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1
KWASHIORKOR MARASMUS
HYPO VITAMINOSIS AND HYPER VITAMINOSIS
DR.ARUN VDEPT. OF ORAL AND MAXILLOFACIAL SURGERY
2
MALNUTRITION
A pathological state due to a relative or absolute deficiency or excess of one or more essential nutrients; clinically manifested or detected only by biochemical, anthropometric or physiological tests.
3
CLASSIFICATION
1.Undernutrition: Marasmus2.Overnutrition: Obesity,Hypervitaminoses3.Specific Deficiency:
Kwashiorkor,Hypovitaminoses, 4.Mineral Deficiencies5.Imbalance: Electrolyte Imbalance
4
Marasmus: weight for age < 60% expected
Kwashiorkor: weight for age < 80% + edema
Marasmic kwashiorkor: wt/age <60% + edema
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Kwashiorkor
Cicely Williams – 1933 Sickness of deposed child
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Between 1-3 yrs oldEtiology:Very low protein intake - following
abrupt weaning. In places where starchy foods are
main staple
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Clinical Manifestations:A. Diagnostic Signs
1. Edema2. Muscle wasting3. Psychomotor changes
B. Common Signs1. Hair changes2. Diffuse depigmentation of skin3. Moon face4. Anemia
C. Occasional Signs:1. Flaky-paint rash2. Hepatomegaly
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Bio chemical and Laboratory findings:
1. Decreased serum albumin2. Potassium deficiency – due to diarrhea
3. Iron & folic acid deficiencies4. Liver biopsy - fatty changes or fibrosis
may occur
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Ketonuria , aminoaciduria , Increased levels of G.H., epinephrine
and steroid .
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Marasmus
Means “to waste”
Common in the 1st year of life characterized by emaciation. Marasmus represents the end
result of starvation where both proteins and calories are deficient.
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Marasmus - an adaptive response to starvation, whereas kwashiorkor represents a maladaptive response to starvation
In Marasmus the body utilizes all fat stores before using muscles
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Etiology
lack of breast feeding and the use of dilute animal milk.
Poverty or famine and diarrhoea Ignorance & poor maternal
nutrition are also contributory
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Clinical Features
1. Weight for age < 60% expected2. Wasting of muscles and s/c fats3. Growth retardation4. Old man’s face5. Mental changes6. No edema7. Diarrhea8. Dry atrophic skin
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low creatinine Hypoglycemia Decreased to normal albumin Normal serum potassium
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Complications of PEM
Hypoglycemia Hypothermia Hypokalemia Hyponatremia Heart failure Dehydration & shock Infections (bacterial, viral &
thrush)
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Marasmic kwashiorkor
State intermediate between marasmus &kwashiorkor when a previously marasmic child develops edema due to higher nutritional requirement
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Treatment
Step1:emergency phase:during 1st 24-48hr A.hypothermia due to less subcutaneous
fat, :gradual warming with blankets B.infection:emperical anti biotics C.hypoglycemia: should be treated D. dehydration : i.v fluid
Step 2 : dietary support
3-4 g protein & 200 Cal /kg body wt/day + vitamins & minerals
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Vitamins
Fat soluble Vitamin A Vitamin D Vitamin E Vitamin K
Water soluble Non B complex – Vitamin C B complex
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Vitamin A
Fat soluble Present in foods of animal origin Pro vitamin beta carotene – found in plants
Retinol Retinal Retinoic acid Beta carotene
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RDA : 3500 IU for men & 2500 IU for women
Sources : Liver, Kidney, egg yolk, milk, cheese, fish liver oil
Yellow and dark green vegetables, carrots , spinach, pumpkin, mango, papaya
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functions
Vision – rhodopsin cycle or Wald’s visual cycle
Protein synthesis Epithelial tissue health Immune system function Carotenoids – anti oxidant Transferrin – iron transport protein
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Hypo Vitaminosis A
Eyes : Night blindness (nyctalopia) Xerophthalmia Bitot’s spots – white triangular plaques
in certain areas of conjunctiva Keratomalacia – destruction of cornea
due to prolonged xerophthalmia and can even lead to blindness
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Hypo Vitaminosis A
Growth : Growth retardation Impaired skeletal formation
Reproduction : Degeneration of germinal epithelium in males
Skin and epithelium: Rough and dry skin Keratinization of epithelial cells of GIT, urinary
tract and respiratory tract(squamous metaplasia) Increased susceptibility to infections
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Hypervitaminosis A
Dermatitis Enlargement of liver Skeletal decalcification Tenderness of long bones Loss of weight Loss of hair Joint pain
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Vitamin D
Anti rachitic vitamin Sun shine vitamin Calciferol
Ergo calciferol (D2) – plant sources Chole calciferol (D3) –animal sources
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7 dehydrocholesterol is converted to chole calciferol on exposure to sunlight
hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol
Concentration of 1,25 DHCC regulated by plasma levels of calcium and phosphate
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Milk, fatty fish and eggs
RDA – 200 – 400 IU
32
Functions
Intestine: Increases calcium binding protein Phosphorus ions absorption through
specific phosphate carrier Alkaline phosphatase (AP) synthesis Muscles
Tonicity and the normal contraction of the muscles
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Functions
Promotes renal calcium re-absorption Stimulates renal phosphate absorption Calcium homeostasis: together with
PTH it mobilises calcium from skeletal stores
In the osteoblasts stimulates calcium uptake and aids in Mineralisation of the growth plate & osteoid
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At risk populations Breastfed infants Older adults People with limited sun exposure
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Deficiency
Rickets Osteomalacia Osteoporosis
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Rickets
Most common during the first year of life.
The first signs of hypocalcaemia are CNS changes- excitation, restlessness, excessive sweating, tremors of the chin and extremities.
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Rickets
Skin and muscle changes- pallor, occipital alopecia, fragile nails and hair, muscular hypotony, motor retardation.
hypocalcemia and hypophosphatemia.
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ACUTE SIGNS
Craniotabes –osteolyses detected by pressing firmly over the occipital or posterior parietal bones,a ping-pong ball sensation will be felt.
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SUBACUTE SIGNS
frontal and temporal bossing False closure of sutures ,in the X-ray
craniosynostosis is absent.
Maxilla in the form of trapezium, abnormal dentition.
Late dental evolution, enamel defects in the primary and permanent dentition.
40
In the chest, knobby deformities results in the rachitic rosary along the costochondral junctions.
The weakened ribs pulled by muscles also produce flaring over the diaphragm, which is known as Harrison groove. The sternum may be pulled into a pigeon-chest deformity
41
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Sub acute signs
Spinal column- scoliosis, kyphosis.
Extremities- bowlegs or knock kness legs.
Deformities of the spine, pelvis and legs result in reduced stature, rachitic dwarfism.
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At the ankle, palpation of the tibial malleolus gives the impression of a double epiphysis (Marfan sign).
greenstick fracture of long bones
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LABORATORY DATA
Decreases in serum calcium, serum phosphorus,, calcitriol, urinary calcium.
Parathyroid hormone, alkaline phosphatase,urinary phosphorus levels are elevated.
46
R/F
1. Osteoporosis of clavicle, costal bones, humerus.
2. widening of the distal epyphysis, fraying and widening of the metaphysis, and angular deformities of the arm and leg bones.
3. Thinning of the cortex, diaphysis and the cranial bones
47
48
Types of Rickets
Nutritional
Nutritional rickets results from inadequate sunlight exposure or inadequate intake of dietary vitamin D, calcium, or phosphorus
49
Vitamin D dependent
Vitamin D-dependent rickets, type I is secondary to a defect in the gene that codes for the production of renal 25(OH)D3-1-alpha-hydroxylase.
Vitamin D-dependent rickets, type II is a rare autosomal disorder caused by mutations in the vitamin D receptor. Type II does not respond to vitamin D treatment; elevated levels of circulating calcitriol differentiate this type from type I
50
Vitamin D resistant
Rickets refractory to vitamin D treatment
Hereditary in nature also known as familial
hypophosphatemic rickets. Normal levels of calcitriol are
found in this disorder.
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1-2% of calcium chloride in milk- 4-6g/day for the first 2 days; after that
1-3g/day continued for1-2wk.
52
1 STAGE
VITAMIN D –2000 IU OD 30 DAYS
2 STAGE
VITAMIN D –3500 IU OD 40 DAYS
3 STAGE
VITAMIN D –- 5000 IU OD 45 DAYS
Then prophylactic dose – 500 IU till the end of the second – third year of life
53
HYPERVITAMINOSIS D
hypotonia, anorexia, vomiting, irritability, constipation, polydipsia, polyuria, sleep disorder, dehydrationJoint & muscle painsDisorientation & coma.renal damage and calcification
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VITAMIN E
Alpha Tocopherol Naturally occuring anti oxidant
Prevents oxidation of RBC Prevents sterility Increases synthesis of heme Helps in storage and synthesis of creatine,
nucleic acids etc Anti cancer vitamin- prevents free radical
formation
55
Increased vitamin E intakes associated with decreased risk of coronary heart disease
Vitamin E delayed or minimized cataract development
Increased vitamin E intakes or blood levels associated with reduced risk of Alzheimer’s disease
56
Vegetable oils Almonds Meat Milk butter
RDA : 10 mg per day
57
Hypovitaminosis E
Neurological symptoms – impaired coordination
Muscle degeneration & weakness Increased risk for sterility Increased fragility of erythrocytes
Hyper vitaminosis E - least toxic vitamin and hence rarely causes overdose effects
58
Vitamin K
German word Koagulation
Phylloquinone: Green leafy vegetables Menaquinone: Intestinal bacteria
Intestinal bacterial synthesis meets the daily requirement of vitamin K even without dietary supplement
Menadione: synthetic form
RDA – 70-120 ug/ day
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Functions
Coenzyme for the synthesis of prothrombin and blood clotting factors VII, IX,X in the liver
carboxylation of glutamic acid residues on vitamin K-dependent proteins. involved in:
1) Coagulation2) Bone Mineralization and 3) Cell growth
60
Deficiency
Uncommon. seen in breast fed infants – can lead
to hemorrhagic disease of new born
long-term antibiotic treatment (loss of colonic bacteria).
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Hemorrhagic disease of the newborn
Bruising tendency, ecchymotic patches
Gingival bleeding, epistaxis, hematuria, melena
Post-traumatic bleeding / internal bleeding
Prolonged prothrombin time
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Osteoporosis due to failed carboxylation of osteocalcin and decreased activity of osteoblasts
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Vitamin C
Ascorbic acid Not synthesized by human body
citrus fruit and juices ( lemons, oranges, peaches, strawberries etc)
Also in cabbage, broccoli, cauliflower, leaf lettuce, tomatoes, potatoes, and beans.
90-100 mg/day
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Protects against immune system deficiencies, cardio vascular disease, prenatal health problems, eye disease, and skin wrinkling.
Helps form collagen in bones, cartilage, muscle, and blood vessels.
Helps in wound healing Helps absorb iron.
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Deficiency –Scurvy Early Symptoms
Appetite loss, weight loss, diarrhea, rapid breathing, fever,
irritability, bleeding, and feeling of numbness
Progressed Symptoms
Bleeding of the gums, loosened teeth, petechial hemorrhage of
the skin and mucous membranes, bleeding in the eye,
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Hypervitaminosis C
Haemochromatosis Renal calculi Erosion of enamel
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Vitamin B1 - Thiamine
Anti beri-beri / anti neuritic vitamin
Sources :
Cereals, pulses, oil seeds Pork, liver, heart,kidney RDA : 1-1.5mg/day
Polishing of cereals removes 80% of thiamine
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Functions
Important coenzyme in energy metabolism
It acts as coenzyme in the production of ribose
TPP – transmission of nerve impulse
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Deficiency
Occurs where polished rice is the only staple
Beriberi (I can’t I can’t)
Weakness, nerve degeneration, irritability, poor arm/leg coordination, peripheral neuropathy, pins and needles sensation in legs.
Edema, heart failure
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Wet Beri Beri
Edema of the legs, circulatory disturbances, hypertrophic cardiomyopathy systolic murmurs and dyspnea may develop.
BP is elevated The pulse is rapid and irregular, and
the neck veins are distended
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Dry Beri Beri Edema does not occur A condition consisting of paresthesia
(prickling or burning) and numbness of the feet and cramps in the legs is present
Muscles become progressively weak
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Infantile beri beri
Caused by inadequate thiamin in the breast milk
Characterized by sleeplessness, restlessness, vomiting, convulsions, dyspnea, cyanosis and cardiac failure
Bouts of screaming that resemble abdominal colic
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Wernicke Korsakoff Syndrome Severe deficiency of thiamin in the
alcoholic individual Characterized by confusion, paralysis
of eye muscles, and loss of memory Peculiar gait and foot and wrist drop
are seen in advanced cases
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Vitamin B2 (Riboflavin)
flavin mononucleotide (FMN) flavin adenine dinucleotide (FAD)
Sources : Milk, liver, heart, and kidney Cheese Eggs Leafy green vegetables
RDA – 1.2-1.7 mg/day
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Functions
Co enzyme in Oxidation reduction reactions – energy production
Assist in the metabolism carbohydrates, protein and fats
Oxidation of most drugs (called the drug vitamin)
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Deficiency symptoms
Gastrointestinal disease that causes vomiting and hypermotility of the gastrointestinal tract
Angular stomatis Glossitis
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Niacin (Vit. B3)
Nicotinamide adenine dinucleotide (NAD) And NAD-phosphate (NADP)
can be synthesized in body (via tryptophan)
Sources : Enriched grains, ready to eat cereals Beef, chicken, turkey, fish Asparagus, peanuts
RDA – 15-20 mg/day
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Deficiency
Pellagra In people whose staple diet is corn characterized as the disease causing 4D’s
Dermatitis Diarrhea Dementia Death
Dermatitis – in sun exposed areas Dementia – anxiety,irritability, poor
memory, insomnia Glossitis and stomatitis
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Over doses
Over doses can lower LDL and TG and increase HDL
80
Pantothenic acid
Chick anti dermatitis factor Metabolic role as co enzyme A
Sources : Egg Liver Meat Milk
RDA – 5-10 mg/day
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Functions
co enzyme A – central molecule in all metabolic pathways and integrates different pathways
initiates the Krebs cycle and releases ATP
It is the starting substance for the biosynthesis of cholesterol
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Deficiency
Rare – due to wide distributed sources
Fatigue Malaise Burning foot syndrome - Burning,
prickling sensations (paresthesia) of the hands and feet, cramping of the leg muscles and impaired coordination
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Pyridoxine (Vit. B6)
Pyridoxal phosphate co enzyme
Meat, fish, poultry Enriched cereals Potatoes,cabbage Milk RDA – 2-2.2 mg/day
84
Functions
Activate enzymes needed for metabolism of CHO, fat , protein
Synthesize amino acid via transamination
Synthesize neurotransmitters – serotinin, GABA and histamine
Synthesize hemoglobin and WBC
85
Deficiency
Neurological symptoms Depression Irritability Convulsons Confusions Peripheral neuropathy Microcytic hypochromic anemia
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Drug induced B6 deficiency Isoniazid – combines with pyridoxal
phosphate and inactivates PLP dependent enzymes – leading to B6 deficiency – peripheral neuropathy
87
Biotin
Anti egg white injury factor Vitamin B7
Rats fed with large quantity of raw egg white- dermatits, neurological symptoms and growth retardation – due to egg white injury factor or avidin- reversed by biotins
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Functions
Carrier of CO2 in carboxylation reactions
Metabolism of CHO and fat Synthesis of glucose, fatty acids,
DNA Help break down certain amino acids
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liver, kidney, milk, egg yolk and yeast
RDA – 100-300 mg
Synthesised by intestinal flora, hence deficiency is rare
But can be seen in prolonged anti biotic therapy
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Dermatitis Glossitis Loss of appetite and sleep Nausea Muscular pains Hyperesthesia (increased skin sensitivity Paresthesia (burning and prickling
sensation) Alopecia
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Folic Acid (Vit. B9)
Active form is tetra hydrofolates
Sources : Liver Kidney Dark green leafy vegetables Asparagus Brocolli Soybeans and nuts
RDA – 200 ug Pregnancy and lactation 400 ug
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Functions
Amino acid and nucleic acid metabolism
maturation of blood cells Necessary for the normal functioning
of the hematopoietic system Prevent anemia, some birth defects
and heart disease
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Deficiency
Most common vitamin deficiency Pregnant and lactating women Megaloblastic anemia of pregnancy Paresthesia Angular cheilosis and gingivitis
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Neural tube defects
Spina bifida Spinal malformation Paralysis
Anencephaly No brain cortex Stillborn or die within hours
Government requires folate enrichment of flour and cereal
May prevent 50% neural tube defects
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Cobalamin (Vitamin B12 )
Anti pernicious anemia vitamin
Synthesized only by micro organisms and not by humans Contains the mineral cobalt
Animal sources and no plant sources Curd Pork Fish Liver
RDA – 3 ug/day
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Role in folate metabolism Maintenance of the myelin sheaths RBC formation
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Deficiency
Pernicious anemia – low Hb levels, decreased number of erythrocytes and neurologiclal manifestations
etiology – Destruction of intrinsic factor needed for
absorption Hereditary malabsorption Gastrectomy Insufficient gastric HCl production
(achlorhydria) Dietary deficiency as seen in pure vegetarians
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weakness, numbness and tingling in the extremities, demyelination of nerves
Patients may have difficulty in walking and coordination of movements
Patient may have a lemon-yellow complexion as a result of jaundice caused by red cell destruction, early graying of hair, fast heartbeat, ankle swelling and peripheral neuritis
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References
Textbook of Pathology By Harsh Mohan – 6th edition
Robbins Basic Pathology – by Vinay Kumar, Abul K. Abbas, Jon C. Aster - 9th edition
Biochemistry By U Satyanarayana – 4th edition
Textbook of Biochemistry for Medical Students By D M. VASUDEVAN – 7th edition
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THANK YOU