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Human Physiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Describe the origins of a neuron.

A

Arisen from multifunctional cells gradually becoming more specialized
Organisms with the ability to detect, other able to monitor and respond, came together with a wiring system connecting these parts
Wiring is the neuron

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2
Q

What is the purpose of the nervous system?

A

To communicate and control with the network of neurons
Uses sensory neurons (afferent), central nervous system (brain and spinal cord) and efferent neurons

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3
Q

Interneurons

A

All of the pieces and structure within the central nervous system (brain and spinal cord), makes up 99% of all neurons

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4
Q

What are the parts of a neuron? Describe

A

Dendrites- receiving end
Cell body (soma)- contains nucleus and other organelles
Axon- sends signals away from cell
Axon terminals- where neurotransmitters are released and stored
Axon hillock- trigger zone, forms action potential

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5
Q

What are the support cells in the nervous system called?

A

Glial cells or Neuroglia

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6
Q

What glial cells form the myelin sheath and how?

A

Schwann cells in peripheral and Oligodendrocytes in the central nervous system
Wrap themselves around the axon

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7
Q

Myelin sheath

A

wrapped around axon to protect and insulate, not all neurons have them but the ones that do propagate action potentials more rapidly

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8
Q

What glial cells form barriers between compartments? Describe how it works

A

Astrocytes and ependymal in central
Create a blood/brain barrier- surround a blood vessel in the brain to protect a toxin from getting to the nervous cells

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9
Q

What glial cells are in charge of clean up? what are they made of and what do they look for?

A

Microglia
modified immune (white blood) cells
Dead cells, metabolic waste

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10
Q

What is the membrane potential at rest of a neuron?

A

-70 mV

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11
Q

What are the two mechanisms of membrane potential and describe?

A

Sodium Potassium Pump- biggest factor, establishes a concentration gradient generating negative potential.
Leak channels- always open, allows Na+ to move back in and K+ to move back out, there is more K+ leaving than Na+ coming back in because there is more potassium channels

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12
Q

Depolarization

A

When movement reduced charge separation/imbalance, approaching neutrality (zero) from the resting potential

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13
Q

Repolarize

A

Movement back toward resting potential, getting more negative

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14
Q

Hyperpolarization

A

development of more negative charge inside the cell, going past resting

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15
Q

Overshoot

A

inside of the neuron becomes positive when Depolarizing

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16
Q

Synapse

A

space between the two neurons where the electrical activity one neuron influences the activity of the other.

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17
Q

Describe Graded potentials

A

When a chemical signal binds to the post-synaptic cell a response is initiated
Produced by the opening of Ligand gated channels producing an electrical charge by the flux of sodium ions. As graded potentials travel they lose strength.

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18
Q

What does the effect of the graded potential depend on? What charge must it have?

A

The strength of the graded potential when it reaches the trigger zone
It must be -55 mV at the threshold to trigger an action potential or a sub-threshold response will be triggered

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19
Q

What are the two types of graded potentials and describe them

A

EPSP- excitatory, bring closer to threshold increasing the chance of an action potential, caused by the opening of ligand gated channels, depolarization
IPSP- hyperpolarization, suppresses the cell making it harder to get an action potential, caused by opening of K+ ligand channels casuing K+ to leave the cell

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20
Q

Define summation, why its needed, list the two types and describe

A

Addition of multiple graded potentials, and additive effect
Rarely can one excitatory graded potential reach threshold
Temporal- graded potentials from the same neuron, occurring over a short time and added together
Spatial- multiple neurons separated by space producing graded potentials at the same time and adding together

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21
Q

What are the steps of an action potential

A
  1. Graded potential above threshold reaches trigger zone
  2. Voltage gates Na+ channels open and Na+ enters the axon, depolarizing the membrane, triggering release of more Na+ channels as it spreading into the negative parts of the cell.
  3. Voltage gated K+ channels open slowly, allowing K+ out as Na+ gates close, repolarizing the membrane
  4. K+ gates stay open hyperpolarizing the membrane
  5. K+ gates close but K+ can still exit through leak channels
  6. Cell returns to resting potential
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22
Q

What is the refractory period, What is its purpose?

A

Reduces the excitability of a neuron, reducing the tendency for an action potential and assures one way propagation of action potentials

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23
Q

Absolute refractory

A

Zero chance for an action potential, inactivation gates are closed, unresponsive to stimulus, the channels are already open

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24
Q

Relative refractory

A

reduced excitably but can get second action potential, would need a stronger graded potential to counteract the hyperpolarization

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25
Q

Saltatory Conduction

A

Action potentials jump from one node to the next as they propagate along a myelinated axon

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26
Q

Nodes of Ranvier

A

Gaps between the myelinated portion of the axon where bare axon is showing
This is the only place where action potentials occur in myelinated neurons

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27
Q

What is conduction velocity and what effects it?

A

Speed of conduction
Myelination- precent is faster than absent
Diameter of axon- increasing the diameter increases the velocity by reducing resistance of ion flow

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28
Q

What are the two types of synaptic transmission?

A

Electrical-uses gap junctions, very fast
Chemical- synaptic cleft, most common, slightly slower

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29
Q

Electrical synapse

A

Permits the flow of electrical signals form the pre to post synaptic neuron across gap junctions.

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30
Q

Gap Junctions and what forms them?

A

Integral membrane proteins that physically connects the cytoplasm of two cells, ions are able to flow directly through.
Connexons- proteins

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31
Q

Chemical synapse and steps

A

action potential reaches terminal triggering release of neurotransmitter form pre-synaptic neuron
1. Action potential depolarizes the axon terminal where neurotransmitters are stored in vesicles
2. Depolarization opens voltage gated Ca ion channel and Ca ions enters the cell (will always be calcium at the axon terminal)
3. Calcium entry triggers exocytosis of synaptic vesical contents by vesicles moving to membrane and anchoring at docking proteins (Synaptotagmin) and wrapped up b SNARE proteins.
4. Neurotransmitter diffuses across synaptic cleft and binds to receptors on postsynaptic cell
5. Neurotransmitter binding (ligand gated channel) initiates a response in post synaptic cell

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32
Q

Classes of Neurotransmitters with examples

A

1.Acetylcholine- most common, muscle contraction, receptors: Muscarinic- GPCR, Nicotinic- ligand gated ion channels
2.Biogenic Amines- Catecholamines derived from tyrosine (dopamine-reward pathway, norepinephrine-alertness, epinephrine-hormone), Serotonin derived from tryptophan mimicking dopamine
3.Amino Acids- glutamate (EPSP), GABA (IPSP), Glycine (IPSP)
4.Neuropeptides- proteins (85) endogenous opioids (beta-endorphins, dynorphins(stimulation), Substance P (pain transmission))
5. Miscellaneous- purines(ATP), gases(NO, carbon monoxide), lipids(prostaglandins), Cannabinoids (anandmide- high affinity for THC)

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33
Q

Nicotine

A

Acetylcholine receptor agonist, stimulant leading to the production of: Norepinephrine (alternes), Dopamine (reward pathway), Beta endorphins (lower anxiety), crosses the blood brain barrier within 10-20 seconds, metabolizing in the liver

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34
Q

MAO

A

Monoamine oxidase
Breaks down Catecholamines
MAO inhibitors- prevents the breakdown
ex: Hydrazine, Nardil, Niamid - treat depression/anxiety

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35
Q

SSRI

A

Slow the reuptake of serotonin, allowing it to remain in synapse for longer
Prozac, Paxil, Celaxa - treat anxiety and depression
Much more specific

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36
Q

Benzos

A

Xanax, Valium, Ambien - reduce anxiety, induce sleep, Anti-seizure
Bind to GABA receptor to induce chloride flux (does not mimic GABA), changes the activity for the receptor, creates hyperpolarization inhibiting effects

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37
Q

Sympathetic vs parasympathetic

A

Both regulate involuntary bodily activates
Has two neurons- preganglionic (acetylcholine), postganglionic
Para- governs bodily activities during restful conditions, rest and digest, post: acetylcholine-short, released from cranial nerves or sacral region
Sym- fight or flight, prepares the body for stressful or emergency situations, pre: norepinephrine/adrenaline -long, thoracic and lumbar.

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38
Q

Synaptic plasticity

A

Change in strength over time and formation of new synapses, strengthen increases graded potential increasing amount of action potential

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39
Q

Long-term potentiation

A

Occurs in the hippocampus, long lasting enhancement of synaptic transmissions following stimulation, changes take place on post-synaptic neuron, stronger graded potential

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40
Q

AMPA

A

Glutamate receptor, Result in EPSP, glutamate binds to ligand gates channel, triggering response

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41
Q

NMDA

A

Glutamate receptor, At rest blocked by Mg ions, post-synaptic cell mush be depolarized to (0 mV) to function, when open allow Ca ion to enter, Ca ion channel

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42
Q

Long-term potentiation mechanism

A
  1. depolarization of post-synaptic cell (AMPA)
  2. Removes Mg ions form NMDA receptor
  3. Ca ion flux into neuron
  4. Phosphorylation and insertion of additional AMPA receptors
  5. Increased amplitude of synaptic response (more likely to cause an action potential)
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43
Q

What is the role of Calcium in LTP

A

induces gene expression and protein synthesis, results in the structural modification of the synapse
Growth or decay of dendric spines

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44
Q

Doogie Mouse

A

Genetically engineered mice that over express NMDA, more LTP because more Ca ions enter the receptors.

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45
Q

What causes migraines?

A

imbalance of brain chemistry, specifically Low levels of serotonin

46
Q

CSD, what region does it target specifically?

A

Cortical spreading depression
A wave of altered electrical energy that occurs before the pain phase
Causes a release of inflammatory mediators leading to irritation of the cranial nerve roots and trigeminal nerve which conveys sensory information
Causes auras, and hypersensitivity to stimulus from an inflammatory response

47
Q

How do inflammatory agents play a role in migraines?

A

If they can be identified and blocked it can reduce or stop this hypersensitivity
Specifically, CGRP (Calcitonin gene-relates peptide) that causes CSP and hypersensitizes the cranial nerves

48
Q

What is the new therapeutic treatments for migraines?

A

Aimovig. TEV-48125
A monoclonal antibody used to bind and neutralize to motivate the immune system to attack CGRP
Individuals didn’t have migraines for 6 months

49
Q

What is a stroke? What is another name for it? What happens?

A

Loss of brain function due to a disruption of blood flow to a portion of the brain
Cerebrovascular accident
Neurons are deprived of oxygen and glucose causing the inability to produce ATP, happen as fast as 60-90 seconds and within an hour irreversible damage can occur

50
Q

What are the two types of strokes

A

Hemorrhagic- rupture in blood vessel in brain that prevents vessels downstream from getting the blood supply they need, minority
Ischemic- clot/blockage in the vessel from plague forming, genetics, diet, exercise play a role, responsible for 80% of strokes

51
Q

What causes the damage in a stroke? How does it happen?

A

Glutamate Excitotoxicity
Lack of blood prevents the removal/breakdown of glutamate in the synapse. Excess causes Ca ions to enter the cell (Glutamate is an ion channel for Na and Ca channels), excess Ca ions in the cell cause apoptosis

52
Q

What are some stroke risk factors and treatments?

A

Advanced age, hypertension, diabetes, high cholesterol, smoking, migraines, previous stroke
Clot busters (thrombolysis), therapy’s, antiplatelet drugs, anticoagulants and statins

53
Q

What is the pathology behind Multiple sclerosis?

A

An autoimmune disease that results in the destruction of the myelin sheath and T lymphocytes destroy oligodendrocytes. Can cause slower propagation or damage to the axon
Reduces sensory and motor impulses to and from the CNS

54
Q

What are the different classifications of MS?

A

Benign- regular flare ups, weak, with some increase of level of disability during but after it is over it does not remain
Relapsing Remitting- flares are stronger, accumulating disability that lasts afterwards (most common)
Primary Progressive- exponential growth of disability, difficult to treat
Secondary Progressive- combination, starts with relapsing remitting and results in progressive

55
Q

What is Huntington’s and what is its pathology?

A

A progressive neurodegenerative disease caused by an autosomal dominant mutation (need one copy of mutation to get it) to the Huntingtin gene
It is caused by an excess in CAG in the gene known as a trinucleotide repeat

56
Q

What protein is misfolded in Huntingdons? What is the protein aggregate?

A

HTT protein
Inclusion bodies (clumping of proteins)

57
Q

What happens in a protein aggregation disorder?

A

Proteins become misfolded due to exposed hydrophobic portions of the protein. These regions of clump to other misfolded proteins, can lead to apoptosis.

58
Q

What is a signature symptom of Huntingtons?

A

Chorea- uncontrollable jerking

59
Q

Describe Parkinsons and its pathology

A

Degenerative disorder resulting from the death of dopamine producing neurons within the brain’s movement control center
Protein aggregation disorder
issues with alpha synuclein which may be associated with vesicles that haul dopamine in the axon terminals like a docking protein

60
Q

What is known as the brain’s movement control center that is affected by Parkinsons?

A

Substantia Nigra

61
Q

What is misfolded protein in Parkinsons? What is the protein aggregation?

A

alpha synuclein
Lewy body

62
Q

Describe Alzheimer’s and pathology

A

Progressive, neurodegenerative disease caused by the death of acetylcholine-producing neurons in regions of the brain important in memory and intellectual function
Protein Aggregation disorder
Amyloid precursor protein gets chopped up to form Amyloid Reta. An accumulation of this protein occurs because it can’t be broken down as fast as it is being made. Extracellular plaques are formed form bunched up protein that kills the neurons

63
Q

What are the misfolded proteins in Alzheimer’s?
What are the Protein aggregations?

A

Amyloid beta, Tau
Amyloid Beta plaques and neurofibrillary tangles

64
Q

What are the 5 classes of sensory receptors and what they are triggered by?

A
  1. Mechanoreceptors- mechanical touch
  2. Thermoreceptors- temperature
  3. Photoreceptors- light
  4. Chemoreceptors- foreign chemicals, internal chemicals
  5. Nocioreceptors- itch and pain
65
Q

Sensory Unit

A

Single sensory neuron and all its receptive endings

66
Q

Receptive Field and how it relates to sensitivity

A

Area of the body that when stimulated leads to activity in an afferent neuron (sensory unit)
More sensitive areas have smaller receptive fields and more dense sensory units

67
Q

Sensory adaptation

A

reduction in response to the continuous presence of a stimulus, preventing sensory overload
Prioritizes new stimulus

68
Q

Lateral inhibition

A

Sharpens contrast in the pattern of action potentials received by the CNS, allowing a finer resolution of stimulus location

69
Q

List Mechanoreceptors, a description and their quickness of adaptation

A

Merkel disks-receive touch stimulus, anything that moves the hair triggers response (slow adapting)
Meisser’s corpuscles- modified nerve ending, touch moves it and channels open (fast adapting)
Pacinian corpuscles- respond to initial pressure, detect deep pressure and vibration (fast adapting)
Ruffini corpuscles- respond to continuous pressure (slow adapting)

70
Q

Define Kinesthesia and what it is detected by

A

Body and limb position (tonic activity)
Muscle spindles- stretch of a muscle, modified muscle fibers, more stretch and more rapid the fire.
Golgi tendon organs- measures muscle tension, the greater the more the firing

71
Q

Tonic Activity

A

constantly firing activity even without stimulation, simulation only alters the firing.

72
Q

What is the role of Substance P and Opioids in Nocioception?

A

Substance P- sends pain signals to the brain
Opioids- block release of substance P

73
Q

Steps of the Gate Control model of Pain Transmission

A
  1. In absence of input form C fiber, a tonically active inhibitory interneuron suppresses pain pathway.
  2. With strong pain, C fiber stops inhibition of the pathway, allowing a strong noxious signal to be sent to the brain.
  3. Pain can be diminished by simultaneous somatosensory input (touch pathway stimulating gate keeper)
74
Q

Referred Pain

A

The sensation of pain at a site other than the injured or diseases tissue caused by sensory convergence confusing the brain

75
Q

Somatosensory cortex
What diagram describes this?

A

Stimulus comes through the thalamus to the parietal lobe to this area where amount of space devoted to each body part is proportional to the sensitivity of that part.
Large for face, hands, fingers
Small for legs and torso
Homunculus

76
Q

Describe the accommodation of the eye

A

The changing of the shape of the lens to focus incoming light so it properly strikes the retina
Ciliary muscles determine the amount of tension of the lens, less tension= more rounded
Zonular Fibers stretch lens to flatten it and it anchors the lens in place, tension is determined by the ciliary muscles

77
Q

Describe how the eye accommodates to see close objects vs far objects

A

Close: rounded lens, ciliary muscles contract, ligaments loosen
Distant- flattened lens Ciliary muscles relax, ligaments to lens stretch.

78
Q

Myopia

A

Nearsightedness
eye is elongated, close objects clear, distant objects out of focus, light is focused on front of retina

79
Q

Hyperopia

A

Farsightedness
Eye is not deep enough, distant objects seen clearly, close objects out of focus, light it focuses behind retina

80
Q

Astigmatism

A

Irregular curvature of the eye causing a scattering of light leading to blurred vision

81
Q

Presbyopia

A

Progressive diminished ability to focus on objects caused by reduced elasticity of the lens, inability to change the shape of the lens

82
Q

Cataracts

A

Lens has become cloudy due to aging caused by the clumping of denatured proteins

83
Q

Glaucoma

A

Pressure caused by cells in the anterior chamber producing aqueous humor and it not getting drained by the canal of Schlemm due to a blockage. This causes pressure to vitreous humor and causes damages retinal cells
Leads to tunnel vision

84
Q

Describe the structure of the retina

A

Light places past the ganglion cell, Amacrine cells, bipolar cells, horizon cells, the rods and cones where excess is absorbed by the pigmented epithelium layer

85
Q

Cone purpose

A

photoreceptor that allows for colored vision and an abundance of light is needed to activate.

86
Q

Rod purpose

A

photoreceptor that allows for monochromatic vision (black/grey/white)
more light sensitive than cones

87
Q

Anatomy of rods and cones

A

Synaptic terminal with bipolar cells, intersegment (typical cell stuff, organelles), outer segment with membrane folds called photo disks, pigment epithelium

88
Q

Photopigments, what they are made of

A

Within the photo disks
Made of opsin which holds in place retinal, the photosensitive molecule of the eye

89
Q

What occurs in the rods and cones in the dark?

A

Retinal is bound to opsin
High levels of cGMP
Promotes opening of sodium channels causing sodium to enter and depolarize the cell
Cell is tonically active (constantly releasing neurotransmitter)

90
Q

What occurs in rods and cones in the light? Recovery phase

A

Light causes photo bleaching which changes the shape of retinal causing opsin to release it
Activates transduction which lowers cGMP levels
Sodium ion channels close, reducing membrane potential
Less neurotransmitter is released
(Light suppresses electrical activity, hyper polarization)
Retinal is released into the pigmented epithelium and is slowly recombining with opsin (delayed night vision)

91
Q

What causes loudness and pitch?

A

Loudness- size of waves (amplitude), louder sounds mean larger waves
Pitch- wave frequency, high voice=more waves

92
Q

Structures of the ear and its main parts

A

External ear- air filled, pinna- funnels sound waves into the ear canal, tympanic membrane- separates external and inner ear (ear drum)
Middle ear- air filled, 3 smallest bones (Malleus, Incus, Stapes), vibrate in characteristics of sound
Inner ear- fluid filled, fluid filled waves caused by oval window in the cochlea

93
Q

What is the structure and function of the organ of corti?

A

Basilar Membrane- anchor and support
Hair cells-the sensory cells that move, opening/closing mechanically gated ion channels, triggering the flux of Potassium into the cell, triggering action potentials
Tectorial membrane-thick membrane structure that moves bends the hairs
Takes the sound waves and converts them into action potentials triggering a response in the brain

94
Q

Steps of sound transmission

A
  1. Sound waves strike the tympanic membrane and become vibrations
  2. Sound wave energy is transferred to the three bones of the middle ear which vibrate
  3. The stapes is attached to the membrane of the oval window, the oval window creates fluid waves within the cochlea
  4. The fluid waves push on the flexible membranes of the cochlear duct. Hair cells bend and release neurotransmitters
  5. Neurotransmitters release onto sensory neurons creates action potentials that travel through the cochlear nerve to the brain
95
Q

How does the ear determine sound pitch?

A

Any pitch (frequency) causes vibrations of only a given segment of the basilar membrane and activation of those hair cells
Thicker portion (closest to oval window) - high pitch sensitivity
Flat/sheet like portion- low pitch sensitivity

96
Q

What are the two types of hearing loss?

A

Conductive- blockages of signal transduction form external canal to organ of Corti (damage to ear drum, infection causing swelling)
Sensorineural- damage to hair cells (cannot be replaced) or vestibulocochlear nerve (loud noises)

97
Q

Vestibular system

A

Detects changes in the motion and position of the head by the use of fluid-filled tubes near each ear. This system is connected to the cochlear duct
Other half of the inner ear

98
Q

List the pieces of the vestibular apparatus

A

Semicircular canals, ampulla, cupula, utricle, saccule, macula, otoliths

99
Q

What are the semicircular canals

A

Posterior- tilt of head towards right or left shoulder
Superior canal- rotation of head front or back
Horizonal- rotation of head left or right

100
Q

Ampulla

A

Boney structure at the base of the semicircular canals

101
Q

Cupula

A

Within Ampulla
Fluid in duct bends the cupula, bending stereocilia, opening channels to allow potassium to flow into the cells

102
Q

Part of the vestibular Apparatus involved with special awareness?

A

Utricle and Saccule have same structure and function

103
Q

Macula

A

Inside Utricle and Saccule
contains hair like cells but is flatter and sheet like
Continas otoliths

104
Q

Otoliths

A

Calcium carbonate crystals within the macula that move the hair cells, opening and closing the ion channels
Moved by gravity and acceleration

105
Q

What causes positional vertigo?

A

When eyes and vestibular apparatus don’t get the same information
An otolith crystal can become dislodged, and it can move through the inner ear, triggering the movement of hair cells even when you are stationary

106
Q

Meniere’s disease

A

reoccurring vertigo, ringing, nausea, fullness of ears caused by excess endolymphatic fluid (Endolymphatic Hydrops) and causing pressure in the semicircular canals and the cochlea.

107
Q

Pathway from vestibular apparatus to brain

A

Vestibular branch of vestibulocochlear nerve to cerebellum or cerebral cortex

108
Q

What are the 5 well characterized tastes and receptor type?

A

Salt Sour - leak/ion channel
Bitter sweet Umami - GCPR

109
Q

Gustatory transduction

A

interaction of tastant molecules in saliva with the receptor cells in the taste buds on the papillae of the tongue; these receptors cells undergo only graded potentials

110
Q

Olfactory receptors

A

neurons with long cilia covered by mucus located in the roof of the nasal cavity
Odorants dissolve in the mucus and bind to the receptors casing the opening of ion channels leading to stimulation that is relayed to the olfactory bulb in the brain

111
Q

What is the structure of a taste bud?

A

taste pore on top, taste cell within, basal cells towards bottom, Gustatory afferent nerve on bottom

112
Q

Structure of Olfactory receptor

A

Olfactory bulb closest to brain, separated by a bony plate, Olfactory receptor cell bodies, and a mucus layer that bind to receptors entering the nasal cavity

Human Physiology (4 decks)

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