CHAPTER 22 Nutrition and MetabolismSTUDENT LEARNING OBJECTIVES

CHAPTER 22 Nutrition and Metabolism
STUDENT LEARNING OBJECTIVES
At the completion of this chapter, you should be able to do the
following:
1.Define and outline the differences between nutrition and
metabolism.
2.Define these terms: assimilation, catabolism, anabolism.
3.Outline the process of carbohydrate metabolism.
4.Discuss the roles of glycolysis, the citric acid cycle, and the
electron transport chain in the production of cellular energy.
5.List the hormones involved in the control of glucose
metabolism.
6.Outline the role of lipids, their transport, and their
metabolism.
7.Outline the role of proteins and their metabolism.
8.Discuss the difference between vitamins and minerals and
their roles in metabolism.
9.Discuss the factors that control and influence metabolic rate.
LANGUAGE OF SCIENCE AND MEDICINE
Before reading the chapter, say each of these terms out loud.
This will help you avoid stumbling over them as you read.
amino acid (ah-MEE-no ASS-id)
[amino NH2, acid sour]
anabolism (ah-NAB-oh-liz-em)
[anabol- build up, -ism action]
antioxidant (an-tee-OK-seh-dent)
[anti- against, -oxi- sharp (oxygen), -ant agent]
appetite center
assimilation (ah-sim-ih-LAY-shun)
[assimila- make alike, -tion process]
ATP synthase (SIN-thays)

[ATP adenosine triphosphate, syn- together, -ase enzyme]
basal metabolic rate (BMR) (BAY-sal met-ah-BAHL-ik)
[bas- basis, -al relating to, metabol- change, -ic relating to]
calcitriol (kal-SIT-ree-ol)
[calci- lime (calcium), -tri- three, -ol alcohol (after 1,25-D3 or
1,25-dihydroxycholecalciferol)]
catabolism (kah-TAB-oh-liz-em)
[catabol- break down, -ism action]
cellulose (SELL-yoo-lohs)
[cell- storeroom (cell), -ul- small, -ose carbohydrate]
chylomicron (kye-loh-MYE-kron)
[chylo- juice (chyle), -micro- small, -on particle]
citric acid cycle (SIT-rik ASS-id SYE-kul)
[citr- citron tree, -ic relating to, acidus sour, kyklos circle]
coenzyme (koh-EN-zyme)
[co- together, -en- in, -zyme ferment]
deamination (dee-am-ih-NAY-shun)
[de- undo, -amin- ammonia compound, -ation process]
electron transport system (eh-LEK-tron TRANZ-port SIS-tem)
[electr- electric, -on unit, trans- across, -port carry, system
organized whole]
essential fatty acid
[acid sour]
free fatty acid (FFA)
[acid sour]
glucose phosphorylation (GLOO-kohs fos-for-ih-LAY-shun)
[gluco- sweet, -ose carbohydrate (sugar), phos- light, -phor-
carry, -yl- chemical, -ation process]
glycolysis (glye-KOHL-ih-sis)
[glyco- sweet (glucose), -o- combining form, -lysis loosening]
hyperglycemia (hye-per-gly-SEE-mee-ah)
[hyper- above, -glyc- sweet (glucose), -emia blood condition]
hypoglycemia (hye-poh-gly-SEE-mee-ah)
[hypo- below, -glyc- sweet (glucose), -emia blood condition]
lipid (LIP-id)
[lip- fat, -id form]

lipogenesis (lip-oh-JEN-eh-sis)
[lipo- fat, -gen- produce, -esis process]
lipoprotein (lip-oh-PROH-teen)
[lipo- fat, prote- primary, -in substance]
macronutrient (MAK-roh-NOO-tree-ent)
[macro- large, -nutri- nourish, -ent agent]
metabolic rate (met-ah-BOL-ik)
[metabol- change, -ic relating to]
metabolism (meh-TAB-oh-liz-em)
[metabol- change, -ism process]
micronutrient (MYE-kroh-NOO-tree-ent)
[micro- small, -nutri- nourish, -ent agent]
mineral
[mineral- mine]
nutrition (noo-TRIH-shun)
[nutri- nourish, -tion process]
oxidative phosphorylation (ahk-sih-DAY-tiv fos-for-ih-LAY-
shun)
[oxi- sharp (oxygen), -id- chemical (-ide), -at- action of (-ate), -
ive relating to, phos- light, -phor- carry, -yl- chemical, -ation
process]
phosphorylation (fos-for-ih-LAY-shun)
[phos- light, -phor- carry, -yl- chemical, -ation process]
satiety center (sah-TYE-eh-tee SEN-ter)
[sati- enough, -ety state]
saturated
(SATCH-yoo-ray-ted)
total metabolic rate (met-ah-BOL-ik)
[metabol- change, -ic relating to]
triglyceride (try-GLISS-er-yde)
[tri- three, -glycer- sweet, -ide chemical]
unsaturated
(un-SATCH-yoo-ray-ted)
vitamin (VYE-tah-min)
[vita- life, -amin- ammonia compound]
WALTER heard that pizza was a complete meal because it

contained all the major macronutrients. “Maybe I could invent a
pizza diet and make millions,” he thought. He went over the
macronutrients in his head, “carbohydrates, lipids… hmm, and
then there are macronutrients such as sodium, carbon, potassium
…”
A friend pointed out that some of his assumptions concerning
nutrients were incorrect. Do you know which ones should not be
part of Walter's list?
Now that you have read this chapter, see if you can answer
these questions about the new “pizza diet” Walter wanted to
invent.
1. Which item doesn't belong in Walter's list?
a. Protein
b. Lipid
c. Vitamin C
d. Carbohydrate
2. Which of the minerals Walter listed is NOT considered a
macronutrient?
a. Sodium
b. Carbon
c. Potassium
d. All are considered macronutrients
3. The olive oil on pizza crust is mostly triglyceride lipids
containing monounsaturated fatty acids. What is the first step in
catabolizing the triglycerides in the olive oil?
a. Conversion to glycerol and three fatty acids
b. Glycolysis
c. Lipogenesis
d. Deamination
To answer these questions, you may have to refer to the
glossary or index, other chapters in this textbook, A&P
Connect, Mechanisms of Disease, and other resources.
Chapter 21 explained the processes of getting nutrients into our
internal environment. This chapter takes the story further by
discussing how our body manages the nutrients after they are

absorbed—that is, how they are stored and how they are used by
the cells of our bodies.
OVERVIEW OF NUTRITION AND METABOLISM
Nutrition refers to the foods that we eat and the types of
nutrients they contain. As you undoubtedly know, healthful
nutrition requires a balance of different nutrients in appropriate
amounts. In contrast, malnutrition is a deficiency or imbalance
in the consumption of food, vitamins, and minerals. As a matter
of convenient communication, many nutrition experts divide the
essential (required) nutrients into two major categories:
1.Macronutrients—usually include those nutrients that we need
in large amounts, such as carbohydrates, fats, and proteins.
Water and minerals that we need in large quantities to remain in
good health are often included among the macronutrients. For
example, sodium, chloride, potassium, calcium, magnesium, and
phosphorus are sometimes considered to be macronutrients.
2.Micronutrients—usually include nutrients that we need in very
small amounts, such as vitamins and some minerals. Minerals in
this group include iron, iodine, zinc, manganese, cobalt, and a
few others. Mineral micronutrients are also called trace
elements.
There are many small differences in individual genetic makeup,
as well as differences in individual lifestyles and envi ronments,
that influence how nutrients affect our bodies. Fortunately, we
have some advice that we can rely on to help us make healthy
choices. For example, the United States government makes use
of an individually customized food pyramid as a general
nutrition guide (Figure 22-1). The Canadian government uses a
similar individualized food guide to advise eating a healthy,
balanced diet.
Now let's see how nutrients and metabolism are related.
Metabolism refers to the complex interactions of chemical
processes that make life possible. It is essentially how the body
uses foods and their nutrients after they have been digested,
absorbed, and transported to the cells of our bodies. Your body
cells use nutrients from food in several ways: as fuel (energy),

as material for growth and maintenance, and for regulation of
body functions. Before they can be used in these different ways,
nutrients have to be assimilated. Assimilation occurs when
nutrient molecules enter cells and undergo many chemical
changes.
Metabolism is a complex process made up of many other
processes. Two of the major metabolic processes are termed
catabolism and anabolism. Each of these processes, in turn,
consists of a series of enzyme-driven chemical reactions known
as metabolic pathways.
Catabolism breaks food molecules down into smaller molecular
compounds and, in so doing, releases energy from them.
Anabolism does the opposite. It builds nutrient molecules up
into larger molecular compounds and, in so doing, uses energy.
Thus catabolism is a decomposition process, whereas anabolism
is a synthesis process. Both catabolism and anabolism take
place inside cells. Both catabolic and anabolic processes go on
continually and concurrently.
Catabolism releases energy in two forms: heat energy and
chemical energy. The amount of heat generated is relatively
large—so large, in fact, that it would effectively “cook” cells if
it were released in one large burst! Fortunately, catabolism is
regulated by enzymes so that heat is released in frequent small
bursts. Most of this heat is used to maintain the
FIGURE 22-1 United States Food Guide Pyramid. Simple
pyramid diagrams help educate the public on building a diet
with a balance of foods from different categories illustrated in
the diagram. This is an abbreviated version of the
comprehensive food guide that can be found at
www.mypyramid.gov. The full version includes recommended
servings per day and other nutrition advice.
FIGURE 22-2 The role of ATP in metabolism. ATP temporarily
stores energy in its last high-energy phosphate bond. When
water is added and phosphate breaks free, energy is released to

do cellular work. The ADP and phosphate groups that result can
be resynthesized into ATP, capturing additional energy from
nutrient catabolism. This cycle is called the ATP/ADP system.
homeostasis of body temperature. In contrast, chemical energy
released by catabolism is more obviously useful. It cannot,
however, be used directly for biological reactions. First, it must
be transferred to the high-energy molecule adenosine
triphosphate (ATP). ATP supplies energy directly to the energy-
using reactions of all cells in all living cellular organisms.
Look now at Figure 22-2. The structural formula at the top of
the diagram shows three phosphate groups attached to the rest
of the ATP molecule, two of them by high-energy bonds.
Adding water to ATP yields an inorganic phosphate group (Pi),
adenosine diphosphate (ADP), and energy, which is used for
anabolism and other cell work. The diagram also shows that Pi
and ADP then use energy released by catabolism to recombine
to form ATP.
Metabolism is not identical in all cells. More active cells have a
higher metabolic rate than do less active cells. In addition,
anabolism in different kinds of cells produces different
compounds. In liver cells, for example, anabolism synthesizes
various blood protein compounds. But in beta cells of the
pancreas, anabolism produces insulin.
Metabolism is a broad and complex mix of biological chemistry.
This chapter discusses only the essential concepts related to the
many and varied metabolic pathways of the human body.
CARBOHYDRATES
Dietary Sources of Carbohydrates
Carbohydrates are found in most of the foods that we eat.
Polysaccharides—such as starches in vegetables, grains, and
other plant tissues—are broken down into simpler carbohydrates
before they are absorbed.
Cellulose, a major component of most plant tissues, is an
important exception. Because we do not make enzymes that
chemically digest this complex carbohydrate, it passes through
our digestive system without being broken down. Also called

dietary fiber or “roughage,” cellulose and other indigestible
polysaccharides mix with chyme and keep it thick enough to
push easily through our digestive system. Most biologists now
agree that a high-fiber diet has many health benefits.
Disaccharides such as those in refined sugar must also be
chemically digested before they can be absorbed.
Monosaccharides in fruits and some “diet foods” are already in
an absorbable form, so they can move directly into the internal
environment without initially being processed. As you will see,
the monosaccharide glucose is the carbohydrate that is most
useful to the typical human cell.
1. Name the two types of metabolism and distinguish between
them.
2. Why must energy in nutrient molecules be transferred to
ATP?
3. Why is cellulose indigestible?
A&P CONNECT
Nutritionists often talk about the “energy value” of food—that
is, how much energy the body can get from that food. Do you
know what it means when a label states that food energy in
calories? Do you know the difference between a calorie and a
Calorie? Or a calorie and a joule or kilojoule? Find answers to
these questions, and also learn the energy values of major
nutrients and the amount of energy expended by different
physical activities, in Measuring Energy online at A&P
Connect.
Carbohydrate Metabolism
The body metabolizes carbohydrates by both catabolic and
anabolic processes. Most of our cells use carbohydrates—
mainly glucose—as their first or preferred energy fuel. When
the amount of glucose entering cells is inadequate for their
energy needs, they may make more glucose by using a pathway
that catabolizes fats or proteins.
As you read through the following sections outlining the basic

process of carbohydrate metabolism, remember the ultimate
result of catabolism: the transfer of energy from a nutrient
molecule to ATP. It is the continued production of ATP, the
energy currency of the cell, which makes nutrient catabolism so
incredibly vital to all of life's processes.
Glucose Transport and Phosphorylation
Carbohydrate metabolism begins with the movement of glucose
through cell membranes. In the interior of a cell, glucose reacts
with ATP to form glucose 6-phosphate, which cannot move back
across the cell membrane. This step, named glucose
phosphorylation, prepares glucose for further metabolic
reactions. Phosphorylation is the process of adding a phosphate
group to a molecule. Depending on their energy needs of the
moment, cells either catabolize (break apart) or anabolize (bind
together) glucose 6-phosphate.
Glycolysis
Glycolysis is the first step in the process of carbohydrate
catabolism. This pathway consists of a series of anaerobic
chemical reactions that take place in the cytoplasm (see Figure
4-13, page 71). In the end, glycolysis breaks apart one glucose
molecule (made of six carbon atoms) to form two pyruvic acid
molecules, each of which has three carbon atoms (Figure 22-3).
As you can see, a specific enzyme catalyzes each of these
reactions. Glycolysis is an essential process because it produces
a small amount of ATP (a net of two molecules for every sugar
molecule) and also prepares glucose for the second step in
catabolism, namely, the citric acid cycle. As we will see below,
glucose itself cannot enter the cycle: It must first be converted
to a compound called acetyl coenzyme A (acetyl CoA).
Citric Acid Cycle
Essentially, the citric acid cycle is a series of chemical
reactions mediated by enzymes that converts the two acetyl
molecules from each six-carbon glucose to four carbon dioxide
and six water molecules (see Figure 4-14, page 72). The citric
FIGURE 22-3 Catabolism of glucose. Glycolysis splits one

molecule of glucose (six carbon atoms) into two molecules of
pyruvic acid (three carbon atoms each). The glycolytic pathway
does not require oxygen, so it is termed anaerobic. The removal
of a carbon dioxide molecule converts each pyruvic acid
molecule into a two-carbon acetyl group that is “escorted” by
coenzyme A (CoA) into the citric acid cycle, where it joins a
four-carbon compound (oxaloacetic acid) to form a six-carbon
compound (citric acid). Now, two more carbon dioxide
molecules (one carbon atom each) are released from each citric
acid molecule formed. The carbon and oxygen atoms in the
original glucose molecule are thus released as waste products.
However, the real metabolic prize is energy, which is released
as the molecule is broken down. Because this part of the
pathway requires oxygen, it is termed aerobic.
acid cycle occurs in the mitochondria (recall that glycolysis
takes place only in the cytoplasm).
Before it can enter the citric acid cycle, each pyruvic acid
molecule combines with coenzyme A, thus forming acetyl CoA.
Coenzyme A then detaches from acetyl CoA, leaving a two-
carbon acetyl group, which enters the citric acid cycle by
combining with oxaloacetic acid to form citric acid. This is
what gives the citric acid cycle its name.
Each pyruvic acid molecule generates three CO2 molecules,
some ATP, and many high-energy electrons while going through
the citric acid cycle. Most of the energy leaving the citric acid
cycle is temporarily “stored” in these high-energy electrons.
The next section describes how these high-energy electrons are
used to generate ATP.
Electron Transport System and Oxidative Phosphorylation
High-energy electrons removed during the citric acid cycle
enter a chain of carrier molecules embedded in the inner
membrane of mitochondria that is known as the electron
transport system.
Figure 22-4 shows that high-energy electrons—along with their
accompanying protons (H+)—are shuttled to the electron
transport system during the citric acid cycle by carrier

molecules called nicotinamide adenine dinucleotide (NAD) and
flavin adenine dinucleotide (FAD). The electrons quickly move
down the chain, from one membrane protein complex to the
next, and eventually to their final acceptor, oxygen.
As the electrons are transported, some of their energy is used to
pump their accompanying protons (H+) to the intramembrane
space between the inner and outer membranes of the
mitochondrion. This creates a concentration gradient of protons,
and the intermembrane space thus becomes a reservoir of
protons. Like water behind a dam, the reservoir of protons
temporarily stores energy. In much the same way as water flows
through a dam and turns wheels to generate energy, the inner
membrane has “proton wheels”—in the form of ATP synthase.
ATP synthase is an enzyme that uses the proton movement down
the concentration gradient to bind together ADP and a
phosphate group to generate ATP (Figure 22-5).
FIGURE 22-4 Electron transport system. This system of energy
transfer takes place entirely within each mitochondrion.
FIGURE 22-5 Generation of ATP by ATP synthase. This
simplified model of the proton “wheel” in the mitochondrial
inner membrane shows how protons (H+) moving down their
concentration gradient drive the rotation of a molecular
machine. The energy of rotation then phosphorylates (adds
phosphate to) ADP to become ATP.
At this time, the low-energy electrons (e−) and their protons
(H+) join oxygen, forming water. This oxygen-requiring joining
of a phosphate group to ADP to form ATP is called oxidative
phosphorylation. As you can see, although oxygen is not needed
until the very last step of aerobic respiration, its r ole is vital.
Without oxygen to oxidize the hydrogen
FIGURE 22-6 Cell machinery for glucose catabolism. 1,
Glycolysis occurs in the cytoplasm. 2, Citric acid cycle takes
place mostly in the mitochondrial matrix. 3, Electron transport

and oxidative phosphorylation occur on the inner membrane of
mitochondria.
FIGURE 22-7 Energy extracted from glucose. Energy released
from the breakdown of glucose is released mostly as heat, but
some of it is transferred to a usable form—the high-energy
bonds of ATP. In most human cells, one glucose molecule
produces enough usable chemical energy to synthesize or
“charge up” 36 ATP molecules. Some cells, such as heart and
liver cells, shuttle electrons more efficiently and may be able to
synthesize up to 38 ATP molecules. This represents an energy
conversion efficiency of 38% to 44%, much better than the 20%
to 25% typical of most machines.
into water, the energy generation pathway would stop. In effect,
oxygen serves as an “electron dump,” ridding the body of spent
electrons derived from the breakdown of glucose.
The breakdown of ATP molecules, of course, provides virtually
all the energy that does cellular work. Therefore, oxidative
phosphorylation is the crucial part of glucose catabolism
(Figures 22-6). The energy extracted during the various steps of
the breakdown of glucose is given for you in Figure 22-7.
FIGURE 22-8 Hormonal control of blood glucose level.
Simplified view of some of the major glucose-regulating
hormones. Insulin lowers the blood glucose level and is
therefore hypoglycemic. Most hormones shown here raise the
blood glucose level and are called hyperglycemic, or anti -
insulin, hormones.
We can now summarize the long series of chemical reactions in
glucose catabolism with one short equation:
C6H12O6 + 6 O2 → 6 CO2 + 6 H2O + 36 (or 38) ATP + Heat
Control of Glucose Metabolism
Levels of sugar in the blood are under hormone control as
shown in Figure 22-8, which shows that most hormones cause
the glucose blood level to rise. These hormones are called
hyperglycemic because they tend to promote a high blood

glucose concentration. The one notable exception is insulin,
which is hypoglycemic (tends to decrease the blood glucose
level). See Box 22-1 for more discussion of blood glucose
problems.
4. What is glycolysis? How much energy is transferred to ATP
through this process?
5. What happens to a nutrient molecule as it proceeds through
the citric acid cycle?
6. What is the purpose of the electron transport system?
7. What is the difference between hyperglycemic hormones and
hypoglycemic hormones?
BOX 22-1 FYI
Abnormal Blood Glucose Concentration
The term hyperglycemia, which literally means “condition of
too much sugar in the blood,” is used anytime the blood glucose
concentration becomes higher than the normal set point level.
Hyperglycemia is most often associated with untreated diabetes
mellitus, but it can occur in newborns when too much
intravenous glucose is given or in other similar situations. If
untreated, the excess glucose leaves the blood in the kidney—
literally “spilling over” into the urine. This increases the
osmotic pressure of urine, drawing an abnormally high amount
of water into the urine from the bloodstream. Thus
hyperglycemia causes loss of glucose in the urine and its
accompanying loss of water—potentially threatening the fluid
balance of the body. Dehydration of this sort can ultimately lead
to death.
In contrast, hypoglycemia occurs when the blood glucose
concentration dips below the normal set point level.
Hypoglycemia can occur in various conditions, including
starvation, hypersecretion of insulin by the pancreatic islets, or
injection of too much insulin. Symptoms of hypoglycemia
include weakness, hunger, headache, blurry vision, anxiety, and
personality changes—sometimes leading to coma and death if
untreated.

LIPIDS
Dietary Sources of Lipids
Recall from Chapter 2 that lipids are a class of organic
compounds that includes fats, oils, and related substances. The
most common lipids in the diet are triglycerides, which are
composed of a glycerol subunit attached to three fatty acids.
Other important dietary lipids include phospholipids and
cholesterol.
Dietary fats are often classified as either saturated or
unsaturated. Saturated fats contain fatty acid chains in which
there are no double bonds—that is, all available bonds of its
hydrocarbon chain are filled (saturated) with hydrogen atoms
(see Figure 2-16, p. 32). Saturated fats are usually solid at room
temperature. Unsaturated fats contain fatty acid chains in which
there are double bonds, meaning that not all sites for hydrogen
are filled. Because the double bonds change the shape of
unsaturated fats, the molecules usually do not “fit” together as
well and so are usually liquid at room temperature.
Triglycerides are found in nearly every food that we eat.
However, the amount of triglycerides in each type of food
varies considerably, as does the proportion of saturated to
unsaturated types. Phospholipids are also found in nearly all
foods because they make up the cellular membranes of all living
organisms. Cholesterol, however, is found only in foods of
animal origin. Cholesterol concentration also varies. For
example, it is particularly high in liver, shrimp, and the yolks of
eggs.
Transport of Lipids
Lipids are transported in blood as chylomicrons, lipoproteins,
and free fatty acids. Chylomicrons are small fat droplets found
in blood soon after fat absorption takes place. Fatty acids and
monoglyceride products of fat digestion combine during
absorption to again form fats (triglycerides, or triacylglycerols).
These triglycerides plus small amounts of cholesterol and
phospholipids compose the chylomicrons.
Lipoproteins are produced mainly in the liver and, as their name

suggests, consist of lipids and protein. Blood contains three
types of lipoproteins: very-low-density lipoproteins, low-
density lipoproteins, and high-density lipoproteins. Usually,
they are designated by their abbreviations: VLDL, LDL, and
HDL, respectively. Diets high in saturated fats and cholesterol
tend to produce an increase in blood LDL concentration, which
in turn is associated with a high incidence of coronary artery
disease (CAD) and atherosclerosis (Figure 22-9 and Box 22-2).
A high blood HDL concentration, in contrast, is associated with
a low incidence of heart disease. You can remember this by
thinking of the LDLs as the “lethal lipoproteins” and the HDLs
as the “healthy lipoproteins.” Considerable evidence indicates
that exercise
FIGURE 22-9 Cholesterol and heart disease. The graph shows a
relationship between the total serum (blood plasma) cholesterol
level and coronary artery disease (CAD).
tends to elevate HDL concentration and reduce the likelihood of
coronary heart disease.
Fatty acids, on entering the blood from adipose tissue or other
cells, combine with albumin to form free fatty acids (FFAs).
Fatty acids are transported from cells of one tissue to those of
another in the form of free fatty acids.
Lipid Metabolism
Lipid Catabolism
Lipid catabolism, like carbohydrate catabolism, consists of
several processes. Each of these processes, in turn, consists of a
series of chemical reactions. Triglycerides are first hydrolyzed
to yield fatty acids and glycerol. Glycerol is then converted to
glyceraldehyde 3-phosphate, which may be converted to glucose
or it may enter the glycolysis pathway directly (see Figure 4-13,
p. 71). Fatty acids are broken down into two-carbon pieces—the
familiar acetyl CoA. These molecules are then catabolized via
the citric acid cycle. The final process of lipid catabolism
therefore consists of the same reactions as does carbohydrate
catabolism. Catabolism of lipids, however, yields considerably

more energy than does catabolism of carbohydrates. Whereas
catabolism of 1 gram of carbohydrates yields only 4.1 kcal of
heat, catabolism of 1 gram of fat yields 9 kcal.
Lipid Anabolism
Lipid anabolism, also called lipogenesis, consists of the
synthesis of various types of lipids, notably triglycerides,
cholesterol, phospholipids, and prostaglandins. Triglycerides
and structural lipids (e.g., phospholipids that make up our cell
membranes) are synthesized from fatty acids and glycerol or
from excess glucose or amino acids. This is why it is possible to
“get fat” from foods other than fat! Triglycerides are stored
mainly in adipose tissue cells. These fat deposits constitute the
body's largest reserve energy source. Enormous amounts of fat
can be stored in our bodies. In contrast, only a few hundred
grams of carbohydrates can be stored as liver and muscle
glycogen.
BOX 22-2 Lipoproteins
As you've seen, high blood concentrations of low-density
lipoproteins (LDLs) are associated with a high risk for
atherosclerosis. Atherosclerosis is a form of “hardening of the
arteries” that occurs when lipids accumulate in cells lining the
blood vessels and promote the development of a plaque that
eventually impedes blood flow and may trigger clot formation.
Atherosclerosis may also weaken the wall of a blood vessel to
the point that it ruptures. In any case, a person with
atherosclerosis of the coronary arteries risks a heart attack when
blood flow to cardiac muscle is impaired. If vessels in the brain
are affected, there is risk of a cerebrovascular accident (CVA),
or “stroke.”
According to a current model (see part A of figure), LDL
delivers cholesterol to cells for use in synthesi zing steroid
hormones and stabilizing the plasma membrane. Most, if not all,
cells have many LDL receptors embedded in the outer surface of
their plasma membranes. These receptors attract cholesterol -
bearing LDL. Once the LDL molecule binds to the receptor,
specific mechanisms operate to release the cholesterol it carries

into the cell. Excess cholesterol is stored in droplets near the
center of the cell. It seems that, in some individuals at least,
cells have so few LDL receptors that they accumulate too much
cholesterol in the blood. Some mechanism in endothelial cells
moves this excess LDL into the wall of blood vessels. This has
been proposed as a cause for the lipid accumulation
characteristic of atherosclerosis.
High blood concentrations of high-density lipoproteins (HDLs)
have been associated with a low risk of developing
atherosclerosis and its many possible complications. Although
the exact details of how this works have yet to be worked out,
scientists have made progress toward that end. According to one
model (see part B of figure), HDL molecules are attracted to
HDL receptors embedded in the plasma membranes. Once they
bind to their receptors, the cell is stimulated to release some of
its cholesterol from storage. The released cholesterol migrates
to the plasma membrane, where it may attach to the HDL
molecule and be whisked away to the liver for excretion in bile.
High blood LDL levels (more than 180 mg LDL per 100 ml of
blood) signify that a large amount of cholesterol is being
delivered to cells. High blood HDL levels (more than 60 mg
HDL per 100 ml of blood) indicate that a large amount of
cholesterol is being removed from cells and delivered to the
liver for excretion from the body. Currently, researchers are
using this information to develop treatments that may prevent—
or even cure—atherosclerosis and the disorders it causes.
Role of blood lipoproteins. A, Simplified diagram of the role of
low-density lipoprotein (LDL) in delivering cholesterol to cells.
B, Proposed role of high-density lipoprotein (HDL) in removing
cholesterol from cells.
Most fatty acids can be synthesized by the body. A certain
number of the unsaturated fatty acids must be provided by the
diet and are thus called essential fatty acids. Some of the
essential fatty acids serve as a source within the body for
synthesis of an important group of lipids called prostaglandins.

These hormone-like compounds, first discovered in the 1930s
from prostate fluids forming semen, have in recent years gained
increasing recognition for their occurrence in various tissues,
where they support a wide spectrum of biological activity.
Certain essential fatty acids are also necessary for
manufacturing the phospholipids in cell membranes (see
Chapter 4) and the myelin in nerve tissue (see Chapter 11).
Control of Lipid Metabolism
Lipid metabolism is controlled mainly by the following
hormones:
▪Insulin
▪Adrenocorticotropic hormone (ACTH)
▪Growth hormone
▪Glucocorticoids
As you may recall, these help regulate fat metabolism such that
the rate of fat catabolism is inversely related to the rate of
carbohydrate catabolism. If some condition such as diabetes
mellitus causes carbohydrate catabolism to decrease below
energy needs, increased secretion of growth hormone, ACTH,
and glucocorticoids soon follows. These hormones, in turn,
bring about an increase in fat catabolism. But, when
carbohydrate catabolism equals energy needs, fats are not
mobilized out of storage and catabolized. Instead, they are
spared and stored in adipose tissue. So, it can be said that
“Excessive carbohydrates have a ‘fat-storing’ effect.”
8. In what forms are lipids transported to cells?
9. How can glycerol and fatty acids enter the citric acid cycle?
10. Which fatty acids cannot be made by the body?
11. Which hormones are involved in lipid metabolism?
PROTEINS
Sources of Proteins
Recall from Chapter 2 that proteins are very large molecules
composed of chemical subunits called amino acids. Proteins are
assembled from 20 different kinds of amino acids. If any one
type of amino acid is deficient, vital proteins cannot be

synthesized—a serious health threat. One way your body
maintains a constant supply of amino acids is by synthesizing
them from other compounds already present in the body.
However, only about half of the required 20 types of amino
acids can be made by the body. The remaining types of amino
acids must be supplied in the diet. Nutritionists often refer to
the amino acids that must be in the diet as essential amino
acids. Table 22-1 lists amino acids according to whether they
are considered essential in the diet or nonessential in the diet
(synthesized by the body). Box 22-3 investigates the link
between blood levels of amino acids and disease.
Proteins are obtained in the diet from various sources. Muscle
meat and other animal tissues particularly high in proteins
contain the essential amino acids. Food from a single plant or
other nonanimal source does not usually contain an adequate
amount of all the essential amino acids. Therefore, it is
important to include meat (or other animal tissues), or a mixture
of different vegetables that provide all the amino acids needed
by the body, in the diet. Plant tissues that are particularly high
in protein content include cereal grains, nuts, and legumes such
as peas and beans.
TABLE 22-1 Amino Acids
ESSENTIAL
NONESSENTIAL
Histidine*
Isoleucine
Leucine
Lysine
Methionine
Phenylalanine
Threonine
Tryptophan
Valine
Alanine
Arginine
Asparagine

Aspartic acid
Cysteine
Glutamic acid
Glutamine
Glycine
Proline
Serine
Tyrosine†
* Essential in infants and, perhaps, adult males.
† Can be synthesized from phenylalanine; therefore,
nonessential as long as phenylalanine is in the diet
Protein Metabolism
Protein Anabolism
Every cell synthesizes its own structural proteins and its own
enzymes using ribosomes to read the DNA code and construct
polypeptides. In addition, many cells, such as liver and
glandular cells, synthesize special proteins for export. For
example, liver cells manufacture the plasma proteins found in
our blood. Any particular cell's genes, under the influence of
signaling mechanisms, determine the specific proteins to be
synthesized for that cell or for other body cells. Protein
anabolism is truly “big business” in our body. For example, red
blood cell replacement alone requires the production of millions
of cells per second and by itself creates huge demands for
protein anabolism.
BOX 22-3 Health Matters
Amino Acids and Disease
Recent research shows that the balance of amino acids
circulating in the blood is associated with various diseases.
High blood levels of homocysteine, one of several alternate
forms of the amino acid cysteine (see Table 22-1), have been
linked to heart disease, stroke, and dementias such as Alzheimer
disease. Whether such abnormalities in homocysteine levels are
the direct cause of these conditions is uncertain. Despite this
uncertainty, many physicians recommend lowering abnormally
high blood homocysteine levels to reduce the possible risk for

these devastating conditions. Homocysteine can be reduced to
normally low blood levels when there is adequate vitamin B6,
B12, or B9 (folic acid) in the diet.
Protein Catabolism
The first step in protein catabolism takes place in liver cells.
Called deamination, it consists of the splitting off of an amino
(NH2) group from an amino acid molecule to form a molecule
of ammonia and one of keto acid. Most of the ammonia is
converted by liver cells to urea and later excreted in the urine.
The keto acid may be oxidized via the citric acid cycle or may
be converted to glucose or to fat. Both protein catabolism and
anabolism go on continually. Only their rates differ from time
to time. With a protein-deficient diet, for example, protein
catabolism exceeds protein anabolism. Various hormones, as we
shall see below, also influence the rates of protein catabolism
and anabolism.
Control of Protein Metabolism
Protein metabolism, like that of carbohydrates and fats, is
controlled largely by hormones rather than by the nervous
system. Growth hormone and the male hormone testosterone
both have a stimulating effect on protein synthesis, or
anabolism. For this reason, they are referred to as anabolic
hormones. The protein catabolic hormones of greatest
consequence are glucocorticoids. They speed up the hydrolysis
of cell proteins to amino acids, their entry into the blood, and
their subsequent catabolism. ACTH functions indirectly as a
protein catabolic hormone because of its stimulating effect on
glucocorticoid secretion.
Thyroid hormone is necessary for and promotes protein
anabolism and therefore growth when plenty of carbohydrates
and fats are available for energy production. Under different
conditions—for example, when the amount of thyroid hormone
is excessive or when the energy foods are deficient—this
hormone may then promote protein mobilization and catabolism.
12. What is meant by the term essential amino acid?

13. What happens when an amino acid is deaminated?
14. What is the purpose of the process of amino acid
deamination?
15. How is protein metabolism controlled?
VITAMINS AND MINERALS
Vitamins
Vitamins are organic molecules needed in small quantities for
normal metabolism throughout the body. Most vitamin
molecules attach to enzymes or coenzymes and help them work
properly. Coenzymes are organic, nonprotein catalysts that
often act as “molecule carriers.” Many enzymes or coenzymes
are not functional without the appropriate vitamins attached to
them. This attachment gives coenzymes the proper functional
shape. For example, coenzyme A (CoA)—an important carrier
molecule associated with the citric acid cycle—has pantothenic
acid (vitamin B5) as one of its major components.
Not all vitamins are involved directly with enzymes and
coenzymes. Vitamins A, D, and E play a variety of different,
but no less important, roles in the chemistry of the body. The
form of vitamin A called retinal, for example, plays an
important role in detecting light in sensory cells of the retina.
Vitamin D can be converted to the hormone calcitriol, which
plays a role in the regulation of calcium homeostasis in the
body. One role of vitamin E (and vitamin C) is to serve as an
antioxidant that prevents free radicals (highly reactive oxygen
atoms) from damaging electron-dense molecules in the cell
membranes and DNA molecules.
All but one vitamin, vitamin D, cannot be made by the body
itself. Recent research suggests that vitamin D supplements may
reduce risks for a range of diseases, including cancers of the
breast, colon, ovaries, and prostrate. Bacteria living in the colon
make two more: vitamin K and biotin. We must eat vitamins, or
molecules we can convert into vitamins, in our food to get the
rest. The body can store fat-soluble vitamins—A, D, E, and K—
in the liver for later use. Because the body cannot store
significant amounts of water-soluble vitamins such as B

vitamins and vitamin C, they must be continually supplied in
the diet. Table 22-2 lists some common vitamins, their sources
and functions, and symptoms of deficiency.
Minerals
Minerals are at least as important as vitamins in our diet.
Minerals are inorganic elements or salts that are found naturally
in the earth. Like vitamins, mineral ions can attach to enzymes
or other organic molecules and help them work. Of course,
minerals such as sodium, chloride, and potassium are essential
in relatively large amounts for maintaining the fluid/ion
composition of the internal fluid environment.
Minerals such as sodium and calcium also function in nerve
conduction and in the contraction of muscle fibers. Without
these minerals, the brain, heart, and respiratory tract would
cease to function. Iron is needed to manufacture hemoglobin in
red blood cells, and iodine is needed to make thyroid hormones
T3 and T4. Calcium, phosphorus, and magnesium are required
to build the strong structural components of the skeleton.
Information about some of the more important minerals is
summarized for you in Table 22-3. Like vitamins, minerals are
beneficial only when taken in the proper amounts.
Recommended adequate intakes (AIs) of minerals can change
over the life span. For example, calcium intake should increase
throughout childhood and remain high throughout adulthood.
However, the actual intake of
FIGURE 22-10 Iron intake requirements. The chart compares
male and female absorbable iron requirements over the life
span.
calcium among females in the United States tends to fall short
during adulthood—thereby increasing the risk for osteoporosis
and other disorders.
TABLE 22-2 Major Vitamins
VITAMIN
DIETARY SOURCE
FUNCTIONS

SYMPTOMS OF DEFICIENCY
Vitamin A
Green and yellow vegetables, dairy products, and liver
Maintains epithelial tissue and produces visual pigments
Night blindness and flaking skin
B-complex vitamins
B1 (thiamine)
Grains, meat, and legumes
Helps enzymes in the citric acid cycle
Nerve problems (beriberi), heart muscle weakness, and edema
B2 (riboflavin)
Green vegetables, organ meats, eggs, and dairy products
Aids enzymes in the citric acid cycle
Inflammation of skin and eyes
B3 (niacin)
Meat and grains
Helps enzymes in the citric acid cycle
Pellagra (scaly dermatitis and mental disturbances) and nervous
disorders
B5 (pantothenic acid)
Organ meat, eggs, and liver
Aids enzymes that connect fat and carbohydrate metabolism
Loss of coordination (rare), decreased gut motility
B6 (pyridoxine)
Vegetables, meats, and grains
Helps enzymes that catabolize amino acids
Convulsions, irritability, and anemia
B9 (folic acid)
Vegetables
Aids enzymes in amino acid catabolism and blood production
Digestive disorders and anemia
B12 (cyanocobalamin)
Meat and dairy products
Involved in blood production and other processes
Pernicious anemia
Biotin (vitamin H)

Vegetables, meat, and eggs
Helps enzymes in amino acid catabolism and fat and glycogen
synthesis
Mental and muscle problems (rare)
Vitamin C (ascorbic acid)
Fruits and green vegetables
Helps in manufacture of collagen fibers; antioxidant
Scurvy and degeneration of skin, bone, and blood vessels
Vitamin D (calciferol)
Dairy products and fish liver oil; also made in the body from
cholesterol
Aids in calcium absorption
Rickets and skeletal deformity
Vitamin E (tocopherol)
Green vegetables and seeds
Protects cell membranes from being destroyed; antioxidant
Muscle and reproductive disorders (rare)
TABLE 22-3 Major Minerals
MINERAL
DIETARY SOURCE
FUNCTIONS
SYMPTOMS OF DEFICIENCY
Calcium (Ca)
Dairy products, legumes, and vegetables
Helps blood clotting, bone formation, and nerve and muscle
function
Bone degeneration and nerve and muscle malfunction
Chlorine (Cl−)
Salty foods
Aids in stomach acid production and acid-base balance
Acid-base imbalance
Cobalt (Co)
Meat
Helps vitamin B12 in blood cell production
Pernicious anemia
Copper (Cu)

Seafood, organ meats, and legumes
Involved in extracting energy from the citric acid cycle and in
blood production
Fatigue and anemia
Iodine (I)
Seafood and iodized salt
Required for thyroid hormone synthesis
Goiter (thyroid enlargement) and decrease in metabolic rate
Iron (Fe)
Meat, eggs, vegetables, and legumes
Involved in extracting energy from the citric acid cycle and in
blood production
Fatigue and anemia
Magnesium (Mg)
Vegetables and grains
Helps many enzymes
Nerve disorders, blood vessel dilation, and heart rhythm
problems
Manganese (Mn)
Vegetables, legumes, and grains
Helps many enzymes
Muscle and nerve disorders
Phosphorus (P)
Dairy products and meat
Aids in bone formation and is used to make ATP, DNA, RNA,
and phospholipids
Bone degeneration and metabolic problems
Potassium (K)
Seafood, milk, fruit, and meats
Helps muscle and nerve function
Muscle weakness, heart problems, and nerve problems
Sodium (Na)
Salty foods
Aids in muscle and nerve function and fluid balance
Weakness and digestive upset
Zinc (Zn)

Many foods
Helps many enzymes
Inadequate growth
Figure 22-10 shows the requirement for iron over the life span
for both men and women. Although both males and females
require a large amount of iron during the spurt of growth in the
teenage years, the iron requirement remains high only in women
during the rest of adulthood. This difference is explained by the
fact that adult women must continually replace the iron lost in
the menstrual flow. Notice that female iron requirements drop
to the level of males after menopause. Notice also that the iron
requirement peaks during pregnancies—when fetal blood
development requires large amounts of iron.
A&P CONNECT
One of the hottest areas in the field of nutrition today is that of
functional foods. Find out what they are and why you may want
to include them in your diet in Functional Foods online at A&P
Connect.
16. What is a vitamin? How do they function in the body?
17. List two functions of minerals in the body.
18. Why should the intake of iron be more important for women
during the childbearing years?
METABOLIC RATES
Metabolic rate refers to the amount of energy released in the
body in a given time by catabolism. Metabolic rates are
expressed in either of two ways: (1) in terms of the number of
kilocalories of heat energy expended per hour or per day, or (2)
as normal or as a definite percentage above or below normal.
Basal Metabolic Rate
The basal metabolic rate (BMR) is the body's rate of energy
expenditure under “basal conditions,” namely, when the
individual is tested under the following conditions:
▪Awake but resting, that is, lying down and, as far as possible,
not moving a muscle.

▪In the postabsorptive state (12 to 18 hours after the last meal).
▪In a comfortably warm environment (the so-called
thermoneutral zone, a temperature range at which metabolism is
independent of ambient temperature).
Note that the BMR is not the minimum metabolic rate. It does
not indicate the smallest amount of energy that must be
expended to sustain life. It does, however, indicate the smallest
amount of energy expenditure that can sustain life and also
maintain the waking state and a normal body temperature in a
comfortably warm environment.
Factors Influencing Basal Metabolic Rate
The BMR is not identical for all individuals because of the
influence of various factors, some of which are described in the
following paragraphs.
Most individuals have the same BMR per square meter of body
surface, if other conditions are equal. However, because a larger
individual has more square meters of surface area than does a
smaller person, the BMR is greater than that of a smaller
individual. Likewise, the higher the ratio of lean tissue to fat
tissue in a person, the higher the BMR (Figure 22-11).
Other factors affecting BMR have to do with sex and age. Men
oxidize their food approximately 5% to 7% faster than women
do. This explains why their BMRs are about 5% to 7% higher
for a given size and age. This gender difference in BMR
probably results from the difference in the proportion
FIGURE 22-11 Body composition. Estimated values in healthy
men and women.
of body fat, which is determined by sex hormones. In general,
the younger the individual, the higher the BMR for a given size
and sex.
Other factors affecting BMR are fever, drugs, and a person's
physiological state. For example, fever increases the BMR. For
every degree Celsius increase in body temperature, metabolism
increases about 13%. A decrease in body temperature
(hypothermia) has the opposite effect. In addition, certain

drugs, such as caffeine, amphetamine, and levothyroxine,
increase the BMR. Other factors, such as emotions, pregnancy,
and lactation (milk production), also influence basal
metabolism.
Total Metabolic Rate
Total metabolic rate is the amount of energy used or expended
by the body in a given amount of time. It is often expressed in
kilocalories per hour or per day. The main direct determinants
of total metabolic rate are as follows:
Factor 1—the basal metabolic rate, which usually constitutes
about 55% to 60% of the total metabolic rate.
Factor 2—the energy used to do skeletal muscle work.
Factor 3—the thermic effect of foods. The metabolic rate
increases for several hours after a meal, apparently becaus e of
the energy needed for metabolizing foods.
Energy Balance and Body Weight
Our bodies maintain a state of energy balance, in which the
body's energy input equals its energy output. Energy input per
day equals the total calories (kilocalories) in the food ingested
per day. Energy output equals the total metabolic rate expressed
in kilocalories. If calorie intake and energy output are not
equal, changes in body weight may occur:
▪Body weight remains constant (except for possible variations
in water content) when the total calories in the food ingested
equal the total metabolic rate.
▪Body weight increases when energy input exceeds energy
output.
▪Body weight decreases when energy input is less than energy
output—when the total number of calories in the food eaten is
less than the total metabolic rate.
Foods are stored primarily as glycogen and fats. Many cells
(except for skeletal muscle) catabolize carbohydrates first, then
fats. If there is no food intake, almost all of the glycogen is
estimated to be used up in a matter of 1 or 2 days. Then, with no
more carbohydrate to act as a fat sparer, fat is catabolized. The
amount of fat available determines the length of time that an

individual can catabolize fat as a reserve source of energy.
Finally, with no more fat available, tissue proteins are
catabolized. Because significant amounts of protein are not
“stored” for use in catabolism, important structural and
functional proteins are quickly depleted. For this reason, severe
starvation will eventually lead to death.
MECHANISMS FOR REGULATING FOOD INTAKE
Mechanisms for regulating food intake are still not clearly
established, though it is understood that the hypothalamus plays
a major role in these mechanisms. A cluster of neurons in the
lateral hypothalamus function as an appetite center—meaning
that impulses from them bring about increased appetite.
It is likely that a group of neurons in the ventral medial nucleus
of the hypothalamus functions as a satiety center—meaning that
impulses from these neurons decrease appetite so that we feel
satiated or, “full.”
The temperature of the blood circulating to the hypothalamus is
important in regulating the action of these centers. Another
factor is blood glucose concentration and the rate of glucose
use.
The hypothalamus also produces several hormones and
neurotransmitters that affect the feeding centers. Some appetite-
altering hormones and neurotransmitters are produced in many
other organs, such as the liver, adipose tissue, pancreas, GI
tract, and vagal nerve. Of course, factors such as daily eating
habits or patterns, emotional responses, the sensations of food,
and many others must also be involved in regulating or
affecting appetite.
19. Give one of the two ways in which metabolic rates can be
expressed.
20. Name three of the factors that influence basal metabolic
rate.
21. Distinguish between basal metabolic rate and total
metabolic rate.
22. In which division of the brain would you find the control

center for regulating food intake?
Cycle of LIFE
The importance of proper nutrition to an individual's well-being
begins at the moment of conception and continues until death.
In the womb, various nutrients must be obtained from the
mother's blood in sufficient quantity to ensure normal growth
and development.
One critical nutrient during fetal development, infancy, and
childhood is protein. Sufficient proteins, containing all the
essential amino acids, are required to permit normal
development of the nervous system, muscle tissues, and other
vital structures.
Another critical nutrient during the early years of life is the
mineral calcium. Large quantities of calcium are needed by a
growing body to maintain normal development of the skeleton
and other tissues. In the womb, a steady supply of calcium in
the mother's blood is maintained by increased levels of
parathyroid hormone (PTH). PTH increases blood calcium
levels by removing it from storage in the bones.
Unless a pregnant woman consumes enough calcium to replace
this calcium lost from bones, she may suffer from the bone-
softening effects of calcium deficiency. If proteins, calcium, or
other necessary nutrients are in short supply anytime before the
beginning of adulthood, the consequences may be permanent.
For example, bone deformities resulting from a lack of calcium
during childhood could become permanent if not corrected or
compensated for before the skeleton ossifies completely.
In late adulthood, the number of food calories needed declines
because the metabolic rate declines due to changes in the
balance of some metabolic hormones. Even though the number
of required food calories declines, the overall balance of
nutrients consumed must be maintained to preserve proper
metabolic function. Some nutrients, such as calcium, may be
needed in greater quantity in older adults to compensate for
age-related bone loss.
The BIG Picture

Every cell in the body must maintain the operation of its
metabolic pathways to ensure its survival. Anabolic pathways
are required to build the various structural and functional
components of the cells. Catabolic pathways are required to
convert energy to a usable form. Catabolic pathways are also
needed to degrade large molecules into small subunits that can
be used in anabolic pathways. These processes require the
correct amounts of carbohydrates, fats, proteins, vitamins, and
minerals in order to produce the structural and functional
components necessary for cellular metabolism.
Various body systems operate to make sure that essential
nutrients reach the cells as needed to maintain metabolism and
homeostasis. For example, the nervous, skeletal, and muscular
systems make it possible for us to take in complex foods from
our external environment. The digestive system reduces these
complex nutrients to simpler, more usable nutrients—then
provides the mechanisms that allow their absorption into the
internal environment. The circulatory and lymphatic systems
transport absorbed nutrients to individual cells for immediate
use or to the liver or other organs for temporary storage. The
endocrine system regulates the balance between immediate use
and storage. The respiratory and circulatory systems provide the
oxygen needed for oxidative phosphorylation to generate ATP.
These two systems also provide a mechanism for removing
waste CO2 generated by the catabolism of nutrient molecules.
Likewise, the urinary system provides a mechanism for
removing waste urea generated by protein catabolism. Even the
integumentary system becomes involved, by producing vitamin
D in the presence of sunlight.
It should be easy for you to see now why metabolism is simply
the sum total of all the biochemical processes required by a
living organism!
MECHANISMS OF DISEASE
Nutritional and metabolic disorders are numerous and
widespread in the United States. A number of inherited
conditions are well known, but not common. Perhaps the most

common disorder is obesity, followed by eating disorders such
as anorexia nervosa and bulimia, which are well known because
of media coverage. Beyond these conditions, however, there are
serious nutritional disorders, including protein-calorie
malnutrition and a number of vitamin deficiency disorders that
were once common in this country and still can be seen in many
developing countries around the world.
Find out more about these nutritional and metabolic disorders
and diseases online at Mechanisms of Disease: Nutrition and
Metabolism.
CHAPTER SUMMARY
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with your iPod or other portable media player, access the Audio
Chapter Summaries online at http://evolve.elsevier.com.
Scan this summary after reading the chapter to help you
reinforce the key concepts. Later, use the summary as a quick
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OVERVIEW OF NUTRITION AND METABOLISM
A. Nutrition refers to the foods that we eat and the types of
nutrients they contain
1. Malnutrition—deficiency or imbalance in the consumption of
food, vitamins, and minerals
B. Categories of nutrients
1. Macronutrients—nutrients that we need in large amounts
a. Carbohydrates, fats, and proteins
b. Water
c. Minerals
2. Micronutrients—nutrients that we need in very small amounts
a. Vitamins
b. Minerals (trace elements)
C. Metabolism—complex, interactive set of chemical processes
that make life possible; the use the body makes of foods and
their nutrients after they have been digested, absorbed, and
transported to the cells of our bodies
1. Assimilation—occurs when nutrient molecules enter cells and
undergo many chemical changes

2. Two major metabolic processes:
a. Catabolism—breaks food molecules down into smaller
molecular compounds; releases energy from them (heat and
chemical)
b. Anabolism—a synthesis process
c. Both catabolism and anabolism go on continually and
concurrently and take place inside cells
3. ATP supplies energy directly to the energy-using reactions of
all cells in all living cellular organisms (Figure 22-2)
CARBOHYDRATES
A. Dietary sources of carbohydrates
1. Polysaccharides—starches found in vegetables, grains, and
other plant tissues
2. Cellulose—major component of most plant tissues; passes
through our digestive system without being broken down
3. Disaccharides—found in refined sugar; must be chemically
digested before they can be absorbed
4. Monosaccharides—found in fruits; move directly into the
internal environment without being processed; glucose
B. Carbohydrate metabolism—body metabolizes carbohydrates
by both catabolic and anabolic processes
C. Glucose transport and phosphorylation—glucose reacts with
ATP to form glucose 6-phosphate
1. Glucose phosphorylation—prepares glucose for further
metabolic reactions
2. Phosphorylation—process of adding phosphate group to a
molecule
D. Glycolysis—first step in the process of carbohydrate
catabolism (Figure 22-3)
1. Occurs in cytoplasm
2. Produces small amount of ATP
3. Prepares glucose for the citric acid cycle
E. Citric acid cycle—series of chemical reactions mediated by
enzymes; converts two acetyl molecules to four carbon dioxide
and six water molecules
1. Occurs in the mitochondria

2. Most of the energy leaving the citric acid cycle is “stored” in
high-energy electrons
F. Electron transport and oxidative phosphorylation
1. High-energy electrons (along with their protons) removed
during the citric acid cycle enter a chain of carrier molecules
(Figure 22-4)
2. As electrons are transported, some of their energy is used to
pump their accompanying protons (H+) to the intramembrane
space between the inner and outer membranes of the
mitochondrion
3. Protons temporarily store energy; move down their
concentration gradient across the inner membrane, driving ATP
synthase
4. Low-energy electrons (e−) and their protons (H+) join
oxygen, forming water; joining of a phosphate group to ADP to
form ATP is called oxidative phosphorylation
G. Control of glucose metabolism—levels of sugar in the blood
are under hormone control (Figure 22-8)
1. Hyperglycemic hormones—promote a high blood glucose
concentration
2. Hypoglycemic hormones—decrease blood glucose level
LIPIDS
A. Dietary sources of lipids
1. Triglycerides—most common lipid; composed of a glycerol
subunit attached to three fatty acids
2. Phospholipids—important lipids; found in nearly all foods
3. Cholesterol—an important lipid; found only in foods of
animal origin
4. Dietary fats
a. Saturated—contain fatty acid chains in which there are no
double bonds
b. Unsaturated—contain fatty acid chains in which there are
double bonds
B. Transport of lipids—lipids are transported in blood as
chylomicrons, lipoproteins, and free fatty acids
1. Chylomicrons—small fat droplets found in blood soon after

fat absorption
2. Lipoproteins are produced by the liver and consist of lipids
and proteins
3. Fatty acids are transported from cells of one tissue to those
of another in the form of free fatty acids
C. Lipid metabolism
1. Lipid catabolism—consists of several processes
2. Lipid anabolism (lipogenesis)—consists of the synthesis of
various types of lipids; triglycerides, cholesterol,
phospholipids, and prostaglandins
D. Control of lipid metabolism—controlled mainly by the
following hormones:
1. Insulin
2. ACTH
3. Growth hormone
4. Glucocorticoids
PROTEINS
A. Sources of proteins
1. Proteins are assembled from 20 different kinds of amino
acids
2. Body synthesizes amino acids from other compounds in the
body
3. Only about half of the required 20 types of amino acids can
be made by the body (nonessential amino acids); rest must be
supplied through diet (essential amino acids)
B. Protein metabolism
1. Protein anabolism—process by which proteins are
synthesized by the ribosomes of the cells
2. Protein catabolism—deamination takes place in liver cells
a. Consists of the splitting off of an amino (NH2) group from an
amino acid molecule to form a molecule of ammonia and one of
keto acid (e.g., alpha-ketoglutaric acid)
3. Control of protein metabolism—protein metabolism is
controlled largely by hormones
VITAMINS AND MINERALS
A. Vitamins—organic molecules needed in small quantities for

normal metabolism throughout the body; attach to enzymes or
coenzymes (Table 22-2)
1. Coenzymes—organic, nonprotein catalysts that often act as
“molecule carriers”
2. The body does not make most of the necessary vitamins; they
must be obtained through diet
B. Minerals—inorganic elements or salts that are found
naturally in the earth; attach to enzymes or other organic
molecules and help them work (Table 22-3)
1. Recommended adequate intakes (AIs) of minerals can change
over the life span (Figure 22-10)
METABOLIC RATES
A. Metabolic rate—refers to the amount of energy released in
the body in a given time by catabolism
1. Metabolic rates are expressed in either of two ways:
a. In terms of number of kilocalories of heat energy expended
per hour or per day
b. As normal or as a definite percentage above or below normal
B. Basal metabolic rate (BMR)—the body's rate of energy
expenditure under these “basal conditions”:
1. Awake but resting
2. In the postabsorptive state
3. In a comfortably warm environment
C. Factors influencing basal metabolic rate—BMR is not
identical for all individuals because of the influence of various
factors
1. Most people have the same BMR per square meter of body
surface, but larger people have larger body surface, so BMR is
greater
2. Gender differences based on proportions of body fat
3. Other factors are age, fever, drugs, physiological state
D. Total metabolic rate—the amount of energy used or
expended by the body in a given amount of time
1. Factor 1—basal metabolic rate
2. Factor 2—energy used to do skeletal muscle work
3. Factor 3—thermic effect of foods

E. Energy balance and body weight—the body maintains a state
of energy balance
1. Energy input equals its energy output
a. Body weight remains constant when the total calories in the
food ingested equals the total metabolic rate
b. Body weight increases when energy input exceeds energy
output
c. Body weight decreases when energy input is less than energy
output
d. In starvation, the carbohydrates are used up first, then fats,
then proteins
MECHANISMS FOR REGULATING FOOD INTAKE
A. Hypothalamus plays a major role in the mechanism of
regulating food intake
1. Appetite center—cluster of neurons in the lateral
hypothalamus function to bring about increased appetite
2. Satiety center—impulses from a group of neurons in the
ventral medial nucleus of the hypothalamus decrease appetite;
we feel satiated, or “full”
REVIEW QUESTIONS
Write out the answers to these questions after reading the
chapter and reviewing the Chapter Summary. If you simply
think through the answer without writing it down, you won't
retain much of your new learning.
1. What is metabolism? Nutrition?
2. What two processes make up the process of metabolism?
3. Does the body digest dietary fiber? Why or why not?
4. Briefly describe glycolysis, the first process of carbohydrate
catabolism.
5. Where does glycolysis occur?
6. How are dietary fats classified?
7. Explain how lipids are transported in blood.
8. List the hormones involved in the control of lipid
metabolism.
9. What are the essential amino acids?
10. What does the term metabolic rate mean?

11. List the various factors that influence basal metabolic rate.
12. Describe various factors that influence the amount of food a
person eats.
CRITICAL THINKING QUESTIONS
After finishing the Review Questions, write out the answers to
these items to help you apply your new knowledge. Go back to
sections of the chapter that relate to items that you find
difficult.
1. How would you describe the mitochondria, and why do you
think they are referred to as the “power plants” of the cells?
2. Can you identify and explain the processes and hormones
involved in maintaining the homeostatic level of glucose in the
blood?
3. State in your own words the process of lipid catabolism. How
is it similar to the carbohydrate pathway?
4. Describe protein catabolism in your own words.
5. How would you compare and contrast the functions of
proteins, carbohydrates, and fats?
6. What is the function of most vitamins in the body? What
examples can you find that do not have this function? What
functions do these vitamins have?
7. What is the difference between basal metabolic rate and total
metabolic rate?
Rubric Detail
Select Grid View or List View to change the rubric's layout.
Content
Name: NRNP_6675_Week2_Assignment1_Rubric
Grid ViewList View
Excellent
90%–100%

Good
80%–89%
Fair
70%–79%
Poor
0%–69%
In the E/M patient case scenario provided:
• Assign DSM-5 and ICD-10 codes to services based upon
the patient case scenario.
Points:
Points Range:
18 (18%) - 20 (20%)

DSM-5 and ICD-10 codes assigned to the scenario are correct,
with no more than a minor error.
Feedback:
Points:
Points Range:
16 (16%) - 17 (17%)

DSM-5 and ICD-10 codes assigned to the scenario are mostly
correct, with a few minor errors.
Feedback:
Points:
Points Range:
14 (14%) - 15 (15%)

DSM-5 and ICD-10 codes assigned to the scenario contain
several errors.
Feedback:
Points:
Points Range:
0 (0%) - 13 (13%)

significant errors, or response is missing.
Feedback:
In 1–2 pages, address the following:
• Explain what pertinent information, generally, is required in
documentation to support DSM-5 and ICD-10 coding.
Points:
Points Range:
23 (23%) - 25 (25%)

The response accurately and concisely explains what pertinent
documentation information is required to support DSM-5 and
ICD-10 coding.
Feedback:
Points:
Points Range:
20 (20%) - 22 (22%)

The response accurately explains what pertinent
ICD-10 coding.
Feedback:
Points:
Points Range:
18 (18%) - 19 (19%)

The response somewhat vaguely or inaccurately explains what
pertinent documentation information is required to support
DSM-5 and ICD-10 coding.
Feedback:
Points:
Points Range:
0 (0%) - 17 (17%)

The response vaguely or inaccurately explains what pertinent
ICD-10 coding, or the explanation is incomplete or missing.
Feedback:
• Explain what pertinent documentation is missing from the
case scenario, and what other information would be helpful to
narrow your coding and billing options.
Points:
Points Range:

23 (23%) - 25 (25%)
The response accurately and concisely identifies the pertinent
misssing information from the case scenario and clearly
identifies what additional information would narrow coding and
billing options.
Feedback:
Points:

Points Range:
20 (20%) - 22 (22%)
The response accurately identifies the pertinent misssing
information from the case scenario and identifies what
additional information would narrow coding and billing options.
Feedback:
Points:

Points Range:
18 (18%) - 19 (19%)
The response somewhat vaguely or inaccurately identifi es the
pertinent misssing information from the case scenario and
billing options.
Feedback:
Points:

Points Range:
0 (0%) - 17 (17%)
The response vaguely or inaccurately identifies the pertinent
misssing information from the case scenario or partially
billing options, or this information is incomplete or missing.
Feedback:
• Finally, explain how to improve documentation to support
coding and billing for maximum reimbursement.

Points:
Points Range:
14 (14%) - 15 (15%)
The response accurately and concisely explains how to
improve documentation to support coding and billing for
maximum reimbursement.
Feedback:

Points:
Points Range:
12 (12%) - 13 (13%)
The response accurately explains how to improve
documentation to support coding and billing for maximum
reimbursement.
Feedback:

Points:
Points Range:
11 (11%) - 11 (11%)
The response somewhat vaguely or inaccurately explains how
to improve documentation to support coding and billing for
Feedback:

Points:
Points Range:
0 (0%) - 10 (10%)
The response vaguely or inaccurately explains how to improve
reimbursement, or response may be incomplete or missing.
Feedback:
Written Expression and Formatting - Paragraph Development
and Organization:
Paragraphs make clear points that support well-developed ideas,
flow logically, and demonstrate continuity of ideas. Sentences

are carefully focused—neither long and rambling nor short and
lacking substance. A clear and comprehensive purpose
statement and introduction are provided that delineate all
required criteria.
Points:
Points Range:
5 (5%) - 5 (5%)
Paragraphs and sentences follow writing standards for flow,
continuity, and clarity.
A clear and comprehensive purpose statement, introduction, and
conclusion are provided that delineate all required criteria.

Feedback:
Points:
Points Range:
4 (4%) - 4 (4%)
continuity, and clarity 80% of the time.
Purpose, introduction, and conclusion of the assignment are
stated, yet are brief and not descriptive.

Feedback:
Points:
Points Range:
3.5 (3.5%) - 3.5 (3.5%)
continuity, and clarity 60%–79% of the time.

vague or off topic.
Feedback:
Points:
Points Range:
0 (0%) - 3 (3%)

continuity, and clarity <60% of the time.
Purpose statement, introduction, and conclusion were not
provided.
Feedback:
Written Expression and Formatting - English Writing
Standards:
Correct grammar, mechanics, and proper punctuation
Points:
Points Range:
5 (5%) - 5 (5%)

Uses correct grammar, spelling, and punctuation with no errors
Feedback:
Points:
Points Range:
4 (4%) - 4 (4%)

Contains 1-2 grammar, spelling, and punctuation errors
Feedback:
Points:
Points Range:
3.5 (3.5%) - 3.5 (3.5%)

Feedback:
Points:
Points Range:
0 (0%) - 3 (3%)

Contains five or more grammar, spelling, and punctuation
errors that interfere with the reader’s understanding
Feedback:
Written Expression and Formatting -
The paper follows correct APA format for parenthetical/in-text
citations and reference list.
Points:
Points Range:
5 (5%) - 5 (5%)

Uses correct APA format with no errors
Feedback:
Points:
Points Range:
4 (4%) - 4 (4%)

Contains 1-2 APA format errors
Feedback:
Points:
Points Range:
3.5 (3.5%) - 3.5 (3.5%)

Feedback:
Points:
Points Range:
0 (0%) - 3 (3%)
Contains five or more APA format errors

Feedback:
Show Descriptions
Show Feedback
In the E/M patient case scenario provided:
• Assign DSM-5 and ICD-10 codes to services based upon
the patient case scenario.
--
Levels of Achievement:
Excellent
90%–100%
18 (18%) - 20 (20%)

DSM-5 and ICD-10 codes assigned to the scenario are correct,
with no more than a minor error.
Good
80%–89%
16 (16%) - 17 (17%)
DSM-5 and ICD-10 codes assigned to the scenario are mostly
correct, with a few minor errors.
Fair
70%–79%
14 (14%) - 15 (15%)
several errors.

Poor
0%–69%
0 (0%) - 13 (13%)
significant errors, or response is missing.
Feedback:
In 1–2 pages, address the following:
• Explain what pertinent information, generally, is required in
--
Excellent
90%–100%

23 (23%) - 25 (25%)
The response accurately and concisely explains what pertinent
ICD-10 coding.
Good
80%–89%
20 (20%) - 22 (22%)
The response accurately explains what pertinent documentation
information is required to support DSM-5 and ICD-10 coding.
Fair
70%–79%
18 (18%) - 19 (19%)
The response somewhat vaguely or inaccurately explains what
pertinent documentation information is required to support

DSM-5 and ICD-10 coding.
Poor
0%–69%
0 (0%) - 17 (17%)
The response vaguely or inaccurately explains what pertinent
ICD-10 coding, or the explanation is incomplete or missing.
Feedback:
• Explain what pertinent documentation is missing from the case
scenario, and what other information would be helpful to narrow
your coding and billing options.--

Excellent
90%–100%
23 (23%) - 25 (25%)
The response accurately and concisely identifies the pertinent
misssing information from the case scenario and clearly
billing options.
Good
80%–89%
20 (20%) - 22 (22%)
The response accurately identifies the pertinent misssing
information from the case scenario and identifies what
additional information would narrow coding and billing options.
Fair
70%–79%
18 (18%) - 19 (19%)

The response somewhat vaguely or inaccurately identifies the
pertinent misssing information from the case scenario and
billing options.
Poor
0%–69%
0 (0%) - 17 (17%)
The response vaguely or inaccurately identifies the pertinent
misssing information from the case scenario or partially
billing options, or this information is incomplete or missing.
Feedback:

• Finally, explain how to improve documentation to support
coding and billing for maximum reimbursement.--
Excellent
90%–100%
14 (14%) - 15 (15%)
The response accurately and concisely explains how to improve
reimbursement.
Good
80%–89%
12 (12%) - 13 (13%)
The response accurately explains how to improve documentation
to support coding and billing for maximum reimbursement.

Fair
70%–79%
11 (11%) - 11 (11%)
The response somewhat vaguely or inaccurately explains how to
improve documentation to support coding and billing for
Poor
0%–69%
0 (0%) - 10 (10%)
The response vaguely or inaccurately explains how to improve
reimbursement, or response may be incomplete or missing.
Feedback:

Written Expression and Formatting - Paragraph Development
and Organization:
Paragraphs make clear points that support well-developed ideas,
flow logically, and demonstrate continuity of ideas. Sentences
are carefully focused—neither long and rambling nor short and
lacking substance. A clear and comprehensive purpose
statement and introduction are provided that delineate all
required criteria.
--
Excellent
90%–100%
5 (5%) - 5 (5%)
continuity, and clarity.
A clear and comprehensive purpose statement, introduction, and
conclusion are provided that delineate all required criteria.

Good
80%–89%
4 (4%) - 4 (4%)
continuity, and clarity 80% of the time.
stated, yet are brief and not descriptive.
Fair
70%–79%
3.5 (3.5%) - 3.5 (3.5%)
continuity, and clarity 60%–79% of the time.
vague or off topic.

Poor
0%–69%
0 (0%) - 3 (3%)
continuity, and clarity <60% of the time.
Purpose statement, introduction, and conclusion were not
provided.
Feedback:
Written Expression and Formatting - English Writing Standards:
Correct grammar, mechanics, and proper punctuation
--

Excellent
90%–100%
5 (5%) - 5 (5%)
Uses correct grammar, spelling, and punctuation with no errors
Good
80%–89%
4 (4%) - 4 (4%)
Fair
70%–79%
3.5 (3.5%) - 3.5 (3.5%)

Poor
0%–69%
0 (0%) - 3 (3%)
Contains five or more grammar, spelling, and punctuation errors
that interfere with the reader’s understanding
Feedback:
Written Expression and Formatting -
The paper follows correct APA format for parenthetical/in-text
citations and reference list.
--
Excellent

90%–100%
5 (5%) - 5 (5%)
Uses correct APA format with no errors
Good
80%–89%
4 (4%) - 4 (4%)
Fair
70%–79%
3.5 (3.5%) - 3.5 (3.5%)

Poor
0%–69%
0 (0%) - 3 (3%)
Contains five or more APA format errors
Feedback:
Total Points:
100
Name: NRNP_6675_Week2_Assignment1_Rubric

Pathways Mental Health
Psychiatric Patient EvaluationInstructions
Use the following case template to complete Week 2
Assignment 1. On page 5, assign DSM-5 and ICD-10 codes to
the services documented. You will add your narrative answers
to the assignment questions to the bottom of this template and
submit altogether as one document.Identifying Information
Identification was verified by stating of their name and date of
birth.
Time spent for evaluation: 0900am-0957am
Chief Complaint
“My other provider retired. I don’t think I’m doing so well.”
HPI
25 yo Russian female evaluated for psychiatric evaluation
referred from her retiring practitioner for PTSD, ADHD,
Stimulant Use Disorder, in remission. She is currently
prescribed fluoxetine 20mg po daily for PTSD, atomoxetine
80mg po daily for ADHD.
Today, client denied symptoms of depression, denied anergia,
anhedonia, amotivation, no anxiety, denied frequent worry,
reports feeling restlessness, no reported panic symptoms, no
reported obsessive/compulsive behaviors. Client denies active
SI/HI ideations, plans or intent. There is no evidence of
psychosis or delusional thinking. Client denied past episodes of
hypomania, hyperactivity, erratic/excessive spending,
involvement in dangerous activities, self-inflated ego,
grandiosity, or promiscuity. Client reports increased irritability
and easily frustrated, loses things easily, makes mistakes, hard

time focusing and concentrating, affecting her job. Has low
frustration tolerance, sleeping 5–6 hrs/24hrs reports nightmares
of previous rape, isolates, fearful to go outside, has missed
several days of work, appetite decreased. She has somatic
concerns with GI upset and headaches. Client denied any
current binging/purging behaviors, denied withholding food
from self or engaging in anorexic behaviors. No self-mutilation
behaviors.
Diagnostic Screening Results
Screen of symptoms in the past 2 weeks:
PHQ 9 = 0 with symptoms rated as no difficulty in functioning
Interpretation of Total Score
Total Score Depression Severity 1-4 Minimal depression 5-9
Mild depression 10-14 Moderate depression 15-19 Moderately
severe depression 20-27 Severe depression
GAD 7 = 2 with symptoms rated as no difficulty in functioning
Interpreting the Total Score:
Total Score Interpretation ≥10 Possible diagnosis of GAD;
confirm by further evaluation 5 Mild Anxiety 10 Moderate
anxiety 15 Severe anxiety
MDQ screen negative
PCL-5 Screen 32
Past Psychiatric and Substance Use Treatment
Entered mental health system when she was age 19 after raped
by a stranger during a house burglary.
Previous Psychiatric Hospitalizations: denied
Previous Detox/Residential treatments: one for abuse of
stimulants and cocaine in 2015
Previous psychotropic medication trials: sertraline (became
suicidal), trazodone (worsened nightmares), bupropion (became

suicidal), Adderall (began abusing)
Previous mental health diagnosis per client/medical record:
GAD, Unspecified Trauma, PTSD, Stimulant use disorder,
ADHD confirmed by school records
Substance Use History
Have you used/abused any of the following (include
frequency/amt/last use):
Substance Y/N Frequency/Last Use
Tobacco products Y ½
ETOH Y last drink 2 weeks ago, reports drinks 1-2 times
monthly one drink socially
Cannabis N
Cocaine Y last use 2015
Prescription stimulants Y last use 2015
Methamphetamine N
Inhalants N
Sedative/sleeping pills N
Hallucinogens N
Street Opioids N
Prescription opioids N
Other: specify (spice, K2, bath salts, etc.) Y reports one-
time ecstasy use in 2015
Any history of substance related:
Blackouts: +
Tremors: -
DUI: -
D/T's: -
Seizures: -
Longest sobriety reported since 2015—stayed sober maintaining
sponsor, sober friends, and meetings
Psychosocial History

Client was raised by adoptive parents since age 6; from Russian
orphanage. She has unknown siblings. She is single; has no
children.
Employed at local tanning bed salon
Education: High School Diploma
Denied current legal issues.
Suicide / HOmicide Risk Assessment
RISK FACTORS FOR SUICIDE:
Suicidal Ideas or plans - no
Suicide gestures in past - no
Psychiatric diagnosis - yes
Physical Illness (chronic, medical) - no
Childhood trauma - yes
Cognition not intact - no
Support system - yes
Unemployment - no
Stressful life events - yes
Physical abuse - yes
Sexual abuse - yes
Family history of suicide - unknown
Family history of mental illness - unknown
Hopelessness - no
Gender - female
Marital status - single
White race
Access to means
Substance abuse - in remission
PROTECTIVE FACTORS FOR SUICIDE:
Absence of psychosis - yes
Access to adequate health care - yes
Advice & help seeking - yes
Resourcefulness/Survival skills - yes
Children - no
Sense of responsibility - yes

Pregnancy - no; last menses one week ago, has Norplant
Spirituality - yes
Life satisfaction - “fair amount”
Positive coping skills - yes
Positive social support - yes
Positive therapeutic relationship - yes
Future oriented - yes
Suicide Inquiry: Denies active suicidal ideations, intentions, or
plans. Denies recent self-harm behavior. Talks futuristically.
Denied history of suicidal/homicidal ideation/gestures; denied
history of self-mutilation behaviors
Global Suicide Risk Assessment: The client is found to be at
low risk of suicide or violence, however, risk of lethality
increased under context of drugs/alcohol.
No required SAFETY PLAN related to low risk
Mental Status Examination
She is a 25 yo Russian female who looks her stated age. She is
cooperative with examiner. She is neatly groomed and clean,
dressed appropriately. There is mild psychomotor restlessness.
Her speech is clear, coherent, normal in volume and tone, has
strong cultural accent. Her thought process is ruminative. There
is no evidence of looseness of association or flight of ideas. Her
mood is anxious, mildly irritable, and her affect appropriate to
her mood. She was smiling at times in an appropriate manner.
She denies any auditory or visual hallucinations. There is no
evidence of any delusional thinking. She denies any current
suicidal or homicidal ideation. Cognitively, She is alert and
oriented to all spheres. Her recent and remote memory is intact.
Her concentration is fair. Her insight is good.
Clinical Impression
Client is a 25 yo Russian female who presents with history of

treatment for PTSD, ADHD, Stimulant use Disorder, in
remission.
Moods are anxious and irritable. She has ongoing reported
symptoms of re-experiencing, avoidance, and hyperarousal of
her past trauma experiences; ongoing subsyndromal symptoms
related to her past ADHD diagnosis and exacerbated by her
PTSD diagnosis. She denied vegetative symptoms of depression,
no evident mania/hypomania, no psychosis, denied anxiety
symptoms. Denied current cravings for drugs/alcohol, exhibits
no withdrawal symptoms, has somatic concerns of GI upset and
headaches.
At the time of disposition, the client adamantly denies SI/HI
ideations, plans or intent and has the ability to determine right
from wrong, and can anticipate the potential consequences of
behaviors and actions. She is a low risk for self-harm based on
her current clinical presentation and her risk and protective
factors.
Diagnostic Impression
[Student to provide DSM-5 and ICD-10 coding]
Double click inside this text box to add/edit text. Delete
placeholder text when you add your answers.
Treatment Plan
Medication:
Increase fluoxetine 40mg po daily for PTSD #30 1 RF
Continue with atomoxetine 80mg po daily for ADHD. #30 1 RF
Instructed to call and report any adverse reactions.
Future Plan: monitor for decrease re-experiencing,
hyperarousal, and avoidance symptoms; monitor for improved
concentration, less mistakes, less forgetful
Education: Risks and benefits of medications are discussed

including non-treatment. Potential side effects of medications
discussed. Verbal informed consent obtained.
Not to drive or operate dangerous machinery if feeling sedated.
Not to stop medication abruptly without discussing with
providers.
Discussed risks of mixing medications with OTC drugs, herbal,
alcohol/illegal drugs. Instructed to avoid this practice. Praised
and Encouraged ongoing abstinence. Maintain support system,
sponsors, and meetings.
Discussed how drugs/ETOH affects mental health, physical
health, sleep architecture.
Patient was educated about therapy and services of the MHC
including emergent care. Referral was sent via email to therapy
team for PET treatment.
Patient has emergency numbers: Emergency Services 911, the
national Crisis Line 800-273-TALK, the MHC Crisis Clinic.
Patient was instructed to go to nearest ER or call 911 if they
become actively suicidal and/or homicidal.
Time allowed for questions and answers provided. Provided
supportive listening. Patient appeared to understand discussion
and appears to have capacity for decision making via verbal
conversation.
RTC in 30 days
Follow up with PCP for GI upset and headaches, reviewed PCP
history and physical dated one week ago and include lab results
Patient is amenable with this plan and agrees to follow

treatment regimen as discussed.
Narrative Answers
[In 1-2 pages, address the following:
· Explain what pertinent information, generally, is required in
· Explain what pertinent documentation is missing from the case
scenario, and what other information would be helpful to narrow
your coding and billing options.
· Finally, explain how to improve documentation to support
coding and billing for maximum reimbursement.]
Add your answers here. Delete instructions and placeholder text
when you add your answers.
References
[Add APA-formatted citations for any sources you referenced]
Delete instructions and placeholder text when you add your
citations.
Page | 2
Walden University, LLC
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