Body Temperature And Its Regulation

Normal Body Temperature : The temperature of the deep tissues of the body which is known as the core temperature remains almost exactly constant except when a person develops a febrile illness.On the other hand the skin temperature rises & falls with the temperature of the surroundings. The core body temperature can be measured either orally or rectally. The oral temperature is normally 0.50C lower than the rectal temp.,

but is affected by many factors including ingestion of hot or cold fluids & mouth breathing. The average normal oral temperature in young adults measured in the morning is 37C with a range between 36.3 and 37.1 C.

Physiological variations in body temperature

1. Normally, the body temp. undergoes a regular circadian fluctuation of about 0.60C being lowest in the morning & highest in the evening. 2. In Woman there is a monthly cycle of temp. variation characterized by a rise in basal temp. of about 0.50 C at the time of ovulation &during the second half of the menstrual cycle.A similar rise occurs during the first trimester of pregnancy.

3. In children temp. regulation is less precise and they may normally have a temp. that is 0.50C above the normal for adults.

4. During exercise, excess heat is produced in the body and the rectal temp. can normally rise to as high as 400C . 5. Emotional excitement slightly increases the body temp. probably due to unconscious tensing of muscles. 6. When the metabolic rate is high the body temp. is chronically elevated by as much as 0.50C and vice verse. 7. Constitutional hyperthermia.

The balance between heat production & heat loss :

The body temp. is kept constant when the rate of heat production in the body is equal to the rate of heat loss. Heat is produced in the body by the basal rate of metabolism, contraction of skeletal muscles, food ingestion and extra metabolism caused by the slow but prolonged effect of thyroxin on the cells and the rapid but short lived effect of epinephrine, nor epinephrine and sympathetic effects on the cells.

Most of the heat produced in the body is generated in the organs especially in the liver, the brain the heart and the skeletal muscles especially during exercise. Therefore, heat loss from the body occurs in two steps :
A. Conduction of heat from the deeper organs and tissues to the skin. B. Transfer of heat from the skin to the surrounding.

Temperature regulating centres :

The temp. of the body is regulated almost entirely by temp. regulating centers located in the hypothalamus. 1. The anterior hypothalamus-preoptic area : The preoptic & anterior hypothalamic nuclei contain two types of neurons : A) Heat Sensitive neurons(receptors) which are present in large numbers.They increase their rate of firing as the temp. rises.

B)Cold sensitive neurons (receptors) which are less in number than the heat
sensitive neurons.Their firing rate increase when the body temp. falls.Both of these types of cells function as temp. sensor for controlling body temp.
2. The posterior hypothalamus : The posterior hypothalamus contains a special area located bilaterally,approximately at the leval of the mammary bodies. This area receives signals from the anterior hypothalamus -preoptic area and from peripheral receptors where they are combined to provide mainly the heat producing and heat conserving reactions. (it is the regulating C., it is the thermostat.)

Peripheral receptors for detection of Temperature

These receptors play an important role in temp. regulation. They are present in the following sites: A) The skin :- Where both cold and warmth receptors are present.However, there are far more cold receptors than warmth receptors. Therefore, skin receptors mainly concerns detection of cold rather than warm temp. of the body surface.

B) Deep body tissues :

Mainly in the spinal cord, in the abdominal viscera, and around the great veins. These receptors detect body core temp. rather than the body surface temperature. Yet . Like the skin receptors they detect cold. Therefore, both the skin and deep body receptors are concerned with preventing low body temperatures.

(1)Normal body temperature

F Axillary 36~37 .4 C Oral 36.7~37.7 C Rectal 36.9~37.9 C

~37~98.6

Normal body temperature homeostasis (2) Elevation of body temperature An elevation of body temperature above the normal amplitude of daily variation(>0.5)

What is normal core body temperature?

Normal core temperature : 37C (98.6F) + 0.8 diurnal variation = 0.6 - 1.1C

maximum temperature

~ 4 - 6 pm.

 Oral - axilla temp < 1C Rectal - oral temp < 1C (generally 0.4C (0.7F) higher than oral readings)1 Tympanic membrane ~ oral temperature (not reliable for < 3 year old children): underestimate core temp by 0.5 C
Axillary temp underestimate core temp 1 C Lower esophageal temp > core temp The standard definition of fever is a rectal temperature of > 100.4F (38.0C). A life-threatening event occurs in approximately 1% of children presenting to an acute care setting with fever.2
1. Harrisons Internal Medicine 2. http://www.emedicine.com/EMERG/topic377.htm

Types of the elevation of body temperature

Physiological elevation the setpoint of hypothalamic thermostat before menstruation severe exercise stress Pathological elevation Fever Hyperthermia

Fever: What, Why, How?

Definition of fever
Common medical sign and patient felt symptom Elevated temperature of > 37.20C (mid-morning oral) or > 37.80C (other times of the day). The core temperature is elevated due to re-setting the thermoregulatory set-point in the hypothalamus. This elevation is controlled hyperthermia/ pyrexia as opposed to uncontrolled hyperthermia which results from failed thermoregulatory mechanisms ie: body produces or absorbs more heat than it can dissipate eg. Heatstroke, NMS and serotonin syndrome with some drugs, overheating while wearing PPE, thyrotoxicosis and pheochromocytoma.

Fever: Whats normal?

Site Axilla Oral Rectal Normal (0C) 36.4 36.8 37.3 Fever (0C) >36.9 >37.3 >37.7

From this we can see there are some places that we shouldnt go near

Skin temp
Hypothalamus thermostat

Core temp
Via lateral spinothalamic tract

Peripheral receptors

Central thermoreceptors

Effector mechanisms that increase/ decrease temp

Fever

Fever is a complicated pathological process characterized by a regulated elevation of core body temperature that exceeds the normal daily variation (>0.5), in which pyrogens cause a temporary upward resetting of the hypothalamic thermostatic setpoint.

Biological role of fever

Fever plays an important role in bodys defences against infection since fever: Activates T-cell production Increases effectiveness of some IFN Limits the replication of some viruses/ bacteria Increases phagocytosis Increased Ig production Some study actually found reduced mortality in those infections with significant fever But you die when temp rises over 430C

(4) Pathogenesis of fever

Pyrogenic activators: infection, microbial toxins, mediators of inflammation, immune reactions

FEVER

Heat conservation, heat production Monocytes/macrophages, endothelial cells, others Elevated thermoregulatory set point

Endogenous pyrogens/ Pyrogenic cytokines IL-1,6, TNF, IFN,MIP-1

Hypothalamus Central mediators of fever

Circulation, etc

Pathophysiology of fever

Raising of the hypothalamic set point in CNS

Infection, CNT disease, Malignancy Reduced by antipyretic & physical removal of heat ASA overdose, hyperthyroidism excessive environmental temperature malignant hyperthermia ectodermal dysplasia, heat stroke anticholinergic drug poisoning

Heat production exceeding heat loss

Defective heat loss

Mechanism of fever production

Exgenous Pyrogens Viruses Endotoxin Bacteria Ag-Ab complexes Fungi Drugs

Antigen+ Sensitized T-Cells

Phagocytic Leukocytes Monocytes Macrophages Neutrophils

Interleukin-1 lymphocyte-activating

Interleukin-1 endogenous pyrogen

Interleukin-2
Proliferation of Helper T-Cells

T-Cell

Preoptic Anterior Hypothalmic Nuclei

Prostaglandins

Fever

Interleukin-1

Phospholipids phospholipase A2
Arachidonic acid Cyclo-oxygenase Endoperoxides Leukotrienes lipogenase

Prostacyclins Prostaglandins (PGE-2) Fever

Thromboxanes

Metabolic and physiologic response

1. HR increase

~ 15 BPM/1C

2. Metabolic Rate 10-12%/1C 3. Insensible water loss : 300-500 ml/m2/day

4. Electrolyte & nutritional consequence

Classification of fever according to etiologic diagnosis

Endogenous Cause

- Infection & Inflammation - Malignancy - CNT Disease Tissue injury - Hereditary : FMF, Ectodermic dysplasia - Metabolic Dz - Kawasaki - Endocrine - CNS (thermoregulatory center) - granulomatous Dz

Exogenous cause

- Drug : cocaine, amphotericin, ATB - Vaccine - Biologic agent : GM-CSF, IL, IFN - Factitious fever

Clinical classification of fever

1. Fever with localizing sign
2. Fever without localizing sign (FWLS)

self-limited fever with localizing sign fever of unknown origin

3. Fever with nonspecific sign 4. Fever of unknown origin

uncommon presentation of common disease Infections (30-50%) CNT disease (10-20%) Neoplasm (5-10%) Miscellaneous (10-20%) Unknown (10-25%)

Causes of fever
Influenza HIV Malaria Pyelonephritis Dengue fever Infective mononucleosis SLE Sarcoidosis IBD Kawasaki disease Leukaemia/ Lymphoma Hepatobiliary sepsis Infective endocarditis PID CMV Drug hypersensitivities

Causes of fever
Persistent fever that escapes diagnosis is called Pyrexia of Unknown Origin (PUO/ FUO) Fevers of less than 3 days duration are often due to self-limiting viral infection of respiratory tract, although pneumonia and UTIs (esp. in females) are also common causes.

Mechanisms of fever
Endogenous pyrogens are also known as cytokines and are part of the innate immune system, as produced by macrophages after their TLRs are activated. The major endogenous pyrogens are IL-1, IL-6 and TNFa. Exogenous pyrogens include LPS and other endotoxins from bacteria. LPS is bound by LPS binding protein (an acute phase protein) and this complex binds to the CD14 receptors of macrophages, resulting in cytokine release (IL1, IL-6 and TNFa). All these cytokines eventually end up interacting with endothelial receptors on vessel walls or microglial cells to activate the arachidonic acid pathway.

Mechanisms of fever

Arachidonic acid Prostaglandin H2 Prostaglandin E2 with the help of COX-2 and PGE2 synthase enzymes

Mechanisms of fever
PGE2 acts on the Prostaglandin EP3 receptors in the preoptic area of the hypothalamus, stimulation of the sympathetic output evoking non-shivering thermogenesis to produce body heat coupled with peripheral vasoconstriction to decrease heat loss.