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Neuro system

James Murdoch Medicine 2 Englisch 4,1Durchschnittliche Bewertung 4,1 von 5 (7 Bewertungen) 200 Karten

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  1. 1Cells that myelinate the nerve cells in the CNS/PNS?Oligodendrocyte/Schawnn cells
  2. 2PSNS vs SNS differences?PSNS longer pre ganglionic neurone
    PSNS neurotransmitter always ACh
  3. 3What decreases the risk of NTD?Folic acid
  4. 4Number of layers in the cortex? Neurones break through which plate to reach cortical plate?6
    Subplate
  5. 5Where do the two dura layers spilt?When brain fissures at falx cerebra
  6. 6The superficial layer is different to the deep layer how?Not continuous with the spinal cord
  7. 7What allows the CSF to drain into the sinuses at the Falx cerebri?Arachnoid Villi
  8. 8Tentorial herniation occurs why? and damages what?SOL (tumour) causing dura to exert pressure on the brain leading to Brainstem/cerebral and cranial nerve damage
  9. 9Collections of arachnoid villi are called?Granulations
  10. 10CSF produced by what cells?Choroid plexus
  11. 11Haemorrhage types and what vessels burst?Extra dural- meningeal arteries
    Sub dural-cerebral veins
    Subarachnoid-Cerebral artery
  12. 12Four differences in CSF and blood?Low glucose and potassium
    Protein and cholesterol
  13. 13Describe CSF circulation?Lateral to 3rd to 4th into subarachnoid space
  14. 14What happens when CSF is continuosly produced?Hydrocephalus
  15. 15What areas lack the BBB?Areas around 3th and 4th ventricle
  16. 16Dicenphalon is?Thalamus/hypothalamus
  17. 17Hypothalamus connected to, functions?Connected to pituitary gland, maintains drinking eating and circadian rhythms
  18. 18Functions of the amygdala and hippocampus?Social behaviour and emotion
    memory
  19. 19Functions of temporal/occipital/parietalAuditory/visual and sensory and motor functions
  20. 20Explain the loop involving the basal ganglia and SMABasal ganglia to the ventral nucleus which is in the thalamus, this directs info to the SMA that distributes it amongst the cortex then back to basal ganglia
  21. 21Lentiform nucleus/striatum are composed of? LN is lateral or medial to the internal capsulePutamen/GP
    Putamen and caudate nucleus
    Lateral, GP most medial then putamen
  22. 22Connections from the BG to the thalamus are?Internal segments of the GP and substantia nigra (pars reticulate)
  23. 23Dopamine containing neurones are?pars compacta
  24. 24Direct and indirect pathways function? Describe each pathway briefly?Direct activate movement
    Indirect inhibit movement
    GABA inhibition of IGP so no longer inhibits thalamus, Glutamate stimulation of IGP so increases tonic inhibition of thalamus
  25. 25Parkinsons disease is caused by degeneration in what part of the brain?Substantia nigra
  26. 26Huntingtons diseaseLost of striatal neurones and then lost of cortical neurones
  27. 27Ballism is caused by?Damage to subthalamic nuclei, and it excites the IGP that inhibits movement.
  28. 28The vertebral arteries branch off where?Subclavian
  29. 29Describe what part of the brain each branch of COW supplies?ACA-Parietal and frontal
    MCA-temporal
    PCA-occipital
  30. 30Lower limb,Upper limb and face motor and sensory arterial supply?Anterior supplies lower limb and middle supplies upper limb
  31. 31Describe a watershed infarct?When perfusion pressure is low can occur where blood supply overlaps?
  32. 32Commonest site for an ischaemic stroke and why?Middle cerebral artery, connected to ICA, so emboli elsewhere in the body can reach the MCA
  33. 33CBF=, how much of the CO does the brain use?CPP/CVR
    15%
    CPP=MAP-ICP
  34. 34Range of brain auto regulation?50-170
  35. 35CBF maintained by what 3 things?Neural/metabolic/myogenic
    Neuronal control is weak
  36. 36PSNS/SNS control arises from where?Facial and superior cervical ganglion
  37. 37Metabolic control?Decreasing pH and increases CO2 pressure causes VD
    Increases in K+ causes VD
  38. 38Reduction in O2 supply triggers production of what chemicalAdenosine within 5 secs
  39. 39Myogenic control does what to vesselsConstricts them
  40. 40Marker used for fMRIgadolinium
  41. 41Final type of brain imagingPET
  42. 42Three components of the skullBrain tissue/blood/csf
  43. 43Average ICP20mmHg
    True is between 5-13mmHg
  44. 44CPP/mean BP/ ICP equationCPP=MAP-ICP
  45. 45Cardiac arrests causes what at watershed zones?Hypoperfusion causes ischeamic
  46. 46Four causes for raised ICP?Edema/hydrocephalus/bleeding/SOL
  47. 47S&S of raised ICP?Headache papillodema vomiting
    Pupil changes/hemiparesis
  48. 48Types of intracranial herniation?Subfalcine/transtentorial/foramen magnum
  49. 49Effects of a transtentorial herniation?Compressed PCA/Crn 3
  50. 50Berry anerysm occurs which intracranial space?Sub arachnoid
  51. 51Secondary tumours of the brain come from where?lung/breast/skin/renal + colon
  52. 52Primary tumours relatively affect which demographic the most?children
    Medulloblastoma
    Pilocytic astrocytoma
  53. 53Two types of hydrocephalus?Non-communicating=blockage
    Communicating=thickening of arachnoid villi
  54. 54Are neurones terminally differentiated?Yes
  55. 55Human brain consumes what % for each of the following: CO/02/Glucose15/20/25 percent
  56. 56The nernst Equation tells us what?The equilibrium potential for to be no net movement of that particular ion
  57. 57Goldmanns equation uses what three variable?Conc gradient
    Voltage gradient
    Membrane permeability
  58. 58If the RMP becomes closer to Nernst potential what has happened to the permability?It has increased for the ion, Na+ it depolarises
  59. 59Where are the action potential generated?Axon hillock
  60. 60For saltatory conduction which is more important for the speed of the impulse myelination or diameter?Diameter
  61. 61Astrocytes have what functions?Metabolising neurotransmitters/bridging between blood vessels and neurones/regulating ionic conc
  62. 62The WBC of the brain are called?Microglia
  63. 63What lines the ventricles?Ependymal cells
  64. 64Number of cells it myelinates Schawnn and oligodendrocytes?1/10
  65. 65Microplagia form amyloid plaques in what disease?Alzheimers
  66. 66Summation allows?Single EPSP not adequate to reach threshold potential
  67. 67How do neurones pass info?By rate of coding, this controlled by the synapse
  68. 68Sensory discrimination is sharpen by?Lateral inhibition
  69. 69EEGS release frequencies what does delta/theta/alpha/beta indicatesleep/memory/restfullness/active concentration
  70. 70Dopamine depletion occurs where?striatum
  71. 71Levodopa is given with what other drug? Commonest side effect with levo dopa?Carbonic anhydrase inhibitor
    dyskinesias
  72. 72+/- of direct dopamine agonists?bypasses nigrostriatal neurons
    activation of peripheral dopamine receptors
  73. 73What cant you consume when on a MAO-B inhibitor such as selegiline?Tyramine/tricylics anti depressants
  74. 74Dopamine depletion leads to what?cholinergic overactivity
    give you dry mouth
  75. 75Deep brain stimulation implant is located where?subthalamic nucleus/GP/thalamus
  76. 76Gene therapy use what?Neurotrophins-BDNF
  77. 77Huntington disease is causes by increases numbers of what codon?Glutamine
  78. 78CAG repeat length determines what?Onset however rate of progression does not!
  79. 79Potential therapies for Hungtindons?coenzyme Q10/creatine(2care crest-e)
  80. 80Somatosensory conveys all sensory to the CNS apart from? Methods of obtaining info?Special senses
    Extero/Intero/Proprio
  81. 81Where do sensory afferent neurones decussate? What cell type? Synapse where?In the spinal cord
    Pseudouni-polar
    Dorsal horn
  82. 82Sensory ganglia are found where? In cranial nerves?Dorsal root ganglion
    trigeminal ganglion
  83. 83Peripheral neuropathy presents in what fashion?Glove and stocking
  84. 84The stimulus strength is indicated by what?The rate of AP
  85. 855 variables for sensory afferent neurones?Modality/Threshold/Adaptation
    Conduction velocity/Receptive field
  86. 86What is an adequate stimulus?Type of energy that the receptors respond to most effectively
  87. 87Low versus high threshold types?Low-touch/warm/cool
    High-Nociceptors
  88. 88Slowly/rapidly adapting fibres?Stretch receptors are SA
    RA react to movement/acceleration
  89. 89Are A fibres myelinated? C fibres run in what?Yes
    Run in remak bundles
  90. 90Receptive field in primary afferent neurones?site of projection of the peripheral terminal
  91. 91Which fibres have the slowest and quickest conduction velocity?Aa fastest
    C slowest
  92. 92Non-nociceptive cutaneous fibre class?AB
  93. 93Pacinian corpuscle?Fibroblasts/modified schwann cell
    RA/deep
  94. 94Meissners corpuscle? What plays the role of these in hairy skinMechanoreceptor and low frequency vibration
    Only in glabrous (no hair)
    RA/superficial
    G cells
  95. 95Merkel cells?Special senses/touch cells
    SA/superficial
  96. 96Ruffini?Tissue stretch sensor
    Deep/slowly adapting
  97. 97LTM stand for and what fibre type?Low threshold mechanoreceptors
    c fibre
  98. 98Two types of muscle afferents, general characteristics?1a dynamic adaptation/change in stretch
    II static adaptation/tonic stretch
  99. 99Type 1&2 tendon and joint receptorsRuffini and Pacinian corpsule
  100. 1004 types of processing in the ascending pathway?Convergence/divergence/lateral inhibition/centrifugal control of neuronal facilitation(accurate transmission of sense/awareness of part of body)
  101. 101Lateral inhibition releases what NT?GABA
  102. 102Define nociception?Detection of stimulus that is potentially harmful
  103. 103Pain is transmitted in what fibres, where to the cell bodies of these sit?C and Adelta
    Dorsal root ganglion/nodose/cranial
  104. 104Cutaneous nociceptors have? Sharp pricking pain versus slow burning pain?Free unmyelinated ending
    Adelta is sharp pain
    C is slow dull pain
  105. 105TRPV-1 is found where? Describe its actionLocated in C-fibre terminals
    Ion channel activated by capsaicin, cation so leads to depolarisation
  106. 106Why does a burn continue to hurt at room temp?TRPV-1 Threshold to heat decreased by prostaglandins/bradykinin/histamine which are released during inflammation. So more are active at lower temperatures
  107. 107Nociceptors release what substances?Glutamate-main excitatory
    CGRP/Substance P-Modulatory role slow EPSP
  108. 108Central sensitisation Where does windup occur?WINDUP constant stimulation of C-fibres that lead to more evoked AP's in WDR neurones
    Lamina V
  109. 109Give a few differences between high and low threshold primary afferents?Nociceptives=smaller/higher threshold/large peptide content (substance P CGRP)
    Slowly adapting
  110. 110Gate control theory stimulates what fibre to counter act pain?AB
  111. 111Spinothalamic tract where does it decussate?Immediately
  112. 112Cortical areas active in pain?Primary sensory cortex/association cortex
    Anterior cingulate cortex
  113. 113Interoceptive activates what?Insular cortex, also where we imagine pain and the intensity of pain
  114. 114PAG/Amydala/hypothalamus role in pain?FIght/flight
    fear/anger/anxiety
    nausea and cvs affects
  115. 115Descending control of nociception?via PAG
    Uses neurotransmitters like serotonin/na/opioid peptides
  116. 116Major sites of analgesic opioid actions?Presynaptic terminal depresses glutamate release
    Post synaptic, inhibits spinothalamic activity K+ channel activation
    PAG
  117. 117Neuropathic pain? De afferentation pain?Stimulus origanates somewhere along pain pathways
    phanton limb
  118. 118Referred pain?Pain is perceived at a location other than the site of painful stimulus
  119. 119Define Hyperalagesia/allodynia?Increased pain from noxious stimulus
    pain from non-noxious stimulus(sunburn)
  120. 120LA two effect on NA Channels?Block Na channels and prolong Na channel inactivation
  121. 121Small or large fibres blocked more readily?Small fibres, pain is transmitted via Ad+C fibres
  122. 122Two drugs that exhibit LA properties at high concentrations?Propanolol/morphine
  123. 123Two pathways that LA use?Hydrophobic/hydrophilic
    Hydrophobic diffuses from cell membrane directly into the receptor.
    Hydrophilic diffuses across the membrane into the cytosol and then binds to the receptor
  124. 124What LA is only used experimentally and give an example of LA that uses the hydrophobic pathway?QX-314 (100% ionised)
    Benzocaine
  125. 125Explain use dependance?The more the nerve fibres fire the greater the effect of the LA
  126. 126Metabolism mechanisms of LA/Does LA VC or VD?Ester-Plasma
    Amide-Liver
    potent VD
  127. 127Clinical uses of LA (6)?Surface/infiltration/IV/Nerve block/spinal/epidural
  128. 128Side effects of LA?Respiratory depression/decreased heart contractility
    Hypersensitivity
    Toxic metabolite-prilocaine causes methaemoglobinaemia
  129. 129Opioid vs Opiate?Opioid acts on opioid receptors
    Drugs derived from juice of opiates
  130. 130Where do C fibres terminate? What tract to nociceptors use?Dorsal horn
    Spinothalamic tract
  131. 131What inhibits pain transmission in substantia gelatinosa? Causes local release of what? System is activated by what drug?PAG
    Dynorphin
    Opiates
  132. 132List the four opioid, what are three inhibited by?MOP/KOP/DOP/NOP
    Naloxone
  133. 133Problem with giving morphine orally? When do u give morphine orally?FPE poor absorption
    Oromorph for cancer patients
  134. 134Side effects of morphine?Miosis(pupil constriction)
    Respiratory depression/alveolar hypoventilation
    anti-tussive
  135. 135With what and where is morphine metabolised, where is it excreted?glucoronic acid, liver.
    In the kidney
  136. 136Most potent, given to help with opioid addiction,prodrug and life saving antagonist?Fentanyl/methadone/codeine/naloxone (much shorter half-life than morphine)
  137. 137Two types of anaesthetics?inhalation and intravenous
    FLURANE=inhalation
  138. 138MAC stands for?Minimum alveolar concentration that produces surgical anaesthia in 50% of patients
  139. 139Entonox? Side effects?N20 mixed with O2 (50%)
    Inactivates B12 neuropathy
    Low solubility in blood so blood becomes easily saturated
  140. 140First halogenated ethers in Uk? Potential side effects of modern fluranes?Halothane no longer in use as causes liver toxicity
    Malignant hyperthermia
  141. 141malignant Hyperthermia is caused by a problem with what receptor?Abnormal ryanodine receptor massive increase in ca2+ in SR
    Give dantrolene
  142. 142What do you give to stop malignant hyperthermia?Dantrolene
  143. 143What drug can you not give to people with a peanut/soya allergy?Propofol
  144. 144Thiopental suppresses what production? Used to treat what?Cortisol
    Status epilepticus
  145. 145What do you give to people with Status asthmaticus?ketamine
  146. 146Side effects of KetamineUlcerative cystitis
  147. 147Two types of NMJ blockers?Depolarising-Sux
    Binds to receptor/4min t1/2/malignant hyperthermia/pseudochol
    Non-depolarising-curium/curonium
    Antagonists/40min t1/2/neostigmine/tachycardia and hypotension
  148. 148Which cranial nerves do not synapse in the brainstem?Olfactory/Optic
  149. 149Edinger Westschal nuclei for which cranial nerve?Oculomotor
  150. 150Functions of the cranial nerves?SSA/SVA/SVE
    GSA/GVA/GSE/GVE
  151. 151Optic and VestibulocochlearOnly associated with SSA
  152. 152Three symptoms of damage to the CR8Ataxia,loss of balance and nystagmus
  153. 153The olfactory nerve is unique cause?Only nerve that is only associated with SVA
  154. 154GSE motor nerves?Hypoglossal/oculomotor/Trochlear/abducens/accesory
  155. 155Ptosis/lateral strabismus is damage to what nerve?oculomotor
  156. 156Hypoglossal nerve palsy deviates to side?Same side as lesion
  157. 1574 nerves that are involved in both sensory and motor? For trigeminal which lesion causes damage to jaw?Trigeminal/facial/Glossopharnygeal/Vagus
    LML
  158. 158Special about the forehead muscles? What causes bells palsy?Bi-lateral innervation
    LML damage of facial nerve
  159. 159What part of the cranial innervates the SCM/traps and what does the other part do?Spinal
    Roots to the pharynx/larynx
  160. 160Bilateral corticonuclear connections present in all cranial nuclei except?Lower part of the face
    Hypoglossal nucleus that supplies the genioglossus muscle
  161. 161Motor neuron location in ventral horns of ventral and dorsal?Flexors-Dorsal
    Extensor-Ventral
  162. 1623 sources of input of the motor a neuron? Difference between A & Y fibres Motor unit? Muscle length determined by what?Inter-neurones/Upper motor neurones/sensory input from muscles
    A innervates skeletal muscle fibres, Y innervate intrafusal muscle fibres/adjust sensitivity of muscle spindles
    Muscle fibres and respective a neurone
    Muscle spindles
  163. 163Monosynaptic reflex maintains what? Exaggerated reflex indicates? Gamma motor neurones do what to the spindles?Muscle tone
    Upper motor lesion
    Cause contraction when the muscle contracts
  164. 164Golgi tendon does what? Helps protect what?Opposite monosynaptic to prevent tendon damage
  165. 165Flexor reflex receives stimulus from what types of fibres? Maintenance of balance is done how? If your left arm flexes your right arm will?Nociceptives (ad+C)
    Crossed extensor reflex, maintained by the central pattern generator (excitatory and inhibitory interneurones)
    Extend
  166. 166Convergence is what, causes three things?Multiple nerves into one nerve
    Summation/Facilitation/Occlusion
  167. 167Basal nuclei function?Initiation and control of movements
  168. 168Rubrospinal synapse?Red nucleus
  169. 169Describe the pathway that the basal ganglia are involvedMotor cortes/PFC to Basal ganglia to ventral tegmental nuclei to SMA then down spinal tracts
  170. 170Striatum is,separated by what? Lentiform nucleus? Output regions of basal nuclei? What is NA involved in and what carries dopamine from substantia nigra?Putamen/caudate internal capsule
    Globus pallidus/Putamen
    Internal segments of GP and pars reticula of SN
    Reward, Pars compacta
  171. 171Which pathway allows movement?Direct
  172. 172Describe basal ganglia pathway?Removes tonic inhibition of IGP on thalamus by the striatum inhibiting it
  173. 173Indirect pathway?Inhibition of the thalamus above normal level, Inhibition of EGP tonic inhibition of Subthalamic nucleus that excites IGP
  174. 174Parkinsons disease causes and symptoms?Loss of pars compact in substantia nigra, trouble initiating movements, bradykinesia
  175. 175Hungtingtons disease?Loss of striatal neurones thus loss of cortical neurones
    dementia/movement problems
  176. 176Damage to subthalamic nucleus causes?Ballism
    cause this excites the IGP so if you remove this you have no control of movements
  177. 177Commonest causes of ballism?Stroke
  178. 178Motor areas can produce movements how?Lowest stimulus intensity
  179. 179Primary motor cortex neurones fire before or at the same time as movement?before
  180. 180Describe the location of the SMA? Pre-SMA differs from SMA proper how?Directly anterior to Primary motor cortex
    Connected to PFC not strongly connected to other motor areas
  181. 181Which pathway lateral or medial controls proximal and distal muscles?Lateral thus medial control axial muscles
  182. 182Lateral pathways/medial pathways?lateral corticospinal/rubrospinal
    Vestibulospinal/reticulospinal/tectospinal/
    corticospinal
  183. 183Percentage of corticospinal neurones that decussate? and where? Lateral innervates what?85% medullary pyramids
    Limbs
  184. 184Corticobulbar fibres involved in cranial nerve functions, what nuclei do not receive bilateral innervation from cortex?Facial muscle below eye and hypoglossal
  185. 185When does rubrospinal tract decussate?What does it innervate?Immediately
    Upper limb
  186. 186Motor that innervate flexors are dorsal or anterior to those that innervate extensors?Dorsal
  187. 187Head orientation is received from tract? Innervation to muscles?Vestibulospinal tract
    bilateral innervation
  188. 188Where does tectospinal tract originate? Function?Superior colliculi
    Control head position
  189. 189Which tract is involved with muscle tone? Ipislateral or contralateral?Reticulospinal tract
    ipislateral
  190. 190Consequences of upper motor injury?Increased muscle tone/hyperactivity
    Barbinski sign/weakness in digits
  191. 191Barbinski sign is normal in infants because?Of lack of myelination of corticospinal tract
  192. 192Most prominent sign of impairment to the corticospinal tract?Weakness in digits
  193. 193In a LML what affect on spasicity and reflexes?Decreases muscle tone and reflexes
  194. 194Difference between decorticate and decerebrate postures?Decorticate-Cerebrum from brainstem
    Arms abducted and flexed (on chest)
    Decerebrate- Separates upper and lower brainstem
    Arms extended/wrist pronated arms are by the side
  195. 195Two things you get with LML that you don't get with UML?Fasciluations/atrophy
  196. 196Left and right hemisphere joined by what? Anterior and posterior lobe separated by what?Median vermis
    Primary fissure
  197. 1974 inputs into the cerebellum? Types of input fibres?3 inferior peduncle vestibular/reticular/inferior olivary nucleus
    1 middle peduncle Cerebral cortex
    Climbing and mossy
    Climbing used for inferior olivary nucleus
  198. 198Number of outputs of cerebellum to the spinal cord? Flocculo-nodular lobe?0
    Loss of balance and co-ordination
  199. 199Hereditary disease associated with the cerebellum?Fredreich's ataxia
  200. 200Clinical signs of cerebellar damage?D-Dyskine
    A-ataxia
    N-nystagmus
    I-intention tremor
    S-Slurred speech
    H-Hypotonia
    P-Past pointing

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Beschreibung
2 Medicine Karteikarten am Neuro system, erstellt von James Murdoch am 07/02/2016.
Erstellt von
James Murdoch
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Durchschnittliche Bewertung 4,1 von 5 (7 Bewertungen)

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