IOD Hypertension Flashcards
Definition?
Hypertension refers to raised blood pressure in the systemic vascular bedtreatment beneficial if >140/90
essential?
95% cases
Essential hypertension -genetic and environmental factors:
- blood pressure has a polygenic inheritance- genes of angiotensinogen, renin and atrial natriuretic peptide receptor genes.
- the most important environmental factors are thought to be stress, diet (eg. increased sodium and alcohol intake both increase blood pressure) and the intrauterine environment (babies with a low birthweight have an increased incidence of hypertension and other cardiovascular disorders in adult life).
secondary ?
5%
• chronic renal disease (the most important cause overall):
• chronic kidney disease of any cause:
• eg. diabetic nephropathy, obstructive nephropathy, chronic glomerulonephritis etc
• renal vessel disease (renal artery stenosis, most commonly due to atherosclerosis-activates RAAS)
• adult polycystic kidney disease
• acute glomerulonephritis (hypertension is one of the presenting features of nephritic syndrome, seen
in IgA nephropathy, post-infectious GN, lupus nephritis)
• autoimmune disease-vasculitis (particularly polyarteritis nodosa), systemic sclerosis
• Coarctation of aorta (mainly due to renal underperfusion and excess renal secretion)
• Endocrine disease
• Cushing’s syndrome, Conn’s syndrome, Phaeochromocytoma, Acromegaly
• Drugs
• eg. steroids, oral contraceptive pill, NSAIDs (COX2) cocaine
• Pregnancy (pre-eclampsia)
link to AS?
accelerates it
hyaline arteriosclerosis?
smooth muscle cells in the media are replaced by collagen -deposition of plasma proteins, together resulting in hyaline change.
This process occurs with increasing age but is accelerated by hypertension (and also diabetes mellitus). Arteriosclerosis increases the rigidity of arteries and so lowers the compliance of the arterial tree- age-related increase in systolic blood pressure and alters tissue autoregulation by shifting the autoregulatory curve to the right.
This makes hypotension much more dangerous as flow drops before 100mmhg and accounts for the increased mortality of shock in elderly patients.
There is also a narrowing of the lumina decreased blood flow-progressive chronic ischaemia of the tissue supplied by the artery/arteriole.
Arteriosclerosis differs from atherosclerosis in that there is no intimal lipid deposition with resultant inflammation.
hyperplastic?
malignant/accelerated hypertension.
The very high systolic blood pressure pressure causes fibrinoid necrosis in the vessel wall. The body’s healing response results in proliferation of the intimal cells. This imparts an “onion-skin” appearance and causes significant narrowing of the vessel lumen. There is sig reduction of blood flow in vessel and ischaemia of tissue.
Hypertensive heart disease?
- it accelerates coronary artery atherosclerosis
- this worsens ischaemic heart disease.
- it causes leP ventricular hypertrophy
- the LV has to push harder against the increased pressure in the systemic circulation in order to eject blood into the aorta. Therefore the LV undergoes compensatory leN ventricular hypertrophy. The patient may be asymptomatic during this period of compensation.
- as the leN ventricular hypertrophy progresses there is increasing metabolic demands of myocardium. However, the heart becomes progressively less able to meet these demands because:
- the myocardial capillary bed does not expand in tandem with the increased myocardial O2 demand, thus increasing distance across which O2/nutrients must diffuse.
- accelerated atherosclerosis (due to hypertension).
- eventually the hypertrophied LV will decompensate and fail (leP heart failure).
Effects of hypertensive heart disease?
• myocardial ischaemia/infarction.
• arrhythmias eg atrial fibrillation (ischaemic muscle is unstable). Hypertension is the commonest cause of atrial fibrillation.
Progressive LeN HF
Why is AF dangerous?
- thrombi may form in the atria as a consequence of stasis. The thrombi may embolise.
- cardiac output may fall because loss of normal atrial contraction can significantly reduce LV filling and stroke vol).
Hypertensive renal disease?
Progressive hyaline arteriosclerosis in the renal arterioles causes chronic and progressive renal ischaemia. This results in tubular atrophy, interstitial fibrosis and progressive glomerular sclerosis. In turn this leads to the development of progressive chronic kidney disease (CKD).
A vicious cycle is established: hypertension causes CKD which in turn worsens the hypertension.
Ultrasound will show small kidneys - they are small because of atrophy and fibrosis.
other complications?
aortic dissection
papilloedema or cotton wool spots
intracerebral haemorrhage-rupture of Charcot-Bouchard aneurysms in arterioles
ischaemic strokes due to AS
subarachnoid haemorrhage due to rupture of berry aneurysm-weakness in media of cerebral vessels
Malignant hypertension?
raised diastolic bp
(usually
>130-140mmHg) and end organ damage.
less than 1% patients with primary-more in secondary
younger people-new cases usually present at 30-40yr of age.
The underlying pathogenesis is poorly understood.
Hyperplastic arteriolosclerosis
There is also
fibrinoid necrosis of small arteries and arterioles.
Consequences of malignant ht?
- acute leN ventricular failure.
- stroke (cerebral haemorrhage).
- acute renal failure.
- blurred vision (due to retinal haemorrhages/exudates and papilloedema).
- hypertensive encephalopathy (headache, irritability, alteration in consciousness).
- microangiopathic haemolytic anaemia and disseminated intravascular coagulation (DIC).
renal damage and encaphelopathy?
due to failure to protect the microcirculation from the increased pressure.
- it is rare in elderly people because the cerebral autoregulatory curve is shifted to the right. Thus, arteriosclerosis protects against the development of the renal damage and encephalopathy. [However, the greatly increased susceptibility to hypotension accounts for the increased mortality of shock in elderly and hypertensive patients].
- it is more common in young people whose arteries are unprotected by arteriolosclerosis
renal damage pathophysiology?
Failure of autoregulation in the kidney transmits increased pressure to the glomeruli, causing fibrinoid necrosis and microaneurysm formation in glomerular capillaries. The pressure also causes fibrinoid necrosis of afferent glomerular arterioles, which may rupture or be associated with luminal thrombosis, resulting in small renal infarcts. Thrombosis causes damage to red blood cells - microangiopathic haemolytic anaemia. Ischaemia of the juxtaglomerular apparatus leads to increased secretion of renin, which further increases blood pressure, leading to a vicious cycle. Together these effects give rise to proteinuria and haematuria.
Similar changes occur in the brain in hypertensive encephalopathy
