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Holtzman Tech IV
NYCC Holtzman final exam spring 2010 includes DeCicco lecture
| Question | Answer |
|---|---|
| Size and concentration of proteoglycans will | decrease with age |
| The Ks/Cs ratio of proteoglycans will _________ with age (kertain sulfate and chondroitin sulfate). | decrease |
| A decrease in Ks/Cs of proteoglycans with age results in decreased ability to bind to water and therefore leads to | water attraction/hydration |
| The nucleus of a disc will ________ in collagen content and thickness with age | increase! |
| The nucleus of a disc will ____________in collagen-proteoglycan binding and _________ in collagen-collagen binding. | increase, increase |
| Because there is more collagen to proteoglycan binding, there is less binding to water. This means that over time, the nucleus pulposis will | dehydrate |
| The annulus will ________ in collagen content, just like the nucleus pulposis, over the lifetime. | increase |
| Unlike the nucleus, the amount of collagen thickness will ___________ over time in the annulus fibrosis. | decrease |
| The annulus will also see a drop in _________ fibers over a lifetime | elastic |
| The entire disc, (nucleus and annulus fibrosis), become more ________, less _________, | fibrous, resilient |
| distinction between the annulus and nucleus pulposis over time | becomes less and less |
| clinical effect of disc changes over time | decreased mobility of the spine |
| Instead of the nucleus cushioning the weight, the greater share goes to the ___________ over time | annulus |
| Increased stresses on the annulus leads to | cracks and fissures |
| Do discs normally increase or decrease in height with age? | Increase up to 10% |
| If the disc is actually increasing in height over time instead of shrinking, where is the height loss coming from? | decrease in vertebral body height |
| What structure around the disc becomes weak over time due to decreasing permeability for nutrients to enter? | vertebral end plate |
| What determines what tissues fail during a compressive load? | Age of patient |
| a child 4-6 compressive load fail | annulus but no crack |
| teen 15-17 compressive load fail | vertebral endplate (resulting in Schmorl's nodes as an uncontrained disc lesion) |
| young adult 20-50 compressive load fail | fusion, annular fibers bear weight, cracks develop in annular lamellae, dehydration, ANNULUS FIBROSIS DISC HERNIATION or disc lesion |
| contained disc herniation | not totally extruded nuclear material |
| sequestered disc herniation | piece of nucleus broken off |
| uncontained disc herniation | totally extruded nucleus pulposis |
| why does bone density increase over time? | the traebecular/spongy bone thickens but also loses mass |
| Why does the load-bearing capacity of vertebral body decrease with age? | traebeculae has changed so cortical/lamellar around perimeter has to take on load |
| how do vertebral body endplates deform? | the endplates bow in, giving the bodies a concave shape |
| when the VBE's bow in, what happens to the discs? | become fish-body shape |
| how do the VBE's continue to change after bowing in? | form osteophyte/spicules at the interface with the disc |
| The sclerosing of subchondral bone and the thickening of articular cartilage happens at the | facet joint |
| When focal areas of erosion and thinning cartilage at the facet occur, what does it use as a filler? | fibro-adipose tissue |
| where do osteophytes form at the facet joint | along attachment sites of capsue and LF to the SAP (ligamentum flavum and Superior articular process) |
| If osteophytes affect the superior articular facets, what happens to the inferior articular facets? | form wrap-around bumpers |
| why do wrap around bumpers occur at the inferior articular facet? | irritation |
| what do wrap around bumpers provide for the inferior articular facet of the joint complex (the superior vertebrae)? | protection against torsional loads |
| Posterior aspect of facet capsules in lumbar spine are actually part of the | ligamentum flavum |
| Posterior facets in lumbar spine are part of the ligamentum flavum and therefore, have more motion. What does this quality allow pathologically? | osteophytes only form on side of the SUPERIOR articular facet |
| facet tropism | any level of asymmetry creating a biomechanically unstable spine |
| Superior articular processes always lie _________ of the inferior articular process | outside |
| imbrucation | facet jamming |
| osteophytes only form around the ___________ articular process and capsule | superior |
| change in length of shape of protenaceous tissue held out of shape for a time | creep |
| the energy change after creep | hysteresis |
| the new shape of the joint after hysteresis | set |
| what may become entrapped/extrapped in the joint capsule? | meniscoid |
| movement wise, there is a progressive decrease in _____ | ROM |
| what is the decrease in ROM of facet joints due to? | increased stiffness in the discs (dehydration and fibrosis) |
| facets show a greater amt of creep and hysteresis but also greater set after deformation. Why? | set because of decreased water-binding capabilities |
| why isn't osteoarthritis/DJD true arthritis? | "itis" means inflammation and there is no inflammation assoc with osteoarthritis/ DJD |
| when DJD occurs to a disc and facet joint, what is it called? | spondyloarthrosis |
| number one cause of disability in the US | arthritis (all forms) |
| most common form of arthritis is osteo. Why is it not considered a true arthritis? | "itis" means inflammation. No inflammation with DJD/osteoarthritis |
| DJD/osteoarthritis is characterized by breakdown of __________ cartilage at synovial joint surfaces, primarily in the weight bearing joints | hyaline |
| in the spine, what joints sufferf from DJD/osteoarthritis loss of hyaline cartilage | zygaphophyseal/facet joints |
| In DJD/osteoarthritis, at the __________ joints (non-synovial), the same sclerotic changes occur at the bony margins. | interbody (non-synovial) |
| DJD leads to further decreases in water and water-binding ____________ | proteoglycans |
| DJD/osteoarthritis leads to dehydration and decreased ability of disc to handle | weight-bearing stress |
| DJD/osteoarthritis can lead to | lumbar-canal spinal stenosis |
| what can lead to lumbar-canal spinal stenosis? | DJD/osteoarthritis |
| what type of DJD/osteoarthritis is fairly common in older adults and slightly more common in males than females? | spinal canal stenosis |
| Spinal canal stenosis can occur centrally or laterally: what happens laterally? | Lateral RECESS stenosis - most common casued by arthritic changes to facet joints. Leg pain, flexing forward mitigates pain. |
| Uncontained disc lesions can _________ the spinal canal | narrow |
| failed surgical back syndrome (post laminectomy) can cause | anklosing spondylitis |
| The cause of DJD is primarily ___________ | mechanical but rarely can be metabolic |
| Is DJD part of the normal aging process? | no! |
| DJD is most commonly found in | middle aged, but can be found in the young |
| Before age 55, what is the incidence of DJD between the sexes? After 55? | even, higher in women after 55 |
| How is DJD diagnosed? | x-ray studies look for narrowing of joint spaces and sclerosing of joint margins, and osteophyte information |
| Big 3 seen on x-ray to diagnose DJD? | narrowing, sclerosing, osteophytes |
| other tests done for DJD? | blood tests by MD's but not for DJD - just to monitor effects of meds they give for DJD. Not a diagnostic tool. |
| Treatment of DJD via medical | NSAID's, Cox-2, Steroids, Synthetic joint fluids, surgical replacement, Glucosamine and chondroitin sulfate |
| surgical treatment of DJD leads to | dislocation, infection, sciatic nerve palsy, fracture of pelvis |
| __________- "It's what we do." | Adjust |
| passive chiro mgmt for DJD | adjust to preserve joint motion and correct biomechanics, Modalities like Manual resistance tech, ultrasound, heat/cold, Exercise and pilates, yoga, Weight loss, Nutrition (glucosamine and chondroitin -don't forget the water!), MSM |
| what IS degenerative joint disease? a disease process? | NO, it is an ACTIVE process, not a disease process. It is an adaptive response to STRESS. A morphological change that progresses with the aging process, but not due to age itself. |
| DJD is not a disease process. It is an __________ process! An adaptive response to stress. | Active |
| DJD can be the adaptive response to the stresses of: __________ or _____________ aberrations. | trauma or biomechanical aberrations |
| Single most common source of DJD? | soft tissue |
| Soft tissue is the single most common source of | DJD |
| what kind of muscles tend to become hypotonic and weak? | phasic (fast twitch) muscles |
| phasic muscles are | fast twitch |
| fast twitch/phasic muscles become hypotonic and weak when __________ muscles become hypertonic and tight | anti-gravity/postural muscles |
| What kind of muscles become hypertonic and tight in the face of gravity? | postural/anti-gravity muscles |
| Degree of hypertonicity or hypotonicity varies between patients but rarely in | distribution |
| increased hypertonicity causes further weakness in the antagonist | Sherrington's Law of reciprocal inhibition |
| Sherrington's Law of Reciprocal Inhibitions states that increased _____________ causes further weakness in the ______________. | hypertonicity, antagonist |
| Quadriceps and Hamstrings would be contenders for Sherrington's Law of Reciprocal Inhibition. Why? | Quad threshold decreases and activity increases(postural, anti-gravity) so hamstring motion (antagonist) is shut out |
| which muscles should you treat first: postural or antagonist? | short, tightened ones before you strengthen the weakened ones |
| Muscular imbalance causes joint ______ and dysfunctional ______ | instability, motion |
| As the threshold of the hypertonic muscle decreases (from being "on" all the time), it's activity __________, shutting out the antagonist's motion altogether. | increases |
| How are postural muscles activated? | movement! |
| poor muscle balance in postural muscles increases | activation |
| Muscles affected by _____lesions are the same muscles that display hypertonicity as a result of poor movement patterns and posture | CNS |
| CNS- difference in control between ______ and _______ muscles | phasic (short-twitch, hypotonic, weak), postural (slow-twitch, anti-gravity, hypertonic) |
| UMN lesions of the CNS affect the same muscles that would be affectex by poor __________patterns and __________. | movement, posture |
| muscle that is a prime mover | agonist |
| stabilizer muscle; allows extremity to return to normal position | antagonist |
| help agonist with desired motion | synergist |
| neutralize agonist motion to create smooth motion | synergist |
| maintain body position to allow motion to occur | stabilizers |
| pectorals | lats |
| anterior deltoids | posterior deltoids |
| traps | deltoids |
| abdominals | erectors |
| quadriceps | hamstrings |
| gastrocs | tibialis anterior |
| biceps | triceps |
| forearm flexors | extensors |
| with Isometric contraction, the stabilizers are/are not changing position? | not |
| no movement takes place, load on the muscle exceeds the tension generated by the contracting muscle | isometric (no movement/stabilizer/antagonist) contraction |
| tension generated by the contracting muscle exceeds the load on the muscle | isotonic (prime mover/agonist) contraction |
| muscle shortens against opposing load | concentric contraction is isotonic |
| muscle lengthens as it resists a load | eccentric contraction is isotonic |
| viscolastic change due to prolonged shortening | Long-term hypertonicity |
| Long-term hypertonicity is not _________ | spasm |
| visco-elastic changes due to prolonged shortening | long-term hypertonicity |
| Can a tight muscle be stretched to its orginal length? Why or why not? | no, there is long term visco-elastic change called adaptive shortening |
| adaptive shortening | joint with decreased ROM, permanently shortened muscle, DJD may result from lack of nutrition from lack of joint movement |
| muscle shortening may be painful upon palpation, does not allow the full joint ROM, and does not register any ________________. | electrical activity during contraction |
| initially, this sort of muscle will be ok but after 20 years will lose the ability to contract. The muscle becomes weak as the result of constant shortening. | tightness weakness |
| in a ________ muscle, the strength intensifies early on (mild to moderate tightness) but the muscle becomes weak as a result of constant shortening. | tightness weakness |
| If tightness weakness occurs in the agonist muscle, what occurs in the antagonist muscle? | stretch weakness - weakness from remaining in an elongated/stretched position |
| Stretching the shortened muscle (actively) will eventually lead to more muscle strength and reduced ? | inhibition of the antagonist |
| sedentary lifestyle, chronic postural overload, bio-mechanically incorrect workstations, repetitive trauma are all causative factors in | muscle tightness |
| what improves the length of the muscle and strength of the antagonist muscle? | stretch |
| a hyper-irritable spot found within a taut band of skeletal muscle or its fascia which, when provocatively compressed, will give rise to characteristic referred pain, tenderness, and autonomic phenomena. | Trigger point definition from Janet Travell |
| where can trigger points occur? | Hypertonic muscles, Hypotonic muscles |
| R belly of soleus is an ipsilateral ______ trigger point | SI |
| how can hypertonic muscle trigger points develop? | painful joints (from sprain/strain), muscle spasm/guarding |
| In hyPOtonic muscles, how do trigger points develop? | reciprocal inhibition (Sherrington's Law), trauma, limbic system hyperactivity (traps), overuse |
| Describe lower (distal) crossed syndrome | anterior pelvic tilt, increased lumbar lordosis, large gut |
| Lower (Distal) Crossed syndrome big 3: | anterior pelvic tilt, increased lumbar lordosis, large gut (basically sway-backed and fat) |
| what muscles are hypertonic in lower crossed/sway back and large gut syndrome: | Psoas and Rectus Femoris due to anterior pelvic tilt so gluteus maximus inhibition. Lumbar erectors hypertonic due to fat so inhibition of rectus abdominis and increased lumbar lordosis. |
| Name the 3 hypertonic muscles of lower crossed syndrome: | psoas, rectus femoris, erector spinae of lumbar |
| Name 2 inhibitors of lower crossed syndrome | gluteus max, rectus abdominis |
| What joints bear the load in lower crossed syndrome? | L4/5, L5/S1 facets |
| How to evaluate for lower crossed syndrome: | hip extension with patient prone (excessive hip extension stress the lumbosacral jt.) |
| Describe upper (proximal) crossed syndrome: | the computer syndrome: forward head carriage, upper cervical extension, lower cervical flexion, elevation and protraction of shoulders, winging of scaps |
| hypertonic muscles of upper crossed syndrome | SCM, upper trap, levator, pecs, suboccipitals |
| what muscles are inhibited in upper crossed syndrome? | deep cervical flexors, rhomboids, serratus anterior, lower and mid traps |
| affects stability, motion, fx of all joints of the shoulder girdle, thoracics, and the cervical spine | upper crossed syndrome |
| what is necessary for normal joint fcn? | normal muscle function |
| Hip extension optimal range | 10-15 degrees of hip ex. is optimal for gait |
| what should happen during hip extension | lumbar spine should engage for stability before any lower extremity movement |
| when patient is prone, external rotation of feet indicates: | gluteus maximus |
| when patient is prone, INternal rotation of feet hanging off table indicates | inhibition of gluteus max |
| Hip extension test | Patient prone, observe feet, ask patient to lift leg 6" off table without bending knee. |
| If lumbar extension occurs with hip extension test, indicates: | gluteals, abdominals or both are weak |
| If patient demonstrates lumbar extension of the spine during hip extension test, what joint is under duress? | L5/S1 |
| Trunk flexion test | patient curls up, flexing head, then chest as if doing abdominal crunch |
| If hip flexion is observed during trunk flexion test, what is pathology? | weak abdominals (ie, in order not engage iliopsoas and do your sit ups with it, you must not raise above the half-crunch level. This ensures rectus abdominis is doing the work) |
| tests for hip abductor stability | Trendelenburg's test |
| what percentage of gait is on one leg? | 85% |
| What is positive Trendelenburg's sign? | if hip shifts anterior (pelvic tilt) and lateral or patient laterally flexes to side of standing leg, test is positive for gluteus medius and minimus weakness |
| when looking for imbalance, note whether or not the body deviates from the norm upon attempted | normal motion |
| when assessing for aberrant motion, one observes whether or not the motion is carried out in the | desired direction |
| If the movement is smooth and at a constant rate, what muscles are functioning properly? | eccentric contraction of the antagonists |
| what kind of contraction guarantees a motion will be smooth and at a constant rate? | eccentric contraction of the antagonists |
| movement follows the _________ path possible | shortest |
| Direction of movement is determined primarily by ___________- and secondarily by _____________ | antagonists, synergists |
| what muscles determine direction? | antagonists, synergists |
| what muscles determine precision? | neutralizers |
| strongest arc degree in nature | 60 degrees (human pelvis, Roman arches, VW bug!) |
| what ligaments provide pelvic stabilization? | posterior SI ligaments, sacrotuberous, sacrospinous |
| describe the posterior SI ligament | sacrum to PSIS, runs laterally with sacrotuberous ligament, medially with thoracolumbar fascia |
| describe sacrotuberous ligament | inferior lateral sacrum to isch tube, MOVES CAUDALLY WITH BICEPS FEMORIS |
| describe sacrospinous ligament | inferior border of sacrum and superior aspect of coccyx to ischial spine |
| posterior movement of the sacral base is restricted by | sacrotuberous and sacrospinous ligaments |
| Anterior movement of the sacral base is restricted by | posterior sacrospinal ligaments |
| which ligament stabilizes L4,L5,S1 | Iliolumbar ligament |
| do muscles surrounding the SI directly contribute to its motion? | no |
| what may be affected by biomechanical changes or stresses in the muscles and vice versa? | mechanical behavior of the muscles |
| impairment in form and force closure leads to | gait problems |
| no external forces necessary for stability (mortise and tenin friction joint) | form closure |
| added lateral compressive forces to reduce shear load | force closure |
| what is at a 90degree orientation to SI joint and provides compression forces? | Gluteus Maximus |
| what is required for SI stability? | ligament and muscle stability |
| why does nutation cause stress on the ligaments of the SI? | because most of them are posterior |
| loads most sacral ligaments | nutation |
| which ligaments of the SI approximated posterior portions of the ilium and cause compression | interosseous |
| ligament that contains excessive nutation | sacrotuberous |
| ligament that restricts counter nutation | long dorsal SACROILIAC |
| swing phase: muscles and fascia pulled caudally | initial step |
| swing phase: ilium moves posterior and PSIS approximates the 2nd sacral tubercle | later step |
| what happens once the first ilium moves posterior in swing phase and the PSIS approximates the 2nd sacral tubercle? | the other ilium moves anterior and the PSIS rotates away from the 2nd sacral tubercle |
| in the swing phase, the sacrum nutates slightly on the side of the _________ ilium rotation | posterior (initial) |
| why does the sacrum nutate on the posterior ilium side during swing phase? | creates pelvic stability for heel strike |
| Flexion restriction of SI or Extension restriction of sacral base on one side makes __________ abnormal | heel strike |
| what SI movements make heel strike irregular or pathological? | flexion restriction of SI or extension restriction of sacral base |
| swing phase: loads sacrotuberous ligament, multifidus, erectors (sacral) | hamstring activation |
| swing phase: contracts to maintain dorsiflexion | tibialis anterior |
| coupled with peroneus longus (like a stirrup) to create a longitudinal sling and transfer energy between pelvis and lower extremity | tibialis anterior |
| During heel strike, initially the _________ inverts and the tibialis anterior moves from _________ to _________ contraction. | calcaneous, concentric, eccentric |
| during middle heel strike phase, the calcaneous is neutral, the tibia-talus bisect the ___________ at 90 degrees to the floor, and the ________ internally rotates. | Achilles, tibia (along with femur) internally rotates |
| How is tibia internal rotation (along with femur) initiated during mid heel strike? | via knee flexion (popliteus) |
| Tibia has medially rotated due to flexion of knee. What happens to fibula during mid heel strike? | drops inferiorly and INCREASES tension on the SACROTUBEROUS ligament and HAMSTRINGS |
| dysfunction of the _____________ increase in tension on the sacrotuberous ligament and hams affects pelvic/spinal biomechanics | fibula |
| Longitudinal muscle sling around talocrural jt: (3) | tibialis anterior, fibularis longus, biceps femoris |
| what muscle extends the femur and rotates the sacrum towards the ilium of stance leg during mid heel strike? | biceps femoris |
| which muscle contributes to early sacral nutation during mid heel strike? | biceps femoris |
| what muscle, besides biceps femoris, will also pull the sacrum into nutation durin mid heel strike? | multifidus |
| To complete the heel strike, the biceps femoris, multifidus and ___________ are added in. | erectors |
| In the final heel strike, the talus engages into __________ flexion, adduction, and internal rotation. | plantar |
| In the final heel strike, the talus engages into plantar flexion, ____________ , and internal rotation. | adduction |
| In the final heel strike, the talus engages in plantar flexion, adduction, and ____________________________ | internal rotation |
| the final heel strike is concurrent with full rear-foot | pronation |
| which bone is the final heel strike dependent upon, if not the talus engaging in plantar flexion, adduction and internal rotation? | the tibia! |
| why is full rear-foot pronation difficult? | conVEX POST facet and concave others on calc |
| what is the final step of heel strike | closed kinetic chain portion of single-support phase |
| continuous tension on latissimus dorsi will cause | upper crossed syndrome |
| positive translation of the head along the ___-axis will occur as the shoulders move anteriorly | z-axis (forward head carriage) |
| what happens when postural fault of anterior head carriage? | shortened stride length, impairment in fx of cardiac and respiratory systems |
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