Life cycle of RBCS and recycling of hemoglobin components

Life cycle of RBCS and recycling of hemoglobin components

Iron (Fe+3) (1)

transported in blood attached to transferrin protein

iron (Fe+3) (2)

stored in liver , muscle, or spleen

stored in liver , muscle, or spleen

iron is stored by attaching protein ferritin and Hemosiderin protein

Iron (Fe+3) (3)

being used for hemoglobin synthesis in bone marrow

Biliverdin (green) converted to bilirubin (yellow)

bilirubin secreted by liver to bile

bilirubin secreted by liver to bile (1)

converted to Urobilinogen then Stercobilin (brown pigment in feces) by bacteria of large intestine

bilirubin secreted by liver to bile (2)

if reabsorbed from intestines into blood is converted to a yellow pigment, urobilin and excreted in urine

polycythemia

an excess of RBCs

polycythemia primary (cause)

Cancer of the erythropoietic (RBC-producing) cells in red bone marrow

polycythemia primary (rbc count)

more than 11 million RBCs/ nanoLiters or hematocrit 80%

polycythemia secondary (cause)

Dehydration, emphysema, high alttiude, or physical conditioning

polycythecemia secondary (rbc coubt)

8million/nanoliters

dangers of polycythemia

INCREASE blood volume, blood pressure, viscosity

Dangers of polycythemia can lead to

embolism, stoke, or heart failure

anemia

not enough RBC’s or defect of RBC’S HB

anemia symptoms

O2- carrying capacity of blood decreases which causes lack of O2 for ATP and heat protection then leads to fatigue, cold intolerance, and paleness

anemia causes

nutritional, bleeding, hereditary and radiation toxin

anemia dangers (1)

tissue O2 decreases then leads to hypoxia

anemia dangers (2)

blood osmolarity decreases then leads to edema

anemia dangers (3)

blood viscosity decreases then leads to heart rate pressure increase (even cardiac arrest)

anemia leads to (1)

kidney failure or insufficient EPO

anemia leads to (2)

iron (FE2+) deficiency anemia

pernicious anemia

short of vitamin b12 folic acids (poor nutrition) or intrinsic factor (stomach problems)

vitamin b12 and folic acids

RBC proliferation in red bone marrow; intrinsic factor help b12 absorption

hereditary hemoglobin defects (1)

sickle cell anemia (mostly among african descent)

hereditary hemoglobin defects (2)

change in hemoglobin chain (6th amino acid) results in its low o2- binding capacity

hereditary hemoglobin defects (3)

malaria parasites die in this type of RBC (selection)

hereditary hemoglobin defects (4)

cells are rigid and sticky , often block small vessels and cause intense pain; can lead to kidney or heart failure, stroke, etc

hemorrhagic anemia

bleeding (ulcers)

hemolytic (lysis) anemia

defects in cell membranes cause RBC rupture

aplastic anemia

destruction of bone marrow (radiation/toxins)

plastic

grow