Hypertensive Vascular Disease

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

Essential hypertension:

  • Approximately 90 to 95% of hypertension is idiopathic which is essential hypertension.

Secondary 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

Malignant hypertension:

  • 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
  1. Gene defects affecting enzymes involved in aldosterone metabolism.

Eg: aldosterone synthase

  1. Mutations affecting proteins that influence sodium reabsorption.

Eg: moderately severe form of salt-sensitive hypertension, called liddle syndrome .

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.

Hyperplastic arteriosclerosis:

  • 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)

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