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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 2. Typical pathological processes.


Theme13: Fever


Chernivtsi – 2008

1.Actuality of the theme. In all hospitals it is obligatory is carried out patients’ thermometria. In the case history there is a temperature list where is the morning and evening temperature, as well as the diagram of its changes. According to type of the curve they define the fever type. It has diagnostical significance because a lot of infectious diseases are accompanied with fever with tupical temperature curve. Fever has mainly protective role. Only in the persons with serious disorders of cardiovascular, nervous and other systems and in children the high temperature (abov 39 °C) can be dangerous. The doctor must evaluate the fever significance in the patient and will plan the treatment.

^ 2.Length of the employment – 2 hours.

3.Aim:

To khow, that fever is a typical pathological process, the main signs of which are changes in thermoregulation and increase of body temperature.

To be able: to analyse of the pathogenetic stages of fiver.

^ To perform practical work: Mechanisms acting IL-1?

1) pyrogenic effect 4) doseness

2) leukocytosis stimulate 5) depressed nervous system

3) myalgia 6) decreased appetite

I L – 1 ? influence on neurons of “Set point”

I L - 1 ?



Increase activity phospholipase A2

thermo Phospholipase

receptor

Lipoid of the membrane of the cells

arachidonic

acid

Arachidonic acid

PG


PG E


4. Basic level.


The name of the previous disciplines


The receiving of the skills

  1. histology

  2. biochemistry

  3. physiology

Thermoregulatory mechanisms.

Biochemical and physical-chemical indexes of metabolism in tissues.


^ 5. The advices for students.

1. Normal thermoregulation.

Temperatures usually do not vary more than 0.5 °C (1 °F) and value the most often used is 37 °C (98.6 °F), average is about 36.7 °C.

Alterations of temperature for a sustained period can have damaging effects and may even be fatal, because most of the cell enzymes function optimally at the level of normal body temperature.

^ 2. Principal mechanisms of human thermoregulation

Common mechanism of termoregulation

Cerebral cortex

Shivering

Behavioral responses

Thermoreceptors

Hypothalamus

Sweat at skin surface

Dermal blood flow

^ 3. Hypothalamic processing in thermoregulation

Anterior hypothalamus sensor

Blood

Core t°

EP*/ drugs

* (endogenous pyrogen)

Peripheral Thermoreceptors

Chemical mediators

Posterior hypothalamus: set point

Various CNS centers

Heat loss or conservation responses

4. What does it fever mean?

Fever is a typical pathologic process, which as a defensive (protective) reaction to the exogenous and endogenous agents and is accompanied by the increase of the core temperature of the human body.

5. What is the etiology of fever?

Pyrogenes are substances which can be the cause of fever.

6. Classify the pyrogens

All the pyrogens may be divided into two groups:

1) infectious (microorganisms, viruses and their toxins)

2) non-infectious (transfusion fever after inflow of the blood, protein and others)

7. ^ Characterize the pathogenesis of fever

The pathogenesis of fever begins with the introduction of exogenous or endogenous pyrogens.

The production and release of interleukin-1 (IL-1), tumor necrosis factor (TNF), IL-6 and interferons occur as exo-bacteria are destroyed by phagocytic cells within the host.

From this you might assume that various external factors can directly influence the thermal regulation center in the hypothalamus to elevate the set point.

FEVER

PATHOGENESIS

Etiological factors PYROGENS

^ PRIMARY EXOGENOUS (MICROBES,VIRUSES)

PRIMARY ENDOGENOUS DISTRUCTION OF THE TISSUE

P do not pass through hemato-encephalic barrier, but in remain in blood

Secondary pyrogens LP, IL-1 (leukocyte origin)

Blood

Changing sensitivity of cooling and heating neurons of hypothalamus

«A resetting of the hypothalamic thermostat» and set point to a higher level

FEVER

PGE other mediators of fever are formed

8. Describe the alterations occurring in fever, hypothermia, and hypothermia.

Fever is not a failure of the normal thermoregulatory mechanism. Instead it is considered «a resetting of the hypothalamic thermostat» to a higher level. The normal thermoregulatory mechanisms are raised so that the thermoregulatory center adjusts heat production, conservation, and loss to maintain the core temperature at a new, higher set-point temperature.

The pathophysiology of fever begins with the introduction of exogenous pyrogens or endotoxins. The production and release of IL-1, TNF, IL-6 and interferons occur as exogenous bacteria are destroyed and absorbed by phagocytic cells within the host. As the set-point is raised the hypothalamus signals increase in heat production and conservation to raise body temperature to the new level.

During fever, arginine vasopressin (AVP), alpha-melanocyte-stimulating hormone, and corticotropin-releasing factor are released and act as endogenous antipyretics to help diminish the febrile response. During this antipyretic effect, as fever breaks, the set-point is returned to normal. The hypothalamus signals a decrease in heat production and an increase to heat reduction.

Fever can be beneficial. Elevated body temperature kills many microorganisms and has adverse effects on the growth and replication of others. Increased temperature cause lysosomal breakdown with auto destruction of cells; this prevents viral replication in infected cells. Heat increases lymphocytic transformation and motility of polymorphonuclear neutrophils, which facilitates the immune response.

Hyperthermia can produce nerve damage, coagulation of cell proteins, and death. At 41°C (109°F), death follows. In hyperthermia, there is no resetting of the hypothalamic set-point. Forms of accidental hyperthermia are heat cramps, heat exhaustion, and heat stroke.

Heat cramps are severe, spasmodic cramps in the abdomen and the extremities subsequent to prolonged sweating and associated sodium loss. Heat cramps usually appear in individuals, who are unaccustomed to heat or in those who are performing strenuous work in very warm climates. Fever, rapid pulse, and increased blood pressure often accompany the cramps.

Heat exhaustion or collapse results from prolonged high body core or environmental temperatures. These high temperatures cause hypothalamic inducement of profound vasodilatation and profuse sweating. Over a prolonged period of elevated temperatures, the hypothalamic responses produce dehydration, decreased plasma volumes, hypotension, decreased cardiac output, and tachycardia.

Heat stroke is a potentially lethal consequence of a breakdown in control of an overstressed thermoregulatory center. The brain cannot tolerate temperatures over 40.5 °C (105°F). In cases of very high core temperatures, the regulatory center may cease to function appropriately. Sweating ceases, and the skin becomes dry and flushed. The individual may become irritable, confused, stuporous, or comatose.

As evaporation of perspiration ceases, core temperatures rise rapidly. High core temperatures and vascular collapse produce cerebral edema, degeneration of the central nervous system, and renal tubular necrosis. Death results unless immediate, effective treatment is initiated.

Treatment requires more than the fluid and electrolyte replacement. Too rapid surface cooling may cause peripheral vasoconstriction, which would prevent core cooling. Children are more susceptible to heat stroke than adults because they produce more metabolic heat when exercising, they have a greater surface area-to-mass ratio, and their perspiring capacity is less than that of adults.

Malignant hyperthermia is a potentially lethal complication of an inherited muscle disorder. The condition is precipitated by the administration of volatile anasthetics and neuromuscular blocking agents. The risk of this muscle disorder may be about 1 in 200 individuals. Malignant hyperthermia causes intracellular calcium levels to rise, producing sustained, uncoordinated muscle contractions. As a result of these contractions, acidosis develops and body temperature may rise 1 °C (1.8 °F) every 5 minutes. Approximately 20 % of those who develop malignant hyperthermia do not survive.

Treatment includes withdrawal on the provoking agents and administration of skeletal muscle relaxants to inhibit calcium release during muscle contraction, treatment of cardiac arrhythmias, sodium bicarbonate administration, and cooling of the body.

Hypothermia slows chemical reactions, increases blood viscosity, slows blood flow, facilitates blood coagulation, and stimulates profound vasoconstriction. Accidental hypothermia, temperature below 35 °C (95 °F), is generally the result of sudden immersion in cold water or prolonged exposure to cold environments. The young and the elderly are at risk because of their less effective thermoregulatory mechanisms.

Individuals with conditions that diminish their ability to generate heat, such as hypothyroidism, hypopituitarism, malnutrition, Parkinson disease, and rheumatoid arthritis are also at risk.

The hypothalamic center stimulates shivering in an effort to increase heat production at core temperatures of 35°C and continues until core temperature drops between 30° and 32°C. Thinking becomes sluggish and coordination is decreased at 34°C. At 30°C, the individual becomes stuporous, heart rate and respiratory rates decline, and cardiac output is diminished. In severe hypothermia, core temperature of 20° to 28°C, pulse and respiration may be undetectable. Acidosis becomes moderate to severe. Ventricular fibrillation and asystole are common.

Depending on the severity of the hypothermia, rewarming of the peripheral tissues may be the only treatment required. Core rewarming is performed when core temperatures have dropped below 30°C or when severe cardiovascular abnormalities appear. Core rewarming may require administration of warm intravenous solutions, gastric or peritoneal lavage, or inhalation of warmed gases. Rewarming generally should proceed at no faster than a few degrees per hour.

9. What is the role of fever?

Fever has a benefit component as it may be actually dangerous to multiplication of many pathogens. Some bacteria and viruses have been shown to reproduce more slowly when the t° is elevated. In experiments with AIDS patients, when the blood t° was raised by circulation and heating it outside of the body, there was a decrease in indicators of infection.

In many cases a moderate fever may enhance the patient’s defensive responses, providing more benefit than would be gained by limiting the fever trying to provide a bit of comfort.

Fever has a harmful accelerating effect on the formation of extracellular fluids in the brain, which can raise cranial pressure.

Normally, fever peaks are at maximum of about 40.5 °C (105°F) following resetting of the hypothalamic set-point. This maximum assumes a healthy functioning hypothalamus. Fever over 41 °C (106 °F) requires emergency medical care.

10. Pharmaceutical intervention in fever.

Salicylate or acetaminophen

Inhibition of prostaglandin production

Depression of elevated set-point

Activation of heat loss mechanisms

^ Key concepts:

1) Long recognized as linked to disease, fever is not an abnormality of thermoregulation but is rather an upward adjustment of its set-point.

2) The skin’s blood flow and sweat gland activity can be altered to cause loss of heat by the way of radiation, conduction, and evaporation or to foster heat retention.

3) Pyrogens induce fever by elevating the temperature set-point of the thermoregulation center in the hypothalamus.

4) Various exogenous pyrogens ( including components of infectious agents) trigger phagocytic cells to release a variety of endogenous pyrogens.

5) Fever seems to enhance host capacities to resist infection or better cope with other forms of injury.

6) Extreme or prolonged fever may result from longstanding injury or from a damaged hypothalamus, posing particular risk to heart and brain.

7) Commonly used antipyretic agents work by suppressing the production or action of the chemical mediators that upwardly adjust the temperature set point in the hypothalamus.

^ 11. Three stages of fever:

1) Stage of increasing temperature (Lat.: St. incrementi) due to:

Decrease of heat loss of due to narrowing of dermal blood vessels, less sweating

Increase of heat production due to muscle contraction and activation of oxidizing processes

2) Stable temperature stage (Lat.: St. fastigii)

Balance

between heat production and heat loss

at a higher level

3) Stage of decreasing t° (Lat.: St. decrementi)

Increase of heat loss profuse sweating, vasodilatation of vessels

Decrease of heat production

OUTCOMES

Critical decrease of t°

Collapse

Lytical decrease of t°

back to normal

REMEMBER!!!

1 °C = 1.8 °F

35 °C = 95 °F

40.5 °C = 105 °F

41 °C = 106 °F

43 °C = 109 °F

^ 5.1. Content of the theme. Normal thermoregulation. Principal mechanisms of human thermoregulation.Common mechanism of termoregulation. Hypothalamic processing in thermoregulation. What does it fever mean? What is the etiology of fever? Classify the pyrogens.Characterize the pathogenesis of fever.Describe the alterations occurring in fever, hypothermia, and hypothermia. What is the role of fever?Pharmaceutical intervention in fever. Three stages of fever.


^ 5.2. Control questions of the theme:

1. Normal thermoregulation.

2. Principal mechanisms of human thermoregulation.Common mechanism of termoregulation.

3. Hypothalamic processing in thermoregulation.

4. What does it fever mean?

5. What is the etiology of fever?

6. Classify the pyrogens.

7. Characterize the pathogenesis of fever.

8. Describe the alterations occurring in fever, hypothermia, and hypothermia.

9. What is the role of fever?

10. Pharmaceutical intervention in fever.

11. Three stages of fever.


^ 5.3. Practice Examination.

1. What are the endogenous pyrogens of nonphagocytic origin?

A. IL-1 (interleukin-1) B. TNF (tumor necrosis factor) C. INF –  (interferon ) D. MIP – 1 (macrophage inflammatory protein)

2. Temperature – related intrahypothalamic signaling depends on:

A. Prostaglandin E B. Monoamines (particularly serotonin) C. GMP (cyclic guanosine monophosphate) D. Interleukin-1 E. AMP(cyclic adenosine monophosphate) F. Nonsteroidal anti-inflammatory agents G. All the above are correct

3. What are not the target cells for interleukin-1

A. Lymphocytes B. Hepatocytes C. Fibroblasts D. Myocyte E. Sinoviocytes

F. All of the above are correct

4. What is true? Antipyretic effect is the cause of the following hormones except

A. Vasopressin B. Alpha-melanocyte-stimulating hormone C. Corticotropin-releasing factor D. Thyroxin

5. Heat loss is accompanied by following processes except

A. Radiation D. Evaporation C. Conduction D. Convection E. Fluctuation of metabolic processes

^ 6. Malignant hyperthermia is caused by:

A. Intracellular calcium levels rise B. Inherited muscle disorder

C. Uncoordinated muscle contractions D. Anaesthetic and neuromuscular blocking agents E. All of the above are correct

7. Interleukin-1:

A. Raises the hypothalamic set-point B. Is an endogenous pyrogen C. Is stimulated by exogenous pyrogens D. None of the above are correct E. A,B,C are correct

8. Increased serum levels of epinephrine increase body temperature by:

A. Increasing vasodilatation B. Decreasing muscle tone C. Increasing heat production D. Decreasing basal metabolic rate

9. In heat stroke:

A. Core temperature usually doesn’t exceed 40°C (101°F)

B. Sodium loss follows sweating

C. Core t° increases as the regulatory center fails

D. Both B and C are correct

10. Which is involved in fever?

A. Tumor necrosis factor B. Endotoxins C. Elevation of the higher set-point in the hypothalamus D. Only A is involved in fever E. A, B, and C are involved in fever.

11. Heat collapse is characterized by:

A. Profuse sweating B. Dehydration C. Hypotension D. Decreased cardiac output E. All of the above are correct

12. Heat stroke depends on:

A. Microbes, viruses

B. Endogenous pyrogen

C. Temperature of the environment

D. «The resetting of the hypothalamic thermostat» to a higher level

E. All of the above are correct

STATE WHAT IS TRUE AND WHAT IS FALSE

Fever can be beneficial due to:

13. Elevated body t° kills many microorganisms.

14. Increased t° has adverse effects on the growth and replication

15. Motility of neutrophils increases

16. Increased lymphocytic transformation

17. Sweating with sodium loss


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.

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