mf3 - hypertension

7/30/2019 MF3 - Hypertension

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HYPERTENSIONDEBBIE ROSE CABANERO


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Doubles the risk of cardiovascular

disease

Coronary heart disease

Congestive heart failurePeripheral arterial disease

Stroke

Renal failure


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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


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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


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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


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Intravascular volume

Primary determinant of arterial pressure overlong 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 bedVascular resistance

Many vascular beds have capacity to autoregulateblood flow


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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


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Autonomic nervous system

Adrenergic reflexes modulate BP over shortterm and long term regulator of arterialpressure

3 endogenous catecholamines Norepinephrine

Epinephrine

Dopamine Neuron neurotransmitter synaptic cleft

receptor sites / target tissue


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RENIN ANGIOTENSIN ALDOSTERONE


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VASCULAR MECHANISM

Vascular radius and compliance of resistance arteriesare important determinants of arterial pressure

Remodeling alterations in vessel wall withoutchanging 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 intracellularcalcium

2nd : increase PH enhances calcium sensitivity increasecontractility


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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


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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 formof hypertension

Low renin volume dependent hypertension


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HYPERTENSION

Home blood pressure are lower than in the clinics

white coat hypertension BP higher in the early morning hrs soon after

walking

Blood Pressure Classification Systolic, mmHg Diastolic, mmHg

Normal


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Secondary hypertension

Renal parenchymal diseases

-renal disease is the most common cause of secondaryhypertension

-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


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Positive study:

1. Decrease relative uptake by involved kidney

2. Delayed uptake on affected side3. Delayed washout on affected side

PRIMARY ALDOSTERONISM

Consequences : sodium retention, hypertension,hypokalemia

3rd- 4th decade of life

Glucose intolerance

Polyuria, polydypsia, paresthesia or muscularweakness, hypokalemia alkolosis

Aldosterone producing adrenal adenoma Tumor unilateral


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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 ofhypertension

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


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Monogenic hypertension

Deficiency in sex hormones and cortisol

Males: pseudohermaphoditism

Females: primary amenorrhea, absent secondary

characteristics


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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 roomtemperature

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


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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 arteryremains 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 nolonger jets through squeezed artery, tapping stops


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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 thenephron, preventing reabsorption of water

Potassium sparing Prevent potassium secretion into distal tubule

Sodium is reabsorbed, potassium is secreted


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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 theperipheral vasculature

Presynaptic adrenergic inhibitors

Inhibits the release of norepinephrine Centrally acting agents

Inhibit sympathetic discharge from the brainstem


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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 incirculating renin

Preventing the adverse structural changes

Calcium channel blockers Block calcium entry into vascular smooth- muscle cells

Inhibit contractile process leading to vasodilation and decreasevascular resistance

T t t


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Treatment


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LIFESTYLE intervention

Weight reduction Attain and maintain BMI < 25 kg/m2

Dietary salt reduction < 6 g NaCl/d

Adapt DASH-type dietary plan Diet rich in fruits, vegetables, and low-fatdairy 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 inwomen

Physical activity Regular aerobic activity, e.g., brisk walking

for 30 min/d


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Blood pressure may be lowered by 30 min of

moderately intense physical activity, such asbrisk walking, 67 days a week, or by more

intense, less frequent workouts

Alcohol use in persons consuming three ormore drinks per day

DASH (Dietary Approaches to Stop

Hypertension) - 8-week period a diet

mf3 - hypertension

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