CH1

secretions from the cell attach to the cell's own surface receptors (one cell to itself)

closely adjacent cells act on each other (cells next to each other)

hormones secreted by endocrine cells reach target through a blood vessel
(takes a 'freeway' to get to destination)

the state of balance between opposing pressures operating in and around a cell or tissue

cell receives nutrients, oxygen, water, and essential materials

by burning some calories derived from nutrients

upkeep the nucleus
for integrity and function of cytoplasm, cell organelles, and plasma membranes

energy

determined by the reactivity of each cell and the ability of the cell to respond to increased demands or stimuli

cell may revert back to original steady state

if the stimulus persists or is severe enough from the beginning, the cell suffers irreversible injury and ultimately cell death

adaptation, reversible injury, and cell death

yes, cells that are nonfunctional due to injury are still viable (but the longer duration may result in irreversible injury and cell death

hydropic change

altered permeability of the plasma membrane

1. swollen microvilli
2. invagination of the cell membrane
3. swollen mitochondria and dilated RER
4. swollen cells lose contact with adjacent cells

consequence of an influx of water in the cytoplasm

gives rise to fluid filled cytoplasmic vacuoles

vacuolar degeneration

Na+ / K+ ATPase pump

Pumps Na+ out (Cl- follows Na+)
K+ in

anoxia or any other form of energy deprivation

ATP dependent

increased anaerobic glycolysis, leading to decreased ATP and decreased energy production

RER dilation and fragmentation
leading to decreased protein synthesis

cytosol pH decreases, so enzyme activity decreases, so metabolism decreases

increase autophagocytosis

decreased energy, decreased protein synthesis, and decreased metabolism

general swelling of cell and organelles
blebbing of the plasma membrane
detachment of ribosomes form the ER
clumping of nuclear chromatin

ATP depletion and decreased ATP synthesis

mitochondria
cell membranes
machinery of protein synthesis and packaging
DNA in nuclei

phagocyte oxidase enzyme in the phagosome membrane generates superoxide (which can be converted to other free radicals)

hypochlorite from reactive oxygen species (ROS)

reversible changes in the size, number, phenotype, metabolic activity, or functions of the cell in response to changes in their environment

irreversible biochemical alterations that cause cell death

during mitochondrial respiration by electron transport chain

H2O2 and hydroxyl (*OH) free radical or to peroxynitrite (ONOO-)

produced by the cell are crucial to normal cellular metabolism but can also damage cells

inflammatory cells (neutrophils)
vascular cells (endothelial, smooth muscle, adventitial fibroblasts)

cell growth, proliferation
apoptosis
inflammatory gene expression
necrosis
matrix regulation

ischemia that results form decreased blood flow

absorption of energy (radiation)
redox reactions (reperfusion)
enzymatic metabolism of chemicals
iron

iron = oxidant
oxidants are inactivated by endogenous or exogenous antioxidants, and the activity of 3 enzymes
disorders that increase free radical production may also result in decreased activity of these antioxidants and enzymes

1. lipid peroxidation
2. alteration of proteins
3. alterations of DNA

showing surface blebs, increased eosinophilia of cytoplasm, and swelling of occasional cells

loss of nuclei and fragmentation of cells and leakage of contents

cells exposed to heavy doses of toxins, anoxia, severe or prolonged hypoxia, or other overwhelming injuries

dead cells release their contents into extracellular fluid
therefore release cytoplasmic enzymes into blood circulation

a. pyknosis
b. karyorrhexis
c. karyolysis

condensation of chromatin

fragmentation of nucleus

lysis of chromatin

circulatory disturbances
inadequate oxygen intake
(myocardial infarction, strangulation)

bacterial exotoxins
direct (viral) cytopathic effect
indirect (immune-mediated) cytotoxicity
(food poisoning and viral infection)

direct and indirect toxicity
(mercury poisoning and carbon tetrachloride poisoning)

action of cytokines and complement
(autoimmune disease)

disruption of metabolic pathways (Lysosomal storage disease, Tay-Sachs)
Abnormal metabolism (diabetes)

short term lack of O2

long term lack of O2

1. interruption of the oxygen supply
2. inhibition of blood oxygenation in lungs
3. inadequate transport of oxygen in circulation
4. inhibition of cellular respiration

oversupply of oxygen may have harmful effect on reversibly damaged cardiac cells resulting in oxygen toxicity from activated oxygen radicals

generation of toxic oxygen radicals which damage cellular membranes and mitochondria
oxygen toxicity can result from activated oxygen radicals)

oxygen consumption by tissues decreases and scavenger enzyme systems are inoperative, leading to excessive formation of oxygen radicals (resulting in tissue loss)

prolonged exposure of cells to adverse or exaggerated normal stimuli evokes adaptations

physiologic atrophy
pathologic atrophy

denotes a decrease in the size of a cell, tissue, organ, or the entire body and reduced metabolism

normal with aging
ex. Thymus atrophies during childhood and 2nd decade of life; ovaries, uterus, and breasts atrophy after menopause

inadequate nutrition, oxygen supply, or hormonal stimulation

ischemic organs are typically small (affected by atherosclerosis)
denervated muscles (leg muscles after spinal cord injury) are flaccid
general body wasting (cachexia)

reversible functional and structural responses to more severe physiologic stresses and some pathologic stimuli, during which new but altered steady states are achieved allowing the cell to survive and function

increased cells and larger

all cells are larger

increase in cells but same size

increased cells and all misshapen

form of adaptation characterized by the change of one cell type into another
represents a reversible change

columnar cells of the bronchial mucosa (when irritated by cigarette smoke) turn into stratified squamous epithelium; once stopped smoking, squamous epithelium should revert back

metaplasia may progress to dysplasia

caused by exogenous injury
vital processes inhibited
affects multiple cells
cells are swollen, ruptured
cell membrane is ruptured
becomes phagocytized by neutrophils

caused by exogenous OR endogenous injury
energy dependent, vital processes active
affects singular cell
cell is rounded up and fragmented (apoptotic bodies)
cell membrane functionally intact
becomes phagocytized by macrophages

apoptosis

incomplete or defective apoptosis

progressive loss of functional capacity characteristic of senescence and ends in death

telomere shortening
environmental injuries
DNA repair defects
abnormal growth factor signaling

directs RNA template-dependent DNA synthesis (nucleotides are added to one strand at the end of chromosome). Lagging strand filled in by DNA polymerase

germ cells and stem cells both contain active telomerase, but only germ cells have sufficient levels of enzyme to stabilize telomere length
normal somatic cells have no telomerase activity and telomeres shorten with successive cell divisions
if not shortened, cell never reaches senescence ...cancer?