1. Hypertension
Arterial blood pressure depends on cardiac
output () and peripheral resistance (R). In people with normal blood pressure
is relatively stable due to the regulatory mechanisms of neural and humoral.
Hypertension occurs when increased cardiac output or increased peripheral
resistance, or increase both factors on which the regulatory mechanisms of the
body is no longer valid.
As defined by the World Health Organization,
an adult is called hypertension as blood pressure ≥ 140 mmHg maximum and / or
blood pressure ≥ 90 mmHg minimum.
1.1. Complications of hypertension
- Complications artery: The first stage only
tone, alone, increased intravascular pressure. Period following injury,
fibrosis is common to the heart arteriolar narrowing or blockage causing
increased peripheral resistance. At this stage, there may be more
atherosclerotic plaques. The collaboration between hypertension and
atherosclerosis promote the development of different and increasingly aggravate
the condition.
- Complications retinal artery: 4 Level:
• Level 1: The narrowing of the arteries,
hard look.
• Level 2: Hard Arteries cross vein, Gunn
sign (+).
• Level 3: Advanced Production and retinal
bleeding.
• Level 4: papilledema.
- Heart Complications: High blood pressure
causes increased pressure in the left ventricle leads to myocardial
hypertrophy, accelerating the progression of coronary atherosclerosis. The
combination of increased demand and decreased oxygen supply to the heart muscle
causes myocardial ischemia leading to high rates of myocardial infarction,
stroke, arrhythmia and heart failure. The cardiac complications in
hypertension: reduction of left ventricular function; left ventricular
hypertrophy; coronary artery disease; myocardial infarction; congestive heart
failure.
- Complications brain: Include expression
transient ischemic, hypertensive encephalopathy, stroke and cerebral infarction
include cerebral hemorrhage, meningitis is fatal and serious sequelae.
- Renal Complications: Exercise is the target
organ complications of hypertension. Clinically, in a long time, patients do
not have symptoms or only subtle symptoms until it has physical damage, kidney
failure to appear, but no signs of aggressive
1.2. The situation of hypertension in some
countries in the world
The prevalence of hypertension in developed
countries are quite high: in Italy
is 38%, Sweden 38%, UK 42%, Spain
47%, Finland 49%, Germany 55%, Switzerland 32%. In the United States
government as a national program to prevent hypertension should be controlled
now at 28%, although still quite high. Asian countries as well as countries in
the region, the rate of hypertension was lower in Europe but also high: 36% of India , Nepal
20%, Singapore 26%, China 27%, Malaysia
24 %, Pakistan 23%, 29% of Hong Kong , Sri Lanka
20%, Korea 34%, Japan 45%. In
Africa Research in Zambia
in 2011 was 34.8% rate of hypertension [69]. In the US , despite a national program from
the 70s of the 20th century, but the rate control blood pressure goal
(<140/90 mmHg) was only 29%. In Canada
the rate is 17%, and Europe at around 10%. In
Canada in 1986 - 1992, studied 2551 people from 20-79 years of age, the rate of
hypertension 21.3% of which 65.7% were treated, 14.7% were treated
intermittently, 19 , 5% of untreated (13.7% of them have no idea hypertension).
A study in the US
in 1999 - 2000 persons in 1565, the rate of hypertension was 28.7%. Research
shows that over 40 million Americans have high blood pressure is not treated.
In China
analysis of 13 studies in 1998 on a 13,500 adults aged 35-59: results showed
that 24% of hypertension in 42% recognize that condition, 31.1% were treated,
6% were control of blood pressure.
1.3. The situation of hypertension in Vietnam
1960, according to a survey of Dang Van
Chung, hypertension rate in Vietnam
is 2-3%. In 1982, according to a survey of Khue Pham et al, the rate of
hypertension in general is 1.95% and the proportion of people over 60 years of
hypertension was 9.2%. By 1992, according to the epidemiological investigation
of Tran Do Trinh et al, sampling over 36,000 people in eight ecological
regions, the rate of hypertension in Vietnam has increased by 11.7%.
Following that investigation, 1999 Pham Gia Khai et al, the rate of
hypertension in Hanoi
increase is 16.05%. The most recent survey (2008) of the Institute of Cardiology Vietnam
as a result of 23% correctly identified the risk of hypertension. In 818 people
diagnosed with hypertension, only 94 people are taking blood pressure and the
rate is 19.1% better control.
2.Ton kidney damage due to hypertension
The initial lesion is functional lesions
occur in a very long time, reversible if treated, only to later stages,
fibrosis developed new lesions appear entity of the renal artery and two
atrophied kidney fibrosis. In hypertension, decreased renal output but
glomerular filtration rate remained help maintain kidney function, but in the
long term damage and progressive end-stage renal failure.
Chronic kidney disease as defined by the
American Nephrology Association 2012 [88] is the status of kidney damage
associated with prolonged expression signs histopathological lesions, signs of
prolonged urinary albumin, change the image of kidney , decline in glomerular
filtration rate below 60 ml / min.
The stages of chronic kidney disease:
- Phase 1: kidney damage, glomerular
filtration rate constant or increases above 90 ml / min.
- Phase 2: kidney damage, glomerular filtration
rate reduction of 60-90 ml / min.
- Phase 3: glomerular filtration rate
decreased on average 30-59 ml / min.
- Stage 4: severe reduction in glomerular
filtration rate 15-29 ml / min
- Stage 5 CKD, reduced glomerular filtration
rate below 15 ml / min
2.1. The pathogenesis of kidney damage caused
by hypertension
Hypertension, chronic systemic arterial blood
vessel damage related to the three mechanisms, such as pressure intravascular
flow, changes in vascular endothelial cells, blood vessels restructuring ..
- Flow with high pressure vessels become
stiffer. Arterial pulse wave propagation hard work faster, so the pressure
vessel ventricular response back from the peripheral arteries earlier. Echo
occurs during diastole, increased pressure in the aorta and left ventricle
during systole. So, hypertension overloading is due to increased peripheral
vascular resistance, due to the hard arteries, reducing the elasticity of the
aorta and early feedback from the periphery.
- Changes in vascular endothelial cells by
increasing the flow pressure: damage including fibrosis and endothelial
thickness, slots between the dilated endothelial cells, endothelial fibrosis
beneath. The smooth muscle cells migrate from the middle class to the lower
layer of endothelial cells, manifested most clearly in that division of the
artery.
- Restructuring angiogenesis and
proliferation of vascular smooth muscle cells: the cells under a layer of
smooth muscle vascular proliferation, thickening of arterial medial migration
and the bottom layer of endothelial cells. The change over to make a thick
arteries become stiffer. Disease progression will appear hyaline layer of the
arterial wall and fibrosis of arteries, causing narrowing of the arteries. Medial
injury continues to evolve, can lead to gangrene and medial aneurysm formation.
The small aneurysm occurs, first place in the branch arteries.
2.2. The role of system rennin - angiotensin
- aldosterone in relation to blood pressure and kidney function
Renin is an enzyme protein, is released from
care organizations access to reduced glomerular extracellular fluid volume.
Renin raise the blood pressure effects of low levels return to normal. Renin
acts on a plasma protein is essentially globulin angiotensinogen to angiotensin
I. The change of NaCl create a signal flow to the kidney marrow cells reach.
The decrease in the concentration of Na + will cause increased nNOS and
COX-conditioned 2, increased synthesis of prostaglandins and catecholamines
PGs, activate the synthesis of cAMP, which was created renin in the kidney
marrow cells reach. Increasing NaCl transport reduces ATP levels and increased
levels of ADO . ADO will diffuse to reach
medulla cells, inactivation of AC and the creation of renin through Gi protein
A1 receptor. The increased transport of NaCl in the wound can also increase the
phenomenon of secretory of ATP and thus can cause inhibition of the secretion
of renin directly through receptor P2Y and activation route Gq-PLC-IP3-Ca2 +
access marrow cells in the kidney. AngII circulation can also inactive renin
secretion via the AT1 receptor. Renin is the decisive factor AngII number will
be generated. It is synthesized, stored and secreted into the systemic
circulation by renal artery access granule cells located in the medulla of the
arteries in the glomeruli.
There are many types of tests including renin
total renin (PRC-plasma rennin Concentration), rennin activity (PRA- plasma
retinal activity), rennin inactivated (IRC-inactive renin Concentration).
Activated renin (PRA) is a form of rennin activity has a direct effect
regulates blood pressure. Normal levels of renin in the blood is 0.29 to 3.7 mg
/ l. Increase in primary hypertension, malignant hypertension, renal artery
disease.
The mechanism of action of angiotensin in
renal directly caused by contraction renal arterioles go, thus increasing the
glomerular filtration rate. This mechanism helps regulate renal blood flow.
Stimulate adrenocortical aldosterone secretion, the hormone increases the absorption
of sodium and water in the renal tubules. Increased water reabsorption in the
kidney (due to the influence of ADH is secreted from the post-yen). Also
Angiotensin also stimulates the thirst center, increases in water and the
response of the central sympathetic system increases blood pressure.
2.3. Histopathological lesions renal
hypertension
In the kidney, early lesions found in the
blood vessels and arteries to glomerulonephritis, including arteries in the
glomeruli. Basic is hyaline lesions of medial arterial wall in the glomeruli,
leading to damage to the glomerular capillary coil section.
Characterized by damage to the
endothelium. Endothelial cells have room peeling off the membrane, creating the
cavity is filled with the material in plasma and collagen, causing narrowing of
the arteries. In addition, the medial necrosis, collapse of the glomerular
capillary tufts anemia.
The first stage of hypertension, found
increased plasma flow through the kidneys, and increased hydrostatic pressure
in glomerular capillaries, which appear microalbuminuria. Later stage
progressive glomerular sclerosis up, reduced glomerular filtration rate and
renal failure.
2.4. Progression of renal disease due to
hypertension
American Society Nephrology 2012 classification
of chronic kidney disease and chronic renal failure in stages as follows:
The first phase is the period of increased
renal ultrafiltration, increased kidney size, characterized by increased
glomerular filtration rate of 20-50% compared with the age of the patient.
Increased pressure within the glomeruli become the cause kidney damage. Most of
the signs outside the blood pressure has no symptoms in other organs such as
the eyes, heart, kidney disease signs also appeared much later.
The next phase progresses silently with
microalbuminuria normal or near normal (20μg / min), appear in 90-95% patients
1-5 years. Glomerular filtration rate is normal in most patients. When
histopathological examination found relaxing capillaries and glomerular
basement membrane thickening. This phase signal microalbuminuria is important
in evaluating patients and treatment monitoring. Each day an adult normal
excretion from 150 to 200 mg of protein in the urine. However, only 10-20 mg of
protein is albumin. If the amount of albumin excretion in urine 30 mg / day,
there are unusual: in the range 30-299 mg / day is called microalbuminuria
amounts (microalbuminuria) and 300 mg / day or more, known as albuminuria
Forest ready (overtalbuminuria). Albuminuria reflects endothelial dysfunction
Body: Urinary Albumin-often seen as a marker of kidney lesions. Especially in
obese patients with diabetes. There are some people with hypertension but never
progressed to hypertensive renal disease. But they can have the stage of kidney
damage manifested, for example, during an acute onset, or after heavy exercise
after a meal rich in protein ... At this point the microalbuminuria may
increase, even with proteinuria, but then returned to normal levels. Urinary
albumin excretion may fluctuate as a result, so only diagnose microalbuminuria
or clinical albuminuria when at least two of three urine samples were taken
over a period of 3-6 months for abnormal results. This change is also one of
the causes of the differences in the incidence of microalbuminuria in patients
hospitalized by a study in the UK ,
the US is about 20%, while
in Europe , with about 12 %. 19% of patients
with disease duration is relatively short (1-5 years), were found to have
microalbuminuria. Many researchers agree that, with hypertension, disease
duration is closely related to the incidence of microalbuminuria, up to 40-50%
positive disease after 30 years. Incidence is usually estimated at about 2%,
this rate will be reduced if good blood pressure control. Factors related to
microalbuminuria is state controlled hypertension, retinopathy, abnormal blood
lipids.
Later stage, vascular relaxation phenomena
and glomerular basement membrane thickness continues to increase. Glomerular
filtration rate began to decline at the end of this period. Microalbuminuria
may at 20-200μg / min (200-300μg / 24 hours). Hypertension is often not treated
well, the numbers are usually higher blood pressure complications with other
agencies.
Then the stage renal disease has manifested a
clear, permanent positive proteinuria (> 0.5 g / 24 hours). This could be
called the clinical stage renal disease. Hypertension is often unstable,
glomerular filtration rate and rapidly declining. Hypertensive renal disease
was considered inevitable progress of all people with hypertension. In fact
research has shown that about 80% of people with hypertension have
microalbuminuria will develop the disease if treated well, but found that
approximately 30% of patients with microalbuminuria, albuminuria back to
normal, 50% still remain with microalbuminuria and only 20% progress to
proteinuria.
The last phase is the period of severe renal
impairment. Pathological lesions characterized by the phenomenon of glomerular
sclerosis. In the case of hypertensive kidney disease, glomerular filtration
rate decreased in parallel with the increased level of microalbuminuria. Speed
reduction dramatically different from one person to another but relatively
constant in each person. Many studies show that the average rate of decline of
glomerular filtration rate is 10-12ml / min / year. Blood pressure is the most
important determining factor affecting the rate of decline in glomerular
filtration rate. Hypertension occurs in approximately 80% - 90% of patients
with chronic renal failure last stage, which often both systolic blood pressure
and diastolic hypertension or isolated systolic hypertension systolic well
dominant than diastolic hypertension. Hypertension is often improved after
dialysis withdraw excess fluid volume. The increase in renin secretion is due
to lack of access glomerular blood, but can also be caused by ataxia, increased
renin production by keeping salt water. Other factors also contribute to
hypertension in renal failure as dependent catecholamine nervous system,
antidiuretic hormone, dysregulated prostaglandin system, the kinin, diuretic
factors atrium.
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