Week 11

  1. What is the mnemonic for the 12 cranial nerves? And meaning?
    • Oh, Oh, Oh to touch and feel virgin girl vagina, ah!
    • Olfactory, Optic, Oculomotor, Trochlear, Trigeminal,Abducens, Facial, Vestibuleocochlear, glossopharyngeal,vagus, spinal acessory, and hypoglossal
  2. What structures pass to or from the neck?
    • Cervical vertebrae
    • Esophagus
    • Trachea
    • Brachial Plexus
    • internal jugular vein
    • common carotid artery
    • vagus nerve
  3. What is different between the components of the cranium and the skull?
    • the skull plus the lower jaw(mandible) creates the cranium
    • the skull does not include the mandible
  4. What is TMJ ?
    the temporomandibular joint. It is a single hinge connecting your jawbone to your skull
  5. WIT Hyoid? WI an important distinguishment about the hyoid.
    U-shaped bone hed in place by strap muscles of the anterior triangle of the neck. It has two superior lesser horns and 2 greater horn It does not articulate with any other bones just muscles and ligaments keep it suspended in the neck.
  6. At what vertebral level is the hyoid located?
    C3
  7. WAT Laryngeal cartilages?
    • 3 unpaired cartilages 
    • epiglottis 
    • thyroid 
    • cricoid
    • 3 paired cartilages
    • arytenoid
    • cuneiform 
    • corniculate
  8. what cartilage in the laryngeal cartilages may be present within the free posterior margins of the thyrohyoid membrane?
    triticeal cartilage
  9. what is the triticeal cartilage?
    an additional laryngeal cartilage present within the free posterior margin of the thyrohyoid membrane
  10. what do the articular processes of the atlas ( first vertebrae) articulate with? And this result in?
    • The occipital condyles 
    • resulting in motion of the skull
    • this forms the atlantooccipital joints
  11. what is the primary motion of the atlantooccipital joint?
    • flex and extend
    • 15-20 degress?
  12. WIT dens?
    • forms the median atlantoaxial joint
    • articulate with he anterior surface of the atlas
    • also provided pivot for atlas rotation
  13. what is the neurocarnium and vscerocranium
    • neuro houses the brain
    • viscero is the face.
  14. how many cranial bones are there? and how are they connected?
    • 22 = 3 from the ear
    • the are connected with sutures
  15. what are fontanelles?which ones are we aware?
    • fibrous softspots between cranial bones
    • these prevent fractures during child birthing and usually ossify after as the child grow
    • there is an anterior and posterior fontanelle
  16. what is the meningeal layers from inside out? and what do they surround?
    • surround the brain and spinal cord 
    • pia mater, arachnoid mater, dura mater
  17. Between which two meningeal layers is the CSF
    the pia mater and the arachnoid mater in the subarachnoid space
  18. What are the three regions of the pharynx?
    • Nasopharynx
    • Oropharlynx
    • laryngopharaynx
  19. What separates the nasopharynx from the oropharnx?
    uvula
  20. What separates the laryngopharynx from the oropharnx?
    epiglottis
  21. What seperate the nasopharynx from the nasal cavity?
    nasal nares
  22. WIT uvula?
    the posterior tip of the soft palate
  23. what is the function of the pharynx
    a common passageway for air, food, and liquids
  24. What is the function of the larynx
    it is a conduit for air, closes off airway. It is also involved in phonation and deglutition
  25. How does the epiglottis work?
    • upon deglutition/aka swallowing the hyoid bone move anteriorsuperior resulting in passive pressure passing through the base of the tongue that bend the epigottis posteriorly 
    • it is one of the unpaired laryngeal cartilages
  26. Steps of ingestion
    • 1- bolus of food enters oral cavity and pushes the soft palate superiorly blocking off the nasal cavity
    • 2- As the bolus moves from the oropharynx to the larngopharx it pushed the epiglottis back simultaneously opening the upper esophageal sphincter 
    • 3- when food passes through the esopheageal everything passively retracts
  27. how ar babies able to drink and breathe at the same time?
    • the larynx and the epiglottis are more superior than adults 
    • this causes the epiglottis and the soft palate to interlock allowing food to pass laterallya nd bypass entry into the airway
  28. what are the 4 paranasal sinuses?
    • Sphenoid
    • frontal 
    • ethmoid 
    • maxillary
  29. what is the function of the paranasal sinuses ? (3)
    • lighten the skull weight 
    • humidify and heat air
    • increase resonance for hearing.
  30. what are some features of the paranasal sinuses?
    • paired 
    • connected to the nasal cavity via ostia
  31. what does the internal carotid supply?
    inside the skull?.
  32. what does the external carotid supply?
    outside of the skull
  33. where does the common carotid comes from and becomes?
    • brachiocephalic trunk ( right) 
    • arch of the aorta (left)
    • splits into the internal and external carotid
  34. What is significant about the bifurcation of the common carotid?
    this is the location of the carotid sinus and carotid body?
  35. WIT carotid body?
    • a chemoreceptor that monitors the o2 levels in the arterial blood. When there are a sign of imbalance such as hypoxia, hypercapnia, or low pH it can trigger a reflex to increase the rate and volume of ventilation via respiratory centers.
    • it is composed of glomus cells.
  36. WIT carotid sinus?
    • a dilated area at the bifurcation of the common carotid and the proximal internal carotid artery
    • it is a baroreceptor (pressure receptor) which monitors changes in arterial blood pressure
  37. what is the carotid body innervated by?
    CN IX glossopharyngeal
  38. WIT pterion?
    is it the thing area junction of the frontal paritel, temporal  an sphenoid bones.
  39. how is visceral affferent fiber information conveyed from the carotid sinus?
    CN IX
  40. WIT clinical relevance of the pterion?
    it overlays the middle meningeal artery and it is thin, thus it there is an injury there is could be life threatning, cause intercranial hemmorage, if middle menengeal art. is ruptures, which leads to a build up of pressure in the brain
  41. what is the first danger zone?
    Pterion
  42. subdural hematoma?
    below the dura mater but above the arachnoid matter
  43. epidural hematoma?
    below skull bone but above the dural matter
  44. Subarachnoid hematoma?
    above pia mater but below arachnoid mater
  45. what does the external jugular vein drain?
    drains temporal (& occiptal regions)
  46. what does the internal jugular vein drain?
    drains face and inside skull
  47. cavernous sinus?
    • split dural venous sinus lateral to the pituitary fossa
    • in the same area as the sphenoid sinus
  48. what is the second danger zone? Why is it clinically significant?
    • the superior and inferior ophthalmic veins. this is int the nose triangle region.
    • because these veins are so close to the brain this can cause infections to spread to the brain.
  49. What are the layers of the cervical fascia?
    • investing fascia
    • pretracheal fascia
    • carotid fascia
    • carotid shealth
    • prevertebral fascia
  50. what does the investing fascia invest ( surround)
    • the SM
    • trapezius
    • submandibular glangs
    • and is continout with the parotid glad capsule
  51. what does the pretracheal fascia invest ( surround)
    esophagus, trachea, and thyroid gland
  52. what does the carotid fascia invest ( surround)
    all of the arteries and veins, lymph nodes, and the vagus nerve
  53. what does the prevertebral fascia invest ( surround)
    all of the vertebrae and the VT muscles
  54. alar fascia
    runs anterior to the preertebral facia
  55. what is the 3rd danger space? why is it important/
    a space between the alar and prevertebral fascia.This space offers a potential route for infections towards the posterior mediastinum and diaphragm
  56. What are the 5 special senses?
    • taste
    • see( vision)
    • hearing
    • olfaction
    • balance
  57. what are the visceral sense fo the 5?
    taste and smell.
  58. what are the three salivary galnds?
    • parotid
    • submandibular
    • sublingual
  59. which salivary gland secreates the most?
    parotid
  60. what is the function of the parotid gland specifically? how does it utilize different parts of the ANS) and how does it bring saliva into the mouth?
    • creates:
    • water saliva( parasympathetic)
    • viscous salvia (sympathetic)
    • saliva travels through the parotid duct and enters mouth via second maxillary molar
  61. how does the submandibular gland bring saliva into the mouth?
    via the submandibular duct, which is deep to the mylohyoid,and opens in the anterior floor of the mouth
  62. how does the sublingual gland bring saliva into the mouth?
    secretions travel superiorly through numerous small ducts
  63. what is the rout of tears?
    • 1-created by lacrimal glands and are secreted through lacrimal ducts
    • 2-tears drain into the lacrimal punctum ( where two canaculi meet) into the lacrimal sac; the inner corners of the eye
    • Lacrimal sacrimal sac drain tears into the nasolacrimal duct,which opens into the nasal cavity
  64. tears that are not lost from eye are drain into the lacrimal punctum then lacrimal sac due to which action?
    blinking?
  65. why do we sniffle when we cry?
    tear drain into the nasal lacrimal duct which opens into the nasal cavity
  66. what are the 3 glands in the deep neck?
    • thyroid
    • paratyroid
    • thymus
  67. WIT thyroid?
    using iodine from food produces thyroxine and thyrocalcitonin ( essential for growth)
  68. what controls the thyroid?
    thyroid-stimulating hormone from the pituitary gland
  69. WIT paratyroid gland?
    • produces paratyroid hormone (PTH) which regulates calcuim and phosphorus metabolism
    • is it usually behind the thyroid and has a set of two on each side of the neck
  70. what controls the parathyroid gland?
    the pituitary and hypothalamus
  71. WIT function of the Tymus?
    produces thymosin that promotes differentiation and maturation in the Tlympocyte precursors transported from the bone marrow
  72. what are the four fibers only found in spinal nerves?
    • GSE
    • GSA
    • GVE
    • GVA
  73. what are the 3 special nerve fiber only found in the head and neck
    • SVA
    • SVE
    • SSA
    • there is no SSE
  74. what are fibers of the SVA for.
    related to taste or smell
  75. what are fibers of the SSA for
    nongut-related special sense fibers such as vision balance or hearing
  76. what are SVE fibers for
    to the brachiomeric muscles derived from segmented pharyngeal arches
  77. CNI
    olfactory nerve
  78. CNIII
    Oculomotor nerve
  79. CnVII
    facial nevre
  80. Cn XI
    Spinal acessory
  81. CNX
    vagus nerve
  82. CN II
    occipital nerve
  83. CN V
    Tigeminal
  84. CN VI
    Abducens
  85. CN IV
    Trochlear
  86. CnVIII
    vestibulocochlear
  87. CnIX
    Glossopharyngeal
  88. CN XII
    hypoglossal
  89. function of abducens?
    abduct the eyes
  90. myotomal nerves
    • occulomotor 
    • trochlear
    • abducens
    • accessory
    • hypoglossal
    • eye movement nerves
  91. Special sensory Nerve SSA and SVA only
    olfactory,occipital, and vestibulocochlear
  92. Branchiomeric Nerves
    • CNV
    • CNVI
    • CN IX
    • CNX
  93. Pharmacodynamics
    • what the drug does to the body
    • The biochemical and physiological effects of drugs and their mechanisms of action
  94. Pharmacokinetics
    • What the body does to/with the drug
    • the movement of drugs in the body over a period of time i.e. absorption,distribution, localization in tissues, biotransformation, and excretion
  95. what determines how quickly and to what extent a drug will appear at its target site
    the absorption, distribution, metabolism, and excretion ADME
  96. what does ADME determine
    how quickly and to what extent drug will appear at its target site
  97. what is the relationship between pharmacokinetics and pharmacodynamics
    the pharmokinetics determines the pharmocdynamics
  98. Pharmacogenomics
    study of genetic variations that cause difference in drug response among individuals or populations
  99. WIT drug
    a substance to brings about a change in the biologica function through its interaction with body components( e.g. receptors being activated or deactivated)
  100. receptor
    a specific molecule in the biological system that plays a regulatory role
  101. effector
    a molecule that ranslates the drug reeceptor interaction into a change in the cellular activity.
  102. what about the drug determines the pharmocokinetics and pharmocodynamics
    the structural features which include but are not limited to size shape, chirality, electrical charge, and lipid solubility
  103. WIT intrinsic activity ?
    • the magnitude of the intensity of the drug
    • the ability of a drug bound to its receptos to actovate downstream effecotr mechanism
  104. WIT structureactivity relationship
    the relationship because the chemical or 3d structure of a mlecules and it activity
  105. receptor affintiy
    • the tendency of a receptor to combine with a drug
    • the strength of the drug receptor interaction
  106. drug specificity
    the degree to which a particular drug gains access to and gind a select receptor type
  107. what are the diferent ways that a drug and receptor can interact?
    • Covalent 
    • electrostatic 
    • Hydrophobic
  108. what is the strongest drug-recptor interaction? why?
    Covalent ; it is often irreversible
  109. what are some example of biological targets of drugs?(6)
    • Regulatory proteins
    • enzymes
    • transport proteins
    • structureal proteins
    • nucelic acids
    • other biological macromolecules
  110. what is the definition of biological target of a drug?
    the cellular macromolecule or macromoelcule cmoplex with which the drug interactsto elicit a cellular response i.e. a chane in cell function
  111. what are some examples of electrostatis drug-receptor interactions (3)
    • van der waals forces( very weak)
    • electrostati forces(relatively strong)
    • hydrogen bonds ( weaker)
  112. whatis hydrophobic drug-receptor interaction?
    • the weakest interactions out of all 
    • weak interactions of lipid soluble drugs with cell membrane
  113. pahrmocokinetics determines which part of the dose relationship?
    • drug dose
    • concentration in bioloical fluid
    • concentration at effector site
  114. pharmocodynamics determines which part of the dose relationship?
    • magnitde of pharmologic effect
    • concentration at effector site
  115. pharmocodynamics ofa drug can either____ or_____ a receptor
    activate or black/inhibit
  116. what are some ways that a drug take action at cytoplasmic receptors?
    • intracellular receptor 
    • activation og cytoplasmic enxyme
    • activation of protein tyrpsine kinase
    • regulation og ion channel
    • activation of g protein signal transduction pathway( protein coupled-receptor)
  117. what are the 4 types od D-R interactions?
    • D+R->D-R complex-> effect
    • D+R->D-R complex-> effector molecule-> effect
    • D+R->D-R complex-> activation gof coupling molecules->effector molecules->effect
    • Drug inihibits the metabolism of an endogenous activator-> increased activator action on effecotr molecules-> increased effect
  118. what are the locationof receptors?
    • ubiquitous
    • limited sitribution
  119. WIT functional capacity of receptors ?
    • common
    • unique
    • vital
  120. what is extent of drug action determined by?
    location and functional capacity  of receptors it interacts with
  121. what kind of effect do ubiquitous receptos and common functional capicity have?
    wife spread effects9 both therapeutic and side effects
  122. what is a example and explanation of limited distribution and unique action?
    • an inhaler
    • it is distributed directly to the lungs and specific for a cerain action ( increae volume capacity of lung)
  123. what is vital function capacity
    an function that is necessary for life for example the heart beating
  124. what 4 things determine the duration of drug action?(4)
    • how long the drug occupies the receptor
    • if there is a second messengers and signal transduction 
    • if drug bind covalently to the receptor 
    • desenitization mechanism
  125. what happens whena drug binds to a non regulatory molecule? give example if this happening?
    • there is no changei n function
    • drug binding to nonreg molecules like plasma serum albumin or tissue marcromocules, so they cannot get to their target receptor
  126. how is drug binding to nonreg molecules important for pharmocokinetics
    since pharmkinetics is all about the Absorption, distribution, metabolisim, and excretion of a drug when it is introduced to the body when a drug bind to a nonreg molecule it affect how the drug is distibuted and the amount of free drug in circulation thus affecting pharmkinetics
  127. which plama protain has one of the highest capacities for binding to protein? how much of the plasa
    albumin, it makes up 60% of total blood plasma
  128. The concentraion of receptors occupied by a drug depends on the
    • drug concentraion
    • drug-receptor assocation rate k+1
    • drug-receptor dissocation rate k-1
  129. the term for the determinants of the concentration of receptors occupied by a drug is
    the receptor occupancy theory
  130. formula for euilibrium dossociation constant? what is the state of the drug at the kd
    • kd=k-1/k+1= [D][R]/[DR]
    • half are free and half bound to a reeptor
  131. kd represents
    the total concentration reuired to saturate 50% of receptors
  132. what is the formula for the affinity constant ( ka)
    • the reciprocal for kd 
    • ka=1/kd
  133. what is the relationship btwn kd and drug affinity?
    the smaller the kd the higher the affinity
  134. what is the type of relationship btwn drug cncentraton and magnitude of effect
    • direct relationship
    • as one increases the other does as well
  135. Ec50
    the concentation of drug that creates 50% of its maximal response
  136. what is Bmax
    total concentraion of receptor sites
  137. what is potency
    the concentration of drug rquired to produce an effect ( reated to drug affinity for its target)
  138. WIT efficacy
    the quantitative ability of a drug to elicit a physiologic response when it interacts with a receptor
  139. when a drug is more potent how will it EC50 be in relationship to another drug that is less potent
    the EC50 will be lower
  140. In regards to dynamics, the drugs efficacy is dependent on_____? and detemines ___?
    the intrinsic activity and determines the efficacy
  141. partial agonist
    a drug that binds to and activates a receptor but does not evoke a meximal response, no matter how high the concentratin of drug
  142. antagonist
    a drug that binds to a receptor , competes with and prevents binding by the other molecules and/or inhibits biological responses by interfering with the agonists ability ti activate the receptor
  143. Intrinsic efficacy
    the relative ability of drug-receptor complex to produce the maximal functional response
  144. inverse agonist
    a drug that has a much stronger affinity for the Ri then the Ra state and stabilizes a large fraction in the Ri-D pool, reducing constitutive activity
  145. agonist
    a drug that binds to and activates the receptor in some fashion, whihc directly or indirectly brings about the effect and/or stimulates the signal transduction pathway
  146. allosteric activator
    a drug that directly activates a recptor by binding to a receptor site distinct from the primary site
  147. allosteric inhibitor
    a drug that binds a receptor at a site distinct from the primary site, inhibits the action of the agonist, and is not overcome by increasni the dose of the agonist
  148. what is pharmacology
    the body of knowledge concerned with the action on chemical on biological systems
  149. what is the fundamental event that initiates the action of the drug
    the interaction o the drug with its receptor
  150. what is the receptor occupancy model
    model for explaining drug behavior assumes that response emanates from a receptor occupied by a dru
  151. the drug effect is proportional to
    the unmer of receptors occupied and eliciting that effect
  152. the receptor occupancy is rleated to
    the ratio of drug concentration and the Kd
  153. what do graded does response curves depicts
    the relationship between the concentration of a drug and the clincially observed response
  154. in regards to dynamics efficacy represent the
    • Emax
    • the max effect of  a drug at the highest olerable dose
  155. potency represents/reflects
    the amount of drug required to caue a specific amountof effect eg EC50for half max effect
  156. what makes a allosteric agonist improve the overal response of the drug
    it stop agonit (drug) from dissocation from the receptor as quickly, in other word it reduces the Kd and increases emax
  157. what is the difference between the allosteric inhibtor and the competitive inhibitor
    • the competetive inhibitor bind to the same site as the agonist
    • the allosteric one binds to anothe site and  causes a conformational chane in the receptor so that the primary site is distorted and the agonist cannot bind
  158. properties of agonst
    have affinity and intrinsic activity
  159. properties of antagonist
    have affinity by lack intrinsic activity
  160. what is the two-state model of receptor actvation
    the theory that receptors occur in exactly 2 conformational states- active and inactive
  161. WIT active conformation of a receptor mean
    in the absence of any agonst, some of the receptor pool must exist in the Ra form some of the time and may produce the same physioloic effect as agonist-induced activity ( consitutive acivity)
  162. WIT inactive conformation of a receptor mean
    the receptor is inactive and produces no effect even if combined with drug
  163. what detemines the extent to which the equilibrium is shifted to ward the active state( Ra)
    the relative affinity of the drug for each of the conformations ( active or inactive)
  164. In regards to receptor conformation, what conformational states does neutral anatagonist hold? and what effect does it hve
    • the antagonist has equal affinity for the active and inactive receptor conformation
    • no effect on net activity and block agonsit since it binds to same spot
  165. how does the inverse agonist stabilise the receptor conformation and what is it affect?
    • similar to competitive antagonist
    • has an affintiy fot eh receptors inactive conformation
    • decrease the rate of signal transduction
  166. how does the partial agonist stabilise the receptor conformation and what is it affect?
    • blocks tha full agonist
    • sub max response
  167. competitive anatagonist
    • you can overcome the effects with increased agonist
    • bind reversibly to same site as agonist
  168. irreversible antagonist
    binds irreversibly to same site as agonst ( usually through covalent bonding
  169. Allosteric noncompetitive anatagonist
    binds to distinct site changint the receptors affinity for the agonist
  170. allosteric activator
    confomrational changes anhacne agonist binding hence effect
  171. how does the competitive inhibitor alter the dose response curve ?
    • shift the curve to the right thus there is a larger concentration need to get to Emax
    • EC50 increases
  172. how does the irreversible antagonist affect the dose respose curve
    • EC50 is reduce, curve shifts to the righ, Emax is reduced
    • can bring e max to 0
  173. how does the allosteric noncompetitive antagonist affect the dose respose curve
    cureve shift to right, Ec50 increased,Emax reduces, and reduce agonist affinty
  174. how does the allosteric activator effect the dose-respose curve
    shift to the left
  175. physiological antoagonist?
    2 drugs that oppose each other in their psychiologcal effect-agonist and antagonist - even though they are acting at 2 distint indepent sites
  176. examples of hysiological anatagonists?
    • antidotes
    • insulin and glucagon
  177. chemical anatagonist
    a compound that directly interacts witht he agonist causing midification or sequestering of the agonist so that it is no linger available to bind to the rceptor.
  178. example of chemical anatoagonist
    protamine sulfate binds to heparin and stop it from anticoagulating
  179. spare receptors
    receptors that are left over or do not have to be used to produce a meximal biological response
  180. how can you tell if there are spare receptors with dynamics
    • lookinh at the Bmax and the E max
    • if the b max is more the right thatn e max this means that there are spare receptors which can be calculated with the differnence in concentrations
  181. how can the spare receptors be demonstrated experimentally
    • using irreversible antagonist to prevent binding to a portion of available receptors
    • the curves emax will stay the same as it shift to the right at a certain poitn emax drops off, this is where the ec50 and kd are approximately equal
    • as antagonist is added the emax remains the same this mean that the EC50, concentation of drug needed to achieve half the mx response is still lower than the kd, the total contration requied to staturate 50% receptos
  182. what are some reason why spare receptors may be present(2)
    • agonist has the ability to bind to plasma membrane recptors activating a NUMBER od downstream intracellular mediators
    • or
    • the duration of the activated signaling intermediate may greatly outlast the agonist-receptor interaction
  183. what some way/mechanism that receptors are regulated
    • -synthesis and degradation
    • -covalent modification so that a new receptor is made to replace the covalently modified one
    • -association w/ regulatory proteins
    • -relocatlization w/in the cell
  184. where will modulatory imput come from?
    • other receptors directly or indirectly
    • feedback regulation by their own signaling outputs
  185. what is the other name for desenitization
    tachyphylaxis
  186. WIT desenitization?
    • attenutated response to the same dose of an agonist over time
    • occurs radily, seconds, minutes or days and is reversible
    • receptors are down regulated
  187. WIT Supersensitivity?
    • increased sensitivity to agonist after prolonged blockabe by an antagonist which is now withdrawn
    • cause an increas ( ur regulation) of receptors induced by antagonist
  188. How to remove the effects of desenitization due to agonist
    remove the agonist and give cell time to recover its capacity
  189. describe the steps in the beta-adrenoceptor agonist desenitization. resensitization and downr egulation
    • desensitization
    • agonist binds to adrenoceptor and signal is initiated
    • GRK phosphorylates and beta-arrestin binds to adrenceptor  reprenting it from interacting with the g protein to carry out the down stream reactions
    • r-arrestin bind to coatedpit and is internalized
    • -Agonist dissociates  receptor is dephosphorylated
    • If it returns to plasma membrane this is resenitization
    • if the receptor is eaten by lysosome/endosome this is Down regulation
  190. what is an adrenoceptor
    a type of g-protein coupled receptor
  191. how doe indidvual respond to drug
    their is variation in the magnitude of responses to the same concentration of a single drug
  192. what is the therapeutic window?
    • is the range of steady state concentratin at which the likelihood o efficacy is hight and the probaility of adverse effects is low
    • this still does not guarentee safety or efficacy because of indivudal variation
    • it is between the Ed50 and ED99
  193. formula for therapeutic index
    ratio of LD50/ED50
  194. what does a a narrow therapeutic window mean?
    • tha that therapeutic dose is close to the toxic dose
    • e.g (digitalis)
    •  the therapeutic index is low/closer to 1
  195. some of the specific parts and descrptions of whatt pharmacoynamic is and what components are involved in it
    • receptors, effectors
    • Dose response curves
    • Agonist,parial agonist, antagonist,inverse agonist
    • signaling mechanism
    • Recptor regulation
    • overall deals with the effect of drugs ont he biological systems
  196. the response elcited by conformation-selective drugs is related to....
    the drugs relaive affinity for teh different receptor conformation states( ie. active vs. inactive state)
  197. when might monitoring plasma drug level be recommended
    • there is a relationship btw plasma conc and clincal effect
    • sinifical pharmocological variability
    • established target conc
    • narrow therapeutic window
  198. what are the two definitions of scoliosis
    a description of a structural alteration, or alterations, that can occur with several conditions, or can occur “idiopathically.”

    a description of a structural alteration, or alterations, that can occur with several conditions, or can occur “idiopathically.”
  199. why is scoliosis also called rotoscoliosis?
    rotoscoliosis, since both the coronal and transverse planes are often  involved
  200. what degree do lateral curves have to be in order to be considered scoliosis
    Lateral group curves equal to or greater than 10 degrees (when the Cobb Method of measurement is used) are called scoliosis
  201. Spinal curves less than 10 degrees are termed
    • spinal or positional asymmetry. These curves have no long-term clinical significance
    • e.g. type ! group curve
  202. scoliosis is named for the side of
    of the convexity of the lateral/coronal plane curve.
  203. The apical vertebra is
    the one that is the most deviated and rotated away from the midline.
  204. Sagittal plane curves are
    kyphotic or lordotic curves
  205. when can significant deformities ossur?
    during times of rapid growth, when the curve will most likely progress and can cause cardiopulmonary compromise.
  206. If three planes are involved, there could be a
    kyphoscoliotic curve
  207. How any children develop scoliosis by age 10-15
    10:200 children
  208. What are screening programs?
    programs that can identify children with scoliosis around these ages
  209. what is controversial about scoliosis screenings?
    the efficacy of the voluntary or state mandated school-based scoliosis screening programs is unproven.

    • critics note that scoliosis lacks the characteristics for a screening program.
    • (e.g. lacks high prevalence, lacks a substantial morbidity and mortality in untreated patients, lacks a highly sensitive and specific screening test for the preclinical phase, etc.)
  210. what do proponents of scoliosis screening programs say?
    Proponents cite that earlier diagnosis allows conservative treatment measures
  211. what is the gender discrepancy between boys and girls?
    In girls, curvatures are ten times more likely to progress, but according to Kuchera, girls and boys are equally affected.
  212. what are the ways to classify scoliosis ?(4)
    • reversibility
    • Severity 
    • Cause
    • Location
  213. what does the reversible classification o scoliosis describe?
    Functional or structural – Structural curves do not go away with rotational, side-bending, or forward bending motions. Functional curves, however, do go away with these motions.
  214. how do you test reversibility of scoliosis?
    Can have patient bend forward until maximal rib hump is visible, then ask patient to swing upper body right then left. Look for reduction of the rib hump with this action.
  215. spinal curves progress during what time period
    puberty ( rapid growth )
  216. what are some ways that scoliotic curves can change from functional to structural?(5)
    • progressive soft tissue shortening
    • body changes
    • disc degeneration
    • fibrosis of ligaments & fascia
    • Decreased active & passive ROM
  217. degrees of mild scoliosis?
    Mild Scoliosis – 10 to 15 degrees
  218. degrees of Moderate scoliosis
    Moderate Scoliosis – 20 to 45 degrees
  219. degrees of severe scoliosis
    more than 50 degrees, and will affect systemic function as well.
  220. which curves affect respiratory function? Cardiovascular function?
    • Thoracic curves >50 degrees affect respiratory function.
    • Thoracic curves >75 degrees affect cardiovascular function
  221. what are some causes of scoliosis
    • Idiopathic 
    • Congenital
    • Acquired
    • Neuromuscular
  222. what percent of curves are idopathic
    – 70% – 90% of all scoliotic curves
  223. what is the most common curve
    idiopathic
  224. what are the subcategories of idopathic classification of scoliosis
    Infantile-Juvenile-Adolescent
  225. What is a cause of Infantile Idiopathic Scoliosis ? and treatment?
    • Possibly due to supine and slight side-lying positioning, allowing gravity to cause plastic deformation of the immature thorax.
    • Ideal treatment is prevention, by lying the kids prone (opposite of back to sleep recommendations)

    Treatment with well fitting orthoses/ casting esp. in early period of skeletal growth.
  226. what is the 
    Important difference between early and late onset scoliosi? and why is this clinically significant?
    • Any child with a significant scoliosis before age 5 can develop cardiorespiratory failure or disabling dyspnea.
    • Reason: the scoliosis decreases the available space for growth of the lungs.
    • Normally, there is a tenfold increase of the alveoli from infancy to 4 years of age, continuing up to 8 years of age.
  227. what is the age range of Juvenile Idiopathic Scoliosis
    Between 4 and 10 years of age.
  228. how is juvenile vs. adolescent idiopathic different in regards to rprogression
    More progressive than adolescent idiopathic scoliosis<20 degrees – observation with examination and PA x-rays every 4 to 6 months.With evidence of progression (5-7 degrees), bracing is indicated.
  229. treatments for juvenile scoliosis
    • Variable success of nonoperative treatment
    • .Crankshaft phenomenon – use anterior and posterior fusion to avoid this.Subcutaneous Harrington Instrumentation to decrease amount of shortening (avg. = 4.5 cm if fusion had been done)
  230. what is AIS and what are the causes
    adolescent idiopathic scoliosis

    Hereditary predisposition with multifactorial causes.
  231. what is AIS associated with
    Association with hypokyphosis, possible CNS defect, increased calmodulin, etc.
  232. what is the connection between AIS and familial relations
    • + genetic contribution supported by high concordance of the incidence and severity of scoliosis seen in monozygotic twins, as compared with dizygotic twins. 
    • Patients with AIS also often have a sibling or parent with scoliosis.
  233. what chromosome are AIS tied to?
    Genetic loci for AIS mapped to chromosomes 17 and 19, with an unclear inheritance pattern.
  234. what are the progression associations of AIS ?(6)
    • Girls > boys;
    • premenarchal;
    • Risser sign of 0;
    • Double > single curves;
    • Thoracic > lumbar curves;
    • severe curves.
  235. what is the second most common classification of scoliosis
    COngenital
  236. what % pf conenital scoliosis is proressive
    . 75% are progressive.
  237. Congenital scoliosis may be associated with?
    congenital defects such as:

    • Wedge vertebrae
    • Failure of segmentation
    • Unilateral (bar)
    • Bilateral (fusion)
    • Fused ribs
  238. examples of acquired scoliosis
    from osteomalacia, sciatic irritability, psoas syndrome, healed leg fracture, from a hip prosthesis, due to irradiation/inflammation, etc.
  239. what are the most common causes of neuromuscular scoliosis
    1.Leg length discrepancy


    2.Neurofibromatosis
  240. Neuromuscular curve disappears with forward flexion or lying down are caused by?
    • Leg length discrepancy
    • Primary postural scoliosis
  241. what is a Double Major Scoliosis
    most frequent is thoracic and lumbar; balanced curves; crossover regions subject to degeneration.
  242. what is Single Thoracic Scolosis
    second most common; if progressive, can affect heart and lungs; quite noticeable
  243. WIT Single Lumbar Scoliosis
    third most common; associated with arthritic change.
  244. WIT Junctional Thoracolumbar Scoliosis
    not a common scoliosis; a longer curve; overstresses the spine; arthritic changes
  245. presentations of scoliosis in children?
    • asymptomatic often
    • asymetey may be noted
  246. presentations of scoliosis in adolescence?
    • often asymptomatic
    • clothing doesn’t fit well, asymmetry may be noted.
  247. presentations of scoliosis in adolescence?
    symptoms of arthritis; backache; neck ache; headache; chest pain; organ dysfunction
  248. at what age are spinal examinating imporant
    around age 10, just before the growth spurt of puberty.
  249. component of a scoliosis evaluation
    • Exclude any underlying etiology
    • Assess the magnitude of the curve
    • Assess the risk for progression
    • History
  250. what components of history are needed for a scoliosis evaluation
    Age of onset, rate of progression, any features of pain, neuromuscular complaints, shortness of breath, family history of scoliosis, current pubertal stage, onset of menarche (girls), any limb trauma history, infection, arthritis.
  251. Forward bending test for scoliosis.
    Patient bends forward with knees extended and then side bends left and then right while physician observes posteriorly for accentuation or improvement of the spinal curve. Functional curves improve or resolve with side bending, whereas structural curves do not.
  252. other name for the pt forward bending test
    the Adams forward bend test
  253. what do you observe and take note of for in a physical examination with spinal examination(8)
    • Observe how arms are hanging by the body
    • Check levelness of occiput, shoulders, iliac crests, PSIS, PIIS, and greater trochanters.
    • Measurement of leg length
    • Run fingers along spinous processes.
    • check for any lower extremity dysfunctions

    • Examination of the skin
    • Any café-au-lait spots and axillary freckling?
    • Any vascular, hypopigmented lesions or a patch or hair overlying the spine?
    • Any skin or joint laxity? Any high arches (pes cavus) or hammer/claw toes?

    • Patient’s height – plot on gender and age specific graph
    • Stage of puberty (Tanner stage)
    • Neurologic examination
    • Normal walking, toe and heel walking, deep squatting, hop on each leg
    • Include abdominal reflex
  254. standing and bent forward at the cervical spine level with chin to chest to assess for scoliosis in the...
    upper thoracic and cervical regions.
  255. upper thoracic and cervical regions.
    thoracic and lumbar spinal regions
  256. Full forward bent position while standing to assess for scoliosis in the....
    thoracic and lumbar spinal regions
  257. How to use scoliometer  and what is its function?
    • The patient is forward bent, for the Adams forward bend test. Then, run the scoliometer along the patient’s spine from cephalad to caudad. If a rib hump is present, the scoliometer ball will deviate away from the midline of the apparatus.
    • It measures the angle of trunk rotation
  258. how does the scoliometer relate to the cobb angle
    • Scoliometer degrees are NOT equivalent to the Cobb angle degrees.
    • General guideline is: angle of trunk rotation of 7 degrees correlates with a Cobb angle of 20 degrees
  259. Inter-rater error for:Thoracic curves
    2 degrees
  260. Inter-rater error for Lumbar curves
    2.2 degrees
  261. Intra-rater error for:Thoracic curves
    1.2 degrees
  262. Intra-rater error for:Lumbar curves
    1.6 degrees
  263. WAT The operator-dependant measurements can include the following sources of error
    • Inconsistent forward bend test performance,
    • Inconsistent localization of the scoliotic curve’s apex
    • The scoliometer degree markings may be poorly visualized due to the size of the deviating ball
  264. what is radiology and what are you looking for with scoliosis?
    standardized standing postural x-ray images

    Looking for any bony pathology, sacral base unleveling, femoral head/iliac crest levelness, and any scoliotic curves – type and severity.
  265. treatment for pt with flexible 20-30 degree curve, with documented progression of 5 degrees or more
    , orthotic treatment is indicated.
  266. Larger curves of 30-40 degrees in growing children, found upon the initial visit, are treated with
    orthotics right away
  267. Treatment for 40-50 degrees curves ? id double major curve?
    surgery or may consider orthotics for double major curves
  268. Treatment for >50 degrees curves
    surgery
  269. how doesw scoliosis affet preganncy
    The scoliotic curve itself does not seem to affect the outcome of the pregnancy
  270. how is scoliosis related to back pain
    slightly increased occurrence of back pain in adults with AIS

    There may be a correlation between the initial magnitude of the curve and later back pain complaints
  271. relationship btwn AIS and degenerative disc changes ?
    Patients with AIS treated with bracing or surgery may also have increased chance of degenerative disc changes.
  272. bracing treatment progression (AIS)
    Bracing treatment, patients followed for 22 years, average coronal curve progression of 7.9 degrees
  273. surgery treatment progression (AIS)
    Surgical treatment, patients followed for 23 years, average coronal curve progression of 3.5 degrees
  274. which curves are less likely to progress?
    <39 degrees
  275. what ratio ofppl have progression with untreated curves?
    2/3
  276. general treatment for scoliosis
    Generally, observation, bracing, and surgery are the main options for treatment.
  277. treatment for mild scoiliosis
    OMT, (Konstantin, per Campell’s Orthopedics) exercises, functional orthotics, education
  278. treatment for moderate scoliosis
    OMT, exercises, education, bracing
  279. treatment for severe scoliosis
    Surgery and adjunctive treatment as above.
  280. OMT goal in the treatment of structural scoliosis is to
    optimize function in the existing structure, not to straighten the curves
  281. OMT treatment for scoliosis d their result
    • Indirect treatment, fascial release, soft tissue treatment to increase general body ROM.
    • Abdominal and Psoas muscle strengthening.Can treat joint somatic dysfunctions as well
  282. what are the two isometric yoga poses that reduce curves in degenretaive IS and AIS
    side plank daily ( Cobb less than 120 and 75

    half moon poses ( complex curves)
  283. For Adolescent Idiopathic Scoliosis (AIS), the goal is spinal curve at skeletal maturity with a Cobb angle of...
    40 degrees or less.
  284. Cobb angle at skeletal maturity is 50 degrees or greater, then these can progress at a rate of..
    1 degree per year after growth ceases.
  285. what is the risser sign for all cures except <20 degrees
    0 to 2
  286. what is the risser sign for <20 cobb angle
    n/a
  287. treatment for <20 degrees
    Observation
  288. treatment for 20 to 29 degrees
    Follow closely
  289. treatment for 20 to 29 degrees with > or = to 5 degrees increase in 3-6 months
    Bracing
  290. treatment for curves 

    30 to 40 degrees
    Bracing
  291. treatment for curves 

    40 to 50 degrees
    Bracing or Surgery
  292. Treatment for curves
    > 50 degrees
    Surgery
  293. contraindication for Bracing
    • Contraindicated in patients who have reached skeletal maturity (Risser 4 to 5, ring apophyses fused)
    • Contraindicated in patients with a Cobb angle > or = to 50 degrees

    Relatively contraindicated in patient’s with a thoracic lordosis
  294. types of braces ? utilization?
    • Underarm arthoses( most comomly used) 
    • Bosoton Brace ( TLSOs; e.g Wilmington plastic jacket, Charleston brace, providence brace) 
    • Milwaukee Breance (CTLSO)( rarely used)
  295. factors that affect Efficacy of bracing
    • more effective with increased hours of daily wear 
    • more effective in females
    • less effective in overweight patients
  296. efficacy of bracing has shown what kind of results
    • mixed 
    • BrAIST” trial is ongoing:randomized trial: comparing bracing and observation in skeletally immature patients
    • Cobb angle between 25 to 40 degrees
  297. Recommended usage for bracing is  and actual usuage?
    Recommended usage of 23 hours per day
  298. why are radiographic of scoiliosis takent
    Is done to confirm presence of scoliosis, to evaluate the type (congenital, neuromuscular, idiopathic) and severity, and to assess the skeletal maturity, in relation to risk for progression
  299. indication for scoiliosis radiograph
    • Scoliometer reading > or = to 7 degrees (may need treatment)
    • Presence of an obvious spinal curve
    • Thoracic or lumbar asymmetry seen on physical examination in skeletally immature children, + family history of scoliosis
    • To monitor progression in patients already diagnosed with AIS
  300. what is the actual percentagle of usage of the brace?
    65%
  301. why would you perform an in-brace radiograph
    look for amount of curve correction
  302. what is the goal for curve reduction of the in brace cobb angle
    20%
  303. when is brace usage stopped? What risser grade?
    • Brace treatment is continued until the end of the growth period;
    • Girls: Two years post-menarche, Risser grade 4 or 5
    • Boys: Risser grade 5
    • Can either stop completely, or wean down to just nighttime usage (orthopedic practitioner clinical choice)
  304. whatis follow-up for post bracing?
    Follow up at six-months post-bracing, and then yearly for a few years. An initial curve collapse (several degrees) will soon stabilize.
  305. What is a poor prognosis of bracing treatment? what is the alternative?
    Progression of the Cobb angle by > or = to 5 degrees during bracing treatment is a poor prognosis for the efficacy of this treatment for the patient, and surgery may be needed in these cases.
  306. how often should bracing be monitored?how should ti be checked? and what is being checked?
    • Monitor the brace treatment every 6-8 months both clinically and with follow up radiographs.
    • Out of brace radiographs are performed to check for any curve progression
  307. what is the orimary and secondary goal for AIS suregry
    • Primary goal = utilizing spinal fusion for prevention of curve progression
    • Secondary goal = partial curve correction, this is frequently achieved
  308. what are the indications for AIS surgery
    • Indications:
    • Skeletally immature patients
    • At diagnosis, patient has curve with Cobb angle of > or = to 50 degrees.
    • Sometimes skeletally immature patients with Cobb angle between 40 to 50 degrees may need surgery.
  309. describe the most common AIS surgery ?
    • Posterior spinal fusion (most common)-
    • Bone grafting and instrumentation
    • Instrumentation has evolved from the Harrington rods (cephalad and caudad spinal connections with hooks), to the modern segmental instrumentation (hooks, screws, wires, rods).
    • Modern instrumentation provides the orthopedic surgeon with more control for positioning of the spine.
    • Most important part of the surgery is obtaining bony fusion
    • Autograft or allograft
  310. Harrington rod implantation is reserved for patients with curves greater than
    45degrees
  311. what is the “crankshaft phenomenon”  and why is it clincally relevant?
    • This phenomenon occurs after a posterior spinal fusion, where the anterior spine continues to grow.
    • This will cause a severe alignment deformity, both rotationally and in the sagittal plane
    • Some evidence that the modern segmental type of instrumentation obviates the need for an anterior spinal fusion
  312. what patients receive posterior spinal fusion with anterior spinal fusion?
    This is sometimes done in skeletally immature patients with open triradiate cartilages.
  313. what is the post operative time pt with Ais surgery have to wat?
    for 9-12 months, sports participation is not recommended.
  314. what sports are not recommened for those with AIS surgery?
    collision sports
  315. what should we look for with staning postural xray
    Looking for any bony pathology, sacral base unleveling, femoral head/iliac crest levelness, and any scoliotic curves – type and severity.
  316. what is a a way to et good spinal mobilization before staning postural xray
    Before sending patient, treat patient with OMT to get good spinal mobilization.Looking for any bony p
  317. why is the standardized standing postural x-ray images use
    Is done to confirm presence of scoliosis, to evaluate the type (congenital, neuromuscular, idiopathic) and severity, and to assess the skeletal maturity, in relation to risk for progression.
  318. Indications for standardized standing postural x-ray images
    • Scoliometer reading > or = to 7 degrees (may need treatment)
    • Presence of an obvious spinal curve
    • Thoracic or lumbar asymmetry seen on physical examination in skeletally immature children, + family history of scoliosis
    • To monitor progression in patients already diagnosed with AIS
  319. Orthopedic referral is not necessary for incidental findings of scoliosis on a chest x-ray, when the Cobb angle measure is
    < 10 degrees.
  320. Indications for REFERRAL to Orthopedic specialist
    • Angle of trunk rotation (scoliometer measurement) of > or = to 7 degrees, and not able to obtain a Cobb angle measurement
    • Cobb angle between 20 and 29 degrees in a premenarchal girl, or a boy age 12 to 14.
    • Cobb angle > or = to 30 degrees in any patient
    • Progression of Cobb angle of more than 5 degrees in any patient
  321. MRI indications
    • Early onset before age 10, with rapid progression.
    • Patient complaints of significant pain associated with the scoliosis:
    • May also need CT or bone scan to rule out bone tumors or infection

    • Associated neurologic s/s:
    • Headache, neck pain, absence of abdominal reflex, asymmetric lower extremity atrophy, pes cavus, midline skin lesions (e.g. vascular, pigmentary, hair patch)
    • Abnormal findings on the plain radiographs:
    • Findings correlating with congenital scoliosis
    • Findings suggestive of intraspinal pathology
    • Increased kyphosis
  322. why is Pa view used for standing postural x-ray for scoliosis
    The PA view minimizes radiation to breasts and thyroid
  323. staning scolisiosi posture xray are taking from what Vt levels?
    From C7 to the sacrum and iliac crest
  324. what position shoudn't standardized standing postural x-ray images be taken in
    supine
  325. How do do Cobb Method
    • A line at the superior border of the highest vertebra inclined towards the concavity, and a line perpendicular to this.
    • A line at the inferior border of the lowest vertebra inclined towards the concavity, and a line perpendicular to this.
    • At the intersection of the two perpendicular lines, the degrees measured here give the Cobb Angle.
  326. a typical curve in AIS is a ..
    double curve, right thoracic and left lumbar
  327. To check for curve progression, it is important at subsequent Cobb Angle measurements to use
    the same vertebrae as the initial evaluation.
  328. examples of neuromuscular etiology
    • Paraspinal masses
    • Hemivertebrae or wedged vertebrae (congenital scoliosis)
    • Vertebral body lucency or erosion of the pedicle
    • Potentially - bone tumor

    • Interpediculate space widening
    • Potentially –
    • Spinal cord tumor
    • Syringomyelia
    • cavitation occurs in the central segments of the spinal cord, usually cervical, with concomitant neurologic deficits, and thoracic scoliosis often present
    • Diastematomyelia
    • abnormal congenital division of the spinal cord by a bony spicule or fibrous band protruding from a vertebrae or two, each of the halves surrounded by a dural sac
    • Spinal dysraphism
    • defective fusion, neural tube
  329. what is the risser sign
    is a visual grading of the degree of ossification and/or fusion present in the iliac apophysis:
  330. Risser sign 0 means?
    – no ossification
  331. Risser sign 1means?
    1 – up to 25% ossification (Risser 1 usually occurs AFTER peak height velocity)
  332. Risser sign 2 means?
    26% to 50% ossification
  333. Risser sign 3 means?
    3 – 51% to 75% ossification
  334. Risser sign 4 means?
    greater than 76% ossification
  335. Risser sign 5 means?
    Full bony fusion of the apophysis
  336. A lower Risser grade, means
    that the patient has quite a bit more growth remaining, and is therefore at a greater risk for a scoliotic curve progression
  337. For bone age/skeletal maturity check x-ray of ( which structures)
    epiphyses of distal radius, ulna, and small bones of the hand (the method of Tanner and Whitehouse)
  338. In girls, the peak height velocity occurs with an
    open triradiate cartilage, before reaching Risser 1
  339. What is the 
    Sauvegrain method:
    Four (4) ossification centers – the lateral condyle, trochlea, olecranon, and proximal radial epiphysis, are scored on a 27-point scale, then plotted on a graph
  340. WIT (simpler) olecranon method
    • The olecranon apophysis is evaluated with regard to the six-month interval radiographic stages observed:
    • Two ossification nuclei
    • Half moon shaped ossification center
    • Rectangular-shaped ossification center (correlates with closure of the triradiate cartilage)
    • Beginning of fusion
    • Complete fusion
  341. which x-ray determines the Risser sign
    Check x-ray of iliac apophysis
  342. which x-ray determines the Tanner and Whitehouse method
    Check x-ray of epiphyses of distal radius, ulna, and small bones of the hand
  343. which x-ray determines the olecranon and simpler method?
    Check x-ray of elbow (assessment of ossification centers in the elbow
Author
Iana
ID
353487
Card Set
Week 11
Description
Head and Neck, Pharm, OMM:Scoliosis, DPR: Cardiovascular, & Physiology of cell signaling and Receptors
Updated