Blood Flashcards
list the functions of blood
Delivers oxygen, nutrients, etc.
Transports metabolic wastes away (CO2, ammonia, etc.)
Maintains body temperature
Maintains body pH (Bicarbonate system)
Maintains fluid volume through exchange (electrolytes)
Prevent blood loss with clotting
Prevents infection (Antibodies, complement proteins, WBC, etc.)
formed elements of blood
were originally living cells, not necessarily still living
erythrocytes
RBC
no longer living
carry respiratory gases (mainly O2)
leukocytes
WBC
immunity
living cells
platelets
little cellular fragments
contain vesicles containing proteins used in clotting
plasma
liquid component
water, proteins, nitrogenous substances
proteins in plasma
albumin globulins, clotting proteins, etc.
Create special amount of osmotic pressure
Colloid osmotic pressure
High concentration in blood, too big to leave
hematocrit
procedure done, finger prick then centrifuged and separated based on mass RBC dense (bottom) Buff layer (leukocytes and platelets) Plasma The length of RBC + entire sample / sample = amount of RBC
Structure and function of RBC
Small Biconcave Anucleate No cell organelles (no DNA) Contain hemoglobin Contain antioxidant enzymes Eliminate free radicals (leakage of charged O2 particles (toxic))
hemoglobin
pigment that gives blood its color
erythropoiesis
RBC production
Subtype of hematopoiesis
All blood cells produced in red bone marrow
erythropoiesis process
Hemocytoblast produces myeloid stem cell
Hemoblasts pluripotent
Myeloid stem cell becomes proerythroblast
Proerythroblast is the committed cell!
Proerythroblast becomes early erythroblast
Early erythroblast becomes late erythroblast
Late erythroblast becomes normoblast
Normoblast loses organelles and nucleus to become reticulocyte
Accumulate hemoglobin
Reticulocyte immature RBC
Reticulocytes mature in bloodstream to become erythrocytes
erythropoietin
hormone produced by kidneys; monitor O2 concentration, stimulated by low O2 to produce more RBC
testosterone role in erythropoiesis regulation
stimulates kidneys to release erythropoeitin
Men have higher RBC count
role of iron in erythropoiesis regulation
from diet, needed to produce functioning RBC
Stored in cells as ferritin and hemosiderin
Transported in blood as transferrin
B vitamins role in erythropoiesis regulation
linked to intrinsic factor to make RBC
dietary nutrients role in erythropoiesis regulation
carbs, AA, etc. to make cellular components
erythrocyte longevity
100-120 days
Old erythrocytes destroyed by macrophages
Old erythrocytes recycled primarily in the spleen
Spleen rich in macrophages
Heme split from globin
Iron bound to proteins and stored
Bilirubin produced
Picked up by liver and secreted as bile into intestine
Pigment degraded and expelled in feces
Globin breakdown to AA
anemias
not enough RBC or something wrong with RBC so it cant carry O2
polycythemia
too many RBC, cant deliver O2 well because blood is so thick, cannot travel efficiently
chemical makeup of hemoglobin
Complex protein, 4 subunits
2 types of subunits: alpha and beta subunits
Globin protein bound to heme pigment
globin
4 polypeptide chains, 2 alpha subunits, and 2 beta
heme
contains oxygen-binding iron, each heme can bind to four O2
oxyhemoglobin vs. deoxyhemoglobin
Can shift between the two
Sigmoidal curve
Shows hemoglobin LOVES O2
When it starts it wants more and doesn’t like to give it up
Saturate quickly and loves to stay saturated
carbaminohemoglobin
carry CO2, binds to the amino acids on the protein
diapedesis
ability of cell to leave circulation and go into interstitial space
RBC cant
Some WBC can
structural characteristics of leukocytes
Complete cells with nuclei and organelles
Living; can reproduce in some cases
Display positive chemotaxis
Positive (more forward)
Ability to move toward certain chemical stimuli
types of granulocytes
neutrophils, eosinophils, basophils
neutrophils
60-70% of WBC, phagocytic function during inflammation
eosinophils
around 20%, two lobe nucleus, granules carry enzymes to fight parasitic worms
basophils
.5-1% granules contain histamine, vasodialator, attract WBC
types of agranulocytes
lymphocytes and monocytes
lymphocytes
in the lymphatic system, active when foreign tissue present
Two types
B= produce antibodies
T= attract own abnormal/infected
monocytes
largest, u shaped nucleus (3-8%), phagocytic cell outside circulation
leukemia
cancer of WBC
Infectious mononucleosis
increase in number of agranulocytes from virus (mono)
leukopenia
not enough WBC
leucopoiesis
Hemocytoblasts give rise to myeloid stem cells and lymphoid stem cells
granulocyte leukopoiesis process
Myeloid stem cells become myeloblasts
Myeloblasts committed to granulocytes
Myelobasts accumulate lysosomes to become promyelocytes
Promyelocytes differentiate into myelocytes
Cell division stops and nuclei arch to form band cells
Nuclei constrict and segment to become mature granulocytes
Agranulocyte Leukopoiesis
Myeloid stem cells become monoblasts
Monoblasts become promonocytes
Promonocytes leave bone marrow and become monocytes in lymph tissue
Lymphoid stem cells become lymphoblasts
Lymphoblasts become prolymphocytes
Prolymphocytes leave bone marrow and become lymphocytes in lymph tissue
Regulation of Leukopoiesis
interleukins and colony-stimulating factor
interleukins
infected cells from virus release these
Colony-stimulating factor
major regulator of WBC
platelets
Anucleated cytoplasmic fragments of megakaryocytes
Granules contain clotting chemicals
Thrombopoiesis
Hemocytoblasts give rise to myeloid stem cells
Myeloid stem cells become megakaryoblasts
Megakaryoblast is committed cell
Megakaryoblasts undergo repeated mitosis but no cytokinesis to form megakaryocytes
Cytoplasmic extensions of megakaryocytes break off to be platelets
* regulated by thrombopoietin*
hemostasis
cessation of bleeding
process of hemostasis
1 Vascular spasm
Blood vessels constrict
2 Platelet plug formation
Accumulate at the site of damage
3 coagulation
“Gel up”
Activation of protein fiberprocess of platelet plug formation
Damage to blood vessels exposes underlying collagen fibers in CT
Also releases von Willebrand factor and thromboxane A2
Willebrand factor is a plasma protein
Thromboxane A2 is a prostaglandin
Creates an environment for platelets to stick
Causes platelets to collect and adhere at the site of damage
Platelets won’t stick to ET
Once attached, thrombin activates platelets to breakdown and release chemical contents
Clotting factors
Intrinsic Pathway to Coagulation
Through platelets themselves
Series of reactions in which clotting factors converted to active forms (13 proteins)
Ultimately aggregated platelets release PF3
PF3 activates other intermediates leading to activation of factor x (10)
Activated factor x complexes with calcium, PF3, and factor V to form prothrombin activator
Prothrombin activator catalyzes the conversion of prothrombin to thrombin
Thrombin catalyzes the polymerization of fibrinogen into fibrin
Thrombin also activates factor xiii (13) which links fibrin strands together
Extrinsic Pathway to Coagulation
From damaged cells
Chemical to go faster
Injured cells release tissue factor
Tissue factor interacts with PF3 to allow shortcut to factor X activation
factors limiting clot formation
Intact endothelial cells secrete PGI2 (prostacyclin) and heparin
PGI2= prostaglandin secreted by intact endothelial cells
heparin= anticoagulant
Vitamin E quinone
Prevents coagulation
clot retraction
Platelets contain contractile proteins
Cause platelets to contract and squeeze out serum to compact clot
Draws ruptured edges of vessel closer together
PDGF stimulates vessel repair
Platelet-derived growth factor
Regeneration
fibrinolysis
Clot accumulates plasminogen
Plasminogen is activated to plasmin
Plasmin digests fibrin
clot limiting factors
Clotting factors carried away from site by circulating blood
Antithrombin 3 inactivates thrombin
Protein c inhibits intrinsic pathway events
Heparin enhances activity of antithrombin 3 and inhibits intrinsic pathway events
Thromboembolic disorders
clot too much
thrombus, embolism
thrombus
blood clot retained at the sight of the damage
Too big, block circulation
embolism
detached blood clot all at once
Stuck and cause blockage
bleeding disorders
dont clot enough
thrombocytopenia and hemophilia
thrombocytopenia
stop producing platelets
Insufficient platelets due to pathology
hemophilia
genetic disease
Missing gene for clot factors
ABO and Rh blood groups
Determined by the presence of agglutinogens (markers)
Specifically ABO and Rh (D)
Directs production of agglutinins (attackers for what you don’t have)
