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Gout & Osteoarthritis
and
Osteoporosis
Gout
 ~10% people with hyperuricemia have gout
 Predominantly middle-aged males
 Due to deposition of uric acid crystals in
joints, causing acute inflammation
 Causes-
 Diet-alcohol, sugar, meat, seafood
 Drugs- diuretics, niacin, aspirin
 Other diseases- obesity, DM, HT, CRI, MPD, hemolytic anemia,
lead toxicity
Clinical features
 s/s-
 Acute, recurrent inflammatory monoarthritis-
most common in 1st
MTP joint, fever common
 Chronic arthritis- in ~10 years, due to tophi
 Tophi- hard non-tender uric acid crystal deposits
 Uric acid urinary calculi- pain, obstruction
 Dx-
 Mono-sodium urate crystals in synovial fluid or tophi,
needle shaped strongly -ve birefringent
 Hyperuricemia ±
 Rx-
 Acute- NSAIDs, steroids, Colchicine
 Prophylaxis- started 1-2 weeks after an acute attack,
Allopurinol, Probenecid- keep UA levels below 6 mg%
Acute gout & tophi
Pseudogout
 Calcium pyrophosphate dihydrate- CPPD-
crystal deposition in joint cartilage
 Cause-
 Age, trauma, hyperparathyroidism, hemochromatosis etc.
 Causes intermittent mono-arthritis, commonly
of knee, hip, wrist
 Dx-
 X-ray
 CPPD crystals in synovial fluid-
rhombus shaped, +vely birefringent
 Rx- NSAIDs, steroids-oral/intra-articular
Osteoarthritis
 A degenerative joint disease
 Primary or Secondary
 Incidence increases with age
 Obesity & trauma increase risk
 Characterized by joint pain related to use,
worse in evening
 Knee & hip joints most commonly involved-
weight bearing
 Heberden’s-DIP & Bouchard’s-PIP nodes
Management
 Dx-
 Clinical
 X-rays to confirm
 Rx-
 Weight loss
 Exercise- to strengthen muscles
 Analgesics- paracetamolNSAIDs
 Arthroscopic intervention
 Joint replacement
Osteoporosis
 A disease of the bones
 Common in post-menopausal females
 Characterized by reduced bone mineral
density- 2.5 SD below peak bone mass
 Leads to an increased risk of fragility
fractures in spine, hip, wrist & ribs
 Affects life expectancy & quality of life
Pathogenesis
 Imbalance between bone formation &
resorption
 Mechanisms-
 Inadequate
 Excessive bone resorption
 Inadequate new bone formation during remodelling
 Trabecular bone is more subject to
remodelling, hence bones with high
trabecular to cortical bone ratio are more
prone for osteoporotic fractures
Risk factors for osteoporotic #
 Non-modifiable-
 Advanced age, female sex
 Family history of osteoporosis or fractures
 Potentially modifiable-
 Chronic heavy alcohol intake, smoking
 Vitamin D deficiency, malnutrition
 Physical inactivity or excess physical activity
Risk factors for osteoporotic #
 Diseases-
 Immobilization, of any cause
 Hypogonadism
 Cushing’s,
hyperparathyroidism,
thyrotoxicosis, acromegaly
 Malabsorption
 Rheumatological disorders
 CRI
 Multiple myeloma
 Parkinson’s disease
 COPD
 Drugs-
 Steroids- Prednisolone,
7.5 mg OD for >3
months
 Barbiturates, Phenytoin
 Thyroxine
 Aromatase inhibitors
 GnRH agonists
 Heparin, Warfarin
 PPI
 Al-containing antacids
 Thiozolidenediones
Management
 Dx-
 DXA- dual energy X-ray absorptiometry- gold standard
 Quantitative CT/US
 X-ray- for diagnosis of fractures or osteopenia
 Rx-
 Anti-resorptive- bisphosphonates, raloxifene, calcitonin,
estrogen/testosterone replacement
 Bone anabolic- teriparatide, calcium & vitamin D
 Others- strontium ranelate, denosumab
 Exercise, any- aerobic, weight-bearing, resistance
Prevention
 Screening- USPSTF
 Females >65 or >60 at increased risk
 Males >80 or >65 with prior fracture
 Prevention-
 Prevent falls
 Smoking cessation, moderation of alcohol intake
 Exercise & good nutrition, specially vit. D & calcium
 Bisphosphonates/Raloxifene/HRT- in post-menopausal females
 Testosterone in hypogonadal men

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Gout & osteoarthritis

  • 2. Gout  ~10% people with hyperuricemia have gout  Predominantly middle-aged males  Due to deposition of uric acid crystals in joints, causing acute inflammation  Causes-  Diet-alcohol, sugar, meat, seafood  Drugs- diuretics, niacin, aspirin  Other diseases- obesity, DM, HT, CRI, MPD, hemolytic anemia, lead toxicity
  • 3. Clinical features  s/s-  Acute, recurrent inflammatory monoarthritis- most common in 1st MTP joint, fever common  Chronic arthritis- in ~10 years, due to tophi  Tophi- hard non-tender uric acid crystal deposits  Uric acid urinary calculi- pain, obstruction  Dx-  Mono-sodium urate crystals in synovial fluid or tophi, needle shaped strongly -ve birefringent  Hyperuricemia ±  Rx-  Acute- NSAIDs, steroids, Colchicine  Prophylaxis- started 1-2 weeks after an acute attack, Allopurinol, Probenecid- keep UA levels below 6 mg%
  • 4. Acute gout & tophi
  • 5. Pseudogout  Calcium pyrophosphate dihydrate- CPPD- crystal deposition in joint cartilage  Cause-  Age, trauma, hyperparathyroidism, hemochromatosis etc.  Causes intermittent mono-arthritis, commonly of knee, hip, wrist  Dx-  X-ray  CPPD crystals in synovial fluid- rhombus shaped, +vely birefringent  Rx- NSAIDs, steroids-oral/intra-articular
  • 6. Osteoarthritis  A degenerative joint disease  Primary or Secondary  Incidence increases with age  Obesity & trauma increase risk  Characterized by joint pain related to use, worse in evening  Knee & hip joints most commonly involved- weight bearing  Heberden’s-DIP & Bouchard’s-PIP nodes
  • 7. Management  Dx-  Clinical  X-rays to confirm  Rx-  Weight loss  Exercise- to strengthen muscles  Analgesics- paracetamolNSAIDs  Arthroscopic intervention  Joint replacement
  • 8. Osteoporosis  A disease of the bones  Common in post-menopausal females  Characterized by reduced bone mineral density- 2.5 SD below peak bone mass  Leads to an increased risk of fragility fractures in spine, hip, wrist & ribs  Affects life expectancy & quality of life
  • 9. Pathogenesis  Imbalance between bone formation & resorption  Mechanisms-  Inadequate  Excessive bone resorption  Inadequate new bone formation during remodelling  Trabecular bone is more subject to remodelling, hence bones with high trabecular to cortical bone ratio are more prone for osteoporotic fractures
  • 10. Risk factors for osteoporotic #  Non-modifiable-  Advanced age, female sex  Family history of osteoporosis or fractures  Potentially modifiable-  Chronic heavy alcohol intake, smoking  Vitamin D deficiency, malnutrition  Physical inactivity or excess physical activity
  • 11. Risk factors for osteoporotic #  Diseases-  Immobilization, of any cause  Hypogonadism  Cushing’s, hyperparathyroidism, thyrotoxicosis, acromegaly  Malabsorption  Rheumatological disorders  CRI  Multiple myeloma  Parkinson’s disease  COPD  Drugs-  Steroids- Prednisolone, 7.5 mg OD for >3 months  Barbiturates, Phenytoin  Thyroxine  Aromatase inhibitors  GnRH agonists  Heparin, Warfarin  PPI  Al-containing antacids  Thiozolidenediones
  • 12. Management  Dx-  DXA- dual energy X-ray absorptiometry- gold standard  Quantitative CT/US  X-ray- for diagnosis of fractures or osteopenia  Rx-  Anti-resorptive- bisphosphonates, raloxifene, calcitonin, estrogen/testosterone replacement  Bone anabolic- teriparatide, calcium & vitamin D  Others- strontium ranelate, denosumab  Exercise, any- aerobic, weight-bearing, resistance
  • 13. Prevention  Screening- USPSTF  Females >65 or >60 at increased risk  Males >80 or >65 with prior fracture  Prevention-  Prevent falls  Smoking cessation, moderation of alcohol intake  Exercise & good nutrition, specially vit. D & calcium  Bisphosphonates/Raloxifene/HRT- in post-menopausal females  Testosterone in hypogonadal men