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Chapter 11 >Lower Spine

>Pelvis
◙Osteoporosis >Cranium
-low bone mass = fragile=Fx ◙Pagetic lesion
-resorption>formation Arthritis Pain rad. From the
-imbalance in osteoclastic and osteoblastic act. Spinal Stenosis spine to the lower
-dec. in cortical thickness Nerve Root impingement extremities
-dec in no. and size o e trabeculae of cancellous
bone Sx:
trabecular plates >Enlargement of the skull
>Kyphotic posture
abnormally perforated/ Fx >Height loss
>Bowing of the long bones
trabecular connectivity is reduced >Vetigo
>Tinnitus Compression of the cranial nerves
t-scope- no. of standard deviation (SD) above or >Heaing loss
below the average BMD (bone mineral density) of >Blindness
young women.
Tx. Mgt:
>Normal- not >1 SD below e young adult ◙Symptomatic
>Osteopenia- 1-2.5 below e young adult mean >Pharmacologic: Analgesics Anti-inflammatory
value drugs >Aspirin
>Osteoporosis- >2.5 SD below e young adult >Plicamyin (Mithracin)-unreponsive to othe Tx.
mean value >Conservative: Heat therapy, massage bracing
>Severe Osteoporosis- more than 2.5 SD below ◙Asymptomatic: No Tx
the young adult mean value >Surgery
>Calcitonin & Etidronate –retard resorption
◙Idiopathic Osteoporosis
- younger men/ premenopausal women ◙Osteomalacia
- widespread decalcification and softening
◙Type 1 Osteoporosis of bones
-postmenopausal 51-75 - dec. calcified bone mass
-accelerated & disproportionate loss of -calcium and phosphorus fails to be
trabecular bone deposited in the bone matrix
- vertebral bodies and distal forearm -deformities in the weight-bearing bones,
common complication distortion in bone shape and
◙Type 2 Osteoporosis pathologic Fx.
-M/F over 70 -deminiralied/ low Vit.D
-Fx in femoral neck, proximal humerus,
proximal tibia & pelvis (cont. cortical and =Spine>Pelvis>LE
trabecular bone) =Bones-Bent/Flattened
◙Etiology =Kyphotic and scoliotic/ Coxa-Vara of the Femoral
-unk/genetic/environment Neck
◙Peak Bone Mass –young adulthood, maximum =Femoral Neck –Commonly under pressure
amount
◙Estrogen deficit/Amenorrhea - bone loss after ◙Precipitating Factors:
menopause, anorexia nervosa >Low Vit.D
>Meds. Phenytoin , Fluoride
◙Risk Factors: >Liver/Kidney Dse.
>Genetic >Malabsrption
>Low estrogen >Gastrectomy
>Amenorrhea > Inflammatory bowel dse
>Meds= thyroid >Renal dse.
meds/corticosteroids/anticonvulsants and >Chronic renal failure
anticoagulant > Tubular Necrosis
>Low Ca > Hypophosphatemia-low phosphate in
>Smoking & Alcoholism blood
>Sedentary lifestyle ◙Tx. Mgt.
>Vertebral Crush Fx >High Ca, Phosphorus, Vit. D Diet
>Hip Fx >KFT
>White, thin small body build >Safety
>Inflammatory arthritis, GI dse/surg. >Sun Bathing
◙Gout
◙Tx. Mgt.
>High Vit.D Ca Purine Cyclosporine,
>Acute Pain= narcotic/analgesics/NSAIDS Lasix Hydrochorthiazide
>Chronic Pain=NSAIDS
>Weight lifting/bearing exercises ↑Uric Acid
>HRT Estro and Proges
>Safety Uric acid concentration in blood

◙Paget’s Disease Hyperuricemia

-d/o in the bone architecture
-inc. rate of bone tissue breakdown (osteoclast) Deposition of crystalline Na Urate
and bone formation (osteoblast) Particularly in the Synovial jt.
◙Pain in
>Femur ◙Primary gout-unk/genetic purine metabolism
>Tibia
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◙Secondary gout-aquired impaired renal fxn, ◙Order of affectations
malignant dse, myeloproliferative d/o and 1. hand joints
hemolytic anemia. 2. wrist joints
◙Clinical Manifestation p254-255 3. metacarpophalangeal joint
4. knee joint
Chapter 12 5. hip joint
◙Osteoarthritis (misnomer) 6. elbow joint
◙Degenerative Joint Disease (a.k.a) ◙Clinical Manifestation p.261
-progressive
-noninflammatory d/o of mobile jts. esp. weight- ◙Swan-Neck deformity
bearing >Extension of the Proximal Interphalangeal
-loss of articular cartilage joint.
◙Primary= aging & Genetic (autosomal recessive) >Flexion of the Distal Interphalangeal joint
◙Secondary= any condition ◙Boutonniere deformity
>Trauma > Extension of the Distal Interphalangeal
Sprain joint
Strain > Flexion of the Proximal Interphalangeal
Dislocation joint
Fractures ◙Hallux Valgus
Avascular necrosis > Lateral deviation of the
Osteonecrosis metatarsophalangeal joint
> Mechanical Stress ◙Ulnar Drift
Athletics > Most common
Hazardous jobs >deviation of the metacarpophalangeal
>Inflammation in joint structures joint to the ulnar side
Autodigestion of joint by enzymes
>Joint instability
> Neurologic d/o Chapter 13
Charcot neuropathy Osteomyelitis- infection of the bone
>Congenital /acquired skeletal deformity ◙Acute Osteomyelitis –initial, <1month
Varus leg ◙Chronic Osteomyelitis – antibiotic therapy failed,
Dislocated hip >4 weeks
Joint laxity ◙DIRECT ENTRY contamination from
Legg-Calve-pertheses disease B-one surgery
>Hematologic/Endocrine d/o O-pen Fx
Hemophilia A-gunshot wound
Hyperthyroidism T-raumatic injury
Hypocalcemia BACTERIA
>Meds.
Collagen-digesting enzymes Arterial supply
Colchicines
Indomethacin Camp Site (bone)
Steroids
◙Clinical manifestations Circulation Slows
Objective: (growing)
popping, cracking, grinding
Limited ROM (DIOJ) Ichemia
Unstable, enlarged (spurs,boggy
synovium joints) Bone dies
Joint deformity ◙INDIRECT INOCULATION (hematogenous) - from a
*loss of articular cartilage blood borne disease like:
*collapse of subchondral B-oils
bone U-pper Respiratory Tract Infections
*Heberden’s nodes T-onsillitis
T-eeht infection
Subjective: S .aurues most common infecting agent
Pain >trauma
Stiffness(inactivity weather >weak immune system
changes)
◙Tx Mgt.
◙Tx. Mgt >Cx & Sensitivity- id. the agent to know the
>NSAIDS appropriate antibiotic
>Steroids >Antibiotic tx- best choice for acute stage as
>Splint-not for long term use long as there is no ischemia
>Heat-suana warm compress >Saucerization-surgical decompression
>Obese-lose some weght - to relieve pressure in the bone
>Sugery: DAAOT - to prevent ischemia
>Grafting- for extensive damage
◙Rheumatoid Arthritis >.Surgical debridement
◙Unknown etiology (may be) >Hemovac/ Jackson-Pratt-removal of
>Infections devitalized tissue
>Autoimmunity >Antibiotic beads Implantation - 6-8 weeks
>Genetics >Amputation- massive infection
>Others
>Autoimmune ◙Septic Arthritis
>Probable familial predisposition -joint ( +bone) cavity invasion
>Great Crippling disease -most rapidly destructive form
>Inflammation of Diarthrodial joint ◙Agents
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N. gonorrhea TB sinus
S. aureus
S.hemolyticus Spread to other parts
D. pneumoniae
Complete destruction of bones and joints
Septic Arthritis cont’d
Pus- Forming organism
◙S/Sx
Synovial membrane Sketetal TB
*Early *Late
Joint space >Night pain >Muscle
dystrophy
Closed-space infection >Muscle spasms >Low
◙Risk factors: grade fever
>Leukemia >Joint swelling >Night sweats
>DM >localized redness, warmth >Anorexia
>Joint trauma /disease *monoarticular involvement >Cough if PTB
>Corticosteroids, ISD intake reactivated >growth def.
>Chronic illness
◙Tx. Mgt.
◙Manifestations: >Pharmacologic: RIPES+C
Fever >Conservative: Bed rest, Traction
Pain >Surgical:
Swelling of joint/s *Focal Fusion- Bone and joint Stability (-) pain
*Arthrodesis- joint fusion (-) pain
*Joint Replacement- not now but later
◙Tx Mgt.
Goal: Spinal TB (Pott’s dse)
>elimination of the pathogen ◙S/Sx
>removal of joint debris
>prevention of deformities *Early
>Antimicrobial Tx >Same
>Hemovac/ Jackson-Pratt –to drain purulent > with peripheral involvement
Synovial effusion >discomfort
>Early immobilization >Dec. in Spinal ROM
>Needle Aspiration *Late
>Arthroscopy >Kyphosis
>Surgical operation >Paraplegia-due to cord
compression
◙TB of bones and joints ◙Tx. Mgt
◙TB of the spine- most common and dangerous >Pharmacologic: RIPES+C
form found in both adults and children >Conservative: Bed rest
◙Lesion in the lower thorax, upper lumbar-usual >Surgical:
cases *spinal Fusion – prev. vertebral collapse and
◙Upper thoracic lesion- seen in most children neurology sequelae in major cases with Neurologic
◙Risk Factors: abnormality, spinal instability and large abcess
>D-irty environment formation
>U-ntreated primary (P)TB
>D-M
>E-SRD
>P-oor nourishment Chapter 12
>T-rauma
◙Pattern of Invasion: starts centrally, spread Osteoarthritis (misnomer)
outward Degenerative Joint Disease (a.k.a)
-progressive
M. tuberculosis (attacks) -noninflammatory d/o of mobile jts. esp. weight-
bearing
Synovial membrane -loss of articular cartilage
Primary= aging & Genetic (autosomal recessive)
Pdxn of excessive secretion, proliferation and Secondary= any condition
thickening >Trauma
Sprain
TB granulation tissue (covers) Strain
Dislocation
Hyaline cartilage and subchondral bone Fractures
Avascular necrosis
Pdxn of caseous necrotic material and TB Osteonecrosis
exudates > Mechanical Stress
Athletics
Build up of pressure within the bone/joint Hazardous jobs
>Inflammation in joint structures
Rupture (releasing) Autodigestion of joint by enzymes
>Joint instability
Cold Abscess containing necrotic debris and > Neurologic d/o
pyogenic pus Charcot neuropathy
>Congenital /acquired skeletal deformity
Bursting in the skin Varus leg
Dislocated hip
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Joint laxity ◙Acute Osteomyelitis –initial, <1month
Legg-Calve-pertheses disease ◙Chronic Osteomyelitis – antibiotic therapy failed,
>Hematologic/Endocrine d/o >4 weeks
Hemophilia ◙DIRECT ENTRY contamination from
Hyperthyroidism B-one surgery
Hypocalcemia O-pen Fx
>Meds. A-gunshot wound
Collagen-digesting enzymes T-raumatic injury
Colchicines BACTERIA
Indomethacin
Steroids Arterial supply
Clinical manifestations
Objective: Camp Site (bone)
popping, cracking, grinding
Limited ROM (DIOJ) Circulation Slows
Unstable, enlarged (spurs,boggy (growing)
synovium joints)
Joint deformity Ichemia
*loss of articular cartilage
*collapse of subchondral Bone dies
bone ◙INDIRECT INOCULATION (hematogenous) - from a
*Heberden’s nodes blood borne disease like:
B-oils
Subjective: U-pper Respiratory Tract Infections
Pain T-onsillitis
Stiffness(inactivity weather T-eeht infection
changes) S .aurues most common infecting agent
>trauma
Tx. Mgt >weak immune system
NSAIDS
Steroids
Splint-not for long term use
Heat-suana warm compress ◙Tx Mgt.
Obese-lose some weght >Cx & Sensitivity- id. the agent to know the
Sugery: appropriate antibiotic
>DAAOT >Antibiotic tx- best choice for acute stage as
long as there is no ischemia
Rheumatoid Arthritis >Saucerization-surgical decompression
Unknown etiology (may be) - to relieve pressure in the bone
Infections - to prevent ischemia
Autoimmunity >Grafting- for extensive damage
Genetics >.Surgical debridement
Others >Hemovac/ Jackson-Pratt-removal of
Autoimmune devitalized tissue
Probable familial predisposition >Antibiotic beads Implantation - 6-8 weeks
Great Crippling disease >Amputation- massive infection
Inflammation of Diarthrodial joint
Order of affectations ◙Septic Arthritis
1. hand joints -joint ( +bone) cavity invasion
2. wrist joints -most rapidly destructive form
3. metacarpophalangeal joint ◙Agents
4. knee joint N. gonorrhea
5. hip joint S. aureus
6. elbow joint S.hemolyticus
Clinical Manifestation p.261 D. pneumoniae
Pus- Forming organism
Swan-Neck deformity
>Extension of the Proximal Interphalangeal Synovial membrane
joint.
>Flexion of the Distal Interphalangeal joint Joint space
Boutonniere deformity
> Extension of the Distal Interphalangeal Closed-space infection
joint ◙Risk factors:
> Flexion of the Proximal Interphalangeal >Leukemia
joint >DM
Hallux Valgus >Joint trauma /disease
> Lateral deviation of the >Corticosteroids, ISD intake
metatarsophalangeal joint >Chronic illness
Ulnar Drift
> Most common ◙Manifestations:
>deviation of the metacarpophalangeal Fever
joint to the ulnar side Pain
Swelling of joint/s

Chapter 13 ◙Tx Mgt.

Goal:
Osteomyelitis- infection of the bone >elimination of the pathogen
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>removal of joint debris >Conservative: Bed rest, Traction
>prevention of deformities >Surgical:
>Antimicrobial Tx *Focal Fusion- Bone and joint Stability (-) pain
>Hemovac/ Jackson-Pratt –to drain purulent *Arthrodesis- joint fusion (-) pain
Synovial effusion *Joint Replacement- not now but later
>Early immobilization
>Needle Aspiration Spinal TB (Pott’s dse)
>Arthroscopy ◙S/Sx
>Surgical operation
*Early
◙TB of bones and joints >Same
◙TB of the spine- most common and dangerous > with peripheral involvement
form found in both adults and children >discomfort
◙Lesion in the lower thorax, upper lumbar-usual >Dec. in Spinal ROM
cases *Late
◙Upper thoracic lesion- seen in most children >Kyphosis
◙Risk Factors: >Paraplegia-due to cord
>D-irty environment compression
>U-ntreated primary (P)TB ◙Tx. Mgt
>D-M >Pharmacologic: RIPES+C
>E-SRD >Conservative: Bed rest
>P-oor nourishment >Surgical:
>T-rauma *spinal Fusion – prev. vertebral collapse and
◙Pattern of Invasion: starts centrally, spread neurology sequelae in major cases with Neurologic
outward abnormality, spinal instability and large abcess
M. tuberculosis (attacks) formation

Synovial membrane

Pdxn of excessive secretion, proliferation and

thickening

TB granulation tissue (covers)

Hyaline cartilage and subchondral bone

Pdxn of caseous necrotic material and TB

exudates

Build up of pressure within the bone/joint

Rupture (releasing)

Cold Abscess containing necrotic debris and

pyogenic pus

Bursting in the skin

TB sinus

Spread to other parts

Complete destruction of bones and joints

◙S/Sx
Sketetal TB
*Early *Late
>Night pain >Muscle
dystrophy
>Muscle spasms >Low
grade fever
>Joint swelling >Night sweats
>localized redness, warmth >Anorexia
*monoarticular involvement >Cough if PTB
reactivated >growth def.

◙Tx. Mgt.
>Pharmacologic: RIPES+C