BIO 313 EXAM 1

Explain why drugs (e.g., aspirin, heparin, and warfarin) that prevent blood clotting can be clinically useful for thromboembolic conditions.

- Aspirin: Inhibits TXA2 formation by inhibiting cyclooxygenase (COX), prevent aggregation of platelets - Heparin: the naturally occurring endothelial-cell cofactor for antithrombin III, can also be administered as a drug, which then binds to endothelial cells and inhibits clotting by inhibiting the production of thrombin, unable to convert fibrinogen into fibrin (unable to form clot) - Warfarin: interferes with Vitamin K-dependent synthesis (production) of some blood clotting factors. So you are unable to initiate blood clotting

· Describe the cardiac conduction system.

- Atrial depolarization & contraction - Ventricular depolarization & contraction -Activity needs to be near simultaneous and coordinated - How is this accomplished? Network of specialized conduction cells facilitate the rapid and coordinated spread of excitation from SA node to rest of heart ("cardiac conduction system")

Explain blood typing.

- Blood typing: Classifying blood based on the type of antigens present on the surface of the RBC - Antigens are substances (proteins, glycoproteins, or glycolipids) that can mobilize the immune system and activate an immune response (can trigger immune response for the production of antibodies). Cell membranes contain surface antigens that enable the immune system to distinguish its own cells from foreign matter. Characteristics of surface antigens are genetically determined - Antibodies are immunoglobulins (gamma globulins, proteins -> specifically recognize antigens) produced by plasma B cells (lymphocytes) in response to an antigen. The antibodies will bind to the antigen and promote the destruction of the cell bearing it. Antibodies mark the antigen for destruction (mechanism of defense). Circulate in plasma, part of plasma protein - "Blood type" is a classification determined by the presence or absence of specific surface antigens on the plasma membrane of RBCs. RBCs have more than 300 kinds of surface antigens - Three antigens are of particular importance: A, B, Rh - Plasma cells produce antibodies. Like al blood cells, plasma cells ultimately originate in the bone marrow; however, these cells leave the bone marrow as B cells, before terminal differentiation into plasma cells, normally in lymph nodes

Identify the type of tissue that blood is and state the primary function of the blood.

- Blood: a specialized type of connective tissue (many cells suspended in a fluid matrix, which is the plasma), tissue made up of cells that perform a common function. Connective tissue - cells are relatively separated from each other, extracellular matrix is the plasma. Primary function: carries oxygen

Describe the cause, prevention, and treatment of hemolytic disease of newborns (HDN)

- Cause: antibodies cross the placenta and destroy the baby's RBCs causing hemolytic disease - Prevention: RhoGAM (anti-Rh antibodies - extrinsic). Administered during last trimester and after delivery (if the 1st baby is Rh+). Destroy fetal RBCs that entered the mother's bloodstream, preventing the mother from making anti-Rh antibodies. Fetal RBC are marked for destruction before immune system is activated, prevent the problem for the next pregnancy

What are platelets (aka thrombocytes).

- Cellular fragments; no nucleus, not true cells, granules in vesicles - release substances to initiate blood clotting - Release substances that initiate blood clotting, to stop bleeding - Developed from the same hematopoietic stem cell, released by megakaryocyte into the bloodstream

Describe the sequence of events leading to the formation of blood clot Phase 1. Describe two reaction pathways that initiate blood clotting cascade. Distinguish the intrinsic and extrinsic pathway. (Note: you do not need to memorize individual clotting factors)

- Coagulation: Blood will be turned to gel after having contact with the platelets - transfer liquid form of blood into gel form making it harder to leak out - Clotting factors are produced in inactive form in the liver - once there is damage (trigger) you will activate one clotting factor, then another, then another, into fibrin clot - Phase 1: two complex pathways lead to the formation of prothrombin activator: - Extrinsic - many clotting factors (all proteins) come from sources external to blood, one of the clotting factor comes from outside of the blood, factor 3 or tissue factor (not located in the blood) located underneath the endothelial. Once tissue is damaged, factor 3 is activated, reaction is faster since there are less factors needed to be activated to reach the damaged spot) - Intrinsic - uses only clotting factors found in the blood, all you need to activate factor 12 to initiate the activation of the other factors. contact activation: if this factor has contact with the surface with negative charges then you can have activation - platelets have the negative charges needed to activate the factor 12) - Both pathways work simultaneously and interact with each other - Prothrombin is inactive in the blood, once activated it is converted into thrombin and. Forms cross link with fibers (fishnet) and is no longer soluble and traps RBC and prevent leaking (fibrin mesh) - fibrinogen (found in plasma, soluble) Once prothrombin activator is formed the following phases (Phase 2 & 3) are common - Prothrombin activator is converted into thrombin and into fibrin - makes a more compact clot - Most clotting factors are produced by the liver - 30-60 mins after formation, platelets induce another process called clot retraction - Brings damage together to signal repairment - Platelets contract and pull surrounding fibrin strands closer together - Serves to strengthen & compact clot and pull damaged edges of vessel closer together

Describe the thromboembolic conditions and the causes.

- Conditions that causes undesirable clot formation in an unbroken blood vessel, blood clot formation when you do not need it, bleeding uncontrollable when damaged vessel - "Thrombus" - clot stays there and doesn't move vs. "Embolus" - clot formed in one part of the body and is transported through the bloodstream to another part of the body - Causes: -Abnormal endothelial surface caused by conditions such as atherosclerosis and/or inflammation (damage of endothelial cells and tissue below due to disease (ex. Atherosclerosis), blood is not leaking out). Showcases collagen fibers attracts platelets - Slowly moving or stagnant blood flow - allows clotting factors to accumulate - Treatment/prevention: aspirin, heparin, warfarin

What is ECG?

- ECF is an electrical conductor - Electrical currents generated by cardiac muscles during depolarization & repolarization spread through body fluid and reach skin surface - These currents can be detected using electrodes placed on skin surface - ECG is a composite of all the action potentials generated by all the cardiomyocytes at a given time - ECG is not the recording of a single action potential

Describe the sequence of events leading to the formation of a platelet plug

- Exposed collagen at site of vessel injury attracts platelets. Platelets adhere to collagen via intermediary called von Willeband factor (vWF). - Platelets release ADP and TXA2, which attracts more platelets (positive feedback mechanism). Platelets attach to broken side of blood vessel - damaged endothelial cells unable to release, platelets attach to collagen fiber, platelets release ADP and thromboxane A2 to recruit more platelets to help make the plug -> temporally block the broken end to prevent the blood from leaking out - positive feedback loop - Do not attach to the normal side of the blood vessel (healthy endothelial cells release prostacyclin and nitric oxide NO - repel platelets and do not let it adhere at all, inhibit platelet aggregation)

Explain what happens to blood clots when they are no longer needed (i.e., the fibrinolytic system).

- Fibrinolysis: dissolving clots once healing has occurred - Following tissue repair, fibrin lots are dissolved in a process mediated by plasmin needed to convert fibrin into soluble fragments. To activate plasminogen, you need tissue plasminogen activator to be released by endothelial cells to release fibrin into soluble fibrin fragments - Synthetic plasminogen activators can be used immediately after a stroke or heart attack to help dissolve clots and restore blood flow.

Define the blood hematocrit. Given a person's body weight and hematocrit, be able to estimate this person's total blood volume and plasma volume.

- Hematocrit: percent of total blood volume occupied by RBC, can give an estimate of patient's RBC count in body (ex. Too low RBC can indicate anemia). Adult males ~ 45 -52%. Adult females ~ 37-48%. - Total blood volume (TBV): blood makes up ~8 of body weight, can calculate by multiplying body weight in kilograms (kg) by 0.08. - Plasma volume: If your blood hematocrit (Hct) is 45%, then: 45% of your TBV is RBCs and 55% of TBV is plasma, plasma volume = TBV x (1-Hct)

Explain the basis of transfusion reactions and the importance of blood testing.

- Importance: need transfusion to meet oxygen needs of patient, if you miss match the blood you cause transfusion reaction - Assume we have a recipient whose blood type is A. The donor's blood type is B. When the donor's type B blood enters the recipient's blood stream, the recipient's anti-B antibody will recognize the antigen and cross link and block the blood flow, agglutination will recruit macrophages to phagocyte cells and destroy the donated RBCs and cause hemolysis

Describe the formation and life history of leukocytes (very general).

- Leukocytes are produced in the red bone marrow by the same hematopoietic stem cells as the RBCs. Can develop into different cell types depending on the signals received - Leukocytes only stay in the bloodstream for a short period of time and then migrate into connective tissues. Lymphocytes will enter the lymphatic system, and back to the bloodstream. Watch for invaders and enter back into bloodstream - Dead leukocytes will be phagocytized by macrophages

Explain what determines a person's Rh blood types (have D antigen: Rh+, lack D antigen: Rh-).

- Many different types of Rh antigens, but the D antigen is by far the most reactive type to cause transfusion reaction. - A person is Rh+ if his/her RBCs have D antigen - will not generate Anti-Rh antibody - Anti-Rh (or Anti-D) antibody belongs to IgG type (smaller molecules that can go through placenta and pass from mother to fetus) - 85% of people in U.S. are Rh+ - In Rh- people, anti-Rh antibodies do not form spontaneously, only be generated when exposed to Rh+ blood. Immune system can be sensitized by initial transfusion. Second exposure can produce strong transfusion reaction. - Importance in childbearing: -An Rh- mother with a Rh+ fetus. The antigens normally cannot cross the placental barrier, thus there are no problems for the fetus and the mother's immune system is not sensitized. (first picture of Rh Blood and pregnancy - >) - Rh- mother carries Rh+ baby OK, but the mother's immune system is sensitized. An Rh- mother with a Rh+ fetus. At delivery, the hemorrhaging that occurs cause fetal blood to mix with maternal blood. Thus the mother's immune system is sensitized to the RH+ antigen. (*picture) - 2nd Rh+ baby will not be OK. Antibodies cross placenta and destroy baby's RBCs. An Rh- mother with a Rh+ fetus. The antibodies that the mother produced as a result of an earlier pregnancy can pass the placental barrier, attack the fetal RBC and cause hemolytic disease of the newborn. (see review sheet for more pictures)

Describe the roles of the liver and vitamin K in blood clotting.

- Most clotting factors are produced by the liver - Vitamin K required by the liver to synthesize some clotting factors

What is ventricular fibrillation?

- Rapid, irregular or uncoordinated ventricular contraction - fatal, circulation stops and brain death occurs - abnormal wave forms - ventricular tachycardia: atrium and ventricle uncoordinated contraction -> not able to pump enough blood out

what is the distribution of autorhythmic cells

- SA node sets up the heart rate, can fire lots of AP at high frequency - in a normal heart, the SA node usually suppresses the ectopic pacemaker activity due to its higher impulse rate - A malfunctioning SA node allows the ectopic pacemakers to generate their rhythm - the other pacemaker cells will determine HR

Describe how global distribution of pathogens (Plasmodium falciparum) influences human evolution in the case of sickle cell anemia.

- Sickle cell anemia: at low oxygen levels, the red blood cells especially in the capillaries the cell becomes sickled. Encoded in the genes of hemoglobin chain. Mutation in the genes at location 6 in beta chain of hemoglobin, low oxygen - unable to maintain shape and integrity of cell. Problems: Tend to get destroyed easily by the macrophages (leads to anemia), can cause blockades of small vessels, and transports less oxygen Val: Valine - no side change with charges Gul: glutamic acid. Glutamate is the ionic or salt form. - A normal RBC is compared to a sickled RBC. As a result of a change in the hemoglobin in the cell, at lower oxygen concentrations, the RBCs change shape, becoming relatively rigid and sharply curved. Sickle cell trait distribution: high frequencies of the sickle cell trait are found in tropical Africa 25% of Nigerians carry HbS allele (heterozygous, AS) 5% born with sickle cell disease (homozygous, SS) Medical puzzle - Malaria: caused by the parasitic microorganisms that feed on RBCs, Plasmodium falciparum. Plasmodium falciparum is a unicellular parasitic protozoan (single-celled eukaryote), transmitted person to person by mosquitoes. People who produce normal RBCs are good hosts. The disease is debilitating and often results in death - People with normal hemoglobin (left of diagram) are susceptible to death from malaria - People with sickle cell disease (right of diagram) are susceptible to death from the complications of sickle cell disease. - People with sickle cell trait, who have one gene for hemoglobin A and one gene for hemoglobin S, have a greater chance of surviving malaria and do not suffer adverse consequences from the hemoglobin S gene. Why? The mechanisms are still not very clear. However, it has been confirmed that the red blood cells that are infected by parasite in AS are cleared by phagocytosis, thus, keep the parasite load relatively low in AS heterozygotes

Explain the functions of leukocytes in general and the individual role of each leukocyte type.

- WBC are the least abundant formed elements in the blood - Have nuclei and organelles (true cells) - Function: protect the body from infection and other diseases, defend body from foreign substances - Can migrate out of blood vessel into connective tissue, use bloodstream to reach tissue with invasion or under attack from bacteria, virus, etc. -Types of WBC: -Granulocytes: neutrophils, eosinophils, basophils, have granules in cell -Agranuolcytes: no granules in cell, lymphocytes, monocytes -Neutrophils: phagocytize (eat) bacteria or virus and release antimicrobial chemicals, part of innate immune system -Lymphocytes: secrete antibodies and serve in immune memory (memorize encounter with specific antigen), different types (B - develop in plasma into specific antibodies and T cells) with specialized functions -Monocytes: differentiate into macrophages (large phagocytic cells of the tissues) when they leave the bloodstream - can directly eat the pathogens, phagocytize pathogens, dead neutrophils, and debris of dead cells, present antigens to activate other cells of immune system, larger cells with crescent shape of nucleus -Eosinophils: phagocytize antigens - antibody complexes (recognize and eat foreign molecules), allergens, and inflammatory chemicals. Release enzymes that weaken or destroy parasites such as worms. Bilobed with red-orange granules. Seen along digestive tract (protect against parasitic entry) -Basophils: secrete histamine (a vasodilator), which increases blood flow to a tissue cause redness of tissue, edema, and weakness of tissue due to increased blood flow. Secrete heparin (an anticoagulant), which promotes mobility of other WBCs by preventing clotting.

Discuss the need for a circulatory system for transport

-The circulatory system ensures the delivery of molecules rapidly over long distance to all cells in the body due to limitations of diffusion, carry nutrients to the cells of the body. With the increase in distance of diffusion, diffusion slows therefore the circulatory system is needed to speed up diffusion and delivery of nutrients. -Capillary: only one layer of cells, small distance for diffusion, smallest vessel

· Describe the three properties of cardiac muscle cells (contractility, automaticity, conductivity).

1. Contractility: 99% of cardiomyocytes, sliding filament theory, cross bridge cycle same as in skeletal muscle (1 ATP/cycle) within each filament the thin filaments slide to the center of the sarcomere due to the cross-bridge cycle, cardiac muscle cells are excitable and are able to contract. Cardiac muscles go through the same process as skeletal muscle (one myosin interacts with one actin using 1 ATP). How to initiate cross bridge cycle - need calcium in cytosol, actin and tropomyosin are blocking the myosin binding sites, troponin will bind to calcium and will change the configuration of the complex - exposes the myosin binding sites to trigger the cross-bridge cycle. To increase cytosolic calcium, you need an AP (excitation-contraction coupling) 2. Automaticity: 1% of cardiomyocytes, generate spontaneous AP (w/o outside stimulus) 3. Conductivity: same group of cells as #2, can tell other cells when to contract, deliver AP. Helps to deliver signals from SA node to have coordinated contractions and relaxation of atrium and ventricles

Describe the three layers of the heart wall.

1. Epicardium: surface, Visceral layer of the serous pericardium. Made of squamous epithelium + thin connective tissue layer. 2. Myocardium: cardiac muscle. Concentric layers wrap around atria - move towards the center, muscle contractions squeeze the blood. Spiral arrangement within walls of ventricles - "wringing action", squeeze the blood upward from the apex of the heart. 3. Endocardium: lines the heart chambers. Made of squamous epithelium + thin connective tissue layer.

Describe the three key components of the circulatory system and their specific roles in transportation.

1. Heart (serves as pump): Four chambers: two atria (receiving chambers), two ventricles (pump -> pump to different parts of the body, work synchronously but do not pump to same location). The right side of the heart receives blood from systemic veins and delivers blood to the lungs, then will get oxygen from the lungs. The left side of the heart receives blood from the lungs and delivers blood to the rest of the body. 2. Blood vessels (serve as conduits, pipes, allow blood to flow). Arteries - carry blood away from heart, more smooth muscle on wall, can maintain high pressure. Veins - collect blood and return it back to the heart, thinner walls, less smooth muscle walls, less pressure. Capillaries - tiny blood vessels with smaller inner diameter, wall is thin (one layer of epithelial cells - short distance of diffusion, exchange of blood with tissues). 3. Blood (serves as carrier): Red color - oxygenated blood; Blue color - partially oxygenated or deoxygenated

Describe the three main functions of the circulatory system.

1. Transport: primary function. Transports substances that enter the body (oxygen and water), transport substances from one part of the body to another part of the body, ex. Circulatory system carries hormones to target cells. Transport materials outside of the body, ex. Carbon dioxide transported to lungs and excreted through exhaling; 2. Protection: Blood plays several roles in inflammation, a mechanism for limiting the spread of infection. White blood cells destroy microorganisms and cancer cells and remove debris from the tissues. Some can directly phagocyte foreign cells. Antibodies and other plasma proteins neutralize toxins and help to destroy pathogens. Platelets secrete factors that initiate blood clotting and minimize blood loss, protect you from losing too much blood when you have a broken blood vessel. 3. Regulation: Blood capillaries help to stabilize fluid distribution between intracellular and extracellular fluid components. Plasma is a part of the extracellular fluid (flows throughout the body). Capillaries walls are leaky, regulate fluid distribution and have enough plasma flowing throughout the body.Blood proteins serve as buffer and stabilize the pH of the extracellular fluids. Body temperature regulation. Heat produced by cell activity and is carried to surface of body and is released through the skin.

Describe the three sequential phases occur during hemostasis.

1. Vascular spasm: smooth muscle contracts, causing vasoconstriction (helps to reduce blood loss). Narrowing vessels, slows the blood flow, therefore reducing the blood flow 2. Platelet plug formation: injury to lining of vessel exposes collagen fibers; platelets adhere. Platelets release chemicals that make nearby platelets sticky; platelet plug forms. Platelets aggregate to form clot 3. Coagulation: fibrin forms a mesh that traps red blood cells and platelets, forming the clot. Blood is transformed from liquid (blood) to gel. Occurs in three phases. (see review sheet for additional images)

how does AP spread through cardiac cells?

AP spreads from pacemaker cells to contractile cells via gap junctions

Describe the functions of the atrioventricular (AV valves) and aortic and pulmonary semilunar (SL) valves.

AV valves only flow from atrium to ventricle and prevent back flow. Opening of valve is due to pressure difference, high pressure closes the valve to prevent eversion. SL between ventricles and major arteries, each have half moon shape, ventricles contract, valve open for blood to flow out into aorta, when it relaxes, the blood will back flow but the valves will close to prevent blood flow. Valves close to control blood flow and make sure it flows in one direction - open and close due to pressure difference. Systole: contraction of ventricles, AV valves close to prevent retrograde flow, SL valves open -> blood to pulmonary trunk and aorta. Blood only exits through aorta. Diastole: relaxation of ventricles, AV valves open -> blood flows in, SL valves close. Pressure drops, blood will tend to backflow but the blood fills the SL cusps and the valve will close.

Describe the activation of B lymphocytes and explain the mechanism of antibody action.

Activation of B Lymphocytes: First activated then differentiate into plasma cells and memory B cells. B lymphocytes produced in red bone marrow, mature, and migrate out into the secondary lymph organs. Germinal center of lymph node - where B cells are activated. Activated by something circulating in the body and reach the lymph node - each of the B cells have different surface receptors and can recognize different types of antigens. Assume one B cell that has the surface receptor to recognize the specific antigen - > the B lymphocyte will be selected and will develop into a clone then into plasma cells. MHC-II protein works to present the antigen to the surface of the body. Helper T cell triggers cloning expansion - cell will be cloned and replicated (identical cells). Plasma cells produce specific antibodies that can be secreted to fight the antigen - will bind specifically to the antigen. 2nd exposure: Memory B cells recognize the known antigen immediately and an immune response is triggered right away. Mechanism of Antibody Action: antibodies do not kill the pathogens directly, inactivate. 1. Neutralization: antigen is suppressed by the antibody (makes it no longer harmful) 2. Agglutination: antibodies will glue to antigen and link together to form monomers, form clump. 3. Precipitation. 4. Complement: involved in a coordinated immune response, outcome is cell lysis

Describe the structure of antibodies.

Antibodies are proteins generated in response to an antigen - Antibody binds to unique parts of the antigen Gamma globulins (five types: IgA, IgD, IgE, IgG, IgM) - All have two heavy chains, two light chains, and variable regions (help to identify different antigens) Secreted by plasma cells (derived form B cells) - Function is to neutralize antigen and tag it for destruction - IgG molecules are relatively small and can pass through the placenta from mother's blood to the baby

Describe the chemical properties of antigens.

Antigens are molecules (or part of molecule) that trigger body's adaptive immune responses and trigger specific antibody production - Uniqueness, enables the body to distinguish its own "self" form foreign "nonself"

Compare the function of the atria and the ventricles, and describe the difference between the function of the right and left ventricles.

Atria is the receiving chamber, ventricles is the discharging chamber. The right ventricle receives deoxygenated blood and sends it to the lungs to get oxygen and nutrients. Left ventricle sends oxygenated blood to aorta and to the rest of the body.

compare and contrast autorhythmic cardiomyoctyes and contractile cardiomyocytes

Autorhythmic: -non-contractile, no actin/myosin/myofilaments, pacemakers cell - unstable resting membrane potential -always depolarized, fire AP then depolarize again - pacemaker potentials initiate APs that spread through the heart (function) - determines heart rate contractile: - contractile cell -stable resting membrane potential (-80 to -90 mV) - stimulated by autorhythmic cells

Explain what determines a person's ABO blood types (A, B, AB, O).

Based on A & B surface antigens, there are four blood types - Type A: RBC have A antigen on surface, Anti-B antibody in plasma - Type B: RBC have B antigen on surface in blood, Anti-A antibody in plasma - Type AB: A and B antigens on surface of RBC, neither Anti-A or Anti-B antibodies, universal recipient, will not attack the Type A or Type B blood when receiving the blood - Type O: no surface antigens (neither A or B antigen on surface), Anti-A and Anti-B antibodies, universal donor - Antibodies to type A or type B antigens are developed spontaneously by the immune system. A person will develop antibodies against the antigen not present in their own RBCs. Ex. A person has type A antigen on the surface of his/her RBCs will develop anti-B antibodies, but not anti-A antibodies - These antibodies begin to appear in plasma when a baby is around 2-3 months old. Antigens appear on the fetus (receive from parents) - Anti-A and Anti-B antibodies belong to IgM type - These antibodies were produced in response to the bacteria in the lumen of the intestine, but cross-react with antigens on the surface of the red blood cells - When there is clumping and cell lysis, the blood has the A antigen for example in the picture above, if clumped on both sides (Type AB blood)

Describe the two main components of the blood and their relative proportions.

Blood = Plasma (liquid portion, 55% of blood) + Formed elements (45% of total blood, some are not true cells, ex. Platelets are not true cells, they are cell fragments; (RBC (>99% of formed elements), WBC <1%, Platelets <1%).

Explain what is blood doping and why it is dangerous.

Blood doping: Artificially induced polycythemia Practiced by some athletes competing in aerobic events (ex. Cyclists, cross-country skiers) How to do it? Remove your own blood month or so before competition then reinject RBCs prior to event (body will have period of time with less RBC to induce more RBC production to compensate then inject them back into the body - more RBC in the body, and more oxygen) or inject EPO Dangers: transfer of blood-borne diseases, infection, increase of blood viscosity (slows blood flow)

What triggers an increase in [Ca2+]i to allow cardiomyocytes to contract?

Calcium is the internal "switch" that turns on cross bridge activity in cardiac muscle cells. Action potentials trigger an increase in calcium to allow cardiomyocytes to contract. Acton potential propagates along the sarcolemma and down to the t-tubules. The action potential triggers calcium release form SR. Calcium levels inside the cardiomyocytes are increased. Calcium triggers cross-bridge cycling. "excitation-contraction coupling"

Describe the two types of cardiac muscle cells: the contractile cells and pacemaker cells.Describe their relative abundancy and distribution in the heart.

Cardiac muscle cell = cardiomyocyte. Not all cardiac muscle cells are the same. A small percent of cardiomyocytes (<~1%), called autorhythmic cardiomyocytes or pacemaker cells, determine the heart rate (HR). These cardiomyocytes do not contract. They are specialized and can generate AP spontaneously - give automaticity to heart to be able to involuntary contract. A much larger group, making up ~99% of the total cells in the heart, constitutes the pumping cardiomyocytes. Their activity determines how strong the heart contracts.

Describe the activation of T lymphocytes and explain the roles of cytotoxic T-cells and helper T-cells in cellular immunity.

Cytotoxic T cells: destroy foreign cells or cancellous cells. Helper T cells: promote the action of other immune cells. Cellular immunity will attack any cells that are being attacked by pathogens or cancerous cells. T-cells are activated occurs in secondary lymphatic organs, Antigens presenting cells (APC) are needed to activate the T cells, foreign antigen is recognized by the T cells. T cell s stimulated to develop a clone (helper or cytotoxic, depending on what T cell you started with), The clone recognizes the antigen and in the meantime the memory T cells are being generated. Recognize the affected cell (generate antigen protein that is presented on the surface using MHC protein). Cytotoxic T cells directly destroy the affected cells or can triggers apoptosis (programmed cell death). T helper cells do not directly attack affected cells or pathogens, helps the T cells, promotes the action of other immune cells.

What is defibrillation? Difference b/w external and internal

Defibrillation: application of electrical current (several thousand volts for a few ms) to the chest to stop ventricular fibrillation. To stop abnormal heart activity - external: defibrillate - hopefully allow pacemaker cells to receive signal to fix abnormal rhythm - internal: implant to detect abnormal heart rate and fix it

· Describe the sequence of events that leads to excitation-contraction coupling in cardiac muscle. Explain why that calcium-induced calcium release from the sarcoplasmic reticulum is important for cardiac muscle contraction.

EC coupling in cardiac muscle cell: Depolarization opens voltage gated Ca2+ channels on sarcolemma. Ca2+ influxes, binds to ryanodine receptor (RyR) on SR and triggers Ca2+ release from SR (calcium induced calcium release). Ryanodine receptors form a class of intracellular calcium channels in various forms of excitable animal tissue like muscles and neurons. It is the major cellular mediator of calcium-induced calcium release (CICR) in animals. The ryanodine receptor is itself activated by cytosolic Ca2+ at micromolar concentrations. Thus, entry of a small amount of Ca2+ into the cytosol causes further Ca2+ release) SERCA:sarcoplasmic/endoplasmic reticulum Ca2+-ATPase, or SR Calcium ATPase, it is a P type ATPase Ca2+ induced Ca2+ release: the entry of extracellular Ca2+ ions cause the release of Ca2+ from the sarcoplasmic reticulum, which accounts to 80-90% of the total Ca2+ Contraction: AP does not directly release Ca2+ from SR (different form skeletal muscle). AP opens voltage gated Ca2+ channels in the cell membrane. · Extracellular Ca2+ enters the cell (following electrochemical gradient) - about 10% of Ca2+ needed for contraction · By calcium-induced calcium release. The influx of Ca2+ triggers the release of large amounts of stored Ca2+ from SR Relaxation occurs when Ca2+ unbinds from tropinin and -is pumped back into SR (primary active transport, SERCA -Calcium pump -> transport calcium against concentration gradient) -is pumped out of cytosol into ECF (secondary active transport) - calcium concentration low - will unbind from troponin

Describe the control of erythropoietin (EPO) secretion and the effect of this hormone on hemopoiesis.

Endocrine cells produce erythropoietin (EPO) secretion and produce new RBC to be released to the bloodstream The process is well regulated Negative feedback regulation method to maintain homeostasis

Describe the structure and function of hemoglobin.

Hb is the major intracellular protein in RBC! Each RBC is basically a bag of Hb molecules. - Hb consists of 4 subunits, each subunit has two parts (heme group, ring with iron in the center, oxygen binds to the iron and globin) Each subunit = globin + heme (contains iron) Each Hb molecule can transport 4 molecules of O2; up to 1 billion O2 molecules/RBC Oxygen is able to dissociate from hemoglobin to be transported to the tissues Globin chains are not the same - in adult, two alpha and two beta chains, heme groups are all the same -> determine the oxygen affinity of the hemoglobin (easy to bind or not, determines oxygen binding) Hb + oxygen = oxyhemoglobin (bright red) Hb without oxygen = deoxyhemoglobin (brown or dark red)

Define hemostasis.

Hemostasis: the stop of bleeding, hemo = blood, stasis = stop

Compare and contrast the properties of cardiac muscle with skeletal and smooth muscle. Describe the structure and function of intercalated disks, including desmosome and gap junctions. Explain why that the heart works like a "functional syncytium".

Histology of Cardiac Muscles: cardiac muscle cells are striated (arrangement of myofilaments), branched, short, interconnected in series via intercalated discs (allow adjacent cells to form together to form the heart. Intercalated disks contain desmosomes and gap junctions: Desmosomes: keep cardiomyocytes from pulling apart during heart contraction, strengthen adjacent cardiac muscle cell connection. Formed by structural proteins that link the two cells together, like zipper to link together. To stay connected to prevent pulling apart during contractions. Gap Junctions: leak channels made by connectin, Made of 6 transmembrane proteins arranged in a ring, Has a water filled pore in the middle that allows materials to pass through, During excitation, gap junctions allow ions to flow between adjacent cardiomyocytes so then cardiomyocytes can contract simultaneously (functional syncytium) allow electrical currents to travel through cells quickly - important to contract together. Cardiac muscle has a sarcolemma (membrane), sarcoplasm, myofibrils (thick & thin filaments that are organized into sarcomeres - A band, I band, Z band), nucleus, mitochondria. Within sarcomere: have protein filaments - thick - myosin (shaft (rod), two heads attached to it on the two ends), thin - actin, troponin, tropomyosin.

Adaptive responses: Contrast humoral and cellular immunity, active and passive immunity, and natural and artificial immunity.

Humoral immunity: B cells, mature in red bone marrow, employs antibodies to tag pathogens for destruction Cellular immunity: T cells, mature in thymus, directly attach and destroy foreign cells or diseased host cells Active Immunity: immunological memory, provide future protection Passive Immunity: no immunological memory, only provide temporary protection Natural Immunity: natural active - infection, contact with pathogen; natural passive - antibodies passed from mother to fetus via placenta; or to infant in her milk (do not have the memory cells, body will not be protected from future illness) Artificial Immunity: active artificial - vaccine; dead or attenuated (weak) pathogens (ex. mRNA, COVID-19), gain immune response without having to have the disease (activate immune system to get memory); passive artificial - injection of exogenous antibodies (gamma globulin, antivenom),

Explain why there is problem when a Rh- mother having a Rh+ baby the second time.

Husband Rh+ and Rh- mother with a Rh+ fetus. First time: no mixture of mothers blood cells with fetus blood cells. Problem when fetal blood enters mothers bloodstream during miscarriage or child birth. This will sensitize the mother's immune system and will remember the anti-Rh antibodies. Problem with second child, antibodies can enter fetal blood circulation and recognize Rh antigen and mark for destruction triggering hemolytic disease in newborns. Antibodies can cross the plasma because it is a protein, RBC cannot. Antibodies that the mother produced as a result of an earlier pregnancy can pass the placental barrier, attack the fetal RBC and cause hemolytic disease of the newborn. (+ image)

Describe the general role of leukocytes in immune response and associate with innate vs. adaptive immune responses.

Immune responses: involved multiple organ systems such as lymphatic system, immune system, and the circulatory system (ex. WBCs). Triggered by damages in the body - cut, pathogens in body, cancerous cells

Identify the body's three lines of defense against pathogens.

Innate defenses: non-specific to pathogen (body will have same reaction regardless of pathogen), local effect (restricted to the region of located pathogen), lacks memory - 1st line - surface barriers like skin and mucous membranes - 2nd line - within the connective tissue, internal defenses like phagocytes, natural killer cells, inflammation, antimicrobial proteins (inhibit microbial reproduction. Two types of antimicrobial proteins are interferons and complement systems (30 or more globulins), fever Adaptive defenses: systemic, antigen-specific, memory - 3rd line - Humoral Immunity (carried by the blood) (antibodies derived from B cells - develop and mature in red bone marrow) and Cellular immunity (T cells - mature in thymus (primary immune organ, attack foreign cells)) - Takes time - need to recognize antigen, then create immune response, but creates memory cells as well for the future exposures (quick response in 2nd exposure)

Explain what the differences between innate and adaptive immunity are.

Innate immunity: nonspecific, local effect, lacks memory Adaptive Immunity: antigen-specific, systemic, memory, takes time and resources

Describe the importance of iron homeostasis in the body and iron distribution.

Iron is essential for hemoglobin synthesis and erythropoiesis Maintain iron homeostasis in the body through diet and body storage Diet: absorbed in the intestine, precisely regulated because the body has no natural way to rid of excess iron (only keep what we need), natural losses of iron is made up through the diet Body storage: Hb (65%); iron in Hb is recycled. Liver, spleen, and bone marrow. Iron is recycled, take iron from dead RBC Transport of iron in blood: bind to transferrin (transport protein), iron tends to combine to other molecules, transferrin is used to transport iron or can attach to albumin Vitamin B12 and folic acid: required for DNA synthesis

Summarize the production, life span, and destruction of erythrocytes.

Lifespan of RBCs is ~120 days Approximately 1% of RBCs are replaced each day, 2 million new RBCs/sec Erythropoiesis: occurs in red bone marrow (in spongy bone, seen in epiphysis of long bone, irregular and flat bones), controlled by erythropoietin (EPO), a hormone produced by the kidneys. A hematopoietic stem cell becomes an erythrocyte colony-forming unit, which has receptors for EPO. Through the developing stage, many developing states, increasing in cell number and are synthesizing many hemoglobin molecules and organelles, then the cells are released into the bloodstream EPO is primarily produced by the liver during the fetal state. After birth, EPO is mainly produced by the peritubular fibroblasts in the renal cortex.

Describe the major causes of anemia.

Low oxygen in tissues The causes of anemia fall into three categories, all result in below normal "O2 carrying capacity" of the blood: - Inadequate erythropoiesis or hemoglobin synthesis: not enough RBC and hemoglobin being produced, low concentration of hemoglobin, Causes: dietary deficiency of iron, folic acid, Vitamin B12, vitamin C; deficiency of EPO secretion, deficiency of intrinsic factor - Pernicious anemia: unable to absorb Vitamin B12 from diet, lack intrinsic factor needed to absorb Vitamin B12 (produced by the stomach - > stomach cancer or stomach removed, not enough cells to produced intrinsic factor). Treat with Intramuscular injection or IV, if you give supplement orally you are unable to absorb Vitamin B12 due to lack of intrinsic factor - Hemorrhagic anemia from bleeding (acute or chronic) - Due to blood loss, trauma, chronic bleeding (gastric cancer, ulcers) - Hemolytic anemia - result from RBC destruction (malaria), break down RBC too often, blood cell lysis (hemolysis), abnormal hemoglobin molecules (sickle-cell anemia)

Name the energetic requirements of cardiac muscle contraction and how these requirements are met.

Mitochondria: many mitochondria (significant % of cell volume). Relies almost exclusively on aerobic metabolism for energy, have more mitochondria than skeletal muscle. Cardiac muscles cannot use anaerobic glycolysis to produce ATP (fast glycolytic fibers) - all use aerobic pathway to make ATP, need lots of mitochondria and lots of blood supply in the heart. Sarcoplasmic reticulum & T-tubules: sarcoplasmic reticulum: store, release, network, active reuptake of Ca2+. Transverse tubules: larger than in skeletal muscle, same function as in skeletal muscle, major function: expel calcium ions from the muscle cell, formed by invaginations of the plasma membrane (sarcolemma), allow AP to reach to the bottom of the cell to be able to trigger the release of calcium.

Innate Immunity (non-specific - does not matter the damage, the body will respond in the same way):

Neutrophils: phagocyte bacteria and fungi, can leave blood stream to phagocyte Macrophages (derived from monocyte) phagocyte bacteria and viruses, come from bloodstream Eosinophil: parasites and allergic reactions, stay underneath mucous membrane (especially in digestive tract to target parasites) NK cells: derived from lymphocytes, detect virus-infected or cancerous cells and mark them for apoptosis Inflammatory cells: Basophil & Mast cell - granules in cell release inflammatory chemicals and initiate inflammation, increase blood flow, trigger pain receptors (redness, swelling, heat, pain), and allergic reactions Adaptive Defenses (specific response, systemic not localized response) Lymphocytes - humoral and cellular immunity

One of the current treatments for COVID-19 is to infuse plasma from recovered COVID-19 patients. Does this make the patient immune "forever"?

No, because the immunity was passive, antibodies are neutralizing the virus, but you do not gain memory B cells, not protecting you from the next infection

Explain the importance of phagocytosis, inflammation, and fever in innate body defense.

Phagocytes: garbage eaters, eat the microbes before they can do further harm in the body. Phagocytosis: prevents the microbes from spreading further in the body Inflammation induces immune response Fever: induces immune response, gives body time to recover and put energy towards fighting infection

what are the steps of action potential in contractile cardiac muscle cells

Phase 0: Voltage gated sodium channels open (same as skeletal muscle) Phase 1: Initial repolariztion is due to transient opening of special potassium channels and inactivation of voltage gated sodium channels Phase 2: Plateau phase of depolarization is due to the slow but prolonged opening of L type voltage-gated calcium channels. K+ and Ca2+ movements have prolonged depolarization (movements cancel out each other roughly). DIFFERENT FROM SKELETAL MUSCLE! Phase 3: Repolarization is due to opening of voltage gated potassium channels and close of voltage gated calcium channels. resting membrane potential ~ -90 mV for cardiac, neuron -70 mV

List the functions of platelets in hemostasis.

Platelets secrete vasoconstrictors, form platelet plug, and secrete clotting factors which promote blood clotting (coagulation)

Describe the two types of polycythemia and their major causes.

Polycythemia: abnormally high RBC number - Why could it be harmful to have a RBC count too high? More RBC means higher blood viscosity (movement of blood flowed slowed down) and slower blood flow which could cause other problems Types: - Polycythemia Vera: a bone marrow cancer, causes unregulated and excessive erythropoiesis in red marrow, hematocrit may be as high as 80% - Secondary Polycythemia: a regulated increase stimulated by EPO (erythropoietin secreted which acts on bone marrow to produce RBC, hormone secreted by kidneys), multiple potential causes such as living at high altitude, chronic lung disease, heart failure -> low oxygen in body, body accommodates by secreting more EPO to compensate for the lost oxygen (constantly stimulate EPO to accommodate)

Describe the two circuits (systemic and pulmonary circuits) through which blood is pumped and their relationships in circulation.

Pulmonary circuit: Blood flow: RA receives low oxygenated blood -> RV pump blood to pulmonary trunk through pulmonary artery -> lungs oxygenated blood returned to heart through pulmonary veins-> LA. Right side of the heart serves as the pump. Function: Pick up O2 and dump off CO2. O2 rich blood runs in the veins and O2 poor blood runs in the arteries. Short, low pressure, low resistance system. Systemic circuit: LA flow -> LV pump blood to the aorta -> arteries branched off of the aorta will deliver oxygen, blood, nutrients to all organs -> RA.Left side of the heart serves as the pump. O2 rich blood runs in the arteries and O2 poor blood runs in the veins. Function: Deliver O2 and nutrients to the tissues and remove metabolic waste, pick up CO2. Key Points: Parallel arrangement of vasculature in systemic circulation ensures: all tissues/organs receive blood of the same composition, adequate perfusion pressure for each tissue, and blood flow to organs adjusted independently. Long, high pressure, and high resistance system (blood needs to travel further throughout the body, need enough pressure to push the blood flow). Circulatory System Key points: close circulation (blood should not get out of the components - in capillaries nutrients diffuse out, but blood stays. Allows you to control the blood flow to organs (volume of blood flow going to each organ to meet their demands), pulmonary & systemic circulations are arranged in series, blood flows in one direction. Equal amounts of blood are pumped to the pulmonary and systemic circuits at any moment. Have to go through pulmonary circulation to go through the systemic circulation, should not be any back flow throughout the circuit. Systemic circulation: serve all the organ systems in the body, many branches all come from the main pipe, all organs are in parallel (to ensure blood composition is the same for all organs). Pulmonary: serves the lungs.

Describe the oxygen status of arterial and venous blood in the systemic versus the pulmonary circulation.

Pulmonary: O2 rich blood runs in the veins and O2 poor blood runs in the arteries. Systemic: O2 rich blood runs in the arteries and O2 poor blood runs in the veins.

Describe the importance of iron recycling when erythrocytes are destroyed.

Red Blood cell turnover: Macrophages (special type of WBC in the tissue) in the spleen, liver, and red bone marrow phagocytize (uptake) old or damaged RBCs and then break down and recycle their component parts. Iron for reuse, globin into amino acids into the blood for reuse to make new proteins for example, heme into biliverdin (metabolic waste, needs to be removed from the body) and then to be processed in the liver - bile stored in the gallbladder, bilirubin is released into the blood and when you eat, bilirubin is squeezed into the lumen of the gut and then is excreted through waste Jaundice: Higher concentration of bilirubin for your liver to uptake from the bloodstream, causes yellowish color of skin

Describe the appearance and relative abundance of each type of leukocyte.

Relative abundance: neutrophils > lymphocytes > monocytes > eosinophils > basophils Appearance: see chart

Describe the path of the spread of excitation from the SA node through the atria and then into the ventricles.

SA node -> atria -> AV node -> AV bundle -> Bundle branches -> Purkinje Fibers -> ventricles muscles

What is serum?

Serum: plasma after removal of clotting factors

Describe the size, location, and orientation of the heart.

Size ~ your fist. Location: thoracic cavity. Orientation: oblique, flat base (superior) directed towards the right shoulder, apex (inferior) points towards left. Well protected; surrounded by and suspended in a membranous sac, called "pericardium".

Innate responses: Describe surface membrane barriers and their protective functions.

Skin, mucous membranes Prevent entry into the body Stratum corneum are water and chemical proof Respiratory tract - mucous membrane: epithelial cells form barrier to entry

Identify structures of the pericardium and state its function.

Structures: Fibrous pericardium (on surface), serous pericardium (inner layer, double layer), parietal layer (serous pericardium), visceral layer (serous pericardium) (epicardium), pericardial cavity (filled with pericardial fluid). Function: reduce friction as heart beats, so the heart will not rub on the membrane when it beats.

What are the problems of the cardiac conduction system?

Suppose the cardiac conduction system (deliver AP to contract at the right time) does not function properly, what would happen? - Arrhythmias: irregular heartbeat (not evenly paced), bradycardia (slow), tachycardia (fast) - Fibrillation: rapid, irregular contractions. Atrial or ventricular fibrillation (more detrimental - unable to fill the ventricle with blood) − Ectopic focus − an abnormal pacemaker takes over the SA node. Premature (atrial or ventricular) contractions. - Heart block - do not allow signals to flow, no longer have coupled contractions. Due to damage to the AV node. Other regions of the heart serving as pacemaker cells -> generate abnormal contractions

Describe the factors that cause vasoconstriction during hemostasis.

Sympathetic-induced vasoconstriction via reflex activated by pain receptors. This only lasts for a few minutes. Induced by endothelin (can also cause smooth muscle contraction) released by damaged endothelial cells and serotonin & thromboxane A2 released by platelets. Multiple factors cause vasoconstriction, reducing blood flow

Describe the chambers, valves, and arteries and veins associated with the heart.

The Four Chambers: Two atria. (LA and RA) - separated by interatrial septum, receiving chambers, separated by interatrium septum. Two ventricles (LV and RV) - separated by interventricular septum, discharging chambers. Great Vessels: each chamber connected with major arteries or veins.Veins return blood to RA: superior vena cava, inferior vena cava, and veins collect together to form coronary sinus (collect venous blood from heart and drain into LA). Veins return blood to LA: four pulmonary veins, bring oxygenated blood. RV pumps blood to pulmonary trunk, pulmonary trunk splits into the lungs. LV pumps blood to the aorta, along the aorta there are many branches that reach the different parts of the body. Internal Structures: chambers. Septa, great vessels, valves (AV, SL): assure that blood flows through heart in one direction. Role of chordae tendineae and papillary muscles in preventing "eversion" of AV valves - due to high pressure blood, Valves also control the direction of the blood flow.

Describe the bleeding disorders and the causes.

Thrombocytopenia: too few platelets, causes spontaneous bleeding, red bone marrow unable to produce platelets Impaired liver function: liver makes most of the clotting factors -> unable to synthesize clotting factors Vitamin K deficiency: required by liver to synthesize some clotting factors. Usually due to problem of fat absorption since vitamin K absorption relies on fat absorption (need bile (produced by liver, needed to absorb fat and therefore vitamin K). Not enough Vit K, hard to produce clotting factors Hemophilia: X-linked genetic disorders in which various clotting factors are absent (recessive, only occurs in males). Excessive bleeding occurs owing to the absence or abnormality of a clotting factor in the blood. Problem producing clotting factors

Differentiate between a primary and a secondary immune response. Define immunological memory.

Titer: amount of antibodies produced in the body. Immunological memory: memory B cells mount a very quick secondary response if re-exposed to the same antigen, body has a stronger immune response and shorter delay during 2nd exposure (IgG is largely generated and can help fight infection right away). IgG is produced during primary and secondary immune responses but more are produced during the secondary response. Booster cells to increase number of memory cells and boost your immune system response.

Explain what keeps blood from clotting in the absence of injury.

Why don't platelets form plugs in undamaged vessels? Prostacycline (PGI2) and nitric oxide (NO), both produced by endothelial cells, inhibits platelet aggregation and therefore prevent the spread of platelet aggregation from a damaged site. TXA2 = Thromboxane A2. (Vander's Human Physiology, 15th Ed.)

The plateau phase of the action potential in a contractile cardiac muscle cell is mainly due to

an influx of calcium ions

Describe the three main types of plasma proteins and their main function.

o Albumin (60%): Responsible for colloid osmotic pressure, main contributor. Major contributor to blood viscosity (resistance of a fluid to flow, internal friction that will slow down the blood flow). Transports lipids (make sure they do not stick to the wall, so they are not water soluble), hormones, calcium, and other solutes, transporter like a cargo ship. Buffers blood pH. Produced by the liver. o Globulins (36%): Three subclasses: alpha, beta, gamma. Transports a variety of solutes.Prothrombin is a type of alpha globulin, promotes blood clotting. Gamma globulins are antibodies, combat pathogens. Alpha and beta are produced by the liver. Gamma are produced by lymphocytes, antibodies. o Fibrinogen (4%): Can be converted into fibrin when blood vessel is damaged to help with blood clotting, the major component of blood clots. Protein that be converted into the active form. Produced by the liver, typically just circulated throughout the body. o Note: most of the plasma proteins are produced by the liver, whereas gamma globulins are produced by plasma cells (descended from B lymphocytes).

•Define blood viscosity and explain the factors in the blood that influence blood viscosity.

o Blood viscosity: the resistance of blood to flow, internal friction that will slow down the blood flow. Erythrocytes are major contributor of blood viscosity, albumin (plasma protein).

What is the structure and function of erythrocytes (RBCs)?

o Function: transport O2 and CO2. o RBC count: 5.1-5.8 million/ul in males, 4.3-5.2 million/ul in females, ~25 trillion in our body (*do not need to memorize the numbers), major contributor of blood viscosity. o Structure: biconcave shape ("biconcave disc"), large membrane surface area relative to volume (keeps diffusion distance short, oxygen has to diffuse across the membrane to reach the hemoglobin within the RBC); lacks nucleus & organelles, short life span (no cellular division, cannot repair damaged RBC); no mitochondria -> can carry large amounts of oxygen but consumes no O2, contains millions of hemoglobin molecules (just a bag of Hb); contain the enzyme carbonic anhydrase, help to transport CO2, reaction is reversible, can occur spontaneously slowly, bicarbonate ion can transport within the blood in that form.

•Describe the major constituents of plasma and their functions. Which solute is present in the greatest concentration?

o Plasma is part of the extracellular fluid (20% of ECF), volume ~ 3L. o Composition of plasma: proteins contribute to colloid osmotic pressure, which favors absorption of interstitial fluid into capillaries o Components: liquid, Plasma proteins (7%), other solutes (1%), water (92%)- transports organic and inorganic molecules, formed elements, and heat o Solutes: ions, electrolytes (ex. sodium, calcium), amino acids, glucose, metabolic wastes (ex. urea)•

•Define colloid osmotic pressure and state the importance of plasma proteins in maintaining colloid osmotic pressure. Describe how the colloid osmotic pressure affects body fluid exchange across the capillary wall.

o Plasma proteins contribute to the colloid osmotic pressure. There is continuous bulk flow of protein-free ECF across capillaries between interstitial fluid and plasma (filtration & absorption). o Proteins cannot leak out of the capillary walls, however they are ionic, and will exert osmolarity and "colloid osmotic pressure" to attract water into the capillary and the plasma, important to regulate fluid distribution to prevent edema (excess fluid in the tissue). o If the plasma protein concentration drops, the water will be pushed out by the hydrostatic pressure and less water will return back due to nothing available to attract the water back. o Plasma proteins exert "colloid osmotic pressure" to attract interstitial fluid and water into plasma. o Starvation and plasma protein deficiency: starvation or other health conditions may cause a deficiency of plasma protein. This will decrease plasma colloid osmolarity. The bloodstream loses more fluid to the tissues than it reabsorbs by osmosis. Tissues become edematous and a pool of fluid may accumulate in the abdominal cavity. (Kwashiorkor - due to plasma protein deficiency, can view thin limbs and fluid distended abdomen).

· Explain how to end the contraction in cardiac muscle cells.

o Relaxation (Calcium role): relaxation occurs when Ca2+ unbinds from troponin and is pumped back into SR (primary active transport) and is pumped out of the cytosol into ECF (secondary active transport)

· Compare the mechanical activities of cardiac muscle with skeletal muscle.

o Skeletal Muscle: recall summation of mechanical activity possible in skeletal muscle (tetanus) due to short duration of AP o Cardiac Muscle: Is summation of mechanical activity possible? Is that good or bad?

· Explain what prevents the cardiac muscle from undergoing tetanic contraction.

o The long Ca2+ plateau of the AP in contractile cardiomyocytes creates a long period of contraction. A prolonged refractory period of cardiac muscle cells prevents tetanus and allows time for ventricles to fill with blood prior to pumping.

Describe action potentials in contractile cardiac muscle cell

repolarization happens slowly(longer duration of AP compared to skeletal muscle), Potassium exits and repolarization slowly starts (plateau when calcium enters and potassium exits) The long Ca2+ plateau of the AP in contractile cardiomyocytes creates a long period of contraction - A prolonged refractory period of cardiac muscle cell prevents tetanus and allows time for ventricles to fill with blood prior to pumping

if we were able to artificially alter the membrane permeability of pacemaker cells of the heart so that sodium influx is more rapid, _______________

the threshold is reached more quickly and heart rate would increase

Are red blood cells true cells?

•RBCs and platelets are not true cells. RBCs do not have nucleus and cell organelles, only contain hemoglobin. Platelets are cell fragments. They only have certain life span. WBCs are true cells. Most blood cells do not divide. The stem cells in the red bone marrow keep making more blood cells to replenish the dead blood cells.