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  1. What is disease?
    A change in the body that interrupts homeostasis and is harmful to the organism.
  2. When does disease occur?
    Disease occurs when the cellular environment changes to the degree that tissues are no longer able to perform their function optimally.
  3. What is pathogenesis?
    It is a sequence of events involving the cellular changes that lead to the disease.
  4. What are Symptoms?
    Evidence of disease that are perceived by the patient such as pain or dizziness.
  5. What are Signs?
    Physical observations that can be made objectively...a fever, a mass, abnormal heart sounds.
  6. What is a Syndrome?
    A group of signs and symptoms characteristic of a specific disorder.  Ex: Chronic Fatigue Syndrome
  7. What is an acute disease?
    An illness that occurs quickly and has a short term duration.
  8. What is a chronic disease?
    A disease that often comes on gradually, persists longer and often has more permanent tissue damage.
  9. What is the meaning of the word Diagnosis?
    The identification of a specific disease through the evaluation of symptoms and signs including lab work and other procedures.
  10. What is a Differential Diagnosis?
    A list of possible diagnoses that follow the signs and symptoms of a patient's illness.
  11. What is etiology?
    The causative factors of the particular disease.
  12. What does idiopathic mean?
    When the cause of the disease is unknown.
  13. What is iatrogenic?
    When a treatment or procedure may actually cause the problem.
  14. What does prognosis mean?
    The probability for recovery or other outcomes of a disease.
  15. What leads a healthcare provider to a prognosis?
    Based on historical data of similar patients and takes into account morbidity and mortality.
  16. What is morbidity?
    An indication of the disease rate within a population.
  17. What is mortality?
    The number of deaths from a particular disease in a given amount of time within a population.
  18. What are some factors to be considered when deciding a treatment plan?
    • Predisposing factors
    • Precipitating factors
    • Perpetuating factors
  19. What are considered predisposing factors?
    • The factors that increase the likelihood of a disorder occurring.
    • Ex: Age, genetics, gender, inherited factors, occupational exposure, smoking, diet.
  20. What are precipitating factors?
    • A factor that may trigger a disease.
    • Ex: An attach of chest pain is precipitated by shoveling snow...this leads to a diagnosis of coronary heart disease.
  21. What are perpetuating factors?
    The lengthening or worsening of a disease due to factors such as diet, smoking, the function of the immune system.
  22. What is treatment?
    A course of action to eliminate or reduce the cause of the disease.  This often includes environmental changes, behavioral changes, and pharmaceutical intervention.
  23. What are examples of pathological causes?
    • Pathogens - 
    • Bacteria
    • Viruses
    • Fungi
    • Protozoa
    • Prions
  24. Bacteria
    • Single cell micro-organisms that are prokaryotes.
    • Have cell walls.
    • Antibiotics are preferred treatment...they destroy the cell wall of the bacteria.
  25. Viruses:
    • Obligate intracellular parasites.
    • Can only reproduce when located inside of a host cell.
    • Work by either killing the cell or altering the cell's protein synthesis.
    • Sometimes can use Antiviral medications but are very limited.
  26. Fungi:
    • Includes both yeast and mold.
    • May cause infection and is then called Mycoses.
  27. Protozoa
    • Unicellular
    • Often motile parasites
  28. Prion:
    • An infectious protein particle.
    • Not a living organism.
    • Transmitted by ingestion of contaminated food.
    • Prefer nervous tissue.
    • Ex: mad cow disease.
  29. Creuztfeldt - Jakob disease
    • A Prion disease.
    • Transmitted between humans through corneal grafts and sometime dural grafts.
  30. KURU disease:
    • A prion disease.
    • Transmitted through cannibalism.
  31. Communicable Disease
    • Disease that spreads from human to human.
    • Transmitted via blood, body fluids, aerosol, etc.
    • Standard precautions help to prevent these from spreading.
  32. What are the stages of infection?
    • 1. Exposure
    • 2. Incubation period
    • 3. Prodromal phase
    • 4. Acute clinical illness
    • 5. Convalescence
  33. Other pathological causes:
    • Toxins
    • Normal inflammatory mediators
    • Protective processes that escape homeostatic control
    • Hypoxia
    • Anoxia
    • Genetics
  34. Define Pathophysiology
    • The study of structural and functional changes in cells, tissues, and organs that cause or are caused by disease.
    • The study of what occurs when in the body when homeostasis is interrupted...beginning at the cellular level.
  35. Eukaryotic cells:
    • This is what humans are made up of.
    • Contain a nucleus, cytoplasm with organelles, and a cell membrane.
  36. Types of cell adaptations:
    • Atrophy
    • Hypertrophy
    • Hyperplasia
    • Metaplasia
    • Dysplasia
    • Intracellular accumulations
  37. Atrophy
    • A decrease in the size of the cells, leading to a decrease in the size of the tissue that they are a part of.
    • Ex: Cachexia
  38. Cachexia:
    • Wasting away of tissue.
    • A serious form of atrophy.
    • Often seen in Cancer, AIDS, Decreased nutrition, etc.
  39. Hypertrophy:
    • Increase in size of tissues - enlargement of individual cells.
    • Normal hypertrophy: enlargement of the skeletal muscles causing them to increase in size.
    • Pathological Hypertrophy: Enlargement of the tissue due to additional work the tissue must do as a result of the pathology.  Ex: Increase in heart size in a person with hypertension.
  40. Hyperplasia:
    • Increase in the number of cells causing an increase in the size of the tissues/organs they are a part of.
    • Ex: Benign Prostatic Hyperplasia (BPH), calluses formed on feet.
  41. Benign Prostatic Hyperplasia:
    A common cause of prostate enlargement and is a normal occurrence as a male ages.  The urethra becomes blocked off, therefore making urination more difficult.
  42. Metaplasia:
    • Change of one cell to another because of injury.
    • Ex: In smokers, their trachea lose the cilia.
  43. Colposcopy:
    A medical diagnostic procedure to examine an illuminated, magnified view of the cervix and the tissues of the vagina and vulva.
  44. Dysplasia:
    • Disorganization of cell arrangement and atypical nuclei and increase in numbers.
    • Often called pre-cancerous cells...Neoplasia (tumor)
  45. Intracellular accumulations:
    As a result of cellular damage, the cell may collect material within it and may or may not cause problems.
  46. Anthracosis:
    • The accumulation of carbon particles within the lung cells of individuals who work in coal mines.
    • Leads to pulmonary pathologies.
    • Begins to disrupt protein synthesis.
  47. Lipid accumulation:
    • AKA: Steatosis
    • The process describing the abnormal retention of lipids within a cell.
    • Ex: a fatty liver.
  48. Heavy Metal Accumulation:
    • Ex: lead poisoning
    • Can affect brain tissue (brain damage), hemopoietic tissue (bone marrow), and the kidneys.
  49. PICA
    The habitual, purposeful, compulsive ingestion of nonfood substance like paint, clay, dirt, etc. as well as children living in old housing with peeling paint on the walls.
  50. What are the two major ways of cell death?
    • Necrosis
    • Apoptosis
  51. Necrosis:
    • Exogenous: (caused from outside the cell) cell death.
    • Often caused as a result of direct or indirect change in oxygen.
    • Toxins can cause necrosis by destroying cell components
  52. What happens to a cell when necrosis occurs?
    • Damage may occur to cellular structures including the mitochondria.
    • Inflammatory response may lead to death of the cell and damage to the tissue.
    • The cells ability to produce ATP is hindered...causing cell death.
    • Enzymes released triggers white blood cells to phagocytize the cell.
  53. Toxins:
    Can cause necrosis by destroying cell components or interrupting metabolic pathways.
  54. Some types of necrosis:
    • Coagulation necrosis
    • Liquification necrosis
    • Caseous necrosis
    • Infarction
    • Gangrene
  55. Coagulation Necrosis:
    • Most common form of necrosis and is typically seen in solid organs like the kidney, heart, liver, and most often seen due to hypoxia.
    • Tissue color turns from being red to a lighter color.
  56. Liquification Necrosis:
    • The dead cells dissolve and liquefy.
    • Often seen in soft tissue like the brain.
    • Ex: Cerebral infarct
  57. Caseous Cheesy Necrosis:
    • Typically seen in tuberculosis and fungal infections.
    • A cheesy-white substance will be found in the affected area that has dies.
    • Common location: the lungs.
  58. Infarction:
    • A term applied to an area of dead cells resulting from a lack of oxygen.
    • After death of an organ, it eventually will be replaced by newly formed tissue or, for tissue that does not go through mitosis, by scar tissue.
    • Ex: Myocardial Infarction
  59. Gangrene:
    • An area of necrotic tissue that has been invaded by bacteria, many times seen in the appendages.
    • Often occur when an infarction has occurred.
    • This tissue must be removed to prevent spread of the bacterial infection to other parts of the body.
    • Wet gangrene (within the body) and Dry gangrene (diabetics, frostbite)
  60. What are some changes that can occur after necrosis has occurred?
    • Scar tissue formation
    • Calcification
  61. Exudate:
    • Rich in protein and blood cells and is typical of inflammation.
    • A type of fluid accumulation in edematous tissues.
  62. Scar tissue formation:
    • Collection of fibrous connective tissue that holds anatomical structure together but does not function as the original tissue.
    • This can be bad in heart scar tissue because the relaxation of the heart function can not occur.
  63. Calcification:
    • Necrotic tissues attract calcium salts and often undergo Dystrophic Calcification.
    • This can been seen in calcification of damaged heart valves...this can hold the valves closed.
  64. Apoptosis:
    • Endogenous cells (from the inside the cell)
    • This is also known as programmed cell death and is based in genetic information found within the cell.
    • Many cells are predetermined to self destruct and that this is seen in normal cell functioning.
  65. Physiological Apoptosis:
    • Seen in normal embryological development of the fingers and toes.
    • During development lysosomes within cells of the webbing burst, releasing their enzymes.
    • This leads to cell death - disintegrating the webbing.
  66. Syndactaly:
    The absence of physiological apoptosis in the webbing formed in normal embryological development of the fingers and toes.
  67. Atresia:
    Lack of apoptosis during the formation of the intestine resulting in a lack of lumen or nonfunctional lumen.
  68. Pathological apoptosis:
    Cell death that occurs because of disease.
  69. Muscular Dystrophy:
    • The skeletal cells undergo apoptosis leading to cell death, sometimes beginning during gestation.
    • Cells form in a normal way and then they destroy themselves.
    • Usually considered a genetic disorder.
  70. Chronic Lymphocytic Leukemia:
    • A mutation of the gene makes the lymphocytes "forget to die".
    • Normally lymphocytes are programmed to live a specific amount of time.  
    • Towards the end of their lifespan, apoptosis occurs and programmed genes are stimulated to be expressed, leading to the death of the cell.
    • Because there is not a normal rate of cell death, they increase in number in the lymph nodes, enlarging them.
  71. What are the components of blood?
    • Plasma
    • Red Blood Cells (RBCs)
    • White Blood Cells (WBCs)
    • Platelets
  72. Hemocytoblasts:
    Formed elements are formed from the same type of cells found in red bone marrow of only a few bones.
  73. What is plasma?
    The straw colored fluid, matrix of blood that the formed elements are suspended in.
  74. What are Red Blood Cells?
    • One of the only mature cells that do not have a nucleus when circulating in the blood.
    • Their primary purpose is to carry oxygen to the cells of the body.
  75. What are White Blood Cells?
    • They are found suspended in plasma and are dedicated to protection of the body.
    • Some will leave the blood and go to the tissues where they achieve their goal of protection.
    • The two types of WBCs are Granulocytes and Agranulocytes.
  76. What is the normal WBC count?
    4500-10,000 per microliter (mcL)
  77. What are granulocytes?
    A WBC that has a lobed nucleus and grains in the cytoplasm that are visible with a light microscope.
  78. What are Agranulocytes?
    • They are WBCs that have a compact nucleus and no visible grains in the cytoplasm.
    • They consist of monocytes (kidney shaped) and lymphocytes (have a large looking nucleus.
  79. Platelets:
    • These are not cells.
    • Portions of large cells found in red bone marrow.
    • Involved in blood clotting.
  80. What is the function of Arteries?
    • A blood vessel that provides oxygenated blood to the rest of the body.
    • The meta-arteriole area does not take in all of the blood.
  81. What happens in the capillaries?
    • Located in the endothelium.
    • This is the location where oxygen moves out of the blood and CO2 moves into the blood to be carried back to become oxygenated.
  82. What is the purpose of veins?
    To bring back deoxygenated blood to the heart.
  83. What is one of the body's methods that offers protection against many pathogens?
  84. What is inflammation?
    • A protective response that is intended to eliminate the initial cause of cell injury.
    • It is a vital reaction, occurring only during life and not death.
  85. What is involved with the process of inflammation?
    • It involves specified cells (mostly WBCs) being brought, by blood, to the area that is infected.
    • These cells often leave the blood and move to the tissue in question.
    • Through this and in conjunction with chemical mediators, the agent is hopefully overpowered.
  86. What is the connection between inflammation and capillary beds?
    The site of inflammation is at the area where substances from the blood can leave or enter the tissue.
  87. What are the cardinal signs of inflammation?
    • 1. redness
    • 2. heat
    • 3. swelling
    • 4. pain
  88. What is happening during inflammation?
    • 1. Smooth muscle of the arterioles (pre-capillary sphincter muscles) relax allowing for an increase in the amount of blood entering the beds, accounting for the redness (erythema) and warmth of the tissue.
    • 2. Edema - the increase in the amount of blood moving into the capillary beds will increase the pressure within these capillaries, forcing more fluid into the interstitial spaces.
    • The edema will irritate nerve endings and pain is felt.
  89. What are the chemical inflammatory mediators?
    • Histamines
    • Bradykinin
    • Cytokines
    • Prostoglandins
  90. Histamines
    • Released early in inflammation primarily by basophils in the blood and mast cells in the interstitial spaces.
    • They stimulate the endothelial cells of the capillary to increase permeability.
  91. Bradykinin:
    • This is a protein that is normally found in an inactive state in the plasma.
    • This will increase permeability of the capillary as well as being responsible for pain that is associated with inflammation.
  92. Cytokines:
    • These are polypeptide products synthesized by many types of cells and will modulate the activity of other cells.
    • Ex: Interleukins, Interferons
  93. Prostoglandins:
    • This is a class of substances found within the membranes of cells and released during inflammatory reactions.
    • Their activities vary, some increasing the permeability of vessels, others responsible for fever.
  94. What happens to the capillary walls during inflammation?
    • Due to tissue factors and other chemical mediators, permeability of the capillaries will increase allowing for the passage of some blood cells out of the vessels into the tissue.
    • An increase in permeability is desired so that WBCs can go out and fight infection.
  95. White Blood Cell response to inflammation:
    Both granulocytes (neutrophils, eosinophils, and basophils) and some agranulocytes (specifically monocytes) are involved with the inflammatory response.
  96. What is Chemotaxis?
    • Active movement of PMNs (polymorphonuclear leukocytes) along a concentration gradient.
    • Ex: When agents get into the tissue, injury occurs to the cells and chemicals (mediators) are released.  These chemicals go from the injury into the blood and attracts WBCs to the ares.
  97. What is diapedesis?
    • Emigration.
    • Many of the WBCs will leave the vessel and by ameboid movement, make their way to the injured tissue.
  98. What action do WBCs taken in reaction to infection?
    • They leave the vessel by ameboid movement and make their way to the injured tissue.
    • The WBCs that reach the injured tissue begin to lose their mobility and begin to destroy the agent that is causing the problem.
    • This is usually by phagocytosis (the release of toxins).
    • Monocytes become macrophages in this process.
  99. What are the indication of inflammation?
    • 1. The 4 cardinal signs of inflammation.
    • 2. An increase in the level of C-Reactive Protein (CRP).
    • 3. An increase in the value of Erythrocyte Sedimentation Rate (ESR).
  100. What is C-Reactive Protein (CRP)?
    • A protein produced in the liver.
    • An increase in the level of CRP can indicate an acute response to inflammation.  The increase can be as great as 500 times normal.
    • It is thought that this protein binds to the surface of the causative agent and targets them for destruction.
    • This can detect different pathologies within the body.
  101. Erythrocyte Sedimentation Rate (ESR):
    • Also called Sedimentation Rate or SED Rate.
    • It is the rate at which red blood cells sediment in a period of 1 hour.  
    • An increase of sediment rate correlates to a more positive chance of internal inflammation.
    • Some of the CRPs attach to the membranes of the RBCs, making them stick together.
    • This is a common hematology rest that is non-specific measure of inflammation.
  102. Etiology of Inflammation:
    Inflammation can be caused by but not limited to: infectious agents like bacteria or viruses, physical changes like extreme temperature, autoimmune responses, trauma or surgery.
  103. What are some types of inflammation?
    • The presence of Exudate.
    • Ulcer (ulcerative inflammation)
    • Peptic ulcer
  104. Define Exudate:
    • Any fluid that is associated with areas of inflammation.
    • Composed primarily of water, plasma proteins, and WBCs.
  105. What are different types of exudate?
    • Serous inflammation - clear liquid
    • Purulent inflammation (PUS) - thick yellow/green; can turn into an abcess.
  106. Abcess:
    A localized collection of pus within an organ or tissue.
  107. What is an ulcer?
    • A type of inflammation that occurs on body surfaces or the mucosa within organs.
    • A defect involving the epithelium but may extend into deeper connective tissue.
    • Peptic ulcer occurs in the stomach, esophagus, or duodenum
    • Decubital ulcer - a "bedsore"
    • Foot ulcer - usually diabetics
  108. Acute inflammation
    Usually will last only a few hours to a few days and will quickly resolve.
  109. Chronic inflammation:
    Occurs for a longer period of time and may be associated with scarring - the replacement of normal cells with collagen and fibroblasts.
  110. Granulomas:
    • May form in areas where there is chronic inflammation.
    • This is a nodule that is composed of WBCs and connective tissue and can eventually cause invasion into blood vessels of the lung tissue, resulting in the coughing up of blood associated with TB.
    • They also occur around foreign bodies like splinters, asbestos.
  111. Localized inflammation
    • When some inflammatory responses occur in a specific organ of the body.
    • This is sometimes responsible for the localized pain a person may be experiencing.
  112. Systemic Inflammation
    • A response that is nonspecific but rather occurs throughout the body.
    • Responses may include: malaise, anorexia, fever, etc.
    • Many autoimmune diseases cause generalized inflammatory reactions.
  113. What is the connection between fever and inflammation?
    • Fever is an elevation in normal body temperature that can be associated with inflammation.
    • Pyrogens are the responsible chemicals for fever.
  114. What is Pyrexia?
    It means fever.
  115. Pyrogens
    • Chemicals that cause fever.
    • They are released by the cell that is involved with the inflammation - both from the blood cells or the tissue cell that is being harmed.
    • They make it to the hypothalamus in the brain and the brain signals the body to bring the body temperature up to a fever.
  116. The course of a fever:
    • 1. Pyrogens are released from the cells or tissues associated with the inflammation and make it to the hypothalamus.
    • 2. The pyrogens cause an increase in the Prostoglandins which results in a "resetting" of the "thermostat".
    • 3. Fever will decrease as soon as the inflammation decreases or if it medically ASA.
  117. What are the stages of fever?
    • 1. prodromal period
    • 2. chills
    • 3. flush
    • 4. defervesence
  118. What does the body do to restore homeostasis once inflammation occurs?
    • The cell cycle and cell division.
    • Healing is the body's attempt to regain homeostasis.
  119. Healing and repair after inflammation:
    • Some tissues may heal completely but others, due to the amount of destruction, may not.
    • The level of healing depends on the type of tissue involved.
  120. Mitosis:
    Cell division that gives rise to new cells that are identical in function and the number of chromosomes as the original cell.
  121. Possibilities of mitosis in the role of healing and repair are:
    • 1. Labile Cells - Cells that continuously divide after birth.  Ex: epithelial cells.
    • 2. Stable Cells - Cells that do not regularly divide but will if necessary.  Ex: Liver cells.
    • 3. Permanent Cells - Cells that lose the ability to go through mitosis at or soon after birth = Post Mitotic Cells.  These don't go through mitosis. Ex: skeletal muscle, cardiac muscle, some smooth muscle.
  122. Since permanent cells do not go through mitosis as a form of repair, what happens in place as a form of healing and repair after inflammation or infection?
    The damaged cells are replaced by fibrous connective tissue (scar tissue).  They keep the organ together but will not function like the original tissue.
  123. What are the factors associate with wound healing?
    • 1. Nutrition
    • 2. Blood flow and Oxygen Delivery
    • 3. Age
    • 4. Size and Location of Injury
    • 5. Proper formation of Granulation Tissue
  124. How does nutrition affect wound healing?
    • Malnutrition slows the healing process and prolongs the inflammatory phase.
    • Successful wound healing depends on amino acids, vitamins, fatty acid stores, and carbohydrates.
  125. How does blood flow and oxygen delivery affect wound healing?
    • For wounds to heal, there needs to be an adequate blood supply to provide for the necessary oxygen, nutrients and removal of wastes, toxins and bacteria.
    • Pre-existing health problems like diabetes involve poor circulation which can compromise wound healing.
  126. How does a hyberbaric oxygen chamber help to heal difficult wounds?
    • 100% oxygen is delivered at least twice the normal atmospheric pressure at sea level.
    • a. An increase in neutrophils = decrease in bacteris
    • b. Decrease in anaerophobic bacteria
    • c. Increase in angiogenesis (formation of more blood vessels)
    • d. Increase in fibroblast activity
  127. How does age factor into the healing process?
    Younger individuals will heal faster than the elderly.
  128. Does size and location of an injury have an effect on the healing process?
    • Large gaping wounds heal slower because it can be impossible to promote wound closure.
    • Some areas of the body get more mechanical stress than others and will allow the wound to be continually disturbed, delaying healing.
  129. What does granulation tissue have to do with wound healing?
    • This is healing of a wound from the inside to the outside of the body.
    • This tissue represents a temporary, makeshift structure that changes over time and results in a scar.
  130. What factors can cause complications in the process of wound healing?
    • a. Delayed healing due to overall health, diet, and age.
    • b. Excessive scarring.  Ex: Keloids, Contractures
  131. What are Keloids?
    • Excessive scars that form due to faulty remodeling of scar tissue.
    • There appears to be a genetic component to this and it is more prevalent in people of color than Caucasians.
  132. What are contractures and what can they lead to?
    • Large scars, especially seen in burns, tend to have an irregular, tightening of the skin, connective tissue including tendons and ligaments.
    • These can lead to a decrease in movement if the occur over joints.
  133. What is primary intention wound healing?
    The healing of a wound caused by sterile surgical cuts/incisions.
  134. What is Secondary Intention would healing?
    Healing of large defects and essentially all infected wounds.
  135. What are some commons ways to treat inflammation?
    • Immediate Treatment
    • Medication
  136. What does R.I.C.E. stand for and what is it used for?
    • Rest
    • Ice
    • Compression
    • Elevation
    • This is immediate treatment of inflammation.
  137. A main type of drug given for out-of-control inflammatory reactions is?
    • Glucocorticoids (aka: Corticosteroids or Steroidal Anti-Inflammatory Drugs...SAIDs)
    • These drugs are synthetic chemicals that are similar to the glucocorticoid hormones (cortisol) produced by the adrenal cortex.
  138. How do Corticosteroids work?
    • They block the release of prostaglandins and similar substances and therefore decrease inflammation.
    • Ex: Prednisone (a prescription drug)
  139. What is the good and bad about Corticosteroids?
    • Good:
    • They decrease capillary permeability.
    • They reduce the number of WBCs around the site, decreasing the release of histamines and prostaglandins.
    • They decrease the immune response.
    • BAD:
    • Side effects such as constant hunger, shaking, weight gain, and insomnia.
    • Atrophy of the lymphoid tissue.
    • Reduced number of white blood cells.
    • Osteoporosis.
    • Delay of healing.
    • Gradual decrease in abrupt stop to taking them
  140. What happens if you suddenly stop taking corticosteroids?
    • The adrenal cortex release of the normal steroid hormones is affected.  It could lead to adrenal insufficiency.
    • Side effects:  vomiting, nausea, headaches.
  141. What are some other anti-inflammatory medications?
    • Aspirin (ASA) and Non-Steroidal Anti-Inflammatory Drugs (NSAIDS).  These include: Ibuprofen, Advil, Motrin.
    • They reduce inflammation by inactivating an enzyme needed for synthesis of prostaglandins.
  142. Analgesic:
    a pain killing drug...relief from pain.
  143. Febrile:
    Referring to a fever.
  144. What is Reyes Syndrome?
    • Primarily seen in children.
    • This happens when aspirin is given to a child to reduce fever.
    • Affects all organs of the body but mostly the brain and the liver - brain edema and steatosis.
    • Personality changes, disorientation, delirium, and convulsions are also experienced and can be fatal.
  145. Tylenol - Acetaminophen
    • Reduces fever but is not an anti-inflammatory and is also considered harmful to the liver.
    • It is an antipyretic.
  146. Are inflammation and an infection the same?
    • These are not the same even though inflammation often results from an infection.
    • Inflammation can become its own pathology.
  147. What are the three lines of defense of the body to protect itself from invaders?
    • 1. Skin, mucosae, and secretions (barrier defense)
    • 2. Innate Immunity - general, non-specific protection.
    • 3. Acquired Immunity - specific and has memory.
  148. Innate Immunity
    • General, non-specific immunity.
    • WBCs involved are granular WBCs and monocytes.
  149. Acquired Immunity
    • This is a group of mechanisms that protect the host against damaging agents (antigens).
    • The immune system is specific and has memory.
    • Lymphocytes are the central cells involved in this process.
  150. What are the two types of lymphocytes?
    • T lymphocytes (T cells)
    • B lymphocytes (B cells)
    • These are agranulocyte cells and are formed in red bone marrow and eventually are released into the blood, some taking up residence in lymphoid tissue and organs like the spleen, tonsils, lymph node, appendix, etc.
  151. Antigen
    Any agent that causes the acquired immune system to respond - a reaction to production of specific antibodies or specifically sensitized immune cells.
  152. What are the three steps T-cells and B-cells go through in order to offer protection against specific antigens?
    • 1. Recognition:Recognize the antigen that they have been programmed against...recognize specific antigens.
    • 2. Prolifertation: Proliferation of specific B or T cells.  An increase in number of the specific lymphocytes programs against the specific antigen.
    • 3. Elimination: Elimination of the antigen, directly or indirectly.
  153. T-Cells
    • Formed in red bone marrow and mature in the thymus gland...they become immunocompetent.
    • Once mature, they leave the thymus and either circulate in the blood or reside in lymph tissue.
  154. Types of T-cells:
    • 1. T-helper cells (T4 cells)
    • 2. Cytotoxic T-cells (T8 cells)
    • 3. Memory T-cells
    • 4. Suppressor T-cells
  155. T-helper cells (T4 cells)
    • These are the central cells in the immune system.
    • They don't directly destroy the antigen but are responsible for the activation of the other lymphocytes by releasing Interleukin 2.
  156. Cytotoxic T-cells (T8 cells)
    These cells, once activated, will eliminate the specific antigen by "cell to cell" contact - they release toxins onto the antigen that destroy it.
  157. Memory T-cells
    These T-cells remain after the elimination, ready to attach the same type of antigen if it is presented at a later date.
  158. Suppressor T-cells
    These cells inhibit the immune response.
  159. B-cells
    • Lymphocytes formed in red bone marrow, but inlike T-cells, B-cells remain in the red bone marrow to gain immunocompetence.
    • Eventually released into the blood and circulate or reside in lymph tissue.
    • They get their assignments in the red bone marrow.
  160. What are the types of B-cells?
    • 1. Plasma cells
    • 2. Memory cells
    • 3. Suppressor B-cells
  161. B-cells - Plasma cells
    Once activated by T-helper cells, B-cells become plasma cells which will form and release antibodies.
  162. Antibody
    • A protein molecule that binds to a specific antigen leading to its elimination.
    • The antibodies are released from the plasma cells within the tissue and will destroy the antigen...B-cells do not directly harm the antigen - the antibodies do.
    • Ex: IgG, IgE, IgA
  163. Major methods that antibodies eliminate antigens
    • a. neutralize the pathogen:  The antibodies and antigens can join together to produce antigen-antibody complexes.
    • b. opsonization: improve phagocytosis to make it more successful.
    • c. activate complement system: 20 circulating proteins that when activated, aid in fighting off causative agent - stimulating the inflammatory process is one thing that antibodies will do.
  164. Opsonization:
    Improves phagocytosis that helps to eliminate antigens more successfully.
  165. Complement System:
    • 20 Circulating proteins that when activated, aid in fighting off causative agents.
    • This can be bad when it begins to affect our own healthy cells...autoimmune disease.
  166. What is a titer blood test looking for?
    Specific antibodies tested for in a person's blood as proof of having exposure to a specific antigen.
  167. B-Memory Cells:
    • Cells that will continue to circulate after the elimination of the antigen.
    • They become plasma cells and release specific antibodies if the body comes into contact with the same type of antigen later.
    • These are the cells that vaccinations work on.
  168. Suppressor B-cells:
    Suppresses immune response after elimination of the antigen.
  169. Hypersensitivity:
    Exaggerated, inappropriate immune system reactions in the body.
  170. Anaphylactic Shock:
    • A sudden, sever, life threatening systemic reaction resulting in a decrease in blood pressure, airway obstruction, edema and hypoxia.
    • An immediate response to an antigen.
  171. What medication is used in response to an anaphylactic episode?
    An injection of epinephrine should be given which will constrict vascular smooth muscle and relaxes respiratory smooth muscle.
  172. Delayed Hypersensitivity:
    An allergic reaction that happens hours after an exposure to the allergen.
  173. What are MHC's?
    • (Major Histocompatibility Complexes)
    • Surface markers on most cells.
    • They are unique to each individual, unless they have an identical twin and are found on all cell membranes except red blood cells.
Card Set:
2014-02-10 04:36:00
This card set is information for pathophysiology BIOL 2305. This is considered a science elective class - not Nursing pathophysiology.
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