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Increment in blood pressure above a level that is harmful to the organs of the body

Optimal 120/ 80

Normal 130 /85

High normal 130–139 /85–89

Stage 1 (mild) 140–159 90–99

Stage 2 (moderate) 160–179/ 100–109

Stage 3 (severe) 180 /110

Isolated systolic hypertension140/ 90

Malignant HTN= accelerated HTN+papilledema

Hypertension can broadly be divided into :

BENIGN HYPERTENSION: 90 – 95% of cases.

Rapidly rising blood pressure that if untreated leads to end organ failure and death within 1 or 2 years.
Clinically - Severe hypertension - diastolic pressure over 120 mm Hg, renal failure, and retinal hemorrhages and exudates, with or without papilledema.

MORPHOLOGY: Blood vessels show fibrinoid necrosis or concentric hyperplasia of smooth muscle-cells – Hyperplastic arteriosclerosis -- onion-skin changes. These hyperplastic changes are accompanied by fibrinoid deposits and acute necrosis of the vessel walls, referred to as necrotizing arteriolitis, particularly in the kidney.


Essential Hypertension
Secondary Hypertension


Acute glomerulonephritis,
Chronic renal disease,
Polycystic disease,
Renal artery stenosis,
Renal artery fibromuscular dysplasia,
Renal vasculitis,
Renin-producing tumors


Adrenocortical hyperfunction (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion)
Hypothyroidism (myxedema)
Hyperthyroidism (thyrotoxicosis)
Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oral contraceptives]

Sympathomimetics and tyramine-containing foods, monoamine oxidase inhibitors
Pregnancy-induced (Pre eclampsia)


Coarctation of aorta,
Polyarteritis nodosa (or other vasculitis),
Increased intravascular volume,
Increased cardiac output,
Rigidity of the aorta
Increased intracranial pressure
Sleep apnea

BP regulation

Complications of HTN

Hypertensive Encephalopathy and Cerebral Atrophy
Sub arachnoid and intracerebral hemorrhage

Hypertensive Retinopathy

Hypertensive Cardiomyopathy

Hypertensive nephropathy: Nephrosclerosis and chronic renal failure

Exacerbation of atherosclerosis

Aortic dissection and aneurysm formation

Resorption, fibrosis


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