hypertension
DESCRIPTION
Hypertension. Definition. Sustained elevated blood pressure in a quiet state is called- hypertension. Diagnostic criteria proposed by WHO. systolic pressure. diastolic pressure. classify. Normal BP.TRANSCRIPT
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Hypertension
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Sustained elevated blood pressure in a quiet state is called- hypertension
Definition
Diagnostic criteria proposed by WHO
classify systolic pressure diastolic pressure
Normal BP <140mmHg <90mmHg
Grade 1 hypertension
Grade 2 hypertension
Grade 3 hypertension
140-159mmHg
160-179mmHg
>180mmHg >110mmHg
100-109mmHg
90-99mmHg
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Types Essential hypertension
Secondary hypertension
Cause Not Yet Clear
Cause Clear
Secondary hypertension is secondary from renal, endocrine and nervous system diseases, much as temporarily, after a good treatment of the primary disease, hypertension will fade away.
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Pathogenesis
Blood pressure is proportional to cardiac output and peripheral vascular resistance.
Any fators that can cause the above two aspects
rising may be concerned with high blood pressure
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Pathogenesis
Major factors
Genetic factors
Dietary factors
Environmental factors
Other factors
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Genetic factors
Familial aggregation: parents: 2-3 times, morbidity of children
single-parent: 1.5 times
Serum hormone-like substance
Inhibition of Na / k-ATP enzyme
activity
Concentration of
intracellular Na, Ca ion rise
Contraction of small artery
Angiotensin gene encoding variability
Influenced by multiple genetic and acquired factors
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Dietary factors
Excessive sodium intake
sodium intake <5g/d
Potassium promote sodium excretion
Eat a lot of vegetables
Calcium can reduce the pressor effect of
sodium
High calcium diet
The three imbalance cause hypertension
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Epidemiological and clinical observations have shown
there is a close relationship between salt intake and
hypertension 。Extracellular fluid volume Cardiac output
Vascular smooth muscle cell Na + Intracellular Ca + +
Vasoconstriction
(peripheral vascular resistance rise)
BP
salt intake
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Environmental factors
Long term mental stress, pressure
Vasomotor regulation be out of control
The vasoconstrictor
effect is dominant
Peripheral resistance
BP
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Other factors
Overweight or obesity
Smoking
Age
Lack of physical activity
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Extracellular fluid
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Types and pathological change
benign hypertension ( chronic hypertension )
malignant hypertension ( accelerated hypertension )
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Process mainly involves small arteries and arterioles , evokes spasm 、 hardening and affects some important organs.
Benign hypertension may be divided into three stages:
benign hypertension
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Dysfunctions period
Arterial system changes period
Visceral lesions period
• small arteries
• arterioles
• elastic arteries
heart
cerebrum
kidney
retina
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Dysfunctions period
•The whole body small arteries and arterioles spasm, no organic disease
•BP increased occasionally
•Clinical symptom appear occasionally, BP will return to normal after a rest
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Arterial system changes period
•Hyaline arteriolosclerosis: Hyaline arteriolosclerosis: Hyaline arteriolosclerosis Hyaline arteriolosclerosis is a major morphologic characteristic.is a major morphologic characteristic.
•Arteriolar sclerosisArteriolar sclerosis
•Elastic arteries appear AS.
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Hyaline arteriolosclerosisHyaline arteriolosclerosis : The arteriolar wall is hyalinized, and the lumen is markedly narrowed
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Arteriolar sclerosis
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Clinical features:
May be associated with AS lesions
Further raise of blood pressure, and continued at high levels. Lose Fluctuation.
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Visceral lesions period
Heart : Left ventricle Compensatory hypertrophy
Concentric hypertrophy
Eccentric hypertrophy
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Normal heart
Concentric hypertrophy wall thickening, heart cavity to narrow
Eccentric hypertrophy wall thickening, heart cavity enlarge
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Microscopically features : cardiocytes are thicker 、 elongate, nucleus is bigger and hyperchromatic.
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Clinical feature
myocardial ischemia , finally progress to heart failure
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kidney : Primary granular contracted kidney
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Microscopically features :•Renal arteriolar sclerosis, hyalinization
•Sclerosis and hyalinization of some glomeruluses. Visible compensatory hypertrophy of the other glomeruluses
•Atrophy and disappearance of some renal tubules. Visible compensatory dilatation of the other renal tubules
•Hyperplasia of interstitial connective tissue, infiltration of lymphocytes
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dilatation of some renal tubules
compensatory hypertrophy of some glomeruluses
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Bilateral renal symmetry reduction. Texture hardening, renal surface uneven, with fine granules
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Cerebral lesion
1 ) Cerebral edema: headache, dizziness, vertigo and so on
2 ) Hypertensive encephalopathy: the syndrome of central nervous dysfunctions caused by acute cerebral edema and intracranial hypertension. Blood pressure increased significantly, severe headache, vomiting, convulsions and coma.
3 ) Cerebral softening: cerebral ischemic infarction
4 ) Cerebral hemorrhage: known as stroke. The most serious complication of hypertension
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Cerebral softening: cerebral ischemia occurs anemic infarct, liquefaction, forming a loose texture mesh lesions. Necrosis of brain tissue repaired by the proliferation of glial cells, because the lesions were smaller, generally do not cause serious consequences.
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loose mesh lesions
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Hypertensive retinopathy
The central artery arteriolosclerosis, ophthalmoscope see vascular tortuosity, reflecting enhancement, arteriovenous crossing compression, papilledema, retinal hemorrhages and exudates.
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Central retinal artery can occur hardening. ophthalmoscope shown vascular tortuosity, pale, with bleeding
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In youth, diastolic pressure is often greater than 130mmhg, can be secondary from chronic hypertension, but often from primary.
features: 1 ) Hyperplastic arteriolosclerosis: intima and smooth muscle cell hyperplasia, collagen fibers increased significantly, the vessel wall, a concentric lamellar thickening, called onion-skinonion-skin change. 2 ) Necrotizing arteriolitis: fibrinoid necrosis of the intima and medial.
Patients death in a year due to uremia, cerebral hemorrhage and heart failure.
malignant hypertension ( accelerated hypertension )
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Hyperplastic arteriolosclerosis (onionskinning) causing luminal obliteration, with secondary ischemic changes
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fibrinoid necrosis
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Benign Malignant
Morbidity high ( 90% ) low ( 10% )
Age The middle-aged or older The young and middle-aged
BP > 150/95mmHg Persistent diastolic pressure
130 ~ 140mmHg
Symptom mild severity
changes Hyaline arteriolosclerosis Hyaline arteriolosclerosis Hyperplastic arteriolosclerosis
Necrotizing arteriolitis
Course of disease > 10years 1 ~ 2 year
cause of death Cerebral hemorrhage, Renal failure,uremia ( 95% ),
heart failure Cerebral vascular accident
The distinction between benign and malignant hypertension