Hypertension and Hyperlipidaemia

Question 1

Stage 1 HTN

Answer 1

Clinic BP >140/90 + ambulatory average >135/85

Question 2

Stage 2 HTN

Answer 2

Clinic BP >160/100 + ambulatory average >150/95

Question 3

Stage 3 HTN (severe HTN)

Answer 3

> 180/100

Question 4

Primary HTN RF

Answer 4

Modifiable (obesity, excess salt, inactivity, excess alcohol, stress, smoking, diabetes)
Non modifiable (age, fHx, ethnicity, males <65, females >65)

Question 5

Secondary HTN causes

Answer 5

Pregnancy
Intrinsic renal disease
Renovascular disease
Endocrine (thyroid dysfunction, phaechromocytoma, conn’s disease, acromegaly, cushings)
Pharmacology (excess alcohol, cocaine use, COC, antidepressants, herbal remadies)
Obstructive sleep apnoea
Aortic coarctation

Question 6

HTN can cause

Answer 6

stroke, IHD, AAA, PAD, HF, vascular dementia, CKD

Question 7

HTN symptoms

Answer 7

Asymptomatic, but primary may cause headache and secondary may show end organ damage

Question 8

Malignant/accererated HTN

Answer 8

> 180/120 developing over short period of time + signs of end organ damage (e.g. cerebral haemorrhage, acute Renal failure, aortic dissection, HF)
Must have papilloedema
Can present as headache and confusion (hypertensive encephalopathy)
Urgent treatment with slow BP reduction (to avoid stroke)

Question 9

End organ damage

Answer 9

• CV events (LVH, diastolic dysfunction and CHF)
• Renal failure/renal disease (glomerular ischaemic changes) and also glomerular hyperperfusion injury. Kidneys atrophy
• Retinal events

Question 10

HTN retinopathy stage 1

Answer 10

Tortuous arteries with shiny walls (copper/silver wiring)

Question 11

HTN retinopathy stage 2

Answer 11

A-V nipping/narrowing as arterioles cross veins

Question 12

HTN retinopathy stage 3

Answer 12

Flame hamorrhages, cotton wool spots

Haemorrhages due to constant high pressure
Cotton wool spots due to inadequate perfusion

Question 13

HTN retinopathy stage 4

Answer 13

Papilloedema (swelling of optic disc)

Question 14

HTN investigations

Answer 14

Confirm BP (ambulatory and clinic)
Assess for secondary cause (cortisol, calcium and renin/aldosterone ratio)
Assess for end organ damage (blood/protein in urine, renal function, renal USS, ECG, fundoscopy)

Question 15

Treatment

Answer 15

Non pharma (lifestyle mods)
But pharma if too high on repeated measurements.
CCB for black/over 55/T2D
ACEi/ARB for everyone else
If no response then switch to ther droup
If no response then combine ACEi+ CCB + thiazide
If not enough then add further diuretic (potassium sparing if potassium is normal) or alpha blocker or beta blocker

Question 16

qrisk2

Answer 16

Looks at age, sex, ethnicity, post code, smoking, Cholesterol: HDL ration, BMI, systolic BP, diabetes, previous CVD, FHx CVD and Hx of HTN

Question 17

Primary Hyperlipidaemia

Answer 17

Familial/genetic

Question 18

Secondary hypercholesterolaemia

Answer 18

Obesity/diet
Hypothyoidism
Anorexia nervosa
Obstructive jaundice
Nephrotic syndrome
Ciclosporin (for autoimmune)

Question 19

Secondary Hypertriglycerideaemia

Answer 19

Obesity/diet
Diabetes
Pregnancy
Renal failure
Alcohol abuse
Hepatitis
Oral contraceptives
Beta blocker
isotretanoin
Protease inhibitor

Question 20

Secondary mixed hyperlipidaemia

Answer 20

Obesity/diet
Thiazides
Steroids

Question 21

Primary hyperlidaemia

Answer 21

Classed according to Frederikson system

Question 22

Most common primary hyperlipidaemia

Answer 22

Combined hyperlipidaemia and isolated raised TGs

Question 23

Familial hypercholesterolaemia indicators

Answer 23

Tendon xanthalasma

Totalcholesterol >7.5mmol/L and FHx of premature CHD.

Question 24

Management of dyslipidaemia

Answer 24

20mg atorvastatin for primary CVD prevention in 10%+ QRISK2.
80mg for Hx of CVD
Aim for 40% non-HDL reduction.
If not achieved, consider adherence/timing, lifestyle and increasing dose.