Blood Basics & Functions
What pH range is normal for human blood?
slightly alkaline, 7.35–7.45 (Slide 5)
What is the typical lifespan of an erythrocyte?
90–120 days (Slide 9)
What antigens are present on Type AB blood?
Both A and B (Slide 18)
What is anemia in general terms?
Low O₂-carrying capacity (Slide 28)
What percentage of blood volume do leukocytes normally make up?
~1% (Slide 41)
What type of cell do platelets originate from?
Megakaryocytes (Slide 50)
What is a thrombus?
Stationary clot in unbroken vessel (Slide 55)
What symptoms are common across most forms of anemia?
Fatigue, pallor, shortness of breath, palpitations (Slide 29)
What percentage of blood volume is plasma and what percent is RBC and what is that called?
~55%, 45%, hematocrit (Slide 7)
What structure in hemoglobin binds oxygen?
Iron atom in heme (Slide 10)
What antibodies are found in the plasma of Type O blood?
Both anti-A and anti-B (Slide 19)
What nutrient deficiency causes pernicious anemia?
Vitamin B12 (Slide 29)
What does the mnemonic “Never Let My Engine Blow” represent?
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils (Slide 43-44)
What is the main function of platelets?
Blood clotting (Slide 50)
What is an embolus and an embolism?
Free-floating clot; embolism = lodged clot (Slide 55)
What is the most common cause of mononucleosis?
Epstein–Barr virus (Slide 49)
Name one transport, one maintenance, and one protection function of blood.
Transport =metabolic waste, respiratory gases, hormones; Maintenance = body, temperature, normal pH, adequate fluid volume; Protection = prevents blood loss, prevents infection (Slide 6)
Define oxyhemoglobin and deoxyhemoglobin.
Oxyhemoglobin = Hb + O₂; Deoxyhemoglobin = Hb without O₂ (Slide 11)
Which blood type is considered the universal donor?
O– (Slide 25)
What genetic mutation causes sickle-cell anemia?
Point mutation in β-globin (Slide 32)
Define leukocytosis and what does it indicate.
WBC count >11,000/µL (Slide 42)
List the three primary stages of hemostasis.
→ Vascular spasm → Platelet plug → Coagulation (Slide 52)
What can a deficiency in Vitamin K lead to?
Impaired liver function, abnormal and severe bleeding (Slide 61)
What is polycythemia, and name one possible cause.
↑ RBCs; causes = altitude, marrow cancer, overproduction of EPO, blood doping (Slide 38)
Which component makes up the majority of plasma, and why is it important?
Water (92%); acts as solvent for the solutes and transport medium (Slide 7-8)
What nutritional requirements are essential for erythropoiesis?
Amino acids, lipids, carbs, iron, vitamin B12 (Slide 14)
Why can a person with Type B blood not safely receive Type A blood?
Anti-A antibodies would attack A antigens (Slide 23)
Explain why iron-deficiency anemia leads to fatigue.
Less Hb → less O₂ transport (Slide 31)
What is diapedesis, and why is it important?
WBCs exit blood to fight infection (Slide 42)
Explain how platelets form a temporary plug.
Adhere to collagen, release chemicals, recruit more platelets (Slide 52)
How does aspirin help prevent clot formation?
Inhibits platelet plug formation (Slide 57)
Why does untreated anemia often cause the heart to work harder?
Low O₂ → heart compensates → arrhythmia/heart failure (Slide 37)
What is serum?
Plasma minus proteins (Slide 18)
What hormone stimulates red blood cell production, and where is it produced?
Erythropoietin (EPO), kidneys (Slide 14-15)
What is agglutination, and why is it dangerous?
Antibody-antigen clumping → blocks circulation, causes hemolysis (Slide 22-24)
Compare and contrast sickle-cell anemia and thalassemia.
Sickle cell = misshapen cells, malaria resistance; Thalassemia = immature RBCs, Mediterranean ancestry (Slide 33)
Compare granulocytes and agranulocytes.
Granulocytes = short-lived, cytoplasmic granules; Agranulocytes = longer-lived, no granules (Slide 45)
What is the role of thrombin in clot formation?
Converts fibrinogen to fibrin (Slide 53)
Compare the actions of heparin and warfarin.
Heparin inactivates thrombin; Warfarin inhibits Vit K–dependent factors (Slide 57)
Explain why living at high altitude can lead to polycythemia.
Low O₂ → stimulates EPO → more RBCs (Slide 38)
Why is blood temperature slightly higher than body temperature?
Heat is generated as a byproduct of metabolism waste (Slide 6)
Explain how hypoxia regulates erythropoietin secretion.
Low O₂ triggers kidney release of EPO (Slide 15)
Explain why an Rh-negative person does not normally have anti-D antibodies
They only form after exposure to Rh+ blood (Slide 21)
Why might athletes use blood doping, and what risks does it pose?
↑ O₂ delivery; risks = clotting, heart strain (Slide 39)
Why are interleukins and colony-stimulating factors important in leukopoiesis?
Stimulate WBC production (Slide 45)
Compare the intrinsic and extrinsic clotting pathways.
Intrinsic = slow, many steps, damage from inside the vessel; Extrinsic = fast, tissue damage triggers it (Slide 53)
Why is DIC both a bleeding and clotting disorder?
Widespread clotting, residual blood unable to clot (Slide 58)
A patient presents with easy bruising. What possible blood disorders should be considered?
Vitamin K deficiency causing liver disease, hemophilia (Slide 61, 63)
Predict what would happen to blood viscosity and oxygen transport if plasma volume decreased significantly.
Viscosity ↑, O₂ transport slowed down and heart strain (Slide 7)
Predict what happens if the body produces too much EPO.
Polycythemia, ↑ viscosity, heart strain (Slide 38–39)
A pregnant woman is Rh– and her fetus is Rh+. Predict what will happen if she is not given immunoglobulins.
Anti-D antibodies cross placenta → hemolytic disease of newborn (Slide 26
What is untreated aplastic anemia and its effect on other formed elements besides RBCs.
↓ WBCs & platelets too (Slide 30)
What is leukopenia and what can cause it.
low WBC count, cancer, illness, medications (Slide 47)
A patient has a genetic defect that prevents fibrin formation. Predict what would happen after an injury.
No stable clot, continuous bleeding (53)
Predict what happens in a patient with hemophilia A after a small injury.
Missing Factor VIII → prolonged bleeding (Slide 62)
Predict the effects of liver disease on blood clotting and explain why.
→ Fewer clotting factors → increased bleeding (Slide 61)
Insufficient hemoglobin causes what issue and what hormone does that trigger?
Hypoxia, Erythropoietin (EPO) (Slide 15)
A patient has a mutation that prevents hemoglobin from binding iron. How would this affect oxygen transport and overall metabolism?
No O₂ transport → tissue hypoxia, metabolic failure (15, 37)
A Type AB+ patient needs an emergency transfusion. Evaluate which blood types could safely be given and why.
All types; no antibodies present in patient → universal recipient (Slide 19)
A patient with thalassemia has high numbers of immature erythroblasts. Analyze why these cells fail to function properly in oxygen transport.
Immature cells lack full Hb → ineffective gas exchange (Slide 29, 33)
Evaluate how leukemia differs from leukopenia in both mechanism and clinical outcomes.
Leukopenia = low count; Leukemia = uncontrolled proliferation, cancer (Slide 47-48)
A patient comes in with small, purple blotches. Why is this happening, what is the diagnosis and what are they deficient in?
Widespread hemorrhage, thrombocytopenia, platelets (Slide 60)
Analyze how X-linked inheritance explains why hemophilia is more common in males.
Males only have one X; mutation always expressed (Slide 64)
A patient complains of fatigue, shortness of breath, and pallor. What is the most likely cause?
→ Anemia (Slide 29)