Classification according to pathophisiological picture

1. Hypovolemic shock secondary to any condition provoking a major reduction in blood volume;

- internal/external hemorrhage;

- severe burns; acute pancreatitis;

- dehydration.

2. Normovolemic shock secondary to capillary damage, arteriovenous shunting and inappropriate vasodilatation:

- septic shock;

- anaphylactic shock.

3. Cardiogenic shock, caused by any form of severe heart failure:

- myocardial infarction;

- acute massive pulmonary embolism;

- heart tamponade due to pericardial enfusion.

Classification according to etiology

- infections,

- toxic,

- anaphylactic,

- hemorrhagic,

- cardiogenic,

- burn.

Pathogenesis. The syndrome of shock is characterized by widespread failure of the capillary system caused by a complex interaction of hemodynamic and toxic factors. Loss of capillary integrity reduces oxygen delivery to the tissues, disturbs local metabolism, and allows fluid to extravasate into the interstitial space. Generalized cell death and further capillary damage occur due to the combined effects of ischemia, acidosis, and the release of toxic metabolites including catecholamines, angiotensin II, and cytokines such as the interleukins and tumor necrosis factor.

Clinical features

- weakness, cyanosis, pallid skin, cold extremities;

- cold clammy skin;

- drowsiness, confusion, irritability;

- rapid shallow respiration;

- tachycardia (> 100 beats per minute);

- thready pulse;

- hypotension (systolic BP <100mmHg);

- oliguria (urine output < 30 ml/hour);

- multi-organ failure.

Complications of shock:

· muscle damage;

· peripheral gangrene;

· visual and cerebral impairment;

· respiratory distress syndrome;

· myocardial dysfunction;

· jaundice, impaired liver function;

· acute renal failure;

· disseminated intravascular coagulation/consumption coagulopathy.

Additional methods of examination

Although clinical evaluation is essential, progress can also be assessed by monitoring certain parameters at the bedside.

Addition methods of examination include:

skin temperature - this reflects cutaneous blood flow and is therefore a useful indirect measurement of peripheral perfusion;

urinary flow - this is a sensitive measure of renal perfusion and can easily be monitored if a urinary catheter is in place;

oxygen saturation - this can be monitored easily using a finger or ear lobe probe. In general, oxygenation is satisfactory if the saturation is greater than 90 %;

ECG - a standard monitor will record rate and rhythm, ST-segment shift, which may be useful in patients with ischemic heart disease;

central venous pressure - using a catheter to measure the right atrial pressure is a useful means of assessing the circulating blood volume and therefore the appropriate rate of intravenous fluid replacement;

pulmonary artery wedge pressure - in most situations the central venous pressure is an adequate guide to the filling pressures of both sides of the heart.

 

Literature

1. Internal diseases an introductory course. - Vasilenko V., Grebenev A. - M.: Mir Publishers, 1990. - 647 p.
2. Propedeutics to internal medicine. Part 1.-Vinnytsya: NOVA KNYHA, 2006.- 424 p.
3. Propedeutics to internal medicine. Part 2.-Vinnytsya: NOVA KNYHA, 2007.- 264 p.
4. Introduction to the course of internal diseases. Book 1. Diagnosis: [Textbook/Zh.D. Semidotskaya, O.S. Bilchenko, et al.].-Kharkiv: KSMU, 2005. -312p.
5. Michael Swash Hutchison’s clinical methods / XIX edition. ELBS, 1989. -618p.
6. Mark H., Beers M.D., Robert Berkow The Merck Manual of diagnosis and therapy / XVII edition.- Published by Merk research laboratories, 1999.- 2833 p.
7. Harrison΄s principles off internal medicine / Fauci, Braunwald, Isselbacher and al.-XIV edition. - Vol. 1 and 2. - International edition, 1998.

 

Topic2. Rheumatism

Class lasts: 3 hours

Chronological class structure:

Control of initial standard of knowledges- 20 min.

Teacher′s demonstration of practical skills - 60 min.

Sudents′ independent work: - 30 min.

Control of ultimate standard of knowledges- 15 min.

Sum up of the class, homework- 10 min.

Questions for theoretical preparation: Rheumatic disease of the heart: etiology, pathogenesis, classification, the clinical picture, and etiology factors. the Jones Criteria for Rheumatic Fever, Updated 199, additional methods of examination

 

ACUTE RHEUMATIC FEVER

Rheumatic fever is a general infectious in which connective tissues, mainly of the cardiovascular system, are affected by inflammation; joints, serous membranes, internal organs, and the central nervous system are often. Rheumatism is a collagenous disease, i.e. a disease characterized by a systemic and progressive derangement of connective tissue.

Rheumatism was classified as an independent disease with typical affections not only of the points but also mainly have the heart in 1835 by a French clinicist Bouillaud and in 1836 by the Russian physician Sokolsky. Until that time rheumatism had been considered a disease of joints.

 

Etiology

The epidemiology of acute rheumatic fever is identical to that of group A streptococcal upper respiratory tract infections. As is the case for streptococcal sore throat, acute rheumatic fever most often occurs in children: the peak age-related incidence is between 5 and 15 years. Most initial attacks in adults take place at the end of the second and beginning of the third decades of life. Rarely, initial attacks occur as late as the fourth decade and recurrent attacks may be seen even later; attacks have been documented in the fifth and sixth decades.

Epidemiologic risk factors classically associated with individual attacks and especially with outbreaks of acute rheumatic fever include lower standards of living, especially crowding; the disease has been more common among socially and economically disadvantaged populations. However, the outbreaks in the United States in the late 1980s and early 1990s cannot be explained entirely by these factors. The large Utah outbreak of almost 300 cases during 7 years affected patients in primarily middle-class families with ready access to medical care. Therefore, one can conclude that the organism itself as well as the degree of host/herd immunity to the prevalent serotypes in an affected community is equally important risk factors.

Studies have shown that approximately 3 percent of individuals with untreated group A streptococcal pharyngitis will develop rheumatic fever. The epidemiology of rheumatic fever is also influenced by the serotypes of group A streptococci present in a population. The concept of "rheumatogenecity" of specific strains is largely based upon epidemiologic evidence associating certain serotypes with rheumatic fever. Mucoid or highly encapsulated strains have been associated with rheumatic fever.

Pathogenesis

More than half a century ago the pioneering studies of Lancefield differentiated beta-hemolytic streptococci into several serologic groups. This ultimately led to the association of infection by the group A organism of the oropharynx (not of other sites) and the subsequent development of acute rheumatic fever. However, the mechanism(s) responsible for the development of rheumatic fever after an infection remains elusive. Historically, approaches to understanding the pathogenesis of rheumatic fever have been grouped into three major categories:

1) direct infection by the group A streptococcus;

2) a toxic effect of streptococcal extracellular products on the host tissues;

3) an abnormal or dysfunctional immune response to one or more as yet unidentified somatic or extracellular antigens produced by all (or perhaps only by some) group A streptococci.

There is insufficient evidence to support direct infection of the heart as the inciting event. Additionally, while toxins such as streptolysin O and others have been postulated to be responsible for this sequel, there is relatively little convincing evidence at the present time. Major efforts have focused on an abnormal immune response by the human host to one or more group A streptococcal antigens. The hypothesis of "antigenic mimicry" between human and bacterial antigens has been studied extensively and has concentrated on two interactions. The first is the similarity between the group-specific carbohydrate of the group A streptococcus and the glycoprotein of heart valves; the second involves the molecular similarity between either streptococcal cell membrane or streptococcal M protein and sarcolemma or other moieties of the human myocardial cell. The possibility of a predisposing genetic influence in some individuals is one of the most tantalizing of the incompletely understood factors that might contribute to the susceptibility to rheumatic fever. The precise genetic factors influencing the attack rate have never been adequately defined. Observations have been described that support the concept that this nonsuppurative sequel to a group A streptococcal infection results from an abnormal immune response by the human host. Thus differences in immune responses to streptococcal extracellular antigens have been reported, with a unique surface marker on non-T lymphocytes of rheumatic fever patients.

Classification

1. Acute rheumatic fever

2. Rheumatic disease of heart (Rheumatic disease of heart – with defect or vice of heart, valvular heart disease).