hypertension Flashcards

1
Q

definition of HTN

A

Defined as systolic BP >140mmHg and/or diastolic BP>85mmHg measured on three separate occasions.

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2
Q

definition of malignant HTN

A

BP >=200/130mmHg.

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3
Q

aetiology of HTN

A

primary - essential/idiopathic HTN - commonest >90% cases

secondary

  • renal - renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal failure, polyarteritis nodosa, systemic sclerosis, atheroma, fibromuscular dysplasia
  • endo - dm, hyperthyroidism, cushings syndrome, conn’s, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly
  • CVS - aortic coarctation, raised intravascular volume
  • drugs - Sympathomimetics, corticosteroids, oral contraceptive pill, MAOI, cocaine, amphetamines
  • preg - pre-eclampsia
  • liquorice
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4
Q

pathology of HTN

A

fibrotic intimal thickening of arteries, reduplication of elastic lamina and smooth muscle hypertrophy

arteriolar wall layers replaced by pink hyaline material with luminal narrowing

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5
Q

white coat and masked HTN

A

white coat hypertension - elevated clinic pressure, normal ABPM. dont treat, but increased risk of developing HTN in future and CVD

masked hypertension is the opposite

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6
Q

malignant or accelarated phase HTN

A

A rapid rise in BP leading to vascular damage (pathological hallmark is fibrinoid necrosis).

  • severe hypertension (eg systolic >200, diastolic>130mmHg) + bilateral retinal haemorrhages and exudates; papilloedema may or may not be present.
  • Symptoms are common, eg headache ± visual disturbance.
  • It requires urgent treatment, and may also precipitate acute kidney injury, heart failure, or encephalopathy, which are hypertensive emergencies.
  • Untreated, 90% die in 1yr; treated, 70% survive 5yrs.
  • It is more common in younger and in black subjects.
  • Look hard for any underlying cause.
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7
Q

epidemiology of HTN

A

Very common.

10–20% of adults in the Western world.

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8
Q

sx of HTN

A

asymptomatic

symptoms of complications

symptoms of cause

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9
Q

sx of accelarated HTN

A

scotomas - visual field loss

blurred vision

headache

seizures

nausea

vom

acute HF

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10
Q

signs of HTN

A

Measure on two to three different occasions before diagnosing hyper-tension and record lowest reading.

loud 2nd heart sound

4th heart sound

examine for causes:

  • radiofemoral delay, weak femoral pulse (aortic coarction)
  • renal artery bruit (renal artery stenosis)
  • palpable kidney
  • cushings

end organ damage - fundoscopy for retinopathy, LVH, proteinuria - indicates severity = worse prognosis

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11
Q

Keith–Wagner classification of retinopathy

A

(I) ‘silver wiring’;

(II) as above, plus arteriovenous nipping;

(III) as above, plus flame haemorrhages and cotton wool exudates;

(IV) as above, plus papilloedema.

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12
Q

Ix for HTN

A
  • blood - UE, glucose, lipids, ca
  • urine dipstick - blood and protein
  • ECG
  • echo - LVH, past MI
  • Ambulatory BP monitoring (BP measured throughout the day)
  • fasting glucose
  • cholesterol
  • Renal ultrasound/arteriography (renal artery stenosis);
  • 24h urinary meta-adrenaline
  • urinary free cortisol
  • renin
  • aldosterone
  • MR aorta - coarctation
    *
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13
Q

ECG for HTN

A

LVH: deep S wave in V1–2, tall R wave in V5–6,inverted T waves in I, aVL, V5–6, left-axis deviation)

ischaemia.

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14
Q

why do ambulatory BP monitoring

A

Excludes ‘white coat’ hypertension,

monitoring of treatment response,

assesses preservation of nocturnal dip.

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15
Q

Mx approach for HTN

A

assessment and modification of CVS risk factors

treat underlying causes

conservative

  • stop smoking
  • lose weight
  • reduce alcohol
  • reduce dietry Na
  • increase exercise

investigate for secondary causes - young patients, malignant hypertension or poor response to treatment

Reduce blood pressure slowly; rapid reduction can be fatal, especially in the context of an acute stroke.

medical

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16
Q

target BP

A

140/80 non-dm

130/80 dm without proteinuria

125/75 dm with proteinuria

150/90 if >80yrs

17
Q

Mx of acute malignant HTN

A

IV b-blocker, labetolol or hydralazine sodium nitroprus-side.

Avoid very rapid lowering which can cause cerebral infarction. bed rest.

Oral therapy unless encephalopathy or CCF

18
Q

approach to encaphalopathy in HTN

A

headache, focal CNS signs, seizures, coma

aim to reduce BP to 110 diastolic over 4hrs

admit

arterial line

Either IV labetalol (eg 50mg IV over 1min, repeated every 5min, max 200mg) or sodium nitroprusside infusion (0.5mcg/kg/min IVI titrated up to 8mcg/kg/min, eg 50mg in 1L glucose 5%; expect to give 100–200mL/h for a few hours only, to avoid cyanide risk).

19
Q

medical Mx of HTN

A
20
Q

complications of HTN

A

HF

CAD and MI

CVA

PVD

emboli

retinopathy

renal failure

hypertensive encephalopathy

posterior reversible encephalopathy syndrome

malignany hypertension

premature death

50% of all vascular deaths

21
Q

Px of HTN

A

good if BP controlled

Uncontrolled hypertension linked with increased mortality (6x stroke risk and 3x cardiac death risk).

Treatment reduces incidence of renal damage, stroke and heart failure.

22
Q

when to treat HTN

A
23
Q

persistent HTN

A

High blood pressure at repeated clinical encounters

24
Q

stage 1 HTN

A

clinic: 140/90 - 159/99

ABPM or HBPM 135/85 - 149/94

25
Q

stage 2 HTN

A

clinic - 160/100 - 180/120

ABPM or HBPM >150/95

26
Q

stage 3 HTN

A

clinic - >180/120