Medicine

Dr. Abdulla Lec: -1-

16.10.2006

Hypertension
• Elevation of pressure in the vascular system above the normal limits that
causes increased morbidity & mortality.

Aetiology:
• In > 95% a specific cause could not be found called ( essential HT).
• The exact cause of essential HT is not known, but explained by
abnormalities in the renal, peripheral vascular resistance & sympathetic
nervous system & mostly multifactorial on genetic bases which is
contributory in 50%.
• It is > in blacks & Japanese.
• Enviromental factors: salt, alcohol,obesity, sedentary life & IUGR & ?
stress.

Aetiology: secondary causes

• Alcohol, obesity, pregnancy( PET).
• Renal diseases: Renal vascular diseases, paranchymal specially
glomerulonephritis,APKD
• Endocrine diseases: pheo,cushing,Conns,
hyperparathyroidism,acromegaly,hypothroidism,
• Cong adrenal hyperplasia.
• Liddle syndrome.
• Coaractation of Aorta.
• Drugs: OC,Anabolic steroid,AXTH, NSAID, Carbenoxole,
sympathomimetics.

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BP Measurement:

• Diagnosing HT means life-long drug treatment, so accurate measure of

BP is essential.
• BP should be made to the nearest 2mm Hg, in sitting position with the
arm supported, repeated after 5 mins if the first reading is high & take 2
measurement at each visit.
• The cuff’s bladder should encircle at least 2/3 of the arm, to avoid false
high readings in obese.
• Use validated calibrated well maintained instrument.
• Measure sitting & additional standing in DM, elderly & suspected
postural hypotension.
• Remove tight clothes from the arm.
• Lower mercury slowly 2mm/second.
• Use phase five for diastolic BP measurement.

HT: Definitions
• Optimal <120/<80
• Normal <130/<85
• High normal 130-139/85-89
• HT (grade 1, mild): 140-159/90-99
• HT ( grade 2, moderate): 160-179/100-109
• HT ( grade 3, severe): = > 180/=>110
• Isolate systolic HT:
• Grade 1: 140-159/<90
• Grade 2 => 160/ <90

Home BP measurement

• White- coat HT:

• Patients may be hypertensive in the doctor’s clinic but not in their home if
they measure BP by automated devices in their home.
• They have less CV Risk than those with sustained HT, but more than
normotensive general population.

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Ambulatory 25 hour BP measure:
• Provides better BP profile than occasional Office measures.
• Correlates better with evidence of end – organ dmage.
• They are about 12/7 mm Hg lower than office measures & average
ambulatory daytime( not 24 hour) measures should be used to guide
treatment.

Home &ambulatory BP measure:

• Specially useful for:

• Patients with labile HT.
• Patients with refractory HT.
• Patient eperiencing symptomatic hyoptension.
• If white-HT suspected.

History:
• Family history of HT.
• Life style: exercise, salt intake, smoking, habits).
• Other risk factors of CV diseases as DM, obesity, lipids.
• Drugs as OCP, alcohol.
• Symptoms of secondary causes as pheo (paroxysmal headache,
palpitation, sweating).
• Complications or end-organ damage of HT: as CAD as angina, dyspnea.

Physical exam:
• Majority of abnormal finding are due to complications of HT: as deviated
apex beat& heave due to LVH,loud S2, 4th heart sound, CHF features,
peripheral vascular disease, hypertensive retinopathy on opthalmoscopic
exam & aortic aneurysm on abdominal palpation.
• Radio-femoral delay: coarctation of aorta.
• Enlarged kidneys: APCK.
• Abdominal bruits( RAS).
• Moon face, buffalo hump & striae: cushing syndrome.
• Evidence of risk factors: obesity, zanthomas of hyperlipidemias.

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Target organ damage:
• Include blood vessels, CNS, Retina, heart & kidneys.

Blood vessels:
• HT accelerates athreosclerosis in the large & medium sized arteries
leading to narrowing of major organ arteries causing CAD, CVA, Renal
artery disease & peripheral vascular disease.
• Atherosclerotic Vascular narrowing further aggravates Hypertension by
increasing total peripheral vascular resistants & by causing renal artery
stenosis.
• HT also contributes to aortic aneuysms & discetions.

CNS:
• Stroke( CVA) is more common in HT either due to haemorrhgae(
intracerebral or suarachnoid) or infarction.
• Carotid atheroma & TIAs are more common in HT.
• Hypertensive encephalopathy: is a rare condition occurs in association
with malignant HT (usually diastolic BP > 120 with papiledema or retinal
haemorrhages or soft retinal exudates) & transient reversible
neruological deficit as transient dysphasia, parasthesia, vision
disturbances, disorientation, fits & CT frequently shows hemorrhages in
& around the basal ganglia.

Retina:
• HT causes retinopathy & degree of retinopathy correlates with severity of
HT.
• Fundoscopic findings can be an indicator of the arteriolar changes in
other parts of the body.
• HT is also associated with central retinal vein thrombosis.

• Grades of hypertensive retinopathy:

• Grade 1: Arteriolar thickening, turtuosity & increased reflectiveness
( sliver wiring).
• Grade 2: Above+ veins constriction at sites of arterial crossings( AV
nipping).
• Grade 3: above + retinal ischemia (flame-shaped or blot hemorrhages&
cotton-wool exudates; indicative of ischemia or infarction fade in few
weeks).
• Grade 4: grade 3+ papiledema.
• Hard exudates & microaneurysma 9 dot hemorrhages) are more
indicative of diabetic retinopathy than of hypertensive retinopathy.

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Heart:
• The high morbidity & mortality of HT is mainly due to excess incidence
of CAD.
• HT causes: LVH, LVF, CHF, CAD, AMI,AF.
• ECG & Echo finding of LVH is highly predictive of CV complication so
very important in risk assessment.
• Sever HT can LVF in the absence of CAD specially when renal function is
impaired causing impaired Na excretion.

Renal:
• Long-standing HT can cause proteinurea & progresive glomeruloscelosis
& renal failure.
• Sometimes it is difficult to find which of them is the cause of the other;
HT or CRF.

Malignant HT:
• Can complicate both essential & secondary HT.
• It is severe HT& rapidly progressive end organ damage with grade 3 or 4
HT retinopathy with or without HT encephalopathy or other organ
failures as acute renal failure or acute LVF.
• High mortality within months if not treated urgently.
• Pathologicly there are fibrinoid necrosis of arterioles 7 small arteries &
intravascular thrombosis.

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Investigations: all
• GUE: for protein, blood & sugar.
• B.Urea, S. Creatinine.
• S. electrolytes: hypokalemia usually is due to use of diuretics but may
indicate hyperaldosteronism.
• FBS.
• Serum total cholesterol & HDL.
• ECG: for LVH & CAD.

Investigations: Selected patients

• CXR: To detect LVH,HF, Coaractation of aorta.
• Ambulatory BP: for borderline or white-coat HT.
• Echo: to detect or quantify LVH.
• Renal angio: for suspected RAS if clinically suspected.
• Urinary catecholamines: for suspected pheochromocytoma.
• Urianary cortisol & DST to detect suspected cushing.
• Plasma renin activity & aldosteron for suspected primary aldosteronism.