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Musculoskeletal System > PTH-01-Disease of Bone > Flashcards

PTH-01-Disease of Bone Flashcards

1
Q

Bone forming

A
  • Osteoblasts

- Osteoclasts

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2
Q

Bone Digesting

A
  • Osteoclast precursors

- Functioning osteoclasts

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3
Q

Regulated by

A

-RANK-RANKL pathway

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4
Q

Inherited Syndromes Affecting Bones(Generalized Situation)

A

Hurler’s syndrome (Mucopolysaccharidosis)

Marfan’s syndrome

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5
Q

Hurler’s syndrome (Mucopolysaccharidosis)

A

Lysosomal storage disease

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6
Q

Marfan’s syndrome

A

Mutation in fibrillin gene required for structural integrity of connective tissue

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7
Q

Congenital for Bone(Specifically)

A
  • Dysostosis

- Skeletal Dysplasia

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8
Q

Dysotosis-Definition

A

Localized developmental abnormalities of migration of mesenchymal cells

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9
Q

Dysostosis-Type

A
  • Aplasia(missing part)
  • Supernumerary digits(+ or - original no)
  • Abnormal fusion of digits
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10
Q

Skeletal Dysplasia-Definition

A
  • Abnormalities in bone or cartilage growth or maintenance

- Due to mutations in signal transduction or in components of extracellular matrix

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11
Q

Skeletal Dysplasia-Type

A

1- Achondroplasia
2- Osteogenesis Imperfecta
3- Osteopetrosis

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12
Q

Achondroplasia

A
  • AD, dwarfism,
  • Point mutation in the fibroblast growth factor receptor 3 → inhibits cartilage proliferation → suppression of growth
  • Shortened proximal extremities, trunk of relatively normal length, enlarged head
  • Normal life span, intellect & reproduction.
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13
Q

Osteogenesis Imperfecta

Brittle Bone Disease

A
  • Defective synthesis of type 1 collagen present in bones, joints, eyes, ears, skin and teeth.
  • Usually AD.
  • It has several subtypes with different outcomes.
  • Bone fragility & bone fractures, blue sclera, hearing defects, thin skull and dental abnormalities.
  • Can be diagnosed in utero
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14
Q

Osteopetrosis

Marble bone disease

A
  • Genetic, AD or RD → reduced bone resorption.
  • Impaired osteoclast function or formation.
  • Dense stone like bone, liable to fracture.
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15
Q

Osteopetrosis-Result

A
  • Cranial nerve problems (compression).
  • Decreased hematopoiesis
  • May benefit from bone marrow transplant
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16
Q

Acquired Diseases of Bone Development

A

1- Osteoporosis
2- Rickets / Osteomalacia
3- Hyperparathyroidism
4- Paget’s Disease Of Bone

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17
Q

Osteoporosis

A
  • Progressive Loss Of Bone Mass
  • Up to 30years. Later,osteoclast activity exceeds osteoblast activity
  • Result :Bone loss of 0.7%/year is normal
  • Governed by several factors e.g. vit.D, parathyroid hormone , level of estrogen….etc.
  • Commonest Disorder of bone;Localized, Generalized
  • Primary or Secondary
  • Mostly affect spine & femoral neck
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18
Q

Primary Osteoporosis

A

Post menapausal in women

Senile in both sexes as an aging process

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19
Q

Secondary Osteoporosis

A

Endocrine disorders
Carcinomatosis , multiple myeloma
GIT disorders: malnutrition, malabsorption, obesity…etc
Drugs : corticosteroids, chemotherapy..
Others : immoblization, pulmonary disease…etc

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20
Q

Factors Affecting Bone Resorption

A 
Age related changes
Hormonal factors
Physical activity
Genetic factors
Nutritional factors
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21
Q

Pathophysiology : Osteoclast Activation

A

Osteoclast precursor→Active Osteoclast in present of RANK-RANKl, M-CSF, inhibited by Osteoprotegerin. (Estrogen prevent this activation by activating OPG)

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22
Q

Primary Post Menapausal

A
  • cytokines and hormones(TNF,IL-1,IL-6), stimulate the expression of RANKL
  • Estrogen deficiency
  • Increase osteoclast activity
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23
Q

Osteoporosis-Morphology

A
  • Thin bone trabeculae
  • Widely separated
  • Notable osteoclast activity
  • Normal mineral bone content
  • Most changes in weight bearing areas in vertebral bodies & femoral neck
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24
Q

Osteoporosis-Clinical Picture

A
  • Post menapausalor senile
  • Often missed until fractures occur
  • Lumbar & Thoracic fractures, Head of femur
  • Diminished height
  • Kyphoscoliosis→Respiratory function
25
Q

Osteoporosis-Diagnosis

A
  • Plain X-ray only after 30-40% bone loss
  • Radiographic measurement bone density
  • Laboratory biochemical markers of bone:
  • Formation (alkaline phosphatase)
  • Resorption (urinary calcium)
  • Rarely , bone biopsy
26
Q

Osteoporosis-Treatment

A
  • Estrogenreplacementtherapy
  • Excercise
  • Calciumand Vitamin D dietary intake& supplements
  • Biphosphonate
27
Q

Rickets / Osteomalacia:

A

•Decrease in vitamin D intake or metabolism
→excess of unmineralized matrix
•Normally almost 100% of bone is mineralized, whereas in these conditions , mineralization may be < 20%
•Histology : thick unmineralized osteoid around more mineralized bone trabeculae
•Weak bones →Bone deformities & Fractures

28
Q

Sign of Rickets

A
  • Soft spot on baby, slow to close
  • Bony necklace
  • Curved bones
  • Big, lumpy joint
  • Bowed leg
29
Q

Hyperparathyroidism

A
  • Primary or Secondary

* ↑parathormone→osteoclast activation →bone resorption→↑calcium

30
Q

Hyperparathyroidism-Result

A
  • Bone cyst in any site
  • BROWN tumor/OSTEITIS FIBROSA CYSTICA in which there are osteoclasts, giant cells, hemosiderin & fibrovascular background
  • Fractures & Deformities
31
Q

Paget’s Disease Of Bone

A
  • Paget disease is a localized disorder of bone remodeling , in middle age
  • Disordered osteoclast hyperactivity with osteoblast activity →increased bone mass
  • Disorganized mosaic of bone weaker bone , larger, less compact, more vascular,
  • Cause : Viral, genetic, inflammatory disorder ???
32
Q

PDB-Phase

A
  • Primary phase of osteoclasticactivity, bone loss & hypervascularity.
  • Phase of mixed osteoclastic& osteoblastic activity.
  • Late osteosclerotic phase with formation of dense mineralized bone.
33
Q

PDB-Pathology

A
  • Focal replacement of the bone marrow by loose vascular connective tissue
  • Bone trabeculae are lined by huge osteoclasts.
  • Osteoblastic proliferation with concomitant bone resorption & new bone formation.
  • Irregular woven bone deposition with bone thickening (mosaic pattern).
34
Q

PDB-Clinical Picture

A

•Often asymptomatic & discovered incidentally.
•↑Alkaline phosphatase , serum calcium & phosphate normal
•Deformities:
-Lower limbs→Bowing of the legs.
-Skull deformed & enlarged→headache

35
Q

PDB-Complication

A
  • Nerve compression →deafness, visual disturbances
  • Increased vascularity in bone marrow leads to arteriovenousshunting →may leads to high output heart failure.
  • Osteosarcoma may develop (1 % )
  • Prognosis good unless complications occur
36
Q

Inflammatory Conditions

A
  • Osteomyelitis
  • Arthritis(Joint)(RA,IA)
  • Osteoarthritis(Degenerative)
  • Gout
  • Pseudogout
  • Tenosynovitis, GCT
37
Q

Osteomyelitis

A
  • Inflammation of the bone and the marrow cavity.

* Usually blood -borne infection

38
Q

Osteomyelitis

A
  • Pyogenic osteomyelitis.
  • Tuberculousosteomyelitis.
  • Syphilitic osteomyelitis.
  • Pott’s disease*
39
Q

Pyogenic Osteomyelitis

A 
•Caused by pyogenic bacteria:
-Staph. Aureus, E. coli, Salmonella
-mixed infection
•Sources: 1-Hematogenous*
2-Direct extension
3-Direct trauma.
4-Iatrogenic
•Mainly affects in metaphysis.
•Infants:Epiphyseal infection→joint
40
Q

PO-Clinical Picture

A
  • Acute : Fever, bone pain, leukocytosis, ↑BMR

* Chronic : Low grade fever, pain, abscess, discharging sinuses

41
Q

PO-Diagnosis

A
  • X-ray : Destructive lytic lesion with new bone formation

* Blood & sinus discharge culture

42
Q

PO-Treatment

A

•Appropriate antibiotic & surgical debridement

43
Q

PO-Pathology

A
  • Acute,subacute,chronic stages
  • Neutrophil infiltration,early bone necrosis (Sequestrum)
  • Spread to periosteum→subperiosteal abscess → rupture into soft tissue →draining sinus
  • Chronic:plasma cells & lymphocytes, reactive new bone ( involucrum), abscess (Brodie’s Abscess)
44
Q

PO-Complication

A
  • Pathological fracture.
  • Septic arthritis.
  • Bacteremia & septicemia.
  • Endocarditis.
  • Amyloidosis.
  • Chronic skin sinus
  • Squamous cell carcinoma of the skin.
45
Q

Tuberculous Osteomyelitis

A
  • May follow pulmonary or GIT tuberculosis.
  • Most common in immunosuppressed
  • Hematogenousor direct from nearby focus
  • May be solitary or multicentric.
  • Long bones & vertebrae most affected
  • Pathology is a caseating granulomatous reaction destroying bone
46
Q

Pott’s Disease

A
  • Tuberculousosteomyelitis affecting the vertebrae → KYPOSIS,SCOLIOSIS ( Hunchback)
  • May drain into soft tissue & adjacent psoas muscle →PSOAS ABSCESS
  • Therapy: Antituberculous therapy, but difficult to treat.
47
Q

Infectious arthritis

A

•Septic-Acute :Staph.,Strep.,Gonococci…..etc
Any joint, inflammation with suppuration .
Heals with antibiotics, or fibrosis & calcification

•Tuberculous: Complication of pulmonary or miliary
Granulomatous inflammation with caseation
destruction of cartilage & deformity.
More in children & spine

48
Q

Rheumatoid Arthritis

A

•F>M, middle age, ? Etiology
•Autoimmune process →T-cell & macrophage reactions in genetically predisposed →TNF→tissue damage & synovial proliferation
•Systemic disease with involvement of small joints of hands & feet, mainly proximal interphalyngeal joints.
Later any joint
•Stiff swollen red joints, later deformity, & fusion of joints(ANKYLOSIS)

49
Q

RA-Pathology

A
  • Acute & chronic inflammatory cells, lymphoid follicles in hypertrophied synovium, extends into joint
  • Later, synovium+ inflammatory cells →‘PANNUS’ →fibrosis →Joint destruction
  • ‘Rheumatoid nodules’ in joints & soft tissue
50
Q

RA-Diagnosis

A
  • Serological tests : Hypergammaglbulinemia
  • Rheumatoid Factor Positive (IgM or IgG autoAB that bind to Fc portion of IgG →immune complexes deposited throughout the body
51
Q

Osteoarthritis

A

•Commonest type. Both sexes.
•Primary degenerative dis.ofcartilage: > 65yrs.
•Secondary in younger patients:
-trauma, obesity, bone deformity
•Genetic causes
•Hips, Knees , Hands & Intervertebral joints →Swelling & decreased mobility

52
Q

OA-Pathology

A
  • Proliferation& disorganization of chondrocytes, ↑water,↓proteoglycans →Cracking of cartilage superficially
  • Loss of cartilage →Exposed smooth subchondral hard bone ( Bone eburnation )
  • Minor fractures→Loose cartilage bodies ’Joint mice’ in joint space
  • Gaps filled by synovial cysts & bony outgrowths ‘osteophytes’. Occasional fibrous Pannus.
53
Q

OA-Clinical Picture

A
  • Morning stiffness
  • Pain & swelling in joints
  • Progressive deformity in joints, but no ankylosis
  • Spinal root compression due to involvement of vertebra by osteophytes
54
Q

OA-Treatment

A
  • Analgesics

* Joint replacement

55
Q

Gout

A

•Accumulation of Uric Acid in soft tissue & joints→acute arthritis→chronic arthritis & renal complications
•Primary is unknown
-Middle aged men with high uric acid level
•Secondary :
-High nucleic acid turnover
-Renal failure
-Inborn error of metabolism

56
Q

Gout-Pathology

A

Repeated attacks of ACUTE ARTHRITIS in small joints, with deposition of MONOSODIUM URATE crystals → severe inflammation

Repeated attacks → ” Tophi”
Tophi are foci of urate crystals surrounded by inflammation with foreign body giant cell reaction.

Chronic Tophaceous arthritis with joint destruction & deformity.
Gouty nephropathy : calculi, pyelonephritis

57
Q

Pseudogout (chondrocalcinosis)

A

Deposition of calcium pyrophosphate with similar pathology to gout
Over the age of 50, often less severe
Acute, subacute, or chronic arthritis of knees, wrists, elbows, shoulders, and ankles.
Cause ?
Some cases are inherited

58
Q

Tumor –Like Lesions in Joints

A

Ganglion :

  • Small cyst near tendon or joint,
  • most around wrist, symptomless

Synovial cyst :
-Herniation of synovium through joint capsule at popliteal fossa ( Baker’s cyst)

59
Q

Pigmented Villo-nodular Tenosynovitis & Giant Cell Tumor of Tendon Sheath

A

PVNS mainly around knee, benign but may be large & aggressive
GCT smaller , painless nodule & around tendon
Cause ? Neoplasm ?
Both have similar morphology :
spindle cells, histiocytes , pigment

Musculoskeletal System (12 decks)

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