Classification of blood pressure.
HTN is classically classified into:
- Essential (95%)
- Secondary (5%)
Acquired disease as a result of a combination of genetic and environmental factors. Genetic factors may include genes encoding for the renin-angiotensin system and renal sodium excretion and vasocontrictive influences. Environmental factors include stress, obesity, smoking, physical inactivity, alcohol and salt intake.
Renal: glomerulonephritis (nephretic syndrome), chronic kidney disease, renal artery stenosis, polycystic kidney disease.
Endocrine: phaechromocytoma, Cushing's syndrome, Conn's syndrome, hyperparathyroidism, hypothyroidism/hyperthyroidism
CVS: coarctation of the aorta
Neurological: stress, increased intracranial pressure, sleep apnoea
Drugs: alcohol, toxins - envenomation
Changes in the blood vesels secondary to HTN
- Accelerates the development of atherosclerosis within the arterial system or damage to sensitive vascular beds particularly in the kidneys and eyes.
- Hyaline arteriosclerosis
- Hyperplastic arteriosclerosis
- Degenerative changes in the large and medium sized arteries that potentiates aortic dissection and cerebrovascular haemorrhage
Homogenous pink hyaline thickening due to plasma proteins leaking into the injured endothelial cells and increased smooth muscle ECM secretion due to chronic stress. Associated with luminal narrowing. In nephrosclerosis the arterial narrowing causes ischaemia and glomerular scarring.
Occurs in severe malignant HTN. Vessels have concentric laminated thickening of the walls secondary to smooth muscle cells with reduplicated BM (onion skin lesions) and luminal narrowing - fibrinoid deposits and vessel wall necrosis can also be seen.
Complications of systemic HTN
Dramatically increased risk of :
- Stroke (haemorrhagic and ischaemic)
- Chronic kidney disease
Changes in the heart secondary to HTN
In pressure loading concentric ventricular hypertrophy occurs. This results in a thickened myocardium that can pump with more force. Transcriptional changes occur which affect the expression of numerous growth factor proteins in the myocytes. This process ultimately decompensates as the heart's ability to increase contractility by this method is limited. This could result in HF.
Outcomes of pulmonary HTN
Results in right sided myocardial hypertrophy, hypertension and eventual right heart fialure known as cor pulmnale.
Right sided heart failure.
Acute cor pulmonale can occur secondary to a massive PE.