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Hypertension: Medicine

This document discusses hypertension (HT), including its definition, causes, risk factors, diagnosis, target organ damage, and investigations. HT is defined as a blood pressure above 140/90 mmHg. The majority of cases are essential HT, while secondary HT can be caused by factors like renal disease or drugs. Accurate blood pressure measurement is important for diagnosis. Home and ambulatory monitoring provide better profiles than occasional office readings. Target organ damage from HT includes effects on blood vessels, brain, eyes, heart, and kidneys. Investigations help identify secondary causes and assess organ damage risk.

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51 views

Hypertension: Medicine

This document discusses hypertension (HT), including its definition, causes, risk factors, diagnosis, target organ damage, and investigations. HT is defined as a blood pressure above 140/90 mmHg. The majority of cases are essential HT, while secondary HT can be caused by factors like renal disease or drugs. Accurate blood pressure measurement is important for diagnosis. Home and ambulatory monitoring provide better profiles than occasional office readings. Target organ damage from HT includes effects on blood vessels, brain, eyes, heart, and kidneys. Investigations help identify secondary causes and assess organ damage risk.

Uploaded by

api-3829364
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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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.

1
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.

2
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.

3
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.

4
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.

5
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.

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