Secondary Hypertension

Secondary hypertension is a type of hypertension which is caused by
identifiable underlying organ system pathologies. According to statistics secondary
hypertension accounts only for 5-10% of total hypertensive patients. Causes of
secondary hypertension with their percentages of prevalence are listed below:
Chronic kidney disease 1.8-5.6%, renovascular hypertension 0.2-3.3%, Cushing’s
syndrome 0.1-0.6%, OCP(oral contraceptive pills) 0.2-1.0%, primary aldosteronism
0.3-1.5%, pheochromocytoma 0.1-0.3%, coarctation of aorta 0.2%.
Secondary main causes of hypertension:
Systolic-diastolic arterial hypetrtension.
Renal
Renal parenchymal (diseases) – acute and chronic glomerulonephritis, chronic
pyelonephritis, polycystic kidney disease, obstructive uropathy, kidney involvement
in systemic diseases and vasculitis, diabetic nephropathy, hydronephrosis,
tuberculosis, Goodpasture syndrome, myeloma cast nephropathy, congenital renal
hypoplasia.
Renovascular – atherosclerosis, fibromuscular dysplasia, thrombosis of renal
arteries, Takayasu’s disease.
Renin secreting kidney tumors
Liddle syndrome
Nephroptosis(floating kidney)
Endocrine
Adrenal – Cushing’s syndrome, congenital adrenal hyperplasia, primary
aldosteronism, pheochromocytoma.
Hyperthyroidism
Hyperparathyroidism
Acromegaly
Carcinoid

Coarctation of aorta
Pregnancy related(preeclampsia, eclampsia)

Neurogenic – psychogenic, diencephalic syndrome, familial dysautonomia,
polyneuritis, acute increased intracranial pressure.
Obstructive sleep apnea
Medications – high dose estrogens, adrenal steroids (exogenous hormones),
appetite suppressants, NSAIDs, cyclosporine, erythropoietin, cocaine, tricyclic
antidepressants.
Hematologic disorders – primary and secondary polycythemia
Alcohol

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hypercalcemia Clinical sings in different nosologies of hypertension Renal hypertension: In renal parenchymal diseases number of working nephrons decreases . tremor. hyperkinetic heart syndrome. Elevation of vasoconstrictors synthesis: endothelin.  Multiple organ system complaints during first visit  Non-symmetric peripheral pulse with low BP in lower extremities  Abdominal bruit over renal artery (with diastolic component)  Target organ damage with II degree or higher retinopathy. patent ductus arteriosus. arteriovenous fistula. thromboxane. Vessels lengthening factor production is disturbed in kidney-endotelial nitrogen oxide. prostaglandins. hypokalemia. Systolic hypertension Aortic valve insufficiency (regurgitation). thyrotoxicosis. which presses the reels and decreases the filtration surface. this brings to activation of sympathoadrenal system and as a result development of arterial hypertension.5mg/dl  Lab analysis – hyperglycemia. Secondary hypertension common sigens  Under 25 and over 55 years of age  Hypertension higher than 180/110mmHg  Sudden onset elevated BP in previously normotensive patient during one year  Refractory hypertension – not responsive to standard treatment methods  Bad response to previously effective treatment  Paroxysmal hypertension accompanied with palpitation. fever. Clinical picture of secondary hypertension usually is similar to that of essential hypertension. growth of glomerulonephritis can be seen. although there are some specificities:  Increase of BP in exacerbation of renal pathologies. pallor. During greels of immune inflammation in the case of acute nephritis there issinterstitial swelling.  Mild decrease in BP at night hours  permanent high diastolic pressure  Exaggerated retinal changes  Hypertension encephalopathy is less expressed 3 . perspiration. and decrease in BP in case of remission. left ventricular hypertrophy  Creatinin > 1.

is the fibro muscle dysplasia of renal artery. cilindruria. proteinuria.to which it's typical  Renal failure in 4th or 6th week of glomerulonephritis development(urine density reduction of . in the case of pieronefrit-bacteruria  Clinical picture of severe inflammation of renal coil (waist pain. hematuria. (resistant hypertension) which in terminal period can be malignant  Typical morphological changes in kidney bioptat  Diagnosing renoparenkhimatoz arterial hypertension the following is taken into consideration. dysuria. The most common reason of Renovascular hypertension in the young . transmission of benign Renovascular hypertensionto malignant 5 . swelling syndrome)  Normalization of blood pressure with the disappearance of clinical and lab phrases  X-ray and ultrasound changes Renovascular hypertension – arterial hypertension with artery lesion is caused because of kidney malnutrition.  Existence of Nephrotic syndromes  Rapid growing glomerulonephritis is considered to be an exception.  The appearance of arterial hypertension parallel with pathology  Possible pyelonephritis  In the case of glomerulonephritis-antistreptococal antibody high title. rapid development of isohyposthenuria.o. The diagnose is based on the following:  Renovascular hypertension development before 25 or after 50 y. failure of Percutaneous Renal Biopsy. fever.increase of blood urea and creatinine)  Severe retinopathy  Expressed arteria hypertension.  Renovascular hypertension development on the background of obliterating disease of peripheral artery  The appearance of refraction to hypertensive therapy.

Aldosterone hyperproduction leads to Na+ and water reabsorption increase in renal tubes.  Kidney unilateral reduction  Long systolic or systole diastole noise discovery in ribs or in round of navel. ulcer/  Joints syndrome Endocrine arterial hypertension Primary hyperaldosteronism . rib-vertebral angels  Sudden disorder of kidney function  Renin activity increase 3-4 days after getting ACE inhibitor  Repeated pulmonary edema during arterial hypertension  The absence of arterial hypertension in family anamnesis  Doppler examination of renal artery blood flow Clinical picture of arterial hypertension in systemic diseases and arteritis  Sudden start and rapid growth of urine syndrome /scleroderma. there is an increase of Na + concentration in blood. Goodpasture's syndrome/  Stable arterial hypertension to the standard treatment  Abdominal syndrome/ abdominal pain. There is hyperplasia of adrenal cortex in 38% of patients.Conn disease develops because of high production of aldosterone. purpura. development of arterial hypertension and hypokalemia. and is distinguished arterial hypertension and hypokalemia. scleroderma/ rheumatoid arthritis  Malign arterial hypertension/ scleroderma. Solitary adenoma of adrenal coil (in 60% cases of primary hyperaldosteronism). SCHOENLEIN-HENOCH. also increases volume of circulating blood. 7 . dynamic disruption of intestine. rheumatoid arthritis/  Renal insufficiency increase.

It is a result of hypokalemia and hypernatremia. which is located in adrenal nuclear sector (90% cases) or sympathic and parasympathic ganglions. Clinical picture is connected to the influence of catecholamines on cardiovascular system.  Due to echo examination bilateral (symmetrical hyperplasia) and unilateral (aldosteronoma)adrenal growing can be seen. second version. From 6% to 8% the arterial hypertension becomes malignant. Clinical types are distinguished 1 permanent artery hypertension /15-25%/ 2 stable arterial hypertension with regular pheochromocytoma crisis /50-60%/ 9 . Neuromuscular syndrome – expressed muscle weakness. growing of U wave. rare permanent arterial hypertension without any crisis process. Renal syndrome – polyuria. which sometimes gets stronger up to paralysis. sense of always being thirsty. paresthesia. increase of QT interval. negative T wave. nicturia. But during the attack blood pressure is normal. arranged to the dystrophic changes of tubular cells.Typical clinical picture: Hypertension syndrome with permanent high blood pressure with crisis. rare shakes. which produce catecholamines.  hypernatremia – 144-148 one/l  hypokalemia – 3-2 mmol/liter  hyperaldosteronism and hyporeninemia  Spironolactone experience – on the 4th day of taking spironolactone calcium level in plasma increases  ECG-hypokalemia symptoms – ST depression. transitory increase of blood pressure during neuromuscular flare.  CT and MRI adrenal neoplasm Pheochromocytoma – tumor consisting of chromaffin cells. Diagnose is based on the following paraclinical data.

systolic also increases. Cushing's syndrome . crimson shade of face skin. diagnose is based on the following paraclinical data Leukocytosis. erythrocytosis. in low and lateral abdomen. 100/110. in women- hypertrichosis. high ESR. excitation.obesity. paresthesies. blood pressure increases up to 180/200. moon face.high blood pressure.tachykardia. glukozuria. hypokalemia and hypoglycemia. crimson strias. pale skin. klofelin experience – normaly klofelin decreases adrenaline level in blood.dry thin hair. straias in axilla. Pheochromocytoma crisis are typical: Acute development of hypertensive crisis and often independent disappearance. 3 regularly emerging pheochromocytoma crisis. α . loss of weight. diabetes or glucose intolerance. 150/110-240/160 Hgmm blood pressure in 80 % cases. Crisis is dangerous for development of stroke. muscle atrophy. hand shaking. in some cases its reason is stress. abdominal and chest pain. blood pressure is normal out of crisis. hyperglycemia.hypercorticism with pituitary adenoma(Cushing's syndrome with high level of ACTH) or adrenal cortex hyperplasia (Cushing's syndrome with low level of ACTH). dexamethasone experience – in healthies after 11 . headaches. weakness. tumor palpatha.high temperature. hyperglycemia – hands shaking. steroid osteoporosis. in breast. but in this case it doesn't. hyperglycemia. Crisis frequency flaps during 2-3 till 10-12 days. heart attack. diffuse diaphoresis. ventricular fibrillation. pallor.paradoxical hypertensive result while using β –blockers. Crisis is expressed with adrenal syndrome. heart beat. arrhythmia.cortisol concentration increase in blood and urine cortisol and addition of 17-OKS excretion. Diagnose is based on the following paraclinical data .high level of catecholamines in blood and urine.recurrent crisis. physical overloading.Clinical syndormes are . mydriasis. lymphocytosis. Usually crisis lasts 10-30 minutes.crisis development and prompting factor connection. ACTH increase in the case of Cushing's deases .blockers are effective if blood pressure exceeds 190/120 mmHg . midriasis abundant urination in the end of crisis. patient’s wellness is satisfactory /25%/ Crisis developes suddenly and often interapts independently.

head.headaches. shoulders and intercostal severe pulsation. often ischemic disease evolves. Aortic valve insufficiency . asymmetrical high blood pressure in the arms (from 150/90 to 250/150 mmHg. cardiac catheterization – systolic pressure changes up and down from narrowness of aorta. permanent noise in ears. it's typical to the pulse above from aortic hypertension narrowness. Diagnose is confirmed with low level of thyroid hormone and with high or low numbers of thyreotropin (primary or secondary hypothyroidism). inhibition. orbs increase- divergent squint. hidroperikard or hidrotorax development. but ACTH in blood is normal or high. it's unchangable in unhealthy ones.  sleep apnea – obesity.dexamethasone injection cortisol quantity decreases by 50% but it's more in comparison I itial volume. MRI is considered to be the best diagnosing method. pulsation in the head. Diagnose is based on the following clinical data . constipation. in Cushing's deases high dose of dexamethasone decreases cortisol level by 50%. SCD. rough facial features. low rude voice. swelling. pulse pressure increases.In Cushing's syndrome case any dose of dexamethasone can't supress cortisol secretion. CT and MRT. lower limbs muscles are atrophic. ischemic disease. Clinical signs are the following – obesity. dry cold skin. diastolic blood pressure decreases due to the blood flow from aorta to the left ventricle. strong pulsation in high sector of aorta. arterial hypertension.systolic hypertension developes as a result of final diastolic backflow to left ventricle volume. In healthy people the quantity of somatotropin in plasma decreases till 2ng/ml 2 hours after taking 75g glucose. hypertrophied muscles of shoulders and upper limbs. systolic murmur in ERB point and aortic point. and ACTH isn't found in blood. Diagnose is confirmed according to high level of somatotropin in blood. accented II sound in aortic point. teeth area increase. low blood pressure in lower limbs).congenital defect of aorta. bradycardia (decreased heart rate). nosebleeds. X Ray – aortal configration. Hypothyroidism – Due to arterial hypertension peripheral vascular resistance increases. tomography of abdomen. pulsation weakness in lower limbs. drowsiness in the afternoon  nervous hypertension – orthostatic changes of blood pressure Coarctation of the aorta . 13 . Acromegalia –grown limbs.

protodiastolic noise in heart listening point which spreads to the top. high systolic noise on the aorta. ekzoftalm.o.systolic hypertension. Diagnose is based on the following clinical and paraclinical data . and according to high or low level of thyrotropin. Diagnose is confirmed according to the high level of thyroid hormones. In 70% cases it’s met in the elderly at the age of 60 y. sweating. calcification and dilatation of aorta. II tone emphasized aorta. atherosclerosis of peripheral artery. which gets higher when hands are up. loss of weight. temperature increase. a-adrenoblockers renal parenchymal ACE inhibitors disease dihydropyridine calcium renovascular hypertension blockers hyperthyrosis B-adrenoblockers primary calcium-retaining diuretic hyperaldosteronism α –adrenoblockers β -adrenoblockers pheochromocytoma acute stress diuretics isolated systolic hypertension 15 . tachycardia.carotid pulsation . Selection of Anti-hypertensive drugs according to type of secondary hypertension Reasons of hypertension Preferable drugs diabetic nefropathia ACE inhibitors obstructive uropatia of Nondihydropyridine calcium growing prostate blockers. – the elderly people. predominantly high systolic pressure.aortic wall elasticity reduction is accompanied with the growth of spread speed of pulse wave which leads to systolic and pulse pressure increase. Aortic atherosclerosis. natural or low diastolic pressure. high and rapid pulse. Hyperthyrosis-. echocardiographic singhs of aortic insufficiency.

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