ANP Midterm 2

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1

Define Homeostasis, giving at least 2 Physiological examples.

The ability of the body "to maintain relatively stable [not unchanging; dynamic] internal conditions even though there is continuous change in the outside world" [Walter Cannon - father of homeostasis]. Once a change is sensed, a response is activated. Involves:

  • adequate blood levels of vital nutrients
  • heart activity/blood pressure monitored and adjusted as needed
  • wastes must not accumulate
  • core body temperature must remain within range
2
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List the 3 Essential Components of each Control Mechanism, defining the Roles of each.

Receptors sense the change [stimulus] and sends the information [afferent pathway] to the control center.

Control centers determine the set point for variable maintenance. It analyzes the information received and determines the correct response.

Effectors provide the means for response [output along efferent pathway]. This reaction brings the particular level back into range.

3

Differentiate between Positive and Negative Feedback.

Negative feedback mechanisms operate on an output that reduces or shuts off the stimulus. This can occur through one or two different hormone(s) or neural pathway(s) regulating a process through occurring in the opposite direction to the original response. The goal is to prevent sudden, severe changes. (blood glucose level, body temperature)

Positive feedback mechanisms operate on an output that further stimulates the stimulus. This change occurs through occurring in the same direction to the original response. The goal is to drive a process in motion. (blood clotting, birth)

4

Define Disease and Aging in terms of Homeostasis.

A disease is a disturbance in homeostasis [homeostatic imbalance] [chemicals are released to drive the body to generate heat leading to a level out of homeostatic range].

Aging is associated with a progressive decrease in our ability to [and time it takes to] maintain homeostasis resulting in greater risk for illnesses.

5

Using a flow chart, indicate the positions of the autonomic and somatic nervous systems in the structural organization of the nervous system as a whole.

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6
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Compare the autonomic and somatic nervous systems in terms of effectors, pathways, use of ganglia, transmitter effects.

Effectors are involved in the somatic [in skeletal muscle] and autonomic [in smooth muscle, cardiac muscle, and glands] nervous systems.

Pathways are neuron(s) involved in the somatic [one thick and myelinated reaching from spinal cord to skeletal muscle producing rapid conduction of impulses] and automatic [two chained [preganglionic neuron - thin and lightly myelinated originating in the CNS, synapses with 2nd motor neuron] [postganglionic - thin and unmyelinated which transmits to effector organ]] nervous systems.

Ganglia [ganglion] are areas of exchange of neurotransmitters from one neuron to the next.

Transmitter effects

7

Distinguish between the PNS and SNS in terms of the types of processes regulated

A parasympathetic division ["resting and digesting system"] is activated in non-stressful situations where the body's energy use is low while regulating "housekeeping" activities. (digestion, defecation, diuresis - "D" system)

A sympathetic division ["fight or flight"] is activated in stressful situations where the body's energy use is high while activating "survival" activities. (exercise, excitement, emergency, embarrassment - "E" system)

8

Define sympathetic tone, parasympathetic tone

A tone is the state of sustained tension in a muscle. Only a certain proportion of muscle fibers are contracted at a given time while the rest are relaxed and recovering.

A sympathetic [vascular] tone is when blood vessels are kept in a state of partial vasoconstriction to direct blood to where it is immediately needed [blood shunting (variations in sympathetic output to specific vessels)].

A parasympathetic tone is when the body works to keep all systems at homeostasis (the contractile activity of the heart and smooth muscle of the GI and urinary tracts). This can be overridden by the sympathetic nervous system.

9

Identify: systems regulated in opposite directions by the SNS and PNS, cooperative effects of the SNS and PNS, unique regulatory roles of the SNS.

Most visceral [internal] organs recieve dual innervations.

The activity of [SNS vs PNS] the heart [INC vs DEC], GI system [DEC vs INC], and respiratory system [INC vs DEC] receive antagonistic interactions.

The regulation of external genitalia during intercourse receives cooperative effects.

The adrenal medulla, sweat glands, arrector pili muscles of the skin, kidneys, and blood vessels involves uniquely the regulatory roles of the sympathetic nervous system. Also thermoregulatory responses to heat and the release of renin from the kidneys.

10

HOW DO THE PNS AND SNS DIFFER

  1. Sites where nerves originate
  2. Relative lengths of pre and post-ganglionic fibers
  3. Locations of ganglia
11

List the 3 levels of regulation of autonomic function, giving examples.

Brainstem and spinal cord controls have direct effects on the anterior nervous system mainly involving the ventro-lateral medulla [motor center] (controls the cardiovascular center - heart rate, blood vessels; also GI, respiratory tract)

Hypothalamic controls have effects on the body's homeostatis regulation mainly involving the hypothalamus [intregation center] (heart activity, blood pressure, body temperature, water balance, endocrine activity; also centers that help mediate emotions and biological drives) *anterior regions = parasympathetic, posterior areas = sympathetic

Cortical controls have a parasympathetic [lowering] effect on autonomic systems. For example, meditation and biofeedback allow for some conscious control over visceral activities (lower heart and breathing rate, oxygen use, metabolic rate). Biofeebback can also improve the management of migraine headaches, stress, and cardiac function.

12

Hormones: define receptor, specifity, affinity.

Receptors are what hormones must bind to in order to influence the target cell function.

Hormones are specific and their level of target cell activation depends on the hormone concentration [amount of hormones in the area], the target cell receptor content [how many receptors are in the area], and the affinity [how strongly something is attracted to another] of hormone for the receptor in order to bind.

13

List 3 structural groups of hormones and differentiate between steroid hormones and protein/peptide hormones in terms of their mechanisms of action

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Hormone's structural groups include amino acids/peptides/proteins [water soluble], steroid hormones [lipid soluble; derivatives from cholesterol], and eicosanoids [form arachidonic acid]

Peptides bind to the surface of cell receptors, activates a G-protein within the cell which dissociates from the receptor and binds to another receptor [adenylate cyclase], ATP activates the second messenger [cAMP] [that was bound to the receptor] which triggers the responses of the target cell [activating protein kinases].

Steroids enter the nucleus of the cell and activate their response [gene transcription].

14

ENDOCRINE SYSTEM

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Composed of clusters of cells in organs that produce hormones that are, once produced, usually transported in the blood. (pituitary gland, hypothalamus, thyroid gland thymus, adrenal cortex, pancreas, ovaries/testicles)

15

HORMONE

A chemical substance released into the ECF that regulates the metabolic function of other cells in the body. Hormones are potent, not needing many for the amount to be sufficient to activate a response. The blood level of a hormone depends on the rate of synthesis and the rate of degradation. The half-life of the persistence of hormones in the blood can be less than a minute to a week. The onset of a hormone action depends on if it is completed through enzyme activation [rapid] or synthesis [slow - turning on transcription and creating protiens]. The duration of a hormone is variable [those with a generalized effect will last longer].

16

MECHANISM OF HORMONE ACTION

Hormones alter levels of cell activity including membrane permeability or potential [use of channels], the synthesis of enzymes within cells, enzyme activation and deactivation, introduction of secretory activity, and the stimulation of mitosis (human growth hormone during childhood)

17

Differentiate between positive and negative feedback as well a between humoral vs neral vs hormonal regulation of hormone release.

Negative feedback sets a specific point while positive feedback sets a goal.

The 3 types of stimuli are humoral [hormone secretion occurs in direct response to change in the blood (level of a nutrient ion, insulin, blood glucose), neural [hormone secretion due to a neural impulse (SNS and epinephrine release by adrenal medulla, hypothalamic neurons and oxytocin release) and hormonal [hormone release due to the presence of hormones (hypothalamic-pituitary axis)] .

18

HORMONAL STIMULI

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Hormones [thyroid-releasing hormone (TRH)] are pumped out of hypothalamus to act on the anterior pituitary gland to release hormones [thyroid-stimulating hormone (TSH)] through to general circulation into the thyroid [thyroid hormones (T3 and T4)].

19
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HYPOTHALAMUS TO PITUITARY GLAND

A neural component of the brain that produces a number of releasing factors [hormones] which travel to the anterior pituitary gland via a hypophyseal portal system [vein to a capillary bed to a vein to a capillary bed]. The posterior lobe contains axon terminals from the hypothalamus [paraventricular and supraopic areas] to produce antidiuretic hormone (SON) [water balance] and oxytocin (PVN) [muscle contraction in the uterus during labour and delivery] to be released into circulation.

20

2 KEY HOMEOSTATIC REGULATORY SYSTEMS

Autonomic Nervous System:

  • parasympathetic vs sympathetic
  • sensory and neural pathways
  • fast response

Endocrine System:

  • hormones released into extracellular fluid and often travel to target organs via the bloodstream
  • slower response time but a longer-lived response
  • different chemical classes of hormones with associated mechanisms of action
21

Describe the composition of blood.

Plasma - salts, plasma proteins, substances transported by blood

Buffy coat + Erythrocytes - formed elements [platelets, red blood cells, white blood cells

22

List the physical characteristics of blood and the types of formed elements found in the body.

Blood is the only fluid tissue in the body. It is formed elements [erythrocytes or red blood cells, leucocytes or white blood cells, platelets] suspended in plasma. It can be scarlet [oxygen rich] or dark red [oxygen poor] in colour. It is more dense and viscous than water. The pH range is tightly controlled between 7.35 and 7.45. It is responsible for 8% of a body's weight.

23

List and briefly describe the 3 main functions associated with blood and the circulatory system

Distribution is the first function including oxygen and nutrients [obtained by the GI tract and goes to tissues], metabolic wastes [CO2 to lungs and other products through urea and feces], and hormones [from where they are produced to where they can affect the body]. Regulation involves body temperature [distribution, conservation, dissipation], pH in body tissues [plasma proteins, bicarbonate reserve], and adequate fluid volume. Protection from anything foreign involves platelets/plasma proteins/blood clotting and antibodies/complement/white blood cells.

24

List the physical characteristics of plasma

Plasma is the fluid volume of blood. It is formed from water and solutes and comes from the liver [where albumin is produced - non specific carrier protein that holds water to keep it dissolved]. It is pale yellow [straw] in colour. Plasma is a carrier of various molecules and is an important blood buffer. Blood constantly adjusts the composition of plasma to keep its composition and keep pH in the range [albumin soaks up extra hydrogen ions].

25

Describe the functional anatomy of an erythrocyte, the structural organization of hemoglobin.

The 7.5 micrometers diameter and biconcave disks [with no nucleus] of erythrocytes allows for a larger surface area for better transportation of oxygen. Proteins maintain the plasmic reticulum and regulate the cell shape of the hemoglobin filled [greater than 97%] cell. Energy is generated anaerobically.

Hemoglobin is composed of 4 polypeptide chains [globin] [that can bind one carbon dioxide of oxygen each], 2 alpha and 2 beta, and 4 iron containing central heme groups [that can bind one molecule of oxygen each]. A cell with full oxygen has a different shape than that which has released oxygen. Hemoglobin is held in erythrocytes to keep it from being fragmented and lost and from contributing directly to osmotic pressure and blood viscosity.

26

Describe the process of erythropoiesis, its regulation and the dietary requirements associated with daily production; outline the life cycle of a red blood cell.

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Erythropoiesis is the process of red blood cell production, occurring in the red bone marrow. Stem cells [hematopoietic stem cell/hemocytoblast] become committed cells [proerythroblast through the presence of hormones [erythropoietin]]. It then goes into the developmental pathway [basophillic erythroblast (ribosome synthesis), polychromatic erythroblast and orthochromatic erythroblast (hemoglobin accumulation), reticulocyte (ejection of the nucleus)] and once it is put into circulation to completes it's specialization [maturation].

27

REGULATION OF ERYTHROPOIESIS

Red blood cell production and destruction is a balance.

*hypoxia = kidneys produce erythropoietin, activation of bone marrow occurs resulting in more mature red blood cells

28

HORMONAL CONTROLS OF BLOOD REGULATION

Erythropoietin is produced in the kidneys and stimulates the specialization of red blood cells. There is always some EPO in blood to compensate for the cells that are being destroyed. More might be needed if there is a shortage of oxygen [hypoxia] due to:

  • excess red blood cell destruction/loss [hemorrhage]
  • high altitude or pneumonia (more difficult for air to circulate)
  • increase demand

*kidney's measure the amount of oxygen in the blood rather than the number of red blood cells

Renal failure is due to lack of EPO

29

Define: anemia, polycythemia and give examples

Anemia presents itself with tiredness, pale skin, shortness of breath, and chills due to not enough red blood cells being produced, significant blood loss, or red blood cells being destroyed too quickly.

Polycythemia is due to too many blood cells being produced making the blood too viscous. This can put someone at risk for blood clots. Examples include:

  • polycythemia vera: cancer within the bone marrow resulting in the production of red blood cells
  • secondary polycythemia: as a result of the environment lacking in oxygen (high altitude)
  • artificial polycythemia: blood doping [infusing concentrated blood cells into the body]
30

Define platelet and summarize the main steps in platelet production.

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Platelets are [anucleate] cytoplasmic fragments of megakaryocytes that contain purple staining granules that contain clotting factors and enzymes. They last about 10 days until they become too old or are used up and total 150,000-400,000 at any one time. Platelet production is regulated by thrombopoietin [hormone from the liver that stimulates stem cells for platelet production].

Platelet production starts at the level of stem cells [hematopoietic stem cell/hemocytoblast] then goes into the developmental pathway [megakaryoblast (stage 1 megakaryocyte), megakaryocyte (stage 2/3), megakaryocyte (stage 4)] and finally pieces break off the megakaryocyte and goes into circulation.

31

Define hemostasis; list the 3 key events involved in the process and describe the processes occurring during each of these 3 events.

Vascular spasma includes the vasoconstriction of the vessel in response to damage. This lasts long enough to slow the blood flow around the area of damage so a clot can form.

Platelet plug formation occurs when the endothelial cells lining the blood cells are damaged which exposes the base membrane [made of collagen] and inhibits the release of NO and PGI2 [prostacycin, plycostinoids] which keep platelets from sticking together. Exposure to collagen stimulates platelets to swell and become spiky and sticky to adhere [von Willebrand facor]. Degranulation also occurs, where the release of ADP [enhances aggregation and degranulation] and serotonin and thromboxane A2 [enhances vascular spasm and agregation] begins.

Coagulation makes blood transform from a liquid to a gel in 3 phases: prothrombin activator form, prothrombin to thrombin, fibrinogen molecules to fibrin mesh. Also involves procoagulants [promote and drive to completion] and anticoagulants [interfere to stop unnecessary clots].

32

2 PATHWAYS TO PROTHROMBIN ACTIVATORS

Intrinsic pathway involves clotting outside the body or in a slightly damaged vessel. This is a slower pathway to factor 10 where extrinsic can simply skip to. Materials that are needed are found in the blood vessel.

Extrinsic pathway involves the clotting of blood associated with the body and blood vessel damage. This causes the release of tissue factor which bypasses many steps in the intrinsic pathway and is thus faster. Needs to use material from outside the body.

*prothrombin activator is the rate limiting step

33

Describe briefly the processes of clot retraction and fibrinolysis.

Clot retraction and repair occurs within 30-60 minutes when platelets contract and exert a pull on surrounding fibrin strands, pulling the edges of blood vessels closer. A serum is squeezed from the clot. Platelet-derived growth factor [PDGF] that is released during degranulation stimulates the smooth muscle cells and fibroblasts to divide and rebuild the wall. Vascular endothelial growth factor [VDGF] multiply endothelial cells to fill the gap in the lining.

Fibronolysis is the removal of the clot once it is no longer needed. Tissue plasminogen activator [tPA] is released by endothelial cell and bind to plasminogen. This forms plasmin which breaks down fibrin.

34

FACTORS LIMITING CLOT GROWTH/FORMATION

The 2 homeostatic mechanisms that limit formation are the swift removal of coagulation factors and the inhibition of activated clotting factors. Clot formation requires procoagulation factors over anticoagulation factors. Normally, the flowing of blood washes away procoagulants.

  • as thrombin forms, it is absorbed onto fibrin threads [limits clot size]
  • antithrombin III [in plasma] inactivates any escaping thrombin
  • antithrombin III and protein C [liver] inactivate many intrinsic pathway procoagulants
  • heparin [basophils and mast cells] enhances the activity of antithrombin III [a type of white blood cell]
  • the smooth endothelial lining of undamaged blood vessels [also endothelial-derived heparin and prosracyclin] has some immune elements to keep unnecessary clots from occurring
35

Define: thrombus, embolus, thrombocytopenia, hemophilia.

A thrombus is a clot that develops and persists in an unbroken blood vessel and can block blood circulation to tissues.

An embolus is a piece of a thrombus that has broken free and can get stuck in a vessel of small diameter [pulmonary or cerebral emboli].

A thrombocytopenia is defined as any condition harmful to bone marrow or any movement leading to bruising.

A hemophilia is defined as hereditary bleeding disorders including hemophilia A [deficiency in factor VIII] and hemophilia B [deficiency in factor IX]. These are both sex-linked disorders requiring transfusions/injections of purified clotting factors.

36

Define the components of the ABO and Rh blood group systems. Describe a transfusion reaction using the terms agglutination and hemolysis

Red blood cell antigens promote agglutination [only ABO and Rh antigens cause serious agglutination problems]

O is the universal donor as it has no antigens to stimulate the production of antibodies. AB is the universal recipient as it has no antibodies. Blood has to have the same antigens

There are 8 kinds of Rh factors. Rh+ have Rh factor on the blood's surface. If exposed to this factor, Rh- blood will produce antibodies which attack donor red blood cells in response to the second and subsequent exposures. Anti-Rh serum [RhoGAM] prevents this from occurring.

37

BODY'S COMPENSATION FOR BLOOD LOSS

Blood vessels can constrict [vasoconstriction] to decrease volume OR may increase the rate of erythropoiesis [making of more red blood cells].

Loss of 15-30% results in weakness and pallor [unhealthy pale appearance]. Loss of more than 30% can induce shock [substantial blood loss or thrombocytopenia [lack of platelets] can be fixed through packed red blood cells].

Blood can be mixed with heparin to reduce clotting [must be held at 4 degrees celcius].

38

TRANSFUSION REACTIONS

*in transfusions, the problem is the recipient's blood as in it's larger quantity it continuously produces antibodies

Agglutination is when small vessels become clogged. Clogged red blood cells rupture or are ruptured by phagocytes and hemoglobin release. The overall result is blocked flow to tissues, reduced oxygen-carrying ability of the blood, and hemoglobin precipitates/clogs kidney tubules [administration of alkaline fluids can dilute and dissolve hemoglobin and prevent kidney failure].

39

Describe the internal and external anatomy of the heart.

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The heart is simply a transport system pump for blood which is provided delivery through hollow blood vessels. It is enclosed within mediastinum [centralized] of the thorax. The layers include the epicardium [connective tissue that protects, anchors and prevents overfilling of the heart; the double layers that make up the fluid-filled pericardial cavity allows mobility], myocardium [the bulk of heart; composed of muscle arranged into bundles that reinforce the myocardium internally and anchor cardiac muscle fibers, provide additional support for great vessels and valves, and direct the spread of action potentials across the heart to specific pathways - coupled together with gap junctions], and endocardium [endothelial cells [endothelium] and connective tissue that are continuous from the blood vessels].

40

Locate the following on diagrams of the heart; chambers, great vessels, coronary circulation, internal muscles, ect.

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*left and right are switched on paper

There are 2 atria and 2 ventricles whereby the right deals with oxygen-poor blood from the body and the left deals with oxygen-rich blood from the lungs. The right artia receives blood from the superior vena cava [head and upper limbs], the inferior vena cava [lower torso and lower limbs], and the coronary sinus [from myocardium [left atrium via 4 pulmonary veins]]. The right ventricle pumps blood received by the tricuspid valve to the pulmonary trunk via the pulmonary valve to the pulmonary circuit [short, low-pressure circulation to and from the heart]. The left ventricle pumps blood received from the mitral [bicuspid] valve to the aorta via the aortic valve to the systemic circuit [long pathway with 5x the resistance].

Pectinate muscles are bundles of muscle to allow stronger contractions with minimal muscle mass.

Fossa ovalis is a depression between the left and right atrium. If this is not closed properly. In a fetus, it is open and called a foramen ovale.

The ventricles are the pumps of the heart and thereby have thicker walls [left more so than right [3x] as it pumps to the whole body rather than to only lungs].

Trabeculae carneae are any bundles of cardiac muscle not attached to valves.

Papillary muscles are any bundles attached to valves via the chordae tendineae and simply keep them from opening the wrong way and also are used to keep the valves closed.

Heart valves are unidirectional and control the direction of flow - opening to allow blood in and closing to assure blood doesn't flow back - through the use of pressure. Valvular insufficiency occurs when the valves do not close 100% and thus pushes blood back on itself, making it need to repeat the process. Stenosis occurs when the valves do not open 100% and makes the heart work more to fill the cavities. These can both start through heart damage.

The 2 exterior grooves include the coronary sulcus [atrioventricular groove] which is located between the 2 atria and ventricles to keep them well anchored as they extend into the deepness of the heart, and the anterior-posterior interventricular sulcus which is located between the two ventricles.

41

Describe the coronary circulation. (pt.1 - arteries)

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Coronary circulation is the shortest, but one of the most important circulations of the body. The left and right coronary arteries begin from the base of the aorta and encircle the heart in coronary sulcus [atrioventricular groove].

Left: circumflex artery, anterior ventricular artery, [anastomosis], posterior inter ventricular artery, [anastomosis], right marginal artery, right coronary artery :Right

42

Describe the coronary circulation. (pt.2 - veins)

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The veins begin with capillaries.

Left: coronary sinus, great cardiac vein, [anastomosis], middle cardiac vein, cs, small cardiac vein, anterior cardiac veins :Right

43

ANASTOMOSIS

An anastomosis is a junction of vessels which provides alternate routes for nourishment if a given artery begins to be occluded, but total occlusion may still occur. Angina pectoris is the medical term for chest pain due to the heart tissues not getting enough blood as it needs. Myocardial infarction is the term for a heart attack when blood flow decreases to a part of the heart, causing damage.

44

Compare the physiological properties of cardiac muscle fibers with those of skeletal muscle cells.

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45

Describe intercalated disks and relate 2 aspects of their structure to the support of cardiac functions

Intercalated disks are connective regions of the heart to help assure it functions as a single functional organ [synchronized contraction of cardiac tissue]. The heart needs only to be stimulated in one location for the whole organ to respond.

Desmosomes are used for strong cell to cell adhesion regions, especially important during contraction.

Gap junctions [functional syncytium] are used for strong electric coupling.

46

Compare the electrical properties of contractile cardiac muscle cells with those of autorhythmic cardiac muscle cells

Heart contraction is stimulated by action potentials [signals] allowing 99% of the cells, contractile cells, to contract. The 1% of autorhythmic cells start the action potential through a leaky sodium channel allowing intake.

47

Special characerisics of cardiac muscle cells.

Cardiac muscle cells stimulate their own contraction through the use of autorhythmic cells [autorhythmicity]. The intercalated disks allow for the heart to contract as a single unit. The influx of calcium from the extracellular fluid triggers the release of calcium from the sarcoplasmic reticulum. The absolute refractory period [amount of time a second action potential cannot be initiated] is longer [250 vs 1-2 milliseconds] to allow contractions to occur following a complete relaxation for blood to flow properly through the heart. The heart relies almost exclusively on aerobic respiration [energy involving the intake of oxygen].

48

ACTION POTENTIAL OF CONTRACTILE MUSCLE CELLS

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1. Depolarization is due to sodium influx through fast voltage-gated sodium channels. A positive feedback cycle rapidly opens many sodium channels, reversing the membrane potential. Channel inactivation ends this phase

2. Plateau phase is due to calcium influx through slow calcium channels. This keeps the cell depolarised because few potassium channels are open.

3. Repolarization is due to calcium channels inactivating and potassium channels opening. This allows potassium efflux which brings the membrane potential back to its resting voltage.

49

Define autorhythmic cell; describe cardiac autorhythmic cell properties that allow them to spontaneously depolarize.

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Autorhythmic cells have unstable resting and by themselves fire faster than the heart beats regularly. In autorhythmic cells, an action potential is due to:

1. Pacemaker potential is the slow depolarization due to both openings of sodium channels and closing of potassium channels. Notice that the membrane potential is never a flat line. Reaching threshold ends this phase and the action potential begins.

2. Depolarization is due to calcium influx through calcium channels.

3. Repolarization is due to calcium channels opening. This allows potassium efflux, which brings the membrane potential back to its most negative voltage.

50

Define sinus rhythm and indicate why SA node is the pacemaker.

The sinus rhythm determines the heart rate in that it determines how quickly the sinoatrial node [SA node] is firing.

51

Explain how the intrinsic conduction system of the heart allows it to function as a pump

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The action potential is generated by the SA node [the right atrium of the heart] and passes to the AV node [above the tricuspid valve]. It then has a short delay as it goes through the 'bottleneck' of the AV bundle [between the top of the left and right ventricles] [this allows time for the atria to fully contract and fill the ventricles before they begin to contract and empt] and then branches into the left and right bundle branches. It then branches into Purkinje fibers that flow up into the papillary muscles [attached to valves through chorae tendineae].

52

Delineate the extrinsic innervation of the heart and contrast the influences of the PNS and SNS on heart rate.

The rate of the SA node depolarization is regulated by the autonomic nervous system through the decrease of the diastolic depolarization rates [parasympathetic] and increase of the depolarization and repolarization rates [sympathetic]. Under resting conditions, tonic parasympathetic output have a dampening effect on heart rate [as the SA node naturally wants to depolarize faster than it does].

Bradycardia is when the heart beats slower than normal. Tachycardia is when the heart rate increases over and above the regulation of the autonomic nervous system. Sinus rhythm is a regular heart rate (120/80).

53

Explain what ECG tracing is and the nature of the information it is encoding.

An electrocardiogram is a record of electrical changes during heart activity, relying on the conductive activity of body fluids. It generally contains a P-wave [atrial depolarization], QRS-wave [ventricular depolarization], and T-wave [ventricular repolarization]

54

ABNORMAL ACTIVATION OF THE HEART

Sinus rhythm is a normal ECG tracing.

Ventricular fibrillation is when each area is being controlled at their own rate; there is no pattern.

2nd-degree heart block is when the SA node fires but the action potential does not always reach the ventricles [only every second time]

Nonfunctional SA node is when the AV node must drive the action potential, therefore there is no P-wave and it is much slower [SA node spontaneously depolarizes the fastest].

55

Explain the events of each phase of the cardiac cycle.

The cardiac cycle involves: atrial systole + diastole = ventricular systole + diastole.

1. Ventricular filling phase [passive followed by atrial contraction]

2. Isovolumetric contraction phase

3. Ventricular ejection phase

4. Isovolumetric relaxation phase

56

Describe the pressure changes responsible for valve opening and closing and like these with resultant volume changes.

1. Period of ventricular filling: mid-to-late diastole is when the pressure in the atria is greater than that in the ventricle so the AV [tricuspid/mitral] valves open and the semilunar [pulmonary/aortic] valves close. After 70% filling, the AV [tricuspid/mitral] valves begin to close [P-wave]. The atria then contracts [atrial systole = 0.1 sec] to fill with the final 30% [atrial diastole for the rest of the cycle].

2. Ventricular systole = 0.3 sec [comprises QRS and T waves]: ventricles begin to contract, increasing the pressure and closing the AV [tricuspid/mitral] valves creating a period of isovolumetric contraction. An increase of pressure opens the semilunar [pulmonary/aortic] valves creating a phase of ventricular ejection.

3. Isovolumetric relaxation: early diastole is when the ventricles relax and the pressure decreases rapidly, closing the semilunar [pulmonary/aortic] valve creating a period of isovolumetric relaxation.

4. Back to [1]: the atria continued to fill through these steps and when pressure builds to be greater than ventricular pressure, AV [tricuspid/mitral] valves open and the steps restart.

*quiescent period = 0.4 sec [from the end of the T-wave to the start of the next P-wave]

57

FEATURES DRIVING THE CARDIAC CYCLE

Blood flow through the heart is controlled entirely by pressure changes.

Blood flows from higher to lower pressure through any available opening.

*the electrical activity of the left and right sides are almost simultaneous

58

Define these terms in relation to a cardiac cycle: systole, diastole, isovolumetric contaction and relazation, dichrotic notch

*whenever there are lines ha cross, there is a valve either opening or closing

Systole is the contraction of the heart, pumping out blood. Diastole is the relaxation of the heart, filling with blood.

Isovolumetric contraction and relaxation are the periods where the volume is constant [not pressure] in a closed system after concentration or relaxation of the ventricle.

The dichrotic notch is when the blood influx from the ventricle is causing the aorta to stretch and the recoil.

59

Indicate the physiological significance of the first and second heart sounds.

The first heart sound is the closure of the AV valves [indicating the beginning of systole/isovolumetric contraction] and the second heart sound is the closure of semilunar valves [indicating the end of systole/isovolumetric relaxation]. Heart sounds are the vibrations of the heart and chest due to valve closure.

60

HEART MURMURS

Heart murmurs may be due to valvular obstruction [high velocity of blood through a narrow opening as they have not opened all the way]. They also may be due to valvular insufficiency [leakage of blood backward in the path causing a sound when there should be silence as they do not close all the way]

61

Define cardiac output in terms of heart rate and stroke volume.

Cardiac output is the amount of blood pumped from the left ventricle into the aorta per minute [average for a male is 5L/min].

CO [cardiac output] =HR [heart rate] x SV [stroke volume]

Stroke volume is the amount of blood pumped from the left ventricle per beat.

SV = EDV [end diastolic volume] - ESV [end systolic volume]

Heart rate is the amount of times a heart beats within one minute.

62

Indicate the influences of exercise of HR and SV.

Cardiac output increases 4-5 [7 in a marathon runner] times in a fit person meaning more blood is being used and reoxygenated.

The notion of cardiac reserve indicates that the heart can pump more blood if needed during an active or stressed state.

Combined effects of heart rate and stroke volume allow for these health benefits.

63

Describe in detail the mechanisms for the regulation of HR and SV.

1. Delineate the effects on HR of: the autonomic ns, epinephrine (adrenal medulla), plasma electrolytes, body temperature.

Heart rate is determined by the rate of spontaneous depolarization of the SA node but can be affected by:

  • autonomic fibers innervating the SA node
  • circulating hormones (nor-epinephrine increases the rate of spontaneous depolarization while acetylcholine decreases this)
  • plasma electrolyte concentration
  • body temperature

*in resting conditions, the parasympathetic nervous

64

Apply the Frank-Starling Law of the Heart to the intrinsic regulation of SV.

Law: within defined limits [a certain range], the heart will pump whatever volume of blood it receives.

Preload is the end-diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions.

65

What are the effects of chronically elevated blood pressure on cardiac muscle cells?

How can this apply to both physical training or a chronic disease?

Elevated blood pressure makes the heart work more, exercising the muscles and making them initially stronger. However, if this persists over time, such as in the case of a chronic disease, the heart does not receive time to rest and repair itself and therefore becomes exhausted and eventually 'wears out'.

66

Define aferload and describe its influence on stroke volume.

Afterload is the pressure that ventricles must overcome to force open valves and eject blood from the heart [approximately 80 mm in the aorta, 10 mm in the pulmonary trunk]. Hypertension reduces the ability of ventricles to eject blood.

67

Describe 2 types of extrinsic influences on stroke volume.

These are factors outside the heart which change vigor of contraction without changing the end diastolic volume. Must not be due to greater initial fiber length but rather involve changes in the strength of contraction due to increased calcium influx.

  • sympathetic stimulation [increases the strength of contraction as well as the rate of contraction and stimulation]
  • drugs [digocin] [increases heart contractility]
  • parasympathetic nervous system [antagonizes sympathetic stimulation]

*norepinephrine increases heart contractility via cyclic AMP