Lectures 8, 9, 10 and 11: Blood Flashcards
Body Fluids
blood and ISF (60% of body)
1/3 of that is ECF
80% Interstital fluid and 20% plasma
Hematology
study of blood and blood disorderw
blood composition
plasma (yellowish, 91.5% water, 8.5% solutes)
fromed elements
Blood Plasma
more than 90% water
makes up 55% of blood
about 7% plasma proteins (made in liver)
Albumins
maintain osmotic pressuer
if dec, conce change, dec ability to get water tto end of caps
can be taken from blood for energy in starvation
Blood Doping
injecting previously stored RBCs to self before atheletic event (most of plama removed first) so you can get more O2 Dnagerous *inc blood viscosity *forces heart to work harder
Globulins
antibodies that bind to forgieners (antigens)
Blood Serum
plasma w/o fibringin and other clotting factors
give this to people so we dont worry about causing clots
Hematocrit Ranges
38-46% W
40-50% Male
Polycythemia
too many RBCs
dehydration, tissue hypoxia, blood doping
Platelets
Thrombocytes clotting irregular shape can send stickiness messages 150,000 to 400,000 platelets per microL blood
Lymphocyte Types
T cells (come from Thymus) and B Cells
Formed Elements
RBCs
Luekocytes
Platelets
RBC shape
biconcave 8 um wide, 2 thick inc SA for O2 binding easily deformed filled with hemoglobin (over 90% of protein in them)
Reoleaux
stacked
larger BVs
RBCs
Parachutter
small arterioles and venules
RBCs
Bullet
in caps
RBCs
Hemoglobin
protein 4 large prteon chains (2 alpha 2 beta) heme group *porphyrin Ring each iron in heme can bind to one O2 molec (total of 4)
porphyrin Ring
surrounds 1 iron molec
complicated structure
Hemoglobin Functions
carry 4 O2 molecs
O2 bound in caps of lungs, transported to cells
Transports 23% of CO2 produced in CELLS
*** DOES NOT BIND WITH HEME (where O2 binds)
Blood concs of hemoglobin in health vs. anemic
16g/dL (g/100mL) in men
14 g/dL in women
diff probably due to body size
hematocrit AND hemoglobin level diagnositc for anemia
Erythropoiesis
RBC formation in Red Bone Marrow after birth, formed by stem cells * which diff into proerythroblasts **Then become erythroblast, then reticulocyte
Erhtydrocyte
when fully mature
no more nucleus!
if anculear pereythrocyte
BAD
means theres a crazy high need for RBCs for infections
Mature reticulocyte
hemoglobin produced, nucleus ejected
RBC formation steps
Hematopoietic stem cell myeloid stem cell proerythroblast erythroblast *** 3 stages Reticulocute (lose nuclus) Erhtyrocyte!
Hemopoetic growth factors
regulate differentiation of proliferation of blood cells
EPO
TPO
Cytokines
Erythropoietin (EPO)
RBCs
produced by kidneys
incs RBC precursors
Thrombopoietin
hormone from liver
stim. platelet formation
* Megakaryocyte created (can create thousnds of platelets)
* sheds parts (platelets form)
Cytokines
local hormones of bone marrow
stim proliferation in other marrow cells
colony stimulating factors (CSFs) and interleukins
stim WBC production
RBC Lifecycle
live 120 days
no repair possible (no culeus!)
breakdown and recycle
removed by macrophages in spleen and liver
Recycling RBCs
globin broken down, recycle amino acids
heme split into iron and biliverdin (green pigment)
* iron to make more hemoglobin
*ring to make bile
Recycled Iron
stored in liver, muscle or spleen
attaches to protein (ferritin or hemosiderin) there
transported to bone marrow to use in hemoglobin synth
Biliberdin
made to bilirubin (green to yellow) from porforin ring excreted by kidneys and intestines *bilirubin-->urobilinogen **some reabsoprbed, becomes urobilin, expredted by KIDNEYS
Medical Use of Growth Factors
recomb EPO effective in treated dec BC production due to kidney disease or cancer
gives O2 carrying capacity lost
stim WBC formation in cancer patients getting chemo, which kills marrow and stem cells
TPO given to prevent platelet depletion during chemo or pregnancy
cells from myeloid stem cells
RBC megakaryocyte eosinophin basophil neutrofil monocyte
Lymphoid stem cells
lymphocyte
T and B cells
very specific in what they attack
Colony Forming Unit E
erythrocyte
CFU Meg
megakaryocyte
CFU GM
nuetrophil
monocyte
number of WBCs
way less
1 for every 700 RBC
if loss of blood, loss of WBCs first (thats their job)
only 2% circling in blood
* rest in lymph fluid, skin, lungs, nodes, and spleen
Leukopenia
low WBC count
radiation, shock, chemo
WBC movement
roll on endothel, stick to it (to see if damage
Selectins
WBC adhesion molecs
placed near injury sites
Integrins
on neutrophils
movement through wall
Neutrophil
60-70% (up in bact. infection) fastest bacteria *lysozomes (digest bact.) defensin proteins (antibiotics, poke holes in bact. cell) release strong oxidants (H2O2)
eosinophil
2-4% (up in allergy, parasite) relases histaminASE *slow inflamation caused by basophil attack worms phagocytizees antibody antigen complexes accidental triggering=allergies
basophil
<`1% (up in allergy, hypothyroid) inflammatory response Mast Cells (how they enter CT) relase histamine, heparin, serotonin inc inflam response, inc blood flow, allergic reactions
lymphocyte
20-25% (up if viral)
Tcell
B cell
Natural Killer Cell
T cell
attack virus, fungi, transplated organs, cancer cells, some bact
differintiates non self cells
Natural Killer Cells
attack many microbes
some tumor cells
kill forgieners with direct attack
B Cell
destory bacteria
turn into plasma cells that produce antiboides
Monocyte
3-8% (up if viral, fungal) slowest, but arrive in larger numbers become macrophages (when they leave the blood) destroy microbes clean up dead tissue
Phagocytosis
neutrophils and monocytes Process: 1. chemotaxis 2. Adherence & ingestion 3. Destruction
Chemotaxis
attract phagocyte to infection site
relase chems from pathogen and/or infected cell (this is what attracts)
Adherence and Ingestion
attachment of phagocyte to pathogen membrane
ingestion by pseudopodia (arm things)
result: phagosome
Destruction
initiated when phagolysome fuse
lysozyme relasesd, destroys membrane of pathogen
fragments removed via excocytosis
Phagolysosome
fusing of phagosome and lysosome
Bone Marrow Transplant Procedure
destroy sick marrow (chemo, radiation)
put donor sample in vein, goes to marrow
success: compatability of donor and recipiant
Bone Marrow Transplant Treatment
leukemia sickel cell breast, ovaria, testicular cancer lymphoma aplastic anemia
Platelet Lifetime and Location
5-9 days
2/3 in circulation
1/3 in spleen
Thrombosis
clot formation
thrombus
a clot
embolus
circulating clot
BAD
lack of blood to area, distal will not live
stroke in brain
hemorrhage
sever, uncontrolled bleeding
Thrombocytopoiesis
myeloid stem–> megakaryocyte
TPO (thrombopoietin) causes frags to fall off mega (2000 to 3000 per cell)
very small platelets (10-20 could fit in RBC)
Hemostasis
reaction to stop bleeding
must be small vessle
depends on plateltes
3 phases of hemostasis
vascular spasms (immediate vasoconstriction in response)
platelet plug formation
coagulation
Vascular Spasm
hemostasis ONLY in vessles with SMOOTH MUSCLE (so NO caps!!!!) also must be small react to injury reduce vessle diameter stop blood flow
Platelet Plug Formation
Platelets dont normally stick do when damage stick to exposed collagen fibers (which it knows shouldnt be there) ADP, seratonin, throboxane 2 relasesd activate more platelets ADP makes sticky, T and seratonin cause contraction of cells result: tight soft platelet plug
Coagulation
13 clotting factors (most from liver)
reactions where blood goes from liquid to gen
intrinsic and extrinsic pathways
(INT slower)
eextrensic blood (hemostasis)
blood vessle
intrinsic (hemostasis)
platelet, blood component
common pathway for clotting
- prothrombinase activated
prothrombin–> thrombin - thrombin
converts firinogen to fibrin (sol to insol)
activate factor XIII (stabilize fibrin network)
Formation of clotting factors
synthed in liver
prothrombin
fibrinogen
factors V, VII, IX, X
Factor II
Thrombin
Vitamin K needed for
making factors II, VII, IX, X
vit K deficiancy can lead to failure of clotting
Lack of VIII
hemophiliacs
Fibrinolysis
clots must be dissolved (so no embolus)
dissolution of clot
things that make plasmin
tissue plasminogen activator, thrombin, plasminogen, make
digest fibrin strands and break clot
