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UofG Medicine Question Bank 2020 > Rheumatology/Osteoporosis/Weightlessness > Flashcards

Rheumatology/Osteoporosis/Weightlessness Flashcards

1
Q

What are potential problems with inflammation?

A

Bystander Damage

Too intense of a response

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2
Q

Why doesn’t everyone get auto-immune diseases?

A

Tolerance (controlled unresponsiveness to self)

Immune system has regulatory checks

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3
Q

What is the 2 hit mechanism of autoimmune disease?

A

Genetic susceptibility-> susceptible genes resulting in failure of self-tolerance
Infection/inflammation

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4
Q

How do RA patients present?

A

Pain, swelling (metacarpal-phalangeal joints, seen when trying to form fist), stiffness
Pain is common in morning and due to inactivity

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5
Q

What sex is more likely to develop autoimmune disease?

A

Women, 2-3x more

Potentially due to fact that women live with foreign material (during pregnancy)

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6
Q

What is palmer deviation?

A

Movement of phalangeal bones laterally/medially.

Way the tendons will pull the bones if RA becomes very severe

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7
Q

What other morbidities may occur alongside RA?

A

Sarcopenia (extreme loss of muscle mass)
Metabolism abnormailities (store fat in liver)
Vessel inflammation (can cause CVD, increase in myocardial infarction)
Fatigue
Depression

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8
Q

Why do people get RA?

A

Born with risk factors

Environmental exposures later in life

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9
Q

What are the phases of RA?

A 
Phase A- Genetic Risk factors
B- Environmental Risk factors 
C- autoimmunity, but no symptoms (tells us maybe RA starts outside the joints and moves there later)
D- symptoms
E- Undifferentiated arthritis 
F- Established RA
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10
Q

What are genetic risk factors? Fix this question.

A 
Genome wide association studies show evidence of immune function contribution displaying it is adaptive
Epigenetic abnormalities (methylation)
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11
Q

What is the strongest risk factor for RA?

A

Smoking.
HLA-DRB1 alleles (the shared epitope, can have 1, or double shared-epitope, more equals larger risk)
If you have the gene and smoke, there is an exponential risk at developing RA.

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12
Q

How does microbiome relate to RA?

A

Prevotella copri bacteria is enriched in early RA

This is where our immune system becomes educated about the environment and learns to tolerate things.

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13
Q

What are 2 important molecules involved in systemic autoimmunity leading to RA?

A 
CCP antibodies (binds to post translational modifications of proteins. CCP is cyclic citrullinate peptide, where citrulline replaces arginine) 
Rheumatoid factor (antibody directed against an self-antibody (FC fragment of IgG or IgM))
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14
Q

Why does RA go to the joints?

A

We don’t know.
We have systemic response, and then we get immune cells that invade joints.
There are defects in CD4 T cells where differentiation of naïve CD4 to Th effector cells happens, and this ‘starts a war’ in the joints.

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15
Q

How do cells within joints change as a result of RA?

A

Fibroblast-like synoviocytes start releasing inflammatory cytokines
Osteoclasts release MMP
DC presentation to:
T cells -> release cytokines
B cells -> release autoantibodies
Both contribute to worsening inflammation

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16
Q

What are some treatments in RA?

A

NSAIDs
Corticosteroids- don’t prevent damage though, used short term
Disease-modifying antirheumatic drugs (DMARDs)- There are conventional synthetics which reduce reactivity of leukocytes helping decrease cytokines, and Biologics ones (monoclonals) which can bind receptors for particular cytokines (typically TNF)

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17
Q

What are some popular Disease Modifying Anti-Rheumatic Drugs?

A 
Methotrexate
Sulphasalizine
Leflunomide
Hydroxychloroquine
Many also have an immune dampening effect.
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18
Q

What are biologic agent DMARDs?

A

Drugs, like monoclonal abs, receptors, or peptides, that are developed rationally by targeting processes important in the disease pathogenesis, i.e. cytokines, t cells, and B cells
They have to be injected

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19
Q

In relation to B cells, what drug can be used to treat RA?

A

CD20 receptor on B cells can be blocked by Anti-C20 monoclonal antibody (rituximab), depleting mature B cell levels and therefore reducing levels of Auto-Ab

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20
Q

How can we treat RA by targeting cytokines?

A

Can interfere with pro-inflammatory cytokines
Anti-6 receptors (TNF, or IL-6)
IL6 and cytokine storm is important

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21
Q

Why is inhibiting JAK kinases not going to work in comparison to blocking cytokines when treating rheumatoid arthritis?

A

JAK 1-3 and TYK2 receptors sit on surface with the tyrosine kinase receptors.
If you block them though, you block all pathways, so you can get a lot of off target effects.

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22
Q

How does the immune and nervous system relate in terms of developing RA?

A

Mice who have had their vagus nerves cut cannot produce TNFa and therefore don’t develop RA.

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23
Q

How does TNFa related to RA?

A

TNF is pro-inflammatory involved largely in bacterial infection (not viral, this is interferons).
Blocking TNFa also reduces further inflammatory cytokines, like IL1.

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24
Q

Is RA and its treatments associated with increased risk of infection?

A

Yes

25
Q

Is RA and its treatments associated with increased risk of malignancy?

A

Yes

26
Q

How much bone density is lost by age 80, and when does most bone loss occur?

A

25-40%

Most loss occurs first 5 years following menopause

27
Q

What is a fragility fracture?

A

Fractures resulting from mechanical force that would not ordinarily result in fracture
Said force equivalent to falling from a standing height or less

28
Q

What fragility fracture is most and least common?

A

Spinal vertebrae, hip (proximal femur), then wrist (distal radius) is least

29
Q

What causes the most hospital admissions in people over 75?

A

Fracture of femur (significantly greater)

Then lumbar/pelvic fracture

30
Q

What people are at highest risk for fragility fracture and are invited for screening?

A

Those who have fragility fractures after 50 years of age
Also carry out fracture-risk assessments (online) to determine people’s risk which will determine risk (if major risk, they should be invited for DXA)

31
Q

How can you maximize peak bone mass?

A 
Regular weight bearing exercise
Healthy diet
Sufficient Vitamin D
Avoid smoking
Responsible alcohol consumption
32
Q

What are the 2 main forms of pharmaceutical treatment for osteoporosis?

A

Antiresorptive- inhibit osteoclasts, but don’t promote building muscle (bisphosphonates, denosumab)
Anabolic- stimulate bone formation via osteoblast (Teriparatide- injection stimulates osteoblasts)

33
Q

How much muscle bulk is lost during aging and when?

A

From 30 years onwards, 3-8% atrophy of muscle fibers per decade is lost
General muscle fibre loss (5% 24-50, then 25% over next 25 years)

34
Q

Can you prevent muscle aging?

A

Yes, by doing weight bearing exercise

35
Q

What is sarcopenia?

A

Progressive and generalized skeletal muscle disorder associated with increased likelihood of adverse outcomes including falls, fractures, physical disability, and mortality.

36
Q

What is the primary parameter in defining sarcopenia?

A

Low muscle STRENGTH, not necessarily muscle loss

37
Q

What declines are more drastic in terms of muscle with aging?

A

More of a decline in muscle strength

Decline of muscle mass is not as drastic

38
Q

What are the two types of sarcopenia?

A

Primary- age related, no cause for sarcopenia

Secondary- activity, disease, or nutritional related declines

39
Q

How do you screen for sarcopenia?

A

Sarc-F screening tool- if they score positive on tool, you look for further investigations

40
Q

How do you diagnose sarcopenia?

A

Muscle function is tested first- look for muscle weakness (grip strength, chair-stand strength, gait speed)
Muscle mass- can use CT/MRI cross sectioning and calculate muscle bulk. Can use DXA scanners.
Bioimpedance analysis- scale and height used to calculate body composition but not reproducible

41
Q

What are the steps of diagnosis of sarcopenia according to the European Algorithm?

A

Suspicion -> Grip strength test -> DXA Scan (will confirm) -> Performance measurements (Gait speed, TUG) -> severity is confirmed

42
Q

What impacts does sarcopenia have on a person?

A

Increased hospitalization
Increased mortality
Increased frailty

43
Q

What is the treatment for sarcopenia?

A 
Exercise- resistant and aerobic
Nutrition attention (increased protein)
Vitamin D supplementation for those deficient
44
Q

What are consequences of musculoskeletal aging?

A

Altered gait and balance leading to falls
Increased injury (fracture)
Chronic pain (50% in community, 80% in long-term care)
Isolation
Loss of independence

45
Q

What changes are seen in both hormone and cell activity in relation to bone ageing

A

Reduction of oestrogen following menopause causes loss of inhibition of resorption leading to increased osteoclast activity -> increased remodelling
Reduction in secretion of and sensitivity to Growth Factors and IGF-B (needed for osteoblast differentiation)
Reduction in osteoblast proliferation and differentiation
Reduced ability of osteoblasts to sense/respond to mechanical force

46
Q

Does osteoporosis cause pain?

A

No, it is painless. Its complications cause pain

47
Q

How does the body respond to weightlessness?

A

It begins to excrete more calcium and phosphate, as the body ‘thinks’ it is not needed.
Muscle fibre loss/weakness occurs

48
Q

What is the turnover rate of bone in young people vs elderly?

A

20% turnover in young

2% in elderly

49
Q

When is peak muscle typically reached?

A

28-29 years.

50
Q

What changes cause bone and muscle mass loss?

A

Linked to endocrines and rates of activity

51
Q

What type of force does gravity create and what resists this?

A

Compressive
Hydroxyapatite resists this force, although collagen aids in the flexibility needed when undergoing compressive force (they reinforce it by allowing for flexion)

52
Q

What drives bone remodelling?

A

Loading forces

53
Q

What hormones/factors help regulate bone remodelling?

A

PTH- increases osteoclast activity via ^RANKL expression (also inhibit PO4 reabsorption in kidney)
Vit D- Increases Ca and PO4 absorption from gut and recovery from renal filtrate
Calcitonin- Lowers plasma Ca by reducing osteoclast activity
FGF23- Reduces PO4 and calcium reabsorption from kidneys
Oestrogen- Inhibits bone resorption

54
Q

How does air quality relate to rickets?

A

Too much fog will reduce sunlight, which will reduce Vitamin D activation.

55
Q

What are the physiological consequences of prolonged space flight?

A

Fluid shifts, fluid and electrolyte loss (change in urine composition)
Negative energy balance (not eating enough calories)
Both points above result in:
-Bone Loss
-Skeletal and (some) cardiac muscle atrophy
Less radiation exposure
These changes are similar to aging

56
Q

What percentage of muscle loss is seen in the lower limbs when in free-fall conditions?

A

6-8% in thigh

4-6% in calf

57
Q

How can we prevent bone loss when in space?

A

Alendronate- form of bisphosphonates which slows bone turnover by being absorbed onto hydroxyapatite crystals
Maintain formation with heavy resistance exercise
Maintain nutrients- vit d supplementation (and other minerals/vitamins like Vitamin K which has role in stabilizing bone)

58
Q

What are physiological impacts observed in astronauts returning to earth?

A

Hypotension (reduced blood volume)
Weakness (sarcopenia)
Bone demineralization (osteopenia)

UofG Medicine Question Bank 2020 (42 decks)

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