Transcript Practice and Optometrists Vascular Risk 2014

Shelagh Cleary
Vascular Programme Manager
Dudley Office of Public Health
Do we need cholesterol?
Where do we get it from?
Lipid breakdown
 Very large and dense lipid molecules are broken down to
release energy for the cells of the body to use.
 As this process continues they get smaller and smaller
and eventually leave the final circulating particles in the
blood stream
 These are the particles we look at when we look at lipid
results from blood test reports
Lipid profile
Final particles
 Total cholesterol is the value given for HDL, LDL and
triglycerides combined – the “total”
 If we just look at the total it does not give us enough
information, because….
High Density Lipids or HDL is anti-artherogenic
Low Density Lipids or LDL is pro-artherogenic
Atheroma build up
 The purpose of analysing lipids is to determine whether
there is likely to be a build up of atheroma in the
arteries.
 Atheroma build up leads to the development of CVD
and to conditions such as heart attack and stroke.
So optimally, we would need:
A high level of the anti-artherogenic particles – HDL
and
A low level of pro-artherogenic particles - LDL
Why?
 Unused LDL is oxidised and then forms atheromatous
plaques on the inside walls of the arteries, causing them
to become narrowed or even blocked.
 HDL absorbs the unused LDL and takes it back to the liver
before it can become oxidised.
 So either a low level of HDL, or a high level of LDL (or
both) causes more atheromatous plaques to be formed Mismatch
So what should the levels be?
Target levels
 Cholesterol - less than 5.0 in primary prevention, but less
than 4.0 in secondary prevention
 HDL - at least 1.0, but at least 1.2 in females and people with
diabetes
 Ratio - less than 4.0 – 5.0
 LDL - less than 3.0 in primary prevention, but less than 2.0
in secondary prevention.
 Triglycerides - less than 1.7
CVD Risk Assessment
 Just looking at total cholesterol does not tell us enough
 We need to understand how much of this total is made
up of the good lipids and how much of the bad
 For primary prevention risk assessment we use the ratio
of total cholesterol to HDL:
Ratio = Total cholesterol  HDL
Importance of ratio
 This gives a better indication than TC alone of the overall
impact of the lipids on the development of
atherosclerosis.
 E.g. work out the ratios….
 55 year old male TC 5.6, HDL 0.8
= 7.0
 55 year old female TC 5.6, HDL 1.2
= 4.6
 55 year old female TC 7.0, HDL 1.5
= 4.6
If the target levels are raised
 The iCAP software will identify anyone with a total
cholesterol or a ratio of 5 or more in the workflow.
Then:
 Explain the results
 Give advice on reducing cholesterol in the diet
 A repeat test is indicated in 3 months time
 If the cholesterol is still raised at 3 months and the CVD
risk is 20% or more, then the GP may commence lipid
lowering medication.
But remember ratio…..
 Remember the ratio is a better guide to the impact of the
lipids and the development of atheroma, so:
 If the total cholesterol is raised but the ratio is normal,
then just give advice on a low cholesterol diet
 If the cholesterol is normal but the ratio is raised, give
advice and follow with a repeat blood test in 3 months to
re-check
Familial Hyperlipidaemia
Hereditary condition - heterozygous (approximately 1 in 500 of the U.K.)
 High levels of lipids are present from birth. The disease is genetic,
autosomal dominant. Children of a person with FH have a 50 per
cent risk of having FH.
 The disease does not skip generations which means that children
and grandchildren of family members who do not have a
defective gene are therefore not at risk from FH
 In all the cells of the body there is a receptor that allows LDL to
be cleared from the bloodstream.
 People with FH have a defect in the gene responsible for this LDL
receptor. This causes an accumulation of LDL in the blood and
ultimately in the arterial vessel walls.
 Well researched area, more than 300 known gene defects that
lead to FH.
Diagnosis of FH – Simon Broome
Criteria
TC >7.5mmol/l LDL>4.9mmol/l, plus
Tendon xanthoma in the person or 1st/ 2nd degree relative
Other signs
 Corneal arcus
 Development of premature CVD
 History of premature familial CVD
Premature CVD:
 Male developing CVD at or below 55 years,
 Female developing CVD at or below 65 years.
Premature Familial CVD:
 Father/brother-developing CVD at or below 55 years
 Mother/sister developing CVD at or below 65 years
N.B. CVD risk calculators or tables cannot be used to asses patients with familial
hyperlipidaemia.
F.H.
Xanthalasma
Tendon Xanthoma
Corneal Arcus
F.H.
 The iCAP software will identify anyone with possible FH.
 ALL patients with suspected F.H. should be referred to the
GP urgently for assessment and possible specialist
referral / assessment of family members
 N.B. The risk calculation software cannot be used to
calculate risk scores for people with FH
 Explain this to the patient – it will be underestimated if
they have FH
What will lower cholesterol?
 Low cholesterol diet – remember the liver makes it too!
 Increasing physical activity and exercise
 Avoiding stress
 What about ..?
 Smoking
 Alcohol
Low cholesterol diet
 Switch to mono or poly-unsaturated fats (30%)
 Reduce saturated fat (10%)
 Butter, cream, full fat milk
 Meat, burgers, sausages
 Processed foods, pies, ready meals
 Cakes, biscuits, chocolate, crisps
 Use healthier cooking methods
Coffee time?
Sweet success with checking blood
glucose results
Type 2 diabetes
 Type 2 diabetes is not a single disorder but part of a much
broader metabolic syndrome:
This consists predominantly of insulin resistance.
 Insulin resistance results from hereditary and lifestyle
factors involving over nutrition and under activity. It is
associated with obesity, particularly abdominal obesity.
 Nature versus nurture?
Insulin resistance
 Insulin resistance causes high levels of glucose and insulin in
the blood
 High levels of insulin cause problems with the lipid profile,
raising triglycerides and LDL and lowering HDL.
 It therefore helps to make more atheromatous plaques
develop
Impaired glucose regulation
 The regulation of glucose can be impaired for several
years before diabetes is diagnosed. This period is called
impaired glucose regulation or a pre-diabetic state.
 Diabetes may be prevented by management of people
with impaired glucose regulation
 Pre-diabetic state …. how do we find it?
Diagnosing IGR
Fasting glucose test
 If the fasting glucose is 6.0 or below, then this is normal
 If the fasting glucose is 6.1 – 6.9, then this may be
impaired fasting glucose or IFG or impaired glucose
tolerance IGT
 If the fasting glucose is 7.0 or more, then this may be
diabetes
Non-Fasting glucose
 Using the point of care finger prick blood test
 Ask when the patient last ate a meal or snack
 If this is more than 2 hours before the glucose should be
6.0 or less
 If it is less than 2 hours the glucose should be no more
than 11.0
 Less than 2 hours
 More than 2 hours
-
6.0 or less
No more than 11.0
What is in iCAP?
 iCAP will highlight any glucose result over 6.0 and
recommend a 2nd test to confirm.
 Explain to the patient that they should see their GP or
practice nurse to arrange a 2nd test if this is required
 Take into account other risk factors for diabetes
 Where a diagnosis is to be considered the practice may
send them for / carry out an oral glucose tolerance test
(OGTT)
Oral Glucose Tolerance test
 An OGTT is requested to confirm either diabetes or
impaired glucose tolerance
 What the test involves:
 Fasting specimen
 Glucose load
 2 hour post load specimen
 This shows any problems with the way that glucose is
processed in the body which may give the diagnosis of
IGT or diabetes
Referral
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So….,
Arrange for a second test for anyone with
A fasting glucose of 6.1 or more, or
A non-fasting glucose which is:
More than 6.0 if they have not eaten in the last 2 hours, or
More than 11.0 if they have eaten in the last 2 hours
 Ask them to see the practice nurse or GP with the results
 Dudley Diabetes Website www.dudleydiabetes.co.uk
Any questions….?
What’s pee got to do, got to do with it…?
Kidney function
 Kidney impairment is a major cause of heart attack and
stroke and is associated strongly with hypertension
 The process by which we measure kidney function is the
rate at which the kidneys are able to filter the arterial
blood stream
 This is called the Glomerular Filtration Rate or GFR.
 It is calculated from levels of creatinine in the blood and
so is called an estimated GFR or eGFR
Chronic Kidney Disease
 A diagnosis of moderate chronic kidney disease is made
when the eGFR is less than 60 mls/min
 An eGFR of 59 or less would possibly indicate a CKD stage
of 3, 4 or 5
 These stages are moderate to severe kidney disease. At
these levels the incidence of cardiovascular disease is 10
fold.
CKD and CVD
 CKD causes blood pressure to rise which causes a heavy
workload on the heart
 CKD causes levels of protein in the urine to become raised
leading to oedema, also causing blood pressure to rise
and further increasing the workload of the heart.
CKD and CVD
 CKD causes calcium to be taken from the bones and into
the blood stream where it is deposited in the arteries and
heart valves. This causes stiff and narrowed vessels and
problems with the pumping mechanism of the heart
 CKD causes anaemia, which increases the workload of the
heart as it has to pump the blood faster to maintain
perfusion. There can also be loss of perfusion to the heart
itself.
What is on iCAP?
 The eGFR result will be displayed.
 If the result is lower than 60 then it will stage the level of
possible CKD, i.e. Possible CKD Stage 3, 4 or 5
 Any result of less than 60 will be included in the workflow
along with the next step of the pathway
 The next step would be to repeat the eGFR test after a
period of 3 months – advise the patient
What about dementia?
 The incidence of dementia rises with age
 The incidence in the UK is rising rapidly
 The risk factors for CVD are the same as for dementia –
especially vascular dementia
 If the patient is over 65, then icap will prompt you to
advise the patient of this additional risk
 Give leaflet supplied by DoH
Any questions….?
So what are the odds…..?
CVD Risk Calculation
 Risk scores are automatically calculated on the iCAP
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software.
The risk is displayed as latest risk, relative risk and target
risk.
Latest risk is the risk calculated on the entries made. This
is also called absolute risk.
Relative risk is what level of risk would be expected for an
individual
Target risk shows what happens to risk when values are
changed, i.e. smoker to non-smoker
Communication of risk
 Risk of 1-9% is low risk
 Risk of 10-19% is moderate risk
 Risk of 20% or more is high risk
 Use odds, e.g. 1 in 5, 1 in 4 etc
 Heart age – probably more meaningful and more
powerful to communicate risk to patients
 Bus queue
 Comparison of absolute risk to relative risk
High risk
 Those found to be at high risk are added to a high risk
register
 They will be called for review annually using the
software.
 People at this level of risk can be prescribed lipid lowering
drugs
 More intensive targeting of risk factors
Referral
 Give advice to:
 Anyone who is high risk, especially where this is unexpected, i.e. where
the relative risk is low and there are clinical indications to account for
this, e.g. raised blood pressure or lipids.
 Anyone who has a higher absolute risk than expected / relative risk
level, even if this is moderate or low
 Risk factors will have been identified which can account for the
increased level of risk
 These risk factors need to be reduced where possible to reduce the
level of risk – use target risk to demonstrate this
So, what are the risk
factors…?
Any questions….?
Wish I’d
done a risk
assessment!
Risk assessment can be a good thing…….