Hypertension Flashcards

1
Q

What is hypertension?

A

-NICE define hypertension as follows:
=a clinic reading persistently above >= 140/90 mmHg, or:
=a 24 hour blood pressure average reading >= 135/85 mmHg

Normal: 90/60 to 140/90

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2
Q

Primary vs secondary hypertension

A

Primary/ essential: 90-95%, series of complex physiological changes which occur as we get older.

Secondary causes
-Renal
=Glomerulonephritis
=Chronic pyelonephritis
=Adult polycystic kidney disease
=Renal artery stenosis
-Endocrine
=Primary hyperaldosteronism
=Phaeochromocytoma
=Cushing’s syndrome
=Liddle’s syndrome
=Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
=Acromegaly
-Other
=Glucocorticoids
=NSAIDs
=Pregnancy
=Coarctation of the aorta
=Combined oral contraceptive pill

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3
Q

Symptoms and signs of hypertension

A

-Hypertension does not typically cause symptoms unless it is very high, for example > 200/120 mmHg. If very raised patients may experience:
=headaches
=visual disturbance
=seizures

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4
Q

Assessing for end organ damage

A

-Fundoscopy: to check for hypertensive retinopathy
-Urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
-ECG: to check for left ventricular hypertrophy or ischaemic heart disease

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5
Q

Investigations in hypertension

A

-24 hour blood pressure is now recommend for the diagnosis of hypertension. If 24 hour blood pressure monitoring is not available then home readings using an automated sphygmomanometer are useful.

-Following diagnosis patients typically have the following tests:
=urea and electrolytes: check for renal disease, either as a cause or consequence of hypertension
=HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease
=lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease
=ECG
=urine dipstick

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6
Q

Clinic BP under 140/90

A

Check BP at least every 5 years and more often if close to 140/90

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7
Q

ABPM/HBPM under 135/85

A

Check BP at least every 5 years and more often if clinic BP close to 140/90
=If evidence of target organ damage, consider alternative causes

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8
Q

Clinic BP 140/90 to 179/119

A

-Offer ABPM (or HBPM if ABPM is
declined or not tolerated)
-Measure BP both arms, higher reading if difference >20, HS to rule out supravalvular AS
If the difference in readings between arms is more than 15 mmHg, repeat the measurements.
If the difference in readings between arms remains more than 15 mmHg on the second measurement, measure subsequent blood pressures in the arm with the higher reading.
-Investigate for target organ damage
-Assess cardiovascular risk

> 150/95= stage 2, treat all patients regardless of age

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9
Q

ABPM/HBPM 135/85 to 149/94

A

STAGE 1
-Age >80 with clinic BP >150/90= offer lifestyle advice and consider drug treatment
-Age <80 with target organ damage, CVD,
renal disease, diabetes or 10-year CVD
risk ≥10%: Offer lifestyle advice and discuss
starting drug treatment
-Age <60 with 10-year CVD risk <10%: Offer lifestyle advice and consider drug
treatment
-Age <40: Consider specialist evaluation of
secondary causes and assessment long term benefits and risks of treatment

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10
Q

Clinic BP 180/120 or more

A

-Assess for target organ damage as soon as
possible:
-If target organ damage, consider starting
drug treatment immediately without
ABPM/HBPM
-If no target organ damage, confirm
diagnosis by:
= repeating clinic blood pressure
measurement within 7 days, or
= considering monitoring using ABPM/
HBPM and ensuring a clinical review
within 7 days

-Admit for specialist assessment if:
=signs of retinal haemorrhage or papilloedema (accelerated hypertension) or
=life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury
-NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)
-If none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG)
=if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM.
=if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days

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11
Q

Assessing for target organ damage

A

-Test for haematuria.
=Urine albumin:creatinine ratio (to test for the presence of protein in the urine).
==HbA1C (to test for diabetes).
=Electrolytes, creatinine, and estimated glomerular filtration rate (to test for chronic kidney disease).
-Examine the fundi (for the presence of hypertensive retinopathy).
-Arrange for a 12-lead electrocardiograph to be performed (to assess cardiac function and detect left ventricular hypertrophy).
-Consider the need for specialist investigations in people with signs and symptoms suggesting target organ damage or a secondary cause of hypertension.
-CVD risk (QRISK), HDL

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12
Q

Indications for referral to same-day specialist review

A

-retinal haemorrhage or papilledema
(accelerated hypertension) or
-life-threatening symptoms or
-suspected pheochromocytoma

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13
Q

ABPM/HBPM 150/95 or more

A

Offer lifestyle advice and drug treatment
Age <40:
* Consider specialist evaluation of
secondary causes and assessment long-term benefits and risks of treatment

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14
Q

What are the stage criteria of hypertension?

A

-Stage 1 hypertension: Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

-Stage 2 hypertension: Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

-Severe hypertension: Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

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15
Q

Describe ACEi

A

-Inhibit the conversion angiotensin I to angiotensin II -SE: Cough, Angioedema, Hyperkalaemia
-First-line treatment in younger patients (< 55 years old)
-Less effective in Afro-Caribbean patients
-Must be avoided in pregnant women
-Renal function must be check 2-3 weeks after starting due to the risk of worsening renal function in patients with renovascular disease
-Drug names end in ‘-pril’

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16
Q

Describe calcium channel blockers (CCB)

A

-Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction -SE: Flushing, Ankle swelling, Headache
-First-line treatment in older patients (>= 55 years old)

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17
Q

Describe thiazide type diuretics

A

-Inhibit sodium absorption at the beginning of the distal convoluted tubule
-SE: Hyponatraemia, Hypokalaemia, Dehydration
-Although technically a diuretic, thiazides have a very weak diuretic action

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18
Q

Describe angiotensin 2 receptor blockers (ARB)

A

-Block effects of angiotensin II at the AT1 receptor -SE: Hyperkalaemia
-Angiotensin II receptor blockers are generally used in situations where patients have not tolerated an ACE inhibitor, usually due to the development of a cough
-Drug names end in ‘-sartan’

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19
Q

Step 1 Antihypertensives

A

-ACEi or ARB: with T2DM, age <55 and not of black African or African-Caribbean family origin
-CCB: without T2DM, age 55+, black African/ African-Caribbean family origin

20
Q

Step 2 Antihypertensives

A

2 of

-ACEi/ARB
-CCB
-Thiazide-like diuretic

21
Q

Step 3 Antihypertensives

A

ACEi/ARB + CCB + thiazide-like diuretic

22
Q

Step 4 Antihypertensives

A

-Confirm resistant hypertension: confirm elevated BP with ABPM or HBPM, check for postural hypotension and discuss adherence
-Consider seeking expert advice or adding a:
=low-dose spironolactone if blood potassium level is ≤4.5 mmol/l
=alpha-blocker or beta-blocker if blood potassium level is >4.5 mmol/l
-Seek expert advice if BP is uncontrolled on optimal tolerated doses of 4 drugs

23
Q

Lifestyle advice

A

a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
caffeine intake should be reduced
the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight

24
Q

When to measure standing and sitting BP

A

-T2DM
-Symptoms of postural hypotension
-Aged 80 and over

25
Q

BP targets

A

-Age <80 years:
=Clinic BP <140/90 mmHg
=ABPM/HBPM <135/85 mmHg

-Age ≥80 years:
=Clinic BP <150/90 mmHg
=ABPM/HBPM <145/85 mmHg

-Postural hypotension:
=Base target on standing BP

-Frailty or multimorbidity:
=Use clinical judgement

26
Q

Secondary hypertension causes

A

-Conn syndrome/ Primary hyperaldosteronism (5-10%, most common secondary cause)
-Cushing’s disease
-Renovascular disease
-Chronic kidney disease
-Phaeochromocytoma
-Obstructive sleep apnoea
-Cortication of aorta

27
Q

Causes of Conn syndrome/ Primary hyperaldosteronism

A

-Bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases
-Adrenal adenoma: 20-30% of cases
-Unilateral hyperplasia
-Familial hyperaldosteronism
-Adrenal carcinoma

28
Q

Features of Conn syndrome

A

-Hypertension
-Hypokalaemia e.g. muscle weakness
-Metabolic alkalosis (elevated bicarbonate level)
-Plasma sodium level greater than 140 mmol/L
-Larger than expected decrease in serum potassium when using a low-dose thiazide-type diuretic

=Muscle weakness, tetany, Nocturia, polyuria

29
Q

Investigations of Conns syndrome

A

-Screening: hypertension with hypokalemia/ treatment-resistant hypertension
-Plasma aldosterone/renin ratio= high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
-HRCT/MRI abdomen and adrenal vein sampling: differentiate between unilateral and bilateral sources of aldosterone excess
=if the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia

30
Q

Management of Conn syndrome

A

-Adrenal adenoma: surgery (laparoscopic adrenalectomy)
-Bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
-CCB can mask features

31
Q

Features of Cushing’s disease

A

-Truncal obesity
-Striae
-Menstrual irregularities
-Easily bruised
-Weakness
-Psychiatric symptoms
-Acne
-Hypokalaemia metabolic alkalosis
-Impaired glucose tolerance/ DM

32
Q

Investigations of Cushing’s Disease

A

-Urine pregnancy test
-Serum glucose elevated
-Late-night salivary cortisol
-Overnight/high-dose dexamethasone suppression test (suppressed cortisol, suppressed ACTH= pituitary tumour secreting ACTH therefore adrenal hyperplasia)
-24-hour urinary free cortisol
-CRH stimulation: if pituitary source then cortisol rises

pituitary tumour secreting ACTH producing adrenal hyperplasia

33
Q

Management of Cushing’s Disease

A

-Trans sphenoidal pituitary adenectomy
-Somatostatin analogue
-Dopamine agonist
-Steroidogenesis inhibitor
-Glucocorticoid receptor antagonist
-Post-surgical corticosteroid replacement therapy
-Pituitary radiotherapy or bilateral adrenalectomy

34
Q

Features of renal artery stenosis

A

-Renal artery stenosis secondary to atherosclerosis accounts for around 90% of renal vascular disease, with fibromuscular dysplasia being the most common cause of the remaining 10%.
-Peripheral vascular disease and an abdominal bruit, or if blood pressure is resistant to treatment.
-Recurrent flash pulmonary oedema

-hypertension
chronic kidney disease
‘flash pulmonary oedema’

35
Q

Investigations for renal artery stenosis

A

-Increased plasma renin level
-Serum creatinine
-Serum potassium
-Urinalysis and sediment evaluation
-Aldosterone-to-renin ratio
-Ultrasound
-CT angiography

36
Q

Management of renal artery stenosis

A

-Normal hypertension management
-Statin, antiplatelets
-Renal artery stenting/ surgical reconstruction

37
Q

Features of pheochromocytoma

A

Phaeochromocytoma is a rare catecholamine secreting tumour. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

bilateral in 10%
malignant in 10%
extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

-Headaches
-Palpitations
-Sweating
-Anxiety
-Intermittently high or labile blood pressure, or postural hypotension
-Unexplained fever and abdominal pains

38
Q

Investigation of phaeochromocytoma

A

24 hr urinary collection of catecholamines/ metanephrines

39
Q

Management of Phaeochromocytoma

A

-Alpha-blocker (e.g., phenoxybenzamine), given before
-beta-blocker (e.g., propranolol)
-Surgery.

40
Q

Presentation of obstructive sleep apnoea

A

Predisposing factors
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome

The partner often complains of excessive snoring and may report periods of apnoea.

Consequence
daytime somnolence
compensated respiratory acidosis
hypertension

Assessment of sleepiness
Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)

41
Q

Investigation of Obstructive sleep apnoea

A

-Sleep studies (polysomnography) - ranging from monitoring of pulse oximetry at night to full polysomnography where a wide variety of physiological factors are measured including EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry

42
Q

Management of obstructive sleep apnoea

A

-Weight loss
-Continuous positive airway pressure (CPAP)
-Intra-oral devices (e.g., mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness
-DVLA should be informed if OSAHS is causing excessive daytime sleepiness

43
Q

Features of cortication of aorta

A

-Heart failure in infancy
-Upper limb hypertension in adults
-Radio-femoral delay
-Mid systolic murmur (maximal over back)
-Apical click from the aortic valve
-Palpable collateral blood vessels in the back muscles
-Notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

-Associations
Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
Coarctation of the aorta describes a congenital narrowing of the descending aorta. It is more common in males, despite an association with Turner’s syndrome.

44
Q

Investigations of cortication of aorta

A

-ECG (LVH/ normal in adults, RVH infants)
-CXR (adults= posterior rib notching from collateral vessel enlargement, infants= cardiomegaly and increased pulmonary vascularity)
-ECHO (discrete narrowing in the thoracic aorta; pressure gradient across narrowing)

45
Q

Management of cortication of aorta

A

-Critical= Prostaglandin E to maintain ductal patency and surgical repair
-Non-critical= percutaneous angioplasty with or without stent implantation/ surgery