DEFINITION: Persistent increase in systemic arterial blood pressure.CLINICAL DEFINITION: When systolic B.P rises above 130mmHg and

diastolic B.P above 85.(reference: Silver-thorn)

Don’t declare a person as hypertensive on 1st clinical reading! (white coat hypertension) but on at least 3 readings at different timings & in different postures; preferably B.P chart should be maintained at home by different

persons thrice or at least twice a day, before labeling the patient !

TYPES OF HYPERTENSION:

PRIMARY / ESSENTIAL SECONDARY PRIMARY HYPERTENSION: Hypertension is of unknown origin. Strong

hereditary tendency. Excess wt gain (65-70% risk, prolong QT interval in obese) & sedentary life style may play a major role.

(C.O, Symp activity, AngII & Aldost increased & renal natriuresis impaired unless art. Pr is high or renal func is improved).

PRIMARY HYPERTENSION TYPES: BENIGN & MALIGNANT / ACCELERATED.

BENIGN PRIMARY HYPERTENSION: In early stages: moderate hypertension 200/100 mmHg In sleep and at rest: normo-tensive. In late stages: does not come back to normal

during rest. Persistent hypertension over years vascular disease or end organ damage (cardiac or renal)

MALIGNANT OR ACCELERATED PRIMARY HYPERTENSION: 250/150 B.P Developed due to combined effect of

primary and secondary hypertension. It produces severe renal disease &

retinal hemorrhage.(end organ damage) causes death in few years.

SECONDARY HYPERTENSION: Due to some underlying disease. Subtypes: CADIOVASCULAR HYPERTENSION ENDOCRINE HYPERTENSION RENAL HYPERTENSION NEUROGENIC HYPERTENSION HYPERTENSION DURING

PREGNANCY

CARDIOVASCULAR SECONDARY HYPERTENSION: ATHEROSCLEROSIS (hardening of

blood vessels) COARCTATION OF AORTA (narrowing

of aorta)

ENDOCRINE SECONDARY HYPERTENSION: Due to hyperactivity of some endocrine

glands. PHEOCHROMOCYTOMA: Tumor in adrenal medulla. HYPERALDOSTERONISM: Excess aldosterone from adrenal cortex. CUSHING SYNDROME: Excess glucocorticoids from adrenal

cortex.

RENAL SECONDARY HYPERTENSION: STENOSIS OF RENAL ARTERIES TUMOR OF JG CELLS EXCESS

ANGIOTENSIN II GLOMERULONEPHRITIS

NEUROGENIC SECONDARY HYPERTENSION: INCREASED INTRACRANIAL

PRESSURE LESION IN TRACTUS SOLITARIUS SECTIONING OF NERVE FIBERS

FROM CAROTID SINUS

HYPERTENSION DURING PREGNANCY: Due to toxemia of pregnancy Low GFR and Salt & water retention

Mechanisms: Autoimmune reaction to pregnancy V.C agents release from placenta Excessive secretion of hormones rise in

B.P Hypertension + convulsions eclampsia

OTHER TYPES OF HYPERTENSION: ‘ONE-KIDNEY’ GOLDBLATT

HYPERTENSION: Hypertension caused by renal artery

constriction of the remaining kidney, when one kidney is removed.

TWO-KIDNEY GOLDBLATT HYPERTENSION:

Hypertension when artery to one kidney is constricted while artery to other kidney is normal

Mechanism: Constricted kidney renin retains salt & water + Angiotensin II +

aldosterone circulate to opposite kidney cause it to retain salt & water both kidneys (but for different reasons) become salt & water retainers hypertension.

Hypertension caused by diseased kidneys that secrete RENIN chronically: Patchy ischemic kidney tissue RENIN

ANGIOTENSIN II remaining kidney mass will retain salt & water.

It is one of the most common causes of renal hypertension in older age.

EFFECTS: Like 2 kidney goldblatt hypertension.

Hypertension in the upper part of the body caused by coarctation of aorta: COARCTATION OF AORTA: Congenital

pathological constriction or blockage of aorta at a point beyond the aortic arterial branches to the head & arms but proximal to the renal arteries.

INCIDENCE: 1 in few thousand babies. Blood flow to lower body by multiple small

collateral arteries, with much vascular resistance b/w upper & lower aorta arterial pr in upper part is 40-50% > the lower body

Mechanism: like 1 kidney goldblatt hypertension. Blood flow in the arms where pr is higher, remains

normal due to long term autoregulation 100% compensation for pr differences.

NEUROGENIC HYPERTENSION: CAUSE: Strong sympathetic stimulation

(excitement, anxiety) excessive symp. Stimulation peripheral V.C ACUTE HYPERTENSION

ACUTE NEUROGENIC HYPERTENSION CAUSED BY SECTION OF BARORECEPTOR NERVES (buffer nerves): ;loss of normal inhibitory effect on VMC extreme activation of VMC MEAN ART. Pr 100 160 mmHg pr normal in 2 days due to ‘resetting’ of receptors (response of VMC to absent baroreceptor signal fades away).

TREATMENT OF HYPERTENSION: LIFE STYLE MODIFICATION: Increased physical activity (20 min walk or yoga

mudra) Wt reduction (avoid saturated fat) Salt & water restriction Quit smoking Avoid tension (don’t jump out of bed, don’t answer

door bell or telephone call at the 1st bell!!) Antihypertensive drugs: Vasodilators Diuretics or natriuretics

Mechanism of action of vasodilators: Sympathatic inhibition to kidneys or

blockage of symp neurotransmitter on renal vasculature V.D

Smooth muscle relaxation of renal vasculature V.D

Blockage of action of renin angiotensin system on renal vasculature or tubules V.D

Mechanism of action of diuretics or natriuretics: Decrease tubular reabsorption of salt &

water decreased blood volume decreased M.S.F.Pr decreased V.R decreased C.O B.P decreased to normal.