Hypertension Flashcards
hypertension epidemiology
Leading global cause of death
Affects 1bn people worldwide
Define hypertension
level of blood pressure above which investigation and treatment do more good than harm
What is teh distribution of BP and hypertension?
BP distribution is unimodal (one maximum) and any distinction between normal and abnormal is arbitary and has changed overtime.
What is ambulatory BP?
Blood pressure automatically recorded at regular interval and averaged to show true mean - 5-10mmHg lower than recorded in surgeries
Blood Pressure and age
- Mean BP rises with age
- Pulse pressure rises with age
- Majority of people above 60 will be expected to be hypertensive.
Therefore the number of people diagnosed as hypertensive increases with age, if you live long enough you will almost certainly become hypertensive.
What is primary/ essential hypertension?
Primary hypertension has an unidentifiable cause
85-95% of cases
What is secondary hypertension?
Hypertension with an identifiable cause. Causes include:
- Renal disease
- Tumors secreting alderostone (to do with sodium reabsorption)
- Tumors secreting catecholamines
- Oral contraceptive pills
- Pre-eclampsia/ pregnancy associated hypertension
- Rare genetic causes
(Aetiology) causes of primary hypertension?
Genetic: monogenic (rare), complex polygenic (common)
Environment: dietary salt, obesity, lack of exercise, alcohol, pre-natal environment, pregnancy (pre-eclampsia), other dietary factors
Genetics and blood pressure
30-50% of variation in blood pressure is attributable to genetic variation but to date identified SNPs only account for <4% of this variance.
Monogenic disease causes <1% of hypertension: Liddle’s syndrome (mutation in gene coding for Na channel) and Apparent mineralcorticoid excess too.
Complex polygenic cases are much more significant; multiple genes with small effects (positive and negative) and interaction with sex, other genes and environment
Blood pressure and age in a low salt environment
Dietary salt intake is a major factor in the rise in BP with age
How do you calculate blood pressure (MAP)?
MAP= CO x TPR
In primary hypertension, its mainly due to elevated peripheral resistance.
Which factors are associated with established hypertension (in terms of CVS)?
- Increased TPR
- Decreased arterial compliance
- Normal CO
- Normal blood volume
- Central shift in volume
- Secondary to reduced venous compliance
What causes elevated TPR in hypertension?
There is active narrowing of the arteries (vasoconstriction)- this is short term
There is structural narrowing of the arteries (growth and remodelling)
Capillary loss (rarefraction)
Isolated systolic hypertension
Systolic BP > 140mmHg and diastolic BP < 90mmHg
Systolic high, diastolic normal
This is a condition of people over the age of 60. It is due to the icnreasing stiffness of medium/ large arteries (no real main cause for this)
Pulse wave reflected and is greater by the time it reaches brachial artery.
This does not mean that the TPR increases.
There is no real treatment for ISH vs normal hypertensive treatments
Pathological mechanisms behind the causes of primary hypertension
All of the following mechanisms increase TPR.
Kidney: key role in BP regulation - salt intake strongly linked to BP, with low salt leading to no increase with age and low BP (monogenic causes usually related to genes affecting renal Na+ excretion)
Endocrine/ paracrine factors: inconsistence evidence
Sympathetic nervous system: high sympathetic activity to development of hypertension
more on the kidney as a cause of hypertension
- Impaired renal function/ perfusion is 2nd commonest cuase of hypertension
- Almost all monogenic causes of hypertension affect renal Na secretion
- And remember people who have a lower salt intake will have no rise with BP with age
Hypertension increases the risk of:
- Coronary heart disease
- Stroke
- Peripheral vascular disease
- Heart failure
- Atrail fibrilation
- Dementia/ cognitive impariment
- Retinopathy
What does hypertension do to the left ventricle?
Increase in LV wall mass and changes in the chamber size
Hypertension and congestive heart failure (CHF)
Prevalence of CHF is increasing (as opposed to other CVD)
Hypertension increases the risk of CHF 2-3 fold and accounts for 25% of all cases of CHF
Hypertension precedes CHF in 90% of cases and most CHF in the elderly is attributable to hypertension
Hypertension and large arteries
High BP also results in changes in large arteries (like common carotid arteries). Typically, hypertension is associated with thickened walls (hypertrophy) of large arteries and acceleration of athersclerosis
This is a compensation mechanism to withstand the increased stress on the walls.
Consequences of the large arteries?
Hypertension can cause arterial rupture or dilations (aneurysms).
This can lead to thrombosis or haemorrhage (stroke)
Hypertension and the eyes
Hypertension adversely affects the microcirculation in the eyes. There will be microvascular damage. The thickening of the walls of small arteriesm, arteriolar narrowing, vasopasm, impaired perfusion and increased leakage into the surrounding tissue (exudates)
Hypertension in microcirculation
Hypertension is associated with reduction in capillary density.
Elevated capillary pressure= damage and leakage
Hypertension and the kidney
Renal damage/ dysfunction is common in hypertension
Increased microalbumin excretion in urine due to a reduced glomerular filtration rate (also decreases with age, BP speeds up rate)
Primary hypertension: Granular capsular surface, cortical thining, renal atrophy
Accelerated hypertension: subcapsular haemorrhages
Extreme (accelerated) hypertension is now rare but leads to rapidly progessive kindey failure.
BP and microalbuminuria
Hypertension causes increased loss of albumin in the urine, it causes reduced glomerular filtration rate.
GFR declines with age even without high BP which speeds up the deteriation.
Lifestyle modification for BP
- weight loss
- exercise
- less alcohol
- quit smoking
What are treatments for hypertension?
ACE inhibitors- angiotensin II cannot be produced. Less alderostone is secreted, less Na is reabsorbed and BP decreases.
ANGIOTENSIN RECEPTOR BLOCKER- AGII cannot have its effects on target organs. It is vital that this is used as AGII can be made by otherways, bypassing the RAAS system.
Another treatment: diuretics
loop dieuretics: Used in hypertensive crisis to block water reabsorption
Thiazide diuretics do not work through diuresis, but slowly reduce PVR (pulmonary vascular resistance)
Beta blockers
Blockage of ß1 receptors in heart, reduced rate and force of contraction and there is reduced CO.
Blockage of ß1 receptors in kidney- reduced secretion of renin and reduced RAAS activity.
Calcium channel blockers
Major mechanism: in vascular smooth muscle to reduce Ca2+ influx to reduce actin-myosin cross bridge cycling
Minor mechanism: inhibition of Ca influx to reduce contractility (negative inotropy) and rate of conduction (negative dromotropy) in the heart
