Chapter 11 - The Blood Flashcards

1
Q

Blood Functions

A

-transport of O2, waste, heat, etc.
-defense
-hemostasis

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2
Q

Blood Statistics

A

-8% of body weight is blood
-blood makes up 25% of ECF

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3
Q

Erythrocytes

A

-red blood cells
-majority of blood cells (99%)
-transport oxygen to tissues and remove carbon dioxide
-biconcave disks with large surface area to volume ratio
-flexible
-fit the diameter of capillaries to reduce diffusion distance

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4
Q

Erythrocyte Internal Anatomy

A

-have no nucleus, mitochondria, or other organelles
-have no DNA or RNA meaning they can’t divide and have a finite lifespan

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5
Q

Glycolytic Enzymes (RBC Enzyme in Cytoplasm)

A

-anaerobic respiration for ATP

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6
Q

Carbonic Anhydrase (RBC Enzyme in Cytoplasm)

A

-critical in CO₂ transport

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7
Q

Hemoglobin

A

-binds oxygen and carbon dioxide to RBCs
-found only in RBCs
-has pigment that contains iron
-appears red when oxygenated
-appears blue when deoxygenated

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8
Q

Globin Portion (of hemoglobin)

A

-proteins composed of four highly folded polypeptide chains

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9
Q

Heme groups (of hemoglobin)

A

-4 iron groups per Hb molecule
-each is bound to one of the polypeptides
-where oxygen binds

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10
Q

Other molecules Hb binds with

A

-CO2 and H+ (not on heme group)
-CO and nitric oxide (vasodilation)

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11
Q

Carbon Monoxide

A

-can be dangerous because CO doesn’t remove from heme and uses up oxygen binding sites

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12
Q

Leukocytes

A

-white blood cells
-immune systems defence units

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13
Q

Thrombocytes

A

-platelets
-cell fragments
-important in hemostasis (clotting)

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14
Q

Plasma

A

-makes up 55% of whole blood
-fluid portion of blood
-92% water and 7% proteins
-1% organic molecules, ions, vitamins

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15
Q

Haematocrit

A

-packed cell volume
-99% of haematocrit is RBCs

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16
Q

Buffy Coat

A

-platelets and leukocytes

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17
Q

Plasma Proteins

A

-remain in the blood
-made in the liver

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18
Q

Albumins (Plasma proteins)

A

-most abundant (60%)
-transports many substances such as fats, bilirubin (yellow pigment made during breakdown of RBC), drugs

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19
Q

Globulins (Plasma proteins)

A

-𝛂 (alpha), β (beta), 𝛾 (gamma)
-𝛂 and β used for: transporting hormones + cholesterol, blood clotting proteins
-𝛾 are immunoglobulins (antibodies)

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20
Q

Angiotensinogen

A

-globulin hormone produced in the liver, kidney, adrenal glands, brain, heart
-cause vasoconstriction and regulate BP
-inactive form

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21
Q

Gammaglobulins

A

-not produced in the liver
-antibodies
-protect body from toxins, bacteria, viruses, etc.

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22
Q

Fibrinogen (Plasma proteins)

A

-forms fibrin threads essential to blood clotting

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23
Q

Erythropoiesis

A

-erythrocyte production
-occurs in red bone marrow
-stem cell in red bone marrow differentiate into different types of blood cells
-cells replaced at 2-3million cells/second

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24
Q

How long do RBCs survive?

A

-about 120 days

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25
Q

Intrauterine Erythropoiesis

A

-first by yolk sac in the embryo
-then liver and spleen when developing
-then bone marrow when developed

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26
Q

Childhood Erythropoiesis

A

-most bones have red bone marrow

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27
Q

Adult Erythropoiesis

A

-only sternum, ribs, upper ends of long bones

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28
Q

Negative Feedback Erythropoiesis Control

A

-kidneys detect reduced O₂ carrying capacity in blood
-kidneys secrete erythropoietin (EPO) hormone
-erythropoietin stimulates erythropoiesis by bone marrow
-blood O₂ carrying capacity increases
-stimulus is relieved

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29
Q

EPO Doping

A

-blood doping
-increased RBC count
-increased O₂ carrying capacity

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30
Q

Effects of increased RBC levels

A

-blood viscosity increases
-TPR increases and can lead to heart damage
-blood clotting issues

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31
Q

Cells Becoming RBCs

A

-increase in numbers/production
-maturation: loss of nucleus, organelles, gain Hb

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32
Q

Blood Types

A

-active immunity
-ABO blood types: named for surface antigens

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33
Q

Type A Blood

A

-contains A antigens
-anti-B antibodies
-can accept type A or type O blood

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34
Q

Type B Blood

A

-contains B antigens
-has anti-A antibodies
-can accept type B or type O blood

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35
Q

Type AB Blood

A

-has both A and B antigens
-universal recipient: can accept all blood types
-no ABO antibodies

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36
Q

Type O Blood

A

-neither A nor B antigens
-universal donor
-can only accept O blood
-has both anti-A and anti-B antibodies

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37
Q

Antibody

A

-binds with the specific antigen against which it is produced
-in plasma?

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38
Q

Agglutination

A

-clumping of particles together
-ie. if A accepts B, the B antibodies will attack the B antigen blood cells

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39
Q

Transfusion Reaction

A

-when blood of incompatible type is given
-most dangerous is AB in plasma for incoming donor RBCs

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40
Q

Rh(esus) Factor

A

-people who have the Rh factor have Rh+ blood
-people lacking the Rh factor have Rh- blood

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41
Q

Rh Antibodies

A

-no natural antibodies against Rh factor
-anti-Rh antibodies are produced by Rh- people if exposed to Rh+ blood

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42
Q

Erythroblastosis Fetalis (Hemolytic Disease of Newborn) HDN

A

-Rh- mother develops antibodies against RBCs of Rh+ fetus
-prevented by giving Rh- mother Rh immunoglobulin

43
Q

Iron

A

-recycled for the synthesis of new Hb
-iron is transported bound to transferrin to red bone marrow
-iron is stored bound to ferritin in the liver, spleen, small intestine

44
Q

Cross-matched Blood

A

-mix donor RBCs with plasma of recipient

45
Q

Role of the Spleen

A

-removes most of old erythrocytes from circulation
-1% of total/day
-macrophages filter blood and phagocytize old RBCs

46
Q

Bilirubin

A

-what hemoglobin broken down is converted into
-iron is removed and recycled
-yellow in colour

47
Q

Anaemia

A

-below normal oxygen carrying capacity of the blood

48
Q

Nutritional Anaemia

A

-iron deficiency in diet

49
Q

Pernicious Anaemia

A

-vitamin B12 deficiency (required for folic acid which makes DNA, RNA, proteins)
-dietary
-lack of intrinsic factor from stomach lining

50
Q

Intrinsic Factor

A

-crucial role in transportation and absorption of B12 in stomach

51
Q

Aplastic Anaemia

A

-insufficient RBC production
-cells don’t have appropriate quantity and function
-can result from destruction on bone marrow from radiation and chemo

52
Q

Renal Anaemia

A

-kidney disease and failure

53
Q

Hemorrhagic Anaemia

A

-wound
-menstrual flow

54
Q

Hemolytic Anaemia

A

-rupture of RBCs
-malaria
-sickle cell disease

55
Q

Sickle Cell Disease

A

-fragile RBCs
-destruction of deformed cells (unable to move around good)
-production unable to keep up with removal
-makes you tired because you receive less O2
-genetic disease

56
Q

Primary Polycythaemia

A

-erythropoiesis at an excessive and uncontrolled rate
-viscosity of blood increases

57
Q

Secondary Polycythaemia

A

-adaptive mechanism (not a disease state)
-results from reduced oxygen
-can be from high altitude, chronic lung disease, heart failure

58
Q

Normal Hematocrit Volume

A

-45% hematocrit
-55% plasma

59
Q

Anaemia Hematocrit Volume

A

-hematocrit lowered to 30%
-plasma is 70%

60
Q

Polycythaemia Hematocrit Volume

A

-hematocrit increased to 70%
-plasma is 30%

61
Q

Dehydration Hematocrit

A

-hematocrit is 70%
-however, plasma volume is significantly decreased and RBC count remains

62
Q

Leukocytes

A

-mobile immune defence units
-least concentration of cells in blood

63
Q

Immune System

A

-made of leukocytes and plasma proteins
-recognize and destroy/neutralize foreign materials

64
Q

Leukocyte Functions

A

-defend against pathogens
-identify and destroy cancer cells
-remove worn out cells and tissue debris

65
Q

Leukocyte Characteristics

A

-colourless because they lack hemoglobin
-larger than RBCs
-have nuclei and granules
-5 different types

66
Q

Leukocyte Production

A

-originate from same cells in red bone marrow
-granulocytes and monocytes produced only in bone marrow
-most are produced by WBCs already on lymphocyte tissue (tonsils and lymph nodes)

67
Q

Granulocytes

A

-cytoplasmic granules that contain chemicals in vesicles that could be released
-neutrophils
-eosinophils
-basophils

68
Q

Agranulocytes

A

-no cytoplasmic granules
-monocytes
-lymphocytes

69
Q

Leukopoiesis

A

-chemical messages from damaged or invaded tissues

70
Q

Colony stimulating factors

A
71
Q

Neutrophils (granulocyte)

A

-destroy bacteria by phagocytosis
-release bacteria-killing chemicals

72
Q

Neutrophil Functions

A

-first defenders on scene
-important for inflammatory responses
-clean up debris
-increased cell count points to bacterial infection

73
Q

Eosinophils (granulocytes)

A

-increase in these cells associated with: allergic conditions (asthma + hay fever) & internal parasite infestations

74
Q

Basophils (granulocytes)

A

-least numerous
-poorly understood
-similar to mast cells

75
Q

Basophil Functions

A

-release histamine in allergic reactions
-release heparin, an anti-clotting agent, anticoagulant drug

76
Q

Monocytes (agranulocytes)

A

-phagocytotic
-emerge from bone marrow
-migrate to tissues and mature to become macrophages
-antigen presentation
-cytokine production
-cytotoxicity
-live several months-years

77
Q

Lymphocytes (agranulocytes)

A

-B cells
-T cells
-bind to antigens and destroy cells
-specifically programmed
-live 100-300 days

78
Q

B Lymphocytes

A

-produce antiBodies
-antibody mediated immunity

79
Q

T Lymphocytes

A

-do not produce antibodies
-destroy target cells by releasing chemicals

80
Q

Platelets

A

-from megakaryocytes
-7-8 day lifespan
-don’t leave blood
-1/3 stored in spleen and released by sympathetic splenic contraction
-no nuclei, some organelles and enzymes
-have granules
-important in blood clotting

81
Q

Thrombopoietin

A

-liver hormone
-increased number of megakaryocytes and platelets per cell

82
Q

Platelet Granules

A

-contain secretory products
-ADP
-serotonin
-epinephrine

83
Q

Hemostasis

A

-stoppage of bleeding from broken blood vessels

84
Q

Steps in Hemostasis

A
  1. vascular spasm
  2. formation of platelet plug
  3. blood coagulation
85
Q

Vascular Spasm

A

-results from damage to blood vessel
-damaged tissue secretions cause contraction (minimize blood loss)
-endothelial layer becomes sticky to aid clotting

86
Q

Formation of a Platelet Plug

A

-platelets activated by exposed collagen (extracellular protein) in damaged vessel wall
-aggregation: platelets release ADP causing other platelets to become sticky

87
Q

Thromboxane A2

A

-synthesized from platelets stimulates further aggregation

88
Q

Platelet Plug Function

A

-decreases blood loss
-maintains BP
-important for blood clot production

89
Q

Blood Coagulation (clotting)

A

-blood converted to clot/thrombus
-occurs around platelet plug
-can take place in absence of all cells except platelets

90
Q

Clot Formation

A

-reinforced platelet plug
-creates non-flowing gel

91
Q

Clotting Factors

A

-always present in plasma in inactive form
-activated in a cascade

92
Q

Clotting Cascade

A

-12 plasma proteins produced in lover
-act as enzyme co-factors
-series of steps
-final conversion of fibrinogen into fibrin mesh
-intrinsic/extrinsic pathway

93
Q

Thrombin

A

-converts fibrinogen to fibrin
-bound to fibrin to prevent systemic clotting
-unbound thrombin is inactivated

94
Q

Intrinsic Pathway

A

-all compounds exist in plasma
-seven steps
-Hageman factor (XII) activated by contact with exposed collagen or foreign surface

95
Q

Extrinsic Pathway

A

-compounds exist in tissues (outside of blood - muscle/liver)
-only 4 steps
-tissue thromboplastin is released from traumatized tissue and activates factor X

96
Q

Clot Retraction

A

-contraction of platelets shrinks fibrin mesh
-squeezing fluid from clot to get rid of it

97
Q

Clot Dissolution

A

-enzyme plasmin dissolves clot
-plasmin is formed from plasminogen which breaks down the fibrin meshwork
-gets rid of clot

98
Q

Thrombus

A

-abnormal clot attached to vessel wall
-can occlude the vessel
-fatal heart attacks

99
Q

Emboli

A

-freely floating clots
-can suddenly block blood flow
-can cause strokes and prevent oxygen to tissues

100
Q

Endothelial Cell Dysfunction

A

-associated with atherosclerosis
-can cause thromboembolism

101
Q

Impaired Liver Function

A

-reduces protein production (clotting factors)
-can cause clot formation disorders

102
Q

Vitamin K Deficiencies

A

-decreased synthesis of clotting factors
-clot formation disorders

103
Q

Hemophilia

A

-lack of clotting factors
-results in excessive bleeding