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Yr3 Medicine- Cardiology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Remind yourself of the difference between primary and secondary hypertension

*For secondary, give some example causes

A
  • Primary: idiopathic
  • Secondary: due to underlying cause e.g.
    • Phaechromocytoma
    • Conn’s disease
    • Cushing’s disease
    • Polycystic kidney disease
    • Renovascular disease
    • CKD
    • Acromegaly
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2
Q

Remind yourself of the different stages of hypertension

A
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3
Q

At what blood pressure should ambulatory bp monitoring be offered?

A

>140/90mmHg

*Home BP monitoring is an alternative. HOWEVER, if pt has severe hypertension treatment should be considerd immediately without need for ABPM or HBPM

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4
Q

State some risk factors for developing hypertension

A
  • Smoking
  • Alcohol
  • Physical inactivity
  • Chronic stress
  • Age
  • Male
  • Diet high in salt, low in K+
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5
Q

What symptoms may someone with hypertension have?

A

People usually asymptomatic or may have:

  • Headaches
  • Sweating & palpitations & anxiety (if hypertension is due to phaechromocytoma)
  • Muscle weakness or tetany (may point to hyperaldosteronism)
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6
Q

What may you find on clinical examination of someone with hypertension?

A
  • High blood pressure
  • Retinopathy
  • Signs of underlying disease e.g. phaemchromocytoma, renal disease, Cushing’s disease
  • Renal bruits
  • Displaced apex beat (due to cardiomegaly)
  • Proteinuria (kidney damage)
  • Radio femoral delay (if coarctation of aorta)
  • Features of acromegaly
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7
Q

What investigations may you do if you suspect hypertension, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • Urine dip (test for blood & protein)
  • Urine sample (test for estimation of albumin:creatinine ratio)
  • Pregnancy test (can elevate BP)
  • BMs
  • Examine fundi for retinopathy *May do this in your examination
  • ECG

Bloods

  • FBC
  • U&E’s
  • Creatinine (kidney damage)
  • eGFR (kidney damage)
  • Serum total cholesterol
  • HDL cholesterol
  • HbA1c (diabetic control)
  • Cortisol (Cushing’s can cause hypertension)
  • Calcium (hyperparathyroidism can cause hypertension)

Imaging *NOT often done

  • Echo (consider echo to see for heart disease)
  • Doppler sonography (assess blood flow in arteries)
  • Renal ultrasound or angiogram

*And offer ABPM or HBPM to pts with bp >140/90

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8
Q

If you suspect a pt to have hypertension, and hence you send them home with ABPM or HBPM, what should you do whilst awaiting confirmation of hypertension?

A
  • Cardiovascular risk assessment
  • Evidence of target-organ involvement
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9
Q

State two tools we can use to assess cardiovascular risk

A
  • QRISK
  • JBS3 risk (Joint British Societies reccommendations on the prevention of cardiovascular disease)
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10
Q

State some factors which are assessed in the QRISK and JBS3 risk calculators/assessments

A

JBS3

  • Age
  • Smoking status
  • BP
  • Cholesterol (total & non-HDL)
  • BMI

QRISK

  • Age
  • Sex
  • Smoking status
  • Systolic BP
  • Cholesterol/HDL ratio
  • Ethnicity
  • Other conditions e.g. Diabetes, angina, stroke or TIA, AF, RA, MI or angina in 1st degree relative
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11
Q

Discuss what is involved in conservative management of hypertension

A
  • Low salt diet is recommended, aiming for less than 6g/day
  • Reduce caffeine
  • Stop smoking
  • Reduce alcohol
  • Weight loss if appropriate
  • Regular exercise
  • Eat more fruit & veg
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12
Q

Discuss the management of stage 1 hypertension

*NOTE: don’t need to include specific drugs in this answer, just discuss whether we treat them or not

A

Conservative management should be offered to all pts. Pharmacological therapy should be offered to those <80yrs with any of:

  • End /target organ damage
  • Established cardiovascular disease
  • Renal impairment
  • Diabetes
  • 10 year risk >10%
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13
Q

Discuss the management of stage 2 hypertension

*NOTE: don’t need to include specific drugs, just discuss whether or not we offer treatment

A

Conservative management AND drug therapy to everyone who has stage 2 hypertension (regardless of age, other conditions etc….)

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14
Q

Discuss the management of stage 3 hypertension

*NOTE: don’t need to include specific drugs just discuss whether or not we treat them

A

Drug therapy immediately and conservative management

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15
Q

State the target blood pressures for the following groups of people:

  • Patients at low-moderate risk
  • Diabetic, previous stroke/TIA, ischaemic heart disease, CKD
  • Over 80yrs
  • Under 80yrs
  • Under 80yrs with systolic bp >160
A
  • Low-moderate risk: <140/90
  • Diabetic, previous stroke/TIA, IHD, CKD: <130/80
  • Over 80yrs: <150/90
  • Under 80yrs: <140/90
  • Under 80yrs with systolic >160: 140-150

*For all pts, diastolic target is <90mmHg except in diabetes where target is <80/85mmHg

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16
Q

Discuss the conservative management of hypertension

A
  • Weight reduction if BMI >25kg/m2
  • Salt restriction (5-6g/day)
  • Minimise alcohol intake
  • Aerobic exercise
  • Smoking cessation
  • Decrease caffeine consumption
  • Increase fruit, vegetables and low fat dairy in diet
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17
Q

Each kg of weight loss yields roughly what reduction in bp?

A

2/3mmHg

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18
Q

Discuss the pharmacological treatment of hypertension ensuring you discuss the different first line treatments for different categories of people e.g. age, diabetes, ethnicity etc…

A

*NOTE: at step do ACEi or ARB and CCB. Then at step 3 add thiazide like diuretic

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19
Q

Discuss how you would treat secondary hypertension

A

Treat underlying cause if possible. If not may have to use bp lowering drugs

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20
Q

State some drugs that can cause secondary hypertension

A
  • Steroids
  • COCP
  • Monoamine oxidase inhibitors
  • NSAIDS
  • Cocaine
  • Nasal decongestants (e.g. ephedrine)
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21
Q

Describe what happens in diabetic nephropathy

A
  • Hypertension causes arteriole thickening through hyaline arteriosclerosis
  • Kidney ischaemia
  • Leading to tubular atrophy and glomerular changes
  • If advanced can lead to renal failure
22
Q

Briefly describe the grading of hypertensive retinopathy

A
  • Grade 1: tortous arteries with thickened, shiny walls (silver wiring)
  • Grade 2: thickened arteries compress the veins they cross
  • Grade 3: rupture of superficial arterioles or small veins (flame haemorrhages). Ischaemia in nerve fibre layer causes axonal damage leading to axoplasmic material deposition (cotton wool spots)
  • Grade 4 “papilloedema”: swollen optic disc with poorly defined margins, haemorrhages adjacent to disk
23
Q

State some complications of untreated hypertension

A
  • Coronary heart disease
  • Kidney disease
  • Visual problems
  • Increased risk of stroke, MI
24
Q

Discuss the difference between a hypertensive emergency and a hypertensive urgency

A
  • Hypertensive emergency: high blood pressure associated with a critical event/signs of end organ damage (e.g. high bp with encephalopathy, pulmonary oedema, AKI, myocardial ischaemia etc..)
  • Hypertensive urgency: high blood pressure without critical illness/ signs of end organ damage (…yet)
25
Q

The absolute value of blood pressure is not vastly important/agreed; however, in a hypertensive emergency & urgency what is the systolic BP usually above?

A

Usually above 180mmHg

26
Q

Patients with a hypertensive emergency won’t seek help because ‘they know they have high bp; they will often seek help as their hypertension is causing alternative pathology. State some pathologies/conditions someone with a hypertensive emergency may present with

A

Pts who have a hypertensive emergency (high bp with end organ damage) often have symptoms related to the end organ damage, such as:

  • Cardiac: ACS, aortic dissection, heart failure, microangiopathic haemolytic anaemia
  • Neurological: stroke, TIA, seizure, hepatic encephalopathy
  • Renal: AKI
  • Lung: pulmonary oedema
  • Visual: changes in sight
27
Q

What is hypertensive encephalopathy?

Dicuss pathophysiology

Discuss symptoms & signs

A

Brain dysfunction due to cerebral oedema which is caused by high blood pressure in hypertensive emergency. CNS usual autoregulation systems fail to work at very high blood pressures. Usually when bp increased, cerebral vessels vasoconstrict to prevent too much blood flow. When bp is outside range for autoregulation vasoconstriction doesn’t occur resulting in lots of blood to brain, increased hydrostatic pressures and cerebral oedema leading to neurological deficits.

28
Q

State some risk factors for hypertensive emergency and urgency

A
  • Usual risk factors for hypertension (smoking, alcohol, physcial inactivity etc..)
  • Untreated/poorly managed hypertension
  • CKD
  • Endocrine disorders e.g. Cushings
  • Renal transplant (when graft failure occurs)
  • Renal artery stenosis
  • Pregnancy & pre-eclampsia
29
Q

Discuss what you may find on examination of someone with hypertensive emergency

A

*Remember: hypertensive emergency is when there is end organ damage

  • Neurological: motor deficit, sensory deficit, dysarthria, cranial nerve damage, abnormal gait
  • Cardiac: palpitations, raised BP
  • Pulmonary: reduced breath sounds or wheeze due to pulmonary oedema
  • Fundoscopy: papilloedema, retinal haemorrhages
  • Abdominal: enlarged kidneys if PKD is cause, renal bruits
30
Q

What investigations would you want to do if you suspect hypertensive emergency or urgency, include:

  • Bedside
  • Bloods
  • Imaging

*HINT: most of your investigations revolve around assessing if there is end organ damage

A

Bedside

  • _​_ECG (check for cardiac damage)
  • Urine dipstick (check for blood, protein to indicate kidney damage)
  • Observations (including continual BP monitoring)

Bloods

  • FBC
  • Smear (check for microangiopathic haemolytic aneamia)
  • U&Es (check renal damage & see if Conn’s)
  • Creatinine & urea (renal damage)

Imaging

  • CXR (check for pulmonary oedema, cardiomegaly, aortic dissecition)
  • ***May consider others dependent on what you think cause or end organ damage could be e.g. thyroid function test, cardiac enzymes, BNP, renal ultrasound, TOE, urine or plasma metadrenaline, cortisol, head CT*
31
Q

What is the aim of treatment in:

a. ) Hypertensive emergency
b. ) Hypertensive urgency

A

a. ) Hypertensive emergency: reduce diastolic BP to 100-110mmHg in 3-12 hours
b. ) Hypertensive urgency: reduce diastolic BP to ~100-110mmHg in 24 hours
* *NOTE: it is important not to reduce BP by no more than 25% in first hour. Then if stable continue to aim for 100-110mmHg diastolic over the next 2-6 hours. exceptions to this include aortic dissection, phaechromocytoma & pre-eclampsia/eclampsia in which bp should be reduced to 140mmHg systolic (or 120mmHg systolic in AD) within an hour*

32
Q

Why must be avoid excessive falls in BP when treating hypertensive crises?

A

Excessive falls in pressure may precipitate renal, cerebral, or coronary ischaemia and so should be avoided.

33
Q

Discuss the management/treatmetn for a hypertensive emergency

A

Pts should be sent to ICU for continual bp and end organ damage monitoring. All medications should be given IV in a hyptensive emergency; the specific drugs depend on the end organ damage present, comorbidities and pts general condition. Drugs you can use (IV) are:

  • Sodium nitroprusside
  • Labetalol
  • GTN
  • Esmolol
34
Q

What is sodium niroprusside?

A

A nitric oxide releasing agent that relaxes arterial and venous smooth muscle (with no effect on duodenal or uterine smooth muscle). Causes vasodilation. Has greater effect in veins than arteries (but this difference is less than the difference observed with nitroglycerin)

35
Q

What is esmolol?

How fast does it work?

How long does it work for?

A
  • Cardioselective (B1) beta blocker
  • Acts within 60s (rapid onset)
  • Duration of action 10-20 mins (short duration of action)
36
Q

Discuss the monitoring that is required for someone who has had a hypertensive emergency

A
  • 1 week after discharge: follow up visit with bp check both arms
  • Monthly: pts should return for follow up visits once a month, or more frequenlty, until target bp (130/80) is achieved
  • Every 3-6 months: once target BP is achieved it should be monitored every 3-6 months. Serum K+ and creatinine should be measured every 6 months
37
Q

What is malignant hypertension?

Is it a hypertensive emergency or urgency?

A

he term ‘accelerated hypertension’ (also known as malignant hypertension) is a subcategory of hypertensive emergency where severe hypertension occurs with retinopathy of grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) or grade IV (papilloedema)

38
Q

How may someone with hypertensive urency present?

A

Pts with hypertensive urgency generally have no symptoms or signs as there is no end organ damage (yet). End organ damage likely if bp stays elevated for a few days

39
Q

What would you find on clinical examination of someone with hypertensive urgency?

A

Hypertenisve urgency has no end organ damage so often only think you will find is high BP (>180 systolic)

40
Q

Dicuss what investigations you may want for someone with hypertensive urgency, include:

  • Bedside
  • Bloods
  • Imaging
A

Any investigations you do are to rule out end organ damage and hence the investigations are the same as what you would do for hypertensive emergency:

Bedside

  • ​ECG (check for cardiac damage)
  • Urine dipstick (check for blood, protein to indicate kidney damage)
  • Observations (including continual BP monitoring)

Bloods

  • FBC
  • Blood smear (check for microangiopathic haemolytic aneamia)
  • U&Es (check renal damage & see if Conn’s)
  • Creatinine & urea (renal damage)

Imaging

  • CXR (check for pulmonary oedema, cardiomegaly, aortic dissecition)

***May consider others dependent on what you think cause or end organ damage could be e.g. thyroid function test, cardiac enzymes, BNP, renal ultrasound, TOE, urine or plasma metadrenaline, cortisol, head CT

41
Q

Discuss the management/treatment of someone with a hypertensive urgency

A

Manage by either adjusting pts maintenance therapy (if already on therapy for hypertension) and/or adding in new anti-hypertensives. Give drugs orally (whereas in hypertensive emergency you give IV).

A combination of ACEi and CCB is effective & well tolerated. You could give:

  • Amlodipine 5-10mg OD
  • Diltiazem 120-300mg OD
  • Lisinopril 5mg OD

Safest & most effective treatment for majority of pts, according to local guidelines, is :

  • Nifedipine 20mg MR BD plus amlodipine 10mg OD for three days
  • Then just continue amlodipine 10mg OD (after initial 3 days)
42
Q

What are the potential complications of hypertensive urgency?

A

End organ damage (e.g. renal, cardiac, neurological, vasculature, visual)

43
Q

What is the classic triad of symptoms in patients with phaeochromocytoma?

Do pts commonly have all 3?

What is a common sign of phaechromocytoma?

A

Classic triad:

  • Episodic headache
  • Sweating
  • Tachycardia

BUT most pts don’t have all three. Classic sign is sustained or paroxysmal hypertension

44
Q

How do we diagnose phaechromocytoma?

A
  • Measure 24hr urinary metanephrines
  • CT or MRI of abdomen & pelvis
  • MIBG scan (if CT & MRI can’t detect)
45
Q

Discuss the treatment of a phaeochromocytoma

A

All pts require surgery to remove tumour, whilst waiting for surgery control BP using alpha- and beta-adrenergic blockade. Important notes:

  • Start with alpha blocker: Phenoxybenzamine is most commonly used. Initial dose=10mg once or twice daily, can increase by 10-20mg every 2-3 days if needed- final dose ends up between 20-100mg typically
  • After adequete alpha-adrenergic blockade achieved then add beta-adrenergic blocker (typically occurs 2-3 days pre-operatively). NEVER start beta first
46
Q

How do you diagnose Cushing’s syndrome?

A

Multiple factors which contribute to diagnosis:

  • Appearance
  • BMs may show hyperglycaemia
  • 24hr urine cortisol will be elevated (3x normal)
  • Low dose dexamethasone supression test (supression >50% would suggest cushing’s disease)
  • Adrenal CT
47
Q

What is primary hyperaldosteronism?

A

Defect in adrenal cortex causing too much aldosterone to be produced. Aldosterone increases Na+ and hence water reabsorption leading to hypertension

48
Q

Who should you suspect primary hyperaldosteronism in (as a cause of their hypertension)?

A
  • Hypokalaemia and high/normal sodium (although up to 50% have normal potassium)
  • Resistant hypertension
  • Family history of premature hypertension
49
Q

Discuss how you diagnose primary hyperaldosteronism

A
  • Aldosterone:renin ratio will be high (should be measured in morning)
  • Adrenal CT
  • Investigated by specialist
50
Q

Discuss the management of orthostatic hypotension

A

Management of orthostatic hypotension (ESC 2018):

  • education and lifestyle measures such as adequate hydration and salt intake
  • discontinuation of vasoactive drugs e.g. nitrates, antihypertensives, neuroleptic agents or dopaminergic drugs
  • if symptoms persist, consider compression garments, fludrocortisone, midodrine, counter-pressure manoeuvres, and head-up tilt sleeping
51
Q

What criteria is used to diagnose orthostatic hypotension?

A
  • symptomatic fall in systolic BP > 20 mmHg
  • symptomatic fall in diastolic BP > 10 mmHg
  • or decrease in systolic BP < 90 mmHg

Yr3 Medicine- Cardiology (12 decks)

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