Exam 1: Ch 2 Flashcards
atrophy
cells decrease in size and activity in response to decreased workload or poor environmental conditions
generally reversible
atrophy in muscle
decrease in oxygen consumption, # of mitochondria, and # of myofilaments
causes of atrophy
disease
denervation
poor nutrition
ischemia
decreased endocrine stimulation (IGF 1)
hypertrophy definition and 2 types
cells increase in size in response to increased workload
physiologic or pathologic
physiologic hypertrophy
increased muscle size with exercise
pathologic hypertrophy
response to disease
Hypertension
Valvular heart disease
excessive hypertrophy is _____
counterproductive
signals for hypertrophy
hormonal (IGF1, EGF, growth factors)
mechanical (HTN)
hyperplasia
increase in the number of cells (usually epithelial or connective tissue)
Tissues with cells capable of mitotic division
3 examples/types of hyperplasia
hormonal: breast enlargement with pregnancy
compensatory: liver cell division after partial hepatectomy
wound healing
metaplasia
change in cell type
results from chronic inflammation/irritation (if untreated can turn into dysplasia)
ex. cilliated columnar epithelium –> stratified squamous in airways of smokers
dysplasia
higher deranged cell growth (usually from inflammation)
precursor to cancer
ex. abnormal pap smear of cervix
intracellular accumulations
cells build up substances they cannot eliminate
categories of substances in intracellular accumulations
normal substances present in excess (jaundice, lipofuscin)
products of abnormal metabolism (lipids in brain –> Tay-Sachs, glycogen in liver —> Von Gierke)
exogenous substances (blue line in gum tissue from lead poisoning)
dystrophic calcification
deposits of calcium phosphate crystals in injured tissue
calcium found in atheroscletotic lesions or heart valves
metastatic calcification
deposits of Ca in normal tissues when serum Ca is high
occurs in lungs, blood vessels, and kidneys
3 causes of metastatic calcification
Paget’s disease (excessive osteoclast activity)
renal failure (phosphate retention)
cancer
Hyperparathyroidism
what can cause cell injury
physical agents
radiation
chemicals
biological agents
nutritional imbalances
cell injury: physical agents
mechanical trauma: damages tissues/blood vessels
temperature: burns, frostbite–destroy blood flow
electrical: disrupt cardiac and nervous system, burn
3 types of radiation
ionizing
nonionizing – thermal damage
UV
ionizing radiation
kills immediately/causes genetic damage
endothelium most vulnerable –> blood vessel damage, burns, enteritis
chronic damage –> fibrosis/scarring
UV radiation
sunburn
increased skin cancer risk (DNA damage)
cell injury: chemicals
drugs: directly toxic/toxic metabolites
lead: paint, old pipes, air, industrial exposure
mercury: industrial/medical sources
lead toxicity
absorbed through GI & respiratory tract
stored in bones and teeth
blocks brain development (demyelization) and is toxic to RBS (anemia)
lead is particularly toxic to _______
children
CDC says blood lead [ ] > 5 micrograms/dL is dangerous
mercury toxicity
interferes with brain development
children/pregnant women at risk
predator fish contain mercury
cell injury: biological agents
viruses
bacteria
parasites
cell injury: nutritional imbalance
excesses or deficiencies
what is a free radical (ROS–reactive oxygen species)
chemical with unpaired electron in outer shell– highly
unstable
product of normal metabolism (convert O2 to ROS)
product of increased reperfusion –> overwhelm protective mechanisms
free radical injury
damages organelles (mitochondria) and DNA
may contribute to ALS, aging, other diseases
which vitamins are free radical scavengers?
C & E
hypoxia
oxygen deprivation
induction of genes for hypoxia inducible factors (HIF) –> increased RBC & angiogenesis
if severe, ATP production is interrupted
hypoxic cell injury
time until damage depends on cell’s energy requirement
permanent damage in 4-6 min for brain
pH falls, Na/K pump fails
hypoxia in rats
epithelial cells of kidney tubules can survive 20-30 min
anything greater than that decreases O2 delivery to tissues and produces hypoxic damage
_____ is important as a 2nd messenger
calcium
impaired calcium movement
levels must be kept very low
ischemia and toxins disrupt the ability of cells to exclude calcium
intracellular enzymes are released/activated and cell destroys itself
reversible cell injury
Na/K pump fails and causes swelling (hypoxic damage)
intracellular fat accumulations: associated with high serum fat
2 types of lethal cell injury
necrosis
apoptosis
apoptosis
programmed cell death
eliminates excess and damaged cells
eventually membrane is disrupted and debris consumed by phagocytes
apoptosis and cancer
important in normal development and destruction of cancer cells
cancer cells learn to escape apoptotic signals
p53 gene inactivated —> cancer
diseases involving overstimulation of apoptosis
ALS
Parkinson’s
Alzheimer’s
2 types of apoptosis pathways
extrinsic
intrinsic
both activate endonucleases –> DNA fragments
extrinsic apoptosis
activation of death receptors like TNF or Fas ligand receptor
death domain activated
procaspases –> caspases (activated form) in cascade
intrinsic apoptosis
multiple inputs damage mitochondria
caspase cascade activated
necrosis
uncontrolled cell death that is not pre-programmed
types of necrosis
liquefaction
coagulation
caseous (form of coagulation)
liquefaction necrosis
cells die but enzymes remain active
dead tissue is soft
seen in infection
ex. flesh eating bacteria (meningococcemia)
coagulation necrosis
area becomes hard
acidosis destroys enzymes
seen in ischemia/infarction
ex. dry gangrene, avascular necrosis
caseous necrosis
fatty infiltrates
seen in interior of TB lesions
gangrene
large mass of necrotic tissue
3 types of gangrene
dry
wet
gas (type of wet)
dry gangrene
type of coagulation necrosis
caused by interruption of arterial blood flow
line of inflammation between healthy/dead tissue
can progress to wet gangrene with infection
wet gangrene
type of liquefaction necrosis from infection
caused by venous obstruction or infection
area cold, swollen, pulseless
rapid spread
gas gangrene
type of wet gangrene (which is a type of liquefaction necrosis)
wound infection from Clodtridium bacteria
commonly following dirty trauma, bowel obstruction/rupture
bacteria product hydrogen sulfide gas –> tissue death
debridement, antibiotics, maybe amputation
cellular aging
normal process that decreases organ system function over time
may reflect accumulation of environmental and genetic damage
replicative senescence
cells can divide a fixed number of times (Hayflick limit)
involves shortening of telomeres
telomerase is active in germ cells/cancer cells
genetic influences on cellular aging
some gene alleles protect against chronic disease (increases longevity)
progeria
genetic defect that causes premature aging
gene
DNA that codes for a protein
cellular adaptation
how cells respond to persistent stress by activating gene pathways
ARDS
acute respiratory distress syndrome
systemic infection
DIC
disseminated intravascular coagulation
systemic infection
clotting factors/platelets get used up – excessive bleeding
