Kwashiorkor, marasmus, hypo & hypervitaminoses

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KWASHIORKOR MARASMUS

HYPO VITAMINOSIS AND HYPER VITAMINOSIS

DR.ARUN VDEPT. OF ORAL AND MAXILLOFACIAL SURGERY

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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.

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CLASSIFICATION

1.Undernutrition: Marasmus2.Overnutrition: Obesity,Hypervitaminoses3.Specific Deficiency:

Kwashiorkor,Hypovitaminoses, 4.Mineral Deficiencies5.Imbalance: Electrolyte Imbalance

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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

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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.

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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

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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.

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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

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Types of Rickets

Nutritional

Nutritional rickets results from inadequate sunlight exposure or inadequate intake of dietary vitamin D, calcium, or phosphorus

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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

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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.

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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

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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

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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

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Vegetable oils Almonds Meat Milk butter

RDA : 10 mg per day

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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

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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

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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

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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

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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

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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

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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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