Pathology Final - Inflammation & Immunity

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Pathology Final - Inflammation & Immunity
2011-11-29 17:54:21

Pathology Final
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  1. What is reversible cellular injury?
    hydropic change –swelling of cytoplasm, influx of sodium and water
  2. What is an irreversible cellular change? What are the 3 types?
    • Plasma membrane ruptures and nuclear changes
    • 3 types:
    • Pyknosis---condensation of chromatin
    • Karyolysis—lysis of chromatin
    • Karyorrhexis---fragmentation of nuclear material
  3. What is necrosis? What are the 5 types?
    • Necrosis: groups of cells; inflammation; non-energy dependent
    • 1. Coagulative-most common—outline of tissue preserved—MI, kidney infarcts
    • 2. Liquefactive---brain infarct, abscess, wet gangrene
    • 3. Caseous---granulomas of tuberculosis/deep fungal
    • 4. Fat necrosis—found with acute pancreatitis or trauma to fat
    • 5. Fibrinoid necrosis—small blood vessels; Systemic lupus
  4. Describe apoptosis
    programmed cell death-involves gene activation and enzyme action; no significant inflammation; single cell; requires energy
  5. Adaptation results from cell injury or chronic stress; important forms of adaptation are? (all are potentially reversible)
    • 1. Hypertrophy—increase in tissue/organ size due to increase in cell
    • size (weight lifter; left ventricle enlargement secondary to HBP)
    • 2. Hyperplasia—increase in tissue/organ size due to increase numbers of
    • cells (endometrium)
    • 3. Metaplasia---replacement of one mature cell
    • type by another—example: Barrett’s esophagus—reversible in most cases
    • 4. Atrophy (pathologic or physiologic)
    • 5. Dysplasia
  6. Lipofuschin
    wear and tear pigment of aging
  7. Dystrophic calcifications are found where?
    found in areas of necrosis
  8. Metastatic calcifications are?
    a consequence of hypercalcemia
  9. Acute inflammation is mediated by what type of cell?
  10. What events are involved in acute inflammation?
    • Hemodynamic changes (brief vasoconstriction, then vasodilatation), increased permeability of vessel walls, and emigration of leukocytes from blood vessels into the tissues.
    • Transudate—clear, protein poor, relatively acellular liquid—seen in renal and heart failure (low protein; spec. gravity < 1.02)
    • Exudate—viscous, protein rich, seen in pus (high protein; specific gravity > 1.02)
    • Anasarca—severe generalized swelling of all subcutaneous tissues (cirrhosis or nephrotic syndrome)
    • Ascites-- edema in peritoneal cavity (end stage liver disease)
  11. What are the main events leading to neutrophils crossing out of a vessel?
    • 1. margination
    • 2. rolling
    • 3. adhesion
    • 4. transmigration
  12. What are the plasma-derived mediators of inflammation?
    • 1. Clotting factors—Hageman, thrombin, fibrinogen
    • 2. Anticoagulants—plasmin
    • 3. Complement proteins
    • 4. Kinins—bradykinin
  13. What are the cell-derived mediators of inflammation?
    • 1. Biogenic amines—histamine and serotonin—from mast cells and platelets
    • 2. Arachidonic acid derivatives prostaglandins and leukotrienes
    • 3. Cytokines
    • 4. Platelet activating factors
    • 5. Nitric acid from endothelial cells and macrophages
  14. Which inflammatory mediators cause vasodilation?
    Prostaglandins & nitric oxides
  15. Which inflammatory mediators cause increased vascular permeability?
    • 1. histamine
    • 2. bradykinin
    • 3. platelet activating factor
    • 4. leukotrienes
  16. Which inflammatory mediators are involved with chemotaxis?
    C5a, leukotriene B4, interleukins
  17. Which inflammatory mediators cause pain?
    prostaglandins and bradyinin
  18. Which inflammatory mediators are involved with phagocytosis?
    Neutrophils, eosinophils, macrophages
  19. What is the complement system and what is it made of?
    • Part of the innate immune system, it causes massive amplification of the response and activation of the cell-killing membrane attack complex (MAC).
    • It is composed of more than 20 plasma enzymes.
  20. What are the two activation pathways of the complement system?
    • 1. Classical path—antigen antibody reactions
    • 2. Alternative path---usually activated by fragment of fungi or bacteria, toxins, foreign substances.
  21. What are the 4 functions of the complement system activation?
    • 1. opsonization of bacteria (coating with IgG and complement C3b)
    • 2. anaphylatoxic action—stimulates release of histamine
    • 3. chemotaxis—C5a attracts neutrophils
    • 4. cytolysisMembrane Attack Complex formed (MAC)
  22. What is the sequence of events in primary healing?
    • 1. Bleeding and clot formation
    • 2. Inflammation
    • 3. Granulation tissue
    • 4. Scarring
    • 5. Restructuring (reorganization) of scar
  23. What is the difference between primary intention and secondary intention wound healing?
    • Primary intention---edges of wound approximated and held in place by sutures
    • Secondary intention----edges of wound are not approximated or are missing (takes longer to heal).
  24. What is a keloid?
    Hypertrophic scar composed of type III collagen; results from defective remodeling of scar tissue
  25. Describe the following types of cells and give examples of each:
    • Permanent: cannot regenerate—neurons, striated muscle of myocardium**(some debate about validity now)
    • Labile: Can readily regenerate---skin, mucosa
    • Stable: can also regenerate (if needed) such as liver or kidney
  26. What are the main causes of edema?
    • Increased intravascular (hydrostatic) pressure
    • Increased permeability of vessel wall
    • Decreased osmotic pressure of plasma (reduced albumin)
    • Sodium retention
    • Obstruction of lymph flow
  27. What causes sodium retention in the body, and what affects does it have?
    Reduced perfusion of kidneys (such as from heart failure) leads to rennin secretion. Renin activates the angiotensin system causing the increased secretion of aldosterone from the adrenal cortex. Aldosterone stimulates the tubules of the kidney to retain sodium. Retention of sodium is accompanied by retention of water which expands the intravascular volume leading to increased hydrostatic pressure and edema.
  28. Hyperemia
    active process—blood influx into tissues—tissue is bright red, warm
  29. Congestion
    passive process-stasis, tissue is dusky red to blue—tissues are cold and clammy
  30. Nutmeg liver
    Chronic passive congestion results in pooling and necrosis of hepatocytes (red-brown). These hepatocytes are replaced by fibrous tissue—uncongested areas appear pale tan--- nutmeg appearance to cut surfaces.
  31. What are the main components of hemostasis?
    • 1. Vascular wall
    • 2. Platelets
    • 3. Coagulation cascade
  32. What are the steps of primary hemostasis?
    • 1. Platelet adhesion and shape change (adhesion mediated by VonWillebrand factor)
    • 2. Secretion and release of granules by platelets—ADP, TxA2
    • 3. Recruitment and aggregation to form hemostatic plug
  33. What does secondary hemostasis involve?
    Activation of the coagulation cascade
  34. What is Virchow's triad?
    • (factors predisposing to thrombosis)
    • 1. Endothelial injury
    • 2. Alteration of blood flow (stasis or turbulence)
    • 3. Hypercoagulability
  35. What are the different fates of a thrombus? (5)
    • 1. Resolution
    • 2. Propagation and eventual occlusion
    • 3. Organization
    • 4. Recanalization
    • 5. Embolization
  36. What is an emboli, and what are the different types?
    • An emboli is a dislodged thrombus.
    • 1. Venous- originate in deep leg veins—carried to lungs
    • 2. Arterial-originate in heart, aorta, or large arteries—carried to various organs
    • 3. Fat emboli—fracture of long bones
    • 4. Paradoxical embolism: goes through a defect in inner ventricular heart wall to bypass pulmonary—behaves as an arterial embolism
  37. What is DIC (disseminated intravascular coagulation)?
    Clotting disorder---Microthrombi in small blood vessels consumes platelets and depletes fibrin. Can be triggered by obstetric complication, shock, gram negative sepsis (whole body inflammation), extensive trauma.
  38. What is shock, and what are the different categorizations of it?
    • 1. Cardiogenic (pump failure)
    • 2. Hypovolemic (wounds, burns, vomiting)
    • 3. Hypotensive (peripheral vasodilation)—bacterial toxins, anaphylactic, neural injury)
  39. What is Tay Sachs disease?
    A lipid storage disease showing deficiency of hexosaminadase A.
  40. What is Gaucher's disease?
    a lipid storage disease showing deficiency of beta glucosidase.
  41. What is Neimann Pick disease?
    Lipid storage disease showing deficiency of sphingomyelinase.
  42. What is Fabry's disease?
    Lipid storage disease showing deficiency of alpha galactosidase.
  43. What is Hurler's disease?
    • Mucopolysaccharidoses
    • deficiency of alpha-L-iduronidase—results in buildup of heparin sulfate and dermatan sulfate
  44. What is Phenylketonuria?
    • abnormality in amino acid metabolism
    • Deficiency of phenylalanine deaminase blocking conversion of phenyalanine to tyrosine.
    • If untreated, mental and neurologic deterioration
  45. What is amyloidosis? What are the complications?
    • Intercellular deposition of a proteinaceous material in beta-pleated sheets; many different amyloid proteins.
    • If deposited in sufficient amounts it can interfere with cell functions, most notably in the heart, adrenal, liver, and kidney (deposits in the glomeruli--nephrotic syndrome).
  46. How does amyloidosis appear histologically?
    Homogenous pink material on H&E sections; green birefringence when stained with Congo red and subjected to polarized light.
  47. In what conditions do we see amyloidosis?
    • Seen in multiple myeloma (AL), medullary carcinoma of the thyroid (A cal—derived from calcitonin molecules), Alzheimer’s disease (AB2); AA amyloid—seen in areas of chronic inflammation)
    • Not currently curable
  48. What is an oncogene? What is a proto-oncogene?
    Oncogenes are cancer-inducing genes; normal genes that may become oncogenes are called proto-oncogenes
  49. What is the Epstein-Barr virus, and what conditions is it associated with?
    • Epstein-Barr virus is a herpes virus.
    • It is associated with: Nasopharygeal carcinoma, Burkitt’s lymphoma, Infectious mononucleosis, Oral hairy leukoplakia.
  50. Which HPV subtypes are associated with cervical cancer? With benign lesions such as condyloma accuminatum?
    • HPV (human papilloma virus) subtypes 16, 18, 33 associated with cervical cancer.
    • Subtypes 6 & 11
  51. What is the most frequent cancer in men?
  52. What is the most frequent cancer in women?
  53. What is the most frequent cause of cancer death?
    Lung cancer (in both men and women)
  54. What is the most common cause of death in the US? The second?
    Cancer is the second most common cause of death in the US, following cardiovascular disease.
  55. What is the single most inportant defining characteristic of malignancy?
  56. What are the 3 major routes of metastasis?
    • hematogenous
    • lymphatic
    • Direct seeding of body cavities
  57. What are the two best known tumor suppressor genes, and what happens if they are lost or mutated?
    • p53, Rb-1 (retinoblastoma)
    • Loss or mutation of these genes can lead to cancer.
  58. Which tumor suppressor genes are associated with Wilm's tumor?
    WT1 & WT2
  59. Which tumor suppressor gene(s) are associated with familial polyposis coli?
  60. Which tumor suppressor gene(s) is associated with breast cancer?
  61. Two hit hypothesis of Knudsen
    two mutagenic events are required to initiate alterations on both chromosomes
  62. What are neuroblastomas associated with?
    gene amplification (N-myc oncogene)
  63. What two cancers are associated with Hereditary cancers?
    • Familial polyposis coli
    • Wilms tumor
  64. What is the most common autosomal disease in the US?
    Neurofibromatosis Type 1 - linked to a defective or missing NF1 gene.
  65. Most neoplasms have what characteristic?
  66. Describe the characteristics/differences between humoral and cellular immunity. (Principle cell, assisting cells, end result, effective against?)
  67. What are the 4 types of hypersensitivity reactions?
    • Type 1 Anaphylactic (IgE Mast cell degranulation - Hay fever, hives, anaphylaxis)
    • Type 2 Cytotoxic (IgG, IgM complement cell lysis - Goodpastures; Graves disease; hemolytic anemia)
    • Type 3 Immune complex--(IgM +complement---antigen-antibody complexes - Serum sickness; Arthus rx; SLE)
    • Type 4 Cell-mediated (delayed) Cellular—lymphokines; cell-mediated toxicity;Tuberculin reaction; contact dermatitis; poison ivy; granulomatous disease
  68. What is another name for a congenital immunodeficiency?
    Primary immunodeficiency
  69. What is the general effect of a primary T cell immunodeficiency?
    Poor response to viruses typically
  70. What is the general effect of a primary B cell immunodeficiency?
    Poor response to bacteria typically
  71. What is DiGeorge disease? What are some distinguishing characteristics?
    • A primary/congenital T cell immunodeficiency.
    • Thymus hypolplasia/ aplasia—no cell-mediated (t-cell) immunity; hypocalcemia
  72. X linked aggamaglobulinemia of Bruton
    • Primary B cell immunodeficiency
    • no plasma cells
  73. Isolated IgA deficiency
    Most common Primary B cell deficiency
  74. Common variable immunodeficiency
    • failure of B cell maturation
    • primary B cell immunodeficiency
  75. SCID
    • Combined Immunodeficiency ("severe")
    • Deficiency of B and T cells
    • Severe infections/ failure to thrive
  76. Wiskott-Aldrich syndrome
    X-linked; characterized by eczema, thrombocytopenia, recurrent infections
  77. HIV characteristics
    • Acquired Immunodeficiency
    • Virion has gp 120 surface protein which binds to CD4 lymphocyte
    • Virus found in blood, semen, vaginal secretions, breast milk, saliva
    • Increased opportunistic infections in late stage: Pneumocystis, Mucor, deep fungal
  78. Important Autoimmune diseases