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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 1 : GENERAL PATHOLOGY.


Contenting module 1. General nosology.


Theme3: Thermal injury. Crush syndrome.


Chernivtsi – 2008

1.Actuality of the theme. The environment factors constantly affect a man. Inadequate nutrition, bad social conditions, toxins influences and other factors decrease organism resistance. Going in for sport, rational labour and rest routine guard of environment raise unspecific organism resistance. Some factors can be used in medicine for prophylaxy of the diseases. For example, hypothermia (hibernation) increases organism resistance to hypoxia and doctors use that at operation on heart and brain.

Regulating mechanisms of the body temperature.

The control of the body temperature is a function of the centers located in the hypothalamus. Thermoreceptors provide the hypothalamus with the information about peripheral and core temperatures. If the temperature is low the body initiates heat conservation, measured by a series of hormonal mechanisms. Heat production begins with the hypothalamic release of TSH (thyroidstimulating hormone) – RH (releasing hormone), which stimulates the release of TSH from anterior pituitary. The TSH causes release of thyroxin from the thyroid gland. This hormone causes the release of the epinephrine (adrenaline) from the adrenal medulla.

Epinephrine causes vasoconstriction, glycolysis, and increased metabolic rates which increase heat production. Warmer peripheral and core temperatures reverse the process. Decreasing the sympathetic pathway produces vasodilatation, decreased muscle tone, and increased perspiration.

^ 2.Length of the employment – 2 hours.

3.Aim:

To khow effect of the thermal factors.

To be able: to analyse of the pathogenesis of the crush syndrome.

To perform practical work: Characterize “vicious circle” in traumatic shock.

Hypoxia – Depression of living important centers




The disturbances of respiratory Excitation of the respiratory

and cardiac function and cardiac centers


4. Basic level.


The name of the previous disciplines

The receiving of the skills

  1. histology

  2. biochemistry

  3. physiology

Physiological reactivity indexes

Physiological thermoregulation mechanisms.

Influence of a temperature on enzyme activity.


^ 5. The advices for students.

1. Describe the effect of the thermal factors.

The effect of the high temperature (when the air temperature elevation varies from 33 °C to 37°C, it is equal to the body temperature) is the development of the overheating (local effect – burn), or the effect of the low temperature – hypothermia.

2. Characterize overheating.

There are two stages:

1) Compensation stage, when normal temperature is preserved.

2) Decompensation stage, when overtension of thermoregulation leads to its exhaustion.

^ 3. Describe hypothermia.

The effect of the low temperature on the body may result in the decrease of the body temperature and the development of pathological condition – hypothermia. There are two stages of overcooling:

1. Compensation stage is directed at limitation of the heat emission.

2. Decompensation stage or hypothermia proper.

^ 4. Explain what is a “crush syndrome”.

Crush syndrome (CS) is a variant of traumatic disease. The main pathogenic factors in CS are:

1) Pain syndrome

2) Intoxication

3) Psychoemotional stress

4) Hypovolemia

5. Characterize the clinical course of crush syndrome.

There are three periods in the clinical course of crush syndrome:

1. Early (to 3 days, with compression and decompression phases)

2. Intermediate (from 8 to 12 days) with the prominence of acute renal insufficiency(ARI)

3. Late (from 12 days to 1-2 months — the period of recovery with the prevalence of local syndromes.

^ 6. Pathogenesis of traumatic shock

I stage

II stage

Extremity injuries, cause severe emotional stress, pain, fear of death, blood loss




Excitation of the brain cortex (delirium, hallucinations)

toxemia

Blood

hypovolemia


The right atrium pressure is lower





Brain cortex inhibition

(loss of consciousness)


ARI, acidosis, hyperkalemia, hyponatremia

The arterial pressure decreases to 80-60 mm Hg

Tachycardia


Hyperkalemia atrioventricular blockade

Disturbances of regional blood flow and microcirculation lead to thrombohemorhagic syndrome.

^ 7. Why the decompression phase of crush syndrome is the critical moment?

Due to massive plasmorrhagia. Blood loss. Hypovolemic shock. Simultaneously many kinds of toxins from the injured tissues enter the bloodstream

5.1. Content of the theme. Describe the effect of the thermal factors. Characterize overheating. Describe the hypothermia. Explain what is “crush syndrome”.Characterize the clinical course of crush syndrome. Pathogenesis of traumatic shock. Why the decompression phase of crush syndromeis the critical moment?

^ 5.2. Control questions of the theme:

1. Describe the effect of the thermal factors.

2. Characterize overheating.

3. Describe the hypothermia.

4. Explain what is “crush syndrome”.

5. Characterize the clinical course of crush syndrome.

6. Pathogenesis of traumatic shock.

7. Why the decompression phase of crush syndromeis the critical moment?


^ 5.3. Practice Examination.

Practice examination N 1

I. Give the correct answer to each question.

Which mechanism of compensation switches on

A. Spasm of the cutaneous vessels B. Dilatation of the peripheral vessels C.Reduction of sweating D. Increasing of sweating E. Tachypnoe F. Tachycardia 1. Hyperthermia 2. Hypothermia

II. As we know, there is a misbalance under the thermal injury between heat production in the organism and its output into the environment. Fill in the correct responses. A. Reduction of the heat production B. Elevation of the heat production C. Increasing output of heat D. Decreasing output of heat E. Normal thermoproduction F. Normal thermooutput 3. Stage compensation of hyperthermia 4. Stage decompensation of hyperthermia 5. Stage compensation of hypothermia 6. Stage decompensation of hypothermia

III. Which is not true? 7. The increase of the body temperature, i. e. hyperthermia is accompanied by: A. Sharp excitation of the nervous system B. Metabolism increase C. Hypoxia D. Tachypnoe E. Disturbance of electrolyte metabolism F. Hyperhydratation on whole organism G. Convulsions H. Reduction of the arterial pressure

8. Reduction of the body temperature, i. e. hypothermia is characterized by:

A. Decrease of the metabolic processes B. Reduction of oxygen consumption C.Bradypnoe D. Bradycardia E. Inhibition of the central nervous system F.Reduction of immunologic reactivity G. Elevation of the arterial pressure

IV. 9. Why hypothermia may be used is surgical practice?

A. Vitally important organs are inhibited B. Oxygen starvation C. Sensitivity of the nervous cells to the lack of oxygen is decreased D. The decrease of the metabolism E. All the above are correct

10. What makes the organism less sensitive to various unfavorable factors (lack of O2 , food, intoxication, the effect of electric current, overloads, etc) under hypothermia: A. Inhibition of the central nervous system B. Disturbances of respiration and whole circulation of the blood C. Reduction of the body temperature D. Decrease of immunity E. All the above are correct

V. Hyperthermia is accompanied by the profuse sweating. Is it good or bad? Characterize by indicating the positive (11) or negative (12) factors:

A. Dehydration B. Loss of chlorides and sodium C. Increased viscosity create additional load on the heart D. Cardiac insufficiency E. Increased heart output

13. Which of the following is not present in the burn?

A. Erythema B. Acute exudative inflammation with formation of the vesicles (blisters) C. Partial necrosis of the skin D. Ulceration, necrosis E. All the above are present

VI. Which signs of the burn are characterized as local pathological process (14) and as general impairment (burn disease) (15).

A. Burn shock (hypovolemic shock) B. Burn toxaemia C. Burn infection D.Dehydration E. Redness of the skin F. Disturbed water-electrolyte metabolism

16. In the burn there are serious disturbances in general metabolism. Which ones characterize it?A. Reduction of activity of the tissue respiratory enzymes B. Loss of proteins C. Increased activity of pro­teolytic enzymes D. Autoimmunity disorders E. Hyperkalemia F. Hyponatremia G. All the above are right

17. What are the complications in burn disease?

A. Cachexia B. Anemia C. Edema D. Dystrophic changes in the inner organs E. Pneumonia F. Glome­rulonephritis G. Exhaustion of the function of the adrenal gland cortex H. All of the above are correct

Practice examination N 2

1. What is the most dangerous complication of crush syndrome?

A. Acute renal insufficiency B. Wounds C. Increased plasma osmolarity D.Hyperglycemia E. Anemia

2. Why does toxemia occur?

A. Release of the toxic substances from the crushed tissues B. The damaged muscular tissues C. Production and penetration of lysosomal enzymes into blood, the so-called “endotoxin”, or “ischemic toxin” D. All of the above are correct

3. Why the decompression phase of crush syndrome is the critical moment?

A. Due to massive plasmorrhagia B. Blood loss C. Hypovolemic shock D. Simultaneously many kinds of toxins from the injured tissues enter the bloodstream E. All of the above are correct


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.- P.28-34.

2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study guide for medical students and practitioners.-Odessa, 2003.- P.10-26.

3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar, Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.

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