Systems 3 review.txt
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What cells and structures are derived from neural tube?
- Ependymal cells
- Choroid cells
- Brain, spinal cord
What cells and structures are derived from neural crest?
- Pia and arachnoid mater
- Choroid stroma
- PNS(spinal&cranial nerves outside brain & SC, schwann cells, ENS ANS)
What cells and structures are derived from mesoderm?
What are the functional divisions of the cerebral cortex?
- Frontal: higher cognitive
- Parietal: spatial and navigation
- Temporal: Auditory, speech and memory
- Occipital: Vision
What are the barriers of the brain?
- 1. Blood brain barrier
- 2. Choroid Cell barrier
- 3. Arachnoid barrier: tight junctions
- 4. Perineurial barrier (
- What is the sulcus limitans?
- Separates developing gray matter into basal(motor,ventral, interneurons) and alar(sensory,dorsal, 2o) plates along spinal cord through mesencephalon.
- Primary 1o sensory neurons come from neural crest
- In brainstem, Separates cranial nerve motor nuclei(medial) from sensorty nuclei(lateral)
What are the neurotransmitter criteria?
- 1. Present in presynaptic cell
- 2. Released by depolarization
- 3. Acts on receptors on postsynaptic cell
What is the primary mechanisms of excitation and inhibition?
- Excitation: generally leads to influx of Na+
- Inhibition: generally leads to influx of Cl-
List some important neurotransmitters.
- Glutamate: major excitatory neurotransmitter in the CNS
- Acetylcholine: excitatory neurotransmitter in the neuromuscular junction
- GABA: major inhibitiry neurotransmitter
- Glycine: another inhibitory neurotransmitter
- Biogenic amines: dopamine, serotonin, norepinhrine, epinephrine, histamine: mostly excitatory
- ATP and purines: excitatory
- Neuroactive peptide: endorphins, enkephalon, substance P, etc.: modulate activities
- Nitric oxide: excitatory and inhibitory
- Peptide transmitters are made in the cell soma, processed to form active portions, transported to axon terminals, and stored in large, dense vesicles
- Other neurotransmitters (amino acid-based, ACh, etc.) are synthesized in the axon terminal and stored in smaller, clear vesicles
Describe the process of neurotransmission at the chemical synapse.
- 1. Transmitter synthesis, uptake & storage in vesicles
- 2. Action potential invades axonal ending
- 3. Opening of Ca2+ channels
- 4. Influx of Ca2+
- 5. Vesicle fusion with presynaptic membrane
- 6. Transmitter release
- 7 & 8. Transmitter acts at postsynaptic receptors
- 9. Change in cell excitability
- 10. Recycling of vesicle
Describe glia and the different types
- Glial cells
- -Outnumber neurons 5-10:1
- -Oligodendrocytes-myelinate CNS axons, multiple oligodendrocytes per axon
- -Schwann cells- Neural crest derived, myelinate PNS axons, one Schwann cell per axon
- -Myelination increases nerve conductance
- -Astrocytes- many different types, play complex roles- surround and modify synapses, trophic support for neurons, capillary blood pressure regulation, nutrient support, injury response
- -microglia- not CNS derived, but rather from blood system (macrophage), act to keep the nervous system clear, are activated and more are recruited into the nervous system in injury response
- -radial glia-astrocyte-like, provide scaffold for migrating neurons in the cortex and other places, often serve another function as neural stem cells
- -Loss of myelination is the underlying cause of several diseases including multiple sclerosis- leads to decreased nerve conductance and eventually loss of neurons
- -astrocyte/oligodendrocyte response to injury can impede axon regrowth;
- but Schwann cell response seem to facilitate axon regrowth (hence peripheral nerves regenerate much better than central nerves)
What are two main factors that affect nerve conductance?
What are the roles of astrocytes?
- (1) Structural support (glia =’glue’)
- (CNS has no extracellular matrix - astrocytes provide support)
- (2) ‘Maintain’ extracellular environment
- K+ uptake
- Glutamate uptake
- (3) Provide energy metabolites essential for neuronal function
- (4) Interact with synapses: influence synaptic activity, plasticity and synapse number
- (5) Regulate blood flow through cerebral vessels
- (6) Blood-brain barrier (induction and repair)
- (7) React to injury
As you go up toward the brain stem what happens to the white matter?
Describe the somatotopic organization of the white matter.
- Medial to Lateral:
- Fasciculus(dorsal column): Gracile (sacral, lumbar), Cuneate (thoracic, cervical)
- Lateral Corticospinal Tract(lateral column): cervical, thoracic, lumbar
- Spinothalmic tracts(ventral column): cervical, thoracic, lumbar sacral
Describe the organization of the gray matter.
Rexed’s Laminae goes from I to IX dorsal to ventral and X forms the central canal connects VII
What is the difference between lower and upper motor neurons?
- Lower Motoneuron
- Typically an -motoneuron whose axon innervates skeletal muscle:
- - soma in CNS, but axon leaves CNS & enters the PNS.
- Upper Motoneuron
- A motoneuron with the soma and axon entirely within CNS (i.e. descending fibers)
- - directly or indirectly innervates lower motoneurons
What is a motor unit?
- All muscles innervated by at least 1 alpha-motorneuron (most 1)
- Vary in size
- Muscle fiber type in a unit is constant (slow, fast-fatigue resistant, fast fatigable)
Describe a typical stretch(myotatic) reflex loop.
- I-alpha afferent senses stretch enters dorsal and synapses with alpha-motor(stimulate extensor) and interneuron(inhibit flexor via gamma motor neuron)
- Homonymous & synergistic muscles stimulated
- Antagonistic muscles inhibited (via interneuron)
Describe an inverse myotatic reflex loop.
- Protects tendon and muscle from injury due to excessive tension
- GTO afferent via Ib neuron
- Interneuron->alpha-motor neuron
Describe the circuitry of the Flexor reflex.
- Protective reflex using multisynaptic relays to maintain posture.
- Stimulus conveyed via A-delta nociceptor
- Reciprocal innervation: Ipsilateral (stimulus side)= flexors excited, extensors inhibited
- Double reciprocal innervation: Conralateral flexors inhibited, extensors excited
- Net effect: stimulus limb flexed, opposite side extended
- Interneurons used for inhibition
Describe the sequelae of Lower MN syndrome
- Damage to ventral horn or cranial motorneurons
- Symptoms: paralysis, paresis(weakness), areflexia, loss of muscle tone & atrophy
- Fibrillations: spontaneous twitches(altered excitability) of denerved muscle fibers
- Fasciculations: spontaneous twitches of motor units, abnormal injured alpha MN
Describe spasticity of Upper MN syndrome
- Damage to descending motor pathways
- Symptoms: increased muscle tone, hyperactive stretch reflex, clonus
- Clonus: oscillatory motor response to muscle stretching)
- Causes of symptoms: removal of inhibitory descending influenced exerted by the cortex and postural centers (vestibular nuclei & reticular formation)
- Ameliorated by lesions to vestibular nuclei and deafferentation (removal of DRG)
- Therefore spasticity represents an abnormal increase in afferent gain.
Briefly describe mechanoreceptors in the DC-MLS.
- Meissner corpuscle: skin motion, slip
- Pacinian corpuscle: high-freq vibration
- Ruffini’s corpuscles: cutaneous stretch
- Merkel’s disks: shape, force and textures
- Free nerve endings: pain
- Superficial: precise, small field
- Deep: broad
What are signs of CN III autonomic damage?
Loss of sphincter pupillae: eyes dilated at rest, no light reflex
What happens if there is a trochlear nerve lesion?
- Rest: eye is elevated and extorted
- Adducted: inability to depress.
What are the symptoms of CN VI lesion?
Lateral rectus abducts eye, therefore when looking straight ahead eye is adducted(crossed)
Which part of the trigeminal does the motor root come from?
V3, mastication (masseter, temporalis, lateral & medial pterygoid, anterior digastric, mylohyoid, tensor veli palatine and tensor tympani
What are the symptoms of Bell’s Palsy?
- CN VII: Loss of facial expression and hyperacusis: loss of muscle to stapedius function
- Also loss of anterior 2/3 taste
If you cannot smile on one side voluntarily but can when told a joke what is the problem?
- Upper lesion in the contralateral side of not smiling
- Stroke injury to descending influences of voluntary RIGHT motor cortex. (left side not smiling)
What happens with hypoglossal nerve damage?
- Defective tongue innervation
- During Extension tongue deviates to damaged or lesioned side and shrivels on that side.
- Lower motor neuron lesion
What are the tools to minimize pain?
- Accurate assessment
- Methodical prevention
- Aggressive treatment
Describe what happens during peripheral sensitization.
- Nociceptors: increased impulses elicited by successive stimuli
- Reduced threshold
- Initiation or increase of ongoing activity
- Arachidoniic acid metabolites: prostaglandins, leukotrienes
Describe what happens during early and late central sensitization.
- Early: neuropetides
- Late: prostaglandins via IL-1 Interleukin 1
What are opiods main mechanisms?
- G-protein coupling decreases adenylyl cyclase, cAMP, PKA, CA2+influx channels and increase K+ efflux
- 1. Decrease Ca2+ flux->dec neurotransmitter rls
- 2. Decrease synaptic transmitter activity
- 3. Hyperpolarize dorsal horn neurons
What are the side effects of opiods?
- Nausea, constipation, orthostatic hypotension, RESPIRATORY DEPRESSION, miosis(pupil constriction, may mask head injury symptoms)
- May suppress immune system
What are the consequences of pain?
- Inhibit immune function
- Enhance tumor growth
What is the difference between naloxone and naltrexone?
- Naloxone: short, non-oral
- Naltrexone: long, oral
What is the difference between tolerance and dependence?
- Tolerance:decreased pharm effect from improper administration
- Dependence: adaptation to reset homeostasis from repeated drugs
What is the technique to avoid withdrawal of opiates?
What is the main interaction to avoid with opiates?
- Further CNS depression.
- MAO inhibitors, phenothiazines, tricyclic antidepressants, local anesthetics
What’s the current alternative to rofecoxib (Vioxx)?
Ibuprofen 800mg x3 x 3 days and PPI
What are the different types of TMD?
- Anterior Disk Displacement w/Reduction: non-painful=no treatment
- Anterior Disk Displacement w/o reduction(close lock): MANIPULATION, PT, arthrocentesis, surgery
- May need splint(NSAIDSs) to stop inflammation
- Splint may alter bite
How far can people open jaw on average?
What is arthritides?
- Achy joint, tender, pain, swelling, malocclusion, crepitus(creaking), reduced joint space, loss of subcortical bone or sclerosis
- Diagnosis: pain, crepitation, pain w/chewing, tomograms, Westergren autoimmune measurements
- Treatment: home care, hinge axis exercise, NSAIDs, corticosteroids, JOINT INJECTED STEROIDS or lube
What are typically myofascial pain referral patterns?
- Masseter to molars
- Splenius: top of head
- Temporalis: temple, orbit, anterior teeth
What is the treatment for myofascial pain?
- Identify triggerpoints (injections), elimate provoking factors, correct posture
- N stretching
- Moist heat and ice
- Decrease muscle load
- Spray and stretch
- Manage stress
What are some neuropathic pain descriptors?
- Sharp, shooting, electric, burning, tingling
- Dysesthesia: abnormal sensatioin
- Allodynia: pain from non-painful stimuli
- Parasthesia: abnormal numbing sensation
What is the difference between peripheral and centralized pain?
- Peripheral: static mechanical allodynia (A-delta and C damage)
- Central: dynamic mechanical allodynia (brain, neurotransmission w/o stimuli)
What are the features of trigeminal neuralgia?
- Stabbing, electrical shock
- Unilateral intermittent, cyclic
- May be due to superior cerebellar artery compression
- MRI REQUIRED
- Rule out MS
- Treatment: anti-seizure(gabapentin), anti-depressants, surgery (cushion artery & nerve), rhizotomy, glycerol, gamma knife
What are intercranial causes of pain?
What are extracranial causes of pain?
What are the neurovascular causes of pain?
- Temporal arteritis
What are the distinguishing features of tension type headaces?
- Most prevalent
- Pressing/tightening, mild
- No physical aggravation or vomiting.
- Treatment: NSAIDs, muscle relaxors, Tylenol, ASA, relaxation
What are the distinguishing features of Migraines?
- UNILATERAL, PULSATING, MODERATE TO SEVERE
- Nausea, vomiting, photo or phonophobia
- Treatment: ASA NSAIDS,Tylenol
- Moderate: triptans, ergotamines, opiates, antiemetics
- Preventative: tricyclics, B blockers, Ca blockers, valproate, topiramate
What are other types of headaches?
- Menstrual Migraine (estrogen withdrawal) use single phase estrogen
- Cluster Headache (autonomic dysfunction)ORBITAL
- Subarachnoid Hemorrhage (headache is the red herring) spinal consequences
- Basilar Migraine (presents with mulitple brainstem dysfunctions)
- Medication Overuse
- Trigeminal Neuralgia (electrical-like, excruciating pain radiating to teeth)
- Venous Sinus Thrombosis (severe symptoms, consider risk factors, unilateral numbness weakness)
- Paroxysmal Hemicrania (cluster-like, gout med indomethacin)
- Sexual Activity
- Low CSF Pressure (associated with position-dependent symptoms chiari malformation)
- Temporal Arteritis with Polymyalgia Rheumatica
- (one sided headache seen mostly in elderly, generalized achiness)
- Tolosa-Hunt Syndrome (cavernous sinus thrombosis affects multiple nerves, especially of orbit)
What is aura?
Visual symptoms, sensory symptoms, dysphasic speech disturbance.
What are the features of aspirin/salicylates?
- Analgesic: peripheral & central, no tolerance/addiction
- Antipyretic: inhibits PG synth in brain
- Antiinflammatory: inhibits PG in brain and periphery
- CV: none
- Adverse: salicylism, bleeding (inhibits platelet aggregation), GI ulcer, renal/hepatic toxicity, asthma, Reye’s
What are the features of analine derivatives?
- Analgesic: peripheral & centeral
- Antipyretic: prevent PG in brain
- Antiinflammatory: not much
- CV: none
- Blood: no inhibition of platelet aggregation
- Adverse: Hepato/nephron toxicity, allergy, blood dyscrasias
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