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NURA 806 Advanced Physiology
Exam 4 Study Guide: Units 11, 12 & 13
Chapter 67:
Glycogenesis = Formation of glycogen
Glycogenolysis = Breakdown of stored glycogen. Using epi or glucagon
Gluconeogenesis = The conversion if amino acids/fatty acids into glucose or glycogen
1. List the basic functions of adenosine triphosphate (ATP).
a. Active transport of molecules across cell membrane
b. Contraction of muscle and performance of mechanical work
c. Various synthetic reactions that create hormones, cell membranes, and many
other essential molecules of the body
d. Conduction of nerve impulses
e. Cell division and growth
f. Many other physiologic functions that are necessary to maintain and propagate
life
2. How much free energy (calories) can one mole of ATP generate in the human body?
(Make sure you understand the difference between calories [with a small “c”] and
Calories [with a big “C” i.e. kilocalories]). P.809/810
a. The amount of free energy liberated by complete oxidation of mole (180 grams)
of glucose is 686,000 calories.
3. Molecules of pyruvic acid are formed at the end of what energy-releasing process? What
is the net ATP gain in this process?
a. Glycolysis 2 pyruvate. NET gain of ATP is 2
4. The conversion of pyruvic acid into acetyl CoA immediately precedes what energyproducing cycle?
a. Tricyclic Acid cycle, Citric acid cycle
5. Oxidative phosphorylation takes place in which cellular organelle?
a. Mitochondria
6. How many ATP molecules (net) are produced from the complete breakdown of a glucose
molecule after all cycles are complete?
a. 38 molecules of ATP
7. What is pyruvic acid converted to under anaerobic conditions?
a. Lactic acid, which diffuses readily out of the cells into the extracellular fluids and
even into the intracellular fluids of other less active cells.
b. The heart is capable of converting lactic acid into pyruvic acid and then using the
pyruvic acid for energy
Chapter 68:
1. How are fats transported from the gastrointestinal tract to the blood?
a. During digestion, most triglycerides are split into monoglycerides and fatty acids.
Then, while passing through the intestinal epithelial cells, the monoglycerides and
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fatty acids are resynthesized into to new molecules of triglycerides that enter the
lymph as minute, dispersed droplets called chylomicrons. Apoprotein B is
adsorbed to the outer surfaces of the chylomicrons preventing the chylomicrons
from adhering to the lymphatic vessel walls. Chylomicrons also contain
Apoprotein B, cholesterol, and phospholipids. The chylomicrons are then
transported upward through the thoracic duct and emptied into the circulating
venous blood at the juncture of the jugular and subclavian veins
2. What is the composition of adipocytes (fat cells)?
a. Modified fibroblasts that store almost pure triglycerides in quanties as great as 8095 percent of the entire cell volume. Triglycerides inside the fat cells are
generally in liquid form.
3. What are three functions of the liver in fat metabolism?
a. The priniciple functions of the liver in lipid metabolism are:
b. (1) degrade fatty acids into small compounds that can be used for energy
(oxidizes triglycerides (fatty acids) for energy. Production of ketone bodies from
triglycerides (FA); exported to other cells as energy source (Acetyl- CoA)
c. (2) synthesize triglycerides, mainly from (glucose) carbohydrates, but to a lesser
extent from proteins (amino acids) as well
d. (3) Synthesize other lipids from fatty acids, especially cholesterol and
phospholipids.
4. What is the function of carnitine relative to fatty acids and mitochondria? CARRRIER
a. Transport of the fatty acid into the mitochondria is a carrier mediated process that
uses canitine as the carrier substance. Fatty acids metabolized ONLY in the
mitochondria. Once inside the mitochondria, fatty acids split away from the
carnitine and are degraded and oxidized.
5. What is the net gain of ATP after the beta-oxidation of one molecule of stearic acid?
a. Net gain of 146 molecules ATP from a steraric acid
b. Steraric acid has an 18 carbon chain that is fully saturated with hydrogen ions.
c. Palmitic acid, which has 16 carbon atoms and is fully saturated.
6. How do epinephrine and norepinephrine affect fat utilization during exercise?
a. Epi/NE released from the adrenal medulla during exercise, as a result of
sympathetic stimulation. These two hormones directly activate hormone-sensitive
triglyceride lipase, which present in abundance in the fat cells, and this causes
rapid breakdown of triglycerides and mobilization of fatty acids.
7. How are phospholipids used in the body?
a. Phospholipids (lecithins, cephalins, and sphingomyelin) are used in the body as:
b. (1) Phospholipids are an important constituent of lipoproteins in the blood and
are essential for the formation and function of most of these, serious abnormalities
of transport of cholesterol and other lipids can occur
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c. (2) Cephalins are used to compose thromboplastin, which is necessary to initiate
the clotting process.
d. (3) Large quantities of sphingomyelin are present in the nervous system acting as
an electrical insulator in the myelin sheath around nerve fibers
e. (4) Phospholipids are donors of phosphate radicals when these radicals are
necessary for different chemical reactions in the tissues
f. (5) And phospholipids are used in the formation of structural elements - mainly
membranes- in cells throughout the body.
Chapter 69:
1. How are proteins absorbed from the digestive tract and handled in the blood?
a. The products of protein digestion and absorption in the GI tract are almost
entirely amino acids (A.A); only rarely are polypeptides or whole protein
molecules absorped from the digestive tract into the blood.
b. Soon after a meal, the A.A. concentration rises in a persons blood to only a few
milligrmas per dL for 2 reasons; (1) Protein digestion and absorption are ususally
extended over 2-3 hours, which only allows small quantites of A.A.’s to be
absorbed at a time. (2) after entering the blood, the excess amino acids are
absorbed within 5-10 minutes by the cells thoughout the body, especially by the
liver. Therefore, almost never do large concentrations of amino acids accumulate
in the blood and tissue fluids.
c. BLOOD: The molecules of all the amino acids are much too large to diffuse
readily through the pores of the cell membranes. Therefore, significant quantities
of amino acids can either move inward or outward through the membranes only
by facilitated transport or active transport using carrier mechanisms is still porrly
understood.
2. Differentiate essential from non-essential amino acids. ( need at least 20-30 gm/day)
a. Essential must be supplied from exogenous source v.s. non-essential produced by
the body
b. Ten of the amino acids normally present in animal proteins can be synthesized in
the cells (non-essentail amino acids), whereas the other 10 either cannot be
synthesized or are synthesized in quantities too small to supply the body’s needs.
(essential amino acids)
c. Use of the word “essential” does not mean that the other 10 “non-essentail” amino
acids are not required for the formation of proteins, but only that the others are
not essential in the diet because they can be synthesized in the body.
3. What happens to excess amino acids in the liver? What potentially toxic end product can
result and how is it handled in the body?
a. Once the cells are filled to their limits with stored protein, any additional amino
acids in the body fluids are degraded and used for energy or are stored main as fat
or secondarily as glycogen. This degradation occurs almost entirely in the liver,
and it begins with deamination.
b. Deamination means removal of the amino groups from the amino acids.
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c. This occurs by transamination, which means transfer of the amino group to some
acceptor substance, which is the reverse of the transamination in relation to
synthesis.
d. Amino acid group  α-ketoglutaric acid  glutamic acid  ammonia
e. To initate the above process, the excessive amino acids in the cells, especially in
the liver, induce activation of large quantities of aminotransferase, the enzymes
responsible for initiating most deamination.
f. The ammonia released during deamination of amino acids is removed from
the blood almost entirely by conversion into urea; 2 moelcules of ammonia and
one molecule of carbon dioxide combine.
g. Urea diffuses into the body fluids/blood and is removed via the kidneys
4. Describe the factors involved in the hormonal regulation of protein metabolism.
a. (Growth hormone ↑)increases the synthesis of cellular proteins
i. an increased transport of amino acids through the cell membranes
b. Insulin is necessary for protein synthesis
i. Insulin accelerates the transport of some amino acids into cells, which
could be the stimulus to protein synthesis
c. Glucocorticoids/Cortisol increase breakdown of most tissue proteins
i. Breakdown of extrahepatic tissue proteins, increased plasma A.A’s.
remember that A.A’s are needed for gluconeogenesis and ketogenisis
d. (Testosterone ↑) increases protein deposition in tissues.
i. Has an upper limit
e. Estrogen also causes some deposition of protein, but not to the effect of
testosterone.
f. Thyroxine increases the rate of metabolism of all cells
i. As a result, indirectly affects protein metabolism. If insufficient carbs
and fats are available for energy, thyroxine causes rapid degradation of
proteins and uses them for energy
Chapter 70:
1. Know the structures of a liver lobule (Figure 70-1).
a. A liver lobule is constructed around a central vein that empties into the hepatic
veins and then into the vena cava
b. The lobule itself is composed prinicipally of many liver cellular plates (2 are
shown) that radiate from the central vein like spokes in a wheel. Each hepatic
plate is usually two cells thick and between the adjacent cells lie small bile
canaliculi that empty into bile ducts in the fibrous septa separating the adjacent
liver lobules
c. In the septa are small portal venules that receive their blood mainly from the
venous outflow of the GI tract by way of the portal vein. From these venules
blood flows into flat, branching hepatic sinusoids that lie between the hepatic
plates and then into the central vein. Thus the hepatic cells are exposed
continuously to portal venous blood.
d. Venous sinusoids are lined by two other cell types: (1) typical endothelial cells
and (2) large Kupffer cells ( also called reticuloensothelial cells), which are
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resident macrophages that line the sinusoids and are capable of phagocytizing
bacteria and other foreign matter in the hepatic sinus blood.
e. Beneath the endothelial lining, lying between the endothelial cells and the hepatic
cells, are narrow tissue spaces called the spaces of Disse. The millions of spaces
of Disse connect with lymphatic vessels in the interlobular septa. Therefore,
excess fluid in these spaces is removed through the lymphatics.
f.
2. Describe lymph drainage from the liver.
a. 50% of body lymph is formed in the liver
b. Porous fenestrations in sinusoidal endothelial cells leak fluid and protein into
“space of Disse” and collects in lymph vessels.
c. The pores in the hepatic sinusoids are very permeable and allow ready passage of
both fluid and proteins into the spaces of Disse, the lymph draining from the liver
usually has a protein concentration of about 6g/dL, which is only slightly less than
the protein concentration of plasma. Also, the high permeability of the liver
sinusoid epithelium allows large quantities of lymph to form. Therefore, about
half of all the lymph formed in the body under resting conditions arises in the
liver.
3. How are ascites formed and what is the approximate composition of ascetic fluid?
a. When the pressure in the hepatic veins rises only 3-7 mmHg above normal – (910 mmHg), excessive amounts of fluid begin to transude into the lymph and leak
through the outer surface of the liver capsule directly into the abdominal cavity.
This fluid is almost pure plasma, containing 80 to 90 percent as much protein as
normal plasma. At vena caval pressures of 10 to 15 mmHg, hepatic lymph flow
increases as much as 20 times normal, and the “sweating” from the surface of the
liver can be so great that it causes large amounts of free fluid in the abdominal
cavity, which is called ascites.
b. Blockage of portal flow through the liver also causes high capillary pressures in
the entire portal vascular system of the GI tract, resulting in the edema of the gut
wall and transudation of fluid through the serosa of the gut into the abdominal
cavity causing ascites.
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4. What is the function of hepatic growth factor (HGF)?
a. Important in causing liver cell division and growth.
b. HGF is produced by mesenchymal cells in the liver and in other tissues, but not
by hepatocytes. Blood levels of HGF rise more than 20 fold after partial
hepatectomy, but mitogenic responses are usually found only in the liver after
these operations, suggesting that HGF may be activated only in the affected
organ.
c. Can donate up to 70% of liver
5. List the essential functions of the liver in carbohydrate, fat and protein metabolism.
a. Carbohydrate Metabolim
i. Storage of large amounts of glycogen
ii. Convert galactose/fructose to glucose
iii. Gluconeogenesis (conversion of lipids/proteins to glucose)
iv. Formation of many chemical compounds from intermediate products of
carbohydrate metabolism
b. Fat Metabolism
i. Oxidation of fatty acids to supply energy for other body functions
ii. Synthesis of large quantities of cholesterol (80% to bile salts, which are
secreted into the bile), phospholipids, and most lipoproteins (20%).
iii. Synthesis of fat from proteins and carbohydrates
c. Protein Metabolism ( most important)
i. Deamination of amino acids
1. ammonia
ii. Formation of urea for removal of ammonia from the body fluids.
iii. Formation of plasma proteins
1. Albumin, Fibrinogen, Globulins
iv. Interconversions of the various amino acids and synthesis of other
compounds from amino acids
1. Non-essential amino acids
6. Describe how old red blood cells are eliminated by the liver.
a. Tissue Macrophages split Hgb (heme and globin)  free iron (transported as
transferrin in blood) and pyrrole nuclei (basis for unconjugated bili)  released
into the plasma/combines with albumin.
b. In the liver bilirubin conjugated to bilirubin glucuronide and other substances
i. Conjugated bili released into intestines and converted by bacteria to
urobilinogen  taken back up into blood and re-excreted in feces and
urine.
c. The hemoglobin is first split into globin and heme, and the heme ring is opened to
give (1) free iron, which is transported in the blood by transferrin, and (2) a
straight chain of four pyrrole nuclei, which is the substrate from which bilirubin
will be eventually formed.
d. The first substance formed is biliverdin, but this is rapidly reduced to free
bilirubin, also called unconjugated bilirubin, which is gradually released from the
macrophages into the plasma. Unconjugated bili combines strongly with plasma
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albumin and is transported in this combination throughout the blood and
interstitial fluids.
e. Within hours the unconjugated bilirubin is absorped through the hepatic cell
membrane. In passing to the inside of the liver cells, it is released from the
plasma albumin and soon thereafter conjugated about 80% with glucuronic acid to
form bilirubin sulfate, and about 10 percent with a multitude of other substances.
In these forms, the bilirubin is excreted from the hepatocytes by an active process
into the bile canaliculi and then into the intestines.
f.
Chapter 72:
1. What is the purpose and benefit of phosphocreatine? For how long can energy from this
source be used during maximal exertion?
a. (1) Energy storehouse; (2) 3-8 times more abundant than ATP; (3) Capable of
exchanging energy with ATP; (4) 1st source of energy when short burst are
needed; (5) Only provides 5-10 seconds of energy (think sprinter or competitive
weight lifter) 
i. ATP-phosphocreatine system  ATP “buffer” system
b. Phosphocreatine is 3-8 times more abundant than ATP.
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c. Also, the high energy bond of phosphocreatine contains about 8500 calories per
mole under standard conditions and as many as 13,000 carolies per mole under
conditions in the body. This is slightly greater than the 12,000 caloires per mole
in each of the two high energy phosphate bonds of ATP.
d. Unlike ATP, phosphocreatine cannot act as a direct coupling agent for energy
transfer between foods and the functional cellular systems, but it can transfer
energy interchangeably with ATP. Phosphocreatine + ADP = ATP + Creatine
e. Extra amounts of ATP available in the cell, its used to synethesize
phosphocreatine, thus building up this storehouse of energy.
2. Understand the relationship between heat production and metabolism in the body. How
much of the energy produced in the body is actually used in a functional way (i.e. not just
lost as heat)?
a. The metabolism of the body simply means all the chemical reactions in all the
cells of the body, and the metabolic rate is normally expressed in terms of the rate
of heat liberation during chemical reactions.
b. Only formed by the body is used for functional about 27 % of energy purposes.
c. On average 35% of the energy in foods becomes heat during ATP formation.
Then, still more energy becomes heat as it is transferred from ATP to the
functional systems of the cells, so even under optimal conditions, no more than
27% of all energy from food is finally used by the functional systems
3. On average, how many Calories (big “C”) are liberated per liter of oxygen used in the
body? Of what benefit is this knowledge in estimating energy used by the body?
a. Big ‘C’ or kilocalorie is equivalent to 1000 calories (small c). Calories/Kilocalorie
is the unit ordinarily used in discussing energy metabolism.
b. Direct calorimetry measures heat liberated from the body.
c. Indirect calorimetry the “Energy Equivalent” of oxygen. Because more than 95%
of the energy expended in the body is derivied reactions of oxygen with different
foods, the whole body metabolic rate can also be calculated with a high degree of
accuracy from the rate of oxygen utilization. When 1 liter of oxygen is
metabolized with glucose, 5.01 Calories of energy are released; when metabolized
with starches, 5.06 Calories are released; with fat, 4.70 Calories; and with protein,
4.60 Calories.
d. On average, the quantity of energy liberated per liter of oxygen used in the body
averages about 4.825 Calories.
e. Using this energy equivulant, one can calculate with a high degree of precision
the rate of heat liberation in the body from the quantity of oxygen used in a given
period of time.
4. How much of daily energy expenditure does basal metabolic rate (BMR) account for?
a. Even when a person is at complete rest, considerable energy is required to
perform all the chemical reactions of the body. This minimum level of energy
required to exist is called the basal metabolic rate
b. It accounts for about 50-70% of the daily energy expenditure in most sedentary
individuals.
c. BMR normally averages about 65-70 Calories per hour in an average 70 kg male
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5. What is the effect of climate on BMR?
a. Adaptation of the thyroid gland—with increased secretion in cold climates and
decreased secretion in hot climates—contributes to the differences in BMRs
among people living in different geographical zones; for example, people living in
artic regions have BMRs 10-20% higher than those of persons living in tropical
regions.
Chapter 73:
1. Identify and define the ways heat is lost from the body.
a. Radiation ( about 60% of total heat loss)
i. Loss in the form of infrared heat rays, a type of electromagnetic wave.
Most infrared heat rays radiate from the body have wave lengths of 5-20
micrometers, 10-30 times the wavelengths of light rays. The body radiates
heat rays in all directions. If the body temperature is greater than the
environmental temperature, then heat is radiated from the body to the
surroundings.
b. Conduction
i. Direct conduction (3%) from the surface of the body to solid objects, such
as a chair or a bed.
c. Convection (15%)
i. The removal of heat from the body by convection air currents is
commonly called heat loss by convection. Actually, the heat must fort be
conducted to the air and then carried away by the convection air currents.
d. Evaporation (22%)
i. When water evaporates from the body surface, 0.58 Calorie (kilocalorie)
of heat is lost for each gram of water that evaporates. Even when a person
is not sweating, water still evaporates insensibly from the skin and lungs at
a rate of about 600-700ml/day. This causes continual heat loss at a rate of
16-19 Calories per hour.
2. What determines the composition of fluid secreted by sweat glands? What is a
“precursor secretion”?
a. The precursor of the sweat gland is primary secretion or precursor secretion; the
concentrations of constituents in the fluid are then modified as the fluid flows
through the duct.
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b. The precursor secretion is an active secretory product of the epithelial cells
lining the coiled portion of the sweat gland. Cholinergic sympathetic nerve
fibers ending on or near the glandular cells elicit the secretion.
c. The composition of the precursor secretion is similar to that of plasma, except that
it does not contain plasma proteins. The concentration of sodium is about
142mEq/L and that of chloride is about 104mEq/L, with much smaller
concentrations of the other solutes of plasma.
d. As the precursor solution flows through the duct portion of the gland, it is
modified by reabsorption of most of the sodium and chloride ions. The degree of
this reabsorption depends on the rate of sweating.
e. When the sweat glands are stimulated only slightly, the precursor fluid passes
through the duct slowly. In this instance, essentially all the sodium and chloride
ions are reabsorbed, and the concentration of each falls to as low as 5 mEq/L.
This reduces the osmotic pressure of the sweat fluid to such a low level that most
of the water is also reabsorbed, which concentrates most other constituents as
urea, lactic acid, and potassium ions are usually very concentrated.
f. Conversly, when the sweat glands are strong stimulated by the symapathetic
nervous system, large amounts of precursor secretion is formed, and the duct may
reabsorb only slightly more than half the sodium chloride; the concentrations of
sodium and chloride ions are then a maximum of about 50 to 60 mEq/L, slightly
less than half the concentration in the plasma. Furthermore, the sweat flows
through the glandular tubules so rapidly that little of the water is reabsorbed.
Therefore, the other dissolved constituents of sweat are only moderately increased
in concentration – urea is about 2x that in the plasma, lactic acid about 4x, and
potassium about 1.2x.
3. Describe the hypothalamus’ function in sensing body temperature. Where else in the
body are cold and warmth receptors found?
a. The principle areas in the brain where heat or cold from a thermode affects body
temperature control are the pre-optic and anterior hypothalamic nuclei of the
hypothalamus. The anterior hypothalamic-preoptic area has been found to
contain large numbers of heat-sensitive neurons, as well as about one-third as
many cold sensitive neurons.
b. Temperature receptors in the skin and in a few specific deep tissues of the body.
The skin has far more cold receptors than warmth receptors – in fact 10x as many
in many parts of the skin. Deep body temperature receptors are fund mainly in
the spinal cord, in the abdominal viscera, and in or around the great veins in
the upper abdomen and thorax. These deep receptors function differently from
the skin receptors because they are exposed to the body core temperature. Yet,
like the skin temperature receptors, they detect mainly cold rather than warmth. It
is probable that both the skin and the deep body receptors are concerned with
preventing hypothermia.
c. The peripheral temperature sensing sensory signals stimulate the posterior
hypothalamus (integration center). The temperature sensory signals from the
anterior hypothalamic pre-optic area are also transmitted into this posterior
hypothalamic area. Here the signals from the pre-optic area and the signals
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from elsewhere in the body are combined and integrated to control the heat–
producing and heat-conserving reactions of the body
4. Describe how the shivering mechanism works.
a. Located in the dorsomedial portion of the posterior hypothalamus near the wall of
the third ventricle is an area called the primary motor center for shivering. This
area is normally inhibited by signals from the heat center in the anterior
hypothalamic-preoptic are but is excited by cold signals from the skin and the
spinal cord. It transmits signals that cause shivering through bilateral tracts
down the brain stem, into the lateral columns of the spinal cord, and finally
to the anterior motor neurons. They increase the muscle tone of the skeletal
muscles throughout the body by facilitating the activity of the anterior motor
neurons. When the tone rises above a critical level, shivering begins. During
maximum shivering, body heat production can rise to four to five times normal.
5. How does non-shivering thermogenesis provide heat? What is the role of
catecholamines?
a. An increase in either sympathetic stimulation or circulating norepinephrine and
epinephrine in the blood can cause an immediate increase in the rate of cellular
metabolism. This effect is called chemical thermogenesis, or nonshivering
thermogenesis. It results at least partially from the ability of NE and epi to
uncouple oxidative phosphorylation, which means that excess foodstuffs are
oxidized and thereby release energy in the form of heat but do not cause ATP
to be formed.
6. How does thyroxine provide chemical thermogenesis?
a. (slides) Cooling anterior hypothalamus increases secretion of thyrotropinreleasing hormone (TRH)  stimulates secretion of TSH from anterior pituitary
 increased thyroxine from thyroid gland  Increases cellular metabolism and
temperature
b. Cooling of the anterior hypothalamic-preoptic area causes a release of
thyrotropin-releasing hormone, this hormone is then carried away via the
hypothalamic portal system to the anterior pituitary gland, which then secretes
thyroid-stimulating hormone. Once at the thyroid gland, the gland is then
stimulated to release thyroxine. As mentioned earlier, thyroxine activates
uncoupling of protein and increases the rate of cellular metabolism
throughout the body, thus increasing heat production. This process takes
several weeks to exposure to the cold. Eventually the body will increase the size
of the thyroid gland 20- 40%. This is only noted in animal experiments.
7. What is the role of cytokines (especially interleukin-1) in the development of a fever?
a. (slides) Pyrogens (released from toxic bacteria) can indirectly reset set-point 
Interleukin-1 released from phagocytes following phagocytosis of blood-borne
pyrogens  IL-1 raises set point by increasing prostaglandin production (mainly
E-2)
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b. Interleukin-1 is released from macrophages into the body fluids and, on reaching
the hypothalamus, almost immediately activates the process to produce fever,
sometimes increasing the body temperature a noticeable amount in only 8-10
minutes.
c. Several experiments have suggested that interleukin-1 causes fever by first
inducing the formation of one of the prostaglandins, mainly PGE-2, or a similar
substance, which acts in the hypothalamus to elicit the fever reaction. Aspirin
reduces fever because it impedes the formation of prostaglandins from
arachidonic acid.
Chapter 74:
1. Identify and define the six chemical messengers and the three general classes of
hormones.
a. Neurotransmitters are released by axon terminals of neurons into the synaptic
junctions and act locally to control nerve cell function
b. *Endocrine hormones are released by glands or specialized cells into the
circulating blood and influence the function of target cells at another location in
the body
c. *Neuroendocrine hormones are secreted by neurons into the circulating blood
and influence the function of target cells at another location in the body.
d. Paracrine are secreted by cells into the extracellular fluid and affect neighboring
target cells of a different type
e. Autocrine are secreted by cells into the extracellular fluid and affect the function
of the same cells that produced them
f. Cytokines are peptides secreted by cells into the extracellular fluid and can
function as autocrines, paracrines, or endocrine hormones
g. Three General Classes
i. Proteins and Peptides, (pituitary, pancreas, parathyroid)
1. including hormones secreted by the anterior and posterior pituitary
gland, the pancreas (insulin and glucagon), the parathyroid gland
(parathyroid hormone), and many others.
ii. Steroids (cortisol, aldosterone)
1. secreted by the adrenal cortex (cortisol and aldosterone), the
ovaries (estrogen and progesterone), the testes (testosterone), and
the placenta (estrogen and progesterone)
iii. Derivatives of the amino acid tyrosine (epi, norepi, thyroid)
1. , secreted by the thyroid (thyroxine and triiodothyronine) and the
adrenal medullae (epi & norepi).
iv. Releasing hormones hypothalamus, secreting hormones from pititutary
(endocrine), anterior adrenohypophysis, posterior neurohypophysis
2. Be familiar with Table 74-1 (you may omit the reproductive hormones LH and FSH since
we are not covering those units in this course).
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3. Understand how negative and positive feedback and cyclical variations influence
hormone secretion.
a. Negative feedback prevents over activity of hormone systems. Ensures a
proper level of hormone activity at the target tissue.
b. Positive feedback occurs when the biological action of the hormone causes
additional secretion of the hormone. Ex. Oxytocin or Leteinizing hormone
4. Which hormones are protein bound in the blood?
a. Steroids and thyroid hormones are bound to plasma proteins, which are the
inactive form. Less than 10% in the plasma exist free in the solution
b. Water-soluble hormones (peptides and catecholamines) are dissoloved in the
plasma and transported from their sites of synthesis to target tissues, where they
diffuse out of the capillaries, into the interstitial fluid, and ultimately into the
target cells
5. Where are hormone receptors located?
a. In or on the surface of the cell membrane. The membrane receptors are specific
mostly for the protein, peptide, and catecholamine hormones
b. Cell Cytoplasm, The primary receptors for the different steroid hormones are
found mainly in the cytoplasm
c. Cell Nucleus, The receptors of for the thyroid hormones are found in the nucleus
and are believed to be located in direct association with one or more of the
chromosomes.
6. Describe the up and down-regulation of hormone receptors.
a. Down Reg: Increased hormone concentration and increased binding with its
target cell recpetors sometimes cause the number of active receptors to decrease.
Thus decreasing the target tissues responsiveness to the hormone
i. Inactivation of some of the receptor molecules
ii. Inactivation of some of the intracellular protein signaling molecules
iii. Temporary sequestration of the receptor to the inside of the cell, away
from the site of action of hormones that interact with the cell membrane
receptors
iv. Destruction of the receptors by lysosomes after they are internalized
v. Decreased production of the receptors
b. Up Reg: Stimulating hormone induces greater than normal formation of receptor
or intracellular signaling molecules by the protein manufacturing machinery of
the target cell, or greater availiblity of the receptor for interaction with the
hormone.
i. Target tissue becomes progressively more sensitive to the stimulating
effects of the hormone. Less drug admin
7. Understand the process of increased protein synthesis stimulated by steroid hormones.
a. (slides) Hormone (lipid soluble) diffuses across cell membrane/binds with
receptor
b. Transported into the nucleus
c. Binds to DNA, creates RNA (transcription)
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d. mRNA travels to cytoplasm to initiate (Translation) protein synthesis in the
ribosomes.
8. What is the basic mechanism of thyroid hormones expression?
a. T3, T4 cause increased transcription of nuclear genes
i. Binds with activated transcription factors in the chromosomes
ii. Activate genetic mechanisms for the production of proteins (enzymes) that
increase cell metabolism (all cells)
iii. Continue to express hormonal control for days/weeks
Chapter 75:
Pituitary gland also called the hypophysis that lies in the sella turcica and is
connected to the hypothalamus by the pituitary stalk. Anterior pituitary =
adenohypophysis (endocrine/hormonal transport in the blood) and Posterior pituitary is
the neurohypophysis (neuroendocrine stimulation)
1. Know which hormones are secreted from the anterior and posterior pituitary gland.
a. Anterior Pituitary
b. Growth hormone: promotes growth of the entire body by affecting protein
formation, cell multiplication, and cell differentiation
c. Adrenocorticotropin: controls the secretion of some of the adrenocortical
hormones, which affect the metabolism of glucose, proteins, and fats
d. Thyroid-stimulating hormone: controls the rate of secretion of thyroxine and
triiodothyronine by the thyroid gland, and these hormones control the rates of
most intracellular chemical reactions in the body
e. Prolactin: promotes mammary gland development and milk production
f. FSH and LH  ovaires and testes
g. Posterior Pituitary
h. ADH: controls the rate of water excretion into the urine, thus helping to control
the concentration of water in the body fluids
i. Oxytocin: helps express milk from the glands of the breast to the nipples during
suckling and helps in the delivery of the baby at the end of gestation.
2. Understand the connection between the neural secretion of hypothalamic releasing and
inhibitory hormones and the hypothalamic-hypophysial portal blood vessels
(Figure 75-4).
a. Secretion by the anterior pituitary is controlled by hormones called hypothalamic
releasing and hypothalamic inhibitory hormones secreted within the
hypothalamus and then conducted to the anterior pituitary through minute blood
vessels called the hypothalamic-hypophysial portal vessels.
i. The anterior pituitary is highly vascular gland with extensive capillary
sinuses amoung the glandular cells. Almost all of the blood that enters
these sinuses passes first through another capillary bed in the lower
hypothalamus. The blood then flows through small hypothalamichypophysial portal blood vessels into the anterior pituitary sinuses.
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ii. Goes from the hypothalamus  median eminence  primary capillary
plexus  hypothalamic-hypophysial portal vessels  superior
hypophysial to anterior pituitary and/or inferior hypophysial artery to
posterior pituitary
b. Special neurons in the hypothalamus synthesize and secrete the hypothalamic
releasing and inhibitory hormones that control secretion of the anterior pituitary
hormones. These neurons originate in different parts of the hypothalamus and
send their nerve fibers to the median eminence and tuber cinereum (an extension
of the hypothalamic tissue into the pituitary stalk. The endings of these fibers
secrete hormones into the tissue fluids (this is different from other neuron endings
that transmit signals between neurons). The hormones are immediately absorbed
into the hypothalmic-hypophysial portal system and carried directly to the sinuses
of the anterior pituitary gland.
3. Know the function of the five hypothalamic releasing/inhibitory hormones.
a. Thyrotropin-releasing hormone (TRH): which causes release of thyroidstimulating hormone (TSH)
b. Corticotropin-releasing hormone (CRH): which causes release of
adrenocorticotropin (ACTH)
c. Growth hormone-releasing hormone (GHRH): which causes the release of
growth hormone, and growth hormone inhibitory hormone (GHIH), also called
somatostatin, which inhibits release of growth hormone
d. Gonadotropin-releasing hormone (GnRH), which cause release of the two
gonadotropic hormones, luteinizing hormone (LH) and follicle-stimulating
hormone (FSH)
e. Prolactin inhibitory hormone (PIH), which causes inhibition of prolactin secretion
4. What are the basic effects of growth hormone (GH) in the system? What conditions
stimulate the secretion of GH?
a. Growth hormone (somatotropic hormone) does not function through a target
gland but exerts its effects directly on all or almost all tissues of the body
i. Increased rate of protein synthesis in most cells of the body
ii. Increased mobilization of fatty acids from adipose tissue, increased free
fatty acids for energy. Uses fat for energy rather than glucose
iii. Decreased rate of glucose utilization throughout the body.
iv. Thus, in effect, growth hormone enhances body protein, uses up fat stores,
and conserves carbohydrates
b.
c.
d.
e.
f.
g.
h.
Stimulation of GH:
Starvation—severe protein deficency
Hypoglycemia—low concentration of fatty acids in the blood
Exercise
Excitement
Trauma
Ghrelin—hormone secreted by the stomach before meals
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5. Describe the neural secretory structure of the posterior pituitary gland (Figure 75-9).
a. Paraventricular (oxytocin) and supraoptic nucleus (ADH) to posterior
hypothalamus. These tracts pass to the neurohypophysis through the pituitary
stalk.
b. The posterior pituitary is also called the neurohypophysis and is composed of
glial-like cells called pituicytes. The pituicytes do not secrete hormones, they just
supply support for many for a large number of terminal nerve fibers and terminal
nerve endings from nerve tracts that originate in the supraoptic and
paraventricular nuclei of the hypothalamus. These tracts pass to the
neurohypophysis through the pituitary stalk
6. What mechanism stimulates the release of anti-diuretic hormone?
a. Increased Extracellular fluid osmolarity stimulates ADH
b. Low blood volume
c. Low blood pressure
d. Pain
e. Stress
f. Drugs
g. Somewhere in or near the hypothalamus are modified neuron receptors called
osmoreceptors. When extracellular fluid becomes too concentrated, fluid is pulled
by osmosis out of the osmoreceptor cell, decreasing its size and initiating the
signal for ADH secretion. So, concentrated body fluids stimulate the supraoptic
nuclei and paraventricular nuclei to immediately transmit impulses into the
posterior pituitary to release large quantities of ADH.
Chapter 76:
1. Describe iodine trapping in the thyroid gland. (50mg a year, 1mg a week)
a. Iodine brought to the thyroid gland via the circulatory system
b. Active transport into the thyroid against a concentration gradient
i. Co-transported with 2 sodium ions
c. Concentrating iodine in the thyroid is called “iodide trapping”
i. Increases with increased levels of TSH
d. Iodide moved into follicle
i. Counter transport with chloride with the help of pendrin
2. What molecule is iodinated in a series of steps to form thyroxine (T4) and
triiodothyronine (T3)? What percentage of T4 and T3 are initially released?
a. Tyrosine (contained by thyroglobulin) by peroxidase
b. 93% thyroxine (T4) and 7% triiodothyronine (T3)
c. About one half of the thyroxine is slowly deiodinated to form additional
triiodothyronine. Therefore, the hormone finally delivered to and used by the
tissues is mainly triiodothyronine, a total of about 35 micrograms of
triiodothyronine per day
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3. State the genomic and non-genomic functions of thyroid hormone.
a. Genomic: attaches to receptors in cell nuclei
i. Binds to DNA
ii. Stimulates formation of mRNA for synthesis of metabolic proteins
1. Increases cell metabolism
b. Non-genomic:
i. Sites: plasma membrane, cytoplasm, organelles (mito)
ii. Activities: regulate ion channels; oxidative phosphorylation (mito); 2nd
messenger signals (cAMP or protein kinase signaling cascades)
4. List the functions of thyroid hormone from pp. 912-914.
a. Increase active transport of ions through cell membranes :
i. ↑ protein synthesis, ↑ catabolism, ↑ growth rate in youth, ↑ mental
processes, ↑ sctivity of other endocrines, ↑ number and activity of
mitochondria  ↑ ATP
b. Stimulation of carbohydrate metabolism
i. ↑ glucose uptake, enhances glycolysis, enhances gluconeogenesis,
enhances GI absorption, ↑ insulin secretion
c. Stimulation of fat metabolism
i. ↑fatty acid mobilzation
d. Effects on plasma and liver fats
i. ↓ cholesterol and bile secretion
e. Increased requirement for vitamins
f. Increased basal metabolic rate
g. Decreased body weight
h. Increased blood flow and cardiac output (↑HR and ↑ contractility)
i. Excites CNS
5. What are the effects of thyroid stimulating hormone (TSH)? What hormone stimulates
the production of TSH?
a. TSH, also known as thyrotropin, is an anterior pituitary hormone, a glycoprotein
with a molecular weight of 28,000
b. Increases the secretion of thyroxine and triiodothyronine by the thyroid gland
i. **Increased proteolysis of the thyroglobulin that has already been
stored in the follicles ** most important
ii. Increased activity of the iodide pump, which increases the rate of
“iodide trapping” in the glandular cells
iii. Increased iodination of tyrosine to form thyroid hormones
iv. Increased size and increased secretory activity of the thyroid cells
v. Increased number of thyroid cells.
c. Production of TSH in the anterior pituitary controlled by TRH
i. From hypothalamus
ii. Activates phospholipase SMS
iii. Cold climate ↑ production of TRH
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Chapter 77:
*Mineralcorticiods have gained this name because they especially affect the electrolytes (the “
minerals”) of the ECF, especially sodium and potassium
*Glucocorticoids have gained their name because they exhibit important effects that increase
blood glucose concentration.
1. Know the three layers of the adrenal gland and what hormones they produce.
a. Zona glomerulosa: aldosterone (mineralocorticoid 90%)
i. Blood levels affected by angiotensin II and potassium
b. Zona fasiculata: cortisol and corticosterone (glucocorticoid 95%)
i. Controlled release by ACTH
c. Zona reticularis: androgens  DHEA, androstenedione, estrogens
i. Controlled by ACTH and possibly other hormones
2. What is the role of cholesterol in the production of steroid hormones?
a. Approximately 80% of the cholesterol used for steroid synthesis is provided by
low density lipoproteins (LDL) in the circulating plasma. The LDL’s which have
high concentrations of cholesterol, diffuse from the plasma into the interstitial
fluid and attach to specific receptors contained in structures called coated pits on
the adrenocortical cell membranes
b. The steps: Cholesterol enters the cell and is delivered to the mitochondria. Then
it is cleaved by the enzyme cholesterol-desmolase to form pregnenolone (this is a
rate-limiting step). It then forms adrenal steroids (so, cholesterol is the initial step
in steroid formation!!).
3. How does plasma protein binding affect adrenal hormones once they are secreted?
a. The degree of binding to plasma proteins slows the elimination of cortisol from
the plasma; therefore, cortisol has a relatively long half life of 60 to 90 minutes.
b. Only about 60% of circulating aldosterone combins with the plasma proteins, so
about 40% is in the free form; as a result, aldosterone has a relatively short half
life of about 20 minutes
c. Binding of adrenal steroids to the plasma proteins may serve as a reservoir to
lessen rapid fluctuations in free hormone concentrations. So if there are brief
periods of stress and episodic secretion of ACTH; there is still stored adrenal
steroids. The plasma protein binding adrenal hormons also helps to ensure a
relatively uniform distribution of adrenal hormones to tissues.
4. What imbalances will mineralocorticoid deficiency produce?
a. Severe renal sodium chloride wasting and hyperkalemia
b. Without mineralocorticoids, potassium ion concentration of the ECF rises
markedly, sodium and chloride are rapidly lost from the body, and the total ECF
voume and blood volume become greatly reduced.
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5. State the basic steps of aldosterone activity at the level of the tubular cell from p. 926.
a. First  Aldosterone diffuses readily to the interior of the tubular epithelial cells
because of the cellular membranes lipid solubility.
b. Second  Once in the cytoplasm of the tubular cells; aldosterone combines with
a mineralcorticoid receptor (MR) protein. This protein allows only aldosterone or
similar compounds to combine with it.
c. Third  The aldosterone-receptor complex or just a product of this complex
diffuses into the nucleus; attaching to DNA and changing this to messenger RNA
d. Fourth  Then the messenger RNA diffuses back into the cytoplasm. It uses
ribosome to form protein. The proteins formed are: one or more enzymes and
membrane transport proteins which act together for the transport of sodium,
potassium, and hydrogen transport through the cell membrane. One of these
enzymes is the Na-K ATPase which helps as the principle part of the pump for Na
and K exchange in the basolateral membrane of the renal tubular cells.
e. Results is that aldosterone has delayed effects on Na transport (waiting for
mRNA) 60-90 minutes
6. What effects does cortisol have on gluconeogenesis? On insulin production?
a. Stimulation of gluconeogenesis (formation of carbohydrate from proteins and
some other substances)
i. Cortisol increases the enzymes required to convert amino acids into
glucose in the liver cells.
ii. Cortisol causes mobilization of amino acids from the extrahepatic tissues
mainly from muscle.
b. Reduced insulin sensitivity of tissues
i. High levels of fatty acids, caused by the effect of glucocorticoids may
produce disturbances of carbohydrate metabolism similar to those found in
patients with excess levels of growth hormone.
7. What effect does cortisol have on fatty acids?
a. Promotes mobilization of fatty acids from adipose tissue. This increases the
concentration of free fatty acids in the plasma, which also increases their
utilization for energy
8. Name five stages of inflammation.
a. Released inflammatory mediators
i. Release from the damaged tissue cells of chemical sunstances that activate
the inflammation process – chemicals such as histamine, bradykinin,
proteolytic enzymes, prostaglandins, and leukotrines
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b. Increased blood flow to damaged areas
i. An increase in blood flow in the inflamed area caused by some of the
released products from the tissues, an effect called erythema
c. Increased capillary permeability
i. Leakage of large quantities of almost pure plasma out of the capillary into
the damaged areas because of increased capillary permeability, followed
by clotting of the tissue fluid, thus causing a nonpitting edema
d. Infiltration of the area by leukocytes
e. Healing, growth of fibrous tissue
i. After several days or weeks, ingrowth of fibrous tissue that often helps in
the healing process.
9. Describe how cortisol prevents inflammation.
a. Cortisol stabilizes the lysosomal membranes: anti-inflammatory effects
b. Cortisol decreases the permeability of the capillaries
c. Cortisol decreases both migration of WBC’s into the inflamed area and the
phagocytosis of the damaged cells
d. Cortisol suppresses the immune system, causing lymphocyte reproduction to
decrease markedly
e. Cortisol attenuates fever mainly because it reduces the release of interleukin-1
from the WBC’s
f. It can block the early stages of the inflammation process before inflammation
occurs
g. If inflammation has already begun, it causes rapid resolution of the inflammation
and increased rapidity of healing
Chapter 78:
1. Differentiate the cell types of the islets of Langerhans and what substances each type
secretes.
2. Describe the half-life and clearance of insulin from the blood.
3. What happens to glucose that is delivered to a non-exercising muscle after a meal?
4. How does insulin cause glucose uptake and storage in the liver? In adipose tissue?
5. What is the relationship between brain cells and insulin with regard to uptake of glucose?
6. List the effects of insulin on protein metabolism.
7. Describe the mechanism by which increased levels of glucose prompt insulin secretion
from the pancreatic beta cells (Figure 78-7).
8. What are two major effects of glucagon on glucose metabolism?
9. What is the effect of somatostatin on insulin and glucagon?
Chapter 79:
1. What are the three forms of calcium transport in the blood and the approximate percent of
each?
2. Describe the composition of bone (matrix, salts and their respective components etc.).
3. What are the functions of osteoblasts/osteoclasts in the deposition/absorption of bone?
4. List the activities of vitamin D.
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5. Describe how parathyroid hormone (PTH) regulates blood calcium levels.
6. What are the functions of calcitonin in humans and how significant are they compared to
PTH?