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Wednesday, December 17, 2014

Functional symptoms of respiratory apparatus

The functional symptoms are the symptoms felt by the patient to suffer from respiratory disease in their patients recalled. In respiratory disease, the main symptoms: chest pain, coughing, shortness of breath, coughing sputum and blood. These symptoms have important implications for diagnosis.
chest pain
mechanisms
No branch pulmonary sensory nerve pain. Chest pain is usually caused by damage to the chest wall (muscles, bones, joints), pleura, pericardium, esophagus and tracheobronchial tree. When the lung tissue damage that occurs due to pleural chest pain in response to this damage.
characteristics
The important point to understand when patients ask:
How onset:
Sudden intense: intense pain without prior notice nature and degree of pain immediately at the maximum.
Persistent pain gradually increased.
Location of pain:
Location pain may suggest organ damage and the nature of the injury.
Pain in the front of the sternum following: Inflammation of the tracheobronchial or mediastinal syndrome.
Pain on the front side: Pneumonia or pleura. Pain in the breast less common in acute pneumonia.
Upper quadrant pain common in pleural disease.
The change of chest pain with breathing movements: The degree of pain when coughing change when changing positions often have little diagnostic value. The pain increases when you cough or breathe deeply.
Characteristics of chest pain according to the agency vulnerable
Chest pain due to lung diseases - the pleura:
Pain is often sudden onset, accompanied by clinical symptoms and x rays.
The pain of acute pneumonia: Sore breasts, increased pain when coughing, often accompanied by other symptoms such as chills, fever, lung examination coagulation syndrome. This pain is encountered in pulmonary embolism.
Tracheobronchitis pain: patients feel a burning pain behind the sternum, increased pain when coughing, may or may not meet sputum in bronchial inflammation caused by influenza gas or smoke inhalation irritation.
Pain due to pleural disease: pain in the side and bottom of the chest, pain intensity changes, increased coughing and deep breathing. Pain spreading to the shoulders and are often associated with dry cough, pain medication less effective and often occur when changing positions. In pleural effusion pain often associated with shortness of breath, chest side fell ill and had to move 3 down syndrome.
Chest pain due to pneumothorax: Sudden, intense "pain stabbing" pain in the side, shoulder, breast orang sometimes like angina. Pain is often accompanied by shortness of breath, coughing when changing positions and the triad of Gaillard. Stabbing pain when faced lung abscesses, abscesses under the diaphragm rupture into the pleura.
In pleurisy in low areas including the periphery of the diaphragm pleura is dominated by six intercostal nerves below, these are the nerves that govern the abdominal wall so as pleurisy in this section may be accompanied by pain in the abdomen. The central part of the diaphragm is controlled by nerve diaphragm (CIII and CIV) as inflammatory diseases in this section
workers may feel pain in the neck or shoulder tip.
Chest pain due to pulmonary tuberculosis is usually dull, nagging.
Chest pain in lung cancer. Pain is not clear, the location may change, but fixed time of day, less analgesic effect, often accompanied by cough, hemoptysis can ... At the peak of lung tumors spread from the chest pain the upper limb.
Pain in the mediastinal disease inflammatory or non-inflammatory:
Pain behind the breastbone can be accompanied by fever.
Chronic pain in mediastinal tumors:
Pain in the mediastinal compression syndrome before: Pain behind the sternum, false angina pain accompanying line jacket, purple and collateral circulation, increasing pressure on the veins of the coughing and straining.
Pain in the mediastinal syndrome pinched between pain type "braces" irregular and often accompanied by shortness of breath hissing, wheezing, cough, voice sometimes backfired cord paralysis due to left, step by compression or mental paralysis business diaphragm.
Pain in the mediastinal compression syndrome following: pain due to intercostal nerve compression. Pain spreading to the arm or by compression of the nerve roots in the arm plexus CVIII - DI.
  Chest pain due to disease: pathology addition of pleural pain in the chest may be caused by:
Bone lesions: Pain due to broken ribs usually persistent, increasing the respiratory movements, changing positions and cough.
Rib cartilage injury (Tietze's syndrome).
Muscle damage, myalgia, myositis.
Intercostal nerve damage: Pain that spreads along the thoracic ribs in half.
Chest pain in people who play sports (tennis).
Pain due to other causes:
Chest pain due to cardiovascular disease:
Pain due to coronary artery disease: Pain behind the breastbone, spreading to the neck and upper limbs.
Pain due to pericardial effusion: pain before the heart, increased exertion, taking a deep breath.
Pathologic esophageal pain: Pain after sternum, appeared to swallow and supine can be combined with difficulty swallowing.
The chest pain caused by disease of the breast: The pain spread to other parts of the chest.
Pain comes from the belly: The pathology of the liver, bile, stomach, pancreas.
Pain from retroperitoneal: nephropathy.
cough
define
Ho is reflective of the respiratory organs, causing cough receptors are stimulated. This is a positive reflection to exclude from airway secretions and foreign material.
mechanisms
Cough reflex arc include: The cause cough receptors in the pharynx, larynx, bronchi large mediastinal pleura and, in addition to other receptors in the liver, uterus, ear canal. Lung parenchyma and small airways at the receptor causes coughing. Medullary cough center, floor 4 intraventricular nerve afferent nerves consisting of strings X backfired, nerve diaphragm, intercostal nerves, abdominal muscles.
characteristics
Analysis of the characteristics of cough may help diagnosis.
Circumstances and time appear cough:
Spontaneous.
Appears on exertion, change posture, swallowing (cough when swallowing is characteristic symptom of esophageal probe - windpipe).
Ho morning waking up, day or night cough.
Paroxysmal or persistent cough, Chronic: Chronic cough is a cough that lasts more than 3 weeks
Rhythm: Ho ho to attack or aggression.
Timbre: cough may be higher or depression.
Him in his hoarse cough or laryngitis. like barking dogs.
Ho voice double: cough at high-downs. Meet the opposite recurrent nerve paralysis.
Cough or sputum: Coughing up phlegm mucus that is coughed prove the quality of bronchial secretions (children and women often do not spit out phlegm that swallowed the stomach).
Value of Symptoms
Dry cough occurs when changes in posture having pleural effusion.
Productive cough with fever, chest pain, dyspnea, pulmonary inflammation
Cough lasts: laryngeal disease, interstitial lung disease, chronic mastoiditis. pharyngitis beads, felt throat disorders, inflammation of the sinuses mountain.
A persistent cough with sputum in chronic bronchitis, bronchiectasis.
Paroxysmal cough: There may encounter due to the following reasons:
Pertussis: a bout ho, ho often limp night, causing vomiting, productive cough flow into wires.
Respiratory viral infections.
Foreign body airway: Tigers first fall in airway foreign bodies previously overlooked - common in children.
Lung cancer in adults: Cough lasts. in smokers symptoms are often ignored by the mistaken idea that cough from smoking.
Tuberculosis: According to national TB programs Vietnam, coughing more than 3 weeks needed medical care whether or not infected with tuberculosis.
Tracheobronchial spasm: Common in bronchial asthma, cough, shortness of breath attacks, but also when asthma attacks only manifested by cough, about dawn, common in children.
Ho led to disorder awareness: Often sudden onset, with one or more coughs caused a temporary sense of gloom or fainting (Cough Syncope), also known as stroke larynx (Ictus Larynge) met in respiratory failure very severe, dyskinesia tracheobronchial atypical.
Cough in heart disease: nocturnal cough accompanied by shortness of breath, asthma, heart in hypertension due to left heart failure, valve stenosis 2 leaves.
gob
define
Sputum is coughing and spitting out the discharge, the product is in airway pathology orang lid glottis.
characteristics
Features phlegm is coughed up from the tracheal tree is very important in the diagnosis and treatment of respiratory diseases. But it must first determine whether the patient actually productive cough or not. It should be noted the following cases are not sputum:
Spit out saliva: white and thinning.
Spit out the substance from the nose and throat, or the quality of esophageal reflux, stomach.
Need to determine the time and number of colors, flavors and ingredients not stink of sputum.
Characteristics of sputum under bronchopulmonary disease
Acute bronchitis: After the cough is productive cough mucus stage latex. yellow or green.
Chronic bronchitis: In the absence of multiple infections; greyish white mucus or phlegm.
Pneumonia:
Level lobe pneumonia in adult pneumococcal: cough sputum usually on day 3 of the illness, difficult to expectorate sputum stick, with less blood and sputum called "rust", along with typical coagulation syndrome. After illness variables in the 9th day of the disease, sputum becomes diluted, easy to cough up, down and out in the 15th.
Klebsiella pneumonia: Sputum color stone tiles.
Pneumonia caused by pseudomonas curling: green sputum stuck.
Sputum in bronchoalveolar inflammation: A green or yellow purulent sputum, mucus.
Viral pneumonia: Usually cough or sputum with white mucus. When multiple infections with purulent sputum mucus.
Lung abscess: sputum is basic symptoms of lung abscess help diagnose, monitor progress and direction pathogens. To monitor the number and nature of sputum daily.
The first phase cough or coughing up mucous sputum.
Phase ộc pus: Usually happens from day 5 to day 10.
Prodrome: Breathing the smell rotten, sometimes with blood concepts.
OC latex bulk: Patients with Severe chest pain feels like chest x, can be passed. Then ho ộc hundreds ml pus comes out through the mouth to the nose sometimes.
OC latex partial Patients cough up different amounts of pus, several times a day.
Sputum knob coin: When patients stop coughing coughing up thick gob, the coin (Crachat nummulaire).
Sputum odor suggesting abscess caused by anaerobic bacteria.
Chocolate colored sputum, or chicle: Abscess by amoeba.
Bronchiectasis:
More productive cough in the morning, when waking up. The total amount of mucus in the day from a few tens to hundreds of milliliters (probably more than 300 ml / 24 hours). Place in a glass cup with 3 layers:
On the mucous layer of foam.
The middle layer is mucus (due to increased bronchial secretion)
The bottom layer of latex.
Asthma:
Sputum in the last bout dyspnea, sputum white sticky or cooked like tapioca, pearls can have phlegm (as described by Laennec).
Pulmonary edema: pink foam sputum, greater numbers.
Tuberculosis: Sputum "top three" white, smooth, sometimes mixed with mucus and blood.
Follicle available for: Sputum diluted, clear, with particles such as millet, color, available for the first tests.
Coughing up blood
define
Coughing up blood is the phenomenon of blood from the lower respiratory tract is escaping through the mouth. Coughing up blood is often a medical emergency.
mechanisms
Common mechanisms are:
Ulcers, broken blood vessels in labor: Rupture of an aneurysm Ramussen, bronchiectasis: breaking the circuit in paragraph stop-Von Hayek, lung cancer.
Due to increased vascular pressure: hemodynamic pulmonary edema, increased permeability of blood vessels in the pulmonary edema lesions.
Damage to the alveolar capillary membrane: Good Pasture Syndrome.
Coagulopathy, bleeding, especially when accompanied by lung disease.
characteristics
Circumstances occur: After exertion, emotion, women in menstrual period or no special circumstances.
Prodrome: A burning feeling behind the breastbone, itchy throat, or mouth fishy tired fainted away.
Coughing up bright red blood, foam, can only pure blood or sputum.
Tail blood summary: the sign had stopped bleeding, common in tuberculosis, blood spitting out little by little, dark red and black again.
Classification level hemoptysis
Currently, the classification of the severity of hemoptysis inconsistent. In fact, there are usually two likelihood that the patient is coughing, coughing up blood in the new few hours or hemoptysis in 24 h.
So to help manage and prognostic classification as follows:
  Mild: Cough each small beach bloody sputum, coughing up blood of <50 ml. pulse and blood pressure normal.
Moderate: Whole blood was coughing up from 50 to 200 ml. rapid pulse, blood pressure was normal, no respiratory distress.
The severity: coughing up blood volume> 200 ml / time or 600 ml / 48 hours, more lung damage, respiratory failure, cardiac arrest.
Ho blood lightning: Appears sudden, large amounts of blood, lungs flooded ngap2 gayngat breathing and death.
Differential Diagnosis: There is a difference hemoptysis with bleeding from the nose, throat, mouth and vomited blood.
Vomiting up blood Coughing up blood
Cough, chest pain epigastric pain
Itchy throat and cough Nausea and vomiting
Bright red blood and sputum, blood and foam food
alkaline pH acid pH
Separate normal (black swallowing blood) black stool
Differential diagnosis between coughing and vomiting blood will be difficult, as patients with hemoptysis accompanied by vomiting bloody vomit, blood swallow down by the stomach. When it needs a thorough examination and lung X-ray, mining engineering history of stomach; if necessary, bronchoscopy or gastroscopy to detect lung injury.
The main causes of hemoptysis
Tuberculosis: The most common cause, all TB can cause coughing up blood from the few to the many. In that tuberculosis has progressed bean pulp necrosis majority. Then came bronchial tuberculosis. very rare in primary employment and labor Statistics. Coughing up blood and sputum residue can usually beans and tail concept blood.
Lung Cancer: A common cause, mainly in primary lung cancer, lung cancer is less common in secondary. Sputum and blood rays, with moderate coughing blood, usually in the morning coughing red purple (plum).
Bronchiectasis: In dry bronchiectasis may be expressed only by coughing up blood, bright red blood, recurrent, easily confused with tuberculosis.
Cardiovascular disease and other diseases: pulmonary infarction, 2 leaves stenosis, congenital heart disease, illness or disease Good Pasture Collagen system. Can meet all levels of hemoptysis. Noting: Blood and pink foam found in pulmonary edema.
Pneumonia: Pneumonia caused by bacteria, lung abscess.
Lobe pneumococcal pneumonia: rust colored sputum.
Klebsiella pneumonia necrosis bloody sputum tile adhesive
The rare cause:
Bronchopulmonary Aspergillus.
U pulmonary blood vessels.
Also see hemoptysis due to injury, and lung injury due to intervention procedures such as bronchoscopy, transthoracic lung biopsy ...
Shortness of breath
define
Difficulty breathing is difficult feelings and problems in the patient's breathing. Trouble breathing alter the performance characteristics of the patient to breathe normally as breathing frequency, duration of the inhalation and exhalation, the coordination and participation of the respiratory muscles. So to describe adequately dyspnea should be combined with patient examinations.
characteristics
Facial appearance:
Acute paroxysmal dyspnea.
Chronic persistent dyspnea.
Circumstances occur:
When you leave or after exertion, infection, trauma.
Appear suddenly or slowly.
Difficulty breathing rhythm types:
Frequency:
Shortness of breath quickly:> 20 times / minute.
Shortness of breath slow: <12 times / minute.
By the breath:
Shortness of breath is inhaled.
Shortness of breath is exhaled.
By location:
Difficulty breathing when lying down.
Shortness of breath when moving from lying to standing position.
Shortness of breath related to environmental factors:
Changing weather, occupational exposure.
Dyspnea accompanied by functional symptoms and other entities:
Cyanosis (a sign of respiratory distress or chronic), cough, chest pain, sputum, or respiratory muscle contraction not the women.
The degree of dyspnea:
Classification of the American Heart Association NYHA (New York Heart. Associatide).
Level I: No limit physical activity.
Level II: Breathlessness on exertion much.
Level III: mild dyspnea on exertion and limited physical activity.
Level IV: Dyspnea stay.
Some special types of dyspnea
Shortness of breath due to heart disease: Appears on exertion or chronic, with symptoms of heart failure.
Shortness of breath due to central nervous system damage and peripheral: Difficulty breathing Biot type: irregular breathing at quickly, sometimes slowly, while shallow, deep time, no see kz cycle of meningitis.
Shortness of breath due to metabolic disorders:
KUSSMAUL Dyspnea: Shortness of breath with 4-stroke cycle: Inhale - stop - breathe out - stop by metabolic acidosis in diabetes.
Dyspnea type Cheyne - Stokes: Yes cycle, amplitude increase - decrease - stop having pulmonary renal syndrome, obesity, some cerebrovascular disease, severe heart failure ...
Cause shortness of breath
Upper airway: Difficulty in breathing accompanied by withdrawal recessed hole on memory and language Stridor, the hiss sounds harsh and prolonged, on the inhale, spasm, edema loaded hoacday sound, object, laryngitis management, cancer, or thyroid to tracheal compression ..
Airway below:
Emphysema in chronic obstructive pulmonary disease, shortness of breath on exertion, gifts, chronic.
Asthma: In a typical asthma attack, attack paroxysmal dyspnea, shortness of breath out slowly, hissing, spontaneously or after bronchodilator use, or relapse when weather changes.
Lung parenchyma:
Pulmonary fibrosis: Progress slowly smoldering, at first appeared after the exertion of chronic appear both stay.
Pneumonia: Shortness of shortness.
Waste Management - Waste inflammation: rapid shallow breathing is difficult, often accompanied by symptoms of respiratory distress, cyanosis, tachycardia, especially in children, the elderly.
Pleural Disease:
Pleural effusion: Shortness of shortness, increases the movement and coughing.
Pneumothorax: sudden shortness of breath, rapid shallow, sometimes accompanied by cyanosis.

U mediastinal tracheal compression: Difficulty breathing when lying down, wheezing.

Diuretics privacy and confidentiality drug

Diuretics password
Distinguish two types:
Diuretics water density (secretin, enhance parasympathetic drugs) increases the excretion of water and electrolytes biliary epithelial cells, causing increased secretion of bile leakage.
Diuretics real honey stimulates liver cells increased excretion of bile bile like physiology. Depending on the source, there are:
Diuretics secret animal origin
It's bile salts, bile acids or bile full eliminates pigment and cholesterol.
Preparations: Bilifluine, 0.1g capsules, take 2 capsules before each lunch and dinner.
Diuretics native vegetation density
  Art, artichoke, boldo. Preparations used a combination of medicinal plants
Diuretics bile synthesis
Cyclovalon: 50 mg tablets, drink 6-12 tablets / day
Anethole trithion: 0,0125g form of drug particles / seeds. Every day drink 3-6 seeds.
Indication of the diuretic common bile
Symptomatic treatment of gastrointestinal disorders: abdominal distention, flatulence, belching, nausea
Adjunctive therapies against constipation
Contraindications: biliary obstruction and severe hepatic impairment
Drug information confidential
As these drugs cause gallbladder contraction, muscle relaxation and round Oddi. Password completely get rid of the gallbladder.
Physiologically, this effect depends on pancreatozinin cholecystokinin (CCK - PZ) due to duodenal lipid and peptide secreted from the stomach into the tea n. Almost all the drug information is confidential due to excretion CCK- PZ.
Indication: digestive disorders such as bloating, indigestion, heartburn, nausea Contraindications: biliary stones, with a history of amoeba.
Drugs: Sorbitol powder 5g package. Each packet in phase 1 hairpin Convention, taken before meals.

Magnesium sulfate: drink 2 5g

Tuesday, December 9, 2014

Change Research glomerular filtration rate in patients with primary hypertension

The study of 30 people with hypertension author Huynh Van Minh result 50% of patients with proteinuria appeared with many different levels. The level of average blood pressure of 166 / 97mmHg correlated with urinary albumin concentration was 71.9 mg / 24 h. Study of Chu Minh Ha in 05 years from 2001 to 2005 have 3306 patients hospitalized for hypertension in total 92 103 inpatient percentage of 3.6%. In hypertensive complications from kidney failure percentage is 5.9%.
In 1996 researchers working group, track 1795 hypertensive patients 10 years Buckalew author comments hypertensive renal function decline as rapidly. Rate and the higher the number, the time of progression to end-stage renal failure as quickly. The author also Ridao 2001 for similar results. The authors conclude that hypertension is one of the most important factors for kidney disease prognosis and treatment of hypertension decided to slow the progression of kidney failure.
  The study of 840 patients with hypertension and nephropathy, author Peterson commented hypertension treatment will prevent coils early kidney disease and hypertension. Treatment of hypertension decided to slow the progression of kidney failure. NHANES III study comparing over 15600 patients and MDRD study found that 40% of hypertension among glomerular filtration rate of 90 ml / min / 1,73m2 lower MDRD study. However, the blood pressure 160/100 mmHg on the same two studies: 20% of patients with glomerular filtration rate: 15-30 ml / min / 1,73m2 2 times higher than the glomerular filtration rate in the group of 30 ml / min / 1,73m2. Puttinger H. 2003, see Fraser 2013 hypertensive kidney disease is the main cause of end-stage renal failure. When kidney function is severely impaired control of blood pressure treatment and maintain kidney function very difficult. This study suggests that blood pressure control achieved the goal of helping patients reduce kidney damage as well as block in other target organs. Redon J. 2006 epidemiological study of the incidence of cardiovascular disease in patients with renal impairment. The authors concluded that in patients with hypertension, the prevalence of cardiovascular disease increased in the same direction with the severity of renal impairment. Glomerular filtration rate test to help predict cardiovascular patients with hypertension. The study's authors Pontremoli in Genoa, Italy in 459 diabetic patients with primary hypertension untreated. The research results show that the incidence of kidney damage is 24%, 12% and microalbuminuria was reduced creatinine clearance was 13%. The presence of kidney damage leading to cardiovascular abnormalities 3.3 times higher than people without kidney damage. If there is simultaneous decline in creatinine clearance and urinary albumin, up to 68% of patients with a high risk. In conclusion, the authors suggest that the role of assessment tests glomerular filtration rate and urinary microalbumin test is the simplest and most important to assess target organ damage in patients with primary hypertension.

Thus most of the studies showed decreased glomerular filtration rate with the increase in the number of both systolic blood pressure and diastolic. Glomerular filtration rate seems to decrease faster in people with hypertension systolic than diastolic hypertension. Time as long hypertension, the risk reduction in glomerular filtration rate increases. Glomerular filtration rate decreased faster in the elderly. And when the glomerular filtration rate decreased cardiovascular events also increased. Thus it can be said glomerular filtration rate is an independent risk factor for hypertension, although the decline in glomerular filtration rate due to hypertensive renal injury. Glomerular filtration rate in patients with kidney damage caused by hypertension or hypertension are due to improved blood pressure control achieved if the target figure. Glomerular filtration rate is stable if good treatment of urinary albumin levels.

Glomerular filtration rate change due to hypertension

As a general rule, at the beginning of the change in pressure alter renal function, has brought about the change in structure. By the time the structural change will affect the functionality. And finally when the original structure is broken, the function will decline. Hypertensive nephropathy occurs in the majority of hypertensive patients not treated.
The first stage does not change anything, MLCT slight increase.
Following stages: Signs persistent microalbumin in urine is an early stage of hypertensive renal disease. Glomerular filtration rate in normal.
If untreated patients with microalbuminuria will progress to clinical proteinuria (urinary albumin> 300 mg / mg creatinine or> 300 mg / 24 hours). Once clinical proteinuria, glomerular filtration rate will decrease rapidly, kidney failure will become increasingly clear.
Currently hypertensive renal disease is second leading cause of diabetes causes of end-stage renal disease should hemodialysis, peritoneal dialysis or kidney transplantation cycle in many countries. Compared with end-stage chronic kidney disease due to other causes, patients with chronic end-stage renal failure due to hypertension had more cardiovascular risk factors other than clear and mortality rates are higher. Preventing the progression of kidney damage is one of the main goals when treating patients with hypertension. Hypertension is a motivating factor in kidney damage progresses faster. Research MDRD (Modification of Diet in Renal Disease) in the kidney due to many different reasons to see patients with controlled blood pressure was positively reduced glomerular filtration rate slower than patients with blood pressure was maintained at normal levels. When aggregating data from nine clinical trials evaluating the effects of antihypertensive treatment on kidney function, the authors found that people with chronic kidney disease have uncontrolled blood pressure (> 140/90 mmHg) decreased glomerular filtration rate of 12 ml / min / year, whereas those with chronic kidney disease have high blood pressure is 130/85 mm Hg under control decreased glomerular filtration rate is only about 2 ml / min / year (equivalent to the reduction of physiological).
Change glomerular filtration rate in patients with renal hypertension when autoregulation mechanism in the kidney (renal autoregulation) no longer works. Normal renal autoregulation of renal blood flow and keep the pressure in the glomerular stable when the average blood pressure change in a wide range from 80 to 160 mm Hg. The mechanism of the self-regulate vasomotor reflexes of arterioles to (afferent arteriole): When the average reduction in blood pressure, arteriolar dilation to, whereas the average increase in blood pressure, arteriolar to co back. The feedback mechanism tubules - glomeruli (tubuloglomerular feedback) is the change in tone of arterioles to meet with tubular NaCl concentration away. In addition, the co arterioles go (efferent arteriole) mediated angiotensin II also contributes to maintain the pressure in the glomerular renal perfusion pressure decreased. Chart 1 below shows the relationship between average blood pressure body with glomerular filtration pressure, factors determining the glomerular filtration rate. Street performers self-regulate pressure in the glomeruli of normal, chronic hypertension who have normal kidney function and chronic hypertension associated with chronic kidney disease
In patients with chronic hypertension, due to endothelial dysfunction and structural changes of the renal arterioles, glomerular pressure starts to decrease at a rate higher than 80 mmHg and started to increase at a rate higher than 160 mmHg. If performing the change of pressure in accordance with changes in glomerular average blood pressure on a chart, we can see in people with chronic hypertension phenomenon curve "misses to the right." Particularly in patients with hypertension associated with chronic renal injury, self-conditioning system disorders glomerular arterioles before losing the ability to stretch. In this the pressure in the glomerular changes almost parallel with the average blood pressure.
The consequence of the reduction in glomerular pressure is decreased glomerular filtration rate, expressed as increases in serum creatinine. Increases in serum creatinine particularly common in patients with hypertension associated with chronic kidney disease. In the first phase the reduced glomerular filtration rate nature hemodynamic not reflect the reality of kidney damage and is usually transient. Glomerular filtration rate will be restored and improved if better blood pressure control improves the structure and function in renal arterioles and shifting autoregulation curve of normal position. If high blood pressure continues to increase, the damage increases renal fibrosis. clinical proteinuria appears constant and glomerular filtration rate will decrease rapidly. The higher the blood pressure, glomerular filtration rate decreases more. Finally, renal fibrosis completely lost filtering function and required replacement therapy.

The process of dialysis in glomerular

1. The rate of glomerular filtration: One of the two kidneys filter 180 liters of services, including 99% of services are reabsorbed in the tubules, forming only 1-1.5 liters of urine excreted with a product of decomposition of the body. In normal in 1 minute with 1200 ml of blood flow through the kidneys (containing 650 ml of plasma) by 21% cardiac output, but only 125 ml of plasma is filtered through the glomerular membrane in which Bowman. Thus, 125 ml of plasma is filtered through the glomeruli in 1 minute called glomerular filtration flow (or glomerular filtration rate). The process of glomerular filtration agents have similar mechanisms of metabolism at the capillary hydrostatic pressure instantly. It is a passive mechanism, depends on the pressure difference between inside and outside the circuit.
Pressure Filter (P¬L) really pushes service glomerular filtration membrane, calculated by the formula:
PL = PH - (PK + PB)
Among them:
PH: hydrostatic pressure of glomerular capillaries (normal is 60mmHg),
PK: glue pressure in the glomerular capillaries (normal is 32 mmHg),
P¬B¬: How Bowman pressure (normal is 18 mmHg).
Thus, the glomerular filtration rate depends primarily on three factors: pressure filter, filtering capabilities and areas of glomerular filtration membrane.
2. Mechanisms regulating glomerular filtration rate
There are two mechanisms regulating automatic glomerular filtration rate: Stretch arterioles to: the reduced glomerular filtration rate, decreased levels of sodium, chloride characteristics to macula DENSA plated layer. The decrease in the concentration of ions causes the arteries to relax, increasing blood flow to the glomeruli, glomerular filtration rate increases and vice versa. Regulating co arterioles go backwards when reduced renal blood flow, with less sodium and chloride to the macula DENSA, as glomerular cells secrete renin edge, leading to the formation of angiotensin II minimizing travel arterioles, increases in glomerular pressure and increased glomerular filtration rate.
Methods exploration of glomerular filtration function
Glomerular filtration rate was calculated using the formula:
MLCT (GFR) = Kf. PL = k.s.PL = Ki. (PH - PB - PK).
In that ultrafiltration coefficient Kf = ks (k: the ability of the membrane filter, s: is the membrane area). Pl is the pressure filter, PH: hydrostatic pressure of glomerular capillaries (normal is 60mmHg), PK: glue pressure in the glomerular capillaries (normal is 32 mmHg), P¬B¬: pressure how Bowman (normal is 18 mmHg).
In fact to calculate glomerular filtration rate it based on renal clearance with a reagent. The concept of clearance (Clearance) is Muler, Van Slyke first introduced in 1928 when the study of kidney function by determining the volume of blood is purified from urea. Clearance of a substance is the mass of purified plasma totally out of that substance in a unit of time. Van Slyke was formulated to evaluate glomerular clearance:



C: Clearance reagent (ml / h)
U: reagent concentrations in urine (mg%)
P: reagent concentrations in serum (mg%)
V: The volume (ml / min)
1.73: The surface area of the body at the high 1,70m, 70kg is 1,73m2.
S: surface area of the patient's actual body (m2)
Techniques to measure glomerular filtration rate requires the use of these substances freely filtered through the glomeruli, not protein bound, not being reabsorbed or excreted by the kidney tubules, and the substance is not metabolized by the kidney, as well as to collect blood and urine correctly in the given time. Inulin is a substance commonly used in the laboratory, but because of the difficulty of the technique should not be widely applied in clinical practice. Endogenous creatinine is now widely used in practice because of its simplicity and ability to perform easily, cheaply. However the downside is that the accuracy is not high in some cases severe renal impairment, children, the elderly ... Now to overcome the limitations of endogenous creatinine reagent, the authors recommend the use of substances cystatin C and beta testing is 2 microglobulin support for measurement using endogenous creatinine. However because of technical complexity, high cost, so they need time to be widely applicable.
Creatinine clearance with 24-hour urine flow (Clcre 24) is often chosen as the main criteria in clinical practice to assess glomerular filtration rate. The main disadvantage of this test is creatinine is excreted by the kidney tubules should add in creatinine clearance greater than 24 typically carry MLCT and retention of urine in 24 hours unavoidable errors.
There are four formulas are used to calculate the MLCT:
- Formula estimated by the Cockcroft Gault MLCT
eClcre CG (ml / min) = [(140- age) x weight (kg)] / (72 x creatinine HT) x 0.85 (for women)
- Recipe of the MDRD estimate MLCT
MDRD eGFR (ml / min / 1.73 m2) = 186 x (HT creatinine) -1.154 x (age) -0.203 x (0.742 if female) x (1.210 if black)
- Formula MLCT estimate of Japan has been modified MDRD
MDRD eGFR Japan (ml / min / 1.73 m2) = 194 x (HT creatinine) -1.094 x (age) -0.287 x (0.739 if female)
- Formula estimates of CKD-EPI MLCT
+ Female: If HT creatinine ≤ 0,7mg / dL: eGFR = 144 x (HT creatinine) -0.329 x (0.993) age; If HT creatinine> 0,7mg / dL: eGFR = 144 x (HT creatinine) -1.209 x (0.993), age
+ Men: If HT creatinine ≤ 0,9mg / dL: eGFR = 141 x (HT creatinine) -0.411 x (0.993) age; If HT creatinine> 0,7mg / dL: eGFR = 141 x (HT creatinine) -1.209 x (0.993), age

  Through a comparative study of formulas to estimate creatinine clearance, estimated creatinine clearance (eClcre) is the appropriate formula in practice on the Vietnamese people. In fact, computerized and not only give the results of blood creatinine but an MLCT help clinicians know directly the value of glomerular filtration function. Since it can be diagnosed early cases of kidney failure, timely intervention and reduced the proportion of patients with chronic end-stage renal failure.

Hypertension and renal injury DO hypertension

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 in the country, the rate of hypertension in our country is 25.1% among those aged 25 years or older. In 1992, Trinh Tran Do surveyed 1716 people with hypertension are unaware 67.5% patients, 15% said the disease but no treatment, 13.5% of treatment but irregular and improper, only 4 % is the right treatment. In 2002, Pham Gia Khai et al 5012 survey of people aged 25 years and older in four provinces in northern 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.