Patho Week 3 Inflammation.txt

  1. Describe the order of the initial response for acute inflammation, including transudate and exudate formation.
    • Transient Vasoconstriction
    • Vasodilation
    • Transudate formation (pitting edema)
    • Increased permeability
    • Exudate formation (non-pitting)
  2. What is the purpose of both acute and chronic inflammation?
    To kill or confine a pathogen
  3. Does the order of the acute response change depending on the injury?
    No, only the magnitude of the response changes
  4. What are the three main effectors cells of acute inflammation? What is the major effector cell?
    • Neutrophils (major because most acute responses are due to bacteria)
    • Lymphocytes
    • Eosinophils
  5. What do neutrophils fight? What about lymphocytes and eosinophils?
    • Neutrophils = bacteria
    • Lymphocytes = viruses
    • Eosinophils = allergic reactions or parasitic infections
  6. Describe the normal axial flow of blood.
    The formed elements of the blood normally travel in the middle of the blood vessel surrounded by the plasma. This, along with the normal teflon-like surface of the endothelial cells keeps the formed elements from sticking to the vessel wall.
  7. In regards to the Sequence of Cellular Events of the Acute response, describe Margination.
    • 1. Normal axial flow of blood
    • 2. Margination: since the hydrostatic pressure has increased (because fluid has left the vessel) the blood is thicker and the endothelial wall is now sticky. The RBCs bump into each other and form aggregates called Rouleaus (rulows) which push WBCs up against the wall where they stick
  8. In regards to the Sequence of Cellular Events of the Acute response, describe Rolling.
    • 1. Normal axial flow of blood
    • 2. Margination
    • 3. Rolling: as the WBCs stick to the wall they form selectins L,P, E form adhesion molecules; however, the adhesion molecules are not tight so the WBC "rolls" along the vessel wall.
  9. In regards to the Sequence of Cellular Events of the Acute response, describe Firm Adhesion.
    • 1. Normal Axial of blood flow; 2. Margination, 3. Rolling
    • 4. Firm Adhesion: as the WBC rolls along the wall, Integrins (which bind to Icam 1)are created which anchor the WBC to the wall, this stops the rolling.
  10. In regards to the Sequence of Cellular Events of the Acute response, describe Emigration
    • 1. Normal Axial flow of blood, 2. Margination, 3. Rolling, 4. Firm Adhesion
    • 5. Emigration: the movement of the WBC across the membrane through a process called Diapedesis
  11. In regards to the Sequence of Cellular Events of the Acute response, describe Chemotaxis.
    • 1. Normal axial flow, 2. Margination, 3. Rolling, 4. Firm Adhesion, 5. Emigration
    • 6. Chemotaxis: after emigration, the WBCs are in the tissue and ready to fight; however, they need to know where to go. Chemotaxis is the chemical attraction of WBCs by chemotaxins through tissue to the site of an infection.
  12. In regards to the Sequence of Cellular Events of the Acute response, describe Phagocytosis.
    • 1. Normal Axial of blood flow, 2.Margination, 3. Rolling, 4. Firm Adhesion, 5. Emigration, 6. Chemotaxis
    • 7. Phagocytosis: eat that shit up... yum yum....
  13. Describe the first stage of Phagocytosis.
    1. Recognition: Opsonization occurs and the bacteria is coated with opsonins like IgG (antibody) or C3b (compliment), this is how the WBCs know what to eat.
  14. Describe the second stage of Phagocytosis. What is the end result?
    Stage 2. Engulfment: the phagocyte wraps its cytoplams around the bacteria; it is now called a Phagosome
  15. What is the third stage of phagocytosis?
    3. Killing/Degradation: now that the bastard is wrapped up in the phagosome, it needs to be digested. The phagocyte contains lysosomes, once the bacteria is exposed to the lysosomes the entire thing is called a Phagolysosome.
  16. What are the two chemical mediators of acute inflammation?
    Cell-derived and Plasma-derived
  17. What three types of cells release histamine?
    Mast, Basophiles, Platelets
  18. Are Mast cells cell-derived mediators or plasma-derived? Describe them. Where are they located?
    Mast cells are cell-derived mediators that release histamine. They are tissue bound, and since they are located near the blood vessel, the histamine is quickly picked up.
  19. Are basophils cell or plasma derived mediators, what do they release, where are they located?
    Basophils are cell-derived mediators that release histamine and are free-floating/circulatory.
  20. Are Platelets cell derived or plasma derived mediators? What do they release?
    Cell-derived, release histamine, free-floating
  21. What are Eicosanoids? Name two types.
    Cell-derived chemical mediators. Prostaglandins and Leukotrienes
  22. What are prostaglandins made from? What causes them to become prostaglandins?
    They are from the breakdown of arachidonic acid and become prostaglandins because they followed the cyclooxygenase pathway.
  23. Describe two types of prostaglandins.
    • 1. Prostacyclin: causes vasodilation and inhibits platelet aggregation
    • 2. Thromboxane: causes vasoconstriction and promotes platelet aggregation
  24. What are leukotrienes a product of and what do they do?
    Leukotrienes are a product of arachidonic acid breakdown through the 5-lipooxygenase pathway. Leukotrienes cause vasoconstriction and bronchospasms. They are related to asthma, that is why vasoconstriction makes sense. Asthma meds are leukotriene blockers.
  25. What is the most powerful chemotaxin in the body?
    Leukotriene B4
  26. Describe the rolls of ROSs and Lysosomal Protease as chemical mediators.
    ROSs are used by inflammatory cells to destroy biological material and Lysosomal Protease is released when WBCs die, this can be dangerous because they can harm neighboring cells.
  27. What are two characteristics of Cytokines?
    They are released in the immediate environment and the signal molecules that affect the function of other cells by stimulating surface receptors.
  28. List five Cytokines
    • Interferons
    • Interleukins
    • Tumor Necrosis Factor
    • Colony Stimulating Factor
    • Chemokines
  29. What is TNF?
    Tumor Necrosis Factor: released by monocytes and macrophages in response to endotoxins. They mediate an inflammatory response and have the ability to cause necrosis in some tumor cells.
  30. What is CSF and what does it do?
    Colony Stimulating Factor: promotes the differentiation of stem cells into blood granulocytes and macrophages.
  31. List two plasma-derived chemical mediators.
    Kinin System and Compliment System
  32. What is important to know about the Kinin System?
    • It is a plasma-derived chemical mediator system and it causes PAIN!!!
    • Bradykinin: powerful vasodilator, stimulates smooth muscle contractions and causes increased permeability
  33. How does the Compliment System work with inflammation?
    The terminating pathway of the compliment system (C5-C9) is the Membrane Attack Complex (MAC). The MAC drills holes in the phospholipid bilayer of bacterial walls.
  34. List 5 local signs of acute inflammation. What is important about each?
    • 1. Redness: caused by vasodilation
    • 2. Heat: not fever heat, fever heat is systemic
    • 3. Swelling: transudate and exudate formation
    • 4. Pain: caused by prostaglandins, bradykinin, swelling against pain receptors, or possible knife wound through a pain receptor
    • 5. Loss of function
  35. What are three systemic manifestations of acute inflammation?
    • 1. Fever
    • 2. Leukocytosis
    • 3. Erythrocyte Sedimentation Rate
  36. Fever is a systemic response to inflammation. Describe what can cause fever.
    • Interferons alpha and beta
    • Interleukins 1 & 6
    • Bacterial products
  37. Leukocytosis is a systemic response to acute inflammation. Describe it.
    Normal leukocyte number is 5,000 - 11,000mm3, normal band is 5%. Any increase in these numbers can reflect a non-specific inflammatory response.
  38. What is ESR and what does it indicate?
    Erythrocyte Sedimentation Rate: During an acute inflammatory response there is an increase in fibrinogen (remember Fibrosis can be an outcome of acute inflammation), the excess fibrinogen causes RBCs to stick together and form Rouleaux. When in a test tube, these Rouleaux sink faster, providing a non-specific inflammatory response.
  39. Describe the four likely outcomes of acute inflammation. Which is most likely?
    • 1. Resolution (most likely): everything back to order, no loss of tissue or function
    • 2. Fibrosis: scar formation
    • 3. Suppuration/abscess formation: if the response cannot rid the body of the foreign substance, it will coat it. An abscess is the foreign substance coated in puss.
    • 4. Chronic Inflammation: if things go wrong
  40. What are five characteristics of chronic inflammation?
    • 1. Insidious, slow onset
    • 2. Increased macrophage activity
    • 3. Vague, non-specific malaise
    • 4. Tissue necrosis
    • 5. Fibrosis
  41. What are the two most common outcomes of chronic inflammation?
    Tissue necrosis and fibrosis
  42. What are four reasons chronic inflammation occurs?
    • 1. acute inflammation was not able to eradicate the injurious agent
    • 2. the injurious agent is a self-molecule; autoimmune
    • 3. the injurious agent is inert; wood, silicone, metal
    • 4. the anatomical structure of the injurious agent is not affected by the acute inflammation; TB, syphilis, Hanson's (leprosy)
  43. What are the four most common Chronic Inflammatory Cells?
    • 1. Macrophages
    • 2. Lymphocytes
    • 3. Plasma Cells
    • 4. Fibroblast
  44. What are the main effector cells of Chronic inflammation?
  45. Provide examples of that can initiate an response by macrophages.
    • IFN-gamma from T-lymphocytes
    • endotoxins
    • chemical mediators of acute inflammation
  46. Describe Plasma Cells.
    Plasma cells are a type of B-lymphocyte that produces antibodies.
  47. What do fibroblast do and what do they release that does it?
    Fibroblast created scar tissue by the release of collagen.
  48. What is the difference in vascular changes between Acute and Chronic Inflammation?
    Acute inflammation includes active vasodilation and increased permeability resulting in edema from exudate formation. Chronic inflammation results in new vessel formation (granulation tissue).
  49. What are systemic signs of acute inflammation vs. systemic sign of chronic inflammation?
    • Systemic Acute: fever, often high
    • Systemic Chronic: low-grade fever, weight loss, anemia
  50. Describe the differences in peripheral blood changes between acute inflammation and chronic inflammation.
    With acute inflammation we see an increase in neutrophils and leukocytosis. Often lymphocytosis as well if it is a viral issue. In chronic inflammation, we see less changes in peripheral blood. However, there could be an increase in plasma immunoglobulins from the plasma cells creating antibodies.
  51. What are three ways intracellular organisms can cause tissue injury from infection.
    • 1. Cell Necrosis: Lytic viruses like HIV and Hep B destroy the host cell as they leave
    • 2. Cellular Swelling: intracellular organisms can disrupt cellular processes inhibiting ATP production
    • 3. Latent Infection: Varicella virus can remain latent and show up later as shingles
  52. What are three ways extracellular organisms can cause tissue injury?
    • 1. Local Vasculitis
    • 2. Release of locally-acting enzymes
    • 3. Release of remotely-acting enzymes
  53. Extracellular organisms can cause tissue injury by local vasculitis, describe this.
    Many highly-virulent organisms, like anthrax, can infect and cause thrombosis in small blood vessels, this causes necrosis at the site of the infection. This may be due to direct invasion by the organism or production of toxins.
  54. Extracellular organisms can cause tissue injury by releasing locally-affecting enzymes, describe this.
    Many bacteria release enzymes that invade tissue, these enzymes break down tissue and can cause injury or necrosis. This is how Clostridium perfringens gets deeper into the tissue.
  55. Extracellular organisms can cause tissue injury by the release of remotely-affecting enzymes, describe this. What are three ways this happens?
    Some bacteria produce toxins that are carried in the circulation to cause cell injury/death to tissues far removed from the point of infection. This can be done by endotoxins, exotoxins or enterotoxins.
  56. What line of defense is inflammation?
  57. Describe Endotoxins.
    • - lipopolysaccharide components of bacterial cell walls released during lysis into the bloodstream
    • - act on small blood vessels to cause vasodilation
    • - fucks up the endothelial cells and promotes the coagulation cascade resulting in clots
    • - can cause Disseminated Intervascular Coagulation (DIC) which is abnormal clotting so you bleed from everywhere
    • - result is septic shock
  58. Describe Exotoxins.
    • - toxins released from living bacteria into bloodstream
    • - highly antigenic so there are lots of antibodies created
    • - heat liable above 60 Celsius
  59. What are enterotoxins?
    Exotoxins that affect the mucosal cells of the intestines. Think about what "entero" means (pertaining to the intestines)
  60. If there are lots of antibodies created, do you think there is an issue with endotoxins or exotoxins?
  61. What is the redness of skin called due to inflammation/vasodilation?
  62. What is the heat from inflammation called?
  63. What is the pain associated with inflammation called?
  64. What is Serous Exudate? What is it called if it's pinkish due to capillary destruction?
    Watery, low-protein exudate similar to blister fluid. Serosanguinous
  65. What is Purulent Exudate? What is a large amount of Purulent exudate called?
    Exudate containing pus; abscess
  66. Metabolic Acidosis: When does metabolic acidosis occur?
    Metabolic Acidosis occurs when kidneys cannot excrete enough metabolic acid, or bincarbonate is lost from the body.
  67. What is the hallmark of metabolic acidosis? What two ways can it happen?
    • Loss of Bicarb.
    • 1. the addition of metabolic acid causing the bicard to be used up
    • 2. the loss of bicarb, usually through the GI tract
  68. What is the anion gap, when does it happen, what is the formula?
    • The anion gap is the amount of excess acid after the bicarb has been used up. It is usually the result of excess acid and NOT the result of loss of bicarb, therefore you can usually rule out GI issues with an elevated gap.
    • Na - (HCO3 + Cl) = anion gap
  69. What is the normal range of the anion gap?
    12 plus/minus 2, but it has to be much,much higher to be of clinical relevance.
  70. What are common reasons we would see metabolic acidosis?
    • DM
    • Lactic acid build-up
    • Starvation
    • Renal Failure
    • Ingesting acid
  71. What are the normal values for Serum Sodium and Osmolarity?
    • Serum Sodium = 134 - 146
    • Osmolarity = 275-295
  72. What are the normal values for Potassium and Calcium?
    • Potassium = 3.5 - 5.1
    • Calcium = 9 - 11
  73. What are the normal values for CO2 and HCO3?
    • CO2 = 35 - 45 (think in relation to Ph 7.35 - 7.45)
    • HCO3 = 22 - 28
  74. What is the normal blood osmolarity?
    275 - 295
  75. True/False: If MAC is activated, then bradykinin is activated. If one system is activated, they all the systems are activated.
  76. What happen when IgG or IgM bind to an antigen?
    Compliment is activated
  77. What is mucousal inflammation called?
    Catarrhal Inflammation
  78. What is a response to liquifactive necorsis of paranchymal cells called?
    Suppurative (purulent) inflammation
Card Set
Patho Week 3 Inflammation.txt
Patho Week 3 Inflammation