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What is the CNS? What is the peripheral nervous system?
What are bundles of neuronal cell bodies called in each? What axons come into/out of each?

1) CNS = brain + spinal cord, communicates via peripheral nervous system
2) peripheral nervous system - everything outside the CNS, convey info b/w peripheral structures and CNS
3) CNS- called nuclei
PNS- called ganglion
4) sensory neurons (afferent) come INTO the CNS and motor axons (efferent) LEAVE the CNS


Somatic/autonomic systems:
functions/signals carried
where are neurons located

1) Somatic- carries signals to/from muscles, tendons, joints, skins; conveys pain, temp, touch, proprioception (self-awareness)
Motor neurons- ventral horn of spinal cord
Sensory neurons- dorsal root (spinal) and cranial nerve ganglia
2) Autonomic- carries signals to/from internal organs; conveys distension
either parasympathetic (dine and recline) or sympathetic (flight or fight)
Motor neurons- preganglionic are in the CNS
postganglionic neurons are in PNS ganglia


What are the classifications for neurons? Classify motor and sensory neurons and where they are located

Multipolar, bipolar, unipolar- number of dendritic processes attached to cell body
Motor neuron (efferent)- multipolar, carry info AWAY from CNS; located in ventral horn of spinal cord
Sensory neuron (afferent)- unipolar, carry info TO CNS; located in dorsal root ganglia or cranial nerve ganglia


What are the spinal cord segments? How do spinal nerves exit?

1) 31 segments/spinal nerves
From top of spinal cord: cervical (8), thoracic (12), lumbar (5), sacral (5), and coccygeal (1)
2) spinal nerves exit the vertebral canal through the intervertebral foramen
C1-C7 exit ABOVE (E.g. C3 exits between C2 and C3)
C8 and below all exit BELOW (e.g. T5 exits between T5 and T6)


How does the spinal nerve attach to the spinal cord? Describe structure and what it innervates

1) Spinal nerve attached to cord via ventral and dorsal roots
ventral- ONLY motor neurons
dorsal- ONLY sensory neurons
2) Dorsal and ventral roots fuse at spinal nerve, which branches again into dorsal ramus and ventral ramus
3) Dorsal rami innervate:
-skin on back
-true back muscles (e.g. erector spinae)
-zygapophyseal joints (joint bw articular processes of two adjacent vertebral processes- allow for flexion/extension of vertebrae)
Ventral rami innervate:
-everything else


What are dermatomes?

Skin slices that divide up the body- each dermatome is innervated by ventral or dorsal rami
They overlap--> for complete anesthesia you need to knock out segments before and after e.g. for T10 dermatomal segment anesthesia, knock out T9, T10, and T11 ventral rami


Describe the parts of the autonomic nervous system and how nerve fibers are distributed

Autonomic nervous system is part of the peripheral nervous system; is comprised of sympathetic and parasympathetic divisions
Sympathetic- fight or flight, nerve fibers distributed with spinal nerves/blood vessels
Parasympathetic- dine and recline, nerve fibers distributed with cranial nerves and pelvic autonomic nerves


Compare motor neurons of somatic and visceral(autonomic) systems

1) Similarities- both multipolar neurons, carry signals away from CNS
2) Differences-
-structures innervated- voluntary skeletal muscle (somatic), smooth muscle and cardiac muscle and glands (autonomic)
-pathway- 1 motor neuron (somatic), 2 motor neurons with preganglionic in CNS and postganglionic in PNC fibers (autonomic)


Compare motor neurons of the sympathetic and parasympathetic system

1) Similarities: require 2 neuron pathway with 1st in CNS, 2nd in PNS
2) Differences:
-functions- fight or flight (symp), dine and recline (parasymp)
-sympathetic have short preganglionic and long post ganglionic
parasympathetic have long preganglionic and short post ganglionic
-location of preganglionic- sympathetic in lateral horn of T1-L2, parasympathetic in brainstem or sacral spinal cord
-location of postganglionic- sympathetic in paravertebral/prevertebral ganglia, parasympathetic in terminal parasympathetic ganglia
*sympathetic neurons all over the body


Describe schematic pathway of sympathetic motor nerve innervation to the trunk

Trunk innervated by T1-L2 postganglionic sympathetic nerve fibers
1) preganglionic cell body of motor neuron in lateral horn
2) axon exits via ventral root, spinal nerve, ventral ramus
3) enters paravertebral ganglion (sympathetic chain of ganglia next to vertebral column) via white ramus communicans
4) preganglion synapses onto postganglionic cell bodies
5) postganglion axon exits via gray ramus communicans into ventral ramus
6) distributed to its final destination


Describe schematic pathway of sympathetic motor nerve innervation to the upper/lower limbs

Upper/lower limbs do not have preganglionic cell bodies nor white rami communicans (white rami for preganglionic neurons)
1) preganglionic cell body of motor neuron in lateral horn
2) axon exits via ventral root, spinal nerve, ventral ramus
3) enters paravertebral ganglion (sympathetic chain of ganglia next to vertebral column) via white ramus communicans
4) does NOT synapse here, either ascends or descends the paravertebral ganglion chain
5) then it synapses on the postganglionic neuron attached to the target spinal cord segment
6) postganglion axon exits via gray ramus communicans into ventral ramus
7) distributed to final destination


Describe general distribution of parasympathetic motor nerve innervation

-More limited distribution than sympathetic system
-Neurons distributed to visceral structures throughout the head, neck, thorax, abdomen, pelvis, and perinuem
-does not innervate smooth muscle/glands associated with somatic structures --> not in trunk or limbs
*Craniosacral outflow


Compare sensory neurons of somatic and visceral (autonomic) systems

1) Similarities: unipolar neurons with cell bodies in a ganglion
same pathway- one motor neuron from dorsal root to dorsal horn
2) Differences:
-structures innervated- skin muscle + joints (somatic), visceral glands + blood vessels (autonomic)
-sensations- pain, temp, touch, prioprioception (somatic), distension, hunger, nausea (autonomic)
-location of cell bodies- dorsal root ganglia from C2-coccyx (somatic), dorsal root ganglia from T1-L2 (autonomic)
*sensory follows same pathway as motor


Why does referred pain occur? Describe the schematic pathway involved in referred pain from the heart

1) Referred pain occurs because visceral/autonomic afferent/sensory fibers synapse on the same neurons in the dorsal horn of spinal cord segments T1-L2 as do somatic afferent/sensory fibers (follow same pathway back)
so the brain is confused whether the pain is coming from the heart or upper arm because those sensory neurons are in the same place
2) Heart --> visceral nerve --> superior cervical ganglion --> descends chain to paravertebral ganglion --> exits via white ramus communicans --> ventral ramus --> spinal nerve --> dorsal root ganglion --> dorsal horn --> SYNAPSES


Where does the spinal cord end? What segment of the vertebral column is present in this region?
What can be done in that area? What is the landmark in that area?

1) Ends at level of L1/L2, tapers at conus medullaris, nerve roots that continue down from there are called cauda equina
*lower sacral segment*
2) Can insert needle to draw fluid
3) iliac crest which you can palpate, is at L4


What is the intervertebral disk? What is its function? What is it composed of?

Why do we get shorter as we get older?

1) cartilaginous joint between vertebral bodies
2) shock absorber, mobility between vertebrae
3) outer lying anulus fibrosis - made of cartilage and connective tissue
inner nucleus pulposus- few cells, lot of ECM with proteoglycans, water-containing (adult remnant of notochord)
*distributes pressure (water squeezed out- shorter end of day)
4) fewer proteoglycans in the np--> less water bound--> shorter


What is the intervertebral foramen? What is its function? What forms its boundaries?

1) space between two spinal vertebrae
2) passageway of spinal nerves in/out of the vertebral column
3) Anterior: vertebrae above, below + intervertebral disk
posterior: superior/inferior processes + facet joint


How are spinal nerves numbered?

Cervical: C3 nerve passes between vertebrae C2 and C3
Thoracic/lumbar: L1 nerve passes through vertebrae L1 and L2


1) What is the most common direction of a herniated nucleus pulposus? Why?
2) When do hernias become symptomatic? How do we trace the cause?

1) Posterior laterally
posterior is where the anulus fibrosis is weakest
there is a posterior longitudinal ligament so the np will be pushed laterally
2) when the spinal nerves/roots become compressed- can trace back which nerves depending on the affected dermatome/myotome
Dermatome symptoms- tingling (paresthesia), pain, reduced sensation
Myotome symptoms- muscle weakness (paresis), paralysis


What can cause impingement of spinal nerves/roots? What number nerve is affected?

1) -herniated nucleus pulposus (on anterior side)
-osteoarthritis at facet joint (on posterior side) - osteophyte bone spurs encroach on foramen
-stenosis (caused by thickening ligamentum flavum or facet joint)
2) number nerve below the intervertebral disk e.g. L5 nerve affected when hernia at IV disk L4/L5
can also affect multiple nerves if the hernia is more medial


What are the types of stenosis?

Central stenosis- entire vertebral canal narrows, can compress nerves/roots, cauda equina, spinal cord
Foraminal stenosis- IV foramen narrows, compresses spinal nerves/roots


What is spondyolysis? What is spondylolisthesis?

Spondyolysis- fracture of the isthmus (neck of the scottie dog)
Spondyolisthesis- breakage of the isthmus
both cause nerve compression


Define electrical conductance, membrane diffusion potential, current , electrogenic, diffusion potential

Membrane potential - voltage difference between inside/outside plasma membrane because of ion concentration gradient
Current- flow of ions
Electrical conductance- ability to conduct current
Electrogenic- ability to create electricity bc of ion gradient--> conduct action potential e.g. pump


Explain distribution of Na+, Cl-, K+ across plasma membrane
Describe action of ATPase and its role

More Na+, Ca2+ outside the cell, more K+ inside the cell
some Na+ will leak inside and K+ outside down their concentration gradient
but ATPase maintains the electrochemical gradient by pumping 3 Na+ out and 2K+ in - so outside of cell is more positive than inside


What is the resting membrane potential (RMP) for a motor neuron? What is it influenced by?

1) -90mV
2) RMP set by K+ concentration gradient; larger the gradient --> more negative the cell


What is the Nernst potential?

Membrane potential at which there is no net flux of a given ion


Describe the phases of an action potential

1) Resting-
2) Depolarization
3) Repolarization
4) Refraction


What happens if you have hyperkalemia?

hyperkalemia- high plasma K+
Acute: depolarizes the cell --> excitability
Chronic: membrane potential clamped --> Na+ voltage gated channels inactive --> impairs excitability--> fewer action potentials --> leads to arrhythmia


Compare and contrast the properties of pacemaker and plateau action potentials

Pacemaker potential (SA node): self-perpetuating without stimulus
gradual depolarization initially due to If and Ca2+ in, K out; Ca2+ channel opening causes action potential, repolarization via K+ channels
Plateau potential (smooth muscle, cardiomyocyte): rapid Na+ depolarization, inward Ca2+ and outward K+ cause plateau phase, then rapid K+ repolarization


How is the action potential propagated along an axon towards the axon terminal?

action potential excites adjacent portions through Na+ migration -- > adjacent membrane depolarization --> Na+ channels opened


What is the impact of motor neurons that are myelinated?

Action potentials move a lot faster because of saltatory conduction as they jump from one unmyelinated part (node of Ranvier) to another
unmyelinated- cable-like, takes longer e.g. pain fiber


Describe the sensation of pain. How do local anesthetics work?

1) Stimulus --> activates nocicepters --> action potential in pain afferents --> Ascend spinal cord --> end in thalamus and relay pain
2) Local anesthetics block the action potential in afferent sensory neurons--> protonated in the cell --> bind to Na+ channels and inactivate --> threshold not reached --> no action potential


Describe differences between electrical and chemical synapses. What are excitatory vs inhibitory neurotransmitters?

Electrical- v rare, in connexons in gap junctions, physical connection
Chemical- use neurotransmitters to relay action potential
e.g. acetylcholine (for neuromuscular)
excitatory- glutamate, aspartate
inhibitory- GABA, glycine


Describe how chemical synapses work. Difference between ionotropic and metabotropic transmission

chemical synapse- where neurons signal to each other or muscle cells (neuromuscular junction)
1) Action potential activates Ca2+ channel in presynaptic membrane
2) Rapid Ca2+ influx
3) Ca2+ dependent signaling cascade
4) synaptic vesicles fuse with presynaptic membrane
5) neurotransmitters released
6) bind with receptor on postsynaptic membrane
7) response
8) transmission terminated when neurotransmitters broken down or taken up again in the presynaptic neuron
Ionotropic- activate ligand -gated ion channels directly - v FAST
metabotropic - includes receptor mediated signaling - much SLOWER


What is synaptic fatigue?

Comes from depletion of neurotransmitters, postsynaptic receptor desensitization, disruption in ion gradient of postsynaptic neuron


Determine effect of each agent on action potential/neurotransmission:
-Nicotine: is not hydrolyzed by cholinesterase.
-alpha toxins: are found in cobra venom and curare;  toxins out-compete ACh for binding to the ACh receptor. Although alpha toxins bind the ACh receptor, they do not activate it.
-beta-bungarotoxin: is a member of the family of cholinesterase inhibitors that are common in various arachnid and snake venoms. Bungarotoxins block the activity of cholinesterase.
-Botulinus toxin A, B, and C; tetanus: each block ACh release.
-Tetrodotoxin: is found in several marine species, It blocks voltage-gated Na+ channels in nerves and cardiac muscle.
-Dendrotoxin: derived from the venom of the green mamba snake, it blocks neuronal voltage-gated K+ channels in motor neurons.

-Nicotine: activation of the ACh receptor is more sustained than that induced by ACh.
-alpha toxins: The activation of ligand-gated Na+ channels within the post-junctional membrane is prevented.
-beta-bungarotoxin: promote highly erratic and abnormal muscle contractions that result in muscle spasm.
-Botulinus toxin A, B, and C; tetanus: prevent muscle contraction.
-Tetrodotoxin: depolarization within nerves is prevented; cardiac failure due to impaired cardiomyocyte contractility.
-Dendrotoxin: AP duration is increased, and this results in the enhanced release of ACh within the neuromuscular junction; hyperexcitability, convulsions may result.


How are action potentials initiated?

any event that depolarizes membrane potential e.g. electrical, chemical, mechanical
subthreshold changes due to subthreshold stimuli = graded potential
graded potentials can sum to reach threshold potential


1) non-vascular circulation
2) cardiovascular
3) lymph vascular

1) Non-vascular circulation - fluid leaves vascular system, gong into extravascular space, and then reenters e.g. CSF, synovial fluid
2) Cardiovascular- 2 way system (heart --> tissues --> heart), heart acts asa pump that creates pressure gradient, in low pressure there are valves
3) Lymph vascular- 1 way system (tissues --> heart), no pump


T/F: All veins have valves

False. Portal veins do not have valves, neither do veins communicating between veins of face/scalp, nor dural venous sinuses within the skull


Lymph vascular system:
What does it do?
What are the pathways of drainage?
What is the clinical relevance re: cancer?
Where are the major lymph node groups?

1) Rid body of waste, toxins; transport lymph, which contains white blood cells
2) LHS of head/neck/thorax, left upper limb, EVERYTHING below diaphragm --> thoracic duct
RHS of head/neck/thorax, right upper limb --> right lymphatic duct
3) Need to know where lymphatic drainage of the breast occurs because cancer spreads through the breast first before metastasizing through the body
4) cervical (neck), axillary (arm), inguinal (groin), popliteal (knee), mastoid (head)


What are the main functions of the cardiovascular system. Describe in particular thermoregulation mechanisms

1) Transportation- O2, Co2, nutrients, waste
2) Communication- hormones
3) Thermoregulation- normally warm blood from artery is brought to cutaneous vasculature (ie skin) and heat is diffused, veins have cooler blood (how body maintains a constant temp)
BUT when its cold, need an A-V shunt; when shunt is open, blood flows from artery to vein without going to skin --> conserve heat, but deprive O2 to the skin --> ischemia --> frostbite
SO you have venae comitantes (paired veins), 2 veins flanking artery which creates thermal gradient --> allows heat to transfer --> conserve heat but dont reduce blood flow to skin e.g. in limbs, chest wall
examples: brachial artery, ulnar artery, radial artery


End arteries
Collateral circulation
What is costal notching

1) End arteries - if you have occlusion--> no blood flow--> cell dies
anatomical - full responsibility for providing blood e.g. in retina
functional- shared responsibility, but cell will still die e.g. coronary artery --> myocardial infarction
2) Collateral circulation - anastomosis (connection) of arteries to have multiple pathways of blood flow --> no cell death *can only happen in veins without valves
e.g. in brain, limbs
3) costal notching - when aorta is occluded but internal thoracic arteries are fine --> intercostal arteries used as collateral pathways--> they grow thicker --> bone resorption (bone broken down) along rib, clinical finding for aorta obstruction


Describe the process of neurulation (ectodermal neural plate --> neuroectodermal tube).
What does the neural tube become?

1) begins at level of first 5 somites - post gastrulation and notochord
TF from mesoderm--> increased FGF, decreased BMP4 (wants to form epidermis)
cranial end --> chordin, noggin
caudal end --> FGF, Wnt, retinoic acid
2) Neural plate hinges and forms neural groove and neural folds
3) neural folds fuse in dorsal midline EXCEPT for rostral and caudal neopores --> forms neural tube
4) First rostral neopore closes, then caudal
5) caudal end formed by secondary neurulation of caudal eminence
*neural tube becomes brain and spinal cord (CNS)


Describe development of neural crest cells. What are their derivatives?

1) Neural crest cells detach rostral to caudal during neurulation and migrate
2) melanocytes, sensory ganglia, schwann cells, adrenal medulla, bones/conn tissue of the face, meninges, etc.


Describe the differentiation of somites (somites = segmented paraxial mesoderm).

1) Somites differentiate under influence of shh
low shh --> Dermomyotome (skin + muscle)
high shh --> sclerotome (bone vertebrae and ribs)
2) sclerotome cells migrate and surround notochord to form vertebral bodies and surround neural tube to form vertebral arches (pedicles + laminae)
somites C5-T1 = upper limb bud (C5 - T1 is brachial plexus)
somites L2-S3 = lower limb bud (L2-S3 is lumbosacral plexus)
# somites = # vertebrae, influences # of spinal nerves
3) dermomyotome splits into dermotome and myotome
myotome - muscles (back, limbs)
dermatome- skin


Describe the types of folding during neurulation and their effects (cephalocaudal folding)

lateral folding- creates gut tube, body cavities, brings embryo into the amniotic cavity
cranial folding- how mouth moves to ventral surface, heart moves down to thorax
caudal folding - establishes reproductive, urinary, digestive systems at caudal ends


Describe the changes in the position of the ending of the spinal cord during devlpt

early fetal devlpt- spinal cord is whole length of embryo
later fetal devlpt- differential growth so formation of cauda equina and filum terminale
birth- spinal cord ends at L3/L4
adult- spinal cord ends at L1/L2


Describe the most common neural tube defects

1) rostral neopore closing defects --> anencephaly
2) caudal neopore closing defects --> spina bifida
occulta- lack of fusion of vertebral arches (tamest) - mesoderm cant migrate between neural tube and ectoderm to establish vertebral arch, there is hair on top
meningocele- multiple vertebrae missing, protrusion of meninges but spinal cord normal
meningomyelocele- protrusion of meninges but spinal cord is not normal --> some neuro deficits
rachischisis- neural tube doesnt fuse- exposed neural tube tissue --> lots of neuro tube defects e.g. paralysis from waist down


Where does spinal cord develop from?

Cervical, thoracic, lumbar regions --> neural tube
*why spina bifidas occur in lumbar region
saccral region--> where old primitive streak was (primitive node to cloacal membrane) is --> mesoderm


Describe the process of limb development and rotation

Limbs formed in lateral plate mesoderm (secretes FGF) and induced by adjacent somites
upper limb bud- C5 to T1 somites, lower limb bud- L2 to S3 (devlps 2 days later)
3 axes:
1) proximo-distal- determines order of limb segments --> apical ectodermal ridge (AER) induced by BMP, leads to proliferation of mesenchymal core of limb buds and differentiation
2) rostro-caudal (anterior/posterior)- determines order of digits --> differentiation through zone of polarizing activity (ZPA) at caudal end which releases shh --> regulate hox gene expression
closest to ZPA --> digit #5
3) dorso-ventral axis- in the upper limb dorsal is extensor and ventral is flexor, switched in the lower limb
this is because lower limb rotates 180 degrees


apical ectodermal ridge
hyaline cartilage model
epiphyseal plate

1) Apical ectodermal ridge- formed at distal end of each limb bud, major signaling center for proper limb development in proximo-distal axis, communicates with limb mesenchyme and ZPA to direct limb devlpt
mesenchyme cells further from AER start to differentiate into cartilage and muscle
2) mesenchymal cells --> chondrocytes--> hyaline cartilage models which undergo endochondral ossification, starting in center of long bone at primary center (diaphysis) and extending outwards towards secondary center (epiphysis)
3) epiphyseal growth plate separates the primary and secondary ossification centers - replaced by growth line when bone has reached its full length (in adults)


Discuss the role of dorsal and ventral mesodermal masses with respect to compartmentalization of the limb, functions of muscles, and innervation patterns

1) Limb musculature when condensations of somitic mesoderm form dorsal and ventral to axial mesenchyme (mesenchyme= conn tissue that forms bones, cartilage, etc)
2) dorsal mass, upper limb- extensor, supinators
dorsal mass, lower limb- extensors, abductors
ventral mass, upper limb- flexors, protonators
ventral mass, lower limb- flexors, adductors
*rotation of lower limb which switches these in the fetus
3) Innervation
upper limb- C5-T1
lower limb- L4-S3
ventral muscle mass --> ventral division of ventral rami
dorsal muscle mass--> dorsal divisions of ventral rami
challenges to innervation: GAGs, dense mesenchyme


Describe the development of the segmental innervation of the limbs

1) dorsal mass muscles innervated by dorsal divisions of primary ventral rami
ventral muscle mass innervated by ventral divisions of primary ventral rami
2) nerves grow along permissive pathways, blocked by dense mesenchyme and GAGs; nerves enter limb buds and come in contact with mesoderm/future muscle cells
3) Motor axons mix to form brachial plexus (upper limb) and lumbo-sacral plexus (lower limb)
4) axon growth cones migrate into limb bud
motor axons- travel along permissive pathway, deviate at decision points
sensory axons- travel along motor axon routes, deviate to innervate specific target organs
5) rotation
lower limb rotates 180 degrees medially - dermatome twisted into spiral


What are the differences in clinical symptoms between pre and post brachial plexus lesions?

Pre plexus: supraclavicular portion injury, weakness of muscles of same segmental innervation, sensory deficit in dermatomal region
Post plexus: infraclavicular injury, paralysis of muscles innervated by same nerve, sensory loss in cutaneous nerve distribution


What does the neural tube develop into? What are glial cells?

Neural tube - brain + spinal cord
initially epithelium with cilia
epithelium --> neurons + glia of CNS
glial cells aka astrocytes provide guidance to migrating neurons, growth factor support


What are the components of a neuron? What are their functions?

neuron- highly polarized cell
soma- cell body, provides protein
axon- transmits info
dendrite- increase surface area through branches and spine protrusions, receive info at synapses and sum all the excitatory/inhibitory info
if excitatory reaches threshold -- action potentials fired down the axon


What are Nissl bodies?

stacks of RER and free ribosomes in the neuronal cell body- produce the proteins for the entire neuron including the axon
dye basophilic purple
Nissl bodies extend to dendrites but are NOT in the axon


What are the types of axonal transport?

Anterograde- cell body to terminal
can be fast when transporting vesicles, mt
is slow process when moving proteins, cytoskeleton

retrograde- terminal to cell body, has both a fast and slow process

fast processes use microtubules (kinesin for anterograde, dynein for retrograde)


What are synapses? What are the different types?

Synapse- spatially discrete membrane specialization which mediates communication between neurons and target cells
Electrical- gap junctions with small pores so ions can pass through, allow 1 cell development to be coordinated with another
Chemical- transmitter signals released into synaptic cleft and received by postsynaptic element
--> Ca2+ influx through channels leads to vesicle release from actin cytoskeleton
--> vesicles dock to presynaptic membrane via VAMP/tSNAREs in process regulated by calcium sensoring proteins
--> vesicle contents released when there is an action potential (Ca2+ influx)
--> vesicles are recycled to early endosome pathway or can be refilled with transmitter (ultimately degraded by lysosome in cell body)
*botulinum/tetanus affects SNAREs


What happens to neurotransmitters after action potential signal is transmitted?

1) diffuse away
2) taken up by glial cell ie astrocyte
3) taken up by presynaptic terminal
4) degraded by enzymes


T/F: Synapses can occur at any point along a neuron

True. focus is on synapses between axon and dendrite of another neuron, but can have synapses between axon-axno, dendrite-dendrite, axon-cell body/soma


Peripheral nervous system:
1) what are groups of neurons called
2) where are the receptors for action potentials
3) What are the support/glial cells and their functions
4) What is the organization

1) Ganglia
2) receptors on neurons or peripheral targets (skeletal muscle, smooth muscle, etc)
3) satellite cells- glial cells, surround cell bodies of neurons and provides physical support
Schwann cells- wraps myelin around the axon/nerve fiber, also produce growth factors and phagocytose debris
one Schwann cell between two nodes of Ranvier (can see nucleus of Schwann cell outside of white myelin sheath)
*Schwann cells surround ALL axons whether or not they are myelinated (1 schwann cell ~ 20 unmyelinated axons)
4) endoneurium around schwann cell --> perineurium around nerve fibers/fasicles --> epineurium around nerve trunk


Types of PNS ganglia and their differences:

1) Sensory/afferent- round nucleus in center, prominent nucleolus, many satellite cells around periphery, no synapses
located in dorsal root ganglion
sensory neurons
2) Sympathetic (part of autonomic)- small multipolar neurons, eccentric nucleus, fewer satellite cells and nerve fibers, have synapses
chain on both sides of vertebral column -- paravertebral column
visceral motor neurons


Central nervous system:
1) What are groups of neurons called
2) where are the receptors for action potentials
3) What are the support/glial cells and their functions

1) nuclei (groups) or cortices (sheets of cell bodies)
2) receptors on neurons or glia
3) oligodendrocytes- produce myelin
astrocytes- star shaped, lie between neurons and capillaries and found at initial segment and nodes of ranvier, provide structural support to nervous system + lots of other functions, linked by gap junctions
ependymal cells- cover surface of brain/central canal of the spinal cord (remnant of original neuroepithelium), allow CSF to enter
microglia- macrophages of brain/spinal cord (do not originate from neuroepithelium/CNS)


What is the choroid plexus? Where is it and what is its structure?

Choroid plexus:
-in ventricles of the brain
-produces CSF - one in each ventricle
-covered by ependymal epithelial cells with tight(/occluding) junctions


What are the functions of astrocytes

Astrocytes- glial cells in CNS
1) structural support to nervous system
2) K+ sinks, regulate ionic environment
3) segregate synapses
4) accumulate neurotransmitters (have the receptors), so could terminate synaptic transmission
*can be regulated by neurotransmitters to change permeability, morphology, content of neurotrophic factors, ability to take neurotransmitter
5) release factors that influence formation of tight junctions between endothelial cells of capillaries --> influence integrity of the blood brain barrier
6) release factors that regulate blood flow in capillaries of the brain
7) immune response- divide during injury and remove neuronal debris


When does myelination occur in the CNS? What is responsible for it?

What is the purpose of the myelin sheath? What are the different parts and their purpose?

What are the similarities/differences with the PNS?

1) Myelination occurs in last trimester but a lot of it happens postnatally
nodes of ranvier are unmyelinated parts between the internodal segments
2) oligodendrocytes produce myelin sheath by sending out processes to wrap axons spirally (as opposed to schwann cells which fully wrap around one axon to form just one internode)
major dense lines- plasma membrane of the process that wraps around the axon
intraperiod line- lighter, when the extracellular faces of the plasma membrane of adjoining wrappings are brought into close contact by PLP proteins
3) myelin sheath - insulating coat of resistance, isolates axon from extracellular electrical influences
4) Nodes of ranvier- unmeylinated/naked, high capacitance/low resistance, lots of ion channels
action potential jumps from node to node down the axon--> saltatory conduction

5) PNS also has major dense lines and intraperiod lines
but the transmembrane protein is P0


What is a potential cause for diseases like multiple sclerosis and alzheimer's?

paranodal region - at the edges of the nodes of ranvier/tip of axon sheath, can see edges of the wrapped oligodendrocyte cytoplasm --> looks like tongues
communication between axon cell membrane (axolemma) + oligodendrocyte
loss of signals can cause diseases like MS or AD


What are major differences between neurons of the CNS and PNS?

1) in CNS unmyelinated axons are naked, in PNS unmyelinated axons are still covered with Schwann cells that are covered by basal lamina
2) no end/peri/epineurium in the CNS
3) in CNS oligodendrocyte can wrap around many axons, in PNS the schwann cell wraps around just one axon to form one internode
4) Transmembrane protein in myelin sheath: PLP in CNS, P0 in PNS


How do CNS/PNS respond to nerve injury?

1) PNS- can have functional regeneration if cell body is not damaged - Schwann cells line up around lesion within basal lamina and produce growth factors so the axon can be directed towards tube, go across lesion site, and grow towards distal stump
2) CNS- microglia and astrocytes phagocytose debris but there is a glial scar --> cant regenerate because of environment
experiment that shows that axons are able to grow along a graft into normal target and conduct AP


Explain the 3 different kinds of joints

1) fibrous- fibrous connective tissue between bones limited movement, e.g. sutures of the skull, teeth
2) cartilaginous- cartilage between bones, fibrous capsule surrounding joint, slightly more movement e.g. intervertebral disk
3) Synovial- cartilage between bones, then synovial cavity, then synovial membrane (synovium), then fibrous capsule surrounding joint, low friction, e.g. shoulder, hip, elbow, knee
*osteoarthritis causes degeneration of articular cartilage at synovial joint


What is a motor unit? What are the mechanisms for gradation of muscle action? What are the gradations of muscle control in the body?

Motor unit- functional unit in muscle- the motor neuron + all the skeletal muscle cells it innervates
all of nothing function- when motor neuron depolarizes and undergoes action potential -- all the muscle cells contract fully
Gradation: based on the number of motor units used
-Muscles for large movement: >500 muscle cells per motor unit --> large gradation of function e.g. shoulder girdle, hip girdle
-Muscles for fine motor movement: small gradation of function e.g. intrinsic hand muscles


Describe the three types of muscle contraction:

Concentric- muscle shortens to cause movement e.g. lift arm
Isometric- muscle length is constant to prevent movement e.g. keep arm elevated
Eccentric- muscle lengthens to resist effect of gravity e.g. lowering arm, deltoid (which is for abduction) prevents adduction of the arm


What is radiodensity and what is the order?

Radiodensity- amount of X ray that a particular material absorbs (more absorption --> more radiodense/radiopaque--> film is less exposed --> film is whiter)
In order of increasing density:
-water density (muscle, cartilage, tendon, blood, conn tissue, nerves, etc)
-foreign heavy metal


Explain superimposition. What are the major radiographic projections? What is the convention of orientation?

1) Bc radiographs are 2D images of 3D- objects can be superimposed
need to take projections from another orientation
2) Anterior projection (PA)- anterior side faces film
posterior projection (AP)- posterior side faces film
left lateral projection- left side faces film
right lateral projection- right side faces film
obliques- at 45 degrees
3) Look at radiograph as if patient is facing you
The target structure should be CLOSER to film to reduce penumbra affect - image will be smaller and sharper


What are the similarities and differences between CT and MRI?

*analyze images as if patient is supine, feet facing you
CT- X rays from many different directions, same greyscale as X rays
use CT for abdomen (cheaper than MRI)
MRI - magnetic resonance; patient surrounded by magnet, radiofrequency pulse and emitted energy analyzed based on realignment with orbit
fat - white, bone- dark OPPOSITE from x-rays
use MRI for things covered in bone e.g. brain


How does the ultrasound machine work?
How can transducers affect frequency?
How do structures appear on US?
What is anisotropy?

1) Computer programmed to transform sound waves/echoes into images; transducer has crystals that vibrate to create sound waves in 1-20 Mhz range
need gel so sound waves can travel through the body
2) High frequency transducers - LOWER penetration but BETTER resolution
lower frequency transducers- BETTER penetration but LOWER resolution (lower frequency waves travel further because of less attenuation/energy loss)
3) More reflective- hyperechoic e.g. bone
not reflective e.g. fluid, fat, cartilage- hypo or anaechoic (black)
4) change in echogeneicity of a structure bc of angle of beam- need to make sure probe is lined up otherwise might appear hyopechoic, esp problem for tendons


For skeletal, cardiac, and smooth muscle:
1) function
2) where is Ca2+ located
3) where does ATP come from

1) Skeletal muscle
ambulation, posture, displacing mass, largest site for glucose storage and post-eating lipid oxidation
Ca2+ is intracellular
ATP is from ox phox, fatty acids, glyolytic, or ATP stores
2) Cardiac muscle
moving blood volume
Ca2+ intra and extracellular
ATP from ox phos, fatty acids
3) smooth muscle
changing lumen diameter for digestion, blood pressure
Ca2+ is intra and extracellular
ATP from ox phos


Explain the entire process of skeletal muscle contraction from AP to contraction

1) Action potential reaches motor nerve terminus
2) voltage dependent Ca2+ channels open
3) Ca2+ influx
4) synaptic vesicles fuse with membrane and release Ach
5) Ach binds to cholinergic nicotinic receptors on post-junctional membrane of muscle cell
6) Na+ influx --> endplate potential (sub-threshold membrane depolarization)
7) Voltage gated Na+ channels open
8) AP in muscle fiber into T tubules (invaginations of sarcolemma that allows AP to travel fast)
9) DHPR receptors open
10) RyR pores open
11) Ca2+ effluxes from sarcoplasmic reticulum (smooth ER) into sarcoplasm (Cytoplasm of skeletal muscle)
12) Ca2+ binds with troponin C on actin
13) reveals tropmyosin on actin
14) actin + myosin binding
15) powerstroke where is released
16) ATP binds so myosin and actin dissociate
17) ATP hydrolysis into ADP + P --> tight binding between myosin + ADP
18) P+ leaves and powerstroke --> 14 to 18 is called crossbridge cycling


How does extracellular calcemic status affect skeletal muscle excitability? What is the pathology?

1) Hypercalcemia --> hypoexcitability because too much extracellular Ca2+ raises membrane potential to open Na+ channels --> Na+ channels dont open as much
2) Hypocalcemia --> hyperexcitability because there is no Ca2+ to stabilize membrane Na+ channels --> Na+ channels excited and open a lot (increased Ina+)
3) Parathyroid hormone PTH stimulates release of Ca2+ from bone or kidneys


What are the sources of intramuscular ATP?

sarcoplasmic ATP (only lasts a few sec) -->
phosphocreatine (creates 1 ATP and creatine, works for short duration) -->
Anaerobic glycolysis (glucose --> 2 ATP + lactate + heat, lasts about a minute) -->
Oxidative phosphorylation of fatty acids, glucose (sustained activity, generates lots of ATP)


How do skeletal muscles relax?

1) primary mechanism: SERCA pumps Ca2+ from sarcoplasm --> SR lumen --> lowers intracellular [Ca2+]
2) facilitory mechanism: NCX channel in sarcolemma --> pumps Ca2+ out of muscle cell and Na+ into cell


What are the two types of muscle contraction?
How do they apply to skeletal muscle contraction?
What is the difference between concentric and eccentric contraction?

1) Isometric- tension without force
isotonic- generation of force by moving load over distance
2) all muscle contractions begin with isometric, can become isotonic if muscle preload> afterload (muscle tissue contracts/shortens)
muscle needs to displace load over a distance (do work) to increase in strength
3) concentric- muscle shortens when it contracts (preload > afterload)
eccentric - when preload


What are the different types of skeletal muscle? What is the order of activation in a contraction?

1) Type 1- slow twitch, well vascularized (dark red), slow oxidative, for endurance (lots of myoglobin + mt)
low resistance endurance training- type I hypertrophy
-Type 2- fast twitch, for power and speed
2a- some oxidative, some anaerobic capacity
2b- anaerobic so less vascularized (white/pinkish), fast glycolytic, short duration (lot of SR but few mt)
high resistance training -- type 2 hypertrophy
*there are all alpha motor neurons

2) Type 1 recruited first, slow buildup
Then Type 2b, which has high max then burns out, then type 2a, which also maxes and burns out
finally type 1 is left and continues to build to its max
*1 motor unit innervates only 1 type of muscle


Explain how the following monitor skeletal muscle contraction:
1) golgi tendon organs (GTOs)
2) muscle spindles

1) GTOs located in musculotendon junctions, senses changes in muscle tension
early warning system/stress sensor for CNS based on muscle tension
*Type 1b fibers exit GTOs and can synapse with stimulator OR inhibitory neurons
load --> increased muscle tension --> more GTO activity --> 1B fibers stimulate inhibitory neurons --> affects alpha motor neuron activity --> ipsilateral agonist muscles blocked AND ipsilateral antagonist muscles stimulated

2) muscle spindles- senses changes in muscle length and provide this info to CNS
sustained muscle contraction --> gamma motor neurons stimulated --> stimulate intrafusal muscle fibers in chain --> bag fibers in middle stretch --> Actives type 1a in middle--> relays info to CNS --> allows muscle contraction to continue --> chain fibers slacken until more sustained contraction needed
*limit of slacking/contracting of intrafusal fibers --> no more isotonic contraction


What is the difference between alpha and gamma skeletal motor neurons?

alpha motor- all voluntary skeletal muscle contraction (aka extrafusal fibers that generate force)
gamma motor- innervate intrafusal muscle fibers only within the muscle spindle (which monitors contraction)


What are the different types of skeletal muscle growth? In whom do they occur?
How does exercise impact muscle growth?

1) Hypertrophy- increase in muscle fiber diameter --> Adults
Hyperplasia - increase in number of muscle fibers --> children
2) Exercise --> increase in mt, creatine kinase--> ATP, glycogen stores, triglyceride stores --> muscle can perform more work --> hypertrophy
if muscle protein synthesis (actin and myosin are protein) > muscle protein breakdown --> hypertrophy


What is the mechanism of skeletal muscle growth?

Satellite cells main source of muscle regeneration and growth, on outside of myofibers and normally quiet
during muscle tear (injury, workout) --> satellite cells differentiate into myoblasts
satellite cells express androgen receptor --> proliferate in response to IGF-1
Clump into myotubules --> fuse with existing myofibers to repair tears --> make muscle stronger than before


How is skeletal muscle an endocrine organ?
What are anabolic factors?
What are catabolic factors?
How is the sympathetic nervous system involved in muscle function?

1) secretes myokines to modulate growth: cytokines (immune mediators), blood sugar regulators, glucoregulation, lipolysis, prevents neurodegeneration
2) anabolic factors:
-androgenic steroids e.g. testosterone and dihydrotestosterone (DHT) --> stimulate satellite cell proliferation, GH secretion, IGF-1 expression in skeletal muscle
-growth hormone (GH)- secreted by anterior pituitary gland, stimulates IGF-1 production
-insulin like growth factor (IGF-1)- works with GH and stimulates regeneration (satellite cell proliferation), proteogenesis, lipolysis
-Ca2+ signaling - need calcium for growth
3) Catabolic factors:
-glucocorticoids- secreted by adrenal cortex, inhibit IGF1, stimulate myostatin, stimulate proteolysis in order to regulate blood glucose levels e.g. cortisol
-myostatin - expressed in satellite cells, inhibits their proliferation and prevents muscle growth
4) Sympathetic nervous system involved in repair mechanisms in muscles through beta adrenergic receptor (Expressed in skeletal muscle)


What is muscle fatigue and its mechanism, including involvement of CNS and PNS nervous systems

Muscle fatigue- reversible decrease in contractile force in response to an increase in stimulation frequency/duration
-free radicals impairs protein function
-increased P from breakdown of phosphocreatine to make ATP + creatine
-decreased glycogen stores
-K+ efflux --> impairs AP generation
-disruption of intracellular Ca2+ homeostasis
-cytokine release --> increased sense of fatigue in brain
-chemo and pain receptors--> impair motor neuron tone
*lactic acid from anaerobic metabolism doesnt have as huge of impact as we thought, biggest impairment of Type 2b fibers (which uses anaerobic)


What is sarcopenia? What does it affect? What is it caused by? When does it start?

1) sarcopenia - age associated loss in muscle mass
2) type 2 fibers more affected- dont know why (cant hit max anymore)
3) caused by: impaired GH/IGF1, inactivity, inadequate dietary protein, impaired anabolic androgens
4) Muscle loss starts at 30 as testosterone starts to decline and GH declines (After age 20)


Smooth muscle:
1) where is it found
2) characteristics
3) types
4) how does contraction differ from skeletal
5) how is smooth muscle contraction activated
6) how is contraction relaxed

1) lining of organs and vessels e.g. GI tract, uterus, urinary tract, lymphatic vessels
2) smaller than skeletal muscle cells, higher actin ratio, unstriated, v little SR, dense bodies attached to actin filaments in oblique arrangement
3) Visceral (single unit)- arranged in sheets/bundles that function as a single unit (called syncytium)
controlled by autonomic neurons
contact through gap junctions
Multiunit- 1:1 synaptic input, fibers act independently
allows for finer control
4) when crossbridge cycling happens, bc actin is attached to dense bodies on cell membrane --> 3D contraction where cell is pulled inward; skeletal muscle- more of 2D contraction
smooth muscle contraction has long duration with low ATP use bc of slow crossbridge cycling
5) need an increase in sarcoplasmic Ca2+ (both intra and extracellular sources e.g. voltage independent channels)
Ca2+ binds with calmodulin --> Activate MLCK kinase --> phosphorylates and activates myosin light chain heads --> actin-myosin binding
6) MLCK phosphatase --> dephosphorylates myosin light chain


What is vascular smooth muscle? What promotes vasoconstriction? What promotes vasodilation?

1) lines arterial (but not venous) walls, under control of sympathetic nervous system, controls blood flow and therefore blood pressure through vasoconstriction/dilation
2) Vasoconstriction (constricting of blood flow --> increased blood pressure): epinephrine/norepinephrine which promotes increased sarcoplasmic Ca2+ and inhibits SERCA
3) Vasodilation (widening of blood vessels --> improved blood flow--> decreased blood pressure): nitric oxide which stimulates Ca2+ pumps for efflux out of cell, stimulates SERCA
*viagra is a vasodilator (improves blood flow to penis for erection)


How is blood pressure maintained in smooth muscle through stress relaxation?

(blood pressure, cardiac output, total peripheral resistance in the vasculature)
Stress relaxation- pressure drops with increase in volume
Pressure = tension / radius
in urinary bladder: low P --> low resistance to filling since T decreases and R increases (like a water balloon)
In vascular smooth muscle: lower stress relaxation, high P since radius doesnt really expand --> allows for propulsion of blood


Histology: characteristics of skeletal, cardiac, smooth muscle

1) Skeletal muscle:
-multi-nucleated syncytium
-peripheral nuclei
-surrounded by basal lamina + satellite cells
-organized CT with endo, peri, epimysium
-cells cant divide - need stem (Satellite) cells which are in the same basal lamina
-voluntary contractions
-triad of T-tubule and 2 terminal cisternae at junction between A and I bands --> v fast APs (looks like a butterfly)
2) Cardiac muscle:
- striated
-short, branched fibers
-1 or 2 central nuclei
-CT not organized, more CT between cells
-cannot divide
-T tubule at Z line
-Purkinje fibers are special cardiac muscles- involuntary control in the heart (large, pale bc lots of glycogen)
-intercalated discs - cell to cell boundaries (fasciae adherentes, desmosomes, gap junctions) -- look like dark lines, made of actin
3) Smooth muscle:
-no striations
-tapered cells
-organized in sheets with very little CT between cells, indistinguishable cell borders-
-one central nuclei (S shaped)
-gap junctions
-No T-tubules, little SR
-have dense bodies on sarcolemma to attach the actin myofilaments (instead of Z lines)
-can secrete proteins of ECM
-cells can divide!
-surround the simple squamous epithelium in blood vessels
-caveolae (invaginations of membrane) form pinocytic vesicles


What determines whether mesenchyme becomes cartilage or bone?
How is cartilage formed?
How does cartilage grow?
What is the difference between territorial vs interterritorial matrix?

1) proximity to vasculature --> bone
avascular --> cartilage
2) mesenchymal condensations become chondroblasts cells --> make ECM --> when trapped in their ECM become chondrocytes
3) Growth is appositional or interstitial
appositional- new chondroblasts form at chondogenic layer of perichondrium connective tissue (other layer is fibroblastic, makes fibroblasts)
interstitial- isogenous groups of chondrocytes that can divide
*no interstitial growth in bones
chondrocytes have lots of RER, Golgi
4) Territorial matrix- immediately around chondrocyte, basophilic staining
interterritorial matrix- further away, acidophilic staining


What are the common features of cartilage? What are the differences in the 3 types?

1) common features
-chondrocytes are in lacunae (ECM depressions)
-all Type II collagen
-ECM is mostly water (nutrition through diffusion)
2) 3 types
I. Hyaline- articular cartilage is at end of bones when they form joints - no perichondrium
nasal/laryngeal/tracheal - perichondrium
II. Elastic- ear, epiglottis, has perichondrium, need special stain to view
III. Fibro- intervertebral disk, menisci, intermixed with dense CT, no perichondrium


What are the similarities and differences between bone and cartilage?

1) Bone is radiopaque, cells are connected to neighbors/blood supply through gap junctions and also processes that go through canaliculi tunnels in the matrix, this is bc matrix is low water content (hostile), vascular
bone is dynamic, can generate in response to stresses
2) Cartilage is radiolucent, cells are not connected, matrix is high water content (use diffusion), avascular
similarity: both have cells in lacunae, both have precursor cells (chondroblasts and osteoblasts)


What are the two ways that bone is formed? Describe the mechanisms. Elaborate on difference between formation of spongy vs compact bone

1) Intramembranous- e.g. flat bones on face, skull
appositional growth: periosteum (like the perichondrium in cartilage, perimysium in muscle) is on the outerlying layer, generates osteoblasts --> become osteocytes in the matrix --> unmineralized matrix is osteoid --> quickly begins mineralization process to become bone
*no interstitial growth in bones

2) Endochondral- uses cartilage scaffold to create complex shapes and lengthen bone e.g. long bones
I. cartilage model surrounded by perichondrium
II. blood vessels invade- the vasculature flips the switch and converts perichondrium --> periosteum
III. Periosteum generates ostoblasts --> osteocytes
IV. osteocytes lay down osteid --> forms bony collar mid-shaft
V. cartilage starts to degrade (dying chondrocytes calcify matrix, resorbed) --> marrow cavity created
VI. blood enters cartilage model, osteoblasts follow --> calcified cartilage replaced by woven bone
VII. woven bone remodeled into lamellar bone (two types: spongy and compact, highly organized, stronger, fewer osteocytes), expands in directions
VIII. hybrid bone/cartilage- bone provides strength, cartilage growth and elongation
*this process happens during development but also at epiphyseal growth plate in adults
for compact bone, which is not as close to the vasculature as spongy bone is --> osteoclasts make Volkmann and Haversian canals to bring blood vessels, endosteum in (need endosteum to make osteoblasts)
osteon- functional unit of compact bone- forms around haversial canal
interstitial lamallae- remnants of old osteon that are lots during formation of new osteon

Life cycle of an endochondral chondrocyte: rest --> proliferation --> hypertrophy --> calcification --> bone replacement


What are osteoclasts? What is their function

osteoclasts are multinucleated bone destroys, play role in remodeling, calcium balance, maturation, repair
consists of 20+ macrophages put together
produced in osteon (lining of inner bone surfaces, also makes osteoblasts/cytes- just like periosteum)
make HCl to dissolve minerals and Cathepsin K to degrade collagen
after osteoclasts break bone down, osteoblasts/cytes replace with higher quality lamellar bone


Describe principles of peripheral nerve regeneration

axon compression --> axon regenerates in a proximo-distal direction at ~1 cm / week following the endoneurium/schwann cell pathway to the deinnervated muscle cell (schwann cells clean the pathway through phagocytosis)
axon laceration --> leaves a gap, the smaller is higher likelihood the axon can regenerate, can also suture the epineurium that holds the entire nerve together


Long thoracic nerve injury (C5-C7):
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) chest crush injury- compression on chest wall
trauma during axillary surgery
2) SALT- serratus anterior long thoracic
limited upward rotation of scapula (with trap) --> limited range of motion in abduction/flexion/protraction
3) no cutaneous sensory innervation
4) winged scapula when patient pushes against the wall - normally serratus anterior holds the scapula to the chest wall but when its not working- you push the scapula away from the chest wall (hence the winging)


Axillary nerve injury (C5-C6):
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) Glenohumeral dislocation - dislocates inferiorly (down) and anteriorly (forward) and tears glenoid labrum, affects axillary nerve
surgical neck fracture -dislocates medially, separates abductors (suprasinatus) from adductors (latissimus dorsi)
2) affects deltoid and teres minor - loss of abduction since deltoid is THE major abductor
3) loss of sensory innervation on skin overlying deltoid (sergeant's patch)
4) bulge where dislocated humerus head is (glenohumeral dislocation), if its chronic there will be deltoid atrophy


Radial nerve injury (C5-C8):
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) Dislocation at head of humerus (glenohumeral dislocation), fracture at mid-shaft of humerus, fracture/dislocation at head of radius, upwards pressure on floor of axilla (eg saturday night palsy), dorsal wrist laceration/compression
2) Radial nerve is all posterior arm/forearm innervation
More proximal injury- greater motor and sensory loss
e.g. at axillary- lose triceps (elbow extension), wrist/finger extension, sensory
at shaft of humerus- would have triceps, still no wrist/finger
at head of radius- weak wrist extension since they insert into distal arm (lateral epicondyle humerus)
3) cutaneous: posterior lateral side of hand (all of thumb to posterior hand below digits 2 and 3)
4) Wrist drop- cant extend to stabilize wrist, cant make a fist for the same reason


Median nerve injury (C6-T1):
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) supracondylar fracture- median runs in front of that region of the humerus with brachial artery/veins, compression by pronator teres (called entrapment neuropathy) e.g. body building,
carpal tunnel compression,
wrist laceration (median nerve exposed before going into carpal tunnel),
lunate dislocation,
colles' fracture (FOOSH, fracture of radius/ulna)
2) distal injury (wrist): cant oppose thumb but can still flex/abduct it because of the longuses (FPL and APL)
claw hand- lumbricals paralyzed
proximal injury (elbow): in addition to above
- sign of benediction (Cant flex digits 2 + 3 bc of lost FDS and FDP)
- no thumb flexion (also lost FPL)
3) most debilitating- no anterior hand sensation for palm + digits 1-3 and half of ring finger
4) sign of benediction (loss of FDS and FDP), claw hand in digits 2+ 3 (loss of lumbricals 1+2)


Carpal tunnel compression:
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) swelling of synovial tendon sheaths (FLP, FDP, FDS) that pass through carpal tunnel compress median nerve
2) loss of lumbricals 1+ 2
3) sensory tingling + pain
4) claw hand, thenar atrophy for chronic injury
can incise flexor retinaculum to free up space


Ulnar nerve (C8-T1):
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) medial epicondyle trauma (passes behind there with superior ulnar collateral artery + vein)
heel of hand trauma- goes through its own canal near the wrist
2) loss of abduction/adduction of digits bc of interossei - patients cant hold paper between pointer and middle finger
3) numbness, tingling in ring and pinky finger
4) Claw hand of digits 4 + 5, interosseus wasting


Upper trunk (C5, C6): Erb's palsy
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) push head and shoulder in opposite directions e.g. fall on shoulder in motorcycle accident, obstetric injury
2) bc of myotome, affects proximal limbs e.g. intrinsic shoulder muscles (for abduction and external rotation)
3) bc of dermatome, cutaneous sensory loss on lateral side of arm and forearm and hand
4) waiter's tip sign- adducted, internally rotated, and extended


Lower trunk (C8,T1): Klumpke's palsy
1) how does it happen
2) what motor functions are affected
3) what cutaneous sensory distributions are affected
4) clinical presentation

1) upwards traction e.g. hanging from tree, obstetric injury, or cervical rib (compresses T1)
2) affects anterior hand muscles (whether median or ulnar nerve innervated) --> clawing, no abduction/adduction of digits
3) bc of dermatome, cutaneous sensory loss on medial side of hand, forearm, arm
4) clawed hand
T1 also part of sympathetic outflow - (T1-L2) --> loss of sympathetic outflow to the head


Describe limb rotation during development:
1) when does it happen?
2) what happens?
3) what are the effects?

1) weeks 6-8 of embryonic development
2) lower limb rotates medially so knees are anterior, big toe is medial
upper limb rotates slightly laterally so that elbow is posterior and thumb is radial
3) ventral muscle mass is in posterior compartment (knee flexors)
dorsal muscle mass in anterior compartment (knee extensors)


What happens if you have a hip fracture (how does it happen, what is torn, treatment)

What happens if you have hip dislocation? (how does it happen, what is torn, treatment)

1) Hip fracture is usually fracture of femoral neck, can result in OR from a fall; need hardware to set it, usually periosteum and medial circumflex femoral artery are torn so there is some avascular necrosis --> need hip resurfacing or replacement

2) Hip dislocation - can be congenital (usually girls on left side, family history) or acquired (traumatic e.g. car accident) and head of femur is driven posteriorly out of acetabulum, fracturing both


Explain the two clinical considerations from the glute:
Trendelenburg gait
piriformis syndrome

1) Trendelenburg gait - weakness in hip abductors (gluteus medius/minimus) due to superior gluteal nerve injury, needed to keep pelvis steady --> lurch towards affected side to reduce force, pelvis on other side drops
2) piriformis compresses sciatic nerve as the muscle exits the greater sciatic foramen --> muscle weakness e.g. foot drop (if you affect the common fibular nerve which goes to anterior/lateral leg and is responsible for dorsiflexion, which is actually extension), can also get tingling down leg


anatomic compartment
example muscles

1) Anterior compartment
knee extension, hip flexion
2) Medial compartment
hip adduction
3) posterior
knee flexion, hip extension


What does the IT band do? What do the ligaments in the hip joint do?

1) IT band stabilizes knee and hip (thickening of the fascia lata, the tensor fascia lata muscle inserts into IT band, so does gluteus maximus)
2) hip joint ligaments (iliofemoral strongest- can see on anterior side) resist hyperextension
if you put on heavy backpack or do lordosis - line of gravity shifts back --> can use hip ligaments to support body weight


What is in the femoral sheath? What bounds this femoral triangle? What complications can arise here?

How do you catheterize to enter left side of heart? Right side?

1) sheath is evagination of the fascia
outside sheath: Nerve
inside sheath: artery, vein, lymphatics
floor of triangle: pectineus
bounded by: sartorius, iliopsoas, adductor longus, and below inguinal
can have femoral hernia if bowel gets into femoral canal - need to remove otherwise blood supply will be cut

2) To enter right side of heart- insert catheter into femoral vein in groin
enter left side of heart - insert catheter into femoral artery


What is the adductor hiatus and what is its clinical significance?

Adductor hiatus- gap in tendon of adductor magnus
femoral artery and vein pass through here
significant amount of artherosclerosis (plaque buildup) can happen here --> becomes calcified and you have to revascularize the limb


Describe the major support structures of the knee joint.

1) Bones- round femoral condyles on flat tibial condyles
knee joint- hinge type synovial joint
2) extracapsular support
-patellar ligament - anterior support
-lateral collateral (LCL)- smaller, resists varus stress
-medial collateral (MCL)- larger, connected to medial mensiscus, resists valgus stress
-popliteal ligaments- resists hyperextension
3) intracapsular support
-medial meniscus- MOST commonly torn--> results in premature knee locking
-lateral meniscus
menisci- shock absorption and mechanics for knee flexion: moral condyles roll on menisci, femoral + menisci translate on the tibial condyles
-anterior cruciate ligament (ACL)- external, taut during extension --> resists anterior displacement of tibia on fixed femur (anterior drawer test)
-posterior cruciate ligament (PCL)- crosses deep to ACL, taut during flexion --> resists posterior displacement of tibia on fixed femur (posterior draer test)


Describe the major movements at the knee joint e.g. knee extension (fixed tibia- getting up from squat)

1) anterior rolling of femur up on tibia in suprameniscal compartment (checked by PCL)
2) posterior translation of femur on tibia in inframeniscal compartment (checked by ACL)
3) near full extension - lateral femoral condyle stops rolling, medial femoral condyle is longer and medially rotates to lock knee into place
4) to unlock knee --> need popliteus muscle to laterally rotate femur on fixed tibia


What is the unhappy tried injured in a valgus stress injury?

-medial meniscus


What are the important ankle and foot bones?

Talus- connection between leg and ankle bones (has trochlea and head)
sits on top of the heel bone- calcaneus (has sustentaculum tail to sustain/support talus)
midfoot is where talus connects to navicular --> allows for twisting and weight transfer while walking
toes have 1 metatarsal and 3 phalanges


What is anterior compartment syndrome?

not a lot of room in leg compartment esp anterior compartment
if there is any swelling or buildup (e.g. overusing muscles suddenly, bleeding, cast) --> increased pressure --> can compress nerves (deep fibular) and vascular supply (anterior tibial artery) and cause ischemia --> potentially irreparable damage
clinical symptom - pain disproportionate to injury, swollen and pale leg


What are the tendons that pass posterior to the medial malleolus?

Tom - tibialis posterior
Dick- flexor digitorum longus
and very nervous- posterior tibial artery, tibial nerve, posterior tibial vein
Harry- flexor hallicis longus


What are the 4 ankle/foot ligaments and what are their functions?

What is the innervation and blood supply to the ankle/foot?

What are common injuries?

1) medial collateral (aka deltoid)- prevents eversion
lateral collateral- prevents inversion
spring- connects sustentaculum talum on calcaneus with navicular tarsal, supports head of talus to propel foot off the ground
plantar fascia- lateral arch support
2) dorsal innervation - (motor) deep fibular (sensory) superficial fibular
plantar (sole) innervation- (motor) lateral plantar (sensory) medial plantar (both are branches of tibial nerve)
dorsal blood- dorsalis pedis (foot pulse) - extending of anterior tibial artery
plantar blood - media/lateral plantar arteries (branch of posterior tibial artery)
3) Ankle sprain- lateral collateral ligament torn
plantar fasciatis- microtears in plantar fascia


What are the three ankle joints and their functions?

1) Ankle joint- talocrural- joints distal leg bones + talus, for dorsi/plantar flexion
2) Transverse talar- between talus and navicular/cuboid, first joint for inversion/eversion
3) Subtalar- between talus and calcaneus, second joint for eversion/inversion


Explain the venous pump and how it relates to DVT and varicose veins

Venous pump- e.g. calf muscle pump - muscles surround deep veins and their contraction helps push the blood up against gravity
if you are immobile (post-op, long flight, etc)- venous pumps are not working--> blood can clot --> can cause DVT
if the clot detaches --> becomes embolus --> can travel to heart and cause PE
blood in perforating vein branches have valves to prevent blood flow from deep --> superficial veins (e.g. great saphenous vein, lesser saphenous vein)
if valves dont work properly and high pressure venous blood enters superficial veins --> causes varicose veins
*great saphenous vein comes off femoral vein outside femoral sheath, small saphenous vein is branch of popliteal vein


What is the difference between pre and post plexus injuries?

preplexus - roots, trunks, and divisions
injury affects dermatome, leads to weakness
Post-plexus - cords, and terminal nerves
injury affects nerve-specific locations, lead to paralysis