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
2
Q
somatic
A
skeletal muscle; automatic
3
Q
autonomic
A
- two responses; sympathetic or parasympathetic
4
Q
sympathetic
A
fight or flight
5
Q
para-sympathetic
A
breeding and relaxing
6
Q
primary motor cortex
A
voluntary movement
7
Q
central sulcus
A
defines the boundary between primary motor cortex and primary somatosensory cortex
8
Q
primary somatosensory cortex
A
process somatic sensations (the position of the body in space, perception of pain, temperature)
9
Q
sensory association areas
A
the processing between the arrival of input in the primary sensory cortices and the generation of behavior
10
Q
visual association areas
A
receive, segment, and integrate visual info
11
Q
primary visual cortex
A
revives visual info from retinas
12
Q
wernicke’s area
A
supports speech production
13
Q
auditory association area
A
responsible for processing acoustic signals
14
Q
glial cells
A
- not neuronal
- glue that holds your brain together
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
16
Q
Oligodendrocytes
A
myelinated your cells and wrap neurons in order to promote conduction, therefore faster connection
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
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
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
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
21
Q
Concussion types
A
- direct impact injury
- acceleration-deceleration injury
- blast injury
22
Q
Concussion Symptoms
A
Loss of balance
Light/noise sensitivity
Fatigue
Headaches
Dizziness
Confusion
Memory loss
Vision disturbance
Difficulty concentrating
Nausea
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)
24
Q
Long Term Potentiation (LTP)
A
how memories are made
25
Forebrain
receiving and processing sensory information, thinking, perceiving, producing and understanding language, and controlling motor function.
26
Brainstem
Controls actions that you don’t think about (ie breathing, blinking, sweating)
27
Cerebellum
helps coordinate and regulate a wide range of functions and processes in both your brain and body
28
Right Side Brain
left body movement, left side sensory perception, spatial orientation, creativity, face recognition, music, dream, imagery, philosophy, and intuition
29
Left Side Brain
right side movement, right side sensory reception, logic, analytical processing
30
Thalamus
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.
31
Cerebral Cortex
o What is hurting and where? Location and intensity
o Sends info through thalamus, then to motor neuron, and finally skeletal muscle
32
Basal Nuclei
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
33
Parkinson’s
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.
34
Hypothalamus
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
35
Medulla
o Cardiac Center – controls heart rate and strength of contraction
o Vasomoter Center – controls blood pressure
o Respiratory Centers – controls
o Digestive Center – controls
36
Reflexes
o A response to a stimulus that occurs without convicts effort
o Four basic classifications of reflexes, but fall into 1-2 subclasses
37
Levels of Neural Processing
spinal
cranial
38
Efferent Division Controlling Effector
somatic
autonomic
39
Developmental pattern
innate
conditioned
40
number of synapses in the pathway
monosynaptic
polysynaptic
41
5 components of reflex arc
- sensory receptor
- afferent pathway
- integrating center
- efferent pathway
- effector
42
the stretch (knee jerk) reflex
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
43
Photoreceptors
vision
modality: photons of light
44
chemoreceptors
taste, smell, pain
modalities: chemicals dissolved in saliva and dissolved in muscles. chemicals in extracellular fluids
45
thermoreceptors
warmth, cold
modalities: increase in temperatures between 30 C and 43 C, decrease in temperatures between 35 C and 20 C
46
mechanoreceptors
vibration, sound, balance/equilibrium
modalities: pressure, sound waves, acceleration
47
synesthesia
A neurological phenomenon in which stimulation of one sensory or cognitive pathway leads to automatic, involuntary experiences in a second escort or cognitive pathway.
48
Sensory Pathways
Primarily a protective mechanism meant to bring a conscious awareness that tissue damage is occurring
49
two point discrimination
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
50
acuity
o Sensory fields overlap
o Which neuron will fire the stimulus?
51
lateral inhibition
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.
52
pain
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
53
nosciceptors
pain receptors
54
SCN9A
stops sodium from coming through (no action potential, no pain). The gene that is mutated with Congential Insensitivity to Pain (CIP)
55
substance P
activates ascending pathways that transmit nociceptive signals to higher levels for further processing
56
glutamate
major excitatory neurotransmitter
57
fast pain (lego pain)
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
slow pain
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
gate control theory
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
endogenous opiates
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
referred pain
o Your brain gets mixed up in where the signal are coming from
o Heart attack (feeling it in your arm/shoulder)
62
cyclooxygenase (COX)
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
COX inhibitors
o Some COX inhibitors
Aspririn
Ibuprofen
Advil/motrin
Tylenol
Celebrex
Aleve
64
Dan Simmons
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
preganglionic fiber
Cell bodies of preganglionic fibers lie in the spinal cord
66
postganglionic fiber
o Fibers synapse with a ganglion
o Sympathetic nervous system has shorter ganglion lengths
o Empanephrin and norepinephrine are responsible for sympathetic responses
67
ganglion
cluster of neuron bodies outside of CNS
68
nictoinic
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
muscarinic
5 different types
Primarily on effector organs in the parasympathetic system
Works through g-linked protein receptors
Can be either excitatory or inhibitory
70
Adrenergic Receptors
o Alpha and Beta
o G-protein linked
o Can be inhibitory or stimulatory
o Many subtypes
o Tuneable, not just on/off
71
Alpha 1
Most vascular smooth muscle, pupils
ME>Epi
Activates IP3
72
Alpha 2
CNS, platelets, adrenergic nerve terminals (auto receptors), some vascular smooth muscle, adipose tissue
NE > Epi
Inhibits cAMP
73
Beta 1
CNS, cardiac muscle, kidney
NE = Epi
Activates cAMP
74
Beta 2
Some blood vessels, respiratory tract, uterus
Epi >> NE
Activates cAMP
75
Beta 3
Adipose tissue
NE = Epi
Activates cAMP
76
Catecholamine Synthesis
postganglionic fibers and adrenal medulla
77
nueromuscular junction
Once generated at the neuromuscular junction, the action potential radiates in all directions over the muscle fiber sarcolemma
78
myasthenia gravis
- 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
t tubules
invaginations in the sarcolemma that extend deep into the muscle cell, running along the myofribrils
80
sarcoplasmic reticulum
specialized ER, stores calcium
81
sarcomere
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
A band
defined by presence of thick filament (myosin); denotes the start to the end of thick filament
83
I band
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
H zone
portion of the A band with only thick filament; denotes the ends of thin filament s within the same sarcomere
85
m line
anchors thick filaments
86
z line
anchors thin filaments
87
thick filament
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
thin filament
Made of many actin, troponin, and tropomyosin proteins
89
actin
globular protein (G-actin) and each has a binding site for myosin and can polymerize to make a fibrous strand (F-actin)
90
tropomyosin
strand-like protein. In resting muscle, covers myosin-binding sites on actin molecules
91
troponin
calcium sensitive. A trimmer of three subunits. One binds calcium, one binds actin, one binds tropomyosin
92
cross bridge cycling
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
latent period
The delay between the start of the action potential and the start of the twitch
94
complete tetanus
AP rapid enough to prevent dip in Ca++/force between twitches
95
tetanus
maximum contraction/force that your muscle cell can generate at any one time
96
fatigue
- The loss or inability to generate force
- sets in usually during high frequency generation and large force generating activities
97
Causes of fatigue
Loss of ATP
Accumulation of metabolites
Loss of nerve signaling
Decreased oxygen
Emotional stress
98
nervous fatigue
loss of the ability to maintain high frequency signals (not painful), depletion of neurotransmitter
99
metabolic fatigue
shortage of available fuel substrates and accumulation of metabiloties (K+, Lactic acid, etc)
100
hypertrophy
Not making new muscles, making existing muscles grow
101
motor unit
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
isotonic contraction
o Muscle is allowed to shorten as it contracts. Measure degree of shortening
o Maintains a constant amount of force
103
isometric contraction
o Change the amount of tension developed but it’s not necessarily associated with movements.
o Consistently the same length
104
muscles are classified by
Speed of contraction: fast or slow
Major pathway of ATP production: glycolysis or oxidative
105
Type 1 - Slow Oxidative
* 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
Type 2A - Fast Oxidative
* 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
Type 2X - Fast glycolitic
* 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
With training and exercise, we lessen the onset of fatigue and reduce ROS (reactive oxygen species) generation through:
o Increase mitochondria
o “supercharge” mitochondria
o Decrease lactate production
The more you exercise, the longer it takes to produce lactate
109
Mitochondrial Biogensis
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
circulatory system
The heart
Blood vessels
Blood
111
pulmonary circulation
driven by right side of the heart Closed loop of vessels between heart and lungs
112
Systemic circulation
driven by left side of heart
Circuit of vessels carrying blood between heart and other body systems
113
causative factors of heart disease
o Alcohol consumption
o High cholesterol
o Genetics
o Obesity
o Smoking
114
autorhymicity
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
The purpose of autonomic innervation of the heart is to
o Increase the rate and strength of contraction (sympathetic)
o Decrease the rate of contraction (parasympathetic)
116
pacemaker cells
initiate action potentials
117
conduction fibers
transmit action potentials throughout the heart for coordination
118
SA Node
o The pacemaker of the heart
o Composed of P-cells
o Don’t have a normal resting potential
o Exhibit “pacemaker potential”
119
Pacemaker Potential
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
systole
ventricular contraction
121
diastole
ventricular relaxation
122
phase 1 heart sounds
Atroventricular valves OPEN
Aortic and pulmonary valves CLOSED
123
phase 2 heart sounds
Atroventricular valves CLOSED
Aortic and pulmonary valves CLOSED
124
Phase 3 heart sounds
Atroventricular valves CLOSED
Aortic and pulmonary valves OPEN
125
phase 4 heart sounds
Atroventricular valves CLOSED
Aortic and pulmonary valves CLOSED
126
p -wave
atrial depolarization
127
QRS complex
ventricular depolarization
128
t wave
ventricular depolarization
129
end diastolic volume
volume of blood in ventricle after filling is complete
130
end of systolic volume
volume of blood left in ventricle after contraction
131
stroke volume
volume of blood ejected from ventricle with each beat
132
cardiac output
heart rate x stroke volume
133
Cardiac Output can be Regulated by:
Regulating Heart Rate
Regulating Stroke volume
