MSS Flashcards
(129 cards)
1
Q
What are the primary functions of the musculoskeletal system?
A
Provide structural support, enable movement, maintain posture, support body weight.
2
Q
What are the main components of the musculoskeletal system?
A
Bones, muscles, joints, cartilage, ligaments, tendons.
3
Q
What functions do bones serve?
A
Protect organs, store calcium and phosphates, produce blood cells, provide structure.
4
Q
Where does linear bone growth occur?
A
At the epiphyseal growth plates between the epiphysis and diaphysis.
5
Q
Which hormones influence linear bone growth?
A
Growth hormone (+++), thyroid hormones (++), androgens (+), oestrogens (±), glucocorticoids (-).
6
Q
What cells are involved in bone remodelling?
A
Osteoclasts (resorption) and osteoblasts (formation).
7
Q
What are the phases of bone remodelling?
A
Activation, Resorption, Reversal, Formation, Quiescence.
8
Q
How does calcium move in and out of bone?
A
Osteoclasts release calcium (resorption), osteoblasts deposit calcium (formation).
9
Q
How does PTH affect bone?
A
Stimulates osteoclasts to increase blood calcium; reduces calcium excretion in kidneys.
10
Q
What is the role of calcitonin?
A
Inhibits osteoclasts and promotes calcium deposition into bone, lowering blood calcium.
11
Q
What are the types of joints?
A
Ball-and-socket (e.g., shoulder) and hinge (e.g., knee).
12
Q
What are the types of cartilage?
A
Hyaline (articular), elastic, and fibrocartilage (meniscus).
13
Q
What is the function of ligaments?
A
Connect bones, stabilize joints.
14
Q
What is the function of tendons?
A
Connect muscles to bones; transmit force for movement.
15
Q
What is sarcopenia?
A
Age-related loss of muscle mass and strength.
16
Q
What is osteoporosis?
A
A condition where bone resorption exceeds formation, leading to fragile bones.
17
Q
What is arthritis and what are its types?
A
Joint inflammation and degeneration; includes rheumatoid arthritis, ankylosing spondylitis, and gout.
18
Q
What is scoliosis?
A
An abnormal lateral curvature of the spine.
19
Q
What are common MSS injuries?
A
Tendonitis, sprains, muscle tears, fractures.
20
Q
Name three congenital MSS disorders.
A
Clubfoot, scoliosis, limb deformities.
21
Q
What is osteoarthritis (OA)?
A
A common, progressive, age-related joint disease with cartilage deterioration, joint pain, and stiffness.
22
Q
What joints are commonly affected in OA?
A
Knees, hips, spine, and hands.
23
Q
What is a classic symptom of OA?
A
Pain worsens at the end of the day and is eased by rest.
24
Q
What are Heberden’s nodes?
A
Hard swellings at the DIP joints caused by osteophytes in OA.
25
What are risk factors for OA?
Age, obesity, joint injury, female gender, family history, occupational overuse.
26
What is the first-line pharmacologic treatment for OA?
Paracetamol, followed by NSAIDs (topical preferred).
27
What non-pharmacologic strategies help manage OA?
Weight loss, physiotherapy, exercise, hot/cold packs, walking aids.
28
What is rheumatoid arthritis (RA)?
A chronic, autoimmune inflammatory disease affecting synovial joints.
29
What joints does RA commonly affect?
Small joints of hands and feet, symmetrically.
30
What is morning stiffness duration in RA?
Typically lasts ≥1 hour.
31
What are key diagnostic criteria for RA?
Morning stiffness, ≥3 joints, hand joint involvement, symmetrical arthritis, RF+, X-ray changes.
32
What is the role of RF and anti-CCP in RA?
RF is positive in 60–70%; anti-CCP is more specific and positive in ~80%.
33
What is the gold standard first-line DMARD in RA?
Methotrexate (MTX).
34
How is methotrexate dosed?
7.5–25 mg once weekly; folic acid given weekly on a different day.
35
What monitoring is required for methotrexate?
FBC, LFTs, creatinine at baseline and regularly during treatment.
36
What is a major caution with methotrexate?
Avoid during pregnancy and breastfeeding; limit alcohol; live vaccines contraindicated.
37
Name other cDMARDs besides MTX.
Leflunomide, sulfasalazine, hydroxychloroquine.
38
What are bDMARD examples used in RA?
TNFα inhibitors (e.g., adalimumab), IL-6 inhibitors (e.g., tocilizumab), and others.
39
What is a key difference between OA and RA symptoms?
OA is worse after activity; RA is worse in the morning and improves with movement.
40
When should a suspected RA patient be referred?
Urgently within 3 working days if small joints or multiple joints affected, even with normal RF.
41
What causes gout?
Elevated uric acid leading to monosodium urate crystal deposition in joints and tissues.
42
What are major lifestyle risk factors for gout?
High meat/seafood diet, alcohol, stress, physical trauma.
43
What enzyme is responsible for converting hypoxanthine to uric acid?
Xanthine oxidase.
44
What is the mechanism of action of allopurinol?
Competitive inhibitor of xanthine oxidase, reducing uric acid production.
45
What is the active metabolite of allopurinol?
Alloxanthine (oxypurinol), with a longer half-life.
46
Why can allopurinol trigger acute gout initially?
Mobilisation of tissue uric acid; colchicine or NSAID co-administered initially.
47
How does colchicine work?
Inhibits tubulin polymerisation, blocking leukocyte migration and reducing inflammation.
48
Which rings in colchicine interact with tubulin?
Rings A and C interact with the β-tubulin C-domain.
49
What are adverse effects of colchicine?
Bone marrow suppression, GI upset, potential for aplastic anaemia with long-term use.
50
What type of drug is hydroxychloroquine?
4-aminoquinoline DMARD used in mild RA; accumulates in lysosomes to stabilise them.
51
What is methotrexate’s primary mechanism in RA?
Inhibits DHFR, disrupting DNA synthesis and B-cell proliferation.
52
What does DHFR inhibition lead to?
Reduced thymidine production, leading to cell cycle arrest and reduced immune activity.
53
Which position on methotrexate must be unsubstituted for activity?
Position 7.
54
What chemical property of uric acid leads to its precipitation in gout?
Low water solubility of the urate monoanion when exceeded in concentration.
55
What form is uric acid predominantly in at physiological pH?
As a urate monoanion (~98–99%).
56
How is uric acid primarily excreted?
Via the kidneys (70%) through URAT1 transporter regulation.
57
What is the SAR requirement for methotrexate’s inhibition of DHFR?
2,4-diamino substitution is essential; 1-N must be basic for strong DHFR binding.
58
Name 3 drug classes linked to preventable hospital admissions.
NSAIDs, anticoagulants, opioids.
59
Who is most at risk from high-risk drugs?
Elderly, patients with kidney problems, on many medicines, or with memory issues.
60
What should be monitored with NSAIDs?
Blood pressure, kidney function, liver function, haemoglobin (if GI risk).
61
List 2 warning signs of NSAID-related GI problems.
Black stools, coffee-ground vomit.
62
Name 2 interactions of NSAIDs.
Increased bleeding with anticoagulants; reduced excretion of methotrexate.
63
What should you always consider with NSAIDs?
Use the lowest dose for the shortest time; consider a PPI.
64
What must patients do after inhaled corticosteroids?
Rinse mouth to avoid infection.
65
List 3 things to monitor with corticosteroids.
Blood pressure, glucose, bone density.
66
What card should patients carry on long-term steroids?
Steroid treatment card.
67
How often is methotrexate taken?
Once a week.
68
What supplement is taken with methotrexate?
Folic acid.
69
Name 2 signs of methotrexate toxicity.
Mouth ulcers, shortness of breath (pneumonitis).
70
Name 2 drugs that increase methotrexate toxicity.
NSAIDs, trimethoprim.
71
What is a serious risk of long-term opioid use?
Addiction.
72
What should be monitored with opioids?
Kidney and liver function.
73
List 2 signs of opioid overdose or addiction.
Drowsiness, taking more than prescribed.
74
How is antidepressant effectiveness monitored?
Using a questionnaire like PHQ-9.
75
Which antidepressants are most toxic in overdose?
Tricyclic antidepressants (TCAs) and MAOIs.
76
Name a key interaction with SSRIs.
With NSAIDs like ibuprofen – can increase bleeding risk.
77
Name one key principle for safe prescribing of high-risk drugs.
Review medicines regularly and monitor bloods where needed (e.g. LFT, U&E, INR).
78
What neurotransmitter is used at the neuromuscular junction (NMJ)?
Acetylcholine (ACh).
79
What type of receptor does ACh bind to at the NMJ?
Nicotinic acetylcholine receptors (Nm type, ionotropic).
80
What enzyme breaks down ACh at the NMJ?
Acetylcholinesterase (AChE).
81
What is Myasthenia Gravis (MG)?
An autoimmune disorder where antibodies target and reduce nicotinic ACh receptors at the NMJ.
82
What symptoms are commonly seen in MG?
Ptosis (drooping eyelids), diplopia (double vision), muscle weakness.
83
How do AChE inhibitors help in MG?
They prolong ACh activity at the NMJ, enhancing muscle stimulation.
84
Name two reversible AChE inhibitors.
Pyridostigmine and neostigmine.
85
Why is pyridostigmine preferred over neostigmine?
Longer duration and fewer muscarinic side effects.
86
What side effects can AChE inhibitors cause?
Salivation, GI upset, sweating, bradycardia (muscarinic effects).
87
What is the role of corticosteroids in MG?
Immunosuppression to reduce autoimmune activity.
88
How does baclofen work as a muscle relaxant?
GABA-B receptor agonist; reduces excitatory neurotransmission at the spinal cord.
89
What is the mechanism of diazepam in muscle relaxation?
GABA-A receptor agonist; increases Cl⁻ influx, enhancing inhibition.
90
How does tizanidine work?
Alpha-2 adrenergic agonist; inhibits presynaptic excitatory neurotransmitter release.
91
What is the mechanism of dantrolene?
Inhibits calcium release in muscle cells, reducing contraction.
92
What triggers muscle contraction after ACh binds to its receptor?
Na⁺ influx → action potential → Ca²⁺ release from SR → contraction.
93
How is ACh formed in the neuron?
Synthesised by choline acetyltransferase (ChAT) from choline and acetyl-CoA.
94
What type of joint is most commonly affected in arthritis?
Synovial joints.
95
What are the components of a synovial joint?
Joint cavity, articular cartilage, synovial fluid, ligaments, sometimes menisci or bursae.
96
What is the function of synovial fluid?
Lubrication and nutrition of the joint.
97
What causes bursitis?
Inflammation of a bursa due to overuse, trauma, pressure, infection, gout, or RA.
98
What is osteoarthritis (OA)?
A degenerative joint disease involving cartilage breakdown, joint space narrowing, and osteophyte formation.
99
Name three risk factors for OA.
Age, obesity, joint injury/misalignment.
100
What is a pannus in RA?
Inflamed, thickened synovial tissue that invades cartilage and bone.
101
What cytokines are involved in RA pathogenesis?
TNF-alpha, interferon gamma, interleukins.
102
What are the first-line DMARDs in RA?
Methotrexate, sulfasalazine, hydroxychloroquine, leflunomide.
103
What antibodies may be detected in RA?
Rheumatoid factor (RF) and anti-CCP antibodies.
104
What is gout?
Inflammatory arthritis caused by deposition of monosodium urate crystals in joints.
105
What causes hyperuricaemia?
High purine intake, obesity, renal failure, genetic factors.
106
What triggers a gout flare?
Urate crystals entering the joint space and triggering immune cell activation.
107
How does colchicine work in gout?
Inhibits neutrophil migration and phagocytosis by disrupting microtubules.
108
How does allopurinol work?
Inhibits xanthine oxidase to reduce uric acid production.
109
What is a uricosuric drug and give an example.
Increases uric acid excretion in urine; example: sulfinpyrazone.
110
What type of crystals cause gout?
Monosodium urate crystals.
111
What is the main cause of symptoms in gout?
Inflammatory response triggered by urate crystals in joints.
112
What is the target serum urate level in chronic gout?
< 360 µmol/L (or < 300 µmol/L in tophaceous gout).
113
Which drugs are first-line for acute gout attacks?
NSAIDs, colchicine, corticosteroids.
114
What should be avoided during an acute gout attack?
Starting urate-lowering therapy (ULT) like allopurinol.
115
When should allopurinol be continued?
Always continue if already taking it, even during an acute attack.
116
What is colchicine’s mechanism of action?
Inhibits neutrophil migration and phagocytosis by disrupting microtubules.
117
What are common side effects of colchicine?
Nausea, vomiting, diarrhoea.
118
What are signs of colchicine toxicity?
Multi-organ failure, bone marrow suppression, cardiovascular collapse.
119
What is the dose limit for colchicine?
Max 6 mg per course; do not repeat within 3 days.
120
How does allopurinol work?
Xanthine oxidase inhibitor – reduces uric acid production.
121
What are key cautions with allopurinol?
Hypersensitivity, rash, renal/hepatic dose adjustment.
122
What is febuxostat?
Non-purine xanthine oxidase inhibitor used if allopurinol is not tolerated.
123
What serious risk is associated with febuxostat?
Increased cardiovascular mortality in patients with a history of CVD.
124
When is uricosuric therapy used?
If XO inhibitors are contraindicated or not tolerated (e.g., sulfinpyrazone).
125
Name three risk factors for gout.
Obesity, alcohol, thiazide diuretics.
126
What lifestyle advice helps manage gout?
Reduce alcohol/purines, lose weight, hydrate, treat flares early.
127
When should a gout patient be referred?
Unclear diagnosis, CKD stage 3b–5, organ transplant, or failed therapy.
128
How should ULT be started?
2–4 weeks after acute attack + colchicine/NSAID cover for ~6 months.
129
Which joints are most commonly affected in gout?
Big toe (podagra), ankle, knee, wrist, elbow.
