Cellular Biology

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Altered Cellular and
Tissue Biology
Chapter 2
1
Cellular Adaptation
Physiologic vs. pathogenic
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
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Cellular Adaptation
3
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Cellular Adaptation
4
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Cellular Injury
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Reversible
Irreversible
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Cellular Injury Mechanisms
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Hypoxic injury
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Ischemia – cut off of blood flow circulation
Anoxia – insufficient oxygen can be due to lowered Hb,
respiration effects, respiratory poisons
Cellular responses
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Decrease in ATP, causing failure of sodium-potassium pump and
sodium-calcium exchange
Cellular swelling
Reperfusion injury
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Cellular Injury Mechanisms
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Free radicals and reactive oxygen species
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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
7
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Cellular Injury Mechanisms
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Chemical injury
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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 toxininterrupts 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
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Blunt force injuries
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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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Contusions and Hematomas
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Unintentional and Intentional
Injuries
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Sharp force injuries
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Incised wounds
Stab wounds
Puncture wounds
Chopping wounds
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Unintentional and Intentional
Injuries
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Unintentional and Intentional
Injuries
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Gunshot wounds
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Entrance wounds
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Contact range entrance wound
Intermediate range entrance wound
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Tattooing and stippling
Indeterminate range entrance wound
Exit wounds
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Shored exit wound
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Gunshot Wounds
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Unintentional and Intentional
Injuries
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Asphyxial injuries
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Caused by a failure of cells to receive or use
oxygen
Suffocation
Strangulation
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Hanging, ligature, and manual strangulation
Chemical asphyxiants- carbon monoxide,
cyanide
Drowning
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Infectious Injury
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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
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Invasion and destruction
Toxin production
Production of hypersensitivity reactions
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Immunologic and Inflammatory
Injury
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Phagocytic cells – immune cells that engulf and
destroy invading microbes and toxins
Immune and inflammatory substances
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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
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Nuclear alterations – mutations and damage to
DNA
Alterations in the plasma membrane structure,
shape, receptors, or transport mechanisms
Examples of genetic diseases
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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
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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
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Hypothermic injury
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Slows cellular metabolic processes
Ice crystal formation and frostbite
Hyperthermic injury
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Heat cramps
Heat exhaustion
Heatstroke
Protein denaturation
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Atmospheric Pressure Changes
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Sudden increases or decreases in atmospheric
pressure
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Blast injury
Nitrogen Narcosis or rapture of the deep
Nitrogen gas has a narcotic effect (laughing gas)
Decompression sickness or caisson disease
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“The bends”
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Ionizing Radiation
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Any form of radiation capable of removing
orbital electrons from atoms
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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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Ionizing Radiation
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Cellular Injury
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Illumination injury
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Mechanical stresses
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Eyestrain, obscured vision, and cataract formation
Caused by light modulation
Physical impact or irritation
Noise – sound can cause tisse and organ trauma
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Acoustic trauma and noise-induced hearing loss –
tinnitus very common among performing rock band
members
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Manifestations of Cellular Injury
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Cellular accumulations (infiltrations)
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Water
Lipids and carbohydrates
Glycogen
Proteins
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Hydropic Degeneration
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Manifestations of Cellular Injury
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Cellular accumulations (infiltrations)
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Pigments
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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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Calcium Infiltration
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Cellular Death
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Necrosis – local cell death by autodigestion
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Sum of cellular changes after local cell death and the
process of cellular autodigestion
Processes
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Karyolysis
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Pyknosis
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Nuclear dissolution and chromatin lysis
Shrinking & Clumping of the nucleus
Karyorrhexis
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Fragmentation of the nucleus
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Cellular Death
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Necrosis
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Coagulative necrosis
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Primarily found in Kidneys, heart, and adrenal
glands
Protein denaturation and increased intracellular
level of Ca
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Coagulative Necrosis
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Necrosis
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Liquefactive necrosis – common after
ischemic events in CNS (stroke)
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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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Liquefactive Necrosis
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Necrosis
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Caseous necrosis
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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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Caseous Necrosis
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Necrosis
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Fat necrosis
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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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Fat Necrosis
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Necrosis

Gangrenous necrosis
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Clinical term
Dry vs. wet gangrene
Gas gangrene
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Gangrenous Necrosis
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from Necrosis in that it is active self
destruction of normal and pathologic
tissue
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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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Apoptosis
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Aging and Altered Cellular
and Tissue Biology
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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
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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
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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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Theories of Aging
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Aging
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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
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Frailty – wastin syndrome of aging due to
decreased protein synthesis and reduced muscle
mass and lowered bone density
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Somatic Death
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Death of an entire person Somatic death with no
respiration or circulation
Postmortem changes
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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
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