A motor unit is a motor neuron and all the muscle fibers it innervates. Motor unit recruitment is increasing the number of muscle fibers that contract within a muscle.

Actin- binds to myosin to contract muscle,

 troponin- calcium binds to it to move tropomyosin,

tropomyosin- blocks actin until it is moved by troponin.

 Ryanodine channels release calcium once it has been opened by the electrical signal.

Creatine kinase is the enzyme that helps our body to store ADP and creatine phosphate because we cannot store a lot of ATP. Creatine phosphate is what our body is able to store while ATP is not needed for use.

  Neuromuscular fatigue occurs when AcH synthesis cannot keep up with demand, and psychological fatigue occurs when motor neuron activity decreases below desired state

Hypertrophy is when there is an increase in muscle fiber diameter due to an increase in myosin and actin synthesis.

Hyperplasia occurs when cells increase in size and then split lengthwise so there is an increase in the number of cells.

 Release calcium once the AP has traveled down the T-tubules

Magnesium helps to hydrolyze the ATP so myosin ATPase can break it down

Calcium ATPase pumps calcium back into its lateral sacs so that muscle relaxation can occur.

 Muscle contractions can vary in strength by changing the number of muscle fibers that contract within a muscle, and the tension developed by each contracting fiber.

 Motor units are recruited and more muscle fibers are stimulated to contract.

Similar to temporal summation in that as long as another AP is generated before the previous AP fully resets, and then the two will summate and create a stronger AP resulting in more tension developed in the muscle fiber.

There is the maximum amount of cross bridges that can be formed by the myosin and actin

In a shortened sarcomere, there is not the optimum number of cross bridges that can be formed, the calcium is not able to be released from the SR, and calcium is not able to bind to troponin because it is being blocked. In a lengthened sarcomere, there is also less than the optimum number of cross bridges that can be formed.

 Isotonic- same tension, but muscle length changes,

 isometric- same muscle length, tension changes

 Lactic acid changes of the pH of the muscle, causing fatigue in the area.

 Slow oxidative type 1 fibers, fast oxidative Type IIA fibers, fast glycolytic type IIB fibers

Myoglobin increases the rate of oxygen transfer from the blood and imparts a red color to the fibers

 They monitor changes in muscle length and tension to regulate it and keep the muscle at optimum length

Increased calcium concentrations, calcium bind to calmodulin, and activate myosin kinase. Myosin kinase phosphorylates myosin allowing it to bind to actin. The thick and thin filaments slide across each other, and the cell collapses or shrinks due to a pulling effect on the dense bodies and the intermediate filaments.

Pacemaker activity occurs when the membrane potential gradually depolarizes due to shifts in passive ionic fluxes, resulting in an AP, Slow Wave potentials occurs when there are alternating depolarizations & repolarizations of the membrane, resulting in an AP if the depolarization is significant enough.

 Skeletal- striated, Smooth- unstriated, Cardiac- striated with intercalated disks.

Varicosities are holes at the end of a motor neuron in which the neurotransmitter is released from. Does not directly innervate receptor but is close enough for neurotransmitter to reach receptor.

Albumins- transports molecules, but makes biggest contribution to colloid osmotic pressure, Globulins- alpha & beta for clotting and gamma for antibodies, Fibrin- for platelet clotting

  hemoglobin is the molecule that carries oxygen in the blood. It is composed of 4 globin molecules and 4 iron containing heme groups which bind to oxygen

Nutritional- iron deficiency which occurs with low hemoglobin synthesis and folic acid which are aberrations in DNA synthesis leading to fewer RBCs dividing and maturing, Renal- Kidney disease which causes low

production of erythropoietin, Hemolytic- excessive rupturing of circulating erythrocytes such as sickle cell anemia and malaria

Primary- tumor like condition in the bone marrow increasing the viscosity of the blood which increases blood pressure,

Secondary- increase in erythropoietin secretions due to environmental conditions such as high altitude, Relative- dehydration in which RBC count is not elevated but hematocrit is high

  Granular contains granules, and agranular does not contain granules

Thrombopoetin is the hormone that regulates platelet production

Platelets possess actin and myosin so they can contract during the platelet plug formation to pack more platelets closer together and make the plug stronger.

Intrinsic- Hageman’s factor is activated when it meets the exposed collagen of the damaged blood vessel. This activates factor X, which causes prothrombin à thrombin. Thrombin then catalyzes fibrinogen à fibrin and activates factor XIII to seal fibrin net.

Extrinsic- Tissue thromboplastin is released by the damaged tissue. This activates factor X, which causes prothrombin à thrombin. Thrombin catalyzes fibrinogen à and activates factor XIII to seal fibrin net.

SA node, AV node, Bundle of His, Left and Right Bundle Branches, Purkinje Fibers

Slow depolarization phase 1- decrease Pk increase to Pna (funny channels), slow depol phase 2- decrease Pna and increase Pca (T-type calcium channels), fast depol- increase Pca (L-type calcium channels), repolarization- decrease Pca increase Pk

Another pacemaker creates a higher AP than the SA node causing an extrasystole (premature heartbeat)

Sharp depolarization due to increase Pna, Plateau phase due to increase Pca and decrease Pna & Pk, repolarization due to increase Pk & decrease Pca

Tachycardia- increased rate > 100bpm, Bradycardia- decreased rate < 60 bpm

1^st heart sound is the AV valve and

2^nd heart sound is the aortic valve

 Stenotic- does not open completely, Insufficient- does not close completely

Large conducting arteries aid in pumping blood (thin walled, more elastic fibers, less smooth muscle) muscular distributing arteries determine where blood is needed and controls overall blood pressure (thick walled, more smooth muscle, less elastic fibers)

 Anchoring filaments attach lymphatic endothelial cells to surrounding tissue. When swelling occurs in the interstitial tissue due to water entering from the blood capillaries, the anchoring filaments are moved due to their attachment to the cells. This movement pulls on the lymphatic endothelial cells, which separates them. Fluid then flows into the lymphatic vessels down a pressure gradient. When fluid is drained, the anchoring filaments move back to original position, and the spaces between endothelial cells close.

 Edema is the swelling of blood vessels due to the invasion of pathogens. It occurs when too much interstitial fluid accumulates. Potential causes: reduced concentration of plasma proteins which reduce water re-absorption, increased permeability of capillary walls allowing more plasma proteins and water to move into the tissue, increased venous pressure which increases capillary pressure and reducing water reabsorption, blockage of lymph vessels in which fluid cannot return to the blood.

 The muscarinic cholinergic receptor and G protein activation, AcH increases SA node permeability to K+ closing the T-type calcium channels and funny sodium channels, hyperpolarizing it and taking it longer to reach threshold. AcH hyperpolarizes the AV node, and decreases atrial contractile strength by shortening plateau phase. Does not modulate stroke volume because it only innervates the atria.

Beta I adrenergic receptors & cAMP 2^nd messenger system, NE increases both sodium funny and T-type calcium channel opening which increases the rate of spontaneous depol. NE reduces AV nodal delay by enhancing the slow, inward (T-type) Calcium. Beta I adrenergic NE increases both atria & ventricular contraction strength by increasing Ca influx through L-Type calcium channels, Ca release from SR increasing myosin ATPase activity & increasing Ca re-uptake to relax faster

 Inability of the cardiac output to keep up with the body’s demands for supplies & removal of wastes.

Adenosine is the control for linking coronary blood flow to the oxygen requirement of the heart

 Systolic- pressure developed by contracting the heart, Diastolic- minimum pressure within the arteries as the blood is draining off into the remainder of the vessels during diastole

 Pressure autoregulation is a bad way to control blood pressure because although it dilates the blood vessels to get more blood to area that needs it, it does not take into account actual blood pressure. It actually only really regulates blood flow. So when MAP decreases, blood flow decreases, arterioles dilate to restore flow, but this causes MAP to also further reduce which is bad for the body, and the opposite is also true.

 Bulk flow is used to determine volume between the vascular and interstitial fluid compartments when moving materials across the capillary wall. It is the ultrafiltration of plasma from the vascular side to the interstitial tissue side due to capillary pressure, which is protein free plasma. It causes reabsorption when inward pressure is greater.

Venous capacity which is the volume of blood the veins can accommodate, and venous return which is the volume of blood entering each atrium per minute

 The distensibility of the veins and any externally applied pressure such as skeletal muscle contraction which decreases capacity and increases venous pressure

  Distensibility can be changed by sympathetic activity, which induces vasoconstriction decreasing the volume and capacity of the veins. This then increases the blood flow back to the heart.

 Hypertension occurs when the blood pressure is above 140/90 mmHg. Primary hypertension occurs more often and has unknown causes, and secondary hypertension occurs less often and is caused by a known or primary pathological problem.

Cardiovascular- hypertension due to atherosclerosis,

Renal- hypertension caused by an increase in overall blood volume due to reduced blood flow to the kidneys (atherosclerosis) and increased salt retention,Endocrine- hypertension caused by Pheochromocytoma which is adrenal medulla tumor caused by excess epinephrine and norepinephrine and Conn’s syndrome which is an increase in aldosterone secretion by the adrenal cortex inducing salt retention, Neurogenic- hypertension due to a defect in nervous control receptors and center, and due to a reduction in blood flow to the brain.

  Hypotension is when blood pressure drops below 100/60 mmHg. Orthostatic hypotension occurs when there is a shift from lying down to coming to an upright position. This is because the reflexes are inadequate, blood pools in the veins, and pressure drops. Baroreceptor reflexes kick in.

 Circulatory shock occurs when tissues cannot be maintained due to low blood pressure.

Hypovolemic shock- fall in blood volume; hemorrhaging; vomiting, Cardiogenic shock- weakened heart making it unable to pump blood, Vasogenic shock- widespread vasodilation due to substances (septic- massive infection; vasodilator substances released by bacteria and anaphylactic- allergic reaction; histamine is released), Neurogenic shock- loss of sympathetic vascular tone resulting in vasodilation and is induced by pain.

 Inflammation, Interferon, Natural killer cells, and the Complement System

  Margination- stickiness of the leukocytes to the inner endothelial lining of capillaries of the affected tissue. Caused by cell adhesion molecules, which protrude through the endothelial lining, Diapedesis- Amoeboid movement of the leukocytes through capillary pores, Chemotaxis- leukocytes are drawn toward their targets by chemotaxins, which are secreted, from the cells of the damaged area.

Humoral immunity occurs when B cells are differentiated into plasma cells to secrete antibodies and cell-mediated immunity is when T cells differentiate into cytotoxic t cells to directly destroy the pathogen.

  Antibody is composed of two light chains and two heavy chains in the shape of a Y, with the light chains on the outside and the heavy chains on the inside. The tips of the Y are where the antigen binding fragments are (Fab) and the tail of the Y is where it interacts with the immune cells (Fc).

Agglutination- antibodies cause the pathogens to clump together preventing proper function, Neutralization- antibodies bind with the pathogen preventing function, Activation of complement system- activation of complement system proteins which attack cell membrane of pathogen, Opsonization- antibody tails bind with phagocytes to enhance phagocytosis, Stimulation of Killer cells- abnormal body cells bound by antibodies recognized by natural killer cells and instantly lyses it

Cytotoxic T cells secrete perforin to the infected cell causing it lyse and leak

Cytotoxic T cells- destroy infected “self” cells via secretion of perforin, Helper T cells- secretes B cell growth factor & T cell growth factor, secretes chemotaxins, macrophage-migration inhibition factor to keep phagocytes from migrating out of the infected area, Suppressor T cells- inhibit the immune response and are slow to develop, Memory T cells- provide rapid mobilization of the immune response if the system is subsequently exposed to the same antigen.

 MHC class I is on all body cells except white blood cells, MHC class II is only on white blood cells

 TH1 stimulates cell mediated response, TH2 stimulates humoral response

   Interleukin 12 stimulates TH1 and Interleukin 4 stimulates TH2

Antibodies are produced to attack the acetylcholine receptors on skeletal muscle