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Week 1 Flashcards

1
Q

Function of neurons?

A
  • Function: transmits electrical via APs and chemical signals via NTs
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2
Q

Define functions of dendrites, cell body, and axon

A
  • Morphological features:
    • Dendrites: diverse structured (inputs)
    • Cell body: protein synthesis occurs
    • Axon: transport signals with Bi-directional transport of proteins
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3
Q

What are the function of glia cells and name the 4 types (differntiate PNS vs CNS)?

A
  • Function: provide metabolic and structural support, respond to infection or damage, or regulate local metabolism
  • Types
    • Astrocytes (CNS) or Satellite cells (PNS) – most numerous cell type in CNS
    • Oligodendrocytes (CNS) or Schwann cells (PNS)
    • Microglia (CNS)
    • Ependymal cells (CNS) - Ciliated barrier between CSF and brain
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4
Q

For: Astrocytes (CNS) or Satellite cells (PNS) – most numerous cell type in CNS

  • What is the structure?
  • Function (4)?
A
  • Astrocytes (CNS) or Satellite cells (PNS) – most numerous cell type in CNS
    • Structure: star like filament processes made from GFAP
    • Function:
      • homeostasis (glycogen energy storage, regulation of vasculature via endfeet)
      • neurotransmission (NT metabolism/reuptake i.e. glutamate)
      • development/plasticity
      • response to injury/infection (via IL-1 → formation of glial scar)
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5
Q

What are 3 associated diseases with astrocyte function and how do they occur?

A
  • Associated Diseases:
    • Alzheimer’s disease ( increased astrocyte activity → toxic)
    • Huntington’s disease (defective astrocyte function)
    • Parkinson’s disease (Alpha-synuclein accumulates in astrocytes leading to neuronal excitotoxicity)
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6
Q
  • For: Oligodendrocytes (CNS) or Schwann cells (PNS)
    • What is the function?
    • Compare Oligodendrocytes (CNS) and Schwann cells (PNS)
      • cell body location
      • embryoloical origin
      • how many cells per axon?
A
  • Oligodendrocytes (CNS) or Schwann cells (PNS)
    • Function: produce myelin (protects and support axon, increases transmissions speeds)
      • Myelin on axon separated by nodes of Ranvier – increases transmission via saltatory conduction
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7
Q

What are two associated diseases of the oligodendrocytes?

A
  • Associated disease:
    • Guillain-Barre Syndrome – inflammatory demyelination of PNS
    • Multiple Sclerosis – autoimmune demyelination of CNS
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8
Q
  • For Microglia (CNS)
    • Description?
    • MOA/Phases?
A
  • Microglia (CNS)
    • Description: resident immune cells derived from macrophages
    • MOA: quiescent phase → activated by injury/disease → phagocytic phase → release of cytokines, ROS
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9
Q

What are 3 diseases associated with microglia? How do they occur?

A
  • Associated Diseases:
    • Alzheimer’s disease ( increased microglia release of amyloid and IL-1)
    • Parkinson’s disease (Increased microglia → dopamine neuron loss)
    • Neuropathic pain (spinal cord injury)
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10
Q

What are the ependymal cells?

A
  • Ependymal cells (CNS) - Ciliated barrier between CSF and brain
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11
Q

What are the 4 functions of the blood brain barrier?

A
  • Isolate and protect the CNS
    • Fluctuations in nutrients, hormones, metabolites, chemical compounds, etc.
    • Allows for optimum neuronal transmission
  • Deliver nutrients, remove metabolites
  • Barrier for ionic currents and hydrophilic compounds
  • Regulates access to drugs
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12
Q

What are three main cellular componenets of the BBB?

A
  • Endothelial Cells (EC)
  • Astrocytes
  • Pericytes
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13
Q

Identify the three cells in this pic at the BBB

A
  • Endothelial Cells (EC) – purple
  • Astrocytes – yellow
  • Pericytes – green
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14
Q

What are the characteristics of endothelial cells at the BBB? How do they differ from peripheral endothelial cells?

A
  • Endothelial Cells (EC) – purple
    • Different than peripheral
      • Tight Junctions
      • Lack pinocytic vacuoles
      • High number of mitochondria
      • Lack fenestrations
      • Selective permeability for lipophilic molecules
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15
Q

Characterstics of astrocytes?

What are end feet?

What do they play a major role in?

A
  • Astrocytes – yellow
    • Attach neurons to blood vessels
    • End feet contain Aquaporin 4 (water channel) and a K+ channel
    • Major role in neuronal metabolism, nutrition, and elimination of used substrates
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16
Q

What are pericytes? What do they do? Structurally, where are they located?

A
  • Pericytes – green
    • Associated with small vessels
    • Separated from EC by the basement membrane
    • Gap junctions allow for contact spots with EC
    • Regulate activity of EC, mediate inflammation, control capillary diameter
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17
Q

What are the three mechanisms of diffusion across the BBB?

A

Simple diffusion, transcytosis, transport proteins

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18
Q

What are the two methods of simple diffusion? How do they work?

A
  • Diffusion
    • Paracellular
      • Between tight junctions of EC’s
      • Allows transport of small water-soluble molecules and ions
    • Transcellular
      • Lipophilic molecules pass freely into out of the EC’s
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19
Q

How does transcytosis across BBB work? Where does it occur and what is it used for?

A
  • Transcytosis
    • Occurs in EC’s
    • For macromolecules
    • Uses pinocytic/endocytic vacuoles
      • Far downregulated compared to systemic EC’s
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20
Q

Name some transport proteins located on the BBB

A
  • Transport Proteins
    • ATP-binding cassette Group
    • Solute Carrier Group
      • Efflux of anions
    • Amino Acid Transport
    • Neurotransmitter Transport
    • Energy Transport
      • GLUT-1 – Brain cannot store glucose
      • CRT – Brain stores Creatinine 180x serum concentration
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21
Q

What is the function of the BBB?

What can the regulation be disrupted by?

How does the BBB affect the administration of brain-targeted drugs?

A
  • The BBB protects the CNS from foreign substances (xenobiotics).
  • The regulation of the BBB can be disrupted by trauma, infection, stroke, systemic disease, tumors, etc.
  • Delivery of drugs into the CNS is made difficult by the BBB
    • Intrathecal drug administration
    • Transport (efflux) inhibition
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22
Q

What are 7 locations outside the BBB?

A
  • Locations outside of BBB
    • Direct Secretion into circulation
      • Pineal Gland: Melatonin
      • Posterior Pituitary: oxytocin, vasopressin
      • Median Eminence of Hypothalmus: pituitary hormones
    • Detection of toxins
      • Area postrema
    • Structural Integrity
      • Subcommisural Organ (SCO)
        • Maintains patency of Sylvian Aqueduct and electrolyte balance
      • Subfornicular Organ (SFO)
        • Maintains osmoregulation, cardiovascular regulation and energy homeostasis
      • Vascular Organ of the Lamina terminalis (OVLT)
        • Osmoregulation
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23
Q

Define localization in terms of clinical neuro? What are the 7 parts to a neuro exam?

A
  • Localization is the process of using knowledge of neuroanatomy and the patient’s presentation) to figure out where the symptom is coming from in the nervous system
  • 7 Parts to the Neurological Exam: MS, CNs, Motor, Sensory, Reflexes, Coordination, Gait
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24
Q

Define CNS vs PNS

A
  • CNS vs. PNS
    • CNS: brain and spinal cord
    • PNS: cranial nerves/ganglia, spinal nerves/dorsal root ganglia, para/sympathetic nerves/ganglia, and enteric nervous system
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25
Q

What is part of each of these: cerebral hemisphere, diencephalon, brainstem, cerebellum?

A
  • Cerebral hemispheres: cerebral cortex and basal ganglia (motor control)
    • Limbic system: emotion, memory, behavior, homeostasis
  • Diencephalon: thalamus (sensory relay) and hypothalamus
  • Brainstem: midbrain (mickey mouse ears), pons, medulla (4 leaf clover shaped)
  • Cerebellum
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26
Q

What does the corticospinal tract do? Basic understanding (more later!)

A
  • Corticospinal Tract: efferent tract for voluntary motor activity
    • UMN starts at primary motor cortex → decussates in medulla → lateral motor nuclei → LMN synapses at anterior horn of spinal cord
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27
Q

What dos the dorsal column medial lemniscal pathway do? Basic level, more on this later!

A
  • Dorsal Column Medial Lemniscal Sensory Pathway: afferent tract for vibration, joint position sense, and fine touch
    • Afferent nerve fibers synapses at dorsal column → decussates at caudal medulla → travels to thalamus → synapses at primary somatosensory cortex
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28
Q

What does the anterolateral (spinothalamic) tract do? Basic understanding, more on this later!

A
  • Anterolateral (Spinothalamic) Sensory Pathway: afferent tract for pain, temperature, and crude touch
    • Afferent nerve fibers synapses at dorsal horn → decussate immediately at spinal cord → travels to thalamus → synapses at primary somatosensory cortex
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29
Q

When would you want to use a CT vs MRI for brain stuff?

A
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30
Q

What kind of membane does the neuron have? What is the function of this? How do ions diffuse?

What determines and influences membrane potential? What is the membrane potential?

A
  • Bilipid membrane layer
    • Acts as a diffusion barrier, regulates movement of solutes
    • Ions diffuse across the membrane via ion channels
    • Number and selectivity of ion channels determines the membrane potential
  • Membrane potential ~ - 60 to - 70 mV
    • Heavily influenced by potassium leak channels
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31
Q

What are 2 types of electrical signals?

A
  • Electrical signals
    • Receptor potentials: activation of sensory neurons by external stimuli
    • Synaptic potentials: transmission of information between neurons
    • Inputs can summate
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32
Q

How is an AP formed? Know all the steps! 5 steps! This includes knowing when activation and inactivation gates close and open!

A
  • Action potentials result from the coordinated activity of voltage gated Na+ and K+ channels
    1. Voltage-gated Na+ channels activation gate closed. Most K+ channels closed
    2. Membrane depolarization opens voltage-gated Na+ channels
    3. Na+ channels inactivate (time-dependent) by closing inactivation gate. Voltage-gated K+ channels open
    4. Inactivation of voltage-gated Na+ channels removed
    5. Baseline state is reached
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33
Q

Where is an AP propagated? How? What allows for the unidirectionality?

A
  • An action potential is propagated along the axon
  • Na+ enters through voltage-gated Na+ channels and passively diffuses through the axoplasm → depolarizes neighboring membrane → opening adjacent voltage-gated Na channels
    • Directionality of AP is due to refractory period caused by inactivated Na channels
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34
Q

What two things can increase propagation speeds? What is the function of the nodes of ranvier?

A
  • AP propagation
    • Increased in diameter of axon correlates with increased speed of conduction
    • Increased myelin sheath correlates with increased speed of conduction
      • Nodes of Ranvier: APs jump from node to node, “saltatory conductance”
      • Able to regenerate APs here because high concentration of Na channels
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35
Q

Explain the following three disorders (including etiology/cause of each!)

  • Guillain-Barre syndrome
  • Multiple sclerosis
  • Experimental allergic neuritis
A
  • Guillain-Barre syndrome: viral exposure → damage to myelin of peripheral nerves, mainly motor nerves
  • Multiple sclerosis: genetic predisposition, environmental exposure → multiple plaques of demyelinated CNS white matter (commonly optic nerve, deep cerebral white matter)
  • Experimental allergic neuritis: lysis of myelin lamellae → gap in myelin sheath → macrophages penetrate the sheath and strip myelin from axon
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36
Q

What are the general concentrations (extra/intracellular) and nernst potentials of each of the four ions?

A
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37
Q

For electrical synapses:

  • What is the structure? What forms it?
  • Characteristics?
  • Advantages?
  • Sites in body
  • Disorders associated
A
  • Electrical synapses – gap junctions allow electrical coupling between cells
    • Structure: cylindrical assemblies of 6 transmembrane proteins (connexins) to form connexons
    • Characteristics: low resistance, instantaneous transmission
    • Advantages: guaranteed transmission of signals, coordinated activity
    • Sites: retina, glial cells, astrocytes
    • Disorders: deafness, cataracts, Charcot-Marie-Tooth disease
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38
Q

What are the advantages of chemical synapse?

A
  • Chemical synapses
    • Advantages: signal is amplified, can be excitatory/inhibitory, can be manipulated pharmacologically
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39
Q

How does chemical synapse work? Provide in depth process!

A
  • Synthesis of neurotransmitter
  • Concentration and packaging of neurotransmitter in the presynaptic terminal
  • Release of neurotransmitter from the presynaptic terminal (Ca dependent process)
  • Binding of neurotransmitter to receptors on the postsynaptic membrane, located directly across the synaptic cleft. This allows for very rapid effect (<200msec)
  • Termination of neurotransmitter action
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40
Q

How is calcium involved in chemical synapse?

A
  • An action potential invades the presynaptic terminal → opening voltage-gated Ca2+ channels
  • Vesicles fuse with the presynaptic membrane and release neurotransmitter into the synaptic cleft
  • Vesicles are recycled in the synaptic terminal
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41
Q

What are the methods of termination for NT action?

A
  • Neurotransmitter binds to the receptor while other mechanisms compete to remove it from the synaptic cleft, including:
    • Reuptake into the presynaptic terminal
    • Uptake into the postsynaptic terminal
    • Uptake into nearby glial cells
    • Enzymatic inactivation of neurotransmitter
    • Diffusion out of synaptic cleft
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42
Q

What are the two main families of NT receptors? Which one is faster?

A
  • Ligand-gated ion channel – fast synaptic transmission
  • G-protein-coupled receptors – slower synaptic transmission
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43
Q

Describe the neuromuscular junction

What is the MOA?

A
  • Neuromuscular Junctions
    • Description: Active zones of synaptic boutons positioned over junctional folds
      • Junctional folds contain receptors for neurotransmitter
    • MOA: ACh released by presynaptic terminal activates nicotinic receptors, ligand-gated cation channels, on the postsynaptic membrane → Ion channel allows influx of Na, efflux of K → Triggers depolarization termed the end plate potential (70mV) → Opens voltage-gated Na channels in junctional folds and trigger action potential
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44
Q

What is this showing?

A

NMJ

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45
Q

What is the green blood supply? The yellow? What tracts are affected with each?

A
  • Green: posterior spinal artery (dorsal column)
  • Yellow: anterior spinal artery (corticospinal and spinothalamic tract)
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46
Q
  • Appreciate the location of the following tracts/nuclei on this pic:
    • Fasiculus cuneatus/gracilis (dorsal column)
    • Lateral corticospinal tract
    • Lateral spinothalamic tract
A

Memorized?

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47
Q
  • What would you expect in a UMN vs LMN lesion for the following:
    • Weakness
    • Atrophy
    • Fasiculation
    • Reflexes (Why does this occur?)
    • Tone
    • Plantar Response
  • What is a caveat?
A

*When a lesion in a UMN pathway occurs there is a loss of inhibition to the LMN which gives rise to characteristic clinical findings

  • With acute UMN lesion (i.e. stroke), reflexes may initially be decreased or absent
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48
Q

Provide the following for the doral/posterior column:

  • Function
  • Decussation
  • Lesion at spinal cord causes what?
  • Blood supply?
A
  • Function: Pressure, Vibration, Fine Touch, Proprioception
  • Decussation: caudal medulla
  • Lesion at spinal cord causes what
    • At spinal cord: ipsilateral loss of dorsal column function distal to lesion
  • Blood supply: posterior spinal a
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49
Q

Provide the following for the spinothalamic tract

  • Function
  • Decussation
  • Lesion at spinal cord causes what?
  • Blood supply?
A
  • Function: Pain, Temperature, Crude Touch
  • Decussation: Immediately at spinal cord 1-2 segments above/below @ anterior commissure
  • Lesion at spinal cord causes what: At spinal cord: contralateral loss of function 1-2 segment below lesion
  • Blood supply: anterior spinal artery
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50
Q

Provide the following for the corticospinal tract

  • Function
  • Decussation
  • Lesion at spinal cord causes what?
  • Blood supply?
A
  • Function: voluntary movement
  • Decussation: Medullary Pyramids @ Caudal Medulla
  • Lesion at spinal cord causes what: At spinal cord: ipsilateral loss of function distal to lesion
  • Blood supply: anterior spinal artery
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51
Q

For dorsal column, provide the following:

  • First order neuron (type)
  • First synapse
  • Second order neuron
  • Second synapse
  • Third order neuron (if applicable)
  • Target
A
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52
Q

For spinothalamic tract, provide the following:

  • First order neuron (type)
  • First synapse
  • Second order neuron
  • Second synapse
  • Third order neuron (if applicable)
  • Target
A
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53
Q

For corticospinal tract, provide the following:

  • First order neuron (type)
  • First synapse
  • Second order neuron
  • Second synapse
  • Third order neuron (if applicable)
  • Target
A
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54
Q

What occurs in 2nd and 3rd weeks for neuroembryology?

A

Gastrulation:

  • Primitive streak (PS) appears at caudal end of embryo → elongates toward cranial end → regresses back to caudal end of embryo → formation of Hensen’s node at cranial end of the PS
    • In the cross-section: endoderm and mesoderm cells move towards midline; remaining epiblast cells become ectoderm
      • Lateral ectoderm: skin; medial ectoderm: CNS
    • Prospective notocordal cells migrate from Hensen’s node inwards to create an invagination→ formation of notochord → formation of nucleus pulposus of intervertebral discs
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55
Q

What occurs in the 3rd and 4th weeks of neuroembryology? BE SPECIFIC.

Name specific cells that form and spaces that form.

What part of the spinal cord do these tissues form?

A

Primary Neurulation (3rd and 4th weeks) – Tissues from C1 to S2

  • Neural plate (pseudostratified columnar epithelium) is attached at cutaneous ends of ectoderm and lie above notochord
  • Formation of neural tube: notochord causes differentiation of neural plates → formation of neural folds/crest cells → convergence of neural folds → apposition and fusion of neural folds → neural tube
  • Neural crest cells: cells between ectoderm and neural tube that migrate during neurulation
    • Contribute to: DRG, autonomic ganglia, Schwann cells, melanocytes, adrenal medulla
  • Neuropores: spaces between the newly-formed neural tube where the neural plate has yet to converge and fuse
    • Closure occurs in multiple waves
    • Last sites to close: cranial neuropore, caudal neuropore
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56
Q

What occurs towards the end of week 4? Be specific.

A

Secondary Neurulation (end of week 4) – Tissues from S2 to caudal end

  • Multi-potent caudal cell mass from Hensen’s node → formation of spinal cord below S2 and filum terminale
    • Secondary neurulation disorders will commonly present with skin attached because secondary neurulation occurs under an intact cutaneous ectoderm
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57
Q

What occurs in the ascent of the conus medullaris? When does this occur?

What are the two processes within this?

A

Ascent of the conus medullaris (begins at day 42)

  • Processes – most ascent is prenatal → ascension to L1-L2 post-natal
    • Retrogressive differentiation (until day 53)
      • Neural tube becomes thinner
    • Differential growth of spinal cord and vertebral column (day 54 and beyond)
      • Cells undergo differentiation
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58
Q

How does the development of basal and alar plates occur?

A

Development of Basal and Alar Plates

  • During neural tube formation: basal plate of neural plate forms ventral side of spinal cord (motor) while the alar plate of neural plate forms the dorsal side of the spinal cord (sensory)
    • Basal and alar plates are separated by sulcus limitans
    • Spinal cord follows this development; brainstem follows this development with modifications
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59
Q

How and when does the development of primary and secondary vesicles occur? Name the primary and secondary vesicles and what makes up each one!!

A

Development of Primary and Secondary Vesicles

  • Day 19: brain is divided into 3 primary vesicles: prosencephalon, mesencephalon, rhombencephalon
  • Day 32: further divides into 5 secondary vesicles:
    • Prosencephalon: telencephalon (olfactory lobes, hippocampus, cerebrum), diencephalon (optic vesicle, epithalamus, thalamus, hypothalamus)
    • Mesencephalon: mesencephalon (midbrain)
    • Rhombencephalon: metencephalon (cerebellum, pons), myelencephalon (medulla)
  • Development of Flexure (4th and 5th weeks): angulation of neural tube during development → forms the shape of the vesicles
    • Mesencephalic flexure (convex dorsally), cervical flexure (convex dorsally), and pontine flexure (convex ventrally)
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60
Q

How does the formation of the pituitary gand occur? What are the two sources?

***VERY IMPORTANT***

A

Formation of Pituitary Gland

  • Pituitary gland derived from two sources
    • Outgrowth of diencephalon (ectoderm) to form posterior pituitary (neurophypophysis)
    • Upward migration of stomodeum (pharynx, endoderm) to form anterior pituitary (adenohypophysis)
  • Infundibular stalk forms from downward migration of neurohypophysis
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61
Q

What happens during modification of the telencephalon?

How does the histogenesis of the nervous system occur? How do cells migrate?

A
  • Modifications of Telencephalon
    • Two halves connected by corpus callosum, anterior commissure, and hippocampal commissures
    • Telencephalon undergoes explosive growth in the direction of the occipital lobe to ultimately overlie the mesencephalon and cerebellum
  • Histogenesis of Nervous System
    • Neuroblasts divide in germinal zone → post-mitotic cells (i.e. neurons, glia) migrate outward to mantle zone (gray matter) → axons project even further outward to marginal zone (white matter) → remaining cells form ependyma
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62
Q

When and how are commisural fiber tracts developed?

A
  • Growth of corpus callosum (day 84-115), growth of anterior commissure (begins day 54), growth of hippocampal commissure (begins week 11)
    • Corpus callosum develops in a specific temporal order (genu → body → splenium → rostrum (anterior most part – reason unknown)
    • Agenesis of CC: spares only anterior CC (exception holoprosencephaly affects ONLY anterior CC)
  • Posterior and habenular commissures develop from diencephalon
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63
Q

For tethered cord syndrome: provide, description, etiology, signs/sx

A
  • Tethered cord syndrome
    • Description: conus is below middle third of L2
    • Etiology: thickened filum due to fat infiltration or congenital tethering (attachment) malformation
    • Signs/Sx: Pain (back or leg), weakness/paralysis/gait issues, bowel/bladder issues, scoliosis/orthopedic foot or leg deformities
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64
Q

For myelomeningocele: provide description, signs/sx

A
  • Myelomeningocele
    • Description: outpouching of spinal cord and meninges due to failure of primary neurulation
    • Signs: exposure of spinal cord with overlying dysplastic skin, possible leakage of CSF
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65
Q

For meningocele: provide description, signs/sx

A
  • Meningocele
    • Description: outpouching of meninges
    • Signs: skin covered sac filled with CSF, not leaking fluid, neurologically normal
66
Q

For spina bifida occulta: provide description, signs/sx, and associated diseases

A
  • Spina Bifida Occulta (SBO)
    • Description: isolated bony malformation due to failure of posterior vertebral fusion of caudal neuropore (commonly involves S1)
    • Signs/sx: dura is intact, no herniation, +/- tuft of hair/dimple
    • Associated with: occult spinal dysraphism
67
Q

For disorder of cerebral histogenesis (tuberous sclerosis): provide etiolog, signs/sx

A
  • Disorder of Cerebral Histogenesis: Tuberous Sclerosis
    • Etiology: autosomal dominant mutation of two genes TS1 (hamartin) and TS2 (tuberin) → disordered neuronal proliferation/migration
    • Sign/sx: triad of cognitive deficiencies, seizures, and skin lesions (adenoma sebaceum)
68
Q

For agenesis of corpus callosum: provide description, etiology, signs/sx

A
  • Agenesis of Corpus Callosum
    • Description: partial or complete absence of corpus callosum
    • Etiology: autosomal recessive or x-linked inherited form OR Arcadi syndrome, CNS infections during gestation, fetal alcohol syndrome, CNS malformations
    • Signs, sx: cognitive issues, seizures
      • Imaging: abnormal ventricle shape, widened occipital horns of lateral ventricles (colpocephaly), bundles of Probst (commissural fibers)
69
Q

What are the regions of the spinal cord?

A
  • Spinal cord – Extends from foramen magnum to second lumbar vertebra
    • Regions: Cervical (8), Thoracic (12), Lumbar (5), Sacral (5), Coccygeal (1)
    • Conus medullaris – tapered inferior end (L1-2)
    • Cauda equina – origin of spinal nerves extending inferiorly from conus medullaris
70
Q

What are the meninges and spaces in between the meninges?

A
  • Meninges – connective tissue membranes surrounding CNS
    • Dura mater – outermost layer
    • Arachnoid mater – middle layer
    • Pia mater – bound to CNS, forms the filum terminale (anchors spinal cord to coccyx)
      • Spaces
        • Epidural – external to dura
        • Subdural space – serous fluid
        • Subarachnoid – filled with CSF
71
Q

What is the general organization of the spine?

A
  • Gray matter (horns): neuron cell bodies, dendrites axons
    • Ventral (motor), Dorsal (sensory), Lateral (sympathetic: T1-L2)
  • White matter (columns): myelinated axons
  • Commissures: connections between left and right halves
72
Q

Describe the afferent and efferent neurons involved in spinal processing

A
73
Q

For Brown Sequard syndrome: etiology, pathophys, signs/sx

A
  • Brown Sequard syndrome
    • Etiology: multiple sclerosis, tumor, lesion to spinal cord
    • Pathophysiology: damage to hemi-section of spinal cord of all three major column tracks
    • Signs/symptoms: ipsilateral LMN spasticity/weakness, ipsilateral vibration/proprioception loss, and contralateral pain/temperature loss distal to lesion
      • Lesion above T1 → ipsilateral Horner’s syndrome
74
Q

For central cord syndrome: etiology, pathophys, signs/sx

A
  • Central Cord Syndrome
    • Etiology: trauma or Arnold-Chiari malformation
    • Pathophysiology: bilateral loss of dorsal column, corticospinal, and spinothalamic tracts
      • Common to spare dorsal column because mainly effects the commissures of the spinal cord body
    • Signs/symptoms: bilateral LMN spasticity/weakness, bilateral vibration/proprioception loss, and bilateral pain/temperature loss distal to lesion
75
Q

For b12 deficiency in spine: etiology, diagnosis/labs

A
  • B12 Deficiency
    • Etiology: B12 Deficiency → demyelination of the dorsal column and/or corticospinal tract
    • Diagnosis/labs: megaloblastic anemia, increased methylmalonic acid, increased homocysteine cord
      • Imaging: thin central/posterior lesion to spinal cord
      • PE: Lhermitte sign (flex neck → irritation of dorsal column → tingling), Uhtoff’s phenomenon (tingling during heat)
76
Q

3 main dermatomes?

A
  • Dermatomes
    • Clavicle – C4
    • Nipple line – T4
    • Umbilicus – T10
77
Q

Know the reflexes, muscles and sensation for C5-T1

A
78
Q

Know the reflexes, strength, and sensation for L2-S1

A
79
Q

What is the major blood supply of the midbrain?

Name some major structures found in the midbrain.

A

MIDBRAIN – Upper most part of brainstem

  • Blood supply: PCA
  • Major structures of midbrain
    • Dorsal surface: superior and inferior colliculi, CN IV (between midbrain and pons), superior cerebellar peduncle
    • Ventral surface: cerebral peduncle, CN III (between cerebral peduncles)
80
Q

Know what is located in the cross section of Midbrain-thalamus junction

A
  • Midbrain-thalamus junction
    • Inferior part of the thalamus can be seen on dorsal side
    • Red nucleus seen centrally on both sides
    • Third ventricle can be seen
81
Q

Know what is located in the cross section of upper midbrain

A
  • Upper midbrain
    • Superior colliculus can be seen on dorsal side (bump)
    • Red nucleus is seen
    • Oculomotor n. seen at this level
82
Q

Know what is located in the cross section of lower midbrain

A
  • Lower midbrain
    • Inferior colliculus can be seen on dorsal side (bump)
    • Decussation of SCP (superior cerebellar peduncles) can be seen centrally
    • Decussation of trochlear nerves on dorsal side
83
Q

What is located in the tectum of the midbrain? What are the functions of these structures?

A
  • Functions of tectum
    • Superior colliculus - Part of visual pathway
    • Inferior colliculus - Part of auditory pathway
84
Q

What two cranial nerves come out of the midbrain?

A

CN III and CN IV

85
Q

What is the parasympahetic pathway for the occulomotor n in the midbrain?

A
  • Oculomotor n.
    • 5 individual nuclei and 1 parasympathetic nucleus (Edinger-Westphal)
    • Preganglionic parasympathetic fibers arise in the Edinger-Westphal nucleus → Ciliary ganglion → Postganglionic fibers → constriction of pupil → light and accommodation reflex
    • Found between superior cerebellar and posterior cerebral arteries
      *
86
Q

What are the etiologies for an occulomotor n lesion? In which would pupil be affected?

What are the sx?

A
  • Oculomotor n.
    • Lesion
      • Etiology: PCOM aneurysm (pupil affected), diabetes (pupil sparing), tumors, cavernous sinus lesions, stroke
      • Sx: ptosis, lateral strabismus, diplopia
87
Q

What is the pathway of the trochlear n innervation? What are the sx with a trochlear n lesion (central or peripheral?)

A
  • Trochlear n.
    • Trochlear nucleus → decussation → superior oblique of opposite eye
    • Lesion
      • Sx: weakness of introversion, diplopia
        • Nerve lesion: head tilts away from lesion
        • Nucleus lesion: head tilts towards lesion
88
Q

What is the blood supply of the pons?

What are imporant structures of the pons?

A

PONS – Middle part of the brainstem

  • Blood supply: basilar a. (superior), ant. inferior cerebellar a. (inferior)
  • Major structures of pons
    • Dorsal surface: pontine nuclei, tegmentum, CN V, CN VI
    • Ventral surface: middle cerebellar peduncle
89
Q

Know what is located in the cross section of the pons: upper pons

A
  • Upper pons
    • Trigeminal n. is seen laterally
    • Corticopontine fibers is seen
    • MLF is anterior to fourth ventricle
90
Q

Know what is located in the cross-section of the pons: mid pons

A
  • Mid pons
    • Abducens nucleus is seen
    • ICP is seen
    • Middle cerebellar peduncle nerve fibers is seen
    • MLF can be seen just anterior to fourth ventricle
91
Q

Know what is located in the cross-section of the pons: Ponto-medullary junction

A
  • Ponto-medullary junction
    • Fourth ventricle can be seen dorsally
    • Superior cerebellar peduncle can be seen on both side of ventricle
    • MLF can be seen just anterior to fourth ventricle
    • At this level, both CN VI, CN VII are seen exiting pons
    • Inferior cerebellar peduncle (ICP) is seen dorsolaterally
    • Centrally, medial lemniscus pathway is seen
92
Q

What are the two cranial nerves that come out of the pons area?

A

CN V and CN VI

93
Q

Explain the spinal trigeminal nucleus pathway

A
  • Spinal trigeminal nucleus (3 neurons): sensory nerves (pain/temp.) from face → synapse on spinal trigeminal nucleus → decussates at the pons → ascends via trigeminal lemniscus → at thalamus synapses at VPM → sensory cortex
94
Q

Explain the main trigeminal nucleus pathway

A
  • Main trigeminal nucleus (3 neurons): sensory nerves (touch/position) from face → synapse on spinal trigeminal nucleus → decussates at the pons → ascends via trigeminal lemniscus → at thalamus synapses at VPM → sensory cortex
95
Q

Expalin the mesencephalic trigeminal nucleus pathway

A
  • Mesencephalic trigeminal nucleus (2 neurons): proprioceptive fibers from jaw → synapses on mesencephalic trigeminal nucleus at pons → fibers spread ipsilateral and contralateral to thalamus → sensory cortex
96
Q

What are the functions of the three parts of the CN V nerve?

What does the motor nucleus do?

A
  • V1 (sensory), V2 (sensory), V3 (motor and sensory)
  • Motor nucleus: supplies muscles of mastication
97
Q

What can occur as a result of the lesion of the trigeminal nerve?

A
  • Lesions
    • Lateral medullary syndrome: damage to spinal trigeminal nucleus fibers → ipsilateral loss of pain and temp
    • Abnormal corneal reflex: lack of afferent limb (V1)
    • Jaw deviation to same side of the paralysis
98
Q

What is the pathway for the abducens n?

A
  • Abducens n.
    • Pathway: fibers from abducens nucleus (located in floor of 4th ventricle in pons) innervate lateral rectus muscle (abduction of eye)
99
Q

What occurs with the lesion of the abducens n? sx and nucleus lesion?

A
  • Lesion:
    • Sx: diplopia w/ lateral gaze, medial strabismus
    • Nucleus lesion: horizontal gaze palsy (ipsilateral eye cannot abduct and contralateral eye cannot adduct)
100
Q
  • Paramedian Pontine Reticular Formation (PPRF)
    • Description? Sx?
A
  • Paramedian Pontine Reticular Formation (PPRF)
    • Description: involved in coordination of eye movement by receiving inputs from superior colliculus and frontal eye fields (region located in the frontal cortex)
    • Sx: same gaze palsy as abducens nucleus lesion
101
Q

What is the function of the MLF? What is the pathway?

A
  • Medial longitudinal fasciculus (MLF) – connects abducens nucleus to contralateral oculomotor nucleus → conjugate horizontal movement
    • Description: left lateral eye gaze → contraction of left lateral rectus → firing of left abducens nerve → synapse on contralateral MLF → firing of right CN III nucleus → contraction of right medial rectus → conjugate gaze
102
Q

What disease occurs as a result of a lesion of the MLF?

A
  • Lesion: Internuclear ophthalmoplegia
    • Medial rectus ipsilateral to lesioned MLF is unable to adduct; lateral rectus contralateral to lesion undergoes nystagmus
103
Q
A
104
Q
  • Osmotic demylenilation syndrome
    • etiology
    • Pathophys
    • Presentation
    • Diagnosis
A
  • Osmotic demyelination syndrome
    • Etiology: rapid correction of hyponatremia
    • Pathophysiology: osmotic destruction of myelin in pons (can happen other places), water leaves the neurons too quickly
    • Presentation: Locked-in syndrome
      • Conscious, tetra/quadriplegic, blink and move eyes only
    • Diagnosis: MRI shows lesion (T1-dark, T2-light)
105
Q

Red nucelus lesion

  • Etiology
  • Presentation
A
  • Red nucleus lesion
    • Etiology: multiple sclerosis (epidemiology: young, slow progression)
    • Presentation: titubation (coarse tremor of head), tremor of limbs, diplopia, dysarthria, urinary incontinence
      • Pertinent negatives: weakness, swallowing problems
106
Q

Benedikt’s Sydrome

  • Pathophysiology
  • Presentation (compare to two other syndromes - Webers and Claude)
A
  • Benedikt’s syndrome
    • Pathophysiology: posterior circulation stroke that affects midbrain and cerebellum
      • Ischemia to: CN III nucleus, red nucleus, corticospinal tracts, brachium conjunctivum, cerebellum
    • Sx: all types have ipsilateral CN III palsy
      • Lateral (Weber’s) – contralateral paralysis/weakness, red nucleus spared
      • Medial (Claude) – contralateral cerebellar ataxia/clumsiness, red nucleus lesion
      • Benedikt’s: both types combined
107
Q
  • Reference ranges for CSF
    • Opening pressure
    • Appearance and color
    • Blood cell count and differential
    • Glucose
    • Total protein
A
  • Reference ranges:
    • Opening pressure – 12-20 cm H2 O (with patient lying in lateral position)
    • Appearance and color - clear, colorless
    • Blood cell count and differential - WBC: < 5 (all mononuclear); RBC: 0
    • Glucose - 50-80 mg/dL
    • Total protein - 15-60 mg/dL
108
Q
  • CSF Volume
    • Total volume:____ mL, Ventricles: ____ mL, 3rd Ventricle ____ mL, exraventricular: _____ mL, rate of formation: _____ ml/min (___ ml/day)
A
  • CSF Volume
    • Total volume: 165 mL, Ventricles: 32 mL, 3rd Ventricle 1 mL, exraventricular: 133 mL, rate of formation: 0.35 ml/min (500 ml/day)
109
Q

What is the breakdown of the cranial vault

A
  • Cranial vault is a structure with fixed volume: brain (80%), blood (12%), and CSF (8%)
    • An increase in one compartment must be offset by an equivalent decrease in another
110
Q

How is CSF produced? What cells and how does it occur?

What decreases CSF production

A
  • CSF production (within choroid plexus of all ventricles)
    • Ependymal cells pump Na into subarachnoid space via ATP → water follows from blood vessels → isotonic (with plasma) CSF fluid
      • CSF is always produced regardless of ICP or cerebral venous pressure
  • Factors that decrease CSF production: carbonic anhydrase inhibitors, corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors
111
Q

What is the CSF circulation pathway?

A
  • CSF circulation
    • Lateral ventricle → interventricular foramen of Munro → 3rd ventricle → cerebral aqueduct of Sylvius → 4th ventricle → exits into either two foramina of Luschka (Laterally) OR one foramen of Magendie (Midline) → subarachnoid space around brain/spinal cord
112
Q

How is CSF reabsorbed?

What factors affect reabsorption?

A
  • CSF resorption (passive: no ATP used)
    • Reabsorbed from subarachnoid space into venous system via villi in arachnoid granulations containing along dural venous sinuses (i.e. superior sagittal sinus)
      • Absorption of CSF is directly proportionate to ICP and inversely proportionate to cerebral venous pressure

Factors affecting reabsorption: blockage of villi (cell debris or fibrosis), tumors/hemorrhage (increased ICP), specific volatile and anesthetic agents

113
Q

Define hydrocephalus

Differentiate between communicating and non-cimmunicating in terms of etiologies.

What are signs/sx

How do you diagnose?

A
  • Hydrocephalus: condition in which there is excess CSF within the intracranial space and intraventricular spaces within the brain → dilation of ventricles
    • Types
      • Communicating/Non-obstructive: no obstruction along CSF pathway (travels freely)
        • Etiology: choroid plexus papilloma (excess CSF produced), arachnoid scarring post-meningitis
      • Non-communicating/Obstructive: obstruction along CSF pathway (blockage)
        • Etiology: tumor, stenosis of cerebral aqueduct, colloid cyst blocking foramen of Munro
    • Signs/sx: global dysfunction (neuro sx from multiple modalities), pressure gradient sx (positional exacerbation of sx – i.e. Vasalva maneuver)
    • Diagnosis: dilated ventricles seen on MRI, may present with tumor if obstructive hydrocephalus
114
Q

For Parinaud’s Syndrome:

  • Description
  • Etiology
  • Sx
A
  • Parinaud’s Syndrome
    • Description: lesion to superior colliculus (part of dorsal midbrain)
    • Etiology: stroke, hydrocephalus, and pinealoma
    • Sx: paralysis of conjugate vertical gaze (cannot look up), light-near dissociation (optic tract fibers are disrupted), convergence-retraction nystagmus (when asked to lookup), eyelid retraction (Collier’s sign), setting sun sign (eyes look like a sunset because they cannot go up)
115
Q

For increased intracranial pressure

  • Etiology
  • Sx
A
  • Increased intracranial pressure
    • Etiology: hydrocephalus
    • Signs/sx: headache, AMS, N/V, papilledema (optic nerve edema due to CSF around nerve → bulging optic disc), visual loss, diplopia, Cushing’s triad (HTN, bradycardia, irregular respirations), possible bilateral CN VI nerve palsy due to increased ICP
116
Q

For medulla: what is the blood supply, what are the major structures, and what is the general fucntion?

A

MEDULLA – Lowest part of brainstem

  • Blood supply:
    • Anterior spinal artery: caudal medulla on the ventral surface
    • Posterior spinal artery caudal medulla on the dorsal surface
    • Vertebral and Posterior inferior cerebellar aa: rostral medulla
    • Paramedian br. of basilar a: extreme rostral medulla
  • Major structures of medulla
    • Decussations at medulla:
      • Corticospinal tract (motor function): decussates at pyramids → descends as cortical spinal tract
      • Posterior column (vibration, position sense): decussates through internal arcuate fibers → ascends as the medial lemniscus
  • Functions of medulla:
    • Unconscious respiratory control, reticular formation (arousal)
117
Q

What important structures are seen in this cross section of the medulla: middle medulla?

A
  • Middle Medulla
    • Gracile (medial) nucleus and cuneatus (more lateral) nucleus are seen dorsally
    • Medial lemniscus is seen centrally
    • Pyramids are seen anteriorly
    • CN XI and XII are seen
118
Q

What important structures are seen in this cross section of the medulla: spino-medullary junction?

A
  • Spino-medullary junction
    • Gracile (medial) nucleus and cuneatus (more lateral) nucleus are seen dorsally
    • Pyramidal decussation of corticospinal tracts are seen anteriorly
119
Q

What is the rule of 4 mnemonic for midbrain anatomy?

A

MNEMONIC FOR MIDBRAIN ANATOMY – RULE OF 4’s

  • 4 CNs
    • Above pons (I and II are outside the midbrain) III, IV localize to midbrain
    • Pons (V), VI, VII, VIII
    • Below pons IX, X, XI, XII
  • 4 CN divide evenly into 12
    • III,IV,VI,XII (all motor nuclei that lie on midline)
  • 4 CN do not divide evenly into 12
    • V, VII, (VIII), IX, XI (nuclei lie laterally)
  • 4 midline columns – the m’s stick together
    • Motor nuclei (CN listed above), Motor pathway (pyramids), MLF, Medial Lemniscus
  • 4 lateral columns (lateral=Side)
    • Sympathetic, Spinothalamic = anterolateral, Sensory (face) – trigeminal nucleus, Spinocerebellar
120
Q

How does the muscle stretch reflex work?

A

MUSCLE STRETCH REFLEX

  • Muscle A stretches (i.e. patellar tendon → quads) → 1a afferent fibers → dorsal root ganglion → synapse with motor axons of muscle A → ventral horn → contraction of muscle A
    • 1a afferent fibers at spinal cord also synapse with inhibitory interneuron → synapse with motor axon of muscle B (normally opposes muscle A) → ventral horn → relaxation of muscle B
121
Q

For deserine syndrome: etiology, sx?

A
  • Dejerine Syndrome – left medial medullary infarct
    • Etiology: stroke of paramedian branches of vertebral a.
    • Sx: contralateral motor deficits, contralateral dorsal column deficits
      • Possible facial nerve deficits, possible trigeminal nerve deficits
122
Q

For pseudobulbar affect, what is it?

A
  • Pseudobulbar affect: abnormal activation of laughing or crying without the accompanying emotion
    • Emotional incontinence: a UMN lesion involving the brainstem nuclei involving laughing and crying
123
Q

What is pseudobulbar palsy? What does it lead to? What are the sx?

A
  • Pseudobulbar palsy: palsy of corticobulbar tract → dysarthria and dysphagia from UMN connections in the brainstem
    • Corticobulbar tract innervates CN V, VII, IX, and X
    • Sx: motor issues of facial/mastication muscles, absent gag reflex, dysphagia
124
Q

What is the pathways of the cerebellum that leads to what sided defects

A
  • Cerebellum provides ipsilateral motor-sensory inputs
    • Pathways: cerebellum → contralateral red nucleus → rubrospinal tract → decussation of rubrospinal tract → descent to periphery (double cross)
125
Q

What does the cerebellum not do?

A
  • Does NOT: initiate movement, control musculature, cause paralysis with lesion
126
Q

What part of the cerebellum is in the vestibulocerebellum?

What is the function? WHat is the output?

A
  • Vestibulocerebellum: encompasses flocculonodular lobe (oldest part)
    • Function: equilibrium and posture
    • Output: vestibular nuclei → lower motor neurons in the spinal cord and brainstem
127
Q

What part of the cerebellum is in the spinocerebellum?

What is the function? What is the output?

A
  • Spinocerebellum: encompasses vermis and paravermis (medial part)
    • Function: maintenance of muscle tone (lesion causes tremor)
      • Vermis (medial): axial (trunk and proximal appendages)
      • Paravermis (lateral): distal appendages
    • Output: Interposed and fastigial nuclei → motor cortex and brainstem
128
Q

What part of the cerebellum is in the cerebrocerebellum?

What is the function? What is the output?

A
  • Cerebrocerebellum: encompasses lateral cerebellum (newest and smartest)
    • Function: fine motor coordination
    • Output: dentate nucleus → premotor cortex (motor planning)
129
Q

What are the two main input pathways to the cerebellum?

A
  • Input:
    • Contralateral frontal-motor cortex → pons → middle cerebellar peduncle → cerebellar cortex
    • Spinal cord → inferior cerebellar peduncle → proprioception info from ipsilateral side
130
Q

What is the output of the cerebllum? What cells are involved? How does the pathway occur?

A
  • Output:
    • The only output of cerebellar cortex = Purkinje cells (always inhibitory) → deep nuclei of cerebellum → superior cerebellar peduncle →
      • VL nucleus of the thalamus → contralateral primary motor and premotor cortex
      • Contralateral red nucleus → rubrospinal tract → decussation of rubrospinal tract → descent to periphery (double cross)
131
Q

What are your deep nuclei (lateral to medial)? Know a mnemonic?

A
  • Deep nuclei (lateral to medial)—Dentate, Emboliform, Globose, Fastigial (“Don’t Eat Greasy Foods”).
132
Q

What can lesions of the cerebellum cause? List some things (we will define them on a different card)

A
  • Lesions of cerebellum can cause the following:
    • Limb ataxia
    • Dysmetria
    • Dysarthria
    • Dysrhythmia (timing)
    • Unsteady gait
    • Truncal ataxia and postural instability
    • Nystagmus
    • Hypotonia
133
Q

Define the following

  • Limb ataxia
  • Dysmetria
  • Dysarthria
  • Dysrhythmia (timing)
  • Unsteady gait
  • Truncal ataxia and postural instability
  • Nystagmus
  • Hypotonia
A
  • Lesions of cerebellum can cause the following:
    • Limb ataxia – movements have a wavering course
    • Dysmetria – movements that “over-shoot” and “undershoot” (finger to nose or heel-shin test)
    • Dysarthria – slurred speech
    • Dysrhythmia (timing) – poor synchrony of multi-joint movements
    • Unsteady gait
      • Perform tandem gait (heel to toe test), Rhomberg test (maintain balance while eyes closed
      • Patients will present with a wide gait
    • Truncal ataxia and postural instability
    • Nystagmus (involuntary eye movements)
    • Hypotonia – decreased tone of muscles
134
Q

Compare and contrast the two types of anesthetics (metabolize, allergic reactions, and examples of each)

Amides and esters

A
  • Amides
    • Metabolize slowly in the liver
    • Rare allergic reactions
    • Ex: Lidocaine, Bupivacaine (toxic), Ropivacaine (Amide has I - these drugs have I’s not including the second one)
  • Esters
    • Metabolized quickly by serum cholinesterases
    • Allergic potential of PABA metabolite
    • Ex: Tetracaine, Chloroprocaine, Procaine, Benzocaine
135
Q

What is the pathway of action of local anesthetics?

Where does this action occur?

A

Mechanism of Action of Local Anesthetics

  • Location: lipid bilayer membrane of axons
  • Pathway: Penetrate epineurium (outer layer of axon) → bind voltage gated sodium channels → prevents conformational changes of channel → no sodium enters cell → stops transmission of action potential
136
Q

What is important to note about the following characteristics of MOA of anesthetics: absorption, distribution, metabolism (know where amides and esters are metabolized), and elimination?

A
  • Drug Action:
    • Absorption: certain locations of the body absorb drugs at a higher rate
    • Distribution: drugs have a different half-life and therefore different clearance
    • Metabolism: removal by circulation, local hydrolysis, and local tissue binding
      • Amides → liver via cytochrome P450AIII
      • Esters → pseudocholinesterase → PABA metabolite
    • Elimination: eliminated in urine as inactive metabolites
137
Q

What are the different routes of administration of anesthetics?

A
  • Topical anesthesia: anesthetics are applied directly (i.e. eye)
  • Infiltration anesthesia: anesthetics are injected subcutaneously
  • Intravenous regional anesthesia: anesthetics are administered through IV
  • Neuraxial blockade: anesthetics are administered through the spine (below L2) or epidurally → blocks all spinal nerves below the point of administration
  • Regional anesthesia: anesthetics are injected directly into nerves plexuses that control parts of your body (i.e. brachial plexus)
    • Supraclavicular, subclavian perivascular, and transarterial approach (goes through the artery to reach underlying nerve)
138
Q

How does local anesthetic toxicity work? How can you manage the sx (which sx do you get?)

A
  • Allergic reactions: super rare in amides and rare in esters
  • Local anesthetic toxicity: worsening sx with increasing dose/concentration of drug (i.e. muscle twitching, convulsions, hypoxia, acidosis, coma)
    • Toxicity is additive (cannot give maximum dose of two separate local anesthetics)
    • Management:
      • Minimize hypoxia, hypercarbia, acidosis
      • Benzodiazepines (Midazolam/diazepam) may increase threshold for convulsions
      • Intralipid 20%, 1.5ml/kg
139
Q

What occurs with the absorption of epi? Why is it added to the dose?

A
  • Absorption of Epinephrine: tachycardia, breathlessness, hot and bothered
    • Added to the dose of local anesthetics to vasoconstrict regional vessels to prolong anesthetic effect
140
Q

Define pain

What case showed the importance of pain?

A

Definition of pain

  • Pain: an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
  • The importance of pain:
    • Deletion of the gene that encodes voltage-gated Na⁺ channel SCN9A (Nav1.7) results in self-mutilation, bone fractures, multiple scars, joint deformities, amputations, and early death due to insensitivity to pain
    • Peripheral neuropathy leads to denervation of joints leading to neuropathic joint disease (Charcot’s joint)
141
Q

What are the receptor types?

A
142
Q

What are three types of nociceptors?

A
  • Nociceptors (pain receptors):
    • Mechanoreceptors
    • Silent nociceptors (respond only in presence of inflammation)
    • Polymodal Mechano-Heat Nociceptors: responds to extreme pressure, temp, and pain
143
Q

What are afferent NT: name excitatory and name inhibitory?

A
  • Afferent (sensory) Neurotransmitters
    • Excitatory: Substance P, Calcitonin Gene Related Peptide, Excitatory Amino Acids
    • Inhibitory: Enkephalins, Endorphins, NE, Serotonin, GABA
144
Q

Describe how pain transmission works with adelta and c fibers.

A
  • Pain Transmission
    • A-delta fibers (myelinated): fast, sharp, well-localized sensation
    • C-fibers (unmyelinated): duller, slower onset, poorly localized sensation
    • Physiology: 1st pain (A-delta) and 2nd pain (c-fibers)
145
Q
  • For nociceptive pain (type I)
    • Description
    • Types
A
  • Nociceptive pain (Type I)
    • Description: early physiologic protective system that is used to minimize contact with acute noxious stimuli (hot, cold, sharp)
      • Uses high-thresholds of pain to elicit withdrawal reflex → quick responses to extreme stimuli
    • Types: somatic (well localized) and visceral (poorly localized)
146
Q
  • Decribe what happens in the following systems with acute pain
    • Cardio
    • Pulm
    • GI
    • Endocrine
    • Heme
    • Immune
A
  • Systemic responses to acute pain
    • Cardiovascular: ↑BP, ↑HR , ↑myocardial oxygen demand
    • Pulmonary: ↓ respiratory function.
    • GI and Urinary: Increases sphincter tone and decreases intestinal and urinary motility.
    • Endocrine: ↑adrenaline/cortisol/glucagon, ↓anabolic hormones (insulin and testosterone), ↑Na⁺ retention, etc.
    • Hematologic: Increase in platelet adhesiveness, decreased fibrinolysis (breaking up of blood clots) à Propensity for clot formation
    • Immune: leukocytosis, inhibition of reticuloendothelial system, increased risk of infection
147
Q

For inflammatory pain:

  • Describe
  • Etiology
  • Physiology (two mechanisms!)
A
  • Description: causes heightened sensory sensitivity after tissue damage
    • Protective mechanism to reduce further risk of damage → promotes recovery
  • Etiology: tissue damage (i.e. UTI, pharyngitis, sunburn)
  • Physiology: Two mechanisms for heighted sensory sensitivity
    • Hyperalgesia: increased pain response to noxious stimuli
      • Phenomenon that occurs immediately around tissue injury
    • Allodynia: non-pain sensory receptors (i.e. mechanoreceptors) synapse with pain receptor ganglion → pain is felt with light touch
      • Phenomenon that occurs to adjacent uninjured skin around areas that experience hyperalgesia
148
Q

For visceral pain (a type of inflammatory pain):

  • Describe and give examples of locations
    Define referred visceral pain and provide pathway
A
  • Visceral Pain
    • Description: visceral organs contain silent nociceptors and are therefore usually insensitive to pain
      • Organs that have active nociceptors: heart, lungs, testes, bile ducts, intestines (respond to muscle spasm)
        • Brain lacks nociceptors, but meningeal layer contains them
    • Referred Visceral Pain
      • Due to embryological development, the body is divided into dermatomes via migration of tissue → convergence of visceral and somatic afferent nerve inputs into CNS
      • Pathway: Afferent sensory fiber from visceral organs detect tissue damage → synapse with afferent fibers from sensory cutaneous tissue → cutaneous pain
149
Q

For pathologic pain (type III)

  • Descirption
  • Types (2): give symptoms for both
A
  • Pathologic Pain (Type III)
    • Description: disease state of the nervous system that causes pain
    • Types:
      • Neuropathic pain: damage to nervous system (central NS or peripheral NS)
        • Classic symptoms of burning quality, hyperpathia, hyperesthesia, allodynia
        • Examples: phantom limb pain, peripheral neuropathy, stroke
      • Dysfunctional pain: nervous system dysfunction without damage (i.e. fibromyalgia, IBS, TMJ disease, interstitial cystitis)
150
Q

For chronic pain:

  • Description
  • Etiologies
  • Complications
A
  • Chronic pain:
    • Description: pain that persists beyond the usual course (>3-4 months) of an acute disease
    • Etiology
      • Non-curable illnesses: diabetes, arthritis, fibromyalgia, cancer, headaches
      • Complications of primary illness (i.e. muscle spasm, nerve damage)
      • Psychological issues: history of child abuse, PTSD
    • Complications: depression
151
Q

Explain and describe gate control theory

A

Gate-Control Theory

  • Description: proposes a balance of input by large A-beta and small A-delta and C fibers
    • Large fiber input inhibits transmission, while small fiber input facilitates spinal cord transmission of painful stimuli
    • The brain can modulate pain at the dorsal horn and brain stem
152
Q

What are some non-pharm treatments of pain

A
  • Non-pharmacological treatment of pain: cold/warm packs, rest/splint, rubbing/massage
153
Q

What are some pharm treatments of pain?

BE SPECIFIC

A
  • Pharmacological treatment of pain:
    • Local anesthetics, ketamine, tricylic antidepressants, anticonvulsants, alpha-2 agonist, dexamethasone
    • Non-opioid: analgesics: acetaminophen (inhibits COX in CNS), NSAIDS (inhibits COX in peripheral CNS)
154
Q

How do opioid analgesics work?

What are the three receptor types and what are their effects?

A
  • Opioids analgesics (brain and dorsal horn):
    • MOA: GPCR → reduces cAMP → activates potassium conductance and inhibits calcium conductance → hyperpolarization → decreased NT release → analgesia
    • Receptor classification effects
      • Mu: analgesia, sedation, bradycardia, N/V, decreased gastric motility (i.e. Tramadol)
      • Delta: spinal and supraspinal analgesia, decreased gastric motility
      • Kappa: spinal analgesia, diuresis, dysphoria
155
Q

What are the sites of action of all the different types of drugs?

A
  • Sites of Action:
    • Brain: opioids, alpha-2 agonists
    • Descending brain fibers: antidepressants (TCA/SNRI), anticonvulsants (gabapentin)
    • Dorsal horn: local anesthetics, opioids, alpha-2 agonists
    • Dorsal root ganglion: anticonvulsants
    • Peripheral nerves: local anesthetics
    • Peripheral nociceptors: local anesthetics, anti-inflammatory drugs
156
Q

Define neurocutaneous syndromes and phakomatoses

A
  • Neurocutaneous syndrome: group of conditions that have both skin and nervous system involvement
  • Phakomatoses: disorders in which there is tendency to form dysplastic lesions and tendency to form tumors, particularly in the nervous system
157
Q

What are all the major featires of tuberous sclerosis? There are a lot.

A
  • Major features (multi-systemic) – mostly potato-like lesions
    • hypomelanotic macules (≥3 at least 5 mm diameter): paler skin areas
    • Angiofibromas (≥3) or fibrous cephalic plaque: acne-like lesions
    • Ungual fibroma (≥2): fibromas around toenails/nails
    • Shagreen patch: elevated patch of skin
    • Cortical dysplasias
    • Subependymal nodules
    • Subependymal giant cell astrocytoma (tumor in brain)
    • Multiple retinal hamartomas
    • Cardiac rhabdomyoma
    • Lung Lymphangioleiomyomatosis (LAM)
    • Renal Angiomyolipomas (≥2)
158
Q

What are the genetics and sx of tuberous sclerosis?

A
  • Genetics: Autosomal dominant (2/3 spontaneous mutations)
    • Tumor suppressor genes in mTOR pathway
      • SC-1: 9q34 hamartin and TSC-2: 16p13 tuberin
  • Symptoms: seizure disorders, intellectual disability, ADHD, autism,
159
Q

For type 1 neurofibromatosis

  • Describe
  • Genetics
  • Major features
  • Diagnostic criteria
A

Neurofibromatosis (NFM)

  • Type 1 – neurocutaneous syndrome involving CNS and PNS
    • Genetics: autosomal dominant (NF1 gene 17q11.2 à encodes neurofibromin)
      • Tumor suppressor gene expressed in Schwan cells
    • Major features
      • Café-au-lait spots: hyperpigmented, flat, smooth borders
      • Freckles: axillary and inguinal spots
    • Diagnostic criteria (2 or more)
      • 6 or more café-au-lait spots, > .5 cm in prepubertal children; > 1.5 cm in postpubertal individuals
      • Axillary or inguinal freckling
      • 2 or more cutaneous neurofibromas (tumors of the nerve sheath cells) or 1 plexiform neurofibroma (arise in spinal root)
      • 2 or more iris Lisch nodules (proliferation of melanocytes à discoloration of the iris), an optic glioma (astrocytoma), a characteristic bony lesion, first degree relative with NF1
160
Q

For type 2 neurofibromatosis, describe and genetics

A
  • Type 2 – characterized by bilateral vestibular schwannomas
    • Autosomal dominant disorder – different than NF-1; chromosome 22; skin findings NOT a prominent feature
161
Q

For Sturge-Weber Syndrome

  • Genetics
  • Pathophys
  • Signs
  • Sx
A

Sturge-Weber Syndrome

  • Genetics: sporadic inheritance
  • Pathophysiology: Impaired cerebral blood flow due to sluggish flow and poor drainage in the leptomeningeal angiomatosis à tortuous veins and engorged choroid plexus
  • Signs: Port Wine Birthmark in trigeminal distribution that is light pink-purple (V1 and V2), leptomeningeal angioma (brain tumor with train-track appearance on CT due to calcifications), glaucoma
    • May present with ischemic brain injury over time
  • Symptoms: epilepsy, glaucoma, stroke-like episodes, cognitive and behavioral issues, migraine
162
Q

For von-Hippel Lindau Syndrome:

  • Genetics
  • Epidemiology
  • Tumors associated with it?
A

von-Hippel Lindau Syndrome

  • Genetics: autosomal dominant condition
  • Epidemiology: average age of presentation 26 years
  • Tumors
    • Hemangioblastomas of the brain (cerebellum) and spine
    • Retinal capillary hemangioblastomas (retinal angiomas)
    • Clear cell renal cell carcinomas (RCCs)
    • Pheochromocytomas
    • Endolymphatic sac tumors of the middle ear
    • Serous cystadenomas and neuroendocrine tumors of the pancreas
    • Papillary cystadenomas of the epididymis and broad ligament

NBS (8 decks)

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