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RACP Written 2018 > Cardiology - Hypertension > Flashcards

Cardiology - Hypertension Flashcards

1
Q

Risk factors for hypertension?

A

Age (systolic increases)
- diastolic decreases over age 60rys

Obesity and weight gain

  • esp centrally located fat
  • for every 9.2kg reduction –> 6/3mmHg

High salt diet

Low potassium diet and calcium
- urine Na:K ratio is stronger correlate to BP than either serum Na or K

Alcohol >=3SD/day

Physical inactivity

Genetics

  • family study inheritability 15-30%
  • twin inheritability 60% male, 30% female
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2
Q

How is adrenergic activity mediated in the autonomic nervous system?

A

Mediated by G proteins stimulated by norad/adrealine and dopamine

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3
Q

What are the adrenergic receptors in the autonomic nervous system?

A

Alpha-1:

  • On post-synaptic cells in smooth muscle. Result in vasoconstriction.
  • On kidneys they increase renal sodium reabsorption

Alpha-2:

  • On post-synaptic cells
  • activation results in noradrenaline –> negative feedback

Beta-1:

  • On myocardium stimulates cardiac contraction and rate
  • in kidneys stimulates renin release

Beta-2:
- Activation by adrenaline stimulates relaxation of vascular smooth muscle and vasodilation

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4
Q

What do alpha-1 receptors do in the autonomic nervous system?

A

Alpha-1: activated by ad/norad/dopamine

  • On post-synaptic cells in smooth muscle. Result in vasoconstriction.
  • On kidneys they increase renal sodium reabsorption
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5
Q

What do alpha-2 receptors do in the autonomic nervous system?

A

Alpha-2: activated by ad/norad/dopamine

  • On post-synaptic cells
  • activation results in noradrenaline –> negative feedback
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6
Q

What do beta-1 receptors do in the autonomic nervous system?

A

Beta-1:

  • On myocardium stimulates cardiac contraction and rate
  • in kidneys stimulates renin release
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7
Q

What do beta-2 receptors do in the autonomic nervous system?

A

Beta-2:

- Activation by adrenaline stimulates relaxation of vascular smooth muscle and vasodilation

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8
Q

What is the baroreflex in autonomic nervous system?

A

Stretch-sensitive nerve endings in carotid sinus and aortic arch

Increased BP –> increased nerve firings –> decreased sympathetic activity

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9
Q

What stimulates renin synthesis in RAAS?

A

Renin is synthesised in renal afferent renal arteriole.

Stimulated by:

1) Decreased NaCl in distal thick ascending LOH at macula densa
2) Reduced pressure/stretch in renal afferent arteriole
3) sympathetic stimulation of renin-secreting cells via Beta-1 Adrenoceptors
4) Blockage of ACE or Angiotensin II Receptor

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10
Q

What inhibits renin secretion in RAAS?

A

1) Increased NaCl in macula densa
2) Increased pressure/stretch in renal afferent arteriole
3) Beta-1 blockade
4) Angiotensin II Type I Receptor on juxtaglomerular cells by angiotensin II

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11
Q

What does Angiotensin II Receptor Type 1 do?

A
  • Stimulates secretion of aldosterone by zona glomerulosa
  • Stimulates vascular smooth muscle cell and myocyte growth
  • Inhibits renin secretion
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12
Q

What does Angiotensin II Receptor Type 2 do?

A
  • Vasodilation
  • Sodium excretion
  • Inhibition of cell growth and matrix formulation
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13
Q

What does aldosterone do in RAAS?

A
  • stimulates amiloride sensitive epithelial sodium channels (ENaC) on apical side of principle cells in renal cortical collecting duct to increase Na reabsorption
  • binds to mineralocorticoid receptors
  • – cardiac fibrosis
  • – nephrosclerosis
  • – left ventricular hypertrophy
  • – vascular inflammation and remodelling
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14
Q

Complications of Hypertension in the Heart?

A
  • LVH and heart failure
  • coronary and microvascular disease
  • cardiac arrythmias
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15
Q

Complications of Hypertension in the brain?

A

Elevated BP is the STRONGEST risk factor for stroke (as per Harrisons)

Associated with late life cognitive decline

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16
Q

Complications of Hypertension in the kidney?

A

1) Hypertension is a RF for kidney injury and ESRF
- systolic BP more strongly associated
- black men more at risk

2) Atherosclerotic hypertension related vascular damage in pre-glomerular arterioles
- and damage to glomerular capillaries secondary to hyperfiltration
- and loss of autoregulation of renal blood flow and GFR

3) Macroalbuminuria (random urine Alb:Cr > 300) or microalbuminuria (random urine Alb:Cr 30 - 300)
4) Proteinuria: micro 50-500mg/day, macro >500mg/day

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17
Q

Complications of Hypertension in the peripheral arteries?

A

Peripheral artery disease

  • ABI <0.90 = PAD associated with 50% stenosis
  • ABI <0.80 = assoc with hypertension
18
Q

Secondary Causes of Hypertension:

Renovascular hypertension - how to diagnose/screen

A

Scren renal blood flow with DTPA scan before and after captopril

Doppler ultrasound
Confirm with angiography

19
Q

Secondary Causes of Hypertension:

Primary aldosteronism - how to diagnose/screen

A

Ensure potassium replete!!!
Screen with plasma aldosterone: renin ratio
(ratio >30:1 has 90% sens+spec)

Needs to be done OFF:

  • aldosterone antagonists (increase renin and may increase aldosterone)
  • ACEi and ARBs (increase renin)

Confirm on FAILURE to suppress aldosterone <150 after 2L isotonic saline over 4 hours

20
Q

Secondary Causes of Hypertension:

Cushings - how to screen

A

24hour urine free cortisol
overnight dexamethasone suppression test
late night salivary cortisol

21
Q

Secondary Causes of Hypertension:

Pheochromocytoma - how to screen

A

24hr urinary metanephrines or plasma fractionated free metanephrines

22
Q

Secondary Causes of Hypertension?

A

Renovascular hypertension

Primary aldosteronism
Cushings Syndrome
Pheochromocytoma

Obstructive Sleep apnoea
Coarctation of aorta

Renin secreting tumours
Polycystic kindey disease

Hyperthyroidism
Hypothyroidism causes DIASTOLIC HTN
Hypercalcaemia

Monogenic forms

23
Q

What is glucocorticoid remediable hyperaldosteronism?

A

Causes secondary hypertension
Autosomal dominant
11beta hydroxylase/aldosterone gene on Ch8

24
Q

What is 17alpha hydroxylase deficiency?

A

Causes secondary hypertension
Autosomal recessive
Mutation on CYP17 on Ch10

In males: pseudohermaphroditism
In females: primary amenorrhoea and absent sex characteristics

25
Q

What is 11beta hydroxylase deficiency?

A

Causes secondary hypertension

26
Q

Which hypertensive syndrome is associated with pregnancy?

A

Autosomal dominant missense mutation with substitution of leucine for serine at codon 10

27
Q

At which alcohol consumption levels do you increase risk for hypertension?

A

> =2 SD/day in males

>=1 SD/day in females

28
Q

When do you treat hypertension?

A

If patients with <10% 5-yr CVD risk: if BP>=160/100

If patients with 10-15% 5yr CVD risk: if SBP>=140 or DSP>=90
Then aim for BP <140/90

If patients >15% 5yr CVD risk: aim for SBP <=120

29
Q

Effect on kidney function from the SPRINT Study?

A

SPRINT compared intensive (SBP <120) vs standard (SBP <140) in HIGH RISK >50yr old patients with BPs 130-180mmHg and risk >15% of 5yr CVD.

Increased AKI

30
Q

Effect on hypotension from the SPRINT Study?

A

SPRINT compared intensive (SBP <120) vs standard (SBP <140) in HIGH RISK >50yr old patients with BPs 130-180mmHg and risk >15% of 5yr CVD.

Increased ED presentations for hypotension
DID NOT change postural hypotension

31
Q

Effect on falls/syncope from the SPRINT Study?

A

SPRINT compared intensive (SBP <120) vs standard (SBP <140) in HIGH RISK >50yr old patients with BPs 130-180mmHg and risk >15% of 5yr CVD.

Increased ED presentations for syncope
DID NOT increase injurious falls

32
Q

Treatment approach to hypertension?

A

Start either thiazide, beta blocker, ACEi/ARB, CCB

If target not reached at 3 months, start 2nd agent

If target not reached at 6 months, add 3rd agent

33
Q

Comparing antihypertensives…which is better to prevent stroke or all-cause mortality from CCB or BB?

A

CCB is better than beta blocker

34
Q

Comparing antihypertensives…which is better to prevent heart failure from diuretic vs BB?

A

Diuretics

35
Q

Comparing hypertensives….which is better to prevent MI from ACEi or BB?

A

ACEi is better to prevent MI

36
Q

What are the NICE guidelines for treatment of hypertension?

A

STAGE 1:
BP>140/90 and subsequent ABPM average >=135/85
–> if <55yrs give ACEi
–> if African American or >55yrs give CCB

STAGE 2:
BP>160/100 and ABPM average >150/95
–>give both ACEi and CCB

STAGE 3:
SBP>180 or DBP>110
–> give ACEi, CCB and Thiazide

Then add spironolactone

37
Q

What is the pathology of malignant hypertension?

A

Associated with diffuse necrotising vasculitis, arteriolar thrombi and fibrin deposition in arteriolar walls

38
Q

What are the clinical features of malignant hypertension?

A

Progressive retinopathy:

  • arteriolar spasm
  • haemorrhages
  • exudates
  • papilloedema

Deteriorating renal function with proteinuria

Microangiopathic haemolytic anaemia

Encephalopathy

39
Q

Treatment of malignant hypertension WITH encephalopathy?

A

Aim to reduce BP by <25% within minutes-2 hours
OR aim for BP 160/100

Treatment options:

  • IV nitroprusside
  • labetolol
  • nicardipine
40
Q

Treatment of malignant hypertension WITHOUT encephalopathy

A
  • frequent captopril, clonidine or labetolol
  • reduce BP over hours or longer
  • aim for <5-15% reduction of BP in every 24 hour period

RACP Written 2018 (167 decks)

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