Worksheet 5 musculosketel PDF

Preview

Summary

worksheet solution...

Description

NUM2409 Adult Health Care 2 TUTORIAL WORKSHEET Module 2 –Musculoskeletal disorders Activity 1 Gina is a 69-year-old woman who leads a reasonably active life despite being diagnosed with Fibromyalgia 10 years ago. Whilst in the garden she tripped over and sustained a # left neck of femur. Gina is admitted to your ward for total hip replacement. As this was a low trauma # it is suspected she may have osteoporosis. A. Review normal bone formation Most bone formation and strength of bones occurs in the first 20 years of life. Normal bone formation is a continuous process of resorption by osteoclasts (chewers) and bone formation by osteoblast (builders) .Soosteoclasts resorb bone (break it down) and in the process releases Calcium from the bone into the blood – RESORPTION. A by-product of this process is the release of substances that recruit osteoblasts to the site to lay down new bone. Osteoclasts also have a receptor on them called RANK ( member of TNF cells) the interaction with its ligand ( molecule which allows and forms a connection) RANKL also impact regulation of bone resorption and increases osteoclasts activity and aids in attaching to the bone . This is where Denosumab works as it inhibits RANBKL and therefore inhibits osteoclast activity Once new bone is laid down by osteoblasts the mature osteoblasts become trapped in the osteoid as it hardens by the minerals during calcification. The process is kept at a homeostatic balance by hormones, vitamins and minerals intake and physical stressors. Calcitonin (thyrocalcitonin) from C cells of thyroid lowers serum calcium levels by stimulating calcium uptake from the blood into the bones andinhibits bone resorbing osteoclasts (the chewers). Parathyroid hormone (PTH) increases serum calcium and decreases serum phosphate.PTH increases osteoclast activity therefore releasing calsciuminot the blood Calcium is inversely related to phosphorus. These hormones areregulated by negative feedback where plasma calcium levels is the stimulus. Oestrogen and to a lesser extent Testosterone both control osteocyte apoptosis (programmed cell death) which keeps the balance of blasts and cytes correct for good bone health. Lower androgen levels are also linked with increased RANKL = increased osteocyte activity Vit D - not really a vitamin it is a steroid. activated in kidney, increases absorption of Ca from gut, sensitizes bone to resorptive action of PTH. Remember Vit D 1

NUM2409 Adult Health Care 2 needed so Ca can be absorbed from the gut in first place this is why Ca supplements without Vit D are not as effective Mechanical forces increase osteoblast activity B. What tests and how would confirm a Dx of osteoporosis for Gina X-ray (on detection 25-30% bone already lost) Measuring bone mineral density (BMD) Dual-energy x-ray absorptiometry (DEXA) Ultrasound, CT scan Serum and urinary markers: Serum Ca, phosphorus and alkaline phosphatase, protein electrophoresis. C. List the risk factors for osteoporosis and discuss how do these risks alter normal bone homeostasis

      

insufficient dietary intake of calcium (dairyproducts ) – lack of calcium will lead to all calcium being required in plasma and not enough to be deposited in the bone sedentary lifestyle (lack of weight-bearing exercise)–weight bearing exercise stimulates osteoblast activity cigarette smoking and alcohol consumption – increase osteoclast activity postmenopausal status–oestrogen controls osteocyte apoptosis rate to maintain balance. Low oestrogen will result in osteocytes living longerand increase bone resorption over bone formation female gender – generally have lower bone density to start with vitamin D deficient. Need Vit D to absorb Calcium Age – bone density generally declines normally after age 30 - 35

D. Discuss pharmacological treatment is used in osteoporosis.



    

Oestrogen (HRT): Oestrogen helps osteoclasts apoptosis (programmed cell death) so its decline is associated with the survival of the bone-removing osteoclasts. Nowadays, benefits don’t outweigh the risks (increases risk of breast cancer, MI, stroke) Raloxifene (SERM): oestrogenic effects, protects against breast and endometrial cancer. Activates oestrogen receptors to provide benefit of oestrogen. Tamoxifen in Aust: used to treat and prevent breast cancer. Bisphosphonates: undergo incorporation into bone, then inhibit bone resorption by decreasing osteoclast activity. Alendronate most widely used: oesophagitis (ulceration) main side effect. Teriparatide: synthetic form of PTH, increases bone formation (increases osteoblasts more than increases osteoclasts)

2

NUM2409 Adult Health Care 2  

Denosumab: is a fully human monoclonal antibody for the treatment of osteoporosis, treatment-induced bone loss, bone metastases, multiple myeloma, and giant cell tumor of bone. Calcitonin-salmon: more potent than human calcitonin, inhibits osteoclast activity, increases tubular excretion of calcium. Not recommended for osteoporosis in Aust.

E. Using the clinical reasoning cycle identify three specific considerations / potential complications you need to consider when planning Gina’s post op care. Compartmentsyndrome from swelling post # and post surgery – need NVO

DVT – PE due to immobility

Dislocation of new joint if adequate abduction not maintainedor too much flexion (>90degree)

Activity 2: Karen a 33 year old married woman with 4 children aged between 11 yrs and 18 months. She has attended her local GP complaining of pain in her hands and feet. On examination her hands display evidence of inflammation; rubra, heat and swelling. On palpation and movement, they cause considerable pain which she rates as 6 – 7 on pain scale of 0 -10. When questioned on when this pain and inflammation first started, she is unable to say, but it has gradually worsened over the past 4 weeks. It is worse in the morning and she is now unable to carry out her normal household routine. She had experienced pain in her right hip which lasted for approximately 3 weeks but resolved spontaneously. Her GP suspect’s Rheumatoid Arthritis (RA). A. Discuss the pathophysiological process of RA and why it causes joint deformity. This gross inflammatory response thantthickens the synovial membrane and reduces blood supply leading to ischaemia (itself an inflammatory mediator) and breakdown of the synovial membrane. The immune system mistakes normal tissue for foreign tissue Synovial membrane becomes inflamed When inflammation occurs body releases cytokines and Tumour necrosis factor that increase inflammation

3

NUM2409 Adult Health Care 2 T cells activate macrophages and B- cell derived antibodies also Causesinflammation , oedema, excessive growth of inflamed membrane, exudate forms a fibrous pannus layer. Immobilisation occurs. Pannus – scar like layer which is specific to RA and distinguishes it from other inflammatory joint conditions. It is the pannus that causes the deformities. Treatment is aimed at reducing limiting the pannus formation Immobilisation occurs due to the ankylosis of joint from the pannus and then subsequent loss of muscle strength and atrophy

4

NUM2409 Adult Health Care 2 B. What diagnostic procedures / tests could be used to confirm the diagnosis of RA. Good physical assessment, look at other joints for inflammation, reduction in function pain etc. What about family history of RA or any other auto immune disease. Rheumatoid factor (RF)although not always present Analysis of synovial fluid Increased C reactive protein and WBC though these are only indicative of inflammation occurring and are not specific. Diagnosis may be made by Karen exhibiting 4 of the manifestations of a classification tool that was developed by the American Rheumatoid Association to aid diagnosis. These include a 6 weeks history of morning stiffness for more than 1 hour, swelling of 3 or more joints, swelling of the wrists and finger joints, any other symmetrical joint swelling, nodules in addition to positive RF and radiological evidence of joint involvement. C. An important component of treatment of RA is to reduce the inflammatory process. Discuss this in specific reference to Karen and what non pharmacological measures can be used to help relieve Karen’s symptoms, and how will they achieve relief. It is vital that the inflammatory process is managed well and minimised. As with any inflammation the end result will be scarring of the joints. As RA primarily attacks the small synovial joints of the hands and feet this scarring can lead to subluxation of the fingers especially leading to deformity and loss of function. Karen is a mother who leads a very busy life and will do for some time as her children are young. Any deformity and loss of function will have a huge impact on her quality of life and that of her family. As she is young she also has a reasonable life expectancy and the aim is to keep her joints functioning optimally for as long as possible so she is able to meet her ADL’s independently. The use of splints especially of her hands. Heat and cold packs to minimise inflammation and aid healing. They will also help with pain management. Use of devices around the home to reduce stress on joints especially hands eg adapted kitchen utensils with large handles, adaptors to reduce effort needed to turn on taps. Home help during periods of exacerbation to allow Karen to rest and minimise joint damage. Support groups Exercise and physiotherapy Good nutrition and hydration Plenty of rest, reduction of both physical and emotional stress. Education on the disease to allow Karen to mange her condition in an informed and autonomous way – give her control.

5

NUM2409 Adult Health Care 2 D. What are DMARDS and how do they work? DMARD’s Methotrexate Non biological

Sulfasalazine Non biological

Antimetabolite of folic acid and interferes with DNA / RNA synthesis and slows cell replication esp. rapidly dividing cells. Specifically inhibits action of B & T cells Anti-inflammatory and immunomodulator y

Etanercept biological Biological DAMRD Neutralises TNF (which is in high levels in the joints of RA)and cytokine activity -

Skin reactions, bone marrow depression, GI ulceration hepatotoxic in large doses or prolonged use.

Onset of action Takes 6 – 8 weeks Good patient education around dosage to prevent ADR. Avoid excessive sunlight as may cause photosensitivity.

Anorexia, nausea Fever, headache erythema, rash Rare – aplastic anaemia and agranulocytosis

Also used for inflammatory bowel disease

Pain swelling at injection site Upper resp infections

Given to patients unreceptive to other DMARD’s Sub cut injection weekly

6

NUM2409 Adult Health Care 2 E. Compare and contrast OA & RA Aetiology

CM & affected joints

Osteoarthritis Biomechanical injuries Loss of cartilage matrix

Genetic disposition Obesity ****** Wear and Tear due to previous trauma, joint malalignment Localised specific joints Pain, swelling loss of function Development of osteophytes Stiffness of < 20 minutes Limited ROM

Alleviating and precipitating factors

Better with rest

DX

CM Imagining – Xray MRI

Tx

Gentle exercise NSAID COX 2 inhibitors Intra articular steroid injections Surgery – joint replacement.

Rheumatoid Arthritis Auto immune disease Joint destruction due to inflammatory process and auto digestion of the synovial membrane and the development of pannus causing joint subluxation Genetic predisposition environmental triggers ? viral infections

Bilateral symmetrical joints Joint swelling Rheumatoid nodules and pannus formation Stiffness > 1 hour Joint deformity – subluxation Limited ROM Better with activity Acute exacerbations

CM Rheumatoid factor usually present Imaging – Xray MRI Gentle exercises Support splints Hydrotherapy NSAID DMARD’s Immunosuppressant’s

7...