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

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Presentation transcript:

HYPERTENSION: 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 1 st 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. 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, Ang-II & Aldost increased & renal natriuresis impaired unless art. Pr is high or renal func is improved). (C.O, Symp activity, Ang-II & Aldost increased & renal natriuresis impaired unless art. Pr is high or renal func is improved). PRIMARY HYPERTENSION TYPES: BENIGN & BENIGN & MALIGNANT / ACCELERATED. 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: 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. 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) 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 1 st bell!!) Antihypertensive drugs: Vasodilators Vasodilators Diuretics or natriuretics 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.