DEVELOPMENT OF BREAST (PHYSIOLOGY)  Calcium and phosphate lost each day and unless the

 Development is stimulated by estrogen during puberty mother is drinking large quantities of milk and
 Estrogen stimulates growth of mammary glands, adequate vit D intake, there could be deficiency
deposition of fat to give mass to the breast
 To supply the need, parathyroid glands
 Much additional growth occurs during pregnancy; only
then does the glandular tissue becomes completely enlarge greatly and the bones progressively
develop for milk production decalcified
 Growth of ductal system is stimulated by estrogen  Human milk provides antibodies and other anti-
 During pregnancy, large quantities of estrogen infectious agent
secreted by the placenta cause ductile system to grow
& branch BREAST (HISTOLOGY)
 Stroma increase in quantity and laid down
w/ fats  Breast/ mammary gland develop as downgrowth of the epidermis
 For estrogen to produce its desired effect it needs:
 Invagination of surface ectoderm along the two ventral
GH, prolactin, adrenal glucocorticoids, insulin
 Development of lobule-alveolar system is stimulated by lines, milk line, from the axillae to the groin
progesterone  15 to 20 lactiferous ducts with lactiferous sinuses open at the tip
 With estrogen plus simultaneous action of of the nipple
progesterone cause growth of lobules, budding of  Each lactiferous duct drains one lobe
alveoli, and development of secretory characteristics  Nipple surrounded w/ connective tissue and smooth
in the cells of the alveoli
muscle cells (with sympathetic nerve fibers) forming
 Prolactin promotes lactation
circular sphincter
 Estrogen and progesterone inhibits milk secretion
 Prolactin induce lactation  Mammary gland contain duct system, lobes and lobules
 Human chorionic somatomammotropin secreted by  Lobule: consist of lactiferous duct and several alveolar
placenta has lactogenic properties acini (tubuloalveolar secretory unit). It opens into a
 Colostrum: the fluid secreted during the last few days lactiferous sinus
and the first few days after parturition  Lobules and lobe are not seen in resting breast
 Secretion of milk requires other hormones: GH,
 Lactiferous duct lined by simple columnar or cuboidal
cortisol, parathyroid hormone and isulin
epithelium surrounded by myoepithelial cells
 Provide amino acid, fatty acid, glucose,
calcium in the milk  In resting or nonlactating state: ends of lactiferous
 Hypothalamus secretes prolactin inhibitory horomone gland are blind
 Hypothalamus stimulates production of other  During pregnancy, ducts branch and end cluster forms
hormones while mainly inhibits prolactin production lobules
 Damage of the hypothalamus often increases prolactin  Mammary gland consist of 10 to 20 separate lobules
while depresses secretion of other hormones
 Dopamine: prolactin inhibitory hormone
 Ovarian cycle and ovulation does not resume for at least first few
months in lactating women
 Diminished estrogen secretion by the ovaries during
lactation
 Uterus of lactating mother involutes & decrease in size
 Preoccupation of the adenohypophysis w/ prolactin
production which reduces the rate of secretion of
other gonadotropic hormone
 After several months of lactation, adeohypophysis
begin to secrete again gonadotropins which does not
necessitate marked reduction in prolactin secretion
 Oxytocin function in the ejection of milk (called milk ejection or
milk let-down
 Suckling > stimulates somatic nerves in the nipples >
send to spinal cord > reach the hypothalamus >
secretion of oxytocin > oxytocin carried to the blood to
the breast > causes myoepithelial cells (which
surrounds the alveoli) to contract > milk is ejected
 Suckling in one breast cause milk to flow in other
breast

 Fats enter the milk each day

 Lactose are lost
NUTRITIONAL REQUIREMENTS  Wellcome classification- concerned with severe, clinically obvious
malnutrition
 Malnutrition:  2 criteria:
 Degree of weight loss (in terms of weight
 Pathological state resulting from a relative or absolute deficiency for age)
or excess of one or more essential nutrients  Presence or absence of edema
 Clinically manifested or detected only by biochemical, Weight for age as Edema No edema
anthropometric and physiological test percentage
 4 forms: 80-60 Kwashiorkor Undernutrition
 Undernutrition- consumption of an inadequate quantity of <60 Marasmic-kwashiorkor Marasmus
food over an extended period of time; starvation: almost
total lack of food that results to rpid development of severe  Waterlow classification- can distinguished between deficits in
undernutrition weight for height (wasting) and deficits in height for age (stunting)
 Specific deficiency- relative or absolute lack of an individual  Wasting- referred to as acute malnutrition
nutrient  Stunting- chronic malnutrition
 Overnutrition- consumption of excessive quantity of food,
caloric excess over an extended period of time Wasting:
 Imbalance- disproportion among essential nutrients, w/ or
without the absolute deficiency of any nutrients
 The highest incidence of malnutrition is in the toddler age group actual weight
x 100

of preschool child (1-5 y/o)
Nutritional deficiency may be:
ideal weight for actual length/height
Classification:
 Primary malnutrition- due to dietary inadequacy
Normal ≥ 90%
 Secondary malnutrition- due to factors other than
Mild 80-90%
from food inadequacy; some physiologic or
Moderate 70-80%
pathological conditions of the body preventing
Severe <70%
adequate ingestion of food or proper metabilsm
Stunting:
 Filipino diet is lacking of in calories
 It increases the requirement of protein w/c barely
meets the minimum actual length/height
 Protein is used for its main function of the body ONLY x 100
when energy needs are fully met
ideal length for age
 Protein lack results in growth retardation and
kwashiorkor Classification:
ETIOLOGY Normal ≥95
 Major factor that contributes to inadequate diet: Mild 90-95
 Low income Moderate 80-90
 Ignorance and erroneous food habits and belief Severe <80
 Scarcity of food supply
 Overpopulation PROTEIN-ENERGY MALNUTRITION
1. Inadequate supply of energy and nutrients to the tissues  PEM- used to describe certain signs and symptoms in infants and
2. Tissue depletion- tissue reserves are drawn to satisfy needs; young children which results from a deficiency of calories and/or
manifested by loss of weight and growth stunting protein in their diets
3. Biochemical changes- lowe blood and urinary levels of nutrients  Includes two major severe clinical syndromes of kwashiorkor and
or their products marasmus
4. Subjective symptoms- weakness, dizziness, fatigability, shortness  2 groups of PEM:
of breath  Mild –moderate PEM: (Latent, hidden or marginal
5. Classical symptoms of deficiency- nightblindness and photophobia malnutrition) 1st and 2nd levels underweight for age
in vit. A (between 90% and 61% of standard weight)
6. Anatomic lesios by physical examination- xerophtalmia  Severe PEM: Cases of 3rd level underweight for age
keratomalacia in avitaminosis A (kwashiorkor, nutritional marasmus and marasmic
 Retardation of growth or loss eight, weakness etc are more kwashiorkor)
widespread, more significant than less common classical A.MARASMUS
symptoms of deficiency (Infantile atrophy, inanition, athrepsia, cachexia, decomposition)
 Presence of keratomalacia or edema indicates long  Withering; severely wasted , underweight young child
standing snd serious condition
 Marginal deficiency states remain unnoticed until infections such Etiology
as measles or gastroenteritis TRIGGER into full blown cases of  Diet which is very low in protein and calories
severe malnutrition  Balanced starvation
 Overall lack of calories
CLASSIFICATION OF MALNUTRITION  Succinctly characterized as “wasting”
 Gomez system- the child’s weight is compared to that of a normal  Can occur at all ages but more common in the 1st year of life (or
child (50th percentile) of the same age earlier)
 Children with 3rd degree usually comprise cases of  Often the result of unsuccessful breastfeeding or insufficient
kwashiorkor and marasmus breast milk supply
 Can occur in bottle-fed because of too dilute milk mixture or
Percent of reference weight for age= [(patients’ weight)/(weight unhygienic preparation resulting to diarrhea
of normal child of the same age)] x 100
Weight for age Status Clinical Manifestation
91-100 Normal  Failure to gain weight > loss of weight > emaciation
76-90 First degree malnutrition  Loss of turgor in skin that becomes wrinkled and loose as
61-75 Second degree malnutrition subcutaneous fat disappears
<60 Third degree malnutrition  Abdomen is distended or flat w/ visible intestinal pattern
  Atrophy of muscles w/ resultant hypotonia  Normal: 3.4-5.4 g/dl
 Potbelly and winged scapulae  ADH is concerned in the pathogenesis of edema
 Muscle wasting seen in buttocks, thighs, scapular  The capacity of liver to normally inactivate
region and upper arms the ADH is impaired in low protein diet
 Facies are pinched and wizened  Muscle wasting w/ retention of some subcutaneous
 May be fretful (alert) but later becomes listless/apathetic, quite, tissue; reduction in upper arm circumference
 Appetite usually good  Looks miserable and does not smile
 No edema or hepatic enlargement in the pure marasmic
syndrome  COMMON SIGN
 Subnormal temperature  Hair luck of luster and pluckability, “flag sign”,
 Slow pulse rate dyspigmentation (light brown, reddish brown, blonde),
 Reduce BMR brittle dry hair, dyschromotrichia (absence of pigment
 Usually constipated in hair)
 Starvation type of diarrhea appear  Long scanty pale hair: prolonged period of
 Frequent small stools containing mucus deprivation
 Hair changes are never marked  Flag sign: alternating light and dark bands
 Light brown and sparse hair indicate alternating periods of protein
 Hair is relatively normal adequacy and deprivation
 There are associated vitamin deficiencies; associated conditions  Depigmentation of the skin
or diseases include:  General lightening of the skin of the face
 Dehydration from diarrhea
 Intestinal parasitism *changes in the skin or hair are not
 Oral moniliasis- yeast infection of the mouth and essential for the diagnosis of kwashiorkor
throat caused by Candida albicans; also known as  Moonface
thrush  Puffiness of the subcutaneous tissue of the
 Tuberculosis face
B. KWASHIORKOR  Rounded cheeks (early sign)
(Protein malnutrition, nutritional edema syndrome, malignant malnutrition,  Anemia
Melnahrschaden (flour malnutrition), plurideficiency syndrome)  Usually due to iron and folic deficiencies
 The disease of the displaced child and may aggravated by hookworm
 Child is weaned to almost entirely carbohydrate infection is some cases
 Appetite usually poor; irritable  OCCASIONAL SIGN
Etiology  Flaky-paint rash or enamel dermatoses
 Occurs in children from 4 mos to 5 yrs of age  If present it is pathognomonic (presence of
 Main incidence between 1 and 3 years particular sign means a particular disease is
 Diet that is low in protein but which contains carbohydrates present beyond any doubt)
 Common in places where starchy foods are the main staple  Seen hidden parts of the body mostly on
 Contributing factors are vit B complex, vit A, certain minerals and buttocks, groin and trunk
amino acid deficiency  Noma or cancrum oris (devastating
 Kwashiorkor is never exclusively dietary in etiology infectious disease w/c destroys the soft and
 Respiratory infections hard tissues of the oral and para-oral
 Diarrhea structures) is the effect of combination of
 Hookworm malnutrition and infection
 Malaria  Hepatomegaly
 Tuberculosis  Enlargement of liver, w/c has a firm,
smooth surface and edge
Clinical manifestation  Fatty liver thought to the impaired hepatic
 Secondary immunodeficiency is one of the most serious and synthesis of the acceptor proteins
constant manifestation necessary for the formation of the
 Measles is benign to normal infant but fatal to lipoprotein that are involved in the
malnourished mobilization of lipids from liver cells
 Infection and parasitic infections are common
 Suggested that the hepatic damage is due
3 categories:
to aflatoxin toxicity and chronic free radical
 DIAGNOSTIC SIGN
exposure, secondary to a lack of antioxidant
 EDEMA is a cardinal sign; should not be diagnosed in
nutrient in the diet (speculative)
its absence
 Associated vitamin deficiency
 Occurs first above the ankle
 Signs like photophobia, keratomalacia,
 Edema becomes generalized in the legs, angular stomatitis
forearm, penis, scrotum, lower back, lower  Associated conditioning infection
part of face
 Passage of 3 or more semisolid stools per
 Protruding abdomen composite of hypotonia of
day
abdominal muscles and the intestine; edema of the
 Inapparent respiratory infection :
abdominal wall
bronchopneumonia manifest as subnormal
 Edema is due chiefly to a lowering of the albumin
temperature or an increase in respiratory
fraction of the serum proteins
rate w/ few auscultatory sign
 Albumin is a protein made by the liver that
Laboratory data
keeps fluid from leaking out of blood
 Lowering of serum albumin level usually below 3 g/dl
vessels, nourishes tissue and transport
 Ratio of essential: non-essential amino acid is reduced to less than
hormones, vitamins, drugs, and substances
2.0. Normal: 3.0-6.0
like calcium
 This ration not lowered in marasmus
 Gross edema: serum albumin levels below  Urinary excretion of urea per gram creatinine is lowered
1.5 g/dl  Hydroxyproline per gram creatine is lowered in both
 Mild edema: above 2 g/dl  Glucose tolerance curves may be diabetic in type
  K deficiency is almost always present
 Serum cholesterol is low
 Diminished activity of pancreatic and intestinal enzyme (return to
normal shortly after onset of treatment)
 Anemia may be normocytic, microcytic, or macrocytic
 Bone growth is delayed
 GH may be increased
Prevention
 Adequate feeding
 Early diagnosis
 Control of infectious diseases
 Good physical hygiene and environment condition
Treatment
 Recovery observed after 2-3 weeks of treatment
 Hospitalization desirable or 1 to 3 mos or more for
desirable recovery
 High calorie, high protein diet
 Note presence of hypovitaminosis A; assess if dehydration is
present
 Acute phase (first week)
 Child is stabilized (treat dehydration and infection)
 Feeding started as soon child is no longer dehydrated
 To provide calories and proteins w/o
provoking vomiting and diarrhea
 Reduce risk of cardiac and liver failure,
possibility of lactose intolerance,
hypoglycaemia and hypothermia
 Full feeding when edema is lost and
appetite returns
 Rehabilitation phase
 High energy feeds are given for catch-up growth
 Caloric intake as high as 150-200 kcal/kg
 Child fed 4-6 times a day
 Recovery expected w/in 4-6 weeks
 Bacterial infection must be treated concomitantly w/ dietary
therapy
 Treatment of parasitic infestation may be postponed
until recovery is under way
Prognosis
 Most clinical manifestations are reversible
 Permanent impairment if malnutrition is severe and
occurs early in life (before 6 mos age)
 First 48 hrs after admission is critical
 Sudden endocrine failure, electrolyte imbalance,
hypoglycemia
PROTEIN EXCESS
 Led to signs of dehydration-protein fever
 Marasmic infants feed w/ high protein develop hyperammonemia
 Protein intoxication in children with liver disease
MORPHOLOGY. Central anatomic changes in PEM are:
1. Growth failure
 Marked in marasmus than in kwashiorkor
2. Peripheral edema
 In kwashiorkor NOT in marasmus
3. Loss of body fat and atrophy of the muscles
 In marasmus
*many hybrid forms share the feature of both
syndrome
 Fatty liver in kwashiorkor
 Small bowel in kwashiorkor
 Mucosal atrophy w/ loss of villi and microvilli and
disappearance of mitosis in the epithelium crypts
 Bone marrow in BOTH are often hypoplastic
 Depressed number od RBC precursor
 Anemia due to iron deficiency worsen by
intestinal worm; dieatary deficiency of folate
 Brain in infants of malnourished mothers show cerebral
atrophy during 1 to 2 yrs of life
VITAMIN DEFICIENCY
 Vitamins
 Organic compounds needed in small quantities found
in large variety of foods
 Serve as catalytic cofactors or prosthetic groups on
enzyme involved in metabolic rxn
 Fat soluble: A,D,E,K
 Water soluble:C and vit B complex
 Vitamins are stored to a slight extent in all the cells
 Some stored to major extent in the LIVER
 Vit A stored in liver may be sufficient up to
6 mos w/o any intake
 Water soluble vitamins is stored relatively slight
 Clinical symptoms of the deficiency can be
recognize w/in a few days
 Endogenous synthesis: Vit D, K, niacin, biotin
Vitamin A
Occurs in:
 Foods of animal origin as Vit A1 & Vit A2 or retinoids
 Retinol, retinal, retinoic acid
 These vit do not occur in foods of vegetable origin
 Vegetable foods as provitamin A
 These are yellow and red carotenoid pigments
 Provide 60% and above of the total vit A
 Utilization depends upon:
 Absorption- reduced if there is inadequate
fat in the diet
 Conversion to vit A in the intestinal mucosa:
b-carotene is the biological active;
absorption takes place in the small
intestine > converted to vi A ester in the
intestinal wall > pass to lymphatics >
bloodstream > stored in the liver > released
when needed
 Ingested carotenoids are nontoxic
 Yellow discoloration of the skin but not in
sclera
 Serum retinol level indicates vit A stores
METABOLISM:
 B-carotene partly absorbed in the intestinal lymphatics
 Remainder is cleaved into 2 molecules of retinol
 Retinyl ester hydrolyze to retinol in the intestine
 Retinol esterified inside the mucosal cell w/ palmitic acid and
stored into liver as retinyl palmitate
 Then, hydrolyze to free retinol for transport in site of
action
 As needed, esters are hydrolyzed; retinol
bound to specific retinol binding protein
(RBP) called transthyretin > transport in the
blood > to the cells > bind to membrane
RBP receptors > cytosolic RBP > transport to
nucleus
 Zinc is required for this mobilization
 Digestion and absorption of carotenes and retinoids require bile
salts, pancreatic enzyme concomitant fat; storage in the liver
 Normal plasma value infant: 15 and 30 microgram
Adult: 30 and 90 microgram
 Daily requirement infant & young children: 1000 IU or 300
microgram
Adults: 3000 IU
Nursing mother: 6000 IU
 Lack of vit A produces eye signs after 1-7 y/o
 Associated w/ diarrhea, measles, PEM and ascariasis
ETIOLOGY
Summarized as:
1. Poor storage of during fetal life
2. Absence of vit A in diet
3. Poor absorption of provitamin A
 4. Low intake of dietary fat and protein
5. Vit A excretion is increased in cancer, urinary tract disease
 Low vit A in liver at birth
 Rapidly increased by intake of milk
 Cow’s milk and breast colostrum are rich source
 Source of vit A: animal liver, kidneys, fat, human/cow’s milk,
butter, egg yolk, fish liver oils
 Provitamin A: yellow sweet potato, papaya, squash, carrots,
mangoes, tisa, orange, tomatoes, bananas, green leafy vegetables
 Deficiency associated w/ PEM (kwashiorkor)
 Loss in cooking, freezing and canning is minimal and do not alter
the Vit A to a significant extent
 Oxidizing agent destroy it
PATHOLOGY
Function of vit A:
 Maintenance of specialized, mainly mucus-secreting epithelia
 Include in the formation of muculopolysaccharides,
maintenance of lysosomal stability and synthesis of
protein
 Provision of critical prosthetic groups in the visual pigment in the
retina
 Enhancement of immunity
 Antioxidant function (carotenoids)
 Putative anticarcinogenic action (regulatory effect on cell growth)
2 photoreceptor system:
1. Rods: sensitive to light of low intensity; night vision
2. Cones: colors and light of high intensity; day vision
 Retinal is the prosthetic group of the photosensitive pigment in
both rods (rhodopsin) and cones (iodopsin)
 Both visual pigments differ in the nature of protein
bound to retinal
 Vitamin A (all-trans-retinol) is the precursor for the
formation of rhodopsin
 All trans-retinal isomerizes in the dark to 11-cis-form
 Combines with opsin to form rhodopsin
 Rhodopsin + light:reconverts 11-cis-retinal
back to all trans-retinal
 Energy exchange, transmitted via the optic
nerves to the brain resulting in visual
sensation
 During dark adaptation, some of the all trans-retinal is
reconverted to 11-cis-retinal, but most is reduced to
retinol and deposited in the retina.
 Delayed if vit A serum is low
Vitamin A in night vision
1. In order for rhodopsin to be formed, vit A MUST be converted to
11-cis-retinal. This occur in two ways:
 All-trans-retinol (isomerisation) > all-cis-retinol
(oxidation) > 11-cis-retinal
 All-trans-retinol (oxidation) > all-trans-retinal
(isomerisation) > 11-cis-retinal
2. 11-cis-retinal + opsin = rhodopsin
3. Rhodopsin + light: reconverts 11-cis-retinal back to all trans-
retinal
 conformational change also occurs in the opsin fragment to
form metarhodopsin II, which is the activated form of
rhodopsin
 The metarhodopsin II then stimulates transducin, a G-
coupled protein
  This activation of transducin causes an activation in cGMP
phosphodiesterase, which will remove the cGMP mediated
activation of cGMP-gated channels that are letting Na+ ions
leak into the rod cytoplasm, resulting in a hyperpolarization
of that rod cell
  Thus, in the presence of light, the blockage of
Na+ movement into the rod cell will result in a
hyperpolarization of that rod cell which then allows
messages about light being seen during night vision to be
sent to the brain.
Clinical manifestation
Eyes sign
 Principal manifestation are in the eye
 Early symptoms is nyctalopia or night blindedness,
inability to see in dim lights
 Later there is photophobia, so that eyelids are kept
firmly closed
 First clinical sign is xerosis conjunctivae
 Thickening, loss of luster producing frequent blinking
 Bitot’s spots may form- well demarcated, superficial,
dry, grayish, silvery or chalk-like, foamy plaques usually
triangular or irregularly circular in shape, lateral to the
cornea
 Next stage is xerosis or xerophthalmia
 Replacement of normal, moist corneal conjuctival
surfaces by nonsecretory squamous, keratinizing
epithelium
 “dry eye”
 Cornea is hazy or opaque, w/ bluish milky appearance
 Later, corneal ulcers- develop in the form of small
erosions
 Then, keratomalacia- cornea becomes soft and
gelatinous
 Irreversible blindness
Skin sign
 Xerosis of the skin w/ desquamation or scaling
 Follicular hyperkeratosis or phrynoderma in the back of the
hands, thighs and buttocks
 Squamous metaplasia of specialized epithelium
 Some epithelia are less severely affected than others
 In intestine, loss of mucus-secreting cells
but no squamous replacement
 Squamous metaplasia is pronounced in cornea and
conjunctiva, upper respiratory tract, urinary tract,
pancreatic and salivary glands
 Respiratory tract:loss of mucociliary
escalator predispose to respi infection
 Urinary tract: nidus for stone formation
 Pancreas and salivary gland: secretory
obstruction and infection
 Sebaceous and sweat gland: cause follicular
hyperkeratosis and predispose to acne
 Increased intracranial pressure w/ wide separation of cranial
bones at the sutures may occur
Diagnosis
 Dark adaptation test
 Plasma carotene concentration falls quickly; retinol decreases
slowly
 Examination of the scrapings from the eye and vagina is
recommended as diagnostic aid
Prevention
 For prophylaxis:
 Infant <12 mos: 55 mg retinol palmitate or 33 mg
retinol acetate (100,000 IU) as liquid or capsule at 6
mos interval
 Older children: 110 mg retinol palmitate or 66 mg
retinol acetate (200,000 IU); capsule or liquid; 4-6 mos
interval
 In vit a prevalence area: 100,000 IU; orally; every 3
mos or 250,000 IU orally evry 6 mos
  Low-fat diets should be supplemented  Cause degeneration of myelin sheath in the
 Water-miscible preparation in amounts severl times the dly peripheral and nervous system
requirement in disorders q/ poor absorption; including the  Polyneuritis: pain radiating along the
premature peripheral nerves
Treatment  Paralysis if severe deficiency
 110 mg retinol palmitate or 66 mg retinol acetate (200,000 IU)  Thiamine and Cardiovascular system
orally OR 55 mg retinol acetate (100,000 IU) IM  Weakens the muscle: heart muscle
 Following day, 110 mg of retinol palmitate or 66 mg retinol  Severe deficiency develops cardiac
acetate (200,000 IU) orally failure
 Another 200,000 IU given oraly if clinical deterioration occurs 2-4  Right side of the heart greatly
weeks later enlarged
 Return of blood to the heart increased
Hypervitaminosis A 3x as normal
 Intoxication results ingesting 300,000 IU or more in single  Deficiency causes peripheral
dose or more thn 50,000 IU/d for several mos vasodilation as a result of metabolic
 Vomiting, drowsiness or irritability deficiency in the smooth muscle
 Bulging of anterior fontanel, diplopia (double vision) and  Peripheral edema and ascites occur
papilledema ( increased pressure in or around the brain with major deficiency
causes the part of the optic nerve inside the eye to swell)  Due to high output
 Serum Vit A range from 20 to 1000 IU/dl  Decreased renal blood flow
 Normal: 50 to 100 IU per Dl leads to vasoconstriction in
 Chronic hypervitaminosis A the vascular bed of the
 Anorexia, pruritus (severe itching), irritability, kidney and retention of salt
tender swelling of the bone w/ limitation of & water
motion  Thiamine and GI tract
 Lack of weight gain  Indigestion, severe constipation, anorexia, gastric
 Skin lesions atony, hyperchlorhyria
 Craniotabes and hyperostosis of the long bones  Overall picture of thiamine deficiency includes, polyneuritis,
 Hepatomegaly and hypercalcemia cardiovascular symptoms, gastrointestinal disorders
Prognosis
 Disappear w/ discontinuing intake Clinical manifestation
2 classifications:
Vitamin B1 (Thiamine) 1. Dry and wet types
Beriberi  Dry
 Operates in the metabolic systems of the body principally as  Peripheral nerves
thiamine pyrophosphate  Appear well but is pale, listless,
 Function as cocarboxylase in conjunction w/ cyanotic and dyspneic
protein decarboxylase for decarboxylation of  Neuritis is observed in older and
pyruvic acid and other a-keto-acids adults
 Thymine hydrochloride  Impairment of motor power follows:
 White crystalline substance flaccid paresis, foot drop, muscular
 Destroyed by heat in neutral or wasting and lateral muscular paralysis
alkaline solution  Heart rate is rapid and liver enlarge
 Thymine deficiency decrease utilization of pyruvic  Wet
acid  Edematous, pale, malnourished,
 Deficiency results in accumulation of dyspneic with vomiting and
pyruvic acid in the tissues tachychardia
 Thymine needed for final metabolism of  May have an acute onset in healthy
carbohydrates and proteins older and adult doing heavy work
 Body stores limited amounts; kidney has no  Heart
known threshold and spill large doses of thymine  Both types occur among women before and after delivery
in urine when rice is the main food eaten and in alcoholics
 Easily destroyed by heat in neutral or alkaline media  Person w/ beriberi complaints of excessive fatigue,
 Polished rice, white flour, white sugar contains little palpitation on exertion and shortness of breath
 Antithiamine: raw, freshwater fish, strong tea and coffee,  Hoarseness or aphonia due to paralysis of the laryngeal
factors in myoglobin and haemoglobin nerve is a characteristic sign
 Reserves are limited and found in: skeletal muscle, heart,  Heart sound exaggerated w/ systolic murmurs and full-
liver, kidney, brain bounding pulse is felt
 2 mechanism of absorption: 2. Three overlapping syndrome
 Passive: when at high concentration  Acute cardiac- 2-4 mos
 Active: when at low concentration  Predominantly cardiovascular in
Pathology nature
The major targets are: heart, peripheral nerves, brain  Aphonic- 5-7 mos
 Thiamine deficiency and CNS
 Hoarseness, dysphonia or aphonia
 CNS depends most entirely on the metabolism of
 Pseudomenigeal- 8-10 mos
carbohydrate
 Apathy, drowsiness, signs of
 Decreased as much as 50-60% in
menigneal irritation and even
thiamine deficiency
unconsciousness
 Neuronal cells frequently show  Found in purely breast-fed infants where mother’s diet is
chromatolysis and swelling that deficient in thiamine
disrupts communication in CNS  General symptoms:
 Thiamine is required for the synthesis of  Excessive crying and screaming
acetylcholine  Vomiting
  Constipation
 Loss of ankle and knee jerk Clinical manifestation
 Calf muscle tenderness  Pellagra may start w/ anorexia, weakness irritability, numbness
 Cardiovascular dysfunction and dizziness
 Edema  Classical picture is triad: diarrhea, dermatitis, dementia
Diagnosis  Feces is pale, foul milky, soapy or at times steatorrheic
 Therapeutic test w/ parenteral thymine  The most characteristic manifestations are cutaneous
 Improves acute cardiac type  Symmetric erythema of the exposed surface that may
 Less striking in aphonic and pseudomenigeal resemble as sunburn
 Elevated blood lactic and pyruvic acid after oral load of glucose  Pellagrous glove: lesion of the hand
 Decreased red cell hemolysate tranketolase  Pellagrous boot: “ on the foot and leg
 High blood/urinary glyoxylate  Casal necklace: around the neck
Diagnosis
Prevention  Difficult to distinguished between pellagra and kwashiorkor
 Infants: 0.4 mg  Urinary levels of N-methyl-nicotinamide are low or absent
Older children: 0.6 to 1.2 mg Prevention
Adults: 1.0 to 1.3 mg  Infants & children <10 y/o: 6-10 mg
Nursing mother: 1.5 mg Older: 10-20 mg
 Thymine requirement increased w/ high carbohydrate diet Treatment
 Cereals, peas , nuts, beans, yeast, green vegetable, roots, fruits,  Diet rich in vit B complex plus 50 to 300 mg of niacin daily
dairy products  Skin lesions treated w/ lotions and protected from irritants
 Pork > beef/lamb (thymine content)  Large doses of niacin is followed by local heat and flushing and
 Improve milling and cooking burning of the skin; may cause cholestatic jaundice or
 Excessive cooking destroy hepatotoxicity
 Sun exposure should be avoided
Treatment
 Daily oral administration of 10 mg for children; 50 mg for adults Vitamin B6 (Pyridoxine)
for several weeks  Vitamin B6 groups:
 Supplementing vit b complexes  Pyridoxine
 Pyridoxal
Vitamin B2 (Riboflavin)  Pyridoxamine
 Present in heat-stable fraction  Pyridoxic acid is metabolic end product
 Yellow crystalline slightly soluble in water but not in fats  Pyridoxal phosphate is a coenzyme involved in:
 Stable to heat and acids; destroyed by alkaline and exposure to  Transamination
light  Deamination
 Act as coenzyme of flavoprotein important in amino acid, fatty  Decarboxylation
acid and carbohydrate metabolism and cellular respiration (FAD)  Racemisation
 Also needed in the eye for light adaptation  Act as coenzyme in the metabolism of glycogen and fatty acids
 Absorption in the intestine  Necessary for the breakdown of kynurenine
 Impaired in achlorydia, diarrhea, vomiting  Appearance of xanthurenic acid if does not occur
 Utilization is great w/ increased metabolism  Important for normal neuronal function and activity
 Storage is limited; excess excreted in urine  Deficiency upsets cerebral metabolism and causes
convulsions
Clinical manifestation  Other clinical condition includes: anemia, hyperemesis gravidum,
 seldom encountered w/o manifestation of other vit B complex cardiac decompensation, etc.
deficiency Etiology
 suggestive signs: angular stomatitis, cheilosis (inflammation and  Pyridoxine is lost from refining, process, cooking and storing
cracking at the angles of the mouth), glossitis, atropic lingual,  Pyridoxine dependency
fissuring of the tongue  Mothers who took pyridoxine supplements for
 skin lesion vomiting during pregnancy develop increase
 ocular sign: photophobia, blurred vision, itching of the eyes, pyridoxine requirement
lacrimation and corneal vascularisation  Antagonism between isoniazid (INH) and pyridoxine
Diagnosis  Nerve tissue and tryptophan metabolism seems to be
 urinary riboflavin and RBC riboflavin test affected
 urinary excretion below 30 microg/24 hr  Those with anti-TB plus INH requires greater
Prevention pyridoxine
 infants and children <10 yrs: 0.6-1.4 mg  Peripheral neuritis produced by INH is not common in
>10 yrs: 1.4-2 mg/day children
Adults: 0.025 mg/gm of protein Clinical manifestation
 eggs, liver, other organs, fish, mil, legumes, green leafy vegetable  Affects skin, mucous membrane, nerve tissue and
Treatment reticuloendothelial system
 2.5 mg orally daily w/ other vit B complex  4 clinical disturbances:
 Convulsion in infants
Vitamin B3 (Niacin)  Peripheral neuritis
 Forms part of 2 enzymes important in ETC and glycolysis (NAD  Dermatitis
&NADPH)  anemia
 Pellagra is the disease caused by low in niacin and/or tryptophan  Irritability, depression, somnolence
 Related to excessive corn consumption especially when stored for  Skin and mucuous membrane lesions
a longer time  Infection respond poorly to antibiotics in vit B deficient
 niacin present in corn is BOUND resulting in nicotinic
acid deficiency
 Human can’t synthesize; depend on exogenous sources
Diagnosis
  Infants with convulsion is suspected with vit B3 deficiency or  Found only in collagen
dependency if:  Made from reaction of proline plus ascorbic acid
 common causes of seizures like hypoglycaemia,  Defect in collagen in vit A deficiency
hypocalcemia, infections has been ruled out  Hemorrhagic tendencies
 if seizures stop after injection of 100 mg pyridoxine, vit  Defective dentin
B6 should be suspected  Loosening of teeth
 Tryptophan load test  Osteoid no longer formed
 Give 100 mg of tryptophan per kg body weight  Endochondral ossification stops
 Large amount of xanthurenic acid is a manifestation  Bones become brittle and fracture easily
Prevention  Subperiosteal haemorrhages w/ lifting of the
 Infant:0.1to 0.5 mg periosteum especially at ends of femur and tibia
Child: 0.5 to 1.5 mg
Adult:1.5 to 2.0 mg Clinical manifestation
 Found in meat, liver, kidney, peas, soybeans, grains  Early stages present vague symptoms
Treatment  Irritability
 100 mg IM for seizures  Progress w/ painful immobile legs
 For pyridoxine dependency: 2.10 mg IM or 10-100 mg (pseudoparalysis)
vit B6 orally  Infant scream when approached
Vitamin B7 (Biotin)  Legs edematous;in “frog-like position” with
 Deficiency is rare; found in those consuming avidin, a biotin occasional mass felt at the distal end of the
antagonist found in raw egg white femur
 Water soluble that act as cofactor for all carboxylase in the body  Digestive disturbance
 Dietary biotin is bound to protein; free biotin is generated in the  Anorexia
intestine  Gums are bluish-purple, swollen and completely conceal teeth
Etiology  Bleeding gums do not occur in the absence of teeth
 Deficiency following avidin ingestion  Scorbutic rosary
 Deficiency appeared to those receiving nutrition parenterally and  Sternum is depressed
infants whose mothers are deficient  More angular w/ sharp angulation
 Rachitic rosary (in rickets)
Clinical manifestation  Smooth and rounded
 Brawny dermatitis  Nodularity at the costochondral junction
 Somnolence  Low grade fever and anemia usually present
 Hallucination  Delay in wound healing and impaired growth and dev
 Hyperesthesia: excessive physical sensitivity, esp of skin
 Accumulation of organic acid Diagnosis
 Roentgenographic findings in long bones
Diagnosis  X-ray changes prominent in knees
 Elevated organic aciduria  Simple atrophy of the bone in early stages
 Trabeculae not distinguish & w/ ground
Prevention and treatment glass appearance
 Biotin content in parenteral solution  Cortex reduced to thickness (pencil point
 10 mg oral administration thinness)
 White line of frankel is irregular &
Vitamin B12 (Cobalamin) thickened representing zone of calcification
 Helps in the production of RBC  Zone of rarefaction under the white line
 Vit B12 deficiency makes the body produce larger than normal  Subperiosteal haemorrhages not seen and
RBC describes as megablastic or macrocytic assumed dumbbell shaped; hemorrhage
 Most common cause is pernicious anemia: autoimmune condition occurs at both ends not in the middle
caused by lack of protein called intrinsic factor that is need for the  Ascorbic acid concentration of the buffy layer of centrifuged
absorption of vit B12 oxalated blood is more accurate test
 Zero in scurvy
Vitamin C (Ascorbic acid)  Diminished excretion of vit C after loading test dose demonstrate
Scurvy deficiency
 Found in guava, papaya, citrus; green leafy vegetables like
tomatoes, fresh tubers Differential diagnosis
 Absent in cereals, most animal products and canned milk  Chronic gingivitis and pyorrhoea
 Small intestine absorptive capacity is limited  Bleeding of gums with associated pus
 Powerful antioxidant & reducing agent  Respond to good dental hygiene not on ascorbic acid
 Easily oxidized and destroy by heating therapy
 Participate in collagen metabolism, biosynthesis of  Poliomyletis
neurotransmitters, carnitine biosynthesis, immune function  Produce flaccid paralysis
Etiology  Absent tenderness of extremities
 Seen at any age but common between 6 and 24 mos  Syphilis
 Breastfed babies rarely suffer  Pseudoparalysis is early manifestation
 Breast milk contains 4 to 7 mg/dl  Look for other signs of this diseases
 Scurvy may develop if mother’s diet lack vit C  Roentgenogram helps differentiate from scurvy
 Clinical findings:  Rheumatic fever
 Gingivitis and bleeding gums (but can be attributed w/  Rare under 2 years
poor oral hygiene)  Supportive arthritis and osteomyelitis
 Improper cooking produced significant loss of vit C.  Should be considered because of tenderness of limbs
and pain when moving
Pathology  Pyogenic infection
 Hydroxiproline  Should have a positive blood culture
  Blood dyscrasias  Vitamin D2 (calciferol)
 Suspected because of bleeding manifestation  Entirely artificial product prepared by irradiating
 Blood examinations help rule out ergosterol
 Rickets
 Because of rosary

Prevention and treatment

 Infant should receive vit C supplements starting from 2nd week of
life
 At least 50mg for lactating mothers
 30mg daily intake for all age levels
 Treatment consist of administration of 200 to 500 mg daily of
ascorbic acid or 100-150 ml fruit juice

Vitamin K
 Abundant in pork, liver, soybean, green leafy vegetables
 Cow’s milk has more Vit K than human milk
 Vit K1- natural
 Participates in oxidative phosphorylation
 Synthesize by intestinal microorganism
 Required for normal clotting of blood; vit K-dependent clotting
factors made in the liver are:
 Prothrombin (except factor V)
 Factor VII, IX, X
 Hypoprothrombinemia
 Usually regarded as synonymous w/ vit K deficiency
but limited to depletion of prothrombin and factor VII
if there is vit K deficiency
 Prothrombin time test
 Most useful test for vit K deficiency
 Normal level excludes vit K deficiency
Etiology
 Dependent of supply prenatally
 After birth source no longer available
 Intestinal flora not yet adaptive
 Vit K required to prevent neonatal decline of vit K-  Food source of vit D is not as important
dependent clotting factor
 Exclusively breastfed have low vit K compared to formula milk
 Administration of antibiotics inhibits intestinal flora,decrease vit K
 Coumarin anticoagulant act as antimetabolites for
normal vit K utilization
 Salicylates
 Infants born to mothers using anticonvulsant
Clinical manifestation
 Hemmorhagic manifestation
 Bleeding from the cord and circumcision site
 Anemia and shock from severe loss
Prevention and treatment
 4 requirements:
 Normal bile composition in the GI tract
 Adequate vit K diet
 Absorptive capacity of small intestine
 Functioning liver capable of synthesizing those blood clotting
factors
 Water miscible natural vit K administered orally or parenterally
 More rapid than synthetic
 Excessive intake should be avoided because of
haemolytic action and tendency to cause
hyperbilirubinemia and G-6-PD
 Early vit K prophylaxis
 0.5-1.0 mg: single parenteral dose
1-2 mg: single oral dose & infants w/ mild prothrombin deficiency
5 mg: severe, daily

Vitamin D
Rickets
 Vitamin D or D3
 Produced from irradiation of the provitamin, 7- Pathology
dehydrocholesterol which is predominantly animal  Rickets
sterol and rarely found in vegetable foods  Retardation or suppression of normal growth of
 Natural vitamin D present only in egg yolk, fish-liver epiphyseal cartilage and of normal calcification
oils, fish-body oils, small quantity in cow’s and human  Decrease in the calcium and phosphorus for
milk mineralization
  Result is frayed, irregular epiphyseal line at
the end of the shaft
 Failure of normal mineralization of osseous and
cartilaginous matrix
 Zone of calcification fails to mineralize
 Newly formed uncalcified osteoid is
deposited resulting in a wide, frayed zone
of nonrigid tissue
 This becomes compressed and bulges
producing flaring of the ends of the bones
and the rachitic rosary
Chemical pathology
 Normal inorganic serum phosphorus: 4.5-6.5 mg/dl
Rachitic infants: 1.5-3.5 mg
 Normal phosphatase: 5 and 15 Bodansky units per 100 mL
Mild rickets: 20 to 30
Severe: 60
Clinical manifestation
 Craniotabes, caput quadratum (head appears like box), soft
border anterior fontanel, rachitic rosary
 Developmental delay such as sitting, standing, walking
 Children above 2 y/o:
 Bowing of lower extremities
 Thick ankles
 Widened wrist
 Knock-knees
 Pronated feet
 Protruding abdomen
 Flabby muscles
 Harrison’s groove- horizontal groove on the posterior
border of thorax
 Pigeon’s breast deformity: sternum and adjacent
cartilage appears to be projected forward
 Slight ot moderate degree of lateral curvature
(scoliosis), kyphosis may appear, lordosis (excessive
inward curve of the spine) may be seen
 Relaxation of ligaments help to produce deformities
 Muscles are poorly developed and lack tone
 Result to delayed standing and walking
 Potbelly bec of weakness in abdominal
muscle, gastric and intestinal wall
Diagnosis
 Serum calcium level may be normal or low
 Parathyroid hormone is secreted when slight calcium
in the blood thus concentration is maintained
 Serum phosphorus below 4 mg/dl
 Because parahormone decreases reabsorption in the
kidney
 Serum alkaline: usually elevated
 Due to increased osteoblastic activity
 X-ray examination shows
 rachitic rosary
 cupping and fraying of the proximal ends of long bones
 not visible epiphyseal plates
 humeral ossification barely vizualized
 shaft is osteoporotic and coarse texture
 Ca and Ph homeostasis depend on the intestinal absorption
 Maximum Ca absorption when calcium phosphorus
ration in diet is 2:1
 Inc phosphate decrease Ca absorption
 Acidity inc Ca absorption
 Inc Ca absorption when lactose is dietary sugar
 Chelating agents and phytates of cereals decrease Ca
absorption
 Dietary Fe may decrease absorption of phosphate
 High stearic and palmitic decrease Ca absorption
 Urinary cyclic AMP is elevated
 Serum 25-hydroxycholecalciferol level is decreased
Complication
 Bronchitis and bronchopneumonia are common
 Pulmonary atelectasis associated w/severe deformities in chest’
 anemia
Prognosis
 heal spontaneously as more sun exposure
Treatment
 100 mg (4000 IU) daily
 Fish-liver oil, artificial irradiation, sunbathing
Vitamin E
 Anti-oxidant that may involved in nucleic acid metabolism
 Diets high in unsaturated fatty acid increase Vit. E requirement
 Excess Fe administration exaggerates sign of vit E deficiency
Clinical manifestation
 Creatinuria, ceroid deposition in smooth muscle, muscle weaknes
 Vit E deficiency has been suggested as a causative factor in the
anemia of kwashiorkor
Diagnosis
 If vit E has been recently administered, after 3 days before
determination of blood levels since oral vit E circulate for 1-2 days
OBESITY
 Is not a disease in itself
 Or overnutrition is the accumulation of fatty subcutaneous tissue
 Overweight
 10% or more above the desirable weight
standard
 Increased body size w/o increased body fat
but increased lean body mass
 Obese
 20% or more above the desirable weight
 Excess accumulation of body fat
 Childhood obesity occurs in a minority of obese adult
 It is not a predictor of obese adult
 Probability of an obese child to become obese adult
decreases with greater time intervals between onset of
obesity and adulthood
 But increases w/ severity of childhood obesity, onset in
adolescent and familial obesity
 Weight-for-age percentile is unsatisfactory measurement for
obesity
 BMI is the most useful index
 Resistant to insulin resulting in increased levels of circulating
insulin
 Insulin decreases lipolysis and increase fat synthesis
and uptake
 During a carbohydrate meal obese respond w/
increased insulin and decreased free fatty acid
utilization
 During weigh-reduction regimen, obese delivers less
food to his cells, owing to decreased mobilization of
free fatty acid
 In starvation, fat is mobilized as insulin level decreases
 Protein is facilitated as brain utilizes ketone
for energy
 Serum alanin decrease, glycine level rise
 Purified sugars and high protein diets may cause greater secretion
of insulin than do complex carbs
Etiology
 Due to excessive intake of food compares to its utilization, rather
than massive overeating
 Other factors like genes, psychic disturbance and insufficient
exercise
 Endocrine and metabolic disturbances
Clinical manifestation
 Appears most frequently in first yr of life, late childhood (5-6 y/o)
& adolescent but may be evident at any age
 Features appear disproportionately fine
 Small nose and mouth w/ double chin
 Adiposity in mammary gland of males
 Abdomen pendulous w/ white or purple striae
 Puberty may occur early
  External genitalia in boys appear disproportionately
small
 External genitalia of females are normal and menarche
is not delayed
 Greater obesity in upper arms and thigh
 Hands relatively small and tapering
 Taller and bone age is advance
 Genu valgum or “knock-knee” is common
Treatment
 Decreasing energy intake and increasing energy output
 Prescribing a restrictive diet will most likely to fail
 Surgery, pharmacotherapy and gastric balloons are
contraindicated in children
 Very low-calorie diets are inappropriate because they may impair
growth and development
 Maintenance of weight during growth spurt (there is a reduction
of weight during the growth spurt in adolescent)
 Screening program cannot support identification of childhood
obesity