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304 Cards in this Set
- Front
- Back
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parts of a neuron
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1. cell body
2. dentdrites 3. Axon 4. Axon collaterals 5. Terminals 6. Varicosities |
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Axon
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process from cell body to target
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Axon collaterals
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branches of axon
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Where does release of NT occur on neuron?
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nerve terminal
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Schwann cells
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make mylin sheath for periphery
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Oligodendrocytes
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make myelin for CNS
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what are between mylin forming cells
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nodes of ranvier
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purpose of myelin
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accelerates conduction velocity along the axon
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what does acceleraton of conduction velocity in a neuron depend on?
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size on the axon and mylination
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multipolar neuron
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has multiple dendritic processes. most tract neurons and neurons with peripheral processes are multipolar
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pseudounipolar cell
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has single stem that bifurcates to make distal and proximal processes that project to the target organ and the central nervous system. This is cell type in DRG
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Unipolar and bipolar cells
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have one or two processes. these are associated with special senses
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Afferent (sensory) neurons
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primary sensory neurons go from body to the CNS
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efferent neurons
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motor. go from CNS to effectors
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Interneurons
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local circuit neurons.
connect neurons within the CNS |
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Nerve
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bundle of axons in peripheral nervous system that contains both afferent and effernt fibers
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Tract
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collection of axons with the orgin (cell bodies) in one area or nucleus that projects to a discrete target
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Funiculus
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Large collection of axons that may contain multiple tracts with many different terminations, but found wi a defined region. (in SC)
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Fasiculus
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discrete collection of axons, usually in the BS or ventral forebrain that contains axons from multiple sites and interconncets multiple areas (many tracts together)
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What makes up largest number of cells in nervous system?
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90% are glial cells
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function of glial cells
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support neurons and maintain ECF
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Oligodendrocytes
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forms mylin sheath around neurons in the CNS
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types of glial cells
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oligodendrocytes
astrocytes microglia ependymal |
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Astrocyte
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maintains ECF, supports metabolic activity of neurons, assist in forming BBB
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Microglia
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Macrophages that partipcipate in immune fuction
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Ependymal cells
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comprise lining of cerebral ventricles and regulate CSF
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Difference in regeneration of axons in CNS and PNS
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severed axon in PNS can regrow to reinnervate the orginal target
Severed axons in CNS do NOT regrow to target; they may sprout new endings, but fuction is not regained |
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Neuronal cell bodies in periphery
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ganglion
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neuronal cell bodies in CNS
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nucleus
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Gray matter in SC
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central butterfly area
contains cellbodies of neurons and glia, dendrites, axonal processes. Appears gray due to lack of mylin |
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white matter in SC
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surrounds gray matter.
consists of axons; those with myelin give the color white look. White matter connects regions of SC or SC with brain |
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how does sensory input reach SC?
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Dorsal root allows afferents to reach the SC bc DR consists of axons of sensory neurons
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DRG
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contains cell bodies of pseudounipolar sensory neurons
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How do efferent leave the cord?
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via the Vental Roots with consist of axons of motor neurons
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What is ventral SC?
Dorsal? |
MOTOR is in ventral
dorsal is sensory |
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how are spinal nerves formed
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by joining dorsal and ventral roots
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number of Spinal nerves
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31 divided into five groups
cervical-8 thoracic-12 lumbar-5 sacral-5 coccygeal-1 |
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what does Brainstem consist of?
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medulla oblongata, pons, and midbrain
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function of BrainStem
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responsible for basic mechansisms of life: regualtion of cardiovascular and respiration, sleep and wake, posture, and balance
relays and integrates info from periphery to brain and vice versa Nuclei of most CN in BS Central core of BS is reticular formation |
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reticular formation
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in central core of BS it is involved in integrating info from all sensory modalities and affecting motor outflow. Biogenic amine nuclei are in the reticular formation
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Function of cerebellum
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coordinates ongoing movement and learns new movements
gets input form all muscles, and other brain regions responsible for movement |
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2 components of cerebellum
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cortex: near surface. output cells from here project mainly to the deep nuclei.
Deep nuclei: deeper in cerebellum, neurons in these nuclei provide output from cerebellum |
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Forebrain
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make you, you!
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2 parts of forebrain
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cerebral hemispheres
cerebral cortex:outer shell of gray matte in each hemisphere, they are about 3mm thick |
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What connect regions of the cerebral cortex and send info from cortex to other brain regions or SC?
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fiber bundles
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What conncest the two sides of the cortex?
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corpus collsum
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Output cells of cortex
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pyramidal cells
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4 lobes of cortex
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frontal
parietal occiptal temporal |
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3 major regions of input to cortex
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thalmus
other parts of cortex reticular formation |
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Major integrating region of brain
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cortex; it makes us, us!
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Subcortical nuclei
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groups of cell bodies deep wi hemispheres; the most prominent are the basal ganglia
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Components of basal ganglia
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caudate n.
putamen globus pallidus |
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Function of basal ganglia
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help control movement, they cell groups also help with higher cortical function such as cognition and emotion
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2 parts of diencephalon
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thalmus and hypothalmus
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thalmus
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major relay station to cortex
most sensory and motor input from body must relay through thalmus before going to the cortex. The thalmus is also involved in arousal and attention |
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hypothalmus
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major endocrine center and is responsible for maintaining homeostatis
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limbic system
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responsibe for emotional responses, learning, memory, and integratoin of autonaumic responses to emotional stimuli
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what does limbic connect to to cause emotion?
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hypothalmus
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cebral ventricles
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4 CSF filled interconnected cavities
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How are lateral ventricles connected third ventricle and third ventricle connected to fourth ventricle?
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they are deep in cortex and connected by foramen Monro to third ventricle wi the diencephalon. the third ventricle is connected by aqueduct of sylvius in midbrain to the fourth ventricle which is between the cerebellum and BS
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meninges
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outer membraneous coverign of brain
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layers of meninges
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dura
arachnoid pia |
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dura matter
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thickest and tougest. next to skull.
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arachnoid
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middle layer of meninge
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pia
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meninge layer adjacent to brain and SC
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where does CSF circulate?
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in subarachnoid space between arachnoid and pia
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chroid plexus
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part of lining of ventricles appears tufted
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What cells secrete CSF?
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ependymal cells wi choroid plexus
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How does CSF return to blood?
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by aracnoid villi which are structures that project from the arachnoid to venous sinuses kinda like lymph
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total % of body blood that brain gets
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15%
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What does glucose need for energy?
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glucose
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what does blood brain barrier consist of?
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endothelial cells of brain/spinal cord capillaries
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Purpose of BBB
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prevent large molecules from entering ECF
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what can cross BBB?
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lipid soluble substances but not lipid insobuble substances
therefore drugs cant cross BBB |
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3 divisions of gray matter
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dorsal horn is sensory
ventral horn is motor intermediate region is interneurons that connects sensory and motor |
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what is in the lumbar SC
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gracile fasiculus
lateral coricospinal tract spinocerebellar tract spinothalmic tract vestibulospinal and reticulsopinal tracts |
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gracile fasiculus
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in SC on dorsal column. Touch input to lower half of body
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lateral corticospinal tract
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fine motor control. without this you would be paralyzed
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spinocerebellar tract
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proprioceptive input from body to cerebellum
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spinothalmic tract
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pain and temp input from body
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vestibulospinal and reticulospinal tracts
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postural motor control
found very medial dorsal |
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what is found in cervical SC?
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gracile fasiculus
cuneate fasiculus lateral corticospinal tract spinocerebellar tract spinothalamic tract vestibulospinal and reticulo. rubrospinal tract |
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cuneate fasciculus
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touch input from upper half of body; part of dorsal column
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rubrospinal tract
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motor input of upper limbs
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where is vestibulospinal and reticulospinal tracts?
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very ventral and medial
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where is spinocerebellar tract?
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very lateral and ventral to lateral corticospinal tract
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Where does corticospinal tract cross over?
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at pyramids in BS
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where is corticospinal tract
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in brain very verntral part
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in brain, what is lateral to cuneate n. and fasiculus?
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spinal trigeminal n. and tract
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medial lemniscus
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where aons from gracile and cuneate cross over. Very medial part of brain
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olfactory nerve
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CNI
sense of smell only sensory |
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pathway of Olfactory nerve (CN I)
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primary sensory neurons in olfactory epithelium in roof of nasal cavity send olfactory info to the olfactory bulb. The fibers are the olfactory n.
the olfactory bulb contains cell bodies of secondary sensory neurons, whose axons comprise the olfactory tract. the olfactory tract converys olfaction to olfactory cortical areas |
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CN II
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optic n.
only sensory |
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pathway of CN II (optic)
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photoreceptors in retina of eye transmit visual info to bipolar cells in the retina, which are the primary sensory neurons
bipolar cells synapse on ganglion cells, whose cell bodies also are in the retina; ganglion cells are secondary sensory neurons axons of ganglion cells leave eye to form the optic nerve the optic nerve crosses at the optic chiasm and becomes the optic tract from the optic chiasm it goes to the lateral geniculate body |
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CNIII
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occulomotor n.
innervates eye muscles has both motor and sensory components exits from the midbrain |
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what muscles does CN III innervate?
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superior rectus
medial rectus inferior rectus inferior oblique levator palpebrae superiosis |
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what adducts the eye?
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medial rectus by CN III
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what moves the eye down?
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inferior rectus CN III and is helped by superior oblique and CN IV
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How does the eye move up?
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by superior rectus and inferior oblique both supplied by CN III
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what allows you to lift your eyelid?
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levator palpebrae superiosis elevates eyelid. It is innervated by CN III
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sensory componenet of CN III
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contains a few fibers that transmit sensory info from muscle sensory receptors; these exit the motor nerves to course mainly in the opthalmic division of the trigeminal
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PS componenet of CNIII
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comes from edinger westphal nucleus
preganglionic neurons project to ciliary ganglion postganglionic fibers inervate constictor pupillaie m. to constrict the pupil, and ciliar muscle to change the shape of the lens |
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Trochlear n.
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exits from caudal midbrain
has afferent and efferent component |
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What does CN IV do?
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innervates superior oblique m
sensory component from m. receptors is similiar to oculomoter |
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how does superior oblique m. move the eye?
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down and lateral, causing inward rotation of the eye
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only CN that exits dorsally and the only the one that crosses!
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trochlear n. CN IV
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Trigeminal n.
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CN V
both afferent and efferent components sensory from face and motor to muscles of mastication |
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where does trigeminal n. arise from?
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arises from pons and courses to the trigeminal ganglion, which contains cell bodies of sensory fibers. the three divisions of the trigem leave the ganglion
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Three divisions of the trigeminal
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opthalmic: sensory input from eye, orbit, forehead, ethmoid, and frontal sinus
maxillary: sensory input from maxilla and overlying skin, nasal cavity, palate, nasopharnx, and some meninges mandibular: sensory input from mouth, lower jaw, and anterior 2/3 of tongue. motor to mastication m. |
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4 brainstem nuclei of CN V
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1. spinal trigeminal: pain and temp (2ary neurons)
2.Trigeminal main sensory nucleus: touch sensation (2ary sensory neurons) 3. Trigeminal mesencephalic n.: cell bodies of primary sensory neurons that transmit info from the chewing muscles trigeminal motor n.: cell bodies of motor neurons that innervate chewing muscles |
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CN VI
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innervates lateral rectus m.
has both motor and sensory component |
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How does lateral rectus move eye?
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innervated by CN VI. moves eye laterally
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Where does CN VI exit brain?
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pontomedullary junction
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sensory of CN VI
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sensory from muscle recepters (like occulomoter)
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CN VII
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facial n.
motor to muscles of facial expression; taste |
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Where does CN VII leave the brain?
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both motor and sensory components exit at pontomeduallary junction
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motor component of CN VII
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somatic motor control of muscles of facial expression
visceral (PS) motor control of salivary glands (except parotid), lacrimal gland, and mucus glands |
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sensory component of CN VII
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sensory input from skin on lower part of ear and behind ear
taste buds from anterior 2/3 of tonge. fibers course in solitary tract and terminate in solitary n. |
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CN VIII
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vestibulocochlear n.
auditory and vestibular info only sensory component |
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where does CN VIII exit brain?
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pontomedullary junction just lateral to CN VII
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auditory component of CN VIII
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hair cells in cochlea transmit info onto primary sensory neurons
primary sensory neurons exit the cochlea from CN VIII and terminate in the cochear n. in the BS |
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Vestibular component of CN VIII
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hair cells in semicircular canals, saccule, and utricle transmit info onto primary sensory neurons
primary sensory neurons exit the structure from CN VIII and terminate in the vestibular n. in the BS |
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CN IX
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glossopharyngeal n.
associated with tase and eating has both motor and sensory |
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where does CN IX exit the brain?
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medulla
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motor component of CN IX
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innervates m. that elevates pharynx during swallowing and speech
PS control of parotid gland |
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sensory component of CN IX
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input from carotid sinus and carotid bodies that monitor blood pressure and blood oxygen levels
sensory input from part of ear and inner ear, and posterior 1/3 of tonge, and upper pharynx(gag) taste from posteior 1/3 of tongue |
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CN X
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most of PS
has both motor and sensory |
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where does CNX exit?
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medulla
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motor of CN X
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smooth m. and glands in pharynx,larynx,thorax,and abdomen(PS)
skeltal m. in pharynx, larynx, and tongue (but not all of em) |
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sensory of CN X
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from all visceral structures innervated by the vagus n; also from BF receptors and chemoreceptors in aortic arch
part of ear,larynx, and pharynx |
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CN XI
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spinal accessory n
motor to sternocleidomastoid m. and traps in neck cell bodies of motor neurons are in upper cervical SC; axons emerge from SC to form a trunk that ascends to medulla and then exits the skull with vagus n. |
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CN XII
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hypoglossal n.
motor control of tongue m. only motor nerve that exits the medulla |
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receptor cell
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specialized cells that sense the environment and then secrete neurotransmitters to excite nerve ending that are closely associated with the receptor cell.
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What does receptor respond to?
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only one sensory modality
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graded potentials
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transduce the stimulus to the neuron
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types of graded potentials
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generator potential
receptor potential |
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generator potential
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potential caused by stimulus to a nerve ending it will then travel to an axon.
the generator potential has to be big enough to cause an AP |
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Receptor potential
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potential caused by a stimulus to a receptor cell but it must reach AP
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describe how the stimulus causes an AP
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opening of ion channels, usually sodium, potassium, or and/or chloride, which cuases a change in membrane potential; this is the same as a EPSP
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describe graded potentials
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decrementing; the amplitude decreases with distance. If the amplitude is hi enough to reach threshold once the potential reaches the first node of Rnavier and AP is generated
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What doew frequency of AP depend on?
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amplitude of graded potential but the amplitude of AP is constant
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A single afferent neuron with all of its branches
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sensory unit
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why are peripheral afferent neurons called primary afferents?
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bc its the 1st neuron in the sensory pathway
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where are primary afferents cell bodies?
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in DRG or other peripheral ganglia associated w/cranial nerves
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describe receptive field
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many brances off sensory neurons
the smaller the receptive field, the higher the sensation |
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what on body has small receptive filds? large?
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fingers have small receptive fields while the back has large receptive fields
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describe specific ascending pathway
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transmits sensation to cerebral cortex
its a 3 neuron pathway usualy 1. primary afferent 2. secondary neuron in SC or BS witch projects to the thalmus 3. tertiary neuron in thalmus which projects to cortex |
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Describe non specific pathways
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used for emotional/autonamic responses
transmits non specific info saying something happened but you dont know what can have many synapses usually relays reticular formation; which is an area that integrates input from a wide variety of sensory modalities; one neuron can respond to many sensations this pathway leads to alternating responses, arousal, and can lead to the affective component of a stimulus (hurts or feels good) |
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somatosensory cortex
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postcentral gyrus, anterior end of parietal lobe
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visual cortex
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posterior part of occiptal lobe
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auditory cortex
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superior part of temporal lobe
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what signals stimulus intensity?
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1.signaled by frequnecy of AP
ex: push down on skin, the harder you push the increase in AP bc its a stronger stimulus 2. signaled by recruitment |
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describe recruitment of new sensory afferents
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stimulus is big enough to excite all of neurons receptive fields and other neurons too bc they overlap so brain sees this as a huge stimulus
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two point discrimination
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with small rceptive fields it is easir to detect two closely spaced stimuli that it is with large receptive fields
areas with large receptive fields dont have good two pt discrimination(feels like one point instead of two) |
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in certain receptive field which area has the greatest response to the stimulus
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the center of receptive field will generate more action potentials bc of denser innervation
(but this cant distinguish between low intensity stimuli at center vs. hi at edge) |
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describe lateral inhibition
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has an effect to focus the info from a stimulus site. Through inhibitory interneurons,input from the periphery of a stimulus is inhibited, so this will focus input to brain on center of the stimulus. Lateral inhibition occurs at different levels of the brain and SC
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what signals stimulus duration?
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duration of the firing of the AP
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adaption
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reduction of frequency of AP despite a constant stimulu. There are two major classes of adaptation patterns in sensory fibers
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slowly adapting receptors
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frequency of AP does not reduce to zero during the duration of a stimulus. theses signal location and intensity of a stimulus
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2 types of rapidly adapting recetpors
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velocity detectors
vibration detectors |
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velocity detectors
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AP frequency is proportional to velocity of stimulus and frequency is zero once velocity is zero. these receptors signal sensation of flutter, low frequency vibration, and movement across skin
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vibration (acceleration) detectors
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AP frequency is proportional to acceleraton of stimus, or change in velocity. typical of hi frequency vibration detectors
the bigger the acceleration the more the AP vibration detectors dont respond to direction or accleration |
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classification of sensory receptors
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superficial: touch,pressure,flutter,
vibration, tickle,warmth,cold,pain, itch deep:postion,kiesthesia,deep pressure,deep pain visceral: hunger,nausea,distension, visceral pin special:vision,auditory,taste olfaction,balance |
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type of axons, location, and function of free nerve endings
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C,A,gamma axons
skin pain,temp,crude touch |
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type of axons, location, and function of meissner's corpuscles
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A,beta
on hairless skin touch pressure |
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type of axons, location, and function of pacinian corpuscles
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A,beta
subcutaneous tissue,viscera, and skin deep pressure,vibration |
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type of axons, location, and function of ruffinis corpuscles
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A,beta
on all skin stretching of skin |
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type of axons, location, and function of muscle spindles
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Ia,II axons
on muscles tells muscle length |
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type of axons, location, and function golgi tendon
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Ib
on tendon tells muscle tension |
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dermatomes
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area of skin innervated by a single dorsal root
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The dorsal column medial leminscal system
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transmits information regarding touch, pressure, and movement of hairs fro mthe body and back of the head
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dorsal column medial leminscus pathway
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primary afferents enter SC along the whole length and ascend in the Dorsal column on the same side(from lower body fibers make up gracile fasciculus from upper body fibers make up cuneate fasciculus)
ascending fibers terminate in the dorsal column nuclei(fibers in gracile fasiculus synapse on the gracile nucleus, fibers in cuneate synapse on cuneate n.) the secondary axons exiting the gracile and cuneate cross to the opposite side in the caudal medulla and ascend to the thalmus in the medial lemniscus fibers in medial lemniscus synaspe in VPL of thalmus tertial fibers then go and synapse in somatosensory cortx. |
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what does spinothalmic tract (anterolateral system)transmit?
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transmits info reguarding pain and temp
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spinothalmic pathway
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primary afferents enter SC along its whole length, and synapse on spinothalmic tracts cells in DH of SC
secondary fibers immediately cross to the opposite side to ascend in the ventrolateral part of the SC in the spinothalmic tract to the BS fibers in spinothalmic tract synapse on cell bodies in the VPL of the thalmus tertiary fibers ascend to synapse in the somatosensory cortex |
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describe trigeminal system
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kinda like dorsal column-medial lemniscal system and spinothalmic system for face
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where do primary afferents enter the BS?
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in CN V,VII,IX, and X
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trigeminal pathway for non nociceptive (touch) info
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primary afferents synapse on neurons in the trigeminal main sensory n.
secondary axons cross to the opposite side and ascend to synaspe on cell bodies in the VPM of the thalmus teritiary fibers ascend to synapse on cell bodies in the face region of the somatosensory cortex |
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trigeminal tract for nociceptive info
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primary afferents synapse on neurons in the spinal trigeminal. n.
secondary axons cross to opposite side and ascend to synapse on cell bodies in the VPM of the thalmus tertiary fibers go to synapse on cell bodies in the face region of somatosensory cortex |
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How is pain sensed?
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by hi threshold receptors on bare nerve endings called nociceptors
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Two components to pain
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short latency prickling pain evoked by noxious stimuli carried by Agamma fibers used for localization of stimulus
long latency pain of burning and less bearable quality carried by C fibers (suffering) |
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stimuli that excite nociceptors
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tissue damaging or potentially damaging stimuli
chemicals can sensitize nociceptors to stimuli |
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what are some chemicals that can sensitize nociceptors to stimuli
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bradykinin
serotonin histamine prostaglandins cytokines |
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hyperalgesia
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enhanced sensation of pain in response to subsequent stimuli when tissues are damaged
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primary hyperglesia
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enhanced sensation of pain at the site of tissue damage
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secondary hyperalgesia
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enhanced sensation of pain in the undamaged area surrounding the damaged area
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describe visceral pain
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commonly expressed as referred pain where pain is referred to somatic structure
poorly localized |
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Modulation of pain
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pain is VERY subjective. there is a psychological component to pain. There are also delayed responses to pain in emergency situations. so there must be a mechanism for altering and reducing pain signal
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The gate Theory
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excitation of large diameter fibers (A beta fibers) either directly or through modulatory systems can reduce the activity in the spinothalmic tract neurons therfore reducing pain transmission.
C fibers however inhibit the inhibtor thereby reducing the interneurons inhibitory effect on the STT cells so you feel pain. Both effects of the C fiber faciliate pain transmission |
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pain descending modulation
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hypothalmus
periaquductal gray locus coeruleus raphe magnus these things release enkephalins to decrease pain at spinothalmic tract or inhibit the presynaptic inhibition to decrease substance P and decrease STT |
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when C fibers come in and release substance P to excite the spinothalmic tract, where do ascending tracts go?
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sharp pain goes to thalmus
there are collateral branches that go to reticular formation for suffering pain (thalmus, pons,medulla) |
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how can pain be prevented
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1. altering the transmission of painful information in the periphery at the level of primary afferents (Agamma or C fiber cut)
2. interrupting the ascending transmission of painful infromation and the processing of the painful information in the SC net effect is to decrease excitation of STT to decrease pain |
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two major mechanism to activate descending inhibitory pathways
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1. brainstem descending pathways excite interneurons in the SC. these interneurons release an opiate NT called enkephalin that inhibits the ascending (spinothalmic tract)
2. some BS descending pathways used enkephalin as their NT. these neurons contatct the presynaptic nerve termainls of primary afferent neurons. substance P is the NT released by primary afferents to excite STT. the release of enkephalin on the presynaptic nerve terminal inhibits the release of substance P, which means that there will be less excitatory input to the STT and therefore less nociceptive to higher centers |
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what does our rxn to painful stimulus depend on?
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1. past experience
2. how other react to pain 3. the emotional content |
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NSAIDS
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non opioid analgesics whose mechanism of action is to block prostaglandin synthesis.
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Primary use of NSAIDS
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treat inflammation,
except for acetominphin of course |
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Purpose of pain and inflam
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protective mechanisms that are essential for survival.
inflammation removes noxious agents from the site of injury to repair tissue damage |
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prostaglandin synthesis
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Tissue Injury
Disturb cell membrane Release of phospholipids arachidonic acid makes both lekotrienes and prostanglandins |
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how do NSAIDS have antiiflam, antipyretic, and analegic properties?
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bc NSAIDS inhibit prostaglandin synthesis by inhibiting cyclo oxygenase
NSAIDS act at the level of the primary sensory neuron (except for acetaminophen) |
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Two isozymes of COX
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COX 1 and COX 2
Cox 1 is made constitutively COX 2 is induced by cytokines, and other inflam processes but it is expressed constituitively in the brain and kidneys |
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Only cox in tummy
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COX 1 so it would be great if we had a drug that just inhibited COX 2 bc NSAIDS cause GI side effects bc they decrease the mucus cells ability to resist acid
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How do NSAIDS block inflam, fever, and pain
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the antiinflam and analgesic effects are due to decreased inflam mediators which also reduces the substance the exicites the nocioceptor
prostaglandins reset the hypothalmus to increase set point of body temp causing fever, COX inhibitors block this process and reduce fever |
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how does aspirin work?
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it is a non cometive inhibitor of COX 1 and COX 2 bc it covalently binds to the COX enzyme. It is the ONLY NSAID to do this. Since it binds covalently, it lasts longer.
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Effects of Aspirin
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antipyretic
Antiinflam analgesic NO CV effect at therapeutic dose GI side effects bc decreases gastric mucosal cells to resist penetration by acid which causes gastrice irritation Increases bleeding time bc it inhibits platelet aggregation and since plateletts cant make new COX, new platelets must be made fefore bleeding time can return to normal |
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Therapeutic uses of aspirin
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Releve Pain
Relieve inflam Reduce fever |
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Describe Acetaminophen (Tylenol)
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has both analgesic and antipyretic activites that are equivalent to that of aspirin but it does NOT relieve inflam!!!
Acetaminophen inhibits COX and prostaglandin synthesis but it has more activity in the CNS and less on prostanglins |
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Therapeutic uses of Acetaminophen
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relieve pain
reduce fever |
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describe pheylpropionic derivitives (Advil, Ibprofin)
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largest aspirin alternative.
they have antiinflam, analgesic, and antipyretic action Fewer GI side effects than aspirin |
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Coxibs
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Celebrex, Vioxx, Bextra
NSAIDS that only inhibit COX 2 so they produce less GI side effects. They are used for treating chronic pain. Very contraversial bc produce sever CV problems. |
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How do local anesthetics work?
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they reversibly block nerve conduction by blocking Na channel at the level of the sensory neuron
causes analgesia , loss of temp, touch, proprioception, and muscle tone |
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what fibers does local anesthetics work best on? Worst?
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Type B and Type C are the best bc they are unmylinated
Type Aalpha,Abeta,Agamma, and Adelta are less susceptible to anesthetic bc of their heavy mylination |
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what is added to local anesthetic solutions?
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vasoconstrictors like epinephrine to decrease systemic absorbtion and prolong duration of action of anesthetic
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Adverse effects of local anesthetics.
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can be absorbed from site of injection and cause problems, most problems due to ODing pt
Bc its lipid soluble, local anesthetics get into PNS and CNS so get lightheaded, dizzy, numb, and disorieted. If blood levels hi can go into convusions, excessive stimulation of CNS followed by resp and CV depression with hi conc of local anesthetic it can cause CV depression Allergic Rxn can occur due to dematitis, asthma, and anaphylactic rxn. allergic rxn occur more frequently with ester local anesthetic |
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3 FUNCTIONAL classifications of opiates
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agonists- opid agonist act on some or all of opoid receptors to produce a biological effect. Examples are morphine, methadone, dermerol, codeine, darvon, hydrocodone
antagonist-opoid antagonists are drugs that bind to all or some of opiate receptors but do NOT produce a biological effect. Examples: Narcan and Trexan Mixed Agonist/antagonists- mixed activate some opiate receptors and block others. the are partial agonists at kappa and competive antagonists at mu receptors, Examples: talwin, stadol, nubain |
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3 opoid receptors
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Mu-analgesia, sedation,miosis,constipation,respiratory depression, phys dependence, and euphoria
Kappa-analgesia, miosis, dysphoria, and sedation delta-analgesia |
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3 families of endogenous opiates
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1.endorphins-neurohormaone that mediates psychologic responses to stress and pain; hi affinity for mu
2.enkephalins-NT that has hi affinity for delta 3. Dynorphins-NT with hi affinity for kappa receptors |
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opoid analgesics and endogenous opiates 3 primary sites of action
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1.SC-opoids inhibit release of NT from primary afferents to inhibit DH neuronal activity
2.Thalmus-Opoids block perception of pain at level of thalmus, reticular foramtion, and limbic to depress pain rxn 3. activation of descending systems: opoids activate descending inhibatory systems which modulate pain transmitted at the level of the SC |
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what pain is treated best with opiates?
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severe dull costant pain is better releived by opoids than sharp pain.
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clinical uses of opiates
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releave pain
antitussive: supress cough antidiarrheal adjuct with anesthesia bc it is sedative and analgesic |
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tolerance
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decreased responsiveness to any pharmacolgic drug as a consequence of prior administration of that drug
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with opiate use, what can you develop tolerance for?
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analgesia
euphoria,dysphoria mental clouding sedation resp depression nausea and vomitting cough suppression |
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Physical dependence
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an abnormal phsyiological state produced by repeated administration of a drug, which then makes its continued use necessary to prevent withdrawl
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Scler
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tough outermost layer of the eye
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cornea
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transpartent surface, major refractive component, continuous with the sclera
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opening the controls the amount of light that reaches the retina
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pupil
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2 muscles of iris
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inner circular m. and outer radial m.
pupillary diameter depends on activity of these muscles. eye color is based on pigment in iris |
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lens
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fine tunes refraction for focosing light on the retina (allows accomodation)
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Ciliary m.
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sphincter like circular m. controls thickness of lens during accomadation
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zonular fibers
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conncects lens to ciliary m.
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what happens to zonular fibers with relax ciliary m?
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tension on these fibers is hi and lens is flat
when ciliary m contracts zonular fibers are more relaxed and lens gets more round |
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choroid
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highly vascularized between the retina and the sclera
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photorecetor area of the ey
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retina
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macula
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center area of retina where light fall if you look straight
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center of macula
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fovea centalis only cones are found here this is the region of greatest acuity
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entrance of optic n.
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optic dist aka blind spot
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visible spectum
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wavlengths in spectrum of 400-700 nm
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where does refraction occur in the eye?
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cornea and lens
the cornea has 3x the refractive ability the lens does! |
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how is refraction measured?
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in diopters. refractive ability equals 1/focal length in meter.
distance from cornea to retina is 0.024 m so 1/.024= 42 diopters lens only has 12 diopters |
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effect of refracton on image in eye
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image will be upside down and reversed from right to left on the retina
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As an object moves closer, what must occur to eye?
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an obj that is closer requires more refraction(diopters) to focus the image on the retina than a far away image. the eye accomodates. the ciliary m, innervated by PS component of CN III contracts releasing stretch on zonular fibers which allows the lens to assume a more spherical shape and increasing its refractive ability
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emmetropic
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normal vision
lens is flat and the refraction is done mainly by the cornea |
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hyperopia
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far sightedness; eye to short
when looking at a distant image, the images is focused behind the retina. The eye uses the lens to add refractive power to shorten the focal length so that the image falls on the retina. this uses up much of the refractive ability of the lens so that near objects cant be focused |
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myopia
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near sightedness; eye ball too long
when looking at a distant object the image is focused in front of the retina. This is no compensatory ability for the eye to increase focal length in this situation so that far objects are ALWAYS out of focus. objects that are closer produce a longer focal lenght bc the light paths diverge rather than stay parallel. this pushes the image back toward the retina so near objects can be focused |
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prebyopia
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with age lens becomes stiffer which prevents it from being able to assume a round configuarion. This reduces accomadation
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Astigmatism
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this is due to uneven curvature of the cornea which has the effect of focusing an object at 2 separate places on the retina, producing blurry vision
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what corrects hyperopia
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convex lens to increase diopters and refraction. the cornea is also convex and increaes diopters
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what corrects myopia
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reduce refraction, use concave lens to decrease diopters
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What type of lens corrects astigmatism?
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cylindrical lens
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visual acuity
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measure of the ability to distinguish between 2 points. the greater the number of photoreceptors, the better the eye's refractive ability, the higher the acuity
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how does a small pupil effect acuity?
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increases depth of field of focus bc by allowing less light to reach retina, fuzzy edges of object that is out of focus become darker so object appears to be in focus.
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path of light through the retina
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in most of retina, light must first pass through regions containing cell bodies and axons of the neurons before reaching photoreceptors
at the fovea, the neurons in front of photoreceptors are pushed laterally so that light has a more direct path to the photorecetprs |
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2 types of photoreceptor cells
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rods; very sensitive to lo light, lo acuity
cones; less sensitive to light, hi acuity, color vision |
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structure of photoreceptor
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outer segment contains light sensing apparatus. infolding of cell membranes make discs; these break off and are free floating in rods, but stay attached to cell membrane in cones
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describe photopigments
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the photopigment molecules are contained within the disc membrane. there are four photopigments; one for rods and 3 for cones.
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What do photopigments consist of?
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light absobing molecule called retinal (Vit A derivative) plus a proteins taht spans the membrane 7 times usually called an opsin which is different in each photopigment
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What is at the end of the photoreceptor opposite from the photopigments?
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machinery for releasing the NT glutamate
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ultimate result of phototransduction
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biochemical changes alterthe release of NT from the photoreceptor
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process in which biochemical events in the photoreceptor alter the electrical properties of the cell
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phototransduction
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2 major functional groups of brainstem descneding pathways
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1. medial systems that primarily influence posture
2. Lateral systems that control fine dextrous movements |
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2 types of medial BS descending pathways
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1. vesibulospinal tracts
2. reticulospinal tracts |
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vestibulospinal tract
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originates in vestibular nuclei and projects to the SC
1. it is ipsilateral 2. it excites extensors and inhibits flexors |
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reticulospinal tracts
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part of medial system
originates in medullary and pontine reticular formation and projects to the SC 1. uncrossed and crossed (contralateral) 2. pontine reticulospinal tract excites extensors and inhibits flexors and medullary reticulospinal tract excites flexors and inhibits extensors |
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2 types of lateral systems of BS descending pathway
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1. corticospinal tract originates in CC and projects to SC
2. Rubrospinal tract originates from red nucleus in midbrain and projects to SC the function of the 2 are coordinated |
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Corticospinal tract
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from cortex To SC
Contralateral excites flexors in distal limbs and digits and inhibits extensors |
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rubrospinal tract
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originates from RN in midbrain and projects to SC
crossed excites flexors in proximal limbs and hands, inhibits extensors |
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what does cerebral cortical motor regions control?
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volunary movements
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what are areas in cerebral cortex that produce movements when electrically stimulated termed?
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motor cortex
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2 major conceptual divisions of motor cortex
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primary motor cortex
premotor cortex |
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primary motor cortex
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low intensity electrical stimulation produces focal movement
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Premotor cortex
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consists of lateral convexity of brain and cingulate motor cortices on medial part of brain. in these regions, electrical stimulation produces movements but intensity required to evoke movement is greater that that needed in primary motor cortex and larger muscle grups are excited. these 3 regions have extensive connection wtih the primary motor cortex
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Are frontal eye fields motor cortex?
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they do not connect with primary motor corex instead they project to regions controlling saccadic eye movements
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area 4
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primary motor cortex
brodmanns area |
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where is brodmanns area?
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anterior of central sulcus. on lateral convexity of brain cortex is in precentral gyrus
primary motor cortex is located in the anterior portion of the brain the paracentral lobule |
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how is cortex somatotopically organized?
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leg is on medial surface. Arm, hand, and face are represented on the lateral convexity from superior to inferior.
there is a large representaion of fingers and thumb and for muscles used in speech |
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describe primary motor cortex contralateral representaion of the body
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primary motor cortex influences unilateral movement. The primary motor cortex provides input to all body and facial m of voluntary movement it also control distal limbs and digits bc there is no backup control for these if lesioin occurs
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what kind of movement is primary motor cortex primarily involved in?
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fractionated movement, finely controlled, dexterous movements across single joint.
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describe supplementary motor cortex
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stimulation on one side produces movements on both sides
it allows coordinated movements of both limbs it allows you to learn new movement sequence and mentally rehease the sequence. once you learn sequence well, the activity in the supplementary motor cortex lessens and primary motor cortex increases |
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2 parts of premotor cortex
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supplementary on medial brain suface
lateral premotor on lateral brain surface these take higher intensity to stimulate and allow more muscles to get excited |
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T or F the supplementary and lateral premotor cortex are both involved in regulating posture
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TRUE
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what has major projection to lateral premotor cortex?
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parietal lobe
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Lateral premotor cortex
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outer surface of brain
reacting to environment. Coordinates unilateral movements. posture adjustment is needed for the movement controls larger muscle groups on contralateral side. Allows reaching movements |
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somatosensory cortex
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recieves somatosensory input and relays info to complementary motor region
modulates sensory input so its appropriate for occasion |
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posterior parietal lobe
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recieves input form somatic sensory areas, visual areas, and premotor areas
coordinates spatial info with movement input to motor region from posterior parietal cortex allows you to move in relation to objects in environment |
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lower motor neuron
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spinal motorneuron or nerves or CN motor neuron
alpha motor neuron |
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what happens if damage to lower motor neuron?
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decrease m. tone
muscle atrophy muscle fasiculation abscence of tendon reflex no babinski sign |
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upper motor neuron
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refers to corticospinal neurons or other descending neurons above SC
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characteristic damage of upper motor neurons
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decrease m. tone then becomes increase m. tone (spacticty) over time
affect GROUPS of muscles enhanced stretch receptors (hyperreflexia) babinski sign |
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What is a babinski sign?
|
stroke lateral foot w/ sharp object:
in normal pt causes flexion toes w/corticospinal damage, big toe invariable extends and other toes fan out (babinski sign) |
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functions of cerebellum
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to produce coordination of movements
learn new movements equilibrium planning and coordination of movement |
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What seperates anterior and posterior lobe of cerebellum?
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primary fissure
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What seperates posterior lobe from flocculondodular lobe?
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posterolateral fissure
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3 major regions of cerebellum
|
1. vestibulocerebellum which consists of flocculondular and adjacent vermis
2. spinocerebellum which consists of most of vermis and paravermal zone 3. Cerebrocerebellum which consists of hemispheric or lateral zone |
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Cerebellar deep nuclei
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1. Fastigial n.
2. Globose + emboliform n. = interposed n. 3. Dentate n. |
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describe vestibulocerebellum
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signal in vestibular ganglia -> vestibular n. -> cerebellar fastigial n. -> sends signals to reticular formation and vestibular n. to aid with postural and balance
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Problem with vestibulocerebellum
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dizzy and when walk drift to that side
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Describe spinocerebellum
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information from all muscles in body go to spinocerebellar tract to the fastigial n and the interposed n. they compare what the muscles are doing with what the muscles should be doing and controls the ongoing movements. the fastigial n. affects posture via the vestibular and reticular n. The interposed n. sends signals to the Red N. and the thalmus which then sends signal to cortex to move arms/fingers
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describe cerebrocerebellum
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input and output form cerebral cortex
dentate n. projects to RN and thalmus to cortex. Cortex sends signal to basilar pons which then projects to cerebellum lateral zone. this is how cortex sends message to cerebellum involved with planning and timing of SKILLED movements |
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what do cerebellar lesions affect?
|
ipsilateral side, unless lesion is in middle, then both sides are affected
asnergia/dysynergia decomp of movement dysmetria ataxia dysdiadochokinesia intension tremor hypotonus nystagmus |
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dysmetria
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inaccurate range and direction of movement
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ataxia
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gait
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dysdiadochonkinesia
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cant perform rapid alternating movements
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hypotonus
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lose faciliation from deep n.
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functions of basal ganglia
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initiate movement
permissive effect on movemnt control gross movement adjust body position for task |
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direct pathway of basal ganglia
|
the cortex activates the putamen which inhibits the globus pallidus allowing the Thalmus to be activated (bc inhibit the inhibitor)
this increases thalmocortical activity increasing muscle excitation by corticospinal tract |
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indirect pathway of basal ganglia
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putamen activates the globus pallidus causing inhibitioni of the subthalmic n. so the globus pallidus is activated and it inhibits the thalmus decreasing thalmocortical activity
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