Exam 2

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Exam 2
2012-02-26 20:55:26

genetics, RBCs, anemias, immunity, cases 1-5
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  1. What are the most abundant cells of the body?
  2. T/F: RBCs have a nucleus.
  3. T/F: RBCs have organelles.
  4. Which blood cells have a great capacity for reversible deformity?
  5. Where do RBCs mature?
    bone marrow
  6. What is the lifespan of a RBC?
    120 days
  7. Where is erythropoeitin produced?
    • peritubular kidney cells
    • hepatic Kupffer cells
  8. What are the two main growth factors for RBCs?
    • erythropoietin
    • Stem cell factor (Steel factor)
  9. What does the spleen do?
    • stores up to 300 ml of blood
    • phagocytize old or damaged RBCs
    • can constrict and release up to 200 mls of blood if there is an injury
  10. What are the 2 types of bone marrow?
    • red
    • yellow
  11. Which bone marrow is active and myeloid?
    red marrow
  12. Which bone marrow is inactive and replaced with fat?
    yellow marrow
  13. Which bone marrow is found in adults, and in flat bones like the pelvis, sternum, ribs, jaw and vertebrae?
    red marrow
  14. What type of cells can differentiate into fibroblasts, adipocytes, or osteoblasts?
    mesenchymal stem cells
  15. What type of cells secrete cytokines?
  16. What are the 2 cytokines that a fibroblast can secrete?
    • M-CSF (macrophage colony stimulating factor)
    • GM-CSF (granulocyte-macrophage colony stim factor)
  17. What do adipocytes secrete?
  18. What does leption do and where does it come from?
    • stimulates mesenchymal cells to differentiate into osteoblasts
    • comes from adipocytes
  19. What are multipotent stem cells in the marrow?
    • intermediate groups of stem cells
    • partially differentiated, but still have the ability to differentiate into different cell types
  20. What is the steel factor?
    a stem cell factor from the stromal cells that help support bone marrow
  21. What is CSF (colony stimulating factor)?
    helps initiate differentiation/maturation
  22. What does "-blast" mean when talking about hematopoiesis?
    immature cell
  23. What can hematopoiesis be accelerated by?
    • erythropoietin
    • faster differentiation of progenitor cells
    • faster proliferation of stem cells into progenitor cells
  24. T/F: epo is secreted more by the kidneys than the liver.
    true dat
  25. What converts yellow marrow to red marrow?
  26. What type of patients would benefit from receiving epo?
    renal failure
  27. What events might trigger the production of more RBCs?
    • decreased RBCs (maybe injury)
    • decreased hemoglobin synthesis
    • decreased blood flow
    • hemorrhage
    • increased oxygen comsumption by the tissues
  28. What is the sequence of a developing RBC? (erythropoiesis)
    • erythroid progenitor
    • committed proerythroblast
    • normoblast (nucleus shrinks)
    • reticulocyte (cell leaves marrow and enters blood stream)
    • erythrocyte (cell fully mature; final shape and size; hemoglobin synthesis stops)
  29. What is the definition of anemia?
    • reduced RBCs
    • reduced quality/quantity of hemoglobin
  30. What are the main causes of anemia?
    • acute blood loss
    • chronic blood loss
    • impaired erythrocyte production
    • increased RBC destruction
    • combo of any of above
  31. What does "cytic" mean?
  32. What does "chromic" refer to?
    hemoglobin concentration
  33. What does anisocytosis mean?
    assuming various sizes
  34. What does poikilocytosis mean?
    assuming various shapes
  35. If compensatory mechanisms to fix anemia fail, what signs and symptoms do you see?
    • dyspnea (shortness of breath)
    • palpitation
    • dizziness
    • fatigue
    • muscle pain (claudication)
    • cardiac angina
    • pail skin and nailbeds
    • low grade fever
    • if acute like with a hemorrhage, vasoconstriction and activate renin-ang response
  36. How might the body compensate if there was blood loss?
    • you would see a shift of fluid from interstitial into vascular space
    • dilutes blood cells and thins blood, but helps maintain volume
  37. How does the heart respond to blood loss?
    • increase cardiac output
    • hypoxemia: systemic arterial dilation- reduces afterload
    • increase heart rate via sympathetic nervous system
  38. How does the respiratory system respond to blood loss?
    • rate increases in rate and depth
    • increase release of oxygen
  39. Why would you get a low grade fever from blood loss?
    b/c ischemic tissues release pyrogens
  40. What is macrocytic normochromic anemia?
    • unusually large stem cells in marrow that mature into unusually large RBCs
    • hemoglobin is normal
  41. What is the most common form of macrocytic normochromic anemia?
    PA (pernicious anemia)
  42. What are two byproducts of RBC destruction?
    • indirect bilirubin (from heme breakdown)
    • lactic dehydrogenase
  43. What % of nursing home patients have anemia?
  44. what are the causes of macrocytic normochromic anemia?
    • decreased precursor DNA synthesis
    • (genetic disorder of DNA synthesis)
    • congenital or acquired deficiency of intrinsic factor (IF)
    • DNA does not clump normally
    • RNA messed up--- unequal growth and development of cytoplasm and nucleus
  45. How do megaloblastic RBCs cause anemia?
    they are phagocytosed and there is a greater chance of them dying b/c they are so large = anemia
  46. What is the main cause of pernicious anemia?
    vitamin B12 deficient
  47. What group of people are more likely to have pernicious anemia?
    vegetarians b/c they don't eat meat, don't get B12
  48. What is a disease that might cause pernicious anemia?
    chronic atrophic gastritis (Type A)
  49. who is at risk for chronic atrophic gastritis and therefore pernicious anemia?
    • over age 50
    • northern europeans
    • blacks
    • hispanics
    • females
  50. What is the cause of chronic atrophic gastritis?
    • lack of IF (intrinsic factor) from gastric parietal cells
    • =pernicious anemia
  51. Why do you need IF and B12 to prevent anemia?
    b/c B12 and IF bind and travel to the ileum, where they are absorbed and the blood needs vitamin B12
  52. What disease is a precursor to pernicious anemia, could be autoimmune, may show in family history, creates antibodies against parietal cells, and may be associated with achlorhydria and lowered digestive enzymes?
    chronic atrophic gastritis type A
  53. What are the major risks for getting pernicious anemia?
    • family history
    • female
    • diet/habits (alcohol, smoking, hot tea)
    • gastrectomy
    • H. pylori infection
    • PPI use
  54. Which anemia has a very slow onset and is hard to diagnose?
    pernicious anemia
  55. what are some signs and symptoms of pernicious anemia?
    • usually occur later in onset
    • atrophic glossitis: sore, beefy tongue
    • irreversible demyelination: loss of position or vibration sensation
    • ataxia
    • spasticity
    • depression
  56. What is the treatment for pernicious anemia?
    B12 injections once a month or high oral doses
  57. What is microcytic hypochromic anemia?
    • small and pale RBCs
    • low hemoglobin concentration
  58. What are the 3 main causes of microcytic hypochromic anemia?
    • disorder of iron metabolism
    • disorder of porphyrin and heme synthesis
    • disorder of globin synthesis
  59. What is the most common type of microcytic hypochromic anemia?
    iron deficiency anemia (IDA)
  60. What is the most common type of anemia in the world?
  61. What are the causes of IDA?
    • malnutrition and blood loss due to gastritis or ulcers
    • lead poisoning
    • NSAIDs
    • diet
    • eating disorders
    • pica (eating lead or minerals)
  62. What disease affects 9% of infants in the US?
  63. What is a major effect that IDA has on the body?
    • can cause irreversible cognitive impairment
    • parasites increase blood loss
  64. What is the treatment for IDA?
    • oral iron replacement
    • IM iron dextran
  65. How do you diagnose IDA?
    • test hemoglobin concentrations in blood
    • serum ferritin
    • check bone marrow iron stores
  66. What are the signs and symptoms of IDA?
    • can be gradual
    • immune impairment
    • brittle, spoon-shaped or concave nails
    • red, sore tongue
    • dry mouth corners: angular stomatitis
    • difficulty swallowing due to web in esophagus
    • neuronal dysfunction
    • irritable
    • HA
    • confusion
    • memory loss
  67. What is the first line of defense?
    • innate immunity
    • (physical, biochemical, mechanical barriers)
  68. What is the second line of defense?
  69. What is the third line of defense?
    acquired immunity (adaptive)
  70. What are some of the physical and mechanical barriers to infection?
    • skin
    • mucus membranes
    • mucus secretions
    • lower temp of extremities
    • directly expelled (cilia in lungs, coughing, sneezing, vomiting, urinating)
  71. What are some biochemical barriers to infection?
    • mucus
    • saliva
    • tears
    • earwax
    • sebaceous glands secrete fatty acids and lactic acids
    • sweat, tears and saliva contain lysozymes that attack the cell walls of gram + bacteria
    • skin is acidic
    • epithelial derived chemicals like defensins and cathelicidins
  72. What is the structure of cathelicidins?
    • linear alpha helix
    • amphipathic (have both hydrophillic and hydrophobic parts)
  73. Where are cathelicidins stored?
    mast cells, epithelial cells, and neutrophils
  74. How do cathelicidins kill bacteria?
    they are able to insert and disrupt membranes because bacteria have cholesterol-free membranes
  75. What type of bacteria can cathelicidins kill?
    gram + and -
  76. What can defensins do that cathelicidins cannot?
    they can activate cells of both the innate and immune system (cathelicidins= only innate)
  77. What is the structure of defensins?
    triple stranded beta sheet
  78. Where are defensins stored?
    mast cells, neutrophils, epithelial cells, monocytes
  79. T/F: cathelicidins and defensins function in a similar manner.
  80. Where is a specific site that was given in class where neutrophils secrete cathelicidins to eradicate bacteria?
    urinary tract
  81. Which epithelial-derived chemicals specifically protect against respiratory infections?
  82. What are collectins made of?
  83. Where are collectins made?
    in the lung
  84. What are the different types of collectins?
    • *mannose binding lectin (MBL)
    • *surfactant proteins A-D
    • resistins
    • BPIs
    • antimicrobial lectins
  85. Which specific collectins are part of the complement system (lectin pathway)?
    mannose binding lectin
  86. What are some of the normal endogenous flora in the GI tract?
    • indols
    • phenols
    • ammonia
  87. What are the triggers for an inflammatory response (innate immunity)?
    • infection
    • ionizing radiation
    • extreme temperatures
    • mechanical damage
    • genetic defects
    • nutritional deprivation
    • immune defects
    • chemical agents
    • oxygen deprivation (ischemia)
  88. What are the 3 parts of the plasma proteins systems?
    • complement system
    • clotting system
    • kinin system
  89. What are the cellular mediators of an inflammatory response?
    • cellular receptors
    • mast cells
    • phagocytes
    • monocytes/macrophages
    • eosinophils
    • natural killer cells
  90. During an inflammatory response, what cellular products are released?
    • cytokines (interleukins, interferons, TNF alpha)
    • chemokines (chemotaxis)
  91. These soluble factors contribute to the regulation of innate or acquired resistance by affecting other neighboring cells and can be pro or anti-inflammatory in nature?
    • cytokines
    • chemokines
  92. The actions of these cellular products are pleiotropic?
    • chemokines
    • cytokines
  93. What are the four visible changes that occur during inflammation?
    • redness
    • heat
    • swelling
    • pain
  94. What are the four chemical mediators of inflammation?
    • histamine
    • bradykinin
    • leukotrienes
    • prostaglandins
  95. What is the overall combined function of the four chemical mediators of inflammation (h, b, l, p)?
    stimulate endothelial cells that line capillaries and veins to retract, creating spaces for cells and plasma to enter tissue
  96. During inflammation, WBCs, plasma proteins, and biochemical mediators at the site of injury work together to do what?
    • cause localized clotting & WBC action to prevent the spread to healthy tissues
    • fluids dilute bacterial toxins and cell debris
    • WBCs attack bacteria
    • adaptive immune system interacts
    • lymphatic drainage by B and T cell activation
    • healing and repair
  97. What are the four main advantages of the complement cascade?
    • it can directly kill pathogens (lysis)
    • causes opsonization (tagging)
    • has anaphylatoxic activity (mast cell degranulation)
    • causes leukocyte chemotaxis (calls in WBCs)
  98. How is the 'classical' complement pathway activated?
    by antibody + antigen
  99. How is the 'lectin' complement pathway activated?
    by bacterial carbohydrates
  100. How is the 'alternative' complement pathway activated?
    by gram - bacterial and fungal cell wall polysaccharides
  101. In summary, what are the four functions of the classical, lectin, and alternative complement pathways?
    • WBC chemotaxis
    • opsonization
    • pathogen lysis
    • anaphylatoxic mast cell degranulation
  102. What molecule is the major player in the alternative complement pathway?
  103. What molecule is the major player in the lectin complement pathway?
    mannose binding lectin
  104. What is the most important result of complement activation?
    the production of small fragments (C4, 2, 3, 5)- small and soluble
  105. What does C2b do?
    • acts on smooth muscle
    • causes vasodilation and increases vascular permeability
  106. What does C3b do?
    • opsonin
    • tags pathogens for destruction by WBCs (primary neutrophils and macrophages)
  107. What does C5a do?
    major chemotactic factor for neutrophils (after one amino acid is removed so it is not anaphylatoxic anymore)
  108. What do both C3a and C5a do?
    • anaphylatoxins
    • induce rapid mast cell degranulation and histamine release
    • vasodilation and increased vascular permeability
    • early part of immune response
  109. What is the clotting cascade's role in inflammation?
    • prevent the spread of infection
    • trap microorganisms and foreign bodies at the site of greatest inflammation
    • form a clot to stop bleeding
    • provide framework for repair and healing
  110. What are the 2 pathways to clotting?
    • extrinsic
    • intrinsic
  111. Where do the intrinsic and extrinsic clotting pathways converge?
    factor ten (X)
  112. What is another name for factor XII?
    hageman factor
  113. What initiates the intrinsic clotting path?
    • hageman factor (XII)
    • blood trauma or collagen
  114. What initiates the extrinsic clotting path?
    • TF (tissue factor)
    • tissue damage
  115. What common ion is needed for proper clotting?
  116. What is the basic pathway in clotting scheme? (start with factor X)
    • Factor X (convergence)
    • Prothrombin
    • Thrombin
    • Fibrinogen
    • Fibrin
    • Clot
  117. In general, what ate the clotting cascasdes (kinin and clotting) triggered by?
    • collagen
    • poteinases
    • kallikrein
    • plasmin
    • bacterial endotoxins and other products
  118. Just like in the complement system, fragments contribute to inflammatio, what are they?
    fibrinopeptides A and B
  119. What do fibrinopeptides A and B do, when are they made?
    • released from fibrinogen when fibrin is made
    • chemotactic for neutrophils
    • increase vascular perm
  120. What is the main role of the kinin system?
    to activate and assist inflammatory cells (and interact with clotting system)
  121. LIke the clotting system, what factor begins the kinin system?
    hageman factor
  122. What does bradykinin do?
    • vasodilates
    • induces pain
    • smooth muscle contraction
    • increases vascular perm
    • may increase leukocyte chemotaxis
  123. What is the general cascade of the kinin system (starting with factor XII)?
    • hageman factor (XII)
    • collagen or other activators
    • prekallikrein activator converts prekallikrein to kallikrein
    • kallikrein converts kininogen into bradykinin
    • bradykinin causes vasodilation, pain, perm
  124. What factor activates both the kinin and clotting cascades?
    Hageman factor (XII)
  125. What are some sources of kinins?
    • kinin system
    • tissue kallikreins in sweat, saliva, tears, urine, feces
    • kallidin
  126. T/F: kinis are slowly degraded.
    false; rapid
  127. Name the cellular receptors of the inflammatory response.
    PRRs (pattern recognition receptors)
  128. T/F: PRRs are part of our innate resistance and are programmed into our DNA.
  129. What do PRRs recognize?
    • PAMPs (pathogen associated molecular patterns)
    • byproducts of cellular damage
  130. Where do we find PRRs?
    • on cells at the interface of self and environment (skin, respiratory tract, GI tract, GU-genitourinary tract)
    • some are secreted too
  131. T/F: PRRs are less specific than antibodies
  132. What are some of the cellular PRRs?
    • toll-like receptors (TLR)
    • complement receptors
    • scavenger receptors
    • glucan
    • mannose
  133. What is one of the secreted PRRs?
    mannose-binding lectin of the complement system
  134. Where might you find toll-like receptors (subtype of PRRs)?
    • on the cell surfaces of neutrophils, macrophages, dendritic cells, epithelial cells,some lymphocytes
    • intracellularly found also: to detect pathogen RNA/DNA
  135. Where are the target sites for toll-like receptors found?
    • fungi
    • bacteria
    • yeast
    • viruses
  136. Where would you find complement receptors (subtype of PRRs)?
    • WBCs
    • platelets
    • RBCs
    • some epithelial cells
  137. What are the 3 complement receptors (subtype of PRR)?
    • CR1
    • CR2
    • CR3 and 4
  138. What does CR1 do?
    binds to C4b, C3b, and breakdown products of C3b
  139. What does CR2 do?
    • found on B lymphocytes
    • recognizes C3b breakdown products and interferon alpha
  140. What does CR3 and CR4 do?
    • they are integrins
    • they recognize C3b breakdown products
    • facilitate phagocytosis by neutrophils and monocytes/macrophages
    • CR3 is found on platelets
  141. Where would you find scavenger receptors (subtype of PRR)?
    on macrophages
  142. What is the function of a scavenger receptor?
    • phagocytosis
    • helps to recognize bacterial pathogens, damaged cells, altered soluble lipoproteins associated with vascular damage like HDL, acetylated LDL or oxidized LDL
  143. What is a specific example of a scavenger receptor? What does it do?
    • SR-PSOX
    • recognizes phosphatidylserine (PS), which is externalized with senescence of RBCs and cellular apoptosis
    • the macrophages that scavenger receptors are found on identify and remove dying RBCs or apoptotic cells
  144. Where are mast cells found?
    • loose connective tissue close to blood vessels
    • in skin
    • lining GI tract
    • lining respiratory tract
  145. If you are looking for mast cells in a blood sample (CBC), will you find any?
    no, you will have to take a tissue sample
  146. What are the 2 effects of mast cells on inflammation?
    • degranulation
    • synthesis of lipid-derived inflammatory mediators
    • also, initiates an allergic response
  147. What are the stimuli for mast cell degranulation?
    • physical injury (heat, trauma, UV light, X-rays)
    • chemical agents (toxin, venom, proteolytic enzymes, antimicrobial peptides)
    • immune reactions (anaphylatoxins, antibodies)
    • activation of toll-like receptors by bacteria or viruses
  148. What substances are released from mast cells immediately following degranulation?
    • tryptase
    • cytokines (TNFalpha, interleukin 3)
    • histamine
    • chemotactic factors (neutrophil chemotactic factors, eosinophil chemotactic factors aka ECF-A)
  149. Is histamine pro or anti inflammatory?
  150. What is histamine?
    • a substance released from mast cells
    • a vasoactive amine
    • pro-inflamm
  151. What is the function of histamine?
    • *causes increased blood flow to the microcirculation by:
    • temporary rapid constriction of large vessels
    • dilation of post-capillary veins
    • *increases vascular permeability: retraction of endothelial cells
  152. What is the function of the H1 receptor?
    • pro-inflammatory
    • found on smooth muscle cells, especially bronchi
    • bronchoconstriction
  153. What is the function of the H2 receptor?
    • anti-inflammatory
    • suppress WBC function
    • found in the stomach on parietal cells
    • stimulate acid secretion
  154. What different mediators of inflammation do mast cells synthesize?
    • factors derived from plasma membrane lipids (leukotrienes and prostaglandins)
    • cytokines
    • factors that stimulate growth and angiogenesis
  155. What do all of the plasma membrane lipid derived mediators of inflammation stem from (the leukotrienes, prostaglandins, platelet act. factor)?
  156. What major chemical do leukotrienes stem from?
    arachidonic acid
  157. What major chemical do prostaglandins stem from?
    • arachidonic acid
    • *cyclooxygenase (COX)
  158. What major chemical does PAF (platelet activating factor) stem from?
  159. Where do leukotrienes originate?
    from mast cells
  160. What molecule do leukotrienes come from?
    • arachidonic acid
    • acidic, sulfur-containing lipids
  161. T/F: leukotrienes have a similar action to histamine.
  162. What do leukotrienes do?
    • smooth muscle contraction
    • increase vascular perm
    • chemotaxis of neutrophils and eosinophils
    • may be important for later stages of inflammation
  163. What 2 mediators of inflammation start from arachidonic acid?
    • leukotrienes
    • prostaglandins
  164. What 2 drugs block prostaglandin synthesis?
    • aspirin
    • NSAIDs
  165. Where do prostaglandins come from?
    mast cells
  166. What do prostaglandins do?
    • similar to histamine
    • smooth muscle contraction
    • increase vasc. perm.
    • chemotaxis of neutrophils
    • pain
    • may inhibit some aspects of inflammation
  167. T/F: prostaglandins have a similar action to histamine.
  168. Where does PAF come from?
    • mast cells
    • neutrophils
    • monocytes
    • endothelial cells
    • platelets
  169. What type of molecule is PAF?
    a lipid
  170. What does PAF do?
    • similar to leukotrienes
    • vascular perm.
    • leukocyte adhesion to endothelial cells
    • platelet activation
  171. What are 'bands' or 'stabs'?
    immature neutrophils
  172. What are 'segs' or 'polys'?
    polymorphonuclear neutrophils (mature)
  173. T/F: it is normal to have a large % of bands in a CBC.
    false; should only have 3-5%
  174. Where would you find phagocytes?
    • circulating in the blood
    • more along vessel walls, but RBCs are in the center
  175. Chemical mediators of inflammation cause expression of _____molecules on WBCs and endothelial cells so that they can move to the site of inflammation (phagocytes)?
  176. What is diapedesis?
    phagocytes emigrating through opened endothelial junctions in vessels
  177. What substance do endothelial cells release during phagocytosis?
    nitric oxide
  178. What are the 3 classes of adhesion molecules involved in phagocytosis?
    • selectins
    • integrins
    • CAMs
  179. Which adhesion molecule is involved in the rolling of phagocytes and have a low affinity?
  180. Which adhesion molecule(s) are involved in margination, diapedesis, and firm attachment during phagocytosis?
    • integrins
    • CAMs
  181. What are some of the many chemotactic factors involved in phagocytosis?
    • bacterial products
    • complement fragments (C3a and C5a)
    • kallikrein
    • plasminogen activator
    • fibrin degradation products
    • chemokines
    • mast cell factors (attact eosinophils and neutrophils)
    • on-site neutrophil factors (attract monocytes)
  182. What are the 5 steps of phagocytosis?
    • 1. opsonization via C3b or antibody
    • recognition of target
    • adherence of phagocyte to the target
    • 2. engulfment
    • 3. phagosome is formed
    • 4. fusion with lysosome
    • 5. destroy target
  183. How do phagocytes kill/destroy the target once it is in the cell?
    • respiratory burst: oxygen-dependent killing mechanism
    • uses superoxide and ROS and H2O2 to kill
  184. Is phagocytosis specific or non-specific?
  185. When are bleaches formed?
    during non-specific phagocytosis (destruction)
  186. What is the purpose of creating reactive oxygen species and bleaches during phagocytic destruction?
    • to kill pathogen
    • creates an acidic environment
  187. What are the 2 types of cationic proteins that attack cell membranes during phagocytosis?
    • cathelicidins
    • defensins
  188. What are the 2 types of enzymes that attack mucopeptides in the microbe wall during phagocytosis?
    • lysozyme
    • elastase
  189. How does inhibition of bacterial growth occur during phagocytosis?
    lactoferrin binding of iron
  190. What 2 acids are formed during phagocytosis?
    • hydrobromous acid
    • hypochlorous acid
  191. What can protect against some of the spilled enzymes that come from a phagocyte dying?
    • alpha1 antitrypsin: an endogenous plasma protein
    • made in the liver
  192. What are all of the types of WBCs?
    • neutrophils
    • monocytes/macrophages
    • eosinophils
    • natural killers
  193. Which type of WBC cannot divide so it doesn't last long?
  194. T/f: neutrophils are aka granulocytes.
  195. Which type of WBC has a segmented or banded nucleus?
  196. Which cell is an early phagocyte in the inflammatory response?
  197. which cell arrives within 6-12 hours of inflammation, but doesn't last long?
  198. What specific chemotactic signals call in neutrophils (3)?
    • some bacterial proteins
    • C3a and C5a
    • mast cell neutrophil chem factor
  199. What do neutrophils do?
    phagocytose bacteria, dead cells, and debris
  200. Which WBCs are killed by the acidic pH of a lesion?
  201. What do monocytes and macrophages do?
    similar to neutrophils, but last much longer and arrive later
  202. What is the largest normal blood cell found?
  203. What does the nucleus of a monocyte look like?
    often indented or horseshoe shaped
  204. Where are monocytes stored?
    bone marrow
  205. When will monocytes arrive after inflammation?
    within 24 hours, usually by 3-7 days
  206. Which cells develop into macrophages?
  207. _____ are phagocytic WBCs that can divide in the acidic environment of inflammation?
  208. What releases the chemotactic factor to call in macrophages?
  209. What are the 4 tissue macrophages?
    • liver: Kupffer cells
    • brain: microglia
    • lungs: alveolar macrophages
    • tissue: tissue macros
  210. What type of WBC can be parasitized by bacteria?
  211. What are some bacteria that can live in macrophages?
    • TB
    • mycobacterium leprae
    • typhoid fever
    • brucella abortus
    • listeria
  212. Once activated, what happens to macrophages?
    • increase in size
    • increase plasma membrane area
    • increase glucose metab
    • increase # of lysosomes
    • increase phagocytic activity
    • release factors to stimulate other inflammatory cells
    • can activate the adaptive immune system
  213. T/F: neutrophils can activate the adaptive immune system.
    false; only macros can
  214. What type of factors do macrophages release to stimulate other inflammatory cells?
    G-CSF (granulocyte-colony stimulating factor)
  215. While monocytes are found in the blood, where are macrophages found (where do monocytes become macros)?
    in tissues
  216. If someone's eosinophils are high, what are the 2 possible issues?
    • allergic response
    • parasite problem
  217. Which WBC is only mildly phagocytic?
  218. Which WBCs release their granules into the extracellular space?
  219. Where are eosinophils found?
    • respiratory
    • intestinal
    • genitourinary
  220. What is the main function of eosinophils?
    • attack parasites
    • help regulate vascular mediators from mast cells (keep inflamm response under control)
  221. What cells can help balance out an allergic response? (not always a bad sign to have large # of)?
  222. Which cells secrete ECF-A (eosinophil chemo factor)?
    mast cells
  223. How does an eosinophil calm an allergic response?
    it has a lysosomal enzyme that degrades vasoactive molecules
  224. What cells get rid of viruses and some cancer cells?
    natural killers
  225. what is the function of NK cells (natural killer)?
    • recognize and eliminate:
    • viruses
    • abnormal host cells (cancer)
    • circulatory > tissue
  226. what are some of the receptors on an NK cell?
    • toll-like recep
    • activating recep
    • inhibiting recep
  227. What are platelets aka?
  228. Where do platelets come from?
    megakaryocytes (huge cells in the marrow)
  229. How do we get rid of old platelets?
    • macrophages
    • about 50% removed by macros in the spleen
  230. T/F: platelets have nuclei.
  231. T/F: platelets cannot reproduce.
  232. What prevents platelets from clotting all the time?
    glycoprotein coat
  233. What cellular machinery do platelets still have even though they can't reproduce?
    • ER
    • golgi (store calcium)
    • mitochondria (make ATP and ADP)
    • enzymes that synthesize PGs
    • have actin, myosin, and thrombosthenin
  234. The membranes of platelets are high in phospholipids that activate what 3 cells?
    • vascular endothelial cells
    • fibroblasts
    • vascular smooth muscle cells
  235. What happens when platelets contact damaged vessels or collagen?
    • calcium influx
    • swell
    • assume irregular forms with psuedopods
    • become sticky
    • adhere to collagen and von Willebrand factor
    • contractions force granule release: ADP and thromboxane A2 (these factors activate other platelets, which adhere to the original platelet)
  236. What is von Willebrand factor related to?
  237. What are all of the cytokines (broad category)?
    • interleukins
    • interferons
    • TNF
    • chemokines
    • CSF
    • classical growth factors
  238. What are the main functions of cytokines?
    • pro/anti inflammatory
    • pleotropic
    • detection
    • recruitment
    • repair
    • regrowth
    • clean-up
  239. What is the general structure of most cytokines?
    soluble peptides
  240. where do you find cytokines?
  241. what are the targets (and sources) of cytokines?
    • leukocytes
    • epithelia
    • fibroblasts
  242. What are the triggers of cytokines?
    • debris
    • cytokines
    • bacteria
    • etc
  243. What are the 5 main functional classes of cytokines?
    • 1. regulate lymphocyte fxn
    • 2. act on innate immunity
    • 3. activate inflammatory cells
    • 4. stimulate hematopoiesis
    • 5. chemotactic for leukocytes
  244. Which molecules can fxn as autocrine, paracrine, or endocrine factors?
  245. What are some things that cytokines release?
    • IL-2
    • TGF beta
    • TNF
    • IL-1
    • interferon gamma
    • macrophages
    • IL-12
    • GM-CSF
  246. ________ are low MW peptides that can be soluble or bound to extracellular glycosaminoglycan carbohydrates?
  247. What are the general fxns of interleukins?
    • pro/anti inflammatory
    • enhance acquired immune response to pathogens and other foreign substances
    • alters adhesion molecules
    • chemotaxis
    • leukocyte proliferation in marrow, some are growth factors
  248. Where do interleukins come from?
    • in response to microorganisms (PAMPs) or products of inflammation
    • macrophages
    • lymphocytes
    • fibroblasts
    • endothelial cells
  249. What is the major difference between interleukin 1 and 10?
    • IL1 is pro inflammatory
    • IL10 is anti inflammatory
    • IL1 comes from macrophages and neutrophils
    • IL10 comes from lymphocytes
    • IL1 produces fever (is an endogenous pyrogen)
  250. What is the function of the interferons?
    • protect uninfected cells against viruses
    • cause uninfected cells to make antiviral proteins
    • modulate the inflammatory response
  251. What type of cytokines are species-specific but not virus-specific?
  252. What is the main target of an interferon?
    uninfected cells
  253. Where do interferons come from?
    • virus infected cells
    • macrophages = IFN alpha IFN beta
    • T-cells = IFN gamma
  254. The release of interferons is triggered by what?
    viral double stranded RNA
  255. What are some of the "other" cytokines?
    TNF: pro-inflammatory
  256. What releases TNF?
    • macrophages
    • mast cells
  257. What type of receptors on macrophages recognize PAMPs and release TNF (a cytokine)?
    toll-like receptors
  258. Which disease is a manifestation of the cytokine TNF?
    Crohn disease
  259. What are the fxns of TNF?
    • enhance adhesion molecule expression
    • induce chemokines
    • endogenous pyrogen
    • acts on liver to increase synthesis of pro-inflammatory proteins
    • prolonged elevation: muscle wasting, thrombosis
  260. What drug is an interferon cytokine?
    Interferon B1 (Betaseron) for MS
  261. What drug is a TNF cytokine?
    Infliximab (Remicade) for Crohn disease
  262. What types of cells release chemokines?
    • macrophages
    • fibroblasts
    • endothelial cells
  263. What triggers the release of chemokines?
    • pro-inflamm cytokines
    • macrophages
  264. What is the general fxn of chemokines?
    • pro-inflammatory
    • call in WBCs (leukocyte chemotaxis)
    • induce leukocyte adhesion
  265. What are the targets of chemokines?
    • monocytes
    • lymphocytes
    • eosinophils
    • neutrophils
  266. What is the difference b/w exudate and transudate?
    transudate does not contain any cells or proteins; filtrate; usually clear
  267. What are the different types of exudate?
    • serous
    • fibrinous
    • purulent (suppurative)
    • hemorrhagic
  268. Which type of exudate usually has a lot of WBCs in it?
    purulent (pus)
  269. Which type of exudate is thick and clotted?
  270. Which type of exudate has RBCs in it?
  271. What are the 3 systemic manifestations of acute inflammation?
    • fever
    • leukocytosis
    • plasma protein synthesis
  272. Which interleukin is an endogenous pyrogen?
    • IL-1
    • causes fever
  273. When is IL1 released?
    • after phagocytosis
    • after exposure to bacterial endotoxins
    • after exposure to antigen-antibody complexes
  274. What is an advantage of fever?
    kills bacteria: syphillis and gonococcal urethritis
  275. What is a disadvantage of fever?
    • enhances responses to endotoxins
    • may cause seizures in kids
  276. What is leukocytosis?
    an increase in the # of circulating leukocytes (especially neutrophils)
  277. What/where is leukocytosis triggered by?
    • in the marrow
    • C3a
    • C-CSF
  278. In leukocytosis, what happens to the neutrophils in a CBC?
    left shift to more bands (which are immature)
  279. What are APRs?
    acute phase reactants
  280. What are APRs triggered by?
    IL1 and IL6
  281. During acute inflammation, plasma protein synthesis stimulates the liver to increase its production of these?
    acute phase proteins (reactants)
  282. When APRs are increased with inflammation, this leads to what kind of sed rate?
    increased RBC sed rate = more inflammation both acutely and chronically
  283. What does a faster sed rate mean?
    more inflammation
  284. What are some of the APRs released during inflammation?
    • coagulation components (Fibrinogen)
    • protease inhibitors (Alpha 1 Antitrypsin)
    • transport proteins (Ceruloplasmin)
    • complement
    • CRP (C-reactive protein)
  285. What are some other signs and symptoms of inflammation (other than APRs, redness, pain, swelling, heat)?
    • somnolence
    • malaise
    • anorexia
    • muscle aches
    • sickness behaviors
  286. What is SIRS?
    systemic inflammatory response syndrome
  287. What characterizes SIRS?
    • hyper metabolic changes
    • must have 2 or more of following: temp above 100.4 or below 96.8, HR above 90bpm, RR above 20, WBCs above 12000 or below 4000, more than 10% immature bands
  288. What is MODS?
    • what happens if SIRS goes untreated
    • Multiple Organ Dysfunction Syndrome
  289. When would you move from acute inflammation to chronic?
    after more than 2 weeks inflamm
  290. what causes chronic inflammation?
    • unresolved acute inflamm
    • persistent bacterial contamination of a wound or object
    • pus and suppuration
    • can arise without previous acute inflammation
    • persistent toxins, chemicals, or physical irritants
  291. What organisms typically cause chronic inflammation b/c they resist clearance?
    • TB
    • syphillis
    • leprosy
    • brucellosis
  292. How does chronic inflammation usually present itself?
    • granulomas
    • dense infiltrations of lymphocytes and macrophages
  293. What is a granuloma?
    a walled off organism or object
  294. When do granulomas form (specifically)?
    when neutrophils or macrophages can't destroy the pathogen
  295. What are some common pathogens that lead to granulomas?
    • brucella
    • listeria
    • fungi: histoplasmosis
    • parasite: leishmaniasis
    • rheumatoid arthritis
  296. What structure can be encapsulated by collagen and could also become calcified?
  297. The center of this may be necrotic and caseous?
  298. The inside of a granuloma contains ______, but is surrounded by________?
    • macrophages inside
    • lymphocytes surround
  299. How long does resolution and repair usually take?
    weeks to years
  300. What is resolution?
    • injured tissue is replaced with tissue of normal struction and fxn
    • only happens if injured tissue is capable of regeneration
  301. What is repair?
    • injured tissue is replaced with SCAR tissue (collagen)
    • not normal fxn
    • occurs when damage is too extensive
    • happens when injured tissue is NOT capable of regeneration
  302. Both resolution and repair begin with what event?
    • phagocytosis
    • 'debridement'
  303. What are the 2 types of healing?
    • primary intension
    • secondary intension
  304. What is primary intension?
    • clean incision
    • close apposition of edges of cut
    • minimal tissue loss
    • little sealing or shrinkage required for healing
  305. What is secondary intension?
    • ulcer like
    • pressure sores
    • slower to heal
    • more tissue damage to fill in
  306. What factors complicate wound healing in neonates and elderly?
    • neonates: deficient in complement and alternative paths, can cause sepsis and meningitis, deficient in collectins, have cutaneous abcesses which harbor staph and candidiasis, impaired chemotaxis
    • elderly: age, chronic illness, medications, decreased fat, decreased capillaries, decreased innate immunity, decreased fibroblast proliferation
  307. What is dehiscence?
    • sutured wound pull apart = gross
    • usually 5-12 days later
    • = sepsis
    • caused by strain, obesity, increased serous drainage
  308. What is a keloid?
    • an overproduction of collagen during wound healing
    • raised scar that goes out of the boundaries of the injury
    • doesn't go away
    • most common in blacks
  309. What are the steps of resolution and repair?
    • reconstruction
    • maturation
  310. This begins within 3-4 days, lasts ~ 2 weeks, the tissue undergoes epithelialization, fibroblasts proliferate, collagen is made, contraction happens, and cells differentiate?
  311. This begins after several weeks, can last up to 2 years, and has continued differentiation, scar formation and remodeling?
  312. What factors are secreted by macrophages during reconstruction?
    • TGF beta (transforming growth factor beta): stimulates fibroblasts, which secrete procollagen
    • Angiogenesis Factors: VEGF(vascular endothelial growth factor), FGF-2 (fibroblast growth factor)
    • Matrix Metalloproteinases (MMPs): degrade and remodel extracellular matrix proteins at injury (collagen and fibrin)
  313. What are the more specific steps of reconstruction?
    • Seal wound with blood clot/platelet plug
    • Dissolve clot, replace with normal tissue or a scar
    • Granulation Tissue
    • Secrete Factors
    • Epithelialization
    • Fibroblasts
    • Wound contraction
  314. What happens during epithelialization?
    • epithelials migrate underneath the scab
    • MMPs unravel collagen as they migrate
    • differentiate into layers
  315. T/F: epithelialization occurs faster if the wound is kept dry.
    false; want it wet
  316. What synthesize and secrete procollagen?
  317. What is the most abundant protein in the body?
  318. what are the cofactors needed for fibroblasts to make collagen?
    • vitamin C
    • oxygen
    • iron
  319. what happens during wound contraction?
    myofibroblasts make parallel fibers that connect smooth muscle
  320. What is the last step of reconstruction?
    wound contraction
  321. What step of wound healing is especially crucial/necessary for secondary intention?
    wound contraction
  322. During what step of res and repair do capillaries disappear until the scar is avascular?
  323. Where does compensatory hyperplasia (wound maturation) naturally occur?
    • liver
    • epithelium
    • marrow
  324. What are some problems that can occur if wound healing is dysfunctional?
    • contractures: burns, cirrhosis of liver, ulcers, esophagus
    • fibrous adhesions: can cause bands, problem in GI, pleural, pericardial cavities, strangulations
    • hemorrhage: impair healing, allow bacteria, add space to fill
    • sepsis: may require surgical debridement or absorbent dressings
  325. What are some contributing factors that would cause dysfunctional wound healing?
    • hypovolemia
    • malnutrition
    • diabetes (glucose, small vessel diseases, glycosylated Hb)
    • hypoproteinemia
    • NSAIDs
  326. Compared to innate immunity, adaptive immunity is....?
    • slower acting
    • very long lived in body
    • more specific
  327. What are the molecules that recognize an antigen?
  328. What is another name for antibody?
  329. What four things determie the immunogenicity of an antigen?
    • foreignness
    • size
    • chemical complexity
    • quantity
  330. What are haptens?
    • small molecules bound to carriers that can be antigens
    • poison ivy
    • penicillins
  331. What are adjuvants?
    • a vehicle that you put vaccines in
    • increases the immunogenicity of vaccines
  332. What are the 3 molecules that can recognize antigens?
    • circulating antibodies
    • BCRs (antigen receptors on B lymphocytes)
    • TCRs (antigen receptors on T lymphocytes)
  333. Are immunoglobulins or antibodies more specific?
  334. What are the 5 most common immunoglobulins?
    • IgG
    • IgA
    • IgM
    • IgE
    • IgD
  335. What is the most abundant immunoglobulin?
  336. Which immunoglobulin can pass from the mother to the fetus?
  337. Which Ig is the largest?
  338. Which If is a pentamer?
  339. Which Ig is produced early in response to an antigen?
  340. Which Ig is made by neonates?
  341. Which Ig is found on B cell surfaces, is in low concentrations in the blood, and has a limited role, and unknown fxn?
  342. Which Ig is the least concentrated and is involved in allergic reponses and with parasites?
  343. What is the valence of an Ig?
    how many paratopes per molecule
  344. Both heavy and light chains of Igs contain what 2 regions?
    • constant region
    • variable region
  345. Which Ig is found in blood and secretions?
  346. Which Ig protects against infections the most?
  347. Which Ig has its own intrinsic resistance to proteolysis?
  348. Which two Igs have Jchains?
    • IgA
    • IgM
  349. Which Igs use the classical pathway?
    • IgG
    • IgM
  350. Which Ig uses the alternative pathway?
  351. What are the 2 necessary molecules involved in intracellular signaling for the BCR complex?
    • Ig alpha
    • Ig beta
    • on actual structure of B cell receptor complex
  352. What is the major accessory protein used for the TCR complex?
  353. What does CD3 do for the TCR complex?
    transmits info to the cell's nucleus for cell activation and differentiation
  354. What is the leading cause of MR and miscarriage?
    chromosomal abnormalities
  355. What are the 2 methods of detecting chromosome abnormalities?
    • amniocentesis
    • chorionic villus sampling