Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Chiro theories

Dr. Well's Chiropractic Theories Exam 1 1st half

What is the 3 phase of model of VSC? Subluxations begin a degenerative process that ends in permanent changes if not corrected. Basis of maintenance and preventative models of care.
What is VSC phase 1? Segmental dysfuction hypothesis
What is VSC phase 2? Instability hypothesis Injury or congenital
What is VSC phase 3? Immobilization Degeneration hypothesis; typically go from 1 to 3 w/o going through 2
What words should you associate w/ VSC phase 1, 2 and 3? 1: inflammation and segmental dysfunction 2: instability 3: stabilization and immobilization
What was Palmer's first hypothesis? The 1st theory was inflammation, which was, "the result of displacement of any body part: n., a., or v., bone, ligament or m.
How did DD refine his hypothesis? "Luxation on bones cause disease". He believed mm. nn. and bones were the key in displacement causing pressure which could be relieved w/ adjustments.
What did DD believe put "pressure" on the nerves? Articular structures most important sources (After Renwick's hot arm).
What does innate mean? Born with
What did DD add to his theory after asserting the superiority of the nervous system? Vibratory theory: nerves vibrated ormally at 200 per minute representing the tone of the NS.
According to DD what causes BOP? Accidents Poisons Toxins Stresses
What were BJ's 4 criteria for subluxation? 1. Misalignment of vertebra in relation to adjacent segments 2. Occlusion of a foramen including the canal 3. Pressure on nerves 4. Interference to transmission of mental impulse supply
What did CO Watkins do for chiropractic history? Advocate of applying the scientific method to chiropractic practice, research and education to show evidence.
What did Marcel and Henri Gillet and do for chiropractic history? Revitalized the LPS concept of lack of proper joint motion.
What did Fred Illi do for chiropractic history? Discovered the intraarticular sacroiliac ligament.
What did Dr. Thomas Brown do for chiropractic history? coined the term "spinal irritation"
What did Dr. J. Evans Riadore do for chiropractic history? Irritation of spinal nerves; probably the contemporary father of the nerve compression hypothesis
What did AR Renwick do for chiropractic history? DD adjusted him b/c right arm was hot but left arm became hot afterwards and DD believed he adjusted him too much.
What did Solon Langworthy, Oakley Smith and Minora Paxson do for chiropractic history? Made LSP text saying BOP model, by Palmer, was too old. Joint fixation a better model to distinguish medicine and osteopathy from chiro.
What did Tom Morris do for chiropractic history? in Morikubo case. Used LSP text to defend that chiropractic used for his client is different from medicine and osteopathy.
What did Joy Lovan do for chiropractic history? Objected DD's introduction of x-ray; left Palmer school w/ 50 students to form Universal College of Chiropractic down the street. Made detailed Meric system.
What did Alva Gregory do for chiropractic history? Accepted the Palmer hypothesis (BOP) w/o metaphysical thinking. He emphasized the effects of mechanical interference on the excitability, conductivity, reflexivity and efferent transmission of nn. at the IVF.
Whad did Verner, CW Weiant and RJ Watkins do for chiropractic history? Admonished chiropractic for dogmatic adherence to Palmerism
What did Irvin Hoff do for chiropractic history? Osteopathic researcher who published data related to axoplasmic flow during nerve compression.
What did Coulter do for chiropractic history? Talked down to chiropractic saying it doesn't look at data that goes against Palmerism. He suggested we research focusing on the body as a self healing organism w/o metaphysical things.
What characteristics count towards a good theory? (5) 1. Predict novel observations 2. Explain observed phenomena 3. Testable/falsifiable 4. Eloquent 5. Should be naturally explained
What is the independent variable (Leach)? The adjustment
What is the mediating variable? SDF (VSC phase 1)
What is the dependent variable? Improvement of pain or function
Clinical trials on the effectiveness of spinal manipulation, have they used the term "subluxation" according to Nelson? No, previous studies have not used subluxation at all.
What sort of reasoning is used when assuming there is a lesion chiropractors treat w/o that lesion being verified? Many chiro.s believe a lesion does exist d/t their education of anatomy, neuro, etc. Based on the article (Nelson) all science and spine related facts are being used to validate the existence of the lesion but proof is never shown.
What does Nelson say about defining subluxation by consensus vs. reality and validity of subluxations? It is useless and all debators are more concerned w/ being right rather than rethinking and applying science (physiology) to their definition.
What doesn't the VSC model accomplish as a proposed theory? (Nelson) Doesn't provide a coherent understanding of relationship b/w spinal dysfcn and health, a clinical phenomenon, predictions can't be made b/c it doesn't draw conclusions, is not testifiable or falsifiable. Can't be shown as false by new evidence = no theory
What are problems w/ Nelson's conclusion that a theory should be falsifiable? A problem is that not all theories can be tested. In order for a theory to be useful in the healthcare sense he does have a point.
What is tautology? A circular type of argument that validates itself by renaming accepted principals or beliefs as a new theory or principle.
In Nelson's view do clinical studies on manipulation offer any insight into subluxations? No, clinical studies just focus on treatment by Chiropractic in comparison to other forms of care.
What are the necessary characteristics that would make a genuine subluxation theory? (6) Should: 1. Bear some resemblance to its history 2. Be testable (no innate) 3. Be consistent w/ current basic scientific precepts and principles 4. Reflect current practice and educ. standards 5. Clincally meaningful 6. Distinct and unique point of v
What were Nelson's modifications to Palmer's original theories on subluxations? (4) 1. Less emphasis on innate 2. The manipulation is not as "almighty" as it once seemed. 3. Expands BOP model 4. Shifted away from pinched nerve theory and into somato-visceral reflexes
What are the 4 testable hypotheses? 1. Differences in health can be related to diff. in spinal fcn 2. Spinal dysfcn at x, y, & z related to more of cond'n w 3. Ability to reliably identify and categorize spinal dysfcn that relate to cond'ns 4. Specific manip. better than nonspecific mani
What occurs in tissue w/ injury? Infiltration of histamine, protein derived factors, eicosanoids, proinflammatory cytokines, NO, degradative enzymes and substance P into tissues are caused by injury.
What are leukotrienes? An eicosanoid, product of arachidonic acid
What are proteoglycans? Product of arachidonic acid. TXA2 vasoconstricts and platelet aggregates and PGI2 does opposite. Inflammation destroys PGs and those pieces induce inflam.
What does platelet activating factor do? Causes platelets to aggregate, mediator in anaphylaxis, inflammation and bronchoconstriction.
What does cyclooxygenase activate? proteoglycan pathway
What does lypooxygenase activate? Leukotriene pathway
What does aspirin do? Blocks cyclooxygenase.
What do cytokines do? Regulate inflammation and immune responses. Says "cell can no longer function and needs to die."
What does interleukin do? Stimulates synthesis of proteases, proteoglycans, NO (vasodilates), and CK (high in joints)
What do tumor necrosis factor, chemokines and tissue growth factor do? Bind to receptors to start processes (autocrine, endocrine, paracrine)
What does substance P do? Neuron protein that functions as nt, associated w/ anxiety, stress, neurogenesis, vomiting, pain or nociception. Stimulates cell growth in culture Potent vasodilator b/c releases NO from endothelium can -> hypotension
What are arthritides? Inflam destroys PGs and those pieces induce inflammation. Inflam includes tissue remodeling which may cause loss of function in long term.
What are the characteristics of acute inflammation? Visible signs, often w/ vascular damage, capillary walls allow exudates. Cell level: mast cell, leukocytes, macrophages (chemotaxis). Histamine (vasoconstrictor), protein derived factors (complement system, kinin system, coagulation system)
What are the characteristics of chronic inflammation? Infiltration of lymphocytes and macrophages w/ angiogenesis and connective tissue proliferation.
What are the clinical characteristics of inflammation? Rubor (redness) Tumor (swelling) Calor (heat) Dolor (pain) Functio Laesa (Loss of function)
What does diapedesis mean? process of WBCs when they penetrate the basement membrane out of a blood vessel and undergo chemotaxis
What does opsonization mean? a function of the complement system, tags bacteria as foreign for macrophages to destroy.
What does autocrine mean? chemicals made from cell to interact w/ itself
What does paracrine mean? Chemicals made from cell to communicate w/ adjacent cells
What does endocrine mean? Chemicals made from cell that act on cells far away (travels a distance)
What is involved if myopathology occurs before segmental facilitation occurs? Afferent and efferent nerves Joint receptors Muscle receptors Posterior facet joints Inflammatory triggers and noninflammatory triggers
Describe Group I afferent nerve fibers. Largest, thickly myelinated, fastest, not in skin, proprioception, kinesthesia
Describe Group II afferent nerve fibers. Medium sized, thickly myelinated, fast, A-beta in skin proprioception, mechanical
Describe Group III afferent nerve fibers. Small, thinly myelinated, slow, A-delta mechanical, heat, cold, nociception
Describe Group IV afferent nerve fibers. Smallest, unmyelinated, slowest, C mechanical, heat, cold, nociception
What are the efferent nerve fibers? (2) Alpha motor neurons: myelinated, innervate force-producing extrafusal muscle; larger, faster Gamma-motor neurons: innervate the intrafusal fibers; smaller, slower
What are the joint receptors? Group II-IV neurons respond to chemical and mechanical changes near facet joints. Some respond to movement w/in physiologic range and others might respond to greater force. Some respond to directions of movement.
With joint receptors describe how nociceptive chemicals can act. Various nociceptive chemicals like substance P can alter the threshold of the mechanoreceptors, causing them to fire in an attempt to modify nociception.
What acts in concert to regulate muscle stiffness? Muscle spindles and golgi tendon organs may act in concert to regulate muscle stiffness. i.e. ratio of muscle tension change to muscle length change
Describe what group Ia does as a muscle receptor. Primary muscle spindle afferents; they respond to stretch and probably signal the rate and magnitude of change in muscle length. They are inhibited by muscle contraction.
What does Group Ib do as a muscle receptor? Golgi tendon organ afferents; respond to muscle tension and low levels of force during active muscle contraction.
What do group II afferents do as a muscle receptor? Mostly secondary m. spindles that respond to m. stretch and are inhibited by m. contraction. Respond to change in m. length (tonic response) but not so much to the rate of change in length (phasic response)
What do non-muscle group II afferents do? Innervate muscle, joints and skin
What do group III and IV afferents do as a muscle receptor? Considered together d/t their similarity. C fibers (IV) most well known pain receptors. Have highly specific responses to chemical and/or mechanical stimuli.
What can SMT do to muscle receptors? Might modify the discharge of group I and II afferents.
How does Golgi Tendon Organ react to SMT? silent at rest and more activated by impulse of SMT than by preload before the thrust.
Describe type I/slow twitch fibers. Have more mitochondria, store O2 in myoglobin, rely on aerobic metabolism, have greater capillary to volume ratio and associated w/ endurance; produce ATP more slowly. Marathon runners tend to have more type I fibers d/t training and genetics.
Describe type II/fast twitch fibers. Fewer mitochondria, capable of more powerful (but shorter) contractions, metabolize ATP more quickly, have a lower capillary to volume ratio, and more likely to accumulate lactic acid. Weightlifters and sprinters have more type II fibers.
What is a motion segment in reference to facets? 2 adjacent vertebrae, IVD, and soft tissues that cross or connect the 2 vertebrae.
What is the anterior part of a motion segment in reference to facets? Vertebral bodies, IVD, and anterior and posterior longitudinal ligaments.
What is the posterior segment in reference to facets? SP, pedicles, lamina and articular facets, posterior paraspinal muscles and ligamentum flavum.
Describe a facet joint. True diarthrodial w/ posterolateral fibrous capsule that has reinforcing strands from the interspinous ligament; there is synovial lining and a medial capsule formed by ligamentum flavum. It has the property of shock absorption.
What is joint derangement d/t ligamentous and capsular instability as a model of facet pathophysiology? Foraminal encroachment; intra-articular synovial fold inclusions; impingement of the superior articular process against the pedicle above and lamina below. (Hadley)
What facet pathophysiology was researched by Schmorl and Junghann? Degenerative change w/in the joint and meniscal "incarceration".
What facet pathophysiology was researched by Jackson? Joint effusion w/ capsular distention.
What facet pathophysiology was researched by Haldemann? Joint effusion w/ direct diffusion as a cause of nerve root pain.
What facet pathophysiology was researched by Farfan? Joint adhesion
What did Giles study in models of facet pathophysiology? Lumbar z-joints and favored release of trapped intra-articular fold and stretching the joint capsule as a likely mechanism for why adjusting the spine works.
What are the models of facet pathophysiology? (6) 1. Joint derangement 2. Degenerative change 3. Joint effusion w/ capsular distention 4. Joint effusion w/ direct diffusion 5. Joint adhesion 6. Z-joints
What are Z-joint meniscoids? Contain variable tissues such as vascular fibroadipose, synovium, calcified tissue, fibrocartilage and chondrocytes in the process of calcification. Might cause chronic SDF; mech. could explain "acute locked back"
What are the hypothesized pathophysiological effects of trapped meniscoid? (4) 1. Joint capsule tension -> more mechanoreceptor activity 2. Capsular adhesions form 2ndary to joint hypomobility 3. Biochem change: GAG lost from cartilage and lig. related to jt 4. Deg. changes occur early as normal stresses apply to the dysfcn'l jo
What are the hypothesized pathological effects of trapped meniscoid? (4) 1. Joint capsule tension 2. Capsular adhesions 3. Biochemical alteration 4. Degenerative changes
What is joint capsule tension as a pathological effect of trapped meniscoid? Results in increased mechanoreceptor activity; results in increased nociception, lowering pain threshold and creates pain-spasm-pain cycle.
What are capsular adhesions as a pathological effect of trapped meniscoid? Form secondary to joint hypomobility; results in capsule contracture and connective tissue growth across the joint space which obliterates the cavity.
What is biochemical alteration as a pathological effect of trapped meniscoid? GAG lost from cartilage and ligament related to the joint including end plates.
What are degenerative changes as a pathological effect of trapped meniscoid? Prematurely occur as normal stresses apply to the dysfunctional joint; results in bone loss w/ increasing hypomobility.
What current research is being done on the pathological effects of trapped meniscoid? Using small animal models is ongoing using rat spine, rat tail and the inducement of facet pathophysiology by fixation.
Created by: kabrown