The patient is diagnosed hypertensive when the
- Systolic pressure is above 89 mmHg
- Diastolic pressure is above 139 mmHg
Types of hypertension:
- Essential hypertension
- Secondary hypertension
- Approximately 90 to 95% of hypertension is idiopathic which is essential hypertension.
- A small number i.e 5% are secondarily hypertensive from an underlying renal or adrenal disease,renal artery stenosis etc.
- The prevalence and vulnerability to complications of hypertension increase with age
- Rapidly rising of blood pressure that if untreated leads to death in 1 to 2 years is malignant hypertension
- Characterised with severe hypertension
- Systolic pressure more than 200mmHg
- Diastolic pressure more than 120 mmHg
Blood pressure regulation:
- Blood pressure is a function of cardiac output and peripheral vascular resistance,both of which are influenced by multiple Genetic and environmental factors.
- Cardiac output is a function of stroke volume and heart rate
- Peripheral resistance is regulated predominantly at the level of the arterioles by neural and hormonal inputs
Factors released from kidney,adrenals and myocardium interact and influence hypertension
Pathogenesis of hypertension:
- The vast majority of hypertension is idiopathic
Pathogenesis of secondary hypertension:
- The underlying pathways are reasonably well understood
- Renovascular hypertension
- Single gene disorders
- Gene defects affecting enzymes involved in aldosterone metabolism.
Eg: aldosterone synthase
- Mutations affecting proteins that influence sodium reabsorption.
Eg: moderately severe form of salt-sensitive hypertension, called liddle syndrome .
- It is caused by gain of function mutations in an epithelial Na+ channel protein.
- That increases distal tubular reabsorption of sodium in response to aldosterone.
Mechanisms of essential hypertension:
- Genetic factors
- Reduced renal sodium excretion
- Vasoconstrictive influence
- Environmental factors
Vascular pathology in hypertension:
- Hypertension not only accelerates atherogenesis but also associated with two forms of small blood vessel disease
Hyaline arteriosclerosis :
- Arterioles show homogeneous,pink hyaline thickening with associated luminal narrowing
- These changes reflect both plasma protein leakage across injured endothelial cells, as well as increased smooth muscle cell matrix synthesis in response to the chronic hemodynamic stresses of hypertension.
- This lesion occurs in severe hypertension; vessels exhibit concentric, laminated (onion skin) thickening of the walls with luminal narrowing.
- The laminations consists of smooth muscle cells with thickened , reduplicated basement membrane;in malignant hypertension , they are accompanied by fibrinoid deposits and vessel wall necrosis (necrotising arteriolitis)