Human Physiology Yr1

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Last updated 4:21 PM on 5/6/26
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63 Terms

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Total Body Fluid & Cellular fluid

13\frac13 Extracellular fluid Eg. Blood plasma

23\frac23 Intracellular fluid

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Fluid mosaic model

Cell membrane - Phospholipid bilayer consisting of Hydrophilic heads & Hydrophobic tails

Transmembrane Proteins to allow for pores - Allow movement of molecules

Permeability to molecules:

  • Very permeable to H2O

  • Increased size = Decreased permeability

  • Lipid soluble

  • Charge = most important, increasing charge = decreased permeability

Impermeability to molecules:

  • Sugars

  • Proteins

  • Inorganic ions

Unless helped

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Diffusion

Random movement from High conc to Low conc (Down Gradient)

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Filtration

Pores allow this process due to size

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Osmosis

Movement of H2O in response to a solute conc Grad

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Osmotic Pressure

The pressure that would stop H2O from moving

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Protein facilitated movement

Carriers/Channels

High to low = Facilitated diffusion

Low to high = Active transport

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Exocytosis

Out of cells

<p>Out of cells</p>
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Endocytosis

In to cells - Proteins and very large molecules

Pinocytosis - Membrane pinches off

Phagocytosis - Arms of cytoplasm encapsulate

<p>In to cells - Proteins and very large molecules</p><p>Pinocytosis - Membrane pinches off</p><p>Phagocytosis - Arms of cytoplasm encapsulate </p>
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Functional anatomy of a Synapse

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Generation of an Action Potential

Nerve cells have a low threshold for excitation

Electrical/Mechanical/Chemical factors impact ion distribution

  1. Local/non-propergated ( Generator potential (EPSP & IPSP))

  2. Propergated ( Action Potential)

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Action potential (Propergated) & Nerve cell structure

All or none law

  • If stimulus is sufficient = Response

Action Potential leads to Na+ , K+ across the membrane

  • Absolute refractory - Cell cannot fire = No more AP ( One way movement)

  • Relative refractory- Only larger than normal Stimuli = New AP

Action potential starts in the Axon Hillsneck

  • Travels in one direction to synapse

Myelinated Axons - Jumps between nodes of Ravier (Ensures Conduction Velocity)

<p>All or none law </p><ul><li><p>If stimulus is sufficient = Response </p></li></ul><p></p><p>Action Potential leads to Na<sup>+  </sup>, K<sup>+ </sup>across the membrane </p><ul><li><p>Absolute refractory - Cell cannot fire = No more AP ( One way movement)</p></li><li><p>Relative refractory- Only larger than normal Stimuli = New AP</p></li></ul><p></p><p>Action potential starts in the Axon Hillsneck </p><ul><li><p>Travels in one direction to synapse</p></li></ul><p></p><p>Myelinated Axons - Jumps between nodes of Ravier (Ensures Conduction Velocity)</p><p></p>
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Neurones & The Transmembrane Resting Potential

Neurones release neurotransmitters across the synapse

Transmission through the movement of charged ions across the cell membrane

Transmembrane Resting Potential = -70mV

This is the electrical gradient between Extra 7 Intracellular fluid

<p>Neurones release neurotransmitters across the synapse </p><p>Transmission through the movement of charged ions across the cell membrane</p><p></p><p>Transmembrane Resting Potential = -70mV</p><p>This is the electrical gradient between Extra 7 Intracellular fluid </p><p></p>
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Voltage Gated ion channels

Closed at rest & play an important role in the generation of action potentials

K+ channels

Sodium potassium pump/ NaKATPase

<p>Closed at rest &amp; play an important role in the generation of action potentials</p><p></p><p>K+ channels</p><p>Sodium potassium pump/ NaKATPase </p>
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K+ channels

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Sodium potassium pump/ NaKATPase

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Post synaptic Potentials

  • Local change in transmembrane potential

  • Not propagated

  • No Refractory

  • Can summate - Add together

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IPSP

Inhibitory Postsynaptic potential

<p>Inhibitory Postsynaptic potential </p>
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EPSP

Excitatory Postsynaptic potential

<p>Excitatory Postsynaptic potential </p>
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Summation of IPSPs & EPSPs

EPSPs synapse mainly on dendrites

IPSPs synapse mainly on cell body

Spatial summation - 2 EPSPs on adjacent membranes add

Temporal summation 2 EPSPs close in time add together

IPSPs / EPSPs can cancel out

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Pre synaptic inhibition

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Peripheral Nervous system

Senses

Somatic:

  • Touch

  • Temp

  • Proprioception

  • Pain

Visceral:

  • BP

  • Internal Temp

  • PH

  • Blood Glucose

Special senses:

  • Smell

  • Taste

  • Hearing

  • Vision

  • Balance

Receptor cells synapse with sensory neurone

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Sensory Pathway

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Somatic Nerves System Pathway

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Nerves system schematic

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Autonomic Nerves system

Subconscious control over internal organs, conditions and homeostasis

EG. HR or Hormones

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Ganglia

Cell bodies of many peripheral autonomic neurons occurring in clusters swell on nerve trunks

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Motor/ Efferent pathways of ANS

Axons that form with ganglionic cells = preganglionic fibres

Axons innervating effector cells = Postganglionic fibres

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ANS Facts

  1. Conveys all outputs from the CNS to the body, other than control of skeletal muscle

  2. Regulates most of homeostasis

  3. The sympathetic and parasympathetic systems work separately

  4. Sympathetic = increase in stress, Parasympathetic = Rest and digest

  5. Influenced by sensory info/ Brain ( control centres)

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Sympathetic Nerves system

Excitement - Adrenaline “ Fight or Flight”

CV response = 89- 155 BPM

Neurotransmitter = Noradrenaline

  • Formed from tyrosine

  • Released across the synapse & taken up by Beta receptors on the postsynaptic cell

<p>Excitement - Adrenaline “ Fight or Flight”</p><p>CV response = 89- 155 BPM</p><p></p><p>Neurotransmitter = Noradrenaline</p><ul><li><p>Formed from tyrosine</p></li><li><p>Released across the synapse &amp; taken up by Beta receptors on the postsynaptic cell</p></li></ul><p></p>
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Other sympathetic pathway

Adrenaline into the blood

<p>Adrenaline into the blood </p>
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Synaptic Receptors

Alpha:

  • Postsynaptic -A1/A2

  • Presynaptic -A1

  • A1 antagonist promotes relaxation

  • A1 Agonist promotes vasoconstriction

Beta:

  • Post synaptic - b1/b2/b3

  • B1 promote heart and muscle function - used for cardiac arrest

  • B2 agonists - Used a as a treatment for asthma - enhance bronchioles

  • B antagonists ( Beta blockers) - Slow heart

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Parasympathetic nervous system

Keeps the body at low energy use

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Parasympathetic contribution to HR

  • Ach (SA node) → M2 receptor = Decreased HR

  • Atrial muscle = Decreased HR

  • AV node = Decreased rate of conduction

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Ach Receptors

  1. Nicotinic - at ganglia/brain/NMJ ( Ionotropic - ion channel receptor controls Na+/K+ transport)

  2. Muscarinic - at autonomic target tissues/brain ( Metabotropic - G protein & 2nd messenger controls k+/Ca+ transport)

  • M1 - Neuronal/gut - Increase gastric acid

  • M2 - Cardiac - Decreased HR/Force

  • M3 - Smooth muscle constriction

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Parasympathetic Neuroeffector pathway

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PNS drugs

Agonists (Increase PNS activity)

  • Pilocarpine

  • Muscarine

  • Nicotine

Antagonists ( Decreased PNS activity)

  • Atropine - Blocks receptors

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Transduction

Converting stimulus into electrical signals

Activation of receptors = movement of ion channels

Sensory neuron - Action potential

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Mechanoreceptors

  • Mostly located on the skin / visceral organs

  • Stimuli = Physical distortion

Free nerve endings

Ruffini corpuscles

Pacunian corpuscles

Merkles disk

Meisser corpuscles

Free nerve endings

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Thermoreceptors

  • Mostly on the skin

  • Stimuli = Temperature

Free nerve endings

  • TRPV1 = Hot

  • TRPV8 = Cold

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Nociceptors

  • Mostly on skin

  • Potential to cause tissue damage (stimuli)

Free nerve endings

  • mechanical, thermal, chemical

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Proprioreceptors

  • Location: Muscles, tendons, ligaments & joints

  • Stimuli = Muscle tension

Subtypes:

  • Muscle spindles

  • Golgi tendon organs

  • Proprioreception in joints

<ul><li><p>Location: Muscles, tendons, ligaments &amp; joints</p></li><li><p>Stimuli = Muscle tension</p></li></ul><p>Subtypes:</p><ul><li><p>Muscle spindles </p></li><li><p>Golgi tendon organs</p></li><li><p>Proprioreception in joints</p></li></ul><p></p>
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Cardiac pumps

Right ventricle = Pulmonary circulation

Left ventricle = Systemic circulation

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Cardiac output

HR x SV

Rest = 5L

Exercise = 12.5 - 30L

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CV response to Exercise

  • Increase venous return due to CO increase/ Compression of veins from skeletal muscle

  • Increased SNS activity

  • Decreased PSNS activity (increased HR)

  • Cardiac hypertrophy from prolonged training (LV enlarges /SV increases)

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Aorta/ Large arteries

  • Thich walls

  • Highly elastic

  • Role = distribution - High pressure - propulsion

<ul><li><p>Thich walls</p></li><li><p>Highly elastic </p></li><li><p>Role = distribution - High pressure - propulsion </p></li></ul><p></p>
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Arterioles

  • Thick walls

  • Muscular

  • Role = Tissue distribution, variable resistance

<ul><li><p>Thick walls</p></li><li><p>Muscular</p></li><li><p>Role = Tissue distribution, variable resistance</p></li></ul><p></p>
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Capillaries

  • Single cell thick

  • Lack of elastin/ muscle

  • Functional for exchange

<ul><li><p>Single cell thick </p></li><li><p>Lack of elastin/ muscle</p></li><li><p>Functional for exchange</p></li></ul><p></p>
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Veins & venules

  • Thin walls

  • Some muscle

  • Valves

  • Reservoir = 60% of blood

<ul><li><p>Thin walls</p></li><li><p>Some muscle</p></li><li><p>Valves</p></li><li><p>Reservoir = 60% of blood</p></li></ul><p></p>
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Equations - Flow rate, velocity & TPR

Flow rate = volume/ unit time

Peripheral res = pressure dif/flow

Velocity = Distance/ unit time

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Cardiac excitation

  • Action potential generated at the SA node

  • Rapid excitation of both atria

  • Reaches AV - slows conduction ( Allows atria to contract/ Ventricle emptying)

  • Excitation down BOH & Purkunje fibres to ensure activity of ventricular cells

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Poiseulle’s law

Factors that affect flow through a vessel:

  • Pressure (pi - po)

  • Length (L)

  • Radius (r4 )

  • Viscosity (n)

<p>Factors that affect flow through a vessel:</p><ul><li><p>Pressure (pi - po)</p></li><li><p>Length (L)</p></li><li><p>Radius (r<sup>4</sup><sub> </sub>)</p></li><li><p>Viscosity (n)</p></li></ul><p></p><p></p><p></p>
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SA node

SA node = Pacemaker - Creates its own action potential for the heart

8mm long/2mm thick - in the right atrial wall

Phases:

0 - Upstroke of action potential is less steep than in myocytes

3 - Plateau is not sustained

4 - Membrane potential deviates from k+ potential

Action potential in SA:

  • Slow depolarisation - Na influx, ca influx, reduced K+ efflux

  • Rapid depolarisation - Ca efflux

  • Repolarisation - K+ Exflux

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Cardiac Contraction

  1. Atrial systole

  • Av valves open + blood into ventricles

  • Atria excitation should be complete before ventricular contraction

  1. Ventricular systole

  • Ventricles contract - pressure increase closes av valves

  • Pressure in ventricles rises above aortic pressure - aortic valve opens + Blood pumped out

  1. Ventricular diastole

  • Pressure falls in ventricles ( Below aortic) - Aortic valves close

  • Pressure continues to fall below atrial pressure - AV valves close

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ECG

4 Events - 3 visable

  1. Arterial depolarisation (P wave)

  2. Ventricular depolarisation ( Masks atrial repolarisation) ( QRS)

  3. Ventricular repolarisation ( T wave)

<p>4 Events - 3 visable </p><ol><li><p>Arterial depolarisation (P wave)</p></li><li><p>Ventricular depolarisation ( Masks atrial repolarisation) ( QRS)</p></li><li><p>Ventricular repolarisation ( T wave)</p></li></ol><p></p>
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Systolic BP

The force the heart exerts on the walls of arteries every time it beats

120mmHg

Determined by:

  • SV - Increased SV = Increased SBP

  • Decreased Aortic elasticity = Increased SBP

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Diastolic BP

Pressure in the arteries during the period when the heart is not beating

80mmHg

Determined by:

  • Increased TPR = Decreased DBP

  • Decreased Aortic elasticity = Decreased DBP

  • Decreased HR = Decreased DBP

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Key measurements of BP

SV = EDV - ESV

CO = HR x SV

Pulse pressure = SBP - DBP

Mean BP = DBP x 1/3 Pulse pressure

Flow ( CO) = Mean BP/TPR

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Why is BP control important

  • Too low = Inadequate supply of o2 to tissues

  • Too high = Excessive strain on heart / increased damage to vascular tissue

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NEXT TOPICS

INFLUNCE BP HR etc EFFECTOR MECHANISM, Detereminaents of blood flow. High bp. Map = co x TPR

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