A genetic defect in cell membranes in primary arterial hypertension leads to:

Candidate genes for the development of arterial hypertension, the expression of which is associated with vasoconstriction, include:

Hypernatremia contributes to the development of arterial hypertension through:

One of the modifying risk factors predisposing to the development of primary arterial hypertension is:

Endothelial dysfunction in arterial hypertension is characterized by an increase in the expression and production of:

Nitric oxide, by activating guanylate cyclase with subsequent activation of cGMP-dependent protein kinase G, contributes to:

The pathogenetic stage of stabilization of arterial hypertension is characterized by:

The stable stage of the pathogenesis of hypertension is characterized by:

A patient complained of headaches, facial swelling, and general weakness. Symptoms appeared three weeks after tonsillitis. Blood pressure was 190/100 mmHg. The urine showed significant proteinuria and microhematuria. The patient developed a form of secondary arterial hypertension. What is the most likely diagnosis?

A patient experienced sharp increases in blood pressure, accompanied by palpitations, muscle tremors, profuse sweating, and pale skin. Elevated catecholamine levels were observed in the urine. A CT scan revealed a tumor on the left adrenal gland. This type of hypertension is characteristic of:

Exogenous form of secondary arterial hypertension can occur when taking:

Which of the following is a first-line therapy for idiopathic bilateral adrenal hyperplasia with symptoms such as severe hypokalemia and elevated 17-hydroxycorticosteroid levels?

The hypotensive effect of beta-blockers is primarily due to their ability to:

Under physiological conditions, coronary blood flow is regulated primarily by:

The pathogenetic basis of ischemic heart disease is:

In coronary insufficiency, increased calcium content in cardiomyocytes is accompanied by:

Coronary factors in the development of absolute coronary insufficiency include:

The cause of absolute coronary insufficiency, which occurs when the blood supply to intact coronary vessels decreases, may be:

In absolute coronary insufficiency, instability (“vulnerability”) of the atherosclerotic plaque is associated with:

Factors leading to the development of relative coronary insufficiency include:

A patient with a myocardial infarction developed shortness of breath, tachycardia, and cyanosis of the visible mucous membranes. The development of hypoxia in this case is associated with:

Patient R., 52, was admitted to the emergency room of the hospital unconscious. According to his relatives, the patient had experienced a severe chest pain approximately five hours earlier, with no response to nitroglycerin. An ECG revealed abnormal Q waves (QS) in leads I, V1, and V2, with ST elevations above the isoline and an upward curve. The following factors are most significant in the development of this typical form of cardiac pathology:

A 38-year-old patient experienced a sharp, crushing pain behind the sternum after emotional stress, radiating to the left arm and under the left shoulder blade. Blood levels of lactate dehydrogenase and creatine phosphokinase were elevated. An ECG showed changes in the ST segment and T wave. Coronary angiography revealed no changes. The most likely cause of cardiac damage in this case is:

Which feature of energy metabolism is observed under conditions of myocardial ischemia?

RAutopsy results revealed that the patient died of myocardial infarction associated with stent thrombosis. Histological examination of the myocardium revealed significant contracture changes in the cardiomyocytes. This is due to the accumulation of ions in the cardiomyocytes:

Patient F., 67, has had a 10-year history of chest pain when walking, which is relieved by nitroglycerin. He smokes 10-15 cigarettes a day. Several hours ago, intense chest pain developed that was not relieved by nitroglycerin. An ECG shows ST segment elevation in leads I, aVL, and V1–V6, along with the formation of a pathological Q wave (with an amplitude greater than 1/4 of the R wave and a duration greater than 0.03 s). To determine the typical form of cardiac pathology, the following cardiac-specific marker must be measured in the blood:

In stable and unstable angina, myocardial infarction, and chronic heart failure of ischemic origin, which of the following is often detected?

Non-coronary myocardial necrosis in young women most often occurs with which of the following?

An increase in the diastolic pressure gradient between the left atrium and the left ventricle is characteristic of which condition?

Following acute rheumatic fever, a patient developed thickening and calcification of the valve leaflets, resulting in decreased left ventricular filling during diastole and increased pulmonary venous pressure. These signs are characteristic of which condition?

The most common complication of mitral stenosis is the development of:

Mitral valve prolapse, papillary muscle dysfunction, and rupture of the chordae tendineae can lead to the development of acquired heart disease, which is characterized by:

Complications of acute severe mitral regurgitation may include the development of:

The patient complains of shortness of breath, increased fatigue, heart pain, irregular heart rhythms, and fainting during exertion. Left ventricular hypertrophy and aortic orifice diameter were detected. The characteristic hemodynamic abnormalities of this heart defect include:

The most common cause of aortic stenosis in younger patients is:

With narrowing of the aortic orifice, an increase in afterload is accompanied by the development of:

A patient with severe infective endocarditis developed rupture of the aortic valve leaflets, leading to heart pain. The mechanism of cardiac pain is as follows:

A patient presents with increased carotid artery pulsation, pupillary pulsation, and head nodding movements corresponding to each systole. The pulse is rapid, high, and systolic blood pressure is 200 mmHg, while diastolic blood pressure is 20 mmHg. These signs are characteristic of:

During which period are congenital heart defects and minor anomalies in the development of the heart formed?

Patent ductus arteriosus with preserved connection between the aorta and pulmonary artery after birth is accompanied by the development of:

What occurs with an atrial septal defect?

The characteristic clinical symptoms of a congenital heart defect include cyanosis and dyspnea. Echocardiography reveals a large ventricular septal defect, pulmonary valve stenosis, right ventricular hypertrophy, and aortic overhang. Pulmonary circulation hemodynamics in this heart defect are characterized by:

The patient's ECG revealed a regular rhythm, with a P wave before each QRS complex and a heart rate of 110 min-1. The primary electrophysiological mechanism for the development of this arrhythmia is:

A patient with a traumatic brain injury was diagnosed with nomotopic arrhythmia with a heart rate of 40-45 bpm. Changes in cardiac automaticity may be associated with

Heterotopic rhythm disturbances associated with changes in impulse formation include:

The electrophysiological basis for the occurrence of arrhythmias associated with the development of trigger activity (trigger automatism) is:

Early afterdepolarizations may be the electrophysiological basis for trigger activity. An important condition for their occurrence is:

The consequence of a prolonged attack of paroxysmal ventricular tachycardia is:

When potassium ions enter the extracellular environment and its concentration in cardiomyocytes decreases, the development of extrasystoles is associated with:

Patient Sh., 68, complains of palpitations and shortness of breath during moderate physical exertion. He has a history of myocardial infarction. Objectively: the heart rhythm is irregular, with an average heart rate of 100 beats per minute and weakened heart sounds. The ECG shows no P waves in all leads, variable RR intervals, and f waves of varying amplitude and shape. These findings indicate a cardiac arrhythmia:

The formation of the micro-re-entry mechanism most often leads to the emergence of:

The patient's ECG shows all P waves associated with QRS complexes, a regular rhythm, and a PQ interval duration of 0.26 seconds. These signs indicate the

A patient with a myocardial infarction underwent 24-hour ECG monitoring, revealing a PQ interval of 0.36 seconds with the loss of every third QRS complex. The heart rate was 40 beats per minute. These signs indicate the patient is developing:

In a patient with ischemic heart disease, the ECG revealed M-shaped QRS complexes (type rsR') in the right chest leads, and widened, jagged S waves in the left chest leads and in leads I, aVL. The development of this type of arrhythmia is associated with dysfunction of:

The pathogenetic basis of cardiac arrhythmia associated with slowing or blocking of impulse conduction is:

The presence of additional abnormal pathways for conducting electrical impulses from the atria to the ventricles contributes to the development of:

Myocardial heart failure occurs when:

The development of the overload form of heart failure, caused by an increase in preload due to an increase in the end-diastolic volume of the ventricle of the heart, occurs when:

Secondary (non-cardiogenic) form of heart failure can occur with:

Heart failure with systolic dysfunction and reduced ejection fraction primarily develops with:

Characteristic hemodynamic signs of systolic heart failure include:

Left heart failure is most likely indicated by changes in the following hemodynamic parameters:

Left ventricular heart failure is characterized by:

The patient was admitted to the hospital in serious condition with a recurrent massive left ventricular myocardial infarction. He was agitated and unaware. His skin was pale, he had a cold, clammy sweat, and acrocyanosis. His respiratory rate was 24 beats per minute, his heart rate was 110 beats per minute, and his blood pressure was 80/50 mmHg. He was also diagnosed with oliguria. These signs indicate the development of:

A patient in the acute stage of myocardial infarction experienced an attack of severe inspiratory dyspnea accompanied by a feeling of fear, frothy sputum, and profuse fine rales in the lungs. The trigger for the development of this typical form of circulatory pathology is:

A patient with an anterior left ventricular myocardial infarction experienced a severe asthma attack. Examination revealed diffuse cyanosis and numerous moist rales of varying caliber. Heart rate was 100 beats per minute, and blood pressure was 120/100 mmHg. The primary pathogenic factor for the development of this complication of myocardial infarction is:

A patient with myocardial infarction has pronounced pallor of the skin and mucous membranes, oliguria, respiratory rate of 28 beats per minute, heart rate of 110 beats per minute, and blood pressure of 100/85 mmHg. In this situation, blood pressure is maintained by compensatory mechanisms such as:

The patient suffered a transmural myocardial infarction. He suddenly lost consciousness. His pulse and blood pressure are undetectable, and his breathing is agonal. The ECG, instead of ventricular QRS complexes, shows frequent (400 per minute) irregular waves of varying shape and amplitude. The treatment method for this heart rhythm disorder is:

With prolonged activation of the sympathoadrenal system, chronic heart failure progresses. What is this due to?

A patient with chronic obstructive pulmonary disease developed tachycardia, severe peripheral edema, ascites, jugular vein distension, acrocyanosis, nausea, decreased appetite, and oliguria. This typical form of circulatory pathology is characterized by the development of:

With myogenic dilation of the ventricles of the heart, characteristic changes in intracardiac hemodynamics are:

After recovering from the flu, a patient with coronary artery disease developed signs of cardiac decompensation, including edema in the lower extremities. What is the initial link in the pathogenesis of edema development?

A patient with chronic heart failure secondary to coronary artery disease (CAD) was diagnosed with pleural effusion. A thoracentesis was performed. Characteristics of pleural effusion in congestive heart failure include: