Download - 3-Causes of Disease-2.pptx
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Causes of Disease
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Review Adaptation Ways to adapt to injury: Atrophy Hypertrophy Hyperplasia
All of these will have consequences for the tissue, organ, and system.
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Hyperplasia Compensatory Hormones Pathologic Atypical
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Compensatory Can’t keep up so increase in cell number (Remember adaptation to injury!) Liver damaged by byproducts of alcohol
metabolism or infection with hepatitis virus
Cells are produced. Liver cells can divide. Some are bi-nucleated.
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Hormonal Stimulation Number of cells increase. Cells of follicle in ovary increase in
response to FSH Endometrium of uterus proliferates in
response to estrogen
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Pathological Hyperplasia Abnormal proliferation of normal cells Tissues in organs as well as organs have
characteristic size For example, no 50 lb. kidneys Physiological mechanisms exist to
regulate size When mechanisms fail, proliferation
occurs
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Abnormal Proliferation Hemangioma Proliferation of capillaries, results in
blood red birth mark Cells are relatively normal
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Hemangioma Too much of a good thing. Lots of blood
close to the surface.
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Atypical Hyperplasia Dysplasia is also used Cells are of abnormal size, shape and/or
organization Mature cells Not adaptation Common in cervix, respiratory tract
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Dysplasia
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Will These Cells Become Cancer??? Experts disagree Abnormal, but not cancer Different degrees of abnormality Can stage them Doesn’t necessarily mean progression
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Metaplasia Meta means change (metamorphosis) Reversible change or replacement of
one normal tissue type with another normal tissue type
Classic example respiratory epithelium can change from ciliated pseudostratified columnar epithelium to stratified squamous epithelium
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Metaplasia
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Metaplasia in Esophagus
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Metaplasia in Respiratory Tract Response to irritation, smoke Can come from cigarettes, cigars, or
industrial smoke Protective mechanism to protect against
irritant
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Relationship Between Cellular Changes and Neoplasia
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Picture of the Smoker Coughs and gurgles in the morning Ciliated epithelium hard at work moving
mucus up to the mouth all day and night Smoker, no elevator for mucus Most noticeable in the morning 2-3 weeks of not smoking, cough goes
away Epithelium reverts to classic respiratory
epithelium
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Smoker and Metaplasia
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Anaplasia Anaplasia-cells lose the morphological
characteristics of mature cells and their orientation with respect to each other and to endothelial cells
Actual dedifferentiation Feature of malignancy
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Normal Versus Abnormal
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Cellular Changes
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Cellular Injury Result of cell’s inability to maintain
balance with environment Injurious agent induces adaptation
mechanisms Adaptation fails Cell can’t carry out biochemical
processes Cellular injury results
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Hypoxic Injury Lack of oxygen and nutrients Oxidation reaction fail Energy production reduced or stops Important processes requiring energy
stop or are reduced Ion pumping, e.g. Osmotic gradient results, cell swell
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Hypoxia Atherosclerosis in femoral artery Cells try to adapt: Atrophy Skin thins Leg hair disappears Cells swell (not edema)
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Swollen Cells Chemical reaction occur as reactants
bump up against each other Cell swell, distance between reactants
increases, reactions slow down Cell function disturbed
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Injurious Agents Chemicals that are toxins or poison Chemical that fits into a reaction
scheme of the cell and blocks reaction Thousands of enzymes that control
reactions Bring reactants together
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Enzyme with Pocket
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Anabolic Reactions Two reactants bind to enzyme, enzyme
changes shape Bond is formed Product formed
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Catabolic Reactions Sucrose binds Enzyme changes shape Bond broken Fructose and glucose are formed
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Enzyme Function
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Cyanide as a Poison Blocks energy producing reactions
(binds to cytochrome c oxidase) Cell gone in seconds Shuts down mitochondria Instantaneous Cyanide hits acid of stomach, forms
cyanide gas
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Infectious Agent Lots of bacteria live in harmony with us
and in us Problem: Some injurious Some cause direct destruction
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Tetanus Fecal material of animal containing
tetanus bacteria contaminate object Object penetrates skin, contaminates
individual Bacteria grow and release toxin Toxin latches onto Acetylcholine
receptor Causes tetanic contraction Eventually locks up respiratory muscles
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Consequences Carbon dioxide builds up Acidic conditions shut down cells
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Excessive Defense Reaction Tuberculosis Bacteria invade, macrophages engulf,
bacteria replicate within endosomes Lymphocytes, macrophages, and
fibrocytes wall off creating granuloma Classified as an granulomatous
inflammatory disease Tissue destroyed, scars form
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Overactive Defense Immune response to an injurious agent Allergies
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Nutritional Imbalance Abnormal mix of amino acids Enzymes not normal or structure not
normal Interferes with function Cell biochemistry abnormal
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Physical Agents Heat, cold Temperature extremes Very hot surface causes damage Coagulation of proteins (think of a hard-
boiled egg)
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Hyperthermia Temperature increases Feel cold as set-point for temperature
regulation in hypothalamus is reset Shivering thermogenesis increases heat
production Look pale, blood vessels constrict Dry skin, no sweat Temp rises to set-point
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Hyperthermia As temp increases, we feel unable to
think clearly Cells malfunction at 101 or 102 At 105, death ensues The obvious signs we observe are those
of the nervous system All other organs and tissues also
malfunction
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Consequences First temperature increase rate of chemical
reactions Speed up molecules, probability of reaction
increases Problem, not all reactions (enzymes) respond
in the same way to a given change in temperature
One part increases more than another, imbalance
Enzymes have an optimal pH and temperature
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Summary The mechanism of injury induces
responses which are aimed to allow adaptation
Failure to adapt results in death
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Physical Agents Continued Atmospheric pressure Rapid extreme changes Explosion: Expansion, compresses air Wave of pressure travels out from site First wave of high pressure followed by
low pressure First a push in then a pull out
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Example of Ear Damage The tympanic membrane responds to
wave effects, moves violently, tears Explosion can tear skin by same
movement Rest of the body is full of water-can’t
compress
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Biggest Problem Airways and lungs full of air Rapidly expand then compress Tears tissue Bleeding occurs Respiratory system fills with blood and
can suffocate
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Example of Pressure Damage Bats near wind turbines die Blades on windmills huge, calculated at
tip as moving at 100’s of miles/hr Cut through air causing compression
and expansion or an extreme pressure gradient
Bats have more delicate alveoli than other birds, severely effected by pressure
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Mechanism of BendsDecompression Sickness Atmospheric pressure increases as we
descend in the ocean Squeezes gas into body fluids Ascend slowly, respiratory compensates
by removing gas as blood goes through respiratory system
Move up fast bubbles form in tissue, tears tissue
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Additional Damage Bubbles in blood block small vessels
causing disturbance in blood flow CNS effect first, confusion, see colors Called nitrogen narcosis
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Example Astronaut moves out of capsule Unpressurized area Must wear pressurized suit or will be
ripped to shreds
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Hyperbaric Chamber Create high pressure Squeeze oxygen into tissues Can kill bacteria like tetanus or gas
gangrene Obligate anaerobes Lack superoxide dismutase Can’t survive oxygen-rich environment
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Ionizing Radiation X-Ray hits molecule, electron bounces
off, creates “free radical” Highly reactive Reacts with another molecule Could bind to an enzyme, inactivate
enzyme Generally not a problem as is on small
scale
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Free Radicals and DNA Free radical joins with DNA DNA contains information about enzyme
and other protein construction Instruction destroyed, cell dies Only one cell not a big problem
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Serious Problem Free radical joins DNA in a way that
leads to uncontrolled division Locks on DNA causing tumor formation Excessive radiation: Nuclear accident-develop cancer
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Which Tissues Effected by Radiation? Skin Bone marrow Epithelia Fetus Primarily male gonads All have rapid division
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Mechanism Resting cell, DNA tightly coiled around
histone proteins Protected against free radicals Replication- uncoiled DNA, expose
nucleotides Free radicals join with part of DNA and
upset control mechanisms Uncontrolled proliferation, tumor
formation
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Results of Cellular Injury Accumulations: Water: Cell injury Energy production
Pumping ion accumulation osmotic pressure swelling reaction rates change
Reactants far apart- imbalance in chemistry of cell
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Hydropic Degeneration Irregular round inclusions Distended organelles: MTC, ER Called vacuoles Path report: hydropic degeneration Due to accumulation of water Reversible change
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Lipid Accumulations Injurious agent causes abnormal
biochemistry Accumulate fat molecules Lipid in water illustrates the condition Lipid comes together and avoids water Obesity, diabetes and alcoholism most
common cause
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Starvation Unable to burn fat Inadequate nutrition, lack of enzymes
due to inability to make protein Can mobilize fat from storage but sits in
liver due to inability to metabolize Liver enlarges
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Genetic Diseases Inherited diseases of metabolism For example: glycogen, galactose,
tyrosine or homocysteine Inborn errors of urea cycle enzymes or
involving mitochondria in FFA oxidation
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Toxic Compounds Alcoholism leads to fatty liver disease Carbon tetrachloride and other organic
solvents can lead to fatty liver Tetracycline, valproic acid, and
salicylate Corticosteroids Can cause microvesicular fatty liver
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Calcium Accumulations Calcium accumulates in cell after injury Due to damaged calcium pump Calcium percipitates and forms crystals
in tissue
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Dystrophic Calcification See in dead or dying tissues Severely damaged cells in
atherosclerosis Smooth muscle cells in arterial wall are
damaged and develop an atheroma which then calcifies
Blood vessel gets stiff and hard Epthelium degenerates, gets rough and
forms clots
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Metastatic Calcification Occurs in many parts of the body Due to hypercalcemia ECF Ca++ concentration is close to
percipitation Change conditions, percipitation occurs Basic or alkaline percipitate For example in bone, normally
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Calcification Change in blood vessel wall, percipitate Opposite is true: change conditions,
decalcification Example: Tumor in marrow cavity,
demineralization, bone can break Can be first sign of disease
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Hyaline Change Accumulation of glassy translucent
crystals Denatured protein Can occur in abnormal condition:
Immune reaction, clumps of antigen-antibody complex
Indicates cell injury
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Cell Death Necrosis is localized cell death while
majority of the animal is alive Visible change Heart attack-can see area of necrotic
tissue
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Autolysis Self-digestion Lysosomes digest tissue Happens immediately, within seconds Study fixed tissue with light microscope,
all appears well Study und electron microscope see
damage Takes too long for fixative to prevent
damage
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Immune Reactions Attack on dead cells Removed by macrophages Pathologist sees pyknotic nuclei Clumped nuclear material Karyolysis then occurs where
membranes degenrate Organelles disappear
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Gross Necrosis What you can see with the naked eye Coagulative Proteins degenerateclumpmaintain
architecture of tissue Heart attack, part of heart wall dies Looks like heart wall Maybe different color, swollen, hard
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Coagulative Necrosis
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Gross Necrosis Occurs in specific tissues due tissue
type, cause of death, and environment conditions
Macrophages invade, inflammation develops
Replaced by scar tissue, gel and fibers
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Liquefactive Necrosis Hydrolytic enzymes dissolve tissue Form pocket of liquid (cyst) Surrounded by healthy tissue or capsule Occurs in brain
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Liquefactive Necrosis No connective tissue in brain Cut off blood supply, no connective
tissue to maintain structure Forms fluid-filled pocket Glial cells move in and form scar
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Liquefactive Necrosis
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Caseous Necrosis Cottage-cheese like Between the two-types Some coagulation, some liquefaction Lumps of tissue with liquid around them Often associated with infections caused
by myobacterium tuberculosis
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Caseous Necrosis
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Fat Necrosis Open up abdomen, white flaky stuff Dry white crystals Caused by leakage of pancreatic
enzymes Lipase breaks down fat FFA combine with sodium and form soap
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Fat Necrosis in Pancreatitis
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Summary Cells are injured Try to adapt May die These mechanisms are common to the
disease process