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Year 4 CCC > Chronic Core Conditions > Flashcards

Chronic Core Conditions Flashcards

1
Q

What % of the population is affected by asthma?

A

5-8%

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2
Q

At what age range does asthma prevalence peak?

A

5-15 years

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3
Q

What is asthma?

A

It is a chronic inflammatory condition of the airways, characterised by recurrent episodes of dyspnoea, cough and wheeze, caused by reversible airway obstruction

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4
Q

What are the three factors that contribute to airway narrowing?

A
  1. Bronchial muscle contraction: triggered by various stimuli
  2. Mucosal swelling/inflammation
  3. Increased mucus production
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5
Q

What causes mucosal swelling and inflammation?

A

Mast cells and basophil degranulation resulting in the release of inflammatory mediators

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6
Q

What happens during an acute flair up of asthma? (2)

A
  1. Bronchospasm

2. Excessive production of secretions (plugging airways)

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7
Q

How can asthma be catergorised?

A
  1. Extrinsic

2. Intrinsic

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8
Q

What is extrinsic asthma?/what are the triggers? (9)

A

Definite cause found - most commonly type of atopy. Possible triggers include:

  1. Dust mite
  2. Pollen
  3. Animal dander and fur
  4. Pollution
  5. Cold air
  6. Exercise
  7. Smoking (including passive)
  8. NSAIDs
  9. Beta blockers (DO NOT GIVE TO ASTHMATICS)
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9
Q

In addition to the extrinsic triggers, what are the risk factors for developing asthma? (5)

A
  1. Inner city environment
  2. Family history of asthma and atopy
  3. Concurrent eczema/hayfever
  4. Maternal smoking
  5. High serum IgE (gene on chromosome 2 called PHF11 that controls IgE synthesis)
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10
Q

What are the symptoms of asthma/how might someone present? (7)

A
  1. Dyspnoea
  2. Wheeze
  3. Cough (nocturnal)
  4. Diurnal variation
  5. Chest tightness
  6. Disturbed sleep (severe asthma)
  7. Sputum production
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11
Q

What are the signs of asthma? (7)

A
  1. Tachypnoea
  2. Widespread bilateral wheeze
  3. Hyperinflated chest
  4. Hyper-resonant percussion note
  5. Diminished air entry
  6. Prolonged expiration
  7. Increased respiratory rate
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12
Q

When would someone with some of the symptoms of asthma be less likely to have a diagnosis of asthma? (6)

A

If they had:

  1. Lack of wheeze
  2. Normal chest examination
  3. Voice disturbance
  4. Symptoms with cold only
  5. Significant smoking history
  6. Cardiac disease
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13
Q

What are the differential diagnoses of asthma? (7)

A
  1. COPD (can coexist)
  2. Pulmonary oedema
  3. PE
  4. Bronchiectasis
  5. Foreign object
  6. Obliterative bronchiolitis
  7. Pneumothorax
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14
Q

What investigations need to be carried out in someone with suspected asthma? (5)

A
  1. Peak flow (PEFR) - recorded as the best of three forced expiratory blows from total lung capacity while standing (if possible)
  2. Spirometry
  3. CXR
  4. FBC
  5. Skin prick test (may identify allergens- don’t routinely test this)
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15
Q

What investigation is preferable to have before diagnosis of asthma?

A

Spirometry

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16
Q

What is the FEV1/FVC ratio expected to be for asthma?

A

<0.7

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17
Q

What defines complete control of asthma? (7)

A
  1. No daytime symptpoms/no night time awakening
  2. No need for rescue medication
  3. No asthma attacks
  4. No exacerbations
  5. No limitations of activity including exercise
  6. Normal lung function
  7. Minimal side effects from medication
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18
Q

When is a step up in medication indicated for people with asthma? (4)

A
  1. Using SABA 3 times a week or more
  2. Symptomatic three times a week or more
  3. Exacerbation in the last 2 years
  4. Waking one night a week
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19
Q

What is the lifestyle advice for people with asthma? (6)

A
  1. Stop smoking
  2. Avoid triggers (e.g. NSAIDs)
  3. Lose weight (if overweight)
  4. Wash spacer once a month in soapy water and leave to drip dry
  5. Monitor PEFR 2x daily
  6. Immunisations
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20
Q

What is the treatment for step 1 of asthma - so mild intermittent asthma? (adults)

A
  1. Inhaled short-acting beta agonist (SABA) 100 micrograms QDS
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21
Q

If the asthma is not controlled simply with a short-acting beta agonist, what is the next step, step 2, of the asthma treatment pathway? (adults)

A
  1. Add inhaled corticosteroid 200-800 micrograms per day

400 micrograms is an appropriate starting dose for more patients

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22
Q

If the asthma is not controlled by step 2, what is step 3 treatment? (2) adults)

A
  1. Add inhaled long-acting beta-agonist (LABA)

2. May need to increase dose of inhaled corticosteroid (to 800 micrograms)

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23
Q

What needs to be done once someone has started on step 3 (and even before now)? (adults)

A

Review the patient to see if LABA is working - if it isn’t, stop this, ensure they are on highest dose of steroid, and start other therapy e.g. leukotriene receptor antagonist

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24
Q

What is step 4 on the treatment pathway for asthma? (2) (adults)

A
  1. Increase corticosteroid up to 2000 micrograms per day

2. Add an extra (4th) drug e.g. leukotriene receptor antagonist or SR theophylline beta-agonist tablet.

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25
Q

What is the 5th and final step in the treatment of chronic asthma? (3) (adults)

A
  1. Use daily steroid tablet (in lowest dose that provides adequate control)
  2. Maintain high dose inhaled corticosteroid
  3. Refer patient to specialist care
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26
Q

In children, the pathway of treatment for asthma is very similar, what are the steps?

A

Step 1 - SABA
Step 2 - inhaled corticosteroid 200-400 micrograms
Step 3 - LABA + up dose of steroid
Step 4 - Inhaled corticosteroid up to 800 micrograms
Step 5 - Daily steroid tablet + corticosteroid 800 micrograms

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27
Q

Give an example of SABA? (2)

A
  1. Salbutamol

2. Terbutaline

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28
Q

Give an example of LABA? (2)

A
  1. Salmeterol

2. Formoterol

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29
Q

Which drugs do SABA/LABA interact with? (2)

A
  1. Digoxin (monitor potassium levels)

2. Corticosteroids, diuretics, theophyllines (monitor potassium levels)

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30
Q

Give example of inhaled corticosteroids (ICS)? (4)

A
  1. Beclometasone
  2. Budesonide
  3. Ciclesonide
  4. Fluticasone
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31
Q

Which oral steroid is given most commonly in the treatment of asthma?

A
  1. Prednisolone (40-50mg OD)
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32
Q

Give an example of two leukotriene receptor antagonists?

A
  1. Montelukast (10mg OD)

2. Zafirlukast (20mg BD)

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33
Q

What are the signs/symptoms of acute asthma/near-fatal asthma? (9)

A
  1. Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures
  2. PEF < 33%
  3. Exhaustion
  4. SpO2 <92%
  5. PaO2 <8kPa
  6. Hypotension
  7. Cyanosis
  8. Silent chest
  9. Poor respiratory effort
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34
Q

What is the treatment of acute/life threatening asthma? (6)

A
  1. Supplementary oxygen (aim for 94-98% sats)
  2. High dose inhaled beta-agonists (salbutamol/terbutaline)
  3. Prednisolone (40-50mg) or Parenteral hydrocortisone (400mg)
  4. Magnesium sulphate
  5. Nebulised ipratropium bromide/tiotropium
  6. IV aminophylline (if poor response to initial therapy)
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35
Q

What % of >40 year olds are affected by COPD?

A

10-20%

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36
Q

When may someone under the age of 35 develop COPD?

A

If they have alpha 1 anti-trypsin deficiency

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37
Q

Which gender is COPD most common in and why?

A

Males, due to the previous smoking trends

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38
Q

COPD is an umbrella term for which two diseases?

A
  1. Emphysema

2. Chronic bronchitis

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39
Q

What is emphysema?

A

It is the enlargement of air spaces distal to the terminal bronchioles and destruction of the alveolar walls

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40
Q

What is chronic bronchitis?

A

It is a cough with/or without sputum production for most days for 3 months in the last 2 years

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41
Q

How is the diagnosis of chronic bronchitis different to emphysema?

A

Chronic bronchitis is a clinical diagnosis, whereas emphysema is a histological diagnosis

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42
Q

What are the characteristics of COPD? e.g. is it reversible?

A

It is a progressive disorder that is not reversible.

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43
Q

How is airway obstruction defined with regards to FEV1:FVC?

A

FEV1/FVC <0.7

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44
Q

As COPD progresses, what happens to the hypercapnic drive to breath?

A

People lose their hypercapnic drive to breath and depend on the hypoxaemic drive

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45
Q

What three mechanisms of COPD limit airflow into the small airways?

A
  1. Loss of elasticity and alveolar attachment of airways - airways collapse during expiration
  2. Inflammation and scarring cause the small airways to narrow - squamous cell metaplasia
  3. Mucus secretions block the airways (increased number of goblet cells)
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46
Q

What are the risk factors for developing COPD?

A
  1. Smoking (active or passive) 90%
  2. Climate or air pollution
  3. Alpha-1-anti-trypsin deficiency - protease inhibitor for enzymes able to destroy alveolar wall
  4. Age-related decline in lung function
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47
Q

What are the symptoms of COPD? (6)

A
  1. Chronic cough
  2. Sputum (purulent during exacerbation, otherwise white)
  3. Dyspnoea
  4. Frequent winter bronchitis
  5. Exacerbated by cold weather and pollution
  6. Weight loss, exercise intolerance, fatigue
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48
Q

What are the signs of COPD? (12)

A
  1. Tachypnoea
  2. Use of accessory muscles
  3. Hyper-inflated poor expansive chest
  4. Hyper-resonant percussive notes
  5. Cor pulmonale
  6. Wheeze or quiet breath sounds
  7. Pursed lip breathing
  8. Cyanosis
  9. Cachexia
  10. Prolonged forced expiratory time
  11. CO2 flapping tremor
  12. No diurnal variation
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49
Q

What are the two phenotypes of presentation of COPD?

A
  1. Pink puffers

2. Blue bloaters

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50
Q

What are the symptoms/signs of ‘pink puffers’? (4)

A
  1. Increased alveolar ventilation (profound emphysema)
  2. Normal PaO2 and normal or low PaCO2
  3. Breathless (accessory muscles) but NOT cyanosed
  4. Progression to type 1 respiratory failure
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51
Q

What are the signs/symptoms of ‘blue bloaters’?

A
  1. Decreased alveolar ventilation
  2. Low PaO2 and high PaCO2
  3. Cyanosed but NOT breathless
  4. May develop right-sided heart failure and type 2 respiratory failure
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52
Q

Why should supplementary O2 be given with caution in patients with COPD?

A

Because they rely on the hypoxic drive to maintain respiratory effort, and therefore could cause respiratory depression

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53
Q

In order for a diagnosis of COPD, what are the criteria that needs to be met? (5)

A
  1. Age older than 35 years old
  2. Presence of a risk factor (e.g. smoking)
  3. Typical symptoms
  4. Absence of clinical features of asthma
  5. Post-bronchodilator spirometry
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54
Q

What investigations are carried out in someone with suspected COPD?

A
  1. Spirometry (gold standard- should be carried out 15-20 minutes post-inhalation of salbutamol)
  2. CXR
  3. Bloods
  4. ABG
  5. ECG
  6. Pulse oximetry
  7. Sputum culture
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55
Q

What would be expected on a CXR in someone with COPD? (4)

A
  1. Hyperinflation
  2. Flat hemi-diaphragms
  3. Large central pulmonary arteries
  4. Reduced peripheral vascular markings
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56
Q

What blood tests are required and why, for someone with COPD?

A
  1. FBC - to identify anaemia or secondary polycythaemia
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57
Q

What would an ABG should of someone with COPD?

A

Low PaO2 +/- hypercapnia

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58
Q

What is the ECG for when investigating COPD?

A

Assessing for cor pulmonale (RHF) signs = right atrial and ventricular hypertrophy

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59
Q

When taking a social history, what is important to note in someone with suspected COPD?

A

Whether the person is a smoker or ex-smoker etc, and calculate pack years

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60
Q

How is the severity of COPD measured/assessed? (3)

A
  1. The degree of airflow obstruction according to the reduction in FEV1
  2. The degree of breathlessness according to the Medical Research Council dyspnoea scale
  3. Presence of right-sided heart failure
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61
Q

How many stages are there in the GOLD classification of severity of COPD?

A

Stage 0 - Stage IV

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62
Q

What does stage 0 of GOLD refer to?

A

At risk; chronic cough and sputum production, but normal spirometry

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63
Q

What does stage 1 of GOLD refer to?

A

Mild COPD; mild airflow limitation, FEV1/FVC <0.7, FEV1 >80%

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64
Q

Stage 2 of GOLD?

A

Moderate COPD - FEV1 50-79%

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65
Q

Stage 3 of GOLD?

A

Severe COPD - FEV1 30-49%

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66
Q

Stage 4 of GOLD?

A

Very severe COPD - FEV1 <30%

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67
Q

What is the Medical Research Council dyspnoea scale?

A

It is a scale based on grades 1 through to 5, measuring the level of activity the individual is capable of

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68
Q

What is grade 1 of MRC dyspnoea scale?

A

Not troubled by breathlessness except during strenuous exercise

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69
Q

What is grade 3 of MRC dyspnoea scale?

A

Walks slower than contemporaries on the same level because of breathlessness, or has to stop for breath when walking at own pace

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70
Q

What is grade 5 of MRC dyspnoea scale?

A

Too breathless to leave the house, or breathless when dressing/undressing

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71
Q

What is the management of COPD?

A
  1. STOP SMOKING (or even cut down if unable to stop)
  2. LTOT - long-term O2 therapy; proven to improve 3yr survival in over 50% in a study
  3. Mucolytics
  4. Flu vaccinations
  5. Pulmonary rehabilitation for patients with MRC dyspnoea grade 3-5
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72
Q

What drugs are prescribed for people with COPD to help cope with breathlessness?

A
  1. SABA or SAMA (short-acting muscarinic antagonist e.g. ipratropium bromide)
  2. LABA or LAMA (tiotropium)
  3. If not controlled, consider: carbocysteine or theophylline
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73
Q

In an acute exacerbation of COPD, what is the treatment? (4)

A
  1. Increase dose of SABA
  2. Prednisolone 30mg orally OD for 7-14 days
  3. Oral abx (if signs of pneumonia)–> amoxicillin 500mg TDS for 5 days OR doxycycline
  4. Oxygen therapy is O2 sats <90%
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74
Q

When is LTOT indicated in someone with COPD? (5)

A
  1. FEV1 <30%
  2. Cyanosis; O2 sats <92%
  3. Polycythaemia
  4. Peripheral oedema
  5. Raised JVP
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75
Q

For how many hours each day should LTOT be used?

A

> 15 hours per day

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76
Q

How can hospital admissions for patients with COPD prone to exacerbations be prevented?

A
  1. Keep abx in the house in case of infection

2. Prednisolone tablets in case of increasing breathlessness

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77
Q

What % of people in the UK with a diagnosis of diabetes, have type 1?

A

10%

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78
Q

How many people in the UK have diabetes?

A

4.5% (2.9 million people)

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79
Q

What features/symptoms/signs suggest type 1 diabetes, rather than type 2? (5)

A
  1. Weight loss with polydipsia and polyuria
  2. Hyperglycaemia despite diet and medications
  3. Islet cell antibodies (ICAs) and anti-glutamic acid decarboxylase (GAD) antibodies
  4. Ketosis: ketonuria on urine dipstick
  5. If older, ketotic and unresponsive to hypoglycaemics, consider LADA and measure above antibodies
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80
Q

What features/symptoms/signs suggest type 2 diabetes as opposed to type 1? (3)

A
  1. Polydipsia and polyuria
  2. Fatigue
  3. Recurrent infections e.g. thrush
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81
Q

What is type 1 diabetes?

A

It is an absolute deficiency in insulin which causes persistent hyperglycaemia.

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82
Q

What causes type 1 diabetes?

A

It is caused by destruction of insulin-producing beta cells in the pancreatic islets of Langerhans. The most common cause of beta cell destruction is autoimmunity.

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83
Q

Diabetes belongs to a family of which autoimmune diseases?

A

HLA-associated immune mediated organ specific diseases. Genetic susceptibility is polygenic and the HLA responsible is DR3+/-DR4)

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84
Q

What is the demographics of patients presenting with type 1 diabetes? (2)

A
  1. Usually juvenile onset, but may occur at any age (young people)
  2. Latent autoimmune diabetes of adulthood (LADA) is a type of T1DM with slower progression into insulin deficiency that occurs in later life and is difficult to distinguish from type 2. (rarely older people)
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85
Q

What is the classic triad in presentation of symptoms in type 1 diabetes?

A

RAPID ONSET over days of weeks with classic triad:

  1. Polyuria (due to the osmotic effect of glucose and ketone bodies in the urine)
  2. Polydypsia
  3. Weight loss (due to the combined effects of dehydration and catabolism)
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86
Q

In addition to the classic triad, what other signs/symptoms may be present in T1DM? (5)

A
  1. Hyperglycaemia (random blood glucose >11mmol/L)
  2. Fatigue
  3. Ketonuria and pear drop breath
  4. Infections e.g. thrush, fungal/bacterial skin infections
  5. Cramps and abdominal pain
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87
Q

What is the clinical presentation of overt DKA? (4)

A
  1. Nausea and vomiting
  2. Kussmauls breathing
  3. Ketones on breath
  4. Abdominal pain
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88
Q

What investigations need to be carried out in someone with suspected T1DM? (6)

A
  1. Fasting blood glucose (>7mmol/L)
  2. Random blood glucose (>11mmol/L)(4-7mmol = normal)
  3. Blood glucose post Oral Glucose Tolerance Test (OGTT)
  4. Urine dipstick (postive for glucose and ketones)
  5. Bloods: FBC, U&Es, LFTs, lipids, HbA1c (>48mmol/L is raised)
  6. Check for auto-antibodies
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89
Q

What are the diagnostic requirements for type 1 diabetes?

A
  1. Classical symptoms + 1 raised glucose OR
  2. No classical symptoms + 2 raised glucose
  3. HbA1c > 48mmol/L but lower doesn’t exclude DM
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90
Q

What are the complications of type 1 DM?

A
  1. Metabolic: DKA, hypoglycaemia, dyslipidaemia
  2. Macrovascular: MI, stroke, peripheral vascular disease (limb ischaemia)
  3. Microvascular: retinopathy, nephropathy, sensory, motor and autonomic neuropathy
  4. Psychological: depression and anxiety
  5. Children and young adults: family conflict, risky behaviour, and poor adherence
  6. Pregnancy: pre-eclampsia, IUGR, macrosomia, congenital malformations, stillbirth
  7. Fungal infections and some skin conditions e.g. granuloma annular or necrobiosis diabeticorum
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91
Q

What is the management plan for someone with suspected T1DM?

A
  1. Immediate referral to secondary care at initial diagnosis
  2. Insulin therapy will be required to self-monitor their blood glucose levels with two goals:
    - prevent hypos and hyperglycaemia and maintain a level of glycemic control
    - prevent and treat the long-term micro and macro - vascular complications of diabetes
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92
Q

Which type of insulin is the only one used in the UK now?

A

Human insulin

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93
Q

What is the only route of administration of insulin?

A

Sub-cutaneous injections

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94
Q

What are the 3 different types of insulin?

A
  1. Short and ultra fast-acting
  2. Intermediate and long-acting
  3. Biphasic premixed
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95
Q

What is the aim of the short and ultra fast-acting insulin’s?

A

To have a rapid onset of action (15 minutes) and short duration of action (4 hours) - used to mimic the physiological secretion of insulin that occurs in response to the glucose absorbed from food and drink (use just after meals)

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96
Q

What is intermediate and long-acting insulin used to mimic?

A

It mimics basal insulin that is secreted continuously throughout the day. Its onset of action is approximately 2 hours and its maximum affect lasts from 4 - 12 hours, but will last up to 42 hours. Normally taken once a day, in the evening.

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97
Q

What is the typical insulin requirement per day?

A

0.3-1 unit/kg/day

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98
Q

Although there is the typical insulin requirement, what does this depend on? (7)

A
  1. Age
  2. Weight
  3. Stage of puberty
  4. Duration and phase of diabetes
  5. Daily routine
  6. Diet
  7. Illness
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99
Q

In general, a half, to two-thirds of total insulin is given to cover what? …and the remainder is to control what?

A

Basal needs and the remainder is to control post-prandial glycaemia

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100
Q

What is the main adverse effect of insulin?

A

Hypoglycaemia

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101
Q

What are the initial effects of hypoglycaemia? (5)

A

Adrenergic:

  1. Sweating
  2. Tachycardia
  3. Palpitations
  4. Pallor
  5. Hunger
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102
Q

What are the later effects of hypoglycaemia? (7)

A

Neuroglycopenic:

  1. Confusion
  2. Slurred
  3. Drowsiness
  4. Yawning
  5. Anxiety
  6. Blurred vision
  7. Numbness of nose, lips and fingers
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103
Q

What is the lifestyle advice that should be discussed with patients with diabetes? (6)

A
  1. Discuss diet taking into account other factors e.g. obesity, hypertension, renal impairment; offer referral to dietician
  2. Regular physical activity
  3. Reduce alcohol consumption
  4. Wear a medical emergency identification bracelet or similar
  5. Notify DVLA, cannot drive more than 2 hours without checking blood glucose levels
  6. Carry insulin in hand luggage when travelling
104
Q

What needs to be monitored in someone with T1DM? (9)

A
  1. Blood glucose control by HbA1c levels (monitored every 2 - 6 months) target = <48mmol/L
  2. Blood pressure (intervene if >135/85 mmHg)
  3. Cholesterol (<4mmol/L)
  4. Weight
  5. Urine albumin:creatinine ratio (ACR)
  6. Abdominal adiposity due to injection sites
  7. Retinopathy screening
  8. Diabetic foot checks
  9. Monitor sexual dysfunction (erectile dysfunction in males)
105
Q

What is the % lifetime risk of developing T2DM?

A

15%

106
Q

What is the pathophysiology behind T2DM? (3)

A
  1. Insulin resistance and relative insulin deficiency (due to beta cell dysfunction) result in persistent hyperglycaemia
  2. There is an increase in glucose production in the liver, due to the inadequate suppression of gluconeogenesis, due to insulin resistance and decrease glucose uptake by peripheral cells
  3. Hyperglycaemia and lipid excess may be toxic to beat cells and so may advance the disease
107
Q

T2DM typically progresses from what and why is this important?

A
  1. IGT or IFG - impaired glucose tolerance or impaired fasting glucose; important is it provides a unique window of opportunity for lifestyle intervention
108
Q

What is MODY?

A

Maturity onset diabetes of the young - it is a rare autosomal dominant form of T2DM

109
Q

What are the risk factors for T2DM? (8)

A
  1. Obesity
  2. Lack of physical activity
  3. Alcohol and calorie excess
  4. Polygenetic influence
  5. History of gestational diabetes
  6. IGT or IGF
  7. Smoking
  8. PCOS (polycystic ovarian syndrome)
110
Q

What are the signs and symptoms of T2DM? (8)

A
  1. Polyuria
  2. Polydipsia
  3. Blurred vision
  4. Weight loss
  5. Lethargy and fatigue
  6. Recurrent and prolonged infections
  7. Genital thrush
  8. May present with complications e.g. retinopathy
111
Q

When is HbA1c not suitable for diagnosis of T2DM? (6)

A
  1. Children and young people
  2. Pregnant women or <2 months postpartum
  3. Suspected T1DM
  4. Those on medications that can cause acute glucose rise
  5. Acute pancreatic damage including surgery
  6. HIV +ve
112
Q

In addition to HbA1c, what else can be measured to diagnose T2DM? (2)

A
  1. OGTT is gold standard (75g of anhydrous glucose given, check blood sugar before and 2 hours after)
  2. Fasting blood glucose is preferable in terms of diagnosis to random
113
Q

What is the HbA1c target for someone with T2DM?

A

48mmol/L

114
Q

Name a group education programme for people with T2DM?

A

DESMOND or XPERT

115
Q

Which drug class does metformin belong to?

A

Biguanides

116
Q

What is the mechanism of action of metformin?

A

Works by decreasing gluconeogenesis (hepatic glucose output) and by increasing peripheral utilisation of glucose. Only effective if there are some residual functioning pancreatic islet cells

117
Q

What are the contra indications for metformin?

A

Impaired renal function (eGRF <30)

118
Q

What is the usual method of initiating metformin treatment?

A

500mg OD with breakfast, increasing by 500mg at intervals of 1-2 weeks according to response.

119
Q

What needs to be monitored when someone is on metformin?

A
  1. Renal function

2. HbA1c

120
Q

What are the side effects that metformin can cause?

A
  1. Non-serious GI side effects e.g. nausea, vomiting

2. Lactic acidosis (rare but potentially fatal)

121
Q

Name the treatment for T2DM that is an insulin secretagogues?

A

Sulfonylureas

122
Q

What is the mechanism of action sulfonylureas?

A

They directly increase insulin secretion from the pancreas and therefore are only effective when some residual pancreatic beta cell function is present

123
Q

What are the first-choice sulfonylureas? (3)

A
  1. Gliclazide
  2. Glimerpiride
  3. Glipizide
124
Q

Do sulfonylureas have a short or long duration of action?

A

Long

125
Q

What is the method of action of meglitinides?

A

These have the same method of action as sulfonylureas - (insulin secretagogues)

126
Q

Do meglitinides have a short or long duration of action?

A

Short and rapid onset

127
Q

When are meglitinides preferred over sulfonylureas?

A

They are indicated for use for people with erratic lifestyles leading to irregular meal times.

128
Q

Name some types of meglitinides? (2)

A
  1. Natglinide (combination therapy with max metformin dose)

2. Repaglinide

129
Q

Name the two types of insulin secretagogues?

A
  1. Sulfonylureas

2. Meglitinides

130
Q

When should meglitinides be taken?

A

30 minutes before a meal

131
Q

When are insulin secretagogues contra-indicated? (2)

A
  1. People who are at risk of hypo’s

2. Pregnancy

132
Q

What are the adverse effects of using insulin secretagogues? (2)

A
  1. Hypoglycaemia - must warn DVLA they are taking them

2. Weight gain 1-5kg

133
Q

Name some examples of DPP-inhibitors (dipeptidyl peptidase-4 inhibitors)? (4)

A

The gliptins..

  1. Sitagliptin
  2. Linagliptin
  3. Saxagliptin
  4. Vildagliptin
134
Q

What is the mechanism of action of DPP-inhibitors?

A

Increase insulin secretion - inhibition of DPP-4 allows increased half-life of incretins which potentiate nutrient-induced insulin secretion

135
Q

What are incretins?

A

Incretins are a hormone which augment the secretion of insulin by a blood glucose-dependent mechanism

136
Q

What are the two forms of incretins?

A
  1. Glucose-dependent insulinotropic peptide (GIP)

2. Glucagon-like peptide-1 (GLP-1)

137
Q

What are the side effects of taking DPP-4 inhibitors? (1)

A
  1. Small risk of hypoglycaemia (don’t need to inform DVLA)

weight neutral

138
Q

When is the use of DPP4-inhibitors contraindicated? (2)

A
  1. Substantial renal/liver disease

2. Pancreatitis

139
Q

What are SGLT2 inhibitors?

A

Sodium-glucose co-transporter-2 inhibitors and they act by reducing the amount of glucose reabsorption in the renal tubules. Therefore more glucose is excreted in the urine and patients lose weight

140
Q

Name some examples of SGLT2 inhibitors? (3)

A
  1. Canagliflozin
  2. Dapagliflozin
  3. Empagliflozin
141
Q

What are the possible side effects of SGLT2 inhibitors?

A
  1. Increased risk of thrush and UTI

2. Hypoglycaemia (small risk)

142
Q

When is the use of SGLT2 inhibitors contra-indicated?

A
  1. Renal impairment and severe liver disease
143
Q

Name some examples of thiazolidinediones?

A
  1. Glitazones
  2. Pioglitazones
  3. Rosiglitazone
144
Q

When is insulin therapy indicated for patients with T2DM?

A

When the other treatments/modifications are insufficient to maintain normoglycemia

145
Q

What is important to stop once insulin therapy has commenced in T2DM?

A

Sulfonylureas should be stopped once insulin has started as there is a severe risk of hypoglycaemia

146
Q

What is the start dose of insulin?

A

8 units

147
Q

What is hypertension?

A

A persistently raised arterial blood pressure

148
Q

What % of adults have a BP that is at least 140/90?

A

30%

149
Q

95% of people have what type of hypertension?

A

Primary essential hypertension

150
Q

What are the causes of secondary hypertension?

A
  1. Renal disorders
  2. Cardiovascular disorders
  3. Endocrine disorders
  4. Drugs
  5. Misc.
151
Q

What are the renal disorders that can lead to secondary hypertension? (6)

A
  1. Chronic pyelonephritis
  2. Diabetic nephropathy
  3. Glomerulonephritis
  4. Polycystic kidney disease
  5. Obstructive uropathy
  6. Renal cell carcinoma
152
Q

What are the cardiovascular disorders that can lead to secondary hypertension? (2)

A
  1. Coarctation of the aorta

2. Renal artery stenosis (BP resistant to treatment)

153
Q

What are the endocrine disorders that can cause secondary hypertension? (6)

A
  1. Primary hyperaldosteronism
  2. Phaeochromocytoma
  3. Cushing’s syndrome
  4. Acromegaly
  5. Hypothyroidism
  6. Hyperthyroidism
154
Q

Which drugs both recreational and medicinal can cause secondary hypertension? (9)

A
  1. Alcohol misuse
  2. Cocaine
  3. COCP
  4. Corticosteroids
  5. Ciclosporin
  6. Erythropoietin
  7. Leflunomide
  8. NSAIDs
  9. Venlafaxine
155
Q

What are the other causes of secondary hypertension, not grouped within CV, renal or drug related? (3)

A
  1. Connective tissue disorders
  2. Retroperitoneal fibrosis
  3. Obstructive sleep apnoea
156
Q

What are the risk factors for developing hypertension?

A
  1. Smoking
  2. Obesity
  3. Alcohol
  4. Occupation –> stress
  5. Diet (high salt) and exercise (lack of)
  6. Family history - BP, heart disease, stroke, diabetes
  7. Low birthweight
  8. Type A personality…?
157
Q

How is hypertension diagnosed?

A

If clinic readings are >140 / >90 or both. Unless they are crazy high, then the recording needs to be taken as a ABPM or HBPM if ABPM not tolerated.

158
Q

What is stage 1 hypertension classed as?

A

ABPM = >135/85 (clinic >140/90)

159
Q

What is stage 2 hypertension classed as?

A

ABPM = >150/95 (clinic >160/100)

160
Q

What is stage 3 aka severe hypertension classed as?

A

Clinic systolic BP = >180mmHg or clinic diastolic BP = >110mmHg

161
Q

What is accelerated hypertension classed as?

A

Clinic BP higher than 180/110mmHg with signs of papilloedema and/or retinal haemorrhage (hypertensive retinopathy) OR BP > 220/120mmHg

162
Q

If someone presents to GP with accelerated hypertension, what is the management plan?

A

Same day referral to specialist!

163
Q

How many measurements are meant to be taken for ambulatory blood pressure monitoring?

A

Between 8am and 10pm, 2 measurements per hour. Use the average of >14 measurements

164
Q

What examinations/obs need to be taken for someone presenting with hypertension?

A
  1. Weight and BMI
  2. Cardiovascular: pulse (rate, rhythm and character), BP in other arm, heart sounds, lungs
  3. Eyes - signs of retinopathy
165
Q

What investigations need to be carried out in someone with a new presentation of hypertension (to exclude co-existing conditions)? (4)

A
  1. CKD; U&Es (urea, creatnine eGFR), urine dipstick (proteinuria, haematuria)
  2. Diabetes; serum glucose, HbA1c
  3. Hypercholesterolaemia; total cholesterol and HDL cholesterol levels
  4. CHD: ECG
166
Q

What lifestyle modifications need to be made to help reduce high blood pressure? (6)

A
  1. Lose weight, aim for BMI <25
  2. Physical exercise
  3. Low fat diet, reduce sodium <6g/day
  4. Reduce alcohol consumption
  5. Reduce consumption of coffee and caffeine
  6. Stop/reduce smoking
167
Q

What is the treatment step ladder for people <55 years old with hypertension who are NOT of afro-caribbean ethnicity?

A
  1. ACE inhibitor or low-cost ARB
  2. Add CCB
  3. Add thiazide-like diuretic
  4. Consider further diuretic / beta- or alpha- blocker
168
Q

If a caucasian female aged 41, who is trying with her partner to become pregnant, requires treatment for stage 1 - 2 hypertension, what is the recommended drug?

A

Beta-blocker

169
Q

What is the treatment step ladder for people over >55 years old or/and people of afro-caribbean ethnicity with hypertension?

A
  1. CCB
  2. Add ACEi or ARB
  3. Add thiazide-like diuretic
  4. Consider further diuretic or alpha/beta- blocker
170
Q

If someone is 51, with stage 1 hypertension and no other co-morbidities, what is the recommended treatment?

A

No medication - lifestyle changes

171
Q

If someone under 40 has stage 1 hypertension, what is the recommended plan?

A

Refer to specialist - likely it could be secondary and this needs to be investigated

172
Q

What co-moribidities would indicate someone with stage 1 hypertension requires medication to treat? (4)

A
  1. Diabetes
  2. Target organ damage
  3. Established cardiovascular disease
  4. A QRISK2 score of greater then 20%
173
Q

What does of ramipril is normally started for someone with hypertension?

A

2.5mg OD - the first dose is taken at night to avoid hypotensive drop and then after that taken every morning

174
Q

What is the maximum dose of ramipril OD?

A

10mg

175
Q

If lisinopril is recommended over ramipril, what is the first/starting dose?

A

10mg

176
Q

What is the maximum dose of lisinopril OD?

A

80mg

177
Q

What are the contra-indications for using ACE inhibitors?

A
  1. Pregnancy/women planning pregnancy/breastfeeding
  2. Angioedema
  3. Bilateraly artery stenosis
178
Q

What are the side effects of taking ACE inhibitors? (4)

A
  1. Dry cough
  2. Hyperkalaemia
  3. Deterioration in renal function (hence this has to be monitored)
  4. Dizziness/headaches
179
Q

Name two CCBs used to treat hypertension?

A
  1. Amlodipine

2. Nifedipine

180
Q

What is the mechanism of action of CCBs?

A

They reduce calcium influx into vascular smooth muscle cells, by interfering with voltage-operated calcium channels in the cell membrane

181
Q

What is the usual starting dose of amlodipine?

A

5mg OD

182
Q

When is the use of CCB contra-indicated? (5)

A
  1. Heart failure
  2. Cardiac outflow obstruction
  3. Second-degree atrioventricular
  4. Hepatic impairment
  5. Renal impairment
183
Q

What are the side effects of CCBs? (5)

A
  1. Ankle swelling
  2. Headache
  3. Nausea
  4. Dizziness
  5. Flushing
184
Q

Which drugs/juices are known to interact with CCBs? (4)

A
  1. Grapefruit juice
  2. Beta-blockers
  3. Enzyme-inducing drugs (e.g. carbamazepine)
  4. Anti-depressants
185
Q

Name two thiazide-like diuretics?

A
  1. Indapamide

2. Bendroflumathiazide

186
Q

What is the mechanism of action of thiazide-like diuretics?

A

They control hypertension in part by inhibiting reabsorption of sodium and chloride ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive sodium/chloride symporter

187
Q

What is the recommended dose of indapamide?

A

2.5mg OD

188
Q

What are the contra-indications for thiazide-like diuretics? (8)

A
  1. Gout
  2. Refractory hypokalaemia
  3. Hyponatraemia
  4. Hypercalcaemia
  5. Severe hepatic impairment
  6. Addison’s
  7. eGFR <30
  8. Pregnancy
189
Q

What are the side effects of thiazide-like diuretics? (6)

A
  1. Excessive diuresis
  2. Hypokalaemia
  3. Gout
  4. Postural hypotension
  5. DM
  6. Dizziness
190
Q

In the annual review for patients with hypertension, what needs to be recorded/discussed? (5)

A
  1. Blood pressure
  2. U&Es; renal function
  3. Lifestyle; diet and exercise
  4. Weight / BMI
  5. Side effects from treatment
191
Q

In people with hypertension who are at risk of cardiovascular disease, what other drugs are often prescribed?

A

Aspirin (anti-platelet) 75mg OD

Atorvastatin (statin) 40mg OD

192
Q

What is a stroke?

A

A acute focal neurological deficit of arterial origin lasting more than 24 hours with a positive scan

193
Q

What % of people who have a stroke, have a preceding TIA?

A

15%

194
Q

What is a TIA?

A

Transient ischaemic attack - is an acute loss of cerebral or ocular function with symptoms lasting <24 hours, caused by an inadequate blood supply as a result of low blood flow, ischaemia, or embolism.

195
Q

What can cause cerebral ischaemia?

A
  1. Atheroma
  2. Thromboembolism
  3. Trauma
  4. Infection
  5. Tumours
196
Q

What % of strokes are ischaemic and haemorrhagic?

A

85% ischaemic

15% haemorrhagic

197
Q

If the stroke is ischaemic, what are the two usual causes?

A

Thrombotic - spontaneous thrombosis in situ
Embolic - clot breaks off from a larger artery and gets lodged there (more likely if AF or carotid artery atherosclerosis)

198
Q

What are the risk factors for a stroke/TIA?

A

Risk factors for atherosclerosis: HTN, smoking, alcohol excess, obesity, DM, hyperlipidaemia, hypercholesterolaemia
Prothrombotic: clotting disorders, polycythaemia, OCP use, CHD, vasculitis
Past TIA or stroke

199
Q

What are the symptoms/signs of a TIA?

A
  1. Attacks are single or many
  2. Always mimc features of a stroke in the same arterial territory
  3. Global events (syncope and dizziness) are not typical of TIAs
  4. If emboli pass to renal artery, may cause amaurosis fugax, progressive unilateral loss of vision (like curtain coming down)
200
Q

What % of ischaemic strokes are a cerebral infarct?

A

50%

201
Q

What are the different cerebral infarcts and signs?

A

ACA - frontal and medial cerebrum –> contralateral weakness with facial sparing
MCA - lateral cerebrum –> contralateral hemiparesis, contralateral homonymous hemianopia (if optic radiation involved), dysphasia (if dominant hemisphere), visuospatial disturbance (if non dominant)
PCA - occipital lobe –> contralateral homonymous hemianopia with macula sparing

202
Q

What % of ischaemic strokes are brainstem infarcts, and what are the signs?

A

25% –> wide range of effects including quadriplegia, visual disturbance, and locked-in syndrome

203
Q

What % of ischaemic strokes are lacunar infarcts, and what are the signs?

A

25% –> ataxic hemiparesis, pure motor or sensory or combination, dysarthria/clumsy hand, intact cognition/consciousness except thalamic

204
Q

What is the scoring system used to assess risk of TIAs?

A

ABCD2

205
Q

What does the scoring system stand for and how many points is each worth?

A

Age >60 years = 1 point
Blood pressure >140/90 = 1 point
Clinical features: unilateral weakness = 2 points, speech disturbance without weakness = 1 point
Duration of symptoms >60 minutes = 2 points, 10-59 minutes = 1 point
Diabetes = 1 point

206
Q

What score would a patient get on the ABCD2 system which would lead to an immediate referral to a specialist?

A

> 4

207
Q

If a patient scores 4 on the ABCD2 system, what is the management?

A

1 week wait referral to specialist

208
Q

What are the indications for a same day specialist assessment of someone experiencing a TIA? (3)

A
  1. More than one TIA in a week
  2. A TIA whilst on anticoagulation
  3. ABCD2 score greater than 4
209
Q

What investigation will be performed on someone who has experienced a TIA in the specialist assessment unit?

A

Carotid ultrasound

210
Q

What is the immediate treatment given to someone who has experienced a TIA?

A
  1. Anti-platelet - aspirin/clopidogrel 300mg loading dose and then 75mg daily alongside a PPI if the person has a GI disease
  2. Start a statin (simvastatin 40mg)
211
Q

When would someone with a suspected TIA be referred for brain imaging? (3)

A
  1. If carotid endarterectomy is being considered when circulatory origin uncertain
  2. Haemorrhage needs to be excluded
  3. Alternative diagnosis is being considered
212
Q

When would someone with a suspected stroke require a head CT within 1 hour/ASAP of arrival? (2)

A
  1. If there is an indication for thrombolysis
  2. High risk of haemorrhage (already of anti-coagulation or known bleeding tendency, GCS <13, papilloedema, neck stiffness, fever or severe headache (SAH)
213
Q

If someone with suspected stroke is not for thrombolysis or suspected haemorrhagic stroke, what is the time frame for recommended brain scan?

A

Within 24 hours of arrival

214
Q

What is the time period for treatment with thrombolysis in someone with ischaemic stroke?

A

4.5 hours from onset of symptoms

215
Q

What is the thrombolysis used?

A

Alteplase - tissue plasminogen activator or tPA

216
Q

In someone with an ischaemic stroke who cannot taken aspirin orally due to dysphagia, what is the route of administration?

A

Rectally

217
Q

If the stroke is haemorrhagic, what treatment can be given to help with clotting?

A

Prothrombin complex and vitamin K to normalise clotting factors

218
Q

When someone who has suffered a stroke has been admitted to a specialist stroke unit, in addition to the immediate treatment, what else needs to be done? (8)

A
  1. Maintain/restore homeostasis e.g. supplemental oxygen if necessary, maintain blood glucose between 4-11mmol/L
  2. Consider surgical referral
  3. Nil by mouth until SALT assess safe swallow
  4. Screen for malnutrition
  5. Facilitate early mobilisation
  6. Pharmacological treatment
  7. Give heparin and then warfarin unless contraindicated
  8. Do not start statins immediately after acute stroke (wait 48 hours)
219
Q

What are the medical management aims in terms of rehab for someone who has suffered a stroke? (7)

A
  1. Cognition
  2. Vision
  3. Hearing
  4. Tone
  5. Strength
  6. Sensation
  7. Balance
220
Q

What lifestyle modifications should be made by anyone who has suffered a stroke? (5)

A
  1. Smoking cessation
  2. Cardioprotective diet including reducing salt intake
  3. Regular exercise
  4. Reduced alcohol consumption
  5. Achieve and maintain a healthy BMI
221
Q

Which professions make up the core multidisciplinary stroke team? (7)

A
  1. Consultant physicians
  2. Nurses
  3. Physiotherapists
  4. Occupational therapists
  5. SALT
  6. Clinical psychologists
  7. Rehabilitation assistants
222
Q

What is epilepsy?

A

A disorder of the brain characterised by a predisposition to epileptic seizures, diagnosed after at least 2 epileptic seizures.

223
Q

What is an epileptic seizure?

A

Spontaneous uncontrolled abnormal brain activity

224
Q

What percentage of people with epilepsy have no anatomically identifiable cause? (idiopathic epilepsy)?

A

66%

225
Q

What % of people with epilepsy have a 1st degree relative with epilepsy?

A

33%

226
Q

In 33% of epileptics, there are anatomical causes, what are they?

A
  1. Structural - cortical scarring from previous head injuries, stroke, vascular malformations, developmental
  2. Tuberous sclerosis, SLE, sarcoidosis
227
Q

What are the non-epileptic causes of seizures?

A
  1. Raised ICP

2. Alcohol withdrawal

228
Q

What are diverticula?

A

Diverticula are sac-like protrusions of mucosa through the muscular wall of the colon. They are usually multiple 5-10mm in diameter and occur in the sigmoid colon in about 85% of people.

229
Q

What is thought to cause diverticulitis?

A

A low-fibre diet - lowers stool bulk, slows transit times and increases intraluminal pressure

230
Q

What is the difference between diverticulosis and diverticular disease?

A

Diverticular disease is a condition where the diverticular cause symptoms, such as intermittent lower abdominal pain, without inflammation and infect. Diverticulosis is the presence of diverticula without symptoms.

231
Q

What is diverticulitis?

A

A condition where the diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding.

232
Q

What is the difference between complicated and uncomplicated diverticulitis?

A

Complicated diverticulitis is associated with complications such as abscess, peritonitis, fistula, obstruction or perforation of the peritoneum. Whereas uncomplicated is localised inflammation.

233
Q

What are the risk factors for developing diverticular disease? (5)

A
  1. Genetic
  2. Low-fibre diet
  3. Smoking
  4. Obesity
  5. Drugs - NSAIDs, opioids, corticosteroids
234
Q

What are the complications of diverticular disease? (5)

A
  1. Haemorrhage - occurs in about 15% of people with all forms of diverticula, 1/3 are massive bleeds requiring emergency transfusion; bleeding stops spontaneously in 70-80%
  2. Intra-abdominal abscess formation
  3. Perforation and peritonitis (leading to sepsis)
  4. Stricture and fistula formation
  5. Intestinal obstruction
235
Q

Diverticulosis is asymptomatic, but what are the symptoms of diverticular disease?

A
  1. Abdominal pain (left lower quadrant especially)
  2. Constipation and diarrhoea
  3. Bloating and passage of mucus rectally
236
Q

What are the differentials for diverticular disease?

A
  1. GI - IBS, appendicitis, colorectal cancer, IBD, ischaemic colitis
  2. Gynae - PID, ovarian cyst, ectopic pregnancy
  3. Urological - UTI with pyelonephritis
237
Q

Which website is useful to direct patients towards who require information on diverticular disease?

A

corechairty.org.uk

238
Q

How much fibre should adults aim to consume every day?

A

30 grams

239
Q

What is the recommended management for diverticular disease? (3)

A
  1. High fibre diet
  2. Bulk forming laxatives
  3. Fluids
    (extras when needed include ABX, analgesia, antispasmodics, aminosalicylates)
240
Q

What are the most common causes of AF?

A
  1. Ischaemic heart disease
  2. Hypertension
  3. Valvular heart disease
  4. Hyperthyroidism
241
Q

Which non-cardiac conditions can cause AF? (9)

A
  1. Drugs (thyroxine, bronchodilators)
  2. Acute infection
  3. Electrolyte depletion
  4. Lung cancer
  5. Pulmonary embolism
  6. Thyrotoxicosis
  7. Diabetes
  8. Excessive caffeine intake
  9. Alcohol excess
242
Q

What are the complications of AF? (4)

A
  1. Stroke and thromboembolism
  2. Heart failure
  3. Tachycardia-induced cardiomyopathy and critical cardiac ischaemia
  4. Reduced quality of life (reduced exercise tolerance and impaired cognitive function)
243
Q

Anticoagulation treatment for AF, reduces the risk of a stroke by how much?

A

Reduces risk by 2/3

244
Q

When should AF be suspected in someone? (before ECG)

A

In anyone with an irregular pulse, with or without the following:

  1. Breathlessness
  2. Palpitations
  3. Chest discomfort
  4. Syncope
  5. Reduced exercise tolerance, malaise, polyuria
245
Q

Why can someone with AF get polyuria?

A

Due to the release of atrial natriuretic peptide during episodes of AF

246
Q

What investigation is best to do in someone with suspected paroxysmal AF?

A

An ambulatory 24-hour ECG (in some places an event recorder ECG is used in people who have symptomatic episodes more than 24 hours apart - Holter monitor)

247
Q

What are the differentials for AF?

A
  1. Atrial flutter (saw-tooth pattern of regular atrial activity)
  2. Ventricular ectopic beats
  3. Sinus tachycardia
  4. Supraventricular tachycardias e.g. Wolff-Parkinson-White syndrome
248
Q

What is the management for patients with AF?

A
  1. Identify and manage any underlying causes/triggers of AF
  2. Treat the arrhythmia
  3. Assess stroke risk - CHADSVASC assessment tool
  4. Assess risk and benefits off anticoagulation - the HAS-BLED assessment tool should be used to assess risk of a major bleed
  5. Arrange follow-up
  6. Provide advice and information
249
Q

How is the arrhythmia treated in AF? (2)

A
  1. A rate-control treatment - beta blockers or CCB
  2. Referral for rhythm-control treatment (card version) for people with:
    - new onset AF
    - AF has a reversible cause
250
Q

What is the CHADVASc assessment tool?

A 
The CHA2DS2-VASC score is for the risk of stroke in someone with AF. 
It takes into account: 
Age
Sex
CHF history
Hypertension history
Stroke/TIA/thromboembolism history
Vascular disease history
Diabetes history
251
Q

How many points on the CHADVASc score means a moderate-high risk of stroke?

A

2 or more points

252
Q

In terms of anticoagulants for stroke prevention in someone with AF, what is the advice that should be offered to help choose between warfarin and NOACs?

A
  1. Stroke risk reduction - both equally preventable
  2. NOACs have a reduced risk of haemorrhagic stroke compared with warfarin
  3. Adherence to treatment - NOACs have a shorter half-life (12-24 hours), whereas warfarin is 48-72 after missing a dose.
  4. NOACs do not require monitoring, whereas warfarin requires regular blood tests
253
Q

If anticoagulant is contraindicated in someone with AF, what other treatment can be offered?

A

Dual-anti-platelet therapy - aspirin and clopidogrel

254
Q

What should the INR be for someone taking warfarin?

A

Between 2 and 3

255
Q

Why might someone taking warfarin have poor anticoagulation control indicated by INR values being too high or too low? (5)

A
  1. Impaired cognitive function
  2. Poor adherence with prescribed treatment
  3. Illness
  4. Use of concurrent medications that may interact with warfarin
  5. Lifestyle factors such as diet and alcohol consumption
256
Q

What advice and information can be given to someone with AF? (4)

A
  1. Leaflets/websites to visit - www.atrialfibrillation.org.uk
  2. Safety net - if symptoms get worse
  3. Driving - inform the DVLA and check car insurance OK
  4. Support groups for AF

Year 4 CCC (17 decks)

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