Musculoskeletal Support Flashcards

1
Q

Define osteoarthritis and the signs/symptoms

A

degenerative arthritis of the articular cartilage, typically affecting the weight bearing (larger) joints and seen mostly > 45 years.

Joint pain worse with activity. Stiffness. Swelling/deformity.

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2
Q

In OA: What is the composition of articular cartilage, and how do chondrocytes contribute to its maintenance?

A

Articular cartilage comprises an extracellular matrix (ECM) containing water, collagen, and proteoglycans, with chondrocytes playing a key role.

Chondrocytes mediate the turnover of matrix components by synthesizing ECM components and proteolytic enzymes.

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3
Q

What are proteoglycans, and how do they contribute to the properties of articular cartilage?

A

Proteoglycans in articular cartilage consist of glycosaminoglycan (GAG) chains, such as chondroitin sulfate, bound to hyaluronic acid. These proteoglycans provide osmotic properties critical for resisting compressive forces on the cartilage.

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4
Q

How do chondrocytes actively contribute to both the synthesis and breakdown of extracellular matrix components in articular cartilage?

A

Chondrocytes in articular cartilage play a dual role by synthesizing extracellular matrix components and proteolytic enzymes responsible for breaking down these components. This dynamic activity allows chondrocytes to maintain the equilibrium and health of articular cartilage.

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5
Q

What are some causes and risk factors associated with osteoarthritis (OA)?

A

Age
mitochondrial
joint trauma leading to inflammation and cartilage degradation, and the direct mechanical load on cartilage associated with overweight/obesity. Chondrosenescence, the age-dependent deterioration of chondrocyte function, is characterized by erosion of telomere length and mitochondrial dysfunction.
T2DM
genetics
metobolic endo
other joint issues

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6
Q

How does insulin in Type 2 diabetes mellitus (T2DM) influence chondrocytes and what role does genetics play in OA risk?

A

Insulin in T2DM stimulates chondrocytes to synthesize proteoglycans.

Chronic inflammation drivers, such as metabolic endotoxaemia, and other joint diseases like gout and rheumatoid arthritis, are additional risk factors.

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7
Q

What are the key radiographic findings in osteoarthritis, and why does the severity determined by X-rays not always correlate with the degree of pain?

A

joint space narrowing, osteophytes, and subchondral sclerosis. However, there is a lack of correlation between X-ray severity and pain

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8
Q

How do NSAIDs impact osteoarthritis symptoms, and what is the drawback associated with their use in managing OA?

A

NSAIDs suppress osteoarthritis symptoms for short-term relief but have drawbacks, as they inhibit collagen matrix synthesis and accelerate cartilage breakdown. This can increase the rate of degeneration, emphasizing the need for alternative approaches to managing OA symptoms.

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9
Q

Natural approach to OA?

A

Anti-Inflam diet
Hydration - syniovial support
Change dietary fats and oils - ↓ AA (↓PGE2 series). use DGLA for PGE1 series/EPA PGE3.
Hydrotherapy
Acupuncture/osteopathy
Exercise - low moderate - swimming, yoga

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10
Q

Supplements and doses in OsteoArthritis?

A

Glucosamine Sulphate (500x3); Proteoglycan synthesis (↑ collagen), ↓COX2/PGE2/NFkb)

Chondroitin Sulphate (200-400): ↑ hylauronic acid, joint lubrication.

MSM (1-4g): Anti-inflam. ↓ NFkb. ↑ proteolglycan/hylauronic acid.

Vit C/E: (5000/200-400): chondrocyte protein synthesios (collagen), antiox

Vit D (2000-10000iu): prevent articular cartilage erosion. Bone/collage T/O

Tart Cherry (3000mg) anti-inflam ↓NFkb/IL6, ↓hsCRP. Antioxident.

K2 (50-100mcg): inhibit cartilage calcification

Tumeric (500-2000): ↓ NFkb/IL1B IL6.
Bswelia (300x3): ↓ 5-lipooxygensage and Leuketriene B4 formation.

Ginger (500-1000mg); ↓TNFa/PGE2/COX2, ↓ infl joint pain.

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11
Q

What characterizes rheumatoid arthritis (RA), and which joints are commonly affected by synovial inflammation in this autoimmune disease?

A

A chronic inflammatory autoimmune disease known for synovial joint inflammation.

It typically affects small distal joints of the hands and feet in a symmetrical polyarthritis pattern, although more proximal joints can also be involved.

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12
Q

What are some specific signs and complications associated with rheumatoid arthritis (RA), beyond joint inflammation?

A

Hand deformities, including swan neck deformity
subcutaneous nodules.

Complications of RA may include:
C1/2 vertebral subluxation, pleurisy, pulmonary fibrosis, kidney disease, Sjögren’s syndrome, and carpal tunnel syndrome.

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13
Q

Explain process of Citrullination in RA

A

Arginine → Citrulline → cytokines → ↑ RANKL → osteoclasts

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14
Q

What are some of the genetic and environmental factors that contribute to the development of rheumatoid arthritis (RA)?

A

Genetics: HLA-DRB1 alleles (30% genetic risk), PTPN22SNP.

Environmental factors: Smoking, silica dust exposure, infectious agents (e.g., Porphyromonas gingivalis, EBV)

Intestinal dysbiosis (Prevotella copri, Collinsella).
SIBO
Metabolic Endo
Intestinal Inflammation

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15
Q

How can rheumatoid arthritis (RA) be diagnosed based on blood test findings, and what are some of the commonly observed markers?

A

Diagnosis through blood tests.
Markers: Raised ESR and CRP, Rheumatoid factor (RF), Anti-citrullinated protein antibodies (ACPAs).

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16
Q

What are key aspects of the natural approach to managing rheumatoid arthritis (RA), including dietary considerations and lifestyle changes?

A

Dietary modifications: CNM Diet, antioxidant-rich foods, AIP, gluten-free diet.

Lifestyle changes: Smoking cessation, stress management, support for gut barrier function, and microbiome.

Interventions: Anti-microbial and biofilm disruptors, oral probiotics (also silver non particle liquid, ginger, turmeric, aloe, clove, garlic, neem), immune support,

Specific measures against infectious agents (EBV). L-Lysine, berberine, resveratrol, turmeric, EGCG.

Additional support: Probiotics, anti-inflammatory herbs (turmeric, ginger), stop smoking

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17
Q

Supplements to support RA

A

Vit D: ↓TH17, T reg diff, ↓ RANKL

Omega 3 (1g):Anti-Inflam ↓TH17, IL17, PGE2, NFkb, TNFa, IL6

GLA (1-2g): forms anti-inflam PGE1. ↓NFkb.

Reservatrol (200): polyphenol. ↓ TH17, NFkb, COX2

Alpha Lipoic Acid (1200mg): fat +water soluble antiox. ↑ gluathione. Anti inflamm ↓ NFkb, CRP.

Green tea (2-3): Anti-inflam ↓ NFkb, NO.

Quercetin (1.5-3g): Anti-inflam; ↓ NFkb, COX2, IL17, TNFa.

Zinc citrate (15-30): ↓ delta-6-desaturase. ↓ NFkb, IL1b, TNFa.

Probiotics lacto casei. Anti-inflamm Herbs; turmeric, devils claw, boswelia, ginger

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18
Q

What are the typical signs and symptoms of gout, and which joint is commonly affected during an acute episode?

A

Monoarticular arthritis, often affecting the 1st metatarsophalangeal joint (big toe).
Pain, swelling, redness, heat, and shiny skin.
Acute episodes may cause fever, malaise, and an inability to use the joint.

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19
Q

Explain the pathophysiology of gout, including the role of hyperuricaemia and the key cytokine involved in inflammation.

A

Hyperuricaemia is a key risk factor and prerequisite for monosodium urate (MSU) crystal formation.

Uric acid, the final purine breakdown product, accumulates, leading to MSU crystal formation.

Interleukin 1β is the primary cytokine mediating inflammation in gout.

20
Q

What are the causes and risk factors related to both uric acid overproduction and underexcretion, contributing to the development of gout?

A

Uric acid overproduction: Dietary purines (meat, organ meat, seafood), high cell turnover disorders, chemotherapy, fructose.

Uric acid underexcretion: Medication side effects, renal insufficiency, alcohol, genetics (ABCG2 SNPs), obesity, insulin resistance, dehydration.

21
Q

How is gout diagnosed, and what is the gold standard for confirming the diagnosis?

A

Diagnosis is mostly based on clinical presentation.

Hyperuricaemia (>6.8 mg/dL) alone doesn’t confirm gout.

Gold standard: Synovial joint microscopy showing urate crystals (not practical for routine diagnosis).

22
Q

What are some conventional medications used in the treatment and prevention of gout, both for acute attacks and long-term management?

A

Prevention: Allopurinol (inhibits xanthine oxidase).
Acute attacks: NSAIDs, colchicine (with a narrow therapeutic window).

23
Q

What are some key elements of the natural approach to managing gout, including dietary considerations and lifestyle changes?

A

CNM Naturopathic Diet with a focus on reducing uric acid levels.

Lifestyle changes: Addressing specific causes, optimizing omega-3:6 ratio, maintaining hydration.

Avoiding excessive protein intake, keeping feet warm, considering castor oil packs.

24
Q

Supplements/herbs for GOUT? Dosages?

A

Quercetin (200-400): XO inhibition. Anti-Inflam

EPA (3g): Anti-infla - ↓ NFkb, TNFa, IL-6.

Methyl Folate (400-800 mcg): ↓ XO

Tart Cherry (3000): Polyphenols. ↓ COX/NFkb, IL-1b. Redcue uric acid levels and Ox Stress,

Celery: ↓ XO and Ox Stress. ↓COX/LOX

Nettle - diuretic/alkasining. urinary excretion ↑.

25
Q

Describe the key symptoms associated with Fibromyalgia (FM), and what are the diagnostic criteria according to the American College of Rheumatology?

A

Key symptoms: chronic widespread pain, fatigue, sleep disturbance, stiffness, headaches, bowel disturbances, anxiety, and depression.

A widespread pain index (WPI) score: 7+
Symptom severity scale (SS) score of 5+,or
a WPI score of 4–6 and SS score of 9+, lasting >3 months with no other explanation for the symptoms.

26
Q

What are the causes and risk factors associated with Fibromyalgia, including the role of trauma, hypothyroidism, intestinal dysbiosis, infections, and nutritional deficiencies?

A

Trauma: Both physical (surgery, accidents) and emotional (bereavement, divorce) with links to early-life adversity. HPAA dyregulation.

Hypothyroidism: Disrupted cortisol levels and altered substance P synthesis in CNS.

Intestinal Dysbiosis: SIBO, altered gut bacteria composition (↓ F Praunitzii +baceteroides spp.), and the modulation of pain through metabolites (nociception).

Infections: e.g., EBV with correlations between high EBV IgG concentrations and pain intensity.

Nutritional Deficiencies: Vit D, B12, Magnesium, Gluten , Genetic SNPs, Heavy metals.

27
Q

Explain the natural approach to managing Fibromyalgia, covering dietary considerations and lifestyle changes.

A

Diet for stress, mitochondrial dysfunction, and chronic fatigue syndrome (CFS).

Gluten-free + low FODMAP diets

Support thyroid, adrenals, and GI function with protocols such as SIBO/5R.

↓ glutamate levels by ↑ GAD co-factors (Mg, B6, Zn, vitamin C, taurine), avoiding glutamate sources, and limiting alcohol.

28
Q

How do infections, specifically the Epstein-Barr virus (EBV), contribute to Fibromyalgia, and what are the implications of genetic variations?

A

Infections: High EBV IgG concentrations correlate with pain intensity and FM symptoms.

Genetic Variations:
MTHFR (C667T SNP): Impaired methylation affecting detox+ neurotransmitter prod.

COMT: Variations associated with low activity influencing pain sensitivity.

GSTM1: Absent gene increases toxic burden (i.e. mercury - reduces glutathione)

29
Q

Provide insights into the role of dietary changes, in managing Fibromyalgia.

A

Follow dietary guidelines outlined for **stress, **mitochondrial dysfunction and CFS
* Gluten-free diets and a low FODMAP show clinical improvements in FM.
* Support the thyroid, adrenals, GIT as needed. E.g., apply a SIBO/ 5Rprotocol; support commensal microbial diversity and SCFA-producers with fibre, polyphenols etc.
* Reduce glutamate levels ―by increasing glutamate decarboxylase (GAD) co-factors (Mg, vitamin B6, Zn, vitamin C, taurine). Avoiding glutamate sources (e.g., MSG) and alcohol (inhibits GAD).

  • Reduce toxic load; support liver detoxification phases and elimination pathways
  • Optimise Metallothionein (binds to heavy metals) ―requires adequate cysteine, zinc, copper, and selenium.
    Optimise Antioxidant enzyme status (e.g., SOD, glutathione peroxidase etc.) with selenium, zinc, etc.
    Optimise Chain-breaking antioxidants (vitamin C, E, flavonoids, carotenoids). Focus on a ‘rainbow’.
  • Optimise glutathione levels ―e.g., NAC, silymarin, resveratrol.
  • Saunas―↑ excretion of toxins incl. mercury.
    Technique: High enough temp to start sweating freely in 15–20 minutes. 20–40 min heavy sweating. Drink before/after (typically ~1 pint / 20 min moderate / heavy sweating.
  • Hydrotherapy―Epsom salts (0.5‒1 kg) with few drops of lavender essential oil in bath. Balneotherapy is well researched for FM
  • Support methylation ―for NT synthesis and detoxification: folate, B12, B6, B2, choline, betaine (TMG, e.g., in beetroot) and zinc; SAMe. Consider methylated B vitamins.
  • **Sleep support **― FM patients demonstrate abnormal α-rhythms and wakefulness during non-REM sleep. Sleep is therefore non-restorative. Sleep deprivation impairs descending pain-inhibition pathways.
30
Q

How can glutamate levels be reduced as part of the natural approach to Fibromyalgia, and why is this important in symptom management?

A

Reduce glutamate levels by enhancing GAD co-factors (Mg, B6, Zn, vitamin C, taurine).

Avoid glutamate sources (e.g., MSG) and limit alcohol, as they inhibit GAD.

Elevated glutamate is linked to increased pain sensitivity in FM.

Support Methylation (methylated B vits, SAMe, choline, betaine, zinc.

Sleep support
Epsom salt baths (1kg) + lavender oil.
Saunas
Antioxidant - Se, Zinc etc.

Aerobic exercise but avoid high intensity.
Support stress.

31
Q

Fibromyaglia supplements and dosages?

A

Mg malate/citrate (200-500): Block NMDA receptor (for excitation). Zinc also.

Vit D - modulate central pain process, Infl cytokines, PGE2

B6 (50-100): GAD cofactor - conversion glutamate to GABA

COQ10 (300): Anti-ox, electron transport chain, mito dysfunction

5-HTP (100-300): precursor serotonin for descending pain regulation and melatonin synthesis.

32
Q

Fibromyaglia herbs

A

Ashwagandha (300-600 1-3x) HPAA/sleep, GABA, Anti-nociceptive

St Johns Wort (600-1200): ↑ serotonin/melatonin. GABA and MAO

Devil’s Claw (3-6g dried herb): ↓inflam cytokines IL-1b, IL-6, TNFa

33
Q

What are the risk factors and causes associated with mechanical back pain, and how does emotional stress contribute to its development?

A

Physical trauma, such as sports injuries and heavy lifting, more common in manual occupations.

Emotional stress leading to increased sympathetic nervous system (SNS) activity, resulting in elevated muscle tone/shortening.

Inflammation induced by poor diet, metabolic endotoxaemia, and obesity.

Contribution of Emotional Stress:
↑ muscle tone and alters neurotransmitter levels in descending antinociceptive pathways.
Negative thoughts (‘catastrophising’) and fear/pain avoidance exacerbate chronic LBP.

34
Q

Explain the natural approach to managing back pain, emphasizing dietary strategies and the role of inflammation mediators.

A

CNM diet. ↓ inflammation (eliminating refined sugar, trans fats, dairy, limited red meat, and increasing omega-3).

Mediterranean diet, polyphenol content with antioxidant and anti-inflammatory actions.

Addressing mediators of chronic inflammation through interventions like gut protocols and sleep hygiene.

35
Q

How does chronic stress contribute to the development and exacerbation of chronic lower back pain (LBP)?

A

Sympathetic nervous system (SNS) activity

Alters neurotransmitter levels associated with descending antinociceptive pathways.

Negative thoughts (‘catastrophising’) and fear/pain avoidance exacerbate chronic LBP.

36
Q

How can essential oils be incorporated into the natural approach for back pain, and which oils are commonly used?

A

Lavender and frankincense for relaxation and anti-inflammatory effects.

Peppermint for its anti-spasmodic properties.

Use carrier oil (eg almond)

37
Q

Supplements for back pain

A

Magnesium (200-400mg): block NMDA receptor - nociception. Muscle relaxing.

Omega 3 (1g+): Anti-inflam, ↓ PGE2, NFkb, TNFa, IL-6

Phospatidylserine (200-400): neuronal cell membran support (myelination). Synergetic with EPA.

Proeolytic enzymes (serrapeptase 75/bromelain 1500): ↓PGE + fibrinolytic (aid fluid drainage)

Bach Flowers (4x4): star of bethleham -Trauma/shock of unexplained back pain.

Nervine herbs: lemonbalm (300-600), passionflower (1 tsp), chamomile (1 tbsp) (GABA).

38
Q

What is Axial Spondyloarthritis, and what are its common signs and symptoms?

A

chronic inflammatory arthritis affecting the spine and sacroiliac joints (SIJs).

Chronic back pain and stiffness, especially in the mornings.

Extra-articular manifestations, such as uveitis, psoriasis, and inflammatory bowel disease (IBD).

Systemic symptoms like fever and fatigue.

39
Q

What are the genetic factors and other risk factors associated with Axial Spondyloarthritis?

A

Genetic Factors:

HLA-B27 gene
IL-23R SNPs and ERAP1/2
Dysfunction in the IL-23/Th17 signaling axis is a key driver of chronic inflammation.

Other Risk Factors:
Biomechanical stress -repetitive strain.
Microbial cross-reactivity- Klebsiella pneumoniae.
GI inflamm/dysbiosis, ↓ F. prausnitzii and ↑ E. coli.
Impaired intestinal barrier ↑ zonulin, LPS and thin mucosal barrier.

40
Q

What are some natural approaches for managing Axial Spondyloarthritis?

A

CNM Diet with dairy exclusion.

Low-starch diet associated with lower ESR levels.

Fasting
Anti-inflamm herbs: Devil’s Claw, turmeric, ginger, boswellia.
Osteopathy) -mobility.
Exercise-Pilates: posture considerations.
Breathing exercises- thoracic mobility.
Contrast showers, Epsom salt baths.

41
Q

Supplements for Axial Spondyloarthritis

A

Vit D - T reg, ↑ Th17/Th1
Reservatrol (200): ↓Th17, Nf-kb, COX2
Omega (1g)

42
Q

What is osteoporosis, and what are its signs and symptoms?

A

Low bone mass, micro-architectural deterioration, and increased bone fragility, leading to a higher risk of fractures.

Signs/symptoms:
Usually asymptomatic until a fracture occurs.
Common fractures: vertebrae, hip, and distal radius.
Vertebral crush fractures-loss of height and kyphosis.

43
Q

Explain the bone remodelling process for osteoporosis.

A

Bone Remodelling:

Osteoclasts (OC) increase bone resorption, while osteoblasts (OB) create a collagen matrix for remineralization.
Various substances like PTH, estrogen, vitamin D, corticosteroids, and acidosis influence this balance.
Osteoporosis results from unbalanced OC bone resorption without sufficient OB bone formation.

44
Q

Explain the causes/risk factors for osteoporosis.

A

Age >25, with age-related bone loss.
Postmenopausal women (estrogen deficiency).
Low body weight
high red meat consumption
nutrient def (e.g., vit D, calcium, mg).
Acidic-forming diets (dairy, carbonated beverages, coffee), caffeine, alcohol, smoking, inactivity.

Hypochlorhydria impairs calcium absorption, inflammation, drugs (e.g., corticosteroids), gut dysbiosis, and certain diseases.

45
Q

What is the natural approach to managing osteoporosis

A

Avoid/limit: Dairy, carbonated beverages, coffee, alcohol; limit red meat intake.

Include: Anti-inflammatory foods, high omega-3 sources, flax/chia seeds, turmeric, ginger.
DGLV for minerals and vitamins, phytoestrogens if post-menopausal, adequate dietary protein, addressing other risk factors.

3 weekly, 30-min weight-bearing sessions promote osteoblast activity.

Options: Walking, weight training, stair climbing, dancing, yoga, Pilates, Tai Chi, hiking.

Resistance exercise is beneficial for tendonous attachments to bone and coordination to prevent falls.

46
Q

Osteoporosis supplements

A

Calcium (food DGLV, seasame, tahini) or 500: must be ionised to be absorbed by intestines - HCI.

Vit D; facilitate Ca absorption, Bone T/O, muscle function/balance.

K2 (50-100): osteocalcin production - draws Ca into bone tissue.

Mg (00-400): co-factor alkaline phosphatase (bone mineralisation(

Zinc: inhibit osteoclast activity

Nettle - nutritive (1 tsp infusion 3x)