-ONLY response in tissue that does NOT divide, like myocardium

Question 17

physiological cause for hypertrophy

Answer 17

increase in muscle mass with exercise
growth factors
hormonal activity (pregnancy)

Question 18

pathological cause of hypertrophy

Answer 18

chronic hemodynamic overload-> hypertrophy of heart muscle in response
normal heart: 350 gm
hypertrophied heart: 700-800 gm

Question 19

pathological hypertrophy of heart muscle

Answer 19

1.) increase size of heart-> increased synthesis of cellular constituents such as proteins and filaments-> permits increase in contraction

Question 20

examples of pathological hypertrophy

Answer 20

• skeletal muscle hypertrophy: exercise
• cardiac muscle: systemic hypertension or aortic valve stenosis-> increase outflow resistance-> chronic hemodynamic overload-> allows for maintenance of cardiac output against outflow resistance

Question 21

left ventricular hypertrophy key features

Answer 21

• chronic hemodynamic overload results in activation of mechanical sensors
• sensors results in autocrine secretion of GF
• other signals such as vasoactive agents-> contribute to hypertension
• activation of transcription factors and nuclear activation
• increase in actin and myosin synthesis
• switch from adult to fetal or neonatal forms of proteins (myosin heavy chain)

Question 22

continued overload of myocardial tissue leads to?

Answer 22

ability of cells to compensate is eventually overcome and degeneration of cells results-> Cardiac dilation or failure

Question 23

hypertrophic response in liver due to alcohol or other drugs?

Answer 23

hypertrophy in ER in hepatocytes because of chronic activation with alcohol or other drugs-> increased capacity to metabolize alcohol but ALSO increases metabolism of other medications and decrease time in circulation

Question 24

hyperplasia

Answer 24

increase in NUMBER of cells

-occurs in ONLY in tissue that have capacity to divide

Question 25

types of hyperplasia

Answer 25

physiological: growth of tissue under normal hormonal control-> lactation, menstrual cycle, puberty pathological: growth of tissue in response to an aberrant hormone secretion, local production of GF, infection with warts, etc. - endometrial hyperplasia b/c of estrogen imbalance secretion - benign nodular hyperplasia of prostate (androgens) - hyperkeratosis of skin - gynecomastia in men secondary to increased estrogen in alcoholism

Question 26

what is hyperplasia normally apart of?

Answer 26

healing and regeneration | -related to chronic injury or inflammation

Question 27

what is compensatory hyperplasia?

Answer 27

replacement of lost tissue due to resection or necrosis | -in that case, cell proliferation occurs but NO increase in size of tissue

Question 28

difference between hyperplasia and neoplasia?

Answer 28

hyperplasia: controlled growth b/c results from production of GF or hormones, or proliferation of mature cells that can divide or increased output of new cells from tissue stem cells, stops when stimulus is withdrawn neoplasia: uncontrolled

Question 29

in what cells does NEITHER hyperplasia or hypertrophy occur?

Answer 29

nerve cells (only in glial cells)

Question 30

regeneration

Answer 30

replacement of injured or lost tissue-> replacement parenchymal through stimulation of cell division results in re-establishment of tissue architecture and function -where parenchymal cells CANNOT divide-> replaced by scar tissue

Question 31

classic model liver regeneration

Answer 31

partial hepatectomy-> DNA synthesis begins 12 hours after procedure-> peaks 1-2 days after-> division declines and regeneration complete after 1-2 weeks normally .5-1% cells divide

Question 32

negative tropic effects

Answer 32

adaptive conservation | atrophy, apoptosis

Question 33

atrophy

Answer 33

reduced size of an organ or tissue from a decrease in cell size

Question 34

in atrophy, loss of tissue size due to decrease in individual cell size, reduction in structural components of cell can be caused by?

Answer 34

1. ) few organelles, myofilaments, reduced RER, reduction in structural synthesis 2. ) increased degradation of cellular components-> - ubiquitin-proteosome pathway (nutritional deficits, ubiquitin ligase) - increase in autophagic vacuoles (residual granules from membrane bound autophagic vacuoles fusing with lysosome-> brown atrophy) 3. ) signals result in decreased cell components or function (dec work load, loss innervation, dec blood supply, aging) 4. ) chronic pressure->impingement by growing tumor (likely from loss blood supply) 5. ) cellular changes-> new equilibrium achieved when decreased metabolic demands meet decreased blood supple, nutrients, atrophic cells can have diminished function, but not be dead, but later led to death

Question 35

Apoptosis

Answer 35

programmed cell death

Question 36

Hypoplasia and Aplasia are not what?

Answer 36

part of adaptive changes, but are decreased or absent tissue, usually development anomalies

Question 37

hypoplasia

Answer 37

too little division-> developmental defect in which the size of a tissue never reaches normal due to failure of the cells to divide, too few cells (small)

Question 38

aplasia

Answer 38

developmental defect in which a tissue fails to develop at all due to absence of a primordium (precursor cells) -Example: aplastic anemia-> loss of stem cells-> resulting in failure to make blood cells from lack of cellular proliferation

Question 39

developmental adaptations

Answer 39

Result in altered tissue differentiation and architecture | Metaplasia, dysplasia, neoplasia

Question 40

Metaplasia

Answer 40

reversible change in which one adult cell type is placed by another adult cell type (usually adaptive response in reaction to chronic stress) - resist further injury from chronic exposure or irritation - function loss-> physiological dysfunction possible - ONLY in cells that have ability to proliferate - REPLACEMENT of damaged cells by new cell type from local tissue stem cells

Question 41

metaplasia due to smoking

Answer 41

normal columnar ciliated bronchial epithelium-> squamous epithelial cells -can induce cancer transformation in metaplastic epithelium

Question 42

metaplasia due to gastric reflux

Answer 42

squamous epithelium-> columnar epithelium in lower third of esophagus -leads to Barrett's esophagus and pre-disposes to esophageal cancer

Question 43

deficiency in vitamin A metaplasia

Answer 43

squamous metaplasia of respiratory tree while excess vit A suppress keratinization

Question 44

metaplasia from chronis infection with schistosomiasis haematobium

Answer 44

transitional epithelium of bladder-> squamous epithelial cells

Question 45

dysplasia

Answer 45

disordering of tissue architecture characterized by loss in the uniformity of the individual cells as well as a loss of their architectural orientation secondary to genetic damage. - PRE-CANCEROUS, but not invariably lead to cancer. - controlled proliferation although disordered

Question 46

Neoplasia

Answer 46

uncontrolled growth of tissue in form of a tissue mass, often preceded by areas of chronic damage resulting in hyperplasia, metaplasia, and or dysplasia - closely associated with proliferation potential of tissue - cancerous - NEVER seen in tissue that due not proliferate.