Dysfunction and pathologies - Osteopathy Flashcards
Lower back pain is a difficult process and a major causes of disabilities. Briefly explain why, and what would be your approach to abord the problem:
- Any structure of the lumbar spine and low back that receive innervation can be source of pain, muscles, ligaments, tendons, fascias, facet joints, disc, dural sleeves of nerves and bone.
- Experimental studies have shown that back muscles, interspinous ligaments, dura mater, zygapophysial joints can produce local and referred pain.
- However proving the exact cause of pain in the low back isn’t a easy tasks and required a multifactorial approach to reach proper diagnostics.
- Rule out serious pathology, tumours, infections or fractures.
- work systematically patient history, screening, and clinical diagnostic test.
Explain the pathology of degenerative disc disease:
Notes: lumbar vertebral highly susceptible of herniation due to tremendous forces, through the movement of the upper body.
DDD is a natural part of ageing, discs exhibits changes in their discs consistent with a greater and lesser degree of degeneration. The degeneration can create a nerve root compression from development of osteophytes. Disc herniation or prolapse can generate both local and radiating pain and nerve compression such as weakness and sensory symptoms in legs and feet.
Often associated with osteoarthritis of the spine which is sometimes referred to as spondylosis. Nociceptive nuclear material tracks and leaks through the outer rim of the annulus which is the main source of discogenic pain. The disc loose its height and the neighbouring structure ligaments flavour, facets joints and the shape of neural foramina begin to degenerate. In consequence, it become the main cause of spinal stenosis and radicular pain.
Tears can be accompanied by endplate separation or failure, interrupting blood supply to the disk and impairing nutritional supply and waste removal. Such changes may be the result of repetitive micro trauma.
Studies suggest proteoglycan destruction may result from an imbalance between the matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1). [4, 5, 6] This imbalance results in diminished capacity for imbibing water, causing loss of nuclear hydrostatic pressure and leading to buckling of the annular lamellae. This phenomenon leads to increased focal segmental mobility and shear stress to the annular wall. Delamination and fissuring within the annulus can result.
Explain the pathophysiology of radiculopathy:
Give examples of lumbar radiculopathy:
- any condition that create nerve root impairment and or inflammation that has progressed to the stage of neurologic symptoms in the areas that are supplied by the affected nerve roots.
- Most common symptom of lumbar readiculopathy is sciatica, from nerve root L4-S3 that radiate along the buttocks, legs and feet. sensory symptoms are more common than motor. Muscle weakness will be sign of a more serious nerve compression. The pain can be dull, aching, difficult to localise, to sharp, burning and easy to pinpoint.
- Radiculopathy can create hypersensitivity to touch as well as numbness in the dermatomes supplied by nerve root.
- Most common nerve root compression is L4-L5 due to the narrowing of the posterior longitudinal ligament at L4-5 segmental level.
- Causes of radiculopathy can be herniation, tumours, exostoses, spinal stenosis or infection.
Describe the process of inflammation:
Inflammation is the response intended to eliminate the initial cause of cell injury, remove damaged tissue and generate new tissue.
It is initiated by the constellation of systemic manifestations generating redness, swelling, heat, and pain.
It is characterised by the exudation of fluid and plasma component and emigration of leukocytes, neutrophils into the extravascular tissue. If chronic, associated with proliferation of macrophages, blood vessels, fibrosis and tissue necrosis.
It includes a vascular phase where there is vasodilation of the arterioles and venules and increase capillary blood flow creating redness and heat.
Cellular phase is the delivery of the leukocytes in the site of injury.
Fibrous tissue will replace its connective tissue by forming new capillaries, generating fibroblasts and residual inflammatory cells and involution of scar tissue.
Explain the pathophysiology of sponylolithesis
- Spondylolisthesis refers to the forward slippage of one vertebral body with respect to the one beneath it. This most commonly occurs at the lumbosacral junction with L5 slipping over S1, but it can occur at higher levels as well. It is classified on the basis of etiology into the following five types [1] :
- Congenital or dysplastic
- Isthmic
- Degenerative
- Traumatic
- Pathologic
- gradual slippage of the L5 vertebra due to gravity and posture.
- The dysplastic type occurs from a neural arch defect in the upper sacrum or L5. In this type, 94% of cases are associated with spina bifida occulta. A high rate of nerve root compression at the S1 foramen exists, though the slip may be minimal
- The pars interarticularis, or isthmus, is the bone between the lamina, pedicle, articular facets, and the transverse process. This portion of the vertebra can resist significant forces during normal motion. The pars may be congenitally defective or undergo repeated stress under hyperextension and rotation, resulting in microfractures. If a fibrous nonunion forms from ongoing insult, elongation of the pars and progressive listhesis results.
- In degenerative spondylolisthesis, intersegmental instability is present as a result of degenerative disk disease and facet arthropathy. These processes are collectively known as spondylosis (ie, acquired age-related degeneration). The slip occurs from progressive spondylosis within this three-joint motion complex. This typically occurs at L4-5, and elderly females are most commonly affected. The L5 nerve root is usually compressed from lateral recess stenosis as a result of facet and/or ligamentous hypertrophy.
Explain the pathophysiology of Lower crossed syndrome
- The lower crossed syndrome (LCS) is the result of muscle strength imbalances in the lower segment. These imbalances can occur when muscles are constantly shortened or lengthened in relation to each other. The lower crossed syndrome is characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body. In LCS there is overactivity and hence tightness of hip flexors and lumbar extensors. Along with this there is underactivity and weakness of the deep abdominal muscles on the ventral side and of the gluteus maximus and medius on the dorsal side. The hamstrings are frequently found to be tight in this syndrome as well. This imbalance results in an anterior tilt of the pelvis, increased flexion of the hips, and a compensatory hyperlordosis in the lumbar spine.
- This muscle imbalance creates joint dysfunction (ligamentous strain and increased pressure particularly at the L4-L5 and L5-S1 segments, the SI joint and the hip joint), joint pain (lower back, hip and knee) and specific postural changes such as: anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, external rotation of hip and knee hyperextension. It also can lead to changes in posture in other parts of the body, such as: increased thoracic kyphosis and increased cervical lordosis
Explain the pathophysiology of arthritis: ankylosing spondylosis
- chronic inflammatory disease of the joints of vertebral column and SIJ.
- pain progressive and stiffening the spine.
- all races and groups.
- late adolescent and early adulthood.
- inflammatory erosion of the sites where tendons and ligaments attach to bones.
- being in the SIJ and involve in the spine.
- fusion of the spine due to the destruction of these joints.
- presence of mononuclear cells in the involve structure suggest immune response.
- genetic and environmental factors play a role.
Explain the pathophysiology of Rheumatoid arthritis
- systemic inflammatory disease
- women more affected
- all age and groups, increase with age.
- genetic predisposition
- joint inflammation
- activation of T-cell mediated response to immunologic trigger.
- aberrant joint immune response leading to synovial inflammation and joint architecture destruction.
- cellular accumulation of neutrophils and macrophages that phagocyte the immune complexes and release lysosomal enzymes causing destructive changes in joint cartilages.
• When chronic, synovial membrane thickens
• Occludes blood flow, compounds problem
• Thickened synovium – contains granular tissue (pannus)
Explain the pathophysiology of Osteoarthritis
- degenerative joint disease
- leading cause of disability and pain in older adults.
- slow and progressive destruction of the articular cartilage weight bearing joints and fingers.
- loss of synovitis
- inflammation due to repair process attempting to heal, creating osteophytes and spurs.
- joint stiffness, pain, limitation of motion, instability and deformity.
- homeostatic mechanism is jam, water increase in the joint with a decreased concentration of proteoglycans with a weakening of collagen fibres.
- inadequate repair, the articular surfaces become eroded due to emptying of synovial fluid in cracks with its surface and micro fractures and loosing smooth component.
- Free floating osteocartilaginous bodies enter the joint cavity and the underlying trabecular bone becomes sclerotic in response to increase pressure decrease its property as shock absorber and forms abnormal bone growth. osteophytes and spurs.
Explain the pathophysiology of Trochanteric bursitis:
- inflammation of the bursa on the superficial greater trochanter of the femur.
- running, physical contact activities, hip surgery, preexisting condition, falling regularly are potentially the causes.
- patients complain of lateral hip pain.
- pain radiate down the lateral aspect of the thigh.
- tenderness in the greater trochanter.
- the joint hip isn’t involved.
- leg-length discrepancy and lateral surgery can be the main cause of bursitis.
Explain the pathology of Avascular necrosis:
- cellular death of been components due to interruption of the blood supply.
- bone structure collapsed resulting in bone destruction, pain, and loss of joint function.
- involves epiphysis of long bones, femoral and humeral head and the femoral condyles.
- patients taking corticosteroids are more in risks to develop AVN.
- interruption of the vascular supply and resultant necrosis of marrow, medullary bone, and cortex can be the causes of the mechanism.
- Other causes:
- Vascular occlusion
- Altered lipid metabolism
- Intravascular coagulation
- Abnormal joint remodelling.
- Mechanical stress.2.
Explain the pathology of congenital hip dysplasia:
- abnormal growth of the hip.
- ligamentous laxity is also believed to be associated with the disorder.
- EG: associated with Marfan Syndrome.
- genetic predisposition appears to be a factor in the disease. Low in asian population. and 10 times higher in people with the same family.
- female sex, first born children and breech on positioning are all associated.
- others muscular disorders of intrauterine malpositioning or crowding, such as metatarsus adducts and torticollis have been reported to be associated with the disorder.
- left more associated than the right.
- the disorder can be associated with neuromuscular disorders. (Eg: cerebral palsy)
- the abnormal development include the acetabulum, the femur, the capsule and the soft tissue..
Explain the pathology of Perthe’s disease:
- avascular necrosis of the proximal femoral head resulting from compromise of the tenuous blood supply to this area.
- children 4-10
- insidious onset.
- may occur after hip surgery.
- caused unknown but most of children have delayed bone growth and shortened in stature.
- can be idiopathic disease resulting from a SCFE, trauma, steroids used, sickle cells crisis, toxic synovitis or congenital dislocation.
- rapid growth occur in relation to development of the blood supply of the secondary ossification centres in epiphyses, causing interruption of adequate blood flow and making these areas prone to avascular necrosis.
Explain the pathology of transient synovitis of the hip:
- most common cause of hip pain in children aged 3-10.
- causes arthralgia and arthritis secondary to inflammation of the synovium.
- biopsy shows nonspecific inflammation and hypertrophy of the synovial membrane.
_ ultrasound demonstrate an effusion that causes bulging of the anterior joint capsule. - an increased of proteoglycans has been noticed as well.
Explain the pathology of the slipped capital femoral epiphysis:
- appears as a varus relation between the head and the neck on radiography.
- sometimes can have valgus position with the epiphysis displaced superiorly in relation to the neck.
- ethology is unknown, some cases associated with a endocrine disorder, renal failure osteodystrophy, previous radiation therapy.
- can lead into deformity or osteoarthrosis if untreated.
- complications = avascular necrosis.
