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MBBS - Year 1 > Clinical Skills - Chronic Diseases > Flashcards

Clinical Skills - Chronic Diseases Flashcards

1
Q

Classification of fibromyalgia

A

Pain for >3 months

11/18 tender points

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2
Q

Where must the pain be to classify it is fibromyalgia

A

The upper and lower body
Right and left sides
Axial skeleton

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3
Q

Tender points in FM

A 
Suboccipital 
Lower cervical 
Trapezius 
Supraspinatus 
2nd rib 
Lateral epicondyle 
Gluteal 
Greater trochanter 
Knee (medial fat pad)
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4
Q

Characteristic features of fibromyalgia

A 
Fatigue 
Sleep disturbance 
Stiffness 
Paraesthesia 
Headaches 
Irritable bowels 
Cold hands 
Depression 
Anxiety 
Daytime restless legs
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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

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6
Q

2010 Fibromyalgia syndrome criteria

A

Widespread pain index
Symptom severity score
Duration >3 months
No other explanation

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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

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8
Q

Fibromyalgia prevalence

A

Fibromyalgia 1 - 10%

Chronic widespread pain 10 - 20%

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9
Q

FM epidemiology

A

3x more common in women
Rises w/ age to a maximum in 60s
Disability level comparable to RhA

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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
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11
Q

Hyperalgesia

A

Abnormally heightened sensitivity to pain

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12
Q

Allodynia

A

Pain is caused by a stimulus that usually doesn’t elicit pain

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13
Q

Examination in FM

A

Tender points are only reliable finding
No myasthenia
No synovial infl

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14
Q

Investigations in FM

A

Normal:
No infl markers
No metabolic or endocrine abnormality
Muscle enzymes and EMG normal

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15
Q

Diseases that overlap w/ FM

A 
CFS
Myofascial pain syndrome 
IBS
Migraine 
irritable bladder 
Post-traumatic syndrome
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16
Q

FM in other diseases

A

Infl rheumatic disease - 30%
Infl myositis and myopathies
Hypothyroidism
MS

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17
Q

Causes of FM

A 
Infection 
Trauma 
Genetics 
Muscle abnormality 
Psychological abnormality 
Sleep abnormality 
Neuroendocrine 
CNS Autonomic sensitisation
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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

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19
Q

Trauma causing FM

A

Association w/ leg fracture, neck fracture, hypermobility

But psychiatric historic history prior to trauma is related

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20
Q

Genetics causing FM

A

Familial clustering
HLA association
But pain behaviour is learned in families and HLA may reflect infl disease

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21
Q

Muscle abnormality causing FM

A

Intrinsic muscle abnormalities have been detected

But likely secondary to inactivity or to pain

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22
Q

Psychological abnormality causing FM

A

Pt looks well and non physical abnormality so must be psychological

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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

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24
Q

Sleep abnormality causing FM

A

Slow wave disruption triggers FM

EEG patterns reported

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25
Q

Neuroendocrine cause of FM

A

Reduced growth hormone, prolactin, SH, CRH response to stress

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26
Q

CNS (autonomic) sensitisation causing FM

A

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

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27
Q

Most plausible explanation for FM

A

Disorder of nociceptive input

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28
Q

Management of FM

A

Anti-infl
Antidepressants
Opiates
Non-drug treatment

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29
Q

Anti-infl for FM

A

No better than placebo

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30
Q

Antidepressants for FM

A

Low dose tricyclic antidepressants
Amitriptyline effective in reducing pain
Serotonin reuptake inhibitors have short term effects

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31
Q

Opiates for FM

A

Tramadol

Ketamaine

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32
Q

Examples of non-drug treatments for FM

A 
Exercise 
PT 
Cognitive therapy 
Biofeedback 
Tender point infections
Hypnotherapy Acupuncture
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33
Q

Prognosis for FM

A

Conflicting

Tertiary centres show little change over decade

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34
Q

Who has the best outcome for FM

A

Younger pt

Lower pain score

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35
Q

Chronic conditions

A

Diseases lasting more than 3 months and some have no cure

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36
Q

What do chronic conditions normally result in

A

Significant adjustment for the individual and increased contact w/ medical services

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37
Q

Examples of chronic diseases

A 
Alzheimer's
Arthritis 
Asthma ]Cancer 
MS 
Epilepsy
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38
Q

Regular reviews of the condition

A

The disease
The treatment
Secondary prevention

39
Q

Regular reviews of the condition - the disease

A

Check patients understanding

Monitor disease progress

40
Q

Regular reviews of the condition - the treatment

A

Check patients understanding

Monitor adherence, effectiveness, side effects, adverse effects

41
Q

Regular reviews of the condition - secondary prevention

A

Check payments understanding of risk of other conditions developing
Assess/ monitor/ treat risk factors

42
Q

Regular reviews of the pt

A

Effects on feelings
Effects on life
Effects on family/ carers

43
Q

Regular reviews of the pt - effects on feelings

A

Sick role, self-esteem , stigma

44
Q

Regular reviews of the pt - effects on life

A 
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
Q

Effects of chronic illness

A 
Physical 
Psychological 
Behavioural 
Social 
Spiritual/ existential
46
Q

Social effects of chronic illnesss

A 
Role 
Employment 
Family 
Financial 
Educational
47
Q

The Dr’s response to chronic illness

A

Curative medicine approach
Sense of failure or feeling overwhelmed as many cannot be cured
Perspective of Palliative Medicine

48
Q

Why may chronic disease co-exist

A

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
Q

Unmodifiable risk factors

A

Age

Genetic (inherited) risk

50
Q

Potentially modifiable risk factors that the MDT monitor

A 
Diet and exercise 
Pollution 
Smoking 
Alcohol consumption 
Social factors e.g. deprivation
51
Q

Team members that may be involved in care of chronic back pain

A 
GP or nurse practitioner community physiotherapist 
Osteopath or chiropractic practitioner 
Radiology service 
Pain clinic 
Orthopaedic surgeon 
Rheumatologist
52
Q

Diff trajectories for chronic illness

A

Chronic disease follows a no. of diff courses w/ consequent differences in the response of the individual to that disease

53
Q

Examples of diff trajectories for chronic illness

A

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
Q

HPA axis

A

Stress stimulates hypothalamus to produce CRH
Pituitary gland stimulated to produce ACTH
Adrenal cortex stimulated to produce cortisol

55
Q

CRH

A

Corticotropin Releasing Hormone

56
Q

ACTH

A

Adrenocorticotropic hormone

57
Q

Compounds cholesterol can metabolise into

A

Aldosterone
Cortisol
Dihydrotestosterone anf oestradiol - sex hormones

58
Q

Aldosterone

A

Helps regulate bp, renal salt and water resorption

59
Q

Diurnal variation of cortisol

A

Increases while we sleep and decreases as our day goes on

60
Q

Physiological effects of cortisol

A

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
Q

Addison’s disease

A

Adrenal glands not working as steroids have been suddenly withdrawn from someone who’s been taking them long-term

62
Q

Features of Addison’s

A 
Low blood pressure
Hyperpigmentation
Fatigue
Muscle weakness
Hypoglycaemia
Low Na / raised K
Nausea, vomiting
63
Q

Addisonian crisis

A

Collapse, hypoglycaemia, abdo pain, D & V, death isn’t uncommon

64
Q

Cushing’s disease/ syndrome

A

Disease - pituitary gland
Syndrome - adrenal glands

Prolonged exposure to elevated endogenous or exogenous glucocorticoids.e.g cortisol

65
Q

Features of Cushing’s disease

A 
Truncal obesity 
Moon face
Striae 
Hypertension
Hirsutism
Osteoporosis
Diabetes
66
Q

Truncal obesity

A

Thin arms and legs but fat. body

67
Q

Striae

A

Purple stretch marks

68
Q

Mechanism of action of steroids

A

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
Q

What does the suppression of COX-2 synthesis do

A

Prevent arachidonic acid being converted to PG and LT

70
Q

Indication of glucocorticosteroids

A

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
Q

Adverse effects of corticosteroids

A

Usually mimic symptoms of Cushing’s disease

The higher the dose, the more quickly people start to experience adverse effects

72
Q

Types of adverse effects of corticosteroids

A 
General 
Infection*
MSK 
Ophthalmic 
GI 
CNS
Dermatological 
Cardiovascular - htn
Diabetes
73
Q

General adverse effects of corticosteroids

A

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
Q

Adverse effects of corticosteroids - infection

A

Bacterial: Staphylococcus, Gram, -ve, TB, Listeria
Viral: Herpes zoster
Fungal: Candidiasis

75
Q

Adverse effects of corticosteroids - MSK

A

Myopathy - usually proximal
Osteoporosis
Osteonecrosis
Tendon rupture, usually happens acutely

76
Q

Osteoporosis

A

Skeletal disorder characterized by compromised bone strength, predisposing a person to an increased risk of fracture

77
Q

Most serious complication of glucocorticoid therapy

A

Osteoporosis, usually manifests as hip fractures tubes or vertebral fractures

78
Q

Adverse effects of corticosteroids - Ophthalmic

A

Cataracts

Glaucoma

79
Q

Cataracts

A

Lens becomes cloudy

80
Q

Glaucoma

A

Increase in pressure in eyes

81
Q

Adverse effects of corticosteroids - GI

A

Peptic ulcer disease: de novo or reactivation, exacerbates ulcerogenic properties of NSAIDs (x2)
Pancreatitis
Perforation
Steatohepatitis

82
Q

Adverse effects of corticosteroids - CNS

A

Psychosis
Depression
Mood and sleep disturbance
Benign Intracranial Hypertension

83
Q

Benign Intracranial Hypertension

A

Increased pressure in CNS and areas surrounding brain

84
Q

Adverse effects of corticosteroids - Dermatological

A 
Acne 
Striae 
Alopecia 
Bruising 
Skin atrophy
85
Q

Adverse effects of corticosteroids - Cardiovascular

A

Fluid retention
Altered lipid profiles
Arrhythmias w/ iv infusion
Accelerated atherosclerosis increasing risk of heart attack

86
Q

Consequences of vertebral fractures

A

Kyphosis
Unable to take deep breaths due to decreased lung volumes
Unable to eat large meals due to abdominal protrusion
Loss of height

87
Q

How does glucorticoids lead to decreased volume

A

Increased bone resorption due to decreased serum PTH and increased serum oestrogen and testosterone
Decreased bone formation

88
Q

What happens if steroids are given to children

A

Causes growth retardation:
Inhibits linear growth
Delay epiphyseal closure
Suppression of growth hormone secretion

89
Q

How do we lessen the effects of steroids on children

A

Alternate day administration

90
Q

How should we use steroids

A

Minimum effective dose for the minimum amount of time via an appropriate route
We NEVER stop steroids suddenly

91
Q

CK test

A

Creatine Kinase can be used to detect muscle damage

92
Q

What is defined as long term steroid use

A

More than 7.5mg for more than 3 months.

93
Q

Why are steroids given in the morning

A

To coincide with peak levels of endogenous cortisol.

94
Q

Surgery for those on long-term steroids

A

Require a higher dose just before surgery

MBBS - Year 1 (93 decks)

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