Hypertension

Alemwosen T.(MD, asst prof in

Pathology)
 Hypertension
Elevated blood pressure
Sustained DBP greater than 90 mm Hg, or a sustained SBP
in excess of 140 mm Hg
25% of persons in the general population are hypertensive
Affects more than 800 million individuals worldwide
Prevalence and vulnerability to complications increase
with age and, for unknown reasons, are high in African
Americans
 Hypertension
Common health problem with occasionally devastating
outcomes
Epidemiologic data indicate that SBP is more important than
DBP as a determinant of CV risk, except in young individuals
Remains asymptomatic until late in its course
Contributes in the pathogenesis of
Coronary heart disease
Cerebrovascular accidents
Cardiac hypertrophy and heart failure (hypertensive heart disease)
Aortic dissection
Renal failure
 Blood Pressure Regulation
Blood pressure is one of the most variable but well
regulated functions of the body
The main determinants of BP are cardiac output
and peripheral vascular resistance
Cardiac output = SV X HR
Peripheral vascular resistance reflects change in the
radius of the arterioles as well as viscosity of the
blood
Poiseuille's equation
TPR = viscosity of blood/(radius of arteriole)4
 Mechanisms of BP Regulation
Short term regulation intended to correct
temporary imbalances in BP such as those that
occur during physical exertion and change in body
position
Neural mechanisms baro receptor reflex and
chemoreceptor mediated reflex
Hormonal mechanisms Renin-Angiotensin aldosterone
mechanism, vasopressin (ADH)
Long term regulation mainly renal mechanisms
Cardiac output
Affected by blood volume,itself strongly dependent on
sodium concentrations
Peripheral resistance
Regulated predominantly at the level of the arterioles
Influenced by neural and hormonal inputs
Normal vascular tone reflects an interplay between
circulating factors that induce vasoconstriction (e.g.,
angiotensin II and catecholamines) and vasodilation (e.g.,
kinins, PGs, and NO)

NB:The integrated function of these systems ensures

adequate systemic perfusion, despite regional demand
differences
 Etiological classification of HTN
Essential hypertension - idiopathic
- 90 % to 95% of HTN
Secondary hypertension
Hypertension as a result of other disorders
5% to 10% of HTN
Primary aldosteronism
Cushing syndrome
Pheochromocytoma
renovascular disease
Coarctation of aorta
Drugs
,etc
Causes of secondary HTN
 Clinical course classification of HTN
1.Benign hypertension (95%)
A chronic and relatively mild increase in systemic arterial
blood pressure (DBP not higher than 110 to 120 mm Hg)
may or may not have an underlying cause
compatible with long life, unless a myocardial infarction,
cerebrovascular accident, or other complication
supervenes
 2. Accelerated or Malignant hypertension
~ 5% of hypertensive persons show a rapidly rising BP
that if untreated leads to death within 1 or 2 years
Clinical syndrome is characterized by:
Severe hypertension (SBP over 200 mm Hg DBP over
120mmHg)
Renal failure
Retinal hemorrhages and exudates, with or without
papilledema.
May develop in previously normotensive persons but
more often is superimposed on preexisting benign
hypertension, either essential or secondary
 Diagnosis of Hypertension
Obtaining one elevated BP record should not constitute
the diagnosis of hypertension
Two or more readings at each of the two or more visits
BP should be taken when person
Relaxed and rested for at least 5 minutes
Has not smoked or ingested caffeine within 30
minutes
 Essential Hypertension
Results from an interplay of multiple genetic and environmental
factors affecting CO and/or peripheral resistance
Although the cause or causes of hypertension are largely unknown
several risk factors have been implicated as contributing to its
development
Risk factors
Family history
Age
Race
Insulin resistance and metabolic abnormalities
Lifestyle factors
Excess alcohol consumption
Oral contracetives
 Reduced renal sodium excretion in the presence of normal
arterial pressure is probably a key initiating event of HTN
 Clinical Manifestations of HTN
Essential HTN is typically an asymptomatic disorder
When symptoms occur they are due to long term effects
of HTN on other organs like kidneys, heart, eyes and
blood vessels (target organ damage)
Hypertension is a major risk factor for atherosclerosis
 Target Organ Damage
Heart
Most common cause of death in HTN patients is
heart disease
Left ventricular hypertrophy
Diastolic heart failure
Coronary artery disease
Cardiac arrhythmia
 Target Organ Damage- contd
Brain
Hypertension is an important risk factor for both
brain infarction and hemorrhage
Malignant HTN failure of cerebral auto regulation
with vasodilatation and hyper perfusion
Presents with severe headache, nausea, vomiting,
focal neurologic signs and altered mental state
If not treated promptly- stupor, coma, seizure and
death within hours
 Target Organ Damage- contd
Kidney
Hypertension is a risk factor for renal injury and
ESRD
HTN also accelerates the rate of progression of
other types of kidney diseases like diabetic
nephropathy (DM pts BP should be maintained <
130/80)
Malignant HTN fibrinoid necrosis of the afferent
arterioles sometimes extending into the glomerulus
and may result in focal necrosis of glomerular tuft
 Target Organ Damage- contd
Vessels
Accelerates atherogenesis
Hypertension-associated degenerative changes in the walls of
large and medium arteries can potentiate both aortic
dissection and cerebrovascular hemorrhage
 Target Organ Damage- contd
Peripheral arteries
Atherosclerotic disease secondary to long standing
HTN
Intermittent claudication is the classic symptom of
peripheral arterial disease
Aching pain in the calves and buttocks while walking that is
relieved by rest
 Target Organ Damage- contd
Small blood vessel
1. Hyaline arteriolosclerosis
Homogeneous pink hyaline thickening of the walls of arterioles
Encountered frequently in elderly patients, whether normotensive or
hypertensive & DM pts
More generalized and more severe in patients with hypertension
Reflect leakage of plasma components across vascular endothelium and
excessive ECM production by SMCs secondary to the chronic
hemodynamic stress of hypertension
 Target Organ Damage- contd
Small blood vessel
2. Hyperplastic Arteriolosclerosis
Related to more acute or severe elevations of blood pressure
Hyperplastic arteriolosclerosis is characteristic of (but not limited to)
malignant hypertension
Associated with "onion-skin," concentric, laminated thickening of
the walls of arterioles with luminal narrowing
Accompanied by fibrinoid deposits and vessel wall necrosis
(necrotizing arteriolitis), particularly prominent in the kidney
 Treatment of Hypertension
Goal of treatment
Maintain BP < 140/90 mmHg
In patients with Diabetes or other renal disease
goal should be to maintain BP<130/80 mmHg
For patients with secondary hypertension
efforts should be made to correct or control
the disease condition causing hypertension
Lifestyle modification
Pharmacologic treatment
 ANEURYSMS
Aneurysm is a localized abnormal dilation of a blood vessel
or the heart
Atherosclerotic, syphilitic, and congenital aneurysms, and
ventricular aneurysms
"true" aneurysm or pseudoaneurysm ("pulsating
hematoma")
 The two most important causes of aortic aneurysms are
atherosclerosis and
cystic medial degeneration of the arterial media
Other causes that weaken vessel walls and lead to
aneurysms include:
Trauma
Congenital defects (e.g., berry aneurysms)
Infections (mycotic aneurysms), or syphilis
systemic diseases, such as vasculitis
 Abdominal Aortic Aneurysm(AAA)
Atherosclerosis is the most common cause of aneurysms
Atherosclerotic aneurysms occur most frequently in the
abdominal aorta
The common iliac arteries, the arch, and descending parts of the
thoracic aorta can also be involved
Hereditary defects in structural components of the aorta can
produce aneurysms (e.g., defective fibrillin production in Marfan
disease affects elastic tissue synthesis)
 The clinical consequences of AAA include:
Rupture= fatal hemorrhage
Obstruction of a branch vessel=infarction
Thrombus - Embolism
Impingement on an adjacent structure
simulates a tumor = palpably pulsating
atherosclerosis in other vascular beds = IHD,stroke
 Aortic Dissection (Dissecting Hematoma)
Catastrophic event characterized by dissection of
blood between & along the laminar planes of the
media
Formation of a blood-filled channel within the aortic
wall
Often ruptures outward, causing massive hemorrhage
 Aortic dissection occurs principally in two
epidemiologic groups:
Men aged 40 to 60 years, with antecedent
hypertension (> 90% of cases of dissection)
Younger patients with systemic or localized
abnormalities of connective tissue affecting the aorta
(e.g., Marfan syndrome)
Clinical Course of aortic dissection
depends strongly on the level of the aorta affected
most serious complications occur with dissections that
involve the aorta from the aortic valve to the arch
classic clinical symptoms of aortic dissection are the
sudden onset of excruciating chest pain
most common cause of death is rupture
 Aortic dissections are classified into two types
Type A dissections
More common (and dangerous)
Proximal lesions involving either the ascending aorta
only or both the ascending and descending aorta
Type B dissections
Distal lesions not involving the ascending part
Usually beginning distal to the subclavian artery