Saturday, January 5, 2008

lecture slides on energectics and body temperature regulation

ENERGETICS AND METABOLIC RATE
 Importance of ATP in metabolism
-large quantity of free energy in its high energy phosphate
bonds (7000cal /mol)

 Transfer of energy from diff foodstuff to functional system of the cell

 Phosphate bonds – release stored energy
PHOSPHOCREATINE
 Storage depot for energy
 Buffering the concentration of ATP
 Most abundant substance that stores energy
 Can’t act as ATP but can transfer energy with ATP
-extra amount of ATP synthesis of phosphocreatine
when ATP is used up energy from phosphocreatine
is transferred back to ATP
- concentration of ATP is maintained at high level-
ATP buffer system
ANEROBIC/AEROBIC ENERGY
 Anaerobic – energy derived from foods without the
use of O2

 Aerobic –energy derived from foods by oxidative
metabolism

 Glycogen storage is the only food for anaerobic
metabolism - glycolysis


 What happens to Pyruvate
 If oxygen is present it is converted to Acetyl-CoA and enters citric acid cycle
 If oxygen is not present is will become lactic acid and /or ethanol

 Oxidative Respiration
 aerobic metabolism
 occurs in mitochondria
 conversion of pyruvate to Acetyl-CoA
 citric acid cycle
 electron transport

 Anaerobic Metabolism (fermentation) occurs when oxygen is not available.
 ethanol fermentation (Yeast)
 Pyruvate is converted to acetaldehyde, by removal of CO2. Which then accepts H from NADH to produce ethyl alcohol.
 Lactic Acid Fermentation
 takes H from NADH and attaches it to pyruvate to produce lactic acid (Muscles)


 Oxidative Respiration
 aerobic metabolism
 occurs in mitochondria
 conversion of pyruvate to Acetyl-CoA
 citric acid cycle
 electron transport

 How Cells Make atp
 by

 PHOSPHORYLATION... adding a phosphate to ADP

 ADP + P ------> ATP
 ) substrate level phosphorylation...

 where a substrate molecule ( X-p ) donates its P to ADP making ATP
 b) chemiosmosis - [Oxidative Phosphorylation of Krebs cycle & ETC]...

 food substrates donate e- & protons to acceptor molecules [NADH], i.e., oxidation.

 NADH gives up electrons & protons are pumped out of mitochondria
 protons diffuse back into mito thru an enzyme - ATPase,

 the ATPase enzyme makes ADP + P --> ATP
 Complex I
 NADH dehydrogenase (or)
NADH-coenzyme Q reductase

 Complex II
 Succinate dehydrogenase (or)
Succinate-coenzyme Q reductase

 Complex III
 Cytochrome C - coenzyme Q oxidoreductase-

 Complex IV
 Cytochrome oxidase
 Complex VATP synthase
ANAEROBIC ENERGY DURING HYPOXIA
 Acute hypoxia – O2 in the lungs/hemoglobin is good only
for 2 mins – glycolysis

 Anaerobic energy usage during strenuous bursts of activity
-energy is derived from
1. ATP already present in the muscle cells
2. phosphocreatine in the cells
3. anaerobic energy from glycolysis
4. oxidative energy from oxidative process
 Max. amount of ATP in a liter of intracellualr fluid – 5 millimoles - can maintain contraction for a second
 Phosphocreatine is 3 to 8 times this amount – can
maintain contraction for few more seconds
 Energy from glycolysis can occur rapidly than from oxidative
process
 Glycogen content of the muscle during exercise is reduced
while lactic acid increases
 After exercise – reconversion of lactic acid to glucose
 Oxygen debt – rapid breathing after exercise

 Excess O2 is used to
1. reconvert lactic acid to glucose
2. reconvert ATP/ phosphocreatine to normal
3. restablished normal conc of O2 in Hg/ myoglobin
4. O2 in the lungs
SUMMARY OF ENERGY UTILIZATION
glycogen energy for
synthesis and growth
Glucose ATP muscular contraction
glandular secretion
Lactic acid pyruvic acid nerve conduction
active absorption
 Acetyl-coA

 Deaminated a.a. phosphocreatine

 Other substrate AMP


CO2 +H2O creatine+phosphate
CONTROL OF ENERGY RELEASE IN THE CELL
 1. rate control of enzyme-catalyzed reaction
 2. role of enzyme conc. in the regulation of
metabolic reaction
 3.role of substrate concentration
 4. rate limitation in a series of reaction
 5. ADP conc. as rate controlling factor
THE METABOLIC RATE
 Metabolism – all chemical reaction in the body
 Heat – end product of energy released in the body
 35% of energy in the foods becomes heat during ATP
formation
 Only 27% of energy from food is utilized by the cell’s
functional system
 But all eventually becomes heat
 Calorie – unit for expressing the quantity of energy released
from foods or expended by diff. functional process
in the body
MEASUREMENT OF METABOLIC RATE
 1. direct calorimetry
-quantity of heat liberated from the body at any
given time(not doing external work)
- uses calorimeter- insulated air chamber
- heat gain by cool water bath

 2. indirect calorimetry- oxygen utilization

 3. metabolator –floating drum with O2 chamber to a
mouthpiece thru 2 tubes
\
 The Formula
 B x 10 x A x C = Your Basic Metabolic Rate
FACTORS AFFECTING METABOLIC RATE
 1. exercise – most dramatic effect
- may increased to 2000%
 2. energy requirements for daily activity
- avg. 70 kg. man lying in bed -1650cal/day
- process of eating and digesting of food- 200cal
- daily requirement for existing – 2000cal/day
 3. effects of diff. types of work
 4. specific dynamic action of protein
 5. age – rate of cellular reaction
 6. sympathetic stimulation- increase cellular activity
increase liver muscle glycogenolysis
-non shivering thermogenesis
 7. male sex hormones
 8. Growth hormones
 9. fever
 10. climate
 11. sleep – decrease muscle tone – sympathetic stimulation
 12. malnutrition
BASAL METABOLIC RATE
 Rate of energy utilization in the body during absolute rest
but while a person is awake

 Conditions for measuring BMR
1. NPO at least 12 hours
2. after a night of restful sleep
3. no strenuous activity preceding 1 hour
4. psychic and physical factors causing excitement be
eliminated
5. temperature of air must be comfortable
METHODS FOR MEASURING BMR
 Expressing BMR in terms of surface area
- percentage above or below normal

 Constancy of BMR in same person
- person to person
BODY TEMPERATURE: REGULATION AND FEVER
 Normal body temperature
-core temperature – deep tissue of the body
-constant
 Skin temperature – rises and falls
 Body temperature – balance of heat production
and heat loss
 Heat production from :
1. BMR of all cells
2. metabolism cause by muscle activity
3. effect of thyroxin
4. sympathetic stimulation
5. increase in temperature
 Heat production – generated in deep organs
liver, brain, heart, skeletal muscle

 Heat transferred to the skin

 Rate of heat loss
1. rate of conduction from core to skin
2. rate of transfer from skin to surrounding tissue
THE INSULATOR SYSTEM OF THE BODY
 Skin, subcutaneous tissue and fat - insulator
 Fat conducts heat only one third as readily
 Effect of blood flow
-venous plexuses below the skin
-arteriovenous anastomosis
-increase rate of blood flow heat loss
 Control of heat conduction to the skin is regulated
by sympathetic nervous system
PHYSICS OF HEAT LOSS FROM SKIN
 1. radiation – in the form of infrared heat rays
- 60% of heat loss
 2. conduction - to objects to air air convection
 3 convection – heat loss thru air currents
- cooling effect of wind
-water adjacent to the skin
 4. evaporation – when water evaporates from the
body heat is also loss
- insensible heat loss
SWEATING
 Its regulation – anterior hypothalamus pre
optic area

 Sweat glands – sympathetic cholinergic fibers –
responsive to epinephrine

MECHANISM OF SWEAT SECRETION
 Sweat gland – tubular – 2 parts
1. deep subdermal – coiled portion
2. duct portion

 Epithelial lining in coiled portion forms the primary or
precursor secretion ( similar to plasma secretion)
 Composition is modified by reabsorption of sodium and
potassium
 Depends on sympathetic stimulation
 Acclimatization of sweat mechanism
 Rarely 700cc/hr if not acclimatized
 Progressive sweating occurs when exposure to hot temperature is increased
-Maximum of 2 liters/ hr

 Decrease sodium chloride loss - 3 – 5 gms/day – due aldosterone
REGULATION OF BODY TEMPERATURE
 Anterior hypothalamus preoptic area
– heat /cold sensitive neurons

 When stimulated
– profuse sweating and vasodilation

DETECTION OF TEMPERATURE
 Receptors from skin and deep tissues
 More cold receptors than warm receptors
 When skin is chilled – reflex reaction
1. shivering
2. inhibit sweating
3. vasoconstriction
 Both receptors are important in prevention of
hypothermia
ROLE OF HYPOTHALAMUS
 Integration of peripheral and central
temperature signals

 Responsible for providing either heat producing
or heat conserving reaction
TEMPERATURE DECREASING MECHANISM WHEN BODY IS TOO HOT
 1. vasodilatation
 2. sweating
 3. decrease heat production

 1. vasodilatation
 2. sweating
 3. decrease heat production

 1. skin vasoconstriction
 2. piloerection
 3. increase in heat production
-shivering- primary motor center in hypothalamus
- sympathetic excitation of heat production
chemical thermogenesis – uncoupled oxidation
-thyroxine secretion- release of thyrotropin-
releasing hormone—throid stimulating hormone
thyroxin chemical thermogenesis

 SET POINT FOR TEMPERATURE CONTROL
 Critical core body temperature --- 37.1 degree centigrade
 Above or below this temperature –
 - change in the rate of heat loss or heat production
 by temperature regulating mechanism of the body

 Heat temperature receptors in the ant hypothalamic-preop-
 -tic area

 Can be altered by temperature signals from the peripheral
 areas of the body

ABNORMALITIES OF BODY TEMPERATURE REGULATION
 Fever – body temperature above normal
- causes: 1. bacterial diseases
2. brain tumors
3. environmental conditions
 Resetting of the hypothalamic temperature regulating center
in febrile conditions

 Illness- effects of pyrogens(Proteins, breakdown products of
proteins,lipopolysacharride,toxins)
- cause set point to increase
- activates mechanism for increasing body temperature

MECHANISM OF ACTION OF PYROGENS IN CAUSING FEVER
 Directly acting on hypothalamic regulating center
 Indirect action – bacterial pyrogens(endotoxin)
bacterial phagocytosis by blood cells digestion
release of interleukin1 hypothalamus

 One 10,000,000th of a gram
 Formation of prostaglandin acts on hypothalamus
fever

 Aspirin – blocks formation of prostaglandin
CHARACTERISTICS OF FEVER
 Change of set point to higher level
-since blood temperature is lower
- body respond to increase temperature
- chills, cold vasoconstriction
- equalized hypothalamic setting
 Crisis or flush
--removal of factor causing fever
--set point returns to normal
--body temperature still high
--heating of hypothalamus from peripheral recptors
--activates temperature regulating mechanism
--sweating
--vasodilatation

The danger of dehydration and heat stroke
 can be life-threatening if left untreated.
What is heat stroke?
What is heat stroke?
 It is the result of long, extreme exposure to the sun, in which a person does not sweat enough to lower body temperature.

 The elderly, infants, persons who work outdoors and those on certain types of medications are most susceptible to heat stroke.

 It is a condition that develops rapidly and requires immediate medical treatment.
 Limits of heat one can withstand – dry/wet
 Limitation of losing heat by heat regulating capacity
 Thalamus is also depressed

 Body temperature of 106-108OF heat stroke
symptoms -dizziness, abdominal distress, delirium
-loss of consciousness, circulatory shock

 Hyperpyrexia – brain damaging
 Could be fatal
 prevention – ice-water bath – uncontrollable
shivering
- sponge or spray cooling

 Harmful effects of high temperature
-local hemorrhages
-parenchymatous degeneration of cells
ACCLIMATIZATION TO HEAT
 Increase maximum rate of sweating
 Increase plasma volume
 Decrease salt loss in sweat and urine
-due to aldosterone
EXPOSURE OF BODY TO EXTREME COLD
 30 mins. exposure to ice water
-heart stand-still or fibrillation
 Loss of temperature regulation at low temperature
 Loss of chemical heat production in the cell
 Sleepiness/coma
-depress cns heat control mechanism
-prevents shivering

 Hypothermia is defined as a core temperature of less than 35 degrees Celcius.

 the clinical state of sub-normal temperature when the body is unable to generate sufficient heat to efficiently maintain functions.
 The healthy individual's compensatory responses to heat loss via conduction, convection, radiation, evaporation and respiration may be overwhelmed by exposure.
 Once hypothermia develops, the heat deficit is shared by two body compartments, the shell and the core.
 Medications may interfere with thermoregulation. Acute or chronic central nervous system processes may decrease the efficiency of thermoregulation
Hypothermia
 Warnings signs of Hypothermia are uncontrollable shivering
 memory loss
 disorientation
 incoherence
 slurred speech
 drowsiness
 and apparent exhaustion.
 Patients cold, stiff and cyanotic, with fixed pupils and no audible heart tones or visible thoracic excursions have been successfully resuscitated.
 The only certain criterion for death in hypothermia is irreversibility of cardiac arrest when the patient is warm.
 Conclusions regarding the potential reversibility of coexisting conditions should be withheld until the patient is rewarmed.

 Resuscitation, including CPR if necessary, should be continued until either failure after hospital rewarming to 35 degrees Celcius or danger through exposure to rescuers exists.
 If medical care is unavailable
 start warming the body slowly
 warm the body core first
 use your own body heat to help
 get the victim into dry clothing
 and wrap them in a warm blanket covering the head and neck.
 Frost bite
-freezing of surface area of the body
-ears, digits of hand/feet
-gangrene
 Protection against frost bite – vasodilatation
 Artificial hypothermia
-sedation
-depress cns temperature regulating mech.
- ice, cooling blankets
- alcohol
ARTIFICIAL HYPOTHERMIA
 Strong sedative-depressing the reactivity of hypothalamic temperature controller
 Cooling with ice
 Used in heart surgery
 Organ transport

No comments: