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CELL 305 midterm 2 > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

Peripheral

A
  • anything outside the brain and spinal cord
  • looking for different types of stimuli
  • takes info back to the CNS
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2
Q

somatic

A

skeletal muscle; automatic

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3
Q

autonomic

A
  • two responses; sympathetic or parasympathetic
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4
Q

sympathetic

A

fight or flight

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5
Q

para-sympathetic

A

breeding and relaxing

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6
Q

primary motor cortex

A

voluntary movement

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7
Q

central sulcus

A

defines the boundary between primary motor cortex and primary somatosensory cortex

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8
Q

primary somatosensory cortex

A

process somatic sensations (the position of the body in space, perception of pain, temperature)

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9
Q

sensory association areas

A

the processing between the arrival of input in the primary sensory cortices and the generation of behavior

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10
Q

visual association areas

A

receive, segment, and integrate visual info

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11
Q

primary visual cortex

A

revives visual info from retinas

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12
Q

wernicke’s area

A

supports speech production

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13
Q

auditory association area

A

responsible for processing acoustic signals

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14
Q

glial cells

A
  • not neuronal
  • glue that holds your brain together
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15
Q

astrocytes

A
  • looks like stars; not a neuron
  • goes to capillaries that feed your brain and will wrap around capillaries
  • acts as gatekeeper for what gets out of capillary; nothing unnatural will get past it
  • also contracts around vessels to regulate blood flow
  • reaches out and wrap around neurons in your brain. it wraps around the synapse between two neurons and turning off the EPSP
  • brain damage affects glial cells as well
  • Exocitocity
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16
Q

Oligodendrocytes

A

myelinated your cells and wrap neurons in order to promote conduction, therefore faster connection

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17
Q

microglia

A

-resident immune cells
Phagocytoses (kills) dead/dying cells and infectious agents
Inactivated vs inactivated
Neurodegenerative diseases is where microglia have issues and just go crazy with it

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18
Q

Ependymal Cells

A
  • form the epithelium called ependyma
  • create CSF
  • contain cilia for the movement of CSF
  • have stem cell qualities
  • slow regeneration
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19
Q

Nueroglycopnia

A

o Glucose is natural lower in CSF
o Plasma glucose affects the CSF glucose levels, where under low plasma concentrations, CSF glucose concentrations drop and cause CNS dysfunction
o Symptoms:
 Drowsiness
 Irritability
 Confusion

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20
Q

Cerebral Spinal Fluid

A

o CSF has nearly the same composition as plasma
o Normal individuals have around 150 ml of CSF in our system
 Recycled 3x a day
o Produce nearly 500 ml/day
o As CSF circulates through the CNS, it makes its way to the subarachnoid space through spendings in the fourth ventricle and is absorbed into the venous blood

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21
Q

Concussion types

A
  • direct impact injury
  • acceleration-deceleration injury
  • blast injury
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22
Q

Concussion Symptoms

A

 Loss of balance
 Light/noise sensitivity
 Fatigue
 Headaches
 Dizziness
 Confusion
 Memory loss
 Vision disturbance
 Difficulty concentrating
 Nausea

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23
Q

What does your frontal lobe do post concussion?

A

 Judgement
 Overrides social judgements
o Repeated concussions caused morphological changes in the brain: Chronic Traumatic Encephalopathy (CTE)

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24
Q

Long Term Potentiation (LTP)

A

how memories are made

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25
Q

Forebrain

A

receiving and processing sensory information, thinking, perceiving, producing and understanding language, and controlling motor function.

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26
Q

Brainstem

A

Controls actions that you don’t think about (ie breathing, blinking, sweating)

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27
Q

Cerebellum

A

helps coordinate and regulate a wide range of functions and processes in both your brain and body

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28
Q

Right Side Brain

A

left body movement, left side sensory perception, spatial orientation, creativity, face recognition, music, dream, imagery, philosophy, and intuition

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29
Q

Left Side Brain

A

right side movement, right side sensory reception, logic, analytical processing

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30
Q

Thalamus

A

o Relay station for all sensory information (except smell)
o Relay station for motor pathways from cerebral cortex.
o Interpretation center for sensory information. Modality of sensation is perceived here, but not location or intensity.

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31
Q

Cerebral Cortex

A

o What is hurting and where? Location and intensity
o Sends info through thalamus, then to motor neuron, and finally skeletal muscle

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32
Q

Basal Nuclei

A

o Inhibition of muscle tone
o Coordination of slow, sustained movements (especially posture)
o Selecting purposeful patterns of movement and suppressing useless patterns of movement
o Diseases of the Basal nuclei can involve movement disorders

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33
Q

Parkinson’s

A

o Shaking, pill rolling, shuffle walk
o Basal nuclei disorder
o Resting, unpurposeful movement is hard
o Black substance releases dopamine. Over time, Parkinson’s loses that. This is when symptoms appear.

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34
Q

Hypothalamus

A

o Regulates body temperature
o Regulates osmolarity of body fluids (intake and excretion of water)
o Regulates food intake (appetite and satiety centers)
o Emotions of rage and aggression
o Regulates anterior pituitary function (endocrine system)
o Regulates uterine contractility and milk ejection (via oxytocin)
o Sleep/wake cycles

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35
Q

Medulla

A

o Cardiac Center – controls heart rate and strength of contraction
o Vasomoter Center – controls blood pressure
o Respiratory Centers – controls
o Digestive Center – controls

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36
Q

Reflexes

A

o A response to a stimulus that occurs without convicts effort
o Four basic classifications of reflexes, but fall into 1-2 subclasses

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37
Q

Levels of Neural Processing

A

spinal
cranial

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38
Q

Efferent Division Controlling Effector

A

somatic
autonomic

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39
Q

Developmental pattern

A

innate
conditioned

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40
Q

number of synapses in the pathway

A

monosynaptic
polysynaptic

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41
Q

5 components of reflex arc

A
  • sensory receptor
  • afferent pathway
  • integrating center
  • efferent pathway
  • effector
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42
Q

the stretch (knee jerk) reflex

A

o When patellar tendon is hit, it cause it to stretch.
o When it stretches, there are stretch receptors that are activated. The stretch receptor takes the action potential to the nervous system.
o The action potential will synapse the efferent pathway, causing the quadriceps to contract.
o MONOSYNAPTIC

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43
Q

Photoreceptors

A

vision
modality: photons of light

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44
Q

chemoreceptors

A

taste, smell, pain
modalities: chemicals dissolved in saliva and dissolved in muscles. chemicals in extracellular fluids

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45
Q

thermoreceptors

A

warmth, cold
modalities: increase in temperatures between 30 C and 43 C, decrease in temperatures between 35 C and 20 C

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46
Q

mechanoreceptors

A

vibration, sound, balance/equilibrium
modalities: pressure, sound waves, acceleration

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47
Q

synesthesia

A

A neurological phenomenon in which stimulation of one sensory or cognitive pathway leads to automatic, involuntary experiences in a second escort or cognitive pathway.

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48
Q

Sensory Pathways

A

Primarily a protective mechanism meant to bring a conscious awareness that tissue damage is occurring

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49
Q

two point discrimination

A

o The smaller you can make the receptive fields, you can tell exactly where.
o The smaller the acuity, the more precise you can tell where something touches

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50
Q

acuity

A

o Sensory fields overlap
o Which neuron will fire the stimulus?

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51
Q

lateral inhibition

A

o The advantage of this setup is that as the action potentials go up, they diverge to three different ends of the termini
o One termini is going to synapse with the second one
o Creates an EPSP with the inter neuron, Will activate the inhibitory interneuron
o Creates presynaptic inhibition. Dumps a bunch of IPSP, it will fight again the presynaptic inhibition.
o The lateral input is dampened to find localization.
o The disparity between the two side neurons is easier for my brain to understand how wide it is.

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52
Q

pain

A

o Primarily a protective mechanism meant to bring a conscious awareness that tissue damage is occurring or is about to occur
o Storage of painful experiences in memory helps us avoid potentially harmful events in the future

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53
Q

nosciceptors

A

pain receptors

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54
Q

SCN9A

A

stops sodium from coming through (no action potential, no pain). The gene that is mutated with Congential Insensitivity to Pain (CIP)

55
Q

substance P

A

 activates ascending pathways that transmit nociceptive signals to higher levels for further processing

56
Q

glutamate

A

 major excitatory neurotransmitter

57
Q

fast pain (lego pain)

A

sharp pain. Usually temporary. Transmitted on fast fibers (A-delta fibers)
* A- delta fibers are mylenated and move action potentials at a speed of 12-30 m/sec

58
Q

slow pain

A

dull, aches pain. Persists chronically. Transmitted on slow fibers (C-fibers)
* C-fibers are unmylenated and move action potentials at speed of 0.2-1.3 m/sec

59
Q

gate control theory

A

o Slow pain inhibits inhibitory internuerons
o Collaterals from other sensory receptors stimulate internurons, blocking pain transmission
o Trying to activate non-pain receptors to inhibite pain

60
Q

endogenous opiates

A

o Brain has built in analgesic system
o Bind to opioid receptors on the postsynaptic neuron and induces am inhibitory membrane potential shift
o Bind to opioid receptors on the afferent nocioreceptors neuron and inhibits the release of substances
o Presynaptic inhbition – IPSP, depress the amount of substance coming from that terminous
o Examples: endorphins, enkephalins, dynorphin

61
Q

referred pain

A

o Your brain gets mixed up in where the signal are coming from
o Heart attack (feeling it in your arm/shoulder)

62
Q

cyclooxygenase (COX)

A

o Gatekeepers of pain
o During tissue injury they will make prostaglandin. Activates PKA and PKC. These will phophoralate the trip channels, which let in Na+ and Ca, which depolarizes the cell.
o This sensitizes your neuroreceptors to feel pain.

63
Q

COX inhibitors

A

o Some COX inhibitors
 Aspririn
 Ibuprofen
 Advil/motrin
 Tylenol
 Celebrex
 Aleve

64
Q

Dan Simmons

A

o Cyclooxygenase-2 (COX2) was discovered at BYU in 1988 by Dr. Daniel L. Simmons
o While aspririn can inhibit COX2, it is a better COX1 inhibitor
o His discoveries added in the development of many different drugs to alleviate pain and inflammation, namely Celebrex from Pfizer.
o Celebrex is used to treat osteoarthritis, rheumatioid arthritis, acute pain, painful menstruation
o Celebrex earned an estimated $35 billion
o Dr. Simmons originally did NOT receive any compensation for his contributions
o In May 2012, BYU and Dr. Simmons won a legal battle for $450 million

65
Q

preganglionic fiber

A

Cell bodies of preganglionic fibers lie in the spinal cord

66
Q

postganglionic fiber

A

o Fibers synapse with a ganglion
o Sympathetic nervous system has shorter ganglion lengths
o Empanephrin and norepinephrine are responsible for sympathetic responses

67
Q

ganglion

A

cluster of neuron bodies outside of CNS

68
Q

nictoinic

A

 4 different types
 Signals between preganglionic and postganglionic fibers in both sympathetic and parasympathetic systems
 Adrenal medulla
 Skeletal muscle
 Induces changes to ion channels opening
 Generally excitatory

69
Q

muscarinic

A

 5 different types
 Primarily on effector organs in the parasympathetic system
 Works through g-linked protein receptors
 Can be either excitatory or inhibitory

70
Q

Adrenergic Receptors

A

o Alpha and Beta
o G-protein linked
o Can be inhibitory or stimulatory
o Many subtypes
o Tuneable, not just on/off

71
Q

Alpha 1

A

 Most vascular smooth muscle, pupils
 ME>Epi
 Activates IP3

72
Q

Alpha 2

A

 CNS, platelets, adrenergic nerve terminals (auto receptors), some vascular smooth muscle, adipose tissue
 NE > Epi
 Inhibits cAMP

73
Q

Beta 1

A

 CNS, cardiac muscle, kidney
 NE = Epi
 Activates cAMP

74
Q

Beta 2

A

 Some blood vessels, respiratory tract, uterus
 Epi&raquo_space; NE
 Activates cAMP

75
Q

Beta 3

A

 Adipose tissue
 NE = Epi
 Activates cAMP

76
Q

Catecholamine Synthesis

A

postganglionic fibers and adrenal medulla

77
Q

nueromuscular junction

A

Once generated at the neuromuscular junction, the action potential radiates in all directions over the muscle fiber sarcolemma

78
Q

myasthenia gravis

A
  • inability to properly signal at the neuromuscular junction
  • autoimmune disease; thymic in origin
  • general muscle weakness but not cardiovascular in nature
  • more common in women
79
Q

t tubules

A

invaginations in the sarcolemma that extend deep into the muscle cell, running along the myofribrils

80
Q

sarcoplasmic reticulum

A

specialized ER, stores calcium

81
Q

sarcomere

A

functional unit of skeletal muscle. Runs Z line to Z line
o Under microscope, skeletal and cardiac muscle are “striated” or striped
o Due to alternating A bands (dark) and I bands (light)

82
Q

A band

A

defined by presence of thick filament (myosin); denotes the start to the end of thick filament

83
Q

I band

A

defined by presence of thin filament (actin) but NOT thick filament; denotes the end of the thick filament to the end of another thick filament from the adjacent sarcomere

84
Q

H zone

A

portion of the A band with only thick filament; denotes the ends of thin filament s within the same sarcomere

85
Q

m line

A

anchors thick filaments

86
Q

z line

A

anchors thin filaments

87
Q

thick filament

A

o Made of many myosin proteins
o Myosin has ATPase activity: breaks down ATP, releases energy
o Myosin orientation is not linear but rather is orientated in many different directions
o Myosin can bind to actin in thin filament (six thin filaments surround each thick filament)

88
Q

thin filament

A

Made of many actin, troponin, and tropomyosin proteins

89
Q

actin

A

globular protein (G-actin) and each has a binding site for myosin and can polymerize to make a fibrous strand (F-actin)

90
Q

tropomyosin

A

strand-like protein. In resting muscle, covers myosin-binding sites on actin molecules

91
Q

troponin

A

calcium sensitive. A trimmer of three subunits. One binds calcium, one binds actin, one binds tropomyosin

92
Q

cross bridge cycling

A

Binding of myosin to actin
o 2. Power stroke
o 3. Rigor (myosin in low-energy form)
o 4. Unbinding of mysoin and actin

93
Q

latent period

A

The delay between the start of the action potential and the start of the twitch

94
Q

complete tetanus

A

AP rapid enough to prevent dip in Ca++/force between twitches

95
Q

tetanus

A

maximum contraction/force that your muscle cell can generate at any one time

96
Q

fatigue

A
  • The loss or inability to generate force
  • sets in usually during high frequency generation and large force generating activities
97
Q

Causes of fatigue

A

 Loss of ATP
 Accumulation of metabolites
 Loss of nerve signaling
 Decreased oxygen
 Emotional stress

98
Q

nervous fatigue

A

loss of the ability to maintain high frequency signals (not painful), depletion of neurotransmitter

99
Q

metabolic fatigue

A

shortage of available fuel substrates and accumulation of metabiloties (K+, Lactic acid, etc)

100
Q

hypertrophy

A

Not making new muscles, making existing muscles grow

101
Q

motor unit

A

one motor neuron plus all of the muscle fibers that it innervates
 Note that muscle fibers in 1 motor unit are spread out in the muscle (not right next to each other)

102
Q

isotonic contraction

A

o Muscle is allowed to shorten as it contracts. Measure degree of shortening
o Maintains a constant amount of force

103
Q

isometric contraction

A

o Change the amount of tension developed but it’s not necessarily associated with movements.
o Consistently the same length

104
Q

muscles are classified by

A

 Speed of contraction: fast or slow
 Major pathway of ATP production: glycolysis or oxidative

105
Q

Type 1 - Slow Oxidative

A
  • Red muscle
  • High oxidative capacity, low glycolysis captacity
  • Speed of contraction is slow
  • Low myosin ATPase activity
  • High mitochondrial acitivty
  • High capillary density
  • High resistance to fatigue
  • Small fiber diameter
  • Low force generating capacity
106
Q

Type 2A - Fast Oxidative

A
  • Mixed muscle
  • High oxidative capacity, intermediate glycolytic capacity
  • Intermediate speed of contraction
  • Intermediate myosin ATPase activity
  • High mitochondrial density
  • High capillary density
  • High resistance to fatigue
  • Intermediate fiber diameter
  • Intermediate force generating capacity
107
Q

Type 2X - Fast glycolitic

A
  • White muscle
  • Low oxidative capacity
  • High glycolytic capacity
  • Fast speed fo contraction
  • High myosin ATPase activity
  • Low mitochondrial density
  • Low capillary density
  • Low resistance to fatigue
  • Large fiber diameter
  • High force generating capacity
108
Q

With training and exercise, we lessen the onset of fatigue and reduce ROS (reactive oxygen species) generation through:

A

o Increase mitochondria
o “supercharge” mitochondria
o Decrease lactate production
 The more you exercise, the longer it takes to produce lactate

109
Q

Mitochondrial Biogensis

A

o ROS goes to JNK
o JNK activates the transcription factor
o Transcription Factor:
 PGC-1a
o The transcription factor creates more mitochondria
o When you have more mitochondria, they aren’t necessarily producing more, they are just less stressed and are functioning better.

110
Q

circulatory system

A

 The heart
 Blood vessels
 Blood

111
Q

pulmonary circulation

A

driven by right side of the heart Closed loop of vessels between heart and lungs

112
Q

Systemic circulation

A

driven by left side of heart
Circuit of vessels carrying blood between heart and other body systems

113
Q

causative factors of heart disease

A

o Alcohol consumption
o High cholesterol
o Genetics
o Obesity
o Smoking

114
Q

autorhymicity

A

o Skeletal muscle requires innervationto contract
o Cardiac muscle contracts automatically without innervation from any neurons. This is called myotonic contraction (compared to skeletal muscle that is considered neurogenic)

115
Q

The purpose of autonomic innervation of the heart is to

A

o Increase the rate and strength of contraction (sympathetic)
o Decrease the rate of contraction (parasympathetic)

116
Q

pacemaker cells

A

initiate action potentials

117
Q

conduction fibers

A

transmit action potentials throughout the heart for coordination

118
Q

SA Node

A

o The pacemaker of the heart
o Composed of P-cells
o Don’t have a normal resting potential
o Exhibit “pacemaker potential”

119
Q

Pacemaker Potential

A

the pacemaker potential is the slow, positive increase in voltage across the cell’s membrane that occurs between the end of one action potential and the beginning of the next action potential.

120
Q

systole

A

ventricular contraction

121
Q

diastole

A

ventricular relaxation

122
Q

phase 1 heart sounds

A

 Atroventricular valves OPEN
 Aortic and pulmonary valves CLOSED

123
Q

phase 2 heart sounds

A

 Atroventricular valves CLOSED
 Aortic and pulmonary valves CLOSED

124
Q

Phase 3 heart sounds

A

 Atroventricular valves CLOSED
 Aortic and pulmonary valves OPEN

125
Q

phase 4 heart sounds

A

 Atroventricular valves CLOSED
 Aortic and pulmonary valves CLOSED

126
Q

p -wave

A

atrial depolarization

127
Q

QRS complex

A

ventricular depolarization

128
Q

t wave

A

ventricular depolarization

129
Q

end diastolic volume

A

volume of blood in ventricle after filling is complete

130
Q

end of systolic volume

A

volume of blood left in ventricle after contraction

131
Q

stroke volume

A

volume of blood ejected from ventricle with each beat

132
Q

cardiac output

A

heart rate x stroke volume

133
Q

Cardiac Output can be Regulated by:

A

Regulating Heart Rate
Regulating Stroke volume

CELL 305 midterm 2 (1 decks)

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