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Muriel Lambert, Ph.D.

December 5, 2003 (Friday)


10:00 am
NUTRITIONAL DISORDERS
There are three broad categories of causes for nutritional imbalances. The first is inadequate or
excessive intake. The second is poor digestion and absorption. The third is an increased requirement
due to physical activity, rapid growth, infection, acute or chronic illness, pregnancy, drug therapy, or
increased loss of nutrients.
In economically under-developed areas calorie and protein deficiencies are presently the most important
nutritional problems. Vitamin deficiencies usually coexist with protein-calorie deficiency. In
economically developed areas, on the other hand, there is excessive intake of certain types of food,
particularly lipids, and inappropriate eating patterns sometimes result in
vitamin deficiencies.
The major nutritional disturbances result from imbalances in (1) proteins, carbohydrates and fats, (2)
vitamins and (3) minerals and water.
I.

PROTEIN, CARBOHYDRATE, AND LIPID IMBALANCES

In addition to a minimal overall intake of protein, carbohydrates, and lipids, there are eight
essential amino acids that are necessary in the human diet. These are: tryptophan, lysine, phenylalanine,
leucine, isoleucine, threonine, methionine and valine. There are also three
essential fatty acids: arachidonic, linoleic and linolenic. Some of the major diseases resulting from
imbalance of these essential nutrients are described below.
A. Protein-Energy Malnutrition
Protein-energy malnutrition is currently an important cause of child death in many parts of the world.
The two main clinical syndromes are kwashiorkor and nutritional marasmus.
1. Kwashiorkor
Kwashiorkor results from a dietary deficiency of protein, usually in the presence of
an adequate caloric intake.
a. Occurrence:
1) Mainly in children 1 to 3 years of age
2) Common in many underdeveloped countries and in poverty stricken areas of
developed countries
3) Most prevalent during the weaning period when the child's diet changes from
maternal milk to primarily carbohydrates

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Clinical Manifestations:
1) Growth failure
2) Edema
3) Hepatomegaly (liver enlargement)
4) Anemia
5) Hair changes - changes in texture, color, strength
6) Dermatoses - wax paper-type desquamation, depigmentation and
hyperpigmentation
7) Apathy, anorexia (loss of appetite), listlessness
8) Impaired intelligence

c. Histopathology
1) Atrophy of the mucosa of the small bowel
2) Erythroid hypoplasia in the bone marrow
3) Decrease in number of lymphocytes
4) Fatty change of the liver
2. Nutritional marasmus
Marasmus is a state of malnutrition resulting from a deficiency of total calories.
a. Occurrence
1) Common in nearly all underdeveloped countries
2) Common in children under 1 year of age
3) May occur secondary to such diseases as hepatic fibrosis, celiac disease or
overwhelming infection
b. Clinical Manifestations
1) Growth failure
2) Wasting - little or no subcutaneous fat, loss of muscle
3) Growth retardation
4) Ravenous appetite
5) Alert mental state
6) Many of the manifestations of kwashiorkor except edema
c. Histopathology
1) Erythroid hypoplasia of the bone marrow
3. Marasmus-Kwashiorkor
Kwashiorkor and marasmus can be regarded as two extremes of protein-calorie
malnutrition; most cases of protein-calorie malnutrition, however, are intermediate
between the two. These patients usually manifest other deficiencies as well,
particularly of dietary vitamins and manganese.

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4. Marasmus-like and kwashiorkor-like syndromes


a) Secondary forms of these two syndromes may develop in chronically or acutely ill
hospitalized patients
b) Takes weeks or months to develop
B. Obesity
This type of malnutrition is prevalent in the U.S. and other developed countries. It is
characterized by:
1. Abnormally increased adipose tissue which is the result of caloric intake greater than
energy expenditure.
2. High mortality rate associated with an increased risk for development of many
diseases (cardiovascular and pulmonary diseases, hypertension, cholelithiasis
(gallstones) and diabetes mellitus.
3. Genetic influences and environmental factors play an important role in human obesity
4. Obese children and adolescents are a major source for the relatively intractable adult
obesity.
C. Lipid Disorders
1. Marked increases in incidence of arteriosclerosis and its complications, particularly
coronary heart disease, are associated with metabolic disorders in which blood lipids
are elevated.
2. Levels of triglycerides and cholesterol are the factors most closely associated with
development of these diseases.
3. Dietary factors are important in determining lipid and cholesterol levels. Serum
cholesterol can be reduced by lowering dietary intake of saturated fats and cholesterol
and increasing the intake of polyunsaturated fats.
4. Inherent metabolic traits are also important factors in determining serum cholesterol
levels.

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II.

VITAMIN IMBALANCES
Vitamins are chemically unrelated organic substances that are required for specific metabolic
reactions; they are not adequately synthesized by the individual and are therefore
essential in the diet in minute amounts.
Traditionally vitamins are classified according to their solubility in water or fat and
physiologically this property determines their patterns of transport, excretion and storage.
A large number of the vitamins form specific coenzymes.
At the present time it is difficult to precisely correlate the biochemical and physiological
functions of individual vitamins with the clinical manifestations of their deficiencies.
A. Water Soluble Vitamins
This group of vitamins is rapidly and readily absorbed from the alimentary canal. Figure
1 shows some of the key roles vitamins play as catalysts in the metabolism of
carbohydrates, fats and proteins. The more important ones, described below, are marked
with an asterisk(*).
*1. Vitamin B1 (Thiamine)
a. Chemistry and Biochemical Function. Thiamine is part of the coenzyme, thiamine
pyrophosphate (TPP), which is an important factor in carbohydrate metabolism.
1) TTP has three important functions: (a) regulates oxidative decarboyxlation of
pyruvate and a-ketoglutrate leading to synthesis of ATP (Fig. 1); (b) involved
in glucose oxidation (pentose phosphate pathway); (c) maintains neural
membranes and normal nerve conduction (chiefly of peripheral nerves).
2) Thus, the organ systems most severely affected by thiamine deficiency are
those most dependent upon carbohydrate metabolism (i.e. the heart and
nervous system).
b. Pathology of Thiamine Deficiency. Thiamine deficiency is widespread in the
orient where the diet of the population consists largely of polished or refined rice.
It is also associated with chronic alcoholism. The best documented thiamine
deficiency state is beriberi. Beriberi in Singhalese means "weakness". The changes
occurring in beriberi are, for the most part, confined to the heart and nervous
system. Beriberi can be divided into several syndromes:
1) Wet Beriberi (Acute)
a) Principally characterized by chronic heart failure; the heart is flabby and
dilated

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1) Wet Beriberi (Acute) - continued


b) Peripheral vasodilatation
c) Extensive edema secondary to cardiac failure
2) Dry Beriberi (Chronic)
a) Peripheral neuropathy, with degenerative changes also ccurring in the
central nervous system
b) Myelin egeneration and disruption of axons
c) Wrist-drop, foot-drop, marked wasting of lower extremities
3) Wernicke's disease - This disease is considered a subtype of dry beriberi and is
mainly associated with chronic alcoholism. It is principally characterized by
degenerative changes in the brain and central nervous systems, oculomotor
disturbances and ataxia.
4) Korsakoff's pyschosis - This is usually associated with Wernicke's disease
(Wernicke-Korsakoff syndrome) and is characterized by loss of memory of
the immediate past and often elaborate confabulation which attempts to
conceal this amnesia, generally without success.
c. Antagonists of thiamine - In certain fish (e.g. carp) a heat-labile enzyme
(thiaminase) has been found which destroys thiamine. In those countries where
large amounts of raw fish are eaten, thiamine deficiency sometimes occurs.
Up to 3% of Japanese are thiamine deficient for this reason.
*2. Vitamin B2 (Riboflavin)
a. Chemistry and Biochemical Function - Riboflavin forms part of the structure of
two coenzymes, flavin mononucleotide (FMN) and flavin adenine dinucleotide
(FAD), which play an important role in both protein and energy metabolism.
They serve as carriers in the electron transport system and participate in the
oxidation of amino acids and purines (Fig. 1).
b. Riboflavin Deficiency - Symptoms first appear in the skin and mucous
membranes. Other clinical signs are also seen.
1) Cheilosis: This is usually the first and most characteristic sign of the
deficiency. It is characterized by cracks or fissures and crusts at the angles of
the mouths which may extend into the mucous membrane inside the mouth.
2) Glossitis: This lesion of the tongue results from atrophy of the mucosa. This
may be accompanied by superficial submucosal inflammation, producing a
bright red or magenta hue.

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b. Riboflavin Deficiency - continued


3) Eye Change: In avascular tissues, such as the cornea oxidation takes place by
means of a riboflavin-containing enzyme. In riboflavin deficiency attempts
at oxygenation occur through neovascularization of these tissues.
4) Dermatitis: A scaling, greasy dermatitis occurs especially over the nasolabial
folds with scrotal and vulvar lesions also common.
5) Retarded intellectual development has been noted in riboflavin-deficient
children.
*3. Niacin (Nicotinic Acid)
a. Chemistry and Biochemical Function - Niacin is metabolically converted to
nicotinamide, a component of the coenzymes nicotinamide adenine dinucleotide
(NAD) and nicotinamide adenine dinucleotide phosphate (NADP) which function
in electron transfer. These coenzymes are of major importance in glycolysis and
cellular respiration where in the reduced state they donate hydrogens to the cell
respiratory chain (Fig. 1).
b. Niacin deficiency
1) Pellagra. This disease is associated with corn (maize) eating peoples. Maize
is poor in usable niacin and very low in tryptophan content (niacin is
synthesized from dietary tryptophan). Pellagra may not be a simple niacin
deficiency; deficiency of several of the other B vitamins may also be involved.
a) Clinical Manifestations - Clinically the disease is characterized by the four
D's - dermatitis, diarrhea, dementia, and death.
i.

ii.
iii.
iv.

Dermatitis - Skin lesions tend to occur in regions of the body


exposed to sunlight or chronic irritation such as the face, neck, hands,
wrists, elbows, and knees. The lesions on the upper chest and lower
neck are known as Casal's necklace.
Diarrhea - This is presumed to be due to mucous membrane lesions,
most prominent in the esophagus, stomach, and colon.
Dementia - Degeneration of the ganglion cells of the brain and the
tracts of the spinal cord occurs.
Death - Pellagra may be quite rapidly fatal.

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4. Pyridoxine (B6)
a. Chemistry and Biochemical functions. Pyridoxine is the accepted name of a group
of three closely related compounds which are converted in the body to the
coenzyme pyridoxal phosphate, whose major function is amino acid or protein
metabolism (Fig. 1), and which is also a cofactor in the production of the
inhibitory amine, a-amino butyric acid.
b. Pyridoxine deficiency.
1) Biochemical evidence of pyridoxine deficiency occurs in uremia and cirrhosis.
It can also occur with pharmacologic agents such as penicillamine. A
significant percentage of women using oral contraceptives have altered
pyridoxine metabolism.
2) The most common cutaneous sign of pyridoxine deficiency is a dermatitis of
the face, scalp, neck and shoulders. Central nervous system alterations such
as somnolence and confusion occur commonly. Pyridoxine deficiency is also
common in chronic alcoholics.
5. Pantothenic acid (B5)
a. Chemistry and Biochemical functions. Pantothenic acid is a component of
coenzyme A (CoA). Pantetheine, a derivative of pantothenic acid, is the
functional unit of coenzyme A and plays a vital role in numerous metabolic
processes.
b. Deficiency of Pantothenic Acid. Though pantothenic acid is of physiological
importance, evidence for lesions in man from deficiency of this vitamin are
inconclusive. The "Burning Feet" syndrome, consisting of severe paresthesias and
tenderness of the feet, observed among prisoners of war (in World War II) and in
malnourished subjects in the Far East, responded to preparations containing
pantothenic acid and probably represents a specific manifestation of deficiency
of this vitamin.
*6. Vitamin B12 (Cyanocobalamin)
a. Chemistry and Biochemical functions. Vitamin B12 is the largest of all the
vitamins and has been isolated in several different forms, of which cyanocobalamin
is the principal one.
1) The absorption of vitamin B12 from the gastrointestinal tract is dependent on a
constituent of the gastric juice designated "intrinsic factor," which is believed
to interact with the vitamin and protect it during its transit to the ileum where
it is absorbed.

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*6. Vitamin B12 (Cyanocobalamin)


2) At least 5 different vitamin B12 coenzymes have been identified. The
mechanism by which the B12 coenzymes function is not clear. Many of their
functions appear to be closely linked with tetrahydrofolic acid (FH4) in the
metabolism of one-carbon groups. Present evidence suggests that they
participate in nucleic acid synthesis, protein synthesis, particularly
biosynthesis of amino acids, and in lipid metabolism.
b. Vitamin B12 Deficiency. Primary dietary deficiency of vitamin B12 is rare.
Deficiency is usually induced by mechanisms which include; (1) inadequate
production of intrinsic factor; (2) interference with B12 or intrinsic factor function;
(3) impaired absorption; or (4) loss in the body.
Deficiency produces cellular changes throughout the body, the most serious
consequences of which is Pernicious Anemia which consists of:
1) Megaloblastic Anemia - characterized by erythroblasts that are larger than
normal and which have an altered nuclear- cytoplasmic ratio. This is related to
defective DNA synthesis.
2) Neurological disorders - Degeneration of the spinal cord (subacute combined
system degeneration) occurs. This will be discussed in more detail in later
lectures.
*7. Folic Acid (Pteroylmonoglutamic acid) (Vitamin M)
a. Biochemistry and Biochemical function. The active form of folic acid is
tetrahydrofolic acid (FH4). This coenzyme is a carrier for and donates one carbon
groups and is mainly involved in the biosynthesis of the nucleic acids necessary
for DNA synthesis. It is necessary for mitosis in actively dividing cells such as
those of the alimentary tract and bone marrow.
b. Folic Acid Deficiency. The typical reaction to folic acid deficiency is a
megaloblastic red cell maturation in the bone marrow with a resulting megaloblastic
anemia which may be accompanied by intestinal malabsorption and glossitis.
Certain vitamin B12 deficiency findings may be attributed to a defect in folate
utilization.

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*8. Vitamin C (Ascorbic Acid)


a. Biochemistry and Biochemical function. Ascorbic acid is a hexose derivative.
1) It functions as a reducing agent required as a coenzyme for the enzymes
proline hydroxylase and lysine hydroxylase, which are important in synthesis
of collagen and intercellular cement substance. Hence, Vitamin C is critical for
growth and tissue repair.
2) Vitamin C has antioxidant properties. It can directly scavenage free radicals in
cells and indirectly regenerate the antioxidant form of vitamin E. Thus
vitamins C and E can act in concert.
b. Vitamin C Deficiency. Gross vitamin C deficiency results in the disease scurvy.
Metabolic stress, such as acute illness or surgery, markedly increases requirements
for vitamin C. Scurvy sometimes occurs in intensive care units. A lack of vitamin
C affects:
1) Capillary Walls. Deficiency of intercellular cement substance and connective
tissue support weakens capillary walls and leads to their rupture and extensive
hemorrhage. Hemorrhages are one of the most striking manifestations of
scurvy. These occur most often in the subcutaneous tissues (producing
petechiae and ecchymoses), joints, nose (epistaxis-nosebleed), and mucous
membranes of the mouth.
2) Bone formation. In scurvy, the principal deficiency is in formation of osteoid
matrix, not, as rickets, in mineralization or calcification. As a consequence,
bone growth, formation and strength are severely disrupted. Deficiencies in
collagen and cement substance also occur and as a result the periosteum
becomes detached and extensive subperiosteal hematomas occur.
3) Wound healing. Ascorbic acid deficiency leads to failure of collagen formation
and as a result impaired wound healing. Also there is a constant turnover of
collagen in old wounds, so that reopening of old wounds may occur in scurvy.
4) Teeth - Resorption of the alveolar bone may cause the teeth to soften, loosen
or fall out.
5) Gingiva - Swelling, hemorrhages and secondary marginal infections of the
gingiva may occur.
A patient with scurvy may have some of the above symptoms and not appear
seriously ill, however, he or she may suddenly collapse and die.

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9. Biotin (Vitamin H)
a. Chemistry and Biochemical function. Biotin is a relatively simple monocarboxylic
acid. Its primary function is as the coenzyme for enzymatic reactions involving
the addition of carbon dioxide to other units (carboxylation reactions). It has also
been attributed an important role in the intermediary metabolism of
carbohydrates, proteins and fats (Fig. 1).
Raw egg white contains avidin, a protein which combines with biotin and acts as
an antagonist. Paradoxically, egg yolk is a very rich source of biotin.
b. Biotin deficiency. Deficiency of biotin can be acquired or genetic. Acquired biotin
deficiency is extremely rare due to its ubiquity among foods and because it is
produced by intestinal bacteria. Occasionally biotin deficiency occurs in an
individual who has for some reason consumed a diet consisting mainly of raw egg
whites. Two forms of genetic biotin deficiency occur, neonatal and infantile.
Exfoliative dermatitis has been observed in these infants. Neuropsychiatric
changes are noted in all forms of biotin deficiency.
B. Fat Soluble Vitamins
This group of vitamins is absorbed in association with dietary fats and requires the
presence of bile salts for adequate uptake from the alimentary canal.
*1. Vitamin A (Retinol)
a. Chemistry and Biochemical function. Vitamin A is a long chain alcohol (retinol)
which exists in a number of isometric forms. Vitamin A can be obtained directly
in the diet or more commonly as the proto-vitamin precursors, the carotenes. The
most important of these carotenoids is B-carotene (which consists of two
covalently linked molecules of retinol). The carotenoids present in the diet are
cleaved within the intestinal wall to form Vitamin A. Vitamin A has a number of
roles, the best understood of which is in vision. The aldehyde of retinol, retinal, is
a constituent of the visual pigments rhodopsin and iodopsin, in the rod and cone
cells, respectively, of the retina.
Vitamin A is necessary for growth and development, and is involved in the normal
functioning of the eyes, skin and gonads.

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b. Vitamin A Imbalance
1) Hypovitaminosis A
a) Night blindness. Visual acuity in subdued light depends on excitation of
rhodopsin in the retina. During the visual process some retinal is degraded,
thus a constantly available source of Vitamin A is necessary in order to
maintain adequate levels of rhodopsin due to retinal loss. Inadequate levels
of Vitamin A result in a loss of vision in low intensity light (night
blindness).
b) Epithelial Metaplasia. By an as yet unknown mechanism vitamin A is
necessary for the maintenance of mucous membranes and epithelial of the
eyes, respiratory, gastrointestinal, and genitourinary tracts, and the lining
of numerous gland ducts. Deficiency leads to atrophy and replacement by
stratified squamous epithelium which keratinizes.
i.
Xerophthalmia - The conjunctional and corneal mucosal surfaces of
the eye become dry and rough, and keratin debris accumulates in
whitish plaques (Bitot's spots). Visual acuity is impaired.
ii.

Keratomalacia. This disease may develop, particularly in children, if


Xeropthalmia is left untreated. The corneal surface ulcerates,
becomes opaque, and softens. Secondary infection may occur leading
to perforation of the cornea and blindness.

iii.
Skin lesions. Even though the skin is normally keratinized, Vitamin A
deficiency may lead to hyperplasia and hyperkeratinization of the
epidermis.
iv.

Squamous metaplasia of epithelium lining the upper respiratory


passages and urinary tract. The epithelium lining is replaced by
keratinizing squamous cells. This predisposes to secondary
pulmonary infections and renal and kidney stones.

c) Immune deficiency. Vitamin A plays some role in host resistance to


infections. It stimulates the immune system. This impairment of
immunity, during vitamin A deficiency, leads to high mortality rates from
common infections such as measles, pneumonia and infectious diarrhea.
2) Hypervitaminosis A
Excess vitamin A can lead to irritability, anorexia, nausea, hepatomegaly,
headaches with increased cerebrospinal fluid pressure leading to
hydrocephalus, and hyperkeratosis and desquamation of the skin.

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*2. Vitamin D (Ergocalciferol, cholecalciferol)


a. Chemistry and Biochemical function. Several forms of Vitamin D exist, all arise
from the irradiation of sterols.
1) In plants, ergosterol is activated by sunlight to form ergocalciferol (D2), and in
animals 7-dehydrocholesterol is activated to form cholecalciferol (D3). Both
forms of vitamin D undergo metabolic transformation in the liver and kidneys
to an active form.
2) Vitamin D deficiency results from three major causes: (1) inadequate intake ,
(2) chronic liver or kidney disease, or (3) inadequate sun exposure.
3) The major function of vitamin D is the maintenance of normal plasma levels of
calcium and phosphorus. Vitamin D facilitates the transport of calcium across
intestinal epithelium and its antirachitic activity appears to be due primarily to
this function.
b. Vitamin D deficiency. The two main vitamin D deficiency disease states are
rickets, which occurs in children, and osteomalacia, occurring in adults, These are
characterized by:
1) Failure of mineralization of osteoid matrix leading to marked skeletal
deformities in children.
2) Progressive loss of calcium from the matrix of long bones. This is usually
evident on X-ray as increased radiolucency of bone. This may lead to:
compression fractures of vertebrae and spontaneous fractures.
c. Hypervitaminosis D. Huge overdoses of Vitamin D lead to hypercalcemia,
metastatic calcification and hypercalciuria. This last abnormality predisposes
toward formation of renal stones. Calcium is also mobilized from the bones with
resulting osteoporosis.
3. Vitamin E (tocopherol)
Vitamin E was first described as an antisterility vitamin in 1922 when it was found to
prevent resorption of fetuses in pregnant female rats and testicular degeneration in
males. The name tocopherol is derived from the Greek tokos (childbirth) and phero
(to bear).
a. Biochemistry and Biochemical function. Several substances, designated
collectively as tocopherols, comprise the vitamin E group.

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a. Biochemistry and Biochemical function - continued


1) Vitamin E serves as an antioxidant that scavenges free radicals throughout the
body.
2) The tocopherols in part protect vitamin A and polyunsaturated
lipids, particularly those in cellular membranes, from destructive oxidation
b. Vitamin E deficiency. The nervous system is a particular target of vitamin E
deficiency, for reasons that are not clear, possibly through effects on cell
membranes. There is degeneration of axons in the posterior columns of the spinal
cord, and loss of nerve cells in the dorsal root ganglia. This leads to depressed or
absent tendon reflexes; ataxia, dysarthria, loss of position and vibration sense,
loss of pain sensation, muscle weakness and disorders of eye movement.
*4. Vitamin K (Naphtoquinones)
a. Biochemistry and Biochemical function. Vitamin K was named from the Danish
word Koagulation. It occurs in several closely related forms, and structurally is
similar to vitamin E.
1) Vitamin K is a required cofactor for a liver microsoma carboxylase which
carboxylates glutamate residues.
2) Vitamin K is essential for the synthesis of prothrombin as well as factors VII,
IX, and X, which all require carboxylation of glutamate residues for functional
activity and in its absence the mechanism for blood coagulation is inadequate.
3) Vitamin K also appears to favor calcification of bone proteins through its
ability to facilitate carboxylation of these proteins.
b. Vitamin K deficiency. Avitaminosis K leads to the production of hemorrhagic
disease. In adults simple deficiency is rare because of the abundance of this
vitamin in common foods and because of its formation by intestinal bacteria.
Usually, deficiency is due to chronic liver disease or biliary obstruction. In
neonates, its most serious manifestation is intracranial hemorrhage.
c. Hypervitaminosis K. Excessive doses of synthetic vitamin K have lead to
hemolytic anemia in infants.

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*4. Vitamin K (Naphtoquinones) Posterior columns of three - continued


d. Antagonists - Dicomarol is a naturally occurring antagonist blocking the action
of vitamin K. It was originally isolated from spoiled sweet clover and shown
to be responsible for hemorrhagic disease observed in cattle and sheep.
Commercially it is used in rat poison and medically in the treatment of
atherosclerotic heart disease, to reduce the risk of thrombosis in the coronary
arteries, and of phlebothrombosis, to reduce new clot formation and
subsequent embolization.
III. MINERAL AND WATER IMBALANCE
A. A number of minerals are essential for maintenance of various biological processes. Some
of these function entirely as components of enzymes or compounds while others act as
structural components and are important in maintaining electrolyte balance. Those
minerals known to be essential and which are present in fairly large quantities are:
calcium, phosphorous, potassium, sodium, chlorine, magnesium and sulfur.
The principal trace elements include; iron, zinc, copper, selenium, iodine, cobalt,
manganese, and molybdenum. The nutritional importance of a few of these are briefly
indicated below:
1. Iron. It is an essential component of hemoglobin. A deficiency in iron can lead to iron
deficiency anemia in which there is inadequate synthesis of hemoglobin.
2. Iodine. This element is absorbed as iodide and quickly oxidized to iodine in the
thyroid, where it becomes a constituent of thyroxine and related compounds. Low
dietary intak may lead to simple goiter and hypothyroidism which is endemic in many
areas of the world.
3. Zinc. A number of metalloenzymes in the body that regulate lipid, protein and nucleic
acid synthesis and degradation require zinc. Premature infants are especially
susceptible to zinc deficiency since they are born with inadequate zinc stores and
decreased absorptive ability. Disorders of zinc metabolism can occur in alcoholics.
Zinc deficiency can also be genetic.
Clinical manifestations of zinc deficiency involve multiple organ systems. Growth
retardation and anorexia can occur. There is a lack of genital and secondary sexual
development. There are also central nervous system changes, gastrointestinal effects,
eye changes, immune abnormalities and severe dermatoses.

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4. Copper. It is a component of a number of enzymes such as cytochrome C oxidase.


Acquired copper deficiency is rare. Deficiency leads to an impairment of copperdependent enzymes. Infants with marked protein-energy malnutrition or those on
strict cow's milk diets constitute the majority of cases. The kinky hair syndrome is
an X-linked recessive disorder of copper metabolism in which hairs have repetitive
twisting. Muscular weakness, severe mental retardation abnormal colagen crosslinking can ocur.
B. Water is the most critical of all nutrients. The human body contains more water than any
other compound. Approximately 70% of the fat-free body is water. Regulation of body
temperature is dependent upon water. Excessive water loss from the body results in
dehydration and loss of electrolytes, and replenishing the body water without concurrent
repletion of electrolytes leads to water intoxication.

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