CT 2 Cardiovascular Risk

Question 1

what are the non-modifiable risk factors for developing heart disease

Answer 1

• age
• male gender
• FHx (ApoB/ApoA1 gene mutation eg means deficient in HDL)

Question 2

what are the modifiable risk factors for CVD

Answer 2

• smoking as smoking can accelerate atherosclerotic
  progression through oxidation of LDL, stimulate inflammatory mediators, and adversely affect
  platelet activation, coronary vasospasm and blood pressure)
• alcohol
• hypertension (a 2mmHg increase can lead to a 7% increase in CVD risk)
• high LDL
• low HDL
• diabetes
• inactivity
• obesity
• drug use (cocaine and methamphetamine)
• stress and deprivation
• polluted air as higher concentrations of fine particles in the air can increase coronary artery
  calcium levels (leading to calcification and plaques), increasing CVD risk

Question 3

what is the QRISK score

Answer 3

risk of developing CVD in the next 10 years

low <10%

moderate 10-20%

high >20%

Question 4

what are the NICE guidelines on reducing CVD risk

Answer 4

◦
A cardioprotective diet, where total fat
intake is less than 30% of total energy
intake, with saturated fat being less than 7%
(and saturated fats should be replaced by
monounsaturated and polyunsaturated fats),
dietary cholesterol intake is less than 300mg
a day, wholegrain starchy foods should be chosen, sugar intake should be reduced, you should
get your 5 a day, and you should have at least 2 portions of fish a week and 4-5 portions of
nuts, seeds and legumes (e.g. beans, peas, lentils) a week
◦
Physical activity, so at least 150 minutes of moderate intensity activity, or 75 minutes of
vigorous intensity activity a week. You should also have at least 2 days a week of whole body
muscle strengthening exercise
◦
Less alcohol intake, so no more than 14 units per week for men and women, and spreading
◦
that drink over 3 or more days, with some days in the week being alcohol free
Less smoking

Question 5

which groups of patients should QRISK not be used in

Answer 5

T1 DM
EGFR of <60mL/min
familial hyperlipidemia
taking meds that cause dyslipidemia (anti-psychotics, steroids, immunosupressants)
autoimmune - lupus

Question 6

familial hyperlipidaemia

Answer 6

If a patient’s cholesterol is very high (over 7.5mmol/l) and there is family history of premature CHD,then familial hyperlipidaemia/hypercholesterolaemia should be considered. Furthermore, patients
with total cholesterol over 9mmol/l, or LDL levels over 7.5mmol/l, should be referred even if there is
no family history of premature CHD

Question 7

what is primary prevention

Answer 7

lifestyle advice: (changes should be made by patients before offering statins, as it can reduce CVD risk without the
need for medication), and if this doesn’t work then offer atorvastatin 20mg to people with a 10% or
greater 10 year risk of developing CVD (moderate and high risk), and also offer for over 85

20mg atorvastatin should also be considered for prevention of CVD in type 1 diabetics who are over
40 years old, have had diabetes for over 10 years, have nephropathy, and have other CVD risk
factors. It should also be considered in patients with CKD, and the dose should be increased if
greater than a 40% reduction in LDL cholesterol is not achieved, or eGFR is 30ml/min or less

Question 8

cautions with statins

Answer 8

Patients should only have statins at night, as that is when cholesterol is synthesised. LFTs should be
checked at baseline, 3 months, and 12 months, as statins are metabolised in the liver, and cause
increases in ALT and AST. Ezetimibe is a cholesterol absorption inhibitor which can treat primary
hypercholesterolaemia in patients where statins are contraindicated (e.g. pregnancy)

Question 9

what is secondary prevention

Answer 9

known disease but aim is to slow disease progression
Atorvastatin 80mg should be started
initially in patients with CVD, but a lower dose
should be used if there are potential drug
interactions, high risk of adverse effects, or
patient preference

Question 10

SE of aspirin

Answer 10

GI irritation, GI ulcers, GI haemorrhage, hypersensitivity reactions (including
bronchospasm), and tinnitus in regular, high-dose therapy

Question 11

MOA of aspirin

Answer 11

NSAID that irreversibly inhibits both COX-1 and COX-2 enzymes to stop them from
ultimately producing inflammatory mediators (i.e. prostaglandins, prostacyclins, thromboxanes). This
differs from other NSAIDs, which are reversible
inhibitors of COX-1 and COX-2

Question 12

contraindications for aspirin

Answer 12

children under 16 (as there’s a risk of Reye’s syndrome, which is
where use of aspirin to treat symptoms during a viral infection causes swelling of the brain and loss
of liver function), people with hypersensitivity to aspirin, and pregnant women in the 3rd trimester.
Caution should also be taken for patients with peptic ulcers (give gastroprotection with the aspirin),
and gout

Question 13

MOA of statins

Answer 13

competitive inhibitors of HMG-CoA reductase, which is an enzyme involved in cholesterol
synthesis. Decreased cholesterol synthesis leads to increased expression of LDL receptors on
hepatocytes, so more LDL uptake, and therefore less LDL in the blood. Statins also reduce
triglyceride levels, and slightly increase HDL levels

Question 14

se of statins

Answer 14

nosebleeds, arthralgia (joint pain), myalgia (muscle pain), hyperglycaemia,
increased risk of diabetes, liver damage and potential liver failure, headaches, GI disturbance,
myopathy (disease of the muscles that leads to muscle weakness), and rhabdomyolysis

Question 15

what combinations increase of rhabdomyolysis with use of statins

Answer 15

statin + ezetimibe

statins + macrolides

Question 16

what are fibrates

Answer 16

PPAR-alpha agonists (an intracellular receptor protein), and activating this receptor
causes lipid and carbohydrate metabolism, increases gene transcription of lipoprotein lipase (which
causes increases catabolism of LDL and increases HDL precursors to increase HDL), inhibits
cholesterol synthesis (to reduce total cholesterol), and increases bile acid excretion

Question 17

SE of fibrates

Answer 17

abdominal pain, abdominal distension, myopathy, increased risk of gallstones,
diarrhoea, nausea and vomiting, anorexia, cholelithiasis, interstitial lung disease, and rhabdomyolysis

Question 18

contraindications for fibrates

Answer 18

gallbladder disease (as increased cholesterol content of the bile increases
risk of gallstones further), pancreatitis, sensitivity to fibrates, nephrotic syndrome, hypoalbuminaemia,
and pregnancy

Question 19

MOA of ezetimibe

Answer 19

selectively inhibits
brush border enzymes in the small intestine, to inhibit the absorption of cholesterol. This decreases
hepatic cholesterol stores, and increases clearance of cholesterol from circulation

Question 20

SE and contraindications for ezetimibe

Answer 20

fatigue, GI disturbance, headaches, and myalgia. Contraindications include
patients with liver disease, patients with unexplained persistent elevation in hepatic transaminase
levels (type of liver enzyme), and pregnant women

Question 21

Outline a strategy to reduce cardiovascular disease in the local community (HS)

Answer 21

Useful strategies include community based activities (e.g. exercise groups, healthy cooking classes,
regular BP and cholesterol screenings), CVD education (including educating people at a younger age
to instil a healthy lifestyle), annual calculations of QRISK2 score, and prescribing 20mg atorvastatin to
patients with a QRISK2 score over 10%