Blood Physiology Flashcards

(84 cards)

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
Kidney disease
reduced level of EPO
26
Hemolytic anemia
increased breakdown due to abnormal shape of RBC
27
Hemorrhagic anemia
blood loss due to injury, ulcers, chronic menstruation
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Sick cell disease
abnormal Hb called HbS, nonflexible membrane and sickle shaped, recessive disease
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2 types of immunity
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)
30
Inflammation
innate immune response to tissue injury cause healing, destruction of non-self, formation of scar tissue (fibrosis)
31
Histamine
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
32
Cellular events of inflammation WATCH VIDEO
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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Chemotaxis
WBC move against concentration gradient in response to their attraction to chemical factors
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Phagocyte
cell that can eat non self pathogen by gulfing with temporary cytoplasm extension called pseudopodia monocytes, macrophages, neutrophils
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Opsonization
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
Neutrophils - oxygen dependent killing
corrosive free radical products are synthesized by body to destroy foreign body
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Neutrophils - oxygen independent killing
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
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Complement proteins (OIL)
Opsonization - opsonins Inflammation mediatory - chemoattractant that attract immune cells to site of inflammation, increasing histamine Lysis - lysis of bacteria
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MAC attack
kill pathogen by forming a membrane attack complex form a pore on bacteria surface innate immune response
40
B cell production
primary: develop in bone marrow, move to blood secondary: move to lymphoid tissue or nodes
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T cell production
primary: start in bone marrow and develop in thymus gland, move to blood secondary: move to lymphoid tissue or nodes
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3 R's of Acquired immunity in B and T cells
Recognize, Respond, Remember
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Antigens
specifically recognized by antibody to form antibody-antigen complex immunogen - activated immune response
44
Antibody
globulin class of plasma proteins Y shaped molecule with two heavy chains and two light chains connected by disulfide bridge
45
Humoral immunity
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
Cellular immunity
involves T cells: cytotoxic T cells, helper T cells, memory T cells
47
Antigen presentation
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
MHC proteins
MHC I: all nucleated cells MHC II: antigen presenting cells like macrophages
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Active immunity
direct exposure to antigen or exposure by vaccination antibodies are self generated not immediate and long term immunity
50
Passive immunity
preformed antibodies are transferred from mother to fetus during pregnancy or nursing immediate and short term immunity
51
Hemostasis
prevention of blood loss - platelets pro-hemostatic factors - prevent blood loss anti-hemostatic factors - keep blood fluid
52
Steps of hemostasis
1. Vasoconstriction - through pain receptors, smooth muscle injury, serotonin 2. Primary - Platelet plug formation - white thrombus 3. Secondary - Blood clotting/coagulation - red thrombus
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Structure of platelets
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
Primary hemostasis - platelet plug formation
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
Inhibits Platelet Plug
adjacent undamaged endothelial cells release prostacyclin, nitric oxide which inhibit spread of plug
56
Arachidonic Acid Metabolites
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
Aspirin
prevent clot formation during heart attacks inhibit COX 1 initially inhibit COX 2 (cyclooxygenase) but will overcome it
58
Secondary hemostasis - formation of blood clot
cascade of clotting factor enzymes activation occurs by proteolytic cleavage formation of gel-like fibrin clot where RBC cells become trapped in red thrombus
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Factors involved in blood clotting
13 factors, all present in inactive plasma proteins in blood, synthesized in liver
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Factor I
Fibrinogen
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Factor II
Prothrombin
62
Factor III
Tissue thromboplastin, tissue factor
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Factor IV
Calcium
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Factor Xa
formation of active thrombin by prothrombin which will turn fibrinogen to fibrin
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Intrinsic pathway for blood clotting
Activation of factor XIII when contacted with damaged blood vessel wall, triggers clotting
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Extrinsic pathway for blood clotting
Activation of factor VII when contacted with tissue factors outside blood vessel. Factor VIIa activates X to facilitate fibrin formation by thrombin production
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Deficiency of factor VII and VIII
serious bleeding
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Deficiency of factor XI
moderate bleeding
69
Deficiency of factor XII
no bleeding problem, but won't clot in vitro
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Roles of Thrombin
activation of platelets converts soluble fibrinogen into insoluble fibrin activates several other clotting factors plays a role in anti clotting pathways
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Regulation of blood clotting
Anticoagulants - prevent clot formation Fibrinolysis - enzymatic breakdown of fibrin in blood clots
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Natural anticoagulants
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
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Clinical anticoagulants
Calcium chelators - remove free ionized calcium Heparin - increases antithrombin 3 Vitamin K - inhibit clotting factors
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Fibrinolysis
breakdown of fibrin in a clot tPA tissue plasminogen activator converts inactive plasminogen to active enzyme plasmin which breaks down fibrin strands
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ABO Blood Type
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
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ABO gene code
DNA will code for enzyme protein that attaches specific carbohydrate molecule to surface proteins of RBC
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Agglutination
surface antigens on RBC are bound to antibodies to form a clump followed by hemolysis or RBC, blood is not matched
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Major cross-match
donors RBC antigens are matched with recipient plasma antibodies
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Minor cross-match
whole blood is transfused where RBC are not separated from plasma which contains antibodies
80
Universal donor
Type O
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Universal recipients
Type AB
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Rhesus blood type
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
Mismatched blood transfusion in Rh system
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
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Rhesus mismatch between mother and child
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