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A and P - Test 2 - Study Guide

by: Kimberly Krause

A and P - Test 2 - Study Guide 2402

Marketplace > Tyler Junior College > Biology > 2402 > A and P Test 2 Study Guide
Kimberly Krause
Tyler Junior College
GPA 4.0

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This study guide covers the last half of Chapter 18 and Chapter 22. Immune System is a big part of the test.
Anatomy and Physiology II
Dr. Cates
Study Guide
immune system, adaptive immunity, Innate Immunity, Hemostasis, Endocrine system
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This 10 page Study Guide was uploaded by Kimberly Krause on Thursday September 29, 2016. The Study Guide belongs to 2402 at Tyler Junior College taught by Dr. Cates in Fall 2016. Since its upload, it has received 139 views. For similar materials see Anatomy and Physiology II in Biology at Tyler Junior College.

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Date Created: 09/29/16
Study guide for Test 2 - Chapters 18 and 22 Color key: Red = Main points to study 1. Hematopoiesis/ Hemopoiesis (Formation of Blood Cells) Steps to making all blood cells 1. Starts in the Red Bone Marrow aka Myeloid tissue 2. Starter cells: Blood stem cells or Hemocytoblasts are the cells that can turn into any type of blood cell. These can make any of the three formed elements of the blood. Listed below: 3. After the new cells are formed they enter the circulatory system. The lymphocytes however, can travel to lymphoid tissue. 1. Erythropoiesis (RBC 2. Thrombopoiesis (Platelets 3. Leukopoiesis (WBC formation) formation) formation) a) Stem cell is a normal cell a) Started with the stem cell a) Starts with that normal stem cell b) Nucleus is ejected b) Turns into a Megakaryoblast b) Makes the leucocytes c) Turns into a Reticulocyte c) Which matures into a c) Which branch off into the different (hemoglobin making - immature Megakaryocyte. WBCs, except lymphocyte. RBCl) d) The little “tails” of the -The lymphocyte is not formed from d) Finally turns into a Erythrocyte megakaryocyte rip off to form the myeloid stem cell, but a lymph platelets.anslational stem cell. 2. Hypoxia (Low oxygen in blood) How your body fixes it 1. Kidneys sense decreased blood oxygen levels. 2. Kidneys release the hormone EPO (erythropoietin) into the blood 3. EPO stimulates red bone marrow make more RBCs (because they carry the oxygen). 4. In 5 days new RBCs (reticulocytes) enter the blood stream 5. More oxygen can be carried by the RBC and O2 levels rise Recycling old RBCs RBCs have a lifespan of 120. After this, they are tattered and need to be recycled. Page 1 of 0 Hemoglobin splits into: Liver and Spleen are the two organs 1. Hem
 a) Iron (toxic- transported to liver by alpha and beta proteins) that clean up the old RBCs. b) Bilirubin (yellow color. Too much can cause jaundice. Liver “catches” the old tattered RBCs in Accounts for the yellow color of bile/feces) order to phagocytize by the ex. Babies might be born with jaundice as liver is not working properly. macrophages in the liver. It can catch Too much bilirubin. Yellow food in small intestine. Large intestine has them because of the unique tissue of the bacteria e. coli that turns poop brown. When babies poop finally the organ. changes to brown, parents rejoice; everything works! ex. Sick dogs eating poop to put e. coli back into gut. Rate of destruction: 3 million RBC/second 2. Globin -protein which gets broken into amino acids can be used again. Rate of creation: 3 million RBC/second 3. Disorders of Varying Blood Levels 1. Leukocytosis (more WBC) -elevated WBC means there’s an infection -The excess WBC’s are immature WBC’s. 2. Leukopenia (less WBC) -Not enough “police force.” 3. Polycythemia (more RBC) -Blood is normally 5x thicker than water, with this condition it’s 8-10x thicker -Thick and gummy like liquid sandpaper. -Can be caused from excessive secretion of EPO and too much RBC production. 4. Anemia (less RBC) -means “not blood” - less oxygen a) hemorrhagic - bleed out -heavy menstrual bleeding -chronic ulcers b) hemolytic - blown up cells -malaria - fever (is exploding RBCs, lots of garbage to clean up) -happens with hypotonic solution c) aplastic - bad form -something is wrong with your bone marrow 5. (Less “good” hemoglobin)
 Fe + O2 = red color. You have to have iron to make hemoglobin 
 ex. Years ago they wanted kids to eat well, so they created Popeye to promote iron intake. a) Fe deficiency b) Pernicious anemia means “vague” and worthless -Can’t digest b12 c) Sickle cell anemia -Genetic (when someone inherits 2 copies of the sickle cell gene) -These will fill up arteries and cause pain in the joints. 4. Hemostasis - Repairing damage to blood vessels Steps to repair the blood vessels 1. Vascular Spasm (figure A) -This means the that the vessel constricts. It’s like when someone were to stick a knife in your gut the first reaction would be to fold over. It constricts so that it can reduce the flow of blood in that area and allow for repair of the damage. Page 2 of 0 2. Platelet Plug Formation (figure B) -The collagen fibers create a sticky film, so when a platelet floats by it sticks to that site. Then more platelets start to stick, created a plug. Platelets secrete a solution that attracts more platelets and plug grows. 3. Coagulation Retraction/Fibrinolysis (figure C and D) -For blood clots you NEED CA++ and Vitamin K (made in large intestines) 1. Prothrombin Activator X (from liver plasma) activates thrombin. 2. Thrombin activates Fibrin. Fibrin floats around in plasma until there’s a damage in the vessel and it gets activated. 3. Fibrin flops over the platelet plug and more fibrins builds up ex. Scotch tape in fan ex. Silly string 4. Fibrin makes the web over the whole thing 5. Fibers in fibrin constrict and squeeze (retraction) it down. Making it a hard-packed clot. 6. The juice that is squeezed out of the clot is called a “serum.” -You can give a patient a serum, which keeps blood volume up without causing a clots. 7. Fibrinolysis is when the “patch” begins to dissolve -If the clot rips off and floats down the blood stream that’s called an embolus. 5. Movement of White Blood Cells Margination: WBC already alerted, traveling through vessel to site of injury. CAMs (Cell-adhesion molecules) on leukocytes adhere to CAMs on capillaries. “Cell velcro.” Diapedesis: means “stepping out” It’s where the WBS changes shape to slip out of the vessel to damaged area. Chemotaxis: Chemo means chemical, so WBCs are like hound dogs sniffing out the inflammatory chemicals (histamine). Histamine is like a smoke alarm or a scream. Phagocytosis: WBCs eat the bacteria. 6. Transportation of Respiratory Gasses (picture to right) 7. Immune System Big Picture Pathogens: -Virus (not a cell, not alive, protein shell with nucleic acid, can take over) -Prions (no nucleic acid, cause disease in nervous tissue, the new “scary”) -*Bacteria (can cause disease, but not most of bacteria) -*Fungus (includes molds, yeasts, and fungi producing spores) -*Protozoan (Malaria) -*Worms (parasites) Page 3 of 0 Immune System Big Picture Innate Defense 
 1st Line: Surface Skin and Mucous Membrane (Born with it) —————————
 ———————————— 2nd Line: Internal Phagocytes, fever, NK cells, Complement Proteins, (When it gets past walls of your Interferons, Inflammation membrane) Adaptive Defense 
 3rd Line: Cellular Immunity T cells (Targets directly) (Developed it because (cells are attacking)
 Ex. like grabbing a flyswatter and killing a cockroach of exposure) 
 directly —————————
 ———— Humoral Immunity B cells (Kills everything in sight) (Humor - means fluid - acting Ex. Fogging a whole house and killing ALL the bugs
 and carries antibody) 
 APC’s Antigen (Target) Presenting Cell 8. Innate Defense - First Line Skin -Made up of Stratified Squamous Epithelium ex. Raincoat -Keratin -Takes 40 days to get new layer of epidermis -Hair -Bacteria gets sloughed off (that’s why it’s a good line of defense) ex. bedsores -Because skin is the first line of defense, we don’t want to use too much Purell hand sanitizer because the alcohol causes the skins to dry, and when the dry skin cracks it allow more bacteria to enter the body. Secretions -Sweat (pH 4-6, salts, IgA, nitrogenous wastes), same composition as urine. IgA - stands for Immunoglobulin which is an antibody. Immunoglobulin is the functional name. Gamma is the of skin structural name. -Sebum (oil, acne likes the sebum) -Cerumen (earwax) ex. Ear infection is caused by wax sealing in water in ear. Mucous -goblet cells, mucus production rates change, cilia membrane Other -Saliva (pH 6, lysozyme, IgA, nitrogenous wastes) secretions -Gastric (pH 2-3, HCI, protein-digesting enzyme) -Lacrimal (lysozyme, IgA) -Vaginal (lactic acid) -lactic acid would retard the bacteria. Sperm cells die in acidic, but the semen can handle it. -Urine (pH 6, nitrogenous wastes) -antiseptic Page 4 of 0 9. Innate Defense - 2nd Line Phagocytes (eating things) 1. Macrophages -100x more effective a) Fixed -ex. Küpffer cells live in sinusoids of liver, waiting to eat old cells b) Free 2. Neutrophils -60% of WBC, like national guard (they get to the battle and hold the fort down) -Components of Pus (Chemicals called defensins, do damage to neutrophils) 3. Eosinophils -Clean up crew after the battle. -Levels go up after an allergic reaction -Fight parasite worms Respiratory burst (Oxidative burst) -A method of killing by releasing a bunch of free radicals. -When the lysosome in the macrophage is digesting the “garbage,” they can kill them quickly by releasing a burst of free radicals. -Vitamin A,C,E neutralizes free radicals. -If you have an excess of free radicals, they can be used to destroy stuff like in this method. Opsonization (To grab a slippery pathogen antigens add handles) Natural Killer Cells Chemicals they use -Perforins (perforate) -released then accumulate on surface, then they poke into cell in a circle. This poked circle opens the pathogen up so it can kill. -Granzymes (shred) -Go into the cell and shred up the organelles and DNA of cell. -The pathogen collapses (called apoptosis -ptosis means drooping) -Deflates cell (can’t explode it, don’t want to spread harmful materials in body) -The phagocytes can come and eat up that deflated cell. Page 5 of 0 Dangers of Inflammation Hyperemia -Caused when there’s too much blood flow Exudate -Too much fluid Cytokines Alarm chemicals 1. Cytokines/kinins (-kine means to activate things) 2.Histamine (secreted from Mast cells) 3. Prostaglandins How they act Autocrine - They act on themselves Paracrine - They act on neighboring cells Endocrine - They circulate the blood (systemic) Major Cytokines Interleukin (IL) Regulates immune cells, between WBCs. T cells make these to alert other cells. Tumor necrosis factor (TNF) Destroys tumor cells Colony-stimulating factor (CSF) Stimulates leukopoiesis in bone marrow to increase synthesis of a specific type of WBCs Interferon (IFN) Antiviral agents Interferon -When virus is released the interferon blocks them from spreading. Complement proteins -Made in liver -Like antibodies (they can do several things, they promote opsonization) -Increase inflammation -Make MAC (Membrane attack complex) that hooks on cell and causes it to lyse. -Just poke holes in membrane, but does not shred organelles. Fever -Dangerous 104 degrees (because that will denature your proteins) Page 6 of 0 -106 degrees brain dies -109 you’re dead -Fever can be brought on by toxins, response to trauma, brain tumors, or drug reactions. -Hypothalamus controls body temp including a fever. Pyrogens (create fires) Events of Fever 10. WBC locations: -Nodules are scattered throughout the body. -Lymph nodes are encapsulated as the lymph comes in it showers over the nodules that make up the nodes. MALT (Mucosa-associated lymphatic tissue) -located in lamina propria of mucosa of the GI tract, respiratory, genital, and urinary tracts. -a collection of lymph nodules in the small intestine are called Peyer Patches. -They have the same function as the other lymphatic nodules. -Tonsils and spleen -take on the invaders. 11. Adaptive Defense 1. Humoral Immunity -B Cells (antibody mediated) -B Cells are APCs. 2. Cellular Immunity T Cells (cell mediated) -T cells need APC’s to start. Antigens 1. Complete antigen (able to start reaction) 2. Incomplete antigen = Hapten (not able to start reaction) Antigenic Determinants -Exact trigger to tell if it is a pathogen. These are located ON the antigen. Autoimmune -Happens when your cells misread something and attack the wrong cell. Self/Non-self (MHC 1 and 2) 1. MHC Class 1 -These tags on the cell are sampling the internal fluid of their cell and putting it in their tag. -all nucleated cells have Class 1 MHCs. -The none nucleated such as a Red Blood Cell does not have one. -The Class 1 MHC tells your body that that cell does belong in the body and to not destroy it. -RBCs don’t have MHC 1s because your liver and spleen need to break down and destroy the old RBCs. 2. MHC Class 2 -These tags are presenting the ripped up pathogen recently phagocytized on the surface of the cell. -When APCs “present” they use the MHC class 2 to display it. Page 7 of 0 MHC 1 and MHC 2 on cells Macrophage B cell Dendrite Cell -APC -APC -APC -BCR -MHC 1 -MHC 1 -MHC 1 -MHC 2 -MHC 2 -MHC 2 -IgD (displays antibody) Red Blood Cell Plasma Cell -Activated B -No MCH 1 or 2 cells make -Activated B cells these make these -Produces antibodies -BCR -MHC 1 -MHC 1 HIV takes over CD4 and CD8’s. Helper T Cells Cytotoxic T Cell -TCR -TCR -MHC 1 -MHC 1 -MHC 2 -MHC 2 -CD4 -TCR -Releases -CD8 (I remember interleukins and the 8 for hate the cell cytokines to it kills) stimulate other -Destroys infected cells cells via apoptosis Page 8 of 0 1. Naive helper T cell has an empty T Cell 12. Activation of Helper T Cells Receptor, and looks for antigen to fill it. 2. An Antigen Present Cell has just engulfed the pathogen and displayed the antigen on the outside. 3. When the APC bumps into the helper T Cell Receptor they connect. 4. CD4 arm clamps down and strengthens that bond. 5. This activates the naive helper T cell and it releases the “alarm chemical” interleukin. 6. This stimulates the cloning of the helper T cells. 13. Activation of Cytotoxic T Cells 1. Naive cytotoxic has a empty TCR looking for antigen. 2. APC is displaying the antigen and looking for the cytotoxic T cell. 3. They bump into each other and they latch on. 4. CD8 latches on to enforce the bond. 5. Cytotoxic T cells clone 6. And now activated, they can go about killing the infected cell by the perforins and granzymes. 14. Activation of B cells 1. B cell bind free antigen 2. B cell engulfs antigen and presents it to a T helper cell 3. Activated helper T cell releases interleukin 4. B cell proliferates into memory B cells and plasma. 5. Plasma cells make the Antibodies Page 9 of 0 15. Antibodies and their functions Immunoglobulin - functional name Gamma globulin - chemical name IgG IgM IgA - At surface IgD IgE 16. Where Lymphocytes are made You can remember this by T Cells and “educated” the acronym God made -T cells are made in the Thymus and they leave as a Naive T Cell. -B cells are made in the bone marrow and educated there. That education is called immunocompetence. It leaves as a Naive B cell. -The “education” is where they have to be tested and learn the 1 antigen determinant. - Naive cells become activated when they bump into their antigen. That first time bump is called an antigen challenge. 17. Primary and Secondary Response 1. B cells bump into antigen 1st day -Lag peak 10th day 2. Launch in immediately - Peak is in 2-3 days. Could remain for weeks and months. Page 10 of 0


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