Chronic Core Conditions Flashcards
(256 cards)
1
Q
What % of the population is affected by asthma?
A
5-8%
2
Q
At what age range does asthma prevalence peak?
A
5-15 years
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
4
Q
What are the three factors that contribute to airway narrowing?
A
- Bronchial muscle contraction: triggered by various stimuli
- Mucosal swelling/inflammation
- Increased mucus production
5
Q
What causes mucosal swelling and inflammation?
A
Mast cells and basophil degranulation resulting in the release of inflammatory mediators
6
Q
What happens during an acute flair up of asthma? (2)
A
- Bronchospasm
2. Excessive production of secretions (plugging airways)
7
Q
How can asthma be catergorised?
A
- Extrinsic
2. Intrinsic
8
Q
What is extrinsic asthma?/what are the triggers? (9)
A
Definite cause found - most commonly type of atopy. Possible triggers include:
- Dust mite
- Pollen
- Animal dander and fur
- Pollution
- Cold air
- Exercise
- Smoking (including passive)
- NSAIDs
- Beta blockers (DO NOT GIVE TO ASTHMATICS)
9
Q
In addition to the extrinsic triggers, what are the risk factors for developing asthma? (5)
A
- Inner city environment
- Family history of asthma and atopy
- Concurrent eczema/hayfever
- Maternal smoking
- High serum IgE (gene on chromosome 2 called PHF11 that controls IgE synthesis)
10
Q
What are the symptoms of asthma/how might someone present? (7)
A
- Dyspnoea
- Wheeze
- Cough (nocturnal)
- Diurnal variation
- Chest tightness
- Disturbed sleep (severe asthma)
- Sputum production
11
Q
What are the signs of asthma? (7)
A
- Tachypnoea
- Widespread bilateral wheeze
- Hyperinflated chest
- Hyper-resonant percussion note
- Diminished air entry
- Prolonged expiration
- Increased respiratory rate
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:
- Lack of wheeze
- Normal chest examination
- Voice disturbance
- Symptoms with cold only
- Significant smoking history
- Cardiac disease
13
Q
What are the differential diagnoses of asthma? (7)
A
- COPD (can coexist)
- Pulmonary oedema
- PE
- Bronchiectasis
- Foreign object
- Obliterative bronchiolitis
- Pneumothorax
14
Q
What investigations need to be carried out in someone with suspected asthma? (5)
A
- Peak flow (PEFR) - recorded as the best of three forced expiratory blows from total lung capacity while standing (if possible)
- Spirometry
- CXR
- FBC
- Skin prick test (may identify allergens- don’t routinely test this)
15
Q
What investigation is preferable to have before diagnosis of asthma?
A
Spirometry
16
Q
What is the FEV1/FVC ratio expected to be for asthma?
A
<0.7
17
Q
What defines complete control of asthma? (7)
A
- No daytime symptpoms/no night time awakening
- No need for rescue medication
- No asthma attacks
- No exacerbations
- No limitations of activity including exercise
- Normal lung function
- Minimal side effects from medication
18
Q
When is a step up in medication indicated for people with asthma? (4)
A
- Using SABA 3 times a week or more
- Symptomatic three times a week or more
- Exacerbation in the last 2 years
- Waking one night a week
19
Q
What is the lifestyle advice for people with asthma? (6)
A
- Stop smoking
- Avoid triggers (e.g. NSAIDs)
- Lose weight (if overweight)
- Wash spacer once a month in soapy water and leave to drip dry
- Monitor PEFR 2x daily
- Immunisations
20
Q
What is the treatment for step 1 of asthma - so mild intermittent asthma? (adults)
A
- Inhaled short-acting beta agonist (SABA) 100 micrograms QDS
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
- Add inhaled corticosteroid 200-800 micrograms per day
400 micrograms is an appropriate starting dose for more patients
22
Q
If the asthma is not controlled by step 2, what is step 3 treatment? (2) adults)
A
- Add inhaled long-acting beta-agonist (LABA)
2. May need to increase dose of inhaled corticosteroid (to 800 micrograms)
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
24
Q
What is step 4 on the treatment pathway for asthma? (2) (adults)
A
- 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.
25
What is the 5th and final step in the treatment of chronic asthma? (3) (adults)
1. Use daily steroid tablet (in lowest dose that provides adequate control)
2. Maintain high dose inhaled corticosteroid
3. Refer patient to specialist care
26
In children, the pathway of treatment for asthma is very similar, what are the steps?
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
27
Give an example of SABA? (2)
1. Salbutamol
| 2. Terbutaline
28
Give an example of LABA? (2)
1. Salmeterol
| 2. Formoterol
29
Which drugs do SABA/LABA interact with? (2)
1. Digoxin (monitor potassium levels)
| 2. Corticosteroids, diuretics, theophyllines (monitor potassium levels)
30
Give example of inhaled corticosteroids (ICS)? (4)
1. Beclometasone
2. Budesonide
3. Ciclesonide
4. Fluticasone
31
Which oral steroid is given most commonly in the treatment of asthma?
1. Prednisolone (40-50mg OD)
32
Give an example of two leukotriene receptor antagonists?
1. Montelukast (10mg OD)
| 2. Zafirlukast (20mg BD)
33
What are the signs/symptoms of acute asthma/near-fatal asthma? (9)
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
34
What is the treatment of acute/life threatening asthma? (6)
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)
35
What % of >40 year olds are affected by COPD?
10-20%
36
When may someone under the age of 35 develop COPD?
If they have alpha 1 anti-trypsin deficiency
37
Which gender is COPD most common in and why?
Males, due to the previous smoking trends
38
COPD is an umbrella term for which two diseases?
1. Emphysema
| 2. Chronic bronchitis
39
What is emphysema?
It is the enlargement of air spaces distal to the terminal bronchioles and destruction of the alveolar walls
40
What is chronic bronchitis?
It is a cough with/or without sputum production for most days for 3 months in the last 2 years
41
How is the diagnosis of chronic bronchitis different to emphysema?
Chronic bronchitis is a clinical diagnosis, whereas emphysema is a histological diagnosis
42
What are the characteristics of COPD? e.g. is it reversible?
It is a progressive disorder that is not reversible.
43
How is airway obstruction defined with regards to FEV1:FVC?
FEV1/FVC <0.7
44
As COPD progresses, what happens to the hypercapnic drive to breath?
People lose their hypercapnic drive to breath and depend on the hypoxaemic drive
45
What three mechanisms of COPD limit airflow into the small airways?
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)
46
What are the risk factors for developing COPD?
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
47
What are the symptoms of COPD? (6)
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
48
What are the signs of COPD? (12)
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
49
What are the two phenotypes of presentation of COPD?
1. Pink puffers
| 2. Blue bloaters
50
What are the symptoms/signs of 'pink puffers'? (4)
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
51
What are the signs/symptoms of 'blue bloaters'?
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
52
Why should supplementary O2 be given with caution in patients with COPD?
Because they rely on the hypoxic drive to maintain respiratory effort, and therefore could cause respiratory depression
53
In order for a diagnosis of COPD, what are the criteria that needs to be met? (5)
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
54
What investigations are carried out in someone with suspected COPD?
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
55
What would be expected on a CXR in someone with COPD? (4)
1. Hyperinflation
2. Flat hemi-diaphragms
3. Large central pulmonary arteries
4. Reduced peripheral vascular markings
56
What blood tests are required and why, for someone with COPD?
1. FBC - to identify anaemia or secondary polycythaemia
57
What would an ABG should of someone with COPD?
Low PaO2 +/- hypercapnia
58
What is the ECG for when investigating COPD?
Assessing for cor pulmonale (RHF) signs = right atrial and ventricular hypertrophy
59
When taking a social history, what is important to note in someone with suspected COPD?
Whether the person is a smoker or ex-smoker etc, and calculate pack years
60
How is the severity of COPD measured/assessed? (3)
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
61
How many stages are there in the GOLD classification of severity of COPD?
Stage 0 - Stage IV
62
What does stage 0 of GOLD refer to?
At risk; chronic cough and sputum production, but normal spirometry
63
What does stage 1 of GOLD refer to?
Mild COPD; mild airflow limitation, FEV1/FVC <0.7, FEV1 >80%
64
Stage 2 of GOLD?
Moderate COPD - FEV1 50-79%
65
Stage 3 of GOLD?
Severe COPD - FEV1 30-49%
66
Stage 4 of GOLD?
Very severe COPD - FEV1 <30%
67
What is the Medical Research Council dyspnoea scale?
It is a scale based on grades 1 through to 5, measuring the level of activity the individual is capable of
68
What is grade 1 of MRC dyspnoea scale?
Not troubled by breathlessness except during strenuous exercise
69
What is grade 3 of MRC dyspnoea scale?
Walks slower than contemporaries on the same level because of breathlessness, or has to stop for breath when walking at own pace
70
What is grade 5 of MRC dyspnoea scale?
Too breathless to leave the house, or breathless when dressing/undressing
71
What is the management of COPD?
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
72
What drugs are prescribed for people with COPD to help cope with breathlessness?
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
73
In an acute exacerbation of COPD, what is the treatment? (4)
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%
74
When is LTOT indicated in someone with COPD? (5)
1. FEV1 <30%
2. Cyanosis; O2 sats <92%
3. Polycythaemia
4. Peripheral oedema
5. Raised JVP
75
For how many hours each day should LTOT be used?
>15 hours per day
76
How can hospital admissions for patients with COPD prone to exacerbations be prevented?
1. Keep abx in the house in case of infection
| 2. Prednisolone tablets in case of increasing breathlessness
77
What % of people in the UK with a diagnosis of diabetes, have type 1?
10%
78
How many people in the UK have diabetes?
4.5% (2.9 million people)
79
What features/symptoms/signs suggest type 1 diabetes, rather than type 2? (5)
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
80
What features/symptoms/signs suggest type 2 diabetes as opposed to type 1? (3)
1. Polydipsia and polyuria
2. Fatigue
3. Recurrent infections e.g. thrush
81
What is type 1 diabetes?
It is an absolute deficiency in insulin which causes persistent hyperglycaemia.
82
What causes type 1 diabetes?
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.
83
Diabetes belongs to a family of which autoimmune diseases?
HLA-associated immune mediated organ specific diseases. Genetic susceptibility is polygenic and the HLA responsible is DR3+/-DR4)
84
What is the demographics of patients presenting with type 1 diabetes? (2)
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)
85
What is the classic triad in presentation of symptoms in type 1 diabetes?
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)
86
In addition to the classic triad, what other signs/symptoms may be present in T1DM? (5)
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
87
What is the clinical presentation of overt DKA? (4)
1. Nausea and vomiting
2. Kussmauls breathing
3. Ketones on breath
4. Abdominal pain
88
What investigations need to be carried out in someone with suspected T1DM? (6)
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
89
What are the diagnostic requirements for type 1 diabetes?
1. Classical symptoms + 1 raised glucose OR
2. No classical symptoms + 2 raised glucose
3. HbA1c > 48mmol/L but lower doesn't exclude DM
90
What are the complications of type 1 DM?
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
91
What is the management plan for someone with suspected T1DM?
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
92
Which type of insulin is the only one used in the UK now?
Human insulin
93
What is the only route of administration of insulin?
Sub-cutaneous injections
94
What are the 3 different types of insulin?
1. Short and ultra fast-acting
2. Intermediate and long-acting
3. Biphasic premixed
95
What is the aim of the short and ultra fast-acting insulin's?
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)
96
What is intermediate and long-acting insulin used to mimic?
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.
97
What is the typical insulin requirement per day?
0.3-1 unit/kg/day
98
Although there is the typical insulin requirement, what does this depend on? (7)
1. Age
2. Weight
3. Stage of puberty
4. Duration and phase of diabetes
5. Daily routine
6. Diet
7. Illness
99
In general, a half, to two-thirds of total insulin is given to cover what? ...and the remainder is to control what?
Basal needs and the remainder is to control post-prandial glycaemia
100
What is the main adverse effect of insulin?
Hypoglycaemia
101
What are the initial effects of hypoglycaemia? (5)
Adrenergic:
1. Sweating
2. Tachycardia
3. Palpitations
4. Pallor
5. Hunger
102
What are the later effects of hypoglycaemia? (7)
Neuroglycopenic:
1. Confusion
2. Slurred
3. Drowsiness
4. Yawning
5. Anxiety
6. Blurred vision
7. Numbness of nose, lips and fingers
103
What is the lifestyle advice that should be discussed with patients with diabetes? (6)
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
What needs to be monitored in someone with T1DM? (9)
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
What is the % lifetime risk of developing T2DM?
15%
106
What is the pathophysiology behind T2DM? (3)
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
T2DM typically progresses from what and why is this important?
1. IGT or IFG - impaired glucose tolerance or impaired fasting glucose; important is it provides a unique window of opportunity for lifestyle intervention
108
What is MODY?
Maturity onset diabetes of the young - it is a rare autosomal dominant form of T2DM
109
What are the risk factors for T2DM? (8)
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
What are the signs and symptoms of T2DM? (8)
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
When is HbA1c not suitable for diagnosis of T2DM? (6)
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
In addition to HbA1c, what else can be measured to diagnose T2DM? (2)
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
What is the HbA1c target for someone with T2DM?
48mmol/L
114
Name a group education programme for people with T2DM?
DESMOND or XPERT
115
Which drug class does metformin belong to?
Biguanides
116
What is the mechanism of action of metformin?
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
What are the contra indications for metformin?
Impaired renal function (eGRF <30)
118
What is the usual method of initiating metformin treatment?
500mg OD with breakfast, increasing by 500mg at intervals of 1-2 weeks according to response.
119
What needs to be monitored when someone is on metformin?
1. Renal function
| 2. HbA1c
120
What are the side effects that metformin can cause?
1. Non-serious GI side effects e.g. nausea, vomiting
| 2. Lactic acidosis (rare but potentially fatal)
121
Name the treatment for T2DM that is an insulin secretagogues?
Sulfonylureas
122
What is the mechanism of action sulfonylureas?
They directly increase insulin secretion from the pancreas and therefore are only effective when some residual pancreatic beta cell function is present
123
What are the first-choice sulfonylureas? (3)
1. Gliclazide
2. Glimerpiride
3. Glipizide
124
Do sulfonylureas have a short or long duration of action?
Long
125
What is the method of action of meglitinides?
These have the same method of action as sulfonylureas - (insulin secretagogues)
126
Do meglitinides have a short or long duration of action?
Short and rapid onset
127
When are meglitinides preferred over sulfonylureas?
They are indicated for use for people with erratic lifestyles leading to irregular meal times.
128
Name some types of meglitinides? (2)
1. Natglinide (combination therapy with max metformin dose)
| 2. Repaglinide
129
Name the two types of insulin secretagogues?
1. Sulfonylureas
| 2. Meglitinides
130
When should meglitinides be taken?
30 minutes before a meal
131
When are insulin secretagogues contra-indicated? (2)
1. People who are at risk of hypo's
| 2. Pregnancy
132
What are the adverse effects of using insulin secretagogues? (2)
1. Hypoglycaemia - must warn DVLA they are taking them
| 2. Weight gain 1-5kg
133
Name some examples of DPP-inhibitors (dipeptidyl peptidase-4 inhibitors)? (4)
The gliptins..
1. Sitagliptin
2. Linagliptin
3. Saxagliptin
4. Vildagliptin
134
What is the mechanism of action of DPP-inhibitors?
Increase insulin secretion - inhibition of DPP-4 allows increased half-life of incretins which potentiate nutrient-induced insulin secretion
135
What are incretins?
Incretins are a hormone which augment the secretion of insulin by a blood glucose-dependent mechanism
136
What are the two forms of incretins?
1. Glucose-dependent insulinotropic peptide (GIP)
| 2. Glucagon-like peptide-1 (GLP-1)
137
What are the side effects of taking DPP-4 inhibitors? (1)
1. Small risk of hypoglycaemia (don't need to inform DVLA)
| weight neutral
138
When is the use of DPP4-inhibitors contraindicated? (2)
1. Substantial renal/liver disease
| 2. Pancreatitis
139
What are SGLT2 inhibitors?
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
Name some examples of SGLT2 inhibitors? (3)
1. Canagliflozin
2. Dapagliflozin
3. Empagliflozin
141
What are the possible side effects of SGLT2 inhibitors?
1. Increased risk of thrush and UTI
| 2. Hypoglycaemia (small risk)
142
When is the use of SGLT2 inhibitors contra-indicated?
1. Renal impairment and severe liver disease
143
Name some examples of thiazolidinediones?
1. Glitazones
2. Pioglitazones
3. Rosiglitazone
144
When is insulin therapy indicated for patients with T2DM?
When the other treatments/modifications are insufficient to maintain normoglycemia
145
What is important to stop once insulin therapy has commenced in T2DM?
Sulfonylureas should be stopped once insulin has started as there is a severe risk of hypoglycaemia
146
What is the start dose of insulin?
8 units
147
What is hypertension?
A persistently raised arterial blood pressure
148
What % of adults have a BP that is at least 140/90?
30%
149
95% of people have what type of hypertension?
Primary essential hypertension
150
What are the causes of secondary hypertension?
1. Renal disorders
2. Cardiovascular disorders
3. Endocrine disorders
4. Drugs
5. Misc.
151
What are the renal disorders that can lead to secondary hypertension? (6)
1. Chronic pyelonephritis
2. Diabetic nephropathy
3. Glomerulonephritis
4. Polycystic kidney disease
5. Obstructive uropathy
6. Renal cell carcinoma
152
What are the cardiovascular disorders that can lead to secondary hypertension? (2)
1. Coarctation of the aorta
| 2. Renal artery stenosis (BP resistant to treatment)
153
What are the endocrine disorders that can cause secondary hypertension? (6)
1. Primary hyperaldosteronism
2. Phaeochromocytoma
3. Cushing's syndrome
4. Acromegaly
5. Hypothyroidism
6. Hyperthyroidism
154
Which drugs both recreational and medicinal can cause secondary hypertension? (9)
1. Alcohol misuse
2. Cocaine
3. COCP
4. Corticosteroids
5. Ciclosporin
6. Erythropoietin
7. Leflunomide
8. NSAIDs
9. Venlafaxine
155
What are the other causes of secondary hypertension, not grouped within CV, renal or drug related? (3)
1. Connective tissue disorders
2. Retroperitoneal fibrosis
3. Obstructive sleep apnoea
156
What are the risk factors for developing hypertension?
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
How is hypertension diagnosed?
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
What is stage 1 hypertension classed as?
ABPM = >135/85 (clinic >140/90)
159
What is stage 2 hypertension classed as?
ABPM = >150/95 (clinic >160/100)
160
What is stage 3 aka severe hypertension classed as?
Clinic systolic BP = >180mmHg or clinic diastolic BP = >110mmHg
161
What is accelerated hypertension classed as?
Clinic BP higher than 180/110mmHg with signs of papilloedema and/or retinal haemorrhage (hypertensive retinopathy) OR BP > 220/120mmHg
162
If someone presents to GP with accelerated hypertension, what is the management plan?
Same day referral to specialist!
163
How many measurements are meant to be taken for ambulatory blood pressure monitoring?
Between 8am and 10pm, 2 measurements per hour. Use the average of >14 measurements
164
What examinations/obs need to be taken for someone presenting with hypertension?
1. Weight and BMI
2. Cardiovascular: pulse (rate, rhythm and character), BP in other arm, heart sounds, lungs
3. Eyes - signs of retinopathy
165
What investigations need to be carried out in someone with a new presentation of hypertension (to exclude co-existing conditions)? (4)
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
What lifestyle modifications need to be made to help reduce high blood pressure? (6)
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
What is the treatment step ladder for people <55 years old with hypertension who are NOT of afro-caribbean ethnicity?
1. ACE inhibitor or low-cost ARB
2. Add CCB
3. Add thiazide-like diuretic
4. Consider further diuretic / beta- or alpha- blocker
168
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?
Beta-blocker
169
What is the treatment step ladder for people over >55 years old or/and people of afro-caribbean ethnicity with hypertension?
1. CCB
2. Add ACEi or ARB
3. Add thiazide-like diuretic
4. Consider further diuretic or alpha/beta- blocker
170
If someone is 51, with stage 1 hypertension and no other co-morbidities, what is the recommended treatment?
No medication - lifestyle changes
171
If someone under 40 has stage 1 hypertension, what is the recommended plan?
Refer to specialist - likely it could be secondary and this needs to be investigated
172
What co-moribidities would indicate someone with stage 1 hypertension requires medication to treat? (4)
1. Diabetes
2. Target organ damage
3. Established cardiovascular disease
4. A QRISK2 score of greater then 20%
173
What does of ramipril is normally started for someone with hypertension?
2.5mg OD - the first dose is taken at night to avoid hypotensive drop and then after that taken every morning
174
What is the maximum dose of ramipril OD?
10mg
175
If lisinopril is recommended over ramipril, what is the first/starting dose?
10mg
176
What is the maximum dose of lisinopril OD?
80mg
177
What are the contra-indications for using ACE inhibitors?
1. Pregnancy/women planning pregnancy/breastfeeding
2. Angioedema
3. Bilateraly artery stenosis
178
What are the side effects of taking ACE inhibitors? (4)
1. Dry cough
2. Hyperkalaemia
3. Deterioration in renal function (hence this has to be monitored)
4. Dizziness/headaches
179
Name two CCBs used to treat hypertension?
1. Amlodipine
| 2. Nifedipine
180
What is the mechanism of action of CCBs?
They reduce calcium influx into vascular smooth muscle cells, by interfering with voltage-operated calcium channels in the cell membrane
181
What is the usual starting dose of amlodipine?
5mg OD
182
When is the use of CCB contra-indicated? (5)
1. Heart failure
2. Cardiac outflow obstruction
3. Second-degree atrioventricular
4. Hepatic impairment
5. Renal impairment
183
What are the side effects of CCBs? (5)
1. Ankle swelling
2. Headache
3. Nausea
4. Dizziness
5. Flushing
184
Which drugs/juices are known to interact with CCBs? (4)
1. Grapefruit juice
2. Beta-blockers
3. Enzyme-inducing drugs (e.g. carbamazepine)
4. Anti-depressants
185
Name two thiazide-like diuretics?
1. Indapamide
| 2. Bendroflumathiazide
186
What is the mechanism of action of thiazide-like diuretics?
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
What is the recommended dose of indapamide?
2.5mg OD
188
What are the contra-indications for thiazide-like diuretics? (8)
1. Gout
2. Refractory hypokalaemia
3. Hyponatraemia
4. Hypercalcaemia
5. Severe hepatic impairment
6. Addison's
7. eGFR <30
8. Pregnancy
189
What are the side effects of thiazide-like diuretics? (6)
1. Excessive diuresis
2. Hypokalaemia
3. Gout
4. Postural hypotension
5. DM
6. Dizziness
190
In the annual review for patients with hypertension, what needs to be recorded/discussed? (5)
1. Blood pressure
2. U&Es; renal function
3. Lifestyle; diet and exercise
4. Weight / BMI
5. Side effects from treatment
191
In people with hypertension who are at risk of cardiovascular disease, what other drugs are often prescribed?
Aspirin (anti-platelet) 75mg OD
| Atorvastatin (statin) 40mg OD
192
What is a stroke?
A acute focal neurological deficit of arterial origin lasting more than 24 hours with a positive scan
193
What % of people who have a stroke, have a preceding TIA?
15%
194
What is a TIA?
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
What can cause cerebral ischaemia?
1. Atheroma
2. Thromboembolism
3. Trauma
4. Infection
5. Tumours
196
What % of strokes are ischaemic and haemorrhagic?
85% ischaemic
| 15% haemorrhagic
197
If the stroke is ischaemic, what are the two usual causes?
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
What are the risk factors for a stroke/TIA?
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
What are the symptoms/signs of a TIA?
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
What % of ischaemic strokes are a cerebral infarct?
50%
201
What are the different cerebral infarcts and signs?
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
What % of ischaemic strokes are brainstem infarcts, and what are the signs?
25% --> wide range of effects including quadriplegia, visual disturbance, and locked-in syndrome
203
What % of ischaemic strokes are lacunar infarcts, and what are the signs?
25% --> ataxic hemiparesis, pure motor or sensory or combination, dysarthria/clumsy hand, intact cognition/consciousness except thalamic
204
What is the scoring system used to assess risk of TIAs?
ABCD2
205
What does the scoring system stand for and how many points is each worth?
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
What score would a patient get on the ABCD2 system which would lead to an immediate referral to a specialist?
>4
207
If a patient scores 4 on the ABCD2 system, what is the management?
1 week wait referral to specialist
208
What are the indications for a same day specialist assessment of someone experiencing a TIA? (3)
1. More than one TIA in a week
2. A TIA whilst on anticoagulation
3. ABCD2 score greater than 4
209
What investigation will be performed on someone who has experienced a TIA in the specialist assessment unit?
Carotid ultrasound
210
What is the immediate treatment given to someone who has experienced a TIA?
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
When would someone with a suspected TIA be referred for brain imaging? (3)
1. If carotid endarterectomy is being considered when circulatory origin uncertain
2. Haemorrhage needs to be excluded
3. Alternative diagnosis is being considered
212
When would someone with a suspected stroke require a head CT within 1 hour/ASAP of arrival? (2)
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
If someone with suspected stroke is not for thrombolysis or suspected haemorrhagic stroke, what is the time frame for recommended brain scan?
Within 24 hours of arrival
214
What is the time period for treatment with thrombolysis in someone with ischaemic stroke?
4.5 hours from onset of symptoms
215
What is the thrombolysis used?
Alteplase - tissue plasminogen activator or tPA
216
In someone with an ischaemic stroke who cannot taken aspirin orally due to dysphagia, what is the route of administration?
Rectally
217
If the stroke is haemorrhagic, what treatment can be given to help with clotting?
Prothrombin complex and vitamin K to normalise clotting factors
218
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)
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
What are the medical management aims in terms of rehab for someone who has suffered a stroke? (7)
1. Cognition
2. Vision
3. Hearing
4. Tone
5. Strength
6. Sensation
7. Balance
220
What lifestyle modifications should be made by anyone who has suffered a stroke? (5)
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
Which professions make up the core multidisciplinary stroke team? (7)
1. Consultant physicians
2. Nurses
3. Physiotherapists
4. Occupational therapists
5. SALT
6. Clinical psychologists
7. Rehabilitation assistants
222
What is epilepsy?
A disorder of the brain characterised by a predisposition to epileptic seizures, diagnosed after at least 2 epileptic seizures.
223
What is an epileptic seizure?
Spontaneous uncontrolled abnormal brain activity
224
What percentage of people with epilepsy have no anatomically identifiable cause? (idiopathic epilepsy)?
66%
225
What % of people with epilepsy have a 1st degree relative with epilepsy?
33%
226
In 33% of epileptics, there are anatomical causes, what are they?
1. Structural - cortical scarring from previous head injuries, stroke, vascular malformations, developmental
2. Tuberous sclerosis, SLE, sarcoidosis
227
What are the non-epileptic causes of seizures?
1. Raised ICP
| 2. Alcohol withdrawal
228
What are diverticula?
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
What is thought to cause diverticulitis?
A low-fibre diet - lowers stool bulk, slows transit times and increases intraluminal pressure
230
What is the difference between diverticulosis and diverticular disease?
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
What is diverticulitis?
A condition where the diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding.
232
What is the difference between complicated and uncomplicated diverticulitis?
Complicated diverticulitis is associated with complications such as abscess, peritonitis, fistula, obstruction or perforation of the peritoneum. Whereas uncomplicated is localised inflammation.
233
What are the risk factors for developing diverticular disease? (5)
1. Genetic
2. Low-fibre diet
3. Smoking
4. Obesity
5. Drugs - NSAIDs, opioids, corticosteroids
234
What are the complications of diverticular disease? (5)
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
Diverticulosis is asymptomatic, but what are the symptoms of diverticular disease?
1. Abdominal pain (left lower quadrant especially)
2. Constipation and diarrhoea
3. Bloating and passage of mucus rectally
236
What are the differentials for diverticular disease?
1. GI - IBS, appendicitis, colorectal cancer, IBD, ischaemic colitis
2. Gynae - PID, ovarian cyst, ectopic pregnancy
3. Urological - UTI with pyelonephritis
237
Which website is useful to direct patients towards who require information on diverticular disease?
corechairty.org.uk
238
How much fibre should adults aim to consume every day?
30 grams
239
What is the recommended management for diverticular disease? (3)
1. High fibre diet
2. Bulk forming laxatives
3. Fluids
(extras when needed include ABX, analgesia, antispasmodics, aminosalicylates)
240
What are the most common causes of AF?
1. Ischaemic heart disease
2. Hypertension
3. Valvular heart disease
4. Hyperthyroidism
241
Which non-cardiac conditions can cause AF? (9)
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
What are the complications of AF? (4)
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
Anticoagulation treatment for AF, reduces the risk of a stroke by how much?
Reduces risk by 2/3
244
When should AF be suspected in someone? (before ECG)
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
Why can someone with AF get polyuria?
Due to the release of atrial natriuretic peptide during episodes of AF
246
What investigation is best to do in someone with suspected paroxysmal AF?
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
What are the differentials for AF?
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
What is the management for patients with AF?
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
How is the arrhythmia treated in AF? (2)
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
What is the CHADVASc assessment tool?
```
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
How many points on the CHADVASc score means a moderate-high risk of stroke?
2 or more points
252
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?
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
If anticoagulant is contraindicated in someone with AF, what other treatment can be offered?
Dual-anti-platelet therapy - aspirin and clopidogrel
254
What should the INR be for someone taking warfarin?
Between 2 and 3
255
Why might someone taking warfarin have poor anticoagulation control indicated by INR values being too high or too low? (5)
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
What advice and information can be given to someone with AF? (4)
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
