MSS Flashcards

1
Q

What are the functions of musculoskeletal system

A

-provide structural framework
-support body’s weights
-maintain posture
-enable movement

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2
Q

what are the components of MSS

A
  • Bones (provide skeleton, protect organs and tissues, store calcium, phosphates and fat, produce blood cells)
    -joints ( join bones, some have range of motion, some only go back and forth)
  • Cartilage (hyaline, elastic, meniscus, protects bones from rubbing against each other, lack nerves, blood, lymphatic system, can not regenerate on its own)
    -ligaments (connect bones, stabilize joints)
    -tendons (connect muscle to bones, tough not strechy)
    -muscles (skeletal, strechy fibres, move the bones, protect joints and hold them in place)
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3
Q

what are mss pathologies

A

-aging (loss of bone density, loss of muscles mass, cartilage deterioration, delayed injury recovery)
-arthritis (cartilage and joints break down, pain, inflammation and joint stiffness)
-back pain, muscle spasms (herniated disk, spinal stenosis, scoliosis)
-injuries (tendonitis, sprains, muscle tears, broken bones)
-congenital abnormalities eg clubfoot (stiffness and reduced range of motion)
-diseases (osteonecrosis, fibrous dysplasia, brittle bone disease, muscular dystrophy, myasthenia gravis, sarcopenia, rhabdomyolysis)
cancer (bone cancer, sarcoma)

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4
Q

what is bone remodeling

A

-bone resorption by osteoclasts
-bone deposition by osteoblasts
-activation (pre-osteoclasts are activated and mature)
-resorption (osteoclasts dig out a cavity in spongy bone- calcium is released into the blood for use)
-reversal: pre-osteoblasts appear
-formation: mature into osteoblasts, release osteoid forming new matrix, new matrix is mineralized with calcium and phosphorous
- quiescence: remains dormant until next cycle

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5
Q

what hormones affect calcium homeostasis

A

-parathyroid hormone: stimulate osteoclasts to break down bone matrix, increase intestinal absorption (increase blood levels)
-vitamin D (increase blood levels)
-calcitonin: inhibit osteoclasts, stimulate bone deposition (decrease blood levels)

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6
Q

what is osteoarthritis

A

-inflammation of joint
-slowly progressive deterioration
-affects weight bearing joints
-loss of articular cartilage
-inflammation may or may not be present
-assymetrical
-worst at the end of the day, after exercise
-pain, stiffness, loss of function, joints swelling (hard, soft)
-risk factors : age, family history, female, occupational overuse, obesity

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7
Q

what is the management of osteoarthritis

A

-education and counselling
-physiotherapy, occupational therapy
-correction of exacerbating factors
-paracetamol, aspirin, NSAID
-corticosteroids (severe inflammation)
-opioids if effusion is present
-topical joint replacement

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8
Q

what is rheumatoid arthritis

A

-a chronic progressive inflammatory systemic disease
-affects any joints
-more common in women
-symmetrical
-worst at the start of the day, exercise can help
-rheumatoid factor positive
-strong immune component
-stiffness, swelling, red, warm, loss of function, fever, malaise

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9
Q

what is the immunopathology of RA

A

-activation of T cells by macrophages- cause cytokine release
-inflammation of the synovium- bone erosion and structural damage (TNF and IL-1 are important in maintenance of inflammation and bone damage

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10
Q

what is the diagnosis of RA

A
  • seven criteria (at least 4 of them for more than 6 weeks)
    -blood test (RF positive)
    -consider anti-CCP antibodies if negative RF
    -x-ray in hands and feet
    -blood (FBC, RFT, CRP)
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11
Q

What is the management of RA

A

-patient education
-physiotherapy
-occupational therapy
-hand exercise program
-psychological interventions
-diet
-smocking cessation
-CVS risk modification
-pharmacological: DMARD (methotraxate, sulfasalazine, leflunomide)- disease progression
corticosteroid (prednisolone), NSAID, paracetamol
-if not effective add a bDMARD
*methotrexate: once a week, give folic acid the day after methotrexate (methotrexate-teratogenic), advised to limit alcohol intake

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12
Q

what monitoring is required for methotrexate
what are the side effects of methotrexate

A

-baseline: FBC, creatinine, electrolytes, lung function
-during treatment: FBC, LFT, creatinine, electrolytes every week for the first 6 weeks then monthly
-S/E: myelosuppresion, cough, dyspnea, GI, skin rash, nephrotoxicity

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13
Q

what is the synovial joint

A

-articular cartilage (protective)
-synovial fluid (lubrication, nutrition)
-allows smooth movement and increased joint mobility
-bones connected by ligaments
-meniscus: between articulating bones (shock absorption)
-bursa: thin connective tissue (outside joints)
filled with fluid (prevent friction)

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14
Q

what is the pathology of osteoarthritis

A

-damage to articular cartilage
-loss of matrix (swelling)
-bones move against each other (more pressure)
-increased production of synovial fluid
-underlying bone tissue thickens

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15
Q

what is the pathology of RA

A

-inflammation of synovial joints
-chronic system autoimmune condition
-inflammation of multiple peripheral joints
-abnormal activation of B and T cells and macrophages
-pannus formation (destructive type of tissue, invades interface between cartilage and bone)
-MMPs released by chondrocytes (degrade cartilage and bone)
- two antibodies present (RF, CCP)

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16
Q

what is the pathology of gout

A

-monosodium urate crystals are deposited
-in cartilage, bone, joint space
-raised plasma uric acid (cytotoxic drugs, radiotherapy, alcohol, purine intake)
-source: catabolism of nucleic acid and purine bases (G, C)
-develops when crystals are shed into the joint space
-macrophages phagocytose crystals- inflammatory response
risk factors: age, male, BP, weight, alcohol, meat intake

17
Q

what is the treatment of acute gout and hyperuricemia

A

-colchicine: interferes with inflammatory activity in gout
:interferes with recruitment and function of neutrophil leucocytes in gouty joint
-inhibits microtubules (phagocytosis of crystals, migration of immune cells)
-hyperuricemia:
xanthine oxidase inhibitors (allopurinol)- inhibit uric acid formation
sulfinpyrazone: inhibit reabsorption of uric acid in kidney

18
Q

what is myasthenia gravis

A

-rare autoimmune disease
-destruction of post-synaptic membrane (interferes with binding of Ach
-reduction of nicotinic N2 receptors
-less depolarization
symptoms: double vision, drooping eyelid

19
Q

what is the treatment of myasthenia gravis

A

-physostigmine (inhibit AchE enzyme)-increases Ach levels
-prednisolone- corticosteroid (reduce inflammation)
-muscle relaxants: (muscle spasms from nerve damage)
Baclofen: GABA B receptor agonist
diazepam: GABA A receptor agonist
tizanidine: alpha adrenergic agonist (reduce excitatory neurotransmitter)

20
Q

what are side effects of methotrexate

A

-nausea, vomiting
-teratogenic
-liver failure
-cough, dyspnea
-nephrotoxicity
*live vaccines must be avoided
*avoid alcohol
*contraception
*avoid breast feeding