GP - Primary Prevention of CVD Flashcards

1
Q

How can you calculate the no. of units in a drink?

A

strength (ABV) x volume (ml) / 1000 = units

e.g. pint (568 ml) of strong larger (ABV 5.2%) = 2.95 units

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2
Q

What age group can have their CVD risk checked/assessed on the NHS? (i.e. blood tests etc)

A

40-74 yrs

(above 74-yrs, age alone is a strong risk factor)

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3
Q

What lifestyle changes can be suggested to patients with Hypertension?

A

Those in bold ↓ risks associated with HTN

  1. Smoking cessation
  2. Diet:
    1. ↓ salt / switch to low-salt
    2. ↓ caffeine
    3. ↓ Fat
  3. ↓ Alcohol intake
  4. ↓ weight
  5. Exercise
  6. Find relaxing hobbies
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4
Q

When taking a Hx to identify CVD risks, what topics are important to discuss?

A
  1. Physical activity
  2. Alcohol
  3. Smoking
  4. Diet - high salt or sat-fats?
  5. Weight
  6. Diagnoses: HTN, DM
  7. FHx of CVD e.g. stroke, IHD, heart failure, HTN etc.
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5
Q

What are the physical activity recommendations for ‘early years’

(birth - 5 yrs)?

A

180 mins / day of physical activity

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6
Q

What are the physical activity recommendations for children and young people aged 5-18 yrs?

A

Average 60 mins / day across the week

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7
Q

What are the physical activity recommendations for adults?

A

at least 150 mins / week (moderate intensity)

OR

at least 75 mins / week (vigorous activity)

Also:

  • Minimise sedentary time (break up periods of inactivity)
  • Strength exercises on at least 2 days / week - helps joints (e.g. yoga, gym, carrying weight)
  • Balance and co-ordination activities in adults > 65-yrs - lowers risk of falls (e.g. dance, tai chi etc)
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8
Q

How many milliliters are in a pint?

A

568 ml

(this is often rounded down to 500 ml when calculating units)

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9
Q

What are the current guidelines on weekly alcohol consumption?

A

< 14 units per week (for both men and women)

  • Units should be spread out across the week
  • Avoid binge-drinking
  • Involve some alcohol-free days
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10
Q

What risk factors can you name for CVD?

A

Non-modifiable risk factors:

  1. Age (older ↑risk)
  2. Male
  3. FHx of CVD e.g. stroke, IHD, heart failure, HTN etc.
  4. Ethnicity - 1.5 x risk of CVD in south asian pts

Modifiable risk factors:

  1. Physical activity
  2. Alcohol
  3. Smoking
  4. Diet - rich in salt, sat-fat, sugars / lacking fruit & veg
  5. Weight
  6. Hypertension
  7. Diabetes
  8. Hypercholestserolaemia
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11
Q

Name some conditions that being Obese is associated with an increased risk of.

A
  • CVD
  • Stroke
  • HTN
  • Diabetes
  • Osteoarthritis
  • Cancer
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12
Q

Is a single measurement of ↑ BP sufficient

to diagnose Hypertension?

A

NO!!

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13
Q

What is the process for determing a patient’s BP in clinc?

A
  1. Measure BP in both arms
  2. If difference in BP is > 20 mmHg –> repeat measurements
  3. If difference remains > 20 mmHg on the 2nd measurement –> measure subsequent BPs in the arm with the higher BP
  4. If BP is measured as 140/90 or higher –> take 2nd measurement during consultation
  5. If 2nd measurement is substantially different from the 1st –> take a 3rd BP measurement
  6. Record the lower of the last 2 measurements (2nd or 3rd) as the BP
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14
Q

How do you confirm a diagnosis of HTN

after a recorded clinic BP of 140/90 or higher?

A
  1. If clinic BP is 140/90 or higher –> offer ABPM (ambulatory blood pressure monitoring) to confirm diagnosis, ensure that:
    • At least 2 measurements per hour - during ususal waking hours
    • Use average of at least 14 measurements to confirm diagnosis
  2. If pt unabale to tolerate ABPM –> HBPM (home blood pressure monitoring), ensure that:
    • For each BP recording, 2 consecutive measurements are taken, at least 1 minute apart and with the person seated
    • BP is recorded twice/day (ideally in the morning and evening)
    • BP recording continues for at least 4 days (ideally for 7 days)
    • Discard measurements taken on the 1st day + use the average value of all the remaining measurements to confirm a diagnosis of HTN
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15
Q

What are the grades for severity of Hypertension?

A
  • Isolated Systolic HTN = >140 / >90
  • Grade 1 (mild) = clinic BP 140-159 / 90-99
    • OR ABPM / HBPM average of > 135/85
  • Grade 2 (moderate) = clinic BP 160-179 / 100-109
    • OR ABPM / HBPM average of > 150/95
  • Grade 3 (severe) = >180 / >110
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16
Q

For what 2 reasons is staging the severity of HTN important?

A

Severity of HTN i.e. grade, impacts:

  1. Risk stratification of patient
  2. Guides next step in management
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17
Q

When a patient’s hypertension is stage 3 (severe) it can result in hypertensive emergency - what is this also known as?

A

Also known as Malignant Hypertension it is severe hypertension (BP ≥ 180/120 mmHg) WITH damage to at least 1 organ

Examples of Organ damage:

  • Brain - cerebral infarction, hypertensive encephalopathy and oedema, spontaneous intracranial haemorrhage
  • Eyes - retinal bleeding, exudate, cotton-wool spots, splinter haemorrhages and papilloedema
  • Heart - pulmonary oedema, CHF
  • Aorta - dissection
  • Kidneys - blood/protein in urine, AKI
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18
Q

Who is malignant hypertension most likely to affect?

A

Epidemiology:

M > F

Affects 1% of those with HTN

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19
Q

What can cause malignant hypertension?

A

Essential HTN:

  • Undiagnosed or inadequately treated essential HTN
  • Pts who have stopped their anti-HTN medication

Secondary HTN:

  • Renal disease - renal artery stenosis, acute glomerulonephritis, kidney transplant
  • Neuro - head trauma, autonomic dysfunction
  • Respiratory - obstructive sleep apnoea
  • Immune - scleroderma, vasculitis
  • Pregnancy - pre-eclampsia / eclampsia
  • Endocrine:
    • primary aldosteronism
    • phaeochromocytoma
    • thyroid disorder
    • Cushing’s syndrome
    • acromegaly
    • hyperparathyroidism
    • carcinoid tumour
    • congenital adrenal hyperplasia
    • renin-secreting tumour
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20
Q

How high in BP in malignant hypertension?

A

VERY HIGH BP!

systolic > 180 or diastolic > 120

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21
Q

Severe hypertension (BP ≥ 180/110 mmHg) WITHOUT target-organ damage is defined as what?

A

Hypertensive urgency (not emergency)

  • BP needs to be ↓ gradually over 24-48 hrs with ORAL antihypertensives
    • as opposed to reduced in mins - 2hrs and IV in hypertensive emergency
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22
Q

What are the signs / symptoms of malignant hypertension?

A

Symptoms / Signs of Malignant HTN:

  • ↑ BP - systolic > 180 and/or diastolic > 120 mmHg
  • Eye signs (seen on opthalmoscopy):
    • Papilloedema (must be present for diagnosis to be made)
    • Retinal haemorrhages
    • Exudates
    • Cotton wool spots
  • Cardiac symptoms:
    • Chest pain - crushing/pressure
    • SoB
    • Pulmonary oedema
  • Neuro symptoms:
    • Abnormal sensory findings
    • Motor weakness
    • Abnormal gait
    • Blurred vision
    • Dizziness
    • ↓ GCS
    • ↑ ICP e.g. headache, nausea & vomiting, seizure
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23
Q

How is malignant hypertension managed?

A

Management:

  • BP - within few mins - 2 hrs with IV anti-hypertensives
  • 1st line = Labetalol (alpha and beta adrenergic antagonist) –> ↓ peripheral vascular resistance via vasodilation (in short term use) + ↓ HR (in long term use)
  • 2nd line = Nicardipine (Ca2+ antagonist) - more selective for cerebral and coronary vessels than other Ca2+ antagonists –> causes vasodilation, ↓ BP
  • 3rd line = Fenoldopam (selective D1 receptor agonist /w arterial vasodilator effects) –> ↓ BP + increases renal perfusion
24
Q

If a pt is considered to be at risk of CVD - what dietary advise can be given i.e. cardioprotective diet?

A

Cardioprotective diet:

  • Total fat intake < 30% of total energy intake
  • Saturated fat intake < 7% of total energy intake
  • Dietary cholesterol < 300 mg/day
  • Increase mono-unsaturated fat intake via olive oil, rapeseed oil or spread based on these (use for food prep)
  • Wholegrain varieties of starchy foods (bread, rice, pasta)
  • ↓ sugar
  • 5 portions of fruit / veg per day
  • at least 2 portions of fish per week (especially oily fish)
  • 4-5 portions of unsalted nuts, seeds and legumes
25
Q

Which 4 organs in the body are common sites of damage/modification

as a result of Hypertension?

A
  1. Eyes
    • Retinopathy/maculopathy
  2. Brain
    • Strokes
    • Microaneurysms
  3. Heart
    • Compensative/adaptive cardiomegaly
    • Ischaemic heart disease
    • CCF (followed by pulmonary HTN)
    • Aortic aneurysms
    • Peripheral vascular disease (not actually related to the heart)
    • PE
    • Sudden death
  4. Kidneys
    • Hypertensive nephropathy (HTN causing kidney pathology)
    • Nephron arteriosclerosis –> ischaemia –> kidney atrophy (small kidneys)
    • Glomerular ischaemia due to renal artery stenosis caused by plaques or stiffening
    • Glomerular HTN can result in glomerular damage –> causing blood and protein leakage into urine
26
Q

What 4 signs on the retina can be produced by

hypertension (seen on Opthalmoscopy)?

A
  1. Papilloedema - optic disc swelling due to ↑ ICP ( which can be caused by malignant hypertension)
    • Venous engorgement (often 1st sign)
    • Blurring of optic disc margin
    • Paton’s lines - concentric/radial lines cascading from optic disc
  2. Flame Haemorrhage - intraretinal haemorrhage (looks like bruise)
    • Feather/flame shape indicates bleed occurs at level of nerve fibre layers
  3. Hard exudates - small white/yellowish lipid deposits with sharp margins, which form due to capillary leakage (i.e. ↑ retinal vascular permeability)
    • Often appear waxy / shiny / glistening
  4. Cotton wool spots - white spots which represent swelling of retinal nerve fibres due to microinfarctions
    • Usually near optic disc
27
Q

What are the 2 causes of Primary Hyperaldosteronism?

What metabolic disturbance does it cause?

A

Two causes of Primary Hyperaldosteronism:

  1. Conn’s Syndrome = Unilateral Aldosterone producing adenoma (~30% of cases) –> adrenalectomy
  2. Bilateral adrenal hyperplasia (~70% of cases) –> spironolactone

Metabolic disturbance due to Hyperaldosteronism:

  1. ↓ K+ and ↓ H+ –> Hypokalaemic Alkalosis
  2. ↑ Na+ and ↑ BP
28
Q

What is Addison’s Disease?

A

Addison’s Disease = autoimmune destruction of adrenal glands causing –> hypoadrenalism (↓ cortisol + ↓ aldosterone)

Causes of Primary Hypoadrenalism:

  • 80% of primary hypoadrenalism = Addison’s Disease
  • TB, metastases, meningococcal septicaemia, HIV, antiphospholipid syndrome

Treatment:

  • Ongoing: hydrocortisone (glucocorticoid) + fludrocortisone (mineralocorticoid)
    • Mineralocorticoid dose is impacted by mineralocorticoid activity of glucocorticoid given
  • Adrenal Crisis: 50-100mg IV every 6 hours for 1-3 days

Features:

  • Lethargy + weakness
  • Anorexia
  • Weight loss
  • Hyperpigmentation (especially palmar creases)
  • ↓ BP
  • ‘Salt-craving’ due to hyponatraemia
  • Nausea / vomiting
  • Hyperkalaemia + acidosis
  • Hypoglycaemia
  • Vitiligo
29
Q

How do you test for Addison’s Disease?

A

Short SynACTHen Test

  1. Administer tetracosactide (synacthen) 250 micrograms IV/IM
  2. Check blood cortisol at time 0 and +30 mins
  3. Cortisol at +30min should be > 600 nmol/L = in normal person
  4. If cortisol < 600 nmol/L –> Addison’s Disease
30
Q

What % of cases are

essential / primary hypertension vs secondary hypertension?

A
  • Essential/primary hypertension = 90-95%
    • Cause unknown
  • Secondary hypertension = 5-10%
    • This is hypertension due to an underlying pathology
31
Q

What are some common causes of Secondary Hypertension?

A

Causes + some signs:

  • Renal diseases: - ↑ creatinine + abnormal urinalysis
    • Polycystic kidney disease (PKD)
    • Chronic glomerulonephritis
    • Pyelonephritis
    • Renovascular disease e.g. renal artery stenosis
      • Presence of atherosclerotic disease elsewhere
      • Asymmetry in renal size of > 1.5cm (without other cause)
      • Renal artery bruit
  • Endocrine diseases:
    • Cushing’s Syndrome - moon face, striae, central obesity, proximal muscle weakness, facial plethora, thin skin, bruising, ↓ libido
    • Primary hyperaldosteronism: (most common cause of secondary hypertension)
      • Conn’s syndrome
      • Bilateral idipathic adrenal hyperplasia
    • Pheochromocytoma
  • Neurological disease:
    • Brainstem lesion
    • Space occupying lesion –> ↑ ICP –> ↑ resistance to cranial bloodflow –> heart ↑ BP to compensate
  • Drugs:
    • Steroids
    • MAO inhibitors (antidepressants)
    • COCP
    • NSAIDs
  • Pregnancy:
    • Pre-eclampsia
  • Aorta coarctation
    • Diminished femoral or left brachial pulse with high BP in right arm (subject to location of coarctation)
  • Obesity
  • Sleep apnoea - ↓ oxygen supply to body –> heart tries to compensate by ↑ BP (noctural ↑BP)
    • Obese men, loud snoring, daytime somnolence, fatigue, morning confusion
  • Licorice (excessive consumption)
32
Q

What is a Pheochromocytoma?

A

A neuroendocrine tumour of the chromaffin cells of the adrenal medulla

  • ↑ BP (HTN) + Hyperglycaemia are common
    • 10% present without hypertension
  • 90% unilateral vs 10% bilateral
  • FHx of such tumours is suggestive of –> Multiple endocrine neoplasia syndromes (MENs)
33
Q

What are the features of Primary Hyperaldosteronism?

A

Features:

  • Hypertension (↑ BP)
  • Alkalosis
  • Hypokalaemia:
    • Muscle weakness & ↓ tone
    • Palpitations
    • Hypokalaemia induced nephrogenic DI –> polyuria + polydipsia
34
Q

How does Hypokalaemia present on an ECG?

A

ECG:

  • Prolonged PR interval
  • ST depression
  • T-wave flattening or inversion
  • Apparent Long QT
    • it only appears to show long QT, but due to fusion of the T+U waves it is actually the QU segement not QT being viewed
  • U-waves (best seen in precordial leads i.e. V1-V6)
35
Q

What does this ECG show?

A

Hypokalaemia

  • ST depression
  • T wave inversion
  • Prominent U waves
  • Long QU interval
36
Q

What causes Primary Hypoadrenalism?

A

Causes of Primary Hypoadrenalism:

  1. 80% of primary hypoadrenalism = Addison’s Disease
  2. 20% is due to congenital adrenal hyperplasia, TB, metastases, meningococcal septicaemia, CMV infection (HIV pts), antiphospholipid syndrome
37
Q

What are the features of Addison’s disease?

A

Features of Addison’s disease:

  • Female
  • Tiredness / weakness
  • ↓ BP
  • Anorexia
  • Weight loss
  • Hyperpigmentation (especially palmar creases)
  • Nausea / vomiting
  • ‘Salt-craving’ (rare but occurs if hyponatremia features)
  • Loss of axillary + pubic hair (women)
  • Hypoglycaemia
  • Hyponatremia & Hyperkalaemia (may be seen)
  • Other signs of autoimmunity e.g. vitiligo, Hashimoto’s thyroiditis, pernicious anaemia
  • Adrenal Crisis:
    • Collapse
    • Shock
    • Fever
38
Q

How is Addison’s Disease managed?

A

Lifetime: ​

  1. Hydrocortisone (glucocorticoid) usually 15-30 mg daily in divided doses - depends on body weight & metabolism
  2. Fludrocortisone (mineralocorticoid) usually 50-300 mg daily - depends on metabolism & exercise
    • Mineralocorticoid dose is impacted by mineralocorticoid activity of glucocorticoid given

Adrenal Crisis:

  • Hydrocortisone 50-100mg IV every 6 hours for 1-3 days
39
Q

When should antihypertensive treatment be offered for the following situations:

  1. Patient < 80yrs old with stage 1 HTN (BP 140-159/90-99) or ABPM/HBPM ≥ 135/85 mmHg
  2. Patient with stage 2 HTN (BP 160-179/100-109) or ABPM/HBPM ≥ 150/95 mmHg
A
  1. Offer antihypertensive in pts < 80yrs + stage 1 HTN who have 1 or more of the following:
    • Target organ damage
    • Established CVD
    • Renal disease
    • Diabetes
    • 10-year cardiovascular risk > 10%
  2. Offer antihypertensive in everyone with stage 2 HTN
40
Q

Describe the NICE pathway for choosing what type of antihypertensive medication to prescribe:

  1. What is the cut-off age that influences drug choice?
  2. If a pt has T2DM + HTN what is the 1st line antihypertensive?
  3. What ethnicity influences drug choice?
  4. What type of diuretic is involved in the pathway?
  5. What drug can be used instead of an ACE-I e.g. if patient is intolerant?
A
  1. 55yrs is the cut-off for guiding drug choice
  2. ACE-inhibitor or ARB
  3. Afro-carribbean origin influence drug choice
  4. Thiazide
  5. Angiotension II receptor blocker (ARB)
43
Q

Common Antihypertensive drugs include; ACE-I, Ca2+ channel blockers, Thiazide diuretics and ARBs

  • What are the common side effects of each drug?
  • What are some important notes, if any for each drug?
A

ACE-inhibitors (end in -pril): e.g. lisinopril, perindopril, captopril, enalapril etc.

  • Cough
  • Angioedema - swelling of lower layer of skin; face, tongue, larynx, abdomen, arms, legs
  • Hyperkalaemia
  • Agranulocytosis (rare)
  • Notes:
    • Avoid in pregnancy
    • Monitoring - renal function check at initiation + 2-3 weeks later + dose changes due to risk of ↓ renal function in renal artery stenosis
    • ↑ in creatinine + K+ may be expected but shouldn’t be > 30% of baseline (creatinine) or > 5.5 mmol/L K+

Ca2+ channel blockers: - side effects for dihydropyridines (end in -pine)

  1. Ankle oedema
  2. Headache
  3. Flushing

Thiazide-diuretics: e.g. Indapamide, chlorthialidone, chlorothiazide, metolazone

  • Dehydration
  • Hyponatraemia (↓ Na+)
  • Hypokalaemia (↓ K+​)
  • Hypercalcaemia (↑ Ca2+​)
  • Postural hypotension
  • ↑ Urea reabsorption –> ↑ Uric acid –> can worsen gout
  • Impotence
  • Rare: Agranulocytosis, thrombocytopenia, photosensitve rash, pancreatitis
  • Notes:
    • Thiazides actually have very weak diuretic action

ARBs (end in -sartan) e.g. candesartan, losartan

  • Hypotension (↓ BP)
  • Hyperkalaemia
  • Note: avoid in pregnancy
44
Q

With treatment what should a patient’s target BP be for:

  1. Age < 80 yrs
  2. Age > 80 yrs
A

< 80yrs:

  • < 140/90 via clinic BP
  • < 135/85 mmHg via ABPM or HBPM

> 80yrs:

  • < 150/90 via clinic BP
  • < 145/85 mmHg via ABPM or HBPM
45
Q

When is Methyl-dopa used to treat HTN?

A

In Pregnant Women

  • Methyl-dopa = compeititve inhibitor of DOPA decarboxylase (which converts L-DOPA –> dopamine)
  • Dopamine is a precursor for noradrenaline + adrenaline
  • Methyl-dopa ↓ dopaminergic + adrenergic neurotransmission –> vasodilation + ↓ BP
46
Q

The plan after a diagnosis of HTN is to

1) Assess CV risk 2) Assess target organ damage.

To do this all pts with HTN should be offered which tests?

A
  1. Urine tests: - check for renal disease
    • Urine sample for albumin:creatinine ratio (tests for proteinuria)
    • Urine dipstick for haematuria
  2. Blood tests:
    • Serum glucose + HbA1c
    • U+Es - looking for electrolyte disturbance
    • Creatinine
    • eGFR
    • Serum cholesterol, HDL and LDL
  3. Fundoscopy:
    • Hypertensive retinopathy
  4. 12-lead ECG
    • Check for left ventricular hypertrophy or ischaemic heart disease
48
Q

What is the ‘normal’ range for Blood Pressure?

A

Between 90/60 - 140/90 mmHg

  • Some sources describe being between 120/80 and 140/90 as ‘pre-hypertensive’
  • BP varies depending on; Age, gender and physiology
49
Q

In which 2 populations of people is HTN more common?

A

Black Afro-carribean

and

Elderly (BP rises with age, up to the 7th decade)

50
Q

What should you do if patient has grade/stage 1 hypertension and is < 40yrs?

A

Refer to specialist

If no evidence of target organ damage, CVD, renal disease or diabetes

51
Q

What are common side effects of ACE-inhibitors?

A

ACE-inhibitors (end in -pril): e.g. lisinopril, perindopril, captopril, enalapril etc.

  • Cough
  • Angioedema - swelling of lower layer of skin; face, tongue, larynx, abdomen, arms, legs
  • Hyperkalaemia
  • Agranulocytosis (rare)
  • Notes:
    • Avoid in pregnancy
    • Renal function check at initiation + dose changes + 2-3 weeks after initiation due to risk of ↓ renal function in renal artery stenosis
    • ↑ creatinine + ↑ K+ may be expected but shouldn’t be > 30% of baseline (creatinine) or > 5.5 mmol/L K+
52
Q

What are common side effects of dihydropyridine Calcium channel blockers?

A

Ca2+ channel blockers: - side effects for dihydropyridines (end in -pine)

  1. Ankle oedema
  2. Headache
  3. Flushing
53
Q

Describe the NICE pathway and the steps for which anti-hypertensive medication to prescribe and what to escalate to.

A
54
Q

What does the QRISK 3 score calculate?

A

Patient’s absolute risk of suffering a; cardiac event or stroke

over the next 10-years

Takes into account:

  • Age
  • Sex
  • Ethnicity
  • BP
  • BMI
  • Cholesterol results
  • Smoking + Diabetes
  • FHx
  • Other existing conditions e.g. RA, migraines, SLE, AF, CKD etc.
55
Q

How do Statins work?

A

Inhibit HMG-CoA reductase

thus ↓ coversion of saturated fat –> cholesterol

56
Q

What are some important contraindications for statins?

A
  1. Macrolide Abx (e.g. erythromycin, clarithromycin)
    • Stop statins until Abx course is completed
  2. Pregnancy
57
Q

What are the side-effects of statins?

A
  • Muscle aches / cramps (common) - consult GP
  • Liver impairment
    • Monitoring - LFTs at baseline, 3-months and 12-months
    • Discontinue statin if serum transaminase (ALT & AST) concentrations ↑ + persist at 3 x upper limit of reference range
  • Muscle pain, tenderness or weakness –> STOP statin now!
    • Can be due to rhabdomyolysis (muscle breakdown)
    • Blood test for ↑↑↑ creatinine kinase

Advise:

  • Avoid Grapefruit juice
  • If starting new medication or OTC - ensure your statin is known about
58
Q

Under what circumstances should a Statin be prescribed?

A
  1. All pts with established CVD e.g. stroke, TIA, ischaemic heart disease, peripheral arterial disease
  2. QRISK 3 > 10 % (i.e. 10-year CVD risk > 10%) AND lifestyle modification is ineffective
  3. T1DM pts if:
    • diagnosed > 10-years ago
    • > 40-yrs old
    • have established nephropathy
    • have other CVD risk factors
59
Q

In which Statins is myopathy (aches, cramps and pain) more common?

A

Myopathy is more common in:

  • Simvastatin
  • Atorvastatin

Myopathy is less common in:

  • Rosuvastatin
  • Pravastatin
  • Fluvastatin
60
Q

Which Statin and dose are 1st line for:

  • Primary prevention of CVD
  • Secondary prevention of CVD
A

Primary prevention:

  • Atorvastatin 20 mg BD

Secondary prevention:

  • Atorvastatin 80 mg OD