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A&P Lecture > "Exam 4" > Flashcards

"Exam 4" Flashcards

1
Q

Conscious Processing

A

Special Senses (vision, hearing, taste, smell, equilibrium)
Somatic senses (touch, temperature, pain, itch, proprioception)

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2
Q

Proprioception

A

3D awareness, sense of body in space around us

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3
Q

Subconscious processing

A

Somatic stimuli (muscle length, tension, proprioception)
Visceral stimuli (BP, GI stretch, blood glucose, core body temp, osmolarity, pH)

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4
Q

Common elements of sensory pathways

A

Stimulus in the form of physical energy (heat, chemical conc., light, sound)
Sensory receptor- converts stimulus to electrical signal (sub-threshold or threshold)

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5
Q

Simple receptors

A

Have free nerve endings (diagram on slide 369)

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6
Q

Complex Receptors

A

Have endings enclosed in connective tissue (diagram on slide 369)

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7
Q

Special Senses Receptor

A

Release NT onto neurons (diagram on slide 369)

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8
Q

4 types of sensory receptors

A

Chemoreceptors, mechanoreceptors, photoreceptors, thermoreceptros

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9
Q

Chemoreceptors

A

Oxygen, pH, various organic molecules like glucose

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10
Q

Mechanoreceptors

A

Pressure, cell stretch, vibration, acceleration, sound

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11
Q

Photoreceptors

A

Photons of light

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12
Q

Thermoreceptors

A

Varying degrees of heat

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13
Q

Transduction

A

Sensory neurons converting physical stimuli to electrical signal
Physical/chemical signal usually opens ion channels and change membrane potential –> lead to graded potential

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14
Q

Convergent Receptive fields

A

Large. Receptive fields of multiple primary sensory neurons overlap to form one large secondary receptive field.
Sum of primary neuron stimuli on secondary neuron to reach threshold and send AP
Found in legs, trunk, arms…

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15
Q

Small recepetive fields

A

Fewer neurons converge, secondary receptive fields are much smaller. One or 2 primary neurons per each secondary neuron.
Found in skin, nose, hands, mouth, spinal cord…

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16
Q

Simple Receptive field

A

One primary sensory neuron synapses onto one secondary neuron
Smaller but more sensitive

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17
Q

Complex Receptive fields

A

Convergent, multiple presynaptic neurons provide input to smaller number of postsynaptic neurons
Larger but less sensitive

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18
Q

Where do spinal cord afferents go

A

Thalamus and then sensory cortex (Diagram slide 405)

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19
Q

Where do special senses go

A

Directed to sensory area like vision cortex (Diagram slide 405)

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20
Q

Perceptual threshold

A

The stimulus intensity necessary for you to be consciously aware of it

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21
Q

Habituation

A

When your brain decreases perception of the stimulus, tune out

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22
Q

Why do we have habituation

A

Efficiency, we have so much to take in we have to pick our battles.

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23
Q

What sense is the only one that does not go through the thalamus

A

Olfactory (Nose)

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24
Q

4 properties of a stimulus for CNS to distinguish

A

Modality, Location, Intensity, Duration

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25
Q

Modality

A

the TYPE of stimulus
touch vs. pain vs. temperature
Labeled-line coding

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26
Q

Labeled-line coding

A

A cold receptor always perceives cold, pain receptor doesn’t send temperature info

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27
Q

Location

A

Where the stimulus originated, depends on receptive field that is activated
Receptors project to specific area of sensory cortex
Lateral inhibition

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28
Q

Lateral Inhibition

A

Isolates the stimulus and increase the sensitivity (contrast) of the signal (diagram slide 407)
Occurs at secondary level
“Noise cancelling headphones”

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29
Q

Intensity

A

Population coding- # of receptors activated
Frequency coding- frequency of action potentials being sent

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30
Q

Duration

A

Duration of AP. Too much info can be disruptive so receptors adapt and dismiss some senses/info
Tonic and Phasic receptors

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31
Q

Tonic receptors

A

Slowly adapting receptors
Fire rapidly at first and then slow down but maintain firing of AP; never turn off
Used for things that constantly need monitoring
Ex: BP, breathing

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32
Q

Phasic Receptors

A

Rapidly adapting receptors
Fire rapidly but cease firing if strength remains constant
Ignore info once it is perceived; turn off
Ex: pain

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33
Q

Sensory receptor overview

A
  1. each receptor is sensitive to particular type of stimulus
  2. A stimulus above threshold indicates AP in a sensory neuron that projects to the CNS
  3. Stimulus intensity and duration are coded in the pattern of APs reaching CNS
  4. Stim location and modality are coded according to which receptors are activated by the timing of activation
  5. Each sensory pathway projects to a specific region of the cerebral cortex dedicated to its particular receptive field.
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34
Q

Four somatic senses

A

Touch, temperature, Nociception (pain), Proprioception (spacial awareness)

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35
Q

where are receptors for somatic sensation found

A

Skin and viscera
Secondary neurons cross the midline in SC or brain stem

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36
Q

Somatosensory cortex

A

Thalamus relays secondary neurons here, recognizes stimulus origin, can be reorganized after loss of digit/limb
The amount of space in the somatosensory cortex devoted to each part of the body is proportional to the sensitivity of that part

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37
Q

The types of physical contact touch receptors respond to and touch receptors structure

A

Stretch, steady pressure, fluttering, vibration, texture
Receptors Structure: Free nerve endings or encapsulated in connective tissue
Skin, hair, under skin

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38
Q

Temperature receptors

A

Free nerve endings embedded in skin
Cold: temps below 37C
Warm: Temps between 37-45C
above 45C activates pain receptors

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39
Q

Nociceptors

A

Free nerve endings that respond to harmful/noxious stimuli (chemical, mechanical, thermal)
Found in Skin, joints, muscles, bones, and some internal organs but not in CNS
Afferent signals carried to CNS by A-delta or C-fibers

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40
Q

A-delta nociceptor

A

faster, myelinated fibers
more intense pain

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41
Q

C-fibers nociceptor

A

slower, unmyelinated
Dull pain

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42
Q

Pain

A

Subjective perception begins with nociceptors
Individual and multidimensional
May vary along with emotional state

43
Q

Fast Pain

A

Sharp, localized pain rapidly transmitted to CNS by A-fibers
ex: sharp initial pain when you stub your toe

44
Q

Slow pain

A

Dull and more diffuse pain transmitted by C-fibers
ex: dull throb after stubbing toe

45
Q

Itch

A

Derived from nociceptors (c-fibers)
antagonistic action against pain, scratching an itch interrupts the itch

46
Q

Chemical effect on nociceptor

A

enhance or dampen
Histamine, K, prostaglandins, substance P will enhance pain (inflammatory)

47
Q

Integration of nociception

A

Spinal reflex pathway
Information does not reach bain
ex: withdraw hand when touch hot

48
Q

Visceral deep pain

A

often poorly localized, hard for brain to tell where pain is coming from
Referred pain: visceral and somatic sensory pain input converges on a single ascending tract

49
Q

Chronic

A

More than nociceptor activation, involves damage and long-term nervous system change

50
Q

Gate-control therapy

A

Pain of modulation
AB fibers synapse on and increase inhibitory neuron activity
Reduces pain sensation
Ex: rubbing pain area to make something feel better
(Diagram slide 425)

51
Q

Autonomic Nervous System

A

Efferent division
Controls smooth & cardiac muscle, many glands
Involuntary system

52
Q

Somatic Motor Nerves

A

Control skeletal muscle
Voluntary system

53
Q

Know the sympathetic vs. parasympathetic effect on select tissue type

A

Diagram slide 433

54
Q

Major subdivisions of ANS

A

Sympathetic- dominant during stress or exercise
Parasympathetic- dominant at rest/during sleep
Balance of both

55
Q

Autonomic control by hypothalamus, pons, and medulla (brain stem)

A

Control centers that receive sensory input
Monitor parameters
Ex: osmolarity, body temp, BP, breathing

56
Q

Autonomic control by Cerebral cortex and limbic (emotion)

A

System can send commands to control centers

57
Q

Autonomic control by spinal cord

A

Mediates some ANS reflexes without brain input
Ex: urination, defecation, arousal

58
Q

Antagonistic control

A

Opposing effects
SNS increase HR while PNS decreases

59
Q

ANS displaying 4 of Canon’s Postulates

A
  1. Preserves fitness of internal enviro
  2. Up/down regulation of tonic control
  3. Antagonistic control
  4. Chemical signals used with different effects on different tissues
60
Q

Preganglionic neurons

A

Originate in CNS project to the autonomic ganglion

61
Q

Postganglionic neurons

A

Originate in the ganglion, project to the target tissue (ANS Ganglion can act as integrating center)
(Diagram slide 439)

62
Q

Divergence in ANS

A

1 preganglionic neuron to synapse on 8-9 postganglionic neurons (up to 32)
Allows for 1 CNS command to control several target tissues

63
Q

Sympathetic pathway Anatomy

A

Originate in thoracic and lumbar regions of spinal cord, ganglia lie close to spinal cord
Short preganglionic, long postganglionic

64
Q

Parasympathetic pathway anatomy

A

Originate in brain stem and sacral regions of spinal cord
ganglia lie close to target tissue
Long preganglionic, short postganglionic

65
Q

Sympathetic postganglionic NT vs. Parasymp

A

Symp: Norepi to an adrenergic receptor
Parasymp: ACh to muscarinic receptor
(diagram slide 442)

66
Q

Neuroeffector Junction

A

The synapse between a postganglionic Autonomic neuron and target cell
The structure is atypical compared to regular neural synapse

67
Q

Varicosities

A

ANS postganglionic axons modified into a series of swollen bulbs that release neurotransmitter
Covers large area
Chemicals can influence activity

68
Q

Synthesis and release of ANS NT

A

NT synthesized in varicosity
Depolarization of varicosity opens calcium channel
Calcium influx triggers vesicle release
NT binds to receptor and triggers response
NT removed like normal (taken back in, diffuse away, degraded)

69
Q

Sympathetic receptor subtypes

A

Adrenergic receptors (bind catecholamines)
Alpha receptors: NE > Epi, activates phospholipase C pathways (GPCR)
Beta: preference depends on subtype, increase cAMP levels
B1 NE=EPI
B2 Epi > NE

70
Q

Parasympathetic receptor subtypes

A

Cholinergic receptors
Nicotinic: ion channels, only on ganglia
Muscarinic: GPCR, on target tissue

71
Q

Adrenal cortex

A

Outside of adrenal gland, true endocrine gland, secretes steroid hormones

72
Q

Adrenal medulla

A

Inner adrenal gland, modified sympathetic ganglion, secretes EPI into bloodstream (no postganglionic), systematic release of epi from SNS activation (once released, any receptor that can bind it, will.

73
Q

Compare PNS and SNS

A

Table slide 455

74
Q

Affect of PNS and SNS on organs

A

Slide 456

75
Q

Types of muscle

A

Skeletal, cardiac, smooth

76
Q

Skeletal muscle

A

Attach to bones via tendons, contract by motor neurons, no endocrine influence
40% body weight (water, protein)

77
Q

Cardiac Muscle

A

Found only in heart, pumps blood, influenced by ANS and endocrine

78
Q

Smooth muscle

A

Muscle of internal organ and hollow tubes, influences by ANS and endocrine

79
Q

Flexors

A

Muscles that bring the center of two bones closer

80
Q

Extensor

A

Muscles that move bones away from one another

81
Q

Flexors

A

Muscles that bring the center of two bones closer

82
Q

Label muscle cell organelles

A

Slide 469

83
Q

T-tubules

A

Extensions of sarcolemma that penetrate into fiber, allow action potentials to move rapidly from exterior to interior and deep into the muscle

84
Q

Glycogen granules

A

storage form of glucose, energy source for extended contraction

85
Q

Myofibril

A

Bulk of muscle, thousands per muscle, composed of several protein types, highly organized and repeated

86
Q

Myosin

A

Motor protein that forms thick filaments

87
Q

Actin

A

Microfilament protein that forms thin filaments

88
Q

Nebulin

A

Helps align actin, connects to Z Disk

89
Q

Titin

A

Provides elasticity and stabilizes myosin

90
Q

Muscle creating tension

A

Sarcomeres shorten, I bands disappear, requires ATP provided by glucose and phosphocreatine

91
Q

Muscle contraction

A
  1. Somatic motor neuron releases ACh at NMJ (chemical –> electrical)
  2. Excitation-contraction coupling- action potentials traveling down t-tubules and release of Ca
  3. Contraction-relaxation cycle- molecular events that lead to sarcomere shortening (actin myosin cross bridge cycle)
92
Q

Initiation muscle action potential

A

Somatic motor neuron releases ACh at NMJ
Na+ enters through nicotinic receptor channel and initiates muscle action potential
Diagram slide 476

93
Q

Full process of muscle contraction

A

Slides 476-485

94
Q

Troponin

A

Calcium-binding protein on actin that regulates position of tropomyosin

95
Q

Tropomyosin

A

Elongated protein that regulates myosin’s ability to bind actin

96
Q

Cross bridge cycle/sliding filament theory (one twitch)

A
  1. ATP binds to myosin (myosin releases actin)
  2. Myosin hydrolyzes ATP, energy from ATP rotates head to cocked position (PE) and myosin weakly binds actin
  3. Power stroke begins when tropomyosin moves from binding site (due to Ca signal)
  4. Actin moves towards m-line, myosin releases Pi and myosin releases ADP at end of power stroke
97
Q

Relaxation Phase

A
  1. Sarcoplasmic Ca-ATPase pumps Ca back into SR
  2. Decrease in free cytosolic [Ca] to unbind from troponin
  3. Tropomyosin re-covers binding site. Elastic pulls filaments back to relaxed position when myosin releases
98
Q

Energy for muscle contraction

A

muscle fibers store enough ATP from 8 twitches, need more from sustained contraction

99
Q

Aerobic respiration

A

Glucose provides ATP, uses oxygen
30-32 ATP

100
Q

Anaerobic respiration

A

Occur when O2 levels fall, metabolism shift and pyruvate converted to lactate; 2 ATP

101
Q

Back up energy

A

Phosphocreatine and creatine kinase, not a long term energy source
Creatine kinase transfers phosphate from phosphocreatine to ADP

102
Q

Fatigue

A

Exercising muscle is no longer able to generate or sustain power
Reversible, variable, influenced by intensity, duration, aerobic/anaerobic, muscle composition

103
Q

Central fatigue

A

One explanation for fatigue; Mechanisms that arise in CNS
Subjective feelings of tiredness and desire to cease activity
1. psychological 2. low pH 3. acidosis 4. lack motivation

104
Q

Peripheral fatigue

A

One explanation for fatigue; molecular based explanation
mechanisms that arise in NMJ or contractile elements
1. Decreased communication at NMJ (pathological) lack of ACh production/release
2. Decreased Ca release
3. Increased free phosphate
4. K+ accumulation in t-tubules hyper polarizes muscle cell

A&P Lecture (3 decks)

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