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HYPERTENSION

DEBBIE ROSE CABANERO

Doubles the risk of cardiovascular disease Coronary heart disease Congestive heart failure Peripheral arterial disease Stroke Renal failure

epidemiology
Varies among countries Present in all populations 6% death worldwide Children and adolescents blood pressure is associated with growth and maturation Average systolic BP ( >140mmHg)
higher for man early adulthood Older women 60 up

Dystolic pressure(>90 mmHg)


Adults increase until 55 yrs then decrease
Consequence is widening of pulse pressure beyond age 60

Both environmental and genetic factors


Obesity/ wt gain High nacl intake Low dietary intake of calcium and potassium Alcohol consumption, psychosocial stress, decrease level of physical activity

Mechanism of hypertension

Cardiac output Stoke volume and heart rate Myocardial Contractility

Size of vascular compartment Peripheral resistance Functional and anatomic Changes in small arteries and arterioles

Intravascular volume
Primary determinant of arterial pressure over long term Extracellular fluid space- composed of vascular and interstitial spaces Sodium- extracellular ion primary determinant of extracellular fluid volume Blood flow = pressure across the vascular bed
Vascular resistance

Many vascular beds have capacity to autoregulate blood flow

Arterial pressure increase = urinary sodium excretion increase and sodium balance maintained Pressure natriuresis phenomenon
Increase glomerular filtration rate Decrease absorbing capacity of renal tubules and hormonal factors

Autonomic nervous system


Adrenergic reflexes modulate BP over short term and long term regulator of arterial pressure 3 endogenous catecholamines
Norepinephrine Epinephrine Dopamine

Neuron neurotransmitter synaptic cleft receptor sites / target tissue

RENIN ANGIOTENSIN ALDOSTERONE

VASCULAR MECHANISM
Vascular radius and compliance of resistance arteries are important determinants of arterial pressure Remodeling alterations in vessel wall without changing vessel volume (hypertrophic, eutrophic) Ion transport contribute to hypertension associated with abnormalities of vascular tone Na+ - H+ exchange increase hypertension
Increase vascular tone 1st: increase in Na entry increase vascular tone by activation Na+ - CA2 + exchange = increase intracellular calcium 2nd : increase PH enhances calcium sensitivity increase contractility

Pathologic consequences of hypertension


Heart
most common cause of death in hypertensive patients Diastolic dysfunction early consequence of hypertension

Brain
Risk factor for brain infarction and hemorrhage Impaired cognition encephalopathy

Kidney
Primary renal disease is the most common etiology of secondary hypertension Direct damage to glomerular capillaries Renal tubules ischemic - atrophic

Peripheral Arteries
blood vessels may be a target organ for atherosclerotic disease secondary to long-standing elevated blood pressure

Clinical d/o of hypertension


Essential hypertension
Aka primary / idiopathic Familial , genetic, environmental Increase w/ age Peripheral resistance increase, cardiac output normal/ decrease High plasma renin activity vasoconstrictor form of hypertension Low renin volume dependent hypertension

HYPERTENSION
Blood Pressure Classification Normal Prehypertension Stage 1 hypertension Stage 2 hypertension Systolic, mmHg <120 120139 140159 160 Diastolic, mmHg and <80 or 8089 or 9099 or 100

Isolated systolic hypertension

140

and <90

Home blood pressure are lower than in the clinics white coat hypertension BP higher in the early morning hrs soon after walking

Secondary hypertension
Renal parenchymal diseases -renal disease is the most common cause of secondary hypertension -proteinuria Renovascular hypertension - Due to obstruction of renal artery ,curable - Pt at risk -Older atherosclerotic pt. who have plaque Obstructing the renal artery -pt with fibromuscular dyplasia (women) - affect bilaterally, distal portion of renal artery - Have abdominal bruit

Positive study: 1. Decrease relative uptake by involved kidney 2. Delayed uptake on affected side 3. Delayed washout on affected side PRIMARY ALDOSTERONISM Consequences : sodium retention, hypertension, hypokalemia 3rd- 4th decade of life Glucose intolerance Polyuria, polydypsia, paresthesia or muscular weakness, hypokalemia alkolosis Aldosterone producing adrenal adenoma
Tumor unilateral <3cm Bilateral adenocortical hyperplasia

Cushing syndrome
S timulation of mineralocorticoid receptors by cortisol and increase secretion of adrenal steroids

obstuctive sleep apnea Coarctation of the aorta


Most common congenital cardiovascular cause of hypertension Occur in children with turners syndrome Dimished and delayed femoral pulses and systolic pressure gradient between right arm and legs Blowing systolic murmur may be heard in the post. Left interscapular areas

Monogenic hypertension
Deficiency in sex hormones and cortisol Males: pseudohermaphoditism Females: primary amenorrhea, absent secondary characteristics

Approach to patient
Measurement of BP
Before taking the blood pressure measurement, the individual should be seated quietly for 5 min in a private, quiet setting with a comfortable room temperature center of the cuff should be at heart level width of the bladder cuff should equal at least 40% of the arm circumference length of the cuff bladder should encircle at least 80% of the arm circumference

Methods in determining BP
Auscultatory method
Stethoscope over antecubital area BP cuff inflated over upper arm Korotkoff sounds Mechanism:
When cuff pressure is higher than systolic P, brachial artery remains occluded As cuff pressure is reduced, blood jets through the artery, hearing tapping sounds from antecubital artery When cuff pressure is equal diastolic pressure, blood no longer jets through squeezed artery, tapping stops

treatment
Diuretics
Increase the formation and excretion of urine Decreasing the fluid within vascular system Often first type of drugs to treat hypertension

Classification
Thiazide
Act a distal tubule of the nephron, inhibit sodium reabsorption

Loop
Act on the ascending limb of the loop of henle. Inhibiting the reabsorption of sodium and chloride from the nephron, preventing reabsorption of water

Potassium sparing
Prevent potassium secretion into distal tubule Sodium is reabsorbed, potassium is secreted

Sympatholytic drugs
Increase sympathetic activity

Beta adrenergic blockers


Decrease BP, mainstay of antihypertensive therapy Primary effect on the heart

Alpha blockers
Decrease in vascular resistance, directly act on the peripheral vasculature

Presynaptic adrenergic inhibitors


Inhibits the release of norepinephrine

Centrally acting agents


Inhibit sympathetic discharge from the brainstem

Ganglionic blockers
Block synaptic transmission at autonomic ganglia, reduce BP by decreasing systemic sympathetic activity Nicotinic cholinergic antagonists block transmission bet. Presynaptic and postsynaptic neurons

Vasodilators
Directly vasoldilate peripheral vasculature Decreasing peripheral vascular resistance Inhibit smmoth muscle contraction

ACE inhibitors
Decrease BP in pt who do not have a substantial increase in circulating renin Preventing the adverse structural changes

Calcium channel blockers


Block calcium entry into vascular smooth- muscle cells Inhibit contractile process leading to vasodilation and decrease vascular resistance

Treatment

LIFESTYLE intervention
Weight reduction Attain and maintain BMI < 25 kg/m2

Dietary salt reduction Adapt DASH-type dietary plan

< 6 g NaCl/d Diet rich in fruits, vegetables, and low-fat dairy products with reduced content of saturated and total fat

Moderation of alcohol consumption

For those who drink alcohol, consume 2 drinks/day in men and 1 drink/day in women Regular aerobic activity, e.g., brisk walking for 30 min/d

Physical activity

Blood pressure may be lowered by 30 min of moderately intense physical activity, such as brisk walking, 67 days a week, or by more intense, less frequent workouts Alcohol use in persons consuming three or more drinks per day DASH (Dietary Approaches to Stop Hypertension) - 8-week period a diet

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