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Pathophys 1

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  1. What is infectivity?
    Aility to enter the host and replicate
  2. What is an example of infectivity?
    coagulase (enzyme that creates a special sticky coating around staphg to protect it from the host's defenses.)
  3. What is pathogenicity?
    ability to produce disease in a healthy host
  4. What is virulence?
    disease-producing potential; potency of pathogen and speed of its replication
  5. Virulence is measured in terms of what?
    in terms of the number of microorganisms required to kill its host
  6. What is  toxigenicity?
    the amount and tye of toxin produced as a byproduct of the disease.
  7. What does the hemolysin byproduct do? and an example?
    • destroys RBC
    • E. Coli
  8. What does the  leukocidin byproduct do? and an example?
    • destroys WBCs
    • Staph aureus
  9. What is an endotoxin and an example?
    byproduct of gram (-) bacteria that cause pyrogenic effects and the resulting disease.  

    • Sugar + fat molecule create disease states.
    • ex = Cholera
  10. Other than coagulase, what are two more examples of infectivity?
    TB & cammo wax
  11. What is an exotoxin?
    Protein enzymes released from living microbes that cause body to swell.
  12. What is an example of an exotoxin?
    Staphylococcus (gram +) can grow and reproduce in salt.  Toxins create the "sickness" we feel.  No smell, no spoilage. Lots of vomiting.
  13. What type of immunity is B-cell immunity?
    Humoral (directed against pathogens in EXTRAcellular fluid)
  14. What do B-cells target?
    bacteria and viruses
  15. What do T-cells do?
    target infected cells and kill tumors!
  16. What is cellular immunity?
    • (aka cell-mediated)
    • directed against pathogens WITHIN the cells (INTRAcellular)
  17. What do b-cells secrete?
    antibodies
  18. What do t-cells secrete?
    cytokines
  19. Where are b-cells found?
    in the spleen
  20. Where are T-cells found?
    blood & lymph nodes
  21. Type of ab (immunoglobulin) that can fix complement.
    IgM
  22. Type of ab (immunoglobulin) that is found mainly in mucus, but also in histamine.
    IgA
  23. Type of ab (immunoglobulin) that is important in activation of B-cell.
    IgD
  24. Type of ab (immunoglobulin) that can crossthe placental   barrier.
    IgG
  25. Type of ab (immunoglobulin) that is involved in allergies.
    IgE
  26. There are fixed macrophages in two of our important body organs. Name the macrophages and the corresponding organ of each.
    • Kupffer cells = LIVVER
    • Microglia = BRAIN
  27. What is chemotaxis?
    • It's how the specialized WBCs know how to get to injury and where exactly to lay down the protein to make a clot;
    • Movement of a cell toward or away from a chemical substance.
  28. Chemotaxis is part of what system?
    The kinin system
  29. How can we give people immunity?
    In the form of an IV (IVG)
  30. What kind of rxn is a type I hypersensitivity?
    anaphylaxis
  31. What kind of rxn is a type II hypersensitivity?
    Specific Cytotoxic Rxn
  32. What kind of rxn is a type III hypersensitivity?
    Immune Complex - A rxn agains soluble antigens in serum.
  33. What kind of rxn is a type IV hypersensitivity?
    Cell-mediated
  34. Explain what (and which) ab do in a type I hypersensitivity rxn.
    IgE ab bind to mast cells & basophils which cause degranulation and a release of histamine
  35. Explain what (and which) ab do in a type II hypersensitivity rxn.
    IgG or IgM bind to an antigenic cell and the cell lyses.
  36. What are two examples of a type II hypersensitivity?
    • Goodpasture's Syndrome; 
    • Blood transfusion rxn (given wrong type of bld)
  37. With a type II hypersensitivity rxn, which ab does the body produce and what do they do?
    • immunoglobulin ab that can damage tissue cells
    • the allergen gets attacked and cells are also destroyed
  38. What is Goodpasture's Syndrome?
    • A type II hypersensitivity rxn (cytotoxic) to Paraquat weed killer, chem in cigs, cocain, benzene, kerosene
    • Defective ab are produced which attack RBCs
  39. What is destroyed and what can it cause in those with Goodpasture's Syndrome?
    Collagen, which clogs the kidneys an lungs and causes renal failure (glomerulonephritis) and widespread hemoptysis
  40. What is an arthus?
    a type III hypersensitivity rxn (immune complex) to a vaccine which causes edema, hemorrhaging and necrosis at the site
  41. How are soluble antigens normally removed and what happens to them in a type III hypersensitivity rxn?
    • normally removed by macrophages in the spleen and liver.
    • they form in lg amts and overwhelm the body immunocomplexes, deposit in tissues and cause inflammation
  42. Which type of cells or ab are involved in a type IV hypersensitivity rxn?
    T-cells. NOT antibodies.
  43. Why is the type IV hypersensitivity rxn delayed a day or two?
    b/c the macrophages and T-cells need time to migrate to the rxn site
  44. Where does the type IV hypersensitivity rxn show up?
    on the skin
  45. What is Stevens-Johnson Syndrome?
    a Type IV SEVERE allergic hypersensitivity to MEDICATION
  46. What happens to the skin in those with SJS?
    • Degloving (secondary to cytotoxic T-cells)
    • epidermal apoptosis
  47. What are the 3 types of autoimmune disorders?
    • Type II (Cytotoxic Rxns)
    • Type III (Immune complex)
    • Type IV (Cell-mediated)
  48. What is Grave's Disease?
    A Type II Autoimmune Disorder in which the body attacks the thyroid (overproduction of thyroid hormone; thyroid swells)
  49. What is Myasthenia Gravis and what does it affect?
    • A Type II Autoimmune Disorder in which ACh receptors are blocked by ab.
    • Muscles that control the eyes, face, neck and limbs are commonly affected. ("tosis" of the eye)
  50. What are two examples of a type II autoimmune disorder?
    • Grave's Disease
    • Myasthenia Gravis
  51. What is Systemic LUPUS Erythematosus?
    • a type III autoimmune DO
    • autoantibodies react agains DNA, blood cells, neurons
    • after apoptosis, immune complexes form under the skin, in kidneys and in joints. 
    • widespread inflammation
  52. What are the symptoms (cluster) of lupus?
    • rash
    • oral ulcers
    • arthritis
    • proteinuria
    • leukopenia
    • thrombocytopenia
    • photosensitivity
  53. What is Rheumatoid Arthritis?
    • a type III autoimmune DO
    • IgM auto ab collect inside joints, cause swelling and heat and damage the joint
  54. What are two examples of type III autoimmune DO and who do they affect?
    • Lupus and arthritis; 
    • primarily women
  55. What is Type I diabetes?
    • A type IV autoimmune DO
    • Insulin Dependent
    • The body attacks its own BETA cells in the PANCREAS = destroys ability to produce insulin
  56. What is MS?
    • A type IV autoimmune DO
    • caused by myelin-reactive T-cells activated by a trigger (infection?)
  57. What are some signs/symptoms of MS?
    • axonal loss & scarring
    • brain atrophy
    • impaired eye movements, blurry vision
    • noncoordination in extremities & gait
    • tremors
    • heat intolerance
    • incontinence, retention, constipation
    • cognitive impairment & confusion
  58. What are two examples of type IV autoimmune DO?
    • Type I DM
    • Multiple Sclerosis
  59. What is the temp range considered to be a sign/symptom of sepsis?
    96 - 101.4
  60. What is the heart rate that is considered to be a sign/symptom of sepsis?
    sustained HR 90 or more bpm
  61. What is the respiratory rate range that is considered to be a sign/symptom of sepsis?
    sustained 20 or more per min
  62. What is the range of WBC count considered to be a sign/symptom of sepsis?
    • less than 4,000/mm3 
    • OR
    • more than 12,000/mm3
    • OR
    • more than 10% immature neutrophils
  63. When is BP a sign of sepsis?
    Severe hypotension (90/40)
  64. What are two signs of sepsis that do not involve numbers?
    • bacteria and toxins are in the blood & growing OOC
    • cytokines produce widespread systemic VASODILATION
  65. At what level of UOP is considered a sign of sepsis?
    No, or minimal UOP (10 cc/hr)
  66. When testing for HIV, and the second HIV test (Blot or IFA) is negative, when do you retest?
    in 6 mos to cover the window of poss seroconversion
  67. The ______ test is used to confirm the _______ HIV test
    • Western Blot
    • ELISA
  68. _____ describes what sets the disease process in motion (initial contact); ______ explains how the disease process evolves (cellular & tissue events after contact).
    • Etiology
    • Pathogenesis
  69. A bacterial infection on top of the flu is an example of what?
    A complication (secondary infection)
  70. Excessive bleeding when injured is an example of what in regards to a person with hemophilia?
    sequelae (consequence)
  71. Decreasing risk factors BEFORE disease occurs.
    Primary prevention
  72. Early detection of the POTENTIAL for dev of a disease.
    Secondary Prevention
  73. Examples of primary, secondary, and tertiary prevention.
    • Primary - immunizations
    • Secondary - Pap smear to detect HPV
    • Tertiary - coctail to treat HIV AFTER diagnosed
  74. Clinical interventions to prevent further deterioration or reduce the complications of a disease once diagnosed.
    tertiary prevention
  75. What are SElye's 3 stages of GAS (General Adaptation Syndrome)?
    • Alarm stage
    • Resistance/Adaptation stage
    • Exhaustion stage
  76. What is the alarm stage of Selye's General Adaptation Syndrome (GAS)?
    • the first stage;
    • generalized stimulation of the sympathetic NS and the HPA axis
    • results in release of catecholamines (NE & Epi)
    • and cortisol
  77. What is the second stage of Selye's General Adaptation Syndrome (GAS)?
    • Resistance/Adaptation
    • body selects most effective & economic channels of defense
  78. During this stage of GAS, cortisol levels drop because they are no longer needed.
    Resistance/Adaptation stage
  79. What is the Endocrine Response #1 to stress?
    • Adrenal MEDULLA dumps epi, dopamine, and sm amts of NE after stimulation by sympathetic NS
    • Liver releases glycogen to increase BGL
    • Heart contraction and CO increase
    • Increase in free fatty acids & serum cholesterol
    • Inhibition of insulin from pancreas = increase in glucose
  80. What is the Endocrine Response #2 to stress?
    • ADH released from post. pit. = water retention
    • CRF in hypoth. stim post pit to release ACTH = stim release of cortisol from adrenal CORTEX
    • PRL & GH also released from Post pit
  81. Main effect of cortisol (hydrocortisone).
    to increase BGL & aa
  82. Other than it's main affect, what else does cortisol do?
    • suppreses B & T cell activity initially while increasing humoral immunity in time
    • supports higher BP
  83. What are the two patterns of reversible cell injury?
    • Cellular swelling
    • Fatty Change
  84. How does cellular swelling occur and what is it?
    • It is a pattern of reversible cell injury
    • occurs with impairment of the Na+/K+ pump, usually as a result of hypoxic cell injury
  85. Fatty changes are linked to __________. When they occur, small vacuoles of fat disperse throughout the _______.
    • INTRAcellular accumulation of fat;
    • cytoplasm
  86. What does a fatty change in cells usually indicate?
    a severe injury
  87. How may fatty changes occur?
    • normal cells are presented with an increased fat load, or
    • injured cells are unable to metabolize the fat properly
  88. How does hypoxia contribute to cellular swelling and membrane damage?
    • It causes an inflammatory response - deprives cell of O2 and interrupts oxidative metabolism and generation of ATP.
    • Reduced ATP causes acute cellular SWELLING

    impairment of Na+/K+ pump causes intracellular K+ levels to decrease, and Na+ and H20 accumulate in the cell (swells!)
  89. Some causes of hypoxia.
    • Inadequate amt of O2 in air
    • Respiratory disease
    • Edema
    • Ischemia
    • Hypermetabolic states
  90. Fatty change occurs mainly in which organ?
    Liver
  91. A protective nonspecific defense response to cell injury.
    Inflammation
  92. What is the purpose of inflammation?
    • To remove the aggravating agent and 
    • to initiate the healing process
    • Limit the injuriuos effect of pathological agent
  93. Inflammation MOST OFTEN occurs when?
    with infection. But also develops as a result of an injury to a cell
  94. In inflammation, the adhesion of WBCs to endothelial lining.
    pavementing
  95. The first responders in the vascular response to inflammatin (chemical mediators).
    • histamine & seratonin;
    • initial vasodilation & capillary permeability
  96. How is redness produced in the inflammation process?
    • dilation of arterioles and increased circulation;
    • localized bluch from capillary distention
  97. How is heat produced in the inflammation response?
    • vasodilation
    • fluid leakage into interstitial spaced
    • increased BF
  98. How is pain produced in the inflammation process?
    • pain receptors are stimulated by swollen tissue,
    • local pH changes,
    • and chemicals excreted during the inflammatory process
  99. How is edema produced in the inflammation process?
    • vasodilation,
    • leakage of fluid into interstium;
    • blockage of lymphatic dranage
  100. How is loss of fxn produced in the inflammation process?
    result of edema & pain
  101. Local or systemic manifestation of inflammation? pyogenic microbes that present infection
    local
  102. Local or systemic manifestation of inflammation?  hemorrhagic
    local
  103. Local or systemic manifestation of inflammation? abscesses
    local
  104. Local or systemic manifestation of inflammation?  leukococytosis
    systemic
  105. Local or systemic manifestation of inflammation?  increase in plasma proteins
    systemic
  106. Why do we feel pain with inflammation?
    the tissue is swollen, full of exudate & presses on the nerves
  107. What biochemical mediators initiate pain in the inflammation process?
    prostaglandins. They also damage nerves.
  108. Chronic inflammation is characterized by infliltration of ______ instead of ______.
    • monocytes and lymphocytes;
    • neutrophils
  109. What are the 3 phases of would healing?
    • Inflammatory
    • Proliferative
    • Remodeling
  110. What happens in the proliferative stage of wound healing?
    • new tissue is built
    • fibroblasts secrete collagen
    • granulation starts forming (pink-red)
  111. Which phase of wound healing includes hemostasis and vascular & cellular phases?
    Inflammatory
Author
MeganM
ID
256554
Card Set
Pathophys 1
Description
Patho
Updated
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