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by: Mikaela Maldonado

BMS260StudyGuide.pdf BMS 260

Mikaela Maldonado
GPA 4.0

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About this Document

All rights go to RV Anthony but all work is my own
Biomedical Sciences
Dr. Russell Anthony
Study Guide
50 ?




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This 14 page Study Guide was uploaded by Mikaela Maldonado on Thursday March 31, 2016. The Study Guide belongs to BMS 260 at Colorado State University taught by Dr. Russell Anthony in Spring 2016. Since its upload, it has received 40 views. For similar materials see Biomedical Sciences in Biomedical Sciences at Colorado State University.

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Date Created: 03/31/16
Muscle Physiology  Skeletal  Voluntary  Multinucleated  Long, linear  Striations  Many mitochondria  Transverse tubules  Myofibrils and sarcomeres  Sarcolemma = plasma membrane, sarcoplasm=cytoplasm, sarcoplasmic reticulum=smooth ER/stores Ca+  Sarcoplasmic reticulum – Ca+ released at resting is 10^-7 M, stimulation 10^-5 M  Connects to T-tubules -2 integral proteins –1 in SR and 1 in T- tubule  T-tubule protein is voltage sensitive Ca+ channel and DHP receptor  SR membrane protein is ryanodine – forms a Ca+channel  Myofibrils  Give striated appearance  Arrangements of thick (myosin) and thin (actin) filaments  Perimysium  Surrounds individual muscle bundles  Epimysium  Outer connective tissue sheet  At ends form tendons  Endomysium  Surround individual myocytes  Innervated at a 1:1 ratio  Sarcomere  From one Z line to the next contractile unit  Z line – non contractile unite  Invaginations in sarcolemma are part of transverse tubule structure  Titin –anchors actin to Z line (non contractile)  I band – actin, titin Z line (light)  A band – myosin, actin (dark)  M line – junction between actin  H zone – thick and thin slide past one another  Contraction Mechanism  Shortening and contraction do not correlate  Activation of force-generation sites -> cross bridges  Sliding Filament Model  Thick and thin filaments are propelled past one another by the cross-bridges  Depends on interactions of actin and myosin  Ca+ binds to troponin on thin filaments that moves tropomyosin out of its blocking position and myosin binds to actin and creates the cross- bridge cycling  Smooth  Involuntary  Spindle shaped  Neuromuscular Junction  Motor unit  Motor neuron and innervated skeletal muscle fibers  1 neuron innervated many fibers, but one muscle fiber is innervated by one motor neuron  one muscle has many MANY motor units  stimulation of nerve fibers to skeletal muscle – only way action potentials are initiated  motor neurons cell bodies are located in brainstem or spinal cord  axon of motor neurons are myelinated and cell body are largest diameters  high velocity propagation  axon terminals have vesicles with acetylcholine  directly under the terminal portion of axon plasma membrane – motor end plate  axon terminal with motor end plate junction = neuromuscular junction  Influence  Electrical activity in the plasma membrane  Neurotransmitters released by autonomic neurons  Hormones  Locally induced changes in chemical composition of extracellular fluid surrounding the cell  Stretch  Involves the binding of calmodulin to Ca+ in the cytosol that creates complex that binds to myosin light chain kinase to phosphorylate myosin cross bridges  Cardiac  Intercalated disks  Striations  Uninucleated  In between voluntary and involuntary  Glycogen  Branching  Myocardiocytes  Heart muscle cells  Single nucleus (center of cell)  No neuromuscular junctions  Striations  Cells separated by intercalated discs (cell-cell communication)  Discs located at the z lines but not all z lines are intercalated discs  Communication through gap junctions  Provides from electrocoupling- range of inherent electrical activity (myogenic)  Arranged in sheets/cords of connective tissue  Ca is the primary inward current instead of Na  Prolonged refractory period  Allows relaxation of muscle to allow blood circulation back into the heart  Have to relax muscle before a new AP  Myocyte or myofiber = muscle cell  Myosin  Heavy and light  Heavy -> globular head + filament actin binding site  Globular head of myosin  Functional ATPase  Converts ATP->ADP + Pi  When ATP binds to myosin -> actin and myosin interaction disrupted  Immediately ATP->ADP  Myosin head carries ADP +Pi it is charged  Myosin binds actin -> release of Pi  Allows myosin head to pivot then ADP is released  2 strand alpha helix of “beads on a string”  contractile protein  G actin has binding site for myosin  Tropomyosin  Regulatory protein  Overlap binding sites on actin for myosin and inhibits interaction when in relaxed state  Form strand that wraps around actin  Stearic blocking model  Physically blocking by tropomyosin  “chemical and physical” conformational blocking  troponins  regulatory protein  “forms a complex with the other proteins of the thin filament (actin and tropomyosin)”  “binds Ca+ reversibly, once bound changes conformation to pull tropomyosin away from the myosin interaction sites”  Ca+ binding regulates contraction because it allows myosin-actin interactions to take place  troponin C – binds Ca+- tethers to allow both to go through a conformational change  troponin I – binds actin  troponin T – binds tropomyosin *taken from R.V Anthony’s lecture  Anatomy of the heart  Atria-thin walled and serve as a holding site  Ventricles are thick walled and serve as a contraction site  Left is bigger because it pumps to the body/ right pumps to the lungs  Pericardium  Parietal pericardium – outer layer  Visceral pericardium – next to myocardium on the outside  Fluid filled sac, reduces friction to reduce heat within the body  If infection, pericarditis – infection/inflammation of pericardial sac  Myocardium  Heart muscle  Papillary muscles  Specializes as wrapped cords within ventricles  Attach to chordae tendineae which then attach to valves  Endocardium  Inside of the heart  Endothelial cells (like what line blood vessels)  Continuous  Valves  Anchored to the inner wall of ventricles  Left -> Atria-ventricular valve – 2 valve flaps (bicuspid) mitral  Right -> atria-ventricular valve 3 flaps (tricuspid)  Right – pulmonary semilunar (dub) and left – aortic semilunar (lub) are both tricuspid and give the lubb dub sounds when closing  Conduction  Parasympathetic input comes from the vagus nerves -> acetylcholine released to muscanaric receptors in atria  Slows down SA node conduction of impulse – brachycardia (vasodialation)  Sympathetic input comes from thoracic spinal nerves-> norepinephrine and epinephrine from the blood stream that stimulate beta adrenergic receptors in both atria and ventricles  Speed up heart rate – tachycardia and works to increase strength of contraction  SA (sinoatrial) node  Myocardiocytes group that has the most unstable resting potential  Can be fixed with pacemaker  AV (atrioventricular node)  Reside in septum, sits on tops of the ventricles – 2 ndmost unstable  Condenses electrical activity across atria  Blocking – troublesome – lengthening distance between P and QRS  Bundle branch blocking – left axial shift – problem when a history of heart disease  SA creates AP -> depolarization -> atria -> AV -> condensed (accumulates activity) -> bundle of His (cord like myocardiocytes)  Pernkinje fibers – branch of bundles and stimulus of contraction from apex to top  AV node can default take care of ventricular contraction if SA node doesn’t work  Ventricle tachycardia – paddle totally depolarize hear so that repolarization will resynchronize with the heart  Cardiac cycle  Vena cava –RA – tricuspid valve – RV – pulmonary valve – pulmonary artery – lungs – pulmonary vein – LA – mitral valve – VV – aortic valve – aorta – body – and back  Diastole – ventricles relax – end volume – greatest volume/pressure  Systole – ventricles contracting – end volume – lower pressure/volume  Vibrations are associated with blood acceleration/deceleration and cause sounds  Isovolumetric contraction  Volume doesn’t change but pressure does increase  Isovolumetric relaxation  Aortic valve closes so volume same, the pressure decreases in ventricles as relax  Stroke volume  Amount of blood ejected from the heart during a cardiac cycle *taken from R.V. Anthony’s lecture  P wave-depolarization and contraction of atria  QRS – depolarization and contraction of ventricles  T – ventricle repolarization  Heart murmurs  Abnormal (louder), during systole/diastole  Stenotic or narrowed valves (stiff)  AV-diastolic murmur  Semilunar –systolic murmur  Leaky, insufficient or incompetent  AV – systolic / semilunar – diastolic  CO (cardiac output) = Heart rate x stroke volume -> amount of blood moved per unit time  Medulla  Cardiac regulatory centers  Cardio inhibitory center  Vagus releases AcH  Vasomotor center (cardio acceletory center) – sympathetic output – release norepinephrine  Basoreceptors  Sense the amount of pressure in circulation (afferent) to the medulla from blood vessels  BP increase = stimulate cardio inhibitory and will have efferent output- vagal nerve  BP decrease = stimulate vasomotor center -> sympathetic output  Increase plasma epinephrine – increase adrenal medulla – increase sympathetic activity –decrease parasympathetic activity–release epinephrine/norepinephrine–B receptors- destabilizes SA node – stroke volume (end diastolic volume – end systolic volume) increase – tachycardia  Starling’s Law of the Heart  Increased stroke volume if you fill ventricles with more blood  Strength of the contractions is directly related to following of filling – “end diastolic volume”  AND deliver sympathetic signals as norepinephrine and epinephrine  Strength of contraction is proportional to the distension of heart chamber at the end of diastole  Guest lecture:  Mitochondria – free radicals  Translational research – can be applied to humans  Echocardiography – study beating of the heart  Arteries leaving the heart have a lot more fibroelastic tissue in their walls  Aorta – baroreceptors, increase pressure of the system  Baroreceptors are located in the aortic arch, carotid sinuses, L+R atria, L ventricle  Arterioles have a lot more smooth muscle  Arteries and arterioles  Smooth muscle  Sympathetic regulation  Tonic constriction  Drop in BP occurs In the arterioles  Capillary  Fragile, leaky tube  No smooth muscles  Endothelial tubes  Exchange  Precapillary sphincters  Decrease BP from arterioles -> capillaries so capillaries (with no muscle) so they don’t burst  Arteriovenous anastomoses  Redirect flow of blood  Allows for shunting of blood  Provides for thermoregulation  Distributing flow slows down speed and pressure with increase area to flow through – capillary structures  Starling’s Law of Filtration  Favor filtration-hydrostatic pressure within the capillary (blood pressure); interstitial colloidal/osmotic pressure of tissue or Bowman’s capsule (essentially is zero)  Oppose filtration – is the hydrostatic pressure of interstitial fluid/tissue (Bowman’s capsule); osmotic/colloidal pressure of blood  Valves in veins set up unidirectional flow – 60% total blood is in the veins  Sympathetically mediated vasoconstriction can increase venous return to the heart  Venous flow is assisted by skeletal muscle pump and tone  Abdominal and thoracic pumps continue flow of the blood through breathing movements  Pressure  Pumping of the heart/resistance  Increase strength/increase pressure  Decrease diameter/increase pressure  Increase vessel length/ increase resistance and pressure  Increase degree of vessel branching/ decrease pressure  Increase blood viscosity/increase pressure  Constrictors  Angiotensin II  Serotonin – released by platelets  Vasopressin/ADH  Epinephrine/norepinephrine - Delta 1 and delta 2 receptors/located primary in veins  Dilators  Nitric oxide  Norepinephrine/epinephrine – B 2 receptors, coronary blood vessels and skeletal muscle arteries  Enteric nerves release nitric oxide locally  Epinephrine is both based on receptors available to bind to and target cell type  Blood composition  Plasma – protein and fluid- serum occurs following clotting  55% plasma, 45% erythrocytes, 5% leukocytes and platelets  erythrocytes – concave, no nucleus, allows to squeeze through tight places  Leukocytes - granulocytes  Neutrophils – 50-70%  Esoniphils – 1-4%  Basophils – 0.1-0.3%  Monocytes – 2-8%  Lymphocyctes – 20-40%  Transportation  Oxygen/platelets  Erythrocytes  Carry oxygen  O2 deprivation – erythropoiesis – decrease o2 to kidneys = increase release of erythropoietin to activate receptor in bone marrow increase erythropoiesis  Clotting a. Damage to the wall of blood vessel b. Exposure surrounding collagen to interior of vessel c. Local vasoconstriction due to myogenic activity of smooth muscle – 20 min – with sympathetic output d. Platelet activation and aggregation – release ADP, serotonin e. Synthesis of thromboxane and discharge of mediators f. Construction of vascular smooth muscle g. Fixes with a platelet plug  Release platelet factor 3 – plasma proteins derived from the liver  Thromboplastin, calcium and platelet factor 3  Combine to form prothrombin activator  Prothrombin -> thrombin  Plasma protein - cleaved by prothrombin activator  Liver needs K+ to make prothrombin  Fibrinogen -> thrombin -> fibrin  Clotting factor 13  Polymerizes loose clot into a firm clot  Plasminogen activators -> plasmogen -> plasmin  Break down fibrin -> soluble fibrin fragments  Lymphatic System  Lymph vessels  Lymph nodes  Spleen  Tonsils  Thymus  Lymph capillaries  Single layer of epithelial cells  Irregularly shaped making walls of lymph capillaries very porous  Left side of the body is the main  Lymph vessels/lacteals empty into the central lacteal/thoracic duct  Then empty into the left subclavian vein  Lymph nodes are honey comb of lymph-filled sinuses with large cluster of lymphocytes and many macrophages  2 efferent vessels  antigen presenting cells  macrophages  B lymphocytes  Stem cells in bone marrow are the source of T and B cells  T cells mature in thymus  B cells when activated by antigens produce antibodies  T cells  Helper T  Interleukin 2  Activates cytotoxic T and plasma B cells  Cytotoxic T  B cell activation  Don’t need maturation in bone marrow  Most go to plasma cells  Memory cells  Cytokines  Interleukins  Interferons  Tumor necrosis factor  Antibody is a large protein that consists of 4 interlocking peptides  Antigen binding sites work in a ligand receptor with antibodies  Antigen internalization by macrophages or B cells allows cells to present antigens to helper T cells  Located on surface of macrophage  Class II Major Histocompatibility Complex  Cells recognize things that the body makes compared to foreign substances  Macrophage engulfs bacterium and produces its helper T cells its antigens which then activates B cells to plasma cells generating antibodies which enter syntenic circulation  Viral DNA in host is present as antigens to attract a lethal attack from cytotoxic T cells  Respiratory System  Lungs  Provide O2  Eliminates CO2  Regulates blood pH  Forms speech sounds  Defense against microbes  Arterial concentrations of messengers by removing pulmonary capillary blood and producing and adding others to the blood  Traps/dissolves blood clots arising from systemic veins  Respiration  Pulmonary ventilation (breathing)  External respiration -> movement of O2 and CO2 within cells  Transport of gases in blood  Internal respiration – movement of O2 out of the body  Airways  Trachea – bronchi – bronchioles – terminal bronchioles – respirator bronchioles-alveolar ducts – alveolar sacs  Conducting zone  Mass movement of air  Respiratory zone  Exchange of gases with blood  Metabolic rate is proportional to relative surface area and is proportional to respiration  Pleural cavity  Pleurae  Thin- double layered serosa  Parietal covers the thoracic wall and superior face of the diaphragm  Visceral pleura covers the surface closest to the lung  Constant negative pressure relative to atmospheric pressure that makes the active form of breathing inspiration  Relative to atmospheric pressure  Expiration = -3mmHg  Inspiration = -10mmHg; maximal = -30mmHg  The site of gas exchange is the alveoli  Type I pneumocytes  Thin, stretched lining of alveolar sacs  Type II pneumocytes  Produces surfactant – reduce surface tension at air barrier interface  Newborns – respiratory distress syndrome  Betamethansone – synthetic glucoticoid  Metabolic rate (O2 consumption)  Proportional to body surface area and alveolar surface area  Capillary endothelium and type I pneumocytes  Comprise diffusion barrier Velocity = K(( pressure differential x gas solubility)/(sqrt (gas density)) K is difusability constance and is proportional to surface area and inversely proportoiinal to diffusion barrier thickness  CO2 is much more soluble than O2 to offset pressure differential in exchange  Hemoglobin  4 peptide subunits  each has a heme group carrying one molecule of Fe  2 alpha and 2 beta globin polypeptides  carry 4 O2 molecules  Affinity:  Decreases with lower ph/increase CO2 presure/increase temp/increase [DPG]  Tidal volume  Normal breathing  Inspiratory reserve volume – deep inhale  Expiratory reserve volume – max exhale  Vital capacity – combination of expiratory/inspiratory reserve volume  Residual volume – air remaining in lungs at all times  Diaphragm is innervated by the phrenic nerve  CPAP – continuous positive airway pressure Renal Functions  Regulation of water, inorganic ions, and acid-base balance  Removal of metabolic waste from blood  Detoxification (removing foreign materials)  In conjunction with the liver  Gluconeogenesis  Making glucose from non carbohydrate precursors  Production of hormones/enzymes  Erythropoietin- erythrocyte production  Tenin- enzyme that controls formation of angiotensin and influences blood pressure and sodium balance  1,25 – dihydroxyvitamin D, influences Ca+ balance  cow has lobulated kidneys and the horse has a heart shaped right kidney  outer cortex – granular in appearance from presence of granular  inner medulla striated in appearance  renal pelvis- collecting area in center  ureter –thick smooth muscle wall  bladder – hollow smooth muscle lining, reservoir; wall is made of transitional epithelium  micturition – emptying of bladder, normally an involuntary event, reflect control  kidney nephron –functional unit  cortical and medullary base on most of presence  renal corpuscle – cortex  site of filtration of blood  glomerulus- afferent/efferent vessels  tuft of capillaries  Bowman’s capsule  Leaving – proximal convoluted tubule which turns into the Loop of Henle  Distal convoluted tubule which will then empty into collecting ducts  Renal Corpuscle  Glomerular endothelium is more porous than normal capillaries  On outside -> podocytes – fenestrations (slits)  Allow capillary fluid to enter Bowman’s capsule in between the glomerulus and podocytes there is a basement membrane  Juxtaglomerular cells – sense osmolarity of materials passing through the distal convoluted tubule. Efferent arteriole into the renal corpuscle  Macula densa – tall columnar DCT cells  Act as chemoreceptors, sense osmolarity of DCT fluid  Decrease osmolarity increase JG cells increase renin production  Renin = increase BP increase Na reabsorption – sympathetic stimulation = renin production  Flow  Glomerular filtration – tubular secretion – tubular absorption  Hormones  Aldosterone (mineral corticoid)  Antidiuretic hormone (vasopressin)  Alcohol majorly inhibits  Na in plasma  Blood pressure  Autonomic nervous system  Glomerular Filtration  180 L/day  GFR (filtration rate) decreases = increased sympathetic output to afferent arterioles = constrict AA  Increase GFR – constrict EA/dialate AA  Proximal convoluted tubule  Nearly all glucose is reabsorbed  SLGT 2 – Na dependent – inhibit for diabetic treatment  85% of H20 is reabsorbed  Loop of Henle  Descending limb – H20 reabsorbed  Ascending limb – Na and Cl reabsorption, H20 reabsorption is blocked  Distal tubule and cortical collecting ducts “fine tuning”  Na and H20 reabsorption  Glucose urea  SGLT 2 inhibition causes glucose in urine at a much lower inhibition  Vasopression/ADH  Stimulate aquaporin 2 molecules  Water transporters  Renin  Enzyme that converts angiotensin -> angiotensin I -> aldosterone  Increase plasma K secretin to drive aldosterone secretion  Atrial naturietic peptide = increase Na excretion = naturieis


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