Se ha denunciado esta presentación.
Utilizamos tu perfil de LinkedIn y tus datos de actividad para personalizar los anuncios y mostrarte publicidad más relevante. Puedes cambiar tus preferencias de publicidad en cualquier momento.
PATHOLOGY OF THE
MUSCULOSKELETAL
SYSTEM
Uploaded by: http://mbbshelp.com
Bone disorders
Metabolic bone disorders
Osteoporosis (primary or secondary)
Osteomalacia and rickets
Paget’s disease
...
Osteoporosis (primary or secondary)
represents an increased loss of total bone
mass due to an imbalance between bone
abso...
Osteoporosis
PATHOGENESIS
Osteoporosis is conventionally classified into 2 major
groups:
Primary osteoporosis results prim...
Risk factors
1. Genetic factors—more marked in whites and
Asians than blacks.
2. Sex—more frequent in females than in male...
Secondary osteoporosis is attributed to a number
of factors and conditions:
endocrine disorders (hyperthyroidism,
acromeg...
Clinical features
The first clinical manifestations of
osteoporosis are pain accompanied
by skeletal fractures: vertebrae...
Osteoporosis weakens the
vertebrae, resulting in
compression fractures of the
anterior aspect of the vertebral
bodies. The...
Osteomalacia
Produce a softening of the bones and do not involve the
loss of bone matrix
Causes of osteomalacia:
1. Insuff...
Clinical features
1.Bone pain, tenderness, and
fractures as the disease progresses,
muscle weakness
2.Deformities (gravity...
This is a classic
pseudofracture and
is pathognomonic
for osteomalacia.
Uploaded by: http://mbbshelp.com
Paget’s disease
Is not a true metabolic disease
Localized disorder of bone remodeling,
resulting in excessive bone resor...
Forms of involvement
1.Monostotic (15%): involving one bone
2.Polyostotic (85%): involving multiple bones
3.Common sites i...
ETIOLOGY
1. Slow-virus infection by paramyxovirus (e.g.
respiratory syncytial virus, measles) in
osteoclasts. However, the...
Clinically, the monostotic form of the
disease may remain asymptomatic and the
lesion is discovered incidentally or on
rad...
 In this image, the calvarium is markedly thickened by
the growth of new bone. Secondly, in both specimens,
the density o...
rat skull, especially bone brain parts, front less
often. In the latter case, a characteristic look
sick-lion's face Uplo...
Infectious diseases of bones
Osteomyelitis
Osteomyelitis represents an acute or chronic
pyogenic infection of the bone.
...
Course of disease:
1.Acute osteomyelitis - sometimes
lightning inflammatory diseases,
trauma, iatrogenic, postradiation.
2...
HEMATOGENOUS OSTEOMYELITIS
Is preceded by staphylococcal or streptococcal
infections of the skin, sinuses, teeth, or middl...
Clinical features: bacteremia - chills,
fever, malaise, leukocytosis; pain on
movement, loss of movement, local
tenderness...
Chronic Osteomyelitis
Develops as a consequence of acute when the
infection persists beyond 6 to 8 weeks and more.
Pathoge...
Tuberculous osteomyelitis
Occurs in 1% of cases of ТВ
Extrapulmonary tuberculosis.
Caused by Mycobacterium tuberculosis...
Osteomyelitis with vascular
insufficiency
Commonly associated with chronic
or ischemic foot ulcers in persons
with longst...
 Hematogenous osteomyelitis
of the fibula of 3 months’
duration. The entire shaft has
been deprived of its blood
supply a...
Classification of primary bone tumors
TissueType BenignNeoplasm Malignant Neoplasm
Bone Osteoid osteoma, Benign
osteoblast...
Diseases of the joints (arthritis)
1. Infectious arthritis
2. Autoimmune
3. Metabolic
4. Degenerative arthritis or arthros...
Degenerative joint disease
Osteoarthritis Syndrome
Osteoarthritis (OA) - formerly called
degenerative joint disease, is th...
Causes of Osteoarthritis
1. Postinflammatory disorders (Rheumatoid arthritis, Septic
joint)
2. Post-traumatic disorders (A...
TYPES AND PATHOGENESIS
Primary OA occurs in the elderly, more
commonly in women than in men. The
process begins by the end...
Secondary OA may appear at any age
and is the result of any previous wear and
tear phenomena involving the joint such as
p...
Pathogenesis
Result from the release of cytokines such as
interleukin-1 and TNF, changes synthesis
protheoglicans and coll...
Clinical Manifestations
- May occur suddenly
- The pain worsens with use or activity and is usually
relieved by rest.
- Cr...
In this image, the knee
joint has been opened
anteriorly under the
patella. For orientation,
the hip is to the right and
t...
A common finding in
degenerative joint disease is
the formation of osteophytes at
the margin of affected joints. In
this i...
Rheumatic disorders (Autoimmune)
Rheumatic disorders are characterized by
inflammation, pain, and stiffness in the
musculo...
Rheumatoid Arthritis
Systemic inflammatory disease; 0.3% to
1.5% of the population
Women affected two to three times mor...
Immunologic derangements
1. Detection of circulating autoantibody called rheumatoid factor
(RF) against Fc portion of auto...
Trigger events
Though the above hypothesis of a possible role
of autoimmunity in the etiology and pathogenesis
of RA is ge...
Immunopathogenesis
In response to antigenic exposure (e.g. infectious agent) in
a genetically predisposed individual (HLA-...
Clinical manifestations
The disease, which is characterized by
exacerbations and remissions, may involve only
a few joints...
 Joint Manifestations - symmetric and polyarticular, any
diarthrodial joint can be involved (most frequently fingers,
han...
 This is a classic presentation
of acute rheumatoid arthritis. It
is polyarthritic, affects the
proximal interphalangeal ...
Metabolic diseases of the joints
Crystal-Induced Arthropathies
Crystal deposition in joints produces arthritis.
Gout
Dise...
The elevation of uric acid can result
from:
1. Overproduction of purines,
2. Decreased salvage of free purine
bases,
3. Au...
Hyperuricaemia of metabolic origin
This group comprises about 10% cases of gout
which are characterised by overproduction ...
Hyperuricaemia of renal origin
About 90% cases of gout are the result of reduced
renal excretion of uric acid. Altered ren...
Pathogenesis
Hyperuricemia → monosodium urate crystals
precipitate in the joint → initiate an inflammatory
response → dest...
Clinical Manifestations
Typical acute attack is monoarticular (first
metatarsophalangeal joint). Acute gout often
begins a...
Gouty node (Tophus)
Uploaded by: http://mbbshelp.com
PATHOLOGY OF LIGAMENT -MUSCLE
APPARATUS
Depending on the etiology of the disease of muscle are divided into the
following ...
MYASTHENIA GRAVIS
PATHOGENESIS.
The basic defect is reduction in the number of
available AChRs at the postsynaptic muscle
...
About 85-90% patients of MG have anti-
AChR-antibodies in their sera. These
antibodies reduce the number of available
AChR...
 The first signs-oculomotor violations (ptosis,
ophthalmoplegia, diplopia)
Uploaded by: http://mbbshelp.com
MYOPATHY
Myopathy or muscular dystrophy is a
group of primary diseases of striated
muscle, which combined a hereditary
nat...
Type Inheritance Age at
Onset
Clinical Features Other Systems Course
1.
Duchenn
e’s type
X-linked
recessive
By age
5
Symme...
4.
Facioscapul
o- humeral
type
Autosom
al
dominant
2nd-
4th
decad
e
Slowly
progressive
weakness of
facial, scapular
and hu...
PATHOLOGY OF THE MUSCULOSKELETAL SYSTEM
Próximo SlideShare
Cargando en…5
×
Próximo SlideShare
Pathology of the musculoskeletal system 1
Siguiente
Descargar para leer sin conexión y ver en pantalla completa.

34

Compartir

PATHOLOGY OF THE MUSCULOSKELETAL SYSTEM

Descargar para leer sin conexión

Pathology of the musculoskeletal system

Uploaded by: http://mbbshelp.com

Libros relacionados

Gratis con una prueba de 30 días de Scribd

Ver todo

PATHOLOGY OF THE MUSCULOSKELETAL SYSTEM

  1. 1. PATHOLOGY OF THE MUSCULOSKELETAL SYSTEM Uploaded by: http://mbbshelp.com
  2. 2. Bone disorders Metabolic bone disorders Osteoporosis (primary or secondary) Osteomalacia and rickets Paget’s disease Genetic disorders (dysplasia): osteopetrosis, achondroplasia, osteogenesis imperfecta, hyperostosis, fibrous dysplasia. Infectious diseases of bones - Osteomyelitis Bone Tumors Bone injury Uploaded by: http://mbbshelp.com
  3. 3. Osteoporosis (primary or secondary) represents an increased loss of total bone mass due to an imbalance between bone absorption and bone formation, most often related to the aging process and decreased estrogen levels inpostmenopausal women. Osteomalacia and rickets represent a softening of bone due to inadequate mineralization of the bone matrix caused by a deficiency of calcium or phosphate. Paget’s disease is a disorder involving excessive bone destruction and repair, resulting in structural deformities of long bones, spine, pelvis, and cranium. Uploaded by: http://mbbshelp.com
  4. 4. Osteoporosis PATHOGENESIS Osteoporosis is conventionally classified into 2 major groups: Primary osteoporosis results primarily from osteopenia without an underlying disease or medication. Primary osteoporosis is further subdivided into 2 types: idiopathic type found in the young and juveniles and is less frequent involutional type seen in postmenopausal women and aging individuals and is more common. Uploaded by: http://mbbshelp.com
  5. 5. Risk factors 1. Genetic factors—more marked in whites and Asians than blacks. 2. Sex—more frequent in females than in males. 3. Reduced physical activity—as in old age. 4. Deficiency of sex hormones—oestrogen deficiency in women as in postmenopausal osteoporosis and androgen deficiency in men. 5. Combined deficiency of calcitonin and oestrogen. 6. Hyperparathyroidism. 7. Deficiency of vitamin D. 8. Local factors—which may stimulate osteoclastic resorptionor slow osteoblastic bone formation. Uploaded by: http://mbbshelp.com
  6. 6. Secondary osteoporosis is attributed to a number of factors and conditions: endocrine disorders (hyperthyroidism, acromegaly, hyperparathyroidism, Cushing’s syndrome, diabetes) malabsorption disorders starvation malignancies (multiple myeloma) alcoholism certain medications (Glucocorticoid, aluminum- containing antacids, corticosteroids and anticonvulsants antiretroviral therapy, large dose of heparin). Immobilization Uploaded by: http://mbbshelp.com
  7. 7. Clinical features The first clinical manifestations of osteoporosis are pain accompanied by skeletal fractures: vertebrae (compression fracture, loss of height and kyphosis), femoral neck (hip fracture), distal radius (Colles fracture) Systemic symptoms such as weakness and weight loss. Uploaded by: http://mbbshelp.com
  8. 8. Osteoporosis weakens the vertebrae, resulting in compression fractures of the anterior aspect of the vertebral bodies. The fractures result in back pain and, over time, shortening of stature, dorsal kyphosis, and cervical lordosis. Loss of bone in osteoporosis is more rapid in trabecular bone than in cortical bone; hence vertebrae, because of their prominent trabecular component, are prone to fracture. Noticeable the variation in the width of the vertebrae, the fractures, and that the bone is very porous. Uploaded by: http://mbbshelp.com
  9. 9. Osteomalacia Produce a softening of the bones and do not involve the loss of bone matrix Causes of osteomalacia: 1. Insufficient calcium absorption from the intestine because of a lack of dietary calcium or deficiency or resistance to the action of vitamin D (among the elderly, biliary tract or intestinal diseases, on long-term anticonvulsant, tranquilizer, sedative, muscle relaxant, or diuretic drugs, during the winter months, probably because of lessened exposure to sunlight, in cultures in which the diet is deficient in vitamin D, such as in northern China, Japan, in strict vegetarians, persons who had a gastrectomy, long-standing primary hyperparathyroidism.) 2. Phosphate deficiency caused by increased renal losses (chronic renal failure, renal tubular defects) or decreased intestinal absorption. Uploaded by: http://mbbshelp.com
  10. 10. Clinical features 1.Bone pain, tenderness, and fractures as the disease progresses, muscle weakness 2.Deformities (gravity, muscle weakness, and bone softening) - dorsal kyphosis in the spine, rib deformities, heart-shaped pelvis, marked bowing of the tibiae and femurs Uploaded by: http://mbbshelp.com
  11. 11. This is a classic pseudofracture and is pathognomonic for osteomalacia. Uploaded by: http://mbbshelp.com
  12. 12. Paget’s disease Is not a true metabolic disease Localized disorder of bone remodeling, resulting in excessive bone resorption followed by disorganized bone replacement, producing thickened but weak bone that is susceptible to deformity and fracture Begins after age 40 years and progresses slowly over many years Uploaded by: http://mbbshelp.com
  13. 13. Forms of involvement 1.Monostotic (15%): involving one bone 2.Polyostotic (85%): involving multiple bones 3.Common sites include the skull, pelvis, femur, and vertebrae. Three stages of Paget disease 1.Osteolytic: osteoclastic activity predominates 2.Mixed osteolytic-osteoblastic 3.Osteosclerotic: osteoblastic activity predominates “burnout stage Uploaded by: http://mbbshelp.com
  14. 14. ETIOLOGY 1. Slow-virus infection by paramyxovirus (e.g. respiratory syncytial virus, measles) in osteoclasts. However, the virus has not been cultured from the osteoclasts of Paget’s disease. 2. Autosomal dominant inheritance and genetic susceptibility have been proposed on the basis of observation of 7-10 fold higher prevalence of disease in first-degree relatives. The susceptibility gene located on chromosome 18q encodes for a member of tumour necrosis factor called RANK (receptor activator of nuclear factor). Uploaded by: http://mbbshelp.com
  15. 15. Clinically, the monostotic form of the disease may remain asymptomatic and the lesion is discovered incidentally or on radiologic examination. Polyostotic form, however, is more widespread and may produce pain, fractures, skeletal deformities, and occasionally, sarcomatous transformation. Typically, there is marked elevation of serum alkaline phosphatase and normal to high serum calcium level. Uploaded by: http://mbbshelp.com
  16. 16.  In this image, the calvarium is markedly thickened by the growth of new bone. Secondly, in both specimens, the density of the bone is very heterogeneous, varying from rarefied foci to dense regions. Uploaded by: http://mbbshelp.com
  17. 17. rat skull, especially bone brain parts, front less often. In the latter case, a characteristic look sick-lion's face Uploaded by: http://mbbshelp.com
  18. 18. Infectious diseases of bones Osteomyelitis Osteomyelitis represents an acute or chronic pyogenic infection of the bone. Inflammation of the bone marrow and other bone items More often affects metaphysis femoral and tibial bone Cause – staphylococci, hemolytic streptococci, Escherichia coli, Mycobacterium, pathogenic fungi. Risk factors - endogenous microflora, acute infectious diseases, dialysis, presence of prosthetic orthopedic apparatus, etc.Uploaded by: http://mbbshelp.com
  19. 19. Course of disease: 1.Acute osteomyelitis - sometimes lightning inflammatory diseases, trauma, iatrogenic, postradiation. 2.Subacute 3.Chronic forms of osteomyelitis- chronic inflammatory diseases of chronic tuberculous osteomyelitis, chronic syphilitic osteomyelitis. Uploaded by: http://mbbshelp.com
  20. 20. HEMATOGENOUS OSTEOMYELITIS Is preceded by staphylococcal or streptococcal infections of the skin, sinuses, teeth, or middle ear→ bacteremia → Osteomyelitis Pathogenesis - consist of bone marrow lesion appearance of serous inflammation. Serous exudate increases pressure in the closed space of bone marrow and gaversov channels → joins thrombosis of arterioles and venules bone blood flow stops (vascular insufficiency) and focal bone necrosis develops (ischemic necrosis of bone) → exudate becomes suppurative inflammation and acquires the character of phlegmon → bone marrow necrosis develops compact bone with formation of underperiosteum abscess and fistula formation Uploaded by: http://mbbshelp.com
  21. 21. Clinical features: bacteremia - chills, fever, malaise, leukocytosis; pain on movement, loss of movement, local tenderness followed by redness and swelling. Forecast - septic form of acute hematogenous osteomyelitis causes patients to death, acute focal osteomyelitis can end with recovery. Uploaded by: http://mbbshelp.com
  22. 22. Chronic Osteomyelitis Develops as a consequence of acute when the infection persists beyond 6 to 8 weeks and more. Pathogenesis and morphogenesis - formation of abscesses of bone marrow, around which the bone resorption, necrosis and sequestration of necrotic areas → a cavity containing bone sequesters. Near the hearth of inflammation of the bone thickens, deforms, fistulas are formed through which bone small sequesters. Periosteum is thickened and sclerosis. The skin is atrophic changes. Complications - pathological fractures, false joints, bleeding from the fistula, secondary amyloidosis, septicemia, tumors. Uploaded by: http://mbbshelp.com
  23. 23. Tuberculous osteomyelitis Occurs in 1% of cases of ТВ Extrapulmonary tuberculosis. Caused by Mycobacterium tuberculosis Bone destruction and abscess formation, caseating granulomas with extensive destruction of the bones. Local symptoms - pain, immobility, and muscle atrophy; common symptoms - swelling, mild fever, leukocytosis, night sweats, weight loss. 50% it affects the vertebrae, also is seen in the hip and knee. Common site: thoracic and lumbar vertebrae (“Pott disease”). Complications - vertebral compression fracture, psoas abscesses, secondary amyloidosis. Uploaded by: http://mbbshelp.com
  24. 24. Osteomyelitis with vascular insufficiency Commonly associated with chronic or ischemic foot ulcers in persons with longstanding diabetes or other chronic vascular disorders Treatment: debridement and antibiotic - good oxygen tension in the infected site, amputation - oxygen tension is inadequate Uploaded by: http://mbbshelp.com
  25. 25.  Hematogenous osteomyelitis of the fibula of 3 months’ duration. The entire shaft has been deprived of its blood supply and has become a sequestrum (S) surrounded by new immature bone, involucrum (Iv). Pathologic fractures are present in the lower tibia and fibula.  A patient with chronic osteomyelitis of the midshaft of the tibia. A large fragment of necrotic cortex is visible deep within the draining sinus (sequestrum). The reactive periosteum has formed a collar of reactive bone (involucrum) around the chronic draining lesion. Uploaded by: http://mbbshelp.com
  26. 26. Classification of primary bone tumors TissueType BenignNeoplasm Malignant Neoplasm Bone Osteoid osteoma, Benign osteoblastoma Osteosarcoma, Parosteal osteogenic sarcoma Cartilage Osteochondroma, Chondroma, Chrondroblastoma Chondromyxoid fibroma Chondrosarcoma Lipid Lipoma Liposarcoma Fibrous and fibroosseous tissue Fibrous dysplasia Fibrosarcoma,Malignant fibrous histiocytoma Miscellaneous Bone marrow Giant cell tumor Malignant giant cell, Ewing’s sarcoma, Multiple myeloma, Reticulum cell sarcoma
  27. 27. Diseases of the joints (arthritis) 1. Infectious arthritis 2. Autoimmune 3. Metabolic 4. Degenerative arthritis or arthrosis 5. Developmental disorders of the joints 6. Tumor 7. Joint (Musculotendinous) Injuries Uploaded by: http://mbbshelp.com
  28. 28. Degenerative joint disease Osteoarthritis Syndrome Osteoarthritis (OA) - formerly called degenerative joint disease, is the most prevalent form of arthritis. Men are affected more commonly at a younger age than women, but the rate of women affected exceeds that of men by middle age. Obesity is a risk factor for OA Uploaded by: http://mbbshelp.com
  29. 29. Causes of Osteoarthritis 1. Postinflammatory disorders (Rheumatoid arthritis, Septic joint) 2. Post-traumatic disorders (Acute fracture, Ligament or meniscal injury, Cumulative occupational or recreational trauma) 3. Anatomic disorders (Hip dysplasia, Avascular necrosis, Paget’s disease, Slipped capital femoral epiphysis) 4. Metabolic disorders (Calcium crystal deposition, Hemochromatosis, Acromegaly, Wilson’s disease) 5. Neuropathic arthritis (Charcot joint) 6. Hereditary disorders of collagen 7. Idiopathic or primary variants Uploaded by: http://mbbshelp.com
  30. 30. TYPES AND PATHOGENESIS Primary OA occurs in the elderly, more commonly in women than in men. The process begins by the end of 4th decade and then progressively and steadily increases producing clinical symptoms. Little is known about the etiology and pathogenesis of primary OA. Genetic factors favouring susceptibility to develop OA have been observed; genetic mutations in proteins which regulate the cartilage growth have been identified e.g. FRZB gene. Uploaded by: http://mbbshelp.com
  31. 31. Secondary OA may appear at any age and is the result of any previous wear and tear phenomena involving the joint such as previous injury, fracture, inflammation, loose bodies and congenital dislocation of the hip. The molecular mechanism of damage to cartilage in OA appears to be the breakdown of collagen type II, probably by IL-1, TNF and nitric oxide. Uploaded by: http://mbbshelp.com
  32. 32. Pathogenesis Result from the release of cytokines such as interleukin-1 and TNF, changes synthesis protheoglicans and collagen type II → stimulate the production and release of proteases (enzymes) → destructive to joint structures → Edema of the extracellular matrix → the cartilage loses its smooth aspect → surface cracks occur allowing synovial fluid to enter and widen the crack → the vertical clefts form in the subchondral bone cartilage → fragments of cartilage to become dislodged → creating osteocartilaginous loose bodies → sclerosis, or formation of new bone (osteophyte) and cysts, usually occurs in the juxta-articular bone. Small osteophytes in the interphalangeal joints-Geberden's nodules Uploaded by: http://mbbshelp.com
  33. 33. Clinical Manifestations - May occur suddenly - The pain worsens with use or activity and is usually relieved by rest. - Crepitus and grinding when the joint is moved. - Joint swelling as a result of chronic inflammation in the periarticular tissues The most frequently affected joints - hips, knees, lumbar and cervical vertebrae, proximal and distal joints of the hand, the first carpometacarpal joint, and the first metatarsophalangeal joints of the feet. - limitations of joint motion and joint instability Uploaded by: http://mbbshelp.com
  34. 34. In this image, the knee joint has been opened anteriorly under the patella. For orientation, the hip is to the right and the foot to the left. There has been extensive destruction of the articular cartilage of the lower end of the femur. The synovium is not hyperplastic, nor is it inflamed. There is no evidence of pannus. Uploaded by: http://mbbshelp.com
  35. 35. A common finding in degenerative joint disease is the formation of osteophytes at the margin of affected joints. In this image, there are three osteophytes projecting from the intervertebral joints. Osteoarthritis of the hip is common. In this typical image, there is marked irregularity and erosion of the articular surface. Very little articular cartilage remains. Uploaded by: http://mbbshelp.com
  36. 36. Rheumatic disorders (Autoimmune) Rheumatic disorders are characterized by inflammation, pain, and stiffness in the musculoskeletal system. Systemic autoimmune rheumatic diseases Systemic autoimmune rheumatic diseases - group of chronic disorders characterized by diffuse inflammatory vascular lesions and degenerative changes in connective tissue that share clinical features and may affect many of the same organs, all of which share an autoimmune systemic pathogenesis. Uploaded by: http://mbbshelp.com
  37. 37. Rheumatoid Arthritis Systemic inflammatory disease; 0.3% to 1.5% of the population Women affected two to three times more frequently than men The ages of 40 and 60 years Cause – uncertain, the disease is initiated in a genetically predisposed individual by the activation of a T cell-mediated response to an immunologic trigger, such as a microbial agent Uploaded by: http://mbbshelp.com
  38. 38. Immunologic derangements 1. Detection of circulating autoantibody called rheumatoid factor (RF) against Fc portion of autologous IgG in about 80% cases of RA. RF antibodies are heterogeneous and consist of IgM and IgG class. 2. The presence of antigen-antibody complexes (IgG-RF complexes) in the circulation as well as in the synovial fluid. 3. The presence of other autoantibodies such as antinuclear factor (ANF), antibodies to collagen type II, and antibodies to cytoskeleton. 4. Antigenicity of proteoglycans of human articular cartilage. 5. The presence of γ-globulin, particularly IgG and IgM, in the synovial fluid. 6. Association of RA with amyloidosis. 7. Activation of cell-mediated immunity as observed by presence of numerous inflammatory cells in the synovium Uploaded by: http://mbbshelp.com
  39. 39. Trigger events Though the above hypothesis of a possible role of autoimmunity in the etiology and pathogenesis of RA is generally widely accepted, controversy continues as regards the trigger events which initiate the destruction of articular cartilage. Various possibilities which have been suggested are as follows: 1. The existence of an infectious agent such as mycoplasma, Epstein-Barr virus (EBV), cytomegalovirus (CMV) or rubellavirus, either locally in the synovial fluid or systemic infection some time prior to the attack of RA. 2. The possible role of HLA-DR4 and HLA-DR1 in initiation of immunologic damage. Uploaded by: http://mbbshelp.com
  40. 40. Immunopathogenesis In response to antigenic exposure (e.g. infectious agent) in a genetically predisposed individual (HLA-DR), CD4+ T cells are activated. These cells elaborate cytokines ( tumour necrosis factor (TNF)-α, interferon (IF)-γ , interleukin (IL)-1 and IL-6). These cytokines activate endothelial cells, B lymphocytes and macrophages. Activation of B-cells releases IgM antibody against IgG (i.e. anti-IgG); this molecule is termed rheumatoid factor (RF). IgG and IgM immune complexes trigger inflammatory damage to the synovium, small blood vessels and collagen. Activated endothelial cells express adhesion molecules which stimulate collection of inflammatory cells. Activation of macrophages releases more cytokines which cause damage to joint tissues and vascularisation of cartilage termed pannus formation. Eventually damage and destruction of bone and cartilage are followed by fibrosis and ankylosis producing joint deformities. Uploaded by: http://mbbshelp.com
  41. 41. Clinical manifestations The disease, which is characterized by exacerbations and remissions, may involve only a few joints for brief durations, or it may be relentlessly progressive and debilitating. - Fatigue, anorexia, weight loss, and low-grade fever - systemic manifestations - The erythrocyte sedimentation rate (ESR) correlates with the amount of disease activity - Anemia - associated with a low serum iron level or low iron-binding capacity is common (resistant to iron therapy) Uploaded by: http://mbbshelp.com
  42. 42.  Joint Manifestations - symmetric and polyarticular, any diarthrodial joint can be involved (most frequently fingers, hands, wrists, knees, feet). Joint pain and stiffness that lasts 30 minutes and frequently for several hours. The limitation of joint motion (pain; later it is caused by fibrosis). Subluxation of the joints.  Extraarticular manifestations - occur in persons with the RF. Rheumatoid nodules (granulomatous lesions around small blood vessels) - tender or nontender, movable or immovable, and small or large. Vasculitis - ischemic areas - ulcerations in the lower extremities, around the malleolar areas; neuropathy; heart, lungs, and gastrointestinal tract, also may be affected. Episcleritis and scleritis, hematologic abnormalities, pulmonary disease, cardiac complications, infection, and Felty’s syndrome (i.e., leukopenia with or without splenomegaly). Uploaded by: http://mbbshelp.com
  43. 43.  This is a classic presentation of acute rheumatoid arthritis. It is polyarthritic, affects the proximal interphalangeal joints, and has produced a fusiform swelling of the soft tissue. The lesion is usually symmetrical.  In this case, there is marked destruction of the epiphyseal bone. The joint spaces are narrowed, because of the destruction of the articular cartilage. In severe cases, the joints become fused by bony ankylosis. Uploaded by: http://mbbshelp.com
  44. 44. Metabolic diseases of the joints Crystal-Induced Arthropathies Crystal deposition in joints produces arthritis. Gout Disease caused by purine disorders Exchange and reflected increased levels of uric acid in the blood (hyperuricemia) and urine (hyperuricuria), the deposition of urates in joints, kidneys and in soft tissues. Almost exclusively men aged 35-50 years old Uploaded by: http://mbbshelp.com
  45. 45. The elevation of uric acid can result from: 1. Overproduction of purines, 2. Decreased salvage of free purine bases, 3. Augmented breakdown of nucleic acids as a result of increased cell turnover 4. Decreased urinary excretion of uric acid. Uploaded by: http://mbbshelp.com
  46. 46. Hyperuricaemia of metabolic origin This group comprises about 10% cases of gout which are characterised by overproduction of uric acid. There is either an accelerated rate of purine biosynthesis de novo, or an increased turnover of nucleic acids. The causes of primary metabolic gout include a number of specific enzyme defects in purine metabolism which may be either of unknown cause or are inborn errors of metabolism. The secondary metabolic gout is due to either increased purine biosynthesis or a deficiency of glucose-6- phosphatase. Uploaded by: http://mbbshelp.com
  47. 47. Hyperuricaemia of renal origin About 90% cases of gout are the result of reduced renal excretion of uric acid. Altered renal excretion could be due to reduced glomerular filtration of uric acid, enhanced tubular reabsorption or decreased secretion. The causes of gout of renal origin include diuretictherapy, drug-induced (e.g. aspirin, pyrazinamide, nicotinic acid, ethambutol and ethanol), adrenal insufficiency, starvation, diabetic ketosis, and disorders of parathyroid and thyroid. Renal disease per se rarely causes secondary hyperuricaemia such as in polycystic kidney disease andleads to urate nephropathy. Reinforced exchange nucleic acids and the purine bases - myelogenous leukemia, hemoglobinорatia and psoriasis Uploaded by: http://mbbshelp.com
  48. 48. Pathogenesis Hyperuricemia → monosodium urate crystals precipitate in the joint → initiate an inflammatory response → destructive changes to the cartilage and subchondral bone → repeated attacks of acute arthritis → chronic arthritis → formation of tophi urici (contain crystalline deposits of monosodium urate) in the synovium, olecranon bursa, Achilles tendon, subchondral bone, and extensor surface of the forearm → chronic tophaceous gout (degradation of subhondral departments of bones, ankilosis) Uploaded by: http://mbbshelp.com
  49. 49. Clinical Manifestations Typical acute attack is monoarticular (first metatarsophalangeal joint). Acute gout often begins at night and may be precipitated by excessive exercise, certain medications, foods, alcohol, or dieting. The attack may last for days or weeks. After the first attack, it may be months or years before another attack. Uploaded by: http://mbbshelp.com
  50. 50. Gouty node (Tophus) Uploaded by: http://mbbshelp.com
  51. 51. PATHOLOGY OF LIGAMENT -MUSCLE APPARATUS Depending on the etiology of the disease of muscle are divided into the following groups:  neurogenic (e.g., muscle atrophy after crossing the nerve);  hereditary-muscular dystrophy (myopathy);  metabolic-endocrine myopathies (such as in hyperthyroidism);  toxic-myopathy caused by salts of heavy metals, alcohol, etc.;  Autoimmune - myasthenia gravis, polymyositis, dermatomyositis;  infectious-viral and bacterial meningitis myositis  traumatic-Lysis syndrome long muscle strength;  tumor and opuholepodobnye muscle diseases. Uploaded by: http://mbbshelp.com
  52. 52. MYASTHENIA GRAVIS PATHOGENESIS. The basic defect is reduction in the number of available AChRs at the postsynaptic muscle membrane. In addition, the postsynaptic folds are flattened. These changes result in decreased neuromuscular transmission leading to failure to trigger muscle action potentials and consequent weakened muscle contraction. The neuromuscular abnormalities in MG are mediated by autoimmune response. Uploaded by: http://mbbshelp.com
  53. 53. About 85-90% patients of MG have anti- AChR-antibodies in their sera. These antibodies reduce the number of available AChRs either by blocking the active sites of the receptors or by damaging the post- synaptic muscle membrane in collaboration with complement. The exact mechanism how autoimmune response is initiated is not completely understood but the thymus appears to play a role in this process. Majority of patients of MG may have either thymoma or thymic hyperplasia; thymectomy is helpful in ameliorating the condition. The thymus possibly sensitises B cells to produce anti-AChR antibodies. Uploaded by: http://mbbshelp.com
  54. 54.  The first signs-oculomotor violations (ptosis, ophthalmoplegia, diplopia) Uploaded by: http://mbbshelp.com
  55. 55. MYOPATHY Myopathy or muscular dystrophy is a group of primary diseases of striated muscle, which combined a hereditary nature of suffering electoral defeat of muscle groups and progressive increasing muscle weakness. Uploaded by: http://mbbshelp.com
  56. 56. Type Inheritance Age at Onset Clinical Features Other Systems Course 1. Duchenn e’s type X-linked recessive By age 5 Symmetric weakness; initially pelvifemoral; later weakness of girdle muscles; pseudo- hypertrophy of calf muscles Cardiomegaly; reduced intelligence Progressi ve; death by age 20 due to respirator y failure 2. Becker’s type X-linked recessive By 2nd decade Slow progressive weakness of girdle muscle (minor variant of Duchenne’s type) Cardiomegaly Benign 3. Myotonic type Autosomal dominant Any decade Slow progressive weakness and myotonia of eyelids, face, neck, distal limb muscles Cardiac conduction defects; mental impairment; cataracts; frontal baldness; gonadal atrophy Benign
  57. 57. 4. Facioscapul o- humeral type Autosom al dominant 2nd- 4th decad e Slowly progressive weakness of facial, scapular and humeral muscles Hypertension Benign 5. Limb- girdle type Autosom al recessive Early child- hood to adult Slowly progressive weakness of shoulder and hip girdle muscles Cardiomyopat hy Variable progressi on 6. Oculo- pharyngeal type Autosom al dominant 5th-6th decad e Slowly progressive weakness of extraocular eyelid, face and pharyngeal muscles — Rarelypro gressive
  • AkanshaArya6

    Oct. 1, 2021
  • HarshitaPatil9

    Aug. 24, 2021
  • raziarazia

    Jul. 14, 2021
  • MayuriGidwani

    Jul. 6, 2021
  • Abdirahmanolol

    Apr. 2, 2021
  • kirtihada

    Feb. 5, 2021
  • DrSunakshiSharma1

    Jan. 28, 2021
  • JUDYANN94

    Jan. 10, 2021
  • kevinekuinte

    Dec. 6, 2020
  • BhatRfn

    Oct. 7, 2020
  • KajalNameirakpam

    Aug. 5, 2020
  • PriyaPampaniya1

    Apr. 2, 2020
  • PushpaTilekar

    Mar. 29, 2020
  • monumuraleedharan9

    Jan. 1, 2020
  • DrHinaDevmurari

    Dec. 23, 2019
  • AmalSPillai

    Dec. 4, 2019
  • FatoH2

    Jul. 25, 2019
  • CHANDAKUMARI11

    May. 7, 2019
  • AasthaJaiswal7

    May. 2, 2019
  • RockChandan

    Feb. 7, 2019

Pathology of the musculoskeletal system Uploaded by: http://mbbshelp.com

Vistas

Total de vistas

5.670

En Slideshare

0

De embebidos

0

Número de embebidos

2

Acciones

Descargas

312

Compartidos

0

Comentarios

0

Me gusta

34

×