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CBL MSK > lectures 3 > Flashcards

lectures 3 Flashcards

1
Q

What is pain?

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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2
Q

Scientific theory of pain

A

Pain direct result of tissue damage
Severity of injury determines amount of pain
Brain passive receptor of signals

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3
Q

Gate control theory of pain

A

Biophycosocial model
Pain input to brain is controlled via a gate in the spinal cord
Gate controlled by pain fibers at site of injury and pain fibers elseqhere

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4
Q

Acute pain
Duration
Aetiology
Purpose

A

Short( <3 months)

Result of injury or disease

Important protective role- know what pain feels like and if stimulus is HARMFUL

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5
Q

Congenital analgesia

A

When you can’t feel pain

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6
Q

Chronic pain
Duration
Aetiology
Purpose

A

Long ( >3-6 months)
Can be related or unrelated to tissue damage
No useful biological function

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7
Q

What do we access when accessing pain

A

SENSORY ASPECTS OF PAIN- e.g. intensity, location, frequency, quality

PHYSICAL FUNCTION- e.g. activity levels, exercise, daily life

EMOTINAL WELL BEING/PHYSCHOLOGICAL IMPACT e.g. pain related distress, depression, coping

ROLEAND INTERPERSONAL FUNCTIONING e.g. work, relationships, social activities

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8
Q

Challenging of using questionnaires to access pain

A

Pain fluctuates over time
Impact of comorbities and pain elsewhere
Adaptation and avoidance strategies

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9
Q

Non verbal pain assessment

A

Some patients may be unable to self report pain

Identify potential causes lf pain
Observe patient behaviours e.g. behabioural pain assessment tools
Surrogate reporting of pain
Analgesic trial – trying to alleviate pain

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10
Q

Stress

A

State of disharmony or threat to homeostasis

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11
Q

Protective factors

A

Factors which enhance coping and resilience and decrease the likelihood that stress will have a negative outcome

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12
Q

Central pain sensitisation

A

development and maintenance of chronic pain

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13
Q

Allodynia

A

non painful stimulus experienced as painful

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14
Q

Hyperalgesia

A

painful stimuli experienced as much more painful than it is

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15
Q

Biophyschosocial approach to health and illness

A

BIOLOGICAL – genetic predisposition, neurochemistry, medications

PSYCHOLOGICAL- learning, emotions, thinking, attitudes, memory, beliefs, stress

SOCIAL- social support, family background, cultural, medical care

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16
Q

Biophychosocial model of pain

A

Biological – intensity and nature of pain
Psychological- distress and health beliefs
Social- effect on daily functioning

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17
Q

How does pain increase stress and increase pain

A

HPA axis – part of endocrine system, controls reactions to stress, regulates the immune system, digestion and energy
Increased cortisol= increased inflammation= increased pain

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18
Q

Coping

A

COPE is a measure of coping

3Subscales

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19
Q

3 types of coping

A

PROBLEM FOCUSED COPING- active coping, planning , suppression of competing activities, restraint coping

EMOTIONAL FOCUSED COPING- acceptance, denial, turning to religion, positive reinterpretation, seeking to support emotional support

LESS USEFUL/ DISENGAGEMENT- focus on + venting of emotions, behavioral and mental disengagement

20
Q

Promoting adaptive coping

A

Sleep
Training e.g knowing how to do CPR if youre a doc
Eating healthy

21
Q

Avoiding maladaptive coping

A 
Blurring of boundaries 
Avoidance and withdrawal 
Negative attitude
Alcohol/drugs 
Hopelessness 
Negative self talk
22
Q

Fear avoidance model of chronic pain

A

Avoiding an activity as fearful pain will increase or will do it again e.g. not doing physio as worried it’ll get worse- muscle gets worse

23
Q

Pain catastrophizing

A

Exaggerated negative orientation toward actual or anticipated pain experiences
Maladaptive beliefs
Without treatment, patients that catastrophise about their pain are at higher risk of developing chronic pain and disability

24
Q

Pyschological innervations

A

Relaxation
Hypnosis
Cognitive behavioral therapy ( CBT)
Graded exposure in vivo for pain related fear

25
Q

Bone growth in children

A 
High velocity (cm/year) in children 
Varies depending on age 
Puberty = fastest rate of growth
26
Q

Bone growth measurement

A

osteoblastic activity

In lab - use enzyme ALKLAINE PHOSPHATASE as a marker of osteoblastic activity

Highest levels of ALP at birth and puberty

27
Q

Green stick fracture

A

Mid-diaphyseal, bone is bent such as to damage the CONVEX surface, fracture is INCOMPLETE

28
Q

Torus fracture

A

Bone buckles but the integrity of the surface of the bone on convex side is maintained
Eg like bending a piece of cardboard
Fractures don’t usually need treatment and bone will remodel over time

29
Q

Salter harris fractures

A 
Fractures including the growth plate 
S- seperated growth plate 
A= above grwoth plate 
L= below growth plate 
T= through grwoth plate 
ER= erasure of grwoth plate
30
Q

Rickets

A 
Osteomalacia in adults 
Prematurity 
Nutrition 
Maternal vit D deficiency 
Lack of sunlight

Features worst where growth is GREATEST e.g. long bones

31
Q

Sarcopaenia

A

Inevitable loss of muscle mass and strength that occurs in ageing muscle
Gradual loss
Muscle replaced by fat

Loose motor neurones
Fewer motor units with more muscle fibers causing loss of coordiantion
Slow muscle reflex
Bad coordination 
Higher chance of fall
32
Q

Factors contributing to age related sarcopeania

A

REDUCED physical activity
Nutritional, hormonal, metabolic and immunologic factors
Decreased motor units and muscle fibers – muscle fiber atrophy

33
Q

osteopaenia /porosis

A

begins as you lose bone mass and your bones get weaker. This happens when the inside of your bones become brittle from a loss of calcium. It’s very common as you age
BONE LOSS, reduced bone mineral density ( BMD), micro architecture deterioration
Bones become more fragile
Vertebrae wrist and hip are most at risk
Previous fracture increases risk of future fracture

34
Q

How do oestrogen and progesterone affect bones

A

Stimulate bone formation
Hormone levels decrease with age
Menopause: bone loss becomes twice as fast in women = loss of hormones
Effect is systemic ( so other factors operate)
Hormone replacement therapy ( hrt) reverses some of effects of menopause
Hormones also affect bone via muscle – increased muscle = increased bone

35
Q

Diet and bones

A

Inadequate dietary calcium is a problem
Vitamin and sunlight help
Alcohol and smoking can decrease bone mass
Low body weight increases risk of low BMD
Diet has less effect than genes, hormones and exercise

36
Q

How does ageing affect fibrous tissues

A

Cell content/morphology changes
Collagen cross links increase and mature – become non reducible – brittle
Non enzymic glycation ( NEG) makes tissue yellow and stiffer
Microdamage accumulated and makes tissue weaker
Cells become less responsive to mechanical stimuli
Ligaments get stiffer

37
Q

Tendons

A

fibrous connective tissue which attaches muscle to bone. Tendons may also attach muscles to structures such as the eyeball.

38
Q

Ligaments

A

fibrous connective tissue which attaches bone to bone, and usually serves to hold structures together and keep them stable

39
Q

Tendon cells

A

Elongated cells with long processes

40
Q

Immature tendon tissue

A

Tenoblasts/fibroblasts - fat

41
Q

Mature tendon tissue

A

tenocytes/ fibrocytes - thin

42
Q

Collagen cross linking

A

Collagen is main component of connective tissue
Cross links increase tissue strength and stiffness
Non enzymatic glaycation( NEG ) makes tissues brittle and yellow
NEG uncontrolled by cells – problem In tissues with LOW turnover
Cross links are REDUCIBLE in young tissue and NON REDUCIBLE in mature tissue

43
Q

Age related changes in cartilage

A

Decreased proteoglycan content
Decreased aggregation of PGs
Increased collagen content and cross linking
Increased levels of non enzymatic glycation
Increased apopotosis
Increased stiffness and decreased flexibility

44
Q

Chondrocytes

A

Produce and maintain Cartlidge
Cartlidge cell density decreases with age
Chondrocytes stop dividing at skeletal maturity

45
Q

Age related changes in spine

A

LOSS OF HYDRATON
Leak out
Damaged
Degraded

46
Q

Vertebral osteoporosis

A

Anterior region of traceulae most affected
Porous
Less connected
Leads to kyphotic deformity

47
Q

Bones under xray

A

look WHITE absorb alot of rays

CBL MSK (6 decks)

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