Question Answer
Plasma and serum plasma is 50% of blood volume. It’s 90% water and serum is the plasma minus the fibrinogen (clotting factors)
WBC in a drop of blood 150,000
RBC in a drop of blood 5 million
HCT 45% RBC/55% plasma water when RBC goes down, Hb goes down
HCT vs Hb The Hct is always 3x the Hb, so if the Hb is 12, the HCT is 36%, if the Hb is 10, the HCT is 30% (anemic- both are low H&H)
What does it mean if the HCT is high? dehydration- as volume of fluid drops, RBC per volume of fluid rises
Hb 10 HCT 45 anemic b/c the Hb is low- low RBC- just dehydrated b/c this is the RBC to total volume- especially in
S/S anemia SOB, pallor, fatigue, low H&H
Polycythemia too many RBC, H&H increase 20 Hb and 60% Hct- aka Absolute polycythemia
Relative Polycythemia Hb 15 and 60% Hct- dehydrated- too little water- normal Hb- any condition of dehydration- diarrhea
Primary Polycythemia vera if bone marrow has a problem- hyper proliferative neoplastic d/o- non-benign- blood is thicker/slower, thrombotic events, DVTs
Secondary Polycythemia Vera smoking too much, COPD, chronic hypoxia- kidney starts to secrete more erythropoietin because of this b/c this is how body responds to chronic hypoxia-NOT d/t bone marrow
Congenital Spherocytosis RBC look like spheres and have rigid cell membranes= result in hemolysis- rupture inside body- a type of hemolytic anemia
Heme and globin globin is a protein, 2 pairs of globin chains, a beta and 2 alpha chains. Heme is colorful and carries the iron- where O2 is attached.
If Iron goes down one iron on each heme- without iron = iron deficiency anemia- one iron carries one O2 so one Hb carries 4 O2
Beta thalassemia when you are missing the 2 beta chains in Hb- congenital- missing just one chain is beta thalassemia minor/2 is major- same for alpha chains- these are hemolytic anemias- normal iron
Major problem in anemia is tissue hypoxia
When a RBC passes through a metabolizing tissue i.e. exercising ph down, releasing CO2, temp up and Hb become more willing to release O2- shifts to the right. In anemia, Hb to compensate, they become more generous as well- to the right
RBC made where in the bone marrow
Erythroblast takes 5-7 days to become a RBC b/c its blue- needs hemoglobin and need iron
Maturation- Immature RBC has… nuclear matter which has to disappear and they need folate and B12- MOST IMPORTANT- and iron
Folate and B12 deficiency RBC will not mature and will have too much nuclear matter and bone marrow will be unable to make RBC-
Low production anemias either missing folate, B12 or iron to become mature RBC- HYPOPROLIFERATIVE
Reticulocyte baby RBC- has nuclear matter- 1-2% of the RBC- if bone marrow if hypofx, it will produce less, if hyperfx, it will produce more
Why would your bone marrow be hyperfx? kidney secreting erythropoietin d/t living in Big bear, COPD, smoking, hypoxia…hemolytic anemia outside the bone marrow
Hemolytic anemia? =high reticulocytes hyper proliferative bone marrow
Low reticulocytes deficiency anemia- folate, iron, B12 deficiency- first thing that’s corrected on the CBC when treated is the reticulocyte count
Heme and globin after 120 days proteins turn into amino acids and the heme> taken back to the bone marrow from spleen via transferrin- iron taken to the liver as ferritin
Ferritin the most important test you want to do in iron deficiency anemia
Heme green broken down by macrophages- yellow indirect bilirubin- cannot swim in water- toxic- carried by albumin to the liver-transform to soluble direct bilirubin to pee
Indirect bilirubin if u have lots of RBC destroyed (hemolysis) in the spleen, indirect bilirubin will go up > 3mg= jaundice- deposited in the gallbladder= stones
Hemolytic anemia s/s jaundice and gallbladder stones d/t breakdown of indirect bilirubin
Hypo proliferative anemia bone marrow hypofx- folate, iron and B12 deficiency- bone marrow not function- chronic kidney dz- reticulocytes DOWN, less than 1-2%
Bone marrow produces RBC and they die prematurely hemolytic anemia (before 120 days up)- hyperproliferative anemia- body hypoxic cause reduced O2 so body releases more erythropoietin- stimulates B. marrow- hyperactive- high retics
Hemolytic anemia destroying RBC and kidney secretes erythropoietin= hyper B. marrow, increase retics= maybe even nucleated ones.
Dx hemolytic anemia low H& H- look at the reticulocytes- high >2%
Biochemical markers of hemolysis elevated indirect bilirubin >3, elevated, LDH, low haptoglobin- together with high reticulocytes >2% (100% sure of hemolytic anemia)
Dx of hemolytic anemia 1st look at s/s (pale), then look at H&H and then the biochemical markers
Intravascular hemolysis in blood vessels- increased bili, inc LDH & low haptoglobin- plasma turns pink- hemoglobinemia & hemoglobinuria & iron in renal cells binds to hemosiderin= hemosiderinuria
Extravascular hemolysis spleen- still see increased bili, inc LDH and decreased haptoglobin
Why did the RBC die young (hemolysis) Intracorpuscular- problem coming from the RBC itself- congenital/intrinsic or extracorpuscular/acquired- medication, autoimmune, toxins, malaria, metallic cardiac valves
Intracorpuscular hemolytic anemia examples congenital, membrane, Hb or enzymes problem i.e. congenital spherocytosis or thalassemia, sickle cell anemia, glucose 6 dehydrogenase deficiency (fava beans)
Medications that cause hemolysis ASA and sulfa
Chronic hemolysis hyperplasia of the bone marrow, short of folate, gallbladder stones
s/s anemia fatigue, pallor , SOB
hypoproliferative, the retics are low
hypoproliferative Renal Failure, Altered hemoglobin synthesis Iron deficiency, Thalassemia, chronic inflammation, Pernicious, Folate, Aplastic anemia, Bone marrow infiltration, Carcinoma/ Lymphoma
hyperproliferation hemolytic- hemorrhage, hereditary spherocytosis, malarial, sickle cell disease, G6PD deficiency
MCV mean corpuscular volume mean of RBC volume 80-100- the size/CBC- pt has low H&H- look at MCV, if low, microcytic <80 (small) , if high, macrocytic (large) >100- also normocytic anemia (80-100) normal size
Microcytic anemia MCV <80= iron deficiency
Macrocytic anemia MCV >100 = B12 deficiency and folate deficiency, B12 is the biggest RBC
Anisocytosis different size cells (RDW)-10-15% variance- not cookie cutter- elevated in Folate/Iron/B12 anemias and cells will be much smaller in size
Macrocytosis vs macrocitic anemia macrocytosis- occurs w/hypothyroidism/drug induced- etoh & anticonvulsants- Depakote and carbamazepine/Tegretol-
Macrocytic anemia (MCV, neuro, megaloblast) B12 (biggest MCV, neuro, megaloblasts), folate (MCV, no neuro, megaloblasts) and etoh (MCV, neuro)
Megaloblasts hypersegmented neutrophils seen in a peripheral blood smear (nucleus has up to 8 lobules- immature)- need B12/folate
B12 deficiency 3 causes low intake (vegan’s), metformin (parenteral), pernicious anemia
Pernicious anemia need intrinsic factor to absorb b12 from small intestine- they have autoimmune gastritis/inflammation- parental B12 is best
Sideroblastic anemia iron is high but cannot absorb it
Who develops folate deficiency? Prego women/ etoh/malnutrition
#1, 2… 9 cause of anemia iron deficiency anemia- 90% of cases
Thalasemis iron levels are normal- problem is in the globin- microcytic anemia
Microcytic anemias iron deficiency, sideroblastic, thalassemia, anemia of chronic dz (kidney)
B6 deficiency can cause (test) microcytic anemic- sideroblastic
B12 can cause (test) macrocytic anemia
Iron deficiency anemia is caused by NSAIDS/ulcers- chronic blood loss- menstruation
3 tests for iron deficiency serum iron (drug-level), serum ferritin (storage form of iron)- liver storage, total iron binding capacity TIBC (high)
Ferritin is an acute phase reactant protein (TEST) (immune lecture too)- generic proteins manufactured by the liver in excess amounts in any condition of inflammation- C-reactive proteins & ferritin goes up- allergies, injured hand, cellulitis= inflammation
Total iron binding capacity TIBC one of the 3 tests for iron deficiency- would be high because you’re missing iron- the binding sites are available
30% of patients with iron deficiency anemia can have normal ferritin (due to inflammatory process which could be happening)- liver will be making more ferritin but serum iron is still low
Iron deficiency serum ferritin is low, TIBC is high, serum iron low
Anemia of chronic disease ACD serum ferritin is normal or high, TIBC low, serum iron low
Thalassemia iron profile is NORMAL
Sideroblastic abnormally high serum iron
Iron deficiency anemia ferritin will tell you BUT in 30% of cases- d/t inflammatory response, this will be normal- c-reactive protein will be high- do with TIBC
“Classic” iron deficiency anemia look at low ferritin
Low ferritin Iron deficiency anemia
High iron Sideroblastic anemia
High TIBC Iron deficiency anemia (Ferritin could be normal in 30% of cases)
Low iron, low TIBC, normal ferritin Anemia of chronic disease
Hemolytic anemia episodes CRISIS- (high retics/LDH), bilirubin increases, jaundiced, H&H down, gallbladder stones, thrombolytic manifestations (sickle cell dz)- pale, splenomegaly
Sickle cell part of spleen gets killed off and dies with each attack- eventually auto- splenectomy d/t thromboembolic manifestations
Sickle cell one amino acid replaces another- valine instead of glutamic acid- happens d/t stress, infx, hypoxia, acidosis… valine bends RBC bends and blocks blood vessels= thrombotic crisis= aplastic crisis- give anbx, infx causes more cycling
Respiratory virus parvo virus High retics help bone marrow compensate until this virus infx cough brings down Hb in aplastic crisis hemolytic anemia- give antibiotics

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