Blood Stuff

how much blood do males have?

5-6 L

how much blood do females have?

4-5 L

color of high O2 blood

scarlet red

color of low O2 blood

dark red

blood pH range

7.35-7.45

function of blood

distribution, regulation, protection

blood composition

55% plasma, 45% erythrocytes,

plasma composition

90% water, dissolved solutes, proteins

proteins in plasma

albumin, globulin, fibrinogen

albumin function

maintain osmotic balance and buffers pH (regulation)

globulin function

immune response and lipids (transportation)

fibrinogen function

blood clot (protection)

average range of leukocytes

4800-10800 / microliter of blood

when is it ok to have more than the normal number of leukocytes?

when fighting infections

diapedesis

white blood cells can squeeze through spaces in capillaries to go fight diseases and pathogens

types of granulocytes

neutrophils, eosinophils, basophils

types of agranulocytes

lymphocytes and monocytes

difference between granulocytes and agranulocytes

granulocytes: visible cytoplasmic granules, multilobe nucleus
agranulocytes: no visible cytoplasmic granules, nucleus with distinct shape

most to least abundant leukocytes

neutrophils, lymphocytes, monocytes, eosinophils, basophils (Never Let Monkeys Eat Bananas)

neutrophils (polymorphonuclear leukocyte, PMN)

very phagocytic

eosinophils

lysosome like granules, associated with allergic reactions, asthma, etc.

basophils

granules contain histamine; vasodilator; if more WBC, move faster

types of lymphocytes

T cells and B cells

T cell function

protect against virus-infected cells

B cell function

antibody production

monocytes

able to migrate into tissues and transform into a macrophage, activates lymphocytes

stem cells of leukocytes

mesenchyme cells -\> hematopoietic cells

what are platelets

cytoplasmic fragments of megakaryocytes (a type of hematopoietic cell)

platelet function

blood clotting

amount of platelets in blood

150,000-400,000 / microliter of blood

platelets regulated by

thrombopoietin

life span of erythrocytes

100-120 days

spectrin

plasma membrane protein that provides flexibility to change shape

amount of erythrocytes in blood

4.2-6.1 million / microliter of blood

parts of a hemoglobin molecule

globin (protein)
heme (contains iron)

oxyhemoglobin

oxygen loading

deoxyhemoglobin

oxygen unloading

carbaminohemoglobin

carbon dioxide loading

carbon dioxide and hemoglobin

20% of carbon dioxide binds to globin chains of hemoglobin

RBC structure and function

high surface area/volume ratio permits high rate of gas diffusion across membrane
flexible structure permits passage through narrow capillaries
no nuclei or mitochondria because uses anaerobic respiration

hematopoiesis

process of making blood

hematocrit

percentage of blood volume occupied by red blood cells

hematocrit of males

47%, +/- 5

hematocrit of females

42% +/- 5

low hematocrit

anemia

what could a high WBC count mean

long term illness

high hematocrit causes

dehydration, polycythemia vera, lung/heart disease (low oxygen \= high RBC)

how many RBCs are produced per second

2 million

tissue hypoxia

low oxygen

cause of tissue hypoxia

low red blood count, high elevation, hemorrhage, increased destruction of RBC, insufficient hemoglobin per RBC

cause of increase blood viscosity

high RBC count

effects of high blood viscosity

slower flow rate, heart has to work harder

erythropoietin (EPO)

hormone secreted by the kidneys that stimulates red blood cell formation (erythropoiesis)

EPO target organ

red bone marrow

testosterone effect on EPO

increases EPO production

EPO trigger

tissue hypoxia

why high altitude leads to a risk of stroke

low oxygen level -\> tissue hypoxia -\> kidney to produce EPO -\> more RBC -\> thicker blood -\> slower flow rate -\> higher blocked artery risk

effects of EPO on erythropoiesis

rapid maturation of committed cells, increase the number of developing cells that are circulating

reason for destruction of RBC

old RBC are less flexible and can get stuck in smaller capillaries, so macrophages engulf dying RBCs

what happens to heme and globin after destruction

they are separated and recycled

iron after hemoglobin destruction

degraded into bilirubin which is secreted by the liver and makes brown feces

globin after hemoglobin destruction

metabolized into amino acids

anemia

blood has abnormally low oxygen carrying capacity

causes of anemia

blood, loss, low RBC production, high RBC destruction (hemoglobin abnormalities)

low RBC production anemia

renal and aplastic anemia

renal anemia

lack of EPO release causes less erythrocytes produces, kidney disease

aplastic anemia

failure of blood cell production in the bone marrow because the organ was not fully developed, destruction or inhibition of bone marrow

high RBC destruction anemia

hemolytic, thalassemia, sickle-cell

hemolytic anemia

Hb abnormalities caused by incompatible transfusion and infections leads to premature RBC lysis (dying)

example of hemolytic anemia

malaria: parasite enters erythrocyte, replicates, and bursts

thalassemia

mostly Mediterranean ancestry, one globin chain is faulty causing RBC to be thin and delicate

sickle cell anemia

one amino acid is wrong causing RBC to be in a crescent shape when oxygen is low, ruptures easily and blocks small vessels

why is sickle cell more prevalent in African malarial belt

impairs parasite's ability to rearrange actin to remove waste and get nutrients

polycythemia vera

bone marrow cancer leads to excess RBC which increases blood viscosity

secondary polycythemia

less oxygen available or and increase in EPO leads to a higher RBC and lower plasma volume

ways to increase RBC count

blood doping, EPO injections, testosterone

blood doping

transfusion of RBC into the body leads to a 50% cell level increase, more RBC \= more oxygen \= less fatigue

why does blood doping cause less fatigue

can engage in more aerobic respiration which leads to more energy

3 steps of stopping blood

vascular spasm, platelet plug formation, coagulation

vascular spasm method

vasoconstriction to reduce blood loss (temporary)

plug formation steps

platelets stick to collagen fibers; von Willebrand factor secures the connection; activated platelets are star shaped, swell, become sticky; release ADP, serotonin, and thromboxane A2 to recruit more platelets

coagulation phase 1

intrinsic pathway triggered by negatively charged surface and extrinsic pathway triggers by exposure of tissue factor, create prothrombin activator

coagulation phase 2

prothrombin uses prothrombin activator to convert to thrombin

coagulation phase 3

thrombin cleaves fibrinogen to create fibrin which converts liquid blood into gel

vessel repair and clot retraction

actin and myosin in platelets contract and bring walls closer together, squeezes serum out of fibrin strands

platelet-derived growth factor (PDGF)

stimulates smooth muscle and fibroblasts to regrow cells and ground substance

vaso endothelial growth factor (VEGF)

helps rebuild outer walls of blood vessels

Fibrinolysis

removes unneeded clot after healing and converts plasminogen into plasmin which breaks down fibrin strands

thromboembolytic condition

floating blood clots in unbroken blood vessels

thrombus

a blood clot attached to the interior wall of an artery or vein

embolus

clot that breaks lose and travels through the bloodstream

embolism

the sudden blockage of a blood vessel by an embolus

thrombocytopenia

low platelet count, takes longer to make plug, can result in petechiae

petechiae

small, pinpoint hemorrhages (internal bleeding)

inability to synthesize procoagulants

cannot make prothrombin activator, impaired liver function

cause of inability to synthesize procoagulants

vitamin k deficiency, hepatitis, and cirrhosis

procoagulants

clotting factors

cirrhosis

chronic degenerative disease of the liver

hemophilia

hard to stop blood clots

hemophilia A

factor VIII deficiency, most common