lecture 12 Flashcards
blood definition
formed elements or cells in a liquid ECM
ECM of blood
blood plasma
what percent of body mass is blood
8%
average amount of blood in males vs females
males - 5-6L
female - 4-5L
blood temperature it must be kept around
38 degrees
components of blood (%)
blood plasma (55%)
formed elements (45%)
formed elements of blood
erythrocytes
platelets
leukocytes
blood plasma % makeup
91.5% water, 8.5% solutes
solutes in blood plasma
albumins (54%)
globulins (38%)
fibrinogen (7%)
other (1.5%)
albumins in blood plasma function
maintain osmotic pressure
globulins in blood plasma function
antibodies and transport proteins for ions, lipids, and vitamins
“other (1.5%)” components of blood plasma
electrolytes
nutrients
enzymes
hormones
gases
metabolic wastes
erythrocytes facts
most abundant
- transport O2 and CO2
- mature cells have no organelles - more hemoglobin
leukocytes facts
many types
fight infection and invasion
platelets
anucleate cell fragments
thrombocytes
nucleated blood cells that form clots in lower verebrates
why might a low or high hematocrit be harmful?
low - less effective transport of O2, CO2, hormones etc
high - thickens blood, risk of blockage, heart works harder
hemopoiesis
process of blood cell formation
pluripotent stem cells
blood cells start as these, will continue development into two lineages (myeloid and lymphoid)
precursor cells
produced by each lineage, step between progenitor cells and formed elements
myeloid lineage produces:
RBCs, platelets, 4 leukocytes (no lymphocytes)
lymphoid lineage produces:
T lymphocytes, B lymphocytes, Natural killer cells
path of an RBC
pluripotent stem cell
myeloid stem cell (CFU-E)
proerythroblast
reticulocyte
RBC
what regulates blood cell formation
hemopoietic factors (hormones)
these include:
erythropoetin
thrombopoetin
cytokines
(more on them later)
erythropoetin
increases number of erythrocyte precursor, increasing RBCs in blood
- synthesized in kidneys
thrombopoetin
stimulates platelet formation
- synthesized in liver
cytokines
stimulate proliferation of leukocytes and lymphocytes
- synthesized in red marrow
RBC structure
biconcave discs
- flexible
- anucleate
- lack most organelles when mature
- no mitochondria
why do RBCs have no mitochondria
makes more space for hemoglobin, and so the mitochondria cannot use the O2 it is carrying in aerobic cellular respiration
RBC count in males and females
4.8 mil in females
5.4 mil in males
how many O2 can hemoglobin bind
4
carbonic anhydrase
enzyme contained by RBCs that converts CO2 into carbonic acid, important as a blood buffer
Nitric oxide (NO)
(released by, causes)
acts as a hormone
- released by endothelial cells during inflammation, causes vasodilation
RBC life cycle
- damaged RBCs die
- globulin + heme parts are seperated
- globulin is recylced
- ferric iron from heme is bound to transferrin
- ferric iron transfered to ferritin for storage in liver
- iron reattached to transferrin
- iron taken to Red marrow
- erythropoiesis
5 steps of erythropoiesis
- starts with proerythroblast
2.. it divides, one cell ejects nucleus - resulting cell - reticulocyte
- nucleus ejection - biconcavity
- RBC leaves marrow
- matures in 1-2 days (loses organs)
negative feedback loop for RBC production
- stimulus - reduced O2 transport to tissues
- sensor - kidney receptors
- control centre - kidney cells
- effectors - proerythroblasts in red marrow
- net outcome - more RBCs = more O2 delivered to tissues
leukocytes structure
all organelles present, no hemoglobin
may be granular or agranular
granular leukocytes
contain special vesicles
- neutrophils
- eosinophils
- basophils
neutrophils
- granular, phagocytic cells
- myeloid lineage
- polymorphonuclear (multilobed nucleus)
eosinophils
- defend against parasites
- granular
- combat effects of histamine
basophils
- release histamine
- granular
- granules obscure appearance
lymphocytes
– agranular
- lymphoid lineage
- T, B, NK cells
monocytes
- agranular
- myeloid lineage
- differentiate into macrophages or fuse into osteoclasts
chemotaxis
permit WBCs to find the site of infection
movement of WBCs to a chemical stimulus
fastest leukocyte to respond to bacterial infection
(and what they do at the site)
neutrophils, they release lysozymes that disrupts bacterial membranes
what happens during infection and invasion?
inflammation
emigration and rolling
chemotaxis
tissue disinfection
tissue healing
emigration
movement of WBCs from blood to the site of tissue damage
rolling
leukocytes sensing where to squeeze through the endothelium
how are platelets formed?
when megakaryoblasts mature into magokaryocytes and break into 2-3k pieces
lifespan of a platelet
5-9 days
hemostasis
process that prevents hemorhage
3 steps of hemostasis
vascular spasm
platelet plug formation
blood clotting
vascular spasm
chemicals released by damaged smooth muscle and activated platelets lead to spasm of smooth muscle around blood vessels
stems bleeding shortly
platelet plug steps
platelet adhesion
platelet activation
ADP makes platelets sticky
blood clot
platelet plug + insoluble protein fibres
coagulation
process of blood clot formation
requires clotting factors like calcium and enzymes
intrinsic blood clotting pathway
activation
activated by damaged endothelial cells sense within blood vessels
extrinsic pathway activation
external substance (tissue factor) enters blood
sickle cell anemia
genetic mutation in the globin gene
- change in amino acid sequence, chances shape of protein folding
- alleles protect against malaria
malaria
caused by parasitic infection of erythrocytes
- sickled RBCs leak potassium which allows malarial parasite to reproduce
hemophilia
inherited disease
- mutation leading to insufficient clotting factors
- minor injury - hemorrhage
- found on X chromosome
- treated by donated plasma + clotting factors
polycythemia
too many RBCs in the blood
- caused by mutation, hormone imbalance, or EPO injection
- leads to thickened blood
both pathways of clotting first activate factor ____, which starts a common pathway
factor X
common pathway in blood clotting
factor X starts common pathway
- prothrombinase activates prothrombin into thrombin
- thrombin activates factor XIII to strengthen fibrin threads between RBCs
