735 Musculoskeletal Flashcards
**Osteoporosis
Affects **
- Osteoporosis affects >10 million the US
- S**mall proportion are diagnosed **& treated
*** 8 million women & 2 million men ( Female Predominantly) - Loss of ovarian function in women around age 50
* Precipitates rapid bone loss (most women meet dx criteria by ago 70 to 80 yrs)
2 million fractures each year occurs in USA due to Osteroporosis
Osteoporosis
characteristics
- Decreased bone strength
- Post menopausal women
- Function of Age: Occurs both M and W as a Function of age due to underlying conditions or major risk factors associate with **bone dimerization **
- Progressive loss of bone tissue: naturally occurs with age
Manifestations & Complications
- Most Common FX: Vertabra and HIP FX , However
- Fractures occur at any skeletal site
- DVT/PE: Fx has high association with DVT/PE
* Mortality: 5 to 20% 1st year after surgery ( if fx occurs can be life debilitation condition )
Osteoporosis
DX
**DX Scan **
* Higly Accurate XRAY
*Measures Bone Mass Measurement
**Bone Mass Measurement **
* All Women by age 65
* Males at age of 70 with absence of risk factors or related fracture
**Vitamin D Leve
*<12 associate with Vit D deficiency (Rickets = Kids and Osteomalacia = in adults
* 12 to 20 - Indadequate
* 21 to 50 Addequate
* 50 potenital adv reaction
* >60 adverse reaction
Osteoprorosis
TX
- **vitamin D3 : **
- 50 K x 8 wks then 2000 daily
- take with Ca supplement
*** PostMenopausal Women ** : Purpose to decrease bone turne over rate and incrase bone mass
Alendronate 70mg pO/weekly st line
Fosamax (Alendronate and vitamin D )
Acute Gaut
Overview
**Metabolic Disorder
**Affects middle aged to Elderly Men
P**ost -Menopausal women
OA, HTN, CKD
**Purines
- Play Crucial role essential compnnet DNA and RNA
- Found in animal and plant products
- Converted to uric acid
- lead to gout if not flushed out
**Typical Characterization **
Acute or chronic arthritis
Deposits of crystals the joints and connective tissue
**
Comlications **
Depostition into kidney interstitium
Uric acid neprholitheais **( kidney stones )
Acute Gouty Arthritis
Clinical Findings
- First Episode
- Evening Hours
- Join pain and sweling
- Warm, red, tender joints
- Early attacks suside 3 to 10 days
*** Precipitating Factors **
Dietary access
trauma
surgery
Excessiv ethnol ingestion
Hyporicemic therapy
serious medical illnessess
**Common Early clinical Manifestations **
Acute arthritis
Affect one joing
Polyarticular in subsequent episodes
Metatasophlangeal joint of 1st toe
Elderly or advnaced disease
finger or advanced disease
Finger joints involvement
Inflamed Heberden’s or Bouchard’s nodes
Gout :
DX
*** Arthrocentesis **
* Neele shaped monosodium urate (MSU ) Crystals
* WBC 2000 to 60, 000
* Cloudy (bacteria) ior Chalky (crystals ) apperace
* Bacterial infections can coexist
* Culture fluids to **r/o Septic Arthritis **
* **Laboratory **
* Serum uric Acid levels : can be normal and lower at the time of acute attack
* UA
* CBC, CMP, LFTs
* All labe to obtain to r/o other dx
* **24 -Hour Urine
For urinc acid
> 800 uric acid (excess of Purring)
> Excess purine
Gout Tx
-
NSAIDs
Naproxen, Ibuprofen, Toradol ( check kidney function and GI disorder )
* Colchicine - 1.2mg stat Then
- 0.6 in 1 HR
- **Glucocorticoids **
- Po or IV
- 30 to 50 mg/day
- **Hyouricemic therapy for maintenance
**Not initiated during acute attack
Alloprnol 100 mg can be incrae to 800 /dau
Caution with Thiazide use or PCN allergy
Life trhetenin Reaction :
Toxic epidermal necrolysis
systemic vasculysis
bone marrow supression
Hepatitis
renal failure
Combine wit colchicine until normouricemic x 6 month unti NORmouricemic; or without Gaut attack for 6 mont or as long as Tofi is present
ICe rest
Colcine - Acute attack
Alloprurinol - maintace
Can be combine aloprorino
**Rheumatoid Arthritis
OVerview **
**Chronic Inflammatory disease **
Unknow Etiology
Most common chronic inflammatory arthritis
No cure or prevention FOUND
**CHaracterization **
Symmeric Polyarthritis
**Disease Process Lead to **
Articular cartilage and bone destruction
Functional disability
CHances increase with AGe
Acquired b/w 25 to 55 age
Plateaus 75
Chance of getting decline after
RA
characteristic
**Presenting symptoms **
* Inflammation of Joints, Tendons, Bursa
* Early morning stiffness
* Eases with Physical Activities
* Earlier Joints Involved
* Hands and feet
*** Pattern of Involvement **
Monoarticular or Polyarticular
Symmetrical distribution
Extraacular manifestation
Fituque
Subcutaneous nodules
Lung involvemenet
Pericarditis
Peripheral Neuropathy
vascultis
Hematologic abnormalties
RA
Work Up and DX
Inflammatory and Biomarkers
* ESR and CRP
* Anti-CCPs (Biomarkers )
* Rheumatoid Factors
* CBC
Anemia
Leukocytosis
Thrombocytosis (High Plt)
**Joint Aspitration **
Conirms Inflammatory nature
Synovia WBC >75 to rarely >100K
Negative cultue
Traslucent to Opaque yellow ( if not other problem )
RA TX
**Primary Objective **
Reduce Inflammatory pain
Prevention of function
Prevention of deformity
Early pharmacologic intervention
**Nonsteroidal anti inflammatory (NSAID) **
Provide relieve
Do Not prevent Erosion
Do not alter disease progression
**Corticosteroids **
Anti inflammatory effect
slow articular erosion rate
Bridge before DMARD
Prednisoen 5 to 10mg/day
DMARDs( Disease modifying anti rheumatic drugs )
RA
Synthetic DMARDs
Synthetic DMARDs
Methotrexate
* 1st choice & well tolerated
* Beneficial effect in 2-3 weeks
* Does have complications
Gastric irritation, stomatitis, cytopenias, hepatotoxicity
Sulfasalazine
* Second line agent
* Does have complications
Hemolysis with G6PD deficiency
Check G6PD level before initiating
* Hydroxychloroquine sulfate
Monotherapy with only mild disease
Combo therapy with conventional DMARDs
Effective combination
Methotrexate + Sulfasalazine + Hydroxychloroquine**
RA TX
Biologic DMARDs
- Tumor necrosis factors Inhibitors (TNF Inhibitor)
- Etanercept, Infliximab, Adalimumab
- Golimumab
- **Most Common Therapy : Methothrexate and TNF factors
- Folic acid with it
- Reduce