Hypertension Flashcards

1
Q

Describe the epidemiology of hypertension

A

Hypertension affects approximately 1 billion people worldwide and is the leading global cause of death

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2
Q

Describe the distribution of BP and hypertension

A

BP distribution is unimodal and any distinction between normal and abnormal is arbitrary.
this leads to the definition of hypertension:
o The level of BP above which investigation and treatment will do more good than harm.
The BP accepted as normal has decreased over time.

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3
Q

Why is the cut-off arbitrary

A

The numbers are fluid- they change all the time.
The criteria are arbitrary as blood pressure varies with age and levels are variable within the population.
Current British guidelines define hypertension as a sustained resting blood pressure above 140mmHg and/or 90mmHg.

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4
Q

What does the risk of CVD increase with

A

Increasing BP, even within the normal range.

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5
Q

Describe ambulatory blood pressure

A

blood pressure automatically recorded at regular interval and averaged to show true mean - 5-10mmHg lower than recorded in surgeries
Push towards this- cheap and reliable- patients take responsibility for their own health.

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6
Q

What is current practice encouraging BP targets of

A

Current practice is tending to lower target systolic BP to 120 mmHg but NOT always well tolerated- people who lower their BP dramatically may feel ill- treat patients not numbers.

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7
Q

Describe the relationship between BP and age

A

Mean BP rises with age
Pulse pressure rises with age (as DBP does not rise much)
The majority of people >60y would be expected to be hypertensive by current definitions, almost everyone hypertensive by >80y
In almost all societies (low salt communities are an exception) mean BP rises with age, pulse pressure also rises after mid-life. This means that the number of people diagnosed as hypertensive increases with age, recent data from the Framingham longitudinal study indicates that if you live long enough you will almost certainly become hypertensive by current definitions.

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8
Q

Is there are reliable threshold for BP and stroke mortality risk

A

ThThis slide plots a population distribution of systolic BP and the relationship between systolic BP and risk of stroke. The relationship between BP and risk is exponential (log linear) and there is no threshold for risk. Every 20mmHg increase in BP results in a doubling in risk of stroke (or CHD – not shown). Similar relationships have been shown for BP and coronary heart disease and other cardiovascular disease.
ere is no reliable threshold for BP risk

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9
Q

What is the consequence of a lack of a threshold

A
  • As there is no threshold, a large burden of disease is on people with a ‘normal’ BP.
    o 50% of attributable burden falls on people with a BP < 141mmHg.
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10
Q

Describe primary hypertension

A

Unidentifiable cause – primary or essential
(85-95% of cases)
they are idiopathic

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11
Q

Describe secondary hypertension

A

secondary 5-15%% e.g.
Renal disease, including renal artery stenosis- decreases renal perfusion- stimulating the RAAS
Tumours secreting aldosterone (Conn’s syndrome) - salt and water retention, increasing blood volume, preload and therefore CO- increasing BP
Tumours secreting catecholamines (phaeochromocytoma)
Oral contraceptive pill
Pre-eclampsia/pregnancy associated hypertension
Rare genetic causes (e.g. Liddle’s syndrome
Coarctaction of the aorta- resistance to flow through the aorta- thus increasing TPR and BP
Hypertension from a disease of which hypertension is a symptom.

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12
Q

Describe the genetic aetiology of hypertension

A
  • Monogenic (single genes causing hypertension) – VERY RARE.
    o Liddle’s Syndrome.
    o Apparent mineralocorticoid excess.
  • Complex polygenic (multiple genes causing hypertension) – COMMON.
    Estimates suggest that the heritability of high blood pressure is around 30-50%.
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13
Q

Describe the environmental aetiology of hypertension

A
Dietary salt (sodium)
Obesity / overweight, lack of exercise
Alcohol
Pre-natal environment (~birthweight)
Pregnancy (pre-eclampsia)
Other dietary factors and environmental exposures?
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14
Q

Describe the genetics behind hypertension

A

Most genes involved in the regulation of Na+ in the Kidney.
Twin and other studies suggest 30-50% of variation in blood pressure is attributable to genetic variation but to date identified SNPs only account for <4% of this variance1.
Monogenic disease causes <1% of hypertension
Liddle’s syndrome
Mutation in amiloride-sensitive tubular epithelial Na channel
Apparent mineralocorticoid excess
Mutation in 11b-hydroxysteroid dehydrogenase

Complex polygenic causes
Multiple genes with small effects (positive and negative)
Interactions with sex, other genes, environment

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15
Q

Describe the importance of dietary salt on BP

A
  • Dietary salt – PRINCIPAL CAUSE in terms of environmental factor
    o With low sodium intake throughout life, there is no rise in BP with age.
    Increased salt excretion= increased DBP- linear relationship.
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16
Q

What is hypertension associated with

A
Increased TPR (major cause)
Decreased arterial compliance
Normal cardiac output
Normal blood volume / ECV
Central shift in volume
Secondary to reduced venous compliance
17
Q

Describe the importance of TPR

A

The relationship between BP, cardiac output and peripheral resistance is key to understanding the haemodynamics of high BP. Numerous studies have shown that in established primary (essential) hypertension the increased blood pressure is due to elevated peripheral resistance.

18
Q

What factors increase the TPR

A

Structural narrowing of the arteries- remodelling- walls get thicker- lumen gets smaller- may be adaptive (not necessarily caused by hypertension)

Active narrowing of the arteries- vasoconstriction- probably short term.

Capillary loss- Rarefaction (reduction in density) (Adaptive? Damage?

19
Q

What is meant by isolates systolic hypertension

A

Systolic BP ≥ 140 mmHg, diastolic BP ≤ 90 mmHg
Condition of people over age 60

There are no specific treatments for ISH as against “standard” hypertension

20
Q

What are the causes of isolates systolic hypertension

A

Due to increasing stiffness of medium/large arteries
Pulse wave reflected and is greater by the time it reaches brachial artery
Does NOT mean that TPR increases
Stiffer arteries reflect the pulse wave and effectively amplify it when they are supposed to cushion it.

21
Q

Describe the role of the kidney in the development of primary hypertension

A

play a key role in salt regulation and so BP regulation (PRINCIPAL CAUSE)

22
Q

Describe the role of the endocrine system in the development of primary hypertension

A

Endocrine/paracrine factors

Inconsistent evidence

23
Q

Describe the role of the SNS in the development of primary hypertension

A

Sympathetic nervous system

Evidence linking high sympathetic activity to the development of hypertension

24
Q

Describe the mechanisms by which the Kidney plays a role in hypertension

A

The kidney exerts a major influence on BP through regulation of sodium/water/extracellular fluid volume1
Impaired renal function or blood flow is the commonest 2º cause of hypertension (e.g. renal parenchymal disease, renal artery stenosis)
Almost all monogenic causes of hypertension affect renal Na+ excretion
Salt intake is strongly linked with blood pressures of human populations. Populations with low salt have low population blood pressures and no rise in BP with age.
Animals with reduced renal Na+ handling (genetic or experimental) develop hypertension. Excess salt intake in many animals results in elevated blood pressure

25
Q

Can hypertension be transplanted

A

In rats hypertension can be ‘transplanted’ with the kidney, there is similar, though incomplete data, in man

26
Q

Describe the damage caused by hypertension

A

coronary heart disease
stroke
peripheral vascular disease/atheromatous- increasing risk of stroke or MI disease
heart failure
atrial fibrillation (arrhythmia)
dementia /cognitive impairment
retinopathy- accessible to the circulation

27
Q

Describe the effects of hypertension on the heart

A

Hypertension is commonly associated with an increase in left ventricular wall mass (LVMI) and changes in chamber size
Increased afterload caused by the raised blood pressure caused LVH- can progress to heart failure.

28
Q

Describe the link between hypertension and congestive heart failure

A

The prevalence of heart failure (CHF) is in
creasing (in contrast to other CVD)
Hypertension increases the risk of CHF 2 -3 fold and probably accounts for about 25% of all cases of CHF
Hypertension precedes CHF in 90% of cases and most CHF in the elderly is attributable to hypertension

29
Q

What may happen with CVD trends in the future

A

When the impact of hypertension adds to the epidemics of obesity and diabetes apparent in younger individuals it seems likely that recent favourable trend in CVD will reverse and that the increase in heart failure will accelerate in future decades.
More deaths from CVD

30
Q

Describe the effects of hypertension on the large arteries

A

Muscular hypertrophy of the media- reduplication of the external lamina and intimal thickening.
Typically hypertension is associated with thickened walls (hypertrophy) of large arteries and acceleration of atherosclerosis.
Not the same as thickening of the arteries.
Hypertension may causes arterial rupture or dilations (aneurysms)- weakening of the walls. This can lead to thrombosis or haemorrhage (e.g. strokes

31
Q

Which two types of aneurysms are associated with hypertension

A
Aortic aneurysm
Charcot Bouchard (cerebrovascular) aneurysm- microvascular
32
Q

Describe the effects of hypertension on the eye

A

The retina illustrates microvascular damage in hypertension. There is thickening of the wall of small arteries, arteriolar narrowing, vasospasm, impaired perfusion and increased leakage into the surrounding tissue (exudates)

33
Q

Describe the effects of hypertension on the microcirculation

A

The retina illustrates microvascular damage in hypertension. There is thickening of the wall of small arteries, arteriolar narrowing vasospasm, impaired perfusion and increased leakage into the surrounding tissue
Hypertension is associated with:
reduction in capillary density (impaired perfusion? increased PVR?)
elevated capillary pressure  damage and leakage

34
Q

Describe the effects of primary hypertension on the kidney

A

Granular capsular surface
Cortical thinning, renal atrophy
Renal dysfunction is common in hypertension
(e.g. increased (micro)albumin excretion in urine)

35
Q

Describe the effects of malignant hypertension on the kidney

A

Extreme (accelerated / malignant hypertension) is now rare but leads to rapidly progressive renal failure

Subcapsular haemorrhages

Hypertension also adversely affects the kidney. The slide shows examples of marked renal damage due to very high (accelerated or malignant) hypertension. This degree of damage is relatively rare nowadays thanks to better treatment and control of hypertension. However more subtle damage to renal function is common in hypertension and is manifest as loss of albumin in the urine (micro- or macroalbuminuria- due to reduced GFR).

36
Q

What is meant by malignant or accelerated hypertension

A

In this condition, blood pressure rises rapidly to very high levels with the DBP exceeding 130-140mmHg. It is more common in secondary hypertension, especially phaeochromocytoma, and it causes rapid development of end organ damage

37
Q

Describe the link between blood pressure and microalbuminuria

A

Hypertension causes increased albumin loss in the urine
Hypertension causes reduced glomerular filtration rate.
GFR declines with age even without high BP, which speeds up deterioration
marker of glomerular damage

38
Q

Describe the lifestyle modifications to reduce BP

A

Weight loss
Eat healthy
Exercise
less alcohol

39
Q

Describe the use of ACE inhibitors as treatment

A

Ang 2- main contributor to increased BP