HYPERTENSION:HYPERTENSION:DEFINITION:DEFINITION: Persistent increase in systemic arterial Persistent increase in systemic arterial

blood pressure.blood pressure.CLINICAL DEFINITION:CLINICAL DEFINITION: When systolic B.P rises above When systolic B.P rises above

130mmHg and diastolic B.P above 85.130mmHg and diastolic B.P above 85.(reference: Silver-thorn)(reference: Silver-thorn)

Don’t declare a person as hypertensive on 1Don’t declare a person as hypertensive on 1stst clinical clinical reading! (white coat hypertension) but on at least 3 reading! (white coat hypertension) but on at least 3 readings at different timings & in different postures; readings at different timings & in different postures;

preferably B.P chart should be maintained at home by preferably B.P chart should be maintained at home by different persons thrice or at least twice a day, before different persons thrice or at least twice a day, before

labeling the patient !labeling the patient !

TYPES OF HYPERTENSION:TYPES OF HYPERTENSION:

PRIMARY / ESSENTIAL PRIMARY / ESSENTIAL SECONDARYSECONDARYPRIMARY HYPERTENSION: PRIMARY HYPERTENSION:

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

(C.O, Symp activity, Ang-II & Aldost increased & renal (C.O, Symp activity, Ang-II & Aldost increased & renal natriuresis impaired unless art. Pr is high or renal func natriuresis impaired unless art. Pr is high or renal func is improved).is improved).PRIMARY HYPERTENSION TYPES:PRIMARY HYPERTENSION TYPES:

BENIGN & BENIGN & MALIGNANT / ACCELERATEDMALIGNANT / ACCELERATED..

BENIGN PRIMARY BENIGN PRIMARY HYPERTENSION:HYPERTENSION:

In early stagesIn early stages: moderate hypertension: moderate hypertension

200/100 mmHg200/100 mmHg

In sleep and at rest: normo-tensive.In sleep and at rest: normo-tensive.

In late stagesIn late stages: does not come back to : does not come back to normal during rest. Persistent normal during rest. Persistent hypertension hypertension over years over years vascular vascular disease or end organ damage (cardiac or disease or end organ damage (cardiac or renal)renal)

MALIGNANT OR ACCELERATED MALIGNANT OR ACCELERATED PRIMARY HYPERTENSION:PRIMARY HYPERTENSION:

250/150 B.P250/150 B.P

Developed due to combined effect of Developed due to combined effect of primary and secondary hypertension.primary and secondary hypertension.

It produces It produces severe renal disease & severe renal disease & retinal hemorrhage.(end organ damage)retinal hemorrhage.(end organ damage)

causes death in few years.causes death in few years.

SECONDARY HYPERTENSION:SECONDARY HYPERTENSION:

Due to some underlying disease.Due to some underlying disease.

Subtypes:Subtypes:

CADIOVASCULAR HYPERTENSIONCADIOVASCULAR HYPERTENSION

ENDOCRINE HYPERTENSIONENDOCRINE HYPERTENSION

RENAL HYPERTENSIONRENAL HYPERTENSION

NEUROGENIC HYPERTENSIONNEUROGENIC HYPERTENSION

HYPERTENSION DURING PREGNANCYHYPERTENSION DURING PREGNANCY

CARDIOVASCULAR CARDIOVASCULAR SECONDARY HYPERTENSION:SECONDARY HYPERTENSION:

ATHEROSCLEROSIS (hardening of blood ATHEROSCLEROSIS (hardening of blood vessels)vessels)

COARCTATION OF AORTA (narrowing of COARCTATION OF AORTA (narrowing of aorta)aorta)

ENDOCRINE SECONDARY ENDOCRINE SECONDARY HYPERTENSION:HYPERTENSION:

Due to hyperactivity of some endocrine glands.Due to hyperactivity of some endocrine glands.

PHEOCHROMOCYTOMAPHEOCHROMOCYTOMA::

Tumor in adrenal medulla.Tumor in adrenal medulla.

HYPERALDOSTERONISMHYPERALDOSTERONISM::

Excess aldosterone from adrenal cortex.Excess aldosterone from adrenal cortex.

CUSHING SYNDROMECUSHING SYNDROME::

Excess glucocorticoids from adrenal cortex.Excess glucocorticoids from adrenal cortex.

RENAL SECONDARY RENAL SECONDARY HYPERTENSION:HYPERTENSION:

STENOSIS OF RENAL ARTERIESSTENOSIS OF RENAL ARTERIES

TUMOR OF JG CELLS TUMOR OF JG CELLS EXCESS EXCESS ANGIOTENSIN IIANGIOTENSIN II

GLOMERULONEPHRITISGLOMERULONEPHRITIS

NEUROGENIC SECONDARY NEUROGENIC SECONDARY HYPERTENSION:HYPERTENSION:

INCREASED INTRACRANIAL INCREASED INTRACRANIAL PRESSUREPRESSURE

LESION IN TRACTUS SOLITARIUSLESION IN TRACTUS SOLITARIUS

SECTIONING OF NERVE FIBERS FROM SECTIONING OF NERVE FIBERS FROM CAROTID SINUSCAROTID SINUS

HYPERTENSION DURING HYPERTENSION DURING PREGNANCY:PREGNANCY:

Due to Due to toxemia of pregnancytoxemia of pregnancy

Low GFRLow GFR and and

Salt & water retentionSalt & water retention

Mechanisms:Mechanisms:

Autoimmune reaction to pregnancyAutoimmune reaction to pregnancy

V.C agents release from placentaV.C agents release from placenta

Excessive secretion of hormones Excessive secretion of hormones rise in B.P rise in B.P

Hypertension + convulsions Hypertension + convulsions eclampsia eclampsia

OTHER TYPES OF OTHER TYPES OF HYPERTENSION:HYPERTENSION:

‘‘ONE-KIDNEY’ GOLDBLATT ONE-KIDNEY’ GOLDBLATT HYPERTENSIONHYPERTENSION::

Hypertension caused by renal artery Hypertension caused by renal artery constriction of the remaining kidney, when constriction of the remaining kidney, when one kidney is removed.one kidney is removed.

TWO-KIDNEY GOLDBLATT TWO-KIDNEY GOLDBLATT HYPERTENSIONHYPERTENSION::

Hypertension when artery to one kidney is Hypertension when artery to one kidney is constricted while artery to other kidney is normalconstricted while artery to other kidney is normalMechanism:Mechanism:Constricted kidney Constricted kidney renin renin

retains salt & water + Angiotensin II + aldosterone retains salt & water + Angiotensin II + aldosterone circulate to opposite kidney circulate to opposite kidney cause it to cause it to retain salt & water retain salt & water both kidneysboth kidneys (but for (but for different reasons) different reasons) become salt & water retainersbecome salt & water retainers hypertension. hypertension.

Hypertension caused by diseased Hypertension caused by diseased kidneys that secrete RENIN chronicallykidneys that secrete RENIN chronically::

Patchy ischemic kidney tissuePatchy ischemic kidney tissue RENINRENIN ANGIOTENSIN IIANGIOTENSIN II remaining kidney remaining kidney mass will mass will retain salt & waterretain salt & water..

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

EFFECTS: EFFECTS: Like 2 kidney goldblatt Like 2 kidney goldblatt hypertension.hypertension.

Hypertension in the upper part of the Hypertension in the upper part of the body caused by coarctation of aorta:body caused by coarctation of aorta:COARCTATION OF AORTA:COARCTATION OF AORTA: Congenital pathological Congenital pathological constriction or blockage of aorta at a point beyond the constriction or blockage of aorta at a point beyond the aortic arterial branches to the head & arms but proximal aortic arterial branches to the head & arms but proximal to the renal arteries.to the renal arteries.INCIDENCE:INCIDENCE: 1 in few thousand babies. 1 in few thousand babies.Blood flow to lower body by multiple small collateral Blood flow to lower body by multiple small collateral arteries, with much vascular resistance b/w upper & arteries, with much vascular resistance b/w upper & lower aorta lower aorta arterial pr in upper part is 40-50% arterial pr in upper part is 40-50% > the > the lower bodylower bodyMechanism:Mechanism: like 1 kidney goldblatt hypertension. like 1 kidney goldblatt hypertension.Blood flow in the arms where pr is higher, remains Blood flow in the arms where pr is higher, remains normal due to normal due to long term autoregulation long term autoregulation 100% 100% compensation for pr differencescompensation for pr differences..

NEUROGENIC HYPERTENSION:NEUROGENIC HYPERTENSION:

CAUSE:CAUSE: Strong sympathetic stimulationStrong sympathetic stimulation (excitement, anxiety) (excitement, anxiety) excessive symp. excessive symp. Stimulation Stimulation peripheral V.C peripheral V.C ACUTE ACUTE HYPERTENSIONHYPERTENSIONACUTE NEUROGENIC HYPERTENSION ACUTE NEUROGENIC HYPERTENSION CAUSED BY SECTION OF BARORECEPTOR CAUSED BY SECTION OF BARORECEPTOR NERVES (buffer nerves): NERVES (buffer nerves): ;loss of normal ;loss of normal inhibitory effect on VMC inhibitory effect on VMC extreme activation extreme activation of VMC of VMC MEAN ART. Pr 100 MEAN ART. Pr 100 160 mmHg 160 mmHg pr pr normal in 2 days due to ‘ normal in 2 days due to ‘resettingresetting’’ of of receptors receptors ((response of VMC to absent response of VMC to absent baroreceptor signal fades awaybaroreceptor signal fades away).).

TREATMENT OF TREATMENT OF HYPERTENSION:HYPERTENSION:

LIFE STYLE MODIFICATION:LIFE STYLE MODIFICATION: Increased physical activity Increased physical activity (20 min walk or yoga)(20 min walk or yoga)Wt reduction Wt reduction (avoid saturated fat)(avoid saturated fat)Salt & water restrictionSalt & water restrictionQuit smokingQuit smokingAvoid tension Avoid tension (don’t jump out of bed, don’t answer door (don’t jump out of bed, don’t answer door bell or telephone call at the 1bell or telephone call at the 1stst bell!!) bell!!)Antihypertensive drugs:Antihypertensive drugs:

VasodilatorsVasodilators Diuretics or natriureticsDiuretics or natriuretics

Mechanism of action of Mechanism of action of vasodilators:vasodilators:

Sympathatic inhibitionSympathatic inhibition to kidneys or to kidneys or blockage of symp neurotransmitter on blockage of symp neurotransmitter on renal vasculature renal vasculature V.DV.D

Smooth muscle relaxationSmooth muscle relaxation of renal of renal vasculature vasculature V.DV.D

Blockage of action of renin angiotensinBlockage of action of renin angiotensin systemsystem on renal vasculature or tubules on renal vasculature or tubules V.DV.D

Mechanism of action of diuretics or Mechanism of action of diuretics or natriuretics:natriuretics:

Decrease tubular reabsorption of salt & Decrease tubular reabsorption of salt & waterwater decreased blood volume decreased blood volume decreased M.S.F.Pr decreased M.S.F.Pr decreased V.R decreased V.R decreased C.O decreased C.O B.P decreased to B.P decreased to normal.normal.