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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%, Cushings
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 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
Renovascular atherosclerosis, fibromuscular dysplasia, thrombosis of renal
arteries, Takayasus disease.
Renin secreting kidney tumors
Liddle syndrome
Nephroptosis(floating kidney)
Adrenal Cushings syndrome, congenital adrenal hyperplasia, primary
aldosteronism, pheochromocytoma.

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
Hematologic disorders primary and secondary polycythemia

Systolic hypertension
Aortic valve insufficiency (regurgitation), thyrotoxicosis, hyperkinetic heart
syndrome, fever, arteriovenous fistula, patent ductus arteriosus.
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, pallor, perspiration,
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, left ventricular
Creatinin > 1.5mg/dl
Lab analysis hyperglycemia, hypokalemia, hypercalcemia
Clinical sings in different nosologies of hypertension
Renal hypertension:
In renal parenchymal diseases number of working nephrons decreases .
During greels of immune inflammation in the case of acute nephritis there
issinterstitial swelling, which presses the reels and decreases the filtration surface;
growth of glomerulonephritis can be seen. Vessels lengthening factor production is
disturbed in kidney-endotelial nitrogen oxide, prostaglandins. Elevation of
vasoconstrictors synthesis: endothelin, thromboxane, this brings to activation of
sympathoadrenal system and as a result development of arterial hypertension.
Clinical picture of secondary hypertension usually is similar to that of
essential hypertension, although there are some specificities:
Increase of BP in exacerbation of renal pathologies, and decrease in BP in
case of remission.
Mild decrease in BP at night hours
permanent high diastolic pressure
Exaggerated retinal changes
Hypertension encephalopathy is less expressed

Existence of Nephrotic syndromes
Rapid growing glomerulonephritis is considered to be an exception,to which
it's typical
Renal failure in 4th or 6th week of glomerulonephritis development(urine
density reduction of , rapid development of isohyposthenuria,increase of
blood urea and creatinine)
Severe retinopathy
Expressed arteria hypertension, (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;
The appearance of arterial hypertension parallel with pathology
Possible pyelonephritis
In the case of glomerulonephritis-antistreptococal antibody high title, in the
case of pieronefrit-bacteruria
Clinical picture of severe inflammation of renal coil (waist pain, fever, dysuria,
hematuria, proteinuria, cilindruria, failure of Percutaneous Renal Biopsy,
swelling syndrome)
Normalization of blood pressure with the disappearance of clinical and lab
X-ray and ultrasound changes
Renovascular hypertension arterial hypertension with artery lesion is caused
because of kidney malnutrition. The most common reason of Renovascular
hypertension in the young , is the fibro muscle dysplasia of renal artery.
The diagnose is based on the following:
Renovascular hypertension development before 25 or after 50 y.o.

Renovascular hypertension development on the background of obliterating

disease of peripheral artery

The appearance of refraction to hypertensive therapy, transmission of benign

Renovascular hypertensionto malignant

Kidney unilateral reduction
Long systolic or systole diastole noise discovery in ribs or in round of navel,
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, rheumatoid


Renal insufficiency increase, scleroderma/ rheumatoid arthritis

Malign arterial hypertension/ scleroderma, purpura, SCHOENLEIN-HENOCH,

Goodpasture's syndrome/

Stable arterial hypertension to the standard treatment

Abdominal syndrome/ abdominal pain, dynamic disruption of intestine, ulcer/

Joints syndrome

Endocrine arterial hypertension

Primary hyperaldosteronism - Conn disease develops because of high production of

aldosterone, and is distinguished arterial hypertension and hypokalemia. Solitary
adenoma of adrenal coil (in 60% cases of primary hyperaldosteronism). There is
hyperplasia of adrenal cortex in 38% of patients. Aldosterone hyperproduction leads
to Na+ and water reabsorption increase in renal tubes, there is an increase of Na +
concentration in blood, also increases volume of circulating blood, development of
arterial hypertension and hypokalemia.

Typical clinical picture: Hypertension syndrome with permanent high blood pressure
with crisis, rare permanent arterial hypertension without any crisis process, second
version; transitory increase of blood pressure during neuromuscular flare. But
during the attack blood pressure is normal. From 6% to 8% the arterial hypertension
becomes malignant.

Neuromuscular syndrome expressed muscle weakness, which sometimes gets

stronger up to paralysis, paresthesia, rare shakes.

Renal syndrome polyuria, nicturia, sense of always being thirsty. It is a result of

hypokalemia and hypernatremia, arranged to the dystrophic changes of tubular

Diagnose is based on the following paraclinical data;

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, negative T wave, growing of U
wave, increase of QT interval.
Due to echo examination bilateral (symmetrical hyperplasia) and unilateral
(aldosteronoma)adrenal growing can be seen.

CT and MRI adrenal neoplasm

Pheochromocytoma tumor consisting of chromaffin cells, which is located in

adrenal nuclear sector (90% cases) or sympathic and parasympathic ganglions,
which produce catecholamines. Clinical picture is connected to the influence of
catecholamines on cardiovascular system. Clinical types are distinguished

1 permanent artery hypertension /15-25%/

2 stable arterial hypertension with regular pheochromocytoma crisis /50-60%/

3 regularly emerging pheochromocytoma crisis, blood pressure is normal out of
crisis, patients wellness is satisfactory /25%/

Crisis developes suddenly and often interapts independently, in some cases

its reason is stress, tumor palpatha, physical overloading. Crisis is expressed with
adrenal syndrome, weakness, paresthesies, abdominal and chest pain, heart beat,
arrhythmia, excitation, headaches, hyperglycemia hands shaking, pale skin,
midriasis abundant urination in the end of crisis. Usually crisis lasts 10-30 minutes,
blood pressure increases up to 180/200, 100/110, systolic also increases. Crisis
frequency flaps during 2-3 till 10-12 days. Crisis is dangerous for development of
stroke, heart attack, ventricular fibrillation.

Pheochromocytoma crisis are typical:

Acute development of hypertensive crisis and often independent

disappearance,high blood pressure,recurrent crisis,crisis development and
prompting factor connection,tachykardia, hand shaking, diffuse diaphoresis,
pallor, mydriasis,high temperature, loss of weight, hyperglycemia,
glukozuria,paradoxical hypertensive result while using blockers.

diagnose is based on the following paraclinical data

Leukocytosis, lymphocytosis, erythrocytosis, high ESR,

hyperglycemia,high level of catecholamines in blood and urine, klofelin
experience normaly klofelin decreases adrenaline level in blood, but in this
case it doesn't, - blockers are effective if blood pressure exceeds 190/120
mmHg .

Cushing's syndrome - hypercorticism with pituitary adenoma(Cushing's syndrome

with high level of ACTH) or adrenal cortex hyperplasia (Cushing's syndrome with low
level of ACTH).Clinical syndormes are - obesity, crimson strias, moon face,
hypokalemia and hypoglycemia,dry thin hair, crimson shade of face skin, in women-
hypertrichosis, straias in axilla, in breast, in low and lateral abdomen, muscle
atrophy, 150/110-240/160 Hgmm blood pressure in 80 % cases, steroid
osteoporosis, diabetes or glucose intolerance.

Diagnose is based on the following paraclinical data - cortisol concentration increase

in blood and urine cortisol and addition of 17-OKS excretion, ACTH increase in the
case of Cushing's deases , dexamethasone experience in healthies after

dexamethasone injection cortisol quantity decreases by 50% but it's more in
comparison I itial volume, in Cushing's deases high dose of dexamethasone
decreases cortisol level by 50%, but ACTH in blood is normal or high.In Cushing's
syndrome case any dose of dexamethasone can't supress cortisol secretion, and
ACTH isn't found in blood, tomography of abdomen, CT and MRT.

Hypothyroidism Due to arterial hypertension peripheral vascular resistance

increases, often ischemic disease evolves. Clinical signs are the following obesity,
swelling, inhibition, dry cold skin, bradycardia (decreased heart rate), hidroperikard
or hidrotorax development, constipation, low rude voice. Diagnose is confirmed with
low level of thyroid hormone and with high or low numbers of thyreotropin (primary
or secondary hypothyroidism).

Acromegalia grown limbs, rough facial features, teeth area increase, orbs increase-
divergent squint, arterial hypertension, ischemic disease, SCD. Diagnose is
confirmed according to high level of somatotropin in blood.

In healthy people the quantity of somatotropin in plasma decreases till 2ng/ml 2

hours after taking 75g glucose, it's unchangable in unhealthy ones.

sleep apnea obesity, drowsiness in the afternoon

nervous hypertension orthostatic changes of blood pressure

Coarctation of the aorta - congenital defect of aorta, it's typical to

the pulse above from aortic hypertension narrowness.

Diagnose is based on the following clinical data - headaches, permanent noise in

ears, pulsation in the head, nosebleeds, hypertrophied muscles of shoulders and
upper limbs, lower limbs muscles are atrophic.head, shoulders and intercostal
severe pulsation, pulsation weakness in lower limbs, accented II sound in aortic
point, systolic murmur in ERB point and aortic point, asymmetrical high blood
pressure in the arms (from 150/90 to 250/150 mmHg, low blood pressure in lower
limbs), X Ray aortal configration, strong pulsation in high sector of aorta, cardiac
catheterization systolic pressure changes up and down from narrowness of aorta,
MRI is considered to be the best diagnosing method.

Aortic valve insufficiency - systolic hypertension developes as a result of final

diastolic backflow to left ventricle volume, diastolic blood pressure decreases due
to the blood flow from aorta to the left ventricle, pulse pressure increases.
Diagnose is based on the following clinical and paraclinical data - carotid
pulsation , protodiastolic noise in heart listening point which spreads to the top,
high and rapid pulse, echocardiographic singhs of aortic insufficiency.

Aortic atherosclerosis- aortic wall elasticity reduction is accompanied with

the growth of spread speed of pulse wave which leads to systolic and pulse pressure
increase. In 70% cases its met in the elderly at the age of 60 y.o. the elderly
people, predominantly high systolic pressure, natural or low diastolic pressure,
atherosclerosis of peripheral artery, II tone emphasized aorta, high systolic noise on
the aorta, which gets higher when hands are up, calcification and dilatation of aorta.
Hyperthyrosis-- systolic hypertension, tachycardia, loss of weight, sweating,
ekzoftalm, temperature increase. Diagnose is confirmed according to the high level
of thyroid hormones, and according to high or low level of thyrotropin.
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, a-adrenoblockers

renal parenchymal ACE inhibitors

disease dihydropyridine calcium
renovascular hypertension blockers

hyperthyrosis B-adrenoblockers

primary calcium-retaining diuretic

hyperaldosteronism adrenoblockers

acute stress diuretics

isolated systolic