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125 Cards in this Set
- Front
- Back
How do we know that neurons are metabolically active cells?
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large nucleus
many organelles a lot of mitochondria produce alot of ATP require an abundant supply of O2 (lack of O2 for more than 4 minutes = cell death) |
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What is the carcinogenic potential for neurons?
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Low - because they are postmitotic
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Characteristics of spinal motor neurons.
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Extend out away from spinal cord, cell body in ventral horn, super long.
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Characteristics of spinal sensory neurons.
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Dorsal root ganglion receives input.
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Characteristics of cranial nerves.
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Motor neurons serving the head and neck, interface with the medulla or brain stem.
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Where are upper motor neurons found?
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cerebral cortex
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What is a ganglia?
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collection of cell bodies of upper motor neurons in the cerebral cortex.
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Dendrites
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bring input into cell body
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Axons
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take information away from cell body
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Synapse
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connection between 2 neurons
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How is communication mediated between neurons at a synapse?
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chemically - with a neurotransmitter
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Neurotransmitter
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substance that is released by a presynaptic neuron (in response to an AP in that neuron) that diffuses across the gap to the postsynaptic neuron, binds to a receptor and elicits a response in the postsynaptic neuron.
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Common examples of neurotransmitters
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acetylcholine, norepinephrine and dopamine are most common examples of neurotransmitters
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The connection between neurons may be ---------- or --------- depending on the events that occur in the postsynaptic cell in response to the neurotransmitter
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The connection between neurons may be excitatory or inhibitory depending on the events that occur in the postsynaptic cell in response to the neurotransmitter
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What is the aim of modern neuropharmacology?
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Modern neuropharmacology is aimed at maintaining or restoring normal neurotransmitter balance within neurons of the brain.
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The support cells of the CNS:
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Glia (neuroglia):
1.astrocytes 2.oligodendroglia 3.Microglia – not discussed 4.ependymal |
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All of the support cells in the CNS are...
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facultatuve mitotic cells
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Astrocytes
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Large star shaped cells, cytoplasmic processes link neurons and blood vessels
1.function in metabolism of neurotransmitters 2.help to form the blood brain barrier (BBB) 3.function to maintain extracellular fluid balance *network of support for neurons because no lymphatic system in brain |
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Oligodendroglia
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Cytoplasmic processes of myelinated nerve fibers. myelin- insulation – make transmitting AP faster
In peripheral nervous system, Schwann cells are equivalent Myelin allows for very rapid conduction of AP’s =Provide support -regulate extracellular fluid like astrocytes -most common glial cell (essentially a lipid layer coating the axon) |
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Myelin
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gray – unmyelinated, neural cell bodies
white – myelinated, cellular processes (no cell bodies) Myelin serves to insulate the neuron and allows for increased speed of the AP propagation *Some disease states affect the myelin sheath - MS |
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What cells line the ventricles and central canal of the spinal cord and have cilia to promote flow of CSF?
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Ependymal Cells
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what makes up the Central Nervous System?
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brain and spinal cord
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What makes up the Peripheral Nervous System?
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Peripheral sympathetic and parasympathetic nerves and the autonomic ganglia.
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What are the 3 distinct brain regions?
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Hindbrain (most primitive, 1st to develop) - medulla, pons, cerebellum
Midbrain Forebrain - cerebrum, thalamus, basal ganglia, hypothalamus |
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What functions is the frontal lobe associated with?
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motor, problem, solving, spontaneity, memory, language, initiation, judgment, impulse control, social and sexual behavior
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Functional regions of the parietal lobe.
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1.sensation and perception
2.integrating sensory input, primarily with the visual system |
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Function of occipital lobe.
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vision and the interpretation of vision
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Function of temporal love.
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auditory sensation, language, and perception
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Function of basal ganglia.
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integration centers for sensory information ascending to the cortex and motor information descending to lower levels;
monitors what SHOULD BE occuring with WHAT IS occuring; Coordinating muscle movement (fine adjustments) |
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Function of amygdala.
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center for emotions (fear, confusion, distrb. awareness, amnesia, rage)
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Function of hippocampus.
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short term memory, spatial orienting/processing info as it enters the brain;
largest neurons-prone to ischemic attack (result: s-t memory loss) |
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Function of thalamus.
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integrating sensory stimuli;
acquisiton of knowledge and awareness |
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Function of hypothalamus.
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integration of temp., HR, BP, thirst, appetite;
releases neurosecretory substances which activate pituitary (via neurons) to release hormones |
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Function of hindbrain.
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1st part to evolve;
reflex circuit low-level processing; pons, medulla oblongata, cerebellum |
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Function of pons, medulla oblongata.
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-most primitive
-visual/auditory reflex ctrs. -cardiac centers -rate/force of contraction -vasomotor center-BV tone -respiratory ctrs. - rate -origin of most cranial nerves |
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Function of the cerebellum.
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major integrator of motor function
-damage to the cerebellum affects coordination of limb and eye movement -compares what should be occurring with what is actually occurring - sends error messages to other areas -determine our position in time and space -damage results in ataxia, dysmetria, diffulting moving quickly, delayed initiation/termination |
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ataxia
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postural instability
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dysmetria
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disturbance of the trajectory or placement of a body part during movement
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Function of the midbrain (mesencephalon).
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all ascending and descending information to or from the cerebral cortex must pass through
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Function of the peripheral nervous system.
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nerves from CNS and the autonomic nervous system, including cranial nerves
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Function of the spinal cord.
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outer white matter and inner gray (opposite of brain tissue)
gray - neuron cell bodies white - myelinated fibers and unmyelinated from ascending sensory or descending motor neurons -motor root - going out -sensory root - coming in dorsal root ganglion - cell bodies for all sensory nerves |
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Function of Meninges.
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protective covering of brain and spinal cord.
Dura Arachnoid Pia (innermost) -brain injury will result in bleeding in at least one of the layers |
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Function of Cerbrospinal Fluid (CSF).
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Produced in choroid plexus (a series of specialized capillaries, it flows throughout the ventricular system and exits through lateral openings or a medial opening into the subarachnoid space (bathes brain, cushions brain).
-Can also enter the central canal of the spinal cord. -Low pressure -fast turnover (3x a day) -distinct composition and pressure - alterations in ions, cells, pressure indicate disease |
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An increase in CSF pressure is caused by ...
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-increased polymorphonuclear leukocytes - bacterial infection (and acute inflammation)
-increased lymphocytes - viral infection (meningitis) -decreased glucose concentration - bacterial infection (meningitis) – bac. use glucose for food |
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Function of Blood Brain Barrier
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-capillary endothelial cells and glial (astrocyte) cellular processes make a thick basement membrane
-glucose, alcohol, amino acids, oxygen and carbon dioxide readily penetrate -diffusion of lipids limited by size - one reason the brain can not metabolize fat to produce ATP – only glucose! -only certain antibiotics gain access to brain: erythromycin and sulfadiazine -insulin cannot cross |
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How is blood supplied to the brain?
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internal carotid --> circle of Willis on base of brain (circles the stalk of pituitary)
vertebral arteries, R & L vertebrals merge to form basilar; serve the pons, medulla, cerebellum |
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3 major branches from the circle of Willis:
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1.Anterior cerebral - supplies structures on the front of the brain
2.Posterior cerebral - supplies the back of the brain 3.Middle cerebral - supplies almost all of the lateral aspects of the brain – the largest portion |
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Aphasia
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Inability to comprehend and integrate receptive language or use language or both.
-∑ associated with lesions to the dominant cerebral hemisphere -extent of the lesion(s) determine(s) the extent of damage |
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Wernicke’s Aphasia
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damage to area where understanding and interpretation of word symbols occurs (in the dominant hemisphere);
lesions result in impairment in comprehension of speech -patient is unaware of a problem -affected persons have fluent, spontaneous speech with normal rhythm and articulation - word salad -comprehension, repetition and naming are impaired |
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Broca’s Aphasia
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Lesion located in frontal lobe just in front of motor area
-individual may not be able to utter a word or have limited speech -fully comprehends spoken word -fully aware - FRUSTRATION |
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Global Aphasia
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-large lesions to both Broca and Wernicke’s area in dominant hemisphere
-DUE TO MAJOR BLOCKAGE OF MIDDLE CEREBRAL ARTERY -all aspects of speech involved -patients usually have hemiplegia and are unable to comprehend or speak |
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Which hemisphere is dominant in most people?
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>90% of right handed people are left hemisphere dominant
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Paralysis
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loss of function and this includes both spastic and flaccid paralysis;
usually defined in terms of injury to upper motor neurons and lower motor neurons -Upper at higher levels of the brain and spinal cord -Lower at the level of the spinal cord OR peripheral nerves |
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2 types of paralysis
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1.Spastic paralysis – muscles are hard, rigid and difficult to move a joint; can exhibit hyperactive reflex activity
2. Flaccid paralysis – muscles flaccid with lack of reflex activity |
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Characteristics of Upper Motor Neuron Injury
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Spastic paralysis, hyperreflexia, Babinski sign, muscle atrophy (develops over a few weeks)
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Characteristics of LMN injury.
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Flaccid paralysis - loss of muscle tone
loss of peripheral reflexes occurs -no Babinski -significant and prompt muscle atrophy |
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What is the most common CNS malformation?
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Neural tube defects - failure of the neural tube to fuse.
-anencephaly -spina bifida |
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When does closure of the neural tube start and finish?
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start: 22nd day, finishes: 28th day of gestation
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This is a catastrophic defect resulting in failure of the brain to develop.
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Anencephaly - cerebrum does not develop, most common neural tube defect (1/500 preg.) May be carried to term but infant dies soon after. Higher in women over 40 (Ireland sees it in 1/200.) preg.)
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A group of neural tube defects in which the area affected is in the lower back.
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Spina Bifida - 4 kinds
Occulta (mildest; hair) Meningocele Myelomeningocele Rachischisis (most severe) |
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What is Spina Bifida Occulta?
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This defect is a lack of development of vertebral arches. Skin usually covers the defect- hair usually seen over the defect. Neural elements are in the normal location.
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What is Meningocele?
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Protrusion of meninges (ballooning) through a defect in the spinal column. Neural elements in normal location.
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What is Myelomeningocele?
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Protrusion of meninges (ballooning) through a defect in the spinal column with protrusion of cord elements.
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What is Rachischisis?
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Most severe form neural tube fails to close and open to the elements, brain is open to infection.
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What nutrient reduces incidence of neural tube defects?
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folic acid - essential for formation of nucelotide base thymine.
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What should women of reproductive age who are sexually active should take a supplement of folic acid?
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Because whether they intend to become pregnant, if they do, defects would occur prior to time woman knows she is pregnant.
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What are the types of traumatic head injury?
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concussion
contusion laceration |
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What is a concussion?
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Blunt head trauma characterized by loss of consciousness; no significant macroscopic or microscopic changes to the brain.
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What is a contusion?
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Disruption of cerebral and/or meningeal blood vessels by severe blunt trauma; associated with considerable mortality.
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What is a laceration?
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Open trauma to the brain tissue; highly fatal.
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What is cerebral edema?
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Fluid accumulation within the brain;
two types: cytotoxic and vasogenic - closely related. |
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What is cytotoxic edema?
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Cellular dysfunction or injury due to loss of cellular ability to regulate water.
Anything that causes loss of ATP to power the pumps will result in cytotoxic edema. If Na/K pump fails then Na accumulates --> water follows. *Intracellular accumulation |
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What can cause the loss of ATP to run Na/K pumps?
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intoxicants
hypoxia metabolic disorders infarction |
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What is vasogenic edema?
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Edema characterized by increased vascular permeability from damage to or dysfunction of cerebral vessels.
-composition of the fluid is similar to plasma – plasma proteins and it accumulates in the interstitial space. -this protein draws fluid by osmotic forces -lack of blood flow results in cytotoxic edema |
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Vasogenic edema results in...
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cytoxic edema.
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What are the clinical signs of cerebral edema?
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increased intracranial pressure --> decreased cerebral blood flow --> decrease in cerebral function --> hernaitions of the brain (through foramen magnum)
-brain appears heavy; wet -sulci are obliterated, ventricles flattened, subarachnoid space lost. |
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This is frequently seen in shaken baby syndrome or following major trauma to the brain.
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Cerebral edema
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This is a lay term for the slow or sudden onset of a series of neurological symptoms; a disease of old age and related to atherosclerosis of cerebral arteries.
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Stroke
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What causes stroke?
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1.Occlusion of cerebral vessels - from atherosclerotic narrowing of an artery, thrombus formation or lodgement of an embolism, or by
2.hemorrhage - from intracerebral, subarachnoid or AVM (arteriovenous malformations) bleeding. |
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What are factors that favor the development of stroke?
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hypertension, diabetes and thromboembolism
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What is the result of stroke?
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ischemia and necrosis to the brain
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What is a TIA?
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Transient Ischemic Attack - lasts for a few minutes to a few hours and the neurological deficits resolve.
-first sign of atherosclerotic narrowing or cerebral vasoconstriction |
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What is occlusive cerebrovascular disease?
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Includes atherosclerosis, cerebral thrombosis (usually of an atherosclerotic plaque) and cerebral embolism
-these have a final common pathway, even though pathogenesis of each is different. |
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What is cerebral atherosclerosis?
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cerebral arteries undergo the process of atherosclerosis -->
formation of an atheroma that projects into the vessel lumen --> inhibits blood flow --> ischemia -primary cause of TIAs -if lesion ruptures --> thrombus forms --> aggravates vessel narrowing |
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What is the leading cause of CVAs?
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Cerebral Thrombosis
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Where do cerebral thromboses usually cause an occlusion?
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curves and bifurcations of vessels - why? turbulence --> endothelial injury
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How quickly can cerebral thrombosis occur?
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gradual: thrombus forms on existing plaque over time causing occlusion
rapid: ischemic infarction from an embolus dislodged from an atherosclerotic plaque that moves to the brain. |
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What is the usual cause of death with cerebral thrombosis?
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cerebral edema (3-5 days later) from both cytotoxic and vasogenic mechanisms
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The clinical presentation of cerebral thrombosis.
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gradual or more rapid occlusion of middle cerebral artery (#1 cause) results in contralateral hemiplegia,
sensory loss, bilateral symmetrical loss of vision in half of the visual field, headache, vertigo, confusion, aphasia, other focal neurological signs -global aphasia can occur if dominant hemisphere affected -GRADUAL ONSET OF SYMPTOMS |
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Characteristics of cerebral embolism.
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-source from heart due to atrial fibrillation, bacterial endocarditis, valvular disease
-also from dislodged thrombus on atherosclerotic lesion -can cause massive infarction -SUDDEN ONSET OF SYMPTOMS |
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What is hemorrhagic cerebrovascular disease?
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intracranial bleeding.
ex: intracerebral hemorrhage, aneurysms |
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What is an intracranial hemorrhage?
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rupture of blood vessel due to congenital abnormality (aneurysm); rupture caused be traume or through other mechanism like HTN.
-4 groups based on location epidural, subdural, subarachnoid, intracerebral |
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What is an epidural hematoma?
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Hematoma located between the skull and dura usually due to tear in a meningial ARTERY.
-causes pressure on brain, coma, and death -DELAY ON ONSET OF SYMPTOMS Tx - drill hole in skull to drain blood |
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What is a subdural hematoma?
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Hematoma located between the dura and the arachnoid layer, usually due to rupture of thin walled bridging VEINS that traverse this area.
-MUCH SLOWER DEVELOPMENT THAN ARTERIAL BLEED (epidural h.) |
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What is a subarachnoid hemorrhage?
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Ruptured cerebral vessels due to: arteriovenous malformations or rupture of berry aneurysms caused by trauma to cerebral vessels on the surface of the brain.
-HIGH MORTALITY -BLOOD IN CSF (arterial bleed in subarachnoid space) |
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What is an intracerebral hemorrhage?
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bleeding within the brain; results from rupture of small vessels damaged by HTN. Common site is basal ganglia.
Presents like cerebral embolism but more dramatic and severe headache. |
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Aneurysm
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Berry Aneurysm - subtype of hemorrhage in the subarachnoid space. A defect of weakness of cerebral arteries --> outpouching. Originate in circle of Willis --> can be silent then rupture with HTN.
S&S: blood in CSF, very different treatment if hemorrhagic (vs. occlusive) |
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Neoplasms of the CNS
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These are relatively rare, and can occur at any age but more prominient in youth and elderly.
50% tumors are primary 50% are metastatic |
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Why are malignant neoplasms of the CNS hard to treat?
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Difficult to differentiate normal brain from the highly infiltrative malignant tumor.
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Why do primary malignant tumors not metastatize?
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Because of the BBB, no lymphatics in the brain.
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Clinical manifestations of intracranial tumors:
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highly variable
headache, vomiting, papilledema (eyes - fundus bulging) paralysis, seizures, memory loss, visual field defects, cranial nerve dysfunction, mental status, speech disorders, tongue dev. to one side |
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Classification of CNS tumors
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tumors of glial cells (75%)
tumors of the meninges (15%) Other 10% |
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Astrocytomas
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a type of astrocytic glioma; occure as
1.solid cerebral tumors in adults 2.cycstic cerebellar tumors in children -slow growing, well-differentiated astrocytes |
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Glioblastoma multiforme
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-Most common CNS malignancy
-more malignant than astrocytomas -peak incidence at age 65 -irregular shape, pooly demarcated from normal brain parenchyma -highly infiltrative and vascular tumor, very rapid growth, no resemblance to parent cell |
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Oligodendrogliomas
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RARE
-in cerebral hemispheres - usually frontal lobe, in middle-age adults -lesions well circumscribed, cystic, calcified (dystrophic) -well-differentiated cells |
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Ependymomas
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tumors derived from ependymal cells
-malignant and benign -ventricular ependymomas in children -spinal ependymomas in young adults S&S: muslce weakness, disuse atrophy, sensory loss |
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Prognosis of gliomas
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gliobastoma multiforme - fatal
astrocytomas - 5 yrs (poor) cerebral oligodendrogliomas & ependymomas - better, but needs early detection |
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Meningioma
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tumor of the meninges
-benign lesion - in women after 70 -S&S: seizures, headache, visual impariment, hemiparesis, aphasia, compression of brain -can be surgically removed; excellent prognosis |
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metastatic tumors
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spread from other sites - usually lung (45%) breast (20%)
-poor prognosis |
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Agents of CNS infection
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bacteria, viral, protozoal, fungal
-acquired by direct extension via the blood, through the blood and via nerves |
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Common bacterial causes of CNS infection:
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N. meningitidis (meningococcus) and S. pneumoniae, E. coli, H. influenzae, T. pallidum
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Common viral causes of CNS infection:
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measles, rubella or adenovirus, CMV, herpes virus, rabies virus, arbovirus (mosquito vector) resulting in various forms of encephalitides (St. Louis, California, Venezuelan, etc), HIV, west Nile Fever, Dengue Fever
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Mad Cow Disease
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at least 2 forms of prions have been identified
-spread in animals by feed infection with neural tissues of infected animals -brain has spongy appearance |
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Encephalitis
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infection of brain parenchyma; usually viral invasion of neural and glial cells
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Meningitis
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inflammation of the meninges
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Viral Meningitis
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T-lymphocytes fight virus --> exudate rich in T cells in subarachnoid space and CSF
-NO change in glucose |
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Bacterial Meningitis
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exudation of neutrophils into subarachnoid space and CSF
-LESS glucose (it is used by the bacteria) -S&S: stiff neck (nerves irritated by the infection) |
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Multiple Sclerosis
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demyelinative disease affects 250,000 Americans, usually women 20-45 of Northern European origin who live in temperate climate zones above the 40th parallel
-clustering (NW Ohio) |
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Clinical Features of MS
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recurrent episodes of neurologic symptoms
-sensory (touch) and motor (weakness) abnormalities -Dx 2 separate sets of CNS symptoms *Upper motor neuron injury +Babinski, hyperreflexes |
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Pathology of MS
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lesions infiltrated with T cells and macrophages in PLAQUES, oligodendroglial cells are gone (no insulation)
-Tx with corticosteroids, immunosupressives to SLOW |
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Neurodegenerative diseases
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neuron cells themselves die (different from MS)
– Parkinson’s – Huntington’s – Alzheimer’s |
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Alzheimer's
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form of dementia - atrophy of the corticol parts of the frontal and temporal lobes
-50-60% of people over 85 -loss of brain neurons that use acetylcholine as a transmitter affected -LONG course, die from some other disease -Dx only with exam of cortex so Dx is with the presence of progressive dementia |
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Parkinson's
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-subcortical (other than the cortex) neurodegenerative disorder
-movement disorders; decreased numbers of dopaminergic neurons in the substantia nigra – a part of the midbrain -tremor, rigidity, bradykinesia postural instability |
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Huntington's
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utosomal (chromosome 4) dominant neurodegenerative disease characterized clinically by choreiform movements and progressive dementia. (Chance 50/50 of getting)
-atrophy of the cortex and subcortical basal nuclei (caudate and putamen) -appears in the 40s and rapidly deteriorates |
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Choreiform
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- irregular, spasmodic involuntary movements of the limbs or facial muscles often accompanied by hypotonia (decreased muscle tone)
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