systemic hypertension

Def:

systemic HTN is diagnosed of the avenge Level of 140/90. SBP is 140 mm Hg DBP is 90 mm Hg or more If SBP is 160 mm Hg a single visit for measurement OR DBP is 105mm Hg sufficient for the diagnosis

Etiology:
1) systolic HTN( SBP 160 mm Hg with Normal DBP). A ) increased LT. ventricular stroke volume: 1- aortic reguige 2- thyrotoxicosis & fever 3- A-V fistula 4- P.D.A 5- hypa Kinetic disease B) decreased aortic compliance aortic atherosclerosis 2) systolic & diastolic HTN a-essential HTN: Commonest form of systemic HTN (> 90% of cases) occurs in middle & late ages. the problem is probably multifactorial as 1. HTN is more common in some ethnic groups - Japanese - American Blacks. 2. in 40-60% is explained by genetic factors 3. important environmental factors:

high salt intake heavy alcohol consumption obesity impaired intrauterine growth b- 2ry HTN (disease or abnormality Na retention or Peripheral V.C.) 1- Alcohol 2- Pregnancy (pre-iclampsia) 3- Renal renal vascular syndrome (R.A.S) parenchymal renal disease : - GN - chronic pyelonephritis polycystic kidney diabetic nephropathy 4- Endocrine Disease: phaeochromocytoma cons syndrome acromegaly Cushing syndrome hyperparathyroidism & 1ry hypothyroidism thyrotoxicosis cong .adrenal hyperplasia Due to - 11B-hydroxypase deficiency or - 17 hydroxypase deficiency 5- drugs oral contraceptive pills anabolic steroids Corticosteroid NSAIDs Sympathomimetic agents. 6- coarctation of aorta. 7- Nervous Disease as incresed I.C tension

8- polycythemia vera.

C/P

A.

uncomplicated HTN:

symptoms:
1- majority of Pts are Asymptomatic there may be Headache dizziness vertigo tinnitus palpitation easy fatigability & it may develop of the pt. has been informed about his HTN due to development of amxiety neurosis.
2-

3-sever HTN occipital Headache which is usually present when pt. awakes & subsides spontaneously often several hours

signs :
1-

Pulse: increased pulse volume in systolic HTN

 2-

decreased pulse volume in systolic & diastolic HTN. blood pressure: increased take care of white coat HTN Severity of HTN:

Normal Person HTN

category *Optimal * Normal Stage 1(mild) Stage 2(Moderate) Stage 3 (sever)

Systolic (mmHg) <120 120-139 140-159 160-179 180

Diastolic (mmHg) <80 80-89 90-99 100-109 110

3-

Cardiac Examination : load A2 aortic systolic ejection click. Systolic ejection murmur due to dilatation of aortic ring with the development of Aortic in competence (functional) Earliest clinical sign of cardiac affection is the appearance of a presystolic gallop .

Note: the majority of deaths due to HTN result from myocardial infarction or congestive heart failure

investigations :
Chest X-ray many reveal prominent aortic knock

) complicated HTN (target organ Damage )

B.

1- cardiac complication: (systolic , Diastolic ) Dysfunction A. L t. Ventricular hypertrophy of subsequent Lt ventricular failure Then Rt . sided failure may follow later on Note: Lt. ventricular hypertrophy is a major risk factor of premature cardio vascular: - morbidity. (or) - mortality. All anti HTN agents reverse the LT ventricular hypertrophy especially ACEI centrally acting " captopril" B.B CCB B.coronary atherosclerosis which may lead to is chemic 2- Vascular Complications: 1- accelerated atherosclerosis 2- Hge e.g.:- epistaxisis Due to rupture of -haematouria small vessels . 4- arterial medial hypertrophy & later on fibrinoid degeneration 5- cystic medial necrosis of the aorta so HTN is implicated in the pathogenesis of : -aortic aneurysm.

-aortic dissection 3cerebral complications: 1- transient ischemic attacks 2- cerebral thrombosis 3cerebral hge (due to rupture of vascular microaneurysm) 4subarachnoid hge 5Hypertensive encephalopathy (mean bp>180 mmhg) Disturbed consciousness Retinopathy with papilloedema I.C.P & seizres focal neurological signs. E.g. Transient disturbances of (speech & rision )

4- Renal complications: Protein urea & Haematouria Due to glomerular injury atherosclerosis of the afferent & efferent arterioles of glomerular capillaries Note. Nephrosclerosis : disturbed glomerular filtration, Tubular dysfunction, Followed by R.F in 10-20 % of pts 5) Retina Hypertensive retinopathy . Grade 1: 1- arteriolar thickening 2- touristy 3- increased reflectivness (silver wiring). Grade 2: 1+ construction of vien's at arterial crossing (A-V nipping).

Grade 3: 2+ evidence of retinal ischemia - flame shaped or blot Hges. - cotton wool exudates. Garde 4: 3+ papilloedema.

Malignant or accelerated phase HTN:

This

rare condition may complicate HTN of any etiology.

It

ccc by accelerated micro vascular damage with necrosis in the wall of small arteries & arterioles (fibrinoid necrosis). intravascular thrombosis. The diagnosis is based on evidence of 1high BP 2- rapidly progressive 3end organ damage as-retinopathy [grade 3,4] -renal failure -HTN encephalopathy. Lt. ventricular failure may Occur & if untreated death within months.

 Investigations:
1) Basic (investigations of all pts): 1- urine analysis for: blood (haematuria). proteinuria glucose glucoseuria. 2- plasma urea & electrolytes Note: hypokalemia alkalosis may indicate Conns but usually due to diuretics. 3- plasma creatinine. 4- plasma cholesterol. 5- ECG: to detect LT. vent. Hypertrophy. Or evidence of coronary artery D. 2) Investigations of selected PTS: 1- chest X-ray to detect : - cardiomegaly. - heart failure. - coarctation of aorta. 2- ambulatory blood pressure recording to assess borderline or white coat HTN. 3- Echocardiogram to detect LT. vent. Hypertrophy.

4- renal U/S to detect possible renal D. 5- renal angiography to detect R.A.S 6- urinary catecholamines to detect phaeochromocytoma. 7- urinary cortisol & dexa methasone suppression test for possible cushing $. 8- plasma rennin activity & aldosterone for conn's $. 9- T3 & T4 & TSH for hypo & hyperthyroidism.

Treatment
1- life style modification [non pharmacological therapy] Avoidance of smoking. Wt. reduction in over wt. PTs. Restriction of alcohol intake. Regular physical activity & relaxation. Moderation of dietary Na to < 6 gm /d (salt restriction). 2- pharmacological therapy:

for stage 1 & 2 HTN:

if BP remains> 140/90 for 3-6 months despite life style modification. Anti Hypertensive drug's should be started with a single drug (monotherapy). Since B.B. & Diuretics can decrease cardiovascular morbidity & mortality. they are proferred far initial drug therapy if ineffective: ACEI & CCB or blocker, b blocker

The lowest doses of the selected drug to avoid their side effects if blood pressure remains uncontrolled for several wks dose gradually if after 1-3 months & the response is still inadequate 3 options: 1) dose of the initial drug to maximal levels. 2) Substitute an agent for another. 3) Add a 2nd drug from another class.

for stage 3 HTN: as above but it's often necessary to add: nd rd - a 2 or 3 agent after short interval. - The maximum dose of 1 drug may be needed. for resistant HTN: def.: blood pressure can't be ed to <160/100 (if it was > 180/115) or 140/90 (if it was < 180/115). despite appropriate, triple drug therapy is nearly maximum doses. the drug therapy should include at least 3 different pharmacological agents including a diuretic consider 2ry HTN ttt of the cause e.g..: repair of renal artery stenosis either by surgically or angioplasty. for HTN emergencies: "acute HTive crises" If severe rise of Bl pressure with symp & sign's of acute severe target organ damage which must be reduced within minutes (typically using parenteral therapy).

If sever rise in Bl pressure with mild or no acute target organ damage which must be reduced within hours (typically with oral therapy).

It includes: Acute HTive encephalopathy. 2) Acute pul. Oedema due to HTive LT. ventricular failure 3) Malignant HTN. 4) Acute dissecting aneurysm of aorta. 5) Eclampsia & Hgic strokewz marked elevation of Bl. Pressure.
1)

In these cases the blood pressure should be lowered only to levels that relieve the immediate crisis Ex.: 160/100 & not more.

If the Bl. Pressure must be lowered immediately then

I.V. in fusion of sodium nitroprusside is the first choice & alternative drugs are nitroglycerin I.V. & Diazoxide.