blood part 1 red blood cells Flashcards
SOAP
S-subjective (personal feelings, observations, symptoms
O- objective (symptoms that can be measured)
A- assessment (diagnosis)
P- plan (tests and treatments)
blood
fluid connective tissue
blood main components
Plasma and formed elements
formed elements
Erythrocytes (red blood cells, or RBCs)
Leukocytes (white blood cells, or WBCs)
Platelets
Hematocrit
Percent of blood volume that is RBCs
hematocrit for males vs females
47% (plus or minus) 5% for males
42% (plus or minus) 5% for females
Physical Characteristics of blood
Sticky, opaque fluid
Color scarlet to dark red
blood: Ph, Temp, and volume (males and females)
pH 7.35–7.45
38 C (100.4 F)
5-6 L male, 4-5 L females
8% body weight
Functions of blood
Distribution
regulation
protection
blood function: distribution
Distribution of
O2 and nutrients to body cells
Metabolic wastes to the lungs and kidneys for elimination
Hormones from endocrine organs to target organs
blood function: regulation
Regulation of
Body temperature
Maintain normal pH using buffers
Adequate fluid volume
blood function: protection
Protection against
Blood loss (clot formation)
infection (antibodies, WBCs, complement proteins)
composition of blood plasma
90% water
8% proteins (mostly produced by liver)
1% extra
blood plasma proteins
60% albumin (helps move small molecules, keeps from leaking)
36% globulins (Ph buffering, transport)
4% fibrinogen (blood clotting)
Blood plasma extra 1%
nitrogenous by products nutrients electrolytes O2 and CO2 hormones
formed elements, which ones are complete and non complete cells
only WBCs are complete cells
RBCs have no nuclei or organelles
platelets are cell fragments
how long do formed elements survive
only a few days
where do most blood cells originate
in bone marrow and don’t divide
what are the major factor contributing to blood viscosity
Erythrocytes
Erythrocytes description
Biconcave discs, anucleate, essentially no organelles
Filled with hemoglobin (Hb) for gas transport
Contain the plasma membrane protein spectrin and other proteins (for flexibility)
in erythrocytes, what Structural characteristics contribute to gas transport
Biconcave shape—huge surface area relative to volume
>97% hemoglobin (not counting water)
No mitochondria; ATP production is anaerobic; no O2 is used in generation of ATP
Erythrocyte Function
respiratory gas transport
hemoglobin binds reversibly with oxygen
Hemoglobin structure
Protein globin (2A 2B)
Heme pigment to globin
iron atom bound to one 02 molecule
how much oxygen can each hemoglobin molecule transport
four O2
Hemoglobin O2 loading in the lungs produces
oxyhemoglobin (ruby red)
Hemoglobin O2 unloading in the tissues
Produces
deoxyhemoglobin or reduced hemoglobin (dark red)
Hemoglobin CO2 loading in the tissues
Produces
carbaminohemoglobin (carries 20% of CO2 in the blood)
HOW DOES BLOOD “KNOW” WHEN TO RELEASE O2?
Binding of oxygen to hemoglobin is affected by CO2 concentration (and pH)
More CO2 changes ph (more acidic), changes hb shape, causes O2 drop
Hematopoiesis (hemopoiesis)
blood cell formation
Hematopoiesis occurs where
Occurs in red bone marrow (spongy bone) of axial skeleton, girdles (shoulder, hip) and proximal epiphyses of humerus and femur
Hemocytoblasts (hematopoietic stem cells)
Give rise to all formed elements
what pushes cells toward specific pathway of blood development
hormones and growth factors
Erythropoiesis definition
red blood cell production
Erythropoiesis steps
A hemocytoblast is transformed into a proerythroblast
Proerythroblasts develop into early erythroblasts
Erythropoiesis phases in development
1) Ribosome made
2) Hemoglobin increase
3) Get rid of nucleus
4) form reticulocytes
5) Reticulocytes then become mature erythrocytes
Too few RBCs leads to
tissue hypoxia
reduced oxygen, bleeding
Too many RBCs increases
blood viscosity
Balance between RBC production and destruction depends on
Hormonal controls
Adequate supplies of iron, amino acids, and B vitamins
Erythropoietin (EPO)
Direct stimulus for erythropoiesis (making RBC)
When is EPO released and in response to what
Released by the kidneys in response to hypoxia
Causes of hypoxia
Hemorrhage or increased RBC destruction reduces RBC numbers Insufficient hemoglobin (e.g., iron deficiency) Reduced availability of O2 (e.g., high altitudes, vigorous exercise, lack of breathing)
Effects of EPO
More rapid maturation of committed bone marrow cells
Increased circulating reticulocyte count in 1–2days
what can also enhance EPO production
testosterone
homeostasis steps for blood level oxygen
stimulus: hypoxia
kidney releases EPO EPO stimulates red bone marrow
increases RBC count
O2 carrying blood ability increases
Dietary Requirements for Erythropoiesis
Nutrients—amino acids, lipids, and carbohydrates
Iron
Vitamin B12 and folic acid—necessary for DNA synthesis for cell division
life span of red blood cells
100–120 days
destruction of red blood cells
Old RBCs become fragile, and Hb begins to degenerate
Macrophages engulf dying RBCs in the spleen
Heme and globin are separated
Heme and globin are separated
Iron is salvaged for reuse
Heme is degraded to yellow the pigment bilirubin
Liver secretes bilirubin (in bile)) into the intestines
Degraded pigment leaves the body in feces
Globin is metabolized into amino acids
Erythrocyte Disorders
anemia
Polycythemia
anemia
blood has abnormally low O2-carrying capacity
A sign rather than a disease itself
Anemia symptoms
Accompanied by fatigue, paleness, shortness of breath, and chills
causes of anemia
insufficient RBCs
Low hemoglobin content
Abnormal hemoglobin
Hemorrhagic anemia
acute or chronic loss of blood
Hemolytic anemia
RBCs rupture prematurely
Aplastic anemia
destruction or inhibition of red bone marrow
hypochromic anemia
Iron-deficiency anemia
iron deficiency anemia causes
Secondary result of hemorrhagic anemia or
Inadequate intake of iron-containing foods or
Impaired iron absorption
Pernicious anemia
Deficiency of vitamin B12
Lack of intrinsic factor needed for absorption of B12
Treated by intramuscular injection of B12
Thalassemias
Absent or faulty globin chain
RBCs are thin, delicate, and deficient in hemoglobin
Sickle-cell anemia
Defective gene codes for abnormal hemoglobin (HbS)
Causes RBCs to become sickle shaped in low-oxygen situations
Polycythemia
excess of RBCs that increase blood viscosity
Polycythemia results from
Polycythemia vera—bone marrow cancer
Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases
Blood doping
