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Blood collected from a superficial vein, such as the median cubital vein in the superficial elbow

Arterial Stick

To obtain a blood sample from an artery such as the radial artery at the wrist or brachial artery at the elbow

Blood PH is typically

7.35-7.45 (slightly basic)

Blood temp is higher or lower than body temp?

Slightly higher at 100.4 vs. 98.6.

3 Blood cellular parts

RBCs, WBCs, and platelets

3 main pasma proteins

Albumin, fibrinogen, and globulin make up 99% of the plasma proteins

Components of whole blood

48% formed elements (47% eurythrocytes, 1% leukocytes and platelets) and 52% plasma

Difference between plasma and serum

serum is the protein rich fluid that is separated from the blood after the blood clots. Serum lacks clotting proteins.

Blood functions

-Delivery oxy and nutrients from digestive tract to body
-Transport metabolic waste products from cells to eliminations site (kidney, lungs)
-Transport hormones to target organs
-Maintain normal pH in body tissues (7 in cyto and instertitial space, 7.3 in blood)
-Maintain and distribute appropriate body temp
-Maintain normal vascular fluid volume

Plasma properties

90% H20, 8% proteins, 2% a.a.s, electrolytes, metabolites.


Made in the liver and released into the blood circulation. Function is to shuttle other proteins around and osmotic pressure.

Origin of plasma protein

Liver makes 90%. Thus liver diseases can alter the composition and functional properties of blood. Some form of liver disease can cause uncontrolled bleeding to the inadequate synthesis of clotting factor fibrinogen.

Blood volume

5-6 L in males and 4-5 L in females


Decreased blood volume (decreased plasma volume)

Hypovolemic shock

elevated pulse, lack of tissue perfusion indicated by pale skin, dizziness, nausea, thirsty, doesn't show up until 20-25% blood loss

Cause of hypovolemic shock

Severe bleeding, severe burns, severe dehydration, diarrhea. Basically the heart doesn't have enough H2O to pump so CO decreases. Heart rate increases, blood vessels constrict, kidney decrease urinary output

Blood loss from donating blood


Normal RBC count

5-6 million per ul of blood in males and 4-5 million per ul in females.


The % of a blood sample that consists of formed elements. Typically refers to amount of RBC's i.e. 47% hematocrit count.

Danger of high hematocrit?

Viscous blood and result is stroke or heart attack


Consists of globin (two alpha and beta polypeptide chains) and 4 heme groups. Each heme contains 1 Fe atom. Each heme can bind to 4 O2. 250 million Hb per RBC so 1 billion O2 in Hb.


Not enough RBC


When max of 4 O2 binds to 1 Hb

Resting partial pressure

100 mm Hg.

Arterial blood

Hb saturation is 98%

Hb saturation as it flows

75% and can drop to 15 mm Hg during exercise.

S curve shifts to the right if

temp/acidity goes up

S curve shifts to the left if

temp/acidity goes down

O2 molecules binding

O2 binds to the Fe ions in the center of the heme units forming oxyhemoglobin

Environmental factors affecting Hb are

the PO2 of the blood, blood Ph, temp


binding ability of oxygen


Low levels of oxygen in the blood. As elevation increases, oxygen levels decrease


Inability to produce sufficient alpha or beta chains of Hbs.

Sickle cell anemia

Mutation in aminoacids of the beta chain of the Hb.

Free iron (Fe)

toxic to cells so the body iron is generally bound to transport or storage proteins. Fe in the blood binds to transferrin. Excess transferins are removed in the liver and spleen. Fe is stored in ferritin protein - Fe complex

Homeopoieses or hematopoiesis

formation of all blood cells


Formation of RBCs. Formed in the liver and spleen from 2nd to 5th month of development. Then switches to bone marrow.

Erythropoiesis formation

Hemocytoblast > Myeloid Stem cell > Proerythroblast > erythroblast (contain nucleus) > reticulocyte (still in bone marrow but lose nucleus and enter stream) > erythrocyte. Blast has nucleus, cyte does not

Retics count

Measures how rapidly reticulocytes are made by the bone marrow. Can be used to determine if treatment for anemia is working. Within a day they become mature RBCs.


Hormone produced by the kidneys. When O2 levels drop, EPO is released to increase RBCs and increase the amount of O2 carried by the blood.

Why is Fe, B12, and folic acid important?

Developing RBCs don't grow and divide without it.

Where is intrinsic factor made?

Stomach. Purpose is for B12 to be absorbed. Without the person develops pernicious anemia.

Dead RBCs

Eaten up by macrophages or spleen. Fe is kept and saved inside liver cells or as Transferrin released to blood. Bilirubin is released into blood bound to albumin. Picked up by liver and secreted to intestine as bile. Metabolizes as sterobilin in gut and excreted in feces. May be converted to urobilinogen and secreted in urine.

Bili lights

Used for newborns with jaundice. Breaks down bilirubin into different forms.


Production of leukocytes. Stimulated by interleukins and colony stimulating factors.

5 Leukocytes



50-70% relative value
Also called Poly


1-3% relative value
Increase in allergy and parasitic infection
Attach objects that are coated with antibodies like bacteria or parasites


.4-1% relative value
Bilobed with purplish black granules
Discharge their granules into the instertitial fluids.
Object is to enhance the local inflammation at the damaged tissue
Attract eosinophils


25-35% relative value
Large, spherical nucleus
Most aren't in blood stream. Either in connective tissues or lymphatic system
3 types:
T cells (directly attack foreign cells)
B cells (secrete antibodies)
NK cells (kills abnormal cells)


4-6% relative value
Kidney shaped nucleus
Also called macrophage
Floats in bloodstream for 24 hours then enters peripheral tissues and becomes macrophage.
Eat things same size or bigger.


Above normal WBCs


Below normal WBCs


Also thrombocytes. They are fragments of larger cells called megakaryocytes (turns into 4000). Responsible for clot formation


Elevated platelets in response to infection, inflammation, or cancer.


Below normal level of platelets

Characteristics of WBCs

Can migrate out of bloodstream called diapedesis
Cabaple of emoebid movement called gliding motion.
Attracted to specific chemical stimuli called chemotaxis
N, E, and M or cabable of phagocytosis


Stopping of bleeding

3 phases of clotting

-Vascular spasm to decrease the diameter. Takes about 30 sec. Endothelian is released to contract smooth muscle cells.
-Platelet adhesion causes platelet activation (serotonin and thrombaxane act as vasoconstrictors). Platelets release ADP which makes them sticky and leads to aggregration to form platelet plug.
-Coagulation which is blood clotting that traps RBCs and platelets forming the clot.

Clotting extrinsic

Blood vessel is damaged. Starts with protein called tissue factor (TF attached to smooth muscle wall) leading to formation of prothrombinase. Faster

Clotting intrinsic

SLower clotting pathway.

Clotting after prothrombinase

Converts to propthrombin then to thrombin. In the presence of Ca thrombin is converted to soluable fibrinogen then to insoluable firbin. 30-40 minutes after clot forms it retracts, pulls the edges of the wound together and is further stabalized.


Clot is no longer needed and is dissolved

Clot retraction

Consolidation and tightening of the fibrin clot so repairs can be made.

Vitamin K in clotting

Required for synthesis of 4 clotting factors.


Fibrin dissolving protein from plasminogen.


Substances that delay or suppress blood clotting such as heparin (released by basophils). Acts by inhibiting thrombin

Hemorrhagic anemias

Due to massive blood loss

Hemolytic anemias

Premature rupture of RBCs. Mismatched blood transfusion.

Aplastic anemia

BM destruction i.e. by drugs

Iron deficiency anemia

Iron deficient. Sometimes with athelets anemia

Pernisious anemia

B12 defiency


A globin chain can be missing

Sickle cell anemia

Sickle shaped RBCs


Many blood cells. Bone marrow cancer due to excessive RBC. Secondary is due to excessive EPO or O2 deficient


Blood clot in unbroken vessel


Thrombus that broke loose


Embolus blocks capillaries and flow


Too few platelets, strawberry shaped rashes

Blood types

A, B, AB (rare, universal recipient), O (most common, universal donor) and Rh+ (most common) RH-(15% of population).


Infection of entire body


bacteria in the body


Cancer of WBCs


Receive from a sibling


Bone marrow collection from peripheral blood

Lymph nodes compared to nodules

Larger, encapsulated, B, T, and macrophages

Lymph nodules compared to nodes

Smaller, non-capsulated

Lymphatic system made up of

Lymphatic vessels and organs and tissues.

What is lymph?

Similar to plasma with less protein and has lymphocytes

Lymph vessels drain into

the right lymphatic duct (drains from upper right arm and right side of head and chest) which drains into right subclavian vein or larger thoracic duct (drains rest of body) drains into left subclavian vein.

Characteristics of lymphatic vessels

Blind Ended
Always directed to heart
Mechanism of pumping is spasm of smooth muscle cells in vessels
Contraction/relaxation of skeletal muscles surrounding the lymph vessels
Flap like valves


Any substance that stimulates IR


A protein made by B cells that binds to an Ag and in the process gets of the Ag or the cell that carries the Ag.

Lymph nodes

Bean like and clustered among lymphatic vessels. Serve as filters for the lymph and can filter out bacteria and other debris to keep it from entering the blood stream. Plays a role in activating the immune system as lymphocytes within the nodes monitor the system for entigens and mount an attack against them. Activation of lymphocytes causes an increase in lymphocyte numbers and thus swelling of the nodes.

Where are lymph nodes usually clustered?

Neck, axillary, and groin area plus lower small intestine area.

Anatomy of lymph node

Surrounded by a fibrous capule and inside the node the fibrous capsule extends to form trabeculae. The substance of the lymph node is divided into the outer cortex and inner medulla. Multiple afferent lymph vessels bring lymph into the lymph nodes. Inside the lymph nodes are B and T cells and macrophages that perform the filtration job. The lymph then enters efferent lymph vessels.


Lymphoid follicle
Germinal center
Subcapsular sinus


Meduliary cord
Medullary sinus

Blood vessels in lymph node

In order to function properly, has to have the ability to dump leukocytes immediately into blood stream.

Lymphoid organs and tissues

Spleen, Tonsils, lymph nodes, Peyer's patches (full of nodules), thymus


Located below rib cage, size of fist. Production of B cells, phagocytizing bacteria, graveyard for RBCs and platelets.


Enlargement of spleen due to hemolytic anemia because spleen becomes hyperfunctional; lymphoma, infectious mononucleosis.


Behind the sternum. Site for maturation of T cells. Starts shrinking and by age 75 is hard to tell it apart.


Gather and remove germs entering the mouth and nasal cavities

Palantine tonsils

Located on either side of the tongue at the back of the oral cavity

Linguinal tonsils

Base of tongue

Pharyngeal tonsils

On posterior wall of the nasopharynx (also called adenoids)


Cancer of blood forming tissue - bone marrow


Cancer of lymph nodes (hodgkins (6) and non-hodgkins (61, more common)). If caught early can be treated 90% of the time.

Classifications of leukemia

Based on how fast it grows.
Acute: Many blast cells in circulation.
Chronic: Elevation of more mature cells.
Lymphocytic leukemia
Myelocytic leukemia

Types of leukemia

Acute/chronic lymphocytic leukemia
Acute/chronic myelogenous leukemia


Most common in children but can occur in adults


Common in both children and adults


Most common for adults. May feel well for years without treatment. Rare in children


Mainly affects adults. May have no symptoms for months or years before entering a phase where it grows more quickly.

Nonspecific system

Skin, inflammatory response, fever, IFN, complement system, neutrophils, macrophages, basophils, eosinophils

Specific system (immunity)

Humoral (antibodies produced by B cells)
Cellular (T cells)

1st line of IS defense

Sweat, saliva, lysozyme

2nd line of IS defense

N, M, and E. Phagocytes, NK cells, inflmmation, antimicrobial proteins, fever

3rd line of IS defense

Lymphocytes (B and T cells)

Nonspecific chemical defenses

Sebaceous secretions, lysozyme (enzyme that hydrolyzes the cell wall of bacteria, in tears and macrophages), High lactic acid and electrolyte concentration in sweat, skins acidic pH, hydrochloric acid in stomach, digestive juices and bile of intestines, semen, vagina has acidic pH


Initiated by circulating pyrogens which reset the hypothalamus to increase bod temp. Signals muscles to increase heat production and vasoconstriction.

Exogenous pyrogens

products of infectious agents

Endogenous pyrogens

liberated by monocytes, neutrophils, and macrophages during phagocytosis

Benefits of fever

Inhibits multiplcation of temp sensitive microorganisms, impedes nutrition of bacteria by reducing the available iron, increases metabolism and stimulates immune reactions and protective physiological processes

Inflammatory response

When skin is penetrated. Start of activation of heat, redness, swelling, and pain.
When the skin breaks open, injured tissues release chemical signals (histamine, kinin, prostaglandis, cytokines, etc...). i.e. histamine is a vasodilator so arterioles increase in diameter so more blood flows to injured site and redness and warming take place. Histamine increases the capillary permeability making the vessels leaky and swelling takes place. Swelling puts pressure on the nerve ending causing pain. Diapedis of the WBCs begin.


Eat up bacteria

2nd mode of bacterial destruction by macrophages

Some bacteria are phagocytized by macrophages but arent destroyed inside the macrophage (i.e, mycobacteria or leishmania).However, somehow, macrophage process some of their proteins into smaller peptides (presumably those bacteria that spontaneously die inside the macrophage). Those bacterial peptide fragments then presented on the cell surface of macrophage in conjunction w MHCII. TCR of T cell recognizes MHCII plus the bacterial peptide, this is called T cell priming which leads to release of a number of cytokines such as IL-2, IFN-gamma. IL-2 helps making T cells and more Ab-producing B cells. IFN-gamma activates microbicidal mechanisms in the macrophage.

Types of interferons

Alpha produced by lymphocytes and macrophages
Beta produced by fibroblasts and epithelial cells
Gamma produced by T cells

Alpha and Beta interferons

Not meant to save the invaded cell but they act as an alarm system to let nearby healthy cells know that a virus is around and stimulate these healthy cells to protect themselves, by expressing antiviral proteins, from being infected by a virus.

Difference between alpha/beta and gamma interferons

Alpha/beta block and gamma gives instructions to kill.

Complement system

Consists of 26 blood proteins that work in concert to destroy bacteria and viruses.
Complement proteins are activated by cleavage (cascade reaction), similar to the system activating blood clotting. Complement proteins are initially inactive and present in the blood circulation. Once proteolytically-activated, a chain reaction (cascade) occurs. The end-product of the chain reaction is the formation of an annular membrane attack complex (MAC). MAC insert itself into the microbial phospholipid bilayer membrane and acts like a channel for electrolytes & H2O. H2O & electrolytes pour into the cell via this channel leading to the microbial cell lysis.

3 pathways for complement proteins

1. Classical pathway
2. Lectin pathway
3. Alternative pathway

Classical complement pathway

activated by the presence of antibody bound to microorganism. Ab has to first bind the surface protein of microbes in order to activate the cascade.

Lectin complement pathway

nonspecific reaction of a host serum protein called mannose-binding protein (MBP)that binds mannan (polymer of the sugar mannose) located on the surface of bacteria, yeasts, parasites, and viruses. In the process, the complement pathway gets activated and destruct the invaders.

Alternative complement pathway

begins when complement proteins bind directly to normal cell wall and surface components of microorganisms and activate the complement cascade to punch a hole in the microorganism and destroy it. Does need an antibody, can directly destroy

Stages in the complement cascade

Regardless of which of the 3 complement pathways are used to destruct the microorganisms, the 3 pathways share the followings:
Amplification and cascade
Membrane attack

B cells and Ab production

Antigen (Ag) - Molecules that stimulate a response by T and B cells. That is the T and B cells see it as foreign. Therefore, an Ag is a chemical and most often they are foreign proteins, i.e, bacterial proteins. When an Ag binds to the surface of a B cell, it causes the B cell to divide & develop into a clone of mature B cells called plasma cells. Each plasma cell produces millions of antibodies AKA (immunoglobulins) (Ig). Igs circulate in blood and lymphs & when they find SPECIFIC Ag, they bind to it. Abs (Igs) don't directly destroy the Ags or kill the microbes carrying the Ag on its surface, rather they identify it for T cells or complement proteins so they can do the destruction.

Plasma cells - B cells

Clone of mature B cells. B cells that have been exposed to Ag and have gained ability to make specific Ab to that Ag.

Clonal selection theory - b cells

When an Ag enters the body, it is confronted by a dazzling array of lymphocytes all bearing different Abs each with its own individual recognition site. The Ag will only bind to those receptors with which it makes a good fit. Lymphocytes whose receptors have bound Ag receives a triggering signal & develop into Ab-forming plasma cells. Becuase we make millions of different Ab molecules, we simply don't have enough room in the body to accommodate them. To get around this, lymphocytes upon contact w Ags, undergo many division to build up a large clone of plasma cells which will be making Ab of the kind for which the parental lymphocyte was programmed.

Memory cells - B cells

Any clone cells that does not develop into plasma cell. Seasoned soldiers that haven't seen war. In lymph tissues and some hide in bone marrow.


The Ab molecule is made up of 2 identical heavy and 2 identical light chains held together by interchain disulfide (S-S) bonds.
The most abundant type of Ab (Ig) is called IgG. In the lab, enzyme papain can be used to break the IgG into 2 Fab fragments and 1 Fc portion.
Is a protein. Does not kill the bacteria but facilitates it.

FAB portion

Antigen binding site at top of Y

FC portion

Bottom of Y

Mechanism of antibody actions

-Neutralization (escorts out without going through liver)
-Agglutination (cell bound antigen) enhances phagocytosis
-Precipitation (soluable antigen) enhances phagocytosis and inflammation
-Complement (floats in blood, waterfall effect until punches hole and explodes)

Primary immune response to antigen

0-10 days

Secondary immune response to antigen

Memory cells become plasma cells with in two days

Active immunity

results when a person is challenged with antigen that stimulates production of antibodies; creates memory, takes time, and is lasting.

Passive immunity

preformed antibodies are donated to an individual; does not create memory, acts immediately, and is short term. Ex, injection of gammaglobulin to someone exposed to hepatitis A. not lasting as it doesn't stimulate one's own immune system.

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