functions of blood Flashcards
when blood is centrifuged, what do we see
-plama layer, buffy coat (has plt, WBC), formed elements (rbc)
what’s the difference between plasma and serum
-plasma contains fibrinogen so serum is plasma without fibrinogen and other clotting factors
what’s the most abundant cation in the plasma and interstitial fluid? why are they not the same if they are both extracellular
- Na for both
- a bit less Na in the interstitial fluid because in the fluid, we have lots of proteins that are negatively charged that cause cations to bind to them
what are the main anions in the plasma and interstitial fluid? what are the main anions in the intracellular fluids?
- Cl for both
- anions- HPO4
what is anion gap
- unmeasured anions in the plasma usually the anions that are from negatively charged proteins
- equation: Na- (Cl+HCO3)
- useful in diagnosing metabolic acidosis
what does hypoalbuninemia do to the anion gap?
-increases the gap
what is the oncotic pressure
- the osmotic pressure
- the amount of solute or molality of the plasma that allows it to keep the solute in and draw fluid in as well
colloid osmotic pressure
- osmotic pressure produced by the plasma proteins
what’s the normal oncotic pressure
25 mmHg
albumin
- makes up the most of plasma and is responsible for approx. 70-80% of colloid pressure
- also important for tx of freee fatty acids, ca, copper, steroids, bilirubin and drugs
- without it =edema
transferrin
-free iron is toxic so it helps to tx iron to bone marrow to make RBC
haptoglobin
-binds free hemoglobin that can enter the plasma after RBC lysis and this complex can’t be excreted by the kidney (too big) so it’s phagocytosed and the iron is conserved and recycled -done in liver
*what would happen to plasma hgb and haptoglobin leels during an episode of increased intravascular hemolysis?
-haptoglobin would decrease b/c it would be binding to Hgb being released into the plama via lysis (so hgb would increase) but the half-life of that complex is only 90 min so we would see a lot of elimination of the haptoglobin vs when it’s not bound and has a half life of 5 days
what is hematopoiesis and what are the steps
- the making of blood cells
- starts from a stem cell and turns into progenitor cells that become one of the cells that is in demand
- when progenitors first maturing, they have proliferative potential but as they mature they get more and more differentiated
what kind of cells do lymphoid progenitor cells differentiate into? Myeloid progenitor cells?
lympohoid- t cells, b cells, nk cells =lymphocytes
myeloid- everything else- neutrophils, basophils, eosinophis, plt, RBC
polycythemia
too many rbcs
how many RBCs are made daily
200 billion
what is the process of RBC synthesis
hemopoetic stem cell-> erythropoietin -> erythroblasts (decrease in nucleus)-> enter blood stream and enter as immature erythrocytines (reticulocytes) -> mature erythrocytes
what indicates a recent increase in erythropoiesis?
increased reticulocytes b/c half life is only 24-48 hr
what produces erythropoietin?
kidneys- does so when it senses decrease in oxygen
how is erythropoietin made in the kidneys? is there anything that regulates this?
- it is made via binding of HIF alpha (hypoxia induced factor alpha) to HIF beta that causes an increase in translation of erythropoietin
- HIF alpha is constantly being made but with enough oxygen (thus no need for more erythropoietin), we have an enzyme that hydroxylates HIFalpha and stops it’s activity by making it bind to hippel landau protein
when rbcs broken down, what is the porphyrin ring turned into
bilirubin
plt
- nucleus free
- secrete factors and change shape for coagulation
- activated when glycoproteins on their surface bind collagen at site of injury
what is the function of thrombopoitin
-stimulates megakaryocyte progenitor cells to begin making plt
what makes thrombopoetin? how are plt made
- THE LIVER and BONE MARROW- (not kidneys like for erythropoietin)
- plt synth- megakaryocyte precursors under go ENDOMITOSIS (mitosis without splitting the cytoplasm so have a bunch of new ones in one megakaryocyte precursor)
- get a mature megakaryocyte that produces 100-1000 plt
what stops plt synth
-plt bind to thrombopoesis and degrade it, stopping plt synth =negative feedback mech
