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163 terms

BIO 242 Test 2

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.
Natural immunity
acquired as part of normal life experiences. You get a virus you make Ab to it.
Artificial immunity
acquired through a medical procedure such as a vaccine.
Cell mediated immunity
T cells are responsible for.
Types of T cells
-T helper. Activates B cells and help them recognize Ag and produce Ab.
-T cytoxicity. Directly attacks infected cells
-T supressor or T reg. When infection is over it supresses the immune system.
-Natural killer. Kills tumor cells and virus infected cells
Mechanism of T-helper cell action
When a foreign Ag is in the body, a macrophage (also here refers to antigen-presenting cell (APC) phagocytizes a bacteria or a virus, somehow breaks it up into small pieces, and then displays the parts of the Ag (peptide fragments in association w HLAII on its surface to TH cell (to TCR on TH cell surface). TH then releases a number of cytokines such as IL-2, IFN-gamma, etc. IL-2 for instance, helps make more T cells and more Ab-producing B cells.
Mechanism of cytotixic T cell killing
Cytotoxic T lymphocytes (CTL) (Tc) are antigen-specific effector cells of the immune system with the ability to lyse target cells such as virus-infected cells, allografted cells, or even parasites in a contact-dependent manner. Like other T lymphocytes, CTL initially differentiate in the thymus, where they acquire the specific T-cell receptor (TCR). The majority of CTL also bears CD8 molecules (CD8+). CTL identify the microbial peptide fragments on the surface of macrophages in context of MHC-I. They release their granular contents (perforins & granzymes) to kill the infected macrophage.
Normal TH
500 - 1600 ul.
Normal TS
375 - 1100 ul.
AIDS in regards to TH
Another method to call it AIDS is if CD4+ is below 200 per ul of the blood. This is when the patients can easily get opportunistic infections, i.e, PCP, yeast. HIV + that is not AIDS yet can have 500 CD4/ul blood.
Another method of AIDS measurement is looking at the CD4 cells percentage. Percentage here means the % of the total lymphocytes that are CD4+. Normal percentage range of CD4+ TH cells in a HIV negative person is 40%. CD4+ less than 20% is AIDS. CD4<14% implies very seriously damaged immune system.
Organ transplants
T cells are involved in rejection of organ transplants.
From another species i.e. temp porcine graft in severe burns. Need to match at least 75% MHC to be successful.
IgA - Against bacteria of skin or floor of GI tract. Abundant in booby milk.
IgG - Most common, strongest and can cross placenta
IgM - Large
IgE - Allergies
IgD - Mostly unknown
Body recognizes protein as an infection. B cells > activated > plasma cells > IgE binds to protein > causes basophils to release histamine granules > histamine makes capillaries more porous and plasma secretes > antihistamine binds to block histamine
Autoimmune diseases
Diabetes Mellitus (Type 1): the body attacks against self-pancreatic cells.
MS: the body destroys its own myelin.
RA: the body attacks synovial tissues in the joints.
Allergies (hypersensitivities): The body see things (i.e, animal dander) as a threat and mount an immune response.
Immediate hypersensitivity & anaphylaxis.