Clinical Skills - Chronic Diseases Flashcards
1
Q
Classification of fibromyalgia
A
Pain for >3 months
11/18 tender points
2
Q
Where must the pain be to classify it is fibromyalgia
A
The upper and lower body
Right and left sides
Axial skeleton
3
Q
Tender points in FM
A
Suboccipital Lower cervical Trapezius Supraspinatus 2nd rib Lateral epicondyle Gluteal Greater trochanter Knee (medial fat pad)
4
Q
Characteristic features of fibromyalgia
A
Fatigue Sleep disturbance Stiffness Paraesthesia Headaches Irritable bowels Cold hands Depression Anxiety Daytime restless legs
5
Q
Criticisms of fibromyalgia diagnosis
A
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
6
Q
2010 Fibromyalgia syndrome criteria
A
Widespread pain index
Symptom severity score
Duration >3 months
No other explanation
7
Q
Symptom severity score
A
A: fatigue, waking unrfreshed, cognitive symptoms
B: list of 40 other wide-ranging symptoms e.g. headaches, itching, change in taste
8
Q
Fibromyalgia prevalence
A
Fibromyalgia 1 - 10%
Chronic widespread pain 10 - 20%
9
Q
FM epidemiology
A
3x more common in women
Rises w/ age to a maximum in 60s
Disability level comparable to RhA
10
Q
Pain in FM
A
'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
11
Q
Hyperalgesia
A
Abnormally heightened sensitivity to pain
12
Q
Allodynia
A
Pain is caused by a stimulus that usually doesn’t elicit pain
13
Q
Examination in FM
A
Tender points are only reliable finding
No myasthenia
No synovial infl
14
Q
Investigations in FM
A
Normal:
No infl markers
No metabolic or endocrine abnormality
Muscle enzymes and EMG normal
15
Q
Diseases that overlap w/ FM
A
CFS Myofascial pain syndrome IBS Migraine irritable bladder Post-traumatic syndrome
16
Q
FM in other diseases
A
Infl rheumatic disease - 30%
Infl myositis and myopathies
Hypothyroidism
MS
17
Q
Causes of FM
A
Infection Trauma Genetics Muscle abnormality Psychological abnormality Sleep abnormality Neuroendocrine CNS Autonomic sensitisation
18
Q
Infection causing FM
A
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
19
Q
Trauma causing FM
A
Association w/ leg fracture, neck fracture, hypermobility
But psychiatric historic history prior to trauma is related
20
Q
Genetics causing FM
A
Familial clustering
HLA association
But pain behaviour is learned in families and HLA may reflect infl disease
21
Q
Muscle abnormality causing FM
A
Intrinsic muscle abnormalities have been detected
But likely secondary to inactivity or to pain
22
Q
Psychological abnormality causing FM
A
Pt looks well and non physical abnormality so must be psychological
23
Q
Psychological abnormalities in FM
A
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
24
Q
Sleep abnormality causing FM
A
Slow wave disruption triggers FM
EEG patterns reported
25
Neuroendocrine cause of FM
Reduced growth hormone, prolactin, SH, CRH response to stress
26
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
27
Most plausible explanation for FM
Disorder of nociceptive input
28
Management of FM
Anti-infl
Antidepressants
Opiates
Non-drug treatment
29
Anti-infl for FM
No better than placebo
30
Antidepressants for FM
Low dose tricyclic antidepressants
Amitriptyline effective in reducing pain
Serotonin reuptake inhibitors have short term effects
31
Opiates for FM
Tramadol
| Ketamaine
32
Examples of non-drug treatments for FM
```
Exercise
PT
Cognitive therapy
Biofeedback
Tender point infections
Hypnotherapy Acupuncture
```
33
Prognosis for FM
Conflicting
| Tertiary centres show little change over decade
34
Who has the best outcome for FM
Younger pt
| Lower pain score
35
Chronic conditions
Diseases lasting more than 3 months and some have no cure
36
What do chronic conditions normally result in
Significant adjustment for the individual and increased contact w/ medical services
37
Examples of chronic diseases
```
Alzheimer's
Arthritis
Asthma ]Cancer
MS
Epilepsy
```
38
Regular reviews of the condition
The disease
The treatment
Secondary prevention
39
Regular reviews of the condition - the disease
Check patients understanding
| Monitor disease progress
40
Regular reviews of the condition - the treatment
Check patients understanding
| Monitor adherence, effectiveness, side effects, adverse effects
41
Regular reviews of the condition - secondary prevention
Check payments understanding of risk of other conditions developing
Assess/ monitor/ treat risk factors
42
Regular reviews of the pt
Effects on feelings
Effects on life
Effects on family/ carers
43
Regular reviews of the pt - effects on feelings
Sick role, self-esteem , stigma
44
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
```
45
Effects of chronic illness
```
Physical
Psychological
Behavioural
Social
Spiritual/ existential
```
46
Social effects of chronic illnesss
```
Role
Employment
Family
Financial
Educational
```
47
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
48
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
49
Unmodifiable risk factors
Age
| Genetic (inherited) risk
50
Potentially modifiable risk factors that the MDT monitor
```
Diet and exercise
Pollution
Smoking
Alcohol consumption
Social factors e.g. deprivation
```
51
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
```
52
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
53
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
54
HPA axis
Stress stimulates hypothalamus to produce CRH
Pituitary gland stimulated to produce ACTH
Adrenal cortex stimulated to produce cortisol
55
CRH
Corticotropin Releasing Hormone
56
ACTH
Adrenocorticotropic hormone
57
Compounds cholesterol can metabolise into
Aldosterone
Cortisol
Dihydrotestosterone anf oestradiol - sex hormones
58
Aldosterone
Helps regulate bp, renal salt and water resorption
59
Diurnal variation of cortisol
Increases while we sleep and decreases as our day goes on
60
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
61
Addison's disease
Adrenal glands not working as steroids have been suddenly withdrawn from someone who’s been taking them long-term
62
Features of Addison's
```
Low blood pressure
Hyperpigmentation
Fatigue
Muscle weakness
Hypoglycaemia
Low Na / raised K
Nausea, vomiting
```
63
Addisonian crisis
Collapse, hypoglycaemia, abdo pain, D & V, death isn’t uncommon
64
Cushing's disease/ syndrome
Disease - pituitary gland
Syndrome - adrenal glands
Prolonged exposure to elevated endogenous or exogenous glucocorticoids.e.g cortisol
65
Features of Cushing's disease
```
Truncal obesity
Moon face
Striae
Hypertension
Hirsutism
Osteoporosis
Diabetes
```
66
Truncal obesity
Thin arms and legs but fat. body
67
Striae
Purple stretch marks
68
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
69
What does the suppression of COX-2 synthesis do
Prevent arachidonic acid being converted to PG and LT
70
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
71
Adverse effects of corticosteroids
Usually mimic symptoms of Cushing's disease
| The higher the dose, the more quickly people start to experience adverse effects
72
Types of adverse effects of corticosteroids
```
General
Infection*
MSK
Ophthalmic
GI
CNS
Dermatological
Cardiovascular - htn
Diabetes
```
73
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)
74
Adverse effects of corticosteroids - infection
Bacterial: Staphylococcus, Gram, -ve, TB, Listeria
Viral: Herpes zoster
Fungal: Candidiasis
75
Adverse effects of corticosteroids - MSK
Myopathy - usually proximal
Osteoporosis
Osteonecrosis
Tendon rupture, usually happens acutely
76
Osteoporosis
Skeletal disorder characterized by compromised bone strength, predisposing a person to an increased risk of fracture
77
Most serious complication of glucocorticoid therapy
Osteoporosis, usually manifests as hip fractures tubes or vertebral fractures
78
Adverse effects of corticosteroids - Ophthalmic
Cataracts
| Glaucoma
79
Cataracts
Lens becomes cloudy
80
Glaucoma
Increase in pressure in eyes
81
Adverse effects of corticosteroids - GI
Peptic ulcer disease: de novo or reactivation, exacerbates ulcerogenic properties of NSAIDs (x2)
Pancreatitis
Perforation
Steatohepatitis
82
Adverse effects of corticosteroids - CNS
Psychosis
Depression
Mood and sleep disturbance
Benign Intracranial Hypertension
83
Benign Intracranial Hypertension
Increased pressure in CNS and areas surrounding brain
84
Adverse effects of corticosteroids - Dermatological
```
Acne
Striae
Alopecia
Bruising
Skin atrophy
```
85
Adverse effects of corticosteroids - Cardiovascular
Fluid retention
Altered lipid profiles
Arrhythmias w/ iv infusion
Accelerated atherosclerosis increasing risk of heart attack
86
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
87
How does glucorticoids lead to decreased volume
Increased bone resorption due to decreased serum PTH and increased serum oestrogen and testosterone
Decreased bone formation
88
What happens if steroids are given to children
Causes growth retardation:
Inhibits linear growth
Delay epiphyseal closure
Suppression of growth hormone secretion
89
How do we lessen the effects of steroids on children
Alternate day administration
90
How should we use steroids
Minimum effective dose for the minimum amount of time via an appropriate route
We NEVER stop steroids suddenly
91
CK test
Creatine Kinase can be used to detect muscle damage
92
What is defined as long term steroid use
More than 7.5mg for more than 3 months.
93
Why are steroids given in the morning
To coincide with peak levels of endogenous cortisol.
94
Surgery for those on long-term steroids
Require a higher dose just before surgery
