Red Blood Cells Flashcards
erythrocyte
- live about 120 days
- flexible biconcave disks, lack a cell nucleus, mitochondria, ribosomes, and they cannot synthesize proteins
- 4.5-6x10^6 men
4-5x10^6 women
-at end of lifespan, become senescent, mis-shapen and removed by macrophages in the spleen or liver (extravascular) or destroyed in blood stream (intravascular)
hemoglobin
- a molecule that can bind to oxygen.
- 14-17g/dL men
- 12-15g/dL women
- 4 globin chains + 4 heme
- give RBCs their color
- synthesis happens during the erythroblast stage in bone marrow
normochromic
RBC staining (due to hemoglobin) is deeper at the periphery of the cell and fades at the center (central pallor).
hypochromic
cells that stain with decreased intensity (because of less hemoglobin)
Rouleaux formation
- in the absence of significant blood flow, RBCs stack due to Plasma proteins—fibrinogen, C-reactive proteins, globulins, albumin
- reversible
hematocrit
- aka Packed cell volume
- Volume occupied by RBCs in blood (normal is 45% men; 40% women)
- 42-49%men
- 38-46%women
- increased hematocrit -> increased blood viscosity -> thrombotic complications e.g. clogged capillaries
Mean Corpuscular Volume
- average volume of single RBCs. Normal MCV is ~85 femtoliters (fl).
- decreased in iron deficiency anemia
- 83-99 fL (femto = 10^-15)
- nucleus (lost before reticulocyte) is about 40 pg
microcytic anemia
- iron deficiency
- reduced MCV
macrocytic anemia
- cobalamin (vit B12) deficiency
- vit B12 needed for DNA synthesis/replication so cells don’t divide fast enough
- increased MCV
Mean Corpuscular Hemoglobin:
- average mass of hemoglobin in each RBC (in picograms)
- 30pg/cell
- 32-36 g/dL
Mean Corpuscular hemoglobin concentration
- average concentration of hemoglobin in a given volume of packed RBCs
[Hb]/hematocrit
reticulocyte %
.5-1.8%, men
.5-2.2% women
50,000-75,000/microliter
decreased reticulocyte
hematopoeisis deficient
increased reticulocyte
increased hematopoeisis (for example, compensatory response to a bleed)
erythropoietin
90% produced by kidney
- chronic renal failure (CRF) -> EPO deficiency -> anemia
- renal cell carcinoma -> increases EPO (increased hematocrit)
10% produced by liver
- hepatocellular carcinoma -> increases EPO
Decreased oxygenation causes EPO synthesis and release within minutes, peaking in 24 hours. Stimuli include hypoxia, severe anemia, high altitude, abnormal hemoglobins that bind O2 tightly and do not release it to tissues
suppresed by increased O2 content
new RBCs within 5 days of EPO stimulus
Polycythemia
- elevated hematocrit due to increased RBCs or decreased plasma volume
- hematocrit > 55%
Physiological Polycythemia.
- High Altitude Living increases EPO
Secondary Polycythemia
occurs when EPO rises in renal or hepatocellular carcinoma, EPO doping, or due to chronic hypoxia (e.g. lung or heart disease).
Polycythemia Vera
is a disease due to over-production of RBCs because of clonal expansion of “abnormal” pluripotent stem cells. The resulting erythroblasts may be hypersensitive to EPO, but the EPO level may be low.
O2 concentration
- decreases 10% per 1000m over sea level
Microcytic Hypochromic Anemia
non-viable or a barely viable red blood cell that is both pale (hypochromic) because of reduced hemoglobin, and small (microcytic)
ferritin
intracellular protein serves to store iron in a non-toxic form, to deposit it in a safe form, and to transport it to areas where it is required
- iron + apoferritin (protein)
- apoferritin is a shell with a central cavity to store iron, six channels go to the cavity. Fully saturated, can hold up to 4500 iron atoms
- releases iron easily
Clinical Features of Iron Deficiency
- pale conjunctiva
- fatigue
- tachycardia
- koilonychia- spoon-shaped nails
- glossitis- sore or swollen tongue
- angular stomatitis- fissuring at lip corners
- gastric atrophy
- esophageal strictures- narrowing of esophagus
- melena- back stool
- pica- craving for starch, clay or ice
treatment of iron deficiency
- ferrous salts
- ascorbic acid ncreases absorption and toxicity
- supplement on empty stomach
- avoid antacids
orthochromaticblast
stage before reticulocyte, when nucleus is shed
iron storage
- liver removes and stores excess iron ~1000mg
- ferriton is main form of storage (65%), hemosiderin (33%)
- human body contains 3-4g of iron
- hemoglobin 1800-2500mg
- liver 0-1000mg
- blood 3mg
- iron deficiency results in accumulation of protoporphyrin IX in RBCs
hemosiderin
- dense aggregate of ferritin crystals formed inside lysosomes of macrophages and hepatocytes so it’s membrane bound
heme
- one iron molecule per heme. Iron is added as last step in the pathway
protoporphyrin IX
important precursor to heme
iron absorption
- In stomach Ferric (Fe3+) -> ferrireductase -> ferrous (Fe2+)
- ferrous absorbed easier
- antibiotics reduce absorption
- absorption takes place in duodenum
- acidic compounds (ascorbic acid/vit C) increase release of iron from food
iron deficiency anemia
- decreases hemoglobin synthesis which decreases:
- MCV, mean corpuscular volume
- MCHC, mean corpuscular hemoglobin concentration
- total arterial O2 concentration
- which increases:
- total iron binding capacity
- free erythrocyte protoporphyrin (bc protoporphyrin IX accumulates)
