PSL301 Blood and Immunity

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What are the 5 functions of blood?

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1

What are the 5 functions of blood?

transportation, regulation, restriction, defence, stabilization/

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2

Hematocrit

percent of total blood volume occupied by packed (centrifuged) red blood cells normal hematocrit = 37-54%

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3

what are the percentages of different proteins in the blood

60% albumins, 35% globulins, 4% fibrinogen

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4

where are most plasma proteins made

liver

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5

role of albumins in blood plasma

colloid osmotic pressure and carriers for hormones

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6

role of globulins in blood plasma

alpha and beta = clotting factors, enzymes, carriers gamma = antibodies

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7

role of fibrinogen in blood plasma

cleaved to form fibrin in blood clotting

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8

granulocytes

neutrophils, eosinophils, basophils

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9

phagocytes

neutrophils and monocytes

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10

how many RBC's are in the blood

5 million RBC/microL of the blood

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11

How many RBCs are made per second?

2-3 million

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12

how long is the lifespan of a red blood cell

120 days

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13

what is the production of red blood cells called

erythropoiesis

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14

Eryhtropoietin

hormone secreted by the kidneys that stimulates red blood cell formation --> produced in response to low oxygen (stabilizes HIF1alpha) and activates erythropoetin gene

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15

what does the process of erythropoiesis require

iron, vit B12, folate

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16

Do mature RBCs have a nucleus?

no, there is no need for new transcription and they undergo anaerobic metabolism

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17

what is the process of making blood cells called

hematopoiesis

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18

what are the percentages of erythrocytes and leukocytes in the bone marrow?

25% developing erythrocytes and 75% developing leukocytes (b/c higher turnover)

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19

what regulates hematopoiesis

cytokines: colony stimulating factor (from endothelial cells and WBCs) and interleukins (from WBCs)

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20

what is the effect of cytokines on hematopoiesis

survival, proliferation and differentiation of different cell type s

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21

Where does hematopoiesis occur in adults?

bone marrow: pelvis, spine, ribs, cranium, proximal end long bones

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22

Where does hematopoiesis occur in embryos?

yolk sac, liver, spleen, bone marrow

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23

What can ulcerative colitis lead to?

contributing to the low production of erythrocytes as it may contribute to low levels of folate absorption

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24

what is the process of RBC removal

90% are engulfed by macrophages and then broken into their amino acids --> the heme groups are converted to biliverdin and then to billirubin which goes to the liver to then either go to the kidneys to be converted to bilirubin derived products for excretion in the urine or to the small/large intestine for excretion -the Fe2+ is either transported in circulation by transferrin or stored in liver as ferritin

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25

Jaundice

yellowing of the skin and the whites of the eyes caused by an accumulation of bile pigment (bilirubin) in the blood --> caused by: high turnover of RBCs, liver disease (can't process it), and bile duct obstruction (pushed back into liver)

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26

causes of low production of RBCs

-destruction of stem cells via drugs and radiation (aplastic anemia) -inadequate nutrients: iron, folic acid, vit B12 (nutritional, pernicious anemia) -low erythropoietin (renal anemia/kidney failure)

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27

causes of high removal of RBCs

-Hemolytic: genetic (defects in proteins), parasitic infections, drugs (antibiotics and anti-seizure drugs), autoimmune reactions -Hemorrhagic: excessive blood loss

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28

Polycythemia

hematocrit is too high (>54%) therefore theres too high of a production of RBC while same removal levels -causes high blood viscosity -result from: mainly abnormal erythrocyte precursors (ie. cancerous) as well as low O2 delivery to tissues

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29

Functions of the immune system

-destroys pathogens, detects and kills abnormal cells, removes debris from body

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30

types of pathogens

parasitic worms, fungi, protozoa, bacteria, viruses

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31

what are the two types of defence against pathogens

  1. Innate immunity = rapid, non-specific

  2. acquired immunity = slower, specific

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32

General Components of the Immune system

tonsils, lymph nodes, spleen, GALT, bone marrow, lymphatic vessels, thymus

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33

Roles of the lymphatics

  1. return excess tissue fluid to blood

  2. transport pathogens + dendritic cells to lymph nodes

  3. transport fat from digestive system to blood

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34

role of lymph nodes and spleen

both contain mature immune cells fro response -nodes = to minor the lymph --> the lymphatics are draining into the lymph nodes -spleen = monitors blood

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35

types of immune cells

lymphocytes (B, T, NK), macrophages, dendritic cells, mast cells ,neutrophils, eosinophils, basophils

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36

Parts of the innate immune response

  1. physical barriers, 2) phagocytes, 3) natural Killer (NK) cells, 4) Antimicrobial proteins, 5) Inflammation, 6) Fever

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37

Physical barriers

epithelium blocks entry (first line), glandular secretions (mucous, enzymes) trap, stomach acidity destroys, mechanical removal (tears, coughing, GI motility) removes

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phagotcytes

at the epithelium, there are cell adhesion molecules when infected (for neutrophils) --> chemotaxins attract cell, cells undergoes diapedesis (moves in), then phagocytosis

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39

two ways for phagocytosis

  1. toll like receptors bind pathogen

  2. sapsule around pathogen --> antibodies bind the capsule (specific) and the phagocyte has antibody/Fc receptor to bind and engulf

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40

What types of cells are antigen-presenting cells (ACP)

macrophages and dendritic cells -fuse phagosome with lysosome and present antigen (class II MHC + antigen)

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41

Natural Killer cells

in the lack of expression of MHC class I receptors (binds NK inhibitory receptor) on infected cells, NK produce interferons and granule release to cause pores to form in target cell to kill

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42

antimicrobial proteins

-interferons: alpha and beta = prevent replication, gamma = activate macrophages -complement proteins: 25 plasma prot, destroy target membranes, stimulate inflammation, attract phagocytes, enhance phagocytosis

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43

Three pathways of complement activation

alternative, lectin, classical -all three end up activating the membrane attack complex (C5-9)

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44

Inflammation

localized response to injury --> swelling, redness, heat, pain Roles = slow spread of pathogens, mobilize defences, sets stage for repair -Kinin cascade leads to formation of bradykinin = vasodilator and stimulates pain receptors -mast cells release histamine and heparin for dilation of vessels and attraction of neutrophils

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45

Fever

Body temp > 32.7˚C caused by pyrogens (bacterial components, interleukin-1 from activated macrophages) which change set point in hypothalamus --> causes increases metabolic activity of host and inhibits some pathogens

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46

Features of Acquired Immunity

specificity, versatility, memory, tolerance

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47

Specificity

activated by and responds to specific antigen -B and T cells have receptors that recognize specific shapes

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48

Versatility

ready to confront any antigen at anytime -different B and T cells have diff receptors

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49

memory

"remembers" any antigen it has encountered -some activated B and T cells are long lasting

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50

tolerance

responds to foreign substances but ignores normal tissues -B and T cells with receptors that recognize self are deleted or not activated

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51

B vs T cell receptors

B = immunoglobulin like receptors (bind extracellular antigens) T = receptors that bind both viral antgen and MHC

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52

Clonal selection

selecting for the cell that has that specific kind of receptor

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53

Clonal expansion

the cell that is recognized becomes activated and you get a lot more of the same kind of cell

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54

Clonal memory

long lived cell and continue to reproduce (can be activated if the body recognizes the antigen again)

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55

Primary vs Secondary Immune Response

1˚ = lag for the activation of the antibodies produced 2˚ = antibody concentration increases straight b/c antibodies are already in system

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56

where do T and B lymphocytes originate

Bone Marrow

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57

where do T cells undergo selection

in the thymus

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58

where do B cells undergo selection

in the bone marrow

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59

every human has between 10^7 and 10^9 different shaped ...

Fabs

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60

the light chain of the antibodies is the .....

light chains

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61

memory

"remembers" any antigen it has encountered

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62

How are B cells activated ?

  1. Antigen binds to specifci B cells

  2. Antigen is internalized, digested and combined with MHC and then transported to the cell surface

  3. and the specific helper T cells recognizes antigen and MHC becomes activated and secretes cytokines

  4. activated B cell divides. some daughter cells becomes plasma cells and secrete antibodies, others become memory B cells

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63

Antibodies protect us

  1. Activates B lymphocytes

  2. Acts as opsonins

  3. Causes antigen clumping and inactivation of bacterial toxins

  4. activates antibodies-dependent cellular activity

  5. triggers mast cell degranulation (release histamine and heprin)

  6. activates complements

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64

how are antibodies classed

grouped into classes based on their F portion (all formed from B cells)

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65

classes of antibodies

IgG, IgM, IgA, IgE, IgD

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66

IgG

most common type of circulating antibody, transferred across the placenta from mother to baby (so baby has same antibodies)

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67

IgM

first type of antibody to be secreted in response to a new antigen, good at causing antigen clumping and activating complement

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68

IgA

crosses epithelial cells, protects epithelial surfaces and present in breast milk

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69

IgE

fights parasites, eosinophils have receptors for the IgE, releases histamines

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70

IgD

unknown role (less clear)

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71

Types of humoral immunity

active vs passive

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72

T cell activation

  1. Cell binds to T lymphocyte (specific interaction)

  2. signal transduction activates T lymphocyte

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73

Helper T cells

-have CD4 to recognize the MHC -binds MHC class II and antigen -releases cytokines that suppress or activate other immune cells -activated T and B cells

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74

Cytotoxic T cells

-have CD8 -bind MHC Class I and antigen -kill infected/cancerous cells -use perforin and granzymes to kill or by activating death receptor, Fas

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75

MHC Class II

located on dendritic cells, macrophages and B cells, present exogenous antigen (some foreign), and activate helper T cells -antigen fragments (from lysosome) get bound to MHC II and then move to surface

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76

activation of helper T cells

costimulation of the APC and inactive CD4 cell to activate and then split into active helper T and inactive memory

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77

cytokines will stimulate ....

helper T cells, cytotoxic T cells and B cells

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78

MHC Class I

located on all nucleated cells (so all but RBC) and present endogenous antigen (any protein made by the cell), activates cytotoxicT cells

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79

activation of cytotoxic T cells

infected cell bind inactive cytotoxic T, cytokines from helper T (IL-2, interferon gamma) further activate -active Tc binds infected cell and1) releases lymphotoxin (disrupt cell metabolism), release cytokine (stim apoptosis), and release perforin (cell membrane)

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80

advantages of the immune system

protective immunity and tumor immunity

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81

disadvantages of the immune system

recurrent infection (deficient response), allergy (immune), rejection (immune), autoimmunity (immune), cancer (deficient)

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82

Percentages of the ABO blood groups

A = 42% B = 9% AB = 3% O = 46%

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83

percentages of Rh blood group in europeans

Rh+ = 85% Rh- = 15%

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84

what type of antibodies does type A blood have

anti-B antibodies

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85

what type of antibodies does type B blood have

anti-A antibodies

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86

what type of antibodies does type O blood have

Anti-A and Anti-B

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87

what is the universal recipient

AB

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88

what is the universal donor

O

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89

hemolytic disease of the newborn

RBC's are being destroyed -anemia, jaundice, enlarged liver and spleen, sever edema (clumping blocks capillaries)

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90

how does hemolytic disease of the newborn develop

any rupture of the blood vessels between the placenta of the mother's blood and fetal blood -the mother (Rh-) mounts an immune response to the first Rh+ baby --> then for the second pregnancy, the mothers immune system has memory and targets the second Rh+ fetus

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91

How can hemolytic disease of the newborn be prevented?

by injecting anti-D antigen antibodies into the Rh- mother during and following her pregnancy, which will bind and remove the fetal RBCs before immune response triggered, thus no memory of the D antigen

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92

what is the half life of platelets

10 days

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93

what is the role of thrombopoetin

increase platelet numbers -is a cytokine which stimulates the development of megakaryocytes and production of platelets

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94

Phases of Hemostasis

  1. Vascular Phse

  2. Platelet Phase

  3. Coagulation Phase

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95

Vascualr phase

after injury, the blood vessels constrict due to neurogenic (neurons in surrounding area) and myogenic control (smooth muscle around vessels) --> reduces blood loss (short lived)

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96

what is the vasocontriction prolonged by

serotonin, endothelin-1, and thromboxane A2

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97

platelet phase

  1. exposed collagen - binds and activates platelets (with adaptor vWf to bind both)

  2. factors released from platelet (eg. ADP, PAF, serotonin, thromboxane A2)

  3. factors attract more platelets

  4. platelets aggregate and form plus

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98

what does PAF stand for

platelet activating factor

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99

differences between inactive vs active platelets

inactive = small, dislike fragments active = spiky, outer surface and adhere to each other

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100

what prevents platelet adhesion with no injury

Prostacyclin (prostaglandin I2, PGI2) and NO are released from intact endothelium and prevent platelet adhesion and are vasodilators

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