1 altered cellular and tissue biology chapter 2. mosby items and derived items © 2006 by mosby,...
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Cellular AdaptationPhysiologic vs. pathogenicAtrophyHypertrophyHyperplasiaMetaplasiaDysplasia
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Cellular Injury Mechanisms Hypoxic injury
Ischemia – cut off of blood flow circulation Anoxia – insufficient oxygen can be due to lowered Hb,
respiration effects, respiratory poisons Cellular responses
Decrease in ATP, causing failure of sodium-potassium pump and sodium-calcium exchange
Cellular swelling
Reperfusion injury
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Cellular Injury Mechanisms Free radicals and reactive oxygen species
Electrically uncharged atom or group of atoms having an unpaired electron
Lipid peroxidation Alteration of proteins Alteration of DNA Mechanisms for the inactivation of free radicals
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Cellular Injury Mechanisms Chemical injury
Lead – CNS toxin – interferes with neurotransmitters causing hyperactivity. Lead paints and children – anemia & lead toxicity
Carbon monoxide – binds irreversibly to Hb Ethanol – cellular toxin kills cells – liver toxin-
interrupts protein transport – pickles cells can cause fetal alcohol syndrome
Mercury – neurotoxin can cause bone deformities Social or street drugs
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Unintentional and Intentional Injuries Blunt force injuries
Application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues
Contusion vs. hematoma – bleeding in skin & underlying layers
Abrasion – removal of superficial skin layers Laceration rip, year or puncture of skin & layers Fractures – broken bones
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Unintentional and Intentional Injuries Sharp force injuries
Incised wounds Stab wounds Puncture wounds Chopping wounds
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Unintentional and Intentional Injuries Gunshot wounds
Entrance wounds Contact range entrance wound Intermediate range entrance wound
Tattooing and stippling
Indeterminate range entrance wound
Exit wounds Shored exit wound
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Unintentional and Intentional Injuries Asphyxial injuries
Caused by a failure of cells to receive or use oxygen
Suffocation Strangulation
Hanging, ligature, and manual strangulation
Chemical asphyxiants- carbon monoxide, cyanide
Drowning
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Infectious Injury Pathogenicity of a microorganism – gram neg or
positive will determine which antibiotics will work best – anti viral agents for viral infections
Virulence of a microorganism – some strains are more dangerous than others
Disease-producing potential Invasion and destruction Toxin production Production of hypersensitivity reactions
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Immunologic and Inflammatory Injury Phagocytic cells – immune cells that engulf and
destroy invading microbes and toxins Immune and inflammatory substances
Histamine (chemical released by injured or infected cells that cause local vasodilation), antibodies (endogenous proteins that combat and identify invading cells and toxins), lymphokines (chemical produced by imune cells), complement, and enzymes
Membrane alterations – leakage of cell contents due to the presence of antibodies and histamines
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Injurious Genetic Factors Nuclear alterations – mutations and damage
to DNA Alterations in the plasma membrane structure,
shape, receptors, or transport mechanisms Examples of genetic diseases
Sickle cell anemia (substitution of one amino acid in Hb structure) and muscular dystrophy (muscle tissue does not function properly
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Injurious Nutritional Imbalances Essential nutrients are required for cells to
function normally inadequate proteins, carbohydrates, fats, vitamins, minerals
Deficient intake – starvation and improper diets – protein deficiency “kwashiokor” most common, Vitamin B 12 deficiency leads to pernicious anemia
Excessive intake - obesity
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Temperature Extremes Hypothermic injury
Slows cellular metabolic processes Ice crystal formation and frostbite
Hyperthermic injury Heat cramps Heat exhaustion Heatstroke Protein denaturation
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Atmospheric Pressure Changes Sudden increases or decreases in atmospheric
pressure Blast injury Nitrogen Narcosis or rapture of the deep
Nitrogen gas has a narcotic effect (laughing gas) Decompression sickness or caisson disease
“The bends”
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Ionizing Radiation Any form of radiation capable of removing
orbital electrons from atoms X-rays, gamma rays, alpha and beta particles Amount of exposure measured in RADS.
People who work with X-rays must wear badge that measures dosees of exposure over time
Mechanism of damage – ionization of chemicals and breakage of chemical bonds
Effects of ionizing radiation
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Cellular Injury Illumination injury
Eyestrain, obscured vision, and cataract formation Caused by light modulation
Mechanical stresses Physical impact or irritation
Noise – sound can cause tisse and organ trauma Acoustic trauma and noise-induced hearing loss –
tinnitus very common among performing rock band members
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Manifestations of Cellular Injury Cellular accumulations (infiltrations)
Water Lipids and carbohydrates Glycogen Proteins
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Manifestations of Cellular Injury Cellular accumulations (infiltrations)
Pigments Melanin, hemoproteins, bilirubin (aging brown spots)
Calcium – can cause hardening of cells and altered membrane permeability
Urate example is gout where urate crystals form in joints and is very painful
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Cellular Death Necrosis – local cell death by autodigestion
Sum of cellular changes after local cell death and the process of cellular autodigestion
Processes Karyolysis
Nuclear dissolution and chromatin lysis
Pyknosis Shrinking & Clumping of the nucleus
Karyorrhexis Fragmentation of the nucleus
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Necrosis Coagulative necrosis
Primarily found in Kidneys, heart, and adrenal glands
Protein denaturation and increased intracellular level of Ca
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Necrosis Liquefactive necrosis – common after
ischemic events in CNS (stroke) Neurons and glial cells of the brain die and are
rich in digestive enzymes Hydrolytic enzymes causes brain tissues to
become soft and liquefy – sometimes walled off and form cysts
These types of cysts also form after bacterial infection due to actions of phagocytic neutrophils and fluid in cyst is called pus.
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Necrosis Caseous necrosis
Found in Tuberculous pulmonary infection Combination of coagulative and liquefactive
necrosis Necrotic debris not completely digested thus
tissues appear granular like clumped cheese
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Necrosis Fat necrosis
Common in Breast, pancreas, and other abdominal organs – breakdown of fats create soaps and referred to as saponification and tissue is opaque or white chalky
Action of lipases – break down fats to FA and glycerols
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Necrosis Gangrenous necrosis
Clinical term Dry vs. wet gangrene Gas gangrene
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Apoptosis a type of cell death different from Necrosis in that it is active self destruction of normal and pathologic tissue Programmed cellular death- found mostly to
occur during development of embryo Mechanisms- specific signaling chemicals
send message to cells programmed to die Necrosis vs. apoptosis- while necrosis usually
effects all cells in an area apoptosis effects scattered cells killing the cells shrink quickly and disappear neatly while necrotic cells swell and lyse
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Aging and Altered Cellular and Tissue Biology Aging vs. disease tissues all have accumulaion of
toxic chemicals and mutation damage over time. Disease can damage and destroys cells quickly due to some pathogenic cause
Normal life span - brain cells live as long as you do and the neurons in CNS once formed by age 6 do not divide. RBC live only 120 days
Gender differences - women live longer than men 78 vs 81 years may be due to genetic superiority
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Theories of Aging Accumulation of injurious events – the more exposure to
dangerous chemicals and pathogens the faster you age Genetically controlled program – some of us are destined to
live longer due to the genetic program in our cells Theories
Genetic and environmental lifestyle factors Alterations of cellular control mechanisms decreased protein
synthesis as you age Degenerative extracellular changes – nutrients and free radicals
important
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Aging Cellular aging all cells can replicate 40 – 60
times max and may be why clones do not live as long as parents
Tissue and systemic aging immune function goes down with age and free radicals damage cells speeding aging Frailty – wastin syndrome of aging due to
decreased protein synthesis and reduced muscle mass and lowered bone density
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Somatic Death Death of an entire person Somatic death with no
respiration or circulation Postmortem changes
Algor mortis drop in body temp such that in 24 hrs same as room temp
Livor mortis blood settles on lowest tissues due to gravity causing discoloration
Rigor mortis – 6 – 12 hours post somatic death stiffening of body due to muscle protein breakdown
Postmortem autolysis bloating and swelling of body due to autolysis