Human Physiology Exam 2

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Last updated 12:25 PM on 3/25/26
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99 Terms

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Neural Pathways

Divergence: e.g. “group text”

  • one neuron affects many post-synaptic cells

Convergence

  • many pre-synaptic neurons affect a smaller number of post-synaptic neurons

  • post-synaptic neuron will integrate these signals and sum into one signal

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Summation of Signals: Spatial Summation

  • Graded potentials from many locations in the neuron are added together

  • total of all potentials determines whether an A.P. is generated

  1. Distance → farther away = less input

  2. Original amplitude → whichever signal is most intense has most input

  3. EPSP or IPSP → if inhibitory signal is closer/stronger, it can cancel excitatory signals

  4. Time of arrival → if the signals are disjointed, there won’t be an action potential

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Summation of Signals: Temporal Summation

  • must arrive at same time to sum

  • two graded potentials will be added if they arrive at the trigger zone in a short timeframe

  • 1st potential hasn’t yet returned to resting potential

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Inhibition at Synapses

Receptor

  • antagonist blocks neurotransmitter → no graded potential generated

Selective Pre-Synaptic

  • axon terminal is inhibited → no voltage-gated Ca2+ channels open

  • sometimes this blocks a response because it needs a coordinated response

Global Pre-Synaptic

  • dendrite is inhibited, no Action Potential is generated in axon

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Ohm’s Law and Electric Signaling

  • electric signals are created when charges flow across the membrane

  • V=IR

  • V = charge gradient → membrane insulates and separates charges

  • I = flow of charge → charges flow through channels

  • R = resistance to flow → membrane insulates, prevents flow of charges

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Electrical Disequilibrium

  • Active transport causes chemical gradients: outside the cell, [Na+] increases. inside the cell [K+] increases

  • many substances are charged

  • Movement across the membrane of a charged substance = e-gradient

  • cell is essentially neutral: there are regions of charge difference

  • opposite charges attract

  • membrane is an insulator

  • charges are moved across the membrane in a selective manner (mediates transport or channels)

  • Resting membrane potential: the electrical disequilibrium which exists while the cell is at rest → only a small number of ions need to move to change the potential

  • Active transport and a mechanism to separate charges are required to establish electrical disequilibrium.

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Resting Membrane Potential

  • Cell = (-) → -40 to -90 mV for neurons and muscle cells

  • selective permeability of membrane → most permeable for K+

  • forms e-gradient

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Equilibrium Potential

  • potential where the electric and chemical gradients are balanced

  • Determined by Nernst Equation, which accounts for: temperature, charge, [inside], and [outside]

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Graded Potential

  • signal is received and transduces through the membrane via an open channel down a gradient → graded potential

  • G.P. arc is summed at axon hillock, if it meets threshold, an AP is generated

  • AP causes Na+ channels to open, Na+ floods into cell, depolarizing membrane. The K+ channels are stimulated to open

  • At peak, Na+ channels close, K+ channels open, and K+ leaves, re-polarizing then hyper-polarizing the membrane.

  • Na+/K+/ATPase pumps help return to resting membrane potential

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Causing an Action Potential

  1. Distance Traveled = farther allows more leak

  2. Original Amplitude = larger means more impact, + vs ++++

  3. EPSP (depolarizing +) increases the chance of an AP, while IPSP (hyper-polarizing -) decreases the chance of an AP

  4. Timing = must arrive at the axon hillock at nearly the same time to be summed

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Peripheral Nervous System

Afferent: Sensory

  • sensory receptors sense external and internal stimuli

  • transduce stimuli into electric signals

Efferent: Somatic

  • skeletal muscle

  • mostly voluntary

Efferent: Autonomic

  • smooth and cardiac muscle

  • adipose tissue

  • glands

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Structural Proteins

Integral → transmembrane

  • Channels, transporters, receptors, structural proteins, enzymes

Peripheral → outside or inside of p.m., connected to another protein

  • receptors, structural support, enzymes

Lipid-anchored

  • receptors, structural support, enzymes

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Long-term Potentiation

  • Used to strengthen synapses, which are used frequently and with intensity

  • increased sensitivity of post-synaptic cell

  • increased release of neurotransmitter by presynaptic cell

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Muscle: Major Functions

  • generate motion and force

  • generate heat

  • maintain homeostasis of body temperature: regulate heat gain and loss

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Muscle Types

Skeletal

  • attached to skeleton

  • allows body movement

Cardiac → shares characteristics of both skeletal and smooth muscle

  • only found in heart

  • pumps blood throughout body

Smooth

  • moves substances in, out, and through body (GI tract, blood vessels, lining of organs)

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Skeletal Muscle

  • Striated = due to regular arrangement of actin and myosin

  • Multi-nucleated = skeletal muscle cells started as many cells → elongated/fused into 1 long cell during development, causing formation of a multi-nucleated cell

  • Voluntary control = can choose to override a reflex = voluntary

  • requires neuronal input: somatic division → somatic motor neurons

  • No Gap Junctions → all other muscle types have gap junctions

  • Ca2+ and troponin

  • Fastest contraction of all muscle types

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Cardiac Muscle

  • Semi-striated

  • single neurons

  • involuntary control

  • stimulated by pacemaker cells → doesn’t need nervous system, regulated by autonomic NS

  • Gap Junctions → Need them to contract bc electric signals pass btw cells, causing contraction at the same time = pump

  • Medium contraction rate

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Smooth muscle

  • no striation

  • mono-nucleated

  • involuntary control → e.g. uterine contractions aren’t controlled

  • stimulated by: hormones, pacemaker cells and have irregular rhythm, chemical changes, autonomic NS, stretch

  • Gap Junctions

  • Ca2+ and calmodulin

  • Slowest contraction of all muscle groups

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Skeletal Muscle Characteristics

  • Attached to bone by tendons in antagonistic pairs

  • flexion: toward body, decreases angle at joint

  • extension: away from body; increases angle at joint

  • origin: stationary bone → typically proximal/medial

  • insertion: mobile bone → typically distal/lateral

  • myofibril: bundle of contractile proteins

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<p>Anatomy of a skeletal muscle fiber</p>

Anatomy of a skeletal muscle fiber

  • blue mesh = sarcoplasmic reticulum → stores Ca2+

  • T-tubules = action potentials travel through here

  • Mitochondria = ATP production

<ul><li><p>blue mesh = sarcoplasmic reticulum → stores Ca<sup>2+</sup></p></li><li><p>T-tubules = action potentials travel through here</p></li><li><p>Mitochondria = ATP production</p></li></ul><p></p>
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  • sarcomere = contractile unit of skeletal and cardiac muscle

  • actin = thin filament

  • myosin = thick filament

  • myosin heads = form cross-bridges

  • nebulin - keeps actin in alignment

  • Titin = provides elasticity and stabilizes myosin → returns sarcomere to original length

<ul><li><p>sarcomere = contractile unit of skeletal and cardiac muscle</p></li><li><p>actin = thin filament</p></li><li><p>myosin = thick filament</p></li><li><p>myosin heads = form cross-bridges</p></li><li><p>nebulin - keeps actin in alignment</p></li><li><p>Titin = provides elasticity and stabilizes myosin → returns sarcomere to original length</p></li></ul><p></p>
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Sliding Filament Theory

  • Actin and myosin slide past each other → shortens sarcomere length (z-disk to z-disk)

  • Myosin heads attach to actin → cross-bridges form

  • Can only occur when Ca2+ is present → allosteric modulation

  • Requires ATP

<ul><li><p>Actin and myosin slide past each other → shortens sarcomere length (z-disk to z-disk)</p></li><li><p>Myosin heads attach to actin → cross-bridges form</p></li><li><p>Can only occur when Ca<sup>2+</sup> is present → allosteric modulation</p></li><li><p>Requires ATP</p></li></ul><p></p>
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Neuromuscular Junction (NMJ)

  • synapse between neurons and skeletal muscle

  • Acetylcholine (ACh) is the neurotransmitter

  • Causes depolarization (Na+ goes in immediately, K+ goes out later) of muscle fibers (myofibers)

  • AP is generated by myofiber →

<ul><li><p>synapse between neurons and skeletal muscle</p></li><li><p>Acetylcholine (ACh) is the neurotransmitter</p></li><li><p>Causes depolarization (Na<sup>+</sup> goes in immediately, K<sup>+</sup> goes out later) of muscle fibers (myofibers)</p></li><li><p>AP is generated by myofiber → </p></li></ul><p></p>
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Release of Calcium

  • ACh is released at NMJ

  • muscle is depolarized bc ACh opens channels; AP is generated

  • AP travels through T-tubules

  • V-gated channels (DHP) linked to Ca2+ release channels

  • ryanodin receptors on SR increase [Ca2+]

<ul><li><p>ACh is released at NMJ</p></li><li><p>muscle is depolarized bc ACh opens channels; AP is generated</p></li><li><p>AP travels through T-tubules</p></li><li><p>V-gated channels (DHP) linked to Ca<sup>2+</sup> release channels</p></li><li><p>ryanodin receptors on SR increase [Ca<sup>2+</sup>]</p></li></ul><p></p>
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Regulation of Contraction

  • binding site = troponin and is blocked by tropomyosin

  • AP depolarizes cell → travels down T-tubules

  • Ca2+ enters cell (via diffusion through channel, fast); binds to troponin → rolls and exposes binding site

  • Troponin pulls tropomyosin off of binding site

  • cross-bridges are formed and start the power-stroke cycle

  • Ca2+ is pumped back into the SR → pump is slow

<ul><li><p>binding site = troponin and is blocked by tropomyosin</p></li><li><p>AP depolarizes cell → travels down T-tubules</p></li><li><p>Ca<sup>2+</sup> enters cell (via diffusion through channel, fast); binds to troponin → rolls and exposes binding site</p></li><li><p>Troponin pulls tropomyosin off of binding site</p></li><li><p>cross-bridges are formed and start the power-stroke cycle</p></li><li><p>Ca<sup>2+</sup> is pumped back into the SR → pump is slow</p></li></ul><p></p>
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Power-Stroke Cycle

  1. ATP binds to myosin, causing it to release actin

  2. Myosin hydrolyzes ATP. Energy from ATP rotates the myosin head to the cocked position. Myosin binds weakly to actin

  3. Power-stroke begins when tropomyosin moves off of the binding site

  4. Myosin releases ADP at the end of the power-stroke

<ol><li><p>ATP binds to myosin, causing it to release actin</p></li><li><p>Myosin hydrolyzes ATP. Energy from ATP rotates the myosin head to the cocked position. Myosin binds weakly to actin</p></li><li><p>Power-stroke begins when tropomyosin moves off of the binding site</p></li><li><p>Myosin releases ADP at the end of the power-stroke </p></li></ol><p></p>
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Muscle relaxation

  • destroying cross-bridges until they’re all gone

  • Ca2+ ATPase pump removes Ca2+ from cytosol, continually pumping it back into the SR

  • once free, Ca2+ is removed, Ca2+ releases from troponin

  • Troponin allows tropomyosin to slip back over actin binding site

  • cross-bridges can no longer be formed

  • muscle is relaxed

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Time and Contraction Events

  • contraction caused by single AP = twitch

  • latent period: start of stimulus (muscle AP) to response to stimulus (contraction/twitch)

<ul><li><p>contraction caused by single AP = twitch</p></li><li><p>latent period: start of stimulus (muscle AP) to response to stimulus (contraction/twitch)</p></li></ul><p></p>
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Time and Contraction Events: The Latent Period

Latent Period: time btw stimulus (AP) and the start of contraction

  • AP travels down the T-tubules

  • Voltage sensor triggers opening of Ca2+ gate

  • Ca2+ release from SR

  • Ca2+ diffuses and binds to troponin

  • Troponin pulls tropomyosin away

  • Cross-bridges can be formed and tension generated

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Energy for Contraction

  • Must have ATP: power-stroke cycle, active transport of [Ca2+] into SR, Na+/K+/ATPase pump to replace Na+/K+ from AP

  • Phosphocreatine

  • Anaerobic glycolysis: glycolysis (Cori/Lactate Cycle)

  • Aerobic metabolism: glycolysis, citric acid cycle, ETS

  • both phosphocreatine and anaerobic glycolysis produce ATP in low [O2] env.

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Aerobic metabolism

Glycolysis → pyruvate + ATP → Citric Acid Cycle → NADH + FADH2 + ATP → ETS → lots of ATP

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Muscle Fatigue

  • physiological → muscle can no longer contract

  • long, lower intensity exertion → depletion of glycogen

  • fast, maximum exertion → build up of Pi, increasing extracellular [K+]

  • prevents P from leaving cell or decreases chance of AP

<ul><li><p>physiological → muscle can no longer contract</p></li><li><p><strong>long, lower intensity exertion</strong> → depletion of glycogen</p></li><li><p><strong>fast, maximum exertion</strong> → build up of P<sub>i</sub>, increasing extracellular [K+]</p></li><li><p>prevents P from leaving cell or decreases chance of AP</p></li></ul><p></p>
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Muscle Fatigue: Neuronal Factors

  • depletion of ACh.

  • Plays a role in disease, abnormal

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Types of Fatigue

  • central: CNS → psychological effects, protective factors

  • peripheral: PNS → decreased neurotransmitter release, decreased receptor activation, change in muscle membrane potential

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Tension and Fiber Type

Fast-Twitch Glycolytic → fatigues easily

  • white (glycogen)

  • glycogen and anaerobic metabolism

  • most force generated

Fast-twitch Oxidative (intermediate)

  • red (myoglobin)

  • glycogen and mix of aerobic/anaerobic

Slow-Twitch Oxidative → fatigue resistant, slow contraction, least amount of force but lasts longer

  • red (myoglobin)

  • oxidative, aerobic metabolism (increased number of mitochondria)

Types are mixed within a muscle, a neuron will only go to one fiber type

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Motor unit

somatic motor neuron + all the fibers it innervates

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Length-Tension Relationships

  • Tension is directly proportional to the number of cross-bridges formed

  • length is related to cross-bridges formed

<ul><li><p>Tension is directly proportional to the <strong><u>number of cross-bridges formed</u></strong></p></li><li><p>length is related to <strong>cross-bridges formed</strong></p></li></ul><p></p>
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Mechanism for Increasing Tension

  1. length-tension curve

  2. mechanical summation

  3. motor unit recruitment

  4. muscle fiber type

  • low length = high number of cross-bridges, but they’re fighting against titin

  • normal people will have muscle length at/around the ideal length bc it’s attached to bone, which prevents over-extending or over-contracting

<ol><li><p>length-tension curve</p></li><li><p>mechanical summation</p></li><li><p>motor unit recruitment</p></li><li><p>muscle fiber type</p></li></ol><ul><li><p>low length = high number of cross-bridges, but they’re fighting against titin</p></li><li><p>normal people will have muscle length at/around the ideal length bc it’s attached to bone, which prevents over-extending or over-contracting</p></li></ul><p></p>
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Tension and Twitch Summation

  • aka mechanical summation/wave summation

  • AP can’t be summed

  • mechanical event (twitch) can be summed. How? v-gated Ca2+ channels

Single twitch

  • muscle relaxes completely between stimuli

  • all Ca2+ is put back into cytosol

Summation

  • stimuli closer together don’t allow muscle to relax fully

  • new Ca2+ is released before old Ca2+ is put back fully, this allows higher [Ca2+] in cytosol and increases binding to troponin, and therefore causes an increase in the formation of cross-bridges

Tetanus: state of constant contraction

  • increase frequency of AP = increased [Ca2+] in cytosol

  • summed twitches generate more tension because they cause increased formation of cross-bridges

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Tension and Recruitment

  • motor units are recruited when tension is generated

  • slow twitch first; fast twitch glycolytic last

  • recruit slow 1st bc they don’t fatigue as fast

  • fast twitch 2nd bc provide most force, but fatigue very quickly

  • this provides more controlled movement

  • Asynchronous: don’t want to recruit all muscle units at the same time bc you want to be able to recruit new units as the old ones fatigue

  • works for all except maximal contractions

<ul><li><p>motor units are recruited when tension is generated</p></li><li><p><strong>slow twitch first; fast twitch glycolytic last</strong></p></li><li><p>recruit slow 1st bc they don’t fatigue as fast</p></li><li><p>fast twitch 2nd bc provide most force, but fatigue very quickly</p></li><li><p>this provides more controlled movement</p></li><li><p><strong>Asynchronous</strong>: don’t want to recruit all muscle units at the same time bc you want to be able to recruit new units as the old ones fatigue</p></li><li><p>works for all <u>except</u> maximal contractions</p></li></ul><p></p>
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Properties of Sensory Systems

Receptive Fields

  • region where sensory info is gathered by a single sensory neuron

  • two-point discrimination test

Sensory unit: sensory neuron and all of its receptors → parallels motor units

  • larger receptive fields = less sensitive area

<p><strong>Receptive Fields</strong></p><ul><li><p>region where sensory info is gathered by a single sensory neuron</p></li><li><p>two-point discrimination test</p></li></ul><p><strong>Sensory unit</strong>: sensory neuron and all of its receptors → parallels motor units</p><ul><li><p>larger receptive fields = less sensitive area</p></li></ul><p></p>
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Sensory Vs Motor Units

Sensory

  • smaller unit = higher sensitivity

  • larger unit = lower sensitivity

  • fewer sensory units/area

Motor

  • smaller units = less strength, more precision

  • larger units = more strength, less precision

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Contraction Type

Isotonic

  • same tension, length changes, causes movement

Isometric

  • same length, tension changes, no movement

All muscle contractions start out as Isometric, then move to Isotonic

<p><strong>Isotonic</strong></p><ul><li><p>same tension, <strong>length changes</strong>, <u>causes movement</u></p></li></ul><p><strong>Isometric</strong></p><ul><li><p>same length, <strong>tension changes</strong>, <u>no movement</u></p></li></ul><p></p><p>All muscle contractions start out as Isometric, then move to Isotonic</p><p></p>
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Role of elastic elements in isotonic vs isometric contractions

  • work = force x distance

  • when there’s enough tension in elastic elements, the muscle will contract (sarcomeres shorten) and lift the load

<ul><li><p>work = force x distance</p></li><li><p>when there’s enough tension in elastic elements, the muscle will contract (sarcomeres shorten) and lift the load</p></li></ul><p></p>
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can isometric contraction perform work?

No, because no movement happens

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Load-Shortening Velocity

  • No load, highest shortening velocity

  • heavy load, slow velocity

  • Power = load x velocity

<ul><li><p>No load, highest shortening velocity</p></li><li><p>heavy load, slow velocity</p></li><li><p>Power = load x velocity</p></li></ul><p></p>
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Skeletal Muscle Disorders

Atrophy

  • loss of muscle mass from lack of use

  • require stimulation from neurons to stay healthy

Neuromuscular Junction

  • botulism decreases ACh release (Botox)

  • Myasthenia Gravis (autoimmune disease) blocks ACh receptors

Both

  • lead to death bc skeletal muscle loss prevents breathing

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Smooth Muscle: Actin and Myosin Arrangement

  • Actin and myosin arrangement is irregular → no striations

  • Contraction still caused by actin and myosin sliding past each other

  • myosin heads still bind to actin and slide past it

  • actin is bound to dense bodies

  • myosin is in middle, actin binds to outside and pulls myosin in opposite directions

<ul><li><p>Actin and myosin arrangement is irregular → no striations</p></li><li><p>Contraction still caused by actin and myosin sliding past each other</p></li><li><p>myosin heads still bind to actin and slide past it</p></li><li><p>actin is bound to dense bodies</p></li><li><p>myosin is in middle, actin binds to outside and pulls myosin in opposite directions</p></li></ul><p></p>
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Smooth Muscle - Regulation of Contraction

  • Cell is depolarized due to Ca2+

  • Ca2+ triggers Ca2+ release from Sarcoplasmic Reticulum → Ca2+ is from the AP coming into the cell

  • Ca2+ binds to Calmodulin; complex activates MLCK → kinase adds P to myosin and causes increased affinity to actin

  • cross-bridges are formed

  • Myosin Light Chain Phosphatase removes P from myosin → decreases affinity to actin and decreases cross-bridges

  • smooth muscle: any hollow organ or tube: blood vessels, GI tract, uterus, bladder, etc

<ul><li><p>Cell is depolarized due to Ca<sup>2+</sup> </p></li><li><p>Ca<sup>2+</sup> triggers Ca<sup>2+</sup> release from Sarcoplasmic Reticulum → Ca<sup>2+</sup> is from the AP coming into the cell</p></li><li><p><u>Ca<sup>2+</sup> </u>binds to Calmodulin; complex activates <strong>MLCK</strong> → kinase adds P to myosin and causes increased affinity to actin</p></li><li><p>cross-bridges are formed</p></li><li><p><strong>Myosin Light Chain Phosphatase</strong> removes P from myosin → decreases affinity to actin and decreases cross-bridges</p></li><li><p><strong>smooth muscle</strong>: any hollow organ or tube: blood vessels, GI tract, uterus, bladder, etc</p></li></ul><p></p>
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Skeletal Muscle Reflexes

Proprioreceptors

  • tells body where it is in space

  • muscle spindles (intrafusal fibers)

  • Golgi Tendon Organ

  • Joint Mechanoreceptors: found in joints and sense mvts

Efferent Pathways

  • Alpha motor neurons → extrafusal fibers

  • Gamma motor neurons → intrafusal fibers

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Mechanoreceptors

  • mechanical stimuli

  • baroreceptors: pressure

  • osmoreceptors: cell stretch

  • hair cells: sound waves

  • nociceptors: pain, tissue damage

  • once the stimulus enters the CNS, it’s directed to a specific

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<p>Properties of Sensory Systems</p>

Properties of Sensory Systems

  • sensory receptors are most sensitive to one type of stimuli, BUT can respond to others

  • sensory information carried to brain based on typical stimulus types

Problems

  • stimulus type will be perceived incorrectly

  • rewiring can course incorrect perception of location of stimulus

Modality

  • type of stimulus

  • wiring (labeled line coding)

Location

  • localization in brain wiring

  • timing: hearing and smell

  • lateral inhibition

<ul><li><p>sensory receptors are most sensitive to one type of stimuli, BUT can respond to others</p></li><li><p>sensory information carried to brain based on typical stimulus types</p></li></ul><p>Problems</p><ul><li><p>stimulus type will be perceived incorrectly</p></li><li><p>rewiring can course incorrect perception of location of stimulus</p></li></ul><p>Modality</p><ul><li><p>type of stimulus</p></li><li><p>wiring (labeled line coding)</p></li></ul><p>Location</p><ul><li><p>localization in brain wiring</p></li><li><p>timing: hearing and smell</p></li><li><p>lateral inhibition</p></li></ul><p></p>
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Stretch Reflex

  • Muscle spindles sense stretch

  • travel to CNS

  • Alpha motor neuron: extrafusal fibers contractions

  • Gamma motor neuron: intrafusal fibers contraction

<ul><li><p>Muscle spindles sense stretch</p></li><li><p>travel to CNS</p></li><li><p>Alpha motor neuron: extrafusal fibers contractions</p></li><li><p>Gamma motor neuron: intrafusal fibers contraction</p></li></ul><p></p>
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Stretch Muscle/Muscle Spindle Reflex

  1. load added to muscle

  2. Muscle and muscle spindle stretch as arm extends. muscle spindle afferents fire more frequently

  3. Reflex control initiated by muscle stretch restores arm position and prevents damage from over-stretching

Generates more tension so you don’t drop the load

<ol><li><p>load added to muscle</p></li><li><p>Muscle and muscle spindle stretch as arm extends. muscle spindle afferents fire more frequently</p></li><li><p>Reflex control initiated by muscle stretch restores arm position and prevents damage from over-stretching</p></li></ol><p>Generates more tension so you don’t drop the load</p><p></p>
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Golgi Tendon Organ Reflex

  • Golgi Tendon organ senses tension → contraction

  • inhibits alpha motor neuron activity

  • protects muscle from injury

<ul><li><p>Golgi Tendon organ senses tension → contraction</p></li><li><p>inhibits alpha motor neuron activity</p></li><li><p>protects muscle from injury</p></li></ul><p></p>
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Inhibition At Synapses

Receptor

  • antagonist blocks NT

Selective Presynaptic

  • axon terminal is inhibited

Global Presynaptic

  • dendrite is inhibited, no AP is generated in axon

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Flexion Reflex and Crossed Extensor Reflex

Nociceptor senses pain

Ipsilateral

  • extensors inhibited

  • flexors contract

Contralateral

  • extensors contract

  • flexors inhibited

<p><strong>Nociceptor</strong> senses pain</p><p><strong>Ipsilateral</strong></p><ul><li><p>extensors inhibited</p></li><li><p>flexors contract</p></li></ul><p><strong>Contralateral</strong></p><ul><li><p>extensors contract</p></li><li><p>flexors inhibited</p></li></ul><p></p>
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Cardiovascular System

Major Function: Transportation

  • Gases: O2 and CO2

  • Nutrients

  • Waste Products

  • Immune cels

  • Hormones

  • Heat

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Anatomical Parts

Heart (Pump)

  • 2 atria

  • 2 ventricles

Blood Vessels

  • Arteries: Carry blood away from heart

  • Capillaries: Site of exchange

  • Veins: Carry blood back to heart

  • Capillaries: site of exchange

  • Veins: carry blood back to heart

Blood

<p>Heart (Pump)</p><ul><li><p>2 atria</p></li><li><p>2 ventricles</p></li></ul><p>Blood Vessels</p><ul><li><p><strong>Arteries</strong>: Carry blood away from heart</p></li><li><p><strong>Capillaries</strong>: Site of exchange</p></li><li><p><strong>Veins</strong>: Carry blood back to heart</p></li><li><p><strong>Capillaries</strong>: site of exchange</p></li><li><p><strong>Veins</strong>: carry blood back to heart</p></li></ul><p>Blood</p><p></p>
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Ohm’s Law

V = IR

  • V = driving force

  • I = flow

  • R = resistance

ΔP = FR

  • P = pressure differences

  • F = flow of blood

  • R = resistance to flow

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Pressure Gradient

Hydrostatic Pressure

  • increased by heart pumping

  • maintained by constriction of arteries

  • decreases with friction

  • decreases over distance

<p>Hydrostatic Pressure</p><ul><li><p>increased by heart pumping</p></li><li><p>maintained by constriction of arteries</p></li><li><p>decreases with friction</p></li><li><p>decreases over distance</p></li></ul><p></p>
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Pressure and Flow

  • Fluid moves from high to low pressure

  • Flow is dependent on DIFFERENCES in pressure

  • pressure and flow are directly proportional

<ul><li><p>Fluid moves from high to low pressure</p></li><li><p>Flow is dependent on DIFFERENCES in pressure</p></li><li><p>pressure and flow are directly proportional</p></li></ul><p></p>
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Resistance

R = 8Ln/πr4

  • L = length of tube

  • n = viscosity of fluid

  • r = radius of tube → inversely proportional to resistance. most important factor, can change at a moment’s notice. main regulatory factor. can control it to its 4th factor

  • The smaller the radius, the greater the resistance

  • vasodilation and vasoconstriction of arteries

<p>R = 8Ln/<span>πr<sup>4</sup></span></p><ul><li><p>L = length of tube</p></li><li><p>n = viscosity of fluid</p></li><li><p>r = radius of tube → inversely proportional to resistance. most important factor, can change at a moment’s notice. main regulatory factor. can control it to its 4th factor</p></li><li><p>The smaller the radius, the greater the resistance</p></li><li><p>vasodilation and vasoconstriction of arteries</p></li></ul><p></p>
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Resistance and Flow

  • Resistance and flow are inversely proportional

  • Radius and flow are proportional

  • the tube with the highest radius and shortest length will have the greatest flow

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Flow

  • Flow rate = volume of blood/time

  • Flow velocity = speed of blood

  • same volume of blood in same period of time

  • the smaller the diameter of the tube, the faster the blood will travel

  • individual capillaries = slow bc gas exchange

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Heart: Generates Pressure Differences

  • 4 Chambers

  • 2 Atria: receives blood

  • 2 Ventricles: sends blood

  • Valves: one way flow

  • left ventricle has more muscle bc it pumps blood to body, which requires more force

  • right ventricle has less muscle bc it’s going to lungs = short distance requires less force

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Flow of Blood Through Body

  • Right Atrium, Right AV Valve (tricuspid), Right Ventricle, Pulmonary semilunar valve

  • Lungs

  • Left Atrium, Left AV Valve (bicuspid or mitral), Left Ventricle, aortic semilunar valve

  • Body

<ul><li><p>Right Atrium, Right AV Valve (tricuspid), Right Ventricle, Pulmonary semilunar valve</p></li><li><p>Lungs </p></li><li><p>Left Atrium, Left AV Valve (bicuspid or mitral), Left Ventricle, aortic semilunar valve</p></li><li><p>Body</p></li></ul><p></p>
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<p>How Does the Heart Pump?</p>

How Does the Heart Pump?

Electrical Stimulus

  • pacemaker cells

  • modified by autonomic NS

  • spreads via gap junctions

Mechanical Contraction

  • linked to electrical stimulus

Contraction Period

  • same as skeletal

  • power-stroke cycle

Relaxation Period

  • Ca2+ returns to SR and ECF by active transport

  • Ca2+ released from troponin and tropomyosin slides back

<p><strong>Electrical Stimulus</strong></p><ul><li><p>pacemaker cells</p></li><li><p>modified by autonomic NS</p></li><li><p>spreads via gap junctions</p></li></ul><p><strong>Mechanical Contraction</strong></p><ul><li><p>linked to electrical stimulus</p></li></ul><p><strong>Contraction Period</strong></p><ul><li><p>same as skeletal</p></li><li><p>power-stroke cycle</p></li></ul><p><strong>Relaxation Period</strong></p><ul><li><p><span>Ca<sup>2+</sup> returns to SR and ECF by active transport</span></p></li><li><p>Ca<sup>2+</sup> released from troponin and tropomyosin slides back</p></li></ul><p></p>
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Overview of Heart Pumping

  1. pacemaker cells create AP

  2. AP travels through T-tubules

  3. Ca2+ from AP→Ca2+ released from SR

  4. Ca2+ binds troponin, pulling tropomyosin

  5. myosin heads bind to actin, forming cross-bridges

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Regulation of Cardiac Muscle Contraction

  • AP enters via gap junctions

  • Ca2+ enters, triggers release of more Ca2+ from SR

  • Ca2+ binds to troponin, moves tropomyosin out of the way

  • Myosin heads can form cross-bridges with actin

  • Ca2+ is re-sequestered into SR and pumped out of cell

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Electrical Stimulation

  • Due to autorhymic cells

  • Permeability of membrane changes, causing depolarization

  • Modified by autonomic division

  • AP spreads through heart via gap junctions

  • SA (sinoatrial node) → set of pacemaker cells

  • internodal pathways → used to send depolarized signal to atria

AV node (atrioventricular) delay → set of pacemaker cells, slower rate SA

  • gives time for atria to top off the ventricle, pushing out the rest of the blood

  • AV bundle → splits into left and right bundle branches. some pacemaker cells have slower rate

  • split into conduction myofibers

AV node follows SA node

  • AV node has its own rhythm, acting as a backup. If atria doesn’t contract, it’s inconvenient, if ventricle doesn’t contract, you die.

<ul><li><p>Due to autorhymic cells</p></li><li><p>Permeability of membrane changes, causing depolarization</p></li><li><p>Modified by autonomic division</p></li><li><p>AP spreads through heart via gap junctions</p></li><li><p>SA (sinoatrial node) → set of pacemaker cells</p></li><li><p>internodal pathways → used to send depolarized signal to atria </p></li></ul><p>AV node (atrioventricular) delay → set of pacemaker cells, slower rate SA</p><ul><li><p>gives time for atria to top off the ventricle, pushing out the rest of the blood</p></li><li><p>AV bundle → splits into left and right bundle branches. some pacemaker cells have slower rate</p></li><li><p>split into conduction myofibers</p></li></ul><p>AV node follows SA node</p><ul><li><p>AV node has its own rhythm, acting as a backup. If atria doesn’t contract, it’s inconvenient, if ventricle doesn’t contract, you die. </p></li></ul><p></p>
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<p>Measuring Electrical Activity</p>

Measuring Electrical Activity

  • Action potential for contractile

  • Depolarization = Na+

  • Plateau = Ca2+

  • Re-polarization = K+

  • Note time frame: hundreds of ms. Skeletal muscle = 10s of ms

  • Electrocardiogram (EKG/ECG)

  • Measures overall electrical activity of heart outside of body

  • Pattern based on position of leads

<ul><li><p>Action potential for contractile</p></li><li><p>Depolarization = Na<sup>+</sup></p></li><li><p>Plateau = Ca<sup>2+</sup></p></li><li><p>Re-polarization = K<sup>+</sup></p></li><li><p>Note time frame: hundreds of ms. Skeletal muscle = 10s of ms</p></li><li><p>Electrocardiogram (EKG/ECG)</p></li><li><p>Measures overall electrical activity of heart outside of body</p></li><li><p>Pattern based on position of leads</p></li></ul><p></p>
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Measuring Electrical Activity:

  • P-wave

  • QRS complex

  • T-wave

P-wave:

  • (E) atrial depolarization

  • (M) atrial contraction (red block)

QRS complex:

  • (E) ventricular depolarization → atrial re-polarization happens during this event

  • (M) ventricular contraction

T-wave:

  • (E) ventricular re-polarization → causes T-wave

  • (M) ventricular relaxation → associated with re-polarization

<p><strong>P-wave: </strong></p><ul><li><p>(E) atrial depolarization</p></li><li><p>(M) atrial contraction (red block)</p></li></ul><p><strong>QRS complex</strong>: </p><ul><li><p>(E) ventricular depolarization → atrial re-polarization happens during this event</p></li><li><p>(M) ventricular contraction</p></li></ul><p><strong>T-wave</strong>: </p><ul><li><p>(E) ventricular re-polarization → causes T-wave</p></li><li><p>(M) ventricular relaxation → associated with re-polarization</p></li></ul><p></p>
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<p>Mechanical Activity</p>

Mechanical Activity

  • AP trigger contraction

  • Cardiac muscle contractions cannot be summed, unlike skeletal muscle

  • No tetanus is possible → mechanism: AP is almost as long as the contraction/relaxation cycle

  • cardiac AP lasts 100s of ms

  • Cardiac muscle contraction lasts 100s of ms

  • Contractions ends about the same time as absolute refractory period

  • relaxation period of cardiac muscle = filling period of the heath

<ul><li><p>AP trigger contraction</p></li><li><p>Cardiac muscle contractions <strong>cannot be summed,</strong> unlike skeletal muscle</p></li><li><p>No tetanus is possible → mechanism: AP is almost as long as the contraction/relaxation cycle</p></li><li><p>cardiac AP lasts 100s of ms</p></li><li><p>Cardiac muscle contraction lasts 100s of ms</p></li><li><p>Contractions ends about the same time as absolute refractory period</p></li><li><p>relaxation period of cardiac muscle = filling period of the heath</p></li></ul><p></p>
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Cardiac muscle vs Skeletal Muscle

Cardiac

  • isovolumic contraction

  • isotonic contraction

Skeletal

  • isometric contraction

  • isotonic contraction

<p>Cardiac</p><ul><li><p>isovolumic contraction</p></li><li><p>isotonic contraction</p></li></ul><p>Skeletal</p><ul><li><p>isometric contraction</p></li><li><p>isotonic contraction</p></li></ul><p></p>
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Measuring Mechanical Activity

  • Use indirect measures of cardiac muscle tension and work

  • Blood pressure (load on heart)

  • stroke volume (movement of blood out of heart) → volume/beat

  • Heart sounds (due to pressure changes) → closing of valves creates noise

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Wigger’s Diagram

P-Wave: atrial depolarization → atrial contraction

  • atrial pressure increases

  • ventricular volume increases

QRS: ventricular depolarization → ventricular contraction

  • left ventricular pressure increases

  • pushes blood out

  • heart sound

  • open aortic semilunar valve

Left Ventricular Volume decreases

  • pressure starts to decrease

T-Wave: relaxation phase

  • rapid drop in ventricular pressure

  • AV valve opens

  • 2nd heart sound

  • ventricular volume increases

<p><strong>P-Wave</strong>: atrial depolarization → atrial contraction</p><ul><li><p>atrial pressure increases</p></li><li><p>ventricular volume increases</p></li></ul><p><strong>QRS</strong>: ventricular depolarization → ventricular contraction</p><ul><li><p>left ventricular pressure increases</p></li><li><p>pushes blood out</p></li><li><p>heart sound</p></li><li><p>open aortic semilunar valve</p></li></ul><p><strong>Left Ventricular Volume decreases</strong></p><ul><li><p>pressure starts to decrease</p></li></ul><p><strong>T-Wave</strong>: relaxation phase</p><ul><li><p>rapid drop in ventricular pressure</p></li><li><p>AV valve opens</p></li><li><p>2nd heart sound</p></li><li><p>ventricular volume increases</p></li></ul><p></p>
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Wigger’s Diagram Summary

  • Diastolic → point A → # closest to point

  • Systolic → heart contracts → highest point

  • end diastolic → heart relaxes → increasing volume

  • end systolic → heart empties → decreases volume

  • electric activity → P-wave, QRS, T-wave

  • heart sounds → valves closing

<ul><li><p>Diastolic → point A → # closest to point</p></li><li><p>Systolic → heart contracts → highest point</p></li><li><p>end diastolic → heart relaxes → increasing volume</p></li><li><p>end systolic → heart empties → decreases volume</p></li><li><p>electric activity → P-wave, QRS, T-wave</p></li><li><p>heart sounds → valves closing</p></li></ul><p></p>
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Calculating Pressures

Blood Pressure

  • Systolic/Diastolic

Pulse Pressure

  • Systolic - Diastolic

Mean Arterial Pressure (MAP)

  • Diastolic + 1/3 Pulse Pressure

  • e.g. 90 + 1/3(30) = 100 mmHg

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Calculating Volumes

Stroke Volume

  • End Diastolic - End Systolic

  • e.g. 135mL - 65mL = 70mL

Cardiac Output

  • Heart rate x Stroke volume

  • e.g. 70bpm x 70mL = 4900 mL/m

Ejection Fraction

  • (SV/EDV) x 100%

  • e.g. (70mL/135mL) x 100 = 51.8%

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Calculating Peripheral Resistance

  • RP = resistance in arteries

  • ΔP = F x R

  • MAP = CO x RP

  • RP = MAP/CO

e.g. 100 mmHg/4.9 L/min → 100 mmHg/5 L/min = 20 mmHg/L/min

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Regulating Mechanical Aspects

  • Measuring blood pressure

  • High pressure blocks flow

  • slowly release pressure

<ul><li><p>Measuring blood pressure</p></li><li><p>High pressure blocks flow</p></li><li><p>slowly release pressure</p></li></ul><p></p>
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What determines systolic and diastolic pressure?

the point at which you hear “quiet flow” is diastolic pressure

<p>the point at which you hear “quiet flow” is <strong>diastolic pressure</strong></p>
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Regulating Blood Pressure

Blood Vessels

  • Arteries have most control over dilation/constriction → most smooth muscle

  • Capillary beds can open and close

  • veins are pliable; serve as blood reservoirs → low smooth muscle, high flexibility

Volume of Blood

  • high volume = high pressure

  • drinking large volumes

  • high [salt] = high osmolarity = high blood volume

  • high heart rate → doesn’t change total volume, but increases the blood in arterial side

<p><strong>Blood Vessels</strong></p><ul><li><p>Arteries have most control over dilation/constriction → most smooth muscle</p></li><li><p>Capillary beds can open and close</p></li><li><p>veins are pliable; serve as blood reservoirs → low smooth muscle, high flexibility</p></li></ul><p><strong>Volume of Blood</strong></p><ul><li><p>high volume = high pressure</p></li><li><p>drinking large volumes</p></li><li><p>high [salt] = high osmolarity = high blood volume</p></li><li><p>high heart rate → doesn’t change total volume, but increases the blood in arterial side</p></li></ul><p></p>
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Regulating Volumes and Flow: Stroke Volume

  • EDV - ESV

Veinous Return

  • amount of blood that returns to the heart

  1. Pocket Valves: prevent blood from flowing backwards

  2. Skeletal Muscle Pump: contract muscle and squeezes blood up. When relaxed, the blood could move down, but the pocket valves prevent that.

  3. Respiratory Pump: creates areas of low pressure. When you inhale, there is a decrease in pressure in the thoracic cavity and heart → helps draw blood from the rest of the body back to the heart.

Contractility of the Heart

  1. Increased Ca2+: can’t do mechanical summation because of the longer AP. Cardiac muscle gets Ca2+ from extracellular fluid, if more channels open, more Ca2+ in → more Ca2+: out of SR → generates more force

  2. Sympathetic Division

  3. Increasing Muscle Fiber Length → Frank Sterling Law

  • increase by changing EDV, increased EDV = increased stretch = increased formation of cross-bridges

  • creates more force

<p><strong><u>Veinous Return</u></strong></p><ul><li><p>amount of blood that returns to the heart</p></li></ul><ol><li><p><strong>Pocket Valves</strong>: prevent blood from flowing backwards</p></li><li><p><strong>Skeletal Muscle Pump</strong>: contract muscle and squeezes blood up. When relaxed, the blood could move down, but the pocket valves prevent that. </p></li><li><p><strong>Respiratory Pump</strong>: creates areas of low pressure. When you inhale, there is a decrease in pressure in the thoracic cavity and heart → helps draw blood from the rest of the body back to the heart. </p></li></ol><p><strong><u>Contractility of the Heart</u></strong></p><ol><li><p><strong>Increased Ca<sup>2+</sup></strong>: can’t do mechanical summation because of the longer AP. Cardiac muscle gets Ca<sup>2+</sup> from extracellular fluid, if more channels open, more Ca<sup>2+</sup> in → more Ca<sup>2+</sup>: out of SR → generates more force</p></li><li><p><strong>Sympathetic Division</strong></p></li><li><p><strong>Increasing Muscle Fiber Length</strong> → Frank Sterling Law</p></li></ol><ul><li><p>increase by changing EDV, increased EDV = increased stretch = increased formation of cross-bridges</p></li><li><p>creates more force</p></li></ul><p></p>
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Regulating Volumes and Flow: Cardiac Output

  • heart rate: autonomic division

  • stroke volume

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Regulating Mechanical Aspects

Feedback Loops

Sensors

  • baroreceptors: pressure

  • increased pressure increases Action Potentials

  • Carotid bodies: in carotid arteries → go to brain

  • Aortic bodies: goes out to body

<p><strong>Feedback Loops</strong></p><p><strong>Sensors</strong></p><ul><li><p>baroreceptors: pressure</p></li><li><p>increased pressure increases Action Potentials</p></li><li><p>Carotid bodies: in carotid arteries → go to brain</p></li><li><p>Aortic bodies: goes out to body</p></li></ul><p></p>
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Baroreceptor Reflex Flow-Chart

knowt flashcard image
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Controlling Blood Flow

Flow to Tissues is determined by:

Dilation/Constriction of arteries

  • O2/CO2 levels

  • H+ levels

  • K+ levels

  • NO

  • Autonomic System

Pre-Capillary Sphincters (PS)

  • When PSs are relaxed, blood flows through all capillaries in the bed

  • if PSs constrict, blood flow bypasses capillaries completely and flows through meta-arterioles

  • PS regulate which capillary beds are open, most often depending on the metabolic needs of the capillary

<p>Flow to Tissues is determined by: </p><p><strong><u>Dilation/Constriction of arteries</u></strong></p><ul><li><p>O<sub>2</sub>/CO<sub>2</sub> levels</p></li><li><p>H<sup>+</sup> levels</p></li><li><p>K<sup>+</sup> levels</p></li><li><p>NO</p></li><li><p>Autonomic System</p></li></ul><p><strong><u>Pre-Capillary Sphincters (PS)</u></strong></p><ul><li><p>When PSs are relaxed, blood flows through all capillaries in the bed</p></li><li><p>if PSs constrict, blood flow bypasses capillaries completely and flows through meta-arterioles</p></li><li><p>PS regulate which capillary beds are open, most often depending on the metabolic needs of the capillary</p></li></ul><p></p>
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Exchange at Capillaries

Characteristics

  • thin walls, small diameters

  • high density of blood vessels

Types

  • continuous: leaky, most common and basically everywhere → fluids, small particles, no cells/proteins

  • fenestrated: more leaky → no cells/proteins → found in GI tract, kidneys

  • sinusoidal/discontinuous: most leaky, least common → leak everything including rbcs, cells, and large proteins → found in bone marrow, spleen, and liver

<p>Characteristics</p><ul><li><p>thin walls, small diameters</p></li><li><p>high density of blood vessels</p></li></ul><p>Types</p><ul><li><p><strong>continuous</strong>: leaky, most common and basically everywhere → fluids, small particles, no cells/proteins</p></li><li><p><strong>fenestrated</strong>: more leaky → no cells/proteins → found in GI tract, kidneys</p></li><li><p><strong>sinusoidal/discontinuous</strong>: most leaky, least common → leak everything including rbcs, cells, and large proteins → found in bone marrow, spleen, and liver</p></li></ul><p></p>
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Filtration and Absorption

  • occur as a result of pressures → constant exchange btw circulatory system and the interstitial fluid

  • filtration at arterial end

  • absorption at venule end

  • excess reabsorbed by lymph system

<ul><li><p>occur as a result of pressures → constant exchange btw circulatory system and the interstitial fluid</p></li><li><p>filtration at arterial end</p></li><li><p>absorption at venule end</p></li><li><p>excess reabsorbed by lymph system</p></li></ul><p></p>
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Pressures Affecting Filtration

Hydrostatic pressure

  • inside and outside of capillary

  • HP pushes away, goes high to low

  • beginning of capillary = high HP

  • end of capillary = low HP

Oncotic (Colloid Osmotic) Pressure

  • pressure in and out of capillary

  • increases osmotic pressure in an area

  • oncotic pulls stuff toward areas of high concentration to dilute them

  • beginning of capillary = low oncotic pressure

  • end of capillary = high oncotic pressure → fluid comes back into capillary

<p>Hydrostatic pressure</p><ul><li><p>inside and outside of capillary</p></li><li><p>HP pushes away, goes high to low</p></li><li><p>beginning of capillary = high HP</p></li><li><p>end of capillary = low HP</p></li></ul><p>Oncotic (Colloid Osmotic) Pressure</p><ul><li><p>pressure in and out of capillary</p></li><li><p>increases osmotic pressure in an area</p></li><li><p>oncotic pulls stuff toward areas of high concentration to dilute them</p></li><li><p>beginning of capillary = low oncotic pressure</p></li><li><p>end of capillary = high oncotic pressure → fluid comes back into capillary</p></li></ul><p></p>
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Imbalances in the Filtration and Absorption

  • Edema results from imbalance in the system

Causes of Imbalances

  • Hydrostatic pressures: higher in cap, lower outside cap

  • high bp, low interstitial pressure

  • Colloid Osmotic Pressures: low in cap, high outside cap

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Blood Components

  • Blood cells (red and white) from bone marrow → carry O2 and function in immune system

  • Plasma: water, salts/ions, proteins/organic molecules, gases → transport cells in fluid

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Blood Cells

Erythrocytes → Red Blood Cells

  • Bind O2 and some CO2

  • Hematocrit; Erythropoietin increases

Leukocytes → Immune System

  • eosinophils, basophils, monocytes, neutrophils

Platelets

  • allows clotting

<p>Erythrocytes → Red Blood Cells</p><ul><li><p>Bind O<sub>2</sub> and some CO<sub>2</sub></p></li><li><p>Hematocrit; Erythropoietin increases</p></li></ul><p>Leukocytes → Immune System</p><ul><li><p>eosinophils, basophils, monocytes, neutrophils</p></li></ul><p>Platelets</p><ul><li><p>allows clotting</p></li></ul><p></p>
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Plasma

Proteins

  • Albumin - bind hormones

  • Globulin - antibodies

  • fibrinogen - clotting

Organic Molecules

  • vitamins

  • glucose

  • nitrogenous wastes

  • lipids

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The Immune System

Major Functions

  • protect against invaders

  • remove dead/damaged cells

  • identify and remove abnormal cells

Major pathogens

  • bacteria

  • viruses

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Bacteria

Structure

  • cell w/ cell wall

  • occasional capsule

Living Conditions

  • anywhere

Reproduction

  • by itself

Antibiotics

  • susceptible when not resistant

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Viruses

Structure

  • DNA or RNA encased by proteins

Living Conditions

  • must have a host

Reproduction

  • must have a host → uses host machinery

Antibiotics

  • not susceptible, it’s a virus

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