the patient Flashcards

(120 cards)

1
Q

Rheumatoid Arthritis and
Osteoarthritis

what is RA

A

Most common autoimmune disease
 Chronic, progressive, systemic inflammatory
disorder
 Affects synovial joints
 Many non‐articular manifestations, some of
which ↓ life expectancy
 Causes significant disability

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2
Q

RA: Who is affected?

A

Affects 1% of UK population
 ↓ in past few decades
 2‐3 times more common in women
 more prevalence with age
 Peak incidence 30‐50 years
 Disease activity varies over time, but about
50% develop serious progressive disease

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3
Q

What causes RA?

A

Not clear
 Genetic
 Hormonal
 Cigarette smoking
 Infection?

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4
Q

RA: Pathophysiology ‐ much simplified

A

Widespread inflammation of synovium
‐ thickens
 Infiltration by inflammatory cells
 Synovium spreads onto the articular cartilage
surface (‘pannus’) isolating it from synovial fluid
 Pannus erodes the articular cartilage; underlying
bone exposed → damage (osteoclasts sƟmulated)
 Key inflammatory cells include T‐cells, B‐cells,
macrophages and plasma cells.
cytokines: IL‐6, IL‐1 and TNF‐α
 Key inflammatory mediators are the cytokines
IL‐6, IL‐1 and TNF‐α
 Autoantibodies such as rheumatoid factor and citrullainated peptides
acƟvate the complement system → sƟmulates macrophages
 Characteristic bone loss is juxtra‐articular – immediately adjacent to both
sides of the joint. Eventually the joint is destroyed and undergoes fusion.

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5
Q

RA: How does it present?

A

Typically: slowly progressive, symmetrical
peripheral polyarthritis, evolving over few
weeks or months
 Pain and stiffness of the small joints of the
hands and feet; patients feels tired and unwell
 Also, wrists, elbows, shoulders, knees and ankles
 Joints are warm and tender, with swelling; stiffness
esp. mornings; limited movement and muscle
wasting
 Occasionally monoarthritis
 Occasionally very sudden

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6
Q

RA of hands

A

Early disease – swelling and early joint damage
 Late disease – deformity &
contractures

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7
Q

RA: Non‐ articular manifestations
symptoms and complications

A

Haematological
Anaemia
Neutrophilia
Thrombocytosis
Felty’s syndrome
 Neurological
Nerve entrapment
Cervical myelopathy
Mononeuritis complex
Peripheral neuropathies
 Pulmonary
Pulmonary nodules
Pleural effusions
Interstitial lung disease
Bronchiolitus oblitrans
 Cardiac
Pericarditis
Pericardial effusion
Conduction defects
Valvular heart disease
Vasculitis
Nail fold
Systemic
 Ocular
Keratoconjunctivitis sicca
Episcleritis
Scleritis
 Cutaneous
Palmar erythema
Pyoderma gangrenosum
Vasculitic rashes
Leg ulceration
Alopecia
 Amyloidosis
 Nodules

The
manifestations are listed to
ensure you understand that
RA is a systemic disease,
that affects a lot more than
joints. dont need to memorise

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8
Q

RA: Co‐morbidities

A

MI, HF, CVA, CVD, HTN
E.g. Patients with RA have a 3‐6 fold ↑risk of
MI
 Lymphoma and lymphoproliferative diseases
 Lung cancer, skin cancer
 Infections (disease & treatment)
 Depression, GI disease, osteoporosis,
psoriasis, renal disease (disease & treatment)

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9
Q

How is RA diagnosed?

A

Patient history
 Presenting symptoms / clinical examination
 American College of Rheumatology classification criteria
(1987) – poor sensitivity for early disease
 Clinical tests
↑ ESR & CRP (not always)
↑ platelet count
Rheumatoid factor – IgM present in 75‐80% of patients
with RA (seropositive) and 5% of patient without RA
Anti‐cyclic citrullinated peptide (anti‐CCP) antibodies is a more
specific test (90‐96% specificity)
Anaemia of chronic disease (normochromic, normocytic)
Radiology – X‐rays, MRI, ultrasound

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10
Q

RA: Monitoring of disease

A

Symptoms and clinical markers (CRP)
 NICE refers to DAS28 – Disease Activity Score
which has 4 parameters:
1. Number of swollen joints out of a total of 28 specified joints
2. Number of tender joints out of a total of 28 specified joints
3. Erythrocyte sedimentation rate
4. Patient’s interpretation of wellbeing, 0 – best, 100 – worst
Disease Activity DAS28
High > 5.1
Moderate > 3.2 – 5.1
Low 2.6 ‐ 3.2
Remission < 2.6

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11
Q

RA: Management

A

Multidisciplinary Team
 Medical – shared care (1° and 2° care)
 Specialist RA nurses
 Pharmacists
 Psychology
 Occupational therapy
 Physiotherapy
 Podiatry
Patient education is very important

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12
Q

RA management

A

Early diagnosis is important
Analgesics and NSAIDs only useful for:
 Symptom relief including pain control
Corticosteroids, DMARDs and biologicals:
 Slowing or prevention of joint damage
 Preserving and improving functional ability
 Achieving and maintaining disease remission

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13
Q

RA: Analgesics and NSAIDs

A

Analgesics – adjunct for pain relief
 NSAIDs ‐ analgesic and anti‐inflammatory effect,
but only provide symptomatic relief
 Use lowest dose possible and withdraw if
possible once patient responses to DMARDs
 Side effects:
Gastrointestinal – consider gastroprotection
Renal
Cardiac / thrombotic

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14
Q

RA: Corticosteroids

A

Inhibit cytokine release
 Rapid relief of symptoms / ↓ inflammaƟon
 Long‐term oral steroids associated with long‐
term side effects
 Oral therapy – bridging therapy until respond
to DMARDs (withdraw slowly)
 Intra‐articular injection into target joints

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15
Q

RA: Disease Modifying Anti‐Rheumatic Drugs

A

The sooner the better to prevent damage
 Ideally within 3 months of start of persistent
symptoms
 NICE – first line treatment is a
combination of DMARDs, unless inappropriate; if
so monotherapy
 Oral methotrexate, leflunomide or
sulfasalazine

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16
Q

RA: Biologic Response Modifiers

A

Huge change in management of RA in past
decade
 Currently only used if DMARDs fail ‐ NICE
 Specialist supervision
 Expensive
 Balance cost of treatment vs cost of disability
Tumour necrosis factor‐α blocker
Adalimumab, Certolizumab, Etanercept, Infliximab
NICE: TNF‐α blockers are the first‐line biologicals
 JAK inhibitor – Baracitinib, Tofacitinib
 Interleukin‐6 antagonist – Tocilizumab, Sarilumab
 T‐cell co‐stimulation modulator ‐ Abatacept
 B‐cell depleting ‐ Rituximab

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17
Q

what are biologics RA

A

Biologic response modifiers (BRMs) are a class of medications used in the treatment of rheumatoid arthritis (RA). They work by targeting specific components of the immune system involved in the inflammatory process, helping to reduce inflammation and prevent joint damage. BRMs are typically prescribed when conventional disease-modifying antirheumatic drugs (DMARDs) have been ineffective or are not well tolerated.

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18
Q

how are biologics given RA

A

Given along with DMARD, e.g. methotrexate
 Assessment using DAS28 at least every 6
months
 Continue if improvement in DAS28 of 1.2
points or more
 Often given by injection – mostly s/c, but some
by infusion (big proteins), except JAK inhibitors
 Different regimens – daily, twice weekly, weekly,
every 2 weeks, every 4 weeks, every 8 weeks
 Not just licensed for RA

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19
Q

RA: Biologic Response Modifiers ‐
Problems

A

↑ risk of infecƟon, parƟcularly with TNF‐α
inhibitors
 Particularly reactivation of latent TB (screen
before commencing Tx)
 Rituximab associated with 3 cases of
progressive multifocal leukoencephalopathy
 Injection site and infusion reactions
 TNF‐α inhibitors C/Id in advanced heart failure

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20
Q

Systemic lupus erythematosus – SLE
“lupus”

A

Autoimmune, multisystem
 90% of patients are female
 Rare – more common in black and Asian
women than white women
 Peak age onset 20‐30 years
 Strong genetic link; triggers
 5 fold increase in mortality compared to
age and gender matched controls, mainly
due to increased risk of premature CVD

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21
Q

SLE – clinical features

A

Typically follows pattern of flares and remissions,
but some patients have active disease for
prolonged periods
 Fever, weight loss and mild lymphadenopathy
during disease flares
 Fatigue and low grade joint pain may be constant
– symmetrical joints typically knees, wrists and
small joint of hands
 70‐90% of patients will have arthralgia and morning
stiffness, but joint swelling is rare
80‐90% of patients have skin manifestations,
e.g. malar rash
 Renal disease – a major determinant of
prognosis
 Vascular ‐ Raynaud’s syndrome is common
 Also affects cardiovascular and pulmonary,
peripheral and central nervous system, GI
systems; ocular disease, haematological
abnormalities, recurrent miscarriages

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22
Q

SLE ‐ treatment

A

Analgesics and NSAIDs
* Hydroxychloroquine – first line maintenance
* Acute & chronic: combination of low and high dose
glucocorticosteroids and immunosuppressants such as
methotrexate, azathioprine, mycophenolate mofetil or
cyclophosphamide
* Biologicals – belimumab
* Management of co‐morbidities
* Non‐pharmacological – sun protection, vit D
supplementation, smoking cessation, exercise

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23
Q

Osteoarthritis: What is it?

A

Most common musculoskeletal condition in
older people
 Chronic, degenerative disorder of the joints
 Most commonly affects knee, hip, spine and
small joints of the hand
 Causes significant pain and functional disability
 Interfers with ADLs, esp hand OA

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24
Q

OA: Who is affected?

A

About 1/3rd of UK population ≥ 45 have
sought Tx for OA
 More common in women
 Steep  prevalence with age
 Knee > Hip > Hand
 Overweight/obese

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25
What causes OA?
Primary OA – no known cause  Secondary OA – link to previous injury to joint, congenital abnormality or inflammatory arthritis such as gout or RA  Aetiology unknown but risk factors pre‐dispose: Age, gender, obesity, bone density, joint injury or disease, occupation, joint abnormalities and genetics.
26
OA: How does it present?
Pain in one or more joints  Gradual onset  Worsened by activity  Only short period of early morning stiffness  Muscle wasting around joints due to avoiding activity  Pain may be episodic, but can become persistent, occurring at rest  OA hands – Heberden’s and Bouchard’s nodes
27
How is OA diagnosed?
No validated diagnostic tool  Combination of Hx of pain symptoms and physical joint findings  X‐ray  Blood tests do not assist  (maybe CRP for inflammation)  X‐ray and blood tests to eliminate 
28
OA: Management
Education  Self‐management plan  Non‐pharmacological treatment is key  Pharmacological intervention is adjunct to non‐pharmacological  Surgery
29
OA: Non‐pharmacological management
Weight loss  Exercise  Physical aids  Joint surgery
30
OA: Pharmacological management
Adjunct to lifestyle interventions  Topical NSAIDs  Paracetamol  Oral NSAIDs or opioids  Topical capsaicin  Intra‐articular corticosteroids X Chondroitin and glucosamine X Intra‐articular hyaluronic acid
31
asthma definition
Asthma is a common long-term condition that affects the airways Central to all definitions is the presence of symptoms (more than one of wheeze, breathlessness, chest tightness, cough) and of variable airflow obstruction. More recent descriptions of asthma in both children and adults have included airway hyper-responsiveness and airway inflammation as components of the disease.
32
asthma symptoms
More than one of the following symptoms: wheeze, breathlessness, chest tightness and cough, particularly if: – symptoms worse at night and in the early morning
33
asthma triggers
Triggers = irritate, tighten and inflame airways: >common cold/infection >allergies to pollen/dust/animal fur >air pollution
34
possible causes of asthma
The airway lining becomes inflamed causing a build-up of sputum. This makes the airways even narrower, so harder to get air in and out of the lungs. ➢ Exercise-induced-asthma ➢ History of atopic disorder ➢ Family history of asthma and/or atopic disorder
35
asthma diagnosis
The amount of air you breathe out is measured by: Spirometry- measures the total amount of air you can breathe out from your lungs and how fast you can blow it out (presence and severity of airflow obstruction) Peak flow meter-measures how fast you can breathe out after you’ve taken a full breath in. Diagnosed in accordance with BTS/SIGN
36
what does spirometry measure
measures the total amount of air you can breathe out from your lungs and how fast you can blow it out (presence and severity of airflow obstruction)
37
what does peak flow measure
peak flow meter-measures how fast you can breathe out after you’ve taken a full breath in.
38
Two Phases of Asthma
Immediate Phase Reaction: on first exposure to antigen Late Phase Reaction: more sustained occurring 3 to 12 hours after early phase
39
Eosinophils??
Eosinophils are a type of white blood cell that protect your body from parasites, allergens, foreign bacteria and outside organisms. Eosinophils are larger than most cells and make up less than 5% of all white blood cells in your body Major cell in the LPR Primarily a secreting cell - Eosinophil Granular Associated Proteins Major Basic Protein (MBP) Eosinophil cationic protein Eosinophil-derived neurotoxin eosinophil peroxidase Platelet Activating Factor (PAF) Peptido leucotrienes (LTC4, LTD4 & LTE4) Free radicals species
40
Inflammatory Mediators asthma
Histamine Cyclo-oxygenase Products Lipoxygenase Products Bronchoconstriction: powerful response in asthmatics Increased Vascular Permeability: very potent PAF>LTD4>>Histamine Increased Mucous Secretion: very potent Bradykinin Platelet Activating Factor - PAF
41
Drug Treatment of Asthma
Asthma is common, incurable but eminently treatable. Asthma is an inflammatory disorder – the inflammatory basis is an important target Relievers (bronchodilators): rapid symptomatic relief in an acute attack. Preventers - prophylactic therapy to suppress immune component of asthma Non-pharmacological and alternative medicine – no convincing data of benefit
42
Aims in chronic asthma
Control of symptoms - preferable no chronic symptoms e.g. no nocturnal dyspnoea, best possible pulmonary function with minimal side-effects Stable long term control - no exacerbations Minimal nocturnal symptoms Minimal use of relievers Peak expiratory flow rate (PEFR) maintained at >80% best. Circadian variation on PEFR <20% Minimal limitations on exercise
43
Chronic Asthma Step 1: mild intermittent asthma
Sort acting inhaled b2-bronchodilator (SABA) on prn basis (but no evidence against regular dosing) Asthma is not controlled at any step if using SABA >3 times a week having symptoms 3 times a week or more waking at least once a week Same strategy for adults and children under 5 years but evidence base best in adults Inhaled b-agonist 30min before exercise is treatment of choice for exercise induced-asthma
44
B-Agonists in Asthma Bronchodilatation
b-receptors on bronchial smooth muscle. Major effect. Most quickly effective agents available. Act as functional antagonists.
45
Cholinergic Nerves B agonsist
some reduction of ACh release (post-ganglionic nerves)
46
b aginists in mucus secretion
some decrease in viscosity leading to increased clearance
47
mast cells b agonists
b-receptors stabilise. No proven anti- inflammatory action. Little change in hyper- reactivity
48
Adverse Effects of b-Agonists
Skeletal Muscle tremor - diagnostic use Cardiac Stimulation -direct b2 and indirect reflex due to peripheral b2-vasodilatation Impaired ventilation/perfusion ratio Hypokalaemia Increased glucose metabolism Increased lipolysis CNS stimulation - variable, typically sleep disturbance
49
b2 agonists choice of agent
All b2-agonists are effective. Pharmacological differences account for differing profile of action Degree of b2-selectivity. Binding affinity: duration of action Binding Kinetics: onset of action Systemic effects can be clinically significant Vascular b: vasodilatation. Reflex tachycardia In high doses break through b1-agonism
50
Short acting b2-selective agonists
None are catecholamines (rapid metabolism) Rapid onset of action (<10min, peak 30-90 min) and relatively short duration 4-8 hours when given by MDI Some may be used orally for prophylaxis (*) Relatively free of CVS effects by inhaled route Examples: Salbutamol Terbutaline
51
Systemic Administration b-agonists
Some active orally. Increase SE profile and little evidence of benefit (unless unable to use inhaler) Parenteral administration used in severe or life- threatening asthma Caution in hyperthyroidism, CVS disease, diabetes. Risk of hypokalaemia – may be serious with systemic administration (via stimulation of skeletal Na+/K+/ATPase pumps coupled to beta receptors)
52
Chronic Asthma Step 2: regular preventer therapy
Chronic Asthma Step 2: regular preventer therapy Low dose Inhaled corticosteroids (ICS) Beclomethasone (BEC) 200mcg BD Budesonide 200mcg BD Fluticasone 100mcg BD Mometasone 200mcg BD NB: above for dry powder inhalers
53
CFC Free Inhalers – HFA propellants
Beclometsaone (BEC): Qvar™ extra-fine particles and more potent than traditional CFC containing inhalers and 2x potent than Clenil Clenil Modulite™ is same potency as dry powder and CFC BEC inhalers. Note: Qvar and Clenil are NOT interchangeable and should be rx by brand (MHRA 2008) Dose conversion advice in BNF Steroid card issued with high dose BEC
54
Alternative Step 2 Strategies asthma
Regarded as less effective therapies Cromones: DSG ineffective in children, nedocromil not effective <5 years. Long Acting Beta-Agonits (LABAs) – have effect but should not be used without steroid therapy (evidence) – so not step 2! Leukotriene antagonists – have some effect. May be useful in children particularly <5 years Theophylline – may have beneficial effect but side effects. Caution
55
Glucocorticoids for asthma
First used early 1950s by systemic route most powerful agents for asthma therapy major systemic actions no direct bronchodilator activity: no immediate relief from symptoms 6 hours before benefit and even with injection, maximum benefit only after 12-24 hours Inhaled administration of topically active steroid At suitable dosage minimises systemic actions – step two “Standard Dose” regimens Now a major component in asthma therapy
56
Inhaled Administration
Agents must have potent topical action Beclomethasone diproprionate (BEC) & Budesonide equipotent Fluticasone (2x potentcy of BEC). No convincing evidence of advantage for any individual agent. Deposition in oropharyngeal tract is a problem (candidiasis, dysphoria can occur even at low dose). may be minimised by use of spacer or prior administration of beta-agonist. Rinse mouth after use. Particularly higher dose schedules
57
Inhaled Steroids - ADRs
Hypothalamic-Pituitary-Adrenal Supression No significant risk BDP < 800g daily adult or 400 g child (but do see in child >400 g daily) Bone Resorbption - some controversy modest effects down to 500g daily in adult Carbohydrate Metabolism/Lipid Metabolism effects minor and not significant <800 g daily Growth Retardation: possible above 400 g daily in children – usually short term. Monitor growth and use lowest possible dose
58
Mode of Action in Asthma
Major effect is suppression of cytokine synthesis and release and so recruitment of inflammatory cells (particulalry eosinophils) Affect many components of inflammatory response Inhibit phosopholipase A2 Inhibit macrophage activation Depress Antibody synthesis Depress activation & recruitment of T lymphocytes and of eosinophilsCheck compliance before action! Add Inhaled LABA to low dose ICS (combination inhaler) Depress release of peptido-leukotrienes. (Little immediate direct effect upon mast cells)
59
Chronic Asthma Step 3: Initial add on therapy
Check compliance before action! Add Inhaled LABA to low dose ICS (combination inhaler)
60
Long Acting b-agonists (LABA)
Slow onset of action, prolonged action Not normally for acute attacks and used on regular bd schedule for control Prolonged functional antagonism at bronchial smooth muscle. Do not replace steroids -no evidence for anti-inflammatory action Very potent (salmeterol 4x Salbutamol) Salmeterol (Serevent). Inhaled route Eformoterol (Foradil - Geigy). Inhaled Bambuterol (Bambec - Astra). Oral. *bis-dimethylcarbamate prodrug, lung conversion, 24hr dose
61
Compound Preparations (ICS+LABA)
Several different combination (see BTS table 12 + 13) Examples: Fostair (BEC and Formoterol – 100/6). Can be used bd at step 3. (Note CFC free). Seretide (Fluticasone/salmeterol – 50, 125, 250) Symbicort (Budesonide/Formoterol – 100/6; 200/6 and 400/12). Used bd at step 3. Also can be used bd plus prn as a combined prophylaxis and acute therapy.
62
Step 4: Additional add-on therapies
Stop LABA if no response and ICS to medium dose (see BTS) If benefit from LABA but NO control continue LABA + ICS If benefit from LABA but NO control continue LABA + ICS + trial of: >leukotriene antagonist
63
Step 5: High dose therapies
Increase ICS to high dose (see BTS) Add 4th agent: leukotriene antagonist m/r theophylline LAMA -Tiotropium (COPD inhalers) oral slow release b-agonist tablet (care with LABA)
64
Leukotriene Antagonists asthma
Montelukast (Singulair - MSD) and Zafirlukast (Accolate – Zeneca) Cysteinyl leukotriene receptor (cysLT1) antagonists Long acting and orally active. Once daily therapy. Licensed for prophylaxis of asthma Montelukast for add on therapy in adults and children (>6 months) Zafirlukast for therapy of asthma adults and children >12 years
65
Clinical Use
Inhibit EPR and LPR. Additive with inhaled & oral corticosteroids and with b-adrenoceptor agonists Not licensed as steroid sparing agents - additive with steroids. Do not replace and given with steroids. Inhibit aspirin induced and exercise asthma Main SE are GI disturbances including pain and headache. Both can induce Churg-Strauss Syndrome Vasculitis and eosinophilia – common background asthma Rare but fatal normally seen on steroid withdrawal. Monitor patients during steroid down-dosing
66
Methylxanthines asthma
Clinical use theophylline - or as aminophylline (theoph./EDTA complex). Effective orally only. Bronchodilator over plasma range 30-100 mol/ml Side-effects at 100 mol/ml and serious at 200 mol/ml (CVS: most serious dysrhythmia) Small VD - little individual dose variation Clearance by hepatic metabolism - variable Increased by enzyme induction (rifampacin, phenobarb, phyenytoin, carbamazepine) Impaired by hepatic disease & inhibitors of metabolism (e.g. oral contraceptives, erythromycin, calcium channel blockers) Low therapeutic index and variable clearance. Plasma levels achieved not easy to predict.
67
Undesirable Properties Methylxanthines asthma
Oral MR products minimise changes in plasma levels but show variable release Side effects Cardiac stimulation - can be marked (inotropic and chronotropic). High risk when by parenteral route – rare now Gastric Irritation - increased release of gastric acid and digestive enzymes CNS disturbances - insomnia, anxiety, nervousness and tremor. Seizure a risk – in children around upper dose range Not normally used in chronic asthma in children unless other therapies fail – specialist advice only
68
Mode of action Theophylline
Mode of action in asthma is still not fully explained. Phosphodiesterase inhibition - likely to be involved but are plasma concns. too low? Adenosine antagonism - but an analogue enprofylline is active yet not an antagonist Inhibition of inflammatory cells - weak and not enough to explain action (< b-agonists) Potentiation of diaphragm contractility - useful action unique to these agents.
69
Anticholinergics in asthma
Oldest drugs for asthma e.g. strammonium All are muscarinic antagonists – none are selective for muscarinic receptor sub-types. Reduce cholinergic tone to bronchial SM and submucous glands Atropine highly effective but marked systemic effects Dryness of mouth; dilation of pupils; cycloplegia; dryness of skin; constipation; urinary retention Airway “selectivity” is achieved by inhaled administration
70
The Anticholinergics asthma
Ipatropium bromide (Atrovent - Boehringer) Oxitropium bromide (Oxivent - Boehringer) Both are quarternary compounds with poor absorption across mucous membranes When inhaled, actions are local in the respiratory tract Slow onset of action but prolonged duration – ipatropium 8hr and oxitropium up to 12hr. No value as add-on in chronic asthma Value in acute asthma
71
New LAMA agents for asthma
LAMA usually for COPD! Aclidinium bromide (Eklira genuair) >Competitive, selective muscarinic receptor antagonist, with a longer residence time at M3 receptors which mediate contraction of smooth muscle in the airways; induces bronchodilation. >Once absorbed it is rapidly broken down in the plasma, resulting in minimal systemic anticholinergic side-effects. Glycopyrronium bromide (Seebri breezehaler) Umeclidinium (Incruse Ellipta)
72
Cromoglycate/Nedocromil for asthma
Derived from original research on khellin from seeds of Amni Visnaga Not bronchodilators Very safe with few side-effects. LD50 in animals >4grams/kg Little clinical Value - NICE Guidelines. No value at stage 3 for adults. Possible alternative to low-dose inhaled steroid (step 2 in children. Have some value in exercise asthma May be considered for occupational asthma – predictable No value in acute asthma. Often termed “mast cell stabiliser”. Decreases mediator release from by Ca dependent mechanism. Not the only mode of action
73
Primary Prevention in asthma
Breast feeding in infants – may also protect development of early asthma Avoidance of tobacco smoke Weight reduction (where obese)
74
Secondary Prevention in asthma
Avoid house dust mites – measures to reduce Immunotherapy where clear antigen
75
Alternative medicine
Buteyko breathing technique
76
No Evidence of Value primary prevention non pgarmacological in asthma
Nutritional Supplementation Immunotherapy Fish oils and fatty acids or electrolytes
77
No Evidence of Value in secondary prevention of non pharmacological in asthma
Air pollution – more research needed
78
No Evidence of Value for complimentary and alternative medicine in asthma
Acupuncture Herbal Medicine Hypnosis Ionisers – definitely not recommended Exercise programmes
79
Other ways to help asthma
Avoid triggers such as smoke, animal fur and dust. Manage asthma by: Maintaining healthy weight Keeping fit and active Having an annual flu jab Quit smoking Breathing exercise programme Supported self-management: 1. Asthma action plans 2. Adherence and concordance
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Acute Asthma
In UK 200 deaths per annum – majority chronically severe asthma Risk factors for acute asthma More than 3 drugs for control Previous acute attacks or poor control Brittle asthma –wide variation in PEFR (Type 1) or sudden severe attacks when apparently controlled (Type 2) Psychiatric illness or treatment Alcohol or drug abuse Social factors e.g. isolation, poverty, stress, abuse
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Acute Severe Asthma signs
Any of: Respiratory rate > 25/min (>30/min child over 5 and >50 child under 5) Pulse rate > 110/min (>125/min child over 5 and >140 under 5) PEFR 33-50% of best Breathlessness - affects speech. Cannot complete sentences
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acute severe asthma life threatening when:
Cyanosis Weak respiratory effort PEFR < 33% of best fatigue, confusion, exhaustion Bradycardia or exhaustion common. Child tachycardia symptom of severe, falling rate a pre-terminal event
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Therapy of Acute Emergency asthma
High flow O2; all patients High Dose b-agonist: Inhaled when possible. Nebulised salbutamol or terbutaline in life threatening. IV used when inhaled impossible. Steroid: oral if possible (40-50mg OD adult) or IV hydrocortisone max 100mg QDS when oral impossible Ipatropium Br: add to nebuliser in life threatening or if bronchodilator response poor Life Threatening: IV Magnesium Sulphate, IV aminophylline. Needs senior medical decision.
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Acute in Children <2 yrs asthma
Additional problems: recurrent cough and wheezes often associated with upper respiratory viral infections. May not indicate worsening of asthma. Diagnosis relies on symptoms - few functional tests. Condition may suddenly worsen. Oral b-agonist not recommended – inhaled best. Metered dose inhaler with spacer and mask. Can use oral steroid in hospital setting. Inhaled ipatropium bromide in combination with inhaled b-agonist can be considered.
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Monitoring in acute asthma
Heart rate Pulse rate Maintain SpO2 >94–98% Peak expiratory flow 15–30 minutes after starting treatment Blood gas measurements Chart PEF before and after giving β2 agonists and at least 4 times daily throughout hospital stay
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COPD definition
Chronic Obstructive Pulmonary Disease (COPD) is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking
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Disease pathology 1 COPD
C-chronic (long term condition) O-obstructive (narrowing of airways) P-pulmonary (affects your lungs) D-disease (its medical condition)
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what is bronchitis
means the airways are inflamed and narrowed. People with bronchitis often produce sputum, or phlegm.
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what is emphysema
affects the air sacs at the end of the airways in the lungs. They break down and the lungs become baggy and full of holes which trap air.
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COPD characterisation
These processes narrow the airways, making it harder to move air in and out as you breathe: - the lung tissue is damaged so there is less pull on the airways - the elastic lining of the airways flops - the airway lining is inflamed
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COPD disease pathology 2
Most likely to develop COPD if >35 years and are, or have been, a smoker Jobs where people are exposed to dust, fumes and chemicals can also contribute to developing COPD Some people are more affected than others by breathing in noxious materials. You have higher risk if respiratory problems run in the family. A rare genetic condition called alpha-1-antitrypsin deficiency makes people very susceptible to develop COPD at a young age.
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COPD demographics
COPD is the second most common lung disease in the UK, after asthma. Around 2% of the whole population – 4.5% of all people aged over 40 – live with diagnosed COPD. Nearly 30,000 people die from COPD each year, making it the second greatest cause of death from lung disease and the UK’s fifth biggest killer. Along with lung cancer and pneumonia, COPD is one of the three leading contributors to respiratory mortality in developed countries such as the UK. An estimated 1.2 million people are living with diagnosed COPD. Men are more likely to be diagnosed with COPD and to die from it than women. COPD is rare under 40 and becomes commoner with age, affecting 9% of those aged >70. COPD prevalence, incidence and mortality rates are highest in Scotland and the north of England. Prevalence and incidence are over twice as great in the most deprived population quintile than in the least.
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signs and symptoms of COPD
getting short of breath easily when doing everyday things (e.g. going for a walk or doing housework) having a cough that lasts a long time wheezing in cold weather producing more sputum or phlegm than usual You might get these symptoms all the time, or they might appear or get worse when you have an infection or breathe in smoke or fumes. In severe COPD = lose appetite, lose weight and ankle swelling COPD is different to asthma; In COPD airways are permanently narrowed and is irreversible
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COPD diagnosis
The diagnosis of COPD depends on thinking of it as a cause of breathlessness or cough. It is suspected on the basis of symptoms and signs and is supported by spirometry. Diagnosis of COPD should be considered for: Patients >35 years and * Smokers (or significant dusty occupation) patients who present with one or more of the following: Exertional breathlessness, Chronic cough, Regular sputum production, Frequent winter ‘bronchitis’ and wheeze. Spirometry is one of the essential lung function investigations in the diagnosis, severity assessment and monitoring of disease progression of COPD. Further investigations for all patients at initial diagnostic evaluation include – 1. Chest radiograph to exclude other pathologies 2. FBC - to identify anaemia or polycythaemia 3. BMI calculated 4. Eosinophilia
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how is COPD different to asthma
In COPD airways are permanently narrowed and is irreversible
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testing COPD
FEV1: forced expiratory flow in 1 second FVC: forced vital capacity
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What is FEV1
It indicates how much air you can exhale in one second, and a low FEV1 implies that your airflow is obstructed.
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what is FVC
Forced vital capacity (FVC) is the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible. It's measured by spirometry
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COPD risk factors
STOP SMOKING! This is the only therapeutic approach other than oxygen therapy that impedes development of the condition. Patients should be given assistance to stop. Unless contraindicated, use NRT or bupriopion (antidepressant) or varenicline (nicotinic receptor partial agonist) as appropriate in support
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fundementals of COPD care
Offer treatment and support to stop smoking Offer pneumococcal and influenza vaccinations Offer pulmonary rehabilitation if indicated Co-develop a respiratory action plan Optimise treatment for co-morbidities
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start inhaled therapies only if: in COPD
if fundemental COPD care has been offered needed to relieve breathlessness compliance with inhalers
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Indacterol (LABA; Onbrez™) COPD
New long acting sympathomimetic agent Single dose duration 24 hours – od dosing Licensed only for maintenance treatment of COPD – not for asthma! Not tested in long term asthma therapy In COPD alternative to salmeterol or formoterol
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Long Acting Muscarinic Antagonist (LAMA) for COPD
Sustained antagonism of muscarinic receptors: high receptor affinity Topically active and administered by inhalation Tiotropium (bromide) powder or solution for inhalation. Licensed only for maintenance treatment of COPD – no value in acute attack. Must stop SAMA when using LAMA
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new LAMA agents for COPD
Aclidinium bromide (Eklira genuair) >Competitive, selective muscarinic receptor antagonist, with a longer residence time at M3 receptors which mediate contraction of smooth muscle in the airways; induces bronchodilation. >Once absorbed it is rapidly broken down in the plasma, resulting in minimal systemic anticholinergic side-effects. Glycopyrronium bromide (Seebri breezehaler) Umeclidinium (Incruse Ellipta)
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LABA/ICS Combinations for COPD
New recommendation 2010 Fostair: beclomethasone diproprionate 100mcg with formoterol fumarate 6 mcg Symbicort: budesonide 100mcg with formoterol fumarate 6 mcg If ICS not tolerated or declined an alternative option is to combine LABA and LAMA e.g. formoterol with Tiotropium
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Inhaler Delivery Systems COPD
Quality statement 2: Inhaler technique (patients should have this assessed when starting treatment and then regularly during treatment) Hand held best if can be used. Consider a spacer MDI first option but can try other inhaler types Spacers must be compatible with inhaler and do not over clean Nebulisers when patients disabled by breathlessness despite max use of inhalers Review and do not continue without evidence of benefit
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Steroid Therapy for COPD
Oral steroids are NOT advised. In advanced COPD may need low dose oral maintenance – dose as low as possible. Watch for SE. ICS not licensed for use alone in COPD - prescribers responsible Oral reversibility tests do not predict inhaled therapy responses and should not be used ICS are to reduce progression of disease and control exacerbations not to improve lung function per se Risk of osteoporosis and other side effects with long term high dose ICS
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Theophylline for COPD
No longer recommended agent – narrow therapeutic index - toxicity Should only be used for patients that cannot use inhaled therapy or if symptoms persist. Offer only after trials of SABA and LABA Can be combined with beta-agonists and muscarinic antagonists No advantage over SABA or LABA and poor side- effect profile-need to monitor plasma levels and interactions
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Long term O2 therapy (LTOT) for COPD
Inappropriate use - respiratory depression possible LTOT for patients PaO2 <7.3kPa (55mmHg) or <8kPa with polycythaemia or nocturnal hypoxaemia (PaO2 < 90% for 30% of time) Consider if FEV1 30-49% predicted. To benefit from LTOT, give for 15hrs/day Need to assess benefit – including arterial blood gas on 2 occasions at least 3 weeks apart for patients who are stable. Ambulatory O2 prescribed when on LTOT to allow movement outside home – may also use short burst O2
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Roflumilast (Daxas) for COPD
Phosphodiesterase type-4 inhibitor Maintenance therapy for COPD particularly associated with recurrent bronchitis with history of frequent exacerbations NICE – currently recommended only as part of a research study in COPD as an add on to bronchodilator therapy NICE recommend that patients should be allowed to continue therapy if benefit is found
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Mucolytic: Carbocisteine in COPD
Considered for patients with a chronic productive cough Facilitate expectoration by reducing sputum viscosity (thickness) Can reduce exacerbations Should be stopped if there is no benefit after a 4-week trial
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Beta-agonists side effects in COPD
angioedema, arrhythmias, headaches hyperglycaemia (when given IV), hypokalaemia (with high doses)
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Antimuscarinics side effects in COPD
constipation, cough, dry mouth, gastro- intestinal-motility-disorder
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steroid side effects in COPD
hoarse voice, oral thrush. Need to reduce the risk by using inhalers correctly and rinsing mouth out with water after using inhaler
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surgery in COPD
Patients with severe COPD who remain breathless with marked restrictions of their activities of daily living, despite maximal therapy (including rehabilitation), should be referred for consideration of lung volume reduction surgery if they meet all of the following criteria: 1. FEV1 more than 20% predicted 2. PaCO2 less than 7.3 kPa 3. Upper lobe predominant emphysema 4. TLCO more than 20% predicted
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not reccomended in COPD
Anti-oxidant therapy – alpha-tocopherol (guess what it is) and beta-carotene (guess what it is) supplements Anti-tussive therapy Prophylactic antibiotic therapy (insufficient evidence) Anti-oxidant therapy – alpha-tocopherol (vit E) and beta-carotene (carrots!) supplements Anti-tussive therapy Prophylactic antibiotic therapy (insufficient evidence) Mucolytics should not be used routinely. Consider in people with productive chronic cough who respond.
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exacerbation of COPD
Symptoms: worsening breathlessness, cough, increased sputum production and change in sputum colour Give bronchodilator therapy via nebuliser +/- oxygen IV aminophylline given if response to nebulised bronchodilators is poor (take levels within 24 hours) Short course of oral steroids (prednisolone 30mg for 5 days) - if increased breathlessness interferes with daily activities Antibiotics – if sputum becomes more purulent or if other signs of infection (usually a macrolide, or a tetracycline)
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other ways of managing COPD better
1. Exercise and pulmonary rehabilitation 2. Controlling breathing (breathing gently, using the least effort, with shoulders supported and relaxed) 3. Eating well and maintaining healthy weight 4. Vaccination (against pneumococcal infection -have this once, and the annual influenza vaccine) 5. Managing flare ups (exacerbations) Top Tip: STOP SMOKING
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