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biology chapter 19

Jaimee Mc Biology Inglês 126 flashcards

Flashcards do conjunto (126)

  1. 1hematology- study of blood, blood forming tissues, and functions and properties of blood
  2. 2blood- a connective tissue with 'cells' suspended in plasma
  3. 3functions and properties of blood- transportation
    - regulation of various body parameters
    - protection
  4. 4blood transport- essential for cellular and whole body homeostasis
    - transports various substances into tissue cells
    - transports substances from body cells
  5. 5transport of various substances to tissue cells- from capillary blood to interstitial fluid then across cell plasma membranes into cytosol
    - substances include: oxygen, nutrients, hormones and regulatory factors, electrolytes
  6. 6transport of substances from body's cells, including:- secretory products
    - glucose
    - cellular waste products
  7. 7blood regulates various body parameters, including:- pH regulation
    - thermoregulation
    - regulation of osmotic pressure
  8. 8pH regulation- achieved by buffers (phosphate & carbonic acid/bicarbonate buffers & plasma proteins)
  9. 9thermoregulation- vasoconstriction/ vasodilation of dermal blood vessels
    ~ vasoconstriction decreases loss of body heat
    ~ vasodilation increases loss of body heat
  10. 10regulation of osmotic pressure- osmotic pressure exerted by blood & interstitial fluid determined by salt & protein content
    ~ water balance between ECT & ICF due to their relative contents of salt and proteins
    - blood colloidal osmotic pressure due to relative amounts of protein in plasma and interstitial fluid
  11. 11protection- blood contains white blood cells and proteins which protect against foreign cells and particles, cancer cells, and toxins
    - hemostasis
  12. 12hemostasis- protection from exsanguination caused by severe traumatic injury
    (prevents you from 'bleeding out')
  13. 13Physical characteristics of blood- average adult male: ~5-6 liters blood
    - average adult female: ~ 4-5 litres of blood
    ~ blood temperature at core: 38*C
    ~ normal blood pH range: 7.35-7.45
  14. 14Components of blood- centrifuges whole anti-coagulated blood separates into blood plasma and formed elements
  15. 15Blood plasma- upper layer of centrifuged blood
    =ECF found within vessels
    - about 55% of whole blood volume
    - about 95% water
    - contains: nutrients, wastes, electrolytes, buffers, gases, hormones, enzymes and other plasma proteins
    - buffers in blood keep pH around 7.4
    - plasma constitutes maintain osmotic pressure
    - plasma proteins: albumins, globulins, fibrinogen
  16. 16plasma proteins include...- albumins
    - alpha and beta globulins
    - gamma globulins
    - blood clotting proteins
  17. 17Albumins= main colloidal osmotic proteins
    - function as transport proteins
  18. 18alpha and beta globulins= transport proteins that carry:
    ~ fats (cholesterol, phospholipids)
    ~> apoproteins of LDL, VLDl, HDL and chylomicrons
    - fat soluble vitamins
    - iron
    ~> transferrin
  19. 19gamma globulins- antibodies - fight infection
    - made by plasma cells, NOT by liver
  20. 20blood clotting proteins- including fibrinogen(I), prothrombin(II), and clotting factors VII, IX and X
    - fibrinogen converted to fibrin that foms blood clot meshwork
  21. 21formed elements- lower layer
    - RBC's and platelets are NOT true cells
    - 45% of whole blood volume
  22. 22hematocrit- precentage of whole blood that is RBS's
    - adult Hct > 60% indicates polycythemia, associated with increased blood viscosity
    - adult Hct < 30% indicates severe anemia
  23. 23formation sites of blood cells: hemopoiesis- continuous process by which blood cells are formed
    - fetal hemopoiesis sites: liver, thymus, spleen and lymph nodes, and eventually red bone marrow
    - in adult red bone marrow is only site
    ~> found in trabecular bone of skull, sternum,ribs, vertebrae, pectoral and pelvic girdles, proximal epiphysis of humerus and femur
  24. 24formation process of blood cells: hemopoiesis- red bone marrow contains pluripontent stem cells that ~> many different cell types
    - during hemopoiesis, red bone marrow stem cells ~> formed elementsof blood
    - hemocytoblast divides and its daughters differentiate into either myeloid stem cell or lymph stem cells, which can divide and self renew
    - myeloid stem cells divide and their daughters differientiate into progenitor cells, aka, colony-forming units (CFU) which can divide but cannot self renew
    ~> CFU's produce blast cells (precursor cells), which divide and ~> formed elements of blood
  25. 25CFU-Eproduce proerythrobasts, which untimately ~> reticulocytes
  26. 26CFU-Meg- produce megakaryoblasts, which ~> megakaryocytes (large nucleus cell), which ~> blood platelets
  27. 27CFU-GMproduce:
    - eosinophilic myeloblasts ~> eosinophils
    - basophilic myeloblasts ~> basophils
    - neutrophilic myeloblasts ~> neotrophils
    - monoblasts ~> monocytes
  28. 28CFU-Mast~> mast cells
  29. 29lymphoid stem cells- divide and their daughter cells dierentiate into:
    T-lymphoblasts which ~> T-lymphocytes
    B-lymphoblasts which ~> b-lymphocytes
    NK-lymphoblasts which ~> natural killer cells
    - mature blood cells collect in blood sinuses which surround red bone marrow and enter general circulation
    - lymphocytes continue their development in thymus gland
  30. 30hemopoietic growth factors include:- erothropoietin (EPO)
    - thrombopoietin (TPO)
    - cytokins
  31. 31erthropoietin (EPO)- EPO stimulates proliferation of RBC progenitor cells (CFU-E), which ~> more RBC's
    - recombinant EPO used to treat uremic patients
  32. 32thrombopotin (TPO)- stimulates myeloid stem cells ~> CFU-Meg that ~> megakaryoblasts that ~> megakaryocytes that ~> blood platelets
    - recombinant TPO used to treat thrombocytopenia
  33. 33cytokines- glycoprotein local hormones
    - made by WBC's red bone marrow, macrophages, fibroblasts and endothelial cells
    - 2 types
  34. 34two types of cytokines- colony-stimulating factors (CSF) ~> proliferating of bone marrow progenitor cells (CFU-GM) that ~> myeloblasts and monoblasts
    - interleukins regulate specific and non-specific immune WBCs responses
  35. 35red blood cells (RBCs)- carriers of oxygen, bound to hemoblobin
  36. 36RBC count- RBCs in a microlitre of blood
    - male: ~5.4 million cells/mm^3 blood
    - female: ~4.8 million ''
    - ~2 million old or damaged RBCs destroyed each second by fixed macrophages
    red bone marrow must replace blood at same rate
  37. 37anemia- inadequate RBCs in blood to supply oxygem to tissues
  38. 38polycythemia- too mant RBCs, making blood too viscous
  39. 39RBC anatomy- 8 microm biconcave, disc-shaped cells without nuclei or organelles
    - cannot divide and very limited metabolic functions
    - not true cells; membrane bags of hemoglobin
  40. 40RBC physiology- make ATP by glycolysis
    - each rbc is ~33% Hb
    - role of Hb = O2 transport
    - Hb transports 23% of total blood CO2
    - Hb transports nitric oxide (NO) = vasodilator
  41. 41role of Hb = O2 transport1) Hb loosely binds O2 in lungs
    - Hb + O2 ~> oxyhemoglibin (oxyHb)
    2) Hb readily releases O2 into tissues
    - slightly acidic enviroment of peripheral tissues is because cells ~> ATP and CO2
    - Hb that has given up a lot of its O2 is called reduced hemoglobin
    - but still contains ~60% of O2 bound in lungs
    *) proportion of Hb that is oxyHb accounts for a difference in color of blood
    a) blood in systemic arteries is bright red
    b) blood in systemic veins is darker red
  42. 42calculation of total Hb content of human body- each RBC contains ~280 million Hb mollecules
    - therefore (5X10^6 RBC/mm^3)(5 litres of blood)(1000ml/liter)(1000microL/mliter)(280 X10^6 Hb molecues/RBC) = 7 X10^21 molecules Hb in body
    - total number of O2 molecules could be 4X that number
  43. 43Hb molecule consists of:1) globin protein
    ~ each Hb molecule has 4 globin protein chains: 2 alpha and 2 beta-globin chains
    2) iron-containing heme
    ~ heme = ring-like sructure that holds iron atom
    ~ each hemecan bond 1 O2 molecule
    ~ Hb molecule has 4 heme groups
    - RBCs also contain enzyme carbonic anhydrase which reversibly catalyzes the following reaction:
    CO2 + H2O <~> H2CO3 <~> H + HCO3
    ~ this enxyme enables 70% of CO2 to be carried to lungs as HCO3
  44. 44average lifespan of red blod cell- ~120 days
  45. 45degregation of old of damaged RBCs- destroyed be fixed macrophages of liver, spleen, and red bone marrow
    - released Hb degregaded into heme and globin
    ~ globin amino acids reused
    ~ iron recycled: transferin, ferritin
  46. 46transferin- iron transport protein of blod
  47. 47ferritin- intracellular iron-storage protein found in muscle, liver cells and fixed macrophages of RES
  48. 48hemochromatosis- inherited iron overload disease, usually seen in males
    ~> excessive iron deposits in organs
    ~> free radical damage to liver, heart, pancreas, ect
  49. 49iron overload disease- excessive GI iron absorbtion exceeds available transferrin and ferritin binding sites, producing deleterious effects like hemochromatosis
  50. 50disposal of heme structure- porphyrin ring broken down by RES macrophages, ~> biliverdin ~> bilirubin
    - bilirubin carried in bloodstream by plasma proteins to liver
    - in liver, bilirubin conjugated with glucronic acid, then excreted into bile
    - bile concentreated within gallbladder and released into small intestine
    - conjugated bilirubin travels to large intestine, converted by colonic bacteria to urobilinogen
    - some urobilinogen reabsorbed, becoming urobilin excreted by kidneys
    - most urobilinogen remains in large intestine, and converted by bacteria into stercobilin
  51. 51erythropoiesis- process by which RBCs formed in red bone marrow
    - if rumber of RBCs too low in blood, tissue hypoxia may result
    erythropoietin (EPO) released ny kidneys whenever blood oxygen levels too low
    - EPO ~> erythropoiesis: EPO stimulates CFU-E progenitor cells to ~> proerythroblasts ~>~> reticuloytes ~> RBCs
    ~ 1-2 days after release into blood, reticulocytes become mature RBCs
  52. 52blood doping- recombinant EPO used by some atheletes to enhance physical proformance
    - EPO-induced polycythemia ~> increased O2-carrying capacity of blood but also increased blood viscosity and ~> rist of hypertension, heart attacks and strokes
  53. 53differance between WBCs and RBCs- WBCs are larger
    - WBCs have nucleus
    - WBCs lack hemoglobin
    ~ to visualize WBCs with microscope, blood smear stained with Wright's stain
    - WBS less numerous
    - WBCs have a major histobombatibility complex antigens on surface
    => cell identity markers
    - WBC lifespan usualy hours or days
  54. 54WBC numbers and diseases- WBC count: 5,000 - 10,000 cells/mm^3
    -leukocytosis: WBC coult exceeds 10,000 cells/mm^3
    - leukopenia: WBC count falls below 5,000 cells/mm^3
  55. 55WBC function- fight infections, infestations, and cancer
  56. 56types of WBCs- granular leukocytes
    - agranular leukocytes
  57. 57granular leukocytes- granular WBCs - prominent peri-nuvlear granules
    - 3 subtypes: neutrophils, eosinophils, basophils
  58. 58neutrophils- most abundant WBCs in blood
    - display small pale lilac-colored granules
    ~ granules have low affinity for acidic and basic dyes of Wright's stain
    - multi-lobed nuclei joined by nuclear threads: 2-5 lobes
    ~ polymorphonuclear leukocytes or PMNs or polys
  59. 59eosinophils- large granules that take up red eosin dye
    - 2-lobed nucleus, connected by strand of nuclear material and not obscured by stained granules
  60. 60basophils- granules great affinity for blue basic dye
    - 2-lobed nucleus obscured by stained granules
  61. 61agranular leukocytes- lack of prominant granules
    - 2 subtypes: monocytes, lymphocytes
  62. 62monocytes- largest WBCs
    - kidney-shaped or horse-shoe shaped nucleus
    - blue-gray or purple-blue foamu-looking cytoplasm
    - migrate from bloodstream nad transform into macrophages
  63. 63lymphocytes- single spherical or slightly-indented nucleus
    ~ thin rim of cytoplasm surrounding nucleus
    - smallest WBCs
    - small lymphocytes (6-9 microm) and large (10-14 microm)
    - 3 subtypes: B-lymphocytes, T-lymphocytes, and NK lymphocytes
  64. 64differential WBC count- useful in diagnosis
    - wuantifies numbers of neutrophils, eosinophils, basophils, monocytes and lymphocytes as a percentage of the total number of WBCs in blod
    - complete blood count (CBC): differential WBC count, RBC and platelet counts, Hematocrit, mean corpuscular hemoblobin concentration (MCHC), and mean corpuscular volume (MCV)
  65. 65function of WBCs: neutrophils- phagocytize nad digest microbes
    - early inflamatory response
    - manufacture chemiclas:
    ~lysosome
    ~ oxidants
    ~ antibiotic-like defensins
    ~lysosomal protease
  66. 66function of WBCs: eosinophils- phagecytize circuating immune complexes
    - combat allergic responses
    ~ release histaminase and other enzymes to destroy imflammatory mediaors
    - kill parasitic worms
  67. 67function of WBCs: basophils- many similarities to mast cells
    - release garnules containing histamine, serotonin and heparine
  68. 68function of WBCs: monocytes- transform into macrophages when they pass from bloodstream into tissues
    ~ fixed macrophages
    ~ wandering macrophages
    ~> later stages of inflammatory response
    ~> enter invasion site ~36 hours injury
    ~> clean up tissue debris, microbes
    - magrophages = antigen-presenting cells (APCs), helping B- and T-lymphocytes
  69. 69lymphocytes- 3 types:
    ~ B-lymphocytes
    ~ T-lymphocytes
    ~ natural killer (NK) lymphocytes
  70. 70function of WBCs: B-lymphocytes- B-cells
    - produce antibody-mediated immunity
    - secrete antibodies targeted to antigens on surface of foreign cell or to toxins
    - differientiate into plasma cells
  71. 71function of WBCs: T-lymphocytes- T-cells
    - produce cell-mediated immunity
    - T-cells directly attack and kill infected cells and tumor cells
    - cause immune rejection of organ transplants
  72. 72function of WBCs: natural killer (NK) lymphocytes- target abnormal MHC cell surface antigens of cancer cells and virus-infected cells
    -release perforins and pro-apoptosis molecules
    ~ cytolysis
  73. 73chemotaxins- chemical attractants of WBCs
    - eg. microbial toxins, kinins, colony stimulating factors
  74. 74response of WBCs to chemotaxins- 2-step process by which WBCs leave circulation: migration (find way to side of vessel and squeeze out) and emigration (will not return to circulation)
    - adhesion molecules
    - monocytes and granular never return to bloodstream
    - lymphocytes are capable of re-entry into circulation via lymph
    ~ only 2% of lymphocytes at any gives time are circulating in blood stream
  75. 75adhesion molecules- selectins on endothelial cell surfaces
    - integrins on WBC surfaces
    - after migration, WBCs squeeze between endothelial cells
  76. 76platelets- fragments of red bone marrow megakaryocytes
    - do not have nuclei, but have granules
    ~ granules contain: platelet thromboplastin, ADP, ATP, calcium, serotonin, COX-2 enzyme, fibrin-stabilizing factor, platelet-derived growth factor (PDGF)
    - survive only 5- days in general circulation
  77. 77normal platelet count- 150,000 - 400,000 platelets/mm^3 of blood
  78. 78thrombocytopenia- too few blood platelets
  79. 79platelets are involved in- hemostasis - immediate stopping of blood flow from injured blood vessel
    ~ platelets aggregate ~> platelet plug
    ~ platelets release cemicals that ~> vasoconstriction of arterioles
    - initiating blood clotting - reinforce platelet plug
  80. 80stem cell transplants from bone marrow adn cord blood- if patient has cancerous bone marrow, it can be destroyed with radiation and chemotherapy, and re-seeded with stem cells from normal bone marrow or cord blood
    - doner bone marrow is heterologous (unrelated doner) or autologus (identical twin or self)
    - transplanted normal bone marrow or cord blood given intravenously to recipient
    - stem cells re-populate recipient's red bone marrow ithin 2-3 weeks
  81. 81disadvantages of heterologous grafts1) graft-versus-host disease: graft T-cells attack recipient's tissues
    2) any surviving recipient's T-cells attack and kill graft
    3) immunosuppressive drug therapy
    ~ lowers immunity, damages kidneys and liver
  82. 82advantages of using neonatal cord blood- abundant, unlikely to be virally-infected and less likely to ~> graft-versus-host disease
  83. 83hemostasis- process of stopping blood flow from injured blood vessel
    - 3 main mechanisms prevent hemorrage:
    - vascular spasm
    - platelet plug formation
    - blood cloting (coagulation)
  84. 84vascular spasm- decreases blood flow through damaged blood vessel if cut via immediate vasoconstriction
    - 3 mechanisms may ~> vasoconstrictor response:
    1) release of platelet serotonin and thromboxane A2
    2) damage to vascular smooth muscle ~> spontaneous contraction
    3) pain receptors trigger vasoconstrictor reflexes
  85. 85platelet plug formation- when blood vessel cet, platelets exposed to collagen and adhere (platelet adhesion), because platelets adhere to negatively-charged surfaces
    - platelet adhesion ~> platelet activation and degranulation
    - platelet plug fills break in blod vessel
    - platelet plug re-enforced with fibrin meshwork
  86. 86blood clotting (coagulation)- assembling of fibrin clot that reinforces platelet plug ad traps formed elements in meshwork
    - 13 blood clotting factors including Ca
    ~most are proenzymes, arranged as activation cascade
    ~> activation of 'early' proenzyme sped up by activation of 'later' enzymes
  87. 87extrinsic and intrinsic pathways- clotting mechanism initiated by:
    a) tissue trauma ~> rapid exrinsic pathway
    b) damage to endothelial cells ~> platelet activation ~> slow intrinsic pathway
    - lipid materials released:
    ~ tissue thromboplastin = lipoproteins and phospholipids
    ~ platelet thromboplastin = phospholipids
    ~ lipids + Ca activate cascade ~> activation of factor V to ~> prothrombinase
  88. 88common pathway- shared by intrinsic and extrinsic pathways
    - prothrombinase converts prothrombin to thrombin in presence of Ca
    - in the presence of Ca, thrombin digests fibrinogen ~> fibrin monomers, which self-assemble into fibrin threads, which produce framework of clot, trapping formed elements
    - blood clot
    - serum
  89. 89blood clot- platelet plug + surrounding fibrin mesh + entrapped formed elements
  90. 90serum- blood plasma without clottign factors
  91. 91during inflammatory reaction- arterioles vasodilate and capillary permiability increases, allowing clotting factors to escape
    - clotting cascade activated in interstitail space ~> fibrin clot
  92. 92clot reaction- process of drawing together edges of damaged blood vessel
    - occures because platelets pull on fibrin threads
    - expedites repair process
    - fibrin-stabilizing factor (Xlll)
  93. 93role of vitamin K in clotting- to synthesize activation clotting factors, liver needs vitamin K
    ~ if diets deficient in vitamin K ~> hemorrage disorders
    ~ anticoaguant warfarin inhibits vitamin K activity
    ~ vitamin K = fat-soluble vitamin found in dark green leafy vegatables
    ~> vitaming K can be converted to vitamin K2 by gut bacteria
    ~> vitamin K2 helps regulate calcium deposition in tissues
  94. 94homeostatic controll mechanisms- fibrinolysis
    ~> plasmin
    ~> plasminogen
    - other controlls on blood clotting
    ~> prostacyclin
    ~> endogenous anticoagulants
    ~> activated protein C
  95. 95fibrinolysis- necessary:
    a) to prevent spread of intravascular clotting
    b) to remove blood clots after vessel repair completed
    - to prevent disseminated intravascular coagulatio, both blood clotting and fibrinolysin mechanisms activatd simultaneously
  96. 96plasmin- aka fibrinolysin
    - destroyes fibrin polymer, dissolving clot
  97. 97plasminogen- inactive form of plasmin
    - thrombin, activated XII and tissue plasinogen activator (TPA) ~> plasminogen activation
  98. 98thrombolytics- TPA-like drugs or recombinant TPA
  99. 99prostacyclin- derived from fatty acids
    - prostaglandin made by endothelial cells and WBCs
    - it inhibits release of thromboxane A2 from platelet membranes, which blocks platelet adhesion and platelet degranulation
    - thromboxane A2 = vasoconstriction and prothrombotic
    - prostacyclin = vasodilator and antithrombotic
  100. 100low dose asprin (ASA)- inhibits vasoconstriction nad platelet aggregation
    - because ASA blocks synthesis of thromboxane A2
    - ASA lowers risk if arteriol occlusion by platelet initiated blood clot
  101. 101endogeneous anticoagulants: antithrombin III and heperin- antithrombin III = protease inhibitor
    - antithrombin III + heperin ~> protein inhubition of thrombin and clotting factors XII, X and II
    - this combination in ~1000X more potent than antithrombin III acting alone
  102. 102activated protein C- produces potent inhibition of clotting factors V and VIII
  103. 103intravascular clotting- thrombosis
    - embolism
  104. 104thrombosis- formation of blood clot in unbroken blood vessel - thrombus
    a) arterial thrombosis
    b) venous thrombosis
  105. 105arterial thrombosis- accures in arteries, especially at sites of endothelial damage, which allow adhesion of platelets, creating a platelet-initited blood clot
    - low-dose ASA reduces risk of such clots
  106. 106venous thrombosis- occures in veins, since blood moves more slowly
    - this may trigger blood clotting ~> a fibrin blood clot
    - risk lessened by taking anticoagulant medications: heparin, warfarin
  107. 107embolism- obstruction of a blood vessel by an embolus (moving plug), moving with the flow
    - many kinds of emboli
    ~ thromboembolus: dislodged blood clot
    - embolus can ~> occlusive event ~> ischemia (holding back blood from tissue cells) ~> possible tissue necrosis
  108. 108ABO blood group- 4 blood types: A,B,AB,O
    - 2 possible antigens on RBC membrane surfaces: antigen A and antigen B
    - blood plasma may contain large IgM antibodies that bins to either antigen A, antigen B or both
    - called anti-A antibody and anti-B antibody
  109. 109type O blood- no antigens (A or B) on RBC surfaces
    - both antibodies (anti-A and anti-B) in plasma
    - universal doners
    ~ can donate RBCs to anyone regardless of ABO blood type - cannot donate plasma to just anyone
  110. 110type A blood- antigen A of RBC surfaces
    - anti-B antibody in plasma
  111. 111type B blood- antigen B on RBC surfaces
    - anti-A antibody in plasma
  112. 112type AB blood- both antigens A + B on RBC surfaces
    - no anti-A or anti-B antibodies in plasma
    - universal recipient
    ~ can recieve packed RBCs from anybody, regardless of doner ABO blood type - cannot recieve plasma from just anyone
  113. 113blood transfusions and agglutination reactions- inportant to consider both the so-called mayor reaction (btw doner RBCs and recipiants plasma) and the minor reaction (btw doner plasma and recipient RBCs
    - mismatch ~> agglutination
  114. 114blood typing- blood sample is mixed with a small quantity of antiserum containing either anti-A antibodies or anti-B antobodies to detect posible agglutination reaction
  115. 115cross-matching- mixign doner RBCs with recipient plasma to detect possible agglutination reactions
  116. 116agglutination reactions- reactions seen when:
    ~ RBCs with A antigens mixed with blood containing anti-A antibodies in its plasma or mixed with antiserum containing anti-A antibodies
    (same for B antigens/ with anti-B plasma or serum)
  117. 117Rh blood groups- Rh+ individuals have Rh antigens on RBC surfaces
    - Rh- individuals have no Rh antigens on RBC surfaces
    ~ Rh- indivuduals will make Rh antibodies if exposed to Rh antigens
  118. 118Rh in pregancy- if mother is Rh- and father is Rh+, fetus may be Rh+
    - diring birth process, fetal Rh+ RBCs may leak into mothers blood, immunizing her agains future Rh+ fetuses
    - when anti-Rh antibodies cross placents into fetal blood ~> hemolytic disease of the newborn (HDN) (erythroblastosis fetalis)
  119. 119prevention of erythroblasosis fetalis- injections containing anti-Rh Abs ~> breif period of passive immunity against Rh+ cells in mothers blood
    ~ this prevents mother from developing active immunity
    - Rh immune globin injections given:
    1) halfway through first pregnancy, and
    2) no later than 72 hours after giving birth to Rh+ child o after miscarriage or abortion
  120. 120disorders: homeostatic imbalances- aminia
    - sickle cell disease
    - hemoplilia
    - leukemia
  121. 121anemia- insufficient numbers of RBCs in blood, or individual RBCs within blood lack sufficient Hb content
    - person feels exhausted, feeling tired and 'run-down' and is intolerant to cold
    - different types of anemia
  122. 122sickle cell disease- sickle cell hemglogin (Hb-S) in inherited as an sotsomal recessive trait
    - if 2 defective copies of Hb-S gene inherited, individule has sickle cell disease
    - when deoxyHb-S formed in blood, RBC Hb-S molecules assume a sickle shape
    - this ~> RBCs to sickle and increase their rendency to rupture
    ~ average RBC lifespan in sickle cell disease is 10-20 days
    ~> causing severe anemia nad possible vascular occlusion, causing ishemia
    - sickle cell crisis
  123. 123sickle cell trait- if only one Hb-S gene is inherited, individule is carrier
    - Hb-S gene can be passed to next generation
    - RBCs of persons with sickle cell trais are mosaics:
    ~ half of RBC Hb normal Hb and half Hb-S
    - Hb-S carriers show survival advantages in areas with malaria epidemic
    ~ intra-erythrocytic stage of malarial organism's life cycle disrupted by Hb-S
  124. 124hemophilia- a recessive X-linked genetic trait
    - hemophilia impairs blood clotting
    - 2 types:
    1) hemophilia A = mutations of factor VIII gene
    2) hemophilia B = mutations of factor IX gene
    - hemophilia ~> prolonged bleeding
  125. 125leukemia- cancer of red bone marrow
    - distrupts hemopoiesis and ~> anemia, infections and excessive bleeding
    - cancerous WBCs spread to liver adn lymphoid tissues
    - cause: usually unclear
  126. 1264 types of leukemia1) acute lymphoblastic leukemia (ALL) = rapidly progressive cancer of lymphoblasts and lymphocytes
    2) acute meylogenous leukemia (AML) = rapidly progressive cancer of meyloblasts
    3) chronic lymphoblastic leukemia (CLL) = slow progressive cancer of lymphoblasts and lymphocytes
    4) chronic meylogenous leukemia (CML) = slow progressive cancer of meyloblasts

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Biology FlashCards sobre biology chapter 19, criado por Jaimee Mc em 19-03-2018.
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Jaimee Mc
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