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170 Cards in this Set
- Front
- Back
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What is pathophysiology?
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Study of abnormal functioning of diseased organs with application to diagnostic procedures and patient care
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How does structure dictate function?
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Diseased function can lead to abnormal structure
ex. myocardial hypertrophy from hypertension |
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What is homeostasis and what are the two things it depends on?
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Homeostasis is having the systems of the body in equilibrium.
It depends on: 1) Health of physiological systems 2) Nature of stress imposed |
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What is health?
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Homeostatic balance; when our physical and mental capabilities can be fully utilized
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Disease
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disruption in homeostasis - unhealthy state of body part, system, or body as a whole
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Etiology
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cause of the disease
ex. bacteria causing strep throat. bacteria is the etiological agent |
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What are the 3 categories of etiology?
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Genetic
Congenital Acquired |
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Genetic Etiology
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Defective genes are responsible for structural/functional defect.
Are passed on the future generations Ex. Cystic fibrosis, sickle cell anemia, PKU, hemophelia |
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Congenital Etiology
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Genetic info is intact, error in prenatal development
Ex. Fetal Alcohol Syndrome, Atrial Sepial Defect, Cleft Palate, Spinal Bifida |
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Acquired Etiology
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Genes and prenatal are both ok, but factors encountered later in life produce the disease
Ex. TB, emphysema, hepatitis, osteoporosis, CAD |
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What is it called if the cause of a disease is unknown?
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Idiopathic
Ex. Alzhemiers, MS, Cancer, etc. |
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What is Medical History and what 4 things does it include?
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taken by medical practitioner before actual physical examination. Description of nature and timing of patients abnormalities
Includes: Signs, Symptoms, Findings, Syndrome |
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What are symptoms?
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Patient may DESCRIBE sensation of pain or malaise, generalized feeling of illness or loss of well being.
Ex. PAIN, pruitis (itching), vertigo, anxiety, fatigue, headache Can't measure; subjective |
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What are signs?
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Detected by the observer, signs emerge during physical examination.
Ex. Elevated blood pressure, irregular heart beat, lesions, excessive sweating (diaphoresis), cyanosis (blue), pallor (pale), fever CAN measure; objective |
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What are findings?
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Results from lab tests, CT imaging, or exploratory surgery that clarify clinical picture.
CAN measure, objective |
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What is a syndrome?
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Combination of signs and symptoms associated with a specific disease.
Ex. Downs Syndrome = characteristic set of symptoms |
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What is pathogenesis?
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Pattern of disease development
(development and progression) Can be ACUTE or CHRONIC |
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What is ACUTE pathogenesis?
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Rapid onset, quickly develops, and usually are short duration.
Ex. viral infection, flu, trauma |
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What is CHRONIC pathogenesis?
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Usually longer duration. Onset can be sudden or insidious (small changes that build on each other)
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What are chronic diseases characterized by?
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Remission: Signs and Symptoms SUBSIDE
Exacerbation: Signs and Symptoms RETURN |
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What is a sequela?
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A condition resulting from disease. Like the aftermath of a disease.
Thickening of artery walls is a sequela of high blood pressure |
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What is a lesion?
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Somatic distribution of damage sites.
Four types: Local & Systemic, Focal & Diffuse |
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What is a local lesion?
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Damage is confined to one region of the body.
Ex. Nerve damage in forearm |
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What is a systemic lesion?
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Lesions are more widely distributed
Ex. Metastazied cancer |
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What is a focal lesion?
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WITHIN diseased organ; damage is confined to one or more distinct sites.
Ex. bronchopulmonary segments of the lungs |
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What is a diffuse lesion?
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If lesions are more uniformly distributed in diseased organ
Ex. entire lung full of cancer |
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Which lesions affect the body as a whole and which are only damage within an organ?
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Local and System: Affect the body as a whole
Focal and Diffuse: Affect an organ |
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What is diagnosis?
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Analysis of signs and symptoms, coupled with knowledge of pathogenesis leads to (diagnosis) IDENTIFICATION of patient's disease
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What is therapy?
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Once diagnosis is established (therapy) TREATMENT of the disease with aim of cure or reducing signs and symptoms to level where near normal functional capacity can be restored
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What is palliative therapy?
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Can't offer cure, but can alleviate pain and suffering
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What is prognosis?
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Assesment of body's response to therapy, knowledge of pathogenesis, and clinical experience all combine for a PREDICTION of patients outcome.
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What are the three causes of cell injury?
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Defciency
Intoxication Trauma |
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Cell Injury - Deficiency
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Lack of substance necessary to cell.
Ischemia, Hypoxia, Nutrional, Infection |
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Ischemia
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A decrease in blood supply due to either OCCLUSION or PUMP FAILURE
Ischemia can lead to hypoxia |
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Hypoxia
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Inadequate oxygenation due to failure of:
Respiratory Cardiovascular System Red Blood Cells |
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How does hypoxia cause cell injury?
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The decreased blood supply leads to decreased aerobic metabolism. This leads to anaerobic metabolism, which increases lactic acid, decreases pH, and causes lysosomal liberation and cell lyse.
Decreased aerobic metabolism also leads to decreases ATP production, which causes the Na/K pump to fail and Na+ to build up in the cell. This causes water to build up inside, and the cells to lyse (burst) |
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Which tissues are most intolerant to hypoxia?
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Nervous tissue (Necrosis after 3 minutes)
Cardiac tissue Kidneys (60-90 minutes) Have high ATP demands so they're quickly affected |
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What causes a nutritional deficiency?
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Lack in diet. Can be primary or secondary.
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What are primary and secondary nutritional deficiencies?
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Primary: Lack in diet; aren't taking it in
Secondary: Taking it in, but body isn't using it |
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Infection caused defciency
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Microorganisms also consume substances essential for normal cell metabolism
- Virus, protozoa, fungi |
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Intoxication
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Presence of substance that interferes with cell function; poisoning
Caused by toxins |
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What are toxins?
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Injurious substances that interfer with normal function.
Two major origins: Exogenous and Endogenous |
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Exogenous Toxins
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Originate outside the cell
can be BIOLOGICAL or NON-BIOLOGICAL |
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Biological Exogenous Toxins
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Produced from microorganisms and can enter cell through infection.
Ex. Bacteria, protozoa, fungi |
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Non-biological Exogenous Toxins
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Injurious chemicals that orginate outside the body.
Ex. Drug overdose, alcohol, lead, CCL4 |
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Endogenous Toxins
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Originate inside the cell.
Can be caused by: genetic defect free radicals impaired circulation ischemia |
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Endogenous Toxin - Genetic Defect
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Produces toxin
Ex. Huntington's disease, toxic substance causes neurological dysfunction. Cystic Fibrosis, PKU |
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Endogenous Toxin - Free Radicals
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Produced by normal cellular processes.
Accumulation can damage DNA, cell membrane, and enzymes |
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Endogenous Toxin - Impaired circulation ischemia
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Allows metabolic byproducts to accumulate to toxic levels
Ex. CO2 and H+ |
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Trauma
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Loss of cell's structural integrity; physical injury
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Types of trauma
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Hyperthermia
Hypothermia Ionizing Radiation Mechanical Pressure Infections |
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Hypothermia
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Due to extreme cold. Ice crystal formation in cytoplasm's water injures cell.
Cells expand and burst Below 95 degrees, abrupt vasoconstriction and cells die Ex. Frostbite |
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Hyperthermia
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Extreme heat damages cells by disrupting and coagulating (denaturing) proteins.
Ex. Burns. Source of heat can be direct contact with source, solar radiation, or electric current. 106 degrees or above |
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Ionizing Radiation
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Can produce toxic chemical fragments called free radicals. Free radicals interrupt normal cellular function and damage proteins, especially DNA, causing problems with cell mitosis and meiosis.
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Mechanical Pressure
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Forces cell membrane to explode or degenerate
Ex. car accident, impact, noise, brain tumor Tumor - causes adjacent cells to die because of pressure |
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Infections
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Microogranisms infect cells or damage cell membrane and lead to immune attack
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Cellular adaption can be broken down into 3 categories:
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1. Altered size or number
2. Altered functional capacity 3. Intracellular Accumulation |
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Altered Size or Number
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Can be hypertrophy, atrophy, hyperplasia, metaplasia, or dysplasia
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Hypertrophy
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Process of cell and organ enlargement do to increased demands.
Ex. Myocardial cells enlarge due to valvular stenosis Normal: From training Pathological: Heart Compensatory: Losing one kidney, other ones gets bigger |
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Atrophy
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Decrease in cell size from disuse or lack of stimulation
Ex. Dementia = atrophy of brain, Bedridden patients lost muscle mass |
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Hyperplasia
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Process of producing new cells by mitosis in response to increased demand
Ex. Cells duplicate |
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Metaplasia
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CHANGE from one cell type to another
A response to chronic irritation or inflammation Ex. In smokers psuedostratified to stratified in trachea |
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Dysplasia
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Disordered growth
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Altered Functional Capabilites
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Alternative Metabolism
Organelle Changes |
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Alternative Metabolism
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In hypoxia, body switches from oxidative phosphorylation to glycolysis. The end result is lactic acid production.
Disruption of glucose switches to fat and/or protein. Ex. in starvation or eating disorders, diabetes |
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Organelle Changes
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Altering the complement of organelles to better meet a demand
Ex. Liver responds to increase levels of toxic chemicals by increasing the amount of smooth ER Ex. Increased levels of mitochondria with increased energy levels |
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Intracellular Accumulation
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Build up of substances that cells do not dispose of. Gives pathological idea about the history of damage.
RESIDUAL BODIES - indicates cells ability to cope with threatening bacteria or deal with damaged organelles Derived from phagosomes Ex. LIPOFUSCION GRANULES are the wear and tear pigment |
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Reversible Cell Injury
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1. Hydrophic Change
2. Fatty Change |
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Hydrophic Change
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- Damage reduces ATP production
- Ion pump fails to remove NA+ - Increases osmotic pressure - Water enters the cell and goes into vacuoles - If enough water enters the CELL SWELLS and cytoplams gets PALE AKA: Cloudy Swelling or Hydrophic Degeneration |
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Fatty Change
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Cell injury causes fat to accumulate. This causes cells to get bigger, which makes organ get big.
Eventually cell ruptures and fat is deposited inside organ Ex. Liver (primary fat deposit) |
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Irreversible Cell Death
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Best indicator of irreversible injury is an ALTERED NUCLEUS
1. Pyknosis: shrink and condense; clumps 2. Karyorrhexis: breaks up into small dispersed fragments 3. Karyolysis: following cell death, nucleus seems to fade and melt into cytoplasm; ghost cell |
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Two Patterns of Cell Death
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1. Apoptosis (Programmed Cell Death)
2. Necrosis |
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Apoptosis
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Cell suicide, or controlled cell death.
Can be NORMAL or PATHOLOGICAL Eliminates cells that are worn out, overproduced, or genetically damaged Genes are activated in the nuclues that tell it to kill itself |
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Necrosis
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Characterized by cell membrane breakdown and tissue death
Always pathological and unregulated After lethal injury: lysosomes release enzymes to speed breakdown and removal of nonfunctional tissue from the scene (spills it on neighboring cells) |
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Coagulation Necrosis
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Retains outlines of cells (seen after hypoxic death)
Firm and relatively intact region of necrosis with relatively normal architecture Most common Ex. Heart Attack |
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Liquefaction Necrosis
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When phagocytes secret enzymes that liquefy tissue, seen often in the brain post anoxia where extracelllular proteins like collagen are lacking
-Phagocytic enzymes digest area and form a cavity -Liquid region of dead cells, tissue fluid, and phagocytes Ex. stroke, brain, spinal cord |
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Caseous Necrosis
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Form of coagulation necrosis often in TUBERCULOSIS
Pale yellow, granular, cheese-like appearance |
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Gangrenous Necrosis
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Complication of necrosis characterized by decay. Especially problematic in the extremities when blood flow is compromised
1. Dry Gangrene 2. Wet Gangrene 3. Gas Gangrene |
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Dry Gangrene
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Extremity becomes dry, and shrinks sustained coagulation - slower spread
Ex. mummified, like frost bite |
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Wet Gangrene
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Body part is cold, swollen, and pulseless
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Gas Gangrene
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infection of the necrotic area with clostridium perfringens
produces foul smelling gas |
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Calcification
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calcium deposition usually occurs with necrosis
1. Dystrophia 2. Metastatic |
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Dystrophic Calcification
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Slow, gradual accumulation of Ca++ leads to rigidity and brittleness in necrotic tissue
Ex. Calcified arteries (hardened arteries) |
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Metastatic Calcification
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Occurs in normal tissue due to hypergcalcemia, high systemic levels of Ca++
Ex. too much calcium in the blood to it deposits in lungs and kidneys Ex. hyperactivity of parathyroid glands secretes too much PTH which liberates Ca++ from bone |
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How do we determine which of the many body cells have been injured and to what extent?
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1. Assesment of functional loss
2. Detection of cell constituents 3. Monitoring of electrical activity |
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Assessment of Functional Loss
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- Functional deterioration of internal organs can be assessed by measuring subtle changes in body fluids
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Detection of Cell Constituents Released from Injured Cell
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- Injured cells may leak substances at faster rate, so high plasma levels may indicate cell injury
- Elevated K+ indicated hemolysis, indicating large-scale cell damage - High levels of creatine phosphate (CPK) indicates skeletal, cardiac, or brain tissue |
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Monitoring of Electrical Activity
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- Electrocardiogram (ECG) for heart
- Electroencephalogram (EEG) for brain - Electromyogram (EMG) for muscle |
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Albumins
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maintain osmotic pressure in blood
produced by the liver |
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Blood Hydrostatic Pressure
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pressure of blood/water
PUSHING POWER Higher near arterial side, so pushes fluid out. The fluid formed is called tissue fluid / interstitial fluid |
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Tissue Osmotic Pressure
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PULLING POWER
outside of vessel is higher, so water moves out |
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Tissue Hydrostatic Pressure
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PULLING POWER
pressure outside of vessel in venous end is higher due to fluid being driven into confined spaces |
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Blood Osmotic Pressure
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PULLING POWER
[plasma proteins] Higher near vein end so water is attracted to blood. Water moves back in at benous side due to higher osmotic pressure with the capillary Most water returns via osmosis |
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Excess interstitial fluid is collected by?
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The lymphatic system
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Extra interstitial fluid causes?
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Edema (swelling)
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Inflammation definition
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protective tissue response to injury or invasion
- "itis" arthritis, tonsilitis, pericarditis Bridge between INJURY and HEALING |
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What can cause inflammation?
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1. Deficiency
2. Intoxication 3. Trauma (same causes of cell injury) |
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The inflammation response
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- Injury causes damage to mast cells, which releases histamine
- Histamine causes two things: vasodilation and increased capillary permeability - VASODILATION causes increase in blood hydrostatic pressure and exudate - INCREASED CAPILLARY PERMEABILITY: albumins leak into tissue and cause an increase in tissue osmotic pressure, which causes exudate |
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What are the cardinal signs of inflammation?
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1. Redness (dilation of vessels, increased blood flow)
2. Heat (increased blood flow) 3. Pain (changes in pH, swelling of inflamed tissues, release of histamine and other chemicals) 4. Swelling (movement of fluid and cells from the blood into the interstitial spaces) 5. Loss of function |
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Function of the Inflammatory Response
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1. Neutralize and/or destroy the noxious agent
2. Limit damage to surrounding tissues 3. Removal of necrotic tissue 4. Aid in healing process |
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VASCULAR RESPONSE
of inflammation (Hemodynamic Response) |
- Triggered by chemical mediators
- HISTAMINE - Causes VASODILATION of arterioles and venules - SWELLING occurs due to increased permeability of capillaries and venules due to increased space between endothelial cells - This exudate helps to dilute the toxic or irritating agent - The fluid out of capillaries causes stagnation of fluid and clotting, therefore the problem becomes localized |
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CELLULAR RESPONSE
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- Movement of leukocytes (WBCs) to the injured arease
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Axial blood flow
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normal pattern of blood flow
elements cluster along long axis of vessel; plasma surrounds column |
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MARGINATION
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As fluid leaves circulation, the viscosity of the blood increases and the WBCs move to the periphery of the blood vessel
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PAVEMENTING
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WBCs adhere to the endothelium walls
flatten out against the wall CAMS - loops and hooks latch on to the wall like velcro |
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EMIGRATION
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through DIAPEDESIS, the leukocytes squeeze between endothelial cells and into the tissues
Release enzymes that digest the vessel wall |
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CHEMOTAXIS
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migration in response to chemical signals
when attracted by chemical mediators, WBCs move to the injured area |
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PHAGOCYTOSIS
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ingestion and digestion of bacteria and cellular debris
Process = REK R: Recognition E: Engulfment K: Killing |
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Two main phagocytes
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Neutrophils and Monocutes
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Inflammatory Mediators
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Histamine, Prostaglandins, Bradykinin, Leukotrienes, Lymphokines/Cytokines
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Histamine
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- Found in mast cells
- Dilates the arterioles, increased capillary permeability, immediate transient response - Degrades in an hour, but very potent |
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Prostaglandins
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- Made from arachadonic acid and stored in the phospholipid bilayer
- Vasodilation, increase capillary permeability, potentiates response of histamine (keeps in going) - Fever (reset hypothalmic set point) |
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Bradykinin
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- Protein found in plasma associated with complement clotting factors
- PAIN - Increase capillary inflammation |
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Leukotrienes
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- Made from arachadonic acid
- Increases capillary permeability and chemotaxis to monocytes |
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Lymphokines
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(Cytokines)
Substances released by lymphocytes that promote chemotaxis |
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Aspirin
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Inhibits prostaglandin synthesis by blocking the first step from aracadonic acid to prostaglandins
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Glucocorticoid Hormones
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(adrenal cortex)
Decrease arachadonic acid |
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Why do we treat inflammation?
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- Inflammation can cause pain, tissue damage, and loss of function
- Many diseases result from excessive inflammatory responses |
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What do we treat inflammation with?
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1. Temperature
2. Elevation and Pressure 3. Drug Therapy |
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Temperature
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- Cold is applied early to damaged area to reduce swelling and exudate formation
(3 days or earlier) - Heat is applied later to enhance phagocytosis |
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Elevation and Pressure
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In limbs, elevation and pressure wraps 1) decrease swelling and 2) promote lymphatic drainage
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Drug Therapy
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- Antihistamines
(only works for sustained injuries, like allergies) - NSAIDS (stop AA > PGA) - Corticosteroids (stop AA formation) |
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What is an exudate?
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Protein rich fluid found in inflamed tissue
(Proteins like Albumins) |
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What are the five types of exudate?
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1. Serous exudate
2. Fibrinous exudate 3. Membranous Exudate 4. Purulent Exudate 5. Hemorrhagic Exudate |
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Serous Exudate
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Mild injury, early in the injury
Mostly plasma, plus leaked albumins Ex. Blister |
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Fibrinous Exudate
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Increased fibrinogen, gets thick, sticky.
Glues structures together, and thereby prevents spread of infection Ex. appendicitis |
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Membranous Exudate
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Mucous membrane surfaces
Forms a false membrane that can be peeled away, can lead to suffication Ex. Oral Thrush |
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Purulent Exudate
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Suppurative Exudate
PUS = WBSc, bacteria, tissue, debris Caused by pyrogenic bacteria ABCESS: local collection of pus that is encapsulated (rupture or drainage) EMPYEMA: pus filled body cavity (pericardial, lungs) Ex. Strep, staff, pimples |
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Hemorrhagic Exudate
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Severe tissue damage to blood cells
RBCs escape to tissue |
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Outcomes of Acute Inflammation
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1. 100% Resolution
2. Chronic Inflammation 3. Scarring |
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Characteristics of Chronic Inflammation
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- A cellular response
- Site of inflammation is infiltrated with LYMPHOCYTES (mainly T cells) and MONOCYTES (with few neutrophils) -Proliferation of fibroblasts with possible scarring or deformity, rather than exudates as in acute response |
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Causes of Chronic Inflammation
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- Persistant irritants; repeated acute inflammation
- Foreign bodies such as asbestos, silica, or suture material - Viruses, bacteria, fungi, parasities - Idiopathic sources |
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What are the two patterns of chronic inflammation?
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Non-specific and Granuloma
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Non-specific Chronic Inflammation
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- Involves diffuse accumulation of macrophages and lymphocytes
- Fibroblasts proliferate secreting collagen with resulting scar formation - Will often result in normal tissue being replaced with scar tissue, which decreases net function of the organ |
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What is a granuloma?
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1-2 mm lesion with macrophages surrounded by lymphocytes
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Granuloma Chronic Inflammation
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- Large accumulation of macrophages called epitheliod cells
- Seen in TB, fungal infections, splinters, and other foreign bodies - Occurs because the noxious agent is poorly digestible and/or difficult to control - Cells may clump = granuloma or coalesce forming large multinucleated giant cells (MGCs) |
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Parenchmya
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Normal functioning tissue
Ex. kidneys > nehphrons |
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Stroma
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Structural framework within tissues
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Fibroblasts
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CT cells that form collagenous matrix
- can withstand hypoxic conditions for hours |
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What are the cell classifications based on regenerative ability?
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1. Labile Cells
2. Stable Cells 3. Permanent Cells |
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Labile Cells
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Regenerate throughout our lifetime
Ex. epithelial cells (skin, mucous membranes, bone marrow) Continuous regeneration |
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Stable Cells
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Stop dividing when growth ceases, but are capable of regeneration if properly stimulated. Underly structural framework must be intact.
Ex. Liver cells Conditional regeneration |
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What are the two patterns of chronic inflammation?
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Non-specific and Granuloma
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Non-specific Chronic Inflammation
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- Involves diffuse accumulation of macrophages and lymphocytes
- Fibroblasts proliferate secreting collagen with resulting scar formation - Will often result in normal tissue being replaced with scar tissue, which decreases net function of the organ |
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What is a granuloma?
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1-2 mm lesion with macrophages surrounded by lymphocytes
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Granuloma Chronic Inflammation
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- Large accumulation of macrophages called epitheliod cells
- Seen in TB, fungal infections, splinters, and other foreign bodies - Occurs because the noxious agent is poorly digestible and/or difficult to control - Cells may clump = granuloma or coalesce forming large multinucleated giant cells (MGCs) |
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Parenchmya
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Normal functioning tissue
Ex. kidneys > nehphrons |
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Stroma
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Structural framework within tissues
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Fibroblasts
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CT cells that form collagenous matrix
- can withstand hypoxic conditions for hours |
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What are the cell classifications based on regenerative ability?
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1. Labile Cells
2. Stable Cells 3. Permanent Cells |
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Labile Cells
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Regenerate throughout our lifetime
Ex. epithelial cells (skin, mucous membranes, bone marrow) Continuous regeneration |
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Stable Cells
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Stop dividing when growth ceases, but are capable of regeneration if properly stimulated. Underly structural framework must be intact.
Ex. Liver cells Conditional regeneration |
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Permanent Cells
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Cells that are unable to divide
Ex. muscle cells (heart after heart attack) and neurons |
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Two ways to heal injured tissue
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1. Regeneration
2. Repair |
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Regeneration
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- Process in which damaged cells are replaced with parenchymal, and normal structure and function are restored
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What are the requirements for regeneration?
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1. The injury must not be too severe
2. The tissue must be mitotic * both have to be met |
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Repair
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When the injury is too severe or the tissue is not mitotic, the parenchymal tissue will be replaced with fibrous CT replacing structure, but sacrificing function
Once fibroblasts lay down scar tissue, the collagen fibers contract After three months, the tissue heals to 70-80% |
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Angiogenesis
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Growing new blood cells
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Revascularization
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New capillaries formed from vessels adjacent to wound
Dividing endothelial cells form buds or cords that extend to damaged area, that eventually meet forming anastomoses |
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Healing with the skin
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- Reepithelialization: replacement of epithelium
- New epithelial cells divide near damage - New cells move to denuded area - Cells secrete a new basement membrane as they migrate - Cells then get anchored to membrane, and dividing cells move up towards surface of tissue |
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What are the two main types of WBCs?
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Granulocytes and Agranulocytes
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Granulocytes
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Neutrophils, Eosinophils, Basophils
- Twice the size of RBCs - Circulating granulocytes are MATURE, meaning they can start defensive tasks right away - Life span hours to several days |
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Neutrophils
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Polymophonuclear Neutrophils
- First to arrive at injury site - 60-70% of WBCs - Increase in bacterial infections - Phagocytosis -Die in 10 hrs, and therefore leukocytosis results |
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Eosinophils
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- Increase during allergic and parasitic reactions
- 1-3% - Terminate the response and detoxify |
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Basophils
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- Contain HISTAMINE (vasodilator) and heparin (anti-coagulator)
- Less than 1% |
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Agranulocytes
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Monocytes and Lymphocytes
- Are immature; have to mature in tissues |
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Monocytes
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- Largest of all WBCs
- Second cells to arrive at site and are the predominat type in 2 days - 3-8% of all WBCs - Phagocytotic - When they leave circulation are called macrophages - Live for months/years |
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Lymphocytes
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Two Types:
T-lymphocytes: antibodies B-lymphocytes: cell mediated immunity - 20-30% of WBCS |
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What are the three sources of free radicals?
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1. Metabolism of Proteins or Lipids
2. Inflammation 3. Smoke, pollutants, radiation |
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What are the 3 areas of the cell that free radicals damage?
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1. Lipid membrane damage
2. Damage DNA 3. Damage proteins |
