idiopathic hypertensia

advertisement
MINISTRY OF HEALTH REPUBLIC OF UZBEKISTAN
CENTRE OF DEVELOPMENT OF A MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
IDIOPATHIC HYPERTENSIA
(The educational-methodical grant on the integrated training
For students of IVcourses of medical institutes)
MINISTRY OF HEALTH REPUBLIC OF UZBEKISTAN
CENTRE OF DEVELOPMENT OF A MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
I "confirm"
The chief of the main department
Science and educational institutions
Ministry of Health
Republic of Uzbekistan
S.E.Atakhanov
___________________________
“____” ________________ 2011
№ the report
IDIOPATHIC HYPERTENSIA
(The educational-methodical grant)
Tashkent - 2011
Composers:
Matchanov S.H. - Associate Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Djuraeva E.R Associate Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Kasimova M.B. – Senior Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Ziyaeva F.K. Assistant Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Sagatova D.R - Assistant Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Sultonova M.X. – Assistant Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Bekenova G.T. – Assistant Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Berdieva D.U. - Assistant Professor and Faculty Hospital Therapy Faculty of
Medicine, and Internal disease and pre ventive health care
department
Reviewers:
A.V.Yakubov -
chair of clinical pharmacology ТМА, professor
M.Z.Zohidova - chair on preparation of the doctor of the general practice of the
Tashkent institute of improvement of doctors, professor
The educational-methodical grantis considered and confirmedat session CМCТМА (the
report № _____ “_____” _____ 2011).
Chairman CМC, professor M.Sh.Karimov
The educational-methodical grant is confirmed on Academic council ТМА and it is
recommended to publication (the report № _____ “_____” _____ 2011г.).
The scientific secretary,
professor G.S.Rakhimbaeva
Conditional abbreviations
АI
Angiotensin I
АII
Angiotensin II
АV
atrioventricular
АH
Arterial hypertension
AP
Arterial pressure
АDH
antidiuretichormone
ACE
angiotensinconvert enzyme
АТ1
angiotensin1
АТ2
angiotensin2
АТF
adenosine triphosphoric acid
CART
The world organisation of public health services
IH
Idiopathic hypertensia
HCMP
Hypertrophic cardiomyopathy
HLV
Hypertrophy of left ventricle
DAP
Diastolic arterial pressure
DCMP
dilatationcardiomyopathy
DOCS
desoxycorticosterone
IHD
ischemic heart disease
IT
Myocardium heart attack
BMI
Body mass index
FDP
Final diastolic pressure
LHD
Lipoproteins high density
LV
Left ventricle
LLD
Lipoproteins low density
MWLV
Muscular weight of left ventricle
МV
Minute volume
IDH
The international department on a hypertension
BW
bodyweights
ОНМК
Sharp infringement of brain blood circulation
TPR
Total peripheral resistance
VCB
Volume of circulating blood
ANUF
Atrialnatriuretic
factor
RAAS
Renin-angiotensin-aldosteron system
SAP
Sistolic arterial pressure
SAS
Simpato-adrenalovaja system
DM
Diabetes mellitus
СССУ
Weakness syndrome синусового knot
RF
Risk factors
ХПН
Chronic nephritic insufficiency
СS
cholesterin
CАМP
Cyclic adenosine monophosphoric acid
CNS
The central nervous system
HR
Heart rate
EHPF
Endothelial the hyperpolarizing factor
ECG
Electrocardiography
ЭchoCG
Echocardiography
JGA
Juxtaglomerular apparatus
РGI2
Prostaglandinum I2
NО
Nitrogen oxide
Theme:IDIOPATHIC
HYPERTENSIA
1. A place of carrying out of employment, equipment
Division of Cardiology, cardiorheumatology and general therapy department laboratory and
instrumental diagnostics, training room.
Blood analyses, serological tests, clinical and biochemical analyses, coagulogram, radiological
researches, an electrocardiogram, EchoCG,learning-supervising tests, thematicpatients, a distributing
material.
Blood tests, serological tests, clinical and biochemical analysis, coagulogram , X-ray examinations, ECG, EhoKS, -control
tests, case-patients, handout.
ТV-video, оверхет, multimedia, tables, slides, the information-computer program.
2. Duration of employment
Time for illumination of the given theme-270 of minutes
3. The employment purpose:
Training of students of an aetiology, pathogenesis, clinical symptomatology, laboratory-tool
diagnostics and rational therapy of idiopathic hypertensia , preventive maintenance of complications,
rehabilitation.
The training purpose - development and strengthening of theoretical knowledge:
The educational purpose -formation in preparation of the doctor of interest corresponding to the
world standards for a speciality, feelings of responsibility, education of interest to expansion of the
knowledge, level formation deontology education, formation of care in the course of performance of
practical work, clearness and responsibility.
The develop purpose - formation at students of independent thinking and discussion, development of
critical thinking in students.
.
Problems
1. Definitionof arterial hypertension.
Aetiologyof arterial hypertensions, concept about idiopathic hypertensia.
Pathogenesis ofidiopathic hypertensia.
Classification of idiopathic hypertensia.
Clinical picture at idiopathic hypertensia: subjective data, the general survey, data of palpation,
percussion and auscultation, the conclusion of laboratory-tool methods of researches.
Differential diagnostics of idiopathic hypertensia.
Main principles of treatment of idiopathic hypertensia.
Current and the forecast of idiopathic hypertensia.
The student should know:
Aetiologyof idiopathic hypertensia
Pathogenesisand haemodynamic infringements at idiopathic hypertensia
Classification of idiopathic hypertensia
Methods of diagnostics of idiopathic hypertensia
Main principles of treatment of idiopathic hypertensia
The student should be able:
To collect the anamnesis, complaints of the patient, to spend the general survey, palpation,
percussion and auscultation
To make the plan of inspection of the patient
To interpret indicators of laboratory data
To interpret data of radiological researches
To prove on steps the clinical diagnosis
To write the recipe on preparations and to explain their mechanism of action and collateral
Actions
4. Motivation
Now studying of idiopathic hypertensia has huge value because it occupies one of the first places
among cardiological diseasesand can lead dangerous to a life of the patient to complications.
5. Interdisciplinary and intradisciplinary communication
Interdisciplinarycommunication:
Idiopathic hypertensia
To integrate with following subjects:
On a vertical
Normal anatomy
Normal physiology
Histology
Pathological anatomy
Pathological physiology
Propaedeutics of internal illnesses
Across
Beamdiagnostics
Normal anatomy
Cardiovascular system
The Cardiovascular system transfers oxygen and nutrients between fabrics and bodies. Besides, it
helps to delete slags from an organism.
Heart, blood vessels and blood form a difficult network on which plasma and uniform elements are
transported in an organism.
These substances are transferred by blood on blood vessels, and blood actuates the heart working as
the pump.
Blood vessels of cardiovascular system are formed by two basic subsystems: vessels of a small
circle of blood circulation and vessels of the big circle of blood circulation.
Vessels of a small circle of blood circulation transfer blood from heart to lungs and back.
Vessels of the big circle of blood circulation connect heart to allother parts of a body.
Blood vessels
Blood vessels transfer blood between heart both various fabrics and body bodies.
There are following types of blood vessels:arteries, arterioles, capillaries, venules and veins.
Arteriesand arterioles bear blood from heart. Veins and venules deliver blood back in heart.
Arteries and arterioles
Arteries bear blood from ventricles hearts in other parts of a body. They have the big diameter and
the thick elastic walls maintaining very a high pressure of blood.
Before incorporating to artery capillaries share on more thin branches named arterioles.
Capillaries
Capillaries are the smallest blood vessels which connect arterioles with venules. Thanks to very thin
wall of capillaries in them there is an exchange of nutritious and other substances (such, as oxygen
and carbonic gas) between blood and cages of various fabrics.
Depending on requirement for oxygen and other nutrients different fabrics have different quantity of
capillaries.
Such fabrics as muscles, consume an oxygen considerable quantity and consequently have a dense
network of capillaries. On the other hand, fabrics with a slow metabolism (such as false skin and a
cornea) at all have no capillaries. The body of the person has many capillaries: if them it was
possible расплести and to extend in one line its length would make from 40000 to 90000 km!
Venules and veins
Venules are the tiny vessels connecting capillaries with veins which are larger venules. Veins settle
down almost in parallel arteries and bear blood back to heart. Unlike arteries, veins have more thin
walls which contain less than a muscular and elastic fabric.
Heart of the person is the muscular pump divided into 4 chambers. Two top chambers are called as
auricles, and two bottom - ventricles.
These two types of chambers of heart carry out different functions: auricles collect the blood
arriving in heart and push it in ventricles, and ventricles push out blood from heart in an artery on
which it gets to all parts of a body.
Two auricles are divided interatrial by a partition, and two ventricles - interventricular a partition. An
auricle and ventricle each party of heart incorporate atrioventricular an aperture. This aperture opens
and closes atrioventricular the valve. Left atrioventricular the valve is known also as mitral the valve,
and right atrioventricularthe valve-asthe three-folding valve.
Normal physiology
Automatism function.Automatism function is an ability of heart to develop electric impulses in the
absence of external irritations.
Conductivity function.Conductivity function is an ability to carrying out of excitation of fibres of
spending system of heart and retractile a myocardium.
Excitability function.Excitability function is an ability of cages of spending system of heart and
retractile a myocardium to be raised under the influence of external electric impulses.
Function contractility. Contractilityfunction - is ability of a cardiac muscle to be reduced in reply to
excitation. This function possesses basically retractile a myocardium.
As a result of consecutive reduction and a relaxation of variousdepartments of heart the basic is
carried out -pump function of heart.
Histology
Myocardium structure.
To light microscopy branching of the fibres consisting from cardiomyocytes is visible to A.Pri. In the
centre of everyone cardiomyocyte there is a kernel.
B.Stroeniecardiomyocyte (submitted electronic microscopy). The set parallel myofibril, consisting of
segments - sarcomereIs visible.
V.Stroeniesarcomere.
G.Raspolozhenie of threads on a cross-section cut sarcomere. In the centre of disk A (zone) is only
thick threads (myosin), in its peripheral departments - both thick, and thin threads (actin), and each
thick thread is surrounded by six thin. In a disk I there are only thin threads.
Pathological anatomy.
Myocardium hypertrophy of LV it is caused first of all by postloading increase that promotes growth
of pressure of wall LV. In hypertrophy formation activation fabric RACES, the leader to increase in
development АII which through receptors АТ2 influences on кардиомиоциты has Great value, as is
known, causing their hypertrophy. Other factors (эндотелины, growth factors etc.) matter also.
In initial stages of formation IG moderate concentric диффузнаяthe myocardium hypertrophy in
most cases develops? LV with identical increase in a thickness of a wall of various segments LV (a
back wall, IVS, tops etc.). Approximately in 1/3 cases the hypertrophy has asymmetric character
when there is primary hypertrophy IVSor back wall LV.
Concentric () and eccentric () a hypertrophy of a myocardium left ventricle at idiopathic
hypertensia
The size of muscular weight LV (ММLV) gradually increases, in a cardiac muscle develops fibrosis.
Infringements diastolic functions For a long time prevail? letter=Д&id_term=35>LV with decrease
in its pliability during time diastoles and redistribution diastolic a blood stream aside larger volume
atrialemission.
In this connection can moderately raise FDP and pressure of filling LV that is quite
often accompanied dilatationLA.
In due course decreases contractility myocardium LV and dysfunction develops it sistolic. There are
signs dilatationLV and the eccentric hypertrophy of a myocardium
<http://medbook.medicina.ru/term.php develops? letter=Г&id_term=34>LV. Insufficiency of blood
circulation develops in late stages of illness, mainly on left ventricular or biventricular to type.
Pathological physiology
Hyperactivation role simpato- adrenal systems (SAS). In most cases AH, especially at early stages of
formation of disease, proceeds with expressed hyperactivationSAS-hipersimpatikotonia which is not
so much result “cardiovascular neurosis” vasomotorcentre, how many reflects disadaptation the system
of blood circulation to usual physiological loadings (physical and emotional).
hipersimpaticotonia initiates the whole cascade регуляторных the infringements anyhow
influencing level the HELL:
The increase LV contractility and HR, that is accompanied by growth of warm emission (MV);
Stimulation норадреналином<http://medbook.medicina.ru/term.php?letter=А&id_term=3>, allocated in
presynaptic cracks, α1-adrenoretseptorov smooth-muscular cages arterioles, that conducts to increase of
a vascular tone and sizes TPR;
Thus, against hyperactivationSAS activity of variety прессорных the mechanisms regulating the
HELL raises: increases MV, TPR
Propaedeutics of internal illnesses
The most typical complaints of patients IG are: headaches of various character and genesis;
dizzinesses, memory infringements, noise in a head, irritability, fast fatigue; flashing of "front
sights" before eyes and other signs of infringement of sight; pains in the field of heart, small pastose
hypodermic fat.
The analysis anamnestic data allows to reveal some features of current AH, more characteristic for
symptomatic AH: youngish age of patients AH; the sharp beginning of disease with fast stabilisation
the HELL on high figures; in most cases - sistolo-diastolichesky character AH, and diastolic the
HELL often exceeds 110-120 mm hg (exceptions make some cases hemodynamic caused AH - aortal
insufficiency, an atherosclerosis of an aorta, etc. for which increase sistolic the HELL is more
characteristic); it is quite often observed refractory to antihypertensiv therapies; fast development of
complications (a stroke, to IT, sight infringements, ХПН, etc.).
Appearance of patients:position - active, except patients transferred ischemic or hemorrhagic stroke,
at late stages - orthopnoe; adiposity - especially adverse in prognostic the relation is so-called
abdominal adiposity type; hypostases of the bottom finitenesses; colour of a skin - hyperemia persons
with unsharply expressed cyanosis, pallor; neurologic semiology - paresises, paralyses, a smoothness
nasolabialfolds, language deviation, pathological reflexes, nystagmus, etc.
Palpation and percussion
I stage - without changes;
II stage - strengthening and displacement to the left a top push, displacement of relative dullness of
heart to the left, expansion of a vascular bunch.
auscultation
I tone loud or "deaf"; accent of II tone over an aorta; in initial stages - on a top pathological IV tone
is listened; in late stages - on a top pathological III tone is listened; functional noise on an aorta; at
relative insufficiency mitral the valve - sistolic noise in a combination to weakened I tone on a top,
spent to the left axillary area.
Arterial pulse
Arterial pulse at IG good filling and pressure, big, firm. The tachycardia and arrhythmia quite often
comes to light.
Beam diagnostics
patients IG degree dilatationLV, and at patients with warm insufficiency - signs of
venous stagnation of blood in a small circle of blood circulation and a pulmonary arterial
hypertensia allows to estimate hearts.
Allocate three degrees of increase LV revealed in the left forward slanting projection:
I degree - back contour LV reaches backbone edge;
II degree - a back contour accumulates on a backbone shade;
III degree - a back contour considerably accumulates on a backbone shade, blocking it.
Roentgenography at
Intradisciplinarycommunication:
The knowledge acquired in the course of employment can be applied at studying of
subjects:cardiology, ophthalmology, endocrinology, neurology, nephrology.
6. The employment maintenance
Theoretical part
IDIOPATHICHYPERTENSION
Essential hypertension (also called primary or idiopathic hypertension) is the form of
hypertension that by definition, has no identifiable cause. It is the most common type of
hypertension, affecting 95% of hypertensive patients, it tends to be familial and is likely to be the
consequence of an interaction between environmental and genetic factors. Prevalence of essential
hypertension increases with age, and individuals with relatively high blood pressures at younger
ages are at increased risk for the subsequent development of hypertension. It can increase risk for
cerebral, cardiac, and renal events.
Contents
1 Classification
2 Risk factors
3 Pathophysiology
4 References
Classification
The variation in pressure in the left ventricle (blue line) and the aorta (red line) over two cardiac
cycles ("heart beats"), showing the definitions of systolic and diastolic pressure.
A recent classification recommends blood pressure criteria for defining normal blood pressure,
prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a
common occurrence among the elderly. These readings are based on the average of seated blood
pressure readings that were properly measured during 2 or more office visits. In individuals older
than 50 years, hypertension is considered to be present when a person's blood pressure is
consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures over
130/80 mmHg along with Type 1 or Type 2diabetes, or kidney disease require further treatment.
Classification
Normal
Systolicpressure
Diastolicpressure
mmHg kPa (kN/m2) mmHg kPa (kN/m2)
90–119 12–15.9
60–79 8.0–10.5
Prehypertension 120–139 16.1–18.5
81–89 10.8–11.9
Stage 1
140–159 18.7–21.2
90–99 12.0–13.2
Stage 2
≥160
≥21.3
≥100
≥13.3
Isolatedsystolic
≥140
hypertension
≥18.7
<90
<12.0
Resistant hypertension is defined as the failure to reduce blood pressure to the appropriate level after
taking a three-drug regimen. Guidelines for treating resistant hypertension have been published in
the UK, and US.
Risk factors
Hypertension is one of the most common complex disorders. The etiology of hypertension differs
widely amongst individuals within a large population. And by definition, essential hypertension has
no identifiable cause. However, several risk factors have been identified.
Hypertension may be secondary to other diseases but over 95% of patients have essential
hypertension which is of unknown origin. Itisobservedthoughthat:


Having a personal family history of hypertension increases the likelihood that an individual
develops HPT.
Essential hypertension is four times more common in black than white people, accelerates
more rapidly and is often more severe with higher mortality in black patients.
More than 50 genes have been examined in association studies with hypertension, and the number is
constantly growing. One of these genes is the angiotensinogen (AGT) gene, studied extensively by
Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence
this may cause hypertension. Twins have been included in studies measuring ambulatory blood
pressure; from these studies it has been suggested that essential hypertension contains a large
genetic influence. Supporting data has emerged from animal studies as well as clinical studies in
human populations. The majority of these studies support the concept that the inheritance is
probably multifactorial or that a number of different genetic defects each has an elevated blood
pressure as one of its phenotypic expressions. However, the genetic influence upon hypertension is
not fully understood at the moment. It is believed that linking hypertension-related phenotypes with
specific variations of the genome may yield definitive evidence of heritability. Another view is that
hypertension can be caused by mutations in single genes, inherited on a Mendelian basis.
Hypertension can also be age related, and if this is the case, it is likely to be multifactorial. One
possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries.
This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in
glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium
excretion. The developing of certain diseases such as renal microvascular disease and capillary
rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental
evidence that suggests that renal microvascular disease is an important mechanism for inducing saltsensitive hypertension.
Obesity can increase the risk of hypertension to fivefold as compared with normal weight, and up to
two-thirds of hypertension cases can be attributed to excess weight. More than 85% of cases occur
in those with a Body mass index greater than 25.[ A definitive link between obesity and
hypertension has been found using animal and clinical studies; from these it has been realized that
many mechanisms are potential causes of obesity-induced hypertension. These mechanisms include
the activation of the sympathetic nervous system as well as the activation of the renin–angiotensinaldosterone system.
Another risk factor is salt (sodium) sensitivity which is an environmental factor that has received the
greatest attention. Approximately one third of the essential hypertensive population is responsive to
sodium intake.When sodium intake exceeds the capacity of the body to excrete it through the
kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular
compartment. This causes the arterial pressure to rise as the cardiac output increases. Local
autoregulatory mechanisms counteract this by increasing vascular resistance to maintain
normotension in local vascular beds. As arterial pressure increases in response to high sodium
chloride intake, urinary sodium excretion increases and the excretion of salt is maintained at expense
of increased vascular pressures. The increased sodium ion concentration stimulates ADH and thirst
mechanisms, leading to increased reabsorption of water in the kidneys, concentrated urine, and thirst
with higher intake of water. Also, the water movement between cells and the interstitium plays a
minor role compared to this. The relationship between sodium intake and blood pressure is
controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is
insufficient to recommend a general reduction in salt intake.
Renin elevation is another risk factor. Renin is an enzyme secreted by the juxtaglomerular apparatus
of the kidney and linked with aldosterone in a negative feedback loop. In consequence, some
hypertensive patients have been defined as having low-renin and others as having essential
hypertension. Low-renin hypertension is more common in African Americans than white Americans,
and may explain why African Americans tend to respond better to diuretic therapy than drugs that
interfere with the Renin-angiotensin system. High renin levels predispose to hypertension by
causing sodium retention through the following mechanism: Increased renin → Increased
angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium
reabsorption in the kidneys (DCT and CD) → Increased blood pressure.
Hypertension can also be caused by Insulin resistance and/or hyperinsulinemia, which are
components of syndrome X, or the metabolic syndrome. Insulin is a polypeptide hormone secreted
by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose
is to regulate the levels of glucose in the body antagonistically with glucagon through negative
feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin
may stimulate sympathetic activity without elevating mean arterial pressure. However, in more
extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity
may over-ride the vasodilatory effects of insulin.
It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors. It has
been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood
pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a
"negative endocrine regulator of the renin-angiotensin system". Hence a deficiency in vitamin D
leads to an increase in renin secretion. This is one possible mechanism of explaining the observed
link between hypertension and vitamin D levels in the blood plasma.
Also, some authorities claim that potassium might both prevent and treat hypertension.
Recent studies claims that obesity is a risk factor for hypertension because of activation of the reninangiotensin system (RAS) in adipose tissue, and also linked renin-angiotensin system with insulin
resistance, and claims that any one can cause the other.
Cigarette smoking, a known risk factor for other cardiovascular disease, may also be a risk factor for
the development of hypertension.
Pathophysiology
A diagram explaining factors affecting arterial pressure
Cardiac output and peripheral resistance are the two determinants of arterial pressure. and so blood
pressure is normally dependent on the balance between cardiac output and peripheral resistance.
Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial
contractility and to the size of the vascular compartment. Peripheral resistance is determined by
functional and anatomic changes in small arteries and arterioles. The pathophysiology of essential
hypertension is an area of research, and until now remains not well understood, but many theories
have been proposed to explain this.
What is known is that cardiac output is raised early in the disease course, with total peripheral
resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased.
Threetheorieshavebeenproposedtoexplainthis:


An overactive Renin-angiotensin system leads to vasoconstriction and retention of sodium
and water. Theincreaseinbloodvolumeleadstohypertension.
An overactive sympathetic nervous system, leading to increased stress responses.
It is also known that hypertension is highly heritable and polygenic (caused by more than one gene)
and a few candidate genes have been postulated in the etiology of this condition.
The new pedagogical technologies applied on employment:
Interactive game «Business game»
At application of "Business game» students are distributed on roles.
For example:
The student - the patient.
The student - the local therapist.
The student - the ambulance surgeon.
The student - the doctor of a reception.
The student - the doctor of an electrocardiogram of an office.
The student - реаниматор
The student - the expert.
The student - the cardiologist
In the course of game the student should play the role correctly. After game the
student the expert estimates errors and lacks at execution by each student of the role.
6.2. An analytical part.
Situational problems
1. At sick 50 years which has addressed to the doctor of the urgent help with complaints to
intensive headaches and a nausea, increase the HELL to 200/115 mm hg In the anamnesis an arterial
hypertensia in a current of 7 years is found out. Constant therapy does not receive.
I. You will appoint What two preparations the patient:
A. Dibazolumin/m
B. Furosemidum in/v*
C. magnesia sulphatein/m
D. papaverinin/m
E. nifedipine*
II. As heart borders change:
A. are displaced to the left and to the right
B. are displaced upwards and to the right
C. are displaced to the left and downwards
D. are displaced upwards, to the right and to the left
2. The patient of 45 years, shows complaints to strong headaches, face skin and neck
reddening, a shiver in hands, palpitation, dizziness, потливость.
Objectively: a condition of average weight. In lungs - vesicularbreath. Tones of heart are muffled, a
tachycardia, II tone over an aorta is strengthened. The HELL of 160/100 mmс.у.т., pulse of 100
blows 1 minute, rhythmical. An electrocardiogram: a sinus rhythm,ЧСС 95 blows 1 minute. Signs of
a hypertrophy left ventricle. Your diagnosis?
A. Sharp heart attack of a myocardium
B.
C.
Sharp infringement of brain blood circulation
Idiopathic hypertensia , hypertensive crisis*
D. Pheochromocytoma
What stage of disease?
A. I
B. II*
C. III
3. In branch of intensive therapy the patient of 45 years with following complaints has
arrived: noise in ears, headaches, dizziness, dimness before eyes, palpitation, fatigue, the general
weakness. Objectively: a condition of average weight. Integuments damp, pure. Pulse 60 1 minute
the rhythmical. The HELL of 170/90 mm hg an electrocardiogram: a rhythm синусовый, ЧСС 58 in
1мин, signs of a hypertrophy left желудочка,AV-blockade of 1 degree.
Your diagnosis:
A. Idiopathic hypertensia *
B. IHD, a myocardium heart attack
C. IHD, a pressure stenocardia
D. Neurocirculatory dystonia oncardial type
What preparation is counter-indicative:
A. Atenololum*
B. Corinfarum
C.
kapotenum
D. Nitrosorbidum
4. The patient 42 years, is on stationary treatment in cardiological branch with the
diagnosis:Idiopathic hypertensia of II degree.
Prospective left border of heart:
A. 5 intercostal space 1,5 sminside from left mediaclavicular lines.
B. 5 intercostal space 1,0 sminsidefrom left mediaclavicular lines
C. 5 intercostal space1,0 smoutside from left mediaclavicularlines
Changes on an electrocardiogram:
A. RI> RII> RIII; RAVL> RAVF; RV5> RV4*
B. RII> RI> RIII; RAVL> RAVF; RV5> RV4
C. RI> RII> RIII; RAVF> RAVL; RV4> RV5
7. A quality monitoring of practical skills and theoretical knowledge.
1. Professional inquiry and survey of the patient with idiopathic hypertensia.
The purpose:
- Reception of the information necessary for diagnostics;
- An estimation of probability of disease;
- Definition of other sources of the information (relatives, other doctors, etc.);
- An establishment of confidential mutual relations with the patient;
- An estimation of the person of the patient and its relation to illness (an internal picture of illness);
- To estimate a condition of consciousness and the mental status of the patient, its position, a general
view, a condition of external covers and separate sites of a body.
Indications: interrogation necessarily for all patients who are in consciousness; survey is spent by all
patient.
Equipment: well shined chambers, offices of doctors, lamps of day illumination.
Performance conditions: absence of extraneous persons, confidential conditions.
Carried out stages (steps):
№
Action
Has not executed
1
Inquiry of nameplate data
2
Gathering of complaints
3
Gathering of the anamnesis of disease
4
Gathering of the anamnesis of a life
5
The epidemiological, allergic anamnesis
6
Objective survey of the patient
7
Will make the inspection plan
8
Correct statement of the diagnosis
9
Differential diagnostics
10
Will make the treatment plan
In total
0
0
0
0
0
0
0
0
0
0
0
Completely has
correctly executed
5
15
20
15
5
5
5
5
20
5
100
2. Drawing up of dietary recommendations and the treatment program.
The purpose: Treatment of illnessand preventive maintenance of complications.
№
2
3
4
5
6
Action
Has not executed
Studying of the characteristic of medical tables on
Певзнеру
Correct choice of a dietary table according to the
diagnosis
Estimation of
full value of a diet
According to the diagnosis, weight of disease and a stage
appointment of the basic therapy
According to the diagnosis, weight of disease and a stage
appointment of symptomatic therapy
Preventive actions
In total
0
Completely
has correctly
executed
10
0
10
0
20
0
20
0
20
0
0
20
100
Tests
1. Not medicamentoustreatment of an arterial hypertensia does not concern:
A. restriction physical activity*
B. sufficient physical activity
C. decrease in superfluous bodyweight
D. restriction of consumption of table salt
2. To блокаторам receptors of angiotensin II do not carry:
A. losartanum
B. valsartanum
C. enalapril*
D. irbesartanum
3. As irrational combinations in treatment of an arterial hypertensia consider:
A. β-adrenoblockers + nondihydropyridine slow calcium channelblockers*
β-adrenoblockers + diuretics
ингибиторыАПФ + slow calcium channelblockers
D. ингибиторыАПФ + diuretics
4. The most exact method of revealing of a hypertrophy left ventricle:
A. percussion
B. ECG
C. EchoCG*
D. radiological research
5. At objective research of the patient with idiopathic hypertensiaof II stage it is found out
A. sistolic noise on the basis of heart on the right
B. accent of II tone over an aorta
C. increase heart borders
D. displacement of borders of heart to the left*
6. On what basis of symptoms III stage of idiopathic hypertensia is defined:
A. a hypertrophy of left ventricle
B. a hypertrophy of right ventricle
C. high proof arterial pressure
D. complications from bodies target*
7. The basic electrocardiograms signs of a hypertrophy left ventricle:
A. absence of tooth Т
B. lengthening of interval Q-T
C. increase R II. V1, V2
D. increase in amplitude of tooth R I. V5, V6, AVL*
8. The choice of a preparation for treatment of idiopathic hypertensia (IG) is always difficult. Most 2
correct principles of selection are:
A. the account of stage IG and degrees of increase the HELL
B. the account of clinical variant IG (the reasons of increase the HELL and its expressivenesses
in each concrete case) *
C. the account pathophysiological variant IG (the reasons of increase the HELL and its
expressivenesses in eachconcretecase) *
D. step selection of appointment of monotherapy in all cases IG
E. sharp medicinal tests
9. Specify 2 basic of a preparation, the most effective in treatment volume-dependent of the form of
idiopathic hypertensia:
B.
C.
A. Obsidanum
B.
C.
clonidine
Triampurcompositum
D. Corinfarum *
E.
*
captopril
10. Under the maintenance renin allocate forms of an arterial hypertensia:
A. normorenin*
B. hyporenin*
C. hyperrenin*
D. normokinetic
E. hyperkinetic
F. hypokinetic
11. In pathogenesisidiopathic hypertensia all listed factors have leading value, except:
A. the hereditary or got infringements of cellular membranes with electrolyticinfringements
B. the raised reactance of sympathetic nervous system
C. deficiency (or exhaustions) depressory systems
D.
hyperactivity of system renin - angiotensin-II - Aldosteronum
decrease in the maintenance of calcium in smooth-muscular cages of walls arterioles*
F. the raised reactance of parasympathetic nervous system *
12. To group of risk of disease of idiopathic hypertensia carry all listed, except:
A. hereditary predisposition
B. superfluous consumption of salt
C. a stomach ulcer *
D. excess weight
E. bronchial asthma*
13. To not selective/Z-adrenoblokatorov carry all preparations, except (3):
A. atenolol*
B. methoprolol*
C. propranolol
D. bisoprolol*
E.
E.
Corvitin
14. Bodies-targets at an arterial hypertensia everything, except (2):
A. liver*
B. kidneys
C. hearts
D. a brain
E. lungs*
15. Increase the HELL can cause long reception of all ЛС, except (2):
A. anaprilin*
B. NSAID
C. inhibitorsMAO
D. peroral contraceptives
E. enalapril*
16. The Alpha-adrenoblokatoramcarry everything, except (2):
A. Reserpinum*
B. Clonidinum*
C.
D.
Prazozinum
E.
F.
diabetes mellitus
doxozinum
17. As contra-indications for appointment inhibitorsACF consider (4):
A. pregnancy*
B. a hypertensive crisis
C. dry tussis*
D. the expressed stenosis of a mouth of an aorta and mitral orifice*
bilateral stenosis of nephritic arteries*
18. InhibitorsАПФ block (2):
A. receptors of angiotensin II
B. transformation of angiotensin I in angiotensin II*
C. transformation of angiotensin II in angiotensin I
D. action of the enzyme, transforming angiotensin I in анигиотензин II*
19. Features of an arterial hypertensia at elderly (4):
A. more expressed reduction brain кровотока*
B. decrease secretory functions kidneys*
C. reduction warm выброса*
D. high total peripheralvascular resistance*
E. anything from the listed
F.
increase in warm emission
increase secretory functions of kidneys
20. For treatment of an arterial hypertensia use the following diuretics (3):
A. Thiazid*
B. loopback*
C. kalium savings*
D. osmotic
8. Criteria of an estimation of the current control
G.
Level of knowledge of the student
The student on the basic questions of a theme and concerning independent
work of students (IWS):
Sums up and makes of the decision
Creatively thinks
Independently analyzes
Puts into practice
Shows high activity, the creative approach at carrying out of interactive
games
Correctly solves situational problems with a full substantiation of the
answer
Understands a question essence
Knows, tells confidently
Has exact representations
Prepares modern informative visual aids or abstracts of high quality
with use of data of last literature from 7-10 sources and the Internet.
The student on the basic questions of a theme and concerning IWS:
Creatively thinks
Independently analyzes
Puts into practice
Shows high activity, the creative approach at carrying out of interactive
games
Correctly solves situational problems with a full substantiation of the
answer
Understands a question essence
Knows, tells confidently
Has exact representations
Prepares modern informative visual aids or abstracts of high quality
with use of data of last literature from 4-6 sources and the Internet.
The student on the basic questions of a theme and concerning IWS:
Independently analyzes
Puts into practice
Shows high activity, the creative approach at carrying out of interactive
games
Correctly solves situational problems with a full substantiation of the
answer
Understands a question essence
Knows, tells confidently
Has exact representations
Prepares modern informative visual aids or abstracts of high quality
Progress in % and points
Estimation
96-100
5
91-95
5
86-90
5
with use of data of last literature from 3-5 sources and the Internet.
The student on the basic questions of a theme and concerning IWS:
Puts into practice
Shows high activity, the creative approach at carrying out of interactive
games
Correctly solves situational problems with a full substantiation of the
answer
Understands a question essence
Knows, tells confidently
Has exact representations
Prepares modern informative visual aids or abstracts of high quality
with use of data of last literature from 3-5 sources and the Internet.
The student on the basic questions of a theme and concerning IWS:
Shows high activity at carrying out of interactive games
Correctly solves situational problems, but a substantiation of the
answer the incomplete
Understands a question essence
Knows, tells confidently
Has exact representations
Prepares modern visual aids or abstracts with use of data of last
literature from 1-2 sources.
The student on the basic questions of a theme and concerning IWS:
Correctly solves situational problems, but a substantiation of the answer
the incomplete
Understands a question essence
Knows, tells confidently
Has exact representations or
The student on the basic questions of a theme and concerning IWS:
Commits errors at the decision of situational problems
Knows, tells uncertainly
Has exact representations on separate questions of a theme
Prepares modern informative visual aids or abstracts of high quality
with use of data of last literature from 7-10 sources and the Internet.
Prepares modern visual aids or abstracts of high quality with use of
data of last literature from 4-6 sources and the Internet.
The student on the basic questions of a theme and concerning IWS:
Understands a question essence
Correctly solves situational problems, but cannot prove the answer
Knows, tells confidently
Has exact representations on separate questions of a theme
The student on the basic questions of a theme and concerning IWS:
Commits errors at the decision of situational problems
Knows, tells uncertainly
Has exact representations on separate questions of a theme
The student on the basic questions of a theme and concerning IWS:
Knows, tells uncertainly
Has partial representations
The student on the basic questions of a theme and concerning IWS:
Has no exact representation
81-85
4
76-80
4
71-75
4
66-70
3
61-65
3
55-60
3
Less than 55
2
Does not know
9. A chronological card of employment.
№
Stages of practical employment
Employment
forms
Opening address of the teacher (theme
substantiation).
Discussion of a theme of practical employment,
check of basic knowledge of students with use of
new pedagogical technologies, a demonstration
material
Duration
270minutes
10
(slides,audio videocassettes,
roentgenograms,
electrocardiogram,
etc.).Interrogation,
explanatories.
Discussion end.
60
20
Distribution of tasks to students for performance
of a practical part of employment. Instructing and
the explanatory under the requirements shown to
practical tasks.
Development by means of the teacher of a
practical part of employment (курация the
thematic patient).
Interpretation of laboratory-tool methods of
researches of the thematic patient, differential
diagnostics, treatment and preventive maintenance
scheduling, extract of recipes, etc.
Discussion of theoretical and practical knowledge
of students, their reinforcement and estimation of
activity of group in respect of achievement of an
object in view of employment.
The conclusion of the teacher on the passed
employment, an estimation of activity of each
student and the announcement of results. Working
out of tasks for preparation for following
employment (the collection of questions).
Independent
exemine patients.
30
Case records,
interactive games,
situational
problems.
Work with klinikolaboratory toolkit.
50
Oral interrogation,
the test,
discussion, check
of results of
practical work.
Questions for
independent work.
40
10. Questions for the control of knowledge
1. An aetiology and патогенез idiopathic hypertensia.
2. Classification of idiopathic hypertensia.
3. A clinical picture of idiopathic hypertensia.
4. Electrokardiografichesky changes at idiopathic hypertensia.
40
20
5. Radiological измененения at. Idiopathic hypertensia.
6. Complications of idiopathic hypertensia.
7. Treatment of idiopathic hypertensia.
8. Preventive maintenance of idiopathic hypertensia.
11. The recommended literature
The basic:
1. Internal illnesses: the textbook in 2t./under the editorship of N.A.Mukhin,
V.S.Moiseyev, A.I.Martynova, 2 изд., испр. And доп.- М: GEOTAR-MEDIA,
2009.- Т.2.592с.: silt.
The additional:
2. Rojtberg G. E, Strutynskij A.V. «Internal illnesses: Cardiovascular system». 856 p.
Moscow, 2007.
3. Okorokov A.N. “Diagnostics of illnesses of internal bodies”.Т.6. Diagnostics of
illnesses of heart and vessels.Moscow,2003 464 p.
4. Okorokov A.N. “Treatment of illnesses of internal bodies”.Т.3, кн.1. Treatment of
illnesses of heart and vessels.Moscow,2005 464 p.
5. Sites: www.ТМА.uz<http://www.ТМА.uz>.,
6. <http://www.meddean.luc.edu>,
7. http://www.embbs.com
References
1. ^Carretero OA, Oparil S (January 2000). "Essential hypertension. Part I: definition and
etiology". Circulation101 (3): 329–35. PMID 10645931.
http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10645931. Retrieved 200906-05.
2. ^Oparil S, Zaman MA, Calhoun DA (November 2003). "Pathogenesisofhypertension". Ann.
Intern. Med.139 (9): 761–76. PMID 14597461.
3. ^ Hall, John E.; Guyton, Arthur C. (2006). Textbook of medical physiology. St. Louis, Mo:
Elsevier Saunders. pp. 228. ISBN 0-7216-0240-1.
4. ^"Hypertension: eMedicine Nephrology". http://emedicine.medscape.com/article/241381overview. Retrieved 2009-06-05.
5. ^"Essential hypertension : The Lancet".
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(07)61299-9/abstract.
Retrieved 2009-06-01.
6. ^ abcChobanian AV, Bakris GL, Black HR, et al. (December 2003). "Seventh report of the
Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure". Hypertension42 (6): 1206–52. doi:10.1161/01.HYP.0000107251.49515.c2.
PMID 14656957. http://hyper.ahajournals.org/cgi/content/full/42/6/1206.
7. ^ Calhoun DA, Jones D, Textor S, et al. (June 2008). "Resistant hypertension: diagnosis,
evaluation, and treatment. A scientific statement from the American Heart Association
Professional Education Committee of the Council for High Blood Pressure Research" (PDF).
Hypertension51 (6): 1403–19. doi:10.1161/HYPERTENSIONAHA.108.189141.
PMID 18391085. http://hyper.ahajournals.org/cgi/reprint/51/6/1403.pdf.
8. ^ abc Dickson ME, Sigmund CD (July 2006). "Genetic basis of hypertension: revisiting
angiotensinogen". Hypertension48 (1): 14–20. doi:10.1161/01.HYP.0000227932.13687.60.
PMID 16754793. http://hyper.ahajournals.org/cgi/content/full/48/1/14.
9. ^ abcLoscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser,
Stephen L; Longo, Dan L. (2008). Harrison'sprinciplesofinternalmedicine. McGrawHillMedical. ISBN 0-07-147691-1.
10. ^Haffner SM, Lehto S, Rönnemaa T, Pyörälä K, Laakso M (July 1998). "Mortality from
coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and
without prior myocardial infarction". The New England Journal of Medicine339 (4): 229–34.
doi:10.1056/NEJM199807233390404. PMID 9673301.
http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9673301&promo=ONFLNS19.
Retrieved 2009-06-08.
11. ^Lindhorst J, Alexander N, Blignaut J, Rayner B (2007). "Differences in hypertension
between blacks and whites: an overview". Cardiovasc J Afr18 (4): 241–7. PMID 17940670.
http://blues.sabinet.co.za/WebZ/Authorize?sessionid=0:autho=pubmed:password=pubmed20
04&/AdvancedQuery?&format=F&next=images/ejour/cardio/cardio_v18_n4_a9.pdf.
Retrieved 2009-06-01.
12. ^ Burt VL, Whelton P, Roccella EJ, et al. (March 1995). "Prevalence of hypertension in the
US adult population. Results from the Third National Health and Nutrition Examination
Survey, 1988-1991". Hypertension25 (3): 305–13. PMID 7875754.
http://hyper.ahajournals.org/cgi/pmidlookup?view=long&pmid=7875754. Retrieved 200906-01.
13. ^Kotchen TA, Kotchen JM, Grim CE, et al. (July 2000). "Genetic determinants of
hypertension: identification of candidate phenotypes". Hypertension36 (1): 7–13.
PMID 10904005. http://hyper.ahajournals.org/cgi/pmidlookup?view=long&pmid=10904005.
14. ^ Williams B et al.; British Hypertension Society; Michael Sutters, MD (2006).
"Hypertension Etiology & Classification - Secondary Hypertension". Armenian Medical
Network. http://www.health.am/hypertension/secondary-hypertension/. Retrieved 2007-1202.
15. ^Kosugi T, Nakagawa T, Kamath D, Johnson RJ (February 2009). "Uric acid and
hypertension: an age-related relationship?".J Hum Hypertens23 (2): 75–6.
doi:10.1038/jhh.2008.110. PMID 18754017.
16. ^ abHaslam DW, James WP (2005). "Obesity". Lancet366 (9492): 1197–209.
doi:10.1016/S0140-6736(05)67483-1. PMID 16198769.
17. ^Rahmouni K, Correia ML, Haynes WG, Mark AL (January 2005). "Obesity-associated
hypertension: new insights into mechanisms". Hypertension45 (1): 9–14.
doi:10.1161/01.HYP.0000151325.83008.b4. PMID 15583075.
18. ^http://www.jstage.jst.go.jp/article/jphs/100/5/370/_pdf A Missing Link Between a High
Salt Intake and Blood Pressure Increase: Makoto Katori and MasatakaMajima, Department
of Pharmacology, Kitasato University School of Medicine, Kitasato, Sagamihara, Kanagawa,
Japan February 8, 2006
19. ^Jürgens G, Graudal NA (2004). "Effects of low sodium diet versus high sodium diet on
blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride".
CochraneDatabaseSystRev (1): CD004022. doi:10.1002/14651858.CD004022.pub2.
PMID 14974053.
20. ^ Lee JH, O'Keefe JH, Bell D, Hensrud DD, Holick MF (2008). "Vitamin D deficiency an
important, common, and easily treatable cardiovascular risk factor?".J. Am. Coll. Cardiol.52
(24): 1949–56. doi:10.1016/j.jacc.2008.08.050. PMID 19055985.
21. ^ Forman JP, Giovannucci E, Holmes MD, et al. (May 2007). "Plasma 25-hydroxyvitamin D
levels and risk of incident hypertension". Hypertension49 (5): 1063–9.
doi:10.1161/HYPERTENSIONAHA.107.087288. PMID 17372031.
22. ^ Eva May Nunnelley Hamilton, M.S., Eleanor Noss Whitney, Ph.d, R.D., Frances
Sienkiewicz Sizer, M.S., R.D. (1991). Fifth Edition Annotated Instructor's Edition Nutrition
Concepts & Controversies. West Publishing Company. ISBN 0-314-81092-7.
OCLC 22451334.
23. ^ Segura J, Ruilope LM (October 2007). "Obesity, essential hypertension and reninangiotensin system". Public Health Nutrition10 (10A): 1151–5.
doi:10.1017/S136898000700064X. PMID 17903324.
http://journals.cambridge.org/abstract_S136898000700064X. Retrieved 2009-06-02.
24. ^ Hasegawa H, Komuro I (April 2009). "[The progress of the study of RAAS]" (in Japanese).
Nippon Rinsho. JapaneseJournalofClinicalMedicine67 (4): 655–61. PMID 19348224.
25. ^Saitoh S (April 2009). "[Insulin resistance and renin-angiotensin-aldosterone system]" (in
Japanese). NipponRinsho. JapaneseJournalofClinicalMedicine67 (4): 729–34.
PMID 19348235.
26. ^Halperin RO et al. (2008). "Smoking and the Risk of Incident Hypertension in Middle-aged
and Older Men". AmericanJournalofHypertension21 (2): 148–152. doi:10.1038/ajh.2007.36.
PMID 18174885.
27. ^Klabunde, Richard E. (2007). "Cardiovascular Physiology Concepts - Mean Arterial
Pressure". http://www.cvphysiology.com/Blood%20Pressure/BP006.htm. Retrieved 200809-29.
28. ^Sagnella GA, Swift PA (June 2006). "The Renal Epithelial Sodium Channel: Genetic
Heterogeneity and Implications for the Treatment of High Blood Pressure".
CurrentPharmaceuticalDesign12 (14): 2221–2234. doi:10.2174/138161206777585157.
PMID 16787251.
29. ^ Johnson JA, Turner ST (June 2005). "Hypertension pharmacogenomics: current status and
future directions". Current Opinion in Molecular Therapy7 (3): 218–225. PMID 15977418.
30. ^ Hideo Izawa; Yoshiji Yamada et al. (May 2003). "Prediction of Genetic Risk for
Hypertension". Hypertension41 (5): 1035–1040. doi:10.1161/01.HYP.0000065618.56368.24.
PMID 12654703.
http://hyper.ahajournals.org/cgi/content/short/01.HYP.0000065618.56368.24v1.
Download