lectures 3 Flashcards
What is pain?
Unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Scientific theory of pain
Pain direct result of tissue damage
Severity of injury determines amount of pain
Brain passive receptor of signals
Gate control theory of pain
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
Acute pain
Duration
Aetiology
Purpose
Short( <3 months)
Result of injury or disease
Important protective role- know what pain feels like and if stimulus is HARMFUL
Congenital analgesia
When you can’t feel pain
Chronic pain
Duration
Aetiology
Purpose
Long ( >3-6 months)
Can be related or unrelated to tissue damage
No useful biological function
What do we access when accessing pain
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
Challenging of using questionnaires to access pain
Pain fluctuates over time
Impact of comorbities and pain elsewhere
Adaptation and avoidance strategies
Non verbal pain assessment
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
Stress
State of disharmony or threat to homeostasis
Protective factors
Factors which enhance coping and resilience and decrease the likelihood that stress will have a negative outcome
Central pain sensitisation
development and maintenance of chronic pain
Allodynia
non painful stimulus experienced as painful
Hyperalgesia
painful stimuli experienced as much more painful than it is
Biophyschosocial approach to health and illness
BIOLOGICAL – genetic predisposition, neurochemistry, medications
PSYCHOLOGICAL- learning, emotions, thinking, attitudes, memory, beliefs, stress
SOCIAL- social support, family background, cultural, medical care
Biophychosocial model of pain
Biological – intensity and nature of pain
Psychological- distress and health beliefs
Social- effect on daily functioning
How does pain increase stress and increase pain
HPA axis – part of endocrine system, controls reactions to stress, regulates the immune system, digestion and energy
Increased cortisol= increased inflammation= increased pain
Coping
COPE is a measure of coping
3Subscales
3 types of coping
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
Promoting adaptive coping
Sleep
Training e.g knowing how to do CPR if youre a doc
Eating healthy
Avoiding maladaptive coping
Blurring of boundaries Avoidance and withdrawal Negative attitude Alcohol/drugs Hopelessness Negative self talk
Fear avoidance model of chronic pain
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
Pain catastrophizing
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
Pyschological innervations
Relaxation
Hypnosis
Cognitive behavioral therapy ( CBT)
Graded exposure in vivo for pain related fear
Bone growth in children
High velocity (cm/year) in children Varies depending on age Puberty = fastest rate of growth
Bone growth measurement
osteoblastic activity
In lab - use enzyme ALKLAINE PHOSPHATASE as a marker of osteoblastic activity
Highest levels of ALP at birth and puberty
Green stick fracture
Mid-diaphyseal, bone is bent such as to damage the CONVEX surface, fracture is INCOMPLETE
Torus fracture
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
Salter harris fractures
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
Rickets
Osteomalacia in adults Prematurity Nutrition Maternal vit D deficiency Lack of sunlight
Features worst where growth is GREATEST e.g. long bones
Sarcopaenia
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
Factors contributing to age related sarcopeania
REDUCED physical activity
Nutritional, hormonal, metabolic and immunologic factors
Decreased motor units and muscle fibers – muscle fiber atrophy
osteopaenia /porosis
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
How do oestrogen and progesterone affect bones
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
Diet and bones
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
How does ageing affect fibrous tissues
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
Tendons
fibrous connective tissue which attaches muscle to bone. Tendons may also attach muscles to structures such as the eyeball.
Ligaments
fibrous connective tissue which attaches bone to bone, and usually serves to hold structures together and keep them stable
Tendon cells
Elongated cells with long processes
Immature tendon tissue
Tenoblasts/fibroblasts - fat
Mature tendon tissue
tenocytes/ fibrocytes - thin
Collagen cross linking
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
Age related changes in cartilage
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
Chondrocytes
Produce and maintain Cartlidge
Cartlidge cell density decreases with age
Chondrocytes stop dividing at skeletal maturity
Age related changes in spine
LOSS OF HYDRATON
Leak out
Damaged
Degraded
Vertebral osteoporosis
Anterior region of traceulae most affected
Porous
Less connected
Leads to kyphotic deformity
Bones under xray
look WHITE absorb alot of rays
