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)
Xenobiotic
Substance foreign to the body
Lead
Most common overexposure found in industry
-houses with older pain = Pb dust = inhaled
-BBB in fetus is immature and vulnerable to lead poisoning
Carbon monoxide
Odourless, colourless, non irritating
-causes Hypoxic injury due to oxygen deprivation = CO attaches to RBC with higher affinity than O2
Ethanol (alcohol)
-liver damage
-nutritional deficiencies (magnesium, VB6)
-absorbed in stomach, then distributed to body tissues and fluids
J shaped effect of alcohol consumption
-light to moderate drinks = lower mortality than non drinkers
-heavy drinkers = high mortality
Mechanism for light to moderate drinkers
-decreased LDL levels
-Dec BP
-decreased atherosclerosis
Mercury
Recognized as a global threat to human and environmental health
Over the counter and prescribed medications
-chemical injury is a major limitation to medication therapy
-leading cause of child poisonings
Direct damage of the medications to cell (on target toxicity)
Chemicals and medications injure cells by combining directly with critical molecular substances
-chemotherapeutic medications
Hypersensitivity reactions
Range from mild skin rashes to immune mediated organ failure
Asphyxiation
Failure of cells to receive or use oxygen
Suffocation
Systemic hypoxia
-no air exchange
Strangulation
Compression
-closure of airway
-causing cerebral hypoxia
Drowning
Fluid fills lungs
-no oxygen exchange
-fluid can pass thru alveolar/capillary interface = massive fluid and electrolyte changes in blood
Chemical asphyxiation
Prevention of oxygen delivery to cells or its utilization
Carbon monoxide binds to
Hb in same positions as oxygen
Treatment for carbon monoxide
Hyperbaric chamber
Cyanide
Blocks utilization of oxygen at electron transport chain, which leads to cardiac arrest
Jones town
Cult members forced to drink cyanide laced fluid
-900 people died
Contusion
Crushing injury to muscle
-mild, causes bruising
Laceration
Irregular cut from tearing
-irregular edges
Incision
Sharp strait wound
Fracture
Broken or shattered bones
Incised wound
Wound is longer than it is deep
Stab wound
Wound deeper than it is long
Puncture wound
Sharp point but not sharp edges
Infectious injury
Invasion of a pathogen
-bacterium, virus or other microorganism
-disease producing potential
What are the disease producing potentials of pathogen
-invasion and destruction
-toxin production
-production of hyper immune reactions
Apoptosis
Cell death that occurs as normal controlled part of an organisms growth and development
-orderly, broken into sections, taken by immune system
Autophagy
Consumption of a cells own contents for fuel to oppose starvation and certain diseases
Necrosis
Swelling and bursting of cell membrane
-due to disease, injury, failure of blood supply
-cellular level
Coagulation necrosis (kidney and heart) is caused by
Ischemia or infarction
-obstruction of blood supply causing death of cell
Ischemic cells can be revived if
Oxygen supplied within twenty minutes
Coagulation is the result of
Protein desaturation
Caseous necrosis (lungs)
Dead tissue resemble clumped cheese (soft and granular)
Caseous necrosis caused by
Tuberculosis
Danger of caseous
Dead cells enveloped by other cells
-increased mall = Dec lung space
Liquefactive necrosis (brain)
Ischemic injury to neurons and glia cells
-transforms tissue into liquid causes infarction
Liquefactive necrosis is caused by
Strep. Or E.coli
Infarction
Blockage of blood supply causing death of cell
Fatty necrosis (breasts and abdominal organs)
Action of lipases
-usually harmless, often left alone and let body absorb it
Gangrenous necrosis
Severe Hypoxic injury often to major arteries in lower leg
-becomes medium for bacterial growth (anaerobic)
Gas gangrene
Due to clostridium (anaerobic bacteria)
-produces gas
-fatal if it enters blood and dismisses oxygen carrying capacity of RBC
Oncosis
Cell death due to swelling
Process of oncosis (diagram)
Cellular aging
Atrophy, decreased function and loss of cells
Tissue and systemic aging
Progressive stiffness and rigidity
-sarcopenia
Sarcopenia
Progressive and generalized loss of skeletal muscle mass and strength
Sarco= flesh
Penia = decreased
Frailty
Mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance, falls, fractures and bone density
