Chapter Four - Altered Cellular And Tissue Biology Class Notes Flashcards
Cellular injury occurs
If cell is unable to maintain homeostasis
-reversible = cell recovers
-irreversible = cell dies
Atrophy
Dec in cellular size
Physio- occurs in early development, thymus gland during childhood
Patho-occurs with dec in stimulation and use, such as aging
Hypertrophy
Increase in cellular size in response to mechanical stimuli
Physio- heart and skeletal muscles
Patho- associated with structural and functional changes,
hyperplasia
Increase in number of cells
Physio- response to injury
Patho-
Metaplasia
Replacement of one type of cell with another
-chronic injury or irritation
-reversible replacement
-after/behind
Dysplasia
Deranged cellular growth
-persistent severe injury or irritation
-usually found in epithelial tissue of cervix and respiratory tract
-bad
Hypoxic injury
Most common cause of cellular injury
-lack of sufficient oxygen within cells
-loss of hemoglobin
-decreased production of RBC
-R and CV disease
-poisoning of oxidative enzymes
Disuse atrophy
Immobilized in bed for prolonged period of time causing skeletal atrophy
Mechanisms of atrophy
-decreased protein synthesis
-inc protein catabolism
Autophagy
Atrophy resulting from chronic malnutrition
-self eating process creating autophagic vacuoles
Compensatory hyperplasia
Adaptive mechanism, enabling certain organs to regenerate
-removal of part of liver, begin to compensate for loss (removal of 70% of liver, regeneration is complete in two weeks)
Hormonal hyperplasia
Occurs in chiefly estrogen dependant organs
-uterus and breast
-estrogen stimulates endometrium to growth and thicken
Pathological hyperplasia
Abnormal proliferation
-pathological endometrial hyperplasia, causing excessive menstraul bleeding
Ischemia
Inadequate blood supply
-most common cause of hypoxia
Reduced O2 to mitochondria
-reduced production of ATP = reduction of cellular energy
Ischemia reperfusion injury
Additional injury caused by restoration of boood flow and oxygen
-oxidative stress, inc IC calcium, inflammation
Cellular response to ischemia
-decrease in ATP
-Causing failure of sodium potassium pump and sodium calcium exchange
-cellular swelling and shrinking
Free radicals
Missing an electron and will attack healthy atom to obtain a replacement electron
-highly reactive + risk of chain reaction
common causes of ischemia injury
Gradual narrowing of arteries, or completely blockage by blood clots
Oxidative stress (ischemia repperfusion injury)
(·OH), (·O2-), (H2O2)
-not producing enough antioxidants to break down current free radicals
Inflammation
Ischemia injury inc inflammation because resident immmune cells release danger signals from cytokines when cells die
How do free radicals develop
Within cells, first by reduction oxidation in normal metabolic processes
-natural byproduct of metabolism
Oxidative stress
Not producing enough antioxidants to break down current free radicals
-major role in chronic and degenerative ailments
Too many free radicals =
Oxidative stress and damage to cells
We’re okay if we have enough
Antioxidants to fix free radicals
How do antioxidants work
Neutralize free radicals
-have an atom to give away and balance them out
inc accumulation of H+ in mitochondria =
breakdown of membrane = inc in IC H+ = loss of mem potential = NECROSIS
Hypoxic injury
Reactive oxygen species
Healthy atoms that have lost an atom due to a free radical
Free radicals and reactive oxygen species
Electrically uncharged atom or group of atoms having unpaired electron
ROS
Subset of free radicals that contain oxygen
Three things free radicals cause
- Lipid per oxidation (free radicals attack lipids, like membrane)
- Alteration of proteins (desaturation)
- Alteration of DNA (mutation)