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Physiology 210 > Blood Physiology > Flashcards

Blood Physiology Flashcards

1
Q

Functions of blood

A
  • transport of substances in blood
  • regulation of ion and pH balance
  • defense and immune protection
  • hemostasis or prevention of blood loss
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2
Q

Blood centrifugation

A

upper layer: plasma 55%
middle layer: buffy coat - white blood cells and platelets <1%
bottom layer: red blood cells 42% females, 47% males

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3
Q

Composition of plasma

A
  • water, electrolytes, organic molecules, trace elements, gases
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4
Q

Functions of plasma proteins

A

Albumins: colloid osmotic pressure of plasma, transport substances in plasma
Globulins: clotting factors, enzymes, antibodies
Fibrinogen: forms fibrinogen threads to blood clotting
Transferrin: transport of iron
Made in liver

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5
Q

3 types of blood cells

A

Red blood cells (erythrocytes): transport of oxygen and carbon dioxide
White blood cells (leukocytes):
Platelets (thrombocytes):

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6
Q

Different types of white blood cells

A

Neutrophils, eosinophils, basophils, monocytes, lymphocytes

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7
Q

neutrophils

A

phagocytes

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8
Q

Eosinophils

A

defense against parasites

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9
Q

Basophils

A

inflammation

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10
Q

Monocytes

A

phagocytes and immune defense, leave blood stream and transformed into macrophages

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11
Q

Lymphocytes

A

B-cell: antibody production and humoral immunity
T-cell: cellular immunity

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12
Q

Hematopoiesis

A

formation of blood cells
before birth - yolk sac, liver, spleen
after birth - bone marrow
all originate from a pluripotent hematopoietic stem cell

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13
Q

Cytokines

A

protein that regulates hematopoiesis
released into blood and act on receptors of cells
erythropoietin - production of RBC
thrombopoietin - production of platelets

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14
Q

Structure of hemoglobin

A

single hemoglobin molecule has 4 globin protein chains (2 alpha and 2 beta chains), 4 heme groups, 4 iron atoms (each hemoglobin can find 4 oxygen)

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15
Q

Manner of oxygen binding

A

relaxed manner means successive oxygen facilitates finding of next oxygen
oxyhemoglobin is hemoglobin bound to oxygen
deoxyhemoglobin has tight binding structure and has given up oxygen

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16
Q

CO inhalation

A

Hb has higher affinity for carbon monoxide so it binds very tightly and cannot bind oxygen and deliver it to body

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17
Q

3 factors needed for RBC production

A

Cytokines: erythropoietin (EPO) stimulates RBC production
Dietary factors: iron needed in Hb, folic acid, vitamin B2
Intrinsic factors: made by cells in stomach to absorb vit B12

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18
Q

EPO RBC production

A

stimulus for EPO secretion comes from low oxygen in kidneys
EPO acts on bone marrow to turn stem cells to RBC
Increases oxygen carrying capacity of blood

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19
Q

Hypoxia

A

low oxygen concentration in blood

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20
Q

Transferrin

A

iron transport protein in blood

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21
Q

Ferritin

A

protein that stores iron in liver

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22
Q

Recycling hemoglobin

A

Heme - iron (absorbed in blood or ferritin), biliverdin (bilirubin secreted into bile and enters small intestine)
Globin: broken down into amino acids

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23
Q

Pernicious anemia

A

lack of intrinsic factor or vit B12

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24
Q

Aplastic anemia

A

damage of bone marrow due to radiation/drugs

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25
Q

Kidney disease

A

reduced level of EPO

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26
Q

Hemolytic anemia

A

increased breakdown due to abnormal shape of RBC

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27
Q

Hemorrhagic anemia

A

blood loss due to injury, ulcers, chronic menstruation

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28
Q

Sick cell disease

A

abnormal Hb called HbS, nonflexible membrane and sickle shaped, recessive disease

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29
Q

2 types of immunity

A

Innate/natural: born with, non-specific defenses, physical or chemical barriers on body, no memory, fast, phagocytes (neutrophils and macrophages)
Acquired/adaptive: acquired over time upon exposure to foreign pathogens (antibodies), has memory, slow, lymphocytes (B and T cells)

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30
Q

Inflammation

A

innate immune response to tissue injury
cause healing, destruction of non-self, formation of scar tissue (fibrosis)

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31
Q

Histamine

A

causes vasodilation which increases blood flow causing redness and heat
causes blood vessels to become leaky and permeable allowing protein and fluid to move to extracellular space causing swelling

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32
Q

Cellular events of inflammation
WATCH VIDEO

A
  1. WBC move to edge of blood vessels
  2. WBC attach to endothelial cells and slow rolling along vessel
  3. WBC activated - expression of proteins on surface of neutrophils and endothelial cells
  4. Neutrophils bind to complementary proteins on endothelial cells and stop rolling
  5. WBC squeeze between cells to exit out of blood vessel into tissue spaces
  6. WBC move to site of inflammation by chemotaxis
  7. Recognition of foreign agents
  8. Phagocytosis of foreign agents
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33
Q

Chemotaxis

A

WBC move against concentration gradient in response to their attraction to chemical factors

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34
Q

Phagocyte

A

cell that can eat non self pathogen by gulfing with temporary cytoplasm extension called pseudopodia
monocytes, macrophages, neutrophils

35
Q

Opsonization

A

coating of bacteria with opsonins (either antibodies or complement type proteins produced by host body which then speeds up attachment and phagocytosis of bacteria

36
Q

Neutrophils - oxygen dependent killing

A

corrosive free radical products are synthesized by body to destroy foreign body

37
Q

Neutrophils - oxygen independent killing

A

use bactericidal enzymes
lysozymes - degrade entire bacteria by proteolytic breakdown
lactoferrin - binds to iron and reduced iron in environment to bacteria cannot grow
defensins - drill holes in bacteria surface

38
Q

Complement proteins (OIL)

A

Opsonization - opsonins
Inflammation mediatory - chemoattractant that attract immune cells to site of inflammation, increasing histamine
Lysis - lysis of bacteria

39
Q

MAC attack

A

kill pathogen by forming a membrane attack complex
form a pore on bacteria surface
innate immune response

40
Q

B cell production

A

primary: develop in bone marrow, move to blood
secondary: move to lymphoid tissue or nodes

41
Q

T cell production

A

primary: start in bone marrow and develop in thymus gland, move to blood
secondary: move to lymphoid tissue or nodes

42
Q

3 R’s of Acquired immunity in B and T cells

A

Recognize, Respond, Remember

43
Q

Antigens

A

specifically recognized by antibody to form antibody-antigen complex
immunogen - activated immune response

44
Q

Antibody

A

globulin class of plasma proteins
Y shaped molecule with two heavy chains and two light chains connected by disulfide bridge

45
Q

Humoral immunity

A

naive B cells in lymph nodes are exposed to foreign antigens
B cell will bind and undergoes mitosis
One group plasma cells - synthesize antibodies specific to antigens and will freely circulate
One group memory cells - retain memory of first exposure for long time

46
Q

Cellular immunity

A

involves T cells: cytotoxic T cells, helper T cells, memory T cells

47
Q

Antigen presentation

A

macrophage engulfs foreign antigen, breaks into smaller pieces, and presents it to T cell in a protein called MHC
T cells will produce cytokines which interact with B cells

48
Q

MHC proteins

A

MHC I: all nucleated cells
MHC II: antigen presenting cells like macrophages

49
Q

Active immunity

A

direct exposure to antigen or exposure by vaccination
antibodies are self generated
not immediate and long term immunity

50
Q

Passive immunity

A

preformed antibodies are transferred from mother to fetus during pregnancy or nursing
immediate and short term immunity

51
Q

Hemostasis

A

prevention of blood loss - platelets
pro-hemostatic factors - prevent blood loss
anti-hemostatic factors - keep blood fluid

52
Q

Steps of hemostasis

A
  1. Vasoconstriction - through pain receptors, smooth muscle injury, serotonin
  2. Primary - Platelet plug formation - white thrombus
  3. Secondary - Blood clotting/coagulation - red thrombus
53
Q

Structure of platelets

A

Contain vesicles called alpha granules (von Willebrand factor) or dense granules (ATP, serotonin, calcium), glycogen, contractile proteins actin and myosin, glycoproteins
Do not contain nucleus

54
Q

Primary hemostasis - platelet plug formation

A
  1. Adhesion - platelets stick to collagen tissue using von Willebrand factor and form a bridge
  2. Activation of platelets - binding triggers release of ADP and serotonin, express fibrinogen receptor to form lattice like structure, prothrombin converts to thrombin
  3. Aggregation of platelets - new platelets adhere to old ones positive feedback which rapidly form plug, actin and myosin tighten plug and seal cut site
55
Q

Inhibits Platelet Plug

A

adjacent undamaged endothelial cells release prostacyclin, nitric oxide which inhibit spread of plug

56
Q

Arachidonic Acid Metabolites

A

Lipoxygenase pathway - arachidonic acid is converted to leukotrienes by enzymes lipoxygenase which initiate swelling
Cyclooxygenase pathway - converted to cyclooxygenase enzyme which prevent blood loss
COX 2 produces prostacyclin
COX 1 produces thromboxane A2

57
Q

Aspirin

A

prevent clot formation during heart attacks
inhibit COX 1
initially inhibit COX 2 (cyclooxygenase) but will overcome it

58
Q

Secondary hemostasis - formation of blood clot

A

cascade of clotting factor enzymes
activation occurs by proteolytic cleavage
formation of gel-like fibrin clot where RBC cells become trapped in red thrombus

59
Q

Factors involved in blood clotting

A

13 factors, all present in inactive plasma proteins in blood, synthesized in liver

60
Q

Factor I

A

Fibrinogen

61
Q

Factor II

A

Prothrombin

62
Q

Factor III

A

Tissue thromboplastin, tissue factor

63
Q

Factor IV

A

Calcium

64
Q

Factor Xa

A

formation of active thrombin by prothrombin which will turn fibrinogen to fibrin

65
Q

Intrinsic pathway for blood clotting

A

Activation of factor XIII when contacted with damaged blood vessel wall, triggers clotting

66
Q

Extrinsic pathway for blood clotting

A

Activation of factor VII when contacted with tissue factors outside blood vessel. Factor VIIa activates X to facilitate fibrin formation by thrombin production

67
Q

Deficiency of factor VII and VIII

A

serious bleeding

68
Q

Deficiency of factor XI

A

moderate bleeding

69
Q

Deficiency of factor XII

A

no bleeding problem, but won’t clot in vitro

70
Q

Roles of Thrombin

A

activation of platelets
converts soluble fibrinogen into insoluble fibrin
activates several other clotting factors
plays a role in anti clotting pathways

71
Q

Regulation of blood clotting

A

Anticoagulants - prevent clot formation
Fibrinolysis - enzymatic breakdown of fibrin in blood clots

72
Q

Natural anticoagulants

A

Tissue factory pathway inhibitor (TFPI) - inhibit factor III tissue factor
Antithrombin 3 - inhibits thrombin
Thrombomodulin - binds to thrombin to prevent clot, expressed on healthy endothelial cells, activates protein C

73
Q

Clinical anticoagulants

A

Calcium chelators - remove free ionized calcium
Heparin - increases antithrombin 3
Vitamin K - inhibit clotting factors

74
Q

Fibrinolysis

A

breakdown of fibrin in a clot
tPA tissue plasminogen activator
converts inactive plasminogen to active enzyme plasmin which breaks down fibrin strands

75
Q

ABO Blood Type

A

A, B, AB, O
surface carbohydrate antigens
Blood group A - antigen A, B antibodies
Blood group B - antigen B, A antibodies
Blood group AB - antigen A and B, no antibodies
Blood group O - no antigens, A and B antibodies
Dominant is A and B antigen

76
Q

ABO gene code

A

DNA will code for enzyme protein that attaches specific carbohydrate molecule to surface proteins of RBC

77
Q

Agglutination

A

surface antigens on RBC are bound to antibodies to form a clump followed by hemolysis or RBC, blood is not matched

78
Q

Major cross-match

A

donors RBC antigens are matched with recipient plasma antibodies

79
Q

Minor cross-match

A

whole blood is transfused where RBC are not separated from plasma which contains antibodies

80
Q

Universal donor

A

Type O

81
Q

Universal recipients

A

Type AB

82
Q

Rhesus blood type

A

protein antigen
Rh positive - presence of D antigen, no D antibodies
Rh negative - absence of D antigen, no D antibodies
dominant is D antigen
anti-D antibodies are immunoglobin G class

83
Q

Mismatched blood transfusion in Rh system

A

Rh- with no D antibodies is exposed to Rh+ and develops D antibodies. Then same Rh- person exposed mistakenly to another Rh+ which leads to clumping

84
Q

Rhesus mismatch between mother and child

A

Rh- woman conceives with Rh+ man, baby will be Rh+
First delivery - fetal Rh+ RBC enters maternal blood through placental rupture
Mom produces D antigens
Second delivery - mom’s D antigens will enter baby’s body and bind to baby RBC and hemolysis
Hemolytic disease of the newborn - enlarged spleen and jaundice
Treatment: after first delivery mom is treated with D antigens that will bind with new Rh+ blood and will be blocked

Physiology 210 (12 decks)

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