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63 Cards in this Set

  • Front
  • Back

Functions (1 of 2)

carry O2 and CO2 btwn tissues and lungs
-review the two sites of gas exchange (lungs and body tissues); know where the two gasses are going to and from
-in lungs, oxygen goes from alveoli to blood, carbon dioxide goes from blood to alveoli (then exhaled)
-in body tissues, oxygen goes from blood to tissue fluid, carbon dioxide goes from tissue fluid to blood


Functions (2 of 2)

-carry nutrients & wastes to and from tissues
-carry hormones
-regulates body temp. by carrying heat to surface
-immune function
-inflammation, antibodies, WBC’s
-clotting
-water balance
-acid and base balance

Main Components

plasma


formed elements


erythrocytes


platelets


leukocytes


plasma

-liquid part of blood
-collected from non-clotted blood (in a tube containing an anticoagulant, such as heparin)


serum

-plasma minus clotting elements
-collected from clotted blood (in a tube that has no anticoagulant; the clotting elements stay in the clot)


erythrocytes

-red blood cells (RBC’s)
-carry oxygen to tissues
-most numerous of the formed elements
-stain light pink, no nucleus


platelets

-are cell fragments
-needed for blood clotting
-stain dark blue, much smaller than other formed elements


leukocytes


white blood cells (WBC’s)
part of the immune system


granulocytes

eosinophils: bi-lobed nucleus, red-stained granules in cytoplasm
-basophils: no visible nucleus, filled with blue-stained granules, no cytoplasm visible
-neutrophils: multi-lobed nucleus
-agranulocytes:
-monocytes: large cell, horseshoe or kidney- shaped nucleus
-lymphocytes: large oval nucleus, some cytoplasm visible


Osmolarity of blood

number of particles
-usually measured in milliOsmos (mOs)
-larger number means more particles

osmosis

H2O moves from hi to lo conc. of H2O


hypotonic

a hypotonic solution has fewer particles, or is more dilute


hypertonic

a hypertonic solution has more particles, or is less dilute


osmolarity in blood controlled by

-electrolytes (such as Na+, K+)
-proteins in blood (albumins, globulins)
-osmolarity due to proteins is blood is colloid osmotic pressure


plasma protein deficiency
-causes:


-protein starvation in diet
-liver disease (affects protein synthesis)
-kidney disease (protein loss in urine)
-severe burns (protein loss at surface)

plasma protein deficiency


effects

-blood osmolarity drops
-tissue fluid increases
-swelling
-ascites = fluid accumulates in abdominal cavity
-bloodstream loses fluid
-low BP
-kwashiorkor
-African word for protein deficiency w/ distended stomach in children
-often occurs when child is no longer breast-fed


ABO Group


blood type derived from antigens on RBC’s.
-proteins on cell membranes
-part of cell identity (self vs. non-self)


blood type/Antigen

A has A antigen; type B has B antigen; type O has neither antigen; type AB has both A and B antigens


body makes antibodies to the antigens not present on the RBC’s


antibodies are in the plasma


blood

-type A has anti-B antibodies only
-type B has anti-A antibodies only
-type O has both anti-A and anti-B antibodies
-type AB has neither anti-A nor anti-B antibodies

universal donor/recipient

-type O is universal donor
-type AB is universal recipient

agglutination

seen if antibodies react with antigens
-caused by antibodies binding to RBC’s


coagulation

not the same as coagulation, which is due to clotting factors


agglutinins

antibodies also called agglutinins

agglutinogens

antigens also called agglutinogens

Rh Group

Rh plus has Rh antigen on RBC’s


Rh minus individual has no Rh antigen and will make anti-Rh antibodies


-important in blood transfusions and in pregnancy
-if mother is Rh minus and father is Rh plus
-Rh plus fetus may be attacked by mother’s anti-Rh antibodies




HDN (hemolytic disease of the newborn)

prevented by giving mother RhoGam
-an immune globulin (an antibody)
-binds to fetal Rh antigens so they cannot stimulate mother’s body to make anti-Rh antibodies
-given to mother in late pregnancy and at birth


Blood Cell Production

hemopoiesis


myeloid hemopoiesis


lymphoid hemopoiesis


hemocytoblasts


hemopoiesis

(aka hematopoiesis) = blood cell (formed elements) production
-useful for understanding blood disorders (anemias, leukemias)
-Note: blood cells often called formed elements because platelets are not cells, but cell fragments

myeloid hemopoiesis

-formation of all formed elements
-occurs in red bone marrow

lymphoid hemopoiesis

-formation of lymphocytes
-occurs in lymph tissues
-thymus, tonsils, spleen, lymph nodes


hemocytoblasts

stem cells
-give rise to all formed elements of blood
-multiply continually to maintain their numbers
-are multipotent: can differentiate into several different cell lines
-differentiation begins when they develop receptors for stimulatory chemicals:
-erythropoietin
-thrombopoietin
-CSFs (colony-stimulating factors)
-once the receptors are formed, they are committed cells


Erythrocyte Production

hemocytoblast


proerythroblast


erythroblast


normoblast


reticulocyte


erythrocyte

erythropoiesis

stimulated by a hormone made by liver and kidneys: erythropoietin
-takes 3-5 days for mature RBC to develop
-2.5 million RBCs made per second; 20ml per day


1-starts as

1-starts as hemocytoblast

2-becomes

2-becomes proerythroblast
-committed cell
-has receptors for erythropoietin


3-becomes

3-becomes erythroblast
-makes hemoglobin


4-becomes

4-becomes normoblast as nucleus shrinks
-when nucleus is gone


5-becomes

5-reticulocyte
-named for ER within
-leaves bone marrow, enters bloodstream


6-becomes

6-becomes erythrocyte when ER disappears
-Note: both reticulocytes (0.5-1%) and erythrocytes found in blood
-# of reticulocytes in bloodstream increases after blood loss

Erythrocyte homeostasis

-maintained by erythropoietin

-example, starting with hypoxemia


(low oxygen in blood):

hypoxemia -> liver & kidneys increase erythropoietin secretion -> stimulates red bone marrow -> increased RBC production -> increased oxygen transport


causes of hypoxemia:


blood loss, high altitude, sudden exercise
-lung damage (like emphysema)
-NOT corrected by increased erythropoiesis
-problem is lack of functioning lung tissue, not lack of RBC’s
-body responds in same way, anyway
-can result in dangerous polycythemia


Polycythemia

-too many RBC’s
-can result from cancer of red bone marrow erythropoietic cells
-can also result from anything can causes hypoxemia
-those mentioned above: lung damage, smoking, high altitude, emphysema
-also caused by dehydration, strenuous conditioning, blood doping
-causes increased blood volume, BP, viscosity
-can strain heart, cause clots
-can result in heart failure, stroke

Leukocyte production


granulocyte-macrophage colony-forming unit


T progenitor


CSFs


1) granulocyte-macrophage colony-forming units become

-become monocytes & granulocytes (eosinophils, basophils, neutrophils)
-monocytes can migrate into tissues and become macrophages

2) T progenitor

2) T progenitor (become T lymphocytes)

3) B progenitor

3) B progenitor (become B lymphocytes)

all 3 committed cell types have receptors for CSFs


-CSFs secreted by mature lymphocytes & macrophages
-secreted in response to immune system challenges

each CSF stimulates a different type of WBC


-bacterial infection produces neutrophils
-allergic response produces eosinophils

Platelet Production

thrombopoiesis


-platelets used to be called thrombocytes



Platelet Production steps

thrombopoietin


megakaryoblast


megakaryocyte


& 4th step



1-hemocytoblast

1-hemocytoblast develops receptors for thrombopoietin
-hormone made by liver and kidneys


2-with receptors

2-with receptors, now called megakaryoblast
-replicates DNA many times w/o cell division
-becomes giant cell called:


3-megakaryocyte

3-megakaryocyte
-has multiple sets of chromosomes
-cell fragments into platelets


4-platelets circulate i

4-platelets circulate in blood; some stored in spleen until needed

polycythemia

too many RBCs

anemia (too few RBCs)


1) inadequate erythropoiesis or hemoglobin production
2) hemorrhagic anemia due to bleeding
3) hemolytic anemia due to RBC destruction


iron-deficiency anemia


hemoglobin contains iron
-when iron is lacking in diet, adequate hemoglobin cannot be made


pernicious anemia

vitamin B12 deficiency (plentiful in meat)
-strict vegetarians need supplements
-intrinsic factor needed for absorption of B12
-made by stomach cells


not enough int. fac. can be hereditary; also commonly occurs with old age



hypoplastic anemia

hypoplastic anemia = decrease in erythropoiesis

aplastic anemia =

complete cessation of erythropoiesis
- both hypoplastic and aplastic can be due to radiation exposure, drugs, poisons (snake venom, mushrooms, arsenic, mustard gas), viruses, autoimmune disease, hereditary causes

medical consequences of anemia:


1-hypoxia of tissues (low oxygen)
-lethargy, shortness of breath, pale-skin
-in extreme, necrosis of tissue & organs
2- reduced blood osmolarity
-more fluid enters tissues -> edema
3- reduced blood viscosity, causing:
-reduced resistance of flow, causing increased heart rate
-can lead to heart failure
-reduced blood pressure