blood Flashcards
plasma
non-fluid matrix
clotting
55% of blood
made up of nutrients, gases, hormones, wastes, proteins, inorganic ions
albumin (60%)
globulins (36%)
fibrinogen (4%)
90% water
blood
made up of plasma, buffy coat (leukocytes and platelets), and erythrocytes
distributes substances (O2, Co2, nutrients, hormones)
regulates blood levels of substances (temp, pH)
protection (antibodies, WBCs, plasma, and platelets)
albumin
substance carrier
blood buffer
major contributor of OP
alpha and beta globulins
produced by liver
transport proteins
bind to lipids, metal ions, and fat-soluble vitamins
gamma globulins
antibodies released by plasma cells
fibrinogen
produced by liver
forms fibrin threads of blood clot
non-protein nitrogen substances
by-products of cellular metabolites that blood gets rid of (urea, uric acid, creatine, ammonium salts)
erythrocytes
make up 45% of blood
biconcave discs (efficient gas transport)
anucleate
possess no organelles
diameters larger than some capillaries
contain spectrin (help change shape)
each contain 250M Hb molecules (gas transport and blood viscosity)
high SA to volume ratio
Hb
composed of 2 alpha and 2 beta chains (globin component)
heme component (gives blood red color)
hematocrit
BV that is RBCs
47% for males
42% for females
erythropoiesis
- myeloid stem cell-> proerythroblast
- proerythroblast->basophilic->polychromic->orthochromatic erythroblast->recticulocytes (within 15 days)
- recticulocytes enter bloodstream
- becomes mature RBC (2 days)
dietary requirements for erythropoiesis
AAs
lipids
carbs
iron
B12
folic acid
life span of erythrocytes
100-120 days
1. Hb in old RBCs degenerate and get trapped in the spleen where macrophages engulf them
2. heme and globin are separated and the iron within them is recycled
3. heme gets degraded to bilirubin in the liver which gets degraded to urobilinogen in the intestines and leaves the body as stercobilin in feces
4. globin gets metabolized into AAs and gets released into the circulation
recticulocyte
indicate rate of RBC formation
low count indicates tissue hypoxia
high count indicated increased blood viscosity
granular leukocytes
neutrophils
eosinophils
basophils
agranular leukocytes
lymphocytes
monocytes
neutrophils
3-6 lobes in nucleus
2x size of RBC
phagocytic
most numerous
contain hydrolytic enzymes (defensins)
eosinophils
bilobed nucleus
granules
lysosome-like
digest parasitic worms
role in allergies and asthma
basophils
rarest
nucleus within 2 constrictions
large granules
contain histamine
similar to mast cells
lymphocytes
2nd most numerous
circular nuclei
T cells (target viruses and cancers)
B cells (produce antibodies)
monocytes
largest
U or kidney shapes nucleus
differentiates into macrophages
targets viruses, intracellular bacterial parasites, and chronic infections
activates lymphocytes
leukopoiesis
production of WBCs from hematopoietic stem cells in red bone marrow
stimulated by interleukins and CSFs
CSFs
chemical messengers named for the WBCs they stimulate
lymphoid stem cells
develop into lymphocytes
myeloid stem cells
develop into all other WBCs
platelets
cytoplasmic fragments of megakaryocytes which are derived from megakaryoblasts
contain serotonin, Ca2+ enzymes, ADP, PDGF
act in clotting process, form temp platelet plug that help seal breaks in blood vessels
inhibited via NO and prostacyclin
degenerate in ~10 days
regulated by thrombopoietin
leukopenia
abnormally low WBC count
drug-induced
leukemia
cancerous leukocytes fill red bone marrow
immature nonfunctional WBCs in bloodstream
leukocytosis
abnormally high WBC count
anemia
reduction below normal in Hb or RBC number
thalassemias
one globin chain absent or faulty
RBCs thin, delicate, deficient in Hb
sickle-cell anemias
1 AA chain wrong in a globin beta chain
RBCs crescent shaped
RBCs rupture easily and block small vessels
polycythemia vera
bone marrow cancer-> excess RBCs and blood viscosity
absolute
secondary polycythemia
less O2 available or EPO production increases-> increased RBC count
absolute
relative polycythemia
temporary
results from diarrhea, vomitting, or diuretics
agglutinogen
antigen that causes the formation of antibodies
agglutinins
antibodies that cause RBCs to clump together
agglutination
clumping of particles together
transfusion reaction
diminished O2-carrying cap
diminished BF beyond blocked vessels
Hb in kidney tubules-> renal failure
crossmatching
detects the presence of antibodies in the recipient against RBCs of the donor to make sure they are fully compatible
erythroblastosis fetalis
occurs only in Rh- mom and Rh+ fetus
baby is healthly first delivery-> mother synthesizes anti-Rh antibodies
during second pregnancy antibodies can cross placenta and destroy RBCs of Rh+ baby
RhoGAM
contains anti-Rh that must be administered w/ a prebirth transfusion and exchange transfusion after birth
buffy coat
<1% of blood
made up of WBCs and platelets
hemorrhagic anemia
rapid blood loss
treated via blood transfusion
chronic hemorrhagic anemia
slight, but persistant blood loss (hemorrhoids, bleeding ulcer)
iron-deficiency anemia
caused by hemorrhagic anemia, low iron intake, or impaired absorption
microcystic, hypochromic RBCs
treated via iron supplements
renal anemia
lack of EPO
accompanies renal disease
treated via synthetic EPO
aplastic anemia
destruction or inhibition of red marrow by drugs, chemicals, radiation, viruses
treated via transfusions (short-term) or transplanted stem cells (long-term)
hemolytic anemia
premature RBC lysis
causes by Hb abnormalities, incompatible transfusions, infections
intrinsic factor
produces vitamin B12 in stomach
pernicious anemia
decrease in RBCs
intestines can’t absorb vit. B12 properly
treated via B12 supplements or B12 injections
vascular spasm
SM in the blood vessel wall constricts
platelet plug formation
platelets stick to exposed collagen
coagulation
intrinsic
extrinsic
common
intrinsic pathway
factor 12->factor 11->factor 9->factor 8->factor 10
extrinsic pathway
TF (factor 3)->factor 7-> factor 10
common pathway
factor 10->prothrombin->thrombin (factor 2)->fibrinogen->fibrin (factor 1)->clot formation
factor 10
activated via factor 5 and ca2+
clot retraction
- actin and myosin in platelets contract
- pulls on fibrin strands, squeezing serum from clots
- draws ruptured blood vessels together
- stabilized clot
fibrinolysis
plasminogen->plasmin via tPA, factor 12, and thrombin->removes unneeded clots after healing
plasmin
fibrin-digesting enzyme
anticoagulants
inhibit blood clotting
ex. heparin, asprin, warafin, dabagatran
heparin
- activates antithrombin 3
- inactivates factor 10 and inhibits the conversion of prothrombin to thrombin
asprin
inhibits thromboxane
warafin
interferes w/ the action of vit. K
dabigatran
inhibits thrombin
CBC
checks formed elements, hematocrit, and hemoglobin levels
SMAC
can detect liver and kidney disorders
fasting glucose levels
70-120 mg/dL (normal)
measures current BG levels
hemoglobin A1C levels
5-7% (normal)
measures past 3 months BG levels
thrombus
clot develops and persists in unbroken blood vessel
blocks circulation
can lead to tissue death
embolus
thrombus freely floating in bloodstream
embolism
embolus obstructing a vessel
thrombocytopenia
deficient number of circulating platelets
petechiae appear due to spontaneous widespread hemorrhage
due to suppression or destruction of red bone marrow
treated via transfusion of concentrated platelets
impairs vit. K and fat absorption prevents liver from producing bile
caused by vit. K deficiency, hepatitis, or cirrhosis
inability to synthesize procoagulants
hemophilia
prolonged bleeding into joint cavities
treated w/ plasma transfusions and injection of missing factors
increases risk of hepatitis and HIV
ex. A, B, C
hemophilia A
most common
factor 8 deficiency
hemophilia B
factor 9 deficiency
hemophilia C
mild
factor 11 deficiency
fibrin
protein backbone of a bloodclot
Rh factor
positive indicates Rh antigen present
negative indicates that Rh antibodies present
pluripotent stem cells
produces neutrophils, basophils, thrombocytes, and lymphocytes
serum
blood plasma w/o clotting factors
