Download Methodological Instruction to Practical Lesson № 8

MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
Approval on methodological meeting
of the department of pathophisiology
Protocol №
Chief of department of the pathophysiology,
professor
Yu.Ye.Rohovyy
“___” ___________ 2008 year.
Methodological Instruction
to Practical Lesson
Мodule 2 : PATHOPHYSIOLOGY OF THE ORGANS AND SYSTEMS.
Contenting module 5. Pathophysiology of blood circulation
and respiratory system.
Theme 8: Hypertension. Hypotension.
Chernivtsi – 2008
1.Actuality of the theme. The disorders of the vasculare tone arise for
action of the various factors of the external and internal environment. It is
distinguished two main groups of such disorders: arterial hypertension and
arterial hypotension. Hypertensive disease as one example of arterial
hypertensions is the important problem of modern medicine. It is necessary to
take into account that fact, that in 50 % of the men and in 75 % of the women,
which suffer by hypertension the decrease of duration of life for 10 years is
revealed fast progress atherosclerosis, symptom of heart ischemic disease. At
the sometime many physicians frequently has deal with the patients in which the
parameters of arterial pressure are sharply reduced (shock, collapse). The
number of such patients in 4 times exceeds frequency of heart-vessels and
malignant diseases, and in connection with acceleration of scientific and
technical progress the tendency to growth of this kind pathology is observed.
2.Length of the employment – 2 hours.
3.Aim:
To khow: Several hypotheses have been proposed to explain the onset of
primary hypertension in individuals at risk. They include (1) increases in blood
volume, (2) inappropriate autoregulation, (3) overstimulation of sympathetic neural
fibers in the heart and vessels, (4) water and sodium retention by the kidneys, and
(5) hormonal inhibition of sodium-potassium transport across cell walls in the
kidneys and blood vessels.
To be able: to analyse the scheme for the pathogenesis of essential
hypertension, implicating genetic defects in renal excretion of sodium, functional
regulation of vascular tone, and structural regulation of vascular caliber.
Environmental factors, especially increased salt intake, potentiate the effects of
genetic factors. The resultant increase in cardiac output and peripheral resistance
contributes to hypertension. ECF, extracellular fluid.
To perform practical work: to analyse the pathogenesis of the
hypertension and hypotension.
4. Basic level.
The name of the previous
disciplines
1.
histology
2.
biochemistry
3.
physiology
The receiving of the skills
Histological structure of vessels wall.
Vascular tone.
Arterial pressure: the factors, defining it level.
Regulation of vascular tone and blood pressure.
Concept about the functional system of blood
circulation.
5. The advices for students.
1. The kinds of arterial hypertension
In the healthy people arterial pressure is within the limits of 100/60-139/89
mm Hg. Despite of difficult complex regulation, in many cases arterial pressure is
increased or decreased. High arterial pressure is called hypertension, low –
hypotension.
Arterial hypertension is constant and prolonged increase arterial pressure. It is
selecting two stages arterial hypertension: boundary hypertension and fixed
(stable) hypertension. Boundary hypertension is called such state, when the
pressure periodically achieves values of 140/90-159/94 mm Hg or constantly stays
in this range. If arterial pressure achieves level of 160/95 mm Hg or exceeds these
digits, it is regarded as stable, fixed hypertension.
Arterial hypertension divide on two groups – primary and secondary. Primary
arterial hypertension is called still essential hypertension, or hypertonic illness. It is
separate nosological unit. Its consist above 80 per cent all arterial hypertensions.
The second group consist secondary hypertension. On them it is about 20 per cent
of hypertensions. It is not separate nosological unit, and only symptoms of some
diseases (from this one more name – symptomatic hypertension).
2. Etiology and pathogenesis of hypertonic disease.
To problem the disease hypertonic to approach easiest on the basis of the
analysis already formula, known for us: AP = СO х PR. All influences, which are
capable to increase cardiac output or peripheral resistance, it is possible to consider
as etiological factors of hypertonic disease. To major etiological factors belong the
following: increase of plasma volume, increase cardiac output, increase activity of
sympathetic nervous system, alteration of kidneys functions, increase peripheral
resistance, hereditary predisposition.
Increase of plasma volume is connected with accumulation of the salt in
organism. It is possible in consumption plenties of salt, or in insufficient selection
it by kidneys (for example, kidney insufficiency). It is considered, that the long
consumption 5 g of salt per day can cause hypertension in the people, which have
hereditary predisposition.
The following scientific observations testify to a role NaCl in occurrence
arterial hypertension. The Japanese population, which lives on sea coast, every
day consumes salt in increased amount with water and food. Among this
population is observed very high morbility by hypertension (40 % of the adult
population the atter 40 years). At the same time among the population, which lives
in mountainous district and consumes less salt, the level of morbility from
hypertonic disease does not exceed 2 %, that is in 20 times is lower. On the other
hand, it is known, that lower-salt diet influences positive medical effect at the
patients with hypertonic disease.
Why the delay of salt promotes in an organism development arterial
hypertension? It is distinguished some mechanisms, which explain this fact. Owing
to accumulation of sodium, volume of extracellular liquid (including – circulatting
blood) is increased, follow the cardiac output increases and as a result is increased
arterial pressure. Compensator response on increase of plasmas volume is the
limitation blood circulation through the organs, and it is achieved by increase
resistance of peripheral vessels and increase pressure. The accumulation sodium
and water in walls of vessels is results of thickening the walls and decrease lumen
of vessels. Finally, the accumulation of sodium in walls of vessels is results of
increase sensitivity myocytes to pressor agents, in particular to angiotensin ІІ.
Increase of cardiac output. The increase volume of plasma increases cardiac
output secondaryly. However there are factors, which are capable directly to
increase cardiac output. Among them – emotional stress, hyperthyroidism. All
these states are accompanied by activation sympathetic nervous system.
Stimulation of cardiac activity is carried out through β-adrenoreceptors of
myocard on adrenaline acts. It increases stroke volume. In combination with
increase cardiac rate it lead to signiticant increase of cardiac output.
Increase sympathetic tonus. One of the factors responsible for development
essential hypertension, can be increase of activity sympathetic nervous system.
This hyperactivity has effect for functions of some organs, which can be
considered as a targe sympathetic influences. To this group belong heart, arteries,
veins and kidney.
Heart changes the activity on the already stated above mechanism: the
frequency of cardiac rate is increased, stroke volume of blood is increased and in a
result the cardiac output is increased.
In pathogenesis of arterial hypertension the special place belongs small-sized
arteries-arterioles. They are named vessels of resistance or taps of vascular
system. The most characteristic property of these vessels is the very high resistance
to blood circulation, for want to it is supported the proper level of arterial pressure.
The high resistance to blood circulation in arterioles is provided with some
structural and functional features them, named: а) a small lumen – 15-70 microns;
б) a thick layer smooth ring muscle; в) the wall of arterioles stays in a state
continuous tonus. Regulation of peripheral resistance and arterial pressure – main
function of resistance vessels.
The influence of sympathetic nerves to arterioles is carried out by two ways –
direct and mediated. From the terminations sympathetic nerves is selected
noradrenaline. It acts to α1-adrenoreceptors of vessels and narrows them. In such a
way it increases peripheral resistance, and arterial pressure.
Other mechanism consists in activation of adrenal gland medullar layer, where are
synthesized catecholamins – adrenaline and noradrenaline. The level of blood
pressure will depend from issue them simultaneous and of different direct action of
both hormones to cardio-vascular system: а) noradrenaline through α1adrenoreceptors of resistance vessels increases them tonus, peripheral resistance
and arterial pressure;
b) adrenaline excites β-adrenoreceptors of myocard,
increases cardiac output and in such way increases blood pressure;
c) simultaneously adrenaline acts to β-adrenoreceptors vessels dilatates throught
them and decrease blood pressure.
The development of arterial hypertension is possible only by following ratio
to effects of noradrenaline and adrenaline: increase of pressure by stimulation
vessels β-adrenoreceptors by noradrenaline plus increase of pressure, stimulated
β-adrenoreceptors of myocard by adrenaline, in the sum should exceed decrease
pressure connected to action adrenaline to vessels β-adrenoreceptors. But such
situation develops only at 20 percent of the patients with hypertonic disease.
Noradrenaline increases tonus not only the arteries, but also the veins. In
their walls is present smooth muscle too. The narrowing of veins causes
redistribution of blood from venous vessels to arterial. The volume of circulatting
blood is increased, the cardiac output is increased and the peripheral resistance is
increased.
3. Renal hypertension. Kidneys functions disturbance. Long spasm of
arterioles includes the following factor of progressive and stabilization hypertonic
disease – renals factor. The narrowing of arterioles is results of pressure falling in
renals capillaries. In the answer the synthesis and selection in blood of proteolytic
enzym renin is increased. It is synthesized by juxtaglomerular apparatus, which
consists of three structures(parts): а) endothelium of afferent arterioles of renals
glomerule; b) epithelioids cells near glomerules, which surround afferent arteriole;
c) the dense stain (macula densa) – epithelial cells of a segment distal convoluted
renal tubules, which envelop afferent arteriole as cuff.
Active renin represents proteolytic enzym with molecular weight 42 KDa. It
influences on α2-globulin (angiotensinogen), which is synthesized in a liver. Renin
breaks off leicin-leicinous connection in a molecule of angiotensin and transforms
it in angiotensin І (decaprotein). Angiotensin І is not active absolutly. It influences
angiotensinconverting enzyme, which is located, mainly, in lung. This enzym
separate from angiotensin І histidilleicin also transforms it in angiotensin ІІ
(octaprotein). Angiotensin ІІ – very powerful pressor agent. In blood it is not
stable. Under influence enzyme of angiotensinases it loses asparagin acid and
turns in angiotensin ІІІ (hectaprotein). It occurs mainly in kidneys. The function of
angiotensinases is executed by many proteolytic enzymes – tripsin, hemotripsin,
pepsin, aminopeptidase. The activity of angiotensin ІІІ makes 30-50 percent
activity angiotensin ІІ.
The action of angiotensin ІІ is very diverse. It includes set of mechanisms,
which increase blood pressure and stabilize arterial hypertension. Major of them:
а) direct action to specific receptors of vessels smooth muscles; b) mediated
action through the central nervous system – some sites of brain trunk are
sensitized to angiotensin ІІ, they stimulate vasomotorial centre; c) through
peripheral sympathetic nervous system – angiotensin ІІ is stimulates secretion of
noradenalin from presynaptic endings; d) through medulla layer of adrenal glands
– angiotensin ІІ stimulates libering of catecholamins; e) through kidneys – by
active reabsorbtion of sodium and delay of water irrespective of aldosterone
mechanism.
Dependent from activity of renin hypertonic disease divide on three forms:
normoreninemal – 55-60 % of all cases, hyporeninemal – 25-30 %, hyperreninemal
- 10-20 %. Thus, and on this parameter hypertonic disease is not homogeneous.
It was clarified further , that the kidneys select not only renin, which
eventually results in increase of blood pressure and stabilization arterial
hypertansion. They have also depressor function. The kidneys select following
depresor substances: phospholipid inhibitor of renin, antihypertension neutral
lipids medullar layer of kidneys, prostaglandins, angiotensinase, alkalized ethers
phosphatidilholin.
The largest interest from these substances is prostaglandins. They are
synthesized in medullar and cortex layers of kidneys. Stimulators synthesis of
prostaglandins in kidneys are considered angiotensin ІІ, vasopressin,
catecholamins, that is those substances, which cause narrowing renals arterioles
and ischemia of kidneys. Depressor property of prostaglandins will be realized due
to the following mechanisms. Prostaglandins, especially PGE2, render natriurtic
action. They dilatate renals arteries, and also directly oppress return transepithelial
transport of sodium chloridum in nefrone. Besides, prostaglandins prevent action
of antiuretic on reabsorbtion of water.
The kidneys start still one more mechanism of stabilization hypertension hormonal. Angiotensin ІІ and ІІІ, being powerful vasocontrictors, simultaneously
stimulate synthesis of aldosterone in glomerulars zone of adrenal glands cortex.
Effect steroids of them is identical. Aldosterone enhances reabsorbtion of sodium
in canaliculus, especially in distal departent. Sodium is accumulated in liquids of
an organism and in smooth muscles of vessels.
Increase of vesseles resistance. It is the defining mechanism. Irrespective of
first reason, in the patients with hypertonic disease almost always increases
peripheral resistance. It is considered, that the essence hypertonic disease just is in
increase of peripheral vessels tonus. Hyperkinetic phase, which is connected to
increase of cardiac output, happens only at early stages of disease and not in all
patients.
4. The hereditary predisposition to essential hypertension.
The hereditary predisposition has concrete confirmation: а) in separate
families the disease meets in some times more often, than in population; b) high
percent concordans monozygotes twins on hypertonic disease is installed; c) it is
established, that if one of the parents suffered by hypertonic disease, for them
children the risk of disease six times is higher, than for children from family not
burdened by that disease.
It is considered, that in a basis of hereditary predisposition to essential
hypertension the lay disturbances transmembran transport of ions. In the particular,
in such patients in cytozole of vessels wall myocyte is accumulated calcium
because of deficiency Ca2+ -ATP-ase. Calcium can not be deleted from myocytes in
intracellular environment. The accumulation increases it contractive ability of
vessels wall myocytes and due to stable increase of peripheral resistance. Once
more possible mechanism – generical conditioned oppression
systems
endotheliocytes of enzymal, which make internal vasodilatators(oxid of nitrogen,
prostacyclin).
5. Secondary hypertensions.
Secondary hypertension represent symptoms of such diseases.
1. Diseases of kidneys: glomerulonephritis (14 %), pielonephritis, interstitial
nephritis due to abusing analgetics, hereditary nephritis (syndrome Alport’s),
polycytosis kidney.
2. Stenosis of renal artery (1 %). Hypertension arises not in each stenosis.
The most often reason of stenosis, caused atherosclerotic platelits(at 70-80 of %),
which damage usually proximal third of renal artery on the one hand. Other reason
of stenosis with hypertension its fibromuscular hyperplasia of an average third of
renal artery. It, as a rule, double-side and more often happens at the women. The
mechanism of hypertension in stenosis of renal artery – hyperproduction of renin.
3. Primary aldosteronism (Cоnn syndrome) – in 1 % of cases. The reasons –
unilateral adenoma glomerular zone adrenal glands or double-side diffuse
hyperplasia of adrenal glands.
4. Paraganglioma (1 %) – tumour from chromaffin cells of medullar layer
adrenal glands or sympathetic nerves, as a rule – benighn. In paraganglioma is
increased both cardiac output, and peripheral resistance.
5. Coarctation of the aorta is an anatomic defect, in which aorta in pectoral or
abdominal department is narrowed to such extend, that it represents serious barrier
for blood circulation. In all vessels, which depart from the aorta proximal of
narrowing, the resistance increases and is increased arterial pressure.
6. Experimental models of arterial hypertension.
Models confirming a role of the nervous factor in increase of arterial pressure:
1. Arterial hypertension owing to an irritation of hypothalamus nucleuses. The
irritation of a back nucleus frequently results to hypertension, connected with
increase of cardiac output. The irritation of a central nucleus causes hyperension
due to of peripheral resistance increase. Electricity stimulation ventro-medial
nucleus gives hypertension, which depends from simultaneously increase of
cardiac output and peripheral resistance.
2. Arterial hypertension from double-side damage nucleus tractus solitarii to
medulla oblongata of rats, where are located primary synapsis of sinuaorticus
baroreceptors. Arterial pressure is increased immediately without change of
frequency of cardiac rate. The reason of hypertension is the sharp increase of
peripheral resistance
3. Reflexogenic hypertension, in dogs and rabbits affter section depressor
nerve Ludvig-Cion or sinus nerves Hering .
Models, which confirm participation renals factor in occurrence and
stabilization of arterial hypertension:
1. Vasorenal hypertension, which is caused by narrowing renals arteries.
Conditions of reproduction: а) arteries should be narrowed only partially, instead
of are blocked completely; b) the narrowing should be double-side; c) the variant is
possible(probable): narrowing arteries of one kidney plus removal of the other
kidney.
2. Renoprival hypertension it arises after removel both kidneys and spending
of animal on dialysis.
Models confirming a role of adrenal glands in fixing arterial hypertension:
1. Mineral-corticoids hypertension – in the case of long introduction of
aldosteron with simultaneously purpose of solution NaCl instead of water.
2. Salty hypertension. Sodium chlorids in a fair quantity even without
additional hormonal effects is capable to cause hypertension.
Model confirming role of the hereditary factor in etiology of hypertonic
disease. Exists genetic (spontaneous) hypertension in rats. In the animal with
spontaneous hypertension is revealed higher, than in normal animals, permeability
ions channels in membranes smoothmuscle cells of arteries. These membrane
defects can have some significance in increase of arteries tonus and regulation of
volume extracellular liquid. They can be considered as one of the factors
pathogenesis hypertonic disease.
7. Collapse. Classification. Ethiology, pathogenesis and consequences.
Collapse is an acute vascular insufficiency which is characterized by fall of a
vascular tone, and also acute reduction of circulating blood volume .
At the collapse there is a reduction of venous blood inflow to heart, decrease
of heart output, fall of arterial and venous pressure, infringement of tissues
perfussion and metabolism, comes hypoxia of brain appears, the vital functions of
an organism are oppressed. It is shown in clinics by short-term loss of
consciousness, general weakness, features of acute vascular insufficiency with
infringements hemodynamics practically in all organs and tissues.
In a basis of development of collapse discrepancy between volume of
circulating blood and capacity of a vascular system lays. The reasons may be
sudden reduction of blood volume (blood loss, dehydratation), and sudden
dilatation of vessels. Collapse develops as complication at heard diseases and
pathological conditions.
8. The infectious collapse develops as complication of acute infectious
diseases: meningoencephalitis, and typhoid fever typhus fever, acute dysentery,
pneumonia, botulism, the Siberian ulcer, virus hepatites, toxic influenza. The
reason of such complication is the intoxication by endo- and exotoxins of
microorganisms, mainly that influence on central nervous system, or receptors of
pre- and postcapillaries.
9. Hypoxic collapse may appear in conditions of reduced partial pressure of
oxygen in air. The direct reason of circulation infringements thus is insufficiency
of adaptive reactions of an organism to hypoxia. To development of collapse in
these conditions may promote also hypocapnia owing to hyperventilation which
leads to expansion of capillaries and vessels, and from here to deposition and
decrease of circulating blood volume.
10. Ortostatic collapse appears at fast transition from horizontal position in
vertical, and also at long time of standing. Thus there is a redistribution of blood
with increase of total amount of a venous system and decrease of inflow to heart.
In a basis of this condition insufficiency of a venous tone lays. Ortostatic collapse
may be observed at recovers after heard diseases of endocrine and nervous system,
in the postoperative period, at fast removal of ascitic liquids or as a result of spinal
and peridural anesthesias. Iatrogenic ortostatic collapse sometimes appears during
wrong use of neuroleptics, ganglioblockers, adrenoblockers, sympatolytics.
Among pilots and cosmonauts ortostatic collapse may be caused by redistribution
of blood at action of acceleration when blood from vessels of the upper half of
body and a head moves into vessels of organs of abdominal cavity and inferior
extremitus, causing hypoxia of brain. Also it may be observed at practically
healthy children and teenagers.
11. Hemorrhagic collapse develops at massive blood loss as a result of fast
reduction of circulating blood.
Collapse also may be observed at acute diseases of internal organs ( peritonitis,
acute pancreatitis, duodenitis, erosive gastritis), at diseases of heart which are
accompanied by acute and fast reduction of strike volume (heart infarction,
infringements of heart rhythm, acute myocarditis or pericarditis with accumulation
of exudation in cavity of pericardium).
It is possible to mark two basic mechanisms in pathogenesis: 1) fall of
veinis and arteriols tone as a result of action of infectious, toxic, physical, allergic
and other factors directly on a vascular wall, vasomotoric centre and on vascular
receptors (sinocarotid zones, arches of an aorta); 2) fast reduction of circulating
blood volume (blood loss,plasma loss). Reduction of circulating blood volume
results in decrease of return of blood to heart by veins of the big circle of blood
circulation and heart output. Thus the system of microcirculation is damaged,
blood accumulates in capillaries, the blood pressure falls, develops circulatory
hypoxia, metabolic acidosis, permeability of vessels increases. It promotes
transition of water and elctrolytes from blood in intercellular space, are damaged
reologic properties of blood, there is a hypercoagulation of blood and pathological
aggregation of erythrocytes and trombocytes, that creates conditions for formation
of microblood clots. At a long lasting collapse as a result of hypoxia and
disturbances of metabolism are released vasoactive substances (histamine, kinins,
prostaglandins) and formed tissue metabolites - lactic acid,adenosine and its
derivatives which cause hypotonia.
Progressing changes lead to infringement of functions of a brain, deepening
of regulatory and hemodynamic disorders. The death at a collapse comes owing to
an exhaustion of power resources of brain, intoxication and disturbances of
metabolism.
5.1. Content of the theme. The kinds of arterial hypertension. Etiology
and pathogenesis of hypertonic disease. Renal hypertension. The hereditary
predisposition to essential hypertension. Secondary hypertensions. Experimental
models of arterial hypertension. Collapse. Classification. Ethiology, pathogenesis
and consequences. The infectious collapse. Hypoxic collapse. Ortostatic collapse.
Hemorrhagic collapse.
5.2. Control questions of the theme:
1.The kinds of arterial hypertension.
2.Etiology and pathogenesis of hypertonic disease.
3.Renal hypertension.
4.The hereditary predisposition to essential hypertension.
5.Secondary hypertensions.
6.Experimental models of arterial hypertension.
7.Collapse. Classification. Ethiology, pathogenesis and consequences.
8.The infectious collapse.
9.Hypoxic collapse.
10.Ortostatic collapse.
11.Hemorrhagic collapse.
5.3. Practice Examination.
1. G. P. is a 50-year-old male who was referred for evaluation of blood pressure.
If he had a high diastolic blood pressure, which of the following readings belongs
to G. P.? A. 140/82 mm Hg B. 160/72 mm Hg C. 130/95 mm Hg D. 95/68 mm
Hg E. 140/72 mm Hg
2. The complications of uncontrolled hypertension include all of the following
except:A. Cerebrovascular accidents. B. Anemia. C. Renal injury. D. Cardiac
hypertrophy. E. All of the above are complications.
3. Primary hypertension: A. Is essentially idiopathic. B. Can be caused by renal
disease. C. Can be caused by hormone imbalance. D. Results from arterial
coarctation. E. B, C, and D are correct.
4. Orthostatic hypotension is caused by all except:A. Increased age. B. Increased
blood volume. C. Autonomic nervous system dysfunction. D. Bed rest. E. Severe
varicose veins.
5. A weak and thin vessel wall or heart chamber that bulges with each systole is
a/an: A. Thrombus. B. Embolus. C. Thromboembolus. D. Aneurysm.
E. Vegetation.
6. Which is a possible cause of varicose veins?
A.Gravitational forces on blood B.Long periods of standing C. Trauma to
the saphenous veins D. Both B and C are correct. E. A, B, and C are correct.
7. A 76-year-old male came to the emergency room after experiencing chest
pain while shoveling snow. Laboratory tests revealed essentially normal blood
levels of SGOT or AST, CPK, and LDH enzymes. The chest pain was relieved
following bedrest and nitroglycerin therapy. The most probable diagnosis is:
A. Myocardial infarction. B. Emphysema. C. Angina pectoris. D. Hepatic
cirrhosis. E. Acute pancreatitis.
8. In pericardial effusion:
A. Fibrotic lesions obliterate the pericardial cavity. B. There is associated
rheumatoid arthritis. C. Tamponade compresses the right side of the heart before
affecting other structures. D. Arterial blood pressure during expiration exceeds
that during inspiration. E. Both C and D are correct.
9. Which is not an expected finding in acute rheumatic fever?
A, History of a pharyngeal infection B. Elevated ASO titer (antistreptolysin 0)
C. Leukopenia D. Fever
10. In unstable angina: A. Pronounced Q waves are evident. B. LDH increases.
C. Vasospasm occurs. D. Plasma enzyme levels are not altered.
11. Secondary hypertension is caused by: A. Sodium retention.
B. Arteriosclerosis. C. Genetics. D. Decreased cardiac contractability. E. Increased
ventricular preload.
12. Select the incorrect statement concerning hypertension.
A. Malignant hypertension is characterized by a diastolic pressure of over 140
mm Hg B. Approximately 90 % of cases are of the essential or primary type. C.
Headache is the most reliable symptom. D. When left untreated, the major risks
include CVAs and cardiac hypertrophy.
13. A 53-year-old male was admitted to the emergency room after experiencing
shortness of breath, weakness, cardiac dysrhythmias, and chest pain that did not
subside following nitroglycerine therapy. Laboratory tests revealed the patient had
an elevated serum CPK and SGOT or AST level. EKG tracings revealed a
prominent Q-wave and an elevated ST segment. The most probable diagnosis is:
A. A transient ischemic attack. B. An acute myocardial infarct. C. An attack of
unstable angina pectoris. D. Prinzmetal angina. E. Coronary artery vasospasm.
14. Complications of an infarcted myocardium could likely include which of the
following? A. Emphysema. B. Heart failure. C. Endocarditis. D. Death. E. Shock.
15. Which of the following statements is true of rheumatic heart disease? A. Is
caused by staphylococcal infections. B. Is caused by hypersensitivity/immunity to
streptococci. C. Damages the tricuspid valve most often. D. Usually damages the
mitral valve.
16. Infective endocarditis differs from rheumatic heart disease because of which
of the following facts? Bacterial endocarditis: A. Is an infection of the heart,
endocardium, and valves B. Always follows rheumatic fever. C. May occur
following dental or other surgical procedures.D. Commonly involves the vena cava
valve. E. Is caused by a type III hypersensitivity.
17. Patients with only left side heart failure would exhibit which of the
following? A. Hepatomegaly. B. Dyspnea. C. Ankle swelling D. Pulmonary
edema E. Peripheral edema
18. In congestive heart failure, the pump or myocardium itself fails because of
which of the following? A. Loss of contractile force of the heart. B. Hypertension.
C. Cardiac dysrhythmias. D. Intermittent claudication from occlusive vascular
disease.
19. Match the valvular dysfunction with the appropriate characteristic:
19.1. Aortic stenosis 19.2..Tricuspid regurgitation 19.3..Mitral stenosis 19.4.
Mitral regurgitation A. Right ventricular hypertrophy B. Left ventricular
hypertrophy C. Right atrial hypertrophy D. Left atrial hypertrophy E. Left
atrial/right ventricular hypertrophy F. Right and left ventricular/left atrial
hypertrophy G. Hypertrophy of all chambers
Literature: 1. Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and
clinical pathophysiology/ Workbook for medical students and practitioners.Odessa, 2001. 2. Gozhenko A.I., Gurcalova I.P. General and clinical
pathophysiology/ Study guide for medical students and practitioners.-Odessa,
2003. 3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay
Kumar, Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney,
Tokyo.-1999.