1.

Anterolateral (spinothalamic) pathway  senses {{c1::non-discriminative (poorly

localized) touch}}, {{c1::pain}} and {{c1::temperature}}
2. DCML pathway senses {{c1::vibration}}, {{c1::proprioception}}, and {{c1::fine touch}}
3. The DCML pathway sends sensory information via {{c1::A-α}} and {{c1::A-β}}
sensory afferent fibers : Large diameter, myelinated (rapid conduction)
4. The anterolateral (spinothalamic)  pathway sends sensory information via {{c1::A-
δ}} and {{c1::C}} sensory afferent fibers 
5. Small diameter, lightly/unmyelinated (slow conduction)
Aδ = lightly myelinated
C = unmyelinated
6. The anterolateral (spinothalamic tract) gives off collateral fibers that go up or
down 2-3 spinal cord segments via the {{c1::Lissauer's tract}}
Sensory afferent neurons fibers of the anterolateral (spinothalamic) tract synapse in
the {{c1::Substantia Gelatinosa}} in the dorsal horn of the spinal cord: A-δ, C fibers →
dorsal root ganglion (1) → substantia gelatinosa of the dorsal horn (2) → decussation →
VPL (3) 
7. DCML pathway:
input (afferent sensory fibers): {{c1::A-α, A-β}}
Afferent cell body #1: {{c1::dorsal root ganglion}}
Afferent cell body #2: {{c1::nucleus gracilis (lower extremity) / nucleus
cuneatus (upper extremity)}}
Decussation: {{c1::caudal medulla}}
Afferent cell body #3 (target): {{c1::VPL}}
8. In the DCML pathway, sensory input from your upper extremities (T6 and
up) goes up the spinal cord via the fasiculus {{c1::cuneatus}} in the dorsal column
9. In the DCML pathway, sensory input from your lower extremities (T6 and
below) goes up the spinal cord via the fasiculus {{c1::gracilis}} in the dorsal column
10. Anterolateral (spinothalamic) pathway:
input (afferent sensory fibers): {{c1::A-δ, C}}
Afferent cell body #1: {{c1::dorsal root ganglion}}
Afferent cell body #2: {{c1::dorsal horn (substantia gelatinosa)}}
Decussation: {{c1::immediately in the anterior white commissure of the spinal
cord (ascends 2-3 segments as decussates)}}
Afferent cell body #3 (target): {{c1::VPL and intralaminar nuclei of the
thalamus}}
11. Spinocerebellar pathways are responsible for {{c1::unconscious}} proprioception
spinocerebellar pathways are {{c1::ipsilateral::ipsilateral or contralateral}} - Most of
the proprioceptive information goes to the cerebellum and does not reach the cerebral
cortex 
12. The dorsal (posterior) spinocerebellar pathway senses {{c1::lower::upper or
lower}} extremity proprioception
13. The ventral (anterior) cuneocerebellar system senses {{c1::upper::upper or
lower}} extremity proprioception
Sensory ataxia refers to a deficit in {{c1::conscious (active)::conscious or
unconscious}} proprioception: Stomping while walking (walking on pillows), improved
when walking with a cane
Rely on visual information for proprioception (very unsteady when eyes are closed)
{{c2::Spinal ataxia}} refers to a deficit in {{c1::unconscious (passive)::conscious or
unconscious}} proprioception: postural deficits (sitting, standing, walking)
{{c2::Spinal ataxia}} refers to a deficit in {{c1::unconscious (passive)::conscious or
unconscious}} proprioception: postural deficits (sitting, standing, walking)
14. Brown Sequard Syndrome (Hemicord Lesion) deficits:
15.
16. Anterior cord syndrome:anterolateral (spinothalamic) pathway AND lateral
corticospinal/dorsal horn is damaged: loss of pain and temperature below the
level of the lesion loss of ALL motor control below the level of the lesion
17. Posterior cord syndrome: damage to DCML pathway 
loss of vibration, fine touch, proprioception below the level of the lesion

18. On an x-ray Black = {{c1::air}}, Bright white = {{c1::metal}}, White = {{c1::bone}},

Dark gray = {{c1::fat}}, Medium gray = {{c1::fluid/soft tissue}}

19. Always order an {{c1::x-ray}} first and then a {{c1::CT}} next

CT will detect almost all pathology related to {{c1::cortical}} bone injury: cortical bone =
external layer of bone (cortex of bone)
20. MRI is used to visualize {{c1::soft tissues (muscles, ligaments, tendons, cartilage)}}
21. What 3 things are always black on MRI?{{c1:: Air Cortical bone/tendons/ligaments
Flowing blood
Bone scans are typically used to detect {{c1::metastatic cancer::what pathology}} :
Asymmetry = abnormal bone scan
Detects increased osteoblast activity (fracture, tumor, infection)
22. Bone scans detect increased {{c1::osteoblast}} activity which is seen in fracture,
tumor, and infection (anything that caues reactive bone activity)
Asymmetry = abnormal bone scan

1. Unfused epiphyses indicates a {{c1::pediatric}} aged patient: Epiphysis

2. Growth plate
3. Metaphysis
4. Diaphysis 

23. When describing a location on a limb, you divide the bone into {{c1::thirds}}
24. Cortical continuity refers to a {{c1::smooth and continuous}} cortex (surface) of the
bone
25. Trabecular alignment refers to the {{c1::linear densities/lines}} on the bone being
straight
26. Fat pad sign should {{c1::ALWAYS}} be treated like a fracture, whether you see a
fracture of the bone or not. Because bone marrow fat and blood are leaking from
the fractured bone.
Typically posteriorly
27. What's the difference between an open fracture and a closed fracture?
Open fracture: break in skin; fracture is exposed to air (laceration or gross exposure).
Closed fracture: no break in skin; fracture not exposed to air
28. What is a pathologic fracture?
Fracture through weakened bone. Bone weakened due to disease (osteopenia,
cancer, etc.)

29. What is a stress fracture? Fracture due to misuse or overuse 

Seen in runners
30. Salter-Harris classifies the probability of  {{c1::growth}}  disturbance due to
{{c1::growth}} plate injuries in pediatric patients.: "how does this fracture affect
growth"
The higher the number the worse the prognosis
31. Physis is another word for {{c1::growth-plate}}
32. Salter Harris I presents with tenderness over the {{c1::physeal plate (growth plate)}}
with a {{c1::normal}} x-ray
"SALTR"
slip (1)
above (2)
low (3)
through (4)
rammed (5)
Salter Harris II is a fracture through the {{c1::physis}} and {{c1::metaphysis}} and may
produce long-bone shortening (significant if in lower extremity): "SALTR"
slip (1)
above (2)
low (3)
through (4)
rammed (5)
33. Salter Harris III is a fracture through the {{c1::epiphysis}} and {{c1::physis}} 
34. "SALTR", slip (1), above (2), low (3), through (4), rammed (5)
Salter Harris IV is a fracture through the {{c1::epiphysis}}, {{c1::metaphysis}}
and {{c1::physis}}, "SALTR"
slip (1)
above (2)
low (3)
through (4)
rammed (5)
Salter Harris V is a complete {{c1::compression (crush injury)}} of the physeal plate:
"SALTR"
slip (1)
above (2)
low (3)
through (4)
rammed (5)
35. Nociception is the purely {{c1::sensory}} component of pain that does not involve
an emotional component.
36. Receptors for the anterolateral system are {{c1::free-nerve}} endings.
37. A-δ fibers transmit {{c1::fast/sharp}} pain. 
C-fibers transmit {{c1::slow, long-lasting, dull, aching, burning}} pain: unmyelinated,
very slow fibers
{{c2::Aδ}} fibers are {{c1::modality}}  specific, meaning that they respond to a specific
type of noxious stimuli and provide {{c1::good}}  stimulus localization (detection of
the injured site): Noxious stimuli modality types: non-noxious, high threshold
pressure, non-noxious temperature, noxious pressure (tissue damage), or noxious
temperature
{{c2::Aδ}} fibers are {{c1::modality}}  specific, meaning that they respond to a specific
type of noxious stimuli and provide {{c1::good}}  stimulus localization (detection of
the injured site): Noxious stimuli modality types: non-noxious, high threshold
pressure, non-noxious temperature, noxious
38. {{c2::C}} fibers are {{c1::poly}}modal and therefore provide {{c1::poor}} stimulus
localization. They are meant to protect the injured site. 
39. {{c2::C}} fibers are {{c1::poly}}modal and therefore provide {{c1::poor}} stimulus
localization. They are meant to protect the injured site. 
Primary hyperalgesia is the result of to {{c1::peripheral::peripheral or
central}} sensitization to pain which leads to pain that occurs {{c1::in the area}} of
the original damage: peripheral sensitization: increased sensitivity of receptors (primary
afferent neurons) to painful stimuli
Secondary hyperalgesia is the result of both {{c1::peripheral}} and {{c1::central}}
sensitization to pain which leads to pain that {{c1::surrounds}} the original damage.:
peripheral sensitization: increased sensitivity of peripheral receptors (primary afferent
neurons) to painful stimuli
central sensitization: increased sensitivity of CNS neurons
40. {{c2::Allodynia}} refers to pain from a normally {{c1::non}}-painful stimuli
41. Ex: when sunburnt, a feather causes pain when it normally wouldn’t
{{c2::Allodynia}} refers to pain from a normally {{c1::non}}-painful stimuli: Ex: when
sunburnt, a feather causes pain when it normally wouldn’t
42. What is the difference between peripheral sensitization and central
sensitization?
43. Peripheral: increased receptor sensitivty (primary afferent neurons) to painful stimuli
44. Central: increased sensitivity of neurons within CNS (neuron sensitivity/excitability,
disinhibition, microglia activation)
45. Peripheral sensitization can occur from the release of {{c1::K+}} and {{c1::ATP}}
from cellular breakdown (damaged cells) and increased {{c1::acidity}}, this activates
channels and contributes to depolarization in nociceptive neurons.
46. Peripheral sensitization can occur from the release of {{c1::bradykinins}},
{{c1::prostaglandins}}, and {{c1::histamine}} released from damaged tissue which
binds to nociceptive receptors
47. Axonal reflex (peripheral sensitization) "wakes up" silent nociceptors (receptors that
don't normally respond to pain) by
1. ) nociceptors release {{c1::substance P}}
2) {{c1::substance P}} then causes the release of {{c1::histamine}}
and {{c1::NGF}} from mast cells
3) {{c1::NGF}} increases # of ion channels in nociceptors which lowers their
threshold for pain: Axonal reflex = neurogenic inflammation → "wakes up silent
nociceptors (nociceptors that don't normally respond to pain)" which lowers its threshold
for pain by increasing channel numbers in neurons 

48. Describe how central sensitization can occur due to increased neuron

sensitivity/excitability (1):
After significant nociceptive stimulation or persistent injury,
activated C and Aδ fibers release neurotransmitters that activate normally
silent {{c1::NMDA glutamate}} receptors of the {{c1::secondary}} afferent
neuron
Activation of the {{c1::NMDA glutamate}} receptor on the
{{c1::secondary}} afferent neuron increases its excitability to transmit pain
to the brain
49. Describe how central sensitization can occur due to disinhibition (2):
{{c1::inhibitory interneuron}} is inhibited so the normally inhibited {{c1::secondary
afferent neurons}} and {{c1::Aβ fibers (DCML) }} can signal pain to the brain
Secondary afferent is usually not activated because it is inhibited by this inhibitory
interneuron (blue)
 
Orange neuron (A-Beta) in DCML can now cause pain when it is not meant to bc
it's no longer inhibited by an inhibitory interneuron 

50. Describe how central sensitization can occur due to microglia activation (2):

Pain activates microglial cells in the dorsal spinal cord which increases
excitability of dorsal horn neurons and promotes {{c1::hyperalgesia}} and
{{c1::allodynia}}
51. The spinothalamic (ANTERIOR-DIRECT) tract is {{c1::unilateral::unilateral or
bilateral}} and involved in {{c1::pain localization}}
52. The paleospinothalamic (LATERAL-INDIRECT/MEANDERING) tract
is {{c1::bilateral::unilateral or bilateral}} and involved in the {{c1::motivational-
affective (emotional)}} aspects of pain because it is linked to the {{c1::limbic}}
system
53. The spinothalamic (ANTERIOR-DIRECT) tract is a direct pathway that
is monosynaptic from the {{c1::dorsal horn}} to the {{c1::thalamus (VPL)}}
54. The paleospinothalamic (LATERAL-INDIRECT/MEANDERING) is an indirect
pathway that is {{c1::multisynaptic::monosynaptic or multisynaptic}}
55. What is referred pain?
{{c1::Pain that originates in a visceral structure (ex: organ like stomach) that can be felt
or referred to in a somatic structure (ex: on the surface of your abdomen)}} - Abdominal
pain, you want to feel it and protect the area 

56. Convergence theory of visceral pain (viscerosomatic convergence)  refers

to visceral afferent neurons and somatic afferent neurons synapsing onto the
same {{c1::interneuron}} in the spinal cord
57. Wha thappens when you hit your thumb with a hammer?
1) You feel a fast sharp pain due to: {{c1::Aδ fibers}} + {{c1::direct
spinothalamic pathway}}
2) Sharp pain is followed by a throbbing pain due to: {{c1::C fibers}} +
{{c1::indirect spinothalamic pathway}}
3) Injured area becomes more sensitive to touch due to {{c1::primary
hyperalgesia}} + {{c1::peripheral sensitization}}
4) Area around the original injury becomes more sensitive due
to {{c1::secondary hyperalgesia}} and {{c1::central sensitization}}
5) You instinctively rub your thumb due to {{c1::gate control theory}}
58. Neutrophils can reduce pain by reducing the level of {{c1::inflammatory cytokines
(prostaglandins)}} by converting them into {{c1::resolvins}}
and by directly inhibiting {{c1::nociceptors}} 
59. {{c2::Inflammatory cells}} and {{c2::keratinocytes}} release {{c1::factors
(endorphins)}} which inhibit nociception.
60. {{c2::Inflammatory cells}} and {{c2::keratinocytes}} release {{c1::factors
(endorphins)}} which inhibit nociception.
61. Interneurons in the spinal cord can reduce pain by
releasing endogenous {{c1::opioids (enkephalins)}}
62. What is the Gate Control Theory (segmental inhibition)
{{c1::Rubbing thumb activates an A-beta fiber (DCML collateral)
which reactivates the inhibitory interneuron which dampens the output of
our secondary afferent therefore reducing pain}}
63. What is the Diffuse Noxious Inhibitory Control (DNIC) in the brainstem
64. Pain inhibits pain Goes up meandering pathway and synapses a on a bunch of
things that have descending pathway that will inhibit neurons
These areas: PAG (periaqueductal gray) and Raphe Nucleis of the medulla
Think of "biting on your hand when feeling pain"
65. Explain the Cerebral Cortex-Brainstem Control and how it reduces the
transmission of pain
66. Our brain has "biological gates" that is meant to reduce the transmission of
pain from the ascending pathways
We have 4 gates ; Periphery (at site of injury); Spinal cord; Brainstem (DNIC) Prefrontal
cortex 

Drugs
 1. Cocaine, Chlorprocaine, Tetracaine, and Benzocaine are {{c1::Esters::drug
class}} Esters have ONE I in its name
2. Lidocaine, Mepivacaine, Bupivacaine, Ropivacaine, Articaine, and
Prilocaine are {{c1::Amides::drug class}}: Amides have TWO I's in its name
3. What's the difference between anesthesia and analgesia?
{{c1::anesthesia = lack of feeling or sensation analgesia = pain relief (without lack of
consciousness)
4. High blood flow leads to {{c1::less::more or less}} of an effect of local
anesthesia: This is because the blood-flow is going to take the blood away from
the site of action: This opposite to "normal" pharmacology where high blood flow
is good because it delivers the drug to its target site of action. 
5. Local anesthetics block the {{c1::intracellular::intracellular or extracellular}}
domain of voltage gated Na+ channels: Therefore, they need to cross the cell
membrane to work
6. Most local anesthetics are weak {{c1::bases::acid or bases}}
7. To have an effective local anesthetic, you have to have a drug that has
a pKa that allows it to be {{c1::unprotonated}} in physiological pH and
{{c1::protonated}} in intracellular pH: The protonated form is the form
that binds to the receptor, however it does not cross membranes well
 So the local anesthetic has to cross in its unprotonated form and then become
protonated once it crosses the membrane.
8. The {{c1::protonated::protonated or unprotonated}} form of local anesthetic is
the form that binds to the receptor,; however protonated molecules don't cross
membranes well
So the local anesthetic has to cross in its unprotonated form and then become
protonated once it crosses the membrane.
You have to have a drug that has a pKa that allows it to
be unprotonated in physiological pH and protonated in intracellular pH

9. Most local anesthetics have a pKa between {{c1::7.5}} and {{c1::9}}

You have to have a drug that has a pKa that allows it to
be unprotonated in physiological pH and protonated in intracellular pH

 This is because when pH = pKa (50% are ionized and 50% are unionized)
 So 50% are able to cross 

10. Benzocaine is the exception with a pKa of {{c1::3.5}}, therefore it is in

its {{c1::unionized::ionized or unionized}} form at physiological pH and crosses
membranes very easily: Therefore, it is only  used topically
11. Most local anesthetics (pKa 7.6) are formulated in acidic solutions (pH 5) for
longer shelf-life and solubility, therefore there is a {{c1::SMALL}} ratio
of unionized to ionized drug which means a {{c1::slow}}  onset of action after
 injection: This can be bypassed by adding BiCarb to bring the drug to
the physiologic pH faster once its injected.Allows drug onset to happen more
quickly by allowing the drug to be in a form that allows it to cross membranes
easier
12. {{c1::BiCarb}} is usually added before local anesthetic injections to speed up the
onset of action
13. Local anesthetic has an higher affinity for {{c1::open}} and {{c1::inactivated}}
voltage gated Na+ channels. Meaning that LA has a higher affinity for neurons
that are {{c1::actively firing action potentials}}; Therefore, LA works better when
you're actively in pain.
14. Local anesthetics have a similar affinity to other channels, enzymes, and
receptors which may contribute to {{c1::adverse}} drug effects
15. Local anesthetic is injected {{c1::outside::inside or outside}} of the nerve
bundle  and therefore requires a very high concentration to be effective
16. Local anesthetics are {{c1::non}}-specific meaning they can impact afferent,
efferent, autonomic, and somatic fibers; This can lead to adverse drug effects
17.  {{c1::Aδ}} and {{c1::C}} fibers are impacted by local anesthetic first; recall: these
are the anterolateral (spinothalamic) fibers for pain and temperature
18. What is the typical order of sensation loss from local anesthetic?
{{c1::pain}}, {{c1::temperature}}, {{c1::touch}}, {{c1::pressure, proprioception}},
{{c1::skeletal muscle tone}} piumi thulasi tharushi play pokeymon on Tuesday.
19. {{c1::Systemic ADME}} diminishes/terminates the local effect of local
anesthetics which can contribute to the duration of action and adverse drug
reactions; Because this is how the LA leaves its tissues and enters systemic
circulation.
20. Ester LA's are {{c1::rapidly}}  metabolized so they have a {{c1::short}}  half-life,
this means that they have a {{c1::shorter}} duration of action
21. Amide LA's are {{c1::slowly}}  metabolized so they have a {{c1::long}}  half-
life this means that they have a {{c1::longer}}  duration of action.
22. {{c2::Amide LA's}} are metabolized by {{c1::CYP450s}} in the liver and
metabolites are excreted in the urine; Has to go through the liver → slow
metabolism (long half-life).
23. Esters are hydrolyzed in the blood by {{c1::plasma esterase}}, hydrolyzed
quickly in the blood → quickly metabolized (short half-life)
24. Both esters and amides bind to serum proteins including {{c1::albumin}} and
{{c1::alpha-1-acid glycoprotein}} which can contribute to significant drug-drug
interactions; WOMEN and CHILDREN have decreased levels of alpha-1-acid-
glycoprotein, therefore LA's are more toxic.
25. WOMEN and CHILDREN have decreased levels of  {{c1::alpha-1-acid-
glycoprotein}}, therefore LA's are more toxic.
26. If local anesthetic gets absorbed into systemic circulation from the
tissues, toxicity is most likely to be seen in the {{c1::brain}} and
{{c1::heart}} because they are highly perfused.
27. Route of administration: topical {{c1::ointment applied on the skin}}
28. Route of administration: infiltration (intradermal or subcutaneously)
{{c1::injected very superficially under skin}}
29. Route of administration: peripheral nerve block; {{c1::injected onto a nerve,
blocking its signaling}}
30. Route of administration: epidural {{c1::injected OUTSIDE of the subarachnoid
space}}
31. Route of administration: spinal {{c1::injected INSIDE of the subarachnoid
space}}
32. Route of administration: Bier block (IV regional) {{c1::Bier block = injecting the
anesthetic IV (dangerous) Tourniquet the area to prevent the anesthesia from
spreading 
33. Route of administration: IV systemic {{c1::infusing LA into systemic circulation
via IV (dangerous)}}
34. Neuraxial anesthesia (injected into spine)  blocks the {{c1::sympathetic}}
nervous system first, then sensory and motor
35. Peak blood level of LA depends on the {{c1::injection site (intercostal reaches
peak blood level quickly)}}
36. Giving {{c1::vasoconstrictors (epinephrine)}} with an LA injection
provides sustained local tissue concentration by reducing blood flow to the
area of injection. ; This also lowers peak plasma levels (preventing systemic
absorption) so it reduces toxicity.
37. Giving {{c1::vasoconstrictors (epinephrine)}} with an LA injection reduces
toxicity by lowering peak plasma levels; Giving vasoconstrictors
(epinephrine) with an LA injection provides sustained local tissue concentration
by reducing blood flow to the area of injection. 
38. Epinephrine receptors are {{c1::adrenergic:: cholinergic or adrenergic}} and
are GPCRs, α1 = {{c1::Gαq}}, α2 = {{c1::Gαi}}, β = {{c1::Gαs}}
39. CNS local anesthetic toxicity is treated with {{c1::Benzodiazepine}}
40. Cardiac local anesthetic toxicity is treated with {{c1::ILE (IV lipid emulsion) }}
41. Systemic LA toxicity can be due to low alpha-1-acid-glycoprotein levels
(means more free LA in plasma) is common in {{c1::children (infants)}} and
{{c1::pregnant women}}
42. Transient neurologic symptoms (due to spinal or nerve injury) are seen
typically due to poor {{c1::injection}} technique
43. Methemoglobinemia occurs when local
anesthetic metabolites oxidize {{c1::ferrous}} irons in heme to its {{c1::ferric}}
state: This makes it so hemoglobin cannot bind oxygen anymore.
44. Methemoglobinemia is treated with {{c1::methylene blue}}: Methylene
blue reduces iron back to its ferrous state. Methemoglobinemia occurs when LA
metabolites oxidize ferrous irons in heme to its ferric state so
hemoglobin cannot bind oxygen anymore
45. Cocaine is an {{c1::ester::ester or amide}} local anesthetic used for the
anesthesia of {{c1::mucous membranes (nose, mouth, ear)}}: Ester = shorter
duration of action Ester = 1 I in name
46. Chloroprocaine is an {{c1::ester::ester or amide}} local anesthetic with
a {{c1::short::short or long}} onset and duration of action. It is used primarily
in {{c1::epidural}} and {{c1::spinal}} anesthesia, Ester = shorter duration of action
Ester = 1 I in name
 47. Tetracaine is an {{c1::ester::ester or amide}} local anesthetic that can be
used {{c1::topically}}, {{c1::ophthalmically}}, or {{c1::spinally}}, It has
a {{c1::long}} duration of action when compared to other esters
Ester = shorter duration of action
Ester = 1 I in name
48. Benzocaine is an {{c1::ester::ester or amide}} local anesthetic that is
very lipophilic and only used {{c1::topically}}: It is also known to cause
{{c1::methemoglobinemia}}
49. {{c1::Benzocaine::Drug}} is known to cause methemoglobinemia: Ester =
shorter duration of action; Ester = 1 I in name
50. Lidocaine is an {{c1::amide::ester or amide}} local anesthetic that has a wide
range  of uses including: {{c1::topical}}, {{c1::ophthalmic}}, {{c1::infiltration
(intradermal or subQ)}}, {{c1::regionally}}, and {{c1::neuraxial nerve block}}
Amide = longer duration of action
Amide = 2 I's in name
51. Mepivacaine is an {{c1::amide::ester or amide}} local anesthetic that is similar to
{{c1::lidocaine}} but has a longer duration of action. It is used primarily in
{{c1::peripheral nerve blocks.}}
It is not used in {{c1::obstetrics (pregnant women)}} because it is
{{c1::slowly}} metabolized by the fetus. 
52. Bupivacaine is an {{c1::amide::ester or amide}} given via {{c1::infiltration
(intradermal or subQ)}}, {{c1::regionally}}, and {{c1::neuraxially}}. 
It has a long duration so it not ideal for {{c1::outpatient}} procedures. It has a long
duration so it not ideal for {{c1::outpatient}} procedures.
Amide = longer duration of action
Amide = 2 I's in name

53. Bupivacaine has a black box warning for high dose use in obstetric

epidurals because it can cause {{c1::cardiac arrest}}
Amide = longer duration of action
Amide = 2 I's in name
54. Ropivacaine is similar to {{c1::bupivacaine}} but is less cardiotoxic, it is primarily
used in {{c1::peripheral}} and {{c1::epidural}} blocks.
Amide = longer duration of action
Amide = 2 I's in name
55. {{c2::Articaine}} and {{c2::Prilocaine}} are used for {{c1::dental/periodontal}}
procedures: Amide = longer duration of action Amide = 2 I's in name
56. {{c2::Articaine}} and {{c2::Prilocaine}} are used for {{c1::dental/periodontal}}
procedures, Amide = longer duration of action, Amide = 2 I's in name
57. What is a eutectic mixture? Mixture of anesthetics that have a lower melting
point than its individual components, Absorbed very readily from the
skin, cannot be used on mucosal tissue due to high systemic toxicity
Eutectic mixtures most commonly have {{c1::Lidocaine}} and {{c1::Prilocaine}} and is
marketed as a drug named {{c1::EMLA}}, EMLA = "eutectic mixture of local anesthetics"
58. What 3 drugs are known to cause methemoglobinemia
{{c1::"BLP"
 Benzocaine
Lidocaine
Prilocaine
59. What drug is associated with cardiac arrest?
{{c1::Bupivacaine}}
60. {c2::EAR (estimated average requirement)}} refers to
the average daily nutritional intake that meets the requirement of {{c1::50%}} of
the population.
61. {{c2::EAR (estimated average requirement)}} refers to
the average daily nutritional intake that meets the requirement of {{c1::50%}} of
the population.
62. With EAR (estimated average requirement), {{c1::50%::%}} of the population is
at risk for nutritional {{c1::inadequacy}}
63. {{c2::RDA (recommended dietary allowance)}} refers to
the average daily nutritional intake that meets the requirement of {{c1::98%}} of
the population.
64. {{c2::RDA (recommended dietary allowance)}} refers to
the average daily nutritional intake that meets the requirement of {{c1::98%}} of
the population.
65. Adequate intake (AI) refers to an estimated average daily nutritional intake and
is used when {{c1::RDA}} cannot be determined
66. What is tolerable upper intake level (UL)?
67. Bioavailability refers to the amount of vitamin that gets {{c1::absorbed}} into
the bloodstream.
68. What is the RDA (recommended daily allowance) for Calcium at ages 4-8, 14-18, 19-
50, >70
69. What is the RDA (recommended daily allowance) for Vitamin D at ages 4-8,
14-18, 19-50, >70
70. % DV (daily value) is a percentage of the {{c1::RDA}} value and is based on a
{{c1::2000}} calorie diet
71. Dietary fiber, phytates, oxalates {{c1::inhibit}} calcium absorption
72. Calcium carbonate (calcium supplement) is {{c1::insoluble}} at pH > {{c1::7.0 }}
73. What calcium supplement has more calcium:
calcium carbonate or calcium citrate? {{c1::calcium carbonate}}
74. Calcium toxicity occurs after intake of greater than {{c1::2000}} mg of calcium
75. Calcium deficiency leads to {{c1::Rickets}} disease in children,
{{c1::osteomalacia}} in adults, {{c1::colon}} cancer, {{c1::hypo}}calcemia, and
{{c1::hypo}}phosphatemia
76. Calcium impedes the absorption of {{c1::iron}}
77. Aging, sunscreen, and obesity {{c1::decrease}} the body's ability to
synthesize vitamin D
78. {{c2::Bowed legs}} and {{c2::beaded ribs}} are hallmark features
of {{c1::Rickets disease}}
79. {{c2::Bowed legs}} and {{c2::beaded ribs}} are hallmark features
of {{c1::Rickets disease}}
 80. {{c2::Rickets disease}} is a result of a {{c1::vitamin D}} deficiency which leads
to failure of {{c1::cartilage}} formation and {{c1::endochondral ossification}}
81. {{c2::Rickets disease}} is a result of a {{c1::vitamin D}} deficiency which leads
to failure of {{c1::cartilage}} formation and {{c1::endochondral ossification}}
82. Hypercalcemia and hyperphosphatameia can be a result of {{c1::vitamin D}}
toxicity
83. 80% of calcium is found within {{c1::cortical}} bone
19% of calcium is found within {{c1::Trabecular}} bone
84. {{c1::Trabecular}} bone is the bone to be affected by calcium deficiency first due
to its high turnover, Trabecular bone is a frequent site of osteoporotic bone
fracture
85. {{c1::Trabecular}} bone is a frequent site of osteoporotic bone fracture
86. The highest rate of calcium absorption occurs in the {{c1::duodenum (acidic
environment)}}
calcium absorption occurs in the small intestine
calcium absorption is efficient in acidic environments

87. The largest amount of calcium absorption occurs in the {{c1::ileum}}

calcium absorption occurs in the small intestine
ileum = large surface area
88. Calcium is absorbed more efficiently in an {{c1::acidic (pH < 7.0}} environment 
89. What is TRPV6? (calcium absorption)
{{c1::Ca2+ channel that transports calcium from the intestinal
lumen into enterocyte (intestine) so it can eventually reach the bloodstream}}
90. TRPV6 is activated by {{c1::Calcitriol (vitamin D)}}
91. What are the 2 mechanisms for calcium absorption from the small intestine into
the bloodstream?
{{c1::TRPV6 transports Ca2+ from the intestinal lumen into the intestine
(enterocyte). Then it is bound to a Calbindin D and transported to a Ca2+
pump that pumps the calcium into the blood}} {{c1::Calcium
gets endocytosed into an endosomal lysosomal component and
then exocytosed into the blood.}}

92. {{c1::30}}% of dietary calcium is absorbed into the bloodstream

Convulsions, arrhythmias, tetany, numbness/paresthesias are symptoms
of {{c1::low::low or high}} calcium levels, Low calcium = "CATS go numb"
93. Constipation, nausea, pain, poor appetite, vomiting, muscle twitches,
weakness are symptoms of {{c1::high::low or high}} calcium levels
Low calcium = "CATS go numb"
94. Vitamin D synthesis begins when {{c1::7-dehydrocholesterol}} is converted
to previtamin D when UV rays hit the epidermis (skin) 
95. 25-hyroxyl vitamin D = {{c1::Calcidiol (inactive form)}}
1,25 dihydroxy vitamin D = {{c1::Calcitriol (active form)}}
96. PTH activates 1-alpha-hydroxylase which converts calcidiol to calcitriol in the
kidneys {{c2::PTH}} activates {{c1::1-α-hydroxylase}} which
 converts calcidiol to calcitriol in the kidneys leading to increased calcium
resorption (less excreted in the urine)

97. {{c2::PTH}} activates {{c1::1-α-hydroxylase}} which

converts calcidiol to calcitriol in the kidneys leading to increased calcium
resorption (less excreted in the urine)
98. {{c2::Calcitriol}} increases absorption of {{c1::Ca2+}} and {{c1::Phosphate}} 
99. {{c1::Calcidiol}} is used to measure Vitamin D levels in patients
CALCITRIOL CAN BE NORMAL IN PATIENTS THAT ARE VITAMIN D
DEFICIENT.
Calcidiol reflects total amount of stored Vitamin D 
This is because Calcidiol (inactive) must be converted to Calcitriol (active) in the
kidneys
100. Calcitriol stimulates:
1) {{c1::calcium absorption in the intestine (TRPV6)}}
2) {{c1::calcium resorption in the kidneys (TRPV5)}}
3) {{c1::↑ bone resorption, ↓ mineralization}}
101. At low calcium levels, {{c1::PTH}} levels rise
102. At high calcium levels, {{c1::calcitonin}} levels rise
103. PTH {{c1::stimulates}} osteoclast activity
104. At low calcium levels, what hormone is released and happens in
the bone, intestine, and kidney?
105. At high calcium levels, what hormone is released and happens in
the bone, intestine, and kidney?
106. PTH stimulates osteoblasts to express {{c1::RANKL}} which binds to
{{c1::RANK}} on premature  osteoclasts resulting into their maturation into
an active osteoclast.
107. PTH {{c1::increases::increases or decreases}} blood calcium levels
108. Calcitonin {{c1::decreases::increases or decreases}} blood calcium
levels
109. Calcitonin {{c1::inhibits}} osteoclast activity
110. Calcitonin promotes {{c1::deposition/storage}} of calcium into bone
111. Calcium and phosphorous are stored in {{c1::hydroxyapatite}} in bone.
112. PTH {{c1::decreases::increases or decreases}} kidney
resorption of phosphate leading to {{c1::decreased::increased or decreased}}
levels of phosphate in the blood
113. High PTH causes {{c1::low::high or low}} levels of phosphorous in the
blood
114. Magnesium deficiency leads to {{c1::osteoporosis}}
115. Calcitonin is released by C-cells in the {{c1::thyroid}} gland
116. PTH is secreted by the {{c1::parathyroid}} gland

Diseases of Bone
1. lities}} are {{c1::genetically}} based and manifest {{c1::early}} in life
(during bone formation)
 2. {{c2::Developmental abnormalities}} are {{c1::genetically}} based and
manifest {{c1::early}} in life (during bone formation)
3. Acquired diseases are detected in {{c1::adulthood}
4. Localized abnormalities such as missing a bone or a digit are
called dys{{c1::ostosis}}, Results from the defects in the formation of
mesenchyme and their differentiation to cartilage
5. Global abnormalities involving the entire body are called dys{{c1::plasia}}
Results from mutations in genes that control development or  remodeling of the
entire skeleton
6. Achondroplasia and Thantophoric
Dysplasia are autosomal {{c1::dominant::dominant or recessive}}
disorders that result in {{c1::dwarfism::what disease}}
7. Thanatophoric Dysplasia is a lethal form of {{c1::dwarfism}}; Individuals
die at birth or shortly after
8. Achondroplasia results in a {{c1::disproportionate::proportionate or
disproportionate}} short stature which is a characteristic morphology
of {{c1::dwarfism::what disease}}, LONG TRUNK, SHORT LIMBS
9. Both {{c2::achondroplasia}} and {{c2::thanatophoric dysplasia}} result
from a {{c1::gain::gain or loss}} of function mutation of
{{c1::FGFR3::gene}}, FGFR3 reduces growth pace by inhibiting cartilage
synthesis (cartilage is the scaffolding for bone formation)
10. What does the FGFR3 gene do and what disease(s) does a gain of
function mutation cause?
 FGFR3 reduces growth pace by inhibiting  cartilage synthesis at the growth
plate (cartilage is the scaffolding for bone formation)
 This leads to decreased endochondral bone formation and premature
ossification of growth plates

11. The fundamental abnormality of osteogenesis imperfecta  ("brittle bone

disease") is not enough {{c1::type I::type}} collagen which leads to "too little
bone" or "weak bone"
12. {{c2::Osteogenesis imperfecta ("brittle bone disease")}} is caused by mutations
in the genes that encode the {{c1::alpha 1}} and {{c1::alpha 2}} chains of {{c1::type
I}} collagen
12. {{c2::Osteogenesis imperfecta ("brittle bone disease")}} is caused by mutations
in the genes that encode the {{c1::alpha 1}} and {{c1::alpha 2}} chains of {{c1::type
I}} collagen
13. Blue sclera, poor dentition, and deafness can be seen in {{c1::Osteogenesis
Imperfecta ("brittle bone disease")::what disease}}
14. Phenotype (intensity/lethality) of osteogenesis imperfecta is based on
the {{c1::location}} of the mutation.
15. Which subtypes of osteogenesis imperfecta ("brittle bone
disease") are lethal and compatible with survival?{{c1::
Autosomal dominant (subtypes I, III, and IV) are compatible with survival
Autosomal recessive (subtype II) is lethal
16. Osteogenesis imperfecta ("brittle bone disease") subtype {{c1::IV}} has
a normal sclera while the others have a blue sclera
17. Bone sclerosis refers to abnormal {{c1::hardening}} of bone
18. {{c2::Osteopetrosis}} is a disease where individuals have abnormally {{c1::hard
(sclerotic)}} bones which is caused by a mutation that causes impaired
function of {{c1::osteoclasts}}
19. {{c2::Osteopetrosis}} is a disease where individuals have abnormally {{c1::hard
(sclerotic)}} bones which is caused by a mutation that causes impaired
function of {{c1::osteoclasts}}
20. Osteopetrosis is caused by mutations in {{c1::CA2}}, {{c1::CLN7}}, and
{{c1::TC1RG1}} which are involved in the {{c2::acidification of the osteoclast resorption
pit}}
21. Osteopetrosis is caused by mutations in {{c1::CA2}}, {{c1::CLN7}}, and
{{c1::TC1RG1}} which are involved in the {{c2::acidification of the osteoclast resorption
pit}}
22. Osteo{{c2::penia}} refers to {{c1::reduced bone mass}}, Osteo{{c2::porosis}} refers
to {{c1::severe osteopenia (severe reduced bone mass)}}
23. Osteoporosis occurs when bone  {{c1::resorption}} >  bone  {{c1::formation}} which
leads to reduced bone mass
24. Explain the pathophysiology of postmenopausal and senile (aging) osteoporosis
Menopause (high turnover): ↓ serum estrogen → ↑ RANK/RANKL →  ↑ osteoclast
activity 
Senile/aging (low turnover): Bone formation is slower than the osteoclast activity.
This is because as you age, you have decreased synthetic activity of osteoblast
25. What is Paget Disease (Osteitis Deformans)?
{{c1::thickened (sclerotic) and structurally disorganized bone caused by an osteoclast
dysfunction (localized disorder of bone remodeling)}}
26. Paget Disease (Osteitis Deformans) affects individuals over {{c1::40}} years old
27. Microfactures and bony overgrowth with warm overlying skin due
to hypervascularity of the affected bone is a classical symptom of {{c1::Paget Disease
(Osteitis Deformans)}}
28. {{c2::Paget Disease (Osteitis Deformans)}} can lead to
{{c1::malignancy (osteosarcoma or fibrosarcoma)::what complication}}
29. Malignancy such as osteosarcoma and fibrosarcoma are associated
with {{c1::Paget Disease (Osteitis Deformans)::what disease}}
30. A {{c1::mosaic}} histological pattern is associated with {{c2::Paget Disease
(Osteitis Deformans)}}
31. A {{c1::mosaic}} histological pattern is associated with {{c2::Paget Disease
(Osteitis Deformans)}}
32. What is osteomyelitis?
{{c1::infection of the bone and bone marrow}}
33. In reference to osteomyelitis, what is the involucrum and sequestrum?

34. What is a Brodie's Abscess?

{{c1:: a type of osteomyelitis that forms an  abscess within the bone.}}

35. Sclerosing osteomyelitis of Garre refers to osteomyelitis of the {{c1::jaw}}
36. What is osteonecrosis (avascular necrosis)?

{{c1::when a bone dies due to lack of blood flow}}

37. Rickets (children) and Osteomalacia (adults) is caused by a {{c1::vitamin D
deficiency}}
38.How does hyperparathyroidism impact bone?

{{c1::↑ PTH → ↑ osteoclast activity → osteoclasts destroy bone}}

39. Dissecting osteitis and brown tumor are hallmark symptoms
of {{c1::hyperparathyroidism}}
40. Generalized Osteitis Fibrosa Cystica is caused by {{c1::hyperparathyroidism}}
41. Renal osteodystrophy refers to skeletal changes due to chronic {{c1::renal
(kidney)}} disease
42. What are the 3 phases of the evolution of Paget Disease 
43. Cartilage is {{c1::avascular}}, therefore diffusion is essential for healing, removal of
waste, etc.

 Healing is slow
 Cartilage must be small and thin because repair elements need to diffuse to
reach the target tissue. If it's too large, it won't be able to make it. 

44. Cartilage consists of {{c1::chondrocytes}} + {{c1::ECM}} 

Chondrocytes secrete factors that support the ECM (allow it to exist)
ECM provides structural support to chondrocytes
45. The extracellular matrix (ECM) consists of

{{c1::Type II collagen fibers}}

{{c1::Proteoglycans}}
{{c1::Glycoaminoglycans (GAGS)}}
ECM has type II collagen fibers that support it
Proteoglycans and GAGs hydrate the ECM
46. What is ground substance?

{{c1::everything in the ECM except collagen fibers}}

47. Chondrocytes secrete factors that {{c1::support}}  the ECM
48. ECM provides {{c1::structural}} support to chondrocytes, ECM cannot survive
without chondrocytes
49. {{c2::Proteoglycans}} and {{c2::GAGs (hyaluronan)}} and have
a high  {{c1::negative}}  charge that attracts  {{c1::water}}, this allows it to keep
the cartilage hydrated, As you age, these proteoglycans/GAGs lose their ability to
attract water, therefore you have brittle and weak cartilage.
50. {{c2::Proteoglycans}} and {{c2::GAGs (hyaluronan)}} and have
a high  {{c1::negative}}  charge that attracts  {{c1::water}}, this allows it to keep
the cartilage hydrated; As you age, these proteoglycans/GAGs lose their ability to
attract water, therefore you have brittle and weak cartilage
51. Clinical Correlation: What would happen if
the chondrocytes became senile or stopped working? What effect would this have on
the cartilage?

{{c1::The ECM will not be supported (recall: chondrocytes support the ECM) and

therefore the cartilage will degrade.

52. Isogenous groups are groups of {{c1::4}} chondrocytes that form because

the chondrocyte recently underwent {{c1::mitotic division.}}
53. Chondrocytes are found in {{c1::lacunae}} that are floating around in the ECM
54. Hyaline cartilage is the typical cartilage and consists of:

{{c1::chondrocytes}}
{{c1::type II collagen (ECM)}}
{{c1::proteoglycans (ECM)}}
{{c1::GAGS (ECM)}}
55. Hyaline cartilage is found in 

{{c1::epiphyseal plates}}
{{c1::articular surfaces}}
{{c1::airway (larynx, trachea, bronchi)}}
{{c1::nasal cartilages}}
56. Hyaline cartilage is protected by an outer fibrous layer called
the {{c1::perichondrium}}
57. Perichondrium is a type of {{c1::dense}} {{c1::irregular}} connective tissue
58. Perichondrium is an outer fibrous layer that surrounds and protects hyaline
cartilage that consists of

{{c1::Fibroblasts}}
{{c1::Type I collagen}}
{{c1::Blood vessel}}
59. In regards to blood supply, what happens if a cartilage has a perichondrium versus
if it doesn't?

{{c1::
If a cartilage DOES have a perichondrium, the perichondrium is going to provide blood
supply to the cartilage

It a cartilage does NOT have a perichondrium, it's going to rely on surrounding blood

vessels for blood supply
60. {{c2::Chondroblasts}} are found towards the outer border of hyaline cartilage,
they secrete {{c1::ECM (type II cartilage)}} and eventually
become {{c1::chondrocytes}}
61. {{c2::Chondroblasts}} are found towards the outer border of hyaline cartilage,
they secrete {{c1::ECM (type II cartilage)}} and eventually
become {{c1::chondrocytes}}
62. Chondroblasts {{c1::build}} cartilage
63. Perichondrium stains {{c1::pink::color}}
64. Hyaline cartilage stains {{c1::purple::color}}
65. {{c1::Articular}} cartilage is the exception that does NOT have a perichondrium
66. Elastic cartilage consists of {{c1::hyaline cartilage (type II collagen)}} + {{c1::elastic
fibers}}
67. Elastic cartilage is found in:

{{c1::external ear}}
{{c1::auditory tube}}
{{c1::epiglottis}}

67. What is cauliflower ear (auricular hematoma)?

Cauliflower ear occurs after consistent trauma to the ear
which separates the elastic fibers from the outer perichondrium. This
allows blood to fill in the area and this signals the body to add scar tissue to
repair the damage.This leads to scar tissue and dense irregular tissue in the
ear 
68. What kind of scar tissue is found in cauliflower ear?
{c1::dense irregular tissue}}
69. Fibrocartilage consists of {{c1::hyaline cartilage (type II collagen)}} + {{c1::type I
collagen (dense regular CT)}}
70. Fibrocartilage {{c1::does NOT::does or does not}} have a perichondrium
71. Fibrocartilage is found in:
{{c1::Annulus fibrosis}}
{{c1::Pubic symphysis}}
{{c1::Menisci}}
{{c1::Joint discs}}
72. What is a way to speed up the healing of meniscus tears?
{{c1::Notice that the blood vessels are far away from the meniscus. This
leads to slow healing.
One way to attempt to fix this is if you poke a hole in the meniscus in hopes
that blood vessels invade it and supply blood to facilitate healing.}}
73. What kind of cartilage is found in meniscus and joint discs?
74. {{c1::Fibrocartilage}}
75. Explain the process of appositional cartilage growth
New cartilage added to the surface of existing cartilage
This occurs when the chondroblasts located on the top layer of the
perichondrium start to secrete ECM, surround themselves with it, and get
added onto the top layer of the cartilage and differentiate into chondrocytes
76. Explain the process of interstitial cartilage growth
When new cartilage is added WITHIN existing cartilage (within itself)
This occurs when chondrocytes undergo mitosis to create isogenous
groups
77. Explain the process of intramembranous ossification to go
from mesenchyme to bone
Intramembranous ossification occurs when mesenchyme turns directly
into bone, There is no cartilage intermediate
78. Explain the process of endochondral ossification to go from mesenchyme to bone
Endochondral ossification occurs when mesenchyme turns into hyaline
cartilage (which creates a scaffolding for where bone is going to be
placed) before turning into bone.
79. What is a periosteum?
Periosteum is an osteogenic connective tissue layer that lines
the outside of bone (the red outline). 
Osteogenic means it has the ability to build bone so you can add bone to
your entire bone via this.
80. What is an endosteum?
Endosteum is an osteogenic connective tissue layer that lines the inside of
bone. Osteogenic means it has the ability to build bone so you can add
bone to the inside of bone via this.
81. Cartilage stains {{c1::purple::color}}
Bone stains {{c1::pink::color}}
82. What are the zones of the growth plate? (proximal to distal)
83. What occurs in the zone of proliferation? (growth plate)
{{c1::Chondrocytes undergo mitosis. This is mediated by growth hormone.}}
84. What occurs in the zone of hypertrophy? (growth plate)
The chondrocytes increase in size (hypertrophy)
This is important because these chondrocytes eventually die which creates
spaces for osteoblasts to come in and build bone (zone of resorption)
85. What occurs in the zone of calcified cartilage? (growth plate)
{{c1::Leftover cartilage (ECM) will calcify (harden)}}
86. What occurs in the zone of resorption? (growth plate)
Chondrocytes undergo apoptosis to create space  for osteoblasts to come in
and build bone. 
The osteoblasts come in and "eat-up" the leftover calcified
cartilage and convert it into bone
87. Achondroplasia is {{c1::dwarfism}} due to early closure of {{c1::growth-plates}}
88. How does pseudoachondroplasia differ from achondroplasia?
{{c1::Dwarfism due to a mutation that kills chondrocytes}}
similar presentation to achondroplasia but different etiology
disproportionate limbs 
Migets ("little people") stop growing due to {{c1::low levels of growth
hormone}} PROPORTIONATE BODY SEGMENTS
89. What's the morphological difference between dwarfism
(achondroplasia) and midgets?
dwarfism: disproportionate body segments (premature closing of growth
plates), midgets: proportionate body segments (low levels of growth
hormones)
90. What is gigantism?
{{c1::Excessive growth hormone BEFORE the growth plate closes. Therefore
the bones continue to ELONGATE.}}
91. What is acromegaly?
Excessive growth hormone AFTER the growth plates close (after puberty).
Therefore the person enlarges without growing taller.
This occurs at the periosteum (bones get wider but not longer)
92. In gigantism, bones get {{c1::longer}}
In acromegaly, bones get {{c1::wider}}
93. Estrogen causes growth plates to {{c1::close}}.
This is why women are typically shorter than men.
Cutting off testes removes estrogen → grow taller

94. Articular cartilage is just {{c1::hyaline (type II collagen)}} cartilage found at the
{{c1::ends of bones (within the synovial joint)::location}}
95. The superficial zone of articular cartilage consists of type II collagen that
is {{c1::parallel}} to the surface that is meant to be a protective {{c1::abrasion}}
barrier
96. The middle zone of articular cartilage consists of type II collagen that
is {{c1::perpendicular}} to the surface and its function is to {{c1::tether}}  cartilage to
bone
97. The deep zone of articular cartilage consists of type II collagen (hyaline
cartilage) that is {{c1::calcified}} and its function is to {{c1::tether}}  cartilage to bone
98. Articular cartilage is {{c1::THICKER}} in a weight-lifter compared to a normal
person
99. The synovial joint capsule consists of 2 layers:
External (fibrous layer) that is comprised of {{c1::dense irregular}} CT and
is continuous with the {{c1::periosteum}}
Internal (synovial layer) that is lined by {{c1::synoviocytes}} that secrete
{{c1::synovial fluid}}
Synovial fluid prevents friction in the joint space.
Synovial macrophages remove debris from the joint. 

100. Osteoarthritis occurs when the {{c1::articular}} cartilage thins between joints

and develops clefts, Damage may activate MMPs which prevent regeneration of
the cartilage 
 Worse with activity as the synovial fluid contains cartilage fragments and
type II cartilage. 

101. Rheumatoid arthritis is caused by an {{c1::autoimmune}}  reaction that

causes synovial  {{c1::macrophages}} to release proinflammatory
cytokines and MMPs; Pain is improved with activity, worse with rest.

Involves multiple joints and is typically bilateral

102. What are the distinguishing factors between osteoarthritis and rheumatoid

arthritis?
osteoarthritis: pain is worse with activity, affects ONE joint
rheumatoid arthritis: pain is improved with activity, affects MULTIPLE joints

103. {{c2::Ulnar deviation}} of the fingers is a classical

presentation of {{c1::rheumatoid arthritis::disease}}
104. Compact bone (cortical bone) is dense/thick/strong and comprises
the {{c1::diaphysis}} and lines the {{c1::epiphysis}}
105. Trabecular bone (spongy bone) has a lot of spaces that are filled
with {{c1::bone marrow/hemapoetic cells}} and is concentrated in the
{{c1::epiphysis}}
106. Compact bone (cortical bone) and trabecular bone (spongy bone) are
comprised of the {{c1::same::same or different}} tissue type that is
organized {{c1::differently}}
107. Osteons are circular layers (onion rings) of {{c1::compact (cortical)}} bone.
Osteons are connected through vessels running through central and perforating
canals.
108. {{c2::Canaliculi}} are hair-like passageways that allow {{c1::osteocytes (in
osteons)}} to communicate with each other
109. To initiate bone formation, osteoblasts secrete osteoid which
is {{c1::unmineralized bone}} that is comprised of type {{c1::I}} collagen
Osteoblasts become osteocytes once they surround themselves with bone.

110. Osteocytes release factors to initiate the crystallization of

{{c1::hydroxyapatite}} which is a storage of calcium and phosphate
111. Calcium/Vitamin D deficiency leads to {{c1::rickets}} in children

Calcium/Vitamin D deficiency leads to {{c1::osteomalacia}} in adults

112. Bone is comprised of type  {{c1::I}} collagen
113. Osteocytes can respond to levels of mechanical stress by becoming:
114. Explain how osteoclasts "cut" bone
115. Osteoclasts can be identified histologically by its {{c1::multiple}} nuclei
116. Periosteum lines the outer layer of bones (except articular surfaces) has
{{c1::osteoprogenitor}} cells that become osteoblasts and allow it to create bone
117. Describe the process of bone fracture healing
Clinical Consideration

1. {{c1::Medial circumflex femoral a.}} is the primary blood supply to the head

of the femur
2. Hip fracture refers to fracture of the {{c1::femoral neck}}
3. What are the attachment points for the anterior cruciate ligament?
{{c1::Lateral femoral condyle → anterior tibia}}
4. What are the attachment points for the posterior cruciate ligament?
{{c1::Medial femoral condyle → posterior tibia }}
5. Swelling of the knee is most likely due to inflammation of what?
Suprapatellar bursae (anterior, communicates with the synovial cavity)
Anserine bursae (anterior, communicates with the synovial cavity)
Articular/synovial cavity
6. What bursae communicate directly with the synovial cavity?
Suprapatellar bursae
 Popliteus bursae
 Anserine bursae
 Gastrocnemius bursae
7. What artery directly supplies blood to the joint capsule and the cruciate ligaments?

{{c1::middle genicular a.}}

8. If the distal fibula moves anteriorly, the proximal fibula moves {{c1::posteriorly}}
If the distal fibula moves posteriorly, the proximal fibula moves {{c1::anteriorly}}
9. Valgus producing force would tear the {{c1::medial collateral ligament}}
and compress the {{c1::lateral meniscus}}
10. Varus producing force would tear the {{c1::lateral collateral ligament}}
and compress the {{c1::medial meniscus}}
11. Knee injuries that involve lateral rotation, the unhappy triad is typically damaged
which consists of 
medial meniscus
medial collateral lig.
anterior cruciate lig.
12. During ankle inversion, what ligaments are torn in what step-wise order?
ACP
13. During ankle eversion, what ligament(s) is damaged?
{{c1::deltoid ligament}}
14. What muscles stabilize the pelvis/hip?
gluteus medius
gluteus minimus
15. What is Trendelenburg Gait and what does it indicate?
{{c1::contralateral hip drop while walking due to damage to the superior gluteal
nerve}} ; innervated by the superior gluteal nerve
16. If a person is standing and is leaning to the side, this is indicative of
{{c1::ipsi}}lateral superior gluteal nerve nerve damage.
innervated by the superior gluteal nerve
17. If the popliteal artery gets blocked, what route can the blood around the knee take to get to
the leg? (both lateral and medial routes)

18. Lower extremity swelling is due to blockage of a {{c1::vein}} 

Veins carry blood UP the body.
19. Bruising (ecchymosis) is due to ruptures of {{c1::veins}}
Veins carry blood UP the body.
20. What artery may supply collateral blood supply to the plantar foot if the posterior
tibial artery is blocked?
21.