Clinical Skills - Chronic Diseases Flashcards
Classification of fibromyalgia
Pain for >3 months
11/18 tender points
Where must the pain be to classify it is fibromyalgia
The upper and lower body
Right and left sides
Axial skeleton
Tender points in FM
Suboccipital Lower cervical Trapezius Supraspinatus 2nd rib Lateral epicondyle Gluteal Greater trochanter Knee (medial fat pad)
Characteristic features of fibromyalgia
Fatigue Sleep disturbance Stiffness Paraesthesia Headaches Irritable bowels Cold hands Depression Anxiety Daytime restless legs
Criticisms of fibromyalgia diagnosis
Criteria are a compromise
There’s no gold standard pathology
Not grounded in any clear pathological process
Fibromyalgia may be just be one end of the spectrum
2010 Fibromyalgia syndrome criteria
Widespread pain index
Symptom severity score
Duration >3 months
No other explanation
Symptom severity score
A: fatigue, waking unrfreshed, cognitive symptoms
B: list of 40 other wide-ranging symptoms e.g. headaches, itching, change in taste
Fibromyalgia prevalence
Fibromyalgia 1 - 10%
Chronic widespread pain 10 - 20%
FM epidemiology
3x more common in women
Rises w/ age to a maximum in 60s
Disability level comparable to RhA
Pain in FM
'It hurts all over' May have a focus, but shifts Burning, radiating, gnawing Moderate of severe Worse than that of RhA Exhibit hyperalgesia and allodynia
Hyperalgesia
Abnormally heightened sensitivity to pain
Allodynia
Pain is caused by a stimulus that usually doesn’t elicit pain
Examination in FM
Tender points are only reliable finding
No myasthenia
No synovial infl
Investigations in FM
Normal:
No infl markers
No metabolic or endocrine abnormality
Muscle enzymes and EMG normal
Diseases that overlap w/ FM
CFS Myofascial pain syndrome IBS Migraine irritable bladder Post-traumatic syndrome
FM in other diseases
Infl rheumatic disease - 30%
Infl myositis and myopathies
Hypothyroidism
MS
Causes of FM
Infection Trauma Genetics Muscle abnormality Psychological abnormality Sleep abnormality Neuroendocrine CNS Autonomic sensitisation
Infection causing FM
Widespread pain follows infectious mononucleosis in 20%
20% have persistent symptoms after Lyme but no sero-epidemiological evidence and Abx trial don’t help post Lyme
Trauma causing FM
Association w/ leg fracture, neck fracture, hypermobility
But psychiatric historic history prior to trauma is related
Genetics causing FM
Familial clustering
HLA association
But pain behaviour is learned in families and HLA may reflect infl disease
Muscle abnormality causing FM
Intrinsic muscle abnormalities have been detected
But likely secondary to inactivity or to pain
Psychological abnormality causing FM
Pt looks well and non physical abnormality so must be psychological
Psychological abnormalities in FM
Greater psychological symptoms, but cannot be differentiated from those attributable to pain
Active psychological illness only 1.5x times commoner
Greater prevalence of depression in family members
No spp personality type
Healthcare seeking behaviour
Sleep abnormality causing FM
Slow wave disruption triggers FM
EEG patterns reported
Neuroendocrine cause of FM
Reduced growth hormone, prolactin, SH, CRH response to stress
CNS (autonomic) sensitisation causing FM
Altered pain threshold on physiological testing at tender points and other sites
Increased heart rate variability
CSF Substance P levels increased
Brain regional blood flow abnormalities in areas related to pain processing
Abnormal temporal summation of pain
Most plausible explanation for FM
Disorder of nociceptive input
Management of FM
Anti-infl
Antidepressants
Opiates
Non-drug treatment
Anti-infl for FM
No better than placebo
Antidepressants for FM
Low dose tricyclic antidepressants
Amitriptyline effective in reducing pain
Serotonin reuptake inhibitors have short term effects
Opiates for FM
Tramadol
Ketamaine
Examples of non-drug treatments for FM
Exercise PT Cognitive therapy Biofeedback Tender point infections Hypnotherapy Acupuncture
Prognosis for FM
Conflicting
Tertiary centres show little change over decade
Who has the best outcome for FM
Younger pt
Lower pain score
Chronic conditions
Diseases lasting more than 3 months and some have no cure
What do chronic conditions normally result in
Significant adjustment for the individual and increased contact w/ medical services
Examples of chronic diseases
Alzheimer's Arthritis Asthma ]Cancer MS Epilepsy
Regular reviews of the condition
The disease
The treatment
Secondary prevention
Regular reviews of the condition - the disease
Check patients understanding
Monitor disease progress
Regular reviews of the condition - the treatment
Check patients understanding
Monitor adherence, effectiveness, side effects, adverse effects
Regular reviews of the condition - secondary prevention
Check payments understanding of risk of other conditions developing
Assess/ monitor/ treat risk factors
Regular reviews of the pt
Effects on feelings
Effects on life
Effects on family/ carers
Regular reviews of the pt - effects on feelings
Sick role, self-esteem , stigma
Regular reviews of the pt - effects on life
Relationships: dependency, sex, parenting Work: early retirement, change in job Finance: income, pension, benefits Other activities e.g. hobbies, holidays Housing: adaptations needed Mobility: walking, driving
Effects of chronic illness
Physical Psychological Behavioural Social Spiritual/ existential
Social effects of chronic illnesss
Role Employment Family Financial Educational
The Dr’s response to chronic illness
Curative medicine approach
Sense of failure or feeling overwhelmed as many cannot be cured
Perspective of Palliative Medicine
Why may chronic disease co-exist
One disease directly causes another e.g. diabetes –> renal damage
Both condns share a common cause e.g. poor diet/ sedentary lifestyle increases risk of range of condns e.g. diabetes and hypertension
Unmodifiable risk factors
Age
Genetic (inherited) risk
Potentially modifiable risk factors that the MDT monitor
Diet and exercise Pollution Smoking Alcohol consumption Social factors e.g. deprivation
Team members that may be involved in care of chronic back pain
GP or nurse practitioner community physiotherapist Osteopath or chiropractic practitioner Radiology service Pain clinic Orthopaedic surgeon Rheumatologist
Diff trajectories for chronic illness
Chronic disease follows a no. of diff courses w/ consequent differences in the response of the individual to that disease
Examples of diff trajectories for chronic illness
Short period of evident decline e.g. cancer
Prolonged dwindling e.g. frailty and dementia
Long term limitations w/ intermittent serious episodes e.g. heart and lung failure
HPA axis
Stress stimulates hypothalamus to produce CRH
Pituitary gland stimulated to produce ACTH
Adrenal cortex stimulated to produce cortisol
CRH
Corticotropin Releasing Hormone
ACTH
Adrenocorticotropic hormone
Compounds cholesterol can metabolise into
Aldosterone
Cortisol
Dihydrotestosterone anf oestradiol - sex hormones
Aldosterone
Helps regulate bp, renal salt and water resorption
Diurnal variation of cortisol
Increases while we sleep and decreases as our day goes on
Physiological effects of cortisol
Effects on mood
Breaks down fats to fatty acids and glycerol
Modulates immune system
Releases catecholamines
Mineralocorticoid effects on bp
Increases gluconeogenesis ans causes insulin resistance
Reduces bone formation and increases resorption
Catabolises tissues to release AA
Addison’s disease
Adrenal glands not working as steroids have been suddenly withdrawn from someone who’s been taking them long-term
Features of Addison’s
Low blood pressure Hyperpigmentation Fatigue Muscle weakness Hypoglycaemia Low Na / raised K Nausea, vomiting
Addisonian crisis
Collapse, hypoglycaemia, abdo pain, D & V, death isn’t uncommon
Cushing’s disease/ syndrome
Disease - pituitary gland
Syndrome - adrenal glands
Prolonged exposure to elevated endogenous or exogenous glucocorticoids.e.g cortisol
Features of Cushing’s disease
Truncal obesity Moon face Striae Hypertension Hirsutism Osteoporosis Diabetes
Truncal obesity
Thin arms and legs but fat. body
Striae
Purple stretch marks
Mechanism of action of steroids
Glucocorticoids enter cell and bind to receptors in cytoplasm
Glucocorticosteroid-receptor complex binds to responsive genes
Increases transcription of anti-infl proteins and blocks transcription of infl cytokines and adhesion molecules
Inhibit phagocytosis
Suppress COX-2 synthesising
What does the suppression of COX-2 synthesis do
Prevent arachidonic acid being converted to PG and LT
Indication of glucocorticosteroids
Steroids are often used in the treatment of a variety of non-infectious medical conditions that involve infl e.g respiratory system, skin and subcutaneous tissue
Adverse effects of corticosteroids
Usually mimic symptoms of Cushing’s disease
The higher the dose, the more quickly people start to experience adverse effects
Types of adverse effects of corticosteroids
General Infection* MSK Ophthalmic GI CNS Dermatological Cardiovascular - htn Diabetes
General adverse effects of corticosteroids
Appearance - truncal obesity, moon face, ‘buffalo hump’
Metabolic changes - glucose (hyperglycaemia, insulin resistance), protein (catabolism in muscle and bone), electrolyte (Na retention and K loss —> oedema)
Adverse effects of corticosteroids - infection
Bacterial: Staphylococcus, Gram, -ve, TB, Listeria
Viral: Herpes zoster
Fungal: Candidiasis
Adverse effects of corticosteroids - MSK
Myopathy - usually proximal
Osteoporosis
Osteonecrosis
Tendon rupture, usually happens acutely
Osteoporosis
Skeletal disorder characterized by compromised bone strength, predisposing a person to an increased risk of fracture
Most serious complication of glucocorticoid therapy
Osteoporosis, usually manifests as hip fractures tubes or vertebral fractures
Adverse effects of corticosteroids - Ophthalmic
Cataracts
Glaucoma
Cataracts
Lens becomes cloudy
Glaucoma
Increase in pressure in eyes
Adverse effects of corticosteroids - GI
Peptic ulcer disease: de novo or reactivation, exacerbates ulcerogenic properties of NSAIDs (x2)
Pancreatitis
Perforation
Steatohepatitis
Adverse effects of corticosteroids - CNS
Psychosis
Depression
Mood and sleep disturbance
Benign Intracranial Hypertension
Benign Intracranial Hypertension
Increased pressure in CNS and areas surrounding brain
Adverse effects of corticosteroids - Dermatological
Acne Striae Alopecia Bruising Skin atrophy
Adverse effects of corticosteroids - Cardiovascular
Fluid retention
Altered lipid profiles
Arrhythmias w/ iv infusion
Accelerated atherosclerosis increasing risk of heart attack
Consequences of vertebral fractures
Kyphosis
Unable to take deep breaths due to decreased lung volumes
Unable to eat large meals due to abdominal protrusion
Loss of height
How does glucorticoids lead to decreased volume
Increased bone resorption due to decreased serum PTH and increased serum oestrogen and testosterone
Decreased bone formation
What happens if steroids are given to children
Causes growth retardation:
Inhibits linear growth
Delay epiphyseal closure
Suppression of growth hormone secretion
How do we lessen the effects of steroids on children
Alternate day administration
How should we use steroids
Minimum effective dose for the minimum amount of time via an appropriate route
We NEVER stop steroids suddenly
CK test
Creatine Kinase can be used to detect muscle damage
What is defined as long term steroid use
More than 7.5mg for more than 3 months.
Why are steroids given in the morning
To coincide with peak levels of endogenous cortisol.
Surgery for those on long-term steroids
Require a higher dose just before surgery
