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Prof . El Sayed Abdel Fattah Eid
Lecturer of Internal Medicine
Delta University
 Definition:
Systemic hypertension is present in an adult (age> 18 years) if
SBP 140 mm Hg or
DBP 90 mm Hg.
 The long term risk of cardiovascular morbidity and mortality
rises in direct relation
to increases in blood pressure
 30% of patients with hypertension are unaware of it (silent
High normal
Stage 1 hypertension
Stage 2 hypertension
Stage 3 hypertension
1 80
1 10
 - The diagnosis of hypertension is based on finding an
elevated blood pressure on at least three separate occasions.
 - Children and pregnant women are slightly lower than
others; However, care must be taken in making the diagnosis
of hypertension in children and adolescents because the
blood pressure normalizes in adulthood.
 - The incidence↑with age
• African-Americans > whites.
• Younger men > women and men = women after the age of
 1-Primary or essential hypertension (Unknown):
• 90%-95% of patients (no identifiable cause).
• Genetic factors (familial patterns of primary hypertension)
• Environmental factors: obesity, sedentary lifestyle, and salt intake
• Pathophysiology:
- Excessive renal sodium retention
- Overactivity of the sympathetic nervous system,
- Excess Renin-angiotensin activity
- Hyperinsulinemia
- Alterations in vascular endothelium 2ry to↓VD substances (nitric
 2-Secondary hypertension: 5% of patients (with identifiable cause).
 1-Thorough history
2- Physical examination
3- Limited laboratoy studies.
 The goals:
1. Assess the patient for the presence and treatment of
hypertensive target organ damage (TOD)
2. Identity clinical factors that may influence the choice of therapy
(renal failure,heart failure)
3. Determine the presence of other cardiovascular risk factors
4. Recognize patients with secondary potentially reversible cause
Thorough history
 * Asymptomatic
* Headaches (occipital) &Blurred vision
* Fatigue & Dizziness
* Epistaxis
* Dyspnea & chest pain.
* History of alcohol.
* Drugs: oral contraceptives, steroids
* Dietary sodium intake * Family history of hypertension
* Secondary hypertension :
-Weakness, polyuria & muscle cramps: hypokalemia in primary
-Weight gain and emotional liability in Cushing’s syndrome
- Headaches, palpitations, anhidrosis in pheochromocytoma.
- Symptoms of tissue organ damage (TOD)
• Congestive heart failure
• Coronary heart diseases
• Cerebrovascular disease
• Uremia
•Aortic dissection.
Physical examination
 1-Check BP & pulse in both arms and legs for radiofemoral delay ( aortic
 2-Fundoscopic examination :
Mild retinopathy (grade I and II): AV nicking” and “copper wire changes”
Retinal hemorrhages and exudates (grade III) and papilledema (grade IV)
reflect severe and life threatening disease.
 3-Evidence of LV failure
 4-Carotid or peripheral vascular disease
 5-Abdominal bruits (renal artery stenosis)
 6-Neurologic examination: old strokes
Initial laboratory scanning
 1.Serum electrolytes
2. Renal function
3.Urine analysis ( to DD function primary renal disease or as a result of
4. Glucose
5. Lipid levels
6.Echocardiography in selected patients.
7. ECG (LVH)
LVH by voltage criteria: S wave in V2 + R wave in V5 > 35 mm
LV strain pattern: ST depression and T wave inversion in the lateral leads
What is the difference between hypertensive urgency and emergency?
 Accelerated hypertension = Hypertensive urgency.
 - Extreme elevations of BP (SBP>200 and or DBP >120 mmHg)
- Usually asymptomatic patients.
- Without evidence of new or progressive end-organ damage.
- Antihypertensive therapy aimed at lowering BP over several hours to several days
by oral doses of fast-acting medications (β blockers, calcium blockers, ACEI)
 Malignant hypertension = Hypertensive Emergency.
- Extreme elevations of BP (SBP200 and or DBP >120 mn Hg)
- Often associated with acute end-organ damage:
- Hypertensive encephalopathy: Confusion, Visual changes, seizures, headaches and
- Death from: (Intracranial bleeding, Unstable angina, Acute MI or Left Ventricular
- Hypertensive GN: proteinuria, hematuria & acute renal failure.
- Hospital admission and therapy aimed at immediate blood pressure reduction to
limit organ damage.
- Acute organ damage may resolve after aggressive BP treatment
Secondary Causes of Hypertension
 1. Renal
- Renal parenchymal disease (GN, polycystic disease, DN)
- Renovascular disease (RAS, fibromuscular dysplasia, vasculitis)
2. Endocrine
- Hypo- or hyperthyroidism, Hyperparathyroidism
- Adrenocorticoid excess (Cushing’s, primary aldosteromsm)
- Pheochromocytoma
- Exogenous hormones (oral contraceptives, estrogen replacement).
3. Neurologic Disorders: (brain tumors, sleep apnea, spinal cord
4. Stress-Induced: Pain, anxiety
5. Toxic/ Pharmacologic: (Alcohol, NSAIDs, Ephedrine, Monoamine
oxidase inhibitors)
6. Miscellaneous: (Aortic coarctation, Carcinoid syndrome or
How can you suspect patients with secondary causes for their hypertension?
 1. Patients with new onset of hypertension at age < 30 or>55 years
2. Patients with poorly controlled blood pressure despite multiple
antihypertensive medications
3. Patients with previous controlled hypertension who develop sudden
increase in their blood pressure
 - Before we start work up for 2ry causes we have to exclude causes of
failure of adequate blood pressure control as:
1. Medical noncompliance
2. Excess dietary sodium intake.
 3.Drugs as oral contraceptives, corticosteroids. NSAID, over-thecounter cold remedies containing ephedrine or sympathomimetics
How can you suspect patients with renal artery stenosis?
 1. Sudden development of severe hypertension in a patient without a
family- history of hypertension
2. Drug-resistant hypertension
3.The presence of diffuse atherosclerotic disease or an abdominal bruit.
4. Renal insufficiency in the settilig of severe hypertension
5. Worsening of renal function after institution of ACE inhihitor
 Diagnosis
1. Plasma renin activity is normal or high and increased after ACE inhibitor.
NB: Low plasma renin excludes RAS.
2. Nuclear renal scan perfusion and after administration of ACE inhibitors
3. US: decreased size’ of the affected kidney.
4. Definitive diagnosis: angiography> MRA.
 Treatment:
 Surgical or balloon angioplasty
Primary hyperaldosteronism:
 - Unilateral adrenal adenoma (Conn ‘s syndrome) & more common in women.
- Bilateral adrenal hyperplasia & more common in men.
- Asymptomatic in most cases.
- Hypokalemia: muscle eramps. Palpitations, polyurria.and polydipsia
 How can you suspect patients with primary hyperaldosteronism?
- Hypertension and spontaneous hypokalemia
- Hypertension and severe hypokalemia after treatment with diuretics
 Diagnosis:
- Low Plasma renin level: screening test
- High urine aldosterone levels
- Definitive diagnosis: high serum aldosterone is not suppressed after saline.
- CT differeniate between adrenal adenomas and hyperplasia.
 Treatment:
 Surgery for solitary adenomas or spironolactone
 - A rare catecholamine-producing tumor arises from the chromaffin
cells of the neural crest. 85% of these tumors are located in the
adrenal medulla
- 10% bilateral, 10% malignant & 10% extra-adrenal (sympathetic
chain) & 10% multiple tumors in familial syndromes MEN 2
- Adrenal pheochromocytomas secrete predominantly epinephrine
=> systolic hypertension, tachycardia, hyperhidrosis, flushing, and
- Extramedullary tumors secrete mainly norepinephrine => systolic
and diastolic hypertension.
- The secretion of catecholamines is episodic = <wild fluctuations in
blood pressure = <Hypetensive crises and strokes
How can you suspect patients with
 The complex of headaches, sweating episodes, and tachycardia.
 Diagnosis:
1- Laboratory diagnosis: ↑ serum or urine catecholamines or their
metabolites (vanillylmandelic acid or metanephrines).
2- Radiological Localization: CT or MRI, nuclear scanning
 Treatment:
- Surgical resection with preoperative: β blockade, α cblockade,
and volume expansion
- Chronic α blockade therapy for unresectable tumors
Treatment of Hypertension
 The goal: Prevent long-term morbidity and mortality.
 Non -pharmacologic therapy for 3 to 6 months (Lifestyle
- Smoking cessation - weight reduction - Regular aerobic exercise Avoid alcohol
- Restriction of dietary sodium intake.
 Pharmacologic therapy
- β Blockers and diuretics are the initial drugs of choice for mild to
- β Blockers for patients with Coronory heart diseases
- Diuretics and ACEI for patients with depressed LV systolic function
or HF.
- ACE inhibitors slow the progression of nephropathy in patients with
Preferred drug
Problematic drug
β B & D in high dose
Systolic HF
β B* & CCB**
diastolic HF
β B & CCB
CCB (short acting
β B & ACEI
CCB (Nifedipine)
Aldomet & Hydralazine
Receptor blockers &
D & ACEI (if creatinine
Receptor blockers &
ACEI & K- sparing D.
* Except Carvedilol
β B : Beta Blocker
D : Diuretic
CCB: Calcium Chanel Blocker
** Except Amlodipine & Felodipine
ACEI : Angiotensin Converting enzyme inhibitor
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Thank You

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